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Pathology block 2 > Hemodynamics II > Flashcards

Hemodynamics II Flashcards

1
Q

Shock:

A

state of systemic (total body) hypoperfusion, cardiovascular collapse

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2
Q

Severe sepsis:

A

sepsis with acute organ dysfunction

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3
Q

Septic shock:

A

severe sepsis with refractory arterial hypotension

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4
Q

AKI :

A

acute (reversible) renal injury due to hypoperfusion or hypoxemia

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5
Q

ATN :

A

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

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6
Q

ALI :

A

acute non-cardiogenic pulmonary edema and alveolar hyaline membranes

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7
Q

ARDS:

A

acute non-cardiogenic bilateral lung infiltrates and severe hypoxemia

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8
Q

What are the 3 most common causes of shock?

A

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

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9
Q

Other than the 3 most common causes of shock, what else can cause it?

A

anaphylaxis,

systemic inflammatory response syndrome (SIRS)

neurogenic causes.

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10
Q

What are the most common types of shock?>

A
  1. hypovolemic shock
  2. cardiogenic shock
  3. septic shock
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11
Q

What can cause hypovolemic shock?

A

bleeding or fluid loss from vomiting, diarrhea, extensive burns

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12
Q

What can cause cardiogenic shock?

A

MI

cardiac arrhythmia messing up signaling mechanism for adequate pump,

pulmondary embolism obstructing output of the right heart

cardiac tamponade=> hemopericardium squeezing cardiac filling chambers, obstructing filling

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13
Q

Septic shock is generally mixed with anaphylaxis to be termed distributive shock. What is a feature of this type?

A

all feature widespread vasodilation

maldistributes the available blood volume diffusely throughout the body in too many places, returning too little to the heart and lungs to oxygenate and pump it to where it is needed.

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14
Q

A patient who suffered a MI and also a ruptured gastric ulcer will have what type of shock?

A

cardiogenic

hypovolemic

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15
Q

How is shock measured?

A

it cannot be measured with a value. It depends on numerous amounts of signs and symptoms to total body hypoperfusion

it affects the patient as a whole person

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16
Q

What is one of the earliest symptoms of shock?

A

agitation

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17
Q

The clinical manifestations of shock include what?

A
  • decreasing mental status,
  • progressing from confusion to lethargy,
  • delirium (sometimes)
  • coma
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18
Q

Patients in hypovolemic or cardiogenic shock have what type of heart rate? skin?

A

a weak rapid (“thready”) pulse

cool, clammy, sometimes cyanotic skin.

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19
Q

Patients in septic shock have what type of skin?

A

warm flushed skin

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20
Q

The importance of differentiating septic shock from other forms of shock is what?

A

every hour of delay in starting effective antibiotic therapy for septic shock was associated with a 7.6% increase in mortality for each of the six hours after the first hour.

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21
Q

Patients in all forms of shock have what sign?

A

decreasing urine output.

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22
Q

T/F vital signs are a good indicator of shock

A

false, they are usually late responders and considerable injury to cells and tissues have occurred

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23
Q

Who should be examined closer, the young trauma patient or the old postoperative patient? why?

A

young trauma patient because of seemingly normal vital signs and physiologic functioning until limits are reached beyond ability to compensate causing a sudden crash that can be irretrievable

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24
Q

How should you treat hemorrhagic hypovolemic shock? septic shock? cardiogenic shock?

A

Hemorrhagic shock needs treatment with blood transfusion.

Septic shock needs treatment with antibiotic therapy.

Cardiogenic shock needs treatment that assists the heart.

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25
Q

Cardiogenic shock usually results from what?

A

the failure of the heart as a pump due to intrinsic heart disease,

bleeding into the pericardial sac can prevent the heart from filling, with resultant shock

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26
Q

What is cardiac tamponade?

A

distant heart sounds

jugular venous distention

bleeding into pericardial sac can prevent heart from filling

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27
Q

Cardiac tamponade due to hemoperidcardium needs urgent treatment. How should you treat?

A

remove blood from pericardial sac

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28
Q

A large pulmonary thromboembolus can obstruct pulmonary trunk. How would this cause shock?

