Endocrinology Flashcards
Define diabetes mellitus
Chronic hyperglycaemia due to insulin dysfunction.
Types of diabetes mellitus
Type 1.
Type 2.
Clinical presentation of diabetes mellitus
Young: 2-6w history of thirst, polyuria and weight loss. Ketoacidosis if not picked up earlier (fruity breath).
Older: Similar, but over longer period.
Also lack of energy and eye problems (blurred vision).
Neuropathy, eventually (glove and stockings).
Diabetes mellitus - note
In practice, both types exist as a spectrum.
Pathophysiology of type 1 diabetes mellitus
Autoimmune destruction of the pancreatic beta cells.
Associated with HLA genetics, but triggered by 1+ environmental antigens.
Autoantibodies directed against insulin and islet cell antigens predate onset by several years.
Polyuria: Blood glucose exceeds renal tubular reabsorptive capacity (renal threshold) -> Osmotic diuresis
Weight loss: fluid depletion,
Insulin deficiency -> Muscle and fat breakdown.
Pathophysiology of type 2 diabetes mellitus
Polygenic.
Env factors (central obesity) trigger onset in genetically susceptible.
Beta cell mass reduced to 50% of normal.
Inappropriately low insulin secretion and peripheral insulin resistance.
Cause of type 1 diabetes mellitus
HLA-DR3/4 affected in >90%.
Autoimmune disease targeting islet cells.
Cause of type 2 diabetes mellitus
Genetic susceptibility, but no HLA link.
Epidemiology of type 1 diabetes mellitus
Onset younger (<30 years).
Usually lean.
More north European ancestry.
Epidemiology of type 2 diabetes mellitus
Onset older (>30 years).
Usually overweight.
More common in African/Asian.
More common in general.
Diagnostic test for diabetes mellitus
Fasting >7 (or random >11.1) plasma glucose (mmol/L).
HbA1c: 6.5% / 48mmol/mol.
C peptide goes down in type 1 but persists in type 2.
Treatments for type 1 diabetes mellitus
Glycaemic control through diet (low sugar, low fat, high starch)
and insulin (twice daily and with meals).
Exercise encouraged.
Treatments for type 2 diabetes mellitus
Diet and exercise changes.
If no change;
- > Biguanide (Metformin)
- >
- sulfonylurea (gliclazide) / DPP4I (sitagliptin)
- >
- insulin
Complications of diabetes mellitus
ketoacidosis/
nephropathy
/neuropathy (-> lack of sensation in feet -> occult foot ulcers)
/diabetic retinopathy,
Hyperosmolar hyperglycaemic nonketotic coma (mostly in type 2s).
Define Graves disease
Hyperthyroidism due to pathological stimulation of TSH receptor.
Define Hashimoto’s thyroiditis
Hypothyroidism due to aggressive destruction of thyroid cells.
How does Graves disease clinically present?
Rapid heart beat, tremor, diffuse palpable goiter with audible bruit.
Eye problems: bulging outwards and lid retraction.
How does Hashimoto’s thyroiditis clinically present?
Insidious onset.
Tiredness, lethargy, intolerance of cold, goitre, slowing of intellectual activity, constipation, deep hoarse voice.
Puffy face, hands and feet.
Pathophysiology of Graves disease
Thyroid stimulating immunoglobulins recognise and bind to the TSH receptor which stimulates T4 and T3
- > thyroxine (T4) receptors in the pituitary gland are activated by excess hormone
- > reduced release of TSH in a negative feedback look
- > Very high levels of circulating thyroid hormones, with a low TSH
Pathophysiology of Hashimoto’s thyroiditis
Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.
Antibodies bind and block TSH receptors
-> inadequate thyroid hormone production and secretion.
Cause of Graves disease
Unclear - some genetic element.
Autoimmune disease.
Associated with other autoimmune diseases, such as pernicious anaemia and myasthenia gravis
Cause of Hashimoto’s thyroiditis
Unknown. Autoimmune.
