Acid base.txt

  1. What is a buffer?
    • Strong base (HCO3-) and conjugate weak acid (H+)
    • HB H+ + B-
  2. What are the 4 main buffers in our body? Start with best! And why?
    • Bicarbonate: high capacity and ease of elimination (CO2)
    • Phosphate
    • Plasma proteins
    • Intracellular buffers eg Hb
  3. How is the osmolar gap calculated?
    • Difference between measured and calculated osmolality
    • Calculated: 2(Na + K) + urea + glucose
  4. What is the significance of osmolar gap?
    The presence of an osmolar GAP in metabolic acidosis indicates presnce of unmeasured osmoles eg methanol, ethanol, ethylene glycol
  5. What are cations? Give eg
    • Positively charged
    • Sodium Na+
  6. What are anions? Give eg
    • Negatively charged particles
    • Chlrodie Cl-
  7. How is anion gap calculated?
    (Na + K) – (Cl + HCO3)
  8. What is the normal range of anion gap?
  9. How will the addition of acid increase the anion gap?
    It will lower the bicarbonate level (think equation)
  10. What does the anion gap indicate?
    Amount of acid added
  11. Why is anion gap useful in clinical practice?
    Monitor patients response to therapy
  12. What is high anion gap MA due to? (principle)
    Acid added endogenously or exogenously lower bicarb concentration less anions greater GAP
  13. What is normal anion gap MA due to? (principle)
    Loss of bicarbonate associated with HYPERCHLORAEMIA so anion gap remains normal! (as Cl- is an anion)
  14. Give the causes of high anion gap metabolic acidosis?
    • Big MUDPILES
    • Biguanides: metformin
    • Methanol
    • Uraemia
    • DKA, alcoholic ketoacidosis (B-hydroxybutyrate, acetoacetate, acetone)
    • Paraldehye (fixative)
    • Isoniazid, iron, infection
    • Lactate
    • Ethylene glycol
    • Salicylates
  15. Give the causes of normal anion gap metabolic acidosis?
    • HARD UP AA
    • Hyperalimentation
    • Acetozolamide (carbonic anhydrase inhibitor)
    • Renal tubular acidosis
    • Diarrhoea
    • Ureto-enteric fistula
    • Pancreatico-duodenal fisutla
    • Addison’s
    • Ammonium chloride ingestion
  16. What are the 2 main categories od normal anion gap metabolic acidosis?
    • GI loss of bicarbonate: small bowel secretions in diarrhoea or pancreatic drainage
    • Renal tubular acidosis
  17. What is type of acidosis do you get with RTA?
    Hypokalaemic Hyperchloraemic metaboic acidosis with normal anion gap
  18. What is type 1 RTA due to?
    Inability to excrete H+
  19. Where does type 1 RTA occur?
    Distal tubule
  20. What is the urinary pH in RTA1?
    Over 5.5 (ie failure to acidify urine)
  21. What are the clinical features of RTA1?
    • 1. Rickets/osteomalacia due to buffering of H+ with calcium in bone
    • 2. nephrocalcinosis with renal calculi leading to recurrent UTI
  22. Why do you get renal stones in RTA1?
    • Hypercalciuria from bone
    • Decreased urinary citrate: as reabsorbed from urine as a buffer for H+
    • Alkaline urine
    • All favour calcium phosphate stone formation
  23. How is type 1 RTA diagnosed?
    • 1. Urinary pH > 5.3 in face of systemic acidosis
    • 2. failure to acidify urine following an oral acid load challenge: alluminium chloride test
  24. What is the treatment of type 1 RTA?
    • Sodium bicarbonate or citrate
    • correct the acidemia and reverse bone demineralisation.
  25. What is the cause of type 1 RTA?
    • Idiopathic
    • Autoimmune: Sjogren’s, SLE
  26. What is type 2 RTA due to?
    Inability to reabsorb bicarbonate (bicarb leak)
  27. Where does type 2 RTA occur?
    Proximal tubule
  28. What are the causes of type 2 RTA?
    • Fanconi syndrome
    • Tubulointerstitial disease: myeloma
    • Drugs: lead
  29. What type of acidosis do you get with type 2 RTA?
    • Hypokalaemic, hyperchloraemic metablic acidosis
    • Normal anion gap
  30. What is the difference in the urine between type 1 and type 2 RTA?
    • In type 2: tubules are able to reabsorb SOME HCO3
    • So urine can acidify during systemic acidosis
  31. Which syndrome is type 2 RTA associated with?
    Fanconi syndrome (generalised dysfunction of proximal tubule cells)
  32. Which is more common type 1 or type 2 RTA?
    Type 1
  33. Why is hypokalaemia common in type 2 RTA?
    Due to osmotic diuretic effect of reduced HCO3 reab increased flow rate to distal tubule increased K+ excretion
  34. How is type 2 RTA diagnosed?
    Iv sodium bicarbonate load: if see high fractional excretion (>15%) of HCO3 = type 2 RTA
