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COMMON METABOLIC DISORDERS

CONTENTS:
1. Recognize signs + symptoms of common endocrine condition
2. Diagnostic test used to investigate endocrine disease
3. Management of pt in corticosteroid therapy
4. Dental relevance of endocrine disorders

TYPES OF METABOLIC DISORDERS

ENDOCRINE PROBLEMS ?
- 3 basic things that can go wrong :
- Excessive / failure to produce hormone
- Swelling - benign / malignant tumour
Adrenocortical Addison’s disease
gland changes Cushing syndrome
Pheochromocytoma

Thyroid gland Hyperthyroidism

changes Hypothyroidism

Pituitary gland Acromegaly

changes

Normal endocrine Pregnancy

changes Menopause
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HYPERTHYROIDISM

WHAT IS IT? WHAT IS THE CAUSES?

Condition caused by unregulated production of thyroid Thyroid nodules
hormones Medications
Thyroiditis
Graves disease
Excessive iodine intake

HISTORY ? OTHER RISK FACTORS?

Personal or family history of thyroid disease Gender, Age
Recent viral illness Smoking
Medication :levothyroxine, triiodothyronine, amiodarone, Trauma to thyroid
contrast dye Major stress
Current recent pregnancy

COMPLICATIONS? WHAT LEADS TO ?

1. Heart disorders 1. Graves disease (TSH rec antibodies)
a. If left untreated, Graves disease can lead to heart 2. Toxic adenoma
rhythm disorders,changes in structure and 3. Subacute thyroiditis
function of heart muscles and heart failure 4. Follicular carcinoma
2. Thyroid storm 5. choriocarcinoma
3. Brittle bones
4. Pregnancy issues
a. Miscarriage ,pre term birth,fetal thyroid
dysfunction,poor fetal growth, maternal HF ,pre
eclampsia

INVESTIGATIONS ? MEDICATIONS?
1. Basic blood test - free T4 ↑ ,TSH ↓ 1. Anti thyroid drugs -methimazole, propylthiouracil
2. Specific diagnostic test - total T3, free T3 ↑ 2. Radioactive iodine
3. IMAGING - radioiodine 123 uptake and scan 3. Beta blocker +potassium iodides
4. Thyroid surgery : in pregnancy,toxic
adenoma,amiodarone induced hyperthyroidism when
therapy fails
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HYPOTHYROIDISM

WHAT IS IT? HISTORY

Defines as decrease in thyroid hormone production and 1. Cretinism (congenital)
thyroid gland function a. Iodine deficiency
Increase TSH, decrease T3 & T4 b. Defective or absent thyroid gland
Autoimmune but due to excessive removal of thyroid gland 2. Myxedema (acquired)
a. Thyroid surgery
b. I-131 treatment
c. Pituitary gland disorder
d. Family history of thyroid disease
e. Therapeutic irradiation of the neck or thorax (mantle)
f. Iodine excess: amiodarone, contrast, kelp, cough syrup
g. Medications: lithium
h. Severe iodine deficiency
i. Pregnancy: recent, complicate

INVESTIGATIONS ? DD?
1. Basic blood test :free T4,TSH - Primary hypothyroidism - low T4,high TSH)
2. Specific diagnostic test : anti TYPO antibody, 1. Hashimoto disease
antithyroglobulin,lipid panel,creatine 2. Subacute thyroiditis : viral,silent,postpartum
phosphokinase,sodium 3. Post thyroidectomy / T-131 therapy
4. Goitrogen induced : lithium,PTU,MTZ
5. Iodine induce : amiodarone
6. Rare cause : iodine deficiency

- Secondary hypothyroidism (low T4, low or normal

TSH)
1. Pituitary or hypothalamic tumors
2. Post pituitary or hypothalamic surgery
3. Granulomatous diseases
4. Other pituitary and hypothalamic disorders

GENERAL MEASURES SPECIFIC THERAPY ?

1. Assess for ass 1. Levothyroxine
disorders,hypothermia,hyponatremia,mental status, 2. Hydrocortisone: use if secondary hypothyroidism or
hypoventilation myxedema coma present
3. Avoid excessive sedative drugs and fluids to decrease
possibility of hyponatremia and coma

ORAL MANIFESTATION OF PT WITH THYROID GLAND DISORDERS

HYPERTHYROIDISM HYPOTHYROIDISM

Accelerated dental eruption in children Delayed dental eruption

Delayed bone formation

Maxillary / mandibular osteoporosis Enamel hypoplasia in both dentition

Enlargement of extra glandular thyroid tissue (mainly in lateral Anterior open bite
post tongue)

Increased susceptibility to caries Macroglossia

Periodontal disease Micrognathia

Burning mouth syndrome Mouth breathing

Thick lips + glossitis

Thyroid enlarged or noticeably palpable Enlarged salivary gland

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PARATHYROID GLAND DISORDERS

➔ Functions for :
◆ Controlling amount of calcium in blood within bones so nervous + muscular systems function properly
◆ Increase blood calcium levels by stimulating osteoclast to break down bone
◆ Increasing resorption
◆ Increase GIT calcium absorption by activating vit D
◆ Increase renal absorption of calcium by kidneys

