Polyuria Flashcards
What are the differentials for polyuria
Diabetes Mellitus Diuretic use e.g. medications, caffeine, alcohol, lithium Heart failure Hypercalcaemia Hyperthyroidism Primary polydipsia Hypokalaemia Hyperuricaemia Diabetes insipidus Chronic renal failure Steroids and Cushing’s
What questions should be asked to a patient with polyuria
How many times a day (+night) do you go - nocturia important
Any fatigue, weight loss, recurrent infections (Diabetes)
LUTS (bladder or urinary tract pathology)
Pain, frequency, change in urine colour and smell (UTI - frequency increases but not polyuria)
What in the past medical history may be important for polyuria
Renal problems
Conditions that precipitate renal failure e.g vascularises, HTN, chronic urinary retention)
Cancer with known bony involvement
Psychiatric disorders (primary polydipsia)
What is important in the drug history for polyuria
Diuretics
Recent changes in medications
Lithium (-> nephrogenic DI)
What is important about family history in polyuria
Diabetes mellitus
Cancer
Diabetes insipidus
What investigations should be ordered for polyuria
Capillary blood glucose (DM)
Urinalysis (+dipstick: rule out UTI (FREQUENCY) | DM)
Fasting plasma glucose Urine osmolality Electrolytes (sodium low in primary polydipsia, high in everything else) Urea, creatinine, eGFR (rule out CKD) Serum calcium Thyroid function
What does the urine osmolality tell you in polyuria
High (>300): inability to reabsorb solutes by the kidneys
Low (<250): inability to reabsorb water due to distal tubule pathology or ADH deficiency
How do you differentiate between cranial and nephrogenic diabetes insipidus
Water deprivation testing with desmopressin
Normal response to water deprivation = urine concentration
DI = urine remains dilute
+Desmopressin
Nephrogenic: urine remains dilute
Cranial: urine concentrates
Test must be stopped if there is a weight loss of >3%
What is the management for cranial Diabetes insipidus
Adequate fluid intake
MRI head to rule out pituitary lesion + endocrine referral
Replacement ADH
What are the causes of diabetic ketoacidosis
Type 1 diabetes mellitus
Non-compliance with insulin
Illness
How does illness cause DKA
In illness the body makes more corticosteroid in response to the stress
Cortisol antagonises the action of insulin, so the normal insulin requirements go up
T1DM patients must increase insulin doses when they are unwell
What investigations should be done for a patient with polyuria, constipation fatigue and bone pain
Serum calcium to confirm hypercalcaemia
Alkaline phosphatase: raised in bone mets, normal in myeloma
Serum and urine electrophoresis: look for paraprotein in myeloma
Lumbar radiograph: lyric lesions where she has the pain
Where is primary polydipsia most commonly seen
Schizophrenics
What is the MOA for biguanides and give examples
Metofrmin
Reduces hepatic glucose production and increases peripheral uptake
Insulin sensitiser
What is the MOA for Glitazones and give examples
Thiazolidinediones e.g. rosiglitazone
Activates PPAR-gamma receptor (nuclear transcription factors that increases lipoprotein lipase, LDL, and fatty acid transporter protein 1 (FATP1) transcription to increase insulin sensitivity)
