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USMLE STEP 1 > Biochem > Flashcards

Biochem Flashcards

1
Q

what amino acids are histones rich in?

A

lysine and arginine (+ charged)

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2
Q

what ties nucleosome beads together on a string?

A

H1 (the only histone that is not in a nucleosome core)

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3
Q

What is methylated during DNA replication

A

template strand cytosine and adenine (allows for mismatch repair)

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4
Q

What inactivates transcription of DNA

A

histone methylation

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5
Q

What relaxes DNA coiling, allowing for transcription?

A

histone acetylation

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6
Q

nucleotides with 2 rings

A

purines (A, G)

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7
Q

nucleotides with 1 ring

A

pyrimidines (C, U, T)

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8
Q

which nucleotide has a ketone?

A

guanine

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9
Q

which nucleotide has a methyl?

A

thymine

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10
Q

what makes uracil?

A

deamination of cytosine

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11
Q

amino acids necessary for purine synthesis

A

GAG (glycine, aspartate, glutamate) and THF

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12
Q

nucleoside

A

base + ribose

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13
Q

nucleotide

A

base + ribose + phosphate (linked by 3-5 phosphodiester bond)

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14
Q

de novo purine synthesis

A

start with sugar + PRPP, add base

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15
Q

de novo pyrimidine synthesis

A

make temporary base (orotic acid), add sugar + PRPP, modify base

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16
Q

what is required for pyrimidine base production

A

aspartate

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17
Q

what is carbamoyl phosphate involved in?

A

de novo pyrimidine synthesis and urea cycle

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18
Q

ornithine transcarbamoylase deficiency

A

accumulation of carbamoyl phosphate, which is then converted to orotic acid; hyperammonemia

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19
Q

hydroxyurea

A

interferes with nucleotide synthesis, inhibits ribonucleotide reductase

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20
Q

6-MP

A

blocks de novo purine sunthesis

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21
Q

5-FU

A

inhibits thymidylatesynthase

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22
Q

methotrexate

A

inhibits dihydrofolate reductase

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23
Q

trimethoprim

A

inhibits bacterial dihydrofolate reductase

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24
Q

what is defective in orotic aciduria?

A

de novo pyrimidine synthesis (can’t convert orotic acid to UMP) because of defect in UMP synthase (phosphoribosyltransferase or orotidine-5-phosphate decarboxylase)

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25
Q

orotic aciduria inheritance

A

autosomal recessive

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26
Q

orotic aciduria treatment

A

oral uridine administration

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27
Q

increased orotic acid in urine, megaloblastic anemia (doesn’t improve with administration of B12 or folic acid), failure to thrive, no hyperammonemia, needle-shaped crystals in urine

A

orotic aciduria

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28
Q

excess ATP and dATP that inhibits ribonucleotide reductase–>prevents DNA synthesis–>decreases lymphocyte count

A

adenosine deaminase deficiency (major cause of SCID)

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29
Q

adenosine deaminase deficiency inheritance

A

autosomal recessive

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30
Q

defective purine salvage due to defective HGPRT–>excess uric acid production

A

Lesch-Nyhan syndrome

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31
Q

Lesch-Nyhan syndrome inheritance

A

autosomal recessive

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32
Q

retardation, self-mutilation, aggression, hyperuricemia, gout, choreoathetosis (spastic cerebral palsy)

A

Lesch-Nyhah syndrome

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33
Q

Lesch-Nyhan syndrome treatment

A

allopurinol (inhibits xanthine oxidase–>reducesgouty arthritis)

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34
Q

which amino acids are encoded by only 1 codon?

A

methionine, tryptophan

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35
Q

splice site mutation

A

frequently results in production of larger proteins with altered function but preserved immune reactivity

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36
Q

unwinds DNA template at replication fork

A

helicase

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37
Q

prevent strands from reannealing during DNA replication

A

SSBP

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38
Q

fluoroquionolones

A

inhibit DNA gyrase (prokaryotic topoisomerase II)

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39
Q

primase

A

makes RNA primer on which DNA polymerase III can initiate replication

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40
Q

DNA polymerase III

A

prokaryotic only; 5–>3 synthesis, 3–>5 exonuclease

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41
Q

degrades RNA primer and replaces it with DNA

A

DNA polymerase I (prokaryotic)

