Endocrinology Flashcards
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
What investigations are needed in Hyperkalaemia?
U+Es
VBG/ABG - show acidosis
ECG - if K+ >6:
K+ >6.0: tented T, prolonged PR.
K+ >6.5: flattened or absent P, wide QRS, bradycardia, ST elevation.
K+ >8.0: even wider QRS, sine wave, VT.
Other tests:
FBC
Ca2+ and CK in suspected rhabdomyolysis.
Glucose if diabetic
Digoxin levels if taking
How should hyperkalaemia be managed? ( mild, moderate , severe)
Consider and treat underlying cause:
Stop drugs: ACEi, K+-sparing diuretics, NSAIDs.
Mild (≥5.5 mmol/L) or moderate (≥6) and normal ECG:
Reduce dietary intake.
If moderate, consider insulin IV + glucose IV ± salbutamol nebs.
GI cation exchangers remove K+ from the body by binding it in GI tract: Calcium Resonium (calcium polystyrene sulfonate), Kayexalate (sodium polystyrene sulfonate), patiromer.
Severe (≥6.5 mmol/L) or ECG changes is an emergency. Monitor ECG, K+, and glucose, and treat with CIGAR:
C- Calcium gluconate IV or calcium chloride IV, to stabilise cardiac membrane - given via central line to reduce risk of irritation / tissue necrosis peripherallty
I - Insulin IV
G - Glucose IV, to shift K+ into cells
A- Airway dilators - salbutamol nebulised - adjunct therapy
R - remove K+ from body
furosemide or – if severe renal impairment – dialysis
What is hypercalcaemia? What values are associated with this
Hypercalcaemia - condition in which the serum calcium levels in the blood are raised to higher than normal levels
Serum calcium levels above 2.5mmol are diagnostic
A serum calcium level of over 3.5 mmol/L requires immediate therapy.
What are the signs/ symptoms of hypercalcaemia?
Bones - bone related complications e.g. osteitis fibrosis cystica, which results in pains and pathological fractures, osteoporosis, osteomalacia, osteoarthritis
Stones - renal stones, nephrocalcinosis,ectopic calcification ( elsewhere e.g. cornea), polyuria, polydipsia ( diabetes insipidus)
Groans - abdominal pain, vomiting, constipation, anorexia
Psychic moans - depression, memory loss, psychosis, ataxia, delirium & coma
What are the causes of hypercalcaemia? (8)
Primary hyperparathyroidism - excessive secretion of PTH via parathyroid gland
increases serum calcium ( increases osteoclastic activity, enhances calcium resorption in nephron, activates vitamin D to increase GI uptake of calcium)
Malignancy - most common
Usually due to increased osteoclastic activity ( bone metastases)- common primary cancers include: breast, kidney, lung, thyroid, prostate, ovary & colon
Humoral hypercalcaemia of cancer - some cancers are secretory and can produce a PTH related peptide that bind to PTH receptors and stimulate the kidneys and bones like PTH
Myeloma
Familial Hypocalciuric Hypercalcaemia (FHH)
-caused by genetic defect in calcium sensing receptors
- differentiated from primary hyperparathyroidism via low urine Ca2+:Cr ratio
Other rarer causes:
- Granulomatous disorders - sarcoidosis, tuberculosis, leprosy
- Vitamin D intoxication - associated with lymphomas
-Thyrotoxicosis - HIV
- Lithium - iatrogenic
What investigations are needed for hypercalcaemia?
Serum Ca2+ levels
PTH levels
Myeloma screen ( if PTH levels are low- urine & serum electrophoresis)
CTAP - find malignancy
LFTs - Alk Phos - raised in cancer & hyperparathyroidism
ECG - prolonged PR, widened QRS, shortened QT
How is hypercalcaemia managed? Acute vs Chronic
Acute hypercalcaemia (symptomatic or ≥3.5 mmol/L):
Normal saline IV, 4-6 L in 24 hrs, to dilute Ca2+
Consider loop diuretic only if fluid overload develops
Bisphosphonate IV (zoledronic acid ideally, otherwise pamidronate) if rehydration fails
Long term treatment depends on cause:
Primary hyperparathyroidism:
many cases can be managed conservatively
Consider surgical excision if Ca2+ ≥2.85 mmol/L, end organ damage (bones or kidney – screen using DEXA and renal US), or severely symptomatic
If surgery is contraindicated, consider cinacalcet, a calcimimetic which activates Ca2+-sensing receptor on PTH gland and lowers PTH levels
Prednisolone for ↑vitamin D or sarcoidosis
What is hypocalcaemia? What values are associated with it?
Hypocalcaemia describes when the serum concentration of calcium in the blood is too low.
Under 1.9 mmol/L
What are the signs and symptoms of mild and severe hypocalcaemia? (SPASMODIC)
Mild- cramps, perioral parasthesia
Severe - SPASMODIC - medical emergency
Spasms - Carpopedal spasm: tetany (involuntary contraction) of feet or hands, carpal spasm - Trousseau’s sign, occurs when inflating BP cuff, laryngospasm
Perioral Paresthesia
Anxious, irritable, irrational
Seizures
Muscle tone - increased in smooth muscles —> colic pain, wheeze & dysphagia
Orientation impaired - time, place, person- confused
Dermatitis ( atopic)
Impetigo herpetiformis ( rare and serious especially in pregnancy)
Chvostek’s sign - corner of mouth twitches when facial nerve is tapped over parotid
Cataracts & Cardiomyopathy - chronic cases
What are the causes of hypocalcaemia? (4)
Hypoparathyroidism - can lead to chronic tetany, deficient PTH hormone due to either autoimmune cause or accidental removal of parathyroid glands during a Thyroidectomy ( occurs in under 3% of cases)
Also caused by DiGeorge syndrome
Pseudohypoparathyroidism- target organ resistance to PTH, meaning calcium levels aren’t affected by PTH ( rare & genetic)
Low Vitamin D levels
- due to reduced sun exposure
- decreased dietary intake, coeliac, gastric bypass
- Liver or kidney failure
Hypomagnesaemia
- causes functional Hypoparathyroidism with normal / low PTH
- low magnesium - caused by: GI losses, alcohol & drugs (PPIs)
What investigations should be considered in hypocalcaemia ?
Bloods
- Serum Calcium
- PTH levels
- Phosphate levels
- Vitamin D levels
- U+Es - renal cause
- LFTs - Alk phos - osteomalacia
XR - osteomalacia
ECG - increased QT interval
How should hypocalcaemia be managed ( acute & chronic)?
1st line - Calcium replacement:
Mild - give calcium 5mmol/6h PO ,check daily plasma levels
Chronic: Ca2+ plus vitamin D PO e.g. Calcichew-D3 Forte once daily, if severe Vitamin D deficiency - give loading doses of cholecalciferol (20,000 IU/week for 7 weeks) followed by maintenance doses
Acute/symptomatic (paresthesia, tetany): 10 ml of 10% calcium gluconate IV in 10 minutes, followed by slow infusion. Monitor Ca2+ twice daily.
If due to Hypoparathyroidism - 1-alfacalcidol or calcitriol
- 0.25 mcg/day - lower calcium levels to prevent nephrocalcinosis
Hypomagnesaemia - stop precipitating drugs, IV MgSO4 24mmol/ 24hrs
What is hyperparathyroidism? How many types are there?
Hyperparathyroidism occurs when one or more parathyroid glands become overactive, leading to elevated serum levels of parathyroid hormone, leading to hypercalcaemia.
There are 3 types:
Primary
Secondary
Tertiary
