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Immunology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

Forces pushing fluid out of a vessel

A

hydrostatic pressure

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2
Q

Osmotic force keeping fluid in a vessel

A

Oncotic pressure

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3
Q

What is normally more than the other?
Forces keeping fluid in vessels or forces pushing/allowing fluid out?

A

Forces pushing/allowing fluid out is slightly greater

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4
Q

Excess interstitial fluid

A

Edema

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5
Q

Excess fluid in a cavity

A

Effusion

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6
Q

Intra-abdominal effusion

A

Ascites

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7
Q

3 reasons for excess fluid

A

Increased hydrostatic pressure
Decreased oncotic pressure
Increased vascular permeability

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8
Q

3 reasons for increased hydrostatic pressure

A

Decreased venous return (may be local or systemic)
Increased plasma volume (kidney failure or increased Na retention)
Decreased lymphatic drainage (tumor, filariasis, scar tissue)

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9
Q

2 reasons for decreased oncotic pressure

A

Decreased protein production (liver failure or malnutrition)
Increased protein loss (kidney failure or diarrheal illness)

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10
Q

Fluid high in protein and cellularity
Seen in situations with high vascular permeability (inflammation, endothelial damage)

A

Exudate

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11
Q

Fluid low in protein and cellularity
Seen in situations with high hydrostatic pressure or low colloid pressure (heart or liver failure)

A

Transudate

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12
Q

Does high or low hydrostatic pressure lead to transudate?

A

High

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13
Q

Disorder of perfusion involving increased intravascular blood due to increased inflow (inflammation)

A

Hyperemia

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14
Q

Disorder of perfusion involving increased intravascular blood due to decreased outflow (heart failure)
May cause hepatomegaly

A

Congestion

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15
Q

Disorder of perfusion involving blood leaving vascular space
Trauma, vascular disease, coagulopathy

A

Hemorrhage

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16
Q

What is hyperemia (increased intravascular blood) due to?

A

Increased inflow

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17
Q

What is congestion (increased intravascular blood) due to?

A

Decreased outflow

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18
Q

Condition that makes someone vulnerable to bleeding with small injury
Can cause hemorrhages
Can involve platelets or coagulation proteins

A

Coagulopathy

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19
Q

Pinpoint hemorrhage in skin or cornea
Due to microvascular rupture

A

Petechiae

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20
Q

Diffuse superficial hemorrhages in skin
Often a confluence; often seen in small vessel disorders

A

Purpura

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21
Q

Larger collection of blood in superficial skin

A

Ecchymosis

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22
Q

Progression of bruise colors due to RBC degradation:
First to appear

A

Hemoglobin (red)

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23
Q

Progression of bruise colors due to RBC degradation:
Second to appear

A

Deoxyhemoglobin (blue-red)

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24
Q

Progression of bruise colors due to RBC degradation:
Third to appear

A

Biliverdin (yellow-green)

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25
Q

Progression of bruise colors due to RBC degradation:
Fourth to appear

A

Hemosiderin (yellow-brown)

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26
Q

Collection of blood in soft tissue of parenchymal organ

A

Hematoma

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27
Q

Collection of blood in anatomic space

A

Hemorrhagic effusion

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28
Q

Normal process to stop hemorrhage
Has three main contributing systems (vascular, platelets, coagulation)

A

Hemostasis

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29
Q

3 main contributing systems to hemostasis

A

Vascular (vascular activities slow or prevent hemorrhage)
Platelets (contribute to clot and help activate coagulation)
Coagulation (produces a fibrin meshwork)

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30
Q

Lining cell of blood vessels

A

Endothelium

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31
Q

Endothelium releases this which is a vasodilator that inhibits platelet aggregation

A

Prostacyclin (PG-I2)

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32
Q

Endothelium releases this which is a vasodilator

A

NO

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33
Q

Endothelium produces this which degrades platelet ADP

A

ADPase

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34
Q

Small disk shaped cytoplasmic buds from bone marrow megakaryocytes

A

Platelet

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35
Q

Platelet are small disk shaped cytoplasmic buds from these

A

Bone marrow megakaryocytes

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36
Q

Thrombocyte is another name for these

A

Platelets

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37
Q

Component with these procoagulant activities:
Provide surface phospholipid for coagulation factors
Provide ADP to activate others
Aggregate to form initial plug

