PEPTIC ULCER

SYSTEM GASTROINTESTINAL TRACT DISEASES PEPTIC ULCER CLASS OF DRUG H ANTAGONIST GENERIC NAME CIMETIDINE FAMOTIDINE RANITIDINE TRADE NAME TAGAMET FAMODINE ZANTAC MECHANISM OF ACTION A cell called parietal cell makes gastric acid H Antagonist are competitive antagonist histamine These agents inhibit gastric acid secretion SIDE EFFECT FAMODINE Dry mouth/skin Loss appetite Confusion Drowsiness Decrease sexual desire CIMETIDINE Dizziness Diarrhea Impotence Joint/Muscle Pain Constipation Dry mouth Insomnia Headache Rash Nausea Diarrhea Prolonged use of agents suppresing gastric acid may result in low vitamin B Allergic reaction Diarrhea Antibiotic induced colitis (inflammation of colon)

PROTON PUMP INHIBITORS

LANSOPRAZOLE OMEPRAZOLE ESOMEPRAZOLE

PREVACID LOSEC NEXIUM

Thse agents inhibit secretion of gastric acid through inhibition of H+/K+ ATPase enzyme at parietal cell Inhibition of this enzyme suppress secretion of hydrogen ions [H+] into the gastric lumen More effective thab H Antagonist in inhibition of acid secretion The healing of ulcer is much better and faster than H Antagonist. Treatment requires combination of several antibiotics, sometimes in combination with a proton-pump inhibitor or H Antagonist Eradication of H. Pylori prevents the return of ulcers Prostaglandin is produced by the gastric mucosa. It inhibits secretion of HCI and stimulates secretion of mucus and bicarbonate (Cytoprotective effects) It is used for prevention of gasttric ulcers induced by NSAIDS ANTACID + HCI SALT + HO Antacid also reduce peptic activity

ANTIBIOTICS

AMOXICILLIN CLARITHROMYCIN METRONIDAZOLE TETRACYCLINE

AMOXICILLIN YSP CRIXAN FLAGYL BEATACYLCINE

PROSTAGLANDIN

MISOPROSTOL

CYTOTEC

Dizziness Headache GI disorders

ANTACID

ALUMINIUM HYDROXIDE CALCIUM CARBONATE MAGNESIUM HYDROXIDE SODIUM BICARBONATE

Sodium bicarbonate can cause systemic alkalization & sodium overload. Calcium carbonate may cause hypercalcemia Magnesium hydroxide produce diarrhea & excessive absorption og Mg+ in patients with renal failure may result in central nervous sustem toxicity

ANTI-HYPERTENSIVE
SYSTEM GASTROINTESTINAL TRACT DISEASES NAUSEA & EMETIC CLASS OF DRUG 5-HT Antagonist GENERIC NAME ONDANSETRON GRANISETRON DOLASETRON TRADE NAME ZOFRANN KYTRIL ANZEMET MECHANISM OF ACTION 5-HT antagonist prevent serotonin from binding to 5-HT receptors at CTZ (block 5HT receptors) Headache Constipation Diarrhea Fatigue Dizziness Anxiety Drowsiness Dry mouth SIDE EFFECT

ANTI CHOLINERGIC

DIMENHYDRINATE

DRAMAMINE

DOPAMINE ANTAGONISTS

METOCLOPRAMIDE DOMPERIDONE PROCHLORPERAZINE

MAXOLON MOTILUM STEMETIL

Dimenhydrinate is Histamine H Antagonist It competes with histamines for H receptor sites at CTZ avoid stimulation of vomiting center. Antiemetic effects occur within 15-30 minutes following oral administration, 20-30 minutes following IM administration, and almost immediately following IV administration. The duraton of action is 3-6 hours It competes with dopamine for D receptor sites at CTZ avoid stimulation of vomiting center Metoclopramide & Domperidone also increase the mitility of the easophagus, stomach and intestine & decrease reflux into the easophagus Gastric emptying time and GI transit time are shortened Reduce Nausea & vomiting

METOCHLOPRAMIDE Fatigue Extrapyramidal effects (adults and children) Hyperprolactinemia DOMPERIDONE Allergic reactions (rash) Abdominal cramps PROCHLORPERAZINE Hypotension Extrapyramidal symptoms Sedation

