Unit=9=Endocrine System=Anesthesia students 2025 AAU

The Endocrine Physiology
[Lecturer,AAU]
[Feb ,2017 E.C]
1

Gland
1.Exocrine gland
2.Endocrine gland
 Hormones
 Functions
 Comparison with Nervous system
 Regulation of Hormonal secretion
 Chemical classification of hormones based on:
1.Solubility
 Lipophilic
 Lipohobic
2.Synthetic origin
 Amine ,Protein (polypeptide) ,Steroid
 MOA
 Site of synthesis [rER or sER] ,release, transport,
metabolism & excretion:
 Endocrine basis of hormone disorders
 Major endocrine glands & tissues
1.Central endocrine glands
1. Pineal gland
2. Hypothalamus
3. Pituitary (hypophysis) gland
2.Peripheral endocrine glands
1. Thyroid glands
2. Parathyroid glands
3. Adrenal (suprarenal) glands
4. Thymus gland
5. Part of pancreas (islet of Langerhans)
6. Gonads (reproductive glands)
1. Testis
2. Ovary
1.Adipose tissue (fat cell/tissue)=
2.Small intestine & Skin=
3.Stomach=
4.Kidney=
5.Heart=ANP
6.Liver =IGF (somatomedin-c)
 Angiotensinogen
 Thrombopoietin
2
Hormone
secretion
as
secondary
function
Learning Objectives

Terminologies
1. Target organ organ that has specific receptors to which the hormone [messenger] binds specifically.
2. Adeno-  Gland
3. Hypophysis  Pituitary  Underneath growth
4. Adenohypophysis  Glandular Pituitary gland [Anterior]
5. Neurohypophysis Neural pituitary gland [Posterior]
6. Neuroendocrine cells  function as the nervous & endocrine systems (dual functions)
7. Hypophyseal portal system[HPS]  Is the conduit that connects the brain to the anterior pituitary.
8. Largest gland thyroid gland
9. Love hormone  oxytocin
10. Stress hormone  cortisol
11. Master gland  pituitary
12. 99% Ca2+ is  stored inside bone
13. Seat of the soul  pineal gland
14. Active form of thyroid hormone is  T3
15. Hashimoto's disease autoimmune disorder of the thyroid gland
3

Glands
 Are specialized cells, or organs synthesize chemical or hormone & release it through
duct or directly into the bloodstream.
1.Exocrine glands: (secret subs likeEnzyme, sweat, saliva ,milk,oil,sebum,tear)
 Are glands secret their products into a canal or ducts that carry these products to
other organs or outside the body.
a) An acinus (in pancreas) is a round cluster of exocrine cells connected to a duct.
b) Sweat G
c) Salivary G (Enzy)
d) Mammary G
e) Lacrimal G
f) Sebaceous G
g) Prostate gland
 Secrete an alkaline fluid (for lubrication & nutrition of sperm cells)
2.Endocrine glands
 Are group of ductless glands that secrete hormones necessary for normal body function (for growth
& development, reproduction, & homeostasis).
 Secret their products directly into the internal env’t (blood stream). 4

What is the Endocrine system?
 It is a system of control ,communication & coordination of body functions
 It uses chemical signals called hormones for cell to cell communication
 Is a collection of ductless glands (endocrine glands) & specific cells that secrete
chemical messengers called hormone [H].
 This chemical messenger is transported (circulated) within the body mostly
through blood.
 It arrives at distant cells within specific target organs.
The target organs have cells possessing appropriate receptors for that H.
5

What are hormones [H]?
 H are chemical messengers or signal molecules:
 Synthesized by ductless endocrine cells
 Released directly in to the blood stream
 Act on target cells that have receptors for that hormone
 Their action is slower & long-term.
6
Circadian rhythm:
• Is a biological processes occurring at 24-hr interval
• Is inherent cycle or a daily rhythmic activity cycle, based on 24-hr intervals, that is exhibited by many organisms.

Functions of hormones
1.Regulation of reproduction: gametogenesis, sexual desire, coitus, fertilization.[T,Estrogen,P]
2.Regulation of body growth & development [GH, T3 & T4]
3.Production, utilization & storage of energy [Insulin, T3 & T4]
4.Growth & development of brain [T3 & T4]
5.Response to stress or injury & infections [Cortisol,]
6.Energy metabolism [T3 & T4]
7.Homeostasis: maintenance of the internal environment in the body.
 Water (fluid)-electrolyte balance=ADH ,Aldosterone
 Regulation of ABP= Renin ,ADH & Aldostrone
 Control of BT [T3&T4], emotion (NE)
 Change in mass of bone [PTH,calcitonin,Estrogen], muscle [T] ,RBCs [T,ErtPO] & fat [Estrogen]
8.Circadian rhythm [Serotonin or melatonin]
 A rhythmic activity cycle, based on 24-hrs interval

Hormone Functions…
Behavior [T,E,P]
Immune system
8
8

Two general regulator of Homeostasis
1.The nervous system: regulates homeostasis through generation of AP & by
releasing chemical messengers called NTs.
2.The endocrine system: Regulates homeostasis by releasing chemical messengers called hormones.
Feature Nervous system Hormone (endocrine) system
Cell involved Neuron Cell in Gland
Form of transmission Communicating using nerve / impulse
(AP)
Hormone
Transmission pathways (carried
by)
Nerve fiber (axon) Blood
Speed of transmission Fast Slow
Duration of effect Short term Long term (slow response )
Response Rapid ,brief in m/seconds slow
Example Reflexes: like blinking eye
movement
Growth ,body development, metabolism,
reproduction, H2O & electrolyte regulation
9

Regulation of hormonal secretion
1.Feed back control of hormone secretion,
A. Negative Feedback
 It prevents over activity of the hormonal system
B. Positive Feedback.
 It occurs when the biological action of the 1st hormone causes additional secretion of the 2nd hormone.
1.Feed back control of hormone secretion,
2.Periodic variations in hormone secretion

11
Regulation of hormonal secretion…
Stress response

Cont‘d
2.Periodic variations in hormone secretion
 Hormone secretion influenced by:
A. Seasonal change [serotonin]
B. Various stages of development [T,E] & aging [E],
C. The diurnal or daytime cycle & sleep cycle or at night or nocturnal.
E.g.
I. The secretion of GH increased during the early period of sleep but is reduced
during the later stages of sleep & at day time.
II. Some hormones more secreted in adolescence stage
III. LH surge at ovulation [around 14 day of 28 days]
12
Regulation of hormonal secretion…

Chemical classification of hormones
Classification based on [Solubility & Synthetic origin]
A. Solubility
1.Lipophilic :(water insoluble=steroid H)
 Are lipid hormone made from cholesterol & are fat soluble
 Easily cross lipid bilayer part of target organ
 Receptor location in cytoplasm or nucleus (intracellular)
 No need of 2ndary messenger
2.Lipophobic:amino acid [aa] based hormone made up of aa
 Either a single modified amino acid or a protein made up of 3-200aa
 Are hydrophilic: amine & peptide hormones
 NB:But thyroid hormones (amine) are water insoluble
 Receptor locationon surface (on cell membrane)
 Bind to a receptor protein on the surface of the target cell & produce
physiological change in the cell.
 But need 2ndary messenger 13
Thyroid hormonesT3 & T4

