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55 > Electrolyte disorders > Flashcards

Electrolyte disorders Flashcards

1
Q

Ions in ICF and ECF

A
  • ICF: K, Mg, PO4, proteins
  • ECF: Na, Cl, HCO3
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2
Q

causes of dehydration and clinical presentation

A
  • cause: Insufficient oral intake, impaired renal concentrating mechanisms
  • pres: Excessive thirst, decreased skin turgor, elevated serum Na and osmolality
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3
Q

Causes and clinical presentation of hypovolemia

A
  • causes: External fluid losses (burns, hemorrhoage, diuresis)
  • pres: dizziness, decreased urine output, hypovolemic shock
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4
Q

fluid management strategies

A
  • Resuscitation: rapid & aggressive fluid replacement to maintain oral perfusion (more so for hypovolemia)
  • Replacement: replace volume loss in addition to maintenance
  • Maintenance: basal fluid requirements, prevent dehydration
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5
Q

symptoms of hyponatremia

A
  • Moderate: headache, lethargy, disorientation, restlessness
  • Severe: seizures, coma, respiratory arrest
  • Other (depends on etiology): dry mucous membranes, tachycardia, hypotension, reduced/increased urine output
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6
Q

cause of hypertonic hyponatremia

A
  • caused by hyperglycemia
  • treat hyperglycemia
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7
Q

cause of isotonic hyponatremia

A

caused by presence of markedly elevated serum lipids or proteins

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8
Q

types of hypotonic hyponatremia

A
  • hypervolemic: Excess of TBW and Na but excess TBW > excess Na
  • euvolemic: Excess of TBW but total body Na is normal
  • hypovolemic: Deficit of TBW and Na but deficit in Na > deficit in TBW
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9
Q

causes and treatment of euvolemic hypotonic hyponatremia

A
  • cause: syndrome of inappropriate ADH secretion (SIADH)
  • treatment: Fluid restriction, treat underlying cause, ADH receptor antagonist
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10
Q

Causes and treatment of hypervolemic hypotonic hyponatremia

A
  • cause: HF, liver cirrhosis, nephrotic syndrome
  • treatment: Na & fluid restriction, diuretics, treat underlying cause
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11
Q

causes and treatment of hypovolemic hypotonic hyponatremia

A
  • causes:
    • Renal losses e.g. diuretic use.
    • Extrarenal losses e.g. GI, skin & lungs
  • treatment: Isotonic &/or hypertonic fluids
  • need to correct both Na and TBW deficit -> hence use NS (0.9% NaCl)
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12
Q

causes of SIADH

A
  • Carcinomas in lung or pancreas
  • Pulmonary disorders e.g. pneumonias, tb
  • CNS disorders e.g. meningitis, shock, trauma, tumor
  • Medications -> stimulate the release of ADH from pituitary gland causing water retention and dilution of body’s Na stores.

meds can incl: (e.g. sulfonylureas, barbiturates, antipsychotics, tricyclic antidepressants, selective serotonin reuptake inhibitors, dopamine agonist)

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13
Q

General treatment for all the hyponatremia

A
  • Treat underlying cause
  • use hypertonic saline (3% NaCl) to inc tonicity
  • Acute: increase serum Na by 6-12mmol/L in 24h
  • Chronic: increase serum Na by 6-8mmol/L in 24h

  • Change in serum Na = (infusate Na – serum Na)/(TBW+1)
  • Too rapid correction -> central pontine myelinolysis (damage to regions of the brain) so rate is impt
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14
Q

causes and signs and symptoms for hypernatremia

A
  • S&S: mental slowing, confusion, hallucinations, intracranial bleeding, coma
  • Causes: dehydration, diabetics insipidus (decreased ADH secretion, opposite condition of SIADH), Na overload
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15
Q

treatment of hypernatremia

A
  • Free water deficit = TBW x ((current Na/desired Na)-1)
  • Administer hypotonic fluids
  • Desmopressin for diabetics insipidus
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16
Q

How is K homeostasis regulated externally

A
  • dietary intake,
  • renal excretion
  • ## extrarenal losses (GI, sweat)

o Renal excretion: K is freely filtered, mostly passively reabsorbed at PCT, secreted in DCT and CD. Regulated by aldosterone

17
Q

how is K homeostasis regulated internally

A
  • Internal: Na-K-ATPase and K+ leak channels.

