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302/308 > Acid base and electrolyte disturbance > Flashcards

Acid base and electrolyte disturbance Flashcards

1
Q

What is urea produced and excreted by

A
  • Produced by liver, excretion of ammonia and breakdown products of amino acids
  • Excreted in urine
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2
Q

When do urea levels decrease

A

Liver disease

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3
Q

When are urea levels raised

A
  • Intravascular depletion
  • Blood meal
  • Renal failure
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4
Q

Effects of high urea levels

A

Urea>20 - Nausea, decreased appetite, itchiness, tiredness, smelly breath, metallic taste in mouth

Urea > 60 - Extreme ureamic frost, uraemic pericarditis, encephalopathy

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5
Q

What is creatinine a product of

A
  • Breakdown product of creatinine phosphate in muscle

- Usually produced at a fairly constant rate by the body

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6
Q

Link between number of nephrons and creatinine levels

A

The less the number of nephrons the more the build up of creatinine - therefore creatinine levels are indicative of kidney function

  • Creatinine is not toxic itself
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7
Q

How affected are creatinine levels by fluid shifts

A
  • Less affected by fluid shifts
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8
Q

What can creatinine levels be used to calculate

A
  • eGFR
  • MDRD
  • Cockcroft and Gault
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9
Q

Normal creatinine clearance rate

A

> 90 mls/min

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10
Q

CKD 1 eGFR

A

> 90 mls/min

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11
Q

CKD 2 eGFR

A

> 60 mls/min

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12
Q

CKD 3a eGFR

A

> 45 mls/min

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13
Q

CKD 3b eGFR

A

> 30 mls/min

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14
Q

CKD 4 eGFR

A

> 15 mls/min

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15
Q

CKD 5 eGFR

A

< 15 mls/min

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16
Q

Location of bulk of water and electrolytes

A
  • Bulk of water and electrolytes are not in the serum but in the cells
  • Integrated homeostatic mechanisms maintain body fluid compositions
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17
Q

What is glomerular filtration diminished by

A
  • Age
  • Renal disease
  • Congestive heart failure
  • Cirrhosis
  • Nephrotic syndromes
  • Volume depletion
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18
Q

Causes of hyponatremia - hypovolemia - renal losses >20mmol/L

A
  • Diuretic excess
  • Mineralocorticoid deficiency
  • Self-losing nephropathy
  • Bicarbonaturia with renal tubular acidosis and metabolic alkalosis
  • Ketonuria
  • Osmotic diuresis
  • Cerebral salt wasting
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19
Q

Causes of hyponatremia - hypovolemia - extrarenal losses <20 mmol/L

A
  • Vomiting
  • Diarrhoea
  • Third spacing of fluids in burns, pancreatitis and trauma
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20
Q

Causes of hyponatremia - euvolemia(no edema) - increase in total body water, no change in total body Na+ (>20 mmol/L)

A
  • Glucocorticoid deficiency
  • Hypothyroidism
  • Stress
  • Drugs
  • SIADH
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21
Q

Causes of hyponatremia - Hypervolemia - >20mmol/L

A
  • Acute or chronic renal failure
22
Q

Causes of hyponatremia - hypervolemia - <20mmol/L

A
  • Nephrotic syndrome
  • Cirrhosis
  • Cardiac failure
23
Q

What is pseudohyponatremia

A
  • A physiologically normal plasma water sodium concentration, but a reduced measured plasma sodium concentration.
24
Q

What can cause pseudohyponatremia

A
  • Hypertriglyceridemia associated with conditions such as diabetes, obstructive liver disease, nephritic syndrome and acute pancreatitis
  • Can also be caused by administering IV immunoglobulins
25
Q

What is translocational hyponatraemia

A

Translocational hyponatremia refers to the translocation of water from the ICF compartment to the ECF compartment usually in the setting of hypertonicity, which dilutes the PNa

26
Q

Potassium distribution

A
  • Wide distribution - extracellular and intracellular
  • The major intracellular cation
  • Primarily distributed intracellularly (100-120mmol/L)
  • Serum K = 3.2-5.1 mmol/L
27
Q

Hypokalaemia causes - redistribution

A
  • Insulin, theophylline, adrenergic use
28
Q

Hypokalaemia causes - non renal loss

A
  • Sweating, vomiting or diarrohea
29
Q

Another cause of hypokalaemia

A

Poor diet

30
Q

Causes of hypokalaemia - renal loss > 20mmol/l

A
  • Drugs, diuretics, aminoglycosides, amphotericin
  • RTA or metabolic acidosis
  • Low BP bartter’s or gittlemans
  • High BP
  • High aldosterone normal cortisol - hyperaldosteronism
  • Low aldosterone normal cortisol liddle’s
  • Low aldosterone high cortisol cushing’s syndrome
31
Q

