Clinical & Chemical Pathology MCQs              Classified, Reorganized And Updated To Shawual 1425 With Short Notes      ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                  BODY FLUIDS            ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                             BODY FLUIDS9.    ****Calcium...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                 CHEMISTRY               ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                 CHEMISTRY      BLOOD GAS...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                        CHEMISTRY19.     ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                   CHEMISTRY28.     Regar...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                            CHEMISTRY33.     *****HBA1c (...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                CHEMISTRY      CALCULATIO...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                        CHEMISTRY50.     ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                 CHEMISTRY57.     ****Ure...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                    CHEMISTRY65.     **Li...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                CHEMISTRY76.     Nature o...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                   CHEMISTRY85.     ***In...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                      CHEMISTRY93.     **...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                          CHEMISTRY98.   ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                       General           ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                            General11.   ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                Hematology               ...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                   Hematology9       ***B...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                              Hematology18     **Skeletal...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                              Hematology28     **In favis...
CLINICAL & CHEMICAL PATHOLOGY MCQ                                                                Hematology35      ****In ...
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
هام  Clinical & chemical pathology mc qs
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هام Clinical & chemical pathology mc qs

  1. 1. Clinical & Chemical Pathology MCQs Classified, Reorganized And Updated To Shawual 1425 With Short Notes By Dr Mohammad A. Emam 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 .................................................................. 64mohammad_emam@hotmail.com 1
  2. 2. CLINICAL & CHEMICAL PATHOLOGY MCQ BODY FLUIDS Body fluids1. **Doctor sending a sample requesting for lecithin 1. (c) Amniotic fluid sample is used to measure spingomyelin ratio what is the sample? lecithin: sphingomyelin ratio (L/S). L/S > 2:1 a. Blood. (or 2.5:1) denotes acceptable lung maturity. b. CSF c. Amniotic fluid. d. Urine2. ***Cytological examination of pleural effusion in a 60 yrs 2. (d) Lung cancer: 75% of malignant pulmonary old man revealed the presence of malignant cells. The effusions are due to 3 causes; lung cancer most likely primary tumor will be: (30%), breast cancer (25%) & lymphoma (20%). a. Lymphoma. Practically, cytological examination only b. Mesothelioma. establishes the presence of malignant effusion, c. Cancer colon. however, in most cases it cannot identify the d. lung cancer. primary site of the tumor. Regarding mesothelioma, it is a rather a rare tumor of the pleura.3. *****Regarding Albustix: 3. (c) Commercial strips for detecting albumin a. Useless if infected urine. (Albustix) use the following formula: b. Gives red color. Tetrabromophenol blue (yellow at 3.0) → c. Not useful if acid is added to urine. shades of green in the presence of protein at the d. Depends on acid precipitation of urinary proteins 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? 4. (c) A reducing substance is the one that reduces a. Glucose. alkaline cupric sulfate to red coprous oxide. b. Galactose. Most important are glucose, lactose, fructose, c. Sucrose. galactoses and pentoses (e.g. ribose, xylose and d. Fructose. arabinose) while sucrose will not reduce alkaline cupric sulfate.5. ***Red urine is due to? 5. b. Rifampicin is a well known drug to cause red a. INH urine. b. Rifampicin c. Pyrizinamide.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? 8. (c) Although also glucose and protein are a. Urea abnormal constituents of urine, yet they b. Glucose normally present in trace amounts below the c. Cholesterol. detection limit of ordinary methods. d. Uric acid e. Protein. mohammad_emam@hotmail.com 2
