Drugs Affecting Gastrointestinal Secretions PDF

DRUGS AFFECTING GASTROINTESTINAL Antacids SECRETIONS – Interact with acids at the chemical Underlying Causes of GI Disorders: level to neutralize them Dietary excess Proton p...

DRUGS AFFECTING GASTROINTESTINAL Antacids SECRETIONS – Interact with acids at the chemical Underlying Causes of GI Disorders: level to neutralize them Dietary excess Proton pump inhibitors Stress – Suppress the secretion of hydrochloric acid into the lumen of the stomach Hiatal hernia Antipeptic agents Esophageal reflux – Coat any injured area in the stomach Adverse drug effects to prevent further injury from acid Peptic ulcer disease Prostaglandins Effect of Drugs on GI Secretions: – Inhibit the secretion of gastrin and Decrease GI secretory activity increase the secretion of the mucous lining of the stomach, providing a buffer Block the action of GI secretions PATIENTS WHO MAY REQUIRE DIGESTIVE Form protective coverings on the GI lining to ENZYME SUPPLEMENTS prevent erosion from GI secretions Saliva supplements Replace missing GI enzymes that the GI tract or ancillary glands and organs can no longer – Stroke produce – Salivary gland disorder PEPTIC ULCERS – Extreme surgery of the head and neck Definition Pancreatic enzyme supplements – Erosions in the lining of the stomach – Common duct problems and adjacent areas of the GI tract – Pancreatic disease Symptoms – Cystic fibrosis – Gnawing, burning pain, often occurring after meals H2 ANTAGONISTS Cause Cimetidine (Tagamet, Tagamet HB): The first drug in this class to be developed – Bacterial infection by Helicobacter pylori bacteria Ranitidine (Zantac): Longer acting and more potent than cimetidine DRUGS USED IN THE TREATMENT OF ULCERS Famotidine (Pepcid, Pepcid AC): Similar to Histamine-2 (H2) antagonists ranitidine, but much more potent – Block the release of hydrochloric acid Nizatidine (Axid): Newest drug in this class; in response to gastrin similar to ranitidine; indicated for patients with liver dysfunction  INDICATIONS FOR H2 ANTAGONISTS FOCUS ON THE PROTOTYPE ANTACID: SODIUM BICARBONATE  Short-term treatment of active duodenal ulcer or benign gastric ulcer  Indications: Hyperacidity; GI  Treatment of pathological bleeding and stress ulcers; hypersecretory conditions such as severe diarrhea; metabolic Zollinger–Ellison syndrome acidosis; certain drug  Prophylaxis of stress-induced ulcers and intoxications; minimize uric acid acute upper GI bleeding in critical crystallization patients  Actions: Neutralizes or reduces  Treatment of erosive gastroesophageal gastric acidity resulting in an reflux increase in gastric pH; inhibits  Relief of symptoms of heartburn, acid the proteolytic activity of indigestion, and sour stomach (OTC pepsin preparations)  Oral route: Onset rapid; peak 30 min; duration 1–3 h TYPES OF ANTACIDS  T½: Unknown; excreted  Sodium bicarbonate (Bell/Ans) unchanged in urine  Calcium carbonate (Calciday-667, PROTON PUMP INHIBITORS Tums, and others)  Magnesium salts (Milk of Magnesia Action and others) – Suppress gastric acid secretion by  Aluminum salts (Amphojel and others) specifically inhibiting H+,K+-ATPase enzyme  Magaldrate (Lowsium, Riopan) system on the secretory surface of the gastric FOCUS ON THE PROTOTYPE ANTACID: parietal cells SODIUM BICARBONATE Types  Indications: Hyperacidity; GI bleeding – Omeprazole (Prilosec), esomeprazole and stress ulcers; severe diarrhea; (Nexium), lansoprazole (Prevacid), metabolic acidosis; certain drug pantoprazole (Protonix), rabeprazole intoxications; minimize uric acid (Aciphex) crystallization ANTIPEPTIC AGENT  Actions: Neutralizes or reduces gastric acidity resulting in an increase in Sucralfate (Carafate) gastric pH; inhibits the proteolytic – Forms a protective coating over the activity of pepsin eroded stomach lining  Oral route: Onset rapid; peak 30 min; duration 1–3 h – Protects it from acid and digestive  T½: Unknown; excreted unchanged in enzymes urine – Aids healing  ANTIEMETIC AGENTS Groups of Centrally Acting Antiemetics Nausea and Vomiting Phenothiazines  Most common and most uncomfortable Nonphenothiazines complaints. Anticholinergics/Antihistamines  Vomiting is a complex reflex reaction to