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Effects of thyroid hormones include all but which one of the following:
The release of thyroid hormones is regulated by the anterior pituitary gland which secretes thyroid-stimulating
hormone (TSH) and the hypothalamus which secretes thyrotropin-releasing hormone (TRH).
The thyroid follicles secrete two hormones; thyroxine (T4) – a prohormone that acts as a plasma reservoir and tri-
iodothyronine (T3) – the active hormone. T3 and T4 synthesis involves the processing of tyrosine and iodine.
About 90% of thyroid hormones are secreted in the form of T4, with the remainder as T3. About 80% of the T4 is
converted to the more active T3 (under stimulation of TSH) in the liver and kidney.
Secretion of the thyroid hormones is stimulated by long-term exposure to cold temperatures acting on the anterior
pituitary, oestrogens acting on the anterior pituitary and adrenaline acting directly on the thyroid gland. Increased
serum levels of T3 inhibit secretion of TSH.
Most of the thyroid hormones in the blood are bound to plasma proteins (of these, 70% are bound to thyroid-binding
globulin (TBG) and 30% are bound to albumin), which allows them to circulate without being broken down by enzymes.
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Only a fraction of the circulating thyroid hormones (about 0.1% of T4 and 1% of T3) are unbound and thus biologically
active. The thyroid hormones act to increase the basal metabolic rate and are important for growth and normal foetal
development. Effects of thyroid hormones include: increased heart rate and stroke volume, and increased lipolysis,
glycolysis and gluconeogenesis.
a) Pseudohypoparathyroidism
b) Hyperthyroidism
c) Pheochromocytoma
d) Addison’s disease
e) Acromegaly
Something wrong?
The commonest causes of hypercalcaemia are primary hyperparathyroidism (most common) and hypercalcaemia of
malignancy.
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
Regarding the position of the pituitary gland, which of the following statements is CORRECT:
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The pituitary gland lies in a bony hollow of the sphenoid bone (the sella turcica), and it is covered by the brous
diaphragma sellae of the dura mater. The optic chiasm lies directly superior to the anterior pituitary. The posterior
pituitary is connected to the median eminence of the hypothalamus by the pituitary stalk (also known as the
infundibulum). The cavernous sinuses (including cranial nerves III – VI) lie lateral to the pituitary gland.
Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds.
Insulin is formed from the cleaving of proinsulin (derived from preproinsulin synthesised in the rough endoplasmic
reticulum) into insulin and C-peptide in the Golgi body of β cells in the islets of Langerhans.
Since insulin and C-peptide are produced in equimolar amounts, C-peptide acts as a useful marker of β cell activity in
diabetics who receive insulin treatment.
Insulin secretion is stimulated directly by high blood glucose levels, but also by metabolites such as amino acids, fatty
acids and ketones, by glucagon, some gastrointestinal tract peptides (e.g. secretin), GH, ACTH and TSH. Insulin
secretion is inhibited by low blood glucose levels, adrenaline, somatostatin, hypocalcaemia and sympathetic
innervation. (N.B. insulin secretion never ceases completely, there is always a basal level of insulin in the blood)
a) Amenorrhoea
b) Failure of postpartum lactation
c) Infertility
d) Loss of libido
e) Erectile dysfunction
Something wrong?
Prolactin acts on the mammary glands and reproductive organs to promote growth of these organs and initiate
lactation.
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lactation.
Prolactin secretion is stimulated by prolactin-releasing factor (PRF) and thyrotropin-releasing hormone (TRH) from
the hypothalamus. Prolactin secretion is inhibited by dopamine secreted by the hypothalamus.
a) Addison’s disease
b) Propranolol
c) Hypothermia
d) Cushing’s syndrome
e) Alcohol
Something wrong?
Hypoglycaemia is de ned as a level of glucose < 3 mmol/L, although generally patients are not symptomatic unless
plasma glucose reaches < 2.2 mmol/L.
overwhelming sepsis
hypothermia
Addison’s disease
insulinoma
malignancy
certain medications e.g. beta blockers or salicylates
inadequate levels of exercise or carbohydrate intake in patients with diabetes mellitus
Symptoms of hypoglycaemia result from a catecholamine surge and include: feelings of hunger, tremor, nausea,
sweating, anxiety/irritability, pallor, tachycardia or palpitations, headaches, tingling in the extremities or lips.
Symptoms of cognitive impairment re ect neuroglycopenia and include confusion, poor concentration, seizures and
ultimately coma.
Patients should be given oral glucose if possible (e.g. Lucozade or Glucogel), or if the oral route is not possible,
intravenous dextrose if there is IV access (e.g. 75-80 ml 20% glucose or 150-160 ml of 10% glucose), or
intramuscular/subcutaneous glucagon (e.g. 1 mg glucagon) if there is not.
The endocrine cells of the pancreas are arranged in small clusters around the larger exocrine cell clusters, called acini.
The endocrine clusters are called islets of Langerhans and within them are four types of cells:
Insulin and glucagon regulate blood glucose levels, somatostatin inhibits the release of both insulin and glucagon,
pancreatic polypeptide inhibits the exocrine functions of the pancreas.
Insulin receptors are present on most cells and they can be sequestered into the cell to inactivate them; they consist of
two extracellular alpha (α) subunits which contain the insulin-binding site and two transmembrane beta (β) subunits.
Insulin must act via cell surface receptors as it is a polypeptide hormone which cannot readily cross the cell membrane.
When insulin binds to the receptor, the beta subunit autophosphorylates and activates tyrosine kinase causing an
intracellular cascade of phosphorylation to bring about its intracellular effects.
a) Addison’s disease
b) Conn’s syndrome
c) Abrupt withdrawal of long-term corticosteroids
d) Hypothyroidism
e) SIADH
Something wrong?
Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A
level < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions or more commonly, due to increased
retention of water relative to sodium which effectively dilutes the concentration of sodium.
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
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Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt and water) and may
be caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention due to the inability to excrete a water
load, which may be caused by:
Hyponatraemia in oedematous patients is actually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
renal failure
congestive cardiac failure
malnutrition
cirrhosis
nephrotic syndrome
What is the most likely diagnosis in a patient who presents with polyuria, polydipsia, a raised
plasma osmolality and a low urine osmolality:
a) Diabetes mellitus
b) Addison’s disease
c) Diabetes insipidus
d) Conn’s syndrome
e) SIADH
Something wrong?
Diabetes insipidus (DI) may result from a de ciency of ADH secretion (cranial DI) or from an inappropriate renal
response to ADH (nephrogenic DI).
As a result, uid reabsorption at the kidneys is impaired, resulting in large amounts of hypotonic, dilute urine being
passed and subsequent polydipsia.
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passed and subsequent polydipsia.
It is associated with elevated plasma osmolality (> 300 mOsm/kg) and low urine osmolality (< 600 mOsm/kg).
An ADH stimulation test can distinguish between cranial and nephrogenic DI, as nephrogenic DI shows an inability to
concentrate urine even after administration of ADH.
a) Haemochromatosis
b) DiGeorge syndrome
c) Hyperphosphataemia
d) Thyroidectomy
e) Magnesium de ciency
Something wrong?
The most common causes are hypoparathyroidism (frequently following surgery), vitamin D de ciency or abnormal
metabolism, chronic kidney disease and hypomagnesaemia.
Patients with adjusted serum calcium > 1.9 are usually asymptomatic but many patients become symptomatic when
levels fall lower than this.
carpopedal spasm in response to in ating a blood pressure cuff to above systolic BP (Trousseau’s sign)
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twitching of the ipsilateral facial muscles in response to tapping on the facial nerve (Chvostek’s sign)
painful and fragile bones
numbness and paraesthesia in hands and feet
muscle cramps and spasms
myopathy
cardiac arrhythmias
cardiac failure
hypotension
prolonged QT interval
seizures
mood changes
cataracts
a) α cells
b) β cells
c) δ cells
d) F-cells
e) Acinar cells
Something wrong?
The endocrine cells of the pancreas are arranged in small clusters around the larger exocrine cell clusters, called acini.
The endocrine clusters are called islets of Langerhans and within them are four types of cells:
Insulin and glucagon regulate blood glucose levels, somatostatin inhibits the release of both insulin and glucagon,
pancreatic polypeptide inhibits the exocrine functions of the pancreas.
a) Adrenal adenoma
b) Ectopic ACTH
c) Primary hyperaldosteronism
d) Pituitary adenoma
e) Exogenous steroids
Something wrong?
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Cushing’s disease refers to the speci c condition of excess corticosteroids as a result of increased ACTH due to a
pituitary adenoma; the negative feedback that normally prevents excess ACTH secretion is absent in the tumour.
Cushing’s disease is associated with hyperpigmentation due to the melanocyte-stimulating action of ACTH.
Glucagon acts to cause all but which one of the following effects:
a) Stimulation of glycogenolysis
b) Increased peripheral tissue glucose uptake
c) Stimulation of lipolysis
d) Stimulation of ketogenesis
e) Stimulation of gluconeogenesis
Something wrong?
Glucagon is synthesised in the pancreatic alpha (α) cells in the islets of Langerhans.
Glucagon secretion is stimulated by low blood glucose, amino acids, adrenaline, some gastrointestinal peptides,
sympathetic and parasympathetic innervation. Glucagon secretion is inhibited by high blood glucose, fatty acids and
ketones, insulin and somatostatin.
stimulate glycogenolysis
inhibit peripheral tissue glucose uptake
inhibit glycolysis
inhibit amino acid uptake and protein synthesis
stimulate lipolysis
stimulate gluconeogenesis
stimulate ketogenesis
Osteomalacia/rickets are associated with all but which one of the following clinical features:
a) Hypocalcaemia
b) Bow-legs
c) Bone pain
d) Bone fragility and increased risk of fracture
e) Hyperphosphataemia
Something wrong?
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Defective mineralisation is mostly due to reduced calcium and phosphate levels in the extracellular uid due to vitamin
D de ciency.
bone pain
bones appear thin on X-ray with localised radiolucencies
increased susceptibility to fractures
features of hypocalcaemia
Graves’ disease is an autoimmune disease, in which autoantibodies against TSH receptors are produced. These
antibodies bind to and stimulate these TSH receptors leading to an excess production of thyroid hormones.
Classically Grave’s disease is associated with hyperthyroidism, pretibial myxoedema, clubbing (thyroid acropachy) and
eye changes.
Graves’ eye disease may include features of: exophthalmos, lid retraction, lid lag, diplopia, corneal ulcers.
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Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
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If the plasma osmolality is normal, then the possibility of pseudohyponatraemia should be considered; this is an
artifactual result due to a reduction in plasma water caused by marked hyperlipidaemia or hyperproteinaemia e.g.
multiple myeloma.
If the plasma osmolality is high, then the possibility of hyperosmolar hyponatraemia should be considered; this may be
due to hyperglycaemia or administration of mannitol amongst other causes and re ects the shift of water out of cells
into the extracellular uid in response to osmotic effects.
a) Aldosterone
b) Cortisol
c) Angiotensin II
d) Renin
e) Antidiuretic hormone
Something wrong?
Diabetes insipidus (DI) may result from a de ciency of ADH secretion (cranial DI) or from an inappropriate renal
response to ADH (nephrogenic DI).
As a result, uid reabsorption at the kidneys is impaired, resulting in large amounts of hypotonic, dilute urine being
passed and subsequent polydipsia.
It is associated with elevated plasma osmolality (> 300 mOsm/kg) and low urine osmolality (< 600 mOsm/kg).
An ADH stimulation test can distinguish between cranial and nephrogenic DI, as nephrogenic DI shows an inability to
concentrate urine even after administration of ADH.
In a patient with hyponatraemia, dehydration and high urinary Na+, which of the following is
the most likely diagnosis:
a) Vomiting
b) Diabetes insipidus
c) Nephrotic syndrome
d) Sweating
e) Diuretics
Something wrong?
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Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
How does parathyroid hormone (PTH) affect the renal handling of Ca2+:
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
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Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
a) Prognathism
b) Spade-like hands
c) Osteoarthritis
d) Glucose intolerance
e) Hypocalcaemia
Something wrong?
Acromegaly is a result of excess growth hormone (GH) secretion from the anterior pituitary gland, most commonly as a
result of a GH-secreting pituitary adenoma.
In a euvolaemic patient with hyponatraemia and a urinary Na+ > 40 mmol/L, which of the
following is the most likely diagnosis:
Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
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Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
Which of the following signs would you NOT expect to see in hypothyroidism:
a) Proximal myopathy
b) Hypore exia
c) Positive Phalen’s test
d) Bradycardia
e) Pretibial myxoedema
Something wrong?
Hypothyroidism is de ned as an underactive thyroid gland leading to de cient thyroid hormones. T3 and T4 levels are
low and TSH levels are usually high.
Causes include:
overtreatment of hyperthyroidism (e.g. radioactive ablation, surgical removal or anti-thyroid drugs e.g.
carbimazole)
drugs e.g. amiodarone, lithium, anticonvulsants, levodopa
Hashimoto’s thyroiditis
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TSH levels are normally elevated, low TSH levels suggest secondary hypothyroidism which is much less common.
a) Cortisol
b) Aldosterone
c) Growth hormone
d) ACTH
e) Prolactin
Something wrong?
