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MOD Midterm > Hemodynamic Disorders, Thromboembolic Disease, and Shock > Flashcards

Hemodynamic Disorders, Thromboembolic Disease, and Shock Flashcards

1
Q

How is edema different from effusion?

A

Edema is the abnormal accumulation of fluid in the interstitial space; effusion is the abnormal accumulation of fluid in a body cavity/ potential space

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2
Q

What are some examples of body cavities/potential spaces where fluid can accumulate?

A

pericardial space, peritoneal space, pleural space, and joint space

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3
Q

what is it called when fluid accumulates in the peritoneal space?

A

ascites

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4
Q

What 4 things are the direct causes of edema/effusions?

A

Increased hydrostatic pressure, decreased colloid osmotic pressure, increased vascular permeability, and lymphatic obstruction

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5
Q

What is hyperemia, what color is it, and is it physiologic or pathologic?

A

Hyperemia is when too much blood is arriving, red/arterial, physiologic

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6
Q

what is congestion, what color is it, and is it physiologic or pathologic?

A

Congestion is when not enough blood is leaving, blue/venous, pathologic

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7
Q

What does congestion usually result in and why?

A

edema- due to increased hydrostatic pressure

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8
Q

why does heart failure lead to edema?

A

there is an increased hydrostatic pressure, which directly leads to edema; there is also a decrease in renal blood flow, which activates the RAAS system, which causes retention of Na+ and H2O, which causes there to be an increase in blood volume- this causes increased hydrostatic pressure and decreased colloid osmotic pressure, which directly causes edema

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9
Q

what are the pulmonary findings associated with heart failure?

A

pulmonary edema and pulmonary effusions

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10
Q

what is the mechanism of heart failure that leads to edema/effusions?

A

there is decreased “pumping activity”- this leads to a “back up” of pulmonary venous circulation (aka congestion); there is also retention of Na+ and H2O- this causes there to be increased blood volume, which causes a decrease in plasma colloid osmotic pressure

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11
Q

what are 2 examples of edema associated with heart failure?

A

pitting edema and pulmonary edema

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12
Q

what are 2 signs of liver failure?

A

ascites and edema

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13
Q

what are the mechanisms of edema/ascites associated with liver failure?

A

there is a decrease in the production of albumin (this causes there to be a decreased in colloid osmotic pressure); there is also portal hypertension, which leads to congestion

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14
Q

what are the two ways that renal failure can result in edema?

A

there is increased retention of Na+ and H2O (this increases intravascular pressure); nephrotic syndrome, which causes there to be excessive loss of proteins in the urine (this causes there to be decreased colloid osmotic pressure)

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15
Q

What is Kwashiorkor?

A

a protein deficiency that results in insufficient production of albumin- this leads to a decreased colloid osmotic pressure

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16
Q

When might you have a protein deficiency that leads to decreased plasma osmotic pressure?

A

protein deficiency (Kwashiorkor), decreased synthesis of proteins (liver failure) or excessive protein loss of proteins in urine (renal disease with nephrotic syndrome)

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17
Q

What could cause localized edema?

A

lymphedema

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18
Q

What are some causes of lymphedema?

A

infection, inflammation, trauma, tumors, surgery, or malformations

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19
Q

What effect does the parasite filariasis have on the body?

A

the organism induces obstructive fibrosis of lymphatic channels and lymph nodes (this could lead to edema of the external genitalia and lower limbs)

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20
Q

What is the difference between exudate and transudate?

A

exudate has a high protein concentration and contains cell debris; transudate has a low protein concentration and no cellular debris, and has a low specific gravity

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21
Q

what does the presence of transudate imply?

A

that there is an increase in hydrostatic pressure (congestive heart failure) or a decreased in colloid osmotic pressure (decreased protein synthesis –> liver failure or increased protein loss–> kidney disease with nephrotic syndrome)

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22
Q

What does the presence of exudate imply?

A

the existence of an inflammatory process that has increased the permeability of small blood vessels

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23
Q

what could cause an increase in capillary permeability?

A

sepsis, infection, and burns

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24
Q

what could chronic congestion lead to?

A

edema–>hemosiderosis–>tissue damage

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25
Q

What is the morphology/pathology of heart failure caused (chronic) pulmonary edema?

A

pulmonary edema from left heart failure results in the accumulation of fluid in the alveolar spaces; chronic congestion shows increased hemosiderin-laden macrophages (aka heart failure cells)

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26
Q

where do you see obstruction of blood flow in cases of hepatic congestion?

