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Step 1 > Heme/Onc Random Facts > Flashcards

Heme/Onc Random Facts Flashcards

1
Q

What is the life span of a thrombocytes.

A

8-10 days

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2
Q

What are the granules in platelets?

A

Dense granules-contain ADP and Ca, alpha-granules contain vWF and fibrinogen

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3
Q

Where is 1/3 of the platelet pool stored

A

In the spleen

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4
Q

What are the granules in neutrophils?

A

Specific granules contain ALP, collagenase, lysozyme, and lactoferrin. Azurophilic granules (lysosomes) contain proteases, acid phosphatase, myeloperoxidase, and beta-glucuronidase

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5
Q

How are macrophages involved in septic shock?

A

Lipid A from bacterial LPS binds CD 14 on macrophages to initiate septic shock

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6
Q

What activates macrophages?

A

Gamma-interferon

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7
Q

What does eosinophilic mean?

A

Pink

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8
Q

What does basophilic mean?

A

Blue/purple

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9
Q

What are the causes of eosinophilia?

A

Neoplasia, asthma, allergy, chronic adrenal insufficiency, parasites

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10
Q

What die the granules in basophils contain?

A

Heparin and histamine. Leukotrienes synthesized and released on demand

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11
Q

What can basophilia be a sign of?

A

Myeloproliferative disease, particularly CML

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12
Q

What’s the universal donor and universal recipient of plasma?

A

AB is the universal plasma donor (because no antibodies in their plasma), O is the universal recipient of plasma (because antibodies have nothing to react with)

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13
Q

How does warfarin work?

A

It inhibits vitamin K episode reductase, which is needed to activate the vitamin K dependent clotting factors

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14
Q

MOA of antithrombin

A

Inhibits activated forms of factors 2, 7, 9, 10, 11, and 12. Principle targets of antithrombin: thrombin and factor Xa

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15
Q

What does tPA do?

A

Converts plasminogen to plasmin

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16
Q

MOA of protein C and S

A

Protein C is converted to activated protein C by thrombin-thrombin insulin complex on endothelial cells, APC is activated by protein S to cleave and inactivate factor Va and VIIIa

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17
Q

MOA of clopidogrel, prasugrel, and ticlipidine

A

Inhibit ADP-induced expression of GpIIb/IIIa

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18
Q

MOA of abciximab, eptifibatide, and tirifiban

A

Inhibit GpIIb/IIIa directly

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19
Q

What is Bernard Soulier syndrome

A

A deficiency of GpIb

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20
Q

What is Glazmann thrombasthenia

A

Deficiency of GpIIb/IIIa

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21
Q

When might you see a failure of agglutination with ristocetun assay?

A

Von Willebrand disease and Bernard-Soulier syndrome

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22
Q

When might you see acanthocytes (“spur cells”)

A

Liver disease, abetalipoproteinemia

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23
Q

When might you see target cells

A

HbC disease, Asplenia, liver disease, thalassemia

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24
Q

What are Heinz bodies?

A

Oxidation do Hb-SH groups to -S–S- causing hemoglobin precipitation with subsequent damage to RBC membrane causing bite cells

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25
Q

What might you see in a reticulocyte in Wright-Giemsa stain

A

Blue staining, represents the residual ribosomal RNA

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26
Q

Where does iron absorption occur?

A

In the duodenum and proximal jejunum so bypassing this in a gastrojejunostomy results in iron deficiency anemia

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27
Q

What is associated with koilonychia?

A

(Spoon nails) iron deficiency anemia

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28
Q

What happens with a four allele deletion in the alpha-globin gene?

A

Hemoglobin Barts (4 Gamma chains) forms. Is incompatible with life

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29
Q

What is hemoglobin H?

A

Four beta chains

30
Q

What ethnicities are associated with alpha and beta thalassemia?

A

Alpha- Asian and African, beta-Mediterranean

31
Q

How is beta thalassemia minor diagnosed?

A

Increased HbA2 on electrophoresis

32
Q

MOA of lead poisoning

A

Inhibits ferrochatase and ALA dehydratase causing decreased heme synthesis and increased RBC protoporphyrin

33
Q

Signs and symptoms of lead poisoning

A

Lead lines on gingivae and metaphysics of long bones on xray, encephalopathy and erythrocytes basophilic stippling, abdominal colic and sideroblastic anemia, drops-wrist and foot

34
Q

What causes hereditary sideroblastic anemia?

A

X-linked defect in delta-ALA synthase gene

35
Q

Causes of sideroblastic anemia

A

Genetic, acquired (myelodysplastic syndromes) and reversible (alcohol, lead, vitamin B6 deficiency, copper deficiency, isoniazid)

36
Q

What is orotic aciduria?

