Anatomy

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Chapter 18

• Anatomy Physiology
• Fifth Edition
• Seeley/Stephens/Tate
• (c) The McGraw-Hill Companies, Inc.

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• Review of the mechanisms of hormonal action
• The action of hormone is usually by activation of
  cytosolic enzymes.
• But, first, the hormones identify the target
  cells by the receptors on the membrane
  (epinephrine, NE, peptide hormones) or in the
  cytoplasm (steroid hormones) or the nucleus (
  thyroid hormones).
• The hormones which attack the target receptors on
  the membrane do not usually permeate through the
  membrane. These are first messengers.
• The first messenger binds the receptor on the
  membrane and triggers the release of the second
  messenger.

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• Hormone-receptor-release of cyclic AMP-activation
  of adenylate cyclase ATP becomes cyclic-AMP.
• Cyclic AMP can activate enzymes specific to a
  cell.
• One hormone can also have an effect on many
  different types of cells.
• Other second messengers are Ca and c-GMP.
• Thyroid and steroid hormones have effects
  directly on the nucleus or indirectly through
  cytosol.
• These hormones affect protein synthesis e.g.
  anabolic steroid hormone.

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• Control of Endocrine Activity
• The regulation of endocrine activity with the
  hypothalamus is a good example of how the nervous
  system and endocrine system integrate.
• In addition, the activity of endocrine cells may
  be in response to its environment by negative
  feedback.
• For ex
• Circulating Ca levels goes down- parathyroid
  hormone is released target cell elevates Ca
  level- increased Ca level- releases calcitonin
  lowered Ca level.

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• The Pituitary Gland
• This small hypophysis (pituitary gland)
• Located under the hypothalamus, excretes 9 major
  peptides hormones which are regulated by
  hypothalamus and exhibits profound effects on
  many tissues and organs.
• The structure
• 1 cm in diameter
• 0.5 1.0 g
• Sits on the sella turcica of the sphenoid bone
  connected to
• hypothalamus through Infundibulum.
• Divided into (18.2)
• Posterior Pituitary (neurohypophysis) lobe
• Anterior Pituitary (adenohypophysis) lobe

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• Posterior Pituitary
• Developmentally it is an extension of the brain.
• Releases neurohormones.
• Anterior Pituitary
• Developmentally traces back to the oral cavity
  called Rathkes pouch.
• Divided into three distinctive areas
• The pars tuberalis
• The pars distalis
• The pars intermedia
• Release regular hormones

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• Regulation of Pituitary by Hypothalamus (18.3)
• In the region where the pituitary connects with
  the hypothalamus and the anterior pituitary,
  there are two capillary networks
• Hypothalamohypophyseal portal system as the
  primary capillary network.
• Secondary capillary network in the anterior
  pituitary.
• The neurohormone released from the hypothalamus
  enter the primary capillary.
• The hormones are carried into the secondary
  capillary and are released into anterior
  pituitary.
• These hormones may either increase or inhibit the
  excretion of hormones from the anterior
  pituitary.
• Hormones from the anterior pituitary, then will
  be carried by the circulatory system.
• Note the number of neurohormones released from
  the hypothalamus that effect the anterior
  pituitary gland (Table 18.1). Most of them are
  small peptides.

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• As for the posterior pituitary, there is no
  connecting portal system.
• The neurosecretory cells from the hypothalamus
  extend to the posterior pituitary through
  hypothalamohypophyseal tract.
• The neurohormones will be released into the
  portal system of the posterior pituitary.

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• Hormones of the Pituitary Glands
• They are mostly peptides, proteins or
  glycoproteins.
• Posterior pituitary hormones
• The posterior pituitary stores and releases two
  polypeptide neurohormones formed in the
  hypothalamus and transmitted through
  hypothalamohypophyseal nerve tract.
• Antidiuretic hormone (ADH) prevents production
  of large quantity of urine (kidneys) It is also
  vasopressin and constricts blood vessels.
• Oxytocin stimulates the smooth muscle cells of
  the uterus. Important for expulsion of fetus,
  also ejection of milk during lactation, and
  during intercourse.
• Does the posterior pituitary gland make its own
  hormone?

