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CVR Week 1 > Drugs Affecting Blood pressure > Flashcards

Drugs Affecting Blood pressure Flashcards

1
Q

what are some non-specific symptoms of hypertension?

A

dizziness
headache

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2
Q

what is hypertension?

A

isolated systolic blood pressure may be due to stiffness ion arteries as you age, unable to accomodate for the sudden increase in BP at systole

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3
Q

what are some of the main causes of hypertension?

A

primary hypertension
-smoking
-obbesity
-diet
-exercise
-genetic
secondary hypertension
-renal hypertension ro pheochromocytoma

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4
Q

what are the effects of chronic hypertension?

A

further cardiovascular disease
-atherosclerosis
-stroke
-myocardial infarction
-heartfailure
-renal failure
-retinopathy

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5
Q

what are the clinical benefits of reducing BP?

A

40% reduction of stroke
25% red in myocardial infarction
>50% red in heart failure

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6
Q

how do we calculate BP?

A

total peripheral resistance x cardiac output

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7
Q

What are the different pathways that can be affected to reduce blood pressure and the drug classes associated?

A

-block of sympathetic NS
-kidneys (reduce blood volume)
-hormones
-vasodilation of peripheral resistance arterioles (Ca2 channel blockers)

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8
Q

how can we block the sympathetic NS to reduce BP?

A
  • reduce effects on heart (b1-blockers)
  • reduce effects on blood vessels (a1-blockers)
  • reduce renin release from kidney (b1-blockers)
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9
Q

how can we use hormones to reduce the BP?

A

inhibit renin-angiotensin-aldosterone system (angiotensin converting enzyme [ACE] inhibitors and angiotensin receptor blockers)

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10
Q

what is the mechanism of action of B-adrenoceptor blockers?

A

comeptitive reversible antagonists
-reduction in blood pressure via blockade of b1 sympathetic tone on heart and reduction in renin release from kidney
-reduction in heart rate and stroke volume (speeds up relaxation, changes in conduction velocity and reduction in ionotropy)
-reduction in cardiac output

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11
Q

what are some B-adrenoceptor blockers?

A

propranolol (b1 and b2)
atenolol (b1 selective)

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12
Q

what are some of the adverse effects of B-adrenoceptor blockers?

A

-exacerbate asthma (block of b2 absolute contraindication)
-even with b-1 selective drugs you wouldn’t prescribe because there is always a bit of a crossover
-intolerant to exercise
-hypoglycaemia
-vivid dreams

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13
Q

what are some examples of A-adrenoceptor blockers?

A

-phentolamine (a1 and a2)
-doxazosin, prazosin (a1 selective)

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14
Q

what are the mechanism of action of A-adrenoceptor blockers?

A

-competitve reversible antagonists
-reduction in blood pressure via reduction in sympathetic tone in arterioles (a1)
-reduction in peripheral resistance

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15
Q

what are some adverse effects of A-adrenoceptor blockers?

A

-postural hypertension (loss of sympathetic venoconstriction)
-reflex tachycardia (via baroreceptors)
-impotence

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16
Q

what are some other uses of alpha 1 receptors?

A

-increased closure of internal sphincter of the bladder
-mydriasis
-vasoconstriction
-increased peripheral resistance
-increased blood pressure

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17
Q

what are examples of ACE inhibitors?

A

captopril and enalapril

18
Q

what is the mechanism of action of ace inhibitors?

A

-angiotensin converting enzyme on vascular endothelial surface converts angiotensin I to the active angiotensin II (very small peptide)

19
Q

how do ACE inhibitors lower blood pressure?

A
  1. Reduced formation of the vasoconstrictor angiotensin II (reduction in peripheral resistance)
  2. Reduced blood volume (loss of angiotensin II-stimulated release of aldosterone, thus reduction of renal reabsorption of Na+ and water)
20
Q

what are some adverse effects of ACE inhibitors?

A

Generally very well tolerated but:
- Sudden fall in BP on 1st dose - given with supervision
- Persistent irritant cough – due to reduced breakdown of bradykinin, a peptide that activates sensory nerves in lung tissue

21
Q

what are angiotensin II receptor blockers?

