Hypertension Flashcards
1
Q
define hypertension:
A
- persistently raised arterial BP (before)
- any increase in BP increasing risk of damage to body systems
2
Q
hypertension problems:
A
- produces no symptoms
- only detected by routine BP measurement (silent killer)
- predisposes heart and kidney disease
- prolonged/ sever hypertension usually lethal
- more Western countries disease
3
Q
hypertension: effects
A
- increases workload of heart leading to hypertrophy (
- additional mm mass, not well vascularised
- eventual outcome = L heart failure, pulmonary oedema
- enlarged myocardial tissue compromised by ischemia (inadequate oxygen supply) increase risk arrhythmias
4
Q
hypertension: risk factor for atherosclerosis
A
- lipids and fibrous tissues in v walls
- narrows lumen of aa decreasing blood flow = ischemia
- increases risk of blood clots + detached fatty plaques = infarcts (blood v, tissue death)
5
Q
hypertension: coronary heart disease
A
- caused by atherosclerosis
- partial blockage of coronary aa
- angina pectoris (chest pain) due to ischemia but can be relieved by vasodilators (release NO)
- heart attack (cardiac infarcts) when emboli block aa = cell death
- infarct can disrupt pumping action/ disrupt normal conduction of AP through heart = fatal arrhythmias
6
Q
hypertension: atherosclerosis of cerebral aa
A
- increase blood clots and cerebral infarcts (ischaemic stroke)
- vessel walls weakened, rupture (hemorrhagic stroke)
- also compromise blood flow to extremities = gangrene
- thinning aa walls = risk aneurysms/ tearing walls
7
Q
hypertension: microcirculation
A
- flow through cap beds decreased (increased vasomotor tone) increased flow washes away locally released metabolites (usually cause vasodilation)
- hypertension also stretches small v and smooth mm of arterioles (during autoreg)
- vessel remodelling: increase wall thickness, decrease lumen diameter of arterioles
- rarefaction: reduced micro vessel density
8
Q
hypertension: vessel remodelling + rarefaction can
A
- increase TPR
9
Q
hypertension: loss functioning in kidney
A
- nephrons
- complex process
- hypertension + previous kidney damage/ genetic disposition/ diabetes = increase risk renal failure
10
Q
hypertension: lowering BP =
A
- reduce risk of stroke, heart disease
11
Q
risk factors for hypertension: age
A
- increases w age
- 41% for 65-69yrs
- 1/3 over 25 have high BP
12
Q
risk factors for hypertension: heredity
A
- 30-50% of variation in BP explained by genes
- genes affect BP: only account less than 2%
13
Q
risk factors for hypertension: ethnicity
A
- african americans in tropical areas: tendancy to salt-sensitive hypertension
- tropical climate: salt scarce = geneticaly salt saving
- high salt diet: RAAS sys can’t maintain normal BP
14
Q
risk factors for hypertension: gender
A
- after menopause 65+ women have more hypertension than men
- oestrogen may inhibit RAAS sys
- ACE treatment decreases BP for women
- clinical trials traditionally only men
15
Q
risk factors for hypertension: diabetes mellitus
A
- produces atherosclerosis, other vessel changes increase risk
- elevated blood glucose lvl drive production of reactive oxidant species (ROS) via multiple pathways reduce NO availability
- advanced glycation end products also alter vessel wall structure/ function
16
Q
risk factors for hypertension: obesity
A
- having high lvls of fat around stomach increase risk of hypert.
