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CMD Block 2 > Hemodynamics 2 (Word Doc) > Flashcards

Hemodynamics 2 (Word Doc) Flashcards

1
Q

3 Most common causes of shock:

A

(1) decreased circulating blood volume (2) decreased cardiac output (3) sepsis

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2
Q

Causes of hypovolemic shock:

A

bleeding or fluid loss from
vomiting
diarrhea
extensive burns

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3
Q

Cause of cardiogenic shock:

A
  • myocardial infarction
  • arrhythmia (compromises pumping)
  • pulmonary embolism (obstructing right heart -output)
  • hemopericardium (obstructing filling)
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4
Q

What is cardiac tamponade?

A

Blood (hemopericardium) pressing downon the chambers of the heart, limiting filling

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5
Q

Why does septic shock cause hypoperfusion?

A

Systemic vasodilation–sends too much blood out, and too little comes back to the heart/lungs

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6
Q

Shock is not a number, but a _____

A

Syndrome

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7
Q

Characterized by the signs and symptoms of systemic hypoperfusion

A

Shock

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8
Q

Progressing cognitive symptoms of shock:

A

Agitation (earliest) –> decreasing mental status –> lethary –> coma

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9
Q

What is an obvious way to distinguish septic shock from cardiogenic/hypovolmic shock?

A

Warm verus cool/clammy skin

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10
Q

Patients in all form of shock have decreased:

A

Urine output

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11
Q

What are two late signs of shock? (When noticed, injury has already occurred)

A

Elevated heart rate (>100) and low blood pressure (<90 systolic or 40mmHg lower than usual)

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12
Q

T/F: A sudden, profound crash is characteristic of old people.

A

F: Young people crash crash suddenly and profoundly and (often) irretrievably because they can compensate longer, thus their vitals are okay

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13
Q

Accurate categorization of shock is important because:

A

treatments are different

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14
Q

Treatment for hemorrhagic shock:

A

Blood transfusion

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15
Q

Treatment for septic shock:

A

Abx

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16
Q

Cardiogenic shock usually results from

A

Pump failure

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17
Q

What are 3 symptoms of cardiac tamponade?

A

shock
distant heart sounds
jugular venous distention

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18
Q

What is the treatment for cardiac tamponade?

A

removing the blood from the pericardial sac

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19
Q

What two conditions are sometimes considered obstructive shock?

A

cardiac tamponade and pulmonary thromboembolus that blocks the pulmonary trunk

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20
Q

What two conditions are sometimes considered vasogenic shock?

A

Anaphylactic shock and septic shock

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21
Q

Condition in which vasodilatation increases the capacitance of the vascular system so much that the too much blood pools in the periphery and too little returns to the heart (for oxygenation and repumping)

A

Septic and Anaphylactic shock

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22
Q

Vasogenic shock associated with spinal cord injury or spinal anesthesia; causes acute loss of sympathetic nervous system maintenance of normal vasoconstriction

A

Neurogenic shock

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23
Q

Why do trauma patients experience shock that is partially hemorrhagic and partially septic?

A

increased production of proinflammatory cytokines (TNF, IL-1 and IL-6)

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24
Q

The dividing line between lethal and non-lethal hemorrhage

A

loss of 50% of blood volume

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25
Q

Percentage of blood loss causing symptoms of compensation

A

15-20%

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26
Q

Percentage of blood loss causing shock

A

25-30%

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27
Q

Percentage of blood loss causing life-threatening shock

A

35-45%

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28
Q

In a healthy person, 50% blood loss can be tolerated if:

A

It occurs over days-weeks (“The more slowly a hemorrhage takes place, the greater a hemorrhage a person can survive”)

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29
Q

T/F: A person’s general health partially determines the amount of blood loss that can be tolerated.

A

T

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30
Q

Patient-as-a-whole syndrome that occurs in response to infection

A

Sepsis

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31
Q

Definition of sepsis:

A

systemic inflammatory response syndrome (SIRS) due to infection, proven or highly suspected

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32
Q

SIRS Criteria (4):

A
  1. Fever (>38 C [100.4F]) or hypothermia (90/minute)

3. Tachypnea (RR >20/minute) or hyperventilation (arterial pCO2 12,000/cu mm) or leukopenia (WBC 10% bands)

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33
Q

Severe sepsis includes:

A

acute organ dysfunction (aka malfunction such that a person cannot maintain homeostasis without intervention)

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34
Q

Refractory arterial hypotension that only adequately responds to fluid replacement

