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PVS > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

List some target sites for drug action

A
  • Biological molecules, most often proteins
  • Enzymes
  • Carrier molecules
  • Ion channels
  • Receptors
  • Structural proteins
  • DNA
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2
Q

Define the term agonist

A

A molecule/drug that binds and activates the receptor

Has affinity and efficacy

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3
Q

Define the term antagonist

A

A molecule/drug that binds and has no effect on the receptor (affinity but no efficacy)

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4
Q

Define the term partial agonist

A

A molecule/drug that binds and has some effect on the receptor (has affinity and reduced efficacy)

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5
Q

Why might a partial agonist be used?

A

A partial agonist may be used where one drug has a strong effect but also leads to strong side effects, whereas the potency of another may be reduced but there are also fewer side effects

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6
Q

What is a dose-response curve?

A

A curve that plots the concentration of a drug (usually the log) against its response

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7
Q

What can a dose-response curve be used for?

A

Can be used to compare drugs acting on the same target to assess affinity, efficacy and margins of safety

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8
Q

Explain the term affinity

A

The tendency of a drug to bind to the receptor

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9
Q

Explain the term efficacy

A

The tendency of a drug to activate the receptor once bound i.e. its ability to give a response

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10
Q

Explain the term EC50

A

Effective concentration

- is the dose required for an individual to experience 50% of the maximal effect

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11
Q

Explain the term ED50

A

Effective dose
is the dose for 50% of the population to obtain the therapeutic effect
- relates to in vivo experiments where the overall effect is assessed

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12
Q

Explain the term therapeutic index

A

The safety margin of a drug

= toxic dose/effective dose

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13
Q

What does a larger therapeutic index mean?

A

Safer, as the toxic dose is much larger than the effective dose used

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14
Q

Explain the term potency

A

The amount of drug required to produce 50% of its maximal effects

  • Used to compare drugs within a chemical class
  • Usually expressed as mg/kg
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15
Q

Explain the term specificity

A

Describes the capacity of a drug to cause a particular action in a population
- Depends on receptor subtype

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16
Q

Describe the actions of a drug of absolute specificity

A

May increase or decrease a specific function of a given gene, protein or cell type, but must do either not both

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17
Q

Explain the term selectivity

A

Relates to a drug’s ability to target only a selective population i.e. a cell/tissue/signalling pathway in preference of others

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18
Q

Explain the term competitive antagonist

A

Competes with the agonist for the receptor binding site. can be overcome

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19
Q

What is the effect of a competitive antagonist on the agonist dose response curve?

A

The curve will be shifted to the right

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20
Q

Explain the term non-competitive antagonist

A

Non-competitive antagonists either bind to a different receptor site or block a chain of events post binding, acting downstream of receptor in the signalling cascade

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21
Q

Explain the term irreversible antagonist

A

An antagonist that dissociates only very slowly or not at all from a receptor, cannot be overcome with additional agonist

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22
Q

What type of bond do irreversible antagonists form with receptors?

A

Covalent bonds

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23
Q

Explain what is meant by the term inverse agonism

A

A drug that reduces the activation of a receptor with constitutive activity. can be regarded as drugs with negative efficacy

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24
Q

Explain the term IC50

A

Concentration of an antagonist to inhibit 50% of the agonist maximal effect. Can be used to measure antagonist drug potency

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25
Q

Define the term tachyphylaxis

A

“Rapid protection”

Increase in drug tolerance which develops after a short period of repeated dosing leading to a decrease in response to the drug

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26
Q

Define the term self-antagonism

A

When a drug becomes antagonistic to its own effects over time

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27
Q

List the ways in which loss of target sensitivity may occur

A
  • Change in receptors
  • Loss of receptors
  • Exhaustion of mediators
  • Increased metabolic degradation
  • Physiological adaptation
  • Drug transporters
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28
Q

Outline how a change in receptors can lead to loss of target sensitivity

A

Become resistant to drug stimulation/conformational changes

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29
Q

Outline how a loss of receptors may occur to lead to a loss of target sensitivity

A

Endocytosis of receptorss

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30
Q

How may exhaustion of mediators occur, leading to a loss of target sensitivity?

A

Degradation/low re-expression level

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31
Q

How may increased metabolic degradation lead to loss of target sensitivity?

