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USMLE World Q Bank > Hematology > Flashcards

Hematology Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the physiology of CO poisoning?

A

Competitive binding of the heme by CO with higher affinity than O2.

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2
Q

Which drug blocks platelet receptors?

A

Abciximab

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3
Q

Try to name some of the proteins involved in Paroxysmal Nocturnal Hemoglobinuria.

A

PIGA -> GPI which is an anchor for DAF(CD55) and CD59. It can lead to myelodysplastic syndrome.

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4
Q

Excessive exposure of the blood to tissue factor can cause…

A

DIC. (ie. abruption placentae)

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5
Q

Describe the pathophysiology of HUS.

A

Post-infectious endothelium affected by Shiga-like toxin causes microthrombi which then hemolyse RBCs. Normal PT/PTT but high bleeding time.

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6
Q

What electrolyte imbalance can be seen after massive blood transfusion?

A

Citrate anticoagulants can chelate Ca++ so we will see a hypocalcemia.

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7
Q

How do tumor cells become resistant to multiple drugs?

A

They can express the MDR1 gene. A transmembrane ATP-dependent transporter.

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8
Q

What can be given to treat a heparin overdose? Coumadin overdose.

A

Protamine Sulfate binds heparin (low MW hep is not bound as well). Vitamin K (long term) or transfusion (short term) of plasma can reverse Coumadin.

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9
Q

What condition is caused by a (t9;22) translocation? What is the pathophysiology?

A

Chronic Myeloid Leukemia caused by the formation of a new oncogene, BCR-ABL. Tx: Imatinib

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10
Q

Which hemoglobin subunit is most similar to myoglobin?

A

Beta. They both have much higher affinity for O2 than hemoglobin itself.

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11
Q

What does a t(15:17) translocation cause?

A

M3 variant of AML. Immature myeloid precursors do not differentiate. PML/RARalpha fusion protein serves as a retinoic acid receptor.

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12
Q

What is the major difference between an acute and a chronic leukemia on a blood smear?

A

Acute = Immature cells, Chronic = Mature cells

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13
Q

What is the major difference between Acute Myelogenous Leukemia and Acute Lymphoblastic Leukemia on a blood smear?

A

The presence of Auer bodies in the cell cytoplasm of AML.

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14
Q

Describe the pathophysiology of myelofibrosis. What is the mutation that causes primary?

A

Myeloproliferation, particularly of megakaryocytes, releases fibroblast growth factor and causes fibrosis of the bone marrow. This causes hepatosplenomegaly and tear-drop RBCs. Primary myelofibrosis is due to a JAK2 V617F mutation that activates the JAK-STAT pathway.

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15
Q

Describe the PI3K/Akt/mTOR signaling pathway.

A

Tyrosine kinases activate PI3K which converts PIP2 to PIP3. PIP3 activates Akt which activates mTOR which goes to the nucleus and promotes proliferation. PTEN converts PIP3 back to PIP2 so it is an inhibitor.

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16
Q

Describe the metabolism of heme into bilirubin.

A

In the reticuloendothelial system heme is converted to biliverdin by heme oxygenase. Biliverdin is converted to bilirubin by bilverdin reductase.

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17
Q

Which drug is used to prevent DVTs in preganacy?

A

Heparin (Warfarin is teratogenic)

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18
Q

What are the complications of Anti-phospholipid antibody syndrome?

A

Seen on SLE, it causes venous thromboembolism, arterial thromboembolism or recurrent miscarriages.

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19
Q

Why should patients with an IgA deficiency not be transfused?

A

The patient’s blood may contain some anti-IgA Ab and this will lead to shock from the small amount of IgA that may be present on the transfusion.

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20
Q

What is methemoglobinemia and how can it be treated?

A

When hemoglobin carries ferric (3+) Fe instead of ferrous (2+). Use METHElyne blue to reduce the iron.

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21
Q

What is 2,3-bisphosphoglycerate?

A

It is a molecule on RBCs that bind the beta hemoglobin and replaces the Oxygen. Therefore it promotes the release of O2 from hemoglobin.

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22
Q

Conversion of homocysteine to cystathione requires which vitamin as a cofactor?

A

B6

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23
Q

Conversion of homocysteine to methionine requires which vitamin as a cofactor?

A

B12 and Folate. That’s why b12 def leads to homocysteinemia.

24
Q

What hematology disease are patients with trisomy 21 more likely to have?

A

ALL

25
Q

What is the presentation of Wiskoff-Aldrich syndrome?

A

Eczema, recurrent respiratory infections thrombocytopenia. With small abnormal platelets. Caused by an X chromosome mutation and seen on 6 month old boys. Deficiency of B and T lymphocytes.

26
Q

Describe multiple myeloma. Etiology, Symptoms, Bone, Labs, and other organs.

A

B cells become IgG secreting plasma cells. Can lead to lytic bone lesions, anemia, and AL Amyloidosis resulting in renal failure.

27
Q

What is the most helpful test in diagnosing hereditary spherocytosis?

