This document provides an overview of a lecture on endocrine physiology. It begins with an introduction to the endocrine system and hormones. It then covers the classification, properties, and mechanisms of action of hormones. The document outlines the major endocrine glands and hormones, including the pituitary gland and hormones of the anterior and posterior pituitary. It discusses disorders of growth hormone and thyroid hormones, including dwarfism, gigantism, acromegaly, cretinism, and myxedema. It concludes with an overview of hyperthyroidism.

1. DEPARTMENT OF HUMAN PHYSIOLOGY,
FACULTY OF BASIC MEDICAL SCIENCES,
COLLEGE OF MEDICAL SCIENCES,
AHMADU BELLO UNIVERSITY, ZARIA
ENDOCRINE PHYSIOLOGY (HPHY301)
LECTURER’S NAME
Dr. Jimoh Abdulazeez
JANUARY, 2020

2. Today’s lecture Outlines:
Introduction
Classification of hormones
Properties of hormones
Mechanism of action of hormones

3. INTRODUCTION
• Endocrine system together with nervous system
control or regulation the body functions.
• Hormones are chemical messenger secreted by
ductless gland (endocrine gland) into circulation,
• travel to the target organ or tissues,
• bind to receptor,
• initiation intracellular cascade of reactions which
leads to physiological action

4. Hormones regulate the following processes:
• Growth and differentiation of cells, tissues, and
organs
• Metabolic pathways
• Digestive processes
• Maintenance of ion concentrations (homeostasis)

7. Exocrine and endocrine glands secretion format

8. The are two kind of hormones
Local hormones e.g Gastrin, Secretin, CCK, Ghrelin,
VIP, Substance P etc.
General hormone: are the major hormones which
their effects are profoundly studied and produced by
well recognized endocrine organs
These organs are: Pituitary gland, thyroid gland,
parathyroid, pancreas, adrenal cortex and medulla,
pineal, thymus, testes and ovary, and hypothalamus

9. All endocrine organs are important but only 3 organs
are essential for life:
Anterior pituitary gland
Parathyroid gland
Adrenal cortex

10. Major endocrine organs

13. Hypothetical view of major endocrine gland

15. Classification of hormone
Generally, hormones are either protein or steroid in
nature
There are 3 classes of hormones
• Amine or amino acid derived hormones e.g
thyroxine, adrenaline, noradrenaline, dopamine,
serotonin etc.
• Peptide or protein hormones: oxytocin, ADH, GH,
Parathyroid hormone, calcitonin, ACTH etc.

16. • Steroid hormones:
Those derived from cholesterol as precursor; the sex
hormones and hormones of adrenal cortex and
reproductive organs

18. THINK ABOUT
HRT

19. Properties of hormones
• They are secreted in minute quantities and the rate of
secretion depends on the body needs
• They have no effect on the secreting gland (general
hormones)
• Hormone are receptor specific
• Some hormones are secreted by more than one glands
• Some hormones affect more than one organ, while some
have specific organ and some have generalized
functions all over the body
• Some hormones initiate chemical reaction which last for
a long period even the hormone has disappeared from
the body.

20. • Some hormone are secreted in an inactive form and
metabolized into an active form e.g. thyroxin.
• Hormone exist in two form in the blood; the
physiological active form, free hormone and
inactive form bound hormone
• Stimulus that triggers the release of one hormone
inhibits the antagonistic hormone
• Some hormones show cyclical or periodic release
over the 24 hours of the day (circadian rhythm)
• Hormones are continuously metabolize and excrete
from the body

21. Mechanism of action of hormones
Hormones function by binding to specific receptors
• Where are receptors in a cell?
• Surface receptors for all protein
• Intracellular receptors
• Cytoplasmic receptors for steroid
• Intra-nuclear receptors for thyroid hormones

22. Hormone bind to receptor
Hormone receptor complex
Second messenger produced (cyclic AMP, IP3,
DAG, cyclic GMP)
protein kinases stimulation or calcium influence
Protein phosphorylation or gene transcription
and desired physiological action produced

31. Measurement of hormone plasma level
• Hormones levels in the blood are measure by
basically two methods:
• ELISA (Enzyme-Linked Immunoassay Assey)
Technique
• Radio-immunoassay Assey Method

32. Pituitary gland and its connections
• It is a small gland about 0.5 – 1 g in weight
• It is situated behind and below the optic chiasma in
sella turcica (pituitary fossa) attached to the 3rd
ventricle through the infudibulum
• In embryonic life, it formed from two sources
Floor of the 3rd ventricle of the brain
Ectoderm of the primitive buccal cavity
It extend between the optic chiasma and the
mammillary body.

