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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
DDP-4 inhibitors should be avoided in patients with what?
pancreatitis
26
what do DDP-4 inhibitors require to be effective?
residual functioning pancreatic beta cell activity
27
example of a sulphonylurea?
gliclazide
28
mechanism of action of sulphonureas?
inhibit ATP-sensitive potassium channel on pancreatic beta cells → ↑ depolarisation → Ca2+ influx → insulin vesicle exocytosis
29
side effects of sulphonylureas?
weight gain | hypoglycaemia
30
how is weight gain mitigated with sulphonylureas?
taken with metformin
31
example of SGLT-2 inhibitor?
dapaglifozin
32
mechanism of action of SGLT-2 inhibitors?
reversibly inhibits SGLT-2 in renal proximal convoluted tubule → ↓ glucose reabsorption → ↑ urinary glucose excretion
33
side effects of SGLT-2 inhibitors?
``` uro-genital infections (increased glucose load) slight decrease in bone formation can worsen DKA hypotension weight loss ```
34
what would cause SGLT-2 inhibitors to be less effective?
renal impairment
35
where is OCT-1 expressed?why is this important?
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
36
pharmacodynamics vs pharmacokinetics?
``` pd = drug actions on body pk = body actions on drug ```
37
4 types of drug targets?
enzymes ion channels transporter protein receptors
38
types of drug-receptor interactions?
electorstatic - eg vdws, h bonds hydrophobic - lipid soluble drugs covalent - least common, irreversible stereospecific
39
affinity and efficacy?
``` a = strength ability of a drug to bind a receptor, ↑ affinity = ↑ receptor occupancy e = ability of a drug to produce an effect once bound ```
40
agonists vs antagonists?
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
41
what is potency?
concentration/dose of a drug required to produce a 50% tissue response (EC50 and ED50)
42
major pharmacokinetic factors?
absorption distribution metabolism excretion
43
what is bioavailability?
the fraction of initial drug dose that gains access to systemic circulation
44
what is the bioavailability of IV administration?
100%
45
forms of drug administration?
``` oral inhlaed dermal/percutaneous intranasal IV ```
46
how are drugs normally transported into tissues?
diffusion across lipid membranes | carrier mediated transport
47
what form of drug is more lipid soluble?
unionised = more likely to diffuse across plasma membrane
48
pKa and pH are equal , what does this mean?
the drug will be 50/50 ionised/unionised
49
weak acids have what pKa range?
3-5
50
as pH decreases what happens to weak acids?
unionised form dominates
51
weak bases have what pKa range?
8-10
52
as pH decreases what happens to weak bases?
ionised form dominates
53
what pHs are best for weak acids and bases to be absorbed?
weak acid - low pH → more unionised → more lipid soluble | weak base - high pH → more unionised → more lipid soluble
54
what factors determine how much drug a tissue is exposed to?
regional blood flow plasma protein binding capillary permeability tissue localisation
55
regional blood flow of tissues? | what factors affect regional blood flow?
liver, kidneys, muscle, brain, heart exercise = more to muscle large meal = more to GI tract
56
which plasma protein is good at binding acidic drugs?
albumin
57
what determines how much of a drug is bound to plasma proteins?
free drug concentration affinity for protein binding sites** plasma protein concentration
58
what kind of capillary structure does the liver have?
discontinuous = allows for easy diffusion of drugs out of blood into liver tissue
59
what kind of capillary structure does the kidney glomerulus have?
fenestrated = allows for passage of some small drugs to pass from blood into kidney tubules = better excretion
60
explain tissue localisation
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
61
what liver enzymes are mainly responsible for drug metabolism?