A

Increased Mean Corposcular Hemoglobin Concentration (MCHC) indicating membrane loos and RBC dehydration.

28
Q

What do Auer Rods stain for?

A

Peroxidase

29
Q

Which hematologic malignant cells stain for Tartrate Resistant Acid Phosphatase?

A

Hairy Cell Leukemia B Cells.

30
Q

What are the size ranges for the different collections of extravasated blood?

A

Petechiae ( 1cm)

31
Q

Which two arachidonic acid derivatives oppose each other? What exactly do they do?

A

Thromboxane A2 decreases blood flow and increases aggregation.
Prostacyclin (or Prostaglandin I2) increases blood flow and decreases aggregation.

32
Q

What is the mechanism of action of Clopidogrel and what is it used for?

A

Blocks platelet ADP receptors. Used in conjunction or in lieu of aspirin.

33
Q

Which malignancy is characterized by Reed-Sternberg cells?

A

Hodgkin Lymphoma, associated with EBV.

34
Q

What is the treatment for an episode of Acute Intermittent Porphyria?

A

Glucose and Heme given IV inhibit ALA Synthase. ALA Synthase creates Aminolevulinic Acid which is part of the Heme synthesis pathway but it is toxic. ALA build up due to the downstream inhibition of Porphobilinogen Deaminase.

35
Q

What is the inheritance pattern of G6PD deficiency?

A

X-Linked Recessive

36
Q

What is the drug therapy for Sickle Cell anemia? How does it work?

A

Hydroxyurea increases HbF (Fetal hemoglobin) production. This drug is also used because it inhibits DNA production in S phase.

37
Q

What what is the path physiology of Nitrite poisoning?

A

Hemoglobin to Methemoglobin

38
Q

What are prolonged PTT and Bleeding time indicative of?

A

vWF deficiency

39
Q

What drug targets CD20?

A

Rituximab

40
Q

For what is painless waxing and waning lymphadenopathy pathomnemonic?

A

Follicular Lymphoma. translocation of Ig heavy chain and bcd-2. t(14:18)

41
Q

What is the mechanism of action of Cromolyn Sodium? What is it used for?

A

Inhibits mast cell degranulation. Used for asthma prophylaxis.

42
Q

What can be used to unequivocally determine whether a lymph node enlargement is due to reactive lymphadenopathy or a lymphoma?

A

All reactive lymph node enlargements are polyclonal while the lymphoma are generally monoclonal. Monoclonal means that only one of the many possible DNA recombinations for Ig or TCR is present.

43
Q

What is the treatment of vonWillebrand Disease? How does it work?

A

Desmopressin analog (DDAVP) increases the release of vWF from the endothelial cells.

44
Q

A 14 month old baby with megaloblastic anemia and elevated Orotic Acid in the serum should be treated with…

A

Uridine. This is due to a Orotate Phosphoribosyl transferase which is part of the Pyrimidine synthesis pathway. Also presents with growth retardation and neurologic abnormalities.

45
Q

What is the mechanism of action of Coumadin (Warfarin)?

A

It inhibits Vitamin K dependent Carboxylation of glutamic acid residues on Factors 10, 9, 7 and 2.

46
Q

What is a common presentation of Sickle Cell in really young patients? (<1 year)

A

Painful swelling of the hands and feet due to vasoocclusive syndrome of the bone marrow.

47
Q

What is the mechanism of action of Dipyridamole and Cilostazol? What are they use for?

A

Phosphodiesterase III inhibitors that act on the platelets to increase cGMP and thus decrease aggregation and vasodilate. They are better than aspirin. Used for Claudication, CAD and stroke prevention.

48
Q

What is the treatment for Heparin Induced Thrombocytopenia?

A

Argatroban. A direct thrombin inhibitor.

49
Q

Which protein specifically causes an increased ESR?

A

Fibrinogen. Which is an acute phase protein so it is stimulated by IL-6

50
Q

What are enoxaparin and dalteparin?

A

Low molecular weight heparin. So they also bind ATIII but they have more affinity for factor Xa.

51
Q

What gene is normally mutated in Polycythemia Vera? What does it do?

A

JAK. It is a non-receptor tyrosine kinase involved in the signal transduction from EPO receptors.

52
Q

What ins the first line drug for Heparin Induced Thrombocytopenia? What is it’s mechanism?

A

Argatroban or bivalirudin (or other hirudin derivatives). They bind the active site of thrombin.

53
Q

What is Rasburicase and what is it used for?

A

It is a recombinant protein from mammals that converts uric acid into Allantoin. Used in tumor lysis syndrome as well as allopurinol.

54
Q

What are three causes of Pure Red Cell Aplasia (PRCA)?

A

Bening Thymoma, Lymphocytic leukemia and Parvovirus B19 infection. EPO deficiency affects more than just RBCs.

55
Q

What is the main side effect of cisplatin based chemo and how can it be prevented?

A

It causes neprotoxicity which can be prevented with Amifostine and aggressive hydration. Amifostine “scavenges” for free radicals.

USMLE World Q Bank (14 decks)

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