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PITUITARY GLAND

Also called as hypophysis Located in sella turcica Connected to hypothalamus by hypophysial stalk Physiologically divisible in 2 parts Anterior pituitary or adenohypophysis Posterior pituitary or neurohypophysis Pars intermedia

EMBRYOLOGICAL ORIGIN

Anterior pituitary from RATHKES POUCH Posterior pituitary from neural tissue outgrowth from hypothalamus

DIFFERENT CELLS OF ANTERIOR PITUITARY

Hypothalamus is the collecting center for information concerning the internal well being of the body and much of this information is used to control secretions of important pituitary hormones.

HYPOTHALAMIC CONTROL OF ANTERIOR PITUITARY

HYPOTHALAMIC-HYPOPHYSIAL PORTAL BLOOD VESSELS

POSTERIOR PITUITARY GLAND

SUPRAOPTIC NUCLEUS PARAVENTRICULAR NUCLEUS Neurohypophysial tract Pituicytes Bulbous knobs

POSTERIOR PITUITARY HORMONES

ANTIDIURETIC HORMONE (ADH) OR VASOPRESSIN formed primarly in supraoptic nuclei OXYTOCIN formed primarly in paraventricular nuclei both hormone are transported in combination with NEUROPHYSINS

PHYSIOLOGICAL FUNCTION OF ADH


KIDNEYS Collecting tubules and ducts become permeable to water only in the presence of ADH MECHANISM OF ACTION 1. ADH attaches with tubular cell membrane receptors V2 receptors. 2. Activates adenylyl cyclase and causes formation of cAMP in tubular cell cytoplasm

cAMP causes phosphorylation of special vesicles and causes these vesicles to insert into apical cell membrane which have highly water permeable pores known as AQUAPORINS

REGULATION OF ADH PRODUCTION

OSMORECEPTORS Modified neuron receptors present in or near hypothalamus and in organum vasculosum in AV wall of 3rd ventricle. when E.C.F becomes too much concentrated, fluid is pulled out of osmoreceptors by osmosis, decreasing its size and sending appropriate nerve signals to hypothalamus and causing release of ADH or vice versa

Effects of ADH on blood vessels

Mechanism of action: Through V1 receptors, activates membrane phospholipid 2nd messenger system

VASOCONSTRICTOR EFFECTS Higher concentration of ADH have more potent effect in causing constriction of arterioles through out the body so increasing arterial pressure thats why it is also called as VASOPRESSIN INCREASING BLOOD VOLUME Atria have stretch receptors that are excited by overfilling, when they are not excited as a result of under filling ,when the blood volume decreases to 15 to 25 %, they send signals to brain to cause release of ADH

OXYTOCIN
MECHANISM IN LACTATION Suckling---sends sensory signals----paraventricular and supraoptic nuclei------release of oxytocin--carried by blood to the breast---causes contraction of myoepithelial cells that form a latticework surrounding alveoli of the mammary gland---milk begins to flow MILK LETDOWN OR MILK EJECTION Acts through phospholipase C 2nd messenger system

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CONTRACTION OF PREGNANT UTERUS Oxytocin powerfully stimulates especially towards the end of gestation. This is supported by In hypophysectomized animal, duration of labor is prolonged Its amount increases especially during last stage of labor Stimulation of pregnant cervix in animal causes increased secretion of oxytocin

GROWTH HORMONE

Somatotropic hormone OR Somatotropin In adults normal concentration is 1.6 to 3 ng/ml In child or adolescent is about 6 ng/ml

FUNCTION OF GROWTH HORMONE


PROTEIN Promotes anabolism Decreased catabolism FAT KETOGENIC CARBOHYDRATE DIABETOGENIC


1.

BONE AND CARTILAGE GROWTH


Increased protein deposition by chondrocytic and osteogenic cells Increased rate of reproduction of these cells Conversion of chondrocytes into osteogenic cells so causing deposition of new bone

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MECHANISM BEFORE ADULT AGE new cartilage at epiphyseal end so increased length AFTER ADULT AGE Increased thickness by osteoblasts

SOMATOMEDINS

Liver, cartilage and many other tissues Insulin-like growth factor 1(IGF-1) OR Somatomedin C causes growth after birth Insulin-like growth factor II (IGF-II) causes growth of fetus before birth Growth hormone has half time in blood is less than 20 minutes Somatomedin C has half time of about 20 hours

REGULATION OF GROWTH HORMONE SECRETION

HYPOTHALAMUS AND GROWTH HORMONE SECRETION

GHRH acts by adenylyl cyclase 2nd messenger system having short term and long term effect

Abnormalities of growth hormone


Catch-up growth Following illness or starvation in children, growth rate is more than normal PANHYPOPITUITARISM Decreased secretion of all anterior pituitary hormones A. During childhood or DWARFISM All the physical parts of the body do develop but the rate of development is greatly decreased and will not develop adult sexual functions

TYPES OF DWARFISM 1. Only growth hormone deficient 2. African Pygmy and Levi-Lorain dwarf Somatomedin C hereditary deficient 3. Achondroplasia Mutation in gene that code for Fibroblast Growth Factor Receptor 3 presents with short limbs with a normal trunk

TREATMENT
Human growth hormone synthesized by Escherichia Coli by DNA recombinant technology

B. PANHYPOPITUITARISM IN ADULTS
Causes are 1. Craniopharyngiomas 2. Chromophobe tumor 3. Thrombosis of pituitary blood vessels Lethargic, gaining weight and lost all sexual functions

ACIDOPHILIC TUMOR

Before adolescence or Gigantism


before epiphyseal fusion excessive growth hormone causes a giant with Upto 8 feet tall Hyperglycemia Degeneration of beta cells of the islets of langerhans

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TREATMENT

Microsurgical removal or irradiation

After adolescence or ACROMEGALY Cannot grow taller but bones become thicker and soft tissues continue to grow and presents with 1. Protrusion of lower jaw 2. Forehead slants 3. Nose increases 4. Size of feet and fingers increases 5. Hunched back or Kyphosis 6. Soft tissues like tongue, liver, kidneys becomes greatly enlarged

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