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Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacodynamics?

A

how the drug affects the body

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2
Q

What is pharmacokinetics?

A

how the body affects the drug: disposition of the compound

absorption > distribution > metabolism > excretion

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3
Q

What is druggability?

A

ability of a protein target to bind small molecules with high affinity

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4
Q

What are the 4 main drug targets?

A

receptors
enzymes
transporters
ion channels

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5
Q

How do receptors work as drug targets?

A

interact with a ligand = initiates a change

ligands are exogenous (drugs) or endogenous (hormones, NTs)

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6
Q

Receptors facilitate communication between chemicals via what?

A

neurotransmitters eg ACh, serotonin
autacoids (locally produced) eg cytokines, hormones
hormones eg testosterone, hydrocortisone

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7
Q

What are the 4 types of receptor?

A

ligand-gated ion channels
g-protein coupled
kinase-linked receptors
nuclear receptors

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8
Q

Give an example of a ligand-gated ion channel?

A

nicotinic ACh receptor

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9
Q

Give an example of a g-protein coupled receptor?

A

beta-adrenoceptors

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10
Q

What ligands can interact with g protein coupled receptors?

A

light energy, peptides, lipids, sugars, proteins

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11
Q

How do g protein coupled receptors work?

A

g proteins transmit signals from GPCRs
g proteins = GTPases are molecular switches
ON = bound to GDP
OFF = bound to GTP

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12
Q

How does the muscarinic ACh receptor (M3R) work?

A

g protein coupled
couples with Gq and PLC
produces 2nd messengers: IP3 or DAG

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13
Q

How do beta-2-adrenoceptors work?

A

g protein coupled
couples with Gs and AC
produces 2nd messenger cyclic-AMP

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14
Q

How do kinase-linked receptors work?

A

ligand binds to receptor on tyrosine kinas
kinase activity is stimulated (enzymatic)
tyrosines are phosphorylated
intracellular proteins bind to phospho-tyrosine docking sites

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15
Q

How do nuclear receptors work?

A

steroid receptors
modify gene transcription
have zinc fingers which bind to DNA

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16
Q

Give 2 examples for how chemical imbalances can lead to pathology?

A 
allergy = increase in histamine
Parkinson's = decrease in dopamine
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17
Q

Give 2 examples of how receptor imbalances can lead to pathology.

A

myasthenia gravis = loss of ACh receptors

mastocytosis = increase in c-kit receptor

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18
Q

What is potency?

A

measure of how well a drug works

highly potent = low concentrations illicit a great response

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19
Q

What is the EC50 of a drug?

A

the concentration that gives half the maximal response

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20
Q

What is the efficacy/intrinsic activity of a drug?

A

the maximum response achievable from a dose (the Emax of a drug)
the higher the Emax, the higher the efficacy

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21
Q

How is intrinsic activity calculated?

A

Emax of partial agonist/Emax of full agonist

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22
Q

What is a full agonist compared to a partial agonist?

A

full agonist can reach a 100% response - their Emax is 100

a partial agonist cannot get a full response and has an Emax below 100

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23
Q

What are antagonists?

A

decrease the effect of agonists

DON’T activate receptors

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24
Q

What is a competitive antagonist?

A

compete with agonist to bind so the agonist has no effect

bind to the same active site

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25
Q

How does a competitive antagonist affect a response graph?

A

shifts right

must increase amount of agonist to illicit same response

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26
Q

What is a non-competitive antagonist?

A

binds to an allosteric site on receptor to prevent it’s activation by an agonist

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27
Q

How does a non-competitive antagonist affect a response graph?

A

shifts right and down

even more agonist needed for the same response

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28
Q

What are the 2 main cholinergic receptor agonists?

A

muscarine (mACh receptor)

nicotine (nACh receptor)

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29
Q

What is the antagonist of muscarine?

A

atropine

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30
Q

What is the antagonist of nicotine?

A

curare

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31
Q

What type of receptor are all histamine receptors?

A

G-protein coupled receptors

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32
Q

What is the agonist for a histamine receptor?

A

histamine

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33
Q

What does histamine do in the gut when it binds to a histamine receptor?

A

contraction fo ileum

acid secretion from parietal cells

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34
Q

What is the antagonist to histamine?