Acromegaly is a result of excess growth hormone (GH) secretion from the anterior pituitary gland, most commonly as a
result of a GH-secreting pituitary adenoma.
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result of a GH-secreting pituitary adenoma.
a) Hypopituitarism
b) Hyperpituitarism
c) Homonymous hemianopia
d) Ophthalmoplegia
e) Hyperprolactinaemia
Something wrong?
Functioning pituitary adenomas usually release prolactin (most common type – about 50% of pituitary tumours), GH
(about 20%) or ACTH (about 5%). TSH, LH and FSH – secreting adenomas are rare.
In addition to endocrine abnormalities, pituitary tumours can present with effects of a space-occupying lesion e.g.
headaches, vomiting and papilloedema due to raised intracranial pressure, hypopituitarism from compression of
normal secretory cells or compression of the portal veins that bring the hypothalamic-releasing factors (secretion of
anterior pituitary hormones is inhibited in a characteristic order: GH, LH, FSH, ACTH, TSH, Prolactin (N.B. unless
compression is severe, prolactin secretion is usually raised)) , visual eld defects (bitemporal hemianopia) from
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compression is severe, prolactin secretion is usually raised)) , visual eld defects (bitemporal hemianopia) from
compression at the optic chiasm and cranial nerve palsies (CN III, IV, V and VI) from compression of the cavernous
sinus.
a) Increases uid excretion by inhibiting reabsorption of sodium in the distal convoluted tubule
b) Increases uid retention by increasing sodium reabsorption in the distal convoluted tubule
c) Vasodilation
d) Increases uid reabsorption in the proximal tubule via the insertion of aquaporin water channels
e) Increases urine osmolality
Something wrong?
Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
What is the most likely diagnosis in a patient who presents with hypovolaemic hypotensive
shock, who is found to have hyponatraemia and hyperkalaemia:
a) Adrenal crisis
b) Thyrotoxic storm
c) Pituitary apoplexy
d) Myxoedema coma
e) Pheochromocytoma
Something wrong?
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Primary insuf ciency of the adrenal cortex is called Addison’s disease, it is characterised by de cient secretion of both
glucocorticoids and mineralocorticoids.
Causes include:
postural hypotension
hyponatraemia
hyperkalaemia
hypoglycaemia
tendency for hypercalcaemia
weight loss
abdominal pain/constipation/nausea
muscle weakness
fatigue
lethargy
dizziness
depression
An acute exacerbation of Addison’s disease is called an adrenal crisis. It is a life-threatening emergency characterised
by: hypotensive shock, hypovolaemic shock and hypoglycaemia.
Acute adrenocortical failure may occur if long-term high-dose steroid treatment is stopped abruptly (as the prolonged
steroid treatment has suppressed natural ACTH release). Secondary adrenocortical insuf ciency may also be caused
by disorders of the hypothalamus and anterior pituitary gland due to de ciency of CRH or ACTH.
a) Adrenaline
b) Sympathetic innervation
c) Parasympathetic innervation
d) Fatty acids and ketones
e) Low blood glucose
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Something wrong?
Glucagon is synthesised in the pancreatic alpha (α) cells in the islets of Langerhans.
Glucagon secretion is stimulated by low blood glucose, amino acids, adrenaline, some gastrointestinal peptides,
sympathetic and parasympathetic innervation. Glucagon secretion is inhibited by high blood glucose, fatty acids and
ketones, insulin and somatostatin.
stimulate glycogenolysis
inhibit peripheral tissue glucose uptake
inhibit glycolysis
inhibit amino acid uptake and protein synthesis
stimulate lipolysis
stimulate gluconeogenesis
stimulate ketogenesis
a) Bronchodilation
b) Increased heart rate
c) Vasoconstriction of the coronary vessels
d) Inhibited insulin release
e) Increased renin release
Something wrong?
cause alertness/agitation/fear/anxiety
stimulate release of ACTH
dilate pupils
increase glycogenolysis
increase renin release
increase lipolysis
increase sweating
increase heart rate and contractility
cause vasoconstriction in most tissues (but vasodilation in the coronary circulation)
increase cardiac output and blood pressure
dilate the bronchioles
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dilate the bronchioles
stimulate ventilation
stimulate glucagon release
inhibit insulin release
decrease proteolysis
increase ef ciency of skeletal muscle contraction
The adrenal cortex is controlled by the pituitary gland, responding to adrenocorticotrophic (ACTH) hormone.
It is functionally and anatomically divided into three zones of tissue which each secrete different steroid hormones:
Which of the following clinical features would you NOT expect to see in hypothyroidism:
Hypothyroidism is de ned as an underactive thyroid gland leading to de cient thyroid hormones. T3 and T4 levels are
low and TSH levels are usually high.
Causes include:
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overtreatment of hyperthyroidism (e.g. radioactive ablation, surgical removal or anti-thyroid drugs e.g.
carbimazole)
drugs e.g. amiodarone, lithium, anticonvulsants, levodopa
Hashimoto’s thyroiditis
De Quervain (subacute) thyroiditis
primary atrophic hypothyroidism
severe iodine de ciency
TSH de ciency from hypopituitarism
disruption of the hypothalamic-pituitary-thyroid axis
TSH levels are normally elevated, low TSH levels suggest secondary hypothyroidism which is much less common.
You are asked to assess a patient with hyponatraemia. They are hypervolaemic and have a low
urinary sodium of < 20 mmol/L, which of the following is the most likely cause of their
hyponatraemia:
a) SIADH
b) Congestive cardiac heart failure
c) Hypothyroidism
d) Chronic kidney disease
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e) Psychogenic polydipsia
Something wrong?
Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
a) Skin
b) Liver
c) Thyroid gland
d) Parathyroid gland
e) Kidneys
Something wrong?
Vitamin D (cholecalciferol) is absorbed by the small intestine as part of the diet or is synthesised from cholesterol in
skin.
Cholecalciferol is converted to calcifediol by 25-hydroxylase in the liver. This is converted to activated vitamin D (1, 25
– dihydroxycholecalciferol or calcitriol) by 1-alpha-hydroxylase in the kidney. The enzyme 1-alpha-hydroxylase is
stimulated by parathyroid hormone (PTH) and by low concentrations of phosphate.
increase calcium and phosphate absorption in the small intestine (the main action)
increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ ATPase pump)
increase renal phosphate reabsorption
inhibit 1-alpha-hydroxylase activity in the kidneys (negative feedback)
affect bone remodelling to bring about the conditions of high calcium and phosphate optimum for bone
remineralisation
dietary de ciency
malabsorption e.g. coeliac disease
lack of sun exposure
chronic kidney disease
liver failure
anticonvulsant therapy
hypoparathyroidism
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Regarding the gonadotropins, FSH and LH, which of the following statements is INCORRECT:
The gonadotropins, luteinising hormone (LH) and follicle stimulating hormone (FSH) act via G-protein coupled
receptors on the gonads.
In the male, LH acts to stimulate production of testosterone, which acts in concert with FSH to support
spermatogenesis. In the female, LH and FSH are essential for normal menstruation and reproduction.
LH/FSH secretion is stimulated by gonadotrophin-releasing hormone (GnRH) from the hypothalamus. GnRH is
released in a pulsatile fashion, which is essential for normal reproductive activity.
LH/FSH secretion is inhibited by prolactin and sex steroids. LH/FSH de ciency results in gonadal insuf ciency
(decreased sex steroids). Excess levels of FSH/LH (extremely rare) results in infertility.
Oxytocin acts on the mammary glands to stimulate milk ejection, and the uterus to stimulate uterine contraction in
childbirth. Oxytocin release is stimulated by stretch receptors in the nipple and the cervix and by oestrogen. Oxytocin
release is inhibited by stress.
a) Mineralocorticoids
b) Glucocorticoids
c) Adrenal androgens
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c) Adrenal androgens
d) Catecholamines
e) Growth hormone
Something wrong?
The adrenal medulla produces catecholamines, and is controlled by and functions in concert with the sympathetic
nervous system.
The chromaf n cells of the medulla secrete noradrenaline (20%) and adrenaline (80%) stimulated by sympathetic
preganglionic neurones located in the spinal cord in response to stress e.g. exercise, pain, shock, hypoglycaemia. These
catecholamines act on alpha- and beta- G-protein coupled receptors , having the same effect in tissues as stimulation
of sympathetic nerves.
Noradrenaline has equal potency at all adrenoceptors, but adrenaline at normal plasma concentrations will only
activate beta-receptors (higher levels do stimulate alpha-receptors).
Noradrenaline is synthesised from the amino acid tyrosine which is then converted to adrenaline in response to
cortisol from the adrenal cortex. Catecholamines circulate mainly bound to albumin and are broken down by
monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) in the liver.
Vitamin D (cholecalciferol) is absorbed by the small intestine as part of the diet or is synthesised from cholesterol in
skin.
Cholecalciferol is converted to calcifediol by 25-hydroxylase in the liver. This is converted to activated vitamin D (1, 25
– dihydroxycholecalciferol or calcitriol) by 1-alpha-hydroxylase in the kidney. The enzyme 1-alpha-hydroxylase is
stimulated by parathyroid hormone (PTH) and by low concentrations of phosphate.
increase calcium and phosphate absorption in the small intestine (the main action)
increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ ATPase pump)
increase renal phosphate reabsorption
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dietary de ciency
malabsorption e.g. coeliac disease
lack of sun exposure
chronic kidney disease
liver failure
anticonvulsant therapy
hypoparathyroidism
Steroid hormones are synthesised from cholesterol. They are small lipid-soluble molecules that can readily cross cell
membranes and that travel in plasma mainly bound to plasma protein. Inside cells, they act on intracellular receptors to
regulate gene expression.
Calcitonin is secreted by the parafollicular cells in the thyroid gland. Calcitonin is secreted in response to rising or high
blood calcium levels and acts to lower circulating levels of calcium.
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blood calcium levels and acts to lower circulating levels of calcium.
Calcitonin acts on the kidneys to inhibit reabsorption of calcium and phosphate and on the bones to inhibit osteoclast
activity and thus bone resorption of calcium and phosphate.
A patient’s blood results show hypernatraemia, with plasma osmolality > urine osmolality,
which of the following is the most likely diagnosis:
a) SIADH
b) Diabetes insipidus
c) Conn’s syndrome
d) Osmotic diuresis
e) Inadequate water intake
Something wrong?
Hypernatraemia is an increase in the serum sodium concentration above the reference interval of 133 – 146 mmol/L.
Hypernatraemia may arise from either excess sodium or much more commonly from water de cit (both are associated
with a raised plasma osmolality).
Hypernatraemia can be thought of in relation to actual total body sodium. The most common group of patients are
those with hypernatraemia with decreased body sodium through loss of both water and sodium, but with a greater
proportion of water loss which may result from:
renal losses e.g. osmotic diuresis in uncontrolled diabetes mellitus, loop diuretics, renal disease
skin losses e.g. burns, excessive sweating in hot climate or exercise
gastrointestinal losses e.g. vomiting, diarrhoea, stulae
Patients with hypernatraemia with normal total body sodium have a pure water de cit which may result from:
inadequate water intake e.g. unconscious patient, dementia, disordered thirst perception in hypothalamic
lesion
excessive pure water loss e.g. diabetes insipidus (where plasma osmolality > urine osmolality)
Hypernatraemia with an actual increase in total body sodium is rare. Mild true hypernatraemia may be caused by
primary hyperaldosteronism, but this is not typical of Conn’s syndrome, other causes include acute salt poisoning e.g.
intravenous sodium bicarbonate, hypertonic saline, high sodium feeds in infants, near drowning in salt water.
If the hypernatraemia is mild (Na ≤ 150 mmol/L) and the patient has obvious signs of dehydration it is likely the
ECF volume is reduced and that the patient has lost both sodium and water. Treatment should aim to replace
the de cit of uid by infusing isotonic saline, or if the de cit is large, hypotonic saline.
With more severe hypernatraemia (150 – 170 mmol/L), pure water loss is likely if the clinical signs of
dehydration are mild in relation to the degree of hypernatraemia – this is because pure water loss is
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distributed evenly throughout the body compartments and the sodium content of the ECF is unchanged.
Treatment should be aimed at replacing water either orally, or with 5% dextrose.
With gross hypernatraemia ( > 180 mmol/L), an excess of sodium is likely, the patient may present with signs of
uid overload. Treatment may be with diuretics, or rarely, by renal dialysis.
What is the most likely diagnosis in a young girl presenting with virilism and hirsutism:
a) Conn’s syndrome
b) Cushing’s syndrome
c) Congenital adrenal hyperplasia
d) Addison’s disease
e) Pheochromocytoma
Something wrong?
Congenital adrenal hyperplasia (CAH) is the result of an inherited enzyme defect in corticosteroid biosynthesis.