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• Anterior Pituitary Hormones
• Hormones secretion is regulated by the
  neurohormones from the hypothalamus.
• Growth hormone (protein) targets may cells and
  over all increase in metabolism.
• Thyroid-stimulating hormone (glycoprotein)
  targets the thyroid gland and increases thyroid
  hormone release.
• Adrenocorticotropic hormone (peptide) targets
  the adrenal cortex and increase glucocorticoid
  hormone secretion.
• Note the others in Table 18.2

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• Tropic hormones are hormones which stimulate or
  regulate the secretion of hormones from other
  endocrine glands.
• Among the anterior pituitary hormones
• Thyroid-stimulating hormone (TSH) is a
  glycoprotein targets the thyroid gland and
  increase thyroid hormone (TH) release.
• Adrenocorticotropic hormone (ACTH) is a peptide
  targets the adrenal cortex and increase
  glucocorticoids hormone secretion.

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• The Thyroid Gland
• Located at the upper portion of the trachea.
• Structure
• Consist of two lobes connected by a narrow band
  of tissue called isthmus.
• Hormones of the thyroid
• The follicular cells of the thyroid gland release
  derivates of tyrosine to which three or four
  iodine molecules are attached, thus,
• triiodothyronine (T3) makes up 10
• Tetraiodothyronine (T4) makes up 90, also
  known as thyroxine.
• Parafollicular cells release calcitonin.

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• Synthesis and release of thyroid hormones
• Thyroid hormone synthesis requires thyroid
  stimulating hormone (TSH) from the anterior
  pituitary and iodine. For further details you may
  refer to figure 18.8.
• Secretion of thyroid hormone is initiated by TSH.
  (18.9) but it stares with the release of TRH from
  the hypothalamus, to the hypothalamohypophyseal
  portal system of the anterior pituitary, where
  TSH is released. TSH reaches the thyroid gland
  through the circulatory system and regulate the
  secretion of T3 and T4.

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• Transporting Thyroid Hormones
• Thyroid hormones are transported through the
  circulatory system bound with thyroxin-binding
  globulin (TBG). The binding helps the half-life
  of the hormones to increase to 1 week in the
  circulatory system. During this period thyroxin
  (T4) may convert to (T3), which is the more
  active form.
• The Targets of Thyroid Hormones
• Thyroid hormones affect many cells, but not
  exactly in the same manner. They affect
  metabolism, growth and maturation. They permeate
  through the membrane and bind with the receptors
  in the nuclei to react with the DNA for protein
  synthesis.
• Thyroid hormone may interact with mitochondria
  and produce more ATP and hence heat production.
• It requires about 1 week for the thyroid hormones
  to take affect.

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• The action of thyroid hormones
• The effects of thyroid hormones are numerous and
  listed in Table 18.4. Some examples are
• Hypersecretion increased metabolic rate, high
  body temperature, weight loss, increased
  appetite, rapid heart rate etc..
• Hyposecretion decreased metabolic rate, low body
  temperature, weight gain, loss of appetite,
  reduced heart rate etc.
• Essential for the normal growth of children.

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• Calcitonin
• Produced from the parafollicular cells.
• Increased level of Ca stimulates the release of
  calcitonin from parafollicular cells.
• Target is bone tissue and deceases osteoclast
  activity, thus increases the life span of
  osteoblast. (negative feedback)
• Therefore, blood calcium levels may be regulated
  with calcitonin.
• Decreases blood levels of calcium.

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• Parathyroid Glands
• The location
• The small packed parathyroid glands are located
  in the posterior part of each lobe of the thyroid
  gland.
• The hormone of the parathyroid gland is a
  peptide.
• Targets and function
• The gland detects blood Ca levels.
• PTH regulates calcium levels and targeted to
  bone, the kidneys and the intestines.
• PTH stimulates, for example
• Osteoclast activity in bone tissue
• Induces Ca reabsorption in the kidneys to
  increase enzyme activity to form vitamin D
• Increased Ca absorption by small intestines.
• Inactive parathyroid glands result in
  hypocalcaemia (low blood Ca)

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• For further homeostasis by PTH you may refer to
  Fig.18.11
• Calcitonin PTH are antagonistic

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• Adrenal Glands
• Location
• The adrenal glands are attached on top of the
  kidney and may be divided, based on the embryonic
  origin, into outer adrenal cortex and inner
  adrenal medulla. (18.12)
• Histology (in the lab)
• Hormones of the Adrenal Medulla
• Two major hormones of amino acids derivatives
• Epinephrine (adrenaline) 80
• Norepinephrine (noradrenaline) 20
• Norepinephrine is a precursor to epinephrine.