A

preventing outflow from the right heart

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29
Q

Septic shock is due to what?

A

vasodilatation increasing the capacitance of the vascular system

this is done so much that the amount of blood pooled in the periphery leaves too little returning to the heart for adequate perfusion of the body as a whole.

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30
Q

What form of shock is neurogenic shock? What causes neurogenic shock?

A

vasogenic shock

vasodilatation due to spinal cord injury or spinal anesthesia causing acute loss of sympathetic nervous system maintenance of a normal level of vasoconstriction.

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31
Q

What type of shock would you expect a trauma patient with a long bone fracture to have? why?

A

hemorrhagic and septic shock

due to increased production of proinflammatory cytokines such as TNF, IL-1 and IL-6

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32
Q

T/F hypovolemic shock is most common of 3 types in surgery and trauma patients

A

true

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33
Q

Other than hemorrhagic shock, what else can cause hypovolemic shock?

A

fluid loss (dehydration) caused by severe diarrhea or extensive burns

severe bleeding (especially retroperitoneum, abdominal cavity, chest or intestines)

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34
Q

What % of blood volume is the threshold for shock? name specifically

A

25% for an older person,

30% for a young one

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35
Q

At what point does blood loss cause life threatening shock?

A

35-45% of person’s blood volume

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36
Q

What is the common dividing line between lethal and non-lethal hemrrhage?

A

50% of one’s blood volume

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37
Q

What is the ultimate factor when dealing with blood loss?

A

time

a 50% decrease over time has a better chance of living than one that is quickly lossed

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38
Q

What is sepsis?

A

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

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39
Q

SIRS must meet 2 of the 4 criteria. Name all 4

A
  1. Fever (temperature over 38 degrees C [100.4 degrees F]) or hypothermia (temperature less than 36 degrees [96.8 degrees F])
  2. Elevated heart rate (over 90/minute)
  3. Tachypnea (respiratory rate over 20/minute)
    or hyperventilation (arterial pCO2 [partial pressure of dissolved CO2 in the blood] less than 32 mm Hg)
  4. Leukocytosis (white blood cell count over 12,000/cu mm) or leukopenia (white blood cell count less than 4,000/cu mm) or bandemia (over 10% bands).
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40
Q

What are the 2 critical subsets of sepsis?

A

severe sepsis

septic shock

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41
Q

What is severe sepsis?

A

sepsis with acute organ dysfunction

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42
Q

What is septic shock wrt sepsis?

A

sepsis with refractory arterial hypotension

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43
Q

acute organ dysfunction qualifying a patient for the category of severe sepsis is what?

A

malfunction such that a person cannot maintain homeostasis without intervention.

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44
Q

What are examples of severe sepsis?

A

acute alteration in mental status

oliguria (low urine output)

lactic acidosis

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45
Q

What is the definition septic shock?

A

sepsis-induced hypotension with systolic BP less than 90 mm Hg or >40 mm Hg lower than baseline,

refractory to adequate fluid resuscitation,

together with acute organ dysfunction.

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46
Q

If you are able to normalize a patients blood pressure with fluid resuscitation. What type of shock do you expect?

A

hypovolemic shock

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47
Q

FACT: Septic shock is a subset of severe sepsis and severe sepsis is a subset of sepsis.

A
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48
Q

SIRS was altered wrt to many ways. name them (haha)

A
  • HR>2 SDs above normal value for age
  • significant edema
  • positive fluid balance >20mL/kg over 24hrs
  • hyperglycemia in absence of diabetes
  • CRP >2SDs above normal
  • procalcitonin >2 SDs above normal
  • mixed venous O2 saturation <70%
  • cardiac index > 3.5
  • arterial hypoxemia
  • acute oliguria
  • creatinine increase >0.5mg/dL
  • INR >1.5
  • partial thromboplastin time >60secs
  • ileus, thrombocytopenia (<100,000/cu mm)
  • bilirubin>4mg/dL
  • lactate >1mmol/L
  • decreased capillary refeal
  • cutaneous mottling
  • 38.3 C
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49
Q

Describe the molecular mechanisms of sepsis and septic shock

A
  1. PAMPS => TLRs on macs, neutro, ECs or GCPR or NODs bind pamps
  2. Binding activates inflamm cells=> produce TNF, IL-1, IL-6, IL-8, IL-12, IL-18, IFN-y, HMGB1
  3. cytokines upregulate expression of EC adhesion moleucles that bind leukocytes to direct to infection
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50
Q

What does sepsis cause in the cell membranes of platelets, ECs, neutrophils, monocytes? what will this do?

