Chapter 18:

The Endocrine System

Primary sources for figures and content:

Marieb, E. N. Human Anatomy & Physiology. 6th ed. San Francisco: Pearson Benjamin Cummings, 2004.

Martini, F. H. Fundamentals of Anatomy & Physiology. 6th ed. San Francisco: Pearson Benjamin Cummings, 2004.

Endocrine System

• Regulates long-term processes:– growth– development– reproduction

Intercellular Communication

1. Direct Communication– Occurs between two cells of the same type through

gap junctions via ions or small solutes2. Paracrine Communication

– Uses chemical messengers to transfer signals between cells in a single tissue

– Messenger = cytokines or local hormones

Intercellular Communication

3. Endocrine Communication– Uses hormones to coordinate cellular activities in

distant portions of the body– Hormones = chemical messengers released from one

tissue and transported in blood to reach target cells in other tissues

– Gradual, coordinated but not immediate4. Synaptic Communication

– Involves neurons releasing neurotransmitter at a synapse close to target

– Immediate but short lived

Mechanisms of Intercellular Communication

Table 18–1

The Endocrine System

• Consists of glands and glandular tissue involved in paracrine and endocrine communication

• Endocrine cells produce secretions released into extracellular fluid enters blood body-wide distribution to find target– Target cell = specific cells that possess receptors

needed to bind and “read” hormonal messages

Figure 18–1

Endocrine System

Endocrine Cells located In:

Hormones

• Can be divided into 3 groups: – amino acid derivatives– peptide hormones – lipid derivatives

Hormones

• Structure1. Amino Acid Derivatives

• Structurally similar to or based on amino acids

• E.g. catecholamines (epinephrine, norepinephrine, dopamine), thyroid hormones, melatonin

Hormones

• Structure2. Peptide Hormones

• Chains of amino acidsA. Peptides

– <200 amino acids– E.g. ADH, oxytocin, GH

B. Glycoproteins– >200 amino acids with carbohydrate side chain– E.g. TSH

Hormones• Structure

3. Lipid DerivativesA. Steroid Hormones

– Structurally similar to/based on cholesterol– E.g. Androgens, Estrogens, Calcitriol

B. Eicosanoids– Derived from arachidonic acid– Not circulating: autocrine or paracrine only– E.g. Leukotrienes: from leukocytes coordinate

inflammation– E.g. Prostaglandins: from mast cells coordinate local

activities (smooth muscle contractions, clotting, etc.)

Figure 18–2

Classes of Hormones

Mechanism of Action

• Hormones circulate in blood contact all cells• Only cause effects in cells with receptors for

hormone called target cells• Receptors present on a cell determines the cell’s

hormonal sensitivity

Hormone stimulus effects in target cells

1. Alter plasma membrane permeability or transmembrane potential by opening/closing ion channels

2. Stimulate synthesis of structural proteins, receptors, regulatory enzymes within cell

3. Activate or deactivate enzymes4. Induce secretory activity5. Stimulate mitosis

Hormone Receptors

• Located on plasma membrane or inside target1. Cell membrane hormone receptors2. Intracellular hormone receptors

Hormone Receptors

1. Cell membrane hormone receptors– Catecholamines, peptide hormones, glycoprotein hormones,

eicosanoids– Bind receptors on cell surface– Indirectly trigger events inside cell via second messengers (cAMP,

Ca++)– 2nd messenger acts as activator, inhibitor, or cofactor for

intracellular enzymes• Enzymes catalyze reactions for cell changes

– Receptor linked to 2nd messenger by G protein (regulatory enzyme complex)

Hormone Receptors

1. Cell membrane hormone receptors– 2nd messenger mechanism results in amplification of

hormone signals• One hormone molecule binds one receptor but can result

in millions of final products

Figure 18–3

G Proteins and Hormone Activity

cAMP Mechanism1. Hormone binds receptor 2. G-protein activated3. Adenylate cyclase

activated4. ATP cAMP5. Kinases activated6. Proteins (enzymes)

phosphorylated7. Enzymes

activated/deactivated

Figure 18–3

G Proteins and Hormone Activity

PIP-Calcium Mechanism1. Hormone binds receptor 2. G-protein activated3. Phospholipase C (PLC)

activated4. Phospholipids (PIP2)

cleaved into diacyglycerol (DAG) and inositol triphosphate (IP3)

