**Endocrine**

NHS Tayside Endocrinology Web

Endocrinology articles Medscape

University of Maryland Center for Diabetes and Endocrinology

Endocrinology An Integrated Approach Nussey and Whitehead 2001 NCBI

 

Thyroid hormone physiology

 

Thyroid function tests

 

Hypothyroidism BMJ 2008;337:a801
Clinical
features
Coarse facies – dry thickened skin on face and hands, puffy eyes, sparse hair on scalp with loss of outer 1/3 eyebrows
Slow croaky monotonous speech
Slow pulse, slow ankle jerks
Primary
hypothyroidism
Commonest cause in the West is autoimmune  Hashimoto’s
Patients almost always test positive for anti-thyroid peroxidase (anti-TPO) and antithyroglobulin antibodies
Secondary
hypothyroidism
low T4 with normal TSH
due to pituitary failure
Subclinical hypothyroidismbmj/337/bmj.a834 Normal free T3 and T4, but elevated TSH.Common condition, affecting about 5-10% of women over the age of 50.Thyroxine should be started if:
Positive anti-TPO or antithyroglobulin antibodies – most will develop overt hypothyroidism eventually.The patient has been treated for Graves’ disease in the past.The patient has another organ-specific autoimmune disease.The TSH is >10 mU/l.If the patient does not fall into any of the above groups, they should  have TFTs repeated every 6 months; there is very little evidence to suggest that they will benefit from thyroxine, and the risks of osteoporosis and atrial fibrillation from unnecessary treatment should be borne in mind.

However, a trial of thyroxine could be considered

if patient symptomatic,

if the TSH is rising,

if strong FH of thyroid disease

if the patient has a goitre

The aim of treatment is to keep the TSH within the normal range

Congenital
Hypothyroidism

 

Thyroxine Replacement

Levothyroxine 50-100 mcg od, before breakfast, adjusted in 50cg steps every 3-4 weeks until normal metabolism maintained

(usual maintainance 100-150 mcg od – 200mcg  if obese).

In cardiac disease, severe hypothyroidism, and patients over 50 years, should be introduced at 25micrograms once daily, adjusted in steps of 25 mcg  every 4 weeks according to response; usual maintenance dose

After changes in dose of thyroxine, thyroid function tests should normally be repeated after approximately 8 weeks allowing steady state to be achieved. The total daily dose can usually be administered as a single dose in the morning.

It takes 6-8 weeks for the thyroid stimulating hormone (TSH) to change in response to an alteration in dosage.

Many patients don’t feel the benefit of treatment for 3 months after thyroxine is started, and complete recovery can take up to 12 months.

Once the patient is stable, their thyroid function should be checked annually.

The aim should be to keep restore free T4/T3 and  TSH within the normal range, (TSH  ideally around 1 mU/l)

 

TREATMENT-INDUCED TSH SUPPRESSION
Some patients feel very well on a dose of thyroxine that keeps the free T4 and T3 within the normal range, but causes the TSH to become suppressed.
Ideally, dose reduction should be attempted, but a proportion of these people will then become symptomatic and may need to stay on the higher dose.
There are potential harmful effects involved in treating patients in this way; there is some evidence that TSH suppression has an adverse effect on bone mass in postmenopausal women and that there is an increased incidence of atrial fibrillation. It is therefore advisable to exclude osteoporosis by ordering a DEXA scan, which may need to be repeated at regular intervals if there is an initial abnormality.
Reduce dose if:
patient develops new-onset AF, angina or heart failure
patient develops osteoporosis
serum T3 concentration is raised.

youtu.be/JYbio13fOA

Armour thyroid

 

