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Path Block 2 > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

Edema

A

Swelling of tissue due to increased fluid in interstitial tissue spaces

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2
Q

What is the most common cause of generalized edema?

A

Heart failure

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3
Q

Hydrothorax

A

Fluid in a pleural cavity

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4
Q

Ascites

A

Fluid in the abdominal cavity

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5
Q

Anasarca

A

Generalized edema

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6
Q

If finger pressure on subcutaneous tissue leaves a temporary impression, it is called ______.

A

Pitting edema

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7
Q

What are the 5 categories of edema?

A
  1. Increased hydrostatic pressure
  2. Decreased plasma oncotic pressure
  3. Lymphatic obstruction
  4. Sodium retention
  5. Inflammation
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8
Q

Where is edema due to increased hydrostatic pressure commonly worse?

A

In the legs when standing and in the sacrum when recumbent

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9
Q

Increased ________ causes retention of sodium, which then causes edema.

A

Aldosterone

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10
Q

Heart failure causes decreased renal blood flow, which activates ________.

A

The renin-angiotensin-aldosterone system

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11
Q

Edema from _________ is a feature of the nephrotic syndrome due to protein loss through the kidneys.

A

Decreased plasma osmotic pressure

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12
Q

What is the major protein maintaining plasma oncotic pressure?

A

Albumin

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13
Q

Hypoalbuminemia sufficiently severe enough to cause generalized edema causes __________.

A

Secondary hyperaldosteronism

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14
Q

T or F: Edema due to sodium retention is always generalized.

A

T

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15
Q

Edema due to sodium retention is usually caused by _________.

A

Heart failure

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16
Q

T or F: Edema due to inflammation is always localized.

A

F: can be generalized or localized

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17
Q

Lymphedema is usually localized and caused by __________.

A

Tumor, inflammation, surgery, radiation, or scar

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18
Q

________ can make the skin resemble an orange peel.

A

Lymphedema due to breast cancer

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19
Q

What is the most common cause of pulmonary edema?

A

Left heart failure

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20
Q

What are the causes of pulmonary edema?

A

Left heart failure, ARDS (acute respiratory distress syndrome), hypersensitivity reactions, pneumonia, and renal failure

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21
Q

What is the major symptom of pulmonary edema?

A

Dyspnea

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22
Q

What is the major sign of pulmonary edema?

A

Pulmonary crackles

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23
Q

T or F: Cerebral edema can be localized or generalized.

A

T

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24
Q

When can cerebral edema be fatal?

A

When herniation of the cerebellar tonsils into the foramen magnum compresses the brainstem

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25
Q

Hyperemia (erythema)

A

Active increase in arterial blood flow

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26
Q

Hyperemia causes an abnormal reddish coloration due to ____________.

A

The presence of excess oxygenated blood in a tissue

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27
Q

What is the most common cause of hyperemia?

A

Inflammation

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28
Q

Congestion

A

A passive decrease in venous outflow

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29
Q

What is cyanosis and what causes it?

A

Abnormal bluish coloration due to the presence of excess deoxygenated blood; congestion is a common cause of cyanosis

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30
Q

Where is cyanosis due to cardiovascular or pulmonary disease tend to be first visible?

A

Around the lips (second is nail beds)

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31
Q

_________ causes passive congestion of the liver due to the backup of blood inadequately pumped by the heart.

A

Right heart failure

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32
Q

Passive congestion is associated with what pathological finding?

A

Nutmeg liver (alternating red and tan tissue)

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33
Q

Chronic sublethal left heart failure causes __________.

A

Hemophages to accumulate in pulmonary alveoli

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34
Q

T or F: Hyperemia and congestion are common and serious.

A

F: Common but not serious

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35
Q

Hemorrhage

A

Extravasation of blood due to blood vessel rupture

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36
Q

Hematoma

A

Hemorrhage enclosed within tissue

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37
Q

Petechiae

A

Tiny hemorrhages due to platelet deficiency (1-2 mm)

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38
Q

Purpura

A

Medium hemorrhages due to vasculitis, vessel fragility, etc. (3-10 mm)

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39
Q

Ecchymoses

A

Larger subcutaneous hemorrhages that go from red-blue to blue-green to gold-brown as the hemoglobin breaks down (over 1 cm)

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40
Q

Ecchymoses are frequently called _____.

