2. Health Care System
Composed of physician (including other medical and dental staffs), pharmacist ,
nurse and other paramedics
Physician ; diagnosis, prescription, monitoring, medical care
Pharmacist; prescription*, dispensing, counseling, monitoring,
pharmaceutical care
Nurse ; administering, monitoring, nursing care
Other paramedics ; their own work
Load to physician & nurse ; high due to the system of "physicians are all in all in
hospital for the treatment of patient, with the help of nurse."
Concept of normal public/patient ; same
11. High Profile Examples
•A patient with leukaemia received Intrathecal vincristine
instead of intravenously. Died beginning of February
2001. 14th such case over the last 16 years.
•Patient being operated for a AAA received bupivicaine
intravenously rather than epidurally. Patient died 3 days
later.
•A 3 year old girl, who had a convulsion post flu vaccine.
Attended hospital to get “checked out”. Received nitrous
oxide instead of oxygen in casualty
12. Elderly lady was prescribed Methotrexate in 1997 for her
rheumatoid arthritis. Dose increased to 17.5mg
WEEKLY over a 6 month period.
•Jan 2000 patient undergoes right TKR in hospital. MTX
given as one tablet a week (only 2.5mg).
Prescription for MTX 10mg/daily written and dispensed.
•30th April patient dies.
13. How does clinical pharmacy differ from pharmacy?
The discipline of pharmacy embraces the knowledge on
synthesis, chemistry and preparation of drugs
Clinical pharmacy is more oriented to the analysis of
population needs with regards to medicines, ways of
administration, patterns of use ,drugs effects on the
Patients,
‘the overall drug therapy management’.
The focus of attention moves from the drug to the single
patient or population receiving drugs.
14. Clinical Pharmacy Requirements
Patient
care
Knowledge of
drug therapy
Knowledge of
the disease
Knowledge of
laboratory
and diagnostic
skills
Communication
skills
Patient
monitoring
skills
Physical
assessment
skills
Drug
Information
Skills
Therapeutic
planning
skills
Knowledge of
nondrug therapy
15. Functions of Clinical Pharmacists
1. Taking the medical history of the patient
2. Patient Education
3. Formulation and management of drug policies
4. Drug information
5. Teaching & training to medical and paramedical staff
16. 6. Research and development
7.Patient counseling
8.Therapeutic drug monitoring
9.Drug interaction surveillance
10.Adverse drug reaction reporting
11.Safe use of drugs
12.Disease management cases
13.Pharmacoeconomics
18. Drug Interaction
Risk Factors for Drug Interactions
High Risk Patients
Elderly, young, malignant, multiple disease
Multiple drug therapy, Renal, liver impairment
High Risk Drugs
Narrow therapeutic index drugs e.g.(digoxin, warfarin,
theophylline)
Recognized enzyme inhibitors or inducers
20. Drug Interaction
Outside the body:
Incompatibilities: reaction of IV drugs resulting in
solutions after mixing that are not longer safe for
the patient alter stability (change the PH) or
structure leading to:
Loss of drug activity.
Formation of precipitates.
Development of toxic product.
21. Drug Interactions outside the body
Penicillin and aminoglycoside should never be
placed in the same infusion fluid because of
formation of inactive complex.
With calcium – ceftriaxone precipitates in the
lung and kidneys premature neonates.
Pheyntoin with infusion fluids particularly
dextrose (ph 4)so care should be taken to follow
the manufacture's instruction including the use
of an in – line filter.
22. Drug Interactions Inside the body
Antibiotics kill a large number of the normal
flora of the intestine:
•Antimicrobials may potentiates Oral Anticoagulant
by reducing bacterial synthesis of vitamin K
•In 10% 0f patients receiving Digoxin…..40% or more
of the administered dose is metabolized by the
intestinal flora - Increase digoxin conc.
and increase its toxicity
23. Drug Interactions Inside the body
gastric emptying Slowed by such as antimuscarinic
drugs and opiate analgesics
anticholinergics + acetaminophen
Impact: delay in absorption of acetaminophen
OR
Accelerated by drugs e.g metclopromide which
hasten gastric emptying
24. Drug Interactions Inside the body
H-2 blockers, anti acid + ketoconazole
Decrease gastric acid, dissolution of ketoconazole
is decreased, resulting in reduced absorption
Therefore, These drugs must be separated by at
least 2h in the time of administration.
