Endocrine Disorders II Flashcards
1. Outline main glands and physiological actions of hormones produced by: thyroid, adrenal gland, parathyroid and pituitary glands 2. Pathologies affecting endocrine glands and their clinical features 3. Interpretation of basic endocrine investigation 4. Dental aspect of common endocrine disorders
Which glands are under the control of the pituitary and hypothalamus
- thyroid and parathyroid
- adrenal glands
- ovaries
- testes
What are the manifestations and aetiology of endocrine disorders
Manifests as
- hormone overproduction or underproduction
- structural defect
It is due to
- primary dysfunction of gland
- secondary dysfunction of gland by over/under stimulation by another gland or exogenous hormone
- receptor dysfunction
What is the most common endocrine disorder after diabetes
Thyroid gland
What are the target organs of the thyroid gland
It produces thyroxine hormones T4 and T3 which target the brain, bones, heart, gut, skin and metabolism
Give examples of hyperthyroidism (7)
= thyroxine overproduction
- Graves’ disease; autoimmune
- Toxic adenoma
- Toxic multinodular goitre
- Exogenous thyroxine
- Pituitary dysfunction (ant. produces XS TSH)
- Amidarone drug used for cardiac arrhythmias
- Thyroiditis; viral post-partum
Give examples of hypothyroidism (7)
- Autoimmune hypothyroidism
- Hashimoto’s disease
- Post thyroidectomy or radioactive iodine
- Congenital
- Secondary due to pituitary dysfunction
- Lithium, chemotherapy and amidarone drugs
- Iodine deficiency
Give examples of thyroid disorders that aren’t associated with the abnormal production of thyroxine (there is a problem with the gland itself)
- Non functioning thyroid nodule
- Multinodular goitre
- Thyroid carcinoma
- Infiltration e.g. lymphoma, TB
What are the clinical features of hyperthyroidism
Cardiovascular = tachycardia, atrial fibrillation Metabolism = weight loss, increased hunger GI = diarrhoea Skin = palmar sweating, hair loss Neurological/psych = anxiety, insomnia, restless Skeletal/muscular = proximal weakness Reproductive = infertility, oligo/amenorrhoea Temperature = heat intolerance
What are the clinical features of hyporthyroidism
Cardiac = bradycardia Metabolism = weight gain GI = constipation Skin = dry, hair loss Neurological/psych = poor concentration/memory, reduced fetal brain development Skeletal/muscle = proximal weakness Reproductive = infertility, oligo/amenorrhoea Temperature = intolerant of cold water
Clinical presentation of Graves’ disease
= hypothyroidism
- Exophthalmos = protruding eyes
- Goiter = enlarged thyroid gland
What is seen in the blood test results of a patient who has hyperthyroidism
Increased T4, T3
Suppressed TSH
Positive Thyroperoxidase Ab
Positive TSH receptor Ab (only in Graves’)
What is seen in the blood test results of a patient who has hyporthyroidism
Low T4, T3
Elevated TSH
Positive Thyroperoxidase Ab
What is given to manage hyperthyroidism
- Beta-blockers to slow HR = propranolol
- Antithyroid medication e.g. carbimazole and propylthiuracil (decreases thyroxine production)
- Radioactive iodine
- Thyroidectomy
- Steroids, lithium (rarely given)
What is given to manage hyporthyroidism
Thyroxine replacement
Give two antithyroid medications
Carbimazole
Propylthiouracil
What is the dental aspect of hyperthyroidism
- increased caries risk
- icreased periodontal disease risk
- enlarged extraglandular thyroid tissue at post. tongue
- burning mouth syndrome
- accelerated dental eruption in children
- osteoporosis (mad. max.)
