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MCB Diseases - 1

Disease for MCB exam 1 Creighton Medical School

anemia low Hb Macrocytic (RBC too big) Microcytic (RBC too small) Anisocytic (uneven RB size)
erythrocytosis/polycythemia too many RBCs
sickle cell anemia point mutation of Glu to Val HbA to HbS HbS aggregates to create sickle-shaped RBC with little flexibility leading to decreased 1/2 life and anemia
aplastic anemia too few cells in bone marrow marrow is mostly adipose with no normal hematopoiesis
acute myelogenous leukemia too many cells in bone marrow marrow has tightly packed myeloblasts with few adipocytes
myasthenia gravis neurmuscular disorder Ab's against Ach receptors on mm cell membrane weakness in mm
osteogenesis imperfecta "brittle bone disease" substitution mutation for Gly in collagen protein
Scurvy vit. C deficiency hydroxypro can't be synthesized causing a decrease in collagen stability
Alzheimer's Disease amyloid B protein aggregates (due to Phe) form amyloid fibrils that degeneration brain tissue
Creutsfeld-Jakob Disease transmissible Spongiform Encephalopathy (TSE) conversion of cellular prion protein to scrabie prions that aggregate and cause brain degeneration
I-Cell Disease Defect in the enzyme in the Golgi that adds M6P to enzymes destined for lysosome Causes an accumulation of autolysosomes in acinar cells
Primary Ciliary Dyskinesia defects in MT's causing immotile cilia leads to chronic ear infections, bronchitis, as well as other defects
Emery-Dreifuss Muscular Dystrophy & Charcot-Marie-Tooth (both are laminopathies) because Lamin A in nuclear pores regulates cell fate, effects of mutations are highly tissue specific (as such EM presents in muscles while Charcot presents in neuro)
Cholchicine anti-mitotic chemothearpeutic binds tubulin to prevent MT growth
Taxol anti-mitotic chemothearpeutic depletes tubulin pool by increasing MT growth and stabalizing MT
Vinblastine anti-mitotic chemothearpeutic depolymerizes MT
diseases associated with mitochondrial malfunction diseases of aging (type 2 diabetes, parkinsons, atherosclerosis, stroke) cause an increase in mitochondria
Lysosomal Storage Diseases primarily effect children and are recessive enzyme loss of fxn disorders cause accumulation of substrate to toxic levels (progressive) treatment = enzyme replacement or substrate reduction
Proteasomal Diseases loss of function in Ub-ligases Exception: HPV = proteasomal-mediated degradation
Zellweger Syndrome defective enzyme transport to perioxisome
X-Adrenoleukodystrophy defective long-chain FA uptake by peroxisome
Metaplasia abnormal stimuli causes one type of epithelia to convert into another type often reversible - only becomes cancerous if chronically exposed to stimuli
Lipoma benign adipose tumor 3 types: Conventional (white adipose), Fibrolipoma (excess fiberous tissue), Angiolipoma (vascularized)
Osteoarthritis damage to articular cartilage Can't repair because cartilage is avascular and chondrocytes have poor mitotic abilities
Osteoporosis imbalance in bone resorption and formation leads to decrease bone mass and density results in increased fracture risk, Dowager's Hump, stomach pouch, and decreased height
Duchene Muscular Dystrophy mutation in Dystrophin (protein that links thin filaments to lamins in CT via dystroglycan intermediate) results in muscle contractions with little to no action at the joint
Created by: c.phill