Neuromuscular Juntion

Question 1

what are the 5 steps of neuromuscular junction

Answer 1

The 5 steps of synaptic Transmission is Synthesis, storage (protect and package), release, activation and inactivation.

Question 2

What is the drug encahcne by direct stimulation

Answer 2

Drugs can enchance synaptic transmission by direct stimulation of post synaptic receptors by natural transmitters or analogues

Question 3

what is the drug enchance synaptic transmission indirect

Answer 3

drugs can enchnace synaptic transmission by indirect action by increased transmitter release and inhibition removal.

Question 4

Drugs can inhibit synaptic transmission

Answer 4

drugs an be inhibit synpatic transmission by blocking synthesis storage or release from the pre synaptic neurone or blocking postsynaptic receptors

Question 5

what is affinity and effiacy

Answer 5

Affinity is the ability of agonists to bind to receptors and efficacy is the ability of an agonist once bound to receptor to initiate a biological response

Question 6

what is the difference between antagonists and agonist

Answer 6

agonist posses affinity and effiacy while antagonsits only have affinity

Question 7

what is cholinoceptors

Answer 7

cholinoceptors are receptors upon which ACh acts

Question 8

cholinergic

Answer 8

Cholinergic is synapses where the presynaptic neurone synthesised and release ACh transmission

Question 9

what is mepp

Answer 9

a mepp is actiation the assoicated nitonic cation open and Na ion flux into the muscle fibre to cause local depolarisation at the endplate region

Question 10

Black Widow Spider

Answer 10

the spider gives a massive ACH release and muscle spasms and after causes depletion of vesicles , inhibition of endocytosis and distended terminal causing paralysis

Question 11

break microelectrode

Answer 11

nerve stimulation cause muscle contraction resulting in glass microelectrode breaking so High Mg2+ and Low Ca2+ buffer solution

Question 12

what is a quantal

Answer 12

The amplitude of the epp is a multiple of the amplitude ofthe mepp, with the smallest epp amplitude equal to that of the mepp amplitude this release is called a quantal

Question 13

what is quantal content

Answer 13

QC = mean EPP ampltiude / mean Mepp ampltiude

Question 14

cholingeric transmission (synthesis)

Answer 14

Choline acetyl transferase(CAT) synthesises ACh fromprecursors choline and AcetylCoenzyme A (Acetyl Co-A)from mitochondria

Question 15

reuptake of choline

Answer 15

Reuptake of choline is Na+-dependent & blocked competitively by hemicholinium 3(not used clinically).There will be less ACh in each vesicle

Question 16

cholingeric transmission of storage

Answer 16

Transport of ACh into vesicles blocked by inhibition of theACh vesicular transporter by VESAMICOL

Question 17

TTX

Answer 17

Tetrodotoxin (TTX)blocks Na+ channels(no action potential– no release, no EPP)

Question 18

cholinergic transmission

Answer 18

Voltage-gated Ca2+ channelsblocked by conotoxins(Ca2+ influx –  release).The epp amplitude decreases; nochange in themepp amplitude. A decreasedquantal content

Question 19

Dendrotoxin

Answer 19

Dendro toxin blocks voltage-gated K+channels prolonged action potential (Ca2+influx release).Increased epp amplitude; mepp amplitude – no change. Quantal content increased.The synthetic drug 4-aminopyridine(4-AP) has a similar mechanism

Question 20

Botulinum Toxin

Answer 20

Botulinum toxin blocks vesicle fusion by cleaving a vesicular protein required for exocytosis– decreased release.EPP amplitude decreases. Mepp amplitude – no change.Quantal content decreases

Question 21

Tubocuraine medically

Answer 21

Tubocurarine is used during surgery to produce skeletal muscle paralysis

Question 22

tubocurarine qualities

Answer 22

Tubocuraine Competitive non-depolarising neuromuscular blocking agent.Used clinically: a skeletal muscle relaxant.Muscle block reversed by anticholinesterases eg.NeostigmineClinically tubocurarine mainly replaced by synthetic drugs e.g. vecuronium

Question 23

a bungarotoxin

Answer 23

a bungarotoxin is not reversed by washout or by anticholinesterases

Question 24

succinylcholine

Answer 24

Succinylcholine used for rapid tracheal intubation and to prevent violent muscle contractions associated with electro convulsant therapy

Question 25

Phase I Block

Answer 25

Phase I Block 1. persistent activation of endplate nicotinic receptors 2. prolonged depolarisation of endplate 3. inactivation of voltage-gated sodium channels

Question 26

Phase II block

Answer 26

Phase II Block 4. desensitisation of endplate nicotinic receptors 5. repolarisation of endplate 6. receptor desensitisation maintains blockade

Question 27

Cholinergic Transmission

Answer 27

ACh is terminated by an enzyme acetylcholinesterase(AChE), which breaks down ACh to acetate and choline. Drugs which inhibitAChE,anti cholinesterases (egnervegases, neostigmine) increase the effects of ACh

Question 28

True Acetylcholinesterase

Answer 28

True - present at cholinergic synapses and bound to the postsynaptic membrane in the synaptic cleft

Question 29

Pseudo cholinesterase

Answer 29

Pseudocholinesterase is important in inactivating the depolarisisng neuromuscular block suzamethonium

Question 30

Atrpoine

Answer 30

ATROPINE counteract effects ofexcessive muscarinic receptorstimulation by ACh

Question 31

Oximes

Answer 31

OXIMESEg. pralidoxime (2-PAM)antidote to Nerve Gasreactivates the AChase But…ageing

Question 32

Organophophates

Answer 32

organophosphates readily absorbed through the insect cuticle