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year 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Name the structures of the blood brain barrier

A
  • astrocyte end feet
  • tight junctions
  • adherens junctions
  • pericytes
  • endothelial cell
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2
Q

Which areas of the brain are not enclosed by the blood brain barrier

A
  • Vascular organ of the Lamina terminalis
  • pineal gland
  • subfornical organ
  • medial eminence and posterior pituitary
  • area postrema
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3
Q

Name a drug that competes with choline re-uptake in presynaptic neurones thus inhibiting synthesis of ACh

A

Hemicholinium

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4
Q

Which drug breaks down SNARE proteins and prevents release of acetylcholine?

A

Botulinum toxin

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5
Q

Name a toxin that promotes exocytosis/release of ACh resulting in depletion of it

A

Black widow spider (alpha latrotoxin)

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6
Q

What is the action of tubocurarine ?

A

tubocurarine

Prevents access of ACh to its Nm receptor thus preventing depolarisation of the motor end plate

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7
Q

Name an example of a depolarising neuromuscular blocking drug

A

suxamethonium

Causes excessive depolarisation of the motor end plate due to excessive stimulation of Nm receptor

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8
Q

which drug reverses the effects of tubocurarine?

A

pyridostigmine

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9
Q

how is tubocurarine administered?

A

intravenously

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10
Q

what are the advantages and disadvantages of intravenous administration?

A

advantages:

  • rapid onset
  • instant plasma peak concentration
  • can be stopped or adjusted if necessary
  • all dose enters systemic circulation

disadvantages:
- skills needed/training
- sterile equipment necessary

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11
Q

name something that is administered subcutaneously ?

A

insulin

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12
Q

what is the difference between subcutaneous and intramuscular administration?

A

subcutaneous is under the skin whereas intramuscular is in the muscle.
generally intramuscular is faster due to a greater blood supply.

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13
Q

which administration routes avoid first pass metabolism?

A

buccal/sublingual
transdermal
intramuscular
inhalation

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14
Q

when is a drug administered rectally?

A

when person cannot swallow the drug due to vomiting or in children suffering from epilepsy and intravenous cannot be used.

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15
Q

which drug is not administered rectally?

a) diazepam
b) aminophyline
c) indomethacin
d) hyoscine
e) prochlorperazine

A

d) hyoscine

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16
Q

give an example of a drug inhaled

A

salbutamol or halothane

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17
Q

list advantages and disadvantages of oral administration

A

advantages:

  • easy
  • no sterile preparations
  • no special skills
  • convenient, generally accepted by patients

disadvantages:

  • not all drugs can be given this way
  • goes through first pass metabolism
  • has to withstand stomach acid
  • withstand enzymes
  • has to be lipophilic to be absorbed well
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18
Q

give an example of a drug administered siblingually

A

trinitrin

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19
Q

what is Evans blue?

A

evans blue is a dye that binds strongly to albumin and is used to determine the plasma volume

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20
Q

what does a low volume of distribution of a drug suggest?

A

low Vd = high plasma concentration = low dose needed

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21
Q

true or false;

CNS drugs have high volume of distribution

A

true

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22
Q

what does a apparent high volume of distribution suggest?

A

Vd greater than total body water amount suggests that the drug is highly lipophilic and has distributed into the extravascular spaces

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23
Q

what are the two phases of drug metabolisation?

A

phase 1: ‘functionalisation’
- involves, oxidation, reduction or hydrolysis of the drug to produce a more polar molecule

phase 2: ‘conjugation’
- involves joining of the phase 1 product to another substance such as glucuronic acid producing a more soluble product more easily excreted in the urine.

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24
Q

what factors determine the concentration of the drug in plasma?

A 
absorption
distribution
metabolism
excretion
rate of elimination
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25
Q

when does a drug dose reach ‘steady state’?

A

when the concentration of drug administered is equal to concentration of drug being eliminated

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26
Q

what methods are used to administer drugs to reach steady state?

A

-loading dose
(a large amount is given, which then lowers to the required concentration)

-multiple dosing
(added to reach therapeutic window)

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27
Q

describe the differences between long and short half-life drugs in multiple dosing

A

long half life: - small fluctuations

                   - easy to maintain within therapeutic window 
                   - takes longer to reach steady state

short half life: - large fluctuations

                - difficult to maintain within therapeutic window
                - rapid onset EG MORPHINE
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28
Q

why are somatic motor reflexes faster than autonomic reflexes?

