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piggy > Biochemistry - Metabolism Part 3 > Flashcards

Biochemistry - Metabolism Part 3 Flashcards

1
Q

Insulin binds to what type of receptor to activate protein phosphatase, which goes on to inactivate glycogen phosphorylase kinase and glycogen phosphorylase?

A

Tyrosine Kinase

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2
Q

An activated glycogen phosphorylase will begin what process?

A

Glycogenolysis

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3
Q

During glycogen metabolism, glucose-1-phosphate is converted to UDP-glucose by which enzyme?

A

UDP-glucose pyrophosphorylase; UDP-glucose is the substrate for glycogen synthase

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4
Q

During glucose metabolism, UDP-glucose is converted to the storage form of glycogen by which enzyme?

A

Glycogen synthase

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5
Q

In which organ does glycogen undergo rapid glycogenolysis during exercise?

A

Skeletal muscle

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6
Q

In which organ does glycogen undergo glycogenolysis to maintain blood sugar within an appropriate range?

A

Liver

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7
Q

What type of bond is found at glycogen branch points?

A

(1,6) bonds

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8
Q

What type of bond is found at side-by-side linkages of glucose in glycogen?

A

(1,4) bonds

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9
Q

What enzyme creates a new branch point when assembling glycogen molecules?

A

Branching enzyme

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10
Q

What enzyme digests glycogen to create a limit dextran?

A

Glycogen phosphorylase

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11
Q

Once a limit dextran has been created, what enzyme is necessary for further digestion of the glycogen molecule?

A

Debranching enzyme

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12
Q

Glycogen digestion in the lysosome occurs through which enzyme?

A

-1,4-glucosidase

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13
Q

What molecules are the end products of glycogenolysis?

A

Glucose and Pi

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14
Q

What conversion must occur for the glucose-1-phosphate produced during glycogenolysis to be converted to glucose?

A

The phosphate group has to be moved from the 1 carbon to the 6 carbon

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15
Q

Which enzyme reacts with a limit dextran (four glucose residues in branched configuration) during degradation of glycogen to form glucose?

A

Debranching enzyme

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16
Q

Which enzyme is responsible for the conversion of glucose-1-phosphate to glucose-6-phosphate?

A

Phosphoglucomutase

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17
Q

Which enzyme degrades glycogen to glucose in the lysosome?

A

Lysosomal acid maltase (-1,4-glucosidase)

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18
Q

Glycogen storage diseases involve an abnormal accumulation of toxic levels of what substance within cells?

A

Glycogen

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19
Q

How many types of glycogen storage diseases are there?

A

Twelve glycogen metabolism enzyme deficiencies have been described in humans

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20
Q

What is another name for glycogen storage disease type I?

A

von Gierke’s disease

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21
Q

A patient has severe fasting hypoglycemia, increased stores of glycogen in the liver, hepatomegaly, and elevated levels of lactate in his blood. What is the likely underlying metabolic deficiency?

A

von Gierke’s disease (glycogen storage disease type I) resulting from glucose-6-phosphatase deficiency

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22
Q

Glycogen storage disease type I results from a deficiency of what enzyme?

A

Glucose-6-phosphatase

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23
Q

What is the prognosis for a child diagnosed with Pompe disease?

A

Early death

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24
Q

Name four glycogen storage diseases.

A

Von Gierke;s disease (type I), Pompe;s disease (type II), Cori;s disease (type III), McArdle;s disease (type V) (remember: Very Poor Carbohydrate Metabolism)

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25
Q

How can you differentiate between a patient with Cori;s disease and one with von Gierke;s disease using blood samples?

A

Patients with Cori;s disease have normal blood lactate levels due to intact gluconeogenesis, whereas those with von Gierke;s have elevated blood lactate

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26
Q

What is another name for glycogen storage disease type II?

A

Pompe’s disease

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27
Q

In a patient with McArdle;s disease, would you expect increased or decreased levels of glycogen on muscle biopsy?

A

Increased levels of glycogen, because the muscle cannot break it down

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28
Q

What is another name for -1,4-glucosidase?

