Ranitidine
Zantac, Zantac EFFERdose, Zantac GELdose, Zantac-75
Action:
Potent anti-ulcer drug that competitively and reversibly inhibits histamine action at H2-receptor sites on parietal cells, thus blocking gastric acid secretion. Indirectly reduces pepsin secretion but appears to have minimal effect on fasting and postprandial serum gastrin concentrations or secretion of gastric intrinsic factor or mucus
Classifications:
GASTROINTESTINAL AGENT; ANTISECRETORY (H2-RECEPTOR ANTAGONIST)
Indication:
Short-term treatment of active duodenal ulcer; maintenance therapy for duodenal ulcer patient after healing of acute ulcer; treatment of gastroesophageal reflux disease; short-term treatment of active, benign gastric ulcer; treatment of pathologic GI hypersecretory conditions (e.g., Zollinger-Ellison syndrome, systemic mastocytosis, and postoperative hypersecretion); heartburn.
Medical use
Relief of heartburn, acid indigestion, and sour stomach.
Short-term and maintenance therapy of gastric and duodenal ulcers
Ranitidine can also be coadministered with NSAIDs to reduce the risk of ulceration. Proton-pump inhibitors (PPIs) are more effective for the prevention of NSAID-induced ulcers
Pathologic GI Hypersecretory Conditions such as Zollinger-Ellison Syndrome
Gastroesophageal Reflux (GERD)
erosive esophagitis
Part of a multidrug regimen for H. pylori eradication to reduce the risk of duodenal ulcer recurrence.
Recurrent postoperative ulcer
Upper GI bleeding
Prevention of acid-aspiration pneumonitis during surgery: Ranitidine can be administered preoperatively to reduce the risk of aspiration pneumonia. The drug not only increases gastric pH, but also reduces the total output of gastric juice. In a 2009 meta-analysis comparing the net benefit of proton pump inhibitors and ranitidine to reduce the risk of aspiration before anesthesia, ranitidine was found to be more effective than proton pump inhibitors in reducing the volume of gastric secretions. Ranitidine may have an antiemetic effect when administered preoperatively.
Prevention of stress-induced ulcers in critically ill patients.
Preparations
Certain preparations of ranitidine are available over the counter (OTC) in various countries. In the United States, 75-mg and 150-mg tablets are available OTC. Zantac OTC is manufactured by Boehringer Ingelheim. In Australia, packs containing seven or 14 doses of the 150-mg tablet are available in supermarkets, small packs of 150-mg and 300-mg tablets are schedule 2 pharmacy medicines. Larger doses and pack sizes still require a prescription.
Dosing
For ulcer treatment, a night-time dose is especially important - as the increase in gastric/duodenal pH promotes healing overnight when the stomach and duodenum are empty. Conversely, for treating reflux, smaller and more frequent doses are more effective.
Ranitidine used to be administered long term for reflux treatment, sometimes indefinitely. However, PPIs have taken over this role. In addition, a fairly rapidtachyphylaxis can develop within 6 weeks of initiation of treatment, further limiting its potential for long-term use
People with Zollinger-Ellison syndrome have been given very high doses without any harm.
Contraindications
Ranitidine is contraindicated for patients known to have hypersensitivity to the drug.
Adverse effects
The following adverse effects have been reported as events in clinical trials
Central nervous system
There have been rare reports of malaise, dizziness, somnolence, insomnia, and vertigo. In severely ill, elderly patients, there have been rare cases of reversible mental confusion, agitation, depression, and hallucinations.Ranitidine causes fewer CNS adverse reactions and drug interactions compared to cimetidine
Cardiovascular
There have been rare reports of arrhythmias such as tachycardia, bradycardia, atrioventricular block, and premature ventricular beats.
Gastrointestinal
All drugs in its class have the potential to cause vitamin B12 deficiency secondary to a reduction in food-bound vitamin B12 absorption.Elderly patients taking H2receptor antagonists are more likely to require B12 supplementation than those not taking such drugs.H2 blockers may also reduce the absorption of drugs (azole antifungals, calcium carbonate) that require an acidic stomach. In addition, multiple studies suggest the use of H2 receptor antagonists such as raniditine may increase the risk of infectious diarrhoea, including traveller's diarrhoea and salmonellosis. Finally by suppressing acid-mediated breakdown of proteins, ranitidine may lead to an elevated risk of developing food or drug allergies, due to undigested proteins then passing into the gastrointestinal tract, where sensitisation occurs. Patients who take these agents develop higher levels of IgE against food, whether they had prior antibodies or not.Even months after discontinuation, an elevated level of IgE in 6% of patients was still found in this study.