Because of the lack of cortisol, negative feedback to the pituitary is absent and ACTH secretion continues to drive
steroid biosynthesis.
Cortisol precursors are secreted in large amounts. Increased stimulation of adrenal androgen production can cause
virilisation in girls and precocious puberty in boys.
Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
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Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
Which of the following symptoms would you NOT typically expect in hyperthyroidism:
a) Tachycardia
b) Constipation
c) Weight loss
d) Heat intolerance
e) Tremor
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e) Tremor
Something wrong?
Hyperthyroidism is de ned as over activity of the thyroid gland, leading to excess thyroid hormone secretion.
Causes include:
Graves’ disease
toxic multinodular goitre
toxic adenoma
ectopic thyroid tissue
drugs e.g. amiodarone
exogenous iodine
hair loss
emotional lability
fatigue
anxiety
restlessness
goitre
palpitations
tachycardia
atrial brillation
proximal myopathy
diarrhoea
increased appetite
weight loss
tremor
heat intolerance
sweating
oligomenorrhoea/amenorrhoea
infertility
reduced libido
osteoporosis
hyperre exia
pretibial myxoedema (in Graves’ disease)
palmar erythema
clubbing
onycholysis
T3 and T4 levels are elevated, and TSH levels are usually low. A raised TSH suggests the fault lies in or above the
pituitary gland.
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a) GH-secreting tumour
b) Catecholamine-secreting tumour
c) Cortisol-secreting tumour
d) ACTH-secreting tumour
e) Aldosterone-secreting tumour
Something wrong?
A pheochromocytoma is a tumour usually of the adrenal medulla that leads to the excess production of
catecholamines. They are usually benign and unilateral.
hypertension
headaches
profuse sweating
palpitations
tremor
postural hypotension
Primary insuf ciency of the adrenal cortex is called Addison’s disease, it is characterised by de cient secretion of both
glucocorticoids and mineralocorticoids.
Causes include:
postural hypotension
hyponatraemia
hyperkalaemia
hypoglycaemia
tendency for hypercalcaemia
weight loss
abdominal pain/constipation/nausea
muscle weakness
fatigue
lethargy
dizziness
depression
An acute exacerbation of Addison’s disease is called an adrenal crisis. It is a life-threatening emergency characterised
by: hypotensive shock, hypovolaemic shock and hypoglycaemia.
Acute adrenocortical failure may occur if long-term high-dose steroid treatment is stopped abruptly (as the prolonged
steroid treatment has suppressed natural ACTH release). Secondary adrenocortical insuf ciency may also be caused
by disorders of the hypothalamus and anterior pituitary gland due to de ciency of CRH or ACTH.
The adrenal medulla produces catecholamines, and is controlled by and functions in concert with the sympathetic
nervous system.
The chromaf n cells of the medulla secrete noradrenaline (20%) and adrenaline (80%) stimulated by sympathetic
preganglionic neurones located in the spinal cord in response to stress e.g. exercise, pain, shock, hypoglycaemia. These
catecholamines act on alpha- and beta- G-protein coupled receptors , having the same effect in tissues as stimulation
of sympathetic nerves.
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Noradrenaline has equal potency at all adrenoceptors, but adrenaline at normal plasma concentrations will only
activate beta-receptors (higher levels do stimulate alpha-receptors).
Noradrenaline is synthesised from the amino acid tyrosine which is then converted to adrenaline in response to
cortisol from the adrenal cortex. Catecholamines circulate mainly bound to albumin and are broken down by
monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) in the liver.
Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
a) Tremor
b) Palpitations
c) Anxiety
d) Polydipsia
e) Perioral paraesthesia
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e) Perioral paraesthesia
Something wrong?
Hypoglycaemia is de ned as a level of glucose < 3 mmol/L, although generally patients are not symptomatic unless
plasma glucose reaches < 2.2 mmol/L.
Symptoms of hypoglycaemia result from a catecholamine surge and include: feelings of hunger, tremor, nausea,
sweating, anxiety/irritability, pallor, tachycardia or palpitations, headaches, tingling in the extremities or lips.
Symptoms of cognitive impairment re ect neuroglycopenia and include confusion, poor concentration, seizures and
ultimately coma.
Patients should be given oral glucose if possible (e.g. Lucozade or Glucogel), or if the oral route is not possible,
intravenous dextrose if there is IV access (e.g. 75-80 ml 20% glucose or 150-160 ml of 10% glucose), or
intramuscular/subcutaneous glucagon (e.g. 1 mg glucagon) if there is not.
What is the most likely diagnosis in a euvolaemic patient who has the following biochemical
abnormalities; hyponatraemia, low plasma osmolality, high urine osmolality:
a) Diabetes insipidus
b) Addison’s disease
c) Conn’s syndrome
d) SIADH
e) Excess diuretic therapy
Something wrong?
Typical biochemistry shows hyponatraemia, low plasma osmolality, high levels of urinary sodium and high urine
osmolality.
Patients are euvolaemic and normotensive with normal thyroid and adrenal function. The potential causes are vast
including:
Neurological:
tumour, trauma, infection, Guillain-Barré syndrome, multiple sclerosis, systemic lupus erythematosus,
intracranial haemorrhage, sinus thrombosis, AIDS, porphyria
Pulmonary:
lung small-cell cancer, mesothelioma, pneumonia, abscess, cystic brosis, asthma, tuberculosis, positive-
pressure ventilation
Other malignancy:
oropharyngeal, stomach, pancreas, leukaemia, lymphoma, thymoma, and genitourinary tract cancers
Drugs:
chlorpropamide, carbamazepine, selective serotonin reuptake inhibitor (SSRI) antidepressants, tricyclic
antidepressants, lithium, MDMA/ecstasy, tramadol, haloperidol, vincristine, desmopressin, uphenazine
Miscellaneous:
idiopathic, hereditary, pain, postoperative, stress, endurance exercise and marathon runners, dermatomal
herpes zoster
Which of the following is NOT a well known cause of secondary diabetes mellitus:
a) Cushing’s syndrome
b) Thyrotoxicosis
c) Pheochromocytoma
d) Acromegaly
e) Diabetes insipidus
Something wrong?
“Fasting levels of glucose are normally 3.9 – 5.5 mmol/L, random levels are normally < 11 mmol/L.
Glucose homeostasis is primarily maintained by the interplay between insulin and glucagon. Insulin is the only
hormone that can lower glucose levels but adrenaline, cortisol and growth hormone, can raise levels in addition to
glucagon (by stimulating glycogenolysis and gluconeogenesis).
Hyperglycaemia is de ned as a fasting level of glucose > 7 mmol/L. (Levels < 6 mmol/L are normal, levels 6 – 6.9 mmol/L
demonstrate impaired fasting glycaemia, and levels >= 7 mmol/L are diagnostic of diabetes).
Hyperglycaemia may occur in diabetes mellitus type 1 due to a de ciency of insulin (due to autoimmune destruction of
β-cells), in diabetes mellitus type 2 due to a insuf ciency of insulin and/or insulin resistance or due to secondary causes
of diabetes.
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of diabetes.
Cushing’s syndrome
thyrotoxicosis
pheochromocytoma
acromegaly
glucagonoma
cirrhosis
chronic pancreatitis
cystic brosis
pancreatectomy
haemochromatosis
pancreatic carcinoma
thiazide diuretics
corticosteroid use.
polyuria
glycosuria
dehydration
polydipsia
tendency to infections
lethargy
weight loss
wasting
blurred vision
weakness
You are asked to assess a patient with hyponatraemia. They are euvolaemic with a low plasma
and urine osmolality and a urinary sodium of < 20 mmol/L, which of the following is the most likely
cause of their hyponatraemia:
a) SIADH
b) Diabetes insipidus
c) Psychogenic polydipsia
d) Hypothyroidism
e) Renal failure
Something wrong?
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Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
a) Potassium reabsorption
b) Sodium reabsorption
c) Potassium secretion
d) Sodium secretion
e) Vasoconstriction
Something wrong?
angiotensin II
a fall in extracellular uid volume (via the RAAS)
a fall in plasma Na+ (via the RAAS)
high plasma K+
ACTH
ACTH is less important as a regulator, so pituitary failure does not severely impair aldosterone secretion. Aldosterone
acts mainly on the distal convoluted tubule (DCT) and the collecting duct of the kidney to cause increased reabsorption
of sodium ions in exchange for potassium and hydrogen ions (via stimulation of Na+ pumps, Na+/H+ antiporters, and Na
+ and K+ channels in principal cells, and H+ ATPase in intercalated cells).
Water is also reabsorbed and blood volume therefore increased. Increased K+ excretion lowers plasma K+ levels.
Aldosterone also stimulates Na+ conservation by the mucosal cells of the colon and gastric glands and by the sweat
and salivary gland ducts.
You are asked to assess a patient with hyponatraemia. They are euvolaemic with a low plasma
osmolality, a high urine osmolality and a urinary sodium of > 40 mmol/L, which of the following is
the most likely cause of their hyponatraemia:
a) Psychogenic polydipsia
b) SIADH
c) Addison’s disease
d) Diabetes insipidus
e) Conn’s syndrome
Something wrong?
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Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
Adrenocorticotropic hormone (ACTH) primarily acts on which of the following target organs:
Adrenocorticotrophic hormone (ACTH) acts on the adrenal cortex to stimulate glucocorticoid and androgen release.
ACTH secretion is stimulated by corticotrophin-releasing hormone (CRH) from the hypothalamus. ACTH secretion is
inhibited by glucocorticoids.
Excess levels of ACTH due to a functioning pituitary adenoma results in Cushing’s disease.
ACTH de ciency results in adrenocortical insuf ciency (decreased cortisol and adrenal androgens).
The adrenal medulla produces catecholamines, and is controlled by and functions in concert with the sympathetic
nervous system.
The chromaf n cells of the medulla secrete noradrenaline (20%) and adrenaline (80%) stimulated by sympathetic
preganglionic neurones located in the spinal cord in response to stress e.g. exercise, pain, shock, hypoglycaemia. These
catecholamines act on alpha- and beta- G-protein coupled receptors , having the same effect in tissues as stimulation
of sympathetic nerves.
Noradrenaline has equal potency at all adrenoceptors, but adrenaline at normal plasma concentrations will only
activate beta-receptors (higher levels do stimulate alpha-receptors).
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Noradrenaline is synthesised from the amino acid tyrosine which is then converted to adrenaline in response to
cortisol from the adrenal cortex. Catecholamines circulate mainly bound to albumin and are broken down by
monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) in the liver.
a) Hypoparathyroidism
b) Thyroid disease
c) Vitamin D de ciency
d) Post-menopausal women
e) Family history of osteoporotic fractures
Something wrong?
Osteoporosis is a disease characterised by low bone mineral density and deterioration of bone suf cient to cause bone
fragility and an increased risk of fracture (particularly hip, spine and distal radius).
It is caused by increased osteoclast activity and decreased osteoblast activity resulting in a shift towards increased
bone resorption.
post-menopausal women
family history of osteoporotic fractures
rheumatoid arthritis
thyroid disease
long-term corticosteroid use
high alcohol intake
smoking
vitamin D de ciency
hyperparathyroidism
a) Increased gluconeogenesis
b) Decreased proteolysis
c) Decreased glycogenolysis
d) Increased lipogenesis
e) Increased glycolysis
Something wrong?
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a) Hyperpigmentation
b) Hypotension
c) Hypoglycaemia
d) Hyperkalaemia
e) Hypernatraemia
Something wrong?
Primary insuf ciency of the adrenal cortex is called Addison’s disease, it is characterised by de cient secretion of both
glucocorticoids and mineralocorticoids.
Causes include:
postural hypotension
hyponatraemia
hyperkalaemia
hypoglycaemia
tendency for hypercalcaemia
weight loss
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abdominal pain/constipation/nausea
muscle weakness
fatigue
lethargy
dizziness
depression
An acute exacerbation of Addison’s disease is called an adrenal crisis. It is a life-threatening emergency characterised
by: hypotensive shock, hypovolaemic shock and hypoglycaemia.
Acute adrenocortical failure may occur if long-term high-dose steroid treatment is stopped abruptly (as the prolonged
steroid treatment has suppressed natural ACTH release). Secondary adrenocortical insuf ciency may also be caused
by disorders of the hypothalamus and anterior pituitary gland due to de ciency of CRH or ACTH.
a) α cells
b) β cells
c) δ cells
d) F cells
e) Acinar cells
Something wrong?
The endocrine cells of the pancreas are arranged in small clusters around the larger exocrine cell clusters, called acini.
The endocrine clusters are called islets of Langerhans and within them are four types of cells:
Insulin and glucagon regulate blood glucose levels, somatostatin inhibits the release of both insulin and glucagon,
pancreatic polypeptide inhibits the exocrine functions of the pancreas.
What is the most likely diagnosis in a 65 year old man presenting with hypertension, a large
jaw and bitemporal hemianopia:
a) Cushing’s disease
b) Acromegaly
c) Graves’ disease
d) Cranial diabetes insipidus
e) Conn’s syndrome
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e) Conn’s syndrome
Something wrong?