A

Acid maltase

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29
Q

What disease is the result of a deficiency of lysosomal -1,4-glucosidase?

A

Pompe’s disease (glycogen storage disease type II)

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30
Q

Pompe;s disease (glycogen storage disease type II) is associated with the enlargement of what organ?

A

The heart (remember: Pompe;s trashes the Pump)

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31
Q

Name three organs affected in Pompe;s disease.

A

Heart, liver, muscle

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32
Q

What is another name for glycogen storage disease type III? What is another name for glycogen storage disease type III?

A

Cori’s disease

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33
Q

What is another name for -1,6-glucosidase?

A

Debranching enzyme

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34
Q

What disease is the result of a deficiency of -1,6-glucosidase?

A

Cori’s disease (glycogen storage disease type III)

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35
Q

What is another name for glycogen storage disease type V?

A

McArdle’s disease

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36
Q

What disease is the result of a deficiency of skeletal muscle glycogen phosphorylase?

A

McArdle’s disease (glycogen storage disease type V)

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37
Q

A patient has painful cramping and myoglobinuria associated with strenuous exercise. What is the likely underlying metabolic deficiency?

A

McArdle’s disease (glycogen storage disease type V) (remember: McArdle’s = Muscle)

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38
Q

What bodily fluid can be used to diagnose McArdle;s in a patient with severe muscle cramping after exercise?

A

A urinalysis will show myoglobinuria

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39
Q

What enzyme deficiency is seen in Fabry;s disease?

A

-Galactosidase A

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40
Q

A patient presents with progressive neurodegeneration, hepatosplenomegaly, and a cherry-red spot on his macula. Histologic examination reveals cells containing lipid droplets, confirming a lysosomal storage disease. What are these cells called?

A

Foam cells; seen in Niemann-Pick disease

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41
Q

A patient presents with peripheral neuropathy, developmental delay, and optic atrophy. Histologic examination reveals multinucleated macrophages, confirming your diagnosis of a lysosomal storage disease. What are these cells called?

A

Globoid cells; seen in Krabbe;s disease

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42
Q

A deficiency of the enzyme -galactosidase A leads to what disease?

A

Fabry;s disease

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43
Q

What substrate is accumulated in Fabry;s disease?

A

Ceramide trihexoside

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44
Q

What type of inheritance does Fabry;s disease demonstrate?

A

X-linked recessive

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45
Q

What is the appearance of the cells that may serve as histologic confirmation of Gaucher;s disease?

A

Gaucher;s cells are macrophages that look like crumpled tissue paper

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46
Q

Name two mucopolysaccharidoses

A

Hunter;s syndrome and Hurler;s syndrome

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47
Q

A patient shows milder symptoms and appearance similar to Hurler;s syndrome but no corneal clouding; what kind of behavior patterns do you expect?

A

Aggressive behavior; this describes Hunter;s syndrome, an X-linked mucopolysaccharidosis

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48
Q

A patient has peripheral neuropathy of the hands and feet, angiokeratomas of the skin, and both cardiovascular and renal disease. These characteristics are typical of which lysosomal storage disease?

A

Fabry;s disease

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49
Q

What substrate accumulates in a patient with a deficiency of -glucocerebrosidase?

A

Glucocerebroside; it accumulates in liver, spleen, and bone in Gaucher;s disease

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50
Q

Name six types of sphingolipidosis.

A

Fabry;s disease, Gaucher;s disease, Niemann-Pick disease, Tay-Sachs disease, Krabbe;s disease, metachromatic leukodystrophy

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51
Q

What substrate is accumulated in Niemann-Pick disease?

A

Sphingomyelin (remember: No man picks [Niemann-Pick]his nose with his sphinger [sphingomyelinase])

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52
Q

What enzyme deficiency leads to Gaucher;s disease?

A

Glucocerebrosidase

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53
Q

A child has progressive neurodegeneration, developmental delay, cherry-red spots on the macula, and lysosomes with onion skinning; he does not have hepatomegaly. These characteristics are typical of which lysosomal storage disease?

A

Tay-Sachs disease

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54
Q

What is the most common lysosomal storage disorder?