33. In human, it divided into two lobes
Anterior lobe (adenohypophysis); it connects to the
median eminence of the hypothalamu through the
vascular connection called hypothalmo-hypophyseal
portal circulation.
Posterior lobe (neurohypophysis) to the magnocellular
nuclei (supraoptic and paraventricular nuclei)

36. Physiology of Hormones from posterior gland
 Synthesis, release and functions of Oxytocin
 Synthesis, release and functions of ADH
• Disorders of ADH
Diabetic insipidus
Syndrome of Inappropiate ADH secretion
(cerebral or pulmonary salt wasting)
• Frequently cause sudden infant death

37. ADH physiology summary
Other factors: pain, exercise, emotion, surgical stress, drugs:

38. OXYTOCIN
• A peptide hormone form by the hypothalamus but
secreted by the posterior pituitary gland.
• It main function is to cause contraction of the
myothepithlial cells of the mammary gland to cause
milk letdown or injection of milk.

39. Oxytocin function
Factors like:
Emotion stimuli
Conditional reflex
Genital stimulation

41. Other functions of oxytocin
• Contraction of uterus in pregnant and non-
pregnant women.
• Sperm transport in the female genital tract
• Sperm discharge in male
• Squeezing of apocrine sweat gland in both sex
• Social interaction and memory and cognition

42. Hormones of anterior gland
Basically there are two kinds of cells found in the
anterior pituitary gland.
Chromophobe cells
Chromophilic cells; this is subdivided into:
Hormones from acidophilic cells are GH and prolactin
Hormones from basophilic cells are ACTH, TSH,
GRH (LH and FSH), gamma-LPH, gamma-MSH

46. Physiology of growth hormone
Functions of growth hormone
 Protein metabolism: stimulates the passing of
amino acids into the cells; activates the synthesis of
proteins, DNA, RNA and positive and phosphate
balance
 Na and K ion (electrolytes) retention: stimulate the
retension of ions by renal tubules. There is also N,
Ca and phosphorous balance resulting from
anabolic effect of GH

47. • Diabetogenic Effect
• Carbohydrate metabolism: activates the insulinase of
liver;
• inhibits the conversion of lipids to carbohydrates;
• activates the exit of glucose from liver;
• inhibits the entry of glucose into the cells.
 lipid metabolism: stimulates lipolisis;
Stimulates the oxidation of fatty acids
Factors stimulating synthesis and release of GH
Sleep, Exercise, Emotion or various psychological
stress, fasting or hypoglycaemia, stress stimuli

48. Dwarfism due to deficient of GH in children

49. DWARFISM
• Is due to decrease secretion of GH.
• Usually occur in children
• Patient usually have a small status but there is
uniformity in the proportion of the body size
• 10yrs old child would have a bodily development of
4-5yrs old.
• It can be treated using synthetic growth hormone.
• Recombinant DNA technology can be used to
synthesize growth hormone and any other ones.

50. Gigantism as a result high level of GH before puberty

51. Clinical Manifestation of Gigantism
• Overgrowth of skeleton to 2 meter or more due to
hypersecretion before the fusion of epiphyseal of
long bone (b/4 onset of puberty).
• Osteoarthritis is common (genetic dx of the joint)
• Diabetes mellitus is common
• Bitemporal hemianopia: loss of vision in the
temporal part of visual face on both side
• Overgrowth of visceral organs
• Infantile gonadism
• Local effect of the tumor

52. ACROMEGALY
• Hypersecretion of GH after the fusion of epiphysis
of long bone (after onset of puberty)
• No linear growth of the body
• There is mark increase in the ACRAL part of the
body including the hands, feet, nose, ear and
mandible
• The hand becomes larger and thicker and look like a
spade.
• Treatment could be achieve using drugs that inhibit
GH secretion and include Somatostatin,
Bromocriptine.