Acromegaly is a result of excess growth hormone (GH) secretion from the anterior pituitary gland, most commonly as a
result of a GH-secreting pituitary adenoma.
Blood glucose levels can be raised by all but which of the following hormones:
a) Cortisol
b) Growth hormone
c) Adrenaline
d) Glucagon
e) Insulin
Something wrong?
Fasting levels of glucose are normally 3.9 – 5.5 mmol/L, random levels are normally < 11 mmol/L.
Glucose homeostasis is primarily maintained by the interplay between insulin and glucagon. Insulin is the only
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hormone that can lower glucose levels but adrenaline, cortisol and growth hormone, can raise levels in addition to
glucagon (by stimulating glycogenolysis and gluconeogenesis).
Hyperglycaemia is de ned as a fasting level of glucose > 7 mmol/L. (Levels < 6 mmol/L are normal, levels 6 – 6.9 mmol/L
demonstrate impaired fasting glycaemia, and levels >= 7 mmol/L are diagnostic of diabetes).
Hyperglycaemia may occur in diabetes mellitus type 1 due to a de ciency of insulin (due to autoimmune destruction of
β-cells), in diabetes mellitus type 2 due to a insuf ciency of insulin and/or insulin resistance or due to secondary causes
of diabetes.
Cushing’s syndrome
thyrotoxicosis
pheochromocytoma
acromegaly
glucagonoma
cirrhosis
chronic pancreatitis
cystic brosis
pancreatectomy
haemochromatosis
pancreatic carcinoma
thiazide diuretics
corticosteroid use.
polyuria
glycosuria
dehydration
polydipsia
tendency to infections
lethargy
weight loss
wasting
blurred vision
weakness
What is the most likely diagnosis in a 35 year old woman who presents with hypertension,
hypokalaemia and metabolic alkalosis:
e) Addison’s disease
Something wrong?
Hyperaldosteronism causes sodium and water retention (with volume expansion and hypertension) with increased
excretion of potassium and hydrogen ions.
hypertension
hypokalaemia
metabolic alkalosis
polyuria and polydipsia
muscle weakness and spasm
N.B. Hypernatraemia rarely occurs due to other regulating mechanisms.
Conn’s syndrome is the most common cause of primary hyperaldosteronism, in which patients have an adenoma of the
zona glomerulosa of the adrenal cortex.
In primary hyperaldosteronism, renin levels will be low due to negative feedback. High renin levels suggest secondary
hyperaldosteronism e.g. secondary to excessive diuretic therapy (most common cause), congestive heart failure, renal
artery stenosis, nephritic syndrome or cirrhosis with ascites.
cause alertness/agitation/fear/anxiety
stimulate release of ACTH
dilate pupils
increase glycogenolysis
increase renin release
increase lipolysis
increase sweating
increase heart rate and contractility
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Hyperaldosteronism causes sodium and water retention (with volume expansion and hypertension) with increased
excretion of potassium and hydrogen ions.
hypertension
hypokalaemia
metabolic alkalosis
polyuria
polydipsia
muscle weakness
spasm
N.B. Hypernatraemia rarely occurs due to other regulating mechanisms
Conn’s syndrome is the most common cause of primary hyperaldosteronism, in which patients have an adenoma of the
zona glomerulosa of the adrenal cortex. In primary hyperaldosteronism, renin levels will be low due to negative
feedback. High renin levels suggest secondary hyperaldosteronism e.g. secondary to excessive diuretic therapy (most
common cause), congestive heart failure, renal artery stenosis, nephritic syndrome or cirrhosis with ascites.
What is the most likely diagnosis in a 32 year old woman presenting with episodes of ushing,
headaches, hypertension and palpitations:
a) Cushing’s syndrome
b) Cushing’s disease
c) Pheochromocytoma
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c) Pheochromocytoma
d) Conn’s syndrome
e) Hyperthyroidism
Something wrong?
A pheochromocytoma is a tumour usually of the adrenal medulla that leads to the excess production of
catecholamines. They are usually benign and unilateral. Features include (paroxysmal): hypertension, headaches,
profuse sweating, palpitations, tremor and postural hypotension.
a) Exophthalmos
b) Lid lag
c) Ptosis
d) Pretibial myxoedema
e) Clubbing
Something wrong?
Graves’ disease is an autoimmune disease, in which autoantibodies against TSH receptors are produced. These
antibodies bind to and stimulate these TSH receptors leading to an excess production of thyroid hormones. Graves’
disease is the most common cause of hyperthyroidism.
hyperthyroidism
pretibial myxoedema
clubbing (thyroid acropachy)
eye changes including: exophthalmos, lid retraction, lid lag, diplopia, corneal ulcers
a) Aldosterone
b) Adrenocorticotropic hormone
c) Angiotensin II
d) Antidiuretic hormone
e) Corticotrophin-releasing hormone
Something wrong?
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“The pituitary gland is primarily divided into two functional lobes, the anterior pituitary (adenohypophysis) and the
posterior pituitary (neurohypophysis).
The following hormones are secreted from the anterior pituitary gland:
This can be remembered using the mnemonic: Fresh Pituitary Tastes Almost Like Guinness.
Antidiuretic hormone (ADH) and Oxytocin are secreted from the posterior pituitary gland.
The following pituitary hormones are matched with their main target tissue(s):
a) Hyponatraemia
b) Low plasma osmolality
c) High urinary sodium
d) High urine osmolality
e) Fluid overload
Something wrong?
Typical biochemistry shows hyponatraemia, low plasma osmolality, high levels of urinary sodium and high urine
osmolality.
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Patients are euvolaemic and normotensive with normal thyroid and adrenal function. The potential causes are vast
including:
Neurological:
tumour, trauma, infection, Guillain-Barré syndrome, multiple sclerosis, systemic lupus erythematosus,
intracranial haemorrhage, sinus thrombosis, AIDS, porphyria
Pulmonary:
lung small-cell cancer, mesothelioma, pneumonia, abscess, cystic brosis, asthma, tuberculosis, positive-
pressure ventilation
Other malignancy:
oropharyngeal, stomach, pancreas, leukaemia, lymphoma, thymoma, and genitourinary tract cancers
Drugs:
chlorpropamide, carbamazepine, selective serotonin reuptake inhibitor (SSRI) antidepressants, tricyclic
antidepressants, lithium, MDMA/ecstasy, tramadol, haloperidol, vincristine, desmopressin, uphenazine
Miscellaneous:
idiopathic, hereditary, pain, postoperative, stress, endurance exercise and marathon runners, dermatomal
herpes zoster
You are asked to assess a patient with hyponatraemia. They are hypovolaemic with a low
plasma osmolality, and a urinary sodium of < 20 mmol/L, which of the following is the most likely
cause of their hyponatraemia:
a) Addison’s disease
b) SIADH
c) Diuretic therapy
d) Gastroenteritis
e) Poor oral intake due to dementia
Something wrong?
Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds.
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Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds.
Insulin is formed from the cleaving of proinsulin (derived from preproinsulin synthesised in the rough endoplasmic
reticulum) into insulin and C-peptide in the Golgi body of β cells in the islets of Langerhans.
Since insulin and C-peptide are produced in equimolar amounts, C-peptide acts as a useful marker of β cell activity in
diabetics who receive insulin treatment.
Insulin secretion is stimulated directly by high blood glucose levels, but also by metabolites such as amino acids, fatty
acids and ketones, by glucagon, some gastrointestinal tract peptides (e.g. secretin), GH, ACTH and TSH. Insulin
secretion is inhibited by low blood glucose levels, adrenaline, somatostatin, hypocalcaemia and sympathetic
innervation. (N.B. insulin secretion never ceases completely, there is always a basal level of insulin in the blood)
Which of the following acts to inhibit ADH release from the posterior pituitary:
a) Adrenaline
b) Aldosterone
c) Angiotensin II
d) Adrenocorticotrophic hormone (ACTH)
e) Atrial natriuretic peptide
Something wrong?
Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
a) Growth hormone
b) Adrenocorticotrophic hormone (ACTH)
c) Thyroid-stimulating hormone (TSH)
d) Prolactin
e) Follicle-stimulating hormone
Something wrong?
Functioning pituitary adenomas usually release prolactin (most common type – about 50% of pituitary tumours), GH
(about 20%) or ACTH (about 5%). TSH, LH and FSH – secreting adenomas are rare.
In addition to endocrine abnormalities, pituitary tumours can present with effects of a space-occupying lesion e.g.
headaches, vomiting and papilloedema due to raised intracranial pressure, hypopituitarism from compression of
normal secretory cells or compression of the portal veins that bring the hypothalamic-releasing factors (secretion of
anterior pituitary hormones is inhibited in a characteristic order: GH, LH, FSH, ACTH, TSH, Prolactin (N.B. unless
compression is severe, prolactin secretion is usually raised)) , visual eld defects (bitemporal hemianopia) from
compression at the optic chiasm and cranial nerve palsies (CN III, IV, V and VI) from compression of the cavernous
sinus.
Vitamin D (cholecalciferol) is absorbed by the small intestine as part of the diet or is synthesised from cholesterol in
skin.
Cholecalciferol is converted to calcifediol by 25-hydroxylase in the liver. This is converted to activated vitamin D (1, 25
– dihydroxycholecalciferol or calcitriol) by 1-alpha-hydroxylase in the kidney. The enzyme 1-alpha-hydroxylase is
stimulated by parathyroid hormone (PTH) and by low concentrations of phosphate.
increase calcium and phosphate absorption in the small intestine (the main action)
increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ ATPase pump)
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increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca ATPase pump)
increase renal phosphate reabsorption
inhibit 1-alpha-hydroxylase activity in the kidneys (negative feedback)
affect bone remodelling to bring about the conditions of high calcium and phosphate optimum for bone
remineralisation
dietary de ciency
malabsorption e.g. coeliac disease
lack of sun exposure
chronic kidney disease
liver failure
anticonvulsant therapy
hypoparathyroidism
a) Conn’s syndrome
b) Pheochromocytoma
c) SIADH
d) Renal artery stenosis
e) Acromegaly
Something wrong?
Which of the following stimulates thyroid-stimulating hormone (TSH) release from the
anterior pituitary:
Thyroid-stimulating hormone (TSH) acts on the thyroid gland to stimulate thyroid hormone (T3 and T4) release.
TSH secretion is inhibited by raised serum levels of T3 or T4, somatostatin, dopamine, glucocorticoids, acute non-
thyroidal illness and increased human chorionic gonadotrophin (e.g. in early pregnancy).
TSH de ciency results in hypothyroidism. Excess TSH (extremely rare) results in hyperthyroidism.
The adrenal cortex is controlled by the pituitary gland, responding to adrenocorticotrophic (ACTH) hormone.
It is functionally and anatomically divided into three zones of tissue which each secrete different steroid hormones:
What is the most likely diagnosis in a 46-year old woman presenting with buccal
hyperpigmentation, postural hypotension and hyperkalaemia:
a) Pheochromocytoma
b) Conn’s syndrome
c) Cushing’s syndrome
d) Congenital adrenal hyperplasia
e) Addison’s disease
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e) Addison’s disease
Something wrong?
Primary insuf ciency of the adrenal cortex is called Addison’s disease, it is characterised by de cient secretion of both
glucocorticoids and mineralocorticoids.
Causes include:
postural hypotension
hyponatraemia
hyperkalaemia
hypoglycaemia
tendency for hypercalcaemia
weight loss
abdominal pain/constipation/nausea
muscle weakness
fatigue
lethargy
dizziness
depression
An acute exacerbation of Addison’s disease is called an adrenal crisis. It is a life-threatening emergency characterised
by: hypotensive shock, hypovolaemic shock and hypoglycaemia.
Acute adrenocortical failure may occur if long-term high-dose steroid treatment is stopped abruptly (as the prolonged
steroid treatment has suppressed natural ACTH release). Secondary adrenocortical insuf ciency may also be caused
by disorders of the hypothalamus and anterior pituitary gland due to de ciency of CRH or ACTH.
a) Sedating antihistamines
b) Amiodarone
c) Carbimazole
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c) Carbimazole
d) Lithium
e) Phenytoin
Something wrong?
Hypothyroidism is de ned as an underactive thyroid gland leading to de cient thyroid hormones. T3 and T4 levels are
low and TSH levels are usually high.
Causes include:
overtreatment of hyperthyroidism (e.g. radioactive ablation, surgical removal or anti-thyroid drugs e.g.
carbimazole)
drugs e.g. amiodarone, lithium, anticonvulsants, levodopa
Hashimoto’s thyroiditis
De Quervain (subacute) thyroiditis
primary atrophic hypothyroidism
severe iodine de ciency
TSH de ciency from hypopituitarism
disruption of the hypothalamic-pituitary-thyroid axis
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TSH levels are normally elevated, low TSH levels suggest secondary hypothyroidism which is much less common.
Acromegaly is a result of excess growth hormone (GH) secretion from the anterior pituitary gland, most commonly as a
result of a GH-secreting pituitary adenoma.