5. DAG opens Ca++ channels on membrane

6. IP3 releases Ca++ from ER7. Calcium binds calmodulin8. Enzymes Activated

Hormone Receptors

2. Intracellular hormone receptors– Steroid hormones, thyroid hormones– Result in direct gene activation by hormone– Hormone diffuses across membrane, binds

receptors in cytoplasm or nucleus– Hormone + receptor bind DNA transcription

translation = protein production metabolic enzymes, structural proteins, secretions

Figure 18–4a

Steroid Hormones

Figure 18–4b

Thyroid Hormones

Target cell activation depends on

1. Blood level of hormone2. Relative number of receptors3. Affinity of bond between hormone and

receptor• If hormone levels are excessively high for too

long cells can reduce receptor number or affinity and become non-responsive to a hormone

Distribution and Duration of Hormones

• Circulating hormones either free or bound to carrier/transport proteins

• Free hormones last seconds to minutes– Rapidly broken down by liver, kidney, or plasma

enzymes in blood• Bound hormones last hours to days in blood• Effect at target cell can take seconds to days

depending on mechanism and final effect, but hormone once bound to receptor is broken down quickly

Interaction of Hormones at Target Cells

• Target cells have receptors for multiple hormones• Effects of one hormone can be different depending

on presence or absence of other hormones• Hormone Interactions

1. Antagonistic = hormones oppose each other2. Synergistic = hormones have additive effects3. Permissive = one hormone is needed for the

other to cause its effect

Control of Endocrine Activity

• Synthesis and release of most hormones regulated by negative feedback

Control of Endocrine Activity

• 3 Major Stimuli for Hormone Release1. Hormonal stimuli

• Ion and nutrient levels in blood trigger release• E.g. PTH released when blood Ca++ is low

2. Neural stimuli (autonomic nervous system)• Nerve fibers directly stimulate release• E.g. sympathetic adrenal medulla = epinephrine

release

Control of Endocrine Activity• 3 Major Stimuli for Hormone Release

3. Hormonal stimuli• Hormones stimulate the release of other

hormones• E.g. Releasing hormones of hypothalamus cause

release of hormones from anterior pituitary– Hormone release turned on by stimuli and off by

negative feedback but can be modified by nervous system

KEY CONCEPT

• Hormones coordinate cell, tissue, and organ activities

• Circulate in extracellular fluid and bind to specific receptors

• Hormones modify cellular activities by:– altering membrane permeability– activating or inactivating key enzymes– changing genetic activity

How could you distinguish between a neural response and an endocrine

response on the basis of response time and duration?

A. Neural responses are quicker and longer lasting.

B. Neural responses are slower and longer lasting.

C. Neural responses are quicker and shorter in duration.

D. Neural responses are slower and shorter in duration.

How would the presence of a molecule that blocks adenylate cyclase affect the activity of

a hormone that produces its cellular effects by way of the second messenger cAMP?

A. It would block the action of the hormone.

B. It would enhance the action of the hormone.

C. It would increase sensitivity to the hormone.

D. It would decrease speed of hormonal changes.

What primary factor determines each cell’s hormonal sensitivities?

A. pH of intracellular fluid

B. life cycle phase of cell

C. presence/absence of necessary receptor complex

D. tissue where cell is found

Endocrine Organs

Figure 18–5

1. Hypothalamus

1. Hypothalamus

• Located at base of 3rd ventricle• Master regulatory organ• Integrates nervous and endocrine systems• Three mechanisms of control

1. Secrete regulatory hormones to control secretion from anterior pituitary

- Hormones from anterior pituitary control other endocrine organs

2. Act as endocrine organ Produce ADH and oxytocin3. Has autonomic centers of neural control or adrenal medulla

Neuroendocrine reflex

Figure 18–6

2. Pituitary Gland

2. Pituitary Gland (Hypophysis)

• Hangs inferior to hypothalamus via infundibulum• In sella turcica of sphenoid• Anterior lobe secretes 7 hormones

