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USMLE1 - Biochemistry > 6. Metabolism 2 > Flashcards

6. Metabolism 2 Flashcards

1
Q

what enzyme converts phenylalanine to tyrosine? what cofactor is used?

A

phenylalanine hydroxylase; tetrahydrobiopterin factor

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2
Q

what converts tyrosine to DOPA? what cofactor is used?

A

tyrosine hydroxylase; tetrahydrobiopterin factor; NADP+

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3
Q

what is dihydroxyphenylalanine ?

A

DOPA

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4
Q

T/F tyrosinase converts tyrosine to DOPA

A

false; tyrosine hydroxylase

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5
Q

which catecholamine has inhibitory action against acetylcholine?

A

dopamine

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6
Q

what converts dihydrobioterin back to tetrahydrobioterin factor? what energy carrier is used? in what reactions is this cofactor used?

A

dihydropterin reductase; NADP+; phenylalanine to tyrosine and tyrosine to DOP

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7
Q

what converts dopa to dopamine? using what cofactor?

A

dopa decarboxylase; B6

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8
Q

where does catecholamine synthesis take place?

A

neural tissue and adrenal medulla

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9
Q

what converts dopamine to norepinephrine? using what cofactor?

A

dopamine beta hydroxylase; vit C

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10
Q

T/F vit c is needed in catecholamine synthesis

A

true! dopamine to norepinephrine

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11
Q

what negatively regulates dopamine to norepinephrine?

A

carbidopa

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12
Q

what enzyme converts norepinephrine to epinephrine? using what cofactor?

A

phenylethanolamine N-methyl transferase; SAM

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13
Q

what is phenylethanolamine N-methyl transferase located?

A

adrenal medulla

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14
Q

T/F phenylethanolamine N- methyl is only located in the adrenal medulla

A

true (epinephrine only made in the medulla)

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15
Q

what is the degradation product of Norepinephrine?

A

VMA

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16
Q

what is the degradation product of dopamine?

A

HVA

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17
Q

what is the degradation product of epinephrine?

A

metanephrine

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18
Q

what two def. most commonly cause phenylketonuria?

A

phenylalanine hydroxylase or tetrahydrobiopterin factor

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19
Q

what two enzymes are in involved in catecholamine degradation?

A

COMT and MAO

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20
Q

what aa becomes essential with phenylketonuria?

A

tyrosine

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21
Q

what explains the excess phenylketones in the urine in phenylketonuria?

A

phenylalanine build up

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22
Q

give an example of how phenylketonuria is pleiotropic.

A

also have fair skin, blond hair, blue eyes, eczema

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23
Q

what are the findings with phenylketonuria?

A

mental and growth retardation; seizures, fair skin, eczema, musty body odor; neurotoxic ketones and acids stimulate vomitting- can lead to pyloric stenosis

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24
Q

what is the treatment for phenylketonuria?

A

decreased phenylalanine, increase tyrosine

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25
Q

what is Maternal PKU?

A

lack of proper dietary therapy during pregnancy resulting in infant’s microcephaly, mental retardation, growth retardation and congenital heart defects

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26
Q

what type of aa is phenylalanine? what implications does this have on the presentation of phenylketonuria?

A

aromatic; musty body odor

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27
Q

what are phenylacetate, phenylactate, and phenylpyruvate?

A

phenylketones that build up in phenylketonuria

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28
Q

what is the mode of inheritance of phenyketonuria?

A

AR

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29
Q

when is phenylketonuria screened? why?

A

2-3 days after birth because maternal enzyme during fetal like might still be there

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30
Q

what does a deficiency in homogentistic acid oxidase result in? what is this also known as?

A

alkaptonuria; ochronosis

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31
Q

what enzyme is involved in the degradation of tyrosine to fumarate?

A

homogentistic acid oxidase

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32
Q

what builds up in the urine in homogentistic acid oxidase deficiency? what does this result in ?

A

urine turns black on standing

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33
Q

what are the findings in alkaptonuria? why do they occur?

A

dark connective tissue, brown pigmented sclera, debilitating athralgias; homogentistic acid builds up and can be toxic to cartilage

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34
Q

name three causes of albinism. what does albinism increased risk of?

