ANS Flashcards

1
Q

Summarise how the ANS works and what it consists of

A
  • ANS consists of sympathetic and parasympathetic NS.
  • They involve 2 synapse pathways - preganglionic + postganglionic (adrenal medulla - one long ganglionic nerve)
  • SNS uses Ach as neurotransmitter and NA at the organ (some exceptions - sweat gland)
  • PSNS uses only Ach at the ganglia and organ
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2
Q

Receptors - ANS

A

Cholinergic:
* Nicotinic
* Muscuranic (m1,m2,m3)

Adrenergic:
* Alpha (a1,a2)
* Beta (B1,B2,B3)

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3
Q

Drugs that increase/decrease nervous system function

A
  • Sympathomimetic - increase/mimic NS function
  • Sympatholytic - decrease/block NS function

same for PSNS

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4
Q

Do ANS drugs have specifcity, selectivity

A

ANS drugs show selectivity but not Specifity. So, a drug affecting one receptor subtype will interact/alter other recptor subtypes.

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5
Q

effects of parasympathomimetic drugs

A
  1. increased salivary/bronchial secretions
  2. increased peristalsis
  3. bronchoconstriction
  4. bradycardia/hypotension (low heart rate, low BP)

Large doses causes over stimulation

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6
Q

Pilocarpine

Parasympathomimetic

A
  • used to treat glaucoma
  • muscuranic acetylcholine receptor agonist
  • eye drops cross conjunctival membrane
  • pupilary constriction, reduction of intraoccular pressure
  • side effects:
  • allergic conjunctivitis, blurred vision, lid twitching
  • nausea, vomitting, bradychardia, bronchoconstriction, hypotension
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7
Q

Bethanechol

parasympathomimetic

A
  • selective mAchR - does not cross BBB
  • Laxative (enhances parasympathetic activity therefore increased GI motility)
  • rarely used due to side effects
  • Side effects on bladder:
  • hypotension/bradycardia
  • increased GI motility/pain
  • bronchconstriction
  • increased salivation/sweating
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8
Q

muscuranic receptor agonist effects

A

Cardiovascular:
1. slowed heart beat
2. decreased cardiac output
3. decreased force of contraction
4. generalised vasodilation

  • Smooth muscle:
  • gastrointestinal
  • detrusor constriction
  • airway constriction

gland stimulation:
1. salivary
2. sweat
3. bronchial
4. pancreatic
5. gastric

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9
Q

Neostigmine

A
  • increases availability of Ach to outcompete muscle relaxant (mr) therefore reversing effects of (mr)
  • carbymalates the enzyme, which takes minutes to hydrolyse/reverse
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10
Q

AchE inhibitors

A

Donepazil - medium acting AchE inhibitor
* limited use due to adverse effects and so benifit must outweigh side effects

Side effects: nausea vomitting, increased GI motility, urinary incontinence, bradycardia

parasympathomimetic and CNS

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11
Q

mAchR antagonists

parasympaholytic

A

These drugs block the M receptors and so produce the oppisit effect of the mAchR agonists

effects:
dry mouth
gastric secretion
bronchial glands - mucus clearance inhibition
increased heart rate
reduced GI motility (constipation)
bronchodilation
urinary tract relaxation

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12
Q

Atropine

A
  • antimuscarinic (mAchR antagonist)
  • used to treat low heart rate by blocking m2 receptors increasing heart rate
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13
Q

Uses of antimuscarinics

A
  • Asthma - short term releif of symptoms (bronchodilation)
  • motion sickness - hyoscine
  • parkinsons
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14
Q

Autonomic ganglia stimulants

A
  • stimulates the nicotinic receptors found at the preganglionic neurones
  • can produce excitatory and inhibitory depending on the receptor classes effected
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15
Q

side effects of autonomic ganglia stimulants

A
  1. gi disturbances
  2. dizziness
  3. flu like symptoms
  4. heart rate

cautions in:
cardiovascular disease
diabetes
peptic ulcers

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16
Q

autonomic ganglia blockers

A
  • produce a bigger effect on SNS as blockage of these receptors = vasodilatory effect, as decreasing release of noradreneline
17
Q

Adrenaline

A

*A&B adrenergic agonist
* caridac arrest - IV
* Anaphylactic shock - IM, IV emergency, EpiPEN
*Used with local anesthetics - allows LA to remain and work in that area for longer, also slowls rate of absorption and prolongs action

18
Q

Alpha adrenergic agonists

A
  • Vascular smooth muscle contraction
  • Skin constriction
  • veins, arteries constriction
  • decreased vascular compliance
  • decreased central venous pressure
  • increased peripheral resistance
  • increased BP initiates baroreceptor reflex
  • cerebral/coronary/pulmanory beds unaffected
  • INCREASED SYSTOLIC & DIASTOLIC BLOOD PRESSURE INCREASED CARDIAC WORK
  • decongestants
19
Q

types of a1 adrenergic agonists

A

a1:
* phenylephrine - contraction of nasal passages

a2:
* Clonidine
* antihypertension & migraine
* centrally acting hypertensive
* decreases cardiac output & peripheral resistance
* cannot withdraw treatment suddenly (hypersensative crisis)

Side effects:
* sedation
* depression
* fluid retention
* constipation

20
Q

B receptor agonists

A
  • works on smooth muscle
  • relaxation
  • GI tract relaxation
21
Q

B adrenergic agonists

NT, H

A

Nerve terminals:
* presynaptic adrenoreceptors are found on both adrenergic and cholinergic nerves
* Main action: a2 adrenoreceptors inhibitory (main action)
* Weak action - B-adrenoreceptor facilitation

Heart:
* B1-adrenoreceptor powerful stimulant action on heart
* heart rate and force of contraction increased
* increased cardiac output and oxygen consumption

22
Q

B adrenergic agonists

A

Metabolism:
B1,B2 adrenoreceptors located in the liver increase availability of glucose

23
Q

B1 adrenergic agonist

A

Dobutamine:
* septic shock
* increased contractility
* IV administration

24
Q

B2 adrenergic agonist

A

Salbutamol:
* bronchial smooth muscle dilated by the activation of B2 adrenoreceptors
* uterine smooth muscle dilated by the activation of the B2 adrenoreceptors
-can delay premature labour

25
Q

B adrenoreceptor antagonists

A

Treatment of cardiovascular disease
* angina
* myocardial infarction
* heart failure
* hypertension

anxiety systems
controls tremor/palpitations

migraines

26
Q

selective a1 antagonist

A

prazosine - first selective antagonist
doxazosine (Longer half life)

Vasodilation and fall in blood pressure
blockade of a1 mediated vasoconstriction
increased cardiac output (reflex to decreased BP)
additional bloackade of a2 adrenoreceptor increases noradrenaline release (enhanced heart rate)

27
Q

B adrenergic antagonists

A

antihypersensative action
- patients with hypertension have gradual fall in arterial pressure
- due to reduction in cardiac output
- reduction of renin release
- central action decreases sympathetic activity

28
Q

Selective B antagonists

A
  • propanolol - non selective B-blocker B1B2
  • atenolol - selective B1 blocker
29
Q

B blocker side effects

A
  • Bronchoconstriction
  • cardiac depression
  • bradycardia
  • hides hypoglycemia symptoms
  • fatigue
  • cold extremities