The Endocrine system
for dental students
DR IBRAHIM HASSAN
ALZAHRANI FRCPath -UK
Chairman of Pathology
Departement
Faculty of Medicine
CONTENTS:
• Pituitary gland
– Hypopituitarism
– Hyperpituitarism
– Posteroir pituitary syndromes
• Thyroid galnd
–
–
–
–
–
Hypothyrodism
Hyperthyrodism
Goiter
Thyrodidtis
Tumors
• Parathyroid glands
– Hyperparathyroidism
– Hypoparathyroidism
• Adrenal gland
– Cortex
– Medulla
. Tumors
• Multiple endocrine neoplasia
• Endocrine pancreas (D.M )
THYROID GLAND
• This is the normal
appearance of the
thyroid gland on
the anterior trachea
of the neck..
Normal thyroid seen microscopically consists of follicles
lined
by a cuboidal epithelium and filled with pink,
homogenous colloid
Hypothyroidism:
• Causes:
– structural or functional
– 95% are due to:
• Surgical or radiation ablation
• Hashimoto’s thyroiditis
• Primary idiopathic hypothyroidism
Cretinism
• This is uncommon disease of
childhood due to failure of thyroid to
synthesize thyroid hormones 
hypothyroidism
Myxedma, cretenism
• Neurologic & myxedematous
patterns
• Clinically:
– mental retardation
– growth retardation (short stature)
– coarse facial features with dry skin and
protruding tongue
– muscle weakness and umbilical hernia
Myxedema
• Hypothyroidism in adult.
• - Clinically:
–
–
–
–
–
appear insidiously & subtle
lethargy & weakness with slow speech
cold intolerance with cool & rough skin
menstrual problems & psychosis
cardiac changes:  cardiac output,
hypertrophy, (myxedema heart), pericardial
effusion
– deposition of mucopolysaccharides in
connective tissue
– atherosclerosis ( cholesterol)
Hyperthyroidism
• Excess thyroid hormone
(Thyrotoxicosis)
• Causes:
– primary diffuse toxic hyperplasia
(Grave’s disease) > 95%
– toxic multinodular goiter
– toxic adenoma
– certain form of thyroiditis
– secondary to pituitary or hypothalamic
lesion
• Clinical features:
•
•
•
•
nervousness and emotional instability
menstrual changes
fine tremors of the hands
heat intolerance with warm skin and
sweating
• weight loss despite a good appetite
• Eye changes: (exopthalmos, widened
palpebral fissures, staring gaze)
• Cardiac changes: (tachycardia,
palpitations, atrial fibrillation and
thyrotoxic cardiomyopathy----- cardiac
failure)
• skeletal muscle atrophy and fatty
infiltration
• lymphadenopathy
• fatty change of the liver
• Osteoporosis
Thyrotoxicosis
Upper, thyrotoxicosis
Lower, after
treatment
Goiter
• Goiter simply means enlarged
thyroid
Diffuse Goiter
• Characterized by diffuse
symmetrical enlargement of thyroid
(200 - 300 gm) with normal thyroid
function.
• Hypofunction may occur early in the
course .
• Usually occurs in: Endemic areas
( iodine & goiterogens) or
• Sporadic (physiological
Multinodular Goiter
• Characterized by
nodular
asymmetrical
enlargement of
thyroid (up to 1000
gm)
• Slowly evolves
from diffuse
goiter.It can be
toxic or non-toxic
Solitary thyroid nodule
•
•
•
•
•
•
Size (symptoms)
Possible hyperfunction
Usually colloid nodule >70%
Adenoma 20-30%
Carcinoma <5%
 - Radioactive iodine (Hot & cold
nodule)
• FNA & biopsy
• Thyroid function
Solitary thyroid nodule
• Invisigations:
• thyroid hormons: (T3,T4,TSH)
• radiological examinations :
* ultrasound (cystic/solid)
* radioactive iodine (cold/hot)
• Fine needle aspiration cytology
GRAVE’S DISEASE
•
•
•
•
Primary Diffuse Toxic Hyperplasia
The most common cause of thyrotoxicosis
It is an autoimmune disease
Classically shows:
– 1-Exopthalmos (proptosis)
– 2-Dermopathy (pretibial myxedema)
– 3-Hyperthyroidism
•
•
•
•
Common in ♀ 3rd & 4th decade
♀ : ♂ = 10 : 1
HLA – DR3 & Familial predisposition
Other autoimmune diseases may occur
•Pathogenesis
• B-cells secrete autoantibodies
against mainly TSH – Receptors
(Abs. against microsomes,
thyroglobulin, T3 & T4 can be
seen)
Morphology
• Gross:
diffuse
symmetrical
enlargement of
thyroid
THYROIDITIS
• Hashimoto’s thyroiditis
• Subacute
(granulomatous,DeQuervian)
thyroiditis
• Chronic lymphocytic (painless)
thyroiditis
• Riedel’s fibrous thyroiditis
Hashimoto’s thyroiditis
• This is an autoimmune most
common type of thyroiditis
characterized by symmetrical
modesty enlarged thyroid
responsible for most cases of
primary goiterous
hypothyroidism.
Pathogenesis
• B cells  autoantibodies against
microsomes and thyroglobulin.
