Professional Documents
Culture Documents
Congenital
Hypertension
- vessel and end-organ damage major risk factor for coronary
heart disease, cerebrovascular accidents, heart failure, renal failure, and aortic
dissection
- Diabetes can lower the threshold for what is deleterious.
Malignant hypertension - 200/120 mm Hg
- renal failure
- retinal hemorrhages.
Vascular resistance is determined primarily at the level of the arterioles
Secondary hypertension
Causes - intrinsic renal disease
- renal artery stenosis (renovascular hypertension)
- endocrine abnormalities
- vascular malformations
- neurologic disorders
- atherosclerosis
- aortic dissection
- cerebrovascular hemorrhage.
Arteriosclerosis
Arteriosclerosis is a term denoting arterial wall thickening and loss of elasticity
1. Arteriolosclerosis primarily affects small and medium-sized arteries and arterioles, and associated with
downstream ischemia (see preceding discussion).
2. Monckeberg medial sclerosis is characterized by medial calcification in muscular arteries typically
occurring after age 50 years. The calcific deposits are non-obstructive and not usually clinically
significant.
3. Atherosclerosis is the most frequent and clinically important (see later discussion).
Atherosclerosis
Atherosclerosis is a slowly progressive disease of large- to mediumsized muscular and elastic arteries.
The lesions are characterized by elevated intimal-based plaques composed of lipids, proliferating SMC,
inflammatory cells, and increased ECM. They cause pathology by:
Mechanically obstructing flow, especially in smaller-bore vessels Plaque rupture leading to vessel
thrombosis Weakening the underlying vessel wall and leading to aneurysm formation
Epidemiology (p. 496)
The prevalence and severity of atherosclerosis and its complications are related to a number of risk
factors, some constitutional and some modifiable. The major classic risk factors emerging from the
Framingham Heart Study are family history, hypercholesterolemia, hypertension, smoking, and
diabetes.264
Systemic Pathology
Constitutional Risk Factors in Ischemic Heart
Disease (p. 496)
Age: Atherosclerotic burden progressively increases with age,
typically reaching a critical mass with clinical manifestations
beginning between ages 40 and 60 years.
Gender: Relative to age-matched men, premenopausal women are
relatively protected against atherosclerosis and its complications.
In postmenopausal women, the risk rapidly increases and can
exceed that for men. Besides affecting the progression to atherosclerosis, female gender also influences hemostasis, infarct healing, and
myocardial remodeling.
Genetics: Family history is the most significant independent risk
sis are predictors of risk for atherosclerotic events.Blood Vessels Pathogenesis of Atherosclerosis (p. 498)
Atherosclerosis is a chronic inflammatory and healing response ofthe arterial wall to EC injury. In turn,
EC injury causes increased endothelial permeability, white blood cell (WBC) and platelet adhesion, and
coagulation activation. These events induce chemical mediator (e.g., growth factors and inflammatory
mediators) release and activation, followed by recruitment and subsequent proliferation of SMC in the
intima to produce the characteristic intimal lesion (Fig. 11-2).
Endothelial Injury (p. 499)
Even without causing EC loss, endothelial injury leads to endothelial cell dysfunction with increased
adhesivity and procoagulant activity; injury mechanisms include hypercholesteromia, hemodynamic
disturbances (e.g., disturbed flow), smoking, hypertension, toxins, and infectious agents. Regardless of
the inciting stimulus, the vessel responds with a fairly stereotyped intimal thickening; in the presence of
circulating lipids, typical atheromas ensue.