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Year 1 IMS > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the definition of pharmaceutics?

A

Creation of the physical product

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2
Q

What is the definition of pharmacokinetics?

A

Getting the drug into the body and to the site of action

The affect of the body on the drug

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3
Q

What is the definition of pharmacodynamics?

A

Getting the drug to do something

The effects of the drug on the body

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4
Q

What is therapeutics?

A

The study of pharmacology in the context of treating and benefits to the patient

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5
Q

What is bioavailability?

A

The proportion of the drug which reaches the systemic circulation

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6
Q

What 4 factors is bioavailability affected by?

A

1) Extent of metabolism before reaching the systemic circulation
2) Lack or presence of food in the GI tract
3) Dissolution and absorption of a drug
4) Stability of drug in the GI tract

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7
Q

What is the half life of a drug?

A

The time required to reduce the plasma concentration of a drug to half of its original value

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8
Q

As a rule of thumb, how many half lives are needed for a drug to get out of the circulation?

A

5

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9
Q

What is the therapeutic index of a drug, in the ideal drug what would be the value of this index?

A

Ratio of ‘dose that causes toxicity: dose that produces a desired effect’
Want the ideal drug to have a high therapeutic index

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10
Q

Can you name any drugs with a low therapeutic index?

A

1) Digoxin
2) Gentamicin
3) Carbamazepine
4) Lithium
5) Phenytoin
6) Theophylline

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11
Q

What do phenytoin and gentamicin require plasma concentrations measurements?

A

Have low therapeutic indices
Want to make sure suppress seizures with phenytoin
Want to prevent toxicity with Gentamicin

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12
Q

What is the volume of distribution (Vd) of a drug and what is it used for?

A

Calculated as a theoretical value and calculated in relation to body compartments
Needed to determine the loading dose of a drug needed, bigger Vd = bigger loading dose

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13
Q

What is clearance of a drug?

A

The amount of plasma from which the drug is completely removed in any given time
eg. if the concentration is 1g/L and the clearance is 1L per hours then the rate of elimination is 1g/hour

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14
Q

What 2 ways can you increase the plasma concentration of a drug?

A

1) Increase the dose

2) Increase the dose frequency

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15
Q

What is an example of a drug in which you have to be careful how you increase the plasma concentration?

A

Dihydrocodeine

You should increase the frequency rather than the dose in order to avoid toxicity

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16
Q

What is meant by a parenteral route of administration?

A

Injection, IV, SC, or IM

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17
Q

What is the difference in routes of administration of Penicillin G and V and why?

A

Penicillin G is unstable in acid so is given IV

Penicillin V is stable in acid so can be given orally

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18
Q

What 3 factors may alter absorption of a drug from the GI tract?

A

1) Gastric emptying
2) GI motility
3) GI disorders (migraine and surgery slow gut movement - broken down in stomach acid before even reaches GI tract)

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19
Q

What is the purpose of enteric coating on drugs?

A

To protect from stomach acids

Stop the drug being ionised by the stomach acid as if it becomes ionised it cannot be absorbed

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20
Q

What is the issue with suppository (rectal) drug administration?

A

Good absorption

Poor retention

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21
Q

What are the 2 methods by which drugs can be excreted?

A 
Renal (filtered out by the kidneys once the drug has reached the systemic circulation and excreted in the urine)
Hepatic clearance (excreted in the bile by the liver, excreted in faeces)
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22
Q

What are the 2 possible methods of drug movement in the body?

A

1) BULK FLOW TRANSFER : in the blood

2) DIFFUSION TRANSFER : molecule by molecule

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23
Q

What is the influence of pH on drug transfer?

A

Many drugs weak acid or bases
Degree of ionisation depends on their environment pH
Acid in the stomach will ionise/dissociate a drug

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24
Q

What happens to the level of ionisation of acidic and basic drugs with increasing pH?

A

1) Acidic drugs become increasingly ionised/dissociate with increasing pH
2) Basic drugs become increasingly unionised with increasing pH

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25
Q

By what 2 methods do drugs pass through the lipid membrane?

