Trace elements

CC2 Midterms Lee3

supposedly

TRACE ELEMENTS BIOLOGIC FUNCTIONS IRON Fe

foundinthebodyinverylittle 1 Electrontransport most abundant T E
concentration onlypresent in a Respiration Ferric Ferrous state
minuteamounts inthebody IRON important inHEMEL important in carryingOz
961 C H ON importantin
Itg at because it is a constituent
3gooa r electrolytes carries Oz of hemoglobinand myoglob
remaining traceelements 3 Hormonal activities important in Oztranspo
can be classified into hormones inthebody
rely on Agent in redox
ESSENTIAL sometraceelements electrontransport
can'tbe synthesized bybody 4Enzyme activator or wfators cofactors cytochrome oxidas
in largeamount cofactors inorganic compounds xanthine oxidase
sometimescansynthesize but enzymes can't dotheir function peroxidase
insufficient w o a Trace element catalase
oftenlyassociated w absorbed in duodenum
metallo
proteins
metalloenzymes 5 protectionfromfree radicals jejunum in Ferrousform
organmalfunction is caused by SODSelenium Transtalbumin transpor
a deficiency of a traceelement Sop superoxide Dismutase stored as Ferretti or
impaired biochemicalprocesses antioxidanteffect Hemosiderin inBMliver
CAUSES of DEFICIENCY scavenger of free radicals spleen
1 f intake of TE composed ofzinc Fe in diet Fe in
2 9secretioninthebody Copper Ferric reductase
Ferrousform
3 impaired absorption

FREDD 02 t Haoz
NON ESSENTIAL Fe acidicpHin
produced bythebody
catalase stomach Stransferr
Hzozpwof.dz H2O molecule witCpresent
not needed in thediet Albumi
or
Toxicity excess concmayleadto Selenium
intoxication glutathione component BMspleen liver
many N essential T Earetoxic regenerates Vit C D
stored asf Hemosiderini
Ferritin
10ESSENTIALTRACEELEMENTS 6 Tissue repair zinc
1 copper mostTraceelements focuson Storage is important because
2 chromium inAbundancy wound healing accumulationoffreeFe inthe
3 cobalt 1 iron inzincsulfate active healers of plasmaistoxic
4 iron 2 Zinc wound healers
5 Manganese 3 Copper 7 Immune system
6 Molybdenum 8 Growthand reproductive process
7 Zinc
8 selenium
9 Iodine others
10Fluorine
mostaremetals
iron iodine hallogens
continuation of IRON DtENC percent saturation
Generalized IronDeficiency IDA Nv 20 551
ERLOAD ChronicLoss hemorrhagic transferrinboundw Fe
toxic prooxidation destruction impairedrelease ofFefromRES 4saturation senime 100
x
ofcells ofDNA storageorgans ofFeiBMliver TBC
spleen
ironcanonly beexcreted ceruloplasminin Disease TiBc transferring.anrationFerritin
blood t ta
duringmenstruation I DA I I
t Fe anemia Acp r p
damaged epithelium y j
not in urineIstool X SIS SerumTransferrin
storedFe BM for fatigue tiredness frequentheadache measured
byNephelometry
shortnessofbreath Increasedsensitivity
hemoppiesis anindex ofironnutritional
Depression to cold status
CAUSES Hairloss Brittlenails
restless Leg FreetransferrinLinsemmlplasmo
Increased RBCdestruction syndrome

Hemolyticanemia 4 Got Directmeasure ofTransferrin

bound wife
hemolysis releases LAB EVAL of Iron serum
_ufgBfdH XO70
Fe Transferrin
Increasedmobilization serum Iron freeiron
of Iron non hemolyzedserum isused mgdL
Amobilization Aceruloplasmin hemolyzed samplewill
give serumFerritin
tuopasmiy T e.inblood FALSE Increaseof Fe ELISAchemiluminescence
facilitatesFemobilization Earlymorningsample 12hrsfasting anindex of Festores
from Ferritin Fe has digging bsetocaeudsepe.errit.in is
marker of Hepatic late morning
necrosis fee afternoon Transferrin Ferritin
Decreased blood cell 1DA T t
formation measure the Freeironnotbound
to ACD j p
usleadsto excess Fe transferrinlalbumin

