PATHOLOGY - 15 - Endocrine Pathology.pdf
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About This Presentation
endocrine pathology, common diseases affecting the endocrine system
Slide Content
Ephraim Imhotep Zulu, BSc BMS, MSc Path
University of ZambiaSchool of Health Sciences,Dept. of Biomedical Sciences,
Pathology
Lecture #15
Endocrine Pathology
| Version 01 | April 2017
Procedural document:
Rare disease nomenclature in English
www.orpha.net www.orphadata.org
University of ZambiaSchool of Health Sciences,Dept. of Biomedical Sciences,
Pathology
Lecture #15
Endocrine Pathology
| Version 01 | April 2017
Procedural document:
Rare disease nomenclature in English
www.orpha.net www.orphadata.org
Lecture Outline
•Diseases of the Pituitary Gland
•Diseases of the Thyroid Gland
•Diseases of the Parathyroid Glands
•Diseases of the endocrine pancreas
•Diseases of the adrenal glands
•Multiple Endocrine Neoplasia Syndromes (MEN)
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY2
•Diseases of the Pituitary Gland
•Diseases of the Thyroid Gland
•Diseases of the Parathyroid Glands
•Diseases of the endocrine pancreas
•Diseases of the adrenal glands
•Multiple Endocrine Neoplasia Syndromes (MEN)
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY2
Learning Objectives:
At the end of this lecture, the student is expected to
•Know and understand the aetiology, and pathogenesis/pathophysiology of
common diseases of the endocrine system
•Appreciate the risk factors associated with common endocrine diseases
•Appreciate the clinical features and complications associated with common
endocrine diseases
•Differentiate/Compare and Contrast the following pairs of terms:
•Hyperpituitarism vs. Hypopituitarism
•Hyperthyroidism vs. Hypothyroidism
•Type 1 diabetes vs. Type 2 diabetes
•Cushing syndrome vs. Addison's Disease
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY3
At the end of this lecture, the student is expected to
•Know and understand the aetiology, and pathogenesis/pathophysiology of
common diseases of the endocrine system
•Appreciate the risk factors associated with common endocrine diseases
•Appreciate the clinical features and complications associated with common
endocrine diseases
•Differentiate/Compare and Contrast the following pairs of terms:
•Hyperpituitarism vs. Hypopituitarism
•Hyperthyroidism vs. Hypothyroidism
•Type 1 diabetes vs. Type 2 diabetes
•Cushing syndrome vs. Addison's Disease
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY3
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY4
The Endocrine
System
The Endocrine
System
Synopsis
•The endocrine system contains a highly integrated and widely distributed
group of organs that orchestrates a state of metabolic equilibrium, between
the various tissues of the body.
•In endocrine signaling, the secreted molecules, which are frequently called
hormones, act on target cells distant from their site of synthesis.
•Endocrine diseases can be generally classified as
•(1) diseases of underproduction or overproduction of hormones and their
resulting biochemical and clinical consequences, and
•(2) diseases associated with the development of mass lesions, which may
be nonfunctional or may be associated with overproduction or
underproduction of hormones.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY5
•The endocrine system contains a highly integrated and widely distributed
group of organs that orchestrates a state of metabolic equilibrium, between
the various tissues of the body.
•In endocrine signaling, the secreted molecules, which are frequently called
hormones, act on target cells distant from their site of synthesis.
•Endocrine diseases can be generally classified as
•(1) diseases of underproduction or overproduction of hormones and their
resulting biochemical and clinical consequences, and
•(2) diseases associated with the development of mass lesions, which may
be nonfunctional or may be associated with overproduction or
underproduction of hormones.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY5
Hyperpituitarism & Pituitary Adenomas
•The most common cause of hyperpituitarism is an adenoma arising in
the anterior lobe.
•Pituitary adenomas can be functional (i.e., associated with hormone
excess and clinical manifestations thereof) or silent (i.e. demonstration
of hormone production at the tissue level only, without clinical
manifestations of hormone excess).
•Pituitary adenomas may also be hormone negative.
•Pituitary adenomas are usually found in adults, with a peak incidence
from the 30s to the 50s.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY6
Diseases of the Pituitary Gland
•The most common cause of hyperpituitarism is an adenoma arising in
the anterior lobe.
