2. Hypothalamic releasing and inhibitory hormones control
anterior pituitary secretion.
1. Thyrotropin-releasing hormone (TRH), which causes
release of thyroid-stimulating hormone.
2. Corticotropin-releasing hormone (CRH), which causes
release of adrenocorticotropin.
3. Growth hormone–releasing hormone (GHRH), which
causes release of growth hormone, and growth hormone
inhibitory hormone (GHIH), also called somatostatin,
which inhibits release of growth hormone.
4. Gonadotropin-releasing hormone (GnRH), which
causes release of the two gonadotropic hormones,
luteinizing hormone and follicle-stimulating hormone.
5. Prolactin inhibitory hormone (PIH), which causes
inhibition of prolactin secretion.
3. Pituitary Gland
The pituitary gland , also called the hypophysis, lies in the sella
turcica, a bony cavity at the base of the brain, and is connected to
the hypothalamus by the pituitary (or hypophysial) stalk.
Physiologically, the pituitary gland is divisible into two distinct
portions:
The anterior pituitary, also known as the adenohypophysis
The posterior pituitary, also known as the neurohypophysis.
The pars intermedia, which is almost absent in the human
being.
4. ANTERIOR PITUITARY(ADENOHYPOPHYSIS)
Gland contains several different cell types that synthesize and
secrete hormones. The five cell types are:
Somatotropes — 50%. The most abundant cell type.
Secrete Human Growth Hormone (HGH) (GH) or
Somatotropin. Growth hormone promotes growth of the
entire body by affecting protein formation, cell
multiplication, and cell differentiation
Corticotropes—10%. Secrete adrenocorticotropin or
adrenocorticotropic hormone (ACTH) which controls the
secretion of some of the adrenocortical hormones, which
affect the metabolism of glucose, proteins, and fats.
Thyrotropes— 5%. Secrete Thyroid-stimulating hormone
(TSH), which controls the growth and rate of secretion of
T4 & T3 by the thyroid gland, and these hormones control
the rates of most intracellular chemical reactions in the
body.
5. Lactotropes— 15 – 20%. Secrete Prolactin (PRL), which
stimulates breast development and milk production.
Gonadotropes— 5 –10%. Secrete Gonadotropic hormones,
which include both Luteinizing Hormone (LH) and Follicle
Stimulating Hormone (FSH). They control growth of the
ovaries and testes, as well as their hormonal and
reproductive activities.
6. EFFECTS OF LH
Males Females
• It is known as ICSH
i.e. interstitial cell
stimulating hormone.
• It stimulates interstitial
cells of Leydig in the
testes for the secretion
of testosterone
• Maturation of graffian follicle
along with FSH
• Induces synthesis of androgens
from growing cells of follicle
• Responsible for ovulation
• Necessary for formation and
activates secretory activity of
corpus luteum
7. EFFECTS OF FSH
IN MALES IN FEMALES
• FSH along with testosterone
accelerate the process of
spermatogenesis.
• It is responsible for
folliculogenesis
• Stimulates theca cells of
graffian follicle and causes
secretion of estrogen
• Promote aromatase activity for
the conversion of androgens
into estrogens
8. GROWTH HORMONE
• GH is a 191–amino acid peptide hormone
• GH is released from the somatotropes, an abundant (50%) cell
type in the anterior pituitary.
• The majority of secretion occurring nocturnally in association with
slow-wave sleep.
ACTIONS OF GH
Effects on growth: It is responsible for growth of almost all
tissues of the body. It actually increases the size and number
of cells by increasing mitotic division. It also causes specific
differentiation of certain cells like bone, muscles etc.
Metabolic actions. It has important effects on protein, lipid
and carbohydrate metabolism
9. EFFECTS ON BONES
In the bones GH acts directly
• By increasing protein synthesis of osteogenic cells and
chondrocytes
• By stimulating osteoblastic activity and helps in formation
of new bones
• By increasing intestinal absorption of calcium.
GH has indirect action on bones which is mediated through
somatomedins [IGF-I & II], secreted by liver. Somatomedins
promote growth of soft tissues as well as bones.
10. METABOLIC ACTIONS OF GH
Carbohydrates Metabolism: GH is antagonistic to insulin and
produces hyperglycaemia. GH stimulates gluconeogenesis,
decreases uptake as well as utilization of glucose by tissues for
energy production i.e. inhibits glycolysis, increase
glycogenesis. Diabetogenic effect in high levels of GH.
Fat Metabolism: GH enhances utilization of fat by promoting
lipolysis from adipose tissues. It causes mobilization of free
fatty acids and make it available for energy production
Protein Metabolism: GH stimulates protein synthesis by
increasing rate of amino acid transport, transcription and
translation processes and by decreasing protein catabolism as
well as rate of amino acid degradation
Mineral Metabolism: GH increase intestinal absorption of
calcium, decreases excretion of sodium, potassium, phosphate
etc.
11. REGULATION OF GH RELEASE
Secretion of GH is regulated by hypothalamus and feedback
control
Hypothalamus regulate by releasing three hormones;
1. GHRH stimulate somatotropes
2. GHRP promotes the release of GHRH
3. GHIH or somatostatin inhibits GH
Hypothalamus in turn influenced by hypoglycemia, fasting,
exercise, starvation, stress, trauma which increase GH
secretion and hyperglycaemia, increase in fatty acids in blood
which decrease GH secretion.
