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USLME Kiss my ass and pray > Biochem Phys > Flashcards

Biochem Phys Flashcards

1
Q

link between glycolysis and TCA cycle

A

Pyruvate Dehydrogenase

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2
Q

nuclear localization signal?

3

A

marks a protein to enter the nucleus made of proline, lysine and arginine

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3
Q

vimentin

Associate w?

A

intermediate filament in connective tissue

sarcomas

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4
Q

desmin

associate w?

A

intermediate filament in muscle

associate w/ myosarcoma- leiomyosarcomas and rhadbomyosarcoma

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5
Q

cytokeratin

associate w/

A

intermediate filament in epithelial cells

Associate w/ carcinoma

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6
Q

GFAP

associate w/

A

intermediate filament in glial cells

Associate w/ astrocytoma and gliobastoma

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7
Q

Neurofilaments

associate w/

A

intermediate filament in neurons

Associate w/ neuroblastoma and primitive neuroectoderma tumors

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8
Q

Nuclear lamina ABC

associate w?

A

intermediate filaments making up the nuclear envelope

associate w/ mutations -> progeria (old age)
and muscular dstrophy

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9
Q

Microfilaments function?

A

actin and myosin

  • cellular motility
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10
Q

Microtubule function

A

movement - cilia, flagella and mitotic spindle

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11
Q

Intermediate filaments function

A

cellular skeleton - differs w/ each ell used to ID cancer etiology

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12
Q

retrograde movement on microtubule

A

dynein

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13
Q

anterograde movement on microtubule

A

kinesin

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14
Q

Tyrosine Kinase receptor Examples and how composition (4)

A

PDG- single pass - transmembrane
Growth factor receptors - single pass trash membrane

Insuling and IGF -1 -
-2alpha bound extras cell and 2 beta w/ tyrosine activity

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15
Q

Improper clathrin and adapt in leads to

A

inability for receptor binding lwading to endocytosis-> can’t bring in

  • recycled
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16
Q

Phosphatydalinositol?

enzyme that acts on it?

A

cell membrane phospholipid that leads to AA

Phosolipase A2

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17
Q

Drug blocking leukotrien production and MOZ

A

Zilueton

blocks lipoxygenase

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18
Q

Of the leukotriene receptor antagonist, which is best to give to a kid

A

Montelukast

Not as much Zafirlukast

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19
Q

Action of Leukotrienes (2)

A

Chemotaxis of PMN- LTB4

Increases bronchial tone - LTC4 and LTD4

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20
Q

Action of prostacyclin (4)

A 
PGI2
Decreases uterine contraction
Decreases platelet aggregation
Decreases brachial tone
Decreases vascular tone
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21
Q

Action of prostaglandins (4)

A 
PGE2 and PGF2A
Increases uterine contraction
Increases gastric mucosa production
Decreases vascular tone (KEEEEPS open)
Decreases bronchial tone
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22
Q

Action of thromboxane (3)

A 
TxA2
Increases platelet aggregation
increases bronchial tone
Increases vascular tone
(opposite of PGI2)
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23
Q

APAP - acetaminophen’s action vs other COX inhibitors

A

Inactivated peripherally thus no anti inflammatory or anti platelet action

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24
Q

BCL-2

A

major anti apoptotic regulator of Mitochondrial permeability

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25
Q

BAX

A

major pro apoptotic regulator of mitochondrial permeability

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26
Q

Cytochrome C

A

Released from mitochondrial membrane for intrinsic apoptosis

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27
Q

3 mech of apoptosis

Ultimat goal

A
  • caspase activation
    1. intrinsic - mitochondrial
    2. extrinsic
  • FAS-R (CD95) and TNF-R
  • T killer cells
    3. p53 recognizing irreversible DNA damage
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28
Q

T killer cells mech of apoptosis(2)

A
  • Perforin pops a hole

- Granzyme B leads to caspase activation

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29
Q

ligand mediated extrinic pathway of apoptosis

A

FAS-r (CD95) or TNF w/ TNF alpha activated ->caspase actiatopn

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30
Q

coagulative necrosis

  • location (3)
  • description
A

heart, liver, lungs

gelatinous low O2 levels-> loss of necucli w/ preserved cell form

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31
Q

liquefactive necrosis

  • location (3)
  • description (3)
A

brain, pleural effusion, bacterial abscess

digestion/hyldolases from microorg and PMNs

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32
Q

Caseous necrosis
-location/causes (2)
description

A

TB and fungi

combine of liquefactive and coagulative

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33
Q

Fatty necrosis

  • location (1)
  • Description
A

peripancreatic fat w/ lipase release

-saponification of fat (Calcification)

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34
Q

Fibrinoid necrosis

  • location (1)
  • description/causes
A

blood vessels

arteritis/autoimmune and malignant HTN

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35
Q

Gangrenous necrosis

Types (2)

A

dry - ischemia coagulative - arteriole occlusion of toes/fingers

wet - bacteria

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36
Q

Reversible cell injury characterized by

A

cellular swelling - noATP -> impaired Na/K

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37
Q

Irreversible change to a cell (5)

A

Nuclear changes
-pyknosis(shrink), karylysis(loss of), karyorrhexis(fragment)
Ca influx
plasma membrane change

lysosomoal rupture
Mito permeability

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38
Q

Superoxide dismutase

A

O2 free radical -> H2O2

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39
Q

Catalase

A

H2O2 -> O2 and H2O

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40
Q

Glutathione peroxidase

A

Also protects from ROS

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41
Q

red infarct

A

Reprofusion therapy -> increased ROS damage, O2 comes in (why we have stroke and MI timing on tPA)

  • collateral circulation (liver, lung, intestine) or reprofusion therapy seen
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42
Q

Pale infarct

A

solid tissue seen w/ not revascularizing

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43
Q

Chromatin is made of

A

Histones

  • 8 binding to DNA H2A, H2B, H3, H4
  • H1 connecting the two

DNA

Each bundle is a nucleosome

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44
Q

What binds DNA to the Histones (3 components)

A

DNA is negatively charged w/ phosphate

Histones are positively charged w/ Lysine and Arginine

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45
Q

Purines are get their N and C from 5 sources

A 
Aspartate -N
Glutamine -N
Glycine -C
CO2- C
THF - C
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46
Q

Pyrimidine gets their N and C from 4 sources

A

Carbamoyl phosphate

  • CO2 - C
  • Glutamine -N
  • ATP - energy

Aspartate - C

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47
Q

Which bond is stronger G-C or A-t

A

G-C due to 3 bonds instead of 2

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48
Q

Whats the difference between Cytosine and uracil?

A

Cytosine is uracil that has been deaminated

Cytosine is in DNA
Uracil is in RNA

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49
Q

Purine vs Pyrimidine synthesis

A

Pyrimidine you make a temporary base (orotic acid) and then add phosphate and sugar to it w/ PRPP and then modify

Purines you make the phosphosphate ribose sugar first w/ PRPP and then you add the base

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50
Q

Enzymes in pyrimidine synthesis enzymes to know (4)

A

Carbamoyl Phosphate Syntase II(rate limiter)

ribonucleuotide reductase (hydroxyurea)
-UDP-> dUDP
Thymidylate syntase (5-FU)
-dUMP ->dTMP 
Dihydropholate reductase (MTX/TMP)
DHF->THF (regeneration)
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51
Q

Enzymes to know in Purine synthesis (2)

A

Glutamine PRPP amidotransferase (rate limiter) (6 mercaptopurine

IMP dehydrogenase (mycophenolate)
-IMP-> GMP

remember easier pathway, though has more ingredients

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52
Q

inhibits ribonucleotide reductase

A

hydroxyurea

UDP->dUDP

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53
Q

inhibits dihydrofolate reductase (2)

A

Methrotexate - eukaryotes
Trimethoprim - prokaryotes

Regenerates DHF -> THF

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54
Q

Inhibits thymidylate syntase

A

5 Fluroracil

dUMP ->dTMP

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55
Q

Inhibits idenosone monophosphate dehydrogenase

A

mycophenalate

IMP -> GMP

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56
Q

Inhibits PRPP amidotransferase

A

6 mercaptopurine

1st step in making a purine with the ribose phosphate transfer

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57
Q

2 types of carbamoyl phosphate syntetase

  • location
  • Pathway
  • N sources
A

CPS-1

  • mitcochondria
  • Urea Cycle
  • ammonia

CPS -2

  • Cytosol
  • Pyrimidine synthesis
  • Glutamine
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58
Q

megaloblastic anemia that does not improve w. folate and B12

A

UMP syntase deficiency (pyrimidine synthesis pathway0

  • > orotic aciduria
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59
Q

patient presents w/ orotic acid in their urine w/o hyper ammonia

presents as?(2)

A

defect in UMP synthase in the pyrimidine synthesis -> build of orotic acid
- can’t convert orotic acid into UMP

FTT
Megaloblastic anemia

Rx w/ uridine administration

VS - OTC deficiency in the urea cycle (Orotic acid in urine and hyper ammonia)

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60
Q

Deficiency in UMP synthesis presents as

A

FTT
Megaloblastic anemia
orotic aciduria w/o hyperammonia

Rx w/ uridine administration

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61
Q

Defect in HGPRT leads to ?

