2.10.2009ellyte.ppt1 disturbances of water & electrolyte metabolism part 1 – water &...

2.10.2009 ellyte.ppt 1

DISTURBANCES OF WATER &DISTURBANCES OF WATER & ELEELECCTROLYTTROLYTE METABOLISME METABOLISM

PART 1 PART 1 – – WWAATER &TER & SOD SODIUMIUM

LLECECTURETURE FROM FROM PATPATHHOOPHPHYYSSIOLIOLOOGGYY

schoschool ol yeayear 2009r 2009/2010/2010

OLIVER RÁCZ OLIVER RÁCZ ININSTSTITUTE OFITUTE OF PAT PATHHOOPHPHYYSSIOLIOLOOGGY,Y,

MEDICAL SCHOOL,MEDICAL SCHOOL, UPJŠ KOŠICE UPJŠ KOŠICE


IIoonn Amount in Amount in bodybody

PlaPlassmama

mmol/lmmol/l

CellsCells

mmol/lmmol/lSodSodiumium, Na, Na++ 92 g92 g

4 mol4 mol141141 1010

Potassium, KPotassium, K++ 100-140 g100-140 g

2,5-3,5 mo2,5-3,5 moll44 155155

Calcium, CaCalcium, Ca2+2+ 1200 g1200 g

30 m30 mooll2,52,5 < 0,001< 0,001

(uneven(uneven in in organellesorganelles))

Magnesium, MgMagnesium, Mg2+2+ 26,5 g26,5 g

1,1 mo1,1 moll11 1515

ChloridChloride, Cle, Cl-- 50 g50 g

1,4 m1,4 mooll103103 88

PhosphatePhosphate(a(ass phphososphphororusus))

775 g775 g

25 m25 mooll11 6565


SodSodiumium – k – kitcitchheenn s saltalt in our dietin our diet

EuropeEurope 10 – 12 g10 – 12 g/d/d 230 – 276 mmol/d 230 – 276 mmol/d RecommendedRecommended 2 – 7 2 – 7 46 – 161 46 – 161 HypertonicHypertonicss << 3,5 3,5 80 80 StrictStrict vegetari vegetariaannss 0,75 0,75 17 17

Ca & Mg dCa & Mg deficieficiency is frequentency is frequent!!

Mg: 300 – 350 mg/d = 12-14 mmol/dmore in puberty, gravidity, lactation& physical exerciseUSA: 143 – 266 mg/d

Ca: 800 mg/d = 20 mmol/dthe same for chidren and younggravidity & lactation – 1200 mg/d!


DISTRIBUTION OF WATER IN HUMAN BODY

CompartmentCompartment Volume, Volume, litreslitres

% of body % of body massmass

% of total % of total waterwater

ICS*ICS* 2828 4040 6767

ECSECS 1414 2020 3333

ISFISF 1111 15,715,7 2626

IVFIVF 33 4,34,3 77

SUMMASUMMA 4242 6060 100100

*1014 cells

Third space! small virtual volume, dynamicexchange – important in pathological conditions


AGE DEPENDENCE OF FLUID HOMEOSTASIS

AGEAGE TOTALTOTAL WWAATERTER, , %%

DAILY DAILY EEXCHAXCHANNGEGE, %, %

nnewbornewborn&& 7979

3-6 m3-6 mo.o. 7070 14-1614-16

7-12 m7-12 moo.. 6060 12-1512-15

adult manadult man 6060 2-42-4

adult womanadult woman 5151 2-42-4

& ECS > ICS, danger of dehydratationIn old age further impaired adaptation, danger of dehydratation


BALANCE & DYNAMICS

intakeintake = = outputoutput++ 1,2 – 1,2 – 1,5 beverage1,5 beverage

++ 1,0 1,0 foodfood

++ 0,3 – 0,5 metaboli0,3 – 0,5 metabolissmm

– – 1,0 – 2,0 urine1,0 – 2,0 urine

– – 0,6 – 0,8 perspirat0,6 – 0,8 perspiratiionon

– – 0,4 – 0,50,4 – 0,5 respirationrespiration

– – 0,10,1 sto stoooll

2,5 – 3,0 lit2,5 – 3,0 liteerrs/days/day

KKIIDNEYSDNEYS = 180 l/d = 180 l/d GITGIT = 8,2 l/d = 8,2 l/d

ssaallivaiva 1,51,5 stomachstomach 2,52,5 panpanccreasreas 0,70,7 bibillee 0,50,5 gutsguts 3,03,0

