JM Chapter 14 Flashcards
TSH receptor antibodies (TR Ab):
Graves disease
Thyroid peroxidase antibodies (TPO Ab):
Hashimoto disease
Thyroglobulin antibody (Tg Ab):
Hashimoto disease
The term refers to the accumulation of mucopolysaccharide in subcutaneous
tissues.
Tiredness +HUSKY VOICE + cold intolerance
Myxoedema
Common causes of primary hypothyroidism include
radioactive iodine treatment, thyroid surgery
and Hashimoto 1thyroiditis
Patients at risk for primary hypothyroidism
Previous Graves disease
Autoimmune disorders (e.g.autoimmune lymphocytic thyroiditis, rheumatoid arthritis, type 1
diabetes)
Down syndrome
Turner syndrome
Drug treatment: lithium, amiodarone, interferon, iodine
Previous thyroid or neck surgery
Previous radioactive iodine treatment of the thyroid
Clinical Features of Primary hypothyroidism
Constipation
Cold intolerance
tiredness/lethargy/somnolence
physical slowing
mental slowing
depression
huskiness of voice
puffiness of face and eyes
pallor
loss of hair
weight gain
is an autoimmune thyroiditis, is the
commonest cause of bilateral non-thyrotoxic goitre in Australia.
firm and rubbery
patients may be hypothyroid or euthyroid
Hashimoto thyroiditis, or lymphocytic thyroiditis
Confirmatory Teats:
(TPO Ab) titre
and/or fine-needle aspiration cytology.
Most common cause
of hyperthyroidsim
(Thyrotoxicosis)
Graves disease
Followed by nodular thyroid disease
What are the other causes of Hyperthryoidism ?
Graves disease (typical symptoms with a diffuse goitre and eye signs)
Autonomous functioning nodules/toxic adenoma
Subacute thyroiditis (de Quervain thyroiditis) viral origin (suspect if painful thyroid and
malaise)
Excessive intake of thyroid hormones thyrotoxicosis factitia
Exogenous iodine excess, e.g. food contamination
Amiodarone (beware of this drug)
What are the Clinical features of Hyperthyroidsm?
Heat intolerance
Sweating of hands
Muscle weakness
Weight loss despite normal or increased appetite
Emotional lability, especially anxiety, irritability
Palpitations
Frequent loose bowel motions
Physical examinations
Hyperthyroidism
Signs are (usually):
agitated, restless patient
warm and sweaty hands
fine tremor (place paper on hands)
goitre
proximal myopathy
hyperactive reflexes
bounding peripheral pulse
+ atrial fibrillation
DxT anxiety + weight loss + weakness
Thyrotoxicosis
Eye signs of
Hyperthyroidism
Lid retraction (small area of sclera seen above iris)
Lid lag
Exophthalmos
Ophthalmoplegia in severe cases
Investigations
Hyperthyroidism
T4 (and T3) elevated
TSH level suppressed
Radioisotope scan
Antithyroid peroxidase (TPO Ab) often positive
Treatment for Hypothyroidism
Levothyroxine (thyroxine) 50-100 mcg daily up to 200 mcg daily
Aim TSH levels of 0.5-2mUL
Treatment of Hyperthyroidism
Radioactive iodine therapy
Thionamide antithyroid drugs (initial doses)
*carbimazole 10-45 mg (o) daily starting with 10-20 mg in divided doses depending on
disease activity
or
*propylthiouracil 200-600 mg (0) daily in divided doses or methimazole
Adjunctive drugs:
beta blockers propranolol 10-40 mg, 6 to 8
hourly); diltiazem or atenolol are alternatives
Lithium carbonate (rarely used when there is intolerance to thionamides)
Lugol’s iodine: mainly used prior to surgery
Surgery
Page 140
What are the surgical treatment for Hyperthyroidism
Subtotal thyroidectomy or Total Thyroidectony
Thyroid enlargement may be diffuse or multinodular. Diffuse causes include physiological,
Graves disease, thyroiditis (Hashimoto or de Quervain), iodine deficiency or it can be hereditary
Goitre
Investigations include
Goitre
TFTs, needle biopsy, ultrasound and CXR.
Management
Goitre
Supportive thyroxine if TSH elevated (may lead to marked regression) and subtotal or total thyroidectomy
It is defined as a discrete lesion on palpation and/or ultrasonography that is distinct from the rest of the thyroid gland.
Thyroid nodules
Causes of Thyroid Nodules
Dominant nodule in a multinodular goitre (most likely)
Colloid cyst
True solitary nodule: adenoma, carcinoma (papillary or follicular)
Investigations
Investigations of Thyroid Nodule
Ultrasound imaging
Fine-needle aspiration cytology
Thyroid function tests
The main presentations of Thyroid carcinoma are
painless nodule,
a hard nodule in an enlarged gland or
lymphadenopathy.