Fe is not incorporated
toformheme Tomeasure freeiron
protoporphyrinring eeseparated Fewreduced FEIcomplexed
frombinding token wi chromogens
importantin RBC proteins
use
venous
useascorbic
lead poisoning acidstrong
not acid TPR CTripyridyl
inhibits the enzyme Tcactriomoro Striazine SBP
aceticacid
ferochelatase sulfolathophenan
throline
seen in Thalassemia Hemochromatosis direct depositionof
raredisease
and Vit 1316deficiency TotalIronBindingCapacity TBC Fein liverspleen
pancreasendo glands
Defectiveironstorage amountofFethat befoundby
can
saturatingthe bindingproteins present
summat causetissue
Pernicious anemia inthe sample damage
Increase rate of absorption Indirectmeasureof serumtransferrin Hemosiderosis disorder characterized
bindsw Fe
in hemosiderosis inthebody bydeposition ofexcessiron
repeatedbloodtransfusion Differentiates IDAfromACD winthebodytissuesthatnorma
don'tcontain ee
bothlutein circulationbutdiff causes

ACD macrophage isoverstimulated I

Topofenitin late apoferritinTFe BOTH
4 Fe in the body
ferritin storedFe
TFerritin feeincirculating indiv
Nv 240 450mg1dL 43.0 80.6mmolIL
 Z l N C Zn
Component of 300enzymes Constituent of production ofneurotransmitters
enzyme can't performfunctionwhen erythrocuptein norepinephrine production
Absorptionisthroughmetallothioniney proteinfound inRBC
in B dopamine monooxygenase

richmetalbindingprotein j
samewicopper thebody Copper as cofactor
ystem contains enzymes important

Albumin alpha 2 macro

globulin for antioxidantactivity of TTOPPEREXCESS
transports zinc RBCs wk is SOD Wilson's disease
considered as a NUTRIENT zn co aka lenticular
hepato
degeneration
promotes
healthyimmunesystem absorbed in small intestine
promoteswoundhealing sometimes stomach YaeffeinasaffeemffPdfishnnhof
Cu
promotesovulationsperm dev't Kayser Fleischerring
DNAsynthesis growthdev't Transcuprein albumin cerusoplasmin
brownpigment in
Metabolism ofprotein glucose transports copper cornea ofeye
because of excess
and cholesterol copper
Copper 4oxidationStates
ZINCLXC.ES T
intoxication is rare
cuprous stable
can beabsorbedby inmetallothianine
not bad intestine stomach nontoxicstorageformofCu
chitidinegluconatecitrateenhance
oxidized absorbed absorption D penicillamine Dimercaprol

FZINC DEFICIENCY Cu Cuprous is liver stomach e inurinaryexcretionofCu

Growth retardation dwarfism Ammoniumtetra
molybdate
Delayedsexualmaturation v inhibitscopperabsorption
ovulation blood
Cubindswitranscuprein 92Nsupplement to b cu
spermdevelopment canlead Liver
to testicular atrophy liver
centers albuminandceruloplasmin absorption
Prolonged woundhealing ascemioplasmin
Acrodermatitisenterophatica WPPERDEFXENC.TT
inherited condition groupof cancarry 6 Cuatoms Menke'skinky Hairsyndrome
Ceruloplasmin
disorders characterized
goy ofCucomes in Defects inCutransport
by dermatitis theformofcemioplasmin kinkyisteelyhairmental
pigmentedlesion
hyper retardation connectivetissue

alopecia OTHERFATES of Cu in the LIVER defects

growthretardation InZn absorption
infection Cu competes when Fe
diaper facialrash inabsorption
I I cu levelin body
impaired wound healing 3 D
COPPER Cu CHROMIUM
potentiatesinsulinaction
enzymes andproteins
Metallo
copperseries as COFACTOR for supplement fordiabeticpatient
the ff metalloenzymes BIOLOGICAL FUNCTION promotescarbs fat cholesterol