A

septic shock

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35
Q

Oliguria

A

low urine output

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36
Q

If blood pressure normalizes when fluids are given, it suggests that shock is:

A

hypovolemic

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37
Q

T/F: Severe sepsis is a subset of septic shock

A

F: Septic shock is a subset of severe sepsis

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38
Q

Most people with sepsis have _____ blood cultures

A

Negative

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39
Q

T/F: Altered mental status is a sepsis/SIRS symptom

A

T

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40
Q

In sepsis/SIRS: CRP is (elevated/decreased)

A

Elevated (>2 standard deviations)

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41
Q

In sepsis/SIRS: procalcitonin is (elevated/decreased)

A

Elevated (>2 standard deviations)

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42
Q

Less than what oxygen saturation % constitutes SIRS?

A

<70%

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43
Q

In sepsis/SIRS: creatinine is (elevated/decreased)

A

elevated

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44
Q

In sepsis/SIRS: PTT is (elevated/decreased)

A

Elevated (>60 seconds)

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45
Q

In sepsis/SIRS: thromobocytopenia is (elevated/decreased)

A

Decreases (<100,000)

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46
Q

In sepsis/SIRS: bilirubin is (elevated/decreased)

A

Elevated (>4)

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47
Q

In sepsis/SIRS: Fever is defined as

A

> 38.3 degrees

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48
Q

What are two SIRS symptoms you would quickly notice after inspecting a patients arms/legs?

A

Mottling and “significant” edema

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49
Q

In sepsis/SIRS: heart rate is (elevated/decreased)

A

Elevated (>2 standard deviations)

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50
Q

Microbial cell wall and internal elements (lipoproteins and LPS, fungal wall components, nucleic acids)

A

pathogen-associated molecular patterns (PAMPs)

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51
Q

What receptors bind PAMPs (3)?

A

Toll-like, NOD1/2, GPCR

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52
Q

What type of receptors react with intercellular pathogens?

A

NOD

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53
Q

What types of receptors are located on macrophages, neutrophils and endothelial cells?

A

Toll like reeptors

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54
Q

Binding of PAMPs activates inflammatory cells, which produce: (8)

A

TNF, IL-1, IL-6, IL-8, IL-12, IL-18, IFN-G, HMGB1

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55
Q

How do cytokines direct leukocytes to the site of infection?

A

Upregulation of the expression of endothelial cell adhesion molecules which bind leukocytes

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56
Q

State of systemic (total body) hypoperfusion + cardiovascular collapse

A

Shock

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57
Q

What type of cell membrane enzyme produces PAF in response to SEPSIS?

A

phospholipase A2

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58
Q

What types of cells produce PAF?

A

platelets, endothelial cells, neutrophils, monocytes

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59
Q

What does PAF do?

A

vasodilation, increased vascular permeability, activates/promotes platelet aggregation, promotes leukocyte migration/degranulation

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60
Q

How do microbes activate the fibrinolytic system?

A

Plasmin

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61
Q

What do CD4 cells secrete in response to antigen and costimulation?

A

IFN-Gamma

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62
Q

What so APC secrete to sustain the expression of costimulatory molecules?

A

IL12

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63
Q

What APC costimulation molecule binds to CD28?

A

CD80

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64
Q

Why was TGN1412 so toxic to the volunteers?

A

anti-CD28

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65
Q

What occurs in response to IL-1 and IL-8?

A

mast cells in the connective tissue adjacent to blood vessels to release large quantities of histamine from granules in their cytoplasm

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66
Q

Histamine causes…

A

dilation of arterioles and increased permeability of venule

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67
Q

What types of cells synthesized prostaglandin?

A

Activated macrophages, neutrophils, endothelial cells and mast cells

68
Q

PGD2, PGE1 and PGE2 cause

A

vasodilation

69
Q

PGD2 and PGE2 cause

A

increased vascular permeability

70
Q

How do activated endothelial cells and activated macrophages/neutrophils use NO differently?

A

activated endothelial cells: potent vasodilator

Activated macrophages and neutrophils: kills microbes by combining with reactive oxygen species

71
Q

Extracellular ROS (in small amounts) can increase expression of:

A

IL8 and endothelial cell leukocyte adhesion molecules

72
Q

Extracellular ROS (in large amounts) will:

A

Damage endothelial cells, which increases vascular permeability and allows fluid to leak out into the tissues–this deceases blood volume

73
Q

T/F: Sepsis leads to shock by a phenomenal number of redundant pathways

A

T

74
Q

2 ways in which NO contributes to sepsis

A

Vasodilation, decreased blood volume (due to increased vascular permeability from endothelial cell damage)

75
Q

Activated Hageman factor initiates what 4 systems?

