Lecture 13 Endocrine System - Linn–Benton Community Collegecf.linnbenton.edu/mathsci/bio/waitea/upload/Lecture_13... · 2017-03-08 · )ljxuh p51$ 1hz surwhlq '1$ +ruprqh uhvsrqvh

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The Endocrine System

Overview Acts with the nervous system (NS)

Major effector of homeostatic systems

Influences metabolic activities using hormones Responses occur more slowly but last longer than NS

Endocrine glands Pituitary, thyroid, thymus, pancreas, parathyroid, gonads,

adrenal and pineal glands

Figure 16.1

Pineal glandHypothalamus

Pituitary gland

Parathyroid glands(on dorsal aspectof thyroid gland)Thymus

Thyroid gland

Adrenal glands

Pancreas

Ovary (female)

Testis (male)

Overview

Nervous System Endocrine System Nerve impulses Neurotransmitters Faster responses Brief effects Acts on specific target

Hormones Slower responses Longer effects Broader influence

Overview Extensive integration between endocrine and nervous

systems Due to neuroendocrine cells

Cells that respond directly to neurotransmitters by releasing hormones Found in many organs (lungs, adrenals) Found extensively in the hypothalamus and pituitary –

considered neuroendocrine organs

Hormones

Chemical substances secreted by cells Very long-distance chemical signals

Secreted directly into the bloodstream Travel in the blood or lymph

Most are amino-acid based or steroid molecules

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Hormones Two main classes

1. Amino acid-based hormones Amines, peptides, and proteins

2. Steroids Synthesized from cholesterol Gonadal and adrenocortical hormones

Copyright © 2010 Pearson Education, Inc.

(a) Humoral Stimulus (b) Neural Stimulus

Capillary (lowCa2+ in blood)

Parathyroidglands

Thyroid gland(posterior view)

PTH

Parathyroidglands

1 Capillary blood containslow concentration of Ca2+,which stimulates...

1 Preganglionic sympatheticfibers stimulate adrenalmedulla cells...

2 …secretion ofparathyroid hormone (PTH)by parathyroid glands*

2 …to secrete catecholamines (epinephrine andnorepinephrine)

Figure 16.4 Three types of endocrine gland stimuli.

Endocrine Gland Stimulation

• Humoral Stimulation• Changes in blood or other

bodily fluids

• Examples: solute

concentration, temperature


(a) Humoral Stimulus (b) Neural Stimulus (c) Hormonal Stimulus


Parathyroidglands


PTH

Parathyroidglands

CNS (spinal cord)

Medulla ofadrenalgland

Preganglionicsympatheticfibers

Capillary



1hormones that...

2the anteriorpituitary glandto secretehormones that…


2 …to secrete catechola-mines (epinephrine andnorepinephrine)

3glands to secrete hormones


• Neural Stimulation• Hormone is released is

directly triggered by a neuron

• Rapid response

• Example: milk ejection reflex

Figure 16.4 Three types of endocrine gland stimuli. Copyright © 2010 Pearson Education, Inc.

(a) Humoral Stimulus (b) Neural Stimulus(c) Hormonal Stimulus


Parathyroidglands


PTH

Parathyroidglands

CNS (spinal cord)

Medulla ofadrenalgland


Capillary

Hypothalamus

Thyroidgland

Adrenalcortex

Gonad(Testis)

Pituitarygland



1 The hypothalamus secreteshormones that...

2 …stimulatethe anteriorpituitary glandto secretehormones that…


2 …to secrete catechola-mines (epinephrine andnorepinephrine)

3 …stimulate other endocrineglands to secrete hormones

Figure 16.4 Three types of endocrine gland stimuli.


• Hormonal Stimulation• One hormone triggers the

release of another

• Example: thyroid-stimulating

hormone stimulates the

release of thyroid hormone

Target Cell Specificity

Target cell = a cell affected by a hormone A single hormone may have more than one type of target cell Specific receptors

Hormone effects are due to alteration of cell’s activity Effects vary


Target cell effects depend on three factors1. Blood levels of the hormone2. Relative number of receptors on or in the target cell3. Affinity of binding between receptor and hormone

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Hormones influence the number of their receptors Up-regulation

Target cells form more receptors in response to the hormone

Down-regulation Target cells lose receptors in response to the hormone


Hormone concentration depends onRate of synthesis and release Speed of inactivation

Mechanism of Action Slow acting Fatty acids or steroids Examples: estrogen,

testosterone, cortisol

Fast acting Proteins or peptides Examples: insulin, oxytocin,

leptin

Thought Questions What is the plasma membrane made of?

