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CHAPTER11 Endocrinology
Thyroiddisease
Interpretation ofthyroid function test results Table 11.6
Table11.6 Interpretation ofthyroid function test results
Results of TFTs Interpretation Notes
TSH d, T4i Hyperthyroid
TSH i, T4d Hypothyroid TSH d if hypothyroidism is secondary to
TSH i, T4
normal
(thyrotoxic)
Subclinical
hypothyroidism
Hyperthyroidism Aects 2% ♀ and 0.2% ♂. Peak age:20– 49y. Causes:
• Graves’ disease
• Toxic nodular goitre— older ♀ with
past history of goitre
Presentation
• Weight loss
• Tremor
• Palpitations
0 In elderly patients, symptoms may be less obvious and include confusion, dementia, apathy, and depression.
Management Refer to endocrinology at presentation. Treatment:
• β- blockers e.g. propranolol, atenolol. Useful for symptom control until
antithyroid drug therapy takes eect
• Carbimazole Inhibits synthesis of thyroid hormones. Ineective for
treatment of thyroiditis. May be given short term to render a patient
euthyroid prior to surgery or treatment with radioactive iodine, or
long term (12– 18mo) to induce remission (but >50% relapse). 3/ 1000
patients have serious adverse eects— agranulocytosis, hepatitis, aplastic
anaemia, or lupus- like syndromes
• Radioactive iodine (
131
Withdraw carbimazole >4d prior to treatment and do not restart until
>3d after. Advise women of child- bearing age to avoid pregnancy for 4mo.
Most become hypothyroid (sometimes years) after treatment. Monitor
TFTs long- term. Associated with small i risk of thyroid malignancy
• Surgery Partial or total thyroidectomy— reserved for patients with large
goitres or who decline radioactive iodine. Carries risk of damage to
recurrent laryngeal nerve or parathyroids
Occasionally T4 is normal but T3 i; request T3
levels if low TSH and normal T
pituitary failure (rare)
If any symptoms (including depression and nonspecic symptoms or hypercholesterolaemia)
consider a trial of treatment.
If no symptoms, repeat after 3– 6mo and then
monitor annually
• Thyroiditis
• Amiodarone
• Kelp ingestion
• Hyperactivity
• AF
• Hyperhidrosis
• Eye changes
• Infertility
• Alopecia
I) Eects take 3– 4mo to become apparent.
4
• Warn all patients starting carbimazole to stop the drug and seek urgent
medical attention if they develop sore throat or other infection.
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THYROIDDISEASE
Hyperthyroid crisis (thyrotoxic storm) E p. 1083
Graves’ disease Most common cause of hyperthyroidism. ♀:♂
85:1. Peak age:30– 50y. Associated with smoking and stressful life events.
Autoimmune disease in which antibodies to the TSH receptor are produced.
Clinical features Hyperthyroidism; diuse goitre ± thyroid bruit due to i
vascularity; extra- thyroid features:thyroid eye disease— 25– 50% (bilateral
in >90%); pretibial myxoedema— 5%; thyroid acropachy (clubbing, nger
swelling)— rare; onycholysis— rare.
Management As for hyperthyroidism.
Thyroid eye disease Presents with:
• Eye discomfort ± protrusion
(exophthalmos and proptosis)
• Lid lag • TFTs can be i or normal.
Management Treat any hyperthyroidism. Refer to ophthalmologist. If d
acuity or loss of colour vision— refer urgently as there may be optic nerve
compression.
• Double vision/ ophthalmoplegia
(especially of upward gaze)
Hypothyroidism (myxoedema) Common— 10% ♀ >60y, ♀:♂ 88:1.
Causes Chronic autoimmune thyroiditis, post
Presentation Onset tends to be insidious and may go undiagnosed for years.
Always consider hypothyroidism when a patient has non- specic symptoms,
depression, fatigue, lethargy, or general malaise. Other symptoms— weight
i, constipation, hoarse voice, or dry skin/ hair. Signs are often absent—
there may be a goitre, slow- relaxing reexes, or non- pitting oedema of the
hands, feet, or eyelids.
Screening Check TFTs in patients:
• With persistent symptoms of tiredness/ lethargy without clear cause
• On amiodarone or with a history of
• With hypercholesterolaemia, infertility, Turner’s syndrome, depression,
dementia, obesity, DM, or other autoimmune disease
Management Patients taking thyroxine replacement are entitled to apply for
free prescriptions in England (E p. 113).