•Pituitary adenomas can be functional (i.e., associated with hormone
excess and clinical manifestations thereof) or silent (i.e. demonstration
of hormone production at the tissue level only, without clinical
manifestations of hormone excess).
•Pituitary adenomas may also be hormone negative.
•Pituitary adenomas are usually found in adults, with a peak incidence
from the 30s to the 50s.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY6
Diseases of the Pituitary Gland
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY7
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY8
Prolactinomas
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY9
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY9
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY10
Hyperprolactinaemia
Hyperprolactinaemia
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY11
Galactorrhea in a young woman (non pregnant of course) is often the expression of an acidophil tumor of
the adenohypophysis.
Galactorrhea in a young woman (non pregnant of course) is often the expression of an acidophil tumor of
the adenohypophysis.
Somatotroph Adenomas
•If a growth hormone-secreting adenoma occurs before the
epiphyses close, as is the case in prepubertal children, excessive
levels of growth hormone result in gigantism.
•This is characterized by a generalized increase in body size, with
disproportionately long arms and legs.
•If elevated levels of growth hormone persist, or present after
closure of the epiphyses, individuals develop acromegaly, in
which growth is most conspicuous in soft tissues, skin, and
viscera and in the bones of the face, hands, and feet.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY12
•If a growth hormone-secreting adenoma occurs before the
epiphyses close, as is the case in prepubertal children, excessive
levels of growth hormone result in gigantism.
•This is characterized by a generalized increase in body size, with
disproportionately long arms and legs.
•If elevated levels of growth hormone persist, or present after
closure of the epiphyses, individuals develop acromegaly, in
which growth is most conspicuous in soft tissues, skin, and
viscera and in the bones of the face, hands, and feet.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY12
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY13
Gigantism. Family
photographs showed that
this young woman had
consistently outgrown her
twin brother and was
always the biggest child in
the school class. She had a
pituitary adenoma
secreting growth
hormone. She is shown
with two staff members,
one short and one tall.
Gigantism. Family
photographs showed that
this young woman had
consistently outgrown her
twin brother and was
always the biggest child in
the school class. She had a
pituitary adenoma
secreting growth
hormone. She is shown
with two staff members,
one short and one tall.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY14
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY15
Hypopituitarism
Hypopituitarism
•Thyroid hormone has diverse cellular effects,
including up-regulation of carbohydrate and lipid
catabolism and stimulation of protein synthesis
in a wide range of cells.
•The net result of these processes is an increase in
the basal metabolic rate.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY16
Diseases of the Thyroid Gland
including up-regulation of carbohydrate and lipid
catabolism and stimulation of protein synthesis
in a wide range of cells.
•The net result of these processes is an increase in
the basal metabolic rate.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY16
Diseases of the Thyroid Gland
Hypothyroidism vs Hyperthyroidism
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY17
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY17
Hyperthyroidism (Thyrotoxicosis)
•A hypermetabolic state caused by elevated circulating levels of free
T3 and T4.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY18
•A hypermetabolic state caused by elevated circulating levels of free
T3 and T4.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY18
Graves Disease
•Is the most common cause of endogenous hyperthyroidism.
•An autoimmune disorder in which a variety of antibodies may be
present in the serum
•Genetic factors are important in the causation of Graves disease.
•Has a peak incidence between the ages of 20 and 40, with women
being affected as much as seven times more commonly than men.
•Laboratory findings in Graves disease include elevated serum free T4
and T3 and depressed serum TSH.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY19
•Is the most common cause of endogenous hyperthyroidism.
•An autoimmune disorder in which a variety of antibodies may be
present in the serum
•Genetic factors are important in the causation of Graves disease.
•Has a peak incidence between the ages of 20 and 40, with women
being affected as much as seven times more commonly than men.
•Laboratory findings in Graves disease include elevated serum free T4
and T3 and depressed serum TSH.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY19
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY20
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY21
Graves Disease..,
Graves Disease..,
Hypothyroidism
•The clinical manifestations include cretinism and
myxedema.
•Cretinism refers to hypothyroidism developing in infancy
or early childhood.
•Hypothyroidism developing in older children and adults
results in a condition known as myxedema or Gull disease.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY22
•The clinical manifestations include cretinism and
myxedema.
•Cretinism refers to hypothyroidism developing in infancy
or early childhood.
