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KN-Pathology Block 2 > Hemodynamics 2 - Nichols > Flashcards

Hemodynamics 2 - Nichols Flashcards

1
Q

Define shock.

A

a state of systemic hypoperfusion and cardiac collapse

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2
Q

What are some causes of shock?

A
  1. decreased circulating blood volume
  2. decreased cardiac output
  3. sepsis
    there are other less common causes: anaphylaxis, SIRS and neurogenic causes
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3
Q

What is hypovolemic shock and what can cause it?

A

shock due to loss of blood volume. Can be caused by bleeding, vomiting, diarrhea or extensive burns

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4
Q

What is cardiogenic shock and what can cause it?

A

shock from decreased cardiac output. Caused by myocardial infarctions, cardiac arrhythmia, pulmonary emoblism obstructiong output of the right heart, hemopericaridum squeezing the cardiac filling chambers (cardiac tamponade).

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5
Q

What is septic shock and what causes it?

A

distributive shock due to infection that results in widespread vasodilation, which maldistributes the available blood volume diffusely throughout the body in too many places, returning too little to the ehart and lungs to oxygenate and pump it where it needs to be.

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6
Q

What is usually the earliest symptom of shock?

A

agitation. They typically become irritable, nervous and fidgetiy with anxiety.

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7
Q

A patient has cool clammy skin and a weak rapid pulse. What type of shock are they likely in?

A

hypovolemic or cardiogenic shock

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8
Q

What type of shock is warm, flushed skin usually a sign of?

A

septic shock

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9
Q

What happens to urine output in shock patients?

A

urine output is decreased for all types of shock

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10
Q

Are vital signs a good indicator of shock?

A

No. They are typically late responders. Even more of a problem in young patients because their body has more ability to compensate and will crash rapidly once the capacity to do so is used up.

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11
Q

How is hemorrhagic shock treated?

A

blood transfusions

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12
Q

How is septic shock treated?

A

antibiotic therapy

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13
Q

A patient has signs of shock, distant heart sounds and jugular venous distention. What should you suscpect? How is it treated?

A

cardiac tamponade due to hemopericardium.

It is treated by reoval of blood from the pericardial sac.

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14
Q

Which cytokines are released after long bone fracture that can cause septic shock?

A

TNF, IL-1 and IL-6 (proinflammatory cytokines)

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15
Q

What percentage of total blood can the average person lose before showing symptoms and signs of compensation?

A

15-20%

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16
Q

What percentage of total blood can the average person lose before entering shock?

A

25-30% (young people 30%)

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17
Q

What percentage of total blood loss is usually considered lethal?

A

50%

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18
Q

What are the required signs to diagnose SIRS?

A

Has “enough” of the following
1. temp over 38
2. HR over 90/min
3. RR over 20/min (tachypnea) or pCO2 less than 32mmHG
4. leukocytosis or leukopenia or bandemia
altered mental status, high C-reactive protein, high procalcitonin, mixed venous oxygen saturation, elevated creatine or bilirubin, cutaneous mottling

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19
Q

What is septic shock?

A

sepsis with refractory arterial hypotension. it is a subcategory of severe sepsis, which is itself a subcategory of sepsis

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20
Q

What must the blood pressure be to diagnose septic shock?

A 
systolic blood pressure < 90 mmHg 
or
more than 40 mmHg lower than baseline
AND
acute organ dysfunction
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21
Q

What innate imune system receptors initiate the molecular mechanism for shock?

A

PAMPs are recognized by TLRs (toll-like) and NODs 1 and 2 (nucleotide oligomerization).

Complement system also activated

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22
Q

In the mechanism for initiating shock, what do NODs and TLRs do after binding PAMPS?

A

they activate inflammatory cells to produce and realease TNF, IL-1, IL-6, IL-8, IL-12, IL-18, IFN-gamma, and HMGB1.
These upregulate expression of endothelial cell adhesion molecules to bind leukocytes

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23
Q

What does phospholipase A2 in the cell membrane of platelets, endothelial cells, neutrophils, and monocytes do during sepsis?

