CASE PRESENTATION

1. CASE PRESENTATION

2. PATIENT’S PROFILE Name: Mr. X Date of Admission: 26/7/2009 Age: 72 years old Race: Malay Gender: Male Diagnosis: COAD, hypertension Weight: Cannot be assessed Height: Cannot be assessed Allergy: Unknown

3. Chronic Obstructive Pulmonary Disease 1 progressive disease narrowing of the airways, leading to the shortness of breath and difficulty in breathing "Progressive" means the disease gets worse over time. • 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition.

4. COPD includes the terms chronic bronchitis (clinical term) and • condition with chronic or recurrent excessive mucus secretion into the bronchial tree with cough1 emphysema(anatomic pathology) • enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls • Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition. • http://www.buzzle.com/articles/pathophysiology-of-copd.html

5. Causes • Cigarette smoking is the primary modifiable risk factor for the development of COPD. • Long-term exposure to other lung irritants, such as air pollution, chemical fumes, or dust, also may contribute to COPD. 5 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

7. Pathophysiology 1 The most important processes causing lung damage are: Oxidative stress produced by the high concentrations of free radicals in tobacco smoke. Cytokine release due to inflammation as the body responds to irritant particles such as tobacco smoke in the airway. Tobacco smoke and free radicals impair the activity of antiprotease enzymes (such as alpha 1-antitrypsin) Protease enzymes damage the cells and tissue of lungs and other supportive tissues, 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

8. Healthy vsCOPD

9. Symptoms 1 • A cough (large amount of mucus) • Chest tightness • Shortness of breath • Wheezing • Low energy http://www.buzzle.com/articles/pathophysiology-of-copd.html

10. Hypertension High blood pressure (HBP) or hypertension means high pressure (tension) in the arteries. Arteries are vessels that carry blood from the pumping heart to all the tissues and organs of the body.5 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

11. Blood pressure is the force applied against the walls of the arteries as the heart pumps blood through the body. The pressure is determined by the force and amount of blood pumped and the size and flexibility of the arteries.1 http://www.healthline.com/sw/khs-understanding-asthma&usg

12. Classification 1 • Essential (primary) - no specific medical cause can be found to explain a patient's condition. 90-95% • Secondary. Secondary hypertension indicates that the high blood pressure is a result of another condition, such as kidney disease or tumours. http://www.nlm.nih.gov/medlineplus/ency/imagepages/9124.htm

13. Classification of BP for Adults 5 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

14. High Blood - Pressure: The Silent Killer

15. PATHOPHYSIOLOGY OF HYPERTENSION Hypertension may result either from a specific cause (secondary hypertension) or from an underlying pathophysiology mechanism of unknown etiology (primary or essential hypertension).1 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

16. Secondary Hypertension 1 Secondary hypertension may cause by chronic kidney disease, Cushing’s syndrome, hyperthyroidism, hyperparathyroidism, primary alsosteronism, pregnancy, obstructive sleep apnea, and coarctation of the aorta. Some drugs that may increase BP: ~ Corticosteroids ~ Estrogens ~ Nonsteroidalantiinflammatory drugs (NSAIDs) ~ Amphetamines ~ Sibutramine ~ Cyclosporine ~ Tacrolimus ~ Erythropoietin ~ Venlafaxine 1 Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

17. Primary Hypertension 1 Multiple factors that contribute to the development of primary hypertension, including: • Humoral abnormalities involving the renin-angiotensin-aldosterone system, natriuretic hormone, or hyperinsulinemia • Pathologic disturbance in the CNS, autonomic nerve fibers, adrenergic receptors, or baroreceptors 1. Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

18. Abnormalities in either the renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction. 1 • Deficiency in the local synthesis of vasodilating substances in the vascular endothelium, such as prostacyclin, bradykinin, and nitric oxide, or increase in production of vasoconstricting substances such as angiotensin II and endothelin I. 1 1. Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

19. High sodium intake and increased circulating natriuretic hormone would inhibit intracellular sodium transport, causing increased vascular reactivity and increased BP. 1 • Increased intracellular concentration of calcium, leading to altered vascular smooth muscle function and increased peripheral vascular resistance. 1 1. Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

20. DIABETES MELLITUS Diabetes mellitus is a group of metabolic disorders of fat, carbohydrate, and protein metabolism that results from the defects in insulin secretion, insulin sensitivity, or both. 1 1. Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

21. There are two major classifications of diabetes mellitus: i) Type 1 DM ii) Type 2 DM They are differ in clinical presentation, onset, etiology, and progression of disease. 1