``` P450 enzymes (phase 1) transferases (phase 2) ```
62
what are the 2 phases to drug metabolism?noverall effect?
phase 1 - add reactive polar group to drug phase 2 - add conjugate to reactive group =↓ lipid solubility = ↑ excretion elimination
63
how can phase 1 metabolism occur?
oxidation ** reduction hydrolysis
64
what are pro-drugs?
drugs that require metabolism in order to become pharmacologically active (parent drugs has no activity)
65
what happens in phase 2 metabolism?
attachment of substituent group to functional group from phase 1 → inactive , ↓ lipid soluble metabolite → facilitates excretion via urine/bile
66
what is first pass metabolism?
orally administered drugs are absorbed in small intestine and enter hepatic portal circulation → first pass through liver → heavily metabolised → ↓ drug reaching systemic circulation
67
solution to first pass metabolism? associated problems?
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
68
3 main methods for drug excretion via kidney?
glomerular filtration active tubular secretion passive diffusion across tubular epithelium
69
what drugs are most likely to be excreted via glomerular filtration?
low molecular weight drugs (<20000) = quicker rate of excretion compared to larger drugs
70
why is active tubular secretion important?
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
what drugs are more prone to passive diffusion in the kidney? what factors influence this?
``` 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
bile excretion is most effective at removing which metabolites?
phase 2 glucuronide metabolites
73
what is enterohepatic recycling?
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
4 core anticonvulsants?
lamotrigine, diazepam. levetiracetam, sodium valproate
75
mechanism of action of lamotrigine?
blocks voltage gated Na+ channels on glutamatergic neurons → prevents Na+ influx → less depolarisation and less glutamate excitotoxicity
76
side effects of lamotrigine?
rash* drowsiness* stevens-johnson syndrome suicidal thoughts
77
how can allergic reactions be avoided with lamotrigine?
introduce gradually
78
mechanism of action of sodium valproate?
inhibits GABA transaminase in inhibitory presynaptic terminal → less GABA breakdown → ↑ GABA conc in synapse
79
side effects of sodium valproate?
``` stomach pain diarrhoea drowsiness weight gain hair loss hepatotoxicity teratogenecity pancreatitis ```
80
what other enzyme does sodium valproate inhibit? what does this mean?
CYP/cytochrome P450 is inhibited → ↑ concentration of any co-administereed drugs
81
mechanism of action of diazepam?
binds to benzodiazepine site on GABA A receptor → ↑ Cl- influx → hyper polarisation of excitatory neurones
82
side effects of diazepam?
drowsiness respiratory depression jaundice haemolytic anaemia
83
why is diazepam not used for long term seizure suppression?
tolerance
84
levetiracetam mechanism of action?
inhibits synaptic vesicle protein SV2A on excitatory presynaptic terminal → prevents vesicle exocystosis → ↓ glutamate secretion
85
side effects of levetiracetam?
dizziness somnolence fatigue headache
86
what is benefit of levetiracetam compared to other anticonvulsants?
no effect on cytochrome P450 → no drug-drug interactions
87
which anticonvulsant should be given with caution to women of child bearing. age?
sodium valproate - teatrogenic, neural tube defects, ↓ IQ, autism
88
4 core drug classes for hypertension? and examples
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
mechanism of action of ACE inhibitors?
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
side effects of ACE inhibitors?
``` cough hypotension hyperkalaemia foetal injury renal failure (esp with renal artery stenosis) urticaria angioedema ```
91
ACE inhibitors are mostly what kind of drug?exception?
prodrugs - require hepatic activation | except lisinopril
92
what needs to be regularly monitored when taking ACE inhibitors?
eGFR | serum potassium
93
mechanism of action of calcium channel blockers?
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
side effects of calcium channel blockers?
``` ankle oedema constipation palpitations fliushing headaches ```
95
mechanism of action of thiazides/thiazide like diuretics?
