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Hematology/Oncology > Hematology (MoD) > Flashcards

Hematology (MoD) Flashcards

1
Q

Normal hemoglobin, hematocrit ranges?

A

Hemoglobin: 12-14 for women, 14-16 for men
Hematocrit: 36 to 50%

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2
Q

Where is iron absorbed?

A

Proximal duodenum

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3
Q

Anemia of chronic disease pathogenesis

A

Inflammatory mediators (Il-6) lead to incr. hepcidin, in turn leading to decreased Erythropoietin

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4
Q

Iron deficiency lab fidnings

A

Nonspecific, but:
• On CBC: RBC count, H/H low, low MCHC
• Anisocytosis (hypochromia, microcytosis, causes incr. RDW)
• Poikilocytosis (elliptical cells, target cells)

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5
Q

Large, hypersegmented (>5 lobes) neutrophils on a peripheral blood smear…

A

Megaloblastic anemia

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6
Q

Megaloblastic anemia peripheral blood smear characteristics

A

Large hypersegmented (> 5 lobes) neutrophils is the most important characteristic, but also: pancytopenia, large hyper chromic oval RBCs, hyperlobated megakaryocytes (platelet precursors)

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7
Q

Where is vitamin B12 absorbed

A

Terminal ileum

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8
Q

What is pernicious anemia? Cause and symptoms?

A

Specific form of megaloblastic anemia caused by autoimmune destruction of gastric parietal cells with Ab to intrinsic factor; large, smooth, beefy, red tongue, also CNS subacute degradation (differentiates from folate deficiency)

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9
Q

Where is folate absorbed

A

Proximal jejunum

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10
Q

Where does folate come from in diet?

A

Green vegetables (poor storage so need to replenish constantly)

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11
Q

Where does vitamin B12 come from in diet?

A

Animal products (strict vegetarians at risk of deficiency)

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12
Q

4 things can cause folate deficiency

A

Decr. intake (e.g. alcoholism, poor diet, infarct), impaired absorption (e.g. intestinal disease), incr. requirement (e.g. cancer), incr. utilization (e.g. methotrexate)

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13
Q

Serum labs increased by B12 deficiency?

A

Homocysteine, methylmalonic acid (MMA)

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14
Q

Diseases associated with aplastic anemia

A

Fanconi anemia, paroxysmal nocturnal hemoglobinuria (also whole body irradiation but that’s less important)

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15
Q

Diseases associated with pure red cell aplasia

A

Neoplasia, parvovirus infection, collagen vascular disease, blackfan-diamond syndrome

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16
Q

Haptoglobin function

A

Bind free hemoglobin

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17
Q

Danger of free heme in bloodstream

A

Kidney damage

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18
Q

Difference between sickle cell disease and hemoglobin C?

A

In sickle cell disease mechanism is substitution of glutamic acid with valine at 6th position of beta globin chain; for hemoglobin C substitution is lysine instead of valine

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19
Q

“Target cells”

A

One of: thalassemia, poikilocytosis or liver disease

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20
Q

What is the Mentzer index and what is it used for?

A

MCV/RBC ratio; distinguish thalassemia from iron deficiency (less than 13 thalassemia, greater than 13 iron deficiency)

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21
Q

Why isn’t alpha thalassemia (generally) more severe than beta?

A

Because beta and gamma globulin chains are more soluble than alpha so hemolysis and ineffective erythropoiesis less pronounced

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22
Q

Test used to diagnose hereditary spherocytosis

A

Osmotic fragility test (spherocytes are more osmotically fragile)

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23
Q

What causes intermittent anemia

A

G6PD deficiency (leads to decr. NADPH, thus decr. glutathione activity, thus reduced ability to handle oxidative stress); also remember pyruvate kinase deficiency causes continuous anemia

24
Q

Peripheral smear findings in G6PD deficiency

A

Heinz bodies, bite cells

25
Q

Mechanism behind and most important test used to diagnose paroxysmal noctural hemoglobinuria

A

RBCs lack proteins necessary to prevent complement-mediated lysis; flow cytometry (demonstrates reduced CD55 and CD59)

26
Q

Difference in mechanisms underlying warm antibody HA and cold agglutinin HA?