Chronic hypokalaemia - cardiovascular complications

A
  • Hypertension

- Ventricular tachyarrhythmias

32
Q

Chronic hypokalaemia - endocrine complication

A
  • Impairs insulin activity and sensitivity
33
Q

Chronic hypokalaemia - muscular complication

A
  • Impairs muscle contraction –> weakness
34
Q

Chronic hypokalaemia - renal complications

A
  • Mild tubulointerstitial fibrosis
  • Renal cyst formation
  • Metabolic alkalosis (increased net renal acid excretion)
  • Polyuria
35
Q

Chronic hypokalaemia - liver complications

A
  • Increases renal ammonia production which may worsen hepatic encephalopathy
36
Q

What does hyperkalaemia indicate

A
  • Kidneys have a large capacity to excrete K+

- Hyperkalaemia indicates impaired renal excretion

37
Q

What causes hyperkalaemia

A

Impaired renal excretion - CKD4/5

  • Drugs impairing secretion - spironolactone, amiloride, ACE-I, ARB
  • Increased K load - rhabdomyolysis, haemolysis, GI bleed
  • Increased dietary intake
38
Q

Pseudohyperkalaemia

A
  • Haemolysis
    During blood collection/storage
    Rheumatoid/infectious mononucleosis
39
Q

Hyperkalaemia - treatment

A

Back into cells
- Salbutamol, insulin and dextrose, sodium bicarbonate(if acidotic)

Stabilisation
- Calcium gluconate

Removal

  • If passing urine, pee it out, iv fluids and diuretics
  • Dialysis
40
Q

Acid-base regulation

A

Body pH maintained 7.35-7.45

  • Essential for functioning of proteins, enzymes etc
  • Large net acid production - 1 mmol H+/kg
41
Q

What regulates co2 tension

A

Resp system

42
Q

What regulates HCO3 tension

A

Kidneys

43
Q

Major sites of hCO3 recovery and H+ excretion

A
  • Proximal tubule NaHCO3 reabsorption

- Secretion of H+ in the alpha intercalated cell of the cortical collecting duct

44
Q

Sodium bicarbonate in severe metabolic acidaemia

A
  • Depends on underlying cause
  • Generally safe to give isotonic NaHCO3 1.26%
  • If pH<7.2, adverse effects of acidaemia may manifest
  • Removing stimulus to production of lactate/ketones will allow oxidative mechanisms to metabolise excess anion
  • Diarrhoea and ingestions: NaHCO3 may be of use if acidaemia severe, and adverse effects are present
  • Exogenous Na load can exacerbate fluid overload and HTN
45
Q

What might metabolic alkalosis be due to

A

Excess alkali - kidney responds rapidly to this, so is usually transient

  • K+ depletion
  • Cl- depletion
46
Q

Calcium

A
  • Serum calcium tightly controlled levels 2.2-2.6mmol/l
  • Absorbed by the gut
  • Excreted in the urine/reabsorbed in the loop of henle and distal tubule
  • Released by bone
  • Controlled by PTH
47
Q

Phosphate

A
  • 0.85 to 1.6mmol/l
  • Excreted by the kidneys
  • Rises in renal failure/less nephrons less excretion
48
Q

What are phosphate levels a good indicator of

A
  • Malnutrition
49
Q

What are high phosphate levels associated with

A
  • Itchy skin
  • Extraosseal calcification
  • Soft tissues and arteries
50
Q

Vitamin D and Ca and Phosphate

A
  • Vitamin D3 from diet and skin –> liver–> 25-0H-D3 –> Kidneys –> 1,25-(OH)2-D3 –> Bone mineralisation, decrease in PTH, increase in Ca/P Gut
51
Q

AKI

A
  • Normal Na
  • High K
  • low bicarb
  • low pH
  • high urea
  • high creatinine
  • oliguria
  • +/- fluid overload
  • normal calcium, phosphate, PTH levels
52
Q

What happens in ESRF

A

Hyperkalaemic and acidotic

  • Treatment restrict K containing foods
  • Sodium bicarbonate tablets

Lack of vitamin D

  • Low calcium
  • Treatment activated vitamin D tablets

Hyperphosphataemia

  • Lack of phosphate excretion from the kidney
  • Extraossial calcification
  • Diet and phosphate binding tablets

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