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Chapters 1-9 - Robbins Pathologic Basis of Disease, 9th Edition > 4 - Hemodynamic Disorders, Thromboembolic Disease, and Shock > Flashcards

4 - Hemodynamic Disorders, Thromboembolic Disease, and Shock Flashcards

1
Q

Cardiovascular disease will primarily affect one or more of what three components of the cardiovascular system?

A

The heart, the blood vessels, or the blood

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2
Q

What are the four major categories of hemodynamic disorders?

A

Edema, effusions, congestion, and shock

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3
Q

What is the name of fluid accumulations in tissues?

A

Edema

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4
Q

What is the name of fluid accumulations in body cavities?

A

Effusions

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5
Q

What two pressures balance fluid extrusion and intake in capillary beds?

A

Hydrostatic pressure and colloid osmotic pressure

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6
Q

Are edema and effusions inflammatory or noninflammatory?

A

They may be both (exudates or transudates).

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7
Q

What type of disorders are the principal causes of increased hydrostatic pressure?

A

Disorders of impaired venous return (congestion)

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8
Q

Loss of what plasma substance is the principal cause of decreased colloid osmotic pressure?

A

Albumin (accounts for ~50% of all plasma protein)

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9
Q

An increase in what plasma substance will lead to increased water retention and circulatory dilution (and thus increased hydrostatic pressure and decreased colloid osmotic pressure)?

A

Salt

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10
Q

What are some causes of hypoproteinemia?

A

Nephrotic syndrome, malnutrition, liver cirrhosis

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11
Q

What are some causes of lymphatic obstruction?

A

Inflammation, neoplasm, surgical removal, irradiation

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12
Q

What categories of tissues are most commonly affected by edema?

A

Subcutaneous, lung, and brain tissues

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13
Q

What is dependent edema?

A

A form of gravity-influenced subcutaneous edema in the legs and pelvis (often due to right-sided heart failure)

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14
Q

What parts of the body are often the first affected by edema in cases of renal dysfunction?

A

Areas with loose connective tissue such as the eyelids (periorbital edema)

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15
Q

What are the main types of effusion?

A

Pericardial (hydropericardium), pleural (hydrothorax), and peritoneal (ascites or hydroperitoneum)

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16
Q

When is pulmonary edema most commonly seen?

A

In cases of left-sided heart failure (but also in renal failure and adult respiratory distress syndrome)

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17
Q

What fluid accumulation often accompanies pulmonary edema of the lung tissue?

A

Pleural effusions further compressing the lungs from the pleural cavity

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18
Q

What is the most common cause of ascites?

A

Portal hypertension

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19
Q

What is a potentially life threatening complication of cerebral edema?

A

Brain herniation (and death following medulla compression or loss of blood supply)

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20
Q

What is the difference between hyperemia and congestion?

A

Hyperemia is an active process of arteriolar dilation; congestion is a passive process resulting from decreased outflow of blood

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21
Q

Ironically, in what adverse tissue event can long-standing, chronic congestion result?

A

Ischemic tissue, hemorrhage, and scarring

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22
Q

Long-standing congestion can result in hemorrhagic foci with what telltale cell clusters?

A

Clusters of hemosiderin-laden macrophages (trying to catabolize the extravasated red blood cells and contained hemoglobin)

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23
Q

What is another name for the clusters of hemosiderin-laden macrophages trying to clean up hemorrhagic foci?

A

Heart-failure cells

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24
Q

Define the term ‘nutmeg liver.’

A

In chronic passive hepatic congestion, the centrilobular regions are grossly red-brown and slightly depressed (because of cell death) and are accentuated against the surrounding zones of uncongested tan liver.

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25
Q

What color will congested tissues turn?

A

a dusky reddish-blue color (cyanosis) due to red cell stasis and the presence of deoxygenated hemoglobin

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26
Q

Define hemostasis.

A

The process by which blood clots form at sites of vascular injury

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27
Q

What are the two categories of disorder of hemostasis (too much and too little)?

