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JL Principles > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

What is pharmacokinetics?

A

What the body does to a drug (absorption, distribution, metabolism and excretion of drugs and their metabolites)

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1
Q

What is pharmacodynamics?

A

What a drug does to the body (biological effects and mechanism of action)

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2
Q

What are the 4 regulatory proteins that most drugs act by binding to?

A

Enzymes
Carrier molecules (transporters and pumps)
Ion channels
Receptors

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3
Q

What are two important additional targets for drugs to act on?

A

RNA

DNA

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4
Q

What are receptors?

A

Receptors are macromolecules that mediate the biological actions of hormones and neurotransmitters

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5
Q

What is an agonist?

A

A drug that binds to a receptor to produce a cellular response

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6
Q

What is an antagonist?

A

A drug that blocks the actions of an agonist

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7
Q

What is the binding step and activation step called?

A

Affinity and efficacy

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8
Q

What is affinity?

A

The strength of association between ligand and receptor

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9
Q

If a drug has a low affinity what will the dissociation rate be like?

A

Fast

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10
Q

What is efficacy?

A

The ability of an agonist to evoke a cellular response

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11
Q

Describe the response that a drug with a high efficacy will produce?

A

A big response

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12
Q

What do antagonists possess and what do they lack?

A

Affinity but lack efficacy

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13
Q

What is the relationship between concentration (or dose) and response of an agonist described as? (on a linear plot)

A

Hyperbolic

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14
Q

What is EC50?

A

The concentration of agonist that elicits a half maximal response

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15
Q

What is the relationship between concentration (or dose) and response of an agonist described as? (on a semi-logarithmic plot)

A

Sigmoidal

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16
Q

What is competetive antagonism?

A

Binding of an agonist and an antagonsit occur at the same time (orthosteric) site and is thus competetive and mutually exclusive

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17
Q

What is non-competetive antagonism?

A

Agonist binds to orthosteric site and antagonsit binds to seperate allosteric site and this is not competetive. Both may occupy the receptor simultaneously, but activation cannot occur when antagonist is bound.

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18
Q

What are the linked processes of metabolism and excretion frequently referred to as?

A

Elimination

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19
Q

Lipid to water partition coefficient: For a given drug concentration gradient across a membrane, the rate of diffusion increases with what?

A

The lipid solubility of the drug

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20
Q

Degree of ionisation: What forms readily diffuse across the lipid bilayer?

A

Unionised forms

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21
Q

What does the degree of ionisation depend on?

A

pKa of the drug and local pH

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22
Q

What is pKa?

A

The pH at which 50% of the drug is ionised and 50% is unionised

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23
Q

What can proportions of ionised and unionised drugs be calculated by?

A

The Henderson-Hasselbalch equation

Acid: pH - pKa = log(A-/AH)
Base: pH - pKa = log(B/BH+)

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24
Q

What happens to acidic drugs as the pH increases?

A

The become increasingly more ionised

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25
Q

What happens to basic drugs as the pH is decreased?

A

They become increasingly more ionised

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26
Q

Name 2 acidic drugs

A

Aspirin and phenytoin

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27
Q

Name two basic drugs?

A

Diazepam and morphine

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28
Q

What is oral availability?

A

The fraction of drug that reaches the systemic circulation after oral ingestion i.e. (amount in systemic circulation/amount administered)

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29
Q

What is systemic avbailability?

A

The fraction that reaches the systemic circulation after absorption i.e. (the amount in systemic circulation/ amount absorbed)

N.B. drugs administered IV have 100% systemic availability

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30
Q

Name the 3 enteral routes of drug administration?

A

Oral, sublingual, rectal

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31
Q

Name the 4 routes of parenteral drug administration?

A

Intravenous
Intramuscular and subcutaneous
Inhalation
Topical

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32
Q

Drug molecules exist in bound or free forms within each body fluid compartment. What is the only type able to move between each compartment?

A

Free drug

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33
Q

What types of drugs can move freely by diffusion?

A

Ionised and unionised drugs that are not bound to protein (albumin)

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34
Q

What types of drugs can move readily by diffusion?