A

tyrosinase deficiency; defective tyrosine transporters; lack of migration of neural crest cells; skin cancer

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35
Q

T/F Albinism is AR

A

false; only the tyrosinase one is- albinism has variable heritability because of locus heterogeneity

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36
Q

T/F Ocular albinism is AR

A

false- X linked recessive

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37
Q

T/F homocysteine gets turned into methionine by homocysteine transferase

A

TRUE

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38
Q

other than being returned to methionine, what else is the fate of homocysteine? through what enzyme? with what cofactor?

A

cystathionine (which then goes to cysteine) via cystathionine reductase; B6

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39
Q

what does SAM turn into after it loses a methyl? how does it get turned back to SAM?

A

homocysteine; homocysteine methyltransferase with B12 and tetrahydrofolate

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40
Q

what three enzyme def. can cause homocysteinura? what is their mode of inheritance?

A

homocysteine methyltransferase, cystathionine reductase, decreased affinity of cystathionine reductase for pyridoxal phosphate; AR

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41
Q

what aa becomes essential with homocystinuria? phenylalaninuria?

A

cysteine; tyrosine

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42
Q

how do you treat homocystinuria due to decreased affinity of cystathionine reductase to B6?

A

by giving high amounts of pyridoxal phosphate in the diet

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43
Q

what are the findings of homocystinuria?

A

increased homocysteine in the urine, mental retardation, osteoporosis, marfanoid habitus, and atherosclerosis

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44
Q

what aa degradation disorder results in atherosclerosis? debiltating arthralgias? osteoporosis?

A

homocystinuria (homocysteine damages endothelial cells); alkaptonuria (tyrosine degradation); homocystinuria

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45
Q

what is the product of odd chain fatty acid synthesis? how does it return to TCA cycle? what cofactor is required?

A

proprionyl coA; through methylmalonyl coA; B12

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46
Q

what is cystinuria due to?

A

hereditary defect of renal tubular amino acid transporter for cysteine , ornithine, lysine and arginine in the PCT of kidnyes

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47
Q

what is the presentation for cystinuria?

A

cystine kidney stones (cystine staghorn calculi)

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48
Q

what is the treatment for cystinuria?

A

acetazolamide to alkalinize the urine

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49
Q

T/F cysteine is a dimer

A

true- of two dimers connected by disulfide bond

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50
Q

what enzyme is necessary for branched aa degradation? what cofactor? what are the branched aa?

A

branche aa alpha ketoacid dehydrogenase; thiamine; Isoleucine, leucine, valine

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51
Q

what builds up in the blood of patients with maple syrup urine disease? urine/poo? what does this cause?

A

alpha ketoacids in the blood; alpha keto acids in the urine/poo smells of maple syrup/burnt sugar

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52
Q

what enzyme is deficient in maple syrup urine disease?

A

branched alpha ketoacid dehydrogenase

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53
Q

what are the findings in maple syrup disease? what should be tried to be given as treatment?

A

CNS defects, mental retardation, death, feeding difficulties, vomiting, hypoglycemia; thiamine

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54
Q

what is hartnup disease? what is the mode of inheritance?

A

defective neutral amino acid transporter on renal and intestinal cells; AR

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55
Q

what aa is most accumulated in hartnup disease? what vitamin becomes deficient?

A

tryptophan; niacin

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56
Q

what is the main clinical presentation of hartnup disease?

A

pellagra

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57
Q

what is the main hormonal regulation of glycogen?

A

glucagon, insulin and epinephrine

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58
Q

T/F the main hormonal regulation of glycogen is glucagon and insulin

A

false- glucagon, insulin and epinephrine

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59
Q

where is glycogen mainly found?

A

liver and skeletal muscle

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60
Q

what is the main use of glycogen?

A

reserve supply of glucose in the fasting state- liver gives to the blood and skeletal muscle uses for itself

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61
Q

T/F increased levels of cAMP results in glycogenolysis

A

TRUE

62
Q

T/F glucagon works on the liver and muscle to activate glycogenolysis by activating adenylyl cyclase

A

false- just liver

63
Q

T/F epinephrine works on liver to activate glycogenolysis by activating adenylyl cyclase

A

false- liver and muscle

64
Q

T/F phosphorylated glycogen phosphorylase is inactive

A

FALSE

65
Q

what is the first enzyme step in glycogenolysis? what activates it ? inactivates?

A

glycogen phosphorylase; phosphorylation and dephosphorylation

66
Q

how does glucagon activate glycogenolysis? what regulator does similar?

A

by activating adenylyl cylase which increases cAMP which increases levels of protein kinase A which activates glycogen phosphorylase kinase; epinephrine

67
Q

how is muscle activity and glycogenolysis coupled in muscle?

