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Endocrinology
Dr Elsanousi M Taher
BDS, MSc., FFDRCSI
E-mail: [email protected]
 All disorders reflect impaired
control/feedback that result in too much
or too little hormones
 Clinical effects may be due to pressure
effects
 Excess hormones level:
– Tumor or hyperplasia produce high level s
– Excretion by liver or kidney is impaired
 Deficit hormones or reduced effects:
–
–
–
–
–
Inadequate tissue receptors present
Antagonistic hormone production is increased
Atrophy
Surgical removal of the gland
Congenital absence
Diagnostic tests in endocrine diseases:
– Blood tests
 Check serum hormone levels
 Check for the hormone target
 Radioimmunoassay
–
–
–
–
Urine tests (pregnancy test)
Stimulation or suppression test s
Scans, ultrasound and MRI
Biopsy
Treatment:
– Replacement therapy
– Excess secretion may be treated by:
 Medications
 Surgery
 Radiation
Pituitary gland
 Consist of two lobes:
– Ant. Pit. (adenohypophysis):
 GH
 TSH
 ACTH
 LH
 FSH
– Post. Pit. (neurohyphphys):
 ADH
 Oxytocin
– The Pit function is under the influence of
hypothalamus releasing factors
Growth hormone
Deficiency of growth hormone:
 May be part of hypopituitrism due to:
– Congenital
– Space occupying lesions affecting pit.
Fossa like craniopharyngioma
– Sheehan syndrome
– In children: failed growth (pit. dwarfism)
– In adults:
 Decreased body mass (lean)
 Poor bone density
 Loss of muscle strength
 Psychological symptoms:
– Poor memory
– Social withdraw
– Depression
 Reduced vitality (may not survive or perform
functions)
Excess Growth hormone:
–
‘Giantism’ in children
–
Acromegally in Adults: both bone and soft
tissue affected
Acromegally

Due to an excess production of GH after
epiphyseal plate closure

Usually caused by adenoma of anterior
pituitary

Rare disease with 30-40 cases per million
prevalence


insidious onset and course
Affected patients between 40-50 years
General effects:

General features: acne, hairsutism

Hand features: enlargement of hands and
fingers (carpal tunnel syndrome with
tingling of fingers)

Facial features: broad nose, frontal
bossing, prominent supraorbital ridges and
enlarged sinuses

Oral features: Mandibular prognathism &
class II malocclusion, teeth spacing,
enlarged lips and tongue with lateral
indentation
General effects:
 Cardiovascular: hypertension, CAD &
Cardiomyopathy
 Metabolic features: sings of type II
diabetes, amenorrhea and galactorrhea
 Direct pressure effects of the tumour:
Signs of hypopituitarism, some symptoms are
due to local effects caused by expanding
tumors (visual fields and raised ICP)
Class III malocclusion
Thick supra-orbital ridges
Diagnosis:

High GH level by radioimmunoassay

Insulin-like growth factor (1GF-1) is decreased.
–
Its production in the liver is stimulated by GH.
It is more
reliable indicator than GH as the level does not fluctuate during the day

Skull x-ray

MRI

CT scan

Glucose GH suppression test
Treatment:
 Medical:
– The primary current medical treatment of acromegally
is to use somatostatin analogues -- octreotide
(Sandostatin) or lanreotide (Somatuline) injections.
– They are potent inhibitors of growth hormone release
 Surgical removal through transphenoidal
approach is the first line of treatment and give
good results in experienced hands
 Radiotherapy
Dental management: to Consider
 Diabetes
 Hypertension
 Cardiomyopathy
 Effect on old denture
 Esthetic problems
Oral manifestations:
–
Dentist may be the first to notice the
disease
–
Spacing of teeth
–
Class III malocclusion
–
Enlarged lips, tongue with indentation
–
Hypercementosis
–
Enlarged sinuses
–
Denture may become ill fitted
Thyroid Gland
Functions of thyroid hormone:
– Increase BMR and heat generation
– Increase gluconeogenesis, glycolysis, glucose
absorption and lipolysis
– Essential for nervous tissue development and
functions
– Increase sensitivity of B-adrenoreceptors of
the heart to the effect of cathecolamines and
hence increase heart rate and force of
contraction
– In growth and development of bones
Goiter
Goiter
Hyperthyroidism (Thyrotoxicosis)
Classified into:

