THE ENDOCRINE SYSTEM - Weebly



REV. 8/15/06 THE ENDOCRINE SYSTEM

TWO GREAT CONTROLLING SYSTEMS

Nervous System . . . . . . . . . . . . . . . . Endocrine System

1) NERVOUS SYSTEM

Regulates activity via action potential impulses ~ AP’s

Impulses carried by specific sensory or motor neurons

Uses “synaptic communication” to carry message

Targets specific cells ~ for specific response

Response is immediate & usually short lasting

2) ENDOCRINE SYSTEM

Controls cell activity by secreting hormones ~ EXCITE

Hormones = “Chemical Messengers”

Secreted into blood & transported throughout body

Generalized Widespread Response ~ Adrenalin or GH

Targeted specific cells: TSH or FSH

Diverse or very specific effects: Insulin ~ specific

Adrenaline ~ diverse

Response on target cells is delayed ~ due to circulation

Delayed, prolonged or continuous response

ENDOCRINE SYSTEM ~ Controlling Spectrum

MAJOR processes controlled by hormone release

Reproduction

Testosterone

Estrogen

Follicle Stimulating Hormone

Leutenizing Hormone

Oxytocin ~ “Post Pit”

Growth & Development

Growth Hormone & Thyroid Hormone

Body Defense Mechanisms

Corticosteroids ~ Cortisone ~ Anti-inflammatory

Anti-Stress ~ Corticosteroids ~ Gluconeogenesis

Electrolyte, Water & Nutrient Balance

Aldosterone ~ Na+ retention ~ water retention

Anti-Diuretic Hormone ~ ADH

Cell Metabolism & Energy Regulation

Insulin & Thyroid Hormone

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Digestive Processes

TWO GLANDULAR SYSTEMS OF BODY

Exocrine Glands . . . . . . . Endocrine Glands

1. EXOCRINE GLANDS ~ Merocrine . . . Apocrine . . . Holocrine

< PUREST ------------------------------ MESSY >

Secreted onto body surfaces ~ via ducts

Secretions are non-hormonal

Secreted & ACT LOCALLY in a target area only

DO NOT secrete into blood or lymphatics

Can be large in size or extensive in numbers ~ millions

Examples of Exocrine Glands Secrete

Mucous Glands Mucous

Sudoriferous Glands Sweat

Sebaceous or Oil Glands Sebum

Salivary Glands Saliva

Mammary Glands Milk

Liver Bile

Enteric Glands Digestion

Reproductive Glands Several

Pancreas ~ Both Exocrine & Endocrine

2. ENDOCRINE GLANDS

“Ductless Glands” ~ produce hormones ~ NO DUCTS

Secrete hormones most directly into blood

Surrounded by many capillaries ~ allows secretion into blood

Hormones travel through body ~ act on specific target organs

Can have a generalized effect or specific target effect

Effects can be short, prolonged or continuous lasting

Small Glands ~ very localized, & few in numbers ~ 12 groups

ENDOCRINE GLANDS

Pituitary Gland Heart

Pineal Gland Small Intestines

Thyroid Gland Kidney

Parathyroid Gland Pancreas

Thymus Gland Gonads – ovaries &

testes

Adrenal Gland Hypothalamus

Other Specialized Cells can produce hormones

Adipose Tissue . . . .Tumors or cancer cells

CHEMISTRY OF HORMONES

Hormones ~ “chemical messengers” ~ “First Messengers”

Control other parts of body from where secreted

“Endocrine Communication” ~ NOT NEURAL

MOST Secreted into blood & circulatory system

Regulate functions of other cells somewhere else

Major Hormone Classifications

1. Amino Acid Hormones ~ MOST COMMON

Most hormones are globular proteins or peptides

2. Lipid Hormones

Steroid Hormones ~ from cholesterol

Gonadal hormones ~ estrogen, testosterone

Adrenalcorticoids hormones ~ corticosteroids

Eicosanoids (eye cos an oids)

Increase inflammation & cause swelling

NON-CIRCULATING hormones ~ act locally only

Released from most cell membranes & have a highly localized response

Prostaglandins ~ most common

MECHANISM OF HORMONE ACTION

Hormones effect target cells ~ alter cell activity

Increase or decrease types & rates of cellular processes

Up-Regulation ~ increased sensitivity to hormone effects

Down-Regulation ~ less sensitive to hormone effects

Activity is very specific on a specific target cell

EG: Epinephrine causes blood vessel walls to contract

It will also cause an increase in heart rate

HORMONE EFFECTS ON TARGET CELLS

1. Change plasma membrane permeability

2. Change electrical charge of plasma membranes

3. Stimulate secretory activity of cells

4. Stimulate mitosis & cell division

MOST 5. Stimulate Enzyme Activation or Deactivation ~ COMMON

Forms NEW proteins within cells

Amino Acid Hormones ~ cAMP Second Messenger

6. Stimulate Gene Activation ~ COMMON

Lipid/Steroid Hormones ~ Form New Proteins

EXAMPLES ~ MECHANISMS OF HORMONE ACTION

AMINO-ACID HORMONES (“PEPTIDES”) ~ MOST COMMON

Utilizes a Second Messenger System

Hormone ~ is the first messenger

Hormone CANNOT penetrate cell membrane ~ to big

Binds to “hormone receptor” site on target cell

Receptor binding ---> activates a “G-protein” --->

which activates an effector enzyme

Effector Enzyme = Adenylate cyclase

Adenylate cyclase generates Second Messenger ~ cAMP

cAMP activates protein kinase - - -> form NEW PROTEINS

inside cell

MANY reactions follow & cause specific cell activities

LIPID ~ STEROID HORMONES “from CHOLESTEROL”