53. Clinical manifestation of Acromagaly
Other
features are:
Headache,
Hypertension
,
Hyperglycae
mia and
glucosuria
resulting in
diabetes
mellitus,
Enlargement
of visceral
organs,
Bulldog scalp
and Gorilla
face

54. PROLACTIN
• A protein with a molecular weight 23,000 and is
secreted by lactotrope and mammotrope cells of the
pituitary gland.
• Physiological action happears when it level rises in a
pregnant or lactating woman
• LACTOGENESIS: stimulates or initiate the
production of milk.
• SYNERGISM: with estrogen to stimulate the
development system of the mammary duct
• PREVENTION of OVULATION: inhibits the
action GRH and gonadotropins and prevention of
ovulation

57. Concept of feedback mechanism

58. Physiology of thyroid hormones(THs)
Synthesis, and Release of THs
• A large tyrosine reach protein called thyroglobulin
with molecular weight 650,000 is expose to iodine
which bind with the tyrosine residue.
• Thyroidperoxidase catalyze oxidation of iodide to
iodine at the interphase of the colloid and its lining
follicular cells where iodine is produce.
• Iodine react with tyrosine 1st to form
monoiodothyrosine (MIT) and Diiodothyrosine
(DIT).

59. • Thyroidperoxidase linked 2 DIT to form T4 or
thyroxine.
• It can also linked MID and DIT to form T3 or
triiodothyronine.
• The follicular cell actively endocytose thyroglobulin
and then lysosomal proteases release T4.
• About 80µg of T4 is been produce/day and about
4µg of T3 is produce/day

60. Transport of THs in THE PLASMA
• THs bind with some serum protein in the plasma.
This include
• Thyroid-binding globulin (TBG): about 1/3 of this
hormone bind TBG.
• The concentration TBG is very low in the plasma
but has high affinity for T4 and T3
• Pre-albumin Binding Thyroxine (transthyretin)
• Albumin: transport 1/10 of the hormone. Only
about 0.02% of T4 and 0.2% of T3 is free in the
plasma.
• ½ life for T4 is about 1wk and ½ life for T3 is 24hr

61. Functions of thyroid hormone (THs)
• The THs affect practically every cell in the body
• THs is the most powerful orchestrator of metabolism
in the whole organism.
• It causes increase in β- adrenergic level in the
myocardium
• It also enhances the action of catecholamine
• Causes an Increase in the expression of the Na+-K+
ATPase.
• Causes increase in sarcolemma Ca++ UPTAKE
• It increases the production of sex steroid binding
globulin

62. • It synergize with growth hormone to cause
ossification of cartilage
• Neuronal Effect: in the neuron it causes
• Cortical growth
• Axonal and dendritic growth
• Causes myelination of the neuron
• Vital for normal brain development
• Auditory and visual sensory system appear to be
depended on T3 (triiodothyronine)

63. • On renal system:
• It causes in renal plasma flow
• in GFR
• in transport maximum in the tubule
• Conversion of carotene to vitamin A
• Growth: Physical, mental, and sexual growths
• Haemopoietic function
• CVS : HR, CO, SBP, PR but decrease DBP
• Respiration: it causes increase in RR
• GIT: appetite, secretion, motility and absorption

64. Causes and manifestation of cretinism
• Hypothyroidism in foetus and children
a. Congenital absence of thyroid gland
b. Iodine deficiency during pregnancy
• Manifestations:
• Physical and mental growth are delay such as
teeth eruption, closure of frontanelles, sitting
and walking
• Bone growth is inhibited, ossification,
proliferation of epiphyseal cartilages, cretin is
disproportionate dwarf

65. • Muscles are week
• Mental growth is retarded: cretin is idiot, speech is
delay, with hoarse voice and incontinence of urine
• Sexual growth is arrested, organs remain infertile
Typical characteristic of cretin child
1. Face:
a. Swollen eyelid with narrow palpebral fissure
b. Occasionally, the tongue becomes so large in
relation to the skeletal growth such that it obstruct
swallowing

66. b. Depress nose with wide nostril
c. Enlarged protrude tongue btw thick lips
2. abdomen: is bulging with umbilical hernia
3. Skin is cold, pale, coarse with scanty hair
4. Height does not exceed 1 meter
• Metabolism
BMR is decrease
Cretin is sensitive to cold
Serum cholesterol is increased
Treatment; thyroid hormone should be given early
after birth

69. Myxoedema cause
Myxoedema is hypothyroidism in adult
Causes:
• Primary hypothyroidism: could be due to auto-
immune disease (Hashimoto’s thyroiditis),
inflammation, radiation, cancer or following
surgical removal of the thyroid gland
• Secondary hypothyroidism: pituitary or
hypothalamic origin.

