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Name: ____RAFAEL, DUNE VIENIS KAREN N.

____ Year & Section: ___BS-


Pharmacy 4A___
Group No.: ______________________________ Date Started:
_____________________
Date Submitted:
___________________

Activity no. 1
DRUG ALLERGY INTERVIEW

I. Objectives
1. Conduct an interview with a fellow group mate regarding any food or
drug allergy
2. Construct an allergy sheet
3. Define allergy and identify the possible causes of allergy
II. Data Output
Printed on the last three pages of this report.
III. Answers to Questions
1. What is allergy? What are the possible causes of allergy?
According to Wikipedia.org (2009):
“Allergy is a disorder of the immune system often also referred
to as atopy. Allergic reactions occur to normally harmless
environmental substances known as allergens; these reactions are
acquired, predictable, and rapid. Strictly, allergy is one of four forms of
hypersensitivity and is called type I (or immediate) hypersensitivity. It
is characterized by excessive activation of certain white blood cells
called mast cells and basophils by a type of antibody known as IgE,
resulting in an extreme inflammatory response”.
2. Give the mechanism of action of any drug used to alleviate allergy.
• Corticosteroids
➢ Prednisone (Oral corticosteroid)
 Glucocorticoids are naturally occurring hormones that
prevent or suppress inflammation and immune
responses when administered at pharmacological doses.
At a molecular level, unbound glucocorticoids readily
cross cell membranes and bind with high affinity to
specific cytoplasmic receptors. This binding induces a
response by modifying transcription and, ultimately
protein synthesis to achieve the steroid's intended
action. Such actions may include: inhibition of leukocyte
infiltration at the site of inflammation, interference in the
function of mediators of inflammatory response, and
suppression of humoral immune responses. Some of the
net effects include reduction in edema or scar tissue, as
well as a general suppression in immune response. The
degree of clinical effect is normally related to the dose
administered. The antiinflammatory actions of
corticosteroids are thought to involve phospholipase A2
inhibitory proteins, collectively called lipocortins.
Lipocortins, in turn, control the biosynthesis of potent
mediators of inflammation such as prostaglandins and
leukotrienes by inhibiting the release of the precursor
molecule arachidonic acid. Likewise, the numerous
adverse effectsrelated to corticosteroid use are usually
related to the dose administered and the duration of
therapy.
➢ Budesonide (Nasal corticosteroid)
 Exhibits potent glucocorticoid activity and weak
mineralocorticoid activity. Inhibits activities against
multiple cell types (eg, mast cells, eosinophils,
neutrophils, macrophages, and lymphocytes) and
mediators (eg, histamine, eicosanoids, leukotrienes, and
cytokines) involved in allergic- and non-allergic-
mediated inflammation.
• Antihistamines
➢ Cetirizine
 The action of all the H1-receptor blockers is qualitatively
similar. However, most of these blockers have additional
effects unrelated to their blocking of H1 receptors; these
effects probably reflect binding of the H1 antagonists to
cholinergic, adrenergic, or serotonin receptors .
• Decongestants
➢ Phenylephrine
 Phenylephrine produces its ophthalmic and systemic
actions by acting on alpha 1 adrenergic receptors in the
pupillary dilator muscle and the vascular smooth musle,
resulting in contraction of the dilator muscle and
contraction of the smooth muscle in the arterioles of the
conjunctiva and peripheral vasoconstriction.
Phenylephrine decreases nasal congestion by acting on
alpha 1 adrenergic receptors in the arterioles of the
nasal mucosa to produce constriction.
• Leukotrienes
➢ Montelukast
 Leukotriene receptor antagonists exert their actions by
binding to the active site of leukotriene receptors.
Montelukast is a selective inhibitior of leukotriene D4
(LTD4) at the cysteinyl leukotriene receptor CysLT1.
• Mast cell stabilizers
➢ Cromolyn sodium
 Prevents the release of mediators that would normally
attract inflammatory cells and because it stabilizes the
inflammatory cells.
1. Discuss the different types of hypersensitivity reactions.
a. Type I hypersensitivity (Immediate hypersensitivity)
– An allergic reaction provoked by reexposure to a specific type
of antigen referred to as an allergen. Exposure may be by
ingestion, inhalation, injection, or direct contact. The difference
between a normal immune response and a type I hypersensitive
response is that in the latter plasma cells secrete IgE. This class
of antibodies binds to Fc receptors on the surface of tissue mast
cells and blood basophils. Mast cells and basophils coated by
IgE are "sensitized." Later exposure to the same allergen, cross-
links the bound IgE on sensitized cells resulting in degranulation
and the secretion of pharmacologically active mediators such as
histamine, leukotriene (LTC4 and LTD4), and prostaglandin that
act on the surrounding tissues. The principal effects of these
products are vasodilation and smooth-muscle contraction.
b. Type II (Cytotoxic hypersensitivity)
– The antibodies produced by the immune response bind to
antigens on the patient's own cell surfaces. The antigens
recognized in this way may either be intrinsic ("self" antigen,
innately part of the patient's cells) or extrinsic (absorbed onto
the cells during exposure to some foreign antigen, possibly as
part of infection with a pathogen). These cells are recognized by
macrophages or dendritic cells which act as antigen presenting
cells, this causes a b cell response where antibodies are
produced against the foreign antigen.
c. Type III (Immune Complex Disease)
– Occurs when antigens and antibodies (IgG or IgM) are present
in roughly equal amounts, causing extensive cross-linking.
– It is characterized by soluble antigens that are not bound to cell
surfaces (which is the case in type II hypersensitivity). When
these antigens bind antibodies, immune complexes of different
sizes form. Large complexes can be cleared by macrophages
but they have difficulty binding to small immune complexes for
clearance. These immune complexes insert themselves into
small blood vessels, joints, and glomeruli, causing symptoms.
– They deposit in tissues and induce an inflammatory response,
and can cause damage wherever they precipitate. The reaction
can take hours, days, or even weeks to develop.
d. Type IV (Delayed-type hypersensitivity)
– The reaction takes two to three days to develop. Unlike the
other types, it is not antibody mediated but rather is a type of
cell-mediated response. CD8+ cytotoxic T cells and CD4+
helper T cells recognize antigen in a complex with either type 1
or 2 major histocompatibility complex. The antigen-presenting
cells in this case are macrophages which secrete IL-12, which
stimulates the proliferation of further CD4+ T cells. CD4+ T
cells secrete IL-2 and interferon gamma, further inducing the
release of other Type 1 cytokines, thus mediating the immune
response. Activated CD8+ T cells destroy target cells on contact
while activated macrophages produce hydrolytic enzymes and,
on presentation with certain intracellular pathogens, transform
into multinucleated giant cells.
e. Type V (Autoimmune Disease)
– Occurs when IgG class antibodies directed towards cell surface
antigens have a stimulating effect on their target.
2. What is the drug of choice for anaphylactic shock caused by drug
allergy? Illustrate the mechanism of action.

