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BDS stage 2 > Basic Pharmacology theme 2 > Flashcards

Basic Pharmacology theme 2 Flashcards

1
Q

What is the sensory nervous system ?

A

afferent towards the spinal chord

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2
Q

What is the autonomic nervous system ?

A

controls smooth muscle outside of voluntary control

efferetn

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3
Q

What is the somatic nervous system ?

A

voluntary motor control
of skeletal muscle
efferent

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4
Q

What are some sympathetic effects ?

A 
pupils dilate
lens adjusted fro far vision 
respiratory rate increases- bronchodialtion
HR increaaes 
Blood vessels to muscles dilate 
blood vessels to organs constrict
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5
Q

What are some parasympathetic effects ?

A 
pupils constrict
lens adjusted for close vision 
airways constrict
HR and respiratory rate decrease
saliva increaes
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6
Q

What are the neurotransmitters in the sympathetic nervous system ?

A

preganglionic- acetylcholine

postganglionic- noradrenaline

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7
Q

What are the neurotransmitters of the parasympathetic system ?

A

both preganglionic and postganglionic use acetylcholine

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8
Q

Which neurotransmitters act on the somatic nervous system ?

A

acetylcholine acts on the NMJ

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9
Q

What are the sympathetic system exceptions ?

A

sweat glands- acetylcholine in preganglionic

Adrenal glands- acetylholine in postaganglionic

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10
Q

What are the fundamentals oof neurotransmission ?

A 
synthesis 
storage 
release - exocyotic 
receptor interaction 
termination
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11
Q

What are the steps in Ach synthesis ?

A

choline precursor made to Ach via choline acetyltransferase

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12
Q

How is Ach stored and released ?

A

stored in vesicles
allows vesicular release in conjunction with action potentials
vesicles fuse with membrane and Ach released into synapse

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13
Q

What is the receptor interaction of Ach ?

A

acts on receptors on post synaptic membrane

muscarinic or nicotinic

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14
Q

How is Ach terminated ?

A

after acting on receptor

Ach disassociates via acetylcholinesterase into choline and acetate

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15
Q

What are the 2 classes of Ach receptor ?

A

muscaranic

nicotinic

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16
Q

What are muscarinic receptors ?

A

located on postganglionic parasymapathetic synapses
on parasmpathetic organs
GPCRs with slow response

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17
Q

What are nicotinic receptors ?

A

neuronal type- acts on brain and autonomic ganglia
muscule type- acts on NMJ- excitatory
ligand gated ion channels - fast repsonse

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18
Q

Where are nictonic receptors located ?

A

sympathetic, parasympathetic and somatic systems

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19
Q

Where are muscuranic receptors located ?

A

present in parasympathetic system only

mainly parasympathetic fibers

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20
Q

What will muscarinic agonists do ?

A

increase pupil cosntriction
contract ciliary muscle
decrease CO
increase GI motiity

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21
Q

What are muscarinic agonists called ?

A

paraympathomimetics

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22
Q

What do muscarinic antagonists do ?

A

increase CO
decrease GI motility
pupil dialtion
decrease sweating

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23
Q

What are muscarinic antagonists called ?

A

parasympatholytics

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24
Q

What are the clinical uses of muscarinic agonists ?

A

pilocarpine
treat glaucoma- build up of tumour in eye- agonist will lead to sphincter muscle contraction- increase drainage
treat xerostomia

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25
Q

What are the clinical uses of muscarinic antagonists ?

A

pupil dilation before surgery
decrease respiratory secretions before oral procedures
adjunct to anaesthesia
resucitation in bradycardia- increase HR
used in asthma to cause bronchodilation
motion sickness - decrease gut motility

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26
Q

Where are neuronal type nicotinic receptors located ?

A

parasymapthetic and sympathetic ganglia
agonists will bind to both systems leading too autonomic confusion
neuronal nicotinic agonists arent useful

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27
Q

What do neuronal nictonic antagonists do ?

A

lead to loss of sympathetic and parasympathetic reflexes

neuronal antagonists dont have good therapeutuc value

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28
Q

Where are muscle type nicotnic receptors located ?

A

in the NMJ

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29
Q

What doe stimulation of a muscle type nicotinic receptor lead to ?

A

depolarisation

skeletal muscle fibre contraction

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30
Q

What will a nicotnic muscle type receptor agonist do ?

A

causes initial depolarisation

and EPP

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31
Q

What is a depolarising block ?

A

giving a synthetic muscle type muscarnic agonist means the drug is not metabolied rapidly by acetylcholinesterase
the fibre is persistently depolarised resulting in loss of further electrical excitability
it is used for paralysis before surgery

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32
Q

What will a muscle type nicotinic receptor antagonist do ?

A

hyperpolarisation
inhibition of EPPs
muscle fibre relaxation

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33
Q

Which drugs can effect Ach release ?

A

botulinum toxin
causes autonomic and motor paralysis
toxin is injected locally to treat muscle spasm and in botox

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34
Q

What does acetylcholinestarase do ?

A

metabolises Ach into choline and acetate

termination of Ach

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35
Q

How can Ach termination be inhibited ?

A

an anticholinesterase

incrases Ach transmission at parasympathetic postanglionic synapses

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36
Q

What is the effect of anticholinesterases at the NMJ ?

A

increase muscle tension

twitiching and at large doses lead to depolarising block

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37
Q

Where in the PNS does NA act as a neurotransmitter ?

A

NA acts on postganglionic fibres of the sympathetic system

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38
Q

What is NA synthesis ?

A

precursor tyrosine
converted to DOPA by tyrosine hydroxylase
DOPA to DA by DOPA decarboxylase
DA to NA by DA beta hydroxylase in vesicle

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39
Q

What is the storage and release of NA ?

A

stored in vesicle until action potential

release vesicles by exocytosis

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40
Q

What is NA receptor interaction ?

A

alpha or beta receptors

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41
Q

What is the termination of NA ?

A

taken back up

NA converted to amines via monamine oxidase

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42
Q

What are the 2 classes of NA receptors ?

A

alpha

beta

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43
Q

What are the alpha noradrenergic family of receptors ?

A

alpha 1

alpha 2

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44
Q

Where are the alpha 1 and 2 noardrenergic receptors located ?

A

organs and targets of the sympathetic system

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45
Q

What type of receptor are the Alpha 1 and 2 noradrenergic ?

A

GPCR

slow response

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46
Q

What are the beta noradrenergic receptors ?

