Biochem Review Flashcards

1
Q

What is the rate-limiting enzyme in purine synthesis? Pyrimidine synthesis?

A

purine - glutamine PRPP amidotransferase

pyrimidine - CPS-2

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2
Q

What are the sources of carbon in the synthesis of purines? In pyrimidine synthesis?

A

purines - CO2, glycine, THF (nitrogen source = aspartate and glutamine)
pyrimidines - aspartate and CO2 (nitrogens = glutamine)

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3
Q

Which medication inhibits ribonucleotide reductase?

A

hydroxyurea

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4
Q

Which medication inhibits dihydrofolate reductase?

A

methotrexate, trimethoprim

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5
Q

Which medication inhibits thymidylate synthase?

A

5-FU

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6
Q

Which medication inhibits inosine monophosphate dehydrogenase?

A

mycophenolate

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7
Q

Which medication inhibits PRPP amidotransferase?

A

6-MP

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8
Q

What accounts for the positive charge of histones? What accounts for the negative charge of DNA?

A

Lysine and arginine on histones

phosphate groups on DNA

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9
Q

How many adenosine residues are found in a molecule of DNA if one strand contains A=2000, G=500, C=1500, T=1000?

A

3000 - 2000 A plus the 1000 from the other strand

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10
Q

A boy with self-mutilating behavior, intellectual disability, and gout

A

Lesch-Nyhan

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11
Q

Orotic acid in the urine elevated serum ammonia

A

ornithine-transcarbamoylase deficiency

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12
Q

Orotic acid in the urine + normal serum ammonia

A

oratic aciduria

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13
Q

Megaloblastic anemia that does not improve with folate and B12

A

oratic aciduria

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14
Q

Lesch Nyhan syndrome

A

defective purine savage due to absent HGPRT (which converts hypoxanthine to IMP and guanine to GMP)
X-linked recessive
Sx = intellectual disability, self-mutilation, aggression, hyperuricemia (orange sand crystals in diaper), gout, dystonia
Tx = allopurinol, febuxostat

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15
Q

oratic aciduria

A

inability to convert orotic acid to UMP because of defect in UMP synthase
Autosomal recessive
megaloblastic anemia refractory to folate and B12; no hyperammonemia (vs ornithine transcarbamylase deficiency)
Tx = uridine monophosphate to bypass mutated enzyme

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16
Q

What strand of DNA nucleotides opposes this DNA strand: 5’-ATTGCGTA-3’?

A

5’-TACGCAAT-3’ (DNA is always written 5’->3’

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17
Q

How does UV radiation damage DNA?

A

pyrimidine dimers on same strand of DNA (usually thymine-thymine, but can be cytosine-cytosine also)

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18
Q

Which eukaryotic DNA polymerase replicates the lagging strand?

A

DNA polymerase alpha for the first 20 bases then DNA polymerase delta

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19
Q

Which eukaryotic DNA polymerase synthesizes RNA primer?

A

DNA polymerase alpha

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20
Q

Which eukaryotic DNA polymerase repairs DNA?

A

DNA polymerase beta

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21
Q

Which eukaryotic DNA polymerase replicates mitochondrial DNA?

A

DNA polymerase gamma

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22
Q

Which eukaryotic DNA polymerase replicates the leading strand of DNA?

A

DNA polymerase alpha for the first 20 bases, then DNA polymerase epsilon

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23
Q

Nucleotide excision repair

A

DNA polymerase and ligase fill and reseal the gap, respectively; repairs bulky helix distorting lesions

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24
Q

What disorder results from a problem in nucleotide excision repair?

A

xeroderma pigmentosum (very susceptible to damage from the sun)

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25
Q

Base excision repair

A

base-specific glycosylase removes altered base and creates AP site; AP endonuclease cleaves 5’ end; lyase cleaves the 3’ end; DNA polymerase beta fills the gap and DNA ligase seals it

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26
Q

Mismatch repair

A

mismatched nucleotides are removed, and the gap is filled and resealed

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27
Q

What disorder results from a defect in mismatch repair processes?

A

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

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28
Q

Nonhomologous end joining

A

brings together two ends of DNA fragments to repair double-stranded breaks

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29
Q

What disorders result from defects in nonhomologous end joining?

A

ataxia telangiectasia
breast/ovarian cancers with BRCA1 mutation
Fanconi anemia

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30
Q

What is Bloom syndrome?

