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5. ADV PHYS > Hypertension > Flashcards

Hypertension Flashcards

1
Q

define hypertension:

A
  • persistently raised arterial BP (before)

- any increase in BP increasing risk of damage to body systems

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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
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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
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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)
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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
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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
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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
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8
Q

hypertension: vessel remodelling + rarefaction can

A
  • increase TPR
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9
Q

hypertension: loss functioning in kidney

A
  • nephrons
  • complex process
  • hypertension + previous kidney damage/ genetic disposition/ diabetes = increase risk renal failure
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10
Q

hypertension: lowering BP =

A
  • reduce risk of stroke, heart disease
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11
Q

risk factors for hypertension: age

A
  • increases w age
  • 41% for 65-69yrs
  • 1/3 over 25 have high BP
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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%

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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
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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
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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
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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
Q

1º hypertension: evidence for kidney role (6)

A
  • 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
Q

1º hypertension: increase of TPR caused by (7)

A
  • 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
Q

1º hypertension: what other systems cont to dev hypertension (4)

A
  • pressure natriuresis
  • sym renal nn
  • RAAS
  • other hormones
28
Q

treatments: initial treatment

A
  • for prehypertension/ stage 1 hypertension
  • weight loss
  • increased exercise
  • sodium restriction
29
Q

treatments: initial treatment not affective if

A
  • BP doesn’t fall
  • hypertension mod/severe
  • comorbidities (diabetes, obesity)

= antihypertensive drugs are used to lower BP

30
Q

treatments: how effective

A
  • 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
Q

treatments: ACE inhibitors features

A
  • Bothrops jararaca kills steep drop in BP
  • active component is peptide inhibiting ACE
  • inhibits RAAS sys and basis of first ACE inhibitor captopril
32
Q

treatments: ACE inhibitors relevance to pressure natriuresis/ diuresis curve

A
  • 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
Q

treatments: ACE inhibitors- angiotensin

A
  • 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
Q

treatments: future directions

A
  • 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
Q

hypertension: normal BP?

A

<120/80 mmHg

36
Q

hypertension: elevated BP

A

120-129/ <80 mmHg

37
Q

hypertension: stage 1 BP

A

130-139/ 80-89 mmHg

38
Q

hypertension: stage 2 BP

A

≥140/90 mmHg

39
Q

mean sleep time systolic: how much lower than day

A

at least 10% lower

5. ADV PHYS (10 decks)

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