  35. What is the treatment of type 2 RTA?
    High doses of bicarbonate (often intolerable)
  36. What is type 3 RTA?
    • Combination of type 1 and 2 RTA
    • Very rare
  37. What is the difference between type 4 RTA and type 1 and 2?
  38. What is type 4 RTA due to?
    Hyporeninaemic, hypoaldosteronism
  39. Why do you get acidosis in type 4 RTA?
    • Low aldosterone causes hyperkalaemia and acidosis
    • As it decreases K+ and H+ secretion
  40. What are the functions of aldosterone?
    • 1. acts on nuclear mineralocorticoid receptors (MR) in distal tubule and collecting duct in kidney to activate Na/K/ATP pump on basolateral membrane of cell. So sodium is reabsorbed into the blood and K+ is secreted into the urine
    • 2. upreg EnaC on apical membrane to increase permeability of Na
    • 3. Cl- reab with Na to maintain electrochemical balance
    • 4. stimulates uptake of K+ into CELLS
    • 5. stimulates H+ secretion in collecting duct, regulating HCO3- levels (acid-base)
    • 6. acts on posterior pituitary gland to release ADH
  41. what are the causes of type 4 RTA?
    • Hypoadrenalism: hypoaldo
    • Mild renal impairment: DM or tubulointerstitial disease
    • Drugs: K+ sparing diuretics, ACEi, ARB, NSAID
  42. What is the treatment of type 4 RTA?
    • Remove cause
    • Fludrocortisone
    • Furosemide
    • Calcium resonium to control hyperK+
  43. What is Fanconi syndrome?
    • Disturbance of proximal tubule function
    • So defective reabsorption of amino acids, K+, phosphate, glucose, bicarbonate (leading to type 2 RTA)
  44. What are the causes of Fanconi syndrome?
    • Idiopathic
    • Inherited: errors of metabolism eg fructose intolerance, GSD
    • Acquired: tubule damage from heavy metal eg lead, mercury
    • Light chain damage: myeloma or amyloidosis
  45. What is the treatment of Fanconi syndrome?
    • Remove cause
    • Replace losses – K+, HCO3-
  46. What are the clinical effects of metabolic acidosis?
    • Air hunger
    • Neuro symptoms coma
    • Impaired cardiac function and state of shock
    • Severe acidosis: cardiac dysrhythmias, cardiac arrest, sudden death
  47. Which values are raised in metabolic alkalosis? What is it compensated by?
    • Raised: pH & bicarbonate
    • Compensated by: rise in CO2
  48. What are the causes of metabolic alkalosis?
    • Loss of H+/retain bicarb
    • Vomit,
    • Renal loss from hyperaldosteronism (Conn’s/Cushing’s): retention of Na+ but loss of H+ into urine
    • Diuretics (thiazide and loop): K+ depletion
    • Burns
    • Retention of bicarbonate: administration of alkali with decreased GFR
    • Posthypercapnic metabolic acidosis (compensatory)
  49. What are the clinical effects of metabolic alkalosis?
    • Orthostatic hypotension
    • Hypokalaemia leading to weakness and hyporeflexia
    • Tetany
    • Neuromuscular excitability: due to reduced free (active) calcium concentration as it is bound to albumin (as H+ is not bound to it)
  50. What are the causes of respiratory acidosis?
    • Hypoventilation and subsequent rise in PCO2
    • CO2 forms carbonic acid = source of H+
    • CO2 + H20 H2CO3 HCO3- + H+
    • Airway obstruction: laryngospasm/bronchospasm cause ACUTE RA, COPD cause CHRONIC RA
    • Respiratory centre depression: sedative overdose, brain lesions
    • Neuromuscular disorder: respiratory muscle diseaes, MS
    • Restriction defect: respiratory muscle disease, pneumothorax, interstitial fibrosis, kyphoscoliosis
  51. What are the clinical effects of respiratory acidosis?
    • Peripheral VASODILATION
    • Increase ICP
    • Confusion
    • Myoclonus
    • Coma
  52. What are the causes of respiratory alkalosis?
    • (Hyperventilation reduces CO2) SHAPS
    • Salicylates: give MIXED acid base too
    • Hypoxia: Congestive cardiac failure, congenital heart disease
Acute asthma (NB if life threatening, may give respiratory acidosis if cant breathe out)
    • Psychogenic hyperventilation: fear, anxiety, PAIN
    • SAH
  53. What are the clinical effects of acute respiratory alkalosis?
    lightheaded, parasthesiae, numbness around the mouth, tingling sensation in the hands and feet. Tetany
  54. Why do salicylates give a mixed acid base disorder?
    • Salicylates stimulate resp centre over ventilate and cause resp ALKALOSIS
    • Get excess production of lactic acid metabolic ACIDOSIS
  55. What is uraemia?
    The illness accompanying renal failure
  56. What are the symptoms of uraemia
    • Asterixis
    • Tremor
    • Hyperreflexia
    • Upgoing planter response
    • Pericarditis
    • Bruising
    • Fall in BP and body temp
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Acid base.txt
acid base