gangguan pada keseimbangan elektrolit
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GANGGUAN PADA KESEIMBANGANELEKTROLIT
dr. Andi Sulistyo Hariboo! S".PD.
SPESIALIS PEN#AKIT DALAM
Pro$ra% Studi P&ndidi'an Do't&r
UNI(ERSITAS ISLAM MALANG
)*+)
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FLUIDS and ELECTROLYTES
ELECTROLYTES
Functions of Electrolytes
Contribute most of the osmotically active
particles in body fluids
Provide buffer systems for pH reulation
Provide the proper ionic environment fornormal neuromuscular irritability ! tissuefunction
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DISTRIBUTION O, ELE-TROL#TES
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-ATIONS AND ANIONS IN BOD# ,LUIDS
Figure 27.2
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DISTRIBUTION O, MAORELE-TROL#TES• Na+ and CL- predominate in extracellular fluids
(interstitial fluid and plasma) but are ver lo!
in t"e intracellular fluid (ctoplasm)
• #+ and $%&'2- predominate in intracellular fluid
(ctoplasm) but are in ver lo! concentration in
t"e extracellular fluids (interstitial fluid and
plasma)
• t bod fluid p$ proteins *%- act as anions,
total protein concentration *%- is relativel
"ig" t"e second most important anion in t"e
ctoplasm *%- is intermediate in blood plasma
but *%- is ver lo! in t"e interstitial fluid
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DISTRIBUTION O, MINORELE-TROL#TES• $C&/- is in intermediate concentrations in all
fluids a bit lo!er in t"e intracellular fluid
(ctoplasm), it is an important p$ buffer in t"e
extracellular comparments
• Ca++ is in lo! concentration in all fluid
compartments but it must be tig"tl
regulated as small s"ifts in Ca++ concentration
in an compartment "ave serious effects
• 0g++ is in lo! concentration in all fluid
compartments but 0g++ is a bit "ig"er in t"e
intracellular fluid (ctoplasm) !"ere it is a
component of man cellular en1mes
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REGULATION O, ELE-TROL#TES 0aor Cations in bod fluids
3odium (Na+)
%otassium (#+)
Calcium (Ca++)0agnesium (0g++)
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PRIN-IPLES O, ELE-TROL#TEDISTURBAN-ES
PRIN-IPLES O, ELE-TROL#TEDISTURBAN-ES
4mplies an underling disease process
5reat t"e electrolte c"ange but see6 t"ecause
Clinical manifestations usuall not specific to
a particular electrolte c"ange e.g.
sei1ures arr"t"mias
4mplies an underling disease process
5reat t"e electrolte c"ange but see6 t"ecause
Clinical manifestations usuall not specific to
a particular electrolte c"ange e.g.
sei1ures arr"t"mias
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PRIN-IPLES O, ELE-TROL#TEDISTURBAN-ES
PRIN-IPLES O, ELE-TROL#TEDISTURBAN-ES
Clinical manifestations determine urgency
of treatment, not laboratory values Speed and magnitude of correction
dependent
on clinical circumstances
Frequent reassessment of electrolytes
required
Clinical manifestations determine urgency
of treatment, not laboratory values Speed and magnitude of correction
dependent
on clinical circumstances
Frequent reassessment of electrolytes
required
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ELE-TROL#TES / THEIR IMBALAN-ES
SODIUM 0NA12
Sodiu% balan3&
Sodiu% 4 %a5or 3ation in &6tra3&llular 7luid 0E-,2
Sodiu% 4 %ost 3o%%on "robl&% it8 &l&3trolyt& balan3&
K&y to balan3&9 in$&stion :ia G;I tra3t 4 &63r&tion :ia 'idn&y Aldost&ron& 3ontrols sodiu% l&:&ls :ia t8& 'idn&y
R&%&%b&r aldost&ron&
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DISORDERS O, SODIUMBALAN-ENa+ is t"e most abundant electrolte in t"e
CF.