A

Gaucher’s Disease

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55
Q

A patient has developmental delay, gargoylism, airway narrowing, and corneal clouding. These characteristics are typical of which lysosomal storage disease?

A

Hurler’s Syndrome

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56
Q

Which three lysosomal storage disorders are Ashkenazi Jews at increased risk for?

A

Tay-Sachs, Niemann-Pick, and some forms of Gaucher;s disease

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57
Q

What type of inheritance does Gaucher;s disease demonstrate?

A

Autosomal recessive

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58
Q

A patient has hepatosplenomegaly, aseptic necrosis of the femur, and abnormal macrophages on histologic examination. These characteristics are typical of which lysosomal storage disease?

A

Gaucher’s Disease

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59
Q

What is the term for macrophages that look like crumpled tissue paper under the microscope and are associated with a lysosomal storage disease?

A

Gaucher’s Cells

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60
Q

What enzyme deficiency leads to Niemann-Pick disease?

A

Sphingomyelinase

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61
Q

A deficiency of the enzyme sphingomyelinase leads to what disease?

A

Niemann-Pick disease

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62
Q

What type of inheritance does Niemann-Pick disease demonstrate?

A

Autosomal recessive

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63
Q

A child has progressive neurodegeneration, hepatosplenomegaly, and a cherry-red spot on his macula. These characteristics are typical of which lysosomal storage disease?

A

Niemann-Pick Disease

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64
Q

What enzyme deficiency leads to Tay-Sachs disease?

A

Hexosaminidase A (remember: Tay-SaX lacks heXosaminidase)

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65
Q

What substrate is accumulated in Tay-Sachs disease?

A

GM2 ganglioside

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66
Q

What type of inheritance does Tay-Sachs disease demonstrate?

A

Autosomal recessive

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67
Q

Name two lysosomal storage diseases that may present with a cherry-red spot on the macula.

A

Niemann-Pick disease and Tay-Sachs disease

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68
Q

What enzyme deficiency leads to Krabbe;s disease?

A

Galactocerebrosidase

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69
Q

What substrate is accumulated in Krabbe;s disease?

A

Galactocerebroside

70
Q

What type of inheritance does Krabbe;s disease demonstrate?

A

Autosomal recessive

71
Q

A patient has peripheral neuropathy, developmental delay, and optic atrophy. These characteristics are typical of which lysosomal storage disease?

A

Krabbe;s disease

72
Q

What enzyme deficiency leads to metachromatic leukodystrophy?

A

Arylsulfatase A

73
Q

What substrate is accumulated in metachromatic leukodystrophy?

A

Cerebroside sulfate

74
Q

What type of inheritance does metachromatic leukodystrophy demonstrate?

A

Autosomal recessive

75
Q

A patient has central and peripheral demyelination with ataxia and dementia. These characteristics are typical of which lysosomal storage disease?

A

Metachromatic leukodystrophy

76
Q

What enzyme deficiency leads to Hurler;s syndrome?

A

-L-iduronidase

77
Q

What substrates accumulates in Hurler;s syndrome?

A

Heparan sulfate and dermatan sulfate

78
Q

What pattern of inheritance does Hurler;s syndrome demonstrate?

A

Autosomal recessive

79
Q

What enzyme deficiency leads to Hunter;s syndrome?

A

Iduronate sulfatase

80
Q

What substrates are accumulated in Hunter;s syndrome?

A

Heparan sulfate and dermatan sulfate

81
Q

What pattern of inheritance does Hunter;s syndrome demonstrate?

A

X-linked recessive

82
Q

A patient has mild developmental delay, gargoylism, and airway obstruction but no corneal clouding. These characteristics are typical of which lysosomal storage disease?

A

Hunter;s syndrome

83
Q

Name the two lysosomal storage diseases that lead to an accumulation of heparan sulfate and dermatan sulfate.

A

Hunter;s syndrome and Hurler;s syndrome

84
Q

Name the two lysosomal storage diseases that show x-linked recessive inheritance.

A

Fabry;s disease and Hunter;s syndrome

85
Q

What is the name of the shuttle that moves acetyl coenzyme A from the mitochondria to the cytoplasm to participate in fatty acid synthesis?

