Use Drugs Mechanism of action Side effects

Heart failure 1. Diuretics Increase Na+ excretion and reduction Loop:Loss of

- Loop diuretics (more in preload
potent)  used more for - Loop: inhibit Na+/K+/Cl- transporter electrolytes:
rapid relief of symptoms in the thick ascending limb of the loop K+, Mg++, Na+, Ca++
of fluid overload / of Henle (orally,IV) in morning due Ototoxicity, Hyperuricemia
emergency cases. to fall risk. (GOUT), Hyperglycemia,
- Thiazade Eg: Fursomide, bumetanide, increase LDL
- k sparing diuretics torsemide. Thiazide: impotence, fatigue,
 when kineys function - Thiazide: act on the distal tubule glucose intolerance, pancreatits
normally, the patient is on Na+/Cl- Spiranolactone: Hyperkalemia &
other medications (ACEI, - Spiranolactone: Aldosterone gynecomatsia
BBs, other D) and still antagonist. (30% mortality reduction)
symptomatic) DON’T DO IT:
DON’T GIVE D WITH NSAIT
 DIMINSH THEIR EFFECT.
2. -blockers(in Antagonizes the effect of the NOT GIVEN IN ASTHMA
chronic situations) sympathetic NS activation and down AND HEART BLOCK
- Metoprolol B1 slective
regulation of -receptors Compliance is imp. Because
- Carveldilol blockers (reduce the mortality/morbidity. sudden stopping of BBs can
used in
- Bisoprelol Combination
Considered after the use of ACEI and lead to complications.
diuretics)
3. ACE inhibitors Reduces angiotensin 2 activity - renal dysfunction,
(prolongs life in HF) Reduces peripheral resistance: Hypotension, hyperkalemia (not
- Captopril reduction in afterload given with sparing diuretics),
- Enalopril Inhibits aldosterone: diuretic effect: dry cough (due to accumulation
- Lisinopril decrease preload. of bradykinin).
Reduces the activation of sympathetic - Renal dysfunction
NS - NSAIDs antagonizes with
PRIL NOT GIVEN DURING PREGNANCY ACE inhibitors
CI: pregnancy/ angioedema.
4. Agiotensin-2 Inhibit angoitesin- 2 receptors NOT given to patients who
receptor blockers cant tolerate ACE inhibitors
(ARBs) and develop angiodema. But
- Valsartan sarta for those who used of ACE
- Candesartan n inhibitors and developed dry
cough.
5. Vasodilators (acute - Nitrates: Vasodialate both arteries Ineffective alone in the
treatment) and veins due to enhancement of treatment of HF (combination
- Nitrates cGMP of vasodilators –nitrates and
* Nitrigylecerine hydralazine reduces mortality
* Isosorbide dinitrate - Hydralazine: relaxes the smooth in HF).
- Hydralazine muscles by reducing the precapillary
resistance Cause reflex increase in heart
rate and Drug-induced lupus
like syndrome.
 6. Positive Inotropes - Digoxin: - Digoxin: arrhythmia, nausea,
(short term acute  increase the rate of vomiting, diarrhea, visual
treatment) contraction of the heart by hallucinations,toxicity
- Digoxin inhibiting Na+/K+ ATPase  hypokalamia  we use anti-
- Phosphdiesterase more Na in the cell  affect digoxin antibodies (FAB),
inhibitors: Milrinone Na/Ca transporter which narrow TW.
- -1 adrenoceptor removes Ca from the cell  - Milrinone: boronchospasm,
agonists: dopamine, increasing intracellular Ca++. arrhythmia, chest pain,
dobutamine  Inhibits vagal nerve  Slows tremor.
the conduction through SA, AV
nodes (for AF).
(No evidence that it affects the
mortality  but it shifts frank
starling relationship up and to the
left).
- Milrinone: inhibits hearts sp.