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42
Q

5–>3 exonuclease activity

A

DNA polymerase I

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43
Q

repairs bulky, helix-distorting lesions

A

nucleotide excision repair

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44
Q

endonucleases that release oligonucleotide-containing damaged bases

A

nucleotide excision repair

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45
Q

absence of UV-specific adonuclease

A

xeroderma pigmentosum (mutated nucleotide excision repair)

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46
Q

glycosylases that recognize and remove damaged bases; important in repair of spontaneous/toxic deamination

A

base excision repair

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47
Q

defective 3–>5 exonuclease activity (defective mismatch repair)

A

hereditary nonpolyposis colorectal cancer

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48
Q

mutated homologous end-joining

A

ataxia telangiectasia

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49
Q

stop codons

A

UGA, UAA, UAG

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50
Q

what makes rRNA

A

RNA polymerase I

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51
Q

what makes mRNA

A

RNA polymerase II (opens DNA at promoter site)

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52
Q

what makes tRNA

A

RNA polymerase III

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53
Q

alpha amanitin

A

found in Amanita phalloides, inhibits RNA polymerase II

54
Q

antibodies to spliceosomal snRNP

A

SLE

55
Q

CCA at 3 end

A

tRNA

56
Q

tertacycline MOA

A

bind 30S preventing attachment of aminoacyl-tRNA

57
Q

prokaryotic 16S rRNA

A

contains sequence complimentary to shine-delgarno sequence on mRNA

58
Q

initiation of protein synthesis

A

activated by GTP hydrolysis

59
Q

aminoglycosides MOA

A

bind 30S and inhibit formation of initiation complex

60
Q

chloramphenicol MOA

A

binds 50S and inhibits peptidyl transferase

61
Q

macrolides MOA

A

bind 50S and prevent release of uncharged tRNA

62
Q

p27 protein

A

cell cycle inhibitor, acts during G1, inhibits CDK

63
Q

CDKs

A

constitutive and inactive

64
Q

main tumor suppressors

A

p53 and hypophosphorylated Rb (inhibit G1-to-S)

65
Q

permanent cells

A

neurons, skeletal and cardiac muscle, RBCs

66
Q

stable cells

A

hepatocytes, lymphocytes

67
Q

rER

A

site of synthesis of secretory proteins, N-linked oligosaccharide addition, synthesize lysosomal proteins

68
Q

Golgi

A

modifies N-oligosaccharide on asparagine, sdds O-oligosaccharides on serine and threonine, ads mannose-6-P for trafficking to lysosomes

69
Q

I-cell disease

A

lysosomal storage disorder, failure of addition of mannose-6-P to lysosome proteins; abnormal N-acetyl glucosaminotransferase in Golgi

70
Q

coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes

A

I-cell disease

71
Q

where does catabolism of very long f.a. and a.a. occur?

A

peroxisome

72
Q

organelle necessary for heme synthesis

A

mitochondria

73
Q

what are microtubules incorporated in

A

flagella, cilia, mitotic spindles

74
Q

retrograde to microtubule

A

dynein

75
Q

anterograde to microtubule

A

kinesin

76
Q

drugs that act on microtubules

A

mebendazole/thiabendazole (antihelminthic), griseofulvin (antifungal), vincristine/vinblastine, paclitaxel (anti-breast cancer), colchicine

77
Q

chediak-higashi syndrome

A

mutation in lysosomal trafficking regulator gene (product is required for microtubule-dependent sorting of endosomal proteins into late multivesicular endosomes)

78
Q

recurrent pyogenic infections, partial albinism, peripheral neuropathy

A

cheidak-higashi syndrome

79
Q

9+2 arrangement of microtubules

A

cilia

80
Q

kartagener’s syndrome

A

immotile cilia due to dynein arm defect

81
Q

male infertility, decreased female fertility, bronchiectasis, recurrent sinusitis, associated with situs inversus

A

kartagener’s syndrome

82
Q

actin and myocin structures

A

microvilli, muscle contraction, cytokinesis, adherens junctions

83
Q

microtubule structures

A

centrioles

84
Q

vimentin stain

A

CT

85
Q

desmin stain

A

muscle

86
Q

cytokeratin stain

A

epithelial cells

87
Q

GFAP stain

A

neuroglia

88
Q

neurofilament stain

A

neurons

89
Q

chromogranin A and enolase stain

A

neuroendocrine

90
Q

MPO stain

A

myeloid cells

91
Q

ouabain

A

inhibits Na/K pump by binding to K site

92
Q

digoxin and digitoxin

A

inhibit Na/K pump–>inhibition of Na/Ca exchange–>increased intracellular Ca–>increased cardiac contractility

