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45 Cards in this Set

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I say Type I Hypersensitivity, you say:
Mast Cells, Basophils, Eosinophils, & IgE
I say Type III Hypersensitivity, you say:
Ag-Ab Complexes, & PMNs/Complement System
I say Type II Hypersensitivity, you say:
Antibody Mediated
What are Urticaria?
Hives
List 3 symptoms of asthma:
Bronchoconstriction, mucus production, & Laryngeal Edema
Name two diseases involved in Type II antibody membrane binding:
Graves Disease & Myasthenia Gravis
I say linear distribution, you say:
Coating in type II hypersensitivity.
What is deposition of Ag-Ab complexes in blood vessels called?
"Vasculitis"
What is deposition of Ag-Ab complexes in a glomerulus called?
Glomerulonephritis
Streptococcus in the kidney causes:
APGN (acute post-streptococcal glomerulonephritis)
What does major basic protein do?
Damages and kills bystander cells.
Early phase type I involves (2):
Recruitment of PMEs & Mast cell degranulation
Late phase type I involves (2):
Major Basic Ptn destruction & Eosinophil degranulation
Give two GI anaphylactic responses:
Vomiting & Diarrhea
What can type I caused vasodilation result in?
Anaphylactic shock
Give three type II vascular reactions discussed in class:
Blood type rejection, Penicillin opsonization, Erythroblastosis fetalis
Linear distribution can be observed in:
Goodpasture's Syndrome (type II hypersensitivity)
Give 4 results of complement activation:
Phagocytosis, MAC (membrane attack), Chemotaxis, & Mast cell degranulation.
Give three things involved in vasculitis:
Microembolisms/Microthrombosis, Fibrin accumulation, Ischemia downstream
Arthritis is a type ____ Hypersensitivity:
Type III
If you see CD4s and CD8s, you're thinking:
Delayed Hypersensitivity (Type IV)
What's the reason for the delay?
CD4s are slow.
Is allergic contact dermatitis granulomatis or non?
Non-granulomatis.
Perivascular accumulation, aka:
"Cuffing"
Macrophages go to ____, which are ____ phagocytic cells present in CT.
Histiocytes are stationary phagocytic cells.
Histiocytes are seen in type ____ hypersensitivity reactions?
Type IV
What are signs of chronic allergic contact dermatitis(2)?
Scales & lichenification
What are signs of acute allergic contact dermatitis(3)?
Redness, Pain, Swelling, etc.
Granular distribution seen in type ____ hypersensitivity?
Type III
What are some symptoms of SLE (7)?
Red eye, joint pain, fatigue, alopecia, Malar rash (butterfly), photosensitivity, & chest pain.
What are some signs of SLE?
Increased: ANA (anti-nuclear antibodies), ESR (erythrocyte sedimentation rate), & anti-Smith Antibodies, Decreased: C5a, C3a
What type of hypersensitivity reaction takes place in SLE?
Type II
What is the pathophysiology behind SLE?
Abnormalities in apoptosis ("An apoptotic event causes blebs which aren’t destroyed (usually they are)")
How can you treat SLE?
Steroids & antimalaria drugs (one can also use immunosuppressants).
What is Raynaud's Phenomenon?
RWB Fingertips seen in SLE ("very patriotic").
What organ systems are affected by SLE the most?
Hematologic (100%), Joints, Skin, CNS (50%), Kidneys, Heart, GI tract, Eye (15%)
What type of hypersensitivity reaction takes place in JRA?
Type III
What is an Ulnar deformity?
Hand cramps from JRA
Can you recall the difference between SLE and JRA mentioned in class?
JRA affects the body more symmetrically than SLE (somewhat random).
What are some symptoms of JRA (4)?
Scleritis/Episcleritis, Bilateral joint pain, Fatigue, no systemic (extra-joint) pain.
What is RF?
Rheumatoid Factor (It is an antibody against the Fc portion of IgG).
What is Sjögren's Syndrome (SS)?
An autoimmune disorder against exocrine glands (lacrimal, meibomian, salivary, urogenital, etc.)
What's the difference between lab tests for Sjögren's Syndrome & SLE?
No anti-Smith Ab in Sjögren's Syndrome (both will have ANA), although SS may arise secondary to SLE/JRA, etc.
Which autoantibody will be present in the serum of an SSA patient?
Antibodies to Ro extractable nuclear antigens.
None
Which autoantibody will be present in the serum of an SSB patient?
Antibodies to La extractable nuclear antigens.
None