TREATMENT OF HYPERLIPIDAEMA

DRUGS

MECHANISM OF
ACTIONS
HMG-CoA reductase inhibitors (statins)
Atorvastatin
Competitive inhibitors of
Fluvastatin
HMG-CoA reductase
Lovastatin
Reducing LDL cholesterol
Pravastatin
Rosuvastatin
Simvastatin
Pitavastatin
Bile acid binding reins
Cholestyramine
Cholestipol

Fibrates
Gemfibrozil
Fenofibrate

SIDE EFFECTS
Hepatotoxicity
Myopathy
Hepatitis
Muscle aches
Myositis
Angio-oedema
Sleep disturbance

Bind to bile acids

Deplete pool of bile acids
Decrease hepatic
cholesterol (more is used
for bile acid production)
Stimulate increase in LDL
receptor
Lower LDL cholesterol

Bloating
Dyspepsia/indigestion
Interfere with absorption of
drugs

Lowering triglycerides

GI disturbance
Elevated liver enzymes

Increase activity of
peripheral lipoprotein
lipase
Reduce VLDL production
Increase hepatic LDL
uptake
Mild increase in HDL

Safest for GI not

absorbed from gut
(child safe drug)

Contraindication:
Gemfibrozil + Statin
= myotoxocity

Interaction with nuclear

transcription factor PPAR
that regulates several
genes involved in lipid
metabolism
Nicotinic acid
Tredaptive
(nicotinic acid+laropiprant)
Fish oils
*no proven benefit, not
used routinely

Plants sterols and

stanols
(cholesterol like plants
extracts)

Raising HDL cholesterol

Omega-3 fatty acids

containing
eicosapentaenoic acid
cause reduced VLDL
synthesis
Lower TG but increase LDL
Inhibit cholesterol
absorption in intestine
Reduce LDL cholesterol

Didnt provide benefit to

Statin alone and in fact
was worse
= Tredaptive recalled

*stenols = saturated
sterols + methyl/ethyl
group
Probucol

ANTIANGINAL THERAPY
DRUGS

MECHANISM OF
ACTIONS

Nitrates
Nitroglycerin
Isosorbide dinitrate
Isosorbide-5mononitrate

CLINICAL USES

-Nitrates
Stable angina
decompose to form Unstable angina
nitric oxide
Myocardial
-Activates guanylyl infarction
cyclase
Heart failure
-Increases
Hypertensive
conversion ATP to
crises
cGMP
cGMP:
1. Leads to
decrease in
intracellular
calcium
2. Activates protein
kinase, in smooth
muscle:
-inactivate myosin
light chain, causes
reduces
phosphorylation
-muscle relaxes
Beta blockers/ beta adrenergic antagonist
Block action of
Stable angina
1. Non selective
adrenaline or
Unstable angina
-Propanolol
noradrenaline on
Myocardial
-Timolol
beta adrenergic
infarction
receptors.
Heart failure
2. Cardioselective
Arrythmias
-Metoprolol
Beta-1-receptors:
-Atenolol
-increase HR
*Propanolol
-increase
-thyroid crises,
3. Alpha-1contractility
tremor
antagonist
-Carvedilol
Beta-2-receptors:
*Carvedilol
-dilate smooth
-heart failure
muscle on blood
vessels and bronchi
Alpha-1- receptors:

SIDE EFFECTS
Headache
Hypotension
Contraindications:
Phosphodiesterase
5 inhibitor
-Sildenafil (Viagra)
-Tadalafil (Cialis)
-Vardenafil (Levitra)
=causes extreme
hypotension

Bronchoconstriction
(block beta-2receptors)
Hypoglycemia
Precipitate heart
failure
Bradycardia
Peripheral vascular
disease
Somnolence/depres
sion
Impotence
Alter lipid profile

-smooth muscle
constriction
Calcium channel blockers
Block L-type
1. Dihydropyridines
calcium channels
-Nifedipine
Decreases calcium
-Amlodipine
entry
Reduces
2. Nonintracellular
dihydropyridines
calcium
-Verapramil
In smooth muscle,
-Diltiazem
causes vascular
smooth muscle
relaxation
In heart, decrease
in contractility

Stable angina
Arrythmias
Hypertension
*Dihydropyridine
s
-affect
vasculature
-decrease BP

Dizzyness
Flushing
Hypotension
Peripheral oedema/
ankle swelling
Bradycardia
Constipation
Precipitate heart
failure

*Non-DHDP
-affect heart
-decrease HR

TREATMENT OF CARDIAC FAILURE

DRUGS

MECHANISM OF ACTIONS
Enhance Na excretion
kidney
Reduce vascular volume
Reduce preload

SIDE EFFECTS
Loss of electrolytes (K, Na,
Mg, Ca)

Loop diuretics
-Furosemide

Act on thick ascending limb

Inhibit Na/K/Cl carrier
Inhibit transport of NaCl
out of tubule
Increase water excretion

Thiazide diuretics

Act on distal tubule

Bind to Na/Cl co-transport

Potassium-sparing
diuretics
Spironolactone

Antagonist of aldosterone
receptor

Depletion of total body Na

Hypokalemia
Increased Mg and Ca
excretion result in
hypomagnesemia and
hypocalcemia
Ototoxocity, deafness,
tinnitus, vertigo
Hyperuricemia leading to
gout
Hyperglycemia
Increase LDL
Decrease systemic venous
capacitance (furosemide)
Increase venous
capacitance, decrease
preload, decrease LV filling
pressure
Low Na, Mg, K
Hyperuricaemia
Hyperglycemia
Hypercholesterolemia
Impotence
Pancreatitis
Hyperkalemia
Gynaecomastia

Diuretics

ACE Inhibitors
-Captopril
-Enalopril
-Lisonopril

-Reduce circulating levels

Causes decrease in
peripheral vascular
resistance (decreased
afterload)
-Prevent release of
aldosterone
Na and water retention
(decreased afterload)

Hypotension
Renal dysfunction
Hyperkalemia
Renal artery stenosis
(rarely, causing worsening
of renal function)
Cough

-decrease sympathetic
nervous system activity
-potentiate effects of
diuretics
Angiotensin 2 receptor
blockers
Hydralazine+Nitrates

Beta blockers
-Metoprolol
-Bisoprolol
-Carvedilol
Inotropes
ANTIARRYTHMIC

Relax smooth muscle in

precapillary resistance
vessels

If hydralazine used alone:

Increase HR and CO
Increase plasma renin
concentration causing fluid
retention