A

calcium and calmodulin activate glycogen phosphorylase kinase

68
Q

T/F inuslin downregulates glycogenolysis by inactivating cAMP

A

false- insulin receptor is not cAMP second receptor but rater tyrosine kinase- which dimerizes and activates a protein phosphatase which de phosphorylates glycogen phosphorylase

69
Q

how does insulin both deactivate glycogenolysis and activates glycogenesis at same time?

A

by activating protein phosphatase which both dephosphorylates glycogen phosphorylase (deactivating) and dephosphorylates glycogen synthase (activating it )

70
Q

T/F insulin acts on the liver to deactivate glycogenolysis

A

false- both liver and muscle (unlike glucagon)

71
Q

T/F glycogen branches have 1,4 bonds and linkages have 1,6 bonds

A

false-opposite

72
Q

T/F glycogenolysis in skeletal muscle maintains blood sugar

A

false; in hepatocytes

73
Q

what kind of linkages does glycogen synthase make? branching enzyme?

A

alpha 1,4 linkages; alpha 1,6 linkages

74
Q

why does branching occur in glycogenesis?

A

branching increases the rate of synthesis and breakdown of glycogen by having more sites to add on to and break off

75
Q

after glucose 6 P is converted to glucose 1 P , what is the next step in glycogenesis? then what?

A

conversion to UDP glucose via UDP glucose pyrophosphorylase; glycogen synthase (rate limiting step )

76
Q

what is the main form of glycogenolysis after glycogen phosphorylase? what happens instead in some lysosomes? does this process use glycogen phosphorylase? in what disease is this enzyme deficient?

A

debranching enzyme; alpha 1, 4 glucosidase; no!; Pompes disease

77
Q

what does glycogen phosphorylase in glycogenolysis create?

A

limit dextrans

78
Q

what are the glycogen storage disease? what they result in?

A

abnormal glycogen metabolism results in accumulation of glycogen in cells

79
Q

T/F all the glycogen storage diseases are AR

A

TRUE

80
Q

what is the fate of glucose from glycogenolysis?

A

glucosekinase to glucose 6 P

81
Q

how do hepatocytes release glucose 6 P from glycogenolysis into the blood ? in what disease is this enzyme deficient?

A

with glucose 6 phosphatase; Von Gierkes disease

82
Q

what is the deficient enzyme in Von Gierkes disease? what are the findings?

A

severe fasting hypoglycemia, very high levels glycogen in liver, high blood lactate, hepatomegaly

83
Q

what is the order of types of glycogen storage disease?

A

Very Poor Carb Metabolism (Von Gierke- Type 1, Pompes- Type II, Cori’s- Type III, McArdles disease- Type IV)

84
Q

What are the findings for Pompe’s disease? what is the deficient enzyme?

A

cardiomegaly and systemic findings leading to early death; lysosomal alpha-1,4-glucosidase (acid maltase)

85
Q

Findings for Cori’s disease? deficient enzyme?

A

milder form of type 1 with normal blood lactate levels; debranching enzyme (alpha-1,6 glucosidase)

86
Q

findings for McArdle’s disease? deficient enzyme?

A

high glycogen in muscle, but cannot break it down, leading to painful muscle cramps, myoglobinuria with strenuous exercise, no increase in lactic acid after exercise; skeletal muscle glycogen phophorylase

87
Q

which glycogen storage disease results in hepatomegaly?

A

von gierkes

88
Q

which glycogen storage disease causes hypertriglyceridemia?

A

von gierkes

89
Q

which glycogen storage disease results cardiomegaly?

A

pompes

90
Q

T/F coris glycogen storage disease has normal lactate levels

A

TRUE

91
Q

which glycogen storage disease results in no lactic acid after exercise?

A

mcardles disease

92
Q

what causes the lysosomal storage diseases?

A

deficiencies in one of the many lysosomal enzymes results in accumulation of abnormal metabolic products

93
Q

which two lysosomal storage disease are XR and not AR?

A

Fabrys Disease and Hunters Syndrome

94
Q

what is the deficient enzyme in Fabry’s disease? accumulated Substrate?

A

alpha galactosidase A; ceramide trihexoside

95
Q

what is the deficient enzyme in Gauchers disease? accumulated Substrate?

A

Beta glucocerebrosidase; glucocerebroside

96
Q

what is the deficient enzyme in Niemann Pick disease? accumulated Substrate?

