You are on page 1of 4

Diuretics:

Name MOA Indication Contra- Adverse effect


indication

⛔ Na -K -2Cl at TAL Loop:


1)⬇️ Reabsorption of this ions along with iso-osmotic water—>⬆️
+ + -
1)Heart failure+Pulmonary Edema*: 1)If hypersensitivity 1)Hypovolemia(IV ad. –can be
2)Acute Hypercalcemia * 2)Over use in H.Shock)

2) Also ⬆️ Mg and Ca excretions


Loss of ions with water 3)Hyperkalaemia hepatic cirrhosis, renal 2)Hypo– kalaemia, calcaemia,

3)⬆️ Renal Prostaglandins —>⬆️renal blood


2+ 2+
4)Acute Renal failure failure, magnesemia

flow—>⬆️GFR—⬆️Urine—Diuresis
Loop Diuretics 5)Anion overdose heart failure 3)Hyperuricemia (lead to gouty
(Frusemide) 6)Other edematous cond.* attack)

✅ Heart failure+Pulmonary edema:


4)Allergic reaction

⬇️Accumulation of Edema in lungs ⬇️Pulmonary vascular congestion,


5)Metabolic alkalosis

⬇️Preload, ⬆️O + improve mycardial function, ⬆️Diuresis, thus


2
prevent both

⛔NaCl transport at DCT:


1)⬇️Reabsorption of NaCl—>⬆️Loss of NaCl with iso-osmotic
1)Hypertension Same as 1)Hypokalemia

water—>Diuresis—>⬇️BV—>⬇️BP
Thiazide 2)Heart Failure Loop diuretics…. 2)Hyponatremia
(Hydro– 3)Nephrogenic Diabetes Insipidus 3)Metabolic alkalosis

2)In long standing therapy—>⬇️Respone to


chlorothiazide) 4)Hyper—uricemia, glycemia,

catecholamines—>Vasodilation—>⬇️PR—>⬇️BP
calcemia, lipidemia, sensitivity

⛔Aldosteron at receptor level at CT by binding with 1)Hyperaldosteronism 1)Hyperkalaemia

⬆️Na excretion and K and H retention


K+ sparing Mineralocorticoid receptor—> (Primary+Secondary) 2)Metabolic Acidosis


+ + +
(Spironolactone) 2)Diuretic (with K loosing) of choice 3)Gastric upset+PUD
Weak diuretic—>most Na is reabsorbed, before CT in Cirrhosis of Liver Gynecomastia,Kidney Stones,Acute
3)Heart Failure Renal Failure, CNS effect, Skin
rash

⛔CA enzyme in the luminal membrane at PCT—>


⬇️Breakdown of CA into H O & CO —>⬆️Accumulation of H —>No
Carbonic Anhydrase 1)Glaucoma Liver Cirrhosis 1)Metabolic acidosis

Na/H exchange—>⬇️Reabsorption of Na & Bicarbonate —>Diuresis


+
Inhibitors 2 2 2)Urinary alkalization 2)Renal stone
(Acetazolamide) 3)Metabolic alkalosis 3)Renal K wasting
4)Acute Mountain Sickness 4)Drowsiness,
5)Epilepsy peresthesia,hypersensitiv.

⛔ADH at PCT and DL of Hanley


⬆️Urine flow rate ⬆️
Osmotic USE: 1)Extracellular volume expansion

⬆️Water Loss then Na loss ⬇️ ❌


(Mannitol) 1) Urine Volume 2)Dehydration, Hyperkalamia,
2) Intracranial & Intraocular Hypernatremia
*Mannitol prevents normal absorption of water pressure
Lipid Lowering Agents:
Name MOA Indication Contra- Adverse effect
indication

⛔HMG-CoA reductase—>
⛔Rate limiting step of cholesterol
1) 1)Pregnancy or women 1)Liver function abnormality

synthesis—>⬇️Cholesterol—>⬇️VLDL—>⬇️LDL
who are likely to 2)Muscle:Myopathy, myalgia
HMG-CoA reductase become pregnant 3)Drug interaction: May increase