Utilizes: Gene Activation ~ NO 2nd messenger system

Smaller & lipid soluble ~ can penetrate cell membrane

Once inside target cells ~ gene activation occurs

DNA is “transcribed” to messenger RNA ~ mRNA

mRNA ~ stimulates production of NEW proteins

HORMONE TARGET CELL ACTIVATION & SPECIFICITY

Major hormones circulate in blood to all tissue

Specific hormones effect only specific tissue cells

Hormone Receptors ~ located on or in cells

Target Cells have specific hormone receptors on cell membranes or inside target tissue that bind hormones

Receptor Binding is required for activity

SOME receptors are found only on/in SPECIFIC CELLS

Example: ACTH stimulates only the adrenal cortex

SOME receptors are found on/in MOST BODY CELLS

Example: Thyroxine stimulates most cells

Insulin affects all cells of body

Target Cell Activation Requirements

Adequate Hormone Blood Levels

Specific Receptor Binding Sites

Adequate Number of Receptors on or within cells

Specific Bonding Affinity between Hormone & Receptor

Any +/- Changes in any of the above results in:

Endocrine Dysfunction ( Up Regulation OR

( Down Regulation

ENDOCRINE DYSFUNCTION

Up-Regulation ~ Sensitization ~ Stimulation

Occurs when target cells form MORE receptors in response to hormone presence

Down-Regulation ~ Desensitization ~ Inhibition

Occurs when prolonged exposure to high hormone levels causes LOSS of receptors

Desensitizes target cells resulting in lower activity

Hormones also STIMULATE or INHIBIT other hormones

EG: Estrogen stimulates Progesterone release

Progesterone antagonizes Estrogen action

DURATION OF HORMONAL ACTIVITY ~ “Half-Life”

Dependent on circulating blood levels of Hormone

1) Rate of Release into the blood

2) Speed of Inactivation & Removal from the body

Methods of Inactivation ~ Removal from body

1) Degradation by enzymes in target cells

2) Removed from blood via Kidney and Liver

3) Excreted in Urine or Feces

HALF-LIFE

Time required to reduce blood concentrations by 50%

Ranges from seconds to minutes to hours or longer

What is the Half-Life? . . . .If blood concentration is 20 units &

. . . . . 15 units remain after 7 minutes

Answer

. . . . . 10 units remain after 14 minutes = HALF-LIFE

. . . . . 5 units remain after 21 minutes

Endocrine Reflexes ~ CONTROL HORMONE RELEASE

Blood levels are precisely controlled for optimal effects

1) POSITIVE FEEDBACK MECHANISM

As hormone is released, target organ stimulates the release of more hormone . . . more . . . more . . . more

EG: Oxytocin ~ Childbirth

MOST

2) NEGATIVE FEEDBACK MECHANISM ~ COMMON

As blood hormone levels rise, target organs inhibit further hormone release ~ on . . . off . . . on . . . off

EG: thermostat in a house

EG: High blood sugar ---> insulin release --->

---> glucose uptake into cells ---> lower blood sugar

TYPES OF ENDOCRINE GLAND RELEASE STIMULI

Endocrine Gland Reflexes

Stimulate glands to produce & release hormones

1) Humoral Stimuli ~ ions & chemicals

2) Neural Stimuli ~ nerve impulses

3) Hormonal Stimuli ~ other hormones

HUMORAL STIMULI

Hormones secreted in direct response to changing blood levels of certain IONS & CHEMICALS

Examples:

Low blood Ca+ ---> parathyroid gland to secrete parathyroid hormone (PTH) ---> higher blood Ca+ --->

reduced secretion of PTH

High blood sugar ---> pancreas to secrete insulin --->

lowering of blood sugar

NEURAL STIMULI

Nerve IMPULSES (AP’s) stimulate hormone release

EG: Stress ---> Sympathetic NS activation

---> Adrenal medulla secretes catecholamines

Adrenalin ~ Norepinephrine & epinephrine

HORMONAL “TROPIC” STIMULI ~ COMMON

Occurs when an endocrine gland releases hormones that stimulate OTHER endocrine glands to release hormones

Hypothalamus ~ highest level of endocrine control

Integrates activities of endocrine & nervous system

Produces Hormones that regulates Pituitary Gland

Pituitary produces other hormones that regulate OTHER glands

Hypothalamic-Pituitary -Target Endocrine Gland

Feedback Loop

SEVERAL Hypothalamus “Regulating” Hormones

Thyrotropic Releasing Hormone (TRH)

Stimulates release of TSH from Ant. Pituitary

TSH stimulates Thyroid Hormone from Thyroid

Corticotropin Releasing Hormone (CRH)

Stimulates release of ACTH from Ant. Pituitary

Stimulates Adrenal Hormones from Adrenals

Gonadortophin Releasing Hormone (GnRH)

Stimulates release of FSH & LH from Ant. Pit.