THIRDTHIRD SSPPACEACE

volume 5 l= 25 5,0/l= 25 5,0/l= 3 0,6/l= 53 10,6/l

Volume change (water loss)

Canges in concentration of solutes without change of the amount!

Compensatory mechanismsretention or excretion of ions adjustment of concentations

OSMOLALITOSMOLALITYY && OSMOTIC GAPOSMOTIC GAP

Osmolality = 2*[Na] + [glucose] + [urea]

Volume 5 4 l= 25 5,0 6,25/l= 25 5,0 6,25/l= 3 0,6 0,75/l= 53 10 13,25/l

Volume change (water loss)

Canges in concentration of solutes without change of the amount!

Compensatory mechanismsretention or excretion of ions adjustment of concentations

OSMOLALITOSMOLALITYY && OSMOTIC GAPOSMOTIC GAP

Osmolality = 2*[Na] + [glucose] + [urea]

Loss of isotonic fluid

Reduction of ECS, thirstno change of ICSnormal plasma sodium

Loss of hypotonic fluid

Reduction of ECS.Hypernatremia compensated through water shift from ICSShrinkage of cells

Salt loss

Hyponatremia compensated through water shift from ECSinto ICS, Reduction of ECS, swelling (oedema) of cells

2.10.2009 ellyte.ppt 13

DISTURBANCES OF THE SYSTEDISTURBANCES OF THE SYSTEMM

No pureNo pure form formss – – loss of water, salt...loss of water, salt...

ImmediateImmediate reactionreaction of comof compenpenssaatory systemstory systems

ECS ECS is in contact both with external environment is in contact both with external environment aand withnd with ICS ICS

ICS ICS is in contact only withis in contact only with ECS ECS

Plasmatic concentrations are not amounts and does Plasmatic concentrations are not amounts and does not inform on dynamics of compoundsnot inform on dynamics of compounds

2.10.2009 ellyte.ppt 14

POSSIBLE CAUSES AND POSSIBLE CAUSES AND MECHANISMSMECHANISMS

ExtrExtreeme me deviations of external environmentdeviations of external environment

DehydratDehydratationation from insufficient water intakefrom insufficient water intake

Disturbances caused by damaged function of effector Disturbances caused by damaged function of effector systemssystems ( (kidneyskidneys, GIT, , GIT, eettc.c.))

DiarrhoeaDiarrhoea, , vomitusvomitus, , kidney diseaseskidney diseases

Disturbances caused byDisturbances caused by erroneouserroneous regul regulationation (CNS, (CNS, ADH, aldosterADH, aldosteroonnee))

Diabetes insipidus, Conn sy., SIADHDiabetes insipidus, Conn sy., SIADH

Heart failure & RAA activationHeart failure & RAA activation

2.10.2009 ellyte.ppt 15

DECREASED WATER INTAKEDECREASED WATER INTAKE

1 – 2 d1 – 2 daysays: hypero: hyperossmotic hypovolmotic hypovoleemiamia

thirthirsstt, , compensated throughcompensated through ADH/RA ADH/RAAA Pespiratio insensibilis 5 ml/hoPespiratio insensibilis 5 ml/hourur

fever and in hot environment In old people and kidney diseases the

concentrating capacity od kidneys is decreased Later: exsicosis, dehydratation, > 20 % death

2.10.2009 ellyte.ppt 16

WATER DEFICIENCY WATER DEFICIENCY – – REDUCTION OF REDUCTION OF ECECSS

CausesCauses Insufficient fluid intakeInsufficient fluid intake Inability to drinkInability to drink ((loss of consciousnessloss of consciousness)) Losses throughLosses through GIT GIT ((diarrhoe, vomitusdiarrhoe, vomitus)) Losses through kidneysLosses through kidneys

((diuretidiureticscs, osmotic diur, osmotic diuresisesis, , kideny diseaseskideny diseases, , m. Addisonm. Addison))

Losses through skinLosses through skin ((increased sweatingincreased sweating, , burnsburns)) Displacement intoDisplacement into t third hird pplacelace (ileus, ascites)(ileus, ascites) Blood lossBlood loss (?) (?)

