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GI II Exam 1 > Biochem CIS > Flashcards

Biochem CIS Flashcards

1
Q

in bloodstream

A

single amino acids

then transpored into cells

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2
Q

amino acid metabolism

A

need to excrete nitrogen - urea

carbon as energy

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3
Q

urea

A

from urea cycle in liver

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4
Q

uric acid

A

from purine bases

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5
Q

creatinine

A

from creatine phosphate

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6
Q

ammonia

A

from glutamine in kidney

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7
Q

bilirubin

A

from heme

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8
Q

nitrogen to be excreted

A 
urea
uric acid
creatinine
ammonia
bilirubin
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9
Q

fed state

A

amino acids brought in by digestion

  • go to liver
  • carbon to glucose of TAGs

to liver - hepatic portal - as single AAs in blood stream

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10
Q

fasting state

A

amino acids released from protein breakdown

release single AAs from proteins in body - major source muscle

shuttles in blood - carrier AAs - glutamine and alanine**

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11
Q

albumin

A

created by liver

-one of main uses of amino acid nitrogen in the liver

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12
Q

glutamine

A

transport of nitrogen to kidney

ammonia

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13
Q

alanine

A

transport of AAs to liver

for urea

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14
Q

case - 21yo M, loss of appetitive, N/V, joint pain, abdomen pain, ice tea colored urine, clay colored stool, caribbean travel recent, jaundice, enlarged and tender liver

ALT and AST very high
alk phos high
bilirubin high
positive IgM anti-HAV

sent home

6 weeks later, vomiting, jerking, grimacing, altered LOC, ALT, AST, alk phos, bilirubin increased - admitted to hosp

A

travel - hepatitis A - from food

sent home - no real tx for Hep A

avoid tylenol - acetaminophen hepatotoxic

at 6 weeks - see necrosis with acetaminophen and the hepatitis
-hyperammonemia

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15
Q

hyperammonemia

A

caused by liver failure - or hepatotoxicity due to inflammation

sx - brain swelling - osmotic imbalance

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16
Q

high ammonia in brain

A

alters osmotic balance - causes brain swelling

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17
Q

high ammonia and glutamate in astrocytes

A

initiates glutamine synthetase and inhibits glutaminase

astrocytes produce glutamine

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18
Q

glutamate

A

central to urea production
-provides nitrogens for urea cycle

one from ammonium ion

one from aspartate

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19
Q

transamination rxn

A

transfer of nitrogen in form

convert amino acid to its alpha-keto acid

is reversible

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20
Q

glutamate

A

produced from alpha-ketoglutarate + any other AA

steal N from AA

glutamate transfers N to other molecule via second transamination
-if to oxaloacetate - to make aspartate

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21
Q

alpha-keto acid of aspartate

A

oxaoacetate

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22
Q

glutamate

A

for transamination rxn

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23
Q

nitrogen carriers

A

alanine

glutamine

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24
Q

alanine

A

specific to muscle
-pyruvate** transaminated to alanine

alanine then to liver

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25
Q

glutamine

A

in liver, muscle, somatic cells

-from glutamate

26
Q

glutamine

A

is one more nitrogen to glutamate

alpha-KG - 0 N
glutamate - 1 N
gultamine - 2 Ns

27
Q

urea cycle

A

in liver
-nitrogen source - ammonium or aspartate

in mito - carbmoyl phosphate from free ammonium ion - react with ornithine
-produce cirtuline - crosses mito membrane to cytosol

in cytosol - aspartate plus citrulline to arginossuccinate - produce agrinine - release urea and regenerate ornithine

28
Q

low blood cirtulline

A

defect in carbamoyl phosphate synthetase and ornithine transcarbamoylase

29
Q

low blood arginine and high cirtulline

A

defect in arginosuccinate synthetase or arginosuccinate lyase

30
Q

high blood arginine and high cirtulline

A

arginase defect

31
Q

orotate

A

produced from excess carbamoyl phosphate

-with ornithine transcarbamoyl phosphate accumulation

32
Q

carbamoyl phosphate

A

created in mito to allow ammonia to enter urea cycle

will build up - with ornithine transcarbamoyl deficiency

results in orotate increase**

33
Q

orotate

A

defect in ornithine transcarbamoylase

34
Q

Case - 12yo male sudden seizure, left side weakness, PMH special eduation group, surgery for downward lens dislocation of eyes