Presentation (5)

A

Lesch Nyhan, defect in purine pathway and can’t recover guanine and hypoxanthine

both become xanthine -> xanthine oxidase enzyme converts to a lot of uric acid

aggression
retardation
Gout
self mutilation
choreathetosis - writhing movements
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62
Q

Adenosine deaminase deficiency leads to

Presents as

A

SCID (diarrhea, recurrent infection, FTT)

Defect in purine breakdown of adenosine -> Inosine in the pathway

Build up of adenosine is toxic to lymphocytes due to decreased DNA synthesis

Auto recessive

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63
Q

DNA polymerase alpha

A

eukaryotic

makes its own primer and builds the lagging strand

~ DNA polymerase III in prokaryotes - except delta makes the leading

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64
Q

DNA polymerase delta

A

eukaryotic

makes the leading strand of DNA

~ DNA polymerase III in prokaryotes - except alpha makes the lagging

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65
Q

DNA polymerase beta

A

eukaryotic

DNA repair

~DNA polymerase III exonuclease function of proofreading

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66
Q

DNA polymerase gamma

A

makes mitochondria DNA

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67
Q

Silent mutation

A

same amino acid despite different base pair

3 BP often a wobble

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68
Q

missense mutation

A

mutation in which the wrong AA is coded leading to dif structure or funciton

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69
Q

nonsense mutation

A

mutation in which the stop codon is made early -

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70
Q

Pyrimidine dimer

A

2 pyrimidines on the same strand of DNA get covalently bonded together

UV light damage -> thymine Thymine binding on the same strand

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71
Q

Nucleotide excision repair steps

A

Damage in SS results in bulky helix

  1. endonuclease - specific
  2. DNA polymerase fills
  3. ligase seals

Damaged in xeroderma pigmentosa; auto recessive

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72
Q

Mismatch repair steps

A

Newly synthesized DNA is recognized as mismatch and removed - Gaps resealed

Damaged in HNPCC

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73
Q

Base excision Repair steps

A

damage to a specific BP, important in spontaneous/toxic deamination

  1. glycosylases recognize damage
  2. endonucleases remove
  3. DNA polymerase fills
  4. Ligase reseals
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74
Q

Nonhomologous end joining

A

dsDNA repair where 2 ends of DNA fragments are put back together after a clean break

No requirement for homology

Mutated in ataxia telangiectasia

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75
Q

Mutated in xeroderma pigmentosa

A

auto recessive

Nucleotide excision repair

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76
Q

Mutated in hereditary nonpolyposis colorectal cancer

A

mismatch repair

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77
Q

Mutated in ataxia telangiectasia

A

non homologous end joining

  • sensitivity to radiation
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78
Q

Mutated in BRCA 1 and 2

A

dsDNA repair mech

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79
Q

DNA is always written

A

5’-3’

even when copying down an alternate strand**
- unless otherwise labeled

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80
Q

AUG

A

Start codon

Methionine

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81
Q

UGA, UAA, UAG

A

stop codons

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82
Q

Eukatyote RNA polymerases (3)

A

RNA polymerase I - rRNA
RNA polymerase II - mRNA
RNA polymerase III - tRNA

no proofreading

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83
Q

alpha amanitin

A

mushroom toxin that inhibits RNA polymerase II -> hepatotoxicity

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84
Q

Prokaryote RNA polymerase

A

RNA polymerase

Does what takes eukaryotes 3 polymerases to do

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85
Q

Operon is composed of(3)

A

on the DNA -> RNA

structural genes that are transcribed

promotor region

all reglulatory genes

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86
Q

Transcription factors bind to (3)

A

proteins that must bind to promoter regions to allow transcription

Always located upstream

  • CCAAT box 75 bp up
  • hodgness/TATA box 25 bp up
  • pribnow/TATAAT box 10 bp up
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87
Q

Operator regions in transcription (2)

located?

A

proteins bind to these regions which are located in areas between the promoter region and structural gene

either binds to a repressor (ex lac operon)

or inducer (starts)

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88
Q

Response elements in transcriptions(2)

located?

A

Enhancer regions that up regulate the RATE of transcription

Repressor regions that down regulate the RATE of transcription

May be located anywhere on the DNA

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89
Q

Structural motifs that interact w/ DNA(4)

A

Helix loop helix
helix turn helix
zinc finger motif
leucine zipper protein

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90
Q

Termination of prokaryotic transcription (2)

A

rho factor - uses RNA dependent ATPase to put energy in the situation and then turns off

GC rich region forms a tight hairpin loop in the RNA that stresses the system and subsequent weak RNA bonds (uracil rich) fall off

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91
Q

Lac operon regulation of beta galactosidase

A

TF CAP is around in the presence of lactose

lac repressor is absent w/out glucose around

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92
Q

hetergeneous nuclear RNA is transformed how? (3)

A

becomes mRNA through

  1. 5’ capping (s adenosyl methinine)
  2. polyadenilation on 3’ (poly a polymerase using polyadenilation signal, no template)
  3. splices out introns (spliceosome)
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93
Q

Enzyme responsible for charging tRNA

What signals location?

A

Aminoacyl tRNA synthetase charges on the 3’ CCA

uses a little ATP

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94
Q

Ribosomes are made of and where? (3)

A

proteins and tRNA - nucleoplasm

rRNA - nucleolus

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95
Q

Steps of protein synths (3)

A

initiation

  • Needs IF factors and assembles 30S and 50S
  • GTP is used

Elongation

  • more aminoacyl tRNA binds to the A site
  • ribozyme (peptidyletransferase) catalyzes the transfer of the growing peptide chain
  • Translocation allows more tRNA to come in

termination
- Runs into a AUG and release factor breaks apart the complex

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96
Q

Sites of action in protein synthesis (3)

A

A - Aminoacyl tRNA incoming binds here
P - accommodates the growing peptide
E - empty and allows exit to the uncharged tRNA

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97
Q

Elongation factors in prokaryotes and eukaryotes

A

function to help tRNA bind and transpeptidase

E2F in euk
G in pro

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98
Q

Antibiotics that bind to 30s and MOA (2)

A

Aminoglycosides - bind early and prevent initiation complex formation

Tetracyclines - bind later and prevent incoming aminoacyl tRNA from binding to the A site

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99
Q

Antibiotics that bind to the 50s site and MOA (6)

A

Macrolides
clindamycin
streptogramins
lincomycin

-all prevent translocation

linozolid - prevent initiation complex from forming

Chloramphenicol - prevent transpeptidase action at 23s

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100
Q

codominance

A

both alleles contribute to the phenotype

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101
Q

variable expressivity

A

means that the SEVARITY of the phenotype varies amongst individuals with a common genotype - ex tuberous sclerosis

Differs from incomplete penetrance in whether or not the EXPRESSION of a phenotype occurs for a common genotype

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102
Q

incomplete penetrance

A

whether or not the EXPRESSION of a phenotype occurs for a common genotype

vs variable expressivity which means the SEVARITY of the phenotype varies amongst individuals with a common genotype

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103
Q

Pleiotropy

A

the phenotypic expression of a gene mutation affects a lot systems

ex PKU

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104
Q

Imprinting

A

the defferences in gene expression depends on the whether the mutation is of maternal or paternal origin