– Function via cAMP 2nd messenger• Posterior lobe secretes 2 hormones

– Function via cAMP 2nd messenger

Figure 18–7

2. Pituitary Gland

2. Pituitary Gland

A. Anterior lobe (Adenohypophysis)– Glandular tissue– Anterior pituitary hormones are all tropic

hormones • Turn on secretion or support function of other

organs– Secretion of the hormones controlled by releasing

and inhibiting hormones from the hypothalamus

2. Pituitary GlandA. Anterior lobe (Adenohypophysis)

– Hormones of the Anterior Lobe

2. Pituitary Gland

A. Anterior lobe (Adenohypophysis)– Disease of Growth Hormone

• Excess– Usually due to pituitary tumor– Before epiphyseal closure = gigantism– After = acromegaly, excessive growth of hands,

feet, face, internal organs• Deficiency

– Pituitary dwarfism: failure to thrive

2. Pituitary Gland

B. Posterior lobe (Neurohypophysis)– Neural tissue– Contains axons of hypothalamus

• Release hormones to posterior lobe for storage– Hormones release by Posterior Lobe

Figure 18–9

The Hormones of the Pituitary Gland

Figure 18–8a

Hypothalamas and Anterior Lobe

• Rate of secretion is controlled by negative feedback

• Hormones “turn on” endocrine glands or support other organs

Figure 18–8b

Prolactin (PRL)

Hormones

• Releasing Hormones (RH) – Stimulate synthesis and secretion of 1

or more hormones at anterior lobe

• Inhibiting Hormones (IH) – Prevent synthesis and secretion of

hormones from anterior lobe

KEY CONCEPT

• Hypothalamus produces regulatory factors that adjust activities of anterior lobe of pituitary gland, which produces 7 hormones

• Most hormones control other endocrine organs, including thyroid gland, adrenal gland, and gonads

KEY CONCEPT

• Anterior lobe produces growth hormone, which stimulates cell growth and protein synthesis

• Posterior lobe of pituitary gland releases 2 hormones produced in hypothalamus: – ADH restricts water loss and promotes thirst– oxytocin stimulates smooth muscle contractions in:

• mammary glands• uterus• prostate gland

If a person were dehydrated, how would the level of ADH released by the

posterior lobe change?

A. More ADH is released.

B. Less ADH is released.

C. It would not change at all.

D. Initially ADH would decrease, then increase until hydration is restored.

A blood sample shows elevated levels of somatomedins. Which pituitary hormone would you expect to be

elevated as well?

A. thyroid stimulating hormone

B. growth hormone

C. oxytocin

D. adrenocorticotropic hormone

What effect would elevated circulating levels of cortisol, a steroid hormone from the adrenal cortex, have on the pituitary

secretion of ACTH?

A. ACTH levels would slowly rise.

B. ACTH levels would increase rapidly.

C. ACTH levels would decrease.

D. ACTH levels would remain the same.

3. Thyroid Gland

Figure 18–10a, b

3. Thyroid Gland• Inferior to larynx• Left and right lobes connected by isthmus• Largest pure endocrine organ• Tissue

1. Follicles Spheres or simple cuboidal epithelium2. Parafollicular cells/C cells between follicles

• Follicles filled with colloid thyroglobulin• Thyroglobulin protein constantly synthesized by follicle cells and

exocytosed into follicle for storage• Upon stimulation by TSH, thyroglobulin is processed into thyroid

hormones (T3/T4)

Formation and Release of Thyroid Hormones

Thyroid Follicles

Figure 18–11a, b

3. Thyroid Gland

• Receptors for thyroid hormones located in all cells except– Adult brain, spleen, testes, uterus, thyroid

• 3 receptors in target cells1.Cytoplasm: hold hormone in reserve2.Mitochondria: increase cellular respiration3.Nucleus: activate genes for enzymes involved

in energy transformation and utilization

3. Thyroid Gland

• Overall effect of thyroid hormones – Increase metabolic rate and body heat production– Regulate tissue growth and development

