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Usmle Rx Qbank 2017 Step 1 Hematology

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Usmle Rx Qbank 2017 Step 1 Hematology Item: 1 of 15 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 3890 ..L a r Previous Next Lab~lu es Notes Calculat o r • 1 • A 29-year-old female is pregnant with a boy. She was diagnosed with a bleeding disorder when she was a teenager and has recurrent gum bleeding IA•A] . 2 when brushing her teeth. She has anemia secondary to severe menorrhagia. The patient's mother and grandmother h ave had similar problems, but the patent's father has no history of any bleeding disorder. The father of the baby boy has no history of any bleeding disorder either. Laboratory tests • 3 show a platelet count of 250,000/ mm•, increa sed bleeding time and partial thromboplastin time, but normal prothrombin time. · 4 • 5 What Is the probability that the unborn boy will inherit the disease? • 6 : A. 0% . 7 · 8 B. 25% . 9 c. 50% • 10 o. 67% • 11 E. 100% • 12 • 13 • 14 • 15 a s 8 Lock Suspend End Block Item: 1 of 15 ~ . I • M k <:] t> al ~· ~ QIO: 3890 .l. ar Previous Next lab 'Vfl1ues Notes Calculator 1 . 2 The correct a nswer is c. 6 1% chose this. • 3 The pregnant woman's history is consistent with von Willebrand disea se (vWD), an autosomal dominant coagulation disorder characterized by mucocutaneous bleeding and often menorrhagia in women. Von Willebrand factor (vWF) is involved in platelet aggregation and is a carrier protein for . 4 factor VIII. Thus, a lack of vW F increa ses the partial thromboplastin time and the bleeding time, wherea s platelet count and prothrombin time remain • 5 normal. We know that the patient is heterozygous for vWD because there was only a history of the bleeding disorder on her mother's side of the family. Because • 6 she has one defective allele and one normal allele, there is a 50% chance that she may pass the defective allele her offspring. Since the father does not . 7 manifest the disea se, he will not pass on a defective allele. Therefore, 50% of the offspring will have 1 defective allele and since it is an autosomal dominant trait, the bleeding disorder will be passed to 50% of her children . • 8 Von Willebrand disease Von Willebrand factor Menorrhagia Prothrombin time Dominance (genetics) Allele Factor VIII Partial thromboplastin time Heterozygous • 9 Platelet Thrombin Autosome Protein Coagulation Coagulopathy Bleeding time Platelet aggregation Mucocutaneous zone • 10 A is not correct. 11% chose this. · 11 There is a 50% chance the unborn child will have the disea se, not 0% . • 12 B is not correct. 13 % chose this • There is a 50% chance the unborn child will have the disea se, not 25% . • 13 D is not correct. 1% chose this • • 14 There is a 50% chance the unborn child will have the disea se, not 67% . • 15 E is not correct. 14 % chose this. There is a 50% chance the unborn child will have the disea se, not 100% . Botto m Line: Von Willebrand disea se is an autosomal dominant bleeding disorder. The chance of a person contracting an autosomal-dominant disorder that only one parent manifests is 50%, assuming the parent with the defective trait is heterozygous for that tra it. Von Willebrand disease Dominance (genetics) Heterozygous Autosome Coagulopathy Genetic disorder 6 s 0 lock Suspend End Block Item: 1 of 15 ~ . I • M k <:] t> al ~· ~ QIO: 3890 .l. ar Previous Next lab 'Vfl1ues Notes Calculator 1 Bottom Line: . 2 Von Willebrand disease is an autosomal dominant bleeding disorder. The chance of a person contracting an autosomal-dominant disorder that only one • 3 parent manifests is 50%, assuming the parent with the defective trait is heterozygous for that trait. Von Willebrand disease Dominance (genetics) Heterozygous Autosome Coagulopathy Genetic disorder . 4 • 5 • 6 lijl;fiiJI•l toryear:[2017 • ] . 7 FI RST AI D FA CTS • 8 • 9 FA17 p 55.1 Modes of inheritance • 10 Autosomal dominant Often due to defects in structural genes. Many Often pleiotropic (multiple apparently unrelated · 11 generations, both males and females are effects) and variably expressive (different • 12 affected. between individuals). Family history crucial • 13 to diagnosis. With one affected (heterozygous) • 14 parent, on average, Y2 of children affected . • 15 Autosomal recessive Often due to enzyme deficiencies. Usual ly seen Commonly more severe than dominant disorders; in only I generation. patients often present in childhood. t risk in consanguineous famili es. '"'ith 2 ca rrier (heterozygous) parents, on average: !4 of ch il dren wi ll be affected (homozygous), 1/., nf roh ilrlrfHl u ;ill h P 1"'•3t"I";Dt"C "l nrl It;. nr ,..h ;)rlrP I"\ 6 s 0 lock Suspend End Block Item: 1 of 15 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 3890 ..L a r Previous Next Lab~lu es Notes Calculat o r 1 p p } p) ••• shows "ragged red fibers" (due to accumulation . 2 of diseased mitochondria). • 3 0 = unaffected male; • = affected male; 0 = unaffected female; e = affected female. · 4 • 5 FA17p 406.1 • 6 Mixed platelet and coagulation disorders . 7 DISORDER PC BT PT PIT MECHANISM AND COMMENTS · 8 von Willebrand t -It Intrinsic pathway coaguJation defect: l v\VF . 