Name Group MoA Effect Indication Side-effects Interactions and

contraindications
glyceryl Organic Convert to NO to activate Vasodilation of All Angina pectoris Bezold-Jarisch reflex (SNS PDE5 (for erectile
trinitrate nitrates guanylate cyclase to increase cGMP veins, muscular and MI activation due to venous dysfunction)
(GTN), to close Ca2+ channels arteries and aorta pooling causing hypotension increases effects
isosorbide dephosphorylation of myosin light Decrease venous Stable angina and brady) severe hypoTN
mononitrate, chain return, decrease pectoris: improves Tolerance due to it being a
isosorbide Low dose: dilate veins more than afterload, exercise tolerance prodrug requiring enzymes
dinitrate arterioles to decrease venous optimises blood and prolongs onset must have drug-free period
return and decrease cardiac flow of angina overnight
hypertrophy Relax other smooth muscle
High dose: venous pooling and Reduction in Tachycardia due to reflex
decrease arteriolar resistance, myocardial O2 against hypotension
decrease CO and BP demand Low dose (non-arteriole-
altering): facial flush, headache
High dose: pallor, weakness,
dizziness
Verapamil Non- Block voltage-gated Ca+2 channels Mainly cardiac SMC Variant (first line) Palpitations, headache, flushing Arrhythmias
dihydropyridi (L-type/slow) to decrease Ca+2 relax negative and stable angina Systolic HF
ne availability in SA node, AV node, inotropic and (second line). Hypotension
ventricular muscle/vasculature chronotropic UA may have some Severe angina
Class IV slow AP propagation effects demand vasospasm so could (dihydropyridines)
antidysryth and supply be an additional Beta blockers and
mic drugs (ejection) approach other drugs that
Diltiazem Cardiac and Dysrythmias: lower HR and BP
arteriolar SMC Cause partial AV Can inhibit CYP3A4/5
relax block to terminate (lots of drugs)
SVT and reduce Ca2+
entry
Prophylaxis of SVT
EAD/DAD to
suppress premature
ectopic beats
Shorten plateau of
AP and reduce force
AF and ventricular
response to it
nifedipine, Dihydropyrid Mainly arteriolar Hypertension
all end in ine SMC relax
ine increase supply
Propranolol, Beta1 Block beta1 adrenergic receptors in Negative inotropic Angina pectoris Tachycardia if stopped abruptly People with COPD,
all end in selective SA and AV nodes and ventricular and chronotropic, Stable angina: (1st Night terrors, severe asthma, HF due to
lol adrenocepor muscle to decrease Ca2+ decrease preload, line) nightmares lack of selectivity
antagonists LV work and O2 Hypertension no hypotension, fatigue, Arrhythmias (Can
For heart consumption to longer first line bronchoconstriction, cold cause fatal
failure: only Class II reduce CO and BP Some heart failure fingers / toes not extremely bradycardia)
carvedilol, antidysryth (decrease selective Other drugs that
bisoprolol mic drugs tachyarrhythmias, decreased HR response to lower HR and BP and
and remodelling of LV, exercise other drugs that
metoprolol inhibit SNS postural hypertension venous interact with
catecholamine- pooling in legs adrenoceptors
induced NSAIDs
cardiomyocyte Hepatically cleared
death) BBs and H2
Arrhythmias blokckers/SSRI
After MI Dont stop abruptly
Phase 4: decrease pacemaker Reduce heart rate Dysrhythmias:
current decrease sinus rate Decrease Ventricles: suppress
Phase 2: decrease Ca current, intracellular Ca SNS activity after MI
decreases repoling K+ and Cl-, overload that cause
decreases Ca stores and Inhibit afterdepol ventricular
spontaneous Ca release and DADs mediated dysrhythmias
automaticity AV node: increase
Prolong repol ARF, prevent
recurrent
supraventricular
tachy (SVT)
Atria: prevent
paroxysmal attacks
of AF due to SNS
Prazosin, all Alpha- alpha1-antagonism Vasodilation Hypertension less postural hypotension due to Many
end in osin blockers decrease common, less blood pooling in legs
peripheral vascular effective with worse headache, drowsiness
resistance side effects
carvedilol Mixed alpha Blocks both beta1,2 and alpha1 Vasodilation due to Hypertension
and beta- receptors alpha1 reduce Heart failure
adrenocepto peripheral vascular Angina (not really)
r antagonists resistance
beta-blockade Blocks both for more
prevents reflex effect but not very
tachycardia with effective nor widely
the net result that used
HR is slightly
decreased
Perindopril, ACE Inhibit ACE from converting AT-I to Vasodilation and Hypertension Dry cough (bradykinins local Angioedema
all end in inhibitors AT-II which would cause lower blood Heart failure mediators cause inflammation (swelling of face)
pril vasoconstriction, aldosterone, volume to decrease (mandatory) and swelling) local mediators
ADH, blood pressure Hypotension (may only be cause inflammation
initially) and swelling
Hyperkalaemia (arrhythmias) renal impairment
Dizziness increases risk of
hyperkalaemia
pregnancy
NSAIDs: reduce
antihypertensive
effect, increase risk
of renal impairment
because also lowers
GFR and
hyperkalaemia
Risk of
hyperkalaemia with
drugs that retain K+
Sartans because they
work in the same
way

Irbesartan, ARBs/Sartan AT1 receptor antagonists - inhibit As per ACE-I Hypertension As per ACE-I without the cough As per ACE-I
all end in s binding of angiotensin II to AT1 Heart failure as it does not stimulate ACE-I because they
sartan Angiotensin receptor (mandatory) bradykinins work in same way
II receptor Like ACE-I without
antagonists cough (just newer)
Frusemide Loop Inhibit NKCC pumps in ascending increase excretion Hypertension, Hypokalaemia or alkalosis: NSAIDs and ACE-I or
diuretics limb of loop of Henle rapid of water and oedema, heart decrease Na+ reabsorption ARBs=triple
decrease in Na, Cl and hence H2O sodium reduce failure (must) increase [Na+] in DCT + CD whammy as they all
Thiazide Inhibit Na/Cl transport in DCT blood volume Hypertension extra Na+ depolarises luminal decrease GFR
diuretics decreased reabsorption of Na/Cl decrease blood (mainly), oedema, membrane which: facilitates K+ renal failure
hence H2O pressure reduce heart failure excretion and increases
heart workload activation of luminal H+-ATPase
pumps on collecting duct cells