1. Hypothyroidism lack of T3/T4A. Myxedema (adults)

• Low body temp, muscle weakness, slow reflexes, cognitive dysfunction and goiters swollen thyroid

– Produce thyroglobulin but fail to endocytoseB. Cretinism (infants) = Genetic defect

• Causes lack of skeletal and nervous system development

3. Thyroid Gland

2. Hyperthyroidism excessive T3/T4– High metabolic rate, high heart rate, restlessness,

fatigue3. Graves Disease

– Autoimmune disorder– Produce antibodies that mimic TSH causing

overproduction of thyroid hormones

3. Thyroid Gland

• Parafollicular cells/C cells– in basement membrane of follicles– Produce Calcitonin

• Calcitonin stimulates decrease in blood calcium levels

– Inhibits osteoclasts– Promotes Ca++ loss at kidneys

– Parafollicular cells respond directly to blood calcium levels, not controlled by hypothalamus

– Ca++ 20% above normal = calcitonin release

Figure 18–10c

3. Thyroid Gland

Rate of Thyroid Hormone Release

• Major factor: – TSH concentration

in circulating blood

Figure 18–11b

Thyroid Gland

Table 18–3

Iodide Ions

• Are actively transported into thyroid follicle cells:– stimulated by TSH

• Reserves in thyroid follicles• Excess removed from blood at

kidneys• Deficiency limits rate of thyroid

hormone production

5. Parathyroid Glands

• Four glands embedded in posterior surface of thyroid gland

Figure 18–12

5. Parathyroid Gland• Two cell types

– Oxyphiles: few, functions unknown– Chief Cells: majority

• Produce Parathyroid hormone (PTH)/Parathormone– Most important regulator of blood calcium– Secreted when blood calcium is low– Acts to raise blood calcium levels by acting on various tissues

1. Bone stimulates osteoclasts and inhibits osteoblasts2. Kidney enhances reabsorption of Ca++

3. Intestines promotes conversion of Vit. D to calcitriol in kidney to enhance Ca++ and PO4

3- absorption in small intestine

4 Effects of PTH

3. It enhances reabsorption of Ca2+ at kidneys, reducing urinary loss

4. It stimulates formation and secretion of calcitriol at kidneys

Parathyroid Glands

• Primary regulators of blood calcium I levels in adults

Figure 18–13

Parathyroid Glands

Table 18–4

KEY CONCEPT

• Thyroid gland produces: – hormones that adjust tissue

metabolic rates – a hormone that usually plays minor

role in calcium ion homeostasis by opposing action of parathyroid hormone

What symptoms would you expect to see in an individual whose diet lacks iodine?

A. increased rate of metabolism

B. increased body temperature

C. rapid response to physiological stress

D. goiter

When a person’s thyroid gland is removed, signs of decreased thyroid hormone

concentration do not appear until about one week later. Why?

A. Thyroid hormone is produced by other endocrine glands.

B. Thyroid hormone remains in circulation for 14 days.

C. Thyroid-binding globulins provide thryoxine reservoirs.

D. Thyroid hormone is used slowly.

The removal of the parathyroid glands would result in a decrease in the blood

concentration of which important mineral?

A. calcium ions

B. phosphate ions

C. sodium ions

D. potassium ions

What effect would elevated cortisol levels have on the level of glucose in the

blood?

A. increased glucose

B. decreased glucose

C. modulated glucose around homeostatic optimum

D. dramatic increase of glucose, then a crash

6. Adrenal Glands

Figure 18–14

6. Adrenal Gland

• 2 glands, in renal fascia, superior to kidney• Glandular adrenal cortex• Medulla mostly nervous tissue• In general adrenal hormones are used to cope

with stressors

6. Adrenal Glands

A. Adrenal Cortex– Produces 24+ corticosteriods

• In target alter gene transcription to affect metabolism

– Glandular– 3 layers1.zona glomerulosa2.zona fasciculate3.zona reticularis

6. Adrenal Glands

A. Adrenal Cortex1. Zona glomerulosa Mineralcorticoids

- Control water and electrolyte balance- 95% Aldosterone

- Stimulates Na+ retention and K+ loss- Released in response to

- Low Na+ or high K+- Angiotension mechanism- Low blood pressure or volume- Excessive ACTH

