salt and water homeostasis

Question 1

distribution of water ic and ec?

Answer 1

Dependant on ions: •ECF: Na+, Cl- , HCO3- •ICF: K+ , PO4- •Concept of osmolality: Ionic concentration of ECF/ICF/Urine •Plasma osmolality: also influenced by urea and glucose concentration

Question 2

movement in exf is dependent on?

Answer 2

Ionic content of ECF Fluids fairly constant •Capillary Hydrostatic Pressure: Drives Fluid out of capillaries •Colloid Oncotic Pressure: Draws Fluid back in to capillaries (Plasma Proteins)

Question 3

info abouut adh?

Answer 3

Posterior Pituitary release Originates from Hypothalamic Supraventricular and Supra-optic nuclei 2. Role: Water Preservation 3. Mode of Action: Binds on to Vasopressin2 (V2) Receptors in the Collecting Duct 4. Consequence: Opens Aquaporin Channels allowing reabsorption of water from urine in to plasma 5.Secretion Triggered by: •Rising Plasma Osmolality (Thirst Reflex) •Detection of low blood pressure (Baroreceptors) •1% change in osmolality vs. 5-10% change in pressure

Question 4

anatomy of kidney/

Answer 4

add pic

Question 5

causes f hyponatraemia?

Answer 5

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Question 6

diabetes insipidus?

Answer 6

Decreased release of ADH (central) •Decreased renal responsiveness to ADH (nephrogenic) – response to treatment with desmopressin limited •Excessive Urination (>3l/day) •Differential Diagnosis: Psychogenic polydipsia •Diagnosis: Water Deprivation Test •Euvolaemia with normo- or hypernatraemia

Question 7

causes of siadh?

Answer 7

NEUROPSYCIATRIC •DRUGS •PULMONARY •ECTOPIC ADH •OPERATIVE? •OTHERS •RX: TREAT CAUSE; DEMECLOCYCLINE

Question 8

causes of diabetes insipidus?

Answer 8

vDecreased release of ADH (central) •Decreased renal responsiveness to ADH (nephrogenic) – response to treatment with desmopressin limited •Excessive Urination (>3l/day) •Differential Diagnosis: Psychogenic polydipsia •Diagnosis: Water Deprivation Test •Euvolaemia with normo- or hypernatraemia

Question 9

water deprivation test?

Answer 9

Administer ddAVP if urine osmolality fails to rise > 300mosmol/l after 3 samples •Test terminated if urine osmolality reaches 700mosmol/l or if failure to respond to ddAVP/pt at risk of dehydration Administer ddAVP if urine osmolality fails to rise > 300mosmol/l after 3 samples •Test terminated if urine osmolality reaches 700mosmol/l or if failure to respond to ddAVP/pt at risk of dehydration

Question 10

tresting insipidus?

Answer 10

CRANIOGENIC: Desmopressin and identify cause •NEPHROGENIC: Identify and treat cause.

Question 11

potasium balance?

Answer 11

>90% of potassium intracellular (muscle, red cells, liver, bone) •Only 2.5% in ECF •Kidney excretes 90-95%; rest is from GI loss •Insulin stimulates movement of Potassium from ECF in to cells (ICF) •Aldosterone promotes potassium excretion in to urine and sodium reabsorption (Distal Convoluted Tubule) •Metabolic Acidosis promotes movement of Potassium from ICF to ECF leading to hyperkalaemia Trends: rate of rise; ECG Changes; Degree of renal impairment (Anuria); chronicity of renal impairment.

Question 12

symptoms of hyperkalaemia and hypo/?

Answer 12

Hyperkalaemia Life-threatening arrhythmias ECG: Peaked T waves, Widening of QRS Complexes, Loss of P-waves, Sinusoidal pattern •Hypokalaemia Muscle weakness

Question 13

causes of siadh?

Answer 13

Neuropsychiatric disorders –Infections: meningitis, encephalitis, brain abscess –Vascular: thrombosis, subarachnoid or subdural hemorrhage, temporal arteritis, cavernous sinus thrombosis, stroke –Neoplasm: primary or metastatic –Skull fracture, traumatic brain injury –Psychosis, delirium tremens –Other: Guillain-Barré syndrome, acute intermittent porphyria, autonomic neuropathy, postpituitary surgery, multiple sclerosis, epilepsy, hydrocephalus, lupus erythematosus.

