Endocrine.ppttttttttttttttttttttttttttttt
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Sep 16, 2025
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About This Presentation
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Slide Content
Dr. Ahmad Itmezeh
The endocrine system comprises two The endocrine system comprises two
main components main components
i.i. The classical endocrine organs e.g. pituitary, The classical endocrine organs e.g. pituitary,
thyroid, adrenal, parathyroid, islet’ of Langerhans thyroid, adrenal, parathyroid, islet’ of Langerhans
in pancreas.in pancreas.
ii.ii. The diffuse endocrine system consist of cells The diffuse endocrine system consist of cells
dispersed singly or in small group throughout dispersed singly or in small group throughout
various non-endocrine organ including G.I.T. lung. various non-endocrine organ including G.I.T. lung.
Skin.Skin.
main components main components
i.i. The classical endocrine organs e.g. pituitary, The classical endocrine organs e.g. pituitary,
thyroid, adrenal, parathyroid, islet’ of Langerhans thyroid, adrenal, parathyroid, islet’ of Langerhans
in pancreas.in pancreas.
ii.ii. The diffuse endocrine system consist of cells The diffuse endocrine system consist of cells
dispersed singly or in small group throughout dispersed singly or in small group throughout
various non-endocrine organ including G.I.T. lung. various non-endocrine organ including G.I.T. lung.
Skin.Skin.
The pituitary gland is a small , bean- shaped structure
that lies at the base of the brain within the confines of the
sella turcica. The pituitary is composed of two
morphologically and functionally distinct components : the
anterior lobe (adenohypophysis) and the posterior lobe
(neurohypophysis).
Diseases of the pituitary , accordingly , can be divided
into those that primarily affect the anterior lobe and those that
primarily affect the posterior lobe.
The pituitary gland and the hypothalamus The pituitary gland and the hypothalamus
that lies at the base of the brain within the confines of the
sella turcica. The pituitary is composed of two
morphologically and functionally distinct components : the
anterior lobe (adenohypophysis) and the posterior lobe
(neurohypophysis).
Diseases of the pituitary , accordingly , can be divided
into those that primarily affect the anterior lobe and those that
primarily affect the posterior lobe.
The pituitary gland and the hypothalamus The pituitary gland and the hypothalamus
1.1.Hyperpituitarism Hyperpituitarism :: This disorder arises from excessive This disorder arises from excessive
secretion of trophic hormones . It most often results from secretion of trophic hormones . It most often results from
an anterior pituitary adenoma, but may also be caused by an anterior pituitary adenoma, but may also be caused by
other pituitary and extra- pituitary lesions .other pituitary and extra- pituitary lesions .
2.2.Hypopitutarism Hypopitutarism :: This is caused by deficiency of trophic This is caused by deficiency of trophic
hormones and results from a variety of destruc- tive hormones and results from a variety of destruc- tive
processes, including ischemic injury, surgery or radiation processes, including ischemic injury, surgery or radiation
and inflammatory reactions .and inflammatory reactions .
Symptoms of pituitary disease can be divided into Symptoms of pituitary disease can be divided into
the following :the following :
secretion of trophic hormones . It most often results from secretion of trophic hormones . It most often results from
an anterior pituitary adenoma, but may also be caused by an anterior pituitary adenoma, but may also be caused by
other pituitary and extra- pituitary lesions .other pituitary and extra- pituitary lesions .
2.2.Hypopitutarism Hypopitutarism :: This is caused by deficiency of trophic This is caused by deficiency of trophic
hormones and results from a variety of destruc- tive hormones and results from a variety of destruc- tive
processes, including ischemic injury, surgery or radiation processes, including ischemic injury, surgery or radiation
and inflammatory reactions .and inflammatory reactions .
Symptoms of pituitary disease can be divided into Symptoms of pituitary disease can be divided into
the following :the following :
Pituitary Adenomas Pituitary Adenomas
1.1.The most common cause of hyperpituitarism is an adenoma The most common cause of hyperpituitarism is an adenoma
arising in the anterior lobe.arising in the anterior lobe.
2.2.Pituitary adenomas are classified on the basis of hormone(s) Pituitary adenomas are classified on the basis of hormone(s)
produced by the neoplastic cells, which are detected by produced by the neoplastic cells, which are detected by
immunohistochemical stains performed on tissue sections immunohistochemical stains performed on tissue sections
Pituitary adenoma are divided into micro adenoma < 10mm Pituitary adenoma are divided into micro adenoma < 10mm
diameter and macro adenoma > 10mm. diameter and macro adenoma > 10mm.
Clinically diagnosed pituitary adenomas are responsible Clinically diagnosed pituitary adenomas are responsible
for about 10% of intracranial neoplasms, and usually found in for about 10% of intracranial neoplasms, and usually found in
adults, with a peak incidence from the 30s to the 50s. adults, with a peak incidence from the 30s to the 50s.
1.1.The most common cause of hyperpituitarism is an adenoma The most common cause of hyperpituitarism is an adenoma
arising in the anterior lobe.arising in the anterior lobe.
2.2.Pituitary adenomas are classified on the basis of hormone(s) Pituitary adenomas are classified on the basis of hormone(s)
produced by the neoplastic cells, which are detected by produced by the neoplastic cells, which are detected by
immunohistochemical stains performed on tissue sections immunohistochemical stains performed on tissue sections
Pituitary adenoma are divided into micro adenoma < 10mm Pituitary adenoma are divided into micro adenoma < 10mm
diameter and macro adenoma > 10mm. diameter and macro adenoma > 10mm.
Clinically diagnosed pituitary adenomas are responsible Clinically diagnosed pituitary adenomas are responsible
for about 10% of intracranial neoplasms, and usually found in for about 10% of intracranial neoplasms, and usually found in
adults, with a peak incidence from the 30s to the 50s. adults, with a peak incidence from the 30s to the 50s.
4.4.Pituitary adenomas can be functional (i.e., associated with Pituitary adenomas can be functional (i.e., associated with
hormone excess and clinical manifestations thereof) or silent hormone excess and clinical manifestations thereof) or silent
(i.e., immunohistochemical and / or ultrastructural (i.e., immunohistochemical and / or ultrastructural
demonstration of hormone production at the tissue level only, demonstration of hormone production at the tissue level only,
without clinical manifestations of hormone excess), or may be without clinical manifestations of hormone excess), or may be
hormone negative, based on absence of immunohistochemical hormone negative, based on absence of immunohistochemical
reactivity.reactivity.
5.5.Both functional and silent pituitary adenomas are usually Both functional and silent pituitary adenomas are usually
composed of a single cell type and produce a single composed of a single cell type and produce a single
predominant hormone, although exceptions are known to occur.predominant hormone, although exceptions are known to occur.
6.6.Some pituitary adenomas can secrete two hormones (growth Some pituitary adenomas can secrete two hormones (growth
hormone and prolactin being the most common combination); hormone and prolactin being the most common combination);
rarely, pituitary adenomas are plurihormonal.rarely, pituitary adenomas are plurihormonal.
7.7.Most pituitary adenomas occur as isolated lesions. In about 3% Most pituitary adenomas occur as isolated lesions. In about 3%
of cases, however, adenomas are associated with multiple of cases, however, adenomas are associated with multiple
endocrine neoplasia type 1 (MEN-1) syndrome. endocrine neoplasia type 1 (MEN-1) syndrome.
hormone excess and clinical manifestations thereof) or silent hormone excess and clinical manifestations thereof) or silent
(i.e., immunohistochemical and / or ultrastructural (i.e., immunohistochemical and / or ultrastructural
demonstration of hormone production at the tissue level only, demonstration of hormone production at the tissue level only,
without clinical manifestations of hormone excess), or may be without clinical manifestations of hormone excess), or may be
hormone negative, based on absence of immunohistochemical hormone negative, based on absence of immunohistochemical
reactivity.reactivity.
5.5.Both functional and silent pituitary adenomas are usually Both functional and silent pituitary adenomas are usually
composed of a single cell type and produce a single composed of a single cell type and produce a single
predominant hormone, although exceptions are known to occur.predominant hormone, although exceptions are known to occur.
6.6.Some pituitary adenomas can secrete two hormones (growth Some pituitary adenomas can secrete two hormones (growth
hormone and prolactin being the most common combination); hormone and prolactin being the most common combination);
rarely, pituitary adenomas are plurihormonal.rarely, pituitary adenomas are plurihormonal.
7.7.Most pituitary adenomas occur as isolated lesions. In about 3% Most pituitary adenomas occur as isolated lesions. In about 3%
of cases, however, adenomas are associated with multiple of cases, however, adenomas are associated with multiple
endocrine neoplasia type 1 (MEN-1) syndrome. endocrine neoplasia type 1 (MEN-1) syndrome.
8.8.Microscopically, pituitary adenomas are composed of Microscopically, pituitary adenomas are composed of
relatively uniform, polygonal cells arrayed in sheets cords, or relatively uniform, polygonal cells arrayed in sheets cords, or
papillae. Supporting connective tissue, or reticulin, is sparse, papillae. Supporting connective tissue, or reticulin, is sparse,
accounting for the soft, gelatinous consistency of many accounting for the soft, gelatinous consistency of many
lesions. The nuclei of the neoplastic cells may be uniform or lesions. The nuclei of the neoplastic cells may be uniform or
pleomorphic. Mitotic activity is usually scanty. This cellular pleomorphic. Mitotic activity is usually scanty. This cellular
monomorphism and the absence of a significant reticulin monomorphism and the absence of a significant reticulin
network distinguish pituitary adenomas from non-neoplastic network distinguish pituitary adenomas from non-neoplastic
anterior pituitary parenchyma.anterior pituitary parenchyma.