Primary hyperthyroidism:

Secondary hyperthyroidism:
Hyperthyroidism (Thyrotoxicosis)
Causes:
– Autoimmune disease (Graves disease): due to
LATS hormone like effect of autoantibodies
(represent 90% of all cases of
hyperthyroidism)
– Toxic adenoma
– Pituitary tumors
– Over treatment by T4
Hyperthyroidism (Thyrotoxicosis)
Clinical features:
 Nervousness, irritability, anxiousness and
maniac behaviors
 Tremor of extended hands
 Loss of weight despite good apatite
 Intolerance of heat
Hyperthyroidism (Thyrotoxicosis)
Clinical features:
 Worm, moist skin
 Diarrhea
 Resting Tachycardia, palpitation, atrial fibrillation
and failure
 Eye signs: lid retraction, exophthalmos, proptosis,
periorbital & conjunctival oedema (these signs seen
more with Grave’s disease
Led retraction
Hyperthyroidism (Thyrotoxicosis)
Diagnosis:





Thyroid function tests (T4, T3, TSH)
Thyroid autoantibodies
Ultrasound scanning
Radioisotope scanning and gland uptake
Biopsy: usually by FNAB
Hyperthyroidism (Thyrotoxicosis)
Treatment:
 Antithyroid drugs: Thiouracil, carbimazole
 Beta blockers: propranolol
 Surgery :
– partial thyroidectomy which usually follow drug
therapy to stabilize the state.
– Thyroidectomy may be complicated by hypothyroidism
 Radioactive iodine
Hyperthyroidism (Thyrotoxicosis)
Oral manifestations and dental management:
– Early exfoliation of primary teeth and early
eruption of permanent teeth
– Thiouracil may cause agranulocytosis and oral
ulceration
– Consult the physician prior to dental treatment
– No elective treatment unless euthyroid
– Routine dental treatment can be done safely in
controlled cases
Hyperthyroidism (Thyrotoxicosis)
Oral manifestations and dental management:
 Care with using adrenaline containing LA ( best to be
avoided in uncontrolled cases)
 Use of sedatives prior to dental treatment may be given
but avoid barbiturates
 The dentist should be ready to deal with thyroid crisis if
it arise in dental office
 Acute oral infection may be precipitate thyroid crisis in
poorly controlled cases
Thyroid crisis (storm)
Explosive form of thyroid signs and symptoms
Causes:
–
Trauma
–
Stress
–
Infection
–
Fatigue
–
Adrenaline injection
Thyroid crisis (storm)
Clinical features:
– Restlessness & tremor
– Nausea and vomiting
– Abdominal pain
– Tachycardia and may be ventricular fibrillation
– Heart failure, pulmonary oedema, hypertension, comma and
death
Thyroid crisis (storm)
Management:
– Refer to hospital immediately
– Thiouracil, propronolol, hydrocortisone, and IV
glucose can be given
– Cold, wet and ice pack application
– Cardiopulmonary resuscitation if necessary (CPR)
Hypothyroidism (myxodema)
In infants and young children it is called
cretinism (growth defect and mental
impairment) and in adult it is called
myxodema


All children have their TSH checked two weeks after
birth as screening process (T4 is to be give if TSH is
high)
Myxodema


It is more common in females: M:F 1:5
Classified into:

Primary:

Secondary: hypothalamic-pituitary disease
Hypothyroidism (myxodema)
Causes of primary myxodema:
– Surgical excision for treatment of hyperthyroidism
– Radiation
– Drugs used for treatment of hyperthyroidism like
carbimazole, amiodazole and lithium
– Hashimoto’s disease
Hypothyroidism (myxodema)
Causes of primary myxodema:
– Iodine deficiency
– Idiopathic atrophy
– Congenital missing of the gland
Hypothyroidism (myxodema)
Clinical features:
 85% of patients are females between 40-70 years
of age and may be undiagnosed for long time
 General features:
– Tiredness
– weight gain
– puffy ‘moon’ face and facial edema
– intolerance of cold
– loss of outer third of eyebrows
– enlarged tongue and soft tissue
 Hematological features: iron efficiency anemia,
pernicious anemia, normochromic and normocytic
anemia
Hypothyroidism (myxodema)
 Cardiovascular features: Bradycardia, angina,
hypertension/hypotension, cardiac failure, pericardial
effusion
 Cutaneous features: Cold, dry skin, loss of body
hair, signs of vitiligo
 Nervous system: Depression, mental sluggishness,
delayed reflexes, cerebellar ataxia and slow poor
memory
 Metabolic features: low BMR, hypercholesterolemia,
hyperglycemia, delayed puberty and mental
retardation
Hypothyroidism (myxodema)
– Muscular-skeletal features: aches pains,
myalgia, carpal tunnel syndrome and muscle
stiffness
– GIT features: constipation
– Goiter in Hashimoto’s disease and iodine
deficiency
Hypothyroidism (myxodema)
Diagnosis:
– Thyroid functions tests
– Immunological tests for Hashimoto’s
disease
Hypothyroidism (myxodema)
Treatment:
– Thyroxin replacement for life 100-200
picogram/day
Hypothyroidism (myxodema)
Dental management:
– Medical consultation in non controlled cases
(treated patients are normal)
– No contraindication to routine dental
treatment in controlled cases taking into
account the usual associated systemic
complications and diseases like IHD,
hypertension and diabetes
– Preventive program to control caries and
periodontal diseases must be adopted for such
patients
Hypothyroidism (myxodema)
Dental management:
– Avoidance the development of myxodema
coma by:
– Reduce stress
– Avoid cold during treatment
– Treat infection promptly
– Avoid use of CNS depressants like sedatives
and narcotics
Myxodema coma
 Hypothermia
 Bradycardia
 Severe hypotension
 Fits
 Management of myxodema coma:
–
–
–
–
Give hydrocortisone (200 mg IV)
Give O2
warming up the patient
Giving T3 or T4 is controversial !!!
Hypothyroidism (myxodema)
Oral manifestations
– In children:
 Delayed eruption of teeth
 Malocclusion
 Enlargement of tongue
– In adults:




Enlarged tongue
Increased incidence of Caries and gingival diseases
Prone to oral candidosis
These patients are prone to depression and may present
with atypical facial pain
Hyperparathyroidism
bone
Hyperparathyroidism
Classified into:
 Primary hyperparathyroidism:
 Adenoma (90% of cases)
 Hyperplasia
 Carcinoma
– Elevated serum calcium level ( much of it mobilized
from bone) plus raised alkaline phosphatase
Hyperparathyroidism
Secondary hyperparathyroidism which is a
reaction to hypocalcemia produced by:

–
Chronic renal failure
–
Calcium malabsorption syndrome
–
Vitamin D deficiency
– Normal or low serum ca level
Hyperparathyroidism

Tertiary hyperparathyroidism (gland
hyperplasia)

Ectopic hyperparathyroidism:

Malignant tumours e.g. bronchogenic
carcinoma and kidney malignancy
Hyperparathyroidism
Primary hyperparathyroidism
 Clinical features:
– Most patients are asymptomatic with no
clinical signs
– “bones, psychic moans, abdo. groans and
stones”
– musculoskeletal:
 weakness
 back pain
 osteolytic lesion (brown tumor)
Hyperparathyroidism
Primary hyperparathyroidism
 Clinical features:
 bones:
– generalized demineralization
– pathological fracture
– cyst like lesions (osteitis fibrosa
cystica)
– fibrosis and anemia
Hyperparathyroidism
 GU system:
– Polyurea caused by osmotic diuresis
– Polydepsia
– Kidney stones, hematuria and UTI
– Renal failure
– Hypertension
 CV system:
– Excitability and dysrrhythmias and
hypertension
 GIT system:
 Pain
 Constipation
 Anorexia
 Peptic ulcer
 Pancreatitis
 Neuro-psychiatric:
 Confusion & drowsiness
 Severe psychosis and EEG changes
Diagnosis:
 Blood chemistry:
 High serum calcium > 10 mg%
 Low serum phosphorus
 High alkaline phosphatase
 High Serum PTH
 Radiography for lesion localization
 Abdominal x-ray to detect any stones and test for renal
function
 Hand x-ray: subperiosteal resorption of the tufts of
distal phalanges
 Serum calcium is very important in differentiating
between primary and secondary hyperparathyroidism as
in later there is low serum Ca, high PO4. and high
Hand x-ray: subperiosteal
resorption of the tufts of
distal phalanges
Osteitis fibrosa cystica in bones
giant cell lesion or brown tumor
Brown tumor
 Bone trabeculae are
missing
 The lesions may be
multiple in single bone
Treatment:
 Usually conservative
 Parathyroidectomy if tumor is large and
the patient is symptomatic
 Vitamin D supplement
Oral manifestations:
 Lose and teeth displacement
 Salivary stones
 Loss of lamina dura
 Loss of medullary trabculation (giant cell
lesion or brown tumor)
– Peripheral
– Central
 Jaw bones may have granular appearance
Dental management:
 Medical consultations
 Consider the management of complication
during dental treatment (dysrrhythmias,
hypertension and renal disease)
 Consider the cause of secondary
hyperparathyroidism
 Patients are prone to fracture
Hypoparathyroidism
 Characterized by low serum calcium
Causes:
 Surgical removal of the parathyroid gland
 Autoimmune (idiopathic ) in young age group
 Di-George syndrome ( thymic aplasia and thyroid
gland are missing) due to agenesis of 3rd & 4th
pharyngeal pouches
Hypoparathyroidism
Causes:
 As part of polyglandular autoimmune
syndrome type 1: which is comprise of
Hypoparathyroidism, Addison’s disease plus
any two of:
 IDDM
 Vitiligo
 Pernicious anemia
 Autoimmune thyroid disease
Hypoparathyroidism
Clinical features:
– Muscular excitability problem (spasm,
stiffness, cramping and tetany)
– Memory loss
– Numbness and tingling of extremities
– Mucocutaneous candidosis
– Dry skin and nail dystrophy
– Malformed and brittle nails
Hypoparathyroidism
Diagnosis:
– Clinical tests:
– Chevostek’s sign: facial muscle twitching
as result of tapping the facial nerve
branches
– Trousseau’s sign: carpopedal spasm due to
reduced blood supply caused by application
of the cuff above systolic pressure for 2
minutes
– Laboratory investigations:
–
–
–
–
Low PTH
Low serum calcium
High serum phosphorus (hyperphosphatemia)
Normal alkaline phosphatase
Hypoparathyroidism
Treatment:
 At present no PTH available
 Supplements of calcium and Vit D
therapy (in emergency give 10-20 ml of
10% ca gluconate IV slow injection)
Hypoparathyroidism
Oral manifestations:
 Enamel and dentine hypoplasia
 Partial anodontia
 Oral candidosis that resist antifungal therapy
Hypoparathyroidism
Dental management is complicated by:
 Tetany
 Epilepsy & dysrrhythmias
 Psychiatric problems
 Management of associated other problems
like hypertension and hypoglycemia
Hypoparathyroidism
(Trousseu's sign)
Adrenal gland
 The adrenal gland consist of two
separate endocrine tissues that are
different structurally, developmentally
and functionally
– Adrenal medulla (Inner part ):
– Adrenal cortex (outer part): consist of:
 Zona glomerulosa: secrete mineralocorticoids
aldosterone
 Zona fasciculata: secrete two glucocorticoids:
– Cortisol
– Corticosterone
 Zona reticularis: secrete androgens or sex
hormones
Effects of glucocorticoids
 Protein metabolism:
 Cause Protein catabolism and increase blood
level of amino acids that can be used for
gluconeogenesis
 Increase osteoclastic activity that result in:
– Osteoporosis
– Mobilization of Ca from bone
 Carbohydrate metabolism: anti-insulin
effect