  3. 3. CLINICAL & CHEMICAL PATHOLOGY MCQ BODY FLUIDS9. ****Calcium in urine stone is present in all of the 9. (b) In 2ry hyperparathyroidism, hypocalcemia following except: due to e.g. chronic renal failure is the cause of a. UTI increased parathormone. Stones due to b. Secondary hyperparathyroidism. 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 Cushings 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: 10. See 7. a. Becomes black. Urine becomes black on standing in cases of b. Urea increases. alkaptonurea (↑homogentesic acid) and c. Urea decreases. methemoglobinurea. d. Creatinine increases11. Myoglobinuria is seen in: 11. Muscle injury (also known as rhabdomyolysis) e.g. in cases of crush injuries and strenuous exercise. mohammad_emam@hotmail.com 3
  4. 4. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY Clinical Chemistry INSTRUMENTATION1. ******Difference between ELISA & RIA is ? 1. (a) Both techniques apply almost the same a. ELISA technique uses an enzyme. methodology, .ELISA technique uses an enzyme b. ELISA is used by bacteriologists while RIA by label and RIA uses radioisotopic label. virologists2. The label in ELISA is? 2. a. Enzyme b. Antibody c. Antigen.3. ***Which of the following not seen in chemistry lab? 3. (d) Electron microscope. a. Analytic balance. b. Centrifuge c. Spectrophotometer d. Electron microscope, e. Turbidimeter.4. **The washing is must in all heterogenous ELISA 4. (b) In ELISA, the first washing is used to techniques because? remove the unbound (free) sample antigen. The a. It remove the excess binding second washing removes unreacted free label b. Increase the specificity (not excess binding in either of the 2 washings) c. Increase the sensitivity. 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? 5. (a) The conjugate is the second antibody a. Conjugate conjugated with the enzyme. b. Microplate c. Buffer.6. **A standard microplate in an ELISA has? 6. (a) 96 wells are present in the microplate (8 a. 96 wells rows x 12 columns).of these, 1 is used for the b. 98 wells blank, 2 for the –ve controls, 2 for the +ve c. 92 wells. 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. 7. (b) According to Beers law, absorbance is The absorbance of 10ml of the same colored solution will proportional to the final concentration (whatever be: the volume is) a. 1.000 b. 0.500 c. 0.2508. a dichromatic analysis is carried to increase: 8. (a) Di- (bi) chromatic photometry measures a. Specificity absorbance of the sample at 2 different b. Linearity wavelengths. This corrects for interfering c. Sensitivity. substances increasing specificity of the method. mohammad_emam@hotmail.com 4
  5. 5. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY BLOOD GASES, PH AND ELECTROLYTES.9. ******PO2 (or gases) is measure in which unit? 9. © mEq/L (mmol in SI) is used for electrolytes a. Mmol e.g. BE, bicarbonate and H+. While mmHg (or b. umol kpa in SI) is used for gases e.g. pCO2 and pO2. c. mmHg11. 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: 12. (c). See 11. a. secrete more H+ in urine. b. Synthesis bicarbonate to ECF c. Both a and b13. **A buffer is made of ? 13. (c) A buffer system is made of a weak acid and a. Strong acid & strong salt its salt with a strong base of a weak base and its b. Strong acid & weak salt salt with a strong acid. c. Weak acid & strong salt d. Weak acid & weak salt.14. ****pH means: 14. Negative log H+ concentration15. ***What is the base: acid ratio at pH 7 for acid of pK6? 15. (d) According to Henderson Hasselbalchs a. 0.01 equation, pH = pK + Log base/acid. By b. 0.1 compensation, Log (base / acid)= 1, thus base: c. 1.0 acid = 10:1.1 d. 10 e. 10016. ***Which is more serious? 16. (c) Critical K+ values are <2.5 or > 6.5 mEq/L a. Glucose 15mmol/l Critical glucose <40mg or >450mg (2.2 & b. pH 7.25 acidosis. 25mmol respectively), c. Potassium 1.5 mmol/l critical pH <7.2 or >2.6 d. Sodium 150 mmol/l critical Na+ <120 or > 160mEq/L17. ******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 mohammad_emam@hotmail.com 5