Acromegaly Acromegaly (GH producing pituitary (GH producing pituitary
adenoma)adenoma), illustrating the thickening of the , illustrating the thickening of the
nose and enlargement of the lower jawnose and enlargement of the lower jaw
Note monomorphic population of cells Note monomorphic population of cells
with little - no nuclear atypia and clear with little - no nuclear atypia and clear
cytoplasm (this one is chromophobic) cytoplasm (this one is chromophobic)
Pituitary adenoma
relatively uniform, polygonal cells arrayed in sheets cords, or relatively uniform, polygonal cells arrayed in sheets cords, or
papillae. Supporting connective tissue, or reticulin, is sparse, papillae. Supporting connective tissue, or reticulin, is sparse,
accounting for the soft, gelatinous consistency of many accounting for the soft, gelatinous consistency of many
lesions. The nuclei of the neoplastic cells may be uniform or lesions. The nuclei of the neoplastic cells may be uniform or
pleomorphic. Mitotic activity is usually scanty. This cellular pleomorphic. Mitotic activity is usually scanty. This cellular
monomorphism and the absence of a significant reticulin monomorphism and the absence of a significant reticulin
network distinguish pituitary adenomas from non-neoplastic network distinguish pituitary adenomas from non-neoplastic
anterior pituitary parenchyma.anterior pituitary parenchyma.
Acromegaly Acromegaly (GH producing pituitary (GH producing pituitary
adenoma)adenoma), illustrating the thickening of the , illustrating the thickening of the
nose and enlargement of the lower jawnose and enlargement of the lower jaw
Note monomorphic population of cells Note monomorphic population of cells
with little - no nuclear atypia and clear with little - no nuclear atypia and clear
cytoplasm (this one is chromophobic) cytoplasm (this one is chromophobic)
Pituitary adenoma
Clinical Manifestations of Pituitary Adenomas Clinical Manifestations of Pituitary Adenomas
•Prolactinomas :Prolactinomas : amenorrhea, galactorrhea, loss of libido, and amenorrhea, galactorrhea, loss of libido, and
infertility.infertility.
•Growth homone (somatotroph cell) adenomas :Growth homone (somatotroph cell) adenomas : gigantism gigantism
(children), acromegaly (adults), impaired glucose tolerance, (children), acromegaly (adults), impaired glucose tolerance,
and diabetes mellitus.and diabetes mellitus.
•Corticotroph cell adenomas :Corticotroph cell adenomas : Cushing syndrome, Cushing syndrome,
hyperpigmentation. hyperpigmentation.
•All pituitary adenomas, particularly nonfunctioning All pituitary adenomas, particularly nonfunctioning
adenomas, may be associated with mass effects and adenomas, may be associated with mass effects and
hypopituitarism. hypopituitarism.
•Prolactinomas :Prolactinomas : amenorrhea, galactorrhea, loss of libido, and amenorrhea, galactorrhea, loss of libido, and
infertility.infertility.
•Growth homone (somatotroph cell) adenomas :Growth homone (somatotroph cell) adenomas : gigantism gigantism
(children), acromegaly (adults), impaired glucose tolerance, (children), acromegaly (adults), impaired glucose tolerance,
and diabetes mellitus.and diabetes mellitus.
•Corticotroph cell adenomas :Corticotroph cell adenomas : Cushing syndrome, Cushing syndrome,
hyperpigmentation. hyperpigmentation.
•All pituitary adenomas, particularly nonfunctioning All pituitary adenomas, particularly nonfunctioning
adenomas, may be associated with mass effects and adenomas, may be associated with mass effects and
hypopituitarism. hypopituitarism.
Posterior Pituitary Syndromes Posterior Pituitary Syndromes
1. Hormones are synthesized in hypothalamus and transported 1. Hormones are synthesized in hypothalamus and transported
via axons to the posterior pituitary.via axons to the posterior pituitary.
A.A.Oxytocin induces uterine contraction during labor and Oxytocin induces uterine contraction during labor and
ejection of milk from mammary alveoli ejection of milk from mammary alveoli
B.B.Antidiuretic hormone (ADH , vasopressin ) promotes Antidiuretic hormone (ADH , vasopressin ) promotes
water retention through action on the renal collecting ductswater retention through action on the renal collecting ducts..
SIADH is most commonly caused by ectopic productionSIADH is most commonly caused by ectopic production
of ADH by various tumors especially of ADH by various tumors especially small cell carcinoma of small cell carcinoma of
the lung the lung
1. Hormones are synthesized in hypothalamus and transported 1. Hormones are synthesized in hypothalamus and transported
via axons to the posterior pituitary.via axons to the posterior pituitary.
A.A.Oxytocin induces uterine contraction during labor and Oxytocin induces uterine contraction during labor and
ejection of milk from mammary alveoli ejection of milk from mammary alveoli
B.B.Antidiuretic hormone (ADH , vasopressin ) promotes Antidiuretic hormone (ADH , vasopressin ) promotes
water retention through action on the renal collecting ductswater retention through action on the renal collecting ducts..
SIADH is most commonly caused by ectopic productionSIADH is most commonly caused by ectopic production
of ADH by various tumors especially of ADH by various tumors especially small cell carcinoma of small cell carcinoma of
the lung the lung
- SIADH results in retention of water with consequent
dilutional hyponatremia reduced serum osmolality and
Inability to dilute the urine
3. deficiency of ADH
A. This results in diabetes insipidus is characterized by
Polyuria with consequent dehydration and polydipsia
Nonfunctioning pituitary tumors:-
1. Nonsecreting pituitary adenomamas are most often
chromophobic
A. Dysfunction results because of local pressure effect
B. These tumors are clinically variable include hypopituitarism ,
headache , visual disturbances due to pressure on optic
chiasm and palsies caused by cranial nerve damage.
dilutional hyponatremia reduced serum osmolality and
Inability to dilute the urine
3. deficiency of ADH
A. This results in diabetes insipidus is characterized by
Polyuria with consequent dehydration and polydipsia
Nonfunctioning pituitary tumors:-
1. Nonsecreting pituitary adenomamas are most often
chromophobic
A. Dysfunction results because of local pressure effect
B. These tumors are clinically variable include hypopituitarism ,
headache , visual disturbances due to pressure on optic
chiasm and palsies caused by cranial nerve damage.
Thyroid gland
The thyroid gland produces 3 hormones :
1. Thyroxine
2. Tri-iodothyronine : It is more potent .
They are not present as free compounds but are
constituents of thyroglobulin in the colloid .
3. Calcitonin : ( c - cells ) It is produced by the parafollicular
cells. It is polypeptides which lower the conc. Of calcium
in the blood by causing deposition of calcium in the bone .
The normal adult gland weights 20-40 gm, & consists of two
lateral lobes connected by isthmus .
Micro. : It consists of thyroid follicles lined by cuboidal
epithelium & containing colloid.
The thyroid gland produces 3 hormones :
1. Thyroxine
2. Tri-iodothyronine : It is more potent .
They are not present as free compounds but are
constituents of thyroglobulin in the colloid .
3. Calcitonin : ( c - cells ) It is produced by the parafollicular
cells. It is polypeptides which lower the conc. Of calcium
in the blood by causing deposition of calcium in the bone .
The normal adult gland weights 20-40 gm, & consists of two
lateral lobes connected by isthmus .
Micro. : It consists of thyroid follicles lined by cuboidal
epithelium & containing colloid.
This is the normal appearance of the thyroid gland on the anterior trachea This is the normal appearance of the thyroid gland on the anterior trachea
of the neck. The thyroid gland has a right lobe and a left lobe connected by of the neck. The thyroid gland has a right lobe and a left lobe connected by
a narrow isthmus. a narrow isthmus.
of the neck. The thyroid gland has a right lobe and a left lobe connected by of the neck. The thyroid gland has a right lobe and a left lobe connected by
a narrow isthmus. a narrow isthmus.
Hormone synthesis in the thyroid gland :
1. The follicular cells of the thyroid gland remove iodide from the
plasma at a rate which is controlled by the plasma / gland iodide
gradient & by TSH .
2. The iodide is oxidized to iodine.
3.The iodine is taken up by a tyrosine component of an
intrathyroid globulin to produce mono-& di-iodotyrosine- this
forms the colloid .
4. Two of these molecules condense to form thyroxine & tri-
iodothyronine, which are coupled to globulin as thyroglobulin.
5. Thyroglobulin is hydrolysed & thyroid hormones are released
into the circulation.
1. The follicular cells of the thyroid gland remove iodide from the
plasma at a rate which is controlled by the plasma / gland iodide
gradient & by TSH .
2. The iodide is oxidized to iodine.
3.The iodine is taken up by a tyrosine component of an
intrathyroid globulin to produce mono-& di-iodotyrosine- this
forms the colloid .
4. Two of these molecules condense to form thyroxine & tri-
iodothyronine, which are coupled to globulin as thyroglobulin.
5. Thyroglobulin is hydrolysed & thyroid hormones are released
into the circulation.
Goiter
It is an enlargement of part or whole of the
thyroid . It may be diffuse or nodular & it may be
associated with a deficient , normal , or excessive
production of thyroid hormone.
Cross Multinodular goiter Micro-Multinodular goiter
Functional disorders of thyroid glandFunctional disorders of thyroid gland
It is an enlargement of part or whole of the
thyroid . It may be diffuse or nodular & it may be
associated with a deficient , normal , or excessive
production of thyroid hormone.
Cross Multinodular goiter Micro-Multinodular goiter
Functional disorders of thyroid glandFunctional disorders of thyroid gland
Types :
1. Nontoxic goiter : ( Simple goiter ) :
a. Sporadic nontoxic
b. parenchymatous
c. Colloid goiter : Diffuse
Nodular
2. Toxic goiter :
I. Primary
II. Secondary.
Simple goiter
The thyroid enlargement is a response to insufficient
iodine intake resulting from a deficient of iodine in the soil &
water. Endemic goiter may be prevented by the addition to the
diet of minute amount of iodine as by the use of iodised salt.
