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CMOD/PCM- Block 2 > Path: Hemodynamics 3 & 4 > Flashcards

Path: Hemodynamics 3 & 4 Flashcards

1
Q

_______ is a state of systemic (total body) hypoperfusion, a state of cardiovascular collapse.

A

Shock

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2
Q

Shock is caused by 3 things, commonly. List them, please.

A

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

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3
Q

Decreased circulating blood volume is known as _______ shock and can be due to bleeding or fluid loss from ________, ________ or ____________.

A

hypovolemic shock; vomiting, diarrhea or extensive burns

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4
Q

Decreased cardiac output is called ________ shock and this can be due to myocardial infarction, but it can also be due to cardiac __________ messing up the signaling mechanism for an otherwise adequate pump, ______________ obstructing the output of the right heart or _____________ squeezing the cardiac filling chambers, obstructing filling (“cardiac tamponade”).

A

cardiogenic shock; arrythmia; pulmonary embolism; hemopericardium

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5
Q

Septic shock and its associations such as anaphylaxis, all feature widespread _______, which 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.

A

vasodilation

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6
Q

Is there a threshold blood pressure that can define a state of shock?

A

No. Blood pressure low enough to cause shock in one pt may be normal for another.

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7
Q

Shock is a constellation of signs and symptoms of total body ________.

A

hypoperfusion

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8
Q

One of the earliest symptoms of shock is _______ .

A

Agitation. A patient with early shock typically becomes irritable, nervous and fidgety, with anxiety. (no, this is not specific to shock)

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9
Q

Patients in _________ or _________ shock have a weak, rapid (“thready”) pulse and cool, clammy, sometimes cyanotic skin.

A

hypovolemic or cardiogenic shock

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10
Q

Patients in septic shock have ______, ______ skin.

A

warm, flushed skin

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11
Q

T/F: patients in all forms of shock have decreased urine output.

A

True

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12
Q

Are vital signs safe indicators of shock of any kind? Why or why not?

A

No. The vital signs are late responders to shock, especially in young people. By the time the heart rate is clearly abnormal (over 100/minute, in an adult) and especially by the time the blood pressure is clearly abnormal (below 90 mm Hg systolic or 40 mm Hg lower than usual), considerable injury to cells and tissue has already occurred.

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13
Q

T/F: It is characteristic of young people with shock to compensate better and longer than old people.

A

True. Young people with shock commonly have deceptively normal vital signs and physiologic functioning until they abruptly reach the limits of their ability to compensate. Then they crash suddenly and profoundly and, frequently, irretrievably.

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14
Q

Cardiac tamponade is characterized by a triad of:

A

shock, distant heart sounds, and jugular venous distension

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15
Q

T/F: septic shock is due to vasoConstriction Decreasing the capacitance of the vascular system so much that the amount of blood pooled in the Core leaves too little returning to the Extremities for adequate perfusion of the body as a whole.

A

False. Due to vasoDilation Increasing the capacitance of the vascular system 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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16
Q

_________ shock is a form of vasogenic shock with vasodilation due to spinal cord injury or spinal anesthesia causing acute loss of sympathetic nervous system maintenance of a normal level of vasoconstriction.

A

Neurogenic shock

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17
Q

Trauma patients, especially those with long bone fractures, can have shock that is partly hemorrhagic and partly more like ______ shock due to increased production of proinflammatory cytokines such as:

A

septic; TNF, IL-1 and IL-6

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18
Q

______ shock is the most common of the three major types, at least in surgery and trauma pts.

A

Hypovolemic

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19
Q

How much blood loss (in %) causes signs and symptoms of hypovolemic shock?

A

25-30% is threshold for shock
25 for older ppl. 30 for younger ppl
loss of 35-45% of a person’s blood causes life-threatening shock. (is treatable)

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20
Q

What is the % loss of blood that is commonly regarded as the dividing line between lethal and non-lethal hemorrhage?

A

50%

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21
Q

Are the % cut-offs for blood loss universal?

A

No. An unhealthy person may die from a blood loss of much less than 50%, especially a person with heart disease.

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22
Q

The consensus definition of sepsis is the ______________ due to infection, proven or highly suspected.

A

systemic inflammatory response syndrome (SIRS)

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23
Q

SIRS requires meeting 2 or more of the following criteria:

A

1- fever (>38C) or hypothermia (90/bpm)
3- tachypnea (RR >20/min)
4- leukocytosis (WBC > 12,000/cu mm) or leukopenia (WBC < 4,000/cu mm) or bandemia (>10% bands)

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24
Q

Name and describe the two critical subsets of sepsis.