Hepatic
There have been rare, reported cases of cholestatic hepatitis, hepatic failure, hepatitis, jaundice. These symptoms require immediate discontinuation of the drug.
Respiratory
Ranitidine and other histamine H2 receptor antagonists may increase the risk of pneumonia in hospitalized patients. They may also increase the risk of community-acquired pneumonia in adults and children.
Hematologic
Thrombocytopenia is a rare but known side effect. Drug-induced thrombocytopenia usually takes weeks or months to appear, but may appear within 12 hours of drug intake in a sensitized individual. Typically, the platelet count falls to 80% of normal, and thrombocytopenia may be associated with neutropenia and anemia.
Interaugmentary
Rash, including rare cases of erythema multiforme. Rare cases of hair loss and vasculitis.
Warnings and precautions
Disease related concerns
With gastric malignancies, relief of symptoms due to the use of ranitidine does not exclude the presence of a gastric malignancy. In addition with renal or hepatic impairment, ranitidine must be used with caution. Finally, ranitidine should be avoided in patients with porphyria as it may precipitate an attack.
Pregnancy
Pregnancy Category B.
Lactation
Ranitidine enters breast milk, with peak concentrations seen at 5.5 hours after the dose in breast milk. Caution should be exercised when prescribed to nursing women.
Children
In children, the use of gastric acid inhibitors has been associated with an increased risk for development of acute gastroenteritis and community-acquired pneumonia. A cohort analysis including over 11,000 neonates reported an association of H2 blocker use and an increased incidence of necrotizing enterocolitisin very low birth weight (VLBW) neonates. In addition, there was an approximately sixfold increase in mortality, necrotizing enterocolitis, and infection ( such assepsis, pneumonia, urinary tract infection) was reported in patients receiving ranitidine in a cohort analysis of 274 VLBW neonates.
Pharmacology
Mechanism of action
Ranitidine is a competitive, reversible inhibitor of the action of histamine at the histamine H2-receptors found in gastric cells. This results in decreased gastric acid secretion and gastric volume, and reduced hydrogen ion concentration.
Pharmacokinetics
Absorption: Oral: 50%
Protein binding: 15%
Metabolism: N-oxide is the principal metabolite.
Half-life elimination: With normal renal function, ranitidine taken orally has a half-life of 2.5–3 hours. If taken intravenously, the half-life is generally 2-2.5 hours in a patient with normal creatinine clearance.
Excretion: The primary route of excretion is the urine. In addition, approximately 30% of the orally administered dose is collected in the urine as non-absorbed drug in 24 hours.
Elderly
In the elderly population, the plasma half-life of ranitidine is prolonged to 3–4 hours secondary to decreased kidney function causing decreased clearance.[26]
Children
In general, studies looking pediatric patients (aged 1 month to 16 years) have showed no significant differences in pharmacokinetic parameter values in comparison to healthy adults, when correction is made for body weight.
History
Ranitidine was first prepared as AH19065 by John Bradshaw in the summer of[when?] in the Ware research laboratories ofAllen & Hanburys Ltd, part of the Glaxo organization. Its development was a response to the first in class histamine H2-receptor antagonist, cimetidine, developed by Sir James Black at Smith, Kline and French, and launched in the United Kingdom as Tagamet in November 1976. Both companies would eventually become merged as GlaxoSmithKline following a sequence of mergers and acquisitions starting with the integration of Allen & Hanbury's Ltd and Glaxo to form Glaxo Group Research in 1979, and ultimately with the merger of Glaxo Wellcome and SmithKline Beecham in 2000. Ranitidine was the result of a rational drug-design process using what was by then a fairly refined model of the histamine H2-receptor andquantitative structure-activity relationships.
Glaxo refined the model further by replacing the imidazole ring of cimetidine with a furan ring with a nitrogen-containing substituent, and in doing so developed ranitidine. Ranitidine was found to have a far-improved tolerability profile (i.e. feweradverse drug reactions), longer-lasting action, and 10 times the activity of cimetidine. Ranitidine has 10% of the affinity that cimetidine has to CYP450, so it causes fewer side effects, but other H2 blockers famotidine and nizatidine have no CYP450 significant interactions.
Ranitidine was introduced in 1981 and was the world's biggest-selling prescription drug by 1988. It has since largely been superseded by the even more effective PPIs, with omeprazole becoming the biggest-selling drug for many years. When omeprazole and ranitidine were compared in a study of 144 people with severe inflammation and erosions or ulcers of the esophagus, 85% of those treated with omeprazole healed within eight weeks, compared to 50% of those given ranitidine. In addition, the omeprazole group reported earlier relief of heartburn symptoms.
