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qbank - biochem Flashcards

1
Q

citrullination

A

tissue inflammation -> arginine residues (e.g. in vimentin) are enzymatically converted -> cirulline -> different shape -> immune response b/c they become Ags. this process is exaggerated in RA, so anti-CCP (cyclic citrullinated peptide) Abs = 95-98% specific for RA

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2
Q

anti-centromere Abs

A

found in majority of CREST syndrome

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3
Q

anti-dsDNA

A

specific to SLE

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4
Q

rheumatoid factors

A

auto-Abs that target Fc portion of human IgG. occur in ~80% of RA patients, ~10% of healthy patients, ~30% of SLE, ~100% of mixed cryoglobulinemia and other inflammatory conditions

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5
Q

ANA

A

antinuclear Abs = Abs to nuclear basic proteins = nonspecific finding in many connective tissue d/os. ANAs occur in IgM form in pts w/RA but less frequently than RF.

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6
Q

anti-phospholipid Abs

A

found in pts w/SLE and antiphospholipid Ab syndrome, which -> hypercoagulability, paradoxical PTT prolongation, and recurrent miscarriages

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7
Q

homocystinuria

A

most common inborn error of methionine metabolism. present at age 3-10 w/lens subluxation, intellectual disability (~50%), marfanoid habitus, osteoporosis, and possibly thromboembolic events. typically caused by cystathionine synthetase defficiency, which requires pyridoxine (B6) as a cofactor. B6 -> enzyme activity and dec. homocysteine levels

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8
Q

vit C

A

necessary cofactor for hydroxylation of proline and lysine in collagen.

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9
Q

excess methionine in homocystinuria pts

A

-> inc. plasma homocyseine b/c it can’t be metabolized to cysteine. therefore, Tx of homocystinuria involved methionine restriction

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10
Q

thiamine

A

B1. deficiency -> dry and wet beriberi and wenicke-korsakoff syndrome

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11
Q

tyrosine

A

nonessential AA. precursor for DA, epi, and NE

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12
Q

vit K fxn

A

post-translational conversion of glutamate -> gamma-carboxyglutamic acid = necessary for fxn of many clotting factors and reg. proteins in coag. cascade

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13
Q

aging effects on skin

A

gradual thinning of epidermis, reduced subQ fat, blood vessels, hair follicles, sweat ducts, and sebaceous glands. dec. subQ fat -> skin becomes atrophic, more vulnerable to damage. dec. dermal collagen and elastin -> dec. reticular support -> sagging, wrinkles

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14
Q

fibrillin-1

A

protein found in lots of connective tissues. aids in dev. of extracellular matrix microfibrils -> scaffolding for elastic fiber deposition. inherited defect -> marfans

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15
Q

KATP channels

A

K channels in pancreatic beta cells that close when ATP/ADP ratio is high -> depolarization -> V-gated Ca channels open -> insulin release. ATP is generated when a lot of glucose enters via GLUT-2 transporters. defects in KATP -> T2DM. sulfonylereas close KATP channels

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16
Q

methemoglobin

A

Hb w/Fe3+. can’t bind O2. O2 affinity of remaining Fe2+ Hb is increased -> left shift of dissociation curve. can be caused by nitrates. -> dusky skin discoloration, dec. O2 content, carrying capacity, and % saturation, normal PO2.

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17
Q

receptors w/intrinsic enzyme activity

A

receptor tyrosine kinase. 3 structures: extracellular domain (binds growth factor), transmembrane domain, and cytosolic domain (enzyme) . MAP-kinase signaling: receptor autophosphorylates and triggers phosphorylation of Ras protein. e.g. growth factor receptors: EGF, PDGF, FGF

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18
Q

receptors w/o intrinsic enzyme activity

A

tyrosine-kinase associated receptor. 3 structures: extracellular domain, transmembrane domain, and cytosolic domain (lacks enzymatic activity). JAK/STAT signaling: receptor activates Janus kinases (JAKs), which phosphorylate STATS (signal transducers and activators of transcription. e.g. receptors for cytokines, growth hormone, prolactin, IL-2

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19
Q

folate fxn

A

crucial for DNA synthesis and conversion of vit B12 -> one of its coenzyme forms. necessary for dTMP production, which is needed to supply the four nucleotide precursors of DNA replication. folate deficiency -> megaloblastosis and erythroid precursor cell apoptosis.

