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M2-2 > PharmacologyANS > Flashcards

PharmacologyANS Flashcards

1
Q

Breakdown of Peripheral NS

A
  • Sensory neurons and motor neurons

- Motor neurons have somatic, autonomic and enteric （腸の）NS

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2
Q

Effectors (muscle/glands) for somatic NS

A

skeletal muscle

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3
Q

Effectors (muscle/glands) for autonomic NS

A

smooth and cardiac muscle, glands

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4
Q

Effectors (muscle/glands) for enteric NS

A

fx: gastrointestinal innervation

smooth muscle, glands and endocrine cells of GI tract

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5
Q

NT released from CNS

A

Ach, nicotinic Ach ONLY!!!

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6
Q

NT released in parasympathetic NS

A

CNS -Ach(nic)—Ach(mus)—> salivary glands etc

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7
Q

NT released in sympathetic NS

A

CNS -Ach(nic)—NA—> blood vessels etc (most common)
CNS -Ach(nic)—Ach(mus)—> sweat glands etc
CNS -Ach(nic)——> adrenal medulla

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8
Q

α-, ß1- or ß2-adrenoceptors

A

Deactivation by reuptake

Adrenaline can be directly released from adrenal medulla

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9
Q

Ach deactivation by

A

acetylcholinesterase

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10
Q

What’s special about penis regarding NT?

A

cavernous nerves release nitric oxide (NO) in the penis.
- relaxes the smooth muscle of the corpora cavernosa via cyclic guanosine monophosphate allowing expansion of the lacunar spaces and erection

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11
Q

All the preganglionic nerve fibres

A

(for both sympathetic and parasympathetic) are myelinated and release acetylcholine from the nerve terminals

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12
Q

How is (post)ganglionic neurons activated?

A

Ach depolarizes the ganglionic neurons by activating nicotinic receptors

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13
Q

Afferent sensory fibres carry info to

A

centers in the hypothalamus and

medulla

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14
Q

IG: What is the drug for erectile dysfunction

A

Sildenafil, used in male sexual dysfunction, inhibits phosphodiesterase type 5 and, by increasing the concentration of cGMP, facilitates erection.

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15
Q

Sympathetic NS characteristics

A
  • Sympathetic from thoracolumbar region (T1-L3)

- synapse either in the paravertebral ganglia or in the prevertebral ganglia and plexuses in the abdominal cavity

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16
Q

Parasympathetic NS characteristics

A
  • the preganglionic fibers leave the central nervous system via the cranial nerves (especially Ill, VII, IX and X) and the third and fourth sacral spinal roots.
  • often travel much further than sympathetic fibers before synapsing in ganglia, which are often in the target regions itself
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17
Q

How do agonist-R complex get activated?

A

AR + transducer -> ART*

arrow represents intrinsic efficacy (Kar)

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18
Q

What is Ach released from and its effect?

A
  • All preganglionic autonomic nerves (i.e. both sympathetic and parasympathetic).
  • Some postganglionic sympathetic nerves (i.e. thermoregulatory sweat glands and skeletal muscle vasodilator fibres).
  • Nerve to the adrenal medulla.
  • Somatic motor nerves to skeletal muscle endplates. Some neurones in the central nervous system.

Effect:
vasodilation
bradycardia (slow down of heart rate)

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19
Q

Ach R/cholinoceptors

A

2 subtypes

1) nicotinic … determined by measuring the sensitivity of various tissues to the drugs nicotine (ligand gated)
2) muscarinic … determined by measuring the sensitivity of various tissues to the drugs muscarine (GPCR)

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20
Q

Postganglionic relationship between NA and Ach

A

NA (sympathetic) and Ach (para) negatively linked to each other
=> inhibitory effect of adrenaline on acetylcholine release

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21
Q

Tissue response (slow/medium/fast) depending on NT from para and sym

A

from para/sym
slow VIP/NPY
medium NO/NA
fast Ach/ATP

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22
Q

Many noradrenergic and cholinergic terminals have

A

presynaptic inhibition

meaning NT excites to other place but have negative feedback to its own NT release (self regulated)