A

3 types- Beta 1

beta 2 and beta 3

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47
Q

Where are the beta adrenergic receptors located ?

A

effector organs and targets of the sympathetic system

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48
Q

What type of receptor are the beta adrenergic ?

A

GPCRs

slow responses

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49
Q

What are sympathetic effects mediated by alpha 1 receptors ?

A

pupil dilation- radial muscle contracts
blood vessels to visceral organs and skin constrict
brain activity increases

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50
Q

What are the sympathetic effects mediated by the alpha 2 receptors ?

A

presynaptic receptors
negative feedback system for NA and other neurotransmitter release
NA released from the presynaptic synapse acts on terminal receptro on the presynaptic neurone
feedback turns off further NA

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51
Q

Do alpha 2 receptors only control NA release ?

A

no they can be autoreceptors affecting NA release from their own neurone
they can be heteroreceptors affecting Ach release from other neurones

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52
Q

What are sympathetic effects mediated by beta 1 receptors ?

A

HR increases

force of contraction increases

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53
Q

What are sympathetic effects mediated by beta 2 receptors ?

A

bronchodialtion
cilary muscle relax - lens for far vision
blood vessels to limbs dilate

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54
Q

What are sympathetic effects medaited by beta 3 receptors ?

A

increase lipolyisis

breakdown of TAGs to fatty acids

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55
Q

What are the effects of adrenaline ?

A

a noradrenergic agonist
1- given locally with LA- vasoconstriction- increase LA effects- injection as destroyed by stomach
2- intramuscular adrenaline to treat anaphlyctic shock

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56
Q

How can adrenaline be used to treat anaphlyactic shock ?

A

anyphalactic shock is cardio collapse and bronchospasm
it hits alpha 1, beta 1 and beta 2 receptors
alpha 1- smooth muscle constriction
beta 1- cardiac stimualtion
beta 2- bronchodialtion

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57
Q

What is clonidine ?

A

alpha 2 agonist

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58
Q

What do alpha 2 receptors normally do ?

A

inhibit further NA release via negative feedback

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59
Q

What are alpha 2 agonists used for ?

A

hypertension - stop noradrenerigc transmission

also has central effect- for morphine withdrawal- stops more NA

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60
Q

What is dobutamine ?

A

beta 1 agonist

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61
Q

What do beta 1 receptors do ?

A

increased cardiac force and rate

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62
Q

What will a beta 1 receptor do ?

A

treat heart failure

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63
Q

What is salbutamol ?

A

beta 2 agonist

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64
Q

What do beta 2 receptors do ?

A

bronchodilation

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65
Q

What will beta 2 agonists do ?

A

lead to bronchodilation so use for asthma

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66
Q

What is clenbuterol ?

A

Beta 2/3 agonist

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67
Q

How was clenbuterol used ?

A

as a beta 2 agonist to treat asthma

but shows affinity for beta 3 which leads to increased lipolysis which is a side effect

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68
Q

What is prazosin ?

A

alpha 1 antagonsist

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69
Q

What do alpha 1 receptors do ?

A

smooth muscle vasoconstriction

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70
Q

What will an alpha 1 antagonist do ?

A

block vasoconstriction

used to treat hypertension as decreased vascular resistance

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71
Q

What is a side effect of using alpha 1 antagonist ?

A

orthostatic and postiral hypotension

due to loss of sympathetic reflexes

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72
Q

What is tamuloson ?

A

alpha 1 antagonist

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73
Q

How can an alpha 1 antagonist treat urianary problems in prostate hyperplasia ?

A

block vasconstriction leading to relaxation of smooth muscle

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74
Q

What is propanolol ?

A

beta 1 and 2 antagonist

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75
Q

What do beta 1 receptors do ?

A

increase CO

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76
Q

What do beta 2 receptors do ?

A

mediate bronchodilation

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77
Q

What can we use beta 1 antagonists for ?

A

to decrease CO in angina

in hypertension

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78
Q

What is the effect of blocking beta 2 receptors ?

A

would lead to bronchocosntriction - not useful and fatal in asthmatics

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79
Q

What is atenolol ?

A

beta 1 antagonist

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80
Q

What do beta 1 receptors mediate ?

A

increased CO and force

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81
Q

What will a beta 1 antagonist do ?

A

treat angina and hypertension

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82
Q

What is the problem with beta 1 anathonists ?

A

removal of the antagonist can cause hypersensitivty

as receptors are supersensitive

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83
Q

What is timolol ?

A

beta 2 antagonist

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84
Q

What can we use beta 2 antagonists for ?

A

treat glaucoma

antagonism will lead to ciliarmy muscle contraction and reduced intraocular pressure

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85
Q

What is the symapthetic innervation of salivary glands ?

A

alpha 1
beta 1
beta 2

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86
Q

What is the indirect innervation of salivary glands ?

A

vascular adrenergic

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87
Q

What do beta 1 receptors in saliva glands lead to ?

A

stimulate protein secretion

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88
Q

What do alpha 1 receptors in saliva glands lead to ?

A

water electrolyre secretions

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89
Q

What does clonidine do ?

A

inhibits NA release leading to xerostomia

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90
Q

How can we use drugs to affect NA synthesis ?

A 
can use false substrate of meDOPA
leads to meDA via DOPA decarboxylase 
leads to meNA by DA beta hydroxylase 
meNA has lower affinity fot NA receptors
decrease in NA transmission- use for hypertesnion
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91
Q

How can we use drugs to effect NA storage ?

A

reserpine disrupts storage of NA in synaptic vesicles
less NA available for release- treat hypertension
lots of side effects tho

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92
Q

How can we use drugs affecting NA release ?

A

NA release subject to inhibitory control by presynaptic alpha 2 receptors
clonidine is alpha 2 agonsit- inhibit NA release
treat hypertesnsion

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93
Q

How can we use drugs to effect NA uptake ?

A

termination of NA action happens via reuptkae
NA uptake blocked by uptake inhinitors
prolongs action of NA in synapse
Reboxetine

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94
Q

How can we use drugs affecting NA metabolism >?

A

NA degraded to amines via monoxamine oxidase
block MO so more NA for release availble
blocker of MO- tranylcypramine

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95
Q

What is the problem with MO inhibitors ?

A

block amine metabolism
amines not degraded
displace NA from the terminal sympathetic system
excess NA released - hypertension

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96
Q

What are noxious stimuli sensed by ?

A

nociceptors

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97
Q

What is nociception ?

A

the process by which noxious stimuli are transmitted to the CNS

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98
Q

What is pain ?