Stimulates Testosterone, Estrogen & Progesterone from Gonad

12 MAJOR ENDOCRINE ORGANS

PITUITARY GLAND

Also called the “Hypophysis” ~ “Master Gland of Body”

Protected by sella turcica of the sphenoid bone

At the base of the brain ~ not a part of nervous system

Infundibulum ~ “stalk” ~ connects pituitary to hypothalamus

Two lobes: Anterior Pituitary ~ “adenohypophysis”

Posterior Pituitary ~ “neurohypophysis”

HYPOTHALAMUS

Located above the brain stem ~ in diencephalon

Controls Autonomic Nervous System

Controls emotion ~ rage, fear, anger, pleasure

Body temperature regulation

Food intake regulation ~ appetite

Water balance & thirst regulation

Controls Endocrine System

Produces Hormones that “regulate” the Anterior Pituitary

Produces two hormones released by the Posterior Pituitary

ADH . . . . . . Oxytocin

HYPOTHALAMUS

Produces “Releasing & Inhibiting” Regulating Hormones

Carried via “Hypophyseal Portal System” to Ant. Pit.

Vascular connection ~ hypothalamus & Ant. Pit

“Releasing” Hormones

Stimulate secretion of Anterior Pituitary Hormones

“Inhibiting” Hormones

Inhibit release of Anterior Pituitary Hormones

Produces 2 “Neuro-Hormones” for Posterior Pituitary

Paraventricular Nucleus ----> Oxytocin

Supraoptic Nucleus ----> Anti-diuretic Hormone ~ ADH

Carried via “Hypothalamic-Hypophyseal Tract”

by axons to posterior pituitary

Neuro-Hormones are secreted by Posterior Pituitary

“Hypophyseal Portal System”

Vascular connection ~ hypothalamus & anterior pituitary

“Hypothalamic-Hypophyseal Tract”

Neural connection ~ hypothalamus & posterior pituitary

ANTERIOR PITUITARY ~ “Master Endocrine Gland”

Anterior Lobe ~ “Adenohypophysis”

Controlled by the hypothalamus via regulating hormones

Hypophyseal Portal System

Fenestrated Capillaries ~ vascular bed connections

Allows hypothalamic hormones to circulate

through the anterior pituitary

Regulating Hormones ~ regulate the secretions of other hormones from anterior pituitary gland

Secretes 6 major hormones ~ ALL ARE PROTEINS

Instantaneous Response ~ NO storage in Anterior Pit.

Tropic Hormones: Hormonal Stimuli

Regulate the secretory action of OTHER endocrine

glands to release other hormones

TSH Thyroid Stimulating Hormone

ACTH Adrenal Corticotropic Hormone

FSH Follicle Stimulating Hormone

LH Leutenizing Hormone

Non-tropic Hormones: Effects NON-ENDOCRINE

glands

GH Growth Hormone

PRL Prolactin

ANTERIOR PITUITARY - “TROPIC” HORMONES

THYROID STIMULATING HORMONE ~ TSH

TRH ~ Thyrotropin Releasing Hormone - Hypothalamus

Stimulates release of TSH from Anterior Pituitary

TSH (tropic) ~ stimulates Thyroid Gland to secrete

Thyroid Hormone

Negative Feedback “Shut Off” Mechanism

Rising blood levels of TH “shuts off” the Hypothalamus & Anterior Pituitary to block further TSH release

Factors releasing TRH from Hypothalamus

Increased Energy Demands

Need to raise metabolic rate

Need to produce & release heat

EG: Pregnancy

Cold temperatures

Exercise

Fever

ANTERIOR PITUITARY - “TROPIC” HORMONES

ADRENOCORTICOTROPIC HORMONE ~ ACTH

CRH ~ Corticotropin Releasing Hormone - Hypothalamus

Stimulates release of ACTH from Anterior Pituitary

ACTH tropic action: stimulates the adrenal cortex to release several other hormones:

1) Gluco-corticoids ~ corticosteroids ~ mostly

2. 2) Gonad-ocorticoids ~ androgens ~ small amount

3.

3) Mineralo-cortacoids ~ aldosterone

Negative Feedback “Shut Off” Mechanism

Rising blood levels of “corticoids” cause Anterior Pituitary & Hypothalamus to block further CRH release

Factors stimulating CRH release:

fever

hypoglycemia

stress

dehydration . . . shock . . . blood loss . . . low blood

pressure

ANTERIOR PITUITARY - “TROPIC” HORMONES

GONADOTROPINS

FSH ~ Follicle Stimulating Hormone

LH ~ Leutenizing Hormone

GnRH ~ gonadotropin releasing hormone from Hypothalamus

Stimulates release of FSH or LH from Anterior Pituitary

FSH and LH ~ action is tropic

Stimulate gonad activity ~ ovaries & testes ~ at puberty

FSH ~ stimulates sperm & egg production

LH ~ cause ovarian follicle maturation & ovulation

~ causes release of Gonadal Hormones

Estrogen ~ Female ~ controls menstrual cycle

Progesterone ~ Female ~ maintains pregnancy

Testosterone ~ Male Testicular Hormone

Negative Feedback “Shut-Off” Mechanism

Rising blood levels of gonad hormones causes the

Hypothalamus to block GnRH release, & inhibits FSH & LH release from Anterior Pituitary

ANTERIOR PITUITARY - “NON-TROPIC” HORMONES

GROWTH HORMONE ~ GH ~ “Somatotropin”

“Anabolic Hormone” ~ stimulates most body cells

to increase in size and divide

GH targets bones & skeletal muscles

Stimulates epiphyseal plate & long bone growth

Increases skeletal muscle mass

“Insulin-growth factor” ~ Somatomedins ~ enhance GH

Protein produced in liver & muscle stimulate growth

GH Actions

1) Stimulates protein synthesis ~ anabolic ~ muscles

2) Stimulates cartilage & bone development

3) Stimulates fats for energy ~ increases glucose

4) Converts glucose to glycogen stores for future

5) Causes a “diabetogenic” effect

Causes glycogen breakdown & release of glucose into blood causing ↑ blood sugar

GROWTH HORMONE ~ GH ~ “Somatotropin”

