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First Aid Chapters > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

what does methylation do to DNA

A

makes it mute- no transcription

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2
Q

acetylation of DNA

A

makes it active

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3
Q

which two bases get methylated on template strand?

A

cytoskine and adenine

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4
Q

3 amino acids needed for purine synthesis

A

glycine, aspartate, glutamine

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5
Q

leflunomide

A

this inhibits dihydroorotate dehydrogenase so you can’t convert carbamoyl phosphate to orotic acid

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6
Q

problem in orotic aciduria

A

can’t convert orotic acid to UMP

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7
Q

hydroxyurea

A

inhibits ribonucleotide reductase. can’t convert UDP to dUDP

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8
Q

5FU

A

inhibits thymidiylate synthase. can’t convert dUMP to dTMP

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9
Q

MTX/ TMP and pyrimethamine

A

inhibits dihydrofoalte reductase in humans, bacteria and protozoa respectively.

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10
Q

6MP

A

inhibits purine synthesis

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11
Q

Mycofenolate and ribavarin

A

inhibits IMP dehydrogenase so can’t make purines

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12
Q

amino acid required for pyrimidine base production

A

aspartate

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13
Q

adenosine deaminase deficiency

A

excess ATP and dATP because can’t convert adenosine to inosine. makes you go through the pathway one way. major cause of autosomal recessive SCID. via negative feedback you get a reduction in activity of ribonucleotide reductase- decreased lymphocyte count

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14
Q

Lesch Nyhan syndrome

A

defective purine salvage due to absent HGPRT. this means you can’t recover them and you end up dumping many more into xanthine then into uric acid. also get increased de novo purine synthesis.

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15
Q

genetics of Lesch Nyhan

A

x linked recessive

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16
Q

findings in lesch nyhan

A

intelectual disability, self mutilfation, aggresion, hyperuricemia, gout, dystonia

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17
Q

difference between DNA pol I and III

A

DNA pol I has an ability to excise the RNA primer in the 5-3 direction- its an exonuclease

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18
Q

Which is the polymerse (DNA) that is seen in eukaryotes

A

DNA pol III

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19
Q

what is the order of the danger of mutations

A

some men never finish

silent< frameshift

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20
Q

disease that is a problem with nucleotide excision repair

A

defective in xeroderma pigmentosum which prevents repair of pyrimidine dimers because of UV light exposre

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21
Q

disease that results from a problem with mismatch repair

A

HNPCC-

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22
Q

how does base excision repair work

A

AP endonuclease leaves the 5’ end
lyase cleaves the 3’ end
DNA polymerase beta fills the gap
DNA ligase seals it

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23
Q

disease from a problem with non homologous end joining

A

ataxia telangiectasia

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24
Q

what direction is DNA or RNA read

A

5 to 3

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25
Q

mRNA start codons

A

AUG

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26
Q

what is the start codon also indicate (which amino acid)

A

methionine in eukaryotes and formeylmethionine in prokaryotes

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27
Q

mRNA stop codons

A

U go away
U are away
U are gone.

UGA
UAA
UAG

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28
Q

what does rna polymerase I make

A

rRNA

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29
Q

what does rna polymerase II make

A

mRNA. the most massive.

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30
Q

what does rna polymerase III make

A

tRNA

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31
Q

how does alpha amanitin in amanita phalloides (mushroom) make people sick

A

inhibits RNA pol II. severe hepatotoxicity if ingested

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32
Q

how is RNA pol different in prokaryotes from eukaryotes

A

only one in prokaryotes. 3 in eukaryotes.

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33
Q

where do the post transcriptional modifications like caping of the 5’ end, polyadenylation and splicing of introns occur?

A

in the nucleus following transcription

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34
Q

what is the mRNA called before it is processed

A

hnRNA or heterogenous nuclear RNA

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35
Q

what are P bodies

A

mRNA quality control- contain decapping enzymes, endonucleases etc.

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36
Q

what diseases are anti splicesome antibodies associated with

A

anti Smith - lupus

anti U1 RNP - mixed connective tissue disease

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37
Q

disease from abnormal splicing (genetic)

A

beta thal

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38
Q

which end of the tRNA is the amino acid bound?

A

CCA on the 3’ end. “can carry aminoacid”

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39
Q

T arm of tRNA

A

binds to the ribosome

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40
Q

D arm of the tRNA

A

allows for recognition of the right aminoacul tRNA synthetase.