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
side effects of thiazides/thiazide like diuretics?
hypokalaemia hypomatraemia metabolic alkalosis due to ↑ H+ excretion hypercalcaemia hyperglycaemia (hyper polarised pancreatic beta cells) hyperuriceamia
97
what happens with thiazides/thiazide like diuretics after 1-2 weeks?
lose their diuretic effects | maintain antihypertensive action due to vasodilation properties
98
mechanism of action of angiotensin receptor blockers?
act as non-competitive antagonists on AT1 receptors on kidneys and vascalature → prevents angiotensin from binding → vascular smooth muscle relaxation → ↓ blood pressure
99
side effects of ARBs?
hypotension hyperkalaemia foetal injury renal failure
100
ARBs are first line for which patients?(as opposed to ACEi)
afrocarribean patients
101
which condition are ACEi contraindicated?why?
bilateral renal artery stenosis | less angiotensin II results in less efferent arteriole vasoconstriction → lower renal perfusion→ acute renal failure
102
what cause hyperkalemia with ACEi?
sodium is not being reabsorbed, normally it would be exchanged for potassium which would be eliminated
103
5 core drugs for asthma?
``` salbutamol - SABA fluticasone mometasone budesonide montelukast ```
104
salbutamol mechanism of action?
agonist of B2 receptors on airway smooth muscle cells → activation reduces ca2+ entry → prevents smooth muscle contraction
105
side effects of salbutamol?
palpitations arrythmias tachycardia hypokalaemia
106
why are cardiac effects seen with salbutamol?
its not selective for the B2 receptor → can act on B1 receptor on cardiac cells
107
what drugs exacerbate the hypokalaemic effects of salbutamol?
corticosteroids
108
mechanism of action of fluticasone, mometasone and budesonide?
acts on glucocorticoid receptors → ↓ eosiniphils, monocytes, mast cells, macrophages and dendritic cells → ↓ cytokines produced eg. IL5&4
109
side effects of fluticasone, mometasone and budesonide?
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
difference between budesonide compared to fluticasone and mometasone?
budosenide has higher oral availability → some systemic absorption via GI tract its less potent
111
montelukast mechanism of action?
antagonist of CysLT1 leukotriene receptor on eosinophils, mast cells and airway smooth muscle cells → ↓ eosinophil migration, ↓ bronchoconstriction & ↓ inflammation induced oedema
112
side effects of montelukast?
``` diarrhoea fever headaches n&v mood changes anaphylaxis ```
113
what type of asthma is montelukast particularly useful for and why?
NSAID induced asthma
114
2 core drugs for gord?
PPIs - omeprazole, lansoprazole | H2 antagonists - rantidine
115
nsaid mechanism of action in gord?
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
3 examples of NSAIDs?
NSAIDS - ibuprofen, naproxen, diclofenac
117
sides effects of nsaids?
``` gastric irritation, ulceration, bleeding, perf ↓ creatinine clearance , neophritis bronchoconstrcition rashes dizziness tinnitus ```
118
mechanism of action of PPIs?
irreversible inhibitors of h+/k+ ATPase pumpkin gastric parietal cells → ↓ gastric acid secretion
119
how is PPI action prolonged?
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
side effects if PPIs?
``` headache diarrhoea bloating rashes abdominal pain \invreased risk of bone fracture ```
121
PPIs can mask symptoms of what?
gastric cancer
122
what enzyme does omeprazole inhibit? relevance?
cytochrome P2C19 → reduced activity of clopidogrel
123
what type of drugs are PPIs?
pro drugs
124
how are PPIs coated?why?
capsules containing enteric coated granules → prevents rapid degradation at low pH
125
mechanism of action of H2 receptor antagonists?
competitive antagonists of histamine H2 receptors on gastric parietal cells → prevent movement ofcAMP dependent movement of H+ ions → ↓gastric acid secretion
126
H2 receptor antagonist side effects?
``` low incidence diarrhoea dizziness muscle pains transient rashes ```
127
which H2 receptor antagonist inhibits cytochrome P450?
cimetidine
128
nsaid mechanism of action in gord?
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
PPIs should be avoided in what disease?
osteoporosis
130
mechanism of action of statins?