A

Hemorrhagic or thrombotic disorders

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28
Q

What are the four steps of hemostasis?

A
  1. Arteriolar vasoconstriction
  2. Platelet plug (primary hemostasis)
  3. Fibrin deposition (secondary hemostasis)
  4. Clot stabilization and resorption
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29
Q

What substance do endothelial cells release to initiate the vasoconstriction seen in hemostasis?

(Hint: don’t say nitric oxide)

A

Endothelin

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30
Q

What is primary hemostasis?

A

Platelet plug formation

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31
Q

What is secondary hemostasis?

A

Fibrin deposition

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32
Q

What two important substances in the ECM are exposed when the blood vessel is damaged?

A

Collagen (binds vWF) and tissue factor (binds Factor VII)

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33
Q

What process makes up platelet adhesion?

A

Glycoprotein Ib binding to vWF which is bound to collagen in the exposed ECM

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34
Q

When do platelets become activated?

A

Only AFTER adhesion (via vWF to the exposed collagen)

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35
Q

What happens during platelet activation following adhesion?

A

The platelets become spiky (increasing surface area), glycoprotein IIb/IIIa is expressed. negatively charged phospholipids serve as calcium anchors and nucleation sites for coagulation factor complexes;

the contents of the alpha and dense granules are then secreted

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36
Q

What triggers platelet activation?

A

Thrombin (through GPCRs) and ADP

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37
Q

ADP activates platelets and is also released from dense granules following activation. Why is this important?

A

A process known as recruitment: activated platelets then activate other platelets.

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38
Q

What occurs following platelet adhesion and activation?

A

Platelet aggregation (GbIIb/IIIa binding fibrinogen)

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39
Q

What happens after platelet adhesion, activation, and aggregation?

A

The platelets contract towards one another and fibrinogen is turned into fibrin, sealing the clot

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40
Q

Describe the clotting cascade in the laboratory setting.

A
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41
Q

Describe the clotting cascade in vivo. How is it different from the laboratory setting?

A
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42
Q

Where does the clotting cascade (in vivo) take place?

A

On phospholipid surfaces (platelet membranes)

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43
Q

Which clotting factors require vitamin K for their production? Which endogenous anticoagulants require vitamin K for their production?

A

II, VII, IX, and X; protein C and protein S

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44
Q

Name a disease for each of the following steps:

Glycoprotein Ib expression

vWF expression

Glycoprotein IIb/IIIa expression

Factor VIII expression

Factor IX expression

Factor XI expression

A

Bernard-Soulier disease (Glycoprotein Ib)

von Willebrand Factor deficiency (vWF)

Glanzmann’s thrombasthenia (Glycoprotein IIb/IIIa)

Hemophilia A (Factor VIII)

Hemophilia B (Factor IX)

Hemophilia C (Factor XI)

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45
Q

Which clotting factor is most important because it is involved in so many different reactions?

A

Thrombin

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46
Q

What do the partial thromboplastin time (PTT) and prothrombin time (PT) tests measure in the laboratory?

A

PTT - the intrinsic pathway (Factors XII, XI, IX, VIII, X, V, II, and fibrinogen)

PT - the extrinsic pathway (Factors VII, X, V, II, and fibrinogen)

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47
Q

What are some of the seemingly contradictory effects of thrombin?

A

Platelet activation, fibrin formation, pro-inflammatory effects, and anticoagulation

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48
Q

What breakdown product is a useful clinical marker for several thrombotic states?

A

D-Dimers

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49
Q

What are some of the methods by which coagulation is inhibited?

A

Endothelial mechanisms, dilution (flowing plasma washes clotting factors away), plasmin cascade

50
Q

What are the anticoagulant effects of the endothelium?

A

Prostacyclin, nitric oxide, and adenosine diphosphatase release; thrombomodulin, protein C and protein S expression; tissue plasminogen activator secretion

51
Q

What is the most valuable source of coagulation limitation?

A

Endothelial mechanisms

52
Q

What are some of the most common causes of mild bleeding tendencies? What are some of the most common causes of severe bleeding tendencies? What lies between?

