PROJECT

IN
CLINICAL PHARMACY
Case Study
Submitted by:
Alduheza, Shynne B.
Villoria, Christy Grace
Submitted to:
Mae Quenie A. Tiro, RPh.

January 2015

ISCHAEMIC HEART DISEASE

Rationale
Ischemic Heart Disease (IHD) belongs to a group of cardiovascular
diseases known as Coronary Artery Disease. CAD remains to be a
major health problem in western countries and the rest of the world
despite the advances in medicine. The reasons for this are
multifactorial and are due to the advancing age of the population.
Background
Ischemic Heart Disease is characterized by reduced blood supply to the heart.
Ischaemia means a "reduced blood supply".The coronary arteries supply blood to the
heart muscle and no alternative blood supply exists, so a blockage in the coronary arteries
reduces the supply of blood to heart muscle. Most ischaemic heart disease is caused by
atherosclerosis, usually present even when the artery lumens appear normal by
angiography.
Initially there is sudden severe narrowing or closure of either the large coronary arteries
and/or of coronary artery end branches by debris showering downstream in the flowing
blood. It is usually felt as angina, especially if a large area is affected. The narrowing or
closure is predominantly caused by the covering of atheromatous plaques within the wall
of the artery rupturing, in turn leading to a heart attack (Heart attacks caused by just
artery narrowing are rare). A heart attack causes damage to heart muscle by cutting off its
blood supply.
Ischemic heart disease (IHD) is the generic designation for a group of closely related
syndromes resulting from myocardial ischemiaan imbalance between the supply
(perfusion) and demand of the heart for oxygenated blood. It comprises not only
insufficiency of oxygen, but also reduced availability of nutrient substrates and
inadequate removal of metabolites. Isolated hypoxemia (i.e., diminished transport of
oxygen by the blood) induced by cyanotic congenital heart disease, severe anemia, or
advanced lung disease is less deleterious than ischemia because perfusion (including
metabolic substrate delivery and waste removal) is maintained.
Clinical Manifestations:
A. Myocardial infarction (MI), the most important form of IHD, in which
the duration and severity of ischemia is sufficient to cause death of
heart muscle.
B. Angina pectoris, in which the ischemia is less severe and does not
cause death of cardiac muscle. Of the three variantsstable angina,
Prinzmetal angina, and unstable anginathe latter is the most
threatening as a frequent harbinger of MI.
C. Chronic IHD with heart failure.

D. Sudden cardiac death.

Epidemiology
Pathogenesiss

CEFUROXIME
I. Drug
Generic Name: Cefuroxime
Chemical/ IUPAC Name:
(6R,7R)-3-{[(aminocarbonyl)oxy]methyl}-7-{[(2Z)-2-(2-furyl)-2-(methoxyimino)
acetyl]amino}-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylic acid; C16H16N4O8S
Brand Name:
a. Oral- Zinnat (GSK), Axet (Microlabs), Zoltax, Cimex, Panaxim
b. Parenteral- Zinacef (GSK), Kefox, Profurex, Ecocef
II. Chemistry and Stability
Pharmacology
- second generation cephalosporin
- antibacterial agent
- broad spectrum
- bactericidal
- good stability against bacterial beta-lactamase
III. Mechanism of Action
- a well-characterised and effective antibacterial agent which has
bactericidal activity against a wide range of common pathogens
- has good stability against bacterial beta-lactamase and active against
many ampicillin-resistant or amoxicillin-resistant strains
- inhibit bacterial cell wall synthesis
Spectrum

