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IHO Week 1 > Krafts IHO Week 6 > Flashcards

Krafts IHO Week 6 Flashcards

1
Q

Pro-Clotting: Blood Vessels Constricts

A

blood loss decreases, platelets and factors meet

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2
Q

Pro-Clotting: Platelets form a plug

A

proteins are exposed, platelets adhese, granules release contents, platelets aggregate, phospholipids are exposed

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3
Q

Pro-Clotting:fibrin seals up plug

A

tissue factor is exposed, cascade begins, cascade makes fibrin, fibrin solidifies plug

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4
Q

Anti-Clotting: 1. Cascade Inhibition

A

TFPI, ATIII, Protein C,S

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5
Q

Anti-Clotting: 2. Clot Lysis

A

t-PA, plasmin

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6
Q

alpha granule

A

fibrinogen, vWF

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7
Q

delta granule

A

serotonin, ADP, Ca2+

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8
Q

Membrane Phospholipids

A

activate coag factors

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9
Q

Membrane GP 1a

A

binds collagen

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10
Q

Membrane GP 1b

A

binds vWF

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11
Q

Membrane GP IIb-IIIa

A

binds fibrinogen

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12
Q

Where does tissue factor (TF) come from?

A

‘hidden’ cells exposed during injury, microparticles floating in blood, endothelial cells and monocytes (during inflammation)

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13
Q

Closure Time

A

-alternative to bleeding time, platelet function analyzer measures how quickly platelets occlude small holes (in vitro bleeding time), better than the bleeding time at detecting aspirin related bleeding and von Willebrand ds

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14
Q

causes of increased PT

A

decreased VII, X, V, II, I or coumadin, heparin and DIC

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15
Q

When to order a PT?

A

NEVER (order an INR instead which is a corrected PT)

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16
Q

Why do you order an INR?

A

to assess liver function, monitor Coumadin therapy, dx DIC and to assess pre-op status

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17
Q

PTT (partial thromboplastin time)

A

plasma + phospholipid, measures intrinsic pathway, APTT=same thing

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18
Q

PTT increased in

A

hemophilia A, hemophilia B, DIC, heparin, inhibitors

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19
Q

When should you a PTT?

A
  1. investigate a hx of abnormal bleeding time 2. monitor heparin therapy 3. dx DIC 4. dx an antiphospholipid antibody 5. assess pre-op status
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20
Q

Thrombin Time

A

Plasma + thrombin, measures conversion of fibrinogen to fibrin, bypasses intrinsic and extrinsic pathways

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21
Q

TT increased in

A

low fibrinogen and high FDPs

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22
Q

When to order a TT?

A

when the PTT is prolonged and you want to r/o a fibrinogen problem (rare)

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23
Q

PTT Mixing Study

A

pooled plasma + patient plasma + phospholipid

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24
Q

If PTT corrects

A

something is missing=factor deficiency

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25
Q

If PTT doesn’t correct

A

inhibitor present

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26
Q

When should you order a mixing study?

A

when PTT is prolonged and TT is normal

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27
Q

Fibrin Degradation Product Assay

A

Measures FDPs (fibrin degradation products), very sensitive

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28
Q

FDPs increased

A

thrombi, minor clotting

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29
Q

When to order an FDP assay?

A

not to rule in a clot, but to RULE OUT a clot

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30
Q

Hereditary Bleeding Disorders

A

von Willebrand disease, Hemophilia A and B, Hereditary platelet disorder

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31
Q

Acquired bleeding disorders

A

DIC, ITP, TTP/HUS

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32
Q

Platelet Bleeding

A

superficial (skin), petechiae, spontaneous

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33
Q

Factor Bleeding

A

Deep (joints), big bleeds, trauma

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34
Q

most common hereditary bleeding disorder, autosomal dominant, vW factor decreased (or abnormal), variable severity

A

Von Willebrand Disease

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35
Q

huge multimeric protein, made by megs and endothelial cells, glues platelets to endothelium, carries factor VIII, decreased or abnormal vW disease

A

von Willebrand Factor

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36
Q

Type 1 Von Willebrand Disease

A

70%, decreased vWF

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37
Q

Type 2 Von Willebrand

A

25%, abnormal vWF

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38
Q

Type 3 Von Willebrand

A

5%, no vWF

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39
Q

mucosal bleeding in most patients, deep joint bleeding in severe cases

A

Von Willebrand Disease

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40
Q

Lab Tests in VW Disease

A

prolonged bleeding time, PTT prolonged that corrects with mixing study, normal INR, vWF level decreased (normal in type 2), platelet aggregration studies abnormal