A

phospholipase A2

generate platelet activating factor (acetyl glycerol ether phosphocholine)

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51
Q

T/F PAF is more potent than histamine. explain

A

true

  • induces vasodilation and increased vascular permeability
  • activates platelets and promotes aggregation
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52
Q

Other than inducing vasodilation and increasing vascular permeability, what else does PAF do?

A

promote leukocyte adhesion to ECs

chemotaxis

degranulation and oxidative burst that allows killing in leukocytes

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53
Q

Microbial components activate the complement cascade. How?

A

both directly and indirectly through the activity of plasmin from the fibrinolytic system.

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54
Q

Activation of the complement cascade yields C3a and C5a. What do these do?

A

increase vascular permeability and cause vasodilation by inducing mast cells to release histamine.

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55
Q

antigen presenting cells present microbial antigens to what cells?

A

T lymphocytes

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56
Q

If these microbial antigens are presented in conjunction with CD3 on the T cell surface and with costimulatory molecules, what is the result?

A

CD4-positive effector T-cells secrete interferon-gamma that activates phagocytic cells to kill intracellular bacteria,

upregulate their own expression of CD40 ligand,

binds to CD40 on the antigen presenting cells,

releases IL-12

sustains the expression of costimulatory molecules.

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57
Q

The costimulatory molecule CD80 binds to CD28 that results in what?

A

T cell activation and proliferation.

58
Q

What will the cytokines IL-1 and IL-8 cause mast cells to do?

A

degranulate

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

59
Q

What all can histamine be released from? what does histamine cause?

A

platelets, mast cells

dilation of arterioles and increased permeability of venules.

60
Q

Activated macrophages, neutrophils, endothelial cells and mast cells rapidly convert arachidonic acid in their cell membranes into what? and what do they bind to?

A

prostaglandins, which are short-lived lipid mediators that bind to G-coupled receptors on many cell types and have a variety of effects.

61
Q

Which prostaglandins cause vasodilation?

A

PGI2 (also called prostacyclin), but also PGD2, PGE1 and PGE2

62
Q

Which prostaglandins cause an increased vascular permeability?

A

PGD2 and PGE2

63
Q

PAF is a phospholipid derived mediator. What releases it and what does it do?

A

activated macrophages, neutrophils, mast cells, endothelial cells and platelets themselves,

increases vascular permeability.

64
Q

activated endothelial cells increase their expression of what molecule? what is the purpose of this?

A

inducible nitric oxide synthetase and production of nitric oxide (NO).

** potent vasodilator.**

65
Q

Activated macrophages and neutrophils also produce NO. What is the action of NO in this regard?

A

kills microbes by combining with reactive oxygen species.

66
Q

Extracellular release of small amounts of reactive nitrogen species and reactive oxygen species can increase the expression of what?

A

IL-8 and other cytokines

endothelial cell leukocyte adhesion molecules.

too much NO or ROS is damaging to ECs

67
Q

If too much NO or ROS is released then ECs are damaged. What is the result?

A

damage increases vascular permeability.

Increased vascular permeability allows fluid to leak out of the blood into inflamed tissues, decreasing the circulating blood volume.

68
Q

decreased blood volume combined with vasodilatation increasing vascular capacitance causes what?

A

septic shock

69
Q

What activates blood clotting?

A

Exposure of clotting factor XII (Hageman factor) to activated platelets, basement membrane or collagen activates it

70
Q

Activated Hageman factor activates what?

A
  1. activates blood clotting,
  2. kallikrein and the kinin cascade,
  3. via both the clotting and kinin cascades, the fibrinolytic system and the complement cascade.
71
Q

Within the clotting system, activated factor X causes what?

