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CBL Year 2 > Intro to pharmacology > Flashcards

Intro to pharmacology Flashcards

1
Q

Drug harms

A

anaphylactic reactions
side effects
terogenicity (he ability to cause defects in a developing fetus)
dependency

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2
Q

what does ADME stand for in pharmacokinetics

A

Absorption
distribution
metabolism
excretion

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3
Q

digoxin drug - what its used for etc.

A

slows conduction at cardiac AV node
used for arrhythmia management and heart failure
really excreted
risk of digoxin toxicity in chronic kidney disease (shows as broad complex bradycardia on an ECG)

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4
Q

what do beta2 adrenoreceptors do

A

causes bronchial smooth muscle relaxation

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5
Q

define pharmacology

A

the branch of medicine concerned with the uses, effects, and modes of action of drugs.

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6
Q

define therapeutic

A

the branch of medicine concerned with the treatment of disease and the action of remedial agents.

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7
Q

define drug selectivity

A

Selectivity refers to a drug’s ability to preferentially produce a particular effect and is related to the structural specificity of drug binding to receptors.

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8
Q

define drug specificity

A

will be used to describe the capacity of a drug to cause a particular action in a population.

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9
Q

define drug dose

A

dose refers to a specified amount of medication taken at one time.

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10
Q

define drug concentration

A

defined as the amount of drug in a given volume, such. as mg/L: 1-1.

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11
Q

drug affinity

A

the extent or fraction to which a drug binds to receptors at any given drug concentration or the firmness with which the drug binds to the receptor.

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12
Q

define agonism

A

A molecule that combines with a receptor on a cell to trigger physiological reaction. An example is an acetylcholine being the agonist that combines with the cholinergic receptor.

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13
Q

define partial agonist

A

partial agonists are drugs that bind to and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist.

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14
Q

Define potency

A

potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity. A highly potent drug evokes a given response at low concentrations, while a drug of lower potency evokes the same response only at higher concentrations.

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15
Q

define efficacy

A

is the capacity to produce an effect (eg, lower blood pressure).

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16
Q

What is the relationship between drug concentration and response?

A

Progressive increases in drug dose (which, for most drugs, is proportional to the plasma drug concentration) produce increasing response but only within a relatively narrow range of dose; further increases in dose beyond this range produce little extra effect.

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17
Q

define desensitisation in pharmacology

A

refers to the common situation where the biological response to a drug diminishes when it is given continuously or repeatedly.

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18
Q

define drug tolerance

A

Drug tolerance or drug insensitivity is a pharmacological concept describing subjects’ reduced reaction to a drug following its repeated use. Increasing its dosage may re-amplify the drug’s effects; however, this may accelerate tolerance, further reducing the drug’s effects.

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19
Q

examples of full agonistic drugs

A

opioids for pain

beta adrenoreceptors for asthma

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20
Q

two types of antagonists

A

competitive and non-competitive

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21
Q

what is a competitive antagonist

A

competitive antagonist binds to the same site as the agonist but does not activate it, thus blocks the agonist’s action.

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22
Q

what is a non-competitive antagonist

A

A non-competitive antagonist binds to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor.

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23
Q

how is antagonism measured

A

The potency of an antagonist is usually defined by its half maximal inhibitory concentration (i.e., IC50 value). This can be calculated for a given antagonist by determining the concentration of antagonist needed to elicit half inhibition of the maximum biological response of an agonist.

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24
Q

examples of antagonism drugs

A

beta blockers and antipsychotic drugs

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25
Q

what is a drug

A

any synthetic or natural chemical substance that can alter biological function; may be used in treatment, prevention or diagnosis of disease

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26
Q

two ways a drug can produce an (adverse) side effect

A

1) target is too widespread -drug is selective for its target but the target is in part of the body where it can give side effects (e.g. aspirin therapeutically is an anti-inflammatory, antipyretic, analgesic, and anti-platelet aggregation but in toxicity causes GI bleeding)
2) the drug hits other targets - drug is not selective and will bind and activate other targets (e.g. morphine therapeutically is an analgesic, but in toxicity can cause respiratory depression, is addictive, can cause vomiting and constipation)

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27
Q

if a drug is hydrophilic what is the best way to administer it?

