3.0 Peripheral Nervous System Flashcards

Question 1

Q

Where does PSNS originate from?

Answer

A

Craniosacral (CNs III, VII, IX and X + pelvic splanchnics)

Question 2

Q

Where does the SNS originate from?

Answer

A

Thoracolumbar (T1 → L2/3)

Question 3

Q

What neurotransmitter is the exception by not being stored in vesicles?

Question 4

Q

What is the releasable pool?

Answer

A

Vesicles that are already docked to the release sites. Able to release contents very quickly (200μs)

Question 5

Q

What is the reserve pool?

Answer

A

Vesicles that are associated with the cytoskeleton. Can augment vesicle population if more than releasable pool is needed

Question 6

Q

What are the different SNAREs?

Answer

A

v-SNARE Synaptobrevin t-SNARE SNAP-25 Syntaxin

Question 7

Q

How many α helices do the following SNAREs have? 1) Synaptobrevin 2) SNAP-25 3) Syntaxin

Answer

A

1) Synaptobrevin - 1 2) SNAP-25 - 2 3) Syntaxin - 1

Question 8

Q

What is the core complex?

Answer

A

Complex of: 1) Synaptobrevin 2) SNAP-25 3) Syntaxin The four α helices come together and form a leucine zipper to bring plasma membranes together

Question 9

Q

What is synaptotagmin?

Answer

A

Ca²⁺ sensor on vesicle Transmembrane region (N terminus) Sequence homology with PKC Binds several Ca²⁺ with low affinity

Question 10

Q

What are synapsins?

Answer

A

Found on surface of vesicles Link vesicle to cytoskeleton Non-phosphorylated → vesicles are immobile Phosphorylated (by PKA + CaM kinase II) → dissociation → vesicles are free to move

Question 11

Q

What are the symptoms of botulinum poisoning?

Answer

A

Somatic muscle weakness (can lead to need for respiratory support) 2. Loss of cholinergic activity (consitipation, blurred vision, dry skin, urine retention) 3. Noradrenergic nerve actions (heart rate slowed)

Question 12

Q

What is the mechanism of Botulinum toxin?

Answer

A

Preferentially effects cholinergic neurons - Has a light chain and heavy chain - C-terminus (heavy chain) binds ganglioside receptor (GT1b) ⟶ endocytosis of complex - N-terminus translocates light chain from the endosomal lumen ⟶ cell cytoplasm (Does so by making a channel in endosomal membrane) - Light chain has peptidase activity ⟶ cleaves target SNARE

Question 13

Q

What is the mechanism of tetanus toxin?

Answer

A

Does not act directly on motor neuron - Retrogradely transported to the cell body ⟶ transfers to inhibitory interneuron ⟶ disables interneuron from releasing its transmitter ⟶ motor neuron becomes more excitable

Question 14

Q

What are the SNARE targets for botulinum and tetanus toxin?

Answer

A

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Question 15

Q

What is the rate limiting step in ACh production?

Answer

A

Supply of choline

Question 16

Q

What protein transports ACh into vesicles?

Answer

A

VAChT (vesicular ACh transporter)

Question 17

Q

What other neurotransmitters are found in ACh vesicles?

Answer

A

ACh + ATP (10:1) Also some VIP sometimes

Question 18

Q

Whats the structure of AChE?

Answer

A

3 x tetramer of AChE bind to a tail via disulphide bonds Tail binds to basement membrane via heparin sulphate proteoglycan

Question 19

Q

What is the mechanism of action of cholinesterases?

Answer

A

AChE + BuChE = Serine hydrolases AChE 2 binding sites: 1) Anionic site (contains glutamate. Binds choline) 2) Esteratic site (Contains Serine + histidine) BuChE Lacks anionic site therefore ↓ affinity for ACh

Question 20

Q

What is the structure of nAChR?

Answer

A

Pentamer 2 x α + combination of 3 other subunits (e.g. βγδ)

Question 21

Q

What are the different muscarinic receptors?