The condition occurs more commonly in females & is
particularly likely to develop at a time when the thyroid gland
is subjected to extra functional stress as in adolescence or
pregnancy .
1. Nontoxic goiter : ( Simple goiter ) :
a. Sporadic nontoxic
b. parenchymatous
c. Colloid goiter : Diffuse
Nodular
2. Toxic goiter :
I. Primary
II. Secondary.
Simple goiter
The thyroid enlargement is a response to insufficient
iodine intake resulting from a deficient of iodine in the soil &
water. Endemic goiter may be prevented by the addition to the
diet of minute amount of iodine as by the use of iodised salt.
The condition occurs more commonly in females & is
particularly likely to develop at a time when the thyroid gland
is subjected to extra functional stress as in adolescence or
pregnancy .
Sporadic goiter may occur due to :
1. Iodine deficiency due to improper dietary habits.
2. Dyshormonogenesis due to one of a group of inherited defects of
the process of thyroid hormone synthesis or secretion.
3. The action of substances which interfere with thyroid hormone
synthesis e.g. the ingestion of certain plant foods containing
goitrogenic substances.
1. Iodine deficiency due to improper dietary habits.
2. Dyshormonogenesis due to one of a group of inherited defects of
the process of thyroid hormone synthesis or secretion.
3. The action of substances which interfere with thyroid hormone
synthesis e.g. the ingestion of certain plant foods containing
goitrogenic substances.
Gross :
The thyroid gland is enlarged which may be diffuse or
nodular. The cut surface is transluscent because of the colloid
material. Degenerative changes are common & there may be
haemorrhage, cyst formation, calcification & fibrosis.
Many of these goiters reach an enormous size & they
may show a retrosternal prolongation .
Micro. :
The goiter consists of a large distended follicles
containing colloid & lined by a low cuboidal or flattened
epithelium. In some cases of simple goiter the thyroid gland is
composed of small follicles without excess of colloid
accumulation. This variety is termed parenchymatous goiter .
The thyroid gland is enlarged which may be diffuse or
nodular. The cut surface is transluscent because of the colloid
material. Degenerative changes are common & there may be
haemorrhage, cyst formation, calcification & fibrosis.
Many of these goiters reach an enormous size & they
may show a retrosternal prolongation .
Micro. :
The goiter consists of a large distended follicles
containing colloid & lined by a low cuboidal or flattened
epithelium. In some cases of simple goiter the thyroid gland is
composed of small follicles without excess of colloid
accumulation. This variety is termed parenchymatous goiter .
Toxic goiterToxic goiter
I. Primary thyrotoxicosis–Graves disease, Exophthalmic goiter:I. Primary thyrotoxicosis–Graves disease, Exophthalmic goiter:
There is a moderate diffuse enlargement of thyroid gland There is a moderate diffuse enlargement of thyroid gland
occurring mostly in females below the age of 40 years , & occurring mostly in females below the age of 40 years , &
associated with evidence of hyperfunction & eye signsassociated with evidence of hyperfunction & eye signs..
Complications :Complications :
1.1.Pressure :Pressure : Especially on the trachea & oesophagus, particularly Especially on the trachea & oesophagus, particularly
when there is retrosternal extension .when there is retrosternal extension .
2.2.Haemorrhage :Haemorrhage : Into the nodules producing a rapid increase in Into the nodules producing a rapid increase in
size. This may increase the pressure symptoms to a dangerous size. This may increase the pressure symptoms to a dangerous
degree & result in asphyxia.degree & result in asphyxia.
3.3.Toxic changesToxic changes
4.4.Malignancy :Malignancy : Carcinoma may develop in a very small percentage. Carcinoma may develop in a very small percentage.
I. Primary thyrotoxicosis–Graves disease, Exophthalmic goiter:I. Primary thyrotoxicosis–Graves disease, Exophthalmic goiter:
There is a moderate diffuse enlargement of thyroid gland There is a moderate diffuse enlargement of thyroid gland
occurring mostly in females below the age of 40 years , & occurring mostly in females below the age of 40 years , &
associated with evidence of hyperfunction & eye signsassociated with evidence of hyperfunction & eye signs..
Complications :Complications :
1.1.Pressure :Pressure : Especially on the trachea & oesophagus, particularly Especially on the trachea & oesophagus, particularly
when there is retrosternal extension .when there is retrosternal extension .
2.2.Haemorrhage :Haemorrhage : Into the nodules producing a rapid increase in Into the nodules producing a rapid increase in
size. This may increase the pressure symptoms to a dangerous size. This may increase the pressure symptoms to a dangerous
degree & result in asphyxia.degree & result in asphyxia.
3.3.Toxic changesToxic changes
4.4.Malignancy :Malignancy : Carcinoma may develop in a very small percentage. Carcinoma may develop in a very small percentage.
Aetiology :Aetiology :
The actual stimulus for the hyperactivity of the thyroid gland is not The actual stimulus for the hyperactivity of the thyroid gland is not
very well known. very well known. Evidence points to an autoantibody to some
cellular components of the thyroid gland which is called long-
acting thyroid stimulator (LATS), It is possible that the globulin
(which is IgG) acts against the normal inhibitor of mitoses in the
thyroid gland. Thus the removal of mitotic inhibition could lead to
hyperplasia followed by hyperfunction.
Macro. :
There is diffuse vascular & fleshy enlargement of the gland with
lack of colloid seen on the cut surface .
Micro. : It is characterized by :
1.The lining epithelium of the thyroid follicles is hyperplastic, tall &
columnar, with papillary processes projecting into the lumen of the
follicles.
2.The follicles are deficient in colloid & show scalloping of the
colloid margins .
The actual stimulus for the hyperactivity of the thyroid gland is not The actual stimulus for the hyperactivity of the thyroid gland is not
very well known. very well known. Evidence points to an autoantibody to some
cellular components of the thyroid gland which is called long-
acting thyroid stimulator (LATS), It is possible that the globulin
(which is IgG) acts against the normal inhibitor of mitoses in the
thyroid gland. Thus the removal of mitotic inhibition could lead to
hyperplasia followed by hyperfunction.
Macro. :
There is diffuse vascular & fleshy enlargement of the gland with
lack of colloid seen on the cut surface .
Micro. : It is characterized by :
1.The lining epithelium of the thyroid follicles is hyperplastic, tall &
columnar, with papillary processes projecting into the lumen of the
follicles.
2.The follicles are deficient in colloid & show scalloping of the
colloid margins .
3. There is increased vascularity & lymphocytic infiltration with
lymph follicle formation .
Effects :
1. General metabolism : The BMR is raised with increased in the
activity of body of body function e.g. weight loss & increased
heat production with sweating
2. Cardiovascular : Tachycardia & raised cardiac output , this
predispose to cardiac failure, especially when atrial fibrillation
develop.
3. Neurological : Exaggeration in the variation of mood with tremor.
4. Eye signs : a. Exophthalmus b. Lid retraction .
II. Secondary thyrotoxicosis: II. Secondary thyrotoxicosis:
Nodular toxic goiter : toxic change occurring in one or more nodules of a nodular colloid
goiter.
lymph follicle formation .
Effects :
1. General metabolism : The BMR is raised with increased in the
activity of body of body function e.g. weight loss & increased
heat production with sweating
2. Cardiovascular : Tachycardia & raised cardiac output , this
predispose to cardiac failure, especially when atrial fibrillation
develop.
3. Neurological : Exaggeration in the variation of mood with tremor.
4. Eye signs : a. Exophthalmus b. Lid retraction .
II. Secondary thyrotoxicosis: II. Secondary thyrotoxicosis:
Nodular toxic goiter : toxic change occurring in one or more nodules of a nodular colloid
goiter.
Note papillary hyperplasia of follicular epithelium and scalloping of colloid
The thyroid in Graves’ disease
The thyroid in Graves’ disease
Hypothyroidism :
It is due to deficiency of circulating levels of thyroid hormones. It
may be :
1. Primary : due to disease of the thyroid.
2. Secondary : To hypopituitarism .
Severe primary hypothyroidism in adults gives rise to
myxoedema, so called because of the characteristic thickening of
the skin by mucoid material. The clinical features are the opposite
of those of thyrotoxicosis i.e. a very slow heart rate & gain in
weight. Most of symptoms can be explained as being due to
deficient tissue oxidation throughout the body. In severe
myxoedema the reduced metabolism may lead to hypothermia .
Causes : a. Idiopathic atrophy of the gland
b. Iodine deficiency
c. Destruction of the gland by Hashimoto's thyroiditis &
post thyroidectomy.
It is due to deficiency of circulating levels of thyroid hormones. It
may be :
1. Primary : due to disease of the thyroid.
2. Secondary : To hypopituitarism .
Severe primary hypothyroidism in adults gives rise to
myxoedema, so called because of the characteristic thickening of
the skin by mucoid material. The clinical features are the opposite
of those of thyrotoxicosis i.e. a very slow heart rate & gain in
weight. Most of symptoms can be explained as being due to
deficient tissue oxidation throughout the body. In severe
myxoedema the reduced metabolism may lead to hypothermia .
Causes : a. Idiopathic atrophy of the gland
b. Iodine deficiency
c. Destruction of the gland by Hashimoto's thyroiditis &
post thyroidectomy.
Cretinism :
The child with hypothyroidism at birth will become a
cretin. in other ward in cretin thyroid function is deficient from
birth. The characteristic features are : coarse puffy face,
protruding tongue & abdomen & the general physical & mental
inactivity .
