Anterior and Posterio Pituitary Gland

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

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PHYSIOLOGY B: PITUITARY GLAND DRA. GAMBOA July 29.2015

ANATOMY

MAJOR TYPE OF CELLS IN THE ANTERIOR LOBE 1. Chromophils o Granulated secretory cells 2 types of Chromophils a. Acidophils – 80%, majority  Somatotrophs – growth hormone (50%)  Lactotrophs – prolactin (1030%) b. Basophils  Gonadotrophs – FSH and LH (20%)  Corticotrophs – ACTH and MSH (10%)  Thyrotrophs – TSH (5%) 2. Chromophobes o Degranulated secretory cells

 Also known as: hypophysis  It’s a small gland with a diameter of 1cm and weighs about 0.5 to 1 gram  Situated at the sella turcica  Connected to the hypothalamus via the Pituitary stalk Pituitary Land has 2 lobes 1. Anterior Pituitary (Adenohypophysis)  Originates embriologically through the invagination of the pharyngeal epithelium or Rathke’s pouch 2. Posterior Pituitary (Neurohypohysis)  Originates from the neural tissue outgrowth from the hypothalamus  Contains large glial cells

POSTERIOR PITUITARY HORMONES  The posterior pituitary gland does not produce any hormone. It only stores the hormones that are secreted by the hypothalamus particularly in the magnocellular neurons (supraoptic and paraventricular). 2 hormones secreted by the posterior pituitary gland: 1. Anti-diuretic hormone – produced in the supraoptic nuclei of the hypothalamus 2. Oxytocin – produced in the paraventricular nuclei of the hypothalamus  This hormones are transported from the hypothalamus to the posterior pituitary gland via axoplasm neuron nerve fibers  The section of posterior pituitary is controlled by the nerve signals that originate from the hypothalamus and terminate in the posterior pituitary

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FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

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 There are no releasing and inhibiting hormones ANJTERIOR PITUITARY HORMONES  The sections in controlled by: o Hypothalamic Releasing Hormones  Released from the hypothalamus and goes to the target endrocrine glands o Hypothalamic Inhibitory Hormones Hormones Thyrotropin – releasing hormone (TRH)

Target gland Anterior Pituitary

Gonadotrophin – releasing hormone (GnRH) Corticotropin – relaeasing hormone (CRH)

Anterior Pituitary

Growth hormone releasing hormone (GHRH) Growth hormone – inhibitory hormone (somatostatin) Prolactin – Inbibiting hormone (PIH)

Anterior Pituitary

Anterior Pituiatry

Action Stimulates secretion of trophic hormones (TSH) Stimulates secretion of gonadotropes (FSH, LH) Stimulates secretion of coticotropes (ACTH) Stimulates secretion of somatotropes (GH)

Anterior Pituiatry

Inhibits secretion of somatotropes (GH)

Anterior Pituiatry

Inhibits synthesis and secretion of lactotropes (prolactin)

ENDOCRINE AXIS Three levels of Endocrine Axis: 1. Hypothalamus 2. Pituitary Gland 3. Peripheral Endocrine Gland

ADRENOCORTICOTROPIC HORMONE (ACTH)  Produced by corticotropes  Stimulates the release of some adrenocortical hormone in the adrenal cortex  Affects 2 zones in the adrenal cortex: Zona Fasiculata (Cortisol) and Zona Reticularis (Androgen)  Affects metabolism of glucose, proteins and fats  Has diurinal pattern with a peak in early morning and a valley in the later afternoon  Secretion of CRH and ACTH is pulsatile Regulators:  Stress (neurogenic: fear and systemic: infection) – stimulates adrenal cortex to release cortisol Hypothalamus -> release CRH -> stimulate pituitary gland -> release ACTH -> stimulates adrenal cortex -> release cortisol Effects:  Decrease in the blood glucose  Increasing the inflammatory response

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THYROID STIMULATING HORMONE (TSH) One of the pituitary glycoprotein hormones (TSH, LH and FSH) Thyrotropes – regulates thyroid function by secreting the hormone thyroid stimulating hormone Release during diurinal rhythm o Highest in overnight o Lowest in dinnertime It is a hetero dimer composed of alpha subunit, called the alpha-glycoprotein subunit and beta subunit o Alpha subunit is common to TSH, FSH and LH o Beta subunit is specific

