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Metabolic biochem Flashcards

1
Q

phosphorylase

A

adds inorganic phosphate w/out using ATP

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2
Q

mutase

A

relocates functional group within a molecule

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3
Q

rate determining step of glycolysis

+ and - regulators

A

phosphofructokinase-1
PFK-1

+: AMP, fructose-2,6-bisphosphate
-: ATP, citrate

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4
Q

rate determining step of gluconeogenesis

+ and - regualtors

A

Fructose-1,6-bisphosphatase

+: ATP, acetyl-CoA
-: AMP, fructose-2,6-bisphosphate

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5
Q

rate determining step of TCA cycle

+ and - regulators

A

Isocitrate dehydrogenase

+: ADP
-: ATP, NADH

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6
Q

rate determining step of glycogenesis

+ and - regulators

A

Glycogen synthase

+: G6P, insulin, cortisol
-: epi, glucagon

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7
Q

rate determining step of glycogenolysis

+ and - regulators

A

Glycogen phosphorylase

+: epi, glucagon, AMP
-: G6P, insulin, ATP

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8
Q

rate determining step of HMP shunt

+ and - regulators

A

G6PD

+: NADP+
-: NADPH

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9
Q

rate determining step of de novo pyrimidine synthesis

A

Carbamoyl phosphate synthetase II

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10
Q

rate determining step of de novo purine synthesis

+ and - regulators

A

glutamine-phosphoribosylpyrophosphate (PRPP) synthetase

-: AMP, IMP,. GMP

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11
Q

rate determining step of urea cycle

+ and - regulators

A

Carbamoyl phosphate synthetase I

+: N-acetylglutamate

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12
Q

rate determining step of FA synthesis

+ and - regulators

A

Acetyl-CoA Carboxylase (ACC)

+: insulin, citrate
-: glucagon, palmiotoyl-CoA

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13
Q

rate determining step of FA oxidation

+ and - regulators

A

Carnitine acyltransferase I

-: malonyl-CoA

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14
Q

rate determining step of ketogenesis

A

HMA-Coa synthase

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15
Q

rate determining step of cholesterol synthesis

+ and - regulators

A

HMA-CoA reductase

+: insulin, thyroxine
-: glucagon, cholesterol

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16
Q

connection between urea cycle and TCA cycle

A

fumarate, a byproduct in the urea cycle can enter TCA to become malate before OAA

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17
Q

connection between glycolysis, TCA, and Fa synthesis

A

acetyl-CoA

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18
Q

NADPH

  • product of what pathway
  • used for what?
  • ROS?
A
  • HMP shunt
  • used in anabolic processes, respiratory burst, cyt p450 system, glutathione reductase
  • creation and neutralization of ROS
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19
Q

Glucokinase

  • where is it found?
  • insulin effect
  • G6P effect
A
  • liver and beta cells of pancreas
  • insulin induces it
  • no feedback inhibition from G6P
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20
Q

Hexokinase

  • where is it found?
  • insulin effect
  • G6P effect
A
  • most tissues, but not liver or beta cells of pancreas
  • insulin doesn’t affect it
  • negative inhibition from G6P
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21
Q

gene mutation a/w maturity onset diabetes of the young (MODY)

A

Glucokinase

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22
Q 
glycolysis yields 
#ATP 
# NADH
A

2 ATP

2 NADH

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23
Q

what step in glycolysis gives NADH

A

G3P or DAG –> 1,3-BPG

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24
Q

pyruvate dehydrogenase reaction

A

pyruvate + NAD + CoA –> acetyl-CoA + CO2 + NADH

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25
Q

what enzymes does the pyruvate dehydrogenase complex contain (3) and what cofactors do they need

what is it activated by

A
  1. pyruvate dehydrogenase (thiamine pyrophosphate (TPP)
  2. dihydrolipoyl transacetylase (lipoate and CoA)
  3. dihydrolipoyl dehydrogenase (FAD and NAD)

increased NAD/NADH; ADP; and Ca

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26
Q

what does FAD need?

A

B2

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27
Q

What does NAD need?

A

B3

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28
Q

what does CoA need

A

B5

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29
Q

pyruvate dehydrogenase complex deficiency

  • leads to?
  • findings?
  • tx?
A
  • buildup of pyruvate that is shunted to lactate and alanine (LDH and ALT)
  • neuro defects, lactic acidosis, increased serum alanine in infancy
  • increase intake of ketogenic nutrients (high fat content or high lysine and leucine content)
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30
Q

what are the only purely ketogenic aa’s?

