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Hematology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

tissue factor aka

A

thromboplastin

(this is what kicks off the coagulation cascade)

don’t confuse with prothrombin (factor II)

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2
Q

tissue factor/thromboplastin activates … and together they activate X to Xa

A

factor VII

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3
Q

Factor IIa is aka

A

thrombin (prothrombin = Factor II)

(don’t confuse w/thromboplastin/tissue factor)

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4
Q

thrombin/IIa is important in the coagulation cascade because…

A

amplifies coagulation cascade and activate Xa

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5
Q

what is unique about factor VIII?

A

circulates bound to vWF to increase plasma half-life

(released in response to injury)

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6
Q

Which 2 multicomponent complexes convert X → Xa?

A
  1. Intrinsic Xase
  2. Extrinsic Xase

(both require phospholipids & calcium. Phospholipid: Occur on surfaces of cells (TF-bearing cells or platelets)

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7
Q

factor XIII role in coagulation?

A

crosslinks fibrin → stabilization of fibrin plug

(Ca required as cofactor, Ca used to be called factor IV)

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8
Q

factor xiii is activated by…

A

thrombin/iia formation

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9
Q

Factor XII/Hageman factor can activate factor …

A

XI (XIa) of the intrinsic pathway

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10
Q

factor… is used in the PTT test

A

Factor XII/Hageman

(activated by contact w/negative charges)

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11
Q

PTT monitors intrinsic and common pathway, reflecting activity of all factors except…

A

VII and XIII

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12
Q

What is the link between kinins, coagulation and inflammation?

i.e. bradykinin

A

kinins are generated by factor XII/Hageman which activates clotting and produces bradykinin

(pre-kallikrein deficiency = XII doesn’t work → markedly prolonged PTT, no bleeding problems. factor XII mainly just the basis for PTT)

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13
Q

Bradykinin is degraded by …

A

angiotensin converting enzyme (ACE)
C1 inhibitor (complement system; deficiency → hereditary angioedema)

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14
Q

3 coagulation inhibitors

A
  1. anti-thrombin III
  2. proteins C & S
  3. tissue factor pathway inhibitor
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15
Q

antithrombin III is primarily a … inhibitor

A

primarily thrombin & xa

(also…1. Serpin (serine proteases): factors II, VII, IX, X, XI, XII)

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16
Q

Endothelium makes … molecules → activate antithrombin III

(Basis for role of heparin drug therapy)

A

heparan sulfate

(Deficiency: Hypercoagulable state. i.e. minimal change diz & nephrotic syndrome)

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17
Q

protein C inactivates factors…

activated protein c = APC

A
  • va
  • viiia
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18
Q

Protein C is activated by …

A

thrombomodulin

(it “modulates the thrombus/clot”)

don’t confuse w/thromboplastin or prothrombin

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19
Q

thrombomodulin is found on … cells

A

endothelial

(thrombomodulin activates protein C (makes APC). Protein S is APC cofactor; together inhibit va and viiia)

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20
Q

protein C is a …(zymogen/active enzyme).
protein S is a … (zymogen/active enzyme).

A

protein C = zymogen
protein S = active enzyme

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21
Q

deficiency of protein C leads to which disease?

A

factor V Leiden = hypercoaguable state

(factor V mutation = resistant to inhibition)

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22
Q

TFPI
(Tissue factor pathway inhibitor) inactivates…

A

Xa

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23
Q

Two mechanisms tissue factor pathway inhibitor inactivates xa:

A

Directly binds Xa
Binds TF/Fviia complex → prevents X activation

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24
Q

plasminogen/plasmin breaks down … (2)

A
  1. fibrin/fibrinogen (breaks down into D-dimers)
  2. clotting factors

(used for tPA)

factor xiii stabilizes fibrin by crosslinkage; opposite of plasmin

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25
Q

which bacterial protein can be used to activate plasminogen to plasmin?

A

streptokinase

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26
Q

Primary Fibrinolysis aka “Hyperfibrinolysis”

A
  • Plasmin overactive (rare): Causes ↑ FDP with normal D-dimer (no d-dimers)
  • depletes clotting factors: Increased PT/PTT with bleeding (like DIC)
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27
Q

ESR is increased in inflammatory conditions because

A

there is an increase in proteins (acute phase reactants) which are “sticky”, they settle faster at the bottom of the tube.