What class of hormones (steroids or amino acid based) should be able to cross it?

Slow Acting Hormones

Steroid hormone crosses lipid-based membrane

Enters nucleus

Interacts with DNA

Changes cell function by initiating gene transcription

Relatively long lasting effects Examples: testosterone and estrogen

Figure 16.3

mRNA

New protein

DNA

Hormoneresponseelements

Receptor-hormonecomplex

Receptorprotein

Cytoplasm

Nucleus

Extracellular fluid

Steroidhormone

The steroid hormonediffuses through the plasmamembrane and binds anintracellular receptor.

Plasmamembrane

1

2

3

4

5

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Figure 16.3

mRNA

New protein

DNA



Receptorprotein

Cytoplasm

Nucleus

Extracellular fluid

Steroidhormone


The receptor-hormone complex entersthe nucleus.

Plasmamembrane

1

2

3

4

5

Figure 16.3

mRNA

New protein

DNA



Receptorprotein

Cytoplasm

Nucleus

Extracellular fluid

Steroidhormone



The receptor- hormonecomplex binds a hormoneresponse element (aspecific DNA sequence).

Plasmamembrane

1

2

3

4

5

Figure 16.3

mRNA

New protein

DNA



Receptorprotein

Cytoplasm

Nucleus

Extracellular fluid

Steroidhormone




Binding initiatestranscription of thegene to mRNA.

Plasmamembrane

1

2

3

4

5

Figure 16.3

mRNA

New protein

DNA



Receptorprotein

Cytoplasm

Nucleus

Extracellular fluid

Steroidhormone




Binding initiatestranscription of thegene to mRNA.

The mRNA directsprotein synthesis.

Plasmamembrane

1

2

3

4

5

Fast Acting HormonesAmino acid-based hormone binds to a receptor protein

(hormone is first messenger)

Activates internal second messenger (cyclic-AMP)

Activates enzymes

Rapid change in cell function

Relatively short term effects May be greatly amplified Examples: glucagon and parathyroid hormone

Figure 16.2

Hormone (1st messenger)binds receptor.

Receptor

G protein (GS)

Adenylate cyclase

Triggers responses oftarget cell (activatesenzymes, stimulatescellular secretion,opens ion channel,etc.)

Hormones thatact via cAMPmechanisms:EpinephrineACTHFSHLH

Inactiveprotein kinase

Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP

GlucagonPTHTSHCalcitonin

1

2 3 4

5

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Figure 16.2


Receptoractivates Gprotein (GS).

Receptor

G protein (GS)

Adenylate cyclase




Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP


1

2 3 4

5

Figure 16.2



G proteinactivatesadenylatecyclase.

Receptor

G protein (GS)

Adenylate cyclase




Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP


1

2 3 4

5

Figure 16.2




Adenylatecyclaseconverts ATPto cAMP (2ndmessenger).

Receptor

G protein (GS)

Adenylate cyclase




Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP


1

2 3 4

5

Figure 16.2




cAMP acti-vates proteinkinases.

Adenylatecyclaseconverts ATPto cAMP (2ndmessenger).

Receptor

G protein (GS)

Adenylate cyclase




Extracellular fluid

Cytoplasm

Activeproteinkinase

GDP


1

2 3 4

5

GPCR second messenger system

Cellular Hormones

Some cells outside the endocrine glands have endocrine capacity Intestine secretin and cholecystokinin Kidney erythropoietin

Pituitary Gland

2 lobes1. Anterior pituitary lobe (adenohypophysis)

Glandular tissue Releases hormones formed within pituitary

2. Posterior pituitary lobe (neurohypophysis) Glial-like supporting cells and nerve fibers Releases hormones formed within hypothalamus

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Figure 16.5b

Hypothalamus

Anterior lobeof pituitary

(releases hormones made within the

pituitary)

Posterior lobe of pituitary

(releases hormones made within the hypothalamus)

Anterior Pituitary Hormones• Growth hormone (GH)

• Thyroid stimulating hormone (TSH)

• Adrenocorticotropic hormone (ACTH)• Follicle stimulating hormone (FSH)

• Luteinizing hormone (LH)• Prolactin

• Melanocyte stimulating hormone (MSH)

Growth Hormone (GH) Stimulates most cells

Main targets = bone & skeletal muscle

Functions Promotes protein synthesis Encourages use of fats for fuel Breakdown of glycogen

Imbalances of Growth Hormone Hypersecretion

Gigantism Acromegaly

Hyposecretion Pituitary dwarfism Simmond’s disease

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Acromegaly

Heaviness of jaw Increased size of digits


Acromegaly?