• <65y and healthy 50– 100 mcg od levothyroxine. Re- check TFTs after 4–
6wk. Adjust dose to keep TSH in the normal range. Once dose is stable
and TSH is within normal range monitor annually and if symptomatic or
worries about compliance
• If elderly or pre- existing heart disease Start 25mcg od levothyroxine
and i dose every 4– 6wk according to TFTs. Consider adding
propranolol if history of CHD as levothyroxine can provoke angina
Withdrawal oflevothyroxine Usually needed lifelong. If diagnosis is in doubt
stop and re- measure TFTs after 4– 6wk.
131
I, thyroidectomy.
131
I administration
Hypothyroid (myxoedema) coma E p. 1083
Information forpatients
British Thyroid Foundation M www.btf- thyroid.org
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CHAPTER11 Endocrinology
Hyper- andhypocalcaemia
• Checking Ca
ings) and correct for serum albumin— for every mmol/ L less than 40, a
correction of 0.02mmol/ L should be added. For example:
Calcium 2.40
Albumin 24
2+
Take an uncued sample (to avoid falsely high read-
Corrected calcium = (40 − 24)× 0.02 + 2.4
= 0.32 + 2.4=2.72
Hypocalcaemia d serum calcium (<2.15mmol/ L). Causes:
• If phosphate i CKD, hypoparathyroidism (may be congenital or
2° to thyroid or parathyroid surgery, or malignant inltration),
pseudohypoparathyroidism (insensitivity to parathyroid hormone)
• If phosphate normal or d Vitamin D deciency (osteomalacia, rickets),
malabsorption, lack of calcium in diet, overhydration, pancreatitis
Presentation May be subtle. Includes:
• Tetany
• Irritability, depression or
psychosis
• Neuromuscular excitability (tapping over parotid causes facial muscles
to contract— Chvostek’s sign)
0 Apparent hypocalcaemia may be an artefact of hypoalbuminaemia.
Management Check vitamin D levels. Supplement with calcium. Referral
may be needed to investigate/ treat the underlying cause.
• Perioral paraesthesia
• Carpo- pedal spasm (wrist exion and
ngers drawn together)
Hypercalcaemia i level of serum calcium (>2.55mmol/ L). Prevalence
81 in 500; ♂:♀ 81:3. Rare <age 50y.
Common causes (90%) Uncommon causes
• Primary hyperparathyroidism
• Malignancy (10% tumours—
usually myeloma, breast, lung,
kidney, thyroid, prostate, ovary
or colon)
Presentation Often very non- specic. May be an incidental nding. Other
symptoms:‘bones, stones, groans, and abdominal moans’.
• Tiredness
• Lethargy
• Weakness
• Mild aches and pains
• Anorexia
Management
• Treat according to cause (Figure 11.4)— malignancy (E p. 1014);
hyperparathyroidism (E p. 337)
• If diagnosis is unclear, refer to endocrinology. Urgency depends on
serum Ca2+ and severity of symptoms
• Hypercalcaemia can be fatal. If Ca2+ >3.5mmol/ L or severe symptoms,
admit for lowering of Ca2+ with forced diuresis + IV bisphosphonate.
• Weight loss
• Low mood
• Stone formation
• Nausea/ vomiting
• Chronic renal failure
• Familial benign hypercalcaemia
• Sarcoidosis
• Thyrotoxicosis
• Milk alkali syndrome
• Vitamin D treatment
• Polyuria and polydipsia
• Abdominal pain
• Constipation
(often intractable)
• Confusion
• Corneal calcication
Hypercalcaemia
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HYPER- ANDHYPOCALCAEMIA
Hyperparathyroidism i secretion of parathyroid hormone (PTH).
• Primary hyperparathyroidism Incidence 0.5/ 1000. Peak age 40– 60y.