A

Platelets

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38
Q

Platelets provide surface ______ for coagulation factors

A

Phospholipid

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39
Q

Coagulation system where:
Vascular injury induces vasoconstriction
Endothelium is activated to secrete vWF
Platelets adhere, activate, aggregate

A

Primary hemostasis

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40
Q

Coagulation system where:
Soluble coagulation factors –> fibrin
Fibrin clot forms to enmesh platelet aggregate

A

Secondary hemostasis

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41
Q

Coagulation system where:
Counter-regulatory measures keep it local

A

Tertiary hemostasis

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42
Q

3 main steps of hemostasis

A
  1. Vasoconstriction
  2. Platelet plug
  3. Coagulation cascade
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43
Q

Damaged endothelium releases this, which leads to vasoconstriction
Transient effect
Promotes smooth muscle constriction
Vessel caliber decreases

A

Endothelin

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44
Q

Endothelin is released by this

A

Damaged endothelium

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45
Q

Endothelin has this effect

A

Vasoconstriction

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46
Q

Platelets adherence to exposed collagen (ECM) is mediated by this interaction

A

Glycoprotein Ib (platelet receptor) binding to von Willebrand factor (which is produced by endothelium and platelets, and binds to exposed collagen)

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47
Q

This is produced by endothelium and platelets
Binds to exposed collagen
Is bound by glycoprotein 1b on platelets

A

von Willebrand factor (vWF)

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48
Q

What is the role of von Willebrand factor (vWF)?

A

Mediates platelets adherence to exposed collagen (ECM)
Is produced by endothelium and platelets
Binds to exposed collagen
Is bound by glycoprotein 1b on platelets

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49
Q

Platelet receptor that binds to vWF during platelets adherence to exposed collagen

A

Glycoprotein Ib

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50
Q

This binds to platelet receptor, changing platelet shape to have “sticky ends” (starfish shape)

A

Thrombin (or ADP or serotonin)

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51
Q

After changing shape due to thrombin, platelet sticky ends have high density of this

A

Glycoprotein 2b/3a

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52
Q

4 steps of platelet activation during primary hemostasis

A

Platelet change shape
Glycoprotein 2b/3a concentrates on tips of filopodia
ADP/serotonin released (activate nearby platelets)
Fibrinogen released

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53
Q

Interaction that causes platelets to aggregate

A

Glycoprotein 2b/3a binds fibrinogen polymer to form connecting bridge between platelets

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54
Q

Role of glycoprotein 2b/3a

A

Binds fibrinogen polymer to form connecting bridge between platelets
Results in platelet aggregation

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55
Q

Role of glycoprotein 1b

A

Binds vWF –> Platelet adherence to ECM

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56
Q

Formation of fibrin clot involves a cascade of these enzymes

A

Serine proteases

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57
Q

Intrinsic pathway of fibrin clot formation starts with this
Begins fibrinolysis

A

Factor XII exposure to negatively charged surface

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58
Q

Factor XII exposure to this starts the intrinsic pathway of fibrin clot formation

A

Negatively charged surface

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59
Q

Factor XII activates this

A

XI –> XIa

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60
Q

XIa activates this

A

IX –> IXa
(X is skipped)

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61
Q

IXa activates this

A

VIII –> VIIIa

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62
Q

Extrinsic pathway of fibrin clot formation starts with this

A

Factor VII exposure to Tissue Factor

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63
Q

Factor VII exposure to this starts the extrinsic pathway of fibrin clot formation

A

Tissue Factor

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64
Q

Tissue Factor activates this

A

Factor VII –> VIIa

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65
Q

Convergence of the intrinsic and extrinsic pathways of fibrin clot formation

A

VIIIa and VIIa can both activates X to Xa

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66
Q

Xa activates this

A

II (Prothrombin) –> IIa (Thrombin)

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67
Q

Factor II aka

A

Prothrombin

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68
Q

Factor IIa aka

A

Thrombin

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69
Q

Prothrombin is this factor

A

Factor II

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70
Q

Thrombin is this factor

A

Factor IIa

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71
Q

Factor II (thrombin) activates these

A

Platelets

72
Q

IIa activates this

A

Factor I (fibrinogen) –> Ia (fibrin)