Prader will and Angelman

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105
Q

Mosaicism

A

when the cell express differed genetic makeup within an organism

due to post fertilization loss or change of genetic info during mitosis

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106
Q

locus heterogeneity

A

many mutations of genotype lead to a common phenotype being expressed

ex - albinisim, Marfans-MEN2B- Homocystinuria are all related

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107
Q

Prader willi syndrome due to

Presentation(4)

A

loss of the paternal allele on chromosome 15 (maternal allele already imprinted and silenced)

hyperphagia -> obesity
mental retardation
hypogonadism -> osteoperosis and delayed menarche
hypotonia and facial abnormalities

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108
Q

Angelman syndrome due to

Presentation(3)

A

loss of the maternal allele on chromosome 15 (paternal allele already imprinted and silenced)

Happy puppet

  • mental challenges
  • ataxia
  • inappropriate laughter
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109
Q

Hardy weinberg equations (4)

A

p + q = 1

p squared + 2pq + q squared = 1

p squared = frequency of allele of p
q squared = frequency of allele of q

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110
Q

PCR steps (3)

A

goal is to create a lot of copies of a DNA to mess around with

  1. Denature- heat gently separate out the DNA strands
  2. Annealing -add DNA primers to set up DNA polymerases to copy target genes
  3. Elongation - heat stable DNA polymerase replicate target gene

repeat

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111
Q

DNA gel electrophoresis basics

A

separates negatively charged DNA by size
+ charge opposite of the wells with a negative charge

the smallest DNA fragments travel the farthest
Can be compared to known DNA wells run alonside

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112
Q

Protein gel electrophoresis basics

A

similar to DNA electrophoresis except have both + and - charges in proteins

Well is put in the middle and opposite charges are placed on either side

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113
Q

Southern blotting

A

Way to visualize your DNA sample using a known radiographic DNA probe that anneals to your target after it has been soaked in a denaturant that separates out the strands

after gel electrophoresis

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114
Q

Northern blotting

A

way to visualize your RNA sample using a known radiographic DNA probe that anneals to your target

after gel electrophoresis

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115
Q

Western blotting

A

way to visualize your protein sample using a known radiographic antibody probe that anneals to your target

after gel electrophoresis

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116
Q

southwestern blotting

A

way to visualize DNA binding proteins using a radiographic oligonucleotide sequence which the desired protein can bind to

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117
Q

Indirect ELISA vs Direct ELISA

A

indirect ELISA uses a known antigen and tests a patients serum for the presence of an Antibody -> color change
-ex HIV

direct ELISA uses a known antigen and tests for the presence of an Antigen in the patients serum -> color change

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118
Q

FISH mech

A

uses fluorescent DNA or RNA probes that bind to specific gene sequences on chromosomes.

Probes that bind mean that the known gene is present

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119
Q

Cloning mech of cDNA (4)

A
  1. find a mRNA of interest and isolate
  2. use a reverse transcriptase to create an cDNA copy
  3. insert the cDNA fragment in a bacterial plasmid to replicate (antibiotics selective for those that do not take up the cDNA)
  4. Those that survive have the cDNA (~gene minus the introns)
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120
Q

Karyotyping

A

looking at chromosomes that have been organized according to morphology, size, arm length and banding pattern

Something you visually look at for gross chromosomal deformity (chromosomal imbalances)

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121
Q

Aerobic metabolism glucose using the malate aspartate shuttle occurs where? Produces how much ATP

A

heart and liver and kidney

32 ATP

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122
Q

Aerobic metabolism of glucose using the glycerol 3 phosphate shuttles

Produces how much ATP?

A

brain and muscle

30 ATP

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123
Q

Glycolytic enzyme deficiency clinical consequence?

What enzyme is deficient?

A

Hemolytic anemia

Usually pyruvate kinase

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124
Q

Phosphorylation of glucose to glucose 6 phosphate is done by (2)?

Where is each one and associated Km and Vmax

A

hexokinase is ubiquitous
- High affinity (low Km) and low capacity (low Vmax)

glucokinase is in the liver and beta islet cells

  • low affinity (high Km) and high capacity (high Vmax)
  • induced by insulin
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125
Q

What is the rate limiting enzyme of glycolysis?

What can up regulate its function(2)

What can down regulate it (2)

A

Phosphofructokinase 1 (PFK 1)

AMP and Fructose 2,6 bis-phosphate (+)

ATP and citrate (-)

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126
Q

What is the most common enzyme deficiency in glycolysis

What up regulates its function? (1)

What down regulates? (2)

A

Pyruvate kinase
–( Phosphoenolpyruvate (PEP)-> pyruvate)

(+) fructose 1, 6 phosphate

(-) ATP and Alanine

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127
Q

Role of Phsophopyruvate kinase 1

products and reactants?

A

It converts fructose 6 phosphate -> fructose 1,6 phosphosphate

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128
Q

Where is energy put into glycoslisis? (2)

Where is energy extracted? (2)

A

w/ hexokinase/glucokinase
-glucose -> glucose 6 phosphate

w/ phosphofructosekinase 1
-> fructose 6 phosphate -> fructose 1, 6 phosphate

(gain)

phosphoglycerate kinase
->1,3 bisphosphoglycerate -> 3 phosphoglycerate

pyruvate kinase
-> Phosphoenolpyruvate (PEP) -> pyruvate

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129
Q

where does the following reactions take place?

Glycolysis
TCA cycle
oxidative phosphorylation

A

Glycolysis - cytolsol

TCA and oxidative phosphorylation - mitochondria

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130
Q

Which GLUT transporter is responsive to insulin

located where(2)

A

Glut 4

in skeletal muscle and adipose tissue

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131
Q

Which glut transporter is responsible for basal levels and independent go insulin

located where (2)

A

Glut 1

RBC and endothelium of BBB

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132
Q

Which Glut is regulatory and bidirectional (high capacity/ low affinity ) sensor

loacted (2)

A

Glut 2

Beta islet cells and hepatocytes

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133
Q

what 2 enzymes are responsible for regulation of glycolysis via Fructose 2, 6 bisphosphate?

A

Phosphofructokinase 2
-fructose 6 phosphate -> fructose 2,6 bisphosphate (encourages PFK1 action and responds to insulin)

Fructose bisphosphatase 2
-fructose 2,6 bisphosphate -> fructose 6 phosphate (encourages gluconeogenesis and responds to glucagon)

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134
Q

Fasting state leads to glucagon

What role dose that have on glucagon receptor and resulting G protein pathway

what G protein

A

Gs pathway - Glucagon receptor

High glucagon:insulin ratio

  • > adenylate cyclase activation
  • > increase in c AMP
  • > protein kinase A activation
  • > phosphorylates process dual enzyme
  • > fructose bisphosphatase 2(active);
  • —>gluconeogenesis (raises blood glucose)
  • > phosphofructokinase 2 (inactivated)
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135
Q

Fed state leads to insulin release

What role dose that have on glucagon receptor and resulting G protein pathway

what G protein

A

Gs Pathway - glucagon receptor

Low glucagon: insulin ratio

  • > less adenylate cyclase activation
  • > less cAMP made
  • > less protein kinase activation
  • > less phophorylation of the dual enzyme
  • > fructose bis-phosphatease 2 is inactivated
  • > phosphofructokinase 2 activated
  • —>glycolysis (encourage PFK 1)
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136
Q

Gibbs free energy equation

A

∆G = ∆H- T ∆S

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137
Q

why do we make glucose with gluconeogeneis?

A

due to the amount of energy gained from glucose molecules relative to ATP using gibbs free energy

PEP: -62 kJ
ATP: -31 kJ
AMP: -14 kJ

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138
Q

What are the 4 irreversible enzymes used in gluconeogenesis

A

pyruvate carboxylase
- pyruvate -> oxelacetate w/ biotin

PEP carboxylase
-oxeloacetate -> PEP

Fructose 1,6 bisphosphatase *
-Fructose 1,6 bisphosphate -> Fructose 6 phophate

Glucose 6 phosphatase
-glucose 6 phosphate -> glucose

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139
Q

Rate limiting step of gluconeogenesis

Modifiers

(1) increases
(2) decreases

A

fructose 1,6 bis phosphatase

ATP increases reaction

AMP and fructose 2, 6 decreases the reaction

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140
Q

What product up regulates pyruvate carboxylase action?

What co factor is needed?

