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Adrenal glands:
The adrenal glands are paired endocrine organs
consisting of both cortex and medulla, which
differ in their development, structure, and
function.
The adrenal cortex synthesizes three different types
of steroids:
(1) glucocorticoids (principally cortisol)
(2) mineralocorticoids, the most important being
aldosterone
(3) sex steroids (estrogens and androgens)
The adrenal medulla is composed of chromaffin
cells, which synthesize and secrete
catecholamines, mainly epinephrine.
Adrenal glands:
Hypercortisolism (Cushing Syndrome)
Exogenous
Endogenous divided into those that are
 ACTH dependent
 ACTH independent
Adrenal insufficiency(hypoadrenalism)
primary (Addison disease)
secondary
Hypercortisolism (Cushing Syndrome)
Pathogenesis:
 This disorder is caused by any condition that
produces elevated glucocorticoid levels. Cushing
syndrome can be broadly divided into exogenous
and endogenous causes.
 The vast majority of cases of Cushing syndrome
are the result of the administration of exogenous
glucocorticoids (“iatrogenic” Cushing syndrome).
 The endogenous causes can, in turn, be divided
into those that are ACTH dependent and those
that are ACTH independent
Depending on the cause of the hypercortisolism the
adrenals have :
In patients in whom the syndrome results from
exogenous glucocorticoids, suppression of
endogenous ACTH results in bilateral cortical
atrophy, due to a lack of stimulation of the adrenal
by ACTH.
In contrast, in cases of endogenous hypercortisolism,
the adrenals either are hyperplastic or contain a
cortical neoplasm.
The main lesions of Cushing syndrome that are found in
the pituitary and adrenal glands:
(Pituitary gland changes in cushing syndrome)
 Crock hyaline changes:
This is the most common change seen in pituitary gland in all
forms of cushing syndrome. In this condition, the normal
granular, basophilic cytoplasm of the ACTH producing cells in
the pituitary is replaced by homogenous, lightly basophilic
material (cytokeratin filaments deposition).
 Pituitary Adenomas or foci of ACTH cell hyperplasia.
Causes of chronic primary hypoadrenalism
(Addison disease)
 Autoimmune diseases.
 Tuberculosis.
 AIDS
 Metastatic diseases
 Fungal infection
 Sarcoidosis
 Systemic amyloidosis.
AddisonDisease.
◦ Is uncommon disorder resulting from
progressive destruction of the adrenal cortex.
◦ Clinical features of Addison disease do not appear
until at least 90% of adrenal cortex has been
destructed.
Morphology of hypoadrenalism
Gross.
In Addison disease, adrenal glands are shrunken; while in
secondary hypoadrenalism (due to diseases of pituitary &
hypothalamus) adrenal glands are reduced to small,
flattened, yellow structure.
Mic.
In Addison disease, the cortex of adrenal glands contains
only scattered residual cortical cells within the network of
connective tissue, with lymphoid infiltration of the cortex.
Clinical features of Addison disease:
 Insidious onset of weakness & easy fatigability.
 ↑K,↓Na,↓BP, due to mineralocorticoid insufficiency.
 Hyperpigmentation in primary hypoadrenalism (due to
increase level of POMC precursor to ACTH and
melanocytes stimulating hormone).
 Nausea, vomiting & diarrhea.
 Hypoglycemia & glycosuria.
 Acute stresses (e.g., trauma or infection)
 can precipitate acute adrenal crisis, with rapid progression
to deathunless corticosteroid therapy is promptly initiated.
Pathology of adrenal medulla.
The most important pathological process in adrenal
medulla is Pheochromacytoma
Pheochromacytoma:
Are neoplasm composed of chromaffin cells, which like
the non neoplastic chromaffin cells synthesize & release
catecholamines (epinephrine, norepinephrine).
Pheochromacytoma can describe by a rule of 10s
 10% of pheochromacytoma are familial.
 10% are extra- adrenal in their sites (Paraganglioma).
 10% of cases are bilateral.
 10% are biologically malignant.
Gross.
◦ Range from small, circumscribed to large hemorrhagic mass.
Mic.
◦ Composed of polygonal to spindle cells with their supporting
cells, which divide the tumor into small nests (zellaballen) pattern
by a rich vascular network.
◦ Cytoplasm of neoplastic cells is granular (due to their contents of
catecholamines granules).
 Even in benign cases, there is vascular & capsular invasion, so the
diagnosis of malignant pheochromacytoma depends on presence
of metastases (to lymph nodes, lung, liver, & bones).
Clinical features.
 The most characteristic clinical feature of pheochromacytoma is
isolated, paroxysmal, episodes of hypertension in 50% of cases,
with associated symptoms like (tachycardia, palpitation, headache,
tremor, sudden abdominal symptoms).
 All these symptoms are due to overproduction of catecholamines
by the neoplastic cells.
 Laboratory data (increase urinary excretion of free catecholamines
& their metabolites like Vanilyl Mndelic Aid (VMA).
