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Pharm Flashcards

1
Q

5 core drugs for depression?

A 
sertraline
citalopram
mirtazapine
venlafaxine
fluoxetine
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2
Q

3 SSRIs? primary mechnaimis?

A

citalopram, sertraline, fluoxetine

act on serotonin reuptake transporter on presynaptic neuron to inhibit serotonin reuptake → ↑ serotonin in synapse

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3
Q

side effects of SSRIs?

A

nausea, diarrhoea
sexual dysfunction
anxiety
insomnia

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4
Q

what other transporter does sertraline inhibit?

A

dopamine transporter (mildly)

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5
Q

citalopram is a mild antagonist of which receptors?

A

muscarinic and histamine

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6
Q

fluoxetine is a mild antagonist of which receptors?

A

5HT2A

5HT2C

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7
Q

when taking fluoxetine caution needs to be taken with which drug?

A

warfarin - could inhibit it’s anticoagulant effect

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8
Q

what are the drug targets of venlafaxine?

A

serotonin and noradrenaline transporters

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9
Q

venlafaxine mechanism of action?

A

inhibits serotonin and noradrenaline reuptake by acting on reuptake transporters (serotonin≥NA) SNRI

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10
Q

side effects of venlafaxine?

A 
nausea, diarrhoea
sexual dysfunction
insomnia
anxiety
hypertension at high doses
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11
Q

what are the drug targets of mirtazapine?

A

alpha 2 receptor
5-HT2 & 3 receptor
H1 receptor

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12
Q

mechanisms of action of mirtazapine?

A

antagonises central presynaptic a2 adrenergic receptors → ↑ serotonin and NA release
antagonises central 5HT2&3 receptors → 5HT1 receptors unopposed → anti-depressant effects

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13
Q

side effects of mirtazipine?

A

weight gain
sedation
may exacerbate REM sleep behaviour disorder
(±sexual dysfunction)

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14
Q

with what drug is citalopram contraindicated? why? (ecg)

A

erythromycin

both associated with prolonging QT interval

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15
Q

why do antidepressants need to be gradually discontinued?

A

risk of drug interactions
serotonin syndrome
withdrawal symptoms
relapse

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16
Q

what receptor is mirtazapine most selective for? what is the side effect of this and how is it offset?

A

histamine H1 receptor
sedation
however at increased doses this is offset by increased NA transmission

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17
Q

4 core drugs for diabetes?

A

metformin
DDP4 (dipeptidyl-peptidase4) inhibitors eg.sitagliptin
sulphonylurea eg. gilclazide
SGLT2 inhibitors eg. dapaglifozin

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18
Q

metformin mechanism of action?

A

activates AMPK in hepatocyte mitochondria → inhibits ATP production → blocks gluconeogenesis → ↓ HGO → restore insulin sensitivity

blocks adenylate cyclase → ↑ fat oxidation → restore insulin sensitivity

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19
Q

side effects of metformin?

A 
abdo pain
diarrhoea
↓appetite
vomitting 
(especially at high doses, slow increase in dose better)
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20
Q

what transporter does metformin require to enter tissues?

A

OCT-1

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21
Q

what makes metformin more effective?

A

presence of endogenous insulin (some residual functioning pancreatic islet cells)

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22
Q

give an example of a DDP-4 inhibitor?

A

sitagliptin

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23
Q

mechanism of action of DDP-4 inhibitors?

A

inhibit DPP-4 action in the vascular endothelium → ↓ metabolism of incretins like GLP1 → more incretins → ↑ insulin secretion & ↓ glucagon production

slow down digestion and ↓ appetite

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24
Q

side effects of DPP-4 inhibitors?

A

upper respiratory tract infections w flu-like symptoms

allergic reactions

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25
Q

DDP-4 inhibitors should be avoided in patients with what?

A

pancreatitis

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26
Q

what do DDP-4 inhibitors require to be effective?

A

residual functioning pancreatic beta cell activity

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27
Q

example of a sulphonylurea?

A

gliclazide

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28
Q

mechanism of action of sulphonureas?

A

inhibit ATP-sensitive potassium channel on pancreatic beta cells → ↑ depolarisation → Ca2+ influx → insulin vesicle exocytosis

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29
Q

side effects of sulphonylureas?