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20
Q

thymidine kinase salvage pathway

A

normally makes 5-10% of dTMP

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21
Q

glutamine

A

major source of N in synthesis of nucleotides, so contributes N atom to biosynthesis of dUMP.

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22
Q

beta-thalassemia

A

microcytic anemia, increased Hb F (alpha2gamma2), and Hb A2 (alpha2delta2). hypochromia and poikilocytes, including target cells. Fe supplements don’t help. mutations -> dec. transcription, processing, and translation of beta-globin mRNA: heme synthesis = normal.

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23
Q

elastin structure

A

plasticity and recoil ability are attributable to unique desmosine crosslinking between 4 different lysine residues on 4 different elastin chains. crosslinking is accomplished by action of extracellular lysyl hydroxylase. mostly made of non-polar AAs glycine, alanine, and valine, which some proline and lysine

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24
Q

alpha1-antitrypsin deficiency

A

alpha1-antitrypsin inhibits the action of endogenous proteolytic enzymes that hydrolyze proteins like elastin, particularly neutrophil-secreted elastase. so deficiency -> excessive degradation of elastin in lungs and liver -> panacinar emphysema and cirrhosis

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25
Q

elasin differs from collagen in 3 main ways

A
  1. very few proline and lysine residuese are hydroxylated in elasin
  2. triple helix formation = basis of collagen, NOT elastin
  3. triple helix formation in collagen is initiated by hydroxylation, glycosylation and interchain disulfide bridges at C-terminus of procollagen molecule. these modifications do not occur in elastin formation
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26
Q

scurvy

A

caused by impaired collagen formation: hemorrhages, subperiosteal hematomas, hemearthrosis, gingival swelling, secondary periodontal infection, anemia, hyperkeratotic papular rashes, impaired wound healing, weakened immune response

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27
Q

ascorbic acid fxn

A

accelerates hydroxylation and amidation reactions: activation of prolyl and lysyl hydroxylase precursors, both necessary for hydroxylation of procollagen. collagen contains lots of hydroxyproline, so quantity and quality = reduced by vit. C deficiency

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28
Q

B1

A

thiamine

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29
Q

B2

A

riboflavin. deficiency: cheilosis, stomatitis, glossitis, dermatitis, corneal vascularization, ariboflavinosis

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30
Q

B6

A

pyridoxine. deficiency: cheilosis, glossitis, dermatitis, peripheral neuropathy

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31
Q

zinc deficiency

A

acrodermatitis enteropathica, growth retardation, infertility

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32
Q

pellagra

A

3 Ds: dermatitis (rough, scaly, sun-exposed), diarrhea (columnar epithelium atrophy), dementia (neuronal degeneration in brain and cord). 2/2 niacin (B3) deficiency

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33
Q

niacin

A

B3. essential component of coenzymes NAD and NADP. pivotal role in intermediary metabolism of cells, accepting electrons and donating H+s. metabolism of FAs, AAs, and carbs, critical in HMP shunt. obtained from diet or made from tryptophan. happens w/corn-based diet, alcoholics, and chronic dz (e.g. HIV).

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34
Q

carotene

A

vit A precursor

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35
Q

tyrosine precursor

A

phenylalanine. necessary for catecholamine synthesis.

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36
Q

arginine = precursor of

A

NO, urea, ornithine, agmatine. necessary for creatine formation

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37
Q

orotic acid

A

precursor of pyrimidine. overproduced from carbamoyl phosphate by CPS II when there is a block in the urea cycle. found in OTC deficiency, citrullinemia, and argininosuccinic aciduria

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38
Q

individual subunits of Hb

A

structurally analogous to myoglobin: hyperbolic oxygen-dissociation curve.

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39
Q

left-shifted O2 dissociation curve

A

high O2 affinity Hb (e.g. fetal) or inc. pH, dec. T, or dec. 2,3-diphosphoglycerate

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40
Q

right-shifted O2 dissociation curve

A

low O2 affinity Hb, e.g. dec. pH, inc. T, inc. 2,3-diphosphoglycerate

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41
Q

ubiquitin

A

protein that undergoes ATP-dependent attachment to other proteins, labeling them for degradation. tagged proteins ender proteasome and are degraded -> peptides. important for muscle wasting, cell cycle regulation, DNA repair, disposal of misfolded proteins/enzymes. impairment of this system can contribute to neurodegenerative d/os, e.g. AD and PD