Most common thyroid malignancy
Papillary carcinoma
is the investigation of choice of Thyroid Carcinoma
Fine-needle aspiration
Hyperprolactinaemia”
main causes (of many) are a pituitary adenoma (prolactinoma; micro- or macro),
pituitary stalk damage, drugs - such as
antipsychotics, various antidepressants, metoclopramide,
cimetidine, oestrogens, opiates, marijuana - and physiological causes such as pregnancy and
breastfeeding.
Clinical features
Hyperprolactinaemia
Symptoms common to males and females: reduced libido, subfertility, galactorrhoea (mainly
females)
Females: amenorrhoea/oligomenorrhoea
Males: erectile dysfunction, reduced facial
Hyperprolactinaemia
Diagnosis
Serum prolactin and macroprolactin assays
MRI:if there is headache
DxT nasal problems + fitting problems (e.g. rings, shoes) + sweating -
acromegaly
Acromegaly
Symptoms of Acromegaly
Symptoms suggestive of acromegaly include:
excessive growth of hands (increased glove size)
excessive growthof tissues (e.g. nose, lips, face)
excessive growth of feet (increased shoe size)
increased size of jaw and tongue; kyphosis
general: weakness, sweating, headaches
sexual changes, including amenorrhoea and loss of libido
disruptive snoring (sleep apnoea)
deepening voice
What is the key test fpr investigating Acromegaly?
IGF-1
Diagnosis of
Acromegaly:
:
Plasma growth hormone excess
Elevated insulin-like growth factor 1 (IGF-1) (somatomedin) the key test
X-ray skull and hands
MRI scanning pituitary
Consider associated impaired glucose tolerance/diabetes
Treatment options of
Acromegaly
Transsphenoidal pituitary microsurgery, drugs and radiotherapy
DxT weakness + polyuria + polydipsia -
diabetes insipidus
impaired secretion of vasopressin (antidiuretic hormone) from the posterior pituitary leads to
polyuria, nocturia and compensatory polydipsia, resulting in the passage of 3-20 L of dilute
urine per day.
Diabetes insipidus
Causes of diabetes insipidus (DI)
The commonest being
postoperative (hypothalamic-pituitary), which is usually transient only. Other causes of cranial
DI include tumours, infections and infiltrations.
is caused by
cancer (e.g. lung,lymphomas, kidney, pancreas), pulmonary disorders, various intracranial
lesions and drugs such as carbamazepine and many antipsychotic agents.
The syndrome of secretion of inappropriate antidiuretic hormone (SIADH)
Management of
SIADH is essentially
Fluid restriction
The treatment of DI is
Desmopressin, usually given twice daily intranasally.
This rare disorder (acute or chronic) should be considered with:
a history of postpartum haemorrhage or head injury
symptoms of hypothyroidism
symptoms of adrenal insufficiency
symptoms suggestive of a pituitary tumour
thin, wrinkled skin: ‘monkey face’
pale ‘alabaster’ skin/hairlessness
Hypopituitarism
Causes: of
HYPOPITUITARISM
Pituitary adenoma, other parasellar tumours and inflammatory/infiltratie lesions.
DXT (female): amenorrhoea + loss of axillary and pubic hair + breast
atrophy -
hypopituitarism
DXT (male): ! libido + impotence + loss of body hair -
hypopituitarism
Investigation of
hypopituitarism
Serum pituitary hormones
imaging (MRI) and
triple stimulation test
Treatment of
hypopituitarism
HRT,
surgery or
radiotherapy
Mineral corticoids, especially aldosterone
Zona glomerulosa
Glucocorticoids
Zona fasciculata
Androgens, especially DHEA
Zona reticularis
epinepherine, norepinephrine
Catecholamines
deficiency of cortisol and aldosterone
chronic adrenal insufficiency (Addison disease
cortisol excess
Cushing syndrome
DXT fatigue + a/n/v + abdominal pain (+/-Skin discolouration)
Addison
disease
The most common cause of Addison
disease
Autoimmune destruction of the adrenals
others are infection, e.g. TB
or fungal
Clinical features of Addison’s Disease
Lethargy/excessive fatigue/weakness
Anorexia and nausea
Diarrhoea/abdominal pain
Weight loss
Dizziness/funny turns, syncope:
hypoglycaemia (rare); postural hypotension (common)
Hyperpigmentation, especially mucous membranes of mouth and hard palate, skin creases of
hands
Diagnosis of Addison’s
Elevated serum potassium, low serum sodium
Low plasma cortisol level (fails to respond to synthetic adrenocorticotropic hormone [ACTH])
The short synacthen stimulation test is the definitive test
Consider adrenal autoantibodies and imaging? calcification of adrenals
Treatment of Addison’s
Corticosteroid replacement-hydrocortisone/fludrocortisone acetate, other options.
It develops because of an inability to increase cortisol in response to stress
which may include intercurrent infection, surgery or trauma.