A

weight gain

hypoglycaemia

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30
Q

how is weight gain mitigated with sulphonylureas?

A

taken with metformin

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31
Q

example of SGLT-2 inhibitor?

A

dapaglifozin

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32
Q

mechanism of action of SGLT-2 inhibitors?

A

reversibly inhibits SGLT-2 in renal proximal convoluted tubule → ↓ glucose reabsorption → ↑ urinary glucose excretion

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33
Q

side effects of SGLT-2 inhibitors?

A 
uro-genital infections (increased glucose load)
slight decrease in bone formation 
can worsen DKA
hypotension
weight loss
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34
Q

what would cause SGLT-2 inhibitors to be less effective?

A

renal impairment

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35
Q

where is OCT-1 expressed?why is this important?

A

OCT-1 allows the polar metformin to enter tissues
found in hepatocytes - allows for distribution
enterocytes of small bowel - for absorption
proximal renal tubules - excretion

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36
Q

pharmacodynamics vs pharmacokinetics?

A 
pd = drug actions on body
pk = body actions on drug
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37
Q

4 types of drug targets?

A

enzymes
ion channels
transporter protein
receptors

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38
Q

types of drug-receptor interactions?

A

electorstatic - eg vdws, h bonds
hydrophobic - lipid soluble drugs
covalent - least common, irreversible
stereospecific

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39
Q

affinity and efficacy?

A 
a = strength ability of a drug to bind a receptor, ↑ affinity = ↑ receptor occupancy 
e = ability of a drug to produce an effect once bound
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40
Q

agonists vs antagonists?

A

no efficacy = antagonist = prevents activation of receptor
partial agonist = affinity for receptor but sub maximal efficacy = partial response
agonist = has affinity for receptor and maximal efficacy

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41
Q

what is potency?

A

concentration/dose of a drug required to produce a 50% tissue response (EC50 and ED50)

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42
Q

major pharmacokinetic factors?

A

absorption
distribution
metabolism
excretion

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43
Q

what is bioavailability?

A

the fraction of initial drug dose that gains access to systemic circulation

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44
Q

what is the bioavailability of IV administration?

A

100%

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45
Q

forms of drug administration?

A 
oral
inhlaed
dermal/percutaneous
intranasal
IV
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46
Q

how are drugs normally transported into tissues?

A

diffusion across lipid membranes

carrier mediated transport

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47
Q

what form of drug is more lipid soluble?

A

unionised = more likely to diffuse across plasma membrane

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48
Q

pKa and pH are equal , what does this mean?

A

the drug will be 50/50 ionised/unionised

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49
Q

weak acids have what pKa range?

A

3-5

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50
Q

as pH decreases what happens to weak acids?

A

unionised form dominates

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51
Q

weak bases have what pKa range?

A

8-10

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52
Q

as pH decreases what happens to weak bases?

A

ionised form dominates

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53
Q

what pHs are best for weak acids and bases to be absorbed?

A

weak acid - low pH → more unionised → more lipid soluble

weak base - high pH → more unionised → more lipid soluble

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54
Q

what factors determine how much drug a tissue is exposed to?

A

regional blood flow
plasma protein binding
capillary permeability
tissue localisation

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55
Q

regional blood flow of tissues?

what factors affect regional blood flow?

A

liver, kidneys, muscle, brain, heart
exercise = more to muscle
large meal = more to GI tract

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56
Q

which plasma protein is good at binding acidic drugs?

A

albumin

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57
Q

what determines how much of a drug is bound to plasma proteins?

A

free drug concentration
affinity for protein binding sites**
plasma protein concentration

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58
Q

what kind of capillary structure does the liver have?

A

discontinuous = allows for easy diffusion of drugs out of blood into liver tissue

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59
Q

what kind of capillary structure does the kidney glomerulus have?

A

fenestrated = allows for passage of some small drugs to pass from blood into kidney tubules = better excretion

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60
Q

explain tissue localisation

A

depends on tissue fat and water content compared to plasma
eg. brain has a higher fat content and plasma has higher water content
for fat soluble drugs the equilibrium is more weighted towards retention in tissue with higher fat content
same for water soluble drugs

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61
Q

what liver enzymes are mainly responsible for drug metabolism?

