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First Aid Biochem > FA Biochem II > Flashcards

FA Biochem II Flashcards

1
Q

what is dominant negative mutation and give an example

A

exerts a dominant effect, a heterozygote produces a nonfxnal altered protein that also prevents the normal gene from functioning, mutation of Tx factor its allosteric site, nonfxning mutant can still bind DNA, preventing wild type Tx from binding

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2
Q

What is linkage disequilibrium

A

tendency for certain alleles at 2 linked loci to occur together more often than expected by chance - varies is different populations

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3
Q

What is mosaicism and give an example

A

occurs when cells in the body have different genetic makeup, can be germline mosaic, which may produce a disease that is not carried by parents somatic cells - lyonization-random X inactivation in females

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4
Q

What is locus heterogeneity and give an example

A

mutations at different loci can produce the same phenotype, marfans, MEN 2B, homocystinuria; all cause marfinoid habitus, also albinism

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5
Q

What is heteroplasmy

A

presence of both nl and mutated mtDNA resulting in mitochondrial inherited disease

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6
Q

What is uniparental disomy

A

offspring receives 2 copies of a chromosome from 1 parent and no copies from the other parent

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7
Q

What is the Hardy Weinberg disease prevalence equation

A

p2 +2pq+ q2 = 1

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8
Q

What is the hardy weinberg allele prevalence

A

p+q = 1

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9
Q

What is the hardy weinber heterozygote prevalence

A

2pq

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10
Q

What is the prevalence of an X-linked recessive disease in males and in females

A

q, q2

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11
Q

What are the 4 assumption of the Hardy Weinberg law

A

no mutation occuring at the locus, no selection for any genotypes at the locus, completely random mating, no migration

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12
Q

Gene imprinting implies that how many alleles are active at a single locus

A

one

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13
Q

If two alleles are present, but the active allele is deleted, what happens

A

disease

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14
Q

What are the characteristics of prader willi syndrome how does it occur

A

mental retardation, hyperphagia, obesity, hypogonadism, hypotonia - deletion of normally active paternal allele on chromosome 15

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15
Q

What are the characteristics of angelmans syndrome and how does it occur

A

mental retardation, seizures, ataxia, inappropriate laughter - deletion of normally active maternal allele

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16
Q

characterize autosomal domint inheritance

A

many generations, both male and female affected - often pleiotropic, can present clinically after puberty

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17
Q

characterize autosomal recessive inheritance

A

1/4 of offspring from 2 carrier parents are affected, often enzyme def, usually only seen in 1 generation - often more sever than AD, presents in childhood

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18
Q

characterize x linked recessive

A

sons of heterozygous mothers have 1/2 half chance of being affected - no male to male transmission, and often more severe in males, heterozygous females may be affected

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19
Q

characterize x linked dominant

A

transmitted through both parents, affected mother may have affected children, affected father will have affected children

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20
Q

What bone disorder has x linked dominant inheritance

A

hypophophatemia rickets - vit D resistant ricketts, inc wasting of phosphate in proximal tubule, rickets like presentation

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21
Q

characterize mitochondrial inheritance

A

transmitted only through mother, all offspring of affected females may show signs of disease

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22
Q

Give an example of a mitochondrial inherited disease

A

lebers hereditary optic neuropathy - degeneration of retinal ganglion cells and axons - leads to acute loss of central vision. Mitochondrial myopathies

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23
Q

cell signaling defect of fibroblast growth factor (FGF) receptor 3, results in dwarfism, short limbs, head/trunk nl size, associated with advanced paternal age

A

achondroplasia

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24
Q

bilateral, massive enlargement of of kidneys due to multiple large cysts

A

ADPKD

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25
Q

How does patients present with ADPKD

A

flank pain, hematuria, HTN, progressive renal failure

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26
Q

90% of ADPKD cases are due to a mutation in what gene

A

APKD1 on chromosome 16

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27
Q

ADPKD is associated with what additional conditions

A

polycystic liver disease, berry aneurysm, mitral valve prolapse

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28
Q

colon becomes covered witih adenomatous polyps after puberty, progresses to colon cancer unless resected

A

FAP

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29
Q

FAP is due to deletion on what gene on what chromosome

A

APC on chromosome 5

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30
Q

elevated LDL due to defective or absent LDL receptor - heterozygotes have cholesterol ~300, homozygotes ~700