various stimuli. Serotonin (5-HT3) Receptor Blockers  In some cases, it may be desired to Substance P/Neurokinin 1 Receptor induce vomiting. Antagonists  In many clinical conditions, the reflex reaction of vomiting is not beneficial. Miscellaneous Group Managing Nausea and Vomiting PHENOTHIAZINES  Emetics Actions Cause vomiting Depresses various areas of the central nervous No longer recommended for at-home system (CNS) poison control Indications  Antiemetics Decrease or prevent nausea and Treatment of nausea and vomiting vomiting Adverse Effects Centrally acting or locally acting Varying degrees of effectiveness Drowsiness Sites of Action of Emetics/Antiemetics NONPHENOTHIAZINES Actions Acts to reduce the responsiveness of the nerve cells in the CTZ to circulating chemicals that induce vomiting Indications Prevention of nausea and vomiting Adverse Effects Drowsiness Fatigue Restlessness Extrapyramidal symptoms  ANTICHOLINERGICS/ANTIHISTAMINES SUBSTANCE P/NEUROKININ 1 RECEPTOR ANTAGONISTS Actions Actions Anticholinergics that act as antihistamines and block the transmission of impulses to the CTZ Act directly in the CNS to block receptors associated with nausea and vomiting Indications Indications Prevention and treatment of nausea and vomiting In combination with other agents to prevent nausea and vomiting Adverse Effects Pharmacokinetics Drowsiness Given orally, metabolized in the liver, and Confusion excreted in urine and feces Dry mouth Adverse Effects Anorexia Anorexia, fatigue, constipation, diarrhea, liver Urinary frequency enzyme elevation, dehydration SEROTONIN (5-HT3) RECEPTOR BLOCKERS MISCELLANEOUS ANTIEMETICS Actions Actions Block those receptors associated with nausea Varies with agent and vomiting in the CTZ and locally Indications Indications Treatment and prevention of nausea and Control of nausea and vomiting vomiting Pharmacokinetics Pharmacokinetics Rapidly absorbed, metabolized in the liver, and Varies according to agent excreted in urine and feces Contraindications Caution Coma Pregnancy and lactation Severe CNS depression Adverse Effects Brain damage or injury Headache, drowsiness, myalgia, urinary Hypotension or hypertension retention, constipation, pain at the injection site Severe liver dysfunction Caution Renal dysfunction Active peptic ulcer disease Pregnancy PROTOTYPE NONPHENOTHIAZINES Lactation Adverse Effects Linked to interference with normal CNS stimulation or response Drowsiness Dizziness Weakness Photosensitivity Hypotension, hypertension, and cardiac arrhythmias Drug-to-Drug Interactions PROTOTYPE ANTICHOLINERGICS/ Alcohol ANTIHISTAMINES PROTOTYPE PHENOTHIAZINES PROTOTYPE SEROTONIN (5-HT3) RECEPTOR NURSING CONSIDERATIONS FOR BLOCKERS ANTIEMETICS Assessment: History and Physical Exam Nursing Diagnosis Implementation Evaluation DRUGS AFFECTING GASTROINTESTINAL MOTILITY Actions of Drugs Used to Affect Motor Activity of the GI Tract Speed up or improve movement of intestinal contents when movement becomes slow or sluggish (constipation) Increase the tone of the GI tract and stimulate PROTOTYPE SUBSTANCE P/NEUROKININ 1 motility throughout the system RECEPTOR ANTAGONISTS Decrease movement along the GI tract when rapid movement decreases the time for absorption of nutrients (diarrhea) Types of Laxatives Chemical Stimulants Chemically irritate the lining of the GI tract Bulk Stimulants Cause the fecal matter to increase in bulk Lubricants Help the intestinal contents move more smoothly Types of Chemical Stimulants Cascara (Generic): Reliable agent that leads to intestinal evacuation Senna (Senokot): Reliable drug, similar to cascara (OTC) Castor Oil (Neoloid): Old standby for thorough Prevent straining when it is clinically evacuation of the intestine undesirable Bisacodyl (Dulcolax): Very popular OTC laxative Evacuate the bowel for diagnostic procedures Types of Bulk Stimulants Removal of ingested poisons Magnesium Sulfate (Epsom Salts) Adjunct in antihelmintic therapy Magnesium Citrate (Citrate of Magnesia) Pharmacokinetics Magnesium Hydroxide (Milk of Magnesia) Only minimally absorbed and exert their therapeutic effect directly in the GI tract Lactulose (Chronulac) Contraindications Polycarbophil (FiberCon) Acute