Somatomedin increase secretion of GHIH and also inhibits
release of GHRP.
14. GIGANTISM.
• Occurs due to hypersecretion of GH during childhood
• Caused due to the development of tumours or excessively active
somatotropes
• The characteristic features are
• All body tissues grow rapidly, including the bones. Growth is
rapid and excessive, but proportionate in all parts of the body
• Abnormal height: If the condition occurs before adolescence,
before the epiphyses of the long bones have become fused
with the shafts, height increases so that the person becomes
a giant— up to 8 feet tall.
• Visual disturbances and headaches are common due to
pituitary tumours
• The giants are usually hyperglycaemic, and is called pituitary
diabetes
15. ACROMEGALY
• It is due to hypersecretion of GH in adults after the fusion of
epiphysis with shaft of the bone. Occurs due to tumour of
somatotropes
• It is the disorder characterized by enlargement, thickening and
broadening of bones especially in the extremities of the body.
• Signs and symptoms:
Acromegalic face: The striking facial features are protrusion of
supraorbital ridges, broadening of nose, thickening of lips and
forehead and protrusion of lower jaw.
Enlargement of hands and feet with bowing of spine or
kyphosis
Enlargement of visceral organs
Hyperactivity of endocrine glands.
Hyperglycaemia and glycosuria
Hypertension
Headache and visual disturbances
16. DWARFISM
• It is a pituitary disorder in children characterized by stunted
growth
• Caused by reduction in GH secretion in infancy or childhood
resulting from deficiency of GHRH, somatomedin – C, atrophy
or degeneration of acidophilic cells.
• Signs and symptoms
• Stunted skeletal growth, but the proportions are almost
normal. Only the head becomes slightly larger
• The maximum height of pituitary dwarf in the adult stage
is only about 3 feet
• No mental retardation or other deformities
• Reproductive function is not affected if there is only GH
deficiency.
17. • Prolactin is secreted
by lactotropes
• Suckling stimulates
the release of
prolactin.
• Prolactin inhibits its
own release by PIH
release from the
hypothalamus.
PHYSIOLOGIC EFFECTS OF PROLACTIN.
18. PHYSIOLOGIC EFFECTS OF PROLACTIN
• The main physiologic effects of prolactin are
Stimulation of growth and development of the mammary
gland, synthesis of milk, and maintenance of milk
secretion .
Prepares the breast for lactation. The production of milk
is prevented during pregnancy by the high progesterone
levels.
Inhibition of GnRH release (results in suppression of
ovarian cycle during nursing)
Stimulates luteal cell hypertrophy during pregnancy.
Modulates reproductive and parental behaviour.
19.
20. • ADH is secreted by supraoptic nucleus of hypothalamus .
• It is then transported to the posterior pituitary through
hypothalamo- hypophyseal tract.
• Its major function is retention of water by acting on
kidneys. The hormone is called so because it can cause
decreased excretion of water by the kidneys (antidiuresis)
• It increases facultative reabsorption of water from
distal convoluted tubules and collecting duct.
• ADH increases water reabsorption by regulating water
channels called aquaporins through V2 receptors.
• ADH act on blood vessels through V1A receptors and causes
vasoconstriction in all parts of the body and in turn increase
blood pressure. The hormone is known as vasopressin
because of these vasoconstrictor effects.
21. DISORDERS OF ADH PRODUCTION
DIABETES INSIPIDUS
A decrease in ADH release or action results in diabetes
insipidus, a clinical syndrome in which the ability to form
concentrated urine is reduced.
It develops due to deficiency of ADH caused by lesions in
hypothalamus, hypothalamo-pituitary tract, atrophy of
posterior pituitary, or nephrogenic DI.
Symptoms
• Diabetes insipidus is characterized by the excretion of
abnormally large volumes of dilute (<250 mmol/kg) urine
and excessive thirst. This condition is polyuria.
• Water loss stimulates thirst centre and leads to intake of
excess water called polydipsia.
• Dehydration also occurs if water intake decreases and the
loss of water is not compensated.
22. TYPE CAUSE
Central DI (the most
common type)
Damage to the pituitary gland or hypothalamus from
head injury, surgery, or tumors. This can lead to a lack
of ADH.
Nephrogenic DI
The pituitary releases enough ADH into the body but
kidneys can’t respond to it. This can result from the
prescription drug lithium, sickle cell disease, or genetic
problems.
Dipsogenic DI
• Excess fluid intake, caused by a problem with thirst
mechanism, or deliberately drinking too many
fluids (may occur with mental illness)
• This can lead to low blood sodium and possible
brain damage.
Pregnancy-related DI A substance made by the placenta that prevents the
mother’s ADH from working.
23. OXYTOCIN
• It is secreted mainly by paraventricular nucleus of hypothalamus
and is then transported to posterior pituitary for storage.
• Actions
• In females it acts on mammary gland and uterus.
• On mammary gland, it causes ejection of milk by the
contraction of myoepithelial cells.