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23
Q

IG: Noradrenergic/cholinergic terminals in heart

A

heterotropic presynaptic inhibition
meaning neurotransmitter X andY give negative feedback to each other while X stimulate another place and Y inhibit the same place (X and Y fight)

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24
Q

IG: Postsynaptic Synergism example

A

examples of non-adrenergic+ non-cholinergic (co-)transmitters

1)Noradrenaline/NPY in blood vessels
X excite a target, Y positively excites it too

2)Noradrenaline/ATP in blood vessels
Ach/GnRH in sympathetic ganglia
Ach/SP in enteric ganglia
One NT X have fast response, while Y have slower response to the same target

3) Ach/VIP in salivary gland
X excites target A (glands), Y excites target B (blood vessel)

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25
Q

Types of parasympathetic drugs

A

parasympathomimetics (increase Ach activity)
and parasympatholytics (decrease)
can act directly or indirectly

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26
Q

Atropine

A

muscarinic receptor blocker

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27
Q

Muscarinic receptor

A
  • Mostly founds on glands and are dose dependent
  • The effects of acetylcholine are usually excitatory, but an important exception is the heart, which receives inhibitory cholinergic fibers from the vagus.
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28
Q

Parasympathetic drugs

A

Drugs that mimic the effects of acetylcholine are called cholinomimetics and can be divided into two groups: drugs that act directly on receptors (nicotinic and muscarinic agonists); and anticholinesterases, which inhibit acetylcholinesterase and so act indirectly by allowing acetylcholine to accumulate in the synapse and produce its effects.

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29
Q

sympathomimetics effects and use @ heart

A

HeartFailure decrease
negative inotropic

symptom: supraventricular tachycardia (too fast heart rate)

30
Q

sympathomimetics effects and use @ gut

A

peristaltic (wave-like movement) increase

symptom: atonia(無緊張（症）、弛緩（症), functional impairment of
the bladder (post op)
31
Q

sympathomimetics effects and use @ glands

A

secretion increase (sweating !)

symptom: Mucoviscidosis - diagnostic (Pilocarpine iontophoresis)

32
Q

sympathomimetics effects and use @ eye

A

miosis, aqueous humor

symptom: glaucoma

33
Q

sympathomimetics side effects

A 
cardiodepression
diarrhea, nausea, emesis
bronchoconstriction, sweating
disturbance of accomodation
even possible if applied locally !
34
Q

sympathomimetics contraindications

A

cardial insuffizience
Asthma bronchiale

KI also for local treatment !

35
Q

Areca nut

A
  • areca nutis chewed along withbetel leafto obtain astimulatingeffect.
  • areca nut chewing is carcinogenic
36
Q

Central effects of sympathomimetics

A

„analeptic“
Stimulation of ventilation
(in high doses vent. arrest)

no therapeutic use

e.g. pilocarpine, arecoline

37
Q

Parasympathetic Nervous system is on…

A

rest and digest

  • pupil contrict!
  • salivation stimulate
  • heart slows
  • constrict breathing!
  • digestion stimulated
  • gallbladder stimulated
  • bladder constricted!
  • sex organ stimulated
38
Q

Atropa BellaDonna

A

debated whether it is a drug or poison

39
Q

muscarinic antagonists

A

atropine, scopolamine

40
Q

Ideal relaxants

A
  • Nondepolarizing
  • Rapid onset
  • Dose-dependent duration
  • No side-effects
  • Elimination independent of organ function
  • No active or toxic metabolites
41
Q

Structural classes of nondepolarising relaxants

A

Steroids: Rocuronium bromide, Vecuronium bromide, Pancuronium bromide, Pipecuronium bromide

Naturally occurring benzylisoquinolines: curare, metocurine

Benzylisoquinoliniums: Atracurium besylate, Mivacurium chloride, Doxacurium chloride

42
Q

IG: Duration of action of neuromuscular blocking agents

A

Ultra-Short: Succinylcholine
Short: Mivacurium
Intermediate: Rocuronium, Vecuronium
Long: Pancuronium, curare, Doxacurium