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• As shown in Fig 18.13, in the hypothalamus
  stimulation by stress, physical activities, low
  blood glucose levels triggers generation of
  action potential through the sympathetic division
  of its ANS. The stimuli release either N or NE
  from the adrenal medulla.
• The results of stimulation are
• Increased release of glucose from liver
• Increased released of fatty acids from fat store
• Increased heart rate
• Increased constriction of visceral blood vessels
  (inc. blood pressure.)

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• Hormones of the Adrenal Cortex
• Three types mineralocorticoids, glucocorticoids,
  and androgens (Table 18.7)
• These lipid soluble steroids are gradually
  released from the cells as they are made and upon
  binding with specific plasma proteins, they are
  distributed through the circulatory system.
• Their target organs and functions are described
  in Table 18.7.

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• Pancreas
• Location and structure
• Located behind the peritoneum between the greater
  curvature of the stomach and the duodenum
• 15 cm long and weighs 85-100g.
• Histology
• Has both exocrines and endocrines
• The exocrine portion consists of Acini that
  produce pancreatic juice and a duct system.
• The endocrine part consists of pancreatic islets
  (islets of Langerhans) separated into
• Alpha cells (glucagon production)
• Beta cells (insulin production)
• Delta cells (somatostatin)

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• Hormones of the pancreas
• Insulin is a protein, glucagon is a polypeptide,
  and somatostatin is a peptide.
• Insulin produced in beta cells in response to
  rising blood glucose and amino acids. Targets the
  liver, adipose tissue, muscles the hypothalamus.
• Insulin binds to the receptor on the membrane and
  stimulates glucose transport into the cell.
  Glucose, once inside the cell, is metabolized to
  make energy, glycogen, amino acids, proteins,
  fats etc Glucose uptake by the liver (glycogen
  synthesis) and brain cells is independent of
  insulin.

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• Glucagon
• Secreted from alpha cells when blood glucose
  levels fall.
• In the liver, it stimulates glycogenelysis
  (glycogen hydrolysis) and releases glucose into
  circulation.
• In adipose tissue it initiates breaking down of
  fats and releases free fatty acids and ketone
  bodies.
• It also responds to blood amino acids after high
  protein meal.

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• Somatostatin
• Produced in delta cells of islets when blood
  glucose and amino acids rise after a meal.
• It behaves as a paracrine secretion ( chemical
  messenger that diffuses to neighboring target
  cells, I.e.alpha and beta cells.
• Thus modulates their activities.
• Regulation of Pancreatic Hormones
• The level of nutrients in blood.
• ANS also controls insulin secretion.
• See Fig. 18.17 for response to a meal.

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• The Pineal Body
• At the roof of thalamus.
• Produces melatonin and arginine vasotocin.
• Collateral from the visual pathways enter the
  pineal body and effect melatonin production.
• Melatonin is made mostly at night.
• Melatonin (decrease GnRH) and vasotocin
  secretions may act on the gonads to inhibit
  reproductive functions

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• Exert from Clinical Focus on Diabetes Mellitus
• Patients with Diabetes Mellitus have difficulty
  in controlling their blood sugar level. The
  causes are attributed to
• Inability to make insulin by pancreatic islet
  cells. Target cells lack membrane receptor for
  insulin on the cells of target tissues.
• The first type is called insulin dependent
  diabetes mellitus (IDDM), since the patients may
  be treated with insulin, or Type I diabetes.
• It accounts for about 3 of the total diabetes
  population.
• It is assumed that the cause is related to the
  loss of insulin production by pancreatic islets,
  possibly due to an autoimmune disease.
• The patients are primarily children.

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• The second type is called non-insulin dependent
  diabetes mellitus (NIDDM), since insulin does not
  improve the condition of the patients, or Type II
  diabetes.
• It accounts for 97 of the total diabetes
  population.
• The target cells of insulin appear to have
  diminished ability to produce insulin receptors,
  thus the effect of insulin is declined.
• The patients are mostly adults and sometimes the
  disease is referred to as adult on set diabetes.
• Genetic link is suspected.
• (REVIEW CLINICAL FOCUS ON DIABETES)

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The End.