2.0 Receptors Flashcards

Question 1

Q

Adenosine

Answer

A

Class = NANC transmitter - Target = A1, A2A, A2B, A3 receptors - Mechanism = Agonist - Steps: - Info: Injected to treat supra ventricular dysrhythmias A1 recetor inhibits renin release

Question 2

Q

Atropine

Answer

A

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

Question 3

Q

B K 8644

Answer

A

Class = Dihydropryridine - Target = L-type voltage gated Ca²⁺ channel - Mechanism = Agonist - Steps: Favours mode 2 of channel opening - Info: Same binding site as nifedipine Only used experimentally

Question 4

Q

Benzylcholine mustard

Answer

A

Class = Modified form of ACh - Target = Muscarinic AChR - Mechanism = Irreversible antagonism - Steps: 1) Irreversibly alkylates muscarinic receptor - Info: Functions in a time dependent manner → progressive blockade of muscarinic receptors

Question 5

Q

Benzocaine

Answer

A

Class = Local anaesthetic - Target = Na⁺ channel - Mechanism = Blocker - Steps: 1) Non charged, therefore enters the cell using hydrophobic pathway 2) Not use-dependent 3) Not affected by pH - Info:

Question 6

Q

alpha-Bungarotoxin

Answer

A

Class = Toxin - Target = nAChR at NMJ - Mechanism = Irreversible antagonist - Steps: - Info: Produced by branded krait snake

Question 7

Q

Cholera toxin

Answer

A

Class = Toxin - Target = Gαs subunit of G protein - Mechanism = Causes increased activation of adenylyl cyclase - Steps: 1) Causes ADP-ribosylation of αs 2) This inhibits GTPase activity → sustained activation of adenylyl cyclase - Info:

Question 8

Q

Diltiazem

Answer

A

Class = Benzothiazipine - Target = L-type voltage gated Ca²⁺ channel - Mechanism = Antagonist - Steps: Act on different sites than DHPs Show use dependence Preferentially targets cardiac tissue (because Ca²⁺ channels here have highest opening frequency) - Info: Ditliazem → ↑ DHP binding

Question 9

Q

d-Tubocurarine

Answer

A

Class = - Target = nAChR - Mechanism = Antagonist - Steps: - Info: Non selective between ganglionic and NMJ Generated by purification of curare Charged therefore not orally active

Question 10

Q

Ethinylestradiol

Answer

A

Class = Steroid - Target = Estrogen receptor - Mechanism = Agonist - Steps: - Info: Used in contraception Estrogen receptor = exception to steroid receptors as it is found in nucleus unbound to ligand

Question 11

Q

Glibenclamide

Answer

A

Class = Sulphonylurea - Target = Sulphonylurea receptor (SUR) - Mechanism = Agonist - Steps: Binds to SUR → closure of K⁺-ATP channel → depolarisation of panreatic β cells → opening of voltage gated Ca²⁺ channel → insulin release (exocytosis) - Info: Used in Type II DM

Question 12

Q

Isoprenaline

Answer

A

Class = β agonist - Target = β₁ + β₂ - Mechanism = Agonist - Steps: β₁ → ↑ heart rate β₂ → bronchodilation - Info: Used to be used for asthma - now stopped because caused tachycardia

Question 13

Q

Lidocaine/lignocaine

Answer

A

Class = Local anaesthetic (tertiary amine) - Target = Na⁺ channel - Mechanism = Blocker - Steps: 1) Binds to and stabilises the inactive conformation of the channel 2) Crosses membrane in uncharged form 3) Blocks channel in charged form 4) Shows use dependence + voltage dependence - Info: Used as LA but also as antidysrhythmic (ventricular problems) Selectivity for smaller and slower conducting fibres (Aδ + C) Fast in-fast out kinetics (more effective at high rates of stimulation)

Question 14

Q

Minoxidil

Answer

A

Class = K⁺ channel opener - Target = ? K-ATP channel? - Mechanism = Opener - Steps: Exact mechanism unknown Opens K⁺ channel → K⁺ efflux → hyperpolarisation → relaxation of smooth muscle (e.g. that surrounding vasculature) - Info: Used in male baldness, hypertension, asthma, IBS - side effect: May cause hyperglycaemia by limiting insulin secretion by pancreatic β cells