43
Q

Sympathetic nervous system is on…

A

FIGHT or FLIGHT

  • pupil dilate!
  • CNS, brain, alertness increase
  • salivation reduce
  • bronchi気管支 dilate
  • skin sweat
  • heart rate increase
  • digestion reduced
  • liver release Glu
  • bladder reduce in muscle, increase in tone
  • muscle increase
44
Q

NE receptor

A

-sympathomimetic agent; it mimics sympathetic effects
There are two types:
-α1 @ postsynaptic… occur in a few tissues, e.g. brain, vascular smooth muscle
-α2 @ presynaptic… stimulation by NE reduce NT release (negative feedback); more common
-β1,2,3
*different types found in different region/tissue

45
Q

NA (sym) and Ach (para) related by

A

negative feedback to each other

46
Q

NA effector

A

sympathetic; smooth muscle

47
Q

Ach effector

A

para; exocrine gland & endothelial cells

48
Q

What does agonists for adrenoceptors do?

A

Agonists at adrenoceptors (direct adrenomimetics) mimic the actions of the naturally occurring catecholamines, NA and epinephrine, and are used for various therapeutic effects

49
Q

Norepinephrine (noradrenaline) prefer which receptor?

A

α1, α2!!! β1 and β3, but not β2 action

50
Q

Epinephrine (adrenaline) prefer which receptor?

A

α1, α2, β1 and β2 and weak β3 action

51
Q

Isoproterenol (isoprenaline) prefer which receptor?

A

β1 and β2, but not α action

52
Q

Action on alpha-adrenoceptors

A

More like constriction but ejaculate
-Contraction of arterioles and veins: raise in BP (α1)-
-Contraction of radial muscules of iris: mydriasis and
decreased aqueous secretion (α1)
-GIT: intestinal relaxation, contraction of sphincters
-Bladder trigone: contraction
-Uterus: contraction
-Splenic capsule: contraction
-Neuromuscular transmission: increased ACh release
-Insulin secretion: inhibited (α2 dominant)
-Mail sex organs: ejaculation
-Salivary glands: K+ and water secretion (α1)
- Nictitating membrane in cats: contraction (α1)

53
Q

Action on beta-adrenoceptors

A

more like parasympathetic but glycogenolysis at liver
-Dilatation of arterioles and veins (β2): fall in BP
-Cardiac stimulation (β1): increased heart rate,
force and conduction velocity
-Bronchodilation (β2)
-Eye: enhanced aqueous secretion
-GIT: intestinal relaxation (β2)
-Bladder detrusor: relaxation
-Uterus: relaxation (β2)
-Neuromuscular transmission: tremor (β2)
-Augmented insulin and glucagon secretion (β2)
-Liver: glycogenolysis (β2)
-Fat – lipolysis (β3), Kidney – renin release (β1)
-Posterior pituitary: ADH secretion (β1)

54
Q

isoproterenol

A

analog of epinephrine

55
Q

bronchodilation

A

Primarily sites of broncho気管支dilation action of inhaled β2-adrenergic agonists is mainly bronchiolar smooth muscle. Atropinic drugs cause bronchodilation by blocking cholinergic constrictor tone, act primarily in large airways

56
Q

β2-adrenomimetics used for

A 
tocolytic effect:
Fenoterol (Partusisten: tab. 5 mg)
Hexoprenaline
Salbutamol (Salbupart)
Terbutaline
57
Q

IG: (a plant) Ephedra equsetina

A

Ephedrine with anti-hypotensive and anti-asthmatic effects AR: tachyphyllaxis

tachyphyllaxis:
rapidly diminishing response to successive doses of a drug, rendering it less effective

58
Q

Drug misuse

A

refers to the use of a drug for purposes for which it was not intended or using a drug in excessive quantities

59
Q

Indirect sympathomimeticswith central

stimulant activity and abuse potential

A

Amphetamine

Cocaine

60
Q

doping with drugs acting in the ANS

A

-beta blockers
beta-blockers have a relaxing effect on muscle function, gaining the drug class a popular reputation as a performance-enhancement drug for athletes
-beta-2-agonists

61
Q

How does beta-blockers work?

