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Pharm S1 > EX 2 Lecture 7: ANS > Flashcards

EX 2 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- releases Ach as neurotrasnmitter
Postganglionic cell body in autonomic ganglia, can use nictonic (Ach), muscarinic (Ach), or adrenergic (epi/norepi)
contains nicotinic receptor to which the Ach binds

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2
Q

neuron pathway

A

sympathetic start in CNS and have a short preganglionic neuron that synapses with postganglionic neurons nicotinic receptor the long post ganglionic nueron then goes to target where it will synapse at muscarinic receptor for sweat glands, releasing ACh and at adrenergic receptors releasing Epi or Norepi for all other autonomic functions
parasympathetic start in CNS and have a long preganglionic neuron that synapses with postganglionic neuron nicotinic receptor releasing Ach, post ganglionic neuron then travels to target and synapses at muscarinic receptor and releases Ach

somatic has one motor nerve that synapses at target muscle via nicotinic receptor releasing Ach

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3
Q

what is the PNS

A

nerves that extend from the spinal cord to the organs and extremities

autonomic and somatic

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4
Q

afferent neuron

A

incoming
internal and external environment TO THE CNS

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5
Q

efferent neuron

A

exit/outgoing
CNS to body
control and integration of visceral function necessary for life/ CO, blood flow distribution, digestion

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6
Q

what does the autonomic nervous system require

A

requires pre and post ganglionic interaction to influence target organ, unlike somatic system

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7
Q

describe myelination of autonomic nerves

A

lightly myelinated preganglionic axons
unmyelinated postganglionic axons

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8
Q

what does the somatic system require

A

only ONE neuron to influence target organ
afferent nerves from environment to CNS and efferent nerves from CNS to muscle
heavily myelinated axons

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9
Q

autonomic nervous system (motor neurons) are for….

A

involuntary movements

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10
Q

somatic nervous system neurons are for

A

voluntary movements

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11
Q

all preganglionic neurons (sympathetic and parasympathetic are)

A

cholinergic ( release ACh at nicotinic receptor)

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12
Q

all parasympathetic postganglionic neurons are

A

cholinergic (release ACh at muscarinic receptor)

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13
Q

all sympathetic postganglionic neurons are____ except ____ which are ______

A

noradrengeric, sweat glands, cholinergic

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14
Q

role of ANS

A

maintain homeostasis
“autonomic takes care of automatic function”
- cardiovascular system (HR, CO, tone vasculature or constricting when dehydrated)
- smooth muscle for GI tract
- glandular function (adrenal, sweat,bladder)

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15
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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16
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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17
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 lateral to the spinal column, while parasympathetic postganglionic neurons are right next to a target organ instead of along vertebral column

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18
Q

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

A

Norepi (which interacts with a variety of receptors)

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

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19
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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20
Q

what does ACh interact with at the target organ in parasympathetics

A

muscarinic receptors

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21
Q

process of acetylcholin

A
  • acetyl coA + choline synthesized by ChAT into Ach
  • Ach transported from cytoplasm into vesicles by vessicle associated transporter VAT
  • action potential arrives at terminal and activated volt. gated Ca++ channels
  • influx of Ca++ triggers release of Ach from vesicle into nerve terminal (synaptic cleft influx)
  • acetylcholinesterase in synaptic celft breaks up Ach to choline and acetate (inactive)
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22
Q

half life of Ach

A

fraction of a second

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23
Q

What breaks down Ach?

A

Acetylcholinesterase

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24
Q

What are the monoamines?

A

Catecholamines, such as dopamine, epinephrine, and norepinephrine

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25
Q

synthesis pathways of monoamines

A

all linked by common synthesis pathway
tyrosine-> dopa->DA-> NE-> Epi

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26
Q

What happens in the terminal pathway (release) of monoamine creation?

A

Formation and release of EPI and NE to take action in the ANS

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27
Q

How are NE effects stopped/removed?

A

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

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28
Q

what is COMT /what does it do

A

liver enzyme that metabolizes endogenous and exogenous EPI and NE

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29
Q

what is MOA/ what does it do

A

enzyme that degrades EPI and NE

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30
Q

What is the amino acid origin of dopamine?

A

Tyrosine

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31
Q

monoamine synthesis pathway

A
  • synthesized from tyrosine to dopamine by tyrosine hydroxylase (TH)in nerve terminal
  • dopamine transported from cytoplasm to vesicles by vesicular monoamine transporter (VMAT)
  • dopamine covnerted to NE
  • action potential arrives at terminal, influx CA++ from volt gate channels
  • influx of Ca++ triggers release of monoamines
  • action termination by reuptake, diffusion, degradation, feedback mechanism
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32
Q

Where do I find muscarinic and nicotinic receptors?

A

Muscarinic(M1,2,3,4,5): GI tract, myocardium, blood vessels, exocrine glands, cerebral vasculature

Nicotinic(Nn, Nm): Skeletal muscle, adrenal medulla

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33
Q

norepinephrine receptors

A

alpha (a1,a2)
beta (b1,b2,b3)

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34
Q

where are a1 and a2 receptors in the body

A

a1- smooth muscle (vasculature-BP)
a2- platelets, lipocytes, smooth muscle

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35
Q

where are b1, b2, b3 receptors in the body

A

b1- heart
b2-lungs, skeletal vasculature (vasculature going to muscles)
b3- adipose tissue

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36
Q

receptors for dopamine and where they are located in the body

A

D1- brain, renal vascular bed
D2- brian, smooth muscle
D3- brain
D4- brain, cardiovascular system

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37
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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38
Q

What is the mnemonic for cholingeric agonist effects?