• On pregnant uterus, oxytocin level increase during labour
and induces contraction of uterus. Oxytocin also stimulates
release of prostaglandins in the placenta[intensify uterine
contraction]
• On nonpregnant uterus, oxytocin facilitates the transport
of sperms through female genital tract up to fallopian tube
by producing uterine contraction during sexual intercourse.
• In males, release of oxytocin occurs during ejaculation. It
facilitates release of sperm in to urethra by contraction of
smooth muscle fibres of vas deferens.
24. • This reflex is initiated by the nervous factors and completed by
hormonal action, it is called neuroendocrine reflex.
• During this reflex, large amount of oxytocin is released by
positive feedback mechanism.
• Plenty of touch receptors are present on the mammary
glands around the nipple.
• The suckling stimulate these receptors and causes signals to
be transmitted through sensory nerves to the hypothalamus
• Results in release of oxytocin by the posterior pituitary
gland.
• The oxytocin causes contraction of myoepithelial cells
surrounding the alveoli of the mammary glands, resulting in
ejection of milk.
MILK EJECTION REFLEX
25. Suckling stimulates touch receptors on the nipple
of the breast
Signals transmitted through sensory nerves to the
hypothalamus
Release of oxytocin by the posterior pituitary
gland
Oxytocin causes contraction of myoepithelial cells
that surrounding the alveoli of the mammary
glands.
Milk begins to flow or milk let-down or milk
ejection occurs
26. • The cellular composition
of the thyroid gland is
diverse, including the
following:
Follicular (epithelial)
cells, involved in
thyroid hormone
synthesis;T3&T4
Parafollicular or C
cells, are found in the
spaces between
follicles. involved in
the production of
calcitonin,
27. METABOLIC ACTIONS
In general thyroid hormones increase BMR in most tissues except
brain, retina, gonads, lungs and spleen
Carbohydrates metabolism: Accelerate all aspects of glucose
metabolism i.e. enhanced glycolysis, gluconeogenesis,
glycogenesis, glycogenolysis
Fat metabolism: Enhances lipolysis by promoting mobilization
of free fatty acids from adipose tissues. Increase in the levels of
fatty acids.
Protein metabolism: In physiological amounts thyroid
hormones, stimulates protein synthesis. But in higher
concentrations, favour protein catabolism
28. OTHER ACTIONS
Effects on growth
Role in normal body growth and skeletal maturation
Helps to maintain the body weight
Promote growth and development of the brain
Effects on kidneys
Increase the size of kidneys, renal plasma flow, GFR, &
tubular transport maximum for various substances
Effect on CVS
Increase in cardiac output, blood volume
Increase in systolic pressure by increasing rate and force of
contraction, but diastolic blood pressure decreases, mean
arterial pressure remains unchanged
Causes vasodilatation and increase blood flow
29. Effects on reproductive system:
• In males lack of thyroid hormones causes complete loss of
libido & excess hormones cause impotence
• In females lack of thyroid hormones cause disturbances in
menstruation
Effects on respiration :
Increase in rate and force of respiration indirectly
Effects on GIT:
Increase appetite and therefore increased food intake
Increase in GIT motility
Increase in rate of secretion of digestive enzymes
Effects on endocrine glands:
GH, Cortisol increased
PTH & calcitriol are decreased
31. HYPOTHYROIDISM
Hypothyroidism is the condition resulting from insufficient
thyroid hormone action. Two main types are distinguished,
primary and secondary hypothyroidism, although the former is
more common.
• Primary hypothyroidism may be associated with thyroid
enlargement, resulting from inflammation as in Hashimoto’s
thyroiditis and increases in TSH due to dietary iodine
deficiency.
• Secondary hypothyroidism is characterized by decreased TSH
secretion and subsequently decreased thyroid hormone
release, and is usually due to hypopituitarism (decreased
anterior pituitary function).
When the decrease in thyroid function occurs in utero, the result
is severe intellectual and developmental delay or CRETINISM
When the decrease in thyroid function occurs in adults, the
condition is called MYXEDEMA
32.
33. CRETINISM
• Caused by extreme hypothyroidism during fetal life, infancy, or
childhood.
• It results from congenital lack of a thyroid gland (congenital
cretinism), from failure of the thyroid gland to produce thyroid
hormone because of a genetic defect of the gland, or from
iodine lack in the diet (endemic cretinism).
• Skeletal growth is characteristically more inhibited than soft
tissue growth. As a result of this disproportionate rate of
growth, the soft tissues are likely to enlarge excessively, giving
the child with cretinism an obese, stocky, and short
appearance.
• This condition is characterized especially by mental retardation
• Occasionally the tongue becomes so large in relation to the
skeletal growth that it obstructs swallowing and breathing,
inducing a characteristic guttural breathing that sometimes
chokes the child.
