Clinical & Chemical Pathology MCQs

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Clinical & Chemical Pathology MCQs Classified, Reorganized And Updated To Shawual 1425 With Short
Contents
Body fluids ................................................................................. 2
Clinical Chemistry .................................................................... 4
INSTRUMENTATION ...................................................................................................................4
BLOOD GASES, PH AND ELECTROLYTES. .............................................................................5
GLUCOSE, HEMOGLOBIN, IRON AND BILIRUBIN. ...............................................................7
CALCULATIONS, QC AND STATISTICS ..................................................................................9
CREATININE, UA, BUN AND AMMONIA ............................................................................... 10
PROTEINS, ELECTROPHORESIS AND LIPIDS ....................................................................... 11
CLINICAL ENZYMOLOGY........................................................................................................ 13
CLINICAL ENCOCRINOLOGY ................................................................................................. 14
General ..................................................................................... 17
Hematology .............................................................................. 19
BASIC HEMATOLOGY CONCEPTS / LABORATORY PROCEDURES ................................ 19
NORMOCYTIC NORMOCHROMIC ANEMIAS ....................................................................... 20
HYPOCHROMIC MICROCYTIC ANEMIAS ............................................................................. 24
MACROCYTIC NORMOCHROMIC ANEMIA ......................................................................... 25
QUALITATIVE / QUANTITATIVE WBC DISOREDERS ........................................................ 26
LYMPHOPROLIFERATIVE / MYELOPROLIFERATIVE DISORDERS ................................. 29
COAGULATION AND PLATELETS .......................................................................................... 35
Immunohematology ................................................................ 40
Immunology ............................................................................. 41
Microbiology ............................................................................ 43
ANTIBIOTICS, ANTIMICROBIALS, STERILIZATION AND DISINFECTION ..................... 43
BASIC TECHNIQUES ................................................................................................................. 44
BASIC BACTERIOLOGY............................................................................................................ 46
GRAM POSITIVE COCCI ........................................................................................................... 47
GRAM NEGATIVE COCCI ......................................................................................................... 49
GRAM POSITIVE BACILLI ........................................................................................................ 49
ENTEROBACTERECIAE & PSEUDOMONAS ......................................................................... 50
RICHETTSIAE, CHLAMYDIA AND MYCOPLASMA ............................................................. 52
SPIROCHETES ............................................................................................................................. 53
BORDETELLA & BORRELIA .................................................................................................... 53
ANEROBIC BACTERIA .............................................................................................................. 54
BRUCELLA ................................................................................................................................. 55
MYCOBACTERIA ....................................................................................................................... 55
MISCELLANEOUS ...................................................................................................................... 56
MYCOLOGY ............................................................................................................................... 57
VIROLOGY ................................................................................................................................. 60
26th Shawual 1425 .................................................................. 64
CLINICAL & CHEMICAL PATHOLOGY MCQ BODY FLUIDS

Body fluids
1.
**Doctor sending a sample requesting for lecithin spingomyelin ratio what is the sample? a. Blood. b. CSF c. Amniotic fluid. d. Urine
1.
(c) Amniotic fluid sample is used to measure lecithin: sphingomyelin ratio (L/S). L/S > 2:1 (or 2.5:1) denotes acceptable lung maturity.
2.
***Cytological examination of pleural effusion in a 60 yrs old man revealed the presence of malignant cells. The most likely primary tumor will be: a. Lymphoma. b. Mesothelioma. c. Cancer colon. d. lung cancer.
2.
(d) Lung cancer: 75% of malignant pulmonary effusions are due to 3 causes; lung cancer (30%), breast cancer (25%) & lymphoma (20%). Practically, cytological examination only establishes the presence of malignant effusion, however, in most cases it cannot identify the primary site of the tumor. Regarding mesothelioma, it is a rather a rare tumor of the pleura.
3.
*****Regarding Albustix: a. Useless if infected urine. b. Gives red color. c. Not useful if acid is added to urine. d. Depends on acid precipitation of urinary proteins
3.
(c) Commercial strips for detecting albumin (Albustix) use the following formula: Tetrabromophenol blue (yellow at 3.0) → shades of green in the presence of protein at the same pH. This reaction is sensitive to 0.03g/L albumin. A false negative result occurs with acidification of urine. Also, a markedly alkaline urine (pH or higher can give false +ve.
4.
****Which is not a reducing sugar in urine? a. Glucose. b. Galactose. c. Sucrose. d. Fructose.
4.
(c) A reducing substance is the one that reduces alkaline cupric sulfate to red coprous oxide. Most important are glucose, lactose, fructose, galactoses and pentoses (e.g. ribose, xylose and arabinose) while sucrose will not reduce alkaline cupric sulfate.
5.
***Red urine is due to? a. INH b. Rifampicin c. Pyrizinamide.
5.
b. Rifampicin is a well known drug to cause red urine.
6.
**Urine strips detect all except
6.
Fat droplets. Occur with glomerulonephritis and nephritic syndrome but are not detected by the routine urine strips.
7.
**If urine is left for long time which is affected more?
7.
Urea. The most labile constituent of urine is urea. Bacterial action decrease urea and increase ammonia and pH.
8.
**Abnormal constituent of urine includes? a. Urea b. Glucose c. Cholesterol. d. Uric acid e. Protein.
8.
(c) Although also glucose and protein are abnormal constituents of urine, yet they normally present in trace amounts below the detection limit of ordinary methods.
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9.
****Calcium in urine stone is present in all of the following except: a. UTI b. Secondary hyperparathyroidism.
9.
(b) In 2ry hyperparathyroidism, hypocalcemia due to e.g. chronic renal failure is the cause of increased parathormone. Stones due to hyperparathyroidism only occur with the 1ry or 3ry disease. Calcium is precipitated in stones with oxalate (at acid or neutral pH), or less commonly with urate (at acidic pH) or with phosphate (at normal urine pH). Causes of hypercalciurea include: - ↑intestinal calcium absorption (↑P level→↑vit D→↑Ca absorption Or in case of hypervitaminosis D. - Lack of renal tubular reabsorption e.g. with furosamide. - Loss of Ca from bone (due to mobilization as in 1ry & 3ry hyperparathyroidism, due to bone destruction or due to Cushing's and thyrotoxicosis) Otherwise, UTI causes stones at alkaline pH where ammonium is high and mixed stones form due to obstructing Ca stone which favors infection and precipitation of ammonia salts.
10.
If urine is kept for a long time: a. Becomes black. b. Urea increases. c. Urea decreases. d. Creatinine increases
10.
See 7. Urine becomes black on standing in cases of alkaptonurea (↑homogentesic acid) and methemoglobinurea.
11.
Myoglobinuria is seen in:
11.
Muscle injury (also known as rhabdomyolysis) e.g. in cases of crush injuries and strenuous exercise.
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Clinical Chemistry
INSTRUMENTATION
1.
******Difference between ELISA & RIA is ? a. ELISA technique uses an enzyme. b. ELISA is used by bacteriologists while RIA by virologists
1.
(a) Both techniques apply almost the same methodology, .ELISA technique uses an enzyme label and RIA uses radioisotopic label.
2.
The label in ELISA is? a. Enzyme b. Antibody c. Antigen.
2.
3.
***Which of the following not seen in chemistry lab? a. Analytic balance. b. Centrifuge c. Spectrophotometer d. Electron microscope, e. Turbidimeter.
3.
(d) Electron microscope.
4.
**The washing is must in all heterogenous ELISA techniques because? a. It remove the excess binding b. Increase the specificity c. Increase the sensitivity.
4.
(b) In ELISA, the first washing is used to remove the unbound (free) sample antigen. The second washing removes unreacted free label (not excess binding in either of the 2 washings) If washing is not complete, this will ↑false high → ↓ specificity. If the question comes as It avoids excess binding, then this will be the choice.
5.
**The enzyme in ELISA is present in the? a. Conjugate b. Microplate c. Buffer.
5.
(a) The conjugate is the second antibody conjugated with the enzyme.
6.
**A standard microplate in an ELISA has? a. 96 wells b. 98 wells c. 92 wells.
6.
(a) 96 wells are present in the microplate (8 rows x 12 columns).of these, 1 is used for the blank, 2 for the –ve controls, 2 for the +ve controls and 4 for the cutoff control (COC). The remaining 85 for tests.
7.
Five ml of a colored solution has an absorbance of 0.500. The absorbance of 10ml of the same colored solution will be: a. 1.000 b. 0.500 c. 0.250
7.
(b) According to Beer's law, absorbance is proportional to the final concentration (whatever the volume is)
8.
a dichromatic analysis is carried to increase: a. Specificity b. Linearity c. Sensitivity.
8.
(a) Di- (bi) chromatic photometry measures absorbance of the sample at 2 different wavelengths. This corrects for interfering substances increasing specificity of the method.
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BLOOD GASES, PH AND ELECTROLYTES.
9.
******PO2 (or gases) is measure in which unit? a. Mmol b. umol c. mmHg
9.
© mEq/L (mmol in SI) is used for electrolytes e.g. BE, bicarbonate and H+. While mmHg (or kpa in SI) is used for gases e.g. pCO2 and pO2.
11.
Acidemia is associated with
11.
Acid in urine and increased HCO2-. Increased hydrogen ion in the blood is termed academia. If the cause is metabolic, there will be compensatory hyperventilation →↓H+ back to normal while HCO3- drops. Furthermore, if renal function is normal, H+ will be excreted. If the cause is respiratory, renal compensation will cause H+ excretion and HCO3- retention and generation lowering H+ back to normal.
12.
***To correct acidosis, the kidneys: a. secrete more H+ in urine. b. Synthesis bicarbonate to ECF c. Both a and b
12.
(c). See 11.
13.
**A buffer is made of ? a. Strong acid & strong salt b. Strong acid & weak salt c. Weak acid & strong salt d. Weak acid & weak salt.
13.
(c) A buffer system is made of a weak acid and its salt with a strong base of a weak base and its salt with a strong acid.
14.
****pH means:
14.
Negative log H+ concentration
15.
***What is the base: acid ratio at pH 7 for acid of pK6? a. 0.01 b. 0.1 c. 1.0 d. 10 e. 100
15.
(d) According to Henderson Hasselbalch's equation, pH = pK + Log base/acid. By compensation, Log (base / acid)= 1, thus base: acid = 10:1.1
16.
***Which is more serious? a. Glucose 15mmol/l b. pH 7.25 acidosis. c. Potassium 1.5 mmol/l d. Sodium 150 mmol/l
16.
(c) Critical K+ values are <2.5 or > 6.5 mEq/L Critical glucose <40mg or >450mg (2.2 & 25mmol respectively), critical pH <7.2 or >2.6 critical Na+ <120 or > 160mEq/L
17.
******Metabolic acidosis can result from:
17.
(a) Ingestion of certain medicines or chemicals e.g. metformin.(glucophage). Metformin causes lactic acidosis. Generally, metabolic acidosis is due to either addition of H+ (↑AG), ↓ excretion of H+ or loss of HCO3-
18.
pH of the blood.
18.
19
Acid base balance.
19
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19. New
H+ homeostasis is altered by; a. Excessive change of pyruvate to lactate.
19. New
In actively contracting muscle, 8% of the pyruvate is utilised by the citric acid cycle and the remaining molecules are reduced to latctate. This lactate is oxidized by the liver to pyruvate which ,through gluconeogenesis, becomes glucose. If lactate is not efficiently reutilized in such a way, it accumulates in the blood causing lactic acidosis.
20,21, 22, 24, 25, 26.
***Main extracellular ions? a. Na & K b. Na & Cl **Main electrolyte in blood is? ***Electrolytes in ECF a. Na is a major cation b. Cl is a major cation d. HCO3 is a major anion. ***Main intracellular cation is; **In serum: a. Sodium is the main cation. b. Bicarbonate. ***Intracellular fluid contains: a. More potassium less sodium than extracellular fluid.. b. Sodium and potassium in equal amount.
20, 21, 22, 24, 25, 26.
b. Na is the major ECF cation, Cl is the major ECF anion, K is the major ICF cation and proteins followed by phosphates are the major anions.
23.
**All causes renal damage except
23.
Hypocalcaemia. Causes of renal damage include; hypovolemia (hemorrhage or dehydration), myoglobulinurea, hypercalciurea, uricosuria, and drugs e.g. aminoglycosides and ACE inhibitors.
27.
Renal tubular injury occurs in
27.
See 23.
28.
Hypernatremia occurs with a. Cushing disease b. Dehydration c. hypothalamic injury d. All of the above
28.
(d) Hypernatremia occurs with: * ↓body Na : due to extrarenal water loss or renal diuresis. * Normal body Na: due to extrarenal loss e.g. hyperthermia or renal loss e.g. DI. * Na retention e.g. steroids or Na intake.
28. New 1
Regarding concentration of urine; a. Proximal tubules return 75% of filtered water. b. Distal convoluted tubules deliver 40-60L of fluid to collecting tubules / day. c. Osmotic pressure in renal cortex is higher than in medulla. d. ADH acts on all parts of nephrone. e. Aldosterone increase Na excretion.
28. New1
a. Approximately 80% of the water and NaCl contenet together with glucose, phosphate, and amino acids are reabsorbed in the proximal tubule. About 20% of the tubular fluid enters the loop of Henle where water is passively aborbed; 6ml per minute of concentrated tubular fluid now enters the distal tubule, where there is an active reabsorption of sodium. The fluid leaves the distal tubule at a rate of approximately 1ml per minute passing into the collecting ducts in the form of urine. Aldosteron is relased due to ineffective arterial pressure in the kidney. It causes sodium reabsorption which raises plasma osmolality. ADH increases permeability of distal and collecting tubules to water→ urine concentration.
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28. New 2
Regarding excretion of Na+ a. Not dependent on aldosterone. b. Major share of GF osmolarity with associated ions. c. It passively diffuses in proximal tubules. d. In distal tubules it is exchanged for K+ e. Coupled with K+
28. New 2
b. Na+ excretion is influenced by mineralocorticoids (mainly aldosterone):↑ reabsorption. The GF is isoosmolar with plasma i.e. Na is the major electrolyte. 90% of Na is actively (not passively) reabsorbed in the PCT. K is excreted from DCT in exchange with Na (not the reverse and not coupled with it).
28. New 3
Regarding buffer systems; b. An acid is a substance that releases H+ c. Buffering involves change of strong acid to base.
28. New 3
b. Acids are substances that tare capable of donating protons. When a strong acid is added to a buffer, the salt reacts with the acid forming weak acid, and its salt (not base).
GLUCOSE, HEMOGLOBIN, IRON AND BILIRUBIN.
10.
Factors affecting glucose level in blood include:
10.
Adrenaline, T4. These together with cortisol, GH and glucagons are the hyperglycemic hormones causing 2ry diabetes in case of excessive secretion.
29.
**Glucose level to diagnose hypoglycemia in newborn is.
29.
- 25-30 g/dl In newborn babies, glucose tends to be lower than in adults. Critical low level in newborn is 30mg/dL
30.
***About GTT, which is correct according to WHO recommendations? a. Should not be done in pregnant women, b. Should not be done after giving heavy carbohydrate diet for 3 days. c. Should be done after 4-6 hrs fasting.
30.
(c) WHO recommendations for GTT include:
31.
**With age renal threshold for glucose? a. Increased b. Decreased c. Not changed
31.
(b) With age, the renal ability to reabsorb filtered glucose is decreased leading to appearance of glucose in the urine at lower plasma levels.
32.
**All are inborn error of glycogen metabolism except? a. Essential fructosuria b. Phenyl ketonuria c. Galactosemia d. Glycogen storage disease
32.
(b) Essential fructosuria is due to aldolase B defect leading to accumulation of fructose-1-P Galactosemia (serious) is due to decreased Galactose-6-P uridyl transferase leading to decreased glycogen synthesis. Types of glycogen storage diseases (GSD) include: Type I (VonGierke's): ↓ G6P Type II (Pompe's): ↓ lysosomal maltase Type III (Cori's) : ↓debranching enzyme. Type IV (Anderson's): Absent debranching enzyme Type V (McArdle's): ↓ muscles phosphorylation.
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33.
*****HBA1c (Glycosylated hemoglobin) is? a. Not present in healthy normal individuals. b. ↑ in prolonged sustained hyperglycemia
33.
(b) GlycHb (RR 4-6%) is formed by non enzymatic attachment of glucose to N-terminal valine of B-chain of Hb. Three types occur, HbA1a, HbA1b, HbA1c, Both total and HbA1a are used. Time averaged blood glucose = GlycHbx33.3-86 (mg/dL) GlycHb reflects 8-12 weeks of blood glucose while fructosamine reflects 2-4 weeks.
34.
***Glycogen differs from starch in:
34.
It is a highly branched structure
35.
**Cellulose is not metabolized in humans because of absence of which enzyme?
35.
Glucose units in cellulose are combined by cellobiose bridges. These are hydrolyzed by cellobiase which is lacking in animal and human gut.
36.
**Xylose test is done to detect the function of: a. Stomach. b. Pancreas. c. Upper small intestine. d. Lower small intestine. e. Large intestine
36.
c. Xylose is absorbed from proximal small intestine independent on pancreas..
37.
****Von Gerke's disease is caused by deficiency of: a. Glucose 6 phosphatase b. Glucose 6 phosphate dehydrogenase
37.
(a) See 32.
38.
What happens if sucrose is given parentrally:
38.
It will be secreted unchanged or metabolized
39.
***Which of these is not a ketone body? a. Acetone. b. Acetoacetic acid. c. Butyric acid. d. B-hydroxy butyric acid. e. None of the above.
39.
(c) Ketone bodies are formed by condensation of 2 acetyl Co A → Acetoacetic acid which gives B hydroxyl butyric acid by reduction or acetone by decarboxylation. Butyric acid is a fatty acid
40.
***In Gaucher's disease; a. Glycoprotein is accumulated. b. Glucocerebrosidase is deficient.
40.
(b) Gaucher's is a glucosylceramide lipidosis (lysosomal storage disease). It is caused by ↓ glucocerebrosidase enzyme leading to accumulation of glucosylceramide → HSM and pigmentation of exposed parts.
41.
Bile duct obstruction can be diagnosed by: a. AST b. T. Bilirubin c. Bilirubin in urine d. Ester bilirubin
41.
(c) Cholestatic hyperbilirubinemia is characterized by conjugated hyperbilirubinemia and hyperbilirubinuria (only the conjugated fraction appears in urine).
42.
*** Increased jaundice is diagnosis by a. T. bilirubin b. AST c. ALT d. ALP
42.
(a) Estimation of jaundice depends on serum bilirubin, other mentioned tests help to identify the cause of jaundice.
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CALCULATIONS, QC AND STATISTICS
43.
**Most of the concentration are calculated using factor, this factor is? a. Std absorbance / std value b. Std value / std absorbance c. Std value x std absorbance
43.
(b) For methods obeying Beer's law, slope of the calibration curve (Cs/As) provides a constant to calculate the unknown concentration. Also depending on the formula: At x Cs = As x Ct, thus, Ct=(Cs/As)x As
44.
**Ten microliters are? a. 0.01 L b., 0.001 L c. 0.0001 L d. 0.00001 L e. non of these.
44.
(d) μL = 10-6L → 10 μL = 10-5L = 0.00001L
45.
**How much water should be added to 500ml of a solution of 10% NaOH to bring it to 75%? a. 666ml b. 125ml c. 166ml d. 250ml e. 375ml
45.
(c) Using the formula: C1 x V1 = C2 x V2 10 x 500 = 7.5 x V2 V2 = 666mL Thus, 166 mL of DW should be added.
46.
When calculated osmolarity can not be accounted as a measurement for osmolarity? a. per 100gm/l b. Urea 20 mm/l
46.
Calculated osmolarity = 2 X Na + Glu + Urea (All in mmol/L) When calculated osmolarity is less than measurement for osmolarity, this denotes increased osmolar gap (OG). This occurs with:
- Factitious hyponatremia (due to decreased water)
- Unmeasured osmotically active compounds e.g. alcohols, sugars, and ketones.
47.
**Calibrator sera are? a. Primary std b. Secondary std c. Tertiary std d. Internal std.
47.
(b) Secondary std? A primary Std is a reference standard. Secondary Std is standardized depending on the primary standard.
48.
**External QC program means? a. An external person come & does the QC test b. A QC person goes to another lab & does the test..
48.
(b) In EQC, participants receive QC material to be tested inside their labs. Results are sent to supplier to be compared to other labs' results. EQC will be most practically implemented during the regular visit of the lab coordinator. This will give opportunity for errors to be investigated on site and corrected rapidly (Monica)
49.
**We select 2SD value to plot LJ curves because? a. They are easy to calculate, b. They cover 97.5% of normal population, c. Patient value rarely go beyond these limits.
49.
(c) QC results follow a Gaussian distribution, thus 95% of these results normally fall within ±5% of the mean. Therefore, 2.5 out of 100 (1:40) are acceptable to be above +2s and 2.5 our of 100 are acceptable below -2s.
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50.
Sensitivity and specificity are a. Directly related. b. Inversely related. c. They mean the same.
50.
(b) Sensitivity & specificity can be adjusted according to cutoff level. Sensitivity can be increased by choosing a higher cutoff to include more TP, this meanwhile will include more FP thus ↓specificity. However, this is not always the case as highly specific highly sensitive tests as well as poorly specific poorly sensitive exist.
51.
A carryover in chemistry analyzer means a disturbance in readings because: a. The analyzer was carried and placed at a different place. b. The previously measured solution was still in the cuvette c. The current solution is overflowing in the cuvette.
51.
(b) Carryover is due to contamination by a previous sample. It is calculated by measuring a high standard and a low standard each 3 times then applying the following formula: Carry over = (contaminated low – actual low) / contaminated high – actual high)
52.
STAT test means: a. Start at. b. Standardize and test. c. Short turn around time
52.
(c) Stat refers to immediate or as initial dose.
CREATININE, UA, BUN AND AMMONIA
53.
***Which of the following result shows renal impairment? a. urea 9 mmol b. creatinine 10 mmol/l c. urates d. cholesterol e. urine osmolarity less than 800 after 12 hrs of water deprivation.
53.
(e) A urine osmolarity less than 800 after 12 hrs of water deprivation denotes renal impairment. Urea 9mmol is high normal (n: 2.9-8.2) and is not a very sensitive measure of GFR. Creatinine, although a sensitive measure of GF, 10umol is normal (n: 53-106) Cholesterol and urates are useless in this regard.
54.
**Low GFR occurs in all except: a. Congestive heart failure. b. Urethral obstruction.
54.
(b) low GFR occurs with: - Hemorrhage. - Dehydration. - Renal loss of fluids e.g. diuretics. - Ineffective blood volume, e.g. ↓CO, systemic VD, renal vasoconstriction.
55.
Diagnosis of RF
55.
GFR is an index and a monitor of increased or decreased renal functions. It is practically estimated from serum creatinine and creatinine clearance.
56.
****Nephrotic syndrome is characterized by all except: a. Hypocholesterolemia. b. Hypoalbuminemia. c. Albuminuria. d. Hypertriglyceridemia. e. None of the above
56.
(a) Nephrotic syndrome consists of: - Heavy proteinuria. - Hypoalbuminemia. - Oedema. - Hypercholesterolemia (Almost always present). Hypertriglyceridemia is present in 50% of cases.
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57.
****Ureate excretion by the kidney is inhibited by: a. Probenecid. b. Thiazide diuretics.
57.
(b) Thiazide diuretics cause relatively urate retention, glucose intolerance and hypokalemia and interfere with water excretion and may cause hyponatremia. Probenecid is a uricosuric agent like allopurinol.
58.
Chronic glomerulonephritis is diagnosed by: a. Blood urea. b. Creatinine. c. Proteinuria d. All of the above
58.
(d) In chronic glomerulonephritis, there is persistent deterioration of renal functions ending with renal failure.
PROTEINS, ELECTROPHORESIS AND LIPIDS
59.
**The protein having molecular wt less then albumin is? a. Beta protein b. B2-microglobulin. c. Lysozyme. d. Benze Jones protein.
59.