Secretion of GH ~ NOT a feedback mechanism

GHRH – GH Releasing Hormone

Hypothalamic hormone - stimulates release of GH

GHIH – GH Inhibiting Hormone – Somatostatin

Hypothalamic hormone - inhibits release of GH

Growth Hormone Imbalances

Hyper-Secretion ~ gigantisms or acromegaly

Gigantism ~ Abnormally large ~ normal proportions

Excess GH from early age ~ Andre the Giant

Acromegaly ~ Abnormally large ~ abnormal

proportions

Excess GH later in life

Hypo-Secretion ~ pituitary dwarfism ~ in children

Midget ~ Usually normal proportions

Corrected by GH replacement therapy as children

ANTERIOR PITUITARY - “NON-TROPIC” HORMONES

PROLACTIN ~ PRL

PRL has direct action on non-endocrine mammary cells

Stimulates milk production by breast (not release)

PRL is controlled by Hypothalamus

PRH ~ Prolactin “Releasing” Hormone = seratonin

Causes prolactin release from Ant. Pituitary

PIH ~ Prolactin “Inhibiting” Hormone = dopamine

Prevents prolactin secretion from Ant. Pituitary

PRL Levels fluctuates in females with ESTROGEN

Low Estrogen stimulates PIH ---> LESS Prolactin

High Estrogen levels stimulates PRH ---> MORE PRL

Menstruation ~ HIGH Estrogen ---> PRH ---> MORE PRL

Breast swelling & tenderness ~ temporary

Generally NO milk production

Pregnancy ~ cause HIGH levels of PRH near term

Infant Suckling ~ stimulates PRH ---> MORE PRL

PRL Hyper-Secretion ~ occurs in nursing mothers

PRL Hypo-Secretion – only occurs in heavy nursers

POSTERIOR PITUITARY

Neurohypophysis ~ Posterior Lobe + Infundibulum

Neural Portion (axons) is an extension of the Hypothalamus

Stores two “neurohormones” produced in the hypothalamus

1) Oxytocin ~ effects uterus & mammaries

2) Antidiuretic Hormone ~ ADH ~ retains water

Neurohormones released into capillary beds of posterior pituitary in response to neural stimulation ~ Humoral

OXYTOCIN ~ “Post pit”

PRODUCED in hypothalamus ~ Paraventricular Nuclei

Uterus & Cervic stretching during childbirth stimulates

Released from Posterior Pituitary ~ Positive Feedback

Effects: Stimulates uterus muscle contraction

Stimulates mammaries to release & “let-down”

Stimulates sexual arousal & organism

Promotes nurturing & cuddling ~ “nesting”

Highest Concentrations ~ during childbirth & nursing

Synthetic Drug ~ induces labor & stimulates milk “letdown”

POSTERIOR PITUITARY

ANTIDIURETIC HORMONE ~ ADH

What is “Diuresis”??? = Excess Urine Production

ADH = “Anti-Urine Hormone” = AGAINST DIURESIS

“Vasopressin” ~ causes vasoconstriction & elevates BP

PRODUCED in hypothalamus ~ Supra Otic Nuclei

Stimulated by need to retain fluids

Dehydration ~ Excess sweating ~ no fluid intake

Hemorrhage ~ Blood Loss

Low blood pressure & Shock

Released from Posterior Pituitary into blood

Effects: Targets Kidneys ----> Water Retention

Prevents urine formation ----> water retention

Reabsorbs water back into blood in kidneys

Increases blood pressure ~ due to vasoconstriction

& retained fluid volume in blood

Controlled by Negative feedback “Shut-Off” Mechanism

Inhibited by High Blood Volume . . . High Blood

Pressure. . . Fluid Retention . . . Over-Hydration

ADH INHIBITORS ~ BLOCK ADH ~ “Diuretics”

Stimulate urine production & fluid loss

Results in copious urine production & output

Flushes water from body ~ Dehydration

Morning after dry mouth & intense thirst ~ drinking

Decreases Blood Fluid Volume ----> lowers BP

Examples of ADH Inhibitors ~ ALL act as DIURETICS

Drinking excessive fluid & Alcoholic beverages

Diuretic Drugs ~ Diet Pills ~ Dexetrene

Hypertension Drugs ~ to lower blood pressure

ADH Hypo-Secretion ----> Diuresis & Fluid Loss

CANNOT retain water ~ CANNOT concentrate urine

----> fluid loss, HIGH urine output, low blood volume

“Diabetes Insipitus” ~ NO ADH

Excess urine ~ polyuria ~ intense thirst ~ fluid loss

Caused by head injury to hypothalamus or Pituitary

Treated by Re-Hydration & fluid therapy

ADH Hyper-Secretion ~ uncommon ~ trauma, tumor, drugs

Fluid retention, LOW urine output, high blood volume

THYROID GLAND

Largest “pure” endocrine ONLY gland in body ~ “Butterfly”

On the trachea . . . Anterior throat area . . . below the larynx

Two lateral lobes connected by a median isthmus

Blood Supply ~ via thyroid artery off common carotid artery

Extremely vascular ~ Surgery very difficult

Internal Thyroid Tissue Histology

1. Follicular Cells - spherical cells ~ surround lumen

Produce thyroglobulin ~ glycoprotein

2. Lumen of follicle ~ stores colloid

Colloid = thyroglobulin + attached iodine

“Iodinated Thyroglobulin”

Precursor for Thyroid Hormone ~ T3 or T4

3. Parafollicular Cells ~ around & between the follicle

Endocrine cells that produce calcitonin

Calcitonin ~ lowers blood calcium levels

Thyroid Gland is Unique . . .