A

1) Passive diffusion

2) Facilitated diffusion

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26
Q

What kind of drugs can pass the membrane by simple diffusion and which require a carrier?

A

Lipophillic can cross membrane

Hydrophillic (polar/ionised) require a carrier

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27
Q

What 4 barriers require a carrier to get drugs across?

A

1) BBB
2) renal tubule
3) GI tract
4) Biliary tract

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28
Q

The body is designed to protect against foreign chemicals entering the blood, in what 3 ways can we alter drugs to get them into the system?

A

1) Change the route of administration
2) Change the formulation eg. injection solutions
3) Alter the physiochemical properties of a drug

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29
Q

What factors affect absorption?

A

1) Compliance
2) Food
3) Formulation (eg. enteric coated/slow release)
4) Route of administration
5) Lack of specific carrier
6) Malabsorption syndromes
7) First pass effect
8) Site of drug absorption
9) Drug interactions

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30
Q

Does the presence of food enhance of impair absorption of ketaconazole?

A

Enhance

Relies on an acid medium for absorption

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31
Q

Does the presence of food enhance or impair the absorption of tetracyline?

A

Impair

Calcium, iron, milk all reduce its absorption

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32
Q

What is the relationship between GI motility and Metoclopramide?

A

Increases GI motility

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33
Q

What is plasma protein binding and how does it affect drug distribution?

A

Competition for protein binding sites (mainly albumin)
Only free drug can act on receptors
Take another drug and knock the first of the binding site, could lead to toxicity

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34
Q

What factors affect drug distribution?

A

1) Plasma protein binding
2) Specific receptor sites in tissues
3) Regional blood flow
4) Lipid solubility
5) Disease

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35
Q

How can liver and renal disease affect distribution?

A

Liver disease - albumin made mostly in the liver

Renal disease - high blood urea levels

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36
Q

Why are water soluble drugs generally injected?

A

Not lipid soluble, cant cross membranes, confined to bodily fluids unless injected eg. gentamicin

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37
Q

Why can reductions in protein binding have different effects on different drugs?

A

If highly protein bound, a reduction of 5% binding will result in a significant increase in unbound drug
If low protein binding, a reduction of 5% binding will only increase the concentration of unbound drug by a negligible amount
Changes in plasma protein binding is significant for drugs which are >90% protein bound

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38
Q

What factors can increase the fraction of unbound drug?

A

1) Renal impairment: increase in urea levels (competes for binding sites)
2) Liver disease: low albumin levels
3) Late pregnancy: Decreased albumin production so fraction unbound increased but diluted by increase in blood volume and it is that that matters
4) Displacement from binding site by other drugs eg. Aspirin, sodium valproate, sulphonamides
5) Saturability of plasma protein binding within therapeutic range eg. phenyotin - dont get a linear increase in fraction unbound drug throughout whole therapeutic range

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39
Q

What 3 things could occur to a drug when it is metabolised in the liver?

A

1) Activation of an inactive drug
2) Production of an active drug from an active drug
3) Inactivation of an active drug

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40
Q

What is the first pass effect?

A

Extent of metabolism when a drug passes through the liver for the first time before it reaches the systemic circulation
May mean that a much higher oral dose (compared to IV dose) is needed to produce the same effect

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41
Q

How can acylation status, a genetic factor, alter the metabolism of drugs and what syndrome can slow acylation status result in?

A

Acylation is a process by which some drugs are metabolised
Slow acylation status will mean certain drugs build up
Slow acylation can result in Steven Johnsons syndrome - skin peels off and lose all fluid

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42
Q

If a drug has a high excretion ratio what does this indicate?

A

The fraction of a drug removed from the blood flowing through the kidney or other organ
High extraction ratio (close to 1) indicates lots of drug removed during a single pass

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43
Q

What is the determining factor in the hepatic clearance of a drug with a high extraction ration?

A

Hepatic blood flow

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44
Q

In drugs with a low extraction ratio which processes are rate limiting?

A

Poor diffusion through hepatocyte membrane

Hepatic clearance is independent of blood flow

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45
Q

Name some enzyme inducing drugs?