A

mutation of helices; affects both DNA replication and repair
Patients are hypersensitive to sunlight, have increased susceptibility to leukemias and lymphomas, immunodeficiency, infertility, and facial anomalies

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31
Q

What is a silent mutation?

A

nucleotide substation but codes for the same amino acid

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32
Q

What is a missense mutation? What is an example of this?

A

nucleotide substitution resulting in changed amino acid

Ex = sickle cell disease (substation of glutamic acid with valine)

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33
Q

What is a nonsense mutation?

A

nucleotide substation resulting in early stop codon (UAG, UAA, UGA); usually results in a nonfunctional protein

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34
Q

What is a frameshift mutation? What is an example of this?

A

deletion or insertion of a number of nucleotides not divisible by 3, resulting in misreading of all nucleotides downstream
Ex = Duchenne muscular dystrophy, Tay-Sachs disease

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35
Q

What does helicase do?

A

unwinds template DNA at the replication fork

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36
Q

What do single-stranding binding proteins do?

A

prevents strands from reannealing

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37
Q

What does DNA topoisomerase do? What are the auto-Abs to it?

A

removes supercoils

Auto Abs = anti-Scl-70 Abs found in diffuse scleroderma

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38
Q

What are the drugs that inhibit eukaryotic DNA topoisomerase? Prokaryotic?

A

eukaryotic - etoposide/teniposide

prokaryotic - fluoroquinolones (also inhibit topoisomerase IV)

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39
Q

What elongates the lagging strand in prokaryotes?

A

DNA polymerase III

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40
Q

What elongates the leading strand in prokaryotes?

A

DNA polymerase III

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41
Q

What does DNA polymerase I do in prokaryotes?

A

degrades RNA primer; replaces it with DNA

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42
Q

What does DNA ligase do?

A

Joins Okazaki fragments

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43
Q

What amino acid is encoded by the most common start codon?

A

methionine

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44
Q

What is the difference between an intron and an extron?

A

introns get spliced out of the mRNA by the spliceosome

externs go into the mature mRNA to be expressed

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45
Q

Production of what enzyme is regulated by the lac operon?

A

beta-galactosidase

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46
Q

What two proteins regulate the lac operon?

A

CAP and lac repressor

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47
Q

What two substrate conditions must be met for the lac genes to be transcribed?

A
  1. presence of lactose in excess (moves repressor)

2. no glucose (CAP presence)

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48
Q

What are the different eukaryotic RNA polymerases?

A

RNA pol I -> rRNA
RNA pol II -> mRNA
RNA pol III -> tRNA

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49
Q

What is the difference between CPS1 and CPS2 enzymes? (location, pathway, nitrogen source)

A

location - CPS1 - mitochondria; CPS2 - cytosol
pathway - CPS1 - urea cycle; CPS2 - pyrimidine synthesis
nitrogen source - CPS1 - ammonia; CPS2 - glutamine

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50
Q

What is the first enzyme in the glycolysis pathway that catalyzes glucose/fructose -> what?

A

hexokinase or glucokinase catalyzes glucose/fructose -> glucose-6-phosphate

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51
Q

What enzyme catalyzes fructose-6-phosphate to fructose-1,6-bisphosphate in glycolysis?

A

phosphofructokinase-1

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52
Q

What stimulates phosphofructose-1?

A

AMP and fructose-2,6-bisphosphate

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53
Q

What inhibits phosphofructose-1?

A

ATP and citrate

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54
Q

What enzyme catalyzes the conversion of phosphoenolpyruvate to pyruvate in glycolysis?

A

pyruvate kinase

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55
Q

What stimulates the enzyme pyruvate kinase?

A

fructose-1,6-bisphosphate

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56
Q

What inhibits the enzyme pyruvate kinase?

A

ATP, alanine

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57
Q

What is the rate-limiting enzyme in glycolysis?

A

phosphofructokinase-1

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58
Q

What is the most commonly deficient enzyme in glycolytic enzyme deficiency? What are the symptoms?

A

most common cause: pyruvate kinase deficiency

presentation: hemolytic anemia because RBC cannot make ATP without glycolysis; glycolysis is their sole source of ATP

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59
Q

A muscle biopsy on a patient of yours reveals elevated glycogen levels, elevated fructose-6-phosphate, and decreased pyruvate. What enzyme deficiency do you suspect most?

A

phosphofructokinase-1

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60
Q

What reaction does PFK-2 catalyze, and when is it active?