Hyperthyroidism
Primary hyperthyroidism
Graves
autoimmune condition  more common in women 40-60.
Most patients will have TSH-receptor antibodies which bind to and stimulate the TSH receptor with a prolonged stimulatory action (LATS)70-80% will be positive for anti-TPO antibodiesMore common in females (8:1).
Hyperkinesia restlessness and fidgeting.
Prominent eyeballs (exopthalmos), lid retraction (staring eyes visible sclera and wide palpebral fissure) and lid lag (delayed movement of upper lid)
May be opthalmaplegia and diplopia, grittiness, discomfort
May be goitre  +/- bruit.
Tachycardia (+/- arrythmia AF, ST, SVT, VEBs)
Fine tremor, hot sweaty palms
clubbing (acropachy)
pretibial myxoedema  (thick raised mauve plaques with peau d’orange appearance over shins and feet)
shoulder muscle wasting (thyrotoxic myopathy- difficulty rising from chair)
Firm, smooth diffuse goitre
Toxic
multinodular
goitre
Secondary hyperthyroidism in already hyperplastic gland.
Predominance of CVS symptoms AF, heart failure
Toxic
adenoma
>eg TSH-producing pituitary adenoma
Thyroiditis Painful form usually viral
Painless especially in the postpartum period.
Usually self-limiting.

 

t3 thyrotoxicosis = normal plasma levels of thyroxine T4 but raised triiodothyronine T3.  Clinically identical

 

Anti-thyroid drugs
 Referral Hyperthyroidism should usually be referred to a secondary care facility to initiate treatment, as management options might include radioiodine treatment.
Initial GP investigations might include LATS antibodies and ultrasound
Carbimazole tablets 5mg, 20mg
Dose: 15-40mg daily, maintained until patient becomes euthyroid, usually 4-8 weeks; the dose may then be progressively reduced to a maintenance of 5-15mg daily.During carbimazole treatment, patients should be advised to report signs and symptoms of infection, especially sore throat, which may indicate bone marrow suppression.
If sensitivity (eg rash) occurs with carbimazole then propylthiouracil is an alternative.
Propylthiouracil tablets 50mg Dose: 200 – 400mg daily.
Maintain this dose until the patient becomes euthyroid.
The dose may then be gradually reduced to a maintenance dose of 50 to 150mg daily
Beta blockers Adjunct for relief of thyrotoxic symptomsNadolol tablets 40mg, 80mg Dose 80-160mg odPropranolol m/r capsules 80mg and 160mg
Dose 80mg od increased as necessary to 240mg dailySome patients may require doses up to 320mg daily (unlicensed)Nadolol produces a more reliable response, it is water soluble and is excreted unchanged.Note that carbimazole and levothyroxine can be given concomitantly in a blocking-replacement regimen, although this is NOT suitable during pregnancy.
Thyrotoxic
Crisis

 

Thyroid swelling / goitre

Midline swelling, moves with swallowing
Retrosternal extension, thyroid bruit
moves with tongue protrusion only = thyroglossal cyst
Neck, eyes, pulse, tremor, skin/hair
Proximal myopathy; reflexes

 

Thyroid screening
Patients are at increased risk of thyroid disease
Patients on lithium and amiodarone should have 6mly TFTs
Women with type 1 diabetes should have TFTs checked in the first trimester of pregnancy and post-delivery (high risk of postpartum thyroid dysfunction)
People with Down’s syndrome, Turner’s syndrome and Addison’s disease should have annual checks, as they are at risk of developing hypothyroidism.
Diabetic patients should also have an annual TFT check
Patients with AF should have a one-off test to exclude hyperthyroidism.
Patients with hyperlipidaemia and macrocytosis should also be tested as a one-off, to exclude underlying hypothyroidism

 

Thyroid cancer

Papillary

Follicular

Medullary

Anaplastic

Lymphoma

 

Parathyroid

parathyroid glands
4 glands from 4th (and 3rd) branchial arch 40 mg in wt 40mm in diameter


nelm Primary hyperparathyroidism

 

 

Hyperparathyroidism
Primary  Increased secretion of parathyroid hormone PTH from parathyroid adneoma(s), hyperplasia or rarely carcinomaMay be mild asymptomatic hypercalcaemia orpolyuria and polydypsia

renal calculi

bone pain

abdo pain

constipation

fatigue

lethargy

Secondary  Increased PTH secretion in response to hypocalcaemia (CKD, Vit D deficiency)signs and symtoms of hypocalcaemia +/- the underlying cause
Tertiary  autonomous PTH secretion following chronic secondary hyperparathyroidism.