A 
P450 enzymes (phase 1)
transferases (phase 2)
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62
Q

what are the 2 phases to drug metabolism?noverall effect?

A

phase 1 - add reactive polar group to drug
phase 2 - add conjugate to reactive group
=↓ lipid solubility = ↑ excretion elimination

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63
Q

how can phase 1 metabolism occur?

A

oxidation **
reduction
hydrolysis

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64
Q

what are pro-drugs?

A

drugs that require metabolism in order to become pharmacologically active (parent drugs has no activity)

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65
Q

what happens in phase 2 metabolism?

A

attachment of substituent group to functional group from phase 1 → inactive , ↓ lipid soluble metabolite → facilitates excretion via urine/bile

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66
Q

what is first pass metabolism?

A

orally administered drugs are absorbed in small intestine and enter hepatic portal circulation → first pass through liver → heavily metabolised → ↓ drug reaching systemic circulation

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67
Q

solution to first pass metabolism? associated problems?

A

give a larger dose of drug to ensure enough reaches systemic circulation
however, amount of first pass metabolism varies between people → drug effects and side effects difficult to predict

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68
Q

3 main methods for drug excretion via kidney?

A

glomerular filtration
active tubular secretion
passive diffusion across tubular epithelium

69
Q

what drugs are most likely to be excreted via glomerular filtration?

A

low molecular weight drugs (<20000) = quicker rate of excretion compared to larger drugs

70
Q

why is active tubular secretion important?

A

remaining 80% of renal plasma passes via proximal tubule
PT capillary endothelial cells have active transport carrier proteins that are effective at transporting acidic and basic drugs against conc gradient

71
Q

what drugs are more prone to passive diffusion in the kidney? what factors influence this?

A 
lipid soluble ones 
drug metabolism - phase 2 metabolites are more water soluble than parent drugs = less well absorbed
urine pH (4.5-8) - acidic drugs better reabsorbed at lower pH and basic drugs better reabsorbed at higher pH
72
Q

bile excretion is most effective at removing which metabolites?

A

phase 2 glucuronide metabolites

73
Q

what is enterohepatic recycling?

A

glucuronide metabolite → bile → small intestine → metabolite hydrolysed via gut bacteria, losing glucuronide conjugate → ↑ lipid solubility → ↑ reabsorption from small intestine → hepatic portal blood system → liver → portion re-metabolised but some may get into systemic circulation → prolonged effects

74
Q

4 core anticonvulsants?

A

lamotrigine, diazepam. levetiracetam, sodium valproate

75
Q

mechanism of action of lamotrigine?

A

blocks voltage gated Na+ channels on glutamatergic neurons → prevents Na+ influx → less depolarisation and less glutamate excitotoxicity

76
Q

side effects of lamotrigine?

A

rash*
drowsiness*
stevens-johnson syndrome
suicidal thoughts

77
Q

how can allergic reactions be avoided with lamotrigine?

A

introduce gradually

78
Q

mechanism of action of sodium valproate?

A

inhibits GABA transaminase in inhibitory presynaptic terminal → less GABA breakdown → ↑ GABA conc in synapse

79
Q

side effects of sodium valproate?

A 
stomach pain
diarrhoea 
drowsiness
weight gain
hair loss
hepatotoxicity 
teratogenecity
pancreatitis
80
Q

what other enzyme does sodium valproate inhibit? what does this mean?

A

CYP/cytochrome P450 is inhibited → ↑ concentration of any co-administereed drugs

81
Q

mechanism of action of diazepam?

A

binds to benzodiazepine site on GABA A receptor → ↑ Cl- influx → hyper polarisation of excitatory neurones

82
Q

side effects of diazepam?

A

drowsiness
respiratory depression
jaundice
haemolytic anaemia

83
Q

why is diazepam not used for long term seizure suppression?

A

tolerance

84
Q

levetiracetam mechanism of action?

A

inhibits synaptic vesicle protein SV2A on excitatory presynaptic terminal → prevents vesicle exocystosis → ↓ glutamate secretion

85
Q

side effects of levetiracetam?

A

dizziness
somnolence
fatigue
headache

86
Q

what is benefit of levetiracetam compared to other anticonvulsants?