Calcitonin is secreted by the parafollicular cells in the thyroid gland. Calcitonin is secreted in response to rising or high
blood calcium levels and acts to lower circulating levels of calcium.
Calcitonin acts on the kidneys to inhibit reabsorption of calcium and phosphate and on the bones to inhibit osteoclast
activity and thus bone resorption of calcium and phosphate.
Which of the following pituitary hormones is NOT paired correctly with its main target
organ(s):
a) Oxytocin – Uterus
b) Luteinising hormone – Gonads
c) Thyroid-stimulating hormone – Thyroid
d) Prolactin – Mammary glands
e) Antidiuretic hormone – Adrenal cortex
Something wrong?
“The pituitary gland is primarily divided into two functional lobes, the anterior pituitary (adenohypophysis) and the
posterior pituitary (neurohypophysis).
The following hormones are secreted from the anterior pituitary gland:
This can be remembered using the mnemonic: Fresh Pituitary Tastes Almost Like Guinness.
Antidiuretic hormone (ADH) and Oxytocin are secreted from the posterior pituitary gland.
The following pituitary hormones are matched with their main target tissue(s):
In the absence of adequate amounts of insulin, the body is unable to use glucose for energy and so fatty acids are
released from adipose tissue and converted to ketone bodies by the liver. The ketone bodies are acidic and result in a
metabolic acidosis (and ketonaemia and ketonuria).
The excess glucose (due to decreased cellular glucose uptake) and the ketone bodies cause an osmotic diuresis
resulting in dehydration and a loss of electrolytes (sodium, potassium, chloride, calcium, magnesium, phosphate).
lethargy
vomiting
anorexia
abdominal pain
acetone smell on the breath
ketonuria
polydipsia
polyuria
dehydration
hyperventilation (Kussmaul breathing)
shock
reduced consciousness
coma
death
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The most common precipitating factors in the development of DKA are infection, myocardial infarction, trauma or
omission of insulin.
The management of DKA requires the administration of insulin, uids and potassium (despite apparently normal serum
potassium levels).
Which of the following is the most common cause of Cushing’s syndrome in adults:
1. excess secretion of ACTH or CRH (e.g. ACTH secreting pituitary adenoma, ectopic ACTH secretion by small-
cell carcinoma of the lung or bronchial carcinoid tumour)
2. excess secretion of cortisol (e.g. adenoma of the adrenal cortex (most common cause of Cushing’s syndrome in
children) or adrenal carcinoma)
3. exogenous steroids (most common cause of Cushing’s syndrome in adults).
hair thinning
male-pattern baldness
cataracts
truncal obesity
striae
dorsocervical fat pad (buffalo-hump)
moon face
acne
hirsutism
hypertension
skeletal muscle weakness and wasting
peptic ulceration
renal calculi
menstrual disturbance
osteoporosis and associated increased risk of fracture/vertebral collapse
skin thinning, easy bruising, tendency to skin infections
ankle oedema
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ankle oedema
glucose intolerance/DM
predisposition to congestive cardiac failure
depression/confusion/insomnia/psychosis
Which of the following hormones is released in direct response to high plasma [K+]:
a) Antidiuretic hormone
b) Aldosterone
c) Cortisol
d) Adrenocorticotrophic hormone
e) Renin
Something wrong?
angiotensin II
a fall in extracellular uid volume (via the RAAS)
a fall in plasma Na+ (via the RAAS)
high plasma K+
ACTH
ACTH is less important as a regulator, so pituitary failure does not severely impair aldosterone secretion. Aldosterone
acts mainly on the distal convoluted tubule (DCT) and the collecting duct of the kidney to cause increased reabsorption
of sodium ions in exchange for potassium and hydrogen ions (via stimulation of Na+ pumps, Na+/H+ antiporters, and Na
+ and K+ channels in principal cells, and H+ ATPase in intercalated cells).
Water is also reabsorbed and blood volume therefore increased. Increased K+ excretion lowers plasma K+ levels.
Aldosterone also stimulates Na+ conservation by the mucosal cells of the colon and gastric glands and by the sweat
and salivary gland ducts.
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Defective mineralisation is mostly due to reduced calcium and phosphate levels in the extracellular uid due to vitamin
D de ciency.
bone pain
bones appear thin on X-ray with localised radiolucencies
increased susceptibility to fractures
features of hypocalcaemia
ADH release from the posterior pituitary is directly stimulated by which of the following:
Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
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stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
Which of the following is the most common cause of Addison’s disease in the UK:
a) Tuberculosis infection
b) Autoimmune adrenalitis
c) Adrenal carcinoma
d) Waterhouse-Friderichsen syndrome
e) Amyloidosis
Something wrong?
Primary insuf ciency of the adrenal cortex is called Addison’s disease, it is characterised by de cient secretion of both
glucocorticoids and mineralocorticoids.
Causes include:
postural hypotension
hyponatraemia
hyperkalaemia
hypoglycaemia
tendency for hypercalcaemia
weight loss
abdominal pain/constipation/nausea
muscle weakness
fatigue
lethargy
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lethargy
dizziness
depression
An acute exacerbation of Addison’s disease is called an adrenal crisis. It is a life-threatening emergency characterised
by: hypotensive shock, hypovolaemic shock and hypoglycaemia.
Acute adrenocortical failure may occur if long-term high-dose steroid treatment is stopped abruptly (as the prolonged
steroid treatment has suppressed natural ACTH release). Secondary adrenocortical insuf ciency may also be caused
by disorders of the hypothalamus and anterior pituitary gland due to de ciency of CRH or ACTH.
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
a) Angiotensin II
b) Renin
c) ADH
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c) ADH
d) Cortisol
e) CRH
Something wrong?
angiotensin II
a fall in extracellular uid volume (via the RAAS)
a fall in plasma Na+ (via the RAAS)
high plasma K+
ACTH
ACTH is less important as a regulator, so pituitary failure does not severely impair aldosterone secretion. Aldosterone
acts mainly on the distal convoluted tubule (DCT) and the collecting duct of the kidney to cause increased reabsorption
of sodium ions in exchange for potassium and hydrogen ions (via stimulation of Na+ pumps, Na+/H+ antiporters, and Na
+ and K+ channels in principal cells, and H+ ATPase in intercalated cells).
Water is also reabsorbed and blood volume therefore increased. Increased K+ excretion lowers plasma K+ levels.
Aldosterone also stimulates Na+ conservation by the mucosal cells of the colon and gastric glands and by the sweat
and salivary gland ducts.
Cushing’s disease refers to the speci c condition of excess corticosteroids as a result of increased ACTH due to a
pituitary adenoma; the negative feedback that normally prevents excess ACTH secretion is absent in the tumour.
Cushing’s disease is associated with hyperpigmentation due to the melanocyte-stimulating action of ACTH.
Graves’ disease is an autoimmune disease, in which autoantibodies against TSH receptors are produced. These
antibodies bind to and stimulate these TSH receptors leading to an excess production of thyroid hormones. T3 and T4
levels are elevated, and TSH levels are low due to negative feedback.
hyperthyroidism
pretibial myxoedema
clubbing (thyroid acropachy)
eye changes
Graves’ eye disease may include features of: exophthalmos, lid retraction, lid lag, diplopia, corneal ulcers.
a) Polyuria
b) Polydipsia
c) Weight loss
d) Palpitations
e) Blurred vision
Something wrong?
Fasting levels of glucose are normally 3.9 – 5.5 mmol/L, random levels are normally < 11 mmol/L.
Glucose homeostasis is primarily maintained by the interplay between insulin and glucagon. Insulin is the only
hormone that can lower glucose levels but adrenaline, cortisol and growth hormone, can raise levels in addition to
glucagon (by stimulating glycogenolysis and gluconeogenesis).
Hyperglycaemia is de ned as a fasting level of glucose > 7 mmol/L. (Levels < 6 mmol/L are normal, levels 6 – 6.9 mmol/L
demonstrate impaired fasting glycaemia, and levels >= 7 mmol/L are diagnostic of diabetes).
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Hyperglycaemia may occur in diabetes mellitus type 1 due to a de ciency of insulin (due to autoimmune destruction of
β-cells), in diabetes mellitus type 2 due to a insuf ciency of insulin and/or insulin resistance or due to secondary causes
of diabetes.
Cushing’s syndrome
thyrotoxicosis
pheochromocytoma
acromegaly
glucagonoma
cirrhosis
chronic pancreatitis
cystic brosis
pancreatectomy
haemochromatosis
pancreatic carcinoma
thiazide diuretics
corticosteroid use.
polyuria
glycosuria
dehydration
polydipsia
tendency to infections
lethargy
weight loss
wasting
blurred vision
weakness
A patient who has been hospitalised with an intracranial bleed has become progressively
more confused. He is found to be euvolaemic and normotensive with a poor urine output and
hyponatraemia. What is the most likely diagnosis:
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Syndrome of inappropriate ADH secretion (SIADH) causes water retention resulting in hypo-osmotic hyponatraemia.
Patients are euvolaemic and normotensive with normal thyroid and adrenal function.
Neurological:
tumour
trauma
infection
Guillain-Barré syndrome
multiple sclerosis
systemic lupus erythematosus
intracranial haemorrhage
sinus thrombosis
AIDS
porphyria
Pulmonary:
small-cell lung cancer
mesothelioma
pneumonia
abscess
cystic brosis
asthma
tuberculosis
positive-pressure ventilation
Other malignancy:
oropharyngeal
stomach
pancreas
leukaemia
lymphoma
thymoma
genitourinary tract cancers
Drugs: chlorpropamide, carbamazepine, selective serotonin reuptake inhibitor (SSRI) antidepressants,
tricyclic antidepressants, lithium, MDMA/ecstasy, tramadol, haloperidol, vincristine, desmopressin,
uphenazine.
Miscellaneous: idiopathic, hereditary, pain, postoperative, stress, endurance exercise and marathon
runners, dermatomal herpes zoster.
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runners, dermatomal herpes zoster.
Calcitonin is secreted by the parafollicular cells in the thyroid gland. Calcitonin is secreted in response to rising or high
blood calcium levels and acts to lower circulating levels of calcium.
Calcitonin acts on the kidneys to inhibit reabsorption of calcium and phosphate and on the bones to inhibit osteoclast
activity and thus bone resorption of calcium and phosphate.
Vitamin D (cholecalciferol) is absorbed by the small intestine as part of the diet or is synthesised from cholesterol in
skin.
Cholecalciferol is converted to calcifediol by 25-hydroxylase in the liver. This is converted to activated vitamin D (1, 25
– dihydroxycholecalciferol or calcitriol) by 1-alpha-hydroxylase in the kidney. The enzyme 1-alpha-hydroxylase is
stimulated by parathyroid hormone (PTH) and by low concentrations of phosphate.
increase calcium and phosphate absorption in the small intestine (the main action)
increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ ATPase pump)
increase renal phosphate reabsorption
inhibit 1-alpha-hydroxylase activity in the kidneys (negative feedback)
affect bone remodelling to bring about the conditions of high calcium and phosphate optimum for bone
remineralisation
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remineralisation
dietary de ciency
malabsorption e.g. coeliac disease
lack of sun exposure
chronic kidney disease
liver failure
anticonvulsant therapy
hypoparathyroidism
angiotensin II
a fall in extracellular uid volume (via the RAAS)
a fall in plasma Na+ (via the RAAS)
high plasma K+
ACTH
ACTH is less important as a regulator, so pituitary failure does not severely impair aldosterone secretion. Aldosterone
acts mainly on the distal convoluted tubule (DCT) and the collecting duct of the kidney to cause increased reabsorption
of sodium ions in exchange for potassium and hydrogen ions (via stimulation of Na+ pumps, Na+/H+ antiporters, and Na
+ and K+ channels in principal cells, and H+ ATPase in intercalated cells).
Water is also reabsorbed and blood volume therefore increased. Increased K+ excretion lowers plasma K+ levels.
Aldosterone also stimulates Na+ conservation by the mucosal cells of the colon and gastric glands and by the sweat
and salivary gland ducts.
a) Stimulates gluconeogenesis
b) Increases proteolysis
c) Stimulates lipolysis
d) Increases calcium reabsorption in the kidneys
e) Suppresses immune cells
Something wrong?
Cortisol is secreted from the zona fasciculata of the adrenal cortex. Cortisol release is stimulated by
adrenocorticotrophic hormone (ACTH) from the anterior pituitary, which in turn is released in response to
corticotrophin-releasing hormone (CRH) from the hypothalamus.
