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Care - Pharmacology 2024 > Lecture 7: ANS > Flashcards

Lecture 7: ANS Flashcards

1
Q

What is the difference between a preganglionic and postganglionic neuron?

A

Preganglionic starts in CNS, only has Ach for its NT
Postganglionic starts in autonomic ganglia, can use nictonic (Ach), muscarinic (Ach), or adrenergic (epi/norepi)

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2
Q

What is the function of the sympathetic nervous system and its other name?

A

Catabolic, fight or flight response
Thoracolumbar system

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3
Q

What is the function of the parasympathetic nervous system and its other name?

A

Anabolic, rest and digest
Craniosacral system

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4
Q

What is the key difference in response for the sympathetic and parasympathetic? Why does it occur?

A

Sympathetic is generally more widespread
Parasympathetic is localized

Sympathetic fibers are located farther from their target organ along the spinal column, while parasympathetic postganglionic neurons are right next to a target organ.

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5
Q

What is the primary NT secreted by postganglionic fibers of the sympathetic NS? What is the exception?

A

Norepi

The exception is the adrenal medulla, which is 80% epi & 20% norepi

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6
Q

What are the differences between epi and norepi?

A

Norepi is faster acting but has lower response in regards to beta stimulation.

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7
Q

What breaks down Ach?

A

Acetylcholinesterase

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8
Q

What are the monoamines?

A

Catecholamines, such as dopamine, epinephrine, and norepinephrine

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9
Q

What happens in the terminal pathway of monoamine creation?

A

Formation of EPI and NE

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10
Q

How are NE effects stopped?

A

Stopped mostly by reuptake of neuron it was secreted from.
Can also be inactivated by liver and brain enzymes.

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11
Q

What two enzymes metabolize/degrade EPI and NE?

A

COMT
MAO

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12
Q

What is the amino acid origin of dopamine?

A

Tyrosine

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13
Q

What is the monoamine synthesis pathway?

A

Tyrosine -> Dopa -> Dopamine -> NE -> Epi

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14
Q

Where do I find muscarinic and nicotinic receptors?

A

Muscarinic: GI tract, myocardium, blood vessels, exocrine glands, cerebral vasculature

Nicotinic: Skeletal muscle, adrenal medulla

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15
Q

What are the effects of a cholinergic agonist?

A

Eye: Miosis (pupil contraction)
Heart: Bradycardia
Respiratory: bronchial constriction + increased secretions
GI: increased motility
GU: relaxation of sphincters and bladder wall contraction
Glands: increased secretions

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16
Q

What is the mnemonic for cholingeric agonist effects?

A

DUMB BELS

Diarrhea
Urination
Miosis/muscle weakness
Bronchorrhea/bronchospasm
Bradycardia
Emesis
Lacrimation
Salivation/Sweating

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17
Q

What are the direct cholinergic agonists and their indications?

A

Bethanecol: Urinary retention
Pilocarpine: angle-closure glaucoma, miosis induction, Sjogren’s syndrome
Nicotine: Nicotine replacement therapy

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18
Q

What are the contraindications of direct cholinergic agonists?

A

Asthma, bradycardia/hypotension, CAD, epilepsy, GI inflammation/spasms, hyperthyroidism, parkinson’s, peptic ulcers, stroke, uncontrolled hypertension

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19
Q

What is the MOA and the PK of a direct cholinergic agonist?

A

Mimicking Ach and acting on muscarinic receptors.
Half life is <5 hours, dosed throughout the day.

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20
Q

What are the Acetylcholinesterase inhibitors and their indications?

A

Donepezil, Galantamine, Rivastigmine (Alzheimer’s)
Malathion: topical tx for lice

Alzheimer’s = the DRUGS are NOT for U, so DRG.

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21
Q

What is the common chemical characteristic of Alzheimer’s?

A

Low presence of Ach, which is why we use acetylcholinesterase inhibitors to prolong Ach.

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22
Q

What are the contraindications of acetylcholinesterase inhibitors?

A

Intestinal/urinary obstruction, bradycardia, or heart block. (Has powerful GI effects, so you need to titrate slowly)

Caution in GI ulcers, COPD, asthma, seizure, and CVD

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23
Q

What are the adverse effects of acetylcholinesterase inhibitors?

A

Muscle fasciculations and weakness in normal people.
Improve muscle strength in people with myasthenia gravis.