A

acetyl Co A - too much going into the TCA cycle

Biotin

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141
Q

Rate limiting step of glycolysis

A

PFK 1 - Phosphofructokinase 1

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142
Q

Rate limiter of TCA cycle

A

isocitrate dehydrogenase

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143
Q

Rate limiter of glycogen synthesis

A

Glycogen synthase

144
Q

Rate limiter of glcogenolysis

A

glycogen phosphorylase

145
Q

Rate limiter of HMP Shunt

A

glucose 6 phosphate dehydrogenase

146
Q

Rate limiter of de novo pyrimidine syntheis

A

carbamoyal phosphate synthetase II

147
Q

Rate limiter of de novo purine synthesis

A

glutamine PrPP amidotransferase

148
Q

Steps in making glycogen (4)

occurs where

A

occurs in both hepatocytes and skeletal- only skeletal muscle is lacking glucose 6 phosphatase so it does not release glycogen to the blood stream but utilizes it

hexokinase/glucokinase
-> glucose 6 phosphate
------------------
phospho-gluco-mutatse interconverts to
-> glucose 1 phosphate

UDP glucose phosphophorylase
-> UDP glucose

Glycogen syntase*
-> alpha 1, 4 bonds

branching enzyme
-> alpha 1, 6 bonds

149
Q

Breakdown of glycogen (glycogenolysis) steps (2 enzymes)

A

Glycogen phosphorylase*
- breaks down alpha 1,4 bonds making “glucose 1 phosphate”

converted to glucose 6 P via phospo-gluco-mutase -> used in cell or if liver lose lose phosphate and exported

De-branching enzyme - 2 functions

  • transferase: 4 alpha D glucotransferase (at 4 glucose residue)
  • break down of last alpha 1-6 bond (alpha 1-6 glucosidase)
150
Q

Regulation of glycogen synthesis

Role of insulin?

Role of glucagon?

Role of epinephrine?

A

glucagon acts at glucagon receptor

  • > adenylyl cyclase
  • > increase in cAMP
  • > Protein kinase A
  • > phosphorylates Glycogen phosphorylase kinase

Active glycogen phosphphorylase

Epinephrine does the same thing through beta 2 activation

Insulin activates a phosphoratase -> dephosphorylates glycogen phosphorylase

151
Q

Which enzyme converts glucose 6 phosphate to glucose?

located where?

A

glucose 6 phosphatase -> liver enzyme mainly, not in skeleton

last step of gluconeogenesis and also in glycogenolysis

152
Q

glycogen phosphorylase deficiency

A

McArdles Type V

153
Q

Glucose 6 phosphatase deficiency

A

Von Gercks disease Type I

154
Q

lactic acidosis, hyperlipidemi, hyper uricemia glycogen storage disease

A

Von Gercks disease (glucose 6 phosphatase)

155
Q

alpha 1,6 glucosidase deficiency

A

Cori’s disease (type III)

156
Q

alpha 1, 4 glucosidase deficiency (Lysosomal)

A

Pompe’s disease (type II)

157
Q

cardiomegaly glycogen storage disease

A

pompe’s disease infantile (type II) alpha 1-4 glucosidase lysosomal disease

158
Q

diaphragm weakness -> respiratory failure glycogen storage disease

A

pomp’s disease - adult (type II ) alpha 1-4 glucosidase lysosomal disease

159
Q

increased glycogen in the liver severe fasting hypoglycemia

A

von gercks disease -glucose 6 phosphatase

160
Q

hepatomegaly, hypoglycemia, hyperlipidemia, (normal kidneys, lactate and uric acid)

A

cori’s disease (type III) alpha 1-6 glucosidase

161
Q

painful muscle cramps, myoglobinuria w/ strenuous exercise

A

McArdles disease (type V) glycogen phosphorylase in skeletal muscle

162
Q

severe hepatospleomegaly and enlarged kidneys glycogen storage disease

A

Von Gercks disease (type I) glucose 6 phosphatase

163
Q

all the glycogen storage disease are acquired

A

auto recessive

164
Q

4 uses of pyruvate

A

lacate (via LDH w/ NAPH)

oxaloacetate (via pyruvate carboxylase w/ ATP (gluconeo))

Alanine (via ALT and N added on )

Acytyl Co A (via pyruvate dehydrogense w/ B1, B2, B3, B5 and lipoic acid)

165
Q

3 enzymes in the Krebs cycle worth knowing (irreversible)

A

citrate syntase
-Acytyl Co A -> Citrate

isocitrate dehydrogenase
-isocitrate -> alpha keto glutarate

alpha ketoglutarate dehydrogenase
-alpha ketoglutarate -> succinyl Co A

166
Q

Regulation of pyruvate dehydrogenase requires what co-enzymes (5)

Same co enzymes w/ what other enzyme

A

TLC For Nobody

Thiamine pyrophosphate -(activated B1)
Lipoic Acid
Coenzyme A - Vit B5
FADH2 - B2
NADH - B3

Also used in alpha ketoglutarate dehydrogenase

167
Q

Arsenic poisoning presentation?(3)

How does it affect the krebs cycle?

A

Garlic breath
vomitting
rice water stools

Blocks pyruvate dehydrogenase and alpha ketoglutarate dehydrogenase coenzyme: lipoic acid

168
Q

Pyruvate dehydrogenase may be due to (3)

presenation?

A

X linked deficiency

Functional

  • Arsenic poisoning(lipoic acid)
  • Thiamine deficiency

presents as neurogenic defects

169
Q

Rx for pyruvate dehydrogenase complex deficiency

A

increase ketogenic nutrients

high fat content of increase lysine and leucine (ketogenic AA

170
Q

Electron transport complexes may be blocked by what?

Complex I (3)

Complex II

Complex III(1)

Complex IV(4)

ATPase (1)

A

Complex I

  • amytoyl - a barbituate
  • Rotenone - fish poison
  • MPP

Complex II

Complex III
-antymycin A

Complex IV

  • Cyanide - CN
  • carbon monoxide - CO
  • Azide - N3
  • hydrogen sulfide (H2S)

ATPase
-oligomycin A

171
Q

where does ATPase get the energy to make ATP

final electron acceptor in the electron chain?

A

from the H gradient built up in the intermenbrane space

1/2 O2 and 2 H-> H20 is the final e- acceptor

172
Q

What substances can increase the inner permeability of the nner mitochondria membrane decreasing ATP synth but increasing heat(3)

A

uncoupling agents

  • ASA
  • Thermogenin (brown fat)
  • 2,4 dinitrophenol (weight loss pill)
173
Q

Cori cycle function?

A

anaerobic glycolysis

pyruvate in cell is made into lactate (via LDH) -> goes into circulation to the liver where Lactate -> pyruvate (via LDH); 6 ATP are then invested to make that glucose again to be shipped out

  • lactate signal O2 starvation
174
Q

Why is there high levels of alanine and glutamine in the serum?

A

main carriers of N from the tissue to the liver and eventual excretion in the urea cycle

175
Q

What is generally involved i transamination?

A

transfer of AA to alpha ketoglutarate to form glutamate (add on one more NH3 to get glutamine)

the remaining deaminated AA is a ketoacid (such as pyruvate and used in energy metab,)

176
Q

pyruvate and alanine are related how?

A

differ in 1 N group on the alanine

177
Q

in addition to substrates what is required by all aminotransferases

A

B6

pyridoxal phosphate

178
Q

what are the 2 most important amino transferases?

A

alanine aminotransferase
-alanine + alpha ketoglutarate glutamate and pyruvate

aspartate aminotransferase
- glutamate + oxaloacetate alpha ketoglutarate + aspartate

transferases named by donor N group.

179
Q

Source of NADPH ?

Uses (4)

A

HMP shunt/ pentose phosphate pathway

  1. Synthesis of cholesterol and FA
  2. Generation of O2 free radicals in phagocytes
  3. Protection of RBCs from oxidative damage
  4. cytochrome p450
180
Q

Rate limiting enzyme of the pentose phosphate pathway

2 major products

A

2 NADPH - used later in several processes

Ribulose 5 Pi (used in ribose backbone)

181
Q

3 enzymes important in the generation of oxidative burst in phagosomes

A

NADPH oxidase
-> makes free oxygen radical

Superoxide dismutase
- free oxygen radical -> H2O2

Myeloperoxidase
- H2O2 -> HClO (hypochlorite /bleach)

182
Q

Why does NADPH oxidase deficiency lead to increased risk of infection

A

Chronic granlumatous disease

Lose the cells ability to make H2O2 and then catalase positive cells degrade environmental H2O2

-> no substrate to make HCLO3 via myeloperoxidase

183
Q

Role of NADPH and RBC health

A

H2O2 and other free radicals are reduced by glutathione while glutathione is oxidized to glutathione disulfide

Glutathione is regenerated w/ glutathione reductase which uses NADPH as an e- donator.

