Nephrology JC070: Electrolyte And Acid-base Disorders Flashcards

1
Q

Physiology of Kidney

A

Proximal tubule:
- Reabsorb ***NaCl, Glucose, a.a., fluids, HCO3
- Secrete drugs, poisons, H

LoH:
- Concentration gradient created for subsequent H2O reabsorption
- Thin Descending limb permeable to H2O only —> **H2O leave into interstitium by osmosis
- Thick Ascending limb permeable to NaCl only —> actively **
pump Na out —> create salty interstitium —> draw H2O from Descending limb + Collecting duct

Distal tubule:
- Fine tuning of electrolyte + acid-base
- some NaCl reabsorption
- ***K, H excretion

Collecting duct:
- **NaCl, **Urea, H2O reabsorption by concentration gradient created by LoH

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2
Q

Common acid-base + electrolyte problems

A

記: pH, Na, K

  1. Acidosis
    - Metabolic
    - Respiratory
  2. Alkalosis
    - Metabolic
    - Respiratory
  3. Na
    - Hypo
    - Hyper
  4. K
    - Hypo
    - Hyper
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3
Q

Definition of Acid-base disorders

A

Acidaemia: [H] > normal
Alkalaemia: [H] < normal

Acidosis: a process leading to ↑ in plasma [H]
Alkalosis: a process leading to ↓ in plasma [H]

Normal pH: **7.4 (7.35-7.45) ([H]: **40 nmol/L)
- lethal: pH <7.1 / >7.7

Compensation mechanisms:
- Lungs: **immediate
- Kidneys: take **
several days

When well compensated:
- no acidaemia / alkalaemia despite an underlying acidosis / alkalosis process

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4
Q

Compensatory mechanisms

A

Primary metabolic acidosis (↓ HCO3):
- stimulate respiratory centre —> ↓ pCO2 —> compensatory respiratory alkalosis

Primary metabolic alkalosis (↑ HCO3):
- suppress respiratory centre —> ↑ pCO2 —> compensatory respiratory acidosis

Primary respiratory acidosis (↑ pCO2):
- kidney compensate by conserving HCO3 —> ↑ HCO3 —> compensatory metabolic alkalosis

Primary respiratory alkalosis (↓ pCO2):
- kidney compensate by excreting HCO3 —> ↓ HCO3 —> compensatory metabolic acidosis

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5
Q

Metabolic acidosis

A

↓ HCO3 (***<22)
- normal [HCO3]: 22-28 mmol/L
- compensated with hyperventilation —> ↓ pCO2

Diagnosis:
1. Ensure this is Metabolic acidosis

  1. Determine Serum **Anion Gap (AG): high / normal
    - Anion gap = **
    Na - Cl - HCO3
  2. Normal Serum AG acidosis
    - determine Urine AG: [Urine Na + Urine K - Urine Cl] (advanced)
    - NaHCO3 infusion / Acid loading test: Proximal / Distal RTA (advanced)
  3. Look for any **Osmolar Gap (OG): Measured osmol - Calculated osmol
    - detect **
    unmeasured osmotically active substances (e.g. toxic alcohols)
  4. Any mixed acid/base disorder (ΔAG vs ΔHCO3)?
    - too advanced for MBBS
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6
Q

Osmolar gap

A

Osmol gap = Measured osmol - Calculated osmol

***Calculated osmol: 2xNa + Urea + Glucose (cation = anion, other cations ~ bounded Na)

↑ Osmol gap: presence of unmeasured ***osmotically active substances (e.g. alcohol-related compounds ingestion)

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7
Q

Anion Gap

A

Universal law: Charges must be balanced
- Total plasma cations = anions

Plasma cations: Na, K, Ca, Mg
- only Na is present in significant + may have great variations

Measured anions: Cl, HCO3

Measured cations - Measured anion = **Unmeasured anion (i.e. AG)
- Anion gap = **
Na - Cl - HCO3
- Normal anion gap: ~8-14

High AG acidosis vs Normal AG acidosis:
- similar Na levels
- both have ↓ HCO3
- **↑ Cl in normal AG acidosis
- **
↑ unmeasured anions in high AG acidosis