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24
Q

What is the key difference between acetylcholinesterase inhibtors vs cholinergic agonists?

A

Acetylcholinesterase inhibitors are designed to prevent Ach breakdown, so it lasts longer and exerts effects longer.

Cholinergic agonists simply work directly on receptors but still get broken down.

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25
Q

What is the MoA and PK for acetylcholinesterase inhibitors?

A

Inhibits the enzyme that breaks down Ach, which allows Ach to stick around and exert its effects.

Short half life of ~5 hours. Requires dosing throughout the day

26
Q

What are the general effects of anticholinergics/cholinergic antagonists?

A

Eye: Mydriasis, blurred vision
Skin: reduced sweating, flushing
GI: reduced motility, secretions
Cardio: increased HR (In high doses)
Lungs: bronchial dilation & decreased secretions
GU: Urinary retention
CNS: drowsiness, hallucinations, and coma

Can’t pee
Can’t see
Can’t spit
Can’t shit/poop

27
Q

What are the antimuscarinic drugs and their indications?

A

Ipratropium: COPD
Tiotropium: COPD, asthma
Umeclidinium: COPD
Scopolamine: motion sickness
Dicyclomine: IBS
Oxybutynin, Solifenacin, Tolterodine: overactive bladder

28
Q

What are the contraindications for antimuscarinics?

A

Glaucoma, gastric retention, urinary retention, ileus
Caution: Beer’s list

29
Q

What is Beer’s list?

A

A list of meds to be cautionary with in the elderly.

30
Q

What is the MOA and PK for antimuscarinics?

A

Competes with Ach for binding to the muscarinic receptors.

Short half life, metabolism is usually hepatic and excretion is renal.

31
Q

What are the neuromuscular blocker drugs?

A

Succinylcholine, cisatracurium, pancuronium, rocuronium, vecuronium (All given IV for rapid sequence intubation/paralytics)

Special: botulinum for prolonged muscle spasm and excessive sweating.
dantrolene for malignant hyperthermia

32
Q

What are the contraindications for neuromuscular blockers?

A

Myasthenia gravis and anyone not actively intubated or about to be intubated.

33
Q

What is the MOA and PK for neuromuscular blockers?

A

Interferes with the postsynaptic action of Ach & blocks action of Ach at nicotinic receptors.
Very short half lives (has a fast onset but fast offset also)

34
Q

What are the adverse effects of neuromuscular blockers?

A

Increased pulmonary vascular resistance, hypertension, hypotension, and tachycardia.

35
Q

What is our main alpha-1 agonist and its indications?

A

Phenylephrine: nasal congestion and hypotension during anesthesia.

36
Q

What is the MOA and PK of our alpha-1 agonist?

A

Powerful postsynaptic alpha-receptor agonist with minimal effect on beta receptors of heart.
Half life of 2-3 hrs via hepatic metabolism and renal excretion.

37
Q

What are the contraindications of an alpha-1 agonist?

A

Narrow-angle glaucoma, severe HTN, VTach, arteriosclerotic CVD, cerebrovascular disease

38
Q

What are the adverse effects of an alpha-1 agonist?

A

Rebound nasal congestion, HTN.
Serious: HTN crisis, heart failure, reflex bradycardia

39
Q

What is the alpha-2 agonist drug we learned? Indications?

A

Clonidine, used mainly for HTN but also used in opioid withdrawal, nictotine dependence, and ADHD.

40
Q

What is the contraindication for clonidine?

A

Hypotension

41
Q

What are the adverse effects of clonidine?

A

Headache
Xerostomia (dry mouth)
Somnolence (Drowsiness/strong desire to fall asleep)
Fatigue

42
Q

What is the MOA and PK of clonidine?

A

MOA: Stimulates alpha-2 receptors in the brain resulting in reduced sympathetic outflow from the CNS and decreased peripheral resistance, renal vascular resistance, heart rate, and BP
Short half life, must discontinue slowly due to rebound HTN, headache, and agitation

43
Q

What is our beta-1 agonist? Indications?

A

Dobutamine, used for decreased cardiac output, heart failure, and septic shock.

44
Q

What is the MOA and PK for dobutamine?

A

Synthetic catecholamine and direct acting inotropic agent. Stimulates beta receptors of the HEART, producing HTN, mild chronotropic, and arrthymogenic effects.
2 minute half-life, necessitating an IV drip.