A

a combination of sensory and emotional componenents

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99
Q

How are most nociceptors triggered ?

A

by chemical stimuli

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100
Q

Which stimuli cause actue pain ?

A

thermal and mechanical

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101
Q

What does a primary neuron do ?

A

stimulus acts on a primary neuron which goes to the dorsal horn of the spinal chord- synapses in the layers of the dorsal horn

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102
Q

What are the afferent pain fibres ?

A

C fibres
A delta
A beta

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103
Q

What are the properties of C fibres ?

A

Non myelinated - low conduction velocity
Nociceptor/thermo and mechanoreceptor
dull pain- synpase in upper layers of the dorsal horn

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104
Q

What are the properties of A-delta fibres ?

A

myelinated
rapid conduction velocity
nociceptor/mechanoreceptor
sharp pain

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105
Q

What do secondary neurones do ?

A

to the thalamus via the brainstem

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106
Q

What do teritiary neurones do ?

A

from the thalamus to the cingulate cortex, limbic system and the somatosensory cortex

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107
Q

What are the descending pathways that tun off the noxious response ?

A

limbic system
periaqueductal grey
rostral ventromedial area

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108
Q

What are chemical mediators ?

A

substances that stimulate the pain endings in skin

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109
Q

What are examples of chemical mediators ?

A

5-HT
Bradykinin
metabolites of intermediate metabolism- lactic acid
capsacnin

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110
Q

What are eicosanoids ?

A

substances like prostaglandins, prostacyclins which are inflammatory mediators that enhance the pain producing effects of other agents

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111
Q

How do the eicosanoids work ?

A

they increase the sensitivity of pathways to bradykinin

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112
Q

What effect does Nitric oxide have on pain transmission ?

A

nitric oxide increases C fibre activity

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113
Q

Which molecules increase C fibre activity ?

A

Chemical mediators
NGF
Neuropeptides

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114
Q

What are NGFs, mediators and neuropeptides a result of ?

A

inflammation

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115
Q

What is the role of enkephalins and GABA ?

A

reduce pain transmission

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116
Q

What is the basic mechanism of NSAID action ?

A

reducing the chemical mediator release

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117
Q

What do opioids do ?

A

stop neuropeptide release

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118
Q

What do opiates do ?

A

increase the descending inhibitory pathways

through 5-HT and NA

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119
Q

What are the properties of NSAIDs ?

A

analgesic
anti inflammatory
anti pyretic
anti platelet

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120
Q

What does anti pyretic mean ?

A

can decrease elevated body temeperature

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121
Q

What is the mechanism of NSAID action ?

A

inhibiting prostaglandin (an ecosanoid) production by inhibitng COX fucntion

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122
Q

What is COX ?

A

cycloxygenase

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123
Q

What are the 2 forms of COX ?

A

COX1- enzyme expressed in most tissue

COX 2- induced in activated inflamamatory cells

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124
Q

What do NSAIDs do to the 2 forms of COX ?

A

therapeutic effects of NSAIDs are due to inhibition of COX2

Unwanted effects of NSAIDS are due to inhibition of COX1

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125
Q

Why is COX2 easy to target ?

A

due to its structure

has a large side pocket which can be bound to by functional groups

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126
Q

What is the prostaglandin synthetic pathway ?

A 
phospholipids in the membrane
phospholipase A2
arachidonic acid- ecosanoids
COX
intermediates
ecosanoids
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127
Q

What are 3 examples of NSAIDs ?

A

aspirin
ibuprofen
paracetamol

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128
Q

How does aspirin work as an analgesic ?

A

decreased prostanoid synthesis

less sensitisation of nociceptors to mediators

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129
Q

What are the characteristics of aspirin ?

A

analgesic
anti inflammatory
anti platelet
anti pyretic

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130
Q

How does aspirin reduce temperature in a fever ?

A

prostaglnadins produced by pathogens alter the thermostat

aspirin decrease prostalglandins synthesis and changing of the thermostat

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131
Q

What is the ADME of aspirin ?

A

oral
hydrolysed rapidly by esterases
short half life- give in high doses
interactions with warfarin can prevent drug metabolism

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132
Q

What are the characteristics of ibuprofen ?

A

anlagesic

anti pyretic

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133
Q

What is the ADME of ibuprofen ?

A

oral, topical and rectal

rapid absorption

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134
Q

What are the characteristics of paracetamol ?

A

analgesic and anti pyretic

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135
Q

What is the ADME of paracetamol ?

A

safe and effective at a therapeutic dose
oral, rectal or IV admin
quick C max so need regularly

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136
Q

What are the cautions with paracetamol ?

A

hepatotoxicity in alcohol overdose

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137
Q

What are the forms of opioids ?

A

morphine analogues

synthetic derivatives

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138
Q

What are opioid neurotransmitters ?

A

enkephalins
endorphins
dynorphins

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139
Q

What are the 3 types of opioid receptors ?

A

U
delta
K

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140
Q

What is the U opioid receptor reesponsible for ?

A

analgesic effects of opioids

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141
Q

How do opioid analgesiscs act ?

A

agonists of the U receptor
stimulate receptor though GPCR
inhibit adenylyl cyclase
hyperpolarisation leads to reduced excitability

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142
Q

What are the therapeutic effects of opioids ?

A

analgesia
euphoria
sedation

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143
Q

Why do opioids have to be given in high doses ?

A

have extensive first pass metabolism

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144
Q

What do we use strong opioids for ?

A

morphine

moderate/severe pain

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145
Q

What do we use weak opioids for ?

A

cough suppressive
moderate pain
diarrhoea

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146
Q

What are the adverse CNS effects of opioids ?

A

drowsiness
sedation
respiratory sedation
nausea

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147
Q

What are the adverse effects on the PNS of opioids ?

A

constipation
histamine release
pinhole pupils

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148
Q

What is morphine used for ?

A

most valuable fro severe pain relief

terminal care

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149
Q

What is pethidine used for ?

A

rapid onset

more lipid soluble than morphine

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150
Q

What is dextropropxyphene used for ?

A

mild analgesic

use with aspirin and paracetamol

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151
Q

What is dyhydrocodeiene ?

A

similar to codeine but more side effects

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152
Q

What is tolerance ?

A

subjects reduced reaction to a drug following repeated use
semsitivity can return after withdrawal
might need to increase dose to have therapeutc effect

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153
Q

What is dependence ?