Only endocrine gland that stores hormones in large quantities ~ in colloid

THYROID HORMONE ~ TH

“Body’s major “metabolic hormone”

Thyroid Hormone is two Iodine containing hormones

T4 Thyroxine ~ STORED FORM ~ NOT ACTIVE

90% of TH ~ secreted by follicle cells

T3 Triiodothyronine ~ NOT stored ~ “ACTIVE”

Formed at target tissues by conversion of

T4 (STORED) > > > T3 (“Active)

Thyroid Hormone affects most cells except:

Brain . . . Spleen . . . Testes . . . Uterus . . . Thyroid

Effects of Thyroid Hormone

1. Stimulates carbohydrate, lipid & protein metabolism

Glucose & fat catabolism ~ energy produced

Protein & cholesterol synthesis ~ growth

2. Increases basal metabolic rate & O2 consumption

Calorigenic Effect ~ burn calories ~ body heat

Promotes normal oxygen use by cells

3. Regulates tissue growth, development, & function

Thyroid Hormone Release ~ “Negative Feedback”

1. Falling blood levels of thyroxin (T4) ----> Hypothalamus to release thyrotrophic releasing hormone (TRH)

2. TRH ----> anterior pituitary to release thyroid stimulating hormone (TSH) into blood

3. TSH ----> Thyroid to release thyroxin (T4 & T3) into blood

4. Thyroxin (T4 & T3) is carried to target organ receptors

T3 is formed at the target tissue by conversion of T4

5. T3 or T4 actively exert effects on the target tissue

6. Rising blood levels of T3/T4 “shuts off” hypothalamus --> inhibits release of TRH (hypothalamus) & TSH (Ant. Pit)

Factors Triggering TSH release from anterior pituitary:

Any conditions increasing body energy requirements

Pregnancy ~ requires energy for fetus

Prolonged Cold ~ requires body heat

Extensive Exercise ~ requires energy & O2

Factors Inhibiting TSH release:

Somatostatin ~ growth hormone inhibitor ~ less energy

Rising levels of glucocorticoids ~ high blood sugar

High blood iodine concentration ~ Stimulates excess TH

----> Shuts off Hypothalamus

THYROID GLAND DISFUNCTION ~ Common

Hypo-Thyroidism ~ “Under-activity of Thyroid Gland”

Thyroid Gland Defects ----> LOW TRH or TSH secretion

Symptoms: Myxedema – mucous area swelling

Low metabolic rate – weight gain

Feeling chilly

Thick dry skin ~ hair thins & loss

Lethargy & sluggishness

Cretinism ~ severe hypothyroidism in infants

Short, disproportionate body, thick tongue & neck, mental retardation ~ irreversible

Cause unknown ~ genetic deficiency???

Prevented by TH replacement therapy

Goiter ~ enlarged thyroid due to lack of iodine ~ common

Follicle cells produce colloid but cannot iodinate colloid (CANNOT MAKE THYROID HORMONE)

-----> Low blood TH ~ NONE produced

NO negative feedback “shut-off” of TSH

-----> Continuous release of TSH

Unusable colloid accumulates in thyroid gland

Treatment: Removal of Thyroid Gland ~thyroidectomy

Oral TH tablets & Dietary Iodine ~Thyroxin

THYROID GLAND DISFUNCTION

Hyper-Thyroidism ~ thyrotoxicosis

“Over activity of Thyroid Gland”

“Graves” Disease

Cause: “Autoimmune disease” ~ against self

Body produces antibodies ~ mimic TSH

Causes continuous production of TH

Symptoms: Elevated metabolic rate

Sweating

Rapid, irregular heartbeat

Nervousness

Weight loss, even with adequate food intake

Treatment: Surgical removal of thyroid

To stop excessive TH release

Oral controlled thyroxin

THYROID GLAND HORMONES

CALCITONIN

Produced by parafollicular cells of Thyroid

Protein hormone ~ lowers blood Ca++

Direct antagonist to parathyroid hormone

Mode of Action:

1. Targets skeletal tissue & bone

2. Inhibits osteoclast activity & bone resorption

3. Inhibits release of ionic calcium from bone

4. 4. Stimulates calcium uptake into bone

5.

6. Stimulates osteoblast activity in bone

Calcitonin Secretion Stimuli:

Cycles up & down with parathyroid hormone

Excessive blood levels of calcium -----> “calcitonin” release ~ to lower blood calcium

Part of “negative feedback” system with “parathyroid hormone” from parathyroid gland

PARATHYROID GLAND

Very tiny ~ on posterior side of thyroid gland . . . two pairs, one on each side ~ numbers can vary

Function is antagonistic to thyroid gland

Thyroid ~ calcitonin lowers blood Ca++

Parathyroid ~ parathyroid hormone raises blood Ca++

Histology of Parathyroid Tissue

1. Chief Cells – round and dark stained

Produce “Parathyroid Hormone” ~ PTH

2. Oxyphil Cells – function unknown ~ egg whites

3. Capillaries - extensive network

Parathyroid Hormone ~ PTH ~ “Parathormone”