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8
Q

***High AG acidosis

A

↑ AG: ↑ unmeasured anion in blood

Causes:
1. **Ketoacidosis: DKA, Alcoholic ketoacidosis
2. **
Lactic acidosis
3. ***Renal failure (SO4, PO4, hippurate, others)
4. Ingestion of salicylate, formic acid (methanol), glycosylate (ethylene glycol)
5. Rhabdomyolysis (release of organic acids)
6. Altered AG in paraproteinaemia (e.g. ↓ in IgG gammopathy, ↑ in IgA gammopathy)

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9
Q

***Normal AG acidosis

A

↑ [Cl]

Causes:
1. Loss of HCO3, with **compensatory ↑ Cl (via **Anion exchanger Cl/HCO3)
- GI loss: **Diarrhoea
- Renal loss: **
Proximal RTA (Type 2: Fail to reabsorb HCO3), ***Carbonic anhydrase inhibitor

  1. Failure to excrete H
    - **Distal RTA (Type 1: Fail to excrete H, reabsorb K —> hypoK acidosis)
    - **
    Type 4 RTA
  2. Ingestion of excessive Cl
    - ***NH4Cl
  3. Increased reabsorption of Cl
    - Ureterosigmoidostomy
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10
Q

***L-Lactic acidosis

A

Overproduction of L-lactate —> ∵ **O2 deficiency (type A)
1. **
Circulatory problems (e.g. hypotension, shock)
2. **Respiratory problem —> hypoxia
3. **
Hb problem (e.g. CO poisoning)
4. ↑ Metabolic demand (e.g. grand mal seizure, severe exercise)

—> Rate of production can be up to 72 mmol/min with total hypoxia in type A (hypoxia)

Reduced metabolism of L-lactate **without hypoxaemia (type B)
1. **
Liver problem
2. **Alcoholism
3. Thiamine deficiency
4. **
Phenformin, Metformin

Diagnosis:
1. ***High AG metabolic acidosis
2. High plasma lactate level (normal <2)

Treatment:
1. Improve O2 delivery to tissue (most effective)
- correct hypotension, hypoxaemia

  1. NaHCO3 therapy ineffective unless lactate production controlled
    - buy time for life saving
    - Na load limits its massive use
  2. Haemodialysis with ***HCO3 dialysis
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11
Q

***General management of Metabolic acidosis

A
  1. Determine cause of acidosis + treat underlying cause:
    - some causes have independent threat to life e.g. methanol poisoning
    - there maybe specific treatment for certain causes e.g. methanol poisoning
  2. Correction of HCO3 by NaHCO3

Risk of NaHCO3 therapy
1. ***HypoK induction
—> shifting K into cells, esp. in patients with existing HypoK / loss of K with contracted ECF resulting normokalaemia (e.g. DKA)

  1. **Hypocalcaemia
    - esp. in CRF patients —> **
    tetany, seizure
  2. Volume expansion form ***Na load
    - 200 mmol NaHCO3 given —> 200 mmol Na given —> >1L of normal saline (156)
  3. ***Paradoxical cerebral acidosis
    - Too rapid correction —> too much HCO3 —> push equilibrium to make more CO2 —> diffuse into CSF from plasma (while HCO3 cannot diffuse through BBB) —> accumulation of CO2 in CSF —> ↑ H —> cerebral acidosis
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12
Q

How to use Urgent IV NaHCO3 replacement appropriately

A
  1. Estimation of HCO3 needed
    - HCO3 deficit = HCO3 deficit in litre x HCO3 space (= BW x 0.6)
    - usually only ***half the amount is given (BW x 0.3)
  2. Give half of dose initially, recheck afterwards
  3. Only replace [HCO3] to safe level acutely (pH ~7.1), then followed by slower correction / correction by other means
  4. Beware of ***fluid overload esp. in oliguric patients
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13
Q

Renal Tubular Acidosis

A

Normal AG acidosis with:
1. Hypo K
- Proximal RTA (type 2: ∵ loss of HCO3 (∵ ineffective reabsorption in proximal tubule))
- Distal RTA (type 1: ∵ failure of H excretion)
- Mixed (type 3)

  1. Hyper K
    - Type 4 RTA (aldosterone deficiency)
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14
Q

Proximal RTA (Type 2)

