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9/5 Pathology of hypertension and aneurysms
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• Describe the causes and identify the pathologic changes of mitral stenosis, mitral regurgitation aortic stenosis and aortic regurgitation.
• Describe the secondary effects of aortic and mitral valvular stenosis and regurgitation.
• Describe and identify the pathology of infective endocarditis and the most common etiologies.
• Describe and identify non-infectious endocarditis and its association
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Outline
What is the difference between "benign" (essential) HTN and "malignant" HTN?
Benign
- diastolic pressure >90 mm Hg or systolic > 140 mm Hg; mild with slow progression over many years and late symptoms, 95% of cases of hypertension.
Malignant (accelerated)
- severe (diastolic pressure >120 mm Hg or systolic > 210 mm Hg) with rapid progression (fatal within 2 years if untreated), 5% of cases of hypertension (about 8 yrs); may occur following benign hypertension (usual) or de novo(rare); occurs with greater frequency in patients with secondary hypertension, compared to patients with primary hypertension.
What are the vascular changes of HTN?
1) Acceleration of
Atherosclerosis
(note: HTN causes atherosclerosis, NOT the other way around)
2)
Hyaline
arteriolosclorosis (morphologic change)
3) Pathological changes unique to HTN:
a) Adaptive changes in benign HTN
- Vasoconstriction (arterioles)
- Medial hypertrophy (large & medium artery)
- Fibroelastic intimal hyperplasia (small artery)
b) Destructive changes in malignant HTN
- Fibrinoid necrosis (arterioles)
- Hyperplastic arteriolitis (and small arteries)
- Microangiopathic hemolytic anemia
What is the early lesion of atherosclerosis?
Fatty streaks in aorta
What is hyaline arteriolosclerosis?
Thickening of small arteries due to collection of protein in the walls of the arteriole
Inspissation of proteinaceous material into the arterial wall (arrow). This shows a renal arteriole. Not specific to benign HTN. Can be seen in diabetes too.
Describe the histologic findings in a normal small artery
Well defined thick media, bordered by internal elastic lamina. Note that internal elastic lamina (borders lumen) is much more well-defined compared to the outer elastic lamina. This is also visible in the inset image.
Red stain in the inset image illustrates the media, which is made up of smooth muscle as well as some elastic fiber
What happens to small arteries in HTN?
Proliferation of myofibroblastic cells and reduplication of elastic fibers in intima
Internal elastic lamina re-duplicates. Also myofibralstic proliferation. Both of these result in a reduced lumen → ↓ blood flow to kidney → ischemia
What is
fibrinoid necrosis
?
One of 3 destructive changes that takes place in malignant HTN
Deposition of fibrin and other plasma proteins in the walls of arterioles, associated with necrosis of endothelial cells (? toxicity of angiotensin II) and necrosis of medial smooth muscle.
What is
hyperplastic arteriolitis
?
One of 3 destructive changes that takes place in malignant HTN
Concentric proliferation of smooth muscle cells and interstitial proteoglycan deposition in small arteries and arterioles (onion skinning); healing of acute lesions of a) and probably driven by growth factorssuch as platelet derived growth factor
What is
microangiopathic hemolytic anemia
?
Shearing off of red cell fragments (resulting in schistocytesor rbc's with "bites"taken out) by passage through fibrin mesh at increased pressures within the lumen of arterioles.
What is the difference between reversible and irreversible changes in vascular resistance?
What are 5 clinical manifestations of benign HTN?
1) Congestive heart failure
2) MI
3) Stroke (cerebral infarction/hemorrhage)
4) Chronic renal failure
5) Subsequent malignant HTN
What are the organ effects of HTN?
Cardiac
: LVH, accelerated coronary atherosclerosis (→ angina, MI, CHF)
Renal
: arteriosclerosis = microvascular disease with glomerular scarring and tubular atrophy (→ chronic renal failure)
Cerebral
: microaneurysms (→ intracerebral hemorrhage), lacunae, rupture of Berry aneurysm
Compare the histology of normal myocytes and hypertrophied myocytes
Same magnification - note hypertrophied heart muscle
Thickening of heart muscle fibers, ↑ in myocytes → ↑ energy requirements → ↓ compliance
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