A

lysine and leucine

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31
Q

Alanine aminotransferase (ALT)

  • needs what?
  • what does it do
A
  • b6 (pyridoxine)

- pyruvate to Alanine carries amino groups to liver from muscle

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32
Q

pyruvate carboxylase

  • needs what
  • what does it do
A
  • b7 (biotin)

- pyruvate to OAA that can replenish TCA or be used in gluconeogenesis

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33
Q

pyruvate dehydrogenase

  • needs what
  • what does it do
A
  • b1, 2, 3, 5, lipoic acid

- transition from glycolysis to TCA

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34
Q

LDH

  • needs what
  • what does it do
A
  • b3 (niacin)

- end of anaerobic glycolysis (used in RBCs, leukocytes, renal medulla, lens, testes, cornea)

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35
Q

NADH makes how many ATP in ETC

what ETC structure?

A

2.5

complex I

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36
Q

FADH2 makes how many ATP in ETC

what ETC structure?

A

1.5

complex II (succinate dehydrogenase)

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37
Q

direct ETC inhibitors

-mechanism

A

rotenon (complex I)
cyanide (complex IV)
antimycin A (complex III)
CO (complex IV)

blocks complexes and prevents production of proton gradient

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38
Q

ATP synthase inhibitors

A

oligomycin

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39
Q

Uncoupling agents

  • what does that mean
  • ex
A
  • lets H leak across inner mito MB, so weaker proton gradient … produces heat
  • 2,4-dinitrophenol, aspirin overdose –> causes fever
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40
Q

irreversible enzymes of gluconeogenesis (4)

  • whats the rxn
  • what do they need
A
  1. pyruvate carboxylase: pyr to OAA (bitoin, ATP, acetyl-CoA)
  2. PEP caryboxykinase: OAA to PEP (GTP)
  3. F1,6BPase: F1,6BP to F6P (citrate)
  4. G6Pase (in the ER): G6P to glucose
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41
Q

HMP shunt

  • provides what? (2)
  • ATP?
A
  1. NADPH for redox rxns
  2. ribose for nucleotide synthesis
  • ATP neither used nor produced
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42
Q

Two phases of HMP shunt

A

oxidative: irreversible; rate-limiting step w/G6P dehydrogenase

non oxidative: reversible, w/pPEP isomerase and transketolases to make Ribulose 5-P from Ribose 5P

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43
Q

respiratory burst

  • what does it involve?
  • what cells?
  • substrate?
A
  • immune response rapid release of ROS
  • NADH oxidase complexes in neutrophils and monocytes
  • O2
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44
Q

myeloperoxidase

  • what color?
  • what is it
A

blue-green heme-containing pigment

gives sputum its color

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45
Q

enzymes of respiratory burst

A
  1. NADPH oxidase (O2 to superoxide)
  2. Superoxide dismutase (superoxide to peroxide)
  3. myeloperoxidase or catalase or diffusion
  4. Glutathione Peroxidase (uses glutathione to cut peroxide)
  5. Glutathione reductase (reduces glutathione using NADPH)
  6. G6PD (reduces NADP+ using G6P)
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46
Q

chronic granulomatous disease

A

pts with the condition cannot generate ROS, so at greater risk of chronic infections by catalse + organisms that can neutralize ROS

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47
Q

G6PD def and ROS

A

it’s the end point of ROS, so without it, cannot properly protect from oxidative damage

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48
Q

oxidizing agents that can damage RBCs in G6PD def pts (4)

A
  1. fava beans
  2. sulfonamides
  3. chemo drugs
  4. primaquine
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49
Q

heinz bodies

  • what are they?
  • where are they seen?
A
  • precipitated oxidized Hb

- G6PD def

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50
Q

Bite cells

- what happened?