A

Sphingomyelinase; sphingomyelin

97
Q

what is the deficient enzyme in Tay Sachs disease? accumulated Substrate?

A

Hexosaminidase A; GM2 ganglioside

98
Q

what is the deficient enzyme in Krabbes disease? accumulated Substrate?

A

Galactocerebrosidase; Galactocerebroside

99
Q

what is the deficient enzyme in Metachromatic leukodystrophy disease? accumulated Substrate?

A

arylsulfatase A; cerebroside sulfate

100
Q

what is the findings in Fabrys disease?

A

peripheral neuropathies of hands/feet; angiokeratomas between umbilicus and knees; cardiovascular/renal disease

101
Q

which is the most common lysosomal storage disease? what are its findings?

A

Gauchers; hepatosplenomegaly, aseptic necrosis of the femur, bone crises, Gauchers cells -crumpled tissue paper looking (fibrillar appearing macrophages in liver, spleen, b.m.)

102
Q

what are the findings in Niemann Pick disease?

A

progressive neurodegeneration (spasticity d/t UMN disease), hepatosplenomegaly, cherry red spot on macula, foam cells

103
Q

what are the findings in Tay Sachs disease?

A

progressive neurodegeneration (spasticity d/t UMN disease), NO hepatosplenomegaly, cherry red spot on macula, lysosomes with onion skin, muscle weakness

104
Q

what are the findings in Krabbes disease?

A

peripheral neuropathy, developmental delay, optic atrophy, globoid cells

105
Q

what are the findings in Metachromatic leukodystrophy?

A

central and peripheral demyelination with ataxia and dementia

106
Q

which two lysosomal storage diseases findings are very similar? how do you differentiate them?

A

Niemann pick and Tay Sachs; hepatosplenomegaly or not

107
Q

what are the mucopolysaccharidoses? which one is XR? AR? what accumulates in them?

A

Hurlers Syndromes;Iduronate sulfatase deficiency; alpha L iduronidase def; heparan sulfate, dermatan sulfate

108
Q

which Hurlers is milder and presents with no corneal clouding?

A

XR - iduronate sulfatase

109
Q

what are the findings in AR Hurlers?

A

developmental delay, gargoylism, airway obstruction (d/t short neck), corneal clouding, CAD, hepatosplenomegaly

110
Q

what lysosomal storage diseases are seen more in Ashkenazi Jew?

A

tay Sachs, Niemann Picks, Gauchers

111
Q

why is there hepatosplenomegaly in many of the lysosomal storage diseases?

A

because cells of mononuclear phagocytic are esp rich in lysosomes

112
Q

which lysosomal storage diseases have enzymes that are def in cells that are neuronal mostly?

A

neimann pick and tay sachs

113
Q

in Fabrys, what accumulates in tissue because fibroblasts express the def enzyme highly?

A

ceramide trihexoside

114
Q

what is the first step in fatty acid synthesis? where does it occur? where does triacylglycerol synthesis occur?

A

citrate shuttle in the inner mitochondrial membrane transports acetyl coA into the cytoplasm; liver; liver and adipose tissue

115
Q

what is the rate limiting step in fatty acid synthesis? what four things inhibit this rate limiting step? what stimulates it?

A

acetyl coA carboxylase converting Acetyl coA into malonyl coA; increased AMP, glucagon, epinephrine, palmitate; citrate

116
Q

where does synthesis of longer chain fatty acids occur? what does it require?

A

SER and mitochondria; NADPH

117
Q

what is palmitate? saturated or unsaturated? what does that meat?

A

a 16C FA! the product in FA synthesis; saturated; no double bonds

118
Q

T/F fatty acid synthase requires NADP+

A

false! NADPH- reductive biosynthesis!

119
Q

what cofactor does acetyl coA carboxylase require? what does it convert?

A

biotin; rate limiting step in fA synthesis- acetyl coA into malonyl coA

120
Q

T/F carnitine shuttle is used to transport acetyl coA out of the mitochondria for fatty acid synthesis

A

false! citrate shuttle; carnitine shuttle takes acyl coA into the mit for fatty acid degradation

121
Q

what does lipolysis generate? and what two regulators activate lipases?

A

triacylglycerols in adipose tissue broken down into glycerol and free fatty acids; growth hormone and epinephrine

122
Q

what is the fate of the two products of lipolysis?