Amiloride Potassium Blocks ENaCs on luminal With another Hyperkalaemia: as it decreases

sparing membrane of CDs decrease Na+ diuretic to decrease blood volume without
diuretics reabsorption but maintain K+ hypokalaemia decreasing K+ conc
reabsorption
Spironolacto Aldosterone Blocks aldosterone receptors on Decrease blood Heart failure
ne antagonists DCTblocks Na/K pumps volume, venous
increase Na+, H2O secretion, return and preload
decrease K+ secretion
Inhibits hypertrophy and fibrosis
of cardiac muscle
Clonidine, Centrally- Stimulate alpha2 adrenoceptors in Lower BP by Hypertension (not Lots: dizziness, sedation, Bradycardia, CAD,
methyldopa acting CNS decrease SNS outflow negative first line) depression, erectile depression, diabetes,
antihyperten chronotropy and Used in hypertension dysfunction, dry mouth, HF
sives inotropy and in pregnancy hypotension (in brain) Other CNS
decrease Opiate withdrawal depressants, beta
peripheral blockers, TCAs
vasoconstriction Avoid abrupt
Moxonidine I1-imidazoline agonist increase Lowers BP by cessation
DAG (2nd messenger) synthesis decreasing
reduce SNS outflow peripheral
vasoconsriction
Bosentan Endothelin Prevents Endothelin-1 (ET-1) from Vasodilation=lower Pulmonary arterial Reduced Hb (must moniter), Hepatic impairment
receptor promoting vasoconstriction, cell s BP hypertension flushing, oedema, headache Contraindicated in
antagonists proliferation and vascular pregnancy due to
remodelling teratogens
Induces CYP2C9 and
CYP3A4 for faster
breakdown
Ivabradine Sinus node Blocks: I(funny) pacemaker Negative Heart failure
inhibitors currents mixed Na/K inward chronotropy Angina
 current initiates depol phase of reduce myocardial
SA node APs O2 demand
Increases
proportion of
cardiac cycle in
diastole increase
LV filling time and
increases coronary
perfusion
Sacubitril Neprilysin Inhibits: neprilysin (endopeptidase) Vasodilation, Heart failure Increases ATII Administered
inhibitors degrades ANP and BNP increases GFR, with valsartan
reduces SNS and Increases bradykinins cough
aldosterone Alzheimers disease
Digoxin Increase vagal activity, inhibit Positive inotropy Heart failure (2nd line
Na/KATPase elevate intracellular to ACE-I, diuretics
Na+/Ca2+ increase contractility and beta-blockers)
of heart AF
Adrenaline, Sympathomi Mimics SNS action including Heart works harder Heart failure
dobutamine metics stimulation of Beta1 receptors to secondary to MI
produce increase rate and force of (short-term but
heart contraction damages heart long-
term), cardiac stress
testing
Class Ia Sodium Blocks Na+ channels by binding to Reduce max rate of Dysrhythmias Procainamide is no longer used
Procainamid channel alpha subunits on the inside of the depol during phase As below: in Aus
e blockers sodium channel (must enter at 0
Class I depol so acts on channels where Doesnt block AP in
dysrhythmia sodium channel is open nodes bc
drug longer)inhibit AP on excitable conductile (Ca)
cells Use dependence:
Binds in depol (active) and can block high freq
dissociates in repol (inactive), As excitation w/o
below: blocking normal
frequency beats
longer depol=more
drug binding
As below:
Class Ib - Equal affinity for active/inactive Most effective in IV to treat Drowsiness, disorientation, Almost completely
Lignocaine state and influenced by length of depolarising tissue: ventricular convulsions due to effect on remove by hepatic
AP so the rate of dissociation At high rates of dysrhythmias in the CNS (excitable tissue) first-pass
during diastole decreases if the firing, where the immediate 2h half-life (Except
RMP is depol as the membrane diastolic is aftermath of MI when hepatic blood
repols effect is removed depolarised (RMP), flow is reduced, ie.
in the parts of the MI), hence reduce
heart where the AP dose if so
is longest
Class Ic - Very slow to associate and Long acting, reduce Suppress ventricular Prodysrhythmic: Sudden death after
flecainide dissociate frequency of ectopic beats MI due to VF (not
ectopic beats Prophylaxis against used after MI)
paroxysmal AF
Amiodarone Potassium Block K+ channels to prolong repol Prolong cardiac AP Dysrhythmias: re- Photosensitive skin rash and
channel and hence ARF entry tachycardia, slate-grey/blue discolouration
blockers suppress ectopic Thyroid abnormalities (similar
Class III activity, Wolf- to thyroxine)
antidysryth Parkinson-Whit Pulmonary fibrosis
mic drugs syndrome tachy Corneal deposits, peripheral
neuropathies, hepatitis
Adenosine Adenosine Acts on A1 adenosine receptor (in Slows rate of Dysrhythmias: Chest pain, shortness of breath, Theophylline and
SA and AV nodes) to activate ACh- pacemaker IV to terminate SVT dizziness, nausea other xanthine
sensitive K+ channels (KACh) potentials alkaloids
hyperpolarisation, more Na and Ca Increases AV nodal (bronchodilator)
trapped in refractoriness inhibit it by blocking
shorten APD, slow automaticity Inhibits DADs A1 receptors
Increase effects of decreased cAMP elicited by SNS Dipyridamole: blocks
with decreased SNS reduces Ca nucleoside
current potentiating
adenosine, hence
prolongs adverse
effects
Cardiac Increase rate of automaticity Hyperpolarisation Dysrhythmias: re- Prodysrhythmic: increase rate
glycosides (phase 4) Shortening of atrial entry involving AV of automaticity due to more
vagotonic: Inhibit Ca current in APs node Na+ increasing phase 4 slope
AV node Increase AV node Ventricular response
Activate ACh mediated K+ current refractory to AF
in atrium
Simvastatin: HMGCoA Mevlonate-like side-chain Inhibit cholesterol Hypercholesterolae Hepatotoxicity: elevation in Fibrates: elevate
all end in reductase competitively inhibits HMG-CoA biosynthesis mia (1st line) hepatic transaminase, no cases statin levels
Statin inhibitors reductase by negative feedback Lower blood of liver failure Some antibiotics and
(statins) increases sterol response cholesterol Myopathy: death due to things which change
element binding proteins (SRBEPs) Other rhabdomyolysis CYP3A4 elevate
to upregulate LDL receptors to cardioprotective statin levels
increase cholesterol uptake from effects:
blood increased LDL removal Enhance NO
from blood lower blood vasodilation action
cholesterol Increase plaque
stability: weaken
fibrous cap and
remove monocytes
Inflammation:
decrease CRP levels
Cholestyrami Bile acid- Bind to bile no cholesterol Reduce cholesterol Hyperlipidaemia Safest not absorbs in Reduces absorption
ne and binding reabsorption decrease blood reabsorption intestines stay in GI tract and of thyroxine, anti-
colestipol resins cholesterol increased LDL Increase cell removed by faeces inflammatories,
receptor synthesis removal of uptake of Interfere with absorption of other fat soluble
cholesterol from blood cholesterol folic acid and fat soluble drugs etc
vitamins etc
Constipation and bloating:
requires laxatives
Nicotinic acid Water-soluble B-complex vitamin Increase HDL-C Hyperlipidaemia Flushing: prostaglandins
niacin functions after conversion to NAD Lowers Dyspepsia: nausea, vomiting,
or NADP triglycerides diarrhoea
Inhibit GPR109A Reduce LDL-C
activationdecrease cAMP
increase hormone sensitive
lipase activity increase
triglyceride lipolysis and FFA
release
Liver: inhibits synthesis of fatty
aciddecrease triglyceride
synthesis reduce VLDL
production decrease LDL
Increase HDL increase VLDL
clearance
 Increase macrophage cholesterol
receptors for HDL mediated
clearance
Clofibrate Fibric acid Activate PPARalpha receptors Increase HDL-C Hyperlipidaemia Myositis: may lead to renal
All end in derivatives More LDL receptorsReduced LDL Reduce LDL-C failure (risk increases with use
fibrate fibrates in blood Lowers of statins
More apoA-1 and apoA2 more triglycerides Increased bile production: gall
HDL Also has stones
Fatty acid oxidation, increase LPL, antithrombolytic
reduced apoC-IIIdecrease effects
triglycerides
The Inhibits NPC1L1 transport Inhibit dietary Hyperlipidaemia
cholesterol protein inhibits luminal cholesterol uptake
absorption cholesterol uptake by jejunal
inhibitor - enterocytes to lower total and LDL
ezetimibe cholesterol
Increases
Reduced intestinal LDL
increased LDL receptors LDL
clearance from plasma
Heparin Anticoagulan Large endogenous molecule Rapid onset Anticoagulant Haemorrhage Protamine sulphate
ts present in mast cells with Inhibits fibrin Subcut or IV Thrombocytopenia (IgM or IgG antidote to form
histamine formation to (degraded in SI, in Abs against HEP-platelet inactive complex
Activates ATIII prevent thrombus hospital to monitor complex bind to platelets) with HEP
Fast but less effective: binds to formation side effects) Hypoaldosteronism (inhibits
ATIII attached to Xa synthesis) hyperkalaemia Pregnancy: high
- Also inhibits IXa, XIa and Osteoporosis, allergy oestrogen and
XIIa increased pressure
Slow but effective: binds to IIa and on veins with
ATIII (both) foetus+placenta
more clotting and
BP
LMW Too small to interact with thrombin Long lasting Anticoagulant
Heparin (second binding site) inhibition of Easy to administer at
Targets factor Xa to prevent thrombin home via SC
thrombin activation activation Longer half life
More predictable
dosing, no need for
hospital monitoring
Warfarin Competitively inhibits Vit K Inhibition of Anticoagulant Pregnancy: Vit K is the antidote
reductase so actions of Vit K activation of 1st trimester bone Metabolised by
inhibited: activation of II, VII, IX and factors II, VII, IX, X development abnormality CYP2C9 if
X 2nd +3rd trimester CNS increased activity
Takes several days to degrade abnormalities (gene
existing carboxylase so delayed Foetal death or miscarriage polymorphism) the
onset patient is not
S-warfarin is 3-5X more potent responsive to
than R-warfarin warfarin due to
more drug
metabolised
VKORC1 if
defective not
responsive as
enzyme doesnt
respond to warfarin
properly
Diet, alcohol, body
mass etc effect
metabolism, hence
high degrees of
variability b/w
patients
Drugs which inhibit
CYP2C9
warfarin
circulating
Loop diuretics and
valproate (anti-
seizure) displace
from protein binding
site
Antibiotics kill
bacteria that
synthesise Vit K
warfarin=toxic
Pregnancy
Vitamin K Anticoagulant
Thrombin Bind irreversibly to thrombin Inhibit fibrin Anticoagulant
inhibitors: activation
Hirudin-like
molecules
Thrombin Dabigatran: direct thrombin Anticoagulant
inhibitors: inhibitor
Serine Rivaroxaban: selective for Xa rather
protease than thrombin
inhibitors
Aspirin Antiplatelets Inhibits AA inhibits Reduce platelet Reduce incidental
cyclooxygenase inhibits TXA2 aggregation thrombus formation
Low dose (100-
300mg)
Adenosine Acts on A2 receptor cAMP Platelet Reduce incidental
Ca uptake into storage activation and thrombus formation
intracellular Ca aggregation
Dipyridamol Blocks adenosine Inhibits platelet Reduce incidental
e reuptakecAMP, PDE activation and thrombus formation
inhibition cAMP degradation, aggregation
activates PGI2 synthesis
Clopidogrel P2Y12 (ADP receptor antagonist) incidental Reduce incidental 8-10 days to be manifested as it
inhibits PI3K activation of thrombus thrombus formation only exerts effects on cells
GP IIb/IIIa complex cross- formation where VW factor has exerted its
linking of platelets affect
Glycoprotein Prevent GP IIb/IIIa cross-linking to incidental Reduce incidental
IIB/IIIA prevent platelet aggregation thrombus thrombus
receptor formation Eptifibatide (cyclic
antagonists peptide)
Tirofiban (non-
peptide absorbs
better but more
expensive)
Abciximab
(monoclonal
antibody against)
expensive, used
locally with
angioplasty and
avoiding thombus
 complications in NV
surgery

