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Pathology > Hemodynamics III & IV > Flashcards

Hemodynamics III & IV Flashcards

1
Q

What are the factors that coumadin affects?

A

8, 9, 10, 2 (1972), protein C and protein S

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2
Q

What is INR?

A

PT pt / PT nl

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3
Q

What pathway does PT measure?

A

Extrinsic pathway

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4
Q

What pathway for PTT measure?

A

Intrinsic pathway

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5
Q

What is the normal range of INR?

A

0.8-1.2

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6
Q

What drugs prolongs the intrinsic pathway (and thus PTT)?

A

heparin, hemophilia, and antiphospholipid antibody

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7
Q

How do you distinguish if someone have a factor deficiency vs an inhibitor?

A

Mix patient’s sample with normal plasma. If clots, then patient has it. If no clot, then there is an inhibitor

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8
Q

What are the two factors not measured by PT or PTT?

A

7 and 13

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9
Q

Low dose heparin has what effect on PT/PTT?

A 
PT = nl
PTT = prolonged
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10
Q

High dose heparin has what effect on PT/PTT?

A 
PT = Prolonged
PTT = Prolonged
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11
Q

Low dose warfarin has what effect on PT/PTT?

A 
PT = Prolonged
PTT = Normal
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12
Q

HIgh dose warfarin has what effect on PT/PTT?

A 
PT = Prolonged
PTT = Prolonged
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13
Q

What happens to the sensitivity of pts to warfarin with age?

A

Increase sensitivity

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14
Q

What are the contraindications to Warfarin?

A

Pregnancy
If hemorrhage is a risk
EtOH abuse
Dementia

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15
Q

What are the signs of warfarin overdose?

A

Hematochezia
Bruising
Epistaxis
Persistent bleeding

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16
Q

What is Warfarin necrosis?

A

Warfarin causes low levels of protein C, causing excessive clotting (hypercoagulable state)

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17
Q

What strategy do we take to prevent Warfarin necrosis?

A

Give heparin first with Warfarin’s first dose

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18
Q

What is heparin-induced thrombocytopenia?

A

Antibodies form against platelet factor 4 (which normally blocks heparin)

This induces a prothrombotic state

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19
Q

What is HIITS?

A

Heparin-induces thrombocytopenia with thrombosis syndrome

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20
Q

What is Bernard-Soulier disease?

A

AR disease where there is a defect of platelet adhesion d/t defect in Glycoprotein Ib

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21
Q

What is Glanzmann Thrombasthenia?

A

Defect of platelet aggregation d/t a defect in glycoprotein IIb/IIIa.(Recall this links platelets together)

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22
Q

What is thrombotic thrombocytopenic purpura (TTP)?

A

Antibodies directed against von Willebrand factor cleaving protease, ADAMTS-13,(this normally breaks up von Willebrand factor)

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23
Q

Are PT/PTT affected in Bernard-Soulier or Glanzmann disease?

A

No

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24
Q

What is idiopathic thrombocytopenia purpura (ITP)? What is the treatment for recurrent?

A

Antibodies directly against platelets, leading to spleen destruction, resulting in thrombocytopenia

Treatment = splenectomy

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25
Q

What is aplastic anemia?

A

Pancytopenia, marrow’s is fibrosed, no more blood cells

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26
Q

What is von Willebrand’s disease?

A

Deficiency of von Willebrands antigen, causing coagulopathies

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27
Q

What are the clinical symptoms of von Willebrand disease?

A

Easily bruised
Epistaxis
Gingival bleeding
Menorrhagia

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28
Q

What is hemophilia A the result of? How is this passed on?

A

Factor 8 deficiency

XR

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29
Q

What is hemophilia B the result of?

A

Factor 9 deficiency

XR

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30
Q

What is hemophilia C the result of? How is this passed on?

A

Factor 11 deficiency

AR

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31
Q

How do you treat hemophiliacs?

A

Recombinant factor, or plasma

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32
Q

What are the major complications with hemophilia?

A

Deep, internal bleeding

Joint damage

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33
Q

What are the problems with transfusions for hemophiliacs?

A

Risk for infx

Adverse immune rxn

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34
Q

Deficiencies with which factors are particularly problematic?