70. Manifestation of Myoedema
General metabolism
BMI is increased, no cold tolerance, Body temperature
is subnormal, body weight is increased
Protein metabolism: proteins are in plasma, liver, and
retention of subcutaneous fluid rich in protein (MP
containing HA and CSA) with non-pitting oedema
Carbohydrate metabolism increase liver glycogen and
decrease glucose absorption from GIT
The hands and face becomes swollen bcos of
accumulation of mucoprotein in the subcutaneous
layer

71. • Lipid metabolism. hyperlipidemia and
cholesterolemia with fatty infiltration of the liver,
artherosclerosis which could cause angina pain
High carotene and low vitamin A – night blindness
• Nervous system:
Depressed mental function, poor memory, and slow
think and speaking
Apathetic and sleep much (somnolence)
Muscle weakness, decreased deep reflexes, slow
movement, myxoedema madness and coma

72. • Cardiovascular system: infiltration of the heart with
myxoedematous tissues and low cardiac metabolism
causes:
• Decreased HR, CO, prolong Circ. Time, artherosc.
• Respiratory system: hypoventilation, obstructive
apnea and deep and hoarse voice.
• GIT: anorexia and constipation
• Decreased sexual function, disturbed menses, milk
secretion

73. Anemia
Skin: Cold, pale, coarse hair and brittle nails
Eye: Swollen eyelids with puffiness of the face
Night blindness due to vitamin A deficiency
Lost of hair from lateral 1/3 of the eyebrows

75. Hyperthyroidism
Cause:
• LATS in case of grave’s disease
• Toxic adenoma of the thyroid gland
• TSH-Secreting tumour from the pituitary gland
Manifestation
• BMI up to 100% and heat intolerance
• Protein catabolism leads to weight loss and
weakness, osteoporosis etc.
• Deplete plasma level of glucose and lipid

76. • Relatively decrease of body vitamins
• Nervous system: patient is irritable, restless,
anxious, emotionally unstable, insomnia.
Fine tremor, deep reflexes are exaggerated
• Cardiovascular system:
HR, PR (water hammer pulse), SBP are all increased
and decreased DBP
• Respiratory system: increased PV, O2 and CO2
• GIT: increased appetite, diarrhoea, liver failure may
occur

77. Skin warm, flush and moist due to vasodilation
Eye: lit retraction of upper eyelid which leads to
widening of palpebral fissure, lid lag, corneal
ulceration.

79. Parathyroid gland
It is essential for life
• The gland contains two types of cells: the chief cells
and the oxyphil cells.
• The plasma level for parathyroid hormone is 20 -
100 ng/dl
Functions of parathyroid hormone
It increase calcium level through 3 sites:
1. On kidneys
Inhibit phosphate reabsorption and decrease calcium
excretion into the urine to maintain solubility
constant.

80. It activate renal 1- hydrolase to for 1, 25-dihydrocholec.
It increase Mg and H ions reabsorption by renal tubules.
On bone:
• Rapid effect
by increasing permeability of osteoclast and osteocyst to
Ca++ in bone fluid
• Slow action
by stimulation of osteoclast activity of formation of new
osteoclast
Inhibit the activity and formation of new osteoblast
Pth activates the collagenase enzyme of osteoclast which
cause breakdown of bone collagen.

81. On intestine:
• Indirectly stimulate reabsorption of both Ca++ and
PO4 from GIT by formation of 1,25-dihydroxycholec.
BODY CHANGES IN HYPOPARATHYROIDISM
Urine and blood
Decrease PO4 in urine and increase in plasma
Decrease plasma level of calcium and increases in
urine but disappear when renal threshold is low 7
mg%

82. Decreased ionized calcium level in plasma causes:
Tetany
Tarchycardia, cardiac arrythmias and prolong S-T
segment and Q-T interval
Opacity of eye lens (cataract)
Hair falls and nails brittle
Intestinal and biliary colics
TETANY
• Is a state of increased neuromuscular excitation due
to decreased ionized Ca++ level in plasma