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
main side effects of statins?
muscle toxicity constipation diarrhoea
132
side effects of aspirin?
dyspepsia | haemorrhage
133
how does aspirin reduce risk of thrombosis?
inhibits COX2 → less thromboxane A2 produced from arachidonic acid → less platelet aggregation
134
which prostaglandin does aspirin reduce that is involved in pain and fever?
PGE2
135
mechanism of action of trimethoprim?
direct competitor of dihydrofolate reductase → inhibits reduction of dihydrofolic acid to tetrahydrofolic acid → less synthesis of purines required for dna and protein synthesis
136
side effects of trimethoprim?
diarhoea | skin reactions
137
what drug is trimethoprim often administered with?
co-trimoxazole to block bactrerial biosynthesis
138
what needs to be monitored with long term trimethoprim use?
blood counts for those at risk of folate deficiency | serum electrolytes for those at risk of developing hyperkalaemia
139
mechanism of action of gentamicin?
binds to bacterial 30s ribosomal subunit → disturbs translation of mRNA → dysfunctional proteins
140
side effects of gentamicin?
ototoxicity (hearing/balance) | nephrotoxicity
141
what class of antibiotic is gentamicin? what does this mean?
aminoglycoside , can pass through gram negative cell membrane in an oxygen dependent manor - ineffective against anaerobic bacteria
142
what conditions is gentamicin commonly administered for?
``` endocarditis sepsis meningitis pneumonia sx propylaxis ```
143
hypertension stages and ranges?
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
what drugs can improve proteinuria?
ACEi ARBs SGLT-2 inhibitors
145
drug used to treat UTIs?
trimethoprim
146
effect of trimethoprim on eGFR?
can falsely lower eGFR as it inhibits the active secretion of creatinine (serum creatinine ↑)
147
effect of ibuprofen on eGFR?
by inhibiting PG synthesis it reduces renal blood flow → ↓ egfr
148
mechanism of action of paracetamol?
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
why can paracetamol not be used as an antiinflammatory?
there is ↑ levels of peroxidase in inflammation so paracaemols ability to inhibit peroxidase is blocked
150
side effects of paracetamol overdose?
liver damage → right subcoatsal pain after 24 hrs n&V ± renal
151
what can paracetamol be used for?
analgesic | antipyretic
152
weak opioids?
codeine | tramadol
153
strong opioids?
morphine | fentanyl
154
why do opioids have an anti-tussive effect?
decrease activation of afferent pathways from relaying cough stimulus from airways to brain
155
opioid drug target?
opiod receptor
156
side effects of opioids?
N&V | constipation
157
opioid over dose?
respiratory depression - bradypnoea miosis loss of consciousness
158
mechanism if action of co-amoxiclav?
amoxicillin binds to penicillin binding protein → prevents transpeptidation clavulanate inhibits beta lactamase
159
what 2 drugs does co-amoxiclav consist of?
amoxicillin | clavulanate
160
mechanism of action of lactulose?
non-absorbable disaccharide causes water retention via osmosis → easier to pass stool also metabolised by colonic bacteria → add laxative effect
161
side effects of lactulose?
abdo pain diarrhoea flatulence nausea
162
what is often prescribed with opioids?
lactulose
163
what is anandamide?
endogenous endocannibinoid → activates descending pathways
164
what is the pain ladder?
mil pain - non-opioid ± adjuvant mild to. moderate - weak opioid ± adjuvant ± non-opioid moderate to severe - strong opioid ± adjuvant ± non-opioid
165
treatment for opioid overdose?
oxygen | naloxone - opioid receptor antagonist
166
what is codeine metabolised to?
morphine (active, slow metabolism) | norcodeine (inactive, fast metabolism)
167
what is the purpose of the modulation pathway in pain?
it inhibits the sensory pain pathway to the brain so less pain is felt
168
mechanism if action of opioids?
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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