A

mepryamine

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35
Q

What effect foes mepryamine have on the gut when it binds to a histamine receptor?

A

reversed contraction of ileum

no effect on acid secretion

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36
Q

What are the main 4 factors governing drug action?

A
  1. affinity
  2. efficacy
  3. number of receptors
  4. signal amplification
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37
Q

What is the affinity of a drug?

A

how well a ligand binds to the receptor

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38
Q

What is the efficacy of a drug?

A

how well a ligand activates the receptor

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39
Q

Do antagonists show affinity and efficacy?

A

does show affinity

has 0 efficacy

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40
Q

What happens when the number of receptors is reduced?

A

more drug is required to illicit the same response

max response can usually still be achieved

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41
Q

What is the receptor reserve?

A

where agonists need to activate only a small number of receptors to reach max response
= spare receptors
holds for full agonist in many tissues but no reserve for partial agonists

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42
Q

How can receptors be inactivated? Give an example.

A

by irreversible antagonists

eg bromoacetyl alprenolol menthane (BAAM) = irreversible B-adrenoceptor antagonist

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43
Q

What is signal amplification in drug action?

A

determines how powerful a response will be depending on the type of tissue the receptor is in
tissues with the same receptor and agonist may have completely different responses

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44
Q

What is allosteric modulation?

A

binding of an allosteric ligand to a receptor can effect an agonist’s effect

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45
Q

What are the 2 types of allosteric modulation?

A

affinity modulation: change in EC50 value

efficacy modulation: change in Emax

46
Q

What is positive and negative allosteric modulation called?

A 
positive = allosteric
negative = orthosteric (binds to actual active site)
47
Q

What is inverse agonism?

A

drug binds to the same receptor as the agonist but induces the opposite response

48
Q

What is tolerance to a drug?

A

a decrease in the effect of an agonist over time

49
Q

How does tolerance to a drug increase?

A

with continuous, repeated high concentrations

50
Q

What is desensitisation of receptors to drugs?

A

decreased responsiveness with chronic or repeated exposure

51
Q

What are the 3 main ways a receptor becomes desensitised?

A
  1. uncoupled: receptor can’t interact with g-proteins
  2. receptor is internalised in a vesicle
  3. receptor is degraded
52
Q

What is specificity?

A

the ability of a drug to produce an action at a specific site

53
Q

What is selectivity?

A

the degree to which a drug acts on a given site relative to other sites

54
Q

What is the drug most commonly used for overdoses in the UK?

A

paracetamol

55
Q

How is a paracetamol overdose treated?

A

activated charcoal

paracetamol binds to it and both leave the body = adsorption

56
Q

What are the 4 categories of physiochemical reactions?

A

adsorption
precipitation
chelation
neutralisation

57
Q

In terms of pharmacodynamics, what is summation? What equation represents this?

A

1 + 1 = 2
different drugs have a proportional effect
e.g. 2 half anaesthetic doses of different drugs will add up to a whole anaesthetic dose

58
Q

In terms of pharmacodynamics, what is synergism? What equation represents this?

A

1 + 1 > 2

the sum of 2 drugs is more than you would expect of them individually

59
Q

Give 2 examples of 2 drugs that have a synergistic effect?

A

paracetamol and morphine: increase effect

propofol and midazolam: lower doses of both below what you would expect

60
Q

How could the synergistic effect of 2 drugs be measured?

A

compare pain score before and after the medication (in the same person)
pain score will decrease more than you would expect

61
Q

In terms of pharmacodynamics, what is anatagonism? What equation represents this?

A

1 + 1 = 0

the opposite of a drug is given to cancel out it’s effect

62
Q

Give 2 examples of 2 antagonist drugs.

A
  1. doxazosin: alpha blocker in peripheral vasculature = decreases BP by vasodilation, very potent so with anaesthetic drugs = no vasoconstriction = decreased BP
    need alpha agonist to bring BP back up
  2. opioids and naloxone: both target opioid receptors
63
Q

In terms of pharmacodynamics, what is potentiation? What equation represents this?

A

1 + 1 = 1 + 1.5

drug A has the same effect but causes effect of drug B to increase

64
Q

Give an example of 2 drugs that show potentiation.