Answer

A

Several different types. Important ones: M1 - Location = Peripheral and central neurons - G-protein = G₁₁/q M2 - Location = Heart + pre-synaptic terminals - G-protein = Gi M3 - Location = Secretory glands + smooth muscle - G-protein = G₁₁/q

Question 22

Q

What is the synthesis pathway for catecholamines?

Answer

A

Tyrosine → DOPA → Dopamine → NA → A 1) Tyrosine hyroxylase 2) Dopa decarboxylase 3) Dopamine beta-hydroxylase 4) PNMT

Question 23

Q

What is the rate limiting step in catecholamine synthesis?

Answer

A

Tyrosine hydroxylase

Question 24

Q

What is the ratio of NA:ATP in noradrenaline vesicles?

Answer

A

4:1 NA:ATP

Question 25

Q

What transporter transports DA and NA into vesicles?

Answer

A

Vesicular monoamine transporter (VMAT2) H⁺ = energy source (2H⁺ extruded for every amine taken into vesicle) ← ATP dependent

Question 26

Q

Which two adrenoreceptors act as auto receptors?

Answer

A

α2 - Main one - Activation → ↓ NA release (main effect is via G protein gated K⁺ channel β2 - Activation → ↑ NA synthesis

Question 27

Q

What are the different types of uptake for inactivation of catecholamines?

Answer

A

Uptake 1 - Uptake into presynaptic neuron - Affects response - High affinity/low capacity - Transporter = NET -Na+ dependent - NA > Adr Uptake 2 - Uptake into postsynaptic neuron - No effect on response - Low affinity/High capacity - Transporter = ENT (OCT3) - Not Na+ dependent - Adr > NA

Question 28

Q

What enzymes are involved in metabolism of catecholamines?

Answer

A

1) MAO - On outer mitochondrial membrane - MAO-A → NA, Adr, DA + 5-HT - MAO-B → DA 2) COMT - In liver and neuronal tissues - Associated with uptake 2

Question 29

Q

What are the G-proteins coupled to the different adrenoreceptors? What are their effects?

Answer

A

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Question 30

Q

What are the affinities for Adr and NA at the different adrenoreceptors?

Answer

A

α1 - NA > Adr α2 - Adr > NA β1 - Same β2 - Adr > NA β3 - Same

Question 31

Q

As well as primary neurotransmitter, what transmitters are also released from: 1) Cholinergic nerves 2) Noradrenergic nerves

Answer

A

1) VIP + NO + ATP 2) ATP + Neuropeptide Y

Question 32

Q

What are the purinoceptors (purinergic receptors)?

Answer

A

P1 Adenosine > AMP > ADP > ATP These are the adenosine receptors P2 ATP > ADP > AMP > Adenosine Divided into: - 1) P2X (ligand gated ion channel) - 2) P2Y (G-protein coupled)

Question 33

Q

What is the structure of P2X receptor?

Answer

A

Trimer of P2X subunit - Non-selective cation channel Important role in fertility

Question 34

Q

What are the different adenosine receptors?

Answer

A

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Question 35

Q

Give examples of peptide neurotransmitters:

Answer

A

1) Substance P 2) VIP 3) Neuropeptide Y 4) CGRP 5) Opioids 6) Vasopressin (ADH)

Question 36

Q

What are different about peptide vesicles?

Answer

A

1) Much larger 2) Vesicles are further away from plasma membrane, thus require larger APs to generate a large enough ↑[Ca²⁺]i

Question 37

Q

How is NO synthesised?

Answer

A

Mainly on endothelial cells and neutrons Ca²⁺ dependent L-arginine → NO + L-ciltrulline (enzyme = NOS)

Question 38

Q

What are the three types of NOS?

Answer

A

1) Neuronal NOS (nNOS/NOS I) CNS + NANC neurons 2) Inducible NOS (iNOS/NOS II) Induced by macrophages etc (IFN-Y + chemokines) 3) Endothelial NOS (eNOS/NOS III) In platelets and endothelial cells

Question 39

Q

Mechanism of action for NO:

Answer

A

Interacts with soluble guanylyl cyclase (GC) → ↑ cGMP → activation of cGMP dependent protein kinase G → relaxation of smooth muscle (esp. blood vessels)

Question 40

Q

How is NO inactivated?

