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Renal biochemistry

Katherine Chin Clinical biochemistry Inglés 15 fichas

Fichas del conjunto (15)

  1. 1What is osmolalityNumber of particles in 1kg of solution
  2. 2What is osmolarity?Number of particles in 1L of solvent
  3. 3How is osmolality calculated?2([Na]+[K]) + [glucose] + [urea]
  4. 4Vasopressin/ADH: Where is it produced? Where does it act? What does it cause? What triggers it?Produced by hypothalamus supra-optic and paraventricular nucleus.
    Acts on collecting duct of kidney.
    Triggers increased water reabsorption via aquaporins and increased urea permeability
    Triggered by osmotic trigger: extracellular osmolality > intracellular
    non-osmotic trigger: hypovolaemic
  5. 5Renin: Where is it produced? Where does it act? What does it cause? What triggers it?Juxtaglomerular cells.
    Angiotensinogen in blood
    Increased H2O uptake due to increased Na+ and Cl- uptake. Increased K+ and H+ excretion
    Triggered by low sodium; low arterial pressure; decreased renal blood flow
  6. 6What is acute tubular necrosis?Occurs due to decreased plasma volume and/or low renal perfusion (so is pre-renal or renal cause).
    The resulting low GFR (hence pre-renal uraemia) requires fluid to be given
    If fluid not given then there is hypoxic damage and ATN occurs
  7. 7What investigations should be done potential ATN?- Serum creatinine
    - Urinary sodium concentration U[Na+]
  8. 8What can U[Na+] be used for?Differentiate between pre-renal uraemia and acute tubular necrosis
  9. 9What sodium levels do we see in pre-renal uraemia and ATN?Pre-renal uraemia: U[Na] <20 as RAAS activated to counteract the low perfusion volume
    ATN: U[Na] >20 and low urinary output as kidneys are no longer responding to aldosterone
  10. 10What are the biochemical and subsequent clinical features of AKI? (4)- Failure to remove nitrogenous waste: malaise, confusion, nausea
    - Retention of potassium: cardiac changes
    - Fluid overload: cardiac failure, oedema, high BP
    - Retention of acidic waste products: acidotic
  11. 11What is Fanconi syndrome?Globular tubular defect that results in loss of many products into urine
  12. 12What are the biochemical changes seen in CKD? Stage 3aHypertension and increased CVD risk
  13. 13What are the biochemical changes seen in CKD? Stage 3bLow Ca as there is less Vitamin D produced.
    2dary hyperparathyroidism occurs
  14. 14What are the biochemical changes seen in CKD? Stage 4Anaemia due to reduced EPO production
    Anorexia
    Increased phosphate as unable to excreted
  15. 15What are the biochemical changes seen in CKD? Stage 5Na and water retention
    Metabolic acidosis: reduced H+ excretion at the proximal tubules
    Hyperkalaemia: reduced excretion as the distal tubular Na/Ke exchange not working

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Clinical biochemistry Fichas sobre Renal biochemistry, creado por Katherine Chin el 06/06/2018.
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Katherine Chin
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