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CRP- Cardiology > Adrenergic Drugs > Flashcards

Adrenergic Drugs Flashcards

1
Q

What is norepinephrine?

A

non-selective direct-acting agonist that hits alpha 1 receptors most (but also some alpha 2 and beta 1)

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2
Q

What will norepinephrine do to systolic and diastolic pressures?

A

raise both, therefore increasing MABP also!

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3
Q

What will norepinephrine do to HR?

A

keep it the same or DEcrease due to reflex bradycardia

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4
Q

When is norepinephrine used?

A

as a pressor in severe hypotensive states (EXCEPT if it is due to a loss of blood, because you will starve the kidneys where are already have reduced blood flow as that is a side affect of norepi)

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5
Q

What is phenylephrine?

A

selective alpha 1 direct-acting agonist used to increase BP (pressor) for hypotension, as a decongestant, or mydriatic (dilates pupils)

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6
Q

What is methoxamine?

A

slective alpha 1 direct-acting agonist used in hospital because it is I.V. only. This is a pressor, and also stimulates the release of NE.

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7
Q

What is pseudoephedrine (SUDAFED)?

A

selective alpha 1 direct-acting agonist used as a decongestant. Now controlled because people used it to make meth.

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8
Q

What are the adverse effects of alpha agonists?

A

anxiety, respiratory difficulty, forceful heart beat, headache (with overdose), severe hypertension, infiltration necrosis (I.V. drugs), and rebound nasal congestion.

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9
Q

What is clonidine?

A

selective alpha 2 direct-acting agonist that causes DECREASED sympathetic outflow and thus HYPOtension, sedation, and bradycardia. It does this by decreasing central outflow of impulses in the sympathetic nervous system by binding to a GPCR that is associated with the G-inhibitory subunit in the nucleus tractus solitatrius.

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10
Q

What mechanism functions with alpha receptors?

A

phosphatidylinosotol secondmessenger system. Agonist binds to alpha 1 receptor stimulating Gq to activate phospholipase C (or Gi for alpha 2; stopping sympathetic outflow), increasing intracellular IP3 and DAG. IP3 will free stored intracellular Ca++ to cause skin and splanchnic vessels along with iris to constrict causing pupil dilation and increased BP.

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11
Q

What is the mechanism for beta 1 receptors?

A

agonist binds to beta 1 receptor activating Gs protein, which uses GTP to activate adenylyl cyclase, which increases intracellular cAMP, activating PKA. This increases intracellular Ca++ in the HEART, thus increasing contractility and increased HR.

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12
Q

What are the the 2 beta 1 agonists?

A
  1. dobutamine= B1

2. isoproterenol= B1, and B2

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13
Q

What does isoproterenol do?

A

because B1 and B2= smooth muscle relaxation, skeletal muscle vasodilation decreasing TPR, increases cardiac output, and stimulates glycogenolysis in skeletal muscles, and relaxes myometrial (uterine) muscles.

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14
Q

What does dobutamine do?

A

selective B1 agonist used to increase CO and SV w/o much change in HR. This is used short term during cardiac surgery, for CHF, or in acute MI

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15
Q

What are the two most common short acting B2 agonists?

A

terbutaline and albuterol for bronchodilation during asthma attacks.

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16
Q

What are the adverse effects of beta agonists?

A

skeletal muscle tremor (B2), tachycardia (B1), hyperglycemia (B2)

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17
Q

What is epinephrine?

A

non-selective direct-acting adrenergic agonist that hits all receptors but in dose dependent manner.
Low dose= beta
High dose= alpha (predominates) and beta
Used to relieve respiratory distress due to bronchospasm, or to prolong the action of a local anesthetic (by constricting the vessels around the nerve)

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18
Q

What is dopamine?

A
  • low dose= activates the dopamine receptor (D1) causing vasodilation of renal, mesenteric, and coronary beds.
  • moderate dose= hits B1 receptor
  • high dose= release of NE
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19
Q

What is ephedrine?

A

mixed-acting adrenergic agonist that hits all receptors and used for nasal congestion, urinary incontinence, hypotension, and asthma.

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20
Q

For what are alpha adrenergic receptor antagonists (alpha blockers) used?

A
  • decrease BP and TPR
  • increase HR and CO (due to baroreceptor reflex)
  • enhance release of NE
21
Q

Are most alpha blockers competitive or non-competitive antagonists?

A

competitive

22
Q

What is phenoxybenzamine?

A

IRREVERSIBLE non-selective alpha blocker that treats pheochromocytoma (tumor of the chromaffin cells of adrenal gland) by inhibiting uptake system. It will decrease BP and cause reflect tachycardia.

23
Q

What are the side effects of alpha blockers?

A

postural (orthostatic) hypotension, tachycardia, inhibition of sperm production and inhibition of ejaculation.

24
Q

What is phentolamine?

A

REVERSIBLE non-selective alpha blocker that is similar to phenoxybenzamine, but shorter acting and doesn’t afffect ejaculation.

