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CVS > Hypertension > Flashcards

Hypertension Flashcards

1
Q

formula for hBP treatment

A
  • BP = CO x TPR (increasing TPR ^ CO wc BP)
  • BP = SV x HR x TPR (since co = sv x hr)
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2
Q

4 main neurohumeral systems

A

renin-angiotensin-aldosterone system SMP ADH partial natriuretic peptide (ANP)

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3
Q

Atrial natriuretic peptides

A
  • promotes Na+ excretion
  • stored and synthesised In arterial myocyte
  • respond to stretching
  • c vasodilation -

high-up c its release and c vasodilaton of afferent arteriole so more Na+ (natriuresis removed from the body so water follows it and overall v BV and v BP

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4
Q

how do adrenal causes result in secondry hypertension

A

Conn’s syndrome= (hyperaldsteronism ) ^ aldosterone

Cushing’s syndrome = at high levels cortsiol can act on aldosterone receptors

Phaechromocytoma = adrnealine and noradrenaline

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5
Q

diuretics

A

–thiazide diuretics; used to increase NA+ and water excretion

  • inhibit NA/CL channels on apical tubule of DCT so na+ can be removed and not reabsorbed so water can follow bv decreased and with it bp
  • spironolactone (aldosterone antagonist) ; decreased bp - block aldosterone

NOT COMMONLY USED FOR HYPERTENSION

  • use beta blockers to slow down HR and SV b1 (only if MI)
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6
Q

bradykinin

A
  • present in lungs
  • bradykinin is broken down into peptide proteins using ACE
  • using ace inhibitors causes bradykinin to build up and hence why you can get a dry cough
  • RAAS allows inhibition of the breakdown of bradykinin the
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7
Q

treatment for HP

A
  • ACe inhibitor
  • AN2 inhibitor /antagonist
  • L-type ca2+ channel blockers (verapamil, nifedipine) c less CA2+ entry so smooth muscles don’t contract as much so vasodilation
  • a1 receptor blockers (doxazosin) since they c vasoconstriction of smooth msucle b you can get postural hypotension hypotension
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8
Q

aldosterone

A
  • acts on the principle cells of collecting such

c Na+/K+ channels c na+ absorption (and k+ excretion) and therefore c water to reabsorbed

  • it also acts on apical na+ channels ENaC (epithelial Na channels)
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9
Q

renovascular disease

A
  • occlusion of the renal artery c decreased perfusion pressure in the kidney
  • so v bp in the kidney so renin released c effects (activation of the RAAS/vasoconstriction/aldosterone)
  • b stenosis still present its continuously activated
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10
Q

renal parenchymal disease

A
  • disease wehre damage to the cells involved in filtrationof blood
  • in early stages you lose vasodilator substances
  • later stages NA+ and water retention inadequate glomerular filtration (volume-dependent hypertesion)
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11
Q

why is it important to treat high bp and whats the effects of intervention

A

c death like MI

every 10mmHg reduction in blood pressure results in;

  • 17% decrease of coronary heart disease
  • 27%decrease of stroke
  • 28% decrease if heart failure
  • 13% decrease in all -cause mortality
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12
Q

describe the short term regulation of blood pressure

A
  • baroreceptors located on the carotid sinus and aortic arch
  • detect changes in b presure (as the receptor fibres are strecthed with ^ BP) and send this info. to the medulla of the brain wc then works to decrease bp
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13
Q

angiotensin

A

Renin released from glandular cells of just angiotensinogen made in the liver need enzyme in lung to convert it into angiotensin 1 then need renin to convert it into angiotensin 2 giving angiotensin 1 enzyme inhibitor can cause cough because that enzyme also work on brdyc

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14
Q

name the neurohumeral system

A
  • RAAS
  • SNS
  • ADH
  • ANP
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15
Q

ace inhibitors

A

preventing convention of AT1 to AT2 to deal with ^bp

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16
Q

what does the SNS do

A
  • ^ Renin release from the juxtaglomerular apparatus ‘s glandular cells
  • activates apical Na\H exchange system and also basolateral NA/K ATPase inPCT
  • vasoconstriction
17
Q

how does decreasing circulating volume stimulate renin release

A

drop in BP in afferent arteriole bp and blood volume ,

since b is moving slowly through the PCT etc there’s moreNA+ being reabsorbed

so by the time you reach DCT there’ll be less NA+

this c release are RENIN too.