Some genetic element.
Triggers; iodine, infection, smoking and possibly stress
Epidemiology of Graves disease
Most common cause of hyperthyroidism.
Epidemiology of Hashimoto’s thyroiditis
More common in Japan
Diagnostic test for Graves disease
High T3+T4,
Lower TSH than normal.
Diagnostic test for Hashimoto’s thyroiditis
TSH levels, usually raised in hypothyroidism.
Thyroid antibodies.
Treatment for Graves disease
Antithyroid drugs (carbimazole or propylthiouracil) with either dose titration
or ‘block and replace’.
Thyroidectomy.
Radioactive iodine.
Treatment for Hashimoto’s thyroiditis
Thyroid hormone replacement (Levothyroxine).
Resection of obstructive goitre.
Complications of Graves disease
Thyroid storm: treat with propylthiouracil.
Complications of Hashimoto’s thyroiditis
Hyperlipidaemia and consequences.
Sequelae of Hashimoto’s thyroiditis
Hashimoto’s encephalopathy.
Define hypothyroidism
Reduced action of thyroid hormone.
Types of hypothyroidism
Primary
Secondary
Transient
How does hypothyroidism clinically present?
Thyroid gland may enlarge rapidly, occasionally with dyspnoea/dysphagia from pressure on the neck.
Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating.
What is primary hypothyroidism a disease associated with?
the thyroid.
What is secondary hypothyroidism a disease associated with?
Pituitary or hypothalamus.
What is transient hypothyroidism associated with?
Treatment withdrawal.
Pathophysiology of primary hypothyroidism
Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.
Antibodies bind and block TSH receptors
-> inadequate thyroid hormone production and secretion
Pathophysiology of secondary hypothyroidism
Reduced release or production of TSH
-> reduced T3 and T4 release.
Pathophysiology of transient hypothyroidism
The thyroid overcompensates until it can re-establish correct concentrations of Thyroid hormone.
Cause of primary hypothyroidism
Autoimmune hypothyroidism (Hashimoto’s),
iodine deficiency,
congenital defects.
Cause of secondary hypothyroidism
Isolated TSH deficiency,
hypopituitarism (due to neoplasm, infection),
hypothalamic disorders (neoplasms, trauma).
Cause of transient hypothyroidism
Withdrawal of thyroid suppressive therapy such as radioactive iodine.
Epidemiology of primary hypothyroidism
12-20 times more frequent in women.
Most common cause of goitrous hypothyroidism.
Diagnostic test for hypothyroidism
Serum free T4 levels low,
thyroid antibodies may be present.
Treatment for primary hypothyroidism
Thyroid hormone replacement (Levothyroxine).
Resection of obstructive goitre.
Treatment for secondary hypothyroidism
Thyroid hormone replacement (Levothyroxine).
Treat underlying cause.
Treatment of transient hypothyroidism
Remits on its own.
Complications of thyroidism
Myxoedema coma: 20-50% mortality.
Reduced level of consciousness, seizures, hypothermia and hypothyroidism.
Define thyroid cancer
Cancer of the thyroid tissue.
Types of thyroid cancer
Papillary
Follicular
Anaplastic
Lymphoma
Medullary
How does papillary, follicular and anaplastic thyroid cancer clinically present?
Usually asymptomatic thyroid nodule (usually hard and fixed).
Possibly enlarged lymph nodes on examination.
How does lymphoma - thyroid cancer - clinically present?
Rapidly growing mass in the neck.
How does medullary thyroid cancer clinically present?
Diarrhoea,
flushing episodes (very similar to carcinoid syndrome)
and itching.
Papillary thyroid cancer - note
Named for the papillae among its cells on microscopy.
Anaplastic thyroid cancer - note
‘One of the most aggressive cancers in humans’.
Pathophysiology of papillary thyroid cancer
Tends to spread locally in the neck, compressing the trachea.
Pathophysiology of follicular thyroid cancer
Follicular cells of the thyroid,
but does not retain original cell features like iodine uptake or synthesis of thyroglobulin.
