Endocrinology Flashcards
(94 cards)
What is hypernatraemia ? What are the diagnostic values?
Electrolyte imbalance resulting in high plasma serum sodium levels
- defined as a concentration of above 145 mmol/L - normal range is 135-145 mmol/L
- Severe - anything above 152 mmol/L
What are the causes of hypernatraemia?
Always associated with serum Hyperosmolarity
1) Free water losses - most common
- osmotic diuresis - renal failure, poor diabetic control, loop diuretics, diabetes insipidus
- GI losses - d&v
- Diaphoresis - exercise, fever, heat exposure
- peritoneal dialysis
2) Inadequate free water intake
- inability to drink water/ access water ( older patients with dementia)
- impaired thirst mechanism
3) Sodium overload
- mineralocorticoid excess - e.g. Cushings, primary aldosterone’s m
- deliberate intake of large amounts of salt ( bleach ingestion)
How do patients with hypernatraemia present?
Usually associated with Hypovolaemia ( dehydration)
Muscle weakness.
Restlessness.
Extreme thirst.
Confusion.
Lethargy.
Irritability.
Seizures.
Unconsciousness.
What investigations should be considered in hypernatraemia?
U+Es
Serum osmolality - compare to urine, check in case of Diabetes Insipidus
Urine osmolality - compare to serum, check in case of Diabetes Insipidus
Urine flow rate
Urine electrolytes
How can we compare urine and serum osmolality to determine the cause of the hypernatraemia?
What is the treatment for hypernatraemia?
1) IV fluids
2) treat underlying cause e.g. treat diarrhoea etc., remove causative medications
3) monitor & remeasure sodium regularly
If central diabetes insipidus - desmopressin
If Nephrogenic diabetes insipidus - thiazide diuretic
What is Hyponatraemia? What are the values associated with this?
Hyponatraemia is defined as a serum sodium concentration of less than 135 mmol/L.
Normal serum sodium concentration is in the range of 135-145 mmol/L.
It is a disorder of water balance reflected by an excess of total body water relative to electrolytes leading to low plasma osmolality (i.e. less than 275 mmol/kg)
It does not always mean there has been Na+ depletion, there may be dilutional Hyponatraemia ( i.e. appears to be low sodium levels due to high water levels)
What are the causes of Hyponatraemia?
3 types:
1) Hypovolaemic Hyponatraemia - water and Na+ loss, disproportionally more Na+ loss > Water
2 types:
A) urinary sodium concentration is less than 20mmol, ergo water and sodium is lost elsewhere not via kidneys
- GI fluid load ( severe diarrhoea & vomiting)
- Third spacing of fluids - too much fluid moves from intravascular space to interstitial space, e.g. pancreatitis, severe hypoalbuminaemia
- Burns
- Trauma
- CF
B) urinary sodium concentration is greater than 20 mmol, ergo water and Na+is lost via kidneys
- Addisons
- Renal failure
- Diuretic excess
- Osmolar diuresis ( increased glucose & urea)
2) Hypervolaemic Hyponatraemia - usually oedematous
- Nephrotic syndrome
- Cardiac failure
- Cirrhosis
- Renal failure
3) Euvolemic Hyponatraemia - aka dilutional, total body Na+ & ECF volume are normal, but TBW is increased
- water overload - psychogenic polydipsia, addisons, severe hypothyroidism - dilute urine
- SIADH - concentrated urine
How does Hyponatraemia present?
Mostly asymptomatic
- if below 120mmol/L - can present with headache, lethargy & nausea
- severe - neurological ( seizures/confusion—>coma), GI symptoms
Signs of fluid depletion - Hypovolaemic hyponatraemia E.g
Low urine output
Weight loss
Orthostatic hypotension
Decreased jugular venous pressure
Poor skin turgor
Dry mucous membranes
Absence of axillary sweat
Absence of oedema.
Signs of fluid retention - Hypervolaemic Hyponatraemia
E.g.
Oedema and/or ascites
Rales or crackles on lung auscultation
Significant weight gain
Raised jugular venous pressure.
What investigations should be ordered when considering Hyponatraemia?
1) Serum sodium concentration - below 135 mmol/l is diagnostic
2) U+Es - may show Renal cause
3) Serum osmolality - hyper or hypovolemic
4) Urine sodium concentration - Hypovolaemia vs euvolaemia
5)Urine osmolality
How is acute hyponatraemia managed?
Severe symptoms (coma/seizures), SALTY:
1 HDU/ICU transfer and 3% SAline 1-2 ml/kg/hr.
2 Loop diuretic (furosemide) if not hypovolaemic.
3 Re-check Na+ every 2 hours. Aim to increase Na+ by 0.5 mmol/L/hr, up to Ten mmol/L/24hr, until 125 mmol/L or clinically well.
4 Y is it happening? Investigate cause once stabilised.
Beware rapid Na+ replacement as there is a risk of osmotic demyelination syndrome (aka central pontine myelinolysis), which can present at 2-5 days with:
◦ Altered mental status: confusion, fatigue, coma.
◦ Motor impairment: pseudobulbar palsy, quadriplegia.
What are the potential complications of rapid correction of hyponatraemia?