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41
Q

Tx of VW Ds: DDAVP

A

raises VIII and vWF levels

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42
Q

Tx of VW Ds: Cryoprecipitate

A

contains vWF and VIII

43
Q

Tx of VW Ds

A

Factor VIII

44
Q

most common factor deficiency, X-linked recessive in most cases (30% are random mutations), factor VIII level decreased, variable amount of ‘factor’ bleeding

A

Hemophilia A

45
Q

Sx of Hemophilia A

A

severity depends on amount of VIII, typical ‘factor’ bleeding (deep joint bleeding and prolonged bleeding after dental work), rarely, mucosal hemorrhage

46
Q

Lab Tests in Hemophilia A

A

INR, TT, platelet count, bleeding time all normal, PTT prolonged that corrects with mixing study, abnormal factor VIII assays, DNA studies abnormal

47
Q

Tx of Hemophilia A

A

DDAVP and Factor VIII

48
Q

factor IX level decreased, much less common than hemophilia A, same inheritance pattern, same clinical and laboratory findings

A

Hemophilia B

49
Q

Rare Factor Deficiencies

A

XI deficiency (bleeding after trauma) and XIII deficiency (severe neonatal bleeding)

50
Q

abnormal Ib, abnormal adhesion, big platelets, severe bleeding

A

Bernard-Soulier Syndrome

51
Q

No IIb-IIIa, no aggregation,severe bleeding

A

Glanzmann Thrombasthenia

52
Q

No alpha granules, big empty platelets, mild bleeding

A

Gray Platelet Syndrome

53
Q

no delta granules, can be part of a syndrome (Chediak-Higashi)

A

delta granule deficiency

54
Q

lots of underlying disorders, something triggers coagulation to cause thrombosis, platelets and factors get used up and cause bleeding, microangiopathic hemolytic anemia

A

Disseminated Intravascular Coagulation

55
Q

Causes of DIC: Dumpers

A

obstetric complications, adenocarcinoma, acute promyelocytic leukemia

56
Q

Causes of DIC: Rippers

A

bacterial sepsis, trauma, burns, vasculitis

57
Q

malignancy, OB complications, sepsis, trauma

A

DIC

58
Q

Sx of DIC

A

Insidious or fulminant, multi-system ds, thrombosis and/or bleeding

59
Q

Lab Tests in DIC

A

INR, PTT and TT prolonged; FDPS increased, Fibrinogens decreased

60
Q

Tx of DIC

A

tx underlying disorder, support with blood products

61
Q

antiplatelet antibodies, acute vs chronic, dx of exclusion, steroids or splenectomy

A

Idiopathic Thrombocytopenic Purpura

62
Q

autoantibodies to GP IIb-IIIa or Ib, bind to platelets, splenic macrophages eat platelets

A

Pathogenesis of ITP

63
Q

Chronic ITP

A

adult women, primary or secondary, insidious (nose bleeds, easy bruising), danger (bleeding into the brain)

64
Q

Acute ITP

A

children, abrupt; follows viral illness, usually self-limiting, may become chronic

65
Q

Lab Tests in ITP

A

signs of platelet destruction (thrombocytopenia, normal/increased megakaryocytes, big platelets), normal INR/PTT, no specific dx test

66
Q

5 Other Causes of Thrombocytopenia

A

aplastic anemia, bone marrow transplant, big spleen, consuptive processes (DIC, TTP, HUS), drugs

67
Q

TX of ITP

A

glucocorticoids, splenectomy, IV Ig

68
Q

all have thrombi, thrombocytopenia and MAHA, include TTP and HUS, can be hard to distinguish from TTP and HUS, something triggers platelet activation, different from DIC

A

Thrombotic Microangiopathies

69
Q

Pentad (MAHA, thrombocytopenia, fever, neurologic defects, renal failure), deficiency of ADAMTS13, big vWF multimers trap platelets, plasmapheresis or plasma infusions

A

Thrombotic Thrombocytopenic Purpura

70
Q

Just-released vWF is unusaually large (UL), UL vWF causes platelet aggregation, ADAMTS13 cleaves UL vWF into less active bits and TTP is dt ADATS13 deficiency

A

Pathogenesis of TTP

71
Q

Clinical Findings in TTP

A

hematuria and jaundice (MAHA), bleeding and bruising (thrombocytopenia), fever, bizarre behavior (neurologic deficits), decreased urine output (renal failure)