(acute phase reactants are usu the result of cytokines)

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28
Q

primary hemostasis is aka

A

thrombus formation

(three steps: activation, aggregation, secretion)

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29
Q

platelet production is regulated by…

(RBC production regulated by EPO)

A

TPO (thrombopoietin)

(TPO made in liver; EPO made in kidney)

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30
Q

3 steps of thrombus formation

A
  1. adhesion
  2. aggregation
  3. secretion
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31
Q

VWF is synthesized by … (2)

(carries factor VIII)

A
  1. megakaryocytes
  2. endothelial cells (stored in Weibel-Palade bodies)

(also stored in alpha granules, found in plasma)

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32
Q

platelet adhesion occures d/t binding of …

A

platelet/GP1b binding vWF → subendothelial collagen

33
Q

platelet aggregation occurs d/t

A

binding of GPIIb/IIIa + vWF or fibrinogen

34
Q

platelet secretion allows for …

A

more activation

35
Q

In platelets…

alpha granules release…
dense granules release…

A

alpha: PF4, vWF, fibrinogen
dense: ADP, calcium, serotonin

36
Q

heparin can cause a rare, life-threatening condition that involves which platelet granule?

hypersensitivity; UFH more likely to cause

A

PF4

(Heparin-Induced Thrombocytopenia (HIT): Ab form to PF4-heparin complex → diffuse thrombosis → platelet overconsumption)

37
Q

serotonin release assay tests for…

A

HIT (heparin-induced thrombocytopenia)

(released from dense granules & released upon platelet activation. if there is over activation, excessive serotonin will be released)

38
Q

ADP is a powerful platelet activator released from dense granules. It does so by binding…

A

P2Y1 and P2Y12 → decreased cAMP → platelet activation

(Phosphodiesterase inhibitors increase cAMP to block platelet activation)

39
Q

When P2Y1 binds ADP (released from dense granule) →

effect on platelet?

A

calcium release, change in platelet shape

40
Q

When ADP binds P2Y12 →

effect on platelet?

A

Platelet degranulation, ↑ aggregation

(Rx that prevents this are called ADP receptor blockers. i.e. clopidogrel, prasugrel, ticlopidine, ticagrelor)

41
Q

prolonged bleeding time indicates … ONLY

A

platelet problem

(superficial cut; only involves platelets, not coagulation cascade)

42
Q

hypercoagulable states ususally involve… (2)

A

inflammation
immobility and/or trauma

(Virchow’s triad: endothelial damage, stasis, hypercoagulability)

cancer can do it also

43
Q

What are 5 other examples of hypercoagulable states?

other than: cancer, trauma, surgery

A
  1. elevated homocysteine (damages endothelial cells)
  2. pregnancy (increases fibrinogen)
  3. OCP + smoking > 15 cigs/day
  4. nephrotic syndrome (urinate out clotting factors)
  5. inherited thrombophilias (less common: factor V Leiden, prothrombin mutation, ATIII deficiency, Protein C/S deficiency)
44
Q

inherited thrombophilia involve venous or arterial thrombus?

A

venous: DVT, PE

45
Q

factor V Leiden mutation causes which dysfunction?

A

can’t inactivate Va & VIIIa

(same as protein S/C deficiency)

46
Q

point mutation in factor V Leiden

A

guanine to adenine in factor V gene

(same point mutation in prothrombin gene = increase in prothrombin)

47
Q

prothrombin gene mutation is d/t … mutation

A

prothrombin 20210

(heterozygotes have 30% increase in prothrombin levels)

48
Q

acquired ATIII deficiency can be caused by … (3)

A
  1. protein losses (nephrotic syndrome)
  2. DIC (consumption)
  3. impaired production (liver disease)
49
Q

A classic presentation of ATIII deficiency is …

(Hint: after treatment has begun)

A

escalating doses of heparin and no/little change in PTT

50
Q

antiphospholipid syndrome criteria

A
  • laboratory criteria: lupus anticoagulant, anti-cardiolipin or β2-glycoprotein
  • clinical criteria: thrombus (venous or arterial), fetal death after 10 weeks or > 3 fetal losses before 10 weeks

(2 positive lab results > 12 weeks apart)

51
Q

what are the three categories of bleeding disorders?

what 3 areas can problems occur in clotting?

A
  1. abnormal coagulation: hemophilia, Vit K def
  2. abnormal platelets: Bernard-soulier, glanzmann, thrombasthenia
  3. mixed: vWD, DIC, liver diz
52
Q

PTT (activated partial thromboplastin time) measures…

A

the intrinsic pathway of the coagulation cascade

(add silica charge to plasma to mimic the exposure of endothelial collagen)

53
Q

PT measures which pathway of the coagulation cascade?

Prothrombin time

A

extrinsic

add tissue factor and plasma

54
Q

What specific deficiencies does Thrombin Time Test (time to clot) identify (2)?