2)⬇️Intracellular Cholesterol due to less synthesis ❌


inhibitors 2)Nursing mother warfarin level, thus increasing

—>⬆️Cell surface LDL receptor—>⬆️Bind LDL


(Atorvastatin/ 3)Children & teenagers. bleeding tendency

—>⬆️Internalization—>⬆️Catabolism—>
Rosuvastatin)

⬇️Plasma level
Anti-Platelets & Anticoagulants :
Name MOA Indication Contra- Adverse effect
indication



Acetylate—> Cyclooxygenase(irriversably)—> 1)MI 1)PUD with bleeding 1)Gastric HIP(Hemorrhage,
Low dose Synthesis of Prostaglandin(mainly TXA2 but not so PGI2)—>No 2)DVT 2)Asthma Irritation, Perforation)
Aspirin platelet aggregation 3)UA 3)COPD 2)Precipitation Asthma
(75-150mg) 4)IA 4)Coagulation D
*COX activity is lost for platelet for life time(8-10d) 5)TIA 5)Pregnancy-1st
6)AF

✅Binds with AT-III—>Conformational Changes


—>⬆️Activity of AT-III—>Binds with C.Factors(IIa, IXa,
1)MI 1)Any bleeding….. 1)Hemorrhage
Low Molecular Weight 2)DVT 2)Hypersensitivity 2)Hypersensitivity

C.Factors—>❌Coagulation….
Heparin Xa)—>Formation of Complex —>Inactivate 3)UA 3)Uncontrolled 3)Thrombocytopenia
(5000 IU) 4)Pulmonary Embolism Hypertension 4)Thrombosis
5)DIC 5)Osteoporosis
6)Angiogram 6)Alopecia

⛔Vit-K epoxide reductase—>⛔Vit-K active—>


⛔Carboxylation of Glutamic Acid Residues in C.Factors(II, VII, IX,
1)MI 1)Pregnency 1)Bleeding Disorder

X)—>❌Activation of C.Fac
2)DVT Etc…. 2)Skin Rash(Purpura, echymosis)

—>❌Coagulation…
Warfarin 3)TIA 3)Skin necrosis
4)AF 4)Infract brest, vein etc
5)Pulmonary Embolism 5)Teratogenicity(Birth defect)
6)Systemic Embolism
DM Drugs:
Name MOA Indication Contra- Adverse effect
indication

⬇️ Blood Glucose By:- 1)Type-I DM 2)Uncontrolled type 1)Hypoglycemia (most common)

⬆️Glycogenesis
II DM 3)All diabetic 2)Insulin—

⬆️Glucose uptake
Diabetic–ketoacidosis, hypersensitivity, resistance, edema

⬆️Glycolysis ❌
nephropathy, neuropathy, 3)Obesity
retinopathy 4)Hypokalemia

⬇️Glycogenolysis
Insulin 4)DM in pregnancy 5)Alopecia

⬇️Gluconeogenesis
5)Per & post–oparetive diabetic
patient
6)DM of infection, RTA
7)Hyperkalamia

⛔ATP sensitive K channel in Beta-pancreatic cell—>


⬇️K Efflux—>Depolarization—>✅VG Ca channels—>
+
Sulfonylureases 1) 1)Type-2 DM (non-obese) 1)Type-1 DM 1)Hypoglycemia

⬆️Intracellular Ca—>⬆️Insulin secretion


+
(Tolazamide 2)Combination with Insulin in 2)Pregnancy 2)Weight Gain
Talbutamide Type-1 and Type-2 DM 3)Lactation 3)Anemia

2)⬇️Serum Glucagon Level


Glipizide 4)Renal & Hepatic 4)GIT upset
Gliclazide insufficiency 5)Hypersensitivity
Glibenclamide) 5)Elderly 6)Teratogenecity

⬇️Glucose absorption
⬇️Renal & Hepatic Gluconeogenesis
1)Type-2 (most common) 1)Renal & Hepatic 1)GIT upset

⬇️Plasma Glucagon level


2)Obese patients insufficiency 2)Lactic acidosis

⬇️
Metformin 3)Insulin resistance syn. 2)Alcoholism 3)Acute kidney Failure
4)Middle aged 3)Chronic cardioP. 4) Vit-B12 abs. (MegaB A.)
4)Diabetic ketoA.