A

Normally HCO3 ***totally reabsorbed in proximal tubule if concentration below reabsorption threshold (~25 mmol/L)

Pathogenesis:
↓ HCO3 reabsorption threshold in proximal tubules
—> loss of HCO3 in urine —> low plasma HCO3
—> **normal AG metabolic acidosis with **compensatory HyperCl
- **alkaline urine despite acidosis, **urine pH usually >6

Effect:
1. **Loss of Na coupling with loss of HCO3
—> Hypovolaemia
—> **
Hyperaldosteronism
—> ***HypoK

  1. Associated with Hyperphosphaturia, Hypercitraturia (preventing nephrocalcinosis / stones), Hyperuricuria
  2. Hyperphosphaturia
    —> Rickets, Osteomalacia
  3. Fanconi syndrome
    - a pan-dysfunction of proximal tubules with **amino-aciduria, **glycosuria on top of RTA, hyperphosphataemia

Summary (↓ HCO3 reabsorption):
- Alkaline urine
- Na: ↓
- K: ↓ (hyperaldosteronism)
- HCO3: ↓
- Hyperphosphaturia —> Rickets, Osteomalacia
- Hypercitraturia
- Hyperuricuria
- Amino-aciduria, Glycosuria (Fanconi syndrome)

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15
Q

Distal RTA (Type 1)

A

Pathogenesis:
***Due to inability to excrete H:
1. Failure of pumping H against concentration gradient
- H/ATPase pump defect

  1. H back leak
    - ↑ H permeability

Effect:
1. ***Urine pH always >6 ∵ failure to maintain a steep plasma-urine H gradient

  1. ↓ H excretion
    —> ↑ K excretion for exchange of Na reabsorption in distal tubule
    —> ***HypoK
  2. Acidosis
    —> ↑ Ca reabsorption from bone + ↓ Tubular Ca, PO4 reabsorption
    —> Hypercalciuria, Nephrocalcinosis / stones

Summary (Inability to excrete H):
- Alkaline urine
- K: ↓ (↑ K excretion for exchange of Na reabsorption)
- Hypercalciuria, Nephrocalcinosis / stones

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16
Q

***Causes of Proximal + Distal RTA

A

Proximal RTA (type 2: HCO3 loss)
Hereditary
1. Cystinosis
2. Galactossaemia
3. ***Wilson’s disease
4. Lowe’s syndrome

Acquired
1. Dysparaproteinaemia
2. Toxins: Heavy metal poisoning
3. Drugs: **Carbonic anhydrase inhibitors
4. Renal disease: **
Amyloidosis, renal transplant rejection, Sjögren’s syndrome
5. HyperPTH, HyperCa

Distal RTA (type 1: Inability to excrete H)
Hereditary
1. **Primary hypercalciuria
2. Marfan syndrome
3. **
Ehlers-Danlos syndrome

Acquired
1. Autoimmune disease: **Sjogren’s, RA, SLE, PBC
2. Drugs: Amphotericin B, Lithium, Analgesic nephropathy
3. Renal disease: **
CRF, urinary tract obstruction, interstitial nephritis, medullary sponge disease
4. **Paraproteinaemia, hypergammaglobulinaemia
5. **
HyperPTH, hyperVit D

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17
Q

Diagnosis of RTA

A

Clinical suspicion when:
1. Normal AG acidosis with **HypoK
- hint: ↑ Cl with normal Na
2. Urine pH >5.5 (
*Alkaline urine) in presence of acidaemia

Confirmatory tests:
1. **Fractional excretion of HCO3 (FE HCO3): Proximal RTA
2. **
Acid loading test (NH4Cl): Distal RTA

18
Q

Fractional excretion of HCO3

A

Test whether there is excessive HCO3 loss in urine

FE HCO3 = (Urine [HCO3] / Plasma [HCO3]) ÷ (Urine [Cr] / Plasma [Cr])

Proximal RTA: **>15% (i.e. HCO3 loss)
- sensitivity ↑ after **
NaHCO3 infusion at 0.5-1.0 mmol/kg/hour to bring up plasma HCO3 level, urine pH >7.5

Distal RTA: normal (i.e. <5%)

19
Q

Acid loading test (NH4Cl)

