Transcript Endocrinology – Shanice Richardson

Endocrinology
Shanice Richardson
www.peermedics.com
Contents
 Hyperthyroidism + thyrotoxicosis crisis
 Hypothyroidism + myxoedema crisis
 Cushing’s Syndrome
 Addison’s Disease
 Hyperaldosteronism
 Multiple Endocrine Neoplasia (MEN)
 Parathyroid pathology (Hypercalcemia)
 Phaeochromocytoma
Thyroid – HPT axis
Hyperthyroidism
 Most common cause is Grave’s disease. Others = Toxic
multinodular goitre & Amiodarone
 Characterised by Low TSH, High T4
Symptoms
• Weight loss
• Restlessness
• Heat intolerance
• Palpitations
• Increased sweating
• Pretibial
myoxedema
• Diarrhoea
• Oligomenorrhea
• Anxiety
• Tremor
• Exopthalmus
Investigations
• TFTs! – TSH + T4
• TSH receptor antibodies (90-100%
present in Grave’s Disease)
• ECG
Treatment
• Propanalol = Can be used to relieve
symptoms
• Carbimazole = anti thyroid function, reducing
thyroid hormone production.
AGRANULOCYTOSIS - Watch out for sore throat
• Radioiodine = destroys thyroid stunts child
growth and unborn fetus
• Surgery = thyroidectomy followed by
levothyroxine
Thyrotoxic Storm
 Life threatening condition
 Precipitated by infection, amiodarone, thyroxine, non
compliance with carbimazole, surgery, DKA, MI, trauma
•
•
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•
•
Symptoms
Hyperthermia
>41oC
Tachy/AF
>140bpm
NVD, Abdo pain
Agitation/psych
osis
Seizure/Coma
Investigations
• BM
• ABG
• TFT
• CRP
• Cultures
• Infection screen
• Chest Xray
• ECG
Treatment
• Immediate IV access and fluids
• IV propanolol C/I in asthmatics – esmolol
• Antithyroid drugs e.g. carbimazole/PTU for 4
hours, followed by Lugol’s solution (iodine)
• Steroids to prevent peripheral conversion of
T4 to T3
• Treat underlyingcause e.g. antibiotics
Hypothyroidism
Primary
 Iodine deficiency, Druginduced
 Hashimoto’s thyroiditis
(goitre)

Subacute thyroiditis (de
Quervains) – painful goitre
and raised ESR
Secondary
 Not enough TSH hypopituitarism
Symptoms
• Big neck (goitre)
• Reflexes reduced/slow
• Ataxia
• Dry, thin hair and skin
• Yawning/drowsy/coma
• Cold hands and reduced temperature
• Ascites +/- non pitting oedema (lids, han
• Round puffy face, obese
• Depression
• Immobile +/- ileus
• CCF
Investigations
• TFTs!
Primary = high TSH, low T4
Secondary (rare) = low/normal TSH, low T4
• Anti-TPO antibodies – positive in 90% of those with Hashimoto’s thyroiditis
Treatment
Levothyroxine (T4) , review at 12 weeks
Myxoedema Crisis
• Ultimate hypothyroid state before death
• Precipitated by: Infection, Trauma/Surgery, MI, Stroke, non compliance to
levothyroxine
Signs and symptoms
• Looks hypothroid
• Hypothermia <35.5oc
• Bradycardia
• Low blood pressure
• Respiratory depression
• Confusion/Psychosis
• Seizure/Coma
• Intestinal obstruction
• Hypoglycaemia
Investigations
• BM
• ABG
• TFT
• CRP
• Cultures
• Infection screen
• Chest Xray
• ECG
Treatment
• ITU for ventilation
• Fluids, oxygen
• Correct hypoglycemia
• IV T3 slowly
• IV hydrocortisone
• Antibiotics to treat infective cause
• ACTIVE WARMING
Cushing’s Syndrome
Chronic glucocorticoid excess from the adrenal glands, resulting in hypercortisolism
Causes
• ACTH dependent = Cushing’s disease (pituitary tumour secreting ACTH
producing adrenal hyperplasia)
• ACTH independent = Steroids, adrenal adenoma
Signs and symptoms

