Clinical Pharmacy PDF

Clinical Pharmacy  Branch of pharmacy where the pharmacists provide Expected outcomes of Pharmaceutical Care patient care that optimizes the use of medications 1. Preventing disease and symptoms and promotes health, wellness and disease 2. Arresting and slowing the dis...

Clinical Pharmacy  Branch of pharmacy where the pharmacists provide Expected outcomes of Pharmaceutical Care patient care that optimizes the use of medications 1. Preventing disease and symptoms and promotes health, wellness and disease 2. Arresting and slowing the disease process prevention 3. Cure a disease  A practice in which the pharmacy utilizes his 4. Elimination or reduction of patient’s symptoms professional judgment in the application of pharmaceutical sciences to foster the safe and PHARMACEUTICAL CARE PROCESS appropriate use of drugs, in or by patients, while 1. Assessment working with members of the health care team.  Asses the patient for drug-related problems  Health science specialty whose responsibility is to  Determine whether drug-related problems are assure the safe and appropriate use of drugs in being treated patients through the application of specialized  Determine whether current drug therapy is knowledge and functions in patient care. appropriate  Determine whether additional drug therapy is Clinical Pharmacist needed 1. Interacts with the healthcare team  Determine if any of the drug-related problems 2. Interview and assess patient information may have been caused by medication 3. Design and implement a therapeutic plan 2. Care Plan 4. Make therapeutic recommendation  Approach normal physiology 5. Monitor patient response to drug therapy  Slow progression of disease 6. Monitor adverse drug reactions  Alleviate symptoms 7. Provide drug information  Prevent adverse effects  Control medication costs Clinical Pharmacy Settings  Educate the patient about his/her medication 1. Hospitals 3. Evaluate of outcome 2. Community pharmacies  Specify patient’s progress 3. Nursing homes  Monitor potential adverse drug reactions 4. Home-based care services  Determine desired end points for each 5. Clinics parameter and the frequency of monitoring 6. Any other setting where medicines are prescribed and used Medicines Optimization Application of Different Scientific Principles  Aims to ensure that the right patients get the right 1. Pharmacology choice of medicine at the right time. 2. Toxicology  The purpose is to help patients take their medicines 3. Therapeutics appropriately and by doing so, avoid unnecessary 4. Clinical pharmacokinetics treatment, improve safety and outcomes and reduce 5. Pharmacogenomics wastage. 6. Pharmacoeconomics Rational Drug Use Pharmaceutical Care  Requires that patients receive medications  Is the responsible provision of drug therapy for the appropriate to their clinical needs, in doses that purpose of achieving definite outcomes that meet their own individual requirements for an improves a patient’s quality of life adequate period of time, and at the lowest cost to  A patient-centered practice in which the practitioner them and their community. assumes responsibility for a patient’s drug-related  Right - drug, disease, dose, dosage form, dosing needs and is held accountable for this commitment schedule, route, cost, and patient Major functions of Pharmaceutical Care Essential Clinical Knowledge 1. Identifying potential and actual drug-related 1. Diagnostic testing problems 2. Disease 2. Resolving actual drug-related problems 3. Drug Therapy 3. Preventing potential drug-related problems 4. Non-drug Therapy Essential Clinical Skills o Consent must be given freely and without 1. Communication coercion 2. Drug Information Provision c. History 3. Therapeutic planning o Chief Complaint (CC) 4. Patient monitoring and physical assessment - reason/s the patient is seeking medical care or attention CLINICAL PHARMACY SERVICES o History of Present Illness (HPI) I. MEDICATION HISTORY TAKING AND - Narrative, current medical problem DOCUMENTATION o Past Medical History (PMH) 1. Patient Medication Profile - Current and previous patient - Written summary of all the medicines taken problems, unrelated