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MD3001 > treatment of hypertension > Flashcards

treatment of hypertension Flashcards

1
Q

hypertension?

A

persistent elevation of BP in the systemic arterial circulation to a level higher than expected for age, sex, race and of the individual.

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2
Q

lifestyle interventions for treatment of hypertension?

A

stage 1 hypertension is usually managed through lifestyle interventions alone
- exercise
- smoking cessation
- dietary modification
(limit alcohol and caffeine intake)

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3
Q

why are the different types of therapeutic agents?

A
  • ACE inhibitors
  • angiotensin 2 receptor blockers (ARBs)
  • diuretics (decrease water retention)
  • calcium channel blocker
  • B1 adrenergic receptor blockers
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4
Q

what is the difference in step 1 therapeutic intervention between:
1- those with diabetes and <55 yrs old
2- >55 yrs old, Afro-caribean descent?

A

1- give ACE inhibitor
2- give CCB

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5
Q

step 1 medical management of hypertension?

A

ACE inhibitor (ramipril) or CCB (candesartan or nifedipine) depending on the group you are treating.

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6
Q

step 2 medical management of hypertension?

A
  • if max dose of step 1 has failed or not tolerated:
    = combine CCB and ACE
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7
Q

if CCB are not tolerated in step 2 what should you give?

A

thiazide diuretic

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8
Q

step 3 medical management of hypertension?

A

add thiazide diuretic

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9
Q

step 4 medical management of hypertension?

A

this is now RESISTANT HYPERTENSION:
- all medications and add a further diuretic or B1 blocker
- seek specialist advise

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10
Q

in step 4, what further diuretic are you going to use?

A

low dose spironolactone
only do this if blood patssium is <4.5mmol/L

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11
Q

patients with hypertension should be monitored for what?

A

patients should be monitored for end organ damage

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12
Q

what is given for CV risk management in patients with hypertension?

A

statins for primary prevention is 10-year CV is >20%

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13
Q

what are the blood pressure targets for:
1- <80 yrs
2- 80 yrs
3- diabetics

A

1- <80 years: clinic BP <140/90 mmHg (or <135/85 AMPM/HBPM)
2- 80 years: clinic BP <150/90 mmHg (or <145/85 AMPM/HBPM)
3- Diabetics: clinic BP <130/80 mmHg

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14
Q

where is blood filtered?

A

glomerulus of the kidney

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15
Q

where does reabsorption of ions take place

A

reabsorption of solutes, ions and water will take place along the length of the tubule

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16
Q

what does the movement of Na do in the kidney?

A

it creates an osmotic gradient for H20 to follow

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17
Q

where in the kidney is bulk reabsorption uncontrolled?

A

the proximal convoluted tubule

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18
Q

1- what does angiotensin 2 bind to?

2- what are its effects on:
- vascular smooth muscle
- hypothalamus
- renal tubules of the kidney

A

1- AT1 receptors

2- increased smooth muscle constriction, increasing TPR

  • on the hypothalamus:
    increased release of vasopressin (ADH), reabsorption of H20 in kidneys, increased ECV
  • renal tubules of kidneys:
    increased secretion of aldosterone from adrenal glands, Na reabsorption in the kidney, increased ECV
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19
Q

angiotensin 2 effect in the proximal convoluted tubule?

A

it stimulates Na reabsorption, particularly here.

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20
Q

what effect does angiotensin 2 stimulating aldosterone release?

A

it will further stimulate Na reabsorption in the cortical collecting duct.

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21
Q

1- ACE inhibitor example?

2- mechanism of action?

A

1- ramipril

2- inhibitor of ACE=
= no angiotensin 2
- decreased vasoconstriction = decreased TPR
- decreased water retention = decreased ECV
- decreased Na retention = decreased ECV
DECREASED BP

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22
Q

what other system is ACE involved in?
what is the function of this system?

A

the kinin-kallikren system
- this will cleave kininogen into bradykinin
- this is a vasodilator

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23
Q

what does ACE do to bradykinin?

A

it breaks in down into an active metabolite

24
Q

what does bradykinin do?

A
  • it binds to B2 receptors
  • vasodilation
  • PGI2 production
  • NO production
25
Q

what can increased bradykinin do?

A

increased bradykinin can cause bronchoconstriction which can give rise to a dry cough.

26
Q

why would ARB be given over ACE?

A
  • due to the specific effects it has on AT1 receptors, there will be no effects on bradykinin., therefore no side effects of cough.
27
Q

1- what are diuretics?
2- what are 3 different types of diuretics?
3- how do they work?