A 
SMOKING
CHRONIC ALCOHOL INTAKE
Phenytoin
Carbamazepine
Phenobabrbitone
Rifampicin
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46
Q

Name some enzyme inhibiting drugs?

A

ACUTE ALCOHOL INTAKE
erythromicin
ciproflaxin
oral contraceptives

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47
Q

What is the digoxin-erythromycin drug interaction?

A

In 10% of the population a substantial amount of digoxin is inactivated by gut bacteria
Erythromycin kills alot of gut bacteria
More active digoxin is absorbed and there is a risk of toxicity

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48
Q

What is the ethinylestradiol (oral contraceptives) - Abx drug interaction?

A

Ethinylestradiol undergoes hepatic recirculation
Its excreted in the bile, and hydrolysed by gut bacteria releasing oestrogen which is then reabsorbed
Abx prevent this and may result in contraceptive failure

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49
Q

What is entero hepatic recirculation?

A

Excreted in the bile
(possibly modified by gut bacteria)
Reabsorbed from small intestine and travels back to liver

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50
Q

Other than in bile and urine how else could drugs be excreted?

A 
Sweat
Breast milk 
Tears
Genital secretion 
Saliva
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51
Q

What is glomerular function?

A

Kidney filtration function

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52
Q

What is the main site of drug excretion?

A

Kidneys

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53
Q

What is a normal GFR and rate of urine production?

A

GFR = 120ml/min

Urine production = 1-2ml/min

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54
Q

What has creatinine got to do with renal function?

A

Creatinine is a protein produced from the breakdown of muscle
It is neither actively secreted or passively reabsorbed from the kidneys
So estimation of creatinine clearance gives us a good estimate of drug clearance at the glomerulus

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55
Q

What is the cockgroft gault equation and what does it measure?

A

Estimation of creatinine clearance in ml/min

= ((140-age) x weight x constant) / (Serum creatinine)

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56
Q

People of which race were found to give false results with the cockgroft gault equation?

A

African-Carribbean patients

57
Q

What does eGFR take into account and how does it differ to the cockgroft gault equation?

A

Serum creatinine, age, sex and race, uses surface area instead of weight (normal surface area is estimated to be 1.73m)

58
Q

What is the difference between absolute GFR and eGFR?

A

Absolute GFR uses a measured surface area rather than an average
Absolute GFR = eGFR/1.73 x (surface area)

59
Q

Which patients tend to have altered renal function?

A

1) Elderly
2) Neonates
3) Acute and Chronic renal impairment

60
Q

Why do elderly patients tend to have reduced renal impairment and at what age does renal function begin to decline?

A

1) Reduced renal mass
2) Reduced renal blood flow
After age of 30 years creatinine clearance reduces by 8ml/min every decade

61
Q

What is the biochemical basis of myasthenia gravis?

A

Autoimmune response against nAChR on the post synaptic membrane at NMJs
Reduced response to ACh
Decreased number of AChRs
Because of this EPPs are smaller

62
Q

What are the 2 forms of myasthenia gravis?

A

1) Effects extra ocular muscles

2) Generalised muscle weakness

63
Q

What is characteristic of myasthenia gravis?

A

Repetitive stimulation leads to decreased contractile strength
Weakness is greatest at the end of the day

64
Q

What neoplasia/tumour is associated with myasthenia gravis?

A

Women afflicted at an early age with hyperplasia of the thymus
Men afflicted later on in life with cancer of the thymus

65
Q

What tests are needed for a diagnosis of myasthenia gravis?

A

1) MRI or CT scan for possible thymoma
2) Chemical test for Ab to nAChR
3) Electromyography test
4) Edrophonium or neostigmine test

66
Q

What is the treatment of myasthenia gravis?

A

1) Directed at enhancing transmission (anticholinesterase)
2) Immunosuppression (corticosteroids)
3) Removal of tumour of the thymus in some cases

67
Q

Histamine receptors exist in the stomach, brain and mucous membranes, what kind exists in each place and how does this explain the side effects of anti histamines?