6. Adrenal GlandsA. Adrenal Cortex

2. Zona fasciculate glucocorticoids- Metabolic hormones

- Control glucose metabolism- Most common = cortisol, hydrocortisone- Secretion controlled by ACTH- Effects

- gluconeogenesis in liver- release of fatty acid from adipose- triggers protein hydrolysis to release free amino acids from skeletal

muscle- triggers body cells to utilize fatty acids and amino acids instead of glucose

- Excess anti-inflammatory, inhibit immune response and healing

6. Adrenal Glands

A. Adrenal Cortex3. Zona reticularis gonadocorticoids

- Mostly androgens, may aid onset of puberty- Excess = androgenital syndrome

Adrenal Cortex

Table 18–5

6. Adrenal GlandsA. Adrenal Cortex – Disease’s that affect the cortex:

1. Cushing’s Syndrome- Excessive corticosteroids

- increase ACTH from pituitary tumor- Results in

- hyperglycemia, decr. Muscle and bone mass, hypertension, edema, poor healing, chronic infections

2. Addison’s Disease- Deficient in corticosteroids- Results in

- Weight loss, hyopglycemia, decr. Na+, incr. K+ in plasma, dehydration, hypotension

6. Adrenal GlandsB. Adrenal Medulla

- Neural, produces catecholamines to enhance effects of other adrenal hormones- Modified ganglionic sympathetic neurons called chromaffin cells release

epinephrine (80%) and norepinephrine (20%) in response to sympathetic stimulation

- Epinephrine effects:- Stimulate heart- Stimulate metabolic activities

- Skeletal muscle – mobilize glucogen reserves, accelerate ATP production- Adipose – promote release of fatty acids- Liver – promotes release of glucose

KEY CONCEPT

• Adrenal glands produce hormones that adjust metabolic activities at specific sites

• Affects either pattern of nutrient utilization, mineral ion balance, or rate of energy consumption by active tissues

Figure 18–15

6. Pancreas

6. Pancreas

• Inferior and posterior to stomach• Mostly exocrine cells pancreatic acini

– Secrete digestive enzymes• 1% endocrine pancreatic islets

6. Pancreas

• Pancreatic Islets cell types1. Alpha cells glucagon increase blood glucose2. Beta cells insulin decrease blood glucose3. Delta cells somatostatin

• Suppresses glucagon and insulin release• Slows enzyme release into intestines

4. F cells pancreatic polypeptide • Regulates production of pancreatic enzymes

6. Pancreas

• Insulin– Secreted in response to high blood glucose or ANS

• Parasympathetic = incr. insulin• Sympathetic = decr. Insulin

– Effect only on insulin dependent cells (have receptors)

– Brain, kidney, GI mucosa, and RBCs• ALL INSULIN DEPENDENT

5 Effects of Insulin

1. Accelerates glucose uptake2. Accelerates glucose utilization

and enhanced ATP production3. Stimulates glycogen formation4. Stimulates amino acid absorption

and protein synthesis5. Stimulates triglyceride formation

in adipose tissue

6. Pancreas• Diabetes mellitus too much glucose in blood

(hyperglycemia)– Type I failure to produce insulin– Type II insulin resistance, sometimes insulin

deficiency– Cells can not utilize glucose ketone bodies produced

too many ketone bodies lead to ketoacidosis• Glucagon

– Secreted in response to low blood glucose or sympathetic stimulation

3 Effects of Glucagons

1. Stimulates breakdown of glycogen in skeletal muscle and liver cells

2. Stimulates breakdown of triglycerides in adipose tissue

3. Stimulates production of glucose in liver

Insulin and Glucagon Effects

Figure 18–16

Table 18–6

Pancreatic Islets

KEY CONCEPT

• Pancreatic islets release insulin and glucagons• Insulin is released when blood glucose levels rise • Stimulates glucose transport into, and utilization

by, peripheral tissues• Glucagon released when blood glucose levels

decline • Stimulates glycogen breakdown, glucose

synthesis, and fatty acid release

7. Pineal Gland

• Posterior of third ventricle• Pinealocytes

– Synthesize melatonin from serotonin• Secretion on diurnal cycle

– High at night, low during dayligh• Melatonin functions

1. Play role in timing of sexual maturation2. Antioxidant free radical protection3. Sets circadian rhythms

Why does a person with Type 1 or Type 2 diabetes urinate frequently and have a

pronounced thirst?