Answer

A

1) Combined with haem in Hb 2) Oxidated to nitrite and nitrate → excreted in urine

Question 41

Q

ADMA (asymmetric dimethyl arginine)

Answer

A

Class = - - Target = Nitric oxide synthase - Mechanism = Endogenous inhibitor - Steps: - Info: • equipotent to synthetic L-NMMA • its concentration is increased in hypercholesterolaemia, aenemia and renal failure

Question 42

Q

Alpha-latrotoxin

Answer

A

Class = Toxin - Target = Neurexins (transmembrane proteins on plasma membrane of nerves) - Mechanism = Causes massive release of ACh - Steps: Bind to neurexins ⟶ formation of Ca²⁺ channels ⟶ massive release of ACh - Info: From black widow spider

Question 43

Q

alpha-methyldopa [methyldopa]

Answer

A

Class = Precursor to false transmitter - Target = - - Mechanism = Becomes false transmitter α-methylnoradrenaline - Steps: • α-methyldopa is taken into noradrenergic nerve ending • Converted by DDC and DBH ⟶ α-methyldopamine and α-methylnoradrenaline • α-methylnoradrenaline is stored in vesibles ⟶ release in place of NA • α-methylnoradrenaline = false transmitter (Less active than NA on α1 but more active on on α2 ∴ less vasoconstriction following SNS stimulation) - Info: Functions as an anti-hypertensive by preferential competitive inhibition on α1 receptors

Question 44

Q

Amitriptyline

Answer

A

Class = Tricyclic antidepressant - Target = NET - Mechanism = Blocker - Steps: 1) Blocks NET to prevent uptake of norepinephrine and 5-HT through uptake 1 - Info: - replaced by SSRIs, which only blocks specific 5-HT transporter -side effects: sedation due to H1 receptor block, postural hypotension, dry mouth, constipation, ventricular dysrythmias

Question 45

Q

Atenolol

Answer

A

Class = Selective β1 antagonist - Target = Selective β1 antagonist - Mechanism = Antagonist - Steps: - Info: Used in Hypertension Less likely to cause bronchoconstriction (compared to propranolol ∵ selective to β1) Also treat dysrhythmias and angina Does not cross BBB (hydrophilic)

Question 46

Q

Atracurium

Answer

A

Class = Quaternary ammonium - Target = nAChR at NMJ - Mechanism = competitive antagonism - Steps: 1. Block end-plate potential in response to nerve stimulation 2. Antagonise the effects of directly applied ACh/other agonist 3. Tetanic fade - in presence of drug teatanus in response to high freq. stimulation is not maintained. This is due to block of autoreceptors which give +ve feedback to maintain transmitter release - Info: -Charged ∴ not orally active -Broken down by plasma esterases (∴ shorter duration of action than pancuronium) - Used in anaesthetics —Produce muscle relaxation —Affect fast (white) muscles > slow (red) (thought to ↓ respiratory depression ∵ respiratory muscles are slow twitch) -Blocking can be reversed by anticholinesterases

Question 47

Q

Atropine

Answer

A

Class = - Target = mAChR receptor (non-selective) - Mechanism = Antagonist - Steps: - Info: Used to be used to induce pupil dilation (but too long lasting, thus now sympathetic agonists used instead)

Question 48

Q

Bethanechol

Answer

A

Class = - Target = mAChR (non-specific) - Mechanism = Agonist - Steps: - Info: Used for urinary retention Poor oral absorption

Question 49

Q

Botulinum toxins

Answer

A

Class = Toxin - Target = SNARE (mainly cholinergic neurons) - Mechanism = Inhibits neurotransmitter release - Steps: 1) Has a light and heavy chain 2) Heavy chain (C-terminus) binds to ganglioside receptor (GT1b) → endocytosis 3) N terminus translocates light chain from endosomal lumen → light chain now in cytoplasm 4) Light chain has peptidase activity and targets its SNARE - Info: Botox B, D, F + G → Synaptobrevin Botox A + E → SNAP-25 Botox C1 → SNAP-25 and Syntaxin