A

following abrupt withdrawal after chronic treatment

abstinence syndrome after acute treatment

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154
Q

What do anaesthetics do ?

A

prevent pain for a limited period of time for surgical procedures

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155
Q

What are local anaesthetics ?

A

prevent localieed pain and prevent tactile sensation

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156
Q

What are general anaesthetics ?

A

induce loss of consciousness and prevent pain

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157
Q

What are the 2 classes of general anaesthetics ?

A

inhaled

intravenous

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158
Q

What are examples of inhaled GA ?

A

halothane

nitrous oxide

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159
Q

What are examples of IV GA ?

A

thiopental

etmodiate

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160
Q

What are the 2 theories of GA action ?

A

ion channel theory

lipid theory

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161
Q

What is the lipid theory ?

A

strong relationship between the potency of the A and t the lipid solubility
A interact with the lipid bilayer leading to membrane expansion and inability of the membrane to signal

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162
Q

What is the ion channel theory of GA ?

A

anaesthetics have different affinities for different types of receptors

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163
Q

Which receptors do GA have an affinity for ?

A

GABAa receptors- these are inibitory receptors that GA act as agonists for
affinity for the excitatory receptors as anatgonists

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164
Q

How is the depth of anaesthesia determined ?

A

concentration in the bran and spinal chord

165
Q

What is the blood/gas coefficient ?

A

measure of blood solubility
low- rapid induction and recovery
high- slow induction and recovery

166
Q

What is the oil/gas coefficient ?

A

measure of lipid solubility
determines the potency as the brain has a high lipophilicity
lower solubility less potent

167
Q

How does vascularisation effect anaesthetics ?

A

determines the level of A in the tissue
brain has high vascularisation so high levels of anaesthetic
body fat- low vascularisation means A doesnt accumulate in fat- problems with obesity and A

168
Q

How does ventilation rate effect A ?

A

effects removal

some A can cause respiratory depression

169
Q

Are inhaled A metabolised ?

A

not entirely

metabolism can lead to hepatotoxicity and nephrotoxicity

170
Q

What are the side effects of inhaled A ?

A 
malignant hyperthermia
cardiovascular 
decreased respiration 
hepatotoxicity
nephrotoxicity
171
Q

What are IV Anaesthetics ?

A

thiopental
etmomidate
ketamine
propofol

172
Q

How do thiopental and etomidate work ?

A

acts on the GABAa receptor
inihibitory NT released- hyperpolarisation
reduced excitabilty

173
Q

What are the benefits of etomidate ?

A

wider TI between anaesthesia and respiratory depression
rapidly metabolised
quick recovery

174
Q

How does Propofol work ?

A

acts on GABAa receptor
an agonist
rapidly metabolised by plasma esterase
daycare

175
Q

How does ketamine work ?

A

on the NMDA receptor - excitatory
as an antagonist
rarely used due to hallucination and psychosis

176
Q

How can neurones alter their membrane potential ?

A

voltage gated sodium channels

crucial for initiation and propagation of APs

177
Q

What is the structure of a voltage gated sodium channel ?

A

3 subunits
hydrophobic sensors
change orientation when voltage varies
orientation controls opening and closing of pore

178
Q

How does LA interact with the voltage gated sodium channel ?

A

interact with the alpha subunit - plug the transmembrane pore and block sodium from entering

179
Q

Where does LA bind to in the sodium channel ?

A

area located in the inner end of the channel

need intracellular access

180
Q

In which form can LA only bind to the binding area ?

A

ionised and hydrophobic form

181
Q

Why is their problem with LA entry ?

A

needs to be unionised to pass lipid bilayer

needs to be ionsied to bind to area

182
Q

How is the LA entry problem overcome ?

A

most anaesthetics are weak bases
pH outside is 7.4- unionised can enter the neurone
inside the pH drops and LA now ionised and can bind to area

183
Q

What is the general structure of LA ?

A

aromatic group
ester/amide
amine

184
Q

What is the function of the LA aromatic group ?

A

lipid solubility

185
Q

What is the function of the LA ester/amide group ?

A

duration of action is limited by hydrolysis of this drug

186
Q

What is the function of the amine group ?

A

basic- allowing ionisation

187
Q

How are esters metabolised ?

A

by plasma esteraes

LA with ester groups have short half life

188
Q

How are amdies metabolised ?

A

in the liver
CYP
leading to longer half life
dont use amides in liver failure patients

189
Q

How is LA adminstered ?

A

weak base
injected as hypochlorite solution in salt
dissolves in solution quicker

190
Q

How can we manipulate LA ?

A

restrict site of action with adrenaline- alpha 1 receptors leading to local vasoconstriction
accelerate the speed of onset using an alkaline solution - assists with absorption into nerve tissue

191
Q

Which type of axon does LA work most effectively in ?

A

small

192
Q

What is the order of axon LA sensitivity ?

A

small myelinated > non myelinated > large myelinated

193
Q

What size are nociceptive and motor fibres and what is the significance of this ?

A

nociceptive- small- sensitive

motor- large- less sensitive

194
Q

What are the side effects of LA due to ?

A

escape into systemic circulation
inhibition of sympathetic activity
inhibition of sodium conductance in cardiac tissue

195
Q

Why is LA not effective in inflamed tissue ?

A

ionised straight away due to acidic environment

196
Q

What is chemotherapy ?

A

elimination of invading cells and microorganisms

197
Q

What are chemotherapic targets ?

A

mechanisms associated with invading species

198
Q

What are effective chemotherapic agents ?

A

are toxic to invading cells and non toxic to host cells

199
Q

What is selective toxicity ?

A

exploiting differneces between species to use therapeutically
Distributonal toxcity - drug accumulates in certain areas can be difficult to control if systemic

200
Q

What are examples of invading cells that can be selectively targeted ?

A

neoplastic cells
bacteria
fungi
viruses

201
Q

What are the 2 reasons for antibiotic use ?

A

treatment and prophylaxis

202
Q

What is antibiotic prophylaxis ?

A

prevent infection following surgery

antibiotics given beforehand to high risk patients

203
Q

Which 2 amino acids does transpeptidase join ?

A

glysine and lysine

204
Q

What are the subunits of prokaryotic ribosomes ?

A

50s and 30s

205
Q

What are the subunits of eukaroyte ribosomes ?

A

60s and 40s

206
Q

What is the mode of action of tetracycline ?

A

stops tRNA binding to the smaller 30s sub unit

this prevents elongtion

207
Q

What is the mode of action of erythromycin ?

