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Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the definition of pharmacokinetics?

A

The fate of a chemical substance administered to a living organism
- what the body does to the drug

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2
Q

What is the definition of pharmacodynamics?

A

The biochemical, physiological and molecular effects of a drug on the body
- what the drug does to the body

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3
Q

What are the four pharmacokinetic processes?

A

Absorption
Distribution
Metabolism
Excretion

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4
Q

What is absorption (of a drug)?

A

The transfer of a drug from the site of administration to the systemic circulation

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5
Q

What are the three mechanisms used to permeate cell membranes and which molecules can cross them?

A
  1. Passive diffusion through hydrophobic membrane (most common) - lipid soluble molecules
  2. Passive diffusion through aqueous pores - small water soluble molecules
  3. Carrier-mediated transport - proteins transporting sugars, amino acids, neurotransmitters, trace metals
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6
Q

What are the factors affecting drug absorption?

A

Lipid solubility
Drug ionisation
Unionised/lipid soluble is able to move across the membrane

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7
Q

What are the factors affecting oral drug absorption in the stomach?

A

Gastric enzymes - could digest drug
Low pH - could degrade molecule
Food - full stomach will slow absorption
Gastric motility - could be altered by disease state or drugs
Previous surgery

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8
Q

What are the factors affecting oral drug absorption in the intestine?

A

Drug structure - unionised/lipid soluble molecule passively diffuse
Medicine formulation - coating of tablet/capsule, modified release controls absorption rate
P-glycoprotein removes substrates and moves them back to GI tract lumen

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9
Q

Where are weak acids best absorbed?

A

The stomach

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10
Q

Where are weak bases best absorbed?

A

The small instestine

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11
Q

Define first pass metabolism

A

Metabolism of drugs preventing them from reaching the systemic circulation

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12
Q

What could do first pass metabolism and how can it be avoided?

A

Enzymes in the intestinal wall
Enzymes in the liver

Can be avoided through the splanchnic circulation routes (rectal)

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13
Q

Define bioavailability (F)

A

The proportion of the administered drug that reaches the systemic circulation

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14
Q

What is bioavailability dependent on?

A

The extent of drug absorption
The extent of first pass metabolism

Not dependent on the rate of absorption

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15
Q

What are the four compartments of the body for drug distribution?

A

Fat
Plasma
Interstitial fluid
Intracellular fluid

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16
Q

What drug properties that affect their ability to move between compartments?

A

Molecule size - smaller increases dist.
Lipid solubility - lipophyllic increases dist.
Protein binding - unbound increases dist.

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17
Q

What is Volume distribution (Vd)?

A

The theoretical volume a drug will be distributed in the body
The volume of plasma required to contain the total administered dose
high Vd = well distributed

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18
Q

Define drug elimination

A

The process by which a drug becomes no longer available to exert its effect on the body

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19
Q

Define drug metabolism

A

Modification of a chemical structure to form a new chemical entity (metabolite)

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20
Q

What happens in phase 1 of drug metabolism?

A

Cytochrome p450 enzymes in the liver oxidise/reduce/hydrolyse to introduce a new reactive group to a structure

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21
Q

What happens in phase 2 of drug metabolism?

A

Conjugation of a functional group to produce a hydrophilic, non-reactive molecule

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22
Q

What is a pro drug?

A

A drug that is metabolised to its active form

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23
Q

What are the three processes of renal excretion?

A
  1. Glomerular filtration - unbound molecules pass through
  2. Active tubular secretion - OAT/OCTclear protein-bound drugs from peritubular capillaries
  3. Passive reabsorption of lipophilic molecules to the peritubular capillaries
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24
Q

What are first order kinetics?

A

Where the rate of elimination is proportional to the plasma drug concentration (a constant proportion of drug is eliminated)

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25
Q

What are zero order kinetics?

A

Where the rate of elimination is not proportional to the plasma drug concentration (a constant amount of the drug is eliminated)

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26
Q

What is Cmax?

A

The maximum plasma concentration

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27
Q

What is tmax?

A

The time taken to reach maximum plasma concentration

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28
Q

What is clearance (CL)

A

The efficiency of irreversible elimination of a drug from the systemic circulation

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29
Q

What is the bioavailability of an IV/IA administered drug?

A

100%

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30
Q

What is half life (t 1/2)?

A

The time taken for the plasma drug concentration to fall 50%

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31
Q

What is half life dependent on?

A

Clearance of a drug
Volume distribution

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32
Q

When is a drug considered cleared?

A

5 x half life

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33
Q

Define steady state

A

The rate of drug input equals the rate of elimination

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34
Q

What is Css?

