Clin Med - Pathophysiology Flashcards
Anaphylaxis - etiology and clinical presentation; type of reaction
Etiology: First exposure - IgE binds mast cells creating sensitization. Second exposure - allergen binds IgE causing mast cells to degraulate.
Clinical presentation: Local - uticaria, erythema, edema, warmth at site. Systemic - uticaria, vomiting, vasodilation, bronchospasm, laryngeal edema, wheezing, anxiety/fear, vascular collapse, shock.
Type of rxn: Immediate (IgE-mediated) hypersensitivity
Autoimmune hemolytic anemia - etiology and clinical presentation; type of reaction
Etiology: Autoantibodies destroy red blood cells. Warm - IgG autoAb bind and lyse RBCs (37C). Cold - IgM autoAB bind and lyse RBCs (<37C).
Clinical presentation: Non-specific sx of anemia.
Type of rxn: Cytotoxic (Type II) hypersensitivity
Poststreptococcal glomerulonephritis - etiology and clinical presentation; type of reaction
Etiology: After recent strep infection, immune complexes plug glomeruli of nephrons. Occurs most in 2-6 year olds with hx of sore throat in cold weather or skin infection in summer.
Clinical presentation: Asymptomatic. Headache, anorexia, N/V, flank/back pain, smokey colored uring, oliguria, edema, hypertension.
Type of rxn: Immune-complex (Type III) hypersensitivity.
Serum sickness - etiology and clinical presentation; type of reaction
Etiology: Immune complexes are deposited in small vessels and tissues causing vasculitis. Caused by administration of non-human protein antigens (antitoxins/venoms, some vaccines, insect stings).
Clinical presentation: Purpuric rash 7-10 days after first exposure (uticarial or macular/papular), fever >38.5C, polyarthalgias or polyarthritis. May present with angioedema or nephritis. Resolves within weeks of D/C of antigen.
Type of rxn: Immune-complex (Type III) hypersensitivity.
Vasculitis - etiology and clinical presentation; type of reaction
Etiology: Immune complexes deposited in vessels. Rare; primary or secondary; limited to skin/organ or multisystem; mild to life-threatening; affects small (Henoch-Schonlein purpura), medium (Kawasaki disease), and large (giant cell arteritis) vessels.
Clinical presentation: Small/medium - purpura, urticaria, ulcers, nodules. Large - tortuous vessels. Systemic - fever, night sweats, fatigue, anorexia, arthalgia, arthritis. Severe - alveolar hemorrhage, mesenteric ischemia, vision loss.
Type of rxn: Immune-comples (Type III) hypersensitivity.
Contact dermatitis - etiology and clinical presentation; type of reaction
Etiology: First exposure - sensitization. Second exposure - allergic reaction.
Clinical presentation: Wheals in distribution of offending agent, pruritis, excoriation.
Type of rxn: Delayed (Type IV) hypersensitivity.
Transplant rejection - etiology and clinical presentation; type of reaction
Etiology: Graft destruction caused by T cell-mediated reaction to allograft histocompatibility antigens.
Clinical presentation: Fever, chills, malaise, arthalgias; usually only present with abnormal lab values (based on organ transplanted).
Type of rxn: Delayed (Type IV) hypersensitivity.
Anaphylaxis: Type of event (in regard to IgE), sensitization requirement, rxn occur on first exposure, amt of exposure needed for rxn, rxn predicted by skin test
Type: IgE-dependent event Sensitization: Required First exposure: No rxn Amt: Very little Skin test: Predicts
Anaphylactoid: Type of event (in regard to IgE), sensitization requirement, rxn occur on first exposure, amt of exposure needed for rxn, rxn predicted by skin test
Type: IgE-independent event Sensitization: Not requried First exposure: Rxn Amt: Usually more than anaphylaxis Skin test: Does not predict
Clinical relevance of anaphylaxis and anaphylactoid rxns
Acute phase - both result in degranulation of mast cells and present the same clinically requiring same tx.
Differentiating important when considering how to prevent/reduce risk of future rxns.
Classical manifestations of IgE-mediated reactions in following body areas: skin, respiratory tract, heart, eyes, GI tract, neuro system
Skin (90%): Hives, pruritis, flushing, angioedmea (deep dermis).
Resp tract (70%): SOB, wheeze/stridor, hoarseness, pain with swallowing, cough.
Heart (45%): Fast/slow heart rate, low BP.
Eyes: Swelling of conjunctiva.
GI tract: Crampy abd pain, diarrhea, vomiting.
Neuro: Lightheadedness, LOC, confusion, HA, anxiety/fear.
Define urticaria and pathophysiology
Define: Swelling of upper dermis. Vascular reaction of skin characterized by wheals surrounded by a red halo or flare.
Pathophys: Antigen binds to IgE on mast cells causing degranulation and release of histamine binding H1 and H2 receptors causing arteriolar dilation, venous constriction, and increased cap permeability leading to swelling of upper dermis. Acute - new 6wks. Can also be non-immunologic - physical stimulus inducing histamine release in absense of IgE-mast cell binding.
Define angioedema and describe pathophysiology
Define: Swelling of deep dermis. Commonly affects face or portion of extremitiy (lips, cheeks, periorbital areas, tongue, bowels).
Pathophys: Antigen binds to IgE on mast cells causing degranulation and release of histamine binding H1 and H2 receptors causing arteriolar dilation, venous constriction, and increased cap permeability leading to swelling of deep dermis. Can also be non-immunologic - physical stimulus inducing histamine release in absense of IgE-mast cell binding.
Distinguish b/t hereditary and acquired angioedema.
Hereditary angioedema: Inherited autosomal dominant genetic mutation which causes either diminished levels or dysfunctional levels of C1 inhibitor (protein in complement activation pathway). Abnormal activation of the complement system leads to excessive production of bradykinin, a vasodilatory mediator. Histamine is not directly involved and therefore antihistamines are not effective.
Acquired angioedema: Rare disorder caused by acquired C1 inhibitor deficiency via neoplastic disorders, immune complex disorders, or if an autoAB is produced by body.
Define atopy
Type I Hypersensitivity. Genetic tendency to develop IgE-mediated responses, multigenic. 20% of population is atopic.