A

through IV or orally

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28
Q

what are transdermal patches for

A

for drugs that are not water soluble

e.g. nicotine patches or HRT

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29
Q

6 molecular targets for drug action

A

receptors (transduce signal from drug)
enzymes (activate or switch off)
transporters (Carry molecules across membranes)
Ion channels (open or close)
nucleic acids (affect gene transcription)
miscellaneous (lipids, metal ions, etc.)

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30
Q

examples of drugs that inhibit enzymes

A

Cyclooxygenase inhibitors for pain relief (usually arthritis)

HMG - CoA Reductase inhibitors for hypercholesteraemia
(atorvastatin [Lipitor] ; pravastatin [pravachol])

Angiotensin converting enzyme (ACE) inhibitors for high blood pressure, heart failure and chronic renal insufficiency (capatopril [capoten] ramipril [altace])

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31
Q

what are Pro-drugs

A

given as a pharmacologically inactive compound that is then metabolised by the body to produce a pharmacologically active compound

( L-DOPA (pro-drug) to dopamine (drug) used to treat parkinsons)
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32
Q

How is drug affinity measured?

A

Affinity is inversely proportional to the potency of a drug 1 Kd , where Kd is the dissociation constant. The strength of the binding (interaction) of a ligand and its receptor can be described by affinity. The higher the Kd value, the weaker the binding and the lower the affinity.

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33
Q

what determines the position of the binding curve along the concentration axis? (drug affinity)

A

Determined by affinity, efficacy and receptor number

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34
Q

what is a receptor reserve

A

This refers to the condition in a tissue whereby the agonist needs to activate only a small fraction of the existing receptor population to produce the maximal system response.

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35
Q

partial agonism by definition

A

occupy ALL receptors to evoke their maximum response

partial agonists have NO spare receptors

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36
Q

example of partial agonist (think beta 2 adrenergic receptors)

A

salbutamol

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37
Q

4 types of antagonism

A

competitive
non-competitive
uncompetitive
physiological

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38
Q

competitive antagonism

A

binds at the agonist recognition site preventing access

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39
Q

non competitive antagonism

A

does not bind at the agonist site but inhibits agonist binding in other ways

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40
Q

uncompetitive antagonism

A

this is when binding occurs to an activated form of the receptor

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41
Q

physiological antagonism

A

when the effect of a neurotransmitter or hormone is countered by the action of another neurotransmitter or hormone

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42
Q

what equation describes competitive antagonism

A

Gaddum-Schild [D1]/[D1] = 1 + ([B]/Kb)
where d1/d1 = concentration ratio
[B] = antagonist
Kb = dissociation constant of antagonist

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43
Q

examples of competitive antagonists in the clinic

A

propanolol - beta adrenoreceptor - lowers HR

Haloperidol - dopamine receptor - antipsychotic

Atropine - muscarinic ACH receptor - dilation of pupils, decreases secretions

Ranitidine - histamine H2 receptor - decreases gastric acid secretion

D-tubocurarine - nicotinic Ach receptor - neuromuscular block

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44
Q

effect of a competitive antagonist on an agonist concentration - response curve

A

shifts the agonist dose response curve to the right with no change in the apparent maximum response obtained

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45
Q

What does ADME relate to

A

dose of drug administered and absorbed
drugs in tissue of distribution
drug in systemic circulation
drug metabolised or excreted

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46
Q

what does pharmacokinetics relate to

A

what the body does to the drug

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47
Q

what does pharmacodynamics relate to

A

what the drug does to the body

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48
Q

4 reasons why ADME is important

A

1) important to know if a drug is going to be absorbed if given by a particular route
2) important to estimate accurate plasma concentrations of drug as a function of time -plasma drug concentration is dynamic it changes with time
3) to know where the drug goes once inside the body- how it distributes
4) Drug metabolism - are the metabolites safe?