A. Glucose in the blood inhibits ADH release.

B. Sugar in the urine prevents kidneys from reabsorbing water.

C. High blood sugar dehydrates the tissues of the mouth.

D. Blood sugar elevates blood volume, increasing urine output.

What effect would increased levels of glucagon have on the amount of

glycogen stored in the liver?

A. increased glycogen

B. decreased glycogen

C. no effect

D. rapid increase of glycogen, with a slow return to homeostasis

Increased amounts of light would inhibit the production of which

hormone?

A. prolactin

B. melanocyte stimulating hormone

C. aldosterone

D. melatonin

Hormones Produced by Specific Organs

Table 18–7

8. Gastrointestinal Tract

• Enteroendorine cells in GI mucosa secrete many hormones coordinate digestive activity

• Mostly paracrine communication– Cholecystokinin– Enterocrinin– Gastric inhibitory peptide– Gastrin– Secretin– Vasoactive intestinal peptide

9. Kidneys

• Various endocrine cells• Three products

1. Calcitrol Steroid hormone• Stimulate Ca++, PO4

3- absorption in GI• Stimulate osteoclast activity• Stimulate Ca++ retention in kidney• Suppress PTH production

2. Erythropoeitin Peptide hormone• Released in response to low O2 in kidney

3. Renin Enzyme

9. Kidneys • Three products

3. Renin Enzyme• Released in response to sympathetic stimulation or decline in

renal blood flow• Converts angiotensin in blood into Angiotensin II (hormone)• Angiotensin II effects

– Stimulate secretion of aldosterone adrenal– Stimulate secretion of ADH pituitary– Stimulate thirst– Elevate BP

» Both aldosterone and ADH restrict Na+ and H2O loss at kidney

Calcitriol

• Stimulates calcium and phosphate ion absorption along digestive tract

Figure 18–17a

The Renin–Angiotensin System

Figure 18–17b

10. Heart

• Some cells of atrial walls secrete Atrial Natriuretic Peptide in response to stretch

• ANP promotes Na+ and water loss at kidney– Inhibits release of renin, ADH, and aldosterone

reduce BP and volume

11. Thymus

• Located deep to sternum• Cell produces thymosin hormones:

– Promote development and maturation of T lymphocytes and the immune response

12. Gonads

A. Testes male– Interstitial cells produce androgens in response

to LH– Testosterone, most common

• Produces male secondary sex characteristics• Promotes sperm production• Maintains secretory glands

12. GonadsB. Ovaries Female

– Follicle cells produce estrogens in response to FSH and LH– Estradiol, most important

• Produce female secondary sex characteristics• Support maturation of oocytes• Stimulate growth of uterine lining

– Surge in LH causes• Ovulation• Follicle reorganizes to form corpus luteum

– Produces estrogens and progestins, especially progesterone

12. Gonads

B. Ovaries Female– Progesterone, most important

• Prepares uterus for embryo growth• Accelerates movement of oocyte/embryo to uterus• Enlargement of mammary glands

13. Adipose

1. Leptin secretion – in response to absorption of glucose and lipids– Triggers satiation in appetite center of

hypothalamus– controls normal levels of GnRH, gonadotropin

synthesis2. Resistin secretion

– Reduces insulin sensitivity

Hormones interact to produce coordinated physiological responses.