Na+ and accompaning anion Cl- areresponsible for normal osmotic activit of t"e
CF.
ll gain8loss of Na+ is accompanied b
gain8loss of !ater.
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H#PONATREMIA $povolemic "ponatremia
• 9omiting
• :iarr"ea
• :iuretics
• drenal insufficienc Normovolemic "ponatremia
• 3ndrome of inappropriate secretion of antidiuretic "ormone
• ;enal failure
•
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-LINI-AL MANI,ESTATIONS O,H#PONATREMIA Neurologic
• 3ei1ure
• Coma
• gitation
=astrointestinal
• norexia
• Nausea8vomiting
0uscular
• Cramps
• !ea6ness
• $eadac"e
• Cerebral edema
• Confusion
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TREATMENT O, H#PONATREMIA Fluid restriction
dministration of "pertonic saline and an
osmotic or loop diuretic
>>>Correction of serum sodium levels too
rapidl can result in neurologic damage and
central pontine melinolsis>>>
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H#PONATREMIA cute smptomatic "ponatremia
Correct no faster t"an ? m@8L per "our for t"e
first A-B m@8L
No more t"an ?-?2 m@8L in first 2' "ours
DE saline is almost never needed
Calculate t"e Na deficit Na m@ (*Na desired - *Na measured) G 5H< 5H< .D or .A G !eig"t in #=
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-AUSES O, H#PERNATREMIA 0ost common cause is !ater deficienc d8tI
• xcessive loss
• 4nade@uate inta6e
lso ma be caused bI
• xogenous Na+ load
• %rimar "peraldosteronism
• :iabetes insipidus• ;enal dsfunction
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-LINI-AL MANI,ESTATIONS O,H#PERNATREMIA
5remulousness
4rritabilit
taxia
0ental confusion
Coma d8t cerebral !ater loss
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TREATMENT O,H#PERNATREMIA
;enal tubular diuretics
$emodialsis
5reat central diabetes insipidus !it"
vasopressin
>>>Correction of serum sodium level too
rapidl can result in neurologic damage
secondar to cerebral edema>>>
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H#PERNATREMIA 5reatment
Severe ECFV depletion is the priority and should
be corrected with NS first. 3ubse@uent fluid
replacement can be "potonic
0aor complication of overl rapid correction is
cerebral edema
3afe rate is no more t"an .D- ? m@8L per "our
3"ould ta6e /A-72 to "ours to completel correct
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H#PERNATREMIA 5reatment
Calculate t"e !ater deficit
$2& deficit 5H< G (*Na meas- *Na des)8*Na
des 4mportant to ta6e into account ongoing losses
insensible losses .D - ? liter82' "ours !it" fever t"ese losses increase b A-Bml82' "rs for
eac" degree Faren"eit
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POTASSIUM REGULATION
0aor electrolte and principle cation in t"e
extracellular fluid;egulates metabolic activities
;e@uired for glcogen deposits in t"e liver ands6eletal muscle
;e@uired for transmission of nerve impulses normal
cardiac conduction and normal smoot" and s6eletal
muscle contraction;egulated b dietar inta6e and renal excretion
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ELE-TROL#TES / THEIR IMBALAN-ES
POTASSIUM 0K 12
Potassiu% balan3& Ma5or intra3&llular 3ation Balan3&9 in$&stion 4 &63r&tion 0:ia 'idn&ys2
Aldost&ron& "ri%arily 3ontrols "otassiu% It &638an$&s "otassiu% 7or sodiu%
Insulin also r&$ulat&s "otassiu% It dri:&s it into 3&lls 0it8 su$ar2 / t8us "rodu3&s
8y"o'al&%ia "H also a77&3ts "otassiu% s&3r&tionA3idosis9 %or& H1 in blood 8i38 7inds its ay into 3&ll
/ "us8&s K 1
into blood Also $&t 'idn&y to &638an$& H1 7or K 1
A3idosis ;$i:&s; 8y"&r'al&%iaAl'alosis9 l&ss H1 in blood
Kidn&ys &638an$& K 1 7or H1> t8us $&t 8y"o'al&%ia
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5"e relation bet!een potassium and "drogen ions in t"e plasma
3aladinJs natom K %"siolog fourt" edition 0c=ra! $ill
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%otassium balance in t"e bod
Costan1o %"siolog second edition 3aunders
POTASSIUM ION REGULATION IN
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POTASSIUM ION REGULATION INE-,
27-/
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H#POKALEMIACauses
• =astrointestinal losses
• 3stemic al6alosis
•
:iabetic 6etoacidosis• :iuretic t"erap
• 3mpat"etic nervous sstem stimulation
• dministration of beta-adrenergic receptor
agonists
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H#POKALEMIA 3purious "po6alemia
0ar6ed leu6octosis
dose of insulin rig"t before t"e blood dra!