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42
Q

acetylation

A

histone acetylation promotes formation of euchromatin

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43
Q

gamma-carboxylation

A

vit K dependent -> clotting factors II, VII, IX, X, proteins C and S. inhibited by warfarin

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44
Q

glucuronidation

A

step 2 of hepatic processing of bilirubin: conjugation of bilirubin w/glucuronic acid in ER. disrupted in Crigler-Najjar

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45
Q

3 steps of hepatic bilirubin

A
  1. carrier-mediated passive uptake of bilirubin and sinusoidal membrane 2. conjugation of bilirubin w/glucuronic acid in ER 3. active biliary excretion of water-soluble, nontoxic bilirubin-glucuronides
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46
Q

phosphorylation

A

adding a phosphate group: commonly involved in regulation of enzyme activity

47
Q

arginase deficiency

A

arginine -> ornithine and urea. spasticity is commonly mistaken for cerebral palsy. Tx w/low protein, arginine-free diet and administration of synthetic essential AA protein

48
Q

glutamine

A

major AA in blood b/c it transports ammonia from peripheral tissues to kidney. in nephron, amide nitrogen is hydrolyzed by glutaminase to regenerate glutamate and free ammonium, which is excreted in urine

49
Q

homocysteinemia

A

occurs w/vit B6, B12, and folate deficiencies. -> atherosclerosis and thrombotic events

50
Q

gamma-aminobutyrate

A

GABA. inhibits presynaptic transmission in CNS and retina. formed by decarboxylation of glutamate catalyzed by GAD

51
Q

PRPP synthetase abnormality

A

-> gout. often X-linked. PRPP synthetase produces activated ribose necessary for de novo purine/pyrimidine synthesis. mutation -> inc. purine -> inc. degradation -> hyperuricemia

52
Q

gout

A

Sx: 1st metatasophalangeal joint or knee. swelling, erythema, exquisite tenderness. rapid onset. Dx: needle-shaped, negatively birefringent crystals. Tx: NSAIDS. colchicine = 2nd line. can use allopurinol for prevention after acute resolution

53
Q

target of gout Tx

A

neutrophils, which phagocytose crystals and release cytokines and inflammatory mediators -> amplified inflammatory response

54
Q

colchicine MoA

A

impairs neutrophil migration and phagocytosis by interfering w/microtubule formation and decreases neutrophil activation

55
Q

eosinophils

A

defend against parasites. pathogenic in asthma, allergy, hypereosinophilic syndromes, and vasculitides (e.g. chrug-strauss)

56
Q

lymphocytes

A

delayed-type hypersensitivity

57
Q

cromolyn sodium

A

inhibits mast cell degranulation. used to treat asthma and allergies

58
Q

primary structure

A

sequence of AAs linked by covalent peptide-bonds

59
Q

secondary structure

A

alpha-delix or beta-sheet due to H-bonding

60
Q

tertiary structure

A

overall shape protein assumes following compact folding of secondary structure. involves many forces: ionic bonds, hydrophobic interactions, H-bonds, and disulfide bonds

61
Q

disulfide bonds

A

very strong covalent bonds between 2 cysteine residues w/in same polypeptide chain. enhance protein’s ability to withstand denaturation

62
Q

RNA polymerase I

A

produces 18S, 5.8S, and 28S ribosomal RNA. fxn: form essential ribosomal components. only operates in nucleolus

63
Q

RNA polymerase II

A

produces mRNA: translated by ribosome to form specific proteins; small nuclear RNA: involved in mRNA splicing & transcription regulation; and microRNA: causes gene silencing via translation arrest or mRNA degradation. most regulated type of RNA polymerase

64
Q

RNA polymerase III

A

produces tRNA: adaptor molecule linking codons w/specific AAs; 5S rRNA: essential component of 60S ribosomal subunit

65
Q

nucleolus

A

site of ribosomal subunit maturation and assembly. RNA polymerase I synthesizes most rRNA from w/in it

66
Q

endonuclease

A

break phosphodiester bond w/in nucleotide chain in DNA and RNA. important in DNA repair and RNA splicing. present throughout nucleoplasm

67
Q

pigment gallstones

A

10-25% of gallstones in US. more common in rural Asians, women, and elderly. arise 2/2 infection of biliary tract -> release of beta-glucuronidase by injured hepatocytes and bacteria -? hydrolysis of bilirubin glucuronides and inc. unconjugated bilirubin in bile. common biliary pathogens = E coli, ascaris lumbricoides, and liver fluke opishtorchis sinensis

68
Q

desmolase

A

catalyzes formation or destruction of C-C bonds w/in a molecule. plays a role in respiration and fermentation

69
Q

7alpha-hydroxylase

A

converts cholesterol -> bile acids, reducing likelihood of cholesterol gallstones

70
Q

aromatase

A

catalyzes conversion of androgens -> estrogens

71
Q

western blot

A

used to identify specific proteins. 1st, proteins are separated by gel electrophoresis, then transferred to nitrocellulose membrane + probed w/specific Ab. Then washed + treated w/Ab marker.

