Pathology of Hypertension - Jarzembowski Flashcards
What are the changes seen in large arteries under hypertensive conditions?
What can this predispose to?
Degenerative changes in vascular walls & accelerated atherogenesis.
Increased risk of aortic dissection/cerebrovascular hemorrhage.
Describe the pathophysiology & appearance of hyaline arteriolosclerosis.
Is it a benign finding?
Hypertension causes leakage of plasma across the endothelium, which stimulates matrix production. The result is a homogenous thickening of the vessel wall with luminal narrowing.
Yes; found in many elderly patients, diabetics…
Describe this hypertensive vascular change.
What causes it?
This is hyperplastic arteriolosclerosis (note onion-skinning / BM duplication).
It is characteristic of malignant hypertension.
What are the vascular findings of malignant hypertension?
Hyperplastic arteriolosclerosis and necrotizing arteriolitis (fibrinoid)
What criteria defines systemic hypertension?
How widespread is it?
>140/90mm Hg (either or)
Very, very widespread. >25% of US population.
Describe the changes that the heart undergoes in systemic hypertension.
LVH (enlarged fibers and nuclei, often in abscence of other CV pathology), left atrial enlargement (due to impaired ventricular filling), and cardiomegaly in general (>1.5cm, 500g+).
What are the long-term effects of systemic hypertension?
Some patients fare well, but generally increased risk of ischemic heart disease, renal damage, stroke, heart failure & sudden cardiac death.
Describe how systemic hypertension can affect the brain.
Cerebral vessels become weakened and are prone to rupture, leading to hemorrhagic stroke eg Lacunar infarcts.
CSF pressure elevates, leading to headaches/confusion/vomiting/convulsions (hypertensive encephalopathy)
Describe how systemic hypertension can affect the kidneys.
If benign: Hyaline arteriolosclerosis results in atrophy; kidney features granular, pitted surfaces. Glomeruli become sclerosed.
If malignant: Hyperplastic & necrotic changes cause pinpoint petechial hemorrhages and microthrombi formation.
What is Cor Pulmonale?
Distinguish between the acute and chronic forms.
Cor pulmonale is failure of the Right heart to overcome pulmonary resistance.
Acute: No RVH, usually originates from PE.
Chronic: RVH due to pulmonary HTN, chronic lung disease, or other pulmonary circuit obstruction.
Describe 3 mechanisms that contribute to heart failure.
Abnormal load on the heart (eg Fluid overload, MI, regurgitation)
Impaired filling (eg RCM, tamponade)
Obstruction due to valve stenosis (eg Rheumatic heart disease)
(You can distinguish between left and right failure by now, right?)
Describe 3 mechanisms that compensate for heart failure.
What are their pitfalls?
Frank-starling mechanism (increases wall tension, oxygen demand)
Neurohormonal activation (bad for long-term loads *ANP?)
Cardiac Hypertrophy (leads to cardiac failure)
What conditions may result in cardiac hypertrophy > 1kg?
600-800g?
Aortic regurgitation, HCM.
Pulmonary HTN, Ischemic heart disease.
Match the following to a concentric hypertrophy:
Overload of (pressure / volume)
Increased (systolic / diastolic) wall stress
(series / parallel) sarcomeric remodeling.
Concentric: Pressure overload > Systolic stress > Parallel remodeling.
Opposite is true of eccentric hypertrophy.
Why does cardiac hypertrophy evolve to cardiac failure?
Increased size means increased demand, which isn’t well met by the decreased density of capillaries. Myocytes may apoptose.
Describe the cells shown. What are they filled with?
How and why do they appear in this piece of lung tissue?
“Heart failure cells”, macrophages engorged with hemosiderin.
Increased pulmonary pressure in heart failure causes alveolar hemorrhaging.