Prostanoids

Streptokinas Fibrinolytics Activates plasminogen plasmin Fibrinolysis Fibrinolysis Derived from beta-haemolytic
e more fibrin being converted to streptococci so problematic in
fibrin degradation products NT and FNQ with strep
infection rate due to secondary
immune response
Widespread haemorrhage
Tissue Serine protease enzyme digests Fibrinolysis Fibrinolysis Safer than streptokinase due to
plasminogen fibrin, fibrinogen, factors II, V and recombinant DNA technology
activators VII and clot-specific (fewer
(alteplase) More active on fibrin-bound haemorrhages) but expensive
plasminogen than plasma
plasminogen only clotting
Carbimazole, thyoureylene Inhibit iodination of thyroglobulin Decrease thyroid Hyperthyroidism Neutropenia and
methimazole s rapid decrease output of T3 hormone Oral administration agranulocytosis (1%)
production Sore throat
Reduce clinical Rash, joint pain, headache,
symptoms in nausea,
several weeks All side effects are reversible
(long life of T4 with cessation of treatment
and large stores)
Radioiodine Destroy thyroxine producing cells hyperthyroidism
as they take up iodine

levothyroxin thyroxine Replacement of deficient thyroxine Identical to natural Hypothyroidism Overdose mimics
e hormone hormone oral, first choice is hyperthyroidism
liothyronine due to
faster onset and
shorter duration
Fluticasone, Glucocorticoi Activate corticosteroid (GR) Asthma Cushing syndrome in prolonged
budesonide, ds receptors migration of receptor admin or sudden cessation (-ve
mometasone complex to nucleus bind to Addisons disease feedback)
glucocorticoid response elements
on DNA reduce expression of
cytokines, reduce inflammation
 Inhibit COX2 induction inhibit
PGE2/PGI2 production constrict
vessels and reduce immune cell
migration and vascular
permeability (oedema)
Upregulate beta2 receptor
expression
Reduce IL3 levels decrease mast
cell numbers
Combined Hypothalamic action: Prevent ovulation: Contraception Clot formation (use P only if Hormone
Oral progesterone frequency of LH and FSH levels Menopause susceptible) replacement should
contraceptiv GnRH pulses lack of pulsatile LH are suppressed, only be used for
e secretion mid-cycle LH surge Breast cancer, CV complication, menopause
Ethinyl Pituitary action: pituitary is absent, adverse effects higher than E treatment for a short
estradiol and responsiveness to GnRH, endogenous alone time to avoid side
levonorgestr oestrogen FSH release during steroid levels effects
el the follicular phase, progestin diminish, ovulation
oestrogen-induced midcycle LH does not occur
surge, prevent ovulation Reduction of
sperm transport in the fallopian fractures in
tube due to progestin producing menopause
thick, viscous mucus in the cervix
Minipill: low Progestin- Thickening of cervical mucus Blocks most Contraception
does only sperm penetration ovulation,
norethindron contraceptiv Endometrial alteration unaccommodating
e/norestrel e implantation uterus, thickening
daily w/o Blocks only 60-80% of ovulation mucus
interruption due to LH pulses
Subdermal
implants of
norgestrel:
slow release,
long action
Crystalline Thickening of cervical mucus
medroxypro sperm penetration
gesterone Endometrial alteration
acetate implantation
(Depo- Blocks GnRH pulses and inhibits
ovulation in virtually all patients
Porvera) IM
3 monthly

Oestrogen Replace oestrogen action to reduce hip fractures Menopause Increased risk of endometrial Hormone
only pill effects of menopause carcinoma, stroke replacement should
only be used for
menopause
treatment for a short
time to avoid side
effects
Tamoxifene, SERMS Antagonist: breasts Tissue-selective Breast cancer
raloxifene (selective Agonist: bone oestrogen oestrogen-sensitive
oestrogen Depends on relative expression of antagonist/agonist tumour
receptor ERalpha and beta, ligand effects on activity Osteoporosis
modulators) receptor, availability of cofactors,
activity of signalling pathways
Clomiphene Oestrogen H12 cannot move to expose Stimulation of
receptor coactivator binding sites on ligand- ovulation (fertility)
antagonists binding domain
Block pituitary ER
GnRH, LH, FSH
Enlargement of ovaries
Ovulation induction
fulvestrant SERDs Destabilises ER and facilitates Tamoxifene resistant
(selective degradation breast cancer
oestrogen Receptor ubiqitination
receptor Destabilisation of receptor
down- Increased proteolytic degradation
regulators of ERalpha but no change in ERbeta
Testosterone Androgens Actions of testosterone Male hypogonadism Suppress endogenous testicular
testosterone Angioedema: decreased Muscle wasting function (no LH and FSH) no
esters, bradykinin submucosal and associated with AIDS sperm, Gynecomastia (T
subcut oedema of resp and GIT Increasing muscle converted to E2), Hepatotoxicity
Muscle mass increasing, external mass and strength and LDL and HDL
genitalia increasing performance production, Virilisation in
enhancing women: Male pattern hair
Angioedema growth, infertility
Flutamide Androgen In conjunction with GnRH Metastatic prostate
receptor analogues (to prevent -ve cancer (T sensitive
antagonists feedback) tumour)
 Hirsutism in women

Cyproterone Androgen In conjuction with GnRH analogues Hirsutism in females

acetate receptor (to prevent -ve feedback) blocks T
antagonists
with
progestin
Dutasteride 5alpha- Block conversion of TDHT (more Prostatic volume Benign prostatic Impotence
reductase active form) decreases, Urinary hyperplasia
inhibitors flow rate increase
Finasteride Applied topically Male pattern Impotence
baldness

Pitocin, Oxytocin OXT receptors (GPCR) Ca2+ uterine Labour: induction, Normally progressing
syntocinon channels sensitivityCa2+ IC contraction during augmentation (when labour
SMC contraction labour cervix is dilated if not (overstimulation
PG productionuterine Uterine contraction progressing causes trauma to
contraction during labour reduces bleeding normally), mother and baby)
postpartum
haemorrhage
Short life
atosiban Oxytocin Inhibit uterine contractions Preterm labour
antagonist

Soluble Insulin: short acts more rapidly but for a shorter T1DM (short acting Weight gain (more glucose into
insulin and acting time than natural insulin with combined cell, only after reaching normal
insulin lispro enabling patients to inject intermediate or glycaemic state)
themselves immediately before long-acting) to be
the start of a meal taken preprandial
Isophane Insulin: forming finely divided amorphous T1DM Weight gain (more glucose into
insulin and intermediate solid or relatively insoluble crystals T2DM cell, only after reaching normal
insulin zinc -acting injected as a suspension from Hyperglycaemic glycaemic state)
suspensions which insulin is slowly absorbed emergencies
Intercurrent events
(eg infection, MI)
Hyperkalaemia
(insulin + glucose)
Insulin Insulin: long- constant basal insulin supply and lowers post- T1DM Weight gain (more glucose into
glargine acting mimic physiological postabsorptive absorptive plasma T2DM cell, only after reaching normal
basal insulin secretion by forming a glucose Gestational diabetes glycaemic state)
micro-precipitateprolonged not controlled by
absorption diet

Exenatide Incretin Stimulates insulin release and
(glucagon- inhibits glucagon release, slows
like peptide- gastric emptying lowers blood
1, GLP1) glucose after a meal
Exendin-4 Slows gastric emptying satiety
(like GLP1) food intake
hepatic fat accumulation
Metformin Biguanides Reduce hepatic glucose production
(decreased gluconeogenesis due to
low glucose in cell)
Activate AMPK (AMP activated
protein kinase) nuclear
receptor that inhibits expression of
genes important for
gluconeogenesis
glucose uptake and use in
skeletal muscle (insulin
resistance)
carb absorption, fatty acid
oxidation, circulating LDL
Tolbutamide Sulfonylurea Stimulate insulin release by binding
to sulfonylurea receptor on ATP-
sensitive K+ channels to depolarise
beta cells
Reduce postprandial
hyperglycaemia
Glitazones eg Thiazolidined hepatic glucose output
rosiglitazone iones effectiveness of insulin
glucose uptake in muscle
PPARgamma nuclear receptor
agonistsPPARy-RXR complex
binds to DNA transcription of
genes important in insulin
Mimics effects of T2DM Weight loss (energy
GLP1 but longer Gestational diabetes expenditure, leptin
acting not controlled by sensitivity, nauseafood
diet intake)
T2DM Weight loss (insulin
First line: low risk of sensitivity, intestinal glucose
hypoglycaemic, dont absorption, gluconeogenesis,
develop resistance energy metabolism (like
like with other drugs exercise), leptin sensitivity,
ghrelin, GLP1, alphaMSH,
NPY)
T2DM Newer drugs are more specific
on pancreatic beta cells K+
channel
Short duration of action reduces
risk of hypoglycaemia
Weight gain (insulin)
Differentiation of T2DM Weight gain (expansion of fat
adipocytes deposits)
Enhances uptake of
fatty acid and
glucose into cells
 signalling in adipose tissue, muscle
and liver