A

Severe sepsis- sepsis with acute organ dysfunction

septic shock- sepsis with refractory arterial hypotension

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25
Q

Define acute organ dysfunction. You got this.

A

Malfunction such that a person cannot maintain homeostasis without intervention. Examples include acute alteration in mental status, oliguria (low urine output) or lactic acidosis.

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26
Q

Septic shock has a consensus definition of sepsis-induced hypotension with systolic blood pressure less than _________mm Hg or _______mm Hg lower than baseline, refractory to adequate fluid resuscitation, together with acute organ dysfunction.

A

90 mm Hg or >40 mm Hg

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27
Q

Normalization of blood pressure with ___________ suggests that shock is hypovolemic rather than septic.

A

fluid resuscitation

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28
Q

The majority of pts with sepsis have positive or negative blood cultures?

A

Negative

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29
Q

Do the majority of pts with Septic Shock have positive or negative blood cultures?

A

Positive

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30
Q

Babies routinely have resting heart rates well above ___/minute and normal range for their white blood cell counts is up to ______/cu mm.

A

90bpm; 18,000/cu mm

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31
Q

Sepsis causes phospholipase A2 in the cell membranes of platelets, endothelial cells, neutrophils, monocytes and other cells to generate acetyl glycerol ether phosphocholine, better known as _________.

A

platelet activating factor (PAF)

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32
Q

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

A

True

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33
Q

What is PAF’s impact on platelets?

A

It activates platelets and promotes platelet aggregation.

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34
Q

Describe PAF’s role in the killing of microbial pathogens as they relate to leukocyte migration and effector function.

A

PAF promotes leukocyte adhesion to endothelial cells, chemotaxis, degranulation and the oxidative burst that enables microbial killing in leukocytes.

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35
Q

Let’s play “Do You Remember from Block 1?”
Activation of the complement cascade yields C3a and C5a, which (increase/decrease?) vascular permeability and cause (vasodilation/vasoconstriction?) by inducing _______ cells to release histamine.

A

increase vascular permeability; vasodilation; mast cells

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36
Q

Let’s play “Do You Remember from Block 1?”
If microbial antigens are presented in conjunction with CD3 on the T cell surface and with costimulatory molecules, CD4-positive effector T-cells secrete ____________ that activates phagocytic cells to kill intracellular bacteria, and upregulate their own expression of CD40 ligand, which binds to ______ on the antigen presenting cells, which releases ______ and sustains the expression of costimulatory molecules.

A

interferon-gamma; CD40; IL-12

37
Q

List the prostaglandins cause vasoDilation.

A

PGI2, PGD2, PGE1/E2

38
Q

Which prostaglandins cause increased vascular permeability?

A

PGD2 and PGE2

39
Q

NO is a long or short acting vasoDilator?

A

Short

40
Q

Describe how NO is used to fight microbial infections.

A

It is a vasoDilator, increasing blood flow and thus infection fighting cell and molecule arrival to site of infection. It is also produced by activated macrophages and neutrophils, killing microbes by combining with reactive oxygen species.

41
Q

T/F: high amounts of ROS and RNS are not damaging to endothelial cells.

A

False. Extracellular release of larger amounts of reactive nitrogen species and reactive oxygen species into the bloodstream is damaging to endothelial cells. This damage increases vascular permeability. Increased vascular permeability allows fluid to leak out of the blood into inflamed tissues, decreasing the circulating blood volume.

42
Q

How is clotting factor XII (aka Hageman factor) activated?

A

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

43
Q

What happens when you activate Hageman factor?

A

Activated Hageman factor (XIIa), in turn, activates blood clotting, kallikrein* and with that, the kinin cascade**, and via both the clotting and kinin cascades, the fibrinolytic system and the complement cascade.

  • Plasma kallikrein liberates kinins (bradykinin and kallidin) from the kininogens,[3][4] peptides responsible for the regulation of blood pressure and activation of inflammation.
  • *kinin system is a poorly understood hormonal system with limited available research. It consists of blood proteins that play a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types.
44
Q

What role does activated factor X have within the clotting system?

A

Factor X causes increased vascular permeability and leukocyte emigration from blood vessels. It also converts Prothrombin to Thrombin, right?

45
Q

The fibrinopeptides generated by thrombin increase or decrease vascular permeability?

A

fibrinopeptides increase vascular permeability

46
Q

Who converts fibrinogen into fibrin?

A

Thrombin

47
Q

T/F: the fibrinopeptides generated by thrombin are chemotactic for leukocytes.