A

PFK2 catalyzes fructose-6-phosphate -> fructose-2,6-bisphosphate; active when insulin is present (fed state)

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61
Q

What reaction does FBPase-2 catalyze, and when is it active?

A

FBPase-2 catalyzes fructose-2,6-bisphosphate -> fructose-6-phosphate; active when glucagon in present (fasting) -> when you’re fasting, you don’t want to breakdown glucose; you want ht liver to make glucose, so you go through gluconeogenesis

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62
Q

What are the irreversible enzymes involved in glycolysis?

A
  1. hexokinase/glucokinase
  2. PFK-1
  3. pyruvate kinase
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63
Q

What are the irreversible enzymes involved in gluconeogenesis?

A
  1. pyruvate carboxylase
  2. PEP carboxykinase
  3. fructose-1,6-bisphosphatase
  4. glucose-6-phosphatase
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64
Q

What enzyme catalyzes the rate-limiting step in gluconeogenesis?

A

fructose-1,6-bisphosphatase

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65
Q

Order the following molecules by how much energy they contain that can be made available to fuel endergonic reactions: pyruvate, adenosine monophosphate, glucose, adenosine, adenosine triphosphate

A

glucose, pyruvate, ATP, AMP, adenosine

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66
Q

What can be turned into pyruvate for the process of gluconeogensis?

A
  1. odd chain FAs -> propionyl-CoA
  2. TCA cycle molecules (oxaloacetate)
  3. amino acids
67
Q

What is the formula for Gibbs free energy?

A

delta G = delta H - T*deltaS

68
Q

What is the enzyme that converts pyruvate into oxaloacetate in the first step of gluconeogenesis?

A

pyruvate carboxylase

69
Q

What is required for the enzyme pyruvate carboxylase in gluconeogenesis? What stimulates this enzyme?

A

biotin is required; stimulated by acetyl-CoA

70
Q

What enzyme turns oxaloacetate into PEP in the 2nd step of gluconeogenesis?

A

PEP carboxykinase

71
Q

What enzyme catalyzes fructose-1,6-bisphosphate into fructose-6-phosphate?

A

fructose-1,6-bisphosphatase

72
Q

What enzyme catalyzes glucose-6-phosphate into glucose or fructose in the last step of gluconeogenesis?

A

glucose-6-phosphatase

73
Q

What is glycolysis?

A

glucose -> pyruvate

74
Q

What is gluconeogensis?

A

pyruvate -> glucose

75
Q

What is glycogenesis?

A

glucose -> glycogen

76
Q

What is glycogenolysis?

A

glycogen -> glucose

77
Q

What is the rate-limiting enzyme for glycogen synthesis?

A

glycogen synthase

78
Q

What is the rate-limiting enzyme for glycogenolysis?

A

glycogen phosphorylase

79
Q

Which enzyme converts glucose-6-phosphate to glucose in glycogenolysis?

A

glucose-6-phosphatase

80
Q

Pompe Dz

A

deficiency of alpha-1,4-glucosidase in lysosomes

  • Infantile form: severe muscle weakness, cardiomegaly, HF, die within 1 year
  • Adult -> no cardiac problems, gradual onset of skeletal muscle weakness, diaphragm weakness -> respiratory failure
81
Q

McArdle Dz

A

cannot breakdown glycogen due to glycogen phosphorylase deficiency -> rhabdomyolysis -> renal failure

82
Q

Von Gierke Dz

A

glucose-6-phosphate deficiency (last step of glycogenolysis and gluconeogenesis); hypoglycemia with fasting, glycogen buildup in liver -> hepatomegaly, enlargement of kidneys, increased serum lactate, uric acid, and triglycerides
feed frequently and fed cornstarch at night

83
Q

Cori Dz

A

alpha-1,6-glucosidase (debranching enzyme) deficiency (glycogenolysis); mild hypoglycemia

84
Q

What four things can pyruvate be made into?

A
  1. oxaloacetate
  2. acetyl-coA
  3. lactate (Cori cycle)
  4. alanine
85
Q

Why are alanine and glutamine found in such high concentrations in the blood?

A

they are two major carriers of nitrogen from tissues

86
Q

What enzyme catalyzes transamination reactions?

A

transaminases transfer the amino group from an amino acid to alpha-ketoglutarate to form glutamine

87
Q

What are the two most important transaminases? What do they catalyze?

