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Pharmacology (Fall) > ANS Con't - Adrenergic Agonists > Flashcards

ANS Con't - Adrenergic Agonists Flashcards

1
Q

What are Adrenergic Agonists?

A

• Stimulators (SYMPATHOMIMETIC) Mimic action of
norepinephrine, dopamine & epinephrine
• Can be selective or non-selective (of site, receptor subtype, tissue location)
• Almost all are at least partially non-selective (majority of side-effects

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2
Q

What are the uses of Adrenergic Agonists?

A

• HEMODYNAMIC compromise (shock, depressed cardiac rhythm)
• BRONCHOSPASMS (asthma)
• Nasal and sinus CONGESTION
• Often used in EMERGENCY situations

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3
Q

What is the prototype of Adrenergic Agonists?

A

• EPINEPHRINE: Also called ADRENALINE.
• Stimulates both alpha and beta receptors
• EMERGENCY drug: asthma, cardiac arrest, anaphylaxis
• Give PARENTALLY: GI tract enzymes destroy the drug.

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4
Q

Describe Epinephrine & what it’s used for

A

• Non-selective agonist. Used for
– Severe, acute bronchospasm
– Anaphylactic shock (type 1 hypersensitivity)
– Cardiac arrest (heart injection)
– Adjunct to anasthetic (why?)
Works fast, but short-acting

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5
Q

What are Epinephrines side effects?

A

•Stimulant effects on brain (anxiety, paranoia, headache, tremor)
• Hypertension-induced hemorrhage • Cardiac Arrythmia
• Hyperglycemia in diabetic

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6
Q

What are other non-selective agonists?

A

norephinephrine & pseudoephedrine

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7
Q

Norepinephrine:

A

Primarily used to treat shock (increases blood pressure)

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8
Q

What is shock?

A

massive drop in BP (faint b/c too much O2 in blood –> hyperventilate)

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9
Q

Pseudoephedrine:

A

Nasal decongestant

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10
Q

Describe brain-targeted non-selective Adrenergic Agonists

A

• Critical role of NE and dopamine in mood and motor control-Imp for depression, anxiety, Parkinson’s Disease
• Adrenergic Agonists (sympathomimetics) –like any drug-must cross the BBB to effect brain
• Many side effects come from undesired peripheral SNS activation

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11
Q

List brain-targeted non-selective Sympathomimetics

A
  • Cocaine
  • Amphetamines
  • Anti-Parkinsons Disease
  • Anti-depressants 1
  • Anti-depressants 2
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12
Q

Describe the brain-targeted Non-selective sympathomimetics: COCAINE

A

Inhibits the reuptake of serotonin, norepinephrine, and dopamine. Non- selective for receptor subtype and organ.
Peripheral activation causes side effects (HR, sweating, Hypertension, etc)

(medically used to stop bleeding locally & its a v. powerful anaesthetic even though its a stimulant)

(euphoric, energetic etc.)

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13
Q

What is the difference b/t cocaine & meth?

A

meth leaks it out so lasts longer (effect is much longer)

(*check to add more)

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14
Q

Describe the brain-targeted Non-selective sympathomimetics: AMPHETAMINES

A

Inhibits uptake and increases NT release (including serotonin and NE)
• Very potent effects in CNS and periphery- • Crystal Meth, RITALIN, MDMA (ecstasy)

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15
Q

Ectasy…the love drug?

A

makes you feel closer & more romantic
- take viagra with it (anti-stimulant)

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16
Q

Describe the brain-targeted Non-selective sympathomimetics: ANTI-PARKINSONS DISEASE

A

Monoamine Oxidase Inhibitor (MAOi) Example:
SELEGILINE (used with LEVADOPA)

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17
Q

What are side-effects of drugs for Anti-Parkinsons Disease
Monoamine Oxidase Inhibitor (MAOi) Example:
Selegiline (used with Levadopa)