22. Based on three criteria 5: Fasting plasma glucose ≥ 126mg/dL A 2-hour value from a 75g oral glucose tolerance test ≥ 200mg/dL Casual plasma glucose level of ≥ 200mg/dL with symptoms of diabetes Diagnosis of diabetes…

23. PATHOPHYSIOLOGY OF DM 1 Type 1 DM Generally develops in childhood or early adulthood and results from immune-mediated destruction of pancreatic β-cells, resulting in absolute deficiency of insulin. 1. Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

24. Type 2 DM 1 Characterized by the presence of both insulin resistance and relative insulin deficiency. Insulin resistance is manifested by increased lipolysis and free fatty acid production, increased hepatic glucose production and decreased skeletal muscle uptake of glucose. 1. Barbara G. Wells, Joseph T. Dipiro, Terry L. Schwinghammer, and Cecily V. Diporo, Pharmacotherapy Handbook, seventh edition

25. Medication Prescribed For Mr. X

26. Cloxacillin Capsule 500 mg qid ¹ • Treatment of lower respiratory tract infections, skeletal infections, surgical prophylaxis and staphylococcal infections. • Beta lactams antibiotic – Act by inhibiting the formation of peptidoglycan cross-links in the bacterial cell wall. • Precaution: - hypersensitivity to b-lactam antibiotic - Renal impairment • Adverse effect: - Neutropenia - Agranulocytosis - GI upsets - rash [1] Charles F.Lacy et.al, 2008. Drug Information Handbook with International Trade Names Index, 17th edition, Lexi-Comp Inc.

27. Interaction: A. Drug – Drug interaction - Co-admin of probenecid or disulfiram may result in higher cloxacillin concentration. - Chloramphenicol and tetracyclineantagonise bactericidal effect of cloxacillin. B. Drug – Food interaction - delayed absorption in the presence of foods.

28. Tablet Pentoprazole 40 mg bd ¹ Pharmacological Category: -Proton Pump Inhibitor Uses: -Treatment and maintenance of healing erosive esophagitis associated with GERD Precaution: -Relief of symptoms does not preclude the presence of a gastric malignancy. -Long term medication will caused biopsy-proven atrophic gastritis(especially caused by the bacterium Helicobacter pylori) • [1] Charles F.Lacy et.al, 2008. Drug Information Handbook with International Trade Names Index, 17th edition, Lexi-Comp Inc.

29. Side Effect: -Chest pain, Headache(9%), Rash(2%), Diarrhea (6%), N/V/C (2%), back pain and Others. Storage: -Store the tablet at controlled room temperature of 20˚C to 25˚C. Mechanism of Action: -Suppresses gastric acid secretion by inhibiting the parietal cell H⁺ / K⁺ ATP pump. Dosage: -40 mg once daily for up 8 weeks (this is for who have erosive esophagitis associated with GERD. -20 mg once daily have been used in mild GERD treatment and maintenance therapy

30. Administration (Oral): -Should be swallowed whole and do not crush or chew. -may be taken with or without food but the best if taken before breakfast (coz of PPI)

31. Tablet Lipitor 10 mg on (atorvastatin) ¹ Pharmacological Category: -Antilipemic agent -HMG-CoA Reductase Inhibitor Uses: -Treatment of dyslipidemias (to reduce elevations in total cholesterol, LDL-C and triglycerides -Primary prevention of cardiovascular disease. Precaution: -Secondary causes of hyperlipidemia should be ruled out prior to therapy. -Liver function must be monitored by periodic laboratory assessment if not may cause hepatic dysfunction. • [1] Charles F.Lacy et.al, 2008. Drug Information Handbook with International Trade Names Index, 17th edition, Lexi-Comp Inc.

32. Side Effect: -Chest pain, Headache(17%), Rash(4%), Diarrhea (4%), N/C (3%), Insomnia and dizziness. Mechanism of Action: -Inhibitor of 3-hydroxy-3-methylgluryl coenzyme A (HMG-CoA) reductase . -Increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism. Dosage: -Initial: 10 to 20 mg once daily (for who have hypercholesterolemia) -then 40 mg once daily for patient >45% reduction in LDL-C

33. Administration (Oral): -Should be swallowed whole and do not crush or chew. -may be taken with food -take the medicine on night Monitoring Parameters: -Lipid level after 2-4 weeks

34. Liquid Paraffin 15 ml tds ² Uses: - constipation • Precaution: • Do not take immediately before going to bed. • -Avoid prolonged use. • -Not be used for who has abdominal pain, nausea and vomiting. • [2] British National Formulary

35. Side Effect: -Rash, Abdominal pain, Nausea and Vomiting. Mechanism of Action: - Liquid Paraffin acts by softening and lubricating the faeces. The faeces can then move more easily through the bowel. By doing this it relieves constipation and reduces the pain of some conditions such as piles Dosage: -Take 15 ml for 3 times a day.