A
  1. alanine transaminase: catalyzes alanine + alpha-ketoglutarate -> glutamate + pyruvate
  2. aspartate transaminase: catalyzes aspartate + alpha-ketolgutarate -> oxaloacetate + glutamate
88
Q

What cofactor is required by all transaminases?

A

Pyridoxal phosphate (derivative of VitB6)

89
Q

What are the major regulatory enzymes of the citric acid (TCA) cycle?

A
  1. citrate synthase
  2. isocitrate dehydrogenase
  3. alpha-ketoglutarate dehydrogenase
90
Q

What is the rate-limiting enzyme of the TCA cycle?

A

isocitrate dehydrogenase

91
Q

What substances are known to inhibit the complexes of the electron transport chain?

A
  1. complex 1 -> amytal (barbiturate) and rotenone (fish toxin)
  2. complex 2 -> nothing
  3. complex 3 -> antimycin A (fish toxin)
  4. complex 4 -> CN-, CO, H2S, N3-
92
Q

What substances can increase the permeability of the inner mitochondrial membrane, thereby decreasing ATP synthesis but increasing heat generation?

A

aspirin toxicity, 2,4-DNP, and thermogenin

93
Q

In patients with G6PD deficiency, ingestion of what substances can induce oxidative damage to RBCs?

A

“Spleen Purges Nasty Inclusions From Damaged Cells”

  • sulfonamides
  • primaquine (anti-malarial)
  • nitrofurantoin (UTIs)
  • isoniazid (TB)
  • fava beans
  • dapsone (leprosy tx; PCP prophylaxis sometimes)
  • chloroquine (malaria tx)
94
Q

Essential fructosuria

A

deficient in fructokinase; autosomal recessive

buildup of fructose -> spilled in urine (benign)

95
Q

Fructose intolerance

A

deficient in aldolase B; autosomal recessive
increased fructose-1-phosphate
decreased phosphate -> inhibit glycogenolysis and gluconeogenesis
-hypoglycemia and vomiting
-hepatomegaly and jaundice
Tx - decreased intake of fructose and sucrose

96
Q

Galactokinase deficiency

A

deficiency in galactokinase -> increased glactitol

- infantile cataracts

97
Q

Classic galactosemia

A
deficient in gal-1-P uridyltransferase
- worse cataracts than galactokinase def
- hepatomegaly and jaundice
- failure to thrive
- intellectual disability
Tx - lactose and galactose exclusion
98
Q

Which tissues of the body use the pentose phosphate pathway?

A

RBCs, liver, adrenal cortex, mammary glands (during lactation)

99
Q

Explain why a deficiency of the enzyme that is the rate limiter for the HMP shunt can result in hemolytic anemia

A

RBCs need NADPH to keep glutathione reduced to detoxify free radicals; so G6PD deficiency (rate-limiting enzyme) -> hemolytic anemia

100
Q

What fuels are produced and used in the post absorptive period?

A

produced - glucose (from hepatic glycogenolysis and gluconeogenesis) and fatty acids (from adipose tissue)
used - muscles brain, and other tissues use predominantly glucose

101
Q

When does gluconeogenesis begin int he post-absorptive period? When does it become fully active?

A

begins 4-6 hours after the last meal

fully active when glycogen stores are depleted (10-18 hours after last meal)

102
Q

How does the pattern of fuel production and usage change in early starvation (24 hours after the last meal)?

A

produced - glucose (gluconeogenesis) - used up glycogen stores; fatty acid being produced from adipose tissue
used - brain uses predominantly glucose; muscles and other tissues use some glucose but predominantly fatty acids

103
Q

In intermediate starvation (48 hours after the last meal), how does the pattern of fuel production and utilization change?

A

produced - glucose, fatty acids, ketones (from liver)
used - brain uses predominantly glucose but also some ketone bodies; muscle and other tissues use predominantly fatty acids but also some ketone bodies

104
Q

What are the main ketone bodies?

A

acetoacetate and beta-hydroxybutyrate

105
Q

What is the rate-limiting enzyme in the synthesis of ketone bodies?

A

hmg-coA synthase

106
Q

What metabolic scenario favors the synthesis of ketone bodies?

A

when production of acetyl-CoA from beta-oxidation fo fatty acids exceeds the oxidative capacity of the TCA cycle

107
Q

Can ketone bodies be used by all body tissues?

A

No, RBCs can only use glucose

108
Q

What is the pattern of fuel production and utilization in prolonged starvation (5 days after last meal)?