A

increased vascular permeability

leukocyte emigration from blood vessels.

72
Q

Thrombin, the king of clotting, generates fibrinopeptides that cause what?

A

increase vascular permeability and are chemotactic for leukocytes.

73
Q

What is the link between the clotting and complement cascades? How?

A

cleaves complement C5 to release C5a

74
Q

How do activated and injured ECs cause shock?

A

if activated/injured by sepsis then they promote vasodilation

increase vascular permeability (decrease vascular volume)

promote thrombosis

75
Q

Sepsis causes increased tissue factor. What is its action?

A

tissue factor promotes clotting.

76
Q

How does sepsis inhibit fibrinolysis?

A

Sepsis causes increased plasminogen activator inhibitor-1, which indirectly promotes clotting by inhibiting fibrinolysis

decreased tissue factor pathway inhibitor,

decreased thrombomodulin

decreased protein C

77
Q

In up to 50% of patients with sepsis, what is the result wrt clotting?

A

unlocalized disseminated intravascular coagulation (DIC) in small blood vessels.

lead to bleeding because of the consumption of clotting factors and platelets in so many blood vessels.

78
Q

Lipoxins are generated from arachidonic acid. What is their role?

A

inhibit neutrophil adhesion to endothelial cells and chemotaxis

79
Q

In the complement system, what do C1 inhibitor (factor H) and DAF (limiter of convertase) serve as?

A

serve to counter-regulate the pro-inflammatory effects of complement activation

80
Q

How do activated macrophages down regulate responses of other activated macrophages?

A

secrete IL-10

81
Q

What anti-inflammatory actions of the immune system cause immunosuppression and can lead to opportunistic infections, GI bleeding, and reactivation of latent infections?

A

poptosis of CD4 and CD8 lymphocytes,

apoptosis of gastro-intestinal epithelial cells

expression of ligands for inhibitory receptors on lung epithelial cells.

82
Q

What is CARS?

A

compensatory anti-inflammatory response syndrome that is a counter regulatory mechanism of sepsis leading to immuno suppression

83
Q

What is MARS?

A

patients swing back and forth between pro-inflamm and CARS

84
Q

There are some therapies against cytokines. What blocks TNF-a?

A

Infliximab (trade name Remicade),

etanercept (trade name Enbrel)

adalimumab (trade name Humira)

85
Q

What does Tocilizumab block?

A

IL-6 receptors

86
Q

How do targeted therapies against some cytokines help treat sepsis and septic shock?

A

they are not helpful due to the redundancy of the pathways involved

87
Q

What is a superantigen?

A

antigen elicits an acquired immune response from multiple clones of lymphocytes

88
Q

What does a superantigen do?

A

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

89
Q

How does toxic shock syndrome toxin-1 work?

A

covers MHC helices and allows binding to any TCR thus activating 5-20% of T cell clones instead of proceeding with normal antigen processing

the clones create a cytokine storm leading to SIRS resulting in toxic shock syndrome

90
Q

Toxic shock syndrome is due to what?

A

nonspecific immunologic over-reaction to a secreted bacterial product, an exotoxin, produced by staphylococci or streptococci,

most notoriously when Staphylococcus aureus has overgrown in a superabsorbent tampon and numerous T lymphocytes are exposed to the exotoxin, eliciting the reaction.

91
Q

Describe mentrual toxic shock syndrome

A

represents a colonization by the bacteria rather than an infection

92
Q

Other than menstral toxic shock syndrome, how else can the syndrome be caused?

A

group A streptococcal infection of the skin or pharynx with strains of Streptococcus pyogenes producing streptococcal pyrogenic exotoxin A (SPEA) acting as a superantigen.

93
Q

FACT: cytokine storm is associated with immunological over-reactions

A
94
Q

T/F genetics plays a role in determining which patients will get a cytokine storm

A

true

95
Q

Multiple organ failure can be from overt shock, what specific types of shock can cause MOF?