Question 14

causes of hypokalaemia?

Answer 14

Renal loss: diuretic therapy, hypomagnesaemia, gentamicin therapy, aminophylline, Conn’s Syndrome, Bartter’s syndrome, excess diuresis after recovery from obstruction and recovery from acute tubular necrosis •Extra-renal loss: Diarrhoea, vomiting, ileostomy •Metabolic or respiratory alkalosis

Question 15

treatment of calcium chloride?

Answer 15

Stabilise myocardium: iv calcium chloride/gluconate •Insulin/dextrose infusion and/or iv salbutamol •Treat acidosis: iv sodium bicarbonate; treat hypercapnia •Oral/PR calcium resonium •Induce diuresis/dialyse •Minimise oral Potassium intake (Dietician) •STOP DRUGS ASSOCIATED WITH HYPERKALAEMIA

Question 16

causes of siadh?

Answer 16

Neuropsychiatric disorders –Infections: meningitis, encephalitis, brain abscess –Vascular: thrombosis, subarachnoid or subdural hemorrhage, temporal arteritis, cavernous sinus thrombosis, stroke –Neoplasm: primary or metastatic –Skull fracture, traumatic brain injury –Psychosis, delirium tremens –Other: Guillain-Barré syndrome, acute intermittent porphyria, autonomic neuropathy, postpituitary surgery, multiple sclerosis, epilepsy, hydrocephalus, lupus erythematosus. Drugs –––––––––––––– Intravenous cyclophosphamide Carbamazepine Vincristine or vinblastine Thiothixene Thioridazine, other phenothiazines Haloperidol Amitriptyline, other tricyclic antidepressants or serotonin-reuptake inhibitors Monoamine oxidase inhibitors Bromocriptine Lorcainide Clofibrate General anesthesia Narcotics, opiate derivatives Nicotine Lung diseases and interventions ––––Pneumonia Tuberculosis Lung abscess, empyema Acute respiratory failure Positive pressure ventilation 4. Perioperative Period - associated with the stress response to injury and pain 5. Ectopic (nonhypothalamic) production of ADH Cancer: Small cell carcinoma of lung (2/3 of patients with small cell have impaired water excretion), bronchogenic, duodenum, pancreas, thymus, olfactory neuroblastoma, bladder, prostate, uterus Lymphosarcoma, reticulum cell sarcoma, mesothelioma, Ewing sarcoma Hodgkin’s disease, leukemia Pulmonary tuberculosis 6. Potentiation of ADH effect Chlorpropamide Carbamazepine Psychosis Intravenous cyclophosphamide Tolbutamide Prostaglandin-synthesis inhibitors (salicylates, NSAIDS) 7. Exogenous administration of ADH Vasopressin, desmopressin Oxytocin Copyright Patrick Neligan 2001-2002

Question 17

causes of cranial and nephro insipidus?

Answer 17

This is generally attributable to an insult to or defect of the posterior pituitary gland: •Idiopathic •Tumour: Usually a tumour of another part of the pituitary gland. There might be evidence of pituitary dysfunction: e.g. adrenal or thyroid dysfunction •Trauma •Infiltration by non-neoplastic cause: Haemochromatosis, Sarcoidosis, Histiocytosis •Genetic: Autosomal Dominant; Very Rare This is generally attributable to an insult to or defect of the posterior pituitary gland: •Idiopathic •Tumour: Usually a tumour of another part of the pituitary gland. There might be evidence of pituitary dysfunction: e.g. adrenal or thyroid dysfunction •Trauma •Infiltration by non-neoplastic cause: Haemochromatosis, Sarcoidosis, Histiocytosis •Genetic: Autosomal Dominant; Very Rare

Question 18

classification of aki?

Answer 18

RIFLE Criteria –Risk/Injury/Failure/Loss/ESRD –GFR loss: 25/50/75% –Creatinine Rise: 1.5x/2x/3x –Urine output: 0.5ml/kg/h for 6h/12h/0.3ml/kg/h for 24h (or anuria for 12h) •AKIN Criteria –Stages 1-3 similar