Sitagliptin, Gliptins Inhibit dipeptidylpeptidase-4 T2DM Weight neutral

vildagliptin (DPP4) potentiating endogenous
incretins lower blood glucose
Alpha- intestinal absorption of starch, Delays T2DM flatulence, loose stools or
glucosidase dextrin and disaccharides by carbohydrate diarrhoea, and abdominal pain
inhibitors inhibiting alpha-glucosidase in absorption and bloating
brushborderprevents breakdown Weight loss (glucose uptake)
of starch and disaccharides
glucose especially
postprandial hyperglycaemia
GLP1 in circulation glucose
Dapagliflozin SGLT2 Sodium glucose co-transporter Lowers BGL T2DM Genito-urinary infections (due
inhibitors (SGLT2/SGLT1) for glucose Other effects: to glucose in urinemore
reabsorption in nephron inhibited No hypoglycaemia bacteria)
removal of glucose from blood (as it only removes Weight loss (glucose loss)
by not allowing glucose to be whats filtered)
reabsorbed Reduction of BP
(polyuriahypovol
aemia)
CV safety
Rimonabant CB1 Endocannabinoid system is Obesity Suicidality withdrawn in 2008
cannabinoid involved in the regulation of
receptor feeding behaviour
antagonist
Sibutramine Inhibits reuptake of 5HT and NA Obesity NASNS+obesityHR
that regulate food intake and BP CV risk recently
food intake, dose dependant suspended due to risk
weight loss, satiety, visceral fat
LDL HDL energy expenditure
Orlistat Lipase Inhibit lipase Intestine fat Modest weight loss Obesity GI effects related to faecal fat
enzyme digestion calorie intake from (starts increasing loss
inhibitor lipids weight loss after 2 years) Stays in intestine so no systemic
effects
Locaserin Selective 5- Stimulates melanocortin release Modest weight loss Obesity
HTc agonist (alphaMSH) MCR4 receptor (starts increasing
stimulation food intake after 2 years)
Phentermine Amphetamin Inhibit VMAT (vesicular Obesity On its own, does not have huge
e-like monoamine transporter) to inhibit effect
psycchostim reuptakemonoamine release
ulant Activate TAAR1monoamine
indirect release
sympathomi NA/DA release
metric hypothalamic neuropeptides
reduce food intake
Phentermine neuronal inhibition + all the Considerable and Obesity
+ topiramate effects for phertermine reasonably
maintained
weightloss
Bupropion Stimulate DAT/NAT (DA/NA Obesity
transporters) Inhibit NA/DA
reuptake and stimulate NA/DA
release POMC, melanocortins
(and beta-endorphin (stimulate
food intake))
reduce food intake
Bupropion + Naltrexone inhibits beta-endorphin Considerable Obesity
naltrexone receptor to inhibit the effect of weight loss
food intake
Liraglutide GLP-1 body weight Obesity (higher dose
agonist daily injection)
(similar to T2DM
exenatide)
Metoclopra D2 receptor Blocks DAs inhibitory action on D2 Prokinetic agent Constipation, Metoclopramide:
mide, antagonists receptor on myenteric motor nausea, vomiting extrapyramidal effects
domperidon neurons so ACh is released for (Parkinsons) galactorrhoea
e excitation peristalsis Domperiodone:
5HT4 receptor agonist, 5HT3 (vagal PRLgalactorrhoea,
and central) antagonist, gynaecomastia, disrupted temp
sensitisation of muscarinic control
receptors on smooth muscle
Reduce nausea and vomiting
through antagonism of D2 Rs in
CTZ
codeine, Opioids Activate opioid receptors in Antimotility, Diarrhoea Constipation, abdo cramps,
diphenoxylat bowelmotility fluid antispasmotic drowsiness, dizziness
e, absorption
loperamide
(Imodium
BBB cross
only a bit)
Cyclizine and H1 Acts centrally on CTZ, Morning sickness
promethazin antagonists antimuscarinic effect
e
Scopolamine Muscarinic Acts on CTZ, inhibits PNS action on Anti-motility, anti- Motion sickness, Dry mouth, blurred vision
antagonists vomiting emetic diarrhoea
mAChR Inhibits PNS action on GI motility
antagonists
Ondansetron 5-HT3 Acts on vagal nerve and CTZ. Post-op, radiation,
e antagonists Prevents serotonin CTZ and cytotoxic drug
vagal vomiting reflex (inhibits nausea
stimuli reaching CTZ)
Antacids (salt Chemically neutralise stomach acid Gastric ulcers, GORD Uraemia, milk-alkali syndrome In renal failure:
combos) NaCO3 rapid neutralising effect, (mild hypercalcemia aluminium can cause
water soluble rapid absorption polyuria/polydipsia/dehydration osteoporosis,
metabolic alkalosis bicarbonate retention encephalopathy and
CaCO3 rapid and effective metabolic alkalosis renal proximal myopathy
neutralising of gastric H+, CO2 calcium retention severe
belching, nausea, abdo distention, hypercalcemia renal failure
flatulence, Ca2+ rebound acid (Burnetts sy.))
secretion
Simethicone Anti-foaming Surfactant to reduce gas in Reduces gas in GIT GORD, bloating,
stomach abdo pain due to gas

