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THomboembolism Shock Flashcards

1
Q

what is a thrombus

A

an Intravascular clot that often impedes or prevents blood flow

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2
Q

what is thrombosis

A

Formation or preence of a thrombus

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3
Q

what may thrombosis result in

A

Infarction

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4
Q

what is the pathogenesis of Thrombosis

A

Endothelial Injury
Alteration in blood flow
Hypercoagulability

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5
Q

what is the enothelial reason for causing THrombosis

A
  • Loss of endothelial cell barrier
  • Increased prothrombotic activity caused by:
    • Hypertension
    • Homocystinuria
    • hypercholesterolemia
    • radition
    • cytokines
    • endotoxin
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6
Q

what may alter blood flow to lead to thrombosis

A

Turbulence
Stasis
Aneurysms, Atherosclerotic plaques

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7
Q

how does turbulence lead to thrombosis

A

Induces endothelial dysfunction and activation

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8
Q

how does Stasis lead to thrombosis

A

creates hypoxic environment
Stasis disrupts laminar flow cuasing platelts to move to the periphery of the vessel
- allows concentration of clotting factors
- activates endothelial cells
- the major factor in venous thrombi and intra-cardiac thrombi

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9
Q

what is hypercoagulability

A

the increased risk of coagulation

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10
Q

what are the inherited conditions that may lead to hypercoagulability

A

Factor V leiden mutation
Porthrombin mutation
Deficiencies of anticoagulant proteins like AT III

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11
Q

what does a Factor V leiden mutation lead to

A

a factor V that cannot be degraded by protein C leading to hypercoagulability

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12
Q

what are the acquired conditions that may lead to hypercoagulability

A

Prolonged bed rest
Extensive tissue damage such as burns or surgery
Cancer
antiphospholipid antibody syndrome (lupus anticogulant
pregnancy
others

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13
Q

where does Arterial thrombi occur at

A

at sites of turbulence of endothelial injury/loss

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14
Q

what does Arterial thrombi look like

A

has a pale (white appearance

distinct lines of zahn

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15
Q

are arterial thrombi occlusal or mural

A

can be both

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16
Q

what does an arterial thrombi lodging in smaller arteries lead to

A

Often leads to infarction

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17
Q

what aresterile thrombi on heart valves

A

Nonbacterial thrombotic endocarditis

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18
Q

what does a venous thrombi look like

A

have a dark maroon color(red)

indistinct lines of Zahn

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19
Q

where do venous thrombi form

A

In the deep veins of the legs

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20
Q

why do venous thrombi tend to form

A

because of slow flow

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21
Q

how do Venous thrombi look like in the vein

A

Congealed jelly clot that is less organized

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22
Q

waht does thrombi in the heart lead to

A

Alternating lines due to degeneration of RBC

- less capacity of heart

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23
Q

what is the problem with deep vein thrombi

A

can grow, propogate and cause problems

- especially if it gets to the lung

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24
Q

what are the possible fates of thrombi

A

Dissolution (resolution)
Propagation
Embolization
Organization/recanalization

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25
Q

what causes Dissolution of thrombi

A

Lysis by fibrinolytic activity

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26
Q

what causes Propagation of thrombi

A

Enlarge by additional fibrin/platelet deposition

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27
Q

what is embolization of thrombi

A

entire thrombus dislodges or piece breaks loose

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28
Q

how does ORganization of thrombi occur

A

Ingrowth of fibroblasts and smooth muscle cells

- leads to deposition of collagen (replacing fibrin) and recantilizaation

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29
Q

what is the result of organization of thrombi

A

May re-establish some flow through the thrombus

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30
Q

what is Disseminated Intravascular Coagulation

A
  • widespread activation of the coagulation cascade and fibrinolytic system
    • leads to depletion of coagulation factors/platelets
    • leads to a lot of Fibrin split products
  • hemorrhage forms and can’t now clot correctly
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31
Q

what are some of the conditions of Disseminated Intravascular Coagulation

A 
Infection (gram negative)
obstetric complication (placenetal abruption, retained dead fetus)
neoplasm - cascade for coagulation
Shock
Massive injury
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32
Q

how does One treat Disseminated Intravascular Coagulation

A

variable

- dependent upon management of underlying disorders

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33
Q

what is an embolism

A

A solid, liquid, or gas carried from one point to another point in the vascular system

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34
Q

what is often the origin of Pulmonary Thromboembolism

A

Embolism; Thrombi from deep veins of the legs (also pelvic veins, right heart chambers, amoung others)

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35
Q

what are the consequences of pulmonary thromboemboli

A 
No clinical manifestations
Pulmonary hemorrhage and hematemesis
Pulmonary infarcation
Suden death
Gradual obstruction of many small pulmonary arteries
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36
Q

why would a pulmonary Thromboemboli have no clinical manifestation

A

Small emboli cause no ischeme due to the double blood supply to the lungs(bronchial and pulmonary arteries)

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37
Q

why would a pulmonary thromboemboli lead to a pulmonary hemorrhage and hematesmesis

A

Ischemic injury without infarcation

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38
Q

how would a pulmonary thrombooemboli lead to sudden death

A

Large emboli obstructing a large pulmonary artery

- straddling the bifurcation of the pulmonary arterial trunk

39
Q

gradual obstruction of many small pulmonary arties causes what problem

A

Overtime can lead to pulmonary hypertension

40
Q

what is a paradoxical embolus

A

An embolus that arises in a systemic vein and crosses a communication from the venous to arterial side of ciculation

41
Q

where does Paradoxical embolus occure

A

usually through the heart via a patent foramen ovale, atrial septal defect, or another anomalous communication

42
Q

what is the origin of systemic embolization

A

left atrium
Left ventricle (heart valve vegetation)
ulcerated atherosclerotic plaque