A

True

48
Q

T/F: Fibrin cleaves C5 to release C5a, linking clotting and the complement cascade.

A

False. Thrombin does this.

49
Q

Sepsis causes Increased ______________, which indirectly promotes clotting by inhibiting fibrinolysis.

A

plasminogen activator inhibitor-1

50
Q

Sepsis results in Decreased ________, _________ and protein ___, all indirectly promoting clotting by decreasing fibrinolysis.

A

tissue factor pathway inhibitor; thrombomodulin; protein C

51
Q

T/F: sepsis is complicated by DIC in up to 50% of septic pts.

A

True

52
Q

Just as blood clotting has a counter-regulatory fibrinolytic system, inflammation has a counter-regulatory anti-inflammatory system. Briefly summarize a few of these mechanisms and then explain what happens when the momentum swings too far in the “counter-regulatory” direction.

A
  • Lipoxins inhibit neutrophil adhesion to endothelial cells and chemotaxis.
  • C1 inhibitor and factor H serve to counter-regulate the pro-inflammatory effects of complement activation.
  • Activated macrophages secrete IL-10, whose major function is to down-regulate the responses of activated macrophages, calming themselves down.
  • Soluble tumor necrosis factor receptor (sTNFR) serves to block TNF.

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.
These counter-regulatory mechanisms cause immunosuppression. The result is opportunistic infections, reactivation of latent infections and gastro-intestinal hemorrhage.

53
Q

What is compensatory anti-inflammatory response syndrome (CARS)?

A

The extreme end of the anti-inflammatory spectrum

54
Q

What is mixed antagonistic response syndrome (MARS)?

A

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

55
Q

List the 3 targeted therapies against cytokines that block TNF-alpha used to treat autoimmunity.

A

Infliximab, etanercept, and adalimumab (Humira)

56
Q

Name the targeted therapy against cytokine IL-6 receptors used to treat autoimmunity.

A

Tocilizumab

57
Q

Explain how superantigens work.

A

Superantigens are molecules that promote T lymphocyte mitosis in a nonspecific way, bypassing antigen receptor specificity. The toxic shock syndrome toxin-1 (TSST-1), for instance, covers half of the flanking MHC alpha-helices of HLA-DR1, allowing it to bind to any T-cell receptor with a V-beta 2 segment, activating 5-20% of T cell clones instead of the 0.001% activated with normal antigen processing. These numerous clones of activated lymphocytes release mass quantities of cytokines, such as IL-1 and TNF, creating a cytokine storm leading to the systemic inflammatory response syndrome. The result is the toxic shock syndrome.

58
Q

The toxic shock syndrome is due to a nonspecific immunologic over-reaction to a secreted bacterial product, an _______, produced by staph or strep.

A

exotoxin

59
Q

Severe sepsis or SIRS is defined as sepsis or SIRS with ________________.

A

acute organ dysfunction

60
Q

The three stages of shock are:

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.

61
Q

Describe the compensatory mechanisms for shock.

A

Sympathetic nervous system responses (vasoConstriction, increase HR), fluid shifts within the body (move H2O from extravascular compartment into blood, kidneys stop making urine, perfuse only vital organs) and neuroendocrine (increase HR, release epi/norepi, vasopressin-adrenal, renin-renal) stress responses.

62
Q

Why does lactic acidosis occur in progressive stages of shock?

A

As the body begins shutting down blood supply to non-essential organs, these organs (such as extremity muscles) have to begin anaerobic metabolism. The product of this is lactic acid, which is released into the blood stream and causes lactic acidosis.

63
Q

T/F: septic shock has a point of no return after which nothing will save a person’s life. Including returning perfusion to organs.

A

True

64
Q

What, actually, are “red neurons”?

A

Neurons begin dying as soon as 4 minutes after losing their blood supply. Starting approximately 12 hours after they die, dead neurons develop condensed cytoplasm rendered hypereosinophilic by the denatured, closely packed cytoplasmic proteins. These are referred to as “red neurons”.

65
Q

The nuclei of dead neurons are hypereosinophilic or hyperbasophilic?

A

hyperbasophilic

66
Q

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

A

septic

67
Q

The serosal surface of ischemic bowel takes on a __________ appearance

A

dusky (dark red)

68
Q

The only way to cure septic shock from ischemic bowel is to __________ it.

A

surgically resect (remove)

69
Q

T/F: acute kidney injury caused by shock is reversible.

A

True

70
Q

Describe the gross pathology of acute kidney injury (AKI).

A

Swollen kidney with pale cortex and congested medulla..