A

probenecid (for malaria) and penicillin: excreted from same place in kidney so they compete
probenecid wins and is excreted, penicillin remains in the body
duration of action for penicillin increases

65
Q

Where are drugs metabolised?

A

mostly liver

also kidney and lungs (ACEi) sometimes

66
Q

What kinds of changes are made to drugs during metabolism?

A

changed so they can be excreted

changes pro-drugs to functional metabolites e.g. codeine to morphine

67
Q

How is bioavailability of an oral drug compared to an IV drug calculated? Define it.

A

draw blood concentration by time graph
area under oral/area under IV
how much of oral medication makes it into the system vs how much IV drug gets into the system when given as a bonus

68
Q

Compare the absorption of oral and IV drugs.

A

IV drugs reach a high blood concentration very quickly and are then excreted very quickly
Oral drugs take a longer route to reach functionality, don’t reach a very high blood concentration and take longer to be excreted

69
Q

What is the bioavailability of paracetamol?

A

100% - oral and IV dose is usually the same

70
Q

What factors slow down the motility of the gut?

A

morphine

anything that effects the parasympathetic NS

71
Q

What happens to drug absorption when gut motility slows?

A

absorption decreases

drugs take longer to get into system

72
Q

Name 2 drugs that increase gut motility.

A

metaclopramide and erythromycin

to increase feeding (need enteral feeling) and drug intake through nasogastric tubes

73
Q

What is the commonest interaction of 2 drugs which cause motility changes?

A

oral contraceptive pill and antibiotics

74
Q

Which part of a drug is able to cross phospholipid bilayers and which is not? Why?

A

drugs are split into an ionised and unionised portion
the ionised drugs can’t cross phospholipid bilayers as they are lipophilic
unionised portions can cross

75
Q

What can change the proportion of ionised drug?

A

changing the acidity of the environment

76
Q

What happens to the proportion of ionised and unionised drug when an acidic drug enters an acidic environment? Or when a basic drug enters and acidic environment?

A

acidic in acidic = increased unionised portion
basic in acidic = increased ionised portion
or vice versa

77
Q

Which types of drugs alter the pH of the stomach? How does the effect drug absorption?

A

PPIs and antacids

alter absorption of other drugs depending on their pH

78
Q

What kind of environment alters the effectiveness of local anaesthetics?

A

don’t work near accesses
environment is too acidic
general anaesthetic often has to be used

79
Q

How does the interaction between anti-retroviral drugs and PPIs effect drug absorption?

A

anti-retroviral drugs can cause heartburn
PPIs given to treat heartburn
also decrease amount of anti-retroviral drug absorbed as it increases the ionised portion of arv drug in the gut > less absorbed > reduced effect

80
Q

Where does a drug go if it has a large volume of distribution? Give an example.

A

goes to random places in the body, binds to proteins
a low proportion goes to the effect site
e.g. propofol

81
Q

Where does a drug go if it has a low volume of distribution? Give an example.

A

stays in blood and most goes to effect site

e.g. muscle relaxants

82
Q

How does protein binding effect the distribution of a drug?

A

alters drug concentration in plasma
decreases distribution
less available for effect

83
Q

What happens when 2 highly protein bound drugs are given together? Explain with an example.

A

2 protein bound drugs can increase hate therapeutic level to a toxic level
warfarin and amiodarone
both highly protein bound > toxic dose of warfarin
warfarin has a narrow therapeutic range
amiodarone increases the international normalised ratio (INR) of warfarin until it is too high
warfarin is an anti-coagulant = higher risk of bleeding

84
Q

Explain enzyme induction in terms of morphine and CYP450.

A

morphine is metabolised to morphine-6-glucuronide via enzymes CYP450
m-6-g is x10 more potent than morphine
m-6-g is able to be excreted quickly so potency doesn’t matter until phenytoin is added

anti-epileptic drug phenytoin is added: increases effect of CYP450 = increases m-6-g = increases potency = more available before excretion

85
Q

What happens when chronic alcoholics are given morphine?

A

enzymes are constantly induced

effect of morphine likely to be potentiated

86
Q

Explain enzyme inhibition in terms of morphine and CYP450.