to present illness. regularly, including over-the-counter and o Family History complementary medicines - Medical history of patient’s first- - Assist to understand and manage medicines by degree relatives informing how, why and when to take medicine. o Review of Systems (ROS) - summary of patient complaints not 2. Medication Reconciliation Process included in HPI - the process of creating the most accurate list o Social History possible of all medications a patient is taking- - Use of tobacco, alcohol, illicit drugs, including drug name, dosage, frequency, and route computing of pack years, occupation, – and comparing that the list against the marital status, sexual history, living physician’s admission, transfer, and/or discharge conditions orders, with the goal of providing correct Computation for pack years: * 1 pack of cigarette = 20 sticks medications. # 𝑜𝑓 𝑠𝑡𝑖𝑐𝑘𝑠 𝑝𝑒𝑟 𝑑𝑎𝑦 - The ideal medication reconciliation process begins 𝑆𝑚𝑜𝑘𝑖𝑛𝑔 𝑝𝑎𝑐𝑘 𝑦𝑟 = x Yrs of smoking 20 𝑠𝑡𝑖𝑐𝑘𝑠 with conducting a thorough patient medication interview and obtaining an accurate list of all d. Physical Examination current medications from the patient/and or o Short description caregiver o Vital Signs (body temperature, pulse rate, respiration rate, blood pressure) 3. Patient Chart o Systemic examination - Also known as Medical Record  Physical Assessment Techniques - Notes by Health Care Professionals  Vital Signs - Communication tool 1. Body temperature (37 ± 0.5 ˚C) - Source of Info, research - Can be measure in: - Quality Assurance Evaluation o Oral- most accessible and accurate o Rectal- accurate but uncomfortable 4. Patient Medical Chart (PMC) o Axillary- least accurate, most safe - Contains all significant clinical information which o Tympanic enables the physician to give effective continuing - Abnormal Findings: care to the patient o Hyperthermia (high temperature) - Used as a basis for drug therapy plan for patient o Hypothermia (low temperature)  Parts of PMC 2. Pulse rate (60-100 beats/min) a. Patients Data Sheet o Radial pulse- most easily accessible o Patient Demographics o Femoral or carotid pulse- palpitate in (Identification/sociological data) emergency cases o Admission and final diagnosis - Abnormal findings: o Condition upon discharge (discharge o Irregular pulse rhythm – bradycardia, summary, autopsy) tachycardia b. Consent Form 3. Respiratory rate (16-20 breaths/min) o Permission or approval given by patient for - Abnormal findings: admission, testing, procedure and access o Prolonged expiration suggesting to health related or personal information narrowing in bronchioles (asthma)  o Sounds: wheezing or stridor o Indirect auscultation - using o Apnea- no breathing stethoscope o Bradypnea, tachypnea 4. Blood pressure (34 = Hyperchromic the bone marrow tells to make more RBC.  < 26 = Hypochromic (IDA or Hypochromic o Effects of Low RBC anemia) a. Iron Deficiency Anemia (IDA)  Hypochromic = RBC have less color than  Hypochromic, microcytic RBC in the normal microscope o Mean Corpuscular Hemoglobin Concentration  Tx: Iron Supplements (MCHC)  RBCs get smaller in size when matured  HgB concentration  How do you know if you have anemia?  Average: 31-37 mg/dl (31-37%)  Low RBC o Mean Corpuscular Volume (MCV)  Low Hemoglobin  HgB volume  Low Hematocrit  Average: 80-100 b. Folate Deficiency Anemia (FDA)  >100 = Macrocytic  Vit B9 (folic acid) deficiency  Vit B9 and B12 deficiencies;  Macrocytic RBC, hypochromic;  < 80 = Microcytic immature cells  Iron Deficiency Anemia (IDA)  Tx: Folic Acid c. Pernicious Anemia RBC Distribution Width (RDW)  Form of Megaloblastic anemia o Reflects RBC size distribution  No intrinsic factor, macrocytic, o Normal= Lymphocytes > Monocytes >  Ptt - measure time it takes for a clot to form Eosinophils > Basophils  Increased Neutrophils  Bleeding time = 15-30s = bacterial, acute infection, inflammation  International Normalized Ratio  Increased Lymphocytes  Normal: 1.0; = viral, chronic infection, inflammation  under anticoagulation therapy 2.0-3.0  Increased Monocytes = inflammation, TB, fungi, endocarditis Warfarin  Increased Eosinophils o Oral = allergies, parasitic reactions o Inhibits