No NADPH, no protection from free radicals for RBC -> hemolysis (problem w/ G6PD deficiency)

184
Q

G6PD is transmitted?

what is seen on a blood smear?(2)

A

X linked transmission -> lack of RBC protection from oxidative damage due to inability to reduce glutathione again

  • > heinz bodies (oxidized hemoglobin in RBCs)
  • > bite cells (splenic macrophages remove the heinz bodies)
185
Q

Drugs and substances that may induce an oxidative crisis in someone w/ G6PD deficiency (9)

A 
Antimalarias - chloroquine + primaquine
Nitrofurantoin
Dapsone
Sulfonamides
Isoniazid
Naphthalene
Fava beans
High dose
-Ibuprofen
-ASA
186
Q

Defect in fructokinase presentation

Called?

A

essential fuctosuria

benign disease w, excess sugars in the blood and urine, some may spill into hexokinase for conversion

187
Q

Enzyme deficient in fructose intolerance?

Rx?

A

Aldose B -> phosphate trapping on fructose (depletion of phosphates impair phosphorylation needed in gluconeogenesis and glycogenolysis

Rx: no fructose or sucrose (glucose and fructose)

188
Q

Fructose intolerance presentation (5)

A

infant presenting 6-7 months (after starting new foods)

hypoglycemia
jaundice
cirrosis
vomiting
hepatomegaly
189
Q

Enzyme deficiency that may lead to infantile cataracts, sugar in the urine, and not much else?

A

Galactokinase deficiency

Galactitol accumulates vis aldose reductase w/ excess galactose -> cataracts

190
Q

Enzyme deficient in classic galactosemia

presentation

A

Galactose 1 phosphate uridyltransferase
- toxic accumulation

jaundice
FTT
hepatomegaly
infantile cataracts
mental retardation
191
Q

Rx for classic galactosemia?

A

no galactose or lactose (galactose and glucose)

192
Q

When are glycogen stores depleted?

A

10-18hrs after the last meal

193
Q

when does gluconeogenisis begin post absorptive?

A

4-6 hrs

194
Q

after 24 hrs since las meal what fuel is being produces and what is being used by what?

A

Glucose(via glycogenolysis- gylcogen is gone)
FA

Brain uses glucose
Muscles and other tissues use some glucose but predom FA

195
Q

When does the body start to make ketone bodies

A

48 hrs after the last meal roughly
-glucose and FA is also made

Brain uses glucose predominantly but some ketones
Muscles use FA - but also some ketones

196
Q

What cell only uses glucose no matter what state of starvation?

A

RBCs

197
Q

What metabolic scenario favors synthesis of ketone bodies?

What are ketone bodies(2)

A

when production of acetyl CoA from FA beta oxidation overwhelms the TCA cycle oxidative capacity

acteto actetate -> Beta hydroxybutrate (w/NADH)

Acetoacetate also spontaneously breaks down into acetone to give fruity odor

198
Q

What is the rate limiting enzyme to ketone body production

A

HMG Co Synthases

199
Q

Urine test for ketone bodies detects

A

beta hydroxybutrate

NOT aceto acetate

200
Q

How long until the brain preferentially uses ketone bodies?

what the muscle primary fuel sure at this time?

A

~5 days

Musclces use FA mainly but some Ketone

RBC still use glucose from gluconeogen

201
Q

Overnight fast vs 3 day fast

% glucose
% ketone

A

overnight
- 90% from glucose - 2/3 glycogen, 1/3 gluconeogen

3 day

  • 60% ketone bodies - 1/2 aceto acetate, 1/3 beta hydroxybutrate
  • 40% glucose - from mostly glucose genesis
202
Q

Why do you become hypoglycemic after having alcohol on an empty stomach

A

alcohol metabolism leads to generation of NADH

NADH presence takes away gluconeogenisis reactants from making more glucose and shunts them to making:

pyruvate -> lactate (acidosis)
oxaloacetate -> malate

leads to FA synthesis and accumulation in the liver

203
Q

Acytyl CoA used in (4)

A

TCA cycle
FA synthesis
cholesterol synthesis
ketone synthesis

204
Q

Kwashiokor cause and presentation

A

protein malnutrition ->

FLAME

  • Fatty Liver
  • Anemic
  • Malnutrition
  • Edema/Ascities

less protein for albumin and rapidly proliferating cells (RBCs and skin - lesions/ hair abnormalities)

205
Q

Marasmus is due to

Presentation (3)

A

energy malnutrition

muscel wasting
lost of sub Q fat
variable edema

206
Q

Refeeding syndrome is due to

Timeline to be concerned

A

rapid reabsorption of Mg, K and phosphate back into the cell w/ the nutrients now in the cell -> arrhythmia risk and neuro problems

Cells originally dumped electrolytes to maintain osmotic balance in the vasculature

starvation for more than 5 days

207
Q

Chylomicrons are packaged where and leave?

A

Packaged in the enterocyte and leave via the lymph system into the blood around the L subclavian

208
Q

Liver takes up chylomicron and LDL via

A

LRP a group of receptors that include LDL receptors

209
Q

CETP

A

cholesteral ester transfer protein

transfers cholesterol picked up by HDL on to VLDL and LDL

210
Q

Liver picks up the TG it needs via what enzyme

A

hepatic triglyceride lipase

211
Q

cells in the periphery take up cholesterol rich LDL via

A

endocytosis, LDL receptor and clathrin coated endocytosis

212
Q

LCAT

A

lecithin cholesterol acyl transferase

takes cholesterol from the periphery and places on HDL to dump on LDL or have it scavenged directly by the liver via SRB1

213
Q

Cholesterol is made out of?

Rate limiting step?

A

made out of acetyl CoA

HMG CoA reductase is the rate limiting step

214
Q

APO E

A

mediates reuptake of remnants

215
Q

APO A I

A

Activates LCAT which leads to maturation of HDL as it takes on cholesterol from the periphery

216
Q

APO C II

A

co factor w/ lipoprotein lipase that removes FFA from the lipid particles (VLDL, Chylomicrons, HDL)

217
Q

APO B 48

A

mediates secretion of the chylomicrons from enterocytes into the lymph

218
Q

APO B 100

A

mediates secretion of VLDL from the liver, binds to LDL receptor

219
Q

LDL transfer of cholesterol vs HDL

A

LDL transports cholesterol to the periphery of cells while HDL transfers it to the lever

220
Q

hyper chylomicronemia

defect (2)

Complications (3)

A

auto recessive defect in either:

  • lipoprotein lipase
  • apolipoprotein CII

(can’t cut -> increase in chylomicrons and TG and cholesterol)

Pancreatitis,
hepatosplenomegaly,
eruptive/puritic xanthomas
(NO increased risk of atherosclerosis)

221
Q

familial hyper cholesterolemia

defect

Complications(4)

A

Auto DOM defect in LDL receptors ->

  • accelerated athersclorisis
  • tendon xanthomas
  • corneal arcus
  • pancreatitis
222
Q

hyper triglyceridemia

defect

complications

A

Auto DOM hepatic overproduction of VLDL,

pancreatitis

223
Q

Abetalipoproteinemia presentation (5)

Defect?

A

auto recessive defect in microsomal triglyceride transfer protein (MTP) gene -> decrease in B 48 and B100; enterocytes overwhelemed w/ triglycerides b/c can’t export

FTT
Streatorrea
acanthocytosis ( spiky RBCs) 
Ataxia 
night blindness (ADEK def)
224
Q

young patient presents w/ ataxia, night blindness and acanthocytosis, and steartorrea

A

Abetatlipoproteinemia

can also have FTT,

histology shows lipid accumulation in the enterocytes due to inability to export w/lack of apo B48 and B100

225
Q

atheromas

A

plaques in the blood vessels due to oxidized LDL -> inflammation

226
Q

xanthomas

preferred location

A

lipid laden histiocytes (dendrites) in the skin

especially
-eyelids (xanthelasma)

227
Q

tendinous xanthoma

preferred location?