(b) B2-microglobulin has a MW 11,800. Betalipoprotein is 380,000. BJ protein is the light chains of immunoglobulins. It's MW is variable from 11,000 for monomers, 22,0000 for dimmers or tetramers. Lysozyme is 14,000. It is used to differentiate AML M4 and M5 and appears as a far cathodal band on serum or urine EP.
60.
******In cystic fibrosis, which is deficient? a. Beta globulin b. Macroglobulin c. Albumin d. Alpha 1 antitrypsin e. Alpha 2 antitrypsin.
60.
(d) Alpha 1 antitrypsin
61.
***Diet rich in phenylalanine should be restricted in? a. Phenyl ketonuria b. Tyrosinemia c. Maple syrup disease
61.
(a) In phenylketonuria, there is ↓ phenylalanine hydroxylase leading to accumulation of phenylpuruvate and its derivatives and their excretion in urine. Diet rich in phenylalanine should be restricted to prevent brain damage.
62.
***In phenylketonuria, diet should be low in: a. Phenylalanine. b. Carbohydrate. c. Lipids.
62.
(a) Phenylalanine (see 61)
62.
Hypoalbuminemia is associated with all except? a. Tetanus b. hypocalcaemia c. oedema d. toxic effect of sulfonamide
62.
(a) Tetanus is clostridial infection caused be C. tetani has nothing to do with albumin.
64.
**Gluconic amino acids include: a. Alanine. b. Methionine. c. Valine. d. Glutamic acid. e. All of the above.
64.
(a) Ketogenic amino acids are: Leucine and lysine, Mixed amino acids are: Isoleucine, phenylalanine, threonine, tryptophan and tyrosine. Gluconic amino acids are all the other amino acids.
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65.
**Lipoprotein related to hypertension?
65.
. LDL
66.
*****Which is important for atherosclerosis? a. ↑HDL b. ↑LDL c. ↑Chylomicrons.
66.
(b)
67.
***In plasma protein electrophoresis, the protein that will go first is (moves furthest from application)?
67.
Albumin.
68.
***Based on behavior of lipoproteins in ultracentrifugation pre-B lipoprotein is? a. HDL b. LDL. c. VLDL d. Chylomicron
68.
On electrophoresis; Chylomicrons and its remnants stay at the origin. VLDL at preβ (=α2 globulin region) IDL at broad β LDL at β (= β globulin region) HDL at α (= α1 globulin region)/
69.
**All of the following are lipoproteins except? a. Phospholipid b. VLDL d. Sphingomylin e. LDL f. HDL
69.
(d) Although phospholipids are not lipoproteins, they are ingredients of lipoproteins, conferring the hydrophilic properties.
70.
What is the proposition of pulmonary surfactant? a. Phospholipid acid b. Dipalmityl lecithin c. Phosphatidyl choline,
70.
(b) Dipalmityl lecithin (a lecithin phospholipid with 2 palmetic acid residues) is the chemical composition of pulmonary surfactant.
71.
**HDL is good cholesterol because? a. It has more protein & phospholipids in it b. It has no cholesterol in it,. c. It has less TG in it.
71.
(a) HDL is composed of 20% cholesterol, 30% phospholipids and 50% proteins.
72.
***Which lipoprotein has highest concentration of cholesterol? a. VLDL b. LDL c. IDL d. HDL
72.
(b) VLDL are the TG rich lipoproteins HDL has 20% cholesterol. IDL has cholesterol and TG in equal amounts. LDL is the richest lipoprotein in cholesterol esters.
74.
****Which is not associated with abetalipoproteinemia: a. Acanthocytes in the peripheral blood. b. Hereditary spherocytosis. c. Malabsorption and fatty stools
74.
(b) Hereditary spherocytosis is due to spectrin deficiency. Abetalipoproteinemia is a lipoprotein abnormality of absent LDL due to autosomal recessive abnormality in the synthesis of apoB + failure of chylomicron formation leading to malabsorption of fats + fat soluble vitamins + adrenal dysfunction. 50-70% of RBCs have spinal projections (acanthocytes)
75.
Chylomicrons: a. Can cause thrombosis. b. Cannot cause thrombosis.
75.
(a) Chylomicrons don't confer an excess cardiovascular risk, however, in LpL deficiency and apoC II deficiency, the patient presents with lipemia retinalis and retinal vein thrombosis.
CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY
mohammad_emam@hotmail.com 13
76.
Nature of apoproteins.
76.
5 major classes of proteins A to E
77.
Saturated vs unsaturated fats (nutritional value)
77.
Saturated
Unsaturated
e.g.
Oleic a (50% of body fat) Palmitic a (25% of body fat) Stearic a (5% of body fat) Acetic a. Butyric a.
Linoleic a Linolenic a (both are Essential) Arachidonic a.
Presence
Adipose
Vegitable oils.
Suffix
Anoic
Enoic
Significance
Arachidonic acid is precursor of Pgs. Although not essential, it depends on essential FA
Chemistry
No double bonds
Double bonds
78.
Which is best for parentral alimentation? a. FFA. b. AA c. lipoproteins
78. 79.
(b) Parentral nutrition is composed essentially of: a) Nitrogen source: synthetic valuable amino acids (9-17g/L N2) b) Energy source: Glucose (mainly) and fat emulsion (additional source to avoid EFA deficiency). c) Electrolytes and trace elements.
79.
Protocol for IV nutrition?
80.
**Regarding lipoprotein metabolism:
80.
Although cholesterol can be synthesized by all nucleated cells, however, cholesterol in VLDL, IDL and LDL is of hepatic origin
82.
Treatment of familial hypercholesterolemia.
82.
These include general management of hypercholesterolemia + cholesterol lowering drugs + oestrogen replacement in postmenopausal women.
CLINICAL ENZYMOLOGY
83.
***The better for diagnosis of acute pancreatitis is? a. Amylase b. Lipase c. ALP d. ACP
83.
(b) Lipase elevation is of a greater magnitude (2-10 xN) and duration than amylase in acute pancreatitis. When lipase method is optimized, the test is more sensitive and specific than amylase for detection of acute pancreatitis.
84.
**Activities of some enzyme increased in some disease conditions because they are? a. Non functional enzymes b. Functional enzymes c. Neither
84.
(b) That’s why enzymes are measured for the most part by their activity rather than concentration.
CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY
mohammad_emam@hotmail.com 14
85.
***In MI, which is the last enzyme to be raised and lasts long? a. CK b. CK-MB. c. AST. d. LDH
85.
(d)
Onset (h)
Peak (h)
Duration (d)
CK
6-12
20-30
2-6
CK-MB
3-10
12-24
1.5-3
AST
6-12
20-30
2-6
LDH
6-12
24-72
7-14
86.
**Isoenzymes:
a. Are physical types of one enzyme.
b. Have different electrophoretic mobility.
c. All of the above
86.
© Isoenzymes have the same catalytic activities and differ in physicochemical properties.
87.
**MI is diagnosed by: a. CKMB b. CKBB c. CKMM d. LDH
87.
(a) CK-MB is specific for cardiac muscle, CK-BB for brain and CK-MM for skeletal muscle.
88.
**Elevation of LDH is caused by: a. Myocardial disease b. Liver disease c. Prostatic disease d. many organ disease because it has many distribution
88.
(d) LDH is present in the cells of the heart, liver, muscles, blood and malignancies.
89.
****Myoglobin ↑ in injury of: a. muscle. b. Liver
89.
(a) muscle whether cardiac or skeletal is the source of myoglobin.
CLINICAL ENCOCRINOLOGY
90.
*****ADH is? a. Produced by posterior pituitary b. Produced in the hypothalamus.
90.
(b) ADH is produced by the hypothalamus and stored and secreted from the posterior pituitary.
91.
**The method used to estimating insulin is? a. Electrophoresis b. Kinetic estimation. c. Spectrophotometer. d. Radioimmuno assay.
91.
(d) Immunoassay (multiple labels) is used for the measurement of insulin.
92.
*****After the insulin dose, the patient soon comatozed due to a. Hyperglycemia b. Hypoglycemia (glucose <3mmol/l) c. ketonuria c. Ketoacidosis is the cause of coma d. Lactic acidosis,
92.
(b) Hypoglycemia (glucose <3mmol/l)
CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY
mohammad_emam@hotmail.com 15
93.
**While using the pregnancy test we are measuring? a. B-HCG b. Total HCG c. B-HCG & LH d. B-HCG & FSH.
93.
(b) α subunit of HCG is very similar to α subunit of TSH and FSH and identical to LH. Although β subunits of HCG and LH are very similar, antibodies can be made to the β subunit of HCG that do not cross react with LH or other pituitary hormones. Most EIA use 2 monoclonal antibodies against different sites of HCG molecule one for carboxyl terminal of β chain and the other to the α chain, i.e. react with intact HCG.
94.
****Water deprivation test is used in the diagnosis of: a. Anterior pituitary disease. b. Posterior pituitary disease. c. Hypothyroidism.
94.
(b) Water intake is restricted the patient loses 3-5% of body weight or until 3 consecutive hourly determination of urine osmolarity are within 10% of each other. Measure urine osmolality, plasma vasopressin and increased urine osmolality with exogenous vasopressin.
Urine osmol
Pl. VP
After VP
Normal
>800
>2
↑
DI
<300
Undetectable
↑
Nephrogenic DI
<300
>5
No change
95.
****24 hours urine for VMA is used for diagnosis of diseases of: a. Adrenal cortex. b. Adrenal medulla
95.
(b) Catecholamines are oxidized to VMA and metanephrins. 24hour urinary metanephrins is the best single test for pheochromocytoma. Specificity and sensitivity approach 100% when both VMA and metanephrines are measured.
96.
***Hypertension is found in all of the following endocrinal diseases except: a. Cushing's syndrome. b. Pheochromocytoma. c. Adrenal medulla hyperplasia. d. Addisson's disease.
96.
(d) Hypertension secondary to endocrinal causes occurs in: - Pheochromocytoma. - Crohn's syndrome - Cushing's syndrome. Addison is associated with hypos (hypotension, hypokalemia, hyponatremia and hypocortisol)
97.
Diabetic coma presents with: a. Ketone bodies in urine b. Blood glucose may be 1000mg or more c. osmotic diuresis present
97.
All. In diabetes, 2 types of coma may occur, DKA and nonDKA. Glucose levels in nonDKA are typically <800 mg/dL. Once hyperglycemia is established, ketonurea & pH should be looked for to differentiate.
98.
**While anti-PSA is coated on to the well in total PSA estimation, the antibodies coated in free PSA is? a. The same antibodies that is coated for total PSA b. Same antibodies in large amount c. Same antibodies in very low amount d. Different antibodies.
98.
(a) different antibodies.
CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY
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98. New
Carcinoid tumors secrete
98. New
5HIAA. Carcinoid tumors originate from the enterocromaffin cells (APUD cells) of the intestine and most commonly occurs in the appendix, terminal ilium and rectum. Presentation may be asymptomatic until metastasis (most cases), appendicitis (10%) or carcinoid syndrome (in5% when there is liver metastasis) as spontaneous flushing on the face and neck, abdominal pain and water diarrhea, cardiac abnormalities and hepatomegally. The tumor secretes a wide variety of amines an peptides including serotonin (5-hydroxytryptamine (5-HT) with its major metabolite 5-hydroxyindoleacetic acid (5-HIAA)), bradykinin, histamine and tachykinins and prostaglandins.
 Neeman Peck disease is due to deficiency of sphengomylinase
 Cholesterol: In LDL, cell membrane, precursor of bile salts and steroid hormones.
CLINICAL & CHEMICAL PATHOLOGY MCQ General
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General
1.
****The difference between plasma and serum is that plasma: a. Contains fibrinogen. b. Doesn’t contain fibrinogen. c. Has more water. d. Has less water.
1.
(a) Plasma contains fibrinogen which is consumed during the clot formation to separate serum.
2.
******Best way to separate the serum? a. leave the blood to clot at R.T for I hr, then centrifuge b. by adding citrate. c. by adding EDTA
2.
(a) leave the blood to clot at R.T for I hr, then centrifuge
3.
**Point of care testing means? a. Complete a test & make a point[interpret], b. Testing the patient at bed side c. Take care in testing
3.
(c) Take care in testing
4.
****Error in the result is expected in which case? a. Glucose on fluoride. b. Glucose on EDTA c. Calcium on oxalate
4.
(c) Oxalate is a divalent cation chelator.
5.
**Cardiac anatomical anomalies associated with Fallot tetralogy include all of the following except: a. VSD b. ASD
5.
(b) Fallot's tetralogy is composed of PS+VSD + Rt aorta + RVH.
6.
Hemolysed blood is unsuitable for performing which tests?
6.
Hemolysis is visible at Hb> 3.1 μmol/L It increases LDH, K, ACP, cholesterol, ALT and AST. Hemolysis don’t increase serum albumin, bilirubin, ALP, amylase, lipase, Ca, Cl, P, Mg, Na, creatinine, glucose, UA or urea.
7.
****Hemolysis causes? a. Increased serum K b. Increased serum Na c. Increased HCO3- d. Decreased K
7.
a.
8.
After hemolysis: a. Sodium leaks out of RBCs. b. K leaks into cells. c. Bicarbonate gets into RBCs.
8.
9.
Effects of fasting
9.
Prolonged fasting increase TG, glycerol, FFA but not cholesterol.
10.
****Fluoride is used to get samples for? a. Blood sugar b. Coagulation c. Electrolyte d. CBC.
10.
a. Blood sugar
CLINICAL & CHEMICAL PATHOLOGY MCQ General
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11.
***Anticoagulant used for glucose is:
11.
Fluoride
12.
**Changes in blood stored more than 5 hrs at room temp. include? a. Decreased glucose & increased lactate. b. Increased glucose & decreased lactate c. Failure of Na & K pump,
13.
(a) Storage of blood has the following effects: 1- ↓CO2, ACP & Glucose 2- ↑pH & ammonia 3- Changes in RBC permeability →↑K,P &Mg 4- Na-K pump is inhibited at 4 °c but not at 25°c. leading to ↑K in refrigerated samples. 5- Phosphorylation→↑P released from organic P. 6- Loss of enzyme activity. 7- Light→↓ bilirubin, δALA and porphyrins.
14.
Plasma or serum should be separated at the earliest for the estimation of glucose because: a. The glucose values decreases with time. b. Glucose value increases with time. c. Lysis of blood occurs.
14.
a. Continued glycolysis cause glucose values to decreases with time unless cells are separated.
 Best place to put a needle for blood collection is puncture proof container.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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Hematology
BASIC HEMATOLOGY CONCEPTS / LABORATORY PROCEDURES
1
** To stain the B/M other than Wright stain which stain usually used? a. PAS stain b. Sudan black stain c. stain for iron.
1
(c) Bone marrow films should be stained with an iron stain e.g. Perl's, Prussian blue, as a routine to demonstrate iron (Dacie)
2
***In addition to routine Romanowsky stain of bone marrow the following stain is also essential: a. Chloroacetate estrase b. Prussian blue.
2
(b).Prussian blue: See 1
3
The needle used for bone marrow biopsy is? a. 18 gauge needle b. Jamshedi needle c. Menghini needle d. Westermani needle,
3
(b) Jamshedi trephine is used for biopsy.
4
**Hyperplastic B.M with M/E ratio 6:1 is seen in: a. Megaloblastic hyperplasia. b. Normoblastic hyperplasia c. Lymphoid hyperplasia
4
(c) Hyperplasia is diagnosed when fat>cells. In hyperplastic BM, an M/E ratio > 2:1 denotes myeloid hyperplasia and <2:1 denotes erythroid hyperplasia.
5
**Best method to assess BM cellularity is: a. Trephine biopsy b. M:E ratio is enough. c. By high power.
5
(a) Trephine biopsy is preferred over bone marrow aspiration in that it demonstrates the architecture of the bone marrow cellularity.
6
***Which Hbs have the same electrophoretic mobility on alkaline cellulose acetate?
6
HbS, C, D and Hb Punjab (also Hb lepore) occur at the same position on cellulose acetate at pH8.6 . Also Hb C, E and C harlum occur at the position of Hb A2
7
Lymphokines & T-cell activation
7
Lymphocytosis promoting factor and histamine sensitizing factor.
8
******When using and electronic cell coulter counter, which of the following results can occur in the presence of cold agglutinins: a. ↑MCV & ↓MCHC b. ↓MCV & ↓MCHC c. ↓MCV & ↑MCHC d. ↑MCV & ↑MCHC e. ↑MCV & decreased RBC f. ↑MCV & normal RBC h. ↓MCV and RBC
8
(d) A high titer of cold agglutinin cause falsely ↑MCV, MCH and MCHC and falsely ↓ RBC count. To correct, incubate at 37°c for 15-30 minutes and rerun the specimen.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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9
***Bone marrow aspiration needles: a. 18 gauge. b. Meninghi. c. Burtolin
9
a. 18 gauge.
10
**RDW is increased in
10
Iron deficiency anemia and megaloblastic anemia while normal in thalassemia.
11
**By coulter, TLC= 22.5x109/L If NRBC are 200 per 100 leucocytes, so corrected leucocytic count equals: a. 11.5 x 109/L b. 22.3 x 109/L c. 22.7 x 109/L d. 7.5 x 109/L
11
(d) using the correction formula : Corrected WBC= WBC X 100 / (NRBC+100) Corrected WBC= 22.5 X 100 / (200 + 100 ) = 7.5 x 109/L
12
****The main antioxidant in RBCs is: a. NADPH b. Reduced glutathione
12
b. Reduced glutathione acts as antioxidant through its SH group.
13
***Newborn with MCV 100fl, is considered. a. Macrocytosis. b. Normal
13
b. MCV in the first week is normally 108fl. After 2 months, it is 96fl.
14
**Perl's stain
14
BM iron stores
14. New
Hemoglobin breakdown takes place in: a. RES b. Hepatocytes. c. Renal tubules.
14. New
a. Normally 6gm of Hb is broken down per day into;
- Globin peptides: hydrolysed and the amino acids enter into the body amino acid pool.
- Iron: reutilized.
- Porphyrin ring: broken down in the reticuloendothelial cells of the liver, spleen and bone marrow to bile pigments.
NORMOCYTIC NORMOCHROMIC ANEMIAS
15
***In Pyruvate Kinase deficiency all correct except? a. Intermittent attach of anemia. b. Splenectomy is a choice of treatment. c. Autosomal recessive.
15
(a) PKA is an autosomal recessive enzymopathy. O2 dissociation curve is shifted to the right, so only mild symptoms occur. Splenectomy improves the condition.
16
**In A sickle cell disease patient under general anesthesia, all true except?
16
Tourniquet should not be avoided. A sickle cell patient needs transfusion to reduce HbS below 30% prior to general anesthesia. During anesthesia, the patient should be hyperoxygenated and rapidly induced. Limb tourniquet should be avoided.
17
**Organism causing osteomylitis in sickle cell patient is
17
Salmonella. In sickle syndrome, infarctions in the spleen leads to autosplenectomy causing more predisposition to pneumococcal infections. Infarctions in the intestine leads to passage of salmonella which infect the bones causing osteomyelitis.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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18
**Skeletal abnormality present in?
18
Fanconi syndrome. Fanconi syndrome consists of:
- Congenital aplastic anemia.
- Skeletal and urinary tract anomalies.
- Microcephaly.
- Altered skin pigmentation.
19
Fanconi's anemia
19
20
***In G6PD decreased which is affected ?
20
NADP-H, reduced glutathione Being the first enzyme in HMP shunt which generates NADPH to maintain reduced glutathione, G6PD deficiency affects NADPH and reduced glutathione
21
**Sideroblastic.a seen in all except? a. Lead poisoning b. Alcohol c. Aspirin d. Chloramphenicol
21
(c) Sideroblastosis occurs due to; - Lead poisoning due to inhibition of enzyme of heme and globin synthesis. - Alcoholism, due to interference with heme and pyridoxal kinase. - Chloramphenicol; inhibits protoporphyrin. - Other causes: ↓vit B6, thalassemia, excessive dietary Fe, anti-TB and cycloserine.
22
****The least drug to cause acquired sideroblastic anemia is: a. Aspirin. b. Lead.
22
a. Aspirin.
23
**In HUS, all are true except: a. occurs mainly in children. b. Is usually preceded by some sort of enteritis. c. Fragmented RBCs are seen. d. Uremia is usual. e. Anti IgG is positive in 10% of cases.
23
(e) HUS occurs in children following VTEC enteritis (also after salmonella, shigella, streptococcal infection, as an autoimmune disease and following drugs e.g. cycloserine. It is charectarized by: - Thrombosis in small vessels. - Fragmentation of RBCs. - Reduced platelets (consumptive). - Uremia.
24
In HUS, all are present except: a. ARF b. ↓ platelets. c. Microangiopathic HA d. Thrombocytosis
24
d. Thrombocytosis
25
HUS
25
26
**In intravascular hemolysis, all are present except:
26
Normal haptoglobin. In intravascular hemolysis serum haptoglobin is decreased or absent due to consumption.
27
***Free plasma Hb is bound to:
27
Haptoglobin (also hemopexin)
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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28
**In favism, the defect is in
28
G6PD. In favism, hemolytic anemia develops whtn the RBCs are exposed to oxidant stress e.g. drugs, infection and favism.
29
**In hereditary spherocytosis all are true except: a. Autosomal dominant. b. Treated by splenectomy. c. Defect is in hemoglobinization of RBCs
29
c. Hereditary spherocytosis is an autosomal dominant membrane defect (anykrin) not due to a defect is in hemoglobinization of RBCs. Parts of the defective membrane is removed by the spleen leading to reduced cell surface and causing spherocytic cells. Splenectomy improves the condition.
30
***Treatment of choice of spherocytosis is:
30
Splenectomy
31
**In sickle cell anemia patient with iron overload, this organism is isolated from blood: a. Salmonella. b. Strept pneumoniae c. yersinia enterocolitica.
31
(c) Yersina enterocolitica occurs in iron overloaded patients treated with desferrioxamine (see p376 Kumar)
32
***Thalassemia major with iron overload this organism can be isolated. a. Streptococcus pneumoniae. b. Salmonella typhemureum c. Yersina enterocolitica.
32
(c).
33
*****Microangiopathic hemolytic anemia is present in all except: a. TTP b. Meningococcal septicaemia. c. HUS
33
(b) In MAHA there is intravascular hemolysis and fragmentation of the RBCs due to abnormal microcirculation leading to fibrin deposition, platelet deposition and vasculitis e.g in; - HUS - TTP - Renal pathology - Preeclampsia - Autoimmune diseases e.g PAN, SLE. - Carcinomatosis. - Septicemia Meningococcal septicaemia.cause thrombosis of small blood vessels leading to petichiae and adrenal failure (Waterhouse-Fridrechson syndrome)
34
****The following enzyme increases in hemolytic anemia: a. Total ACP b. LDH c. ALP
34
(b) LD1&2 are characteristically increased in HA. ACP although is present in high concentration inside RBCs (tartarate resistant) is not characteristically increased.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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35
****In G6PD deficiency avoid all the following drugs except: a. Salicylic acid b. Primaquine. c. Dapsone. d. Trimethoprim. e. Folic acid
35
(e) Agents causing HA in G6PD deficiency include: - Antimalareals e.g. primaquine. - Sulphonamides and Sulphones (dapsone). - Analgesics e.g. salicylic acid - Antihelmenthics e.g. niridazol. - Miscellaneous e.g. vitamin K analogues, probanecid.
36
***A patient with hemolytic anemia has all the following exept: a. Bilirubinemia. b. Dark urine. c. Hypertension.
36
(c) In hemolytic anemia there is; - Hyperbilirubinemia and hemiglubinuria. - ↑urobilinogen and stercobilinogen→ dark urine. - ↓ Haptoglin and hemopexin. - Hemosiderinemia and hemosiderinuria. - Methemoglobenemia.
37
****Aplastic anemia cause
37
pancytopenia.
38
RAEB
38
Myelodysplastic syndromes (MDS) are classified into:
Peripheral blood
BM
Refractory anemia
<1%blasts
<5%blasts
RA with sideroblasts
<1%blasts
<5%blasts
RA with excess blasts (RAEB)
>5%
20-30%
CMML
↑monocytes
↑promonocytes
39
**Manifestations of HbSS a. Ischemia to femoral artery. b. Infarction of phalanges.
39
(b) Infarction of phalanges.
