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
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
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
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
Hemosiderin- laden macrophages *SEE SLIDE 4.1
A
Heart-failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
13
Q
It is an ACTIVE process resulting from augmented blood flow due to arteriolar dilation. Affected tissue is redder than normal, because of engorgement with oxygenated blood.
A
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84 *SEE SLIDE 4.2
14
Q
It is a passive process resulting from impaired venous return out of a tissue.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 *SEE SLIDE 4.3
15
Q
Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage. *SEE SLIDE 4.4
A
Acute pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
16
Q
Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces. *SEE SLIDE 4.5
A
Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
17
Q
The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration. The periportal hepatocytes are better oxygenated. *SEE SLIDE 4.6
A
Acute hepatic congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
18
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). *SEE SLIDE 4.7
A
Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
19
Q
Presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage and hemosirin-laden macrophages
A
Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
20
Q
Extravasation of blood from vessels into the extravascular space.
A
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
21
Q
Accumulation of blood within a tissue.
A
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86 *SEE SLIDE 4.8
22
Q
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
A
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86 *SEE SLIDE 4.8
23
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 *SEE SLIDE 4.8
24
Q
1-2cm subcutaneous hematomas/bruises.
A
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86 *SEE SLIDE 4.8
25
Pathologic form of hemostasis.
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
26
It occurs after an initial injury, as a result of reflex neurogenic mechanisms.
Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
27
A potent endothelium-derived vasocontrictor.
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
28
Receptors responsible for platelet adhesion.
GpIb receptors on platelet, Von Willebrand factor on endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
29
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
30
Deficiency of GpIIb-IIIa receptors.
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
31
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
32
Two substances essential for the formation of a primary hemostatic plug.
ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87
33
Formation of a hemostatic plug due to platelet aggregation. Reversible.
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
34
Hemostasis characterized by activation of thrombin through the coagulation cascade. Irreversible.
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
35
Most important initiator of the coagulation cascade.
Tissue factor(TOPNOTCH)
36
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)
37
Components of Virchow's triad?
Endothelial injury, Stasis, Hypercoagulability(TOPNOTCH)
38
It is a major contributor to the development of VENOUS thrombi.
Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
39
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
40
Alteration in blood flow that contributes to arterial and cardiac thrombosis 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
41
Any alteration of the coagulation pathway that predisposes to thrombosis.
Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
42
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
43
Apparent laminations seen in a thrombus, representing pale platelet and fibrin layers alternating with darker erythrocyte-rich layers. \*SEE SLIDE 4.9
Lines of Zahn(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
44
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
45
Thrombi occuring in heart chambers or aortic lumen
Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
46
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
47
Thrombi on heart valves.
Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
48
Sterile, verrucous endocartidis occuring in patients with SLE.
Libman-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96 \*SEE SLIDE 4.10
49
Vegetations occuring in the presence of non-infected valves in hypercoagulable states.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96 \*SEE SLIDE 4.10
50
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
51
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
52
Fates of a thrombus (4)
Propagation, Resolution/Dissolution, Organization and recanalization, Embolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
53
Most common site of venous thrombosis.
Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
54
Most common sequelae of deep venous thrombosis.
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
55
Tumor-associated procoagulant release largely 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
56
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
57
Embolus occluding a bifurcation in the pulmonary tree.
Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
58
A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.
Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
59
Most common symptom of pulmonary embolism.
None/ Asymptomatic (60-80%) (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
60
Right Ventricular failure secondary to pulmonary hypertension.
Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
61
Emboli in the arterial circulation.
Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
62
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
63
Most common origin of systemic thrombi.
Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
64
Major site of arteriolar embolization.
Lower extremities (75%), brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
65
Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma. Can lead to pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia.
Fat embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
66
Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.
Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
67
Amount of air in the circulation which produces clinical effects of air embolism.
\>100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
68
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
69
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
70
Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.
Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
71
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
72
Treatment of choice for decompression sickness.
Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
73
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins. 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
74
White or red infarct?Venous occlusion
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
75
White or red infarct?Lung infarction
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100 \*SEE SLIDE 4.11
76
White or red infarct?Intestinal infarct
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
77
White or red infarct?Myocardial infarction
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
78
White or red infarction?Splenic infact
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100 \*SEE SLIDE 4.11
79
White or red infarction?Wedge infarct
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100 \*SEE SLIDE 4.11
80
Red or white infarct? Tend to occur in previously congested tissues, or when flow is reestablished after an infarction (ie, after angioplasty of obstructed artery)
Red infarct(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.92
81
Red or white infarct? Tend to occur in solid organs with end-arterial circulations.
White infarct(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.92
82
Red or white infarct? Tend to occur in loose tissues and in those with dual circulations.
