Pathology (all) Flashcards

1
Q

definition of edema

A

Swelling.
Excessive fluid accumulation in tissues or body cavities.
Capillary/lymphatic leak.

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2
Q

severe generalized edema

A

anasarca

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3
Q

intraalveolar fluid

A

pulmonary edema

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4
Q

fluid accumulation in pleural space

A

pleural effusion/ hydrothorax

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5
Q

fluid accumulation in peritoneal cavity

A

ascites

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6
Q

transudate (associated with ?, appearance, specific gravity, glucose levels)

A
associated with increased hydrostatic pressure.
Clear, sterile, few cells.
Low specific gravity.
Low protein content.
Glucose content near serum levels.
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7
Q

exudate (associated with ?, appearance, specific gravity, glucose levels)

A
associated with malignancy/inflammation.
Turbid/bloody/opaque.
Many cells.
High specific gravity.
High protein content.
Low glucose levels (cells consume it)
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8
Q

acute pulmonary congestion

A

SUDDEN pulmonary capillary engorgement/dilation.
Leakage of fluids –> alveolar edema.
Seen in sudden cardiac/ventricular arrhythmia with left ventricular insufficiency

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9
Q

chronic pulmonary congestion

A

Chronic capillary engorgement –> slow leakage of fluid edema into alveolar spaces.
Hemosiderin-laden macrophages (ingested RBCs) = heart failure cells.
Seen in long-standing left ventricular insufficiency.

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10
Q

hemosiderin-laden macrophages

A

Ingested RBCs.
Heart failure cells.
Seen in chronic pulmonary congestion.

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11
Q

petechiae

A

small punctuate bleedings from capillaries

thrombocytopenia

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12
Q

purpura

A

Small bleedings larger than petechiae.

Associated with blood extravasation from small arterioles, vasculitis.

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13
Q

ecchymoses

A

Larger cutaneous bleedings. (basically normal bruises)
Due to trauma.
Seen in the elderly.

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14
Q

myocardial ischemia

A

symptom: angina pectoris
Coronary blood flow does not meet myocardial oxygen demand.
Most frequent cause: coronary artery stenosis.

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15
Q

cerebral ischemia

A

Symptom: TIA
Short, temporary dysfunction of brain (neurological deficit)
Most frequent cause: decreased arterial supply due to arterial occlusion.

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16
Q

lower extremity ischemia

A

Symptom: claudicatio intermittens.

Decreased blood flow to lower extremities.

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17
Q

ischemia can lead to _____

A

Ischemia can lead to INFARCT.
Ischemic necrosis of tissue.
Caused by occlusion of arterial supply or venous drainage (thrombosis)

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18
Q

hemostasis definition

A

response to vascular injury resulting in formation of a hemostatic plug

No hemorrhage.
Blood still flows.

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19
Q

endothelium produces:

A

procoagulant, and anticoagulant factors

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20
Q

platelets cause ______ by production of __________

A

Platelets cause AGGREGATION (of platelets) by production of ADP/ATP, epinephrine, serotonin, fibrinogen, von Willebrand Factor

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21
Q

basic steps of hemostatic plug formation

A

platelet activation/adhesion, secretion, aggregation

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22
Q

end result of coagulation cascade

A

Fibrin formed (fibrinogen cleaved by thrombin)

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23
Q

fibirin

A

Large, insoluble, forms clot.

Product of coagulation cascade.

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24
Q

thrombosis

A

Pathologic activation of clotting mechanism with formation of a thrombus.

In UNINJURED vasculature.
Results in VASCULAR OCCLUSION.

