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General > Principles Pharmacology Outcomes > Flashcards

Principles Pharmacology Outcomes Flashcards

1
Q

Define pharmacodynamics.

A

Pharmacodynamics describes a drugs biological effects and mechanism of action.

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2
Q

Define pharmacokinetics.

A

Pharmacokinetics describes what the body does to a drug, e.g. absorption, distribution, metabolism and excretion.

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3
Q

Define drug.

A

Narrowly: any substance used in the treatment, prevention or diagnosis of a disease.

Broadly: everyday substances e.g. caffeine/alcohol. Illicit substances, e.g. cannabis, heroin. Food additives.

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4
Q

Define the term agonist.

A

Agonists are drugs which bind to a receptor to produce a cellular response. They possess affinity and efficacy.

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5
Q

Define the term antagonist.

A

Antagonists are drugs that block the action of an agonist. They possess affinity, but lack efficacy.

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6
Q

Define the term ligand.

A

A ligand is a substance which forms a complex with a biomolecule for a biological purpose.

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7
Q

Define affinity.

A

affinity is the strength of association between ligand and receptor.

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8
Q

Define efficacy.

A

Efficacy is the ability of an agonist to evoke a cellular response.

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9
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.

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10
Q

What is the EC50 of an agonist?

A

EC50 is the concentration of an agonist that elicits a half maximal response.

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11
Q

What is meant by competitive antagonism?

A

Binding of an agonist and antagonist at the same orthosteric site, and is thus competitive, and mutually exclusive.

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12
Q

What is meant by non-competitive antagonism?

A

Agonist binds to orthosteric site, and the antagonist binds to a separate allosteric site. They may both simultaneously occupy receptors, but activation cannot occur while an antagonist is bound.

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13
Q

Provide a description of the effect of a competitive antagonist upon the concentration response curve for an agonist acting at the same population of receptors.

A

Competitive antagonists cause a parallel rightward shift of the agonist concentration response curve, with no depression of the maximal response.

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14
Q

Provide a description of the effect of a non-competitive antagonist upon the concentration response curve for an agonist acting at the same population of receptors.

A

Non-competitive antagonists depress the slope and maximum of the concentration response curve, but do not cause a rightward shift.

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15
Q

Describe the determinants of drug disposition in the body: absorption, distribution, metabolism, excretion (ADME).

A

A: Absorption- the process by which drugs enter the body from its site of administration.

D: Distribution- the process by which a drug leaves site of administration to enter blood and tissues.

M: Metabolism- process by which tissue enzymes catalyse the chemical conversion of a frequently lipid soluble drug to an often less active, more polar form, more readily excreted.

E: Excretion- processes that remove the drug/its metabolites from the body.

NB: metabolism+excretion is commonly referred to as elimination.

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16
Q

Describe the factors, that influence the absorption of a drug from its site of administration.

A

Solubility, chemical stability, lipid to water partition coefficient and degree of ionisation.

GI motility, pH at absorption site, blood flow to stomach, how the drug is manufactured, rate may be altered by presence of calcium rich foods, presence of transporters in membranes of epithelial cells of the GI tract.

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17
Q

Define the term oral availability.

A

Oral availability describes the fraction of a drug that reaches the systemic circulation after oral ingestion.

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18
Q

Define the tern systemic availability.

A

It is the fraction of drug that reaches the systemic circulation after absorption.

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19
Q

Describe the principle routes of drug administration, noting their advantages and disadvantages.

A

Oral: simple, convenient non-sterile and good absorption for most drugs.
It may cause inactivation, variable absorption, first pass metabolism, difficulty swallowing.

Inhalation: lungs have huge surface area, good for volatile agents, ideal for local effect.
Requires manual dexterity.

Buccal/sublingual: rapid absorption, bypasses portal system avoiding first-pass.
Infrequent, few preparations available.

Transdermal/Subcutaneous: ideal for certain drugs, with few disadvantages.

Intravenous: rapid onset, continuous, complete availability, used in drugs that cause local tissue damage.
Sterile, risk of sepsis and embolism, high drug levels at the heart.

Rectal: nocturnal administration, good for when oral route is compromised.
Infrequent, variable absorption.

Intramuscular: rapid onset, slow prolonged release.
Painful, may damage tissue, variable absorption.

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20
Q

Name the major fluid compartments of the body and describe the factors that determine the distribution of drugs into these compartments.

A

Plasma water, interstitial water, intracellular water, transcellular water.

