drugs and the vasculature Flashcards

1
Q

what does the sympathetic nerve have along its length?

A
  • varicosities

- primarily release NA to stimulate vasoconstriction

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2
Q

name some VSM mediators that can inc. Ca and stimulate VSM contraction? What receptors do they bind to?

A
  • AngII –> AT1r
  • PGG2, PGH2 –> T-prostanoid receptor
  • ET1 –> ETA/B
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3
Q

name some endothelial cell agonists that can stimulate a relaxation from an inc. in Ca

A
  • NO
  • CNP (C type naturietic peptide)
  • PGI2
  • EDHF (endothelial hyperpolarising factor)
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4
Q

what is BP mediated by?

A

CO and TPR

BP = CO x TPR

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5
Q

which vessels contribute the most to BP regulation?

A
  • arterioles contribute the greatest to BP regulation
  • these vessels have vascular tone
  • so always display partial state of constriction
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6
Q

in terms of vascular tone, what do hypertensive patients have?

A

have a raised base vascular tone
= more TPR
= more BP

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7
Q

define hypertension

A

> 140/90mmHg

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8
Q

describe the treatment overview

A

step 1: single therapy (U55 - ACEi or ARB, O55/ Afro-carribbean - CCB or thiazide diuretic)
Step 2: Dual therapy (ACEi and CCB or ACEi and thiazide diuretic)
Step 3: Triple therapy (ACEi, CCB, thiazide diuretic)
Step 4: Symptomatic relief (low dose spironolactone, beta/alpha blockade)

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9
Q

name an ACEi

A

Enalapril

often have -ipril endings

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10
Q

what is RAS stimulated by?

A
  • low renal Na reabsorption
  • low renal perfusion pressure
  • High SNS activation
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11
Q

what do ACEi do?

A
  • dec. AngII production

- inc. bradykinin

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12
Q

what are some uses of ACEi?

A
  • hypertension
  • HF
  • Post MI
  • diabetic nephropathy
  • progressive renal insufficiency
  • high CVS disease risk patients
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13
Q

how are ACEi effective in hypertension treatment?

A
  • reduce TPR (more bradykinin and less AngII –> reduces TPR via less AT1R-mediated vasoconstriction and more bradykinin vasodilation)
  • sodium retention (less Na retention in kidneys via blocked actions of AngII and less aldosterone secretion)
  • thirst drive (less SNS activation of thirst in brain via AT1R)
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14
Q

how are ACEi used to treat HF?

A
  • reduced TPR (less vasoconstriction via AT1R in vasculature so less afterload = dec. ionotropic effects)
  • reduce preload (venodilation means less preload)
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15
Q

what do ARBs (Angiotensin Receptor Blockers) do?

A

e.g. Losartan

prevent binding of AngII to AT1 receptors

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16
Q

what are the uses of ARBs?

A
  • hypertension

- HF

17
Q

what are the side effects of ARBs?

A
  • hypotension
  • hyperkalaemia (aldosterone promotes K loss so aldosterone inhibtors produce hyperkalaemia)
  • foetal injury
  • renal failure
18
Q

what are the side effects of ACEi?

A
  • cough
  • urticaria/angiooedema
  • hypotension
  • hyperkalaemia
  • foetal injury
  • renal failure
19
Q

describe the process of smooth muscle contraction

A
  • membrane depolarisation opens VGCC
  • Ca enters and binds Calmodulin (CaM)
  • Ca-CaM complexes activated MLCk
  • MLCk mediated phosphorylation –> VSM contraction
20
Q

what are the 2 types of CCBs?

A
  • dihydropyridines (DHPs) = non rate limiting

- non-DHPs = rate limiting

21
Q

name a DHP

A

amlodipine

no negative ionotropic effect

22
Q

name a Non-DHP

A

negative ionotropic effect

23
Q

which CCB is used to treat hypertension and why?

A

amlodipine as it doesn’t have an ionotropic effect on the heart
DHPs inhibit Ca entry itno VSMCs so less contraction of cells –> less TPR –> less BP

24
Q

why are ACE or ARBs first line drugs?

A

due to good patient adherence

higher adherence = less side effects

25
Q

why do afro-carribeans have a different drug schedule?

A
  • due to low plasma renin activity

- so ACEi doesn’t work as well

26
Q

name 2 alpha blockers and what they do

A

they block alpha 1 mediated vasoconstriction

  • prazosin is alpha 2 antagonist
  • phentolamine is alpha 1/2 antagonist
27
Q

how can phentolamine lead to inc. HR (not reflex)?

A

action against alpha 2 blocks -ve feedback of NA release
so there is ehanced NA release and SNS response
can lead to inc. HR