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NURS 2004 Final: N2004- Pharmacology Final Exam
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Department
Nursing
Course
NURS 2004
Professor
R.Crossman
Semester
Winter

Description
PEPTIC ULCER DISEASE Peptic Ulcer Disease Group of upper GI disorders characterized by varying degrees of erosion of gut wall (common in lesser curvature of stomach and duodenum). Develop when any region is exposed to acid’s pepsin and when an imbalance exists between mucosal defensive factors and aggressive factors Signs and Symptoms of PUD - Abdominal discomfort - Weight loss - Poor appetite - Bloating - Belching - N/V - GI bleeding Defensive Factors - Mucous - Bicarbonate - Blood flow - pGs Aggressive Factors - H-pylori - NSAIDs - Gastric Acids/ Pepsin - Smoking Goal of PUD therapy: - Alleviate symptoms - Promote healing - Prevent complications - Prevent recurrence Drugs do not alter the disease process, they create conditions conductive to healing H2 Receptor Antagonist MOA: suppresses secretion of gastric acid by Ranitidine (Zantac) blocking H2 receptors on gastric parietal cells of the stomach, thus decrease both the volume of gastric juice and decrease hydrogen ion concentration Early H2 receptor antagonist was Cimetidine (Tagamet) had more side effects due to distribution Proton Pump Inhibitor MOA: undergoes conversion to its active Omeprazole (Prilosec) form within parietal cells of the stomach. It causes irreversible inhibition of H-K ATPase, the enzyme that generates gastric acid Antacids Give relief and promote healing. They alter pH which affects dissolution and absorption of other drugs Mucosal Protectant MOA: prevents NSAID induced gastric ulcers Misoprostol (Cytotec) by serving as a replacement for endogenous pGs Sucralfate/ Carafate MOA: under slightly acidic conditions, forms a viscous and sticky gel that adheres to ulcer, promoting healing by protecting against gastric acid pepsin and bile salts LAXATIVES Constipation Difficult, incomplete, or infrequent evacuation of dry, hardened feces from the bowels. Determined by altered consistency more than frequency Causes of Constipation: - Excessive alcoholic beverages, white flour, dairy products, chocolate - Aging slows fecal transit time - Drugs that decrease intestinal motility Laxatives Used to ease or stimulate defection - Soften stool - Increase stool volume - Hasten fecal passage through intestine - Facilitate evacuation from the rectum Indications for Mild Laxatives - True diagnosis of constipation - If it causes hemorrhoids and bleeding - If straining, can increase myocardial demand (Valsalva Maneuver: pass out) - For prevention of impaction with bedridden patients Indications for Cathartic Laxatives - Treatment/ procedure/ preparation - Removal of poisons Contraindications of Laxatives - Abdominal pain, cramps, nausea - Acute surgical abdomen - Fecal impaction or obstruction (perforation) - Habitual use Bulk- Forming MOA: swell in water viscous gel soften Psyllium (Metamucil) fecal mass and increase bulk stretches intestinal wall mildly stimulates peristalsis Surfactant MOA: decrease surface tension of stool Docusate sodium (Colace) slowing water to blend with stool; inhibit fluid absorption by intestinal walls; stimulate secretion of water and electrolytes into intestine Stimulant/ Contact MOA: increase water and electrolytes in Biscodyl (Dulcolax) intestine; stimulate intestinal motility Often abused Osmotic MOA: made of poorly absorbed salts, draws Magnesium Hydroxide (Milk of Magnesia) water into intestinal lumen by osmotic action, Magnesium Citrate water causes fecal mass to swell which stimulates peristalsis Likely to cause diarrhea and cramping Contraindication: heart failure and hypertension ANTI-DIARRHEAL Diarrhea Excessive volume, fluidity and frequency of bowel movements Causes of Diarrhea - Infection - Poor digestion - Inflammation - Medication side effect (antibioitcs) - Substances (lactose) - Disorders (IBS, Crohn’s, Ulcerative Colitis) Bismuth Subsolioylate (Pepto-Bismol) MOA: inhibit the pGs responsible for GI hypermotility