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IBI Test 3 > B3.049 Disorders of Coagulation > Flashcards

B3.049 Disorders of Coagulation Flashcards

(61 cards)

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1
Q

why is the vascular wall important in hemostasis?

A

anchor to which platelets bind

mediated by vWf

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2
Q

what are some of the functions of platelets in in hemostasis

A

form plug
have granules with coag factors
have stores of Ca2+
has a phospholipid surface where secondary cascade gets activated (flip flopping)

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3
Q

what prevents vWF and platelets from interacting in circulation?

A

not conformationally compatible

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4
Q

what happens to stimulate vWF and platelet interaction?

A

conformational change
can happen due to chem or phys means
turbulence or cytokines both important
turbulence set off bc of injury to vessel wall

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5
Q

describe the physical characteristics of vWF

A

large protein; enzyme cleaves large protein into functional units
multiple active domains
anchor platelets to subendothelial collagen

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6
Q

what mediator connects vWF to platelets

A

Gp1b

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7
Q

what is the function of Gp2b3a?

A

binds to fibrinogen to help stick platelets together

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8
Q

where is vWF synthesized?

A 
endothelial cells (WP bodies)
platelets (alpha granules)
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9
Q

what protein processes vWF multimers?

A

ADAMTS-13 in plasma

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10
Q

what function outside of platelet adhesion does vWF have?

A

stabilization of factor 8

without it, factor 8 degrades quickly and you have the appearance of a factor 8 deficiency

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11
Q

what factors initiate clotting in vivo?

A

TF and factor 7

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12
Q

what is the purpose of factor 7 after the initiation of clotting?

A

nothing

after initiation, clotting is potentiated by a positive feedback loop stimulated by thrombin

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13
Q

what factors does thrombin activate?

A

8, 9, 10

these must be stopped to stop fibrin clotting (NOT 7)

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14
Q

what is the function of activated factors?

A

serine proteases

can cleave downstream factors

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15
Q

which factor is the PT test more sensitive for?

A

factor 7

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16
Q

what are the vitamin k dependent coag proteins?

A

2, 7, 9, 10

protein C and protein S

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17
Q

why is vitamin k necessary?

A

required for post translational gamma-carboxylation of glutamic acid residues, forming gamma-carboxyglutamic acis (gla)
gla binds to Ca2+ in active site and allows protease reactions to proceed

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18
Q

what is the mechanism of warfarin?

A

inhibits the recycling of vitamin K

inhibits production of functional clotting factors

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19
Q

what is the only mechanism of D-dimer production?

A

breakdown of CROSS LINKED FIBRIN

had to have had a thrombus

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20
Q

causes of an abnormal PT?

A

liver disease
vitamin K def
warfarin

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21
Q

how can you distinguish between liver disease or vitamin K def in a patient w abnormal PT?

A

test 1 liver dependent factor and 1 vitamin K dependent factor separately

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22
Q

what is the function of the INR?

A

to compare PT values across institutions

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23
Q

causes of an abnormal PTT?

A 
hemophilia A and B
vW disease
heparin therapy
liver disease (severe)
vitamin K def (severe)
warfarin (if supra-therapeutic)
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24
Q

discuss the diagnostic utility of the D-dimer test

A

high sensitivity for DIC
low specificity (many many causes for D-dimer elevation)
high negative predictive value for PE
-if you don’t have D-dimer, you don’t have a clotting issue
-if you do have D-dimer that’s not super diagnostically helpful