Red infarct(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.92
83
The dominant histologic characteristic of infarction.
Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
84
Histologic characteristic of brain infarcts.
Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
85
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
86
Most common sequelae of septic infarcts.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
87
Neurons undergo irreversible damage when deprived of their blood supply for \_\_\_\_\_\_\_.
3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
88
Myocardial cells undergo irreversible damage after ______ minutes of ischemia.
20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
89
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
90
End results of shock (3)
Hypotension, Impaired tissue perfusion, Hypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
91
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
92
This type of shock results from loss blood or plasma volume.
Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
93
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
94
True or false: Systemic bacteremia must be present to induce septic shock.
False: Host inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102
95
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
96
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
97
Septic shock caused by gram negative bacilli.
Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
98
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
99
Adrenal changes in shock.
Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
100
Kidney changes in shock.
Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
101
Gastrointestinal changes in shock.
Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
102
Lung changes in shock.
Diffuse alveolar damage if due to bacterial sepsis and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
103
The main mechanism of edema in inflammatory disease is:
increase vascular permeability (TOPNOTCH)
104
Sudden death in pulmonary embolism is due to:
Acute right heart failure (TOPNOTCH)
105
Accumulation of fluid within tissues
Edema (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 113
106
Accumulation of fluid within body cavities
Effusion (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 113
107
Patient presented with pain, swelling, and tenderness of left leg. What is the mechanism of edema in this condition?
Increased hydrostatic pressure. It is caused by impaired venous return as a result of DVT.(TOPNOTCH)
108
Patient presented with dyspnea, orthopnea, easy fatigability, and bipedal edema. The mechanism of edema in this condition is.
Increased hydrostatic pressure (TOPNOTCH)
109
Patient presented with periorbital edema and ankle edema. Lab result shows high lipid levels, and low serum albumin. What is the mechanism of edema in this condition?
Reduced plasma oncotic pressure secondary to protein/albumin loss (case of Nephrotic syndrome) (TOPNOTCH)
110
Mechanism of edema in severe liver disease
Reduced plasma osmotic pressure due to reduced protein synthesis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 114
111
Mechanism of edema caused by Wuchereria bancrofti
Lymphatic obstruction(in Filariasis)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 114
112
A chronic alcoholic male presented with easy fatigability and orthopnea. Chest radiograph showed bilateral pleural effusion, while abdominal ultrasound showed ascites and small liver. What is the mechanism of effusion in this condition?
Reduced plasma oncotic pressure (TOPNOTCH)
113
Patient X presented with pitting edema of the legs, jugular vein distention, and elevated transaminases. If the liver showed a nutmeg appearance, the patient most likely have: \*SEE SLIDE 4.7
Chronic passive congestion of the liver secondary to congestive heart failure (TOPNOTCH)
114
Patient with left-sided heart failure may develop pulmonary edema because of what mechanism?
Increased hydrostatic pressure (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th ed., p. 114
115
Assay that assesses the function of proteins in the extrinsic pathway (factors VII, X, V, II, fibrinogen)
Prothrombin time (PT) (TOPNOTCH) RobbIns Basic Pathology, 9th ed., p. 119
116
Assay that screens the function of proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)
Partial thromboplastin time (PTT) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 119
117
Most important coagulation factor, its various enzymatic activities control diverse aspects of hemostasis
Thrombin (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 119
118
Prostacyclin, nitric oxide and adenosine diphosphatase action: platelet activation or platelet inhibition?
Platelet inhibition(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 121
119
Patient presents with epistaxis and GI bleeding. Lab result showed low platelet count. The patient may have defect in \_\_\_\_\_. Primary or secondary hemostasis?
Primary hemostasis (TOPNOTCH)
120
Patient presented with knee joint and swelling after a soccer game. However, no physical evidence of injury was noted. He is most likely suffering from what defect in hemostasis?
Secondary hemostasis. Bleeding into joints following minor trauma is particularly characteristic of hemophilia. (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 122
121
Fatal and most feared complication of severe thrombocytopenia
Intracerebral hemorrhage (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 122
122
Patient was on anticoagulation therapy for the treatment of arterial thromboembolism. However, few days later she was noted to have blood in the urine and reddish spots on her legs. Platelet count was 20. What is the pathophysiologic mechanism for this condition?
Formation of antibodies against complexes of heparin and platelet factor 4 on platelet surface resulting to platelet activation, aggregration, and consumption. (HIT)(TOPNOTCH)
123
Syndrome presenting with recurrent thromboses, repeated miscarriages, cardiac valve vegetation, and thrombocytopenia.
