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Medical Boards February 2013 > IV - Hemodynamic Disorders, Thrombosis and Shock > Flashcards

IV - Hemodynamic Disorders, Thrombosis and Shock Flashcards

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USMLE® Step 1 flashcards
1
Q

Extravasation of fluid into interstitial spaces due to increases in vascular volume or pressure, decreases in plasma protein content or alterations in endothelial function.

A

Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81

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2
Q

It is a severe and generalized edema with profound subcutaneous tissue swelling.

A

Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81

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3
Q

The edema fluid occuring with volume or pressure overload or under conditions of reduced plasma protein.

A

Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82

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4
Q

Edema secondary to increased vascular permeability and inflammation.

A

Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82

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5
Q

The serum protein most responsible for maintaining intravascular colloid osmotic pressure.

A

Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83

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6
Q

In breast cancer, infiltration and obstruction of superficial lymphatics can cause edema of the overlying skin, called _______ appearance.

A

Peau d’ orange(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83

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7
Q

Microscopically, it is reflected primarily as a clearing and separation of the extracellular matrix elements with subtle cell swelling.

A

Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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8
Q

Diffuse edema usually more prominent in certain body areas as a result of the effects of gravity.

A

Dependent edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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9
Q

True or false:Dependent edema is a prominent feature of left-sided heart failure.

A

False.Dependent edema is a feature of right-sided HF, while pulmonary congestion is a feature of left-sided HF.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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10
Q

Edema due to renal dysfunction which manifests disproportionately in tissues with loose connective tissue matrix, e.g. Eyelids.

A

Periorbital edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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11
Q

Finger pressure over significantly edematous subcutaneous tissue displacing the interstitial fluid, leaving a finger-shaped depression on the skin.

A

Pitting edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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12
Q

Condition wherein the lungs weigh 2-3x the normal, and on sectioning reveals frothy, sometimes blood-tinged mixture of air, fluid and extravasated red cells.

A

Pulmonary edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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13
Q

Condition wherein the brain is grossly swollen, with narrowed sulci and distended gyri showing signs of flattening against the underlying skull.

A

Brain edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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14
Q

It is an active process resulting from augmented blood flow due to arteriolar dilation.

A

Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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15
Q

The affected tissue is redder than normal, because of engorgement with oxygenated blood.

A

Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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16
Q

It is a passive process resulting from impaired venous rturn out of a tissue.

A

Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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17
Q

Tissue has a blue-red color due to accumulation of hemoglobin in the affected tissue.

A

Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

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18
Q

Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage.

A

Acute pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

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19
Q

Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.

A

Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

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20
Q

Hemosiderin- laden macrophages

A

Heart- failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

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21
Q

The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration. The periportal hepatocytes are better oxygenated.

A

Acute hepatic congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

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22
Q

The central regions of the hepatic lobules are grossly red-brown and slightly depressed and are accentuated against the surrounding zones of uncongested tan, sometimes fatty liver (nutmeg liver).

A

Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

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23
Q

Presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage and hemosirin-laden macrophages

A

CPC of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

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24
Q

Extravasation of blood from vessels into the extravasclar space.

A

Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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25
Q

Accumulation of blood within a tissue.

A

Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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26
Q

1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.

A

Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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27
Q

3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.

A

Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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28
Q

1-2cm subcutaneous hematomas/bruises.

A

Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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29
Q

It is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.

A

Normal hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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30
Q

Pathologic form of hemostasis.

A

Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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31
Q

It occurs after an initial injury, as a result of reflex neurogenic mechanisms.

A

Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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32
Q

A potent endothelium-derived vasocontrictor.

A

Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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33
Q

Receptors responsible for platelet adhesion.

A

GpIb receptors- plateletVon Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

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34
Q

Deficiency of GpIb receptors.

A

Bernard-Soulier syndrome(TOPNOTCH)

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35
Q

Deficiency of GpIb receptors.

A

Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

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36
Q

Deficiency of GpIIb-IIIa receptors.

A

Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

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37
Q

Deficiency of Factor VIII.

A

Von Willebrand Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

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38
Q

It is a membrane-bound procoagulant glycoprotein synthesized by endothelium, which becomes exposed at the site of injury.