B.Synthetic origin (derived from tyrosine , tryptophan,cholestrol)
 3 general classes of hormones:
1.Protein & polypeptide hormones: amino acids linkage
2.Steroid hormones :synthesized from cholesterol in a series of rxns
3.Amine hormones :(derivatives of a single amino acid like tyrosine, tryptophan)
1. Derivatives of the amino acid  Amine hormones
Are hormones derived from amino acids tyrosine or tryptophan
Their receptor found on cell surface BUT thyroid hormones in nucleus
 Includes : hormones secreted by
Thyroid gland ((thyroxin (T4) & triiodothyronine (T3)) = (lipid soluble)
Adrenal medulla (epinephrine & norepinephrine)
Pineal gland (melatonin & serotonin)
Hypothalamus dopamine
14
Chemical classification of hormones…
Catecholamines (E,NE,Dopamine) hormones used as neurotransmitter [NT]

Cont’d
2.Proteins & polypeptides hormones
 Made up of small to many amino acids
 Their receptor found on cell surface
 Includes : hormones secreted by
 Anterior & posterior pituitary gland
 Pancreas (insulin & glucagon)
 Parathyroid gland (PTH)
 Hypothalamic hormones but dopamine is
amine
3. Steroids hormones
 These are lipids derived from cholesterol.
 Their receptor found intracellular (in target
organ cytoplasm or nucleus)
 Includes :hormones secreted by:
 Adrenal cortex :(cortisol & aldosterone,
androgen)
 Ovaries & Placenta :(estrogen &
progesterone)
 Testes: (testosterone)
 Vit-D3 [calcitriol]
15
T3 & T4 Tyrosine
Serotonin,melatoninTryptophan

Hormone class Components Example
Amine H
 Catecholamine
Amine H
 Thyroid hormones
• Amino acid with modified group
• Receptor location =on Plasma membrane [PM]
• Amino acid with modified group
• Receptor location =in nucleus
• NE,E,Dopamine,melatonin
• Serotonin [precursor of melatonin]
T3,T4
Peptide H • Chain of linked amino acids • Oxytocin
• ADH
• Insulin/glucagon
• PTH,GH etc.
Steroid H • Derived from the lipid cholesterol
• Can freely pass through PM
• Receptor location = in Cytoplasm or nucleus
• Testosterone (androgen)
• Progesterone, Estrogen
• Cortisol, aldosterone
• Vit-D
16

Mechanisms of Action of Hormones
 The first step of a hormone's action is to bind to specific receptors at the target cell [organ].
 Cell that lack receptors for the hormones does not respond.
 The locations of receptors for the different types of hormones are:
1. Receptors on the surface of the cell membrane.
 Such receptors are specific mostly for the protein, peptide, & catecholamine hormones. &
 Act through 20 messengers
 20 messengers can be:
1. cAMP,DAG
2. cGMP
3. IP3 (inositol 1,4,5 triphosphate)
4. Ca2+ etc.
17

2. Receptors in the cell, either:
A. In the cell cytoplasm
 The primary receptors for the different steroid hormones found mainly in the
cytoplasm. Or
B. In the nucleus
 Are receptors for thyroid hormones
 Located in direct association with one or more of the chromosomes.
 Such hormones are,
 Lipid soluble

 Readily cross cell membrane &

 Interact with receptors in the cytoplasm or nucleus 18
Mechanisms of Action of Hormones…

Cont’d
19

20

Hormone: synthesis, release ,
transport,metabolism & excretion
 Site of synthesis :(in the cell, cell body or soma)
 Protein/peptide hormones: in the rER
 Steroid hormones: in the sER
 Release: Exocytosis
 Transport: hormones are transported in blood in two forms:
a. In the free form (dissolving in plasma)have short half life
b. In combination with plasma proteins (or carrier proteins :albumin & globulin).
Have long half life
 Metabolism: metabolized in the liver or by target cells [organs]
 Excretion: urine, feces, sweat
21

1.Over production of hormones
a.Gigantism (childhood),Acromegaly (adult )GH
b.Hyperthyroidism  Grave’s disease (toxic goiter or exophthalmic goiter) [T3 &T4]
c.Cushing’s syndrome adrenal cortex (cortisol) "buffalo hump") "moon face")
d.Galactorhea  prolactin [PRL]
e.Conn’s disease  Aldosterone
2.Under production of hormones
a. Dwarfism  GH
b. Hypothyroidism  Cretinism, myxedema ,Goiter (endemic) & Hashimoto's disease [ T3 &T4]
c. Addison’s disease  adrenal cortex [ cortisol & Aldosterone]
d. Diabetes mellitus (IDDM or Type 1-DM)  Insulin
e. Diabetic insipidus  Posterior pituitary  ADH [alcohol]
f. Osteoporosis  Estrogen (woman >45yrs) & calcitonin
3.Non-functional receptors for the Hormones
 Target cells become insensitive to the hormone
 Eg. Diabetes mellitus (NIDDM or type II)
22
Endocrine basis of hormone disorders
RicketsIn Children
Osteomalacia In Adult

The principal endocrine glands & endocrine tissues of the body
1. Hypothalamus
2. Pineal gland
3. Pituitary
4. Thyroid
5. Parathyroid
6. Thymus
7. Adrenal gland
8. Pancreas
9. Ovaries
10. Testes
1. HeartANP
2. KidneyErpo, vit-D (calcitriol),Rennin
3. StomachGastrin, Ghrelin [appetite]
4. Small intestine Motilin,Secretin,CCK, neuropeptide-Y,histamin
5. Adipose tissue (fat cell/tissue)Leptin [appetite]
6. Liver IGF (Somatomedin-c),Angiotensinogen ,Thrombopoietin
Endocrine tissues Or organs
23
Endocrine glands
23
Gonads

24
A. Central endocrine glandsincludes;
1. Hypothalamus
2. Pituitary gland (hypophysis)
3. Pineal gland melatonin  amine hormone  sleep & weak cycle
(as circadian rhythm or as body biological clock].
B. Peripheral endocrine glands includes:
1. Thyroid glands
3. Thymus gland
4. Adrenal gland
5. Pancreas
6. Gonads (Ovaries & Testes)
Endocrine glands: divided in to 2; Central & Peripheral

1.Hypothalamus (HT)
I. Location
II. Cells
III.Hormones
IV.Functions
V. Disorders
VI.Relationship with Pituitary Gland
25

 Location [HT]
 HT is part of the diencephalons, which forms the floor & the lateral wall of the
3rd ventricle Or found just under the thalamus. Or
 Found above the pituitary gland
 It is extremely complex part of brain
 It contains many regions (nuclei) with highly specialized functions
 HT represents less than 1% of the brain mass, about 5gm (so small but so
important area of brain)
 Regardless of its size, it plays most important roles in controlling homeostasis
 It is the main brain structure involved in regulating hormonal levels in the body
26
Hypothalamus (HT)…

 Functions,
 Some functions of different parts or regions of HT:
 Regulates temperature :(it gives response to cold & heat)  for thermal regulation
 It has hunger & satiety center if they damaged  hyperphagia or starvation.
 It has thirst center it regulates drinking
 Regulate sexual behavior :(it has sex drive center)
 Control circadian rhythms :(control sleep & wake cycle)
 Control autonomic NS : (sympathetic vs parasympathetic regulation)
 Endocrine function:(HT Releases or secrets hypothalamic releasing & inhibiting hormones)
 In turn, those hormones {H} stimulate pituitary H secretion
Etc.[many]. 27
Hypothalamus (HT)...

 HT:Relationship with pituitary gland :
 The most important function of the HT is to link the nervous system to the
endocrine system via the pituitary gland.
 HT is the main coordinating center b/n the endocrine & nervous system.
 HT synthesizes & secretes certain neuro-hormones called hypothalamic –
releasing & inhibiting hormones &

 These in turn stimulate or inhibit the secretion of pituitary hormones
 The hypothalamus & pituitary gland have both anatomical & functional relationships.
28
Hypothalamus (HT)...

