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Pharmacology > Sympatholytics/ Adrenergic Modulators > Flashcards

Sympatholytics/ Adrenergic Modulators Flashcards

1
Q

What is the MAO for β-Receptor antagonists (β -blockers), what is the site of action, and what are the key β-blockers we need to know

A

β-blockers work by inhibition of cardiac and renal β1-receptors.

  • This reduces HR and force of contraction, so reduces cardiac output (CO=SVxHR)
  • Reduces juxtaglomerular renin secretion
  • (Reduces NA secretion by CNS, alteres baroreceptor sensitivity with chronic use)

β-blockers site of action is at cardiac and JG baroreceptors.

  1. Metaprolol
  2. Atenolol
  3. Propanolol
  4. Carvedilol
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2
Q

What are the 3 classes of Adrenergic modulators which are being covered?

And what are the drugs we need to know under each class

A
  • Beta Blockers (β1 for cardioselectivity)
    • Metoprolol, Atenolol, Propranolol, Carvedilol
  • Alpha 1 Blockers
    • Doxazosin
  • Alpha 2 Agonists
    • Clonidine, α-Methyldopa
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3
Q

What is cardiac output controlled by?

A
  • Rate & force of cardiac contraction (ANS)
  • Blood volume (kidneys & RAA system)
    • Blood viscosity
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4
Q

Which systems control peripheral resistance?

A
  • Sympathetic controlled vascular tone (Rapid since controlled by ANS)
  • RAA control of tone (slow onset & more sustained) (Endocrine system, slow but sustained)
  • Substances released from endothelial cells (e.g. NO, prostacyclin)
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5
Q

What factors control mean arterial pressure?

A

Cardiac output and peripheral resistance

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6
Q

How does the ANS speed up the heart?

A

Speeds it up with sympathetic stimulation

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7
Q

How does the ANS slow down the heart?

A

Parasympathetic stimulation

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8
Q

How does the ANS determine whether to speed up or slow down the heart?

A

Recieves information from the baroreceptors

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9
Q

In sympathetic innervation of the heart, which receptors does Noradrenaline act on?

A

Noradrenaline acts on beta receptors (primarily B1)

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10
Q

Describe the sympathetic innervation of blood vessels

A

Noradrenaline acts on alpha receptors

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11
Q

Describe the parasympathetic innervation of the heart

A

Acetylcholine acts on muscarinic receptors

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12
Q

How does the endocrine system influence the control of cardiac output & vascular tone?

A

Circulating adrenaline affects beta 1 & 2 receptors, and at high conc. it will also affect alpha receptors

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13
Q

What does chonotropy (chronotropic) relate to?

A

Rate of contraction

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14
Q

What does inotropy (Inotropic) relate to ?

A

Force of contraction

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15
Q

Which receptors is vasoconstriction mediated by?

A

α adrenorecptors

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16
Q

Which receptors is HR & force of contraction primarily mediated by?

A

β1 adrenoreceptors

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17
Q

What receptor mediates decreased HR & force of contraction?

A

M2 receptor

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18
Q

What does sympathic innervation to the kidney do?

A

Increased renin production (mediated by β1 adrenoreceptors)

The release of renin leads to angiotensin II production - this is a vasoconstrictor

The kidney also releases aldosterone, this controls water and salts in the body

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19
Q

What is a risk indicator for coronary heart disease in people under age 50?

A

Diastolic blood pressure is a more potent risk factor for coronary heart disease than systolic blood pressure until age 50.

After age 50 systolic blood pressure is a more potent indicator (increased arterial stiffness is the vascular phenotype of systolic hypertension, especially of large ateries)

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20
Q

Describe how systolic and diastolic pressure change over the course of a life

A

Incidence of hypertension increases progressively with age. Systolic blood pressure increases throughout life, and diastolic blood pressure increases until approximately 50 yrs old, then it levels off and begins to decrease.

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21
Q

What is the first line of defence for people with HTN in NZ?