A

Only unionised drugs

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35
Q

What is the volume of distribution (Vd)?

A

The apparent volume in which a drug is dissolved

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36
Q

For a drug administered intravenously: what is the equation of volume of distribution?

A

Vd = dose/plasma concentration

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37
Q

What does a volume distribution of less than 5L mean?

A

Implies the drug is retained in the vascular compartment [e.g. drug extensivly bound to protein (glibenclamide) or too large to cross the capillary wall (heparin)]

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38
Q

What does a vilume of distribution of less than 15 L sugggest?

A

Suggests that the drug is restricted to extracellular water [e.g. permanently charged compounds (tubocurarine)]

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39
Q

What does a volume of distribution of more than 15L indicate?

A

Distribution throughout total body water (or concentration in certain tissues) [e.g. highly lipid soluble drugs (ethanol)]

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40
Q

Where do efferent signals travel?

A

Away from the CNS

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41
Q

Where do afferent signals travel?

A

Towards the CNS

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42
Q

What two divisions is the autonomic nervous system split into?

A

Sympathetic division

Parasympathetic division

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43
Q

What does the autonomic nervous system do?

A

Regulates visceral functions that are largely involuntary and which do not require conscious effort

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44
Q

The transmitter in the preganglionic neurones of the sympathetic and parasympathetic ANS is?

A

Acetylcholine (ACh)

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45
Q

What does the sympathetic division post ganglionic neurone release?

A

Usually noradrenaline (NA)

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46
Q

What does the parasympathetic division postganglionic neurone release?

A

Acetylcholine (ACh)

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47
Q

What does sympathetic stimulation and parasymathetic stimulation do to the heart?

A

Sympathetic - increases heart rate and force of contraction

Parasympathetic - decreases heart rate

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48
Q

What does sympathetic and parasympathetic stimulation do to the bronchi?

A

Sympathetic - relaxes bronchi (via release of adrenaline) and decreases mucus production (lowers airway resistance)
Parasympathetic - constricts bronchi and stimulates mucus production (increasing airway resistance)

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49
Q

What does sympathetic and parasympathetic stimulation do to GI motility?

A

Sympathetic - reduces motility, constricts sphincters

Parasympathetic - Increases motility and relaxes sphincters

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50
Q

What does sympathetic and parasympathetic stimulation do in relation to the penis?

A

Sympathetic - ejaculation

Parasympathetic - erection

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51
Q

What are the 9 stages of neurochemical transmission?

A
  1. Uptake of precursor
  2. Synthesis of transmitter
  3. Storage of transmitter
  4. Depolarisation by action potential
  5. Calcium influx through voltage-activated calcium channels
  6. Calcium induced release of transmitter (exocytosis)
  7. Receptor activation
  8. Enzyme-mediated inactivation of transmitter
  9. or Reuptake of transmitter
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52
Q

Sympathetic division: Once the action potential has travelled to the presynaptic terminal of the preganglionic neurone what happens?

A

It triggers calcium ion entry and the release of ACh

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53
Q

Sympathetic division: Once the preganglionic neurone has released ACh what happens?

A

ACh opens ligand-gated ion channels (nicotinic ACh receptors) in the postganglionic neurone, causing depolarisation and the generation of action potentials that travel to the presynaptic terminal of the neurone, triggering calcium entry and the release of noradrenaline.

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54
Q

Sympathetic division: Once noradrenaline has been release from the presynaptic terminal of the neurone - what happens?

A

Noradrenaline activates G-protein coupled adrenoceptors in the target cell memnbrane to cause a cellular response

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55
Q

Parasympathetic division: what does ACh activate?

A

G-protein -coupled muscarinic acetylcholine receptors in the target cell membrane to cause a cellular response

56
Q

What do ligand-gated ion channels consist of?

A

Consist of seperate glycoprotein subuinits that form a central, ion conducting, channel.

57
Q

What do ligand-gated ion channels allow and do?

A

They allow rapid changes in permeability of membrane to certain ions and rapidly alter membrane potential

58
Q

In relation to G-protein-coupled receptors: what can be said about the receptor, G-protein and effector?