A

familial hypercholesterolemia, hyperlipidemia type IIA

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31
Q

What are the complications/signs of familial hypercholesterolemia

A

sever atherosclerotic disease early in life, and tendon xanthomas on the achilles, MI may develop before 20

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32
Q

telangiectasia, recrrent epistaxis, skin discolorations, AVMs

A

hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

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33
Q

spheroid RBCs due to spectrin or ankyrin defect, hemolytic anemia, inc MHCH, splenectomy is curative

A

hereditary spherocytosis

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34
Q

depression, progressive dementia, choreiform movements, caudate atrophy and dec levels of GABA and ACH in the brain

A

Huntingtons

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35
Q

What trinucleotide repeat in Huntingtons and what chromosome is it found on

A

CAG, 4

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36
Q

fibrillin defect leading to connective tissue disorder affecting skeleton, heart, and eyes

A

marfans

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37
Q

what findings are associated with marfans

A

tall with long extremeties, pectus excavatum, hyperextensive joints, arachnodactyly

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38
Q

Describe the pathophys of the aorta in a pt with marfans, and the eyes

A

cystic medial necrosis of aorta leading to aortic incompetence and dissecting aortic aneurysms, floppy mitral valve, subluxation of lenses

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39
Q

several distinct syndromes characterized by familial tumors of endocrine glands including pancreas, parathyroid, pituitary, thryoid and adrenal medulla - disorders and gene association

A

MEN - 2A and 2B with ret gene

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40
Q

café au lait spots, neural tumors, lisch nodules, skeletal disorders, optic pathway gliomas

A

neurofibromatosis type 1 (von Recklinghausens disease)

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41
Q

What chromosome is the NF gene on

A

17, 17 letters in von Recklinghausen

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42
Q

bilateral acoustic schwannomas, juvenile cataracts

A

NF2 on chromosome 22

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43
Q

facial lesions, hypopigmented “ash leaf spots,” cortical and retinal hamartomas, seizures, mental retardation, renal cysts, renal angiomyolipomas, cardiac rhabdomyomas, inc risk of astrocytomas

A

tuberous sclerosis

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44
Q

deletion of VHL gene on chromosome 3 leading to hemangioblastomas of retina/cerebellum/medulla bilateral RCC - dz and overexpression product

A

von hippel lindau, 3

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45
Q

What do albinism, ARPKD, CF, glycogen storage diseases, hemochromatosis, mucopolysaccharidoses (except Hunters) PKU, sickle cell, sphingolipodoses (except Fabrys) thalassemias have in common

A

autosomal recessive diseases

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46
Q

CF, is AR deletion in what gene on what chromosome resulting in a deletion inf what

A

CFTR gene, 7, Phe 508

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47
Q

What does the CFTR channel do in the lungs, GI tract and skin

A

active secretion in lungs and GI, reabsorbs in skin

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48
Q

What does a defective Cl channel do

A

secretion of abnl thick mucus that plugs lungs, pancreas, liver

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49
Q

recurrent pulmonary infxns in CF are due to what organisms

A

pseudomonas and s aureus

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50
Q

What are the results of pancreatic insuff in CF

A

malabsorption and steatorrhea (ADEK)

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51
Q

What are the results of CF on male fertility

A

males are infertile due to bilateral absence of vas deferens

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52
Q

How do you diagnose CFTR

A

inc Cl- in sweat

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53
Q

What does the mutation in the gene cause in protein synthesis

A

abnormal protein folding, degradation before reaching cell surface

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54
Q

What is the TX for CF and what does it do

A

N-acteylcysteine, cleave disulfide bonds within mucus glycoproteins

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55
Q

Name as many x-linked recessive disorders as you can

A

bruton’s agammaglobulinemia, wiskott-aldrich, fabrys disease, G6PD def, ocular albinism, Lesch-Nyhan syndrome, Duchenne and Becker Muscular Dystrophy, hunter’s syndrome, hemophilia A and B

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56
Q

What leads to the deletion of the dystrophin gene in duchenne’s muscular dystrophy

A

x linked frame shif mutation

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57
Q

what does the deletion of the dystrophin gene lead to

A

accelearted muscle breakdown

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58
Q

What is pseudohypertrophy in the calf a result of, and what are the cardiac manifestations

A

fibrofatty replacement of muscle, cardiac myopathy

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59
Q

What is Gowers maneuver

A

assistance of upper extremities to stand up

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60
Q

What is the mutation in beckers muscular dystrophy, what is the severity and time of onset