 The pituitary gland [PG]: is connected to the hypothalamus by stalk like structure called infundibulm.
 PG is divided into an anterior lobe (adenohypophysis) & posterior lobe (neurohypophsis).
 So, HT exerts its effects on pituitary gland in 2 different ways:
A. Hypothalamo-neurohypophysial axis
B. Hypothalamo-adenohypophysial axis
Hypothalamus & Pituitary
29
29

Cont’d
 Posterior pituitary: an outgrowth of the hypothalamus composed of neural tissue.
 Hypothalamic neurons pass through the neural stalk & end in the posterior pituitary.
 Neuroendocrine cells from 2 nuclei in hypothalamus synapse directly on to blood
vessels in posterior pituitary.
 These 2 nuclei are:
 Supraoptic nucleus (SON) = secrets ADH (5/6th =83% )
 Paraventricular nucleus (PVN) = secrets Oxytocin (5/6th =83% )
30
A. Hypothalamo-neurohypophysial axis
Posterior Pituitary Gland [Neurohypophysis]
 Is composed mainly of glial-like cells called pituicytes
 It does not synthesize hormones, but
Store & secrete 2 hormones:
a. ADH also called ‘Vasopressin’
b. Oxytocin
ADH
Oxy

(SON)
(PVN)
SON produces
 5/6th of total ADH
 1/6th of total Oxytocin
PVN Produces
5/6th of total Oxytocin
 1/6th of total ADH
Fig. Hypothalamic control of neurohypophysis through hypothalamo hypophysial axis
Cont’d
31
Hypothalamo-neurohypophysial axis…

Functions
 Regulates water balance
 Increase water reabsorption by increasing permeability of kidney ducts to
water  Reduce volume of urine (diuresis)
 That is why it is named as antidiuretic hormone.
 Cold & alcohol inhibit the ADH secretion & function means produce high urine output
 Factors stimulating release of ADH:
 Hyperosmolality (high solute content of blood)
 Change in blood volume (high K+)
 An increased in Ang-II 32
ADH
Oxytocin
a.ADH

Cont’d
 Hyposecretion of ADH:leads to
 Diabetes insipidus=DI :can be neurogenic or nephrogenic
Is caused by deficiency of ADH or ADH receptor insensitivity in Nephron
 Manifestation of DI: polyuria & polydipsia
 Two types of DI
1. Neurogenic DI
Due to a genetic defect that blocks ADH production
The hypothalamo-hypophysary system is damaged by surgery or disease.
2. Renal [nephrogenic] DI
The renal tubule cells are insensitive to ADH
33

Cont’d
for parturition & lactation
Function
1.Facilitates transport of sperm in both males & females ductile system
2.Promotion of maternal behavior toward the neonate
 In nonhuman mammals, injection of oxytocin induces maternal behavior
3.Induces uterus contraction [Parturition]
 Stimulating contraction of the pregnant uterus
 Especially toward the end of gestation
34
b.oxytocin

4. Oxytocin also plays an important role in lactation
 Baby crying stimulates Oxytocin secretion
 Oxy induces myoepithelial contraction (lactation) for milk let-down or milk
ejection in the lactating breast.
 In lactation, oxytocin causes milk to be expressed from the alveoli into the ducts
of the breast  the baby can obtain it by suckling
 Mechanism of milk ejection reflex by oxytocin:
Suckling stimulus on the nipple by the baby

Signals transmitted through sensory nerves to oxytocin neurons in PVN
& SON nuclei in the hypothalamus

 Release of oxytocin by the posterior pituitary gland  Carried by the blood to
the breasts Causes contraction of myoepithelial cells of breast  milk ejection
35

Cont’d
 Special neurons [heterogeneous] in hypothalamus synthesize & secrete neurohormones:
a. Releasing hormones (Librins)
 Increase the secretion of hormones from anterior pituitary
b. Inhibiting hormones (Statins)
 Inhibit or decrease the secretion of hormones from anterior pituitary
 These hormones are carried by hypothalamohypophysial portal vein into adenohypophysis
 In the anterior pituitary, librins & statins act on the glandular cells
 To control secretion of the anterior pituitary hormones
 For each anterior pituitary hormone there is a releasing hormone
 For some there is also an inhibiting hormone [GHIH & PRLIH]
36
B. Hypothalamo-adenohypophysial axis [HPA]

The Hypothalamo-anterior pituitary axis…
 A complex communication system b/n the nervous system & the endocrine system.
1. Hypothalamus
2. Pituitary gland
3. Endocrine glands
37
Negative feedback from the primary target gland modulates the secretion of both
pituitary & hypothalamic hormones.
37
1
Hypothalamo-adenohypophysial axisThe Hypothalamo –anterior Pituitary Axis=HPA
[target gland]
1

 The adenohypophysis is connected to HT by a system of blood vessels called the adenohypophyseal portal system. But
 The neurohypophsis is connected to HT by a bundle of nerve fibers, called hypothalmo-neurohypophyseal tract.
 The anterior pituitary is regulated by hormones secreted by the hypothalamus. However
The posterior pituitary simply stores & releases hormones that are actually produced by the hypothalamus.
 Secretion of pituitary is controlled by hypothalamus [HT]
38
Cont’d
2

Hypothalamo-hypophyseal portal system 39
39
Cont’d
3

Hormones of Hypothalamus
 HT: Produces Or secretes 9 main hormones
 7 hormones that travel through portal system & regulate the anterior lobe.
 5 of these trigger hormone release & 2 of them inhibit hormone release by the anterior lobe.
 The hypothalamus synthesizes oxytocin and ADH that are stored in the posterior pituitary
& released in response to nerve signals.
1. TRH
2. CRH
3. GnRH
4. GHRH
5. PRH
6. GHiH (somatostatin=SST=anti-GH)
7. PIH (Dopamine or anti-prolactin)
8. ADH
9. Oxytocin
40
4

41
PRH
PRL
Milk


(PIH)

(-)
(-)
Dopamine
(GHIH)
41
Cont’d
5
Hormones of Hypothalamus…

Cont’d
PIH GHIH
PRH
(GHIH) (-)
(PIH) (-)
ADH Oxy
42
Uterus
6 7

Cont’d
 Neuroendocrine cells in the hypothalamus:
 Has axon tract [nerve] on pituitary glands (on both anterior (shorter) & posterior pituitary [longer])
8
[SON & PVN]
Heterogeneous [different types of] neurosecretory cells

L & S hormones that regulate the anterior pituitary (glandular cells)
Hypothalamic hormone Effect on pituitary
1.Corticotrophin releasing hormone (CRH) Stimulates ACTH secretion by corticotropes
2.Thyrotropin releasing hormone (TRH) Stimulates TSH secretion by thyrotropes
3.Growth hormone releasing hormone (GHRH)
4.Prolactin releasing hormone (PRH)
Stimulates GH secretion by somatotropes
5.Gonadotropin releasing hormone (GnRH)
1.Growth hormone inhibitory hormone [GHIH=Somatostatin=SST]
Stimulates LH & FSH secretion by gonadotropes
2.Prolactin inhibiting hormone [PIH=dopamine] Inhibits PRL secretion
44
Stimulates Prolactin secretion by lactotropes
Inhibits GH secretion
Releasing=R & Inhibiting=I
Hypothalamic: Librins =L & Statins=S  44

 Location
 Pituitary gland (AKA hypophysis) is a small gland (about the size of a pea)
 Lies in the sella turcica, a bony cavity at the base of the brain Sphenoid bone [butterfly-shaped bone]
 1cm in diameter & 4gm weight
 Is Master gland
 Connected to the HT by a stalk of tissue called the infundibulum (hypophysial stalk)
 Physiologically, the pituitary gland is divided into 2 distinct portions:
1. Anterior pituitary (AKA adenohypophysis)
 Glandular anterior lobe (has endocrine cell or secretory cells)
2. Posterior pituitary (neurohypophysisis an extension of hypothalamus or is a neural tissue)
 Neuronal posterior lobe.
45
2.Pituitary gland