♀:♂ 82:1. Circulating level of PTH is inappropriately high. Most
patients are hypercalcaemic (but may be normocalcaemic if coexistent
vitamin D deciency). Due to i secretion of PTH from one or both
parathyroid glands. Refer. Treatment is usually surgical. Drug treatment
(e.g. with cinacalcet) may be an option if unsuitable for surgery
• Secondary hyperparathyroidism i PTH in response to chronic
hypocalcaemia or hyperphosphataemia. Treat the underlying cause
• Tertiary hyperparathyroidism Inappropriately i PTH l iCa2+. Follows
prolonged secondary hyperparathyroidism. Most common in patients
with chronic kidney disease (especially if on dialysis) or chronic
malabsorption. Treatment may be either surgical or medical (e.g. with
cinacalcet or paricalcitol)
Familial benign hypercalcaemia Asymptomatic. Inherited condi-
tion in which serum calcium concentrations are mildly i throughout life.
Conrm (if possible) by demonstrating i Ca2+ in other family members. No
adverse consequences and no treatment needed.
Milk alkali syndrome Usually due to ingestion of OTC indigestion
remedies (e.g. Rennie® tablets). Ca2+ levels revert to normal on stopping. Investigate the reason why the patient is taking these remedies (?
peptic ulcer). Sometimes also caused by calcium supplements taken with
bisphosphonates for prophylaxis of osteoporosis— stop the calcium
supplement.
Albumin i
Urea i
Dehydration—
rehydrate and
recheck
Cued specimen—
repeat uncued
Urea normal
Albumin normal or d
d
Phosphate
or normal
Urea normal
Primary or
tertiary hyperparathyroidism
Phosphate i
or normal
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Alk phos i
Bone metastases
Sarcoidosis
Thyrotoxicosis
Figure11.4 Guide to the diagnosis of cause of hypercalcaemia (must be taken in
clinical context)
ALGRAWANY
Alk phos normal
Myeloma
Vitamin D excess
Milk alkali syndrome
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CHAPTER11 Endocrinology
Adrenaldisorders
Disorders of the adrenal cortex The adrenal cortex produces
3classes of steroids:
• Glucocorticoids e.g. cortisol
• Mineralocorticoids e.g. aldosterone
• Sex hormones e.g. androstenedione, testosterone, and oestrogen
Disorders result from disturbance in production of these steroids:
Cushing’s syndrome In the majority of cases, Cushing’s syndrome is
iatrogenic— caused by exogenous administration of prednisolone or other
corticosteroids. Non- iatrogenic Cushing’s syndrome is much rarer with annual incidence of 1– 2/ million (♀:♂ 83:1):
• 80% have a pituitary adenoma which secretes adrenocorticotrophic
hormone (ACTH) causing hypersecretion of glucocorticoids and sex
hormones (Cushing’s disease)
• 20% are due to ectopic ACTH secretion by other tumours (e.g. small
cell lung cancer) or hypersecreting tumours of the adrenal cortex
Presentation Cushing’s syndrome has high morbidity and mortality. Clinical
features include:
• Moon face (90%)
• Truncal obesity (85%)
• Hypertension (80%)
• Menstrual disturbance (80%)
• Striae and bruising (60%)
• Osteoporosis (60%)
Management
• Stop/ minimize exogenous steroids
• If no exogenous steroids and Cushing’s syndrome is suspected,
request a dexamethasone suppression test— dexamethasone 1mg po
at midnight then serum cortisol measured at 9 a.m. If <50mmol/ L
excludes diagnosis unless cortisol secretion is episodic. If ≥50mmol/ L,
check ACTH level and 24h urinary free cortisol and seek expert advice
Adrenal insuciency (Addison’s disease) May be:
• Primary— resulting from adrenal disease/ failure or
• Secondary— resulting from inadequate pituitary or hypothalamic
stimulation of the adrenal glands
In the UK, most cases result from autoimmune disease, surgery, cessation
of therapeutic corticosteroids, or failure to i steroid dose to cover stress.
Worldwide TB and AIDS are major causes.
Clinicalfeatures
• Tiredness (95%)
• Weakness (95%)
• Anorexia (95%)
• Pigmentation (buccal, palmar creases, new scars— 90%)
Presentation Can be dramatic with coma and severe hypoglycaemia
(E p. 1083— admit as an emergency) or insidious. 50% patients with
• Weight loss (90%)
• Abdominal pain (30%)
• Myalgia/ arthralgia (20%)
• Lethargy/
depression (60%)
• Hirsutism
• Acne
• Pigmentation
• DM
• Feminization in ♂
• Polyuria and
• Psychosis
• Postural hypo-
tension/ fainting (15%)
• Nausea
polydipsia
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ADRENALDISORDERS
autoimmune Addison’s disease have or will develop another autoimmune
disease (e.g. Graves’ disease, pernicious anaemia) and 5% of women develop premature ovarian failure.