A

no effect on cytochrome P450 → no drug-drug interactions

87
Q

which anticonvulsant should be given with caution to women of child bearing. age?

A

sodium valproate - teatrogenic, neural tube defects, ↓ IQ, autism

88
Q

4 core drug classes for hypertension? and examples

A

ACE inhibitors - rami,lisino,perindo pril
calcium channel blockers - amlo,felo dipine
thiazide/thiazide like diuretics -bendroflumethiazide, indapamide
angiotensin receptor blockers - lo, irbe, cande sartan

89
Q

mechanism of action of ACE inhibitors?

A

inhibit angiotensin converting enzyme (lung and renal endothelium) → prevents conversion of angiotensin I to II → vasodilation, less salt and water retention, less aldosterone secretion

90
Q

side effects of ACE inhibitors?

A 
cough
hypotension
hyperkalaemia
foetal injury
renal failure (esp with renal artery stenosis)
urticaria
angioedema
91
Q

ACE inhibitors are mostly what kind of drug?exception?

A

prodrugs - require hepatic activation

except lisinopril

92
Q

what needs to be regularly monitored when taking ACE inhibitors?

A

eGFR

serum potassium

93
Q

mechanism of action of calcium channel blockers?

A

block L type calcium channels on vascular smooth muscle → ↓ calcium influx → inhibition of myosin light chain kinase → prevention of cross bridge formation → vasodilation → ↓ peripheral resistance

94
Q

side effects of calcium channel blockers?

A 
ankle oedema
constipation
palpitations
fliushing
headaches
95
Q

mechanism of action of thiazides/thiazide like diuretics?

A

block the sodium calcium cotransporter in the early distal convulsed tubule → inhibited ca+ and na+ reabsorption → ↑ osmolarity of tubular fluid → ↓ osmotic gradient for water reabsorption in collecting duct → ↑ na+ and water loss

96
Q

side effects of thiazides/thiazide like diuretics?

A

hypokalaemia
hypomatraemia
metabolic alkalosis due to ↑ H+ excretion
hypercalcaemia
hyperglycaemia (hyper polarised pancreatic beta cells)
hyperuriceamia

97
Q

what happens with thiazides/thiazide like diuretics after 1-2 weeks?

A

lose their diuretic effects

maintain antihypertensive action due to vasodilation properties

98
Q

mechanism of action of angiotensin receptor blockers?

A

act as non-competitive antagonists on AT1 receptors on kidneys and vascalature → prevents angiotensin from binding → vascular smooth muscle relaxation → ↓ blood pressure

99
Q

side effects of ARBs?

A

hypotension
hyperkalaemia
foetal injury
renal failure

100
Q

ARBs are first line for which patients?(as opposed to ACEi)

A

afrocarribean patients

101
Q

which condition are ACEi contraindicated?why?

A

bilateral renal artery stenosis

less angiotensin II results in less efferent arteriole vasoconstriction → lower renal perfusion→ acute renal failure

102
Q

what cause hyperkalemia with ACEi?

A

sodium is not being reabsorbed, normally it would be exchanged for potassium which would be eliminated

103
Q

5 core drugs for asthma?

A 
salbutamol - SABA
fluticasone
mometasone
budesonide
montelukast
104
Q

salbutamol mechanism of action?

A

agonist of B2 receptors on airway smooth muscle cells → activation reduces ca2+ entry → prevents smooth muscle contraction

105
Q

side effects of salbutamol?

A

palpitations
arrythmias
tachycardia
hypokalaemia

106
Q

why are cardiac effects seen with salbutamol?

A

its not selective for the B2 receptor → can act on B1 receptor on cardiac cells

107
Q

what drugs exacerbate the hypokalaemic effects of salbutamol?

A

corticosteroids

108
Q

mechanism of action of fluticasone, mometasone and budesonide?

A

acts on glucocorticoid receptors → ↓ eosiniphils, monocytes, mast cells, macrophages and dendritic cells → ↓ cytokines produced eg. IL5&4

109
Q

side effects of fluticasone, mometasone and budesonide?

A

local: (more in inhaled adm)
sore throat, hoarse voice, oral infections

systemic: (more in oral administration)
growth retardation in children
hyperglycaemia
reduced bone mineral density
immunosuppression
mood effects
110
Q

difference between budesonide compared to fluticasone and mometasone?