73
Q

Fibrinogen is this factor

A

Factor I

74
Q

Fibrin monomer is this factor

A

Factor Ia

75
Q

Factor I aka

A

Fibrinogen

76
Q

Factor Ia aka

A

Fibrin monomer

77
Q

Acute phase reactant that is secreted by pIt and endothelium
Produced as the end of the serine protease cascade during fibrin clot formation

A

Factor I = fibrin

78
Q

These form polymers to enmesh platelets
Are cross-linked via Factor XIIIa

A

Fibrin

79
Q

Fibrin is cross-linked to enmesh platelets via this

A

Factor XIIIa

80
Q

Regulatory protein that inhibits Factor Va

A

Protein C

81
Q

Protein C inhibits this

A

Va

82
Q

Cofactor for Factor Xa
together they cleave prothrombin (factor II)

A

Va

83
Q

Va is a cofactor for this

A

Factor Xa
together they cleave prothrombin (factor II)

84
Q

Protein C has this cofactor

A

Protein S
Together they inactivate Factor Va

85
Q

Protein S is a cofactor for this

A

Protein C
Together they inactivate Factor Va

86
Q

Expressed by intact endothelium
Binds thrombin (IIa), together they activate Protein C (which inactivates V)

A

Thrombomodulin

87
Q

Thrombomodulin is expressed by this

A

Intact endothelium

88
Q

Thrombomodulin binds this, and together they activate Protein C

A

Thrombin (factor IIa)

89
Q

Thrombomodulin binds Thrombin (IIa), and together they activate this

A

Protein C

90
Q

Protein C receptor is expressed by this

A

Intact endothelium

91
Q

Expressed by intact endothelium
Inhibits thrombin, Factors 9-12

A

Antithrombin III

92
Q

Antithrombin III is expressed by this

A

Intact endothelium

93
Q

Antithrombin III inhibits these

A

Thrombin, Factors 9-12

94
Q

Factor XIIa cleaves

A

Plasminogen to plasmin

95
Q

This cleaves plasminogen to plasmin

A

Factor XIIa

96
Q

This is expressed by endothelium into clot and activates plasminogen to plasmin

A

Tissue plasminogen activator (tPA)

97
Q

This cleaves fibrin polymers back to monomers
Clot dissolves

A

Plasmin

98
Q

Mucosal bleeding, skin bleeding, severe thrombocytopenia are defects in this

A

Primary hemostasis

99
Q

Soft tissue bleeds (hematomas) and hemarthroses (blood in joint space) are defects in this

A

Secondary hemostasis

100
Q

Thrombosis and hypercoagulability are defect in this

A

Tertiary hemostasis

101
Q

Intravascular (including intra-cardiac) blood clot formation

A

Thrombosis

102
Q

Term for 3 factors that promote thrombus formation

A

Virchow’s triad

103
Q

Define Virchow’s triad

A

3 factors that promote thrombus formation
(Endothelial injury, Blood stasis or turbulence, Hypercoagulability)

104
Q

Activated endothelium (due to injury) down regulates these 3 things to promote a procoagulant state

A

Thrombomodulin
Protein C receptor
Tissue plasminogen activator (tPA)

105
Q

This is a major factor in arterial thrombosis

A

Endothelial injury

106
Q

Endothelial injury is a major factor in _______ thrombosis

A

Arterial

107
Q

Stasis is a major factor in _______ thrombosis

A

Venous
low flow state and stasis allows factor accumulation

108
Q

Turbulence is a major factor in _______ thrombosis

A

Arterial or venous

109
Q

Hypercoagulability is a major factor in _______ thrombosis

A

Venous

110
Q

Example of hypercoagulability involving decreased function of anticoagulant force

A

Factor V Leiden (genetic mutation)

111
Q

Example of hypercoagulability involving increased function of pro-coagulant force

A

Prothrombin G20210A (genetic condition)

112
Q

4 clinical states that can produce Virchow’s Triad and clotting

A

Estrogenic states (hypercoagulability)
Pregnancy (hypercoagulability)
Atrial fibrillation (turbulent blood flow)
Coronary atherosclerosis (turbulent blood flow)