34. MYXOEDEMA
• Hypothyroidism in adults
SYMPTOMS
i. Weight gain without an appreciable food intake
ii. Hypothermia or cold intolerance and decreased sweating
iii. Thickened features; dry thick skin, sparse hair, periorbital
edema
iv. Swelling of hands and feet without indentation i.e. non
pitting edema
v. Delayed muscle contraction and relaxation
vi. Decreased initiative, lethargy
vii. Slowing of mental function, impaired memory, slow speech
viii. Delayed tendon reflexes
ix. Reduced stroke volume and heart rate, decreased cardiac
output, enlarged heart, pericardial effusion, pleural and
peritoneal fluid accumulation
x. Somnolence
xi. Abnormal menstrual flow
35. GRAVE’S DISEASE[TOXIC GOITER OR THYROTOXICOSIS]
• Grave’s disease is an autoimmune condition leading to the
stimulation of TSH receptor by TSH-like antibodies called thyroid-
stimulating immunoglobulins (TSI).This produces marked increase
in T4 and T3 secretion and enlargement of the thyroid gland
(goiter).
• Another hallmark of Graves disease is the occurrence of swelling
of tissues in the orbits, producing protrusion of the eyeballs
(exophthalmos). This occurs in 50% of patients
36.
37. The symptoms of hyperthyroidism are
1. Intolerance to heat
2. Increased sweating and greater water intake
3. Mild to extreme weight loss (sometimes as much as 100
pounds) despite an increased food intake
4. Varying degrees of diarrhoea
5. Muscle weakness
6. Nervousness or other psychic disorders
7. A high state of excitability
8. Tremor of the hands
9. Extreme fatigue but inability to sleep
10. Sinus tachycardia even during sleep, arrhythmias
11. Polycythemia
12. Marked increase in BMR
13. Palpable enlarged thyroid gland
14. Infiltrative ophthalmopathy or EXOPHTHALMOS
38. GOITRE
Goitre is defined as an overall enlargement of the thyroid gland,
associated with either decreased or increased thyroid function.
Endemic goitre:
• Inhibition of synthesis of hormones occurs due to iodine
deficiency. Low levels of T4 &T3 causes the pituitary to
secrete excessively large quantities of TSH. Absence of
normal suppression of TSH production by the anterior
pituitary makes the follicles and the thyroid gland may
increase to 10 to 20 times normal size
Idiopathic nontoxic colloid goitre:
• Enlarged thyroid glands can also occur in people who do
not have iodine deficiency. These goitrous glands may
secrete normal quantities of thyroid hormones.
39. THYROIDITIS
• Thyroiditis, or inflammation of the thyroid gland, may lead to
abnormalities in thyroid hormone state.
Chronic thyroiditis (Hashimoto’s thyroiditis, chronic lymphocytic
thyroiditis, autoimmune thyroiditis)
• Hashimoto’s thyroiditis is the most common cause of adult
hypothyroidism
• It is an autoimmune disease of the thyroid gland
characterized by lymphocyte infiltration and circulating
autoimmune antibodies.
• These antibodies inhibit the Na+/I− symporter, preventing
iodide uptake and consequently thyroid hormone synthesis.
• It is more prevalent in women than in men, and peaks at the
age of 30–50 years.
40. CALCITONIN
• Synthesized by parafollicular cells or C cells of thyroid
gland
• Released in response to rise in plasma calcium
concentration
• The major effects of calcitonin is to lower the plasma
calcium ion level and decrease phosphate ion
concentration
• It is done by following actions;
ACTION ON BONES
• Stimulates osteoblastic activity and facilitate deposition
of calcium on bones
• It suppresses the activity of osteoclasts and inhibit bone
resorption
• It also inhibit development of new osteoclasts
41. ACTION ON KIDNEYS
• Increases excretion of calcium and phosphate through urine
inhibiting their reabsorption from renal tubules
ACTION ON INTESTINE
• Prevents intestinal absorption of calcium and phosphate
42. • The four parathyroid
glands lie immediately
behind the thyroid gland.
• Two types of cells are
found
• The oxyphil cells:
may be modified or
depleted chief cells
that no longer
secrete PTH.
• The chief cells
synthesize and
secrete PTH
PARATHYROID GLAND
43. PARATHYROID HORMONE
• It is also called parathormone [PTH]
• Synthesized from its precursor form , prepro-PTH
• Released by chief cells of parathyroid glands
• Stimulus is decrease in plasma calcium concentration
• The primary action is to elevate plasma calcium
concentration and decrease phosphate concentration by
acting directly on bones and kidneys and indirectly on GIT
ACTIONS ON BONES
• PTH stimulates bone resorption i.e. it causes
decalcification or demineralisation of bones. PTH
stimulates osteoclasts and causes release of proteolytic
enzymes and acids which dissolve the organic matrix of
the bone.
• PTH increases membrane permeability for calcium ions of
osteoblasts and osteocytes
44. ACTION ON KIDNEYS
• PTH causes increase in calcium reabsorption of kidneys
• Inhibit reabsorption of phosphate in PCT
• Inhibit magnesium, sodium and bicarbonate reabsorption by
renal tubules
• Stimulates synthesis of 1,25(OH)2D
ACTION ON INTESTINES
• The activation of vitamin D3 [1,25(OH)2D or calcitriol] is
necessary for intestinal calcium absorption.
• The activity of 1α-hydroxylase, enzyme responsible for
activation of vitamin D3 is stimulated by PTH
46. • Provitamin D (7-dehydrocholesterol) in the skin is converted to
cholecalciferol by ultraviolet (UV) light.