A

They are all sepserate proteins. The G-protein couples receptor activation to effector modulation.

59
Q

Basic structure of G-protein coupled receptors and G protein:

Describe 3 things about the receptor structure

A
  1. Integral membrane protein
  2. Single polypeptide with extracellular NH2 and intracellular COOH termini
  3. Contains seven transmembrane spans joined by 3 extracelliular and 3 intracellular connecting loops
60
Q

Basic structure of G-protein-coupled receptors and G-proteins:

Describe 3 things about G-protein (Guanine nucleotide binding protein)

A
  1. Peripheral membrane protein
  2. Consists of 3 polypeptide subunits (alpha, beta and gamma)
  3. Contains a guanine nucleotide binding site in the alpha subunit that can hold guanosine triphosphate (GTP) or guanosine diphosphate (GDP)
61
Q

G-protein coupled receptor:

What is happening when there is no signalling - in relation to the receptor, G-protein and effector?

A

Receptor - unoccupied
G-protein - alpha subunit binds GDP
Effector - not modulated

62
Q

G-protein coupled receptors:

When the signal has been turned on what 5 steps occur?

A
  1. Agonist activates receptor
  2. G-protein couples with receptor
  3. GDP dissociates from, and GTP binds to the alpha-subunit
  4. G-protein dissociates into seperate alpha and beta-gamma subunits
  5. G-protein alpha subunit combines with, and modifies, activity of effector
63
Q

G-protein coupled receptors:

When the signal is turning off what 2 steps occur?

A
  1. The alpha-subunit acts as an enzyme (a GTPase) to hydrolyse GTP to GDP and Pi. The signal is turned off
  2. The G-protein alpha-subunit recombines with the beta-gamma subunit completing the G-protein cycle.
64
Q

What do nicotinic acetylcholine (ACh) receptors consist of?

A

5 glycoprotein subunits that form a central, cation conduction, channel (sodium, potassium and calcium)

65
Q

Name 4 well characterised subtypes of nicotinic acetylcholine receptors

A
  1. Skeletal muscle (alpha1)2betagammaE - peripheral
  2. Ganglionic alpha3beta4 - peripheral
  3. Alpha4Beta2 - CNS
  4. Alpha7 - CNS
66
Q

Describe the 9 steps in cholinergic transmission

A
  1. Uptake of choline via transporter
  2. Synthesis of ACh via choline acetyltransferase (CAT)
  3. Storage of ACh via transporter (concentrates)
  4. Depolarisation by action potential
  5. Calcium influx through voltage-activated calcium channels
  6. Calcium-induced release of ACh (exocytosis)
  7. Activation of ACh receptors (nicotinic or muscarinic) causing cellular response
  8. Degradation of ACh to choline and acetate by acetylcholinesterase (AChE) - terminates transmission
  9. Reuptake and reuse of choline
67
Q

Drugs that affect cholinergic transmission at ganglia:

Ganglionic transmission is selectively blocked by what?

A

Hexamethonium (the first effective antihypertensive agent). It works by open channel block - a form of non-competetive antagonism.

68
Q

Cholinergic transmission at parasympathetic neuroeffector junctions:

After synthesis and storage of ACh as previously described what are the 6 next steps?

A
  1. Depolarisation by action potential
  2. Calcium influx through voltage-activated calcium channels
  3. Calcium induced release of ACh (exocytosis)
  4. Activation of muscarinic ACh receptor subtypes (M1-M3) causing cellular response (tissue dependent)
  5. Degradation of ACh to choline and acetate by acetylcholinesterase (AChE) - terminates transmission
  6. Reuptake and reuse of choline
69
Q

G-protein coupled muscarinic ACh receptor subtypes at parasympathetic neuroeffector junctions:

M1 - Gq =
M2 - Gi =
M3 - Gq =

A

M1 Gq = stimulation of phospholipase C (increased acid secretion)
M2 Gi = inhibition of adenylyl cyclase; opening of K channels (decreased heart rate)
M3 Gq = stimulation of phospholipase C (increased saliva secretion + contraction of bronchioles)