Cont’d
Hormones
1.Anterior pituitary hormones : 6 peptide hormones
1. Growth hormone (GH)
2. Prolactin (PRL)
3. Adrenocorticotropic hormone (ACTH)
4. Thyroid stimulating hormone (TSH)
5. Gonadotropic hormone: Luteinizing hormone (LH) and
6. Gonadotropic hormone: Follicle-stimulating hormone (FSH)
2.Posterior pituitary store & secrets 2 hormones,
 ADH (Arginine vasopressin)
 Oxytocin
46
Pituitary gland…

Anterior pituitary cells & hormones (products)
1. Corticotrophs
 Adrenalcorticotrophic (ACTH)
2. Gonadotrophs
 Leutinizing Hormone (LH) and
 Follicle Stimulating Hormone (FSH)
3. Thyrotrophs
 Thyroid Stimulating Hormone (TSH)
4. Lactotrophs
 Prolactin
5. Somatotrophs
 Release Growth Hormone (GH)
 The first 4 directly stimulate other endocrine glands and are known as tropic hormones.
47
Cont’d
47
Pituitary gland…

Anterior pituitary cells ,hormones & target
Cell type Pituitary
population
Product (Hormone) Target
Corticotropes 15-20% ACTH Adrenal gland
Thyrotropes 3-5% TSH Thyroid gland
Gonadotropes 10-15% LH, FSH Gonads
Somatotropes 40-50% GH Liver & All tissues
Lactotropes 10-15% PRL Breasts, gonads
48 48
Cont’d Pituitary gland…

Anterior pituitary hormones & functions
Hormones Functions
GH Promotes growth & metabolism
PRL Promotes milk secretion, breast growth, & maintains lactation
ACTH Stimulates adrenal cortex to produce aldosterone & cortisol
TSH Stimulates the thyroid gland to synthesize & secret Calcitonin/ T3/T4/
[For Thermogenesis & metabolism]
LH Promotes ovulation, luteinization
Stimulates Leydig cells for testosterone secretion
FSH Stimulates growth & maturation of ova
Stimulates spermatogenesis
Stimulates secretion of estrogen
49
Cont’d
Pituitary gland…

a. GH
b. Physiological effect of GH
c. Disorders of GH
 Hypo & hyper secretion of GH
50
Growth hormone (GH)

Growth hormone (GH)…
a. Growth hormone (GH)
 Is an anterior pituitary hormone
 Also known as somatotropic hormone.
 All the major anterior pituitary hormones, except GH, exert their principal effects
by stimulating target glands.
 In contrast ‘GH’ exerts its effects directly on all or almost all tissues of the body.
=IGF-1
Fig. Effects of GH 51
Somatomedin-cIGF-1
IGF-1 Insulin like growth factor-1

b.Physiological effect of GH
 Promotes protein deposition in tissues
 Stimulates amino acid uptake & protein synthesis in muscle & other tissues.
 Stimulates Cartilage & Bone Growth
 Enhances [] Fat Utilization for Energy
 Carbohydrate utilization
GH has hyperglycemic effect b/c of the beta cells of the islets of
Langerhans prone to degenerate because they become overactive owing to
the hyperglycemia.
 Consequently, in about 10% of giants eventually develop diabetes mellitus [DM]
52
GH Hyperglycemic Hormone

Cont’d
Metabolic role of GH
 On CHO metabolism
 ↓Glucose utilization
 ↑Gluconeogenesis ↑BGC ( Hyperglycaemic hormone)
 ↑Glycogenolysis
 On protein metabolism (protein anabolic)
 ↑amino acid transport through the cell membrane
 ↑DNA transcription
 ↑RNA translation (protein synthesis)
 ↓Protein catabolism
 On Fat metabolism
 ↑Lipolysis
 ↑FFA in plasma
 ↑Ketogenesis
 ↑β-oxidation
 Other Roles of GH
 ↑RBC formation
 ↑Metabolic Rate, thermogenic
 Insulin secretion (Diabetogenic effect of GH)
 ↑Secretion of Somatomedin-C (IGF)
 On Electrolytes
 ↑Absorption of Na+, K+ & Ca2+
53

Cont’d
C.Disorders (abnormalities of GH secretion)
Hyposecretion
Dwarfism
 Hypo-secretion (deficiency) of GH during childhood.
 All the physical parts of the body develop inappropriate proportion to one another
 Rate of development is greatly decreased.
 This abnormality resulting in short limbs & short stature
54
54

Cont’d
Hypersecretion: excessive GH secretion
1. Gigantism (during active growth)
Caused by over-production of GH during childhood
Somatotrops become excessively active
Usually caused by a tumor on the pituitary gland of the brain (Tumor of
somatotrops)
All body tissues grow rapidly
It causes over growth of the hands, face, & feet
2. Acromegaly (after)
 Results when the anterior pituitary gland produces excess GH after epiphyseal
plate closure at puberty (occurs after adolescence)
 That means after the epiphyses of the long bones have fused with the shafts
 The person cannot grow taller (no vertical growth), but the bones can become
thicker & internal soft tissues continue to grow
 Enlargement of nose & ear due to excessive growth of cartilages
 Prominent eye brow & face 55
55

Acromegaly…
 Marked enlargement in the bones of the:
 Hands, jaw and feet
 Cranium, nose, forehead, supraorbital ridges
 Changes in the vertebrae - hunched back (kyphosis)
 Projection of the lower jaw (prognathism)
 Enlargement & broadening of hands & feet
56
56

 Is anterior pituitary lactogenic hormone
Function of PRL
 It Promotes growth & development of breast (mammary glands)
 It Stimulates & maintains the secretion of milk (maintain lactation after parturition)
 It Delays ovulation & suppresses fertility by inhibiting the action of LH & FSH.
57
Prolactin [PRL]

3.Pineal gland [Also called epiphysis]
 Is located in the brain
 A small, cone-shaped organ in the brain of vertebrates
 Secretes the hormone melatonin (derived from serotonin)
 Serotonin is precursor for melatonin
 Formed from tryptophan
 Melatonin is involved in:
 Circadian rhythm (biorhythms)
Sleep & wake cycle [body clock = biological clock]
Seasonal breeding of animals (reproductive cycle)
58
Serotoninmelatonin
Pineal gland  Is a tiny gland in the midbrain. It regulates mating behaviors & day-night cycles.
Pineal gland circadian rhythm & sleep induction. In animals it is known to play a major role in sexual development & seasonal breeding.

