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FoM > Cell Signalling + Drug Action > Flashcards

Cell Signalling + Drug Action Flashcards

1
Q

Adrenaline (sympathetic OR para?)
adrenoreceptors (what kind of receptor)

A

sympathetic
GPCR

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2
Q

Insuline receptor (What kind)

A

Kinase-linked

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3
Q

Where is ACh released in the body?

A
  1. NMJ (peripheral NS)
    - by motor neurons in NMJ (connections bn nerves + cells)
    - causing voluntary muscle contraction
  2. Autonomic NS (autonomic regulation)
    Primarily PARA, but also SYMPA
    - SYMPA: released by preganglionic neurons, connecting the spinal cord to ganglia (after the ganglia neurotransmitter often switches to norepinephrine for further signalling)
    - PARA: main neurotransmitter, promoting relaxation resposnes e.g. slowing HR, Increasing digestion, stimulating gland secretion

3.CNS (Brain)
primarily within BASAL FOREBRAIN + BRAINSTEM neurons
- cognitive function role e.g. attention/memory/learning
- influences REM, arousal, sensory perception

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4
Q

Nicotinic ACh receptors

A

Ligand gated ion channels
nonspecific cation channels
permeable to Na+ / K+ / Ca2+, depending on subunit composition

found at NMJ
post-ganglionic neuronal cells in the ANS

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5
Q

Varenicline

A

Medication - partial agonist at a4b2 nAChRs. Stimulating these receptors enough, inhibiting x’s ability to bind fully, easing withdrawal symptoms

x= Nicotine

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6
Q

GPCR
Adrenaline binding to b2-adrenoreceptors

A

Bronchodilation

b2 = broncho
2= 2 lungs

Gas
adenylyl cyclase
ATP => cAMP -> PKA - MLCK

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7
Q

GPCR
Adrenaline binding to a2-adrenoreceptors

A

Relaxation of GI tract
GI = 2 words = a2

Gai
adenylyl cyclase
ATP => cAMP -> PKA - MLCK

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8
Q

Salbutamol

A

MEDICATION
binds/activates selectively b2 adrenoreceptors = Bronchodilation, desired therpautic effect for asthma

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9
Q

GPCR
Adrenaline binding to a1-adrenoreceptors

A

Vasoconstriction
Vaso = 1 word = a1

Gaq
c - c
Phospholipase C (NOT adenylyl cyclase)
PIP2 -> DAG + IP3, Ca2+

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10
Q

Theophylline

A

phosphodiesterase inhibitor
INDICATED for COPD
Medication

(terminating action of cAMP)
b2 adrenoreceptor

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11
Q

Aldosterone

A

A steroid hormone
produced by adrenal glands
-> binds to Aldosterone receptor / mineralocorticoid receptor (MR)

role in regulating electrolyte balance, BP, fluid balance, by controlling levels of Na+ and K+ in the body

part of the RAAS + acts mainly on the kidneys to promote reabsorption of Na+ back into the bloodstream

when Na+ is reabsrobed, water follows due to osmosis, increasing blood volume and helping raise BP

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12
Q

another name for Aldosterone receptor = nuclear receptor

A

mineralocorticoid receptor (MR) = nuclear receptorH

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13
Q

Hypokalaemia (

A

lower than normal potassium level in you bloodstream is called…

so body will conserve Na+ at the expense of K+

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14
Q

Thiazides

A

a class of diuretic medications that are commonly used to treat high blood pressure (hypertension) and manage fluid retention (edema) associated with conditions like heart failure, liver disease, and certain kidney disorders.

work by affecting the kidneys’ handling of salt and water, promoting increased urine output, which helps to lower blood pressure and reduce excess fluid in the body.

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15
Q

Function of prostaglandins

A

protect the stomach lining
promote blood clotting
maintain kidney function

involved in PAIN, FEVER, INFLAMMATION at site of injury

SYNTEHSISES BY COX ENZYMES

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16
Q

COX 1 - constitutive enzyme
COX2 - inducible enzyme

A

1 - generates prostaglandins, to protect the stomach lining —- stimulates mucus and bicarbonate production, providing gastric protection

2- generates prostaglandins in repsonse to inflammation —- by increasing blood flow, recruiting immune cells and sensitizing nerve endings –> PAIN, INFLAMMATION

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17
Q

Ibuprofen

A

NSAI drug

inhibits both COX1 + COX2 enzymes, thereby reducing production of prostaglandins

Blocking cox1 -> reduce protective prostaglandins in the stomach, increasing risk of gastric irritation + ulceration

Blocking cox2 -> relieve pain + inflammation at injury site

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18
Q

Overdose of Ibuprofen side effects

A

-> Gastric Ulcers (open sores)
inhibition of COX1, which reduced protective prostaglandins in the stomach lining
cause pain, neausea, serious bleeding

-> blood in stool (GI bleeding)
ulcers erode blood vessels

-> gastroprotective mechanism compromised
inhibition of prostaglandin production that protect the stomah lining, which is a protective barrier (mucus + bicarbonate secretion)
mucosal damage + bleeding

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19
Q

pyrexia synonym

A

fever

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20
Q

NSAIDs - nonsteroidal anti-inflamamtory drugs
e.g. Ibuprofen

A

members of a therapeutic drug class which reduces pain, decreases inflammation, decreases fever, and prevents blood clots.

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21
Q

Amlodipine

A

Drug -> Calcium channel blocker
antihypertensive
antagonist at Ca2+ channels.