A

1) Mucous membranes and brain = H1
2) Stomach cells = H2
Drowsiness due to acting on the brain receptors

68
Q

What are the 2 main catagories of Cholinergic receptors?

A

1) Nicotinic

2) Muscarinic

69
Q

What are the 5 main types of noradrenergic receptors and what do they respond to?

A

Respond to NA and ADR
Alpha 1 and 2
Beta, 1, 2 and 3

70
Q

What receptor is found at the ganglion and effecter sites of sympathetic and parasympathetic nerves?

A

1) Sympathetic ganglion = nAChR
2) Sympathetic effecter = NA receptor
3) Parasympathetic ganglion = nAChR
4) Parasympathetic effector = mAChR

71
Q

Nerves to the adrenal medulla release ACh to act on the nAChR on the adrenal medulla, how does the adrenal medulla respond?

A

Release NA or ADR into the blood stream

72
Q

Does the adrenal medulla have a ganglion?

A

No

73
Q

What kind of receptor is found on the post synaptic membrane of an NMJ?

A

nAChR

74
Q

Other than on post synaptic membranes of synapses and NMJs where else are mAChRs found?

A

Endothelial cells of blood vessels

Not innervated by cholinergic fibres but are sensitive to circulating molecules

75
Q

What kind of receptors are mAChRs?

A

GPCRs

76
Q

What secondary messenger are M1, M3 and M5 linked to?

A

Activate PLC

Increasing IP3 and DAG

77
Q

What secondary messengers are M2 and M4 linked to?

A

Negatively coupled to AC

Reduce cAMP

78
Q

What kind of receptor to parasympathetic fibres is found on the heart and what does its activation lead to?

A

M2

Reduced cAMP and reduced heartrate

79
Q

Muscarinic antagonists, IV atropine, Tropicamide (eye drops), Oral Hyosine, inhaled iprtropium and oral dicyclomine are used to treat what>

A

Atropine: treatment of sinus bradychardia
Tropicamide: to dilate the pupils
Hyosine: prevent motion sickness
Iprtropium: used in Asthma
Dicyclomine: Relaxation of GI smooth muscle

80
Q

NA and ADR are catecholamines synthesised from what?

A

Tyrosine

81
Q

When NA is released from a post ganglionic sympathetic nerve terminal what other substance is released that can act on post synaptic receptors?

A

ATP

82
Q

How are alpha and beta adrenergic receptors classifies?

A 
alpha = NA >ADR > isoprenaline
beta = isoprenaline > ADR > NA
83
Q

What kind of receptors are adrenergic receptors?

A

GPCRs

84
Q

What is the second messenger of alpha 1, alpha 2 and all types beta receptors?

A

alpha 1 = activate PLC = increase DAG and IP3
Alpha 2 = inhibit AC = cAMP decreases
Beta (all types) = activate AC = cAMP increases

85
Q

What does alpha 1 receptor activation lead to? (4 thing)

A

1) Vasoconstriction
2) Relaxation of GI smooth muscle
3) Salivary secretion
4) Hepatic glycogenolysis

86
Q

What does alpha 2 receptor activation lead to? (4 thing)

A

1) Inhibition of NA or ADR release (receptor in charge of autoinhibition on pre synaptic nerves)
2) Platelet aggregation
3) Vasoconstriction
4) Inhibition of insulin release

87
Q

What does Beta 1 activation lead to? (2 things)

A

1) Increased cardiac rate and force

88
Q

What does beta 2 activation lead to? (5 things)

A

1) Bronchodilation
2) Vasodilation
3) Relaxation of visceral smooth muscle
4) Hepatic glycogenolysis
4) Muscle tremor

89
Q

What does beta 3 activation lead to? (1 thing)

A

1) Lipolysis

90
Q

What is SALBUTAMOL and what is it used for?

A

Selective beta 2 agonist

Used as a bronchodilator in Asthma

91
Q

What is PROPANOLOL?

A

Blocks beta 1 and beta 2 receptors equally

92
Q

What is ATENOLOL?

A

Selective beta 1 antagonist

93
Q

What is the collective name for PROPANOLOL AND ATENOLOL?

