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Water metabolism disorders Dr Olcay Evliyaoğlu. Plasma osmolality is tightly between 275-295 mOsm/kg Thirst enhance water ingestion Arginin vasopressin.

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Presentation on theme: "Water metabolism disorders Dr Olcay Evliyaoğlu. Plasma osmolality is tightly between 275-295 mOsm/kg Thirst enhance water ingestion Arginin vasopressin."— Presentation transcript:

1 Water metabolism disorders Dr Olcay Evliyaoğlu

2 Plasma osmolality is tightly between 275-295 mOsm/kg Thirst enhance water ingestion Arginin vasopressin (AVP)enhance water output Both systems work together for the regulation of plasma osmolality

3 Extracellular fluid regulationRenin-angiotensin-aldosterone Na reabsorbstion Osmolality regulationThirst and AVP system Regulation of water intake and output

4 Body water and electrolytes Term newborns and infants % 75-80 of body weight is water % 45-50 of body weight is extracellular water % 30 of body weight is intracellularwater In the first days of life 7 % of the total body water is excreted from extracellular compartment by rapid diuresis

5 % 40 of BW is intracellular % 20 of BW is extracellular % 60 of BW is total water Adult type water distribution is achieved through childhood

6 Daily water ingestion and excretion can be 10 times different between individuals. It also can be different at different times in the same individual. Water losses: respiratory system skin digestive system urine İnsensible losses

7 Urine volumeSolute load that should be excreted Urine concentration that should excrete the solute load Daily solute excretion approx is 500 mOsm/m2 For urine with mean concentration of 500-600mOsm/kg 900ml/m2/day urine is necessary Respiration and via skin 750ml/m2/day Digestive system 100ml/m2/day Water oxidation occuring during enery metabolism 250ml/m2/day 1500ml/m2/day

8 Daily electrolyte needs ElectrolyteAmount Na20-50mEq/m2/day K20-50mq/m2/day Ca Term NB50-75mg/kg/day Infants600mg/day Children800mg/day Adolescents1200mg/day

9 If IV fluid therapy is planned for a short interval (hours- few days) anions with Na and K will be adequate If IV fluid therapy is for a long interval Ca, Mg and P should be added

10 Osmolality differences between the compartments will be equalized Cell membranes are impermeable to electolytes like sodium and chloride Extracellular solute load Cell membranes are permeable to potassium and phosphate Intracellular solute load

11 Osmotic gradient Water pass through compartments

12 Chronic changes is cell osmolality Adaptation mech of cell Intracellular impermeabl solutes increase or decrease Attention to hyper and hyponatremia treatment

13 Physiology of osmotic regulation Serum 275-295mOsm/kg Neurol and biochemical path ways to bring the osm to normal Sensitive mech that can sense osm changes

14 Osmosensors in central nervous system regulate to effector system Thirst Posterior pituitary AVP secretion

15 Vasopressin •AVP cyclic nonapeptide. Structure is like oxytosin. •Synthesized as preprohormone. •Gene is on chromosome 20. •Synthesized in bilateral hypothalamic supraoptic and paraventricular nucleus neurons. •Magnocellular neuron’s axons end at pituitary stalk and posterior pituitary. •AVP containing granulles are stored in nerve endings. •Nerve impulse results in Ca influx and exocitosis of granulles. •AVP is stored in a complex with neurophysin II in granulles •Neurophysin II is functional in AVP folding, oligomerization and transmission •In plasma neurophysin II seperates from AVP leaving it free.

16 Vasopressin secretion and thirst regulation Osmotic regulation İncrease in plasma osmolality İncrease in intravascular volume Emesis Pharmocologic agents Vasopressin secretion Sodium Chloride Glucose (insulin def) Osmotic loads

17 Hypertonic stimulus Osmo rec activated Depolarization of supra optic nucleus AVP secretion Osmo sensors and AVP secreting neurons are anatomically distinct Osmo sensors are outside of blood brain barrier Lamina terminalis- organ vasculosum (OVLT) Subfornical organ (SFO) Preoptic hypothalamus ( outside BBB) Osm res

18 Serum osmolality < 280 mOsm /kg Plasma AVP secretion < 1 pg/ml Serum osmolality >283mOsm/kg (threshold for AVP secretion) AVP secretion increase according to serum Osm. At serum osm of 320 mOsm/kg AVP reaches it’s max con of 20pg/ml

19 Emesis Hypotension Hypovolemia Vasovagal stimulus Hypoglycemia due to insulin Serum AVP > 5pg/ml Peak antidiuretic effect 5 pg/ml

20 More complicated cortical activities are needed for thirst Osmotic stim Angiotensin II Stimulates thirst center For thirst and AVP secretion same osmo sensors are used Threshold for thirst is 10 mOsm/ kg more than AVP secretion Serum Osm 293 mOsm/kg Threshold for thirst