Pituitary Dwarfism

Large head

Normal size torso

Short arms and legs

Twin boys


Simmond’s Disease

Caused by atrophy or destruction

of anterior pituitary

Extreme, progressive emaciation,

loss of body hair, premature aging

• Underlying cause must be addressed

(usually a pituitary tumor)

• Hormone replacement therapy is

effective, may come with side

effects (complicated where infertility

is involved)

Figure 16.6

Growth hormone

Feedback Inhibits GHRH releaseStimulates GHIHreleaseInhibits GH synthesisand release

Anteriorpituitary

Liver andother tissues

Indirect actions(growth-promoting)

Direct actions(metabolic,anti-insulin)

Insulin-like growthfactors (IGFs)

ExtraskeletalSkeletal FatCarbohydratemetabolism

Increased cartilageformation and

skeletal growth

Increased proteinsynthesis, andcell growth and

proliferation

Increasedfat breakdown

and release

Increased bloodglucose and otheranti-insulin effects

EffectsEffects

Produce

Hypothalamussecretes growthhormone—releasinghormone (GHRH), andsomatostatin (GHIH)

Initial stimulus

Physiological response

Result

Increases, stimulates

Reduces, inhibits

Growth Hormone Treatment rHGH used to treat a number of conditions Most common: HGH deficiency in children Wasting caused by AIDS Turner Syndrome Chronic renal failure

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Growth Hormone in Sports

Use without a prescription is illegal Suspected high level of abuse in all sports Supposed benefits: lean body mass, increased muscle

mass, injury resistance Drawbacks: lower stamina,

fatigue, no increase in muscle strength despite increased mass, increased risk of diabetes, joint and muscle pain, hypertension, osteoporosis

Growth Hormone in Agriculture

rBGH has been legal to be injected into dairy cows in the US since 1993

Increases milk production by ~15% Nutritionally identical (almost) Increased incidence of mastitis Different hormonal profile

Thyroid-Stimulating Hormone (TSH)

Produced by the anterior pituitary Stimulates the normal development and secretory

activity of the thyroid Regulation of TSH release

Stimulated by hypothalamus (thyrotropin-releasing hormone) Inhibited by rising blood levels of thyroid hormones

Copyright © 2010 Pearson Education, Inc. Figure 16.7

Hypothalamus

Anterior pituitary

Thyroid gland

Thyroidhormones

TSH

TRH

Target cellsStimulates

Inhibits

Adrenocorticotropic Hormone (ACTH)

Secreted by the anterior pituitary Stimulates the adrenal cortex to release corticosteroids

Gonadotropins (FSH & LH)

Follicle-stimulating hormone (FSH) and luteinizing hormone (LH or ICSH)

Secreted by the anterior pituitary Regulate function of ovaries and testes

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Gonadotropins (FSH & LH) Regulation of gonadotropin release

Triggered by gonadotropin-releasing hormone (GnRH) Absent from the blood in

prepubertal boys and girls

Suppressed by gonadal hormones Estrogen Progesterone Testosterone

NegativeFeedback

NegativeFeedback

Prolactin Secreted by the anterior pituitary

Stimulates milk production Blood levels rise toward the end of pregnancy Suckling stimulates PRH release and promotes continued milk

production

Prolactin Contributes to spermatogenesis in men

Hypersecretion may suppress gonadal hormones Amenorrhea in females Infertility, impotence in men

Plays a role in neurogenesis, fetal lung development, and

immune tolerance of fetus Production rises with use of MDMA (ecstasy)

Melanocyte Stimulating Hormone

Stimulates melanocytes• Stimulates melanocytes = darkening of skin• May influence brain activity

• Appetite, arousal

Control of Anterior Pituitary HormonesPituitary-Hypothalamic Relationships

Hypophyseal portal system Capillary plexuses Hypophyseal portal veins

Allows hormones to be sent from the hypothalamus to the pituitary via the bloodstream without being diluted in general circulation

Figure 16.5b

1

2

3

When appropriatelystimulated, hypothalamic neurons secrete releasing and inhibiting hormones into the primary capillary plexus.