PUD Drugs:
Name MOA Indication Contra- Adverse effect
indication

PPI(Proton Pump ✅—>Convert into Active TSC(Thiophilic sulfonamide cation) in parital 1)PUD—> 1)General: Diarrhoea, Headache,

—>React with H/K ATPase(PP) by Disulfied Linkange—>⛔PP—>❌PP ❌ ⬇️


Inhibitors) cell H. pylori, NSAID, Perforation Abdominal pain

⬆️
(Omeprazol 2)GERD 2) Vit-B12 level

❌HCL by Parital Cell….


Esomeprazol —> 3)Non-ulcer dyspepsia 3) Infection
Pentoprazol 4)Stress ulcer 4)Potential problem has no
Rebeprazol) 5)Zollinger Ellison syndrome evidence (Carcinoid, Colon Ca etc..)
Anti-Hypertensive :
Name MOA Indication Contra- Adverse effect
indication

ACEI. ⛔ACE—>⛔Conversion of Ang-1 to Ang-2—>⬇️Ang-2 1)Hypertension 1)Renal Failure 1)Dry cough 8)S. Rash

⬇️Ang-2 mediated effect —>Vasodilation—>⬇️PR,


(Captopril —>—>—>—>—>—>:- 2)MI 2)Pregnancy 2)Angioedema, 7)ARF

⬇️Output of sympathetic nervous system—>


Lisinopril 3)Diabetic nephropathy(T-1 DM) 3)Hyperkalamia 3)First dose hypoten..

⬇️Adr/NorAdr—>⬇️Aldosteron—>⬇️Retention of Na &
Enalapril 4)Cardiac Hypertrophy 4)Bilateral Renal 4)Hyperkalamia

Water—>⬆️Bradykinin—>Vasodilation—>⬇️BP
+
Ramipril) 5)Chronic HF Stenosis 5)Teratogenecity
6)Fetal R. Shutdown,

ARB ⛔Ang-2 Receptor—>Ang-2 cannot binds with receptors 1)Hypertension 1)Hypotension

⬇️Ang-2 mediated effect —>Vasodilation—>⬇️PR,


(Losartan —>—>—>—>—>—>:- 2)Pat. With Ashtma 2)Hyperkalamia

⬇️Output of sympathetic nervous system—>


Valsartan 3)CHF & MI (Valsartan) Same as ACEI. 3)ARF

⬇️Adr/NorAdr—>⬇️Aldosteron—>⬇️Retention of Na &
Olmesartan 4)Diabetic nephropathy 4)Teratogenecity

Water—>⬆️Bradykinin—>Vasodilation—>⬇️BP
+
Telmisartan) &Prophylaxis of Stroke
(Losartan)

✅MOA in Cardiac Muscle:-


Binds with L-Type Ca channel—>⬇️Frequency of Open VG CC—>⬇️Influx:-
Ca2+ Channel 1)Hypertension 1)Cardiac arrest Same as Contraindications…..

⬇️SV rate & AV Conduction—>⬇️HR


Blockers(CCB) 2)Angina 2)HF & Block

⛔Actin+Myosin—>⬇️FoC
(Amlodipine 3)Arrithmias 3)Bradycardia Nausea, dizziness, Flushing etc…

⬇️Cardiac Outpur—>⬇️BP
Nifedipine 4)Migraine 4)During Labour

✅MOA in Vessels Smooth Muscle:-


Nicardipine 5)Cardiomyopathy 5)Constipation

Binds with L-Type Ca channel—>⬇️Frequency of Open VG CC—>⬇️Influx:-


Verapamil 6)Raynad's phenomenon

❌Ca -Calmudolin com.—>❌Actin+Myosin—>❌MC


Diltiazem)
2+

⬇️PR—>⬇️BP
—>Vasodilation(peripheral vessels, arterioles)—>

You might also like