• Cell-mediated destruction of the
gland
• ♀ : ♂ = 10 : 1 middle-aged
• Higher incidence of autoimmune
disease
Clinical Course
• Euthyroid---  hypothyroid
• Moderate goiter
• Hashitoxicosis(hyperthyroidism)
occasionally
• 5% - B cell lymphoma or rarely
papillary carcinoma of thyroid
THYROID TUMOURS
1-BENIGN:
Follicular adenoma
2-MALIGNANT:
• Carcinoma of thyroid
–
–
–
–
Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Anablastic carcinoma
–Lymphoma
Others – rare (sq. ca, sarcomas, metastasis)
ADENOMA
• Always follicular adenoma
•
•
•
•
No papillary adenoma of thyroid.
Solitary & encapsulated.
No capsular invasion.
Histology: Follicles –> macro (colloid), micro
(fetal), normal size (simple), trabecular
(embryonal).
• Sometimes composed of Hürthl cells
(oncocytic)
Hurthle cell adenoma.
ADENOMA
ADENOMA
CARCINOMA OF
THYROID
• Causes:
– Ionizing radiation
– Hashimoto’s thyroiditis
– Grave’s disease?
Papillary Carcinoma
60-70%
• The most common type
• Young age 20-50y , F:M=3:1
• Forming papillae and psammoma bodies
• Cells typically show ground-glass
appearance with clear grooved nuclei
“Orphan Annie” and intranuclear inclusion
• 50% at presentation  Cervical LN
metastasis
• Haematogenous spread is rare (not
common)
•Follicular variant of
papillary carcinoma :
No papillary formation .
The nuclei shows typical nuclear
ground glass appearance of papilary
crcinoma.
•Grow slowly with indolent course
•Occult microscopic variant
Papillary Carcinoma
Follicular Carcinoma
• Macroscopically often encapsulated
similar to adenoma
• Histologically : composed of follicles
with no papillary formation and no
groundglass nuclear changes.
• sometimes the cells are oncocytic
(Hurthle cell carcinoma).
Follicular Carcinoma
• Haematogenous spread (lung, bone, liver.
.)
• Poorer in prognosis than papillary
carcinoma.
• Represent approximatly 15%
• Most patients are >40y
• TYPES:
1- minimally invasive FC.
2- widely invasive FC.
Medullary Carcinoma of
thyroid <5%
• Derived from calcitonin – secreting
C-cells
• Characterized by formation of
amyloid material from calcitonin,
surrounded by small to medium sized
cells with round to spindle shaped
nuclei forming sheets, nests or cords
Medullary Carcinoma
amyloid
Medullary Carcinoma
• It has slow but progressive growth
• Both lymphatic and hematogenous
metastasis occurs
• 10-20% are familial, multicenteric in
young age, associated with MEN 2&3
• Immuno: +ve calcitonin
• 80-90% sporadic, solitary, old age
Anablastic carcinoma 5-10%
0ccurs in patient > 60 y
• Poorly differentiated, highly malignant tumour
usually forms bulky necrotic mass often
disseminate extensively through blood
• death occurs within 1-2 years (<10% survive for
10y)
•Histological variants:
• Giant cells, spindle cells(sarcomatoid), squamoid
cells
PARATHYROID GLAND
PARATHYROID GLAND
Hyperparathyroidism
- Primary Hyperparathyroidism:
Increase
PTH due to parathyroid lesion
(Adenoma/hyperplasia)
 Hypercalcaemia
PTH  Hypercalcaemia :
–
–
–
–
 osteoclast to mobilize Ca++ from bone
 Ca++ reabsorption in the kidney
 Ca++ absorption in Git .through vit .D.
 excretion of phosphate in urine .
• Part of MEN I & II
• F : M = 3 : 1 > 40y
Clinical features
• Asymptomatic (lethargy&weakness)
• Bone pain (osteomalacia, osteoporosis &
osteitis fibrosa cystica/brown
tumor)
• Renal stones (nephrolithiasis)
• Nephrocalcinosis
• Metastatic calcification (blood vessels, soft
tissue & & joints)
• Abdominal pain (peptic ulcer,pancreatitis) and
mental change
Parathyroid adenoma
adenoma
normal
Adenoma & Hyperplasia
In adenoma one gland, Hyperplasia >one gland
• Frozen section (intraoperative consultation)
required to confirm presence of parathyroid
tissue.
*
Carcinoma of parathyroid:
Rare
– Invasion and metastasis
– Bands of collagen in the stroma
– High mitotic figures.
Parathyroid carcinoma
MULTIPLE ENDOCRINE
NEOPLASIA
MULTIPLE ENDOCRINE
NEOPLASIA (MEN)
• MEN are syndromes characterized by
hyperplasic or neoplastic involvement of
at least two endocrine glands and
sometimes associated with non-endocrine
lesions.
• MEN I:
–
–
–
Wermer ’ s Syndrome
Parathyroid adenom/hyperplasia .
Pituitary adenoma .
Pancreatic lesions (hyperplasia
adenoma , carcinoma )
– Mutant gene(MEN1) locus at 11q13
– Autosomal dominnant
• MEN II (IIa): Sipple
–
–
–
Syndrome
Medullary carcinoma of thyroid
Pheochromocytoma .
Occasionally parathyroid lesion
(30%)
–
Mutant gene locus at 10q11.2
(RET proto-oncogen)
–
Autosomal dominant
• MEN III (IIb):William syndrome:
similar to MEN II plus
–
–
–
Marfanoid bodily habitus
Multiple mucocutanenous
ganglioneuromas
Parathyroid involvement :
(none/rare).