Pathology (all) Flashcards
definition of edema
Swelling.
Excessive fluid accumulation in tissues or body cavities.
Capillary/lymphatic leak.
severe generalized edema
anasarca
intraalveolar fluid
pulmonary edema
fluid accumulation in pleural space
pleural effusion/ hydrothorax
fluid accumulation in peritoneal cavity
ascites
transudate (associated with ?, appearance, specific gravity, glucose levels)
associated with increased hydrostatic pressure. Clear, sterile, few cells. Low specific gravity. Low protein content. Glucose content near serum levels.
exudate (associated with ?, appearance, specific gravity, glucose levels)
associated with malignancy/inflammation. Turbid/bloody/opaque. Many cells. High specific gravity. High protein content. Low glucose levels (cells consume it)
acute pulmonary congestion
SUDDEN pulmonary capillary engorgement/dilation.
Leakage of fluids –> alveolar edema.
Seen in sudden cardiac/ventricular arrhythmia with left ventricular insufficiency
chronic pulmonary congestion
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.
hemosiderin-laden macrophages
Ingested RBCs.
Heart failure cells.
Seen in chronic pulmonary congestion.
petechiae
small punctuate bleedings from capillaries
thrombocytopenia
purpura
Small bleedings larger than petechiae.
Associated with blood extravasation from small arterioles, vasculitis.
ecchymoses
Larger cutaneous bleedings. (basically normal bruises)
Due to trauma.
Seen in the elderly.
myocardial ischemia
symptom: angina pectoris
Coronary blood flow does not meet myocardial oxygen demand.
Most frequent cause: coronary artery stenosis.
cerebral ischemia
Symptom: TIA
Short, temporary dysfunction of brain (neurological deficit)
Most frequent cause: decreased arterial supply due to arterial occlusion.
lower extremity ischemia
Symptom: claudicatio intermittens.
Decreased blood flow to lower extremities.
ischemia can lead to _____
Ischemia can lead to INFARCT.
Ischemic necrosis of tissue.
Caused by occlusion of arterial supply or venous drainage (thrombosis)
hemostasis definition
response to vascular injury resulting in formation of a hemostatic plug
No hemorrhage.
Blood still flows.
endothelium produces:
procoagulant, and anticoagulant factors
platelets cause ______ by production of __________
Platelets cause AGGREGATION (of platelets) by production of ADP/ATP, epinephrine, serotonin, fibrinogen, von Willebrand Factor
basic steps of hemostatic plug formation
platelet activation/adhesion, secretion, aggregation
end result of coagulation cascade
Fibrin formed (fibrinogen cleaved by thrombin)
fibirin
Large, insoluble, forms clot.
Product of coagulation cascade.
thrombosis
Pathologic activation of clotting mechanism with formation of a thrombus.
In UNINJURED vasculature.
Results in VASCULAR OCCLUSION.
hemostasis vs thrombosis
hemostasis: physiologic; does not block blood flow; in injured vasculature
thrombosis: pathologic; blocks blood flow; in uninjured vasculature
virchow’s triad
three factors involved in thrombus formation:
1) endothelial injury
2) abnormal blood flow
3) hypercoagulability/thrombophilia
endothelial injury (virchow’s triad)
Exposed ECM leads to platelet activation, coagulation cascade.
Could also be caused by dysfunctional endothelium (DM, smoking, hypercholesterolemia)
abnormal blood flow (virchows triad)
Turbulence esp. at bifurcation sites, areas of atherosclerotic plaques.
Stasis: slowing of blood
Hyperviscosity: increased cellular elements of blood.
hypercoagulability/thrombophilia
Disorder in coagulation pathway.
fates of thrombi
1) thrombolysis (clot removed by fibrinolytic system)
2) organization (remodeling, recanalization)
3) embolization
paradoxical embolism
Emboli that cross from venous to arterial circulation via septal heart defects (ex: patent foramen ovale)
arterial thromboembolism
Emboli that originate within arterial circulation (bacterial growth/clot formation in heart valve/chambers, vegetation on valves due to metastatic cancer/treatment)
types of emboli
Amniotic fluid emboli.
Septic emboli (cardiac valve vegetations).
Air emobli.
Fat emboli
suspect thrombophilia if:
<60 years old.
Family history.
Spontaneous/massive DVT/VTE
Risk factors for acquired thrombophilia
Immobilization. Major surgery/fracture/burns. Malignancy. MI. Heparin. Pregnancy/estrogen. Smoking.
types of hereditary thrombophilia
Mutation in factor V Leiden. Prothrombia gene mutation. Antithrombin III deficiency. Protein C deficiency. Protein S deficiency. Hyperhomocystinemia.
arteriosclerosis
Umbrella term.
Hardening of the arteries.
Types: atherosclerosis, monckeberg medial calcific stenosis, arteriolosclerosis
atherosclerosis
Formation of lipid rich fibrous plaques in intima.
Affects ELASTIc/MUSCULAR arteries
monckeberg medial calcific stenosis
No clinical significance.
Calcification in tunica media.
arteriolosclerosis
Disease of small arteries/arterioles.
Associated with DIABETES MELLITUS/HYPERTENSION.
Most often in KIDNEYS.
hyperplastic arteriolosclerosis
hyperplasia of smooth muscle
onion skin appearance
Most often in kidneys with malignant hypertension.
hyaline arteriolosclerosis
Leakage of plasma proteins, excess ECM production –> narrowed lumen
Associated with hypertension/diabetes
epidemiologic significance of atherosclerosis
Leading COD in US for both males and females.
More prevalent among developed nations.
non-modifiable major risk factors of atherosclerosis
age sex men > women (estrogen is protective) family history genetic abnormalities
modifiable major risk factors of atherosclerosis
hyperlipidemia hypertension smoking diabetes CRP
minor risk factors of atherosclerosis
obesity physical inactivity stress homocysteine post menopause alcohol lipoprotein a unsaturated fat intake
fatty streak
Lipid filled foam cells.
T lymphocytes.
Extra cellular lipids.
Precursor to atheromatous plaque
intimal thickening
White, thickened areas at branch points.
Smooth muscle cells, CT (no lipids)
Precursor to atheromatous plaque
atheromatous plaque
Smooth muscle cells, macrophages, leukocytes.
CT, ECM.
Intracellular and Extracellular lipid deposits.
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
a complex lesion can lead to
1) aneurysm and rupture
2) occlusion by thrombosis
3) critical stenosis
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
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
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.
thromboangiitis obliterans (Buerger’s Disease)
Small and intermediate arteries, sometimes veins, of EXTREMITIES.
Untreated leads to gangrene, autoamputation.
Associated with heavy cigarette smoking.
aneurysm definition and risks
dilatation due to weakened vascular wall
Risks: rupture, thrombosis & embolism, erosion of adjacent structures
abdominal aortic aneurysm
Intrinsic/acquired defect in wall
>65 years
Usually below renal arteries and above iliac bifurcation
risk factors for AAA
atherosclerosis
smoking
family history of AAA
Risk of rupture increases with size
rupture triad (symptoms of AAA rupture)
1) severe, sudden back pain
2) hypotension
3) pulsatile abdominal mass
berry aneurysms
At bifurcations of circle of willis.
etiology:
genetic, SMOKING, HTN, PCKD
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)
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
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)
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
