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Osha 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is a drug?

A

A medicine or other substance which has a physiological effect when ingested/introduced into the body.

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2
Q

What is druggability?

A
  • the ability of a protein target to bind to small molecules with high affinity
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3
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects

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4
Q

What is the difference between an exogenous and endogenous ligand?

A

Exogenous: drugs
Endogenous: hormones/neurotransmitters

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5
Q

What are the 4 drug targets?

A
  • Receptors
  • Enzymes
  • ion channels
  • transporters
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6
Q

What chemicals allow receptors to communicate?

A
  • neurotransmitters e.g. Ach, serotonin
  • autacoids: cytokines, histamine
  • hormones: testosterone, hydrocortisone
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7
Q

What is the action of competitive inhibitors?

A

bind at the active site and reversibly reduce efficacy, affinity is unchanged. The action can be overcome by increasing the dose of the agonist. E.g. naloxone for opioid receptors.

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8
Q

What is the action of non competitive inhibitors?

A

bind away from the active site, irreversibly reducing both efficacy and affinity. E.g. ketamine at the NMDA-glutamate receptor.

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9
Q

What are the 4 types of receptors?

A
  • Ligand gated ion channels
  • G protein coupled receptors
  • Kinase-linked receptors
  • Cytosolic/nuclear receptors
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10
Q

What are ligand gated ion channels?

A
  • Molecule that sits in cell membrane and controls a pore opening and closing
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11
Q

How do G protein coupled receptors work?

A
  • guanine nucleotide-binding proteins- hydrolyse GTP to GDP
  • G proteins (GTPases) act as molecular switches
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12
Q

What is the 2 state model?

A

Drugs activate receptors by inducing or supporting a conformational change in the receptor from off to on

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13
Q

What is the definition of physicochemical?

A

2 drugs react completely independently of what is happening in the body

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14
Q

What is the definition of pharmacodynamics?

A

The effect a drug has on the body

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15
Q

What is the definition of pharmacokinetics?

A

The effect of the body on the drugs

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16
Q

What is an additive drug reaction?

A

2 drugs that have the same pharmacodynamic effect and the total effect is the sum of the 2. E.g. 2 drugs that cause bp to drop > summative drug reaction. 1 + 1 = 2

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17
Q

What is a synergistic reaction?

A

when 2 drugs are put together, the effect they have is more than the effects of the individual drugs 1 + 1 > 2

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18
Q

What is an antagonistic reaction?

A

when 1 drug cancels out the effect of the other drug to give no overall effect. 1 + 1 = 0

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19
Q

what is the potentiation effect?

A

Give drug A then give drug B. The effect of drug A is increased, the effect of drug B is as expected. 1 + 1 = 1.5 + 1

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20
Q

In which way are most drugs metabolised and excreted?

A

Hepatically metabolised and renally excreted

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21
Q

What is bioavailability and what is it for IV drugs?

A

how much of a drug is available over a given time period, 100% for IV

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22
Q

How is gut motility affected by drugs?

A

Reduced gut motility leads to reduced oral drug absorption

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23
Q

How is drug absorption affected by acidity?

A
  • Drugs are either ionised or unionised
  • unionised particles can pass through phospholipid bilayer but ionised can’t
  • highly acidic environments form more ionised drugs making them less effective
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24
Q

What is the effect of protein bound drugs?

A
  • No effect
  • drugs with lower protein binding affinity will have more effect as there is a greater free concentration in the plasma
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25
Q

What is an adverse drug reaction?

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug. Noxious and unintended.

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26
Q

What is the difference between ADRs and side effects?

A
  • Side effects is unintended but can be beneficial
  • ADRs are always unpleasant
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27
Q

What is the type of effect of the drug if the dose is beyond, within or below the therapeutic range?

A
  • Toxic effects (beyond)
  • Collateral effects (within range)
  • Hyper-susceptibility effects (below)
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28
Q

What is a hyper-susceptibility reaction?

A
  • Receiving sub therapeutic range doses
    e.g. Anaphylaxis and penicillin
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29
Q

What are some patient risk factors for ADRs?

