Hypersensitivity types

1. Week 2
• HSR type 4
• HSR type 3
• HSR type 2
• HSR type 1
• Anaphylactic shock (and how to differentiate it from angioedema)
• Shock
• Summary
• Asthma as an example of HSR type 1 or 4

2. CONTACT GLUTENDELAYED
Antigen:
Insect venom
Mycobacteriae
Response:
Swelling, induration,
erythema
Wheal and flare
Antigen:
Haptens, e.g.:
Poison ivy, rubber,
nickel
Response:
Erythema, vesicles
Infiltrate and abcesses
HSR type 4: mediated byT-cells
Antigen:
Gliadin
Peptides in prolamins
Response:
Villous atrophy
Malabsorption

3. HSR type 4: mediated byT-cells

4. HSR type 3: Immune complexes
•HSR TYPE 4
•HSR TYPE 3
•HSR TYPE 2
•HSR TYPE 1
•ANAPHYLACTIC SHOCK
•SHOCK
Example:Arthus reaction hemorrhage, necrosis

5. HSR type 2
CYTOTOXIC NON-CYTOXIC
example: erythroblastosis fetalis example: myasthenia gravis

7. HSR type 1: Hypersensitivit-e
•HSR TYPE 4
•HSR TYPE 3
•HSR TYPE 2
•HSR TYPE 1
•ANAPHYLACTIC SHOCK
•SHOCK

10. HSR type 1: Anaphylaxis
Immediate
phase
Late
phase

12. Differential diagnoses if someone seems anaphylactic:
angio-edema (which can be idiopathic, after minor trauma, or after starting an ACE)
(systemic mastocytosis)
(malignant carcinoid syndrome)
(medullary thyroid carcinoma)
Differentiate between anaphylaxis and angioedema:
Plasma C1, C2, C4 will be decreased in angio-edema
Further treatment for anaphylaxis:
1.epinephrine - anti-histaminergics (H1 and H2) - glucocorticoids (hydrocortisone, ...)
2.1-2 IV fluid - request tryptase levels, which indicate risk of bleeding
3.if Pt takes ACE-inhibitors, stop ACE inhibitors
4.intubate if necessary

13. Further treatment for angioedema:
Fresh frozen plasma - Ecallantide - Androgens: danazole and stanazole
Duration of stay in hospital:
Discharge after stabilisation and evaluation of severity
Evaluation of severity, HOW?
PAF-levels
Further recommendations:
Advice Pt to carry an epi-pen, instruct the patient how to use an epi-pen
Avoid known triggers
Consider desensitization therapy (not always possible)

14. Hypovolemic
Cardiogenic
Neurogenic
Septic
Anaphylactic
Principle: Hypoperfusion, Cells go anaerobic, metabolic
acidosis
Shock
•HSR TYPE 4
•HSR TYPE 3
•HSR TYPE 2
•HSR TYPE 1
•ANAPHYLACTIC SHOCK
•SHOCK

15. Summary

16. Episodic and reversible airway disease (most cases)
Primarily targets the bronchi and its subdivisions and nonrespiratory bronchioles
Most common chronic respiratory disease in children
More common in children than adults
Majority (50%–80%) develop symptoms before 5 years of age
ASTHMA

17. Type I HSR with exposure to extrinsic allergens
Typically develops in children with an atopic family history
to allergies
Initial sensitization to an inhaled allergen
Stimulate induction of helper T cells (CD4 T H 2) that
release interleukin (IL)-4 and IL-5
Inhaled antigens cross-link IgE antibodies on mast
cells on mucosal surfaces, leading to:
(a) Release of histamine and other preformed mediators
(b) Functions of mediators:
(a) Stimulate bronchoconstriction, mucus production, influx of
leukocytes
EXTRINSIC ASTHMA

18. INTRINSIC ASTHMA
Non immune
Causes:
(1) Virus-induced respiratory infection
• Examples—rhinovirus, parainfluenza virus, respiratory syncytial virus
(2) Air pollutants
(3) Aspirin or nonsteroidal drug (NSAID) sensitivity
• The above drugs block cyclooxygenase activity and therefore inhibit formation of
prostaglandins and thromboxanes. This leaves the lipoxygenase pathway open for
production of leukotrienes (bronchoconstrictors).
(4) Stress, exercise, and cigarette smoke

19. INTRINSIC ASTHMA
Non immune
Causes:
(1) Virus-induced respiratory infection
• Examples—rhinovirus, parainfluenza virus, respiratory syncytial virus
(2) Air pollutants
(3) Aspirin or nonsteroidal drug (NSAID) sensitivity
• The above drugs block cyclooxygenase activity and therefore inhibit formation of
prostaglandins and thromboxanes. This leaves the lipoxygenase pathway open for
production of leukotrienes (bronchoconstrictors).
(4) Stress, exercise, and cigarette smoke

20. TREATMENT OF ASTHMA

21. TREATMENT OF
ASTHMA