clotting factors 1972 (X, IX, VII, II)  Increased Basophils o Monitor: Prothrombin time, INR = rarely increased; hypersensitivity, allergy o Increased Warfarin = bleeding o Bands - immature form of neutrophils o Antidote: Vit K, fresh frozen plasma Heparin  Corrects: o Parenteral  Hypokalemia: Kalium Durule o Inhibits thrombin (clotting)  Increase: forces inward influx of potassium o Monitor: Activated Partial Thromboplastin Time o Insulin-glucose (aPTT) o Bicarbonate o Increased Heparin = Bleeding o Salbutamol o Antidote: protamine sulfate o Ca gluconate (heart protectant) o Can be used by pregnant women o Chloride CLOTTING FACTORS  Acid - base balance I - Fibrinogen  Increased Cl: II - Prothrombin  Hyperchloremia - renal hypercholeremic III - Thromboplastin acidosis: kidneys are unable to excrete IV - Calcium chlorides properly V - Labile Factor  Decreased Cl: VI - Acclerin  Hypocholeremia: the loss of chlorides from VII - Stable the serum means that more bicarbonate VIII - Antihemophilic factor must be retained to replace the lack of IX - Christmas Factor negative ions, thus contributing to the X - Stuard Prower development of metabolic alkalosis XI - Plasma thromboplastin antecedent (PTA) XII - Hageman o Bicarbonate XIII - Fibrin Stabilizing Factor  Second most abundant extracellular anion  Part of both electrolytes and arterial blood gases ELECTROLYTES  Carbon dioxide combining power or total carbon dioxide is often used as an indirect measurement of serum bicarbonate o Magnesium  Increased Mg: Renal failure  Decreased Mg: Diarrhea, Malabsorption diuretics, hyperaldosteronism o Calcium o Sodium  40% bound to albumin  More refractive of fluid status  Increased Ca:  Increased Na:  Malignancy - Metastasis, some tumors  Dehydration, Impaired Renal function release Parathyroid hormone-related  Decreased Na: protein (PTHrP)  Diarrhea, Overhydration, Na depletion  Hyperparathyroidism – Osteoporosis = (mineralocorticoid deficiency) porous bone  Corrects:  Paget’s disease - Increase breakdown of  Body fluid: using Lactated Ringer’s bone, disorganized reformation  Hyponatremia: NSS > LR  Diuretics - Loop-loose Ca (hypocalcemia); thiazide takes Ca (hypercalcemia) o Potassium  Vitamin D intoxication  Excitability of nerve and muscle tissue  Decreased Ca:  Cardiac function and acid base balance  deficiency in parathyroid or Vitamin D  Increased K:  Excessive cellular breakdown (hemolysis), o Phosphate Acidosis  Increased P:  Decreased K:  Renal dysfunction  Diuretic, Vomiting, Diarrhea, Alkalosis  Hypervitaminosis   Hypothyroid End-Stage Renal Disease (ESRD)  Decreased P: o Renal replacement therapy  Aluminum antacids o Dialysis (stage 5)  Renal losses o Renal transplant  Hyperparathyroidism (osteopenia/osteomalacia) Dialysis o A - acidosis Bone and Mineral Homeostasis o E - electrolyte imbalance (K/PO4) o Ca/PO4 - major constituents of bone o I - intoxication o 2 principal regulatory hormones: o O - Overload of fluid  PTH = Increase bone resorption, mineralization o U - uremia  Vitamin D = produced from skin; stimulated intestinal Ca and PO4 transport and absorption o Creatinine Kinase (CK) o Secondary Regulators  Enzyme in tissues that cleave phosphocreatinine  Calcitonin - inhibits resorption  Subunit B - brain type; M - muscle type  Glucocorticoids - antagonize vitamin D;  Normal Volume: stimulates renal excretion of Ca  Male: 60-400 units/L;  Estrogen - reduce bone resorption of PTH  Female: 40-150 units/L (maintain the Ca inside the bone)  Types: o SERM (Selective Estrogen Receptor Modulators)  CK - BB: Brain  RALOXIFENE  CK - MM: Skeletal Muscles - MOA: agonistic in bones, antagonistic on  CK - MB: Cardiac Muscles breast and uterine cells  Elevation:  CK-BB: Cerebrovascular Accidents (CVA) or Arterial Blood Gas Strokes o Acid-base balance  CK-MM: Rhabdomyolysis o Oxygenation  CK-MB: Myocardial Infarction o Normal levels  CK is more useful than the troponins to detect  pH: 7.4 reoccurrence infarction as troponins remain in  pCO2: 40 mmHg the bloodstream for 5 days or longer after the  HCO3: 24 mEq/L initial infarction 3. Blood Chemistry o Lactate Dehydrogenase (LDH) o Blood Urea Nitrogen  Intracellular enzyme  