A

Citrate shuttle (remember: SYtrate = SYnthesis)

86
Q

The addition of carbon dioxide to acetyl coenzyme A during fatty acid synthesis yields what molecule?

A

Malonyl coenzyme A

87
Q

In acyl-CoA dehydrogenase deficiency, dicarboxylic acid levels _____ (increase/decrease) and glucose and ketone levels _____ (increase/decrease).

A

Increase; decrease

88
Q

A deficiency of which enzyme in fatty acid metabolism causes an increase in dicarboxylic acids and a decrease in glucose and ketones?

A

Acyl-CoA dehydrogenase deficiency

89
Q

What cofactor is required for the conversion of acetyl-CoA to malonyl-CoA during fatty acid synthesis?

A

Biotin; it donates the CO2 group

90
Q

Where does fatty acid degradation occur? Where are the products of degradation consumed?

A

Both occur in the mitochondrion

91
Q

What is the name of the shuttle that moves long-chain fatty acids from the cytoplasm to the mitochondria to participate in fatty acid degradation?

A

Carnitine shuttle (remember: CARnitine = CARnage of fatty acids)

92
Q

After breakdown of fatty acids, the resulting acetyl-CoA groups can be put to which uses?

A

Ketogenesis or citric acid cycle

93
Q

In which direction does the citrate shuttle move acetyl-CoA across the mitochondrial membrane?

A

From the mitochondria to the cytoplasm

94
Q

In which direction does the carnitine shuttle move fatty acids across the mitochondrial membrane?

A

From the cytoplasm to the mitochondria

95
Q

A deficiency of what substance will result in hypoketotic hypoglycemia?

A

Carnitine

96
Q

What are the clinical sequelae of carnitine deficiency?

A

Weakness, hypotonia, and hypoketotic hypoglycemia due to toxic accumulation of long-chain fatty acids

97
Q

Name two ketone bodies derived from acetyl-CoA. (These are found in individuals who have experienced prolonged starvation and diabetic ketoacidosis.)

A

Acetoacetate and -hydroxybutyrate

98
Q

In a patient with high levels of circulating ketone bodies, what does the breath smell like?

A

Acetone (a fruity odor)

99
Q

Which two precursors can be made into ketone bodies?

A

Amino acids and fatty acids

100
Q

What is the precursor molecule to acetoacetate?

A

HMG coenzyme A

101
Q

In alcoholism, the citric acid cycle is stalled due to excess NADH, causing a shunting of glucose and free fatty acids toward formation of _______ _______.

A

Ketone bodies

102
Q

Which two organs can use ketone bodies as fuel during starvation?

A

Muscle and brain

103
Q

Which ketone body cannot be detected by a urine test?

A

-Hydroxybutyrate

104
Q

A patient with a history of alcoholism presents to the emergency department intoxicated. Excess NADH and the shunting of oxaloacetate to malate may result in finding what substance in his urine?

A

Ketone bodies

105
Q

Where in the body are ketones synthesized?

A

Liver

106
Q

In which two pathological states will the body produce large amounts of ketones?

A

Starvation and ketoacidosis

107
Q

The brain can convert one ketone body into two of what type of molecule?

A

Acetyl-CoA for use in the tricarboxylic acid cycle to generate adenosine triphosphate

108
Q

1 gram protein or carbohydrate = ____ kcal

A

4

109
Q

1 gram fat = ___ kcal

A

9

110
Q

During the first three days of fasting, which four processes maintain the blood glucose level?

A

Hepatic glycogenolysis, adipocyte free fatty acid release, muscle and liver free fatty acid use (instead of glucose), and hepatic gluconeogenesis

111
Q

What molecules do skeletal muscles contribute for hepatic gluconeogenesis in order to maintain the blood glucose level?

A

Lactate and alanine

112
Q

What are the only triacylglycerol molecules that can contribute to gluconeogenesis?

A

Glycerol, propionyl-CoA (from odd-chain free fatty acids)

113
Q

Which compounds do adipose tissues contribute for hepatic gluconeogenesis in order to maintain the blood glucose level during the first three days of starvation?