A 
beta-blockers have a relaxing effect on muscle function, gaining the drug class a popular reputation as a performance-enhancement drug for athletes who benefit from the adrenaline-blocking effects of the medication.
e.g. less tremor
62
Q

How does beta-2-agonists work?

A

All beta-2 agonists are prohibited at all times (training and competition). Four active substances are approved for inhalation: formoterol, salbutamol, salmeterol, terbutaline. The inhalative administration of the four beta-2-agonists is allowed. Their use for treatment is subject to a Therapeutic Use Exemption (TUE)

63
Q

IG: Pilocarpine

A 
muscarinic agonist
(as eye drops) is sometimes used to reduce intraocular pressure in patients with glaucoma
64
Q

IG: Bethanechol

A

muscarinic agonist

used to stimulate the bladder in urinary retention, but it has been superseded by catheterization

65
Q

Anticholinesterases

A

relatively little effect at ganglia and are used mainly for their nicotinic effects on the neuromuscular junction. They are used in the treatment of myasthenia gravis and to reverse the effects of competitive muscle relaxants used during surgery

66
Q

Muscarinic antagonists

A

block the effects of acetylcholine released from postganglionic parasympathetic nerve terminals. Parasympathetic effector organs vary in their sensitivity to the blocking effect of antagonists. Secretions of the salivary, bronchial and sweat glands are most sensitive to blockade.
Higher doses of antagonist dilate the pupils, paralyze accommodation and produce tachycardia by blocking vagal tone in the heart. Still higher doses inhibit parasympathetic control of the gastrointestinal tract and bladder.

67
Q

What are Catecholamines

A

NE and epinephrine

68
Q

Catecholamines

A

Involved in sympathetic nervous system
Inactivated by reuptake
Sympathomimetics: drugs that partially or completely mimic the actions of norepinephrine and epinephrine

69
Q

Sympathomimetics

A
  • drugs that partially or completely mimic the actions of norepinephrine and epinephrine
  • Act either directly on a- and/or β-adrenoceptors or indirectly on the presynaptic terminals, usually by causing the release of norepinephrine.
  • For example, ß2-Adrenoceptor agonists cause bronchial dilatation and are used in the treatment of asthma. They are also used to relax uterine muscle in an attempt to prevent preterm labour
70
Q

Adrenoceptor agonist

A

(e.g. dobutamine) are sometimes used to stimulate the force of heart contraction in severe low-output heart failure. α1-agonists (e.g. phenylephrine) are used as mydriatics and in many popular decongestant preparations.
Agonists, notably clonidine and methyldopa (which acts after its conversion to αmethylnorepinephrine, a false transmitter), are centrally acting hypotensive drugs

71
Q

Amfetamine

A

Sympathomimetic amines that act mainly by causing norepinephrine release (e.g. amfetamine) have the selectivity of norepinephrine, in addition to causing norepinephrine release. Amfetamine also has a direct action. Its effects are similar to these of epinephrine, but last much longer. Ephedrine is a mild central stimulant, but amfetamine, which enters the brain more rapidly. has a much greater stimulant effect on mood and a depressant effect on appetite. Amfetamine and. similar drugs have a high abuse potential and are rarely used.

72
Q

ß-blockers

A

ß-Adrenoceptor antagonists (ß-blockers) are important drugs in the treatment of hypertension, angina, cardiac arrhythmias, heart failure and glaucoma. α-Adrenoceptor antagonists (α-blockers) have limited clinical applications. Prazosin, a selective αI-antagonist, is sometimes used in the treatment of hypertension. Phenoxybenzamine, an irreversible antagonist, is used to block the α-effects of the large amounts of catecholamines released from tumours of the adrenal medulla (phaeochromocytoma). Phentolamine, a shortacting drug, is used during surgery of phaeochromocytoma

M2-2 (10 decks)

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