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MSC: Disease of major orgns > Potassium > Flashcards

Potassium Flashcards

1
Q

What are the reference ranges for potassium?

A

Ref range 3.5 – 5.3 mmol/L (serum)

  • Maintained within narrow limits
  • Plasma may be slightly lower
  • RCPath Guidance urgent communication if < 2.5mmol/L or >6.5mmol/L
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2
Q

Why is membrane potential important?

A

Membrane potential is vital for many functions

  • Propagation of action potentials – nerve, muscle , cardiac
  • Hormone secretion
  • Acid-base Etc.
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3
Q

What causes potassium to shift into cells?

A
  • Insulin
  • Beta Agonists
  • Alkalosis
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4
Q

What causes potassium shift out of cells?

A
  • Cell lysis
  • Exercise
  • Hypertonicity
  • Alpha Agonists
  • Acidosis
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5
Q

Which organs are involved in potassium control?

A

Renal

  • Extracellular K+ balance occurs mainly in the kidney
  • Predominant control is in the distal tubule ( up to 95% reabsorbed by DCT)

Extrarenal Control

  • GI
  • Sweat
  • Skin
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6
Q

How does renal control of the kidneys occur?

A
  • Hypokalaemia leads to reduced renal excretion
  • Acidosis (preferential excretion of H+)
  • Aldosterone porduction is stimulated high K+ which leads to excretion of potassium
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7
Q

What are lab investigations when there s abnormal potassium?

A

Sodium • Urea & Creatinine • Magnesium • Calcium & Phosphate • Glucose • Bicarbonate • Blood Gases • Urine Potassium

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8
Q

What are signs and symptoms of hypokalemia?

A
  • Cardiovascular: ECG changes, Arrhythmias, Myocardial necrosis (extreme)
  • Neuromuscular: Weakness, pain, tenderness, cramps, rhabdomyolysis
  • Neuropsychiatric: Lethargy, apathy, depression, confusion
  • Renal: Polyuria, sodium retention
  • Gastrointestinal: Constipation, decreased gastric acid secretion
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9
Q

What are ECG changes for hypokalemia?

A
  • Depressed ST
  • Inverted T waves
  • Prominent U waves
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10
Q

How is hypokalaemia managed?

A

Oral / IV (Remember 40 mmol/day will only replace obligatory losses)

  • >2.5 mmol/L - Oral replacement (max 80 mmol/day)
  • <2.5 mmol/L - IV K+ in normal saline

Replace slowly never with a bolus. Plan 48 hr/72 hr replacement.

Check K+ regularly

Higher rates may be given in an ITU setting with cardiac monitoring

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11
Q

What are fluid compartments within the body?

A

Intracellular Fluid (ICF) – 60-70%

Extracellular Fluid (ECF) – 30 – 40%

  • Intravascular space (plasma volume ~7%)
  • Interstitial space (lymph)
  • Transcellular fluid (pleural, pericardal, CSF, gastrointestinal)
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12
Q

What is involved in the sodium potassium pump?

A
  • 3 Sodiums are transported out of the cells and 2 Potassium is transported into the cells
  • Uses ATP
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13
Q

What are obligatory losses of Potassium?

A

Obligatory Losses

  • Renal = 10-20mmol/24h
  • Extra renal = 20 mmol/24h
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14
Q

Describe RAAS

A

RAAS

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15
Q

What are categories for causes of Hypokalaemia?

A
  • Redistribution
  • True Deficits
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16
Q

What are resdistribution causes of hypokalemia?

A

In vitro (spurious)

  • Uptake by WBC
  • Heat

In vivo

  • Alkalosis (cause / effect)
  • Insulin – i.e. post infusion
  • Beta adrenergic agonists – salbutamol
  • Chemicals – toluene
  • Hypokalaemic periodic paralysis
17
Q

What are some true deficit causes of Hypokalaemia? (extrarenal)

A

Normal Acid:Base

  • Poor intake
  • Depletion
  • Anorexia
  • Sweating
  • Cisplatin
  • Cell synthesis
  • Aminoglycosides
  • Laxative abuse

Metabolic Acidosis

  • Diarrhoea
  • Fistula
  • Villous Adenoma
18
Q

What are some true deficit causes of Hypokalaemia? (renal)

A

Metabolic Acidosis

  • Renal tubular acidosis (T1 & T2)
  • Acetazolamide (Carbonic anhydrase inhibitor) induced RTA
  • Urinary tract diversion
  • DKA

Variable Acid:Base

  • Hypomagnasaemia
  • Antibiotics
  • Amphotericin B tox
  • Diuretic phase of ARF
  • Leukaemia

Metabolic Alkalosis

  • Diuretics
  • Severe K+ depletion
  • Bartter Syndrome
  • Gitelman syndrome
  • Liddle Syndrome
  • Vomiting/gastric drainage
  • Chloride loosing diarrhoea
  • Cushing syndrome
  • Exogenous mineralcorticoids
  • Conn’s Syndrome
  • Renovascular hypertension
  • Malignant hypertension
  • Renin-secreting tumour
19
Q

What is Bartter’s syndrome?

A
  • Hyper-reninaemic hyper-aldosteronism
  • Usually presents in childhood
  • Mutations of genes encoding proteins that transport ions across renal cells in the thick ascending limb of the nephron
20
Q

What is Gitelman’s Syndrome?