Inflammation of Thyroid (THYROIDITIS)
A. Bacterial :
1. Acute thyroiditis :
It is rare caused by bacterial infections e.g. staph or
strepto which reach the thyroid gland by one of the following
ways : haematogenous, lymphatic or direct from near by focus.
Pathology : The gland is swollen & congested with interstitial
inflammation .
Results : 1. Resolution or
2. Suppuration with abscess formation .
The child with hypothyroidism at birth will become a
cretin. in other ward in cretin thyroid function is deficient from
birth. The characteristic features are : coarse puffy face,
protruding tongue & abdomen & the general physical & mental
inactivity .
Inflammation of Thyroid (THYROIDITIS)
A. Bacterial :
1. Acute thyroiditis :
It is rare caused by bacterial infections e.g. staph or
strepto which reach the thyroid gland by one of the following
ways : haematogenous, lymphatic or direct from near by focus.
Pathology : The gland is swollen & congested with interstitial
inflammation .
Results : 1. Resolution or
2. Suppuration with abscess formation .
2. Granulomatous thyroiditis :
Specific granulomatous inflammation due to TB, sarcoidosis ,
syphilis (gumma ) may occur .
B. Non-bacterial :
1. Hashimoto's thyroiditis :
The disease process is due to autoimmunity which is
produced by the release of thyroid follicle constituents into the
interstitial tissue & formation of auto antibody against them.
Sex : M : F 1 : 9 .
Serological tests :
There may be circulating antibodies :
a. Antithyroglobulin antibody
b. Microsomal antibody : It is antibody against a lipoprotein
of the membrane of the endoplasmic reticulum(microsome)
of the thyroid epithelial cells.
Specific granulomatous inflammation due to TB, sarcoidosis ,
syphilis (gumma ) may occur .
B. Non-bacterial :
1. Hashimoto's thyroiditis :
The disease process is due to autoimmunity which is
produced by the release of thyroid follicle constituents into the
interstitial tissue & formation of auto antibody against them.
Sex : M : F 1 : 9 .
Serological tests :
There may be circulating antibodies :
a. Antithyroglobulin antibody
b. Microsomal antibody : It is antibody against a lipoprotein
of the membrane of the endoplasmic reticulum(microsome)
of the thyroid epithelial cells.
Macro. :
There is diffuse enlargement of the gland which is smooth,
firm & lobulated. The cut surface is lobulated, pale with
diminished or absent colloid.
Micro. :
a. Lymphoid infiltration with lymph follicle formation .
b. Diffuse plasma cell infiltration
c. Epithelial metaplasia with large eosinophilic thyroid
epithelial cells --- Askanazy cells .
d. Diminished colloid in the follicles .
e. Increase fibrous tissue producing a lobulated pattern.
Result :
The patient might develop myxodema.
There is diffuse enlargement of the gland which is smooth,
firm & lobulated. The cut surface is lobulated, pale with
diminished or absent colloid.
Micro. :
a. Lymphoid infiltration with lymph follicle formation .
b. Diffuse plasma cell infiltration
c. Epithelial metaplasia with large eosinophilic thyroid
epithelial cells --- Askanazy cells .
d. Diminished colloid in the follicles .
e. Increase fibrous tissue producing a lobulated pattern.
Result :
The patient might develop myxodema.
Hashimoto’s thyroiditis
Note prominent lymphoid infiltrate with germinal centers and thyroid follicles with bright
eosinophilic cytoplasm (Hurthle cell change)
Note prominent lymphoid infiltrate with germinal centers and thyroid follicles with bright
eosinophilic cytoplasm (Hurthle cell change)
2. Subacute Granulomatous thyroiditis “De Quervain” :
* It is rare self-limiting disease presented by fever, pain in the
throat & thyroid enlargement.
* It is believed to be caused by a viral infection.
* Microscopically, it show focal granulomatous inflammation
with foreign body giant cells, often engulfing colloid material.
3. Riedel's thyroiditis :
* It is very rare lesion of unknown etiology, characterized by
enlargement of the thyroid by fibrous tissue, which extend to
the surrounding neck structures
* It is hard in consistency which clinically simulate a thyroid
neoplasm
* The presence of circulating antithyroid antibody in most
patients suggests an autoimmune etiology.
* It is rare self-limiting disease presented by fever, pain in the
throat & thyroid enlargement.
* It is believed to be caused by a viral infection.
* Microscopically, it show focal granulomatous inflammation
with foreign body giant cells, often engulfing colloid material.
3. Riedel's thyroiditis :
* It is very rare lesion of unknown etiology, characterized by
enlargement of the thyroid by fibrous tissue, which extend to
the surrounding neck structures
* It is hard in consistency which clinically simulate a thyroid
neoplasm
* The presence of circulating antithyroid antibody in most
patients suggests an autoimmune etiology.
4. Subacute lymphocytic thyroiditis 4. Subacute lymphocytic thyroiditis
** Often occurs following a pregnancy (post-partum thyroiditis) Often occurs following a pregnancy (post-partum thyroiditis)
** It is typically painless. It is typically painless.
** Diffuse lymphoplasmacytic infiltration with Germinal center Diffuse lymphoplasmacytic infiltration with Germinal center
formation.formation.
** Hurthle cell changes is not seen Hurthle cell changes is not seen
** Thyroid auto a.b. is present. Thyroid auto a.b. is present.
** It represent an early precursor form of Hashimoto’s thyroiditis. It represent an early precursor form of Hashimoto’s thyroiditis.
** Often occurs following a pregnancy (post-partum thyroiditis) Often occurs following a pregnancy (post-partum thyroiditis)
** It is typically painless. It is typically painless.
** Diffuse lymphoplasmacytic infiltration with Germinal center Diffuse lymphoplasmacytic infiltration with Germinal center
formation.formation.
** Hurthle cell changes is not seen Hurthle cell changes is not seen
** Thyroid auto a.b. is present. Thyroid auto a.b. is present.
** It represent an early precursor form of Hashimoto’s thyroiditis. It represent an early precursor form of Hashimoto’s thyroiditis.
Auto immune thyroid diseasesAuto immune thyroid diseases
This group of disease “Hashimoto’s thyroiditis, primaryThis group of disease “Hashimoto’s thyroiditis, primary
myxoedima, and Graves diseases are generally characterized by :myxoedima, and Graves diseases are generally characterized by :
1.1. Lymphoid infiltration of thyroid tissue. Lymphoid infiltration of thyroid tissue.
2.2. Presence of circulating auto-a.b. to various component of Presence of circulating auto-a.b. to various component of
thyroid follicular cells e.g. “anti-microsomal, anti-thyroid follicular cells e.g. “anti-microsomal, anti-
thyroglobulinthyroglobulin..
3.3. There is a familial association between the thyroid There is a familial association between the thyroid
autoimmune disease and other organ specific auto immne autoimmune disease and other organ specific auto immne
disease including Addison’s disease, type I. D.M. pernicious disease including Addison’s disease, type I. D.M. pernicious
anemia. anemia.
This group of disease “Hashimoto’s thyroiditis, primaryThis group of disease “Hashimoto’s thyroiditis, primary
myxoedima, and Graves diseases are generally characterized by :myxoedima, and Graves diseases are generally characterized by :
1.1. Lymphoid infiltration of thyroid tissue. Lymphoid infiltration of thyroid tissue.
2.2. Presence of circulating auto-a.b. to various component of Presence of circulating auto-a.b. to various component of
thyroid follicular cells e.g. “anti-microsomal, anti-thyroid follicular cells e.g. “anti-microsomal, anti-
thyroglobulinthyroglobulin..
3.3. There is a familial association between the thyroid There is a familial association between the thyroid
autoimmune disease and other organ specific auto immne autoimmune disease and other organ specific auto immne
disease including Addison’s disease, type I. D.M. pernicious disease including Addison’s disease, type I. D.M. pernicious
anemia. anemia.
Tumours of the thyroid gland Tumours of the thyroid gland
1.1. Benign and malignant thyroid tumour usually present Benign and malignant thyroid tumour usually present
clinically as solitary nodule and majority of them are clinically as solitary nodule and majority of them are
cold on thyroid scan.cold on thyroid scan.
2.2. It can arise from both follicular epithelium and C cells It can arise from both follicular epithelium and C cells
where the majority are follicular adenoma while the where the majority are follicular adenoma while the
malignant tumour of the follicular cells origin fall into malignant tumour of the follicular cells origin fall into
two main group, papillary and follicular carcinoma two main group, papillary and follicular carcinoma
which behave differently, while the medullary carcinoma which behave differently, while the medullary carcinoma
arise from C cells.arise from C cells.
1.1. Benign and malignant thyroid tumour usually present Benign and malignant thyroid tumour usually present
clinically as solitary nodule and majority of them are clinically as solitary nodule and majority of them are
cold on thyroid scan.cold on thyroid scan.
2.2. It can arise from both follicular epithelium and C cells It can arise from both follicular epithelium and C cells
where the majority are follicular adenoma while the where the majority are follicular adenoma while the
malignant tumour of the follicular cells origin fall into malignant tumour of the follicular cells origin fall into
two main group, papillary and follicular carcinoma two main group, papillary and follicular carcinoma
which behave differently, while the medullary carcinoma which behave differently, while the medullary carcinoma
arise from C cells.arise from C cells.
Thyroid adenomasThyroid adenomas
They are benign neoplasm derived from follicular epithelium. They are benign neoplasm derived from follicular epithelium.
The criteria for adenoma are :The criteria for adenoma are :
1.1.Complete encapsulationComplete encapsulation
2.Homogenous texture throughout
3.Variation of tissue of adenoma from that outside the capsule.
4.Compression of adjacent thyroid tissue.
They are benign neoplasm derived from follicular epithelium. They are benign neoplasm derived from follicular epithelium.
