Chapter 1. Cell Injury - Free Radicals Flashcards Preview

MSII Pathology > Chapter 1. Cell Injury - Free Radicals > Flashcards

Flashcards in Chapter 1. Cell Injury - Free Radicals Deck (6)
Loading flashcards...
1

how do drugs like acetaminophen make free radicals? how is this harmful? what is a good treatment method?

acetaminophen is converted into acetaminophen FR in the liver
-may cause diffuse chemical hepatitis
--liver cell necrosis initially occurs around central vein (zone III) and can occur at nontoxic levels in alcoholics
--produces transient decrease in functional factor VII to prolong PT
--treat with N-acetylcysteine to increase glutathione synthesis
-may cause renal papillary necrosis (NSAIDs)

2

how does carbon tetrachloride make FRs? how is this harmful?

converted into CCl3 FRs in the liver
-produces liver cell necrosis with fatty change

3

what FR does cigarette smoke make?

-quinone/hydroquinone FRs made from tar
-makes NO, which reacts with other reactive species to make more FR

4

how are free radicals neutralized? (5 ways)

1. superoxide dismutase (SOD)
-converts superoxide to peroxide and O2
2. glutathione peroxidase in PPP
-neutralizes H2O2, hydroxyl, and acetaminophen FR
3. catalase (in peroxisomes)
-degrades peroxide into O2 and water
4. vitamins
-E prevents lipid peroxidation in membranes and neutralizes ox-LDL
-C is best neutralizer of hydroxyl FR in smokers
5. selenium
-neutralizes FRs in cytosol

5

what might happen if you treat RDS (respiratory distress syndrome) with an O2 concentration > 50%?

retinopathy of prematurity (blindness)

6

how are Fe VS Cu overload disorders similar and different in regards to FR injury?

Fe: intracellular Fe makes HO. FRs that damage parenchymal cells to cause cirrhosis, exocrine/endocrine pancreatic dysfunction
Cu (Wilson's disease): inability to excrete Cu into bile
-excess in hepatocytes increases production of HO. FRs to cause cirrhosis