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41
Q

what is responsible for the accuracy of amino acid selection

A

amionacyl tRNA synthetase and binding of charged tRNA to the codon

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42
Q

what is the function of aminoacyl tRNA synthetase

A

to add the amino acid to the tRNA molecule

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43
Q

energy source for tRNA activation

A

ATP

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44
Q

energy source for tRNA translocation

A

GTP

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45
Q

function of P53 and rb in cell cycle

A

they are normally present to inhibit G1 to S migration.

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46
Q

Li-Fraumeni syndrome

A

this is a mutation in the Rb or P53 genes such that there is unrestrained cell division

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47
Q

cell type- neurons, skeletal muscle, cardiac muscle and RBCs

A

permanent

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48
Q

stable but quiescent cells

A

Heptocytes and lymphocytes. normally in Go but can enter G1 if stimulated to do so

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49
Q

I cell disease

A

inherited lyososomal storage disorder. defect in phosphotransferase which means failure of the golgi to phosphorylate mannose residues (doesn’t put the mannose 6 phosphate on that would signal it to the lysosome) so the proteins are excreted instead of being sent to the lysosomes. coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes. fatal.

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50
Q

proteins accumulating in the cytoplasm?

A

signal recognition particle (SRP) absent or dysfunctional. this normally traffics to the rough ER

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51
Q

COPI I

A

golgi to golgi or golgi to ER

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52
Q

COPI II

A

golgi to golgi or ER to golgi

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53
Q

Clathrin

A

trans golgi to lysosomes or endosomes or plasma membrane.

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54
Q

kartagener syndrome

A

this is primary ciliary dyskinesia. immotile cilia due to a dynein arm defect. results in infertility, immotile sperm, fallopian tube issues, bronchiectasis, recurrent sinusitis, situs inversus

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55
Q

vimentin

A

connective tissue

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56
Q

Desmin

A

muscle

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57
Q

cytokeratin or keratin

A

epithelium

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58
Q

GFAP

A

neuroglia

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59
Q

Neurofilaments

A

neurons

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60
Q

type I collagen

A

most abundant. bone, skin (dermis), tendon, dentin, fascia, cornea, scar

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61
Q

deficiency in type I collagen

A

osteogenesis imperfecta

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62
Q

Type II collagen

A

cartilage, vitreous body, nucleus pulposus

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63
Q

Type III collagen

A

reticulin, epidermis, blood vessels, uterus, fetal tissue, kidney, GRANULATION TISSUE

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64
Q

deficiency in type 3 collagen?

A

EDS vascular type

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65
Q

Type IV collagen

A

basement membrane, basal lamina, lens

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66
Q

problem wit type IV collagen

A

defective in alport syndrome. targeted by antibodies in good pasture syndrome

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67
Q

what is the most common aa in collagen

A

glycine

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68
Q

what are the other two aa in collagen

A

proline and lysine

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69
Q

what disease has an issue with collagen hydroxylation

A

scurvy. hydroxylation of specific proline and lysine residues. requires vitamin C.

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70
Q

what disease has a problem with glycosylation of collagen

A

pro alpha chain is turned into pro-collagen via hydrogen and disulfide bonds. this turns it into a triple helix called procollagen. problems with this are seen in osteogenesis imperfecta

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71
Q

proteolytic cleavage of collagen

A

cleavage of disulfide rich terminal regions of procollagen turning it into insoluble tropocollagen.

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72
Q

cross linking of collagen

A

re-inforcement of many staggered tropocollagen molecules by lysyl oxidase. requires Cu as a co factor to make the collagen fibrils. this is defective in EDS and menkes disease.

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73
Q

what is the most common problem in osteogenesis imperfecta

A

decreased production of otherwise normal collagen type 1

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74
Q

pneumonic for Southern, Western, Northern blot

A

SNoW DRoP

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75
Q

indirect ELISA tests for

A

antigen

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76
Q

direct ELISA test for

A

antibody

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77
Q

pleiotropy

A

one gene effects multiple phenotypes like PKU causing light skin, intellectual issues and musty body odor

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78
Q

locus heterogeneity

A

mutations at different loci can produce a similar phenotype like with albinism

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79
Q

allelic heterogeneity

A

different mutations in the same locus produce the same phenotype such as with beta thal

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80
Q

prader willi

A

chromosome 15. paternal is deleted or mutated while maternal is imprinted. can be caused by maternal uniparental disomy

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81
Q

angelman syndrome

A

chromosome 15. maternal is deleted or mutated and paternal is imprinted.