25. Drug Interactions Inside the body
–Orlistat (Xenical) Inhibits pancreatic lipases,
preventing hydrolysis of ingested fat)
fat soluble vitamins (A,D,E,K)
– Addition of vasoconstrictors e.g adrenalin
to local anesthetics delay absorption and
prolong local anesthesia
26. Drug Interactions Inside the body
Sodium valproates displaces phyentoin from its
binding site on plassma albumin in addition to
inhibit its metabolism.
27. Drug Interactions Inside the body
Effect on drug metabolism
Enzyme induction:the drug called(inducer)
A drug may induce the enzyme that is responsible for
the metabolism of another drug or even itself e.g:
Carbamazepine (antiepileptic drug ) increases its own
Metabolism
Phenytoin increases hepatic metabolism of Oral
Contraceptives Leading to decreased level Reduced
action and Unplanned Pregnancy
Phenobarbital + warfarin increase metabolism of
warfarin (danger of thrombosis)
28. Drug Interactions Inside the body
Most important enzyme inducers:
1. Carbamazipine.
2. Phenytoin.
3. Phenobarbital.
4. Rifampicine.
29. Drug Interactions Inside the body
Enzyme inhibition:
It is the decrease of the rate of metabolism of a drug by
another one.
This will lead to the Increase of the concentration of the
target drug and leading to the increase of its toxicity .
Quinolones (Ciprofloxacin) + Theophylline Inhibit oxidative
metabolism of theophylline
30. Drug Interactions Inside the body
Most important enzyme Inhibitors
1. Cimetidine.
2. Erythromycine.
3. Quinolones.
4. Sodium valproate.
31. Drug Interactions Inside the body
•hydralazine + digoxinhydralazine increases the
renal clearance of digoxin
•probenecid + penicillin Decreases tubular
secretion of Penicillin
•sodium bicarbonate + salicylates or Methotrexate
(weak acid)
decrease reabsorption and Increase excretion of
salicylates
32. Drug Interactions Inside the body
•Carbapenems may decrease the serum concentration
of Valproic Acid and Derivatives.
Unclear mechanism may be due to:
1. include decreased intestinal absorption,
2. decreased hepatic hydrolysis of the valproate
glucuronide,
3. increased valproate glucuronidation,
4. increased renal clearance of valproate
glucuronide, and
5. increased distribution of valproate into red blood
cells.
33. Drug Interactions Inside the body
ACE Inhibitors may enhance the nephrotoxic effect
of CycloSPORINE
The cyclosporine causes reduced renal blood
flow due to afferent vessel vasoconstriction,
increasing the kidney's reliance on angiotensin II to
maintain adequate perfusion. The subsequent
addition of an ACE Inhibitor would decrease
angiotensin II concentrations.
34. The Accident Causation Model
(Adopted from Reason & Dean)
Active
Failures
- Slips&lapses
- Mistakes
Error
producing
conditions Accident
Defences
Latent
Conditions
35. Sources of Error
•Prescribing error - selecting the wrong or inappropriate
drug/dose/formulation/duration etc
•Communicating those instructions
•Supply error - timely; wrong drug, dose, route; expired
medicines, labelling.
•Administration error - timing; wrong route; wrong
rate/technique.
•Lack of user education - actions to take.
36. Drug therapy assessment
Six types of problems which may result in treatment
failure
1.Inappropriate selection of medication
2.Inappropriate formulation of medication
3.Inappropriate administration of drug therapy
.14.Inappropriate medication-taking behaviour
5.Inappropriate monitoring of drug therapy
6.Inappropriate response to drug therapy
43. Patient Assessment Questions
Does the patient need this drug ?
Is this drug the most effective and safe ?
Is this dosage the most effective and safe ?
If side effects are unavoidable does the patient need
additional drug therapy for these side effects?
Will drug administration impair safety or efficacy ?
Are there any drug interactions ?
Will the patient comply with prescribed regimen ?
44. Lab Interpretation
• Polycythemia ↑ RBCs count
• High altitudes/ Strenuous physical activity
• Medications, such as gentamicin and methyldopa
• Smoking
• COPD
Anemia
• Hemorrhage
• Pernicious or sickle cell anemia/ Thalassemia
• Chemotherapy or radiation
• Medications, such as sulfa & azithromycin
45. Lab Interpretation
Hematocrit % of RBCs in the plasma of.
Pregnancy: decreased hematocrit, especially in the last
trimester as plasma volume
• The average range of values for hematocrit is 37-54%
• Critical values include:
• A hematocrit <15% can cause cardiac failure
• A hematocrit >60% can cause spontaneous blood clotting
Hemoglobin
• The average range of values for hemoglobin is 12-17.5 g/dL.