A

In warm Ab HA, IgG binds to RBCs which are then phagocytksed by splenic macrophages; in cold agglutinin HA IgM binds RBCs, then fixes complement

27
Q

Diseases associated with cold agglutinin HA

A

B cell neoplasms and infections (esp mycoplasma pneumoniae)

28
Q

Universal RBC donor type

A

O-

29
Q

Universal plasma donor type

A

AB+, AB-

30
Q

Presumed effect of “one unit” of blood on an “average” patient

A

Incr. Hgb by 1 gm/dL and Hct by 2-3%

31
Q

Presumed effect of “one unit” of fresh frozen plasma

A

Incr. any factor level by 2-3%

32
Q

For what reason is irradiation performed (with regards to transfusion)? What samples do not need to be irradiated

A

Prevent GVHD (in the immunocompromised, hematologic disorders, intrauterine transfusions and Hodgkin’s disease); FFP, cryoprecipitate/coagulation factors

33
Q

Possible metabolic complications of transfusion

A

Citrate toxicity, hyperkalemia, hypothermia, volume overload

34
Q

Platelet’s delta (dense) granule contents

A

ATP, ADP, serotonin, ca++

35
Q

Platelet’s alpha granule contents

A

PF4, PDGF, P-selectin, platelet fibrinogen, VWF, thromboglobulin, thrombospondin

36
Q

Where is GP IIb/IIIa found and what is it?

A

Platelets; receptor for VWF and fibrinogen

37
Q

What is GP Ib/V/IX and where is it found?

A

Receptor for VWF; platelets

38
Q

How is VWF crucial for both primary and secondary hemostasis?

A

Binds collagen to platelets in primary hemostasis, binds to factor VIII (thus stabilizing it) in secondary hemostasis

39
Q

ADAMTS13 function

A

Metalloprotease that lyses VWF (don’t want it to be active forever, only large multimers have hemostatic activity)

40
Q

What form of VWF has hemostatic activity?

A

Only the large multimers

41
Q

Plavix (clopidogrel) mechanism of action

A

ADP receptor inhibitor (ADP activates platelets)

42
Q

Bernard-Soulier syndrome underlying mechanism

A

Deficiency in Ib (Ib/V/IX)

43
Q

Glanzmann thrombasthenia underlying mechanism

A

Deficiency in IIb/IIIa compromises fibrinogen cross linking

44
Q

Cause and symptoms of thrombotic thrombocytopenic purpura

A

Loss of ADAMTS13 causes ultra-large VWF multimers, leading to widespread platelet activation and microvascular thrombosis; classic pentad - fever, thrombocytopenia, microangiopathic HA, mental status changes, renal failure

45
Q

Bacterium associated with Hemolytic Uremic Syndrome

A

E coli (specifically d/t shiga-toxin)

46
Q

Test used to diagnose antiphospholipid syndrome?

A

dilute Russell Ciper Venom test (dRVVT), also remember aPTT can be elevated but it isn’t a bleeding disorder

47
Q

Underlying mechanism behind Heparin-induced thrombocytopenia

A

Antibodies to PF4+ heparin lead to platelet activation and microvascular occlusion

48
Q

Fibrinogen factor number

A

Factor I

49
Q

Prothrombin factor number

A

Factor II

50
Q

What factor deficiencies do NOT cause bleeding

A

XII, prekallikrein, HMWK

51
Q

Intrinsic, extrinsic, common pathway factors

A

Intrinsic: HMWK, prekallikrein, VIII, IX, XI, XII
Extrinsic: VII, Tissue factor
Common: I, II, V, X

52
Q

Describe the role of platelets in secondary hemostasis

A

PF3 present on activated platelets, plays a role in the activation of factors IX, X, prothrombin

53
Q

What clotting factors are vitamin K dependent? How so?

A

II, VII, IX, X, S, C; necessary for carboxylation of gamma carbon of glutamic acid of Glands domain (remember ca++ crucial for this process)

54
Q

What factors does thrombin play a role in activating?

A

I, V (leads to more thrombin), VIII, XI (positive feedback on intrinsic pathway), XIII (cross-links/stabilizes fibrin)

55
Q

TFPI action

A

Blocking extrinsic pathway by compromising interaction of TF with factor VII

56
Q

Heparin mechanism of action

A

Inactivates IIa

57
Q

Disseminated intravascular coagulation labs

A

Incr. PT, PTT, TT
Decr. fibrinogen and platelets
Incr. FSP D-dimers

Hematology/Oncology (3 decks)

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