A

they’re RBCs that have had chunks taken out in attempt to remove Heinz bodies

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51
Q

Enzymes of fructose metabolism (3)

  • where does it occur
A
  1. fructokinase: fructose to F-1P
  2. Aldolase B: F-1P to DHAP or Glyceraldehyde
  3. Triose kinase: Glyceraldehyde to G-3P
  • liver
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52
Q

Essential fructosuria

  • inheritance
  • what is it
  • sxs
A
  • AR
  • defect in fructokinase
  • basically asymptomatic
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53
Q

Fructose intolerance

  • inheritance
  • what is it
  • sxs
  • why?
A
  • AR
  • def in aldolase B
  • hypoGly, jaundice, cirrhosis, vomiting
  • accumulation of F-1P in liver
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54
Q

Enzymes of galactose metabolism (3-4)

A
  1. Galactokinase: galactose to Gal-1P
  2. Uridyltransferase: Gal-1P to Glu-1P
  3. Aldose reductase: galactose to galactitol (the alcohol counterpart)
  4. 4-Epimerase: involved in the switching of UDP-Gal and UDP-Glu
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55
Q

Galactokinase deficiency

  • inheritance
  • what enzyme involved
  • what happens
A
  • AR
  • hereditary def of galactokinase
  • accumulation of galactitol, which acts as an osmotic agent so can get inftaile cataracts
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56
Q

Classic galactosemia

  • inheritance
  • what is what enzyme involved
  • what happens
  • what can it lead to
A
  • AR
  • absence of Gal-1P uridyltransferase
  • accumulation of Gal-1P and galactitol in lens and liver
    jauntice, MR, cataracts, FTT
  • can lead to E. Coli sepsis in neonates
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57
Q

Sorbitol

  • what is it
  • purpose?
  • enzymes involved in its metabolism (2)
A
  • glucose’s alcohol counterpart
  • traps glucose in cells
  • Aldose reductase (glucose to sorbitol using NADPH) + Sorbitol dehydrogenase (sorbitol to fructose using NADP+)
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58
Q

What cells have both enzymes of sorbitol metabolism (3)

A
  1. liver
  2. ovaries
  3. seminal vesicles
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59
Q

what cells have only the first enzyme of sorbitol metabolism (3)

A
  1. schwann cells (so can get peripheral neuropathy)
  2. Retina (so you can get retinopathies)
  3. renal cells
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60
Q

types of lactase deficiency (3)

A
  1. primary
  2. secondary
  3. congenital lactase deficiency
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61
Q

Primary lactase deficiency

A

age-dependent decline after childhood (absence of lactase-persistent allele) common in Asians, AfAms, and NatAms

62
Q

Secondary lactase deficiency

A

loss of brush border 2/2 gastroenteritis (rotavirus), autoimmune disease etc

63
Q

Congenital lactase deficiency

A

rare… 2/2 defective gene

64
Q

stool of lactase def pts

65
Q

Types of esssential AA’s (3)

A
  1. glucogenic
  2. glucogenic/ketogenic
  3. ketogenic
66
Q

glucogenic AA’s (3)

A

Met, Val, His

67
Q

ketogenic AA’s (2)

68
Q

keto/glucogenic AA’s (4)

A

Ile, Phe, Thr, Trp

69
Q

Acidic AA’s (2)

- what’s their charge?

A

Asp and Glu

- negatively charged at body pH

70
Q

Basic AA’s (2)

  • what’s most basic
  • what’s their charge
A

Arg, Lys, His
Arg most basic
no charge at body pH

71
Q

Carbamoyl phosphate synthetase I

  • what cycle is it a part of
  • what reaction
  • cofactor
A
  • urea cylce
  • CO2 and NH3 to Carbamoyl phosphate
  • N-acetylglutamate
72
Q

where is excess nitrogen converted to urea

where is it excreted

A

liver

kidney

73
Q

Order of urea cycle

A 
1. Co2+NH3
add N-acetylglutamate
2. carbamoyl phosphate 
add ornithine
3. citrulline
add Aspartate and ATP
4. Argininosuccinate
deposit fumarate
5. Arginine
deposit urea
6. ornithine 
back to mitochondria
74
Q

what amino acids required for periods of growth? (2)

A

Arg and His

75
Q

Ammonia shuttling

  • what aa’s important
  • from where to where
  • 2 cycles
A
  • glutamate and alanine
  • NH3 from aa’s to urea for excretion
  • muscle to liver
  • alanine and cori cycle
76
Q

alanine cycle of ammonia shuttle

A
  1. pyruvate to Ala by acquiring NH3 from glutamate as it becomes a-KG
  2. alanine leaves muscle and goes to liver
  3. in liver: Ala to pyruvate by giving a-KG NH3 to become glutamate
  4. pyruvate becomes glucose
  5. glucose sent to muscles
  6. glucose becomes pyruvate
    REPEAT
77
Q