Hypothalamic-Pituitary-Thyroid Axis Hypothalamus -> release TRH -> stimulates the anterior pituitary -> release TSH -> stimulate the thyroid gland -> release thyroid hormones T3, T4 Effect  Thyrotropin control the rate of section of T3 and T4 which control the rate of most intracellular reactions in the body If there is a release of T4, peripherally it will be converted into T3. Target tissues: Heart, liver, gonads, CNS. If there is an increase T3 and T4 there will be a negative feedback to the pituitary gland and the hypothalamus  TSH also has a strong tropic effect and stimulates hyperthrophy, hyperplasia, and survival of thyroid epithelial cells GONADOTROPIN RELEASING HORMONE (GnRH)  Gonadotrope secretes FSH and LH  Secreted in a pulsatile manner

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Secretions: 1 pulse per hour – increase in LH secretion (luteal phase) 1 pulse in 3 hours – increase in FSH secretion (follicular phase) Continuous infusion – down regulation/decrease of receptors

Hypothalamic-Pituitary-Gonadal Axis Hypothalamus -> release GnRH (LHRH) -> stimulates anterior pituitary -> release of LH and FSH -> stimulates gonads (ovaries and testis) -> release of estrogen, progesterone, testosterone, inhibin  The FSH will stimulates the ovaries/testis to produce Inhibin  Increase levels of Inhibin will cause a negative feedback to the hypothalamus and pituitary gland  In women, progesterone and testosterone has a negative feedback on the gonadotropic function at the level of hypothalamus and pituitary Estrogen levels  A low dose of estrogen – negative feedback on FSH and LH secretion  High estrogen levels – maintained for 3 days cause a surge in LH (ovulation will occur) and to a lesser extent, FSH secretion (positive feedback)

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PROLACTIN Produced by Lactotrope Structurally related to GH and HPL (Human Placental Lactogen) Acts on non-endocrine cells: mammary gland It is normally under tonic inhibition by the hypothalamus: Dopamine It is one of the many hormones released in response to stress Stimulated by TRH and PRH

Actions:  Physiological development of the breast and

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FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B milk production  Increase prolactin will increase dopamine thus inhibiting GnRH. This will decrease FSH and LH and will inhibit ovulation  Inhibits spermatogenesis via decrease in GnRH Factors that increase Prolactin Secretion o Breastfeeding o Dopamine Antagonist o Sleep o Strees o Estrogen

Factors that decreases the Prolactin Secretion o Dopamine o Dopamine Agonist o Somatostatin o Increase prolactin will cause a negative feedback Abnomalities of Prolactin Secretion: 1. Hypoprolactinemia - Failure to lactate 2. Hyperprolactinemia - Galactorrhea - Inhibition of GnRH will cause amenorrhea that will cause failure to ovulate - A decrease in testosterone will cause a loss of potency and libido GROWTH HOROMONE  Produced by somatotropes  Also called as somatotrophic hormone or somatotropin  Half-life: 6-20mins  Plasma lever is higher in infants and children than in adults.  Has diurinal rhythm: peak is in morning before awakening and lowest during the day  Secretion is pulsatile  One of the stress hormone  Also released during stress

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Hypothalamus -> release GHRH -> stimulated the anterior pituitary -> release of GH -> targets: bones, tissues, muscles and the liver Metabolic Effects of Growth hormone: 1. Anabolic o Stimulates transport of amino acids into the cell thus increasing cell CHON which will be used information of proteins and represses proteolysis 2. Diabetogenic o Inhibits utilization of free fatty acids o Increase insulin secretion -> beta cells exhaustions -> insulin resistance 3. Ketogenic o Lipolysis -> increase breakdown of stored fat -> increase free fatty acids ->ketosis o Increase acetoacetic acid in the liver Direct Effects of Growth Hormone: 1. Decrease glucose uptake and utilization by the cells 2. Increase lipolysis 3. Increase protein synthesis in muscle cells thus increasing the lean body mass 4. Production of IGF-1 in the liver Insulin-like growth factor type 1 (IGF-1)  Stimulate uptake of amino acid in the target cells that promotes protein synthesis thus promoting linear growth  Increase protein synthesis in muscle cells will increase body mass  Increase protein synthesis in most organs will increase organ size Effect on Adipose tissue  Stimulates lipolysis – breakdown of stored fat

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FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B realeasing now the Free Fatty Acids GH releases Ghrelin  Ghrelin – is found in the stomach. It increased your appetite

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ABNORMALITIES OF THE PITUITARY GLAND 1. Panhypopituitarism - Affects both anterior and posterior pituitary gland - Decrease secretion of all anterior pituitary hormones - It can be: congenital, occurs suddenly or slowly at any time during life, results from a pituitary tumor A panhypopituitarism in adult - Conditions could be: craniopharyngiomas/chromophobe tumor - General Effects: hypothyroidism, decrease production of glucocorticoid, suppressed secretion of gonadotropic hormones