A
  • Hypochloremic metabolic alkalosis, hypokalaemia and hypocalciuria.
  • Hypomagnasaemia is present in many but not all cases
  • Inactivating mutations in the SLC12A3 gene resulting in a loss of function of the encoded thiazide-sensitive sodium-chloride co-transporter (NCCT). This cell membrane protein participates in the control of ion homeostasis at the distal convoluted tubule portion of the nephron.
21
Q

What is involved in attacks of Familial hypokalaemic periodic paralysis (FHPP) and Hypokalaemic periodic paralysis with thyrotoxicosis (HPP)?

A
  • Attack involve flaccid paralysis on limbs & trunk which can last for up to 24 hrs
  • Attacks can be provoked by exercise, high CHO diet, hypothermia, high sodium intake
  • Cardiac arrhythmias may also be present
  • Caused by mutation in the skeletal muscle voltage-gated calcium channel α-1 subunit
22
Q

What are difference between HPP and FHPP?

A

FHPP

  • AD, Caucasian, M:F 3:1

HPP

  • Chinese or Japanese population, M:F 20:1
  • Clinical presentation identical to FHPP but condition remits when patient becomes euthyroid
23
Q

What are reference ranges for Hyperkalaemia?

A
  • Mild (5.5 - 5.9 mmol/L)
  • Moderate (6.0 - 6.4 mmol/L)
  • Severe (≥6.5 mmol/L)
24
Q

What are signs and symptoms of Hyperkalaemia?

A

Neuromuscular

  • Parasthesia weakness
  • Paralysis

Renal

  • Natriuresis
  • Decreased reabsorption of HCO3
25
Q

What are ECG changes in Hyperkalaemia?

A

Cardiovascular

  • Tall T waves
  • Prolonged PR interval
  • Flat P waves
  • Widening of QRS complex
  • VF
  • Asystole
26
Q

What are causes of Hyperkalaemia?

A
  • Redistribution (Acidosis, Insulin deficiency with high glucose (DKA), Drugs (beta-blockers), Acute tissue damag, Hypoxia, Tumour lysis, Hyperkalaemic periodic paralysis)
  • Increased Intake (supplement, Herbal medicines, IV Fluids
  • Decreased Output (chronic renal failure, obstructive nephropathy, renal transplant, drugs, syndromes of hypoaldosteronism)
  • Syndromes of Hypoaldosteronism
  • Pseudohyperkalaemia (EDTA contamination, IV contamination, In vitro redistribution, haemolysis, cold, delayed centrifugation, release from WBC & platelets, Fragile cell syndrome)
27
Q

Which drugs can induce hyperkalaemia?

A

Reduce aldosterone secretion

  • ACE inhibitors,
  • Angiotensin II receptor blockers
  • NSAIDS, heparin
  • Antifungals (ketaconazole, flucanazole)
  • Cyclosporin, tacrolimus

Alter transmembrane K+ movement

  • Beta blockers
  • Digoxin
  • Hyperosmolar solutions (mannitol, glucose & saline)
  • Suxamethonium

Inhibit activity of epithelial sodium channel

  • Potassium sparing diuretics (amiloride, tramterene)
  • Trimethoprim
  • Pentamidine

Block aldosterone binding to mineralocorticoid receptor

  • Spironolactone
  • Eplerenone
  • Drospirenone
28
Q

What is Hyperkalaemic Periodic Paralysis (HYPP)?

A
  • Rare AD condition. Presents with muscle weakness and K+ up to 8.0 mmol/L
  • Attacks variable, provoked by high K+ intake, glucocorticoids, hypothermia & recovery after exercise
  • ECG show tall T waves but cardiac arrhythmias are rare
  • Mutations in skeletal muscle voltage-gated sodium channel X subunit (SCN4A)
  • Management salbutamol inhalers
29
Q

What are laboratory investigations for Hyperkalaemia?

A
  • Exclude spurious causes: Time / Date / Storage / WCC/ Plt /Ca/EDTA contamination
  • Assess eGFR
  • Assess acid-base status & glucose
  • Check drug therapy
  • Consider cortisol
  • Check renin & aldosterone: Caution – high K+ stimulates aldosterone but suppresses renin. As eGFR falls – aldo increases & renin decreases
30
Q

How is Hyperkalaemia managed?

A
  • If plasma K>6.0mmol/l then check for EDTA contamination to ensure it is not an artefact.
  • Ask for ECG to be done urgently in such patients.
  • Calcium gluconate or chloride (i.e 10ml of 10% over 10mins may rpt until ECG improves) is used to stabilise the myocardium – ECG changes
  • Salbutamol (10-20mg) is used for redistribution into cells – adjuvant severe & moderate. Insulin + Glucose – (10 units insulin in 25g glucose)If potassium remains high a continuous infusion of insulin and glucose may be required.
  • Excretion is increased with Dialysis or Calcium resonium.
  • Reduction in potassium load through medication review. Stop K+ supplement, ACE-i and K+ sparing diuretics
31
Q

How is Excretion of potassium controlled?

A

Haemodialysis may be required in:

  • Persistent hyperkalemia (>7mmol/l)
  • Severe or worsening metabolic acidosis (pH <7.2)
  • Uraemic pericarditis, encephalopathy, refractory pulmonary oedema.

Calcium resonium (mild/moderate)

  • 15g four times daily or 30g enema in 100ml may be given in asymptomatic hyperkalemia. This takes a few days to take effect.

MSC: Disease of major orgns (23 decks)

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