A
  1. deficiency in fibrinogen/factor I
  2. enzymes against factor IIa/thrombin
55
Q

mucosal bleeding/petechiae indicate abnormal… function
joint bleeding indicates abnormal … function

in the coagulation cascade

A

superficial = platelet
deep = coagulation factors (i.e. hemophilia)

56
Q

is PT or PTT elevated in hemophilia?
vit K deficiency?

A

PTT: intrinsic pathway
PT/INR:

57
Q

why is desmopressin used to tx hemophilias?

A

increases vWF & factor VIII (released from Weibel-Palade bodies in edothelial cells)

ADH w/o pressor activity

58
Q

what are the 2 Rxs used for hemophilias?

A
  1. Desmopressin: increases vWF & FVIII
  2. Aminocaproid acid: inhibits plasminogen activation → allows the factors VIII & IX that are present to work
59
Q

which clinical scenario indicates tx w/cryptoprecipitate?

old tx for hemophilia, factor VIII is used now

A
  1. DIC
  2. Massive trauma w/blood transfusions

(PPT that forms when FFP is thawed, then used for the factor VIII & fibrinogen inside)

60
Q

auto-antibodies to coagulation factors (MC: Factor VIII) may be triggered by which 3 conditions?

A
  1. malignancy
  2. post-partum
  3. auto-immune disorders
61
Q

auto-immune reaction to coagulation factors can present similar to hemophilia. What is a key difference in tx?

A

auto-immune tx = prednisone

hemophillia = factor VIII & vWF,

62
Q

auto-immune reaction to coagulation factors can present similar to hemophilia. How is can you distinguish diagnostically?

A

mixing study = corrects hemophilia, but NOT coagulation factor inhibition d/t auto-immune reaction

63
Q

Common causes of vitamin K deficiency?

A

warfarin (antagonizes vit K)
inability to absorb fat
GI bacteria disruption or absence (abx, newborns)

64
Q

list the 3 inherited platelet disorders

A
  1. glanzman: GBIIb/IIIa receptor→ no aggregation/clumping
  2. bernard-soulier: GP1B receptor → large platelets
  3. wiscott-aldrich: immune def → T-cell cytoskeleton dysfunction
65
Q

What are the key differences between the clinical presentation of the inherited bleeding disorders?

WAS, BS, Glanzman

A

Glanzman: bleeding
BS: bleeding, thrombocytopenia
WAS: thrombocytopenia, eczema, immune dysfunction

66
Q

what are the acquired platelet disorders?

A
  1. ITP: anti-GPIIb/IIIa Ab → splenic MF eat them
  2. TTP: anti- ADAMTS12 Ab → vessel obstruction
  3. Uremia: uremic toxins →TTP of the kidneys

(inherited: glanzman, BS, WAS)

67
Q

function of ADAMTS13 enzyme

A

metalloprotease keeps the vWF multimers from aggregating so they can spread out and bind to platelets

68
Q

microangiopathic hemolytic anemia is caused by…

A

shearing of RBC as they pass through thrombi in small vessels → schistocytes

(seen in TTP, HUS & DIC)

69
Q

thrombocytopenia = platelet counts less than…

A

10,000

70
Q

MC initial presentation of vWD

A

menorrhagia

71
Q

vWD will have increased PT or PTT?

A

PTT (factor VIII)

(increased bleeding time as well, vWD = mixed bleeding disorder - both platelets and coagulation dysfunction)

72
Q

What is the ristocetin cofactor activity assay

A

mix ristocetin with patients serum → aggregation if vWF is present and normal

(no aggregation if absent or defective; ristocetin causes binding of vWF and GP1B)

73
Q

vWD treatment?

(hint: same as hemophilia)

A
  1. desmopressin: increases factor VIII
  2. aminocaproic acid: preserves clots that are formed
74
Q

Heyde’s syndrome is primarily GI bleeding a/w which pathology?

A

aortic stenosis

(d/t vascular malformations of GI tract and vWF deficiency)

75
Q

Heyde’s syndrome is caused by which 2 dysfunctions?

GI bleeding a/w aortic stenosis

A
  1. GI vascular malformation
  2. vWF deficiency → high shearing forces activate ADAMTS12 → uncoiling of vWF multimers

(improves post-aortc valve surgery)

76
Q

both TTP & HUS have which blood profile?

platelets, hemolytic anemia, PT/PTT

A
  1. both have normal PT/PTT
  2. thrombocytopenia
  3. hemolytic anemia

(also TTP presents w/fever/confusion and HUS is a/w childhood GI illness)

77
Q

list the 4 classes of anti-platelet Rx

A
  1. aspirin
  2. anti-GPIIb/IIIa
  3. ADP blocker
  4. phosphodiesterase inhibitor
78
Q

Reye’s syndrome affects which 2 systems?

A
  1. liver failure
  2. encephalopathy

Hematology (6 decks)

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