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IMS > Pharmacology and pharmodynamics > Flashcards

Pharmacology and pharmodynamics Flashcards

1
Q

Pharmacology can be split into two what are they?

A
  1. Pharmacodynamics – specific to drug or drug class (interaction with cellular component, concentration/effect relationship, modification of disease progression)
  2. Pharmacokinetics – non-specific, general processes (absorption from site of administration, time to onset of effect, elimination from the body)
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2
Q

Pharmaceutics

A

Drug designed into a dosage that can be given to a patient

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3
Q

Pharmacokinetics

A

Drug gets into the body and reaches site of action

Pharmokinetics -what body does to the drugs

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4
Q

Pharmacodynamics

A

Drug acts to produce its effect on the body

Pharmodynamics- what drug does to the body

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5
Q

Routes of drug administration

A

Oral, intramuscular, subcutaneous (under the skin), intravenous, buccal (relating to the cheek), transdermal (medicine through the skin) e.g. a patch, inhalational, intrathecal (occurring within or administered into the spinal theca), epidural (introduced into the space around the dura mater of the spinal cord), topical (application to body surfaces such as the skin or mucous membranes).

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6
Q

Pharmacokinetics what it tells us

A

Pharmacokinetic knowledge tells us – what dose to give, how often to give it, how to change the dose in certain medical conditions and how some drug interactions occur.

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7
Q

What is ADME?

A
  • Absorption
  • Distribution
  • Metabolism
  • Excretion
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8
Q

Absorption- how are drugs transferred?

A

Transfer of the drug from the site of administration into the general or systemic circulation
• Absorption from the gut

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9
Q

Factors affecting oral absorption

A
  • Particle size and formulation
  • GIT (Gastrointestinal tract) enzymes/acid
  • GIT motility
  • Physicochemical
  • Food
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10
Q

pH & drug absorption

A

• Drugs are either acids or bases- depends what charge they have to cross cell membrane
• Have to be uncharged to cross cell membrane and lipid soluble
• Acids are compounds that can dissociate to donate one or more protons
HA ↔ H+ + A-
• Bases are proton acceptors
BH + ↔ B + H+
• The degree of ionisation, therefore, is dependent on the pH of their environment

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11
Q

ACIDS & BASES: DRUG ABSORPTION- what happens if you increase the pH?

A

Increasing pH- stomach is more acidic and intestine isn’t- acids become more ionised, bases becomes less ionised. Drugs that are bases are better at absorption.

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12
Q

How are drugs distributed?

A

The process by which the drug is transferred reversibly
• from the general circulation into the tissues as concentrations in blood increase
• from the tissues into blood as blood concentrations decrease

Mainly occurs by passive diffusion of un-ionised form across the cell membrane
Needs to be in unionised form.

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13
Q

Volume of distribution

A

VOLUME OF DISTRIBUTION- Volume of plasma that accounts for total amount of drug

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14
Q

What is the volume of distribution used for?

A
  • Used to determine the loading dose necessary for a desired blood concentration of a drug- how well drug reaches the body
  • Also used for estimating a blood concentration in the treatment of overdose
  • Higher VD- will be well perfused- so use this to determine drug dosing
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15
Q

Factors affecting drug distribution

A
  1. Plasma protein binding (competition for protein binding sites)
  2. Specific drug receptor sites in tissues- needs to bind to right receptor
  3. Regional blood flow- if area well perfused- get more drug to that region- some conditions like diabetes can cause detrimental effects as hasn’t been controlled
  4. Lipid solubility
  5. Disease
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16
Q

Drug-protein binding

A
  • Binding of drugs with albumin and glycoproteins
  • Reversible structure
  • Administration of a drug that becomes highly protein bound to a patient who is already taking a drug that is highly protein bound
  • Results in displacement of drug already bound to protein
  • Produces increased unbound concentration of drug and biological activity

If drug is widely distributed in tissues, the increase in unbound drug is rapidly redistributed to body tissues and unbound plasma concentration rapidly returns to negligible amount.

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17
Q

How is drug-protein binding affected by changes in plasma protein binding?

A

Changes in plasma protein binding are significant for drugs which are greater than 90% bound to plasma proteins.

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18
Q

How do drugs cross membranes?

A
  • Only molecules not bound to protein can cross cell membrane
  • Cell membranes may be crossed by:
  • Passive diffusion
  • Transporters
  • Membrane pores
  • Vesicle mediated transport (Pinocytosis)

Passive and facilitated diffusion, AT and pinocytosis.

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19
Q

What are the four roles for drug metabolism?

A

Process to alter drugs to facilitate their removal from the body.