A

mutated dystrophin gene, less severe, adolescence

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61
Q

What is the physiologic role of dystrophin

A

anchor muscle fibers, primarily in skeletal and cardiac muscle

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62
Q

What is used to diagnose muscular dystrophies

A

inc CPK and muscle biopsy

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63
Q

what gene is implicated in fragile X syndrome, and what is the mutation

A

FMR1 gene, methylation, associated with chromosomal breakage

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64
Q

What are the physical findings of fragile x syndrome

A

mental retardation, macro-orchidism, long face with large jaw, large everted ears, autism, and mitral valve prolapse

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65
Q

What is the trinucleotide repeat in fragile X

A

CGG

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66
Q

trinucleotide repeat for huntingtons

A

CAG

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67
Q

trinucleotide repeat fo myotonic dystrophy

A

CTG

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68
Q

nucleotide repeat for fragile x

A

CGG

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69
Q

nucleotide repeat for fredreich’s ataxia

A

GAA

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70
Q

What are the findings in Down’s syndrome

A

mental retardation, flat facies, prominent epicanthal folds, simian crease, gap between 1st 2 toes, duodenal atresia, congenital heart disease (ASD), inc risk of ALL and Alzheimers

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71
Q

What causes Down syndrome

A

meiotic nondisjunction of homologous chromosomes (associated with advanced maternal age) leading to trisomy 21

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72
Q

A small proportion of Down syndrome is due to what two genetic events

A

robertsonian translocation and mosaicism

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73
Q

What are the fetal screening measures for Down

A

dec AFP, inc betahCGH, dec estradiol, inc inhibin - inc nuchal translucency on US

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74
Q

What causes Edwards syndrome and what is it

A

trisomy 18, severe mental retardation, rocker bottom feet, micrognathia, low set ears, clenched hands, prominent occiput, congenital heart disease, death usually within the first year

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75
Q

What causes patau’s syndrome and what is it

A

trisomy 13, severe mental retardation, rocker bottom feet, micophthlamia, microcephaly, cleft lip/palate, holoprosencephaly, polydactyly, congenital heart disease, death usually within the first year

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76
Q

Describe robertsonian translocation

A

nonreciprocal chromosomal translocation that commonly involves chromosome pairs 13, 14, 15, 21, 22

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77
Q

Do balanced translocations cause abnl phenotype

A

no

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78
Q

What are the results of unbalanced translocation

A

miscarriage, stillbirth, chromosomal imbalance (down, patau)

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79
Q

congenital microdeletion of short arm of chromosome 5 with microcephaly, moderate to severe mental retardation, high pitched crying/meying, epicanthal folds, cardiac abnl

A

cri du chat

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80
Q

congenital microdeletion of long arm of chromosoe 7 with findings of elfin facies, mental retardation, hypercalcemia, well developed verbal skills, extreme friendliness with strangers, cardiovascular problems

A

williams syndrome

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81
Q

What does CATCH 22 stand for and what causes is

A

aberrant 3rd and 4th branchial arches causing 22q11 deletion - cleft palate, abnl facies, thymic dysplasia, cardiac defects, hypocalcemia secondary to parathyroid aplasia

82
Q

What defects characterize DiGeorge syndrome

A

thymic, parathyroid and cardiac

83
Q

What defects characterize velocardiofacial syndrome

A

palate, facial and cardiac defects

84
Q

What are the fat soluble vitamins and what does their absorption depend on

A

ADEK, dependent on gut (ileum) and pancreas -accumulate in fat and can cause toxicity

85
Q

Broadly, what can cause fat-soluble vitamin deficiencies

A

malapsorption syndromes like sprue or CF or mineral oil intake

86
Q

What are the water soluble vitamins, which ones are stored

A

B(1, 2, 3, 5, 6, 12) C, biotin and folate (B12 and folate are stored)

87
Q

What do B-complex vitamin deficiencies often result in

A

dermatitis, glossitis, and diarrhea

88
Q

What are the functinos of vitamin A

A

antioxidant, constituent of visual pigment, essential for nl differntiation of epithelial cells into specialized tissue (pancreatic cells, mucus secreting cells) used to treat measles

89
Q

What are the symptoms of vit A def

A

night blindness, dry skin

90
Q

What are the symptoms of vit A excess

A

athralgias, fatigue, headaches, skin changes, sore throat, alopecia

91
Q

What are the teratogenic effects of vit A and what test must be ordered before starting a woman on isotreitinoin for severe acne