SymptomsSymptoms: hypoten: hypotensionsion, tachy, tachyccardia, ardia, dry skindry skin, , thirstthirst, , oligoliguuria ria && decreased sodium excretiondecreased sodium excretion, , increase of increase of hematohematoccritrit

2.10.2009 ellyte.ppt 17

WATER RWATER RETENETENTIONTION – ECS – ECS EXPANSION EXPANSION

CausesCausesIncreasedIncreased fluid intakefluid intake

Increased intake &Increased intake & disturbed disturbed regulregulatatiionon – SIADH – SIADHkidney failurekidney failurenenephphrotic sy.rotic sy.heart failureheart failureliver cirrhosisliver cirrhosis

SymptomsSymptoms:: OeOeddeemmaa. .

2.10.2009 ellyte.ppt 18

HHypernatrypernatraaeemimiaa >150 / 160 mmol/l>150 / 160 mmol/l

Low osmolality of urineLow osmolality of urine – diabetes insipidus – diabetes insipidusOsmolalitOsmolalityy of urineof urine pla plassmmaa – osmotic diur – osmotic diuresisesis

(diabetes mellitus)(diabetes mellitus)OsmolalitOsmolality of uriney of urine > pla > plassmmaa – dehydrat – dehydratationation

diarrhoea, vomitus sweatingdiarrhoea, vomitus sweatingConn syndrConn syndroommee (hyperaldo (hyperaldossteroniteronissm) m)

hypernatrhypernatreemia, hypokalmia, hypokaleemiamia

2.10.2009 ellyte.ppt 19

HHyponatryponatraaeemimiaa <130 / 120 mmol/l<130 / 120 mmol/l

Plasma oPlasma osmolalitsmolalityy highhigh hypergly hyperglycecemia ?!mia ?!Plasma oPlasma osmolalitsmolalityy lowlow

Na Na in urinein urine > 20 mmol/l > 20 mmol/l && hypovol hypovoleemiamiam. Addison, diuretim. Addison, diureticscssalt losing salt losing nenephphritisritis

Na Na inin urineurine << 20 mmol/l 20 mmol/l && hypovol hypovoleemiamiadiarrhoea, vomitus, sweating with diarrhoea, vomitus, sweating with inadequate fluid replacementinadequate fluid replacement

Na Na inin urineurine << 20 mmol/l 20 mmol/l && oedemaoedemaheart failure,heart failure, cir cirrrhhosis,osis, ne nephphrotic sy.rotic sy.SIADHSIADH

2.10.2009 ellyte.ppt 20

DISTURBANCES OF ADH SECRETION DISTURBANCES OF ADH SECRETION AND EFFECTSAND EFFECTS – – I.I.

Diabetes insipidus, neurogenDiabetes insipidus, neurogenicic (AD) (AD)AVP gene mutationAVP gene mutation

Acquired formsAcquired forms – – damage ofdamage of hypot hypothhalamualamussCCompletomplete & partial formse & partial forms

Diabetes insipidus, renDiabetes insipidus, renaal (X-l (X-related &related & AR) AR)Receptor Receptor (X) (X) or water channel protein (AR)or water channel protein (AR) gene mutationsgene mutations

AcquiredAcquired – – kidney diseaseskidney diseases

2.10.2009 ellyte.ppt 21

DISTURBANCES OF ADH SECRETION DISTURBANCES OF ADH SECRETION AND EFFECTSAND EFFECTS – – IIII..