•Hypothyroidism developing in older children and adults
results in a condition known as myxedema or Gull disease.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY22
Hypothyroidism.,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY23
The endocrine system
456
are shown in Table 17.4. There is weight gain and general
lethargy with cold intolerance. Skin and hair are dry and accu-
mulation of mucopolysaccharides in connective tissue result
in a thickening of the skin, hoarseness, and pain and paraes-
thesia when nerves are trapped. There is intellectual impair-
ment. Change of mood may progress to psychosis. In severe
deficiency, hypothermia and coma can develop. Raised blood
cholesterol levels increase the risk of cardiovascular disease.
(Figure 17.9). Occasionally, simple goitre may produce signs
or symptoms suggestive of tumour. When one nodule is
larger than the others (dominant nodule), fine needle aspir-
ation cytology or even partial thyroidectomy is required to
distinguish the two. Occasionally, there may be compression
of trachea, oesophagus or recurrent laryngeal nerve.
On an epidemiological basis, two forms are defined:
!Endemic goitre affects more than 10% of the popula-
tion, occurring in areas with absolute deficiency of
iodine, usually far from the sea, reflecting seafood as the
major source of iodine. These areas include the Andes,
Himalayas and Alps. The introduction of iodized salt
has reduced the incidence. Goitre usually develops in
childhood, and the sexes are equally affected.
!Sporadic goitre is due to a relative lack of iodine in indi-
viduals. It reflects inadequate intake; inherited abnor-
malities in thyroid hormone production; and ingestion
of goitrogens, i.e. substances that interfere with hormone
synthesis. These include vegetables of the Brassicafam-
ily, excessive fluoride, or drugs such as p-aminosalicylic
acid and sulphonylureas. Some people also suggest that
autoimmune mechanisms may be involved.
(A)
(B)
FIGURE17. 9(A) A cut section through a multinodular goitre showing gross
asymmetrical enlargement. (B) Nodularity is clear on histological assessment.
TABLE17. 4Causes of hypothyroidism
•Autoimmune thyroid disease
Hashimoto’s thyroiditis
primary myxoedema
•Severe iodine deficiency
•Dyshormonogenesis
•Following thyroid surgery or radio-iodine therapy
•Ingestion of goitrogens
•Hypopituitarism
Cretinism is due to severe hypothyroidism in infancy.
Thyroid hormones are critical for normal brain develop-
ment, and these children show signs of mental retardation,
neuromuscular abnormalities, deaf-mutism and retarded
growth. There is a goitre when it is caused by severe iodine
deficiency, or by inherited defects of the enzymes involved
in thyroid hormone synthesis. Rarely, thyroid agenesis or
hypoplasia occurs, and in these cases goitre is absent. It is
extremely important to make an early diagnosis because
hormone replacement permits normal development.
Functional Disorders
Non-toxic Nodular Goitre
Non-toxic nodular goitre is the most common lesion in thy-
roid pathology. When there is absolute or relative iodine
deficiency, reduced levels of thyroid hormones result in
increased TSH secretion by the pituitary.This induces hyper-
plasia in an attempt to increase thyroid hormone output.
The demands are usually intermittent, and the gland under-
goes cycles of growth and involution, resulting in the well-
recognized picture of multinodular goitre, with nodules
consisting of follicles of varying size, fibrosis, haemorrhage
and focal inflammation. Enlargement is usually asymmet-
rical, and the gland may weigh up to several hundred grams
Key Points
•Non-toxic nodular goitre is the most common
thyroid disease.
•It is either endemic or sporadic.
•There is nodular enlargement of the thyroid gland.
•Affected individuals may be either euthyroid or
hypothyroid.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY23
The endocrine system
456
are shown in Table 17.4. There is weight gain and general
lethargy with cold intolerance. Skin and hair are dry and accu-
mulation of mucopolysaccharides in connective tissue result
in a thickening of the skin, hoarseness, and pain and paraes-
thesia when nerves are trapped. There is intellectual impair-
ment. Change of mood may progress to psychosis. In severe
deficiency, hypothermia and coma can develop. Raised blood
cholesterol levels increase the risk of cardiovascular disease.
(Figure 17.9). Occasionally, simple goitre may produce signs
or symptoms suggestive of tumour. When one nodule is
larger than the others (dominant nodule), fine needle aspir-
ation cytology or even partial thyroidectomy is required to
distinguish the two. Occasionally, there may be compression
of trachea, oesophagus or recurrent laryngeal nerve.