Pathophysiology of anaplastic thyroid cancer
May infiltrate neck,
but greater propensity to metastasise to lung and bones relative to papillary.
Pathophysiology of lymphoma - thyroid cancer
Almost always non-hodgkins lymphoma.
Pathophysiology of medullary thyroid cancer
Parafollicular calcitonin-producing C cells.
Produce large amounts of peptide such as calcitonin.
Epidemiology of papillary thyroid cancer
70% of thyroid cancer.
Young people.
Three times more common in women.
Epidemiology of follicular thyroid cancer
20% of thyroid cancer.
Middle age.
Tends to be in areas of low iodine.
Epidemiology of anaplastic thyroid cancer
<5% of thyroid cancer.
Epidemiology of lymphoma - thyroid cancer
2% of thyroid cancer.
Often associated with Hashimoto’s thyroiditis.
Epidemiology of medullary thyroid cancer
5% of thyroid cancer.
More sporadic than hereditary.
Cause of medullary thyroid cancer
Often familial.
Diagnostic tests for thyroid cancer
Fine needle aspiration.
Differences: Medullary; elevated serum calcitonin.
Treatment of papillary and follicular thyroid cancer
Total thyroidectomy
-> ablative radioactive iodine.
Treatment of anaplastic and lymphoma - thyroid cancer
External radiotherapy to provide relief (largely palliative).
Treatment of medullary thyroid cancer
Total thyroidectomy
and prophylactic central lymph node dissection.
Define Cushing’s syndrome (Hypercortisolism)
Persistently and inappropriately elevated circulating glucocorticoid (cortisol).
Define Acromegaly
Overgrowth of all organ systems due to excess GH
Define Conn’s syndrome (primary hyperaldosteronism)
High aldosterone levels independent of renin-angiotensin system.
How does Cushing’s syndrome (Hypercortisolism) clinically present?
Obesity (fat distribution central, buffalo hump),
plethoric complexion,
rounded ‘moon face’,
thin skin, bruising, striae, hypertension, pathological fractures.
How does Acromegaly clinically present?
Slow onset (old photos).
Larger hands/feet.
Large tongue, prognathism, interdental separation, spade-like hands.
How does Conn’s syndrome (primary hyperaldosteronism) clinically present?
Hypertension (possibly low urine output),
hypokalaemic.
Cushing’s syndrome (Hypercortisolism) - note
Cushing’s disease:
When elevated glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary.
Acromegaly - note
If before fusion of epiphyseal plates (children); gigantism.
Conn’s syndrome (primary hyperaldosteronism)
Hyperaldosteronism due to high renin levels is called Secondary hyperaldosteronism.
Pathophysiology of Cushing’s syndrome (Hypercortisolism)
Many features due to protein-catabolic effects of cortisol; thin skin, easy bruising, striae.
Excessive alcohol consumption can mimic the clinical and biochemical signs (Pseudo-Cushings’s), but resolves on alcohol recession.
Pathophysiology of Acromegaly
GH acts directly on tissues such as liver, muscle bone or fat,
as well as indirectly through induction of insulin like growth factor.
Excess causes uncontrolled growth of organ systems.
Pathophysiology of Conn’s syndrome (primary hyperaldosteronism)
Aldosterone causes an exchange of transport of sodium and potassium in the distal renal tubule.
Therefore, hyperaldosteronism causes increased reabsorption of sodium (and water) and excretion of potassium
Cause of Cushing’s syndrome (Hypercortisolism)
ACTH (adrenocortiotropic hormone) dependent disease:
excessive ACTH from pituitary,
ACTH producing tumour or excess ACTH administration
Non-ACTH dependent: adrenal adenomas, adrenal carcinomas, excess glucocorticoid administration (most common)
Cause of Acromegaly
Usually excessive GH secretion by a pituitary tumour.
Other GH releasing tumours possible (hypothalamus, specific lung cancers).