CAT scan - small infarction - right cerebral hemisphere

3 days - left sided weakness cleared

osteopenia, waddling gait, increased length of long bones and scoliosis

high methionine
no cystine
elevated homocystine and homocysteine
normal B12 and folate

24 hour urine homocystine elevated

A

probably congenital

defect in pathway to form cystine

homocystinuruia

35
Q

homocystinuria

A

auto recessive

deficient in cystathione synthase

CV disease and developmental anomalies, mental retardation

marfanoid habitus - says not vit deficienct - probably not that chronic

36
Q

no cystine, elevated methioneine, elevated homocysteine

A

homocystinuria

defect in cystathione synthase

37
Q

methionine and cystine

A

has sulfur

methionine - essential AA

38
Q

B12 and folate

A

for homocysteine methyltransferase - homocysteine** to methionine

defect - see low methionine and high homocysteine

39
Q

PLP

A

pyrodoxal phosphate

-activated vit B6

40
Q

cystathione beta-synthetase

A

requires PLP - vit B6

homocysteine** to cystathione

41
Q

degradation of AAs

A

glucogenic - to glucose

  • intermediates of TCA cycle
  • all the non-essential AAs

ketogenic - to ketone bodies
-acetyl-CoA and acetoacetate

42
Q

lysine and leucine

A

strictly ketogenic**

43
Q

positive nitrogen balance

A

growth

incorporated exceeds excreted

44
Q

negative nitrogen balance

A

malnutrition

excreted exceeds incorporated

45
Q

Case 24 month old to clinic, Uganda, edema, distended abdomen, hypopigmented hair, dry skin

given oral rehydration for 12 hours

given infant formula and MTVs

A

malnutrition

kwashiorkor

46
Q

marasmus

A

total calorie reduction

low weight, loss of body fat and muscle

47
Q

kwashiorkor

A

protein malnutrition

adequate calorie - but protein deprivation

normal body weight

child has edema

48
Q

arginine

A

only essential AA during period of growth

not in adults

49
Q

non-essential AAs

A

from glucose

tyrosine from phenylalanine

50
Q

tx of homocystinuria

A

PLP - vit B6

required for transamination rxns

51
Q

methionine synthesis

A

vit B12 and folate

52
Q

Case 47yo M to ED, alcoholic, binging without eating, slurred speech, sweating, HR 110, grand mal seizure

blood glucose - low
blood ethanol - elevated

A

alcoholic hypoglycemia

metabolism of alcohol - rapid to acetaldehyde - to acetate
-requires NAD+

NAD + is also required for gluconeogenesis - so this cannot occur with lots of ethanol

53
Q

alcoholic hypoglycemia

A

metabolism of alcohol utilizes NAD+

no gluconeogenesis can occur - bc also requires NAD+

occurs with increased NADH/NAD+ ratio

54
Q

maintenance of blood glucose levels

A

by liver
-glycogenolysis - fasting - 12 hours

-gluconeogenesis - starvation - only source after 24 hours of fasting

55
Q

gluconeogenesis and glycolysis

A

most steps are reverse of one another

precursors lactate, alanine, glycerol 3 P

56
Q

lactate

A

oxidized to pyruvate

from anaerobic glycolysis

57
Q

alanine

A

converted to pyruvate

alanine aminotransferase

from breakdown of proteins

58
Q

glycerol 3 P

A

oxidized to DHAP by glycerol 3 P DH

from FAs - adipose tissue

59
Q

irreversible steps in glycolysis

A

4 rxns

PEP to pyruvate

  • OAA reduced to malate
  • requires NAD+

one more?

fructose 1,6 hisphosphatase

glucose 6 phosphatase

60
Q

glucose 6 phosphatase

A

only in liver - so only place for gluconeogenesis

converts glucose to enter bloodstream

61
Q

alpha 1, 6 bonds

A

branching of glycogen

GI II Exam 1 (29 decks)

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