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82
Q

symptoms of angelman syndrome

A

seizures, atazxia and severe intellectual disability with inappropriate laughter- always happy puppet

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83
Q

AD mutations are usually

A

defects in structural genes

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84
Q

AR mutations are usually…

A

cause enzyme deficiency

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85
Q

myopathy with ragged red fibers

A

this is mitochondrial myopathy- myopathy with lactic acidosis, failure in oxidative phosphorylation.

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86
Q

huntington disease chromosome

A

4

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87
Q

PKD1 mutations in ADPKD chromosome

A

number 16

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88
Q

PKD2 mutations in ADPKD chromosome

A

number 4

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89
Q

FAP chromosome

A

5

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90
Q

hereditary hemorrhagic telangiectasia

A

also known as osler weber rendu syndrome- inherited blood vessel disorder- telangiectasia, recurrent epistaxis, skin discoloration, avms, GI bleed, hematuria,

91
Q

neurofibromatosis type 1 mutation

A

NF1 gene on chromosome 17

92
Q

neurofibromatosis type 2 mutation

A

NF2 on chromosome 22

93
Q

what is unique about tuberous sclerosis

A

incomplete penetrance with variable expression- numerous benign hamartomas.

94
Q

Von hippel lindae disease

A

chromosome 3 mutation

95
Q

what is the mutation in CF

A

delta 508 mutation - phenylalanine deletion.

96
Q

treatment for CF

A

N acetylcystine to break up the mucous plugs and dornase alfa (DNAse) to clear leukocytic debris

97
Q

pneumonic for X linked recessive

A

He Said He Only Fought With GOLD B

98
Q

mutation in duchene muscular dystrophy

A

frameshift mutation. truncated dystrophin protein. get pelvic girdle muscle weakness first and then it spread. fibro fatty replacement of muscles.

99
Q

gower maneuver

A

patients with duchene muscular dystrophy use their hands to help them stand up

100
Q

common cause of death in duchene muscular dystrophy

A

dilated cardiomyopathy

101
Q

function of dystrophin

A

anchors muscle fibers, primarily in skeletal and cardiac msucle. connects intracellular cytoskeleton (actin) to the transmembrane proteins alpha and beta.

102
Q

lab values elevated in duchene muscular dystrophy

A

increased CPK and aldolase

103
Q

Becker muscular dystrophy

A

this is an X linked point mutation in dystrophin gene (not a frameshift like in duchene. both can be caused by a deletion.

104
Q

myotonia, msucle wasting, frontal balding, cataracts, testicular atrophy and arrythmia

A

myotonic type 1 dystrophy. this is a CTG repeat.

105
Q

large testicles, long face, large jaw, large everted ears, autism, MVP

A

fragile X syndrome

106
Q

4 trinucleotide repeat diseases

A

Huntington, fragile X, mytotonic dystrophy, friedrich ataxia

107
Q

mutations causing downs syndrome

A

non disjunction in meiosis 1 > RObertsonian translocation > mosaicism (no maternal association, post fertilizaton mitotic error)

108
Q

first trimester findings in downs

A

increased nuchal translucency, decreased PAPP A and increased bHCG

109
Q

findings in edwards syndrome

A

this is trisomy 18. rocker bottom feet, small jaw, cross-over of fingers, low set eras, prominent occiput, congenital heart disease. low PAPP A and low BHCG

110
Q

findings in patau syndrome

A

rocker bottom feet, micropthalmia, microcephaly, cleft lip, cleft palate, holoprosencephaly, poydactylyl, congenital heart disease. increased nuchal tranlucency but decreased bHCG and decreased PAPP A

111
Q

what types of chromosomes do you see robertsonian trans locations on

A

acrocentric chromosomes - centromeres near the end. if balanced, then no problem. the issue is with unbalanced.

112
Q

cri du chat

A

chromosome 5. microcephayl, moderate to severe intellectual issues, high pitched crying/mewing, epicanthal folds, cardiac abnormalities like VSD.

113
Q

what chromosome is responsible for Williams syndrome

A

7

114
Q

what mutation is responsible for DiGeorge syndrome and Velocardiofacial syndrome

A

22q11. due to abberant development of the 3rd and 4th branchial pouches.