Buffalo neck hump

Moon face – facial plethora

Central obesity - “lemon on a
stick”

Purple striae

Acne

Hirsutrism

Cellulitis

Thin skin

Bitemporal hemianopia

Osteoporosis

Tiredness

Depression

Diabetes

Hyperpigmentation
(Ahmed Al-Naher)
Investigations
• Dexamethasone suppression test
• 24hr urinary free cortisol
• MRI pituitary
Treatment
• If iatrogenic, remove steroids
• Medications = ketoconazole/metyrapone acts as a cortisol inhibitor
• Surgery - leading cause is cushing’s disease, removal of pituitary adenoma
Addison’s disease
Adrenal insufficiency, caused by autoimmunity in 80% of cases.
Global glucocorticoid and mineralocorticoid insufficiency. (reduction in cortisol and aldo
Signs and symptoms
• Hyperpigmentation
• Tiredness
• Tearful, weakness
• Anorexia
• Faints
• Depression
• N+V
• Abdominal pain
• Postural hypotension
• Hypoglycaemia
Investigations
FBC/U&E – low Na+ and high K+ due to lack of mineralcorticoid (aldosterone)
Glucose – reduced due to a lack of cortisol
Short synacthen (ACTH) test - Adrenal insufficiency is generally excluded if:
The 30 minute increment in serum cortisol is >200 nmol/L
The maximum serum cortisol level is >550 nmol/L
Treatment
• Replace glucocorticoids with hydrocortisone 15-25mg daily
Must warn patients of abruptly stopping steroids.
Steroid intake should be increased before strenuous activity/exercise
• Replace mineralocorticoids with fludrocortisone daily
Hyperaldosteronism
Excess production of aldosterone independent of the RAAS system.
Commonly caused by Conn’s syndrome or bilateral idiopathic adrenal hyperplasia
Role of aldosterone
• Na+ and Cl- reabsorption
• K+ excretion
• H20 retention
Condition will result in increased
sodium and water retention aswell as
decreased renin production.
Signs and symptoms
Polyuria
Polydipsia
Hypertension
Signs of hypokalemia – weakness, tiredness, muscle cramps
Alkalosis
Investigations
• U&Es, Renin and aldosterone levels – if on diuretics, anti-hypertensives,
steroids, potassium or laxatives, withhold for 4 weeks before testing
• High resolution CT abdomen
• Adrenal vein sampling
Treatments
Conn’s : Laparascopic adrenalectomy
Bilateral adrenocortical hyperplasia: aldosterone anatagonist e.g.
spironalactone/amiloride/eplerone
Parathyroid
• Parathyroid hormone
• Reduction in serum calcium/increased phosphate
• Increases serum calcium, decreases phosphate via the bones,
kidney and small intestine
Hyperparathyroidism
Primary
 80% solitary adenoma, 20% hyperplasia of all 4 glands
 Associated with MEN
Secondary
 Parathyroid hyperplasia and a result of low calcium,
normally always caused by chronic renal failure
Tertiary
 A result of ongoing secondary hyperparathyroidism, but the
secondary cause has been resolved. Usually 4 gland
hyperplasia
Signs and Symptoms
 Depends if primary/secondary, and how long it has been
going on for, but for exam purposes…
“BONES, STONES, ABDOMINAL GROANS and
PSYCHIC MOANS”
 Bone pain/Fracture
 Renal stones
 Peptic
ulceration/constipation/pancreatitis
 Polydipsia/Polyuria
 Hypertension
 Depression
Investigations
Bloods – FBC, U&E

high Ca2+

high PTH

low phosphate (unless in renal
failure)