  6. 6. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY19. H+ homeostasis is altered by; 19. In actively contracting muscle, 8% of the pyruvateNew a. Excessive change of pyruvate to lactate. New 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, ***Main extracellular ions? 20, b. Na is the major ECF cation, Cl is the major ECF21, a. Na & K 21, anion, K is the major ICF cation and proteins22, b. Na & Cl 22, followed by phosphates are the major anions.24, **Main electrolyte in blood is? 24,25, ***Electrolytes in ECF 25,26. a. Na is a major cation 26. 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.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 28. (d) Hypernatremia occurs with: a. Cushing disease * ↓body Na : due to extrarenal water loss or b. Dehydration renal diuresis. c. hypothalamic injury * Normal body Na: due to extrarenal loss e.g. d. All of the above hyperthermia or renal loss e.g. DI. * Na retention e.g. steroids or Na intake.28. Regarding concentration of urine; 28. a. Approximately 80% of the water and NaClNew a. Proximal tubules return 75% of filtered water. New contenet together with glucose, phosphate, and1 b. Distal convoluted tubules deliver 40-60L of fluid to 1 amino acids are reabsorbed in the proximal tubule. collecting tubules / day. About 20% of the tubular fluid enters the loop of c. Osmotic pressure in renal cortex is higher than in medulla. Henle where water is passively aborbed; 6ml per d. ADH acts on all parts of nephrone. minute of concentrated tubular fluid now enters e. Aldosterone increase Na excretion. 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. mohammad_emam@hotmail.com 6
  7. 7. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY28. Regarding excretion of Na+ 28. b. Na+ excretion is influenced byNew a. Not dependent on aldosterone. New mineralocorticoids (mainly aldosterone):↑2 b. Major share of GF osmolarity with associated ions. 2 reabsorption. The GF is isoosmolar with plasma c. It passively diffuses in proximal tubules. i.e. Na is the major electrolyte. 90% of Na is d. In distal tubules it is exchanged for K+ actively (not passively) reabsorbed in the PCT. K e. Coupled with K+ is excreted from DCT in exchange with Na (not the reverse and not coupled with it).28. Regarding buffer systems; 28. b. Acids are substances that tare capable ofNew b. An acid is a substance that releases H+ New donating protons. When a strong acid is added to a3 3 c. Buffering involves change of strong acid to base. 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/dL30. ***About GTT, which is correct according to WHO 30. (c) WHO recommendations for GTT include: 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.31. **With age renal threshold for glucose? 31. (b) With age, the renal ability to reabsorb filtered a. Increased glucose is decreased leading to appearance of b. Decreased glucose in the urine at lower plasma levels. c. Not changed32. **All are inborn error of glycogen metabolism except? 32. (b) Essential fructosuria is due to aldolase B defect a. Essential fructosuria leading to accumulation of fructose-1-P b. Phenyl ketonuria Galactosemia (serious) is due to decreased c. Galactosemia Galactose-6-P uridyl transferase leading to d. Glycogen storage disease decreased glycogen synthesis. Types of glycogen storage diseases (GSD) include: Type I (VonGierkes): ↓ G6P Type II (Pompes): ↓ lysosomal maltase Type III (Coris) : ↓debranching enzyme. Type IV (Andersons): Absent debranching enzyme Type V (McArdles): ↓ muscles phosphorylation. mohammad_emam@hotmail.com 7
  8. 8. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY33. *****HBA1c (Glycosylated hemoglobin) is? 33. (b) GlycHb (RR 4-6%) is formed by non a. Not present in healthy normal individuals. enzymatic attachment of glucose to N-terminal b. ↑ in prolonged sustained hyperglycemia 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 structure35. **Cellulose is not metabolized in humans because of 35. Glucose units in cellulose are combined by absence of which enzyme? 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: 36. c. Xylose is absorbed from proximal small a. Stomach. intestine independent on pancreas.. b. Pancreas. c. Upper small intestine. d. Lower small intestine. e. Large intestine37. ****Von Gerkes disease is caused by deficiency of: 37. (a) See 32. a. Glucose 6 phosphatase b. Glucose 6 phosphate dehydrogenase38. What happens if sucrose is given parentrally: 38. It will be secreted unchanged or metabolized39. ***Which of these is not a ketone body? 39. (c) Ketone bodies are formed by condensation of 2 a. Acetone. acetyl Co A → Acetoacetic acid which gives B b. Acetoacetic acid. hydroxyl butyric acid by reduction or acetone by c. Butyric acid. decarboxylation. d. B-hydroxy butyric acid. Butyric acid is a fatty acid e. None of the above.40. ***In Gauchers disease; 40. (b) Gauchers is a glucosylceramide lipidosis a. Glycoprotein is accumulated. (lysosomal storage disease). It is caused by ↓ b. Glucocerebrosidase is deficient. glucocerebrosidase enzyme leading to accumulation of glucosylceramide → HSM and pigmentation of exposed parts.41. Bile duct obstruction can be diagnosed by: 41. (c) Cholestatic hyperbilirubinemia is characterized a. AST by conjugated hyperbilirubinemia and b. T. Bilirubin hyperbilirubinuria (only the conjugated fraction c. Bilirubin in urine appears in urine). d. Ester bilirubin42. *** Increased jaundice is diagnosis by 42. (a) Estimation of jaundice depends on serum a. T. bilirubin bilirubin, other mentioned tests help to identify the b. AST cause of jaundice. c. ALT d. ALP mohammad_emam@hotmail.com 8
