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Pharmacology > Foundations of medicine > Flashcards

Foundations of medicine Flashcards

1
Q

What determines the severity of the effect a drug has on the body; Time in body, OR time bonded to receptor?

A

Time in body.

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2
Q

What is an agonist?

A

A substance that can bind to a receptor and produce a response.

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3
Q

What is Efficacy?

A

The ability of the agonist to produce a cellular response - e.g. high efficacy means it produces more of a response.

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4
Q

What is Affinity?

A

The ability of an agonist to bind to a receptor.

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5
Q

If one drug is more potent than another what does that mean?

A

The more potent drug produces the same response at a lower dose.

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6
Q

What is Pharmacovigilance?

A

The detection, assessment, understanding and prevention of adverse side effects in association with a drug.

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7
Q

What does a wide therapeutic index mean? why?

A

That very few people taking an effective therapeutic dose (for the intended effect) will also experience adverse side effects.

This is because the efficacy of the drug in relation to the adverse side effect is much less than in relation to the therapeutic effect.

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8
Q

What is drug selectivity?

A

When a drug has a higher affinity and efficacy for one type of receptors over another type (which may cause a side effect)

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9
Q

What is a competitive (reversible) antagonist?

A

Does not produce a biological effect directly but competes with an agonist for binding.

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10
Q

When a competitive reversible antagonist is in effect at a receptor how can a full response still be achieved?

A

Increase the concentration of agonist.

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11
Q

A competitive reversible antagonist decreases what in the agonist?

A

Its potency

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12
Q

An antagonist that permanently stops an agonist from binding to a receptor is what kind of Antagonist?

A

A non-competitive antagonist.

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13
Q

If a non-competitive antagonist is present can a full response still be achieved? Therefore what is reduced in the agonist?

A

No. It’s efficacy.

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14
Q

What is an allosteric antagonist?

A

An antagonist that changes the shape of the receptor so that the agonist cannot bind, a type of non-competitive antagonist.

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15
Q

What two ways might a pharmokinetic antagonist work?

A
  • by reducing its distribution.

- increasing its excretion.

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16
Q

What is a partial agonist?

A

An agonist in which the full response cannot be achieved even if 100% of receptors are occupied, due to low efficacy.

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17
Q

if a partial agonist is in the presence of a full agonist what happens?

A

The partial agonist acts as an antagonist and the full response is not achieved as easily if at all.

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18
Q

Three divisions of the autonomic nervous system?

A

Sympathetic

Parasympathetic

Enteric (GI tract - no CNS involvement)

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19
Q

What is one of the reasons a multi-organ response can be achieved in the sympathetic nervous system? to do with post-ganglionic neurones.

A

Multiple post ganglionic neurones can be stimulated by one preganglionic neurone.

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20
Q

Give some examples of the effects of stimulating the sympathetic nervous system? (6)

A

Heart-rate increases

Blood vessels constrict apart from those in muscles.

Gi motility decreases

Pupils dilate

Salivary glands are stimulated and produce amylase.

Liver starts gluconeogenesis and glycogenolysis.

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21
Q

Effects of stimulating the parasympathetic nervous system?

A

Heart rate decreases - no effect on blood vessels.

Increased GI motility.

Pupil constriction.

Salivary glands secrete amylase

Liver and kidney are unaffected.

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22
Q

What is the receptor and neurotransmitter used when an impulse is transmitted at a ganglion in an efferent neurone in the autonomic nervous system.

A

Acetylcholine, type 1 nicotinic receptors.

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23
Q

Describe the two types of nicotinic receptors.

A

Both types are made up of 5 subunits.

Binding of Acetycholine to the å submits allows the influx of Na+

Both respond to Acetylcholine but differ in response to other neurotransmitter.

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24
Q

What is the receptor and transmitter at all parasympathetic post-ganglionic nerve endings?

A

Muscarinic receptors, and acetylcholine.