A

hypovolemic

cardiogenic

96
Q

Describe the 3 stages of shock

A

1) non-progressive, with reflex compensatory mechanisms that maintain perfusion of vital organs,
2) progressive, with manifestations of decompensating organ function,
3) irreversible, with resultant death even if the cause of shock is reversed.

97
Q

The compensatory mechanisms for shock include what 3 things?

A

sympathetic nervous system responses,

fluid shifts within the body

neuroendocrine stress responses

98
Q

How do tissues with inadequate blood perfusion maintain their BP and perfusion?

A

constrict their arterioles

99
Q

How does blood loss decrease the level of inhibition of arteriolar vasoconstriction?

A

Blood loss causes decreased baroreceptor stimulation in large arteries

sends a reflex neural signal to the brainstem

decrease the level of inhibition of arteriolar vasoconstriction.

100
Q

Molecular mediators of the neuroendocrine response to shock include what? name source too

A

epinephrine and norepinephrine from the adrenal medulla,

vasopressin (also called antidiuretic hormone [ADH]) from the pituitary

renin from the kidneys.

101
Q

Describe the fluid shift response to hypovolemic shock

A

moves water from the extravascular compartment into the blood, which makes it dilute, but restores the volume

kidney stops making urine.

102
Q

Describe the lactate present In the progressive stage of shock,

A

it is worse (higher concentration) due to cells deprived of adequate oxygen resort to anaerobic metabolism, generating lactic acid.

103
Q

The level of lactate in the blood provides a measure of what?

A

measure of the degree of tissue hypoxia

104
Q

gross and microscopic pathologic manifestations of shock include

A
  • cerebral necrosis with red (dead) neurons and cerebral edema,
  • hemorrhagic ischemic enteritis,
  • renal acute tubular necrosis,
  • adrenal cortical lipid depletion and necrosis,
  • centrilobular hepatic necrosis,
  • pulmonary diffuse alveolar damage
  • myocardial necrosis.
105
Q

How long does it take neurons to start dying after losing their blood supply?

A

Neurons begin dying as soon as 4 minutes after losing their blood supply.

106
Q

Starting approximately 12 hours after they die, dead neurons develop what?

A

condensed cytoplasm rendered hypereosinophilic by the denatured, closely packed cytoplasmic proteins.

referred to as “red neurons”

107
Q

Describe what cells undering pyknosis means

A

the cells shrink and their nuclei become shrunken, condensed, hyperbasophilic

108
Q

What cells are most rapidly killed by ischemia?

A

neurons

109
Q

What is anoxic encephalopathy?

A

patients who are resuscitated from shock or cardiac arrest from other causes to have return of all organ functions except those of the brain.

110
Q

T/F The body’s compensatory mechanism of shutting off perfusion of the bowel can convert hypovolemic shock into septic shock.

A

true

111
Q

During septic shock, why does the bowel turn green?

A

Ischemic bowel mucosa becomes leaky and sticky.

Bile pigment leaks into the intestinal lining, turning it green,

stool sticks to the lining, presumably due to proteins such as fibronectin that have leaked into the bowel lumen.

112
Q

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

A

surgically resect it

113
Q

Why does a septic bowel turn dark red in appearance?

A

As the ischemia worsens, blood leaks into the mucosa and then deeper layers.

The intestinal mucosa breaks down, allowing bacteria from the lumen to invade.

The serosal surface of such ischemic bowel takes on a dusky (dark red) appearance.

114
Q

T/F acute kidney injury (AKI) is caused by shock and is reversible

A

true

115
Q

The gross pathology of AKI is what?

A

swollen kidney with pale cortex and congested medulla.

116
Q

AKI is primarily seen in what part of the kidney? What is it manifested by?

A

primarily to the tubules

  1. attenuation and loss of proximal tubule epithelial cell brush borders,
  2. epithelial cell swelling and vacuolization,
  3. epithelial cell necrosis and sloughing into the tubular lumen
117
Q

AKI is also associated with leukocytes where?

A

in the vasa recta (the small straight blood vessels of the renal medulla).

118
Q

The pathologic manifestations of shock in the adrenal glands progress how?

A

from cortical lipid depletion to necrosis and hemorrhage

119
Q

What does shcok stimulate the adrenal cortical cells to do?