A

somatic motor neurones are myelinated whereas the post ganglionic motor neurones of ANS are non myelinated

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29
Q

which division of the ANS is related with the cranio-sacral outflow?

A

parasympathetic

cranial nerves 3 (oculomotor), 7 (facial), 9 (glossopharyngeal) and 10 (vagus)
sacral nerves S1-S3

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30
Q

what are the anatomical differences between symp and parasymp divisions?

A

parasympathetic:
long preganglionic fibres + short postganglionic fibres
their autonomic ganglia are located nearer the target organs
release of Ach from post ganglion
fewer branches

sympathetic:
short preganglionic + long postganglionic
release of NA from postganglion
many branches

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31
Q

what neurotransmitter do the preganglionic neurones in the ANS release?

A

Ach

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32
Q

name an organ with dual innervation from both para and symp NS which have antagonistic control

A

the heart
sympathetic NS : releases NA = increase HR
parasympathetic NS: release of Ach = decrease HR

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33
Q

what is the enteric nervous system?

A

the plexus of nerves controlling the GIT

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34
Q

how is acetylcholine synthesised?

A

acetyl Co A and choline join together. catalysed by acetyl choline transferase

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35
Q

what is pseudocholinesterase?

A

enzyme in plasma made by liver that breaks down Ach but much more slowly

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36
Q

how is Ach broken down?

A

by acetylcholinesterase
enzyme has two sites on active site: anionic site (-ve) and ester site that has a serine protein (OH group)
attracts the positive choline and acetic acid (hydrogen bond)

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37
Q

name an irreversible acetylcholinesterase inhibitor

A

dyflos

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38
Q

name a reversible antagonist of AchE

A

neostigmine

physostigmine

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39
Q

what are the receptors that Ach can bind to and what are their subclasses?

A

nicotinic : Nm= skeletal muscles
Nn= neuronal type

muscarinic :
M1 - Gq - GIT motility + acid secretions, CNS
M2 - Gi - cardiac (decrease rate and force)
M3 - Gq - smooth muscle contraction and increase gland secretions

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40
Q

which one is NOT a muscarinic antagonist?

a) hyoscine
b) ipratropium
c) pilocarpine
d) benzhexol
e) tropicamide

A

c) pilocarpine is an agonist

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41
Q

name a nicotinic antagonist

A

hexamethonium

mecamylamine

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42
Q

list some nicotinic antagonist effects

A
  • vasodilation
  • dilation of pupils
  • decreased HR
  • dry mouth
  • reduced sweating
  • reduced GIT motility
  • urinary retention
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43
Q

what are the main sympathetic ganglia ?

A

celiac
superior mesenteric
inferior mesenteric
inferior hypogastric

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44
Q

to which structure in the body does the sympathetic innervation not pass an autonomic ganglion?

A

adrenal medulla

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45
Q

list the enzymes needed in synthesis of adrenaline

A

tyrosine hydroxylase
dopa decarboxylase
dopamine beta decarboxylase
phentolamine N-methyltransferase

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46
Q

how is catecholamine neurotransmitter production modulated?

A

tyrosine hydroxylase is modulated by end product inhibition
depolarisation activates TH activity
activation of TH involves reversible phosphorylation

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47
Q

which enzyme is found in the vesicle during neurotransmitter synthesis?

a) tyrosine hydroxylase
b) dopa decarboxylase
c) dopamine beta decarboxylase
d) phentolamine N-methyltransferase

A

c) dopamine beta decarboxylase

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48
Q

which enzymes metabolise catecholamines?

A 
monoamine oxidase (MAO)
catechol-O-methyl transferase (COMT)
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49
Q

name a non specific MAO inhibitor

A

phenelzine

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50
Q

name a MAO(B) inhibitor

A

selegilin - used in Parkinsonism

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51
Q

name a COMT inhibitor

A

tolcapone - long acting

entacapone - short acting

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52
Q

name a 5-HT uptake blocker

A

fluvoxamine

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53
Q

name a NA and dopamine reuptake blocker

A

imipramine

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54
Q

what is the action of guanethidine?