Most important hormone controlling blood calcium levels

PTH Secretion & Release Stimuli

Low blood calcium levels (hypo-calcemia) ---->

Stimulate Parathyroid Hormone release

High blood calcium levels (hyper-calcemia) ----> inhibits Parathyroid Hormone release

Main Effect of PTH ~ increases blood calcium ion levels

Direct antagonist to calcitonin (lowers blood Ca++)

Parathyroid Hormone ~ PTH

Blood Calcium Balance ~ needed for many body functions

Nerve impulse transmission

Muscle contraction

Blood clotting

Bone development & maintenance

Mode of Action ~ Parathyroid Hormone

1. Skeletal Tissue ~ stimulates bone cells (osteoclast)

to release calcium from bone into blood

2. Kidney ~ enhances reabsorption of calcium into blood

3. Kidney ~ activates Vitamin D -----> increases intestinal

absorption of Ca++

Parathyroid Gland Dysfunction

Hyper-parathyroidism ~ rare ~ Parathyroid Gland Tumor

Hypo-parathyroidism ~ Parathyroid Hormone Deficiency

Causes: Parathyroid trauma

Thyroid gland removal with parathyroid

Symptoms: Hypocalcemia ~ low blood calcium

Loss of nerve function

Muscle twitches

Convulsions . . . Respiratory paralysis . . .

Death

ADRENAL GLAND ~ the “Stress Gland”

Paired ~ pyramid shaped ~ On top of each kidney

“Suprarenal glands” ~ above the kidney

Each adrenal gland ~ two distinct glands in one

Adrenal Medulla – smaller interior part

Adrenal Cortex – larger portion surrounds medulla

Each produces different types of hormones

BOTH are stimulated in response to stressful situations

“GOOD/glomerulosa FAMILY/fasciculata RULES/reticularis”

Adrenal Cortex Hormones Function

Zona glomerulosa Mineralocorticoids Mineral &

(Aldosterone) water balance

Na+ retention

Zona fasciculata Gluco-corticoids Gluconeogenesis

Cortico-steroids Energy Metabolism

Cortisone Anti-inflammatory

Cortisol) Immune Suppression

Zona reticularis Gonado-corticoids Sex Hormones

(Androgen)

Adrenal Medulla Hormones Function

Adrenal Medulla Catecholamines Increases BP

Hormones Adrenalin Increases HR

Epinephrine Dilates Bronchioles

Nor-Epinephrine Decrease Peristalsis

ADRENAL CORTEX

MINERALOCORTICOIDS ~ Aldosterone

Aldosterone ~ 95% of mineralo-corticoids

Produced in Zona Glomerulosa

Regulate Na+ concentration in body fluids & blood

Retains Na+ ~ most vital ion causing fluid retention

Sodium retention causes fluid retention ~ EDEMA

Retains water & fluid ~ same effect as ADH

Aldosterone Effects

Reduces Na+ excretion from body

Retains Na+ from urine in kidney tubules

Retains Na+ from perspiration & saliva

Water follows sodium > > > fluid retention

Aldosterone Secretion Stimuli

Anything Requiring Fluid Retention

Decreased Na+ blood levels

Decreased blood volume Shock

Dehydration

Decreased blood pressure Blood Loss

Aldosterone Release Mechanisms

Renin- Angiotensin- Aldosterone Mechanism ~ MAJOR

1. Low blood pressure or lost blood volume is sensed by juxtaglomerular apparatus in kidney

2. Kidney releases Renin into blood

3. Renin ----> Angiotensin I in blood

Angiotensin I ----> Angiotensin II in blood

4. Angiotensin II stimulates adrenal cortex to release Aldosterone which ----> Na+ retention in the kidney

5. Na+ & water retained in the blood ---->increasing

Blood volume & blood pressure ~ decreased urine

Other Aldosterone Release Mechanisms ~ MINOR

ACTH ~ adrenocorticotropic hormone

Severe stress ----> hypothalamus secretes corticotropin releasing hormone ----> anterior pituitary to secrete ACTH ----> release of Aldosterone ----> Sodium Retention Effects

Atrial Natriuretic Peptide ~ ANP ~ inhibits aldosterone

Increased blood pressures stimulates heart to release ANP which inhibits the renin- angiotensin mechanism

----> Na+ & water excretion & lower blood pressure

ADRENAL CORTEX HORMONES

GLUCOCORTICOIDS ~ “Cortisone”

Produced in Zona Fasciculata

Cortisol ~ hydrocortisone ~ most significant

Cortisone ~ produced in liver from cortisol

Glucocorticoids Effects ~ MANY

1. Reduces stress ~ prepares body for crisis

Thru gluconeogenesis & glycogenoslysis

“Diabetogenic” Effect ~ ↑ blood sugar

Converts glycogen to glucose

Converts fats to glucose

2. Stimulates protein breakdown to amino acids

3. Anti-Inflammatory ~ reduces swelling ~ “cortisone”

4. Suppresses immunity ~ organ transplants

5. Stimulates appetite ~ “cortisol”

6. Used as a synthetic drug ~ allergy & inflammation

Cortisone . . . Prednisone . . . Hydrocortisone

Glucocorticoid Hormone Release - stimulated by stress

Physical & Emotional trauma . . . Hemorrhage . . . Illness

Severe stress ----> hypothalamus secretes corticotropin releasing hormone ----> anterior pituitary to secrete ACTH ----> stimulates release of Cortisol & Cortisone