113
Q

Thrombi that occur in cardiac chambers, usually a result of turbulence of stasis

A

Mural thrombi

114
Q

Thrombi frequently associated with atherosclerotic plaque
Often occlusive

A

Arterial thrombi

115
Q

Thrombi frequently associated with stasis and hypercoagulable states
“Always” occlusive
Form lines of Zahn

A

Venous thrombi

116
Q

Alternating zones of cell-rich and platelet/fibrin rich areas
Form in states of flowing blood
Form in venous thrombi

A

Lines of Zahn

117
Q

This type of plaque predisposes to an arterial thrombus (produces turbulent blood flow due to plaque distorting shape of blood vessel)

A

Atherosclerotic

118
Q

Thrombus propagation:
Retrograde growth from attachment site

A

Arterial

119
Q

Thrombus propagation:
Anterograde growth from attachment site

A

Venous

120
Q

When fragment thrombus fragment dislodges and travels downstream

A

Embolization

121
Q

4 stages of the thrombus life cycle

A

Propagation
Embolization
Dissolution due to fibrinolytic system
Organization

122
Q

Thrombus obstruction involving congestion, edema, and pain due to inflammation (thrombophlebitis)

A

Venous thrombus obstruction

123
Q

Thrombus obstruction involving ischemia and possible death or organ receiving blood

A

Arterial thrombus obstruction

124
Q

What is thrombophlebitis?

A

Venous thrombus obstruction

125
Q

Loose intravascular material carried by blood stream

A

Embolism

126
Q

Detached thrombus; most common form of embolism

A

Thromboembolism

127
Q

Where do venous thromboembolism end up?

A

Lung
(Right atrium –> right ventricle –> lung)
= Pulmonary embolism

128
Q

Pulmonary embolism that begins in deep veins of leg

A

Deep vein thrombosis

129
Q

Result of a large clot that obstructs pulmonary vasculature

A

Sudden death

130
Q

Result of a smaller clot that obstructs pulmonary vasculature

A

Asymptomatic or chest pain
Infarction is uncommon

131
Q

Type of embolism usually due to long bone fractures
Source = bone marrow
Multiple small emboli lodge in lung and/or systemic circulation (which could go to brain)
Produces endothelial injury and platelet aggregation (leading to low platelet counts)

A

Fat embolism

132
Q

Source of fat for fat embolism

A

Fat embolism

133
Q

This can occur during a fat embolism, causing respiratory distress, dyspnea, or mental status changes

A

Multiple small emboli lodge in lung and/or systemic circulation (which could go to the brain)

134
Q

Type of embolism that involves platelet aggregation, leading to low platelet counts
Results in thrombocytopenia

A

Fat embolism

135
Q

This is often an earlier sign of a fat embolism

A

Platelet aggregation, leading to low platelet counts (thrombocytopenia)

136
Q

Introduction of gas into vasculature
Mechanisms: vessels open to air + negative pressure
Iatrogenic causes (neurosurgery, obstetrics, thoracic), or from trauma (chest wall especially) or decompression sickness

A

Air embolism

137
Q

Obstetric complication where uterine vasculature opens during placental separation
Amniotic fluid enters circulation and contains baby’s epithelial cells/debris
Lodged in narrowed points of circulation
Foreign material produces intravascular coagulation of mother

A

Amniotic fluid embolism

138
Q

Amniotic fluid embolism causes damage when amniotic fluid enters circulation, gets lodged in narrowed points of circulation or the foreign material produces this

A

Intravascular coagulation of mother

139
Q

Tissue necrosis due to ischemia
Most due to arterial atherosclerosis and/or thromboemboli

A

Infarct

140
Q

This type of blood supply is more resistant to infarcts

A

Dual blood supply (e.g. lungs)

141
Q

2 examples of tissues that have short duration ischemia –> infarct

A

CNS and myocardium

142
Q

Tissue type that survives many hours of ischemia

A

Fibrous tissue

143
Q

Infarcts are usually this shape

A

Wedge shaped

144
Q

Color of infarct if end-arterial organ (e.g. spleen, bone)