- aerobe gram-negative, aerobe gram-positive, anaerobe

- Clostridium difficile, Psedomonas, Camphylobacter, Listeria
monocytogenes, MRSA, Legionella, Enterococcus, Proteus vulgaris,
Enterobacter, etc.
IV. Pharmacokinetics
A. Absorption
- slowly absorbed from the gastrointestinal tract
- rapidly hydrolysed in the intestinal mucosa and blood to release
cefuroxime into the circulation
- optimum absorption: after meals
- bioavailability: 37% (empty stomach), 52% (with food)
B. Distribution
- 33-50% bound to proteins
- distributed throughout the extracellular fluid
C. Elimination/Excretion
- not metabolised
- half-life: 80 minutes
- excreted by glomerular filtration and tubular secretion
- excreted unchanged in urine 66-100% approximately 50% of the administered
dose is recovered in the urine within 12 hours
V. Uses
- upper respiratory tract infections: ENT infections, otitis media,
tonsilitis, pharyngitits, sinusitis
- lower respiratory tract infections: pneumonia, acute bronchitis
- genito-urinary tract infections: pyelonephritis, cystitis, urethritis
- skin ans soft tissue infections: impetigo, furunculosis, pyoderma
- gonorrhea, acute uncomplicated gonococcal urethritis, cerviciti
- Lyme disease
VI. Caution
A. Adverse Drug Events
- Gastrointestinal Disorders: diarrhea, nausea, abdominal pain,
vomitting
- Nervous System: headache, dizziness
- Hepatobiliary Disorders: transient increase of liver enzymes
(SGPT,SGOT,LDH)
- Infections: Overgrowth of Candida
- Blood and Lymphatic Disorders: eosinophilia, positive coombs test,
increased erythrocyte sedimentation rate
- Others: skin rashes, urticaria, pruritus, erythema multiforme,

jaundice, hepatitis
B. Contraindications
- hypersensitivity to cephalosporins
C. Warnings and Precautions
- may cause dizziness: caution among those who would drive and
operate machinery
- if there is no improvement within 72 hours, parenteral administration
of treatment must be continued
D. Pediatric
- tablets should not be crushed and unsutiable for children
- oral suspension may be used
- no experience of using in children under 3 years of age
E. Pregnancy
- pregnancy category B
- no experimental evidence of embryopathic or teratogenic effect
- administered with caution during early months of pregnancy
- excreted in human milk: discontinue in nursing mothers
- reproduction studies have been performed in mice at doses up to 3,200 mg/kg/day (14
times the recommended maximum human dose based on mg/m2) and in rats at doses up
to 1,000 mg/kg/day (9 times the recommended maximum human dose based on mg/m2)
- no evidence of impaired fertility or harm to the fetus due to cefuroxime
- should be used when needed
F. Chronic Toxicity
- low toxicity
G. Acute Toxicity
- low toxicity
H. Drug Interactions
- drugs that reduce gastric acidity: lower bioavailability of Cefuroxime
- oral contraceptives: lower estrogen absorption and reduce efficacy of
oral contraceptives
- aminoglycosides and diuretics: renal toxicity
- anticoagulants: risk of increased side effects by cefuroxime
- ferricyanide test: false negative result
VII.
A. Pharmaceutical Dosage Form
- tablet, powder for suspension, parenteral

B. Dosage
- 7-day treatment
- with food
C. Missed Dose
- If you miss a dose of cefuroxime, use it as soon as possible. If it is almost time for your next
dose, skip the missed dose and go back to your regular dosing schedule. Do not use 2 doses
at once.
- Skipping doses or not completing the full course of therapy may decrease the effectiveness
of the immediate treatment and increase the likelihood that bacteria will develop resistance
and will not be treatable.
D. Administration
- oral, IV, IM
E. Preparation
- 250 mg and 500 mg tablet
- 125/5 and 250/5 powder for suspension
- 250 mg and 750 mg vial
F. Storage Conditions
- Tablet: not exceeding 30C and protect from light
- Suspension: not exceeding 30C (unreconstituted), refrigerated
immediately from 2-8C kept up to 10 days (reconstituted)
- Parenteral: 24 hours
VII. Clinical Studies Done
A. Title:
B. Phase: I
C. Methodology:
D. Rationale:
E. Results:

PATIENT PROFILE