A

generate acetyl glycerol ether phosphocoline – aka – platelet activating factor (PAF)

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24
Q

What does PAF do?

A

it is 1000x more potant than histamine in inducing vasodilation and increased vascular permeability. It also promotes leukocyte adhesion to endothelial cells, chemotaxis, degranulation and the oxidative burst.

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25
Q

Which anaphylatoxins produced by the complement cascade promote vasodilation and vascular permeability?

A

C3a and C5a are the most potent because they induce mast cells to degranulate

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26
Q

What type of cells use CD40?

A

Macrophages need it to become activated.

APCs use it to activate them.

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27
Q

Which cytokine do macrophages release upon activation?

A

IL-12 to sustain the expression of costimulatory molecules like CD80, which binds to C28 on T cells.

IL-10, whose major function is to down-regulate the responses of activated macrophages.

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28
Q

Which cells have CD28?

A

T cells. It binds to CD80 on macrophages

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29
Q

What do IL-1 and IL-8 do in the sepsis pathway?

A

they cause mast cells in the connective tissue adjacent to blood vessels to release large quantities of histamine from granules in their cytoplasm. Histamine is also released from platelets

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30
Q

What does histamine do?

A

causes dilation of arterioles and increased permeability of venules

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31
Q

Which prostaglandins cause vasodilation?

A

PGI2 (prostacyclin) and PGD2, PGE1 and PGE2

32
Q

Which prostaglandins increase vascular permeability?

A

PGD2 and PGE2

33
Q

What can activate clotting factor XII (hagemann factor)?

A

activated platelets, basement membranes or collagens.

34
Q

What does activated hagemann factor (XIIa) do?

A

initiates blood clotting, kallikrein, and the kinin cascade via the kinin, clotting cascade and complement cascade.

35
Q

What does activated factor X do?

A

causes increased vascular permeability and leukocyte emigration from blood vesses.

36
Q

What does thrombin do?

A

generates fibrinopeptides that increase vascular permeability and are chemotactics for leukocytes. It also cleaves C5 to release C5a, linking the clotting and complement cascades.

37
Q

What would you expect to happen to the serum level of plasminogen activator inhibitor-1 during sepsis? What does it do?

A

It is upregulated during sepsis. Indirectly promotes clotting by inhibiting fibrinolysis

38
Q

What would you expect to happen to tissue factor pathway inhibitor levels during sepsis? What does it do related to sepsis?

A

decreases.

It indirectly promotes clotting by decreasing fibrinolysis

39
Q

What would you expect to happen to thrombomodulin levels during sepsis? What does it do related to sepsis?

A

decreases.

It indirectly promotes clotting by decreasing fibrinolysis

40
Q

What would you expect to happen to protein C levels during sepsis? What does it do related to sepsis?

A

It indirectly promotes clotting by decreasing fibrinolysis

41
Q

How can DIC cause bleeding?

A

unlocalized disseminated intravascular coagulation in small blood vessels can consume a large portion of the bodies clotting factors and platelets, leaving it vulnerable to bleeding in other vessels

42
Q

What percentage of sepsis patients have complications from DIC?

A

50%

43
Q

What do lipoxins do?

A

inhibit neutrophil adhesion to endothelial cells and chemotaxis

44
Q

What does C1 inhibitor do?

A

counter-regulates the pro-inflammatory effects of complement activation

45
Q

What does factor H do?

A

limits convertase formation and counter-regulates the pro-inflammatory effects of complement activation

46
Q

What does DAF do?

A

decay accelerating factor limits convertase formation and counter-regulates the pro-inflammatory effects of complement activation

47
Q

What does sTNFR do?

A

soluble tumor necrosis factor receptor serves to block TNF.

48
Q

How can sepsis and shock counter-regulatory pathways leave a patient vulnerable to opportunistic infections?

A

counter-regulatory mechanisms lead to apoptosis of CD4 and CD8 lymphocytes , apoptosis of gastro-intestinal epithelial cells, and expression of ligands for inhibitory receptors on lung epithelial cells

49
Q

What is CARS?

