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PNS > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is hypertension?

A

Clinic BP above 140mmHg (Sytolic) and/or 90mmHg (Diastolic)

Or ambulatory mean BP (ABPM):
Above 135/85mmHg.

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2
Q

Why is Hypertension bad?

A

Stress on tubular systems like kidney, eyes, nerves….

Endothelial cell damage which promotes atherosclerosis.

Extra strain on the heart = raised TPR.
= Left ventricular hypertrophy leading to pulmonary oedema.
= Can lead to CHF - peripheral oedema.

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3
Q

What are the risk factors of Hypertension

A

Smoking, high salt diet, alcohol, lack of exercise, obesity, dyslipidaemias, diabetes… being a man.

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4
Q

What are the causes of different types of hypertension?

A

Essential/primary = no apparent cause.

Secondary hypertension -

Pheochromocytoma = Adrenal medulla tumour = excessive catecholamines.
Cushing’s syndrome - increased ACTH.
Hyperaldosteronism = Conn’s syndrome.

Kidney diseases.
Drugs: corticosteroids, the pil., sibutramine, sudafed.

White-coat hypertension - when getting BP taken.

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5
Q

What are the different stages of hypertension?

A

Stage 1 = More than 140/90 or 135/85mmHg
= life style changes, or consider changes if any organ damage, risk of CVD, kidney diseases, diabetes…

Stage 2 = 180/120mmHg
= Start treatment right away.

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6
Q

What is the formula for calculating BP…
And for Cardiac Output?

A

BP = CO * TPR.

CO = HR * Stroke volume.

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7
Q

What are the general ways to reduce BP?

A

Reduce TPR and cardiac afterload = arteriodilation.

Reduce Stroke volume - lower blood volume and cardiac preload (venous return) = venodilation.

Reduce HR…

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8
Q

How does the juxtaglomerular apparatus respond to changes in BP and tubular content?

A

Granular cells in the afferent arteriole secrete pro-renin, which is converted to renin by endothelial peptidases.

  • in response to decreased BP detected by baroreceptors in afferent arteriole…
  • Leads to increased sympathetic stimulation via B1 ARs..

Macula Densa cells in the DCT detect reduced tubular NaCl - stimulating the release of PGE2 by COX-2.

PGE2 acts on granular cells to release more pro-renin.

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9
Q

How are the different angiotensins formed?

A

Pro-renin secreted by Granular cells (in response to decreased BP and from PGE2 released by DCT Macula Densa) is converted to renin.

Renin cleaves angiotensinogen into Angiotensin I.

Angiotensin II formed by ACE in lung endothelial cells.

Aminopeptidases A and N cleave AngII further into Ang III and Ang IV = which have central effects.

AngIII = thirst, natriuresis with aminopeptidase A expressed in brain + kidneys.

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10
Q

What is the role of ACE2?

A

ACE2 hydrolyses Angiotensin II into Angiotensin I-7….
Angiotensin 1-7 have opposite effects to AngII:
Acting on Mas receptor to promote vasodilation, hypotension, apoptosis…

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11
Q

What are the effects of Ang II?

A

Angiotensin II acts on AT1 receptors - Gq11 coupled.

PLC produces IP3 + DAG, opens intracellular Ca2+ stores = vascular SM contraction…. = vasoconstriction.

Stimulates NA release from sympathetic peripheral nerves - indirect vasoconstriction..

Stimulates aldosterone release from adrenal cortex…. = salt retention by increasing NHE action in PCT.

Long term = vascular growth - hypertrophy, fibrosis + hyperplasia.

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12
Q

What are the therapeutic uses of ARBs and ACEi’s

A

First choice treatment of systemic hypertension in younger (less than 55), white people and patients with Type 2 diabetes.

Used in first line therapy for congestive HF.

Myocardial infarction, diabetic nephropathy..

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13
Q

What are the ACE inhibitors?

A

Captopril - the first developed - but is short acting and poorly tolerated so not used…

Enalapril = prodrug with carboxyl moiety removed to become active… Long acting and better tolerated…

ACEIs end with pril…

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14
Q

What are common side effects of ACEi’s and ACEi specific side effects?

A

Hypotension, reflex tachycardia, hyperkalaemia (reduced aldosterone)..

Persistent dry cough!
Angioedema w/ prolonged use!!! = swelling.

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15
Q

How are bradykinins involved with RAAS?

A

ACE converts Angiotensin I to Ang II…. But it also degrades bradykinin…

Bradykinin is a potent vasodilator by agonising B2 adrenoceptors…

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16
Q

How do ACEi’s affect bradykinin?

A

By blocking the actions of ACE, there will be less bradykinin degradation and increased bradykinin levels.

