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BDS2; CHHD > Endocrine Disorders II > Flashcards

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

1
Q

Which glands are under the control of the pituitary and hypothalamus

A
  • thyroid and parathyroid
  • adrenal glands
  • ovaries
  • testes
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2
Q

What are the manifestations and aetiology of endocrine disorders

A

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
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3
Q

What is the most common endocrine disorder after diabetes

A

Thyroid gland

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4
Q

What are the target organs of the thyroid gland

A

It produces thyroxine hormones T4 and T3 which target the brain, bones, heart, gut, skin and metabolism

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5
Q

Give examples of hyperthyroidism (7)

A

= thyroxine overproduction

  1. Graves’ disease; autoimmune
  2. Toxic adenoma
  3. Toxic multinodular goitre
  4. Exogenous thyroxine
  5. Pituitary dysfunction (ant. produces XS TSH)
  6. Amidarone drug used for cardiac arrhythmias
  7. Thyroiditis; viral post-partum
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6
Q

Give examples of hypothyroidism (7)

A
  1. Autoimmune hypothyroidism
  2. Hashimoto’s disease
  3. Post thyroidectomy or radioactive iodine
  4. Congenital
  5. Secondary due to pituitary dysfunction
  6. Lithium, chemotherapy and amidarone drugs
  7. Iodine deficiency
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7
Q

Give examples of thyroid disorders that aren’t associated with the abnormal production of thyroxine (there is a problem with the gland itself)

A
  1. Non functioning thyroid nodule
  2. Multinodular goitre
  3. Thyroid carcinoma
  4. Infiltration e.g. lymphoma, TB
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8
Q

What are the clinical features of hyperthyroidism

A 
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
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9
Q

What are the clinical features of hyporthyroidism

A 
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
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10
Q

Clinical presentation of Graves’ disease

A

= hypothyroidism

  1. Exophthalmos = protruding eyes
  2. Goiter = enlarged thyroid gland
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11
Q

What is seen in the blood test results of a patient who has hyperthyroidism

A

Increased T4, T3
Suppressed TSH
Positive Thyroperoxidase Ab
Positive TSH receptor Ab (only in Graves’)

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12
Q

What is seen in the blood test results of a patient who has hyporthyroidism

A

Low T4, T3
Elevated TSH
Positive Thyroperoxidase Ab

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13
Q

What is given to manage hyperthyroidism

A
  1. Beta-blockers to slow HR = propranolol
  2. Antithyroid medication e.g. carbimazole and propylthiuracil (decreases thyroxine production)
  3. Radioactive iodine
  4. Thyroidectomy
  5. Steroids, lithium (rarely given)
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14
Q

What is given to manage hyporthyroidism

A

Thyroxine replacement

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15
Q

Give two antithyroid medications

A

Carbimazole

Propylthiouracil

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16
Q

What is the dental aspect of hyperthyroidism

A
  • 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
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17
Q

What is the dental aspect of hyporthyroidism

A

Congenital hypothyroidism (cretinism)

  1. Delayed dental eruption
  2. Macroglossia
  3. Microganthia
  4. Malocclusion
  • Glossitis = swollen red inflamed smooth tongue
  • Dysgeusia = distorted unpleasant taste perception (metallic)
  • Poor wound healing
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18
Q

Describe the anatomy of the adrenal gland

A

They are 2 suprarenal glands

  • have 2 parts which produce hormones
  • cortex produces androgens
  • medulla produces cortisol, aldosterone and adrenaline
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19
Q

What are the primary and secondary diseases caused by adrenal insufficiency

A

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
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20
Q

Outline how the feedback mechanism is disrupted in primary adrenal insufficiency

A

Addisons disease

  1. Adrenal gland doesn’t produce cortisol
  2. So no negative feedback between adrenal cortex and hypothalamus + pituitary gland
  3. Thus increased levels of ACTH circulating
  • these patients have low cortisol levels
  • and high circulating ACTH
21
Q

What are the physiological actions of cortisol (3)

A

Cortisol is a glucocorticoid = steroid hormone

  1. Anti-inflammatory and immunosuppressive actions
  2. Stress response
  3. Metabolism (gluconeogenesis)
22
Q

What happens when there is excess steroid hormone in the body (5)

A

e.g. Cushing’s syndrome

  1. Stimulates hepatic gluconeogenesis and glycogenlysis (increases blood glucose causing diabetes)
  2. Stimulates proteolysis = muscle wasting
  3. Sodium retention and potassium loss = limb/facial swelling
  4. Stimulates lipolysis = dyslipidaemia
  5. Hypertension
23
Q

What are the clinical features of Addison’s disease

A

Primary adrenal insufficiency = decreased cortisol and increased ACTH

  1. Hypotension
  2. Hypoglycaemia
  3. Weight loss
  4. Lethargy
  5. Anorexia
  6. Abdominal pain
  7. Skin and oral pigmentation
24
Q

Why is there increased skin and oral pigmentation in Addison’s disease

A

Because there is increased MSH and ACTH which stimulates melanocytes to produce melanin causing hyperpigmentation

25
Q

Why does secondary adrenal insufficiency occur

A

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
26
Q

Addisonian crisis

A

New presentation precipitated by infection

  • non-compliance with medication
  • poor absorption of steroids (diarrhoea)
  • life threatening if untreated
27
Q

Dental aspect of primary adrenal insufficiency

A
  1. Oral infections must be managed aggressively to prevent Addisonian crisis
  2. Steroid cover for major procedures (IM hydrocortisone 1hr before treatment, double oral dose 3-5 days before)
  3. Steroid cover for minor procedures
28
Q