A
  • gender (more common in women)
  • elderly/neonates
  • polypharmacy
  • genetics
  • hypersensitivity
  • hepatic/renal problems
  • adherence problems
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30
Q

What are some drug risk factors for ADRs?

A
  • steep dose-response curve
  • low therapeutic index (small difference between therapeutic and toxic doses)
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31
Q

What are possible toxic effects of ADRs?

A

nephrotoxicity/ototoxicity, ataxia, cerebellar signs and symptoms

32
Q

What are the types of time dependent reactions from ADRs?

A
  • rapid reactions
  • 1st dose
  • early
  • intermediate
  • late
  • delayed
33
Q

What is A in the Rawlins Thompson classification?

A

Augmented: predictable, dose dependent, common. Is an extension of the primary effect and can cause secondary effect

34
Q

What is B in the Rawlins Thompson classification?

A

Bizarre, not predictable or dose dependent. can’t be readily reversed, is less common but still serious

35
Q

What is C in the Rawlins Thompson classification?

A

Chronic: osteoporosis and steroids. Is uncommon but related to the cumulative dose.

36
Q

What is D in the Rawlins Thompson classification?

A

Delayed: malignancies that occur after immunosuppression. Usually dose related and shows some time after first use

37
Q

What is E in the Rawlins Thompson classification?

A

End of treatment: occurs after abrupt drug withdrawal. e.g. opiates

38
Q

What is F in the Rawlins Thompson classification?

A

Failure of therapy. Common and dose related, caused by drug interactions

39
Q

What should be reported in yellow card reactions?

A

Reactions that are:
- fatal
- life threatening
- disabling/incapacitating
- hospitalisation

40
Q

When do ADRs most commonly occur?

A
  • Soon after a new drug is started
  • An increase in dosage use
  • Symptoms disappearing when the drug is stopped and reappearing when the drug restarts
41
Q

What is the autonomic nervous system?

A

Controls all unconscious movement e.g. regulatory control in vascular, airway and visceral smooth muscle; HR; energy metabolism

42
Q

What are the divisions of the autonomic nervous system?

A

sympathetic: fight or flight - dilates pupils + bronchi, inhibits GI motility, relaxes bladder
parasympathetic: rest and digest - constricts pupils, stimulates digestive juice secretion

43
Q

What is the structure of the autonomic nervous system (where are the longer ganglia)?

A

sympathetic: ganglia near spinal cord with longer post ganglionic fibres
parasympathetic: ganglia near target organs with short post ganglionic nerves

44
Q

What are the 2 main neurotransmitters?

A

noradrenaline: acts on adrenergic receptors in the SNS
acetylcholine: acts on muscarinic receptors in the PSNS

45
Q

What neurotransmitters does the sympathetic nervous system use?

A

pre ganglionic: acetylcholine on nicotinic receptors
post ganglionic: noradrenaline on α and β adrenoreceptors

46
Q

What neurotransmitters does the PSNS use?

A

pre ganglionic: ACh on nicotinic receptors
post ganglionic: ACh on muscarinic receptors

47
Q

What are the exceptions to the neurotransmitters of the autonomic nervous system?

A

Sweat glands: sympathetic post ganglionic fibres use ACh on muscarinic receptors
Nitric oxide: released from PSNS post ganglionic termini in blood vessels

48
Q

What do M2 muscarinic receptors control?

A
  • heart
  • activates SA node: decreases HR
  • AV node: decreases conduction velocity, induces AV node block and increases PR interval
49
Q

What do M3 muscarinic receptors control?

A
  • organs with PSNS innervation
  • produces mucus and induces smooth muscle contraction (bronchoconstriction)
  • GI: Increases saliva production, GI motility, promotes biliary secretion
  • Skin: causes sweating
  • Urinary: contracts detrusor, relaxes int urethral sphincter
  • Eye: causes myosis, secretion of tears
50
Q

Where is ACh present outside the autonomic nervous system?

A

Acts on N1 nicotinic receptors in the somatic nervous system

51
Q

What is dopamine?

A

The precursor of adrenaline and noradrenaline

52
Q

What is an agonist?

A

Agonists have full affinity and full efficacy, thereby increasing activation of receptors, e.g. morphine

53
Q

What is an antagonist?