A

lipid accumulation in the tendon

especially the achilles

228
Q

corneal alcus

A

lipid deposition in the cornea (nonspecific

229
Q

FA synthesis precursors?

Rate limiting step and location

A

acetyl CoA

acytyl CoA carboxylase in the cytoplasm

230
Q

FA metabolism rate limiting step and location

A

occurs in the mitochondria after getting in with the carnitine shuttle

Carnitine acyltransferase 1 (carnitine palmitoyl transferase 1)

most commonly deficient is Acyl CoA dehydrogenase

Breaks down into: ketone bodes and TCA cycle

231
Q

Carnitine deficiency is?

Presentation(3)

A

inability to transfer LCFA into the mitochondria for degradation

causes:
- weakness
- hypotonia
- hypoketoic hypoglycemia

232
Q

hypoketoic hypoglycemia be suspicious of

A

defect in FA beta oxidation

most common enzyme acyl CoA dehydrogenase- 1st step in beta oxidation

233
Q

Essential AA(9)

A

PVT TIM HaLL

Phenylalanine
Valine
Threonine

Tryptophan
Isoleucine
Methionine

Histidine
Leucine
Lysine

234
Q

Acidic AA (2)

A

Aspartic Acid
Glutamic acid

(- charge at body pH)

235
Q

Basic AA (3)

A

Histidine
Arginine
Lysine

Arg and His -> growth
His and Arg -> histones and nuclear localization

236
Q

Catecholamine synthesis (6 steps)

A

phenylalanine -> tyrosine
-phenylalanine hydroxyase

tyrosine-> DOPA
-tyrosine hydroxylase

DOPA -> Dopamine
-DOPA decarboxylase

Dopamine -> NE
- vitamin C

NE -> Epi
- SAM

237
Q

hormone that encourages Epi formation

A

cortisol

238
Q

Thyroxine derived from

A

catecholamine pathway

- branch off tyrosine

239
Q

melanin derived from

A

catecholamone pathway

- branch off dopamine

240
Q

Tryptophan makes? (2)

A

Niacin (via B6) -> NAD/NADH

Serotonin (via BH4) -> melatonin (in pineal gland)

241
Q

Niacin derived from what AA

A

Tryptophan (w/ B6)

242
Q

Serotonin derived from what AA

A

Tryptophan

243
Q

Histidine makes (1)

A

Histamine (via B6)

244
Q

Histamine derived from what AA

A

Histitidine (w/B6)

245
Q

Glycine makes (1)

A

Porphyrin(via B6) -> heme

246
Q

heme and porphyrin precursor derived from what AA

A

glycine w/ B6

247
Q

Arginine makes (3)

A

Creatine
Urea
Nitric oxide

248
Q

Creatine is derived from what AA

A

Arginine

Urea, NO

249
Q

Urea is derived from what AA

A

Arginine

Creatine, NO

250
Q

NO is derived from what AA

A

Arginine

Creatine, Urea

251
Q

Glutamate makes what (2)

A

GABA (via B6)

glutathione

252
Q

GABA is derived from what AA

A

glutamate (w/ B6)

253
Q

glutathione is derived from what AA

A

glutamate

254
Q

Methionine makes what?

A

S Adenosyl methionine

255
Q

S adenosyl methionine is derived from what AA

A

methionine

256
Q

Rate limiting step in the Urea cycle?

where does it occur?

A

Carbamoyl phosphate syntetase I

in the liver (mart in the mitochondria part in the cytosol)

257
Q

what AA can donate NH4 directly to the urea cycle

What AA is a found as a substrate in the urea cycle

A

Aspartate

Arginine
- step before arginase cleaves off urea w/ hydrolysis to create ornithine

258
Q

Urea is made of what?

Where is the products sources?

A

Urea is made of 2 NH2 molecules attached to a C that has a double bond to O

1 NH2 is from aspartate
1 NH2 is from NH4 (dropped off by glutamine in the mitochondria)

259
Q

Ornithine transcarbamolysis is important where?

A

in the urea cycle
transports NH4 containing Carbamoyal phosphate and combines it w/ ornithine to create citulline

May be deficient in a X linked recessive disorder interfering w/ ammonia excretion

260
Q

Presentation of ornithine transcarbamoylase deficiency?

2 things in seen w/ labs

A

first few days of life w/ excess carbamoyal phosphate is converted to orotic acid (from pyrimidine synthesis pathway)

thus have orotic acid in blood and serum AND hyper ammonia -> Decreased BUN w/ no urea being made

Symptoms of hyper ammonia -> tremor, slurring of speech, somnolence, vomiting, cerebral edema, blurred vision

261
Q

Ammonia toxicity may be due to (2)

Presents as? (6)

A

Liver disease (hepatocyte damage -> impaired urea cycle)

Congenital abnormality in urea cycle (ornithine transcarbomolase deficiency - X linked)

Hepatoencephalopathy (TCA cycle inhibited due to alpha ketoglutarate depleated w/ excess NH4)

  • tremor (asterixis/ liver flap)
  • slurring of speech
  • somnelance
  • vomitting
  • cerebral edema
  • blurred vision
262
Q

Rx for hyperammonia

4

A

decrease protein diet

Benzoate
phenylbutrate

biotin -> stimulate ornithine transcarbamoylase

263
Q

Patient comes in w/ mental retardation, seizures, fair skin, and musty odor, a few days after birth

What are the 2 causes?

Dietary modifications?

A

Phenylalnine hydroxylase deficiency or BH4 (tetrahydrobiopterin deficiency)

Decreased diet in phenylaine (low aspartame and protein)

Increased tyrosine +/- BH4 if deficient

264
Q

Presentation of PKU (6)

A

Auto recessive deficiency in phenylalanine hydroxylase

Fair skin (less melanin from catecholamine pathway)
musty odor
siezures
mental retardation
growth disorder
eczema
265
Q

Patient’s urine turns black when left out over extended periods and has arthralgias and maybe brown pigmented sclera

defect in?

A

alkaptonuria(ochronosis)

autosomal recessive defect in homogentisic acid oxidase deficiency (tyrosine degradation pathway -> homogentisic acid -X -> fumarate)

Homogentisic acid builds up in connective tissue, sclera, urine and cartilage -> arthralgia

Benign

266
Q

alkaptonuria is a defect in what enzyme

A

homogentisic acid oxidase
-> build up up homogentisic acid which turns things brown/black (sclera, skin, urine) -> arthralgias

Tyrosine is not broken down as well

267
Q

Homogentisic acid oxidase deficiency ->

A

Alkaptonuria (ochronosis) tyrosine breakdown issues

black urine left standing
brown/dark sclera/connective tissue
arthralgia w/ homogentisic acid buildup

268
Q

phenylacetate, phenylpyruvate and phenyl acetate seen in the urine- be concerned w?

Presentation

A

PKU

Mousy odor
Siezures,
Mental retardaiton,
eczema
fair skin
269
Q

Maternal PKU results in?

A

microcephaly
mental retardation
growth retardation
congenital heart defects

Phenylalanine build up is toxic to the babe

270
Q

Albinism may be due to a few causes (3)

What is this called

A

Locus heterogeneity

Tyrosinase deficiency - auto recessive (can’t make melanin from tyrosine)

Defective tyrosine transporters ( less tyrosine in melanocytes)

Failure of melanocyte migration

271
Q

S adenosyl methionine acts as what

important in what 2 synthesis pathways

A

acts as methyl donator
- ATP and methionine make SAM -> homosystine post CH3 donation

Important in

  • NE -> Epi
  • synth of phosphocreatine
272
Q

Regeneration of methionine in order to make SAM need ((3)

A

Folate
B12

deficiency leads to decrease anabolic pathways in CH3 donation

273
Q

Homocystinuria is due to (3) auto recessive issues?

A

cystathione synthase deficiency
- converts homocysteine -> cystathione -> cysteine (AA)

decreased affinity of cystathione synthase for pyridoxal phosphate (B6)

homocysteine methyltransferase deficency

  • (maybe low B12)
  • Converts homocysteine to regen methionine which combines w/ATP to make SAM
274
Q

Subluxation of the lens is a finding in 2 congenital issues

A

Marfans (upward deviation)

Homocystinuria (downward deviation)

275
Q

Findings in homocystinuria (7)

A 
homocysteine in the urine
tall
kyphosis
lens subluxation
atherosclerosis
mental retardation
osteoperosis

(due to cystathione synthase def, low B6 affinity, or homocysteine methyltransferase def)

276
Q

Rx for each of the 3 causes of homosysenuria

A

cystathionine synthase deficiency

  • low Methionine
  • increased cysteine (essential now)
  • increased B12 and B6

low affinity for pyridoxal phosphate by cystathionine synthase
-increase B6

homocystein methyltransferase def
- increase B12

277
Q

Cystinuria is due to ?