A

Bruises

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41
Q

Hemopericardium

A

Hemorrhage into the pericardial space

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42
Q

Hemoperitoneum

A

Hemorrhage into the abdominal cavity

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43
Q

Hemarthrosis

A

Hemorrhage into a joint

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44
Q

Hemostasis (2)

A
  1. Maintenance of blood in a free-flowing liquid state in normal blood vessels
  2. Formation of a blood clot at a site of vascular injury
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45
Q

What is hemostasis regulated by (3)?

A

Vascular wall (endothelium), platelets, and the coagulation cascade

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46
Q

What do platelets contain (6)?

A
  1. ADP
  2. Fibrinogen
  3. Clotting factor V
  4. Clotting factor VIII
  5. Calcium
  6. Epinephrine
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47
Q

What are the four stages of hemostasis at site of vascular injury?

A
  1. Vasoconstriction
  2. Primary hemostasis
  3. Secondary hemostasis
  4. Thrombus and antithrombotic events
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48
Q

What regulates vasoconstriction at a site of vascular injury?

A

Reflex neurogenic mechanisms augmented by vasoconstrictors such as endothelin

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49
Q

What mediates platelet adhesion to thrombogenic extracellular matrix?

A

von Willebrand factor, which binds to their GpIb receptors

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50
Q

How does platelet aggregation occur?

A
  1. Platelets adhere to the extracellular matrix (mediated by von Willebrand factor), which binds to their GpIb receptors
  2. Platelet changes shape from smooth surfaced discs to spheres with long spiky projections (facilitates aggregation)
  3. Change in the shape of the platelets allows a conformational change in their GpIIb/IIIa receptors, making them bind fibrinogen
  4. Fibrinogen binds to the altered receptors on adjacent platelets, linking them in an aggregate
  5. Release of ADP and thromboxane A2 causes additional platelet recruitment and aggregation, resulting in a primary hemostatic plug
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51
Q

Coagulation cascade is activated by ____________.

A

Tissue factor and platelet factors

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52
Q

The coagulation cascade culminates in ________.

A

The conversion of fibrinogen to fibrin by thrombin

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53
Q

What all does thrombin do? (4)

A
  1. Converts fibrinogen to fibrin
  2. Stimulates platelets to release thromboxane A2
  3. Activates monocytes and lymphocytes
  4. Stimulates endothelial cells to adhere to neutrophils and to release NO, tissue plasminogen activator, and prostacyclin
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54
Q

In what stage of hemostasis is a semi-permanent plug of aggregated platelets and polymerized fibrin formed?

A

Stage 4

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55
Q

What counter-regulatory mechanism limits the hemostatic plug to the site of injury?

A

Expression of thrombomodulin on the surface of endothelial cells

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56
Q

Thrombomodulin binds thrombin and together they activate ________.

A

Protein C

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57
Q

What is von Willebrand disease?

A

Deficiency of von Willebrand factor that leads to excess bleeding with surgery or menstruation

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58
Q

What is thrombotic thrombocytopenic purport?

A

Overactive von Willebrand factor causes a tendency to clot in small blood vessels then bleed from having used up too many platelets and clotting factors

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59
Q

What is Bernard-Soulier syndrome?

A

Deficiency platelet GpIb receptors for von Willebrand factor, which causes a bleeding tendency

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60
Q

What is Glanzmann thrombasthenia?

A

Deficiency of platelet GpIIb/IIIa receptors that causes a bleeding tendency due to deficient platelet aggregation

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61
Q

What does clopidogrel do?

A

Blocks platelet ADP receptors and is taken orally by patients who have suffered clotting of their critical coronary or cerebral arteries

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62
Q

Thrombosis

A

Inappropriate formation of a blood clot in a blood vessel

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63
Q

What are the three predisposing factors to thrombosis?