 

Secondary hyperparathyroidism 10 Cs
calcium low
cramps
carpopedal spasm
chvostek
convulsions
cataracts
caries/cavities
crazy
cardiac arrythmias
cranial pressure raised

 

Hypoparathyroidism

  • Congenital
  • Autoimmune
  • Post thyroidectomy or parathyroidectomy
  • Pseudohypoparathyroidism
  • Hypomagnaesaemia
  • iron overload
  • Wilsons Disease

 

Pituitary

Pituitary Hormones
Anterior Pituitary  Posterior Pituitary
those giant gonads prolong the action
TSH
GH
Gonadotrophins FSH/LH
PRL
ACTH
ADH
Oxytocin
produced in the hypothalamus

 

Hypopituitarism

 

HPA Dysfunction

 

Acidophil adenoma

 

Pituitary tumours

Prolactinomas NEJM 2010;362:1219

 

Chromophobe adenoma

 

Acromegaly / gigantism
Arthropathy
Big boggy hands
CTS
DM / glycosuria
Enlarged tongue heart and throat
Fields (bitemporal hemianopia)
Gynaecomastica galactorrhoea greasy skin
Hypertension
Increasing shoe/ring/dentures/ size
Jaw enlargement and prognathism

Excess GH secretion (> 10ng/ml fasting)  from acidophilic or less commonly  chromophobic adenoma (rarely histologically normal pituitary) causing excess growth of viscera, bones, soft tissuesof the hand, supraorbital ridges, sinuses and lower jaw.

May present with: headaches, visual disturbance, paraesthesia in hands and feet, change  in hat ring or shoe size, arthralgia, sweating, DM or hypertension.

 

Diabetes insipidus

Presents like DM with polydypsia and polyuria.

May be cranial (head injury, pituitary tumours and infiltrations, meningitis and encephalitis, strokes, idiopathic and familial) or nephrogenic (CKD, lithium, electrolyte disturbance, or familal)

Diagnosis

– exclude other causes of polydisia and polyuria ( DM, hypercalcaemia, CRF, diuretic abuse, psychogenic)

– check glucose, electrolytes, Ca, U&E, plasma and urine osmolarity. (Nigh Na increased plasma osmolarity but low urine osmlolarity)

–  water deprivation test

–  CXR  – sarcoid TB

youtu.be/4iSiOyhq1l0

youtu.be/1ECDmWuqgEI

youtu.be/f0jMsVT6mVI

Diabetes Insipidus Medscape

 

SIADH
Paraneoplastic syndromes
Ca Bronchus kidney brain tumour lymphoma
Lung disease
bronchiectasis atypical Pneumonia
Cranial abnormalities
infections
head injuries
vascular
Porphyria
hypothyroidism
Drugs
chemotherapy – vincristine cyclophosphamide
neuroleptics
carbamazepine
chlorpropamide
opiates
idiopathic

Inappropriate salt excretion in prescence of hyponatraemia

Symptoms – fatigue, anorexia and weight loss.

Diagnosis
low plasma sodium and plasma osmolality
inappropriately high urine osmolality (1.2-2x plasma)
high urine Na > 20 mmol/l
urine volume 0.5-1.5l per 24hrs
no oedema
normal renal, adrenal  and thyroid function

youtu.be/SYX6-YE4jmI

youtu.be/2X9yZtftQto

youtu.be/SdbQrz7ljCo

youtu.be/mK6nQchMF9c

 

Cushings Glucocorticoid excess
ACTH dependant  ACTH independant
Hypersecretion of adrenal glucocorticosteroids
– bilateral adrenal hyperplasia due to ACTH from pituitary adenoma
– or rarely paraneoplastic syndrone
Glucocorticoid secreting primary adrenal tumouralso long term steroid use

ACTH levels suppressed – no pigmentation

Moon shaped round plethoric face.
Buffalo hump due to prominent supreaclavicular and dorsal cervical fat pads.
Truncal obesity
Purple abdominal striae.
Purpura and spontaneous bruises over extremeties
Acne and hirsuites
Hypertension

24 hr urinary cortisol
Midnight Cortisol
9 am cortisol
Dexamethasone suppression test
Plasma ACTH

 

Primary Hyperaldosteronism

Excess autonomous mineralocorticoid/aldosterone  production from adrenal adenoma with suppression of renin – Conns syndrome (also rarely Ca or Bilateral adrenal hyperplasia).