A

metronidazole inhibits CYP450
causes CYP450 to convert morphine to m-6-g much slower
m-6-g won’t work as effectively

87
Q

How can enzyme inhibition still allow morphine to have a potent effect?

A

may cause morphine to stay in the body for longer

so body still experiences an effect from morphine not just m-6-g

88
Q

What is the drug most commonly used for overdose around the world?

A

aspirin

89
Q

How can excretion of aspirin be increased?

A

it is an acidic drug

if an alkali is given in the blood, excretion occurs quicker

90
Q

What is renal excretion dependent on?

A

pH

91
Q

Give 4 examples of drugs which are weak acids. How do you speed up excretion?

A

aspirin, ibuprofen, paracetamol, warfarin

alkalinise urine

92
Q

Give 3 examples of drugs which are weak bases.

A

less common

amphetamine, salbutamol, atropine

93
Q

What does warfarin do?

A

inhibits vitamin K factors in the coagulation cascade

anti-coagulant

94
Q

What are the 2 factors that effect warfarin the most?

A

LOTS of interactions

  1. protein binding: other protein bound drugs increase its effect
    2a. enzyme induction: phenytoin leads to faster warfarin breakdown = has less of an effect
    b. enzyme inhibition: mentranidazole leads to slower warfarin breakdown = increased INR = increased risk of bleeding
95
Q

What drug does grapefruit juice interact with?

A

warfarin
effects protein binding and CYP450
shouldn’t be drank when on warfarin

96
Q

What 4 groups of drugs contribute to acute kidney injury? What are the 2 most common?

A
  1. NSAIDs
  2. Furomeside
    gentimicin
    ACEi
97
Q

How are drug effects altered in acute kidney injury?

A

effects are prolonged as they can’t be excreted when kidneys aren’t working

98
Q

Gentimicin and furosemide increase the risk of what?

A

deafness: ototoxic

especially when given together or too fast

99
Q

What type of drug are statins? What do they do?

A

HMG-CoA reductase inhibitors

block rate-limiting step in the cholesterol pathway = lower LDL = lowers risk of CVD

100
Q

What are the 3 A benefits of NSAIDs?

A

analgesic, anti-pyretic, anti-inflammatory

101
Q

What enzyme do NSAIDs inhibit? What pathway does this block?

A 
inhibit cyclooxygenase (COX) by competitive inhibition
prevents arachidonic acid reaching COX active site and forming prostaglandin H2
102
Q

What is special about how aspirin acts on COX?

A

it irreversibly inhibits COX

non-selective so can inhibits both forms of COX

103
Q

COX has 2 isoforms. What are they?

A

COX-1: normal and widespread around body
COX-2: induced, found in inflammation
some drugs are specific to one of these

104
Q

Name 2 examples of ACE inhibitors.

A

captopril, enalapril

105
Q

What do ACE inhibitors treat?

A

hypertension

106
Q

How do ACE inhibitors work? What pathway do they inhibit?

A

ACE is required to convert angiotensin I to angiotensin II
when inhibited: less angiotensin II binds to AT1 receptors
reduces vasoconstriction and aldosterone production = REDUCES BP

107
Q

What are the main symptoms of Parkinson’s?

A 
hypokinesia: reduced motor movement
tremor at rest
muscle rigidity, motor intertia
cognitive impariment
degenerative disease of basal ganglia
early degeneration of dopaminergic neutrons in nigrostriatal pathway = autonomic dysfunction and dementia
108
Q

What pathway do drugs for Parkinson’s have to target?

A

dopamine pathway

must be able to cross blood brain barrier

109
Q

What are the 3 different types of protein port?

A
  1. uniporter: uses ATP to pull molecules in
  2. symporter: uses movement of 1 molecule to pull in another against it’s concentration gradient
  3. antiporter: one substance moves down its gradient using energy from the 2nd substance moving down its gradient
110
Q

Give an example of a symporter and a drug that inhibits it.

A

Na-K-Cl cotransporter (NKCC): functions in organs that secrete fluids
furosemide: loop diuretic for hypertension and oedema
inhibits luminal NKCC in thick ascending limb of loop of Henle
causes Na, Cl and K loss in urine
reduces hyperosmolarity and reduces water diffusion out of CD into blood = water loss = dehydration

Phase 2a (5 decks)

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