A

Test whether urine can be acidified: i.e. whether a steep H gradient across plasma and urine can be maintained

***Oral NH4Cl 0.1g/kg to bring acidosis

Normal: urine pH <5.5
***Distal RTA: urine pH remains >6.0 (i.e. Inability to excrete H)
Proximal RTA: variable

20
Q

Type 4 RTA

A

Characterised by:
- Normal AG metabolic acidosis + ***HyperK (vs other RTA: HypoK)

Pathogenesis:
- ***Aldosterone deficiency / resistance

Aldosterone promotes distal K + H secretion, Na reabsorption
- Retention of K —> HyperK
- ↓ H excretion —> Acidosis (usually mild)
- Urine pH variable

Causes:
1. Drugs
- **ACEI, ARB
- **
K sparing diuretics (spironolactone, amiloride, triamterene)
- Cyclosporin A, Tacrolimus

  1. ***Hyporeninism
    - DM nephropathy
  2. ***Renal failure
  3. ***Mineralocorticoid deficiency
  4. Kidney transplant rejection - tubulitis
21
Q

Management of RTA

A

Type 1 and 2 RTA:
1. **Oral NaHCO3 to correct acidosis
- **
very high dose is required in proximal RTA ∵ loss of HCO3 in urine
- **K citrate is a better alternative for Distal RTA (citrate —> HCO3 by liver)
2. **
K supplement for HypoK
3. ***Steroid for Distal RTA due to Sjogren

Type 4 RTA:
1. Stop / ↓ inciting drugs
2. ***Loop diuretics + Low K diet for HyperK

22
Q

Metabolic alkalosis

A

Causes:
1. Loss of H
- GI loss: **vomiting, nasogastric drainage
- Renal loss
—> **
Diuretics (Loop, Thiazide), **HypoK
—> **
Mineralocorticoid excess: primary / secondary
—> Bartter’s / Gitelman’s syndrome

  1. Retention of HCO3
    - Intake of NaHCO3
    - Milk-alkali syndrome

Treatment:
1. If ECF contracted, **expand with saline —> HCO3 will ↓ with expansion
2. Correct HypoK
3. If ECF expanded, correct alkalosis with **
IV HCl / ***oral NH4Cl

23
Q

Na homeostasis

A

[Na] does **NOT reflect absolute content of Na in body but **amount of solvent: H2O
- primarily an ***extra-cellular cation

In the absence of Na loss / retention:
- HypoNa —> H2O retention
- HyperNa —> H2O depletion

Situation will be complicated when concomitant Na loss / retention

Na in kidney:
- ***67% reabsorbed in PCT
- 25% reabsorbed in Ascending LoH
- 5% reabsorbed in DCT
- 3% reabsorbed in Collecting duct

24
Q

Pseudohyponatraemia

A

↓ Serum [Na] but normal osmolality
- ∵ occupation of large amount of non-water (e.g. Fat, Paraprotein) in plasma
—> ↑ plasma volume while actual plasma water Na is normal
—> [Na] appears to be low

Causes:
1. **Hyperglycaemia
2. **
↑↑ TG
3. ***Paraproteinaemia
4. ↑↑ WCC

Clue:
- Check serum osmolality —> normal

Confirmation:
- Check plasma water [Na]