On an epidemiological basis, two forms are defined:
!Endemic goitre affects more than 10% of the popula-
tion, occurring in areas with absolute deficiency of
iodine, usually far from the sea, reflecting seafood as the
major source of iodine. These areas include the Andes,
Himalayas and Alps. The introduction of iodized salt
has reduced the incidence. Goitre usually develops in
childhood, and the sexes are equally affected.
!Sporadic goitre is due to a relative lack of iodine in indi-
viduals. It reflects inadequate intake; inherited abnor-
malities in thyroid hormone production; and ingestion
of goitrogens, i.e. substances that interfere with hormone
synthesis. These include vegetables of the Brassicafam-
ily, excessive fluoride, or drugs such as p-aminosalicylic
acid and sulphonylureas. Some people also suggest that
autoimmune mechanisms may be involved.
(A)
(B)
FIGURE17. 9(A) A cut section through a multinodular goitre showing gross
asymmetrical enlargement. (B) Nodularity is clear on histological assessment.
TABLE17. 4Causes of hypothyroidism
•Autoimmune thyroid disease
Hashimoto’s thyroiditis
primary myxoedema
•Severe iodine deficiency
•Dyshormonogenesis
•Following thyroid surgery or radio-iodine therapy
•Ingestion of goitrogens
•Hypopituitarism
Cretinism is due to severe hypothyroidism in infancy.
Thyroid hormones are critical for normal brain develop-
ment, and these children show signs of mental retardation,
neuromuscular abnormalities, deaf-mutism and retarded
growth. There is a goitre when it is caused by severe iodine
deficiency, or by inherited defects of the enzymes involved
in thyroid hormone synthesis. Rarely, thyroid agenesis or
hypoplasia occurs, and in these cases goitre is absent. It is
extremely important to make an early diagnosis because
hormone replacement permits normal development.
Functional Disorders
Non-toxic Nodular Goitre
Non-toxic nodular goitre is the most common lesion in thy-
roid pathology. When there is absolute or relative iodine
deficiency, reduced levels of thyroid hormones result in
increased TSH secretion by the pituitary.This induces hyper-
plasia in an attempt to increase thyroid hormone output.
The demands are usually intermittent, and the gland under-
goes cycles of growth and involution, resulting in the well-
recognized picture of multinodular goitre, with nodules
consisting of follicles of varying size, fibrosis, haemorrhage
and focal inflammation. Enlargement is usually asymmet-
rical, and the gland may weigh up to several hundred grams
Key Points
•Non-toxic nodular goitre is the most common
thyroid disease.
•It is either endemic or sporadic.
•There is nodular enlargement of the thyroid gland.
•Affected individuals may be either euthyroid or
hypothyroid.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY24
SECRETORY MALFUNCTION17
407
Hypothyroidism (myxoedema) is the clinical syndrome
resulting from inadequate levels of circulating T
3 and T
4. The
metabolic rate is lowered and mucopolysaccharides accumu-
late in the dermal connective tissues to produce the typical
myxoedema face (Fig. 17.21). The general features of
hypothyroidism are summarised in Figure 17.22. If hypothy-
roidism is present in the newborn, physical growth and
mental development are impaired, sometimes irreversibly;
this condition is known as cretinism. Cretinism may be
endemic in geographical areas where the diet contains insuf-
ficient iodine for thyroid hormone synthesis. Sporadic cases
are usually due to a congenital absence of thyroid tissue, or
to enzyme defects blocking hormone synthesis.
The commonest cause of acquired hypothyroidism in
adults is Hashimoto’s thyroiditis (see below), but occasional
cases are iatrogenic, for example, due to surgical removal of
Fig. 17.20 Histological features of Graves’ thyroiditis. There
is hyperplasia of the follicular epithelium with nuclear irregularity,
depletion of colloid and focal lymphoid aggregates (arrowed).
Fig. 17.21 Myxoedemic face. The skin is coarse and puffy due
to accumulation of mucopolysaccharides; the outer third of the
eyebrows is lost.
! Syndrome due to insufficient circulating T
3 and T
4
! If congenital, causes cretinism
! Commonest cause is Hashimoto’s thyroiditis, an
autoimmune disorder
Functioning adenoma
Functioning adenomas of the thyroid may cause thyrotoxi-
cosis, but less than 1% of adenomas show enough secretory
activity to do so. Histologically, the tumour is composed of
thyroid follicles and is sometimes so small that it is visual-
ised only on an
131
I radioisotope scan. Occasionally it may
present as a solitary thyroid mass.