70
Q

Noradrenergic transmission at sympathetic neuroeffector junctions:

Give the 8 steps involved:

A
  1. Synthesis of NA (multiple steps)
  2. Storage of NA by transporter (concentrates)
  3. Depolarisation by action potential
  4. Calcium influx through voltage-activated calcium channels
  5. Calcium-induced release of NA
  6. Activation of adrenoceptor subtypes causing cellular response (tissue dependent)
  7. Reuptake of NA by transporters uptake 1 (U1) and uptake 2 (U2)
  8. Metabolism of NA by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)
71
Q

G-protein coupled adrenoceptor subtypes at sympathetic neuroeffector junctions:

Beta-1 Gs =
Beta-2 Gs =
Alpha-1 Gq =
Alpha-2 Gi =

A

Beta-1 Gs = Stimulation of adenylyl cyclase (increased heart rate and force)
Beta-2 Gs = Stimulation of adenylyl cyclase (relaxation of bronchial and vascular smooth muscle)
Alpha-1 Gq = Stimulation of phospholipase C (contraction of vascualr smooth muscle)
Alpha-2 Gi = Inhibition of adenylyl cyclase (Inhibition of NA release)

72
Q

What do presynaptic autoreceptors mediate?

A

Negative feedback inhibition of transmitter release. Agonists decrease release, antagonists increase release.

73
Q

Examples of drug action in the autonomic nervous system:

Cocaine

A

Blocks U1, increasing the concentration of NA in the synaptic cleft, resulting in increased adrenoceptor stimulation

Peripheral actions cause vasoconstriction [alpha1 stimulation] and cardiac arrhythmias [beta1 stimulation]

74
Q

Examples of drug action in the autonomic nervous system:

Amphetamine

A

A substrate for U1 and enters the noradrenergic terminal where it inhibits MAO, enters the synaptic vesicle and displaces NA into the cytoplasm. NA exits the terminal on U1 ‘running backwards’ and accumulates in the synaptic cleft causing increased adrenoceptor stimulation.

Peripheral actions largely as for cocaine

75
Q

Examples of drug action in the autonomic nervous system:

Prazosin

A

Selective, competetive, antagonist of alpha-1.

Vasodilator used as an anti-hypertensive agent.

76
Q

Examples of drug action in the autonomic nervous system:

Atenolol

A

Selective, competetive antagonist of beta-1.

Used as an anti-anginal and anti-hypertensive agent.

77
Q

Examples of drug action in the autonomic nervous system:

Salbutamol

A

Selective agonist at beta-2.

Used as a bronchodilator in asthma.

78
Q

Examples of drug action in the autonomic nervous sytem:

Atropine

A

Competetive antagonist of muscarinic ACh receptors.

Blocks all muscarinic ACh receptors with equal affinity (1-3) - exerts widespread effects by blockade of the parasympathetic division of the ANS.

Used to reverse bradycardia following MI and in anticholinesterase poisoning.

79
Q

What is MED - minimum effective concentration?

A

The critical concentration a drug must reach in the plasma to achieve an effect.

80
Q

What is the MTC - maximum tolerated concentration?

A

The concentration of drug in the plasma that would cause significant unwanted effects.

81
Q

What size of therapeutic window does a safe drug have?

A

A large therapeutic window (Therapeutic window is between MTC (top) and MEC (bottom)

82
Q

What size (high or low) of therapeutic ration do ‘safe’ drugs have and give two examples?

A

High ratio

Penicillins and Benzodiazepines

83
Q

What size of therapeutic ration (high or low) does an ‘unsafe’ drug have and give 2 examples?

A

Low ratio

Cardiac glycosides
Barbiturates

84
Q

Most drugs exhibit first-order kinetics which is?

A

Where the rate of elimination is directly proportional to drug concentrations

85
Q

For drugs that exhibit first order kinetics, the dose administered changes the plasma concentration in direct proportion but does not affect what?

A

The rate of elimination or the half-life

86
Q

What is clearance?

A

The volume of plasma cleared of drug in unit time

A constant relating the rate of elimination to plasma concentration.