Loss of what AA?(4)

A

defeciency in renal tubular AA transporter

Lose COLA

  • Cysteine
  • Ornithine
  • Lysine
  • Arginine
278
Q

Cystinuria presents as?

Rx?

A

hexagonal crystals and stag horn calculi in a kid due to excess cysteine in the urine which precipitate out

Rx - alkalinize the urine w/ acetazolamide; good hydration

Lose COLA w/ renal tubular AA transporter def

  • Cysteine
  • Ornithine
  • Leucine
  • Arginine
279
Q

defect in alpha ketoacid dehydrogenase presents as?(4)

A

maple syrup urine disease
- can’t break down branched chain AA: Leucine, isoleucine and valine

CNS disorders
mental retardation
death
sweet smelling urine

280
Q

maple syrup urine disease is due to?

what AA pathway is disrupted

A

alpha ketoacid dehydrogenase deficiency leads to inability to break down branched chain AA: leucine, isoleucine and valine

CNS defects, mental retardation , death, sweet smelling urine

281
Q

Hartnup disease is due to?

presentation?(3)

A

deficiency in neutral AA transporter in the kidney -> loss of tryptophan in urine

-> can’t make niacin -> pellagra

dementia, diarrhea, dermatitis

282
Q

kid shows up to an ER w/ hematemisis and abdominal pain

A couple 6-72 hrs later the patient is in metabolic acidosis, what is going on?

A

Kid got into his mom’s iron fortified vitamins

Cell death due per oxidation of membrane lipids

283
Q

Acute and chronic presentation of iron poisoning

A

Acutely - hematoemesis -> hypo volumetric shock; Ab pain

Chronically - metabolic acidosis (6-72 hrs); GI scarring and obstruction 2-8 wks out

284
Q

What is ferritin?

2 functions

A

it is an iron protein complex (ferric acid and apoferritin)

Used in cellular storage of iron in the hepatocyte
Acute phase reactant released into serum w/inflammation and infection -> less Fe for bacteria

285
Q

What is transferrin?

iron deficiency has what effect on transferrin?

A

protein that binds to ferric molecules and transports them in plasma

1/2 life = 8 days

increased in iron def (body makes more decease it wants to shuffle Fe around in def)

286
Q

Zinc is important in what? (3)

essential in what 2 enzymes?

A

formation of zinc fingers (TF motif) -> protein formation in times of synthesis (like healing)

essential for carbonic anhydrase and lactic dehydrogenase

immune system

287
Q

Zinc deficiency manifests as(11)

A 
delayed wound healing*
less adult hair
hypogonadism
less responsive immune system
anorexia/diarrhea
dysgenisa - taste
anosmia - smell
depressed mental function 
Rash - around eyes, nose, mouth and anus (Acrodermatitis  enteropathica)
Impaired night vision 
Infertility
288
Q

Patient presents w/ decreased night vision a new rash located around the eyes, mouth and anus and has cut that just does not seem to heal - Whats going on

A

maybe zinc deficiency

delayed wound healing*
less adult hair
hypogonadism
less responsive immune system
anorexia/diarrhea
dysgenisa - taste
anosmia - smell
depressed mental function 
Rash - around eyes, nose, mouth and anus (Acrodermatitis  enteropathica)
Impaired night vision 
Infertility
289
Q

basophilic stippling and microcytic anemia seen in?

A

lead poisoning

290
Q

Signs of lead poisoning

A

Low IQ
hearing problems
impaired growth
impaired peripherla nerve function - wrist/foot drop
Lead lines (gingival- burtons lines; bone, teeth
anemia
cholic/ ab pain

291
Q

Lead poisoning leads to inhibition of what 2 enzymes?

presents as

A

ferrochelatase and ALA dehydratase
- both involved in heme synthesis -> anemia

-> inhibits rRNA degradaion in RBC -> basophilic stippling

292
Q

Sideroblastic anemia

A

see iron laden mitochondria w. defect in heme synthesis

microcytic

can be hereditary( X linked ALA synth defect)

Reversible - alcohol, lead, isoniazid

293
Q

Rx for lead poisoning (3)

A

dimercaprol - severe

EDTA
Succimer

294
Q

Kid has abdominal pain, decreased mental IQ and peripheral nerve path (wrist/foot drop), w/ burtons lines

Ask about what living situation

A

lead paint chips at home

burtons lines -> lead accum in gingiva

295
Q

D2/ergocalciferol

A

ingested from plants

296
Q

D3/cholecalciferol

A

consumed in milk or synthesized in skin

297
Q

Vitamin D measured in serum?

A

25 hydroxycholecalciterol;
25 OH D3 -> storage form

Made by liver

298
Q

active form of Vitamin D?

made by

A

calcetriol
1,25 (OH)2 D3

Made by the kidney

299
Q

3 functions of Vitamin D

A

increased Ca, Phos and Mg absorption from the intestine

increased PTH dependent reabsorption of Ca in the distal tubule

increased bone mineralization

300
Q

3 causes of Vit D deficency

A
  1. lack of Vit D in diet
  2. impaired hydroxylation of vit D to active form
  3. reduced response to vitamin D
301
Q

Vitamin D deficiency presentation in kids and adults?

A

Rickets - kids
-bone pain, bowing, path fractures, dental issues (increased PTH to raise serum levels leads to pathology)

*note: breast milk is deficient in Vit D - Supplement

Osteomalacia - adults
- hypocacemic tetany, muscle weakness and bone pain

302
Q

Causes of Vit D excess (2) and presentation(3)

A

excess supplementation or sarcoidosis( increased activation of Vit D by epitheliod macrophages)

have hypercalcemia, loss of appetite and stupor

303
Q

alpha tocopherol

A

Vitamin E

304
Q

Vitamin Es function

A

antioxidant - prevents nonenzymatic oxidation of cell components by oxygen free radicals

  • especially protective of RBCs (hemolytic anemia if absent)
305
Q

patient presents w/ muscle weakness, hemolytic anemia and ataxia be thinking of?

A

Vitamen E deficiency/alpha tocopherol

306
Q

Vit E deficency presents as(3)

A

hemolytic anemia - erythrocyte fragility

peripheral neuorpathy -> muscle weakness

spinocerebellar tract demylination -> Ataxia

307
Q

vitamin K’s function

made into active form where?

A

serves as a cofactor for gamma carboxylation of glutamic acid -> coagulation factors II, VII, IX, X, Protein C and S

synthesized by intestinal flora

308
Q

Why are neonates given a shot of Vit K at birth

A

Breast milk does not contain Vit K

309
Q

Deficiency of Vitamin K in neonates presents as

Why are they susceptible to deficiency?

A

neonatal hemorrhage w/ increased PT and aPTT
- normal bleeding times

Neonate intestines are sterile thus no Vit A synthesis

310
Q

What can cause Vit K deficiency in adults (3)

A

warfarin toxicity
Antiepileptics - phenytoin
antibiotics - disrupts normal flora that makes Vit K

311
Q

gamma carboxylation of glutamic acid importance?

