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Phase 2a > ICS - Pharmacology > Flashcards

ICS - Pharmacology Flashcards

1
Q

What is synergy?

A

Interaction of drugs such that the total effect is greater than the sum of the individual effects

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2
Q

What is antagonism?

A

An antagonist is a substance that acts against and blocks an action (2 drugs opposed to each other)

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3
Q

What is summation?

A

Different drugs used together to have the same effect as a single drug would

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4
Q

What is potentiation?

A

Enhancement of one drug by another so that the combined effect is greater than the sum of each one alone

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5
Q

Define pharmacodynamics

A

The effect the drug has on the human body

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6
Q

Define pharmacokinetics

A

What the body does with the drug (the disposition of a compound within an organism)

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7
Q

What are the 4 pharmacokinetic mechanisms within the body?

A

Absorption, distribution, metabolism, excretion (ADME)

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8
Q

How can absorption reduce drug effectivity?

A

Motility - if the gut has slowed digestion, the drugs won’t work as well
Acidity - pH and pHa interactions
Complex formation

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9
Q

What is the significance of distribution in regards to drug interaction?

A

Drugs can go into the proteins, other tissues or to the effect site
If you give 2 highly protein bound drugs, they will make each other stronger and increase their effect, so you always have to Make sure what drugs the patient already takes before giving new drugs

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10
Q

What effect does the metabolism have on drug interaction?

A

Inhibition - drug A blocks metabolism of drug B, leaving more free drug B in the plasma so it has an increased effect

Induction - Drug C induced CYP450 isoenzyme leading to increased metabolism of drug D so it has a decreased effect

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11
Q

What effect does excretion have on drug interaction?

A

Weak bases - cleared faster if urine acidic

Weak acids - cleared faster if urine alkali

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12
Q

Name 2 examples of drug interactions to be aware of

A

Warfarin (lots of interactions)

Acute Kidney Injury - NSAIDs and ACEi

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13
Q

Define drug

A

A medicine or other substance which has physiological effect when ingested or otherwise introduced into the body

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14
Q

What proteins in the body are targets for drugs?

A

Receptors, enzymes, transporters, ion channels

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15
Q

Give an example of a condition caused by imbalance of chemicals

A

Parkinson’s = reduced dopamine

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16
Q

Give an example of a condition caused by imbalance of receptors

A

Myasthenia Gravis = loss of Ach receptors

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17
Q

What are the two types of cholinergic receptor?

A

Nicotinic and Muscarinic

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18
Q

Define signal transduction

A

A basic process involving the conversion of a signal from outside the cell to a functional change within the cell

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19
Q

Define signal amplification

A

To increase the strength of a signal

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20
Q

What makes an inhibitor reversible?

A

It binds non-covalently

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21
Q

What changes occur in RAAS when ACE is inhibited?

A

Angiotensin II production is reduced, causing a reduction in blood pressure

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22
Q

Define active transport

A

Ions move from a lower concentration to a higher concentration

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23
Q

What are the 3 main types of protein ports in cell membranes?

A

Uniporters - use energy from ATP to pull molecules in
Sympoters - Use the movement in of one molecule to pull in another against a concentration gradient
Antiporters - one substance moves against its gradient, using energy from the second substance moving down its gradient

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24
Q

Give 3 examples of how we develop drugs

A

Medicines from plants
Organic molecules
Stereoisomers
Immunotherapy antibodies

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25
Q

Define adherence

A

The extent to which the patient’s actions match agreed recommendations

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26
Q

Give 4 impacts of good patient-doctor communication

A

Better heath outcomes
Higher adherence to therapeutic regimens in patients
Higher patient and clinical satisfaction
Decrease in malpractice risk

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27
Q

Give 2 examples of how a drug might pass across a membrane

A

Passive diffusion through the lipid layer

Carrier mediated processes

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28
Q

What obstacles must drugs overcome before they reach the systemic circulation?

A

Drug structure - must be lipid soluble to be absorbed from the gut
Drug formulation - tablet must dissolve
Gastric emptying - rate of emptying determines how soon a drug is delivered
First pass metabolism - drugs must pass metabolic barriers (intestinal lumen, liver, lungs)

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29
Q

What is a limitation of inhalation absorption?

A

Risks of toxicity to alveoli

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30
Q

How are drugs eliminated from the body?

A

Through the metabolism or excretion

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31
Q

Describe the 2 phases of drug metabolism

A

Phase 1 - transformation of the drug to a more polar metabolite
Phase 2 - formation of a covalent bond between drug and an endogenous substrate

32
Q

How are drugs/metabolites excreted?

A

Fluids - urine excretion: total excretion = glomerular filtration + tubular secretion - reabsorption
Solids - faeces
Gases - expired air (volatiles)

33
Q

Define first order kinetics

A

Change in concentration at any time is proportional to the concentration

34
Q

Define zero order kinetics

A

The change in concentration per time is a fixed amount of drug per time, independent of concentration

35
Q

Define half life

A

The time takes for a concentration to reduce by one half

36
Q

Define bioavailability (F)

A

Fraction of the administered drug that reaches the systemic circulation unaltered

37
Q

What bioavailability do IV drugs have?

A

F = 1 has 100% of drug reaches circulation

38
Q

What bioavailability do oral drugs have?

