Paediatrics: Part 2 Flashcards
What structures produce ADH
Suproptic and paraventricular nuclei of the anterior pituitary gland -> stored in posterior.
Role of ADH
Causes re-absroption of water at the collecting ducts and vasoconstriction (i.e., vasopressin!)
What receptor does ADH bind o and what happens
V2, causes aquaporins to embed into the cell membrane, only allowing water to move back into the blood to improve blood osmolality
This makes urine more concentrated
What is Diabetes Insipidus
When too little water is re-absorbed from the urine. Leads to polyuria
Why do we get polydipsia in diabetes insipidus
Because of reduced osmolality in the blood, causing osmoreceptors to stimulate the thirst centre in the medulla.
Central Diabetes Insipidus vs Nephrogenic Diabetes
Lack of ADH -> Central Diabetes Insipidus
REDUCED ADH response by the kidneys -> Nephrogenic Diabetes
What structures contribute to central diabetes inspidus
Hypothalamus can’t produce ADH
Pituitary gland can’t store ADH
Causes of central diabetes insiipidus
- Pituitary Tumours
- Head Trauma
- Head Surgery
- Ischaemic Encephalopathy
What causes nephorgenic Diabetes Insipidus
More often than not, Hereditary Genetic defects in receptors.
Lithium - Reduces production of aquaporin proteins in collecting duct
Hypokalaemia
Hypercalcaemia
Demeclocycline (aquaporine receptor antagonist)
Symptoms of Diabetes Inspidius
- Polyuria (>3L of dilute urine/day)
- Polydipsia
Increase in plasma osmolality: Fatigue, nausea, poor concentration and confusion
How to diagnose DI
- Blood osmolality Test (>290)
- Urine specific Gravity <10006 (too dilute)
- Low Hyperosmotic volume concentration
- Water Deprivation Test to measure hourly measurements of urine volume (osmolality will stay dilute <300)
- Desmopressin test: Causes an increase in urine osmolality by 50% (central), if no change (nephrogenic)
Central vs nephrogenic
Low ADH vs Normal or High ADH
Treatment of central DI
Desmopressin and water
Treatment of nephrogenic DI
- Thiazide Diuretics to get rid of Na+
2. Or Amiloride (potassium sparing)
What is SIADH
The body makes too much ADH
What causes SIADH
- Ectopic ADH secretion from small cell lung carcinoma
- CNS surgeryy or head trauma that releases all stored ADH in pituitary gland.
- Pneumonia, COPD
- Cyclophosphamide (increases ADH receptors on principal cells)
Pathophysiology caused by SIADH
- Increase in ADH = Increased water reabsorption
ECF expands and water moves into ICF to correct but ECF still has a lot of extra cellular fluid = dilution hyponatraemia (Na+ amount is normal but in larger fluid) = euovolaemic hyponatraemia.
NO oedema as. Na+ is the same.
Impacts of SIADH on the body
- Increased blood volume and pressure
- More ANP or BNP to dilate BP and improve GFR to excrete water and Na+
- Reduced Renin release from kidneys = less aldosterone and angiotensin 2 to reduce sodium and water reabsorption
Cerebral oedema and Seizures = most important complication
Diagnosis of SIADH
- Hyponatraemia
- Reduced serum osmolality
- Increased urine osmolality
How to treat SIADH
- Tolvaptan which antagonises vasopressin receptors.
- FLuid Resus and IV hypertonic saline.
SLOWLY to prevent osmotic demyelination syndrome.
What food can cause red urine
Beetroot
What drug may cause red urine
Rifampicin
What is proteinuria in children
Over 0.15g/24hrs
What threshold defines a UTI
> 10 ^ 5 microorganisms