Toxic nodular goitre
Rarely, one or two nodules in a nodular goitre may develop
hypersecretory activity, a condition termed toxic nodular
goitre.
Hypothyroidism
Fig. 17.22 Systemic features of hypothyroidism (myxoedema).
The features in brackets are neither common nor essential.
Slow cerebration
Dry hair
Myxoedemic face
Typical complexion
Gruff voice
Ischaemic
heart disease
ECG changes
Bradycardia
Constipation
Carpal tunnel
syndrome
Dry, cold skin
Prone to
hypothermia
Psychosis
Loss of outer third
of eyebrows
(Deafness)
(Goitre)
Diminished
sweating
Weight gain
Menorrhagia
(Muscle
weakness)
Slowing of activity
SECRETORY MALFUNCTION17
407
Hypothyroidism (myxoedema) is the clinical syndrome
resulting from inadequate levels of circulating T
3 and T
4. The
metabolic rate is lowered and mucopolysaccharides accumu-
late in the dermal connective tissues to produce the typical
myxoedema face (Fig. 17.21). The general features of
hypothyroidism are summarised in Figure 17.22. If hypothy-
roidism is present in the newborn, physical growth and
mental development are impaired, sometimes irreversibly;
this condition is known as cretinism. Cretinism may be
endemic in geographical areas where the diet contains insuf-
ficient iodine for thyroid hormone synthesis. Sporadic cases
are usually due to a congenital absence of thyroid tissue, or
to enzyme defects blocking hormone synthesis.
The commonest cause of acquired hypothyroidism in
adults is Hashimoto’s thyroiditis (see below), but occasional
cases are iatrogenic, for example, due to surgical removal of
Fig. 17.20 Histological features of Graves’ thyroiditis. There
is hyperplasia of the follicular epithelium with nuclear irregularity,
depletion of colloid and focal lymphoid aggregates (arrowed).
Fig. 17.21 Myxoedemic face. The skin is coarse and puffy due
to accumulation of mucopolysaccharides; the outer third of the
eyebrows is lost.
! Syndrome due to insufficient circulating T
3 and T
4
! If congenital, causes cretinism
! Commonest cause is Hashimoto’s thyroiditis, an
autoimmune disorder
Functioning adenoma
Functioning adenomas of the thyroid may cause thyrotoxi-
cosis, but less than 1% of adenomas show enough secretory
activity to do so. Histologically, the tumour is composed of
thyroid follicles and is sometimes so small that it is visual-
ised only on an
131
I radioisotope scan. Occasionally it may
present as a solitary thyroid mass.
Toxic nodular goitre
Rarely, one or two nodules in a nodular goitre may develop
hypersecretory activity, a condition termed toxic nodular
goitre.
Hypothyroidism
Fig. 17.22 Systemic features of hypothyroidism (myxoedema).
The features in brackets are neither common nor essential.
Slow cerebration
Dry hair
Myxoedemic face
Typical complexion
Gruff voice
Ischaemic
heart disease
ECG changes
Bradycardia
Constipation
Carpal tunnel
syndrome
Dry, cold skin
Prone to
hypothermia
Psychosis
Loss of outer third
of eyebrows
(Deafness)
(Goitre)
Diminished
sweating
Weight gain
Menorrhagia
(Muscle
weakness)
Slowing of activity
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY25
Goiter
Goiter
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY26
Goiter.,
Goiter.,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY27
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY28
Neoplasms of the Thyroid
•Several clinical criteria provide a clue to the nature of a given thyroid nodule:
•Solitary nodules, in general, are more likely to be neoplastic than are
multiple nodules.
•Nodules in younger patients are more likely to be neoplastic than are those
in older patients.
•Nodules in males are more likely to be neoplastic than are those in females.
•A history of radiation treatment to the head and neck region is associated
with an increased incidence of thyroid malignancy.
•Nodules that take up radioactive iodine in imaging studies (hot nodules) are
more likely to be benign than malignant.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY29
•Several clinical criteria provide a clue to the nature of a given thyroid nodule:
•Solitary nodules, in general, are more likely to be neoplastic than are
multiple nodules.