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability
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64
Q

What is the most important factor predisposing to thrombosis?

A

Endothelial injury

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65
Q

T or F: Thrombosis is more common in veins and more serious in arteries

A

T

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66
Q

What is the most common inherited hyper coagulable state?

A

Factor V Leiden mutation – makes clotting factor V resistant to activated protein C, resulting in the loss of an important clot-limiting counter regulatory mechanism

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67
Q

What is the second most common inherited hyper coagulable state?

A

Prothrombin G20210A mutation

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68
Q

What is antiphospholipid antibody syndrome and how does it present?

A

A rare but life-threatening acquired hypercoagulable state – it causes arterial thrombosis and is most common in young females
Presentation: recurrent miscarriages, deep vein thromboses, cerebral infarctions, migraine headaches, cardiac vegetations, ischemic hands or feet, and thrombocytopenia

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69
Q

T or F: Most patients with a lupus anticoagulant do not have lupus and all patients with the anticoagulant are hypercoagulable.

A

T

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70
Q

What are the three types of thrombi?

A

Arterial, venous, and mural

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71
Q

Arterial thrombi tend to be rich in _______ and venous thrombi tend to be rich in ______.

A

Arterial: Platelets (white thrombi)
Venous: Erythrocytes (red thrombi)

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72
Q

Where are mural thrombi located?

A

On the wall of the heart

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73
Q

Arterial thrombi are usually where?

A

At sites of endothelial injury

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74
Q

Venous thrombi are usually where?

A

At sites of stasis

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75
Q

How is deep vein thrombosis typically diagnosed in the legs?

A

By ultrasound examination

76
Q

Vegetations

A

Thrombi on heart valves

77
Q

What are the four fates of thrombus?

A
  1. Dissolution
  2. Propagation
  3. Embolization
  4. Organization (and recanalization)
78
Q

Organization

A

Ingrowth by fibroblasts, who convert thrombus to fibrous tissue, with ingrowth of new capillaries, which can coalesce to reanalyze a thromboses blood vessel

79
Q

Embolus

A

Detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin

80
Q

Fat embolism is most commonly from ______.

A

Long bone fractures

81
Q

Air embolism can be caused by ________.

A

Getting air into an intravenous infusion, a sudden change in atmospheric pressure, chest wall injury, or back surgery in a prone position

82
Q

Amniotic fluid embolism can be caused by ________.

A

Tears in the placental membranes during the course of labor and delivery

83
Q

An infarct is usually due to ___________.

A

Thrombotic or embolic occlusion of an artery

84
Q

White anemic infarcts are typical of organs with __________.

A

End-arterial circulation

85
Q

Red hemorrhagic infarcts are typical with _______.

A

Venous occlusion, dual or anastomosing blood supply, or reperfusion

86
Q

What determines the likelihood of an infarction? (4)

A
  1. An organs vulnerability to hypoxia
  2. The rate of development of vascular occlusion
  3. The nature of an organs blood supply
  4. Oxygen content of the blood
87
Q

What 5 aspects should you use to describe an infarct?

A
  1. Size
  2. Shape
  3. Color
  4. Consistency
  5. Its relationships
88
Q

Shock

A

State of systemic (total body) hypo perfusion, cardiovascular collapse

89
Q

Shock is mainly caused by _________ (3).

A
  1. Decreased circulating blood volume
  2. Decreased cardiac output
  3. Sepsis
90
Q

Less common causes of shock include ________.

A

Anaphylaxis, SIRS, and neurogenic causes

91
Q

__________ shock can be due to bleeding or fluid loss from vomiting, diarrhea, or extensive burns.

A

Hypovolemic

92
Q

________ shock can be due to myocardial infarction, cardiac arrhythmia, or pulmonary embolism.

A

Cardiogenic

93
Q

What types of shock make up the distributive shock group?

A

Septic shock, anaphylaxis, and other less common types of shock

94
Q

What is the main feature associated with distributive shock?

A

Widespread vasodilation

95
Q

T or F: Shock is defined by blood pressure below 100/60.

