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pathology > IV - Hemodynamic Disorders, Thrombosis and Shock > Flashcards

IV - Hemodynamic Disorders, Thrombosis and Shock 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
Accumulation of blood within a tissue.
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
26
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
27
3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.
Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
28
1-2cm subcutaneous hematomas/bruises.
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
29
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.
Normal hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
30
Pathologic form of hemostasis.
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
31
It occurs after an initial injury, as a result of reflex neurogenic mechanisms.
Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
32
A potent endothelium-derived vasocontrictor.
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
33
Receptors responsible for platelet adhesion.
GpIb receptors- plateletVon Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
34
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)
35
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
36
Deficiency of GpIIb-IIIa receptors.
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
37
Deficiency of Factor VIII.
Von Willebrand Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
38
It is a membrane-bound procoagulant glycoprotein synthesized by endothelium, which becomes exposed at the site of injury.
Thromboplastin/Factor III(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
39
Formation of a hemostatic plug due to platelet aggregation
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
40
Hemostasis characterized by activation of thrombin through the coagulation cascade.
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
41
True or false:The primary aggregation of platelets is irreversible.
FalseReversible(TOPNOTCH)
42
Two substances essential for the formation of a primary hemostatic plug.
ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87
43
True or false:Activation of the coagultion cascade and subsequent thrombin formation is reversible.
FalseIrreversible(TOPNOTCH)
44
Substance that activates the coagulation proteins.
Calcium(TOPNOTCH)
45
Substance that medites further platelet aggregation and degranulation.
ADP(TOPNOTCH)
46
Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.
TXA2(TOPNOTCH)
47
Most important initiator of the coagulation cascade.
Tissue factor(TOPNOTCH)
48
A protein found on endothelial cells involved in the breakdown of blood clots which catalyzes conversion of plasminogen to plasmin.
Tissue plasminogen activator (t-PA) and Urokinase(TOPNOTCH)
49
Components of Virchow's triad?
Endothelial injuryStasisHypercoagulability(TOPNOTCH)
50
It is a major contributor to the development of VENOUS thrombi.
Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
51
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.
Laminar flow(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
52
This contirbutes to arterial and cardic thrombisis by causing endothelial injury or dysfunction as well as formation of countercurrents and local pockets of stasis.
Turbulence(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
53
Any alteration of the coagulation pathway that predisposes to thrombosis.
Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
54
A detached, intravascular solid, liquid or gaseous mass that is carried by the blood distal to its point of origin.
Embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
55
Apparent laminations seen in a thrombus, representing pale platelet and fibrin layers alternating with darker erythrocyte-rich layers.
Lines of Zahn(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
56
Significance of Lines of Zahn?
Represents thrombosis in the setting of blood flow, seen in antemortem clots.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
57
Thrombi occuring in heart chambers or aortic lumen
Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
58
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.
Postmortem thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
59
Thrombi on heart valves.
Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
60
Sterile, verrucous endocartidis occuring in patients with SLE.
Limban-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
61
Thrombi occuring in heart chambers or in aortic lumen.
Mural thrombi(TOPNOTCH)
62
Vegetations occuring in the presence of non - infected valves in hypercoagulable states.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
63
Fate of a thrombus wherein the thrombus accumulates additional platelets and fibrin, eventually causing vessel obstruction.
Propagation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
64
Fate of a thrombus wherein it may dislodge or fragment and transported elsewhere in the vasculature.
Embolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
65
Fate of a thrombus as a result of of fibrinolytic activity leading to rapid shrinkage and even total lysis of recent thrombi.
Dissolution(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
66
Fate of a thrombus wherein it may induce inflammation and fibrosis and establish some degree of blood flow.
Organization and recanalization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
67
True or false:Therapeutic administration of fibrinolytic agents is generally effective only within a few hours of thrombus formation.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
68
Most common site of venous thrombosis.
Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
69
Most common sequelae of deep venous thrombosis.
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
70
Tumor-associated procoagulant release largey responsible for the increased risk of thromboembolic phenomena seen in disseminated cancers.
Migrating thrombophlebitis or Trousseau's syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
71
Hardening or thickening of the arteries as a result of the accumulation of fatty materials, macrophages, platelets and other inflammatory mediators.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
72
Fates of a thrombus (4)