A

produced - glucose, fatty acids, ketone bodies
used - brain uses predominantly ketone bodies; muscles and other tissues use predominantly fatty acids but also some ketone bodies and glucose for RBCs

109
Q

What percentage of energy comes from glucose and ketone bodies during an overnight fast? What about after a 3 day fast?

A

overnight fast - 90% of energy comes from glucose (2/3 from glycogen breakdown, 1/3 from gluconeogensis); 5% comes from ketone bodies
3 day fast - 60% of your energy comes from ketone bodies (1/2 acetoacetate, 1/2 beta-hydroxybutyrate); 40% from glucose (mostly gluconeogenesis)

110
Q

What is the primary energy source in a patient that has not eaten in two days?

A

fatty acids

111
Q

A stressed physician comes home from work, consumes seven or eight shots of tequila in rapid succession before dinner, and becomes hypoglycemia. Why did she become hypoglycemic?

A

liver is breaking down the ethanol, which generates a lot of NADH, which shunts pyruvate to production of lactate and oxaloacetate to production of malate; pyruvate and malate no longer available for gluconeogenesis

112
Q

What are some of the hallmark features of kwashiorkor?

A
MEALS
M - malnourished
E - edema
A - anemia
L - liver (fatty)
S - skin/hair depigmentation
113
Q

What does VLDL do?

A

delivers hepatic TGs to peripheral tissue

114
Q

What do chylomicrons do?

A

deliver dietary TGs to peripheral tissues

115
Q

What does IDL do?

A

formed in the degradation of VLDL; delivers TGs and cholesterol to liver

116
Q

What does LDL do?

A

delivers hepatic cholesterol to peripheral tissues

117
Q

What does HDL do?

A

mediates reverse cholesterol transport from periphery to liver

118
Q

What is abetalipoproteinemia? mutation, deficiency, symptoms, tx?

A

autosomal recessive mutation in MTP gene
chylomicrons, VLDL, LDL absent
deficiency in ApoB48 and ApoB100
Infants present with fat malabsorption, steatorrhea, failure to thrive
Later Sx - retinitis pigments, spinocerebellar degeneration due to VitE def, progressive ataxia, acathocytosis, night blindness
Treatment: large doses of vitE

119
Q

What deficiency causes familial hypercholesterolemia?

A

LDL receptors

120
Q

Which apolipoprotein activates LCAT?

A

ApoA-1

121
Q

Which apolipoprotein mediates chylomicron secretion?

A

ApoB-48

122
Q

Which apoplipoprotein mediates VLDL secretion?

A

ApoB-100

123
Q

Which apolipoprotein is a cofactor for lipoprotein lipase?

A

ApoC-11

124
Q

Which apolipoprotein mediates uptake of remnant particles?

A

ApoE

125
Q

What is the rate-limiting enzyme for fatty acid synthesis?

A

acetyl-CoA carboxylase

126
Q

What is the rate-limiting enzyme for beta oxidation of fatty acids?

A

carnitine acyltransferase I

127
Q

What is the rate-limiting enzyme for ketone body synthesis?

A

HMG-CoA synthase

128
Q

What is the rate-limiting enzyme for cholesterol synthesis? Which drug class inhibits it?

A

HMG-CoA reductase; statins

129
Q

What are the essential amino acids?

A
PVT TIM HaLL
phenylalanine
valine
threonine
tryptophan
isoleucine
methionine
histadine
leucine
lysine
130
Q

What amino acid is a precursor to histamine?

A

histidine

131
Q

What amino acid is a precursor to porphyrin/heme?

A

glycine

132
Q

What amino acid is a precursor to nitric oxide?

A

arginine

133
Q

What amino acid is a precursor to GABA?

A

glutamate

134
Q

What amino acid is a precursor to S-adenosyl-methionine (SAM)?

A

methionine

135
Q

What amino acid is a precursor to creatine?

A

arginine

136
Q

What enzyme does carbidopa inhibit?