9 disease - t PTf (v\VF acts to carry/protect factor • 10 VIII). in platelet plug formation: l v\VF • 11 Defect - defect in platelet-to-v\VF' adhesion . • 12 utosomal dominant. ~ Tild but most common • 13 inherited bleeding disorder. No platelet • 14 aggregation with ristocetin cofactor assay . • 15 Treatment: desmopressin, which releases ,,Wf stored in endothelium. Disseminated t t t Widespread activation of clotting - deli eiency intravascular in clotting fa ctors - bleeding stale. coagulation Causes: Sepsis (gram 8 ), Trauma, Obstetric com pi ications, acute Pancreatitis, \lalignancy, J\'ephrotic syndrome, Transfusion (STOP ~ l aking ~ ew T hrombi). a s 8 Lock Suspend End Block Item: 1 of 15 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 3890 ..L a r Previous Next Lab~lu es Notes Calculat o r 1 .... defect in platelet-to-vWF' adhesion. • • 2 Au tosomal dominant. ~ !ild but most common • 3 inherited bleeding disorder. 'o platelet aggrega ti on with ri stocetin cofactor assay. · 4 Treatment: desmopressin, which releases • 5 ' WF' stored in endothelium . • 6 Disseminated t t t Widespread acti\'ation of clotting .... defi ciency . 7 intravascular in clott ing factors .... bleeding slate. · 8 coagulation Causes: Sepsis (gram 8), Trauma, Obstetric . 9 complications, acute Pancreatitis, phrotic syndrome, • 10 \lalignancy, :\'c Transfusion (STOP ~laking :-.. ew T hrombi). • 11 Labs: schistocrtes, t fibrin degradation • 12 products (o-dimers), ~ fi brinogen, ~ factors • 13 and VII I. • 14 • 15 FA17 p 56.1 Autosomal dominant Achondroplasia, autosomal dominant polycystic kidney disease, fam ilial adenomatous polyposis, diseases familial hypercholesterolemia, heredi tary hemorrhagic telangiectasia, heredita ry spherOC) tosis, Huntington disease, Li-F'raumeni S) ndrome, Jvlarfan syndrome, multiple endocrine neoplasias, neurofibromatosis type l (von Recklinghausen disease), neurofibromatosis type 2, tuberous sclerosis, \'On Hippel-Lindau disease. a s 8 Lock Suspend End Block Item: 2 of 15 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 3190 ..L a r Previous Next Lab~lu es Notes Calculat o r 1 • A 16-year-old girl visits her physician for a routine check-up. She has mild pharyngitis on physical examination, as well as tender axillary . 2 lymphadenopathy. She reports increased tiredness while at school for the past 3 weeks. A complete blood count shows the following: • 3 Hemoglobin: 13.0 g/dl Hematocrit: 41% · 4 Mean corpuscular volume: 88 fl • 5 Platelet count: 300,000/ mm• WBC count: 9000/ mm• • 6 A rapid streptococcus test is negative. However, reactive heterophile antibodies that agglutinate horse red blood cells are found in the patient's serum. The . 7 physician also not1ces that large lymphocytes with prominent nucleoli are present In the patient's b shownlood, as in the image. · 8 . 9 • 10 • 11 • 12 • 13 • 14 • 15 a s 8 Lock Suspend End Block • 5 • 6 . 7 · 8 . 9 • 10 • 11 • 12 The virus that causes the infection described above is associated with what other disease? • 13 : • 14 A. Acute glomerulonephritis • 15 B. Cervical carcinoma C. MALT lymphoma D. Nasopharyngeal carcinoma E. Rheumatic heart disease a s 8 Lock Suspend End Block Item: 2 of 15 ~ . I • M k <:] t> al ~· ~ QIO: 3190 .l. ar Previous Next lab'Vfllues Notes Calculator 1 The correct a nswer is D. 64% chose this. 2 This patient appea rs to be suffering from infectious mononucleosis, most commonly caused by Epstein-Ba rr virus ( EBV). It is characterized classically by fever; malaise, pharyngitis, hepatosplenomegaly, and lymphadenopathy. The peripheral smea r shown in the vignette image indicates atypical lymphocytes • 3 (abnormal circulating cytotoxic T lymphocytes). It is diagnosed by the Monospot test, wherein heterophil antibodies are detected by agglutination of . 4 sheep or horse RBCs. It is transmitted by personal contact, typically through saliva , hence its name "the kissing disea se." EBV infection can be complicated by splenic rupture, and patients should be counseled to avoid contact sports until splenomegaly resolves. EBV infection is associated with • 5 nasopharyngea l carcinoma, which manifests with nasal obstruction with epistaxis, neck mass from metastasis, and hea dache from cranial nerve involvement, typically in an Asian male. EBV infection is also associated with CNS lymphoma and Hodgkin lymphoma . • 6 Infectious mononucleosis Nosebleed Epstein-Barr virus Splenic injury Nasopharynx cancer Splenomegaly Pharyngitis lymphadenopathy Hepatosplenomegaly . 7 lymphocyte Malaise Metastasis Antibody T cell Virus Cranial nerves Headache lymphoma Saliva Central nervous system Hodgkin's lymphoma Spleen • 8 Cytotoxicity Cytotoxic T cell Primary central nervous system lymphoma Carcinoma Pharynx Nasopharynx Infection Fever • 9 A is not correct. 7% chose this • Infectious mononucelosis is not associated with acute glomerulonephritis. Poststreptococcal glomerulonephritis ( PSGN ) is a common acute • 10 glomerulonephritis that occurs after infection with group A streptococcus, most typically a skin infection.
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