Cori cycle

A

muscle: glucose –> pyruvate –> Lactate
lactate travels to liver
liver: Lactate –> pyruvate –> glucose
glucose goes to muscle

REPEAT

78
Q

hyperammonemia

  • depletes that?
  • therefore that is inhibited?
A
  • alpha-Ketoglutarate

- TCA cycle inhibited

79
Q

what treats hyperammonemia by binding and excreting aa’s

A

benzoate or phenylbutyrate

80
Q

mechanism of lactulose

A

acidifies GI tract to trap NH4+ for excretion

81
Q

Ammonia intoxication s/s’s

A

asterixis, slurring, somnolence, vomiting, cerebral edema, blurry vision

82
Q

N-acetylglutamate

  • required for what enzyme
  • what cycle
  • what happens if there’s def?
A
  • carbamoyl phosphate synthetase I
  • urea cycle
  • hyperammonemia
83
Q

How to differentiate b/w N-acetylglutamate def and carbamoyl phosphate synthetase I def?

A

normal urea cycle enzymes, but elevated ornithine levels

84
Q

Ornithine transcarbamylase

- what does it do

A

combines ornithine and carbamoyl phosphate into citrulline in the urea cycle

85
Q

most common urea cycle d/o?

A

ornithine transcarbamylase def

86
Q

Ornithine transcarbamylase def

  • inheritance
  • what accumulates
  • what is it converted to, in what pathway
  • findings?
A
  • XRecessive
  • excess carbamoyl phosphate
  • converted to orotic acid in pyrimidine synthesis pathway
  • elevated orotic acid in blood and urine; sxs of hyper-ammonemia; decreased BUN (b/c can’t get to urea)
87
Q

connection b/w urea cycle and pyrmidine synthesis pathway

A

carbamoyl phosphate

88
Q

difference in findings b/w ornithine transcarbamylase def and orotic aciduria

A

orotic aciduria has megaloblastic anemia b/c it’s a defect in the nucleic acid synthesis pathway

89
Q

difference b/w orotic aciduria and b12 deficiency

A

both have megaloblastic anemia 2/2 NT synthesis def, but orotic aciduria will be unresponsive to B12 therapy

90
Q

essential amino acid derivative of catecholamines

- what is it turned into in the body to serve as the starting aa for catecholamines

A

phenylalanine

tyrosine

91
Q

essential amino acid derivative of NAD/NADP

A

tryptophan

92
Q

essential amino acid derivative of melatonin

  • what makes melatonin
A

tryptophan

  • tryptophan –> 5-HT –> melatonin
93
Q

essential amino acid derivative of heme

  • what’s in b/w that and heme
A

glycine

porphyrin

94
Q

essential amino acid derivative of GABA and glutathione

95
Q

essential amino acid derivative of creatine

96
Q

essential amino acid derivative of urea

97
Q

essential amino acid derivative of nitric oxide

98
Q

what co-factor most used while taking amino acid derivates to their biological workers

A

vitamin b6 (pyridoxine)

99
Q

phenylalanine hydroxylase

  • what reaction
  • a/w what condition
  • how to treat that condition
A
  • phenylalanine to tyrosine (catecholamine synthesis)
  • PKU (phenylketonuria) b/c excess phenylalanine
  • need exogenous Tyrosine and decrease phenylalanine
100
Q

why musty odor in PKU?

A

phenylalanine is an aromatic amino acid that accumulates –> leads to odor

101
Q

what must pts with PKU also avoid?

- what dietary thing has phenylalanine?

A

artificial sweeteners

102
Q

how does phenylalanine get to TCA cycle?

A

Phe –> Tyr –> homogentisic acid –> methylacetoacetic acid –> TCA

103
Q

how is albinism a/w catecholamine synthesis?