Epinephrine is the drug of choice for anaphylactic shock caused by


drug allergy. Epinephrine acts directly on α or β receptors, producing effects
similar to those that occur following stimulation of sympathetic nerves or
release of the hormone epinephrine from the adrenal medulla.
3. Describe or illustrate the mechanism
of action of prednisone in blocking the production of IgE.

Prednisone is biologically inert and converted to the predominantly


prednisolone in the liver. It decreases inflammation by suppression of
migration of polymorphonuclear leukocytes and reversal of increased capillary
permeability; suppresses the immune system by reducing activity and vol of
the lymphatic system; suppresses adrenal function at high doses. Indications
and dosage are same as those for prednisolone.

4. Submit the following:


a. Patient Drug Profile
b. Filled Allergy Sheet
c. White Allergy Card.
II. Conclusion

Therefore, allergy is a disorder of the immune system often also


referred to as atopy. Allergic reactions occur to normally harmless
environmental substances known as allergens; these reactions are
acquired, predictable, and rapid. It is divided into different 5 types.
Corticosteriods, antihistamines, decongestants, leukotriene inhibitors and
antagonists and mast cell stabilizers are drugs used to alleviate allergy. In
cases of anaphylactic shock, epinephrine is used.
MARY IMMACULATE HOSPITAL
PATIENT DRUG PROFILE

Patient Name: Fanny Urmeister Address: 24555 Colonial


Estates
Age: 79 Height: 5’2 Weight: 178 lbs Sex:
Female

Route of
Drug Frequenc Date
Dosage Administratio Diet
Description y/Time Ordered
n
Flecainide 50 mg Oral i bid 10/5/2009 On soft diet
acetate tab
(Tambocor)
Docusate 100 mg Oral ii hs 10/5/2009
IV Fluids
tab
Aspirin 325 mg Oral i q AM 10/5/2009
(Ecotrin) tab
Coumadin 2.5 mg Oral i q AM 10/5/2009
tab
Nicoderm Transdermal ut dict 10/5/2009
patches Patch
Procan SR 500 mg Oral i qid 10/26/2009 Discontinu
tab ed
Medication
Isordil 20 mg Oral I q 6h 10/26/2009 10/26: D/C
tab Tambocor
Isuprel Nasal ut dict 11/02/2009 11/5: D/C Procan
SR
inhalation 11/5: D/C
Imodium
Dimetane 4 mg Oral iq8h 11/02/2009
tab
Quinidex 300 mg Oral iq8h 11/05/2009
tab
Robitussin- 120 ml Oral i tsp q 4 h 11/05/2009
DM susp.

Imodium 2 mg Oral ut dit 11/05/2009

PRN Medications Drug History Allergies


• Routinely taking Aspirin
Centrum
Multivitamins as her
daily dietary
supplement. Adverse Reactions
• Used Dermovate for Headache, nausea and
her eczema last June vomiting
to July 2009.
Diagnostic Impressions
Arrythmia secondary to
status post NSTEMI,
smoking and obesity.

MARY IMMACULATE HOSPITAL


Drug and Food Allergy Information Sheet

Patient Name: Fanny Urmeister Address: 24555 Colonial


Estates
Age: 79 Height: 5’2 Weight: 178 lbs Sex:
Female

Drug Classification Name of Drug/Food


Antibiotics None
Analgesics, Aspirin
Antipyretics
Antirheumatics None
Sulfas None
Local Anesthetics None
X-ray Dye for IVO, IV None
Cholangiogram,
others
Food Chicken
Others None
MARY IMMACULATE HOSPITAL

ALLERGY CARD

Name: Fanny Urmeister


Address: 24555 Colonial Estates, Coon Rapids MN
Age: 79

EMERGENCY CONTACT NUMBER:

241-1722
ingested, I carry an Epipen™ and please take me to the nearest hospital. Tha