A

Dry mouth
Constipation
Tachycardia

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18
Q

Describe the brain-targeted Non-selective sympathomimetics: ANTI-DEPRESSANTS 1

A

Monoamine Oxidase Inhibitor
• Example: PHENELZINE

19
Q

What are side effects (among others) of Anti-depressants 1
Monoamine Oxidase Inhibitor
• Example: Phenelzine

A

Dry mouth, constipation, urinary retention, mydriasis, hyperthermia, sweating, hypertension,

(act of SNS)

20
Q

Describe the brain-targeted Non-selective sympathomimetics: ANTI-DEPRESSANTS 2

A

Tricyclic Antidepressants (TCA)
• Example: Amytriptyline

21
Q

What are the Contraindications of brain-targeted Non-selective sympathomimetics: ANTI-DEPRESSANTS 2

A

Urinary retention
Pregnancy
Myocardial infarction
Congestive heart failure

22
Q

Describe Selective sympathomimetics

A

• Even if selective, almost always some “leaky” effect on other receptor types
▪ alpha1, beta1, beta2 Recall that alpha2 receptors inhibit sympathetic response, so activating alpha2 is not sympathomimetic

23
Q

Describe Peripheral sympathomimetics a1 agonist

A

• PRIMARY function of a1 is vasoconstriction, so drugs will be usually geared to this:
– Nasal decongestant- reduces blood flow, thus fluid release
– Increases peripheral resistance, thus increasing blood pressure (trauma, bleeding, shock)
– Example PHENYLEPHRINE

24
Q

What are side effects of a1 activation?

A

STIMULANT EFFECTS! Cocaine, nicotine,
caffeine, meth all stimulate adrenergic – Sweats, manic behavior, anxiety, paranoia – Increased thinking speed and reflexes
(any stimulant will increase IQ for time you’re on it (state-dependent))

Others:
Weight loss, hyperglycemia, impotence, hypertension, GI effects, exacerbation of prostatic urinary inhibition, bradycardia (hypertensive response)

25
Q

Describe B1 agonists

A

• Beta 1 activation causes:
• Increases: Heart rate, Force of contraction, Velocity of conduction
in AV node
– DOBUTAMINE: Increases – cardiac output- used in – congestive heart failure

26
Q

Describe B2 agonists

A

2 activation causes:
– Bronchial dilation, Relaxation of uterine muscle,Vasodilation,Glycogenolysis
– Almost exclusively found as inhalers – Bronchial dilation:
• SHORT ACTING: ALBUTEROL (SALBUTAMOL, VENTOLIN)-asthma, COPD (may increase death in COPD)
• LONG ACTING- SALMETEROL Works 12 hr vs 2 hr for albutarol – Other use- IV inhibition of preterm labor

27
Q

a1 primarily causes _______. So, agonists __________

A

vasoconstrictor

raise blood pressure and decrease local blood flow (PHENYLEPHRINE)

28
Q

B1 primarily ___________, so use to _______

A

stimulates the heart

increase cardiac activity (DOBUTAMINE)

29
Q

B2 primarily causes _________, so use for _________

A

bronchodilation

asthma & COPD (Salmeterol)

30
Q

What do Anti-Adrenergic Drugs do?

A

• INHIBIT OR BLOCK the effects of sympathetic nerve stimulation.
• Not naturally occurring: SYNTHETIC drugs
• Most block (ANTAGONIST action) alpha 1,
beta 1 and beta 2 receptors
• Alpha 2 agonists are adrenergic antagonists

31
Q

Alpha2-Adrenergic agonists are….

A

adrenergic antagonists

a2 agonists treat HTN.
• Despite being an AGONIST, produce BLOCKING OF RELEASE OF SYMPATHETIC neurotransmitter.
• INHIBIT RELEASE of norepinephrine in CNS
• Lower blood pressure
• CLONIDINE

32
Q

Describe a1 antagonists

A

Remember- a1 causes vasoconstriction and constriction of prostate neck
• Thus inhibition would….

