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. HYPER-SENSITIVITY REACTIONS:
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{1} Type "1" (IMMEDIATE):
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. Ex. Acute atopic dermatitis.
. Highly pruritic papules, vesicles & plaques.
. Light microscopy -> Spongiosis (edema of the epidermis).
{2} Type "2" (ANTIBODY MEDIATED):
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. IgM or IgG + ANTIGEN.
. Ex. Immune hemolytic anemia & Rh hemolytic disease of the newborn.
{3} Type "3" (IMMUNE COMPLEX MEDIATED):
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. Ag + Ab + COMPLEMENT.
. Ex. Serum sickness.
{4} Type "4" (CELL MEDIATED):
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. Dermal inflammation after direct contact with allergen.
. Ex. Tuberculin skin test & Allergic contact dermatitis.
. TRANSFUSION REACTIONS:
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. 1 . ABO INCOMPATIBILITY:
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. Acute symptoms of hemolysis WHILE the transfusion is occuring.
. Ex -> DURING a transfusion, the pt becomes hypotensive & tachycardic.
. Back & chest pain & dark urine.
. ++ LDH & bilirubin.
. -- Haptoglobin.
. 2 . TRANSFUSION RELATED ACUTE LUNG INJURY (TRALI) = LEUKO-AGGLUTINATION REACT
ION:
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. Acute Shortness of breath from antibodies in the donor blood against the repi
ent WBCs.
. Ex -> 20 mins after a pt. receives a blood transfusion, the pt becomes short
of breath.
. Transient infiltrates on CXR.
. All symptoms resolve spontaneously.
. 3 . IgA DEFECIENCY:
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. presents with anaphylaxis !
. In the future, use blood donations from an IgA defecient donor or washed RBCs
.
. Ex -> As soon as the pt. received transfus., he becomes SOB, hypotensive & ta
chycardic.
. NORMAL LDH & BILIRUBIN.
. 4 . MINOR BLOOD GROUP INCOMPATIBILITY:
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. To kell, Duffy, Lewis or Kidd antigens or Rh incompatibility !
. Delayed jaundice.
. No specific therapy.
. Ex -> A few days after transfusion, the pt becomes jaundiced.
. The hematocrit doesn't rise with transfusion & he is generally without sympto
ms.
. 5 . FEBRILE NON-HEMOLYTIC REACTION:
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. Small rise in temperature.
. No ttt required.
. Reaction against donor WBCs antigens.
. prevented by using filtered blood transfusions in the future to remove WBCs a
ntigens.
. Ex -> A few hours after transfusion, the pt becomes febrile with rise 1 degre
e in temp.
. No evidence of hemolysis.
. RHINITIS:
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{A} ALLERGIC RHINITIS:
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. Watery rhinorrhea & sneezing with more prominent eye symptoms.
. Early age of onset.
. Identifiable trigger (animals - environmental exposure).
. Usually seasonal symptoms but can be persistent throughout year.
. Nasal mucosa can be normal, pale blue or pale on exam.
. Associated with allergic disorders e.g. eczema & asthma.
. Tx -> Allergen avoidance.
. Tx -> Topical intra-nasal glucocorticoids.
{B} NON-ALLERGIC RHINITIS = VASOMOTOR RHINITIS:
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. Nasal congestion - Rhinorrhea - Postnasal discharge (postnasal drip = dry cou
gh).
. Late age of onset > 20 ys.
. Can't identify clear trigger !
. Symptoms throughout the year but sometimes worse with seasons change.
. Nasal mucosa may be normal or erythematous.
. Less commonly associated with allergic disorders e.g. asthma or eczema.
. Routine allergy testing isn't necessary prior to initiating empiric ttt.
. May respond to 1st generation oral H1 antihistaminics (Chloramphenicol),
. Never ever responds to antihistaminics without anticholinergic properties (Lo
ratidine)!
. Tx -> TOPICAL INTRANASAL GLUCOCORTICOIDS.
. The 3 most common causes of CHRONIC COUGH (> 8 weeks):
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. UPPER AIRWAY COUGH $YNDROME (Post-nasal drip).
. BRONCHIAL ASTHMA.
. GERD.
. UPPER AIRWAY COUGH $YNDROME = POST-NASAL DRIP:
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. NON-smoker.
. Caused by rhino-sinusitis conditions.
. Dry cough is most likely due to post-nasal drip associated with allergic rhin
itis.
. Dx -> Confirmed by improvement of the nasal discharge & cough with H1 Anti-hi
staminics.
. Chlorpheniramine is an H1 receptor blocker that decreases the allergic respon
se.
. Decrease in NASAL SECRETIONS is most likely to significally improve symptoms.
. ALLERGIC REACTIONS:
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{1} . ANAPHYLAXIS = ANAPHYLACTIC SHOCK:
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. Type 1 hypersensitivity reaction.
. Pts usually have prior exposure to the offending substance.
. Pts have preformed Ig E -> Histamine mediated peripheral vasodilatation.
. Bee stings - food & medications are the most common allergens.
. Acute onset of hypotension & tachycardia.
. Dangerous allergic reaction may progress to respiratory failure & circulatory
collapse.
. Allergen exposure -> Sudden onset of symptoms in more than one system,
. Cutaneous (hives - flushing - pruritis).
. GIT ( Lip / tongue swelling - vomiting).
. Respiratory (Dyspnea - wheezing - stridor - hypoxia).
. Cardiovascular (Hypotension).
. It is a medical emergency.
. Tx -> INTRA-MUSCULAR EPINEPHRINE into the THIGH.
{2} . ANGIO-EDEMA:
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. H/O of ICU pt on ACEIs e.g ENALAPRIL.
. Edema in the face, mouth, lips.
. Absence of pruritis & urticaria.
. Laryngeal edema may occur causing airway obstruction.
. occurs due to BRADYKININ release.
. it may occur at any time not just at the start of drug intake.
. Dx----> Low levels of C2 & C4.
. Tx----> STOP ACEIs + FRESH FROZEN PLASMA + Secure the airway.
. HERIDITARY angioedema:
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. C1 esterase inhibitor defeciency.
. usually follows an infection, dental procedure or minor trauma.
. N.B. The most common cause of acquired isolated angioedema is ACE inhibitors
use.
. N.B. C1q is NORMAL in heriditary angioedema.
. N.B. C1q is DEPRESSED in aquired angioedema.
. C4 levels are depressed in all forms !
{3} . URTICARIA:
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