A

Thromboplastin/Factor III(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

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39
Q

Formation of a hemostatic plug due to platelet aggregation

A

Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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40
Q

Hemostasis characterized by activation of thrombin through the coagulation cascade.

A

Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

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41
Q

True or false:The primary aggregation of platelets is irreversible.

A

FalseReversible(TOPNOTCH)

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42
Q

Two substances essential for the formation of a primary hemostatic plug.

A

ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87

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43
Q

True or false:Activation of the coagultion cascade and subsequent thrombin formation is reversible.

A

FalseIrreversible(TOPNOTCH)

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44
Q

Substance that activates the coagulation proteins.

A

Calcium(TOPNOTCH)

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45
Q

Substance that medites further platelet aggregation and degranulation.

A

ADP(TOPNOTCH)

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46
Q

Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.

A

TXA2(TOPNOTCH)

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47
Q

Most important initiator of the coagulation cascade.

A

Tissue factor(TOPNOTCH)

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48
Q

A protein found on endothelial cells involved in the breakdown of blood clots which catalyzes conversion of plasminogen to plasmin.

A

Tissue plasminogen activator (t-PA) and Urokinase(TOPNOTCH)

49
Q

Components of Virchow’s triad?

A

Endothelial injuryStasisHypercoagulability(TOPNOTCH)

50
Q

It is a major contributor to the development of VENOUS thrombi.

A

Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94

51
Q

Type of blood flow found in normal blood vessels, wherein platelets flow centrally in the vessel lumen, separated from the endothelium by a slow moving clear zone of plasma.

A

Laminar flow(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94

52
Q

This contirbutes to arterial and cardic thrombisis by causing endothelial injury or dysfunction as well as formation of countercurrents and local pockets of stasis.

A

Turbulence(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94

53
Q

Any alteration of the coagulation pathway that predisposes to thrombosis.

A

Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95

54
Q

A detached, intravascular solid, liquid or gaseous mass that is carried by the blood distal to its point of origin.

A

Embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95

55
Q

Apparent laminations seen in a thrombus, representing pale platelet and fibrin layers alternating with darker erythrocyte-rich layers.

A

Lines of Zahn(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

56
Q

Significance of Lines of Zahn?

A

Represents thrombosis in the setting of blood flow, seen in antemortem clots.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

57
Q

Thrombi occuring in heart chambers or aortic lumen

A

Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

58
Q

Gelatinous thrombi with a dark red dependent portion where red cells have settled by gravity with a yellow “chicken fat” supernatant. Usually unattached to underlying wall.

A

Postmortem thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

59
Q

Thrombi on heart valves.

A

Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

60
Q

Sterile, verrucous endocartidis occuring in patients with SLE.

A

Limban-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

61
Q

Thrombi occuring in heart chambers or in aortic lumen.

A

Mural thrombi(TOPNOTCH)

62
Q

Vegetations occuring in the presence of non - infected valves in hypercoagulable states.

A

Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

63
Q

Fate of a thrombus wherein the thrombus accumulates additional platelets and fibrin, eventually causing vessel obstruction.

A

Propagation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

64
Q

Fate of a thrombus wherein it may dislodge or fragment and transported elsewhere in the vasculature.

A

Embolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

65
Q

Fate of a thrombus as a result of of fibrinolytic activity leading to rapid shrinkage and even total lysis of recent thrombi.

A

Dissolution(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

66
Q

Fate of a thrombus wherein it may induce inflammation and fibrosis and establish some degree of blood flow.

A

Organization and recanalization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

67
Q

True or false:Therapeutic administration of fibrinolytic agents is generally effective only within a few hours of thrombus formation.

A

True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

68
Q

Most common site of venous thrombosis.

A

Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

69
Q

Most common sequelae of deep venous thrombosis.

A

Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

70
Q

Tumor-associated procoagulant release largey responsible for the increased risk of thromboembolic phenomena seen in disseminated cancers.

A

Migrating thrombophlebitis or Trousseau’s syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98

71
Q

Hardening or thickening of the arteries as a result of the accumulation of fatty materials, macrophages, platelets and other inflammatory mediators.

A

Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98

72
Q

Fates of a thrombus (4)

A

PropagationResolution/DissolutionOrganization and recanalizationEmbolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98

73
Q

Embolus occluding a bifurcation in the pulmonary tree.

