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1. ANAPHYLAXIS
AND DRUG
THERAPY
SUBJECT-General medicine
PRESENTOR- Diya Sharma(3rd BDS)

2. Anaphylaxis: introduction
■ Anaphylaxis is a severe allergic reaction. It can lead to a potentially fatal
condition known as anaphylactic shock.
■ Anaphylaxis happens when the body reacts to a foreign substance as if it were a
serious threat.
■ The most common trigger for these reactions are medications, foods, and insect
stings.
■ Any substance that causes an allergic reaction is called an allergen. For some
people, even minimal exposure to traces of an allergen can cause a severe
reaction.

3. Some foods that often trigger allergic reactions include:
■ milk
■ eggs
■ fish
■ crustacean shellfish
■ wheat
■ soy
■ peanuts
■ tree nuts

4. What happens during anaphylaxis?
In its reaction to an allergen, the body
produces large amounts of
histamine — a signaling molecule that
can trigger an inflammatory response.
This response can lead to:
•dilation of the blood vessels
•a sudden drop in blood pressure
•loss of consciousness
•shock

5. ■ In a person experiencing anaphylaxis, the airways often become narrow, making
breathing difficult.
■ In addition, the blood vessels may leak, causing edema, a type of swelling that
results from the accumulation of fluid.
■ The reaction may happen immediately after contact with the allergen or within
hours of contact. Very occasionally, it happens days later.

6. ANAPHYLAXIS
■ Anaphylaxis is a type I IgE mediated rapidly developing systemic allergic
reaction.
■ Exposure to an antigen results in the formation of specific IgE which binds with
the mast cells.
■ Once IgE is bound to the surface of mast cells, the individual is primed to
develop type I hypersensitivity reaction.
■ Repeated exposure to same antigen in the sensitized individual can lead to the
activation of IgE bound mast cells and release of a number of mediators such as
histamine, serotonin, leukotriens and prostaglandins .

7. ■ These mediators cause bronchoconstriction, vasodilatation, fluid exudation and
smooth muscle contraction which are responsible for clinical features of the
anaphylactic reaction.
■ Anaphylactoid reaction: Certain substances can cause activation of mast cells
directly (non-IgE mediated) and lead to similar clinical picture. This is known as
anaphylactoid reaction. Radio-contrast media are the most common cause of
anaphylactoid reaction.

9. CAUSES

10. Clinical Manifestations
■ The manifestation may be mild, very severe or life threatening.
■ Type I reaction can occur as systemic disorder (anaphylaxis) or local reaction
(urticaria and/or angioedema).
■ [ANGIOEDEMA-painless swelling under skin triggered by an allergy to animal
dander,pollen,drugs,venomm,food or medication.URTICARIA AKA HIVES- a
skin rash triggered by reaction to food,medicine or other irritants.]
■ Serious manifestations occur within seconds to minutes after exposure to
antigen. Sometimes, the reaction is delayed be few hours.

11. (A)Skin lesions in the form of urticaria or angioedema may occur.
In mild cases, this could be the only manifestation.
• Urticaria is a raised flat-topped well demarcated skin lesion with surrounding
erythema. Individual lesions usually last from minutes to hours.They are
localized or disseminated and are pruritic.
Angioedema is a deeper cutaneous process causing areas of localized
nonpitting swelling. It most often involves lips, tongue and eyelids

12. ■ (b) Respiratory distress may Patient may have a feeling of tightness of chest,
stridor and wheezing
( c) Hypotension and shock can occur. Patients have cold extremities,
decreased urinary output, peripheral cyanosis and altered sensorium.
■ ( d)Gastrointestinal manifestations include abdominal cramps, nausea, vomiting
and diarrheaoccur due to laryngeal edema, laryngospasm or bronchospasm.

13. Diagnosis
■ The diagnosis of anaphylactic reaction is clinical, based on the history of
exposure to the triggering agent and appearance of symptoms and signs within
minutes of exposure. An elevated serum tryptase during an episode confirms
the diagnosis of anaphylactic reaction.

14. Treatment
■ Prompt recognition and management of anaphylactic reactions is a must as
death may occur within minutes.
■ Upon any suspicion of anaphylaxis, airway, breathing and circulation are
assessed.

15. ■ The drug of choice is adrenaline (epinephrine).
■ This is given in a dose of 0.3-0.5 mg (0.3-0.5 ml of 1:1000 solution)
intramuscularly or subcutaneously.
■ Repeated injections can be given at 20 minutes intervals if necessary.
■ Patients who are already being treated with beta adrenergic blocker drugs are
refractory to epinephrine.
■ A higher dose of adrenalin is required for the desired effect.

16. ■ Glucagon is also beneficial in such patients
■ Epinephrine causes bronchodilatation and vasoconstriction and prevents further
mast cell degradation.
■ This can also be given sublingually, intravenously or via an endotracheal tube in
patients with hypotension and airway compromise.
■ Airway management should be a priority.

17. ■ Hundred percent oxygen should be administered.
■ Endotracheal intubation may be necessary.
■ If laryngeal edema does not respond to epinephrine, tracheostomy may be
required.
■ Inhalation of β2 adrenergic agonist (terbutaline, salbutamol) and intravenous
aminophylline are helpful in bronchospasm.
■ Intravenous fluids are given to maintain intravascular volume.
■ The amount of fluid to be given is adjusted according to the blood pressure and
urine output.