;edistribution "po6alemial6alosis (# decreases ./ for ever .? increase in
p$)
4ncreased Heta2 adrenergic activit
5"eop"lline toxicitFamilial
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H#POKALEMIA xtrarenal depletion
diarr"ea
laxative abuse
s!eat losses fasting or inade@uate inta6e
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H#POKALEMIA ;enal potassium depletion
urine potassium 2 m@82' "rs
spot urine !it" 2 m@ #8gram creatinine
classified !"et"er t"e occur !it" a metabolical6alosis vomiting8N= suction diuretic tx 0ineralocorticoid excess sndromes
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H#POKALEMIA ;enal losses
metabolic acidosis ;5 5pe 4 and 44 :# Carbonic an"drase in"ibitor t"erap Mreterosigmoidostom
No acid-base disorder 0g deficienc
:rugs
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-LINI-AL MANI,ESTATIONS O,H#POKALEMIA utonomic neuropat"
36eletal muscle !ea6ness
4ncreased sensitivit to :igoxin
Cardiac
• :ecreased mocardial contractilit
• lectrical conduction abnormalities• rr"t"mias
• 5ac"cardia
• 9entricular fibrillation
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POTASSIUM
Copyright 2008 by Pearson Education, Inc.
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H#POKALEMIA AND THE EKG• %rolonged %; interval
• %rolonged 5 interval
•
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TREATMENT O, H#POKALEMIA 3lo! 49 potassium supplements
nest"esia related concernsI
• 4ncreased ris6 of mocardial irritabilit #+ O2.A• void "perventilation of t"e lungs
• void glucose containing 49 solutions
• void rapid infusion of 49 #+ supplements
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H#PERKALEMIA 3evere "per6alemia is a medical emergenc
Neuromuscular signs (!ea6ness ascending
paralsis respirator failure)
%rogressive C= c"anges (pea6ed 5 !avesflattened % !aves prolonged %; interval
idioventricular r"t"m and !idened ;3
complex sine !ave pattern 9 fib)
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H#PERKALEMIACauses
• 4ncreased total bod potassium
• ;enal failure
• %otassium-sparing diuretics
• xcessive 49 #+ supplements
• xcessive use of salt substitutes
• ltered distribution of potassium
• 0etabolic or respirator acidosis
• :igitalis intoxication• 4nsulin deficienc
• $emolsis
• 5issue and muscle damage after burns
• dministration on succinlc"oline
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-LINI-AL MANI,ESTATIONS O,H#PERKALEMIA
reflexia
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H#PERKALEMIA AND THE EKG• Narro!ing and pea6ing of 5 !aves
• ?st degree 9 bloc6
• ;3 !idening
• 35 segment depression
• %rogression to merging of ;3 an
5 !aves to a sine !ave
• 5ac"cardia
• 9entricular fibrillation
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H#PERKALEMIAH#PERKALEMIA
tiolog P renal failure
transcellular s"ifts cell
deat" drugspseudo"per6alemia
0anifestations P
cardiac neuromuscular
tiolog P renal failure
transcellular s"ifts cell
deat" drugspseudo"per6alemia
0anifestations P
cardiac neuromuscular
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TREATMENT O, H#PERKALEMIA%rimar goal