Cause of Conn’s syndrome (primary hyperaldosteronism)
Adrenal adenoma secreting aldosterone in Conn’s syndrome (or possibly bilateral adrenal hyperplasia).
Epidemiology of Cushing’s syndrome (Hypercortisolism)
10/1,000,000.
Higher incidence in diabetes.
2/3 cases are Cushing’s disease.
Epidemiology of Acromegaly
1/200,000.
Average 40 yrs.
Diagnostic tests for Cushing’s syndrome (Hypercortisolism)
Confirm raised cortisol: 48 hour low-dose dexamethasone: Fail to suppress cortisol.
Urinary free cortisol over 24hrs.
Late night salivary cortisol.
Establishing cause: CT and MRI of renal and pituitary.
Diagnostic test for Acromegaly
Glucose tolerance test: IGF-1 raised.
GH raised.
Diagnostic test for Conn’s syndrome (primary hyperaldosteronism)
Plasma aldosterone and renin.
Treatment of Cushing’s syndrome (Hypercortisolism)
Tumours: Surgical removal
Cortisol synthesis inhibition: metyrapone, ketoconazole.
Treatment of Acromegaly
Transsphenoidal resection surgery.
Dopamine agonists (cabergoline), somatostatin analogues (octreotide)
and GH receptor antagonists (pegvisomant).
Treatment of Conn’s syndrome (primary hyperaldosteronism)
Adenoma: Surgical removal
Hyperplasia: aldosterone antagonist (spironolactone).
Complications of Cushing’s syndrome (Hypercortisolism)
Hypertension,
obesity,
death.
Complications of Acromegaly
Hypertension,
diabetes.
Untreated adenoma can impact the optic chiasm -> blindness,
colorectal cancer.
Sequelae of Cushing’s syndrome (Hypercortisolism)
Rare remission.
Define Adrenal insufficiency (hypoadrenalism).
Destruction of the adrenal cortex
-> reduction in adrenal hormones
Define Adrenal hyperplasia.
Defective enzymes mediating the production of adrenal cortex products.
Types of Adrenal insufficiency (hypoadrenalism)
Primary insufficiency (Addison’s disease).
Secondary.
How does primary adrenal insufficiency (Addison’s disease) clinically present?
Insidious.
Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.
Postural hypotension.
Thin, tanned, tired and tearful.
Hyperpigmentation.
How does secondary adrenal insufficiency clinically present?
Insidious.
Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.
Postural hypotension.
Thin, tired and tearful.
How does adrenal hyperplasia clinically present?
In severe forms; salt loss.
Female: Ambiguous genitalia with common urogenital sinus.
Male: no signs at birth, bar subtle hyperpigmentation and possible penile enlargement.
Primary adrenal insufficiency (Addison’s disease) - note
Destruction of adrenal cortex
-> Less cortical products.
Excess ACTH
- > stimulates melanocytes
- > hyper pigmentation.
Secondary adrenal insufficiency - note
Reduction of adrenal cortex stimulation
-> Less cortical products.
Low ACTH
- > less melanocytes stimulation
- > no pigmentation.
Adrenal hyperplasia - note
Low cortisol,
maybe low aldosterone,
high androgen.
Pathophysiology of Primary adrenal insufficiency (Addison’s disease)
Autoimmune destruction of the entirety adrenal cortex.
Associated with other autoimmune conditions.
Loss of cortex -> reduction in ability to produce cortisol and/or aldosterone.
Excess ACTH stimulates melanocytes -> pigmentation.
Pathophysiology of Secondary adrenal insufficiency
Inadequate pituitary or hypothalamic stimulation of the adrenal glands.
No pigmentation, since ACTH levels are low.
Pathophysiology of Adrenal hyperplasia
Defective 21-hydroxylase -> disruption of cortisol biosynthesis.
This causes cortisol deficiency, with or without aldosterone deficiency and androgen excess.
In severe forms, aldosterone deficiency -> salt loss.