• A hemoglobin < 5 g/dl can cause heart failure
• A hemoglobin > 20 g/dl can cause hemoconcentration and clotting
47. Lab Interpretation
Causes of ↑Na+( > 147mmol/L)
• Hypernatremia and hyperchloremia are related. Causes include:
• Dehydration/ Any process that causes ↓free fluid results in ↑
Na+ conc. (such as vomiting , diarrhea)
• Increased insensible water loss (Fever, extensive burns,
mechanical ventilation)
• Impaired renal function
• Congestive heart failure
48. Lab Interpretation
Causes of↓ Na+ (< 125mmol/L)
• Prolonged use of D5W –or Over hydration
• Syndrome of inappropriate ant diuretic hormone (SIADH)
• Addison’s disease
• Water retention : like in renal failure, hepatic failure,
• Diuretics
• Drugs that increase ADH secretion (carbamazapine, chlofibrate,
narcotics, nicotine, vincristine)
• Drugs that have ADH-like action or potentiate ADH renal effect
(acetaminophen, ADH analogs, cyclophosphamide, diuretics,
NSAIDS-)
49. Lab Interpretation
Causes of ↑ K+( > 5.6mmol/L)
Potassium levels can be falsely elevated with hemolyzed blood
samples.
• Over-administration of potassium supplements
• Renal failure
• Potassium-sparing diuretics
• ACE inhibitors, beta-blockers (both affect potassium balance)
• Trauma/bruising/bleeding (cell breakdown causes potassium loss)
54. Lab Interpretation
Hyperglycemia
• Uncontrolled Diabetes mellitus
• Over-administration of glucose
• Pregnancy (gestational diabetes)
• Medications- particularly steroids/ asparaginase
Hypoglycemia
• Over-administration of insulin/ Over-production of insulin, such
as insulin-secreting tumors
• Liver disease such as hepatitis, cirrhosis, liver cancer
• Medications, including beta-blockers, oral hypoglycemic agents
55. Lab Interpretation
• Hypoalbuminemia
• <3.5 g/dL. Causes may include:
• Poor nutrition
• Liver disease
• Impaired renal function
• Burns
• Lymphatic disease or cancer
56. Lab Interpretation
Creatinine
• serum creatinine is a very reliable indicator of renal function( as
the amount of creatinine produced per day is constant and
dependant upon the body’s muscle mass.)
• Causes of Creatinine Elevation
• Hemoconcentration (dehydration)
• Decreased excretion (UT obstruction, renal dysfunction)
• Muscular dystrophy, myasthenia gravis)
• Nephrotoxicity due to drugs (aminoglycosides, amphotericin B,
cistplatin, cyclosporine, dextran, hydroxyurea, lithium,
methoxyflurane, nitrofurantoin, pentamidine, plicamycin,)
• Causes of Creatinine depletion Decreased muscle mass –
cachexia/ muscle atrophy/ Spinal cord injuries/ coma
58. Case…
9 yrs pt. diagnosed as CML on aplastic crisis /
Ph Ch. +ve post chemotherapy ( HD cytarabine
+ Mitoxantrone) e’ history of MRSA 3 months
before..
• Started triple agent antibiotics ( tazocin+
amikacin + vancomycin)
• B.C mixed g –ve E-coli ( ESBL)+ g+ve
streptococci
• Had meropenem + vancomycin 14 d
59. • Had acyclovir empirically for oral mucositis 13
days.
• Imatinib held 3 days d.2. thrombocytopenia
then resumed on reduction.
• Pt. suffered a tonic-clonic convulsion CT &
MRI brain revealed PRES.
• Started AED levitracetam 10mg/kg/ 12hr &
imatinib held
• No fits occurred and imatinib resumed on
reduction.
60. Case 2…
• 2 yr old pt. her wt. is 10 kg admitted to ICU e’
tachyepnia, tachycardia & bld stream G+ve
infection MRSA sensitive to vancomycin.
• Pt. ttt e’ piperacillin/tazobactam + amikacin+
vancomycin for 7 days.
• On week end pt had +ve balance 1000ml/d
urine output diminished to 500ml/d
• Bili D/T 1.5, 2.7 respectively, & Scr. doubled
61. • A new bld clt drawn & G-ve carbapenem
producer MO (Kl. Pneumonie) appeared.
• IV fluids decreased to 10ml/hr, medications
prepared as minimal dilution & lasix shots on
1mg/kg/ 6hrs administered.
• Antibiotics shifted to: HD meropenem on long
infusion + levofloxacin ( e’ MIC < that of
amikacin) + colistin.
• Vancomycin discontinued after 12 days