Cortisol has a negative feedback effect on the hypothalamus and the anterior pituitary gland. Cortisol release displays
a circadian rhythm, with the highest levels in the early morning, peaking around 6 a.m. ACTH and thus cortisol release
is stimulated by physical and psychological stressors (e.g. trauma, haemorrhage, fever).
raise blood glucose by stimulating gluconeogenesis and inhibiting peripheral glucose uptake
increase protein breakdown in skeletal muscle, skin and bone to release amino acids
stimulate lipolysis to increase fatty acid levels in the blood
suppress the action and production of immune cells
suppress the secretion of the anterior pituitary hormones
weakly increase retention of sodium and water (a predominantly mineralocorticoid action)
regulate calcium levels by decreasing calcium absorption from the gut
increasing calcium excretion from the kidneys and increasing calcium resorption from bone
in uence behaviour and cognitive function
Hyperaldosteronism causes sodium and water retention (with volume expansion and hypertension) with increased
excretion of potassium and hydrogen ions.
hypertension
hypokalaemia
metabolic alkalosis
polyuria and polydipsia
muscle weakness and spasm
N.B. Hypernatraemia rarely occurs due to other regulating mechanisms.
Conn’s syndrome is the most common cause of primary hyperaldosteronism, in which patients have an adenoma of the
zona glomerulosa of the adrenal cortex.
In primary hyperaldosteronism, renin levels will be low due to negative feedback. High renin levels suggest secondary
hyperaldosteronism e.g. secondary to excessive diuretic therapy (most common cause), congestive heart failure, renal
artery stenosis, nephritic syndrome or cirrhosis with ascites.
Pituitary insuf ciency (hypopituitarism) often presents with insidious onset depression, tiredness and hypogonadism.
compression of the pituitary by a non-functioning pituitary macroadenoma (most common type of pituitary
tumour)
compression of the pituitary by other local tumours e.g. craniopharyngioma, glioma, meningioma or
metastases (particularly from the breast, bronchus and kidney)
infarction of the pituitary gland e.g. Sheehan’s syndrome caused by hypovolaemic shock during obstetric
haemorrhage
empty sella syndrome
in ammatory/in ltrative processes e.g. sarcoidosis
haemochromatosis
infective processes e.g. TB, syphilis
pituitary hypoplasia or aplasia
head injury
congenital e.g. Kallman’s syndrome
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Vitamin D (cholecalciferol) is absorbed by the small intestine as part of the diet or is synthesised from cholesterol in
skin.
Cholecalciferol is converted to calcifediol by 25-hydroxylase in the liver. This is converted to activated vitamin D (1, 25
– dihydroxycholecalciferol or calcitriol) by 1-alpha-hydroxylase in the kidney. The enzyme 1-alpha-hydroxylase is
stimulated by parathyroid hormone (PTH) and by low concentrations of phosphate.
increase calcium and phosphate absorption in the small intestine (the main action)
increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ ATPase pump)
increase renal phosphate reabsorption
inhibit 1-alpha-hydroxylase activity in the kidneys (negative feedback)
affect bone remodelling to bring about the conditions of high calcium and phosphate optimum for bone
remineralisation
dietary de ciency
malabsorption e.g. coeliac disease
lack of sun exposure
chronic kidney disease
liver failure
anticonvulsant therapy
hypoparathyroidism
You are asked to assess a patient with hyponatraemia. They are hypovolaemic with a low
plasma osmolality, and a urinary sodium of > 20 mmol/L, which of the following is the most likely
cause of their hyponatraemia:
Hyponatraemia is de ned as a serum sodium concentration of below the reference interval of 133 – 146 mmol/L. A Na
+ concentration < 120 mmol/L is considered severe.
Hyponatraemia can arise either because of a primary loss of sodium ions (in excess of water loss) or more commonly,
due to increased retention of water relative to sodium which effectively dilutes the concentration of sodium (both are
associated with a decrease in plasma osmolality).
Patients with hyponatraemia can be divided into three categories on the basis of their ECF volume.
Hyponatraemia in hypovolaemic patients results from a true sodium de cit (following loss of salt > water) and may be
caused by:
Hyponatraemia in euvolaemic patients results from excessive water retention either due to:
increased intake of pure water (where urine osmolality is low and urinary Na+ < 20 mmol/L) for example:
psychogenic polydipsia
inappropriate intravenous dextrose administration
inability to excrete a water load (where urine osmolality is high and urinary Na+ > 20 mmol/L) which may be
caused by:
SIADH
chronic renal disease
severe hypothyroidism
glucocorticoid de ciency e.g. anterior pituitary disease or abrupt withdrawal of long-term glucocorticoids
Hyponatraemia in oedematous patients is usually associated with a high total body sodium, but there is a greater
volume of water retained relative to sodium. Causes include:
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Diabetes insipidus (DI) may result from a de ciency of ADH secretion (cranial DI) or from an inappropriate renal
response to ADH (nephrogenic DI).
As a result, uid reabsorption at the kidneys is impaired, resulting in large amounts of hypotonic, dilute urine being
passed and subsequent polydipsia.
It is associated with elevated plasma osmolality (> 300 mOsm/kg) and low urine osmolality (< 600 mOsm/kg).
An ADH stimulation test can distinguish between cranial and nephrogenic DI, as nephrogenic DI shows an inability to
concentrate urine even after administration of ADH.
angiotensin II
a fall in extracellular uid volume (via the RAAS)
a fall in plasma Na+ (via the RAAS)
high plasma K+
ACTH
ACTH is less important as a regulator, so pituitary failure does not severely impair aldosterone secretion. Aldosterone
acts mainly on the distal convoluted tubule (DCT) and the collecting duct of the kidney to cause increased reabsorption
of sodium ions in exchange for potassium and hydrogen ions (via stimulation of Na+ pumps, Na+/H+ antiporters, and Na
+ and K+ channels in principal cells, and H+ ATPase in intercalated cells).
Water is also reabsorbed and blood volume therefore increased. Increased K+ excretion lowers plasma K+ levels.
Aldosterone also stimulates Na+ conservation by the mucosal cells of the colon and gastric glands and by the sweat
and salivary gland ducts.
a) Rheumatoid arthritis
b) Alcohol
c) Prolonged corticosteroid therapy
d) Bisphosphonate therapy
e) Smoking
Something wrong?
Osteoporosis is a disease characterised by low bone mineral density and deterioration of bone suf cient to cause bone
fragility and an increased risk of fracture (particularly hip, spine and distal radius).
It is caused by increased osteoclast activity and decreased osteoblast activity resulting in a shift towards increased
bone resorption.
post-menopausal women
family history of osteoporotic fractures
rheumatoid arthritis
thyroid disease
long-term corticosteroid use
high alcohol intake
smoking
vitamin D de ciency
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vitamin D de ciency
hyperparathyroidism
a) Hypertension
b) Hypokalaemia
c) Metabolic alkalosis
d) Hyponatraemia
e) Polyuria
Something wrong?
Hyperaldosteronism causes sodium and water retention (with volume expansion and hypertension) with increased
excretion of potassium and hydrogen ions.
hypertension
hypokalaemia
metabolic alkalosis
polyuria and polydipsia
muscle weakness and spasm
N.B. Hypernatraemia rarely occurs due to other regulating mechanisms.
Conn’s syndrome is the most common cause of primary hyperaldosteronism, in which patients have an adenoma of the
zona glomerulosa of the adrenal cortex.
In primary hyperaldosteronism, renin levels will be low due to negative feedback. High renin levels suggest secondary
hyperaldosteronism e.g. secondary to excessive diuretic therapy (most common cause), congestive heart failure, renal
artery stenosis, nephritic syndrome or cirrhosis with ascites.
The release of thyroid hormones is regulated by the anterior pituitary gland which secretes thyroid-stimulating
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The release of thyroid hormones is regulated by the anterior pituitary gland which secretes thyroid-stimulating
hormone (TSH) and the hypothalamus which secretes thyrotropin-releasing hormone (TRH).
The thyroid follicles secrete two hormones; thyroxine (T4) – a prohormone that acts as a plasma reservoir and tri-
iodothyronine (T3) – the active hormone. T3 and T4 synthesis involves the processing of tyrosine and iodine.
About 90% of thyroid hormones are secreted in the form of T4, with the remainder as T3. About 80% of the T4 is
converted to the more active T3 (under stimulation of TSH) in the liver and kidney.
Secretion of the thyroid hormones is stimulated by long-term exposure to cold temperatures acting on the anterior
pituitary, oestrogens acting on the anterior pituitary and adrenaline acting directly on the thyroid gland. Increased
serum levels of T3 inhibit secretion of TSH.
Most of the thyroid hormones in the blood are bound to plasma proteins (of these, 70% are bound to thyroid-binding
globulin (TBG) and 30% are bound to albumin), which allows them to circulate without being broken down by enzymes.
Only a fraction of the circulating thyroid hormones (about 0.1% of T4 and 1% of T3) are unbound and thus biologically
active. The thyroid hormones act to increase the basal metabolic rate and are important for growth and normal foetal
development. Effects of thyroid hormones include: increased heart rate and stroke volume, and increased lipolysis,
glycolysis and gluconeogenesis.
Fasting levels of glucose are normally 3.9 – 5.5 mmol/L, random levels are normally < 11 mmol/L.
Glucose homeostasis is primarily maintained by the interplay between insulin and glucagon. Insulin is the only
hormone that can lower glucose levels but adrenaline, cortisol and growth hormone, can raise levels in addition to
glucagon (by stimulating glycogenolysis and gluconeogenesis).
Hyperglycaemia is de ned as a fasting level of glucose > 7 mmol/L. (Levels < 6 mmol/L are normal, levels 6 – 6.9 mmol/L
demonstrate impaired fasting glycaemia, and levels >/= 7 mmol/L are diagnostic of diabetes).
Hyperglycaemia may occur in diabetes mellitus type 1 due to a de ciency of insulin (due to autoimmune destruction of
β-cells), in diabetes mellitus type 2 due to a insuf ciency of insulin and/or insulin resistance or due to secondary causes
of diabetes.
Cushing’s syndrome
thyrotoxicosis
pheochromocytoma
acromegaly
glucagonoma
cirrhosis
chronic pancreatitis
cystic brosis
pancreatectomy
haemochromatosis
pancreatic carcinoma
thiazide diuretics
corticosteroid use.
polyuria
glycosuria
dehydration
polydipsia
tendency to infections
lethargy
weight loss
wasting
blurred vision
weakness
Growth hormone (GH) acts on the liver to stimulate insulin-like growth factor (IGF) production and to oppose the
actions of insulin (amongst other effects).
GH secretion is stimulated by growth hormone-releasing hormone (GHRH) from the hypothalamus e.g. in response to
hypoglycaemia and by thyroid hormones from the thyroid gland. GH secretion is inhibited by growth hormone-
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hypoglycaemia and by thyroid hormones from the thyroid gland. GH secretion is inhibited by growth hormone-
inhibiting hormone (or somatostatin) and IGF-1.
Excess levels of GH e.g. due to a functioning pituitary adenoma results in acromegaly in adults and gigantism in
children (if excess GH occurs prior to epiphyseal fusion). GH de ciency results in dwar sm in children or adult GH
de ciency syndrome in adults.
Glucagon is synthesised in the pancreatic alpha (α) cells in the islets of Langerhans.
Glucagon secretion is stimulated by low blood glucose, amino acids, adrenaline, some gastrointestinal peptides,
sympathetic and parasympathetic innervation. Glucagon secretion is inhibited by high blood glucose, fatty acids and
ketones, insulin and somatostatin.
stimulate glycogenolysis
inhibit peripheral tissue glucose uptake
inhibit glycolysis
inhibit amino acid uptake and protein synthesis
stimulate lipolysis
stimulate gluconeogenesis
stimulate ketogenesis
a) α cells
b) β cells
c) δ cells
d) F-cells
e) Acinar cells
Something wrong?
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The endocrine cells of the pancreas are arranged in small clusters around the larger exocrine cell clusters, called acini.
The endocrine clusters are called islets of Langerhans and within them are four types of cells:
Insulin and glucagon regulate blood glucose levels, somatostatin inhibits the release of both insulin and glucagon,
pancreatic polypeptide inhibits the exocrine functions of the pancreas.
a)
Normovolaemic patients with hyponatraemia usually require replacement of sodium in the form of isotonic saline.
b) Rapid correction of hyponatraemia is associated with central pontine myelinolysis.
c) Neurological dysfunction resulting from hyponatraemia re ects crenation of cerebral cells.
d) Seizures and focal neurological signs are commonly seen in hyponatraemia of 120 mmol/L or less.
e)
Hypovolaemic patients with hyponatraemia usually require replacement of sodium in the form of hypertonic saline.
Something wrong?
Symptoms due to hyponatraemia re ect neurological dysfunction resulting from cerebral overhydration (with
progressive cell swelling and cytolysis) induced by hypo-osmolality.
They are non-speci c symptoms and include nausea, malaise, headache, lethargy, muscle cramps and weakness, ataxia
and reduced level of consciousness. Seizures, comas and focal neurological signs are not usually seen until the sodium
concentration is less than about 115 mmol/L.
In cases of hyponatraemia due to sodium depletion, there are usually signs of volume depletion. In cases of
hyponatraemia due to uid retention, patients may be euvolaemic or uid overloaded.
Hypovolaemic patients are sodium-depleted and should be given sodium in the form of isotonic saline initially.