Peripheral Endocrine glands-include
1. Thyroid glands
3. Thymus gland
4. Adrenal gland [add + renal]
5. Pancreas
6. Gonads [sex organs= reproductive organs]
59

1.Thymus gland
 Located in the mediastinum superior to the heart  Behind the sternum & b/n
our lungs.
 Unlike most organs, it is larger in children (it is only active until puberty).
 After puberty, the thymus starts to shrink & become replaced by fat.
 The thymus is the site of T cell differentiation, development & maturation.
 T cells originate (born) in the bone marrow & soon after their born they migrate
to the thymus gland.
 T-cells mature in the thymus gland & in the lymph nodes. Since the thymus is
only 10-15% functional in the adult, the lymph nodes take on greater
importance in the maturation process.
60

Cont’d
 Hormones in the thymus stimulate the production, differentiation ,development ,
multiplication & maturation of disease-fighting T cells into different types.
 Into:
 T-Helper, regulatory, cytotoxic ,natural killer & memory T cells
 The thymus gland produces (secrete) hormones like:
1.Thymopoietin
2.Thymosin
3.Thymulin
 They regulate the development & later activation of disease fighting blood cells
called T lymphocytes.
61
Thymus gland…

2.Gonads (ovaries & testes)
Gonads important for :
1.Gonadal cells development
 Female ovum
 Male sperm cells
2.Hormone secretion (sex hormones)
 Female Estrogen & Progesterone
 Male  Testosterone
62

1. Oogenesis formation & maturation of the egg
2. Hormonogenesis: Estrogen [E] & progesterone [P]
 Control growth & development of female reproductive system or organ
Estrogen [E]
 For egg maturation & for dev’t of 20 sexual characteristics
 Body hair growth , narrow shoulder, broad hip, converging thigh.
 Stimulates growth of breasts, particularly of the ductal part of breast.
 ↑Osteoblastic activity→↑rate bone growth
 ↑Bone matrix, ↑Ca2+ + Phosphate deposition inside bone.
Progesterone [P]
 Thickens uterine lining or endometrium (Prepare the uterus to receive a fertilized egg)
Ovary for

1. SpermatogenesisFormation & development of sperm or spermatozoa
2. Hormone → Testosterone
 It regulates sperm cell production
 It controls growth & development of male reproductive system
 For dev’t Male secondary sexual characteristics
 Stimulation of growth of pubic + Facial + axillary hair
 Maintain sexual drive activity
64
Testes for

 Pancreas has 2 major types of cells,
 Acini  produce pancreatic juices
 Islets of Langerhans  produce hormones
Islets contain 4 types of cells
1. Alpha  Constituting about 25% of the total
 Secretes glucagon
2. Beta  Constituting about 60%
 Lie mainly in the middle of each islet
 Secrete insulin
3. Delta  about 10% of the total
 Secrete somatostatin [SS]
 SS Has paracrine depressant effect on both insulin & glucagon secretion
4. PP cells present in small numbers in the islets
 Secretes pancreatic polypeptide
 A hormone of uncertain function 65
3.Endocrine pancreas

Insulin and Its metabolic Effects
 Affects carbohydrate , fat & protein metabolism
Effects of insulin on carbohydrate
 Insulin is secreted in great quantity in response to high glucose concentration.
 It increases cellular uptake of glucose
 It causes glucose to be stored as glycogen mainly in the liver & muscles
 Excess glucose that cannot be stored as glycogen are converted into fat,
 Fat under the stimulus of insulin stored in the adipose tissue.
 Insulin has a direct effect in promoting amino acid uptake by cells &
conversion of amino acids into protein
 It inhibits breakdown of proteins 66
Effects of insulin on carbohydrate
Effects of insulin on Fat [adipose]
Effects of insulin on proteins
Endocrine pancreas…
Insulin and Its metabolic Effects

Cont’d
 Normal blood glucose level (fasting level) is 70-110mg/dl of blood [90mg/dl]
 When the blood [glucose] falls too low, into the range of 20-50mg/dl,

 Symptoms of hypoglycemic shock develop,
 Characterized by;
 Progressive nervous irritability that leads to fainting, seizures, & even coma.
 In the absence of insulin
 Fat breakdown and use for providing energy are greatly enhanced.
 This occurs even normally b/n meals when secretion of insulin is minimal,
 But it becomes extreme in diabetes mellitus when secretion of insulin is almost zero.
 The brain cells are permeable to glucose:
 Use glucose as the only energy source without the intermediation of insulin
67
Insulin & Its metabolic Effects…

Cont’d
 Insulin is The Only Hormone that Can Lower Blood Glucose
 Muscle, fat & liver tissues require insulin to transport glucose into the cells;
 In these tissues insulin the # of ‘GLUT2 transporter’ in the cell membrane
 Many other tissues, like brain, do not require insulin to transport glucose
 Insulin also activity of enzymes [glycogen synthase]that cause storage of sugar as glycogen or lipid
 After a meal blood sugar rises  stimulates the release of insulin;
 Insulin then causes the sugar to enter the cells & Extra become stored as glycogen.
68
Insulin and Its metabolic Effects…
Several Hormones Can Raise Blood Glucose:
5 major hormones raise blood glucose are:
Glucagon, Cortisol, E(NE), GH & T3 & T4 [TH]
In vigorous exercise all of these hormones increase.

Cont’d
 Insulin secretion is associated with energy abundance.
 When there is greater amount of energy-giving foods in the diet, especially
excess amounts of carbohydrates [CHOs], insulin is secreted in great quantity.
 BCZ insulin plays an important role in storing this excess amount.
 In the case of excess CHOs, Insulin causes them to be stored as glycogen
mainly in the liver & muscles.
 Also, under the stimulus of insulin, excess CHOs converted into fats & stored
in the adipose tissue.
69

70

Factors Affecting Insulin Secretion
Increase insulin secretion Decrease insulin secretion
• Increase blood glucose
• Increase blood free fatty acids & amino
acids
• Insulin resistant state
• Glucagon ,cortisol,GH,TH,E & NE
• Decrease blood glucose
• Fasting
• Somatostatin [SST]
71

 Glucagon is secreted by alpha () cells of the islets of Langerhans
 When the blood [glucose] falls:

 Diametrically oppose the function of insulin
Effects of glucagon on Metabolism
 The major effects of glucagon on glucose metabolism are:
1. Breakdown of liver glycogen (glycogenolysis) to glucose
2. Increase gluconeogenesis in the liver
 Both of these effects greatly enhance the glucose availability to the other organs of the body
 And increase blood glucose concentration.
72
Glucagon and Its Functions
Effects of glucagon on Metabolism

 Is a syndrome of impaired carbohydrate, fat, & protein metabolism
 Caused by:
 Either lack of insulin secretion or
 Decreased sensitivity of the tissues to insulin.
a. Type I diabetes, also called insulin-dependent diabetes mellitus (IDDM)
 Is caused by sever, absolute lack of insulin secretion
Results from reduction in the  cell mass
 Due to autoimmune destruction of  cells
 Assumed to occur following an environmental trigger in genetically
susceptible individuals
 Age of onset is <20 years, hence called juvenile onset DM
 In type I diabetes, plasma insulin levels are very low or undetectable during fasting & even
after a meal.
There are 2 general types of DM:
Diabetes Mellitus (DM)

b. Type II diabetes: non-insulin-dependent diabetes mellitus (NIDDM),
 Age of onset usually > 30 years
 Is caused by decreased sensitivity of target tissues to the metabolic effect of
insulin.
 This reduced sensitivity to insulin is often called insulin resistance.
 Is More common than type I
 Is about 90% of all cases of DM.
 Type II , in contrast to type I, is associated with increased plasma [insulin]  hyperinsulinemia
 The in insulin sensitivity weakens carbohydrate utilization & storage,
 Raising blood glucose & stimulating a compensatory increase in insulin secretion.
74
There are 2 general types of DM…

75
 Classical features of DM
 Glucose in the urine exerts osmotic gradient that draws water with it

 Glucosuria

 Polyuria & Polydipsia
 B/c polyuria results in water loss  thirst  polydipsia
 Polyphagia
 B/c glucose is lost via urine causing high demand for fuel  polyphagia
 Muscle Wasting
 To meet the challenge of high demand of fuel endogenous proteins are
catabolized into glucose.
 This causes loss of muscle mass
Classical features of DM
Paresthesia
Poor wound healing

76
1. For type I DM administer enough insulin
2. In persons with type II DM, dieting & exercise are usually recommended
 Weight loss will reverse the insulin resistance.
 If this fails, drugs may be administered Metformin [Glucophage]
To increase insulin sensitivity (type 2)
Treatment of Diabetes

