Hypertension Flashcards
RAAS: what does it stand for
renin angiotensin aldosteron system
- regulates longterm bp and extracellular fluid
- activated when loss of blood volume ot drop in bp
RAAS explained
1) angiotensinogen is released from liver which stimulates the release of renin from kidneys
2) angiotensinogen + renin = angiotensin I
3) angiotensin I causes ACE to be released from lungs
4) angiotensin I + ACE = angiotensin II
5) angiotensin II causes adrenal gland to release aldosterone, adrenal gland also causes vasoconstriction
what does aldosterone do
- increase the reabsorption of Na, water sucks so bp inc
when is angiotensinogen released
low bp and changes in blood volume (usually response to changes in Na levels)
what stimulates the kidneys to release renin
low fluid volume
what does the release of renin cause
the liver to convert angiotensinogen to angiotensin I
what does angiotensin I do
travels to lung where its converted into angiotensin II by ace
what converts angiotensin I to II
ACE: angiotensin converting enzyme
what does angiotensin II act on
the adrenal gland which will release aldosterone
angiotensin II is a _____ ____
potent vasoconstrictor
RAAS can also be activated by…
- decreased renal perfusion
- pathologic ways
- some have hypersensitivity to angiotensin II or high secretors of renin
- stress can elevate angiotensin II, stimulates renin
other mechanisms that stimulate bp
- baroreceptors: found in the carotid sinus, aorta and LV that sense BP and will alter HR accordingly; can also impact vasocon/dil
- vascular auto regulation: helps maintain consistent levels of tissue perfusion, regulates mean arterial pressure, alters resistance, helps keep consistent BP at tissue level
primary HTN
- aka essential HTN
- occurs when there is no known cause (no underlying disease)
- occurs due to complicated interactions of genetics and env, involving neurohormonal effects
risk factors for primary HTN
- smoking
- excessive Na intake
- sedentary lifestyle
- hyperlipidemia
- stress
- fam history/genetics
- obesity / insulin resistance
- over the age of 60
- blacks
- high alc consumption
- men more likely before age 55
secondary HTN
known cause of HTN, known underlying disease
- treatment = treat underlying disease like
– renal disorders, adrencortical tumors, adrenomedullary tumors, drugs (oral contraceptives, corticosteroid, cocaine)
causes of primary vs secondary HTN
- primary: excess salt, abnormal arteries, inc blood vol, genetic disorder, stressful life
- secondary: health conditions, certain meds, recreational drugs, pregnancy, hormonal therapy
s/s of HTN
none, it is a silent killer
- can do screenings for it
- might see signs of end organ damage like
– chest pain, headache, weakness/pain in extremeties
long term outcomes of HTN (cardiac)
inc LV work
- hypertrophy of LV due to excess pressure it has exerted to pump blood
- accelerated progression of atherosclerosis
- increased risk for aortic aneurysm (weakened vessel walls)
long term outcomes of HTN (kidney)
primary cause of end stage renal disease
long term outcomes of HTN (brain)
higher risk for stroke, aneurysm, hemorrage
long term outcomes of HTN (eye)
retinopathy, blindness
long term outcomes of HTN (lower extremeties)
gangrene, intermittent claudication
hypertensive crisis
rapidly progressive HTN
- sbp over 180 and/or dbp over 120
- occurs more often in primary HTN
- types: urgency vs crisis
HTN urgency
- no s/s of end organ damage (pt feels normal)
- BP over 180/120
- treated w oral agents to gradually bring BP down in usually hrs
- often caused by anxiety, pain, abrupt w/drawl
HTN emergency
- s/s of end organ damage like headache, blurred vision, stroke, brain hemorrhage, chest pain, etc>
- BP greater than 180/120
- treated aggressively w IV meds to bring down in mins to hrs