A

F: Shock is not defined by blood pressure below any particular level

96
Q

One of the earliest symptoms of shock is _______.

A

Agitation

97
Q

Patients in _________ shock have cool, clammy skin.

A

Hypovolemic or Cardiogenic

98
Q

Patients in _______ shock have warm flushed skin.

A

Septic

99
Q

You want to quickly start antibiotic therapy for _______ shock.

A

Septic

100
Q

T or F: Young people in shock typically have deceptively normal vital signs until they reach the limits of their ability to compensate.

A

T

101
Q

Why is accurate categorization of shock important?

A

Because the treatments are different

102
Q

Hemorrhagic shock needs treatment with __________.

A

Blood transfusion

103
Q

Cardiogenic shock needs what treatment?

A

Treatment that assists the heart

104
Q

What is cardiac tamponade?

A

Bleeding into the pericardial sac prevents the heart from filling, which results in shock, distant heart sounds, and jugular venous distention.

105
Q

Some would put shock from pulmonary embolism or cardiac tamponade into a category of shock known as ________.

A

Obstructive shock

106
Q

What is neurogenic shock?

A

A form of vasogenic shock with vasodilation due to spinal cord injury or spinal anesthesia causing acute loss of SNS maintenance of a normal level of vasoconstriction

107
Q

Trauma patients can have shock that is partly hemorrhagic and partly septic due to increased production of _______________.

A

Proinflammatory cytokines like TNF, IL-1, and IL-6

108
Q

What is the most common form of shock?

A

Hypovolemic

109
Q

The loss of about ______% of a person’s blood volume is the threshold for shock.

A

25-30%

110
Q

The loss of ____% of one’s blood volume is commonly regarded as the dividing line between lethal and non-lethal hemorrhage.

A

50%

111
Q

What is sepsis?

A

The patient-as-a-whole syndrome of response to infection

112
Q

SIRS requires meeting two or more of what criteria?

A
  1. Fever or hypothermia
  2. Elevated heart rate (>90/min)
  3. Tachypnea (>20/min)
  4. WBC count high or low
113
Q

What are the two subsets of sepsis and what differentiates them?

A
  1. Severe sepsis (sepsis with acute organ dysfunction)

2. Septic shock (sepsis with refractory arterial hypotension)

114
Q

T or F: The majority of patients with sepsis have positive blood cultures.

A

NO WAY

115
Q

What does sepsis have to do with phospholipase A2?

A

Sepsis causes phospholipase A2 in the cell membranes of platelets, endothelial cells, neutrophils, monocytes, and other cells to generate platelet activating factor (PAF)

116
Q

T or F: PAF is 100-1000 times more potent than histamine in inducing vasodilation and increased vascular permeability.

A

T

117
Q

What are PAF’s functions?

A

It induces vasodilation and vascular permeability, activates platelets(obvi), promotes leukocyte adhesion to endothelial cells, chemotaxis, degranulation, and oxidative burst

118
Q

What is TGN1412?

A

A superagonist anti-CD28 monoclonal antibody that produced a systemic inflammatory response when administered to humans

119
Q

Which cytokines cause mast cells to release histamine?

A

IL-1 and IL-8

120
Q

Which prostaglandins cause vasodilation?

A

PGD2, PGE1, PGE2

121
Q

Which prostaglandins cause vascular permeability?

A

PGD2 and PGE2

122
Q

Extracellular release of small amounts of reactive nitrogen species and reactive oxygen species can increase the expression of _________.

A

IL-8 and other cytokines, and endothelial cell leukocyte adhesion molecules

123
Q

Greatly decreased blood volume combined with vasodilation increasing vascular capacitance causes __________.

A

Septic shock

124
Q

Within the clotting system _______ causes increased vascular permeability and leukocyte emigration from blood vessels.

A

Activated factor X

125
Q

What cleaves complement C5 to release C5a, linking clotting and the complement cascade?

A

Thrombin

126
Q

T or F: Sepsis causes increased tissue factor, which promotes clotting.

A

T

127
Q

Sepsis causes increased ________, which indirectly promotes clotting by inhibiting fibrinolysis.