  9. 9. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY CALCULATIONS, QC AND STATISTICS43. **Most of the concentration are calculated using factor, 43. (b) For methods obeying Beers law, slope of the this factor is? calibration curve (Cs/As) provides a constant to a. Std absorbance / std value calculate the unknown concentration. Also b. Std value / std absorbance depending on the formula: c. Std value x std absorbance At x Cs = As x Ct, thus, Ct=(Cs/As)x As44. **Ten microliters are? 44. (d) μL = 10-6L → 10 μL = 10-5L = 0.00001L a. 0.01 L b., 0.001 L c. 0.0001 L d. 0.00001 L e. non of these.45. **How much water should be added to 500ml of a solution 45. (c) Using the formula: of 10% NaOH to bring it to 75%? C1 x V1 = C2 x V2 a. 666ml 10 x 500 = 7.5 x V2 b. 125ml V2 = 666mL c. 166ml Thus, 166 mL of DW should be added. d. 250ml e. 375ml46. When calculated osmolarity can not be accounted as a 46. Calculated osmolarity = 2 X Na + Glu + Urea measurement for osmolarity? (All in mmol/L) a. per 100gm/l When calculated osmolarity is less than b. Urea 20 mm/l 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? 47. (b) Secondary std? a. Primary std A primary Std is a reference standard. b. Secondary std Secondary Std is standardized depending on the c. Tertiary std primary standard. d. Internal std.48. **External QC program means? 48. (b) In EQC, participants receive QC material to a. An external person come & does the QC test be tested inside their labs. Results are sent to b. A QC person goes to another lab & does the test.. 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? 49. (c) QC results follow a Gaussian distribution, a. They are easy to calculate, thus 95% of these results normally fall within b. They cover 97.5% of normal population, ±5% of the mean. Therefore, 2.5 out of 100 c. Patient value rarely go beyond these limits. (1:40) are acceptable to be above +2s and 2.5 our of 100 are acceptable below -2s. mohammad_emam@hotmail.com 9
  10. 10. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY50. Sensitivity and specificity are 50. (b) Sensitivity & specificity can be adjusted a. Directly related. according to cutoff level. Sensitivity can be b. Inversely related. increased by choosing a higher cutoff to include c. They mean the same. 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 51. (b) Carryover is due to contamination by a readings because: previous sample. It is calculated by measuring a a. The analyzer was carried and placed at a different place. high standard and a low standard each 3 times b. The previously measured solution was still in the cuvette then applying the following formula: c. The current solution is overflowing in the cuvette. Carry over = (contaminated low – actual low) / contaminated high – actual high)52. STAT test means: 52. (c) Stat refers to immediate or as initial dose. a. Start at. b. Standardize and test. c. Short turn around time CREATININE, UA, BUN AND AMMONIA53. ***Which of the following result shows renal impairment? 53. (e) A urine osmolarity less than 800 after 12 hrs a. urea 9 mmol of water deprivation denotes renal impairment. b. creatinine 10 mmol/l Urea 9mmol is high normal (n: 2.9-8.2) and is c. urates not a very sensitive measure of GFR. d. cholesterol Creatinine, although a sensitive measure of GF, e. urine osmolarity less than 800 after 12 hrs of water 10umol is normal (n: 53-106) deprivation. Cholesterol and urates are useless in this regard.54. **Low GFR occurs in all except: 54. (b) low GFR occurs with: a. Congestive heart failure. - Hemorrhage. b. Urethral obstruction. - 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: 56. (a) Nephrotic syndrome consists of: a. Hypocholesterolemia. - Heavy proteinuria. b. Hypoalbuminemia. - Hypoalbuminemia. c. Albuminuria. - Oedema. d. Hypertriglyceridemia. - Hypercholesterolemia (Almost always e. None of the above present). Hypertriglyceridemia is present in 50% of cases. mohammad_emam@hotmail.com 10