The criteria for adenoma are :The criteria for adenoma are :
1.1.Complete encapsulationComplete encapsulation
2.Homogenous texture throughout
3.Variation of tissue of adenoma from that outside the capsule.
4.Compression of adjacent thyroid tissue.
1.1. They are the commonest thyroid neoplasm presenting most They are the commonest thyroid neoplasm presenting most
frequently in women over 30 year as solitary nodules.frequently in women over 30 year as solitary nodules.
2.2. Adenoma are usually encapsulated and compress the Adenoma are usually encapsulated and compress the
surrounding normal gland, hemorrhage, necrosis, fibrosis may surrounding normal gland, hemorrhage, necrosis, fibrosis may
occur.occur.
3.3. Histologically most show microfollicular pattern with little colloid Histologically most show microfollicular pattern with little colloid
storages “fetal colloid adenoma”. Some are composed of hurthle storages “fetal colloid adenoma”. Some are composed of hurthle
cell “Hurthle cell adenoma which consist of cell with abundant cell “Hurthle cell adenoma which consist of cell with abundant
eosinophilic cytoplasm or “trabecular adenoma composed of eosinophilic cytoplasm or “trabecular adenoma composed of
cords or trabecular pattern and lastly, papillary form “papillary cords or trabecular pattern and lastly, papillary form “papillary
adenoma” which consist of papillary structure.adenoma” which consist of papillary structure.
4.4. It is often difficult distinguish clinically and histologically It is often difficult distinguish clinically and histologically
between adenoma and carcinoma in the absence of capsular between adenoma and carcinoma in the absence of capsular
and/or blood vessel and/or blood vessel invasioninvasion..
Types of thyroid adenomasTypes of thyroid adenomas
frequently in women over 30 year as solitary nodules.frequently in women over 30 year as solitary nodules.
2.2. Adenoma are usually encapsulated and compress the Adenoma are usually encapsulated and compress the
surrounding normal gland, hemorrhage, necrosis, fibrosis may surrounding normal gland, hemorrhage, necrosis, fibrosis may
occur.occur.
3.3. Histologically most show microfollicular pattern with little colloid Histologically most show microfollicular pattern with little colloid
storages “fetal colloid adenoma”. Some are composed of hurthle storages “fetal colloid adenoma”. Some are composed of hurthle
cell “Hurthle cell adenoma which consist of cell with abundant cell “Hurthle cell adenoma which consist of cell with abundant
eosinophilic cytoplasm or “trabecular adenoma composed of eosinophilic cytoplasm or “trabecular adenoma composed of
cords or trabecular pattern and lastly, papillary form “papillary cords or trabecular pattern and lastly, papillary form “papillary
adenoma” which consist of papillary structure.adenoma” which consist of papillary structure.
4.4. It is often difficult distinguish clinically and histologically It is often difficult distinguish clinically and histologically
between adenoma and carcinoma in the absence of capsular between adenoma and carcinoma in the absence of capsular
and/or blood vessel and/or blood vessel invasioninvasion..
Types of thyroid adenomasTypes of thyroid adenomas
Folicular adenoma of the thyroid. A solitary, well-circumscribed nodule is seen Folicular adenoma of the thyroid. A solitary, well-circumscribed nodule is seen
Mic.Mic. Folicular adenoma well-differentiated Folicular adenoma well-differentiated
folicles resemble normal thyroidfolicles resemble normal thyroid
Hurthle cell adenoma. it composed of cells Hurthle cell adenoma. it composed of cells
with abundant eosinophilic cytoplasm with abundant eosinophilic cytoplasm
Mic.Mic. Folicular adenoma well-differentiated Folicular adenoma well-differentiated
folicles resemble normal thyroidfolicles resemble normal thyroid
Hurthle cell adenoma. it composed of cells Hurthle cell adenoma. it composed of cells
with abundant eosinophilic cytoplasm with abundant eosinophilic cytoplasm
Thyroid CarcinomaThyroid Carcinoma
Which include the following :Which include the following :
1.1.Papillary carcinoma 70-85%.Papillary carcinoma 70-85%.
2.2.Follicular carcinoma 10-20%.Follicular carcinoma 10-20%.
3.3.Medullary carcinoma 5%.Medullary carcinoma 5%.
4.4.Anaplastic carcinoma 5%.Anaplastic carcinoma 5%.
Both genetic and environmental factors Both genetic and environmental factors ““exposure to ionizing exposure to ionizing
radiationradiation”” are implicated in the pathogenesis of thyroid carcinoma. are implicated in the pathogenesis of thyroid carcinoma.
Which include the following :Which include the following :
1.1.Papillary carcinoma 70-85%.Papillary carcinoma 70-85%.
2.2.Follicular carcinoma 10-20%.Follicular carcinoma 10-20%.
3.3.Medullary carcinoma 5%.Medullary carcinoma 5%.
4.4.Anaplastic carcinoma 5%.Anaplastic carcinoma 5%.
Both genetic and environmental factors Both genetic and environmental factors ““exposure to ionizing exposure to ionizing
radiationradiation”” are implicated in the pathogenesis of thyroid carcinoma. are implicated in the pathogenesis of thyroid carcinoma.
Pathology of papillary carcinomaPathology of papillary carcinoma
1.1. It is predominant form of thyroid cancer and can occur at any age It is predominant form of thyroid cancer and can occur at any age
but most often in 3rd to 5but most often in 3rd to 5
thth
decade “20-40” year. With female decade “20-40” year. With female
preponderance 75-85%.preponderance 75-85%.
2.2. Because papillary carcinoma have tendency for invading Because papillary carcinoma have tendency for invading
lymphatic, they often appear multifocal tumour and regional L-lymphatic, they often appear multifocal tumour and regional L-
node metastases are present at times of diagnosis in 50% of node metastases are present at times of diagnosis in 50% of
cases.cases.
3.3. Histologically the tumour is rarely encapsulated and it range from Histologically the tumour is rarely encapsulated and it range from
those that are predominantly papillary to those that are in some those that are predominantly papillary to those that are in some
part follicular in appearance 30% (follicular variants), to lesion part follicular in appearance 30% (follicular variants), to lesion
have equal part of papillary and follicular architecture all have equal part of papillary and follicular architecture all
papillary carcinoma reveal some branching papillae which have papillary carcinoma reveal some branching papillae which have
fibrovascular stalk covered by single or multiple layer of fibrovascular stalk covered by single or multiple layer of
cuboidal epithelium cells which range from well differentiated cuboidal epithelium cells which range from well differentiated
cells to anaplastic variety.cells to anaplastic variety.
1.1. It is predominant form of thyroid cancer and can occur at any age It is predominant form of thyroid cancer and can occur at any age
but most often in 3rd to 5but most often in 3rd to 5
thth
decade “20-40” year. With female decade “20-40” year. With female
preponderance 75-85%.preponderance 75-85%.
2.2. Because papillary carcinoma have tendency for invading Because papillary carcinoma have tendency for invading
lymphatic, they often appear multifocal tumour and regional L-lymphatic, they often appear multifocal tumour and regional L-
node metastases are present at times of diagnosis in 50% of node metastases are present at times of diagnosis in 50% of
cases.cases.
3.3. Histologically the tumour is rarely encapsulated and it range from Histologically the tumour is rarely encapsulated and it range from
those that are predominantly papillary to those that are in some those that are predominantly papillary to those that are in some
part follicular in appearance 30% (follicular variants), to lesion part follicular in appearance 30% (follicular variants), to lesion
have equal part of papillary and follicular architecture all have equal part of papillary and follicular architecture all
papillary carcinoma reveal some branching papillae which have papillary carcinoma reveal some branching papillae which have
fibrovascular stalk covered by single or multiple layer of fibrovascular stalk covered by single or multiple layer of
cuboidal epithelium cells which range from well differentiated cuboidal epithelium cells which range from well differentiated
cells to anaplastic variety.cells to anaplastic variety.
4.4. The characteristic hallmark of papillary neoplasm can be found in The characteristic hallmark of papillary neoplasm can be found in
cell nuclei “nuclear features” even in the absence of papillary cell nuclei “nuclear features” even in the absence of papillary
architecture which include :architecture which include :
a.a. Hypochromatic “empty” nuclei devoid of nucleoli giving rise Hypochromatic “empty” nuclei devoid of nucleoli giving rise
to the designation ground glass “Orphan Annie eye”. to the designation ground glass “Orphan Annie eye”.
b.b. Nuclear grooves. Nuclear grooves.
c.c. Eosinophilic intra nuclear inclusion from cytoplasmic Eosinophilic intra nuclear inclusion from cytoplasmic
invagination (pseudo-inclusion).invagination (pseudo-inclusion).
5.5. Psammoma bodies usually with the core of papillae which are Psammoma bodies usually with the core of papillae which are
never found in follicular or medullary carcinoma.never found in follicular or medullary carcinoma.
6.6. Area of sequamous metaplasia, Lymphocytic infiltrates may be Area of sequamous metaplasia, Lymphocytic infiltrates may be
found.found.
cell nuclei “nuclear features” even in the absence of papillary cell nuclei “nuclear features” even in the absence of papillary
architecture which include :architecture which include :
a.a. Hypochromatic “empty” nuclei devoid of nucleoli giving rise Hypochromatic “empty” nuclei devoid of nucleoli giving rise
to the designation ground glass “Orphan Annie eye”. to the designation ground glass “Orphan Annie eye”.
b.b. Nuclear grooves. Nuclear grooves.
c.c. Eosinophilic intra nuclear inclusion from cytoplasmic Eosinophilic intra nuclear inclusion from cytoplasmic
invagination (pseudo-inclusion).invagination (pseudo-inclusion).
