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Phase 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Name the routes of administration

A

Enteral - through GIT
Oral (PO), rectal (PR)

Parenteral - non GIT
SC
IM
IV
Sublingual
Inhalers (INH)

Local effect
Transdermal e.g. patches
Topical cream e.g. steroid

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2
Q

Define agonist

A

Full affinity and full efficacy
∴ ↑ activation of receptor

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3
Q

Define antagonist

A

Full affinity and zero efficacy
∴ ↓ activation of receptor

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4
Q

Define affinity

A

How well ligand bind to receptor

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5
Q

Define efficacy

A

How well a ligand successfully activates its receptor

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6
Q

Define potency

A

The relative strength of drug
i.e. lower dose needed for response = more potent

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7
Q

Describe the mechanism of a competitive inhibitor

A

Binds at the active site
∴ ↓ Efficacy
Reversible, affinity is unchanged
∴ Less potent

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8
Q

Describe the mechanism of a non-competitive inhibitor

A

Binds away from active site, changing its shape
∴ ↓ Efficacy
Irreversible, affinity is reduced
∴ Less potent

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9
Q

Define bioavailability

A

How much drug is uptaken systemically for effect
IV route = always 100%
Other routes = suboptimal

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10
Q

What is a therapeutic range?

A

Upper and lower of safe doses of a drug
Narrowe range = reqs more care in dispensing

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11
Q

Name some drug targets and examples of each

A

Receptor action - ARBs, BBs, salbutamol, tamoxifen, alpha blockers
Enzymes - ACEi, 5-alpha reductase inhibitors
Ion channels - CCB
Transporters - PPI

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12
Q

Define pharmocodynamics

A

Effect of drug on the body

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13
Q

Define pharmacokinetics

A

Effect of body on the drug
(when it’s being broken down)

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14
Q

State the 4 aspects of Pharmacokinetics

A

ADME

Administration (route)
Distribution
Metabolism! (IV skips this!)
Excretion (hepatically or renally)

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15
Q

Describe GIT metabolism

A

Mechanical and chemical digestion

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16
Q

Describe renal metabolism

A

Simple, already soluble molecules. Easy to pee out directly

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17
Q

Describe hepatic metabolism

A

More complex, hydrophobic molecules. Undergo phase 1 and/or phase 2 reacns

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18
Q

Describe Phase 1 reactions

A

NON-conjugation. Aims to slightly increase hydrophilicity.
By microsomal enzymes e.g. CYP450

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19
Q

Descrive Phase 2 reactions

A

Conjugation. Adds functional groups
e.g. glucuronidation to massively increase hydrophilicity

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20
Q

Name the 2 main receptors of cholinergic pharm

A

Nicotinic and muscarinic

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21
Q

Describe Nicotinic receptors

A

Usually pre-synpatic

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22
Q

Describe Muscarinic receptors

A

Usually post-synaptic

M1 = BRAIN
M2 = HEART
M3 = LUNGS

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23
Q

What condition is related to disrupted Ach Transmission at NMJ?

A

Myasthenia Gravis

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24
Q

Side/Effects of XS acetylcholine stimulation

A

SLUDGE

Salivation
Lacrimation
Urination
Defecation
GI distress
Emesis

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25
Q

Name the receptors of adrenergic pharm

A

alpha 1 & 2
beta 1
beta 2

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26
Q

Where are alpha 1 & 2 found?

A

On vessels and sphincters (e.g. bladder neck)

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27
Q

Example of alpha 1 block and its use + mechanism

A

Tamsulosin
1st line med for BPH
Relaxes bladder neck ∴ easier urine flow

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28
Q

Where is beta 1 found?

A

On heart

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29
Q

Give an example of a beta 1 agonist and its use + mechanism

A

e.g. Dobutamine - Cardiogenic shock, increases force and rate of cardiac contraction

30
Q

Give an example of a beta 1 antagonist and its use + mechanism

A

Beta blockers - decrease force and rate of cardiac contraction

31
Q

Another word for force of contraction

32
Q

Another word for rate of contraction

A

Chronotropy

33
Q

When are BBs CI?

34
Q

Where are beta 2 receptors found?

35
Q

What does a beta 2 agonist do?

A

Bronchodilation of airways
SABA !!