Only free drugs may move between compartments.
ionized and unionized drugs not bound to protein may move freely by diffusion.
Only unionized drugs move readily by diffusion.

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21
Q

what is meant by the ‘apparent volume of distribution’ of a drug?

A

It is the volume of distribution (Vd), i.e. the volume into which, a drug appears to be distributed with a concentration equal to that of plasma.

For drugs administered via IV: Vd=dose/plasma concentration.

More generally, Vd = amount of drug in body/plasma concentration.

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22
Q

Define minimum effective concentration(MEC).

A

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

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23
Q

Define maximum tolerated concentration (MTC).

A

The concentration, above which, the drug will begin to cause significant unwanted effects,

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24
Q

Define therapeutic ratio (TR).

A

TR= MTC/MEC.

It is the drugs therapeutic window, i.e. between MEC and MTC.

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25
Q

what is meant by first order elimination of a drug?

A

The rate of drug elimination is directly proportional to the drug concentration.

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26
Q

What is meant by the half-life of a drug?

A

The half-life (t1/2) is the time taken for a drug’s concentration at a point in time (Ct), to fall by 50%.

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27
Q

what is meant by clearance (Cl) of a drug?

A

It is the volume of plasma cleared of drug, in unit time. It is a constant, relating the rate of elimination to plasma concentration.

Cl determines the maintenance dose rate.

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28
Q

What is the rate of elimination of a drug?

A

It is the product of its plasma concentration and its clearance.

Rate of elimination = Cl x Cp l/hr.

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29
Q

What are the principles of dosing to steady state?

A

At steady state, the rate of drug administration = the rate of drug elimination.

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30
Q

What is meant by volume of distribution, and why is it important in calculating a loading dose?

A

It is a proportionality constant relating the plasma concentration (Cp) to the amount of drug in the body (Ab).
Ab = Vd x Cp.

Vd may change in disease, requiring adjustment of a loading dose, and subsequent dosages.

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31
Q

Define loading dose. Why is it useful?

A

An initial higher dose of a drug given at the beginning of treatment, before stepping down to a lower maintenance dose.

It is useful as it decreases the time taken to reach steady state in drugs with long half lives.

32
Q

Define zero-order elimination.

A

Some drugs are initially eliminated a constant rate, rather than at a rate proportional to their concentration.

33
Q

What is the main organ of drug metabolism?

A

The liver.

34
Q

What role does the liver play in drug metabolism?

A

Produces more polar metabolites, that are more readily removed from the body via renal excretion than hydrophobic compounds.

35
Q

Describe the 2 phases of drug metabolism. What do these collectively achieve?

A

Phase I: oxidation, reduction and hydrolysis of a drug in order to make it more polar.

Phase II: Conjugation with e.g. glucuronyl, sulphate, methyl, acetyl- to increase polarity.

Collectively they produce a more polar metabolite, that is more readily excreted.

However, some drugs are excreted unchanged.

36
Q

What role do CYP450 monoxygenases and UDP-glucuronyl transferase have in phase I & II metabolism, respectively?

A

CYP450 mediates oxidation reactions of many lipid soluble drugs in phase I.

UDP-glucuronyl transferases usually produce inactive products in phase II.

37
Q

By which processes does the kidney excrete drugs & metabolites?

A
  1. Glomerular filtration (only unbound drugs).
  2. Active tubular secretion (very effective elimination, can secrete drugs that are highly protein bound).

If they are not excreted (due to high lipid solubility, low polarity, urinary pH), then passive reabsorption by diffusion across the tubular epithelium occurs.

38
Q

True or false? Drugs that are highly protein bound can be excreted by tubular secretion that is mediated by specific transporters that are saturable.

A

True.

39
Q

What factors influence the tubular reabsorption of drugs and their metabolites?

A

Lipid solubility - high = extensive reabsorption + slow secretion.

Polarity = high polarity -> excretion without reabsorption.

Urinary flow rate = diuresis decreases reabsorption.

Urinary pH = alkaline- increases acid excretion. Acidic - increases base excretion.

40
Q

Define depolarization.

A

depolarization is where the membrane potential becomes less negative or even positive.

41
Q

Define hyperpolarization.

A

Hyperpolarisation is where the membrane potential becomes more negative.

42
Q

what is meant by the driving force upon an ion?

A

A force which acts upon the ion, causing it to flow in or out of the cell.

It is quantified by the difference between the membrane potential and the ion equilibrium potential (VDF = Vm − Veq.).

43
Q

Describe how the opening of Na+- and K+-selective ion channels influences the membrane potential.