A

budosenide has higher oral availability → some systemic absorption via GI tract
its less potent

111
Q

montelukast mechanism of action?

A

antagonist of CysLT1 leukotriene receptor on eosinophils, mast cells and airway smooth muscle cells → ↓ eosinophil migration, ↓ bronchoconstriction & ↓ inflammation induced oedema

112
Q

side effects of montelukast?

A 
diarrhoea
fever
headaches
n&v
mood changes
anaphylaxis
113
Q

what type of asthma is montelukast particularly useful for and why?

A

NSAID induced asthma

114
Q

2 core drugs for gord?

A

PPIs - omeprazole, lansoprazole

H2 antagonists - rantidine

115
Q

nsaid mechanism of action in gord?

A

inhibit cycloxygenase in peripheral nociceptive nerve endings → inhibits production of prostaglandins and thromboxane from arachdonic acid → analgesic, anti-inflammatory and antipyretic actions (COX-2)

116
Q

3 examples of NSAIDs?

A

NSAIDS - ibuprofen, naproxen, diclofenac

117
Q

sides effects of nsaids?

A 
gastric irritation, ulceration, bleeding, perf
↓ creatinine clearance , neophritis
bronchoconstrcition 
rashes
dizziness
tinnitus
118
Q

mechanism of action of PPIs?

A

irreversible inhibitors of h+/k+ ATPase pumpkin gastric parietal cells → ↓ gastric acid secretion

119
Q

how is PPI action prolonged?

A

they are weak bases so accumulate in the acid environment of canaliculi of parietal cells (more ionised so less lipid soluble so less diffusion)

120
Q

side effects if PPIs?

A 
headache
diarrhoea
bloating
rashes
abdominal pain
\invreased risk of bone fracture
121
Q

PPIs can mask symptoms of what?

A

gastric cancer

122
Q

what enzyme does omeprazole inhibit? relevance?

A

cytochrome P2C19 → reduced activity of clopidogrel

123
Q

what type of drugs are PPIs?

A

pro drugs

124
Q

how are PPIs coated?why?

A

capsules containing enteric coated granules → prevents rapid degradation at low pH

125
Q

mechanism of action of H2 receptor antagonists?

A

competitive antagonists of histamine H2 receptors on gastric parietal cells → prevent movement ofcAMP dependent movement of H+ ions → ↓gastric acid secretion

126
Q

H2 receptor antagonist side effects?

A 
low incidence
diarrhoea
dizziness
muscle pains
transient rashes
127
Q

which H2 receptor antagonist inhibits cytochrome P450?

A

cimetidine

128
Q

nsaid mechanism of action in gord?

A

nsaid targets COX 1 enzyme on gastric mucosal cells → inhibit prostaglandin production → inhibition of pg-mediated protection of gastric mucosa (bicarb release, mucus prod. & blood flow)

129
Q

PPIs should be avoided in what disease?

A

osteoporosis

130
Q

mechanism of action of statins?

A

selective competitive inhibitor of HMG-CoA reductase → less HMGCoA to malevonate → less hepatic cholesterol synthesis → upreg of LDL receptors → increased hepatic uptake of LDL cholesterol from circulation

131
Q

main side effects of statins?

A

muscle toxicity
constipation
diarrhoea

132
Q

side effects of aspirin?

A

dyspepsia

haemorrhage

133
Q

how does aspirin reduce risk of thrombosis?

A

inhibits COX2 → less thromboxane A2 produced from arachidonic acid → less platelet aggregation

134
Q

which prostaglandin does aspirin reduce that is involved in pain and fever?

A

PGE2

135
Q

mechanism of action of trimethoprim?

A

direct competitor of dihydrofolate reductase → inhibits reduction of dihydrofolic acid to tetrahydrofolic acid → less synthesis of purines required for dna and protein synthesis

136
Q

side effects of trimethoprim?

A

diarhoea

skin reactions

137
Q

what drug is trimethoprim often administered with?

A

co-trimoxazole to block bactrerial biosynthesis

138
Q

what needs to be monitored with long term trimethoprim use?

A

blood counts for those at risk of folate deficiency

serum electrolytes for those at risk of developing hyperkalaemia

139
Q

mechanism of action of gentamicin?

