Hypokalaemia Flashcards

1
Q

Definition?

A

Hypokalemia (low serum potassium) is a common electrolyte disorder that is typically caused by potassium loss (e.g., due todiarrhea, vomiting, ordiureticmedication).

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2
Q

RF?

A
• Old age
• Low intake of Potassium
• Female
• Eating disorders
• Alcoholism
Bariatric surgery
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3
Q

ddx?

A

pseudohypokalaemia-poor sample
congenital-hypotension or mutations
metabolic acidosis-ketoacidosis, polyuria, increased thirst and vomiting
Cushing syndrome-pituitary adenoma on imaging, signs

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4
Q

Epidemiology?

A

Age: Older
Sex:
Ethnicity:
P: 1% general population

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5
Q

Aetiology?

A

GI loss
Renal loss
IC shift
insufficient intake

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6
Q

GI loss?

A
vomiting,
diarrhoea
adenoma
laxatives
bentonite
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7
Q

renal loss?

A
primary-
RTA T1/2
Cushings
renin-secreting tumours
Fanconi syndrome
Genetic disorders-CAH, Bartter, Gitelman, Liddle
Secondary-
diuretics
B2 agonists
glucocorticoids, catecholamines, ABs,
antifungals, theophylline
endocrine causes-high aldosterone, high cortisol
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8
Q

IC shift

A
alkalosis
insulin
hyposmolality
increased glycogenesis and SNS-SNS use, phaeochromocytoma, alcohol, MI, head trauma
familial periodic paralysis
thyrotoxicosis
hypothermia
intoxication
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9
Q

insufficient intake

A

older
alcohol abuse
eating disorders

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10
Q

CP?

A

Patients may be asymptomatic, particularly if the deficiency is mild. Symptoms usually occur if serum K+levels are< 3.0 mEq/Land/or decrease rapidly.[2]
• Cardiovascular manifestations
• Symptoms ofcardiac arrhythmias(e.g.,palpitations, irregularpulse,syncope)
• Hypotension
• Neuromuscular manifestations
• Muscle cramps and spasms[5]
• Muscle weakness, paralysis
• Respiratory failure secondary to paralysis of the respiratory muscles
• Rhabdomyolysis
• Decreaseddeep tendon reflexes
• Gastrointestinal manifestations
• Nausea, vomiting[5]
• Constipationorileus
• Fatigue
• Other manifestations
• Hyperglycemia[6]
• Polyuria[7]
• Symptoms of underlying causes, including:
○ Dehydrationingastroenteritis
○ Tachycardiaand tremors inalcohol withdrawal
○ Symptoms of thyrotoxicosis
Symptoms ofdigoxin toxicityin patients treated withdigoxin

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11
Q

Patho?

A
  • Too little potassium in blood
  • External balance shift-increased K excretion-less in blood
  • Internal balance shift-more in cells
    • Excess insulin-more glucose uptake-high pump-more K in cells
    • Alkalosis-H/K pump more-more k in and H out
    • Not affected in resp
    • B2 agonists and alpha-blockers-Na/K pump and Ca channels
  • External balance-low intake
  • Anorexia, fasting or specific diets
  • Aldosterone excess-Primary hyperaldosteronism-excess use of Na/K pump-more into tubule and urine
  • CHF, cirrhosis
  • Diuretics-loop and thiazide-inhibit sodium absorption upstream, increased absorption downstream-more K tubule as gradient bt principle cell and tubule
  • Vomiting and diarrhoea-more lost in faeces
  • Sweat-exercise
  • Less positive electrochemical gradient- hyperpolarised and so less reactive to stimuli
  • -constipation, weakness and cramps, resp depression, arrhythmias and arrest
  • Hypomagnesemia-less magnesium to bind to renal outer medullary K channels- More K + out into lumen
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12
Q

Investigations-first line?

A

Laboratory studies
• Electrolytes andkidneyfunction
• Serum K+levels
• Basic metabolic panel
• Serum calcium,magnesium,phosphate
• Blood gas (venous or arterial): may showmetabolic alkalosis
• Urinary potassium: Consider measuring to narrow down underlying etiology[9][10][11]
• Methods
○ Spot urine: rapid assessment, indicated in urgent cases, less reliable than24-hourcollections
○ 24-hoururinecollection: less practical, indicated for chronic cases and uncertain diagnoses, more accurate thanspot urine
• Findings
○ Renal loss:spot urine> 15–20 mEq/L(24 hourcollection> 15 mEq/L)[10][1]
○ Extrarenal loss:spot urine< 15–20 mEq/L(24 hourcollection< 15 mEq/L)[11]
Consider confirming abnormal serum potassium levels with a repeat blood draw.
ECG

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13
Q

ECG findings?

A
  • Mild to moderate hypokalemia
    • T-waveflatteningorinversion
    • ST depression
    • ProlongedPR interval
  • Moderate to severe hypokalemia
    • Presence ofU waves: small waveform following theT wavethat is often absent but becomes more pronounced in hypokalemia orbradycardia[2]
    • T andU wavefusion
    • QT prolongation[12]
  • Dysrhythmias
    • Premature atrial and ventricular complexes
    • Sinusbradycardia
    • Paroxysmalatrial orjunctional tachycardia
    • Ventricular dysrhythmias, e.g.,Torsades de pointes
    • PEA/asystole
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14
Q

Management?

A

• If mild:
• (>2.5mmol/L, no symptoms.) Give oral K+supplement (≥80mmol/24h, eg Sando-k® 2 tabs/8h). Review K+after 3 days. If taking a thiazide diuretic, and K+>3.0 consider repeating and/or K+-sparing diuretic.
• If severe:
• (<2.5mmol/L, and/or dangerous symptoms.) Giveivpotassium cautiously, not more than 20mmol/h, and not more concentrated than 40mmol/L. Do not give K+if oliguric.
Nevergive K+as a fast stat bolus dose.

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15
Q

Prognosis?

A
  • Can be life-threatening

* Need monitoring

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16
Q

Complications?

A

• Cardiac arrhythmias
• Paralysis
Rebound hyperkalaemia