41
****Major adult Hb is
41
HbA (97%) HbA2 (2.5%) and HbF (0.5%)
41. New
Which is true regarding DAT a. It is positive in all IHA. b. may detect complement attached to RBCs.
b. DAT involves testing patient's cells without prior exposure to antibody in vitro. For investigation of AIHA, antiglobulin reagents specific for IgG, IgM and IgA are available. Monoclonal antibodies specific for the complement C3d is also available. 2-6% of AIHA are DAT- negative. This may be due to nature of antibody or its presence in below detection levels. In such patients diagnosis depends on careful screening of a concentrated ether eluate made from the patient's RBCs or by manual polybrene test or by more complex techniques e.g. RIA, complement fixing antibody consumption (CFAC) test and ELISA and enzyme linked antiglobulin test (ELAT). A positive DAT does not necessarily mean that the patient has AIHA. Causes of positive DAT include; 1. An auto-antibody on the red cell surface with or without hemolytic anemia.
2. An allo-antibody on the red cell surface, e.g.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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in HDN or after incompatible transfusion. 3. Antibodies against drugs or against normal globulins damaged by drugs adsorbed on RBCs e.g. cephalothin. 4. Interaction between the antiglobulin sera and anti-T, as with polyagglutinable RBCs. 6. Anti-albumin and anti-transferrin antibodies in antiglobulin sera giving rise to false-positive reaction. 7. adsorption of immune complexes to the cell surface in 8% of hospital patients in a wide variety of disorders. 8. Sensitization in vitro (due to incomplete cold antibodies and complement from normal serum obtained by clotting or defibrination (not EDTA or CDA).. 9. In apparently perfectly healthy individuals for unknown reason.
HYPOCHROMIC MICROCYTIC ANEMIAS
42
***A case of iron deficiency under Microscope is
42
hypochromic, microcytic
43
**Iron deficiency anemia seen in all except? ***Iron stores are deficient in all except: a. B-thalassemia major b. chronic disease,
43
d. B-thalassemia major
44
**Hb variant with fusion of delta and beta gene segments is:
44
Hb Lepore is the result of fusion of β & δ chains which combine with α chain (β δ2,α2) Other abnormal patterns include HbH (β4) and HbSS (Bs, Bs)
45
**Normal Hb pattern?
45
HBA ( α2, β2) Other Hb patterns: HbA2 (α2, δ2), HbF (α2,γ2)
46
****In iron deficiency anemia, all are present except: a. ↑ iron absorption. b. Microcytis hypochromic blood film,
46
None or choose something appropriate. Iron absorption is adjusted to body needs. It is increased in iron deficiency anemia and pregnancy.
47
****Regarding iron
47
60-70 % of body iron is present in Hb. 15-30 % in bone marrow, 1% in transferring and 4% in myoglobulin.
48
Iron status in anemia of chronic disease.
48
In ACD there is:
- ↓serum iron and TIBC.
- Normal ferritin and bone marrow iron.
49
**Iron deficiency anemia cause, except
49
Thrombocytopenia. Actually there is raised platelet count in IDA
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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50
**Anemia of chronic diseases includes: a. Vit B12.deficiency. b. Pernicious anemia c. Increased secretion of erythropoitic factors. d. All of the above. e. None of the above.
50
e. None of the above.
Regarding erythropoietic factors, in ACD there is increased secretion of TNF and IL-1 reduce Epo production.
51
***Hb H disease.
51
Choose Alpha thalassemia, or none HbH = β4 and occurs when 4α genes are deleted in α thalassemia.
51. New
In β-Thalassemia, which is true? a. It presents with severe anemia at the age of 6 months. b. Blood transfustion may be required as frequent as every 9-12 months.
a. In β thalassemia major, anemia presents at the age of 3-6 months when the switch from γ to β chain synthesis normally occurs. Milder cases present later (up to age of 4 years). The regularity of blood transfusiton depends on both the baby's general condition and pattern of development AND stability of hemoglobin level to avoid unnecessary overtransfusion of children who may be later categorized as having thalassemia intermedia OR undertransfusion in demanding cases with subsequent imparierd growth, failure to thrive, poor feeding and other symptoms of anemia (at hb <7g/dl)
1- If the hemoblibin remains at this level for several weeks, and there is clear evidence of disability, then a regular transfustion regime should be started.
2- Two four-weekly transfusions are given at a rate of 2-3h for each unit, to keep hemoglobin level > 9-10 g/dl but <14g/dl.
3- The mean yearly Hb should not be >12.5 g/dl.
4- Splenectomy should be considered if annual blood consumption > 200ml/kg (calculated by dividing total annual volume transfused by the wt in the mid of the year). In splenectomized patients, the rate of Hb fall is 1g/week, in non splenectomized patients it is 1.5g/week.
MACROCYTIC NORMOCHROMIC ANEMIA
52
**Folate store are enough for a period of
52
2-4 months. Fr vitamin B12, stores are enough for 2-4 years.
53
**All are correct about magaloblastic anemia except
53
Defective Hb synthesis. Megaloblastic anemia is associated with delated nuclear development due to defective DNA synthesis not defective Hb synthesis.
54
**Folate is affected by
54
Cooking Steaming and frying causes loss of 90%, boiling for 8minutes causes loss of 80% of folate.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
mohammad_emam@hotmail.com 26
55
A patient after partial gastrectomy a. Has no nutritional deficiency. b. Has IF deficit.
55
IF deficiency. Total or partial gastrectomy causes vitamin B12 defeciency.
56
**Hypersegmented neutrophils present in?
56
Megaloblastic.a Hypersegmentation = shift to the right. Other causes include;
- liver disease.
- Uremia.
- Infection and toxemia.
Hyposegmentation = shift to the left occurs in;
- Leucocytosis.
- Thyroid disease.
- Pelger Huet
57
****Macrocytosis is present in: a. Alcoholism. b. ↑Retics. c. All of the above.
57
c. All of the above. Macrocytosis occurs in; Alcoholism, aplastic anemia, liver disease, myxedema, MDS, retics, cytotoxic, MM and normally in neonates and pregnants.
58
Urinary excretion of radioactive Vit B12 after oral and parenteral administration
58
After a loading dose of IV B12, oral radioactive B12 is given and amount absorbed is measured by total body counting or 24h urine sample. Radioactive B12 may be given alone or + IF. Dicopac test uses 2 isotopic forms of B12, one bound to IF and one unbound. Interpretation: B12 aborbed is low and corrected by IF in PA. B12 abroption is low and not corrected by IF in intestinal causes.
59
Which drug causes megaloblastic anemia.
59
Vit B12 defeciency
Folate deficiency
- Cytotoxic.
- Metformin.
- Colchicin.
- Anticonvulsants.
- Paraaminosalicylic acid.
- Neomycin.
Occurs with;
- Salazopyrine.
- Cholestyramine.
- Triamterene.
- Anticonvulsants.
- Anti TB
QUALITATIVE / QUANTITATIVE WBC DISOREDERS
60
***Regarding cold agglutinins: a. it is IgM b. It has specific anti I ab. c. It works at 4ْ C d. None of the above e. a and c
60
e. a and c Cold agglutinins are IgM, work at 4°c. It is anti I in IMN and in idiopathic type, or both anti I and anti i in lymphocellular disorders.
61
***T lymphocytes found in? a. Cortical area of L.N b. Germinal center c. spleen d. L.N sinusoid e. Paracortical area of LN
61
e. Paracortical area of LN
Follicles and germinal center (B-cells)
Paracortex (T-cell)
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62
***Infectious mononucleosis al are ture except? a. Heterophil antibodies agglutinate Ox RBCs, b. Abnormal level of anti-1 specific IgG antibodies, c. Spontaneous rupture of spleen, d. Lymphadenopathy & atypical lymphocytes,
62
(c) or (b) In IMN the following occur; a. Heterophil antibodies agglutinate Ox RBCs, b. Abnormal level of anti-1 specific IgM (not IgG antibodies), c. Splenomegally: mild to moderate (spontaneous rupture unlikely). d. Lymphadenopathy & atypical lymphocytes,
63
Responsible for immunity for pneumocystis carinii
63
B cells (x) Impaired granulocytes → staph. abscesses. Impaired antibody formation → pneumonia by pyogenic organisms. Impaired cellular immunity → mycobacteria, nocardia, fungi e.g. pneumocystis carinii & candida, viruses, parasites.
64
**Neutrophil inclusions of variable size + thrombocytopenia + neutropenia occur in a case of: a. Chediak-Higashi syndrome b. Alder-Reilly syndrome. c. Pelger-Huet syndrome
64
a. Chediak-Higashi syndrome is an autosomal recessive diseases. WBCs show giant granules + neutropenia but normal neutrophil function. Also there is thrombocytopenia and albinism. Alder-Reilly syndrome is an autosomal recessive disease with prominent granules containing excessive polysaccharides. Pelger Hǔet is an autosomal dominant anomaly with hyposegmented neutrophils.
65
**In IMN, which is not present?
65
Neutrophilia. In IMN there is;
- TLC 12-18
- Atypical lymphocytes.
- Neutrophilia (early) followed by neuropenia).
- ± Thromobytopenia.
66
**Activated T-cells secrete:
66
Lymphokines
67
Neutrophil deficiency =
67
Hereditary granulomatous disease of childhood.
68
****Chronic granulomatous disease is due to immunodeficiency of which of the following? a. T-cell member b. Defective neutrophil function. c. Hypocomplementemia. d. Defeceient immunoglobulins. e. ↓ neutrophils
68
b. Defective neutrophil function. Chronic granulomatous disease is an X-linked disease that manifests in the second year of life with ↑susceptibility to organisms of low virulence e.g. staph. epidermidis, serratia, aspergillus, due to phagocytic disfunction. Complement may be elevated and neutrophils are usually elevated even without infection. There is hypergammaglobulinemia. T-cell function is normal
69
****Regarding the function of T cells, which is correct?
69
regulates immunoglobulins production by B cells
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70
Which is wrong : ***. Regarding the function of T-cell, which is correct? a. IL-1 is produced early in the immune response. b. T cells donot respond to IL-2 early in the immune response.
70
b. T cells donot respond to IL-2 early in the immune response.
71
***Large granulocytic lymphocytes act as:
71
NK cells These are not B nor T-cells, though are CD8+. They characteristically have prominent granules and are often large granular lymphocytes.
72
Where can you find hypogranular leucocytes?
72
In myeloid leukemia (M3 varient)
73
IL1 & 2.
73
74
Toxic granulation and Dohle bodies.
74
In toxic granulation, granules are heavy dark red. This occurs with infection, toxemia and irradiation. Dohle bodies are small round blue peripheral granules that occur with infection and May-Hegglin syndrome.
75
***Pertussis infection, is associated with:
75
Marked leukocytosis with an absolute lymphocytosis. In pertussis, lymphocytosis is characteristic due to lymphocyte promoting factor produced by the organism.
76
**SAEP cause
76
Giant neutrophils
77
Granulocyte production is increased by:
77
GM-CFU Also G-CFU
78
Lymphocytes are derived from
78
Pleuripotent stem cells in thymus (x). T & B lymphocytes both arise from a subset of hemopoietic cells in the bone marrow. A committed marrow progenitor called lymphoid stem cell serves as a common precursor for T & B cells. B-cell development take place entirely in the bone marrow. T-cells develop from immature precursors that leave the marrow and mature in the thymus.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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LYMPHOPROLIFERATIVE / MYELOPROLIFERATIVE DISORDERS
79
**Prognosis of M4 is
79
Poor (x)
Prognostic Factors in AML Favorable Unfavorable young age older age: Age >60 is usually considered a poor prognostic factor because older patients generally don't tolerate therapy & higher likelihood of having unfavorable prognostic factors e.g. special cytogenetic abnormalities. FAB types M2, M3, M4 FAB type M7 t(8;21) and t(15;17) abnormality bnormalities of chromosome 11 at band q23 inversion of chromosome 16: usually associated with type M4 and marrow eosinophilia. This syndrome has an excellent prognosis for remission induction and duration deletion of all or part of chromosomes 5 and/or 7 trisomy 8 reactivity with CD2(T1): The presence of certain cell surface markers such as CD2 appears to be associated with a favorable prognosis. Hyperleukocytosis prior treatment prior heamtologic disorder low labeling index/aneuoploidy Infection
Types M2, M3, and M4 have the best prognoses, types M5 and M6 have variable prognoses, and type M7 has the worst prognosis.
80
****Chronic monocytic leukemia: a. better prognosis. b. bad prognosis
80
b. bad prognosis
81
*****Bone marrow transplant indicated in all except? a. ALL b. AML c. Acclertaed case of CML d. blast phase of CML e. Paget’s disease f. Osteogenesis imperfecta g. B thalassemia major
81
c. Paget’s disease
Indications for BMT are:
- ALL.
- AML
- Chronic or accelerated phases of CML.
- Severe aplastic anemia.
- Selected cases of:
MDS, Lymphoma, MM, CLL Thalassemia major, sickle cell disease. Severe inherited metabolic disease e.g. adenosine deaminase deficiency and Hurler's syndrome.
82
**Bone marrow transplantation is not indicated in: a. CML phase. b. CML in chronic phase. c. B thalassemia major.
82
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83
All are very bad prognostic factors in ALL except? a. Very high TLC count b. CNS involvement c. Children less than 1 year old
83
None Bad prognostic factors in ALL are; a. TLC > 50x109/L b. CNS involvement c. Age <1 or >50 year old d. Boys. e. t(1;19) f. T immunophenotype in children and myeloid antigen in adults. g. Blasts in peripheral blood on day 7 h. >5% blasts in bone marrow on day 14 i. No complete response on day 28
84
**Acute monocytic leukemia is associated with? a. Lymphadenopathy b. soft tissue involvement c. Good prognosis compared with other leukemias, d. More lysozyme level in urine & serum e. +ive for non specific estrase,
84
e. Monoblasts are +ve for NS & butyrate estrase. There is also tissue infiltration (gums with hypertrophy)
85
**All may cause leukemia except: a. Ionising radiation. b. Methotrexate. c. Down's syndrome. d. Benzene. e. Fungus.
85
(b) Alkylating agents (not methotrexate) are the chemotherapeutics known to predispose to leukemia. Ionising radiation predispose to AML. Down's syndrome is associated with increased incidence of ALL. Benzene & petroleum derivatives are associated with increased incidence e.g. showmakers. In 1999, three different children with leukemia suddenly go into remission upon receiving a triple antifungal drug cocktail for their secondary fungal infections. In 1997 a clue was found that leukemia, whether acute or chronic, is intimately associated with the yeast, Candida albicans. 50 years ago, it was stated that "it has been established that histoplasmosis and such reticuloendothelioses as leukemia, Hodgkin's disease, lymphosarcoma, and sarcoidosis are found to be coexistent much more frequently than is statistically justifiable on the basis of coincidence." It is believed by some that cancer is a "chronic, intracellular, infectious, biologically induced spore (fungus) transformation disease." Grains such as corn, wheat, barley, sorghum, and other foods such as peanuts, are commonly contaminated with cancer-causing fungal poisons, or "mycotoxins." One of them, called aflatoxin, just happens to be the most carcinogenic substance on earth. If this is indeed a problem, Kaufmann asserts, then cereal for breakfast and soda pop for dinner may not be conducive to a cancer-free lifestyle.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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86
****In FAB classification, M3 =
86
Promyelocytic leukemia FAB HISTOCHEMISTRY M1 Occasional peroxidate+ granules, PAS- M2 Strongly peroxidase+, PAS- M3 Strongly peroxidase+, PAS- M4 Strongly peroxidase+, some cells may be PAS+ M5 Many be peroxidase+ and PAS+, nonspecific esterase stains are strongly + and inhibited by NAF M6 Red cell precursors are PAS+, ringed sideroblasts are seen with iron stains M7 Variable, platelet peroxidase can be demonstrated by electron microscopy
87
***In acute promyelocytic leukemia, which is wrong? a. In FAB classification it is M4 morphology. b. DIC. c. Multiple Auer rods.
87
b. In FAB classification promyelocytic leukemia is M3 not M4 morphology
M0 = Undifferentiated by morphology & cytochemistry, myeloid by immunophenotype. M1 = Little differentiation >90% blasts. M2 = Differentiated 30-90% blasts. M3 = Promyelocytic, hypergranular (M3) or hypogranular (M3variant). M4 = Myelomonocytic. M5 = Monocytic without differentiation (b) or with differentiation (a). M6 = Erythroid differentiation >50% are erythroid. M7 = Megakaryocytic.
88
****Neutrophil ALP is increased in all except:
88
CML NAP occurs in mature neutrophils. High score (35-100) occurs in normal subjects and in liver diseases, Down's syndrome, PCV, aplastic anemia, HD, ALL) Intermediate score in M5, M4 and CLL. Low score occur in AML, lymphosarcoma and PNH
89
In acute promyelocytic leukemia: a. It belongs to M4 type. b. Abnormal coagulation. c. Leukocyte cell markers common.
89
b. Promyelocytic leukemia is M3, It is associated with DIC
90
Hairy cell leukemia.
90
HCL is a B lymphoid CLL characterized by;
- Splenomegaly.
- Lymphocytosis and hair cells with no nucleoli.
- Dry tap on aspiration.
- Spaces around cells.
- Immunologically mature (Normal Igs)
- Strong SmIg
- -ve mouse rousette.
- CD25 +ve
- Tartarate – ACP resistant (TRAP)
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91
**Chromosomal abnormality of t(8:21) is associated with: a. CML, ALL. b. M1 c. M2 d. M4 with eosinophilia. e. M5b
91
c. M2 associates t(8:21), M3 associates t(15:17) and CML t(9:22) (9 becomes Philadelphia chromosome.
92
Chromosomal abnormality in M3 is:
92
t(15:17)
93
**Chromosomal translocation in case of CML is: a. t(8:21) b. t(9:22) c. t(11:14) d. t(8:22)
93
b. t(9:22)
94
**HTLV except
94
transmitted by blood transfusion (x). HTLV may be transmitted by blood transfusion. In UK, it is under consideration for serodetection in blood donors.
95
**Antigen used for the detection of leukemia:
95
CD antigen
96
**Blood malignancy least encountered in children: a. Wilm's b. Neuroblastoma
96
ALL constitutes 75% of childhood hematological malignancies followed by AML (20%) and CML (5%). Least common hematological malignancies in children are CLL followed by CML then AML. Wilm's is a renal tumor and neuroblastoma is a nervous tumor
97
****Paraprotiens are?
97
A group of identical Ig moving as bumdle on electrophoresis.
98
**A 68 years old man with TLC of 23,000 has the following markers, CD1…%, CD2…% kappa chain +, what is the diagnosis? a. Adult T cell leukemia b. CLL c. Lymphosarcoma cell leukemia
98
b. Adult T cell leukemia (CD25 and CD5)
99
***In CLL: a. RAI classification III is either I or II with hemolytic anemia. b. 5% terminate by Richter's syndrome. c. 30% of lymphocytes agglutinate RBCs
99
? According to RAI classification, III is 0 or I or II but Hb is < 11g/dl due to marrow failure not hemolysis.
100
***TRAP stain is helpful in diagnosis of:
100
Hairy cell leukemia Tartarate resistant alkaline phosphatase (TRAP) is used for diagnosis of HCL
101
*****Bone marrow necrosis occurs with: a. Metastatic carcinoma. b. Chrome lymphoproliferative disorder. c. Hodgkin
101
c. Hodgkin or a. Metastatic carcinoma***?
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102
*****In MM, extramedullary plasmacytoma is likely to be present in: a. Lungs. b. CNS
102
b. Extramedullary plasmacytoma occurs most commonly in nasopharyngeal sinuses. Heart, lung and kidney (nodular glomerulosclerosis) originate from tissues underlying mm of GIT and URT.
103
*****In lymphocyte predominant CLL: a. Reed Sternberg cells are abundant. b. Bad in prognosis. c. Lymph node effacement may be nodular or diffuse.
103
c. Lymph node effacement may be nodular or diffuse. In lymphocyte predominant HL according to Rye classification;
- Nodal architecture is lost
- Small homogenous lymphocytes.
- RS cells are little with no nucleoli.
***In CML *(AML)treatment, which is true: a. Folinic acid protects against the megaloblastic effects of methotrexate . b. Citrovorum and folinic acid are synonymous. c. Trimethoprim if used frequently causes folic acid deficiency or megaloblastic anemia. d. There is ↓ methyl THF in B12 deficiency.
a. Folinic acid protects against the megaloblastic effects of methotrexate .
105
***According to international working formulation, poorly differentiated lymphoma is: a. small cleaved cell lymphoma. b. small non-cleaved lymphoma. c. diffuse mixed cell diffuse lymphoma. d. Large cell follicular lymphoma.
b. b. small non-cleaved lymphoma.
Working Formulation for Non-Hodgkin's Lymphomas (NHL)
Classifiable non-Hodgkin's lymphomas
Unaccounted-for non-Hodgkin's lymphomas
Low-grade
Small lymphocytic (CLL)
Mucosa-associated lymphomas, CD5–, CD10–
Follicular, predemoninantly small-cleaved cell
Follicular mixed, small-cleaved and large-cell
Intermediate-grade
Follicular, predominantly large-cell
Diffuse small-cleaved cell
Mantle-cell lymphoma CD5+, CD23–, t11;14 PRAD1
Diffuse mixed small- and large-cell epithelioid component
Lennert's lymphoma T-cell+
Diffuse large-cell cleaved, T-cell variants, non-cleaved
Transformed from low grade NHL, t14;18+
High-grade
Large-cell, immunoblastic plasmacytoid, clear-cell, polymorphous, epithelioid
Anaplastic large-cell lymphoma,T-cell (rare B), Ki-1(CD30)+, t2;5
Small non-cleaved cell, Burkitt's Follicular areas
Miscellaneous
Composite
Other T-cell NHL
Mycosis fungoides/Sézary syndrome
HTLV-1 lymphoma T-cell CLL
Histiocytic
Angioimmunoblastic lymphadenopathy with dysproteinemia
Unclassifiable
Angiocentric-type Polymorphic reticulosis Lymphomatoid granulamatosis
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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106
**BM transplantation and graft vs host disease
106
All (skin, liver, GIT damage) In GVHD, lymphocytes (allogenic) cause skin rash, liver damage, and diarrhea. Acute if occurs <100days chronic if after 100 days (scleroderma like syndrome).
107
Haploid transplantation.
107
Haploid identical match is when the donor is a parent and genetic match is at least 1/2 identical Synergic transplantation is an all allogenic transplant from identical twin. UBMT or MUD = unrelated BM transplant = matched unrelated donor.
108
Use of P32 for PRV.
108
P32 is a β emitter which is taken up by bone and may be used to give prolonged myelo-suppression (2yrs) in old patients. Effect may take 2-3 months and lasts 6-36 months. But due to side effects, it shouldn’t be used below 70 years. Single dose is sufficient to reduce spleen size. Little risk of neutropenia and thrombocytopenia.
109
Serum erythropoietin antibodies in PRV.
109
110
**Which kind of lymphoma occurs in children?
110
Burkitt's lymphoma. NHL is more common in children than HL. Burkitt's is a NHL.
111
Bone marrow transplantation
111
112
**Waldenstrom's macroglobulinemia: a. Proliferation of cells that resemble lymphocytes rather than plasma cells. b. They produce IgM molecules and often excess of light chains. c. All of the above
112
c. All of the above
113
In myelosclerosis all are ritght except: a. Hepatomegaly. b. Pancytopenia c. Hypocellular BM
113
c. Myelosclerosis is characterized by splenomegally, extramedullary hemopoiesis, leucoerythrocytic blood picture + replacement of BM by collagen fibrosis. Hepatomegally is requent. BM shows ↑ cellularity (not hypocellularity).
114
Myelofibrosis and myelosclerosis.
114
Same
115
CLL when reach LN resemble which type of LN?
115
Low grade small cell Hodgkin lymphoma. CLL are small mature uniform. Well differentiated lymphoma has small mature lymphocytes.