A

cleft palate, cardiac abnl, pregs test

92
Q

What is Retin A used topically for

A

wrinkles and acne

93
Q

Where is vit A found in the diet

A

liver and leafy veggies

94
Q

What is the name and function of vit B1

A

thiamine, in thiamine pyrophosphate a cofactor for pyruvate dehydrogenase (glycolysis), alpha ketoglutarate dehydrogenase (TCA cycle), transketolase (HMP shunt), and branched-chain AA dehydrogenase

95
Q

What is the results of vit B1 def

A

impaired glucose breakdown leading to ATP depletion; highly affected aerobic tissues like brain and heart affected first

96
Q

What 3 syndromes are associated with vit B1 def

A

wernicke-korsakoff, dry and wet beriberi

97
Q

What is the wernicke-korsakoff clinical picture

A

confusion, opthalmoplegia, ataxia, confabulation, personality changes and memory loss

98
Q

What neuroanatomical strutures are injured in wernicke-korsakoff

A

medial dorsal nucleus of thalamus, mamillary bodies

99
Q

What happens with dry beriberi

A

polyneuritis, symmetrical muscle wasting

100
Q

What happens with wet beriberi

A

high output cardiac failure, dilated cardiomyopathy, edema

101
Q

What is the name and function of vit B2

A

riboflavin, cofactor in oxidation and reduction (FAD and FMN are derived from riboflavin)

102
Q

What happens in vit B2 def

A

cheilosis - inflammation of lips, scaling and fissures at the corner of the mouth, corneal vascularization

103
Q

What is the name is fxn of vit B3

A

niacin, constituent of NAD and NADP, derived from tryptophan

104
Q

Synthesis of vit B3 requires what other vitamin

A

B6

105
Q

What does vit B3 def result in

A

glossitis - severe = pellagra - diarrhea, dermatitis, dementia

106
Q

what disease can cause pellagra

A

hartnup disease - dec tryptophan absoprtion, malignant carcinoid syndrome (inc tryptopha metabolism) and INH (dec vit B6)

107
Q

What can excess vit B3 cause

A

facial flushing

108
Q

What can vit B3 be used to treat

A

hyperlipidemia

109
Q

What is the name and fxn of vit B5

A

pantothenate, essential component of CoA, a cofactor for acyl transfers and fatty acid synthase

110
Q

What is the result of vit B5 def

A

dermatitis, enteritis, alopecia, adrenal insuff

111
Q

What is the function and name of vit B6

A

pyroxidine, converted to pyroxidine phosphate a cofactor used in transamination, decarboxylation, glycogen phosphorylase, cystathionine synthesis and heme synthesis - required for synthesis of niacin and tryptophan

112
Q

What is the result of vit B5 def

A

convulsions, hyperirritability, peripheral neuropathy, deficiency inducible by INH and oral contraceptives, sideroblastic anemais

113
Q

What is the name and fxn of vit B12

A

cobalamin - cofactor of homocysteine and methyltransferase, methylmalonyl CoA mutase

114
Q

Where is vit B12 found

A

animal products, synthesized only by microorganisms, large reserve pool, mainly in liver

115
Q

What happens in a B12 def

A

macrocytic, megaloblastic anemia, hypersegmented PMNs, neurologic symptoms, (parasthesias, subacute combined degeneration) due to abnl myelin, prolonged becomes irreversible

116
Q

What causes B12 def

A

malabsorption (sprue, enteritis) lack of intrinsic factor from pernicious anemia, gastric bypass surgery or absence of terminal ileum as in Crohns

117
Q

Infection with what organism can cause B12 def

A

diphyllobothrium latum

118
Q

What test is used for B12 def

A

Schilling test

119
Q

What is the function of folic acid

A

converted to THF, a coenzyme for one-carbon transfer/methylation reactions, important for synthesis of nitrogenous bases in DNA and RNA

120
Q

What is the main source of folate

A

foliage, small reserve in liver, eat green leaves

121
Q

What happens in folate def

A

macrocytic, megaloblastic anemia, no neurologic sx, most common vit def in the US, seen in EtOH and pregs