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25
Q

What is the receptor and transmitter at most sympathetic post-ganglionic nerve endings?

A

Noradrenaline and Adrenergic receptors.

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26
Q

Two examples of exceptions in the receptors and neurotransmitters used normally in the sympathetic nervous system?

A

Sweat glands - acetylcholine and muscarinic receptors are used.

Adrenal medulla - As adrenaline and noradrenaline produced here the neurotransmitter is acetylcholine and the receptor is nicotinic type 1.

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27
Q

Neurotransmitter and receptor in the somatic nervous system in efferent neurones to muscle fibres?

A

Acetylcholine and nicotinic.

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28
Q

Describe the synthesis and release of Acetylcholine at synapses.

A
  1. When action potential arrives vesicles containing Acetylcholine fuse with the presynaptic membrane and are released into the synaptic cleft.
  2. Acetylcholine interacts with muscarinic or nicotinic receptors.
  3. Acetylcholine is rapidly broken down by acetylcholinesterase.
  4. Choline is taken back into the presynaptic neurone and acetylated.
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29
Q

Examples of two drugs that mimic Acetylcholine and their uses.

A

Pilocarpine - used as eye drops to treat glaucoma.

Bethanecol - stimulates muscle contraction, occasionally used to return normal GI function after anaesthesia.

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30
Q

Four examples of drugs that block Acetylcholine and their uses.

A

Atropine - reduces secretions.

Ipatropium - bronchodilator.

Hyoscine - Motion sickness or to facilitate endoscopy.

Tropicamide - eyedrops to induce mydriasis (pupil dilation).

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31
Q

Will a drug that affects the synthesis, packaging, release or reabsorption of Acetylcholine affect Parasymapthetic/somatic/both? Why?

A

Both, due to the fact both use Acetylcholine as a neurotransmitter despite different receptors.

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32
Q

Give two examples of drugs that affect acetylcholinesterase.

A

Edrophonium - short acting - to diagnose myasthenia gravis (weakness of certain muscles)

Neostigmine - medium acting - to treat myasthenia gravis.

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33
Q

In what situation is Noradrenaline used as a neurotransmitter?

A

Stimulating blood vessels in sympathetic system and in cranial parasympathetic system, but not sacral parasympathetic system.

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34
Q

How is noradrenaline synthesised and released?

A

Synthesised as tyrosine is taken into the cell and converted to noradrenaline, then packaged into vesicles and released into the synaptic cleft.

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35
Q

How is noradrenaline removed? (3)

A

Metabolised by monoamine oxidase (MAO) when spare in the cytosol.

Taken back into the cell by specific transport mechanism when free in the synaptic cleft.

Also taken back into neighbouring cells and metabolised by catechol-O-methyl transferase (COMT)

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36
Q

Three drugs that affect noradrenaline synthesis or uptake?

A

Reserpine - blocks the packaging of Noradrenaline into granules

Amphetamine - displaces noradrenaline from the blood vessels.

Cocain and some antidepressants block the reuptake of NA from the synapse.

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37
Q

Drugs that block the metabolism of NA? their effects?

A

MAO inhibitors - Antidepressant - Atropine like affects (dry mouth, blurred vision)

COMT inhibitors - Used in parkinsons to stop the breakdown of dopamine.

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38
Q

Difference in pharmacodynamics and pharmacokinetics?

A

Dynamics is the study on what the drug does to the body and kinetics is the study of what the body does to the drug.

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39
Q

When would you use a rectal pill?

A

Vomiting patient.

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40
Q

When would you deliver drugs as a syrup?

A

Paediatrics

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41
Q

Whats an enteral formulation and a parenteral formulation?

A

Enteral - undergoes first pass metabolism in the liver before reaching the systemic circulation.

Parenteral - does not undergo first pass metabolism in the liver before reaching systemic circulation.

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42
Q

Two Parenteral formulations?

A

Liquid, and lyophilized (freeze-dried).