43
Q

where can a systemic embolization travel

A

To any systemic artery

44
Q

how may a fat emboli occure

A

Fracture of large long bone, soft tissue injury

45
Q

what may cause of air emboli

A

Chest way injury

46
Q

what can an air emboli cause

A

Decompression sickness due to bends and caisson disease

47
Q

why would amniotic fluid cause an emboli

A

Rare, and often associated with DIC

48
Q

what is Atherosclerotic amboli

A

Debris from the central core of an atherosclerotic plaque

49
Q

what is an infarcation

A

An ischemic necrosis involving all cell types in a part of an organ or entire organ

50
Q

why does an infarct occur

A

Most often due to arterial obstruction
less often due to vessel twisting, venous obstruction or slow flow
- also shock

51
Q

what is infarcation a major contributor to the mortality of what disease

A

Cardiovascular disease

52
Q

Types of Infarctions

A

Red

White

53
Q

What type of INfarction is hemorrhagic

A

Red- Hemorrhage

54
Q

what casues a Red infarction

A

Venous
loose tissue (lung)
Dual circulation or extenisve overlap of arterial supply (lung, small intestine)
Previous congestion
Infarcation followed by a reflow of blood to the area

55
Q

where do White infarcts occur

A

With arterial occlusions in solid

- where tissue density limits blood seepage from adjacent vascular beds

56
Q

what shape do infarcts tend to have

A

Wedge-shaped with the point of the wedge at the obstruction

57
Q

when do histo changes of coagulation necrosis occur due to INfarcts

A

begin within several hours

peaks at 2-3 days

58
Q

how does healing of infarcts occur

A

granulation tissue growth

, beginning at the infarct, followed by scar formation

59
Q

what do infarcts in the brain lead to

A

liquefactive (non- coagulative) necrosis

60
Q

how do Infarcts in the brain heal

A

formation of a cystic space

61
Q

what can impact infarct development

A

Nauter of the vascular supply
Rate of development of occlusion
Vulnerability to hypoxia
O2 capacity of blood

62
Q

what is beteer to limit the influence of an infarct, dual or single artery supply

A

Dual

63
Q

where is dual supply found

A

Lungs
Liver(hepatic artery and portal vein flow)
Forearm (radial and ulnar arteries)

64
Q

how does Rate of development of the infarct affect the infarct

A

Slow occlusion allows time for opening of collateral vessels

65
Q

what tissues are more/less vulnerable to hypoxia

A 
More vulnerable (heart, brain)
Less vulnerable (arm, leg)
66
Q

why would the blood be less good at carrying Oxygen

A

Anemia
Shock
Lung diseases
Congestive heart failure

67
Q

what is Shock

A

Systemic hypoperfusion of tissue

68
Q

what is Cardiogenic shock

A

The loss of pumping capacity of the heart

69
Q

what is Hypovolemic shock

A

Blood loss

70
Q

what is septic shock

A

BActerial infection

71
Q

what is anaphylactic shock

A

Hypersensitivity reaction

72
Q

what mediates Anaphylactic shock

A

IgE

73
Q

what is neurogenic shock

A

Loss of vascular tone

74
Q

what may cause Neurogenic shock

A

Anesthesia

Spinal cord injury

75
Q

what is the numnber 1 cause of death in the ICU

A

septic shock -20% mortality with 750,000 death annually

76
Q

what kinds of bacteria cause septic shock

A

Gram-positive or gram-negatiec bacteria associated with PMPS

77
Q

what do PAMPS bind to

A

Bind to toll-like receptors (monocytes and neutrophils) with release of IL-1, TNF
- secondary release of IL-1 and TNF

78
Q

what happens if you have too much PAMPS

A

leads to septic shock that may lead to DIC

79
Q

what is the last response when going to Septic shock

A

Vasodilation
Hypotension
Endothelial cell activation and injury
reduced myocardial contractility

80
Q

what are the stages of Shock

A

Nonprogressive
Progressive
Irreversible

81
Q

why would shock be nonprogressive

A

Compensatory mechanisms maintain tissue perfusion by tachycardia, renal conservation of water, redistribution of blood to vital organs and away from skin by peripheral vasoconstriction

82
Q

what are the compensatory mechanisms that allow nonprogressive shock to maintain tissue perfusion

A

Catecholamines
Renin
ADH
sympa nervous system stimulation

83
Q

what is Progressive shock

A

when inadequate perfusion with metabolic imbalance(acidosis) reduces vasomotor response to symp stimulation
- lead to pooling of blood and reduced perfusion

84
Q

what does hypoxic injury to epithelium during progressive shock lead to

A

DIC

85
Q

what is Irreversible shock

A

Tissue injury that can not be reversed by reperfusion

86
Q

what happens to brain in shock

A

Ischemic necrosis of neurons (hippocampus and cerebelum)

87
Q

what happens to the heart in shock

A

Contraction band necrosis in the heart

88
Q

what happens in the kidney during shock

A

Necrosis of tubular epithelial cells

89
Q

what happens to the lungs in shock

A

Diffuse alveolar damage in the lungs due to endothelial injury

90
Q

what is it called when sock cuasese endothelial injury in the lungs

A

Adult respiratory distress syndrom (ARDS)

91
Q

what happens to the intestinal tract in shock

A

Mucosal hemorrhage and necrosis

92
Q

what happens to the liver in shock

A

Centrizonal necrosis in the liver

93
Q

what are the clinical manifestations of shock

A 
Tachycardia
Tachypnea
Hypotension
Cool clammy skin
Decreased urinary outpur
Confusion
Low blood pH with elevated lactic acid
94
Q

what type of shock does not result in cool clammy skin

A

Spetic shock

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