116
Mycosis fungoides:
116
seen in epidermis , dermis
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117
**Sizary cell leukemia a. T-cell leukemia lymphoma b. Cutaneous T cell lymphoma
117
Both Sezary syndrome is a T-lymphoid leukemia, a skin lymphoma with leukemic phase. Seizary cells are small with highly convoluted nucleus. Epidermis is involved.
118
Binet clinical staging of lymphoma stage IIB
118
Lymphocytosis and Involvement of 2 or more chains. Lymphocytosis is not included.
118 New1
In Hodgkin disease all are true except
118 New1
Chest X ray is rarely helpful Staging in HL influences both treatment and prognosis. Clinical staging is followed by cervical, thoracic, abdominal and pelvic XR, CT or MRI scanning. BM aspirate and trephine are performed to detect marrow involvement.
118 New2
In Non Hodgkin disease, which is true? a. Most are T cells. b. Good risk patients are sensitive to chemotherapy. c. BM is uncommonly involved. d. Histological classification is not as important as in HD. e. None of the above.
118 New2
e. Most NHL are B cell in origin. Paradoxically, aggressive tumors respond more dramatically to treatmet and are more likely to be cured than indolent tumors. Bone marrow is commonly involved leading to BM failure. Treatment of NHL depends principally on the histological classification (more than six histological classifications for NHL).
118 New3
In CML, which is not present? a. NAP is highly positive. b. Splenometally is present in 80% of cases. c. WBC is commonly 500x109 at presentation. d. BCR +ve but Philadelphia negativecases may occur.
118 New3
a. In CML NAP score is low (<20, whereas an elevated or normal score (20-130) occurs in a leukemoid reaction), splenomegally (often massive) occurs in over 90% of cases, WBC are often greater than 100x109 or more at presentation. 5% of CML are Ph-negative and about half of these patients have a BCR-ABL gene that is molecularly identical to the BCR-ABL gene of Ph-positive CML.
COAGULATION AND PLATELETS
119
******In Acute DIC there is?
119
Hypofibrinogenemia. In DIC there is the triad of hypofibrinogenemia, thrombocytopenia and FDPs.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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120
**The following inhibits thrombus formation except
120
thromboxan. Thromboxane is a platelet aggregator. Inhibitors of coagulation include; Serpentines: ATIII Heparin co factor II α1 antitrypsin C1 estrase inhibitor α2 antiplasmin α2 macroblobulin Protein C system Protein C Protein S Thrombomodulin C4b binding protein.
121
***Thrombocytosis seen in all except? a. Hemolysis b. Hemorrage c. spleenectomy d. fanconi’s syndrome.
121
d. Fanconi’s syndrome. Fanconi syndrome is congenital aplastic anemia with pancytopenia and absent megakaryocytes.
122
**ITP affects
122
Females> males
123
****In TTP all are present except
123
Leucopenia In TTP, there is absence of platelet protease that cleaves vW → macro vW → thrombosis in microcirculation + cell fragmentation (HA) + fever + liver dysfunction. It occurs in adults + AI or pregnancy. May be fatal.
124
ITP in child
124
Sudden remission. ITP follow infection. It is characterized by immune complexes absorbed on platelets → aggregations which are removed by spleen. There is defective megakaryocytic budding. It is self limited.
125
***Antiplatelet antibodies are present in a. SLE. b. scleroderma. c. Carcinomatosis d. CLL e. All of the above
125
e. All of the above 2ry auto immune thrombocytopenia occurs secondary to:
- Blood disease (evan's syndrome)
- General AI disease (SLE, RA)
- Lymphoprolyferative (CLL and lymphoma)
- Solid tumors.
- HIV, chemoradiotherapy and BMT
- Post viral infection.
126
Thrombocytopenia is immune mediated in:
126
SLE.
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127
****Qualitative disorder of platelets may be caused by:
127
Aspirin Platelet dysfunction are;
 ↓ adhesion:
- vW
- Pseudo vW
- Bernard Soulier syndrome.
 ↓ release:
- SPD:
SPD Wiscott Aldrich syndrome Hermanskey syndrome Chediak Hegashi syndrome TAR syndrome
- ↓αgranules: Grey platelet syndrome.
- ↓ TXA2
 ↓aggregation:
- Glanzmans syndrome
- Afibrinogenemia.
 Aquired:
- myeloproliferative
- renal
- FDPs
- Drugs: Aspirin
- Chronic hypoglycemia.
128
Effect of splenectomy on platelet count.
128
Increased
129
***ITP occurs in all except: a. hypersplenism, b. Sarcoidosis. c. SLE. d. Quinidine. e. All of the above.
129
??e. All of the above. ITP has no identifiable antecedent. The question may be about autoimmune thrombocytopenia not ITP See 124.
**In purpura: a. Hemorrhage in deep muscles. b. Hemorrhage in mucus membrane. c. Hemarthrosis.
b. Hemorrhage in mucus membrane.
131
In Bernar Soulier syndrome, all are right except: a. Normal aggregation with ristocetin b. Giant platelets c. ↓glycoprotein
131
a. Normal aggregation with ristocetin In Bernard Soulier syndrome there is ↓ adhesion (due to ↓ GPIb receptor that binds FVIII→ ↓ ristocetin adhesion. On blood film there is large megathrombocytes. Swiss cheese platelets are seen on EM
132
**In vW disease, all are true except: a. BT is prolonged. b. PT is normal. c. PTT is normal d. Platelet aggregation is normal
132
c. In vW disease there is: ↑PTT ↑BT (variable) ↓ platelet aggregation with ristocetin
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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133
*****In Hemophilia A which is correct? a. APTT is prolonged. b. PT is prolonged. c. BT is prolonged. d. CT is prolonged.
133
a. APTT is prolonged.
134
*****Treatment of vW disease: a. Factor VIII b. Cryoprecipitate. c. FFP
134
b. Cryoprecipitate contains FVIII, vWF and FVIIIc stimulating factor. vW disease is also treated with DDAVP.
135
**Which test is used to diagnose factor XIII deficiency? a. PTT. b. PT c. Thrombin time d. Clot stability with urea
135
d. In FXIII deficiency there is normal clotting by extrinsic and intrinsic tests and TCT. However clots are friable and dissolve in 5M urea within few houls.
136
To differentiate between hemophilia A and B? a. Individual factor assay. b. ↑PT c. ↑PTT
136
a. Individual factor assay. Also, thromboplastin generation test (TGT) and plasma correction tests can be used.
137
****Which is wrong regarding heparin? a. Acts on thrombin. b. its action can be reversed by vit K
137
b. its action can be reversed by vit K . Heparin acts on ATIII (potentiates its action and directly binds thrombin).
138
****Regarding protein C. which is wrong? a. Acts on thrombomodulin. b. acts independent on protein S.
138
b. protein C inactivates FV and VIII and activates thrombolysis. Protein S is a cofactor of activated protein C.
139
Cumarin (Oral anticoagulant) acts by
139
↓ factors II, VII, IX Vitamin K antagonism leads to synthesis of immunologically detectable but biologically inactive factors +50%↓ the level of vitK dependent factors.
140
Regarding protein C all wrong except:
140
Its main function is inactivation of F Va and VIIIa
NB: Questions from 85 to 104 were found in papers named Anne/Hematology Quiz and may not be encountered in previous exams unless labeled by star (*)
A blood smear shows 80 nucleated red cells per 100 leukocytes. The total leukocytic count is 18 x 109 /μl. The true WBC expressed in SI units is: a. 17.2 x 109 /L b. 9.0 x 109 /L c. 10.0 x 109 /L d. 13.4 x 109 /L
c. 10.0 x 109 /L
Which of the following tests is used to monitor red cell production? a. PCV b. TIBC c. Schilling test. d. Reticulocytic count.
d. Reticulocytic count.
CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology
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Which of the following conditions will increase ESR? a. Erythrocytosis. b. Increased fibrinogen level. c. Decreased IgG level. d. Reticulocytosis.
b. Increased fibrinogen level.
The formula for cell count using hemocytometer is?
When making a blood film by Wdge technique, increasing the angle of the spreader slide results in the film being: a. Longer and thicker. b. Longer and thinner. c. Shorter and thicker. d. Shorter and thinner.
What information is required in order to calculate the MCHC? a. Hemoglobin and erythrocytic count. b. Hemoglobin, MCV and RBC c. Hematocrit and erythrocyte. d. Hemoglobin and MCV e. None of the above.
e. None of the above.
If a case of mismatched indices occurs on the electronic blood analyzer, which is the most sensitive parameter to be affected and why?
If your hematology electronic cell counter requires bleaching, which CBC parameters would be affected and why?
List the most common causes of an inaccurate automated platelet count.
Describe the principle of the latest hematology analyzer you have used.
If you suspect a cold agglutination is present in the specimen you are processing, which 2 parameters would be affected and what course of action could be taken to resolve the problem?
What are the major morphological features that distinquish P. falciparum from P. vivax?
.
What is your interpretation of mixing studies in coagulation testing?
Summarize the steps you would take before reporting patient results if your control was outside acceptable limits?
Explain the difference between suspect flags and definitive flags on your last hematology analyzer.
Briefly describe how to perform a WBC and platelet smear estimate.
How does RDW relate to RBC morphology?
What are Auer rods?
Define The following terms as it pertains to the hematology analyzers: a. Histogram / Threshold.
What do we mean by hydrodynamic focusing and what is the advantage it gives in automated cell counting?
 Hemophilia A male married normal female, incidence in offspring: females are carriers, normal males
CD antigens
CLINICAL & CHEMICAL PATHOLOGY MCQ Immunohematology
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Immunohematology
1.
Serum of donner + RBC of patient is called: a. minor cross matching b. major cross matching
1.
a. minor cross matching = donor serum + recipient cells. Major cross matching = donor cells + recipient serum.
2.
**Acute intravascular hemolysis occur in blood in
2.
ABO incompatibility.
3.
****A patient received 2 bags of blood intraoperatively, after 5 hours he developed fever and rigors. This is likely due to: a. Platelet antibodies. b. Leucocyte antibodies c. Bacterial infection.
3.
b. Febrile reactions due most frequently to WBC reactive antigens and rarely to platelet antiesn occur after 30min to 90 minutes after starting transfusion.
4.
Unsuitable donor.
4.
5
****All diagnose hemolytic disease of new born except: a. Retics count. b. bilirubin c. DAT d. Porphyrins.
5
d. In HDN there is polychromasia and NRBCs in peripheral blood of the baby.
Tests done on cord blood
Tests done on maternal blood
- ABO & D group - DAT -Hb - Bilirubin
- ABO & D group - Ab screen - Kleinhauer test.
6
**For hemolytic disease all are true except? a. It is autoimmune disease, b. Child RBC have to cross the placenta to produce the antibody response, c. First born child unaffected. d. Can be diagnosed even in utero, d. Severity is proportional to antibody titer
6
a. HDN is an alloimmune (not autoimmune) disease.
7
****Investigations useful in HDN: a. Retics count. b. Bilirubin. c. DAT (+ve in alloimmune antibodies)
7
All (see no 5)
8
HDN which is not of value?
8
Cord Hb (x see 5)
9
****Blood transfusion can transmit: a. HIV b. HBV c. CMV d. All of the above
9
d. All of the above
10
The blood donor in KSA can not be with all of the following except: a. donor infected with HIV b. donor infected with hepatitis c. donor infected with syphilis d. donor infected with malaria e. previous pregnancies
10
e. previous pregnancies Possibly transmissible infections not routinely tested are:
- B. burgdorferi.
- Y. enterocolitica
- P. falciparum.
CLINICAL & CHEMICAL PATHOLOGY MCQ Immunology
mohammad_emam@hotmail.com 41
Immunology
1.
**Antigen & antibody reaction is? a. Agglutination b. precipitation c. immunodiffusion,
1.
b. Immunodiffusion is the process of diffusion in semisolid media to detect amount of antibody to neutralize antigen. Agglutination necessitates an indicator system e.g. RBCs or latex particles.
2.
**Hook effect in immune assay occurs because the concentration of antibodies in the well is? a. Too low b. Too high c. Optimum
2.
b. The hook effect is the result of very high antigen levels giving lower than expected result in a double antibody sandwich assay.
3.
**Antigen & antibody complex are? a. Weakly bound b. strongly bound c. no bound at all.
3.
4.
***Reaginic antibody is: a. IgG b. IgM c. IgD d. IgE
4.
d. Reagenic or anaphylactic mechanism refers to events following combination of antigen with IgE molecule specific for it upon the surface of mast cells.
5.
Arthus phenomenon results from: a. Antigen excess. b. Antibody excess. c. Antigen and antibody in equal proportions.
5.
??b. Antibody excess. In arthus phenomenon, a high antigen concentration is attacked by a high antibody concentration→ excess antigen antibody complexes followed by local tissue damage.
6.
**Lysis in complement fixation test means the test is? a. Positive b. negative c. invalid.
6.
b. In CFT, absence of hemolysis indicates that complement was fixed in antigen antibody reaction so specific antibody was present.
7.
**All tube for serial dilution for CRP test contain 0.5ml of saline & 0.5ml of serum is added to Tube 1 & 0.5ml is transferred through the row of tubes & agglutination is demonstrate in tube 7, If sensitivity of the test is 6mg/l the concentration of CRP in serum is? a. 36mg b. 42mg c. 6mg d. 48mg e. 384mg..
7.
None (something missed in the question). The titer in the 7th tube = 27 = 128 So, the concentration of CRP= 128x6= 768mg.
8.
**CRP is tested because it is increased in? a. Bacterial infection b. viral infection c. other infection.
8.
b. CRP is a sensitive non specific indicator of acute injury, bacterial infection or inflammation.
9.
In infectious monopnucleosis antibodiesare? .________
9.
Anti (I)
CLINICAL & CHEMICAL PATHOLOGY MCQ Immunology
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10.
******Which of the following reagin test for syphilis? a. VDRL b. TPHA c. TPT
10.
a. Reagin = Antibody against cardiolipin. Reagenic tests are VDRL, RPR and Wassermann (CFT).
11.
**Antigenic detection is useful in diagnosis of all of the following escept: a. B hemolytic Streptococci. b. H. influenza. c. Listeria monocytogenes.
11.
c. Because L. monocytogens is an intracellular organism.
31.
****Antigenic methods are useful in diagnosis of all of the following cuases of meningitis except: a. Strept B hemolyticus. b. H. influenza c. E. coli e. listeria
31.
12.
**Autoimmune disease contain all except? a. Lesion in B/M b. low complement level in serum c. immune complex in serum d. low Ig in serum.
12.
d. In AI diseases there is ↑ autoantibodies → immune complex formation → complement fixation → ↓ complement. Also there is cell death or altered function.
13.
***Tuberculine test is type.
13.
IV hypersensitivity
14.
Cell mediated immunity =
14.
Candida Defective CMI → candidiasis.
15.
****Which of the following detects type IV cell mediated immunity?
15.
Tuberculin
16.
***Mantox test is a method for
16.
Tuberculin
17.
Immune complex deposits.
17.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 43
Microbiology
ANTIBIOTICS, ANTIMICROBIALS, STERILIZATION AND DISINFECTION
1.
**Antibiotic used for each organism are a. Pneumonia b. Legionella c. S. pyogens d. H.infuenza. e. P. enterocolitis
1.
. a.-penicillin b-erythrocin c. penicillin d-ceftriaxone e- vancomycin
2.
**Tetracycline is identical in action with –
2.
Aminoglycoside Aminoglycosides act on 30s ribosomal subunit.as tetracyclines.
3.
**Which is effective against penicillinase producing organism.
3.
Nfcillin or dicloxacillin.
4.
The best chemical disinfectant in a TB lab? a. Gluteraldehyde b. ethanol c. phenol d. hypochlorate,
4.
a. Phenol, although effective against TB, is rarely used being too caustic. Ethanol is not effective (TB are alcohol resistant). Glutaraldehyde is used to sterilize respiratory equips and is effective against TB.
5.
***What is lab safety level you will employ for the culture of brucella? a. Routine precaution b. bio safety level 1, c. bio safety level 2 d. bio safety level 3 e. no specific measure
5.
d. Biosafety levels are designed according to risk group of the lab;
Risk group
Description
Biosafety level
1
Organisms are low risk to lab workers and community (common organisms)
1
2
Moderate risk to lab workers limited risk to community e.g. staph, strept., vibrio
2
3
High risk to labo workers, low risk to community (don’t spread rapidly) e.g. brucella, TB, Salmonella
3
4
Viruses, high risk to lab and community
4
6.
β-lactamase resistant penicillin for staph
6.
Cloxacillin.
7.
*****Sterility is achieved by: a. Pasteurization. b. Disinfection. c. asepsis. d. All of the above. e. None of the above
7.
c. Sterilization means killing or removal of all microorganisms including spores e.g. autoclaving, ethylene oxide, filtration. Disinfection means killing of many (not all) microorganisms e.g. phenol, ethanol, iodine (antiseptics).
8.
***Intrinsic resistance for vancomycin is present in: a. Penicillin-resistant bacteria b. C. deficile. c. Staph sensitive to cloxacin.
8.
a. Penicillin-resistant bacteria (both act on cell wall) Most important use of vancomycinis against staph aureus that are resistant to penicillinase resistant penicillin e.g. nafcillin.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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9.
***Which of the following is not an aminoglycoside? a. amykacin. b. Erythromycin. c. Neomycin. d. Sissomycin
9.
b. Erythromycin.
10
**Pasteurization gives guarantee of: a. Kills spores sterilization. b. Disinfection. c. Saponification. d. None of the above
10
a. Kills spores sterilization.
11.
For penicillin resistant pneumococci, which is used? a. Ampicillin. b. Ceftriaxone. c. Cefuroxime + Rifampicin. d. Ampicillin + Rifampicin
11.
b. Ceftriaxone.
12.
Cephalosporin resistant bacteria producing beta lactamase is: a. E.coli. b. Y. Enterocolitica
12.
a. β lactamases are produced by; B. fragilis. N. gonorrhoea. H. influenza. Legionella Enterobactereceae
13.
Which of the following denote sterilization?
13.
14.
TB contamination can be disinfected by
14.
Glutaraldehyde. Or phenolic
15.
**A pre-operative medication of antibiotics is indicated in: a. Acute appendicitis. b. Gangerous obstructed loop. c. Abdominal hernia.
15.
b. Gangerous obstructed loop.
16.
Bronchoscope
16.
Glutaraldehyde
17.
***- Which is the best way to sterilize a bronchoscompe? a. Autoclave. b. Ethylene-oxide. c. Gamma rays. d. None
17.
a. Autoclave.is used for heat resistant parts but ethylene-oxide may be used for heat labile parts.
BASIC TECHNIQUES
18.
**Castanida medium for blood culture contain?
18.
Both liquid & solid media in same bottle.
19.
**Medium for each: a. TB ***b. Gonoccoci c. C. Diphtheria d. Staph. Aureus
19.
a. L.J medium b. Chocolate agar or Thayer martin media c. Löefflers media d. Blood agar
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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20.
**If you forget iodine step in gram stain staph aureus will be seen?
20.
Red
21.
**Significant bacterial count is
21.
100,000. (105) 104-105 = Equivocal <104 and mixed = probable contamination
22.
***Anti-coagulant for blood culture ?
22.
Na-phosphonaphthol sulpfonate Also known by abbreviation SPS
23.
***In CLED all bacteria grow except? a. Enterobacter, b. salmonella c. klebsiella d. enterococci.
23.
None On CLED; Salmonella gives flat blue colonies. Klebsiella gives mucoid yellow colonies. Enterococci give yellow translucent colonies.
24.
***Gram stain best done in? a. Lag phase b. log phase c. static phase d. death phase.
24.
b. Growth of bacteria on media follows the following phases; - Lag phase; phase of accommodation to medium. No net growth - Log phase; phase of maximum growth. - Stationary phase; growth equilibrates death - Decline phase; phase of exhaustion of medium components. Growth declines.
25.
***Microaerophilic atmosphere means? a. 10% CO2 b. anaerobic c. trace of free O2
25.
c. trace of free O2
26.
**Which agar concentration is the best to detect bacterial mobility? a. 0.01% b. 0.5% c. 1.5% d. 2% e. 4%
26.
b. 0.5% For solid medium 1.5-2% concentration is used.
27.
***Best time to read oxidase test is within: a. 5 seconds. b. 10 seconds. c. 1 minute. d. 2 minutes. e. 5 minutes.
27.
b. 10 seconds
28.
***In ZN staining used for M. leprae, the decolorizing agent used is: a. 5% acetone. b. 5% acid alcohol. c. 5% hydrochloric a. d. None of the above
28.
d. None of the above. 5% H2SO4 or 3% acid alcohol.
29.
***Which of the following is a chemical fixative? a. Formalin. b. Mercuric chloride c. Methyl alcohol d. All of the above
29.
c. Methyl alcohol
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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30.
****When urine is preserved for culture it should be: a. preserved at room temperature. b. Preserved in refrigerator. c. preserved with nitric acid. d. Preserved with sulfuric acid. e. Preserved with boric acid.
30.
e. (check also for b.) If a delay > 1-2 hours is unavoidable multiplication of bacteria can be prevented by; - Storage in refrigerator at 4°c - Collected and transported in a container of boric acid at a concentration of 1.8%
31.
Suitable medium for many pathogenic bacteria
31.
Brain heart infusion.
32.
Blood culture is indicated in the following: a. Mycobacterium b. Diphtheria c. Staph. Aureus d. None of the above
32.
??d. None of the above ?? c. Staph. aureus may cause septicemia.
33.
Solid media include: a. Slant. b. Streak plates. c. Pour plates. d. All of the above
33.
d. All of the above
BASIC BACTERIOLOGY
34.
**Cell wall is absent in? a. mycoplasma b. bacteria c. fungi c. viruses
34.
a. Mycoplasma is the smallest organism capable of self replication. It possesses cell constituents of bacteria except cell wall. Instead, there is a triple layer cytoplasmic membrane.
35.
**Sterol is the main constituent of cell wall of: a. Mycoplasma. b. Rickettsia. c. Chlamydia. d. Leptospira. e. Staph.
35.
a. Unlike the cell wall of bacteria, mycoplasma cell membrane contains cholesterol or carotenol in addition to the usual mural and phospholipids.
36.
***Which of the following contains more peptidoglycan? a. G+ve bacilli. b. G-ve bacilli. c. Chlamydia. d. Richetsiae.
36.
a. The peptidoglycan layer is much thicker in Gram positive than in Gram negative bacteria. Richetsia cell wall similar to that of Gram negative bacteria. Chalmydia cell wall is similar to that of Gram negative bacteria but no muramic acid.
37.
***Sedimentation constant of bacterial ribosomes is: a. 40s b. 60s c. 70s d. 80s
37.
c. 70s Bacteria has 70s ribosomes with 30s &50s subunits. Mammalian ribosome has sedimentation coefficient of 80s with 60&40s subunits.
38.
***Endotoxins are chemically: a. Mucopeptides. b. Proteins. c. Lipopolysaccharides. d. Polysaccharides.
38.
c. Endotoxins are integral part of G-ve bacteria. They are LPS whereas exotoxins are polypeptides.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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39.
***L forms differ from parent cells in all of the following except: a. Lack rigid cell wall. b. Lack regular shape. c. Cannot grow and multiply on nutrient medium. d. Lack regular size.
39.
c.
40
***Bacterial genes are transferred by all of the following means except: a. Transformation. b. Transduction. c. Mutation. d. Conjugation.
40
c. The transfere of genetic information between bacterial cells can occur by 3 methods: conjugation, transduction and transformation (see table p16 Jawetz review).
41.
**Sepsis cause
41.
Toxic granulomas.
41. New
Which is not a super antigen? a. TSSA b. Psuedomonas exotoxin A. c. Tetanus toxin. d. Diphtheria toxin.
41. New
b. Psuedomonas exotoxin A.
GRAM POSITIVE COCCI
42.
Cell wall of staph.
42.
Teichoic acid Gram posititve cell wall is composed of peptidoglycan and teichoic acid (no lipid A or polysaccharide as in gram negative cell wall)
43.
**Food poisoning by staph aureus is due to.
43.