void adverse cardiac effects 4nsulin and glucose to s"ift #+ into cells 49 calcium to antagoni1e cardiac effects of
"per6alemia
nest"esia related concernsI serum #+ of D.Dm@8L is upper limit for elective
procedures
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H#PERKALEMIA 5reatment
3top potassium>
=et and C=
Hyperkalemia with ECG changes is a medical
emergency
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H#PERKALEMIA 5reatment
First p"ase is emergenc treatment to
counteract t"e effects of "per6alemia 49 Calcium
5empori1ing treatment to drive t"e potassium
into t"e cells glucose plus insulin
Heta2 agonist
Na$C&/
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H#PERKALEMIA 5reatment
5"erap directed at actual removal of potassium
from t"e bod sodium polstrene sulfonate (#aexalate) dialsis
:etermine and correct t"e underling cause
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ELE-TROL#TES / THEIR IMBALAN-ES
-AL-IUM 0-A112
-al3iu% balan3& -al3iu% is %ost abundant %in&ral in body
-al3iu% is i%"ortant as an &6tra3&llular 3ation
-al3iu% / "8os"8orus 8a:& a r&3i"ro3al r&lations8i"
-al3iu% balan3& is d&"&nd&nt on9
Parat8yroid 8or%on& 0PTH2
-al3itriol 0a3ti:& :ita%in D2
-al3itonin 07ro% t8yroid2
?@ o7 3al3iu% r&absorb&d at t8& 'idn&ys
-al3iu% 7un3tions Stru3tural str&n$t8 7or bon&s / t&&t8
Maintains stability o7 n&r:& %&%bran&
R&uir&d 7or %us3l& 3&ll 3ontra3tion
N&3&ssary 7or blood 3lottin$
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REGULATION O, -AL-IUM IONS
;egulated !it"innarro! rangelevated extracellular
levels prevent
membranedepolari1ation:ecreased levels lead
to spontaneous actionpotential generation
5erms$pocalcemia$percalcemia
%5$ increases Ca2+
extracellular levels
and decreases
extracellular
p"osp"ate levels 9itamin : stimulates
Ca2+ upta6e in
intestines
Calcitonin decreases
extracellular Ca2+
levels
27-D
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REGULATION O, -AL-IUM IONS
27-D?
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H#PO-AL-EMIACausesI
• :ecreased serum albumin concentration
• C"elation of calcium b citrate
• ;"abdomolsis
• $poparat"roidism
• %ancreatitis
• ;enal failure
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-LINI-AL MANI,ESTATIONS O,H#PO-AL-EMIA
Neuromuscular irritabilit• 5etan
• Larngospasm
•
$peractive deep tendon reflexes
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TREATMENT O, H#PO-AL-EMIACalcium replacement
4ntraoperative P "perventilation and
respirator al6alosis
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H#PER-AL-EMIACausesI
• Calcium mobili1ation from bone due to
immobilit
• 5umors
• $perparat"roidism
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-LINI-AL MANI,ESTATIONS O,H#PER-AL-EMIA
norexia
Nausea
Constipation
Cognitive depression#= c"anges
• %rolonged %; interval
• 3"ortened 5 interval
• %9CJs
TREATMENT O,
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TREATMENT O,H#PER-AL-EMIA5reatment of underling cause
9olume expansion
4ntraoperative "percalcemia s"ould be
managed !it" administration of ade@uatefluids and maintenance of urine output.
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Copyright 2008 by Pearson Education, Inc.
