Pathophysiology of HTN - Hefnawy Flashcards
(21 cards)
pulse pressure
- becomes wider as you age
- systolic increases and diastolic decreases
stage 1 HTN
- systolic 130-139
- diastolic 80-89
stage 2 HTN
- systolic >/=140
- diastolic >/= 90
mean arterial pressure (MAP)
MAP = CO x TPR
-TPR depends on vasoconstriction/dilation and compliance of blood vessels (hypertrophy of smooth muscle BV decreases compliance, increasing TPR)
cardiac output (CO)
CO = SV x HR
alpha2 receptor
- act centrally
- inhibit sympathetic tone
kidney - long term regulation of BP
- activate RAAS from high sympathetic tone, low bp, or low Na+ delivery to kidney*
- release renin –> converts angiotensinogen to angI –> ACE converts angI to angII –> vasoconstrict blood vessels and aldosterone release –> Na+/fluid retention –> increase CO and BP
- angII also release ADH in brain
- renin in glomerular afferent arteriole
- ACE in endothelial lining (lungs)
angII
- smooth muscle vasoconstriction, aldosterone/ADH release
- also remodels blood vessels and myocytes* –> thicken blood vessels decreasing compliance and lead to heart failure
excess aldosterone effects
- excess Na+ retention –> HTN
- CV disease, renal damage, myocardial fibrosis, BV inflammation*
insulin resistance diabetes
-toxic effects on blood vessels
- vascular smooth muscle hypertrophy –> decrease compliance –> HTN
- endothelial dysfunction from hyperlipidemia –> atherosclerosis –> HTN
- sympathetic activation –> prevent vasodilation and augment constriction –> HTN
essential HTN - unknown
- genetic
- environment (ex. activating SNS releasing cortisol)
- behavior
- physiology
baroreflex resetting HTN*
- prolonged HTN makes arterial baroreflexes reset the threshold to the new normal –> further increase sympathetic tone and arrhythmias when giving a vasodilator*
- initial treatment is hardest bc carotid sinus tries to bring it back up to new “normal”
HTN effect on kidney
- decrease renal function and glomerulosclerosis
- HTN –> damage to kidney –> more HTN
- failed Na+ regulation
- mesangial cell proliferation (less filtration slits)
- sclerotic glomeruli due to HTN induced atherosclerosis
- thicken basement membrane
secondary HTN causes
- renal disease most common* (BUN/creatinine levels)
- drugs
- diabetes - insulin resistance, hyperlipidemia
- pheochromocytoma - flushing and headache due to excess catecholamines
- renal artery stenosis - activate RAAS
- conn’s disease
- cushing - high cortisol contraceptives/pregnancy
- congenital adrenal hyperplasia - high aldosterone
- coarctation of aorta
renal parenchymal HTN
- damage to kidney affects glomerular filtration rate
- assess GFR and creatinine to look at the functional nephrons
-ex. chronic nephritis, polycystic kidney, diabetic nephropathy, etc.
renovascular HTN
- stenosis of renal artery –> + RAAS –> exacerbate HTN
- good success rate if treated within 1st 5 years
what is main reason for renal artery stenosis?***
atherosclerosis
complications of HTN
- heart
- great afterload –> LV hypertrophy, failure
- working harder –> myocardial ischemia, MI - CNS
- risk of stroke* - renal
- mesangial hypertrophy, thicken glomerular membrane, infarction - vascular
- endothelial damage, aortic aneurysm/dissection
what can lead to papilledema?
- HTN leading to intracranial pressure
- hemorrhage
malignant HTN - hypertensive emergency**
- acute BP > 180/110*
- neurological and cardiac issues
- do a fundoscopic eval and CT scan
1 med to try for HTN
- thiazides
- use meds in essential HTN
- don’t give diuretics during pregnancy
-always promote healthier lifestyle for secondary HTN