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49
Q

most common route of drug administration

A

oral

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50
Q

2 examples of drugs that are administered sublingually

A

GTN spray

ondansetron (for migraines)

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51
Q

why are drugs administered sublingually

A

rapid onset

only suitable for drugs that are lipid soluble so they can cross the membrane

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52
Q

why are drugs administered rectally

A

in order to be absorbed into general systemic system or localised
usually give diazepam rectally if patient is unconscious or seizing or for a small child whose veins might be too small

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53
Q

what does enteral mean in terms of drug administration

A

it means that it is via the GI tract

54
Q

What does parenteral mean in terms of drug administration

A

that it does not go via the GI tract

55
Q

What does bolus mean

A

all at once

56
Q

what does infusion mean

A

over a length of time (usually hours or days)

57
Q

Benefits/downfalls of IV

A

rapid and can be given over a long period
(also associated with drug abuse)
(can cause an air embolism)

58
Q

Benefits/downfalls of IM

A

released in an aqueous vehicle to allow for rapid distribution

59
Q 
Fluphenazine (drug)?
what type of administration is used
used to treat what
dissolved in what
released how
A

depot injection - used to treat schizophrenia
dissolved in an oily vehicle
released slowly into blood from muscle over a few weeks

60
Q

Enteral routes of drug administration

A

oral
sublingual
rectal

61
Q

parenteral routes of drug administration

A 
IV
IM
Subcutaneous
Intradermal
Intranasal
Inhalation
Epidural
Transdermal
Topical
62
Q

examples of drugs administered intravenously

A

thiopentone (barbiturate, used to help you relax before you receive general anesthesia with an inhaled medication.)

Vanomyocin (antibiotic medication used to treat a number of bacterial infections.)

63
Q

examples of drugs administered intramuscularly

A

morphine (pain medication of the opiate family)

fluphenazine (high-potency typical antipsychotic medication)

64
Q

examples of drugs administered subcutaneously

A

insulin ( any pharmaceutical preparation of the protein hormone insulin that is used to treat high blood glucose. )

Humira (is a prescription medicine used to treat moderate to severe Crohn’s disease (CD) in adults and children 6 years of age and older.)

65
Q

examples of drugs/things administered intradermally

A

flu vaccine

allergy testing

66
Q

examples of drugs administered intra-nasally

A

sumatriptan (medication used to treat migraine headaches and cluster headaches, serotonin agonist)

beclometasone (for hay fever and cold-like symptoms caused by common allergies (rhinitis))

67
Q

examples of drugs administered through inhalation

A

isoflurane (can be used to start or maintain anesthesia, however other medications are often used to start anesthesia rather than isoflurane, due to airway irritation with isoflurane)

salbutamol (brand name Ventolin among others, is a medication that opens up the medium and large airways in the lungs. It is a short-acting β₂ adrenergic receptor agonist which works by causing relaxation of airway smooth muscle.)

68
Q

examples of drugs administered through epidural

A

bupivacaine (medication used to decrease feeling in a specific area. In nerve blocks, it is injected around a nerve that supplies the area, or into the spinal canal’s epidural space)

69
Q

examples of drugs administered transdermally

A

nicotine - patches

Buprenorphine (opioid used to treat opioid use disorder, acute pain, and chronic pain.)

70
Q

examples of drugs administered topically

A

latanoprost (brand name Xalatan among others, is a medication used to treat increased pressure inside the eye)

Steroid cream - hydrocortisone

71
Q

what is oral bioavailability

A

the fraction of the oral dose that reaches the systemic circulation

72
Q

give an example of a drug with high oral bioavailability and one with low

A

high - diazepam
low - morphine

(Bioavailability refers to the extent and rate at which the active moiety (drug or metabolite) enters systemic circulation, thereby accessing the site of action. )

73
Q

3 factors affecting the oral bioavailability of a drug

A

1) poor absorption from the gut
2) breakdown of drug in gut
3) first pass effect

74
Q

what is the first pass effect of drugs

A

phenomenon in which a drug gets metabolized at a specific location in the body that results in a reduced concentration of the active drug upon reaching its site of action or the systemic circulation

75
Q

Describe the use of pro-drugs in medicine

A

can be used to improve drug delivery or pharmacokinetics, to decrease toxicity, or to target the drug to specific cells or tissues. Ester and phosphate hydrolysis are widely used in prodrug design because of their simplicity, but such approaches are relatively ineffective for targeting drugs to specific sites.

76
Q

why might a pro-drug be used for a patient

A

may be used to improve how selectively the drug interacts with cells or processes that are not its intended target. This reduces adverse or unintended effects of a drug, especially important in treatments like chemotherapy, which can have severe unintended and undesirable side effects.