Cimetidine, Histamine Competitively inhibit H2 basal and food- Gastric and duodenal gynaecomastia, decreased
ranitidine H2 receptor receptorshistamine and stimulated acid ulcers libido, impotence
antagonists gastrin stimulated acid secretion secretion by 90%
Omeprazole Proton pump Activated by proton-driven 80-90% reduction Gastric and duodenal Abdo pain, constipation, Metabolised by
inhibitors conversion to sulfenic acid and in acid secretion ulcers flatulence, diarrhoea, CYP2C19 interferes
sulfenamide in the acidic secretory that only returns impotence, gynaecomastia, with action of
canaliculi of the parietal cells upon enzyme mental confusion, arthralgia clopidogrel (reduce
sulfenamide interacts covalently replacement risk of bone fractures and anti-platelet action)
with sulfhydryl groups in H+/K+ infections
Reduces B12 absorption
 ATPase pump Irreversibly
inhibits
Long lasting (24-48 hours) t1/2 is
2hrs but accumulates in canaliculi
and irreversibly inhibits enzymes
Misoprostol Mucosa Pro-drug converted to misoprotol PG analogue Gastric and duodenal Diarrhoea, abdo pain Pregnancy: causes
cytoprotectiv acid in liver and parietal cells (mucosa cyto- ulcers uterine contractions
e agent activates EP3 prostaglandin Rs protective agent) Exacerbates
cAMP, gastric acid secretion inflammatory bowel
AND activates EP2/4cAMP, disease
mucin and bicarb secretion
Sucralfate Mucosa Sucrose + aluminium creates cross- Gastric and duodenal constipation Prevents absorption
cytoprotectiv linked polymer in acid =physical ulcers of some drugs
e agent barrier in stomach adjust timing of dose
Renal failure (Al)
PPI + triple H. Pylori
Amoxicillin + therapy X 1-
metronidazol 2weeks
e/(or)clarithr
omycin
Alprazolam Benzodiazepi Allosteric interactions with Anxiolytic effects Generalised anxiety Sedative, hypnotic, anaesthetic, Patients with
(xanax) nes benzodiazepine-GABAA receptor disorder anticonvulsant, muscle relaxant personality disorders
Chlordiazepo complex Use for short Panic disorder effects (alpha1) or hx of substance
xide (Valium) GABAA receptors comprised of periods of time Situational anxiety Impair cognitive performance abuse are
Diazepam, alpha1,2,3,5 subunits with immediate Drug withdrawal and memory particularly
any zepam Alpha2 mediates anxiolytic effects effect and in Adversely affect muscle control susceptible to
to enhance inhibitory effects of conjunction with Potentiate effects of other abuse/dependence/
GABAinhibit amygdala activity other meds (SSRIs) sedatives (like alcohol) habituation
(alpha1 mediates sedative effects) or psychotherapy Habituation, dependence,
abuse
Tolerance (chronic) need
higher dose abuse
Buspirone Agonist for presynaptic serotonin Effective following Generalised anxiety No benzodiazepine side effects Increases symptoms
5-HT1a and 5-HT2 Rs and partial chronic treatment disorder (not others) Heightened anxiety at start of of panic disorder
agonist for postsynaptic Rs as it first increases treatment (increase firing rate
Presynaptic: causes full inhibition inhibition before of locus coeruleus
acutelyserotonin preventing imp. In panic)
downregulate receptors inhibition of 5-HT
presynaptic inhibition chronically release
 + stimulates post-synaptic
response to 5-HT always

Propranolol Beta Treats physical symptoms such as Peripheral Performance anxiety Hypotension
and other adrenergic sweating, tremor, tachycardia (eg public speaking)
lols antagonists Lipophilic so it can have CNS action
(but mainly PNS response)
Fluoxetine Selective Serotonin regulating amygdala and Antidepressant Anxiety (1st line) Nausea, anorexia, insomnia, Dont use in
(Prozac) Serotonin (5- locus coeruleus in anxiety Anxiolytic following Depression loss of libido, failure to orgasm, combination with
HT) reuptake Blockade of 5-HT reuptake both chronic treatment suicidal ideation (stimulation of TCAs inhibit
inhibitor pre- and post- synaptically 5- wrong 5-HT receptor or in hepatic CYP2D6
(SSRIs) HT downregulation of 5-HT1a Rs wrong region of brain) enzyme impaired
(autoreceptors)5-HT Not suitable for children<18 TCA metabolism
releasedpost-synaptic receptor Fluvoxamine=obsessive TCA toxicity
activation antidepressant compulsive disorder only
post-synaptic receptor Some increase in anxiety at first
downregulation side-effects start low and go slow
Dont cause cheese reaction like
MAOs
Less effective than TCAs in
treating severe depression

Venlafaxine 5-HT/NA Serotonin regulating amygdala and Antidepressant Anxiety (1st line) Some increase in anxiety at first
reuptake locus coeruleus in anxiety Anxiolytic following Depression start low and go slow
inhibitors Metabolised to desvenlafaxine chronic treatment Neuropathic pain Lack major receptor-blocking
(SNRIs) antidepressant and fibromyalgia actions fewer side effects
Duloxetine Serotonin and NA modulate pro- compared to TCAs
nociceptive and anti-nociceptive Less risk of cardiac effects (safer
effects from the brain stem (pain) in overdose compared to TCAs)
Bupropion Noradrenalin active metabolites Inhibits Depression Unlike cocaine/amphetamines
e reuptake NA/DA uptake Nicotine dependence does not cause euphoria (no
inhibitors abuse potential)
Reboxitine (NARIs) Highly selective NA uptake ADHD
and inhibitors but efficacy for
atomoxetine depression is less that TCAs
Tricyclic Block the uptake of NA/5-HT/(DA) Antidepressant Depression related Sedation, confusion, motor
antidepressa by nerve terminals to anxiety incoordination (wear off in 1-2
nts (TCAs) 5-HT: emotional symptoms Depression weeks)
NA: biological symptoms Interference with autonomic
Metabolites of TCA differ in action control: atropine-like (mACh)
 dry mouth, blurred vision,
constipation and urinary
retention; postural hypotension
(adrenergic transmission in
medullary vasomotor centre);
sedation; ventricular
dysrhythmias, QT interval
Mirtazapine Monoamine blocks 2 adrenoceptorsNA, 5- Antidepressant Depression
receptor HT blocks 5-HT2C,2A,3 receptors
antagonists reduce unwanted SEs
alpha2 block histamine H1 receptors
adrenergic sedation
Trazadone 5-HT2a/2c receptor antagonists
with 5-HT reuptake inhibition