Causes renal sodium retention, K and H+ loss — hypertension, hypokalaemia, metabloic alkalosis.

youtu.be/cWMIGaGAOA4

 

Secondary Hyperaldosteronism

Renal hypoperfusion (RAS, heart failure, cirrhosis) causing raised renin levels (also rarely Renin producing tumour)

 

Friederckson Waterhouse

bilateral hemorrhage into the adrenal glands in meningococcal septicaemia leading to adrenal insufficiency

 

Adrenal Failure

Primary adrenal failure – Addisons – glucocorticoid and mineralocorticoid deficiency

Secondary adrenal failure – isolated ACTH deficiency in pituitary disease

causes glucocorticoid deficiency only

  • Causes
  • Autoimmune
  • Infiltrations – amyloid haematochromatosis
  • Infections – TB fungi
  • Haemorrhage – anticoagulants, meningococcal septicaemia
  • CAH
  • Adrenal Mets

Hypotension, hyponatraemia, hypokalaemic acidosis.

Pigmentation in buccal mucosa, scar tissue, and palmar crease due to xs ACTH

youtu.be/IYDKd75E

Other causes of buccal pigmentation
Peutz-Jegher syndrome  – AD  + multiple small intestine polyps

 

Addisonian crisis

Shock
Hypotension
Hypoglycaemia
Stupor
Terminal Coma

Seen in known cases of Addisons and meningococcal septicaemia.
Give IV hydrocortisone 100mg dextrose saline (taking blood for baseline electrolytes) and transfer ITU.

 

Phaeochromocytoma
10% multiple
10% malignant
10% adrenal / bilateral
10% extra adrenal
10% in children
10% in children

Episodes of palpitations, sweating, pallor headache associted with marked hypertension.

Catecholamine producing tumour of adrenal medulla.

Diagnosed by raised 24 hr urinary catecholamines.

May be part of  Multiple endocrine neoplasia syndrome, Von Hippel Lindau and neurofibromatosis

youtu.be/esv0u2AnID8

youtu.be/2ihZICnCQdM

 

MEN
MEN1  MEN2
PPP
parathyroidhyperplasia
pancreatictumours gastrinoma insulinoma
pituitary adenomas – prolactinoma acromegaly
TAP
Thyroid– medullary ca
Adrenal– phaechromocytoma
Parathyroid – primary hyperparathyroidism

 

Carcinoid
Cyanosis
Asthma
Rubor
Cor pulmonale
Incompetent tricuspid / pulmonary valves
Noisy Abdomen
Oedema
Indoles in stool
Diarrhoea

Facial flushing esp after alcohol /spicy food, diarrhoea. Symptoms suggest liver involvement.

Due to neuroendocrine tumour secreting serotonin and tachykinins usulally in the intestine, occ in the lung.

Rised  24 hr urinary 5 hydroxyindole acetic acid (5 HIAA) a serotonin metabolite and plasma chromogranin A.

youtu.be/HNse0G320XU

 

Adrenogenital syndrome CAH

Autosomal Recessive enzyme defects affecting synthesis of steroid hormones

eg 21 alpha hydroxylase deficiency 

Cortisol deficiency (addisonian crisis)

Aldosterone deficiency (sodium loss and hypotension)

ACTH oversecretion then excess production of 17 OH progesterone – causing virilisation.

 

or 11 beta hydroxylase deficiency

increased androgens causing virilistion

increased coticosterone and hypertension

 

Paraneoplastic syndromes (endocrine)

hacking-medschool/paraneoplastic-syndromes-oncology

Paraneoplastic syndromes Medscape

Paraneoplastic syndromes ninds.nih.gov

 

CFS Fatigue TATT MUSE

NICE CG53 CFS ME Aug 2007

QRG

Chronic fatigue syndrome could be costing UK economy £100m a year BMJ Sep 2011

CFS Medscape

MUSE Guidance

CFS BMJ 2010

CFS iTunes U University Minnesota

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