A

glycerol goes to liver for gluconeogenesis; free fatty acids bind to albumin in blood and travel to cells to be used as for energy

123
Q

T/F Fatty acid coA synthetase is used in FA synthesis

A

false- FA degradation

124
Q

what is the first step in FA degradation in the cytosol?

A

FA coA synthetase combines coA with FA to make acyl coA

125
Q

what is required to get Acyl coA in FA degradation into the mitochondria for beta oxidation to acetyl coA groups?

A

carnitine shuttle

126
Q

what is carnitine deficiency and what does it result in?

A

inability to transport LCFA into mitochondria results in their build up and causes weakness, hypotonia AND HYPOKETOTIC HYPOGLYCEMIA

127
Q

what is deficient in someone with hereditary hypoketotic hypoglycemia?

A

carnitine shuttle

128
Q

why does fa degradation occur in the mitochondria? what does FA degradation produce? what is the fate of this product?

A

because that is where the products will be consumed; acetyl coA; TCA cycle of ketone body production

129
Q

what is acyl coA dehydrogenase used in? what does a deficiency in this enzyme produce?

A

fatty acid (acyl coA) oxidation to acetyl coA; increase in dicarboxylic acids, and decreased glucose and ketones

130
Q

walk through the process that adipose tissue makes triacylglycerol.

A

lipoprotein lipases take FA from VLDL and chylomicrons which are then combined with glycerol 3 P (a carb intermediate) to make triacylglycerol

131
Q

what is the main source of FA? where else can they be released from?

A

synthesis in liver and then hydrolysis of chylomicrons and VLDLs by capillary lipoprotein lipase in peripheral tissue; adipose tissue by lipases

132
Q

T/F the liver uses ketone bodies for energy

A

false- only muscle and brain have transferase enzyme that converts ketone bodies to acetyl coA

133
Q

where are ketone bodies made? what is the rate limiting enzyme? what are they made from?

A

mitochondria in liver; HmG CoA synthetase; amino acids and beta oxidation of FA

134
Q

what does the brain do with ketone bodies?

A

metabolizes them with transferase enzymes to acetyl coA

135
Q

what are three ketone bodies? which is not detected in urine? which do you see most in alcoholic ketoacidosis?

A

b hydroxybutyrate, acetone, acetoacetate; beta hydroxybutyrate; beta hydroxybutyrate

136
Q

what is the impetus for ketoacidosis in starvation? alcoholism?

A

oxaloacetate depleted for gluconeogenesis; excess NADH shunts oxaloactetate towards malate

137
Q

what causes fruity odor in ketoacidosis?

A

acetone

138
Q

how many calories does one gram of protein generate? carb? fat?

A

4,4,9

139
Q

T/F HMG coA reductase is used in KB synthesis

A

false- HMG coA synthase; cholesterol synthesis uses HMG coA reductase

140
Q

in a 100 meter sprint what is used as energy? in general what is the rule with exercise? what is used in 1000 meter run?

A

Stored ATP, creatine phosphate, anaerobic glycolysis; as distances increase, ATP is obtained from additional resources; above plus ox phos

141
Q

what is used in a marathon?

A

glycogen and FFA oxidation- glucose conserved for final sprinting!

142
Q

what are the priorities in fasting and starvation?

A

to supply sufficient glucose to the brain and the RBCs and to preserve protein

143
Q

what is the source of ATP after a meal?

A

glycolysis and aerobic respiration

144
Q

what is the source of ATP when you are fasting (in between meals)?

A

hepatic glycogenolysis (mostly), also hepatic gluconeogenesis, adipose release of FFA (minor)

145
Q

after how long of starvation do glycogen reserves deplete? after this occurs, how are blood glucose levels maintained?

A

1 day; adipose release of FFA, hepatic gluconeogenesis from peripheral tissue lactate and alanine and from adipose tissue glycerol and propionyl coA

146
Q

what does adipose tissue contribute for hepatic gluconeogenesis during starvation? muscle?

A

glycerol and propionyl coA; lactate and alanine

147
Q

after day 3 of starvation, what is the main source of energy?

A

adipose tissue for brain and heart (ketone bodies) and then go to vital protein degradation (organ failure)

148
Q

what is the rate limiting step in cholesterol synthesis? what does it do?

A

HMG CoA reductase; converts HMG CoA to mevalonate

149
Q

how much of plasma cholesterol is esterified? and by what?

A

2/3; LCAT (lecithin cholesterol acyltransferase)

150
Q

what do statins inhibit?

A

HMG CoA reductase

USMLE1 - Biochemistry (6 decks)

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