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heme/onc > platelets > Flashcards

platelets Flashcards

1
Q

Anucleate cells derived from megakaryocytes

in the bone marrow

A

platelets

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2
Q

platelets:

  1. production
  2. nl count
  3. circulation lifespan
A
  1. production: GM-CSF, IL-3, IL-6, TPO
  2. nl count: 150,000- 400,000
  3. circulate in the inactive state for 7-10 days
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3
Q

Alpha granules:

  1. fibrinogen
  2. thrombospondin
  3. vWF
  4. Factor V
  5. Platelet factor 4
  6. Beta thromboglobulin
  7. PDGF (platlet derived growth factor)
  8. P-selectin
A
  1. fibrinogen- aggregation
  2. thrombospondin- aggregation
  3. vWF- adhesion/aggregation
  4. Factor V- fibrin clot
  5. Platelet factor 4- heparin antagonist–promotes fibrin clot
  6. Beta thromboglobulin- recruits fibroblasts
  7. PDGF (platlet derived growth factor)- recruits fibroblasts
  8. P-selectin- adhesion of activated platelets to phagocytes
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4
Q

dense granules

  1. ADP and ATP
  2. Serotonin (5-HT)
  3. calcium
A
  1. ADP and ATP- platelet activation and recruitment
  2. Serotonin (5-HT)- vasoconstriction
  3. calcium- cofactors for factors forming fibrin clot
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5
Q

lysosomes

A

are granules that contain hydrolytic enzymes which phagocytose debris

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6
Q

Glycoprotein (GP) Ib (Ib/IX/V):

A

vWF receptor

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7
Q

Glycoprotein Ia/IIa:

A

collagen receptor

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8
Q

Glycoprotein IIb/IIIa:

A

fibrinogen receptor

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9
Q

procoagulant activity (2)

A
  1. thrombin receptor

2. phospholipids

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10
Q

P-selectin (activated platelets only)

A

leucocyte adhesion

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11
Q

bound to the collagen in the subendothelium of the damaged vessel wall, binds to platelets via GPIb complex, acting as a bridge

A

vWF

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12
Q

in the damaged vessel wall can bind to the platelet via GPIa/IIa

A

collagen

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13
Q

involved in adhesion for platelets (2)

A
  1. vWF

2. collagen

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14
Q

activating agents in platelets (6)

A
  1. thromboxane A2
  2. thrombin
  3. epinephrine
  4. ADP
  5. collagen
  6. arachidoinic acid
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15
Q

three actions of the activating agents

A
  1. enhances cell interaction (GPIIb/IIIa)
  2. induces platelet shape change and secretion
  3. phspholipids on plasma membrane activate clotting on the external surface
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16
Q

shape change with platelets

A

change from discoid to spherical- develop long pseudopods

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17
Q

where do the granules release their contents?

A

into the canalicular system

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18
Q

in aggregation the platelet-platelet interaction mediated by ______ and promoted by thombospondin

A

GPIIb/IIIa with fibrinogen

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19
Q

what does ADP and thromboxane A2 do in aggregation?

A

swelling, membrane adhere and further release reaction

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20
Q

exposure of membrane ___ for coagulation

A

PL

21
Q

_____ stimulates vascular smooth muscle cells, hasten healing

A

PDGF

22
Q

Clot retraction:

tenase complex

A

FIXa, VIIIa and X = FXa

23
Q

clot retraction:

prothrombinase complex

A

FXa, Va, and II = thrombin

24
Q

laboratory studies:

  1. quantitative
  2. qualitive
A
  1. quantitative: platelet count and morphology

2. qualitative: aggregation and PFA100

25
Q

Anticoagulated whole blood under high sheer rate passes through an aperature with two membranes coated with either collagen/epinephrine or collagen/ADP

A

PFA-100

26
Q

PFA-100 affected by

A

thrombocytopenia and to some degree anemia

27
Q

PF-100:

  1. collagen/epi:
  2. collagen/ ADP:
A
  1. collagen/epi: nl<180 sec

2. collagen/ ADP: nl<116 sec

28
Q

thrombocytopathies

A

abnormal platelet function

29
Q

thrombocytopenia

A

platelet count<150,000

30
Q
  1. GPIb (vWF receptor)
  2. abnormal adhesion/agglutination
  3. prolonged bleeding time
    thrombocytopenia with large platelets
A