GLUCOCORTICOID DYSFUNCTION

Hyper-Secretion of Cortisone ~ Cushing’s Syndrome

Caused By: Over usage of cortisone ~ MOST

ACTH tumor of the anterior pituitary

Symptoms: Persistent Hyperglycemia ~ high

blood sugar

Wasting Away ~ Lost muscle mass

Na+ & H2O retention ~ excessive thirst

High Blood Pressure

Severe edema ~ moon faced

Poor wound healing ~ anti-inflammatory

Susceptible to infection ~ Immune

Suppression

GLUCOCORTICOID DYSFUNCTION

HYPO-Secretion of Cortisone ~ Addison’s Disease

Caused By: Deficiency of both glucocorticoids & mineralocorticoids ~ aldosterone

Symptoms: Low blood glucose ~ hypoglycemia

Weight loss ~ no glucose for energy

Na+ loss ~ cannot retain fluid

Dehydration (cannot retain fluid)

Hypotension ~ loss of fluid volume

“Polyuria” ~ excess urine production

GONADOCORTICOIDS ~ Sex Hormones

Produced in Zona Reticularis of Adrenal Cortex

Mainly Androgen ~ male sex hormone ~ Testosterone

Some Estrogen ~ female sex hormone

Lower concentrations than ovaries & testis

Significant levels ~ up to puberty ~ between ages of 7-13

Hyper-secretion could cause masculinization in children

Early hair ~ beard

Deeper voice

Sexual aggressiveness

ADRENAL MEDULLA

Centrally located in adrenal gland ~ smaller portion

Secretes CATECHOLAMINES - effects Sympathetic NS

80% Epinephrine & 20% Norepinephrine = Adrenaline

Release: Stress stimulates the sympathetic nervous system ~ prepares body for crisis

Immediate Response ~ “short acting”

Sympathomimetic Effects:

Blood sugar rises

Heart beats faster

Blood pressure increases

Bronchioles dilate ~ more air

Pupils dilate ~ more light

Digestion & Peristalsis Slows

Visceral Vasodilation & Peripheral Vasoconstriction diverts Blood to where it is needed

From skin & digestive organs to brain, heart & skeletal muscle

MAJOR ENDOCRINE ORGANS

PANCREAS

Large, soft, triangular - posterior to stomach

Mixed gland: Endocrine & Exocrine function

Exocrine Pancreas ~ 99%

Ascinar Cells ~ epithelial cells ~ 99% of gland

Digestive enzymes ducted into small intestine

Amylase ~ carbohydrate breakdown

Lipase ~ lipid breakdown

Protease ~ protein breakdown

Endocrine Pancreas ~ 1%

Islets of Langerhans~ 1% of Gland

Tiny island cluster cells among Ascinar cells

Alpha cells ~ secrete Glucagon

Beta cells ~ secrete Insulin

Both regulate blood glucose ~ effects are opposite

Glucagon ~ raises blood glucose ~ hyper-glycemic

Insulin ~ lowers blood glucose ~ hypo-glycemic

GLUCAGON

Protein produced in alpha cells ~ (islets of langerhans)

Potent hyper-glycemic effects: ( Blood Sugar

Glucagon Secretion ~ Humoral Stimuli

Stimulated by: Falling blood sugar levels

Inhibited by: Rising blood sugar levels

Effects of Glucagon ~ Glucagon ( Blood Sugar

1. Breaks down glycogen to glucose ~ glycogenolysis

2. Stimulates Glucose Synthesis from fats & amino acids

“Gluconeogenesis”

3. Stimulates Release of glucose from liver into blood

( Blood sugar

4. Stimulates breakdown of protein to Amino Acids

“Catabolic Effect”

INSULIN

Small protein ~ made in beta cells ~ islets of langerhans

Potent hypoglycemic effects ( Blood Sugar

Insulin Secretion ~ Humoral Stimuli

Stimulated by: Rising blood sugar levels

Eating a meal

Other hyperglycemic hormones

Glucagon Growth Hormone

Thyroxin Glucocorticoids

Adrenalin

Inhibited by: Lower blood sugar levels

Major Effects of Insulin ~ opposite of glucagon

1. Enhances glucose uptake & utilization by all cells

2. Stimulates glycogen storage in muscle & liver

Inhibits Glycogenolysis ~ lowers blood sugar

3. Inhibits conversion of fats & amino acids to glucose

Inhibits Gluconeogenesis ~ lowers blood sugar

4. Stimulates protein synthesis from amino acids

“Anabolic Effect”

5. Stimulates Glucose conversion to fat for storage

PANCREATIC DYSFUNCTION

HYPO-GLYCEMIA ~ low blood sugar

Causes: Glucagon Deficiency

Insulin overdose - very common

Symptoms: Persistent low blood sugar

Anxiety - - - > Nervousness - - - > Tremors

- - - > Weakness - - - > Convulsions - - - >

Diabetic Coma - - - > Unconscious - - - > Death

Treatment: dietary sugar . . . candy bar . . . orange

juice

HYPER-GLYCEMIA ~ high blood sugar ~ COMMON

Causes: Insulin Deficiency ~ “Diabetes Mellitus”

Cells cannot utilize glucose

Symptoms: Nausea & Anxiety

Glucosuria ~ high urine sugar spill over

Ketouria ~ ketones in urine from FA

Ketoacidosis ~ drop in blood pH → ↑ H+

Rapid breathing ~ blow off carbon dioxide

to increase blood pH ~ Hyperpnea

Severe depression, coma, death

Three Cardinal Signs of Diabetes Mellitus ~ “3 P’s”