A

central vein

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27
Q

what is hepatic congestion most often caused by?

A

advanced heart failure

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28
Q

what is the pathology/morphology of acute hepatic congestion?

A

the central vein and sinusoids are distended–> centrilobular hepatocytes may undergo ischemic necrosis

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29
Q

what is the pathology/morphology of chronic hepatic congestion?

A

the centrilobular regions are grossly red-brown and slightly depressed (because of cell death) and are accentuated against the surrounding zones of uncongested tan liver (nutmeg liver)

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30
Q

What is the initial step in hemostasis?

A

vasoconstriction

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31
Q

how does the initiating step of hemostasis-vasoconstriction- occur?

A

it is a reflexive neurogenic process that is further mediated by endothelin

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32
Q

what is the purpose of the initiating step of hemostasis- vasoconstriction?

A

it reduces the surface area affected and it reduces the blood flow

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33
Q

What are the steps of primary hemostasis?

A

adhesion, activation, and aggregation

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34
Q

what does the subendothelial surface have that allows platelets to bind?

A

von Willebrand Factor

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35
Q

what do the platelets have that allow them to bind to the subendothelial surface?

A

GpIb

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36
Q

What is a significant source of von willebrand factor?

A

Weibel Palade bodies

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37
Q

What does lack of functional vWF cause?

A

von Willebrand disease

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38
Q

what does lack of GpIb receptor cause?

A

Bernard-Soulier Syndrome

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39
Q

what do the platelets look like in Bernard Soulier syndrome?

A

they are giant

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40
Q

what 2 things occur during platelet activation?

A

conformational change and secretion

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41
Q

during the stage of activation what is there a conformational change of?

A

the actual platelet- makes it a negatively charged surface, and the GpIIb-IIIa changes shape

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42
Q

during the stage of activation, what is there secretion of? and what is this secretion initiated by?

A

secretion of ADP and Thromboxane A2; secretion is initiated by thrombin

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43
Q

what does secretion of ADP cause?

A

more activation of platelets

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44
Q

what does secretion of Thromboxane A2 cause?

A

more aggregation of platelets

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45
Q

what is the effect of administration of aspirin?

A

aspirin is going to inhibit thromboxane A2 (so there will not be aggregation of platelets)

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46
Q

what does the conformational change of the GpIIb-IIIa in activated platelets allow for?

A

bivalent binding of fibrinogen, which leads to cross linking of platelets

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47
Q

what do you get if there is a deficiency in GpIIb-IIIa complex?

A

disorder of platelet aggregation- Glanzmann thrombasthenia

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48
Q

How do we know if something is wrong with primary hemostasis clinically?

A

Mucocutaneous bleeding

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49
Q

What are some common clinical signs of someone with a disorder of primary hemostasis/mucocutaneous bleeding?

A

petechiae, ecchymoses, purpura, hemorrhagic bullae

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50
Q

symptoms of disorders of primary hemostasis depends on platelet levels. What symptoms do you get if you have 20-50k platelets?

A

petechiae and ecchymoses following mild trauma

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51
Q

symptoms of disorders of primary hemostasis depends on platelet levels. What symptoms do you get if you have less than 10k platelets?

A

risk for intracranial hemorrhage and spontaneous generalized mucocutaneous bleeding

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52
Q

symptoms of disorders of primary hemostasis depends on platelet levels. What symptoms do you get if you have less than 2k platelets?

A

widespread ecchymoses, hemorrhagic bullae, and retinal hemorrhage

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53
Q

How do we know if something is wrong with primary hemostasis in the laboratory?

A

platelet quantity (CBC); platelet quality (function)

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54
Q

what are some modern techniques to test platelet function?

A

flow cytometry and PFA-100

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55
Q

What is the mechanism of disease in thrombocytopenia?

A

loss or impaired production of platelets

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56
Q

what is the platelet count for thrombocytopenia?

A

low

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57
Q

Is there still platelet adhesion in cases of thrombocytopenia?
Is there still platelet aggregation in cases of thrombocytopenia?

A

yes and yes

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58
Q

what is the mechanism of disease in Von Willebrand disease?

A

inherited lack of vWF

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59
Q

What is the platelet count in cases of von willebrand disease?

A

normal

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60
Q

is there platelet adhesion in cases of von willebrand disease?
Is there platelet aggregation in cases of von willebrand disease?

A

no platelet adhesion

yes platelet aggregation

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61
Q

what is the mechanism of disease for bernard-soulier disease?

A

abnormal GpIb

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62
Q

What is the platelet count for bernard-soulier disease?