HYPERPARATHYROIDISM

CLINICAL FEATURES?
1. Nausea, vomiting or loss of appetite
2. Tiring easily or weakness
3. Abdominal pain
4. Bone and joint pain
5. Fragile bones that easily fracture
6. Kidney stones
7. Excessive urination
8. Depression or forgetfulness
9. Frequent complain of illness with no apparent cause

PRIMARY : parathyroid adenoma

SECONDARY : physiological to low calcium
TERTIARY : parathyroids hyperplasia
DENTAL RELEVANCE ?
1. Bone tumour of the mandible or maxilla
2. Loss of lamina dura around teeth
3. Osteopenia ( prone to pathological fractures)
4. Associated with autoimmune disorders
TREATMENT?
1. Treat the underlying cause )
2. Hyper: Lower calcium levels essentially by rehydration
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HYPOPARATHYROIDISM

Decreased function SYMPTOMS ?

Underproduction of PTH leads to low levels of calcium in 1. Fatigue / weakness,dry coarse skin, brittle nails
blood 2. Tingling / burning on fingertips,toes and lips
Can be inherited but also encountered after thyroid or 3. Anxiety or nervousness , headaches
parathyroid surgery 4. Muscle aches or cramps affecting legs,feet ,abdomen
or face
5. Twitching or spam of muscles , particularly around
mouth hands arms or throat
6. Depression, mood swings
7. Memory problems

DENTAL RELEVANCE TREATMENT ?

1. Candidiasis of the mouth and hand 1. ( Treat the underlying cause )
2. Neuromuscular instability , circumoral paraesthesia , 2. Hypo : Acute - IV calcium gluconate (10%)
seizures Maintenance therapy - alfacalcidol
3. Laryngospasm and Bronchospasm
4. Chvostek sign and Trousseau’s sign – Hypocalcemia

ORAL MANIFESTATION OF PT WITH PARATHYROID GLAND DISORDERS

HYPERPARATHYROIDISM HYPOTHYROIDISM

1. Dental abnormalities 1. Dental abnormalities

a. widened pulp chambers a. Enamel hypoplasia in horizontal lines
b. development defects b. Poorly calcified dentine
c. alterations in dental eruption c. Widened pulp chambers
d. weak teeth d. Dental pulp calcifications
e. malocclusions e. Shortened roots
f. loss of lamina dura on radiographs f. Hypodontia
g. giant cell lesions g. Delay or cessation of dental development
2. Brown tumor 2. Mandibular tori
3. Loss of bone density 3. Chronic candidiasis
4. Soft tissue calcification 4. Paresthesia of tongue or lips
5. Alterations in facial muscles

PITUITARY GLAND : ACROMEGALY

➔ Caused by growth hormone excess
➔ Result of pituitary tumour producing characteristic appearance due to prolonged increased levels of circulating GH

HISTORY ? CLINICAL FEATURES ?

1. Enlargement of hands and feet 1. Acne, Hirsutism and excessive sweating
2. Prognathism and loose teeth 2. Facial features : coarse, with broad nose and brow
3. Increased sweating ridges, thick lips, macroglossia , prognathism and
4. Sleep apnea and snoring malocclusion
5. Diabetes mellitus 3. Headache, arthralgia, skin tags , large spade like
6. Coarsening change in facial appearance hands and feet
7. Frontal bossing 4. Impotence , Decreased libido, Galactorrhea in some
8. Carpal tunnel syndrome women
9. Infertility 5. Visual field cut , bitemporal hemianopia
10. Amenorrhea or oligomenorrhea 6. Increase risk of diabetes, hypertension ,
11. Family history of pituitary tumor cardiomyopathy and atherosclerosis
12. Excessive linear growth (in children)

DIAGNOSIS? TREATMENT?
1. Basic blood studies :check plasma level of 1. Surgery : trans sphenoidal surgery or radiotherapy
a. Insulin like growth fac -1 (IGF 1 ) single best 2. Medical therapy
test a. Octreotide and lanreotide (somatostatin
b. GH 1 hr after 75 g glucose load : <5ng/dl in analogues)
normal (glucose tolerance test) b. Dopamine agonists (bromocriptine or
2. Ancillary blood tests: cabergoline): may lower IGF-I and GH
a. LH,FSH ,prolactin,free T4,TSH,testosterone, 3. Radiation therapy if surgery and medical therapy fail
Estradiol 4. Observation with repeated pituitary MRI to determine
b. GH releasing hormone if tumor is growing
c. Fasting serum glucose ,HgA1c
d. Pituitary MRI - to detect tumour
@wolfiestudy

ADRENAL GLAND DISORDERS

➔ Overproduction or underproduction of secretory
products
➔ Responsible to produce adrenal steroids,
mineralocorticoids and norepinephrine

ETIOLOGY? GLUCOCORTICOID INSUFFICIENCY

- Related to primary endocrinopathies as well as autoimmune, 1. Divided into 2 categories :
infectious, neoplastic or iatrogenically induced disorders a. Primary : result from proggresive destruction of
- Overproduction due to tumour adrenal glands
- Underproduction due to destruction of one both adrenal b. Secondary : result from hypothalamic-pituitary
glands disease and suppression by chronic exogenous
- Primary adrenal insufficiency known as Addison disease steroid administration

ADDISON DISEASE

- Due to destruction of adrenal cortex (lack of function) CLINICAL FEATURES?