25
Q

What are the uses for alpha 1-selective blockers?

all names end with -osin

A

primary systemic hypertension, but side effects follow first-dose phenomenon (postural hypotension and syncope, but tolerance develops).

26
Q

What are prazosin, terazosin, doxazosin?

A

selective alpha-1 blockers that decreases TPR, thus decreasing preload and thus BP. There is NO effect on baroreflex.

27
Q

What is Yohimbine?

A

selective alpha-2 blocker that will INCREASE BP (remember alpha-2 is opposite) and HR, but used to treat psychogenic impotence (i.e. ED).
*Side note: this is found in some supplements, so be sure to ask a pt. if they are taking any supplements that may contain this if they begin to experience cardiac symptoms.

28
Q

What are the effects of beta blocking drugs?

all names end with -olol

A
  • decrease HR and contractility, thereby decreasing CO and BP :)
  • these also reduce O2 demand (increasing O2 supply) by decreasing the work of the heart
  • Thus they increase the mechanical efficiency.
  • they also influence rhythm by decreasing sinus (SA node) rate, decrease ectopic pacemakers, and decrease conduction in atria and AV node by increasing effective refractory period of the AV node.
  • This is what gives beta blockers their antiarrhythmic efficacy :)
  • they also attenuate release of renin (lowering BP)
  • decrease release of NE
  • decrease glycogenolysis (decrease glucose)
29
Q

What are the non-selective beta blocking drugs?

A

propranolol, timolol, nadolol, pindolol, cartelol, and penbutolol

30
Q

Would you use non-selective beta blocking drugs in an asthmatic?

A

no because it inhibits beta-2 receptors also (preventing bronchodilation).

31
Q

What is unique about propranolol?

A

it is the most lipid soluble, has HIGHEST membrane stabilizing effect, and has no partial agonist activity.

32
Q

What is unique about timolol?

A

NO intrinsic sympathomimetic activity (no partial agonist activity), NO membrane stabilizing effect, and used as ophthalmic solution to lower intraocular pressure in glaucoma.

33
Q

What is unique about nadolol?

A

similar to timolol, but longer lasting.

34
Q

What is unique about pindolol?

A

has intrinsic partial agonist (sympathomimetic) activity, like propranolol, but this one has LOW membrane stabilizing effect.

35
Q

What is unique about carteolol and penbutolol?

A

they both have some intrinsic partial agonist (sympathomimetic) activity.

36
Q

What makes beta-1 selective blockers better than non-selective?

A

These can be used with patients who have respiratory problems because they don’t block bronchodilation.

37
Q

What is metoprolol?

A

beta-1 selective blocker that has NO intrinsic sympathomemetic activity; complete blocking action. Also has low membrane stabilization.
*Most commonly used.

38
Q

What is unique about atenolol?

A

beta-1 seletive blocker that has NO intrinsic sympathomemetic activity and NO membrane stabilization

39
Q

What is unique about esmolol?

A

VERY FAST acting selective beta-1 blocker (I.V. only) for SVT emergencies.

40
Q

What are the adverse effects of beta blockers?

A

occur when dose is too high: CHF, bradyarrhythmia, bronchoconstriction (non-selective), and blunt the recogonition of hypoglycemia (in diabetics) so they don’t realize it, while delaying recovery from hypoglycemia.

41
Q

What is Labetalol?

notice spelling change -alol

A

nonselective beta-blocker that ALSO blocks alpha-1 receptors allowing greater affects of BP reduction (I.V. in hypertensive emergencies) by relaxing arterial smooth muscle, and because of beta-1 blockade you won’t see reflex tachy :)

42
Q

What is reserpine? (old drug)

A

adrenergic neuronal blocker that depletes adrenergic nerve endings of catecholamines by blocking transport into storage vesicles and MAO metabolizes it within the cytoplasm.

43
Q

What is guanethidine?

A

adrenergic neuronal blocker that blocks release of NE and thus NE will be metabolized by MAO (like reserpine). Very potent and used for sever hypertension.

44
Q

What is bretylium?

A

prevents release of NE from terminal and used as an antiarrhthymic.

45
Q

What is methyldopa?

A

DOPA with a methylated alpha carbon enters biosynthetic pathways forming methyl-NE which acts as a “false neurotransmitter.” Acts like alpha-2 agonist.

46
Q

What is tyramine?

A

displaces transmitter from axonal terminal acting as a sympathetic agonist.

47
Q

What are the MAO inhibitors?

A

Pargyline, Tranylcypromine, and Phenelzine, which all irreversibly inactivate MAO, thus increasing levels of catecholamines and serotonin (5-HT).
They are used as antiparkinsonian drugs and to treat atypical depression (due to increased serotonin).

48
Q

What is a major side effect of MAO inhibitors?

A

hypertensive crisis.
*Because many foods have tyramine in them, this will exacerbate this drug and therefore a dietician should be brought on board when using MAO inhibitors.

49
Q

What foods have lots of tyramine (contraindicated with use of MAO inhibitors)?

A

european beers, cheese, wines

CRP- Cardiology (49 decks)

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