A

vWF defects, aspirin intake, uremia (renal failure);

aortic dissection, abdominal aortic aneurysm rupture, heart rupture during AMI;

the hemophilias

53
Q

What is a feared complication of severe thrombocytopenia?

A

Cerebral hemorrhage

54
Q

How do platelet disorders and vWF defects usually manifest (dysfunction of primary hemostasis)?

A

Small bleeds in the skin and mucosal membranes, petechiae and purpura, epistaxis

55
Q

How do coagulation factor disorders usually manifest (dysfunction of secondary hemostasis)?

A

Bleeding into soft tissue (e.g. muscle) and joints (hemarthrosis)

56
Q

What type of bleeding is more typical of defects in small vessels (e.g. vasculitis, scurvy)?

A

Palpable purpura, echysmoses, and small hemorrhages (1-2 cm) and hematomas

57
Q

In healthy adults, is the rapid loss of 20% of their blood supply usually a severely dangerous situation?

A

No.

58
Q

What factors make up Virchow’s Triad?

A

Stasis, hypercoagulability, and endothelial damage

59
Q

What is the end result of Virchow’s Triad?

A

Thrombosis

60
Q

What effect do inflammation and noxious stimuli have on the endothelium?

A

It shifts the endothelium to a prothrombotic state

61
Q

Do cells and platelets normally bump into the endothelial walls as they travel through circulation (in laminar conditions)?

A

No, a layer of slower moving plasma separates the contents from the vessel walls

62
Q

What effect can turbulence have in arterial blood flow?

A

It creates pockets of stasis and increases the likelihood of vessel damage and thrombosis

63
Q

What can cause turbulence in the arteries?

A

Aneurysms, vessel damage, cardiac valvular stenosis or malformation, ulcerated atherosclerotic plaques, left ventricular dilatation

64
Q

What is another term for hypercoagulability?

A

Thrombophilia

65
Q

Hypercoagulability is very important in what system of circulation? What are the two general categories of hypercoagulability?

A

The venous system;

Primary (genetic) and secondary (acquired)

66
Q

What are the two most common causes of primary (genetic) hypercoagulability?

A

Point mutations in Factor V and prothrombin

67
Q

What percentage of Caucasians carry a Factor V mutation?

A

2 - 15% (predisposing them to DVT, etc.)

68
Q

What are some causes of secondary (acquired) hypercoagulability?

A

Bed rest and immobility, MI, atrial fibrillation, tissue injury, cancer, DIC, heparin-induced thrombocytopenia, and antiphospholipid antibody syndrome

(Also, smoking, oral contraceptive pills, pregnancy)

69
Q

When should inherited cases of hypercoagulability be considered in diagnosis?

A

When a patient younger than 50 years old presents with thrombosis

70
Q

Describe Heparin-Induced Thrombocytopenia Syndrome.

A

HIT occurs following the administration of unfractionated heparin, which may induce the appearance of antibodies that recognize complexes of heparin and platelet factor 4. Binding of these antibodies to platelets results in their activation, aggregation, and consumption (hence the thrombocytopenia in the syndrome name). This effect on platelets and endothelial damage induced by antibody binding combine to produce a prothrombotic state, even in the face of heparin administration and low platelet counts.

Low-molecular-weight heparin preparations induce HIT less frequently, and other classes of anticoagulants such as direct inhibitors of factor X and thrombin may also obviate the risk.

71
Q

Describe some of the effects of Antiphospholipid Antibody Syndrome.

A

Recurrent thromboses, repeated miscarriages, cardiac valve vegetations, and thrombocytopenia

——>

Pulmonary embolism, pulmonary hypertension, stroke, bowel infarction, renovascular hypertension

72
Q

Why do patients with Antiphospholipid Antibody Syndrome have repeated miscarriages?

A

Fetal loss does not appear to be explained by thrombosis, but rather seems to stem from antibody-mediated interference with the growth and differentiation of trophoblasts, leading to a failure of placentation.