• Cholecalciferol are transported to the liver, where they undergo
the hydroxylation at C-25 to 25-hydroxy vitamin D [25(OH)D]
• The second hydroxylation step, at C-1, occurs in the kidney and
results in the hormonally active 1,25(OH)2D or calcitriol,
mediated by 1α-hydroxylase.
• The activity of 1α-hydroxylase is stimulated by PTH.
• Decreased activity of 1α-hydroxylase favours C-24 hydroxylation
and formation of the less active 24,25(OH)2D.
47. EFFECTS OF 1,25(OH)2D
• Increases bone resorption,
• Increases calcium absorption from the intestine (the major
effect),
• Increases renal calcium reabsorption, and
• Decreases the production of PTH by the parathyroid glands.
The overall effect of 1,25(OH)2D is to increase plasma calcium
concentrations.
48.
49. Signs and symptoms of hypocalcemic tetany
1. Overactive reflexes
2. Convulsions
3. Carpopedal spasm in hand and feet
4. Laryngeal stridor means abnormal loud crowing sound during
inspiration occurs due to laryngospasm
5. Cardiovascular changes
i. Dilatation of heart
ii. Prolonged duration of ST segment and QT interval
iii. Arrhythmias
iv. Heart failure
6. Other features
i. Decreased membrane permeability
ii. Dry skin with brittle nails
iii. Hair loss
iv. Seizures
v. Mental retardation or dementia
50. • The classic clinical sign is known as the Chvostek’s sign, which is
twitching or contraction of the facial muscles in response to
tapping the facial nerve at a point anterior to the ear and above
the zygomatic bone.
51. CARPOPEDAL SPASM or trousseaus sign.
• It is the spasm of hand that is developed after 3 minutes of
arrest of blood flow to lower arm. Occurs usually during BP
measurement.
• The hands adapt a peculiar posture in which there occurs
flexion at wrist and metacarpophalangeal joints, extension at
interphalangeal joints and opposition of thumb.
52. Regulation of blood calcium level is done mainly by these
hormones;
1. Parathormone secreted by parathyroid glands and its main
function is to increase the blood calcium level. It is done by
stimulating bone resorption, formation of new osteoclasts,
increasing renal calcium reabsorption, stimulating secretion of
calcitriol from kidneys and intestinal absorption of calcium.
2. Calcitonin is secreted by parafollicular cells of thyroid gland and
hypocalcemic in action. It reduces blood calcium level by
inhibiting osteoclastic activity, stimulating osteoblastic activity,
stimulate calcium excretion by kidneys and inhibit intestinal
calcium absorption.
3. Calcitriol secreted by kidneys increase calcium level mainly
increasing intestinal absorption of calcium.
4. Growth hormone increase blood calcium level by increasing
intestinal calcium absorption
5. Cortisol decrease calcium blood level by inhibiting intestinal
absorption and renal excretion of calcium
54. Adrenal glands.
• The adrenal glands are
composed of a cortex
and a medulla
• The adrenal medulla is
made of cells derived
from the neural crest;
• The adrenal cortex is
made of cells derived
from mesodermal
tissue.
• The cortex is divided
into three zones:
reticularis, fasciculata,
and glomerulosa.
55. I. Mineralocorticoids:
• Zona glomerulosa secrete mineralocorticoid
• Plays an important role in electrolyte balance
i. Aldosterone
ii. Deoxycorticosterone
iii. 18 hydroxydeoxycorticosterone
II. Glucocorticoids:
• Secreted mainly by Zona fasciculata, small amounts
by zona reticularis
• act on glucose and protein metabolism
i. Cortisol
ii. Corticosterone
iii. Cortisone
56. III. Adrenal androgens:
• mainly secreted by Zona
reticularis, small amounts
by zona fasciculata
• Responsible for masculine
features
i. Dehydroepiandrostero
ne(DHEA)
ii. Androstenedione
iii. Testosterone
57. METABOLIC ACTIONS OF CORTISOL
• Effects of cortisol on carbohydrate metabolism [anti-insulin
effect ]
1. Elevated Blood Glucose Concentration occurs due to
Stimulation of Gluconeogenesis.
2. Decreased Glucose Utilization by Cells.
ACTIONS OF CORTISOL
• Effects of cortisol on fat metabolism
1. Lipolytic effects: Along with epinephrine, it promotes
mobilization of fatty acids from adipose tissue.
2. Lipogenic effects: Cortisol in excess stimulates lipogenesis.
• Effects of cortisol on protein metabolism
1. Cortisol enhances release of aminoacids by proteolysis in
extrahepatic tissues
2. Cortisol increases proteins synthesis in liver and increase
plasma proteins.