A

uses Vit K -> coag factors

312
Q

4 Functions of Vit C

A
  1. Hydroxylation of proline and lysine in synthesis of collagen
  2. Co factor in the synthesis of Dopamine -> NE
    - dopamine hydroxylase uses
  3. Facilitates absorption of Fe ( keeps Fe in reduced Fe2+ state) - drink Fe sup w/ orange juice
  4. Antioxidant (used w/ Vit E)
313
Q

ascorbic acid

A

Vit C

314
Q

Scurvy presentation (7)

A 
swollen gums
purpura eccymycoses/bruising
swollen joints
bleeding into joints -> hemarthrosis
anemia
poor wound healing
weak immune system
315
Q

Vitamin A functions (4)

A

Antioxidant
maintains epithelial and mucous secreting membranes
immune system
Eye maintenance

316
Q

Vitamin A is used in the Rx of (3)

A

Acne - tretinoin, isotretenoin
Measles
AML M3

317
Q

Deficiency in vitamin A (4)

A

decreased night vision
xerophthalima - conjunctival dryness - ulceration
keratomalacia - wrinkling/ cloudy cornea
bitot spots - dry silver grey bulbar conjunctiva

318
Q

Beta carotene

A

2 retinols bound together

319
Q

keratomalcia and bitot spots may hint at

- maybe corneal ulceration

A

Vit A deficiency

Cornea wrinkling,

dry silver/grey bulbar conjunctiva

320
Q

Female patient presents w/ a HA after too much Vitamin A- > wants the diagnosis

A

pseudotumor cerebri

321
Q

Vitamin A toxicity

A 
N/V
HA
intracranial pressure - pseudotumor cerebri
teratogen
aloplecia
\+/- cirrosis
stupor
skin changes
322
Q

What much be done before prescribing Vit A

A

pregnancy test

323
Q

thiamine is essential for what 4 reactions?

A

pyruvate dehydrogenase
-pyruvate -> acetyl CoA

Alpha ketoglutarate dehydrogenase
-alpha ketoglutarate -> Succinyl CoA

Transketolase ( HMP shunt/ pentose phosphate)
- Ribulose 5Pi -> Ribose 5Pi

Branched chain AA dehydrogenase

324
Q

Deficiency in thiamine presents as (4 main presentations)

A

impaired glucose breakdown and ATP depletion worsened after glucose infusion (heart and brain first)

Wernicke Encephalopathy

  • enecphalopathy
  • occulomotor dysfunction
  • gait ataxia

Korsakoff

  • memory loss
  • confabulation

Dry beri beri
-polyneuritis w/ myelin degeneration

Wet beri beri
- cardiomyopathy and cardiac failure

325
Q

Causes of thiamine deficiency - 3 clinical pictures

A

Malnutrition
- alcoholism

Malabsorbtion

Loss of water soluble vitamins
- dialysis

326
Q

Wernicke encephalopathy presentation(3 main) and cause

A

acute thiamine deficiency -> medial dorsal nucleus of thalamus and mammalary body degradation

Encephalopathy
occulomotor dysfunction
gait/ataxia
stupor 
coma
hypotenison
hypothermic
327
Q

korsakof presentation (4) and cause

A

chronic thiamine deficiency -> medial dorsal nucleus of the thalamus and mammalary body degradation

memory loss - retrograde/anterograde
confabulation
apathy
personality changes

328
Q

dry beri beri presentation(4) and cause

A

thiamine deficiency -> polyneuropathy w/ myelin degeneration (w/ lack of glucose breakdown)

toe/wrist/foot drop
muscle weakness
hyporeflexia
arreflexia

329
Q

Wet beri beri presentation (4)and cause

A

thiamine deficiency -> lack of ATP w/ glucose breakdown halted

high output cardiac failure
edema
peripheral vasodialation
high output cardiac failure

330
Q

Vitamin Cofactor in oxidation reduction reactions (2)

A

Riboflavin B2

Niacin B3

331
Q

Riboflavin B2 function

deficiency presents as (3)

A

cofactor in oxidation/reduction reactions

  • if it has dehydrogenase in its name
  • > FMN and FAD

Cheilosis - angular fissures in the mouth
corneal vascularization
glossitis

332
Q

Vitamin B3 used in ?

Deficiency presents as?

A

Niacin -> reduction/oxidation reactions

  • in diet or made from tryptophan
  • > NAD and NADP
Glossitis
Pellagara
-Dermitis
-Delerium
-Diarrhea
333
Q

3 causes of Vitamin B3/ niacin deficiency

A

Hartnup disease - neutral AA transporter deficiency in kidney (less tryptophan)

Carcinoid syndrome (Tryptophan used up)

INH
(decrease in B6 and B3)

334
Q

Vitamin given to raise HDL and lower LDL

symptom?

A

Niacin

Symptom of flushing

335
Q

Vitamin B5/Pantothenate used in?

Deficiency leads to? (4)

A

component of CoA and FA synthesis

Dermatitis,
enteritis,
aloplecia,
adrenal insufficiency

336
Q

Vitamin B6 used in?(4)

Deficiency leads to? 95)

A

pyridoxal phosphate is

  • a cofactor in transamination (ALT/AST)
  • Deamination
  • Synthesis of AA
  • ->cystathione, heme, niacin, histamine,
  • Synthesis of NT
  • -> 5HT, Epi, NE, GABA, Dopamine

Deficiency leads ->

  • convulsion,
  • hyper irritability,
  • peripheral neuropathy
  • glossitis/angular cheilosis
  • sideroblastic anemia w/out heme
337
Q

Patient presenting w/ convulsions, hyper irratability and glossitis may be deficient in what?

A

B6-> pyridoxal phosphate

less GABA leads to convulsions

338
Q

Deficiency in B6 may be due to use of what?

A

INH

339
Q

Vitamin B7/ Biotin is used in?

Deficiency presents as

A

carboxylation reactions- add on 1 C
- like pyruvate carboxylase and acetyl CoA carboxylase

deficiency is rare (maybe if eating egg whites (Avidin))
-> dermatitis, aloplecia, enteritis

340
Q

Patient is a body builder and insists on diet containing pure egg whites, what is he at risk for

A

Biotin deficiency due to avidin in eggs binding and decreasing availability

341
Q

Vitamin B9 is also known as?

Active form?

A

Folic acid

tetrahydrofolate (THF)

342
Q

Importance of B9/folic acid?

deficiency leads to ?(7)

A

synthesis of and repair of the nitrogenous bases in DNA

  • especially in rapidly dividing and growing cells
  • > B9 is a coenzyme for 1 C transfer/methylation
deficiency leas to macrocytic megaloblastic anemia*
- NO neuro symptoms vs B12
growth failure
neural tube defects if pregnant*
glossitis
diarrhea
depression 
confusion
343
Q

megaloblastic anemia is found in? (2)

differ how (4)

Means?

A

folic acid and B12 deficiency

B12 has neuro symptoms, low serum levels, high homocysteine levels and increased MMA

megaloblastic means large cells - keep growing due to impaired DNA synthesis and can’t divide

  • > seen in the bone marrow and peripheral smear
  • > anemia in Macrocytic RBC
  • > hypersegmented PMNs
344
Q

Deficiency in Folic acid may be due to (4)

A

Drugs

  • methotrexate
  • phenytoin
  • sulfonamides
  • trimethoprim
345
Q

Most common vitamin deficiency in the US?

A

Folic acid

-alcoholism and pregnancy

346
Q

Vitamin that has cobalt associated w/ it?

A

B12 - cobalamin

347
Q

Function of Cobalamin? (2 reactions)

Deficiency(2)

A

cofactor for :
homocysteine methytransferase
–>(homocysteine-> methionine and THF)
–> very important in DNA synthesis

methylmalmonyl CoA mutase
-> methylmalonyl CoA -> succinyl CoA

Deficiency leads to

  • macrocytic megaloblastic anemia (hyper segmented PMNs)
  • neurologic symptoms : paresthesis, subacute degeneration, dementia, memory loss, weakness)
348
Q

Clinical picture for B12 deficiency(4)

A

Strict vegans/vegetarians

malabsrobtion

  • celiac sprue
  • enteritis
  • diphyllobothrium datum

intrinsic factor deficiency

  • pernicious anemia
  • Gastric bypass

absence of terminal ileum
-Crohns

349
Q

Pernicious anemia is due to ?

test for it how?

A

autoimmune attack of the parietal cell or intrinsic factor leads to a deficiency in B12

350
Q

Schilling test used for detecting?

A

used for detecting radioactive B12 uptake

- if limited fluorescent B12 is in the urine then there is pernicious anemia

351
Q

Where is B12 absorbed

A

in the terminal illium bound to intrinsic factor

352
Q

peripheral neuropathy and glossitis? (2)

A

B12 and B6

353
Q

pernicous anemia due to deficiency in?

A

B12

354
Q

used in carboxylation reactions

A

Biotin B7

355
Q

used by pyruvate dehydrogenase and alpha ketoglutarate

A

B1 thiamine

356
Q

Vitamins critical for DNA synthesis

A

B9 and B12

USLME Kiss my ass and pray (33 decks)

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