Antioxidant defense soocan cu metabolism

cemioplasmin tyrosinase
cytochrome lysyoxidase CollagenFormation Chromiumlevels
in hairishigher
dopamine
Coxidase hydroxylase Lysioxidase Ccuascofactor thanserum
Sop cev crosslinksproteinintolarger Brewer'syeast from
metallothionine fiber forcollagenformation Saccharomycescerevisiae
critical forreduction of Fe in Melaninproduction
home synthesis tyrosinase Ca ascofactor
 FLUO RI NE SEL E NI UM
incorporatedintobonecrystals naturally present insoil root
crops
uscorrects calciumdeficiency vegetables
prevents osteoporosis regenerates vit E C imostpotent
Enhancesboneformation likeCa tofightcancercellformation
Replace Ca in abonedensity Glutathione peroxidase
Excess discoloration ofelementsin Sereno
cysteine
teeth partofcellularantioxidant defense
presence of crackedmotley mechanism against feeradicals
teethelement
SELENIUM EXCESS
C O B AL T Acuteoralexposure GIT cardiovascular

component of vitamin B12 symptoms

re 2n co Bia Chronicoralexposure dermaleffects
Absorbed
bythesamemechanismas neurologic problems
iron
SELENIUM DEFICIENCY
M A N GA NE SE s Keshan Disease
Highdosage is except aka Endemicmyocardiopathy
wheninhaled injuvenilecardiomyopathy
acutemanganeseaerosolintoxication destruction of cardiac cells
auramanganica manganese Kashin Beckdisease
madness common inminers aka endemic osteoarthritis
in Mn in plasma manifestschondronecrosis
necrosis of cartilage
MRIpatients Mndepositioninbrain
important tothe ff enzymes
pyruvatecarboxylase
mitochondrialSOD

arginase
glucokinase
Chronicmanganese toxicity
Parkinsons disease
characterized
by
akinesia rigidity tremors
masklikefaces
Liverdisease inMnlevel because
of f Mnexcretion

M OLY BD ENUM
Basis of treatment ofWilson'sdse
Inhibits Cu Feabsorption
important for the ft enzymes
xanthine oxidase
xanthine dehydrogenase
sulfiteoxidase
aldehyde oxidase
molybdopterin
 porphyrias
02 Midterms Lee3
pt 2
supposedly

P o R P Hy RlNS POR PHY R 1 AS PPcontinuation

Metabolicintermediatesinthe canbe acquired or inherited can be mistaken w lead
e
hemoglobin synthesis alsomyoglobin poisoning because there isalso
ee pp
Esse plumbo
porphyria
uro foundinurine of Ap Acuteintermittentporphyria 4 ALA
cupro stool urine CEP congenitalErythropoietin porphyria Dithiothreitollsulfhydryl reagent
PROTO differentiates Leadpoiso
stoolonly gpEfPCT porphyriacutanea Tard ning
Redviolet to redbrownincolorgg HEP HepatoengthropoieticPorphyria from
PI
Porphyrias EP Erythropoietinporphyria t v
ammua of porphy gµcp Here anygpwpo.my gqqyggge.gr nggyqqya.ua
T willdenote porphyrias q VP Variegate proto
porphyria ALAD
abnormalhemesynthesis

PP POT bothacquired therestare 2 Alp AcuteIntermittent

PORPHYRINOGENS hereditary porphyria
functionalformof compound DeficientHydroxymethylbilane
used inhemesynthesis ErythropoieticPorphyria synthase AMBS
unstable over
prod of precursors inBM a.k.aPBGD Porphobilinogen
doesnot fluoresce Hepatic porphyria deaminase
colorlesswhen measured
w in liver
congenital Erythropoie
wood lamp or UVlamp Ep porphyria
cutaneous symptoms Deficient UroporphyrinogenlI
photosensitivity cosynthase
blisters notlimited a.k.a Gunther'sDisease
tothese Inmortalityrate
fanyapaterphaigrmentation