Mianserin Blocks H1, 5-HT2a and alpha2 Bone marrow depression

adrenoceptors requiring regular blood counts
use declined
Phenelzine, Monoamine Irreversible, long-acting, non- Antidepressant Depression related Postural hypotension (SNS Cheese reaction:
tranylcypro oxidase selective between MAO-A/B to anxiety block), atropine-like effects (see tyramine-containing
mine inhibitors MAO breaks down monoamines Major depression TCAs), weight gain, CNS food (cheese, beer,
(MAOIs) that has not stimulation restlessness, wine etc) because it
responded to other insomnia, hepatotoxicity and usually removed by
treatment neurotoxicity MAO, converted to
Moclobemid Reversible, short-acting, MAO-A Unresponsive major NA hypertension
e selective: Cheese reaction less depression
severe and shorter lasting than Social phobia
with
Aspirin, NSAIDs Inhibit COX2 Ibuprofen: good for Pain Due to inhibition of COX1
ibuprofen, Suppression of prostanoid inflammation housekeeping enzyme:
paracetamol synthesis in inflammatory cells Paracetamol: good GI: dyspepsia, nausea, vomiting,
(not Anti-inflammatory: PGE2 and for pain gastric ulcers, (suppression of
traditionally, prostacyclin vasodilation and gastroprotective prostaglandins
mainly oedema in gastric mucosa
central Analgesic: PG generation Reversible renal insufficiency in
effects) sensitisation of nociceptive nerve susceptible individuals due to
endings to inflammatory mediators compensatory PGE2 mediated
such as bradykinin and 5-HT vasodilation being inhibited
Antipyretic: prevent IL1 from Inhibition of COX2 in macula
releasing PGs in CNS reduce densa hypertension
 hypothalamic set point for temp
reduce fever
Celecoxib
(coxibs)
Opioids Presynaptic: Activate mueGPCRs
cAMP and block Ca2+ channels
Ca2+ entryinhibit NT release
Removal of inhibitory influence
causing excitation disinhibition
Postsynaptic: K+ conductance
Inhibit neuronal firing
Morphine Mue opioid R agonist
Analgesia, euphoria and sedation,
suppression of cough
Codeine mue opioid R agonist
Metabolised to morphine to exert
analgesic effect
Tramadol Weak mue opioid R agonist
(1/6000 of morphine action
substance P, enhances
inhibitory pathways
Also inhibits NA and 5HT reuptake
Pethidine mue opioid R agonist but less
potent than morphine. Faster
acting when delivered orally
compared to IV/SC
Aspirin-sensitive asthma
bronchospasm
Selective COX2 Remove GI side effects but still
inhibitors effects healing of existing ulcers
Reduce nociceptive Due to acting on other GPCR
signal transmission subclasses: delta and kappa
Reward and abuse potential:
disinhibition of ventral
tegmental area to enhance
dopamine release in nucleus
accumbens
Moderate to severe Respiratory depression: Gall stones
pain sensitivity to PCO2 and inhibit (contraction of
Soft tissue pain resp rhythm generation, gallbladder and
Not neuropathic pain depression of CV function constriction of
GI effects: tone motility of sphincterpressu
MI GIT constipation, delay in re in biliary tract)
(painmyocardi gastric emptying, nausea and
al O2 demand) vomiting
pupillary constriction
histamine release
bronchoconstriction and
hypotension
Moderate to severe CP450 2D6 deficient
pain people will not
experience analgesic
effect
Mild to moderate
pain (as effective as
morphine or
pethidine)
Muscle spasms
(OBGYN)
Hydromorph mue opioid R agonist Moderate-severe
one 8X as potent as morphine pain
Generally used in
severe pain and
opioid tolerant
patients
Oxycodone mue opioid R agonist Pain associated with Strong abuse potential
equivalent to morphine malignancies
Moderate severe
pain (in conjunction
with non-opioid
analgesics)
Fentanyl mue opioid R agonist, 80X more Severe pain Shorter duration of resp
potent than morphine depression effects
High dose muscle rigidity
Lignocaine Local Bind reversibly to a receptor site Sensory nerve Treat/prevent acute Risk of systemic toxicity:
anaesthetic within the pore of the Na+ fibres (C and pain hypotension, bradycardia,
channels in nerves block ion Adelta) with small Diagnosis and respiratory depression
movement through the pore diameter and slow treatment of
reversibly block AP responsible for conduction velocity persistent pain
nerve conduction can cause are most
both sensory and motor paralysis susceptible Modes of admin:
in area innervated (large diameter topical, infiltration,
Lignocaine binds preferentially to motor neurons are intrathecal, epidural
inactivates state of channel and least effected)
stabilises it here
Weak base and worked best in
charges form but passes across to
inside of cell in uncharged form
Use dependence: rate of block of
Na+ channels by lignocaine
depends on rate at which nerve is
stimulated block is faster if
channels are opening frequently
Hydrophilic pathway: charges LAs
(use-dependent) ending inside
channel
 Some LAs (e.g. benzocaine) are
uncharged rate and extent of
block are pH independent
Hydrophobic pathway: no use-
dependence within membrane
Carbamazepi Anticonvulsa dampens down abnormal neuronal Bipolar Trigeminal neuralgia Serious side effects
ne, sodium nts old activity that follows nerve injury
valproate Na+ channel blockade
Gabapentin, Anticonvulsa work by blockade of presynaptic Not anti-epileptics Neuropathic pain
pregabalin nt - new voltage gated calcium channel
NT release
Chlorpromaz Antipsychoti Block D2 dopamine receptors with Relieves +ve Schizophrenia, Motor disturbances
ine, c 1st gen disproportionate D2 affinity symptoms of Parkinsonian features = acute
haloperidol schizophrenia dystonia, tardive dyskinesia
Mania of Bipolar: Antipsychotic malignant
olanzapine given syndrome: muscle
with fluoxetine rigiditybody tempmental
(antidepressant) confusion
2nd gen drugs with PRL= (DA PRL via
lithium or valproate tuberoinfundibular pathway
(effective against with D2 receptors. Blocking D2
mania) breast swelling, pain,
lactation) effect is maintained
Anticholinergic symptoms:
block muscarinic receptor
blurred vision, intraocular
pressure, dry mouth + eyes,
constipation, urinary retention
Reduced pleasure (D2 in