A

Oral drugs may have F<1 if they are incompletely absorbed or undergo first pass metabolism

39
Q

Define tolerance

A

Down regulation of the receptors with prolonged use. Need higher doses to achieve the same effect

40
Q

Name 3 side effects of opioids

A

Nausea and vomiting
Immune suppression
Respiratory depression

41
Q

What is cholinergic and adrenergic pharmacology responsible for?

A 
Control of blood pressure
Control of heart rate
Anaesthetic agents
Regulation of airway tone
Control of GI function
42
Q

Where are each of the 5 muscarinic receptors located?

A

M1 - brain
M2 - heart
M3 - glandular and smooth muscle
M4/5 - CNS

43
Q

Name 4 side effects of anticholinergics

A

Brain - worsen memory, cause confusion

Peripherally - constipation, worsening of glaucoma

44
Q

What is the effect of alpha 1 activators?

A

Raise blood pressure - causing vasoconstriction

45
Q

What is the effect of alpha 2 activators?

A

Lower blood pressure

46
Q

What are the uses of beta agonists?

A

Beta 1 - activation will increase HR and chronotropic effects
Beta 2 - activation is life saving in asthma
Beta 3 - agonists can reduce over-active bladder symptoms

47
Q

What is the effect of beta blockers?

A

Lower blood pressure, reduce cardiac work, treat arrhythmias

48
Q

When would beta blockers be used?

A

Angina, MI prevention, high BP, heart failure

49
Q

What are some side effects of beta blockers?

A

Tiredness, bronchoconstriction, bradycardia, heart failure

50
Q

Define allergy

A

An abnormal response to harmless foreign material

51
Q

What cells are involved in the pathogenesis of allergies?

A

Mast, eosinophils, lymphocytes, dendritic, smooth muscle, fibroblasts, epithelia

52
Q

Name 3 examples of allergic disease

A

Anaphylaxis, allergic asthma, food allergies, contact dermatitis

53
Q

Define adverse drug reactions

A

Unwanted or harmful reactions following the administration of drugs or combination fo drugs under normal conditions of use and is suspected to be related to the drug

54
Q

What are the causes for ADRs?

A

Pharmaceutical variation, receptor abnormality, drug-drug interactions

55
Q

Name 3 common ADRs

A

Confusion, diarrhoea, constipation, hypotension

56
Q

What 4 pieces of critical information are included on a yellow card?

A

Suspected drug, suspect reaction, patient details, reporter details

57
Q

Describe a type 1 hypersensitivity reaction

A

IgE mediated
Acute anaphylaxis after prior exposure to the antigen
IgE becomes attached to mast cells or leukocytes, expressed as cell surface receptors

58
Q

Describe a type 2 hypersensitivity reaction

A

IgG mediated cytotoxicity
Body treats it as a foreign protein and forms antibodies. Antibodies combine with the antigen and complement activation damages the cells

59
Q

Describe a type 3 hypersensitivity reaction

A

Immune complex deposition
Small blood vessels are damaged or blocked
Leucocytes attracted to the site of reaction release pharmacologically active substances leading to an inflammatory process

60
Q

Describe a type 4 hypersensitivity reaction

A

T cell mediated
Lymphocyte mediated
Antigen specific receptors develop on T-lymphocytes

61
Q

Define anaphylaxis

A

An acute allergic reaction to an antigen to which the body has become hypersensitive

62
Q

What are the main features of anaphylaxis?

A

Exposure to drug, immediate rapid onset rash
Swelling of lips, face, oedema, central cyanosis
Hypotension
Cardiac arrest

63
Q

What is the difference between tolerance and desensitisation?

A

Tolerance - reduction in drug effect over time (continuously repeated high conc)
Desensitisation - receptors become degraded/ uncoupled/ internalised

64
Q

What class of drug is Candesartan?

A

Angiotensin II Receptor Blocker

65
Q

In what respiratory condition are beta blockers contraindicated and why?

A

Asthma - beta blockers cause bronchoconstriction

66
Q

What do NSAIDs inhibit and what is the result?

A

Cyclo-oxygenase enzyme, prevents the conversion of arachidonic acid to prostaglandin H2

67
Q

What are the different types of ADR?

A 
A - augmented 
B - bizarre e.g. allergy
C - chronic use
D - delayed e.g. malignancy after immunosuppression
E - end of treatment - withdrawal
68
Q

What is the steady state?

A

Constant drug conc in blood/site of effect for therapeutic use

69
Q

What is the loading dose?

A

High initial dose to shorten time to reach steady state

70
Q

What is druggability?

A

The ability of a protein target to bind to small molecules of high affinity

71
Q

What is affinity?

A

How well a ligand binds to a receptor

72
Q

What is efficacy?

A

How well a ligand stimulates a receptor

73
Q

What is the effect is stimulating adrenergic alpha 1 receptors?

A

Smooth muscle contraction

74
Q

What is the effect is stimulating adrenergic beta 1 receptors?

A

Increased chronotropic/ inotropic effects

75
Q

What is the effect is stimulating adrenergic beta 2 receptors?

A

Smooth muscle relaxation

76
Q

What is the effect is stimulating adrenergic beta 3 receptors?

A

Increase lipolysis and relaxes detrusor muscle

Phase 2a (16 decks)

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