Four roles:

  1. Activation of inactive drug
  2. Production of active drug with increased activity from active drug
  3. Inactivation of active drugs- once drug had an effect- want it to stop
  4. Change in the nature of the activity
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20
Q

What is first pass metabolism?

A

Metabolism occurs prior to and during absorption.
Drugs have to pass 4 major metabolic barriers before they reach the general circulation.

  • Intestinal Lumen- Digestive enzyme secreted by the mucosal cells and pancreas- Certain enzymes break down proteins and stop them from being absorbed
  • Intestinal Wall- Rich in enzymes that further metabolise drugs
  • Liver-Major site of drug metabolism
  • Lung-Cells of the lung have high affinity for many drugs and are the site of metabolism for many local hormones
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21
Q

What are the phases of metabolism?

A

Lipophilic (fat soluble) drug–> Phase 1 reaction (oxidation, reduction and hydrolysis) –> More reactive drug –> Phase 2 reaction (conjugation) –> Hydrophilic (water soluble) drug –> Excreted by kidneys

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22
Q

Factors affecting drug metabolism

A
  • First pass effect
  • Hepatic blood flow
  • Liver disease
  • Genetic factors
  • Other drugs
  • Age
  • Alcohol
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23
Q

What is the Cytochrome P450 (CYP450) system

A

A large family of enzymes and individual one is called an isoenzyme

24
Q

Substrate

A

Drug metabolised by isoenzyme

25
Q

Enzyme Inducers

A
  • Enhance production of liver enzymes which breakdown drugs

* Faster rate of drug breakdown- not enough drug to have the effect

26
Q

Enzyme Inhibitors

A
  • Inhibit production of enzymes which breakdown drugs

* Reduced rate of drug breakdown- more drug in the system

27
Q

How is paracetamol metabolised?

A

Paracetamol undergoes two phase metabolism, phase one, oxidation/reduction/hydrolysis, phase 2 conjugation.

Paracetamol poisoning- Receptors in liver become saturated so paracetamol can’t go by conjugation route.

Body tried to metabolise ingested paracetamol by oxidation, which produces a toxic metabolite NAPQI- toxic metabolite-liver can’t deal with high levels of paracetamol.

28
Q

Bioavailability

A

Proportion of a dose that reaches systemic circulation

29
Q

Bioequivalence

A

Two or more chemically or pharmaceutically equivalent products.

This means that it may be appropriate to replace one product with another without causing clinical problems.

30
Q

How are drugs eliminated?

A

DRUG ELIMINATION VIA THE LIVER- once drug more hydrophilic

Depends on
• Blood flow to the liver
• Activity of the enzymes in the liver
• Liver enzymes will chemically alter the drug to form ‘metabolites’ which are:
• Inactive or equally or more active than the parent drug

31
Q

Clearance

A

Volume of blood/plasma cleared of drug per unit time – amount of blood/plasma removed not drug removed.

32
Q

Half life (T ½)-

A

Time taken for the concentration to reduce by 50%.

Drug undergoes five half-life’s=no drug in the system

33
Q

Evaluating renal function

A
  • Creatinine is a substance produced in skeletal muscle which is excreted through the kidneys
  • Creatinine is muscle breakdown
  • It is neither passively reabsorbed nor actively secreted
  • Estimation of creatinine clearance, estimates clearance of drugs filtered at glomerulus
34
Q

EGFR (estimated glomerular filtration rate)- is a test for what?

A

Tests for kidney function

35
Q

What is the Cockcroft Gault equation?

A

Estimated Creatinine Clearance in mL/min

= (140-Age) x Weight x Constant/ Serum Creatinine

36
Q

Properties of Drugs

A

High affinity= strongly bound
Efficacy= how effective the drug will be
Potency= how strong the drug has to be

37
Q

Agonist

A

Something that mimics a drug.

  • Drug that binds to receptors and initiates a cellular response
  • It has high affinity and efficacy- binds strongly to receptors and elicits a big response
38
Q

Partial Agonists

A

Act on the same receptor but do not produce the same maximal response- partial affinity and efficacy.

39
Q

Inverse Agonist

A

Acts on the same receptor but produces an opposite effect- high affinity and efficacy but just doesn’t produce same response.

40
Q

Antagonist

A

Stops the reaction in the body
• Drug that binds to receptors but does not initiate a cellular response
• It has affinity (as binds) but no efficacy (as no response)

41
Q

Competitive antagonist

A

Binds to the same site as the agonist but does not activate it.

42
Q

Non-competitive antagonist

A

Binds to an allosteric site to prevent activation of the receptor.