Source : Wikipedia
Tag :
Drug Study,
Folic Acid
Action:
Vitamin B complex essential for nucleoprotein synthesis and maintenance of normal erythropoiesis. Acts against folic acid deficiency that impairs thymidylate synthesis and results in production of defective DNA that leads to megaloblast formation and arrest of bone marrow maturation.
Classification:
Vitamin B9
Indication:
Folate deficiency, macrocytic anemia, and megaloblastic anemias associated with malabsorption syndromes, alcoholism, primary liver disease, inadequate dietary intake, pregnancy, infancy, and childhood.
TABLE
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Drug Name
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Dosage & Route
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Action
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Indication
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Adverse Effects
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Contraindication
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Nursing Responsibility
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FOLIC ACID (VITAMIN B9, PTEROYLGLUTAMIC ACID)
(fol'ic)
Classifications
Vitamin B9
|
Therapeutic
Adult: PO/IM/SC/IV  1 mg/dChild: PO/IM/SC/IV 1 mg/dMaintenance Adult: PO/IM/SC/IV 0.4 mg/dChild: PO/IM/SC/IV <4 y, 0.3 mg/d; >4 y, 0.4 mg/dInfant: PO/IM/SC/IV 0.1 mg/d |
Vitamin B complex essential for nucleoprotein synthesis
and maintenance of normal erythropoiesis. Acts against folic acid deficiency
that impairs thymidylate synthesis and results in production of defective DNA
that leads to megaloblast formation and arrest of bone marrow maturation.
|
Folate deficiency, macrocytic anemia, and megaloblastic
anemias associated with malabsorption syndromes, alcoholism, primary liver
disease, inadequate dietary intake, pregnancy, infancy, and childhood.
|
Reportedly nontoxic. Slight flushing and feeling of warmth
following IV administration.
|
Folic acidalone for pernicious anemia or other vitamin B12
deficiency states; normocytic, refractory, aplastic, or undiagnosed anemia.
|
Assessment & Drug Effects
|
Tag :
Drug Study,
Albuterol
Salbutamol, Ventolin, Ventolin Rotocaps, Volmax
Action:
Synthetic sympathomimetic amine and moderately selective beta2-adrenergic agonist with comparatively long action. Acts more prominently on beta2 receptors (particularly smooth muscles of bronchi, uterus, and vascular supply to skeletal muscles) than on beta1 (heart) receptors. Minimal or no effect on alpha-adrenergic receptors. Inhibits histamine release by mast cells.
Classifications:
autonomic nervous system agent; beta-adrenergic agonist (sympathomimetic); bronchodilator (respiratory smooth muscle relaxant)
Indication:
To relieve bronchospasm associated with acute or chronic asthma, bronchitis, or other reversible obstructive airway diseases. Also used to prevent exercise-induced bronchospasm.
TABLE
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Drug Name
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Dosage & Route
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Action
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Indication
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Adverse Effects
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Contraindication
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Nursing Responsibility
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ALBUTEROL
(al-byoo'ter-ole)) Accuneb, Novosalmol  , Proventil,
Proventil HFA, Proventil Repetabs, Salbutamol, Ventolin, Ventolin Rotocaps,
Volmax
Classifications: autonomic nervous system agent; beta-adrenergic agonist
(sympathomimetic); bronchodilator
(respiratory smooth muscle relaxant)
|
Bronchospasm
Adult: PO 2–4 mg 3–4 times/d, 4–8 mg sustained release 2 times/d Inhaled 1–2 inhalations q4–6h Child: PO 2–6 y, 0.1–0.2 mg/kg t.i.d. (max: 4 mg/dose); 6–12 y, 2 mg 3–4 times/d; Inhaled 6–12 y, 1–2 inhalations q4–6h |
Synthetic sympathomimetic amine and moderately selective
beta2-adrenergic agonist with comparatively long action. Acts more
prominently on beta2 receptors (particularly smooth muscles of
bronchi, uterus, and vascular supply to skeletal muscles) than on beta1
(heart) receptors. Minimal or no effect on alpha-adrenergic receptors.
