woo
In the fed state, what can the liver do to amino acid metabolism intermediates
convert them into glycogen and triacylglycerols
True or false: histamine uses H1 receptors and H2 receptors to cause vasodilation, bronchoconstriction, and increase gastric acids
true
If I am taking an antidepressant what amino acid am I also taking
serotonin comes from tryptophan
so does melatonin
Which type of hyperbilirubinemia is pre hepatic (UCB not taken up by hepatocytes)
hemolytic anemia, rotor syndrome
which reaction takes acetyl coA to ketones
ketogenesis
Carbon skeletons of amino acids get converted into these 7 products
Name the breakdown products of glutamate
Where do the catabolic pathways for the three branches chain amino acids occur?
BONUS:What are these amino acids
occurs in extrahepatic tissues
valine, isoleucine, leucine
Name 2 hepatic hyperbilirubinemias
neonatal physiologic jaundice (treat with phototherapy and has kernicterus toxic encephalopathy)
toxic hyperbilirubinemia: can be caused from acetaminophen, hepatitis, amanita mushroom poison
Is transamination irreversible?
No. it is reversible and occurs everywhere.
Deamination occurs in the liver and is irreversible
Which amino acids are glycogenic and ketogenic?
Heather always gets this wrong, so give her a high five if she gets it right
Ile, Phe, Trp, Tyr
When tyrosine synthesis is disrupted, what happens and how can we screen this?
buildup of Phe, screen with Guthrie bacterial inhibition assay
If someone has maple syrup urine disease, what enzyme is deficient? What happens to urine? Symptom? How do we screen it?
deficiency in branched chain a-ketoacid DH; maple syrup urine odor; abnormality in brain function, screen with 2,4 dinitophenylhydrazine
What is post hepatic hyperbilirubinemia
blockage of hepatic or common bile ducts due to gallstones or pancreatic cancer
What pathway is impaired in DKA? Why?
glycolysis, increased acetylene coa leads to increased ketone bodies, and now our pH is low
what can be oxidized to oxalate, which in the presence of calcium, can become kidney stones
glyoxylate
Difference between classic and non classic PKU
classic: deficiency in phenylalanine hydroxylate
non classic: dihydropteridine reductase
In this porphyria, there is a mutation in prophobilinogen deaminase. They also have symptoms of a painful abdomen and port wine-colored pee. What is going on and how do we treat it?
acute intermittent porphyria and treat with hemin and glucose.
2 sources we get from PPP
NADPH and ribose 5 phosphate
______ is a biochemical process that converts essential amino acids into non-essential amino acids
transamination fr
What does asparaginase do
hydrolyzes asparagine to liberate ammonia and aspartate
Cystathione B-synthase deficiency is called ___ and causes deficiency of folate, B6, B12
homocystinemia
What porphyria causes a defect in uriporphyrinogen decarboxylase and causes photosensitivity and hyperpigmentation
porphyria cutanea tarda
Which reaction takes fatty acids to acetyl coa
beta oxidation
contain both catabolic and anabolic