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Osha 2a > Pharmacology > Flashcards

Pharmacology Flashcards

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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
What is an adverse drug reaction?
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.
26
What is the difference between ADRs and side effects?
- Side effects is unintended but can be beneficial - ADRs are always unpleasant
27
What is the type of effect of the drug if the dose is beyond, within or below the therapeutic range?
- Toxic effects (beyond) - Collateral effects (within range) - Hyper-susceptibility effects (below)
28
What is a hyper-susceptibility reaction?
- Receiving sub therapeutic range doses e.g. Anaphylaxis and penicillin
29
What are some patient risk factors for ADRs?
- gender (more common in women) - elderly/neonates - polypharmacy - genetics - hypersensitivity - hepatic/renal problems - adherence problems
30
What are some drug risk factors for ADRs?
- steep dose-response curve - low therapeutic index (small difference between therapeutic and toxic doses)
31
What are possible toxic effects of ADRs?
nephrotoxicity/ototoxicity, ataxia, cerebellar signs and symptoms
32
What are the types of time dependent reactions from ADRs?
- rapid reactions - 1st dose - early - intermediate - late - delayed
33
What is A in the Rawlins Thompson classification?
Augmented: predictable, dose dependent, common. Is an extension of the primary effect and can cause secondary effect
34
What is B in the Rawlins Thompson classification?
Bizarre, not predictable or dose dependent. can't be readily reversed, is less common but still serious
35
What is C in the Rawlins Thompson classification?
Chronic: osteoporosis and steroids. Is uncommon but related to the cumulative dose.
36
What is D in the Rawlins Thompson classification?
Delayed: malignancies that occur after immunosuppression. Usually dose related and shows some time after first use
37
What is E in the Rawlins Thompson classification?
End of treatment: occurs after abrupt drug withdrawal. e.g. opiates
38
What is F in the Rawlins Thompson classification?
Failure of therapy. Common and dose related, caused by drug interactions
39
What should be reported in yellow card reactions?
Reactions that are: - fatal - life threatening - disabling/incapacitating - hospitalisation
40
When do ADRs most commonly occur?
- 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
What is the autonomic nervous system?
Controls all unconscious movement e.g. regulatory control in vascular, airway and visceral smooth muscle; HR; energy metabolism
42
What are the divisions of the autonomic nervous system?
sympathetic: fight or flight - dilates pupils + bronchi, inhibits GI motility, relaxes bladder parasympathetic: rest and digest - constricts pupils, stimulates digestive juice secretion
43
What is the structure of the autonomic nervous system (where are the longer ganglia)?
sympathetic: ganglia near spinal cord with longer post ganglionic fibres parasympathetic: ganglia near target organs with short post ganglionic nerves
44
What are the 2 main neurotransmitters?
noradrenaline: acts on adrenergic receptors in the SNS acetylcholine: acts on muscarinic receptors in the PSNS
45
What neurotransmitters does the sympathetic nervous system use?
pre ganglionic: acetylcholine on nicotinic receptors post ganglionic: noradrenaline on α and β adrenoreceptors
46
What neurotransmitters does the PSNS use?
pre ganglionic: ACh on nicotinic receptors post ganglionic: ACh on muscarinic receptors
47
What are the exceptions to the neurotransmitters of the autonomic nervous system?
Sweat glands: sympathetic post ganglionic fibres use ACh on muscarinic receptors Nitric oxide: released from PSNS post ganglionic termini in blood vessels
48
What do M2 muscarinic receptors control?
- heart - activates SA node: decreases HR - AV node: decreases conduction velocity, induces AV node block and increases PR interval
49
What do M3 muscarinic receptors control?
- 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
Where is ACh present outside the autonomic nervous system?
Acts on N1 nicotinic receptors in the somatic nervous system
51
What is dopamine?
The precursor of adrenaline and noradrenaline
52
What is an agonist?
Agonists have full affinity and full efficacy, thereby increasing activation of receptors, e.g. morphine
53
What is an antagonist?
Antagonists have full affinity and zero efficacy, thereby decreasing the activation of receptors, e.g. calcium channel blockers.
54
What is the action of α-1 receptors?
- vasoconstriction in the skin and splanchnic beds - contraction of smooth muscle
55
What is the action of α-2 receptors?
- mixed effects on vascular smooth muscle - exist in brain and peripherally - reduces vascular tone and reduces BP
56
What is the action of α-1 antagonists?
- lower BP
57
What occurs at β-1 receptors?
- Found in heart, kidney, fat cells - agonism leads to tachycardia, inc in stroke vol, renin release, lipolysis, hyperglycaemia
58
What is the action of β-1 blockers?
- reduce HR - reduce SV - reduce myocardial oxygen demand, help in remodelling in heart failure and post-myocardial infarction
59
Where do β-2 receptors act and what is their role?
- bronchi: bronchodilaton - bladder wall: initiates micturition - uterus: inhibition of labour - skeletal muscle: inc contraction speed - pancreas: insulin and glucagon secretion
60
What drugs act at β-2 receptors?
- agonist drugs e.g. salbutamol - useful in COPD and asthma
61
What is the effect of β-3 receptors?
enhances lipolysis and relaxes the bladder detrusor
62
What is an inverse agonist?
- 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
What is affinity vs efficacy?
- Affinity: How well a ligand binds to the receptor - Efficacy: how well a ligand activates the receptor
64
What is the difference between tolerance and desensitisation?
- Tolerance: reduction in agonist effect over time due to continuously, repeated high concentrations - Desensitisation: uncoupled, internalised, degraded. is more rapid.
65
What are the 3 types of protein ports?
- 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
How do opioids work?
- 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
What is potency?
whether a drug is 'strong' or 'weak' relates to how well it binds to the receptor/its binding affinity
68
What happens in the metabolism of morphine?
- 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
What is the bioavailability of oral morphine vs IM/IV/s/c?
- due to first pass metabolism by the liver: 50%
70
What type of receptor is a muscarinic/nicotinic Ach receptor?
Muscarinic: G protein coupled receptor Nicotinic: ligand gated ion channel
71
What are the possible routes of drug administration?
- Oral - IV - Subcutaneous - Intramuscular - Topical - Rectal - Sublingual/buccal - Inhalation
72
What are the stages of drug development?
- lead compound identification - pre-clinical research - filing for regulatory status - clinical trials on humans - marketing of the drug
73
What are some examples of β-adrenoreceptor blockers (in order of β-1 receptor selectivity)?
- bisoprolol - atenolol - propanolol
74
What are the main clinical indications for β blockers?
- IDH: angina - heart failure - arrhythmia - hypertension
75
What are the main clinical indications for ACE inhibitors and give an example of a drug?
- hypertension - heart failure - diabetic nephropathy - e.g. ramipril
76
What are the main clinical indications for angiotensin II receptor blockers (ARBs) and give an example of a drug?
- Hypertension - Diabetic nephropathy - Heart failure (when ACE-I contraindicated) - e.g. candesartan

Osha 2a (15 decks)

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