A

DOPA decarboxylase

137
Q

PKU

A

autosomal recessive
due to decreased phenylalanine hydroxyls of decreased tetrahjydrobiopterin (BH4); tyrosine becomes essential
increased phenylalanine -> excess phenyl ketones in urine
Sx - intellectual disability, growth retardation, seizures, fair skin, eczema, musty body odor
Tx: decreased phenylalanine and increased tyrosine in diet; tetrahjydrobiopterin supplementation

138
Q

Maple Syrup Urine Disease (MSUD)

A

autosomal recessive
Blocked degradation of branched amino acids (Isoleucine, Leucine, Valine) due to decreased branched-chain alpha-ketoacid dehydrogenase
Sx - severe CNS defects, intellectual disability, death
Tx - restriction of isoleucine, leucine, valine in diet & thiamine supplementation
(I Love Vermont maple syrup)

139
Q

Alkaptonuria

A

autosomal recessive
congenital deficiency of homogentisate oxidase in the degradative pathway of tyrosine to fumarate -> pigment-forming homogentisic acid accumulates in tissue
Sx - bluish-black CT< ear cartilage, and sclera; urine turns black on prolonged exposure to air; may have debilitating arthralgias
Tx - add vita; avoid phenylalanine and tyrosine

140
Q

Homocystinuria

A
autosomal recessive
cystathione synthase deficiency or methionine synthase deficiency
Sx - HOMOCYstinuria
increased homocysteine in urine
osteoporosis
marfanoid habitus
ocular changes
cardiovascular effects -> stroke and MI
kyphosis
intellectual disability
141
Q

Cystinuria

A

autosomal recessive
hereditary defect of renal PCT and intestinal amino acid transporter that prevents reabsorption of COLA (cystine, ornithine, lysine, and arginine)
excess cystine in urine = recurrent hexagonal cystine stones
Tx - acetazolamide

142
Q

What are some of the clinical effects of Zinc deficiency?

A
delayed wound healing
decreased immune response
rash around eyes, mouth, nose and anus (acrodermatitis enteropathica)
anorexia and diarrhea
growth retardation
decreased mental functioning
impaired night vision
infertility
143
Q

Bluish colored lines of gingivae

A

Burton lines (iron toxicity)

144
Q

What organs are primary affected by an excess of mercury? What are other symptoms?

A

kidneys and brain
acrodynia - peeling of the fingertips
peripheral neuropathy, tremor, excitability and insomnia

145
Q

What are the symptoms of VitA toxicity?

A
N/V
vertigo
blurred vision
bone and joint pain
alopecia
dry skin
hepatic toxicity and enlargement
arthralgias
pseudotumor cerebri
ataxia
HA
teratogenic -> cleft palate and cardiac abnormalities
146
Q

What clinical features would lead you to suspect that a patient has scurvy?

A
bleeding gums
poor wound healing
bruising/petechiae
anemia
hemarthrosis
cork screw hair
loose teeth
147
Q

Vitamin C is necessary for the hydroxylation of which amino acids in collagen synthesis?

A

lysine and proline

148
Q

Which enzymes are used to convert cholecalciferol (Vit D3) to calcitriol? (1,25-OH-D3)

A

25-hydroxylase (liver) and 1-alpha-hydroxylase (kidney)

149
Q

A patient presents with convulsions and irritability. What vitamin deficiency is causing these symptoms?

A

Vit B6 (produces GABA) (pyridoxine)

150
Q

Where is Vit B12 absorbed into the circulation?

A

distal ileum

151
Q

Which vitamin deficiency is associated with peripheral neuropathy and glossitis?

A

Vit B12 and Vit B6

152
Q

Which vitamin deficiency is associated with dermatitis, diarrhea, and dementia?

A

Vit B3 (niacin)

153
Q

Which vitamin deficiency is associated with megaloblastic anemia?

A

Vit B9, Vit B12

154
Q

Which vitamin deficiency is associated with pernicious anemia?

A

Vit B12

155
Q

Which vitamin is used in oxidation/reduction reactions?

A

Vit B2 (riboflavin), B3

156
Q

Which vitamin is used in carboxylation reactions?

A

Vit B7 (biotin), VitK

157
Q

Which vitamin requires intrinsic factor for absorption?

A

Vit B12

158
Q

Which vitamin is used by pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase?

A

Vit B1

159
Q

Which vitamin deficiency can be caused by isoniazid use?

A

Vit B6, Vit B3

160
Q

Which vitamin contains cobalt?

A

Vit B12 (cobalamin)

161
Q

Which vitamin is critical for DNA synthesis?

A

Vit B9 and B12

162
Q

Dilated cardiomyopathy, edema, polyneuropathy

A

Wet beriberi (Vit B1 def)

163
Q

What is dry beriberi?

A

Vit B1 def - polyneuritis, symmetrical muscle wasting