Bernard Soulier disease

31
Q
  1. GPIIb/IIIa (fibrinogen receptor)
  2. abnormal aggregation and PFA-100
  3. prolonged bleeding time
A

Glanzmann’s thrombasthenia

32
Q

acquired thrombocytopathy (3)

A
  1. drugs- ASA, NSAID
  2. renal insufficiency- uremia
  3. myeloproliferative disorders/ myelodysplastic syndromes
33
Q

ASA (aspirin) irreversibly, NSAID’s reversibly acetylate and thus inhibit ______, resulting in reduced ________ synthesis and granule release

A

ASA (aspirin) irreversibly, NSAID’s reversibly acetylate and thus inhibit cyclo-oxygenase, resulting in reduced thromboxane A2 synthesis and granule release

34
Q

powerful vasoconstrictor and potentiates aggregation

A

Thromboxane A2

35
Q

autosomal dominant, large platelets, dohle bodies in the wbc’s

A

May-Hegglin anomaly -

36
Q

X-linked recessive, eczema, immune dysfunction

A

Wiskott-Aldrich syndrome –

37
Q

autosomal recessive, abnormal hand/wrist, cardiac lesions

A

Thrombocytopenia with absent radii (TAR) –

38
Q

autosomal dominant, interstitial nephritis, deafness, large platelets

A

Epstein’s/Alport syndrome –

39
Q

stem cell disorder, can also be acquired

A

Megakaryocytic hypoplasia/aplastic anemia –

40
Q

acquired thrombocytopenia due to decreased production (4)

A
  1. infiltrative process- malignancy
  2. infectious- viral
  3. drugs- chemotherapy
  4. toxins- radiation
41
Q

acquired thrombocytopenia due to increased destruction (7)

A
  1. drugs- heeparin/HIT
  2. immune thrimbocytopenic purpura/ ITP
  3. thrombotic thrombocytopenic purpura (TTP)/ hemolytic uremic syd=ndrime (HUS)
  4. disseminated intravascular coagulation/DIC
  5. APLA
  6. HELLP syndrome/pre-eclmapsia
  7. hyperspenism
42
Q

auto-immune disorder, antibody:antigen complex on the surface of the platelet which targets it for removal by the RES

A

Immune thrombocytopenic purpura (ITP):

43
Q

1.Adults
2.Fever, thrombocytopenia
microangiopathic anemia, acute renal failure, neurologic dysfunction
3. ADAMTS13-destruction or deficiency which leads to ultra large vWF multimers and aggregation of platelets and thrombosis
4. Normal PT/PTT
5. Rx: plasma exchange

A

Thrombotic thrombocytopenic purpura

44
Q
  1. Children
  2. Diarrhea infection often E. coli strain
  3. Microangiopathic anemia, thrombocytopenia
    severe renal failure
  4. ADAMTS13 – normal
  5. Normal PT/PTT
  6. Rx: supportive care
A

Hemolytic Uremic Syndrome

45
Q

Disseminated intravascular coagulation:

  1. Consumptive coagulopathy associated with
  2. Initiated by
  3. Clinical –
  4. Lab –
A
  1. Consumptive coagulopathy associated with thrombocytopenia, excessive fibrinolysis and reduced coagulation factors
  2. Initiated by endotoxin, infections (meningococcemia, etc), tissue factor release, tissue injury, proteases, toxins, malignancy, obstetrical complications
  3. Clinical – bleeding and thrombosis
  4. Lab – microangiopathic HA, thrombocytopenia, prolonged PT/PTT, TT, decreased fibrinogen, increased d-dimer
46
Q

does the extrinsic pathway depend of platelets?

A

Nope, the extrinsic pathway is only made up of FVII

47
Q

gray platelet syndrome

A

there is a decreased or absent number of alpha granules.

48
Q

Chediak-Higashi syndrome is a

A

white blood cell disorder due to a failure of phagolysosome formation.

heme/onc (30 decks)

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