21 Water balance AVP secretion Thirst mechanisms Decrease water loss İncrease water intake Both systems work together. One system is enough for the maintance of serum Osm. AVP deficient, thirst intact 5-10 ml/m2 urine output can be compensated by water ingestion Thirst disorder, AVP intactCompensated by AVP secretion

22 Vasopressin secretion and thirst regulation Nonosmotic regulation Right and left atrium Aortic arch (carotid sinus) Activates baroreceptors İncrease in intravascular volume and vascular wall tension Brain stem nucleus tractus solitarius Vagus Glossofarengeal Hypothalamic paraventricular and supraoptic nucleus İnhibit AVP secretion Noradrenergical bundles

23 Small changes (1%) in serum Osm Big changes in intravascular volume Effect AVP secretion 8 % decrease in blood volume can increase AVP secretion

24 Glucocorticoids İnhibit AVP secretion Directly increase free water excretion Cortisol deficiency AVP secretion increase Free water excretion decrease Decrease urine output İncrease urine out put

25 AVP t1/2: 5-10 min Degradation by vasopressinase Desmopressin Aminoterminal part is resistant for degradation t1/2 8-24 saat

26 Vasopressin receptors G protein associated cell membrane receptors V1 V3 (V1b) Vascular smooth muscle (vascular contraction) Hepatocytes Anterior pituitary corticotrophs Increase ACTH (fofotidil inositol yolu ile) secretion Smiliar to V1 and oxytocin rec structure

27 V2 Kidney collector tubulles Thick asccending Henle loop Periglomerullar tubulles Some systemic vessel endotelial cells (vasodilation via NO synthase stimulation) Stimulation of Von Willebrand factor Stimulation of factor VIIIa Stimulation of tissue plazminogen activator Consists of 370 aminoasits G protein associated res. Functions via cAMP Gene on long arm of chromosome X (Xp28)

28 AVP effect at kidnesys VP+VP2Rİncrease cAMP Microflamend and cellular stuctural changes in the microtubules Water channels enter the membrane. Water permeability of the membrane increase

29 V1a andV1b Join with phospholipase C and acts by intracellular Ca and phosphotidilinositol signal pathways V2 Joins with Gαs and acts by cAMP

30 Activation of V2 recaquoporine molecules enter apikal membrane Water permeability increase in luminal epithelial membrane ( 100 times)

31 Vasopressin deficiency •Polyuria ( >2L/m2/day) •Polydipsia •Diabetes Insipidus

32 •Serum Osm:(Serum Na + K)x2 + Gluc/18 +BUN/3 •Urine Osm: (1.86 x Na) + Glucose/16 + BUN/2.8 + 9 •Urine Osm/ Serum Osm <1,5  DI

33 Diabetes Insipidus Primary polidipsia Nephrogenic Central

34 Water deprivition test Response - yes Urine Osm > 1000 Urine Osm > 600(at least 2 meas) Primary polydipsia Partial nephrogenic DIPartial central DI Response - no Serum Osm > 300( Na>146mmol/L) Urine Osm < 600 Central DINefrogenic DI DI differential diagnosis

35 AVP test Response-yes Δ urine Osm > %50 Central DI Response-no Δ urine Osm < %50 Nephrogenic DI

36 Central DI •Pituitary –Genetic •Otosomal dom (VP-neurophysin gene) •Otosomal rec (VP-nörofizin gen) •Otosomal rec (Wolfram synd)(chromosome 4p WFS 1 gene) •X-linked res (chrom Xp28) –Congenital malformations •Midline craniofacial disorders •Holoprosencephaly •Pituitary hypogenesis –Acquired •Trauma •Neoplasms ( craniyofarengioma,disgerminoma,meningioma) •Granulomas •Infections •Inflamatory- lenphocytic infundibuloneurohipophysitis •Vascular •İdiyopathic Clinical disorders of the posterior pituitary In Pediatric Endocrinology

37 Nephrogenic DI •Genetic –X- linked rec (AVP-V2 rec) –Ot rec (aquaporin-2) –Ot dom (aquaporine-2) •Acquired –Drugs •Lithyum •Foscarnet •Demeclocycline •others –Metabolic •Hiperglisemi •Hiperkalsemi •Hipokalemi •Protein malnütrisyonu –Renal •Chronic renal failure •İskemic injury •Medullary disfunction •Obstructions

38 Primary polydipsia •Psychogenic polydipsia •Dipsogenic polydipsia •Iatrogenic polydipsia

39 İnappropriate AVP secretion •ADH secretion inappropriate to plasma osm ( lower than the threshold) •Dilutional hyponatremia

40 •Tumors (bronkogenic Ca) •Drugs •CNS disorders •Non malign lung disorders •Postoperative •Adrenal insufficiency •Hypothyroidism İnappropriate AVP secretion

41 Cerebral salt loss •Any CNS disorder can result in hyponatremia and increase in urine Na •With Na there is also water loss, DH


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