A

Clotting, fibrinolytic, complement, kinin

76
Q

Activated factor X causes:

A

Increased vascular permeability and leukocyte emigration from blood vessels

77
Q

Fibrinopeptides are generated by ______ and function in (2):

A

Thrombin

Increase vascular permeability, leukocytes chemotaxis

78
Q

How does thrombin affect the complement cascade?

A

Cleaves C5 to release C5a (links clotting and the complement cascade)

79
Q

A decrease in these indirectly promotes clotting in sepsis by decreasing fibrinolysis: (3)

A

tissue factor pathway inhibitor, thrombomodulin and protein C

80
Q

An increase in these promotes clotting in sepsis: (3)

A

tissue factor, plasminogen activator inhibitor-1 (inhibits fibrinolysis)

81
Q

Sepsis-related clotting seen in 50% of patients with sepsis

A

disseminated intravascular coagulation

82
Q

Major function of IL10:

A

Down-regulate the responses of activated macrophages (“calm them down”)

83
Q

Counter-regulate the pro-inflammatory effects of complement activation: (3)

A

C1 inhibitor, factor H (limits convertase formation) and decay-accelerating factor
(limits of convertase formation)

84
Q

How do lipoxins counter inflammation?

A

inhibit neutrophil adhesion to endothelial cells and chemotaxis

85
Q

Blocks TNF

A

Soluble tumor necrosis factor receptor (sTNFR)

86
Q

Mixed antagonistic response syndrome (MARS):

A

Alternation of pro-inflammatory response syndrome and a compensatory anti-inflammatory response syndrome

87
Q

What are 3 counter-regulatory mechanisms causing immunosuppression?

A
  • apoptosis of CD4 and CD8 lymphocytes
  • apoptosis of gastro-intestinal epithelial cells
  • expression of ligands for inhibitory receptors on lung epithelial cells
88
Q

What results from CARS immunosuppression?

A

opportunistic infections, reactivation of latent infections and GI hemorrhage

89
Q

To treat autoimmune disease, Infliximab (Remicade), etanercept (Enbrel) and adalimumab (Humira) block:

A

TNF-alpha

90
Q

To treat autoimmune disease, Tocilizumab blocks

A

IL6 receptors

91
Q

Why do burns, acute pancreatitis and multi-organ ischemic necrosis cause SIRS?

A

tissue death

92
Q

Tissue death (necrosis) elicits an:

A

inflammatory response

93
Q

Extensive necrosis elicits a:

A

SYSTEMIC inflammatory response

94
Q

Superantigens

A

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

95
Q

Toxin that can bind to any TCR with a V-beta 2 segment (activates 5-20% of T cells instead of the 0.001%)

A

toxic shock syndrome toxin-1 (TSST-1)

“covers 1/2 of the flanking MHC alpha-helices of HLA-DR1”

96
Q

What is a toxic shock storm?

A

An abnormally large number of T cells are activated by TSST1; these release mass quantities of cytokines, such as IL-1 and TNF (cytokine storm)

97
Q

Nonspecific immunologic over-reaction to a bacteria-secreted exotoxin

A

Toxic Shock Syndrome

98
Q

What bacteria are most associated with Toxic Shock Syndrome?

A

staphylococci or streptococci

99
Q

Toxic Shock Syndrome

A

Nonspecific immunologic over-reaction to a bacteria-secreted exotoxin

100
Q

T/F: Menstrual toxic shock syndrome is an infection caused by Staph aureus.

A

F: colonization by the bacteria; When Staph aureus overgrows in a tampon, numerous T cells are exposed to the exotoxin (eliciting the reaction)

101
Q

Almost all menstrual cases (and 50% of nonmenstrual cases) of toxic shock syndrome are associated with:

A

TSST-1

102
Q

T/F: TSS can be caused by a group A strep infection of the skin or pharynx, with strains of Strep pyogenes producing streptococcal pyrogenic exotoxin A and acting as a superantigen.

A

T (sorry, didn’t know how else to include this)

103
Q

What influences the likelihood of a patient experiencing a cytokine storm?

A

Their genetics (90% TSS occurs in whites)

104
Q

What makes sepsis or SIRS “severe”?

A

Acute organ dysfunction

105
Q

What causes skeletal muscle dysfunction in severe SIRS/sepsis?

