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MCBM > Mitsouras > Flashcards

Mitsouras Flashcards

1
Q

Allosteric regulation of enzyme activity

A

Reversible & transient effects; fast-acting and short-range

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2
Q

Covalent modification of enzyme activity

A

Reversible & transient effects; fast-acting and long-range

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3
Q

Hormonal control

A

Permanent effects; slow-acting and long-range

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4
Q

Gluconeogenesis

A

the synthesis of glucose from non-glucose precursors

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5
Q

Gluconeogenesis

A

the synthesis of glucose during starvation when liver glycogen stores are depleted

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6
Q

Which metabolic fuels are generated and how during the fed state?

A

Insulin: causes organs/tissues to uptake glucose;

mm and liver store excess

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7
Q

Which metabolic fuels are generated and how during the fasting state?

A

Glucagon;

glycogenolysis and gluconeogenesis in liver

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8
Q

Which metabolic fuels are generated and how during the starvation state?

A

Glycogen stores are depleted so gluconeogenesis is only source of glucose

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9
Q

How are FA and ketone body levels in circulation during fasting?

A

equal!

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10
Q

How are FA and ketone body levels in circulation during starvation?

A

more ketone bodies than FAs (ketone bodies left free in blood for brain)

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11
Q

Absorption of monosaccharides

A

From intestinal epithelium into circulation

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12
Q

Transport of monosaccharides

A

From circulation into cells

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13
Q

During what state does digestion of dietary carbohydrates result in increased blood glucose levels?

A

Fed state (about 30 min after a meal)

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14
Q

GLUT1

A

Tissues: Most cell types (RBCs, brain) but not kidney or SI
Function: Glucose & galactose transporter; High affinity; Basal glucose uptake ***** Low capacity

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15
Q

GLUT2

A

Tissues: Hepatocytes, pancreatic b-cells, SI & kidney
Functions: Glucose, galactose & fructose transporter; High capacity & low affinity; Glucose-sensor; Exports glucose into blood after uptake from lumen of SI**

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16
Q

GLUT3

A

Tissues: Most tissues/ organs (brain, testes, placenta)
Functions: Glucose & galactose transporter; High affinity; Basal glucose uptake **low capacity

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17
Q

GLUT4

A

Tissues: Skeletal muscle & adipocytes
Functions: Glucose transporter; High affinity; Insulin-dependent**
Imp in lowering blood glucose levels. Insulin increases number of receptors on cell-surface

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18
Q

GLUT5

A

Tissues: SI, sperm, kidney, brain, muscle, adipocytes
Functions: Fructose transporter; High affinity

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19
Q

GLUT7

A

Tissues: Membrane of ER in hepatocytes
Functions: Glucose transporter; Transports free glucose from ER to cytoplasm for release into blood by GLUT2 (during gluconeogenesis)

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20
Q

SGLUT1

A

Tissues: Epithelial cells of SI & apical surface of kidney tubules
Functions: Glucose, galactose co-transporter with Na+ (same direction); Uptake of sugar from lumen of SI against gradient, ATP Dependent
SGLT1 and SGLUT1: Na+Dependent Co-transporters

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21
Q

Anaerobic glucolysis

A

glucose –> 2 lactate, 2 ATP produce (no NADH)

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22
Q

Allosteric regulation of glucokinase

A

activated by glucose

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23
Q

Allosteric regulation of hexokinase

A

inhibited by glucose-6P

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24
Q

Allosteric regulation of PFK-1

A

inhibited by ATP, citrate

activated by AMP, fructose-2,6-BP

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25
Q

Allosteric regulation of pyruvate kinase

A

inhibited by ATP

activated by fructose-1,6,-BP

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26
Q

Hormonal regulation - induction by insulin of

A

glucokinase, PFK-1 and pyruvate kinase

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27
Q

Hormonal regulation - repression by glucagon of

A

glucokinase, PFK-1 and pyruvate kinase

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28
Q

Lactic acidosis

A

Results from a buildup of lactate in the cytoplasm caused by anaerobic glycolysis;
Caused by strenuous exercise

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29
Q

Alcohol intoxication causes

A

impaired gluconeogenesis

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30
Q

Leukemia/metastatic carcinoma

A

anaerobic glycolysis by tumor cells

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31
Q

How does pyruvate kinase deficiency result in hemolytic anemia?