- Resulting in failure of production of cortisol and aldosterone 1. Bronzing of the skin , as well as melanotic macules on oral
mucosa (hyperpigmentation) because of stimulation of
melanocytes,
2. Vitiligo
3. Anorexia and weight loss
4. Diarrhoea and vomiting
5. Abdominal pain, arthralgia and myalgia
6. Dizziness, confusion and depression
7. Postural hypotension
8. Oral candidiasis secondary to Addison's disease, Addison
crisis

ADDISON CRISIS CHARACTERISTIC SYMPTOMS

1. Long term Addison's disease or pt on long term 1. Sudden penetrating pain in legs,lower back or abdomen
corticosteroids 2. Severe vomit and diarrhea resulting in dehydration
2. Indicates adrenal insufficiency 3. Hypoglycemia, Hyponatremia, Hyperkalemia ,Hypercalcemia
3. Medical emergency and life threatening situation requiring 4. Shock - tachycardia,peripheral vasoconstriction,
immediate emergency treatment hypotension,oliguria ,coma

INVESTIGATIONS?
1. Treatment should not be delayed to wait for results in pt with suspected acute adrenal crisis
2. Random blood sample should be stored for subsequent measurement of cortisol
3. Spend 30 mins performing short ACTH stimulation test before administering hydrocortisone
4. Investigation performed before treatment given who present with features of chronic adrenal insufficiency
@wolfiestudy
ADRENOCORTICAL SUPPRESSION LIKELY IF:
1. Systemic corticosteroids > 10 mgs prednisolone or equivalent, taken regularly during past 3 months
2. Corticosteroids taken for > 1 month in past year
3. No corticosteroids for > 3 months considered to have full recovery and require no supplementation

DENTAL RELEVANCE ? TREATMENT?

1. Oral pigmentation -light brown to black Treat underlying cause
2. Occur in BM, associated with bite line Steroid replacement therapy - corticosteroid, prednisolone,
dexamethasone
3. Increased to oral infection
4. Hypotension / fainting episodes may occur
5. Pt must be given steroid cover (pre op considerations)

CUSHING SYNDROME

Result of excess glucocorticoid production secondary to HISTORY ?

adrenal hyperplasia or prolonged corticosteroid therapy 1. Osteoporosis, fracture , bone pain, loss of height,
ACTH dependent 80% renal stones
Pituitary adenoma secreting ACTH -70% 2. Muscle weakness / atrophy/cramps
Ectopic ACTH syndrome -10% 3. Hypertension, DM, metabolic syndrome,polyuria
4. History of exogenous glucocorticoids administration
5. Alcoholism
6. Family history of Cushing syndrome
7. Cigarette smoking, weight loss

CLINICAL FEATURES?
1. Women : hirsutism, virilism, thinning of scalp hair,
acne, amenorrhea/menstrual irregularity
2. Men: decreased libido, gynecomastia, impotence •
Moon face , Buffalo hump
3. Central obesity and wasting of proximal limb muscles,
resulting in a ‘lemon on sticks’ shape
4. Hypertension, acne, hirsutism , easy bruising,
hyperpigmentation, striae , fragile skin

DIAGNOSIS? TREATMENT?
1. Check plasma or urine cortisol level : elevated or not 1. Treat underlying cause
by dexamethasone suppression test a. Surgery : surgical removal of adrenal /
2. Normal / elevated in pituitary corticotrophic pituitary tumour
adenoma b. Medical therapy
3. Normal to marked elevation in ectopic ACTH 2. Enzymatic inhibitors of cortisol synthesis
4. Plasma ACTH helps distinguish pituitary causes from 3. Hydrocortisone replacement if steroidogenic
adrenal causes blockade complete
5. MRI of pituitary or adrenal gland : to localise the 4. Mineralocorticoid excess : spironolactone
tumors
6. Ectopic (non pituitary) Cushing : CXR, chest CT

DENTAL MANAGEMENT ?
1. Pt with primary adrenal insufficiency or chronic exogenous steroids may be enable to increase endogenous steroid
production to respond app to stress of invasive /extensive dental proc
2. Routine procedures can be performed without medic
3. If untreated , condition evolved into shock,coma and death
4. Life supportive measures including administration of glucocorticoids indicated