43
Q

General Mechanisms of Drug Action- Action on receptors-Ligand-Gated Ion Channels

A

A group of transmembrane ion channel proteins which open to allow ions to pass through the membrane in response to the binding of a ligand such as a neurotransmitter.
Structural change of ion channel- allows ions across

44
Q

General Mechanisms of Drug Action- Action on receptors- G-Protein- Coupled Receptors

A
  • These receptors are linked to their responses by regulatory Guanosine Triphosphate (GTP)-binding proteins or G proteins
  • This complex induces conformational change in the G protein
  • Polypeptide chain across membrane 7 times- 7 TM unit- binding site that’s extracellular- the drug will bind to this
45
Q

Second messengers

A
  • Allow signals conduction to be amplified
  • Enzymes that produce second messengers include:
  • adenyl cyclase – involved in activation of protein kinase
  • Phospholipase C – involved in production of inositol triphosphate (IPS3) and diacyglycerol (DAG)
46
Q

General Mechanisms of Drug Action- Action on receptors- Receptor Kinases

A
  • Activate cascades of intracellular signals
  • Most are receptor tyrosine-kinases and are activated by growth factors
  • E.g. Insulin, growth factors
  • Receptor kinase domains bind together
  • Intracellular and extracellular components- lipid forms a bilipid becomes activated, phosphorylated and becomes active
47
Q

General Mechanisms of Drug Action- Action on receptors- Nuclear receptors

A
  • The receptor is entirely intracellular
  • Ligand must be lipid soluble
  • Primary targets are transcription factors
  • E.g. steroid hormones
  • Receptor site in organ
  • Moves into nucleus
48
Q

General Mechanisms of Drug Action- Action in the Nerve Synapse: Antidepressants

A 
E.g.  Selective Serotonin Reuptake Inhibitors (SSRIs  - sertraline, citalopram)
Tricyclic Antidepressants (TCAs – amitriptyline, imipramine)

SSRIs block reuptake of serotonin. TCAs block reuptake of both serotonin and noradrenaline (red).
5HT- causes increase in serotonin and noradrenaline within the synapse.

49
Q

General Mechanisms of Drug Action- enzyme action

A
  • Macromolecules, usually proteins that act on specific molecules called substrates
  • Lock & Key Concept – enzyme and substrate bind temporarily to form enzyme-substrate complex
50
Q

General Mechanisms of Drug Action- enzyme action- drugs that inhibit enzymes: Non-steroidal anti-inflammatory drugs (NSAIDs)- look at word document

A

NSAIDs block cyclooxygenase activity (COX)

Cytoprotective prostaglandins- lots of platelets, lots of acid

Inhibitors for Cox 1- Non-selective NSAIDs, Aspirin and Diclofenac

Selective inhibitors for Cox 2

51
Q

Renin-Angiotensin Aldosterone System (RAAS)

A

Role in regulating BP, Na conc. and making sure there is enough water within the blood. Drop in BP, kidneys detect the change in water conc. In the blood, releases renin. Converts angiotensin to angiotensin I by the liver. Goes to the lungs where an enzyme called angiotensin-converting enzyme (ACE) produces angiotensin II. Make blood vessels smaller and BP to go back up. Angiotensin II works on adrenal cortex to release aldosterone, role in water reabsorption.

52
Q

General Mechanisms of Drug Action- Inhibit cell transport

A

Carrier Molecules/Transporters

Transportation of substance across a membrane may require a carrier protein.

Drugs Affecting Cell Transport: Calcium Channel Blockers
e.g. amlodipine, diltiazem, verapamil

  • Bind to calcium channels on smooth muscles, blocking the influx of calcium causes smooth muscle relaxation and decreased heart rate
  • 3 classes of CCBs
  • Dihydropyridines (amlopdipine, felodpine) – most smooth muscle selective
  • Phenylalkylamine (verapamil) – selective to myocardium and less effective as a vasodilator
  • Benzothiazepine (diltiazem) – has both cardiac depressant and vasodilator actions
53
Q

Local aesthetics (LA)

A
  • Produce a transient and reversible loss of sensation in restricted area of the body without loss consciousness
  • Causes depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves
  • Process is reversible
54
Q

Local anaesthetics- how it works

A
  • Local anaesthetics disrupt ion channel function in neurone cell membrane
  • Prevent transmission neuronal action potential
  • Specific binding local anaesthetic molecules (ionised form) to Na channels
  • Inactive state = no depolarisation
55
Q

ED50

A

Dose produces 50% max response

56
Q

Ceiling

A

Lowest dose max effect

57
Q

Agonists vs antagonists on log graphs

A

Competitive antagonist is a drug that binds to the same receptor site as drug, non-competitive antagonist is a drug that binds to a different receptor and changes the structure completely.

Presence of competitive antagonist, shift dose response curve to right as takes longer to have an effect.

Add a non-competitive antagonist, never reach maximum response as change receptor structure so much it will never have an effect with the drug.

IMS (13 decks)

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