-
Bacterial endocarditis
- Bacterial colonies develop on the cusps of the aortic valve (MC) or mitral valve (2nd MC)
- Colonies are loosely attached & can be dislodged into the circulation causing an ischemic stroke due to embolism
- More common in young women
-
Common portals of entry for bacterial endocarditis
- Dental infections
- Tonsillitis
- Genitourinary infections (ovaries/prostate)
- Strep cutaneous infections
- Pulmonary infections
- Gallstones
-
Predisposing lesions for bacterial endocarditis
Congenital or acquired biscupid aortic valve, small ventricular septal defect, tetralogy of fallot, patent ductus arteriosus, mild residual changes of rheumatic mitral valve stenosis
-
Acute bacterial endocarditis
- Caused by staph aureus
- More dangerous
-
Subacute bacterial endocarditis
- Caused by strep viridans (aka strep mitis)
- More benign
-
Manifestations of bacterial endocarditis
- Clubbing of the fingernails
- Nail hemorrhages
- Hemorrhages of the retina
- Petechial rash of the hands, mouth, kidneys, & spleen
- Enlarged distal phalanx
-
Complications of bacterial endocarditis
- Perforation of heart valves by bacterial enzymes
- Bacterial embolism leading to ischemic infarction
- Lung infarction due to non-obliterated ductus arteriosus- vegetations of bacteria in the pulmonary trunks can go into the lungs, very painful
- Complete obliteration of the ductus arteriosus-> fatal
- Ischemic-hemorrhagic stroke
-
Ischemic hemorrhagic stroke
- Ischemic stroke caused by bacterial embolus
- Once the bacterial embolus settles, the bacteria release destructive enzymes that perforate the blood vessels-> hemorrhage
-
Arteriosclerosis
loss of artery wall elasticity
-
Atherosclerosis
Plaquing of the arterial wall
-
Monckeberg's medial calcific sclerosis
- Ring like calcification within the media of medium to small muscular arteries of obscure cours
- Occurs in people over 50
- Typically the femoral, tibial, ulnar, & radial arteries & the arteries to the sexual organs
- Never results in lumen narrowing
-
Hyaline arteriosclerosis
- Glass like protein deposits in the wall of small vessels (due to increase pressure)
- Homogenous enlargement/thickening of vessel under microscope
- Long term hypertension is a risk factor
- Vessel may undergo obstruction or rupture
- May occur in elderly w/o hypertension
- Common in diabetes mellitus
- Causes benign nephrosclerosis- kidney contraction (especially in diabetics)
- Narrowing of lumen
- Can happen in young people
-
Hyperplastic arteriosclerosis
- Thickening of the basement membrane; hyperplasia of smooth muscle cells (looks like onion)
- Malignant hypertension (diastolic > 120, can't be controlled, increase mortality rate, 1-2 years)
- Appears laminated under microscope
- Causes necrotizing arteriolitis of the kidneys (development of fibronoid necrosis within vascular walls
-
Ischemic heart disease/coronary artery disease
- A group of closely related disorders which are caused by the imbalance b/w myocardial oxygen demands & blood supply
- Caused primarily by atherosclerosis- formation of plaques in the subentimal layer of the vessel wall-> lumen obstruction (MC arteries- coronary, cerebral, mesenteric, & arteries of lower extremities)
- 75% of vessel obstruction (critical stenosis) needed for clinical manifestations
- Leads to MI
-
Controllable risk factors of Ischemic heart/coronary artery disease
- Smoking (60/1000)
- Hypercholesterolemia or hypertension (60/1000)- both together (90/1000), both + smoking (200/1000)
-
Critical areas of atherosclerosis
- Brain- stroke
- Kidneys- extrarenal stenosis
-
Pathogenesis of ischemic heart disease
- 1. Acute changes in heart morphology (atheroma)
- 2. Platelet aggregation (formation of a platelet plug)
- 3. Coronary artery thrombosis
- 4. Coronary artery vasospasm aka Prinzmetal's variant- increased concentration of vasoconstrictors (thromboxane) that are released w/ sympathetic activity-> causes death
-
Atheroma
- 1. Calcification
- 2. Ulceration & breaking of plaques
- a. debris may go into opening-> emboli
- b. hemorrhage into atheroma-> ballooning of atheroma-> obstruction (immediate death)
- c. thrombosis-> MC & most serious- activation of von Willebrand factor
- 3. Roughening of wall leading to injury of passing cells-> promotes formation of thrombis
- 4. Lumen narrowed-> turbulent blood flow-> thrombosis
-
3 components of atheromas
- Fat
- Connective tissue cap
- RBC's & smooth muscle cells
|
|