March 25 - Other Flashcards
Hepatitis B immunopathogenesis
Hep B has NO viral cytopathic effect. Immune system is what does damage.
- Proliferative phase: HBsAg and HBcAg are expressed on MHC class I. CD8+ cells kill the infected hepatocytes.
- Integrative phase: HBV DNA is incorporated into the genome of surviving hepatocytes. What causes risk for hepatocellular carcinoma.
Antibody response neutralizes virus before it enters hepatocytes, so is protective but does not cause hepatocellular damage.
Immune complexes cause some of non-hepatic symptoms such as arthralgias of acute disease and glomerulonephritis and vasculitis of chronic disease
Hereditary angioedema
Autosomal dominant. Episodes of painless non-pitting edema. Low serum C1 esterase inhibitor- can’t inactivate C1 or kallikrein. Kallikrein converts kininogen to bradykinin which causes the angioedema
Calcineurin inhibitors
Cyclosporine and tacrolimus. Normally calcineurin is activated and then dephosphorylates NFAT. NFAT can then enter nucleus and stimulate IL-2 production. IL-2 stimulates the growth and differentiation of T cells. Calcineurin inhibitors thus block T cell proliferation
Scarlet fever presentation
Fever, malaise, abdominal pain, sore throat.
Swollen edematous pharynx that may be covered by gray-white exudate.
Strawberry tongue due to inflammation of the papillae.
Red rash with sandpaper like feel
Tryptase
Enzyme released by mast cells in anaphylaxis. Can be measured after event to support diagnosis
Hypertensive retinopathy findings
Flame hemorrhages
Thickened retinal arteriolar walls and AV nicking
Cotton-wool spots: small white foci of retinal ischemia
Wilson disease
Kayser fleischer rings: copper deposition in cornea
Damage and atrophy of basal ganglia
Aqueous humor flow
Secreted by ciliary body to posterior eye chamber. Then flows through pupil to anterior chamber. Then diffuses through trabecular network to canal that drains to veins.
Open angle glaucoma pathophysiology
Increased IOP due ot problem with travecular meshwork that blocks outflow of aqueous humor. Results in increased IOP that is painless, chronic, and slowly progressive. Pale optic disc and enlarged optic cup on eye exam.
Closed angle glaucoma pathophysiology
Increased IOP due to physical obstruction of outflow canals by the narrow angle between the iris and the cornea. Results in painful, acute, sudden vision loss.
Treatment of closed angle glaucoma
Mannitol or carbonic anhydrase inhibitor to rapidly lower IOP. Laser or surgery if ineffective.
Cholinergic agonist
-M receptors in ciliary body and iris. Agonist casuses constriction which opens the angle, increasing aqueous humor outflow
Treatment of open angle glaucoma
- Beta blockers
- decrease aqueous humor production by antagonizing B1 receptors in ciliary body - Latanoprost
- prostaglandin analog. Opens canal improving outflow.
- side effect is darkening of iris