72
Q

Tx of TTP

A

acquired: plasmapheresis, hereditary: plasma infusions

73
Q

MAHA and thrombocytopenia, epidemic (e.coli) v non-epidemic, toxin or damages endothelium, tx supportively

A

Hemolytic Uremic Syndrome

74
Q

Pathogenesis of HUS-Epidemic

A

E.coli O157:H7 (raw hamburger), makes nasty toxin, injures endothelial cells

75
Q

Pathogenesis of HUS-Non epidemic

A

defect in complement factor H, inherited or acquired, does does this activate platelets

76
Q

Epidemic HUS Clinical findings

A

children, elderly, blood y diarrhea and then renal failure and is fatal in 5% of cases

77
Q

Non-epidemic HUS Clinical findings

A

renal failure, relapsing-remitting course, fatal in 50% of cases

78
Q

Tx of HUS

A

supportive care, dialysis, NOT abx as may increase toxin release

79
Q

Thrombosis Risk Factors

A

Endothelial damage (atherosclerosis-HTN, hyperlipidemia, obesity, smoking) and Stasis (immobilization, varicose veins, cardiac dysfunction) and Hypercoagulability (trauma/surgery, carcinoma, estrogen/postpartum, thrombotic disorders)

80
Q

Hereditary Thrombotic Disorders

A

Factor V Leiden, ATIII deficiency, protein C deficiency, protein S deficiency, factor II gene mutation, homocysteinemia

81
Q

Acquired Thrombotic Disorders

A

Antiphopholipid Ab

82
Q

most common cause of unexplained thromboses, point mutation in factor V gene (can’t be cleaved by protein C), factor V can’t be turned off, need genetic testing for dx

A

Factor V Leiden

83
Q

Risk of Clot with Factor V Leiden

A

Heterozygotes 7x, homozygotes 80x, normal risk is 1-2 pts per 1000 per year

84
Q

a natural anticoagulant (inhibits IIa, VIIa, IXa and XIa), potentiated by heparin, lots of gene mutations exist, very rare

A

Antithrombin III Deficiency

85
Q

Mutated Gene in ATIII

A

produces LESS ATIII, rara avis (1%), can’t do genetic testing

86
Q

Risk of Getting a Clot in ATIII

A

homo: can’t survive, hetero half get clots, heparin won’t work and antithrombin concentrates required

87
Q

natural anticoagulants, fibrinolytic and anti-inflammatory, wafarin induced skin necrosis, purpura fulminans, rare

A

Protein C Deficiency

88
Q

natural anticoagulants, wafarin induced skin necrosis, super rare

A

Protein S Deficiency

89
Q

Describe Protein C

A

anticoagulant (inactivates Va and VIIIa), fibrinolytic (promotes t-PA action) and anti-inflammatory (keeps cytokines low)

90
Q

Risk of Clot with Protein C Deficiency

A

hetero: 7x normal

91
Q

What does coumadin inhibit?

A

II, VII, IX, X and C and S

92
Q

thrombotic state and vascular injury to skin necrosis, associated with protein C and S deficiency and sepsis, tx may include administering protein C

A

Purpura Fulminans

93
Q

mutated gene makes too MUCH prothrombin, rare in non-caucasians, 5% of caucasians, clot risk 2-20 times normal

A

Factor II (prothrombin) Gene Mutation

94
Q

Too much homocysteine leads to

A

thromboses

95
Q

amino acid, made from methionine, maintains myelin and converts dietary folate

A

Homocysteine

96
Q

rare metabolic disorder, deficient trans-sulphuration enzyme, increase homocytsteine in blood and urine, increase thrombosis, premature atherosclerosis

A

Homocysteinuria

97
Q

MTHFR gene mutation or B12/folate deficiency

A

Homocysteinemia

98
Q

Negatives of Homocysteine

A

toxic to endothelium (ROS) and interferes with NO (a vasodilator and antithromboitc)

99
Q

Risk of thrombosis with heterozygous homocysteinemia

A

venous 2.5x and arterial 10x

100
Q

autoantibodies against phospholipids, falsely prolong INR, may cause thromboses

A

Antiphospholipid Antibodies

101
Q

anticardiolipin antibodies, lupus anticoagulants, antibodies against other molecules

A

IgG antibodies to phospholipids

102
Q

recurrent thrombosis, recurrent spontaneous abortions, increased risk of stroke, pulmonary HTN, renal failure

A

antiphospholipid antibody syndrome

103
Q

How to detect Antiphospholipid Antibodies

A
  1. PTT 2. if prolonged order PTT mixing study 3. if normal, antibody may still be present and need to order fancy tests

IHO Week 1 (16 decks)

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