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organ systems > Heme/onc just a bit > Flashcards

Heme/onc just a bit Flashcards

1
Q

Rostocetin

A

activates vWF to bind GpIb (GpIb is on the platelet) and VwF other side binds to exposed collagen upon endothelial damage

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2
Q

Orotic aciduria

A
  • inability to convert orotic acid to UMP (de nova pyrimidine synthesis pathway)
  • defect in UMP synthase
  • Autosomal recessive

present:
megloblastic anemia that cannot be curred by folate or B12 with failure to thrive
-no hyperammonemia
-hypersegemented neutorphils, glossitis, orotic acid in urine

treat: give UMP

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3
Q

what are the lab findings in anemia of chronic disease?

A
  • decrease iron and TIBC
  • increase ferritin

recall release more hepcidin, so less iron is reasbsorbed and released into the system via the GI, so it builds up in the ferritin

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4
Q

What precipitates sickling in sickle cell?

A

-low oxygen
-dehydration
-acidosis
deoxygenated HbS sickles

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5
Q

What are some renal consequences of sickle cell?

A

-renal papillary necrosis (due to low O2 in papilla, also seen in heterozygotes) and microhematuria (medullary infarcts)

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6
Q

Autoimmunie hemolytic anemia:

Warm agglutinin IgG

A

assoc with SLE, CLL, alpha methyl dopa

coombs positive

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7
Q

Autoimmunie hemolytic anemia:

Cold agglutinin IgM

A

acute anemia triggered by cold

assoc. CLL, mycoplasma pneumonia infections or infectious mononucleosis

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8
Q

Direct coombs test

A

detects antibodies that are bound directly to surface RBC

-add an anti-Ig antibody to patients srum, the RBC agglutinate if the RBC already are coated with Ig

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9
Q

Indirect coombs test

A

detects free floating antibodies in the serum

-take normal RBC and add then to patients serum. Agglutinate if the patients serum has anti RBC surface Ig

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10
Q

corticosteroids cause neutrophilia but eosinopenia and lymphopenia

A
  • decrease the activation of neutrophil adhesion molecules, impairing migration out of the vasculature to sites of inflammation
  • corticosteroids sequester eosinophils in lymphnodes and cause apoptosis of lymphocytes
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11
Q

Lead poisoning

A
  • inhibit ferrochelatase (last step in mitochondria) and ALA dehydratase (second step) (cytoplasm)
  • protoporphyrin and ALA accumulate

present: GI and kidney disease, children –> mental deterioration
adults: memory loss, demyelination

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12
Q

Lead poisoning clinical

A
  • lead lines on gingivae (burtons)
  • encephalopaty and erythrocyte basophilic stippling
  • abdominal colic and sideroblastic anemia
  • drops - wrist and foot drop
  • dimercaporl and EDTA are 1st line treatment
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13
Q

Chelation for lead for kids

A

succimer

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14
Q

chelation for lead in adults

A

dimercaprol

EDTA

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15
Q

acute intermittent porpyria

A
  • prophobilinogen deaminase defective
  • build up of porphorobilinogen, ALA and coporphobilinogen in the urine

symptoms 5p’s

  • painful abdomen
  • port wine colored urine
  • polyneurapath
  • psychological disturbances
  • precipitated by drugs, alcohol and starvation

treatment: glucose, heme (inhibit ALA synthase)

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16
Q

porphyria cutanea tarda

A
  • uroporphrinogen decarboxylase is the defect
  • uroporphyrn accumulates and causes tea colored urine
  • most common!!!
  • blistering cutaneous photosensitivity
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17
Q

Bernard-soulier

A
  • defect in GPIb needed for platelet to vWF adhesion
  • decreased paltelt count
  • increased bleeding time
18
Q

Glanzmann thrombasthenia

A
  • Defect in GpIIb/IIIa leads to a defect in platelet to fibrin to platelt aggregation
  • blood smear shows no platelet clumping
  • increased bleeding time
19
Q

immune thrombocytopenia

A

autoimmune to GpIIb/IIIa leads to splenic macrophage consumption of platelet/antibody complex.