Question 50

Q

beta-Bungarotoxin

Answer

A

Class = Toxin - Target = Nerve ending and K⁺ ion channels - Mechanism = Blocks ACh released by destroying nicotinic nerve endings - Steps: Consists of two chains: Chain 1 ⟶ binds to K⁺ ion channels, targeting 2nd chain to nerve terminal Chain 2 ⟶ a phospholipase A₂ which destroys the terminal - Info: Released from krait snake

Question 51

Q

Butaxamine/Butoxamine

Answer

A

Class = β1 and β2 blocker - Target = β1 and β2 adrenoreceptors - Mechanism = antagonist - Steps: - Info: • >selectivity for β2 • No clinical use

Question 52

Q

Caffeine

Answer

A

Class = A1 receptor antagonist /PDE inhibitor - Target = Non-selective drug: A1 receptor and phosphodiesterase (PDE) - Mechanism = Antagonist/Inhibitor - Steps: Antagonism of A1 ⟶ wakefulness + increase heart rate Inhibition of PDE ⟶ ↓ break down of cyclic nucleotides ⟶ ↑ rate and force of heart contractions (mainly due to cAMP) - Info: Waking action is most prominent after prolonged wakefulness

Question 53

Q

Carbidopa

Answer

A

Class = - - Target = DOPA decarboxylase - Mechanism = Antagonist - Steps: 1) Given with L-DOPA in treatment of Parkinsons disease 2) L-DOPA is given as it can cross blood-brain barrier (DA cannot) 3) L-DOPA alone gives off-target side effects ∵ ↑ DA in periphery 4) Carbidopa cannot cross BBB ∴ inhibits DOPA decarboxylase peripherally to prevent peripheral side effects of L-DOPA

Question 54

Q

Clonidine

Answer

A

Class = Adrenoreceptor agonist - Target = Slightly selective α2/l1 agonist - Mechanism = Agonist - Steps: • stimulation of presynaptic alpha2 receptors reduces NA release (by downregulating PKA activity presynaptically) and thereby reduces blood pressure -it also stimulates I1 receptors (in brain), which may have a more predominant role in clonidine’s ability to act as an anti-hyerpertensive - Info: • Has been used as an antihypertensive (effect is achieved by stimulating receptors in hind brain) • Missing one dose ⟶ rebound hypertension Not used in UK

Question 55

Q

Clorgiline [clorgyline]

Answer

A

Class = MAO inhibitor - Target = MAO-A - Mechanism = Inhibitor - Steps: - Info: -selective blocker of MAO-A, thereby preventing breakdown of presynaptic 5-HT -used in the treatment of depression -exacerbation of the cheese effect from tyramine-containing foodstuffs - excessive stimulation causing tremor and insomnia, muscarinic effects (dry mouth, constipation).

Question 56

Q

Cocaine

Answer

A

Class = - Target = NET - Mechanism = Blocker - Steps: 1) Blocks NET to prevent uptake of norepinephrine through uptake 1 2) This results in prolonged NA-dependent signalling - Info:

Question 57

Q

D-amphetamine [dexamfetamine]

Answer

A

Class = Indirectly acting sympathomimetic amines - Target = - - Mechanism = Displaces NA from vesicles - Steps: • Taken up into storage vesicles • ∵ it is a weak base ⟶ ↑vesicular pH ⟶ ↓ pH gradient that is required for VMAT2 to function ⟶ prevention of uptake of further NA to vesicle • Displaced NA leaves cell through nerve endings ⟶ stimulate receptors - Info: • Substrate for uptake 1 • Dexamfetamine has an α-methyl group ∴ it is • not metabolized by MAO (it is actually a weak inhibitor) • Can reduce appetite

Question 58

Q

Darifenacin

Answer

A

Class = - Target = Selective M3 muscarinic receptor - Mechanism = Reversible antagonist - Steps: - Info: Reduces bladder constriction in the treatment of urinary incontinence to decrease the urge to urinate