71
Q

Histologically, where is the greatest hit to kidneys in acute kidney injury (AKI)? Describe this microscopic manifestation.

A

Renal tubules.
Manifested by attenuation an loss of proximal tubule epithelial cell brush borders, then epithelial cell swelling and vacuolization, and finally epithelial cell necrosis and sloughing into the tubular lumen. In addition, there may be tubular obstruction by casts of eosinophilic hyaline material, principally Tamm-Horsfall protein, which is a urinary glycoprotein normally secreted by particular portions of the tubules. If shock (or trauma causing shock) has resulted in rhabdomyolysis (skeletal muscle breakdown), there may also be an element of tubular obstruction by myoglobin casts. AKI is also associated with leukocytes in the vasa recta

72
Q

Describe shock’s gross and histological effect on the adrenal glands.

A

Progress from cortical lipid depletion to necrosis and hemorrhage. Resting adrenal cortical cells normally have abundant clear cytoplasm on routine H&E stain, cleared of cholesterol, the precursor for cortisol, aldosterone and the other steroid adrenal hormones. Shock stimulates the adrenal cortical cells to deplete their cholesterol making these stress hormones, which are then secreted into the bloodstream. With progressive shock, adrenal cells die and this adrenal necrosis is frequently accompanied by hemorrhage.

73
Q

What is 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.

74
Q

Describe the gross pathological impact of shock on the liver.

A

Nutmeg liver* spanning multiple lobules.

*hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas

75
Q

Vulnerability of hepatocytes to ischemia is directly proportional to their proximity to the hepatic __________ veins.

A

lobular central veins

76
Q

Describe the gross pathological impact of shock on the lungs.

A

Shock lung is typically enlarged and transformed from an air-filled pink-grey sponge into a firm, solidified, edematous, congested, beefy red organ.

77
Q

Describe the microscopic pathological impact of shock on the lungs.

A

Microscopically, perhaps the earliest finding is increased numbers of neutrophils in the capillaries in the septa (walls) between alveoli.

78
Q

Shock’s effect on the lungs:
As soon as half an hour after the lung insult, pulmonary alveolar macrophages produce increased amounts of ___________, which is a strong neutrophil chemotactic and activating agent.

A

interleukin-8 (IL-8)

79
Q

In relation to shock’s effect on the lungs:
Release of IL-8 and such proinflammatory cytokines as ______ and _____ activates endothelial cells and leads to sequestration of neutrophils in small pulmonary blood vessels.

A

TNF and IL-1

80
Q

Shock’s impact on the lungs:
Neutrophils activated by ____ and ______ upregulate their expression of adhesion molecules that bind to receptors on activated endothelial cells.

A

IL-8 and TNF

81
Q

Shock’s impact on the lungs:
Activated neutrophils release a variety of substances, including: (4 things) that damage the alveolar epithelial cells and increase the permeability of the barrier between the airspaces and the bloodstream.

A

oxidants, proteases, platelet activating factor and leukotrienes

82
Q

Shock’s impact on the lungs:
With severe injury, breakdown of the ______________ allows whole blood to leak into the alveoli. With less severe (more typical) injury, the alveolar edema fluid condenses into ____________ membranes lining the airspaces.

A

alveolar-capillary barrier; eosinophilic hyaline

83
Q

Acute lung injury is associated with pulmonary infiltrates on CXR. In severe cases, CXR show complete dense opacification of the lungs referred to as “_______” of the lungs.

A

“white-out”

84
Q

The ____________ is the severe end of a spectrum with acute lung injury.

A

acute respiratory distress syndrome (ARDS)

85
Q

What is the consensus definition of ARDS?

A

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

86
Q

If a person in shock sustains a subendocardial myocardial infarction, but is successfully resuscitated, they tend to have a circumferential infarct involving the anterior left ventricle (name the artery), lateral left ventricle (name the artery) and posterior left ventricle (name the artery).

A

left anterior descending coronary artery; left circumflex coronary artery; right coronary artery

87
Q

Compare and contrast the contraction band form of necrosis in cardiomyocytes with coagulation necrosis

A

In contrast to coagulation necrosis of the myocytes, which produces diffusely dense hypereosinophilia of the cytoplasm, contraction band necrosis features transverse bands of dense eosinophilic hypercontracted sarcomeres separated by relatively cleared spaces of cytoplasm.

88
Q

It is thought that what causes the hypercontraction of sarcomeres in contraction band necrosis?

A

The hypercontraction of the sarcomeres is thought to be due to the 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.

CMOD/PCM- Block 2 (41 decks)

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