  11. 11. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY57. ****Ureate excretion by the kidney is inhibited by: 57. (b) Thiazide diuretics cause relatively urate a. Probenecid. retention, glucose intolerance and hypokalemia b. Thiazide diuretics. and interfere with water excretion and may cause hyponatremia. Probenecid is a uricosuric agent like allopurinol.58. Chronic glomerulonephritis is diagnosed by: 58. (d) In chronic glomerulonephritis, there is a. Blood urea. persistent deterioration of renal functions ending b. Creatinine. with renal failure. c. Proteinuria d. All of the above PROTEINS, ELECTROPHORESIS AND LIPIDS59. **The protein having molecular wt less then albumin is? 59. (b) B2-microglobulin has a MW 11,800. a. Beta protein Betalipoprotein is 380,000. b. B2-microglobulin. BJ protein is the light chains of c. Lysozyme. immunoglobulins. Its MW is variable from d. Benze Jones protein. 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? 60. (d) Alpha 1 antitrypsin a. Beta globulin b. Macroglobulin c. Albumin d. Alpha 1 antitrypsin e. Alpha 2 antitrypsin.61. ***Diet rich in phenylalanine should be restricted in? 61. (a) In phenylketonuria, there is ↓ phenylalanine a. Phenyl ketonuria hydroxylase leading to accumulation of b. Tyrosinemia phenylpuruvate and its derivatives and their c. Maple syrup disease excretion in urine. Diet rich in phenylalanine should be restricted to prevent brain damage.62. ***In phenylketonuria, diet should be low in: 62. (a) Phenylalanine (see 61) a. Phenylalanine. b. Carbohydrate. c. Lipids.62. Hypoalbuminemia is associated with all except? 62. (a) Tetanus is clostridial infection caused be C. a. Tetanus tetani has nothing to do with albumin. b. hypocalcaemia c. oedema d. toxic effect of sulfonamide64. **Gluconic amino acids include: 64. (a) Ketogenic amino acids are: Leucine and a. Alanine. lysine, b. Methionine. Mixed amino acids are: Isoleucine, c. Valine. phenylalanine, threonine, tryptophan and d. Glutamic acid. tyrosine. e. All of the above. Gluconic amino acids are all the other amino acids. mohammad_emam@hotmail.com 11
  12. 12. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY65. **Lipoprotein related to hypertension? 65. . LDL66. *****Which is important for atherosclerosis? 66. (b) a. ↑HDL b. ↑LDL c. ↑Chylomicrons.67. ***In plasma protein electrophoresis, the protein that will 67. Albumin. go first is (moves furthest from application)?68. ***Based on behavior of lipoproteins in 68. On electrophoresis; ultracentrifugation pre-B lipoprotein is? Chylomicrons and its remnants stay at the a. HDL origin. b. LDL. VLDL at preβ (=α2 globulin region) c. VLDL IDL at broad β d. Chylomicron LDL at β (= β globulin region) HDL at α (= α1 globulin region)/69. **All of the following are lipoproteins except? 69. (d) Although phospholipids are not lipoproteins, a. Phospholipid they are ingredients of lipoproteins, conferring b. VLDL the hydrophilic properties. d. Sphingomylin e. LDL f. HDL70. What is the proposition of pulmonary surfactant? 70. (b) Dipalmityl lecithin (a lecithin phospholipid a. Phospholipid acid with 2 palmetic acid residues) is the chemical b. Dipalmityl lecithin composition of pulmonary surfactant. c. Phosphatidyl choline,71. **HDL is good cholesterol because? 71. (a) HDL is composed of 20% cholesterol, 30% a. It has more protein & phospholipids in it phospholipids and 50% proteins. b. It has no cholesterol in it,. c. It has less TG in it.72. ***Which lipoprotein has highest concentration of 72. (b) VLDL are the TG rich lipoproteins cholesterol? HDL has 20% cholesterol. a. VLDL IDL has cholesterol and TG in equal amounts. b. LDL LDL is the richest lipoprotein in cholesterol c. IDL esters. d. HDL74. ****Which is not associated with abetalipoproteinemia: 74. (b) Hereditary spherocytosis is due to spectrin a. Acanthocytes in the peripheral blood. deficiency. b. Hereditary spherocytosis. Abetalipoproteinemia is a lipoprotein c. Malabsorption and fatty stools 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: 75. (a) Chylomicrons dont confer an excess a. Can cause thrombosis. cardiovascular risk, however, in LpL deficiency b. Cannot cause thrombosis. and apoC II deficiency, the patient presents with lipemia retinalis and retinal vein thrombosis. mohammad_emam@hotmail.com 12
  13. 13. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY76. Nature of apoproteins. 76. 5 major classes of proteins A to E77. Saturated vs unsaturated fats (nutritional value) 77. Saturated Unsaturated e.g. Oleic a (50% of Linoleic a body fat) Linolenic a Palmitic a (25% (both are of body fat) Essential) Stearic a (5% of Arachidonic a. body fat) Acetic a. Butyric 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 Double bonds bonds78. Which is best for parentral alimentation? 78. (b) Parentral nutrition is composed essentially a. FFA. 79. of: b. AA a) Nitrogen source: synthetic valuable amino c. lipoproteins 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 origin82. Treatment of familial hypercholesterolemia. 82. These include general management of hypercholesterolemia + cholesterol lowering drugs + oestrogen replacement in postmenopausal women. CLINICAL ENZYMOLOGY83. ***The better for diagnosis of acute pancreatitis is? 83. (b) Lipase elevation is of a greater magnitude (2- a. Amylase 10 xN) and duration than amylase in acute b. Lipase pancreatitis. When lipase method is optimized, c. ALP the test is more sensitive and specific than d. ACP amylase for detection of acute pancreatitis.84. **Activities of some enzyme increased in some disease 84. (b) That’s why enzymes are measured for the conditions because they are? most part by their activity rather than a. Non functional enzymes concentration. b. Functional enzymes c. Neither mohammad_emam@hotmail.com 13