25
***Approach to HypoNa
睇3樣野: Serum osmolarity (判定係咪True HypoNa) —> Volume status + Urine Na (3x2表) 1. ***Serum Osmolarity - low —> true HypoNa 2. ***Volume status 3. Urine osmolarity (>100 = ADH is working, appropriate?) 4. ***Urine Na level (>20 = inappropriate i.e. SIADH) HypoNa —> Serum osmolarity (+ RFT, TFT, cortisol, Urine osmolarity, Urine Na) —> ↓ Serum osmolarity —> True hyponatraemia —> Volume status 1. Hypovolaemia (***Na depletion) —> ↓ Na intake —> Renal (Urine Na ↑) —> Extra-renal loss (Urine Na ↓) 2. Hypervolaemia (Dilutional) —> Urine Na ↓ + Urine osmolarity ↑ —> CHF, cirrhosis, nephrotic syndrome —> Urine osmolarity ↓ —> Primary polydipsia 3. Euvolaemia —> SIADH
26
Causes of SIADH
CL Lai: 記any CNS + respiratory diseases 1. CNS - ***Meningitis, Encephalitis, Brain abscess - ***Head trauma, SAH, CVA, ↑ ICP 2. Respiratory - ***CA lung - ***Chest infection - Positive pressure breathing 3. Drugs - ***SSRI - Ecstasy 4. ***Hypothyroidism
27
SIADH vs Addison's disease
SIADH: - Everything is low - Low K Addison's disease: - Normal / High K - High eosinophil count (∵ cortisol promote eosinophil migration into BM)
28
Treatment of SIADH (CL Lai)
1. Fluid restriction 2. Furosemide 20mg 3. Vaptan 4. IV Na (beware of central pontine myelinolysis)
29
HypoNa
S/S: - ***Non-specific (e.g. malaise, lethargy, headache) - ***Confusion, convulsion, coma - More serious with acute hypoNa Acute: - <48 hours - more serious symptoms, severe symptoms at [Na] <120 - less complications if corrected rapidly Chronic: - >72 hours - symptoms may not develop even [Na] <110 - ***more prone to CNS complications with rapid correction Management: - Rate of correction should be ***slow for chronic hypoNa (>2 days) —> <0.5 mmol/L/hr or <12 mmol/L/day - Too rapid correction —> ***Central pontine myelinolysis - Treat according to ECF volume status —> estimate amount of H2O + Na needed - ***Hypertonic saline should only be used in very experienced hands! - ***Demeclocycline / ***V2 antagonist can be considered in SIADH Clinical features of Central pontine myelinolysis (CL Lai): - Cranial nerve deficits - Quadriparesis
30
H2O + Na replacement in contracted ECF
1. Assess degree of volume depletion / excess - mildly dehydrated: loss of skin turgor: 5% BW loss - moderate: postural hypotension: 10% BW loss - severe: shock: 15% loss - mild edema: 5% in excess 2. ***Replace volume depletion with normal saline cautiously - initial 1/3 can be given in first 8 hours, reduce speed afterwards - monitor [Na] regularly
31
Approach to HyperNa
睇3樣野: Volume status —> Serum osmolarity, Urine osmolarity (Ratio) Serum osmolarity, Urine osmolarity, RFT, CaPO4, Plasma renin + aldosterone, 9am cortisol 1. Hypervolaemia (Salt gain) —> ***Primary hyperaldosteronism / ***Cushing’s syndrome / ***Acute salt loading 2. Isovolaemia / Hypovolaemia - Urine osmolarity >> Serum osmolarity (Serum osmolarity太低有問題) —> ***Extrarenal fluid loss (most common) - Urine osmolarity < Serum osmolarity (Urine osmolarity太低) —> Water deprivation test / DDAVP test —> No change in urine osmo —> ***Nephrogenic DI —> ↑ urine osmo —> ***Cranial DI
32
Management of HyperNa
In pure H2O loss —> calculate H2O deficit - Water deficit = TBW x ([Na]/140 - 1) Rate of volume replacement - 1/3 rule: —> 1/3 in first 8 hours —> 1/3 in second 16 hours —> 1/3 in third 24 hours - Rmb to replace any ongoing H2O loss Rate of [Na] correction - too rapid will lead to ***cerebral edema ∵ rapidly reduced plasma osmolality —> influx of H2O into cells - maximal ↓ of 12 mmol / 24 hours unless seriously symptomatic
33
K homeostasis
***Intracellular cation (diffuse slowly outwards, Na-K ATPase pumps K into cells) - Normal serum K 3.5-5 (intracellular: 150) - Highly influenced by ***acid-base status (acidosis —> K moves ***out of cells, vice versa) - Severe HypoK + HyperK are life-threatening electrolyte disturbances —> Cardiac arrhythmia
34