A

Pale

145
Q

Color of infarct if organ with dual blood supply (e.g. lung, liver)

A

Hemorrhagic

146
Q

Typical type of necrosis of infarct

A

Coagulative necrosis

147
Q

Infarct is hemorrhagic if due to this

A

Venous obstruction

148
Q

This type of margins often occur in infarcts

A

Hyperemic

149
Q

Usual result of this type of infarct is congestion and edema
Less common
Collaterals allow tissue survival

A

Venous infarct
Infarct occurs if enough hemorrhage occurs to obstruct arterial flow

150
Q

2 mechanisms of ischemic injury

A

Lack of ATP
Generation of ROS/free radicals (mitochondrial damage or lack of O2)

151
Q

Increased tissue damage and inflammation due to blood flow restoration
Should provide O2 to reversibly damaged cells and allow survival, but sometimes this causes increased cell death

A

Reperfusion injury

152
Q

3 mechanisms of reperfusion injury cell death

A

Damaged mitochondria (increased ROS, release of cytochrome C)
Blood flow brings WBCs to sites attracted by DAMPs –> increase ROS
Blood flow brings Ca2+ to damaged cells –> pro-death pathways

153
Q

What is contraction band necrosis?

A

Increased Ca2+ causes contraction of actin-myosin

154
Q

Circulatory failure with decreased perfusion and global cellular hypoxia

A

Shock

155
Q

These are the 3 main mechanisms of this:
Inadequate pumping
Too little intravascular volume
Vasodilation

A

Shock
Cardiogenic shock
Hypovolemic shock
Septic/anaphylactic/neurogenic shock

156
Q

Type of shock caused by vasodilation involving bacterial infection

A

Septic shock

157
Q

3 phases of shock

A

Compensated phase
Decompensated phase
Irreversible phase

158
Q

Low renal blood flow results in release of this during shock

A

Renin

159
Q

Renin release due to low renal blood flow has these two effects

A

Angiotensin release –> vasoconstrictoin
Aldosterone release –> kidneys increase sodium and water retention

160
Q

Low hypothalamic blood flow results in release of this

A

ADH

161
Q

These are symptoms of this:
Low pressure, fast pulse
Pale (parenchymal/skin vasoconstriction)
Renal vasoconstriction and renal water retention

A

Compensated phase of shock

162
Q

Phase of shock involving organ hypoperfusion
Goal is to maintain cardiac output and blood pressure

A

Compensated phase

163
Q

These decrease parasympathetic stimulation during the compensated phase of shock, leading to increased cardiac pumping

A

Baroreceptors

164
Q

Baroreceptors lead to this characterization of the compensated phase of shock

A

Increased cardiac phase (fast pulse)

165
Q

Phase of shock involving cerebral, renal, liver, cardiac, and muscle hypoperfusion
Cellular metabolism shifts to anaerobic metabolism (increased lactic acid)

A

Decompensated phase of shock

166
Q

Why is there increased creatinine during the decompensated phase of shock?

A

Renal hypoperfusion

167
Q

Why is there increased AST/ALT during the decompensated phase of shock?

A

Liver hypoperfusion

168
Q

Why is there increased lactic acid during the decompensated phase of shock?

A

Cellular metabolism shifts to anaerobic metabolism

169
Q

Phase of shock where organ damage is too extensive to reverse
Progresses to multiorgan system failure
Cardiac ischemia –> decreased cardiac output
Intestinal ischemia –> bacteremia –> sepsis

A

Irreversible phase

170
Q

Especially severe form of shock due to systemic infection

A

Septic shock

171
Q

Type of microorganism that most prominently causes septic shock

A

Gram positive > gram negative > fungal infection

172
Q

During septic shock, there is widespread ______ activation

A

Endothelial

173
Q

These are factors of this:
Microbial products activate innate immune system
Generalized cytokine release
Widespread endothelial activation (NO synthase, anticoagulant factors decreased)
Complement activation

A

Septic shock

174
Q

During septic shock, these factors are decreased

A

Anticoagulant factors decreased, promoting a procoagulant state

175
Q

During septic shock, a procoagulant state is promoted by these 3 things

A

Decreased thrombomodulin
Decreased protein C
Tissue Factor released

Immunology (21 decks)

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