A

binds to 50s subunit and prevent translocation- movement of the mRNA along the ribosome

208
Q

What type of antibiotic are tetracycline and erythromycin ?

A

macrolides

209
Q

What is the mode of action of fluoroquinolones ?

A

target topoisomerase II

DNA gyrase

210
Q

What are other ways to target bacterial nucleic acid synthesis ?

A

inhibit synthesis of nucleotides
alter base pairing of DNA template
inhibit DNA/RNA polymerase
inhibit DNA

211
Q

What are some examples of herpes virsues ?

A

herpes simplex
varicella zoster
epstein barr- glandular fever

212
Q

What is the mode of action of herpes virus ?

A

re stimulated in sensory ganglia by external stimuli and replicate- often around the mouth

213
Q

What is an antiviral agent that shows selective toxiciyt ?

A

aciclovir

214
Q

What is the structure of aciclovir ?

A

synthetic guanosine analogue - nucloetide structure

215
Q

What does aciclovir have a high specificity for ?

A

herpes simplex

216
Q

What are the properties of aciclovir ?

A

high therapeutic index

prodrug- needs to be activated via intracellular phosphorylation to become active

217
Q

Describe the metabolic activation of aciclovir ?

A

aiclovir enters HSC infected cell
phosphorylated once- monophosphate aciclovir bia Herpes simplex thmidine kinase
cellular kinase adds more phosphates

218
Q

Which form of aciclovir shows antiviral function ?

A

triphosphate aciclovir

219
Q

What is the mode of action of aciclovir triphosphate ?

A

DNA chain terminator

inhibitor of viral DNA polymerase

220
Q

What are fungal infections ?

A

superficial- candidosis, dermatomycoses

systemic- systemic candidiasis in immunocompromised patients

221
Q

Why has there been an increase in fungal infections recently ?

A

widespread antibiotic use

increase in immunocompromised individuals

222
Q

What do fungal cell membranes contain ?

A

ergesterol

223
Q

What are the 3 classes of anti fungal agents ?

A

azoles
polyenes
mitotic inhibitors

224
Q

What is the mode of action of azoles ?

A

affect membrane lipid synthesis
blocks 14 alpha demethylase
needed in synthesis of ergesterol

225
Q

What does a decrease in ergesterol lead to ?

A

inhibition of replication
effects membrane functions
increased permeability

226
Q

What are the subclasses of the azoles ?

A

imidazoles- ketocozanole, miconazole

triazoles- flucozanoles

227
Q

What is ketocozanole ?

A

given orally
inhibits reactions catalysed by cytochrome p450- leads to drug-drug interactions
can cause hepatotoxicity so use safer alternative

228
Q

What is miconazole ?

A

used topically/orally/IV

can also inhbit drug metabolism

229
Q

What is fluconazole ?

A

a triazole- nitrogen containing
given orally
well distributed across the BBB- into CSF- use in gungal meningitis

230
Q

What are polyenes ?

A

form pores in the membrane
bind to sterols in the membrane and form an ion channel
leads to leakage of intracellular ions

231
Q

How are polyenes selective ?

A

Higher affinity for ergesterol rather than cholesterol

232
Q

Why are polyenes poorly absorbed ?

A

protein bound

233
Q

How can we administer polyenes ?

A

liposome on outside

234
Q

What are mitotic inhibitors ?

A

inhibits cell division by interfering with spindle formation
selectively uptaken by cells that synthesis keratin- dermatomycoses

235
Q

What are anxiolytic drugs ?

A

alleviate fear and anxiety

236
Q

What are sedatives ?

A

alleviate fer and anxiety and produce amnesia and analgesia

237
Q

What are hypnotic drugs ?

A

induce sleep

238
Q

What are signs of anxiety ?

A 
uneasiness
apprehension 
tension 
headache
palpitation 
flushing
239
Q

What odes conscious sedation do ?

A

helps you to relax as a sedative and anaesthetic to block pain - allows verbal contact and protective reflexes to be intact

240
Q

What is deep sedation ?

A

general anaesthesia

241
Q

What is an inhalation sedation drug used in dentistry ?

A

nitrous oxide- entonox

242
Q

What is an oral sedative ?

A

benzodiazepines- also use IV

243
Q

Does sedation control pain effectively ?

A

no use LA as well

244
Q

What are the characteristics of NO as a sedative ?

A

light ad rapid absorption
50% NO in oxygen recovery in 4 minutes
mild nausea and vomiting as sie effects

245
Q

What are the limitation so NO as an inhalation sedative ?

A

expensive
limited patient use- cant use in high risk patient
prolonged exposure can change bone marrow and lead to teratogenic risk

246
Q

What are the dose dependent effects of sedatives ?

A

relief of anxiety
sedation
hypnosis
GA

247
Q

What are barbiturates ?

A

positive allosteric modulator of GABAa receptor

248
Q

What are the actions of barbiturates ?

A

block AMPA receptor and stop glutamate release- an excitatory NT
bind to GABAa chloride channel complex and encourage GABA to bind

249
Q

How do barbiturates produce their pharacological effects ?

A

increasing duration of chloride channel opening

250
Q

What are BDZs used to treat ?

A

panic disorders
general anxiety disorders
phobia

251
Q

How do BDZS work ?

A

increase frequency of chloride channel opening

252
Q

What should be given to patients with autonomic symptoms ?

A

b adrenorecpetor antagonist- propanolol

253
Q

What is the structure of BDZs ?

A

7 membered ring fused to an aromatic ring with 4 main substituent groups - can be modified

254
Q

What is the variety of the BDZs ?

A

there are 20 varieties of each compound

255
Q

What are the main pharmacological effects of the BDZs ?

A 
sedation 
reduction of anxiety and aggression 
muscle relaxation 
anti convulsant 
amnesia
256
Q

How exactly to BDZ affect sleep ?

A

decrease time taken to get to sleep
increase duration of sleep
reduce dreaming and decease deep sleep

257
Q

What is the mode of action of the BDZs ?

A

BDZ act on specific regulatory site of the GABA/chloride channel receptor
enhance GABA binding - incrrease GABA affinity
dont open the chloride channel themselves
increase frequency

258
Q

Where does GABA bind on the GABAa receptor ?

A

A and B subunits

259
Q

Where does BDZ bind on the GABAa receptor ?

A

Alpha and gamma subunits

260
Q

Which 4 things can bind to the GABAa receptor ?

A

GA
BDZ
Barbiturates
GABA

261
Q

When are BDZ well abosrbed ?