A

low-normal

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63
Q

is there platelet adhesion in cases of bernard-soulier disease?
Is there platelet aggregation in cases of bernard-soulier disease?

A

no platelet adhesion

Yes platelet aggregation

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64
Q

what is the mechanism of disease for Glanzmann’s thrombasthenia?

A

abnormal GpIIb-IIIa

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65
Q

what is the platelet count in cases of Glanzmann’s thrombasthenia?

A

normal

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66
Q

is there platelet adhesion in cases of Glanzmann’s thrombasthenia?
is there platelet aggregation in cases of Glanzmann’s thrombasthenia?

A

Yes platelet adhesion

No platelet aggregation

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67
Q

What is secondary hemostasis?

A

the coagulation cascade

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68
Q

What is the overall purpose of the coagulation cascade?

A

to form the fibrin clot

69
Q

where does the coagulation cascade start for the intrinsic pathway?/ what kicks off the intrinsic pathway?

A

a negatively charged surface

70
Q

where does the coagulation cascade start for the extrinsic pathway?/ what kicks off the extrinsic pathway?

A

tissue factor (factor III)

71
Q

What is reflected in the laboratory for the intrinsic pathway?

A

aPTT

72
Q

what is reflected in the laboratory for the extrinsic pathway?

A

PT

73
Q

What factors are involved in the intrinsic pathway?

A

XII, XI, IX, VIII

74
Q

What factors are involved in the extrinsic pathway?

A

VII

75
Q

What factors are involved in the common pathway?

A

X

76
Q

what happens once thrombin binds to the heparin-like molecule?

A

it inactivates thrombin (and factors IXa and Xa)

77
Q

What is another name for factor II?

A

prothrombin

78
Q

what is another name for factor VIII?

A

Antihemophilic A Factor (AHF)

79
Q

What are the prothrombotic functions for thrombin?

A

it stabilizes fibrin, it activates platelets, and it activates receptors on inflammatory cells and endothelium

80
Q

What are the vitamin K dependent factors?

A

II, VII,IX, X

81
Q

what is the function of Coumadin (warfarin)?

A

it blocks the vitamin K dependent carboxylation- so the factors II, VII, IX, X remain inactive

82
Q

What are the clinical signs of a defect in hemostasis? (most common in platelet dysfunction)

A

dermatologic manifestations–> petechiae, purpura, and ecchymosis

83
Q

what type of problem with hemostasis might you have if there is visceral and intracranial bleeding?

A

factor deficiencies or profound thrombocytopenia

84
Q

what should a normal aPTT be?

A

32-45 seconds

85
Q

what should a normal PT be?

A

10-14 seconds

86
Q

if there is a prolonged aPTT what might you have?

A

factor deficiency in VIII, IX, XI, or XII

87
Q

if there is a prolonged PT what might you have?

A

factor VII deficiency

88
Q

if there is a combined abnormal aPTT and PT, what might you have?

A

taking anticoagulants, DIC, liver disease, vitamin K deficiency, massive transfusion, or a factor X, V, and II defect

89
Q

what is the function of plasmin?

A

it breaks apart fibrin (the fibrin clot duh)

90
Q

where do we get t-PA?

A

the non-injured endothelial cells release the t-PA

91
Q

what is the function of t-PA?

A

it is going to activate plasmin (from plasminogen)

92
Q

how does intact endothelium have an antithrombotic effect?

A

there is no exposed tissue factor; there is also platelet inhibition

93
Q

what molecules are platelet inhibitors?

A

adenosine diphosphatase, prostacyclin, nitric oxide

94
Q

what enzyme is responsible for fibrinolysis?

A

plasmin

95
Q

what does thrombin bind to on uninjured endothelial cells?

A

thrombomodulin

96
Q

what happens once thrombomodulin binds thrombin?

A

it activates protein C

97
Q

what happens once protein C is activated?

A

it inactivates factors Va and VIIIa

98
Q

what happens once thrombin binds to the heparin-like molecule?

A

it inactivates thrombin (and factors IXa and Xa)

99
Q

What are the primary mechanisms that lead to thrombosis?

A

endothelial injury, abnormal blood flow, and hypercoagulability of the blood

100
Q

What section of virchow’s triad would you place hypercholesterolemia or inflammation?

A

under endothelial injury

101
Q

what section of virchow’s triangle would you place stasis (a fib or bed rest) or turbulence (atherosclerotic vessel narrowing)?

A

abnormal blood flow

102
Q

what section of virchow’s triangle would you place factor V Leiden or disseminated cancer?

