Pathology Of HTN Flashcards
Difference between results from hypotension and hypertension
Hypotension effects = results in inadequate organ perfusion, organ dysfunction and possible ischemic tissue
Hypertension effects =. End-organ and vessel damage and atherosclerosis
Direct kidney influences on peripheral resistance
Sodium excretion/retention through the renin-angiotensin system
*renin is release in response to low blood pressure, elevated levels of catecholamines or low sodium levels to afferent arterioles.
Results in angiotensin 1 and angiotensin 2 production which results in reabsorption of Na+ and water as well as vasoconstriction of Afferent arterioles
Ultimately end result is increasing peripheral resistance and increased blood volume/stroke volume =. Increased blood pressure
How does renin -> angiotensin 2?
Renin cleaves plasma angiotensinogen (inactivated angiotensin 1) into angiotensin 1
Angiotensin 1 -> angiotensin 2 via conversion from the angiotensin-converting enzyme (ACE).
How does angiotensin 2 specifically raise blood pressure
Induces vasoconstriction of arterioles
Stimulates aldosterone secretion by the adrenal gland
Increases tubular sodium resorption
Aldosterone specific effects on BP
Adrenal aldosterone increases sodium and water resorption in DCTs of kidneys (increases blood volume)
Drives potassium excretion
Natriuretic peptides specific effect on blood pressure
Myocardial natriuretic peptides are released from atrial and ventricular myocardium in response to volume expansion
Ultimately inhibit sodium resorption and lead to sodium and water excretion. (Lowers blood volume) also induces vasodilation
Epidemiology of hypertension
Usually >130/>80 mmHg BP
- some places have it >140/>90
Roughly 50% of individuals in America are hypertensive
- increased age and being black raises your odds naturally (not a lot though)
Malignant hypertension
HTN that rapidly rises idiopathically or from untreated severe HTN and affects multiple organ systems
- usually results in SBP of >200mmHg and/or >120mmHg
- associated with renal failure and spontaneous retinal hemorrhage
- leads to death within 1-2 yrs
Which more common, primary or secondary HTN
Primary (essential)= 95% of cases
- is idiopathic/genetic/ environmental based
Secondary (non-essential) = 5% of cases
- due to primary renal disease, renal artery atherosclerosis or adrenal disorders.
Renovascular hypertension
HTN caused by renal artery stenosis
- results in decreased glomerulur flow and pressure in the afferent arterioles
- this results in overall increased renin secretion in response which overall increases blood volume and vasoconstriction*
Liddell syndrome
Gain of function mutations in epithelial Na+ channel proteins that increase the DCT reabsorption of sodium in response to aldosterone
- leads to HTN easily
Gene defects in aldosterone enzymes
Aldosterone synthase
11B-hydroxylase
17a-hydroxylase
*leads to increased secretion of aldosterone which leads to increased sodium resorption and water which ultimately leads to increased BP
What two factors contributes to esssential hypertension
Altered renal sodium handling (reabsorbs too much/ decreases renal sodium excretion in the presence of normal pressure)
Increased vascular resistance
(Easier triggering of vasoconstriction or structural issues within vessel walls themselves)
Hyaline arteriolosclerosis
Benign hypertension That is caused by homogeneous thickening of the anterior walls with hyaline cartilage.
- causes lumen narrowing which increases systemic vascular resistance
Leads to nephrosclerosis (glomerular scarring)
- marked by histology slides showing arteriolar wall thickening with hyaline cartilage*
Hyperplastic arteriolosclerosis
Typically found with severe hypertension
Vessels will exhibit “onion skin” apperence with thickening of the arteriolar walls and luminal narrowing.