A

when given orally

262
Q

How do we get BDZ into systemic circulation ?

A

bound strongly to plasma proteins- give a different form to get into systemic circulation

263
Q

What does BDZ high lipid solubiltiy mean ?

A

accumulation on body fat

264
Q

How are BDZ excreted ?

A

inactivated by metbaolism and excreted as glucoronides in urine

265
Q

What are the 2 forms of acting BDZs ?

A

short acting

long acting

266
Q

What are short acting BDZs?

A

they are metabolised to inactive compounds

short half life

267
Q

What are the long acting BDZs ?

A

metabolised to pharmacologically active metabolites
long half lives
diazepam-nordiazepam

268
Q

What are the unwanted effects of BDZs ?

A

interaction with alcohol leads to further CNS depression
long lasting hangover
development of dependence- higher dose to get same efffects
sexual fantasies

269
Q

What are b adrenoreceptor antagonists ?

A

propanolol
anxiolytic but not sedative
inhibit autonomic responses due to less NA transmission
bradycardia

270
Q

What is the 5 HT agonist ?

A 
agonist of inhibitory autoreceptro- serotonin 
anxiolytic not sedative 
takes long time to develop anti anxiety 
less withdrawal effects 
buspirone
271
Q

What are depression and schizophrenia thought to be caused by ?

A

dysregulation in monoamine oxidase NT function

272
Q

What are the monoamine NTs ?

A

5 HT
dopamine
serotonin

273
Q

/What are the steps in 5 HT biosynthesis

A

tryptophan taken into neurone by amino acid transporter
converted to 5HTP via trytophan hydroxylase
5HT via decarboxylase AADC
stored in vesicles
released in response to APs
act on 5HT receptors
termiantion via reuptake and metabolism

274
Q

What are the steps in DA biosynthesis ?

A 
Tyrosine taken up 
convered to LDOPA by tyrosine hydroxylase 
LDOPA to DA via DOPA decarboxylase 
stored in vesicles 
released onto receptors when AP
reuptake and recycle
275
Q

What is the DA theory of schizophrenia ?

A

schizophrenia is assocaited with increased DA fucntion

276
Q

What are the 3 DA pathways in the brain ?

A

nigrostriatal
mesocortical
tuberoinfindubular

277
Q

What is the nigrostriatal pathway ?

A

DA neurones extend from the substantianigra to the dorsal striatum
controls fine movement
problems lead to Parkinsons

278
Q

What is the mesolimbic pathway ?

A

DA neurones from the ventral tegmental area to the cortex and ventral striatum
cortex controls modd
ventral striatum controls reward/addiction

279
Q

What is the tuberoinfindubular pathway ?

A

DA from the hypothalamus to the pituitary stalk

results in tonic inhibition of prolactin secretion

280
Q

What is the prolactin pathway ?

A 
suckling 
hypohalamic nuclei 
anterior pituitary 
mammary tissue 
milk production
281
Q

What do hypothalamic nuclei release when suckling ?

A

release prolactin releasing factor

282
Q

What does DA act as in the proloactin pathway ?

A

prolactin release inhibiting factor

283
Q

What can we use to target schizophrenia ?

A

D2 antagonists

284
Q

How are d2 receptor antagonists effective as being antipsychotics ?

A

they are potent- have a high affinity at low doses

285
Q

What does D2 antagonism in the nigrostriatal pathway lead to ?

A

extrapyrimidal side effects - movement disorders

286
Q

What are the movement disorders that are EPS ?

A

parkinsons disease

tardive dyskinesia

287
Q

What are the symptoms of parkinsons disease ?

A

tremor
muscle rigidity
loss of facial expression

288
Q

What are the symptoms of tardive dyskinesia ?

A

repetitive rhythmical involuntary movements

289
Q

What does D2 antagonism in the tuberoinfindubular pathway lead to ?

A

galactorrhoea- spontanaeous milk flow in females

gynaecomastea - man boobs

290
Q

Why do antipsychotics have affinity for other receptors besides DA ones ?

A

tricyclic structure
affintity for histamine receptors
M1 receptors
adrenergic receptors

291
Q

What are the H1 mediated side effects of antipsychotics ?

A

sedation and weight gain

292
Q

What are the M1 mediated side effects of antipsychotics ?

A

sry mouth
blurred vision
constipation

293
Q

What are the alpha 1 mediated side effects of antipsychotics ?

A

postural hyptension

294
Q

What is the classification of antipsychotics ?

A 
phenothiazenes- class I,II,III
thioxanthenes
butyrophenes - no tricyclic structure so selective for D2- no sedatio as o muscarninic or histamine activity
295
Q

What are the limitations of the classical antipsychotics ?

A

not all schizophrenic patients will respond
limited efficacy against negative symptom s
side effects and compliance issue

296
Q

What are the ideal characteristics for antipsychotics ?

A

lower EPS

effective against negative and positive symptoms

297
Q

What are positive symptoms of schizophrenia ?

A

disorganised behaviour
hallucinations
paranoia

298
Q

What are the negative symptoms of schixphrenia ?

A

blunted emotions
social withdrawal
loss of energy

299
Q

What are the characteristics of the atypical antipsychotic drugs ?

A

better EPS profile
high metabolic effects though- weight gain
lower affinity fro the D2 receptor

300
Q

How are atypical antipsychotics effective if they have alowe D2 affinity ?

A

they have a faster dissociation rate from the D2 receptor - loose binding

301
Q

What are the 2 types of DA release ?

A

phasic- high bursts then low- nigro

tonic- constant- meso

302
Q

What does phasic DA transmission do ?

A

drugs displaced by phasic bursts of DA transmission

less distortion of DA signalling

303
Q

What are the 3 types of antidepressant drugs ?

A

TCAs- tricyclic antidepressants
selective serotonin reuptake inhibitor- SSRIs
Monoamine oxidase inhibitors

304
Q

What is the role of TCAs ?

A

inhibit 5 HT and NA uptake
affinity for other receptors- side effects
often feel worse before better
imipramine

305
Q

What are the SSRIs ?

A

include SNRIs and NARIs
selective for 5HT and NA transporter - dont have postsynaptic receptor affinity
better side effect profile than TCAs

306
Q

What are the 2 forms of MAO ?

A

MAOa- breakdown 5HT and NA

MAOB- breakdown DA

307
Q

What do old MAOIs do ?

A

irreversibly bind to both isoforms leading to stimulant effects

308
Q

What do new MAOISs do ?