Question 15

Q

Nicorandil

Answer

A

Class = K⁺ channel opener - Target = ? K-ATP channel? - Mechanism = Opener - Steps: Exact mechanism unknown Opens K⁺ channel → K⁺ efflux → hyperpolarisation → relaxation of smooth muscle (e.g. that surrounding vasculature) - Info: Used in HTN and angina (causes ischaemic preconditioning) Also an NO donor - side effect: May cause hyperglycaemia by limiting insulin secretion by pancreatic β cells

Question 16

Q

Nifedipine

Answer

A

Class = Dihydropryridine - Target = L-type voltage gated Ca²⁺ channel - Mechanism = Antagonist - Steps: Favours mode 0 of channel opening (inactive state) Preferentially stabilises inactive channel, thus favours tissues which are constitutively depolarised (e.g. vascular smooth muscle) Use dependence - Info: Same binding site as Bay K 8644 Used for HTN and angina Reduces aldosterone secretion

Question 17

Q

Norethisterone

Answer

A

Class = Steroid - Target = Progesterone (progestagen) receptor - Mechanism = Agonist - Steps: - Info: Used in contraception

Question 18

Q

Pertussis toxin

Answer

A

Class = Toxin - Target = Gαi subunit of G protein - Mechanism = Causes increased activation of adenylyl cyclase - Steps: 1) Causes ADP-ribosylation of αi 2) This prevents GDP→GTP exchange 3) Prevents activation of Gαi → ↑ PKA activity - Info: ↑ PKA activity → loss of water through intestine → severe dehydration

Question 19

Q

Prednisolone

Answer

A

Class = Steroid - Target = glucocorticoid receptor - Mechanism = Agonist - Steps: - Info: Used for inflammatory/autoimmune conditions Has a lymphocytic effect (useful against leukaemias) Administered as prodrug prednisone (converted to prednisolone in liver)

Question 20

Q

Quinidine

Answer

A

Class = Local anaesthetic - Target = Na⁺ channel - Mechanism = Blocker - Steps: 1) Shows use dependence 2) Slow in-slow out kinetics therefore shows use dependence at lower rates of stimulation - Info: Also used as antidysrythmic (Class 1A)

Question 21

Q

Spironolactone

Answer

A

Class = K⁺ sparing diuretic - Target = Aldosterone (mineralocorticoid) receptor - Mechanism = Antagonist - Steps: Spironolactone is metabolised to canrenone in the liver Canrenone and its K+ salt (potassium canrenone) work as K+ sparing diuretics Spironolactone/canrenone compete with aldosterone binding site on cytoplasmic receptor Antagonism → ↓ expression of Na⁺/K⁺ ATPase and ENaC → ↓ Na⁺ reabsorption - Info: Acts on distal tubule Rate of onset of diuresis is slow

Question 22

Q

Tamoxifen

Answer

A

Class = Estrogen antagonist - Target = Estrogen receptor - Mechanism = Competitive antagonist - Steps: Has lower affinity than oestrogen. Reduces the transcription of estrogen response genes. - Info: Used for breast cancer Can have agonist effects in bone and uterus

Question 23

Q

Tetradotoxin

Answer

A

Class = Toxin (guanidium) - Target = Na⁺ channel - Mechanism = Blocker - Steps: Contains guanidium group Blocks Na⁺ channel from outside No use-dependence - Info: Puffer fish Does not affect cardiac channels because of the presence of cysteine residues in the cardiac Na⁺ isoform

Question 24

Q

Tyrphostins

Answer

A

Class = RTK inhibitors - Target = Receptor tyrosine kinase - Mechanism = Inhibition - Steps: - Info: Potential use in the treatment of neoplasms by blocking RTKs implicated in cellular proliferation. Example = Glivec for treating CML

Question 25

Q

Verapamil

Answer

A

Class = Phenylalkylamine - Target = L-type voltage gated Ca²⁺ channel - Mechanism = Antagonist - Steps: Act on different sites than DHPs Show use dependence Preferentially targets cardiac tissue (because Ca²⁺ channels here have highest opening frequency) - Info: Verapamil→ ↓ DHP binding

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2.0 Receptors Flashcards

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