Normovolaemic patients are likely to have normal total body sodium but are retaining uid and should be uid
restricted.
Oedematous patient have an excess of total body sodium and water, and should be given a diuretic to induce
natriuresis and be uid restricted.
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natriuresis and be uid restricted.
In acute symptomatic hyponatraemia, the use of hypertonic saline should be considered with specialist input.
Correction should not be too rapid, especially in chronic hyponatraemia, as this is may result in central pontine
myelinolysis.
a) Aldosterone
b) Angiotensin II
c) Renin
d) Antidiuretic hormone
e) Insulin
Something wrong?
Diabetes insipidus (DI) may result from a de ciency of ADH secretion (cranial DI) or from an inappropriate renal
response to ADH (nephrogenic DI).
As a result, uid reabsorption at the kidneys is impaired, resulting in large amounts of hypotonic, dilute urine being
passed and subsequent polydipsia.
It is associated with elevated plasma osmolality (> 300 mOsm/kg) and low urine osmolality (< 600 mOsm/kg).
An ADH stimulation test can distinguish between cranial and nephrogenic DI, as nephrogenic DI shows an inability to
concentrate urine even after administration of ADH.
a) Insertion of aquaporins
b) Stimulates release of renin
c) Upregulation of Na+/K+ ATPase
d) Decreases GFR by afferent arteriole vasoconstriction
e) Upregulation of Na+ channels
Something wrong?
Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
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called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
a) Pituitary adenoma
b) Hyperthyroidism
c) Polycystic ovary syndrome
d) Domperidone
e) Pregnancy
Something wrong?
Prolactin acts on the mammary glands and reproductive organs to promote growth of these organs and initiate
lactation.
Prolactin secretion is stimulated by prolactin-releasing factor (PRF) and thyrotropin-releasing hormone (TRH) from
the hypothalamus. Prolactin secretion is inhibited by dopamine secreted by the hypothalamus.
Antidiuretic hormone acts primarily at which of the following locations in the renal nephron:
a) Proximal tubule
b) Thick ascending limb of loop of Henle
c) Thin ascending limb of loop of Henle
d) Descending limb of loop of Henle
e) Collecting ducts
Something wrong?
Antidiuretic hormone is synthesised in the hypothalamus and stored in secretory granules in the posterior pituitary.
The main action on the kidneys is to increase the permeability of the distal tubule and the collecting duct to reabsorb
water and thus increase water retention and concentrate urine.
ADH binds to V2 receptors on renal principal cells and increases cAMP, causing the incorporation of water channels
called aquaporins into the apical membrane. It also has a potent vasoconstriction action at high doses.
ADH is rapidly removed from plasma, falling by about 50% in about 10 minutes, mainly due to metabolism in the liver
and kidneys.
ADH release is stimulated by raised plasma osmolality (detected by osmoreceptors in the hypothalamus which also
stimulate thirst) and a fall in blood pressure/plasma volume (detected by cardiac and vascular baroreceptors). The
osmoreceptor system is more sensitive than the baroreceptor system.
ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide
(ANP).
ADH de ciency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in
syndrome of inappropriate ADH secretion (SIADH).
Which of the following signs would you NOT expect to see in hyperthyroidism:
a) Hypore exia
b) Palmar erythema
c) Clubbing
d) Onycholysis
e) Irregularly irregular pulse
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Something wrong?
Hyperthyroidism is de ned as over activity of the thyroid gland, leading to excess thyroid hormone secretion.
Causes include:
Graves’ disease
toxic multinodular goitre
toxic adenoma
ectopic thyroid tissue
drugs e.g. amiodarone
exogenous iodine
hair loss
emotional lability
fatigue
anxiety
restlessness
goitre
palpitations
tachycardia
atrial brillation
proximal myopathy
diarrhoea
increased appetite
weight loss
tremor
heat intolerance
sweating
oligomenorrhoea/amenorrhoea
infertility
reduced libido
osteoporosis
hyperre exia
pretibial myxoedema (in Graves’ disease)
palmar erythema
clubbing
onycholysis
T3 and T4 levels are elevated, and TSH levels are usually low. A raised TSH suggests the fault lies in or above the
pituitary gland.
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The release of thyroid hormones is regulated by the anterior pituitary gland which secretes thyroid-stimulating
hormone (TSH) and the hypothalamus which secretes thyrotropin-releasing hormone (TRH).
The thyroid follicles secrete two hormones; thyroxine (T4) – a prohormone that acts as a plasma reservoir and tri-
iodothyronine (T3) – the active hormone. T3 and T4 synthesis involves the processing of tyrosine and iodine.
About 90% of thyroid hormones are secreted in the form of T4, with the remainder as T3. About 80% of the T4 is
converted to the more active T3 (under stimulation of TSH) in the liver and kidney.
Secretion of the thyroid hormones is stimulated by long-term exposure to cold temperatures acting on the anterior
pituitary, oestrogens acting on the anterior pituitary and adrenaline acting directly on the thyroid gland. Increased
serum levels of T3 inhibit secretion of TSH.
Most of the thyroid hormones in the blood are bound to plasma proteins (of these, 70% are bound to thyroid-binding
globulin (TBG) and 30% are bound to albumin), which allows them to circulate without being broken down by enzymes.
Only a fraction of the circulating thyroid hormones (about 0.1% of T4 and 1% of T3) are unbound and thus biologically
active. The thyroid hormones act to increase the basal metabolic rate and are important for growth and normal foetal
development. Effects of thyroid hormones include: increased heart rate and stroke volume, and increased lipolysis,
glycolysis and gluconeogenesis.
What is the most likely diagnosis in a 70 year old woman with rheumatoid arthritis who
presents with weight gain, moon face and resistant hypertension:
a) Cushing’s syndrome
b) Cushing’s disease
c) Pheochromocytoma
d) Conn’s syndrome
e) Renal artery stenosis
Something wrong?
1. excess secretion of ACTH or CRH (e.g. ACTH secreting pituitary adenoma, ectopic ACTH secretion by small-
cell carcinoma of the lung or bronchial carcinoid tumour)
2. excess secretion of cortisol (e.g. adenoma of the adrenal cortex (most common cause of Cushing’s syndrome in
children) or adrenal carcinoma)
3. exogenous steroids (most common cause of Cushing’s syndrome in adults).
hair thinning
male-pattern baldness
cataracts
truncal obesity
striae
dorsocervical fat pad (buffalo-hump)
moon face
acne
hirsutism
hypertension
skeletal muscle weakness and wasting
peptic ulceration
renal calculi
menstrual disturbance
osteoporosis and associated increased risk of fracture/vertebral collapse
skin thinning, easy bruising, tendency to skin infections
ankle oedema
glucose intolerance/DM
predisposition to congestive cardiac failure
depression/confusion/insomnia/psychosis
Anterior pituitary hormones are released under the control of hypothalamic releasing or inhibiting hormones
originating from small neurones with their cell bodies in the hypothalamus.
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originating from small neurones with their cell bodies in the hypothalamus.
These hypothalamic hormones are transported directly to the anterior pituitary via hypophyseal portal vessels to
stimulate or inhibit release of anterior pituitary hormones e.g. corticotrophin-releasing hormone (CRH) stimulates
release of ACTH, thyrotropin-releasing hormone stimulates release of TSH (and prolactin) and dopamine inhibits
release of prolactin.
The anterior pituitary hormones (and the hormones released by their target organs) inhibit further release of
hypothalamic and anterior pituitary hormones by negative feedback mechanisms.
The posterior pituitary is really a direct extension of the hypothalamus. Oxytocin and ADH are manufactured in the
cell bodies of neurones in the hypothalamus and are transported down the axons of these cells to their terminals on
capillaries originating from the inferior hypophyseal artery within the posterior pituitary gland.
When these neurones are activated, they release oxytocin or ADH into the general circulation. ADH release is
controlled by negative feedback mechanisms, oxytocin however is involved in positive feedback mechanisms.
a) Hypopituitarism
b) Hashimoto’s thyroiditis
c) Iodine de ciency
d) Carbimazole
e) Amiodarone
Something wrong?
Hyperthyroidism is de ned as over activity of the thyroid gland, leading to excess thyroid hormone secretion.
Causes include:
Graves’ disease
toxic multinodular goitre
toxic adenoma
ectopic thyroid tissue
drugs e.g. amiodarone, lithium rarely
exogenous iodine
hair loss
emotional lability
fatigue
anxiety
restlessness
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goitre
palpitations
tachycardia
atrial brillation
proximal myopathy
diarrhoea
increased appetite
weight loss
tremor
heat intolerance
sweating
oligomenorrhoea/amenorrhoea
infertility
reduced libido
osteoporosis
hyperre exia
pretibial myxoedema (in Graves’ disease)
palmar erythema
clubbing
onycholysis
T3 and T4 levels are elevated, and TSH levels are usually low. A raised TSH suggests the fault lies in or above the
pituitary gland.
a) Adrenaline
b) Sympathetic innervation
c) Low blood glucose
d) Somatostatin
e) Secretin
Something wrong?
Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds.
Insulin is formed from the cleaving of proinsulin (derived from preproinsulin synthesised in the rough endoplasmic
reticulum) into insulin and C-peptide in the Golgi body of β cells in the islets of Langerhans.
Since insulin and C-peptide are produced in equimolar amounts, C-peptide acts as a useful marker of β cell activity in
diabetics who receive insulin treatment.
Insulin secretion is stimulated directly by high blood glucose levels, but also by metabolites such as amino acids, fatty
acids and ketones, by glucagon, some gastrointestinal tract peptides (e.g. secretin), GH, ACTH and TSH. Insulin
secretion is inhibited by low blood glucose levels, adrenaline, somatostatin, hypocalcaemia and sympathetic
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secretion is inhibited by low blood glucose levels, adrenaline, somatostatin, hypocalcaemia and sympathetic
innervation. (N.B. insulin secretion never ceases completely, there is always a basal level of insulin in the blood)
What is the most likely diagnosis in a 65 year old patient presenting with polyuria, polydipsia,
renal failure and deteriorating sight:
It can occur in diabetes mellitus type 1 due to a de ciency of insulin (due to autoimmune destruction of beta-cells) or in
diabetes mellitus type 2 due to a insuf ciency of insulin and/or insulin resistance or in secondary causes of diabetes.
Cushing’s syndrome
thyrotoxicosis
pheochromocytoma
acromegaly
glucagonoma
cirrhosis
chronic pancreatitis
cystic brosis
pancreatectomy
haemochromatosis
pancreatic carcinoma
thiazide diuretics
corticosteroid use
Features of hyperglycaemia include polyuria, glycosuria, dehydration, polydipsia, tendency to infections, lethargy,
weight loss, wasting, blurred vision, weakness.
Osteoporosis is a disease characterised by low bone mineral density and deterioration of bone suf cient to cause bone
fragility and an increased risk of fracture (particularly hip, spine and distal radius).
It is caused by increased osteoclast activity and decreased osteoblast activity resulting in a shift towards increased
bone resorption.
post-menopausal women
family history of osteoporotic fractures
rheumatoid arthritis
thyroid disease
long-term corticosteroid use
high alcohol intake
smoking
vitamin D de ciency
hyperparathyroidism
Fasting levels of glucose are normally 3.9 – 5.5 mmol/L, random levels are normally < 11 mmol/L.
Glucose homeostasis is primarily maintained by the interplay between insulin and glucagon. Insulin is the only
hormone that can lower glucose levels but adrenaline, cortisol and growth hormone, can raise levels in addition to
glucagon (by stimulating glycogenolysis and gluconeogenesis).
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Hyperglycaemia is de ned as a fasting level of glucose > 7 mmol/L. (Levels < 6 mmol/L are normal, levels 6 – 6.9 mmol/L
demonstrate impaired fasting glycaemia, and levels >= 7 mmol/L are diagnostic of diabetes).
Hyperglycaemia may occur in diabetes mellitus type 1 due to a de ciency of insulin (due to autoimmune destruction of
β-cells), in diabetes mellitus type 2 due to a insuf ciency of insulin and/or insulin resistance or due to secondary causes
of diabetes.
Cushing’s syndrome
thyrotoxicosis
pheochromocytoma
acromegaly
glucagonoma
cirrhosis
chronic pancreatitis
cystic brosis
pancreatectomy
haemochromatosis
pancreatic carcinoma
thiazide diuretics
corticosteroid use
polyuria
glycosuria
dehydration
polydipsia
tendency to infections
lethargy
weight loss
wasting
blurred vision
weakness
a) Male-pattern baldness
b) Osteoporosis
c) Cataracts
d) Pancreatitis
e) Glucose intolerance
Something wrong?