•Nodules in younger patients are more likely to be neoplastic than are those
in older patients.
•Nodules in males are more likely to be neoplastic than are those in females.
•A history of radiation treatment to the head and neck region is associated
with an increased incidence of thyroid malignancy.
•Nodules that take up radioactive iodine in imaging studies (hot nodules) are
more likely to be benign than malignant.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY29
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY30
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY31
Thyroid Carcinomas
Thyroid Carcinomas
Diseases of the Parathyroid Glands
•The activity of the parathyroids is controlled by the level of free
(ionized) calcium in the bloodstream rather than by trophic
hormones secreted by the hypothalamus and pituitary.
•Tumors of the parathyroid glands, unlike thyroid tumors, usually
come to attention because of excessive secretion of parathyroid
hormone (PTH) rather than mass effects.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY32
•The activity of the parathyroids is controlled by the level of free
(ionized) calcium in the bloodstream rather than by trophic
hormones secreted by the hypothalamus and pituitary.
•Tumors of the parathyroid glands, unlike thyroid tumors, usually
come to attention because of excessive secretion of parathyroid
hormone (PTH) rather than mass effects.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY32
Diseases of the Parathyroid Glands
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY33
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY33
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY34
Endocrine Pancreas
Endocrine Pancreas
Diabetes Mellitus
Is a group of metabolic disorders sharing the common underlying feature of
hyperglycemia. Hyperglycemia in diabetes results from defects in insulin secretion,
insulin action, or, most commonly, both.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY35
Is a group of metabolic disorders sharing the common underlying feature of
hyperglycemia. Hyperglycemia in diabetes results from defects in insulin secretion,
insulin action, or, most commonly, both.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY35
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY36
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY37
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Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY44
Major Risk Factors For DM2
Major Risk Factors For DM2
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY45
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY46
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY47
Pancreatic Endocrine Neoplasms
•AKA "islet cell tumors," are rare in comparison with
tumors of the exocrine pancreas, accounting for only 2%
of all pancreatic neoplasms.
•They are most common in adults, may be single or
multiple, and benign or malignant, the latter
metastasizing to lymph nodes and liver.
•Pancreatic endocrine neoplasms have a propensity to
elaborate pancreatic hormones, but some may be totally
nonfunctional.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY48
•AKA "islet cell tumors," are rare in comparison with
tumors of the exocrine pancreas, accounting for only 2%
of all pancreatic neoplasms.
•They are most common in adults, may be single or
multiple, and benign or malignant, the latter
metastasizing to lymph nodes and liver.
•Pancreatic endocrine neoplasms have a propensity to
elaborate pancreatic hormones, but some may be totally
nonfunctional.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY48
Hyperadrenalism
•Just as there are three basic types of corticosteroids
elaborated by the adrenal cortex (glucocorticoids,
mineralocorticoids, and sex steroids), so there are three
distinctive hyperadrenal clinical syndromes:
•(1) Cushing syndrome, characterized by an excess of cortisol;
•(2) hyperaldosteronism; and
•(3) Adrenogenital or virilizing syndromes, caused by an excess
of androgens.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY49
Adrenal Cortex
•Just as there are three basic types of corticosteroids
elaborated by the adrenal cortex (glucocorticoids,
mineralocorticoids, and sex steroids), so there are three
distinctive hyperadrenal clinical syndromes:
•(1) Cushing syndrome, characterized by an excess of cortisol;
•(2) hyperaldosteronism; and
•(3) Adrenogenital or virilizing syndromes, caused by an excess
of androgens.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY49
Adrenal Cortex
Hypercortisolism (Cushing Syndrome)
This disorder is caused by any condition that produces an elevation in
glucocorticoid levels.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY50
This disorder is caused by any condition that produces an elevation in
glucocorticoid levels.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY50
Hypercortisolism (Cushing Syndrome)
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY51
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY51
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY52
The disorder affects women about five
times more frequently than men, and it
occurs most frequently during the 20s and
30s.
The biochemical sine qua non of adrenal
Cushing syndrome is elevated levels of
cortisol with low serum levels of ACTH.
The disorder affects women about five
times more frequently than men, and it
occurs most frequently during the 20s and
30s.