58. PHARMACOLOGICAL ACTIONS OF CORTISOL
• Anti-inflammatory effects : Cortisol inhibits the release of
proteolytic enzymes, inhibits migration of circulating
leucocytes to site of inflammation
• Anti-immunity effects: Inhibits both cellular and humoral
immunity by decreasing proliferation of T&B cells
• Anti-allergic effects : Reduces the number of circulating
basophils and eosinophils
PERMISSIVE ACTION
It refers to execution of action of some hormones only in the
presence of glucocorticoids. E.g. are
1. Calorigenic effects of glucagon
2. Lipolytic effects of catecholamines
3. Pressor effects of catecholamines
4. Bronchodilator effects of catecholamines
59. Other PHYSIOLOGICAL ACTIONS
• On muscle : Excess cortisol causes decrease in muscle mass
and strength results in thinning
• On bone : Increased bone resorption and inhibition of
bone formation
• On CVS: Maintaining normal blood pressure
• On kidneys : Increase in GFR
• On CNS: Effects on limbic system and modulate excitability,
mood and behaviour
• On GIT: Increase gastric secretion
• On blood cells: Decrease eosinophils, basophils,
lymphocyte. Increase RBC, neutrophils and platelets
IMMUNOSUPPRESSIVE EFFECTS
• Cortisol suppress immune system by decreasing the number
of circulating T lymphocytes
60. ROLE OF GLUCOCORTICOIDS IN FETAL LIFE
• Facilitate maturation of CNS, retina, skin and lungs
ROLE OF GLUCOCORTICOIDS IN STRESS
• During stress conditions like trauma, cold, infection etc.
ACTH production increases which in turn increases the
secretion of glucocorticoids.
• Glucocorticoids enhance the resistance against stress by
following actions; immediate release of proteins amino
acids and fatty acids, enhancement of vascular reactivity
which are necessary to withstand the stress.
61. FUNCTIONS OF ALDOSTERONE
• Mineralocorticoids act on mineral metabolism particularly
sodium and potassium.
• 90% of mineralocorticoid activity is done by aldosterone.
• Secreted by zona glomerulosa of adrenal cortex
• The primary function is sodium retention and potassium
excretion
• Aldosterone increases reabsorption of sodium and
simultaneously increases secretion of potassium by the
renal tubular epithelial cells especially collecting tubules
and, to a lesser extent, in the distal tubules and collecting
ducts.
• Aldosterone also stimulates sodium reabsorption from
colon and potassium excretion through faeces
• Aldosterone helps sodium conservation by facilitating
sodium reabsorption from sweat glands and salivary
glands.
62. • Secondary actions of aldosterone
Sodium retention and potassium excretion are the
primary functions of aldosterone, and it may result in
following action;
1. Hypokalemia: Decrease in potassium level
2. Hypernatremia: Increase in sodium level
3. Hypertension: When sodium ions are reabsorbed
from renal tubules almost equal amount of water is
also reabsorbed. It result in increase in ECF volume
and blood volume finally leads to increase in blood
pressure.
63. Functions of ADRENAL ANDROGENS
• Adrenal cortex secretes sex corticoids mainly by zona
reticularis and in small amounts by zona fasciculata.
• Most of them are androgens or male sex hormones. But small
quantities of estrogen and progesterone are also secreted.
• DHEA is the most active adrenal androgen.
• In adult males, adrenal androgens has no significant role. It
helps in development of male sex organs and secondary
sexual characteristics in males.
• In adult females adrenal androgens in excess leads to
development of masculine features
64. REGULATION OF SECRETION OF CORTISOL
HYPOTHALAMUS
ANTERIOR PITUITARY
ADRENAL CORTEX
CRH
ACTH
CORTISOL
65. CUSHING’S SYNDROME
• Hypersecretion by the adrenal cortex causes abnormal amounts
of cortisol, but excess secretion of androgens may also cause
important effects.
• It can be separated into two categories depending on its etiology.
• ACTH-independent Cushing’s syndrome ( adrenal origin)is
usually due to an adrenal neoplasm or excess exogenous
glucocorticoid therapy
• ACTH-dependent Cushing’s syndrome has two causes:
• Cushing’s disease caused by excess secretion of ACTH by
pituitary corticotrope tumours.(pituitary origin)
• ACTH production may also be ectopic (derived from
extrapituitary tissue), most frequently because of small
cell lung carcinoma.
66. Characteristic features are
Mobilization of fat from the lower part of the body, with
extra deposition of fat in the thoracic and upper
abdominal regions, giving rise to
• Truncal or centripetal obesity
• Buffalo hump due to accumulation of fat at upper back
• Pot belly due to accumulation of fat at abdomen
• Moon face due to accumulation of fat on face
Occurrence of Purple striae: increased protein catabolism,
results in thinning of skin and subcutaneous tissues. In
addition excessive fat deposition in abdomen causes
stretching and rupture of sub dermal tissues producing
purple striae
Sodium and water retention leads to hypotension
Hyperglycaemia and glucosuria(adrenal diabetes)
Muscle weakness and back aches
67. Hirsutism (facial hair growth)
Susceptibility to osteoporosis and fractures
Susceptibility to infection and poor wound healing
Susceptibility to peptic ulcers
Blackening or hyperpigmentation especially on neck
Thinning of extremities, skin and subcutaneous tissues.
68. ALDOSTERONE EXCESS/HYPERALDOSTERONISM
Increased secretion of aldosterone
Two types
Primary hyperaldosteronism, also known as Conn’s
syndrome, is a condition in which autonomous benign
tumors of the adrenal glands hypersecrete aldosterone.