115
Q

which vitamin prevents squamous metaplasia

A

vitamin A

116
Q

what two diseases can be treated with vitamin A

A

measles and AML subtype M3 (APL)

117
Q

what is keratomalacia

A

thickening of the cornea from vitamin A deficiency

118
Q

three things thiamine is used for

A

ATP so alpha ketoglutarate dehydrogenase, Transketolase and pyruvate dehydrogenase

119
Q

how to test for Wernike Korsakoff syndrome

A

increased RBC transketolase with B1 administration

120
Q

classic triad of Wernike Korsakoff

A

confusion, opthalmoplegia, ataxia

121
Q

vitamin used in succinate dehydrogenase reaction

A

riboflavin B2

122
Q

two things deficiency of B2

A

chelosis and corneal vascularization

123
Q

what vitamin can you treat lipid issues with

A

niacin. reduced VLDL and increases HDL

124
Q

what is needed to make thiamin?

A

derived from tryptophan, need B2 and B6

125
Q

diseases that can cause pellagra

A

this is a vitamin B3 deficiency.
hartnup disease (tryptophan decreased absorption)
malignant carcinoid syndrome
isoniazid

126
Q

niacin toxicity

A

facial flushing from prostaglandins

127
Q

vitamin for coA

A

pantothenate

128
Q

vitamin that is for transamination reactions

A

B6

129
Q

vitamin assocaited with carboxylation

A

B7 or biotin

130
Q

deficiency of biotin

A

rare- antibiotic use or ingestion of raw egg whites

131
Q

how to differentiate B12 def from folate

A

folate normal MMA and B12 has increased MMA

132
Q

3 drugs that can cause folate deficiency

A

MTX, sulfonamides, phenytoin

133
Q

bug that likes to eat B12

A

diphyllobothrium latum

134
Q

what two things require vitamin C

A

hydroxylation of lysine and proline for collagen synthesis and conversion of dopamine to nor epi. this is the dopamine Beta hydroxylase enzyme

135
Q

what can you use vitamin C to treat

A

methemoglobinemia- converts Fe3+ to Fe2+

136
Q

what two things are not in breast milk

A

vitamin D and vitamin K

137
Q

neurologic symptoms of B12 deficiency but NO megaloblastic anemia (hemolytic anemia instead)

A

think about vitamin E deficiency

138
Q

two reactions that alcohol pushes

A

it increases NADH so it pushes pyruvate to lactate and oxaloacetate to malate. both of these reactions require NADH and push you away from gluconeogenesis. also make more glycerol 3 phosphate.

139
Q

fomepizole

A

inhibits alcohol dehydrogenase

140
Q

disulfram

A

inhibits acetaldehyde dehydrogenase- makes you sick bc the acetaldehyde is not pleasant.

141
Q

glucokinase

A

found in liver and beta cells of the pancreas. high Km (means low affinity) and high V max means high capacity. not inhibited by G6P and it is induced by insulin. it is what is responsible for MODY diabetes

142
Q

5 enzymes required for pyruvate dehydrogenase

A

Thiamine TPP, FAD, NAD, CoA and Lipoic acid

143
Q

how does arsenic work

A

this inhibits the lipoic acid so you make no ATP. produces garlic breath, vomiting and rice water stools.

144
Q

pyruvate dehydrogenase deficiency

A

buildup of pyruvate that leads to alanine increase and increase in lactic acid production. treat with lysine and leucine- only purely ketegenic amino acids

145
Q

what is pyruvate carboxylase

A

this is the enzyme that converts pyruvate to oxaloacetate for gluconeogenesis. requires biotin.

146
Q

what inhibits complex 1 in ETC

A

rotenone

147
Q

what inhibits complex III in ETC

A

antimycin A

148
Q

what inhibits complex IV in ETC

A

cyanide, CO

149
Q

what inhibits complex V in ETC

A

oligomycin

150
Q

what is complex 2

A

succinate dehydrogenase (part of the krebs cycle)

151
Q

what is oligomycin

A

ATP synthase inhibitor

152
Q

2,4 dinitrophenol

A

this is used as an uncouplig agent- illegally for weight loss. aspirin toxicity can also cause this as can thermogenin in brown fat

153
Q

where is glucose 6 phosphatase located

A

in the ER. turns glucose 6 phosphate into glucose

154
Q

do even or odd chain fatty acids get used for gluconeogenesis

A

only odd chain fatty acids can be used. even ones are broken down to only yield acteyl CoA

155
Q

first enzyme in respiratory burst that is defective in CGD

A

NADPH oxidase.