A

ACE inhibitors are used first, but in other countries thiazide diuretics are used (they reduce plasma volume, reducing blood pressure)

22
Q

What are the current hypertension guidelines? (what treatments should be done first)

A
  1. A low dose of ACE inhibitor/ ARB(angiotensin receptor blockers)
  2. Or a thiazide diuretic
  3. Or calcium channel antagonists (dihydropyridine)
  4. β-blockers not suitable for ISH (isolated systolic hypertension) control (perdominantly in elderly) - since ISH is caused by arteriolar/artery stiffening, whereas β-blockers impact upon the heart

If a single agent doesn’t work, then use two together

A single agent controlls BP in 40-50% of patients

23
Q

What treatments should be given to treat HTN for someone with heart failure?

A

β-blocker

  • Diuretic
  • ACE inhibitor
  • ARB
  • Aldosterone antagonist
24
Q

What treatments should be given for HTN post-myocardial infarction?

A
  • β-blocker
  • ACE inhibitor
  • Aldosterone antagonist
25
Q

Which treatments should be given for HTN in someone with high coronary disease risk?

A
  • Diuretic
  • β-blocker
  • ACE inhibitor
  • CCB (calcium channel blockers)
26
Q

What treatment should be given for HTN for a patient with diabetes?

A
  • Diuretic
  • β-blocker
  • ACE inhibitor
  • ARB
  • CCB
27
Q

What treatment should be given for HTN in a patient that has chronic kidney disease?

A
  • ACE inhibitor
  • ARB
  • Diuretic
28
Q

What treatment should be given for HTN for recurrent stroke prevention?

A
  • Diuretic
  • ACE inhibitor

+/- statins

29
Q

How do β-blockers (β- Adrenergic receptor Antagonists) work?

A

They prevent the binding of NA and Adr to β receptors

In the CVS they inhibit cardiac β1-receptors

30
Q

What determines the level of response for someone taking β blockers?

A

Degree of response is proportional to the level of sympathetic stimulation (e.g. during exercise or stress)

31
Q

What are the 1st, 2nd and 3rd generation β-blockers?

And what is it contra-indicated by?

A

1st generation - Propranolol - blocks both β1 and β2 receptors, contraindicated in people with asthama or COPD (since β2 receptors are found in the airway)

2nd generation - Metoprolol (and Atenolol): β1 - selective, non-respiratory airways, but NOT exempt from cross-reactivity

3rd generation - Carvedilol: β1, β2 &

α1 antagonist (is also a vasodilator capability)

32
Q

Describe how β-blockers decrease CO and B.P

A

They have a negative chronotropic action (decreases rate of contraction) and they have negative inotropic effects (decreases force of contraction), and it decreases renal renin output

β-blockers primarily antagonise Cardiac and Renal β-adrenorecepots

33
Q

We know β-blockers reduce CO and B.P, do how does it have its antihypertensive effect?

A
  • they cause a reduction in CO (initially)
  • Inhibition of β1-stimulated renin release from juxtoglomerular cells
  • Chronic use decreases peripheral resistance (but β-blockers may increase it initially (the initial drop in CO will produce an initial increase in TPR, but this adjusts)

the pimary action is on cardiac output, but long term treatment ultimately decreases peripheral vascular resistance

34
Q

How do β-blockers control have their negative chonotrope effects?

And how do they decrease the work of the heart?

A

By inhibiting cardiac β1 receptors, results in decreased rate of contraction

The negative ionotropic and chronotropic effects causes a reduced oxygen consumption from the heart, due to the decreased work of the heart

35
Q

What is the main therapeutic use of β-blockers for cardiac rate control?

A

It’s used as an antiarrhythmic drug to treat atrial fibrillation

36
Q

What is the main therapeutic use of β-blockers for angina?

A

The negative inotropic and chronotropic effects reduce cardiac oxygen consumption, reducing the amount of angina

37
Q

How can β-blockers treat Glaucoma and anxiety?

A

Glaucoma- Timolol in eye drops to reduce intraocular pressure

Anxiety - Condition associated with tremors and increased HR.

38
Q

What are the adverse effects of β-blockers?