122
Q

What drugs can cause folate def

A

phenytoin, MTX, and sulfonamides

123
Q

Giving folate during early pregnancy is important to prevent what birth defects

A

neural tube

124
Q

What components come together to make S-adenosyl methionine

A

ATP and methionine

125
Q

What does SAM do

A

transfers methyl units

126
Q

What is regeneration of methionine depedent on

A

B12 and folate

127
Q

What catacholamine step is SAM required for

A

conversion of NE to epi

128
Q

What is the function of biotin

A

cofactor of carboxyltion enzymes: pyruvate carboxylase, acetate-CoA carboxylase, and propionyl-CoA carboxylase

129
Q

What substance in egg whites binds biotin

A

Avidin

130
Q

pyruvate carboxylase catalyzes what rxn

A

pyruvate to oxaloacetate (3C to 4C)

131
Q

Acetyl-CoA carboxylase catalyzes what rxn

A

acetyl-CoA to malonyl-CoA (2C to 3C)

132
Q

What rxn does propionyl-CoA carboxylase catalyze

A

propionyl-CoA to methylmalonyl-CoA (3C to 4C)

133
Q

What does biotin def cause

A

dermatitis, alopecia, enteritis

134
Q

What causes biotin def

A

antibiotic use or excessive ingestion of raw eggs

135
Q

What are the names and sources of the two types of vit D found in nature

A

D2 = ergocalciferol -ingested from plants D3 = cholecalciferol - ingested from milk, formed in sun exposed skin

136
Q

How is vit D stored

A

25OHD3

137
Q

What is the active form of vit D

A

1,25 OH2 D3 = calcitriol

138
Q

What is the fxn of vit D

A

inc intestinal absorption fo calcium and phosphate, inc bone resorption

139
Q

What happens in vit D def

A

rickets in kids -bending bones, osteomalacia in adults, hypocalcemia tetany, breast milk has dec vit D (supplement in dark skinned patients)

140
Q

What happens in vit D excess

A

hypercalciuria, loss of appetite, stupor, seen in sarcoidosis from activation fo vit D by epithelioid macrophage

141
Q

What are the function of vit C

A

antioxidant, facilitates iron absorption by keeping iron in the Fe2+ reduced state, necessary for hydroxylation of proline and lysine collagen bridges, necessary for dopamine beta hydroxylase which converts DA to NE

142
Q

What does vit C def cause

A

scurvy - swollen gums, bruising, hemarthrosis, anemia, poor wound healing, weakened immune response

143
Q

What is the fxn of vit E

A

antioxidant, protects RBCs and membrances from free radical damage

144
Q

What does vit E def cause

A

inc fragility of RBC, hemolytic anemia, muscle weakness, posterior column and spinocerebellar tract demyelination

145
Q

What is the fxn of vit K

A

gamma carboxylation of glutamic acid residues on various proteins concerned with blood clotting, synthesized in intestinal flora

146
Q

What clotting factors require vit K

A

II, VII, IX, X (1972) protein C and S

147
Q

What happens in vit K def

A

neonatal hemorrhage with inc PT and PTT, but nl bleeding time, can also occur after prolonged use of broad spectrum Abx

148
Q

How does warfarin work

A

vit K antagonist

149
Q

What is the function of Zinc

A

essential for the activity of over 100+ enzymes, important in the formatio of zinc fingers,

150
Q

What happens in zinc def

A

delayed wound healing, hypogonadism, dec in adult hair, dysguesia, anosmia, may predispose to EtOH cirrhosis

151
Q

What two enzymes are involved in EtOH metabolism

A

EtOH dehydrogenase and acetaldehyde dehydrogenase

152
Q

Where is EtOH dehydrogenase located

A

cytosol

153
Q

Where is acetaldehyde located

A

mitochondria

154
Q

What is the limiting reagent in EtOH metabolism

A

NAD+

155
Q

What order kinetics does EtOH dehydrogenase have

A

zero

156
Q

what does fomepizole do

A

inhibits EtOH dehydrogenase and is an antidote for methanol and ethylene glycol poisoning

157
Q

What is disulfiram used for

A

inhibits acetaldehyde dehydrogenase and contributes to hangover symptoms

158
Q

how does ethanol induce hypoglycemia

A

inc NADH/NAD ratio in liver, causing diversion of pyruvate to lactate and OAA to malate, inhibiting gluconeogenesis and stimulating fatty acid synthesis. Leads to hypoglycemia and hepatic fatty liver change seen in chronic EtOH users