End product of protein metabolism  Diagnosis of MI, hepatic and lung disease  Normal range: 8-18mg/dL  Normal Value: 110-210 units/L  Increase of BUN are manifestations of renal dysfunction, high protein intake, and upper GI o Lactic Dehydrogenase Isoenzymes bleeding  LDH1 = primarily from the heart and erythrocytes o Creatinine  LDH2 = comes mostly from the  Major constituent of muscle, excreted renally reticuloendothelial system  Creatinine Clearance: GFR approximation  LDH3 = from the lungs and other tissue  Cockroft and Gault ( if healthy renal  LDH4 = comes from the placenta, kidneys, and function) pancreas  Jellife Method (with renal problems)  LDH 5 = largely from the liver and striated muscle o Cardiac Troponin (CTn)  Gold standard in the diagnosis of myocardial infarction Detected 6 - 12 hours after MI, peaks after 24 hours gradually decreasing over the following weeks   Types: o Alanine Aminotransferase  cTnT = binds to TROPOMYOSIN, CARDIAC  Former name: AND SKELETAL  Serum glutamic-pyruvic transaminase  cTnl = binds to active site, CARDIAC MUSCLE (SGPT)  cTnC = binds to CARDIAC AND SKELETAL  Found in the largest concentration in liver tissue MUSCLE  More liver specific  Increased SGPT:  Sever hepatitis, infectious mononucleosis, shock, reye’s syndrome, congestive heart failure, and preeclampsia o Aspartate Aminotransferase  Former name:  Serum glutamic-oxaloacetic transaminase (SGOT) o Alkaline Phosphatase  Found predominantly in heart, liver and muscle  Found in the tissues of the liver, bone, intestine, tissue kidneys and placenta  Aminotransferase are very important to energy  Children have higher levels than adults, and transformation, in the highest amounts of them because the placenta is a rich source of ALP, a are found in high-energy cells such as the heart, high level of this enzyme is also normal in liver and skeletal muscle pregnancy  Alcohol induced  ALP from liver tissue is normally excreted into the bile, so biliary obstruction causes an increase  Increased SGOT: in ALP  Hepatitis, shock, trauma, or cirrhosis  May be the first indication of an adverse reaction o Bilirubin to a drug and indicates that the drug should be stopped  Breakdown product of hemoglobin  If Increased:  Bound to albumin, conjugated in the liver  general warning bone or liver abnormality  ↑ Unconjugated bilirubin (Paget’s disease, metastatic bone cancer,  parenchymal liver disease, hemolysis hyperparathyroidism and vitamin D or  ↑ Conjugated bilirubin calcium deficiencies, liver dysfunction,  obstruction to bile flow (stones, tumors) opioid, estrogens and phenothiazine use  If Decreased: o Amylase  hypothyroidism, celiac disease, cystic  Nonspecific salivary and pancreatic enzyme fibrosis or chronic nephritis, premature bone loss, scurvy, malnutrition or excessive o Lipase vitamin D  Pancreatic enzyme (more specific)  > 3 = Acute Pancreatitis o Acid Phosphatase  treatment: hydration and pain medication  Acid phosphatase is found in high concentrations in the prostate gland, erythrocytes and platelets o Albumin (oncotic pressure)  Excreted in the seminal fluid, a test for acid  Systemic function of liver phosphatase is sometimes performed on vaginal  Consider therapeutic monitoring secretions as supportive evidence for alleged  Oncotic Pressure = osmotic pressure induced by rape plasma proteins that causes a pull on fluid back  Increase in Acid phosphatase: into the capillary  increase of chances in Benign Prostatic  If Decreased Albumin: hyperplasia and cancer  Liver disease  PEM (protein energy malnutrition) o Kwashiorkor (decrease protein) o Marasmus (decrease calories)   Edema  Ascites (peritoneal fluid accumulation) o Uric Acid  End-product of nucleoprotein metabolism  If Increased:  gout, neoplastic disorder, drugs  Symptoms: gouty arthritis, uric acid stones  Drugs:  Colchicine – for acute gout  Allopurinol – for maintenance o Fasting Blood Sugar  Fast for 8-12 hrs  65-110 mg/dL o HBa1c  Control of Diabetes Mellitus  3 months blood sugar control o CRP & ESR  C-Reactive Protein and Erythrocyte Sedimentation Rate  Nonspecific indicator of inflammation * LDL = statins * HDL = Niacin * Triglycerides = fibrates