A

Decreased ATP = impaired membrane of RBC –> cane the shape of cells –> cell lysis

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32
Q

Fructose

A

Glyceraldehyde-3-phosphate is the glycolitic intermediate and substrate for gluconeogenesis;
It can go into glycolysis or gluconeogenesis

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33
Q

Galactose

A

Glucose-6-phosphate is the glycolytic intermediate and the intermediate in gluconeogenesis;
Can proceed to glycolysis if the body is in the fed state or to glucose

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34
Q

Fructokinase deficiency

A

inability to metabolize fructose; causes build up of fructose in blood (benign and asymptomatic); build up excreted in urine

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35
Q

Hereditary fructose intolerance

A

aldolase B deficiency; vomiting, hypoglycemia, hepatomegaly; causes liver failure and death

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36
Q

Non-classical galactosemia

A

galactokinase deficiency; build up of galactose in blood and urine; leads to cataracts

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37
Q

Classical galactosemia

A

GALT deficiency; buildup of galactose-1-P; liver damage and mental retardation

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38
Q

What are the two main products of HMP and which pathways utilize them?

A

NADPH and ribose-5-phosphate;
NADPH is used for FA synthesis, cholesterol and steroids;
Ribose is used for nucleotide synthesis

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39
Q

Where is HMP active?

A

ovaries, testes, mammary gland, adrenal cortex, adipose tissue and liver

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40
Q

What is the role of NADPH in RBCs?

A

partcipates in the reactions for the formations of reduced glutathione from oxidized glutathione by glutathione reductase

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41
Q

What is the role of glutathione in RBCs?

A

needed for detoxification of hydrogen peroxide which is important in RBCs because it stabilizes the plasma membrane to maintain hemoglobin in the a reduced state

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42
Q

Inherited deficiency of G6PD

A

reduces the amount of NADPH produced in RBCs by making them more susceptible to hemolysis

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43
Q

Wernicke-Korsakoff encephalopathy

A

due to decrease in thiamine

sx: ataxia, confusion, eye paralysis, learning and memory deficits

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44
Q

How is PDH activity regulated?

A

AcetylCoA and NADH inhibit PDH through feed-back inhibition;
Activated by Ca++
Inhibited by ADP and pyruvate

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45
Q

The TCA cycle provides

A

CO2 and GTP for the ETC

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46
Q

What are the 2 types of anaplerotic reactions

A
  1. 4 and 5 carbon acids replenished via amino acid degradation
  2. Oxaloacetate regenerated from pyruvate by pyruvate carboxylase
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47
Q

What does the chemiosmotic hypothesis do?

A

couples the ETC to ATP synthesis

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48
Q

Uncouplers of ETC

A

DNP, UCP1, ASA;

Uncouple electron flow from ATP synthesis

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49
Q

Inhibitors of ETC

A

Block electron flow at different positions on the ETC

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50
Q

Free radicals

A

molecules with highly reactive unpaired electrons that can exist independently

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51
Q

Antioxidant defense enzymes

A

Catalase, superoxide dismutase, GSH, glutathione peroxidase

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52
Q

Antioxidant vitamins

A

Vitamin C, Vitamin E, Beta-carotene

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53
Q

Metal sequestration

A

Transition metal

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54
Q

What is the role of glycogenesis in the homeostasis of blood glucose levels?

A

Helps prevent hyperglycemia by sequestering blood glucose

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55
Q

Insulin stimulates glycogenesis by:

A

Increasing glucose transport into muscles cells by GLUT4;
Increasing glucose transport into liver by GLUT2;
Inhibits glycogenolysis

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56
Q

Glyocgen synthase

A

UDP-glucose attaches to non-reducing ends of glycogen

57
Q

Branching enzyme

A

removes 6-8 gluce segment from non-reducing end

transfers this segment to an internal position

58
Q

Insulin turns these things on

A

Glycogen synthase and Glycogenesis

59
Q

Glucagon turns these things off

A

Glycogen synthase and Glycogenesis

60
Q

Phosphorylase

A

breaks alpha 1-4 via phospholytic cleavage using Pi to produce G1Pq

61
Q

Debranching enzyme

A

transfers 3 glucose residues from the end to the no-reducing end of the glycogen chain

