IV - Hemodynamic Disorders, Thrombosis and Shock Flashcards Preview

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Flashcards in IV - Hemodynamic Disorders, Thrombosis and Shock Deck (119)
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91

Underlying cause of amniotic fluid embolism.

Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

92

Presence of marked pulmonary edema, diffuse alveolar damage, and presence of squamous cells in the pulmonary circulation shed from fetal skin, lanugo hair, fat and mucin.

Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

93

White or red infarct?Venous occlusion

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

94

White or red infarct?Lung infarction

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

95

White or red infarct?Intestinal infarct

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

96

White or red infarct?Myocardial infarction

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

97

White or red infarction?Splenic infact

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

98

White or red infarction?Wedge infarct

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

99

The dominant histologic characteristic of infarction.

Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

100

Histologic characteristic of brain infarcts.

Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

101

This occurs when bacterial vegetations from a heart valve embolize or when microbes seed an area of necrotic tissue.

Septic infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

102

Most common sequalae of septic infarcts.

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

103

Major determinants of the eventual outcome of an infarct. (4)

Nature of vascular supplyRate of development of occlusionVulnerability to hypoxiaOxygen content of blood(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

104

Neurons undergo irreversible damage when deprived of their blood supply for _______.

3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

105

Myocardial cells undergo irreversile damage after ______ minutes of ischemia.

20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

106

It is the final common pathway for severe hemorrhage, extensive trauma, burns, large MI, pulmonary embolism and sepsis.

Shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

107

End results of shock (3)

HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

108

This type of shock results from failure of the cardic pump which maybe caused by MI, ventricular arrythmias, cardiac tamponade or outflow obstruction.

Cardiogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

109

This type of shock results from loss blood or plasma volume.

Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

110

This type of shock is caused by microbial infection, caused by gram negative and gram positive bacteria and fungi

Septic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

111

True or false:Systemic bacteremia must be present to induce septic shock.

FalseHost inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102

112

Type of shock which occurs in the setting of an anesthetic accident or spinal cord injury as a result of loss of vascular tone and peripheral pooling of blood.

Neurogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

113

This type of shock represents systemic vasodilation and increased vascular permeability caused by IgE hypersensitivity reaction.

Anaphylactic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

114

Septic shock caused by gram negative bacilli.

Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103

115

Criteria for SIRS.

Temp 38 CelciusHR >90 bpmRR >20 or PaCO2 12,000 cells/mm3 or 10% bands(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103

116

Adrenal changes in shock.

Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

117

Kidney changes in shock.

Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

118

Gastrointestinal changes in shock.

Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

119

Lung changes in shock.

Diffuse alveolar damage if due to bacterial sepsi and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106