Short Synacthen
250mcg Synacthen® (synthetic ACTH) IV or IM; take a further blood sample
for serum cortisol levels ½h later. If 30min cortisol level is:
• >600nmol/ L— adrenal insuciency is excluded
• 400– 590nmol/ L— the result is equivocal— repeat
• <400nmol/ L— adrenal insuciency is conrmed— check ACTH (if d
investigate pituitary function; if i investigate cause of adrenal disease)
Otherinvestigations
• Biochemical abnormalities— i K+, d Na+, d glucose (may not be
symptomatic), uraemia, i Ca2+, abnormal LFTs
• FBC— normocytic anaemia, eosinophilia, lymphocytosis
Management Refer to endocrinology, urgency depends on clinical state.
Treatment usually involves replacing decient steroids with hydrocortisone
and udrocortisone. 0 Warn patients not to stop steroids abruptly, to
tell any doctor treating them about their condition and wear Medic- Alert/
Medi- Tag bracelet in case of emergency. Double dose of hydrocortisone
prior to dental treatment or if intercurrent illness (e.g. URTI). If vomiting,
replace hydrocortisone po with IM hydrocortisone.
®
test Take 9 a.m. blood for serum cortisol levels; inject
Hyperaldosteronism Suggested by presence of i BP resistant to treat-
ment together with d K+— but normokalaemic cases are also described.
May be primary (2 out of 3 have an aldosterone- secreting adenoma), when
termed Conn’s syndrome, or secondary to excess renin secretion (e.g.
due to renal artery stenosis). If suspected, refer for endocrine assessment.
Treatment depends on the cause. 0 Rarely excess liquorice consumption
can mimic Conn’s syndrome.
Congenital adrenal hyperplasia E p. 873
Disorders ofthe adrenalmedulla
Phaeochromocytoma Rare but serious disorder aecting 0.1% hypertensive
patients. Usually caused by catecholamine- secreting tumours— 10% are bilateral, 10% extra- adrenal; 10% occur in children; 10% are malignant. May
present with a huge array of symptoms and signs. i BP may be sporadic or
sustained. Suspect in patients who:
• Are young with i BP
• Have very labile BP or sudden- onset hypertension
• Have i BP and associated headaches, sweating, and/ or palpitations
• Have other associated conditions (e.g. neurobromatosis)
Check 24h urine catecholamine/ metabolite levels (follow local laboratory
protocol). If conrmed, or strong suspicion despite −ve test, refer for specialist opinion. Treatment is usually surgical if tumour is found.
Patient advice and support
Addison’s Disease Self Help Group M www.addisons.org.uk
The Pituitary Foundation F 0117 370 1320 M www.pituitary.org.uk
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CHAPTER11 Endocrinology
Pituitaryproblems
Hypopituitarism d production of all pituitary hormones (ACTH,
growth hormone, FSH, LH, TSH, and prolactin). Causes:
• Iatrogenic— surgery/ irradiation • Infection— TB
• Tumour (may be non- secreting or secrete 1 pituitary hormone with d
secretion of the others)
• Sheehan’s syndrome— pituitary necrosis following postpartum
haemorrhage
Presentation
• Hypothyroidism
• Hypogonadism
• Anorexia
Management If suspected refer to neurology or endocrinology for further
investigation and advice on treatment.
Pituitary tumours 10% intracranial tumours. Almost all are benign.
Classied by histological type (chromophobic, acidophilic, or basophilic) or
by the hormone secreted:
• No hormone (30%)
• Prolactin (35%)
• Growth hormone (20%)
• ACTH (7%)
• Prolactin and growth hormone (7%)
• LH, FSH, and TSH (1%)
Presentation Present with symptoms caused by:
• Local pressure— bilateral hemianopia, cranial nerve palsies, headache
• Hormone secretion, and/ or
• Hypopituitarism (see earlier in this topic)
Management If suspected, refer for specialist management.
Pituitary apoplexy Rapid expansion of a pituitary tumour due to infarction
or haemorrhage. Suspect if sudden onset of headache in a patient with
a known pituitary tumour. Admit as a medical/ neurosurgical emergency.
