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Introduction to Clinical Sciences > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacokinetics?

A

How the body affects the drug - absorption, distribution, metabolism and excretion of the drug

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2
Q

What is pharmacodynamics?

A

How the drug affects the body

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3
Q

What are the different kinds of receptors?

A

GPCRs e.g. beta-adrenoceptors
Ligand-gated ion channels e.g. nAchR
Kinase-linked receptors e.g. VEGFR
Cytosolic/nuclear receptors e.g. oestrogen receptor

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4
Q

What is an agonist?

A

A compound that binds to receptors and activates it; it can reverse the effect of an antagonist in competitive inhibition

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5
Q

What is an antagonist?

A

A compound that reduces the effect of an agonist; it does not activate the receptor and can reverse the effects of an agonist in competitive inhibition.

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6
Q

What is EC50?

A

The concentration of the drug that gives half the maximal response.

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7
Q

What is Emax?

A

The maximum possible effect of the agonist

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8
Q

What is intrinsic activity?

A

Intrinsic activity = Emax of partial agonist + Emax of full agonist

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9
Q

What is affinity?

A

How well a ligand binds to a receptor; it is a property shown by both agonists and antagonists

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10
Q

What is efficacy?

A

How well a ligand activates a receptor; only agonists have efficacy

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11
Q

What is tolerance?

A

A reduction in drug effect over time with continuous, repeated high concentrations of the drug. This is a clinical description.

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12
Q

What is desensitisation?

A

The mechanism through which tolerance occurs. It happens though:
Desensitisation of the receptors either by uncoupling them, internalising them or degrading them.

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13
Q

What is receptor-reserve?

A

An integrative measure of the response-inducing capacity of an agonist and of the signal amplification capacity of the corresponding receptor.

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14
Q

What are the three phases of plasma levels?

A

Uptake into plasma
Distribution from plasma
Elimination from plasma

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15
Q

What is the rate of diffusion for a dissolved drug?

A

Rate of diffusion is proportional to the concentration gradient (first order process with respect to concentration)
1/ distance to diffuse
Rate of diffusion is proportional to temperature

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16
Q

What are the compartments of the body and how much fluid is in there?

A

Plasma - 5L
Interstitial - 15L
Intracellular - 45L

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17
Q

What are the different mechanisms of movement?

A 
Simple diffusion
Facilitated diffusion
Active transport
Through extracellular spaces
Non-ionic diffusion
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18
Q

What is bioavailability?

A

The amount of drug taken up as a proportion of the amount administered.

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19
Q

What are the two main routes of elimination for drugs?

A

Hepatic elimination and renal elimination.

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20
Q

What is clearance?

A

The volume of plasma that can be completely cleared of the drug per unit of time.
The rate at which the plasma drug is eliminated per unit of plasma concentration.
Both are measures of efficiency and are measured in ml/min

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21
Q

How are water soluble molecules eliminated in the kidneys?

A

They pass through the glomerular endothelial gaps and are eliminated by glomerular filtration.

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22
Q

How are larger water soluble eliminated in the kidneys?

A

Through active tubular secretion

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23
Q

How is clearance calculated?

A

The rate of appearance in urine / plasma concentration

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24
Q

What does clearance assume?

A

The rate of elimination is equal to the rate of appearance in the urine

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25
Q

What causes impaired renal clearance?

A

Acutely - reduced perfusion causing AKI

Chronically - HTN or DM causing CKD

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26
Q

What effect does hypoalbuminaemia have on drug clearance?

A

Lipid soluble drugs have higher freely diffusible fractions and greater effects. Elevated plasma creatine and urea compete for lipid binding sites on protein and displace more drug.

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27
Q

What adjustments need to be made for renal impairment?

A

Choose drugs not eliminated renally
Avoid nephrotoxic drugs
Measure plasma concentrations if there’s a toxicity risk
Haemodialysis and give normal doses as usual

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28
Q

How are drugs eliminated renally?

A

Through active transport systems; they vary in efficiency for different compounds.

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29
Q

What is the hepatic extraction ratio?

A

The proportion of the drug that is removed by one pass through the liver.

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30
Q

How are drugs with a high HER limited?

A

By perfusion

31
Q

How are drugs with a low HER limited?

A

By diffusion

32
Q

What are phase I reactions?

A

Non-specific reactions that attack specific side chains on large molecules

33
Q

What does cytochrome P450 do?

A

Catalyses oxidative hydroxylation in the liver

34
Q

What are phase II reactions?

A

Conjugation reactions to glucaronic acid

35
Q

How much liver needs to function needs to be lost for it to have an effect on drug metabolism?

A

More than or up to 70% of functioning liver

36
Q

Why are IV drugs used?

A

For drugs that are ineffective administered by other routes or for patients who can’t absorb oral medications

37
Q

What features does the ideal IV drug have?

A

Small VD
Drug is broken down by tissue/plasma enzymes irrespective of liver or renal function
Obvious and predictable dose response relationship
Low risk of toxicity
High therapeutic window
Easy to assay plasma drug concentration quickly

38
Q

For drugs with a high VD, what is needed before a constant infusion?

A

A loading bolus dose to speed up the saturation of all compartments.