ANTI-HYPERTENSIVE
SYSTEM Gastrointestinal Tract DISEASE DIARRHEA CLASS OF DRUG Anti Motility GENERIC NAME DIPHENOXYLATE LOPERAMIDE TRADE NAME LOMOTIL IMODIUM MECHANISM OF ACTION It reduce diarrhea by slowing the bowel movement Decrease transit time, allow time for water and electrolyte to be absorbed Use with caution, as diarrhea is one of the bodys defense mechanism. Slower bowel movement, mean slower clearance of pathogen from body Adsorb intestinal toxins and microorganisms Bind to the causative bacteria or toxin which is then eliminated through the stool SIDE EFFECT Drowsiness Dizziness Euphoria Nausea Paraesthesia Toxic Megacolon Atropine effect ;Hyperthermia, dry skin, tachycardia, urinary retention ACTIVATED CHARCOAL Constipation Dark Stool DIOCTAHEDRAL SMECTITE Constipation **Can decrease the absorption of other drugs taken within 2 hours before other medications Abdominal Discomfort Flatulence Bloating Electrolyte & metabolic disturbances (hypokalemia, hypocalcemia etc) Excess fluid loss and dehydration Senna : medication may cause the urine to turn pink, red or brownish in color. Dark pigmentation of the colon (long term) **Long term use may result in laxative dependence, chronic constipation and loss of normal colon function Abdominal pain Nausea & vomiting Flatulence

ADSORBENTS

ACTIVATED CHARCOAL DIOCTAHEDRAL SMECTITE

BIOCARBON SMECTA

LAXATIVE

BULK FORMING

STIMULANT LAXATIVE

ISPAGHULA HUSK METHYLCELLULOSE PSYLLIUM SENNA BISACODYL

FYBOGEL CITRUCEL METAMUCIL SENOKOT DULCOLAX

Increasing faecal mass which stimulates peristalsis Stimulant laxatives induce bowel movements by increasing the contraction of muscles in the intestines

OSMOTIC LAXATIVES

LACTULOSE MAGNESIUM SALTS MACROGOLS

DULPHALAC

Osmotic laxatives work by pulling large amounts of water into the large intestine from surrounding body tissues or by retaining the fluid they were administered with. This provides a soft stool mass and a rapid increase in bowel action Action occurs within 1-6 hours

ANTI-HYPERTENSIVE
SYSTEM CARDIOVASCULAR DISEASE ANTI HYPERTENSIVE CLASS OF DRUGS ACE INBIHITORS GENERIC NAME CAPTOPRIL ENALAPRIL PERINDOPRIL TRADE NAME CAPOTEN RENITEC COVERSYL MECHANISM OF ACTION ACE INBIHITORS BLOCK ACE > ANGIOTENSIN 1 CANNOT CONVERT TO ANGIOTENSIN 2 CANNOT STIMULATE ALDOSTERONE > REDUCE THE SODIUM &WATER REABSORBTION IN KIDNEY > REDUCE BLOOD VOLUME > REDUCE IN BP SIDE EFFECT -RASH -DYSGEUSIA -HEADACHE -DRY COUGH -HYPOTENSION

- DIURETIC THIAZIDE - DIURETIC LOOP

HYDROCHLOROTHIAZIDE FUROSEMIDE

AMIZIDE LASIX

ANGIOTENSIN 2 RECEPTOR ANTAGONIST (ARBs)

LOSARTAN VALSARTAN, IBERSARTAN, TELMISARTAN

COZAAR VODIUM

- BLOCKER

PROPRANOLOL METOPROLOL

INDERAL BETALOC

CALCIUM CHANNEL BLOCKER

AMLODIPINE NIFEDIPINE DILITIAZEM VERAPAMIL

AMTAS-5 ADALAT HERBESSER ISOPTIN

INCEREASE ELIMINATION OF SODIUM AND WATER > BLOOD VOLUME DECREASE > REDUCE PRIPHERAL RESISTANCE > REDUCE IN BP INHIBIT BINDING OF ANGIOTENSIN 2 TO ITS RECEPTORS (INHIBIT THE FORMATION OF ANGIOTENSION 2) > INHIBIT ALDOSTERONE SECRETION (DECREASE STIMULATION OF ALDESTRONE SECRETION) > REDUCE THE SODIUM &WATER REABSORBTION IN KIDNEY > REDUCE BLOOD VOLUME > REDUCE IN BP IT REDUCE THE ACTIVATION OF -ADRENORECPTOR ON THE HEART > REDUCE CARDIAC OUTPUT IT INHIBIT THE RELEASE OF RENIN FROM THE KIDNEYS > DECREASE THE FORMATION OF ANGIOTENSIN 2 & ALDOSTERONE CA2+ IS ESSENTIAL FOR THE MUSCULAR CONRACTION CALCUIM CHANNEL BLOCKERS WORK BY BLOCKING CALCIUM CHANNEL IN MUSCLE CELLS OF THE HEART AND BLOOD VESSELS THIS PREVENTS CALCIUM CHANNEL LEVELS FROM INCREASING AS MUCH IN THE CELLS TO LESS MUSCLE CONTRACTION

-SIMILAR TO THOSE ACE INBIHITORS -ALTOUGH THE RISKS OF COUGH IS SIGNIFICANTLY DECREASEED -DROWNSINESS - INSOMNIA - FATIGUE -DIMINISHED SEXUAL ABILITY -HEADACHE -CONSTIPATION -HYPOTENSION -PRIPHERAL EDEMA