45
Q

What is the contraindication for dobutamine?

A

Afib
(Dobutamine is an arrhythmogenic drug)

46
Q

What are the adverse effects of dobutamine?

A

CP, HTN, tachyarrhythmia, headache

47
Q

What are the two kinds of beta-2 agonists? Examples and indications?

A

SABA (Short acting beta agonist): Albuterol and Levalbuterol. AKA rescue inhalers

LABA (Long acting beta agonist): Salmeterol, Vilanterol, formoterol, indacaterol, olodaterol. AKA daily inhalers.

LABAs are used for COPD. SABAs are used for asthma.

48
Q

What is the MOA and PK of beta-2 agonists?

A

Sympathomimetic beta-2 adrenergic agonists that result in bronchial smooth muscle DILATION &
INHIBITION of the release of immediate hypersensitivity mediators from mast cells.
PK: SABAs last 4 hours while LABAs last around 12-24. They are all inhaled.

49
Q

What are the contraindications for beta-2 agonists?

A

Asthma for LABAs. LABAs require an additional inhaled corticosteroid if they are treating asthma.
SABAs can be used alone.

50
Q

What are the adverse effects of beta-2 agonists?

A

Tachycardia (SABAs), nausea, anxiety, tremor, bronchitis (misuse), and cough

51
Q

What are the 3 mixed adrenergic agonists and their different indications/effects?

A

EPI: Mix of all alpha and beta 1+2, used as a vasopressor (raise BP) in shock and anaphylaxis.

NE: Mix of all alpha and beta 1, used as a vasopressor to maintain MAP (Mean arterial pressure) in shock. AKA levophed

Isoproterenol: Mix of beta 1+2, uses lower peripheral vascular resistance and diastolic pressure, positive inotropic and chronotropic effects and prevention of bronchoconstriction.

52
Q

What are the alpha-1 blockers and their common indications?

A

Prazosin: HTN and night terrors.

Terazosin, Doxazosin, Tamsulosin, Alfuzosin: BPH (benign prostatic hyperplasia) AKA hard to pee

Note that all of these end with -sin

53
Q

What is the MoA for an alpha-1 blocker and its effects?

A

Block alpha 1 receptor, causing:
Decreased peripheral vascular resistance
Bladder neck smooth muscle
Prostate relaxation

54
Q

What are the contraindications for an alpha-1 blocker?

A

Hypotension

55
Q

What are the adverse effects of alpha-1 blockers?

A

Postural hypotension, reflex tachycardia, headache, abnormal ejaculation, and rhinitis

56
Q

What are the cardioselective betablockers and why are they cardioselective? Indications?

A

They select beta 1 only. Causes lowering of the heart rate. Indicated for arrhythmias and tachycardia

Atenolol
Bisoprolol
Esmolol (IV only)
Metoprolol

57
Q

What are the non-selective beta blockers? Why are they non-selective?

A

Propranolol
Nadolol (Portal HTN)
Timolol (Ophthalmic eye drops)

If taken systemically, they can cause bronchoconstriction at high dosages.

CONTRAINDICATED IN ASTHMA AND COPD

58
Q

What are the mixed alpha and beta blockers? What else do they do extra?

A

Labetalol
Carvedilol

Have mixed activity at alpha and beta receptors. They can cause decreased BP effects.

Note: these two end in -lol instead of -olol

59
Q

What are the indications and contraindications for BBs? (Beta blockers)

A

CHF (congestive heart failure)
Arrhythmias (including Afib)
Post-MI (Myocardial infarction)
HTN

Contraindications:
Cardiogenic shock
Decompensated HF
2nd/3rd degree heart block (brady arrhythmia)
Severe bradycardia
SSS (Sick Sinus Syndrome)

60
Q

What are the adverse effects of BBs? (Beta blockers)

A

Bradycardia, diarrhea, dyspnea, and fatigue.

61
Q

What 3 BBs (beta blockers) have reduced morbidity and mortality in HFrEF (Heart failure with reduced ejection fraction) patients?

A

Metoprolol succinate (This is the extended, once daily version of metoprolol)
Carvedilol
Bisoprolol.

Note: HFrEF is systolic heart failure, while HFpEF (heart failure with PRESERVED ejection fraction) is diastolic heart failure

Care - Pharmacology 2024 (18 decks)

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