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25
hemostasis vs thrombosis
hemostasis: physiologic; does not block blood flow; in injured vasculature thrombosis: pathologic; blocks blood flow; in uninjured vasculature
26
virchow's triad
three factors involved in thrombus formation: 1) endothelial injury 2) abnormal blood flow 3) hypercoagulability/thrombophilia
27
endothelial injury (virchow's triad)
Exposed ECM leads to platelet activation, coagulation cascade. Could also be caused by dysfunctional endothelium (DM, smoking, hypercholesterolemia)
28
abnormal blood flow (virchows triad)
Turbulence esp. at bifurcation sites, areas of atherosclerotic plaques. Stasis: slowing of blood Hyperviscosity: increased cellular elements of blood.
29
hypercoagulability/thrombophilia
Disorder in coagulation pathway.
30
fates of thrombi
1) thrombolysis (clot removed by fibrinolytic system) 2) organization (remodeling, recanalization) 3) embolization
31
paradoxical embolism
Emboli that cross from venous to arterial circulation via septal heart defects (ex: patent foramen ovale)
32
arterial thromboembolism
Emboli that originate within arterial circulation (bacterial growth/clot formation in heart valve/chambers, vegetation on valves due to metastatic cancer/treatment)
33
types of emboli
Amniotic fluid emboli. Septic emboli (cardiac valve vegetations). Air emobli. Fat emboli
34
suspect thrombophilia if:
<60 years old. Family history. Spontaneous/massive DVT/VTE
35
Risk factors for acquired thrombophilia
``` Immobilization. Major surgery/fracture/burns. Malignancy. MI. Heparin. Pregnancy/estrogen. Smoking. ```
36
types of hereditary thrombophilia
``` Mutation in factor V Leiden. Prothrombia gene mutation. Antithrombin III deficiency. Protein C deficiency. Protein S deficiency. Hyperhomocystinemia. ```
37
arteriosclerosis
Umbrella term. Hardening of the arteries. Types: atherosclerosis, monckeberg medial calcific stenosis, arteriolosclerosis
38
atherosclerosis
Formation of lipid rich fibrous plaques in intima. | Affects ELASTIc/MUSCULAR arteries
39
monckeberg medial calcific stenosis
No clinical significance. | Calcification in tunica media.
40
arteriolosclerosis
Disease of small arteries/arterioles. Associated with DIABETES MELLITUS/HYPERTENSION. Most often in KIDNEYS.
41
hyperplastic arteriolosclerosis
hyperplasia of smooth muscle onion skin appearance Most often in kidneys with malignant hypertension.
42
hyaline arteriolosclerosis
Leakage of plasma proteins, excess ECM production --> narrowed lumen Associated with hypertension/diabetes
43
epidemiologic significance of atherosclerosis
Leading COD in US for both males and females. | More prevalent among developed nations.
44
non-modifiable major risk factors of atherosclerosis
``` age sex men > women (estrogen is protective) family history genetic abnormalities ```
45
modifiable major risk factors of atherosclerosis
``` hyperlipidemia hypertension smoking diabetes CRP ```
46
minor risk factors of atherosclerosis
``` obesity physical inactivity stress homocysteine post menopause alcohol lipoprotein a unsaturated fat intake ```
47
fatty streak
Lipid filled foam cells. T lymphocytes. Extra cellular lipids. Precursor to atheromatous plaque
48
intimal thickening
White, thickened areas at branch points. Smooth muscle cells, CT (no lipids) Precursor to atheromatous plaque
49
atheromatous plaque
Smooth muscle cells, macrophages, leukocytes. CT, ECM. Intracellular and Extracellular lipid deposits.
50
progression of atherosclerotic lesions
1) initial lesion/dysfunction 2) isolated/few macrophages 3) fatty streaks, intimal thickening, intracellular lipid accumulation 4) increase in extracellular lipid 5) atheroma (plaque) 6) fibroatheroma (fibrous plaque) 7) complex lesion
51
a complex lesion can lead to
1) aneurysm and rupture 2) occlusion by thrombosis 3) critical stenosis
52
vasculitis (general)
Inflammation of vessel wall due to infection or other causes (immune complex rxn) May affect any vessel, but most commonly small vessels. Types: giant cell arteritis, polerarteritis nodosa, thromboangitis obliterans
53
giant cell (temporal) arteritis
Giant cells and lymphocytes. Intimal fibrosis. Unknown cause (immune??) Blindness if opthalmic artery involvement. Sx: pain/tenderness over temporal head, jaw pain Tx: prednisone
54
polyarteritis nodosa
Systemic and segmental involvement of SMALL and MEDIUM arteries. Causes necrotizing inflammation, swarms of lymphocytes. 30% have HEPATITIS B in system. Young adults, mostly males.
55
thromboangiitis obliterans (Buerger's Disease)
Small and intermediate arteries, sometimes veins, of EXTREMITIES. Untreated leads to gangrene, autoamputation. Associated with heavy cigarette smoking.
56
aneurysm definition and risks
dilatation due to weakened vascular wall Risks: rupture, thrombosis & embolism, erosion of adjacent structures
57
abdominal aortic aneurysm
Intrinsic/acquired defect in wall >65 years Usually below renal arteries and above iliac bifurcation
58
risk factors for AAA
atherosclerosis smoking family history of AAA Risk of rupture increases with size
59
rupture triad (symptoms of AAA rupture)
1) severe, sudden back pain 2) hypotension 3) pulsatile abdominal mass
60
berry aneurysms
At bifurcations of circle of willis. etiology: genetic, SMOKING, HTN, PCKD
61
aortic dissection (definition, symptoms, most common cause)
entry of blood into wall of aorta through tear in tunica media, subsequent pushing apart of wall layers (tunica media) Sx: abrupt onset severe chest /back pain, "tearing pain" Most common cause: chronic HTN Associated with CT disorders (Marfans, Ehler-Danlos, coarctation, bicuspid aortic valve)
62
sequelae of AAA
1) rupture into surrounding soft tissues 2) rupture into pericardial space 3) rupture into pleural space 4) re-entry into aortic lumen 5) compression of branch ostia
63
hemangioma
benign vascular tumors with increased number of normal and abnormal vessels. usually in head/neck, sometimes internal organs Present at birth and SPONTANEOUSLY regress over time (no treatment/surgery)
64
angiosarcoma
Rare malignant neoplasm arising from endothelial cells of blood vessels. Soft tissue, skin, breast, bone, liver, spleen Can develop after radiation Tx for another cancer