Causes of Primary adrenal insufficiency (Addison’s disease)
Organ specific autoantibodies in 90% of cases.
Rarely; adrenal gland tuberculosis,
surgical removal or haemorrhage.
Causes of Secondary adrenal insufficiency
Hypothalamic-pituitary disease
or from long term steroid therapy leading to hypothalamic-pituitary-adrenal suppression.
Cause of Adrenal hyperplasia
Genetic
21-hydroxylase deficiency is the cause of about 95% of cases.
Epidemiology of Primary adrenal insufficiency (Addison’s disease)
1/10,000
Epidemiology of Secondary adrenal insufficiency
200/1,000,000.
Diagnostic tests for Primary adrenal insufficiency (Addison’s disease)
Sodium reduction, potassium elevation.
Cortisol taken across multiple time points.
Diagnostic test for Secondary adrenal insufficiency
Long ACTH test (synacthen test) to distinguish from primary:
ACTH raised in primary, lowered in secondary.
Diagnostic test for Adrenal hyperplasia
Serum 17-hydroxyprogesterone (precursor to cortisol) levels: high.
Treatment of Primary adrenal insufficiency (Addison’s disease)
Hormone replacement (glucocorticoid (hydrocortisone)
and mineralocorticoid (fludrocortisone).
Treatment of Secondary adrenal insufficiency
Hormone replacement (just hydrocortisone).
If from steroid therapy; remove steroids very slowly.
Treatment of Adrenal hyperplasia
Glucocorticoids: Hydrocortisone Mineralocorticoids:
Control electrolytes
If salt loss: Sodium chloride supplement.
Complications of Primary adrenal insufficiency (Addison’s disease)
Adrenal crisis, reduced QOL.
Define diabetes insipidus
Hyposecretion or insensitivity to ADH.
Types of diabetes insipidus
Cranial.
Nephrogenic.
How does diabetes insipidus clinically present?
Polyuria,
compensatory polydipsia.
Cranial diabetes insipidus - note
Hyposecretion.
Nephrogenic diabetes insipidus - note
Insensitivity.
Pathophysiology of cranial diabetes insipidus
Disease of the hypothalamus, where ADH is produced -> Insufficient ADH production.
Interestingly, damage to the Posterior Pituitary gland, does not lead to ADH deficiency, as it can still ‘leak’ out.
Pathophysiology of nephrogenic diabetes insipidus
Depends on the aetiology.
Can be due to disruption of the channels,
damage to the kidney
-> Lack of appropriate response to ADH.
Causes of cranial diabetes insipidus
Neurosurgery, trauma, tumour, infiltrative disease, idiopathic
Genetic: Mutations in the ADH gene
Cause of nephrogenic diabetes insipidus
Hypokalaemia, hypercalcaemia, drugs, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease.
Genetic: Mutation in ADH receptor.
Epidemiology of diabetes insipidus
1/25,000.
Diagnostic tests for diabetes insipidus
Urine volume: Confirm polyuria.
Water deprivation: Confirm DI.
U&Es: Confirm not a more common cause of polyuria
MRI of hypothalamus: Confirm CDI
Treatment of cranial diabetes insipidus
Mild cases: thiazide diuretics, carbamazepine and chlorpropramide to sensitise the renal tubules to endogenous vasopressin.
Desmopressin.
Treatment of nephrogenic diabetes insipidus
Treatment of the cause.
Define Syndrome of inappropriate ADH secretion
Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume.
How does Syndrome of inappropriate ADH secretion clinically present?
Nausea, irritability and headache with mild dilutional hyponatraemia.
Fits and coma with severe hyponatraemia.
Pathophysiology of Syndrome of inappropriate ADH secretion
Ectopic production increases the amount of ADH produced, beyond mechanisms of control.
Causes of Syndrome of inappropriate ADH secretion
Disordered hypothalamic-pituitary secretion, or ectopic production of ADH.
Neurological: Tumour, trauma, infection
Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis.
Diagnostic test for Syndrome of inappropriate ADH secretion
FBC.
