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Exam 3 Pathophys - Complete

Exam 3 Pathophys - Complete

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Published by kkonci01

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Published by: kkonci01 on Nov 03, 2009
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Hey everyone,The following is a list of all the diseases discussed in this unit (quite a bit morethan last time). It is alphabetized, so you can look stuff up easily, and be able to comparediseases with similar names. I believe all the information is accurate, but if you guys findany glaring mistake, please send it out to the yahoogroup so that no one gets confused. Iam still trying to wrap my mind around all of Dr. White’s material, so you might findmore complete info in his notes, or in “Beeman’s”.Forgive my random side notes, they are completely the product of being tired and preferring to look crap up on google instead of actually study.I hope this helps, and good luck!-Pat Clements
- genetic recessive- lack of ceruloplasmin (a copper feroxidase, helps w/ Fe release)- iron accumulation
organ and tissue damage- often seen with other conditions (i.e. thalasemia and alcoholism)
- defective homogentisate oxidase
accumulation of homogentisitc acid
urine- urine turns black when it contacts O2.- joint damage, cardiovasc/urinary damage- red ochre to skin
Anderson’s Disease
- defective branching enzyme (glycogenesis)- causes irregular, long unbranched chain of glucose(Think: you gotta go to Anderson’s to buy a saw to cut that longchain)
- morphologic classification (cell shapes, see specific examples)- Kinetic classification:- Decreased RBC production – improper marrow functionhypoplastic and aplastic anemia*to remember, “plastic is something you make”(__plastic disorders involve making RBC’s)- Increased RBC destruction – i.e. hemolytic anemia--causes hyperplasia – increased RBC production, because RBC’s will have short lifespan.- Ineffective erythropoiesis- apoptosis of RBC precursors- i.e. β-thalesemia (see for more information)- anemia leads to increased iron uptake(low circulating iron, and high reticuloendothelial stores)- overactive hepcidin activity** See iron deficiency anemia for more **
Anemia of Chronic Disease
- observed with infections, inflammation
cytokine mediated- normal RBC size (though can be microcytic)- Increased hepcidin
Fe trapped in MACsalso decreased iron absorbtion in gut (blocked ferroportin)- poor response to supplemental iron- low serum EPO
- partial loss of circulation to heart muscle
chest pain, chronic condition
- hardening of the arteries (general term)
- form of arteriosclerosis- LDL goes into endothelium of arteries- reacts with oxygen free radicals (products of respiration)- modified LDL recognized by scavenger receptor on monocytes- become foam cells, with cholesterol ester droplets(between endothelial and tunica media layers)- inflammatory disease
- Thiamine deficiency- wasting disorder, leads to weakness and paralysis- carbohydrate metabolism is disrupted- test: transketolase (since TPP is a cofactor)
Branched chain keto aciduria
- aka Maple Syrup Disease- lack of α-keto acid dehydrogenase complex
no oxidative decarboxylation-accumulation of α-keto intermediates
can’t metabolize valine, isoleucine, leucine- urine smells like maple syrup- (Think: maple trees have branches)- mental retardation
Cancer and RAS
- mutant RAS = oncogenic- unable to hydrolyze bound GTP
signal always on
activates downstream cell growth
uncontrolled cell growth = cancer 
- caused by a toxin, produced by
Vibrio cholera
- irreversibly modifies Gs subunit of adenylate cyclase- stuck in GTP bound state (active)
cAMP levels, PKA activation
PKA regulated Cl- channel disrupted
loss of water to intestine
Crigler-Najjar Syndrome
- rare, recessive- extremely reduced/absent UDP-glucoronosyl transferase
buildup of unconjugated bilirubinType I: Severe Jaundice- may require liver transplant- Kernicterus (brain damage
cerebral palsy & hearing loss)Type II: Moderate Jaundice- may respond to inducers (i.e. Phenobarbital)
- defective cysteine transport- produces crystals
renal failure (crystals destroy kidneys)
- cystine excretion (S=S)

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