A
  • Bronchospasm (β2 interaction, need to avoid in asthma)
  • Heart failure
  • Reduced exercise tolerance and fatigue
  • Peripheral vasoconstriction (cold peripheries)
  • Worsening heart block (cardiac conduction pathways)
  • CNS effects (nightmares)
  • Worsening lipid profiles (may increase VLDL, LDL/ decrease HDL - increasing LDL:HDL ratio)
    • Non-selective β-blockers may blunt catecholamine induced hepatic gylcogenolysis in response to hypoglycaemia (delay hypoglycaemic recovery in diabetes)
39
Q

Why aren’t 1st and 2nd generation β-blockers not used as a first line for HTN treatment?

A

1st & 2nd gen β-blockers reduce BP through -ve chronotropic and inotropic effects without producing vasodilation (Whilst adversly affecting lipid profiles)

Should use 3rd gen β-blockers, as they have vasodilating capabilities (carvedilol: a1-block, nebivolol: NO release) without major adverse effects on HR, lipids etc

40
Q

Describe the pharmokinetics of hydrophilic drugs

A
  • Lack of hepatic first-pass effets lowers the chance of drug interactions and food interference
  • Often results in longer T1/2
  • Low penetrability into CNS
41
Q

Describe the pharmokinetics of lipophilic drugs

A
  • Have an improved oral absorption
  • They go through hepatic metabolism
  • Greater chance of significant first-pass effect
  • Often have shorter half life
  • Larger vol of distribution, resulting in ADRs
  • Higher penetrability into the CNS
42
Q

Describe the pharmokinetics of Metaprolol/Propanolol

(these are lipophilic drugs)

A
  • They are lipophilic, allowing BB barrier penetration - causing nightmare, hallucinatory effects
  • High oral absorption
  • Extensive 1st pass metabolism producing poor (25-50% bioavailability)
43
Q

Describe the pharmokinetics of Atenolol (Hydrophilic)

A
  • Lower lipid-solubility, Does not cross BB barrier, resulting in few CNS side effects
  • Largely excreted unchanged through renal route
  • Longer T1/2 and can be given once daily
44
Q

What are the main α2 agonists used?

A

Clonidine

α-Methyldopa (broken down into α-methyl NA)

45
Q

What is the action of Clonidine?

A

It has action on the pre-synaptic cells (Sympathetic neuron), this reduces sympathetic and parasypathetic outflow from the medulla.

During the depolarisation of pre-synaptic sympathetic neurons the synaptic bouton is depolarised, and NA is released to move across the cleft to bind to alpha and beta adrenergic receptors. There is a feedback pathway in place, where the NA stimulates the pre-synaptic α2A receptors, and tells the system to stop releasing NA (sufficent NA stops further NA output). Clonidine binds to the α2 receptors and does the same thing as NA, it reduces NA output.

α2B receptors are found in the vasculature, so when a patient takes chlonidine for the first time vasoconstriction can occur (need to be careful of patients BP increasing rapidly with first small doses) - so when clonidine binds to α2B vasoconstriction occurs. This is why you need to start at small doses and build it up over time slowly so it builds up in the brain and doesn’t spread to the vasculature. When binds to α2A in the brain, vasodilation occurs.

46
Q

What therapeutic effects does Chlonidine have?

A

Reduces BP by reducing sympathetic effect on cardiac output and peripheral vasculature

47
Q

What is α-methyldopa, and what’s is mechanism?

A

α-methyldopa is broken down to α-methyl NA (α2 agonist)

It binds to the same receptor as clonidine, and reduces NA output, thus reducing sympathetic activity to cause vasodilation

48
Q

What is Doxazocin?

What acute and chronic effects does it have?

A

It’s a selective vascular α1 blocker

  • Used to treat mild to moderate HTN
  • Acts as a vasodilator: less reflex tachycardia than non-selective α blockers
  • Acute effects: reduce arteriolar resistance and increase venous capacitance, may cause reflex increase in HR and plasma renin activity
  • Chronic effects: Doxazosin will continue to reduce arterial resistance and hyperplasia but other effetcts return to normal
49
Q

What are side effects of α1 blockers? (Doxazosin)

A
50
Q

What are the pharmokinetics of Doxazosin?

A

Good oral absorption, good bioavailability but highly protein bound, undergoes hepatic metabolism

Also has a better LDL/HDL profile comapred to adrenergic modulators

51
Q
A

Pharmacology (13 decks)

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