77
Q

6 factors affecting drug absorption at a membrane

A

1) pKa of a drug (pH at which is it 50% ionised)
2) pH at absorbing site
3) Drug preparation
4) area of absorbing surface
5) Rate of blood flow to other side of absorbing surface
6) presence of food, drugs that can affect stomach emptying/gut motility

78
Q

pH of stomach

A

2

79
Q

pH of plasma

A

7.4

80
Q

pH of small intestine

A

8

81
Q

what is ion trapping

A

ion trapping is the build-up of a higher concentration of a chemical across a cell membrane due to the pKa value of the chemical and difference of pH across the cell membrane.

82
Q

why is pH and pKa important in drugs

A

because many drugs are either weak acids or weak bases, and so can exist in ionised or un-ionised forms depending on pKa of drug or pH of solution
If membrane is present which separates different pH solutions it can lead to ion trapping

83
Q

define drug distribution

A

penetration of a drug into tissues and organs from the blood

84
Q

what does the degree of drug distribution depend on

A

lipid solubility
plasma protein binding (like albumin)
rate of blood flow

85
Q

How can drug distribution be measured

A

by apparent volume of distribution (Vd) - volume of water in which drug would have to be distributed to give its plasma concentration

also written as (amount of drug in body/Cp)
where Cp is plasma concentration

86
Q

can volume of Vd (apparent volume of distribution of a drug) exceed the total body water content

A

yes

87
Q

two uses of Vd (apparent volume of distribution of a drug)

A

partly determines plasma half-life of the drug

used in pharmacokinetic calculations to determine dosing schedules

88
Q

what is plasma drug binding important for?

A

distribution
as drugs that are bound to plasma proteins (such as albumin) cannot leave the blood
drugs that are tightly and extensively bound to plasma proteins tend to have a small Vd (drugs like anticoagulant warfarin)

89
Q

how does drug redistribution work in the body

A

extent of drug distribution into tissues depends on the degree of plasma protein and tissue binding. In the bloodstream, drugs are transported partly in solution as free (unbound) drug and partly reversibly bound to blood components (eg, plasma proteins, blood cells).

90
Q

what is elimination of a drug

A

overall removal of drug from the body, can be done by excretion or metabolism

91
Q

what is excretion of a drug

A

movement of a drug or metabolite from inside to outside the body

92
Q

what is metabolism of a drug

A

chemical change of drug structure

93
Q

5 main excretive methods of drugs

A

urine, faeces, milk, bile, vomit

94
Q

4 main organs for drug metabolism

A

liver
kidney
lungs
blood plasma

95
Q

what is plasma half-life of a drug (T0.5)

A

time it takes for plasma concentration (Cp) to fall to half its initial value

96
Q

what does a short drug half life mean

A

that the body eliminates the drug quickly and that oral doses have to be given more often than drugs with longer half lives

97
Q

give an example of a drug with a very short, short, medium, long, and very long half -life

A

very short - remiphentanil (15 mins), patient-controlled analgesia (PCA)

Short - proprananol (beta-blocker, 3-4 hrs), medication of the beta blocker class.

medium - tetracycline (antibiotic) (10hrs)

long - amphotericin (anti-fungal) (18hrs)

very long - digoxin (40hrs)

98
Q

equation for rate of elimination of a drug

A

rate of elimination = clearance x Cp

99
Q

what is clearance of a drug

A

equal to the amount of plasma which is cleared of its drug content in a unit time

100
Q

as the rate of drug absorption decreases what 3 things happen (think graph)

A

peak Cp decreases

time to peak increases

drug persists in body longer

101
Q

which drugs are excreted by the kidney

A

drugs that are not lipid soluble

102
Q

how can changes in urinary pH alter drug excretion

A

for a weak acid, urinary excretion can be increased by making the urine more alkaline (e.g. with sodium bicarbonate)

for a weak base, urinary excretion can be increased by making urine more acidic (e.g. with ammonium chloride)

103
Q

explain first order drug elimination

A

occur when a constant proportion of the drug is eliminated per unit time. (key here is proportion of drug not amount)

104
Q

explain zero order drug elimination

A

a constant amount of drug is eliminated per unit time

key here is amount not proportion

105
Q

difference between IV bolus and IV infusion

A

bolus achieves a very high peak which only lasts 5–6 hours. The infusion achieves steady levels after an initial delay. An infusion produces a steady level which can be varied and is exactly what is needed, for example during and after surgery.

106
Q

what is a loading dose in comparison to a maintenance dose

A

a loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose. A loading dose is most useful for drugs that are eliminated from the body relatively slowly, i.e. have a long systemic half-life.

