• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Sherwood 18
 

Sherwood 18

on

  • 1,098 views

 

Statistics

Views

Total Views
1,098
Views on SlideShare
1,098
Embed Views
0

Actions

Likes
0
Downloads
14
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Sherwood 18 Sherwood 18 Presentation Transcript

    • Chapter 18 The Central Endocrine Glands Human Physiology by Lauralee Sherwood ©2007 Brooks/Cole-Thomson Learning
    • Outline • General Principles of Endocrinology – Free vs. bound, disorders, receptors • Hypothalamus and pituitary – Relationship – Anterior pituitary – Posterior pituitary • Endocrine control of growth • Pineal gland and circadian rhythms
    • GENERAL PRINCIPLES OF ENDOCRINOLOGY • Hormones exert a variety of regulatory effects throughout the body. • The effective plasma concentration of a hormone is normally regulated by changes in its rate of secretion. • The effective plasma concentration of a hormone is influenced by its transport, metabolism, and excretion. • Endocrine disorders result from hormone excess or deficiency or decreased target-cell responsiveness. • The responsiveness of a target cell can be varied by regulating the number of hormone-specific receptors.
    • Pineal Solely endocrine function Mixed function Hypothalamus Complete function uncertain Pituitary *Know* Parathyroid Hormones Thyroid function regulation Thymus transduction Heart Testes in male Stomach Adrenal gland Pancreas Duodenum Kidney Skin Ovaries in female Placenta in pregnant female Fig. 18-1, p. 654
    • Table 18-2a, p. 659
    • Table 18-2b, p. 660
    • Table 18-2c, p. 660
    • Table 18-2d, p. 661
    • Table 18-2e, p. 661
    • Hormones • Two distinct groups of hormones based on their solubility properties – Hydrophilic hormones (Proteins, peptides) • Highly water soluble • Low lipid solubility – Lipophilic hormones (Steroids) • High lipid solubility • Poorly soluble in water • Peptides/catecholamines/iodinated tyrosines
    • Fig. 4-23, p. 116
    • Fig. 4-22, p. 115
    • Fig. 4-26, p. 122
    • NH2 NH2 COOH COOH S S S A-chain S S S B-chain A chain and B-chain C- peptide Fig 15-4, pg 456
    • Tyrosine Growth hormone Monoiodotyrosine (MIT) Diiodotyrosine (DIT) T4 (thyroxine) Serotonin Insulin T3 (c) 2003 Brooks/Cole - Thomson Learning
    • Fig. 4-24, p. 118
    • Fig. 4-25, p. 119
    • Endocrine System • Overall functions – Regulate organic metabolism and H2O and electrolyte balance (think of resting potentials) – Induce adaptive changes to help body cope with stressful situations (what is stress?) – Promote smooth, sequential growth and development (hypo/hyper) – Control reproduction (birth control/agriculture) – Regulate red blood cell production (EPO) – Along with autonomic nervous system, control and integrate both circulation and the digestion and absorption of food
    • Tropic Hormones • Regulates hormone secretion by another endocrine gland • Stimulates and maintains their endocrine target tissues • Example – Thyroid-stimulating hormone (TSH) secreted from anterior pituitary stimulates thyroid hormone secretion by thyroid gland • Also maintains structural integrity of thyroid gland
    • Vascular Link Between the Hypothalamus and Anterior Pituitary PIF/PRF GnRH TRH CRF GHRH/somatostatin Gonadotropic Thyroid- Prolactin hormones stimulating ACTH Growth (FSH and LH) hormone hormone Two methods of transport Portal System = connects two secondary capillary beds Neurosecretory = from an axon
    • Hormones • Plasma concentration of each hormone is normally controlled by regulated changes in rate of hormone secretion • Direct regulatory inputs that influence secretory output of endocrine cells – Neural input – Input from another hormone • Effective plasma concentration also influenced by – Rate of removal from blood by metabolic inactivation and excretion – Rate of activation or its extent of binding to plasma proteins – Being bound or free. Many hormones are not transported in their active form. They can be bound to a carrier or chemically modified
    • Fig. 18-2, p. 655
    • Fig. 18-3, p. 656
    • N = noon M = midnight Light Dark Fig. 18-4, p. 656
    • Hormone Influence at Target Cell • Hormone can influence activity of another hormone at given target cell in one of three ways – Permissiveness • One hormone must be present in adequate amounts for full exertion of another hormone’s effect – Synergism • Occurs when actions of several hormones are complimentary • Combined effect is greater than the sum of their separate effects – Antagonism • Occurs when one hormone causes loss of another hormone’s receptors • Reduces effectiveness of second hormone