156
Q

second enzyme in oxidative burst

A

superoxide dismutase

157
Q

third enzyme in oxidative burst

A

myeloperoxidase.

158
Q

in orer to break down H2O2 you need glutathione redutctase. what element does this require

A

selenium

159
Q

essential fructoseria

A

defect in fructokinase. this is basically asymptomatic

160
Q

fructose intolerance

A

this is a deficiency in aldolase B so you have a buildup of fructose 1 P and this makes peope sick. hypoglycemia, vomiting, cirrhosis.

161
Q

how to treat fructose intolerance

A

no fructose or sucrose (fructose plus glucose)

162
Q

galaktokinase deficiency

A

this basically leads to a buildup of galactose which can be converted to galactitol. may cause infantile cataracts which present with failure to follow a finger

163
Q

classic galactosemia

A

absence of galactose i phosphate uridyltransferase. accumulation of galactitol and galactose 1 phosphate. can lead to sepsis with Ecoli in neonates

164
Q

treatment of classic galactosemia

A

eclude galactose and lactose from the diet. lactose = glucose plus galactose.

165
Q

aldose reductase

A

converts glucose to sorbitol

166
Q

sorbitol dehydrogenase

A

converts the sorbitol into fructose

167
Q

cells that do not have sorbitol dehydrogenase and therefore get a buildup of sorbital

A

schwann cells, retina, and kidneys. lens has very little

168
Q

essential amino acids that are glucogenic only

A

methionine, histmaine, valine

169
Q

essential amino acids that are ketogenic only

A

lysine and leucine

170
Q

essential amion acids that are both glucogenic and ketogenic

A

isoleucine, phenylalanine, tryptophan and threonine

171
Q

which amino acid is the most basic

A

arginine

172
Q

which amino acid has no charge in the body but is basic

A

histmaine

173
Q

function of ornithine transcarmylase

A

takes carbamoyl phosphate plus ornithine and makes citruline as part of the first step in the urea cycle

174
Q

what is an important cofactor for the carbamoyl phosphate synthetase I reaction?

A

N acetylglutamate

175
Q

what enzyme is defective in phenylketonuria

A

phenylalnine hydroxylase and or tetrahydrobiopterin cofactor (malignant pKU). tyrosine becomes essential in this disease.

176
Q

symptoms of pKU

A

intellectual issues, growth retardation, seizures, fair skin, eczema, musty or mousy body odor

177
Q

what is alkaptonuria

A

this is a congenital defect in homogentisate oxidase which is part of the pathway to breakdown tyrosine to fumarate

178
Q

findings in alkaptonuria

A

dark conenctive tissue, brown pigmented sclerae, urine that turns black on prolonged exposure to air. may get arthalgias

179
Q

homocystinuria

A

this is either a problem with cystathione synthase or homocystine methyltransferase

180
Q

findings in homocystinuria

A

homocystine in the urine, intellectual issues, osteoporosis, tall stature, kyphosis, lens subluxation (down and inward), thrombosis and atherosclerosis.

181
Q

cystinuria defect

A

defect in the proximal convoluted tubule and can’t recover COLA
cysteine, ornithine, lysine, and arginine
excess cystine in the urine can lead to hexagonal cystine stones

182
Q

what does urinary cyanide nitroprusside test diagnose

A

cystinuria

183
Q

what is cystine

A

this is made by two cysteines connected with a disulfide bond

184
Q

maple syrup urine disease

A

can’t break down chain amino acids because of a problem with alpha ketolutarate dehydrogenase. this requires b1 normally. increase in alpha ketoacids in the blood. branched ones are isoleucine, leucine and valine

185
Q

increased ornithine with otherwise normal urea cycle enzymes and hyperammonemia

A

this is most likely N acetylglutamate deficiency

186
Q

increased orotic acid in blood and urine

A

check for megaloblastic anemia- this is orotic aciduria and if not, then check for decreased BUN and increased ammonia levels- ornithine transcarbamylase deficiency

187
Q

why does ornithine transcarbamylase deficiency cause increased orotic acid

A

because there is excess carbamoyl phosphate which can be converted to orotic acid in part of the pyrimide synthesis pathway.

