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Pathology > Hemodynamics II > Flashcards

Hemodynamics II Flashcards

1
Q

What is shock?

A

Total body hypoperfusion; cardiovascular collapse.

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2
Q

What is severe sepsis?

A

Sepsis with acute organ dysfunction.

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3
Q

What is septic shock?

A

Severe sepsis with refractory arterial hypotension.

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4
Q

What is acute kidney injury (AKI)?

A

Acute, reversible renal injury due to hypoperfusion or hypoxemia.

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5
Q

What is acute tubular necrosis (ATN)?

A

AKI severe enough to cause necrosis of renal tubules.

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6
Q

What is acute lung injury (ALI)?

A

Acute, non-cardiogenic pulmonary edema with damage to alveolar hyaline membranes.

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7
Q

What is acute respiratory distress syndrome (ARDS)?

A

Acute, non-cardiogenic bilateral lung infiltrates and severe hypoxemia.

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8
Q

What are the 3 most common types of shock?

A
  1. Septic
  2. Hypovolemic
  3. Cardiogenic
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9
Q

T or F. Shock is a syndrome, NOT a number.

A

T.

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10
Q

What are the 4 clinical manifestations of shock?

A
  1. Decreasing mental status
  2. Decreasing urine output
  3. Pulse
  4. Skin characteristics
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11
Q

What is the pulse and skin like in a patient in either hypovolemic or cardiogenic shock?

A

Pulse: weak, rapid, thready. Skin: cool, clammy, cyanotic.

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12
Q

What is the skin like in a patient in septic shock?

A

Warm, flushed skin.

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13
Q

T or F. The vital signs are late responders to shock, especially in young people.

A

T.

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14
Q

Why is it important to figure out what type of shock a patient is in?

A

Different types require different treatment.

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15
Q

Shock caused by bleeding is treated how?

A

Blood transfusion and stopping the bleed.

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16
Q

What percentage of a patient’s blood volume is the dividing line between lethal and non-lethal hemorrhage?

A

50%.

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17
Q

T or F. Septic shock is a subset of severe sepsis which is a subset of sepsis.

A

T.

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18
Q

Septic shock is severe sepsis with addition of what?

A

Refractory hypotension.

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19
Q

Is sepsis a positive blood culture?

A

Helllllllllllllllllllllllllllllllllllllllllllllllllll NO!

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20
Q

What stimulates the release of inflammatory mediators that cause vasodilation and leaky blood vessels in septic shock?

A

PAMPs bind TLRs and other receptors on immune cells which activates them stimulating release.

21
Q

What are the 3 initial major cytokines in sepsis and septic shock? Others?

A

TNF, IL-1, and IL-6. IL-8, -12, -18, IFN-gamma, HMGB-1.

22
Q

What other molecules play a role in sepsis and septic shock?

A

PAF, C3a, C5a, PGI2, PGD2, PGE1, PGE2.

23
Q

What clotting factor is activated in sepsis that activates both the kinin and clotting cascades?

A

Factor X11a (Hageman factor).

24
Q

What protein activates the fibrinolytic system?

A

Kallikrein, a product of the kinin cascade.

25
Q

What fibrinolytic protein activates the complement cascade?

A

Plasmin.

26
Q

Kallikrein also activates what factor resulting in autocatalytic amplification of cascades in sepsis?

A

Factor XII.

27
Q

How do sepsis, severe sepsis, and septic shock lead to disseminated clotting in small vessels throughout the body?

A

Since they are pro-coagulant states, many clotting factors are activated.

28
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

Widespread fibrin thrombi in arterioles, capillaries, and venules.

29
Q

DIC is a complication of what 4 things?

A
  1. Severe infection
  2. Advanced malignancies
  3. Massive trauma
  4. Various obstetric crises
30
Q

Where is DIC the worst?

A

Brain, heart, lungs, and kidneys.

31
Q

How does DIC sometimes lead to bleeding?

A

Thrombi consume clotting factors resulting in consumptive coagulopathy.

32
Q

Counter-regulatory mechanisms of sepsis lead to what 2 things?

A
  1. Immunosuppression

2. Compensatory Anti-inflammatory Response Syndrome (CARS)

33
Q

What 5 things can result in a syndrome that closely resembles sepsis?

A
  1. Extensive burns
  2. Extensive trauma
  3. Acute pancreatitis
  4. Extensive tissue necrosis
  5. Toxic shock syndrome
34
Q

What are the 3 stages of shock? Describe each of them.

A
  1. Non-progressive: reflex compensatory mechanisms maintain perfusion of vital organs
  2. Progressive: worsening lactic acidosis, etc.
  3. Irreversible: death results even if cause of shock is reversed
35
Q

What is the histological manifestation of shock in the brain?

A

Red dead neurons.

36
Q

When do red neurons become visible histologically? What do they look like?

A

After 12 hours. Shrunken and hypereosinophilic.

37
Q

In the early phase (first day) of ALI, what is present?

A

Alveolar edema: bubbly white fluid.

38
Q

In the intermediate phase (first week) of ALI, the edema is condensed into what?

A

Alveolar hyaline membranes.

39
Q

What is seen histologically in shock heart?

A

Myocardial coagulation necrosis or contraction band necrosis.

40
Q

What causes contraction band necrosis?

A

Reperfusion allows calcium in the cell which causes sarcomeres to hypercontract.

41
Q

Histologically, myocytes lack what 2 things after an acute MI?

A
  1. Striations

2. Nuclei

42
Q

What is the earliest finding of AKI?

A

Tubular epithelial edema.

43
Q

In later stages of a worse injury to the kidney, what is seen histologically?

A

Acute tubular necrosis.

44
Q

Can tubular epithelial cells regenerate and be replaced?

A

Yes.

45
Q

What 3 things are associated with shock liver?

A
  1. Centrilobular necrosis
  2. Sinusoids leak blood
  3. High ALT and AST levels
46
Q

What 3 things are associated with shock bowel?

A
  1. Hemorrhagic ischemic enteritis
  2. Serosa appears dusky
  3. High lactate and amylase levels
47
Q

What happens to adrenal glands in shock?

A

Cortical lipid depletion.

48
Q

If a patient is in septic shock due to meningococcus complicated with DIC, hemorrhage can do what to the adrenal glands? What does this do?

A

Completely wipe out adrenals. Massively contribute to shock b/c there is no source of epinephrine, cortisol, etc.

49
Q

What is Waterhouse-Friderichsen Syndrome?

A

When the adrenal glands are wiped out.

Pathology (6 decks)

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