SIADH – inadeSIADH – inadequatequate se seccrretion ofetion of ADH ( ADH (lack of suspensionlack of suspension))ExpanExpanssiion of on of ECSECShyponatrhyponatreemia, hypoosmolalitmia, hypoosmolalityyHigh urineHigh urine osmolalit osmolality &y & high high Na Na in urinein urine IncreasedIncreased ANP ANPRenRenaal l && endo endoccrinrinee func functtiions ions inntacttact

Hereditary forms and stressHereditary forms and stress ??!! ??!!

2.10.2009 ellyte.ppt 22


PART PART 22 – POTASSIUM– POTASSIUM





2.10.2009 ellyte.ppt 23

POTASSIUM HOMEOSTASIS

Serum concentration: Serum concentration: 3,8 – 5,5 mmol/l3,8 – 5,5 mmol/l** Total amount depends on muscle massTotal amount depends on muscle mass

(young > old;(young > old; mman > woman > womenen) )

37 – 52 mmol/kg 37 – 52 mmol/kg body massbody mass IntakeIntake: : 2-6 g/d2-6 g/d = 50-150 mmol/d= 50-150 mmol/d Excretion through kidneysExcretion through kidneys 10 – 20 mmol/d 10 – 20 mmol/d

(0,4 – 0,8 g/d). (0,4 – 0,8 g/d). Inverse association with Na excretionInverse association with Na excretion GIT GIT excretion iexcretion iss important in kidney failure important in kidney failure a andnd inin

patpathhologicologicalal conditionsconditions ( (diarrhoeadiarrhoea))

*Depends on method. Preanalytic errors - hemolysis!

2.10.2009 ellyte.ppt 24

FUNCTIONS OF POTASSIUM & INTERPRETATION OF RESULTS

FunctionsFunctions intraceintracelllullulaar osmotic r osmotic pressurepressure resting & action resting & action potenpotenttiiaal l enzenzyymme activitye activity, proteosynt, proteosynthesishesis

ProblProbleemmss: :

1.1. assesment of cell homeostasis from extraassesment of cell homeostasis from extracecelllullulaar r cconcentroncentrationation

2.2. pHpH changes changes: : exchangeexchange H H//K K betweenbetween EC ECFF/IC/ICFF

2.10.2009 ellyte.ppt 25

INTERNAL & EXTERNAL BALANCE

acidosis: Hacidosis: H++ enters the cells, K enters the cells, K+ + out into ECFout into ECF alkalalkalosisosis: : HH++ into into ECFECF, K, K+ + enters the cellsenters the cells KK++ entry into cellsentry into cells: in: inssululiinn (together with glucose) (together with glucose), ,

aldosteraldosteroonnee, adrenaline, adrenaline rapid cellular proliferatiom (treatmentrapid cellular proliferatiom (treatment of of perniciperniciousous ana anaeemia mia

with with BB1212 vitamin vitamin cell necrosis, hemolysiscell necrosis, hemolysis (crush sy, (crush sy, malignanciesmalignancies), ), KK++ intinto o

ECFECF

kidney or GIT retentionkidney or GIT retention//losseslosses, parenter, parenteraal l intakeintake dietary dietary deficideficiency/excess as an additional factorency/excess as an additional factor

internal – ECF/ICF

external – ECF/environment

2.10.2009 ellyte.ppt 26

HYPOKALAEMIA - SYMPTOMS

hypokalaemiahypokalaemia < 4,0 mmol/l < 4,0 mmol/l significantsignificant < 3,5 mmol/l < 3,5 mmol/l dangerousdangerous < 3,0 mmol/l < 3,0 mmol/l

Membrane hMembrane hyperpolariyperpolarisationsation Weakness, constipation, ileus, hypotoniaWeakness, constipation, ileus, hypotonia Depression, confusionDepression, confusion Arrhytmia, potentiation of digitalis toxicityArrhytmia, potentiation of digitalis toxicity ADH resistance, pADH resistance, polyuria, polydipsiaolyuria, polydipsia EECCG G flat/inversedflat/inversed T T, prolonged PR, prolonged PR, ,