Diagnose by serum concentrations.
Treatment of Syndrome of inappropriate ADH secretion
Underlying cause.
Water restriction.
Demeoclocycline; inhibition of ADH.
Define Hyperparathyroidism
Excessive secretion of PTH
Define Hypoparathyroidism
Low levels of PTH
Types of hyperparathyroidism
Primary
Secondary
Tertiary
How does primary hyperparathyroidism clinically present?
70-80% asymptomatic.
Bone pain, renal calculi, nausea, neuropsychiatric.
(Bones, stones, abdominal groans and psychic moans)
How does secondary hyperparathyroidism clinically present?
Kidney disease,
with skeletal or cardiovascular complications.
How does tertiary hyperparathyroidism clinically present?
Bone pain, renal calculi, nausea, neuropsychiatric.
(Bones, stones, abdominal groans and psychic moans).
How does hypoparathyroidism clinically present?
Increased excitability of muscles and nerves.
Numbness around the mouth/extremities, cramps, tetany, convulsions.
Chvostek and Trousseau signs.
Primary hyperparathyroidism - note
One parathyroid gland produces excess PTH.
Secondary hyperparathyroidism - note
Increased secretion of PTH to compensate hypocalcaemia.
Tertiary hyperparathyroidism - note
Autonomous secretion of PTH,
due to CKD.
Hypoparathyroidism - note
Hypocalcaemia
and hyperphosphataemia.
Pathophysiology of Primary hyperparathyroidism
Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH.
Pathophysiology of Secondary hyperparathyroidism
Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia.
Pathophysiology of Tertiary hyperparathyroidism
Glands become autonomous,
producing excess of PTH even after the correction of calcium deficiency.
Pathophysiology of Hypoparathyroidism
PTH stimulates the activation of vitamin D,
which facilitates intestinal calcium absorption,
renal reabsorption of calcium as well as calcium release from bone.
Phosphate reabsorption is inhibited by PTH.
In disease, these processes do not occur.
Causes of Primary hyperparathyroidism
Single parathyroid adenoma
or hyperplasia.
Causes of Secondary hyperparathyroidism
CKD (any condition with hypocalcaemia, such as vitamin D deficiency).
Cause of Tertiary hyperparathyroidism
Develops from secondary hyperparathyroidism.
Cause of Hypoparathyroidism
May be transient.
Most commonly follows anterior neck surgery.
Genetic: Can be due to defects in PTH gene.
Can be autoimmune.
Epidemiology of Primary hyperparathyroidism
Third most common endocrine disorder.
Epidemiology of Hypoparathyroidism
Rare.
Diagnostic test for Primary hyperparathyroidism
Bloods: Hypercalcaemia.
Diagnostic test for Secondary hyperparathyroidism
Bloods: low serum calcium.
Diagnostic test for Tertiary hyperparathyroidism
Bloods: Raised calcium, raised PTH.
Diagnostic test for Hypoparathyroidism
Bloods: Calcium and PTH low, phosphate high.
Treatment of Primary hyperparathyroidism
Surgical removal of adenoma.
Potentially bisphosphonates.
Treatment of Secondary hyperparathyroidism
Calcium correction.
Treat underlying condition.
Treatment of Tertiary hyperparathyroidism
Calcium mimetic (Cinacalcet),
total or subtotal parathyroidectomy.
Treatment of Hypoparathyroidism
Acute: IV calcium
Persistent: Vitamin D analogue (alfacalcidol).
Complication of Primary hyperparathyroidism
Hypercalcaemia
Complication of Secondary hyperparathyroidism
Development into tertiary hyperparathyroidism.
Complication of Tertiary hyperparathyroidism
Transient hypocalcaemia follows parathyroidectomy.
Complication of Hypoparathyroidism
Overtreatment with vitamin D
-> hypercalcaemia.
Define Hypercalcaemia
Excess of calcium
Define Hypocalcaemia
Deficiency of calcium
How does Hypercalcaemia clinically present?