Secondary hyperaldosteronism occurs due to extra adrenal
causes like congestive heart failure, nephrosis, liver cirrhosis
or toxaemia of pregnancy.
Signs and symptoms
Increase in ECF volume and blood volume
Hypertension
Depletion of potassium leading to kidney damage and
muscular weakness
Metabolic alkalosis leading to hypocalcemia and tetany
69. ADRENOGENITAL SYNDROME
• An occasional adrenocortical tumor secretes excessive
quantities of androgens that cause intense masculinizing effects
throughout the body.
• If this occurs in a female, she develops male characteristics,
including growth of a beard, a much deeper voice, masculine
distribution of hair on the body and the pubis, growth of the
clitoris to resemble a penis, and deposition of proteins in the
skin and especially in the muscles to give typical masculine
characteristics.
• In the prepubertal male, adrenal tumor causes the same
characteristics as in the female plus rapid development of the
male sexual organs.
70. HYPOADRENALISM-ADDISON’S DISEASE
Addison’s disease results from failure of the adrenal cortices to
produce adrenocortical hormones, and this in turn is most
frequently
• caused by primary atrophy of the adrenal cortices
• caused by autoimmunity against the cortices.
• caused by tuberculous destruction of the adrenal glands or
invasion of the adrenal cortices by cancer.
The disturbances in Addison’s disease are as follows.
• Mineralocorticoid Deficiency: Lack of aldosterone secretion
greatly decreases renal tubular sodium reabsorption and
consequently allows excretion of sodium ions, chloride ions,
and water. The net result is a greatly decreased extracellular
fluid volume with hypotension
71. • Glucocorticoid Deficiency: Loss of cortisol secretion causes
inability to synthesize significant quantities of glucose by
gluconeogenesis. Lack of cortisol reduces the mobilization
of both proteins and fats from the tissues, thereby causing
weight loss, anorexia, nausea, vomiting ,muscle weakness.
• Loss of androgens causes sparse hair in females
• Addisonian crisis or acute adrenal insufficiency is a fatal
condition in which exposure to even a mild stress like
infection, causes sudden collapse associated with an
increase in need for large quantities of the glucocorticoids
• Melanin Pigmentation: Another characteristic of most
people with Addison’s disease is melanin pigmentation of
the mucous membranes and skin.
73. HORMONES OF THE ADRENAL MEDULLA
• The adrenal medulla consists of cells called chromaffin
cells or phaeochrome cells that synthesize and secrete the
catecholamines
74.
75. Metabolic actions of Catecholamines
Adrenaline influences metabolic functions more then
noradrenaline
• Increase in BMR (calorigenic effect)
• Increases oxygen consumption and carbondioxide output
• Epinephrine produce hyperglycaemia and make glucose
available for brain and other tissues to meet emergency. It is
done by increasing glycogenolysis.
• Catecholamines in the presence of cortisol increase lipolysis
Physiological action
• On GIT: Epinephrine decrease motility and contraction of
sphincters of gut resulting in constipation. Mild increase in
salivary secretion.
• On urinary bladder: Epinephrine causes retention of urine
by relaxing detrusor
• On skin: Piloerection
ACTIONS OF CATECHOLAMINES
76. • On skeletal muscle: During exercise vasodilatation
• On eyes: Dilatation of pupils and increase in secretion of tears
• On respiration: Bronchodilation, increase in rate and force of
respiration
• On blood: Reduces blood coagulation, increase RBC count, Hb,
Neutrophils, plasma proteins and PCV.
• On CNS: Activate RAS and leads to arousal and alertness
• On endocrine system : Insulin and somatostatin decreased.
Glucagon and pancreatic polypeptide increased. Thyroid
hormones secretion is enhanced. Renin and aldosterone
increases
• On CVS: Epinephrine increases heart rate, cardiac output and
systolic blood pressure. Decreases diastolic BP, peripheral
resistance. Norepinephrine instead increases systolic and
diastolic BP thereby mean arterial pressure, peripheral
resistance. Decreases heart rate, cardiac output
77. • Dopamine is secreted by adrenal medulla
• In brain it is secreted by dopaminergic neurons in
basal ganglia and act as a neurotransmitter
• Its deficiency leads to parkinsonism
• Injected dopamine causes
• Vasoconstriction and vasodilatation
• Increase in heart rate
• Increase in systolic blood pressure
78. PHAEOCHROMOCYTOMA
• Disorder caused by chromaffin cell tumour ,usually found in the
adrenal medulla
• Excessive secretion of epinephrine and norepinephrine
• Present with signs of excess catecholamine effects, such as
sustained or paroxysmal hypertension associated with
headache, sweating, or palpitations.
79. Embedded within the acini
are richly vascularized,
small clusters of endocrine
cells called the ISLETS OF
LANGERHANS, in which two
endocrine cell types (β and
α) predominate.
1. The β-cells (73–75% of
the total mass of
endocrine cells) secrete
insulin.
2. The α-cells(18–
20%)secrete glucagon.
3. The δ-cells (4–6%)
secrete somatostatin.
4. The F OR PP cells (1%)
secrete pancreatic
polypeptide.