A

taken up by uptake 1 =depletes NA stores in neurone

55
Q

which drug blocks tyrosine hydroxylase?

A

metyrosine

56
Q

which drug blocks uptake of dopamine into vesicles?

A

reserpine

57
Q

which adrenoreceptors cause renin release from kidneys?

A

beta 1

58
Q

which adrenoreceptors stimulate insulin release from pancreatic cells?

A

beta 2

alpha 1 inhibit release

59
Q

what does stimulation of beta 3 receptors cause?

A

lipolysis

60
Q

in the eye what does stimulation of alpha 1 and beta 2 receptors cause?

A

alpha 1 = contraction of pupil

beta 2 = relaxation for far vision

61
Q

what effects does beta 1 and beta 2 stimulation have in the cardiac system?

A

beta 1 = increase HR

beta 2 = bronchodilation

62
Q

name a beta 2 agonist

A

salbutamol

63
Q

what effects do Beta 2 stimulation have?

A 
urinary bladder wall relaxation
uterus relaxation when non-pregnant
insulin release
decreased GIT motility
bronchodilation
vasodilation
64
Q

name a drug used for hypotention

A

phenylephrine - alpha 1 agonist = vasoconstriction

65
Q

what is the difference between alpha 1 and 2 adrenoceptors?

A

alpha 1: post-synaptic
Gq coupled

alpha 2: pre-synaptic
Gi coupled

66
Q

what does beta 3 stimulation cause?

A

lipolysis

67
Q

what does alpha 2 stimulation cause to pancreatic beta cells?

A

inhibition of insulin release

68
Q

what does beta 1 receptor stimulation cause in the kidneys

A

renin release

69
Q

which receptor stimulation causes decrease in GIT motility?

A

alpha 2 and beta 2

70
Q

which receptor types in the eye control the ciliary muscle and the radial muscle?

A

radial : alpha 1

ciliary : beta 2

71
Q

which drug is a non selective beta adrenoceptor antagonist

A

propanolol

72
Q

where is acetylcholinesterase found?

A

synaptic basal lamina of post synaptic neurone

73
Q

which drug inhibits reuptake of choline?

A

hemicholinium

74
Q

which drug prevents Ach transport into a vesicle?

A

vesamicol

75
Q

what is the difference between tubocurare and suxamethonium

A

both are agents that prevent Ach depolarisation of the motor end plate

tubocurarine: non depolarising antagonist
flaccid paralysis
tetanus contraction is not maintained

suxamethonium: depolarising agonist
spastic paralysis
tetanus contraction sustained

76
Q

how can you reverse the effects of tubocurarine?

A

neostigmine

AchE inhibitor = more Ach levels therefore more Ach competes for Nm receptor (tubocurarine is a competitive antagonist)

77
Q

explain the mechanism of action of suxamethonium

A

phase 1
binds to receptor causes opening of Na+ channels = depolarisation
depolarisation does not stop

phase 2
continuous depolarisation causes desensitisation of receptor

78
Q

can neostigmine be given to reverse the effects of suxamethonium ?

A

no, neostigmine is a AchE inhibitor = more Ach
suxamethonium is a depolarising agonist therefore increasing Ach levels will make it worse

the action is terminated by plasma cholinesterase (pseudocholinesterase)

79
Q

what is a partial agonist?

A

only produces an effect if no full agonist is present

if full agonist is present, acts as an antagonist

80
Q

what are spare receptors?

A

if a maximal response is being elicited but not all the receptors are occupied

81
Q

low dose of a non-competitive irreversible antagonist causes a shift in the concentration curve to the right, without changing the Emax and EC50. why?

A

because of spare receptors

82
Q

what is the ‘potency’ and ‘efficacy’ of a drug?

A

potency is the concentration needed to produce half of the drugs maximal effects (EC50)

efficacy: the maximal effect produced once drug is bound to its receptor

83
Q

what is the therapetuic index?

A

the difference between LD50 and ED50

LD50 =lethal dose
ED50= effective dose to produce 50% of maximal response

84
Q

what is physiological antagonism?

A

two drugs producing opposing effects, cancelling each other out

85
Q

what is pharmacokinetic antagonism?

