1.

Loop
Furosemide
Bumetanide
2. Thiazides
Hydrochlorothiazide
Indapamide
Bendroflumethiazide
3. Carbonic Anhydrase Inhibitors
4. K+ Sparing
Spironolactone (SEs!)
Eplerenone
5. Very Osmotic diuretics
(urea, mannitol)
2Cl/Na/K, Hypocalcaemia, hypokalaemia, metabolic alkalosis (na/h)
Na/H, hypercalcaemia, metabolic acidosis
Block formation of H+ which disables the H/Na channel, metabolic acidosis, weak diuretic
Aldosterone antagonist, hyperkalaemia
Calcium Channel Blockers
Dihydropyridines; Nifedipine
Benzothiazepines; Diltiazem
Phenylalkylamines; Verapamil
Vasodilator Nitrates;
Non-selective (effects on the heart)
Sublingual nitroglycerin
Isorbide Dinitrate
5 Isobride mononitrate (100% BA)
Beta blockers
Hydrophilic; Atenolol
Hydrophoic; Propanolol
Alpha and Beta
blocking; Carvedilol
Others;
Nocorandil; Opens the ATP-ase
channel to allow rapid
depolarisation and inhibit the
voltage gated L-Ca channels. (fat
soluble) opposing drug would
be Digoxin.
Ranolazine (CYP); Closes the
funny sodium channel to limit
the Na/Ca co-transporter and
hence lower intracellular Ca.
Ivadabrine; Blocks the funny
sodium channel to decrease the
HR. Selectively inhibits the sinus
node. Good for those who are
intolerant to BBs.
Recall the different types of angina;
(a) Stable
(b) Vasospastic
(c) Unstable
Ace-inhibitors
Beta Blockers
Ca Channel Blockers
Diuretics
ACE INHIBITORS
(ARBS)*
Lisonopril
Atenolol
Propanolol
Candesartan*
Larsartan*
Beta Blockers
Carvedilol
(non-selective)
Bisoprolol
(B1 Selective)
Nebivolol
(NO effect)
Verapamil (Phenyl)
Diltiazem (Benzo)
Nifedipine (DHP)
Ca Channel
Blockers
Thiazides
Hydrochlorothiazide
Indapamide
Bendroflumethiazide
1. Statins; Pravastatin (weakest but no CYP interaction), Atorstatin
(strongest) CRP guide to prognosis.
2. Bile Acid Sequesterants; Interfere with enterohepatic circulation
Decrease TAG syn and LDL (But fat soluble vitamin absorption is also
impeded!) low compliance due to GI side effects
3. Ezetimibe; Like the above except no interference in vitamin
absorption.
4. Nicotinic Acid; Increase HDL and prevent TAG and cholesterol
synthesis in the peripheries
5. Fibrates; (Clofibrate and Gemfibrozil) Bring about lipolysis and Beta
oxidation by interacting with peroxisomes and PPAR alpha receptors
(decrease Apo CII levels)
6. Fish Oils; Shown to lower LDL and slightly increase HDL.
Gemfibrozil and
statins Adverse
effects such as
Rhabdomolysis
Thyroid Pharmacology
HYPERTHYOIDISM;
(1)Anti-thyroid synthesis (ie. Peroxidase
antagonists) Propylthiouracil, Carbimazole
(2) Radioactive Iodine
(3)Blocking thyroid secretion; KI Decreases
thyroid size and vascularity (pre-surgery)
(4)Anion inhibitors; percholates, thiocyanates
(5)Beta Blocking (usually to remove the
palpitations in thyroid storm) Also inhib
peripheral conversion. .


HYPOTHYROIDISM;

Levothyroxine; synthesised T3
HYPERPARATHYROIDISM;

Estrogen to preserve bone
Calcitonin to decrease plasma Ca
Bisphosphates to inhibit osteoclasts
Human osteoprotegerins
Some loop diuretics for acute Hyperpara


HYPOPARATHYROIDISM;

Ca salts
Vitamin D
Thiazide diuretics
Surgery - transplant
Diatrizoate; Inhibits peripheral conversion of T4 to T3
HyperT- lid lag, exopthalamos, palpitations
Liver toxicity, agranulocytosis, anthralga, vasculitis
Primary, secondary, tertiary

DIABETES TYPE I
LISPRO, GLULISINE, ASPART
Rapid Acting (Bolus)
GLARGINE/DETEMIR
Long Acting (Basal)

DIABETES TYPE II
METFORMIN (Bigaunides)
1
ST
choice!
Reduce hepatic glucose output
Incr. insulin sensitivity
No weight gain or loss
SULFONYUREAS
Stimulate insulin release
Risk of hypoglycaemia
Weight gain (so not for obese)
THIAZOLIDINEDIONES
Improve insulin sensitivity
in adipose tissue
Weight gain
No hypoglycaemia

ACARBOSE
Disaccharidase inhibitor
INCRETIN-BASED THERAPIES
(Raise insulin and decrease glucagon)
GLP1 ANALOGUES;
E.G liraglutide
DPP4 Inhibitors;
E.G. Saxagliptin
SGLT-2 Inhibitors;
Prevents glucose
reabsorption in
the PCT
NO
hypoglycaemia or
weight loss
Decrease in BP
(osmotic effect)
Eg. Dapagliflozin
Potential risk of pancreatitis
Dipeptidy pepidase 4
NB/
Amylin: Promotes satiety; slows gastric emptying.
Incretin hormones: Increase insulin, decrease glucagon and promote satiety