Taresutro
andWPRO
PP and Alp accumulates especially

neurologic symptoms in theteeth

manifestationsabdominalpain teethfluorescered
Erythrodentia
vomiting constipationand tachycardia manifestations infant
and hypertension
increase ALA and PBG inurine cutaneous sensitivity
aminotevinicacid TPophobilinogen
mainSITE Liver BM urine red brown
RAWMATERIALS glycine t
Black1Red in color porphyria outanea
FORHEME synthesis andsuccinyl
co a urine dark
browninother
books pcy Tarda
Deficiency ofthe Deficient Uroporphyrinogen
PORPHYRIA converted
enzymes MPBG inurine porphyrin rep decarboxylase
converted also
deficientinHEP
reduction in enzymelevelresults PBO porpnobilin Black mostcommonporphyria
inexcessproduction in 1 ormore toairaight
exposure MANIFESTATIONS Blisters
ofurinesample
precursor substance
fragility insight exposed
skin abnormalgrowth of
DPP Rumboporphyria gaunD hair
Deficient Aminolevulinicaciddehydratase A IsocopRO MURO
a k a ALADdeficiency Type I restrictedto liverftp.qq.ee
sometimes aurine ALA f PBGexcretion type ienzyme deficiency
found in alltissues
 Type1 r
hands ofindividual is exposed Cutaneous symptoms
toOz sunlight air formation avoidsunlight usesunblock
offree radicals oxidative takehematin medicationusedtotreat
damage toskin blisters in
hand symptoms thatoccurswthese
Hepatoengthropoietic
HEP porphyria porphyrins
Deficient uroporphyrinogen decreasehomeload givetherapeutic

decarboxylase phlebotomy
MANIFESTATION notlimited tothese
Photosensitivitybeginsinchildhood
hepaticdiseaseon taterstage
a facial hair
scarring ofhands face
A ISOCOPRO MURO
something inserthere
e
EP Erythropoietin Porphyria
Deficient Ferrochelatase
secondmost common porphyria
T FEP zn PROTOinRBC
plasma andstool Secondary Porphyria
evenin 2nA inRBC don4 urias
Porphyrin
expert Fe is not R R excretion of Urinary Porphyrins
last enzymeinvolved inheme Not a defect inthebiochemical synthesis of hemebut0h
synthesis Otherdisorder
symptomsIMAMFESTATIONS a toxin
photosensitivity Drug interferinghemesynthesis
zburnining iitching in ALA normal PBG
painfulsensation inskin
mostCOMMON burning LABORATORY DETERMINATION
of light exposedskin porphyrias
PBG ALA test interfering
HCP Hereditary Coproporphyria method substancewhen
Deficient Corproporphyrinogen guy youwantto
or 1 Watson Schwartz measure
oxidase 8 inextractionmethodisdone porphobilinogen
a

f
lighterformof AIP t we Butanolchloroformisused useEhrlichreagentfirst
increasecoppo
ygyqggg.is qq.peog
15
a qua a we screeningtest na detect and cuffed
PBGfromUnbilinogen orindole
A ALA PBG of gates
Hardero
porphyria e s reagent sodiumacetate pinkIredcolor
rare erythropoietin in urine t of porpholurobilinogen
form of HCP 2 Addchloroform1butanolon theTestSoln in step 1
3 If redcolorformsinaqueouslayer PORPHOBILINOGEN
VP Variegate proto porphyria red pinkcolorformsin Shutoff rm VROBILINOGEN
ayer
Deficient protoporphyrinogen oxidase 2 HoeschTest confirmatory to WlsTest
SouthAfricanporphyria inPx PBGformsred orangecolorwhenmixed w
same as Alp Ehrlich'sreagent PDAB para
Hallmark is A PROTO GOPROin dimethylbenzaldehydew1HCL
stool Ct Red Orangecolor
neurologicdysfunction PBGandALA in urine
dermatitis
cutaneous symptom photo Quantitative iron exchange
 Prophyrins porphyrins
screeningIquali test andquantitest
canbedone
specimen 24 hoururine WholeBlood
7
g fecal stool
samole
UROWPRO PROTO urine
UVlamp1Woodslamp screening1quail
t orange red fluorescence
proceed to quantitativetests

METHODS
Fluorometry confirmatory
HPLC qualitativetests
Hp TLC
Excitation wv 400 405nm
Emission 594 598nm

Aafrom recordingandlecture

JGBardelosa 412112020