The biochemical sine qua non of adrenal
Cushing syndrome is elevated levels of
cortisol with low serum levels of ACTH.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY53
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY54
The major causes of
primary
hyperaldosteronism
and its principal
effects on the kidney
Hyperaldosteronism
Excessive levels of
aldosterone cause sodium
retention and potassium
excretion, with resultant
hypertension and
hypokalemia.
The major causes of
primary
hyperaldosteronism
and its principal
effects on the kidney
Hyperaldosteronism
Excessive levels of
aldosterone cause sodium
retention and potassium
excretion, with resultant
hypertension and
hypokalemia.
Adrenogenital Syndromes
•Excess of androgens may be caused by a number of diseases,
including primary gonadal disorders and several primary adrenal
disorders.
•Unlike gonadal androgens, adrenal androgen formation is regulated
by ACTH; thus, excessive secretion can occur either as a "pure"
syndrome or as a component of Cushing disease.
•The adrenal causes of androgen excess include adrenocortical
neoplasms and an uncommon group of disorders collectively
designated congenital adrenal hyperplasia (CAH).
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY55
•Excess of androgens may be caused by a number of diseases,
including primary gonadal disorders and several primary adrenal
disorders.
•Unlike gonadal androgens, adrenal androgen formation is regulated
by ACTH; thus, excessive secretion can occur either as a "pure"
syndrome or as a component of Cushing disease.
•The adrenal causes of androgen excess include adrenocortical
neoplasms and an uncommon group of disorders collectively
designated congenital adrenal hyperplasia (CAH).
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY55
Adrenogenital Syndromes..,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY56
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY56
Adrenogenital Syndromes..,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY57
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY57
Adrenogenital Syndromes..,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY58
•Adrenogenital syndrome. F/21. These patients have pseudohermaphrodite genitalia because of hypertrophy of the clitoris. The condition is caused by enzyme deficiency in the adrenal gland,
resulting in overproduction of androgens.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY58
•Adrenogenital syndrome. F/21. These patients have pseudohermaphrodite genitalia because of hypertrophy of the clitoris. The condition is caused by enzyme deficiency in the adrenal gland,
resulting in overproduction of androgens.
Adrenogenital Syndromes..,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY59
Precocious puberty
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY59
Precocious puberty
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY60
Adrenocortical insufficiency,
or hypofunction, may be
caused by either primary
adrenal disease (primary
hypoadrenalism) or
decreased stimulation of the
adrenals resulting from a
deficiency of ACTH
(secondary
hypoadrenalism).
Adrenal Insufficiency
Adrenocortical insufficiency,
or hypofunction, may be
caused by either primary
adrenal disease (primary
hypoadrenalism) or
decreased stimulation of the
adrenals resulting from a
deficiency of ACTH
(secondary
hypoadrenalism).
Adrenal Insufficiency
Adrenal Insufficiency.,
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY61
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY61
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY62
Adrenocortical Neoplasms
•Functional adrenal neoplasms may be responsible for any of the various
forms of hyperadrenalism.
•While functional adenomas are most commonly associated with
hyperaldosteronism and with Cushing syndrome, a virilizing neoplasm is
more likely to be a carcinoma.
•Adrenocortical carcinomas are rare neoplasms that may occur at any age.
•Two rare inherited causes of adrenal cortical carcinomas include the Li-
Fraumeni syndrome and the Beckwith-Wiedemann syndrome.
•The median patient survival is about 2 years.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY63
•Functional adrenal neoplasms may be responsible for any of the various
forms of hyperadrenalism.
•While functional adenomas are most commonly associated with
hyperaldosteronism and with Cushing syndrome, a virilizing neoplasm is
more likely to be a carcinoma.
•Adrenocortical carcinomas are rare neoplasms that may occur at any age.
•Two rare inherited causes of adrenal cortical carcinomas include the Li-
Fraumeni syndrome and the Beckwith-Wiedemann syndrome.
•The median patient survival is about 2 years.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY63
Multiple Endocrine Neoplasia Syndromes (MEN)
•Are a group of inherited diseases resulting in proliferative lesions
(hyperplasias, adenomas, and carcinomas) of multiple endocrine
organs.
•endocrine tumors arising in the context of MEN syndromes have
certain distinctive features that contrast with their sporadic
counterparts:
•These tumors occur at a younger age than sporadic cancers. They
arise in multiple endocrine organs, either synchronously or
metachronously. Even in one organ, the tumors are often multifocal.