Bradykinin is a potent vasodilator - and will act on sensory nerves, triggering a dry cough, as well as causing angioedema via peripheral vasodilation…

This is on top of existing vasodilation from reducing Ang II formation…

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17
Q

Why were AT1 selective blockers developed?

A

To prevent the excess generation of bradykinins that is observed with ACE inhibitors - which leads to excessive vasodilation = dry cough + angioedema…

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18
Q

What are ARBs?

benefits vs ACEi’s?

A

AT1 receptor blockers…

Losartan and Valsartan.

= no persistent dry cough, reduced risk of angioedema and improved tolerance in patients,…

-Sartan suffix.

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19
Q

What is Aliskiren?

A

A non-peptide renin inhibitor…

That is used when ACEinhibitors or AT1 blockers aren’t ideal.

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20
Q

What are the contradictions of drugs acting on RAAS?

A

RAAS acting drugs can be teratogenic - so must not be used in pregnancy for pre-eclampsia.

Not first choice therapy for elderly people (over 55 YO).
Nor african-american/caribbean origin

Thse patients have lower activity of RAAS…

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21
Q

What are the direct-acting vasodilator classses?

A

CCBs
K+ channel openers.
Hydralazine.

Drugs acting on sympathetic NS:
Beta blockers.
A2 agonists.
I1 agonists.
A1 antagonists
Adrenergic ganglion blocking drugs.

22
Q

How can CCBs be used to treat hypertension?

A

Block L-VACCs in vascular SM.

Causing Arterio and Venodilation.
= reduced TPR, afterload, preload + central venous pressure.

Dihydropyridine CCbs are vascular selective L-VACC blockers.
= Nifedipine (fast acting), Amlodipine (slow acting)

23
Q

What are the selectivities of CCBs?

A

Dihydropyridines = Nifedipine + Amlodipine = vascular selective.

Benzothiazepines = Diltiazem = Cardio + vascular selective.
= can’t use diltiazam with Beta blockers for stable angina.

Phenylalkylamines = Verapmili = Cardiac.

24
Q

Which + when are CCB’s are used for hypertension?

A

AS first line treatment for elderly + african-american/caribbean origin + pre-eclampsia = where RAAS acting drugs would be less effective + unsafe.

Nifedepine = pre-eclampsia.
Amlodipine = hypertension.

25
Q

What are the adverse effects of CCBs?

A

Hypotension, postural hypotension, reflex tachycardia, peripheral oedema + constipation.

26
Q

What anti-hypertensives are first-line treatment for Type 2 diabetes?

A

ACEi/ARB = Enalapril/Captopril or Losartan/Valsartan.

If this doesn’t work? add on CCB or thiazide-like diuretic…

27
Q

What drugs are added onto first-line treatment if it fails?

(AFrican american/caribbean or elderly)

A

If CCB (dihydropyridine like amlodipine/nifedipine) fails = add on ACEi/ARB or thiazide-like diuretic.

Captopril/enalapril or losartan/valsartan…. or thiazide-like (Indipamide/chlortalidone)

28
Q

What if all available treatments don’t work?

A

Patient has resistant hypertension.
When ACEi/ARB, Thiazide-like + CCB fails to treat hypertension…

You need to use Potassium channel activators.

29
Q

What is the MoA and anti-hypertensive MoA of Potassium channel activators?

A

Open ATP-sensitive K+ channels (Katp) in vasculature.
These channels are regulated by ATP;ADP ratio…
High ATP keeps channel closed.

Activation of these Katp channels causes membrane hyperpolarisation = closing L-VACCs and inducing vasorelaxation!

30
Q

How do Katp channels relate to diabetes?

A

Katp channels are targets for anti-diabetic treatments.

But Katp channels in vascular SM is different to Katp channels in pancreatic Beta cells…

Vascular SM = Kir6.1/SUR2B.
which are sensitive to activators, as opposed to Kir6.2/SUR1 in pancreatic beta cells, which are more sensitive to inhibitors…

31
Q

What are the Potassium channel activators?

Therapeutic uses?

And adverse effects?

A

Minoxidil = used to activate Katp channels in vascular SM, causing membrane hyperpolarisation, closure of L-VACCs and causing vasorelaxation.

Used to treat severe resistant hypertension….

= hypotension, reflex tachycardia, diabetes mellites, excessive hair growth!!! and fluid retention.
= diabetes mellites by impairing insulin release!!!!!

Fluid retention = add diuretic.
Tachycardia = add Beta blocker.

32
Q

What is Hydralazine?

What are its therapeutic uses?

A

Unknown MoA…

Causing artery and arteriole dilation, reduced TPR and cardiac afterload.