Approach to HypoK
Rule out intracellular K shift: - ***Insulin - ***Catecholamine - ***β2 agonist - ***Metabolic alkalosis - ***Hypokalaemic periodic paralysis HCO3 ↑ (***Metabolic alkalosis) - TTKG <3 (trans-tubular potassium gradient) (i.e. Extra-renal loss) —> ***Vomiting - TTKG >=3 (i.e. Renal loss) —> Normal BP —> ***Diuretics, ***Bartter’s syndrome, ***Gitelman’s syndrome - TTKG >=3 (i.e. Renal loss) —> ↑ BP —> ***Renal artery stenosis, ***Primary aldosteronism, ***Cushing’s syndrome, Liddle’s syndrome HCO3 ↓ (***Metabolic acidosis) —> Normal AG —> Urine AG -ve —> ***Diarrhoea, ***Proximal RTA —> Urine AG +ve —> ***Distal RTA
35
TTKG
Transtubular K gradient: - Attempt to over-ride interference from urinary concentration to determine urinary K loss TTKG: - Tubular [K] / Serum [K] or - (Urine [K] / Serum [K]) ÷ (Urine osmo / Serum osmo) (∵ Tubular [K] = Urine [K] x Serum osmo / Urine osmo) In presence of HypoK, TTKG >4: - high [K] in terminal cortical collecting duct (i.e. ***renal loss)
36
HypoK
Risk / Complications / Symptoms 1. ***Muscle weakness, paralysis (proximal muscle myopathy) 2. ***Cardiac arrhythmia, particularly when [K] <2.0 3. ECG changes (記) - Large U wave - ***Loss of T wave - ***Prolonged QT interval 4. ***Ileus, constipation 5. Rhabdomyolysis 6. Polyuria Management: 1. Oral replacement when mild 2. ***IV KCl - oral not possible e.g. vomiting - moderate to severe hypoK (e.g. <=2.5) - ***always rmb to dilute IV KCl in NS 3. Exact amount of K needed cannot be calculated ∵ - largely intracellular - discrepancy between ICF and ECF [K] - initial distribution in ECF only - 40 mmol K will ↑ [K] 1.5 mmol/L
37
Approach to HyperK
Exclude ***PseudohyperK (e.g. ***haemolysis) + ***Drugs (e.g. K supplement, NSAID, ***ACEI, ARB, ***K-sparing diuretics, salt substitute) 1. ***Renal failure 2. ***Hypoaldosteronism 3. Shift from cells
38
HyperK
S/S 1. ***Muscle weakness (usually when >8) 2. ***Cardiac arrhythmia - may occur when >6 - rate of ↑ of K important —> more tolerable with chronic HyperK - ECG changes (記) —> ***Peak T —> ***Widening of QRS —> ***Loss of P (—> prolonged PR intervals, sinusoidal)
39
Diagnosis of HyperK
1. History - Diet - ***Drug history 2. Repeat [K] if no apparent cause found (pseudohyperK? ***Haemolysis) 3. P/E: volume depleted? 4. ***Renal function test 5. TTKG <6 indicates inappropriate renal response to hyperK
40
Management of HyperK
Emergency? (Arrhythmia, ECG changes) 記: Resonium, IV insulin, NaHCO3, Loop diuretic 1. ***IV Calcium - effect within several mins - stabilise cardiac membrane —> protects heart (↑ threshold potential) but not ↓ [K] - may repeat injection 5 mins later if effect not seen 2. ***NaHCO3 infusion - shift K into cells - effect within 30 mins, last for several hours 3. ***IV insulin / dextrose - 10 units to 30g glucose (60ml D50) —> shift K into cells (self notes: Insulin stimulate Na/K-ATPase) - effect within 1 hour, but effect may last for only 5-6 hours 4. Urgent haemodialysis - most effective in removing K - but takes time to to set up Non-emergency: 1. ***Cation-exchange resin - Na/Ca resin - oral / enema - e.g. ***Resonium 2. ***Loop diuretics if not oliguric 3. Remove underlying cause - remove drugs - volume expansion for depletion 4. ***Correct metabolic acidosis (by NaHCO3) 5. Dialysis (for end stage renal disease / chronic renal failure, HD / PD) 6. Low K diet (Resonium (web): - Insoluble polymer cation-exchange resin - Exchange with H in stomach —> H exchange with K from intestinal cells 1. Resonium A (Na) - exchange H with Na 2. Resonium C (Ca) - exchange K with Ca)
41
Bartter syndrome, Gitelman's syndrome (Self notes)
Bartter syndrome: Defective NKCC (~Loop diuretic) Gitelman's syndrome: Defective NCCT (~Thiazide)