STST depression depression, , prominent prominent UU

2.10.2009 ellyte.ppt 27

HYPOKALAEMIA - CAUSES

Disorders of externalDisorders of external b baalancelance GIT – diarrhoea, vomitus, tumors of colon, rectum, GIT – diarrhoea, vomitus, tumors of colon, rectum,

pancreaspancreas KidneysKidneys - - diuretics, polyuric stage of renal failure, diuretics, polyuric stage of renal failure,

hereditary tubulopathieshereditary tubulopathies,, PrimPrimaary ry && secondary hyperaldosteronism, abuse of secondary hyperaldosteronism, abuse of

liquoriceliquorice, , Cushing, ectopic ACTH productionCushing, ectopic ACTH production

Glycyrrhiza glabra. GlycyrrhizinGlycyrrhiza glabra. Glycyrrhizin, a sweet substance, a sweet substanceWeakWeak ccortiorticcomimetic omimetic && fitoestrog fitoestrogeenn effect effect Component of herb teas, nonalcoholic drinks and beerComponent of herb teas, nonalcoholic drinks and beer

2.10.2009 ellyte.ppt 28

HYPOKALAEMIA - CAUSES

Disorders ofDisorders of intern internalal b baalancelance Treatment of Treatment of diabetic hyperglydiabetic hyperglycaecaemimiaa with with ininssululiin n

((KK+ + entry into cells together with glucoseentry into cells together with glucose)) AlkalosisAlkalosis Rapid cellular proliferationRapid cellular proliferation Familiar hypokalaemic periodic paralysis (hereditary) Familiar hypokalaemic periodic paralysis (hereditary)

2.10.2009 ellyte.ppt 29

HYPERKALAEMIA - SYMPTOMS hyperkalaemiahyperkalaemia < < 55,5 mmol/l,5 mmol/l

significantsignificant < < 66,5 mmol/l,5 mmol/l dangerousdangerous < < 77,5 mmol/l,5 mmol/l

Low resting potential, short cardiac action potential, Low resting potential, short cardiac action potential, increased speed of repolarization increased speed of repolarization

Can kill without warningCan kill without warning Ventricular fibrillation and cardiac arrest may be the first Ventricular fibrillation and cardiac arrest may be the first

signs! (if you do not check K & ECG)signs! (if you do not check K & ECG) EECG: abnormal/absent P; broad QRS, CG: abnormal/absent P; broad QRS,

peaked Tpeaked T,, ST depressionST depression

2.10.2009 ellyte.ppt 30

HYPERKALAEMIA - CAUSES

Disorders ofDisorders of extern externalal b baalancelance Decreased excretion.Decreased excretion. UnderUnder GFR 15 ml/min GFR 15 ml/min alwaysalways. .

AAnnuuriria: Ka: K increaseincrease 1 mmol/l d1 mmol/l dailyaily

In mild impairment of kidney function only when other In mild impairment of kidney function only when other factors are presentfactors are present

Increased intake (infusions, NaCl substitution) only in the Increased intake (infusions, NaCl substitution) only in the case of impaired kidney functioncase of impaired kidney function

m. Addison, adrenogenitm. Addison, adrenogenitaal sy., inhibl sy., inhibiitortors ofs of angioten angiotensinsin cconvertonvertinging enz enzyymmee

2.10.2009 ellyte.ppt 31

HYPERKALAEMIA - CAUSES

Disorders ofDisorders of intern internalal b baalancelance AAcidcidosisosis Cell necrosis - rhabodmyolysis, burns, cytostatic treatment Cell necrosis - rhabodmyolysis, burns, cytostatic treatment

of malignanaciesof malignanacies Digitalis overdosisDigitalis overdosis Hyperkalaemic periodic paralysis (hereditary)Hyperkalaemic periodic paralysis (hereditary) Malignant hypertermia (hereditary)Malignant hypertermia (hereditary)

2.10.2009 ellyte.ppt 32


PART PART 33 – CALCIUM– CALCIUM & & MAGNESIUM MAGNESIUM





2.10.2009 ellyte.ppt 33

CALCIUM

Total body Total body 1200 g 1200 g 30 mol30 mol ECFECF 0,9 g 0,9 g 22,5 mmol22,5 mmol PlasmaPlasma 0,36 g 0,36 g 9,0 mmol 9,0 mmol Bone / ECF exchange Bone / ECF exchange 500 mmol/d500 mmol/d Daily losses Daily losses 25 mmol/d (1g)25 mmol/d (1g)

urineurine 6 mmol (240 GF – 234 reabsorbtion)6 mmol (240 GF – 234 reabsorbtion) faeces 19 mmol (+25 food, 12 in, + 6 secr.)faeces 19 mmol (+25 food, 12 in, + 6 secr.) skin 0,3 mmolskin 0,3 mmol

