PATHO FINAL Flashcards
patho information
Type 1 Hypersensitivity
“IgE Mediated Reaction”
Type 2 Hypersensitivity
Cytotoxic Reaction
Type 3 Hypersensitivity
Immune Complex Reaction
Type 4 Hypersensitivity
Delayed Hypersensitivity
Type 1 Hypersensitivity key facts:
-Immediate Reaction (15-20 min)
-Needs previous exposure (bee sting)
-Involves: allergens, IgE, mast cells, mediator release –> Antigen –> b-cell–> matures to plasma–>IgE–>attaches to mast cells–> WAIT–>allergen comes along again–>binds to IgE on mast cells–> release response (mediator).
Examples: bee sting, shellfish, contrast dye, nuts
Type 2 Hypersensitivity key facts:
-Occurs on surface of cell.
-Blood transfusions, Rh pregnancy; autoimmune; drug reactions.
-Immune cells involved–>
IgG & IgM clump to foreign cells–> complement fixes to the foreign cell–>lysis to it–>WBCs (phagocytes) clear up the debris.
Transfusion Reaction
-Check temperature before and 15 minutes after starting blood transfusion.
-Watch for:
fever, chills, flushing
increased HR; decreased BP
N/V, H/A
Restlessness
chest and back pain.
Stop immediately.
Type 3 Hypersensitivity key facts:
INFLAMMATION!!! (Occurs on inside of tissue)
IgG & IgM clump with antigen to form complex structure–> inflammation occurs inside the tissue–> destroys the tissue.
-Involved: antibodies IgG & IgM, complement, neutrophils, mast cells.
-RA
-glomerulonephritis
-systemic lupis
Type 4 Hypersensitivity key facts:
NO ANTIBODY INVOLVEMENT!!!
Involves: T-cells (delayed reaction); cytokines; mast cells & macrophages.
-Delayed T-cell activation
-peaks 48-72 hours
-poison ivy, TB skin test.
Cataracts
The cataracts blocks the light from passing through the lens & scatters the light–> preventing crisp focus of retina.
- Cloudy lens with gradual onset.
- Painless
- Blurry vision
- If left untreated –> may lead to blindness.
Treatment for Cataracts
No pharm treatment; only surgery.
Cataracts Risk Factors:
Older age
Eye trauma
Congenital risk
DM
Corticosteroid use
Smoking & EtOH
Retinopathy
Damage to blood vessels in the retina.
-40% of patients with DM over the age of 40 have diabetic retinopathy.
Proliferative Retinopathy
Advanced retinopathy, new blood vessels are fragile and leaky.
Nonproliferative Retinopathy
Capillary microaneurysms; retinal swelling; hard exudate; macular edema-plasma leaks from macular blood vessels; capillaries rupture–> “dot or blot” hemorrhaging.
Hypertensive Retinopathy
Increased BP creates blockages in retinal blood vessels.
-Initially no vision change
-Sustained, severe HTN can cause sudden vision loss related to swelling of optic disc & nerve.
-Normal vision is restored with HTN tx.
-See eye providers regularly.
Retinal Detachment
Retina has a tear or leak; vitreous humor flows behind the retina; rapid, progressive detachment from the choroid.
-Usually spontaneous.
Retinal Detachment risk factors:
-Increase occurrence in people with myopia (near sighted)
-Over 40
-Trauma to head
-eye tumor
-complication/history of cataracts surgery
Retinal Detachment: what happens:
-sudden, unilateral vision loss
-painless
-may see floaters
-flashes of light
-curtain effect.
Macular Degeneration
MOST common cause of IRREVERSIBLE vision loss in people >60 in US.
-Vision does not improve; treatment is limited. (meds injected into eye).
-2 types!
Dry (non-exudative) macular degeneration
most common (90%)
yellow deposits in the retinal pigment epithelium.
Wet (exudative) macular degeneration
less common (10%)
Growth of the new, leaky blood vessels in an abnormal location of the retina.
Macular degeneration risk factors:
Retinal aging
fam fx
genetics
UV light
hyperopia
smoking
light-colored eyes
-dark leafy veggies are protective.
Symptoms of macular degeneration
Early: none
Later: blurry, darkened vision, blind spots (scotomas), distorted vision (metamorphopsia)