A

deplete their cholesterol making these stress hormones, which are then secreted into the bloodstream.

120
Q

Wrt the adrenals and progressive shock, what occurs and what accompanies it?

A

adrenal cells die and this adrenal necrosis is frequently accompanied by hemorrhage.

121
Q

What is the Waterhouse-Friderichsen syndrome?

A

Septic shock, especially when due to Neisseria meningitidis infection in children, can lead to massive adrenal hemorrhage and necrosis,

obliterating the important adrenal contribution to counteracting shock.

122
Q

Shock liver features a pattern of what?

A

alternating red and brown (or tan or yellow or green) tissue resembling the cut surface of a nutmeg

123
Q

Grossly visible nutmeg liver usually shows what?

A

hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas.

124
Q

In mild cases of nutmeg liver, there is coagulative necrosis of hepatocytes in the center of hepatic lobules. Why?

A

both the oxygen-rich arterial blood and nutrient-rich portal venous blood diffuse through the lobules from the portal tracts around the periphery.

125
Q

Outflow of venous blood with oxygen and nutrients extracted and toxic metabolites added for a trip to the kidney starts where?

A

at the lobular central veins,

126
Q

vulnerability of hepatocytes to ischemia is directly proportional to what?

A

their proximity to the hepatic lobular central veins.

127
Q

Shock lung or ALI is characterized by what?

A

diffuse alveolar damage

128
Q

Grossly, How would shock lung present?

A

enlarged and a firm, solidified, edematous, congested, beefy red organ.

129
Q

Microscopically, what is the earliest finding of shock lung?

A

increased numbers of neutrophils in the capillaries in the septa (walls) between alveoli.

130
Q

About how long does it take pulmonary alveolar macrophages to produce IL-8? What wll the result be?

A

as quickly as 30 minutes

IL-8 is a strong neutrophil chemotactic and activating agent

IL-8 and other pro-inflammatories activate ECs and lead to sequestration of neutrophils in small pulmonary blood vessels

131
Q

Neutrophils activated by IL-8 and TNF do what wrt ECs?

A

upregulate their expression of adhesion molecules that bind to receptors on activated endothelial cells (ECs)

132
Q

Activated neutrophils release a variety of substances that do what to the lung?

A

damage the alveolar epithelial cells

increase the permeability of the barrier between the airspaces and the bloodstream

133
Q

With severe injury, breakdown of the alveolar-capillary barrier allows what action?

A

allows whole blood to leak into the alveoli.

hemorrhage

134
Q

With less severe (more typical) injury, the alveolar edema fluid does what?

A

condenses into eosinophilic hyaline membranes lining the airspaces.

135
Q

How does alveolar edema and hyaline membrane result in hypoxemia? what is hypoxemia?

A

pose a block to the diffusion of oxygen

decreased oxygen loading of the blood passing through the lungs

136
Q

How can ALI be viewed on x rays? severe cases?

A

pulmonary infiltrates

severe=> complete dense opacification of lungs (white out)

137
Q

What is acute respiratory distress syndrome (ARDS)?

A

an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary edema.

138
Q

Subendocardial myocytes begin dying as early as how long after blood supply is absent?

A

20 minutes after their blood supply has been cut off

139
Q

If a person in shock sustains a subendocardial myocardial infarction, but is successfully resuscitated, they tend to have what?

A

a circumferential infarct involving the anterior left ventricle (left anterior descending coronary artery territory),

lateral left ventricle (left circumflex coronary artery territory)

posterior left ventricle (right coronary artery territory).

140
Q

The resuscitation may be reflected in hemorrhage from reperfusion of the infarct via what 2 things?

A

broken-down blood vessels

in the contraction band form of necrosis.

141
Q

coagulation necrosis of the myocytes produces what microscopically?

A

diffusely dense hypereosinophilia of the cytoplasm

142
Q

The hypercontraction of the sarcomeres is thought to be due to what?

A

influx of calcium brought in by reperfusion, causing the sarcomeres to make one last extreme contraction from which they cannot relax since they have no energy source.

Pathology block 2 (6 decks)

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