5.5. Psammoma bodies usually with the core of papillae which are Psammoma bodies usually with the core of papillae which are
never found in follicular or medullary carcinoma.never found in follicular or medullary carcinoma.
6.6. Area of sequamous metaplasia, Lymphocytic infiltrates may be Area of sequamous metaplasia, Lymphocytic infiltrates may be
found.found.
Micro-Papillary carcinomaMicro-Papillary carcinoma
Micro. Papillary carcinoma Psammoma body Micro. Papillary carcinoma Psammoma body
Micro. Papillary carcinomaMicro. Papillary carcinoma
"Orphan Annie eye" clear nuclei "Orphan Annie eye" clear nuclei
Micro. Papillary carcinoma Psammoma body Micro. Papillary carcinoma Psammoma body
Micro. Papillary carcinomaMicro. Papillary carcinoma
"Orphan Annie eye" clear nuclei "Orphan Annie eye" clear nuclei
Follicular carcinomaFollicular carcinoma
1.1. It composes 10-20% of all thyroid cancer and more common in It composes 10-20% of all thyroid cancer and more common in
female with peak incidence in fifth decade.female with peak incidence in fifth decade.
2.2. Distant blood borne metastasis occur particularly to bone and Distant blood borne metastasis occur particularly to bone and
lung with poor prognosis.lung with poor prognosis.
3.3. Microscoplically most follicular carcinoma are composed of Microscoplically most follicular carcinoma are composed of
fairly uniform cells forming small follicles. Hurthle cell variant fairly uniform cells forming small follicles. Hurthle cell variant
of follicular carcinoma may be seen. of follicular carcinoma may be seen.
4.4. F. carcinoma can be divided into two group F. carcinoma can be divided into two group
a.a. widely invasive tumour which spread throughout normally widely invasive tumour which spread throughout normally
gland. gland.
b.b. microscopic invasion of fibrous capsule and blood vessels. microscopic invasion of fibrous capsule and blood vessels.
1.1. It composes 10-20% of all thyroid cancer and more common in It composes 10-20% of all thyroid cancer and more common in
female with peak incidence in fifth decade.female with peak incidence in fifth decade.
2.2. Distant blood borne metastasis occur particularly to bone and Distant blood borne metastasis occur particularly to bone and
lung with poor prognosis.lung with poor prognosis.
3.3. Microscoplically most follicular carcinoma are composed of Microscoplically most follicular carcinoma are composed of
fairly uniform cells forming small follicles. Hurthle cell variant fairly uniform cells forming small follicles. Hurthle cell variant
of follicular carcinoma may be seen. of follicular carcinoma may be seen.
4.4. F. carcinoma can be divided into two group F. carcinoma can be divided into two group
a.a. widely invasive tumour which spread throughout normally widely invasive tumour which spread throughout normally
gland. gland.
b.b. microscopic invasion of fibrous capsule and blood vessels. microscopic invasion of fibrous capsule and blood vessels.
Medullary carcinomaMedullary carcinoma
1.1. It account for 5-10% of thyroid cancer with 10-20% familial It account for 5-10% of thyroid cancer with 10-20% familial
tendency.tendency.
2.2. Sporadic type (80%) is usually unilateral and in old age “while Sporadic type (80%) is usually unilateral and in old age “while
the familial variant is usually bilateral and multifocal arising on the familial variant is usually bilateral and multifocal arising on
background of c cell hyperplasia and occur before the age of 25 background of c cell hyperplasia and occur before the age of 25
years.years.
3.3. Histologically it consist of solid irregular group and cords of Histologically it consist of solid irregular group and cords of
polygonal to spindle shaped cells which may form nests and even polygonal to spindle shaped cells which may form nests and even
follicles.follicles.
4.4. Calcitonin immunoreactivety, can be demonstrated in all cases. Calcitonin immunoreactivety, can be demonstrated in all cases.
A cellular Amyloid deposits are present in the stroma.A cellular Amyloid deposits are present in the stroma.
5.5. Spread by blood and lymphatic. Spread by blood and lymphatic.
It is neuroendocrine neoplasm derived from parafollicular C-cell It is neuroendocrine neoplasm derived from parafollicular C-cell
1.1. It account for 5-10% of thyroid cancer with 10-20% familial It account for 5-10% of thyroid cancer with 10-20% familial
tendency.tendency.
2.2. Sporadic type (80%) is usually unilateral and in old age “while Sporadic type (80%) is usually unilateral and in old age “while
the familial variant is usually bilateral and multifocal arising on the familial variant is usually bilateral and multifocal arising on
background of c cell hyperplasia and occur before the age of 25 background of c cell hyperplasia and occur before the age of 25
years.years.
3.3. Histologically it consist of solid irregular group and cords of Histologically it consist of solid irregular group and cords of
polygonal to spindle shaped cells which may form nests and even polygonal to spindle shaped cells which may form nests and even
follicles.follicles.
4.4. Calcitonin immunoreactivety, can be demonstrated in all cases. Calcitonin immunoreactivety, can be demonstrated in all cases.
A cellular Amyloid deposits are present in the stroma.A cellular Amyloid deposits are present in the stroma.
5.5. Spread by blood and lymphatic. Spread by blood and lymphatic.
It is neuroendocrine neoplasm derived from parafollicular C-cell It is neuroendocrine neoplasm derived from parafollicular C-cell
(Medullary carcinoma of thyroid) (Medullary carcinoma of thyroid)
The tumor contain amyloidThe tumor contain amyloid
Homogeneous extracellular materialHomogeneous extracellular material
H and E stain H and E stain
The tumor contain amyloidThe tumor contain amyloid
Homogeneous extracellular materialHomogeneous extracellular material
H and E stain H and E stain
Anaplastic CarcinomaAnaplastic Carcinoma
1.1.Anaplastic carcinoma of the thyroid are among the most Anaplastic carcinoma of the thyroid are among the most
aggressive human neoplasms,aggressive human neoplasms,
2.2.Individuals with anaplastic carcinoma are older than those with Individuals with anaplastic carcinoma are older than those with
other types of thyroid cancer, with a mean age of 65 years. other types of thyroid cancer, with a mean age of 65 years.
3.3.About half of the patients have a history of multinodular goiter.About half of the patients have a history of multinodular goiter.
4.4.Microscopically, these neoplasms are composed of highly Microscopically, these neoplasms are composed of highly
anaplastic cells, which may take on several histologic patterns, anaplastic cells, which may take on several histologic patterns,
including large pleomorphic giant cells, spindle cells with a including large pleomorphic giant cells, spindle cells with a
sarcomatous appearance, mixed spindle and giant cell lesions sarcomatous appearance, mixed spindle and giant cell lesions
and lastly small cells, resembling those seen in small-cell and lastly small cells, resembling those seen in small-cell
carcinomas at other sites. carcinomas at other sites.
1.1.Anaplastic carcinoma of the thyroid are among the most Anaplastic carcinoma of the thyroid are among the most
aggressive human neoplasms,aggressive human neoplasms,
2.2.Individuals with anaplastic carcinoma are older than those with Individuals with anaplastic carcinoma are older than those with
other types of thyroid cancer, with a mean age of 65 years. other types of thyroid cancer, with a mean age of 65 years.
3.3.About half of the patients have a history of multinodular goiter.About half of the patients have a history of multinodular goiter.
4.4.Microscopically, these neoplasms are composed of highly Microscopically, these neoplasms are composed of highly
anaplastic cells, which may take on several histologic patterns, anaplastic cells, which may take on several histologic patterns,
including large pleomorphic giant cells, spindle cells with a including large pleomorphic giant cells, spindle cells with a
sarcomatous appearance, mixed spindle and giant cell lesions sarcomatous appearance, mixed spindle and giant cell lesions
and lastly small cells, resembling those seen in small-cell and lastly small cells, resembling those seen in small-cell
carcinomas at other sites. carcinomas at other sites.
PARATHYROID DISEASES
Parathyroid hormone:
Secretion is not under pituitary control
The parathyroid glands are responsive to plasma concentration of
ionized calcium, decreased calcium concentration stimulates PTH
production
Hyperparathyroidism:
1.Primary hyperparathyroidism: is the most common cause of
asymptomatic hypercalcemia.
Parathyroid hormone:
Secretion is not under pituitary control
The parathyroid glands are responsive to plasma concentration of
ionized calcium, decreased calcium concentration stimulates PTH
production
Hyperparathyroidism:
1.Primary hyperparathyroidism: is the most common cause of
asymptomatic hypercalcemia.
Most often due to parathyroid adenoma , few cases
are caused by primary parathyroid hyperplasia,
Carcinoma is rarely a cause.
Parathyroid adenomas are solitary while hyperplasia
is typically a multiglandular process.
Less often the cause is production of PTH like hormone
by non parathyroid malignant tumors such as
bronchogenic squamous cell carcinoma.
are caused by primary parathyroid hyperplasia,
Carcinoma is rarely a cause.
Parathyroid adenomas are solitary while hyperplasia
is typically a multiglandular process.
Less often the cause is production of PTH like hormone
by non parathyroid malignant tumors such as
bronchogenic squamous cell carcinoma.
Laboratory findings:
Hypercalcemia & hypercalciuria
Increased serum alkaline phosphatase
Decreased serum phosphorus
Increased serum PTH
Hypercalcemia & hypercalciuria
Increased serum alkaline phosphatase
Decreased serum phosphorus
Increased serum PTH
Clinically:
Skeletal manifestation: include bone resorption ,osteitis fibrosa
cyctica and brown tumors.
Metastatic calcification affecting various tissues especially the kidney
(nephrocalcinosis) and renal stones
Peptic ulcer .
Skeletal manifestation: include bone resorption ,osteitis fibrosa
cyctica and brown tumors.