A

The drug plasma concentration at steady state

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35
Q

What is time to Css considered to be?

A

5 x half life

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36
Q

What are the boundaries of the Css?

A

Maximum safe concentration (MSC) and minimum effective concentration (MEC)

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37
Q

What happens if the plasma concentration is above the maximum safe concentration?

A

Risk of toxicity and harm increases

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38
Q

What happens if the plasma concentration is below the minimum effective concentration?

A

Subtherapeutic - treatment won’t be effective

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39
Q

What is a loading dose?

A

A larger initial dose to speed up the time to steady state

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40
Q

When and why is therapeutic drug monitoring (TDM) used?

A

In drugs with a narrow therapeutic window to avoid toxicity and ensure efficacy

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41
Q

Define pharmacogenomics

A

The use of genetic and genomic information to tailor pharmaceutical treatment to an individual

42
Q

What are the four types of drug targets?

A

Receptors
Enzymes
Transporters
Ion channels

43
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 ligand observed effects

44
Q

What is a ligand?

A

A molecule that binds to another molecule. Could be endogenous or exogenous

45
Q

What are the four types of receptors targeted?

A
  1. Ligand-gated ion channels
  2. G protein Coupled Receptors
  3. Kinase-linked receptors
  4. Nuclear/cystolic receptors
46
Q

What is an agonist?

A

A compound that binds to a receptor to activate it

47
Q

What is an antagonist?

A

A compound that reduces/reverses the effect of an agonist

48
Q

What is the two state model?

A

Drugs can activate receptors by inducing or supporting a conformational change in the receptor

49
Q

Define potency

A

How well a drug works

50
Q

What is EC50?

A

The concentration that gives half the maximal response.
A measure of potency

51
Q

What is a full agonist?

A

An agonist that gives 100% of a response

52
Q

What is a partial agonist?

A

An agonist that illicit a response but not a full response

53
Q

Define Efficacy

A

How well a ligand activates a receptor
The maximum response achievable (Emax)

54
Q

Define intrinsic activity (IA)

A

The ability of a drug-receptor complex produce a maximum functional response

55
Q

What is competitive antagonism?

A

When an antagonist binds to the same site as the agonist

56
Q

What is non-competitive antagonism?

A

When an antagonist binds to an allosteric (non-agonist) site on a receptor to prevent activation of the receptor

57
Q

Define affinity

A

How well a ligand binds to a receptor
Agonists and antagonists have affinity

58
Q

Do agonists and antagonists show efficacy?

A

Agonists do
Antagonists don’t because they don’t activate receptors

59
Q

What is receptor reserve?

A

Spare receptors after full agonists have produced a maximum response

60
Q

What are irreversible antagonists?

A

Antagonists that permanently bind to a receptor

61
Q

What are the four factors affecting drug action?

A

Affinity
Efficacy
Receptor number
Signal amplification

62
Q

What is allosteric modulation?

A

When an allosteric ligand binds to a second site on the receptor and affects the agonist’s affect
Could change EC50 (affinity modulation), Emax (efficacy modulation)

63
Q

What is an inverse agonist?

A

A drug that binds to the same receptor as an agonist but induces the opposite pharmacological response to that of the agonist

64
Q

Define tolerance

A

A reduction in the agonist’s effect over time

65
Q

What is desensitisation?

A

Sudden failure to get a response/effect

66
Q

Which nervous system do cholinergic receptors affect?

A

Parasympathetic

67
Q

What is the neurotransmitter for cholinergic receptors?

A

Acetylcholine (ACh)

68
Q

What are the two subtypes of cholinergic receptors?

A

Nicotinic and muscarinic

69
Q

Describe nicotinic cholinergic receptors

A

Between pre- and postsynaptic neurones
Nerve and muscle types
Ligand gated
Stimulated by ACh
Stimulate action potential in postsynaptic neuron or stimulate muscle contraction

70
Q

Give an example of a drug affecting nicotinic cholinergic receptors

A

Botulinum - inhibits ACh release at neuromuscular junction causing paralysis
Curare - antagonist, muscle relaxant

71
Q

Describe muscarinic cholinergic receptors

A

G protein Coupled Receptors
Post-synaptic
5 types: M1, 2, 3, 4, 5

72
Q

Describe M1 muscarinic receptors

A

Cholinergic
Stimulator
Found in brain and stomach
When activated: HCl is released, pepsinogen is released, greater cognition and memory

73
Q

Describe M2 muscarinic receptors

A

Cholinergic
Inhibitor
Found in heart
When activated: Hr decreases, force of contractility reduces