A

Higher concentration of drug is required to exert an effect due to increased elimination of the drug

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32
Q

How may physiological adaptation lead to a loss of target sensitivity?

A

Cross talk between body systems allowing organs to compensate for discrepancies in others

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33
Q

How may drug transporters lead to a loss of target sensitivity?

A

Drug is removed from the receptor site before the effect can occur

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34
Q

What are the potential outcomes of drug-drug interaction?

A
  • Action of one or more drugs is enhanced
  • Development of totally new effects
  • Inhibitory effects on one drug from another
  • No change
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35
Q

What are some cases where drug-drug interaction may be likely?

A
  • Pregnancy
  • Chronic cases
  • Elderly
    as there is commonly polypharmacy in these cases
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36
Q

What are the 3 mechanisms of interaction between drugs?

A
  • Pharmaceutical
  • Pharmacokinetic
  • Pharmacodynamic
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37
Q

What is meant by pharmaceutical interactions between drugs?

A

Related to the physiochemical properties and formulation

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38
Q

What is meant by pharmacokinetic interactions between drugs?

A

Related to interactions within ADME

Absorption, distribution, metabolism, excretion

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39
Q

What is meant by pharmacodynamic interactions between drugs?

A

Related to interactions within receptor signalling

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40
Q

What causes pharmaceutical interactions between drugs?

A

Due to chemical or physical incompatibility/interaction

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41
Q

Give examples of drugs that have pharmaceutical interactions

A
  • Sodium bicarbonate and calcium
  • Insulin is denatured by glucose
  • Diazepam binds to plastics (syringes)
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42
Q

Outline how absorption may be affected by drug interactions

A
  • One drug may alter the acidity or motility of the stomach, affecting absorption of drugs taken orally
  • May also have gastric emptying
43
Q

Outline how chemical alterations may occur and affect drug-drug interactions

A
  • pH may be altered by one drug and thus affect another as many are pH dependent
  • Oxidation/reduction
  • Loss of drug potency
  • Complex formation
44
Q

Outline how distribution may be affected by, and affect drug-drug interactions

A
  • Some drugs reduce circulation and may therefore reduce clearance and elimination of others
  • Competition for binding sites on plasma proteins (albumin most common)
45
Q

Outline the pharmacodynamic effects of drug-drug interaction

A
  • Agonist/antagonist negate an effect
  • Agonist/antagonist induce harmful effect
  • Syngergistic effects
46
Q

What is meant by summation of effect?

A

When 2 drugs are administered together, effect seen is equal to sum of individual effects of each drug
1+1=2

47
Q

What is meant by potentiation of effect?

A

When a drug or food increases the effect of another drug, but has no effect when administered alone
1+0=2

48
Q

What is meant by synergism of effect?

A

When 2 drugs are administered together producing effects that are greater than would be produced if either drug was administered individually or would be seen with summative effects
1+1=3

49
Q

What is meant by Ki?

A

The dissociation constant for inhibitor binding and is an indicator of enzyme affinity for inhibitor

50
Q

What is the significance of Ki?

A

Can be used to establish at what concentration an agonist will overcome the inhibitor

51
Q

What is meant by enteral routes of drug administration?

A
  • Administration via the gastrointestinal tract

- Includes sublingual, swallowing and rectal

52
Q

Where does absorption take place with enteral administration?

A

Along the length of the GI tract

53
Q

What is meant by parenteral routes of drug administration?

A

Routes other than oral, go into blood stream

54
Q

Give examples of parenteral routes of drug administration

A
  • Topical
  • Intradermal
  • Subcut
  • Intramuscular
  • Intravenous
  • Inhalation
55
Q

Outline the effects of topical administration at different sites

A
  • Skin: local, slow and sustained effects (hours to weeks e.g. patches)
  • Eye drops: local effect, renew frequently
  • Nasal instillation: local systemic effect
56
Q

Compare the rates of absorption between intradermal, subcutaneous and intramuscular absorption

A
  • ID: slow
  • Subcut: faster (but fat layer may trap lipid soluble compounds)
  • IM: very fast absorption
57
Q

How does formulation of an injectable drug affect drug absorption?