Central pontine myelinolysis - rapid rise in Na+ concentration causes water to move out of brain cells —> raised ICP —> Brain damage / bleeds
Osmotic demyelination - destruction of myelin sheaths of brainstem can lead to locked in syndrome - same as CPM
- Altered mental state, confusion, fatigue, coma
Motor impairment - quadriplegia & psuedobulbar palsy
What is hypokalaemia? What values are associated with this?
Low serum potassium, classified as mild (<3.5 mmol/L), moderate (<3 mmol/L), or severe (<2.5 mmol/L).
Main pathological effect is muscle weakness
How does hypokalaemia present? (Signs & symptoms)
Cardiovascular symptoms:
May be asymptomatic but have ECG changes.
Arrhythmia: palpitations, light-headed.
Neuromuscular:
Confusion and lethargy.
General muscular symptoms: weakness, ↓reflexes, ↓tone, tetany, cramps, myalgia, rhabdomyolysis.
Organ-specific: shallow breathing and respiratory failure, constipation/ileus, polyuria.
Other:
Metabolic alkalosis.
Interstitial nephritis.
↓Insulin secretion.
Carbohydrate intolerance.
↓Growth.
What is the pathophysiology of hypokalaemia? ( 4 types)
GI:
Loss of K+ : diarrhoea, vomiting (inc. gastroenteritis, eating disorders, pyloric stenosis), fistula.
Decreased intake
Kidney:
Diuretics: thiazide, loop.
Metabolic alkalosis
DKA: hyperosmolarity and ↓insulin → K+ leaves cells → lost in urine. Overall body deficit though serum levels may remain high.
Movement of K+ from ECF→ICF:
Insulin
β-2 agonists
Alkalosis
Hypokalemic periodic paralysis: congenital, periodic, 72 hr long ↓K+
Other causes:
↑Mineralocorticoids: Conn’s, Cushing’s
↓Mg2+, which can be due to alcoholism
Tubular disease
What is the pathophysiology of hypokalaemia? What effects does this have on the body?
↓K+ in the serum (extracellular fluid, ECF) which leads to ↑chemical gradient with intracellular fluid (ICF), causing K+ to enter the cells
Increased K+ leakage from ICF → hyperpolarisation of myocyte membrane (inc. cardiac) → ↓muscle excitability.
Other effects:
↓GFR
↑NH4+ production.
↑HCO3- reabsorption.
↓Insulin secretion.
Worsens digoxin toxicity.
What investigations are needed in hypokalaemia?
ECG
Bloods:
U&E, plus Mg2+, Ca2+, and PO43-
↓Na+ suggests thiazides as a cause
Glucose
ABG
Consider urine tests:
Urine K+ to distinguish between renal and non-renal losses.
Urine osmolality to interpret K+ level.
What changes can be seen on an ECG with hypokalaemia?
P widening
T flattening or inversion
ST depression
Prominent U, especially V4-6.
QT may appear prolonged, but this is due to flattened T merging into U (long QU).
If severe: SVT, VT, VF, Torsades de Pointes (i.e. long QU is as dangerous as long QT).
How is hypokalaemia managed?
K+ replacement:
K+ <3.5: no treatment, or consider K+ Per orally (e.g. Sando-K).
K+ ≤3.0: K+ Per orally
K+ ≤2.5 or severe symptoms: K+ IV. Give slowly – less than 10 mmol/hr – and don’t give if oliguric.
Peripheral administration must be diluted – e.g. 40 mmol in 1 L – while central administration doesn’t need to be – e.g. 40 mmol in 40 ml.
Other considerations:
Replace Mg 2+ if also low
What are the complications of hypokalaemia?
Arrythmias —> MI
Periodic paralysis
Respiratory failure
Gastroparesis
What is Hyperkalaemia? What values are associated with it?
Hyperkalaemia is defined as an elevated serum potassium, greater than 5.5 mmol/l
Moderate: K+ ≥6.0 mmol/L.
Severe: K+ ≥6.5 mmol/L
What is the pathophysiology of Hyperkalaemia?
Increase in K+ in the serum (extracellular fluid, ECF) leads to ↓chemical gradient with intracellular fluid (ICF)
↓K+ leakage from ICF → increased myocyte membrane depolarisation (inc. cardiac) → ↑excitability initially → later cells unable to repolarise fully so ↓excitability
Other physiological effects: ↓NH4+ production, ↑insulin secretion.
How do patients with hyperkalaemia present?
CV:
May be asymptomatic but have ECG changes.
Arrhythmias: altered HR, palpitations, light-headed.
Neurological:
Parasthesia
Flaccid weakness.
↓Reflexes
What causes hyperkalaemia? (3 types)
Decreased excretion of K+:
Kidney failure – AKI or CKD – and its causes e.g. hypovolaemia, sepsis
Drugs: spironolactone, amiloride, ACEi, A2RB, NSAIDs.
Addison’s
Metabolic acidosis
Movement of K+ from ICF→ECF:
Acidosis
Tissue damage: rhabdomyolysis (e.g. from trauma, intense exercise), tumour lysis syndrome
Drugs: digoxin, mannitol, suxamethonium, β-blockers
↑Intake of K+:
KCl (iatrogenic).
Salt substitutes
Large blood transfusions