A

As Na+ channels open, the membrane potential is driven towards ENa (+60mV).

As K+ channels open, the membrane potential is driven towards EK (-80mV).

44
Q

Provide a description of an action potential (employing the terms, threshold, upstroke, downstroke, overshoot and undershoot).

A

Action potentials are brief electrical signals in which the nerve cell membrane’s polarity is momentarily reversed (2msec).

APs are generated when threshold is reached.
Upstroke is the depolarizing phase, and mediated by voltage-activated Na+ channels.
Downstroke is the repolarizing phase, and is due to the opening of voltage-activated K+ channels, and inactivation of Na+ channels.
Overshoot: AP above 0mV.
Undershoot: AP below resting potential (-70mV), occurs due to delayed closure of K+ channels.

45
Q

Describe the properties of action potentials in neurons.

A

APs propagate along nerve cell axons with constant magnitude and velocity, allowing signaling over long distances.

46
Q

describe the closed, open and inactivated states of voltage-activated Na+ channels.

A

Closed Na+ channels open in response to depolarization.
In the open state, they begin conducting, and sodium ions flow into the cell.
However, during maintained depolarization, they enter a non-conducting, inactivated state.
Repolarisation then occurs, and the channel returns to its closed state, and the cycle begins again.

Inactivation contributes to the repolarizing phase of an AP, and is responsible for the refractory period.

47
Q

Define absolute refractory period.

A

A period, during which, no stimulus, however strong, can elicit a second action potential. All Na+ channels are inactivated.

48
Q

Define relative refractory period.

A

A period, during which, a stronger than normal stimulus may elicit a second action population. Membrane is hyperpolarized, and there is a mixed population of inactivated and closed channels.

49
Q

Compare impulse propagation in nonmyelinated and myelinated nerve fibres.

A

Conduction in myelinated axons (salutatory conduction) is much faster than in nonmyelinated axons (passive current spread) of the same diameter.

50
Q

State the overall functions of the autonomic nervous system (ANS).

A

ANS is responsible for carrying CNS output to the whole body, with the exception of skeletal muscle.

Regulates visceral functions that are largely involuntary. Training enables a degree of conscious control of some ANS functions, e.g. urination.

51
Q

Describe the basic organisation of the efferent neurones in the ANS.

A

The autonomic ganglion synapses with the preganglionic neurone of the CNS.

The postganglionic neurone of the ANS then reaches the effector cell, e.g. cardiac or smooth muscle cell.

52
Q

What is the transmitter of the preganglionic neurons of the sympathetic and parasympathetic ANS?

A

ACETYLCHOLINE (ACh).

53
Q

What is the transmitter of the postganglionic neurons of the sympathetic division of the ANS?

A

NORADRENALINE.

54
Q

What is the transmitter of the postganglionic neurons of the parasympathetic division of the ANS?

A

ACETYLCHOLINE

55
Q

State the effect of sympathetic and parasympathetic stimulation upon selected tissues and organs.

A

HEART
Sympathetic: increase heart rate and force of contraction.
Parasympathetic: decreases heart rate.

PENIS:
Sympathetic: ejaculation.
Parasympathetic: erection.

56
Q

Describe the overall process of neurochemical transmission

A

A precursor is taken up, resulting in the synthesis and storage of a transmitter.

Depolarisation by an AP occurs, resulting in Ca2+ influx, and inducing transmitter release (exocytosis).

The receptor is then activated, resulting in one of two options:

  1. Enzyme-mediated inactivation of the transmitter.
  2. Reuptake of the transmitter.
57
Q

Provide an overview of neurochemical transmission in the sympathetic division of the ANS.

A

AP originating in the CNS triggers release of ACh at the preganglionic neurone. ACh then causes depolarization and generation of APs triggering Ca2+ entry and release of noradrenaline by postganglionic neurones.

Noradrenaline then activated G-protein-coupled adrenoceptors in target cell membranes to cause a cellular response.

58
Q

Provide an overview of neurochemical transmission in the parasympathetic division of the ANS.

A

AP originating in the CNS triggers release of ACh at the preganglionic neurone. ACh then causes depolarization and generation of APs triggering Ca2+ entry and release of ACh by postganglionic neurones.

ACh then activated G-protein-coupled muscarinic acetylcholine receptors in target cell membranes to cause a cellular response.

59
Q

Outline the operation of a ligand-gated ion channel.

A

They consist of glycoprotein subunits that form a central, ion conducting channel.

They allow rapid changes in the permeability of the cell’s membrane, to certain ions and rapidly alter membrane potential.