  • what enzyme
A

Melanin comes from this cycle (from DOPA; from Tyrosine; from Phe) via Tyrosinase

104
Q

enzymes of catecholamine synthesis

A

phenylalanine hydroxylase, tyrosine hydroxylase, tyrosinase, DOPA decarboxylase

105
Q

carbidopa blocks what

  • what disease used for
  • why does it work for that dz
A
  • blocks DOPA decarboxylase
  • used in Parkinson’s
  • blocks peripheral conversion of levodopa to dopamine so that there’s max delivery of levodopa to CNS
106
Q

findings of PKU

A
  • Mr, growth ret, sz, fair skin, eczema, musty odor
107
Q

3 of the phenylketones

A
  1. phenyl - acetate
  2. phenyl - lactate
  3. phenyl - pyruvate
108
Q

Alkaptonuria

  • what is it
  • findings
  • d/o of metabolism of what
A
  • congenital def in homogentisate oxidase
  • dark connective tissue, brown sclera, urine black on air exposure
  • maybe joint issues b/c homogentisic acid toxic to cartilage
  • tyrosine to fumarate into TCA
109
Q

Homocystinuria vs. Cystinuria

A
  • cystinuria is just renal issues so you get crystals

- homocystinuria is metabolic issue of homocysteine metabolism, so more disease

110
Q

Homocystinuria

  • def enzymes
  • s/s’s
A
  • cystathione synthase
    OR
    homocysteine methyltrasnferase def
  • homocystinuria, MR, osteoporosis, kyphosis, thrombosis, atherosclerosis 2/2 endothelial injury
111
Q

Treating cystinuria

A
  • urinary alkylinzation (w/K-citrate or acetazolamide)
  • chelating agents
  • good hydration
112
Q

Maple syrup urine disease

  • inheritance
  • what is blocked
  • what enzyme affected
  • presentation
  • tx
A
  • AR
  • degradation of branched AAs is blocked
  • alpha-ketoacid dehydrogenase (B1)
  • elevated ketoacids in blood; MR, death, CNS defects
  • dietary restriction and thiamine supplementation
113
Q

Cystathionine synthase

  • what reaction
  • what does it need
A
  • homocysteine to cystathionine

- Serine and Vit B6

114
Q

homocysteine methyltransferase

  • what reaction
  • what does it need
A
  • homocysteine to methionine

- Vit B12

115
Q

what are the branched AA’s

A

Isoleucine
Leucine
Valine

“I Love Vermont Maple tree branches”

116
Q

glycogen metabolism

- what enzymes what do they do

A
  • PKA: activates glycogen phosphorylase kinase
  • glycogen phosphorylase kinase: activates glycogen phosphorylase
  • glycogen phosphorylase: glycogen to glucose
  • glycogen synthase: glucose to glycogen
117
Q

what bonds do glycogen branches have

A

alpha (1,6)

118
Q

what bonds to glycogen linkages have

A

alpha (1,4)

119
Q

glycogenolysis

  • what cells have it
  • what’s the reaction
A

glycogen to glu-1P

muscles and liver

120
Q

debranching of glycogen

A
  1. phosphorylase takes off G-1Ps from branches until 4 left
  2. Debranching enzyme (4-alpha-glucanotransferase) takes 3 off and adds it to linkage
  3. Debranching enzyme (alpha-1,6-glucosidase) takes off the last one
121
Q

Fatty acid synthesis: what shuttle

- what enzymes

A

Citrate shuttle
“SYtrate” = “SYNthesis”

  • ATP citrate lyase
122
Q

Fatty acid degradation: what shuttle

what enzymes

A

Carnitine
“CARNitine = CARNage”

  • FA CoA synthetase
  • beta ox enzymes (acyl-CoA dehydro, etc, thiolase)
123
Q

Carnitine def

  • inability to?
  • presents with?
A
  • inability to break down long FA’s … so toxic accumulation
  • weakness, hypotonia, hypoketotic hypoglycemia
124
Q

Acyl-CoA dehydrogenase def

  • inability to?
  • presents with?
A
  • inability to start beta-oxidation in the mitochondria

- low acetyl-CoA, therefore low fasting glucose, low TCA and low ketones

125
Q

Malonyl-coa in synthesis and degradation of FA

A

synthesis: acetyl-coa into malonyl-coa before formation of FA’s
degradation: malonyl-coa negatively inhibits carnitine shuttle

126
Q

Ketone bodies

  • examples (3)
  • made in? from?
  • used for?
A
  • acetoacetic acid
  • beta-hydroxybutyric acid
  • acetone
  • made in liver from FA degradation and AA’s metabolism
  • acetoacetic acid and beta-hydroxybutyric acid used as energy for brain, heart, muscle in low glucose states
127
Q

What is depleted during starvation and DKA states to undergo gluconeogenesis

  • what is built up
A

OAA

  • acetyl-coa –> ketone bodies
128
Q

how does alcoholism lead to ketonosis

A

excess NADH from lactate dehydrogenase –> shunts OAA to malate

buildup of acetly-coa –> ketone bodies

129
Q

beta oxidation

- acetyl-coa products go where?