mesolimbic reward pathway)
Worsened -ve symptoms
(cortical D2)
Clozapine, Antipsychoti Blocks D2 dopamine receptors but Metabolic syndrome (weight
risperidone c 2nd gen also acting on other receptors to gain, risk of T2DM and CVD):
side-effects H1, 5HT and muscarinic
Nigrostriatal pathway: Anticholinergic symptoms
5HT2aDA release Sedation: H1
Hypotension: alpha-
adrenoceptor blockade
 Mesolimbic: D2 and 5HT2a Clozapine: agranulocytosis
antagonism counteract DA Phenothiazines: obstructive
function (would +ve symptoms) jaundice due to drug-induced
Mesocortical pathway: D2, oedema of the bile ducts
5HT2a and glutamate release
-ve symptoms
5-HT2a, muscarinic, histamine H1
and alpha-adrenergic activity to
reduce extrapyramidal side effects
Quetiapine: 5HT1a agonist 5-
HTDA release in striatum and
prefrontal cortex-ve
symptoms
Olanzapine: inhibit cholinergic
interneurons in striatum that have
inhibitory D2 receptors. Inhibition
of D2muscarinic side effects
but when it inhibits both there are
few side effects except for
muscarinic antagonist effects
Lithium Mimics role of Na+ in excitable Bipolar Li toxicity: Monitoring plasma
tissues (targets voltage-gated Na+ Prophylaxis and nausea, vomiting, diarrhoea, concentration is
channels for AP generation) treatment of mania tremor, weight gain, hair loss, essential (Excreted
Inhibition of inositol and prophylaxis of thyroid enlargement w/ by kidneys from 12h-
monophosphatase blocks bipolar or unipolar hypothyroidism, cognitive 2weeks.
phosphatidyl inositol (PI) pathway disorder (manic impairment, cerebellar effects Accumulates slowly
where inositol phosphate is depression or renal: polyuria (+ thirst) through over 2 weeks before
hydrolysed to free inositol reccurent inhibition of ADH nephrogenic a steady state is
PIblocks inositol triphosphate depression) diabetes insipidus; reached.
formation through PI-linked aldosteroneNa+ 1.5mmol/L=toxic)
receptors (Gq protein) blocks 0.5-1mmol/l IN retention; renal tubular damage Na+ depletion Li
effects (Ca2+) PLASMA for several with chronic treatment, renal excretion due to Li
Inhibition of glycogen synthase weeks = clinical failure (MUST monitor renal reuptake in proximal
kinase 3 (GSK3) isoforms efficacy function regularly) tubule.
(downstream of insulin, BDNF etc) >1.5mmol/L=toxic acute lithium toxicity: various Diuretics acting
no GSK3 inhibitory effects Oral neurological effects, progressing distal to proximal
downstream activation of Narrow therapeutic from confusion and motor tubule also have this
neuroplasticity genes window and long impairment to coma, effect
duration of action convulsions and death if the
 neuroplastic changes and synaptic plasma concentration reaches Renal disease = Li
remodelling functioning 3-5 mmol/l toxicity
Direct: competes with Mg
Indirectly: stimulates PI signalling
so PIP3 AKT inhibits GSK3
Valproate, Antiepileptic Elevate synaptic GABA (inhibitory) Acute attacks of
carbamezapi drugs tone mania. Long-term
ne MOA valproate: treatment of bipolar
expression of glutamate Valproate is given
decarboxylase (GAD67) in with lithium
brainGABAergic transmission Trigeminal pain
protein kinase C (PKC) in manic
patients
Inhibits GSK3 (see lithium)
Lamotrigine Antagonism of glutamate Preventing
recurrence of mania
and depression in
bipolar
Gabapentin, Block Ca2+ channels Adjunct therapies to
pregablin glutamate treat chronic pain
and anxiety with
bipolar
Can also be used for
Anxiety disorders
Neuropathic pain
Levodopa + Levodopa synthesised to dopamine DA synthesis Parkinsons Disease
carbidopa by DOPA decarboxylase (early stage as DA
Carbidopa prevents SNS uptake of cells still need to be
L-DOPA as it inhibits DOPA present)
decarboxylase but does not pass
BBB (prevents side-effects of L-
DOPA without preventing MoA)
Tolcapone COMT Prevent DA breakdown to 3MT by DA at synapses Parkinsons Disease Does not have huge effect
inhibitor COMT (then to HVA by MAO-B) (early stage as DA because DA releasing cells need
cells still need to be to be present for the DA to be
present) made/released/cause an action
Seligiline MAO-B Prevent DA breakdown to DOPAC DA at synapses Parkinsons Disease And does not prevent
inhibitor by MAO-B (then to HVA by COMT) progression surgery needed
 (early stage as DA
cells still need to be
present)
pramipexole DA receptor Stimulate D1 and D2 postsynaptic Postsynaptic Parkinsons Disease
agonists receptors in striatum dopaminergic (early stage as DA
response cells still need to be
present)
Donepezil Cholinestera Non-competitively inhibits AChE to Slight improvement Alzheimers disease Do not prevent progression of
se (AChE) Prevent breakdown of ACh into of cognitive Mild-severe the disease
inhbitors acetate and choline to compensate function
for the loss of cholinergic
transmission
Memantine NMDA Weak noncompetitive antagonist Reduces rate of Alzheimers disease
antagonists (binds to Mg2+ binding site of the clinical Moderate-severe
channel) of the NMDA-type deterioration
glutamate receptor to prevent
excessive activation while
preserving normal function
Barbiturates Antiepileptic GABA-A channel modulator GABA activity Epilepsy
influx of Cl- to hyperpolarise cell Corrects
prolongs duration but not mismatch of GABA
frequency of GABA channel and
opening (like a chemical stent) Glutamatepreve
Limits sustained repetitive firing at nts seizure
higher conc generation
Clonazepam Benzodiazepi Allosteric modulator of GABA-A GABA activity Epilepsy
and nes receptors stimulate GABA Corrects Treatment of acute
diazepam transmission mismatch of GABA seizures
and Glutamate Diazepam: status
epilepticus
Valproate Antiepileptic Weak inhibition of GABA GABA activity Epilepsy most Higher incidence in
transaminase (reuptake) forms including teratogenesis
Some effect on Na+ and T-type absence seizures
Ca2+ channels
Potentiation of GABA activity post-
synaptically
Gabapentine GABA analogue with high lipid GABA activity Epilepsy Drowsiness, dizziness, ataxia,
solubility (not an agonist) fatigue
 augment GABA release from
synaptic terminal)