Metastatic calcification affecting various tissues especially the kidney
(nephrocalcinosis) and renal stones
Peptic ulcer .
Secondary hyperparathyroidism :
Compensatory parathyroid hyperplasia occurs in
response to decreased serum ionized calcium
It is most often cause by renal failure ,malignancies are
most important cause of symptomatic hypercalcemia
which result from osteolytic metastasis or release of
PTH related protein from non parathyroid tumors.
Compensatory parathyroid hyperplasia occurs in
response to decreased serum ionized calcium
It is most often cause by renal failure ,malignancies are
most important cause of symptomatic hypercalcemia
which result from osteolytic metastasis or release of
PTH related protein from non parathyroid tumors.
HYPOPARATHYROIDISM
The most common cause is accidental surgical excision during
thyroidectomy ,In rare cases this disorder is associated with
congenital thymic hypoplasia (DiGeorge Syndrome).
Severe hypocalcaemia manifest clinically by increased
neuromuscular excitability and tetany is characteristic .
The most common cause is accidental surgical excision during
thyroidectomy ,In rare cases this disorder is associated with
congenital thymic hypoplasia (DiGeorge Syndrome).
Severe hypocalcaemia manifest clinically by increased
neuromuscular excitability and tetany is characteristic .
ENDOCRINE PANCREAS
Type 1 diabetes: is an autoimmune disease
characterized by progressive destruction of islet cells,
β
leading to absolute insulin deficiency. Several immune
mechanisms probably contribute to -cell damage,
β
including T cells, cytokines, and autoantibodies.
Type 2 diabetes
has no autoimmune basis; instead, features
central to its pathogenesis are insulin resistance
and -cell dysfunction, resulting in relative insulin
β
deficiency.Obesity has an important relationship
with insulin resistance (and hence, type 2
diabetes), probably mediated by cytokines
released from adipose tissues (adipocytokines).
has no autoimmune basis; instead, features
central to its pathogenesis are insulin resistance
and -cell dysfunction, resulting in relative insulin
β
deficiency.Obesity has an important relationship
with insulin resistance (and hence, type 2
diabetes), probably mediated by cytokines
released from adipose tissues (adipocytokines).
The Adrenal gland
1.Glucocorticoids "principally cortisone" which are synthesized primarily in
the Zona fasciculata.
2.Mineralo corticoids, the most important being aldosterone which is generated
in the zona glomerulosa.
3.Sex steroid "eostrogens and androgens", which are produced largely in the
zona reticularis.
The adrenal glands are paired endocrine organs consisting of both cortex
and medulla, which differ in their development, structure, and function. The
cortex being mesodermal and the medulla of neural origin.
The adrenal cortex synthesizes three different types of steroids :
The adrenal medulla is composed of chromaffin cells which synthesize and
secrete catecholamines, mainly epinephrine.
1.Glucocorticoids "principally cortisone" which are synthesized primarily in
the Zona fasciculata.
2.Mineralo corticoids, the most important being aldosterone which is generated
in the zona glomerulosa.
3.Sex steroid "eostrogens and androgens", which are produced largely in the
zona reticularis.
The adrenal glands are paired endocrine organs consisting of both cortex
and medulla, which differ in their development, structure, and function. The
cortex being mesodermal and the medulla of neural origin.
The adrenal cortex synthesizes three different types of steroids :
The adrenal medulla is composed of chromaffin cells which synthesize and
secrete catecholamines, mainly epinephrine.
Pathology of adrenal cortex
I-Adrenocortical hyperfunction "Hyperadrenalism" As there are
three basic types of corticosteroid, elaborated by the adrenal cortex
"glusocorticoids, mineralocorticoid, and sex steroids", So there are
distinctive hyper adrenal clinical syndromes."
1.Cushing syndrome characterized by an excess cortisone.
2.Hyperaldosteromism.
3.Adrenogenital or virilizing syndrome characterized by excess
androgen.
I-Adrenocortical hyperfunction "Hyperadrenalism" As there are
three basic types of corticosteroid, elaborated by the adrenal cortex
"glusocorticoids, mineralocorticoid, and sex steroids", So there are
distinctive hyper adrenal clinical syndromes."
1.Cushing syndrome characterized by an excess cortisone.
2.Hyperaldosteromism.
3.Adrenogenital or virilizing syndrome characterized by excess
androgen.
Causes of "Cushing syndrome" Causes of "Cushing syndrome"
This conditions is caused by any condition that produces This conditions is caused by any condition that produces
an elevation in glucocorticoid levels. an elevation in glucocorticoid levels.
1.In clinical practice most cases of Cushing syndrome are caused by the
administration of exogenous glucocorticoids.
2.The remaining cases are endogenous and include the following:
a.Primary hypothalamic-pituitary diseases associated with hyper secretion of
ACTH "Cushing disease" account for 50%.
b.Primary adrenocortical hyperplasia or neoplasia "10-20%".
c.The secretion of ectopic ACTH by nonendocrine neoplasma e.i.g." oat cell
carcinoma of lung, medullary thyroid carcinoma carcinoid tumour, islet cell
tumour of the pancreas.
This conditions is caused by any condition that produces This conditions is caused by any condition that produces
an elevation in glucocorticoid levels. an elevation in glucocorticoid levels.
1.In clinical practice most cases of Cushing syndrome are caused by the
administration of exogenous glucocorticoids.
2.The remaining cases are endogenous and include the following:
a.Primary hypothalamic-pituitary diseases associated with hyper secretion of
ACTH "Cushing disease" account for 50%.
b.Primary adrenocortical hyperplasia or neoplasia "10-20%".
c.The secretion of ectopic ACTH by nonendocrine neoplasma e.i.g." oat cell
carcinoma of lung, medullary thyroid carcinoma carcinoid tumour, islet cell
tumour of the pancreas.
Various forms of Cushing syndromeVarious forms of Cushing syndrome
The Pathology of Cushing syndrome The Pathology of Cushing syndrome
The main lesions of Cushing syndrome one found in the
pituitary and a adrenal glands, in pituitary, the normal granular,
basophilic cytoplasm of ACTH-producing cell in anterior pituitary is
replaced by homogonous, lightly basophilic material, due to
accumulation of intermediate keratin filaments in the cytoplasm.
"Crooke hyaline change, while the adrenal glands show either,
cortical atrophy, diffuse or nodular hyperplasia or adenoma and
rarly a carcinoma.
Clinically cushing cyndrome manifested by :Clinically cushing cyndrome manifested by :
a.a.Systemic hypertension.Systemic hypertension.
b.b.Obesity of face, neck and trunk. Obesity of face, neck and trunk.
c.c.Striae of the abdomin.Striae of the abdomin.
d.d.Facial hair.Facial hair.
e.e.Thin and wasting of skeletal muscles Thin and wasting of skeletal muscles
f.f.Increased tendency for bacterial infection.Increased tendency for bacterial infection.
The main lesions of Cushing syndrome one found in the
pituitary and a adrenal glands, in pituitary, the normal granular,
basophilic cytoplasm of ACTH-producing cell in anterior pituitary is
replaced by homogonous, lightly basophilic material, due to
accumulation of intermediate keratin filaments in the cytoplasm.
"Crooke hyaline change, while the adrenal glands show either,
cortical atrophy, diffuse or nodular hyperplasia or adenoma and
rarly a carcinoma.
Clinically cushing cyndrome manifested by :Clinically cushing cyndrome manifested by :
a.a.Systemic hypertension.Systemic hypertension.
b.b.Obesity of face, neck and trunk. Obesity of face, neck and trunk.
c.c.Striae of the abdomin.Striae of the abdomin.
d.d.Facial hair.Facial hair.
e.e.Thin and wasting of skeletal muscles Thin and wasting of skeletal muscles
f.f.Increased tendency for bacterial infection.Increased tendency for bacterial infection.
The Pathology of Hyperaldosteronism The Pathology of Hyperaldosteronism
Excessive levels of aldosterone cause sodium retension and
potassium excretion, with resultant hypertension and
hypokalemia.
Hyperaldosteronism may be primary "Conn syndrome"
associated with aldosterone-secreting adenoma in one adrenal
gland.
Primary hyperaldosteronism indicate a primary autonomous over
production of aldosterone with resultant suppression of the
rennin-angiotensin system with decreased plasma rennin activity.
Excessive levels of aldosterone cause sodium retension and
potassium excretion, with resultant hypertension and
hypokalemia.
Hyperaldosteronism may be primary "Conn syndrome"
associated with aldosterone-secreting adenoma in one adrenal
gland.
Primary hyperaldosteronism indicate a primary autonomous over
production of aldosterone with resultant suppression of the
rennin-angiotensin system with decreased plasma rennin activity.
Secondary hyperaldosteronism due to an extraadrenal cause
where aldosterone release occurs in response to activation of
rennin-angiotensin system, where plasma rennin level increased
in many condition like
I.decreased renal perfusion (renal artery stenosis).
II.congestive heart failure, cirrhosis, nephrotic syndrome
III.Pregnancy (oestrogen increase plasma rennin).
where aldosterone release occurs in response to activation of
rennin-angiotensin system, where plasma rennin level increased
in many condition like
I.decreased renal perfusion (renal artery stenosis).
II.congestive heart failure, cirrhosis, nephrotic syndrome
III.Pregnancy (oestrogen increase plasma rennin).
Pathology of adreno-genital syndromes Pathology of adreno-genital syndromes
- The adrenal cortex can secrete excess androgens in two setting
a. adrenocortical neoplasma "usually virilizing carcinoma".
b. congenital adrenal hyperplasia "CAH"
- Cong. Adrenal hyperplasia is a group of autosomal recessive disorders
characterized by defects in steroid biosynthesis usually cortisol, the
common subtype is caused by deficiency of the enzyme 21-hydroylase.