Enterotoxin This acts by stimulating relase of IL1 and IL2.
44.
**Enterotoxin of staph. Aureus is heat.
44.
stable
45.
***Differentiate between pathogenic & non pathogenic staphylococci use
45.
coagulase test. Pathogenic staph is aureus species.
46.
**Most streptococcus infection to human is
46.
A & B hemolyticus.
47.
***To differentiate A & B hemolytic streptococci we use a. bacitracin b. optochin c. ampicillin
47.
a. Group A strept is bacitracin sensitive while group B is bacetracin resistant. Optochin is used to differentiate αhemolytic strept (pneumococci are sensitive and strept viridans is resistant)
48.
**Commonest disease caused by streptococcus pyogenes is.
48.
sore throat Strept pyogenes cause three types of diseases; - Pyogenic (pharyngitis and cellulites) - Toxigenic (TSS and scarlet fever) - Immunogenic (Rheumatic fever and AGN)
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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49.
**Food poisoning symptom [vomiting] 4 hrs after ingestion of food seen in? a. E.coli b. staph aureus enterotoxin c. salmonella typhi d. vibrio cholera
49.
b. staph aureus enterotoxin
50.
***Strept pyogenes cause all except: 118. Streptococcus cause all except:
50.
Toxic shock syndrome (check this answer because pyrogenic exotoxin A of strept pyogenes is similar to TSST of staph).
51.
Pneumococci are typed by
51.
Optochin, bile solubility, Quellung test Pneumococci are optichin sensitive, bile soluble and Guellung test positive.
52.
Antigen protective for pneumococci is
52.
Capsular polysaccharides. The capsular polysaccharides is antigenic. Other protective mechanisms of pneumococci include enzyme IgA protease, toxin and SSS.
53.
**Diagnosis of metastatic staphylococcal lesions: a. Protein A Ab. b. Anti DNase. c. Endotoxins
53.
a. Staph don’t produce endotoxins (being gram positive). Anti Dnase is used mainly for strept. Protein A antibody methods are diagnostic for staph disseminated lesions.
54.
*****The following differentiates between staph. Pyogenes and strept epidermidis:
54.
Novobiocin. Novobiocin is used to differentiate staph epidermidis (sensitive) from staph saprophyticus (resistant). To differentiate staph pyogenes
55.
***The epidemiological marker used most frequently in strain differentiation of Staph. aureus is: a. Phage typing. b. Biotyping. c. Serotyping. d. Bacteriocin typing
55.
a. Phage typing.
56.
**All of the following species of streptococcus are B hemolytic except: a. Strept. Pyogenes. b. Strept infrequens. c. Strept. avium d. Strept. salivarius
56.
b. Strept. pyogenes is β hemolytic, Strept. avium is α hemolytic, Strept. salivarius is non-hemlytic.
57.
**Which organism grow on NaCl concentration 6gm/L?
57.
Streptococcus. Strept fecalis grows on 6% NaCl while strept bovis don’t.
58.
Staph.
58.
Catalase test Staph is catalase positive.
59.
Test used to differentiate staph. aureus a. Catalase b. Coagulase c. Dnase d. ASOT
59.
b. Coagulase is used to diagnose staph aureus (positive) from other staph and strept. Catalase is used to differentiate staph from strept., Dnase and ASOT are used to diagnose strept.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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60.
**ASOT is used to detect:
60.
Strept. pyogenes.
GRAM NEGATIVE COCCI
61.
***Differenciation of N. gonorrhaea from N. Meningitis by sugar fermentation?
61.
N. Gono N.Menin Maltose - + Glucose + + Sucrose - -
62.
****In N. gonorrhoea causing dissiminated lesion (systemic manifestation), which of the following is incorrect. a. Sensetive to penicillin (G+ve only) b. Resistant to ampicillin
62.
a. Oral penicillin, cirprofloxacin or doxycycline are used in gonococal arthritis.
63.
Meningococcemia causes:
63.
Waterhouse Fredrichson syndrome.
64.
Neisseria gonorrhoea can cause which of the following? a. Osteomyelitis. b. Artheritis. c. Septicemia.
64.
b. N. gonorrhoea may cause septicemia and suppurativeartheritis and hemorrhagic skin papules.
GRAM POSITIVE BACILLI
65.
**Gm +ve bacilli arrange in Chinese letter pattern is
65.
Diptheria bacilli,
66.
**Pseudomembrane cause by a
66.
diphtheria
67.
*******Which test is used to ascertain toxigenicity of C. iphtheria? a. Dick test. b. Elick's test. c. Schick test. d. None of the above.
67.
b. Elick's test is in vitro plate test for toxin production. Schick test in an ID test for susceptibility to diphtheria, if immune →-ve (no reaction).
68.
******A memberane on the pharynx on removal it leaves a bleeding surface occurs with: a. Diphtheria. b. IMN c. Vincent's angina. d. candida. e. streptococcal infection. f. All of the above. g. None of the above
68.
a. Diphtheria.
69.
***A CSF culture revealed an organism that is G+ve at 37ْ
c and no growth at room temperature. This is most likely to be:
69.
Listeria. Something missed in this question; Listeria is motile at 25°c not at 37°c. It grows on a wide range of temperature (3-43°c)
70.
Neonatal meningitis G+ve rods.
70.
L. monocytogens.
71.
Listeria monocytogens.
71.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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72.
**Growth of actinomyces israeli on gram stain shows
72.
gm +ve branching rods with club ends.
73.
**Actinomycosis is caused by?
73.
Actinomyces israelii & arachnia propionica
74.
**Madura foot have all except? a. Fever. b. bone involvement c. Draining sinus tract d. granules in discharge e. Caused by fungus or bacteria.
74.
a. Madura food is a subcutaneous infection with fungi (e.g. eumycates) or actinomyces. There is discharge from sinus tract, bone involvement follow. Systemic symptoms are uncommon, and so is LN.
ENTEROBACTERECIAE & PSEUDOMONAS
75.
**Mobile bacilli are?
75.
E.coli, V.cholera, salmonella, pseudomonas, proteus,
76.
**Proteus is
76.
Motile gm –ive bacilli, NLF, produce swarming on BA.
77.
**Most common agent causing UTI is? a. E.coli b. klebsiella c. proteus d. seudomonas,
77.
a.
78.
**IMViC reaction of E.coli & klebsella are?
78.
E. coli is ++-- Klebsiella is --++
79.
**Example of NLF colonies on MacConkey agar ? 28. Examples of LF colonis on MacConkey agar?
79.
NLF (produce pale colored colonies): Salmonella, shegella, seudomonas, proteus LF (produce pink colored colonies):E.coli, Klebsiella.
80.
**The following proteous are indole +ive except
80.
P. mirabilis While M. morganii, P. vulgaris, and seudomonas are all positive.
81.
**Klebsiella pneumoniae produces.
81.
mucoid colonies
82.
**IMViC reaction of E.coli is
82.
.[++--]
83.
**Which of the following is urease +ve
83.
proteus. Also, Klebsieall and pseudomonas.
84.
Urease present in all except? a. Brucella.abortus, b. Brucella.melitensis, c. shigella sonni,
84.
c. Not only sh. Sonni, but also Shigella A,B and C.
85.
**Which strain of E. coli cause HUS? a. VTEC O157, H7 b. EPEC O157:H7
85.
a. EHEC 157 = VTEC 157
86.
E. coli, Klebsiella and proteus are
86.
Commensals of GIT
87.
E.coli is indole?
87.
Positive Also proteus is indole positive.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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88.
**Psuedomonas infections include?
88.
May cause UTI, otitis media & eye infection, Bed sore, burns,
89.
**Psuedomonas is?
89.
Motile gm –ive bacilli, NLF, produce pigmented colonies
90.
**Psuedomonas aerogenosa produce?
90.
Blue green pigments, Pyocyanin & biovirdin.
91.
Contamination of sterile fluid is
91.
pseudomonas.
92.
**An abscess with bluish green discharge caused by? a. Staphlococcus b. proteus c. seudomonas.
92.
c.
93.
****Hospital fluids are usually contaminated by: ****120. Organism of medical fluids is: a. Pseudomonas. b. Staph. c. Strept.
93.
a. Pseudomonas are able to grow in water with traces of nutrients.
94.
Pigments of pseudomonas aerogenosa
94.
Both Fluorescin (pyovirdin) and pyocyanin
95.
**Widal test used in the diagnosis of? a. Typhoid fever b. malaria c. malta fever d. brucellosis
95.
a. Typhoid fever
96.
**Enriched medium for salmonella is?
96.
Salenite broth
97.
**On Wilson Blair media salmonella produce?
97.
S.typhi large black colonies with metallic sheen after 24hours, S.paratyphi produce green colonies after 48hours.
98.
**Media used for the isolation of salmonella are?
98.
MacConkey, DCA, Wilson blair, Also XLD and selenite broth.
99.
***Culture of choice in the first week of typhoid fever? a. Feces. b. urine. c. blood. d. CSF
99.
c. Blood culture are usually positive 90% in the first week of fever, thereafter rate of posistivity decreases. Stool culture are positive throughout the course of disease. However, it is of less significant being positive in carriers and dignose gastroenteritis not enteric fever.
100.
**Color of salmonella & shigella on MacConkey agar is?
100.
NLF
101.
*******Salmonella & shigella are differentiated by?
101.
Motility
102.
Seroprofile of salmonella typhi?
102.
O-9,12, H-1,2
103.
Diagnosis of typoid fever in 1st week is done by
103.
blood culture
104.
Differentiate between E. coli and salmonella
104.
Salmonella is NLF and E.coli is LF
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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105.
****All of the following is correct regarding enteric fever except:
105.
Localized gut disease.
106.
**Microscopic appearance of Yersinia pestis is?
106.
G-ve coccobacilli.
107.
******Dog bite G-ve bacilli isolated is propably: a. Pasteurella multucida b. H. influenza. c. B. Abortus d. toxocara cannis
107.
a. Pasteurella multucida
108.
**Cholera is caused by? a. V. cholera b. E.coli c. proteus d. seudomonas.
108.
a. V. cholera
109.
***Enriched media for V.cholera is ?
109.
Alkaline peptone water [pH8.6],
110.
****Loss of fluid in cholera is due to?
110.
Adenyl cyclase system activation This leads to ++cAMP → Chloride and water loss.
111.
***Mode of action of vibrio is by: a. irritation of intestinal mucosa by vibrio. b. attack of intestinal mucosa by the toxin. c. stimulation of membrane bound adenylecyclase
111.
c. stimulation of membrane bound adenylecyclase
112.
Vibrio vulnificus.
112.
This is halophilic cholera i.e. lives in salted water, infects wounds of shellfish handlers causing cellulistis (may cause septicemia in immunocompromized patients).
RICHETTSIAE, CHLAMYDIA AND MYCOPLASMA
113.
**Rickettsial pox is transmitted by
113.
mites. Causative organism is R. akari.
114.
**Stain for rickettsia is.
114.
Giemsa stain Giemsa gives rickettsia blue to purple color, Gimenes stain it red, Machiavillo stain it red inside blue cells and IF gives better sensitivity and specificity.
115.
Organism associated with atherosclerosis:
115.
Richetssia (x) Chlamydia pneumoniae (see Kumar 686).
116.
**Lymphogranuloma venerum is caused by.
116.
Chlamydia Sero D-K hlamydia trachomatis
117.
**Mycoplasma are resistant to action of
117.
antimicrobial.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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SPIROCHETES
118.
**Specific or non specific test for syphilis?
118.
Non-specific- RPR, VDRL Specific- TPI, FTA-ABS, TPHA, MHA-TP
119.
**Treponema pallidum is a?
119.
Spirochate, can be demonstrate by dark field microscopy.
120.
**Treponema pallidum causes? a. Syphilis b. TB c. meningitis d. AIDs
120.
a. Syphilis
121.
***Bejel is characterized by all except? a. Non veneral transmission b. Caused by ariant of Treponema pallidum.
121.
Both are OK. Bejel is non venereal disease caused by T. pallidum endemicum. It is a highly infectious skin in fection.
122.
*****Which of the following accurately don't describe 3ry syphilis: a. Ulcerative skin lesions. b. Gummas in internal organs. c. Rare spirochetes in lesions with limited tissue damage..
122.
a. Ulcerative skin lesions.
123.
**Yaws disease
123.
Caused by Treponema pertenue Characterized by ulcerating papule, scar forming and may cause bone destruction.
HEMOPHILUS
124.
**Hemophilus grows uxuriantly on?
124.
Chocolate media.
125.
****Satellitism is exhibited by? a. H. influenza. b. N. meningitides. c. mycobacteria
125.
Hemophilus influenza around staph. Aureus
126.
**Hemophelus influenza require?
126.
X & V factors for their growth
127.
**H Ducrii causes.
127.
soft chancre Soft chancre is also called chancroid. H. Ducreii don’t require V factor
128.
**Bacteria shows satellism.
128.
H. Influnzae
129.
**Factor V & X are essential for growth of.
129.
H. Influenza
130.
H. influenza meningitis occurs most frequently in :
130.
children. 1/2 to 4 years old.
131.
Satellism helps to diagnose?
131.
H.influenza
BORDETELLA & BORRELIA
132.
**Bordetella pertusis are?
132.
Strictly aerobes.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 54
133.
Bordetella exotoxin =
133.
Single Ag previously termed Islet activity protein. It resembles cholera toxin in structure and action.
134.
***What type of fever caused by borrelia? a. Relapsing fever. b. Q fever c. Rheumatic fever. d. enteric fever.
134.
a. B. recurrentis and duttoni casue replapsing fever. B. burgdorferi cause lyme disease and Q fever is caused by coxiella burnetti.
ANEROBIC BACTERIA
135.
**Gm +ve bacilli with terminal round spores resembling match stick are
135.
Clostridium welchii, Also called perfrengins.
136.
**Nagler reaction used for
- Rapid identification of Cl. Welchii
Lecithenase (Negler's)
L
G
C. deficile & botulinum
-
-
+
Lecithinase –ve Saccharolytic NLF
C. perfringens
+
+
+
Lecithinase +ve Saccharolytic LF
C. tetani
-
-
-
Lecithinase –ve asaccharolytic NLF
137.
**Clostridia are
137.
Gm +ve anaerobic bacilli
138.
**Bacteroid is resistant to? a. Penicillin b. metronidazole c. aminoglycoside d. chloramphenicol.
138.
c. aminoglycoside. Also to penicillin (a), neomycin and kanamycin. Chloramphenicol is highly effective.
139.
**Stormy fermentation is seen in? a. Cl. Histolyticum b. Cl.prefrenges c. Cl.septicum.
139.
b. Cl. Perfringens in litumus milk medium produces A&G, the acid clots milk and the gas breaks the clot producing stormy fermentation.
140.
**Bacteria that can be best identified best by direct Gram's film is? a. Vincent bacillus b. campylobacter
140.
a. Vincent bacillus
141.
*****The following combination is isolated from pus from deep pyonidal sinus: a. B. fragilis.and streptococcus milits. b. B. fragilis and B. abortus. c. Strept B.hymolitic and streptococcus.
141.
a. B. fragilis.and streptococcus.
142.
Suitable medium for anerobic bacteria
142.
Blood (selective or non selective), others include;
- Cooked meat broth (CMB)
- Thyoglycolate.
- BHI
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 55
143.
**Which one has non clostridium crepitation?
143.
Cl. perfrengens (X) Clostridia producing gas gangarene are; - .Cl. perfringens (mainly). - Cl. Novyi. - Cl. septicum - Cl. histolyticum.
144.
Crepitant cellulites is caused by:
144.
Clostridia.
BRUCELLA
145.
**Malta fever is caused by?
145.
Brucella species Also called undulant fever.
146.
A young Saudi male came with fever & myalgia your diagnosis is? a. Brucella b. staphylococcus c. streptococcus d. gonorrhea
146.
a. Other symptoms and signs include; - Arthralgia - Sweating - Heptatosplenomegally.
147.
**Bacteremia is seen in: a. Brucella. b. Tetanus. c. shigellosis
147.
a. Both tetanus and shigellosis are localized infections. Brucella enters through the mouth, lung or skin to local lymph nodes to blood to liver, spleen and bone marrow to cause type IV hypersensitivity.
MYCOBACTERIA
148.
**Mycobacterium Leprae
148.
can not be culture artificially in the laboratory
149.
**L.J medium is used for culturing?
149.
T.B,
150.
**Mycobacterium Leprae are?
150.
Acid fast [5% H2SO4]
151.
**Mycobacterium .T.B is?
151.
Acid fast [20% H2SO4], alcohol fast,
152.
***TB culture takes a. 2-4 days. b. 12 days. c. 3-6 weeks. d. 6-10 weeks.
152.
d. 3-6 weeks.
153.
**Most sever form of leprosy is
153.
Lepromatous
154.
**Mycobacteria are acid-alcohol fast because
154.
they resist to decolorized by acid & alcohol.
155.
**In lepromatous leprosy immunity is
155.
very low. Almost nil
156.
*******Which of the following mycobacteria is related to MTB complex? a. Mycobacterium Africanum. b. M. leprae
156.
a. MTB complex include TB, M. africanum, M. bovis, BCG and M. microtti..
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 56
157.
Acid fast bacilli in stool =
157.
TB
158.
*****Diagnosis by direct staining: a. TB b. Hemophylus
158.
a. Acid fast smear is number one rapid test for mycobacterium TB. Positive smear has a predictive value of 96%.
159.
Which of the following belongs to PTB family? a. M. Kanasasi. b. M. Bovis. c. M. intracellulare. d. M. africanum.
159.
a. MOTT (mycobacteria other than TB) are classified into; - Photochromogens: M. kansasii, M. marinum. - Scotochromogens: M.scrofulucian, M. szulgai. - Nonpigmented: M. avium cellular complex (MAC) M. phlei, M. fortuitum
MISCELLANEOUS
160.
**Malignant pustule is caused by.
160.
Bacillus anthracis
161.
**Plague is by
161.
rat flea.
162.
****Vaginal discharge is absent in? a. Gardnerella infection b. trichomonas vaginalis c. Chlamydia d. ryptococcus.
162.
d. G.vaginalis produce fishy smelling discharge, TV produce thin bubbly fishy smelling discharge, Chlamydia produce thin discharge. Cryptococcus is a lung infection.
163.
**Sterile pyuria not seen in? a. TB b. non specific urithritis c. urine collection by suprepubic puncture d. prior treatment with antibiotic
163.
c. Causes of sterile pyuria; TB Mycoplasma Leptospirosis Vaginal contamination Antibiotics, L forms Abacterial cystitis Non infectious disease e.g. tumour, FB
164.
**Diagnosis of bacterial endocarditis? a. Urine culture b. blood culture
164.
b. blood culture
165.
*****Aspergelloma: All correct except: a. Lungs are the most common site. b. no organism is present in lesion. c. Affect children.
165.
b. Aspergelloma is a ball of aspergillous growth. It may affect children with preexisting pulmonary condition.
166.
**Which combination is wrong?
166.
Non-specific urethritis: Penicillin.
167.
Zoonotic disease
167.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 57
MYCOLOGY
168.
******Candida is identified by
168.
germ tube test.
169.
**An oval to spherical budding cause by.
169.
C neoformans
170.
**Tinea versicolor is caused by.
170.
M.Furfur
171.
*****Tenia capitis is caused by: a. Microsporum. b. Trichophyton. c. Candida
171.
a. Microsporum ausdonii cause tenia capitis. Trychophyton causes tenia pedis or unguium.
172.
*****T. vaginalis may be mistaken for: a. White cells. b. RBCs. c. Candida.
172.
a. White cells.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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PARASITOLOGY
173.
**Malaria affecting large RBC-
173.
P.vivax. In P. vivax, infected cells are enlarged with schuffner's dots. In P. ovale infected RBCS are enlarged without Schuffner's dots. P. malariae cause normal or even reduced sized RBCs. In P. falciparum cells are normal with Maurer's clefts.
174.
**Leishmania id transmitted by
174.
Sand fly.
175.
****Dwarf tape worm is.
175.
H.Nana
176.
***Hematuria in Egyption Patient think of,
176.
Schistosoma hematobium.
177.
**Sporozoites are present in
177.
reticuloendothelial system (X). Sporozoits are the infective stage in the mosquito. The merozoit is the form inside the infected RBC. Such RBC is called schizont.
178.
**A parasite can ingest RBC & present in stool-
178.
E.Histolytica.
179.
***Entrobius vermicularis is diagnosed by.
179.
anal swab
180.
**Larva is present in fresh stool?
180.
Strongyloid stercoralis.(rhabdatiform larva)
181.
**Malaria with multiple infection?
181.
P. Falciparum (X). Vivax and ovale due to preerythrocytic schizogony cause multiple infection.
182.
**Anchovy sauce pus is ?
182.
E. Histolytica
183.
**Visceral leishmaniasis best diagnosed by? a. B//M biopsy b. Serology
183.
a. B//M biopsy
184.
**Cutaneous leishmaniasis diagnosis by? a. Skin biopsy b. Culture,
184.
a. Skin biopsy
185.
The following parasite doesn’t not involve GIT in man? a. Ascaris b. cysticercosis c. H.nana d. Tenia
185.
b. cysticercosis
186.
The cigar glycogen is in
186.
I. buchlii, but if cigar shaped chromatoid it is E. histolytica (immature cyst)
187.
**The arthropod vector of malaria is: a. Female anopheles mosquito. b. Culex mosquito. c. Tsetse fly. d. None of the above
187.
a. Female anopheles mosquito.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 59
188.
Cryptosporidium
188.
Intestinal coccidian infection with AIDS
189.
A warm that infects man and pass eggs around the anus is
189.
Oxyurius vermicularis.
190.
Giardia lamblia is diagnosed in stool by the presence of
190.
Cysts or trophozoit
191.
**Which is caused by skin penetration:
191.
Schistosoma hematobium. Also ankylostoma duodenal, strongyloides and N. americanus.
192.
Serology of E.H except
192.
IFAT Also, CFT, IHA & ELISA.
193.
Stains for stool include: a. Iodine. b. Fluorescent. c. Trichrome d. All of the above
193.
d. All of the above
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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VIROLOGY
194.
*******HAV all are correct except: a. Infection in adults is more severe than children, b. There is chronic carrier state in young children. c. Vaccination is recommended for high risk group.
194.
b. There is chronic carrier state in young children.
195.
**Best sample for the diagnosis for recovery of polio is
195.
feaces. Also from throuat and spinal fluid.
196.
**Virus & living cells resemble in
196.
reproduction.
197.
**Latent infection seen in all except? a. Herpes virus b. adeno virus c. coxsackie virus d. retorvirus.
197.
a. Herpes virus (?? HS causes latent infection)
198.
**Which of the following virus causes systemic effect? a. Poliovirus b. adenovirus c. rhinovirus d. Influenzea virus.
198.
There may be a missing "except" in this question because adeno cause RTI and hemorrhagic cystitis and GE. Influenza and polio also cause systemic effect. Rhino is an exception.
199.
***Which is not correlating?
199.
RSV keratitis in AIDS patients.
200.
****Which combination is wrong? a. Rubella: arthritis in young women. b. Mumps: Antigenic shift c. Coxsackie: Meningitis. d. EBV: Heterophil Abs.
200.
b. Antigenic shift is a character of influenza virus
201.
*****Which of the following can pass to fetus transplacentally? a. HSV. b. VZV. c. CMV
201.
c. CMV
202.
***Who of the following is supposed to transmit CMV infection to hospital staff? a. pregnant woman having a skin rash in second trimester. b. HIV patient c. HCV patient. d. Neonate with congenital defect due to CMV infection
202.
d. Neonate with congenital defect due to CMV infection.
203.
**All diagnose viral infection except: **Which diagnose viral infection? a. IgM Ab is one serum only. b. High IgG titre in serum in acute and convalescent stage. c. 2 fold increase in IgG d. 4 fold increase in viral specific IgE in acute and convalescent stage. e. All of the above
203.
a. IgM Ab is one serum only. A high IgG titre in serum in acute and convalescent stage may be due to immunization. 2 fold increase in IgG ??. IgE is regain of allerty not infection.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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204.
