Autoimmune & Hypersensitive Rxns Flashcards

1
Q

What are the 4 Major types of Autoimmune Disorders &Hypersensitivity Reactions?

A
*Type I Hypersensitivity
“Allergies”
*Type II Hypersensitivity
Reactions to Self-Antigens
*Type III Hypersensitivity
Immune Complex Formation
*Type IV Hypersensitivity
Cell-Mediated
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2
Q

What is IgE?

A

immunoglobulin

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3
Q

Describe the histology of an allergic response.

A

Occur within minutes of exposure to antigen
Antigens combine with IgE antibodies
IgE binds to mast cells and basophils, causing them to undergo degranulation and release several chemical mediators:
Histamine: dilates and increases permeability of blood vessels (swelling and redness), increases mucus secretion (runny nose), smooth muscle contraction (bronchi).
Prostaglandins: Contraction of smooth muscle of respiratory system and increased mucus secretion.
Leukotrienes: Bronchial spasms.

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4
Q

What is stridor?

A

kind of croup sound, with breath

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5
Q

What are some symptoms of Anaphylaxis

A

Swelling of conjuctiva, runny nose, swelling lips and throat, lightheaded, unconsciousness, confusion, headache, anxiety, bradycardia or tachycardia, hypovolemia, skin (hives, flushing, itching), shortness of breath, weezing, stridor, diarrhea, vomiting, cramps, loss of bladder control.

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6
Q

Common food triggers of anaphylaxis?

A

Foods
Wasp/bee stings
Medications
Exercise

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7
Q

What are medications for anaphylaxis?

A

epinephrine (emergent); corticosteriods; antihistamines; IV fluids/ airway protection

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8
Q

Describe Type II (Cytotoxic) Reactions?

A

Involves antibodies (IgG or IgM) binding to antigens on the cell surface
Antigen may be intrinsic (i.e.: “self”) OR extrinsic (adsorbed onto the cells during exposure to some foreign antigen/ pathogen)
Antigenic cell is lysed/ phagocytized
Examples: transfusion reactions; Graves Disease; Myasthenia Gravis

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9
Q

What is Graves Disease ?

A

hyperactive thyroid, producing an excessive amount of thyroid hormones
Antibodies attach to TSH receptors on thyroid gland stimulating production & secretion of thyroid hormone
Hyperthyroidism

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10
Q

what is Myasthenia Gravis?

A

Neuromuscular disease leading to weakness & rapid fatigue

Antibodies blocks postsynaptic acetylcholine receptors, disrupting neuromuscular transmission

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11
Q

Describe Type III (Immune Complex) Reactions

A

Involve reactions against soluble antigens circulating in serum. Usually involve IgG & IgM antibodies. Antibody-Antigen immune complexes are deposited in blood vessels, joints and renal glomeruli resulting in symptoms.
Complexes activate complement.
Result –> prolonged inflammation with resultant damage. Common Disorders:
Systemic lupus erythematosus (SLE)
Rheumatoid arthritis (RA)
Extrinsic allergic alveolitis (Hypersensitivity pneumonitis)
Glomerulonephritis

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12
Q

What is Systemic Lupus Erythematosus (SLE)?

A
Multisystem autoimmune disease
Diffuse inflammation involving 
Skin, joints, brain, kidneys, heart, lungs, serous membranes
Common symptoms:
Skin:  rash (malar rash=butterfly rash)
Eyes:  photosensitivity
Neurologic:  headaches; memory loss
Musculoskeletal:  persistent joint pain & swelling
Extremities:  Raynaud’s
Fatigue & Obesity
Osteopenia/osteporosis
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13
Q

what are the Demographics of SLE?

A
Age: 15-45 years peak frequency
15-20% are children and have worse disease
Sex: 9:1 F>M
1 in 250 African-American females
Males have worse disease
Race: Nonwhite/white ratio 3:1
Nonwhites have worse disease
Total number: 1.4 million (250,000 severe)
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14
Q

What does SLE do to the heart?

A

Vasculitis (inflammation) affecting coronary arteries  Atherosclerosis/ CAD
↑ risk for conduction abnormalities (dysrhythmias)
HTN: ↑ risk for cardiomegaly & heart failure

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15
Q

What does SLE do to the Lungs?

A

Pleuritic chest pain
Interstitial lung disease
Decreased diffusion capacity and restrictive pattern on PFT’s
Diaphragmatic weakness leading to dyspnea

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16
Q

Should patients with SLE exercise?

A

Exercise yes! Good outcomes for strength, endurance etc.

17
Q

Describe Type IV Delayed (Cell-Mediated) Reactions.

A

Not antibody mediated but cell mediated
Involve reactions by memory cells.
First contact sensitizes person.
Subsequent contacts elicit a reaction.
Reactions are delayed by one or more days (“delayed hypersensitivity”).
Delay is due to activation/ migration of macrophages and T cells to site of foreign antigens.
Reactions are frequently displayed on the skin: itching, redness, swelling, pain.
Tuberculosis skin test (Mantoux screening test/ PPD (purified protein derivative)
Poison ivy
Metals
Latex (3% of health care workers)
Anaphylactic shock may occur.

18
Q

Describe the pathogenesis of type IV hypersensitivity?

A

Sensitization Phase:
Step 1: antigen absorbed by the skin (or injected)
Step 2: APC (e.g.: dendritic cell; macrophages) process antigen
Effector Phase:
Step 3: Previously sensitized cells recognize antigen on 2nd presentation
Step 4: Macrophages/ cytotoxic T cells attracted to site
Step 5: Activated macrophages/ cytotoxic T cells cause inflammation by releasing cytokines & toxic chemicals locally resulting in damage