- weight loss lowers BP
- type II diabetes occur in overweight obese individuals
17
Q
risk factors for hypertension: diet
A
- rich in saturated fat, cholesterol, salt increases risk
- fish, fruit, veggies, nuts lower risk hypertension
- fish + nuts= rich omega 3 fatty acids
18
Q
risk factors for hypertension: exercise
A
- limits obesity, increase cardiovascular capacity, slows dev of arteriosclerosis (hardening of aa)
- reduces risk
19
Q
risk factors for hypertension: stress
A
- low socioeconomic groups higher tendency of hypert and assoc diseases: depression, social isolation, poor diet, lack social support
20
Q
risk factors for hypertension: smoking
A
- active/passive smoking increases BP nicotine enhances sym vasoconstriction
- vessel damage from tobacco
21
Q
risk factors for hypertension: excessive alcohol
A
- heavy drinkers abstain from drinking BP falls within few days
- effect not well documented, but moderate drinking may lower risk
22
Q
risk factors for hypertension: birth weight
A
- low birth rate at full term increases chances of hypertension dev as individual matures and ages
23
Q
hypertension: types
A
essential hypertension: (90-95%) aka 1º hypertension cause not know
2º hypertension: causes- adrenal gland tumours (excess aldosterone produces v high Na reabsorption by kidney), kidney tumours excrete excess renin, golblatt hypertension (stenosis of renal aa = renal baroreceptors see falsely low BP and release excess renin)
24
Q
1º hypertension: 2 features
A
- kidneys ability to excrete Na at given P reduced (high BP needed for normal urinary output of Na, water)
- TPR elevated
25
1º hypertension: evidence for kidney role (6)
- hypertension, kidney requires higher P for excretion of Na and water
- effective hypertensive drugs (ACE inhibitors etc.) act of kidney reduce P
- absence of angiotensin II (AT1) receptors in kidney prevents dev of hypertension
- animal exp reduced renal function seen first before other signs (eg. TPR)
- hypertension follows kidney transplantation
- stopping sym input to kidney (nn ablation) lowers BP in hypotensive patients
26
1º hypertension: increase of TPR caused by (7)
- increased oxidative stress in PVN and RVLM of medulla (brain stem) increases symp output
- initial vasoconstriction due to increased sym input to smooth mm of arterioles, other resistance vessels
- increased hypertension-induced tissue perfusion will be opp by local effects (autoregulation) again = vasoconstriction
- vasoconstriction result of angiotensin II, endothelin 1 etc.
- vasocon increase tone (contraction) in small aa, arterioles walls
- maintenance of increase tone -> vessel remodelling = increase wall thickness, reduce diameter of lumen
- antihypertensive drugs w vasodilator action (Ca channel blockers, ACE inhibitors, angiotensin II receptor antagonists) help reverse v remodelling
27
1º hypertension: what other systems cont to dev hypertension (4)
- pressure natriuresis
- sym renal nn
- RAAS
- other hormones
28
treatments: initial treatment
- for prehypertension/ stage 1 hypertension
- weight loss
- increased exercise
- sodium restriction
29
treatments: initial treatment not affective if
- BP doesn't fall
- hypertension mod/severe
- comorbidities (diabetes, obesity)
= antihypertensive drugs are used to lower BP
30
treatments: how effective
- 50% patients normal BP not restored
- cardiac/ renal/ vascular changes can't be reversed
- patient noncompliance: pre high as AH drugs expensive, side effects, life sentence, don't address symptoms
- death by stroke/ coronary heart disease decreased by 50% in last 20yrs (due to drugs, dietary changes)
31
treatments: ACE inhibitors features
- Bothrops jararaca kills steep drop in BP
- active component is peptide inhibiting ACE
- inhibits RAAS sys and basis of first ACE inhibitor captopril
32
treatments: ACE inhibitors relevance to pressure natriuresis/ diuresis curve
- hypertension shifts curve to R= higher BP needed to secrete sufficient salt/ water to maintain normal ECF/ plasma vol
- inhibiting RAAS sys will shift curve L
- when RAAS sys inhibited Na excretion increase lowering ECF/ plasma vol and BP
33
treatments: ACE inhibitors- angiotensin
- ang II: is vasoconstrictor
- causes 'endothelial dysfunction'
- ang increase production of damaging reactive oxidant species (promote inflammation in v walls, dev atherosclerotic plaques)
- ang II: breaks down NO (vasodilator) increasing release of paracrine endothelin 1
= all these lead to vessel remodelling, increasing wall thickness of resistance v and decreases radii = increase TPR
34
treatments: future directions
- people respond more/less favourably to hypertensive drugs
- trial and error
- possibly find genetic variation causing hereditary hypert.
- 20 gene mutations cause large effects on BP (monogenic effects) have been identified
- monogenetic variations very rare tho (minute fraction of effected)
- hypert. polygenic, multifactorial trait
- v long way to use specific genetic characteristics to tailor drug treatments for each individual
35
hypertension: normal BP?
<120/80 mmHg
36
hypertension: elevated BP
120-129/ <80 mmHg
37
hypertension: stage 1 BP
130-139/ 80-89 mmHg
38
hypertension: stage 2 BP
≥140/90 mmHg
39
mean sleep time systolic: how much lower than day
at least 10% lower