2_2019_05_04!10_09_05_AMtyvvgģgggggggggg
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Home assignment II on Spectroscopy 2024 Answers.pdfHome assignment II on Spectroscopy 2024 Answers.pdf
Home assignment II on Spectroscopy 2024 Answers.pdf
 

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  • 3. Adrenal glands: The adrenal glands are paired endocrine organs consisting of both cortex and medulla, which differ in their development, structure, and function. The adrenal cortex synthesizes three different types of steroids: (1) glucocorticoids (principally cortisol) (2) mineralocorticoids, the most important being aldosterone (3) sex steroids (estrogens and androgens) The adrenal medulla is composed of chromaffin cells, which synthesize and secrete catecholamines, mainly epinephrine.
  • 4. Adrenal glands: Hypercortisolism (Cushing Syndrome) Exogenous Endogenous divided into those that are  ACTH dependent  ACTH independent Adrenal insufficiency(hypoadrenalism) primary (Addison disease) secondary
  • 5. Hypercortisolism (Cushing Syndrome) Pathogenesis:  This disorder is caused by any condition that produces elevated glucocorticoid levels. Cushing syndrome can be broadly divided into exogenous and endogenous causes.  The vast majority of cases of Cushing syndrome are the result of the administration of exogenous glucocorticoids (“iatrogenic” Cushing syndrome).  The endogenous causes can, in turn, be divided into those that are ACTH dependent and those that are ACTH independent
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  • 7. Depending on the cause of the hypercortisolism the adrenals have : In patients in whom the syndrome results from exogenous glucocorticoids, suppression of endogenous ACTH results in bilateral cortical atrophy, due to a lack of stimulation of the adrenal by ACTH. In contrast, in cases of endogenous hypercortisolism, the adrenals either are hyperplastic or contain a cortical neoplasm.
  • 8. The main lesions of Cushing syndrome that are found in the pituitary and adrenal glands: (Pituitary gland changes in cushing syndrome)  Crock hyaline changes: This is the most common change seen in pituitary gland in all forms of cushing syndrome. In this condition, the normal granular, basophilic cytoplasm of the ACTH producing cells in the pituitary is replaced by homogenous, lightly basophilic material (cytokeratin filaments deposition).  Pituitary Adenomas or foci of ACTH cell hyperplasia.
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  • 12. Causes of chronic primary hypoadrenalism (Addison disease)  Autoimmune diseases.  Tuberculosis.  AIDS  Metastatic diseases  Fungal infection  Sarcoidosis  Systemic amyloidosis.
  • 13. AddisonDisease. ◦ Is uncommon disorder resulting from progressive destruction of the adrenal cortex. ◦ Clinical features of Addison disease do not appear until at least 90% of adrenal cortex has been destructed.
  • 14. Morphology of hypoadrenalism Gross. In Addison disease, adrenal glands are shrunken; while in secondary hypoadrenalism (due to diseases of pituitary & hypothalamus) adrenal glands are reduced to small, flattened, yellow structure. Mic. In Addison disease, the cortex of adrenal glands contains only scattered residual cortical cells within the network of connective tissue, with lymphoid infiltration of the cortex.
  • 15. Clinical features of Addison disease:  Insidious onset of weakness & easy fatigability.  ↑K,↓Na,↓BP, due to mineralocorticoid insufficiency.  Hyperpigmentation in primary hypoadrenalism (due to increase level of POMC precursor to ACTH and melanocytes stimulating hormone).  Nausea, vomiting & diarrhea.  Hypoglycemia & glycosuria.  Acute stresses (e.g., trauma or infection)  can precipitate acute adrenal crisis, with rapid progression to deathunless corticosteroid therapy is promptly initiated.
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  • 17. Pathology of adrenal medulla. The most important pathological process in adrenal medulla is Pheochromacytoma Pheochromacytoma: Are neoplasm composed of chromaffin cells, which like the non neoplastic chromaffin cells synthesize & release catecholamines (epinephrine, norepinephrine). Pheochromacytoma can describe by a rule of 10s  10% of pheochromacytoma are familial.  10% are extra- adrenal in their sites (Paraganglioma).  10% of cases are bilateral.  10% are biologically malignant.
  • 18. Gross. ◦ Range from small, circumscribed to large hemorrhagic mass. Mic. ◦ Composed of polygonal to spindle cells with their supporting cells, which divide the tumor into small nests (zellaballen) pattern by a rich vascular network. ◦ Cytoplasm of neoplastic cells is granular (due to their contents of catecholamines granules).  Even in benign cases, there is vascular & capsular invasion, so the diagnosis of malignant pheochromacytoma depends on presence of metastases (to lymph nodes, lung, liver, & bones).
  • 19. Clinical features.  The most characteristic clinical feature of pheochromacytoma is isolated, paroxysmal, episodes of hypertension in 50% of cases, with associated symptoms like (tachycardia, palpitation, headache, tremor, sudden abdominal symptoms).  All these symptoms are due to overproduction of catecholamines by the neoplastic cells.  Laboratory data (increase urinary excretion of free catecholamines & their metabolites like Vanilyl Mndelic Aid (VMA).