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

B3.049 Disorders of Coagulation Flashcards

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
Q

purpura

A

bleeding within skin or mucous membranes

26
Q

petechiae

A

pinpoint bleeding of skin or mucous membranes

27
Q

ecchymosis

A

large confluent area of bleeding within skin, larger than petechiae

28
Q

hematoma

A

a collection of blood in organ, space, or tissue

29
Q

hemarthrosis

A

bleeding into the joint space

30
Q

bleeding patterns associated with primary hemostasis issues

A

skin or mucosal bleeds
purpura, petechiae, ecchymosis
spontaneous bleeding

31
Q

bleeding pattern associated with secondary hemostasis issues

A

bleeds into soft tissue, muscle, joints
hemarthrosis
bleeding with trauma

32
Q

vW disease epidemiology

A

variable age of onset
m = f
prevalence 1-5 per 1000

33
Q

type 1 vWf disease

A

partial quantitative deficiency

autosomal dominant

34
Q

type 2 vWf disease

A

qualitative deficiency
types: factor 8 binding issue, binds to gp1b too much, no multimers
varying degrees of clinical manifestations

35
Q

type 3 vWf disease

A

complete quantitative deficiency

autosomal recessive

36
Q

pathologic features of vW disease

A 
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
Q

treatments for vWf disease

A

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
Q

classic triad of thrombosis

A

abnormal blood flow (stasis or turbulence)
hypercoagulability (inherited or acquired)
endothelial injury (hypercholesterolemia)

39
Q

what causes venous thromboembolism?

A

inherited risks
OR
acquired risks

40
Q

what causes arterial thrombosis

A

platelet and vessel wall abnormalities

most commonly atherosclerosis

41
Q

acquired risk factors for venous thromboembolism (by risk)

A 
major surgery, trauma
history
lupus anticoagulant
pregnancy
cancer
hospitalization w/ illness
oral contraceptives
hyperhomocysteinemia
anticardiolipin antibodies
hormone replacement
obesity
42
Q

inherited risk factors for venous thromboembolism (by frequency)

A 
Factor 5 leiden (heterozygous)
elevated factor 8
hyperhomocysteinemia
prothrombin G20210A
protein c deficiency
protein s deficiency
antithrombin deficiency
factor 5 leiden (homozygous)
dysfibrinogenemia
43
Q

what is the function of protein C

A

inactivates 8 and 5

44
Q

what is the function of protein S

A

cofactor of protein C

45
Q

what is the function of antithrombin

A

inactivates 10, 2, others

46
Q

what is factor 5 leiden

A

point mutation leading to decreased proteolytic inactivation by protein C

47
Q

where does DVT occur

A

deep veins of legs
pulmonary arteries
cerebral veins, mesenteric veins, hepatic veins

48
Q

clinical features of DVT

A

leg swelling
different in calf circumference between legs
redness, warmth, tenderness, palpable cord in calf

49
Q

diagnosis of DVT

A

compression ultrasound of proximal leg veins (+ if noncompressible)
D-dimer
venography

50
Q

prognosis of DVT

A

PE

post-thrombotic syndrome

51
Q

clinical features of PE

A 
dyspnea, wheezing
chest pain (pleuritic)
hemoptysis
right sided heart failure (cor pulmonale)
hypoxemia
52
Q

diagnosis of PE

A

spiral CT- high PPV, low NPV
D-dimer- high NPV, low PPV
ventilation-perfusion (V-Q) scan, pulmonary angiography

53
Q

prognosis of PE

A

mortality 15%, usually due to right heart failure

chronic pulmonary hypertension

54
Q

prothrombin gene mutation

A

point mutation in 3’ untranslated region leading to increased stability of mRNA
increased prothrombin levels

55
Q

antiphospholipid syndrome

A

autoantibodies against phospholipid binding proteins; mechanism of thrombosis not entirely clear
venous and arterial thrombosis
treat w anticoagulation if you have recurrent symptoms

56
Q

heparin induced thrombocytopenia

A

autoantibodies against heparin-platelet factor 4 complex cause platelet activation and thrombosis
worse with higher MW heparin types

57
Q

clinical features of heparin induced thrombocytopenia

A 
4 T's
timing- 5-7 days after heparin
thrombocytopenia- 50% decrease
thrombosis- venous, arterial
exclude oTher causes
no bleeding
58
Q

what is DIC

A

intravascular activation of coagulation without a specific localization and arising from different causes
can cause damage to microvasculature and produce organ dysfunction

59
Q

clinical features of DIC

A

bleeding

thrombosis

60
Q

pathologic features of DIC

A 
hyaline microthrombi of microvessels
platelet and fibrin rich thrombi
thrombocytopenia
prolonged PT and/or PTT
decreased fibrinogen
elevated D-dimer
microangiopathic hemolysis (schistocytes)
61
Q

management of DIC

A

manage underlying disorder
blood product as clinically indicated
antifibrinolytic agents- if bleeding predom
heparin- if clotting predom

IBI Test 3 (19 decks)

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