1. Location
2. Cells
3. Hormones
4. Functions & metabolism
5. Disorders
 Hypo & hyper secretion
Location:
 Located immediately below the larynx on each sides anterior to the trachea
 Has 2 lobes connected by thyroid tissue called isthmus
 The largest endocrine gland
 Is well vascularized has highest rates of blood flow per gram of tissue
 Weighing 15 to 20 grams in adults
Hyoid bone
77
4.Thyroid gland

Cells & Hormones
 Have 2 secretary cells (many spherical sacs called thyroid follicles)
 The interior of follicles contains a protein rich fluid called colloid.
 The major constituent of colloid is thyroglobulin, which contains the thyroid hormones.
A. Follicular cells
 Secretes 2 major hormones: thyroxine (T4) & triiodothyronine (T3)

 in T4 &T3, the basal metabolic rate of the body to 60-100% above normal
B. Para follicular cells
 Secrete Calcitonin  regulates Ca2+ homeostasis
 Which plasma Ca2+ concentration
 bone Ca2+ (bone resorption)
78
2 secretary cells thyroid follicles (sacs)  colloid  thyroglobulin [TG]  thyroid hormones
Cells & Hormones of [thyroid gland]

Formation & secretion of thyroid hormones [TH]
 Thyroid follicles accumulate iodide from blood & secrete into the colloid
 Iodide oxidized to iodine & attached to amino acid tyrosine within
thyroglobulin
 The attachment of 1 iodine to tyrosine produces monoiodotyrosine(MIT)
 The attachment of 2 iodine to tyrosine produces diiodotyrosine(DIT)
 MIT + DIT produces triiodothyronine (T3)
 DIT + DIT produces tetraiodothyronine (T4) or thyroxine
T3 has 3 iodine atoms and T4 has 4 iodine atoms
Dietary iodine is essential for the normal production of TH
 More T4 [93%] than T3 [7%] is secreted from thyroid cells 79

On body metabolism & Energy formation
  Cellular metabolic activities of almost all the tissues of the body.
  The rate of cellular respiration
 TH:  basal metabolic rate (BMR)
  Oxygen consumption
  Number & activity of mitochondria
  The rate of formation of ATP to energize cellular function
  Heat production
  The rate of utilization of foods for energy [Appetite]
On heart
  Cardiac output & heart rate ( blood flow ,vasodilatation in most tissues)
  Heart strength (force of contraction)
Sympathetic Effects
Pulmonary effects
  The rate and depth of respiration.
Hematopoietic Effects:
  Cellular demand for O2 leads to
  Production of erythropoietin & RBC production (erythropoiesis).
Physiologic Functions of Thyroid hormone [TH]
80

TH:Effects on Protein, Lipid & Carbohydrate Metabolism
On CHO metabolism
 Glycogenolysis
 Gluconeogenesis (Hyperglycemic effect)
 Glucose absorption from the GIT
On protein metabolism
 Transcription of large numbers of genes  high protein synthesis [like GH]
On fat metabolism
 Increase lipolysis (lipids mobilization)
81

 Required for:
 Normal development & maturation of NS (brain) in the fetus & infants
 Normal functioning of nervous system [NS] in adults
 Normal body growth & development
Secretion of GH
82
Thyroid hormones [TH=T3 & T4]

Regulation of TH secretion
84
84

 Hypo & hyper secretion
 Diseases of the thyroid can be primary or secondary in nature
1. Primary disease is one in which the gland itself is affected.
2. Secondary Disease is when the anterior pituitary or the hypothalamus is not
functioning properly.
Disorders of the Thyroid can be:
1. Thyroid gland enlargement
2. Hormone deficiency, or hypothyroidism
3. Hormone excess, or hyperthyroidism
 Deficiency mentally retarded & physically slow [lethargic]
 Low BMR, cold intolerant, lack of appetite
 Excess  restlessness, irritability, anxiety, insomnia
 High BMR, heat intolerant 85
Disorders
Hypo & hyper secretion

1.Hypothyroidism
 thyroid hormones (T3 & T4)endemic goiter
Mechanism for dev’t of endemic colloid goiter
 Iodine is a raw material for production of T3 & T4
 Lack of iodine prevents production of both T3 & T4
 No T3 & T4 to inhibit production of TSH
 Secretion of excessively large quantities of TSH

TSH continuously stimulates thyroid cells [gland] to secrete TH,

The gland grows larger & larger
 But because of lack of iodine, T3 & T4 production does not occur

 Therefore no T3 & T4 normal negative feedback suppression of TSH production

 Follicles become large in size, & thyroid gland may increase to 10-20x normal size
86
 Iodine,T3,T4TSH endemic Goiter
1.Hypothyroidism
Mechanism for dev’t of Endemic colloid goiter

Cretinism
 Congenital abnormal extreme hypothyroidism during fetal life, infancy, or childhood
 Characterized by failure of body growth (stunted growth, deformity) & mental retardation
 Resulted from:
 Inborn lack of thyroid gland or
 Failure of the thyroid gland to produce thyroid hormone
 Because of a genetic defect of the gland AKA congenital cretinism
 Genetic defect of the gland,
 Unless the cretinism is treated within a few weeks after birth,

 Mental growth remains permanently retarded (mental handicap , disability)
 Disordered Or a low metabolism.
Myxedema - extreme adult hypothyroidism [caused by decreased activity of the thyroid gland in adults]
 Develops in the patient with almost total lack of thyroid hormone function.
 Characterized by bagginess under the eyes & swelling of the face.
 Swellings around the lips & nose, mental deterioration, & slow metabolism (BMR).
87
1.Hypothyroidism…
Myxedema:
• Low levels of thyroid hormone in adults, either due to: thyroid-gland removal,
lack of function, or atrophy, or secondary to a pituitary-gland disorder.

 Secretion of high levels of thyroid hormones [T3 & T4=TH]
Symptoms of Hyperthyroidism:
 A high state of excitability & ↑ HR
 Intolerance to heat
 Increased sweating
 Nervousness or psychic disorders & inability to sleep
 Etc.
88
2. Hyperthyroidism

 Hyperthyroidism (thyrotoxicosis, Graves' Disease  Toxic Goiter)
 Is excessive secretion of thyroid hormones (T3 & T4)
 Characterized by an enlarged thyroid gland
 Protrusion of the eyeballs, a rapid heartbeat, & nervous excitability.
 Result in:
 2-3 times normal size of the thyroid gland, with tremendous hyperplasia

 The number of cells are increased greatly [T3 & T4]

 Increased rate of thyroid hormone secretion [T3 & T4]
 But plasma [TSH] is less than normal
2. Hyperthyroidism…

 Graves' diseaseaccounts for about 80% of all cases of hyperthyroidism
 In these patients there is immunoglobulin that have actions similar to TSH
 It is called Thyroid-stimulating immunoglobulin (TSI)
 Occur as a result of autoimmunity that has developed against thyroid tissue

 TSI binds with the same receptors that bind with TSH
 Induce continual activation of the follicular cells
 This Results development of hyperthyroidism
TSI is not precisely subjected to negative feedback [unlike TSH]
 i.e No negative feedback relationship b/n TH (T3 & T4) & TSI
90
T3,T4TSH ,but TSIToxic Goiter
2. Hyperthyroidism…

Exophthalmos
 Is protrusion of the eyeballs due to hyperthyroidism (thyrotoxicosis)
 Occurs in most people with hyperthyroidism
 Can be so severe that the eyeball protrusion stretches the optic nerve damage vision
 Eyes damage can also be due to;
 Eyelids do not close completely when the person blink or sleep