GH secretion is increased by: o Decrease blood glucose (hypoglycemia) – most potent stimulator o Decrease blood free fatty acid o Starvation or fasting o Ghrelin o Protein Deficiency o Trauma, stress, excitement o Exercise o Testosterone o Estrogen o Deep Sleep (stage II and IV) o GHRH

GH secretion is decreased by: o GHIH – Somatostatin o Increased somatomedin o Obesity o Hyperglycemia o Aging o Increased blood Free Fatty acid o Exogenous GH

2. Frolich’s Syndrome - Adipogenitalis syndrome (involves hypothalamus and pituitary gland) Adiposogenital Dystrophy - Usually associated with tumours of the hypothalamus causing increased appetite and depressed secretion of gonadotropin - Rare childhood metabolic disorder characterized by: obesity, growth retardation and retarded development of the genital organs. 3. Simmond’s Disease - Destruction of hypothalamus and pituitary gland 4. Sheehan’s Syndrome - Destruction of adenohypophysis during pregnancy due to massive bleeding thus causing necrosis of the pituitary gland ABNORMALITIES ASSOCIATED WITH GROWTH HORMONE Dwarfism  Pre-pubertal GH deficiency  Generalized deficiency of anterior pituitary

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secretion Well-proportional Does not pass through puberty No hypothyroidism No mental retardation Could have sexual infantilism Cute dwarf

Other Dwarfism 1. Laron Dwarfism - GH insensitivity due to a defect in GH receptors and a marked decrease in IGF-1 2. African Pygmies - Rate of GH secretion is normal or high but IGF-1fails to increase at the time of puberty 3. Glucocorticoid excess 4. Cretinism - Thyroid hormone deficiency - Ugly dwarf Excess in Growth Hormone 1. Gigantism - Excessive GH secretion before adolescence -> giant - Full blown diabetes mellitus -> increase blood glucose level (hyperglycemia) 2. Acromegaly - Acidophilic tumors occur after adolescence - Bone can become thicker, soft tissues can continue to grow - Enlargement of hands and feet - Course facial features - Visceralomegaly (tongue, liver, kidney) - Skin thickening

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ANTI-DIURETIC HORMONE (ADH) Short polypeptide, 9 amino acid residue Uses the following receptors o V1a – vasoconstrictive effects o V2 – antidiuretic effects Half-life = 15-20mins Essential for water balance Affects facultative water reabsorption in the

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kidneys (DCT nad CD) Excitatory Stimuli for ADH Release o Increased ECF osmolality o Hypotension o Pain o Emotion, Stress o Exercise o Warm/Hot Environment o Standing o Angiotensin o Nicotine, Clofibrate, Carbamazipine Decrease H20 -> increase ECF osmolality -> increase secretion of ADH -> increase H20 permeability in DCT and CD -> decrease urine volume, increase urine tonicity, decrease ECF osmolality to normal Inhibitory Factors for ADH Release o Decrease ECF osmolality o Overhydration o Hypertension o Hypervolemia o Alcohol intake o Cold/cool environment Excess body H20 -> decrease osmolality -> inhibition of ADH secretion -> decrease H2O reabsorption in DCT and CD -> increase urine volume, decrease urine tonicity and ECF osmolality increases to normal

DISORDERS OF ADH SECRETION 1. Central Diabetes Insipidus - Decrease ADH secretion 2. Nephrogenic Diabetes Insipidus Absence of receptors for ADH in the DCT and CD Clinical Features:    

Polyuria Polydipsia Hypotension Dilute Urine

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FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B  Hypernatremia  Increase ECF osmolality 3. Syndrome of Inappropriate Secretion of ADH - Increase secretion of ADH - Possibly due to tumors, bronchogenic cancers

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Positive Feedback Loop Stimulus: baby sucking the nipples -> suckling sends impulse to your hypothalamus -> produce oxytocin -> secrete in the posterior pituitary ->hypothalamus will signal posterior pituitary to release oxytocin -> oxytocin will be released into the blood stream -> stimulate milk ejection from the mammary gland -> milk is released into the baby

Clinical Features  Water retention and weight gain  Edema  Hypertension  Serum dilution OXYTOCIN  Increased oxytocin will stimulate estrogen that will dominates uterus to contract and initiate labor  Orgasm will stimulate oxytocin release thus contracting uterus to facilitate transport of sperm  Suckling the nipple Actions of Oxytocin 1. Contraction of the myoepithelial cells in the mammy glands - Milk is forced from the alveoli into the ducts and delivered to the infant - Mechanism: Milk letdown or Milk Ejection 2. Contraction of the uterus - During pregnancy the number of oxytocin receptors increases as parturition approaches

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