Anterior and Posterio Pituitary Gland

Download (0)

Full text

(1)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

ANATOMY

 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

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 (10-30%) b. Basophils  Gonadotrophs – FSH and LH (20%)

 Corticotrophs – ACTH and MSH (10%)

 Thyrotrophs – TSH (5%)

2. Chromophobes

o Degranulated secretory 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

PHYSIOLOGY B: PITUITARY GLAND

DRA. GAMBOA

(2)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

 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 Target gland Action

Thyrotropin – releasing hormone (TRH) Anterior Pituitary Stimulates secretion of trophic hormones (TSH) Gonadotrophin – releasing hormone (GnRH) Anterior Pituitary Stimulates secretion of gonadotropes (FSH, LH) Corticotropin – relaeasing hormone (CRH) Anterior Pituitary Stimulates secretion of coticotropes (ACTH) Growth hormone - releasing hormone (GHRH) Anterior Pituiatry Stimulates secretion of somatotropes (GH) Growth hormone – inhibitory hormone (somatostatin) Anterior Pituiatry Inhibits secretion of somatotropes (GH) Prolactin – Inbibiting hormone (PIH) 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

(3)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

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

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)

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:

(4)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

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

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

(5)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

realeasing now the Free Fatty Acids

GH releases Ghrelin

 Ghrelin – is found in the stomach. It increased your appetite

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

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

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

(6)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

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

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

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

(7)

FEU-NRMF INSTITUE OF MEDICINE: PHYSIOLOGY B

SEC 1G

 Hypernatremia

 Increase ECF osmolality

3. Syndrome of Inappropriate Secretion of ADH

- Increase secretion of ADH

- Possibly due to tumors, bronchogenic cancers

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

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

Figure

Updating...

References