A

under hypercoagulability

103
Q

What is the result of endothelial dysfunction?

A

decreased nitric oxide activity; which leads to endothelial activation, causing an increase in adhesion molecules

104
Q

what are the prothrombotic changes that occur with endothelial activation?

A

there is a down regulation of both thrombomodulin and activated protein C; there is also an elaboration of plasminogen activator inhibitors (PAIs)

105
Q

what is the effect of plasminogen activator inhibitor (PAIs)?

A

they will limit fibrinolysis

106
Q

when might there be alterations in blood flow?

A

normal bifurcations, dilated vessels (aneurysms or hemorrhoids), internal obstruction, external compression, or inadequate heart chamber function

107
Q

how can hypercoagulability be divided?

A

primary (genetic) or secondary (acquired)

108
Q

What are the 3 most common causes of primary (genetic) hypercoagulability?

A

factor V mutation, prothrombin mutation, or increased levels of factors VIII, IX, XI, or fibrinogen

109
Q

what are the 3 rare primary (genetic) causes of hypercoagulability?

A

antithrombin III deficiency, Protein C deficiency, protein S deficiency

110
Q

what are 2 very rare primary (genetic) causes hypercoagulability?

A

fibrinolysis defects or homozygous homocystinuria

111
Q

who is at strong risk for a secondary (acquired) hypercoagulability?

A

those on prolonged bed rest, MI, A fib, tissue injury, cancer, prosthetic cardiac valves

112
Q

What are some other risks factors for secondary (acquired) hypercoagulability?

A

hyperestrogenic states (pregnancy and postpartum), oral contraceptive use, smoking, sickle cell anemia

113
Q

What happens if the deep vein thrombosis dislodges?

A

it becomes an embolus and will lodge itself in the pulmonary arterial circulation

114
Q

when might you suspect a primary hypercoagulable state?

A

if there is an initial event (DVT or PE) with no provoking factors, they have young age (40-50), and a strong family history

115
Q

what tests might you run if you want to rule out a primary hypercoagulable state?

A

ATIII levels, Protein C levels, Protein S levels, Factor V Leiden mutation

116
Q

In the coagulation cascade, what does calcium bind to?

A

the gamma-carboxylated glutamic acid residues that are present in factors II, VII, IX, and X

117
Q

the enzymatic reactions that produce gamma-carboxylated glutamic acid uses what as a cofactor?

A

vitamin K

118
Q

What is found to be more common in factor deficiencies rather than primary hemostasis issues?

A

hemarthrosis (hemophilia)

119
Q

Following secondary hemostasis: the coagulation cascade, what is the final step of hemostasis?

A

fibrinolysis and limitation of clot formation

120
Q

What are the ways our body limits coagulation?

A

through blood flow (blood washes away activated clotting factors); there is no more platelet surface; and through plasmin

121
Q

What is the most common genetic cause of thrombosis?

A

a factor V Leiden mutation

122
Q

what population is more susceptible to a factor V leiden mutation?

A

Caucasian/ Europeans

123
Q

what is the mechanism of action of a factor V Leiden mutation?

A

the mutated factor V makes it essentially unable to be cleaved by activated protein C

124
Q

What are two ways you can see if a patient has a factor V Leiden mutation?

A

by doing a direct genetic test or by using the functional test: APC resistance (APCR) testing

125
Q

How do you perform the APCR test?

A

you give samples of activated protein C to a patient; the patient should have an elevated clot time; however, if they have a factor V Leiden mutation, they will continue to thrombose

126
Q

What are two common acquired (secondary) hypercoagulable states?

A

1) Heparin-induced thrombocytopenia and 2) antiphospholipid antibody syndrome

127
Q

what is the prothrombotic state caused by in heparin-induced thrombocytopenia?

A

antibodies to PF4 heparin

128
Q

what does heparin bind to when administered?

A

to PF-4

129
Q

what type of antibodies are produced against the heparin-PF4 complex in some people?

A

IgG

130
Q

what do the anti-heparin + PF-4 IgG bind to?

A

platelet Fc receptors

131
Q

what happens once the antibody complex binds to the platelet Fc receptors?

A

there is going to be activation and aggregation of the platelets leading to a thrombotic event; but there is also going to simultaneously be dropping out of the platelets from circulation, which leads to thrombocytopenia

132
Q

what does a patient scenario with heparin-induced thrombocytopenia typically look like?

A

we put a patient on heparin and then a few days later their platelet count drops, they might even have a thrombotic event

133
Q

how do we test to see if a patient has heparin-induced thrombocytopenia?