Craniopharyngioma Tumour originating from Rathke’s pouch. 50%
present as children with local pressure eects (see ‘Pituitary tumours’).
Refer as for pituitary tumours.
Hyperprolactinaemia The most common pituitary disorder resulting
from pituitary adenoma (prolactinoma).
Presentation Tends to present earlier in ♀ than ♂. Symptoms are due to
pressure eects or i prolactin. Symptoms of i prolactin:
• ♀:loss of libido, weight gain, apathy, vaginal dryness, menstrual
disturbance, infertility, galactorrhoea
• ♂:impotence, d facial hair
Investigation Check basal plasma prolactin (ask the laboratory for conditions under which they would like the sample taken).
• Headache
• Depression
• Hair loss
• Hypotension
• Visual eld defect
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PITUITARYPROBLEMS
Other causes ofiprolactin
• Pregnancy
• Breastfeeding
• Stress
• Sleep
• Hypothyroidism
Management Exclude other causes of i prolactin. If no obvious other
cause, suspect prolactin- secreting pituitary adenoma and refer for specialist
opinion.
• Drugs— phenothiazines, metoclopramide,
domperidone, SSRIs, methyldopa,
oestrogens
• Chronic kidney disease
• Sarcoidosis
Acromegaly Rare condition due to a growth hormone secreting pitu-
itary tumour. Typical age at presentation:30– 50y.
Presentation
• Local pressure symptoms
• Changes in appearance— coarse oily skin; change in facial appearance
with coarsening of features; i foot size; i teeth spacing
• Other eects— deepening of voice, sweating, paraesthesiae, proximal
muscle weakness, progressive heart failure, goitre
• Complications— DM, i BP, cardiomyopathy, large bowel tumours
Investigation and management Check growth hormone levels. Refer to
endocrinology.
Diabetes insipidus (DI) Caused by impaired water resorption by the
kidney. 2 mechanisms:
• Cranial DI d ADH secretion from the posterior pituitary. 50%
idiopathic. Other causes:head injury, tumour, infection, sarcoidosis,
vascular, inherited
• Nephrogenic DI Impaired response of the kidney to ADH.
Causes:drugs (e.g. lithium), hypercalcaemia, pyelonephritis,
hydronephrosis, pregnancy (rare)
Presentation Polydipsia, polyuria, dilute urine, dehydration.
Investigations U&E (Na+ is often i), plasma and urine osmolality (plasma
i, urine d— ratio >1). Specialist investigations (e.g. water deprivation test)
conrm diagnosis.
Management Treat the cause.
• Cranial DI may be treated with intranasal desmopressin or surgery
• Nephrogenic DI may be treated with dietary restriction of protein and
salt and/ or bendroumethiazide
Syndrome ofinappropriate ADH (SIADH) Important cause of
hyponatraemia. Diagnosis is made by nding a concentrated urine (sodium
>20mmol/ L) in the presence of hyponatraemia (<125mmol/ L) or low
plasma osmolality (<260mmol/ kg), in the absence of hypovolaemia, oedema, or diuretics. Always requires specialist management. Causes:
• Malignancy e.g. small cell lung cancer; pancreas; lymphoma
• CNS disorders e.g. stroke; subdural haemorrhage; vasculitis (SLE)
Patient advice and support
The Pituitary Foundation F 0117 370 1320 M www.pituitary.org.uk
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Chapter12
Gastrointestinalmedicine
Assessment of abdominal pain 344
Vomiting and diarrhoea 346
Gastroenteritis and food poisoning 348
Constipation 350
Other abdominal symptoms and signs 352
Dyspepsia and H.pylori 354
Oesophageal conditions 356
Gastro- oesophageal reux and gastritis 358
Peptic ulceration 360
Gastro- oesophageal malignancy 362
Hernias 364
Appendicitis and small bowel disease 366
Colorectal cancer screening 368
Colorectal cancer 370
Other large bowel conditions 372
Anal and perianal problems 374
Patients with ostomies 376
Chronic diarrhoea and malabsorption 378
Faecal incontinence 380
Coeliac disease 382
Inammatory bowel disease 384
Irritable bowel syndrome 388
Jaundice and abnormal liver function 390
Fatty liver disease 392
Hepatitis 394
Liver failure and portal hypertension 396
Other liver disease 398
Gallbladder disease 400
Pancreatitis 402
Pancreatic tumours 404
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