A

Glycerol and propionyl-CoA (from free fatty acid metabolism)

114
Q

What two metabolic processes does the liver undergo to maintain blood glucose level in the first three days of fasting/starvation?

A

Gluconeogenesis and glycogenolysis

115
Q

Name the organ: After the third day of fasting, ketone bodies formed in the _____ supply the _____ and the ______ with energy.

A

Liver; brain; heart

116
Q

What role does adipose tissue play in maintaining blood glucose levels in the first three days of fasting/starvation?

A

Release of free fatty acids that can be metabolized into contributions for hepatic gluconeogenesis

117
Q

Which tissues contribute the compounds required for hepatic gluconeogensis in order to maintain the blood glucose level during the first three days of fasting?

A

Peripheral tissue (lactate and alanine) and adipose tissue (free fatty acids)

118
Q

True or False? More muscle protein is degraded during days 1-3 of starvation than after several weeks of starvation.

A

True; ketone bodies become the main source of energy for the brain after several weeks of starvation and so less muscle protein is degraded compared to the first three days

119
Q

After several weeks of starvation, survival time is determined by the amount of _____ (muscle/fat) stores.

A

Fat

120
Q

Once fat stores are depleted after several weeks of starvation, _____ (protein/glucose/free fatty acid) degradation accelerates, leading to organ failure and death.

A

Protein

121
Q

What are the sources of adenosine triphosphate for muscles during brief exercise?

A

Stored adenosine triphosphate, creatine phosphate, and anaerobic glycolysis

122
Q

In addition to the sources that can be used in seconds, from which sources do muscles derive adenosine triphosphate during exercise that lasts at least several minutes?

A

Stored adenosine triphosphate, creatine phosphate, anaerobic glycolysis, and oxidative phosphorylation

123
Q

Which sources of adenosine triphosphate does the body use during exercise that lasts for hours?

A

Glycogen and free fatty acid oxidation

124
Q

What are the purposes of the metabolic changes the body undergoes during starvation?

A

To supply glucose to the brain and preserve protein structures

125
Q

What is the enzyme that esterifies plasma cholesterol?

A

Lecithin-cholesterol acetyltransferase

126
Q

What category of drugs inhibits HMG coenzyme A reductase?

A

Statins

127
Q

What enzyme catalyzes the rate-limiting reaction in cholesterol synthesis?

A

HMG-CoA reductase

128
Q

What are the two essential fatty acids?

A

Linolenic acid and linoleic acid

129
Q

What acid becomes essential in the absence of linoleic acid?

A

Arachidonic acid

130
Q

The formation of eicosanoids is dependent on the consumption of which fatty acids?

A

Essential fatty acids: linolenic and linoleic acid

131
Q

Which enzyme is responsible for the degradation of dietary triglycerides?

A

Pancreatic lipase

132
Q

Which enzyme is responsible for the degradation of triglycerides that are circulating as chylomicrons?

A

Lipoprotein lipase

133
Q

Which organs take up low-density lipoproteins from the circulation?

A

The liver and peripheral tissues with low-density lipoprotein receptors

134
Q

Which enzyme is responsible for the degradation of triglycerides circulating as intermediate-density lipoproteins?

A

Hepatic triglyceride lipase

135
Q

What is the enzyme responsible for converting nascent high-density lipoproteins into mature high-density lipoproteins?

A

Lecithin-cholesterol acetyltransferase

136
Q

What enzyme is responsible for the degradation of triglycerides that are stored within adipocytes?

A

Hormone-sensitive lipase

137
Q

What enzyme transfers cholesterol esters from high-density lipoproteins to other lipoproteins?

A

Cholesteryl ester transfer protein

138
Q

What organ releases chylomicrons into the circulation?

A

The gastrointestinal tract

139
Q

Name three lipoproteins that receive cholesterol esters from high-density lipoprotein via cholesteryl ester transfer protein.

A

Very-low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein

140
Q

What enzyme converts chylomicrons into chylomicron remnants?

