Biochemistry Exam 3 - Ucimed

Front 1

Essay: Conditional Knockout

Back 1

in nervous system ^G in blood
neg feedback of HPA axis req. G
-less anxious-->role of G in learning, anxiety, memory in neurons

Front 2

Essay: Knock-in

Back 2

-mutation causing failure of receptor dimerization and DNA binding.
-mice survived
-suggests G ^imp't Prot/Prot int.
-reg. of xscrip factors

Front 3

Essay: Mutation in Human: disease and treatment

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-Adrenal Hyperplasia & ^ ACTH (-->^GR)
-from a pituitary tumor (Cushing's)
-Adrenal Neoplasia
-^ use of glucocorticoid

Front 4

Essay: What happens in nucleus

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GR bound by cortisol (g-coritcoid):
1. binds GRE: represses or activates xscription
2. protein:protein interaction - regulates xscrip. factors (AP1&NF-kB)

Front 5

Essay: Mechanism of action

Back 5

stress (physical: infection/injury or emotional)
-->hippocampus, amygdala-->hypothalamus -(CRF&AVP)-> Pituitary -(ACTH)-> Adrenal Glands --> secrete glucocorticoid (inhib. ACTH&CRF) --> cyto. G receptor --> nucleus

Front 6

Essay: Syndrome, causes, symptoms

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Cushing Syndrome
causes ^glucocorticoid (hypercortisolism)
symptoms: obesity, hypertension, osteoporosis, diabetes

Front 7

Physiological Jaundice

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^ unconjugated bilirubin in newborns due to low UDP-glucuronyltransferase (b/c liver not fully developed)
--mild form doesn’t req’ treatment & improves
--severe form needs treatment: fluorescent light
However, if there’s ^ levels of conjugated bilirubin, means impaired removal (ie liver damage, bile duct obstruction)

Front 8

Jaundice
Reason #2 for Decreased Excretion

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1.bile duct obstruction(obstructive or posthepatic jaundice) 2. decreased bilirubin excretion (note:rate of bilirubin excretion correlates w/ rate of bile flow) 3.^conjugated bilirubin

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Jaundice
Decreased Excretion b/c of:

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1. liver damage(hepatocellular or intrahepatic jaundice) 2.decreased bilirubin uptake and conjugation 3.^levels of unconjugated bilirubin (dangerous! Unconjugated bilirubin in excess of albumincapacity„³binds lipids; impairs membrane funct. esp. in nervous system)

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bilirubin turnover

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By labeling glycine*
early-early
Heme turnover in liver (15%)

early-late \
in liver and bone marrow
(poorly incorporated or
easily released from RBC)
^ w/ diseases ie. pernicious anemia
, thalassemia

late
in RBC’s (85%)

Front 11

HEME DEGRADATION

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RBC’s>Heme>biliverdein>bilirubin>complexedw/albumin>conjugated w/glucuronic acid>bile>unconjugated bilir.>urobilinogen>urobilin(stercobilin in feces) or urobilin in kidney.

Front 12

HEME: what makes it up and location of steps

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-4 pyrrole rings, 4methylene bridges, synthesized mostly in Liver & bone
-marrow, of the 8 steps, the 1st & last 3 steps are in the mitochondria, 2nd –
5th steps are in cytosol, only Uroporphyrin III is acceptable to body (it’s
assymetrical w/A’s(acetate) & P’s (propionate).

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HEME : Found in

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: 1.hemoglogin (binds O2) 2.myoglobin 3. cytochromes (e- carrier
(p450) 4. catalase(part of active site)

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Phy Active Amines: characteristics

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1.All are neurotransmitters 2. All are excitatory except GABA,Gly, Taurine(inhibitory).
a.a.--------------------„³amines
1.Decarboxylation w/PLP cofactor (and/or)
2. Hydroxylation w/ BH4

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NITRIC OXIDE

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NO
R--------------„³Citrulline
NO synthase

NADPH NADP+

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NO char

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1.diffuses freely through membranes 2.short ½
life 3.reactive 4. cell signal molec. 5. smooth muscle relaxer 6.prevents platelet aggre. 7.nuerotransmitter 8.made in macrophages as a bacterial/cancer killer

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SERATONIN: MNEM

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“Small Wimpy Trashy Person is Depressed” so he “Pax” his “Prosac”

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GABA (γ-aminobutyric acid): MNEM

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someone who “GAB”s a lot can be “inhibited” by “GluEing” their mouth shut.

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Glutamate(E) characteristics

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is excitatory and found in all neurons GABA is inhibitory and found in only inhibitory neurons. They’re opposites! Some epileptics have decreased GABA levels—treated w/ Valproic Acid = ^GABA

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Heme synthesis: overall rxn

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8 glycine + 8 succinyl CoA + Fe 2+ ---„³ ---„³ Heme

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ALA locations

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ALA 1 in liver & ubiquitous, ALA 2 in bone marrow

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PORPHYRIAS: Enzymatic abnormalities:

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Hepatic & neuropsychiatric effects

Causes ^ALA & PBG and/or with decreased heme in cell body fluids.

Front 23

CREATINE: MNEM

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you want to “Create” (Creatine) or “GROw” muscle ever since you “Met” “SAM” the trainer

Front 24

GSH: MNEM

Back 24

lowers ROS’s, analogs increase tumor sensitivity to ROS from irradiation

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Bilirubin in blood =

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unconjugated / indirect bilirubin (w/ colorimetric RXN in methanol.

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Bilirubin in bile =

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conjugated/ direct bilirubin (w/ colorimetric RXN in aqueous solution)

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Heme Sources:

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85% RBC’s, 15% immature RBC turnover; liver and other extraerythroid tissue.

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JAUNDICE

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Yellowing of skin and white of eye from bilirubin deposition… caused by 1.^production or 2. decreased excretion

Front 29

jaundice:
Increased Production b/c of:

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1.excess hemolysis(hemolytic/prehepatic jaundice) 2. insufficient conjugation or complexing 3. ^levels of unconjugated bilirubin (dangerous!)

Front 30

Essay: Knockout

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die shortly after birth due to low production of surfactants--> respiratory failure