72
Q

northern blot

A

used to identify specific RNA sequences. separated by gel electrophoresis, transferred to membrane, hybridized w/probe containing complementary mRNA sequence

73
Q

southern blot

A

used to identify specific DNA sequences. DNA is extracted, fragmented using restriction endonucleases, separated by gel electrophoresis, transferred to membrane, cross-linked to membrane w/UV exposure, hybridized w/complementary probe. mutations at restriction sites alter DNA fragment lengths, altering electrophoresis migration patterns

74
Q

southwestern blot

A

used to identify DNA-binding proteins. similar to southern and western technique. DNA-binding proteins are recognized by their ability to bind specific oligonucleotide probes

75
Q

microarray

A

similar to southern and northern blot, but involves hybridization of large number of probes at once.

76
Q

gluconeogenesis

A

becomes principal energy source after 12-18 hrs of fasting. uses many bidirectional enzymes involved in glycolysis. initial committed step = conversion of pyruvate -> oxaloacetate, then oxaloacetate to phophoenolpyruvate.

77
Q

glycogenolysis

A

lasts only until glycogen stores are depleted: 12-18 hrs. first step = breakage of 1-4 glycosidic linkage -> G1P.

78
Q

palmitic acid

A

1st fatty acid produced from acetyl CoA during lipogenesis in fed state. during prolonged fasting, lipolysis -> generation of glycerol and FAs.

79
Q

lac operon

A

= lactose operon. regulated by 2 distinct mechanism: negatively by binding of the repressor protein to the operator locus and positively by cAMP-CAP binding upstream from the promoter region. constitutive expression of the structural genes of the lac operon occurs w/mutations that impair the binding of the repressor protein (Lac I) to its regulatory sequence in the operator region

80
Q

nitrogen carriers

A

alanine and glutamine

81
Q

glutamine

A

produced by most body tissues, catabolized by gut and kidney for maintenance of cellular metabolism and acid-base regulation. can be converted -> alanine -> bloodstream

82
Q

glucose-alanine cycle

A

helps remove excess nitrogen. glucose is converted -> alanine by muscle to pick up nitrogen from catabolized AAs. the liver then converts this alanine into glucose and urea

83
Q

alpha-ketoglutarate

A

accepts the amino group in almost all aminotransferase rxns, including alanine aminotransferase. amino groups are funneled from alanine to glutamate during protein catabolism.

84
Q

heme oxygenase

A

converts heme -> biliverdin, a pigment that makes buises greenish after several days

85
Q

ferrochelatase

A

final enzyme in heme synthesis. inhibited by lead.

86
Q

uroporphyrinogen decarboxylase

A

enzyme in heme synthetic pathway that is defective in the most common type of porphyria, PCT

87
Q

bilirubin glucuronyl transferase

A

enzyme necessary for conjugation of bilirubin to glucuronic acid. problems with this enzyme (genetic or drugs) impairs liver’s ability to conjugate bilirubin

88
Q

methemoglobin reductase

A

catalyzes reduction of methemoglobin to hemoglobin via NADH oxidation. unclear physiological significance. activated by methylene blue

89
Q

methionine formation

A

methyl-tetrahydrofolate donates a methyl group to homocystine to form methionine and tetrahydrofolate. cobalamin (B12) is a necessary cofactor. tetrahydrofolate rapidly accepts 1C moieties and re-enters cycle. so in B12 deficiency, tetrahydrofolate can’t be regenerated, impairing folate metabolism

90
Q

why does B12 deficiency affect neurons, while folate deficiency doesn’t?

A

only B12 is responsible for conversion of methylmalonyl CoA -> succinyl coA. this results in incorporation of nonphysiologic FAs into neuronal lipids. both show elevated homocysteine, only B12 has elevated methylmalonyl CoA.