Phosphodiaesterase 3: increase
contraction, heart rate and
vasodilatation, cAMP and intracellular
calcium
Nitrates Prodruge: converted into NO that - Extreme hypotension: interaction

5
- Isosorbide dinitrate activates guanylyl cyclase convert GTP into
- Nitroglycerine cGMP. Resulting in activation of kinases with phosphdiesterase
- Isosorbide-5-mononitrate that reduces intracellular Ca++ and inhibitors used to treat erectile
reducing the phosphorylation of myosin dysfunctions
light chain  relaxation of the SMs. Contraindicated in patients who
HOWEVER, increased cAMP levels  high use nitrates.
Ca (PDE3I = milirinone) ! - Reflex tachycardia at high
doses (overcome by BBs)
- Headache, hypotension,
metheamogolbineamia
-blockers They reduce the oxygen demand by Bronchoconstriction, depression,
Anti-Anginal - Non-selective: reducing the rate, contractility and the mask the symptoms of
therapy * propranolol, timolol afterload because they reduce BP. hypoglycemia, precipitate the HF
- Cardio-selective: effects, bradycardia, impotence,
+ Aspirin * metoprelol, atenolol Contraindicated in: asthma, peripheral alter lipid profile, exacerbate
- 1 antagonistic activity: vascular disease… etc peripheral vascular disease
* carveldilol
Ca++-channel blockers Used in chronic stable angina. Block L- Dizziness, hypotension, flushing,
- Dihydropyirindine: type Ca++ channels, promoting relaxation bradycardia, peripheral edema,
* nifedipine, amlodipine and reducing contractility: constipation, precipitates HF
Dihydropyirindine: reduce the afterload
- None-dihydropyirindine: * (BP)
verapramil, diltiazem None- dihydropyirindine: reduce the heart
rate
Antiarrhythmics Class: Procaninamide: hypotension, SLE
Vaughn William Class 1a: Sodium channel blockers Disopyrimide: Anti-cholinergic
classification - Disopyramide Class 1a: reduces the upstroke (phase 0 effect.
- Quinidine of AP) and prolongs the action potential. Quinidine: CNS S/e (tinnitus,
- Procainamide For ventricular and supraventricular hearing loss, dizziness, visual
tachycardia. disturbances, psychosis)
Based on cellular Class 1b: Class 1b: ventricular arrhythmias. CNS toxicity.
properties of - Lignocaine IV ONLY Phenytoin: for seizures; used to treat
normal Purkinje Rapidly metabolized atrial & ventricular tachycardia caused by
fibers. digoxin.
- Mexiletine Class 1c: LIFE THREATENING ventricular
Ability of the Class 1c: No effect on AP and supraventricular tachycardia
drug to BLOCK duration. ONLY IF ARRYTHMIAS FAILED TO
certain - Propafenone BB effects RESPONSE TO OTHER DRUGS!
channels/ B adr. - Flecanide PROARRYTHMIC
Receptors. Class 2: -blockers Block B1 receptors in the heart Treat Bronchoconstriction, heart block
• Act on SA and AV ventricular and supraventricular and heart failure
ADVANTAGES nodes predominantly arrhythmia
DIS
- Propranalol
- Atenolol
Class 3: Prolongs the repolarisation by effecting K+ Amiodarone: only in life
- Amiodarone: SVT, Vent. channels threatening cases. It has a long
Arrth. Amiodarone: effecting purkije and t1/2 and it accumulates in the
- Dronedarone less t1/2  ventricular muscle adipose tissues so it has a
less s/e compared to Bretylium: ICU, recurrent refractory persistent effect. Thyroid
amiodarone. ventricular tachyarrythmias. disorders, pulmonary alveolitis,
- Bretylium Sotalol: ventricular arrhythmias liver damage, photosensitivity, skin
- Sotalol discoloration and corneal deposits.
Bretylium: hypotension
Sotalol: beta-blocker effects
Class 4: L-type Ca++ channel blockers
- Verapamil Effects only U CANT GIVE BBs+CCBs in
- Diltiazem
SUPRAVENTRICULAR combination. WHY? They work by
Prolongs conduction the same mechanism and increase
tachycardia and NOT ventricular
and refractoriness in the risk of heart block.
tachycardia.
AV node, slows rate
of conduction of SA
node
Adenosine slows
Others -Adinosine: supraventricular tachycardia
the AV node
(effecting K+ channels; prolongs
conductance
hyperpolarization) it is a vasodilator.
NOT used in Digitalis -Digitalis glycoside: atrial fibrillation
Digitalis reduce
reduce the
the AV
AV
node (Na+/K+
conductance by APTase)
heart block increasing
node conductance
increasing its
by
refractory
-Adrenaline:
its refractory cardiac arrest
period 
period  controls
controls
ventricular - Atropine: sinus bradycardia
ventricular raterate (because
(because
It also causes the aim is to -Calcium
prevent
the aim is to prevent the the chloride: ventricular tachycardia

bronchospasmfibrillation
fibrillation from
-Magnesium chloride: ventricular
from
progressing
progressing to to the
the ventricle
ventricle
CI in asthmaticbut
but itit doesn’t
fibrillation
doesn’t terminate
terminate the
the
and digoxin toxicity
patients atrial
atrial flutter
flutter itit self.
self.