A

1- substances that help to body get rid of water (targeting Na absorption to do this)

2- loop diuretics, thiazide diuretics, K sparing diuretics

3- they will reduce BP by decreasing ECV

28
Q

describe loop diuretics?

A
  • most powerful of diuretic
  • inhibits NKCC2 (Na/K/2Cl co transporter) in Thick acedning loop of henle
29
Q

when will loop diuretics be used?

A

only used when treatment of hypertension where renal function is impaired
- sometimes used in other fluid overload condition

30
Q

examples of loop dietetics?

A

furosemide
bumetanide

31
Q

example of thiazide diertics?

A

bendroflumethiazide
indapamide

32
Q

describe thiazide diuretics?

A
  • less powerful than loop diuretics
  • inhibits NCC in the distal convoluted tubule (Na/Cl co transporter)
  • this is a 2nd/3rd line of treatment
33
Q

describe K sparing diuretics?

A
  • it has limited diuretic action alone, but powerful in combination with loop/thiazide diuretics
  • inhibits ENaC in the cortical collecting duct (epithelial Na channel)
34
Q

why are k sparing diertics rarely used?

A

due to the fact that is also blocks K excretion (coupled to ENaC), causing hyperkalaemia

35
Q

what are the 2 types of K sparing diuretics?

A

1- aldosterone antagonists (eg: spironolactone, eplerenone)

2- ENaC inhibitors (amiloride, triameterne)

36
Q

function of CCB?

A

inhibits contraction of cardiac muscle and vascular smooth muscle

37
Q

describe the movement of calcium and sodium in the heart?

A
  • Na enters via slow Na channel in pacemaker cells (funny current)
  • causing a call depolarisation
  • Ca enters via T-type voltage gated Ca channels
  • further depolarisation
38
Q

what does the movement of Na and Ca cause to the heart?

A
  • depolarisation spreads through gap junctions to both pacemaker and contractile cells
  • depolarisation will occur in neighbouring cells
39
Q

what do the contractile cells contain?

A

they contain L-type Ca channels
- calcium is further released from the SR via RyRs
- causing contraction of the cardiomyocyte

40
Q

what do CCB do?

A

they inhibit L-type voltage gated Ca channels
- this is the same concept as vascular smooth muscle

41
Q

what are the 2 different types of CCB and what which one is most commonly used?

A

1- non dihydropyridines and dihydropyridines

2- dihyropryridines are most commonly used

42
Q

2 types of non dihyropridines?

A

phenylalkylamines (verapamil)
benzothiazepines (diltiazem)

43
Q

examples of dihyrodypridines?

A

amlodipine
felodipine

44
Q

effects of non-dihydropyridines?

A

Cardiac effects:
- decreased contractility
- decreased hr
- decreased conduction
- decreased CO
- decreased PB

smooth muscle effects:
- decreased coronary artery constriction
- decreased peripheral vessel constriction
- decreased TPR
- decreased BP

45
Q

effects of dihydropridines?

A

smooth muscle effects:
- decreased coronary artery constriction
- decreased vessel constriction
- decreased TPR
- decreased BP

46
Q

side effects of CCB?

A

flushes
headaches
ankle oedema
dizziness

47
Q

side effects of thiazide diuretics?

A

hypokalaemia
hyponatraemia
gout

48
Q

side effects of ACE inhibitors?

A

persistent dry cough
dizziness
tiredness
headaches

49
Q

side effects of ARB’s?

A

dizziness
headaches
renal impairment
back/leg pain

50
Q

side effects of K sparing diuretics?

A

hyperkalaemia
renal impairment
GI upset

51
Q

what are the side effects of non-selective B-adrenoreceptor antagonists?

A

bronchoconstriction (bad for asthmatics)

52
Q

examples of B1 selective antagonists?

A

bisoprolol
atenolol

53
Q

how do B1 selective antagonists work?

A
  • decrease force of contraction
  • decrease CO
  • decrease BP
  • decrease TPR
  • decrease ECF
  • decrease BP
  • also inhibits renin release from granular cells= decrease in angiotensin 2= decrease in vasoconstriction, Na and H20 retention
54
Q

why are b1 blockers not the first line of treatment for hypertension?

A
  • less effective than comparators in reducing CV risk
  • less effective then ACE’s and CCB’s at reducing the risk of diabetes
  • less well tolerated than ACE inhibitors/ARB’s
55
Q

when will B1 adrenoreceptor antagonist be used?

A

they are useful antihypertensive patients with additional need for B blockade including angina and heart failure.

MD3001 (56 decks)

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