Antiphospholipid antibody syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.124
124
Most common site of arterial thrombi
Coronary arteries (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 125
125
True or False. Saphenous vein thrombosis often cause embolization.
False. Superficial vein thrombosis rarely embolize. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126
126
Lower extremity DVT are often associated with\_\_\_\_. Turbulent blood flow, endothial injury or hypercoagulable state?
Hypercoagulable state (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126
127
Major cause of arterial thromboses
Atherosclerosis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126
128
Systemic activation of thrombin leading to widespread formation of thombi in microcirculation, and consumption of platelets and coagulation factors.(TOPNOTCH)
Disseminated Intravascular Coagulation/Consumptive coagulopathy(TOPNOTCH)
129
Patient X fractures his right femur after falling from a height of 10 meters. After 2 days of hospitalization, he developed sudden onset of dyspnea, tachycardia, and restlessness. Diffuse petechial rashes was noted on his trunk. What is the most likely diagnosis?
Fat emboli (TOPNOTCH)
130
A 60 y/o female, bed-ridden, was admitted to the hospital with shortness of breath and hemoptysis. Physical examination finds the patient to be afebrile, tachycardic, calf tenderness and widely split S2. What is the most likely diagnosis?
Pulmonary embolism (TOPNOTCH)
131
A 30 year old female experienced dyspnea and edema after being injected with antibiotic. She later lost consciousness and BP rapidly declined, and later went into shock. The is due to:
Anaphylactic shock (TOPNOTCH))
132
A bedridden elderly patient experienced sudden onset of dyspnea and hemoptysis. The underlying lesion that led to this complication was most likely located in which site?
Veins lof lower extremity. It is the most common site of DVT leading to pulmonary embolism. (TOPNOTCH)
133
Exudate or transudate? Inflammation
Exudate(TOPNOTCH)
134
Exudate or transudate? Nephrotic syndrome
Transudate(TOPNOTCH)
135
Exudate or transudate? Chronic liver disease
Transudate(TOPNOTCH)
136
A stillborn baby with Turner syndrome is found to have generalized edema and a large lymphangioma around her neck at autopsy. Heart and aorta findings were unremarkable. What is the mechanism for her edema? (A) Reduced oncotic pressure (B) lymphatic obstruction (C) sodium retention (D) inflammation
Lymphatic obstruction (TOPNOTCH) Robbins Basic Pathology 8th ed. pp82-83
137
Which of the following will most likely produce pulmonary edema? (A) mitral valve stenosis (B) pulmonary hypertension (C) tricuspid stenosis (D) subpulmonic valve stenosis
mitral stenosis (TOPNOTCH) Robbins Basic Pathology 8th ed. P 84
138
In which of the following cases would cerebral edema be more generalized? (A) a meningioma on the parietal cortex (B) viral encephalitis (C) occlusion of the right cerebral artery (D) frontal abscess
viral encephalitis (TOPNOTCH) Robbins Basic Pathology 8th ed. P84
139
A patient with congestive heart failure dies. At autopsy, his liver appears grossly similar to nutmeg. Which describes an expected microscopic finding? (A) lymphocytic infiltrates in the portal tracts (B) hepatocyte necrosis around central veins (C) hepatocyte necrosis around hepatic arterioles (D) vacuolated hepatocytes and giant cell formation
hepatocyte necrosis around central veins (TOPNOTCH) Robbins Basic Pathology 8th ed., p. 85.
140
A Stage IV breast cancer patient on prolonged bed rest suddenly develops difficulty of breathing and dies. At autopsy, a blood clot in the main pulmonary artery is found. Which of the following supports a thromboembolic origin, rather than a postmortem clot? (A) pale platelet and fibrin layers alternating with darker erythrocyte-rich layers (B) gelatinous consistency, with a dark dependent portion and a yellow supernatant (C) chicken fat appearance (D) lines of Kahn
pale platelet and fibrin layers alternating with darker erythrocyte-rich layers (lines of Zahn) (TOPNOTCH) Robbins Basic Pathology 8th ed, p96
141
In pure hypovolemic shock, which of the following organs will manifest the least cellular changes? (A) brain (B) adrenals (C) kidneys (D) lungs
Lungs (TOPNOTCH) Robbins Basic Pathology 8th ed. P 105.
142
Clotting factors that are exclusive members of the EXTRINSIC PATHWAY
Tissue factor (aka Factor III, Thromboplastin) and Factor VII (TOPNOTCH) Robbins Basic Pathology 9th ed. P 83.
143
Clotting factors that are exclusive members of the INTRINSIC PATHWAY
Factor XII, XI, IX, VIII (TOPNOTCH) Robbins Basic Pathology 9th ed. P 83.