A

compensatory anti-inflammatory response syndrome. - when patients overshoot the counter-regulation

50
Q

What is MARS?

A

a back and forth cycle between sepsis and CARS

51
Q

What cytokines could be targeted to try and prevent MARS?

A

TNF-alpha and IL-6 receptors.

52
Q

How does TSS occur via TSST-1?

A

TSST-1 is a toxin superantigen that can by itself activate T cells. It activates anywhere from 5-20% of T cells instead of the normal 0.001%.

53
Q

What cytokines are massively released during the cytokine storm in TSS?

A

IL-1 and TNF

54
Q

What race do 90% of TSS cases occur in?

A

whites

55
Q

What are the three stages of shock?

A
  1. non-progressive, with reflex compensatory mechanisms to maintain organ function
  2. progressive, with manifestations of decompensating organ function
  3. irreversible, with resultant death even if the cause of shock is reversed. Game Over
56
Q

What typically happens to heart rate during shock?

A

increases, but you cant count on this because by the time it does it’s getting pretty serious

57
Q

What is another name for ADH?

A

vasopressin

58
Q

What happens to body pH during shock?

A

it drops and becomes acidic because of lactic acid buildup

59
Q

What biomarkers can be tested to determine the severity of shock (getting close to point of no return)?

A

TNF-alpha, IL-1 and IL-6

60
Q

What color are neurons change to after dying from shock?

A

red (dead) neurons

61
Q

What happens to the brain in shock?

A

red (dead) neurons, cerebral edema

62
Q

How long can neurons survive without oxygen?

A

4 min

63
Q

How much time has to pass before hypoxic cerebral damage is visible microscopically?

A

12 hours

64
Q

What is anoxic encephalopathy?

A

when a person recovers from shock, but has brain damage

65
Q

What does the bowel do during shock?

A

perfusion of the bowel is shut off. This can turn hypovolemic shock into septic shock when ischemic bowel turns green, becomes leaky, bleeding. (dusky bowel)

66
Q

How do you treat septic shock caused by ischemic bowel?

A

surgically remove it.

67
Q

What is AKI?

A

acute kidney injury. Kidney is swollen with pale cortex and congested medulla. It primarily damages the tubules where the epithelial cell brush borders are lost.

68
Q

What is Tamm-Horsfall protein?

A

it is a glycoprotein in the kidney that is normally secreted by particular portions of tubules, but during shock, can obstruct tubules.

69
Q

What happens to the adrenals in shock?

A

cortical lipids are depleted, the necrosis and hemorrhaging occur.

70
Q

What is Waterhouse-Friderichsen syndrome?

A

when Neisseria meningitidis infects children and leads to massive adrenal hemorrhage and necrosis, obliterating adrenal contribution to counteracting shock

71
Q

What happens to the liver during shock?

A

shows a pattern of alternating red and brown tissue (nutmeg liver).

72
Q

Which hepatic cells are most vulnerable to shock?

A

those closes to the lobular central veins

73
Q

What happens to the lungs during shock?

A

DAD (diffuse alveolar damage) and acute lung injury (ALI). Lungs become enlarged and become solid, edematous, and red. Neurotphils increase in the capillaries between alveoli.
Blood and water leak into alveoli.

74
Q

What is the actute respiratory distress syndrome (ARDS)?

A

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

75
Q

How long can the heart survive without oxygen?

A

20 min

76
Q

If a person in shock sustains a subendocardial myocardial infarction, but is successfully resuscitated, where would you expect an infarct?

A

circumferential infarct involving the anterior left ventricle (left anterior descending coronary artery), lateral left ventricle (left circumflex artery) and posterior left ventricle (right coronary artery)

77
Q

The cytoplasm of necrotic heart cells is hypereosinophilic. Did it likely die from coagulation necrosis or contraction band necrosis?

A

coagulation necrosis results in hypereosinophilic cells.

Contraction band happens after shock and the cytoplasm is clear and shrunken do to hypercontraction.

KN-Pathology Block 2 (10 decks)

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