83. It is characterized by attacks of splasmodic
contractions which may involve the laryngeal and
respiratory muscles
Causes of tetany
Hypocalcaemia
• Hypothyroidism
• Diminished calc. intake
• Increased calc. need as in pregnancy and lactation
• Defective reabsorption of Ca in fatty diarrhoae,
deficiency of vitamin D, administration of oxalate of
citrate and during alkalinity of the intestine which
precipitate Ca++

84. Types of tetany
Manifest tetany – ca level is below 7 ng/dl – increased
neuronal memb. Permeability to Na increase excitation
of the cns and peripheral neurones
It’s xterized by:
Fibrillary twitch of skeletal muscles – clonic and tonic
contraction
Carpopedal spasm- obstetrician hand or accoucheur’s
hand or carpal spasm
Spasmodic contraction of the laryngeal muscle and
respiratory muscles result in asphyxia- < 4 mg%

87. Latent tetany- Ca level is above 7 but below 9 mg%
Manifest. are absent at rest. They appear when there
is increased body needy for calcium
Test for latent tetany
1. Determination for ionic level of Ca
2. Troussear’s sign
3. Chvostek’s sign
4. Erb’s sign

88. Treatment of tetany
• Calcium gluconate
• Vitamin D
• Acidify salt (NHCl4)
• PTH IV
• 1,25-Dihydroxycholecalciferol-chronic renal failure

89. Hyperparathyroidism
• Increases calc. level in plasma, low in plama po4
and its increase in urine
• Decalcification of bone- multiple cyst
• Decrease neuromuscular excitability
• Renal changes- polyuria due hyper- calciurina and
• hyperphosphatemia lead to renal stone and renal
failure
• Duodenal ulcers- 15% of patients- hypercal.
Stimulate gastrin hormone.

90. Adrenal Glands
Consist of two layers; outer cortex and inner medulla
Cortex is derived from mesonephron and medulla is
neural in origin (from neural crest cell)

91. Zona glomerulosa –
groups of cell in oval or arch pattern (glomeruli)
Can form new cortical cells for regeneration of the
other 2 zones
Secrete mineralocorticoid: aldosterone and
deoxycorticosterone (DOC); they function in
controlling Na,+ K+ and H2O metabolism

93. Zona fasciculata- large cell arranged in columns or
cord (fascicles) and separated by venous sinuses
Rich in vitamin c and lipid
Secrete glucocorticoid: cortisol and corticosterone 7:1,
these hormones control, protein, carbohyd. and lipid
metabolism
Zona reticularis – columns of cells arranged in a
reticular manner
Secrete sex hormones; mainly androgen (DHEA) and
small amount of estrogen and progesterone

94. Synthesis, transport and metabolism of cortical
steroid hormones
They are all synthesized from cholesterol by
steroidogenesis to form C19 or C21; C19 has androgen
activity while C21 has both mineralocorticoid and
glucocorticoid activities.

97. • They exist in free and bound forms e.g. cortisol
10% free and 90% with transcortin (CBG, 75%)
and 15% to albumin

98. Physiological actions of mineralocorticoid
Main action is on kidney
• Aldosterone stimulate Na & water reabsorption and
k excretion in the DCT and CD which results:
• High Na and low K in plasma and increased ECF
volume due to Na and water retention
• Other effects are: Na reabsorption in the duct of
glands caused decreased Na content in sweat, saliva,
gastric juice and milk
• Na reabsorption and k secretion by the intestine and
colon

99. Action of glucocorticoids
Metabolic effects:
• In extrahepatic tissues- it mobile aa into the plasma
and their uptake (not extrahepatic tissues e.g.
muscles and bones) by liver to produce plasma and
liver pr-
• Pr- catab. In bone is associated with ca mobilization
and demineralization of bones
• It caused hyperglycaemia by gluconeogenesis, anti-
insulin effect and stimulates G6P

100. • Fat metabolism: it causes lipolysis, lipaemia,
ketogenesis, mobile fats from tissues and deposit
them on the face, neck or cervical, supraclavicular
and trunkal regions
Water and electrolytes balance
• It has diuretic action- it accelerate ADH inactivation
in liver, move water into plasma from tissues,
increase GFR, urine out
• Glucocort. Is C21- it has little mineralocort. active;
causes Na retention and k excretion in urine