A

Beta blockers

94
Q

What are the clinical uses for beta blockers (propanolol and atenolol) and what are there side effects?

A 
Clinical uses:
1) Hypertension
2) Angina pectoris
3) Cardiac dysrhythmmias
4) Post MI
Side effects:
1) Bronchoconstriction: important in Asthmatics!
2) Cold extremeties, insomnia depression
3) Cardiac failure
4) Bradychardia
5) Hypoglycaemia (key in poorly controlled diabetics!)
6) Fatigue
95
Q

Kinase linked receptors are key receptors for what hormones?

A

Insulin and GH

96
Q

GABA receptor is what kind of receptor?

A

Ligand gated ion channel

97
Q

Nuclear receptors are key receptors for what kind of hormones?

A

Steroid and Thyroid hormones

98
Q

What is the affinity of a drug?

A

Describes the binding of the drug to the receptor

Describes the ‘goodness’ of fit and how tightly the drug is bound

99
Q

What is the efficacy of a drug?

A

Describes the ability of a drug once bound to a receptor to activate the receptor and produce a response
eg. full agonists have full efficacy

100
Q

What is the potency of a drug?

A

The dose of a drug necessary to produce a desired effect

101
Q

What is a partial agonist?

A

A drug that no matter how high the dose is can never produce a full response

102
Q

What is an inverse agonist?

A

Drug that binds to a receptor to produce an effect opposite to the of an agonist - stabilisers receptors in the inactive state

103
Q

On graded dose curves what is the threshold?

A

Dose of a drug that produces a just noticeable effect

104
Q

On a graded dose curve what is the ED50 value?

A

Dose that produces 50% of max response

105
Q

On a graded dose curve what is the ceiling?

A

The lowest dose that produces a maximal effect

106
Q

What is the specificity of a drug?

A

The ability of a drug to bind to one specific receptor

No drug is truly specific but many have relative selectivity

107
Q

What is the equation of the classical receptor occupancy theory?

A

L + R -> LR -> Stimulus -> Response
Ka = association (of L and R) rate constant
Kd = dissociation rate constant

108
Q

The relative potency of 2 drugs a and b is calculated how?

A

ED50a / ED50b

eg. one may be 10 times more potent than the other

109
Q

Which beta blocker is to be avoided in Asthma?

A

Propanolol

Atenolol is probably still best avoided as its selectivity for beta 1 receptors is only relative

110
Q

What is the enzyme and substrate involved in the formation of prostaglandins?

A

Arachidonic acid

Cyclo-oxygenase

111
Q

Which enzyme is inhibited by NSAIDs?

A

Cyclo oxygenase 1 and 2

112
Q

Which COX enzyme is inducible and controls pain and inflammation and which is a normal constituent?

A

COX 2 = inducible, responsible for pain ad inflammation

COX 1 = normal constituent found in stomach, intestine, kidneys and patelets

113
Q

Aswell as leading to inflammation what other 2 effects do prostaglandins have?

A

1) Reduce acid production and increase mucous in the stomach

2) Increase blood flow to the kidneys

114
Q

What side effects of NSAIDs can be anticipated?

A

Peptic ulceration
Salt and water retention
In elderly reduced blood flow to the kidneys can lead to renal failure

115
Q

Why was a selective COX 2 inhibitor pulled from the market?

A

Found to cause cardiovascular problems

116
Q

Why can ACE inhibitors lead to hypersensitivities in the lungs which can become intolerable?

A

ACE responsible for break down of bradykinin to an inactive protein
Can thus get a build up of bradykinin which can lead to these hypersensitivities

117
Q

What do monoamine oxidase inhibitors do and what are they used to treat and what are the possible side effects?

A

Used as anti depressants
Inhibit the breakdown of monamines in the synapse
Monoamines present in some foods, levels can build up, possible strokes, bleeds, massive headaches

118
Q

What do tricyclic anti depressants do?

A

Inhibit the re uptake of all chemicals in the synapse

119
Q

What is Prozac?