87
Q

What does clearance determine?

A

The maintenance dose rate (dose per unit time required to maintain a given plasma concentration)

88
Q

What is the time to reach dosing steady state determined by?

A

Half-life but not the infusion rate.

89
Q

how many half-lives pass until dosing steady state is reached?

A

Approximately 5 half-lives

90
Q

What is the equation for the amount of drug in the body, using volume of distribution and plasma concentration?

A

Ab = Vd x Cp

91
Q

What is a loading dose?

A

A loading dose is an initial higher dose of a drug given at the beginning of a course of treatment before stepping down to a lower maintenance dose. It is emplyed to decrease time to steady state for drugs with long half-lives (e.g. digoxin, phenytoin)

92
Q

For IV administration of a drug, how can the loading dose be calculated?

A

LD = Vd x target Cp

93
Q

For oral administration of a drug , how can the loading dose be calculated?

A

LD = (Vd x target Cp)/ F

94
Q

What is the half-life dependent upon?

A

Vd and Clearance

95
Q

What are zero order (or saturation) kinetics?

A

A few drugs (ethanol, phenytoin) are initially eliminated at a constant rate, rather than a rate that is proportional to their concentration (this can occur, for example, when the plasma concentration of a drug is greater than the Km of an enzyme that metabolises it)

96
Q

What is the main organ of drug metabolism?

A

The liver

97
Q

Drug metabolism often proceeds in two sequential phases: what are they?

A
  1. Makes drug more polar, adds a chemically reactive group ‘a handle’ permitting conjugation.
  2. Adds an endogenous compound increasing polarity
98
Q

What 3 processes are involved in phase 1 of drug metabolism?

A

Oxidation
Reduction
Hydrolysis

99
Q

In aspirin metabolism: what conjugate group is added on?

A

Glucuronyl

100
Q

What drug is faster in renal excretion - penicillin or diazepam?

A

Penicillin

101
Q

What 3 basic processes are involved in the clearance of drug (products made from parent compound) from the blood?

A
  1. Glomerular filtration
  2. Active tubular secretion
  3. Passive reabsorption by diffusion across the tubular epithelium
102
Q

What (only) type of drug molecules can enter the filtrate via gomerular filtration?

A

Unbound drug molecules

103
Q

What is the equation for clearance by filtration (CLfil)?

A

CLfil = GFR x fraction of drug unbound in plasma (fup)

Where GFR is the glomerular filtration rate - normally 120 mil min

104
Q

Up to 20% of renal plasma flow is filtered through the glomerulus, but where does the remaining 80% get delivered to?

A

The peritubular capillaries of the proximal tube

105
Q

What do epithelial cells of the proximal tubule contain?

A

Two, independent transporter systems that actively secrete drugs into the lumen of the nephron

106
Q

What are the names of the two epithelial cell proximal tubule transporter systems?

A
  1. Organic anion transporter

2. Organic cation transporter

107
Q

What does the organic anion transporter do?

A

Handles acidic drugs (penicillins) endogenous acids (uric acids) and the marker for renal plasma flow (i.e. paraaminohippuric acid; PAH)

108
Q

What does the organic cation transporter do?

A

Handles basic drugs (e.g. morphine)

109
Q

What can tubular secretion of drugs do?

A

Concentrate drugs in the tubular fluid against an electrochemical gradient

110
Q

What type of process is tubular secretion of drugs?

A

Is a saturable process, each carrier has a transport maximum (Tm) for a particular drug

111
Q

Tubular secertion of drugs allows some ‘special’ drugs to be secreted. What is bounded to these drugs?

A

These drugs are highly protein-bound

112
Q

What substances and drugs does the organic anion transporter secrete?

A 
Penicillins
Probenecid
Acetazolamide, frusemide, thiazides
Uric acid
Glucoronic acid, glycine and sulphate conjugates of phase II metabolism
113
Q

What substances and drugs are secreted by organic cation transporters?

A

Morphine
Neostigmine
Amiloride, triamterene

114
Q

What are the 4 factors that influence reabsorption of drugs across the distal tubule by diffusion?