PropagationResolution/DissolutionOrganization and recanalizationEmbolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
73
Embolus occluding a bifurcation in the pulmonary tree.
Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
74
True or false:A patient who has had one pulmonary embolus has a decreased risk of developing another embolus.
False.The patient is at risk of developing more pulmonary emboli.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
75
A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.
Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
76
Most common symptom of pulmonary embolism.
None/ Asymptomatic (60-80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
77
Right Ventricular failure secondary to pulmonary hypertension.
Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
78
Emboli in the arterial circulation.
Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
79
Most common origin of systemic thrombi.
Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
80
Major site of arteriolar embolization.
Lower extremities (75%)Brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
81
Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma.
Fat embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
82
Symptoms of pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia characterize what syndrome?
Fat embolism syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
83
Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.
Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
84
Amount of air in the circulation which produces clinical effects of air embolism.
>100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
85
This occurs when individuals are exposed to sudden changes in atmospheric pressure (e.g. Deep sea divers, scuba divers).
Decompression sickness(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
86
The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and around joints causing pain.
Bends(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
87
Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.
Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
88
More chronic form of decompression sickness where persistence of gas emboli in the bones leads to multiple foci of ischemic necrosis.
Caisson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
89
Treatment of choice for decompression sickness.
Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
90
Underlying cause of amniotic fluid embolism.
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)
91
Underlying cause of amniotic fluid embolism.
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
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.
Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
93
White or red infarct?Venous occlusion
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
94
White or red infarct?Lung infarction
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
95
White or red infarct?Intestinal infarct
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
96
White or red infarct?Myocardial infarction
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
97
White or red infarction?Splenic infact
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
98
White or red infarction?Wedge infarct
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
99
The dominant histologic characteristic of infarction.
Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
100
Histologic characteristic of brain infarcts.
Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
101
This occurs when bacterial vegetations from a heart valve embolize or when microbes seed an area of necrotic tissue.
Septic infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
102
Most common sequalae of septic infarcts.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
103
Major determinants of the eventual outcome of an infarct. (4)
Nature of vascular supplyRate of development of occlusionVulnerability to hypoxiaOxygen content of blood(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
104
Neurons undergo irreversible damage when deprived of their blood supply for _______.
3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
105
Myocardial cells undergo irreversile damage after ______ minutes of ischemia.
20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
106
It is the final common pathway for severe hemorrhage, extensive trauma, burns, large MI, pulmonary embolism and sepsis.
Shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
107
End results of shock (3)
HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
108
This type of shock results from failure of the cardic pump which maybe caused by MI, ventricular arrythmias, cardiac tamponade or outflow obstruction.
Cardiogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
109
This type of shock results from loss blood or plasma volume.
Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
110
This type of shock is caused by microbial infection, caused by gram negative and gram positive bacteria and fungi
Septic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
111
True or false:Systemic bacteremia must be present to induce septic shock.
FalseHost inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102
112
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.
Neurogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
113
This type of shock represents systemic vasodilation and increased vascular permeability caused by IgE hypersensitivity reaction.
Anaphylactic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
114
Septic shock caused by gram negative bacilli.
Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
115
Criteria for SIRS.
Temp 38 CelciusHR >90 bpmRR >20 or PaCO2 12,000 cells/mm3 or 10% bands(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
116
Adrenal changes in shock.
Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
117
Kidney changes in shock.
Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
118
Gastrointestinal changes in shock.
Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
119
Lung changes in shock.
Diffuse alveolar damage if due to bacterial sepsi and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

pathology (24 decks)

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