• Treat hypertension: PRAZOSIN, DOXASIN- Competitive blockers of a1, causing decreased blood pressure
(stronger & faster than clonidine)

• Treat prostatic hypertrophy and vasospastic
(urinary) problems- TAMSULOSIN (more selective for a1A receptors on prostate)

• IN CONGESTIVE HEART FAILURE - Causes decreased preload and afterload by decreasing peripheral resistance (vasodilation)
– Means the heart has less resistance to contract against, leading to increased cardiac output,
decreased pulmonary congestion- PRAZOSIN
– So we can use one drug to ACTIVATE a SNS receptor subtype found on the heart (B1), to increase cardiac output, and a different drug to INHIBIT a SNS receptor subtype found on peripheral vessels (a1) to decrease peripheral resistance, to treat the same condition

33
Q

What are side effects to blocking a1 receptors?

A

Early on, causes massive orthostatic hypotension (fainting when standing - v. rapid drop in BP), so start with low doses
• Vertigo
• Sexual dysfunction
• Reflex Tachycardia (b/c of drop in BP)
• “floppy Iris Syndrome”

34
Q

What are Beta Blockers?

A

Used to treat rapid pulse arrhythmias, hypertension, MI, other heart problems
• DECREASE CONTRACTILITY, cardiac output, heart rate and blood pressure.
• REDUCE OXYGEN DEMAND on the heart.
• SLOW CONDUCTION through the AV node, slow the ventricular response (therefore, slow the heart)

(to reduce heart activity)

(when you have heart probs like this, you may also have changes in BP)

35
Q

What are the generations of B-blockers?

A

• 1st generation- Non selective (B1 and B2)
- block heart & lungs

• 2nd generation- Cardioselective (B1)
- selective to heart

• 3rd generation- Partially selective (with a1 inhibition)

36
Q

Describe nonselective beta blockers. & what they cause

A

block both beta 1 (heart) and beta 2 (lung) receptors.- Example PROPRANOLOL

• Can cause BRONCHOSPASMS: not for use with asthma (side effect on lungs)

37
Q

1st generation-Non-selective beta blocker - PROPANOLOL

A

– Decreases cardiac output

– Reflex peripheral vasoconstriction (slow decrease in hypertension)

– Bronchoconstriction (danger to asthmatics and COPD)

– Decreased glycogenolysis and glucagon secretion-this amplifies the effect of insulin on hypoglycemia.

38
Q

What are propanolol uses?

A

• Reduced hypertension through decreased cardiac output, decreased renin and decreased peripheral resistance (long term)
• Angina and Myocardial infarction from reduced oxygen demands
• Blocks the effect of hyperthyroidism on adrenergic system

39
Q

Other non-specific beta blockers:

A

TIMOLOL- Used for glaocoma by decreasing production of aqeous humor and intraocular pressure

40
Q

Describe a typical response to stress

A
  1. During stressful situation, brain tells adrenal glands to produce adrenaline
  2. Adrenaline flows through blood vessels to heart
  3. Adrenaline enters heart’s cells through receptors
  4. Heart rates goes up, producing fight-or-flight rxns
41
Q

Describe how beta-blockers short-circuit stress

A
  1. Beta-blockers enter the bloodstream through gastro-intestinal tract
  2. Beta-blockers prevent adrenaline from attaching to the receptors on the heart’s cells
  3. Heart rate stays normal; fight-or-flight rxns do not occur
42
Q

Describe 2nd generation- B1 specific blockers

A

• These are developed to specifically avoid
the BRONCHOCONSTRICTION of B2 receptors
• Used to treat hypertension- reduced pulmonary, vascular, and blood glucose effects
• Especially good for diabetic hypertensive patients (very common co-morbidity- DIABETIC OBESE HYPERTENSION)
• Example: ATENALOL

43
Q

Describe 3rd generation. Partial B1 receptor blockage (with examples described)

A

• Reduction in a receptor leads to reduced peripheral resistance, less load on heart

• CARVEDILOL: Higher affinity for b1 and b2, so reduces HR significantly and may exacerbate asthma

• LABETALOL: Higher affinity for a1, so reduce BP w/o large effect on resting HR. Used for pre-eclampsia and emergency

44
Q

B2 specific antagonists?

A

?

Pharmacology (Fall) (28 decks)

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