91
Q

leptin

A

protein hormone produced by adipocytes in proportion to quantity of fat stored. acts on arcuate nucleus of hypothalamus to inhibit production of neuropeptide Y (decreasing appetite) and stimulates production of alpha-MSH (increasing satiety). mutations -> hyperphagia + profound obesity

92
Q

transamination rxns

A

occur between AA and alpha-keto acids. amino group is transferred to alpha-deto acid, which becomes an AA. pyridoxical phosphate B6) serves as a cofactor in AA transamination and decarboxylation rxns

93
Q

thiamine

A

B1. coenzyme for transketolase, alpha-ketoglutarate dehydrogenase, and pyruvate dehydrogenase

94
Q

riboflavin

A

B2. used in dehydrogenase rxns involving FMN and FAD

95
Q

niacin

A

B3 = nicotinic acid. enables dehydrogenases to form NAD and NADP. deficiency -> pellagra: 4 Ds: dermatitis, diarrhea, dementia, death

96
Q

biotin

A

B7. water-soluble cofactor for all 4 carboxylase enzymes. involved in synthesis of FAs, isoleucine, valine, and gluconeogenesis.

97
Q

HbF

A

= alpha2gamma2. dominates in newborns. high affinity for O2, produced during the final 7 months of gestation. switch to HbA (alpha2beta2) occurs during first 6 months of life

98
Q

HbA2

A

= alpha2delta2. normal variant that comprises 2-5% of normal adult Hb

99
Q

Hb Gower

A

zeta2epsilon2 = earliest Hb found in fetus. synthesized by yolk sac, replaced by Hb Portland, then Hb Gower 2 before HbF production begins at 10-12 wks

100
Q

Hb Bart

A

= gamma4. found in homozygous alpha-thal, where 0 alpha chains are synthesized. very high O2 affinity, does not release it to tissues -> hypoxia -> hydrops fetalis -> death in utero

101
Q

HbS aggregates

A

in deoxygenated state. HbS polymers form fibrous strands that reduce RNC membrane flexibility and promote sickling. sickling occurs under all conditions associated w/anoxia: low pH, high 2,3-DPG. also low blood volume

102
Q

SS mutation

A

nonpolar valine replaces charged glutamate at position 6 of beta-chain

103
Q

2,3-DPG

A

ionically binds 2 beta chains and stabillizes the taut (T) deoxygemoglobin. this binding decreases O2 affinity of Hb and facilitates O2 release to tissues. when 2,3-DPG is depleted, O2 affinity increases -> O2 uptake

104
Q

Kozak sequence

A

defined by the sequence: (gcc)gccRccAUGG, where R = adenine or guanine. when AUG is positioned near beginning of mRNA w/in Kozak, it serves as an initiator (-> ribosome binding). if A or G at R is replaced by C or G, initiation won’t work right (e.g. in thalassemia intermedia).

105
Q

translocation

A

catalyzed by elongation factor eEF2, requires FTP hydrolysis

106
Q

peptide bond formation

A

catalyzed by peptidyl transferase on eukaryotic ribosomes. defect in mRNA coding for ribosomes would interfere w/this fxn

107
Q

termination of polypeptide sequence

A

occurs at stop codons. happens early when mutations create misplaced stop codons

108
Q

protein targeting

A

achieved by AA sequence of N-terminal section of formed protein. often removed from final protein once it reaches it’s destination

109
Q

thalassemia intermedia

A

form of beta-thal that is clinically less severe than beta-thal major. hypochromic, microcytic anemia = classic lab finding of thalassemia.

110
Q

thalassemia RBC morphology

A

variable depending on type, but can include anisopoikilocytosis, target cells, tear drop cells, and/or heintz bodies

111
Q

spherocytosis

A

caused by variety of molecular defects in genes encoding RBC membrane proteins, e.g. spectrin, ankyrin, band 3 protein, protein 4.1

112
Q

mitochondrial biochemical processes

A

b-oxidation of FAs, ketogenesis, TCA cycle, parts of urea cycle (carbamoyl phosphate synthetase 1 and ornithine transcarbamoylase) and pyruvate carboxylation

113
Q

transketolase

A

enzyme of pentose phosphate pathway. uses B1 as a cofactor. all pentose phosphate pathway rxns occur in cytoplasm

114
Q

pyruvate carboxylase

A

catalyzes initial step in gluconeogenesis by converting pyruvate to oxaloacetate. requires biotin as a cofactor. fxns w/in mitochondria

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