A

block MAOa only and reversible - safer in overdose

309
Q

What has to be done when taking MAOIs ?

A

avoid food rich in amine (cheese and marmite) as the dietary amines can trigger NA release - normally MAOa would get rid of- but inhibited
hypertensive crisis

310
Q

What is a hormone ?

A

a hormone is a chemical substance synthesised by cells and secreted into blood where it is carried to non adjacent sites in the body where it exerts its action

311
Q

What is a nerotransmitter ?

A

chemical substance synthesised by a neurone and secreted directly onto adjacent neurones where it exerts its action

312
Q

What is the HPA axis ?

A

hypothalamus- CRH
anterior pituitary- ACTH
adrenal gland - cortisol

313
Q

What is the negative feedback of cortisol ?

A

cortisol acts on the anterior pituitary and the hypothalamus

314
Q

What activates the HPA axis ?

A

physical and mental stress

315
Q

What is the role of cortisol ?

A

increase and maintains normal blood glucose
increases gluconeogeneis
decrease muscle and adipose glucose uptake
decrease in protein synthesis- use the amino acids for glucoeogenesis

316
Q

What are the causes of cushings syndrome ?

A

iatrogenic glucocorticoid therapy

adrenal tumour

317
Q

What are the side effects of cushings syndrome ?

A 
loss of protein synthesis- skin thinning 
immunosupression 
high lipid redistribution 
muscle wasting 
buffalo hump
318
Q

What is the treatment of cushings syndrome ?

A

remove tumour

inhibit synthesis of cortisol using mettyropone

319
Q

What is the synthesis of cortisol ?

A

11 beta deoxycortisol to cortisol

via 11 beta dehydroxylating enzyme

320
Q

How does metyrapone work ?

A

block 11 beta dehydroxylating enzyme

less cortisol for secretion

321
Q

How can cortisol be used therapeutically ?

A

as an immunosupressor and for its anti inflammatory effects

322
Q

Why is the insulin glucose axis

A

high blood glucose leads to insulin release from the pancreas
insulin acts on receptors in the liver and muscle

323
Q

Where is insulin synthesised and secreted from ?

A

beta islets of langerhans

stored in insulin granules

324
Q

What is the effect of insulin ?

A

conversion of glucose into glycogen

inhibition of fat breakdown

325
Q

How is insulin released from the islets of langerhans ?

A

cells take up glucose and convert to ATP in glycolysis
ATP binds to potassium ion channel
leads to depolarisation and opening of calcium channels
exocytotic release of insulin

326
Q

What is type I diabetes ?

A

insulin dependent
insulin hyposecretion due to lack of beta cells-autoimmune
treat with insulin substitutions

327
Q

What type of insulin is best for the background ?

A

intermediate acting insulin

328
Q

What is the best insulin for after a meal ?

A

short term

fast acting

329
Q

What is type 2 diabetes ?

A

non insulin dependent
functioning beta cell
receptor insensitivity
not enough glucose to meet with metabolic demands of obesity

330
Q

How do we treat type 2 diabetes ?

A

with sulphonylureas

331
Q

What are the 3 types of insulin preparation ?

A

short term acting
intermediate
long term

332
Q

What is the short term acting insulin ?

A

soluble
rapid onset
subcutaneous (normally) and IV (emergen

333
Q

What is intermediate acting insulin ?

A

insulin complexed with zinc or protamine

slowly released from particles

334
Q

What is long term acting insulin ?

A

insulin complexed with larger molecules like zinc
very slowly released
known as glargin/determir

335
Q

How do sulphonylureas work ?

A

block ATP sensitive K channels in the beta cells
cause depolarisation
increase in insulin secretion

336
Q

What is an example of a sulphonylureas ?

A

glibencalmide

337
Q

What is the HPO axis ?

A

Hypothalamus- GRH
Pituitary- LH and FSH
Ovaries- Oestrogen and progesterone

338
Q

What are the effects of oestrogen ?

A

responsible for uterus development
makes LH cells in the pituitary more sensitive
allows proliferation of the endometrium
inhibits FSH - regulate the cycle

339
Q

What are the effects of progesterone ?

A

renders endometrium suitable for implanting a fertilised ovum
inhibit further FSH LH and GRH

340
Q

What is progesterone secreted by ?

A

corpus leteum

341
Q

What happens when there is no fertilisation ?

A

corpus luteum regresses
progesterone levels drop
endometrium levels cant be maintaned so menstruaion
clamp on FSH LH and GRH is released so a follicle can develop again

342
Q

What happens if the ovum is fertilised ?

A

ovum secretes human chorionic gonadotrophin
stimulates corpus luteum to keep secreting progesterone
maintains the endometrium for the ovum
inhibits further secretion of GRH FSH and LH
prevents further follicles developing

343
Q

What are the action of oral contraceptives ?

A

they target negative feedback of progesterone
mimic pregnant state
2 types - combined and progesterone only

344
Q

What is the action of the combined pill ?

A

oestrogen inhbits FSH via negative feedback - stop follicle development
progesterone inhibits LH secretion
progesterone makes cervical mucus to stop sperm passage

345
Q

What is the action of the progesterone only pill ?

A

main effect is cervical mucus
doesnt stop ovulation
irregular periods
less reliable

346
Q

Why is is not recomended to take amoxicillin with a contraceptive pill ?

A

drug is glucoronidated by liver to excrete into bile by the duodenum
normal flora cleave the glucoronide with glucoronidase - drug can be reabsorbed again in the gut and create a reservoir
normal flora removed by antibiotic- reserovoir taken away-

347
Q

Which 2 processes do anti coagulant drugs target ?

A

blood coagulation

platelet adhesion

348
Q

Which state are patients in who take anti coagulant drugs ?

A

on the edge of haemorrhagic state

349
Q

What is haemostasis ?

A

spontaenous arrest of blood loss from a damaged vessel

required subendothelial exposure

350
Q

What are the 3 processes in haemostasis ?

A

vasconstriction
platelet adhesion and aggregation
conversion of fibrinogen to fibrin in the clot

351
Q

What is thrombosis ?

A

unwanted formation of haemostatic plug - thrombus

within a blood vessel or the heart

352
Q

Why can thrombosis occur >

A

vascular disease
prosthetic heart valves
atrial fibrilation

353
Q

What are the consequences of thrombosis ?

A

deep vein thrombosis
pulmonary embolism
myocardial infarction

354
Q

Where does the blood clot form ?

A

in vitro- outside

355
Q

What is the structure of a blood clot ?