****RSV all correct except: a. Rectal sample gives the highest yield of the virus. b. Form a syncetium in tissue. c. Causes lower respiratory illness in children. d. Related to paramyxoviruses.
204.
a. RSV is a paramyxovirus. It is the most important cause of pneumonia and bronchiolitis in infants.
205.
**In a patient with rabies infection, the main histological characteristic in the brain is: a. Lewi bodies. b. Durel bodies. c. Negri bodies. d. Amyloid plague
205.
c. Negri bodies.
206.
Enteroviruses cannot be isolated from which of the following specimens? a. Throat swab. b. Fecal specimens. c. Gastric fluid. d. Urine. e. CSF.
206.
d. enteroviruses isolated from throat e.g. polio, from feces e.g. polio and hepatitis, from CSF e.g. coxsachie virus. Enteroviruses resist gastric acidity.
207.
Herpes zoster
207.
Localised
208.
Regarding rotavirus, all are correct except: a. DS-RNA virus b. cause majority of infant diarrohea c. diagnosed in feses by ELISA
208.
None Rota virus is a dsRNA virus, it is diagnosed in feces by ELISA. It causes a significant proportion of infant diarrohea.
209.
Ebola virus causes
209.
Fever, myalgia, diarrhea, rash, lymphadenitis, complicated with hemorrhage, encephalitis.
210.
Polio virus is transmitted by which rout?
210.
Feco-oral
211.
**Which of these is not dangerous in contact with AIDS patient?
211.
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
mohammad_emam@hotmail.com 62
If glucose is fermented , TSI reaction is: KIA
 Fungus with acid fast bacilli stain positive: Nocardia.
 Plague causative agent: Yersinia pestis
 Disinfection: Partial destruction of living organisms:
 All sporocidal except: Ethanol.
 Trophozoites on Wright's stained film: Signet ring.
 Ring form with gametocytes seen in F. falciparum.
 Best for collecting urine is dewling catheter, aseptically aspirate 5ml of urine from the catheter tubing.
 Best to disinfect tables contaminated with blood is: Phenol.
 70% alcohol cause protein denaturation and cell membrane damage.
 Transmission of HIV: All
 Fungal infection is not diagnosed by culture because etiologic agent is difficult to grow
 Malaria donot grow in plasma
 Food poisoning is caused by S. enteretidis.
 Strept through all
 First line of body defence against strept is phagocytosis
 Renal impairment except galactosemia
 Don not produce B hemolysis on blood agar: Klebsiella and strept viridans.
 N. gonorrhea infect other than genital tract: vaginintis.
 UTL with indole +ve: E. coli
 Rota: not correct is hemorrhagic conjunctivitis and cardiac disease.
 Respiratury infection cause by: Coxacki B and parainfluenza.
 All G+ve except: Neisseria and mycobacterium
 Specimen examined directly: CSF
 BR that differentiate Neisseria species is sugar fermentation.
 Bacillary dysentery: Shigella.
 Transport media for stool: Carry Blair.
 For nosocomial outbreaks of pseudomonas: pyocin typing.
 Organism that gives metallic sheen on EMB
 Specimen for anerobic culture: Pleural fluid and --- abscess.
 Destruction of microbes except by: Centrifugation.
 Cause of opthalmia neonatorum: N. gonorrheae
 G+ve in cuboidal packages: Sarciniae
 For bacterial motility except: H*E
 BHI with addition of antibiotics for: N (histo.plasma and fungi)
 Choice of media depend on except: one selective plating medium
 TSI gives the following reactions: All (Provedentia K/AG, E. coli K/AG, Citrobacter K/AG, Proteus K/A
 In SS agar, source of carbon is lactose
 Tryptophan is the basis of Indole test.
 Antibiotic sensitivity tes commonly by disc diffusion
 Meningitis in neonates: L. monocytogens.
 New world hook worm: Necator americanus.
 High concentration of liquid or gaseous germicidal chemical sterilization.
 Routine bacterial culture is examined after 5-10 hr, 18-24 hr.
 Routine bacterial culture is incubated at 35ْ C.
 Rapid method for detecting significant bacteria is by microscopy.
 Mycoplasma media is PPLO
 Flukes = Trematodes
 Ribbon like worms = Nematodes
 Most common helminthes are nematodes.
 Largest protozon = B. coli
 Tape worm = cestodes.
 Asexual forms of malaria= Merozoite, asexual cycle in man, sexual cycle in Mosquito
 Ascaris egg migrate from lung to small intestine
CLINICAL & CHEMICAL PATHOLOGY MCQ Microbiology
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 Parasite in blood smear = plasmodium
 Thrush= C. Albicans.
 Flagellates except: S. mansoni.
 Toxo diagnosed by: Fluorescent antibody sera
 Swarming G+ve bacilli = Clostridium
 Protozoa of endemic and epidemic disease = G. lamblia.

 Entrobius diagnosed by Scotch tape method
 Schffner's dots = P. vivax
 Hemoflagellates = Leishmania and trypanosomes
 General term of worms = Helmenth
CLINICAL & CHEMICAL PATHOLOGY MCQ Shawual 1425 Exam
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26th Shawual 1425
1.
****Calcium in urine stone is present in all of the follwing except: a. UTI b. Secondary hyperparathyroidism.
See Q9 body fluids
2.
Acidemia is associated with
See Q 11 Chemistry.
3.
***To correct acidosis, the kidneys: a. secrete more H+ in urine. b. Synthesis bicarbonate to ECF c. Both a and b
See Q 12 Chemistry
4.
***What is the base: acid ratio at pH 7 for acid of pK6? a. 0.01 b. 0.1 c. 1.0 d. 10 e. 100
See Q 15 Chemistry
5.
******Metabolic acidosis can result from:
See Q 17 Chemistry
6.
**All causes renal damage except
See Q 23 Chemistry
7.
***Main extracellular ions? a. Na & K b. Na & Cl **Main electrolyte in blood is? ***Electrolytes in ECF a. Na is a major cation b. Cl is a major cation d. HCO3 is a major anion. ***Main intracellular cation is; **In serum: a. Sodium is the main cation. b. Bicarbonate. ***Intracellular fluid contains: a. More potassium less sodium than extracellular fluid.. b. Sodium and potassium in equal amount.
See Q 20,21, 22, 24, 25, 26.Chemistry
8.
Glycogen differs from starch in: a. Cellulose is not metabolized in humans because of absence of enzyme b. Repeating units.
See Q 34 & 35 chemistry
9.
**Xylose test is done to detect the function of: a. Stomach. b. Pancreas. c. Upper small intestine. d. Lower small intestine. e. Large intestine
See Q 36 chemistry
10.
****Von Gerke's disease is caused by deficiency of: a. Glucose 6 phosphatase b. Glucose 6 phosphate dehydrogenase
See Q 37 chemistry
11.
What happens if sucrose is given paretnrally:
See Q 38 chemistry
CLINICAL & CHEMICAL PATHOLOGY MCQ Shawual 1425 Exam
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12.
***Which of these is not a ketone body? a. Acetone. b. Acetoacetic acid. c. Butyric acid. d. B-hydroxy butyric acid. e. None of the above.
See Q 39 chemistry
13.
***Which of the following result shows renal improvement? a. urea 9 mmoll b. creatinine 10 mmol/l c. urates d. cholesterol e. urine osmolarity less than 800 after 12 hrs of water deprivation.
See Q 53 chemistry
14.
**Low GFR occurs in all except: a. Congestive heart failure. b. Urethral obstruction.
See Q 54 chemistry
15.
**Gluconic amino acids include: a. Alanine. b. Methionine. c. Valine. d. Glutamic acid. e. All of the above.
See Q 64 chemistry
16.
***Which lipoprotein has highest concentration of cholesterol? a. VLDL b. LDL c. IDL d. HDL
See Q 72 chemistry
17.
***In MI, which is the last enzyme to be raised and lasts long? a. CK b. CK-MB. c. AST. d. LDH
See Q 85 chemistry
18.
**Isoenzymes:
a. Are physical types of one enzyme.
b. Have different electrophoretic mobility.
c. All of the above
See Q 86 chemistry
19.
*****ADH is? a. Produced by posterior pituitary b. Produced in the hypothalamus.
See Q 90 chemistry
20.
****Error in the result is expected in which case? a. Glucose on fluoride. b. Glucose on EDTA c. Calcium on oxalate
See Q 4 general
21.
***In Pyruvate Kinase deficiency all correct except? a. Intermittent attach of anemia. b. Splenectomy is a choice of treatment. c. Autosomal recessive.
See Q 15 hematology
22.
**In A sickle cell disease patient under general anesthesia, all true except?
See Q 16 hematology
CLINICAL & CHEMICAL PATHOLOGY MCQ Shawual 1425 Exam
mohammad_emam@hotmail.com 66
23.
**In favism, a. The defect is in b. which is affected
See Q 20 & 28 hematology
24.
***Free plasma Hb is bound to:
See Q 27 hematology
25.
**In hereditary spherocytosis which is false: a. It is autosomal dominant disease. b. Treated by splenectomy. b. Thin underhemoglobinized RBCs are seen in blood film.
See Q 29 hematology
26.
**Normal Hb pattern?
See Q 45 hematology
27.
****Chronic granulomatous disease is due to immunodeficiency of which of the following? a. T-cell member b. Defective neutrophil function. c. Hypocomplementemia. d. Defeceient immunoglobulins. e. ↓ neutrophils
See Q 68 hematology
28.
****Paraprotiens are?
See Q 97 hematology
29.
***In CLL, all are true except:: a. RAI classification III is either I or II with hemolytic anemia. b. 5% terminate by Richter's syndrome. c. 30% of lymphocytes agglutinate RBCs
See Q 99 hematology
30.
***In CML treatment, which is true: a. Folinic acid protects against the megaloblastic effects of methotrexate . b. Citrovorum and folinic acid are synonymous. c. Trimethoprim if used frequently causes folic acid deficiency or megaloblastic anemia. d. There is ↓ methyl THF in B12 deficiency.
See Q hematology
31.
****All diagnose hemolytic disease of new born except: a. Retics count. b. bilirubin c. DAT d. Porphyrins.
See Q 5 immunehematology
32.
***Tuberculine test is type.
See Q 13 immunology
33.
Cell mediated immunity =
See Q 14 immunology
34.
β-lactamase resistant penicillin for staph
See Q 6 Microbiology
35.
**Sterol is the main constituent of cell wall of: a. Mycoplasma. b. Rickettsia. c. Chlamydia. d. Leptospira. e. Staph.
See Q 35 Microbiology
36.
**Which strain of E. coli cause HUS? a. VTEC O157, H7 b. EPEC O157:H7
See Q 85 Microbiology
CLINICAL & CHEMICAL PATHOLOGY MCQ Shawual 1425 Exam
mohammad_emam@hotmail.com 67
37.
Organism associated with atherosclerosis: a. Chalmydia trachomatis. b. Chlamydia pneumoniae d. Mycoplasma
See Q 115 Microbiology
38.
***TB culture takes a. 2-4 days. b. 12 days. c. 3-6 weeks. d. 6-10 weeks.
See Q 152 Microbiology
39.
*****Aspergelloma: All correct except: a. Lungs are the most common site. b. no organism is present in lesion. c. Affect children.
See Q 165 Microbiology
40.
******Candida is identified by
See Q 168 Microbiology
41.
*******HAV all are correct except: a. Infection in adults is more severe than children, b. There is chronic carrier state in young children. c. Vaccination is recommended for high risk group.
See Q 194 Microbiology
42.
***Which is not correlating?
See Q 199 Microbiology
43.
****Which combination is wrong? a. Rubella: arthritis in young women. b. Mumps: Antigenic shift c. Coxsackie: Meningitis. d. EBV: Heterophil Abs.
See Q 200 Microbiology
44.
***Who of the following is supposed to transmit CMV infection to hospital staff? a. pregnant woman having a skin rash in second trimester. b. HIV patient c. HCV patient. d. Neonate with congenital defect due to CMV infection
See Q 202 Microbiology
45.
**All diagnose viral infection except: **Which diagnose viral infection? a. IgM Ab is one serum only. b. High IgG titre in serum in acute and convalescent stage. c. 2 fold increase in IgG d. 4 fold increase in viral specific IgE in acute and convalescent stage. e. All of the above
See Q 203 Microbiology
46.
In β-Thalassemia, which is true? a. It presents with severe anemia at the age of 6 months. b. Blood transfustion may be required as frequent as every 9-12 months.
See Hematology 51 new
47.
Which is true regarding DAT a. It is positive in all IHA. b. may detect complement attached to RBCs.
See Hematology 41 New
CLINICAL & CHEMICAL PATHOLOGY MCQ Shawual 1425 Exam
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48.
Regarding concentration of urine; a. Proximal tubules return 75% of filtered water. b. Distal convoluted tubules deliver 40-60L of fluid to collecting tubules / day. c. Osmotic pressure in renal cortex is higher than in medulla. d. ADH acts on all parts of nephrone. e. Aldosterone increase Na excretion.
See Chemistry 28 New
49.
H+ homeostasis is altered by; a. Excessive change of pyruvate to lactate.
See Chemistry 19. New
50.
Hemoglobin breakdown takes place in: a. RES b. Hepatocytes. c. Renal tubules.
- See Hematology 14.New
51.
Carcinoid tumors secrete
See chemistry 98 New
52.
Which is not a super antigen? a. TSSA b. Psuedomonas exotoxin A. c. Tetanus toxin. d. Diphtheria toxin.
See microbiology 41. New
53.
In Hodgkin disease all are true except
See Hematology 118 New1
54.
In Non Hodgkin disease, which is true? a. Most are T cells. b. Good risk patients are sensitive to chemotherapy. c. BM is uncommonly involved. d. Histological classification is not as important as in HD. e. None of the above.
See Hematology 118 New2
55.
In CML, which is not present? a. NAP is highly positive. b. Splenometally is present in 80% of cases. c. WBC is commonly 500x109 at presentation. d. BCR +ve but Philadelphia negativecases may occur.
See Hematology 118 New3
56.
In enzymopathies, which is false:
57.
Regarding excretion of Na+ a. Not dependent on aldosterone. b. Major share of GF osmolarity with associated ions. c. It passively diffuses in proximal tubules. d. In distal tubules it is exchanged for K+ e. Coupled with K+
See Chemistry 28. New 2
58.
Regarding buffer systems; b. An acid is a substance that releases H+ c. Buffering involves change of strong acid to base.
See Chemistry 28. New 3


Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com

CLINICAL BIOCHEMISTRY

Clinical Biochemistry is one of the most rapidly advancing areas of laboratory and clinical
medicine. The marked increase in the number and availability of laboratory diagnostic
procedures has helped in the solution of clinical problems. Individual laboratory tests are
rarely ordered and reported singly; usually combinations of lab tests are used. The physician
should however be judicious in selecting the tests that really give a clue to the diagnosis of a
disease. Some biochemical investigations however are done routinely for most patients e.g.
qualitative tests with urine.
A trend is also emerging to conduct certain biochemical investigations, which could reveal
predisposition to specific disease processes in healthy individuals. The physician can then
suggest preventive measures to the person e.g. elevated levels of plasma cholesterol
persisting for a long time contribute to the development of coronary artery disease and
increased blood pressure. These individuals should be advised to avoid cholesterolcontaining
food so that the development of a serious disease could be retarded. However,
one must be careful in interpreting these investigations and bear in mind the concept of
normal variation from individual to individual.
Metabolic changes associated with specific disorders may give rise to a change in the
biochemical profile of a particular body fluid, e.g. blood glucose in diabetes mellitus; glucose
levels in the cerebrospinal fluid in bacterial meningitis (which are greatly reduced). Hence,
specific parameters are looked for in a specific body fluid when a disease is suspected.
From a clinical point of view, one purpose of performing a test could be corroborating a
particular diagnosis or ruling it out. Other tests may be done to assess the severity of a disease
process or monitor its progress. Still others may evaluate or monitor the effectiveness or
potential side effects of a particular therapeutic regimen; and certain tests can give a clue
about the prognosis or probable outcome of a disease.
The final interpretation of the results of investigations, whether biochemical or of any other
category, should be in total context of the disease process and the clinical profile of the
patient.
This chapter deals with common units and abbreviations used; the importance of quality
control; and automation in a clinical laboratory. Analysis of the various body fluids and their
role in clinical diagnosis is discussed in detail.
Units and abbreviations
1. Metabolites (glucose, urea etc) are expressed as mg / dL or mmol/L.
2. Electrolytes (Na+, K+) as mmol/L or meq/L (earlier terminology)
3. Enzymes as Units/L
Enzymes are sometimes expressed in conventional units (e.g. Amylase - Somogyi units,
Phosphatase in King-Armstrong Units)
Chemical units
1. Molar Solutions: Contain 1gm molecular weight of the solute / L of solution. 1 Molar
solution of H2SO4 contains 98.08 gm H2SO4/L (Mol .Wt of H2SO4 = 98.08).
3
2. Normal Solution: Contain 1gm equivalent weight of the solute / litre of solution. 1
mole HCl, 0.5 mole H2SO4, 0.333 mole H3 PO4 in 1000 ml of solution in water are
one Normal solutions. No. of moles x valency = No. of equivalents; Molarity x
valency = Normality
The following equations define the expression of concentrations:
No of moles of solute
Molarity of a Solution = ————————————
No of litres of solution
No of gm equivalents of solute
Normality of a Solution = ———————————————
No of litres of solution
The units of measure commonly used to express the concentrations of electrolytes in plasma
is milliequivalents (mEq)/L or millimoles(mmol)/L.
Mass (g) x 1000 Mass (g) x 1000 x valency
No. of mEq = ——————————— =
equivalent weight (g) MW
No. of mmol = Mass (g) x 1000
MW
mg/100 ml can be converted to mEq/L or mmol/L as follows:
mg / 100 ml x 10 x valency mg / 100 ml x 10
mEq/L = ————————————— mmol/L =
Atomic or molecular mass atomic or molecular mass
Example: If serum sodium is 322 mg/100 ml [3220 mg/L].
Atomic wt. of Na = 23, Valency = 1
m Eq/L = (322 x 10 x 1) / 23 = 140
Sodium concentration in plasma is also expressed as mmol/L.
Interpretation of results
Value obtained with a particular parameter is interpreted as increased, decreased or within
normal (reference) range.
Reference values: Values obtained from individuals who are in good health as judged by
other clinical and laboratory parameters, after suitable standardization and statistical analysis,
under definite laboratory conditions.
4
Normal (Reference) Range: Values within which 95% normal healthy person’s fall. The cut
off values are set as mean reference value +/- N times standard deviation, of a normal healthy
population; where N varies between 1, 2 and 3.
Quality Control
A major role of the clinical laboratory is the measurement of substances in body fluids or
tissues for the purpose of diagnosis, treatment or prevention of disease, and for greater
understanding of the disease process. To fulfil these aims the data generated has to be reliable
for which strict quality control has to be maintained. Quality control is defined briefly as the
study of those sources of variation, which are the responsibility of the laboratory, and the
procedures used to recognize and minimize them.
Quality control involves consideration of a reliable analytical method. Reliability of the
selected method is determined by its accuracy, precision, specificity and sensitivity; with
major emphasis of QC being laid on monitoring the precision and accuracy of the
performance of analytical methods.
Accuracy has to do with how close the mean of a sufficiently large number of determinations
on a sample is to the actual amount of substance present and is dependent on the
methodology used.
Precision refers to the extent to which repeated determination on an individual specimen
vary using a particular technique and is dependent on how rigorously the methodology is
followed.
Specificity is the ability of an analytical method to determine solely the analyte it is required
to measure.
Sensitivity is the ability of an analytical method to detect small quantities of the measured
analyte.
Analytical methods require calibration, the process of relating the value indicated on the scale
of the measuring device to the quantity required to be measured. Calibration is done using
standard, the solution with which the sample is compared to arrive at the result.
Standard solutions refer to the known amount of a substance in a solution in which its
concentration is expressed in terms of moles or in weights per unit volume.
Uses:
1. For preparing a standard calibration graph, for e.g. a glucose standard solution is used
in the estimation of glucose in blood, CSF and urine.
2. A standard can also be used to estimate the unknown concentration by comparing the
absorbance of standard and test solutions which is measured using a colorimeter
concentration of unknown substance
T – B
= X Concentration of Standard
S – B
where S, T and B are the absorbance of standard test and blank solutions respectively.
5
3. Preparation of buffers: Standard buffer components like acid and its conjugate base
are prepared as standard solutions and mixed in different proportions to attain the
required pH of the standard buffer.
4. Standard solutions of total protein, glucose, urea, creatinine, albumin etc. obtained
from commercial sources, are used to calibrate auto analyzers.
Two major types of errors may occur in a laboratory:
Random errors that arise due to inadequate control on pre-analytical variables, patient
identity, sample labelling, sample collection, handling and transport, measuring devices etc.
Systemic errors that occur due to inadequate control on analytical variables; e.g. due to error
in calibration, impure calibration material, unstable/ deteriorated calibrators, unstable reagent
blanks etc.
The performance of a method routinely used in a laboratory must be monitored continuously
by quality control techniques in order to detect any change in accuracy or precision and take
corrective action. Quality control is of two kinds: internal quality control, the procedure
making use of results of only one laboratory for quality control; and external quality control
in which the results of several laboratories which analyse the same sample(s) are used.
Internal quality control (QC) programme may be formulated considering the following
points:
1. Clinical correlation of test with the disease the patient is suspected to be suffering
from.
2. Within-assay variation: The same sample is analysed twice during an assay and the
outcome noted. Results should be identical if no error exists; a large variation
suggesting one or more errors.
3. Intra-laboratory duplicates: Samples may be analysed in duplicates for 2 days and
reproducibility of the four values checked.
4. The results of a test may be compared with the results of the same tests previously
conducted on the patient. The values are expected to increase with disease progression
and vice versa. A deviation from this pattern indicates error.
External QC programme: The concerned laboratory is provided with vials of controls
without reference values for analysis under the conditions of that lab. The results obtained
would be sent to the reference laboratory for verification. Internal QC programme is suitable
to determine the reproducibility of result (precision). External QC programme is useful to
assess the closeness of a result to the actual value (accuracy).
If the result of the presently used method widely deviates from the majority of the other
methods which agree with one another, the method should be immediately replaced by
another. Revaluation of calibration standards, reagents, pipettes and measuring devices must
be considered in case of any kind of deterioration.
Manual vs automation in clinical laboratory
Automation in clinical laboratory is a process by which analytical instruments perform many
tests with the least involvement of an analyst. The International Union of Pure and Applied
Chemistry (IUPAC) define automation as “the replacement of human manipulative effort and
facilities in the performance of a given process by mechanical and instrumental devices that
6
are regulated by feedback of information so that an apparatus is self-monitoring or selfadjusting”.
Presently no currently available clinical instrument fully meets this definition,
however the term ‘automation’ is applicable to the individual steps in many analytical
processes and modern instrumentation is improvising with more and more intelligence built
into new generations of laboratory analyzers to soon come up to the IUPAC definition.
Automated instruments enable laboratories to process a much larger workload without a
relative increase in manpower. Automation in clinical laboratories has evolved from fixed
automation whereby an instrument performs a repetitive task by itself, and has progressed to
programmable automation, which permits it to perform a variety of different tasks. Intelligent
automation has recently been introduced into a few individual instruments or systems to
enable them to self-monitor and respond appropriately to changing conditions. Instead of
resorting to manual means automation leads to reduction in variability of results and error of
analysis by doing away with jobs that are repetitive and monotonous for an individual and
that can lead to boredom or casual attitude. However, the improved reproducibility attained
by automation is not necessarily associated with improved accuracy of test results since
accuracy is mainly influenced by the analytical methods used. The significant improvement
in quality of laboratory tests in recent years is due the combination of well-designed
automated instrumentation with good analytical methods and effective quality assurance
programs. Automation may initially incur high costs for procurement of the equipments but is
economical in the long run due to the reduction in the manpower required to perform the
tasks.
Automated analyzers usually include the mechanized versions of basic manual laboratory
techniques and procedures, and several ways have been developed for automating them.