A

5, 7, 8, 9, 11

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35
Q

How do we monitor factor deficiencies?

A

PTT/PT

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36
Q

What are the factor deficiencies that are usually not clinically significant?

A

Factor 12

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37
Q

How do platelet deficiencies appear clinically?

A

Purpura, petechiae, or ecchymosis

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38
Q

What is DIC? What does this lead to?

A

Systemic problem of coagulation where tiny fibrin thrombi form throughout the body.

Leads to thrombocytopenia

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39
Q

What is meant by the term consumptive coagulopathy?

A

All of the platelets are used up

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40
Q

What causes DIC? What two things does this cause?

A

Activation of thrombin systemically, causing fibrin formation and consumption of platelets

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41
Q

Why does DIC result in organ failure?

A

Clots form in organs, leading to cut off blood supply

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42
Q

Why does DIC result in bleeding?

A

All the platelets are used up

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43
Q

What are schistocytes? What causes these?

A

Sheared RBCs, caused by strands of fibrin in capillaries cutting them.

(this is seen in DIC)

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44
Q

What does a D-dimer measure?

A

Measures plasma cleaved insoluble cross-linked fibrin

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45
Q

What is the treatment for DIC?

A

Treat underlying cause

Use blood products

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46
Q

What are the components of Virchow’s triad?

A

Hypercoagulable state
Endothelial injury
Circulatory stasis

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47
Q

What is the dominant influence on thrombosis?

A

Endothelial injury

48
Q

What happens to fibrinogen to fibrin conversion during thrombus formation?

A

Increased markedly

49
Q

What causes endothelial injury?

A

LDL cholesterol buildup
Smoking
HTN
DM

50
Q

What is the most common hypercoagulable state?

A

Factor 5 leiden

51
Q

What does prothrombin mutations lead to?

A

Hypercoagulable state

52
Q

What are the rare deficiencies that result in a hypercoagulable state?

A

Antithrombin III
Protein C
Protein S

53
Q

What are pts with Factor 5 leiden susceptible to?

A

DVTs

54
Q

What is the problems with factor V leiden?

A

Resistance of factor V to Protein C

55
Q

What is the amino acid change involved with factor V leiden?

A

Q substitutes for R at 506 position

56
Q

What is the primary risk for thrombosis?

A

Bedrest or long periods of immobility

57
Q

What are the two heart problems that pose a risk for thrombosis?

A

A fib and MI

58
Q

What is antiphospholipid antibody syndrome?

A

Serum antibody against anionic phospholipids, causing a hypercoagulable state

59
Q

What pts have antiphospholipid antibody syndrome?

A

SLE pts

60
Q

What is turbulence?

A

Disruption of the normal, laminar flow of blood

61
Q

Why is blood turbulence problematic?

A

Forms countercurrents of blood, causing local pockets of stasis, and prevents dilution of clotting factors

62
Q

What can cause turbulence?

A

Ulcerated atherosclerotic plaques
MI
Afib

63
Q

What is hyperviscosity syndrome?

A

Polycythemia

64
Q

What does turbulent flow cause to endothelial cells to secrete (3)?

A

Secreted angiotensin II
Endothelin 1
PDGF

65
Q

What does turbulent flow cause to the amount of migration of immune cells?

A

Increases

66
Q

venous thrombi usually occur as a consequence of what?

A

Stasis

67
Q

Arterial thrombi occur where?

A

At sites of endothelial injury

68
Q

What are the two major problems with arterial thrombosis?

A

Occlusion

Emboli

69
Q

Where do clots form that cause strokes?

A

Carotid bifurcation

70
Q

What are arterial thrombi composed of?

A

Platelets
Fibrin
RBCs
Leukocytes

71
Q

What is gruel?

A

The foam cells in the endothelium

72
Q

Stenting is indicated for AAA when they are how big?

A

5 cm or greater

73
Q

What are lines of Zahn?

A

Lines in a thrombus, indicating alternating layering of platelets, fibrin, and erythrocytes

74
Q

What cells do venous thrombi contain more of?

A

Erythrocytes

75
Q

Where do venous thrombi usually occur?

A

Deep veins in the leg

76
Q

Where is the turbulence found in veins?