Addisonian crisis
Clinical features
Addisonian crisis
Nausea and vomiting
Acute abdominal pain
Severe hypotension progressing to shock
Weakness, drowsiness progressing to coma
Urgent management
Addisonian crisis
Establish IV line with IV fluids
Hydrocortisone sodium succinate 100 mg IV initially and 50-100 mg 4-6 hourly until stable
Arrange urgent hospital admission
Clinical features of Cushings
Proximal muscle wasting and weakness
Central obesity, buffalo
hump on neck
Cushing facies: plethora, moon face, acne
Weakness
Hirsutism
Abdominal striae
Thin skin, easy bruising
Hypertension
Hyperglycaemia (30%)
Menstrual changes (e.g. amenorrhoea)
Osteoporosis
Psychiatric changes, especially depression
Backache
DxT plethoric moon face + thin extremities + muscle weakness -
Cushing
syndrome
Cushing syndrome
The five main causes are:
iatrogenic- chronic corticosteroid administration
pituitary ACTH excess (Cushing disease)
bilateral adrenal hyperplasia
adrenal tumour (adenoma, adenocarcinoma)
ectopic ACTH or (rarely) corticotrophin-releasing hormone (CRH) from non-endocrine
tumours (e.g. oat cell carcinoma of lung).
Diagnosis (apart from iatrogenic cause
Cushing syndrome
Cortisol excess (plasma or 24-hour urinary cortisol)
Dexamethasone suppression test
Late night salivary cortisol (2 measurements)
Inferior petrosal sinus sampling
Serum ACTH
Radiological localisation; MRI for ACTH-producing pituitary tumours; CT scanning for
adrenal tumours
Management
Cushing syndrome
Transsphenoidal excision of pituitary tumour
Ketoconazole (o) is first line.
.
Most commonly due to an adrenal adenoma
Primary hyperaldosteronism
Conn syndrome
Usually asymptomatic and hypertensive but any symptoms are features of hypokalaemia:
weakness, headaches
palpitations
cramps
paraesthesia
polyuria and polydipsia
Investigations
Conn syndrome
Aldosterone (serum and urine) 1
Plasma renin !
Plasma aldosterone to renin activity ratio
Na t, K !, alkalosis
Imaging (MRI or CT scan) of adrenals
Treatment
Conn syndrome
Spironolactone to prepare for
surgery.
DxT episodic headache + sweating + tachycardia -
Phaeochromocytoma
Investigations
Phaeochromocytoma
Series of three 24-hour free catecholamines 1 VMA
Abdominal CT or MRI scan (both highly sensitive)
Treatment
Phaeochromocytoma
Excise tumour cover with alpha and beta blockers
An AR condition with 21-hydroxylase deficiency being the most common of several forms,.
There is inadequate synthesis of cortisol and aldosterone with increased androgenisation.
Major
problem is adrenal failure + salt-losing state (SLS).
In females, ambiguity of external genitalia
and hirsutism before puberty usually occurs.
Males may have normal urogenital development but
SLS is a concern.
Infants of either sex may present with failure to thrive or vomiting and
dehydration (SLS).
Congenital adrenal hyperplasia (adrenogenital
syndrome)
Treatment
Congenital adrenal hyperplasia (adrenogenital
syndrome)
Lifelong glucocorticoid treatment (e.g. prednisolone) is required.
DXT weakness + constipation + polyuria
hypercalcaemia
DXT cramps + confusion + tetany
hypocalcaemia
is caused by an excessive secretion of parathyroid hormone and is usually
due to a parathyroid adenoma.
The classic clinical features
Due to the
effects of hypercalcaemia.
Classic mnemonic: bones, moans, stones, abdominal groans
Primary hyperparathyroidism’
Diagnosis
Primary
hyperparathyroidism
Exclusion of other causes of hypercalcaemia
Serum parathyroid hormone (elevated)
TC-99m Sestamibi scan to detect tumour
Causes include parathyroid injury, autoimmune hyperparathyroidism, severe vitamin D
deficiency and neonates of mothers with hypercalcaemia,
This usually presents with tetany or
more generalised neuromuscular hyperexcitability and neuropsychiatric manifestations.
The
sensory equivalents are paraesthesia in the hands, feet and around the mouth (distinguish from
tetany seen in the respiratory alkalosis of hyperventilation).
There may be seizures and cramps.
Hypocalcaemia
Hypocalcaemia
The diagnosis is by
measurement of serum total calcium concentration in relation to serum
albumin (s. calcium <2.10 mmol/L).
Hypocalcaemia
Two important signs are:
occlusion of the brachial artery with BP cuff precipitates carpopedal spasm
(wrist flexion and fingers drawn together
Trousseau sign: )
Hypocalcaemia
Two important signs are
tapping over parotid (facial nerve) causes twitching in facial muscles
Chvostek sign:
It is the most common cause of hypocalcaemia.
Causes include postoperative
thyroidectomy and parathyroidectomy, congenital deficiency (DiGeorge syndrome) and
idiopathic (autoimmune) hypoparathyroidism.
The main features are neuromuscular
hyperexcitability, tetany and neuropsychiatric manifestations.
Hypoparathyroidism
Hypernatreamia >145mmol/L
Hyponatreamia <135mmol/L
Hyperkalemia >5.5 mmol
Hypokalemia <3.5 mmol