A
  • Liquid > suspension > emulsion
  • Thinner formula = faster absorption
  • Can extend half life by altering formulation
58
Q

Outline the pros/cons of intravascular administration

A
  • Accurately control body concentration of drugs e.g. narrow therapeutic window
  • BUT cannot be recalled and slow admin needed to avoid side effects
59
Q

Discuss the absorption of drugs administered via inhalation

A
  • Rapid systemic effect
  • Dependent on tidal volume and size of aerosol particle
  • Smaller more likely to reach alveolar ducts and sacs
60
Q

What are the chemical properties of drugs that are rapidly absorbed?

A
  • Low degree of ionisation
  • High lipid/water partition in the non-ionised form
  • Low MW (<1000)
  • Biological affinity with transporters/facilitated diffusion
61
Q

What are the chemical properties of drugs that are not rapidly absorbed?

A
  • High degree of ionisation
  • Higher affinity to water vs lipid in the non-ionised form (flows with perisaltic mvt and eliminated or need transporters)
  • Large MW
  • Degraded by specific enzymes
62
Q

Explain the importance of the charge of a drug

A
  • In a protonated environment, acids neutral and bases charged so higher membrane permeability for acids
  • In non-protonated environment, acids charged and bases neutral, higher membrane permeability for bases
63
Q

Compare the absorption of enteral and parenteral drug administration

A
  • Enteral absorbed along entire GIT, goes through first pass metabolism
  • Parenteral bypasses first pass metabolism
64
Q

Explain the importance of the first pass metabolism in drug absorption

A
  • Occurs in the liver
  • Only affects orally administrated drugs
  • Many compounds inactivated and excreted via biliary system
65
Q

What is meant by first pass metabolism?

A

When a drug is metabolised before it reaches the systemic circulation

66
Q

Describe the movement of drugs through the first pass metabolism

A
  • From the portal vein from the GI tract, to the hepatocytes where they can be metabolised, then hepatic vein and into circulatory system
  • Can be recycled several times via the biliary system before entering the systemic circulation
67
Q

What processes occur in phase I of hepatic metabolism of drugs?

A
  • Oxidation
  • Reduction
  • Hydrolysis
  • I.e. catabolic processes
68
Q

What process occurs in phase II of hepatic metabolism of drugs?

A
  • Synthetic conjugation

- I.e. anabolic processes

69
Q

What is the most significant enzyme regarding drug metabolism?

A

CYP450

70
Q

What is the function of the CYP450 enzyme?

A
  • Acts in phase I of metabolism

- Adds hydroxy molecules to make drug more polar

71
Q

Where are mammalian CYPs found?

A
  • Majority in liver but can be present in wall of intestine

- Membrane bound to endoplasmic reticulum

72
Q

What enzymes are important in phase II of drug metabolism?

A
  • Transferases

- Esp glucoronyl transferase

73
Q

What is the function of the transferase enzymes?

A

Attach water soluble, endogenous molecules to make the drug more soluble
E.g. glucoronyl transferase adds glucoronic acid to make molecules very water soluble

74
Q

What are some potential results of drug metabolism?

A
  • Detoxification
  • Production of metabolites with similar activity to drug
  • Metabolite with different activity to drug
  • Production of toxic metabolites
75
Q

List variables that may affect drug absorption via enteral routes

A
  • Individual variation
  • Age
  • Temperature
76
Q

Outline how individual variables may affect drug absorption via enteral routes

A
  • Amount of food eaten
  • Peristaltic movement
  • Metabolic rates/organ function (age and size related)
77
Q

Outline how age may affect drug absorption via enteral routes

A
  • More chronic illness = more chance for adverse reaction
  • Elderly have less proteins and water in body
  • Infants more water (human)
  • pH of GIT may change with age
78
Q

Outline how temperature may affect drug absorption via enteral routes

A

Cold blooded animals have variable metabolism that may change depending on season and with environment

79
Q

What are the main routes of drug excretion?

A
  • Kidneys (mechanical)
  • Hepatobiliary system
  • Lungs (volatile compounds e.g. gas)
80
Q

What are some secondary routes of drug excretion?

A
  • Milk

- Sweat

81
Q

What is the function of phase I in liver metabolism of drugs?

A

Make drug more polar

82
Q

What is the function of phase II in liver metabolism of drugs?

A

Make molecule inactive and water soluble and thus excretable by the body

83
Q

What are the 3 processes of renal excretion of drugs?