 Epithelial surfaces of the eyes become dry , irritated & often infected,

 Resulting in ulceration of the cornea of eye
91
OphthalmosEye
Exophthalmos

Thyroid disorders
Hypersecretion Hyposecretion
Hyperthyroidism Hypothyroidism
1. Graves’ disease 1. Myxedema adult
2. Exophthalmos goitor 2. Cretinism fetal & infant
3. Goiter (toxic goiter)
4. Thyrotoxicosis
5. Protrusion of eye ball
3. Goiter (non-toxic goiter, endemic goiter)
4. Hashmoto’s disease
T4 T3
Thyroid gland synthesizes 93% of T4 Thyroid gland synthesizes 7% of T3
Not active Functionally Active
T4 Functionally active when liberate one iodine in target organ
tissue By iodinase enzyme to T3
Active
T3 Vs T4
92

 Location:
Located immediately behind the thyroid gland
 6mm long, 3 mm wide & 2 mm thick
 Difficult to locate during thyroid operations
Since they often look like just another lobule of the thyroid gland
 Hormone:
 The gland contains mainly chief cells & a small number of Oxyphil cells
 Chief cells secrete parathyroid hormone [PTH]
 Function of the Oxyphil cells is not certain,
 But believed to be modified or depleted chief cells that no longer secrete hormone
93
5.Parathyroid gland

1. Chief cells produce PTH
2. Oxyphilsfunction unknown
Fig. Parathyroid gland & its cells
94
Cont’d

1. Bone :
 It increases the movement of Ca2+ & phosphate from bone into ECF [Blood].
 Stimulates osteoclasts & depresses osteoblasts
 The net effect is ↑[Ca2+] in the plasma [blood]
2. Kidney :
 ↑Reabsorption of Ca2+ in the DT & CD BUT Reabsorption of phosphate
 ↑Formation of 1,25-dihydroxyvitamin D (1, 25 (OH)2 D3)
Role of 1, 25 (OH)2 D3
 ↑Release of Ca2+ from Bone,SI & Renal tubules to blood
3. Gut : ↑Absorption of Ca2+ & Phosphate in small intestine
 The effects of PTH on 3 target tissues result in a higher Ca2+ blood concentration.
PTH: a hypercalcemic hormone 95
The major physiological effects of PTH on 3 Target organs

Calcitonin
 Secreted by the parafollicular cells of the thyroid gland
 Has effects opposite to that of PTH.
 Calcitonin lowers the blood Ca2+ & phosphate levels.
 Action: it is a hypocalcemic hormone (↓Ca2+ level in blood)
 Target organs: bone, renal tubules & GIT
1. Effect of Calcitonin on renal tubules: ↓Reabsorption of Ca2+
2. Effect of Calcitonin on GIT: ↓Absorption & transport
3. Effect of Calcitonin on bone:
 ↓activities of osteoclasts
 ↓formation of new osteoclasts
 ↑activates osteoblasts 96
Net effect ↓ Ca2+ level in blood

Calcium regulator hormones [3]
 3 hormones are primarily concerned with the regulation of Ca2+ metabolism
1. 1,25-Dihydroxy-cholecalciferol [active form of vitamin-D] vitamin-D3
 It increases Ca2+ absorption from the intestine
2. Parathyroid hormone [PTH]
 Reabsorbs Ca2+ & increases urinary phosphate excretion.
3. Calcitonin
 Inhibits bone resorption [Inhibits osteoclast activities]
 Stimulates osteoblasts & bone calcification or formation.
97
97

 Excess PTH causes rapid resorption of Ca2+ from bones  hypercalcemia
 Hypofunction of parathyroid glands Hypocalcemia
 Often with resultant tetany [muscular spasms & tremors]
Hypoparathyroidism
Causes:
 Autoimmune disease to the gland
 Surgical removal of PTGs along with thyroid gland
 During thyroidectomy or Para thyroidectomy
 Congenital absence of the gland
Consequences:
 ↓Plasma Ca2+ level hypocalcemia
 Among the muscles of the body especially sensitive to tetanic spasm are the laryngeal muscles
 Spasm of these muscles obstruct respiration,
 Is common cause of death in tetany unless appropriate treatment is applied
Disorders
98
Low PTH

Hyperparathyroidism
1.Primary PTH excess (primary hyperparathyroidism)
 Causes:
 Due to parathyroid gland adenoma or hyperplasia
 Leads to:
 Bone resorption
 Hypercalcemia
 Kidney stones formation [Ca2+ Precipitate formation]
2.Secondary Hyperparathyroidism
 High level of PTH occur as a compensation for hypocalcemia rather than as a
primary abnormality of the parathyroid glands
 Caused by vitamin D deficiency or chronic renal disease
 For example, damaged kidneys  unable to produce sufficient amounts of active form
of vitamin D (due to chronic renal disease].
Disorders…

 Results from Ca2+ or phosphate deficiency in ECF
 In which the bones soften ,bend & deformed caused by
 An inadequate intake of vitamin-D &
 Insufficient exposure to sunlight [lack of vitamin-D]
 7-dehydrocholesterol in the skin by UV to vitamin-D3,
Activated vitamin D3 prevents rickets
By promoting Ca2+ & phosphate absorption from the intestines [GIT]
 Children who remain indoors do not receive adequate quantities of vitamin-D
100
Osteomalaciasoftening of the bones a deficiency of vitamin D or Ca2+ .
RicketsVitamin-D Deficiency
Osteomalacia 
Rickets

 Prolonged rickets  compensatory increase in PTH secretion

Extreme resorption of bone (mobilization of Ca2+ from bone to blood)

Causes bone to become progressively weaker
Treatment of rickets
 Supplying adequate Ca2+ & phosphate in the diet
 Administering large amounts of vitamin-D
101
Rickets-Vitamin D Deficiency…

 PTH greatly enhances both Ca2+ & phosphate absorption from the intestines
 This is by increasing the formation of 1,25-dihydroxycholecalciferol from vitamin-D in the kidneys
7-dehydrocholesterol in the skin
UV  light
Fig. Role of PTH in intestinal
absorption of Ca2+
102
PTH Increases Intestinal of Ca2+ & Phosphate Absorption

6.Adrenal gland [AG]
Location
 Suprarenal glands
 Two adrenal glands,
 Each of which weighs about 4 grams,
 Placed at the superior poles of the two Kidneys  suprarenal glands
 Hormones
 AG Composed of 2 distinct parts
1. adrenal medulla (inner] 20%)
 Functionally related to the sympathetic nervous system [SNS]
 Medulla secretes amine E & NE in response to sympathetic stimulation
 These hormones cause almost the same effects as SNS in all parts of the body
2. adrenal cortex (outer zone)
 Secretes steroid hormones collectively called corticosteroids (corticoids).
 These hormones are all synthesized from the steroid cholesterol.
103

104
Cont’d
 Different parts of adrenal gland & their secretion
Cont’d

A. adrenal medulla
 Hormones of Adrenal Medullary Hormones
 Cells in the adrenal medulla synthesize & secrete,
 Epinephrine &
 Norepinephrine.
These hormones bind adrenergic receptors on target cells
They induce the same effects as sympathetic nervous stimulation.
Help the body to prepare for "fight-or-flight" reactions.
105

Action of E & NE
1.On cardiovascular system
Heart (β1): ↑Inotropic activity (contractility)=contraction
↑Chronotropic activity (heart rate)=time
Blood vessels: α1-R = Vasoconstriction
2.On Respiratory system:
β2-R = Bronchodilation
3.On GIT: Inhibit GI activity
4.On CNS : ↑Mental alertnessLeads to nervousness in excess
106