73
Q

What organs does Antiphospholipid Antibody Syndrome often damage?

A

The kidneys, the lungs, the placenta (as well as infarctions to the brain, bowel, and heart)

74
Q

Where do arterial and cardiac thrombi usually start?

A

Areas of turbulence and/or endothelial damage

75
Q

Where do venous thrombi usually start?

A

Areas of stasis

76
Q

What name is given to thrombi forming in the heart chambers or aortic lumen?

A

Mural thrombi

77
Q

What conditions predispose a patient to thrombi forming in the heart chambers or aortic lumen?

A

Abnormal myocardial contraction (arrhythmias, dilated cardiomyopathy, or myocardial infarction) or endomyocardial injury (myocarditis or catheter trauma) promotes cardiac mural thrombi;

ulcerated atherosclerotic plaque and aneurysmal dilation are the precursors of aortic thrombi

78
Q

What is a term for thrombi on heart valves?

A

Vegetations

79
Q

What are some fates that a thrombus may undergo?

A

Propagation, embolization, dissolution

(i.e. growth, travel, or dissolvement)

80
Q

Are older or younger thrombi more resistant to lysis?

A

Older (so fibrinolytics must be given with hours)

81
Q

What is the eventual fate of a thrombus?

A

Fibrosis and recanalization

82
Q

In what percentage of individuals are DVT asymptomatic and only noticed after PE?

A

50%

83
Q

Which sites of venous thrombosis or most predisposing to pulmonary embolism? Which are less predisposing?

A

Femoral, iliac, and popliteal veins;

saphenous veins (superficial and varicose veins)

(Although all the above veins may be sites of DVT)

84
Q

Define embolus.

A

a detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or infarction.

85
Q

What are some sources of emboli?

A

Thrombi, fat, air, bacteria, tumors, amniotic fluid

86
Q

Where do most pulmonary emboli arise?

A

The deep leg veins

87
Q

What is a common result of a small embolus in the pulmonary tree?

A

Wedge-shaped infarction and localized tissue death

88
Q

What is a common result of a large embolus in the pulmonary tree? (≥ 60% of the tree obstructed)

A

Collateral circulation prevents complete infarction, but blood flow is inhibited and right-sided heart failure can ensue

89
Q

What percentage of pulmonary emboli are silent due to their small size?

A

60 - 80%

90
Q

Define infarction.

A

An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage

91
Q

What underlies the vast majority of infarctions?

A

Arterial thrombosis or embolism

92
Q

Where do red infarcts (blood collecting in the infarcted zone) generally occur?

A

In venous occlusions (e.g. testes), loose spongy tissues (e.g. lungs), and tissues with dual circulation (e.g. intestines and lungs)

93
Q

Where do white infarcts occur?

A

Solid organs with end-arterial circulation (e.g. spleen, heart, kidney)

94
Q

What factors help determine if a case of thrombosis will turn into an infarction?

A

Collateral circulation, speed of thrombosis, blood oxygenation, tissue susceptibility

95
Q

What are the three general categories of shock?

A

Cardiogenic;

Hypovolemic;

Shock associated with systemic inflammation

96
Q

Describe cardiogenic shock.

A

Cardiogenic shock results from low cardiac output due to myocardial pump failure.

This can be due to intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade; or outflow obstruction (e.g., pulmonary embolism).

97
Q

Describe some of the causes of cardiogenic shock.

A

Intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade), or outflow obstruction (e.g., pulmonary embolism)

98
Q

Describe hypovolemic shock.

A

Results from low cardiac output due to low blood volume, such as can occur with massive hemorrhage or fluid loss from severe burns

99
Q

What are some causes of the widespread release of inflammatory mediators that result in shock associated with systemic inflammation?

A

Microbial infections, burns, trauma, pancreatitis

100
Q

How can systemic inflammation lead to shock?

A

The common pathogenic feature is a massive outpouring of inflammatory mediators from innate and adaptive immune cells that produce arterial vasodilation, vascular leakage, and venous blood pooling.