A

one drug affecting the absorption, metabolism or excretion of another how does

86
Q

in a dose response curve, how does addition of a competitive antagonist affect the curve?

A

shifts to the right without change to EC50 and Emax

takes more [agonist] to reach Emax

87
Q

in a dose response curve, how does the addition of a non competitive irreversible antagonist affect the curve?

A

small dose = shift to the right without change to EC5 or Emax

large dose: decrease in EC50 and Emax

88
Q

why is salbutamol used in treating asthma?

A

salbutamol is a Beta 2 agonist.
beta 2 stimulation of lungs causes bronchodilation

it also reduces mediator release,

and reduces vascular leakage

89
Q

which drug inhibits the enzyme 5-lipoxygenase in treatment of asthma?

A

zileuton

90
Q

which drug binds to IgE on mast cells?

A

omalizumab

91
Q

what is the role of sodium cromoglycate in asthma treatment?

A

prevents mediator release by stabilising membranes

92
Q

which drug inhibits phospholipase A in treating asthma?

A

beclamethasome diproprionate

93
Q

what causes bronchial hyperresponsiveness in asthma?

a) release of LTC4 by inflammatory cells
b) Release of LTD4 by inflammatory cells
c) release of neuropeptides by PAF
d) damage of epithelial lining by eosinophiles

A

d) damage of epithelial lining by eosinophiles

94
Q

what is the action of ipratropium bromide

a) decrease cGMP
b) decrease cAMP
c) decrease PIP2 levels
d) decrease IP3

A

decrease PIP2

because it blocks M3 receptors that are Gq coupled

95
Q

why is ipratropium not absorbed well?

A

quaternary ammonium = charged ion

96
Q

which antimicrobial inhibits RNA polymerase?

a) Erythromycin
b) Metronidazole
c) Penicillin G
d) Rifampicin
e) Vancomycin

A

d) Rifampicin

97
Q

what causes resistance to beta-lactams such as penicillin?

A

bacteria have enzymes called beta-lactamases that break down beta-lactum ring

98
Q

name a compound that can inhibit beta-lactamase enzymes in bacteria

A

clavulanic acid

99
Q

how can microorganisms develop resistance to antimicrobial agents?

A
  • alter target (where drug attaches)
  • alter uptake (altered entry into cell or efflux mechanism)
  • drug inactivation (eg beta-lactamases)
100
Q

what to dilution tests determine for antibiotics?

A
  • minimum inhibitory concentration

- minimum cidal concentration

101
Q

which one is NOT an antifungal agent?

a) nystatin
b) amphotericin B
c) aciclovir
d) itraconazole
e) miconazole

A

c) aciclovir - this is an antiviral agent

102
Q

which antibacterial agent inhibits DNA replication?

a) Erythromycin
b) Metronidazole
c) Nalidixic acid
d) Rifampicin
e) Vancomycin

A

c) Nalidixic acid

103
Q

which antibacterial contain a beta-lactam ring ?

A

all penicillins

and cephalosporins

104
Q

what are the consequences of uncontrolled hypertension?

A
  • stroke
  • coronary heart disease
  • cardiac failure
  • progressive renal failure
  • retinal vascular disease
105
Q

what does stimulation of alpha2 adrenoceptors in the CNS cause?

A

decrease in sympathetic tone = vasodilation and reduction in heart rate

106
Q

what does stmulation of beta receptors cause?

A

increase in blood pressure

because increase in HR, increase renin release

107
Q

what does production of cGMP cause in smooth muscles?

A

vasodilation

108
Q

how do hydralazine and sodium nitroprusside work to reduce blood pressure?

A

they stimulate the production of cGMP = vasodilation

109
Q

how do inhibitors of RAAS reduce blood pressure?

A 
- reduce production of angiotensin II
=
↓ ADH secretion
↓ Na+/Cl- reabsorption 
↓ aldosterone
↓ sympathetic tone
↓ vasoconstriction
110
Q

which drug is not a RAAS inhibitor?

a) captopril
b) propanolol
c) atenolol
d) hydrochlorothiazide
c) losartan

A

d) hydrochlorothiazide

works by reducing Na+/Cl- reabsorption at the DCT and collecting duct

111
Q

how does clonidine act to treat hypertension?