A

amorphous

356
Q

Where does the thrombus form ?

A

in vivo

357
Q

What is the structure of the thrombus ?

A

white head and red tail
arterial- large head of platelets
venous- large tail that breaks off to form emboli

358
Q

What are active blood clotting factors made from ?

A

zymogen precursors

359
Q

What is required for the instrinsic pathway ?

A

collagen exposure

subendothelial damage

360
Q

What happens in the intrinsic pathway ?

A

factor XII is activated
factor 11
factor 9
factor 10

361
Q

What is needed for the extrinsic pathway ?

A

damaged tissue which exposes factor III

362
Q

What happens in the extrinsic pathway ?

A

factor 3 exposed
factor 7 activated
activates factor 10

363
Q

What happens in the common pathway ?

A

factor 10 converts prothrombin to thrombin
thrombin converts fibronogen to fibrin
thrombin activates factor 13
factor 13 cross links the clot

364
Q

What is the structure of heparin ?

A

sulphated mucopolysaccharides

365
Q

Where are heparins found ?

A

mast cells

same as histamine

366
Q

What do the sulphate groups on heparins allow ?

A

binding to ATIII

367
Q

What does heparin binding to ATIII allow ?

A

interact with other clotting factors

inactivate 9 10 11 12

368
Q

What are LMWHs ?

A

consistent activity
only bind to ATIII
longer action but not as broad

369
Q

How is heparin adminstered ?

A

not orally- has to be given by IV or SC

370
Q

How can we treat heparin overdose ?

A

give protamine- strongly basic protein
protamine will bind to heparin and sequester it
stop heparin binding to other clot factors

371
Q

What is an example of an oral anticoagulant ?

A

warfarin

372
Q

What is the action of warfarin ?

A

inhbits the sythesis of vit K dependent clotting factors

373
Q

What are the vit K dependent clotting factors ?

A

2
7
9
10

374
Q

How does warfarin act ?

A

it doesnt act immediately
has a lag time
takes 1-2 days to see the effects

375
Q

How can we treat warfarin overdose ?

A

vitamin K

frozen plasma

376
Q

Which enxyme is needed to activate the Vit K dependent clotting factors ?

A

glutamic acid to carboxyglutamic acid

via gamma carboxyglutamate

377
Q

What does the activation of vit K dependent clotting factors require ?

A

oxidation of vit K

hydroquinone to epoxide

378
Q

What has to happen to allow the activation of Vit k dependent clotting factors to activate again ?

A

vit K has to be reduced back to the reduced form via Vit K reductase

379
Q

How does warfarin effect the vit K process ?

A

inhibit vit K reductase

stops activating clotting factors

380
Q

How is warfarin administered ?

A

orally

381
Q

What is the Vd of warfarin ?

A

small

highly plasma protein bound

382
Q

What is the absorption of warfarin like ?

A

easily absorbed

383
Q

How do we start anti coagulation therapy ?

A

combination of warfarin and heparin
heparin is fast acting- initial effects
warfarin has lag time
once warfarin starts working the heparin is withdrawn

384
Q

How do we measure the clotting ability of warfarin ?

A

INR

385
Q

How do we measure the clotting ability of heparin ?

A

partial thromboplastin time

386
Q

How do we calculate INRs ?

A

PT (patient)/ PT (ref)

should be 2-4

387
Q

What are the new direct oral anticoagulants ?

A

factor 10 inhibitors- Rivaroxabin and Apixaban

Factor 11 inhibitors- dabigatran

388
Q

How do the new direct oral anticoagulants work ?

A

interact with clotting factors directly

dont require anti thrombin - bind to thrombin directly to stop fibrin production

389
Q

Which drugs potentiate the effects of anti coagulants ?

A

drugs which decrease platelet aggregation- aspirin
inhibit cytochrome p450S- Co- trioxazole
inhibit vit K reductase- antibiotics

390
Q

Which drugs decrease the effect of anti coagulants ?

A

induce cytochrome p450s

reduce absorption

391
Q

What does aspirin do to inhibit platelet aggregation ?

A

aspirin inhibits eicosamoid production and hence inhbits platelet aggregation

392
Q

What are the 2 eicosanoids that can effect platelet aggregation ?

A

PGI2- endothelium derived

TXA2- promotes aggregation

393
Q

What does aspirin do to the eicosanoids ?

A

stops cox mediated synthesis of both

394
Q

What is the effect of aspirin on the eicosanoids ?

A

reduced both
but TXA2 cant regenerate quickly
net effect is increase in PGI2- platelet inhibition

395
Q

What is aspirin useful in ?

A

arterial thrombosis

396
Q

What are the implications of anticoagulation therapies on dental patients ?

A

patients are on edge of haemorrhagic state
local haemostatic measures- sutures, pressure packs and vit k packs
antibiotics enhance anti coagulation effect
increased risk of bleeding with aspirin

397
Q

What is the primary target for sulphonamide antibacterials ?

A

folic acid synthesos

398
Q

What is the target process for TCAs in the treatment of anti depression ?

A

reuptake

399
Q

The volume of distribution of Paroxetine is 300L . The fraction unbound in the plasma is 0.06. The plasma concentration when 30 mg of the drug id given would therefore be ?

A

Vd- dose/plasma conc at 0

plasma= dose/Vd

30/300
0.1

400
Q

What could be a potential side effect of giving polyene type anti fungals ?

A

hypokalaemia

induced by increased cell permeability

401
Q

What is a barrier to glomerular filtration but not active tubular secretion ?

A

plasma protein binding

402
Q

Serum levels of warfarin can be increased using which drug ?

A

ibuprofen

403
Q

Local anaesthetics with an amide bonde have a longer duration of action than an ester bond ?

A

true

404
Q

Steroidal anti inflammatories induce lipocortin which inhibits the activity of phospholipase A2 ?

A

true

405
Q

The higher the blood/gas coefficient of a an Inhalation GA the more rapid the induction and recovery ?

A

false

406
Q

The volume of distribution of a drug is 300L, the amount in the body when the plasma concentration is 0.2 is ?

A

Vd= dose/plasma conc
dose= Vd x plasma conc
300 x 0.2= 60

407
Q

if youa administer codeine and the patient returns with shortness of breath and increased tiredness what is the likely cause ?

A

reduced adenylate cyclase activity following K receptor binding

408
Q

What is the order of gram measurements ?

A

mg ug ng

x 1000 to get smaller

BDS stage 2 (28 decks)

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