An agonist binds, the channel opens, and ions flow.

60
Q

What is a G-protein?

A

A peripheral membrane protein consisting of 3 polypeptide subunits.

It contains a guanine nucleotide binding site in its α subunit, that can hold GTP or GDP.

61
Q

What is a receptor?

A

It is an integral membrane protein. A single polypeptide with extracellular NH2 and intracellular COOH termini.

It consists of seven transmembrane spans, joined by 3 extracellular and 3 intracellular connecting loops.

62
Q

Outline the process of signaling via G-protein coupled receptors.

A

An agonist activates a receptor, to which the G-protein then couples.

GDP dissociates from the G-protein, enabling GTP to bind to the α subunit.

The G-protein then dissociates into separate α and βγ subunits.

The α subunit binds to, and modifies the acitivity of the cells effector, to turn on a signal.

63
Q

What is the effector of a cell?

A

it is the enzyme or ion channel.

64
Q

Give an example of a g-protein coupled receptor.

A

Muscarinic ACh receptors.

65
Q

How is G-protein signaling “turned off”?

A

α subunit acts as an enzyme, hydrolyzing GTP to GDP + Pi, turning off the signal.

The G-protein α subunit then recombines with the βγ subunit.

66
Q

There are numerous subtypes of nicotinic acetylcholine receptor in the body, how do they differ? Give an example.

A

They differ in subunit composition, location, physiological and pharmacological properties.

Skeletal muscle and ganglionic (of the peripheral nervous system).

67
Q

Describe the key processes in cholinergic transmission.

A

Choline is taken up at the nerve terminal of a pre-synaptic neurone via a transporter. This stimulates synthesis of ACh via choline acetyltransferase (CAT). ACh is stored via the transporter.

Depolarisation occurs via an AP, resulting in Ca2+ influx and inducing release of ACh.

ACh (nicotinic or muscarinic) receptors are then activated, evoking a cellular response.

Degradation of ACh to choline and acetate by ACHe terminates transmission, and the reuptake and reuse of choline.

68
Q

Describe the key features of ganglionic transmission.

A

Pre-ganglionic neurone terminals release ACh, causing Na+ influx to post-ganglionic neurone dendrites and cell bodies.

This causes a graded depolarization.

I got bored here, sorry.

69
Q

List the 4 main adrenoceptor subtypes. State their G-protein and enzyme coupling, and representative tissue locations and actions.

A
  1. a1: binds to Gq. Stimulates phospholipase C. Causes contraction of vascular smooth muscle.
  2. a2: binds to Gi. Inhibits adenylyl cyclase. Causes inhibition of NA release.
  3. b1: binds to Gs. Stimulates adenylyl cyclase. Increases heart rate and force of contraction.
  4. b2: binds to Gs. Stimulates adenylyl cyclase. Causes relaxation of bronchial and vascular smooth muscle.
70
Q

Receptors exist presynaptically, why is this important?

A

They mediate negative feedback inhibition of transmitter release. Agonists decrease release, and antagonists increase release.

71
Q

Describe the actions of cocaine within the ANS, and its molecular targets.

A

Cocaine causes increased adrenoceptor stimulation. It causes vasoconstriction [a1], and cardiac arrhythmias [b1].

72
Q

Describe the actions of amphetamine within the ANS, and its molecular targets.

A

It displaces noradrenaline into the cytoplasm, accumulating in the synaptic cleft and causing increased adrenoceptor stimulation.

It causes vasoconstriction [a1], and cardiac arrhythmias [b1].

73
Q

Describe the actions of prazosin within the ANS, and its molecular targets.

A

Selective, competitive, antagonist of a1. Does not block a2, b1, or b2. Vasodilator used as an anti-hypertensive agent.

74
Q

Describe the actions of salbutamol within the ANS, and its molecular targets.

A

Selective agonist at b2. Does not activate, b1, a1, or a2. Used as a bronchodilator in asthma.

75
Q

Describe the actions of atenolol within the ANS, and its molecular targets.

A

Selective, competitive, antagonist of b1. Does not block b2, a1, or a2. Used as an anti-anginal and anti-hypertensive agent.

76
Q

Describe the actions of atropine within the ANS, and its molecular targets.

A

Atropine is a competitive antagonist of muscarinic ACh receptors (1, 2 and 3), and does not block nicotinic ACh receptors.

It blocks the parasympathetic division of the ANS, and is used to reverse bradycardia following an MI, and in anticholinesterase poisoning.

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