Used in pre-eclampsia alongside beta blocker + diuretic.

With nitrates in heart failure in african-american origin.

33
Q

What are the side efefcts of Hydralazine?

A

Lupus-like syndrome - skin rashes.

Tachycardia, hypotension, peripheral oedema…

34
Q

What beta blockers are used for hypertension?

A

Nebivolol - B1 selective and stimulates NO release in vascular endothelium.

Pindolol - B1 selective + partial agonist at low sympathetic activity.

Labetatol -
Carvediolol:
Both non-selective Beta blockers with a1 antagonism.

35
Q

What is the MoA of Nebivolol?

A

Nebivolol = B1 selectie antagonist + stimulates NO release in vascular endothelium.
= causing vasodilation and less fatigue/bradycardia risk.

36
Q

MoA of Pindolol?

A

B1 selective + partial agonist at low sympathetic activity.
= Less bradycardia in cardiac dysrhythmic patients
= reduces HR but stops from getting TOO low.

37
Q

MoA of carvedilol and labetalol?

A

Non-selective beta blockers with a1 antagonism.
= Causing vasodilatation + decreased TPR BUT little change to HR + CO!!!

38
Q

What are the uses of beta blockers for hypertension?

A

Resistant hypertension = beta blockers added onto first-line drugs + diuretics.

Pre-eclampsia = Labetalol (Nifedipine first?

Pindolol = hypertension treatment if tachy arrythmic as slows down HR but not TOO much.

39
Q

Adverse effects of Beta blockers for hypertension?

A

With labetalol/carvedilol = bronchoconstriction risk greater.

Bradycardia.

Masks hypoglycaemia symptoms.

Negative inotrope!!, but less than usual since vascular selective.

ED!
Fatigue

40
Q

What are the roles of A1 adrenoceptor antagonists in hypertension?

A

Inhibit post-synaptic a1 adrenoceptors on vascular SM.

A1 adrenoceptors on vascular SM induce constriction.

= cause arterial and veno dilatation.
= reduced TPR, afterload, preload and stroke volume.

For severe restistant hypertension add on to first line drugs.

= Azosin drugs

41
Q

What are the a1 adrenoceptor antagonists?

A

Doxazosin
Prazosin.

azosin drugs.

42
Q

What are the adverse effects of a1 antagonists?

A

Postural hypotension dizziness, fatigue…

BUT
less reflex tachycardia compared to non-selective alpha blockers.

43
Q

What are the central-acting drugs to treat hypertension?

A

A2 adrenoceptor agonists - Clonidine and a-methyldopa.

Imidazoline receptor agonists = Monoxidine.

= Act on A2 autoreceptors in the medulla to decrease sympathetic outflow mostly.

44
Q

How do central-acting antihypertensives reduce BP?

A

In the medulla, a2 autoreceptors on NTS are agonised by clonidine and a-methyldopa.

The NTS inhibits the RVLM - which is where imidazoline receptors are - which monoxidine agonises.

= This reduces sympathetic outflow through depleting NA release at synapses…

45
Q

When are central-acting anti-hypertensives used?

A

Monoxidine = imidazoline receptor agonist = resistant hypertension.

a-methyldopa = pre-eclampsia.

Clonidine - mostly used for migraines, opoiod detox and insomnia…

46
Q

What are the side effects of central-acting antihypertensives?

A

Rebound hypotension when stop use.

Dry mouth.

Sedation + drowsiness - less so with moxonidine.

Clonidine causes respiratory depression.

47
Q

What is trimetaphan?

Adverse effects?

A

Competitive inhibitor to nicotinic ACh receptors in autonomic ganglia.
= acting to inhibit BOTH sympathetic + parasympathetic action.

Reflex tachycardia, postural hypotension, cyclopegia!!!

48
Q

What is guaenethedine?

A

Taken up by NET and VMAT - to deplete vesicles of NA in adrenergic synapses…
= used to treat hypertensive crisis… rarely now.

49
Q

What is reserpine?

A

Taken into adrenergic synapse by NET, but irreversibly inhibits VMAT = preventing uptake of NA in vesicles and in the synapse!!
= causes depression!

50
Q

IF everything fails?

A

Ablate sympathetic nerves!

51
Q

How does methyl dopa work??

A

Methyldopa is metabolised to methyl-NA.
= False precursor molecule so reduces NA synthesis.
= A2 agonist = reduced NA release at sympathetic ganglia.
= Inhibits DOPA decarboxylase = reduces peripheral NA/Dopamine.

= PREFERRED TREATMENT FOR Pre-ECLAMPSIA….

PNS (14 decks)

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