increase glycogenolysis in liver
Decrease the uptake of glucose by tissue
(except heart & brain)
 Fat metabolism:
– Mobilize fat from adipose tissue
– decrease hepatic lipogenesis so it increase
blood level of FFA
 Effect on blood cells:
– Decrease number of eosinophils, basophils
and lymphocytes (Lymphopenia)
– Increase the number of neutrophils,
platelets and RBCs
 Effect on CNS:
 Changes in EEG
 Mode changes: psychosis, irritability
 Permissive action on other hormones:
catecholamines and glucagon
 Resistance to stress:
 Not completely understood
 Stress is always associated with increase in
cortisol and ACTH
 Stresses include: trauma, surgery, infection,
acute hypoglycemia, fear, anxiety
 Anti-inflammatory effect:
 Decrease chemotaxis & phagocytosis
 Stabilization of Lysosymal proteins and thereby
decreasing the release of proteolytic enzymes
from PMNs & monocytes
 Decrease phospholipase A
 Inhibit formation Leukotrienes and interleukins
 Decrease capillary permeability
 Anti-allergic effect:
– Preventing release of histamine from mast
cells
 Effect on other hormones:
– Decrease secretion of GH & TSH
Steroid
inhibition
NSAID
inhibition
 The anti-allergic and anti-inflammatory
effect are produced only by large doses
(pharmacological effect)
 Diurnal (circadian) of ACTH:
– Highest concentration at early morning
– Lowest concentration at midnight
 Cushing's syndrome:
– is a hormone disorder caused by high
levels of cortisol in the blood.
– This can be caused by taking glucocorticoid
drugs, or by tumors that produce cortisol
or ACTH or CRH
 Cushing's disease:
– Refers to one specific cause of the
syndrome: a tumor (adenoma) in the
pituitary gland that produces large amounts
of ACTH, which in turn elevates cortisol.
Cushing’s syndrome & disease
Causes:
 Excess production of ACTH due to Pit.
tumors (Cushing disease )
 Excess production of cortisol due to adrenal
adenoma
 Excess and long term exogenous steroid
 Ectopic: as in oat cell carcinoma of the lung
and kidney and pancreas malignancies
Cushing’s syndrome & disease
Clinical features:
 The onset is very gradual over many months or years
 Truncal or centripetal obesity (involve trunk and
abdominal wall) but not the limbs
 “Buffalo hump”
 “Moon face” caused by water retention
 Purple abdominal striae
 Poorly developed muscles and weakness
Cushing’s syndrome & disease
Clinical features:
 Atrophic skin and tendency to bruise (effect of
protein catabolism)
 hairsutism in women and acne
 Cushing’s due to ACTH cause hyperpigmentation
 Hypertension: due to water and Na retention and
effect on blood cells
 Diabetes
Cushing’s syndrome & disease
Clinical features:
 Depression, euphoria and psychosis
 Osteoporosis and vertebral collapse due to decrease
in ca absorption from intestine and increased
catabolic effect on connective tissue
 Thrombo – embolism diseases
 Infection tendency
 Poor healing of wounds and fractures
Cushing’s syndrome & disease
Diagnosis:
 Urea and electrolytes determination (high Na, low K)
 Serum cortisol & ACTH
 Dexamethasone suppression test: 2 mg of
Dexamethasone is given 6-hourly for 48 hours.
 The results indicates the site of the pathology:
plasma cortisol suppression occurs in adrenal
hyperplasia but no suppression occurs in adrenal
adenoma or carcinoma.
 MRI and CT scan (for adrenal gland ant. Pituitary)
which can give a good localization of tumor site
Moon or cushinoid face
Moon or cushinoid face
Centripetal or truncal
distribution of fat
Thin skin that lead to telangiectasia
Purplish straiae
Easy bruising
ecchymosis
Cushing’s syndrome & disease
Treatment:
 Depend on the cause:
 Partial or complete adrenalectomy
 Trans- sphenoidal surgery for selective pituitary
tumor removal
 Pituitary radiation
Cushing’s syndrome & disease
Oral manifestations:
 Oral infections: increased periodontal and
fungal infection
 Moon face and Buffalo hump
 Facial telangiectasia
 Oral pigmentation in some cases
Dental management:
 Elective treatment should only be done only after
the cortisol level is brought to normal
 Careful handling and mobilization of the patient to
avoid fracture due to osteoporosis
 Impaired wound and fracture healing
 Dental management may be complicated by:
 Hypertension
 Cardiovascular diseases