A
  • Passive filtration
  • Secretion
  • Reabsorption
84
Q

What influences renal passive filtration of drugs?

A
  • GFR

- Plasma protein binding (bound will not be filtered)

85
Q

What influences renal secretion of drugs?

A
  • Affinity for transporters (OATs, OCTs)

- Lipophilicity, polarity

86
Q

What influences renal reabsorption of drugs?

A
  • Lipophilicity
  • Polarity
  • Urine pH
87
Q

Explain the role of transporters in renal secretion of drugs

A
  • Some membrane transporter recognise weak acids, others weak bases
  • Can put drug into proximal tubule to then be excreted
  • OAT: organic anion transporters
  • OCT: organic cation transporters
88
Q

Outline the process of renal reabsorption of drugs

A
  • Distal tubule
  • Only neutral molecules
  • Reabsorbed into blood
89
Q

What is the net renal excretion?

A

Filtration + secretion - reabsorption

90
Q

How is filtration excretion calculated?

A

GFR xfu

- where fu = drug plasma free fraction = 1-fraction of drug bound to plasma

91
Q

What is the significance of a renal excretion > GFRxfu?

A

Active secretion is taking place

92
Q

What is the significance of renal excretion

A

Net reabsorption is taking place

- may still have secretion but there is more reabsorption

93
Q

What are the consequences of metabolic acidosis on drug excretion?

A
  • pH of urine > pH of blood
  • Urine non-protonated in comparison
  • Acids in form of H+ i.e. charged, trapped in urine and excretion increased
  • Bases in neutral form, reabsorbed, excretion reduced
94
Q

What are the consequences of metabolic alkalosis on drug excretion?

A
  • pH urine < pH blood i.e. acidic urine
  • urine protonated
  • Acids in neutral form, reabsorbed and excretion reduced
  • Bases in charged form so cannot be reabsorbed, trapped, excretion increased
95
Q

How may drug interactions occur?

A
  • Pharmaceutical interactions i.e. interaction prior to administration
  • Pharmacokinetic i.e. tissue/plasma levels of a drug altered by another
  • Pharmacodynamic: action of one drug altered by a second
96
Q

What are the potential outcomes of drug interactions?

A
  • Action of one or more drugs is enhanced
  • Development of new effects
  • Inhibitory effects of one drug on another
  • No change
97
Q

Give examples of some pharmaceutical drug interactions

A
  • Chemical or physical incompatibility/interaction
  • E.g. sodium bicarbonate and calcium
  • Insulin denatured by glucose
  • Diazepam binds to plastics so cannot be used in plastic syringes
  • Insolubility e.g. amphotericin B precipitatesin electrolyte solutions
  • Chemical incompatibilities e.g. pH, oxidation/reduction, complex formation between 2 drugs
98
Q

How may pharmacokinetic interactions between drugs occur?

A
  • Absorption
  • Excretion
  • Reduced circulation
  • Metabolism
99
Q

Outline how drugs may interact to affect absorption

A
  • Change in gastric pH
  • Alteration in bacterial flora
  • Competition for binding sites on plasma proteins
  • Decreased gastric emptying (more absorption)
100
Q

Outline how drugs may interact to affect excretion

A
  • Sodium bicarb makes urine more alkaline and thus increases excretion of weak acids
101
Q

Outline how drugs may interact to affect circulation

A
  • e.g. alpha-2 agonists reduce circulation

- May reduce clearance and elimination

102
Q

Outline how drugs may interact to affect metabolism

A
  • Enzyme inhibition/induction
  • Inhibiting the enzyme will slow rate of metabolism, extend half life
  • e.g. grapefruit juice inhibits subtypes of CYP450
  • Some drugs induce CYP450 and increase metabolism of other substances, can lead to adverse reactions e.g. hepatitis
103
Q

Outline some pharmacodynamic mechanisms of drug interaction regarding receptor sites

A
  • Agonist/antagonist can negate and effect e.g. vit K is an antidote to coumarin anticoagulant
  • Agonist/antagonist can induce a harmful effect e.g. alpha-2 agonist and alpha-2 antagonist
  • Synergistic effects: combination of drugs may produce therapeutic/toxic effect greater than sum of each drug’s action

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