Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NAS > WEEK 9 > Flashcards

WEEK 9 Flashcards

1
Q

Give 10 actions of Sympathetic innervation throughout the body

A

1) dilates pupils
2) inhibits saliva production
3) bronchodilation
4) raises heart rate
5) inhibits activity of digestive organs
6) inhibits activity of the pancreas
7) inhibits the gall bladder
8) stimulates the adrenal medulla to release adrenaline and noradrenaline
9) relaxes urinary bladder
10) stimulates orgasm in genitals of M+F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give 9 actions of Parasympathetic innervation throughout the body

A

1) constricts pupils
2) increases saliva production
3) bronchoconstriction
4) reduces heart rate
5) stimulates activity of digestive organs
6) stimulates activity of the pancreas
7) stimulates activity of gall bladder
8) constricts urinary bladder
9) stimulates erection of genitals of M+F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the neurotransmitter in the SNS from the Pre-G to the Post-G?

A

Acetylcholine (ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the receptor in the SNS from the Pre-G to the Post-G?

A

nicotinic Acetylcholine receptor (nAChR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the neurotransmitter in the SNS from the Post-G to the effector?

A

Noradrenaline (NAd)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the receptor in the SNS from the Post-G to the effector?

A

adrenergic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the neurotransmitter in the PNS from the Pre-G to the Post-G?

A

Acetylcholine (ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the receptor in the PNS from the Pre-G to the Post-G?

A

nicotinic Acetylcholine receptor (nAChR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the neurotransmitter in the PNS from the Post-G to the effector?

A

Acetylcholine (ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the receptor in the PNS from the Post-G to the effector?

A

muscarinic Acetylcholine receptor (mAChR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the small difference in the nicotinic cholinergic receptors in ganglia compared to at the NMJ?

A

At NMJ, the main receptor alpha-subtype is alpha-1. In the NS, it’s alpha-2-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is hexamethonium?

A

An antagonist for the neuronal subtype of nAChRs that is not competitive-blocks pores that open due to ligand binding (ACh can still bind)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the result of hexamethonium?

A

It blocks all effects of autonomic stimulation (both Symp. and Parasymp. effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the structure of muscarinic receptors?

A

7 transmembrane segments

5 subtypes, of which the first 3 (M1-M3) are particularly important in the periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are muscarinic agonists referred to as?

A

“Parasympathomimetic drugs” due to exposure mimicking effects of PNS activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the effects of parasympathomimetics?

A

Cardiovascular=decreased HR
Smooth muscle=contraction, although vascular smooth muscle dilates via endothelium->EDRF (endothelial derived relaxing factor)=nitric oxide
Exocrine glands=increased secretions (sweating/lacrimation/salivation/bronchial secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is muscarine?

A

A muscarinic agonist found in many mushrooms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the adverse effects of muscarine poisoning?

A

Bradycardia, vasodilation=decreased BP
Increased gut motility (colicky pain), bronchoconstriction, pupillary constriction (miosis)
Salivation, lacrimation, airway secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the treatment for muscarine poisoning?

A

Muscarinic antagonist (atropine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is pilocarpine?

A

A muscarinic agonist used to treat glaucoma

21
Q

What is the route of administration of pilocarpine?

A

Topical to the eye (eye drops)

22
Q

What is the mechanism of action of pilocarpine?

A

Acts on M3 receptors on ciliary muscles, improving aqueous humour drainage, dropping intraocular pressure

23
Q

What is the classification of muscarinic antagonists based on?

A

The binding to different receptor subtypes

24
Q

What are the 3 main classes of muscarinic antagonists?

A

M1: stomach, salivary glands
M2: cardiac muscle
M3: smooth muscle

25
Q

Which muscarinic antagonists are more common?

A

Less specific antagonists (eg. atropine, hyoscine)

26
Q

Give six clinical uses of antimuscarinic drugs

A

1) Asthma (ipratropium)
2) To treat bradycardia (atropine)
3) During operations: decreasing secretions, AChEI side effects (atropine)
4) To dilate pupils (tropicamide)
5) Urinary incontinence (oxybutynin or tolterodine)
6) Motion sickness (hyoscine)

27
Q

Detail and summarise the 5 main adrenoreceptor subtypes LOOK AT FULL TABLE IN NOTES

A

alpha1: contract smooth muscle (vasoconstriction)
alpha2: pre-synaptic auto-inhibition, direct vasoconstriction, central inhibition of sympathetic outflow
beta1: increased HR and contractility
beta2: relax smooth muscle (bronchodilation, vasodilation)
beta3: relax smooth muscle (bladder), stimulate lipolysis

28
Q

What are the main uses of alpha-adrenoceptor receptor agonists?

