Pathophysiology of

endocrine system

Victoria Rotaru
Ph.D. associate professor
 Cell Surface Receptors
 Antibodies may destroy or block the receptor proteins
 Increased or decreased hormone levels induce changes in the
activity of the genes that regulate receptor synthesis
 Nuclear Receptors
 They modulate the synthesis of enzymes, transport proteins, or
structural proteins
 The receptors for thyroid hormones are directly associated with
controlling the activity of genes located on the chromosomes
Control of Hormone Levels
Feedback Regulation
Negative feedback control
Negative feedback control
Positive feedback
Pituitary gland
 Disturbances of
endocrine function
Hypo function
Hyper function
 Hypo function

 Congenital defects (absence, impaired

development of the gland or the absence of an
enzyme needed for hormone synthesis )
 Acquired diseases (disruption in blood flow,
infection, inflammation, autoimmune responses
or neoplastic growth)
 Atrophy as the result of drug therapy
 Endocrine deficient states associated with
receptor defects
 Receptor defects
 The absent of hormone receptors
 The receptor binding of hormones may be
defective
 The cellular responsiveness to the
hormone may be impaired
 Hyper function
 Excessive hormone production
(excessive stimulation and hyperplasia of
the endocrine gland or from a hormone –
producing tumor of the gland)
 Ectopic tumor can produce hormones
(bronchogenic tumors produce hormones
such as antidiuretic hormone (ADH) and
adrenocorticotropic hormone (ACTH)
 Primary, secondary disorders
 Primary defects
in endocrine function originate in the target gland
responsible for producing the hormone
 Secondary disorders
of endocrine function, the target gland is
essentially normal, but its function is altered by
defective levels of stimulating hormones or
releasing factors from the pituitary system
 Tertiary disorders
Results from hypothalamic dysfunction
(as may occur with craniopharyngiomas
or cerebral irradiation), thus, both the
pituitary and target organ are
understimulated
 Clinical Manifestations of
Pituitary Disease

causes of causes of
hyperpituitarism hypopituitarism

 pituitary adenoma  ischemic injury,

 hyperplasia and surgery or radiation,
carcinomas of the  inflammatory
anterior pituitary reactions, and
 secretion of hormones nonfunctional pituitary
by nonpituitary  adenomas.
tumors
 hypothalamic
disorders
 Hypopituitarism
Is characterised by a
decreased secretion of
pituitary hormones (70%-
90%)
Causes of hypopituitarism
 The manifestations of
hypopuitarism
 Chronically unfit
 Weakness –ACTH deficiency
 Fatigue
 Loss of appetite
 Impairment of sexual function
 Cold intolerance
 Weakness

ACTH deficiency:

Nausea
Fever

Anorexia

Postural
hypotension
Pituitary Tumors
 Growth hormone disorders
 Is produced by somatotropes in the anterior
pituitary
 Is necessary for linear bone growth in children
 It also stimulates cells to increase in size and
divide more rapidly
 It enhances amino acid transport across cell
membranes and increases protein synthesis
 It increases the rate at which cells use fatty acids
and decreases the rate at which they use
carbohydrates
 GROWTH HORMONE
 The effects of GH on linear growth requires
insulin-like growth factors (IGFs), which are
produced mainly by the liver.
 GH deficiency in children interferes with linear
bone growth, resulting in short stature or
dwarfism
 In children , GH excess results in increased linear
growth or gigantism;
 In adults it results in overgrowth of the
cartilaginous parts of the skeleton, enlargement
of the heart and other organs, and metabolic
disturbances in fat and carbohydrate metabolism
 Short Stature in
Children
GH deficiency in children interferes with
linear bone growth , metabolism and
tissue development, known as pituitary
dwarfism
 Growth Hormone Deficiency in
Children
 Idiopathic GH deficiency (lack the hypothalamic
GHRH but have adequate somatotropes, whereas
children with pituitary tumors or agenesis of the
pituitary lack somatotropes.
 Congenital GH deficiency ( decreased birth
length, followed by a decrease in growth rate
that can be identified by careful measurement
during the first year and that becomes obvious
by 1 to 2 years of age)
 Manifestations of GH deficiency
 Normal intelligence
 Short stature
 Obesity with immature facial features
 Delay in skeletal maturation
 Puberty is delayed
 Males have microphallus (abnormally
small penis)
 Growth Hormone Deficiency in
Adults
 GH deficiency that was present in
childhood
 GH deficiency that developed during adult
hood
 Growth hormone
Excess in Children
Fusion of the epiphyses of the
long bones results in
gigantism
 Growth Hormone
Excess in Adults
Excess GH in adulthood or after
the epiphyses of the long bones
have fused-acromegaly
 The causes of acromegaly
 Somatotrope adenoma
 Excess secretion of GHRH by hypothalamic
tumors
 Ectopic secretion of GH by nonendocrine
tumors
Disorders of Adrenal
Cortical Function
 Adrenal Cortical Hormones :

 mineralcorticoids (aldosterone, which function

in sodium, potassium, and water balance)
 glucocorticoids (cortisol, which aid in regulating
the metabolic functions of the body and in
controlling the inflammatory responce, and are
essential for survival in stress situations)
 adrenal sex normones (androgens, which serve
mainly as a source of androgens for women)
 Glucocorticoids
 stimulate gluconeogenesis in the liver
 Inhibit glucose uptake in peripheral cells
 Stimulate lipolysis and
 Promote breakdown of proteins in the
periphery,
 Cause mobilization of fatty acids
 the formation of plasma proteins
 (e.g., angiotensinogen) in the liver
 Promote the formation of erythrocytes,
thrombocytes and neutrophil granulocytes
 suppress inflammation
 Mineralocorticoids
 further renal retention of Na+ and water.
 They
 thus facilitate a rise in blood pressure
 stimulate renal elimination of K+, Mg2+,
 and H+ and simultaneously the
intracellular
 uptake of potassium
Adrenocortical Hyperfunction
 (1) Cushing syndrome, characterized by
an excess of cortisol;
 (2) hyperaldosteronism,as a result of
excessive aldosterone;
 (3) adrenogenital or virilizing
syndromes, caused an excess of
androgens.
Hypercortisolism (Cushing syndrome)
 Exogenous  Endogenous
 1. ACTH dependent
 2. ACTH
independent
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