abdominal disorders Psyllium (Metamucil) Caution Types of Lubricating Laxatives Pregnancy or lactation Docusate (Colace) Adverse Effects Has a detergent action on the surface of the intestinal bolus, making a softer stool GI effects - Diarrhea, abdominal cramping, and nausea Glycerin (Sani-Supp) CNS effects – Dizziness, headache, and Hyperosmolar laxative used to gently evacuate weakness the rectum without systemic effects higher in the GI tract CV effects – Sweating, palpitations, flushing, and fainting Mineral Oil (Agoral Plain) Cathartic dependency Forms a slippery coat on the contents of the intestinal tract Drug-to-Drug Interactions Laxatives Some interfere with the timing or process of absorption Actions Types of Gastrointestinal Stimulants Work in three ways: Dexpanthenol (Ilopan) Direct chemical stimulation of the GI tract Increases acetylcholine levels and stimulates Production of bulk or increased fluid in the the parasympathetic system lumen Metoclopramide (Reglan) Lubrication of the intestinal bolus to promote passage through the GI tract Blocks dopamine receptors and makes the GI cells more sensitive to acetylcholine Indications Leads to increased GI activity and rapid Short-term relief of constipation movement of food through the upper GI tract  Gastrointestinal Stimulants Loperamide (Imodium): Has a direct effect on the muscle layers of the GI tract; slows Actions peristalsis and allows increased time for Stimulate parasympathetic activity within the absorption of fluid and electrolytes GI tract Opium Derivatives (Paregoric): Stimulates Increase GI secretions and motility spasm within the GI tract, stops peristalsis and diarrhea Indications Antidiarrheal Drugs Rapid movement of GI contents is desirable Actions Pharmacokinetics Slow the motility of the GI tract through direct Rapidly absorbed action on the lining of the GI tract Metabolized in the liver Indications Excreted in the urine Relief of symptoms of acute or chronic diarrhea Contraindications Reduction of volume of discharge from Allergy ileostomies GI obstruction Prevention and treatment of traveler’s diarrhea Caution Pharmacokinetics Pregnancy Vary depending on agent Lactation Contraindications Adverse Effects Allergy Nausea, vomiting, diarrhea, intestinal spasms, Caution cramping, decreased blood pressure and heart Pregnancy rate, weakness, and fatigue Lactation Drug-to-Drug Interactions History of GI obstruction Digoxin History of acute abdominal conditions Cyclosporine Diarrhea due to poisonings Alcohol Adverse Effects Types of Antidiarrheal Drugs Constipation Bismuth Subsalicylate (Pepto-Bismol): Coats the lining of the GI tract and soothes irritation Abdominal distension stimulating local reflexes to cause excessive GI Abdominal discomfort activity and diarrhea Nausea Dry mouth Prototype Lubricant Laxative Toxic megacolon Fatigue Weakness Dizziness Drug-to-Drug Interactions Depends on the drug Prototype Chemical Stimulant Laxative Prototype Gastrointestinal Stimulants Prototype Bulk Laxative  Prototype Antidiarrheal Drugs THYROID AND PARATHYROID AGENTS Actions of the Thyroid Gland Produces two thyroid hormones using iodine found in the diet: – Tetraiodothyronine or levothyroxine (T4) = increase production, converted to T3 – Triiodothyronine or liothyronine (T3) = more active Removes iodine from the blood, concentrates it, and prepares it for attachment to tyrosine, an amino acid Nursing Considerations for Laxatives Functions of Thyroid Hormones Assessment: History and Physical Exam Regulate the rate of metabolism ( rate at which Nursing Diagnosis energy is burned in all cells ) Implementation Affect heat production and body temperature Evaluation Affect oxygen consumption, cardiac output, Nursing Considerations for Gastrointestinal and blood volume Stimulants Affect enzyme system activity Assessment: History and Physical Exam Affect metabolism of carbohydrates, fats, and Nursing Diagnosis proteins Implementation Regulate growth and development ( esp. within the reproductive & nervous system ) Evaluation Types of Thyroid Dysfunction Nursing Considerations for Antidiarrheal Drugs Hyperthyroidism Assessment: History and Physical Exam – Overactivity Nursing Diagnosis – Thyroid is overstimulated by TSH ( thyroid can’t Implementation make sufficient thyroid hormone to turn Evaluation off the hypothalamus & ant. pituitary )  viral infection Hypothyroidism overtreatment w/ antithyroid drugs – Underactivity surgical removal or irradiation of – Most common type of thyroid thyroid gland dysfunction - S / Sx : – Common finding in the elderly lethargy pale & coarse HYPOTHYROIDISM skin Absence of the thyroid gland intolerance to cold thickening Lack of sufficient iodine in the diet to produce of tongue & vocal chords the needed level of thyroid hormone hypoactive reflexes Lack of sufficient functioning thyroid tissue due hypotension to tumor or autoimmune disorders bradycardia loss of hair Lack of TRH related to a tumor or disorder of ↓ sexual function sterility the hypothalamus Replacement Hormone Products for Treating ♦ Goiter Hypothyroidism - enlargement of the thyroid gland Levothyroxine (Synthroid, Levoxyl, Levo-T, - occurs when thyroid is overstimulated by Levothroid): Synthetic salt of T4 TSH Thyroid desiccated (Armour Thyroid and ♦ Cretinism others): Prepared from dried animal thyroid glands and contains both T3 and T4 - children born without a thyroid gland or Liothyronine (Cytomel): Synthetic salt of T3 have a nonfunctioning gland Liotrix (Thyrolar): Synthetic preparation of T4 - if left untreated : poor growth & and T3 in a standard 4:1 ratio development Focus on the Replacement Hormone mental retardation ( lack of thyroid Prototype: LEVOTHYROXINE hormone stimulation ) most frequently used replacement hormone ♦ Myxedema Indications: Replacement therapy in - severe adult hypothyroidism hypothyroidism; pituitary TSH suppression in - develops gradually as the thyroid the treatment of euthyroid goiters, slowly stops functioning management of thyroid cancer; thyrotoxicosis in conjunction with other therapy; myxedema - causes : coma autoimmune disease ( Hashimoto’s disease ) Actions: Increases the metabolic rate of body – intolerance to heat - tissues, increasing oxygen consumption, amenorrhea - weight loss respiration, and heart rate; the rate of fat, Treatment protein, and carbohydrate metabolism; and growth and maturation - surgery PO route: Onset slow; peak 1–3 weeks - radiation to destroy parts or all of the gland IV route: Onset 6–8 h; peak 24–48 h - drug treatment to block the T½: 6–7 days; metabolized in the liver and production of thyroxine in thyroid gland excreted in the bile Antithyroid Agents Brandnames: - used to block production of thyroid hormone Synthroid, Levoxyl, Levothroid, Unithroid, & to treat hyperthyroidism Tirosint Thioamides Synthetic salt of T4 Propylthiouracil (PTU) = most frequenly used Most frequently used replacement hormone thioamide due to its predictable bioavailability and reliability = DOC for pregnancy ( inform mother the risk of cretinism ) Dessicated thyroid Armour Thyroid) is prepared from dried animal thyroid glands and contains Methimazole (Tapazole) = more common both T3 and T4 adverse effects but less GI effects than PTU Liothyronine (Cytomel, Triostat)which is a Iodine solutions synthetic of T3 Prototype: METHIMAZOLE HYPERTHYROIDISM Indication: Treatment of hyperthyroidism Definition Action: Inhibits the synthesis of thyroid – Excessive amounts of thyroid hormones hormones are produce and released into the Pharmacokinetics: circulation PO onset 30-60 minutes duration 2-4 hours Cause T ½ 6 to13 hours, excreted in the urine – Graves’ disease Adverse Effects: Paresthesia, neuritis, vertigo, Signs and symptoms drowsiness, skin rash; urticarial, skin – Increased body temperature - pigmentation, nausea, vomiting, epigastric tachycardia - thin skin - goiter distress, nephritis, bone marrow suppression, arthralgia, myalgia, edema – palpitations - hypertension - flushing  Prototype: STRONG IODINE SOLUTIONS – Most likely to occur with the accidental removal of the parathyroid glands Indications: Adjunct therapy for during thyroid surgery hyperthyroidism; thyroid blocking in a radiation emergency Hyperparathyroidism Actions: Inhibits the synthesis of thyroid – The excessive production of hormones and inhibit the release of these parathormone hormones into the circulation – Can