Question 59

Q

Dipyridamole

Answer

A

Class = - Target = Adenosine uptake mechanism/PDE V - Mechanism = Prevents adenosine uptake into cells - Steps: - Info: • Blocks adenosine uptake to prevent termination of adenosine-dependent signalling • By amplifying the effects of endogenous adenosine on A2A and A2B receptors, dypyridamole is a potent vasodilator • PDE V inhibition → ↑ cGMP Causes coronary steal

Question 60

Q

Dobutamine

Answer

A

Class = Beta agonist (β1) - Target = Selective β1 agonist - Mechanism = Agonist - Steps: Effects on β1 ⟶ ↑ heart rate + ↑ inotropy (effect on isotropy > chronotropy) - Info: Used in cardiogenic shock Post heart surgery In heart failure (without HTN)

Question 61

Q

D-tubocurarine [curare/tubocurarine]

Answer

A

Class = - Target = nAChR (non-selective between ganglion and NMJ) - Mechanism = Antagonist - Info: Generated through purification of curare Charged ∴ not orally active

Question 62

Q

Dyflos [diisopropyl fluorophosphate/DFP]

Answer

A

Class = Long acting antiChE - Target = acetylcholinesterase (AChE) - Mechanism = Irreversible inhibitor of AChE - Steps: • Organophosphorous compound • Forms strong covalent bond between phosphorous atom and the serine residue at esteratic site - Info: Used to treat glaucoma

Question 63

Q

Edrophonium

Answer

A

Class = Short acting antiChE - Target = acetylcholinesterase (AChE) - Mechanism = Reversible inhibitor of AChE - Steps: • Quaternary compound • Binds to anionic site in the active site of AChE through electrostatic intereactions - Info: Used to diagnose myasthenia gravis

Question 64

Q

Entacapone

Answer

A

Class = COMT inhibitor - Target = COMT - Mechanism = Inhibitor - Steps: - Info: Used in Parkinson’s disease

Answer 64

A

Class = - Target = - Mechanism = Blocks release of NA - Steps: •Taken into nerve by Uptake 1 ∴ compete with NA • ∴ can potentiate exogenously applied NA • Large doses ⟶ behave as indirectly acting sympathomimetic amines (as described above) • Repeated low doses ⟶ block the release of NA evoked by APs (spontaneous release is unaffected, showing that vesicle release processes are intact) - Info: Used to be used for HTN not any more

Answer 65

A

Class = - - Target = Na⁺/Choline cotransporter - Mechanism = Blocker - Steps: Hemicholinium blocks the symporter →↓ ACh production in pre-synaptic terminal - Info: Only reduces neurotransmission with high rates of stimulation

Answer 66

A

Class = - Target = nAChR at autonomic ganglion - Mechanism = Channel pore blocker - Steps: Use-dependent blocker of open channel pore - Info: Previously used for treatment of HTN but discontinued ∵ 1. Caused loss of both SNS (wanted effect ⟶ ↓ vascular tone) and PSNS (lead to Hexamethonium man) 2. It has a double positive charge ∴ needed frequent administration via injection

Answer 67

A

Class = α1 and α2 blocker - Target = α1 and α2 adrenoreceptors - Mechanism = antagonist - Steps: - Info: • >selectivity for α2

Answer 68

A

Class = Tricyclic antidepressant - Target = NET - Mechanism = Blocker - Steps: 1) Blocks NET to prevent uptake of norepinephrine and 5-HT through uptake 1 - Info: - replaced by SSRIs, which only blocks specific 5-HT transporter -side effects: sedation due to H1 receptor block, postural hypotension, dry mouth, constipation, ventricular dysrhythmias

Answer 69

A

Class = Beta agonist - Target = Non-selective β agonist - Mechanism = Agonist - Steps: causes bronchodilatation through an action on B2 and increased heart rate through B1 - Info: Was used more in asthma (replaced now by β2 selective agonists) Effects on β2 ⟶ bronchodilation but effects on β1 ⟶ ↑ heart rate which was undesired 10x more potent than adrenaline NOT A SUBSTRATE FOR UPTAKE 1

Answer 70

A

Class = Combined α and β blocker - Target = alpha1, beta1, beta2 adrenoreceptors - Mechanism = antagonist - Steps: Has 4 isomers with different actions: 1. R,R - β blocker + weak α1 blocker 2. R,S - no activity 3. S,R - α1 blocker + very weak β blocker 4. S,S - α1 blocker - Info: Used to treat hypertension in pregnancy