and inflammation Caution: hypersensitivity to ASA, diabetes, gout, anticoagulatants, pregnancy Opioid MOA: activate opioid receptors in GI tract, Diphenoxylate (Lomotil) decrease motility, decrease secretion of fluid into small intestine, increase absorption of fluid and salt Morphine effects with high doses Opioid MOA: suppress fluid secretion in intestinal Loperamide (Imodium) lumen No opioid effects ANTI-EMETICS Emetic Response Vomiting Response - Direct stimulation: brain, senses, ears - Indirect stimulation: CTZ first (stomach or drugs) Serotonin Receptor Antagonist MOA: blocks type 3 serotonin receptors on Ondanestron (Zofran) vagal nerve in CTZ For vomiting induced by cancer drugs, radiation Dopamine Antagonist MOA: blocks dopamine and serotonin Metoclopradmine (Reglan) receptors in CTZ activated by stomach or drugs (also GI motility) For post op N/V, emesis from cancer drugs, opioids, toxins, radiation Muscarinic Antagonist MOA: suppresses nerve impulses between Scopolamine inner ear and vomiting centre Most effective for motion sickness Patch Anti- Histamine MOA: blocks receptors for Ach and H1 Diemnhydrinate (Gravol) DIABETES MELLITUS Type 1 Diabetes Loss of pancreatic Beta cells; no insulin produced (immune abnormality/ autoimmune disorder) - Diagnosed in childhood/ adolescence - Abrupt onset/ symptoms come quickly - No insulin production - Requires exogenous insulin Type 2 Diabetes Insulin resistance (impaired insulin secretion) - May or may not need insulin - Diagnosed middle aged/ later life Long term complications Macrovascular - Hypertension - Stroke - Heart disease Microvascular - Nephropathy: kidney disease - Neuropathy: nerve injury/ disease - Retinopathy: eye injury/ disease Amputations Sexual impotence Gastroparesis: delayed emptying of stomach and GI tract Hgb A1C Goal <7% In order to achieve require: - Fasting/ before meals glucose should be 4.0-7.0 - Post meals (2 hrs) should be 5.0-10.0 Diabetes Goals Short Term - Eliminate symptoms and metabolic stabilization Long Term - Maintain normal physical and psychological functioning - Prevent complications - Normoglycemia - Hb A1C with (N) limits Insulin The mechanism by which glucose is taken up into the cell. Stays in the blood if it cannot get in Insulin MOA: binds to insulin receptors on cell membranes of muscle and fat tissue Check pts blood sugar before giving insulin. They need to eat after giving them insulin Indications: hyperglycemia, insulin stimulates the liver to store glucose in form of glycogen Contraindications: hypoglycemia Adverse Effects: - Lipodystrophies (scar tissue where injections are given) - Allergic reaction Rapid Acting Insulin Quick Onset, Short Duration Mimics bodies responses - Lispro (Humalog) - Aspart (Novolog, Novarapid) - Insulin Glusine (Synthetic Human Analog) Regular Insulin - Humulin R - Novolin R Intermediate Duration (NPH) - Humulin N - Novolin N - Iletin 2 NPH (pork) - Insulin Levemir (dose dependent) Long Duration Effects last 24 hours - Glargine insulin (Lantus)- steady levels, no discernable peak Insulin Dosing Doses are guided by blood glucose levels or grams of carbs eaten Teenagers need more insulin during growth spurts When adjust doses: - One type of insulin is changed by very small amount at a time - Based on 2-5 days of glucose values Oral Hypoglycemics MOA: Binds to sensitive K+ channels ATPase in pancreatic Glyburide (Diabeta, cell membranes; enhance insulin secretion in response to high Micronase)- Sulfonylureas blood glucose levels; increase sensitivity of insulin receptors Excreted in bile Contraindications: lack of endogenous insulin, pregnancy, stressful conditions, allergy to sulpha drugs Oral Hypoglycemics MOA: binds to liver; decrease production of glucose in the Metformin (Glucophage) liver; enhances glucose uptake and use in the muscles Oral Hypoglycemics MOA: decreases insulin resistance or ability to target cells to Rosigliatzone (Avandia) respond to insulin; may improve beta cell function (preventing Proglitazone (Actos) complication), may also decrease lipids BP and prevent atherosclerosis Diabetic Ketoacidosis- Signs - Kussmauls respirations and Symptoms - Dehydration - Stomach pain - HPA activation- diaphoresis Diabetic Ketoacidosis- - Water and sodium replacement Management - Insulin replacement - Bicarbonate for acidosis - Potassium replacement - Normalization of glucose levels Glucagon MOA: promotes the breakdown of glycogen, decrease glycogen synthesis and stimulates biosynthesis of glucose to increase glucose levels st IV glucose (D5W) is 1 choice for severe hypoglycemia ASTHMA Asthma Chronic inflammation disorder of the airway. Caused by immune response from allergy or irritant. Allergen Hypersensitive agent Signs and Symptoms of Asthma - Sense of breathlessness - Chest tightness - Wheezing - Dyspnea - Cough Inhaled asthma medication - Therapeutic effects are enhanced (delivered benefits directly to the site of action) - Systemic effects are minimized - Rapid onset of action Metered Dose Inhalers Small and hand held pressurized devices (aerosol canisters) that provides measured doses; requires one minute between puffs; inhale prior to activating the device and requires hand- lung coordination. Only 10% of drugs reaches lungs (use spacers); must lost in oropharynx Dry Powder Inhalers Used to deliver drugs in the form of a dry micronized powder directly to the lungs; no propellants used and breath activated. Delivers 20% to lungs Nebulizers Small machine used to convert a drug solution into a mist; finer particles, easily absorbed; used via face mask; takes long to administer Beta- 2 Adrenergic Agonists MOA: selectively activates Beta-2 receptors on smooth Ventolin (Albuterol) muscle in the lungs; causes bronchodilation (decrease Serevent (Salmeterol) Histamine, increase ciliary action) Terbeutaline (Breathin) Can also activate Beta-1 receptors in the heart (stimulate SA node to increase HR) Indications: acute bronchospasms, exercise induced bronchospasm Side Effect: - Tachycardia (stimulates SA node) - Increase FOC (effect on myocardial smooth muscle) - Vasoconstriction - Angina (s/t increase oxygen demand in patient with CAD) Used as a rescue inhaler Methylxanthines MOA: produces bronchodilation by relaxing bronchial Theophylline (Theodur) smooth muscle, inhibits an enzyme which increase intercellular levels of cyclic AMP Indications: chronic asthma, maintenance therapy Dangerous! Narrow therapeutic range (should be less <20 mcg) Mild (20-25) to severe effects (>25) Glucocorticoids MOA: bind to and stabilize mast cells to decrease Pulmicort synthesis and release of inflammatory mediators (blocks Flovent phospholipase A) Most effective anti-asthma drug Indications: prophylaxis of chronic asthma Adverse Effects: - Adrenal suppression - Oropharyngeal candidiasis- rinse after using - PUD - Dysphonia - Reserved for adult unless severe (stunts children’s growth) Anti-Inflammatory MOA: suppresses inflammation, not a bronchodilator; Cromolyn (Intal) stabilizes the membrane of mast cells Indications: - Prophylactic treatment - Exercise induced bronchospasm - Allergic rhinitis Inhalation only HYPERTENSION Cardiac Preload Pressure in right side of heart as blood returns Cardiac Afterload Pressure the heart must pump against to eject blood (PVR) BP Formula BP= CO x PVR (or) FOC x PVR Hypertension Systolic BP >140; Diastolic BP >90 Goal is BP <140/90 Diuretics MOA: decrease volume, decrease of arterial resistance Thiazide Adverse Effects: - Hypokalemia (messes up heart rhythm and nerve functions) - Dehydration - Hyperglycemia - Hyperuricemia Beta Blockers Non selective Propanolol (Inderal) MOA: binds to Beta 1 and Beta 2 receptors in the heart and lungs - Decrease HR, FOC, impulse conduction at AV node, decrease renin Adverse Effects: - Bradycardia - Reduced CO - Precipitation of heart failure - AV heart block - Bronchoconstriction - Inhibition of glycogenolysis Can get rebound cardiac excitation with abrupt withdrawal Beta Blockers Cardio-selective Metoprolol (Lospressor) MOA: binds to Beta 1 receptors in the heart - Slows depolarization, decrease HR and FOC decrease CO decrease BP and decrease oxygen
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