occur as a result of parathyroid Pharmacokinetics: tumor or certain genetic disorders PO onset 24 hours peak 10-15 days duration 6 Prototype: CALCITRIOL weeks Indications: Management of hypocalcemia in T ½ Unknown; metabolized in the liver and patients on chronic renal dialysis,management excreted in the urine of hypocalcemia associated with hypoparathyroidism Adverse Effects: Actions: A vitamin D compound that regulates Hypothyroidism the absorption of calcium and phosphate from Iodism (metallic taste and burning in the the small intestine, mineral resorption in bone, mouth,and throat, sore teeth and gums, and reabsorption of phosphate from the renal diarrhea, cold symptoms, stomach upset, tubules, increasing the serum calcium level diarrhea) Route: PO slow onset peak 4 hours duration 3- Staining of teeth 5 days Skin rash T ½ 5 to 8 hours; metabolized in the kidneys and other body tissues, excreted in the bile and Development of goiter feces Swelling of salivary glands Adverse Effects: Weakness, headache, nausea, Actions of Parathormone (PTH) vomiting, dry mouth, constipation, muscle Stimulation of osteoclasts or bone cells to pain, bone pain, metallic taste release calcium from the bone Antihypercalcemic Agents Increased intestinal absorption of calcium - drugs used to treat parathyroid hormone Increased calcium resorption from the kidneys excess or high levels of serum calcium Stimulation of cells in the kidney to produce  Bisphosphonates calcitriol  Calcitonin ( human & salmon )  Gallium Parathyroid Dysfunction Prototype Biphosphonates: ALENDRONATE Hypoparathyroidism Indications: Treatment and prevention of – The absence of parathormone osteoporosis in postmenopausal females and in males; treatment of glucorticoid-induced osteoporosis; treatment of Paget’s disease in Exocrine gland certain patients. – Releases sodium bicarbonate and Actions: Slows normal and abnormal bone pancreatic enzymes directly into the resorption without inhibiting bone formation common bile duct to be released into and mineralization. the small intestine Pharmacokinetics: PO, slow onset, duration for – Neutralizes the acid chyme from the days stomach and aids digestion T ½ Greater than 10 days; not metabolized but Insulin excreted in the urine Definition Adverse Effects: Abdominal pain, constipation, nausea, diarrhea, increased or recurrent bone – Hormone produced by the beta cells of the pain, esophageal erosion islets of Langerhans Prototype: CALCITONIN SALMON Action Indications: Paget’s disease, postmenopausal – Released into circulation when the levels of osteoporosis, emergency treatment of glucose around these cells rise hypercalcemia – Stimulates the synthesis of glycogen, the Actions: Inhibits bone resorption; lowers conversion of lipids into fat stored in the form elevated serum calcium in children and of adipose tissue, and the synthesis needed patients with Paget’s disease; increases the proteins from amino acids excretion of filtered phosphate, calcium, and Metabolic Changes Occurring When sodium by the kidney Insufficient Insulin is Released Hyperglycemia: Increased blood sugar ANTIDIABETIC HORMONES Glycosuria: Sugar is spilled into the urine Function of the Pancreas Gland: : glucose concentration in blood too Endocrine gland ↑ for complete reabsorption – Produces hormones in the islets of Polyphagia: Increased hunger Langerhans : hypothalamic centers can’t take 1. alpha cells = produce glucagon, in in glucose & sense they are starving response to ↓ blood sugar Polydipsia: Increased thirst 2. beta cells = produce insulin, in response to ↑ blood sugar : tonicity of the blood is ↑ owing to the ↑ glucose & waste products in the blood 3. delta cells = produce & the loss of fluid with glucose in the urine somatostatin, blocks the secretion of insulin & glucagon Lipolysis: Fat breakdown : body breaks down stored for energy because glucose is not usable Ketosis: Ketones cannot be removed Type 2, non–insulin-dependent diabetes effectively mellitus (NIDDM) Acidosis: Liver cannot remove all of the waste – Usually occurs in mature adults products – Has a slow and progressive onset Acid = primary waste product Clinical Signs and Symptoms of Hyperglycemia Diabetes