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1. excess secretion of ACTH or CRH (e.g. ACTH secreting pituitary adenoma, ectopic ACTH secretion by small-
cell carcinoma of the lung or bronchial carcinoid tumour)
2. excess secretion of cortisol (e.g. adenoma of the adrenal cortex (most common cause of Cushing’s syndrome in
children) or adrenal carcinoma)
3. exogenous steroids (most common cause of Cushing’s syndrome in adults).
hair thinning
male-pattern baldness
cataracts
truncal obesity
striae
dorsocervical fat pad (buffalo-hump)
moon face
acne
hirsutism
hypertension
skeletal muscle weakness and wasting
peptic ulceration
renal calculi
menstrual disturbance
osteoporosis and associated increased risk of fracture/vertebral collapse
skin thinning, easy bruising, tendency to skin infections
ankle oedema
glucose intolerance/DM
predisposition to congestive cardiac failure
depression/confusion/insomnia/psychosis
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Adrenal androgens are secreted from the zona reticularis of the adrenal cortex. The main adrenal androgens are
dehydroepiandrosterone (DHEA) and androstenedione. Adrenal androgens have only weak biological activity but they
are converted to more active androgens, such as testosterone, by aromatase and other enzymes in peripheral tissues.
Aldosterone primarily acts at which of the following sites in the renal nephron:
a) Proximal tubule
b) Descending limb
c) Thick ascending limb
d) Thin ascending limb
e) Distal convoluted tubule and collecting ducts
Something wrong?
angiotensin II
a fall in extracellular uid volume (via the RAAS)
a fall in plasma Na+ (via the RAAS)
high plasma K+
ACTH
ACTH is less important as a regulator, so pituitary failure does not severely impair aldosterone secretion.
Aldosterone acts mainly on the distal convoluted tubule (DCT) and the collecting duct of the kidney to cause increased
reabsorption of sodium ions in exchange for potassium and hydrogen ions (via stimulation of Na+ pumps, Na+/H+
antiporters, and Na+ and K+ channels in principal cells, and H+ ATPase in intercalated cells).
Water is also reabsorbed and blood volume therefore increased. Increased K+ excretion lowers plasma K+ levels.
Aldosterone also stimulates Na+ conservation by the mucosal cells of the colon and gastric glands and by the sweat
and salivary gland ducts.
a) ACTH
b) ADH
c) GH
d) TSH
e) Prolactin
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Something wrong?
Anterior pituitary hormones are released under the control of hypothalamic releasing or inhibiting hormones
originating from small neurones with their cell bodies in the hypothalamus.
These hypothalamic hormones are transported directly to the anterior pituitary via hypophyseal portal vessels to
stimulate or inhibit release of anterior pituitary hormones e.g. corticotrophin-releasing hormone (CRH) stimulates
release of ACTH, thyrotropin-releasing hormone stimulates release of TSH (and prolactin) and dopamine inhibits
release of prolactin.
The anterior pituitary hormones (and the hormones released by their target organs) inhibit further release of
hypothalamic and anterior pituitary hormones by negative feedback mechanisms.
The posterior pituitary is really a direct extension of the hypothalamus. Oxytocin and ADH are manufactured in the
cell bodies of neurones in the hypothalamus and are transported down the axons of these cells to their terminals on
capillaries originating from the inferior hypophyseal artery within the posterior pituitary gland.
When these neurones are activated, they release oxytocin or ADH into the general circulation. ADH release is
controlled by negative feedback mechanisms, oxytocin however is involved in positive feedback mechanisms.
What is the most likely diagnosis in an otherwise healthy 25 year old woman who presents
with polyuria and polydipsia, with no history of weight loss. She has a past medical history of a
traumatic brain injury:
Diabetes insipidus (DI) may result from a de ciency of ADH secretion (cranial DI) or from an inappropriate renal
response to ADH (nephrogenic DI). Cranial DI may be the result of hypoxic encephalopathy, neurosurgery,
autoimmunity or cancer, or sometimes without an underlying cause (idiopathic).
As a result, uid reabsorption at the kidneys is impaired, resulting in large amounts of hypotonic, dilute urine being
passed and subsequent polydipsia.
It is associated with elevated plasma osmolality (> 300 mOsm/kg) and low urine osmolality (< 600 mOsm/kg).
An ADH stimulation test can distinguish between cranial and nephrogenic DI, as nephrogenic DI shows an inability to
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Which of the following is the most common cause of Cushing’s syndrome in children:
1. excess secretion of ACTH or CRH (e.g. ACTH secreting pituitary adenoma, ectopic ACTH secretion by small-
cell carcinoma of the lung or bronchial carcinoid tumour)
2. excess secretion of cortisol (e.g. adenoma of the adrenal cortex (most common cause of Cushing’s syndrome in
children) or adrenal carcinoma)
3. exogenous steroids (most common cause of Cushing’s syndrome in adults).
hair thinning
male-pattern baldness
cataracts
truncal obesity
striae
dorsocervical fat pad (buffalo-hump)
moon face
acne
hirsutism
hypertension
skeletal muscle weakness and wasting
peptic ulceration
renal calculi
menstrual disturbance
osteoporosis and associated increased risk of fracture/vertebral collapse
skin thinning, easy bruising, tendency to skin infections
ankle oedema
glucose intolerance/DM
predisposition to congestive cardiac failure
depression/confusion/insomnia/psychosis
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Something wrong?
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
What is the most likely diagnosis in a 55 year old woman presenting with atrial brillation,
tremor and exophthalmos:
a) Acromegaly
b) Cushing’s disease
c) Graves’ disease
d) Hashimoto thyroiditis
e) Pheochromocytoma
Something wrong?
Graves’ disease is an autoimmune disease, in which autoantibodies against TSH receptors are produced. These
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Graves’ disease is an autoimmune disease, in which autoantibodies against TSH receptors are produced. These
antibodies bind to and stimulate these TSH receptors leading to an excess production of thyroid hormones. Graves’
disease is the most common cause of hyperthyroidism.
hyperthyroidism
pretibial myxoedema
clubbing (thyroid acropachy)
eye changes including features of: exophthalmos, lid retraction, lid lag, diplopia, corneal ulcers
Insulin acts to cause all but which one of the following effects:
a) Stimulation of glycogenesis
b) Stimulation of glycolysis
c) Inhibition of proteolysis
d) Stimulation of lipolysis
e) Inhibition of gluconeogenesis
Something wrong?
Which of the following hormones is NOT secreted by the anterior pituitary gland:
a) Follicle-stimulating hormone
b) Prolactin
c) Oxytocin
d) Luteinising hormone
e) Growth hormone
Something wrong?
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The pituitary gland is primarily divided into two functional lobes, the anterior pituitary (adenohypophysis) and the
posterior pituitary (neurohypophysis).
The following hormones are secreted from the anterior pituitary gland:
This can be remembered using the mnemonic: Fresh Pituitary Tastes Almost Like Guinness.
Antidiuretic hormone (ADH) and Oxytocin are secreted from the posterior pituitary gland.
The following pituitary hormones are matched with their main target tissue(s):
You are asked to assess a patient with hypernatraemia, they are dehydrated with a raised
plasma osmolality and a serum Na+ of 160 mmol/L, which of the following is the most likely
diagnosis:
a) Conn’s syndrome
b) SIADH
c) Near-drowning
d) Addison’s disease
e) Osmotic diuresis in uncontrolled diabetes mellitus
Something wrong?
Hypernatraemia is an increase in the serum sodium concentration above the reference interval of 133 – 146 mmol/L.
Hypernatraemia may arise from either excess sodium or much more commonly from water de cit (both are associated
with a raised plasma osmolality).
Hypernatraemia can be thought of in relation to actual total body sodium. The most common group of patients are
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those with hypernatraemia with decreased body sodium through loss of both water and sodium, but with a greater
proportion of water loss which may result from:
renal losses e.g. osmotic diuresis in uncontrolled diabetes mellitus, loop diuretics, renal disease
skin losses e.g. burns, excessive sweating in hot climate or exercise
gastrointestinal losses e.g. vomiting, diarrhoea, stulae
Patients with hypernatraemia with normal total body sodium have a pure water de cit which may result from:
inadequate water intake e.g. unconscious patient, dementia, disordered thirst perception in hypothalamic
lesion
excessive pure water loss e.g. diabetes insipidus (where plasma osmolality > urine osmolality)
Hypernatraemia with an actual increase in total body sodium is rare. Mild true hypernatraemia may be caused by
primary hyperaldosteronism, but this is not typical of Conn’s syndrome, other causes include acute salt poisoning e.g.
intravenous sodium bicarbonate, hypertonic saline, high sodium feeds in infants, near drowning in salt water.
If the hypernatraemia is mild (Na ≤ 150 mmol/L) and the patient has obvious signs of dehydration it is likely the
ECF volume is reduced and that the patient has lost both sodium and water. Treatment should aim to replace
the de cit of uid by infusing isotonic saline, or if the de cit is large, hypotonic saline.
With more severe hypernatraemia (150 – 170 mmol/L), pure water loss is likely if the clinical signs of
dehydration are mild in relation to the degree of hypernatraemia – this is because pure water loss is
distributed evenly throughout the body compartments and the sodium content of the ECF is unchanged.
Treatment should be aimed at replacing water either orally, or with 5% dextrose.
With gross hypernatraemia ( > 180 mmol/L), an excess of sodium is likely, the patient may present with signs of
uid overload. Treatment may be with diuretics, or rarely, by renal dialysis.
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
a) The adrenal glands are located on the inferior pole of each kidney.
b) The adrenal glands are intraperitoneal organs.
c) The adrenal glands are enclosed in renal fascia.
d) The adrenal medulla comprises about 60% of the gland.
e) The adrenal gland is divided into two functionally distinct regions, the right and the left lobe.
Something wrong?
The adrenal glands are located on the superior pole of each kidney. The glands are retroperitoneal, covered in
perinephric fat and enclosed in renal fascia. The adrenal gland is divided into two functionally distinct regions, the
outer larger region (comprising about 90% of the gland) is called the adrenal cortex and the inner, much smaller region
is called the medulla.
The adrenal cortex is controlled by the pituitary gland, responding to adrenocorticotrophic (ACTH) hormone.
It is functionally and anatomically divided into three zones of tissue which each secrete different steroid hormones:
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It is functionally and anatomically divided into three zones of tissue which each secrete different steroid hormones:
Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to
falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium
and thereby effective reduction of blood calcium levels).
increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity)
increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the
apical membrane and the Ca2+ ATPase pump on the basolateral membrane)
increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron
inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium
from plasma proteins
stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D
indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D)
Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.
What is the most likely diagnosis in a 34 year old man presenting with a hypochloraemic
metabolic alkalosis, low serum renin and a mass in the adrenal gland:
Hyperaldosteronism causes sodium and water retention (with volume expansion and hypertension) with increased
excretion of potassium and hydrogen ions.
hypertension
hypokalaemia
metabolic alkalosis
polyuria and polydipsia
muscle weakness and spasm
N.B. Hypernatraemia rarely occurs due to other regulating mechanisms.
Conn’s syndrome is the most common cause of primary hyperaldosteronism, in which patients have an adenoma of the
zona glomerulosa of the adrenal cortex.
In primary hyperaldosteronism, renin levels will be low due to negative feedback. High renin levels suggest secondary
hyperaldosteronism e.g. secondary to excessive diuretic therapy (most common cause), congestive heart failure, renal
artery stenosis, nephritic syndrome or cirrhosis with ascites.
Hypernatraemia is an increase in the serum sodium concentration above the reference interval of 133 – 146 mmol/L.
Hypernatraemia may arise from either excess sodium or much more commonly from water de cit (both are associated
with a raised plasma osmolality).
Hypernatraemia can be thought of in relation to actual total body sodium. The most common group of patients are
those with hypernatraemia with decreased body sodium through loss of both water and sodium, but with a greater
proportion of water loss which may result from:
renal losses e.g. osmotic diuresis in uncontrolled diabetes mellitus, loop diuretics, renal disease
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Patients with hypernatraemia with normal total body sodium have a pure water de cit which may result from:
inadequate water intake e.g. unconscious patient, dementia, disordered thirst perception in hypothalamic
lesion
excessive pure water loss e.g. diabetes insipidus (where plasma osmolality > urine osmolality)
Hypernatraemia with an actual increase in total body sodium is rare. Mild true hypernatraemia may be caused by
primary hyperaldosteronism, but this is not typical of Conn’s syndrome, other causes include acute salt poisoning e.g.
intravenous sodium bicarbonate, hypertonic saline, high sodium feeds in infants, near drowning in salt water.
If the hypernatraemia is mild (Na ≤ 150 mmol/L) and the patient has obvious signs of dehydration it is likely the
ECF volume is reduced and that the patient has lost both sodium and water. Treatment should aim to replace
the de cit of uid by infusing isotonic saline, or if the de cit is large, hypotonic saline.
With more severe hypernatraemia (150 – 170 mmol/L), pure water loss is likely if the clinical signs of
dehydration are mild in relation to the degree of hypernatraemia – this is because pure water loss is
distributed evenly throughout the body compartments and the sodium content of the ECF is unchanged.
Treatment should be aimed at replacing water either orally, or with 5% dextrose.
With gross hypernatraemia ( > 180 mmol/L), an excess of sodium is likely, the patient may present with signs of
uid overload. Treatment may be with diuretics, or rarely, by renal dialysis.
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