Long
Long QT
QT syndrome
syndrome :: AD
AD disease,
disease, recessive
recessive association
association with
with deafness.
deafness. (life
(life threatening
threatening Vent.
Vent. Arryth.)
Arryth.)
Treatment:
Treatment: BB,
BB, ICD,
ICD, sympathetic
sympathetic denervation
denervation

Brugada
Brugada syndrome:
syndrome: AD AD disease
disease the
the structure
structure of
of the
the heart
heart is
is normal
normal but
but ST
ST segment
segment is
is elevated.
elevated.
Susceptible
Susceptible to
to vent.
vent. tachy.
tachy.
Treatment:
Treatment: ICD.
ICD.
Hypertension - ACE-inhibitors Alpha blockers:  fatigue
2As, B, C, D - Angiotensin-2 Blocking 1 adernoceptors resulting in  Postural hypotension
antagonists vasodilatation (normally when we stand
*alpha blockers: doxazosin our vessels constrict so
- Beta-blockers blood goes to the vital
organs, here, it is not
Non-selective: Propranolol the case)
B1 selective:
 Raynaulds phenomenan
Atenolol,metoprolol, bisoprolol.
VOCC: L-
+ vasodilatation effect
type Vascular SMs
Nebivolol (BB+NO release) Dihydro. (prine)
Carvedalol (BB+ alfa1 Blocker)
Pindolol (B1 antagonist, B2
agonist)
LOCC: T-type
Cardiac myocytes
Nondihydro.
- Ca++ channel blockers
- Diuretics
(hydrochlorothiazide).

Hypolipidemics Statins Competitive HMG-coA reductase inhibitors - S/E: GI, hepatitis, Mayopathy,
* Natural: (involved in the rate limiting step in the Moyitis, Rhadomyalyais, Sleep
- Pravastatin synthesis of cholesterol, converts HMGcoA disturbances, angiodema.
-Simvastatin to Mevalonic acid). Most effective in - Contraindicated in pregnancy and
-Lovastatin reducing LDL. breast feeding.
* Synthetic: Increase LDL receptors in cell membrane - Severe S/E: high doses of
- Fluvastatin and increase clearance of LDL from the potent statins, liver disease, co-
- Atorvastatin blood. administration with fibrates
- Rosuvastatin Decrease cholesterol, death, stroke, CAD.