A

Selective serotonin uptake inhibitor

120
Q

What are calcium channel blockers used for?

A

Anti hypertensives

Good in people with Low renin where you cant use blockage of RAAS

121
Q

What is the mode of action of local anaesthetics?

A

1) Block transmission of nerve impulses between the peripheral pain receptors and the CNS
2) In the unionised form they diffuse through the lipid membrane
3) Low pH in the cell generates the ionised form
4) Ionised LA blocks the sodium channel
5) Impulses stopped
6) Slowly returns to normal and impulses return as block ends

122
Q

What determines whether a local anaesthetic is an ester or an amide and what is the characteristics of each?

A

Made up of lipid soluble aromatic group and attached to a charged amine group
Bond between these 2 determines classification
Esters: Rapidly hydrolysed and the breakdown product is associated with allergic and hypersensitive reactions
Amides: relatively stable and hypersensitivity reactions are rare
Amides for these reasons are more commonly used than esters

123
Q

How are esters and amides metabollised differently and how can this lead to toxicity?

A

Esters: rapidly metabollised by plasma cholinesterase, toxicity less likely
Amides: Metabolised by liver and as a group are more likely to be toxic, slowly broken down by amidases in the liver

124
Q

What factors affect anaesthetic affect?

A

1) Small diameter fibres more sensitive than large diameter ones
2) Action is dose dependent
3) Action is pH dependent (inflammed tissues are acidic and resistant to local anaesthetics)

125
Q

What are the possible adverse effects of local anaesthetic on the heart, CNS and peripheral tissues?

A

1) heart: block Na channels in conducting system of heart - myocardial depression and vasodilation
2) CNS: restlessness and at high doses convulsions
3) Addition of adrenaline causes constriction of peripheral blood vessels, lessening the distribution and prolonging the action and producing a relatively bloodless field

126
Q

Name 3 types of drugs with non specific action?

A

1) Antacids eg. Aluminium hydroxide
2) Emollients - moisturise the skin
3) General anaesthetics - reduce CNS function

127
Q

What is the mode of action of Beta Lactam antibiotics eg. Penicillins?

A

Inhibit cell wall synthesis

128
Q

What is the mode of action of macrolides eg erythromycin?

A

Inhibit bacterial protein synthesis

129
Q

What is the mode of action of antifungal agents eg. nystatin?

A

Inhibit ergosterole in fungul cell membrane (used by fungi how we use cholesterol)

130
Q

What is the mode of action of anti helminthics ascaracides for worm infestation?

A

Paralyses worm by affect on nervous system

131
Q

How is dose rate calculated?

A

Clearance x plasma conc

132
Q

What is saturable drug metabolism?

A

Some drugs at therapeutic conc. overwhelm the metabolising enzymes
When metabolism becomes saturated the relationship between dose and plasma conc is no longer linear
When metabolism becomes saturated drug clearance changes from first order to zero order

133
Q

What is the difference in volume of distribution between highly polar drugs such as penicillin and highly lipid soluble drugs and why?

A

Highly polar distribute in central compartments - lower Vd
Highly lipophillic distribute more widely = higher Vd
Rule of thumb the body fills up
Blood -ECF - Intracellular fluid - muscle - fat

134
Q

What could we assume about a drug with a Vd which is the same as ECF volume?

A

Drug that doesnt pass readily through cell membranes

135
Q

What does enteral refer to?

A

A drug with systemic effects which is administered via the GI tract

136
Q

When should all drugs be avoided if possible in pregnancy?

A

During the first tri mester

137
Q

Why might salbutamol be used in premature labour?

A

Activation of beta 2 receptors leads to relaxation of smooth muscle, and can be used to prevent contraction of uterine muscles and thus premature labour

138
Q

What is allopurinol used for?

A

Block xanthine oxidase which converts purines to uric acid

Build up of uric acid leads to gout

139
Q

What is the difference between a suspension and a solution?

A 
Suspension = lipid droplets suspended in fluid, not dissolved but suspended
Solution = completely dissolved, they are already dissolved so form of a drug most easily absorbed

Year 1 IMS (14 decks)

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