  14. 14. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY85. ***In MI, which is the last enzyme to be raised and lasts 85. (d) long? Onset (h) Peak (h) Duration a. CK (d) CK 6-12 20-30 2-6 b. CK-MB. CK-MB 3-10 12-24 1.5-3 c. AST. AST 6-12 20-30 2-6 d. LDH LDH 6-12 24-72 7-1486. **Isoenzymes: 86. © Isoenzymes have the same catalytic activities a. Are physical types of one enzyme. and differ in physicochemical properties. b. Have different electrophoretic mobility. c. All of the above87. **MI is diagnosed by: 87. (a) CK-MB is specific for cardiac muscle, CK- a. CKMB BB for brain and CK-MM for skeletal muscle. b. CKBB c. CKMM d. LDH88. **Elevation of LDH is caused by: 88. (d) LDH is present in the cells of the heart, liver, a. Myocardial disease muscles, blood and malignancies. b. Liver disease c. Prostatic disease d. many organ disease because it has many distribution89. ****Myoglobin ↑ in injury of: 89. (a) muscle whether cardiac or skeletal is the a. muscle. source of myoglobin. b. Liver CLINICAL ENCOCRINOLOGY90. *****ADH is? 90. (b) ADH is produced by the hypothalamus and a. Produced by posterior pituitary stored and secreted from the posterior pituitary. b. Produced in the hypothalamus.91. **The method used to estimating insulin is? 91. (d) Immunoassay (multiple labels) is used for a. Electrophoresis the measurement of insulin. b. Kinetic estimation. c. Spectrophotometer. d. Radioimmuno assay.92. *****After the insulin dose, the patient soon comatozed 92. (b) Hypoglycemia (glucose <3mmol/l) due to a. Hyperglycemia b. Hypoglycemia (glucose <3mmol/l) c. ketonuria c. Ketoacidosis is the cause of coma d. Lactic acidosis, mohammad_emam@hotmail.com 14
  15. 15. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY93. **While using the pregnancy test we are measuring? 93. (b) α subunit of HCG is very similar to α a. B-HCG subunit of TSH and FSH and identical to LH. b. Total HCG Although β subunits of HCG and LH are very c. B-HCG & LH similar, antibodies can be made to the β subunit d. B-HCG & FSH. 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: 94. (b) Water intake is restricted the patient loses 3- a. Anterior pituitary disease. 5% of body weight or until 3 consecutive hourly b. Posterior pituitary disease. determination of urine osmolarity are within c. Hypothyroidism. 10% of each other. Measure urine osmolality, plasma vasopressin and increased urine osmolality with exogenous vasopressin. Urine Pl. VP After VP osmol Normal >800 >2 ↑ DI <300 Undetectab ↑ le Nephrogeni <300 >5 No change c DI95. ****24 hours urine for VMA is used for diagnosis of 95. (b) Catecholamines are oxidized to VMA and diseases of: metanephrins. 24hour urinary metanephrins is a. Adrenal cortex. the best single test for pheochromocytoma. b. Adrenal medulla Specificity and sensitivity approach 100% when both VMA and metanephrines are measured.96. ***Hypertension is found in all of the following endocrinal 96. (d) Hypertension secondary to endocrinal causes diseases except: occurs in: a. Cushings syndrome. - Pheochromocytoma. b. Pheochromocytoma. - Crohns syndrome c. Adrenal medulla hyperplasia. - Cushings syndrome. d. Addissons disease. Addison is associated with hypos (hypotension, hypokalemia, hyponatremia and hypocortisol)97. Diabetic coma presents with: 97. All. a. Ketone bodies in urine In diabetes, 2 types of coma may occur, DKA b. Blood glucose may be 1000mg or more and nonDKA. Glucose levels in nonDKA are c. osmotic diuresis present 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 98. (a) different antibodies. 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. mohammad_emam@hotmail.com 15
  16. 16. CLINICAL & CHEMICAL PATHOLOGY MCQ CHEMISTRY98. Carcinoid tumors secrete 98. 5HIAA.New New 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. mohammad_emam@hotmail.com 16