- Sjogren’s/SLE = associated autoimmune conditions
- Mouth ulcers due to antithyroid medication
What is the dental aspect of hyporthyroidism
Congenital hypothyroidism (cretinism)
- Delayed dental eruption
- Macroglossia
- Microganthia
- Malocclusion
- Glossitis = swollen red inflamed smooth tongue
- Dysgeusia = distorted unpleasant taste perception (metallic)
- Poor wound healing
Describe the anatomy of the adrenal gland
They are 2 suprarenal glands
- have 2 parts which produce hormones
- cortex produces androgens
- medulla produces cortisol, aldosterone and adrenaline
What are the primary and secondary diseases caused by adrenal insufficiency
The under production of cortisol and aldosterone (rare and life-threatening) causes
Primary = Addison’s disease
- autoimmune
- infiltration e.g. TB, sarcoidosis, primary/secondary malignency
Secondary
- pituitary disease causing ACTH deficiency
- exogenous steroids
Outline how the feedback mechanism is disrupted in primary adrenal insufficiency
Addisons disease
- Adrenal gland doesn’t produce cortisol
- So no negative feedback between adrenal cortex and hypothalamus + pituitary gland
- Thus increased levels of ACTH circulating
- these patients have low cortisol levels
- and high circulating ACTH
What are the physiological actions of cortisol (3)
Cortisol is a glucocorticoid = steroid hormone
- Anti-inflammatory and immunosuppressive actions
- Stress response
- Metabolism (gluconeogenesis)
What happens when there is excess steroid hormone in the body (5)
e.g. Cushing’s syndrome
- Stimulates hepatic gluconeogenesis and glycogenlysis (increases blood glucose causing diabetes)
- Stimulates proteolysis = muscle wasting
- Sodium retention and potassium loss = limb/facial swelling
- Stimulates lipolysis = dyslipidaemia
- Hypertension
What are the clinical features of Addison’s disease
Primary adrenal insufficiency = decreased cortisol and increased ACTH
- Hypotension
- Hypoglycaemia
- Weight loss
- Lethargy
- Anorexia
- Abdominal pain
- Skin and oral pigmentation
Why is there increased skin and oral pigmentation in Addison’s disease
Because there is increased MSH and ACTH which stimulates melanocytes to produce melanin causing hyperpigmentation
Why does secondary adrenal insufficiency occur
Due to prolonged exogenous steroids
- there is suppression of the hypothalamic-pituitary-adrenal axis through negative feedback
- there is risk associated with abrupt discontinuation of steroids causing an adrenal crisis
- drugs must be tapered down gradually
Addisonian crisis
New presentation precipitated by infection
- non-compliance with medication
- poor absorption of steroids (diarrhoea)
- life threatening if untreated
Dental aspect of primary adrenal insufficiency
- Oral infections must be managed aggressively to prevent Addisonian crisis
- Steroid cover for major procedures (IM hydrocortisone 1hr before treatment, double oral dose 3-5 days before)
- Steroid cover for minor procedures
What steroid precautions are in place for patients with primary adrenal insufficiency
- Steroid card/bracelet
- Emergency IM hydrocortisone pack
- Sick day rules = double dose of steroids if feeling unwell
What is the parathyroid gland and describe its role
There are 4 parathyroid glands adjacent to thyroid galnd and these are not under the influence of the pituitary/hypothalamus
It is important in calcium homeostasis
- PTH causes resorption of bone to increase Ca2+ in blood
- PTH causes increased Ca2+ reabsorption from the kidneys to increase levels in the blood
- Vitamin D causes increased Ca2+ absorption from the intestine
When vitamin D levels are low, there is increased PTH to maintain normal blood calcium levels
Give examples of primary and secondary hyperparathyroidism
= XS parathyroid hormone production
Primary
- parathyroid adenoma
- parathyroid hyperplasia including genetic familial HP, MEN
- parathyroid carcinoma
Secondary
- vit D deficiency
- chronic renal failure
What are the clinical features of hyperparathyroidism
These present with symptoms of hypercalcimea = moans, stones, bones, grones and psychiatric overtones
- Abdo pain, constipation
- Renal stones
- Bone pain, osteopaenia and osteoporosis
- Lethargy, fatigue
- Confusion, memory impairment, depression, hallucinations
Osmotic symptoms = polyuria, polydipsia, urinary frequency and nocturia
What are the results of testing for primary hyperparathyroidism