•These tumors are usually more aggressive and recur in a higher
proportion of cases than similar endocrine tumors that occur
sporadically.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY64
•Are a group of inherited diseases resulting in proliferative lesions
(hyperplasias, adenomas, and carcinomas) of multiple endocrine
organs.
•endocrine tumors arising in the context of MEN syndromes have
certain distinctive features that contrast with their sporadic
counterparts:
•These tumors occur at a younger age than sporadic cancers. They
arise in multiple endocrine organs, either synchronously or
metachronously. Even in one organ, the tumors are often multifocal.
•These tumors are usually more aggressive and recur in a higher
proportion of cases than similar endocrine tumors that occur
sporadically.
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY64
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY65
References & Credits
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY
•Barone J, Castro M.A. (2016), USMLE Step 1 Pathology Lecture Notes, Published by Kaplan
Medical, a division of Kaplan, Inc. 750 Third Avenue, New York, NY 10017: ISBN: 978-1-
5062-0772-8
•Cooke A.R, Stewart B (2004) Colour Atlas of Anatomical Pathology (3rd Edition) Elsevier
Science Limited Churchill Livingstone, UK
•Harsh Mohan, (2010). Textbook of Pathology (6th Edition). Jaypee brothers medical
publishers (p) ltd, India
•Juan Rosai, (2011), Rosai and Ackerman's Surgical Pathology. 11th edition Elsevier
Science Limited Churchill Livingstone, UK
•Levison D.A., Reid R, Burt A.D., Harrison D.J., Fleming S., (2008), Muir’s Textbook of
Pathology, 14th Edition, Edward Arnold (Publishers) Ltd
•Riede U.N, and Werner M, (2004). Color Atlas of Pathology. Pathologic Principles ·
Associated Diseases · Sequela. Thieme, Stuttgart - New York, USA
•Robbins SL and Kumar V (2013). Basic Pathology (9th Edition).WB Saunders Co. London.
•Rubin E, Rubin R, Strayer D.S. (2012) Rubin`s Pathology: Clinicopathologic Foundations
of Medicine (6th Edition), Lippincott Williams & Wilkins, a Wolters Kluwer business.
Philadelphia, PA.
•Underwood, J.C.E and Cross, S. S (2009). General and Systematic Pathology (5th Edition).
Churchill-Livingstone, Edinburgh. ISBN: 978 0443068881
66
References & Credits
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY
•Barone J, Castro M.A. (2016), USMLE Step 1 Pathology Lecture Notes, Published by Kaplan
Medical, a division of Kaplan, Inc. 750 Third Avenue, New York, NY 10017: ISBN: 978-1-
5062-0772-8
•Cooke A.R, Stewart B (2004) Colour Atlas of Anatomical Pathology (3rd Edition) Elsevier
Science Limited Churchill Livingstone, UK
•Harsh Mohan, (2010). Textbook of Pathology (6th Edition). Jaypee brothers medical
publishers (p) ltd, India
•Juan Rosai, (2011), Rosai and Ackerman's Surgical Pathology. 11th edition Elsevier
Science Limited Churchill Livingstone, UK
•Levison D.A., Reid R, Burt A.D., Harrison D.J., Fleming S., (2008), Muir’s Textbook of
Pathology, 14th Edition, Edward Arnold (Publishers) Ltd
•Riede U.N, and Werner M, (2004). Color Atlas of Pathology. Pathologic Principles ·
Associated Diseases · Sequela. Thieme, Stuttgart - New York, USA
•Robbins SL and Kumar V (2013). Basic Pathology (9th Edition).WB Saunders Co. London.
•Rubin E, Rubin R, Strayer D.S. (2012) Rubin`s Pathology: Clinicopathologic Foundations
of Medicine (6th Edition), Lippincott Williams & Wilkins, a Wolters Kluwer business.
Philadelphia, PA.
•Underwood, J.C.E and Cross, S. S (2009). General and Systematic Pathology (5th Edition).
Churchill-Livingstone, Edinburgh. ISBN: 978 0443068881
66
References & Credits
Tuesday, July 30, 2024Ephraim Zulu - PATHOLOGY
End of Lecture
Ephraim Imhotep Zulu
Pathology
67
End of Lecture
Ephraim Imhotep Zulu
Pathology
67
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