A

AR defect in UMP synthase, presents as FTT, developmental delay, and megaloblastic anemia refractory to folate and B12. NO hyperammonemia (vs ornithine transcarbamylase deficiency)

37
Q

Tx of orotic aciduria

A

Uridine monophosphate to bypass mutated enzyme

38
Q

What might have an abnormal eosin-5-maleimide binding test

A

Hereditary spherocytosis

39
Q

Pyruvate kinase deficiency

A

AR, causes decreased ATP causing rigid RBCs and extra vascular hemolytic anemia. Hyperplasia of the red pulp of the spleen

40
Q

Mutation in HbC disease

A

Glutamic acid to lysine in beta-globin, causes extravascular hemolysis

41
Q

Triad, labs, and tx in PNH

A

Triad: Coombs - hemolytic anemia, pancytopenia, and venous thrombosis, labs: CD55/59 neg RBCs on flow cytometry, tx: eculizumab

42
Q

Warm agglutinin

A

Chronic anemia seen in SLE and CLL and with certain drugs (alpha-methyldopa), IgG

43
Q

Cold agglutinin

A

IgM, acute anemia triggered by cold, seen in CLL, mycoplasma and infectious mononucleosis

44
Q

What is the direct Coombs test

A

Anti-Ig antibody added to patient’s blood. RBCs agglutinate if RBCs are coated with Ig

45
Q

Indirect Coombs

A

Normal RBCs added to patients serum. If serum has anti-RBC surface Ig, RBCs agglutinate when Coombs reagent is added

46
Q

Effect of corticosteroids on neutrophils, eosinophils, and lymphocytes

A

Neutrophilia from demargination, eosinopenia from sequestration in lymph nodes, lymphopenia from apoptosis

47
Q

Enzyme inhibited in acute intermittent porphyria

A

Porphibiligen deaminase

48
Q

Enzyme deficient in porphyria Cutanea tarda

A

Uropirphyrinogen decarboxylase

49
Q

Pathogenesis of ttp

A

Inhibition or deficiency of ADAMTS13 (vWF metalloprotease) causes large vWF multimers which causes increased platelet adhesion, which causes platelet aggregation and thrombosis

50
Q

Pentad of ttp

A

Neurologic and renal sx, fever, thrombocytopenia, and MAHA

51
Q

When might you give cryoprecipitate

A

For coagulation factor deficiencies involving fibrinogen and factor VIII

52
Q

High leukocyte alkaline phosphatase means what?

A

Leukemoid reaction

53
Q

What are Dohle bodies?

A

Light blue (basophilic) peripheral granules in neutrophils seen in a leukemoid reaction

54
Q

What is Hodgkin lymphoma associated with?

A

EBV

55
Q

Cell markers in reed Sternberg cells

A

CD15 and CD30

56
Q

Genetics of Burkitt lymphoma

A

T(8;14) translocation of c-myc and heavy-chain Ig

57
Q

What is commonly involved in diffuse large B cell lymphoma

A

Waldeyer’s ring (oropharyngeal lymphoid tissue) and GI tract

58
Q

Genetics of follicular lymphoma

A

T(14;18)-translocation of heavy-chain Ig and Bcl-2. Cleaved nuclei on histo

59
Q

Genetics of mantle cell lymphoma

A

t(11;14)-translocation of cyclin D1 and heavy chain Ig

60
Q

Cerebriform nuclei

A

Mycoses fungoides/Sezary syndrome

61
Q

Rouloux formation

A

Multiple myeloma

62
Q

Neutrophils with bilobed nuclei seen after Chen

A

Pseudo-Pelger-Huet anomaly

63
Q

Child with lytic bone lesions and skin rash or as recurrent otitis media with a mass involving mastoid bone

A

Langerhans cell histiocytosis. Calls express S100 (mesodermal origin) and CD1a. Bit beck granules (tennis rackets on EM)

64
Q

T(12;21)

A

Better prognosis ALL

65
Q

Smudge cells

A

Small lymphocytic lymphoma/CLL

66
Q

Tx for CML

A

Imatinib (a small molecule inhibitor of the bcr-abl tyrosine kinase)

67
Q

Mechanism of HIT

A

Development of IgG Ab against heparin bound platelet factor 4. The antibody-heparin-PF4 complex activates platelets causing thrombosis and thrombocytopenia

68
Q

Direct thrombin inhibitors

A

Argatroban, bivalirudin, dabigatran

69
Q

MOA of cilostazol, dipyridamole

A

Phosphodiesterase III inhibitor. Increases cAMP in platelets, resulting in inhibition of platelet aggregation; vasodilators

70
Q

MOA of hydroxyurea for cancer

A

Inhibits ribonucleotide reductase

71
Q

Clinical use for cytarabine

A

Leukemias (AML), lymphoma

72
Q

Use and toxicity of Busulfan

A

CML. Also used to ablate patient’s bone marrow before bone marrow transplantation. Toxicity: severe myelosuppression

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