74
Q

Describe M3 muscarinic receptors

A

Cholinergic
Stimulator
Found in glands and smooth muscle
When activated: tears, saliva, bronchial secretions, digestive enzymes (pancreas), insulin release, GI mucus secretion, pupil constriction, bronchial constriction, peristalsis, detrusor muscle contraction (urination), uterine contractions

75
Q

Give an example of an M3 antagonist

A

Ipratropium - stops bronchoconstriction in asthma and COPD

76
Q

What are the side effects of agonising/activating cholinergic receptors

A

Diarrhoea
Urinary excretion
Miosis - pupil constriction
Bronchoconstriction
Bradycardia
Emesis - vomiting
Lacrimation
Sweating
Salivation

77
Q

Which nervous system do adrenergic receptors affect?

A

Sympathetic

78
Q

What is the neurotransmitter for adrenergic receptors?

A

Acetylcholine and noradrenaline

79
Q

What are the subtypes of postganglionic adrenergic receptors?

A

alpha 1, alpha 2, beta 1 and beta 2 receptors

80
Q

Describe alpha 1 receptors

A

Adrenergic
Stimulatory
Found in smooth muscle, organs and glands except cardiac muscle and juxtaglomerular cells
When activated: vasoconstriction, pupil dilation

81
Q

Describe beta 1 receptors

A

Adrenergic
Stimulatory
Found in cardiac muscle and juxtaglomerular cells
When activated: increases force of contraction of heart, HR, electrical conduction, renin release (and therefore blood pressure)

82
Q

Describe alpha 2 receptors

A

Adrenergic
Inhibitory
Found in preganglionic membranes
When activated: inhibits noradrenaline release so self-inhibits

83
Q

Describe beta 2 receptors

A

Adrenergic
Inhibitory
Found in smooth muscle, organs and glands except preganglionic membranes
When activated: bronchodilation, vasodilation, reduced GI motility

84
Q

Give an example of an adrenergic receptor drug

A

Adrenaline in anaphylaxis - agonist of a1, B2 and B2
Salbutamol in asthma - agonist of B2 receptors
Propranolol - B1 and B2 antagonist

85
Q

How do opioids work in analgesia?

A

Opioids activate G Protein Coupled Receptors on nerve cells
This inhibits the release of pain transmitter at spinal cord and midbrain, blocking the descending transmission
This modulates pain at the higher centres, changing the emotional perception of pain and causing euphoria

86
Q

How is tolerance caused in opioids?

A

Prolonged use causes down regulation of receptors

87
Q

What is dependence in opioids?

A

Psychological effect - craving euphoria

88
Q

What is morphine metabolised to in the liver?

A

Morphine 6 glucuronide

89
Q

Why does codeine need to be metabolised?

A

It is a prodrug

90
Q

What are the side effects of taking opioids?

A

Respiratory depression
Sedation
Nausea and vomiting
Constipation
Itching
Immune suppression
Endocrine effects

91
Q

What is an opioid antagonist?

A

Naloxone - in respiratory depression, give IV, diluted with saline

92
Q

What is a drug interaction?

A

When a substance (drug, food or toxin) alters the expected performance of a drug

93
Q

What are pharmacodynamic drug interactions?

A

When drugs act on the same receptor/physiological system

94
Q

What are the two types of pharmacodynamic drug interactions?

A

Synergistic - two drugs having the same effect
Antagonistic - two drugs cancelling each other out

95
Q

What are the types of pharmacokinetic drug interactions?

A
  1. Affecting the rate or extent of drug absorption by changing the GI pH, complex formulation, induction or inhibition of p-glycoproteins
  2. competition for protein binding affecting drug distribution
  3. inducing or inhibiting metabolic enzymes
  4. competition for OATs/OCTs in renal tubule affecting excretion
96
Q

What is an adverse drug reaction?

A

a response to a medicinal product (or a combination of medicinal products) that is noxious or unintended

97
Q

What are the two classifications of ADRs?

A

ABCDEFG or DoTS

98
Q

What are the ABCDEFG classes of ADRs?

A

Augmented
Bizarre
Chronic
Delayed
End of use/withdrawal
Failure of treatment
Genetic

99
Q

What is the DoTS classification of ADRs?

A

Dose-relatedness - hypersusceptibility, side effects, toxic effects
Timing - time independent, time dependent
Susceptibility - groups of people that may be more susceptible

100
Q

Describe the standard drug development process

A
  1. Target identification
  2. Target assay construction and screening
  3. Target validation and medicinal chemistry safety
  4. Phase I - safety
  5. Phase II - efficacy and safety
  6. Phase III - efficacy and safety
  7. FDA/MHRA review and approval

Phase 2a (9 decks)

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