Decreases electrical excitabiltiy of cardiac muscle cells
(contraction of vascular smooth muscle cells requires influx of Ca2+ intracellularly via Ca2+ VG Ca2+ channels, leading to activation of myosin and actin.

22
Q

GABA

A

primary inhibitory neurotransmitter in the CNS

23
Q

Citalopram

A

antagonist at SERT

24
Q

Sodium Valproate

A

antiepileptic drug
with multiple MOAs

  • increases GABA levels
  • blocks VG Sodium channels
  • Inhibits T-type Calcium channels ( particualrly in the thalamus which is beneficial in treating absence seizures)
  • Alters Histone Deacetylase activity ( implications on gene expression, might contribute to its mood-stabilizing effects)
25
Q

amitriptyline

A

TCA (tricycline antidepressant) with a lot of side effects, due to its non-selective mechanism of action on multiple receptors, beyond its effects on SERT (serotonin transporter)

works by inhibiting the reuptake of both serotoning (SERT) and norepinephrine (NET) at synapses in the brain - dual inhibition

ALSO - side effects:
1. Blocks mAChR, reducing parasympathetic activtiy (Rest and digest), having anticholinergic effects (dry mouth, constipation, urinary retention, blurred vision, confusion)
2. Histamine H1 Receptor Blockade
having sedative effects – can be therapeutic for insomnia
3. a1 adrenergic receptor blockadecausing blood vessels to relax, decreasing blood pressure

26
Q

Role of Histamine

A

This neurotransmitter is involved in wakefulness and appetite regulation.

27
Q

propranolol
metoprolol

A

non-selective b-blockers
- partial agonsists (dont have full efficacy, attenuating the effect of adrenaline)
contraindicated for people with asthma

P because it also has affinity for b2 adrenoceptors will block the action of salbutamol, exacerbating the symptoms for an asthmatic patient + reducing the therapeutic effect of salbutamol intended to alleviate the symptoms

28
Q

carbachol

A

agonist for…

its antagonist is atropine

reversible competition

29
Q

atropine

A

antagonist for…

its agonist is atropine

reversible competition

30
Q

isopernaline

A

drug binding to b1 adrenoceptor (agonist)

its beta blocker is propranolol

revesrible competition

31
Q

Aspirin

A

drug example of a reversible competitive antagonist at COX1 + 2, preventing the conversion of arachidonic acid to prostaglandins by covalently bidnign to the active site of hte COX enzymes

similar effect to IBUPROFEN (but this is a NSAID, which inhibtis COX1 +2, thereby reducing hte produciton of prostaglandins , and hence pain, fever, inflammation

32
Q

pindolol

A

partial agonist of b1 adrenoceptors

33
Q

aspirin

A

COX inhibitor

now used as a cardio drug, not so much as an analgesic

34
Q

ibuprofen

A

COX inhibitor
decreases blood flow by inhibtion of prostaglandins which would normally evoke vasodilation

– pain + inflammation in rheumatic disease and other musculoskeletal disorders

35
Q

stomach pH
plasma pH
aspirin pKa
Codeine pKa

A

1.5
7.4
3.5
9.2

36
Q

weak bases accumulate in compartments with … pH

A

low

37
Q

weak acids accumulate in comparmtents with … pH

A

high pH

38
Q

Atenolol

A

low LogP - i.e. not so much lipophilic

39
Q

Log P of propranolol

A

high i.e. lipophilic

40
Q

Codeine

A

weak base

41
Q

Aspirin

A

weak acid

42
Q

bioavailability

A

the amounf ot drug that eventually reaches systemic irculation, and hence is available for frug action on the target // of an administered dose of the drug

link to metabolism

this is always compared to route of adminsitration without absocpriotn, without metabolism, ie IV

expressed as % of IV

i.e. area under curve of IV / area under curve of Oral

43
Q

common enzymes in Phase 1 metbaolism

A

cytochrome P450 enzymes –
oxidation

44
Q

Metabolism of Paracetamol overview - PHASE 1

+ Overdose

A

Cytochrome P450 2E1 –> NAPQI metabolite is toxic (very reactive) ——– so it is nullified by Phase 2 metabolism (excreted as paracetamol cysteine – enzyme involved in glutathione S-trasnferase)

————— OVERDOSE : saturation, leading to NAPQI accumulation, irreversible liver damage

______________________________________________
PHARMACOLOGICALLY INERT METABOLITES OTHERWISE:
1. x glururonide
2. x sulfate

45
Q

Phase 1 metabolism of aspirin

A

metabolite is pharmacologically inert

46
Q

what is required for Phase 1 metabolism by the monooxygenase P450 system? (Drug oxidation)

A
  1. Drug
  2. P450 enzyme
  3. Oxygen
  4. NADPH
  5. Flavoprotein
47
Q

Processes taking place in Phase 2 metabolism

A

Conjugation
excretion via kidney, once metabolit becomes water soluble

making non-toxic metabolites, pharmacologically inert

– glucuronidation
- sulphation
– acetylation
— methyaltion
– glyucine conj
– glutathione conj

48
Q

exceptions of drugs that go directly to phase 2 metabolism and have pharmacologically active metabolites

A

Codeine (analgesic)

CYtochrome P450 2D6 –, metabolises codeine to morphine (PHASE 1) ,
—> most analgesic effect modulated by amount of morphien you hae from metabolism

morphine glycyronide (PHASE 2) can still bind to opioid receptor and activate it

49
Q

synonym for amoxicillin

A

penicillin

50
Q
A

FoM (14 decks)

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