A

Behind the valves

77
Q

What is a phlebothrombosis?

A

Venous thrombosis

78
Q

What are the problems with superficial thrombi in the legs?

A

Varicose veins–NOT PEs

79
Q

What percent of pts with DVTs have symptoms in their leg?

A

50%

80
Q

What are the risk factors for venous thrombosis?

A

CHF
Trauma
Surgery
Pregnancy

81
Q

What is trousseau syndrome?

A

Thrombi form in larger veins in different parts of the body d/t S proteases released by tumors, that activates factor 10.

Also membrane vesicles released that are prothrombotic

82
Q

What are the five fates of a thrombus?

A 
Emboli
Resolution
Propagate
Recanalized
Incorporated into the wall
83
Q

What do emboli usually occur from?

A

Dislodged thrombus

84
Q

What are the common causes of arterial emboli?

A

A fib
Mitral stenosis
Endocarditis

85
Q

What is the most common type of thrombus?

A

Intracardiac mural thrombi

86
Q

Where do arterial emboli usually go?

A 
Lower extremities (75%)
Brain (10%)
87
Q

What are paradoxical emboli?

A

Rare condition in which an embolus originating from the venous circulation passes through an interatrial or interventricular defect to gain access to the systemic circulation

88
Q

What percent of PEs are caused by DVTs?

A

95%

89
Q

What is a saddle embolus?

A

Lodge across the pulmonary vessel bifurcation

90
Q

Where do medium emboli usually end up?

A

Medium sized branches

91
Q

Where do small emboli end up?

A

Peripheral vessels, usually silent

92
Q

What do recurrent emboli cause?

A

Cor pulmonale

93
Q

Wedge like infarcts are caused by what sized emboli?

A

Medium

94
Q

What is a V/Q mismatch?

A

Different between ventilation and circulation

95
Q

What are fat emboli? What do they usually come from?

A

Fat, usually from fractures of large bones or burns

96
Q

What do fat emboli look like microscopically?

A

Clear vacuoles w/in the vessels

97
Q

True or false: fat emboli usually have no effect

A

True (90% no effect)

98
Q

What is the stain used to identify fat emboli?

A

Oil red O stain

99
Q

What are the symptoms of a fat emboli? (3)

A

Tachypnea/dyspnea
Diffuse petechial rash
CNS symptoms if fat there

100
Q

What are air embolisms caused by?

A

Obstetric procedures

Vascular procedures

101
Q

How much air is needed to cause air embolisms?

A

> 100 cc

102
Q

What is decompression sickness?

A

Sudden changes in atmospheric pressure causes N gas embolize

103
Q

What is the bends?

A

Decompression sickness in skeletal muscles and around joints

104
Q

What are the chokes?

A

Gas emboli in the lungs d/t decompression

105
Q

What is the treatment for decompression sickness?

A

Slow decrompression

106
Q

What is an amniotic fluid embolism?

A

If amniotic fluid gets into the maternal blood, causes severe clots

107
Q

What does amniotic fluid emboli consist of?

A

Epithelial cells from fetus

Lanugo hair

108
Q

What are four causes the infarction, besides thrombus?

A

Vasospasm (cocaine)
Hemorrhage
Compression of vessel
Twisting of vessel

109
Q

venous causes of infarct are more likely in organs with what?

A

Single venous outflow

110
Q

Venous thrombosis usually induces only congestion, not infarction. Why?

A

Usually have more than one venous outflow

111
Q

What is the most critical factor in determining if an infarct will develop?

A

Anastomoses

112
Q

Why are the spleen and kidney particularly susceptible to infarction?

A

End arterial system

113
Q

What is a red infarct? Shape?

A

Infarct with a hemorrhage in them

Usually wedge shaped

114
Q

What causes a red infarct?

A

venous occlusions
Loose tissues
Tissues with dual circulation

115
Q

What causes a white infarct?

A

Type of arterial occlusions in solid organs with limitations of blood flow into areas of ischemic necrosis

116
Q

What is a septic infarct?

A

Infarct where the origin of the embolus is an infected tissue

117
Q

What is the major source of septic infarcts?

A

Vegetations from bacteria on heart valves

Pathology (32 decks)

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