A

Lipoprotein lipase

141
Q

What organ takes up chylomicron remnants from the circulation?

A

The liver

142
Q

What organ releases very-low-density lipoprotein into the circulation?

A

The liver

143
Q

What enzymes convert intermediate-density lipoproteins into low-density lipoproteins?

A

Hepatic triglyceride lipase and lipoprotein lipase

144
Q

What enzyme converts very-low-density lipoproteins into intermediate-density lipoproteins?

A

Lipoprotein lipase

145
Q

Which apolipoprotein activates lecithin-cholesterol acyltransferase?

A

Apolipoprotein A-I Activates LCAT

146
Q

Which apolipoprotein binds to the low-density lipoprotein receptor on the liver?

A

Apolipoprotein B-100 Binds the LDL receptor

147
Q

What apolipoprotein mediates very-low-density lipoprotein secretion?

A

Apolipoprotein B-100

148
Q

Which apolipoprotein acts as a cofactor for lipoprotein lipase?

A

Apolipoprotein C-II is a Cofactor for LPL

149
Q

Which apolipoprotein mediates remnant uptake?

A

Apolipoprotein Emediates Extra (remnant) uptake

150
Q

What molecules do lipoproteins contain?

A

Cholesterol, triglycerides, and phospholipids

151
Q

Which lipoprotein delivers dietary triglycerides to peripheral tissues?

A

Chylomicrons

152
Q

Which lipoprotein is secreted only by intestinal epithelial cells?

A

Chylomicrons

153
Q

Which apolipoprotein mediates the secretion of chylomicrons from the gastrointestinal tract?

A

Apolipoprotein B-48

154
Q

Which lipoprotein delivers hepatic triglycerides to peripheral tissues?

A

Very-low-density lipoprotein

155
Q

Which organ secretes very-low-density lipoprotein into the bloodstream?

A

The liver

156
Q

Name the two major lipoprotein carriers of cholesterol

A

Low-density lipoprotein and high-density lipoprotein

157
Q

What lipoprotein carries cholesterol from the liver to the tissues?

A

Low-density lipoprotein (remember: LDL is Lousy)

158
Q

What lipoprotein carries cholesterol from the tissues to the liver?

A

High-density lipoprotein (remember: HDL is Healthy)

159
Q

Which apolipoprotein on low-density lipoprotein mediates uptake into the liver?

A

Apolipoprotein B-100

160
Q

Which lipoprotein delivers dietary cholesterol to the liver?

A

Chylomicrons (as chylomicron remnants)

161
Q

Which lipoprotein mediates the transport of cholesterol from the periphery to the liver (reverse transport)?

A

High-density lipoprotein

162
Q

Name four apolipoproteins found on chylomicrons.

A

B-48, A-IV, C-II, and E

163
Q

Which lipoprotein acts as a reservoir of apolipoprotein C and apolipoprotein E?

A

High-density lipoprotein

164
Q

Which lipoprotein is formed by the degradation of very-low-density lipoprotein in the periphery by lipoprotein lipase (via IDL as an intermediate)?

A

Low-density lipoprotein

165
Q

What three apolipoproteins are found on very-low-density lipoprotein?

A

Apolipoprotein B-100, apolipoprotein C-II, and apolipoprotein-E

166
Q

Which lipoprotein is formed by the degradation of very-low-density lipoprotein?

A

Intermediate-density lipoprotein

167
Q

What lipoprotein is secreted by both intestinal epithelial cells and the liver?

A

High-density lipoprotein

168
Q

Which lipoprotein delivers triglycerides and cholesterol to the liver for degradation into low-density lipoprotein?

A

Intermediate-density lipoprotein

169
Q

What are the two apolipoproteins found on intermediate-density lipoprotein?

A

B-100 and E

170
Q

What is another name for type I dyslipidemia?

A

Hyperchylomicronemia

171
Q

An altered apolipoprotein C-II that does not function properly produces which type of familial dyslipidemia?

A

Type I (hyperchylomicronemia); C-II is a cofactor for lipoprotein lipase and if altered, the body is unable to metabolize chylomicrons

piggy (83 decks)

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