Serum phosphate = low Vitamin D = high Alkaline phosphate = high Serum calcium = high Serum parathyroid hormone = high
What are the results of testing for secondary hyperparathyroidism
Serum phosphate = high Vitamin D = low Alkaline phosphate = high Serum calcium = low Serum parathyroid hormone = high
Outline treatment for primary hyperparathyroidism
- If due to parathyroid adenoma = parathyroidectomy
2. If due to hyperplasia = cinacalet drug treatment
Outline treatment for secondary hyperparathyroidism
Treat underlying cause; increase vitamin D to normalise PTH levels
What are the oral manifestations of primary hyperparathyroidism
- Alliteration of pulp chamber by pulp stones
- Alterations in dental eruption times
- Loosening and drifting of teeth; spacing of teeth
- Malocclusion
- Partial loss of lamina dura
- Periodontal ligament widening
- Teeth become sensitive to percussion and mastication
- Floating teeth
- Brown tumour = giant cell focal region
- Rarification of jaw
- Soft tissue calcifications and hypercalcemia leads to sialolithiasis = stones in salivary ducts
- Mandibular tori = bony outgrowths on lingual mandibular surface
- Vague jaw bone pain
What are the oral manifestations of secondary hyperparathyroidism
- Enamel hypoplasia = underdeveloped tooth enamel
- Delayed eruption
- Hypodontia and macrodontia
- Poorly calcified dentin
- Widened pulp chambers
- Dental pulp calcifications
- Shortened roots with blunt apex
- Malformed roots
- Maloclusion
- Ankylosis = stiffening and immobility
- Caries
- Chronic candidiasis
- Parethesia of tongue and lips (tingling burning)
- Alteration in facial muscles
What is a brown tumour
Associated with hyperparathyroidism
- benign radiolucent tumour
- due to abnormal bone metabolism
- there is extensive bone resorption and replacement by fibrovascular tissue and giant cells
What hormones are released by the pituitary gland
Anterior
- ACTH, TSH, GH, Prolactin, gonadotrophins (LH + FSH)
Posterior
- ADH, oxytocin
There is negative feedback from the hypothalamus
What is acromegaly and what are the clinical presentations
Excess growth hormone due to pituitary adenoma
- enlarged mandible and spacing of teeth
- macroglossia
- coarse facial features; broad nose, prominant naso-labial angle
- large spade like hands and feet
- osteoarthritis
- goitre
- diabetes
- loss in visual feild
What is given to treat acromegaly
- Transphenoidal surgery
- Radiotherapy
- Drugs = dopamine agonist, somatostatin analogues, pegvisomant
What is the aetiology of Cushing’s syndrome
- Adrenal Cushing’s syndrome = adrenal adenoma so XS cortisol production
- Pituitary Cushing’s syndrome = pituitary adenoma so XS ACTH production so XS cortisol
- Ectopic ACTH production = due to lung malignancy
What are the treatments of Cushing’s syndrome
- surgery (transphenoidal surgery, adrenalectomy)
- drugs = metyrapone and ketoconazole
- radiotherapy if the lesion is inoperable
What drugs are given to patients with Cushing’s syndrome
Metyrapone
Ketoconazole to reduce cortisol
What modifications should be made in dentistry for patients with XS cortisol
- Hypertension so blood pressure should be monitored
- Peptic ulcers so aspirin and NSAIDs should be avoided as increases risk of GI bleeding and ulcers
- Diabetes mellitus so regular assessment of periodontal health due to increased risk of oral infection and periodontitis
- Osteoporosis and myopathy so dentures may need frequent readjustment to accomodate for limited motility
- Immunosupression so need to assess and treat for opportunistic infections
- Poor wound healing so need adequate antibiotic cover following major surgery
What is phaeochromocytoma and paragengliona and what are the clinical presentations
It is the XS production of catecholamines (adrenaline)
- Phaeochromocytoma = adrenal
- Paragengliona = extra adrenal
Clinical presentations include
- high blood pressure and tachycardia
- heavy sweating
- headache
- heartburn
- tremours
- pallor
- dyspnoea = shortness of breath
- pre-syncope or syncope
- feeling of impending doom
What are the treatments of phaeochromocytoma and paragengliona
Drugs = alpha-blockers followed by beta-blockers Surgery = adrenalectomy or removal of paraganglioma
Describe the clinical presentation of Cushing’s syndrome
LEMONS ON STICKS
- Red cheeks, moon face
- Fat pads and buffalo hump
- Thin skin, easy bruising, ecchymosis, poor healing
- High BP
- Red striation on abdomen
- Pendulous abdomen
- Thin arms and legs
- Osteoporosis (compression of vertebrae)