101
Q

What is the leading cause of death in ICUs?

A

Septic shock

102
Q

What is the mortality rate of septic shock?

A

Over 20%

103
Q

What are the principal causes of septic shock?

A

Gram-positive bacteria, gram-negative bacteria, fungi

104
Q

What is septic shock?

A

A subtype of ‘shock associated with systemic inflammation’ that results from microbial infections

105
Q

Is the pathogenesis of septic shock fully understood?

A

No.

106
Q

What are some of the factors believed to play a major role in septic shock development?

A

Inflammatory and counter-inflammatory responses;

endothelial activation and injury;

induction of a procoagulant state;

metabolic abnormalities;

organ dysfunction

107
Q

Describe septic shock.

A
108
Q

What are the three stages of shock?

A

(1) Nonprogressive (compensated), (2) progressive (uncompensated), (3) irreversible

109
Q

Describe the nonprogressive stage of shock.

A

An initial nonprogressive phase during which reflex compensatory mechanisms are activated and perfusion of vital organs is maintained

110
Q

Describe the progressive stage of shock.

A

A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including lactic acidosis

111
Q

Describe the irreversible stage of shock.

A

An irreversible stage that sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible

112
Q

How are cardiac output and blood pressure maintained during the nonprogressive stage of shock?

A

Neurohumoral mechanisms

113
Q

What are some of the neurohumoral mechanisms that maintain cardiac output and blood pressure during the nonprogressive stage of shock?

A

Baroreceptor reflex, catecholamine release, renin-angiotensin activation, ADH release, and generalized sympathetic stimulation

114
Q

What are the effects of the neurohumoral mechanisms in nonprogressive shock?

A

The net effect is tachycardia, peripheral vasoconstriction, and renal conservation of fluid.

Cutaneous vasoconstriction, for example, is responsible for the characteristic coolness and pallor of the skin in well-developed shock (although septic shock can initially cause cutaneous vasodilation and thus present with warm, flushed skin). Coronary and cerebral vessels are less sensitive to the sympathetic response and thus maintain relatively normal caliber, blood flow, and oxygen delivery.

115
Q

What happens if the underlying causes of nonprogressive shock are not treated?

A

If the underlying causes are not corrected, shock passes imperceptibly to the progressive phase, during which there is widespread tissue hypoxia.

In the setting of persistent oxygen deficit, intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid. The resulting lactic acidosis lowers the tissue pH and blunts the vasomotor response; arterioles dilate, and blood begins to pool in the microcirculation. Peripheral pooling not only worsens the cardiac output, but also puts endothelial cells at risk for developing anoxic injury with subsequent disseminated intravascular coagulation. With widespread tissue hypoxia, vital organs are affected and begin to fail.

116
Q

What occurs following progressive shock (if not corrected)?

A

In severe cases, the process eventually enters an irreversible stage. Widespread cell injury is reflected in lysosomal enzyme leakage, further aggravating the shock state.

If ischemic bowel allows intestinal flora to enter the circulation, bacteremic septic shock may be superimposed. At this point, the patient may develop anuria as a result of acute tubular necrosis and renal failure (Chapter 20), and, despite heroic measures, the downward clinical spiral almost inevitably culminates in death.

117
Q

Of otherwise healthy patients in hypovolemic shock, what percentage survive with appropriate management?

A

> 90%

118
Q

What are the symptoms of hypovolemic or cardiogenic shock?

A

Hypotension; a weak, rapid pulse; tachypnea; and cool, clammy, cyanotic skin

119
Q

How is septic shock different from cardiogenic or hypovolemic shock?

A

In septic shock, the skin may initially be warm and flushed because of peripheral vasodilation

120
Q

What are some of the major organs first affected in shock?

A

Rapidly, shock begets cardiac, cerebral, and pulmonary dysfunction, and, eventually, electrolyte disturbances and metabolic acidosis exacerbate the dire state of the patient further

121
Q
A

Chapters 1-9 - Robbins Pathologic Basis of Disease, 9th Edition (9 decks)

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