Affected by:
- Insulin :stimulates Na-K-ATPase to drive K into cells
- Catecholamines
- acid-base disorders
- hyperosmolarity -> drags water out of cell
- exercise

  • in metabolic acidosis, there is high plasma H+ so exchange with K+ in cells to maintain electrical neutrality -> hyperkalemia.
  • In metabolic alkalosis, CO2 is removed via respiration so there will not be exchange of H+ and K+ -> no hypokalemia
18
Q

Etiology of hypokalemia

A
  • Insufficient dietary intake, excessive renal and GI losses e.g. diarrhoea and vomiting, drug-induced, hypomagnesemia
  • Shift of K+ into ICF
  • Aldosterone inhibit Na reabsorption, K secretion (Na, K exchanger)
  • diuretics inhibit upstream Na reabsorption –> reabsorb Na downstream and secrete K+
19
Q

CLinical presentation of hypokalemia

A

Mild: often asymptomatic.
Moderate-severe: cramp, weakness, malaise, myalgia
- Signs: can show as ST-segment depression in ECG (for severe), low serum K

20
Q

treatment of hypokalemia

by severity

A
  • Mild: Initiate pharmacologic therapies depending on S&S
  • Moderate: PO K supplement
  • Severe: IV K supplement, correct hypomagnesemia if present (can increase renal excretion of K+)
21
Q

dosage of oral KCl supplement

how much to take

A
  • PO:600mg SR tablets (8mmol) and 500mg/5ml solution (6.7mmol/5ml)
  • Mild-mod hypoK: 10-20mmol 2-4 times daily
    o Prevention: 20mmol daily
    o Total daily dose divided into 2-4 doses to avoid GI irritation
    o Starting dose is lower for renally impaired

o Prevention: 20mmol daily
o Total daily dose divided into 2-4 doses to avoid GI irritation
o Starting dose is lower for renally impaired

22
Q

dosage for IV KCl

how much to take

A
  • IV: 10mmol in 100ml of NS/water infusion via peripheral line. Avoid dilution in dextrose-containing solution.
  • For severe hypoK, pts who cannot tolerate oral therapy or exhibiting S&S
  • Monitoring of ECG, serum K and if any phlebitis and pain at site of infusion recommended
23
Q

etiology of hyperkalemia

A
  • increased K intake,
  • decreased renal excretion of K,
  • tubular unresponsiveness to aldosterone (sickle cell anemia, SLE, amyloidosis),
  • redistribution of K into ECF (metabolic acidosis, DM, CKD)

  • Falsely elevated serum K can occur due to extravascular hemolysis of RBC
24
Q

clinical presentation of hyperkalemia

A

heart palpitations, ECG ST elevation, serum K

25
Q

treatment of hyperkalemia flow of thinking

A
  1. if abnormal ecg –> calcium gluconate (if not then monitor)
  2. if hyperglycemia: give insulin, if not give insulin and glucose
  3. consider albuterol
  4. bicarbonate if acidic
  5. exchange resis/consider dialysis
  6. follow K every 2h until < 5mEq/L
26
Q

drugs that shift K into cells

A
  • insulin IV and dextrose (inc NA K ATPase activity, with dextrose to avoid hypoglycemia)
  • NaHCO3 IV (for metabolic acidosis, but can cause hyperna and overload)
  • Salbutamol IV / nebulisation (stimulate NaKATPase)
27
Q

Drugs that increase K elimination

A
  • Sodium polystyrene (SPS) (Resonium)
    • MOA: ion (Na and K) exchange resin in large intestine, PO/rectal, 4h prn
    • SE: Na load, intestinal necrosis
  • Sodium zirconium cyclosilicate (Lokelma)
    • Exchanges Na for K throughout entire GIT
    • Administered PO
    • Separated from other PO medications that exhibit pH-dependent solubility for at least 2h
    • SE: edema from Na exchange
28
Q

etiology of hypomagnesemia

A
  • GI: Reduced intake, reduced absorption (e.g. PPI when used in long run), increased loss (e.g. vomiting, diarrhoea)
  • Renal: primary tubular disorders, drug-induced (e.g. AGs, ampho B, diuretics, cyclosporin etc.), primary HPT, aldosteronism
29
Q

Magenesium supplement dosings

PO and IV

A
  • PO: for mild(Mg>0.5). Most common SE: diarrhoea
  • IV: for symptomatic (< 0.5). Often given as 2-4g in 50-100ml infused over 1h
  • Dose is reduced in renally impaired pts
30
Q

Etiology and treatment of hypermagnesemia

A
  • decreased renal excretion (e.g. AKI), excessive intake, others such as Lithium therapy
  • treatment: reduce Mg intake, increase elimination, calcium gluconate to reduce symptoms

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