hypertension Flashcards
what is hypertension
persistently elevated arterial blood pressure
how does BP link to circadium rhythm
rises at the start of the day and is the lowest in the evening
what is primary hypertension
chronically elevated blood pressure with no identifiable cause
what is secondary hypertension
has an identifiable cause either disease or drugs
what is pseudohypertension
- falsely elevated BP measurement
- vessels are stiff and thick because of calcification and resist compression from BP cuff
what is white coat hypertension
clinical BP > home bp
what is masked hypertension
home bp > clinical bp
what is hypertensive emergencies
hypertension with acute end organ damage
what is hypertensive urgencies
hypertension without acute end organ damage
what causes hypertension during pregancy
- preeclampsia-eclampsia
- chronic hypertension
superimposed preeclampsia - gestational hypertension
what are risk factors of hyperenstion
- age
- smoking
- DM
- dyslipidaemia
- obesity
- physical inactivity
what is stage 1 BP
140/90 - 159/99
what is stage 2 bp
160/100- 179/199
what is stage 3 bp
> 180/120
what is arterial blood pressure
the pressure in the arterial wall between blood flow and the resistance of blood flow
what is arterial BP calculation
ABP = CO x PVR
what falls under peripheral resistance
arterial tone
what falls under cardiac output
- heart rate
- contractility
- filling pressure
- blood volume
- venous tone
what does abnormal neuronal mechanism affect in BP
- overactive sympathetic nervous system
- resetting of baroreceptor reflex systems
what abnormalities lead to hypertension development
- abnormal neuronal mechanism
- malfunctions in humoral mechanisms
- defects in peripheral autoregulation
- altered vascular endothelial mechanisms
what is the affects of humoral mechanisms malfunctions
- overactive RAAS
- insulin resistance and hyperinsulinemia
what is the SNS heart regulation of BP
- increase heart rate
- increase force of contraction
- increase CO
- adrenaline and noradrenaline bind to B1
what is the SNS blood vessel regulation of BP
- alpha 1 vasoconstrict increase PVR
- beta 2 vasodilate decrease PVR
what is the SNS kidney regulation of BP
- increase renin secretion
- increase ang II
- increase BP
how does altered vascular endothelial mechanism affect BP
- endothelial cells has vasodilating substances and vasoconstricting substances
- deficiencies can cause excess vasoconstriction
how does insulin resistance and hyperinsulinemia affect BP
- increased insulin increases Na, increasing SNS
- can induce hypertrophy of vascular smooth muscle
- increase intracellular Ca, increase vascular resistance
how does the kidney regulate BP
BP drop kidney increases Na and water retention to increase BP
what do defects in peripheral autoregulation affect BP
increased Na retention means more water retention so increased BP
what are the stages of baroreceptor reflex with increasing BP
- BP above normal range
- baroreceptors in carotid sinuses and aortic arch are stimulated
- increase impulses inhibit cardio stimulatory and vasomotor centre
- decrease sympathetic impulse, decrease HP and CO
- decrease vasomotor to vasodilate
- decrease CO and PVR
what are the stages of baroreceptor reflex with decreasing BP
- decreased BP above normal range
- baroreceptors inhibited
- decreased baroreceptors activates cardio stimulatory and vasomotor centre
- increase sympathetic impulses to heart increase HR and CO
- vasomotor impulses vasoconstrict
- increase CO and PVR
what increases renin release
- decreased renal perfusion
- sympathetic neural activity catecholamines
- low Na
- hyperkalaemia
what does the RAAD system do
regulates sodium, potassium and blood volume
where is renin secreted from
juxtaglomerular cells in the kidney
how does RAAS affect the adrenal gland
- cortex stimulate aldosterone secretion increase Na reabsorption
- medulla stimulate release of catecholamines
how does the RAAS system affect the heart
- inotropic and chronotropic effects
- cardiac hypertrophy - increases stiffness
how does RAAS affect blood vessels
- ang II is a vasoconstrictor
- acts directly on vascular smooth muscle
- facilitates sympathetic transmission through presynaptic angiotensin
how does RAAS affect the CNS
- stimulation of central sympathetic tone
- release of ADH inhibits diuresis
- stimulation of drinking
what are the stages of the RAAS system
- angiotensinogen binds with renin from the kidneys
- makes angiotensin I
- ang I is altered by ACE
- makes angiotensin II
- creates AT1 which vasoconstricts and AT2 which vasodilates
- AT1 triggers aldosterone release
- increase Na and water retention and K excretion