A

Plasminogen activator inhibitor-1

128
Q

Sepsis results in decreased __________ (3), and all of these indirectly promote clotting by decreasing fibrinolysis.

A

Tissue factor pathway inhibitor, thrombomodulin, and protein C

129
Q

Sepsis is complicated by _______ in up to half of septic patients. (sorry this one’s vague.)

A

DIC – disseminated intravascular coagulation

130
Q

__________ inhibit neutrophil adhesion to endothelial cells and chemotaxis.

A

Lipoxins (generated from arachidonic acid)

131
Q

What components of the complement system counter-regulate the pro-inflammatory effects of complement activation.

A

C1INH, Factor H, DAF

132
Q

What is the major function of IL-10? What kind of cell secretes it?

A

To down regulate the responses of activated macrophages; secreted by macrophages (so they calm themselves down)

133
Q

What does soluble tumor necrosis factor receptor (sTNFR) do?

A

It blocks TNF

134
Q

Counter-regulatory mechanisms for sepsis and shock cause _______.

A

Immunosuppression

135
Q

What are the 4 main risk factors for gallstones?

A

Fat, Female, Fertile, Forty

136
Q

The anti-inflammatory counter-regulatory mechanism for sepsis and shock is known as __________.

A

Compensatory anti-inflammatory response syndrome (CARS)

137
Q

What is a mixed antagonistic response syndrome (MARS)?

A

When patients swing back and forth between a pro-inflammatory response syndrome and a compensatory anti-inflammatory response syndrome.

138
Q

Which therapies block TNF-alpha?

A

Infliximab, etanercept, and adalimumab

139
Q

What therapy blocks IL-6 receptors?

A

Tocilizumab

140
Q

T or F: Trauma/burns, acute pancreatitis, and extensive multi-organ ischemic necrosis can also cause SIRS.

A

T

141
Q

Extensive necrosis induces a _______ inflammatory response.

A

Systemic

142
Q

What are super antigens?

A

Molecules that promote T lymphocyte mitosis in a nonspecific way, bypassing antigen receptor specificity

143
Q

What is significant about toxic shock syndrome toxin-1 (TSST-1)?

A

It can bind to any T-cell receptor with a V-beta 2 segment, activating a lot of T cell clones which produce enough cytokines for a cytokine storm.

144
Q

When TSST-1 causes a cytokine storm leading to SIRS, the result is _________.

A

Toxic shock syndrome

145
Q

Toxic shock syndrome is due to ________.

A

A nonspecific immunologic over-reaction to a secreted bacterial product

146
Q

T or F: Genetics plays a role in determining which patients exposed to an antigen will get a cytokine storm due to their immune systems over-reacting.

A

T

147
Q

What defines severe sepsis or SIRS?

A

Sepsis or SIRS with acute organ dysfunction

148
Q

Patients with severe sepsis may have skeletal muscle dysfunction due to _______.

A

Buildup of lactic acid due to anaerobic metabolism

149
Q

What are the three stages of shock?

A
  1. Nonprogressive
  2. Progressive
  3. Irreversible
150
Q

What’s going on in the non progressive stage of shock?

A

Reflex compensatory mechanisms are still maintaining perfusion of vital organs

151
Q

What’s going on in the progressive stage of shock?

A

Manifestations of decompensating organ function

152
Q

What’s going on in the irreversible stage of shock?

A

Death is inevitable

153
Q

The compensatory mechanisms for shock include _________.

A

Sympathetic nervous system responses, fluid shifts within the body, and neuroendocrine stress responses

154
Q

The sympathetic nervous system and neuroendocrine response (increase/decrease) the heart rate.

A

Increase

155
Q

What are the molecular mediators of the neuroendocrine response to shock?

A

Epi, norepi, vasopressin, renin

156
Q

What stage of shock do you get lactic acidosis? Why?

A

Progressive; you get lactic acidosis because cells deprived of adequate oxygen resort to anaerobic metabolism, generating lactic acid

157
Q

_______ provides a measure of the degree of tissue hypoxia?

A

Level of lactate in the blood

158
Q

What biomarkers can tell you when you’ve reached the irreversible stage of shock?