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43
Q

Examples of topical formulations?

A

Cutaneous (skin) Cream, ointment, gel, paste

Inhaled: Metered Dose inhaler (MDI), Breath actuated device, Nebuliser.

Eye drops, Nasal Sprays, Vaginal, urethral suppositories.

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44
Q

For most oral drugs where is the greatest absorption of a drug?

A

The small intestine (not the stomach).

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45
Q

What is Gastric emptying and how does it affect the absorption of drugs?

A

The amount of time it takes to empty the contents of the stomach. increased gastric emptying slows the absorption of the drug.

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46
Q

Ways in which gastric emptying is slowed?

A

A solid meal (distension)

High fat meal.

High protein meal,

Low gastric pH.

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47
Q

What’s first-pass metabolism?

A

When drugs undergo various degrees of metabolism in the liver before reaching the systemic circulation, Travels from the intestine in the portal vein and then out from the liver through the hepatic vein.

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48
Q

Disadvantages of Oral administration?

A

Delay in drug onset

Drug exposed to gastric acid and digestive enzymes

Portal vein —> The liver before reaching systemic circulation, where some drugs undergo first-pass metabolism.

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49
Q

Enteral routes that avoid first-pass metabolism?

A

Rectal, Buccal (mouth), sublingual (under tongue).

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50
Q

Three types of Parenteral routes? and their features?

A

Intravenous - instantaneous onset, high peak concentration (effect not over a long time)

Intramuscular - immediate onset, small volumes only, oil based depot formulations give a very long duration.

Subcutaneous - small volumes only, very slow onset.

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51
Q

What is intraosseous?

A

Injection into bone.

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52
Q

Disadvantages of Parenteral routes?

A

Avoid the GI tract and first-pass metabolism.

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53
Q

Features of transdermal topical administration?

A

Very slow onset, prolonged action.

Requires highly lipophilic drug.

Local irritation possibly.

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54
Q

Features of a topical inhaled administration? (5)

A

Rapid delivery.

No first-pass metabolism.

Acts locally.

Allows low-dose to local site.

Rarely used for systemic drugs.

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55
Q

What are the variables passive diffusion across a membrane depends on?

A

The concentration gradient across a membrane. C1-C2.

Area of the membrane available for diffusion (A)

Thickness of the membrane.

Permeability of the membrane to the drug.

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56
Q

What is the equation to calculate simple diffusion across a membrane

A

(C1-C2) x Area x permeability.
Diffusion= ——————————-
Thickness

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57
Q

How does a lipid-soluble drug cross a membrane?

A

Diffuses through the lipid membrane,

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58
Q

How does a Water-soluble drug with a molecular weight below 200 pass through a cell membrane?

A

Diffusion through an aqueous channel.

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59
Q

How does a water-soluble drug that resembles a natural molecule pass through the cell membrane?

A

Down it’s concentration gradient through a carrier molecule (facilitated diffusion).

Against it’s concentration gradient by energy-dependent (ATP) channel (active transport).

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60
Q

If a weak acid drug is at a low pH will it be non-ionised or ionised and therefore will it diffuse across membranes and be absorbed?

A

Weak acid at low pH will be mostly non ionised and will therefore diffuse effectively across the lipid membrane.

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61
Q

If a weak base drug is at a low pH will it be non-ionised or ionised and will it therefore diffuse across membranes and be absorbed?

A

Will be ionised (accepted H+) and will not be effectively absorbed across the lipid membrane.

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62
Q

In a drug concentration by time graph what does the area under the graph represent?

A

Bioavailability.

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63
Q

What is the definition for bioavailability?

A

The fraction of the drug reaching the circulation as the active drug. 1 represents an intravenous dose (fully available) 0 would be not available.

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64
Q

Whats the symbol for bioavailability?

A

F

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65
Q

How do you calculate the bioavailable dose?

A

Administered does in mg (D) X Bioavailability (F)

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66
Q

What affects oral bioavailability?

A

Drug solubility.

Extent of drug binding to gut contents.

Drug absorption.

Extent of drug degradation.

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67
Q

Name three drugs that mimic the effect of Noradrenaline on the sympathetic nervous system? their effects and uses? their collective name?

A

Salbutamol. Bronchdilator used in asthma.

Adrenaline. used in cardiac arrest, and in local anaesthetics to reduce diffusion

Dobutamine. stimulates heart.

Sympathomimetics.

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68
Q

Effects of Noradrenaline on the body?

A

Relaxation of smooth muscle.

Tachycardia - increased heart rate and force.

Decreased blood flow to the skin and GI tract.

Increased blood flow to the muscles.

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69
Q

Effect of decreasing NA levels on the body?

A

Bradycardia - slowing of the heart rate.

Hypotension - reduced cardiac output.

increased blood flow to skin and GI tract.

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70
Q

Name two drugs that block the actions of NA on the sympathetic nervous system? Their effects and uses?

A

Propranolol -used for angina, hypertension, anxiety.

Prazosin - Resistant hypertension and benign prostate hypertrophy.

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71
Q

How are peripheral adrenoreceptors divided up?

A

Alpha1 and alpha2

Beta1 and beta 2

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72
Q

What peripheral adrenoreceptors does NA affect?

A

Alpha adrenoreceptors, not very effective on B adrenoreceptors.

73
Q

What peripheral adrenoreceptors does Adrenaline act on?

A

Both alpha and beta receptors.

74
Q

Where are Alpha1 adrenoreceptors found?

A

Blood vessels and smooth muscle.

75
Q

Where are Alpha2 adrenoreceptors found?

A

Found on presynaptic cells, inhibiting the release of neurotransmitters.

76
Q

Where are Beta2 adrenoreceptors found?

A

Bronchial and uterine smooth muscle.

77
Q

Where are Beta1 adrenoreceptors found?

A

Found on the heart where they increase the rate and force of contraction.

78
Q

What is perfusion?

A

The level of blood flow to a particular organ.

79
Q

some examples of well perfused tissue and badly perfused tissue?

A

Well perfused (a selection of some of will do):

Liver
Lungs (the most)
Kidney
Brain
Heart

Badly perfused:

Fat
Bone
Muscle

80
Q

Two plasma proteins that bind to drugs reversibly?

A

Albumin

Alpha-1 acid glycoprotein.

81
Q

How many total litres of blood are there in the body?

A

5 Litres.

82
Q

How do you calculate the volume of distribution (Vd) ?

A

Drug Dose
Vd = —————————–
Plasma concentration

83
Q

What is the percentage of body weight that is total body water?

A

50-60%

84
Q

If the Vd was 5 litres in a 70kg man where is the drug likely to have distributed to?

A

In the plasma .

85
Q

If the Vd was 12 litres in a 70kg man where is the drug likely to have distributed to?

A

Extracellular water.

86
Q

If the Vd was 40 litres in a 70kg man where is the drug likely to have distributed to?

A

Total body water.

87
Q

Where are the two areas of the body where the Vd appears so large it seems impossible? Why is this so?

A

Fat (Vd of 140) and Bone (Vd >500)

It is possible as the drug could be absorbed or sequestered very strongly, giving the appearance of a very large Vd.

88
Q

What is the blood-brain barrier made up of?

A

Astrocytes.

Tight junctions.

89
Q

What is the function of the Blood Brain barrier?

A

Excludes Large drug molecules and Water-soluble drugs.

90
Q

When might the blood-brain barrier be deficient?

A

Inflammation, and infectious.

Newborns (6 weeks)

91
Q

How can the tight junctions of the Blood Brain Barrier be opened to allow large drugs or water-soluble drugs through.

A

Therapeutically using intracarotid mannitol.

92
Q

How does the body metabolise lipophilic drugs?

A

Makes them more water-soluble, so they can be excreted by the kidneys.

93
Q

What is the main organism of metabolism?

A

Liver

94
Q

How are metabolites excreted from the liver?

A

Returned to the general circulation or in bile.

95
Q

Do drugs only go through the liver once? what is this called?

A

No will pass through many times 1st pass metabolism and 2nd src etc…

96
Q

2 Phases of metabolism? examples?

A

Inactivation. e.g. Oxidisation, reduction, hydrolysis.

Solubilisation. e.g. conjugation

97
Q

What is cytochrome P450?

A

A family of membrane-bound enzymes that are involved in catalysing reactions in both phase one and phase two metabolism (in phase two they cooperate with other enzymes).

98
Q

Where are P450 isoenzymes found?

A

Mainly on the smooth ER of hepatocytes.

99
Q

Where are the secondary enzymes involved in phase two of metabolism found?

A

mainly in cytoplasm.

100
Q

What will glucoronidation conjugation produce?

A

Drug-glucuronide

101
Q

What will sulphination conjugation produce?

A

Drug-sulphate

102
Q

Acetyl-‘drug’ is produced from what?

A

Acetylation.

103
Q

Methylation conjugation will produce what?

A

Methyl-drug

104
Q

Amino-acid conjugation will produce what?

A

Amino-acyl-drug

105
Q

Consequences of metabolism?

A

Can generate active metabolites from active drugs e.g. in diazepam it becomes nordiazepam or active drugs from pro drugs.

Can generate toxic metabolites e.g. in paracetamol.

106
Q

What are pharmacogenetic differences in CYP2D6?

A

will convey different rates of metabolism of metaprolol (a beta-blocker)

107
Q

What secondary messenger does the G-protein on beta 1 adrenoreceptors activate?

A

Phospholipase C

108
Q

How does activation of alpha-1 adrenergic receptors cause an increase in systolic and diastolic arterial blood pressure?

A

constriction of vascular smooth muscle in the arterioles, arteries and veins, leading to peripheral resistance decreased vascular compliance and increased central venous pressure.

109
Q

An example of an alpha-1 adrenoreceptor antagonist and what it can be used to treat?

A

Doxazosin - used to treat resistant hypertension.

Also benign prostatic hypertrophy. (relaxes smooth muscle improving urinary flow).

110
Q

how are alpha-1 adrenergic receptor agonists used in anaesthetics?

A

used to reduce the spread of the injection in local anaesthetics - e.g. inject with adrenaline causing vasoconstriction.

111
Q

How does a drug such as pseudo ephedrine decrease nasal secretions?

A

Constricts blood vessels in the nose.

112
Q

How do alpha-2 adrenoreceptors act in an inhibitory manner?

A

located in the presynaptic cell and able to inhibit adenylate cyclase reducing cAMP levels in the cell.

113
Q

What do all beta-receptors do to adenylate cyclase?

A

Activate it!

114
Q

Where are B-1 adrenoceptors found?

A

heart!

115
Q

What are the adrenoceptors on the lungs called?

A

B-2 adrenoceptors.

116
Q

What is the effect of stimulating beta-1 adrenoceptors?

A

Increased heart rate, and force of contraction.

Reduced cardiac efficiency.

Can disturb cardiac rhythm.

117
Q

an example of a beta-1 adrenoceptor agonist used to stimulating a failing heart?

A

Dobutamine.

118
Q

The effect of stimulating B-2 agonists?

A

Relax airway smooth muscle, by increasing intracellular cAMP. levels

119
Q

An example of an b2 adrenoceptor agonist?

A

Salbutamol.

120
Q

Weaknesses in using b2 adrenoceptor agonists such as Salbutamol in treating asthma?

A

Doesn’t treat underlying airway inflammation, over-reliance should be avoided.

121
Q

How are B2 adrenoceptors used in premature labour?

A

Agonists such as salbutamol can be given to relax uterine smooth muscle, delay delivery, and then steroid therapy can be used to mature the baby’s lungs.

122
Q

How are adrenoceptor antagonists used?

A

To treat heart dysrhythmias, by improving oxygenation of the heart muscle.

123
Q

Side effects of B-blockers?

A

Bradycardia

Hypoglycaemia - glucose release in response to adrenaline.

Fatigue

Cold extremities

124
Q

Can Beta blockers be used by those who use beta agonists for symptomatic relief?

A

No, as they would interfere.

125
Q

What is the name of the process which removes introns from the primary RNA transcript?

A

Splicing.

126
Q

Can eukaryotic DNA contain a sequence coding for more than one protein? What can?

A

No, prokaryotic DNA can however.

127
Q

Three ways in which The primary RNA transcript is processed?

A

Spilcing

Polyadenylation

Addition of a 5’ cap

128
Q

How is a 5’ cap added to mRNA, what is the function of this?

A

Adding a methylated Guanine (G) residue to the terminal base of the transcript.

This helps the cell distinguish mRNA from other RNA’s, which helps mRNA be properly processed and exported from the nucleus.

129
Q

what is polyadenylation, what is it’s function?

A

The addition of a string (around 200) Adenine (A) nucleotides to the 3’ end of the RNA transcript.

This stops transcription (proteins can bind to the tail to stabilise the RNA.

130
Q

What is the DNA code for polyadenylation?

A

AAUAAA

131
Q

What defines the beginning and end of introns?

A

Splice sites, which are consensus sequences of DNA that are transcribed into the pre-mRNA.

132
Q

What is the splicosome?

A

A large complex of non-coding RNA and proteins. It removes introns from the primary transcript.

133
Q

How does the splicosome remove introns from the primary transcript?

A

Through the formation of a lariat.

134
Q

What do metabolism and excretion contribute to in pharmacokinetic terms?

A

Elimination.

135
Q

What is zero order elimination?

What is an example and why is this so?

A

When the drug is eliminated at a constant rate, there is a constant concentration per unit time producing a ‘straight line’ on a concentration time graph.

Alcohol, this is due to saturation of the liver and all enzymes working at a maximal rate.

136
Q

What is clearance?

A

The volume of blood plasma cleared of a drug per unit time in a particular organ.

137
Q

Why are exponential or ‘first order’ graphs produced?

A

Due to the elimination of the drug reducing as more of the drug is cleared. This is because there is less of the drug in the blood plasma.

138
Q

How do you calculate total clearance?

A

Total clearance = CL(liver) + CL(kidney) + CL(Lung).

139
Q

Is Total clearance constant for a particular drug? does it depend on drug dose and concentration?

A

It is constant and is independent of drug dose and concentration.

140
Q

What is the equation for rate of elimination?

A

Rate of elimination (mg/h) = Total clearance (l/h) x Plasma Concentration (mg/l)

141
Q

What is half-life?

A

The time taken for the concentration of the drug to fall by 50% (T1/2)

142
Q

What is special about the half-life in an exponential curve?

A

It remains constant.

143
Q

What is the symbol for half life?

A

T1/2

144
Q

is Half Life (T1/2) inversely or directly proportional to Clearance?

A

Inversely - as half life increases clearance decreases.

145
Q

Is Vd inversely or directly proportional to T(1/2)?

A

Directly - as Vd increases so does T(1/2)

146
Q

Is T(1/2) dependent or independent of the dose?

A

Independent.

147
Q

What is the relationship between T(1/2) and dose frequency

A

Inversely proportional, as half life increases the dose frequency can be reduced.

148
Q

What is The steady state plasma concentration or (Css)?

A

When the plasma concentration is constant, the drug has fully distributed through it’s Vd and the rate of drug elimination = the rate of drug infusion.

149
Q

How do you calculate rate of drug infusion (if constant infusion is to be given)?

A

Drug infusion = Drug elimination = CL x Css

So CL x Css

150
Q

How do you work out the rate of dosage in oral situations?

A

Oral dose (D) x Bioavailability (F)/ Time interval between doses (T) = CL x Css

151
Q

How do you calculate the loading dose?

A

Vd X Css

152
Q

What is the difference in loading dose and maintenance dose?

A

Loading dose is a large dose so that Css is reached quickly, the maintenance dose is required to maintain the Css.

153
Q

How do you work out % w/v ?

A

It is just number of grams in 100ml.

154
Q

What is classical conditioning?

A

pairing of an unconditioned stimulus with a conditioned stimulus.

155
Q

How do you work out molarity of a solution?

A

Just number of moles in one litre.

156
Q

Why is clearance a constant value?

A

Clearance only measures the VOLUME of plasma cleared of drug per unit time, so that never actually changes.

157
Q

What are the intracellular effects of dobutamine binding to B-1 receptors?

A

Activates andenylyl cyclase Increasing intracellular levels of cAMP.

158
Q

What are the intracellular effects of salbutamol binding to B-2 receptors?

A

Activates adenylyl cyclase increasing levels of intracellular cAMP.

159
Q

What type of interactions do agonists bind to receptors with?

A

Transient interactions.

160
Q

What is ED50?

A

The dose required for a half-maximal response.

161
Q

what type of relationship exists between ED50 and potency?

A

ED50 is inversely proportional to potency.

162
Q

On a dose-response curve which is x and Which is Y?

A

X - dose

Y - response

163
Q

What effect does latarotoxin have on the nervous system?

A

Causes the release of Acetylcholine.

164
Q

What effect does botulinum toxin have on the nervous system?

A

Inhibits the release of Acetylcholine.

165
Q

What effect does neostigmine have on the nervous system?

A

potentiates the action of Ach

166
Q

The effects of pilocarpine and bethanecol (2 or so)? What causes these effects?

A

Activates muscarinic receptors

pupil constriction, salivary secretions, reduced heart rate increased GI motility, bladder wall contraction.

167
Q

The effects of Atropine? what causes these effects?

A

Muscarinic antagonists:

Pupildilation, reduced secretions.

168
Q

What does MAO do?

A

Metabolises noradrenaline in the presynaptic cell.

169
Q

What does COMT do?

A

Metabolises noradrenaline in the postsynaptic cell.

170
Q

What is adrenaline?

A

A hormone, activates adrenergic receptors.

171
Q

What receptors are involved in pupil dilation and what nervous system division?

A

a1 receptors, sympathetic nervous system.

172
Q

What nervous system regulates adrenoceptors?

A

Sympathetic nervous system.

173
Q

What is the difference in enteral and parenteral

A

Enteral is through the gut.

174
Q

What does a kinetic interaction mean?

A

A kinetic interaction alters the amount of another drug.

175
Q

The two stages of metabolism?

A

Inactivation

Solubilisation

176
Q

In what situations would you monitor drugs in patients?

A

Narrow Therapeutic index

Nasty side effects

Unusual pharmacokinetics

Vulnerable groups, e.g. children, pregnant.

177
Q

How could you monitor a drug in a patient?

A

Measure drug e.g. blood samples

Measure the effects, e.g. blood pressure

Ask the patient.

178
Q

CRAP GPS mnemonic?

A

C - Carbemazepine
R - Rifampicin
A - Alcohol
P - phenytoin

G - Dont worry
P - Don’t worry
S - Sulphonylureas

179
Q

SICKFACES.COM G mnemonic?

A 
S - Don't worry
I - Don't worry
C - Don't worry
K - Don't worry
F - Don't worry
A - Alcohol
C -Cimetidine 
E - erythromycin
S - sulphonamides
.
C - Chlorophenicol
O - Don't worry
M - Don't worry

G - Grapefruit juice

Pharmacology (1 decks)

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