Answer 71

A

Class = Long acting antiChE - Target = acetylcholinesterase (AChE) - Mechanism = Irreversible inhibitor of AChE - Steps: • Organophosphorous compound • Forms strong covalent bond between phosphorous atom and the serine residue at esteratic site - Info: Used as an insecticide to kill lice

Answer 72

A

Class = - Target = nAChR at autonomic ganglion - Mechanism = Antagonist - Steps: Use-dependent blocker of open channel pore - Info: Use-dependent, as mecamylamine requires access to the channel

Answer 73

A

Class = - Target = mAChR (non-specific) - Mechanism = Agonist - Steps: - Info: No clinical use

Answer 74

A

Class = Medium acting antiChE - Target = acetylcholinesterase (AChE) - Mechanism = Reversible inhibitor of AChE - Steps: • Binds to the esteratic site and carbomylates the enzyme • It is hydrolysed by the enzyme (but much slower than ACh ∴ enzyme is inactivated for many minutes) - Info: Orally ⟶ myasthenia gravis IV ⟶ reverse neuromuscular blockade after surgery

Answer 75

A

Class = - - Target = nAChR - Mechanism = Agonist (can cause depolarising block) - Steps: Two phases of block 1) Phase I block Long lasting nature of stimulation ⟶ inactivation of voltage gated Na⁺ channels on post-synaptic cell ∴ post-synaptic cells cannot be stimulated 2) Phase II block Membrane repolarised as nictonic receptors become desensitised ∴ stimulation of preganglionic nerve will not excite postganglionic cell Because Na⁺ channels are relieved from inactivation, postganglionic cell can be directly stimulated by electrical means - Info:

Answer 76

A

Class = NO donor - Target = soluble guanylyl cyclase - Mechanism = Activator - Steps: - Info: • Causes actiation of sGC in vascular smooth muscle, leading to smooth muscle relaxation and vasular dilatation • Preferentially causes dilatation in collateral vessles. This reduces the amount of ischaemic myocardial tissue. • Used in acute angina • Must be taken sublingually

Answer 77

A

Class = Quaternary ammonium - Target = nAChR at NMJ - Mechanism = competitive antagonism - Steps: 1. Block end-plate potential in response to nerve stimulation 2. Antagonise the effects of directly applied ACh/other agonist 3. Tetanic fade - in presence of drug teatanus in response to high freq. stimulation is not maintained. This is due to block of autoreceptors which give +ve feedback to maintain transmitter release - Info: -Charged ∴ not orally active -Not broken down by plasma esterases (∴ longer duration of action than atracurium) - Used in anaesthetics (∵ longer duration) —Produce muscle relaxation —Affect fast (white) muscles > slow (red) (thought to ↓ respiratory depression ∵ respiratory muscles are slow twitch) -Blocking can be reversed by anticholinesterases

Answer 78

A

Class = Alpha antagonist - Target = Non-selective α antagonist - Mechanism = Non-selective α antagonist - Steps: - Info: Obsolete in hypertensive treatment ∵ cause reflex tachycardia Can cause reflex hypotension

Answer 79

A

Class = Adrenoreceptor agonist - Target = Selective α1 agonist - Mechanism = Agonist - Steps: - Info: Used to ↑ BP in acute hypotension

Answer 80

A

Class = - Target = mAChR (non-selective) - Mechanism = Agonist - Steps: - Info: Used in treatment of glaucoma Causes contraction of ciliary body ⟶ produces traction on trabecular meshwork ⟶ facilitates aqueous humour drainage ⟶ ↓ intraocular pressure

Answer 81

A

Class = - - Target = acetylcholinesterase (AChE) - Mechanism = Reverses inhibition of AChE imposed by organophosphates - Steps: • Phosphate group on the serine residue (of inhibited enzyme) is transferred to the oxime group of pralidoxime ⟶ relieving inhibition • This reversal can only occur before the process of ‘aging’ occurs of the acetycholinesterase-inhibitor complex (occurs after a few hours ⟶ chemical rearrangement meaning that the bond is no longer susceptible to nucleophilic attack)