107
Q

what are the different types of metabolites formed from drug metabolism

A

Two different phases:
phase I: by oxidation, reduction, or hydrolysis
phase II: by conjugation (joining together) species formed in Phase I with polar molecules, making metabolite less lipid soluble, and hence easier to excrete in urine

108
Q

how does enzyme induction affect how drugs are metabolised

A

refers to an increase in the rate of hepatic metabolism

this leads to a decrease in the concentrations of drugs metabolised by the same enzyme

109
Q

how does enzyme inhibition affect how drugs are metabolised

A

reduces metabolism

110
Q

genetic polymorphism

A

are defined as the occurrence of multiple alleles at a locus, where at least two alleles occur with a frequency greater than 1%.

example is blood groups - ABO

111
Q

how does genetic polymorphism affect how drugs are metabolised

A

it varies - it can affect the gene that metabolises drugs

known to cause people variations

112
Q

describe the toxicity of paracetamol in overdose

A

may cause varying degrees of liver injury over the 2 to 4 days following ingestion, including fulminant hepatic failure. Rarely, massive overdose may initially present with coma and severe metabolic acidosis.

113
Q

What is an adverse drug reaction

A

unintended, harmful events attributed to the use of medicines – occur as a cause of and during a significant proportion of unscheduled hospital admissions.

114
Q

1mM in M

A

1 x 10-3 M

115
Q

1nM in M

A

1 x 10-9M

116
Q

1µM in M

A

1 x 10 - 6 M

117
Q

1pM in M

A

1 x 10 - 12 M

118
Q

• 300µg/ml with initial volume of 0.5ml, diluted to final volyme of 10ml. Concentration?

A

○ 15µm/ml

C1V1=C2V2

119
Q

• 1ml stock volume diluted to 20ml. Final solution has concentration of 20µg/ml. concentration?

A

○ 400µg/ml

120
Q

liquid drug calculations ( how to do them)

A

○ Volume needed=mass needed x (mass/volume)
○ Need 500mg dose of Y
§ Y comes in 250mg/50ml
§ 500mg x (50ml/250mg) = 100ml

121
Q

Drug C comes in 15% w/v how much solution is needed to provide 30g of C?

A

200ml

30/0.15

122
Q

Drug C comes in 15% w/v how much solution is needed to provide 22.5g of C?

A

150ml

22.5/0.15

123
Q

Drug C comes in 15% w/v how much solution is needed to provide 90g of C?

A

600ml

90/0.15

124
Q

Patient has been taking 2 tablets per day of clarithromyocin, each tablet contains 250mg. They are switched to liquid form of the drug which is 5% (w/v). How much liquid do they need to take per day.

A

500mg in g is 0.5g
0.5/0.05 = 10
so answer is 10ml

125
Q

Patient takes 20ml of 2% (w/v) solution of drug x. They are switched to taking tablets that are 200mg of drug. How many tablets do they need to take a day.

A

0.4g a day
0.4 g to mg is 400mg
so 2 tablets a day

126
Q

Patient needs 20µg/kg of drug Y. They weigh 80kg. Tablets contain 0.4mg of drug Y. How many tablets do they need?

A

80 x 20 = 1600
1.6 mg
4 tablets

127
Q

What is meant by Kd

A

the equilibrium dissociation constant -

Think of equation P = [D]/([D] +KD)

128
Q

opioid toxidrome definition

A

opioid agonism leading to pinpoint pupils (miosis) and CNS and respiratory depression

129
Q

sedative hypnotic toxidrome

A

group of drugs that cause CNS depression

benzodiazepines and barbiturates are most commonly used

130
Q

serotenergic toxidrome

A

a potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (CNS). It is seen with therapeutic medication use, inadvertent interactions between drugs, and intentional self-poisoning

131
Q

anticholingeric toxidrome

A

results from competitive antagonism of acetylcholine at central and peripheral muscarinic receptors. Central inhibition leads to an agitated (hyperactive) delirium - typically including confusion, restlessness and picking at imaginary objects - which characterises this toxidrome.

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Q

cholinergic toxidrome

A

represents the acute phase of cholinesterase inhibitor poisoning. It results from the accumulation of excessive levels of acetylcholine in the synapses, glands, smooth muscles, and motor end plates where cholinergic receptors are found.

CBL Year 2 (14 decks)

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