A

Antagonists have full affinity and zero efficacy, thereby decreasing the activation of receptors, e.g. calcium channel blockers.

54
Q

What is the action of α-1 receptors?

A
  • vasoconstriction in the skin and splanchnic beds
  • contraction of smooth muscle
55
Q

What is the action of α-2 receptors?

A
  • mixed effects on vascular smooth muscle
  • exist in brain and peripherally
  • reduces vascular tone and reduces BP
56
Q

What is the action of α-1 antagonists?

A
  • lower BP
57
Q

What occurs at β-1 receptors?

A
  • Found in heart, kidney, fat cells
  • agonism leads to tachycardia, inc in stroke vol, renin release, lipolysis, hyperglycaemia
58
Q

What is the action of β-1 blockers?

A
  • reduce HR
  • reduce SV
  • reduce myocardial oxygen demand, help in remodelling in heart failure and post-myocardial infarction
59
Q

Where do β-2 receptors act and what is their role?

A
  • bronchi: bronchodilaton
  • bladder wall: initiates micturition
  • uterus: inhibition of labour
  • skeletal muscle: inc contraction speed
  • pancreas: insulin and glucagon secretion
60
Q

What drugs act at β-2 receptors?

A
  • agonist drugs e.g. salbutamol
  • useful in COPD and asthma
61
Q

What is the effect of β-3 receptors?

A

enhances lipolysis and relaxes the bladder detrusor

62
Q

What is an inverse agonist?

A
  • has the opposite effect to an agonist but still binds to the same receptor binding site. It depresses a receptor whereas antagonists return receptors to their basal activity.
63
Q

What is affinity vs efficacy?

A
  • Affinity: How well a ligand binds to the receptor
  • Efficacy: how well a ligand activates the receptor
64
Q

What is the difference between tolerance and desensitisation?

A
  • Tolerance: reduction in agonist effect over time due to continuously, repeated high concentrations
  • Desensitisation: uncoupled, internalised, degraded. is more rapid.
65
Q

What are the 3 types of protein ports?

A
  • uniporters: use energy from ATP to pull molecules in
  • symporters: use movement of one molecule in to pull another against its conc grad
  • antiporters: one moves against its gradient using energy from the second moving down its gradient
66
Q

How do opioids work?

A
  • use existing pain modulation pathways
  • Inhibit the release of pain transmitters at the spinal cord and midbrain, modulating pain perception in higher centres changes the emotional perception of pain
67
Q

What is potency?

A

whether a drug is ‘strong’ or ‘weak’ relates to how well it binds to the receptor/its binding affinity

68
Q

What happens in the metabolism of morphine?

A
  • metabolised to morphine 6 glucoronide: more potent than morphine and really excreted
  • in renal failure, it builds up causing resp depression
  • use oxycodone instead
69
Q

What is the bioavailability of oral morphine vs IM/IV/s/c?

A
  • due to first pass metabolism by the liver: 50%
70
Q

What type of receptor is a muscarinic/nicotinic Ach receptor?

A

Muscarinic: G protein coupled receptor
Nicotinic: ligand gated ion channel

71
Q

What are the possible routes of drug administration?

A
  • Oral
  • IV
  • Subcutaneous
  • Intramuscular
  • Topical
  • Rectal
  • Sublingual/buccal
  • Inhalation
72
Q

What are the stages of drug development?

A
  • lead compound identification
  • pre-clinical research
  • filing for regulatory status
  • clinical trials on humans
  • marketing of the drug
73
Q

What are some examples of β-adrenoreceptor blockers (in order of β-1 receptor selectivity)?

A
  • bisoprolol
  • atenolol
  • propanolol
74
Q

What are the main clinical indications for β blockers?

A
  • IDH: angina
  • heart failure
  • arrhythmia
  • hypertension
75
Q

What are the main clinical indications for ACE inhibitors and give an example of a drug?

A
  • hypertension
  • heart failure
  • diabetic nephropathy
  • e.g. ramipril
76
Q

What are the main clinical indications for angiotensin II receptor blockers (ARBs) and give an example of a drug?

A
  • Hypertension
  • Diabetic nephropathy
  • Heart failure (when ACE-I contraindicated)
  • e.g. candesartan

Osha 2a (15 decks)

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