Mellitus Fatigue – Characteristics Lethargy Complex disturbances in metabolism Irritation Affects carbohydrate, protein, and fat Glycosuria metabolism Polyphagia Clinical signs Polydipsia – Hyperglycemia (fasting blood sugar level greater than 126 mg/dL) Itchy skin – Glycosuria (the presence of sugar in Signs of Impending Dangerous Complications the urine) of Hyperglycemia Disorders Associated With Diabetes Fruity breath as the ketones build up in the system and are excreted through the lungs Atherosclerosis: Heart attacks and strokes related to the development of atherosclerotic Dehydration as fluid and important electrolytes plaques in the vessel lining are lost through the kidneys Retinopathy: With resultant loss of vision as Slow, deep respirations (Kussmaul’s tiny vessels in the eye are narrowed and closed respirations) as the body tries to rid itself of high acid levels Neuropathies: With motor and sensory changes in the feet and legs and progressive Loss of orientation and coma changes in other nerves as the oxygen is cut off Hypoglycemia Nephropathy: With renal dysfunction related Definition to changes in the basement membrane of the – Blood sugar concentration lower than Classifications of Diabetes Mellitus 40 mg/dL Type 1, insulin-dependent diabetes mellitus Occurrence (IDDM) – Starvation – Usually a rapid onset; seen in younger people – Lowering the blood sugar too far with treatment of hyperglycemia – Connected in many cases to viral destruction of the beta cells of the pancreas Types of Insulin Delivery Biguanide- Metformin Past Dipeptidyl Peptidase-4 Inhibitors (DPP-4 inhibitors)-Linagliptin – Subcutaneous injection Meglitinides-Repaglinide Present Sodium-Glucose Cotransporter-2 Inhibitors – Subcutaneous injection, insulin jet (SGLT-2 Inhibitors)-Canagliflozin injector, insulin pen, extended insulin pump, long-acting insulin Thiazolininediones-Pioglitazone Future TYPES OF GLUCOSE-ELEVATING AGENTS – Implantable insulin pump, insulin Diazoxide (Proglycem) patch, inhaled insulin – Can be taken orally ORAL ANTIDIABETIC AGENTS Glucagon (GlucaGen) Sulfonylureas – The hormone produced by the alpha – First oral agents introduced cells of the pancreas to elevate glucose levels – Stimulate the pancreas to release – Can be given only parenterally; insulin preferred for emergency situations Nonsulfonylureas IV, onset in 1 minute, peak of action is 15 minutes, duration 9-20 minutes – Introduced more recently – Act to decrease insulin resistance or alter glucose absorption and uptake Advantages of Second-Generation ANTI-INFECTIVES Sulfonylureas ANTI-INFECTIVES Excreted in urine and bile, making them safer - are drugs that are designed to act selectively for patients with renal dysfunction on foreign organisms that have invaded & Do not interact with as many protein-bound infected the body of a human host drugs as the first-generation drugs do Have a longer duration of action; can take Antibiotics = treat bacterial infections them only once or twice a day, increasing compliance Antivirals = treat viruses DRUGS?? Walang nakalagay sa ppt eh Antifungals = treat fungus Glimepiride (Amary),glipizide (Glucotrol), and Antiprotozoal = treat specific protozoal glyburide(DiaBeta) infections including malaria Sulfonylureas- Glyburide Antihelmintics = treat infections caused by worms Alpha-Glucosidase Inhibitors-Acarbose Antineoplasics = treat cancers, diseases caused Bactericidal = drugs that are so active against by abnormal cells the infective microorganisms causing cell death Bacteriostatic = drugs not so active & interfere with the ability of the cells to reproduce or Paul Ehrlich = first scientist to work on divide developing a synthetic chemical that would be effective only against infection – causing cells, Human Immune Response not human cells, in 1920’s. - involves a complex interaction between chemical mediators, leukocytes, lymphocytes, antibodies & locally released enzymes & Goal: reduction of the population of the chemicals invading organism to a point where the human immune response can take care of the Immunocompromised Patients infection - immune system may be incapable of dealing Mechanism of Action: effectively with the invading organism. 