High ALP
Imaging

Osteopenia

Erosion of terminal phalangeal
tufts

Sub periosteal resorption

Renal osteodystrophy
(secondary)
Management
Conservative:
• Increase fluid intake to prevent stones
• Avoid thiazides
• Reduce calcium and vit D intake
Surgery indications (primary):
• Elevated serum calcium >1mg/dL above
normal
• Hypercalciuria >400mg/day
• Creatinine clearance <30% compared with
normal
• Episode of life threatening hypercalcemia
• Nephrolithiasis
• Age <50 years
• Neuromuscular symptoms
• Reduction in BMD , T score lower than -2.5
Excision of adenoma or all 4 glands
S/E: Hypoparathyroidism, recurrent laryngeal
nerve damage
Secondary
Phosphate binders
Vit D
Multiple Endocrine Neoplasia
Autosomal dominant inheritance, causing the formation of functioning hormoneproducing tumours in multiple organs
3P’s
MEN1
gene
Parathyroid (95%)
Pituitary (70%)
Pancreas (50%) insulinoma,
gastrinoma
Most common presentation is
symptoms of:
Hypercalcemia
Acromegaly
Cushings
Prolactinoma
Anaemia
Weight loss
Raised plasma glucose
MEN type IIa
RET
oncogen
e
2P’s, 1T
Parathyroid (60%)
Phaechromocytoma
Medullary Thyroid Cancer (70%)
Most common presentation is
symptoms of:
Thyroid mass
Diarrhoea
Agression
Raised plasma calcitonin
Hypercalcemia
MEN type IIb
RET
oncogen
e
1P, 1T
Phaechromocytoma (50%)
Medullary Thyroid Cancer (100%)
MARFANOID
NEUROMAS
Most common presentation is
symptoms of:
Visible lumps
Muslce hypotonia
Chronic constipation
Phaechromocytoma
symptoms
MEN management
 Most treatable form of pancreatic neoplasia and
hypercalcemia
 Surgical exicision of tumours where possible, plus
symptomatic relief
 Surveillance for development of additional tumours
 Family screening by serum calcium in MEN1, and
genetic testing for RET mutations in MEN2
Phaeochromocytoma
Catecholamine producing tumour of the
adrenal cortex (adrenaline,
noradrenaline,dopamine)
Symptoms
Severely hypertensive – episodic or sustained
Headaches
Palpitations
Sweating
Anxiety
Investigations
24hr urine collection
CT imaging?
Management
Surgery with alpha & beta blockade
Quiz
1) Name 5 (or more) signs/symptoms of Cushing’s
Syndrome
2) A 33 year old female is referred by her GP with
thyrotoxicosis. Following a discussion of
management options she elect to have
radioiodine therapy. Which one of the following is
the most likely adverse effect?
1) Hypothyroidism
2) Thyroid Malignancy
3) Agranulocytosis
4) Oesophagitis
3) A 36 year old woman presents feeling cold all
the time. On examination a firm, non-tender
goitre is noted. Blood test reveal:
TSH 34.2 mU/l (0.5-5.5mu/l)
Free T4 5.4 pmol/l (9-18pmol/l)
What is the most likely diagnosis?
1) Primary atrophic hypothyroidism
2) Pituitary failure
3) De Quervain’s thyroiditis
4) Iodine deficiency
5) Hashimoto’s thyroiditis
4) A 20 year old woman presents to the ED
feeling drowsy and with generalised abdominal
pain. Her blood pressure is 94/30mmHg. U&Es
show:
1) Gastroenteritis
2) Addisonian crisis
3) Intra-abdominal haemorrhage
4) Ecstasy abuse
5) T1DM
Which one of the following is most likely to be
seen in a patient with multiple endocrine
neoplasia (MEN) type 1?
1) Phaeochromocytoma
2) Insulinoma
3) Marfanoid body habitus
4) Medullary thyroid carcinoma
5) RET gene