Inhibits histamine release by mast cells.
|
To relieve bronchospasm associated with acute or chronic asthma, bronchitis, or other reversible obstructive airway diseases. Also used to prevent exercise-induced bronchospasm. |
Body as a
Whole: Hypersensitivity reaction. CNS: Tremor, anxiety, nervousness, restlessness,
convulsions, weakness, headache, hallucinations. CV: Palpitation, hypertension,
hypotension, bradycardia, reflex tachycardia. Special
Senses: Blurred vision, dilated pupils. GI: Nausea, vomiting. Other: Muscle cramps, hoarseness.
|
Pregnancy (category C), lactation. Use of oral syrup in
children <2 y.
|
|
Tag :
Drug Study,
Furosemide
Fumide , Furomide , Lasix, Luramide
Action:
Rapid-acting potent sulfonamide “loop” diuretic and antihypertensive with pharmacologic effects and uses almost identical to those of ethacrynic acid. Exact mode of action not clearly defined; decreases renal vascular resistance and may increase renal blood flow.
Classification:
ELECTROLYTIC AND WATER BALANCE AGENT; LOOP DIURETIC
Indication:
Treatment of edema associated with CHF, cirrhosis of liver, and kidney disease, including nephrotic syndrome. May be used for management of hypertension, alone or in combination with other antihypertensive agents, and for treatment of hypercalcemia. Has been used concomitantly with mannitol for treatment of severe cerebral edema, particularly in meningitis.
TABLE
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Drug Name
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Dosage & Route
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Action
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Indication
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Adverse Effects
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Contraindication
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Nursing Responsibility
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FUROSEMIDE
(fur-oh'se-mide)
Fumide , Furomide , Lasix, Luramide
Classifications: electrolytic and water balance agent;
loop diuretic
|
Edema
Adult: PO 20–80 mg in 1 or more divided doses up to 600 mg/d if needed IV/IM 20–40 mg in 1 or more divided doses up to 600 mg/d Child: PO 2 mg/kg, may be increased by 1–2 mg/kg q6–8h (max: 6 mg/kg/dose) IV/IM 1 mg/kg, may be increased by 1 mg/kg q2h if needed (max: mg/kg/dose) Neonate: PO 1–4 mg/kg q12–24h IV/IM 1–2 mg/kg q12–24h Hypertension Adult: PO 10–40 mg b.i.d. (max: 480 mg/d) |
Rapid-acting
potent sulfonamide "loop" diuretic and antihypertensive with
pharmacologic effects and uses almost identical to those of ethacrynic acid.
Exact mode of action not clearly defined; decreases renal vascular resistance
and may increase renal blood flow
|
|
CV: Postural hypotension, dizziness with excessive diuresis, acute
hypotensive episodes, circulatory collapse. Metabolic: Hypovolemia, dehydration, hyponatremia hypokalemia, hypochloremia metabolic alkalosis,
hypomagnesemia, hypocalcemia (tetany), hyperglycemia, glycosuria, elevated
BUN, hyperuricemia. GI:
Nausea, vomiting, oral and gastric burning, anorexia, diarrhea, constipation,
abdominal cramping, acute pancreatitis, jaundice. Urogenital: Allergic interstitial
nephritis, irreversible renal failure, urinary frequency. Hematologic: Anemia, leukopenia,
thrombocytopenic purpura; aplastic anemia,
agranulocytosis (rare). Special
Senses: Tinnitus, vertigo, feeling of fullness in ears, hearing loss
(rarely permanent), blurred vision. Skin:
Pruritus, urticaria, exfoliative dermatitis, purpura, photosensitivity,
porphyria cutanea tarde, necrotizing angiitis (vasculitis). Body as a Whole: Increased perspiration;
paresthesias; activation of SLE, muscle spasms, weakness; thrombophlebitis,
pain at IM injection site.
|
History of hypersensitivity to furosemide or sulfonamides; increasing oliguria, anuria, fluid and electrolyte depletion states; hepatic coma; pregnancy (category C), lactation. |
·
Observe patients receiving parenteral drug carefully; closely
monitor BP and vital signs. Sudden death from cardiac arrest has been
reported.
·
Monitor BP during periods of diuresis and through period of
dosage adjustment.
·
Observe older adults closely during period of brisk diuresis.
Sudden alteration in fluid and electrolyte balance may precipitate
significant adverse reactions. Report symptoms to physician.
·
Lab tests: Obtain frequent blood count, serum and urine
electrolytes, CO2, BUN, blood sugar, and uric acid values during
first few months of therapy and periodically thereafter.
·
Monitor for S&S of hypokalemia.
·
Monitor I&O ratio and pattern. Report decrease or unusual
increase in output. Excessive diuresis can result in dehydration and
hypovolemia, circulatory collapse, and hypotension. Weigh patient daily under
standard conditions.
·
Monitor urine and blood glucose & HbA1C closely
in diabetics and patients with decompensated hepatic cirrhosis. Drug may
cause hyperglycemia.
|
Tag :
Drug Study,