A

-two receptor subtypes: AT1 and AT2
useful antihypertensive agents
-side effect profile appears good - no irritant cough as seen with ACE inhibitors

22
Q

what do AT1 receptors mediate?

A

vasoconstriction anf aldosterone releasing actions of angiotensin II

23
Q

what kind of drugs are losartan and candesartan?

A

AT1 blockers

24
Q

what is the mechanism of action of diuretics?

A
  • Lower blood pressure by reducing blood volume
  • Mechanism is through reduced renal reabsorption of Na+ and water
  • (additional vasodilator action may also contribute: reduced peripheral resistance)
25
Q

what is an example of a diuretic?

A

bendroflumethiazide (a thiazide)

26
Q

what are some adverse effects of diuretics?

A

Reduction in plasma K+ - hypokalaemia
Potassium-sparing may be favoursed
Hypokalaemia may also affect effectiveness of digoxin

27
Q

what are some examples of calcium channel blockers?

A

verapamil, diltiazem and nifedipine

28
Q

what is the mechanism of action of calcium channel blockers?

A

L-Type Voltage Operated Calcium Channels
- open upon membrane depolarisation
- calcium entry into cardiac and vascular smooth muscle (therefore TPR effect)
Some have more of an effect on cardiac muscle:
Reduce Ca2+ entry into vascular smooth muscle and cardiac muscle by blocking L-type voltage-operated calcium channels

29
Q

what is the different mechanisms of action of calcium channel blockers?

A
  1. Open channel block (cork in a bottle!)
    • verapamil and diltiazem work this way
  2. Allosteric modulation - bind at allosteric site and reduce channel opening
    - nifedipine works this way
30
Q

what is the tissue selectivity of calcium channel blockers?

A

smooth muscle: nifedipine > diltiazem > verapamil
cardiac muscle: verapamil > diltiazem > nifedipine

31
Q

how do calcium channel blockers reduce bloop pressure?

A
  1. Reducing peripheral resistance (block of Ca2+ entry into vascular smooth muscle 4 vasodilatation)
  2. Reducing cardiac output (block of Ca2+ entry into cardiac muscle - heart rate and stroke volume both reduced)
32
Q

what are non rate limiting agents?

A

Dihydropyridines examples include amlodipine and lercanidipine

33
Q

what are Dihydropyridines?

A

They are more effective vasodilators and more vascular-selective because they exhibit voltage-dependent blockade
Cardiac conducting cells are relatively hyperpolarised whereas vascular smooth muscle is relatively depolarised.
So Dihydropyridines do not reduce heart rate and may cause an indirect tachycardia
A new agent called cilnidipine combines L/N blockade and causes less reflex tachycardia.

34
Q

what are rate limiting channel modulators?

A

examples include verapamil and diltiazem

They have more marked effects directly on the cardiac conduction pathways and cardiac muscle.

They slow the heart rate and reduce conduction and contractility; this is more noticeable with verapamil than diltiazem

35
Q

what are some adverse effects of calcium channel blockers?

A

headache- dilation of cerebral blood vessels
constipation - relaxation of GI smooth muscle
heart block due to reduced calcium and therefor cardiac failure
gingival hyperplasia

36
Q

what is step one of NICE treatment for hypertension (under age 56)?

A

ACE inhibitor or low cost angiotensin II receptor blocker

37
Q

what is step one of NICE treatment for hypertension (over 65 or ethnic origin of any age)?

A

calcium channel blocker

38
Q

what is step 2 of NICE treatment for hypertension?

A

ACE inhibitor or angiotensin II receiptor blocker + calcium channel blocker

39
Q

what is step 3 of NICE treatment for hypertension?

A

ACE inhibitor or angiotensin II receptor blocker + calcium - channel blocker +thiazide like diuretic

40
Q

what is step 4 of NICE treatment for hypertension?

A

ACE inhibitor or angiotensin II receptor blocker + calcium- channel blocker + thiazide like diuretic + consider further diuretic or alpha blocker or beta blocker

41
Q

Which hypertensive drug reduces BP without affecting vascular remodelling?

A

Atenolol (beta blocker) no effect on angiotensin system

42
Q

Which neurotransmitters cause vasoconstriction?

A

ATP

CVR Week 1 (8 decks)

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