When initially introduced, automation mimicked manual test procedures and was applied to
those tests requested most often. All the individual steps in the procedure are duplicated.
Analytical methods, which are quicker and with fewer steps as well as modification of
existing protocols are being developed as the manufactures have integrated computer
hardware and software into analyzers to provide automatic process control and data
processing capabilities.
Types of analyzers
Semi-auto analyzer: Here, the samples and reagents are mixed and read manually (Figs.1 &
2).
Figure-1: Semi-Autoanalyzer Figure-2: Semi-Autoanalyzer
7
Batch analyzer: The reagent mixture is mixed and fed automatically. One reagent is stored
in the machine at a time enabling one batch of a specifc test to be automatically conducted
e.g. RA 100.
Random Access autoanalyzers: These analyzers can store more than one reagent. Samples
are placed in the machine and the computer is programmed to carry out any number of
selected tests on each sample e.g. Hitachi 912 (Fig. 3).
Fig. 3: Autoanalyzer
Some of the terms commonly used in autoanalysers are:
Batch analysis wherein several samples are processed for analysis in the same analytical run.
Sequential analysis, where each sample in the batch enters the analytical process one after
another and the results are printed in the sequential order that they are fed.
Continuous flow analysis Here the samples of one batch are sequentially subjected to the
same analytical reactions at the same rate, each sample being separated from the previous one
by air.
Single channel analysis (single test analysis) each of the samples is analysed by a single
process. Result of a single parameter is produced.
Multiple channel analysis( multiple test analysis) Each of the samples is subjected to multiple
analytical processes and sets of test results are obtained.
Random access analysis Any sample may be analysed at random by a signal to the processing
system. eg. of such systems are Ektachem, Hitachi 912 etc.
The following are the steps in the automated systems:
1. Sample identification: The tube containing each of the samples is labelled at the time
of collection of blood or other fluids for analysis. On reaching the lab where it is to be
tested, the sample is recorded by computerized procedure after which the samples are
processed. (Glass and plastic wares using in laboratories Figs. 4 & 5).
8
Fig. 4: Vacutainers used for blood collection and storage
Fig. 5 Pipettes: Demonstration of how to use a pippete
Bar coding: The bar coding technology for sample identification is available in
several analytical systems. A bar coded label is placed onto the sample containers and
is read by the bar readers placed at key positions in the analytical train. The
information that is read by the reader is transfered to and processed by the system
software.
2. Sample preparation: The clotting of blood, centrifugation and transfer of serum causes
delay in the specimen preparation. To eliminate these problems the use of whole
blood for analysis and automation of specimen can be done.
3. Sample handling, transport and delivery: The containers (tubes) holding the samples
are kept covered till the time of analysis to avoid evaporation or spillage. For analysis,
the sample is loaded on loading zone of the analyzer.
4. Sample processing: Automation of the analysis of analytes requires the capability of
removing the interfering substances from blood for the analyte to be tested
9
5. Reagent handling and delivery: Reagents should be stored in 4°C refrigerator till the
assay as per requirement, and the instrument may also be pre-cooled.
6. Chemical reaction: The samples undergo chemical reactions in the analyzers in the
presence of the appropriate reagents and optimum conditions set.
7. Measurement, signal processing and microprocessing: The measurements and output
signals are automatically processed and the results are made available in form of
readings/ graphs as per the requirements input initially.
The demand for increased efficiency and cost effectiveness in health care has led to the
production and commercial availability of a number of sophisticated automated analyzers
to analyze blood, urine and CSF samples. Depending on the specific requirements and
workload, laboratories opt for a combination of automatic, semiautomatic and manual
mode of analyses.
Collection and preservation of biological fluids
The different body fluids that are used for biochemical investigations are given below:
Body Fluid Investigation
Performed
Method of Collection
WHOLE
BLOOD
Blood gases
Glucose
Urea
Obtained by arterial or venepuncture;
collected with anticoagulants like
heparin
PLASMA Enzymes
Metabolites
Electrolyte
Blood with anticoagulants centrifuged
at 2000 rpm, the supernatant is plasma
SERUM Enzymes
Metabolites
Electrolyte
Blood collected in plain glass
container, without any anticoagulant,
centrifuged at 2000 rpm after clotting,
the supernatant is serum
URINE Sugar
Proteins
Bile salts
Pigments
Blood steroids
Directly passed into a glass container,
sometimes a catheter is introduced in
the bladder
CEREBRO
SPINAL FLUID
Sugar, Protein
Chloride
Lumbar puncture from Subarachnoid
space
Anticoagulants
Chemical agents that prevent coagulation are routinely used when whole blood or plasma is
required. Some of the commonly used anticoagulants are:
(1) Heparin (2) Salts of Ethylene diamine tetra acetic acid (EDTA)
(3) Oxalates (4) Sodium Fluoride
1. Heparin: It may be considered to be a natural anticoagulant because it is already
present in the blood, but in concentrations less than that required to prevent clotting in
10
freshly drawn blood. Heparin prevents coagulation by increasing the activity of
antithrombin III, an inhibitor of thrombin. This anticoagulant is used in a
concentration of 0.2 mg / ml of blood and since its molecular weight is large, it
produces no change in erythrocyte volume.
2. Salts of Ethylene diamine tetracetic acid (EDTA): It is an anticoagulant which acts
by virtue of removing calcium ions by chelation. A concentration of 2 mg of the
disodium salt/ml of blood is sufficient. Concentrations even greater than this produce
no detectable change in erythrocyte volume.
3. Oxalates: Lithium, sodium and potassium oxalates act as anticoagulants by removing
calcium ions essential for blood coagulation. Potassium oxalate (K2C204.H20) is
commonly used. 1-2 mg of salt / ml of blood is required.
The disadvantage of the use of oxalate is the alteration of concentrations of plasma
components. Shrinkage of erythrocytes results from a water shift from the
erythrocytes to plasma. This shift increases with increasing anticoagulant
concentration, and if used in the same concentration on a weight basis, all
anticoagulants will have this effect inversely proportional to their molecular weight.
Aside from the water shift there may be alteration of erythrocyte permeability, which
may explain the varied and inconsistent effects of oxalates and other salt
anticoagulants on certain plasma constituents. Because of the difficulty, at times, in
obtaining satisfactory preparation of heparin commercially, Heller and Paul
introduced in 1934, a balanced oxalate mixture for use in hematocrit and
sedimentation rate determinations. It consists of three parts by weight of ammonium
oxalate, which causes swelling of the erythrocytes, balanced by two parts of
potassium oxalate which causes shrinkage. NH4+ & K+ oxalate mixture in the ratio
of 3:2, and 2 mg / ml of blood is the required amount.
4. Sodium Fluoride: It is used when blood is collected for glucose estimations. In the
erythrocytes (RBC), it specifically inhibits the enzyme enolase of the glycolytic
pathway, preventing the consumption of glucose by the RBC’s if blood is left
standing at room temperature. Though it has a weak anticoagulant action, it is usually
combined with another anticoagulant such as potassium oxalate.
Preservation of samples
Alteration in the concentration of a constituent in a stored specimen can result from various
processes such as:
1) Adsorption on to the glass container
2) Evaporation if the constituent is volatile
3) Water shift due to the addition of anticoagulants
4) Metabolic activities of the erythrocytes & leucocytes (accelerated by haemolysis)
Inducing O2 consumption and CO2 production, hydrolysis, glycolysis and finally
degradation.
5) Microbial (fungal / bacterial) growth
11
Changes in concentration of volatile substances such as O2 and CO2 are prevented or at least
hindered by collection and storage of samples under anaerobic conditions.
The problem of microbial growth appears when the sample is to be stored for longer than one
day either at room or refrigerator temperature. This can be solved by four alternative courses
of action:
a) Collection and storage under sterile conditions
b) Freezing of the sample
c) Extreme alteration of pH
d) Addition of an antibacterial agent.
Lyophilized samples are stable with respect to many constituents for periods of at least as
long as ten years.
Samples can be stored at room temperature 18-37oC, refrigerator temperature (4oC) and
frozen state (-10oC or lower). With few exceptions, lower the temperature, greater the
stability. Further, microbial growth is considerably less at refrigerator temperature than at
room temperature and is completely inhibited in the frozen state. Even in the frozen state,
however, some components of plasma deteriorate.
Chemical preservatives
They can be classified into two groups:
1) For prevention of chemical changes such as glycolysis
2) For prevention of microbial growth.
Sander in 1923 introduced the combination of 10 mg Sodium fluoride + 1 mg Thymol / ml of
blood. The presence of Thymol effectively controlled microbial growth so that non-sterile
specimens were stable for all determinations (except non-protein nitrogen) for at least two
weeks.
Monochlorobenzene and monobromobenzene have also been coupled with fluoride and have
been claimed to be superior to thymol.
Antibiotics can be used to prevent bacterial growth 1 mg of streptomycin base / 10 ml of
blood has been used for preservation of blood for Haemoglobin and Urea determinations.
The common preservatives for urine specimen are formaldehyde, thymol, toluene and
chloroform. All these act primarily as antimicrobial agents.
Safety
Safety is each person’s responsibility even in a small clinical laboratory. Even then every
clinical laboratory must have a formal safety program. It is a good practice to assign a
specific person the title of safety officer with the duties of administering the safety program
and keeping it current.
It should be ensured that laboratory environment meets the accepted safety standards (Fig. 6)
which should include, but not be limited to attention to such items as:
12
1) Proper labelling of chemicals
2) Types and location of fire extinguishers
3) Hoods that are in good working condition
4) Proper working and grounding of electrical equipment
5) Providing means for proper handling and disposal of bio-hazardous materials
including all patient specimen.
Fig. 6: Safety measures to avoid hazards
To prevent chemical, electrical and biological hazards following universal precautions should
be followed:
1) Proper storage and use of chemicals is necessary to avoid chemical hazards. Thus
knowledge of the properties of chemicals in use and of proper handling procedures
greatly reduces dangerous situations.
2) All the electrical equipment should be grounded using three-point plugs and use of the
extension cord should be prohibited.
3) Every laboratory should have the necessary equipment to put out a fire in the
laboratory, as well as to put out a fire on the clothing of an individual. Easy access to
safety showers should be made.
4) Biological Hazards can be avoided by following precautions called universal
precautions. (Figs. 7 & 8).
All specimens should be treated as if they are potentially infectious:
a. Avoid performing mouth pipetting and never blow out pipettes that contain
potentially infectious material, for example serum.
b. Do not mix potentially infectious material by bubbling air through the liquid, which
leads to aerosol formation.
c. Barrier protection such as gloves, mask and protective eyewear and gowns must be
Laboratory corridors
should be free of
obstruction
13
available and used when drawing blood from a patient. This includes removal and
handling of all patient specimens. Disposable, non-sterile latex or vinyl gloves
provide adequate protection.
d. Wash hands whenever gloves are changed.
e. Facial barrier protection should be used if there is a significant potential for the
spattering of the blood or body fluid.
f. Avoid re-using syringes and dispose off needles in rigid containers without touching
these, using one-handed technique.
g. Dispose off all sharp objects appropriately.
h. Wear protective clothing, which serves as an effective barrier against potentially
infective materials. When leaving the laboratory, protective clothing should be
removed.
i. Make a habit of keeping your hands away from your mouth, nose, eye and any other
mucous membranes. This will reduce the possibility of infection.
j. Minimize spills and spatters.
k. Decontaminate all surfaces and reusable devices after use with appropriate registered
hospital disinfectant.
l. No warning labels are to be used on patient specimens.
m. Before centrifuging tubes, inspect them for cracks. Inspect the inside of caps for signs
of erosion or adhering matter. Be sure that rubber cushions are free from all bits of
glass.
n. Never leave a discarded tube or infected material unattended or unlabelled.
o. Periodically clean out freezer and dry ice chests to remove broken ampules and tubes
of biological samples. Use rubber gloves and respiratory protection during this
cleaning.
Fig.7: Biosafety measures
14
Fig. 8: Use of exhaust hood for biosafety measures
Chemical composition of blood
Introduction
Blood is a suspension of cells. Erythrocytes, leucocytes and platelets in fluid plasma,
circulating virtually in a closed system of blood vessels. The cellular fraction constitutes 45%
of the volume of blood and plasma constitutes 55% of the volume of blood.
Normal pH of arterial blood is 7.4. The various chemical constituents of blood include the
proteins (albumin, globulin, fibrinogen, lipids, glucose, amino acids, urea, uric acid,
creatinine, hormones and vitamins and the electrolytes Na+, K+, Ca++, Mg++(among cations)
and CI-, HCO-
3, HPO--
4(among anions))
Collection of blood
Venous blood is collected usually from antecubital vein or some other prominent veins of the
forearm under aseptic conditions. Arterial blood is required rarely. This may be collected
from radial, brachial or femoral artery. Capillary blood may be collected from the tip of the
thumb or finger or from the ear lobe.
Experiments
Centrifuge a sample of oxalated blood. Observe that the cells are sedemented and plasma is
separated. What is the color of the plasma? Normally it is pale yellow.
1. Add 10 drops of 2.5% CaCI2 solution to 10ml-oxalated blood. Mix and let stand. The
15
blood clots. Calcium is clotting factor. Oxalate removes it as insoluble calcium
oxalate, preventing clotting. When additional calcium ions are added, clotting occurs.
Keep the clotted blood for an hour. A fluid separates while the clot retracts. Transfer
the fluid to a centrifuge tube and briefly centrifuge. The clear supernatant is serum,
note its color. Normally, it is light yellow. Plasma and serum are chemically same
except that serum lacks fibrinogen.
2. Test for proteins
a) Globulins: To 2 ml serum, add 2 ml saturated (NH4)2SO4 solution. (Half
saturation)
b) The globulins are precipitated. Filter. Test the filtrate by Biuret reaction using
40% NaOH. The test is positive. The filtrate contained serum albumin that was
not precipitated by half saturation.
c) Albumin: Fully saturate with ammonium sulphate crystals the filtrate of the above
experiment. Precipitation will be observed which is due to albumin.
d) Fibrinogen: Mix 0.5 ml plasma, 15 ml water and 0.5 ml of 2.5 CaCI2 solution in a
small beaker. Allow it to stand for 20 mts at 37°C in the incubator. After
incubation, insert a tapered glass rod into the solution and feel the transparent clot
formed and collect it by pressing against the walls of the beaker. The clot is fibrin,
the insoluble form of fibrinogen. Suspend the fibrin clot normal saline to remove
the adhering proteins and dissolve in 5 ml of 5% NaOH. Perform biuret test with
the solution. It is positive. Fibrin is a protein.
Test for-inorganic constituents
Deproteinisation of serum: Take 10 ml serum in a test tube. Add a few drops of 2% acetic
acid. Keep in boiling water for 5 mts. The proteins coagulate, Filter. The filtrate is the protein
free of serum containing all the inorganic constituents except proteins. Use this filtrate for the
following experiments:
1. Test for chlorides: To 1 ml filtrate, add 2 drops of conc. HNO3 and 2 drops of 3%
AgNO3. A white precipitate of AgCI shows presence of chlorides in serum.
Principle: chlorides react with silver nitrate forming a white precipitate of silver
chloride. Nitric acid prevents the precipitation of salts other than chlorides.
2. Test for Phosphates: To 2 ml filtrate and 2 ml of ammonium molybdate reagent and
a few drops of conc. HNO3. Warm, if necessary, to get a canary yellow color which is
due to the presence of phosphates in serum.
Principle: in the presence of nitric acid, phosphours reacts with ammonium
molybdate to form a yellow ppt of ammonium phosphomolybdate.
3. Test for Calcium: To 2 ml filtrate add 1 ml of saturated ammonium oxalate. A white
cloudiness is due to the precipitation of calcium oxalate, which indicates presence of
calcium.
Principle: ammonium oxalate reacts with calcium to form a white precipitate of
calcium oxalate.
Test for organic constituents in the filtrate
(a) Test for Glucose: To 0.5 ml filtrate add 1 ml of Folin’s alkaline copper sulphate
solution mix and keep in boiling water for 5 mts. Coll. Add 5 ml of phosphomolybdic
acid reagent. A deep blue color shows the presence of glucose.
(b) Test for urea: To 0.6 ml filtrate add 0.2 ml of aqueous horsegram suspension (10%).
16
Mix and keep in warm water for 10 mts. Add 5 ml water, mix and filter. To the filtrate
add 2 ml Nesseler’s reagent. A brownish yellow color indicates presence of urea.
Principle: The enzyme urease present in horsegram converts urea in to ammonium
carbonate, which gives color with Nesseler’s reagent.
(c) Test for Uric acid: To 0.5 ml filtrate add 1 ml of 10% Na2CO3 and 1 ml of
phosphotungstic acid, dilute (Folin & Denis). A blue color develops due to uric acid.
(d) Test for Creatinine: To 1 ml filtrate add 0.5 ml of 1% picric acid followed by 0.5 ml
of 10% NaOH. The yellow color changes to orange due to the presence of creatinine.
(This is known as Jaffe’s reaction, which is quantitative for the estimation of
creatinine in serum and urine).
Chemical analysis of urine
Urine is an excretory product of the body and presence of certain substances in the urine
reflects the metabolic state of the body. Since it can be easily collected and examined,
routine and microscopic examination of urine are preliminary and important in diagnosis of
various pathological conditions.
Collection of specimen and its preservation
Like all biological specimens, urine has to be collected and adequately preserved to prevent
contamination and bacterial overgrowth since it is a very good culture medium. The type of
urine specimen to be collected is determined by the test to be performed:
1) A clean, early morning, fasting specimen is generally the most concentrated specimen
and preferred for microscopic examination and for detection of abnormal amounts of
constituents e.g. protein.
2) A clean, timed specimen is one obtained at specific times of the day or during certain
phases of the act of micturition.
-First 10ml of urine voided is most appropriate to detect urethritis.
-Midstream specimen is best for bacteriological study.
3) Catheter specimens are used for microbiological examination in critically ill patients
or in urinary tract obstruction, only.
Preservatives used
1) The most satisfactory form of preservation is refrigeration at 40C combined with
chemical preservation.
2) Commonly used forms of preservation used earlier were formalin (2 drops of 40% in
30 ml of urine) or Thymol (0.1mg per 100ml of urine sample). Nowadays tablets
containing a mixture of chemicals are widely used. They act by lowering the pH and
by releasing formaldeyde.
3) For Ketone bodies: Investigation is to be done immediately or within 2 hours of
collection or it should be refrigerated with adequate preservative.
Physical examination of urine
Colour
Normally the urine is colourless to straw coloured (due to urochrome).
Deep Yellow: Mild to severe dehydration, Jaundice, B complex therapy (due to
17
riboflavin).
Red to brown: Haematuria, haemoglobinuria, myoglobinuria, porphyria
(erythropoetic type).
Brown to black: Alkaptonuria, methaemoglobinuria.
Appearance
Normal urine is perfectly clear and transparent when freshly voided. It may become
turbid if exposed for long time due to the urea being acted upon by bacteria and
converted into ammonium carbonate or due to separation of mucoproteins.
Turbidity
Phosphate excretion in alkaline urine
Pus cells
Specific gravity
Measured by Urinometer - implies the capacity of kidney to concentrate urine.
Normal value: 1.002-1.028
Depends upon - State of hydration & solute load
Values more than 1.028 imply - Severe dehydration
- DM (diabetes mellitus)
- Adrenal insufficiency
Values less than 1.002 indicates - Increase water intake
- Diabetes insipidus
- Chronic Nephritis
Important: A low fixed specific gravity even on fluid restriction denotes loss of
concentrating ability by the kidneys and is usually found is Chronic Renal Failure
(CRF). The specific gravity is fixed at 1.010, a condition known as isosthenuria.
Volume
Normal value- 700 - 2000 mL / day
Depends upon - Fluid intake
- Solute load
- Loss of fluid by skin or otherwise.
-Climatic condition
Some important terms:
Polyuria: More than 3L/day
Conditions- Diabetes Mellitis, Diabetes Insipidus, Recovery from acute renal
failure (ARF), Diuretic therapy
Oliguria: Less than 500 ml/day.
Conditions- ARF, Vomiting, Fever, Burns.
Anuria: Less than 50 ml per 12 hours.
pH
Normal range is 4.5 to 8.5. Average 6.0 in 24 hrs sample.
pH 8.5 or more found- After heavy meals, Proteus infection
pH 4.5 or less found- After heavy exercise, Metabolic Acidosis, Chronic Respiratory
acidosis.
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Chemical Examination
1. Proteins
Normal adults excrete upto 150mg proteins/day (5 to 15mg Albumin, 50 to 70mg Tamm
Horsfall mucoproteins, a product of epithelial lining of the tubules, and the rest different
plasma proteins or glycoproteins).
Nephrotic Syndrome is a clinical condition when kidney loses more than 3.5gm
proteins/day/1.73 m2 with hypoalbuminemia, edema, hyperlipidemia, lipiduria and
hypercoagulability.
Microalbuminuria: It is a condition characterized by urinary albumin excretion rates
between 20-200 μg/min or 30-300 mg per 24 hours. This is shown to precede the overt
renal disease and is an indicative of increased risk for development of diabetic
nephropathy.
2. Glucose / Reducing Substances
Normal urine has reducing sugars in the concentration of 1-1.5 g / L. Of this, Glucose is
200-300mg.
Glycosuria: Glucose in the urine beyond the normal range.
Renal threshold: In normal persons, so long as the blood glucose is less than 160-
180mg/dL, glucose is not excreted by the kidney in amounts which are detected by the
routine tests used. This level is termed the renal threshold for glucose.
Renal glycosuria: It is a condition in which the renal threshold for glucose decreases so
that glucose is present in urine in the presence of normal blood sugar levels.
Physiological renal glycosuria is seen in pregnancy.
3. Ketone Bodies
Ketone Bodies are- β-OH butyrate (78%),
- Acetoacetate (20%) and
- Acetone (2%)
Normal blood levels 0.5-1.5mg%.
Normal amounts in urine are 50mg/day.
Ketonuria seen in- Diabetic ketoacidosis, Starvation, Severe vomiting, Glycogen storage
disorders, high fat diet.
4. Blood
Presence of RBC in urine is called Haematuria.
Hematuria seen in - Nephrolithiasis (Stones in the urinary tract)
- Malignant hypertension
- Sickle Cell Anemia
- Coagulation abnormalities
- Malignancy of Kidney, Urinary tract, and Bladder.
Haemoglobinuria: Presence of free Hb in urine, seen in intravascular hemolysis when
the binding capacity of Haptoglobin is exceeded.
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Myoglobinuria: Presence of Myoglobin in urine, seen in crush injuries and Muscular
disorders.
5. Bilirubin
A freshly voided specimen is required since bilirubin is very unstable. Unconjugated
bilirubin does not cross the Glomerular basement membrane as it is non polar and water
insoluble. Conjugated passes freely as it is water-soluble.
6. Urobilinogen
It is a colourless compound formed in the intestine by the action of gut flora on bilirubin
and is reabsorbed by enterohepatic circulation and excreted in urine.
Increased in: Haemolytic jaundice and Hepatocellular jaundice.
Decreased in: Broad-spectrum antibiotic therapy (by killing gut flora) and Obstructive
jaundice.
Microscopic Examination
1. Cells
a. RBC - ≥2/HPF is abnormal unless it is collected by catheterization.
b. WBC or Pus cells - ≥2/HPF is abnormal and is found in UTI (urinary
tractinfection).
c. Epithelial cells - Normal desquamation from urinary tract.
d. Bacteria, if any.
2. Crystals
Associated with renal calculi, commonly is Oxalate in acidic urine and Phosphate in
alkaline urine.
3. Casts
These are masses of agglutinated proteins in the form of cylindrical moulds of
tubular lumen. Many types are found but commonly seen are:
a. Hyaline casts: Contain mainly proteins and no cells. Cylindrical and transparent,
seen in Pre-renal causes of acute renal failure.
b. Cellular casts: Casts coated with various cells
i. RBC casts are diagnostic of acute glomerulonephritis.
ii. WBC casts are seen in chronic pyelonephritis.
iii. Epithelial casts are seen due to desquamation of tubular epithelial cells. As
the cellular casts travel the tubules they are degraded to granular and then
to waxy casts, which may be seen in diseases, associated with tubular
stasis.
