L2:Immunopathology

Question 1

Atopic Dermatitis/Mucositis

Answer 1

=Urticaria (hives)

• Type I Hypersensitivity reaction - Local, Atopic Dermatitis
• Immunogens: Pollen, fungi, animal allergens, dust mites
• Pruritic (itchy) elevated areas on the skin/mucosa that are redder or paler than the surrounding skin (wheal)
• Angioedema (swelling fo subcutaneous/submucosal tissues of the lips, tongue or eyes

Question 2

Angioedema

Answer 2

=Subset of atopic dermatitis/mucositis where the swelling occurs in sucutaneous/submucosal tissues

• Lips, tongue or eyes severely swollen. May block airways or ability to see.
• Caused by allergens
• Histologically see lots of open vessels in submucosal tissues as well as a higher than normal concentration of eosinophils (pink staining)

Question 3

Allergic Rhinitis/Allergic Conjunctivitis (Hay Fever)

Answer 3

=Local, Type I hypersensitivity reaction

• Immunogens: Pollen, foods, drugs, insect venom
• Mucosal Edema, Erythema, Enhanced mucous secretion
• Histologically: Secretions & mucous contain large numbers of eosinophils
• Symptoms:
  
  • Red, itchy, watery eyes
  • Sneezing, congestion, runny nose
  • Itchy or soar throat, post nasal drip, cough
  • Itchy ears, buzzing sound

Question 4

Bronchial (Atopic/Extrinsic) Asthma

Answer 4

=Allergic, hyper-reactive airways leading to bronchoconstriction
-Localized form of type I hypersensitivity reaction
-Immunogens:
-“environmental” antigens, dust, pollen, animal dander
and foods
-Clinical Presentations:
-Dyspnea, coughing and wheezing triggered by
bronchospasm
-Over-distended lungs & occlusion of bronchioles w/
mucous plugs seen in severe cases
-Histopathology:
-Edema
-Increased size of submucosal glands
-Hypertrophy of bronchial wall smooth muscle
-Large numbers of eosinophils
-Pathogenesis:
-Genetic Factors &Environmental factors lead to Atopy,
which is the predisposition of allergic hyper-sensitivity
in airways, likely due to increased production of IgE
-Chronic Asthma
-Caused by intraepithelial mast cells, which present IgE
to the lumen of airways, undercutting the normal
requirement that allergens must first pass through the
epithelial barrier in order to cause an immune
response. This allows lower levels of allergen to more
frequently cause attacks

Question 5

Systemic Anaphylaxis

Answer 5

Type I hypersensitivity Reaction (Systemic IgE reaction)
-Clinical Presentation
-Widespread edema, respiratory distress & vascular
shock
-Itching hives & skin erythema
-Contraction of respiratory bronchioles leading to
respiratory distress
-Laryngeal edema leads to hoarseness & possible
obstruction of the airway
-GI Symptoms: Vomiting, abdominal cramps, diarrhea
-Patient may go into shock w/in 1 hr due to hypotension
-Etiologic Agents: Anything that can get into the peripheral circulation has potential to initiate anaphylaxes
-Foods, Meds, Venoms, Latex, Vaccines & Blood Comps
-Pathogenesis: Systemic, IgE mediated Mast Cell degranulation
-Heart & Vascular system: Increased capillary
permeability, Loss of blood pressure, reduced oxygen
to tissues, Irregular heartbeat, Anaphylactic shock due
to hypotension
-Respiratory Tract & GI Tract Symptoms due to Mast
Cell mediated smooth muscle contractions

Question 6

Mismatched Blood transfusion

Answer 6

=Hemolytic reaction secondary to ABO mismatch
-Antibody mediated agglutination & lysis of RBCs
-Type II hypersensitivity reaction b/c being mediated by the binding of antibodies to cells & the subsequent activation of the complement system.
-If type A blood given to person w/ type B (or O) blood, Anti-A IgM will bind to the foreign RBCs and activate the C1 complex, resulting in Classical pathway activation & amplification leading to RBC lysis
-Clinical Manifestations:
-Mild: Fever & Chills
-Severe: acute kidney failure or complete vascular
collapse & death
-Disseminated intravascular coagulation (DIC) –> Death

Question 7

Hemolytic Disease of the Newborn (Erythroblastosis Fetalis)

Answer 7

• Mechanism:
  1) Rh-negative mother produces anti-D antibody following a pregnancy with a Rh-positive fetus or transfusion with Rh-positive blood
  2) During SECOND pregnancy with an Rh-positive fetus, anti-D IgG crosses the placenta and binds to fetal RBCs, activates complement leading to hemolysis of RBCs
• Mild hemolysis: Jaundice & Mild Anemia
• Profound Hemolysis: Increased billirubin, severe anmeia, heart failure, CNS damage, enlarged liver, generalized swelling & respiratory swelling, hydrops fetalis & death