Carbamazepi Use-dependent block of Na+ Inhibits Na+ Epilepsy most Sedation, ataxia, mental Strong liver inducing
ne channels channel function forms except disturbances, water retention agent many
prevents spread absence seizures interactions
Particularly
psychomotor
epilepsy
Neuropathic pain:
trigeminal neuralgia
Bipolar disorder
Drug withdrawal
Phenytoin Use-dependent block of Na+ Inhibits Na+ Epilepsy not Saturation kinetics so plasma Interactions are
channels, time for recovery of channel function absence seizures concentration can vary widely common
voltage-gated NA+ channels prevents spread monitoring is recommended
repetitive neuronal firing, affect Confusion, skin rashes,
Na+ excretion during refractory anaemia,
(alters sensitivity of neuron to Occur in all AEDs but worse
hyperexcitation due to change in with phenytoin:
RMP) gum hyperplasia (in children
and young adolescents: altered
collagen metabolism),
teratogenesis: spina bifida,
cleft palate, congenital heart
defects, microencephaly
Ethosuximid Block T-type Ca2+ channels Inhibits of T-type Absence seizures; Nausea, anorexia
e Ca2+ channel may exacerbate
function other forms
Disulfiram Inhibits ALDH (alcohol Abstinence is Alcoholism
dehydrogenase) reinforced to avoid
acetaldehyde after drinking the resulting
toxic feeling very unpleasant adverse reaction
Naltrexone Mu opioid receptor antagonist feelings of Alcoholism
effects of endogenous opioids reward with
alcohol/craving
Mu opioid receptor antagonist effects of street Opiate addiction No agonist effect so will not
Competitively blocks the binding of heroin satisfy craving or relieve
heroin protracted withdrawal
symptoms
 Does not appeal to most heroin
addicts

acamprosate Weak antagonist of NMDA mild protacted Alcoholism

receptors and activator of GABA-A abstinence
receptors syndromes
feeling of
needing alcohol
Nicotine Maintains blood nicotine level Suppresses Nicotine addiction
replacement symptoms of
nicotine
withdrawal to
allow abstinence to
last longer
Buproprion antidepressa Enhances both NA and DA abstinence rates Nicotine addiction
nt transmission via reuptake Depression
inhibition DA levels Obesity (with
naltrexone)
Varenicline Partial agonist at the alpha4beta2 Reduces cravings; Nicotine addiction Risk of suicidal ideation
subtype of the nicotinic ACh prevents
receptor withdrawal
symptoms
Methadone Opioid agonist maintains Suppress the Opiate withdrawal:
stimulation of receptors symptoms of detoxification
opiate withdrawal

Replaces the Opiate addiction

effects of street
heroin
Clonidine Alpha2 adrenergic agonist Alleviates Opiate withdrawal:
adrenergic neurotransmission symptoms of detoxification
from the locus coeruleus opioid withdrawal
Mimics opioid effects
Acupuncture Activation of endogenous opioid Opiate withdrawal: Not yet found to be practical
system without medication detoxification

Buprenophin Partial Opioid agonist Replaces the Opiate addiction

e maintains stimulation of receptors effects of street
heroin