A

(side effects when using these drugs)
DUMB BELS

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

FAUCET ON- wet/fluid

39
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

(also cevimeline and methacholine)

40
Q

adverse effects of direct acting cholinergic agonists

A

DUMBBELS

41
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

42
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.

43
Q

What are the Acetylcholinesterase inhibitors and their indications?

A

Donepezil, Galantamine, Rivastigmine (Alzheimer’s- slow progression of memory loss)
Malathion: topical tx for lice

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

44
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.

start with very low dose and increase slowly bc of GI upsets- throat tears from emesis can occur

45
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

46
Q

What are the adverse effects of acetylcholinesterase inhibitors?

A

DUMBBELS …due to action at nicotinic receptors they cause…
Muscle fasciculations and weakness in normal people.
Improve muscle strength in people with myasthenia gravis( increases msucle control bc they have a problem there).

47
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.

48
Q

What is the MoA and PK for acetylcholinesterase inhibitors?

A

Inhibits the enzyme that breaks down Ach (into choline and acetate), which allows Ach to stick around and exert its effects

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

49
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
FAUCET OFF- everything dries up

50
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

51
Q

What are the contraindications for antimuscarinics?

A

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

52
Q

What is Beer’s list?

A

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

53
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.

54
Q

what are the adverse effects of antimuscarinics?

A

anticholinergic side effects (cant pee, cant see, cant spit, cant shit)

55
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

56
Q

What are the contraindications for neuromuscular blockers?

A

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

57
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)

58
Q

What are the adverse effects of neuromuscular blockers?

A

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

59
Q

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

A

Phenylephrine: nasal congestion and hypotension during anesthesia(not as intense as NE).

nasal congestion is our body’s response of inflammation and vasodilation- this drug constrict back down and decreases congestion (dayquil)

60
Q

effect of adrenergic agonist at A1 receptor

A

constriction of vascular smooth muscle (increase BP)

61
Q

effect of adrenergic agonist at A2 receptor

A

decrease blood pressure through central action (brain tells body to decrease BP)

62
Q

effect of adrenergic agonist at B1 receptor

A

increase heart rate (beta blocker to decrease HR)

63
Q

effect of adrenergic agonist at B2 receptor

A

relax respiratory and uterine smooth muscle (asthma, COPD)

64
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.

65
Q

What are the contraindications of an alpha-1 agonist?

A

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

66
Q

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

A

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

67
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 (and sleep).

68
Q

What is the contraindication for clonidine?

A

Hypotension

69
Q

What are the adverse effects of clonidine?

A

Headache
Xerostomia (dry mouth)
Somnolence (Drowsiness/strong desire to fall asleep- advantage for ADHD)
Fatigue

70
Q

when is clonidine usually used

A

after other drugs have been tried, toward bottom of usage pole

71
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

72
Q

What is our beta-1 agonist? Indications?

A

Dobutamine, used for decreased cardiac output, heart failure, and septic shock (if results in cariogenic shock).

73
Q

What is the MOA and PK for dobutamine?

A

Synthetic catecholamine and direct acting inotropic agent(increase force contraction of heart). Stimulates beta receptors of the HEART, producing HTN, mild chronotropic (increase speed of heart), and arrthymogenic (arrthymia) effects.
2 minute half-life, necessitating an IV drip.

74
Q

What is the contraindication for dobutamine?

A

Afib (or other fatal arrythmias)
(Dobutamine is an arrhythmogenic drug)

75
Q

What are the adverse effects of dobutamine?

A

CP, HTN, tachyarrhythmia, headache

76
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.

77
Q

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

A

Sympathomimetic beta-2 adrenergic agonists that result in bronchial smooth muscle DILATION (relaxation) &
INHIBITION of the release of immediate hypersensitivity mediators from mast cells.( decrease mast cells)

PK: SABAs last 4 hours while LABAs last around 12-24. They are all inhaled.

78
Q

What are the contraindications for beta-2 agonists?

A

Asthma for LABAs. LABAs require an additional inhaled corticosteroid if they are treating asthma (in same formula).
SABAs can be used alone.

79
Q

What are the adverse effects of beta-2 agonists?

A

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

80
Q

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

A

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

NE: Mix of alpha 1 +2 and beta 1, used as a vasopressor to maintain MAP (Mean arterial pressure) in shock. AKA levophed (common IV vasopressor in ICU)

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

81
Q

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

A

Prazosin: HTN and night terrors (esp with hx PTSD).

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

Note that all of these end with -sin

82
Q

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

A

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

83
Q

What are the contraindications for an alpha-1 blocker?

A

severe hypotension

84
Q

What are the adverse effects of alpha-1 blockers?

A

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

85
Q

What are the beta 1 selective 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

86
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 (will cause bronchoconstriction at B2)

87
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

88
Q

What are the indications for BBs? (Beta blockers)

A

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

89
Q

what are the contraindications of BBs

A

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

90
Q

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

A

Bradycardia, diarrhea, dyspnea, and fatigue.

91
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

92
Q

why is it important to wean patients off of beta blockers

A

rebound tachycardia

93
Q

what would be a good choice for someone who has atrial fibrilation and hypertension

A

cevedolol (only 2 times per day)/ levatolol ( more often)

decrease HR and BP

Pharm S1 (18 decks)

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