What steroid precautions are in place for patients with primary adrenal insufficiency

A
  1. Steroid card/bracelet
  2. Emergency IM hydrocortisone pack
  3. Sick day rules = double dose of steroids if feeling unwell
29
Q

What is the parathyroid gland and describe its role

A

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

30
Q

Give examples of primary and secondary hyperparathyroidism

A

= XS parathyroid hormone production

Primary

  • parathyroid adenoma
  • parathyroid hyperplasia including genetic familial HP, MEN
  • parathyroid carcinoma

Secondary

  • vit D deficiency
  • chronic renal failure
31
Q

What are the clinical features of hyperparathyroidism

A

These present with symptoms of hypercalcimea = moans, stones, bones, grones and psychiatric overtones

  1. Abdo pain, constipation
  2. Renal stones
  3. Bone pain, osteopaenia and osteoporosis
  4. Lethargy, fatigue
  5. Confusion, memory impairment, depression, hallucinations

Osmotic symptoms = polyuria, polydipsia, urinary frequency and nocturia

32
Q

What are the results of testing for primary hyperparathyroidism

A 
Serum phosphate = low 
Vitamin D = high 
Alkaline phosphate = high 
Serum calcium = high 
Serum parathyroid hormone = high
33
Q

What are the results of testing for secondary hyperparathyroidism

A 
Serum phosphate = high 
Vitamin D = low 
Alkaline phosphate = high 
Serum calcium = low 
Serum parathyroid hormone = high
34
Q

Outline treatment for primary hyperparathyroidism

A
  1. If due to parathyroid adenoma = parathyroidectomy

2. If due to hyperplasia = cinacalet drug treatment

35
Q

Outline treatment for secondary hyperparathyroidism

A

Treat underlying cause; increase vitamin D to normalise PTH levels

36
Q

What are the oral manifestations of primary hyperparathyroidism

A
  1. Alliteration of pulp chamber by pulp stones
  2. Alterations in dental eruption times
  3. Loosening and drifting of teeth; spacing of teeth
  4. Malocclusion
  5. Partial loss of lamina dura
  6. Periodontal ligament widening
  7. Teeth become sensitive to percussion and mastication
  8. Floating teeth
  9. Brown tumour = giant cell focal region
  10. Rarification of jaw
  11. Soft tissue calcifications and hypercalcemia leads to sialolithiasis = stones in salivary ducts
  12. Mandibular tori = bony outgrowths on lingual mandibular surface
  13. Vague jaw bone pain
37
Q

What are the oral manifestations of secondary hyperparathyroidism

A
  1. Enamel hypoplasia = underdeveloped tooth enamel
  2. Delayed eruption
  3. Hypodontia and macrodontia
  4. Poorly calcified dentin
  5. Widened pulp chambers
  6. Dental pulp calcifications
  7. Shortened roots with blunt apex
  8. Malformed roots
  9. Maloclusion
  10. Ankylosis = stiffening and immobility
  11. Caries
  12. Chronic candidiasis
  13. Parethesia of tongue and lips (tingling burning)
  14. Alteration in facial muscles
38
Q

What is a brown tumour

A

Associated with hyperparathyroidism

  • benign radiolucent tumour
  • due to abnormal bone metabolism
  • there is extensive bone resorption and replacement by fibrovascular tissue and giant cells
39
Q

What hormones are released by the pituitary gland

A

Anterior
- ACTH, TSH, GH, Prolactin, gonadotrophins (LH + FSH)

Posterior
- ADH, oxytocin

There is negative feedback from the hypothalamus

40
Q

What is acromegaly and what are the clinical presentations

A

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
41
Q

What is given to treat acromegaly

A
  1. Transphenoidal surgery
  2. Radiotherapy
  3. Drugs = dopamine agonist, somatostatin analogues, pegvisomant
42
Q

What is the aetiology of Cushing’s syndrome

A
  1. Adrenal Cushing’s syndrome = adrenal adenoma so XS cortisol production
  2. Pituitary Cushing’s syndrome = pituitary adenoma so XS ACTH production so XS cortisol
  3. Ectopic ACTH production = due to lung malignancy
43
Q

What are the treatments of Cushing’s syndrome

A
  • surgery (transphenoidal surgery, adrenalectomy)
  • drugs = metyrapone and ketoconazole
  • radiotherapy if the lesion is inoperable
44
Q

What drugs are given to patients with Cushing’s syndrome

A

Metyrapone

Ketoconazole to reduce cortisol

45
Q

What modifications should be made in dentistry for patients with XS cortisol

A
  1. Hypertension so blood pressure should be monitored
  2. Peptic ulcers so aspirin and NSAIDs should be avoided as increases risk of GI bleeding and ulcers
  3. Diabetes mellitus so regular assessment of periodontal health due to increased risk of oral infection and periodontitis
  4. Osteoporosis and myopathy so dentures may need frequent readjustment to accomodate for limited motility
  5. Immunosupression so need to assess and treat for opportunistic infections
  6. Poor wound healing so need adequate antibiotic cover following major surgery
46
Q

What is phaeochromocytoma and paragengliona and what are the clinical presentations

A

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
47
Q

What are the treatments of phaeochromocytoma and paragengliona

A 
Drugs = alpha-blockers followed by beta-blockers
Surgery = adrenalectomy or removal of paraganglioma
48
Q

Describe the clinical presentation of Cushing’s syndrome

A

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)

BDS2; CHHD (32 decks)

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