Tests
1. For Proteins
a) Heat test: Based on the principle of heat coagulation and precipitation of proteins.
Procedure: Fill half the test tube with urine and heat the top 1/2 of the sample. Look for
any turbidity at the upper part of the tube by comparing with the lower part of the tube. If
20
any turbidity appears, add 2 drops of 33% acetic acid. (Acidification is necessary because
in alkaline medium heating may precipitate phosphates). If the precipitate is due to
proteins, it will increase on acidification and if it is due to phosphates, it will dissolve
again.
Observation Semiquantitative
Barely visible turbidity 5mg/100ml
Distinct turbidity 10-30mg/100ml
Moderate turbidity 40-100mg/100ml
Heavy turbidity 200-500mg/100ml
Bence Jones proteins are light chains of IgG that are excreted in the urine in cases of
multiple myeloma. On heating a sample of urine at 60oC turbidity appears and again
disappears on further heating.
b) TCA test: Add 1ml of 3% of TCA to 5 ml of clear urine. Protein appears as a white
precipitate.
2. For Sugars
Benedict’s Tests: It is a semiquantitative test based on reduction of Cu++ ions by reducing
sugars in hot alkaline medium.
Hot alkaline medium
Cu2+ Cu+ Cu2O (ppt.)
Reducing sugar
Procedure: To 5ml of Benedict's reagent add 8 drops of urine. Heat to boiling point for 3
minutes, keep on stand for 2 minutes and note the colour of precipitation formed.
Observation Report Interpretation
Clear blue/green Nil -
Green ppt. 1+ 100-300mg%
Yellow ppt. 2+ 300-1000mg%
Brown ppt. 3+ 1-1.5g%
Orange-red ppt. 4+ 1.5g%
A false positive test with Benedict's reagent is found with thymol, formaldehyde,
Chloroform, Lactic acid, Vitamin C, Dextrin.
3. For Blood/Haemoglobin
Benzidine test
Procedure: Add 2ml of urine and 1ml of 3% H2O2 to 3ml of fresh saturated solution of
benzidine in glacial acetic acid. Blue colour within 10 min is suggestive of occult blood.
Principle: H2O2 is catalysed by Hb to give (O2), which oxidizes benzidine to a coloured
derivative.
21
4. For Ketone bodies
a) Rothera’s nitroprusside test
Procedure: Saturate 5ml of urine with solid ammonium sulphate and add 0.2ml freshly
prepared sodium nitroprusside solution. Mix well and slowly add 0.5ml of ammonia. A
purple ring at the junction of the liquids indicates the presence of Ketone bodies.
Principle: In alkaline media (by ammonia and ammonium sulphate), freshly prepared
Sodium nitroprusside soln. forms a purple colored compound in reaction with acetoacetic
acid and acetone (α-ketones). Note: β-Hydroxybutyrate does not give a positive Rothera’s
test.
b) Gerhardt’s Test
Procedure: Add 10% FeCl3 solution drop by drop to 5 ml of urine in a test tube until no
more ppt is formed. A purplish colour is given by acetoacetic acid. Similar colour is
given by salicylate, phenol and antipyrine. If urine is heated and then tested, there is no
colour if the original colour was due to ketone bodies.
5. For Bile Salts
Hay’sTest
Principle: Bile salts are surface tension lowering agents. So in presence of bile salt sulphur
powder will sink.
Procedure: Sprinkle a little dry sulphur powder on the surface of fresh clean urine taking
distilled water as control. If the particles sink, bile salts are present in urine
6. For Bile Pigments
Fouchet’sTest
Procedure: Add a pinch of MgSO4 to 10 ml of urine followed by addition of 5ml of 10%
BaCl2, solution to 10ml urine and filter. BaSO4 acts as absorbent for bilirubin and helps in
concentrating it. Dry the filter paper and add a drop or two of Fouchet’s reagent (25g of
Trichloroacetic acid, 10ml of 10% FeCl3 and 90ml water) at the edge of the ppt. A greenish
blue color denotes the presence of bilirubin (due to oxidation of bilirubin to biliverdin by
FeCl3).
Analysis of Cerebrospinal Fluid
Cerebrospinal fluid (CSF) is a clear, colourless fluid filling the ventricles and subarachnoid
space. CSF production is a result of the combined processes of diffusion, pinocytosis and
active transfer. The majority is produced by selective dialysis of blood plasma by a
specialized sponge-like structure called the "choroid plexus" of third, lateral and fourth
ventricles but about 30% comes from' other brain capillaries and seeps into the system via the
extracellular fluid.
The anatomy of the ventricular system allows for movement of CSF in and around all the
major structures of the brain. From the lateral ventricles located within the cerebral
hemisphere, it circulates through the foramina of Monro into the third ventricle. At its caudal
end, the third ventricle is connected by aqueduct of Sylvius to the fourth ventricle. CSF then
flows into the basal cisterns and subarachnoid space by two lateral foramina of Lusckha and
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median foramina of Magendie. From the cisterns the CSF flows / throughout the
subarachnoid space and over the hemispheric convexities and around the spinal cord. The
total volume of CSF is about 150 ml and the rate of CSF production is about 550 ml per day
thus, turnover rate is about 3.7 times a day. CSF is reabsorbed into the venous system by
numerous microscopic arachnoid villi and larger but less common arachnoid granulations
(pacchinian bodies). Villi and granulations represent outpouchings of the arachnoid
membrane that penetrate gaps in the dura and protrude within the venous sinuses. These
projections act as valves, which permit single direction bulk, flow (direct flow) of CSF into
the venous blood about 500 ml per day with additional amounts through diffusion into
cerebral blood vessels and through the cribriform plate of ethmoid bone into the nose. The
reabsorption of CSF occurs along the entire neuraxis. In the SA space CSF comes in contact
with perivascular spaces around the blood vessels entering and leaving the brain where cells
and protein leak during inflammation. It must be remembered that there is no lymphatic
drainage system in the central nervous system CNS), hence only 2 pathways are available for
the elimination of wastes -capillary drainage and excretion via CSF. CSF secretion is an
active process overall but production is independent of intraventricular pressure and
resorption is proportional to it. A blood CSF barrier exists for many substances like bilirubin
and certain drugs, so that their concentration in CSF is lower than in plasma.
Composition
The composition of CSF is essentially same as that of brain ECF and is largely determined at
the cell surfaces on which it is produced (choroid plexus), where it is absorbed (arachnoid
villi and pacchinian granulation ). Its ionic composition is the same as that of plasma for
some components and different for others. In general CSF glucose concentration is 60% of
serum, sodium chloride and magnesium are same or greater than serum but potassium,
calcium and glucose are lower than serum. Active transport in and out of the CSF space is
probably responsible for maintaining this difference.
Total volume = 150 ml (30ml within cerebral ventricles, 120ml in SA
space), (85 ml in spinal part and 35 ml in cranial part)
Specific gravity = 1.006-1.008
pH = 7.31 -7.40 (7.33)
Normal pressure = 110-130 mm Ringer's solution, or 7-10mm Hg
Color = colorless
Transparency = clear, free of clots ; Osmolarity = 292-297mOsm/l
Cellularity = nil or less than 5 lymphocyte or monocyte / mm3
Glucose = 50-80 mg/dl
Protein = 15-50 mg/dl
Bilirubin = nil
Na+ = 138-150 mEq/L
CI - = 116-122 mEq/L ; HCO3 = 20-24 mmol/L
The normal A:G ratio in CSF proteins is 3:1.
Ratio of serum: CSF protein is 200:1.
Functions
1. mechanical support (cushion effect)
2. removal of waste metabolic products
23
3. transport of biologically active compounds which may function as chemical
4. maintenance of the chemical environment of brain
Pathological states in which examination of CSF may be required
A wide range of disorders can produce change in CSF composition and the type and extent
and extent of change is often not specified for a single pathological condition.
Cerebral dysfunction
I. Infections: Meningitis (purulent, aseptic)
Encephalitis
Neurosyphylis (acute)
TB meningitis
2. Cerebrovascular
Sub-arachnoid haemorrhage
3. Dementia and degenerative
Alzheimer’s disease
4. Neoplastic
Meningial carcinomatosis
Secondary deposits
5. Demyelinating
Multiple sclerosis
6. Autoimmune Sarcoid
7. Others Normal pressure hydrocephalus
Pseudotumour cerebri
Cranial nerve dysfunction
1. Miller Fischer variant of GBS
2. Lyme's disease
Motor neuron:
Amyotrophic lateral sclerosis (ALS)
Cerebellar: Cerebellitis
Sensory dysfunction
Neuropathy: Diabetic
CIDP (Chronic Inflammatory Demyelinating Polyradiculopathy)
Trauma
Head injury
Fractured vertebrae
Acquisition
Quinke first developed the technique of LP or spinal tap in 1891. CSF is collected by lumbar
puncture in which a fine bore needle (22 or 24 L.P needle) is passed between the 3rd and 4th
lumber vertebrae into the subarachnoid space with the patient lying in the lateral position and
the fluid allowed to flow automatically. The bevel of the needle should be parallel to the long
axis of the spine. The whole procedure is done under strict asepsis. The first few drops of the
24
fluid are discarded and the rest of the fluid is “collected in sterile containers. There are
specific indications and contraindications for lumbar puncture.
The specimen is divided into 3 aliquots for:
a) Chemistry and Serology
b) Bacteriology
c) Microscopy
Protocol for investigation:
1. Pressure (Opening and closing pressure)
2. Appearance
color
turbidity
coagulum
3. Cytological examination
direct examination
staining of the centrifuged deposit (e.g.Leishman's stain)
4. Microbiological investigations
staining of centrifuged deposit (gram stain, AFB)
culture and sensitivity
5. Biochemical investigations
Total proteins (Lowry method or turbidometry)
Qualitative test for gamma globulin (Pandy's test)
Quantitation of glucose
Quantitation of chloride
Misc. enzymes (LDH, CK),
bicarbonates, urea, calcium, copper, folate.
It must be borne in mind that CSF samples must always be centrifuged prior to analysis in
order to precipitate any cells otherwise falsely high values for CSF protein will be obtained.
The utmost caution must be exercised while pipetting and handling CSF samples.
Changes in CSF in diseased states
Physical Analysis
Pressure: Normally 60-150 mm of water in recumbent position.
Low opening pressure: 10- 20 cm H2O normal- CSF leak or spinal SA obstruction. Elevated
opening pressure: More than 20 cm H2O Mass occupying lesion, diffuse cerebral
inflammation.
Appearance: Normal CSF is clear and colorless and gives no coagulum or sediment on
standing.
Color: Changes only in pathological conditions, whereas the term xanthochromia means
yellow colour. It has been used for the presence of other colours as well
Yellowish tinge --markedly increased protein >200%.
Yellowish --bilirubin
Blood may be present due to bleeding from L.P. site, pathological subarachnoid hemorrhage,
ventricular hemorrhage, or neurosurgical operations. When hemolysis occurs in CSF the
hemoglobin liberated is converted to bilirubin and that gives a yellow coloration to the CSF
25
(more visible after centrifugation) called xanthochromia. Bilirubin is detected after 10 hours
of subarachnoid bleeding.
Turbidity: CSF may occasionally clot if the ratio of blood to CSF is high. Usually due to
fibrin clot (e.g., tubercular meningitis a cobweb coagulum appears by keeping CSF for 12-15
hours). Turbidity can also be due to microscopic fat globules (fat embolism).
Cell count: Normal CSF should contain no more than 5 lymphocytes or monocytes / mm3.
Nature and number of cells are noted. Presence of RBCs indicate hemorrhage. Presence of
WBCs predominantly polymorphs indicate bacterial meningitis. In viral infection and chronic
infections a lymphocytic response is obtained.
Biochemical analysis
1. Proteins: found in CSF ordinarily originate from serum and reach the cerebral space by
endocytosis across the capillary endothelium. An increase in total proteins is the
commonest chemical abnormality in CSF and results from a breakdown of the blood CSF
and brain-CSF barriers usually as a consequences of an inflammatory reaction but on
occasion, if the flow of CSF is obstructed. Albumin is the predominant protein to be
increased, globulins appear in varying amount. If the permeability of the barriers is
markedly increased, fibrinogen is present which in the test tube forms a clot or coagulum.
High protein content accompanied by xanthochromia is referred to as Froin' s syndrome
(associated with tumours and spinal compression).
Examination of CSF protein is done mainly to detect:
a. Increased blood-brain barrier permeability to plasma protein (80%)
b. Increased intrathecal IgG secretion (20%).
Increase in CSF protein occurs in
a. Hemorrhage (trauma, neoplasm, ruptured aneurysm).
Note: A false result may occur from a "bloody tap" -rupture of a blood vessel during
LP (presence of 1000RBCs -increase protein I mg / ml).
b. Inflammation, meningitis especially bacterial (meningococcal), may be as high as
2000mg/dl.
c. Other causes: encephalitis, polio. Decrease in CSF protein occurs in
Children (6 months -2 years) -Pseudotumour cerebri
Tests for globulins
Pandy‘s test: 2 drops of CSF are added to 2ml of reagent (10g phenol + 150ml water)
and the degree of opalescence is noted-slight opalescence, opalescence, marked
opalescence or turbidity.
Normal CSF remains clear (no opalescence). Marked opalescence is observed in multiple
sclerosis and neurosyphilis.
2. Glucose
CSF glucose concentration is 60% of the normal plasma glucose. Blood and CSF glucose
equilibrate only after a lag period of 4hours so that CSF glucose at a given time reflects
blood glucose level during the past 5 hr. When glucose determination is critical. LP and
blood glucose should be obtained only after the patient has been fasted for the last 4 hr.
26
Equilibrated CSF glucose is definitely abnormal when it is less than 40% of
simultaneously determined blood glucose-values of 40mg/dl are almost always abnormal.
Decreased CSF glucose (Hypoglycorrachia)
Markedly decreased in pyogenic meningitis (e.g., 10-20 fig/dl); in tuberculous meningitis
it is 30-50mg/dl; in viral meningitis it is normal.
Note that intrathecally administered streptomycin used in the treatment of tuberculous
meningitis can reduce the alkaline copper reagent often used in glucose determination.
Specialised Tests:
1. Increased lactate Bacterial meningitis
2. Increased glutamine Hepatic encephalopathy
3. Increased LDH Bacterial meningitis,
4. Increased CK-BB Parenchymal damage
5. Increased adenosine deaminase Tuberculous meningitis
Protocol for Protein Estimation in CSF
Add I ml each of test CSF, standard and distilled water in respective tubes. Then add 4ml
coomassie Brilliant Blue G-250 colour reagent (commercially available). Add 2.5ml of 1M
NaOH to sample in all tubes (NaOH need not be added if you use commercially available
colour reagent). Mix. keep for 10 mins. Read at 595nm Standard protein concentration -
50mg/dl.
Note: Either use commercially available Brilliant Blue G-250 or prepare by dissolving 100mg
of coomassie Brilliant Blue G-250 in 50ml ethanol. To this add 100 ml of phosphoric acid
(85% w/v) and dilute to 1 litter with water.
Protocol for estimation of CSF glucose
Place 0.1ml of CSF into 7.8ml of isotonic solution in a centrifuge tube. Mix well. Add 0.1ml
of sodium tungstate solution. Mix and centrifuge at 2000 rpm for 10 min. Take 2ml each of
the supernatant, standard and isotonic solution in the respective tubes. Then add 2ml of
alkaline copper sulphate reagent in all tubes. Mix well and heat in boiling water for 10 min,
cool and add 2ml of arsenomolybdic acid reagent in all tubes. Mix and wait for 5 min. Read
at 540 nm.
Concentration of standard: 1.25 mg/dl.
Renal Function Test
Renal function tests are specialized tests and are advised when medical history, examination
and routine tests like urine analysis are suggestive of some renal disease. Estimation of renal
function is important in a number of clinical situations, including assessing renal damage and
monitoring the progression of renal disease. Renal function should also be calculated if a
potentially toxic drug is mainly cleared by renal excretion. The dose of the drug may need to
be adjusted if renal function is abnormal.
I. Complete medical history, physical examination, routine tests including urine analysis.
27
II. Renal Function tests: Renal function tests may be grouped into (a) those which assess
the glomerular function, and (b) those, which study the tubular function.
Glomerular function tests Tubular function tests
Blood Urea
Blood creatinine
Inulin clearance
Creatinine clearance
Urea clearance
PAH clearance
Proteins in urine
Urine concentration test
Urine dilutional test
Urine acid excretion
Amino acids in urine
III. Tests for structural integrity
a.) Renal biopsy
b) Renal imaging
Plain abdominal X-Ray, Intravenous pyelogram (IVP)
Renal angiogram, Renal ultrasound, Computerized tomography (CT scan)
Magnetic resonance imaging (MRI)/angiogram (MRA)
Radionuclide renal scan
Renal function tests are only for the analysis of the functional capacity of kidneys. Renal
function tests do not give any information about the structural integrity or the structural
pathology. For structural details renal imaging and biopsy has to be done.
The functional unit of the Kidney is the nephron, which is composed of the Glomerulus,
Proximal convoluted tubules (PCT), loop of henle, Distal convoluted tubules (DCT) and the
collecting tubules.
Quantitation of overall function of the kidneys is based on the assumption that all functioning
nephrons are performing normally and that a decline in renal function is due to complete
functional loss of nephrons rather than to compromised function of nephrons.
Tubular function
Renal tubules make up 95% of the renal mass, do the bulk of the metabolic work and modify
the ultrafiltrate into urine. They control a number of kidney functions including acid-base
balance, sodium excretion, urine concentration or dilution, water balance, potassium
excretion and small molecule metabolism (such as insulin clearance). Measurement of tubular
function is impractical for daily clinical use (performed only when there are specific
indications) therefore tubular function tests are not discussed further in this chapter.
Glomerular Filtration Rate: Glomerular filtration rate (GFR) is the rate (volume per unit
of time) at which ultrafiltrate is formed by the glomerulus. Expressed in ml/min ≈125ml/min
Renal Plasma Flow: Volume of plasma flowing through the kidney per min. Expressed in
ml/min. 25% of the total cardiac output.
28
Filtration fraction: Fracion of renal plasma flow which is filtered through glomeruli.
Expressed as percentage.
Clearance: Clearance of a substance is the volume of plasma cleared of the substance per
unit time. It is expressed in ml/min.
Clearance (C) = U (mg/dL) X V (ml/min)
P (mg/dL)
where U is the urinary concentration of a marker x, V is the urine flow rate and P is the
average plasma concentration of x.
Substance filtered neither
(reabsorbed nor secreted)
Clearance = GFR Inulin
Substance filtered
(reabsorbed and secreted)
Clearance ≈ GFR Uric acid
Substance filtered
(partially reabsorbed)
Clearance < GFR Urea
Substance filtered
(secreted and not reabsorbed)
Clearance > GFR PAH
Glomerular Function tests
GFR is the most sensitive and reliable parameter to assess the glomeular function.
1. Exogenous markers
(a) Inulin - inulin clearance is accurate reflection of GFR
(inconvenient-requires intravenous infusion)
(b) Iothalamate nuclide - gold standard for GFR in clinical research
2. Endogenous markers
(a) Creatinine
- derived from muscle creatine; production is usually constant
- plasma concentration is stable for a given individual
- creatinine clearance (Ccr) ≈ GFR when GFR is close to normal.
Creatinine clearance (Ccr) = Ucr X V (ml/min) ≈ GFR
Pcr
Identical plasma creatinine concentrations in two separate patients
may reflect very different GFR.
Case A: P=1.5mg/dl, V=2ml/min, U=90mg/dl
Case B: Pt who is older and lean and thin
has lower steady-state creatinine production and excretion
P=1.5mg/dl, V=2ml/min, U= 60mg/dl
- When GFR is low, Ccr overestimates the GFR
29
(a) Creatinine clearance test
Procedure for creatinine clearance test: Give 500ml of water to the patient to promote
urine flow. After about 30 minutes ask patient to empty bladder and discard the urine.
Exactly after 60 minutes, again avoid the bladder and collect the urine, and note the volume.
Take one blood sample creatinine level in blood and urine are tested and calculated.
Reference value for creatinine clearance is 90-130ml/min.
Interpretation of creatinine clearance
A decreased creatinine clearance is a very sensitive indicator of reduced glomenilar filtration
rate. A creatinine clearance value upto 75% of the average normal value may indicate
adequate renal function. In older people the clearance is decreased.
Significance of determining creatinine clearance is in the early detection of functional
impairment of kidney without overt signs and symptoms. Small changes in plasma creatinine
which may not apparently indicate abnormal function may show gross changes in the value of
clearance. For example, the plasma creatinine level is 1mg/dl and the clearance is
100ml/minute, a rice in plasma creatinine to 2mg/dl will decrease the clearance value by
50%.
Creatinine clearance test is useful in long-term monitoring of patients with renal insufficiency
under a protein restricted diet, creatinine clearance is altered by body muscle mass, drugs,
age, sex and nature of diet.
Modified creatinine clearance
Corrected GFR
Uncorrected GFR has a +ve correlation body wt, height, BSA and male gender and
- ve correlation with age.
Corrected GFR correlates with age alone
30
= Ucr (mg/dL) X V (ml/min) X 1.73
Pcr (mg/dL) BSA
Calculated creatinine clearance
The most well-known formula is the Cockcroft-Gault formula, which is relatively simple to
use and reasonably accurate.
(140-age in years ) X 2.12 X Weight (Kg) X K
Pcr (mg/dL) X BSA (m2)
K= 0.85 for women and 1 for men
BSA = Body surface area
(b) Urea Clearance: Urea clearance is the number of ml of blood which contains the urea
excreted in a minute by the kidneys. Since 40% of urea is reabsorbed by the tubules after
filtration, the clearance of urea is highly dependent on urine flow rate. Therefore, urea
clearances (Curea) is not useful for estimation of GFR by itself. For example in the hydrate
state, urine floe rate is high and the Curea may be >70% of GFR whereas in a dehydrated state,
Curea may be <30% of GFR.
Maximum Urea Clearance
V
Urea clearance = U X
P
Where U=mg of urea per ml of urine; P= mg of urea per ml of plasma and V= ml of urine
excreted per minute. This is the maximum urea clearance and the reference range is 60-
100ml/minute.
Standard Urea Clearance
Urea clearance value is decreased when the volume of urine (V) is less than 2ml/minute. It is
then called standard urea clearance, where the normal value is found to be 54ml/minute.
Interpretation of urea clearance value: If the value is below 75% of the normal, it is
considered to be abnormal. The values fall progressively with increasing renal failure. Urea
is reabsorbed from renal tubules (urea clearance < GFR) and therefore tubular function also
affect urea clearance. Hence creatinine clearance test is more preferred.
BUN (Blood Urea Nitrogen): Plasma Creatinine (Pcr) ratio
Normal BUN/Pcr ratio ≈ 12-16 : 1
High BUN/Pcr ratio Low BUN/Pcr ratio
prerenal azotemia severe liver failure
high protein diet low protein diet
catabolic states (e.g. sepsis) anabolic states
gastrointestinal bleeding rhabdomyolysis
medications (e.g. corticosteroids)
Renal plasma flow
- It can be estimated by clearance of PAH
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- > 90 % of the PAH is removed from the kidney by tubular secretion and glomerular
filtration.
PAH is infused to constant plasma conc. and its clearance is calculate.
Nowadays it is estimated using I131 iodohippurate or other radionuclides ex. diodrast.
Filtration fraction: it is the ratio of filtered plasma out of total renal plasma flow.
Normal Values:
- Plasma creatinine – 0.9-1.3 mg/dl (men), 0.6-1.1mg/dl (women)
- Plasma Urea – 15-40 mg/dl
- Inulin clearance-
Men- 125 + 25ml/min
Women- 119 + 12 ml/min.
- Creatinine clearance- 90-130 ml/min
- Urea clearance (when V=2ml/min) = 60-100 ml/min
- PAH clearance
Men - 650 + 160 ml/min
Women- 590 + 100 ml/min
Suggested Reading
1. Tiets text book Clinical Chemistry, fourth edition, Ed: Carl A. Burtis and Edward R. Ashwood.

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