A

Blood levels of TNF-alpha, IL-1, and IL-6

159
Q

What are red neurons?

A

Dead neurons that develop condensed cytoplasm that is hypereosinophilic because of the closely packed cytoplasmic proteins

160
Q

What is anoxic encephalopathy?

A

Patient has return of all organ functions except those of the brain

161
Q

The body’s compensatory mechanism of shutting off perfusion of the bowel can convert ______ shock into ________ shock.

A

Hypovolemic into septic

162
Q

What is the only way to cure septic shock from ischemic bowel?

A

Surgically remove it

163
Q

What does ischemic bowel look like?

A

Serosal surface has a dusky/dark red appearance

164
Q

What is the gross pathology of acute kidney injury (AKI)?

A

Swollen kidney with pale cortex and congested medulla

165
Q

What part of the kidney does AKI affect most?

A

The tubules

166
Q

What are the steps of AKI?

A
  1. Attenuation and loss of proximal tubule epithelial brush borders
  2. Epithelial cell swelling and vacuolization
  3. Epithelial cell necrosis and sloughing into the tubular lumen
167
Q

What may obstruct the tubules in AKI?

A
  1. Tamm-Horsfall protein, a urinary glycoprotein normally secreted by particular portions of the tubules
  2. Myoglobin casts if shock has resulted in rhabdomyolysis
168
Q

What is Waterhouse-Friderichsen syndrome?

A

Septic shock leads to massive adrenal hemorrhage and necrosis, obliterating the important adrenal collection to counteract shock

169
Q

What do normal resting adrenal cortical cells look like?

A

They have clear cytoplasm on H&E stain because they’re cleared of cholesterol, the precursor for cortisol, aldosterone, and other steroid adrenal hormones

170
Q

What does shock liver look like grossly?

A

Nutmeg liver – pattern of alternating red and brown tissue; alternating hemorrhagic necrosis and steatotic areas

171
Q

The vulnerability of hepatocytes to ischemia is directly proportional to _________.

A

Their proximity to the hepatic lobular central veins

172
Q

What is the most characteristic histological manifestation of shock lung?

A

Alveolar hyaline membranes

173
Q

What does shock lung look like grossly?

A

It’s typically enlarged and transformed from an air-filled pink-grey sponge into a firm, solidified, edematous, beefy red organ

174
Q

What is the earliest finding of ALI?

A

Increased numbers of neutrophils in the capilarries in the walls between alveoli

175
Q

What does IL-8 do?

A

Its a strong neutrophil chemotactic and activating agent

176
Q

In shock lung, release of ________ activates endothelial cells and leads to sequestration of neutrophils in small pulmonary blood vessels.

A

IL-8, TNF, and IL-1

177
Q

What is the result of alveolar edema and hyaline membranes in the alveolar spaces?

A

Hypoxemia – decreased oxygen loading of the blood passing through the lungs

178
Q

________ is the severe end of a spectrum with ALI.

A

Acute respiratory distress syndrome (ARDS)

179
Q

What is ARDS?

A

An acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia without evidence for cardiogenic pulmonary edema

180
Q

What are the features of contraction band necrosis of the heart?

A

Transverse bands of dense eosinophilic hyper contracted sarcomeres spa rated by relatively cleared spaces of cytoplasm

181
Q

In shock, the hyper contraction of sarcomeres is thought to be due to ________.

A

The influx of calcium brought in by reperfusion

182
Q

If a patient’s urine output falls, what should you do before you order a diuretic?

A

Examine the patient for evidence of bleeding

183
Q

T or F: The bigger the clot, the less likely dissolution becomes.

A

T

184
Q

What is the relationship of vein and catheter size with clot size?

A

The bigger the vein and the length of the catheter in it, the bigger the clot that inevitably forms around it.

185
Q

T or F: The longer a foreign body catheter remains in a vein, the less likely the clot will dissolve without a trace.

A

T

Path Block 2 (2 decks)

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