A 
Vasoconstrictors with LA (mainly alpha1)-adrenaline, noradrenaline
Nasal decongestants (mainly alpha1)-phenylephrine
Hypertension (central alpha2)
Facial erythema of rosacea (alpha2: direct vasoconstriction)-brimonidine
29
Q

Describe the process of alpha1 adrenoreceptor coupling to Phospholipase C-beta (PLC-beta) LOOK AT FULL TABLE IN NOTES

A

noradrenaline binds to alpha1 receptor, receptor activation causes G protein dissociation, Gq protein activates PLC-beta which produces a series of signalling molecules (IP3, DAG), IP3 has IP3 receptors on endoplasmic reticulum, when IP3 binds to these receptors Ca2+ is released and causes effect->contraction (vasoconstriction)

30
Q

What are the main uses of alpha-adrenoreceptor antagonists?

A

Hypertension (alpha1)-doxazosin

Benign prostate hyperplasia (alpha1)-tamsulosin

31
Q

What are the main uses of beta-adrenoreceptor agonists?

A 
Cardiogenic shock (beta1)-adrenaline, dobutamine
Anaphylactic shock (alpha/beta)-adrenaline
Asthma/Delay of premature labour (beta2)-salbutamol
32
Q

What are the main uses of beta-adrenoreceptor antagonists?

A

Metoprolol (beta1):
Angina, cardiac arrhythmias, hypertension, anxiety states, (chronic) heart failures
Timolol:
Locally for glaucoma

33
Q

What is responsible for noradrenaline uptake into vesicles?

A

tyrosine->dihydroxyphenylalanine (DOPA)->dopamine: travels into vesicles in the varicosities via VMAT (vesicular monoamine transporter) and forms noradrenaline

34
Q

What causes noradrenaline release?

A

Ca2+ intake results in vesicle fusion to the membrane and release of noradrenaline

35
Q

Where is noradrenaline uptaken after release from varicosities and how is it degraded in these cells?

A

In muscle and other cell types and degraded by Catechol-O-methyltransferase (COMT)

36
Q

How is noradrenaline uptaken into varicosities?

A

Via noradrenaline transporters (NAT)-main mechanism for terminating noradrenaline actions

37
Q

What is the role of monoamine oxidase (MAO)?

A

It degrades noradrenaline in the varicosities

38
Q

What does NAT cotransport?

A

Na+, Cl- and catecholamine

39
Q

What inhibits NAT?

A

Cocaine and tricyclic antidepressants (desipramine)

40
Q

What do NAT inhibitors do?

A

Enhance the effects of sympathetic activity by inhibiting noradrenaline uptake

41
Q

What is the action of desipramine?

A

Major action on CNS with adverse effects being bradycardia and dysrhythmia

42
Q

What is the action of cocaine?

A

Euphoria and excitement (CNS action) with adverse effects being tachycardia and increased BP (peripheral), also a local anaesthetic

43
Q

What are MAO inhibitors (MAOI) clinically used as?

A

Antidepressants

44
Q

Give some examples of MAO inhibitors

A

Phenelzine, tranylcypromine, moclobemide (reversible comp. inhibitor)

45
Q

What is the result of MAO inhibitors?

A

Increased levels of noradrenaline, dopamine and 5-HT in the brain and peripheral tissues

46
Q

What are the adverse effects of MAO inhibitors?

A

Postural hypotension, weight gain, restlessness, insomnia, cheese reaction

47
Q

What is the mechanism of action of indirectly acting sympathetic amines?

A

They are structurally related to noradrenaline and therefore transported into nerve terminals via NAT and into vesicles via VMAT, displacing noradrenaline which leaks out via NAT (similar effect on dopamine and 5-HT in CNS)

48
Q

What is the effect of indirectly acting sympathetic amines?

A

Long-lasting effects that mimic those of noradrenaline: bronchodilation, vasoconstriction, +ve inotropy, raised BP

NAS (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions