Pharmacology Flashcards

1
Q

What is pharmacodynamics

A

how the drug affects the body

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2
Q

What is pharmacokinetics

A

the distribution of a compound within the organism, according to it’s ADME (absorption, distribution, metabolism, excretion)

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3
Q

What is ‘druggability’

A

The ability of a protein to bind small molecules with high affinity (10-15% of the genome)

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4
Q

Define receptor

A

Component of a cell which interacts with a ligand and initiates a chain of biochemical events leading to the ligands observed effects

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5
Q

Define neurotransmitter

A

small molecular mass molecule associated with transmitting a neural response

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6
Q

Define autacoids

A

molecules associated with transmitting a signal locally eg histmaine or cytokines

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7
Q

Define hormones

A

molecules which transmit a biological signal from one cell to another elsewhere in the body, using the blood

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8
Q

Name an example of a ligand gated ion channel

A

Nicotinic ACh

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9
Q

Name an example of a G protein coupled receptor

A

Beta adrenoceptor

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10
Q

Name an example of a kinase linked receptor

A

Growth factor receptor

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11
Q

Name an example of a cytosolic receptor

A

Steroid hormone receptor

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12
Q

Which conformational state is the receptor in when the G protein binds GDP

A

Open

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13
Q

Which conformational state is the receptor in when the G protein binds GTP

A

Closed

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14
Q

What is a heterogenic G protein coupled receptor

A

One which binds to two different molecules

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15
Q

Muscarinic (M3) receptors are associated which protein, enzyme and second mesengers

A

Gq, phospholipase c, IP3/DAG

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16
Q

Adrenergic (B2) receptors are associated with which protein, enzyme and second messengers

A

Gs, adenly cyclase and cyclic AMP

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17
Q

What is needed to activate a kinase linked receptor

A

A ligand in dimer form

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18
Q

What is the function of zinc fingers in nuclear receptors

A

As part of the DNA binding domain they identify DNA motifs

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19
Q

Which disease is caused by loss of ACh receptors

A

Myasthenia Gravis

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20
Q

Which disease is caused by an increase in ckit receptors

A

Mastocytosis

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21
Q

Agonist definition

A

A compound which binds to a receptor and activates it

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22
Q

Antagonist definition

A

A compound which reduces the effect of an agonist

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23
Q

What shape is the agonist response curve on a linear scale

A

Logarithmic

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24
Q

What shape is the agonist response curve on a log scale

A

Sigmoidal

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25
Q

What is EC50

A

The concentration which gives half the maximal response and achieves potency

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26
Q

What is efficacy (Emax)

A

The maximum response achievable from a dose

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27
Q

What is a partial agonist

A

A drug which binds to a receptor but only has partial efficacy relative to a full agonist

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28
Q

How can you classify receptors

A

using competitive antagonists or agonists which a range of potencies

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29
Q

What is the antagonist to the nAChR receptor

A

Atropine

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30
Q

What is the antagonist to the mAChR receptor

A

Curare

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31
Q

What are H1 receptors associated with

A

Allergy

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32
Q

What are H2 receptors associated with

A

Gastric acid secretion

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33
Q

What is a H2 antagonist and its role

A

mepyramine and it causes ileum relaxation and has no affect on parietal cells

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34
Q

What is a H2 agonist and its role

A

histamine and it causes ileum contraction and acid secretion from parietal cells

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35
Q

What are H3 receptors associated with

A

CNS disorders

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36
Q

What are H4 receptors associated with

A

Immune systema nd inflammatory responses

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37
Q

Define affinity

A

Describes how well a ligand binds to a receptor

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38
Q

Define efficacy

A

Describes how well a ligand activates a receptor

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39
Q

What are tissue related factors which affect drug action

A

Signal amplification and receptor number

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40
Q

What is the affinity and efficacy of a succesful competitive antagonist

A

Affinity must be equal or better than the agonist and efficacy is zero

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41
Q

What is the functional reserve of a receptor

A

The number of receptors free when maximal response is acheived

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42
Q

What is an inverse agonist

A

An agent which deactivates a receptor

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43
Q

What is the name of the primary receptor site

A

Arthosteric site

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44
Q

What is the action of an agonist

A

To cause activation of a receptor

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45
Q

What is the action of an antagonist

A

To prevent activation of a receptor

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46
Q

What is the action of an invesrse agonist

A

To cause deactivation of a receptor

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47
Q

Define tolerance

A

A reduction in the drug agonist effect over time after continuously repeated high doses

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48
Q

What is an enzyme inhibitor

A

A molecule which binds to an enzyme and reduces its activity

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49
Q

Active transport definition

A

The movement of a molecule across a membrane, from an area of low to high concentration using energy

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50
Q

What is fureosemide

A

a loop diuretic which targets NKCC symporters in the ascending tubule. Causes sodium, pottasium and chloride loss

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51
Q

Which ion channels are involved in the treatment of heart failure

A

Epithelium sodium

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52
Q

Which ion channels are involved in the treatment of nerve arrythmia

A

Voltage gated calcium/sodium

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53
Q

Which ion channels are involved in the treatment of diabetes

A

metabolic pottasium

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54
Q

Which ion channels are involved in the treatment of epilepsy

A

Receptor activated chloride

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55
Q

Which antihypertensive targets transmembrane sodium channels

A

Amiloride

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56
Q

Name an angioselective calcium channel blocker

A

Amlodipine

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57
Q

Define action potential

A

A momentary change in electrical potential on the surface of a cell, which occurs when it is stimulated and results in transmission of an electrical impulse

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58
Q

Name an antiarrythmic drug which acts by blocking sodium channels and action potentials

A

Lidocaine

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59
Q

What are the three possible states of a voltage gated sodium and pottasium channel

A

Open, Closed, Innactivated

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60
Q

Name type 2 diabetes drugs which block pottasium channels causing insulin release

A

Repaglinide and nateglinide

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61
Q

What is an ionotropic receptor

A

A receptor directly linked to an ion channel

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62
Q

What is the role of barbiturates

A

Increase the permeability of the channel to chloride

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63
Q

How does digoxin treat AF, HF and atrial flutter

A

It inhibits Na/K ATPases, this increase cardiac Na and therefore Ca levels, increasing the length of the cardiac action potential and reducing heart rate

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64
Q

What is a heterodimeric protein and name an example

A

A protein which is the product of two genes such as Gastric K/H ATPase

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65
Q

Name an irreversible cholinesterase inhibitor and where it is found

A

Organophosphates, found in insecticides and nerve gases

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66
Q

Define xenobiotics

A

Compounds foreign to an organisms biochemistry such as any drug or poison

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67
Q

Define absorption

A

Process of transfer from the site of administration into the general or systemic circulation

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68
Q

Name 4 ways a drug can pass through a membrane

A

Passive diffusion through lipid layer, diffusion through pores or channels, carrier mediated processes, pinocytosis

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69
Q

Define carrier mediated transport

A

Carries molecules against their concentration gradient into cells using ATP

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70
Q

What is Verpamil

A

A Pgp inhibitor, increases concentration of anticancer drugs in cytoplasm and therefore increases their action

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71
Q

What is Probenecid

A

A OAT1 inhibitor, increases uric acid (and penicillin) secretion in urine

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72
Q

Define pinocytosis

A

Intake of small droplets of fluid by a cell by cytoplasmic engulfment

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73
Q

Name a drug which is a weak acid

A

Aspirin

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74
Q

Name a drug which is a weak base

A

Propanolol

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75
Q

What two factors determine the ionisation of a drug

A

The strength of the ionised groups, the pH of the solution

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76
Q

Which ionisation extent is more lipid soluble

A

Less ionised

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77
Q

What is pKA

A

The ionisation constant, the point at which 50% are ionised

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78
Q

Where are weak acids best absorbed

A

An acidic environment, eg the stomach

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79
Q

Where are weak bases best absorbed

A

A basic environment, eg the intestines

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80
Q

What is useful about olsalazine’s structure

A

As it is highly polarised it is only partially absorbed in the small intestine, so can pass to the colon and treat IBD

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81
Q

What factors increase the rate of gastric emptying

A

Gastric surgery

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82
Q

What factors decrease the rate of gastric emptying

A

Food, trauma or drugs (Antimuscarinics - oxybutinin)

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83
Q

What causes poor absorption of a drug from the small intestine

A

Short gut syndrome

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84
Q

What are the four barriers an orally taken drug must pass

A

IILL. Intestinal lumen, intestinal wall, liver, lungs

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85
Q

How does the lumenal wall limit absorption

A

Lumenal enterocytes have efflux transporters which transport drugs back into the lumen

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86
Q

How can you avoid the livers metabolism

A

Deliver the drug to part of the GI tract which isnt drained by the splanchnic circulation such as the mouth or rectum

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87
Q

Which absorption routes have a 1 minute absorption time

A

IV and interosseous

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88
Q

Which absorption routes have a 3 minute absorption time

A

Endotracheal and inhalation

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89
Q

What is the sublingual route absorption time

A

3-5 minutes

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90
Q

Which absorption routes have an absorption time of around 30 minutes

A

Intramuscular, subcutaneous, rectal, ingestion and transdermal

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91
Q

When is the intraosseous route used

A

In paediatric trauma where the IV is hard to find

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92
Q

What are the 3 criterion of a transcutaneous drug

A

Lipid soluble, potent and not an irritant

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93
Q

What factors cause increased removal of a drug from an IM site

A

Increased blood flow or water solubility

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94
Q

What is a depot

A

A slow acting store of lipophilic formulation, given intramuscularly it is useful in patients with poor compliance

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95
Q

What are the disadvantages of inhalation as a route of administration

A

Risk of alveolar toxicity and non volatile drugs must be given as aerosols or dry powders

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96
Q

Which drugs easily pass through the BBB

A

Lipid soluble

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97
Q

Define distribution

A

Process by which a drug is reversibly transferred from the general circulation to the tissues, dependent on a concentration gradient out of the blood

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98
Q

Which organs are well perfused and will therefore receive a high dose more quickly

A

Brain, liver, lungs

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99
Q

Define bolus

A

A large dose of a drug administered by rapid injection rather than infusion

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100
Q

Define first order kinetics

A

Exponential decline in concentration, a constant fraction of the drug is eliminated per unit time

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101
Q

Define zero order kinetics

A

Rate of removal is constant and unaffected by changes in concentration; seen in saturated enzyme systems

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102
Q

Define half life

A

Time taken for a concentration to reduce by one half

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103
Q

Define bioavailability

A

The fraction of the administered drug which reaches the systemic circulation unaltered

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104
Q

Define distribution

A

Rate and extent of drug movement into and out of tissues from the blood

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105
Q

What determines distribution of water soluble drugs

A

The rate of passage across membranes

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106
Q

What determines distribution of lipid soluble drugs

A

The rate of blood flow to tissues accumulating the drug

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107
Q

What is volume distribution

A

Total amount of drug in the body (dose)/plasma concentration
(amount needed to have dose in plasma)

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108
Q

Define clearance

A

The volume of blood or plasma cleared of a drug per unit time

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109
Q

Define steady state (Css)

A

Equilibrium between drug input and elimination

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110
Q

How do you shorten the time taken to reach steady state in drugs with a long half life

A

By giving a loading dose

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111
Q

Why is intraoccular pressure controlled

A

To prevent glaucoma causing blindness

112
Q

Why is airway tone controlled

A

To prevent bronchospasm (constriction)

113
Q

Which output from the CNS to the body isnt controlled by the autonomic nervous system

A

Skeletal muscle control

114
Q

Which CNS nerve has a role in the innate immune system

A

Vagus

115
Q

Define enteric nervous system

A

part of the peripheral nervous system, a plexus of nerves around the gut

116
Q

Define somatic

A

One neurone comes from the CNS to innervate muscle

117
Q

Where are parasympathetic nerve ganglia

A

Near the target organ

118
Q

Where are sympathetic nerve ganglia

A

Near the spinal cord

119
Q

What is the sarcral outflow

A

Parasympathetic, innervates pelvis and does contain some sympathetic

120
Q

Parasympathetic neurotransmitter and receptor at tissues

A

ACh and muscarinic

121
Q

Sympathetic neurotransmitter and receptor at tissues

A

Noradrenaline and adrenergic

122
Q

Which organs only have sympathetic innervation

A

Blood vessels and sweat glands

123
Q

Which organs only have parasympathetic innervation

A

Bronchial smooth muscle and the eye

124
Q

Which organs have both sympathetic and parasympathetic innervation

A

Heart, gut, bladder

125
Q

Parasympathetic neurotransmitter and receptor at ganglion

A

ACh and Nicotinic

126
Q

Sympathetic neurotransmitter and receptor at ganglion

A

ACh and nicotinic

127
Q

Parasympathetic NANC post ganglionic substances

A

NO, Vasoactive Intestinal Peptide

128
Q

Sympathetic NANC post ganglionic substances

A

ATP and neuropeptide Y

129
Q

Where are M1 receptors found

A

The brain

130
Q

Where are M2 receptors found

A

The heart

131
Q

Where are M3 receptors found

A

Glandular and smooth muscle

132
Q

Where are M4 receptors found

A

The CNS

133
Q

Where are M5 receptors found

A

The CNS

134
Q

What is glaucoma

A

Increased intraoccular pressure results in nerve fibre loss from the optic nerve

135
Q

What is ipratropium bromide (atrovent)

A

SAMA to M3 for bronchoconstriction

136
Q

What is tiortropium

A

LAMA to M3 for bronchoconstriction

137
Q

Name uses of anticholinergics/antimuscarinics

A

Bronchoconstriction, overactive bladder, dilate eye for examination, Intestinal and bowel spasms, raise heart rate

138
Q

Name roles of Acetylcholine outside the autonomic nervous system

A

Memory and sickness

139
Q

What causes ACh defecit

A

Botulin toxin release, nicotinic blockers, myasthenia gravis

140
Q

What are nicotinic blockers

A

Given in surgery to relax muscles, pancuronium and suxamethonium

141
Q

What are consequences of ACh defecit

A

Bad memory, confusion, constipation, drying, worsening of glaucoma and blurred vision

142
Q

What are causes of ACh surplus

A

Organophosphate insecticides and nerve gases are irreversible insecticide inhibitors

143
Q

What are consequences of ACh surplus

A

Muscle paralysis and twitching, salivation, confusion, adaption and desensitivity to high levels

144
Q

Which protein is associated with alpha 1 adrenoceptors and what is it’s affect

A

Gs, increases intracellular calcium

145
Q

Which protein is associated with alpha 2 adrenoceptors and what is it’s affect

A

Gi, inhibits cAMP generation

146
Q

What is the effect of alpha 1 adrenoceptor activation

A

vasoconstriction especially in the skin and splanchnic beds

147
Q

Where are alpha 1 adrenoceptors agonists used

A

For septic shock and topically for nasal decongestion

148
Q

Where are alpha 1 adrenoceptor antagonists usead

A

To lower BP, targetting alpha 1A can be used to treat hypertrophic prostate

149
Q

Name an alpha 2 agonist and its effects

A

Clonidine, lowers BP treats ADHD and anxiety

150
Q

What affects do beta 1 adrenoceptors have

A

Increased chronotropic (rate) and inotropic (strength) effects on the heart

151
Q

What is the affect of Beta 2 adrenoceptor activation

A

Relaxes smooth muscle, bronchodilation, delay of laboiur

152
Q

what is the affect of beta 3 adrenoceptor activation

A

enhanced lipolysis and bladder detrusor relaxation, used to alleviate overactive bladder symptoms

153
Q

Which adrenoceptors are involved in lipid and carbohydrate metabolism

A

Beta 1 and 3 (2 surpresses awareness)

154
Q

Which receptors does propanolol act on

A

Both Beta 1 and 2

155
Q

Which receptors does atenolol act on

A

Just Beta 1

156
Q

Name some beta blocker side effects

A

tiredness, cold extremities, bronchoconstriction, bradycardia, hypoglycaemia and cardiac depression

157
Q

What is preeclampsia

A

pregnancy induced hypertension with proteinuria (and/or oedema)

158
Q

What is methyldopa and how does it work

A

last resort hypertensive used in preeclampsia which blocks noradrenaline synthesis

159
Q

What are MAOIs and how do they work

A

Monoamine oxidase inhibitors, are antidepressants which prevent NAd breakdown

160
Q

Which adrenoceptors are influenced in COPD management

A

M3 antagonist, B2 agonist

161
Q

Which adrenoceptors are influenced in bladder instability management

A

B3 agonist

162
Q

Which adrenoceptors are influenced in cardiac disease (angina, AF) management

A

B1 blocker

163
Q

Which adrenoceptors are influenced in pneumonia management

A

NAd, septic shock. B2 agonist for wheeze

164
Q

Which adrenoceptors are influened in anaphylaxis treatment

A

Adrenaline

165
Q

Which adrenoceptors are influenced in cardiac arrest treatment

A

Atropine (nAChR antagonist) for bradycardia

166
Q

Name some naturally occuring opioids

A

Morphine and codeine(weak)

167
Q

Name some chemical modifications of natural opioids

A

Diamorphine, oxycodeine, dihydrocodeine

168
Q

Name some synthetic opioids

A

Pethidine and fentanyl

169
Q

Name an opioid antagonist

A

Naloxone

170
Q

When are slow release opioids given

A

Bidaily in palliative care

171
Q

Name some morphine side effects

A

Sedation and respiratory depression

172
Q

What does the term parenteral mean

A

Bypasses the mouth and gut

173
Q

Define potency

A

A measure of drug activity, expressed in terms of the amount required to produce an effect of given intensity

174
Q

Define tolerance

A

A reduction or loss of the normal response to a drug or other substance that usually provokes a reaction in the body

175
Q

Define dependence

A

The physical or psychological effects produced by the habitual taking of certain drugs - characterised by a compulsion to continue taking the drug

176
Q

What are endorphins

A

endogenous morphines which are involved in the fight or flight response

177
Q

What are enkephalins

A

point to point peptide messengers

178
Q

Why are there problems with opioids

A

They were designed for the fight or flight response, not sustained activation and there are therefore problems with tolerance and addiction

179
Q

What are the four types of opioid receptor

A

Mu opiate peptide, Kappa opiate peptide, Delta opiate peptide, Noiceptin opiate peptide

180
Q

What is the first way opioids inhibit pain

A

inhibit action potential generation at noiceptive afferents

181
Q

What is the second way opioids inhibit pain

A

Inhibit transmission of pain in the dorsal horn

182
Q

What is the third way opioids inhibit pain

A

Inhibit descending GABA release from interneurons in periaqueductal grey

183
Q

What is another way opioids inhibit pain

A

Influence the cortex, changing emotional interpretation of pain

184
Q

Should you give lumbar puncture epidural opiates

A

They give precise treatment but opiates need to work on the brainstem too so must be given systemically

185
Q

Why shouldnt opioids be given in chronic non cancer pain

A

As the opioids lose their effectiveness within weeks

186
Q

Whats the difference between prescribed and drug dealer opiates

A

Drug dealers use much more potent derivatives which are highly toxic

187
Q

Which enzyme is involved in the bioactivation of codeine and tramadol

A

CYP2D6

188
Q

Why should you be careful about prescribing codeine

A

CYP2D6. 10-15% caucasians have reduced action, 10% of these are lacking the enzyme. 5% have overactive

189
Q

When should you be careful about prescribing tramadol

A

To those on antidepressents, as it inhibits Serotonin and Noradrenaline reuptake, so interacts with SSRIs, MAOIs and tricyclic antidepressants

190
Q

When should you be careful about prescribing morpheine

A

In those with renal function below 30%, as the more potent metabolite (morpheine 6 glucorinide) will build up

191
Q

What is a teratogen

A

agent which causes disturbance to the development of foetus

192
Q

Define antibiotic

A

An agent produced by microorganisms that kills or inhibits the growth of other microorganisms in high dilution

193
Q

What is the MIC

A

Minimum inhbitory concentration, the concentration required of a bacteriostatic antibiotic to get no microbial growth (determined using increasing turbidities, in reality the antibiotic must occupy the sites and for long enough)

194
Q

Which antibiotic is good for staphylococcus

A

Flucoxacillin

195
Q

Which antibiotics show concentration dependent killing and what is it

A

Aminoglycosides and quinolones, peak concentration/MIC ratio key parameter

196
Q

Which antibiotics show time dependent killing and it is it

A

Beta lactams, macrolides and oxazolidonones. Time spent above MIC most important

197
Q

Name some penicillins, what do they do and when are they used

A

Amoxicillin, coamoxiclav, target peptidoglycan in cell walls and are used in pneumonia and UTI

198
Q

What is vancomycin

A

A glycopeptide, targets gram positive and used in endocarditis, osteomylitis or antibiotic associated colitis (C. dificile)

199
Q

What are polymyxins

A

Polymixin B has a toxic effect of bacterial cell membranes, used against gram negative in E Coli and P Aerguinosa infection

200
Q

What are trimethopims

A

Trimethoprim is a folate antagonist and is used against gran negative bacteria in UTIs

201
Q

What are fluroquinolones

A

Ciprofloxacin targets bacterial topoisomerase and is primarily used against p aerguinosa and second line for UTI, GI and LRTIs

202
Q

What is rifampicin

A

Targets RNA polymerase, used to treat TB, leprosy and legionairres

203
Q

What are aminoglycosides

A

Gentamycin targets protein synthesis in Gram negative aerobes, used in severe sepsis, endocarditis, pyelonephritis and complex UTIs

204
Q

What are macrolides

A

Erythromycin and clarithromycin inhibit protein synthesis and are used in respiratory, soft tissue and skin infections (with other drugs for pneumonia and H pylori)

205
Q

What is clindomycin

A

Targets protein synthesis, using in the treatment of necrosing fascitis as it counters gram positive toxins. Also used in cellulitis of penicillin allergens

206
Q

What are tetracyclines

A

Doxycycline blocks protein synthesis and is used in the treatment of skin conditions, atypical pneumonias and chlamydial infection (pelvic inflammatory disease)

207
Q

Define adverse drug reaction

A

An unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected

208
Q

Define primary adverse effect

A

Consequence of the drug’s primary pharmacological effect (Beta blockers causing heart block and bradykinia)

209
Q

Define secondary adverse effect

A

accessory to the intended therapeutic consequences of drug adminitstration (Beta blockers causing bronchospasm)

210
Q

What is a side effect

A

A reaction from a dose within the therapeutic range

211
Q

What is a toxic effect

A

A reaction from a dose beyond the therapeutic range

212
Q

What is a hyper susceptibility effect

A

A reaction from a dose blow the therapeutic range

213
Q

What are the symptoms of Cushings disease

A

Moon face, central obesity and skin features

214
Q

What is pinocomelia and what causes it

A

Hands and feet close to the trunk, caused by thalidomide in first trimester

215
Q

Name three common ADRs

A

Pencillin allergy (ranging from rash to anaphylaxis), insulin as a hypoglycaemic and NSAIDS affecting kidneys

216
Q

What are patient risks in ADRs

A

Female, elderly (or neonate), genes, renal/hepatic failure, poor adherence, polypharmacy, atopy

217
Q

What are the drug risks in ADRs

A

Steep dose response curve, low therapeutic index and a common cause of ADRs

218
Q

What are prescriber risks of ADRs

A

Rushed, knowledge gaps, mistakes, wrong route or direction

219
Q

What are black triangle drugs

A

Drugs which are undergoing additional monitoring

220
Q

What is considered a serious reaction

A

Fatal, life threatening, disabling, results or prolongs hospitalization

221
Q

Penecillin allergy is an example of which type of hypersensitivity

A

Type 1

222
Q

How does adrenaline stop the release of inflammatory mediators from mast cells and basophils, in anaphylaxis treatment

A

Increases the intracellular cAMP

223
Q

Define drug interaction

A

A change in a drug’s effect on the body when the drug is taken with a second drug

224
Q

Define drug synergy

A

The drugs work together to create a greater overall effect

225
Q

Define drug antagonism

A

The addition of a drug, works against the first drug and decreases the overall effect

226
Q

What is the meaning of narrow therapeutic index

A

A fine line between therapeutic and harmful effect

227
Q

Which drugs increase the motility of oral contraceptive pills

A

antibiotics

228
Q

Patients weighing less than what weight should be given half the noramal dose

A

50kg

229
Q

Which enzyme does ginger effect

A

Increased thromboxane synthetase

230
Q

Why does grapefruit juice affect drugs

A

Affects CYP3A4 and increases bioavailability, and potentiates potential side effects

231
Q

Which drugs interact with grapefruit juice

A

Antiarrythmic, antihistamines, Ca2+ antagonists, statins and immunosurpressants

232
Q

Which are drugs are weak bases

A

Pain killers and warfarin

233
Q

Warfarin shouldnt be prescribed with

A

erythromycin, clarithromycin, tramadol and amiodorone

234
Q

SSRIs shouldnt be prescribed with

A

tricyclic antidepressants and tramadol

235
Q

What is rhabdomyolysis

A

Rapid breakdown of skeletal muscle following injury

236
Q

Interactions with which drug can cause bleeding

A

Warfarin

237
Q

Interactions with which drug can cause rhabdomyolysis

A

Simvastatin

238
Q

Interactions with which drug can cause serotonin syndrome

A

SSRIs

239
Q

Interactions with which drugs can cause renal failure

A

NSAIDs or Cox2 inhibitors, ACE inhibitors and dehydration or furosemide

240
Q

Define patient compliance

A

The extent to which the patient’s behaviour (in terms of taking medications, following diets or other lifestyle changes) coincides with medical or health advice