1. Interfere with the biosynthesis of the ex. malnutrition, age, AIDS, use of immune bacterial cell wall. Ex. Penicillin suppressant drugs 2. Prevent the cells of the invading difficult to treat infection organism from using the substance essential to Reasons: growth and development no cell division cell death 1. Anti-infective drugs cannot totally eliminate the pathogen without causing severe toxicity in 3. Interfere with the steps in protein the host synthesis ex. Aminoglycosides, macrolides & chloramphenicol 2. These patients do not have the immune response in place to deal with even a few 4. Alter permeability of cell membrane invading organism allowing essential cellular components to leak out cell death ex. Antibiotics, antifungals, Intervention: prevention of infection & proper antiprotozoala nutrition RESISTANCE Broad spectrum of activity = drugs that - Ability of bacteria over time to adapt to an interfere with biochemical reactions in many antibiotic and produce cells that are no longer different kinds of microorganisms useful in affected by the drug treatment of a wide variety of infections Reasons: Narrow spectrum of activity = drugs that are 1. Microorganisms produce an enzyme that so selective in their action that they are deactivates the antimicrobial drug. ex Penicillin effective only against only a few penicilinase microorganisms with very specific metabolic pathway or enzyme 2. Changing cellular permeability to prevent the drug from entering the cell or altering transport systems to exclude the drug from 3. Combination Therapy active transport into the cell. to interfere with its cellular structure in 3. Altering binding sites on the membrane or different areas or developmental phases ribosomes that then no longer accept the drug Reasons : 4. Producing a chemical that acts as an 1. May use smaller dosage of each drug -> antagonist to the drug. fewer adverse effects Prevention: 2. Some drugs are synergistic ( more powerful 1. Limit the use of antimicrobial agents to the when given in combination ) treatment of specific pathogen known to be 3. Infections may be caused by more than one sensitive to the drug being used. organism & each pathogen may react to a 2. Dosage should be high enough and the different anti-infective agent duration of drug therapy should be long 4. Sometimes, combined effects of different enough to eradicate even slightly resistant drugs delay the emergence of resistant strains microorganism. 3. Avoid indiscriminate use of anti-infectives. ADVERSE REACTIONS to ANTI-INFECTIVE THERAPY TREATMENT of SYSTEMIC INFECTIONS 1. Kidney damage 1. Identification of the Pathogen = direct toxic effect on the fragile cells in the = culture of infected area ( bacteria ) kidney -> renal dysfunction -> full blown renal failure = fecalysis ( parasites ) = ex aminoglycosides = microscopic ( fungal & protozoal ) = close monitoring & prevent accumulation, by 2. Sensitivity of the Pathogen hydrating well throughout the course of drug = start broad spectrum antibiotic after a therapy culture is taken but before the exact causative 2. GI toxicity organism has been identified = direct toxic effects on the cells lining the GI = do sensitivity testing on the cultured tract microbes = mild : nausea, vomiting, stomach upset or shows which drugs are capable of diarrhea controlling the particular microorganism = severe : hepatitis & liver failure particularly important with microorganisms having known resistant strains = death of microorganism -> release of toxins - > stimulate CTZ ( chemoreceptor trigger zone in medulla ) -> induce nausea & vomiting 3. Neurotoxicity = ex. aminoglycosides affect 8th CN ( vertigo, dizziness & loss of hearing ) = damage or interfere with function of nerve tissue esp. in areas where drugs tend to accumulate in high concentration 4. Hypersensitivity Reactions = induce antibody formation in susceptible people 5. Superinfections = destruction of normal flora -> opportunistic pathogens invade tissues -> infection = Proteus & Pseudomonas ( vagina or GI yeast infections ) PROPHYLAXIS - using antibiotics to prevent infections before they occur -- Sama nyo nalang sa review nyo yung naka table na antibiotics hehe