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25
purpura
bleeding within skin or mucous membranes
26
petechiae
pinpoint bleeding of skin or mucous membranes
27
ecchymosis
large confluent area of bleeding within skin, larger than petechiae
28
hematoma
a collection of blood in organ, space, or tissue
29
hemarthrosis
bleeding into the joint space
30
bleeding patterns associated with primary hemostasis issues
skin or mucosal bleeds purpura, petechiae, ecchymosis spontaneous bleeding
31
bleeding pattern associated with secondary hemostasis issues
bleeds into soft tissue, muscle, joints hemarthrosis bleeding with trauma
32
vW disease epidemiology
variable age of onset m = f prevalence 1-5 per 1000
33
type 1 vWf disease
partial quantitative deficiency | autosomal dominant
34
type 2 vWf disease
qualitative deficiency types: factor 8 binding issue, binds to gp1b too much, no multimers varying degrees of clinical manifestations
35
type 3 vWf disease
complete quantitative deficiency | autosomal recessive
36
pathologic features of vW disease
``` prolonged closure time on PFA-100 prolonged PTT (30% of patients) decreased vWf activity (in all types) decreased vWf antigen (types 1 and 3) normal vWf antigen (in type 2) ```
37
treatments for vWf disease
humate P, best option: vWf concentrate, blood derivative (pathogen inactivated) cryoprecipitate: good source of vWf, blood product (not pathogen inactivated) desmopressin (ADH): stimulates endothelial cells to release remaining vWf stores
38
classic triad of thrombosis
abnormal blood flow (stasis or turbulence) hypercoagulability (inherited or acquired) endothelial injury (hypercholesterolemia)
39
what causes venous thromboembolism?
inherited risks OR acquired risks
40
what causes arterial thrombosis
platelet and vessel wall abnormalities | most commonly atherosclerosis
41
acquired risk factors for venous thromboembolism (by risk)
``` major surgery, trauma history lupus anticoagulant pregnancy cancer hospitalization w/ illness oral contraceptives hyperhomocysteinemia anticardiolipin antibodies hormone replacement obesity ```
42
inherited risk factors for venous thromboembolism (by frequency)
``` Factor 5 leiden (heterozygous) elevated factor 8 hyperhomocysteinemia prothrombin G20210A protein c deficiency protein s deficiency antithrombin deficiency factor 5 leiden (homozygous) dysfibrinogenemia ```
43
what is the function of protein C
inactivates 8 and 5
44
what is the function of protein S
cofactor of protein C
45
what is the function of antithrombin
inactivates 10, 2, others
46
what is factor 5 leiden
point mutation leading to decreased proteolytic inactivation by protein C
47
where does DVT occur
deep veins of legs pulmonary arteries cerebral veins, mesenteric veins, hepatic veins
48
clinical features of DVT
leg swelling different in calf circumference between legs redness, warmth, tenderness, palpable cord in calf
49
diagnosis of DVT
compression ultrasound of proximal leg veins (+ if noncompressible) D-dimer venography
50
prognosis of DVT
PE | post-thrombotic syndrome
51
clinical features of PE
``` dyspnea, wheezing chest pain (pleuritic) hemoptysis right sided heart failure (cor pulmonale) hypoxemia ```
52
diagnosis of PE
spiral CT- high PPV, low NPV D-dimer- high NPV, low PPV ventilation-perfusion (V-Q) scan, pulmonary angiography
53
prognosis of PE
mortality 15%, usually due to right heart failure | chronic pulmonary hypertension
54
prothrombin gene mutation
point mutation in 3' untranslated region leading to increased stability of mRNA increased prothrombin levels
55
antiphospholipid syndrome
autoantibodies against phospholipid binding proteins; mechanism of thrombosis not entirely clear venous and arterial thrombosis treat w anticoagulation if you have recurrent symptoms
56
heparin induced thrombocytopenia
autoantibodies against heparin-platelet factor 4 complex cause platelet activation and thrombosis worse with higher MW heparin types
57
clinical features of heparin induced thrombocytopenia
``` 4 T's timing- 5-7 days after heparin thrombocytopenia- 50% decrease thrombosis- venous, arterial exclude oTher causes no bleeding ```
58
what is DIC
intravascular activation of coagulation without a specific localization and arising from different causes can cause damage to microvasculature and produce organ dysfunction
59
clinical features of DIC
bleeding | thrombosis
60
pathologic features of DIC
``` hyaline microthrombi of microvessels platelet and fibrin rich thrombi thrombocytopenia prolonged PT and/or PTT decreased fibrinogen elevated D-dimer microangiopathic hemolysis (schistocytes) ```
61
management of DIC
manage underlying disorder blood product as clinically indicated antifibrinolytic agents- if bleeding predom heparin- if clotting predom

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