-BLOCKER

PRAZOSIN TERAZOSIN

MINIPRESS HYTRIN

DECREASE THE PRIPHERAL RESISTANCE AND LOWER BLOOD PRESSURE BY RELAXINTION OF BOTH ARTERIAL AND VENOUS SMOOTH MUSCLE

-POSTURAL HYPOTENSION -HEADACHE -G1 UPSET -EDEMA

ANTI-HYPERTENSIVE
SYSTEM CARDIOVASCULAR DISEASES HEART FAILURE CLASS OF DRUGS CARDIAC GLYCOSIDES GENERIC NAME DIGOXIN TRADE NAME LANOXIN MECHANISM OF ACTION DIGITALIS INHBIBITS NA+/K+ ATPASE PUMP THE CONCETRATION OF INTACELLULAR NA+ INCREASES INCREASE NA+ DECREASES THE DRIVING FORCE FOR THE NA+/CA2+ EXCHANGER SO THERE IS DECREASED EXTRUSION OF CA2+ INTO THE EXTRACELLULARSPACE > CA2+ CONCETRATION IS STILL HIGH INSIDE THE CELL SIDE EFFECT -DYSRHYTHMIA -NASUEA & VOMITTING -CONFUSION -HEADACHE -FATIGUE -CONFUSION -ANOREXIA

PHOSPHODIESTERASE INBIHITORS (PDE)(

MILRINONE

PRIMACOR

PDE INBIHITORS PREVENT CONVERSION OF Camp to AMP BY PHOSPHODIESTERASE ENZYME (PDE) INCREASE THE INTRACELULULAR CONCENTRATION OF CAMP CAMP ACITIVATES PROETIN KINASE , WHICH IN TURN PHOSPHORYLATES A CALCIUM CHANNEL PHOSPHORYLATION OF A CALCIUM CHANNEL INCREASES CALCIUM FLOW INTO THE CELL, CAUSING INCREASED FORCE OF CONTRACTION OF HEART MUSCLE

-HEADACHE -HYPOTENSION

-ADRENEGIC AGONIST

DOBUTAMINE

DOBUTREX

B-ADRENERGIC AGONIST BIND TO B-ADRENERGIC RECEPTOR ACTIVATES ADEDNYLYL CYCLASE, WHICH PRODUCE CAMP CAMP ACTIVATES PROTEIN KINASE , WHICH IN TURN PHOSPHORYLATES A CALCIUM CHANNEL PHOSPHORYLATION OF A CALCIUM CHANNEL INCREASES CALCIUM FLOW INTO THE CELL , CAUSING INCREASED FORCE OF CONTRACTION OF HEART MUSCLE

-INCREASED HEART RATE -HEADACHE -NAUSEA -SHORTNESS OF BREATH

ANTI-HYPERTENSIVE
SYSTEM CARDIOVASCULAR DISEASES HEART ATTACK TYPES OF DRUGS ORGANIC NITRATES GENERIC NAME GLYCERYL TRINITRATE (GTN) ISOSORBIDE DINITRATE ISOSORBIDE MONONITRATE TRADE NAME ANGISED ISORDIL IMDUR MECHANISM OF ACTION DILATE LARGE VEIN POOLING BLOOD IN VEIN DIMINISH PRELOAD (VENOUS RETURN TO THE HEART) REDUCE THE WORK OF HEART IT REDUCE THE ACTIVATION OF ADRENORECPTOR ON THE HEART > REDUCE CARDIAC OUTPUT IT INHIBIT THE RELEASE OF RENIN FROM THE KIDNEYS > DECREASE THE FORMATION OF ANGIOTENSIN 2 & ALDOSTERONE CA2+ IS ESSENTIAL FOR THE MUSCULAR CONRACTION CALCUIM CHANNEL BLOCKERS WORK BY BLOCKING CALCIUM CHANNEL IN MUSCLE CELLS OF THE HEART AND BLOOD VESSELS THIS PREVENTS CALCIUM CHANNEL LEVELS FROM INCREASING AS MUCH IN THE CELLS TO LESS MUSCLE CONTRACTION SIDE EFFECT -HEADACHE -DIZINESS -FACIAL FLUSHING -WEAKNESS -DROWSINESS -DIMINISHED SEXUAL ABLITY -FATIGUE -INSOMNIA -HEADACHE -CONSTIPATION -HYPOTENSION PRIPHERAL EDEMA

BETA ADRENERGIC BLOCKERS

PROPANOLOL METOPLOL

INDERAL BETALOC

CALCIUM CHANNEL BLOCKERS

NIFEDIPINE DILITIAZEM VERAPAMIL

ADALAT HERBESSER ISOPTIN

ANTI-HYPERTENSIVE