62
Q

Glucagon turns these things on

A

glycogen phosphorylase and glycogenolysis

63
Q

Insulin turns these things off

A

glycogen phosphorylase and glycogenolysis

64
Q

Type I

A

Glucose-6-phosphate

65
Q

Type II

A

a-1,4-glucosidase

66
Q

Type III

A

debranching enzyme

67
Q

Type IV

A

branchign enzyme

68
Q

Type V

A

glycogen phosphorylase

69
Q

Type VII

A

phosphofructokinase

70
Q

Type VIII

A

phosphorylase kinase

71
Q

Bypass I of gluconeogenesis

A

Pyruvate –> oxaloacetate by pyruvate carboxylase

72
Q

Bypass II of gluconeogenesis

A

Fructose-1,6-B,P –> fructose-6-P by F-1,6-BPase

73
Q

Bypass III of gluconeogenesis

A

Glucose-6P –> glucose by gluco-6-phosphatase

74
Q

How is the energy required for gluconeogenesis supplied?

A

FAs and glycerol from lipolysis

ATP and NADH from FA oxidation

75
Q

What is on/off at low energy charge?

A

Gluconeogenesis is OFF

Glycolysis is ON

76
Q

What is on/off at high energy charge?

A

Glycolysis is OFF

Gluconeogenesis is ON

77
Q

DM Type 1

A

Lack of insulin results in repression of PEPCK –> gluconeogenesis is stimulated and glucose is produced –> hyperglycemia
Loss of pancreatic B cells

78
Q

Insulin in liver activates/inhibits:

A

Activates: FA synth, glycolysis, glycogenesis, protein synth, HMP
Inhibits: gluconeogenesis, glycogenolysis

79
Q

Insulin in adipose activates/inhibits:

A

Activates: TAG storage, glycolysis, HMP
Inhibits: lipolysis

80
Q

Insulin in muscle activates/inhibits:

A

Activates: protein synth, glycogenesis, glycolysis

81
Q

Glucagon in liver activates/inhibits:

A

Activates: glycogenolysis, gluconeogenesis, beta-oxidation, ketogenesis
Inhibits: glycolysis, glycogenesis, FA synth

82
Q

Glucagon in adipose activates/inhibits:

A

Activates: beta-oxidation, lipolysis

83
Q

Glucagon in muscle activates/inhibits:

A

Activates: protein degradation, beta-oxidation, ketolysis

84
Q

Catecholamines in liver and muscle:

A

Activates glycogenolysis

Inhibits glycogenesis

85
Q

Catecholamines in adipose:

A

Activates lipolysis

86
Q

DM Type II

A

Non-insulin dependent diabetes

Insulin resistance combined w/inadequate insuline secretion

87
Q

FISH

A

used to visualize labeled probes using fluorescence microscope

88
Q

Chromosome painting

A

mixture of proves for a given chromosome

89
Q

M-FISH or SKY

A

allows for simultaneous visualization of al chromosomes

90
Q

Array CGH

A

compare pt DNA to control to determine abnormalities

91
Q

Ploidy

A

change in chromosome number due to non-disjunction of sister chromatids during meiosis 1 or 2

92
Q

Aneuploidy

A

gain of loss of individual chromosomes (gain is viable, loss if not)
ex: trisomy 13, 18, 21

93
Q

Polyploidy

A

gain of entire chromosome set (not viable ever)

94
Q

Downs syndrome

A

Trisomy 21; mental retardation, small stature, respiratory infections, characteristic facial appearance

95
Q

Patau syndrome

A

Trisomy 13; congenital heart defects, seizures, hypotonia, cleft lip and palate, polydactyly

96
Q

Edwards syndrome

A

Trisomy 18; low set and malformed ears, rocker bottom feet, clenched fist

97
Q

Turner syndrome

A

45, X or 45XO; viable but not fertile; short, no secondary sex characteristics, mild mental retardation

98
Q

Klinefelter syndrome

A

47, XXY most common; viable but not fertile; hypogonadism, elongated limbs

99
Q

Reciprocal translocation

A

complete exchange of fragments between two broken non homologous chromosomes

100
Q

Robertsonian translocation

A

translocation involving two acrocentric chromosomes; ex: Down’s syndrome!