39
Q

How is ACh synthesised?

A

At the NMJ through choline acetyltransferase

40
Q

What enzyme breaks ACh down?

A

Acetylcholinesterase

41
Q

How does botox work?

A

It inhibits ACh release at the NMJ causing paralysis, it is a protease. It degrades vesicle proteins preventing the vesicle fusing to the presynaptic membrane.

42
Q

What are reversible cholinesterase inhibitors used for?

A

Treating myasthenia gravis as if increases the amount of ACh at the NMJ.

43
Q

What are mAChR agonists used to treat?

A

Glaucoma

Urinary retention

44
Q

What are the adverse effects of mAChR agonists?

A 
Diarrhoea
Urination
Miosis - excessive constriction of the pupil
Bradycardia
Emesis
Lacrimation
45
Q

What are mAChR antagonists used to treat?

A

Eye examinations to dilate the pupils
Used in asthma and COPD as bronchodilators
Used to treat urinary frequency

46
Q

How many alpha adrenoceptors are there?

A

Two

Alpha1 and alpha2

47
Q

How many beta adrenoceptors are there?

A

Three

beta1, beta2 and beta3

48
Q

What effects do beta 1 adrenoceptors have upon activation?

A

Cardiac effects - increased force, rate and contraction

Renal effects - increased renin secretion and BP

49
Q

What effects do beta 2 adrenoceptors have upon activation?

A

Bronchodilation, vasodilation and decreased GI motility

50
Q

What effects do beta 3 adrenoceptors have upon activation?

A

Increased lipolysis and relaxation of the bladder

51
Q

What are the three classifications of pain?

A

Acute, chronic non-cancer pain and cancer pain

52
Q

How long does acute pain generally last?

A

<1 week

53
Q

What causes acute pain?

A

Activation of nociceptors, pain is carried by A-delta fibres and C fibres

54
Q

What are the effectors of acute pain?

A

Behaviour, reaction and emotions

55
Q

What are the different types of noxious stimuli?

A

Mechanical, thermal and chemical

56
Q

What kind of pain do C fibres carry?

A

Diffuse, dull, intense pain

57
Q

What kind of pain do A-delta fibres carry?

A

Localised, sharp pain

58
Q

What is wind-up?

A

A perceived increase in pain intensity over time; stimulation by non-noxious input can suppress pain

59
Q

How do local anaesthetics work?

A

They’re sodium channel blockers which block the conduction of nerve impulses that carry the pain signal.

60
Q

What is chronic pain?

A

Ongoing, persistent pain >3-6 months in duration

61
Q

What are the principles of chronic pain treatment?

A

Pain perception, function/mobility, sleep, emotional and psychological consequences of pain and quality of life

62
Q

What are adverse drug reactions?

A

A response to a drug which is noxious and unintended

63
Q

What are augmented adverse drug reactions?

A

An extension of the clinical effect of the drug. It is predictable, dose-related and self-limiting. They can occur in patients with renal or hepatic impairment or elderly patients.

64
Q

What are bizarre adverse drug reactions?

A

They’re unrelated to dosage and not expected from the known pharmacological action. They’re unpredictable and have mostly immunological mechanisms - hypersensitivity.

65
Q

What are chronic adverse drug reactions?

A

Drug reactions that occur after long term therapy, they may not be immediately obvious with new medicines.

66
Q

What are are delayed adverse drug reactions?

A

They also occur after long term therapy but the adverse reaction is delayed, for example teratogenesis or neoplasia.

67
Q

What are end of use adverse drug reactions?

A

Withdrawal reactions that are serious complications related to the clinical effect. They occur after relatively long use.

68
Q

What are the symptoms of anaphylaxis?

A

Rash, characteristic blotches, swelling of lips, face, oedema, central cyanosis, wheeze, hypotension, cardiac arrest

69
Q

What are the blood markers for drug allergy?

A

Type A - serum concentration

Type B - tryptase, RAST, urine methyl histamine

70
Q

What are the different types of drug interaction?

A

Synergy e.g. clavulanic acid and amoxicillin
Antagonist
Other

71
Q

What are the risk factors for a drug interaction?

A 
In patients:
Polypharmacy
Old age
Genetics
Hepatic disease
Renal disease

In drugs:
A narrow therapeutic index
Steep dose/response curve
Saturable metabolism e.g. paracetamol or alcohol

72
Q

How does pharmacodynamics play a role in drug interactions?

A

Receptors:
Agonists of the same receptor e.g. benzodiazepines and alcohol so the effect is potentiated
Partial agonists e.g. buprenorphine for opioid addiction
Antagonist e.g. beta blockers and asthma

73
Q

How does pharmacokinetics play a role in drug interactions?

A

Absorption e.g. motility, acidity, solubility, complex formation or direct action on enterocytes
Distribution e.g. protein binding
Metabolism e.g. CYP450 - alcohol dehydrogenase and metronidazole
Excretion e.g. renal or biliary

74
Q

What are the side effects of opioid analgesics?

A 
Respiratory depression
Sedation
Nausea and vomiting
Constipation
Itching
Immunosuppression
Endocrine effects

Introduction to Clinical Sciences (4 decks)

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