هام -Clinical & Chemical Pathology MCQs

8/9/2019 Clinical & Chemical Pathology MCQs- هام

1/68

[email protected] 1

Clinical & Chemical Pathology MCQsClassifi ed, Reorganized And Updated To Shawual 1425 With Short Notes

By Dr Mohammad A. Emam

ContentsBody 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


2/68

CLINICAL & CHEMICAL PATHOLOGY MCQ BODY FLUIDS

[email protected] 2

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 alkalin

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 increas

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.


3/68

CLINICAL & CHEMICAL PATHOLOGY MCQ BODY FLUIDS

[email protected] 3

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 (a

acid or neutral pH), or less commonly with urat(at acidic pH) or with phosphate (at normal urin

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 formdue 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.


4/68

CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY

[email protected] 4

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 samemethodology, .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. Spectrophotometerd. 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 antibodyconjugated 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.


5/68


[email protected] 5

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 6.5 mEq/L

Critical glucose 450mg (2.2 &

25mmol respectively),

critical pH 2.6

critical Na+ 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 eitheraddition of H+ (↑AG),↓ excretion of H+ or

loss of HCO3-

18. pH of the blood. 18.

19 Acid base balance. 19


6/68


[email protected] 6

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 witha. 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.New

1

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.


7/68


[email protected] 7

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 ofglucose 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 debranchingenzyme

Type V (McArdle's):↓ muscles

phosphorylation.


8/68


[email protected] 8

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 glucosewhile 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.


9/68


[email protected] 9

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 V2V2 = 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.


10/68


[email protected] 10

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.


11/68



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. oedemad. 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.


12/68



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, conferringthe 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 autosomalrecessive 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.


13/68



76. Nature of apoproteins. 76. 5 major classes of proteins A to E

77. Saturated vs unsaturated fats (nutritional value) 77. Saturated Unsaturatede.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 precursorof 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 ofhypercholesterolemia + 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.


14/68



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


15/68



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 HCGmolecule 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


16/68



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%) orcarcinoid 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.


17/68

CLINICAL & CHEMICAL PATHOLOGY MCQ General


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


18/68

CLINICAL & CHEMICAL PATHOLOGY MCQ General


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.


19/68

CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology


Hematology

BASIC HEMATOLOGY CONCEPTS / LABORATORY PROCEDURES

1 ** To stain the B/M other than Wright stain which stainusually used?

a. PAS stain

b. Sudan black stain

c. stain for iron.

1 (c) Bone marrow films should be stained withan 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 needlec. 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


20/68



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.


21/68



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. Itis 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)


22/68



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 toa 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.


23/68



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) areclassified into:

Peripheral blood BM

Refractory

anemia


24/68



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 antibodiesin 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


25/68



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 havingthalassemia intermedia OR undertransfusion in

demanding cases with subsequent imparierd

growth, failure to thrive, poor feeding and other

symptoms of anemia (at hb 9-10 g/dl but 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 delatednuclear 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.


26/68



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 4

C

d. None of the abovee. 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)


27/68



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 H ǔet 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


28/68



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 cellsThese 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.


29/68



LYMPHOPROLIFERATIVE / MYELOPROLIFERATIVE DISORDERS

79 **Prognosis of M4 is 79 Poor (x)

Prognostic Factors in AMLFavorable Unfavorable

young age

older age: Age >60 is usually

considered a poor prognostic

factor because older patientsgenerally 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 typeM4 and marrow eosinophilia.

This syndrome has an

excellent prognosis forremission 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 CD2appears 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 diseaseIndications 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


30/68



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 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 leukemiasuddenly go into remission upon receiving a tripleantifungal 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 wasstated that "it has been established that histoplasmosisand such reticuloendothelioses as leukemia,Hodgkin's disease, lymphosarcoma, and sarcoidosis

are found to be coexistent much more frequently thanis 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 mostcarcinogenic 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 acancer-free lifestyle.


31/68



86 ****In FAB classification, M3 = 86 Promyelocytic leukemiaFAB HISTOCHEMISTRY

M1 Occasional peroxidate+ granules, PAS-M2 Strongly peroxidase+, PAS-

M3 Strongly peroxidase+, PAS-

M4Strongly peroxidase+, some cells may bePAS+

M5Many be peroxidase+ and PAS+,nonspecific esterase stains are strongly +and inhibited by NAF

M6Red cell precursors are PAS+, ringedsideroblasts are seen with iron stains

M7Variable, platelet peroxidase can bedemonstrated 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)


32/68



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 thefollowing 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***?


33/68



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 ordiffuse.

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 PRAD1Diffuse 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 NHLMycosis fungoides/Sézary

syndrome

HTLV-1 lymphoma

T-cell CLLHistiocytic Angioimmunoblastic

lymphadenopathy with

dysproteinemia

Unclassifiable

Angiocentric-type

Polymorphic reticulosisLymphomatoid granulamatosis


34/68



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


35/68



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 morechains.

Lymphocytosis is not included.

118New

1

In Hodgkin disease all are true except 118New

1

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.

118New

2

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.

118New

2

e. Most NHL are B cell in origin. Paradoxically,

aggressive tumors respond more dramatically to

treatmet and are more likely to be cured thanindolent 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).

118New

3

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.

118New

3

a. In CML NAP score is low (


36/68



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 antitrypsinC1 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. spleenectomyd. 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 byimmune 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.


37/68



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


38/68



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 andFVIIIc 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.↑PTc.↑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 (Or

Documents

هام -Clinical & Chemical Pathology MCQs