93
Q

most abundant protein in body

A

collagen

94
Q

type I collagen

A

bone, skin, tendon, cornea, late wound repair, defective in osteogenesis imperfecta

95
Q

type II collagen

A

cartilage, vitreous body, nucleus pulposus

96
Q

type III collagen

A

reticulin: skin, blood vessels, uterus, fetal tissue, granulation tissue. Defective in ehlers-danlos

97
Q

type IV collagen

A

basement membrane. Defective in Alport syndrome

98
Q

fine skin wrinkles

A

appear secondary to decreased synthesis and net loss of dermal collagen and elastin

99
Q

the most abundant a.a. in collagen

A

glycine

100
Q

collagen synthesis inside fibroblasts

A

translation of alpha chain Gly-X-Y (proline or lysine); hydroxylation of proline and lysine (requires vitamin C); glycosylation and triple helix formation (defect–>osteogenesis imperfecta); exocytosis

101
Q

collagen synthesis outside fibroblasts

A

cleavage of disulfide-rich terminal–>insoluble tropocollagen;c terminal propeptide removal; covalent lysine-hydroxylysine cross-linkage (need Cu; defect–>ehlers-danlos)

102
Q

osteogenesis imperfecta

A

autosomal dominant with abnormal type I collagen

103
Q

multiple fractures, blue sclera (translucency of CT over choroidal veins), hearing loss, small teeth (lack of dentin)

A

osteogenesis imperfecta; defective bone metrix formation

104
Q

ehlers-danlos syndrome

A

hyperextensible skin, tendency to bleed, hypermobile joints, berry aneurysms, organ rupture

105
Q

alport syndrome

A

abnormal type IV collagen, usually X-linked recessive

106
Q

progressive hereditary nephritis and deafness, associated with ocular disturbances

A

alport syndrome

107
Q

which a.a. is elastin rich in?

A

proline and glycine (nonhydroxylated forms)

108
Q

elastin

A

cross-linking takes place extracellularly; broken down by elastase (inhibited by alpha1 antitrypsin)

109
Q

marfan’s syndrome

A

defect in fibrillin (extracellular matrix protein)

110
Q

elastin’s plasticity and ability to recoil

A

attributable to desmosine cross-linking between lysine residues

111
Q

best method for determining whether a gene is being expressed

A

northern blot

112
Q

southwestern blot

A

identifies DNA-binding proteins

113
Q

microarrays

A

used to profile gene expression levels, detect SNPs

114
Q

indirect ELISA

A

uses test antigen to see if Ab is present

115
Q

direct ELISA

A

uses test Ab to see if antigen is present

116
Q

FISH

A

used for specific localization of genes

117
Q

cre-lox system

A

can inducibly manipulate genes at specific developmental points using Ab-controlled promoter

118
Q

pleitropy

A

one gene contributes to multiple phenotypic effects

119
Q

imprinting

A

differences in gene expression depend on whether mutation is of maternal or paternal origin

120
Q

loss of heterozygosity

A

if there is a mutation in tumor suppressor gene, complementary allele must be deleted before cancer develops

121
Q

chimeric pt

A

derived from 2 zygotes that subsequently fuse

122
Q

locus heterogeneity

A

mutations at different loci can produce the same phenotype

123
Q

heteroplasmy

A

presence of both normal and mutated mtDNA

124
Q

mitochondrial syndromes

A

leber hereditary optic neuropathy: bilateral vision loss; myoclonic epilepsy with ragged red fibers: myoclonic seizures and myopathy associated with exercise; MELAS

125
Q

uniparental disomy

A

2 copies of a chromosome from 1 parent. heterodisomy–> meiosis 1 error; isodisomy–>meiosis 2 error or postzygotic chromosomal duplication. Prader-Willi, Angelman

126
Q

frequency of X-linked recessive disease

A

males=q, females=q2

127
Q

prader-willi syndrome

A

paternal allele is not expressed (chromosome 15)

128
Q

mental retardation, hyperphagia, obesity, hypogonadism, hypotonia, short stature

A

prader-willi syndrome

129
Q

angelman’s syndrome

A

maternal allele is not expressed (chromosome 15)

130
Q

mental retardation, seizures, ataxia, inappropriate laughter

A

angelman’s syndrome

USMLE STEP 1 (21 decks)

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