Small changes in fluxes can have profound effect of Small changes in fluxes can have profound effect of plasma Caplasma Ca

2.10.2009 ellyte.ppt 34

FUNCTIONS OF CALCIUM

StructuralStructural NeuromuscularNeuromuscular

BloodBlood Signal systemsSignal systems

Bone, teethBone, teeth Control of excitability;Control of excitability;

Neurotransmitter Neurotransmitter releaserelease

Muscle contractionMuscle contraction Coagulation (Coagulation (§§ 22) 22) MessengerMessenger

2.10.2009 ellyte.ppt 35

PLASMA CALCIUM

TOTAL

2,25 – 2,60 mmol/l

diffusible 54 % protein-bound 46 %

free - ionized 47 %

7% complexed

CLINICAL CHEMISTRY: TOTAL OR IONIZED ?

pH!

2.10.2009 ellyte.ppt 36

EC CALCIUM REGULATING HORMONES

PTH & calcitriol!PTH & calcitriol! Calcitonin is of minor importance. Calcitonin is of minor importance. Also regulation of phosphorus and perhaps magnesium Also regulation of phosphorus and perhaps magnesium o PTH – a 84 AA peptide from 115 AA precursor. AAs 1-PTH – a 84 AA peptide from 115 AA precursor. AAs 1-

34 are active34 are activeo Short half lifeShort half life Calcitriol is a steroid hormone derived from vit. DCalcitriol is a steroid hormone derived from vit. D The 2The 2ndnd hydroxylation in liver is strictly controlled hydroxylation in liver is strictly controlled Calbindin D in gutCalbindin D in gut Receptors in other tissues – role in cellular Receptors in other tissues – role in cellular

proliferation and differentiation and in immune proliferation and differentiation and in immune response ?response ?

2.10.2009 ellyte.ppt 37

FUNCTIONS OF PTH

BONEBONE Release of calcium Release of calcium [Ca [Ca2+2+]] Osteoclastic resorptionOsteoclastic resorption

KIDNEYKIDNEY Calcium reabsorbtion Calcium reabsorbtion [Ca [Ca2+2+]] 22ndnd hydroxylation of vit.D hydroxylation of vit.D Ca, P absorbtion Ca, P absorbtion PhosphaturiaPhosphaturia [PO[PO44] ]

Decrease of HCODecrease of HCO33-- reabsorbtion reabsorbtion pHpH

2.10.2009 ellyte.ppt 38

HYPOCALCAEMIA - CAUSES HypoparathyroidismHypoparathyroidism

Congenital (with Di George sy.)Congenital (with Di George sy.) Acquired – autoimmune, surgery, hemochromatosis, Acquired – autoimmune, surgery, hemochromatosis,

tumorstumors PseudohypoparathyroidismPseudohypoparathyroidism

2 hereditary disorders of PTH signaling pathway (cAMP 2 hereditary disorders of PTH signaling pathway (cAMP dependent)dependent)

Magnesium deficiency (pseudo ?)Magnesium deficiency (pseudo ?) DeficiencyDeficiency of of vit vitaminamin D (!) D (!) DDisorders of vitisorders of vitaminamin D metabolism D metabolism – end stage renal disease – end stage renal disease Acute pancreatitis, transfusions with citrate, neonatalAcute pancreatitis, transfusions with citrate, neonatal

2.10.2009 ellyte.ppt 39

HYPOCALCAEMIA - SYMPTOMS

Stupor, numbness, paraesthesiaStupor, numbness, paraesthesia Muscle cramps and spasms „tetany“Muscle cramps and spasms „tetany“ Laryngeal stridorLaryngeal stridor ConvulsionsConvulsions ChvostekChvostek+ Trousseau+, long QT on ECG+ Trousseau+, long QT on ECG Cataract in chronic hypocalcaemiaCataract in chronic hypocalcaemia Rickets (rRickets (rachitisachitis)) in vitamin D deficiency in vitamin D deficiency

OSTEOPOROSIS ???