A

we test for PF-4 Antibodies

134
Q

what is a common sign in patients if HIT is not treated quickly?

A

digital gangrene

135
Q

what population of people are more susceptible for antiphospholipid antibody syndrome?

A

it is a relatively common situation especially in younger-middle aged women in the US

136
Q

what can antiphospholipid antibody syndrome occur in the presence of?

A

systemic lupus erythematosis

137
Q

what occurs in antiphospholipid antibody syndrome?

A

you get antibodies against plasma proteins that bind to phospholipids

138
Q

What are the various presentations for a patient with antiphospholipid antibody syndrome?

A

Vascular: arterial or venous thrombosis (stroke, pulmonary emboli, digital gangrene); obstetric: unexplained miscarriage/stillbirth

139
Q

What are the four fates of the thrombus?

A

propagation, embolization, dissolution, or organization/recanalization

140
Q

What is propagation of a thrombus?

A

the growth of the thrombus and eventually it is going to occlude and create symptoms

141
Q

What are the 5 different types of emboli?

A

Thromboemboli, amniotic fluid emboli, fat emboli, air emboli, and septic emboli

142
Q

What is it called when a thromboemboli lodges itself right at the bifurcation of the pulmonary arteries?

A

saddle pulmonary embolus: INSTANTANEOUSLY LETHAL

143
Q

How might a patient with a medium sized pulmonary emboli present?

A

SOB and decreased oxygen saturation

144
Q

what causes the instantaneous death during a saddle pulmonary emboli?

A

acute right heart failure

145
Q

How can you tell if a thrombus/embolus occurred during active blood flow (when the patient was still alive)?

A

lines of Zahn

146
Q

What leads to a fat emboli?

A

fracture or trauma to bones (think recent ortho surgery or chest compressions that broke ribs)

147
Q

What are the symptoms of a fat embolism determined by? and what are some examples?

A

As the marrow lodges it creates a situation that manifests based on where it is lodged; respiratory distress or mental status changes

148
Q

What are two causes of air emboli?

A

cardiac catheterization and decompression sickness

149
Q

An amniotic fluid embolism is caused when?

A

there is introduction of fetal material into maternal circulation; when these cells and materials get introduced it creates a shock situation

150
Q

When might a septic emboli occur?

A

in endocarditis (valve vegetations break off and manifest in other sites)

151
Q

what are the microemboli associated with endocarditis/ septic emboli?

A

skin microemboli, retinal microemboli, and vascular damage in the nail bed

152
Q

Where do white thrombi occur and what are they rich in?

A

arterial vessels; rich in platelets

153
Q

A lot of these white thrombi are occurring in a setting of what?

A

atherosclerosis

154
Q

when you think about white thrombi, what arteries should you think of?

A

coronary arteries and cerebral arteries (carotid artery)

155
Q

what type of drugs are good for treating CAD?

A

anti-platelet drugs

156
Q

where do red thrombi occur and what are they rich in?

A

venous vessels; red cell rich

157
Q

a lot of these red thrombi are occurring in the setting of what?

A

stasis

158
Q

when you think of red thrombi, what should you think of?

A

DVT

159
Q

Infarctions are typically occurring because of what?

A

arterial thromboembolic disease

160
Q

What determines if an infarct is going to be red versus white?

A

the anatomy of the vascular supply

161
Q

what is an example of an organ that would have a white infarct?

A

the spleen

162
Q

What are some examples of an organ that would have a red infarct?

A

lungs and the intestines

163
Q

Why does the rate of an occlusion matter?

A

because if a thrombus grows slowly enough, collateral blood vessel formation may occur

164
Q

What are 3 different factors that influence infarcts?

A

anatomy of the vascular supply, rate of the occlusion, and the tissue vulnerability to hypoxia

165
Q

what is shock?

A

when tissue oxygen and nutrient delivery is inadequate to meet physiologic needs

166
Q

What are the 5 different types of shock?

A

cardiogenic, hypovolemic, shock associated with systemic inflammation (SIRS), neurogenic, and anaphylactic

167
Q

what happens when PAMPs on the pathogenic bacteria/fungi interact with TLRs on innate immune cells?

A

there will be a release of inflammatory mediators and activation of complement

168
Q

What is the final result of septic shock?

A

hypotension, hypovolemia, thrombosis; decreased tissue oxygenation

169
Q

as septic shock progresses, how does it manifest?

A

manifestations of hypoxic tissue injury

MOD Midterm (22 decks)

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