PANCREAS
80. EFFECTS OF INSULIN
METABOLIC EFFECTS
• The major target for insulin action are muscle, liver, adipose
tissue
On carbohydrate metabolism: hypoglycaemic action
i. Increase uptake of glucose in target cells
ii. Increase glucose utilization by promoting glycolysis in
muscle and liver and by increasing glycogenesis
iii. Decrease glucose production by inhibiting
gluconeogenesis and glycogenolysis
On lipid metabolism
i. Enhance storage of lipids by blocking mobilization
and oxidation of fatty acid favouring lipogenesis,
decreasing lipolysis and in turn ketogenesis
On protein metabolism
i. Facilitates protein synthesis and inhibits protein
degradation
81. OTHER EFFECTS OF INSULIN
• Increase reabsorption of potassium, phosphate and sodium
• Promotes normal growth
• Directly by stimulating synthesis of macromolecules in
tissues
• Indirectly by stimulation of other growth factors include
somatomedins, epidermal growth factor, nerve growth factor
and relaxin
82. METABOLIC EFFECTS OF GLUCAGON
On Carbohydrate Metabolism (Hyperglycaemic Action )
The principal target tissue for glucagon is the liver.
Glucagon’s main physiologic effect is to increase plasma
glucose concentrations by stimulating gluconeogenesis and
glycogenolysis and decreasing glycolysis.
On Lipid Metabolism [Lipolytic Agent, Also Ketogenic ]
In the adipocyte, glucagon activates lipase, the enzyme that
breaks down triglycerides (stored fat) into diacylglycerol and
free fatty acids, releasing them into the circulation.
Glycerol released into the circulation can be utilized in the
liver for gluconeogenesis or for reesterification.
Free fatty acids are used as fuel by most tissues,
predominantly skeletal muscle and liver.
In the liver, free fatty acids can undergo β-oxidation and
converted into ketone bodies.
83. On protein metabolism
Increase uptake of amino acids by liver cells and promote
gluconeogenesis.
Calorigenic effects: in the presence of glucocorticoids and
thyroid hormones, it increase hepatic deamination of
aminoacids
OTHER EFFECTS OF GLUCAGON
Inhibit sodium reabsorption by renal tubules
Moderate increase in force of contraction of heart
Stimulates secretion of growth hormone insulin and
somatostatin
Glucagon regulate appetite
Glucagon in very high concentrations enhances the
strength of the heart; Increases blood flow in some
tissues, especially the kidneys. Enhances bile secretion.
Inhibits gastric acid secretion.
84. SOMATOSTATIN
Somatostatin is a 14–amino acid peptide hormone produced by
the δ-cells of the pancreas.
Somatostatin has the same chemical substance as GHIH
Somatostatin has multiple inhibitory effects as follows:
1. Somatostatin acts locally within the islets of Langerhans
themselves to depress the secretion of both insulin and
glucagon.
2. Somatostatin decreases the motility of the stomach,
duodenum, and gallbladder.
3. Somatostatin decreases both secretion and absorption in
the gastrointestinal tract
85. PANCREATIC POLYPEPTIDE
Pancreatic polypeptide is a 36–amino acid peptide hormone
It is produced in the endocrine type F cells located in the
periphery of pancreatic islets.
The effects of pancreatic polypeptide include inhibition of
pancreatic exocrine secretion, gallbladder contraction,
modulation of gastric acid secretion, and gastrointestinal
motility.
Pancreatic polypeptide crosses the blood–brain barrier and has
been postulated to play a role in regulating feeding behaviour.
86. DIABETES MELLITUS
The most common disease resulting from impaired insulin
hormone release or sensitivity is diabetes mellitus.
It is characterized by high blood sugar level.
The two forms of diabetes mellitus,
• type 1 (T1DM) or insulin dependent diabetes
mellitus(IDDM) is due to deficiency of insulin. Also called
juvenile diabetes. Caused by degeneration of beta cells.
• type 2 (T2DM) or noninsulin dependent Diabetes mellitus
(NIDDM) occurs due to absence or deficiency of insulin
receptors. It is called maturity or adult onset diabetes. Beta
cells and insulin level is normal, but receptors are absent.
87. Signs and symptoms
1. Glucosuria
2. Polyuria
3. Polydipsia
4. Polyphagia
5. Asthenia or generalized weakness or fatigue
6. Acidosis
7. Acetone breathing and kussmaul breathing
8. Circulatory shock
9. Coma
10.Cardiovasular complications like hypertension and MI
11.Diabetic Retinopathy
12.Diabetic Neuropathy
13.Diabetic Nephropathy
88. TYPE I Diabetes Mellitus TYPE II Diabetes Mellitus
Accounts for 2–5% of cases Accounting for about 90 per cent of all
cases
Juvenile diabetes, onset before 40 years Adult-onset diabetes.onset after 40
years
A complete lack of insulin secretion due
to autoimmune destruction of the islet
cells.
Insulin receptors are absent, is
associated with increased plasma
insulin concentration
(hyperinsulinemia). Insulin resistance is
common i.e. Inability to target tissues
to utilize insulin
Not obese Usually overweight / obese
Symptoms appear rapidly Symptoms develop slowly
Characterized by the development of
ketoacidosis
Ketoacidosis not present
Insulin therapy is effective Insulin therapy may not be effective