Hypothalamus

Hypothalamic neuroncell bodies

Hypophysealportal system

Superiorhypophyseal artery

(b) Relationship between the anterior pituitary and the hypothalamus

Anterior lobeof pituitaryTSH, FSH, LH, ACTH, GH, PRL, MSH

• Primary capillaryplexus

• Hypophysealportal veins

• Secondarycapillaryplexus

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Figure 16.5b

1

2

3


Hypothalamic hormones travel through the portal veins to the anterior pituitary where they stimulate or inhibit release of hormones from the anterior pituitary.

Hypothalamus









Figure 16.5b

1

2

3


Hypothalamic hormones travel through the portal veins to the anterior pituitary where they stimulate or inhibit release of hormones from the anterior pituitary.

Anterior pituitaryhormones are secreted into the secondary capillary plexus.

Hypothalamus









Releasing Factors

Releasing factors Growth Hormone Releasing Hormone Thyroid Hormone Releasing Hormone

Inhibiting factors Identified for prolactin and GH

Negative feedback

Posterior Pituitary

Contains axons of hypothalamic neurons

Hormones produced by hypothalamus

Stores antidiuretic hormone (ADH) and oxytocin Released in response to nerve impulses

Copyright © 2010 Pearson Education, Inc. Figure 16.5a

1

2

3

4

Hypothalamicneuronssynthesize oxytocin and ADH.Paraventricular

nucleus Supraopticnucleus Optic chiasma

Hypothalamus

Inferiorhypophyseal artery

OxytocinADH

Infundibulum (connecting stalk)Hypothalamic-hypophysealtract

Axon terminalsPosteriorlobe ofpituitary


1

2

3

4

Hypothalamicneuronssynthesize oxytocin and ADH.

Oxytocin and ADH aretransported along the hypothalamic-hypophyseal tract to the posterior pituitary.

Paraventricularnucleus Supraopticnucleus Optic chiasma

Hypothalamus


OxytocinADH



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1

2

3

4



Oxytocin and ADH arestored in axon terminals in the posterior pituitary.


Hypothalamus


OxytocinADH




1

2

3

4



Oxytocin and ADH arestored in axon terminals in the posterior pituitary.

Oxytocin and ADH are released into the blood when hypothalamic neurons fire.


Hypothalamus


OxytocinADH



Oxytocin

Stimulates uterine contractions during childbirth Synthetic versions used to induce labor

Also triggers milk ejection

(“letdown” reflex) in lactating women Plays a role in sexual arousal and

orgasm in males and females

“Bonding” hormone

Antidiuretic Hormone (ADH) Hypothalamic osmoreceptors respond to changes in the

solute concentration of the blood…

Solute concentration is high

Osmoreceptors transmit impulses to hypothalamic neurons

ADH synthesized and released

Urine formation inhibited

or…

Antidiuretic Hormone (ADH) Hypothalamic osmoreceptors respond to changes in the

solute concentration of the blood…

Solute concentration is low

ADH inhibited

Increased urine production

Homeostatic Imbalances of ADH

Diabetes insipidus* = Low ADH Huge output of urine and intense thirst Treated with ADH administration

* Not the same as excessive thirst and urine output caused by diabetes

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Figure 16.1

Pineal glandHypothalamus

Pituitary gland


Thyroid gland

Adrenal glands

Pancreas

Ovary (female)

Testis (male)

Thyroid Gland

Saddle bag shaped gland Largest endocrine gland in the body 3 hormones

Thyroxine (T4) Triiodothyronine (T3) Calcitonin

Thyroid hormone

Figure 16.8

Site of T3, T4

synthesis

Site of calcitoninsynthesis

Thyroid Hormone (TH)

Actually two related compounds T4 (thyroxin) 2 tyrosine molecules + 4 bound iodine atoms 90% of what is produced Converted to T3 in target cell

T3 (triiodothyronine) 2 tyrosines + 3 bound iodine atoms 4X more active than T4

Thyroid Hormone (TH)1) Iodide enters body

2) Converted to iodine by thyroid gland in the colloid

3) Iodine binds to tyrosines (part of thyroglobulin) in the colloid4) Iodinated tyrosines and are endocytosed by follicular cells and

combined w/lysosomes

5) Enzymes cleave T3/T4 from thyroglobulin6) Thyroglobulin freed and recycled while T3/T4 diffuses into

blood7) T3/T4 bind to thyroxin-binding globulin in blood

8) At tissue receptors, T4 is converted to active T3 by enzymes(See video on instructor website)

Figure 16.9

To peripheral tissues

T3

T3

T3

T4

T4

Lysosome

Tyrosines (part of thyroglobulinmolecule)

T4

DIT (T2)Iodine

MIT (T1)

Thyro-globulincolloid

Iodide (I–)

RoughER

Capillary

Colloid

Colloid inlumen offollicle

Thyroid follicle cells

Thyroglobulin is synthesized anddischarged into the follicle lumen.

