Cardio-path-hypertension Flashcards
Kidney damage from HTN can result in low renal pressure, what can be the result of this?
A false sense that there is low blood pressure throughout the body which can lead to release of renin that converst angiotensinogen to angiotensin I then II that promotes release of aldosterone and smooth muscle vasoconstriction and then increase BP
Renin is produced by
renal juxtaglomerular cells.
Kidneys influence peripheral resistance and sodium excretion/retention primarily through?
the renin-angiotensin system.
Renin is released in response to 3 things:
low blood pressure in afferent arterioles, elevated levels of circulating catecholamines, or low sodium levels in the distal convoluted renal tubules
low sodium levels in the distal convoluted renal tubules are sensed in response to
when the glomerular filtration rate falls (eg, when the cardiac output is low) because a higher fraction of the filtered sodium is resorbed in the proximal tubules.
What converst angiotensin I to II?
angiotensin-converting enzyme (ACE) in the periphery.
Where does the angiotensin I to II conversion mostly take place?
endothelium of the lungs
Angiotensin II raises blood pressure by:
- Inducing vascular smooth muscle cell contraction,
- Stimulating aldosterone secretion by the adrenal gland, and
- Increasing tubular sodium resorption.
Aldosterone increases blood pressure by its effect on blood volume; aldosterone increases sodium resorption (and thus water) in the distal convoluted and collecting tubules, what effect does it have on K+?
driving potassium excretion into the urine.
What hormones are released by from atrial and ventricular myocardium in response to volume expansion?
Natriuretic peptides
What is the role of natriuretic peptide?
these inhibit sodium resorption in the distal renal tubules, thus leading to sodium excretion and diuresis.
๏ They also induce systemic vasodilation.
Vascular resistance is regulated at the level of which vessel?
arterioles
What is essential HTN?
manifests in an acute aggressive form, high blood pressure is typically asymptomatic for many years.
HTN can increase the risk for :
and lead to:
risk for stroke and atherosclerotic coronary heart disease
cardiac hypertrophy and heart failure, aortic dissection, multi-infarct dementia, and renal failure.
What results from the interplay of several genetic polymorphisms and environmental factors, which conspire to increase blood volume and/or peripheral resistance?
essential hypertension
What is the cutoff BP for diagnosing HTN?
130/80
A small percentage of hypertensive patients (approximately 5%) present with a rapidly rising blood pressure that, if untreated, leads to death in within 1 to 2 years called?
malignant hypertension
malignant hypertension usually is severe, ie, systolic pressures over mmHg or diastolic pressures over 120mmHg, and frequently is associated with failure and hemorrhages, with or without papilledema.
200; renal; retinal
Concerning pathogenesis, most cases of hypertension are:
primary (idiopathic) or essential
Secondary hypertension, are due to:
primary renal disease, renal artery narrowing (renovascular hypertension), or adrenal disorders.
renovascular hypertension can cause renal artery , which causes increased/decreased glomerular flow and pressure in the afferent arteriole of the glomerulus.
stenosis; decreased
Because of the false sense of systemic blood pressure brought on by renovascular hypertension, this can induce secretion, which, as already discussed, increases vascular tone and blood volume via the angiotensin-aldosterone pathway
renini
Rare forms of HTN can be caused by gene disorders
single
Gene defects affecting which enzymes involved in aldosterone metabolism can lead to hypertension?
- aldosterone synthase
- 11β-hydroxylase
- 17α-hydroxylase
Gene defects affecting enzymes involved in aldosterone metabolism (e.g., aldosterone synthase, 11β-hydroxylase, 17α-hydroxylase) can lead to an increase/decrease e in secretion of aldosterone, increased salt and water resorption, plasma volume expansion and, ultimately, hypertension.
increase
There are also mutations affecting proteins that influence sodium reabsorpton caused by gain-of-function mutations in an epithelial Na + channel protein that increase distal tubular reabsorption of sodium in response to aldosterone called:
Liddle syndrome
Although the specific triggers are unknown, it appears that both altered renal sodium handling and increased vascular resistance contribute to hypertension.*
essential
What is the key pathogenic feature of essential hypertension?
Reduced renal sodium excretion in the presence of normal arterial pressure, which can lead to high BP
Increased vascular resistance may stem from:
vasoconstriction or structural changes in vessel walls
not only accelerates atherogenesis
๏ HTN
HTN causes degenerative changes in the walls of large- and medium-sized arteries that can lead to dissection and hemorrhage.
aortic; cerebrovascular
Which small blood vessel disease is associated with benign hypertension?
Hyaline arteriolosclerosis -homogeneous, pink hyaline thickening of the arteriolar walls, and luminal narrowing
How does hyaline arteriolosclerosis form:
lesions stem from leakage of plasma components across injured endothelial cells into vessel walls, and increased ECM production by smooth muscle cells in response to hemodynamic stress
What happens to the kidneys with hylaline arteriosclerosis in the small blood vessels:
leads to diffuse vascular compromise and nephrosclerosis (glomerular scarring)
Which can also cause false sense of low BP leading to RAS
hyaline arteriolosclerosis is found in older and those with HTN but also with people diagnosed with
diabetic microangiopathy
however, in this disorder, the underlying etiology is hyperglycemia associated EC dysfunction.
Hyperplastic arteriolosclerosis is more typical of hypertension.
severe
What is being demonstrated in this example of Hyperplastic arteriolosclerosis?
“onion skin”, concentric, laminated thickening of arteriolar walls and luminal narrowing.
What do the onion skin layers of this artery related to “onion skin” Hyperplastic arteriolosclerosis consist of:
laminations consist of SMCs and thickened, reduplicated basement membrane.
In malignant hypertension, these changes are accompanied by fibrinoid deposits and vessel wall necrosis called:
necrotizing arteriolitis- which occurs mainly in the kidney
note: the dark pink surrounding the vessel are fibrin deposits