159
Q

protein malnutrition resulting in skin lesions, edema and liver malfxn

A

kwashiorkor - small child with swollen belly

160
Q

energy malnutrition resulting in tissues and muscle wasting, loss of subQ fat, variable edema

A

marasmus - muscle wasting

161
Q

What metabolic rxns occur in the mitochondria

A

fatty acid oxidation, acetyl-Coa production, TCA cycle, OXPHOS

162
Q

What metabolic rxns occur in the cytoplasm

A

glycolysis, fatty acid synthesis, HMP shunt, protein synthesis (RER), steroid synthesis (SER)

163
Q

What metabolic rxns occur in both the cytoplasm and mitochondria

A

heme synthesis, urea cycle and gluconeogenesis - HUGs take two

164
Q

what does a kinase do

A

uses ATP to add high energy phophate group onto substrate

165
Q

What does a phosphorylase do

A

adds an inorganic phosphate onto substrate without using ATP

166
Q

what does a phosphatase do

A

removes phosphate group from substrate

167
Q

what does a dehydrogenase do

A

oxidizes substrate

168
Q

what does a carboxylase do

A

adds 2 carbon with the help of biotin

169
Q

What is the rate determining enzyme (RDE) of glycolysis

A

phosphofructokinase 1

170
Q

What is the RDE of gluconeogenesis

A

fructose 1,6 bisphosphate

171
Q

What is the RDE of TCA cycle

A

isocitrate dehydrogenase

172
Q

What is the RDE of glycogen synthesis

A

glycogen synthase

173
Q

What is the RDE of glycogenolysis

A

glycogen phosphorylase

174
Q

What is the RDE of the HMP shunt

A

glucose 6 phosphate dehydrogenase (G6PD)

175
Q

What is the RDE of de novo pyrimidine synthesis

A

carbomoyl phosphate synthetase II

176
Q

What is the RDE of de novo purine synthesis

A

glutamine PRPP amidotransferase

177
Q

What is the RDE of the urea cycle

A

carbomoyl phosphate synthetase I

178
Q

What is the RDE of fatty acid synthesis

A

Acetyl-CoA carboxylase (ACC)

179
Q

What is the RDE of fatty acid oxidation

A

carnitine acyltransferase I

180
Q

What is the RDE of ketogenesis

A

HMG-CoA synthase

181
Q

What is the RDE of cholesterol synthesis

A

HMG-CoA reductase

182
Q

How many ATP are created by aerobic metabolism of glucose in the heart and liver via what shuttle

A

32, malate aspartate shuttle

183
Q

How many ATP are created by aerobic metobolism of glucose in muslce via what shuttle

A

30, glycerol-3-phosphate shuttle

184
Q

How many ATP are produced by anearobic glycolysis per molecule of glucose

A

two

185
Q

How is ATP used by the cell

A

ATP hyrdolysis couple to energetically unfavorable rxns

186
Q

What is the activated carrier for phosphoryl

A

ATP

187
Q

What is the activated carrier for electrons

A

NADH, NADPH, FADH2

188
Q

What is the activated carrier for Acyl

A

coenzyme A, lipoamide

189
Q

What is the activated carrier for Co2

A

biotin

190
Q

What is the activated carrier for 1 carbon units

A

THFs

191
Q

What is the activated carrier for methyl groups

A

SAM

192
Q

What is the activated carrier for aldehyddes

A

TTP

193
Q

What is NAD+ generally used for

A

catabolic processes to carry reducing equivalents away as NADH

194
Q

What is NADPH used for

A

anabolic processes as a supply of reducing equivalents

195
Q

What produces NADPH

A

HMP shunt

196
Q

NADPH are used in what 4 things

A

anabolic processes like steroid and fatty acid synthesis, respiratory burst, P-450, glutathione reductase

197
Q

phosphorylation of glucose to yield glucose 6 phosphate serves as the 1st step of what rxns and what enzymes catalyze it

A

glycolysis and the glycogen synthesis in the liver - hexokinase or glucokinase

198
Q

Where is hexokinase found, what is its Km and Vmax and what uninduces it

A

ubiquitous, low Km, high affinity, low capacity low Vmax, uninduced by insulin

199
Q

Where is glucokinase found, what are the Km and Vmax, and what induces it

A

liver and beta cells of pancreas, low affinity, high Km, high capacity, high Vmax, induced by insulin

200
Q

What feedback inhibits hexokinase

A

glucose-6 phosphate

First Aid Biochem (3 decks)

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