A

Anaerobic metabolism and lactic acid build up

106
Q

Stages of pathophysiological stock: (3)

A

1) nonprogressive, with compensation
2) progressive, with manifestations of decompensating organ function
3) irreversible, with resultant death even if the cause of shock is reversed

107
Q

Compensatory mechanisms for shock:

How does the brainstem respond to the blood loss signaled by baroreceptors?

A

Decreases the level of inhibition of arteriolar vasoconstriction

108
Q

Compensatory mechanisms for shock:

Why do the sympathetic nervous system and neuroendocrine response increase heart rate?

A

Since there is less blood to carry oxygen and other nutrients, it needs to be pumped faster

109
Q

Molecular mediators of the neuroendocrine response to shock: (4)

A
  1. epi (adrenal medulla)
  2. norepinephrine (adrenal medulla)
  3. vasopressin or ADH (pituitary)
  4. renin (kidneys)
110
Q

How does the fluid shift response to hypovolemic shock restore volume?

A

moves water from the extravascular compartment into the blood (it’s dilute, but at least it’s there)

111
Q

Compensatory mechanisms for shock:

How do the kidneys respond to hypovolemia?

A

Stop making urine

112
Q

Compensatory mechanisms for shock:

How does blood perfusion change as shock worsens?

A

Body shuts down perfusion of less vital organs: toes -> feet -> legs -> pelvic organs -> organs below diaphragm -> arms -> heart/brain

113
Q

Why does shock induce lactic acidosis?

A

cells deprived of adequate oxygen resort to anaerobic metabolism, generating lactic acid

114
Q

What blood level provides a measure of the degree of tissue hypoxia?

A

Lactate

115
Q

Biomarkers of the irreversible stage of shock:

A

TNF-alpha
IL-1
IL-6

116
Q

T/F: Shock is irreversible only when the patient is dead.

A

F: Shock has a point of no return after which nothing will save a patient’s life

117
Q

Cerebral pathology of shock:

A

necrosis with red (dead) neurons and cerebral edema

118
Q

Neurons begin dying ___ minutes after their blood supply stops.

A

4

119
Q

Dead neurons with condensed (hypereosinophilic) cytoplasm contains denatured, closely-packed proteins.

A

Red neurons (occurs after 12 hours)

120
Q

Pyknosis

A

Nuclei shrinking and condensation (hyperbasophilic)

121
Q

Why do resuscitated patients often regain all organ function but not brain function (“anoxic encephalopathy”)?

A

neurons are the cells most rapidly killed by ischemia (by a wide margin) and they do not regenerate

122
Q

What is a possible result of shutting off perfusion of the bowel (a compensatory mechanism)?

A

hypovolemic shock can convert into septic shock

123
Q

Describe the process of bowel ischemia. (4)

A
  1. Bile enters through the leaky, ischemic bowel
  2. Stool sticks to the walls (probably due to some of the proteins that leaked in)
  3. As ischemia worsens, blood leaks into the mucosa and then deeper layers
  4. Intestina mucosa breaks down, and the bacteria from the lumen can invade
124
Q

What does the serosal surface of ischemic bowel look like?

A

“Dusky”, dark red

125
Q

The only way to cure septic shock from ischemic bowel:

A

Resection (removal of the ischemic portion)

126
Q

A particularly common site of ischemic bowel

A

cecum

127
Q

When resuscitating a patient, refractory lactic acidosis should tell you to go looking for…

A

Dusky bowel

128
Q

Gross pathology of AKI: (3 characteristics)

A
  1. swollen
  2. pale cortex
  3. congested medulla
129
Q

T/F: Acute kidney injury is always irreversible.

A

F: reversible

130
Q

Rhabdomyolysis

A

skeletal muscle breakdown

131
Q

In AKI, where may leukocytes be found?

A

vasa recta–the small straight blood vessels of the renal medulla

132
Q

What portion of the kidney is the most affected by AKI?

A

Tubules

133
Q

Manifestation of AKI: (3)

A
  1. Attenuation/loss of proximal tubule epithelial cell brush borders
  2. Epithelial cell swelling and vacuolization
  3. Epithelial cell necrosis and sloughing into the tubular lumen
134
Q

Two causes of tubular obstruction:

A
  1. Myoglobin resulting from shock-induced rhabdomyolysis
  2. Eosinophilic hyaline material (mostly Tamm-Horsfall protein, a urinary glycoprotein normally secreted by parts of the tubules)
135
Q

Pathologic manifestations of shock in the adrenal glands:

What causes cortical lipid depletion?

A

Shock stimulates the synthesis of cortisol, aldosterone and other steroid hormones

136
Q

Pathologic manifestations of shock in the adrenal glands:

What typically follows adrenal cell necrosis?