B. adrenal Cortex [AC]
Has 3 Distinct Layers
1. The zona glomerulosa
 A thin outer layer
 Secrets mineralocorticoids (aldosterone)
 Essential to the maintenance of ‘minerals 'of the ECF (Na & K balance) & ECF volume
2. The zona fasciculata
 Secrete the glucocorticoids (cortisol )
 Are steroids & have effects on the metabolism of CHO ,fat & protein
3. The zona reticularis (Gonadocorticoids)
 Are deeper layer of the cortex,
 Secretes the adrenal androgens dehydroepiandrosterone (DHEA)
 Exert minor effects on reproductive function.
 Adrenocortical [AC] secretion is controlled primarily by ACTH from the anterior
pituitary.
107

Cont’d
Corticosteroids from the adrenal cortex includes:
1. Mineralocorticoids
2. Glucocorticoids &
3. Gonadocorticoid [Adrenal androgens DHEAS]
Abnormalities of Adrenal gland Secretion
1. Cushing’s Syndrome hypersecretion of corticosteroids (cortisol)
2. Addison’s Disease hyposecretion of corticosteroids (cortisol & aldosterone)
3. Conn's syndromeexcess secretion of aldosteronedisturbances in salt-water
balance
4. Adreno-genital syndromehyposecrtion of adrenal androgen
5. Pheo-chromocytomais tumor of adrenal medulla which causes
hypersecretion of E & NEleads to Hypertension [BP]
108

1.The zona glomerulosa
Functions,
 These cells are responsible for secreting aldosterone [Aldo].
 Aldosterone ↑ the reabsorption of Na+ & removal of K+ & H+ from the kidney tubules.
 The secretion of these cells is controlled mainly by Ang II & K+
 Both of them stimulate aldosterone secretion.
Hypersecretion of Aldo,
 Excess aldosterone increases ECF volume & ABP
 Cause a serious in the plasma K+ concentration hypokalemia.
Hyposecretion of Aldo,
 If low , large amounts of salt (like NaCl) will lost in the urine.
 It results in severe ECF depletion & low blood volume, leading to circulatory shock.
 ECF K+ & H+ concentration can rise far above normal ,blood acidosis & hyperkalemia.
109

 4 factors play essential roles in the regulation of aldosterone.
Aldosterone secretion will when:
1. K+ concentration in the ECF
2. Angiotensin II
3. ACTH from the anterior pituitary gland &
4. Na ion conc/n in the ECF
110
Cont’d

2. The zona reticularis (inner)
Hormone
Adrenal Androgens
 It is male sex hormone.
 It also exert mild effects in the female (responsible for sex drive )
 Some of the adrenal androgens can converted to testosterone & estrogens.
Function of adrenal androgen [AA]:
 Initiate the development of 2ry-sexual characteristics includes:
 Enlargement of genital organs
 Voice change
 Growth of hairs in the axillary & Pubital areas
 But the concentration of AA is so low & its effect is almost insignificant.
 Androgen is high in the Testis.
111
2. The zona reticularis (inner)

3.The zona fasciculata
Functions
 Is the middle & widest layer,
 Constitutes about 75 % of the adrenal cortex &
 Secretes mainly cortisol but also lesser adrenal androgens & estrogens.
 Secretion controlled by (ACTH) from the pituitary gland.
112

1.On Carbohydrate Metabolism
1. Stimulation of Gluconeogenesis by the liver
2. Decreased Glucose Utilization by Cells.
 Elevated Blood Glucose Concentration
 Both the of its effects cause the blood glucose concentrations to rise.
 This high levels of cortisol reduce the sensitivity of tissues to the
stimulatory effects of insulin on glucose uptake & utilization.
 The condition is called adrenal diabetes.
113
Physiological effects cortisol

Cortisol…
2. Effects of Cortisol on Protein Metabolism
 Increased catabolism of protein (decreased protein synthesis)
 Cortisol promotes amino acid mobilization from muscle.
3.Effects of Cortisol on Fat Metabolism
A. Mobilization of Fatty Acids [FA]
 Cortisol promotes mobilization of FA from adipose tissue.
 This increases the concentration of free FA in the plasma, which also
increases their utilization for energy.
B. Obesity Caused by Excess Cortisol.
 Excess cortisol secretion develop abnormal type of obesity, with excess
deposition of fat in the chest & head regions of the body

 Giving a buffalo-like torso (trunk, chest, upper body) & a rounded “moon face.”
114

Cortisol…
4.Cortisol is Important in Resisting Inflammation
 It has anti-inflammatory effects [Anti-allergic Or Anti-stress]
 It suppresses (block) inflammatory reactions by
 Stabilizes lysosomal membrane
 Inhibits formation of inflammatory mediators
5. Immunosuppressant action [side effect of cortisol]
 Inhibits activation & proliferation of both T-lymphocytes & B-lymphocytes
 Leads to a general depression of Immunity
115
• Cortisol :as anti-inflammatory , as Anti-allergic Or Anti-stress BUT it has side effects [depress our Immunity]
• Cortisol enhances synthesis & release of catecholamines

Summary for the effect of cortisol on metabolism
A. On CHO metabolism
↑Gluconeogenesis ↑BGC
↓Glucose utilization
B. On Protein metabolism D. Fat metabolism
↑Protein catabolism ↑Lipolysis
↓Protein synthesis ↑Mobilization of fat & deposition to unusual area
↓Amino acid uptake
C. Anti-inflammatory action [Anti-stress]
Regulation of Cortisol Secretion By:
a.ACTH
 Stimulate Cortisol Secretion
b.Stress
 Stress increase secretion of ACTH & Cortisol
116
↑BGC
{Hyperglycemia}

Hypoadrenalism  Addison’s Disease
 Results from failure of the adrenal Cortex to produce aldosterone & cortisol.
Causes
 Autoimmune problem or infection to the gland
 Damage or surgical removal of the gland
117
Disorders
1.Hyposecretion

Mineralocorticoid [aldosterone] deficiency
 Lack of aldosterone secretion
 Hyponatremia/Hypotension ,Hyperkalemia & plasma volume falls (ECF depleted)
 CO decreases
 Acidosis develops BCZ of failure of H ions excretion.
Glucocorticoid [cortisol] deficiency
 Lack of cortisol secretion
 Highly susceptible for different types of stress, & even a mild respiratory
infection can cause death.
Gonadocorticoid [Androgen] deficiency
 Lack of androgen secretion
 Fail secondary sexual characteristics (but insignificant effect)
118
Hypo-secretion…

HyperadrenalismCushing’s Syndrome
 Hypersecretion of glucocorticoids (cortisol)
Clinical features of Cushing’s disease
 Obesity: moon face, buffalo hump (torso), trunkal obesity (enlarged abdomen)
 Hyperglycemia: adrenal diabetes mellitus [DM]
 Poor (delayed) wound healing, susceptible to infection
119
2.Hypersecretion

 Excessive secretion of aldosterone
 Two types:
1.Primary aldosteronism (Conn’s syndrome)
Tumor of the zona glomerulosa cells secretes large amounts of aldosterone.
2.Secondary aldosteronism
↑↑Ang-II ↑↑ Aldosterone
Clinical features:
Hypertension & hypokalaemia
Aldosteronism =excessive secretion of aldosterone
120
Excessive secretion of aldosterone

122
122
Gland/Tissue Hormones Major functions Chemical
structure
Summary…

123
123
Cont’d
Summary…
Gland/Tissue Hormones Major functions Chemical structure

124
124
Gland/Tissue Hormones Major functions Chemical
structure
Cont’d
Summary…

Unit=9=Endocrine System=Anesthesia students 2025 AAU

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