1) Polyuria ~ excessive urine output

High glucose in blood causes spill over into acts as diuretic ~ draws water into urine

Concentrated urine ~ high Specific Gravity > 1.035

Decreased blood volume & dehydration ~ fluid loss

2) Polydipsia ~ excessive thirst

Severe dehydration due to fluid loss ---->

Stimulates hypothalamus thirst centers

------->>> Excessive thirst

3) Polyphagia ~ excessive appetite

Body cannot utilize glucose ~ thinks it’s starving

Excessive hunger & food intake

Treatment of Diabetes Mellitus:

Type I ~ Juvenile ~ Insulin Dependent Diabetic ~ 10% of

cases

Treat with Synthetic Insulin

Type II ~ Non-Insulin Dependent ~ 90% of cases

Treat with Proper Diet, Weight Loss & Exercise

OTHER ENDOCRINE ORGANS

PINEAL GLAND

Tiny pine cone shaped . . . in epithalamus of diencephalon

Soft tissue landmark ~ pineal sand/calcium for brain X-rays

Endocrine function is a mystery ~ biorythms/sleep-wake/temp

MELATONIN ~ pineal gland hormone

Peak levels at night make us drowsy

Stimulation of pineal gland related to visual light

Influences sleep/wake cycle, body temperature, & appetite ~ biorythms

THYMUS

Large in infants & children ~ provides immunity in children

Located deep to sternum in upper thorax at base of heart

Becomes adipose tissue & connective tissue with age ~ scars

Secretes hormones: Thymopoitens

Thymosins

Effect: Normal development of T-lymphocytes ~ T-cells

Important in the immune response ~ infant & young

OTHER ENDOCRINE ORGANS

GONADS

Male Gonads ~ Testis Female Gonads ~ Ovaries

Produce more sex hormones than the adrenal cortex . . .

Release regulated by FSH & LH gonadotropins from pituitary

OVARIES ~ Two oval shaped . . . Posterior abdominal cavity

Produce ova or eggs for fertilization

Produce female ovarian hormones

ESTROGEN ~ release influenced by FSH

Released from follicle cells of ovaries

Causes maturation of reproductive organs

Female secondary sex characteristics ~ puberty

Menstrual cycle ~ uterus cyclic changes

PROGESTERONE ~ release influenced by LH

Released from corpus luteum ~ old follicle

Maintains pregnancy ~ secreted for months

TESTES

Two ~ Located in “extra-abdominal” sac ~ scrotum

Produce sperm (influenced by FSH) & male sex hormone

Testicular Hormones ~ male hormone ~ androgens

TESTOSTERONE ~ release influenced by LH

Produced in interstitial cells of testis

Causes maturation of male reproductive organs

Male secondary sex characteristics & sex drive

Necessary for normal sperm production

OTHER HORMONE PRODUCING STRUCTURES

Not really endocrine glands . . . but have other endocrine cells

HEART

Atrial wall stretched by excess fluid volume & pressure

Releases: Atrial Natriuretic Peptide ~ ANP

Effects of ANP:

Inhibits Aldosterone release by adrenal cortex

Inhibits sodium & fluid retention

Reduces blood volume & lowers blood pressure

GASTROINTESTINAL TRACT (GIT) ORGANS

Several Hormones Released to aid digestion

Hormone Source Target Organ & Effect

Gastrin Stomach Stomach HCL release

Serotonin Stomach Stomach contraction

Intestinal Duodenum Inhibits stomach HCL

Gastrin Slows GI Motility

Secretin Duodenum Inhibits gastric secretions

Release bicarbonate from

pancreas & liver

Cholecystokinin Duodenum Pancreatic juices & bile

Amylase ~ CHO

Lipase ~ Fats

Protease ~ Proteins

KIDNEY

Erythropoietin ~ EPO Influences bone marrow to

produce more RBC’s

Renin Stimulates Aldosterone

SKIN

Cholicalciferol Precursor to Vitamin D3

Intestine absorb of Ca++

HORMONES INVOLVED IN GROWTH

Involves coordination of several endocrine organs

Important Hormones: Growth Hormone

Thyroid Hormone

Insulin

Parathyroid Hormone

Calcitrol ~ for Ca++ absorption

Reproductive Hormones

HORMONES INVOLVED IN AGING

Few functional changes with age ~ most work until death

Major changes involve decline of reproductive hormones

Decline in Growth Hormone

Other changes due to disease processes ~ i.e., diabetes

HORMONES INVOLVED IN STRESS

Stress Activates the General Adaptation Syndrome

Involves: Hypothalamus . . . Adrenal Gland . . . Organs

General Adaptation Syndrome Phases

Alarm Phase ~ immediate fight or flight ~ adrenaline

Neural Stimulation ~ immediate ~ short acting

Catecholamines: Epinephrine & Nor-epinephrine

Sympathetic Effects: ↑ BP . . . ↑ HR . . . ↓ Digestion

Resistance Phase ~ longer term response

Involves several endocrine organs

Anterior Pituitary ~ ACTH ~ stimulates adrenals

Growth Hormone ~ mobilizes energy reserves

Kidney releases Renin ~ stimulates aldosterone

Gluconeogenesis ~ ↑ glucose for energy

Na+ & fluid retention ~ ↑ Blood Pressure

Exhaustion Phase ~ organ & TOTAL system failure

It’s over!!!

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