A

Ketone bodies

or

TCA

130
Q

urine test for ketones tests for which one

A

acetone and acetoacetic acid

131
Q

how long can glycogen reserves last?

132
Q

how many days starvation before degrading vital proteins?

133
Q

HMG-CoA reductase

  • reaction
  • insulin effect
A
  • HMG-CoA to mevalonate

- insulin induces it

134
Q

LCAT?

A

lectithin-cholesterol acyltransferase

2/3 of plasma cholesterol is esterified by this

135
Q

which lipoproteins carry most choletserol (2)

A

LDL and HDL

136
Q

lipoproteins made of what?

A

cholesterol
TGs
phospholipids

137
Q

chylomicron

  • delivers what
  • where to where
  • how does it get to liver
  • excreted how
A
  • dietary TGs
  • GI to peripheral tissue
  • chylomicron remnants
  • intestinal epithelia
138
Q

VLDL

  • delivers what
  • where to where
  • excreted how
A
  • hepatic TGs
  • liver to peripheral tissue
  • liver
139
Q

IDL

  • how formed
  • delivers what where to where
A
  • formed in degradation of LDL

- delivers TG and cholesterol to liver

140
Q

LDL

  • delivers what
  • where to where
  • formed by?
A
  • hepatic cholesterol
  • liver to peripheral tissue
  • hepatic lipase mod’s IDL in peripheral tissue

LDL-Rec endocytosis

141
Q

HDL

  • delivers what
  • where to where
  • secrete where?
  • alcohol effect
A
  • cholesterol
  • peripheral tissue to liver
  • secreted from liver and intestine
  • increases HDL synthesis
142
Q

Apolipoproteins (5)

A
  1. E
  2. A-I
  3. C-II
  4. B-48
  5. B-100
143
Q

ApoE

  • function
  • which lipoproteins?
A
  • mediates remnant uptake

- chylo, chylo remnant, VLDL, IDL, HDL

144
Q

ApoA-I

  • function
  • which lipoproteins
A
  • activates LCAT

- chylo, HDL

145
Q

ApoC-II

  • function
  • which lipoproteins
A
  • LPL (lipoprotein lipase) cofactor

- chylo, VLDL, HDL

146
Q

ApoB-48

  • function
  • which lipoproteins
A
  • mediates chylomicron secretion

- chylo, chlyo remnant

147
Q

ApoB-100

  • function
  • which lipoproteins
A
  • binds LDL rec

- VLDL, IDL, LDL

148
Q

Familial dyslipidemias in First AID (3)

A
  1. I-hyperchylomicronemia
  2. IIa-familial hypercholesterolemia
  3. IV-hypertriglyceridemia
149
Q

I-hyperchylomicronemia

  • inheritance
  • high levels of what in blood
  • 2/2?
  • presentation
A
  • AR
  • chylomicron, TG, cholesterol
  • LPL or ApoC-II def
  • HSM, pancreatitis, pruritic xanthomas, no atherosclerosis
150
Q

IIa-familial hypercholesterolemia

  • inheritance
  • high levels of what in blood
  • 2/2?
  • presentation
A
  • AD
  • Chol, LDL
  • absent or mutated LDL receptor
  • atherosclerotic dz, tendon xanthomas, corneal arcus
151
Q

IV-hypertriglyceridemia

  • inheritance
  • high levels of what in blood
  • 2/2?
  • presentation
A
  • AD
  • TG, VLDL
  • hepatic overproduction of VLDL
  • pancreatitis
152
Q

Glucagonoma

  • what cells does it arise from
  • presentation (3)
  • dx
A

-alpha cells pancreas

    1. necrolytic migratory erythema
      1. DM
      2. GI sxs (diarrhea, anorexia, abd pain
  • elevated glucagon

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