A

alpha 2 agonist = ↓ sympathetic tone
↓ HR
- vasodilation

112
Q

how does propanolol act to treat hypertention?

A

beta receptor antagonist= ↓ renin release

↓ sympathetic tone

113
Q

when does coronary perfusion occur?

A

at diastole

114
Q

describe plaque formation

A

damage to endothelium cells causes lipids and cholesterol to accumulate at site
↓
the cholesterol oxidises
↓
inflammatory response triggered = release of cytokines from endothelial cells attract Monocytes
↓
monocytes differentiate into macrophages upon activation by oxidised cholesterol
↓
macrophages engulf the cholesterol = becoming foam cells
↓
foam cells accumulate and form plaque
↓
smooth muscle cells multiply and migrate to the plaque surface, forming a fibrous cap

115
Q

what does atherosclerosis result in?

A
  • development of collateral vessels
  • angina (pain due to limited blood flow to cardiac muscle)
  • myocardial infarction = heart attack
116
Q

what are the types of angina?

A
  • stable
  • unstable (pre-infarction)
  • variant (Prinz Metal) = spasm of coronary arteries
  • intractable/refractory =persists after treatment
  • silent ischemia
117
Q

what does the work load of the heart depend on?

A
  • preload (venous return)
  • afterload (peripheral resistance)
  • sympathetic stimulation
118
Q

define heart failure

A

a state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body

119
Q

list the symptoms of heart failure

A
  • tiredness
  • coughing
  • swelling in ankles/legs
  • swelling in abdomen
  • pleural effusion (excess fluid around lungs)
  • pulmonary oedema
120
Q

what are the body’s response to heart failure?

A
  • drop in arterial pressure = baroreceptor reflex = vasocontriction
-  ↓  blood flow to kidneys = ↑ renin production
= renin = angiotensin II 
= ↑ ADH
   ↑ aldosterone 
=(↑ water reabsorption)
  • ↑ catecholamines in blood cause structural remodelling of the heart
  • oedema
121
Q

how does heart failure cause oedema?

A

decrease in cardiac output = ↓ BP

↓ blood flow to kidneys = ↑ renin release

= ↑ angiotensin II = ↑ water reabsorption = oedema

also cardiac remodelling = left ventricle hypertrophy = pulmonary oedema

122
Q

what is the difference between GABAa and GABAb receptors?

A

GABAa
= ionotropic
= open Cl- channels allowing Cl- to go into cell = hyperpolarisation = no action potential

GABAb
=metabotropic (G protein coupled)
= cause K+ channels to open , K= moves out of cell = hyperpolarisation = no action potential

123
Q

what is the mechanisms of action of benzodiazepines?

A

positive allosteric modulator

binds to allosteric site on GABAa receptor
increased affinity for GABA for its receptor
increased frequency of Cl- channels opening

124
Q

what are benzodiazepines used for ?

A

muscle relaxant
anxiolytic
sedative
anticonvulsant

125
Q

how are most benzodiazepines excreted?

A

in the urine as glucuronides or oxidised metabolites

126
Q

which drug antagonises the effects of benzodiazepines?

a) triazolam
b) chlordiazepoxide
c) flumazenil
d) flurazepam
e) temazepam

A

c) flumazenil

127
Q

what are the two steps that drugs undergo during metabolism?

A
  • hydroxylation

- conjugation (usually with glucaronic acid to make it more polar)

128
Q

which part of the brain do benzodiazepines work on?

A

limbic system

129
Q

which dopaminergic pathway is associated with positive symptoms of schizophrenia?

A

mesolimbic pathway

130
Q

which dopaminergic pathway is associated with negative symptoms of schizophrenia?

A

mesocortical

131
Q

name some of the positive symptoms of schizophrenia

A
  • hallucination
  • delusions
  • disorganised thoughts + speech
132
Q

list some of the negative symptoms of schizophrenia

A

blunt emotions
poor focus
loss of pleasure
social withdrawal

133
Q

why does chlorpomazepine cause extra pyramidal side effects?

A

it is a neuroleptic that blocks D2 receptors which means theres a block in the nigrostriatal pathway and so the decreased dopamine stimulus to the striatum increases Ach release causing n increase of stimulation of extra pyramidal tracts

year 1 (8 decks)

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