188
Q

what does phenylalnine make

A

tyrosine, then dopa, then dopamine, then NE and epi

189
Q

what does tryptophan make

A

seratonin and niacin

190
Q

what does histadine make

A

histamine

191
Q

what does glycine make

A

porphyrin (heme)

192
Q

what oes glutamate make

A

glutathione and GABA

193
Q

what does arginine make

A

creatine, urea and NO

194
Q

what is the enzyme deficiency in albinism

A

tyrosinase which is converting dopa to melanin

195
Q

enzyme deficiency in Von Gierke

A

glucose 6 phosphatase. severe fasting hypoglycemia, increased glycogen in the liver, increased blood lactate

196
Q

enzyme deficiency in Pompe disease

A

alpha 1,4 glucosidase (this is the enzyme in the lysosomes that breaks down some glycogen) acid maltase. leads to cardiomyopathy and systemic findings

197
Q

cori disease enzyme deficiency

A

alpha 1,6 glucosidase- this is the debranching enzyme that removes the last glycogen. milder disease with normal blood lactate levels. gluconeogenesis is intact

198
Q

enzyme deficiency in mcardle disease

A

glycogen phosphorylase in skeletal muscle. this is a muscle disease. it is also known as myophosphorylase. leads to increased glycogen in the muscle that cannot be broken down.

199
Q

fabry enzyme deficiency

A

alpha galactosidase A

200
Q

what builds up in fabry

A

ceramide trihexodase

201
Q

gauchers disease- enzyme deficiency

A

glucocerebrosidase (beta glucosidease)

202
Q

gauche what builds up

A

glucocerebroside

203
Q

symptoms of gauche-

A

lipid laden macrophages, hepatomegaly, pancytopenia, aseptic necrosis of the femur, bone crises

204
Q

enzyme deficiency in Neimen pick

A

sphingomyelinase

205
Q

what builds up in Neimen pick

A

sphingomyelin

206
Q

symptoms of neimen pick

A

progressive neurodegeneration, cherry red macula, foam cells- lipid laden macrophages

207
Q

enzyme deficiency in tay sachs

A

Hexosaminidase A

208
Q

what builds up in tay sachs

A

Gm2 ganglioside

209
Q

symptoms of tay sachs

A

cherry red spot on the macula and lysosomes with onion skin, NO HEPATOSPLENOMEGALY (contrast to Neimen pick)

210
Q

krabbe disease enzyme deficiency

A

galactocerebrosidase

211
Q

krabbe dsiease- what builds up

A

galactocerebroside and pyshocine

212
Q

metachromatic leukodystrophy what enzyme is deficient

A

arylsulfatase A

213
Q

metachromatic leukodystrophy what builds up

A

cerebroside sulfate

214
Q

enzyme deficiency in hurler syndrome

A

alpha L iduronidase

215
Q

enzyme deficiency in hunter syndrome

A

iduronate sulfatase

216
Q

what builds up in hunter and hurler syndrome

A

heparan sulfate and dermatan sulfate

217
Q

how to differentiate hunter and hurler

A

hunters see clearly (no corneal clouding) and it is X linked recessive

218
Q

liproprotein lipase deficiency or CII alteration

A

this causes type 1- hyper–chylomicronemia. causes pancreatitis, hepatosplenomegaly and xanthomas

219
Q

defective LDL receptors

A

this causes type 2a familial hypercholesterolemia. they get very high LDL and cholesterol- heart attacks at an early age etc. can have tendon xanthomas and corneal arcus

220
Q

hepatic overproduction of VLDL

A

this is type 4 hypertriglyceridemia. you get an increase in VLDL and TG. it can cause pancreatitis.

221
Q

what is B48 for?

A

this is a marker for chylomicron secretion- on chylomicrons and chylomicron remnants

222
Q

B100 marker

A

this is somethign that binds to the LDL receptor. it is on the VLDL, LDL and IDL

223
Q

what is CII marker for?

A

this is a cofactor for lipoprotein lipase. it is on chylomicrons and VLDL. it is also in HDL.

224
Q

what is A1 for?

A

this activates LCAT which esterifies the cholesterol and turns iit into mature choelsterol. found just on the chylomicron and HDL. mostly an HDL thing.

First Aid Chapters (8 decks)

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