2.10.2009 ellyte.ppt 40

HYPERCALCAEMIA - CAUSES

COMMON (COMMON (90%90% of all of all)) Primary hyperparathyroidismPrimary hyperparathyroidism Malignancies – bone metastasis (?), PTHrP and other Malignancies – bone metastasis (?), PTHrP and other

humoral factorshumoral factors LESS COMMONLESS COMMON

ThyrThyreeotoxicosis, sarcoidosisotoxicosis, sarcoidosis UNCOMMONUNCOMMON

Lithium treatment, tbc, immobilisation, adrenal failure, renal Lithium treatment, tbc, immobilisation, adrenal failure, renal failure, hereditaryfailure, hereditary

BUT ALSO HYPERPARATHYROIDISM WITHOT BUT ALSO HYPERPARATHYROIDISM WITHOT HYPERCALCAEMIAHYPERCALCAEMIA Compensatory in vitamin D deficiency, renal diseaseCompensatory in vitamin D deficiency, renal disease

2.10.2009 ellyte.ppt 41

HYPERCALCAEMIA - SYMPTOMS

Weakness, tiredness, weight lossWeakness, tiredness, weight loss Imparied concentration, drowsiness (coma)Imparied concentration, drowsiness (coma) Anorexia, nausea, vomiting, constipationAnorexia, nausea, vomiting, constipation Polyuria, dehydrationPolyuria, dehydration Renal calculi, nephrocalcinosisRenal calculi, nephrocalcinosis short QT, arrhytmiasshort QT, arrhytmias

2.10.2009 ellyte.ppt 42

MAGNESIUM 60 % 60 % in bones, higher in in bones, higher in ICFICF than in ECF than in ECF OnlyOnly 0,3 % 0,3 % in blood,in blood, 30% prote 30% proteiinn bound bound SerumSerum 0,7 – 1,0 mmol/l 0,7 – 1,0 mmol/l Regulator is not knownRegulator is not known! ! adadrerenal medullanal medulla, in, inssululiin, n,

parathormparathormoon ???n ??? RegulaRegulatedted resorb resorbtion fromtion from GIT ? GIT ? 8 mmol/d is enough ? Is deficiency common ?8 mmol/d is enough ? Is deficiency common ? Excretion through urine and stoolExcretion through urine and stool

2.10.2009 ellyte.ppt 43

MAGNESIUM

Neuromuscular excitability (inhibition – Neuromuscular excitability (inhibition – mediated through decreased secretion of mediated through decreased secretion of acetylcholine?) acetylcholine?)

Bone structureBone structure Enzyme activity, energy production, Enzyme activity, energy production,

transport mechanisms, ribosomestransport mechanisms, ribosomes Regulation of haemocoagulation and Regulation of haemocoagulation and

membrane functionmembrane function

2.10.2009 ellyte.ppt 44

MAGNESIUM

Cardioprotective antiischemic, antihypoxic Cardioprotective antiischemic, antihypoxic effectseffects

Sedative effect on NSSedative effect on NS AntihypertensiveAntihypertensive AntithromboticAntithrombotic

2.10.2009 ellyte.ppt 45

MAGNESIUM

Deficiency associated with soil and plant deficit Deficiency associated with soil and plant deficit Þ grass tetany of cattle

Some drugs and stress can increase excretion Unhealthy diet (alcohol) High doses of calcium (!)

CONSEQUENCES Spasmophilia is more often a consequence of Mg deficiency

as of Ca Tiredness, irritability, tremor Dysmenorea, preeklampsia arrythmias

2.10.2009ellyte.ppt1 disturbances of water & electrolyte metabolism part 1 – water &...

Documents

space slide

water shift

total water ics

na glucose urea slide

danger of dehydratation

ecs ics

water sodium lecture

pure forms loss of water