36
Q

What are beta blockers known as and why?

A

Cardioselective drugs
Mostly act on cardiac tissue ∴ beta 1 only blockers prescribed

37
Q

State the types of adverse drug reactions

A

Augmented (common)
Bizarre
Chronic use
Delayed
End of use

38
Q

What should you do if you witness an adverse drug reaction?

A

Report to MHRA! Using Yellow card scheme!!

39
Q

What is the bioavailability of opioids?

40
Q

Generally, when do you use opioids?

A

For chronic severe pain
usually cancer pain

41
Q

5mg diamorphine is equivalent to

A

10 mg morphine = 100 mg pethidine

42
Q

Main SE of opiate use?

A

Constipation

43
Q

How do you treat an opiate overdose?

A

IV Naloxone

44
Q

Complications of paracetamol overdose

A

Fulminant liver failure
Shutdown of basic physiological systems e.g. shock
Can lead to death!

45
Q

How is paracetamol metabolised? (check)

A

Hepatic metabolism

Phase 2 - 95%
Phase 1 - 5%

46
Q

Describe the pathophysiology behind a paracetamol overdose

A

Phase 2 pathway gets overwhelmed
∴ increase of Phase 1 pathway

This route includes production of NAPQI = hepatotoxic !!
∴ ↑ Phase 1 metabolism = ↑ NAPQI
∴ Liver failure !!

47
Q

DOAC mechanism and examples

A

Inhibits factor 10a
Apixaban, Rivaroxaban

48
Q

Warfarin mechanism

A

Inhibits 10, 9, 7, 2 (1972 - Vit K dependent factors)

49
Q

LMWH mechanism

A

Inhibits 10 and thrombin

50
Q

Alteplase (IV) mechanism

A

Fibrinolytic.
Essentially tPa - activates plasmin to eat fibrin mesh

51
Q

Antiplatelet mechanism and examples

A

Inhibits P2Y12 - affects primary platelet plug
Clopidogrel, ticagrelor

52
Q

NSAIDs mechanism

A

Inhibits arachidonic acid pathway Cox-1 and Cox-2

53
Q

Cox-1 role and s/e of its inhibition

A

Involved in prostaglandin synthesis, protects gastric mucosa
Peptic ulcer!!

54
Q

Describe Cox-2 pathway

A

Targeted pathway
Activation of Cox-2 is involved in inflammation

55
Q

Example of selective Cox-2 inhibitor

56
Q

Mechanism of Loop Diuretic

A

Acts on ascending limb of loop, inhibits NKCC2 channels

57
Q

Example of Loop Diuretic

A

Furosemide

58
Q

Mechanism of thiazide diuretic

A

Acts on DCT, inhibits Na-Cl co-transporter

59
Q

Example of thiazide diuretic

A

Bendroflumethiazide

60
Q

Mechanism of aldosterone antagonist

A

K+ sparing diuretic, acts on aldosterone receptors of collecting duct
Increases Na+ excretion and retains K+

61
Q

Example of aldosterone antagonist

A

Spironolactone

62
Q

Give examples of anti-hypertensives

A

ACEi - ramipril
CCB - amlodopine, verapamil

63
Q

What do PPIs do and give an example

A

Reduces acidity of GI lumen
e.g. Lanzoprazole

64
Q

Main S/E of ACEi
Why does this happen?

A

Dry cough
Build up of bradykinin

65
Q

Difference between tolerance and dependence

A

Tolerance = Physiological
Dependence = Psychological

66
Q

Main S/E of CCB
What condition is this sometimes mistaken for?

A

Ankle swelling
Heart failure!

67
Q

1st Line treatment for anaphylaxis

A

Adrenaline, 500 mcg, IM

68
Q

Prophylaxis for MI

A

ACAAB
ACEi (maintain BP)
CCB (BP)
Aspirin
Atorvastatin
BB (reduce HR to prevent shearing of coronary arteries)

69
Q

Acute Tx for MI

A

MONAC
Morphine, Oxygen (IF NEEDED), Nitrates, Aspirin, clopidogrel

70
Q

1st line Tx for T2DM
Why?
Main S/E

A

Biguanide - Metformin
Increases peripheral tissue sensitivity to insulin
GI distress and stomach pain

Phase 2 (24 decks)

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