IV - Hemodynamic Disorders, Thrombosis and Shock Flashcards Preview

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Flashcards in IV - Hemodynamic Disorders, Thrombosis and Shock Deck (119)
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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
2
Q
It is a severe and generalized edema with profound subcutaneous tissue swelling.
A
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
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
4
Q
Edema secondary to increased vascular permeability and inflammation.
A
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
5
Q
The serum protein most responsible for maintaining intravascular colloid osmotic pressure.
A
Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
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
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
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
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
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
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
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
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
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
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
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
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
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
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
20
Q
Hemosiderin- laden macrophages
A
Heart- failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
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
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
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
24
Q
Extravasation of blood from vessels into the extravasclar space.
A
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
25
Q
Accumulation of blood within a tissue.
A
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
26
Q
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
A
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
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
28
Q
1-2cm subcutaneous hematomas/bruises.
A
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
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
30
Q
Pathologic form of hemostasis.
A
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
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
32
Q
A potent endothelium-derived vasocontrictor.
A
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
33
Q
Receptors responsible for platelet adhesion.
A
GpIb receptors- plateletVon Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
34
Q
Deficiency of GpIb receptors.
A
Bernard-Soulier syndrome(TOPNOTCH)
35
Q
Deficiency of GpIb receptors.
A
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
36
Q
Deficiency of GpIIb-IIIa receptors.
A
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
37
Q
Deficiency of Factor VIII.
A
Von Willebrand Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
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
39
Q
Formation of a hemostatic plug due to platelet aggregation
A
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
40
Q
Hemostasis characterized by activation of thrombin through the coagulation cascade.
A
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
41
Q
True or false:The primary aggregation of platelets is irreversible.
A
FalseReversible(TOPNOTCH)
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
43
Q
True or false:Activation of the coagultion cascade and subsequent thrombin formation is reversible.
A
FalseIrreversible(TOPNOTCH)
44
Q
Substance that activates the coagulation proteins.
A
Calcium(TOPNOTCH)
45
Q
Substance that medites further platelet aggregation and degranulation.
A
ADP(TOPNOTCH)
46
Q
Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.
A
TXA2(TOPNOTCH)
47
Q
Most important initiator of the coagulation cascade.
A
Tissue factor(TOPNOTCH)
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

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