this is detected by macular dense cells in the DCT,

they are chemoreceptors and measure conc of NA+

  • innervation of the SMP b we want to ^ bp so we can deliver more b to muscles
18
Q

what type of angiotensin 2 receptors are there?

describe these receptors

A
  • 2 AT1 and AT2
  • main actions usually via AT2
  • G-protein coupled receptor
19
Q

classficiatio

A

STAGE 1;

  • BP = >140/90mmHg
  • ABPM / HBPM (ambulatory/house b p measure) >135/85

STAGE 2;

  • BP = >160/100
  • ABPM/HBPM >150/95

STAGE 3:

  • >180/110 OR >110 diastolic
20
Q

dopamine

A
  • can be formed locally in the kidneys from circulating L-DOPA
  • dopamine receptors can be located in the renal b vessels of the PCT and TAL
  • c vasodilation and increases renal b flow
  • reduces reabsorption of NAcl by inhibiting Na/K ATPA and NHX in the principal cells of the TAL and PCT
21
Q

hypertension

A

^ afterlod so LV works harder and undergoes hypertrophy LV then fail c HF ^ demand for O2 so arterial damage

22
Q

what does ADH do

A
  • vasoconstriction
  • increases water reabsorption to increase blood volume and so blood pressure
23
Q

what does AT2 do

A
  • vasoconstrictor (general) c ^ BP
  • c smooth muscles of the efferent arteriole to constrict increasing filtration rate as b backs up, ^ glomerular filtration rate this c less Na+ to be reabsorbed in CT AND CD, so overall more NA+ at DCT
  • c adrenal cortex to release aldosterone wc c distal DCT to remove Na+ back into body c water to follow c ^ Bv and ^ BP
  • hypothalamus c ADH released from PPG wc goes to DCT and CD to reabsorb water back into body to ^BV and therefore ^ BP
24
Q

what released renin

what c renin release

A

there are specialised cells on the afferent arteriole = granular cells ofthe juxtaglomerular apparatus JGA

  • reduced nacl dleivery to macula densa cells of the distal tubule
  • reduced renal perfusion
  • sympathetic nervous system stimualtesthe JGA
25
Q

normal b

A

90/60 and 120/80

26
Q

how is blood pressure regulated? what’s the formula

A
  • mean ABP= CO X TPR

CO = SV X HR

- baroreceptors short term and then medium/long term regulation = neurohumeral and sodium balance

27
Q

c of hypertension

A

95% primary

5% secondary d CHAPS ( cushing’s sydnrome, Hyperaldosteronism (conn’s syndrome) , Aortic Coarctation, Phaechromocytoma, Stenosis of the renal arteries)

28
Q

prostaglandins

A

local mediators and can act as vasodilators

  • they enhance glomerular filtration to reduce NA+ reabsorption
  • act as a buffer d ^ SNS and RAAS system c too much vasoconstriction
  • important when levels of A2 are high
29
Q

what does renin do briefly

A

renin causes angiotensiosngen to AN 1 , ACE made my lung converted A1 to A2 and A2 c vasoconstriction, stimulates Na+ reabsorption to increase perfusion and c aldosterone release from the adrenal cortex

30
Q

medium and longer term control of blood pressure

A
  • neurohumoral responses
  1. RAAS
  2. SYMPATHETIC NERVOUS SYSTEM
  3. ADH
  4. ANP (atrial natriuretic peptide)
  • direct control of sodium levels (sodium balance
31
Q

hypertension

A

sustained high b pressure

32
Q

upon renin release what happens

A
  • goes into systemic circulation
  • liver produced and stores ANGIOTENSINOGEN, wc is inactive and released into b stream.
  • meets R w enzyme and activates it creating AT1
  • gets to lungs where there’s ACE (angiotensin converting enzyme)
  • ACE converts A1 to A2

CVS (23 decks)

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