Bile acid binding residues Resins bind to the anion (lipids) making Use in patients with high
- Cholestyramine them less absorbable) Sequester bile acids cholesterol and normal TAG. Used
- Coleseptol in the small intestine, reducing exogenous with statins if statin alone fails
cholesterol by inhibiting reabsorption in thus reducing the CHD events.
the enterohepatic circulation. Increase
LDL receptor expression and clearance. GI effects, abdominal fullness,
Useful in type 2a (high LDL) + type constipation, nausea. Reduces
2b(hight LDL+VLDL) absorption of Vit A, D. Drug
malabsortion (Follic acid+statins).
HyperTAG.
Fibrates Effective at reducing TAG. - Abdominal pain, nausea, myositis
- Fenofibrates PPAR- receptor agonist receptor (with statins), increased liver
- Gemfribrazol activation leads to  Increases - enzymes, gallstones.
oxidation in liver, reduce TAG secretion. - Contraindicated in sever renal
increase activity of lipoprotien lipase, and liver disease.
reducing VLDL and increasing HDL. - USED IN COMBINATION to
avoid resistance.
Nicotinic acid(vitamin: niacin) Effective at increasing HDL cholesterol. Flushing, hyperglycemia,
Given at high doses, useful in Inhibits peripheral fatty acid mobilization, hyperurecemia, GI upset,
types 2-5 reduces hepatic TAG synthesis, VLDL, and hepatotoxicity, rash.
LDL. Increase HDL Contraindicated: severe gout, liver
disease, peptic ulcer.
 Fish oils Omega-3 FAs. NOT USED because low
Lowers VLDL, TAG, but increases LDL. association of VLDL with CAD,
increasing LDL.
Probucols Lowers LDL, and HDL. Used as anti- GI disturbances
oxidant. Sudden death (NOT PRESCRIBED)
Steriols/Stanols Inhibits absorption of cholesterol from
the intestine. Lowers cholesterol and LDL
Respiratory Symptoms Treated:
Distress Rapid labored breathing, grunting sounds when - Natural/artificial surfactant
syndrome breathing, nasal flaring, cyanosis - Beta-methasone for mother prior pre-term birth
(formation of patchy atelectasis and pulmonary (Cortisol)
edema) - oxygen therapy /intubation
Acute mountain - High alt. cerebral edema: headache, ataxia, Treated:
sickness nausea, vomiting, coma - Acetazolamide: carbonic anhydrase inhibitor
- High alt. pulmonary edema: dry cough, resp. - Dexamethasone
ditress, dyspnea, tachypnea
Bronchodilators Bronchodilators Stimulation of adenylyl cyclase S/E:
* 2-agonists to increase cAMP. Activation - Tremor
- Short acting: Salbutamol, PKA which activate of many - Palpitation
Terbutalin, Formoterol other effector pathways: - Tachycardia
- Long acting: Salmeterol - Myosin light chain - Hypokalemia
phosphatase - Receptor down-regulation (Tolerance)
- Inhibition of Ca++ release from
intracellular stores
* Muscarinic3 antagonists Inhibition of Ach action on M1, Acilidinium Bromide is favorable for
- Ipratropium Bromide M2, M3 receptors causing cardiovascular profile.
- Tiotropium Bromide bronchodialation, and reduction
- Aclidinium Bromide in mucus secretion.
- Glycopyrronium Bromide
* Xanthines Naturally accruing Narrow TI:
- Theophylline, caffeine bronchodilators in coffee, tea, GI: nausea, diarrhea
- Theobromine and coca. Cause bronchial CV: arrhthmias
- Aminophylline smooth muscle relaxation by CNS: nervouseness, tremors and
- Enprofylline inhibiting phosphdiesterase and siezures
increasing cAMP and cGMP.
Have anti-inflammatory effect
Anti-inflammatory Inhibition of expression of Inhaled: Dysphonia, Oral candidiasis
* Glucocorticiods genes involved in inflammation Systemic S/E:
- Beclomethasone by promoting deacetylation of Infection, osteoporosis, adrenal
- Budesonide histones suppression, hypertension, electrolyte
- Fluticasone *SHORT TREM: inactivation of imbalace, myopathy and growth
- Prednisolone (oral) inflamitory cells, inhibition of retardation.
- Hydrocortisone (IV) prostaglandins and
luekotrienes, reduction on
mucosal edema, up-regulation of
adrenoceptors
*LONG: reduction in T-lymph
activation, eosinophil + mast cell
predisposition, reduction in
goblet cell hyperplasia.
 * Cromones Anti-inflammatory: - Cough
- Sodium cromoglycate - Mast cell stabilization by - Wheeze
- Nedocromil sodium inhibition of Ca++ influx and
degranulation 1st choice in children
- Inhibition of sensory C- fiber
neurons
- Inhibition of eosinophil
accumulation
- Reduction in IgE production
* Anti-luekotrienes - Effective against excersize - Headache
- Inhibitors of Lipoxigenase induces boronchoconstriction - GI upset (dyspepsia)
- Receptor antagonists - Cold-induces
(CycLT1) bronchoconstriction
- Aspirin/NSAID induced
bronchoconstriction
COPD Bronchodilators
- 2-agonists:
Short term: Salbutamol, Albuterol1
Once daily: formeterol, Indacaterol, carmoterol
- M3 antagonists
Ipratropium Bromide
Tiotropium Bromide
- Xanthines
Theophylline
Anti-inflammitory drugs
- Selective phosphdiesterase inhibitors 4: Roflumilast, Cilomilast
- Inhaled glucocorticoids (resistance due reduced histone deacetylase resulting NF-B inflammation)
- Histone deacetylase promoters: Theophylline and antioxidants
Expectorants For dry cough. Increases the fluidity of the secretions
Use for gastric mucosa irritant
- Iodide
- Guaiacols
- Creosotes
Mucolytic For heavy mucus cough, breaks down mucus.
agent Viscosity depentednt on: presence of mucoprotiens, di-sulfide bonds, DNA.
2 types:
* Disulfide bond breaker:
- Carbocysteine
- Acetylcysteine
* DNA tangle breaker (DNase)
- Dornase 
Anti-tussives Opioids used as anti-cough medication (reduce sensitivity of cough receptors by acting as local anesthetic;
thez reduce muccilliary clearance and secretions)
- Codeine
- Dextromethorphan (opioid only)