  • may be triggered by viral illness
  • decreased platelet survival
  • decreased platelet count, increased bleeding time and increase baby megakaryocytes on bone marrow to offset the loss
20
Q

Thrombotic thrombocytopenic purpura

A
  • inhibition of deficiency of ADAMTS 13 vWF metalloprotease
  • so vWF multimers build up
  • increases platelet adehesion and platelet aggregation and thrombosis
  • decreases platelet survival
  • decreased platelets and increase bleeding time
    labs: schistocytes and increased LDH
  • fever, thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms and renal symptoms
    treat: exchange transfusion and steroids
21
Q

prothrombin gene mutation is an activating mutation

A

-mutation in 3’untranslated region –> increased production of prothrombin and increase plasma levels and venous clots

22
Q

antithrombin deficiency

A

has no effect on PT/PTT or thrombin time

  • but diminishes the increase in PTT one would normally observe following heparin administration
  • recall antithrombin helps inhibit 2,7,9,10,11,12 but mainly 2 and 10
  • antithrombin can also be lost in the urine during renal failure or nephrotic syndrome
23
Q

protein C or S deficiency

A
  • inability to inactivate facors V and VIII
  • skin and subcutaenous tissue necrosis after warfarin administration. recall warfarin inhibit vitamin K production of 2,7,9,10 C and S. remember activated C breaks down V and VIII so they are antiplatelet. But if there is no C and S at all, then nothing to cancel coagulation and warfarin is tooo effective
24
Q

leukomoid reaction

A
  • acute inflammatory response to infection
  • increase WBC with increased neutorpils and bands left shift, increase in neutrophil ALP (being release by mature neutrophils for the infection)

but in CML there is a decrease in ALP because there are too much proliferation of mylo and not enough maturation and they are not activated so no release of ALP

25
Q

What are the CD on Reed stern berg cells?

A

CD 15 and 30

26
Q

Nodular sclerosing type is most common in?

A

men and women equally

27
Q

What has the best prognosis in hodgkins?

A

lymphocyte rich
mixed or depleted have worst prognosis

there is a good prognosis with strong stromal or lymphocytic reaction against RS cells

28
Q

What is Waldenstrom macroglobulinemia

A
  • seems like MM but its not!
  • m spike, IgM not gamma
  • hyperviscosity symptoms
  • NO lytic bone lesions
29
Q

t (9:22)

A

CML bcr-abl hydrid

tyrosine kinase gone crazy

30
Q

t (8:14)

A

Burkitt lymphoma

c-myc

31
Q

t(11:14)

A

mantle cell lyphoma (cyclin D1 activation)

32
Q

t (14:18)

A

Follicular lymphoma
bcl2
waxing waning

33
Q

t(15:17)

A

M3 AML all-TRA responsive

34
Q

Langerhans cell histiocytosis

A
  • proliferative disorders of dendrites from monocytic lineage
  • child as lytic bone legion and skin rash, otitis media with mass involving the mastoid bone
  • cells are functionally immature and do not efficiently stimulate primary T lymphocytes via antigen presentation
  • cells express S100 (mesodermal origin) and CD1a

see birbeck granules (tennis rackets on EM)

35
Q

LMW heparins:

enoxaparin and dalteparin

A

act more on Xa, better bioavailablity, longer t1/2

36
Q

Directly inhibit thrombin:

Argatroban, bivalirudin, lepirudin

A
  • derivatives of hirudin an anticoagulant in leeches

- use instead if patients get HIT

37
Q

Direct factor Xa inhibitor:

Apixaban and rivaroxaban

A

treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis with patients with AF

38
Q

Name and ADP receptor inhibitor known for neutropenia side effect?

A

ticlopidine

39
Q

Thrombolytics:

altepase tPA, reteplase rPA and tenecteplase TNK-tPA

A

directly or inderiectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots

40
Q

Cliostazol and dipyrimadole

A

-phosphodiesterase III inhibitor—-> vasodilation and increased cAMP which inhibits platelet aggregation

organ systems (25 decks)

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