 DM
 Psychosis
 Immunosuppression
Hypoadrenocorticism
Primary (Addison’s disease):
– Rare ( 4 in 100,000 cases)
Causes:
– Autoimmune (represent 90% of cases, organ specific and
may be associated with DM, thyroid or pernicious anemia)
– TB and Sarcoidosis
– Hemorrhage and infarcts
– Tumors
– Surgery
Hypoadrenocorticism
Secondary:
 It is more common than primary type
 Usually caused by:
 Long term steroid therapy
 Hypothalamus or pituitary disease (Sheehan’s
syndrome)
 No volume depletion and no hypotension because
aldosterone secretion is normal
 No pigmentation
Hypoadrenocorticism
Clinical features:
 Rare and slow onset over months
 Lethargy, fatigue, weakness and loss of apatite
 Nausea and vomiting
 Hypotension
Hypoadrenocorticism
Clinical features:
 Hypoglycemia
 Loss of body hair
 Skin and oral pigmentation (in primary type)
 Depression
 If left untreated circulatory collapse may occur
Hypoadrenocorticism
Investigations:
 U & E
 ACTH, cortisol and blood sugar
 Synacthan test
Oral pigmentation
Oral pigmentation
Palm of hand skin pigmentation
Hypoadrenocorticism
Treatment:
 Corticosteroid replacement for life long
(20-30 mg/day)
 Mineralocorticoids
supplement (fludrocortisone)
Hypoadrenocorticism
Oral manifestations:
 Oral pigmentations
Hypoadrenocorticism
Dental management:
 Steroid cover on stressful situation (surgery, trauma and
infections)
 Medical consultations before surgery
 Stress reduced protocol before dental procedures
 Antibiotic prophylaxis
 Ability to manage steroid crisis (acute adrenal insufficiency) if
arise:
 Hypotension, Hypovolemic shock and hyponatremia
 Vomiting
 Eventual coma
Steroid alert
Corticosteroids
Corticosteroids used as:
– As a replacement therapy
– As an immunosuppressant agents
Corticosteroids
Indications for steroids
 Allergic reactions: like asthma, allergic dermatitis and
others
 CT diseases: Rheumatoid arthritis, SLE
 Renal diseases: nephrotic syndrome, kidney transplant
 GIT disorders: ulcerative colitis and Crohn’s disease
 Inflammatory conditions: cerebral oedema, Sarcoidosis
Uses of steroids
– Infections: chronic active hepatitis
– Blood diseases: idiopathic thrombocytopenia
and lymphoblastic leukemia
– Adrenal insufficiency: as in Addison’s
disease and adrenalectomy
– Mucocutaneous conditions: pemphigus and
MMP
Corticosteroids
 Anti-inflammatory actions of steroids:
 Effects on leukocyte traffic:
– Lymphocytopenia
– Decrease eosinophils & basophils
– Increase in circulating PMNs by decreasing
migration and chemotaxis
Complications of steroids
 Immunosuppressive
– Increased susceptibility to infection
– Opportunistic infections (especially Candida
spp)
– Reactivation of dormant tuberculosis
 Cardiovascular
–
–
–
–
Hypertension
Myocardial infarction
Cerebrovascular accidents
Hypotensive crises
 Metabolic
– Hypothalamic-pituitary-adrenal (HPA) suppression
– Impaired glucose tolerance & diabetes mellitus
– Growth retardation
– Sodium and potassium loss
– Osteoporosis
– Fat redistribution (moon face & buffalo hump)
 GIT
– Peptic ulcer
 Neurological/Psychological
– Mood changes
– Psychosis
 Cataracts
 Dermatological
– Acne
– Striaea
– Bruising
Corticosteroids
Possible steps for steroid withdraw:
 Reduce the steroid dose gradually over one week
 Observe the patient for few days
 Proceed only if the disease does not flare up
 Withdrawal of the steroid is usually based on clinical
judgment
 It may be safer to increase the dosing interval
rather than to stop steroid abruptly
 If any acute problems arise after withdrawal it is
safer to assume insufficiency and treat with steroids
Corticosteroids
Adrenal suppression occurs if:
 High dose is given ( exceed normal physiological dose
of 7.5 mg/day of prednisolone)
 Prolonged administration (5 days course may cause
cessation for 1 week)
 Multiple doses throughout the day is given (single
morning dose is preferable)
– Alternate days course is advisable if the clinical condition
allows
 Before giving steroids, the following should be
checked:
 Weight
 BP
 Blood glucose
 Chest x-ray
 Make sure that there is no contraindication
to its use
 Better to give as a single morning dose and
on alternate days
 Do not stop abruptly
 Dose is to increased if there is infection or
trauma