STEROIDS
SYNTHETIC HORMONES
DEXAMETHASONE
Used in the treatment of Congenital Adrenal
Hyperplasia in pregnancy
BETAMETHASONE
Long acting drug
25-40 anti-inflammatory
0 salt retention
METHYLPREDNISOLONE
5 Anti-inflammatory
0 Salt retention
Cortisol about 1 salt retention

HYDROCORTISONE
Acute treatment of Addissons
No need for mineralcorticoid
Average salt retaining ability
FLUDROCORTISONE
12 Anti-inflammatory
250 Salt retention
Supplementary for chronic Addisons
PREDNISOLONE
Chronic treatment of Addisons

N.B. FLUDROCORTISONE
Antiarrhythmic
Drugs

Class Ia;
Quinidine
Disopyrimide
Procainimide
Class Ib;
Lignocaine
Melixetene
Class Ic;
Flecainide
Propafenone
Class II;
Propanolol
Bisopropyl (Selective
B1)
Atenolol
Carvedilol (non-sel)


Class III;
Amidarone
(beware)
Dronedarone
Sotolol
Ibutilide
Vernakalent
Class IV;
Adenosine
Digoxin(Increases HR)
Drug
Class
Main mechanism of
action
Main Electrophysiological effect
IA Na channel blocker Slows phase 0 depolarization in
ventricular muscle fibres
IB Na channel blocker Shortens phase 3 repolarization in
ventricular muscle fibres
IC Na channel blocker Markedly slows Phase 0
depolarization in ventricular muscle
fibres
II Beta-blocker Inhibits phase 4 depolarization in SA
and AV node
III K channel blocker Prolongs phase 3 repolarization in
ventricular muscle fibres
IV Ca channel blocker Inhibits action potential in SA and
AV node
BB + Calcium channel blockers = Heart block
Heart Failure;
1. Diuretics; Loop, thiazide
2. ACE inhibitors; Lisonopril
3. Mineralcorticoid receptor antagonists/ Aldosterone antagonists eg.
Spironolactone, eplerenone NB. Prevents collagen deposition
(fibrosis)
4. Beta Blockers; Propanolol, atenolol
5. ARBs; Candesartan, Larsartan
6. Digoxin; Last resort (inhibits NA/K channel)

(1) Anti-Metabolites
(a) Anti folates; Methotrexate
(b) Nucleic acid syn inhibitors; Purines 6 Mercaptopurine, 6 Thioguanine
Pyrimidines 5 flurouracil
(2) Alkylating Agents;
(1) Nitrogen Mustard Gas
eg. Cyclophosphamide
(2) Nitrosoureas; eg.
Carmustine (BBB)
(3) Other Alkylating agents
eg. Cisplatin
(3) Cytotoxic Antibodies;
Anthracyclines, Doxorubicin
(4) Plant Alkaloids
Vinca Alkaloids
Vinchristine
Vinblastine

Taxanes
Docetaxel
Paclitaxel
Oestrogens
Natural: Oestradiol, Oestriol, Ostradone
Synthetic: Mestranol, Stilbestrol, Ethinylestradiol
Anti: Tamoxifen (Breast cancer) , Clomifene
(induce ovulation for infertility) - (SERMS)
ERA &ERB
Progestogens
Natural & derivative: Hydroxyprogesterone,
Noragestrol, Desogestrol
Anti; Mifepristone with misoprostol (Prostaglandin)
Tibolone- both oestrogenic and prostogenic - HRT
Anti- Androgens
Cyproterone
Flutamide
5 alpha reductase inhibitors
Hormonal contraceptives;
Combined pill
Norethisterone
Progesterone only
Lelevonorgestrel

Oral contraceptive pills = CYP450
Pharmacology of Asthma
(1) BRONCODILATORS (2) ANTI-INFLAMMATORIES
(A) B2 agonists; cyclic AMP to bring
about bronchodilation.
Turbutalene (short), Salmetrol
(long)
(B) M3 Antagonists; Inhibit the
binding of acetylcholine to the M3
receptor to prevent
bronchoconstriction. Ipatropium
Bromide, Tiotropium
(C) Xathines; Theophylline, caffeine!
They are phosphodiesterase
inhibitors. This raises the cyclic
AMP level for longer periods of
time therefore causing
bronchodilation. (CYP450)
(A) Corticosteroids; Induce histone
deacetylase to prevent transcription
of anti-inflammatory agents.
Inhalation; beclamethasone, oral;
prednisolone, IV; Hydrocortisone
(B) Cromones; Weak, used for kids. They
increase the threshold sensitivity of
the C fibres to prevent reflex
bronchoconstriction and coughing.
Also decrease lung eosinophil and
IgE production
(C) Leukotriene synthesis inhibitors;
There are ones that block lipo-
oxygenase eg. Zileuton. Others that
block the leukotriene receptor eg.
Zifirlukast.
B2 also increase the mucociliary escalator, M3 decrease mucus
secretion. Xanthines have cardiac side-effects,
Considerations
Considerations
Corticosteroids have kidney suppression side-effect (feedback) also
mineralocorticoid interactions.
Anti-tussives
Codeine acts on the medulla and decreases the sensitivity threshold for
mediating the cough reflex. Pain killer and addictive
Dexamethorphan is much the same as above except it is NOT addictive!
Cystic Fibrosis;
Muccolytics; Carbocysteine (little evidence), Dornase Alpha ( breaks up the
DNA in the mucus)
Expectorants; increase the fluidity of the secretions to minimise blockage;
Iodides, Creasotes.
Alpha 1 anti-trypsin deficiency;
Potential treatments; replace alpha 1 anti-trypsin, inhibit neutrophil action,
gene therapy (more for the future)