18. ■ Vasopressor drugs (dopamine, norepinephrine) are used if the patient remains
hypotensive.
■ H2 receptor antagonists (diphenhydramine, promethazine) are useful in relieving
skin symptoms (pruritus, urticaria and angioedema) and abdominal cramps.
■ Addition of H2 receptor antagonists (ranitidine) may provide better effects.
■ Glucocorticoids have no immediate significant effect but may reduce prolonged
reactions or relapses.

19. ■ Hydrocortisone (200 mg) or methylprednisolone (125 mg) can be given
intravenously.
■ The patient is observed for 24 hours as the late phase reactions can cause
reappearance of symptoms.

20. Prevention of Recurrent Anaphylaxis
■ Identification and avoidance of the offending agent is crucial for the prevention
of anaphylactic reaction.
■ Self-administered epinephrine therapy is advocated for those who develop
recurrent anaphylaxis to a food or Hymenoptera sting.
■ Venom immunotherapy is tried in patients with anaphylaxis to hymenoptera
sting.

21. Treatment of Urticaria and
Angioedema
■ These represent mild type I hypersensitivity reactions.
■ 1. Ideal treatment is identification and avoidance of specific cause, such as
medications, cosmetics, foods.
■ 2. Antihistaminics (H1 blocking agents) are given for the control of symptoms.
■ Second generation antihitaminics like fexofenadine, cetrizine, levocetrizine,
rupatadine, loratidine, desloratidine are used as first line agents.
■ Classic antihistaminics such as hydroxyzine is added as a evening dose for
better control of the lesions or in refractory cases.
■ H2 blocking agents (ranitidine) may be added in refractory cases.

22. ■ 3. Oral corticosteroids are given to patients with severe symptoms who have not
responded to antihistaminics.
■ 4. Use of ACE inhibitors and ARBs can be associated with the onset of
angioedema. They should be discontinued if angioedema develops.

23. DRUG ALLERGY
Basis of drug allergy:
i. Idiosyncratic
ii. Toxic
iii. Immunological
NOTE- immunological reaction can be of various types and occur with relatively
low dose. These occur usually after re-exposure to drug in individual who has
already been sensitized by previous exposure.
 SKIN TEST predicts IMMEDIATE HYPERSENSITIVTY REACTION.
 IF TEST IS NEGATIVE, IMMEDIATE HYPERSENSITIVTY REACTION WILL
NOT DEVELOP THESBUT DELAYED NON IgE MEDIATED REACTION MAY
STILL DEVELOP IN E CASES.

25. Cutaneous reaction
■ MOST COMMON MANIFESTATIONS OF DRUG ALLERGY.
1. Urticaria- commonly seen with:
A. PENICILLIN
B. CEPHALOSPORIN
C. SULPHONAMIDE
2. Fixed drug eruptions- these are discrete macular or bullous non pruritic lesions
which occur at same place each time drug is administered.
Drugs commonly implicated are:
A. TETRACYCLINE
B. SULPHONAMIDE
C. PENICILLIN

26. 3. Photodermatitis- bright erythematous eruption/ eczematoid lesions in area exposed
to UV light.
DOXYCYCLINE,coal tar derivatives and psoralens are important drugs causing
photodermatitis.
4. Contact dermatitis- local application of neomycin and PABA can lead to dermatitis
5. Febile mucocutaneous syndromes- these are ERYTHEMA MULTIFORME,
STEVEN JOHNSON SYNDROME, TOXIC EPIDERMAL NECROLYSIS.
Common drugs implicated:
A. RIFAMPICIN
B. PHENOBARBITONE
C. PHENYTOIN
D. TRIMETHOPRIM SULPHAMETHOXAZOLE

27. ■ Steven johnson syndrome- severe form of erythema multiforme and present as
popular,urticarial,vascular or purpuric lesions involving 2 or more mucosal
surface.
■ Lyell syndrome- presents as-
 Epithelial bullae
 Subsequet desquamation

28. ■ ERYTHEMA MULTIFORME: characterized by target lesion on skin.
– Sloughing of dermis and mucous membrane occurs in Steven johnson
syndrome and toxic epidermal necrolysis.(10-30% of body involvement of
ody surface area)
– Offending drug which has resulted in above reaction should not be given
again and future skin testing with offending drug is absolutely
contraindicated.

29. • Hepatic syndrome: presents as-
a) Hepatocellular damge: PHENYTOIN & HALOTHANE
b) Cholestatic jaundice: ERYTHROMYCIN, PHENOTHIAZINE & AZATHIOPRIME
• Renal syndrome- presents as INTERSTITIAL NEPHRITIS (fever, pyuria,
hematuria, proteinuria, rash and eosinophilia).
 Drugs implicated-
I. METHICILLIN
II. SULPHONAMIDES
III. CEPHALOSPORINS

30. ■ Pulmonary syndromes- presents as PULMONARY INFILTRATION{
NITOFURANTOIN, GOLD}, BRONCHOSPASM {ASPIRIN, NSAIDS}
■ IMPORTANT-
– High degree of cross reactivity exists between- PENICLLIN,
CARBAPENEM,IMIPENEM

31. IMPICATIONS ON DENTAL
PRACTICE
1. Swelling of the lips and floor of the mouth may occur in angioedema.
2. Dry mouth and drowsiness may occur in patients taking antihistaminics.
3. Patients should be in supine position when injections are given. Fainting after
injection is common and can be confused with anaphylaxis.

32. References
■ A.K.TRIPATHI’S ESSENTIALS OF MEDICINE FOR DENTAL STUDENTS-2nd
edition