A

hemorrhage

137
Q

Waterhouse-Friderichsen syndrome

A

Septic shock due to Neisseria meningitidis infection in kids; can lead to adrenal hemorrhage and necrosis, which eliminates the adrenal contribution to counteracting shock

138
Q

Nutmeg liver looks like…

A

Tissue with alternating red and brown (or tan or yellow or green)

139
Q

The grossly colored regions in nutmeg liver reflect:

A

Hemorrhagic necrosis and steatosis

140
Q

Why is there coagulative necrosis of hepatocytes in the center of hepatic lobules?

A

Both the oxygen-rich arterial blood and nutrient-rich portal venous blood diffuse through the lobules, starting from the portal tracts around the periphery;
The venous blood headed for the kidneys (with oxygen and nutrients extracted and toxic metabolites added) starts at the lobular central veins

141
Q

T/F: The peripherally located hepatocytes are more likely to become ischemic.

A

F: “The vulnerability of hepatocytes to ischemia is directly proportional to their proximity to the hepatic lobular central veins”

142
Q

Shock lung is typically:

A

enlarged and firm

143
Q

In ALI, the earliest finding is:

A

increased numbers of neutrophils in the capillaries, in the septa between alveoli

144
Q

Half an hour after the lung insult, what do pulmonary alveolar macrophages produce?

A

Increased amounts of IL8 (strong neutrophil chemotactic and activating agent)

145
Q

What results from the increase of proinflammatory cytokines in the lungs?

A
  1. Activation of endothelial cells (leads to sequestration of neutrophils in small pulmonary blood vessels)
  2. Up-regulation of adhesion molecules on neutrophils
  3. Water and plasma proteins (vascular) leak into the interstitium and airspaces
146
Q

What causes damage the alveolar epithelial cells, and what is the result?

A

Oxidants, proteases, PAF and leukotrienes from activated neutrophils; increase the permeability of the barrier between the airspaces and bloodstream

147
Q

In severe injury, what leaks into alveoli?

A

Whole blood

148
Q

Where does fluid collect in less severe ALI?

A

Alveolar edema fluid condenses into eosinophilic hyaline membranes lining the airspaces

149
Q

What causes ALI-related hypoxemia?

A

alveolar edema and hyaline membranes block the diffusion of oxygen

150
Q

In ALI, this will be seen in a chest XR:

A

pulmonary infiltrates

151
Q

Bilateral pulmonary infiltrates and severe hypoxemia (no evidence of cardiogenic pulmonary edema)

A

acute respiratory distress syndrome (ARDS)

152
Q

Subendocardial myocytes begin dying as early as _____ after their blood supply has been cut off.

A

20 minutes

153
Q

What causes hypercontraction of sarcomeres in reperfused cardiac cells?

A

Influx of calcium brought in by reperfusion; since they do not have an energy source, they are unable to relax

154
Q

If a person in shock has a subendocardial MI but is successfully resuscitated, where will the “circumferential infarct” be?

A

anterior left ventricle (L anterior desc coronary artery)
lateral left ventricle (left circumflex coronary artery)
posterior left ventricle (right coronary artery)

155
Q

Why will hemorrhage occur in the heart after resuscitation?

A

blood vessels have broken-down

156
Q

Coagulation necrosis of the myocytes produces ______ cytoplasm.

A

Hypereosinophilic

157
Q

Contraction band necrosis features transverse bands of dense eosinophilic _______ ________ separated by relatively cleared spaces of cytoplasm.

A

contracted sarcomeres

158
Q

Hypovolemic shock, combined with an MI, “adds an element of”:

A

Cardiogenic shock

159
Q

T/F: If a patient has low urine output, order a diuretic.

A

F: Go look at the patient first, so you don’t kill him/her in the same way Dr. Nichols tried to kill those dogs.

160
Q

ALI

A

acute non-cardiogenic pulmonary edema and alveolar hyaline membranes

161
Q

ARDS

A

acute non-cardiogenic bilateral lung infiltrates and severe hypoxemia

162
Q

ATN

A

AKI severe enough to cause (reversible) necrosis of renal tubules

163
Q

ALI

A

acute non-cardiogenic pulmonary edema and alveolar hyaline membranes

164
Q

ARDS

A

acute non-cardiogenic bilateral lung infiltrates and severe hypoxemia

165
Q

ATN

A

AKI severe enough to cause (reversible) necrosis of renal tubules

CMD Block 2 (38 decks)

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