  17. 17. CLINICAL & CHEMICAL PATHOLOGY MCQ General General1. ****The difference between plasma and serum is that 1. (a) Plasma contains fibrinogen which is plasma: consumed during the clot formation to separate a. Contains fibrinogen. serum. b. Doesn’t contain fibrinogen. c. Has more water. d. Has less water.2. ******Best way to separate the serum? 2. (a) leave the blood to clot at R.T for I hr, then a. leave the blood to clot at R.T for I hr, then centrifuge centrifuge b. by adding citrate. c. by adding EDTA3. **Point of care testing means? 3. (c) Take care in testing a. Complete a test & make a point[interpret], b. Testing the patient at bed side c. Take care in testing4. ****Error in the result is expected in which case? 4. (c) Oxalate is a divalent cation chelator. a. Glucose on fluoride. b. Glucose on EDTA c. Calcium on oxalate5. **Cardiac anatomical anomalies associated with Fallot 5. (b) Fallots tetralogy is composed of PS+VSD + tetralogy include all of the following except: Rt aorta + RVH. a. VSD b. ASD6. Hemolysed blood is unsuitable for performing which 6. Hemolysis is visible at Hb> 3.1 μmol/L tests? 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? 7. a. a. Increased serum K b. Increased serum Na c. Increased HCO3- d. Decreased K8. After hemolysis: 8. a. Sodium leaks out of RBCs. b. K leaks into cells. c. Bicarbonate gets into RBCs.9. Effects of fasting 9. Prolonged fasting increase TG, glycerol, FFA but not cholesterol.10. ****Fluoride is used to get samples for? 10. a. Blood sugar a. Blood sugar b. Coagulation c. Electrolyte d. CBC. mohammad_emam@hotmail.com 17
  18. 18. CLINICAL & CHEMICAL PATHOLOGY MCQ General11. ***Anticoagulant used for glucose is: 11. Fluoride12. **Changes in blood stored more than 5 hrs at room temp. 13. (a) Storage of blood has the following effects: include? 1- ↓CO2, ACP & Glucose a. Decreased glucose & increased lactate. 2- ↑pH & ammonia b. Increased glucose & decreased lactate 3- Changes in RBC permeability →↑K,P &Mg c. Failure of Na & K pump, 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 14. a. Continued glycolysis cause glucose values to estimation of glucose because: decreases with time unless cells are separated. a. The glucose values decreases with time. b. Glucose value increases with time. c. Lysis of blood occurs.  Best place to put a needle for blood collection is puncture proof container. mohammad_emam@hotmail.com 18
  19. 19. CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology Hematology BASIC HEMATOLOGY CONCEPTS / LABORATORY PROCEDURES1 ** To stain the B/M other than Wright stain which stain 1 (c) Bone marrow films should be stained with usually used? an iron stain e.g. Perls, Prussian blue, as a a. PAS stain routine to demonstrate iron (Dacie) b. Sudan black stain c. stain for iron.2 ***In addition to routine Romanowsky stain of bone 2 (b).Prussian blue: See 1 marrow the following stain is also essential: a. Chloroacetate estrase b. Prussian blue.3 The needle used for bone marrow biopsy is? 3 (b) Jamshedi trephine is used for biopsy. a. 18 gauge needle b. Jamshedi needle c. Menghini needle d. Westermani needle,4 **Hyperplastic B.M with M/E ratio 6:1 is seen in: 4 (c) Hyperplasia is diagnosed when fat>cells. In a. Megaloblastic hyperplasia. hyperplastic BM, an M/E ratio > 2:1 denotes b. Normoblastic hyperplasia myeloid hyperplasia and <2:1 denotes erythroid c. Lymphoid hyperplasia hyperplasia.5 **Best method to assess BM cellularity is: 5 (a) Trephine biopsy is preferred over bone a. Trephine biopsy marrow aspiration in that it demonstrates the b. M:E ratio is enough. architecture of the bone marrow cellularity. c. By high power.6 ***Which Hbs have the same electrophoretic mobility on 6 HbS, C, D and Hb Punjab (also Hb lepore) occur alkaline cellulose acetate? at the same position on cellulose acetate at pH8.6 . Also Hb C, E and C harlum occur at the position of Hb A27 Lymphokines & T-cell activation 7 Lymphocytosis promoting factor and histamine sensitizing factor.8 ******When using and electronic cell coulter counter, 8 (d) A high titer of cold agglutinin cause falsely which of the following results can occur in the presence of ↑MCV, MCH and MCHC and falsely ↓ RBC cold agglutinins: count. a. ↑MCV & ↓MCHC To correct, incubate at 37°c for 15-30 minutes b. ↓MCV & ↓MCHC and rerun the specimen. c. ↓MCV & ↑MCHC d. ↑MCV & ↑MCHC e. ↑MCV & decreased RBC f. ↑MCV & normal RBC h. ↓MCV and RBC mohammad_emam@hotmail.com 19
  20. 20. CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology9 ***Bone marrow aspiration needles: 9 a. 18 gauge. a. 18 gauge. b. Meninghi. c. Burtolin10 **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 11 (d) using the correction formula : leucocytes, so corrected leucocytic count equals: Corrected WBC= WBC X 100 / (NRBC+100) a. 11.5 x 109/L Corrected WBC= 22.5 X 100 / (200 + 100 ) b. 22.3 x 109/L = 7.5 x 109/L c. 22.7 x 109/L d. 7.5 x 109/L12 ****The main antioxidant in RBCs is: 12 b. Reduced glutathione acts as antioxidant a. NADPH through its SH group. b. Reduced glutathione13 ***Newborn with MCV 100fl, is considered. 13 b. MCV in the first week is normally 108fl. a. Macrocytosis. After 2 months, it is 96fl. b. Normal14 **Perls stain 14 BM iron stores14. Hemoglobin breakdown takes place in: 14. a. Normally 6gm of Hb is broken down per dayNew a. RES New into; b. Hepatocytes. - Globin peptides: hydrolysed and the amino c. Renal tubules. 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 ANEMIAS15 ***In Pyruvate Kinase deficiency all correct except? 15 (a) PKA is an autosomal recessive a. Intermittent attach of anemia. enzymopathy. O2 dissociation curve is shifted to b. Splenectomy is a choice of treatment. the right, so only mild symptoms occur. c. Autosomal recessive. Splenectomy improves the condition.16 **In A sickle cell disease patient under general anesthesia, 16 Tourniquet should not be avoided. all true except? 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. mohammad_emam@hotmail.com 20