101. Blood cell and lymphatic tissues
• Decrease lymphoc. Eosinophils, basophils count
• Increase neutrophils, RBC and platelet count
• Decrease lymphocyte and antibodies formation
• Decrease the size of lymph nodes, spleen, and
thymus- inhibit mitotic division and interleukin II
Anti-inflammatory effect:
• Stabilization of lysosomal membrane
• Inhibit release of kinins

102. • Decrease capillary permeability and oedema
formation
• Inhibit diapedesis
• Suppress the immune system espec. the T-lymp.
• Lowering of fever by inhibit production and release
of interleukin I.
• Inhibit fibroblast proliferation and collagen
formation
The message is that is contraindicated in pt with
immune compromised- TB, AIDS

103. Anti-allergic effect
Inhibit histamine release from mast cell
Decrease the oesinophil and lymphocyte level
Block synthesis of postaglandins and leukotriene
• Resistance to stress
Increase vascular reactivity
Extrahepatic mobilization of aa for liver to produce
essential substance needed in stress
Mobilization of fatty acid as a source for energy
during emergency

104. • Maintenance of plasma volume
 Inhibit prostacyclin-VD- which cause drop of A.B.P.
 Permissive action to glucagon and catecholamines
Other actions-
increase appetite, stimulate HCl and pepsin secretion-
not good in ulcer, Surfactant formation, strengthen
skeletal and cardiac muscle contraction, increase brain
cell excitability, inhibit gh and tsh release, suppres
conversion of T4 to T3

105. Disorder of adrenal cortex
Hypofunction of adrenal cortex (Addison Disease)
Causes:
Autoimmune mechanism
Tuberculosis or tumour
Hypopituitarism simmond’s disease secondary to
decreased ACTH
Manifestations are due to deficiency of GLUC &
MCC
Hypotension
Hypoglycaemia

106. • Hyperkalaemia
• Hyperpigmentation in 2o to ACTH increased; in
face, groins, axilla, nipples, and areas exposed to
sunlight, scars as umbilicus
• Asthenia- muscle weakness due to low Na and high
k
• gastrointestinal disturbance- loss of appetite
vomiting and diarrhoae
• Loss of body weight, low resistance to stress, sexual
disturbance, metabolic acidosis,
• Addisonian crisis in acute adrenocortical
insufficiency

107. Treatment of addisonism
Adrenocortical hormones: ALDOSTERONE AND
CORTISOLARE GIVEN
Diet rich in glucose and NaCl and poor in K
causes of addisonian crisis
1. Sudden withdrawal of glucocorticoid after long
therapy
2. Disease causing acute bilateral adrenal damage
3. Patient with addison disease subjected to stressful
conditions e.g operation, infection, k depletion etc.

108. Hyperfunction of adrenal cortex
3 syndromes are involved
• Conn’s disease: due to high aldosterone secretion
• Cushing’s syndrome: due over activity of zona
fasculata and high glucocorticoid production
• Adrenogenital syndrome: over secretion of sex
hormones (virilization or feminization)

109. Hyperaldosteronism or Conn’s syndrome
Cause- excess secretion of Aldosterone due to adrenal
hyperplasia or tumour
Manifectations:
Hypokalaemia, hypernatraemia, hypervolemia but no
edema due to escape phenomenon in 1o aldosteronism
but occur in secondary i.e couple CHF, TP, NS, CLD

110. CUSHING’S SYNDROME
Causes: primary due to tumour of adrenal cortex, high
level of cortisol but low level of ACTH
Secondary due to pituitary tumour, high ACTH and
high cortisol
Manifestations:
Increased pr- catabolism leads to muscle wasting and
weakness, thin skin, hair and subcutaneous tissues,
osteoporosis, lymphoid tissue hypoplasia

111. Abnormal fat distribution: moon face, buffalo hump,
trunkal obesity, purple striae due to strength of
abdominal skin
Hyperglycaemia, hypertension, androgenital
manifestation
Blood changes: polycythaemia, metabolic alkalosis,
decreased lymphoc. Eosinop. Basop. Counts
Mental abnormalities- insomnia, euphoria, psychosis
Skin pigmentation may occur in secondary cushing’s
syndrome

114. Adrenogenital syndrome
Excessive production of adrenal androgen mainly and
female sex hormones
1. virilism or virilization: development of masculine
(male) secondary sex xteristics which may occur in
males before puberty (precocious puberty) and
females due to pathological over secretion of adrenal
androgen
Symptoms varies with sex and age