241
Q

What is the necessity-concerns framework

A

The two categories why patients dont take drugs: Necessity beliefs (perceptions of the personal need for treatment) and concerns (about a range of potential adverse consequences)

242
Q

What is the theory of concordance

A

A consultation is a negotiation between equals, there is a therapeutic alliance with openness, reality and respect for the patient’s agenda

243
Q

What is antibiotic stewardship

A

The systematic education of prescribes to follow evidence based prescribing to reduce antibiotic overuse and therefore antibiotic resistance

244
Q

What are the four ways bacteria develop resistance

A

Change antibiotic target site, destroy antibiotic, prevent antibiotic access, remove antibiotic from bacterial membrane

245
Q

Define substance use

A

Ingestion of a substance affecting the CNS which leads to behavioural and psychological changes. Implicitly non therapeutic changes

246
Q

Define acute intoxication

A

Disturbances in the level of consciousness, cognition, perception, behaviour, affect and other psychophysiological responses and functions

247
Q

Define at risk (hazardous) drinking

A

a pattern of drinking which brings about the risk of physical or psychological harm - screening tools

248
Q

Alcohol abuse (harmful) drinking

A

A pattern of drinking which is likely to cause physical or psychological harm

249
Q

Define substance abuse

A

A set of behavioural, cognitive and physiological responses that can develop after repeated substance use

250
Q

Define acquired resistance

A

Bacteria which was previously susceptible obtains the ability to resist the activity of a particular antibiotic

251
Q

What is conjugation

A

Sharing of extrachromosomal DNA plasmids via a sec pillus

252
Q

What is transduction

A

Bacteriophages carry donor bacterium DNA in a virus particle to a recipeint bacterium during infection

253
Q

What is transformation

A

Free DNA is taken up from the environment and incorporated into their chromosome

254
Q

Which antibiotics are used as a last resort

A

Carbapenams - primaxin

255
Q

Define stereoisomer

A

Same molecular formula and sequence of bonded atoms but differ in three dimensional orientations and their atoms in space

256
Q

Which element is commonly used in anticancer drugs

A

Platinum

257
Q

What are monoclonal antibodies

A

-mab, all have specificity to the same epitope

258
Q

What is infliximab

A

MAB which targets TNF alpha and is used to treat autoimmune disease. By extracellular neutralisation and inhibits lymphocyte proliferation

259
Q

What are murine antibodies and their suffix

A

mice omab

260
Q

What are chimeric antibodies and their suffix

A

from a mix of organisms, ximab

261
Q

What are humanized antibodies’ suffix

A

zumab

262
Q

What is the human antibody suffix

A

umab

263
Q

What is the brambell receptor

A

Intestinal FCRN receptor for orally absorption of antibodies form breast milk in the neonate

264
Q

wWhat are FCRN receptors

A

Systemic receptors which absorb IgG into cells protecting them from metabolism

265
Q

Is IgG filtered by the kidneys

A

No, 150kD

266
Q

Name three drugs sourced from animals

A

Insulin, thyroxine and steroids

267
Q

How is insulin prescribed

A

In units which are based on hypoglycaemic activity in rabbits, 25units/mg

268
Q

What does mitogenic mean

A

Triggers mitosis

269
Q

How does shorter acting insulin work

A

Insulin lipro turns on lyseine and proline residues preventing insulin dimer/hexamer formation

270
Q

How does long acting insulin work

A

Can bind to albumin and insuline glargine fors aggregats in ECF at neutral pH

271
Q

What is cachexia

A

Wastage of tissue

272
Q

Name recombinant proteins in clinical use

A

Insulin, EPO, GH, IL, gamma interferon, IL-1 receptor agonist

273
Q

Mineralocorticoid adverse effects

A

HTN, fluid retention, K+ loss, Ca2+ loss

274
Q

Glucocorticoids adverse effects

A

Diabetes, cushings syndrome, osteoporosis, muscle wasting, peptic ulcer

275
Q

What is pathogenicity

A

Ability to cause disease

276
Q

What is immunogenicity

A

Ability to provoke an immune response