A

Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

74
Q

True or false:A patient who has had one pulmonary embolus has a decreased risk of developing another embolus.

A

False.The patient is at risk of developing more pulmonary emboli.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

75
Q

A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.

A

Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

76
Q

Most common symptom of pulmonary embolism.

A

None/ Asymptomatic (60-80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

77
Q

Right Ventricular failure secondary to pulmonary hypertension.

A

Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

78
Q

Emboli in the arterial circulation.

A

Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

79
Q

Most common origin of systemic thrombi.

A

Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

80
Q

Major site of arteriolar embolization.

A

Lower extremities (75%)Brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

81
Q

Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma.

A

Fat embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

82
Q

Symptoms of pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia characterize what syndrome?

A

Fat embolism syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

83
Q

Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.

A

Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

84
Q

Amount of air in the circulation which produces clinical effects of air embolism.

A

> 100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

85
Q

This occurs when individuals are exposed to sudden changes in atmospheric pressure (e.g. Deep sea divers, scuba divers).

A

Decompression sickness(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

86
Q

The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and around joints causing pain.

A

Bends(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

87
Q

Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.

A

Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

88
Q

More chronic form of decompression sickness where persistence of gas emboli in the bones leads to multiple foci of ischemic necrosis.

A

Caisson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

89
Q

Treatment of choice for decompression sickness.

A

Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

90
Q

Underlying cause of amniotic fluid embolism.

A

Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)

91
Q

Underlying cause of amniotic fluid embolism.

A

Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

92
Q

Presence of marked pulmonary edema, diffuse alveolar damage, and presence of squamous cells in the pulmonary circulation shed from fetal skin, lanugo hair, fat and mucin.

A

Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

93
Q

White or red infarct?Venous occlusion

A

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

94
Q

White or red infarct?Lung infarction

A

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

95
Q

White or red infarct?Intestinal infarct

A

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

96
Q

White or red infarct?Myocardial infarction

A

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

97
Q

White or red infarction?Splenic infact

A

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

98
Q

White or red infarction?Wedge infarct

A

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

99
Q

The dominant histologic characteristic of infarction.

A

Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

100
Q

Histologic characteristic of brain infarcts.

A

Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

101
Q

This occurs when bacterial vegetations from a heart valve embolize or when microbes seed an area of necrotic tissue.

A

Septic infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

102
Q

Most common sequalae of septic infarcts.

A

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

103
Q

Major determinants of the eventual outcome of an infarct. (4)

A

Nature of vascular supplyRate of development of occlusionVulnerability to hypoxiaOxygen content of blood(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

104
Q

Neurons undergo irreversible damage when deprived of their blood supply for _______.

A

3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

105
Q

Myocardial cells undergo irreversile damage after ______ minutes of ischemia.

A

20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

106
Q

It is the final common pathway for severe hemorrhage, extensive trauma, burns, large MI, pulmonary embolism and sepsis.

A

Shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

107
Q

End results of shock (3)

A

HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

108
Q

This type of shock results from failure of the cardic pump which maybe caused by MI, ventricular arrythmias, cardiac tamponade or outflow obstruction.

A

Cardiogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

109
Q

This type of shock results from loss blood or plasma volume.

A

Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

110
Q

This type of shock is caused by microbial infection, caused by gram negative and gram positive bacteria and fungi

A

Septic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

111
Q

True or false:Systemic bacteremia must be present to induce septic shock.

A

FalseHost inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102

112
Q

Type of shock which occurs in the setting of an anesthetic accident or spinal cord injury as a result of loss of vascular tone and peripheral pooling of blood.

A

Neurogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

113
Q

This type of shock represents systemic vasodilation and increased vascular permeability caused by IgE hypersensitivity reaction.

A

Anaphylactic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

114
Q

Septic shock caused by gram negative bacilli.

A

Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103

115
Q

Criteria for SIRS.

A

Temp 38 CelciusHR >90 bpmRR >20 or PaCO2 12,000 cells/mm3 or 10% bands(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103

116
Q

Adrenal changes in shock.

A

Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

117
Q

Kidney changes in shock.

A

Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

118
Q

Gastrointestinal changes in shock.

A

Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

119
Q

Lung changes in shock.

A

Diffuse alveolar damage if due to bacterial sepsi and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

Medical Boards February 2013 (24 decks)

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