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Water metabolism disorders

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Presentation on theme: "Water metabolism disorders"— Presentation transcript:

1 Water metabolism disorders
Dr Olcay Evliyaoğlu

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

3 Extracellular fluid regulation
Renin-angiotensin-aldosterone Na reabsorbstion Osmolality regulation Thirst and AVP system Regulation of water intake and output

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

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

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 volume Solute 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 mOsm/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 ml/m2/day 1500ml/m2/day

8 Daily electrolyte needs
Amount Na 20-50mEq/m2/day K 20-50mq/m2/day Ca Term NB 50-75mg/kg/day Infants 600mg/day Children 800mg/day Adolescents 1200mg/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 mOsm/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
Posterior pituitary AVP secretion Thirst

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 Osmo rec activated Hypertonic stimulus 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. 5-10 ml/m2 urine output can be compensated by water ingestion AVP deficient, thirst intact Thirst disorder, AVP intact Compensated by AVP secretion

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

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

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

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

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 V2 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+VP2R İncrease 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 rec aquoporine 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/ Urine Osm/ Serum Osm <1,5  DI

33 Diabetes Insipidus Primary polidipsia Nephrogenic Central

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

35 DI differential diagnosis
AVP test Δ urine Osm > %50 Response-yes Central DI Δ urine Osm < %50 Response-no 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 Acquired 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 İnappropriate AVP secretion
Tumors (bronkogenic Ca) Drugs CNS disorders Non malign lung disorders Postoperative Adrenal insufficiency Hypothyroidism

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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