- Reduction in cortisol production causes a compensation increase in ACTH
secretion, which in turn stimulate androgen production Androgens have
virilizing effects include
I. Muscalinization in females (ambiguous genitalia, oligomenorrhoea,
hirsutism.
II. Precocious puberty in males.
Hypotension with salt (sodium) wasting
There is bilateral hyperplasia of adrenal cortex.
- The adrenal cortex can secrete excess androgens in two setting
a. adrenocortical neoplasma "usually virilizing carcinoma".
b. congenital adrenal hyperplasia "CAH"
- Cong. Adrenal hyperplasia is a group of autosomal recessive disorders
characterized by defects in steroid biosynthesis usually cortisol, the
common subtype is caused by deficiency of the enzyme 21-hydroylase.
- Reduction in cortisol production causes a compensation increase in ACTH
secretion, which in turn stimulate androgen production Androgens have
virilizing effects include
I. Muscalinization in females (ambiguous genitalia, oligomenorrhoea,
hirsutism.
II. Precocious puberty in males.
Hypotension with salt (sodium) wasting
There is bilateral hyperplasia of adrenal cortex.
Adrenal insufficiency Adrenal insufficiency
Adrenal insufficiency "hypofunction" may be considered
under the following headings :
1.Primary acute adrenocortical insufficiency "adrenal crisis"
2.Primary chronic adrenocorticol insufficiency addison disease.
3.Secondary adrenocortical insufficiency and the following table
summarize the types and cause of adrenocortical insufficiency.
Adrenal insufficiency "hypofunction" may be considered
under the following headings :
1.Primary acute adrenocortical insufficiency "adrenal crisis"
2.Primary chronic adrenocorticol insufficiency addison disease.
3.Secondary adrenocortical insufficiency and the following table
summarize the types and cause of adrenocortical insufficiency.
Pathology of Addison Disease Pathology of Addison Disease
It is rare disease caused by chronic destructive process in the
adrenal cortex,
it is characterized by :
1.90% of the case are due to autoimmune process or T.B. minor
case are due to amyloidosis, adrenal heamorrhage, metastatic
tumor, heamochromatosis.
2.The outstanding features are weakness, lethering, hypotension
with anorexia and weight loss.
3.Libido is usually diminished.
4.Skin pigmentation particularly of the exposed part, external
genitalia, scar
It is rare disease caused by chronic destructive process in the
adrenal cortex,
it is characterized by :
1.90% of the case are due to autoimmune process or T.B. minor
case are due to amyloidosis, adrenal heamorrhage, metastatic
tumor, heamochromatosis.
2.The outstanding features are weakness, lethering, hypotension
with anorexia and weight loss.
3.Libido is usually diminished.
4.Skin pigmentation particularly of the exposed part, external
genitalia, scar
Pheochromocytoma Pheochromocytoma
I.Are neoplasms composed of chromaffin cells which synthesize and
release catecholamine which is associated with cotecholamine.
Induced hypertension.
II.10% of pheo arise in association with one of several of familial
syndromes like MEN 2 A and MEN 2 B, type I neurofibromatosis.
III.10% of pheo are extra adrenal occurring in sites such an carotid
body, organ of Zukerkandl, and Called usually paraganglioma.
IV.10% of adrenal plaeo are bilateral.
V.10% of adrenal pheo are biologically malignant.
VI.Microscopically phco are composed of polygonal to spindle shaped
chromaffin cells and their supporting cells compartmentalized into
small nests Zellballen by rich vascular network, the cytoplasm of
neoplastic cell is granular, mitosis is scanty. Vascular and capsuler
invasion may be seen in benign neoplasm, therefore the definitive
diagnosis of malignancy in pheo is based exclusively on the
presence of melastasis.
I.Are neoplasms composed of chromaffin cells which synthesize and
release catecholamine which is associated with cotecholamine.
Induced hypertension.
II.10% of pheo arise in association with one of several of familial
syndromes like MEN 2 A and MEN 2 B, type I neurofibromatosis.
III.10% of pheo are extra adrenal occurring in sites such an carotid
body, organ of Zukerkandl, and Called usually paraganglioma.
IV.10% of adrenal plaeo are bilateral.
V.10% of adrenal pheo are biologically malignant.
VI.Microscopically phco are composed of polygonal to spindle shaped
chromaffin cells and their supporting cells compartmentalized into
small nests Zellballen by rich vascular network, the cytoplasm of
neoplastic cell is granular, mitosis is scanty. Vascular and capsuler
invasion may be seen in benign neoplasm, therefore the definitive
diagnosis of malignancy in pheo is based exclusively on the
presence of melastasis.
Pheochromocytoma, demonstrating Pheochromocytoma, demonstrating
characteristic nests of cells characteristic nests of cells
(“Zellballen”) with abundant cytoplasm (“Zellballen”) with abundant cytoplasm
Extra-adrenal
pheochromocytoma
characteristic nests of cells characteristic nests of cells
(“Zellballen”) with abundant cytoplasm (“Zellballen”) with abundant cytoplasm
Extra-adrenal
pheochromocytoma
Multiple Endocrine Neoplasia Syndromes Multiple Endocrine Neoplasia Syndromes
The MEN syndromes are group of inherited diseases resulting The MEN syndromes are group of inherited diseases resulting
in proliferative lesions (hyperplasia, adenomas and carcinomas) of in proliferative lesions (hyperplasia, adenomas and carcinomas) of
multiple endocrine organs in the same individual or in members of multiple endocrine organs in the same individual or in members of
family. It is characterized by : family. It is characterized by :
1.1.These tumour, occur of a younger age than sporadic cancers. These tumour, occur of a younger age than sporadic cancers.
2.2.They arise in multiple endocrine organs, They arise in multiple endocrine organs,
The MEN syndromes are group of inherited diseases resulting The MEN syndromes are group of inherited diseases resulting
in proliferative lesions (hyperplasia, adenomas and carcinomas) of in proliferative lesions (hyperplasia, adenomas and carcinomas) of
multiple endocrine organs in the same individual or in members of multiple endocrine organs in the same individual or in members of
family. It is characterized by : family. It is characterized by :
1.1.These tumour, occur of a younger age than sporadic cancers. These tumour, occur of a younger age than sporadic cancers.
2.2.They arise in multiple endocrine organs, They arise in multiple endocrine organs,
Classification Classification
I. MEN.I. I. MEN.I.
I.Parathyroid (95%) where hyperparathyroidism arising from
multinodular parathyroid hyperplasia is the most consistent
feature of MEN I.
II.Pancrease Endocrine tumours of the pancreas are the leading
cause of death in MEN 1 eig Zollinger Ellision syndrome
associated with gastrinoma and hypoglycemia related to
insulinoma.
III.Pituitary prolactin-secreting adenoma is most frequent
manifestation rarely acromegaly develop.
I. MEN.I. I. MEN.I.
I.Parathyroid (95%) where hyperparathyroidism arising from
multinodular parathyroid hyperplasia is the most consistent
feature of MEN I.
II.Pancrease Endocrine tumours of the pancreas are the leading
cause of death in MEN 1 eig Zollinger Ellision syndrome
associated with gastrinoma and hypoglycemia related to
insulinoma.
III.Pituitary prolactin-secreting adenoma is most frequent
manifestation rarely acromegaly develop.
2. MEN II a :this include : 2. MEN II a :this include :
1.1.Medullary thyroid carcinoma which occur in the first decades of life.Medullary thyroid carcinoma which occur in the first decades of life.
2.2.Pheochromocytoma occur in 50% of cases .Pheochromocytoma occur in 50% of cases .
3.3.Hyperparathyroidism, approximately a third of patient develop Hyperparathyroidism, approximately a third of patient develop
parathyroid hyperplasia .parathyroid hyperplasia .
4.4.it has been linked to mutation on chromosome 10.it has been linked to mutation on chromosome 10.
3. MEN II b or 3. MEN II b or ““IIIIII”” (sipples syndrome) (sipples syndrome)
11.This syndrome includes pheochromocytoma , medullary thyroid .This syndrome includes pheochromocytoma , medullary thyroid
carcinoma and multiple mucocutaneous neuromas or carcinoma and multiple mucocutaneous neuromas or
ganglioneuromas ganglioneuromas
22.In contrast to MEN IIa it does not induce hyperparathyroidisim..In contrast to MEN IIa it does not induce hyperparathyroidisim.
33. Its linked to different mutations in the ret oncogene compared to . Its linked to different mutations in the ret oncogene compared to
MEN IIaMEN IIa . .
1.1.Medullary thyroid carcinoma which occur in the first decades of life.Medullary thyroid carcinoma which occur in the first decades of life.
2.2.Pheochromocytoma occur in 50% of cases .Pheochromocytoma occur in 50% of cases .
3.3.Hyperparathyroidism, approximately a third of patient develop Hyperparathyroidism, approximately a third of patient develop
parathyroid hyperplasia .parathyroid hyperplasia .
4.4.it has been linked to mutation on chromosome 10.it has been linked to mutation on chromosome 10.
3. MEN II b or 3. MEN II b or ““IIIIII”” (sipples syndrome) (sipples syndrome)
11.This syndrome includes pheochromocytoma , medullary thyroid .This syndrome includes pheochromocytoma , medullary thyroid
carcinoma and multiple mucocutaneous neuromas or carcinoma and multiple mucocutaneous neuromas or
ganglioneuromas ganglioneuromas
22.In contrast to MEN IIa it does not induce hyperparathyroidisim..In contrast to MEN IIa it does not induce hyperparathyroidisim.
33. Its linked to different mutations in the ret oncogene compared to . Its linked to different mutations in the ret oncogene compared to
MEN IIaMEN IIa . .
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