Can be asymptomatic.
More severe: malaise, depression, bone pain, abdominal pain, nausea, constipation.
Occasionally renal calculi and CKD.
Polyuria and polydipsia.
How does Hypocalcaemia clinically present?
Increased excitability of muscles and nerves.
Numbness around the mouth/extremities, cramps, tetany, convulsions.
Chvostek and Trousseau signs.
Hypercalcaemia - note
Shortening of the QT interval.
Hypocalcaemia - note
QT prolongation (primarily by prolonging the ST segment).
Pathophysiology of Hypercalcaemia
Ectopic secretion of PTH is very rare.
Tumour related hypercalcaemia tends to work by a secretion of a peptide with PTH-like activity,
direct invasion of bone and production of local factors for calcium mobilisation.
Pathophysiology of Hypocalcaemia
CKD
- > Increased phosphate
- > Microprecipitation of calcium phosphate in tissues
- > Low serum level of calcium.
CKD
-> Inadequate production of active vitamin D.
Cause of Hypercalcaemia
> 90% of cases; primary hyperparathyroidism and malignancy.
Primary hyperparathyroidism is caused by a single parathyroid gland adenoma, occasionally hyperplasia.
Cause of Hypocalcaemia
Increased serum phosphate: Chronic kidney disease (most common), Phosphate therapy
Reduced PTH function: Post thyroidectomy and parathyroidectomy
Vitamin D deficiency: Reduced exposure to sunlight
Epidemiology of Hypercalcaemia
30/100,000
Diagnostic test for Hypercalcaemia
Bloods: Raised calcium
Diagnostic test for Hypocalcaemia
History.
eGFR to search for CKD.
PTH,
Vitamin D.
Treatment of hypercalcaemia
Loop diuretic to return calcium to normal.
Primary hyperparathyroidism: surgical removal.
Treatment of hypocalcaemia
Acute: IV calcium
Persistent: In vitamin D deficiency, vitamin D supplement.
If hypoparathyroidism; alfacalcidol.
Complication of hypocalcaemia
Death.
Define hyperkalaemia
Excess of potassium.
Define hypokalaemia
Deficiency of potassium.
How does hyperkalaemia clinically present?
Few symptoms until it can cause MI.
Impaired neuromuscular transmission (muscle weakness and paralysis).
How does hypokalaemia clinically present?
Usually asymptomatic, possibly muscle weakness.
Increased risk of cardiac arrhythmias.
Polyuria.
Hyperkalaemia - note
Tall tented T waves
Hypokalaemia - note
T wave inversion, prominent U wave(?)
Pathophysiology of Hyperkalaemia
Renal impairment can lead to retention of potassium in the nephron.
This is possible with potassium sparing diuretic.
Pathophysiology of Hypokalaemia
Excessive loss of potassium through the kidneys in response to aldosterone or diuretic therapy.
GI fluid loss
- > less chloride
- > increase in aldosterone
- > Decreased potassium reabsorption
Cause of Hyperkalaemia
Renal impairment (most common) and drug interference with potassium excretion.
Elevated without either of these may be artefactural.
Cause of Hypokalaemia
Diuretic treatment and hyperaldosteronism.
Possibly due to loss of GI fluids by constant vomiting/diarrhoea.
Diagnostic test for Hyperkalaemia
Bloods: Check potassium.
Recheck unexpected result.
ECG: peaked T waves, prolonged PR, widened QRS and reduced P
Diagnostic test for Hypokalaemia
Bloods: low magnesium and potassium
ECG: Flat T waves, ST depression, prominent U waves.
Treatment of Hyperkalaemia
Dietary potassium restriction
and loop diuretic.
Treatment of Hypokalaemia
Treat underlying cause.
Withdraw harmful medication.
Normalise magnesium as well as potassium.
Complications of Hyperkalaemia
Myocardial infarction
-> Death
Complications of Hypokalaemia
Cardiac arrhythmia
and sudden death.