101
Q

Allele

A

different version of a gene in a population

102
Q

Allele frequency

A

frequency of allele in population

103
Q

Genotype

A

genetic makeup of a cell

104
Q

Genotype frequency

A

proportion of individuals with a specific genotype

105
Q

Autosomal dominant

A

every generation affected; males and females equally

106
Q

Autosomal recessive

A

unaffected parents can have affected or unaffected kids; males and females equally

107
Q

X-linked dominant

A

every generation affected; affected father only transmits to daughters; males and females equally

108
Q

X-linked recessive

A

males more than females; unaffected males do not transmit; carrier women transmit to sons

109
Q

Penetrance

A

the % of individuals w/the same genotype who express that phenotype

110
Q

Expressivity

A

range of phenotypes produced by the same genotype

111
Q

Locus heterogeneity

A

mutations in different loci that produce the same phenotype/disorder

112
Q

Allelic heterogeneity

A

different mutations in the same locus that produce phenotypes of differing severity

113
Q

Anticipation

A

progressively earlier age of onset and increased severity of sx (correlates w/increased number of trinucleotide repeats)

114
Q

Multifactorial inheritance

A

disease process that has influence stemming from genetics and environmental interactions

115
Q

Risk

A

disease susceptibility conferred by genes alone

116
Q

Liability

A

factors affecting disease development

117
Q

SNP

A

a DNA sequence variation occurring commonly w/n a population

118
Q

Sanger DNA sequencing

A

for known and unknown mutations;

can identify SNPs/point mutations, deletions, insertions

119
Q

Exome sequencing

A

for unknown mutations;

whole genome coverage

120
Q

Microarray hybridization

A

for unknown and known mutations;

screen entire genome

121
Q

Southern blotting

A

DNA;
for known mutations;
used for detection of relatively larger rearrangements on single gene;
used for trinucleotide repeat disorders

122
Q

PCR amplification

A

for known mutations

123
Q

RFLP analysis

A

for known mutations

124
Q

ARMS PCR/allele-specific PCR

A

for known mutations

125
Q

Biosynthetic pathway affected

A

the end product is usually important for cellular function and thus a decrease in levels is very detrimental

126
Q

Catabolic pathway affected

A

a decrease in end product not as detrimental

127
Q

Degradative pathways affected

A

accumulation of substrate is very detrimental

128
Q

Screening

A

performed on healthy individual who might be at risk for developing disease

129
Q

Diagnostic

A

performed on symptomatic individual to establish or confirm a diagnosis

130
Q

Types of tx for metabolic disorders:

A
  1. Avoidance
  2. Enhancement (of residual enzyme activity)
  3. Protein replacement
131
Q

Phenylketonuria (PKU)

A

Defect in phenylalanine metabolism –> elevated serum phenylalanine levels;
Sx: mental retardation, seizures, autistic behavior
Tx: dietary restriction

132
Q

Hyperphenylalanemia

A

Defect in biosynth of cofactor required for phenylalanine hydroxyls activity;
Sx: muscle rigidity, dystonic movements, myoclonic seizures, drooling, microcephaly
Tx: not responsive to phe-free diet; supplement w/L-dopa and 5-OH tryptophan to restore neurotransmitter balance

133
Q

Extensive metabolizers

A

normal activity and normal metabolism

134
Q

Intermediate metabolizers

A

slightly reduced activity and slightly slower than normal metabolism

135
Q

Poor metabolizers

A

low/no activity and almost no metabolism

136
Q

Ultra-rapid metabolizers

A

higher than normal activity and faster than normal metabolism

137
Q

Oncotype DX breast cancer assay

A

gene expression profile of 21 gene panel used to calculate recurrence score w/n 10 yrs of initial diagnosis and assess whether women will benefit from certain types of chemo

138
Q

Mammaprint breast cancer assay

A

gene expression profile of 70 gene panel used to predict risk of metastasis over 10 years

139
Q

Prevenio lung RS test

A

gene expression profile of 14 genes associated w/known molecular pathways in non-small-cell lung cancer

MCBM (11 decks)

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