Answer 82

A

Class = Alpha antagonist (α1) - Target = Selective α1 antagonist - Mechanism = Antagonist - Steps: - Info: Used in hypertension Can cause postural hypotension

Answer 83

A

Class = Non-selective β antagonist - Target = β1 and β2 antagonist - Mechanism = Antagonist - Steps: - Info: Was used for hypertension but replaced by β1 selective blockers

Answer 84

A

Class = - - Target = VMAT2 - Mechanism = Blocks amine binding site on VMAT2 - Steps: • Blocks amine binding site ⟶ prevention of uptake of NA ⟶ depletion of stored NA (and 5-HT in brain) • Depletion occurs ∵ there is some leak and MAO in cytoplasm metabolises the neurotransmitters • Acts on periphery and CNS • Recovery requires synthesis of new vesicles - Info: Use as a hypertensive stopped ∵ lead to profound depression (5-HT depletion)

Answer 85

A

Class = Beta agonist (β2) - Target = Selective β2 agonist - Mechanism = Agonist - Steps: Effects on β2 ⟶ bronchodilation - Info: Used in asthma

Answer 86

A

Class = MAO inhibitor - Target = MAO-B - Mechanism = Inhibitor - Steps: - Info: - used in the treatment of parkinson’s disease, since is it MOA-B that is responsible for dopamine metabolism in the substantia nigra

Answer 87

A

Class = PDE inhibitor - Target = PDE V - Mechanism = Inhibition - Steps: - Info: • Inhibition of PDE V ⟶ persistence of cGMP in smooth muscle cells ⟶ smooth muscle relaxation, specifically of vascular smooth muscle in the penis • It is used in treating impotence and can also be used in pulmonary arterial hypertension

Answer 88

A

Class = Depolarising blocking agent - Target = nAChR at NMJ - Mechanism = Agonsit but causes depolarising blockage - Steps: 1. Phase I Anitcholinesterases ⟶ deepen bloackade ∵ prolonged ACh signal ⟶ enhanced depolarisation ⟶ blockade of transmission at more junctions Non-depolarising blockers can be used in this phase to reverse blockade 2. Phase II Anitcholinesterases ⟶ reverse blockade - Info: - Only depolarising blocker with clinical use - Duration of action = short ∴ used for short procedures (e.g. intubation) - Ester ∴ rapidly broken down by plasma BuChE - Some people have deficiency of this enzyme ⟶ prolonged action

Answer 89

A

Class = Toxin - Target = Synaptobrevin - Mechanism = Inhibits neurotransmitter release - Steps: Indirectly affects motor neurons Retrograde transport to cell → disables inhibitory interneuron Causes motor neuron to be more excitable - Info:

Answer 90

A

Class =MAO inhibitor - Target = MAO-A and MAO-B - Mechanism = Inhibitor (irreversible) - Steps: - Info: - non-selective MOA inhibitor → preventing the breakdown of adrenaline, noradrenaline, dopamine and histamine -used in the treatment of refractory depression

Answer 91

A

Class = Indirectly acting sympathomimetic amines - Target = - - Mechanism = Displaces endogenous NA from vesicles - Steps: • Transported to nerve endings and vesicles • Displaces NA from vesicles • Some NA escape MAO action and reach extracellular space ⟶ activate adrenoreceptors - Info: • Substrate for uptake 1 • Found in food (cheese, red wine, pickled herring, yeast [marmite], soya beans) • Large ingestion ⟶ large NA release ⟶ widespread vasoconstriction ⟶ HTN • HTN can be fatal (cheese effect) Especially likely in people taking MAO inhibitors (MAOI) ⟵ warned about high tyramine foods Can be converted to octopamine by DBH (octopamine = false transmitter)

Answer 92

A

Class = - - Target = Selective α2 agonist - Mechanism = Agonist - Steps: - Info: Used in vetinary medicine for sedation (effect is on receptors in CNS)

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3.0 Peripheral Nervous System Flashcards

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