clinical presentation of anaphylaxis
- Cutaneous: Flushing, pruritis, hives, urticaria, angioedema, periorbital swelling
- Respiratory: Dyspnea, cough, nasal itching, congestion, wheezing, throat itching, tachypneic, stridor
- Cardiovascular: Chest pain/tightness, palpitations, dizziness, tachycardic, hypotensive
- GI: Nausea/vomiting, crampy abdominal pain, diarrhea
- CNS: Headache, confusion, fear of impending doom
Sensitization to allergen
-APC + antigen -naïve CD4+ T-helper cells in lymph node - CD4+ to Th2 (IL4, IL5) - Th2 releases IL4 -IL4 activates B-cells to mature into IgE secreting plasma cells -IgE attaches to surface of mast cells—now ready to respond to subsequent exposure to allergen -Th2 also releases IL5 which activates eosinophil degranulation
Subsequent exposure to allergen
-Mast cell IgE receptors cross-link to allergen - immediate degranulation of pro-inflammatory mediators (histamine, eosinophils)—causes continued immune response even after allergen is gone
first-line emergency anaphylaxis vs second-line therapies
o 1st line = IM EPI, O2 and albuterol—maintain airway
o 2nd line = Normal saline IV, Antihistamines, Corticosteroids, Bronchodilators, Ranitidine
Mechanism of Epi
o Alpha-1: ↑ vasodilation, ↓ mucosal edema in upper airway
o Beta 1: ↑ heart rate
o Beta 2: Bronchodilation; ↓ release of inflammatory mediators by mast cells
Why is epinephrine used for the long-term management of severe allergy?
so patient w/anaphylactic potential always has immediate access to EPI in anaphylactic emergency to prevent severity
-EPI-Pen = fixed dose EPI, administered IM in lateral thigh
role of IgE allergen testing
Testing for IgE antibodies in response to exposure to specific antigen/allergen is useful to establish diagnosis of a hypersensitive reaction.
Describe the clinical presentation of cellulitis with furuncle
o Localized erythema, tenderness, warmth
o Inflammation
o Furuncle:infected hair follicle causing small abscess
o Systemic symptoms: fever, malaise
Mechanism by which fever develops and its role in an acute bacterial infection
- Macrophages release cytokines in response to bacterial infection—IL-1 induces fever
- bacteria and virus can only survive at certain temps and increasing temp can help to weaken/kill them
Clinical significance of lymphadenopathy
- Indicative of infection
- APCs carry antigens to lymph node which causes inflammatory mediators and causes activation of T-cells which then causes swelling before drainage
Summarize the etiology and mechanisms behind neutrophilia
- Macrophages phagocytose bacteria and release cytokines recruiting neutrophils
- Neutrophils phagocytose bacteria
- Eventually neutrophils lyse, releasing contents into tissues, damaging it
- Also secrete PTX3 for complement induced opsonization
Relate the finding of pus to the body’s response to bacterial infection
-pus is build-up of dead/lysed neutrophils and contents
Clinical application of C-reactive protein in the evaluation of a bacterial infection
C-reactive protein = early inflammatory marker produced mainly by liver that binds to surface of bacteria; enhances activation of alternative pathway of complement (enhances inflammation)
pathogenesis of Staphylococcus aureus (S. aureus) infection
- S. aureus is commonly present in healthy individual’s normal skin microbiome
- Break in skin/barrier can allow S. aureus to invade and infect tissue
how are Gram stain and culture with sensitivity utilized in the laboratory to isolate and identify bacteria
- Gram stain differentiates Gram (+) (purple) from Gram (-) (pink/red) bacteria, which aids in identification of causative organism.
- Culture sensitivity aids in antibiotic selection
when to use prophylactic, empiric, and definitive antimicrobial therapies in the infection progression timeline
- Prophylactic therapy is used preventatively prior to infection
- Empiric antimicrobial therapies: broad-spectrum antibiotics used before bacteria has been identified—based on clinical judgment
- Definitive: antibiotic specific to identified causative agent
Rationale for using empiric antibiotics to manage Gram-positive bacterial infections
most Gram (+) bacteria can be treated using the same small group of antibiotics
how S. aureus becomes methicillin-resistant
Bacteria acquires gene for penicillin-binding protein (PBP)-2a, unique from regular PBP, inhibiting -cillin antibiotics from being able to bind