  21. 21. CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology18 **Skeletal abnormality present in? 18 Fanconi syndrome. Fanconi syndrome consists of: - Congenital aplastic anemia. - Skeletal and urinary tract anomalies. - Microcephaly. - Altered skin pigmentation.19 Fanconis anemia 1920 ***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 glutathione21 **Sideroblastic.a seen in all except? 21 (c) Sideroblastosis occurs due to; a. Lead poisoning - Lead poisoning due to inhibition of enzyme of b. Alcohol heme and globin synthesis. c. Aspirin - Alcoholism, due to interference with heme and d. Chloramphenicol 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 22 a. Aspirin. is: a. Aspirin. b. Lead.23 **In HUS, all are true except: 23 (e) HUS occurs in children following VTEC a. occurs mainly in children. enteritis (also after salmonella, shigella, b. Is usually preceded by some sort of enteritis. streptococcal infection, as an autoimmune c. Fragmented RBCs are seen. disease and following drugs e.g. cycloserine. It d. Uremia is usual. is charectarized by: e. Anti IgG is positive in 10% of cases. - Thrombosis in small vessels. - Fragmentation of RBCs. - Reduced platelets (consumptive). - Uremia.24 In HUS, all are present except: 24 d. Thrombocytosis a. ARF b. ↓ platelets. c. Microangiopathic HA d. Thrombocytosis25 HUS 2526 **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) mohammad_emam@hotmail.com 21
  22. 22. CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology28 **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: 29 c. Hereditary spherocytosis is an autosomal a. Autosomal dominant. dominant membrane defect (anykrin) not due to b. Treated by splenectomy. a defect is in hemoglobinization of RBCs. Parts c. Defect is in hemoglobinization of RBCs 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 Splenectomy31 **In sickle cell anemia patient with iron overload, this 31 (c) Yersina enterocolitica occurs in iron organism is isolated from blood: overloaded patients treated with desferrioxamine a. Salmonella. (see p376 Kumar) b. Strept pneumoniae c. yersinia enterocolitica.32 ***Thalassemia major with iron overload this organism 32 (c). can be isolated. a. Streptococcus pneumoniae. b. Salmonella typhemureum c. Yersina enterocolitica.33 *****Microangiopathic hemolytic anemia is present in all 33 (b) In MAHA there is intravascular hemolysis except: and fragmentation of the RBCs due to abnormal a. TTP microcirculation leading to fibrin deposition, b. Meningococcal septicaemia. platelet deposition and vasculitis e.g in; c. HUS - 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: 34 (b) LD1&2 are characteristically increased in a. Total ACP HA. ACP although is present in high b. LDH concentration inside RBCs (tartarate resistant) is c. ALP not characteristically increased. mohammad_emam@hotmail.com 22
  23. 23. CLINICAL & CHEMICAL PATHOLOGY MCQ Hematology35 ****In G6PD deficiency avoid all the following drugs 35 (e) Agents causing HA in G6PD deficiency except: include: a. Salicylic acid - Antimalareals e.g. primaquine. b. Primaquine. - Sulphonamides and Sulphones (dapsone). c. Dapsone. - Analgesics e.g. salicylic acid d. Trimethoprim. - Antihelmenthics e.g. niridazol. e. Folic acid - Miscellaneous e.g. vitamin K analogues, probanecid.36 ***A patient with hemolytic anemia has all the following 36 (c) In hemolytic anemia there is; exept: - Hyperbilirubinemia and hemiglubinuria. a. Bilirubinemia. - ↑urobilinogen and stercobilinogen→ dark b. Dark urine. urine. c. Hypertension. - ↓ 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 <1%blasts <5%blasts anemia RA with <1%blasts <5%blasts sideroblasts RA with excess >5% 20-30% blasts (RAEB) CMML ↑monocytes ↑promonocytes39 **Manifestations of HbSS 39 (b) Infarction of phalanges. a. Ischemia to femoral artery. b. Infarction of phalanges.41 ****Major adult Hb is 41 HbA (97%) HbA2 (2.5%) and HbF (0.5%)41. Which is true regarding DAT b. DAT involves testing patients cells withoutNew a. It is positive in all IHA. prior exposure to antibody in vitro. For b. may detect complement attached to RBCs. 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 patients 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. mohammad_emam@hotmail.com 23

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