A
  1. Lipid solubility - drugs with high lipid solubility will be extensively reabsorbed and excreted slowly
  2. Polarity - highly polar drugs will be excreted without reabsorption
  3. Urinary flow rate - diuresis decreases reabsorption
  4. Urinary pH - the degree of ionisation of weak acids and bases can strongly influence their reabsorption
115
Q

What does an alkaline pH do to the excretion of acids?

A

Increases it

116
Q

What does an acidic pH do to the excretion of bases?

A

Increases it

117
Q

Define depolarisation

A

The membrane potential becomes less negative (or even positive)

118
Q

Define hyperpolarisation

A

The membrane potential becomes more negative

119
Q

The direction of the change in potential (i.e. depolarisation or hyperpolarisation) depends on 2 things - what are they?

A
  1. The direction of the movement of the ion (influx) or (efflux)
  2. The charge carried by the ion (positive, or negative)
120
Q

What is passive movement of an ion through an ion channel driven by?

A

The electrochemical gradient for that ion

121
Q

What does Vm stand for?

A

The membrane potential

122
Q

If a cell membrane sodium selective channel opens what happens?

A

Na flows inwardly (generating an inward current) because:

The concentration gradient is inward, the electrical gradient is inward and quantitively, the membrane potential is negative to the quilibrium potential for Na given by the Nernst equation.

123
Q

What can simply define the driving force for Na influx?

A

(Vm - ENA) - when negative inward movement of Na occurs

124
Q

What is the expression for the current carried by Na (INA)?

A

INA = gNA (Vm - ENA)

gNA - Na conductance
ENA - Driving force
INA - Na current

125
Q

What happens to K+ in response to the opening of cell membrane potassium-selective channels?

A

K+ flows outwardly (generating an outward current) because:

The concentration gradient is outward and has an energy which exceeds that of the electrical gradient which is inward. Quantitively, the membrane potential is positive to the equilibrium potential for K+ given by the Nernst equation.

126
Q

What is the driving force for K+ efflux simply defined as?

A

(Vm - Ek) - When positive outward movement of K+ occurs.

127
Q

What is the current carried by K+ (IK) given as an expression?

A

Ik = gK (Vm - Ek)

128
Q

What are the two ion channels responsible for the action potential in neurones?

A
  1. Voltage-activated Na+ channels (Nav) (depolarising)

2. Voltage-activated K+ channels (Kv) (hyperpolarising)

129
Q

What to action potentials possess as they propagate along nerve cell axons?

A

Constant magnitude and velocity allowing signalling over long distances

130
Q

The activation of Na+ channels is self-reinforcing. What does this mean?

A

The opening of a few channels causes further channels to open, causing further depolarisation. This is positive feedback.

131
Q

The activation of K+ channels is self-limiting. What does this mean?

A

Outward movement of K+ causes repolarisation which turns off the stimulus for opening. This is negative feedback.

132
Q

What do voltage-gated Na+ channels initially open in response to?

A

Depolarisation

133
Q

During the maintained depolarisation, what to voltage-activated Na+ channels enter?

A

A non-conducting, inactivated state

134
Q

What is required for a voltage-activated Na+ channel, sitting in the inactivated, non-conducting state, to reopen?

A

Repolarisation

135
Q

There is no stimulus for the absolute refractory period but, what can it elicit?

A

A second action potential

136
Q

The distance over which current spreads depends upon what two things?

A
  1. Membrane resistance (rm)
  2. Axial resistance of the axoplasm (ri)

INCREASING THE RATIO INCREASES the length constant. The longer the length constant, the greater the local current spread. Greater local current spread increases AP conduction velocity.

137
Q

What are 2 strategies to increase passive current spread and thus action potential velocity?

A
  1. Decrease (ri) - possible by increasing axon diameter
  2. Increase rm - possible by adding an insulating material - myelin - provided by Schwann cells in the PNS and oligodendrocytes in the CNS.
138
Q

In saltatory conduction in myelinated axons what does the AP jump to and from?

A

One node of Ranvier to the next

JL Principles (12 decks)

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