    • Fig. 4-21, p. 112
    • Endocrine Control of Growth • Growth depends on growth hormone but is influenced by other factors as well – Genetic determination of an individual’s maximum growth capacity – An adequate diet – Freedom from chronic disease and stressful environmental conditions – Normal levels of growth-influencing hormones • Including insulin, thyroid and steroid hormones
    • Fig. 18-12, p. 673
    • Growth Rate • Not continuous • Factors responsible for promoting growth are not the same throughout growth period • Fetal growth – Promoted largely by hormones from placenta – GH plays no role in fetal development • Postnatal growth spurt – Displayed during first two years of life • Pubertal growth spurt – Occurs during adolescence
    • Normal Growth Curve
    • Growth Hormone • Primarily promotes growth indirectly by stimulating liver’s production of somatomedins – Primary somatomedin is insulin-like growth factor (IGF-1) • Acts directly on bone and soft tissues to bring about most growth-promoting actions • Stimulates protein synthesis, cell division, and lengthening and thickening of bones • Inhibits apoptosis • Exerts metabolic effects not related to growth – Increases fatty acid levels in blood by enhancing breakdown of triglyceride fat stored in adipose tissue – Increases blood glucose levels by decreasing glucose uptake by muscles
    • Fig. 18-11, p. 671
    • Articular cartilage Bone of epiphysis Epiphyseal plate Bone of diaphysis Cartilage Marrow cavity Calcified cartilage Bone Fig. 18-11a, p. 671
    • Cartilage Bone of epiphysis Calcified cartilage Resting Bone chondrocytes Chondrocytes undergoing Causes cell division thickening Epiphyseal plate of Older chondrocytes epiphyseal enlarging plate Calcification of extracellular matrix (entrapped chondrocytes die) Dead chondrocytes cleared away by osteoclasts Diaphysis Osteoblasts swarming up from diaphysis and depositing bone over persisting remnants of disintegrating cartilage Fig. 18-11b, p. 671
    • Endocrine Dysfunction • Can arise from a variety of factors • Most commonly result from abnormal plasma concentrations of a hormone caused by inappropriate rates of secretion – Hyposecretion • Too little hormone is secreted – Hypersecretion • Too much hormone is secreted
    • Hyposecretion • Primary hyposecretion – Too little hormone is secreted due to abnormality within gland – Causes • Genetic • Dietary • Chemical or toxic • Immunologic • Other disease processes such as cancer • Iatrogenic • Idiopathic (spontaneously) • Secondary hyposecretion – Gland is normal but too little hormone is secreted due to deficiency of its tropic hormone
    • Hypersecretion • Causes – Tumors that ignore normal regulatory input and continuously secrete excess hormone – Immunologic factors • Primary hypersecretion – Too much hormone is secreted due to abnormality within gland • Secondary hypersecretion – Excessive stimulation from outside the gland causes oversecretion
    • Growth Hormone Abnormalities • Growth hormone deficiency – Due to pituitary defect or hypothalamic dysfunction – Hyposecretion of GH in child is one cause of dwarfism – Deficiency in adults produces relatively few symptoms • Growth hormone excess – Most often caused by tumor of GH-producing cells of anterior pituitary – Symptoms depend on age of individual when abnormal secretion begins • Gigantism – Caused by overproduction of GH in childhood before epiphyseal plates close • Acromegaly – Occurs when GH hypersecretion occurs after adolescence
    • The world's tallest man, Bao Xishun, who stands 2.36 meters (7.9 feet), shakes hands with He Pingping, who only measures 73 centimeters (2.4 feet),in Baotou, China's Inner Mongolia Autonomous Region Friday, July 13, 2007. Nineteen-year-old He is applying for the Guinness World Record as the world's shortest man. (AP Photo) CHINA OUT
    • Fig. 18-14, p. 675
    • Growth • Other hormones besides growth hormone are essential for normal growth – Thyroid hormone • Growth severely stunted in hypothyroid children • Hypersecretion does not cause excessive growth – Insulin • Deficiency often blocks growth • Hyperinsulinism often spurs excessive growth – Androgens • Play role in pubertal growth spurt, stimulate protein synthesis in many organs • Effects depend on presence of GH – Estrogens • Effects of estrogen on growth prior to bone maturation are not well understood poorly