A

binds to bacterial 30s ribosomal subunit → disturbs translation of mRNA → dysfunctional proteins

140
Q

side effects of gentamicin?

A

ototoxicity (hearing/balance)

nephrotoxicity

141
Q

what class of antibiotic is gentamicin? what does this mean?

A

aminoglycoside , can pass through gram negative cell membrane in an oxygen dependent manor - ineffective against anaerobic bacteria

142
Q

what conditions is gentamicin commonly administered for?

A 
endocarditis
sepsis
meningitis
pneumonia
sx propylaxis
143
Q

hypertension stages and ranges?

A

under 135/85 = monitor every 5 years
135/85 - 149/94 = stage 1 = drugs of organ damage, CVD, renal disease, diabetes, CVD risk ≥10%
over 150/95 = stage 2 = drugs

144
Q

what drugs can improve proteinuria?

A

ACEi
ARBs
SGLT-2 inhibitors

145
Q

drug used to treat UTIs?

A

trimethoprim

146
Q

effect of trimethoprim on eGFR?

A

can falsely lower eGFR as it inhibits the active secretion of creatinine (serum creatinine ↑)

147
Q

effect of ibuprofen on eGFR?

A

by inhibiting PG synthesis it reduces renal blood flow → ↓ egfr

148
Q

mechanism of action of paracetamol?

A

may inhibit a peroxidase enzyme involved in conversion of arachidonic acid to prostaglandins
activation of descending serotenergic pathways
inhibits reuptake of endogenous endocannibinoids → ↑ activation of cannabinoid receptors → activate descending pathways (↑ pain modulation)

149
Q

why can paracetamol not be used as an antiinflammatory?

A

there is ↑ levels of peroxidase in inflammation so paracaemols ability to inhibit peroxidase is blocked

150
Q

side effects of paracetamol overdose?

A

liver damage → right subcoatsal pain after 24 hrs
n&V

± renal

151
Q

what can paracetamol be used for?

A

analgesic

antipyretic

152
Q

weak opioids?

A

codeine

tramadol

153
Q

strong opioids?

A

morphine

fentanyl

154
Q

why do opioids have an anti-tussive effect?

A

decrease activation of afferent pathways from relaying cough stimulus from airways to brain

155
Q

opioid drug target?

A

opiod receptor

156
Q

side effects of opioids?

A

N&V

constipation

157
Q

opioid over dose?

A

respiratory depression - bradypnoea
miosis
loss of consciousness

158
Q

mechanism if action of co-amoxiclav?

A

amoxicillin binds to penicillin binding protein → prevents transpeptidation
clavulanate inhibits beta lactamase

159
Q

what 2 drugs does co-amoxiclav consist of?

A

amoxicillin

clavulanate

160
Q

mechanism of action of lactulose?

A

non-absorbable disaccharide
causes water retention via osmosis → easier to pass stool
also metabolised by colonic bacteria → add laxative effect

161
Q

side effects of lactulose?

A

abdo pain
diarrhoea
flatulence
nausea

162
Q

what is often prescribed with opioids?

A

lactulose

163
Q

what is anandamide?

A

endogenous endocannibinoid → activates descending pathways

164
Q

what is the pain ladder?

A

mil pain - non-opioid ± adjuvant
mild to. moderate - weak opioid ± adjuvant ± non-opioid
moderate to severe - strong opioid ± adjuvant ± non-opioid

165
Q

treatment for opioid overdose?

A

oxygen

naloxone - opioid receptor antagonist

166
Q

what is codeine metabolised to?

A

morphine (active, slow metabolism)

norcodeine (inactive, fast metabolism)

167
Q

what is the purpose of the modulation pathway in pain?

A

it inhibits the sensory pain pathway to the brain so less pain is felt

168
Q

mechanism if action of opioids?

A

binds to the mu receptor on presynaptic neurones → uncouples G protein → ↑ K+ efflux → hyper polarisation → less likely to fire AP
inhibits influx of Ca2+ → ↓ vesicle exocytosis
inhibits adenylate cyclase → ↓cAMP
→→ less transmission of pain

activates inhibitory modulatory pathways → less pain felt

brs 2 (12 decks)

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