115. In males:
Fetus: develops macrogenitosomia precox- enlarged
external genitalia
Prepubertal: leads to precocious puberty but no
spermatogenisis
Adult: Shows increased masculinisation
In female: in fetus b4 12th week of pregnancy can lead
to female pseudohermaphrodism

116. Typical features of virilism
Hirsutism
Deeping of voice
Increased muscularity
Atrophy of breast and external genitalia (except
clitoris)
Enlarged clitoris
Psychological disturbance and homosexuality

118. Feminization: rarely occurs due to excess oestrogen
secretion from zona reticularis
Symptoms varies with sex
Male: show breast enlargement (gynaecomastia),
diminished sexual power and testicular atrophy
Female:
Prepubal stage: girls show precocious maturation of
secondary sexual organs and xter
Adult: the condition is unusually notice

120. Pancreatic Gland

121. PANCREAS
• It consists of two type of tissues
• The pancreatic acini (exocrine gland) that secrets
pancreatic juice that aid in digestion
• The islets of Langerhans (endocrine gland) which
contain the following 4 type of cells
• A (alpha) cells (20%): secrets glucagon hormone
• B (beta) cells (70%) secrets Insulin hormone
• D (delta) cells (8%) secrets somatostatin
• F cells (2%) secrets pancreatic polypeptides

122. INSULIN
• Glucose lowering polypeptide hormone that consist
of 2 chain of amino acids (A and B).
• A contain 21 AA and B contain 30 AA.
• Both chains are linked by disulphide bridge at
position 7 and 19, 20 and are held together by C-
peptide (pre-insulin in endoplasmic reticulum).
• Cleavage of C-peptide releases insulin that is being
packages in Golgi apparatus.

123. Type 1 diabetes (juvenile diabetes)
• Type 1 diabetes happens when the pancreas does not
make enough, or any, insulin. Without insulin, the
cells cannot get enough energy from food.
• This form of diabetes results from the body's
immune system attacking the insulin-producing beta
cells in the pancreas. The beta cells become
damaged and, over time, the pancreas stops
producing enough insulin to meet the body's needs.
• People with type 1 diabetes can rebalance their
blood glucose levels by receiving insulin injections
or wearing an insulin pump every day.

124. • There is no clear cause of type 1 diabetes.
Some evidence suggests that it results from
genetic or environmental factors. An
estimated 1.25 million people in the United
States are living with type 1 diabetes.
• Type 2 diabetes
• This type occurs when the body builds up a
resistance to insulin. While the pancreas may
still produce the hormone, the body's cells
cannot use it effectively.
• As a result, the pancreas produces more
insulin to meet the body's needs, and it is
often unable to keep up with the increased

125. • With an insufficient amount of insulin in the body,
diabetes develops. Over time, the beta cells become
damaged and may stop producing insulin altogether.
• As with type 1 diabetes, type 2 can cause high blood
sugar levels and prevent the cells from getting
enough energy.
• Type 2 diabetes may result from genetics and family
history. Lifestyle factors, such as obesity, lack of
exercise, and poor diet also play a role. Treatment
often involves increasing levels of exercise,
improving the diet

126. • Gestational diabetes
• Pregnancy can cause type 2 diabetes, known as
gestational diabetes. This can result from
complications during pregnancy and delivery.
• After giving birth, gestational diabetes usually goes
away, though it increases the risk of developing type
2 diabetes later in life

127. GLUCOSE HOMEOSTASIS
• Main source of glucose is CHO
• Other source is through gluconeogenesis and
glycogenolysis in the liver
• Amount of glucose absorbed in the GIT is about 20-
25g/hr through 20 active transport
• Kidney to some extend due take part in
gluconeogenesis after prolonged starvation and
fasting
• Normal plasma glucose level is about 90-120mg/dL
• Glucose is excreted in urine if the renal threshold
exceed 180mg/dL (glucosuria)

128. MANIFESTATIONS OF DM
• Polyuria
• Polydipsia (could result into obesity)
• Hyperphagia/Polyphagia
• Rapid fatiguability
• Loss of weight
• Decrease resistance to bacteria infection (due to
hyperglycemia)
• Increase lipolysis (diabetic ketoacidosis)
• Diabetic nephropathy
• Diabetic retinopathy
• Diabetic neuropathy

129. THANK YOU FOR YOUR PATIENCE, LISTENING
AND UNDERSTANDING