JM Chapter 14 Flashcards by Sheila Sarmiento

TSH receptor antibodies (TR Ab):

Graves disease

How well did you know this?

Not at all

Perfectly

Thyroid peroxidase antibodies (TPO Ab):

Hashimoto disease

How well did you know this?

Not at all

Perfectly

Thyroglobulin antibody (Tg Ab):

Hashimoto disease

How well did you know this?

Not at all

Perfectly

The term refers to the accumulation of mucopolysaccharide in subcutaneous
tissues.

Tiredness +HUSKY VOICE + cold intolerance

Myxoedema

How well did you know this?

Not at all

Perfectly

Common causes of primary hypothyroidism include

radioactive iodine treatment, thyroid surgery
and Hashimoto 1thyroiditis

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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.

How well did you know this?

Not at all

Perfectly

Most common cause
of hyperthyroidsim
(Thyrotoxicosis)

Graves disease
Followed by nodular thyroid disease

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

DxT anxiety + weight loss + weakness

Thyrotoxicosis

How well did you know this?

Not at all

Perfectly

Eye signs of
Hyperthyroidism

Lid retraction (small area of sclera seen above iris)
Lid lag
Exophthalmos
Ophthalmoplegia in severe cases

How well did you know this?

Not at all

Perfectly

Investigations
Hyperthyroidism

T4 (and T3) elevated
TSH level suppressed
Radioisotope scan
Antithyroid peroxidase (TPO Ab) often positive

How well did you know this?

Not at all

Perfectly

Treatment for Hypothyroidism

Levothyroxine (thyroxine) 50-100 mcg daily up to 200 mcg daily

Aim TSH levels of 0.5-2mUL

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

What are the surgical treatment for Hyperthyroidism

Subtotal thyroidectomy or Total Thyroidectony

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Investigations include
Goitre

TFTs, needle biopsy, ultrasound and CXR.

How well did you know this?

Not at all

Perfectly

Management
Goitre

Supportive thyroxine if TSH elevated (may lead to marked regression) and subtotal or total thyroidectomy

How well did you know this?

Not at all

Perfectly

It is defined as a discrete lesion on palpation and/or ultrasonography that is distinct from the rest of the thyroid gland.

Thyroid nodules

How well did you know this?

Not at all

Perfectly

Causes of Thyroid Nodules

Dominant nodule in a multinodular goitre (most likely)

Colloid cyst

True solitary nodule: adenoma, carcinoma (papillary or follicular)
Investigations

How well did you know this?

Not at all

Perfectly

Investigations of Thyroid Nodule

Ultrasound imaging
Fine-needle aspiration cytology
Thyroid function tests

How well did you know this?

Not at all

Perfectly

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