Hormone Interactions

1. Antagonistic (opposing) effects2. Synergistic (additive) effects3. Permissive effects:

– 1 hormone is necessary for another to produce effect

4. Integrative effects: – hormones produce different and

complementary results

Hormones Important to Growth

1. GH2. Thyroid hormones3. Insulin4. PTH5. Calcitriol6. Reproductive hormones

Growth Hormone (GH)

• In children:– supports muscular and skeletal

development

• In adults:– maintains normal blood glucose

concentrations– mobilizes lipid reserves

Thyroid Hormones

• If absent during fetal development or for first year:– nervous system fails to develop normally– mental retardation results

• If T4 concentrations decline before puberty:– normal skeletal development will not

continue

Insulin

• Allows passage of glucose and amino acids across cell membranes

Parathyroid Hormone (PTH) and Calcitriol

• Promote absorption of calcium salts for deposition in bone

• Inadequate levels causes weak and flexible bones

Reproductive Hormones

• Androgens in males, estrogens in females

• Stimulate cell growth and differentiation in target tissues

• Produce gender-related differences in:– skeletal proportions– secondary sex characteristics

Insulin lowers the level of glucose in the blood, and then glucagon causes glucose

levels to rise. What is this type of hormonal interaction called?

A. additive

B. antagonism

C. permissive

D. integrative

The lack of which hormones would inhibit skeletal formation?

A. GH, thyroid hormone, PTH, gonadal hormones

B. prolactin, FSH, LH, GH

C. thyroid hormone, melatonin, PTH, calcitonin

D. GH, TSH, ACTH, FSH

Why do levels of GH-RH and CRH rise during the resistance phase of the general

adaptation syndrome?

A. to bolster immune response

B. to decrease excess blood volume

C. to increase needed supplies of blood glucose

D. to heighten sensory perceptions

Generaladaptation syndrome.

General Adaptation Syndrome (GAS)

• Also called stress response

• How bodies respond to stress-causing factors

Figure 18–18

General Adaptation Syndrome (GAS)

• Is divided into 3 phases: 1. alarm phase 2. resistance phase3. exhaustion phase

Alarm Phase

• Is an immediate response to stress• Is directed by ANS• Energy reserves mobilized

(glucose)• “Fight or flight” responses• Dominant hormone is epinephrine

7 Characteristics of Alarm Phase

1. Increased mental alertness2. Increased energy consumption3. Mobilization of energy reserves (glycogen and lipids)4. Circulation changes:

– increased blood flow to skeletal muscles– decreased blood flow to skin, kidneys, and digestive organs

5. Drastic reduction in digestion and urine production6. Increased sweat gland secretion7. Increases in blood pressure, heart rate, and respiratory rate

Resistance Phase

• Entered if stress lasts longer than few hours

• Dominant hormones are glucocorticoids

• Energy demands remain high• Glycogen reserves nearly

exhausted after several hours of stress

Effects of Resistance Phase

1. Mobilize remaining lipid and protein reserves

2. Conserve glucose for neural tissues3. Elevate and stabilize blood glucose

concentrations4. Conserve salts, water, and loss of

K+, H+

Exhaustion Phase

• Begins when homeostatic regulation breaks down

• Failure of 1 or more organ systems will prove fatal

• Mineral imbalance

Aging Related Changes

• Very little change in most hormone levels• Adverse effects due to changes in target tissue

– Prevent reception or response to hormone• Gonads decrease in size and hormone production

Review: Endocrine System

• Provides long-term regulation and adjustments of homeostatic mechanisms:– fluid and electrolyte balance– cell and tissue metabolism– growth and development– reproductive functions– assists nervous system response to stressful

stimuli through general adaptation syndrome

SUMMARY

• Paracrine communication• Endocrine communication• Classes of hormones:

– amino acid derivatives– peptide hormones– lipid derivatives, including steroid hormones and

eicosanoids• Secretion and distribution of hormones• Endocrine reflexes• Hypothalamus regulation of the endocrine system• The pituitary gland:

– the anterior lobe– the posterior lobe

SUMMARY

• Releasing hormones• Inhibiting hormones• The thyroid gland:

– thyroid follicles– thyroid hormones

• The parathyroid glands• The adrenal glands:

– the adrenal cortex and adrenal medulla• The pineal gland• The pancreas:

– the pancreatic islets– insulin and glucagons

SUMMARY

• Endocrine tissues in other systems• Hormonal interaction• Role of hormones in growth• Hormonal response to stress• Effects of hormones on behavior• Effects of aging on hormone production