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REGULATION O, -HLORIDE /MAGNESIUM IONS C"loride ions%redominant anions in CF
0agnesium ions
Capacit of 6idne to reabsorb is limitedxcess lost in urine:ecreased extracellular magnesium results in
greater degree of reabsorption
27-DQ
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MAGNESIUM REGULATION ssential for en1me activities Neuroc"emical activities
Cardiac and s6eletal muscle excitabilit
;egulation :ietar
;enal mec"anisms
%arat"roid "ormone action
D P AE of magnesium contained in bones ?E in CF
0inimal amount in cell
REGULATION O, BLOOD
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REGULATION O, BLOODMAGNESIUM
27-A?
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H#POMAGNESEMIA 3erum magnesium less t"an ?.Dm@8L
CausesI• 4nade@uate inta6e of magnesium
• 5%N
• =astrointestinal losses
• %ancreatitis
• %arat"roid "ormone disorders
• $peraldosteronism
• #etoacidosis• C"ronic alco"olism
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-LINI-AL MANI,ESTATIONS O,H#POMAGNESEMIA
CN3 irritabilit• 3ei1ures
•
$perreflexia
• 36eletal muscle spasm
TREATMENT O,
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TREATMENT O,H#POMAGNESEMIA
49 administration of magnesium sulfate
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H#PERMAGNESEMIA 3erum magnesium level greater t"an 2.D
m@8L
CausesI• 4atrogenic administration
• %reeclampsia
• ntacids8laxatives
• ;enal failure
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-LINI-AL MANI,ESTATIONS O,H#PERMAGNESEMIA
CN3 depression stupor coma
36eletal muscle !ea6ness respirator failure
:ecreased perip"eral vascular tone
:ecreased mocardial contractilit
5ocolsis
H#PERMAGNESEMIA AND THE
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H#PERMAGNESEMIA AND THEEKG%rolonged % interval
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TREATMENT O,H#PERMAGNESEMIA 3upportive care
Fluid loading
:iuresis
cute "permagnesemia P49 calcium to
counter t"e elevated magnesium levels
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ANIONS -ONT
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PHOSPHATE
27-7
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OTHER ELE-TROL#TE DE,I-ITS-A! POC! MG
OTHER ELE-TROL#TE DE,I-ITS-A! POC! MG
0a produce serious but nonspecific cardiac
neuromuscular respirator and ot"er effects
ll are primaril intracellular ions so deficits
difficult to estimate
5itrate replacement against clinical findings
0a produce serious but nonspecific cardiac
neuromuscular respirator and ot"er effects
ll are primaril intracellular ions so deficits
difficult to estimate
5itrate replacement against clinical findings
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PHOSPHATE
4nvolved in acidPbase buffering sstem 5%production and cellular upta6e of glucose
0aintenance re@uires ade@uate renal functioning
ssential to muscle ;HCs and nervous sstem
function
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H#PERPHOSPHATEMIA
$ig" serum %&'/−
caused bcute or c"ronic renal failure
C"emot"erap
xcessive ingestion of p"osp"ate or vitamin :
0anifestationsCalcified depositionI oints arteries s6in 6idnes
and corneas
Neuromuscular irritabilit and tetan
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H#PERPHOSPHATEMIA
0anagement 4dentif and treat underling cause
;estrict foods and fluids containing %&'/−
de@uate "dration and correction of "pocalcemic
conditions
H#POPHOSPHATEMIA
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H#POPHOSPHATEMIA
Lo! serum %&'/−
caused b0alnouris"ment8malabsorption
lco"ol !it"dra!al
Mse of p"osp"ate-binding antacids
:uring parenteral nutrition !it" inade@uate
replacement
H#POPHOSPHATEMIA
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H#POPHOSPHATEMIA
0anifestationsCN3 depression
Confusion
0uscle !ea6ness and pain
:sr"t"mias
Cardiomopat"
H#POPHOSPHATEMIA
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H#POPHOSPHATEMIA
0anagement&ral supplementation
4ngestion of foods "ig" in %&'/−
49 administration of sodium or potassium p"osp"ate
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+??
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Saya akan perlakukan teman sejawat saya seperti saudarakandung
)*+*
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