36. DRUG USED FOR COPD

37. Combiventnebulizer 8 hourly • Combivent- Salbutamol and ipratropium • Salbutamol- Act on β2 receptors β2 receptors stimulation activate adenylcyclase increase in intracellular cyclic adenosinemonophosphate (cAMP) relax bronchial smooth muscle • Ipratropium- competitively inhibit cholinergic receptor in bronchial smooth muscle block acetylcholine reduce cyclic guanosinemonophosphate (cGMP) relax brochial smooth muscle • Precaution: immediate hypersensitivity reactions may occur after administration, as demonstrated by rare cases of urticaria, angioedema, rash, bronchospasm. • Drug-drug interaction: • # Ipratropium-increase toxicity with anticholinergic or drug with • anticholinergic effects (eg: atropine, TCA, antipsychotic drug). • # Salbutamol- refer to MDI salbutamol

38. Adverse drug reaction: (Ipratropium) # Glaucoma # Hypersensitivity reaction # Urinary retention # Blurred vision

39. Metered dose inhaler salbutamol 2 puff + prn • Bronchodilator • Short acting selective β2- adrenergic agonist • Act on β2 receptors β2 receptors stimulation activate adenylcyclase increase in intracellular cyclic adenosine monophosphate (cAMP) bronchial smooth muscle relaxation • Precaution: # hypertension # cardiac disorders (eg: arrhythmia, CHF) # diabetes # elderly patients.

40. Drug-drug interaction: • # salbutamol + nonpotassium sparing diuretics (eg: furosemide) • hypokalemia • # α- blocker, β-blocker decrease effect of sulbutamol • Drug-food interaction: • # Avoid or limit caffeine- may cause CNS stimulation • Adverse drug reaction: # CNS stimulation # Arrhythmia # Seizure # Hyperglycemia # Hypokalemia

41. Step For Using Metered Dose Inhaler Take off the cap and shake the inhaler. Breathe out all the way to empty the lungs as much as possible. Hold the inhaler 1 - 2 inches in front of your mouth (about the width of 2 fingers). Start breathing in slowly through your mouth, and then press down on the inhaler one time. (If you use a spacer, first press down on the inhaler. Within 5 seconds, begin to breathe in slowly.) Keep breathing in slowly, as deeply as you can. Hold your breath as you count to 10 slowly, if you can. This lets the medicine reach deep into your lungs.

42. Wait about 1 minute between puffs for inhaled quick-relief medicine (beta-agonists). There is no need to wait between puffs for other medicines. Rinse your mouth - help reduce unwanted side effects.

43. Tablet prednisolone 20mg OD • Systemic corticosteroid • Antiinflammatory mechanism; beneficial effect- reduction in capillary permeability to decrease mucus, inhibition of release of proteolytic enzymes from leukocytes, and inhibition of prostaglandin. • Precaution: # Use with caution in patients with thyroid disease, hepatic impaired, renal impairment, cardiovascular disease, diabetes, patients at risk of osteoporosis, patients at risk of seizure, patients at risk of GI disease (peptic ulcer). • Drug-drug interaction: # CCB (nondihydropyridine), azole antifungal, macrolide- may increase the • serum level of prednisolone • # Prednisolone may increase the hypokalemia effect of potassium wasting • diuretic (loop or diuretic)

44. # Concurrent use of NSAIDs and salicylate with corticosteroid- may increase GI • adverse effect. • # Antacids may reduce absorption of corticosteroid- separate administration by 2 • hours. • # Prednisolone may cause reduction in warfarin effect. • Drug-food interaction: • #Avoid ethanol- may increase gastric mucosal irritation. • # Prednisolone interfere with absorption of calcium. • # Limit caffeine. • Adverse drug reaction: # Increase appetite # Weight gain # Peptic ulcer # Hypokalemia # Convulsion # Diabetes mellitus

45. Actrapid HM PenfillHuman Insulin Solution for injection

46. What are the differences between the types of insulin?

47. COMPOSITION • Active substance: Human insulin, ( recombinant DNA produced in Saccharomycescerevisiae) • 1 IU is corresponds to 0.035mg of anhydrous human insulin.

48. INDICATIONS • Treatment of diabetes mellitus. • Initial stabilization of diabetes especially in diabetes emergencies.

49. MODE OF ACTION The blood glucose lowering effect of insulin is due to : • Facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells. • Simultaneous inhibition of glucose output from the liver.

50. An average action profile after subcutaneous injections indicates: Onset: within half hour Maximum: between 1 and 3 hours Duration: approximately 8 hours.