Golgiapparatus

1

2

3

4

5

6

7

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Figure 16.9


T3

T3

T3

T4

T4

Lysosome


T4

DIT (T2)Iodine

MIT (T1)


Iodide (I–)

RoughER

Capillary

Colloid



Iodide (I–) is trapped(actively transported in).


Golgiapparatus

1

2

3

4

5

6

7

Figure 16.9


T3

T3

T3

T4

T4

Lysosome


T4

DIT (T2)Iodine

MIT (T1)


Iodide (I–)

RoughER

Capillary

Colloid



Iodideis oxidizedto iodine.



Golgiapparatus

1

2

3

4

5

6

7

Figure 16.9


T3

T3

T3

T4

T4

Lysosome


T4

DIT (T2)Iodine

MIT (T1)


Iodide (I–)

RoughER

Capillary

Colloid






Iodine is attached to tyrosinein colloid, forming DIT and MIT.

Golgiapparatus

1

2

3

4

5

6

7

Figure 16.9


T3

T3

T3

T4

T4

Lysosome


T4

DIT (T2)Iodine

MIT (T1)


Iodide (I–)

RoughER

Capillary

Colloid



Iodinated tyrosines arelinked together to form T3

and T4.





Golgiapparatus

1

2

3

4

5

6

7

Figure 16.9


T3

T3

T3

T4

T4

Lysosome


T4

DIT (T2)Iodine

MIT (T1)


Iodide (I–)

RoughER

Capillary

Colloid




and T4.


Thyroglobulin colloid isendocytosed and combinedwith a lysosome.




Golgiapparatus

1

2

3

4

5

6

7

Figure 16.9


T3

T3

T3

T4

T4

Lysosome


T4

DIT (T2)Iodine

MIT (T1)


Iodide (I–)

RoughER

Capillary

Colloid




and T4.


Thyroglobulin colloid isendocytosed and combinedwith a lysosome.

Lysosomal enzymes cleaveT4 and T3 from thyroglobulincolloid and hormones diffuseinto bloodstream.




Golgiapparatus

1

2

3

4

5

6

7

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Thyroid Hormone (TH)

Major metabolic hormone (catabolism) Regulates tissue growth and development Increases reactivity of mature nerve cells Regulates heart rate Regulates movement of gastrointestinal tract

Figure 16.7

Hypothalamus

Anterior pituitary

Thyroid gland

Thyroidhormones

TSH

TRH

Target cellsStimulates

Inhibits

Imbalances of Thyroid Hormone

Goiter Cretinism Myxedema Graves disease

Figure 16.10

Goiter• Enlargement of thyroid

• Due to inflammation or hyperplasia

• Caused most commonly by iodine deficiency• Can also be caused by Hashimoto’s disease, ingestion of

goitrogens• Associated with both hypo

and hyperthyroidism

Cretinism• Congenital hypothyroidism

• Usually caused by maternal iodine deficiency during pregnancy

• Severely stunted physical growth, developmental delay

Myxedema• Hypothyroidism in adults

• Lethargy, low body temperature, swollen face, leathery skin

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Graves Disease• Hyperthyroidism

• Often treated by destruction or removal of thyroid tissue

Calcitonin

Made in parafolicular cells Lowers serum calcium

Inhibits bone resorption Stimulates uptake by the bone matrix

Antagonist to parathyroid hormone (PTH) Regulated by Ca2+ concentration in the blood

Negative feedback mechanism Falling Ca2+ in the blood inhibits calcitonin release

Parathyroid Glands

4-8 tiny glands embedded in the posterior aspect of the thyroid Parathyroid hormone (PTH)

Most important hormone in Ca2+ homeostasis

Figure 16.11

(b)

Capillary

Chiefcells

(secreteparathyroidhormone)

Oxyphilcells

Pharynx(posterioraspect)

Thyroidgland

Parathyroidglands

Trachea

Esophagus

(a)

Parathyroid Hormone Functions

Stimulates osteoclasts to digest bone matrix Enhances reabsorption of Ca2+ by the kidneys Increases absorption of Ca2+ by intestinal mucosa

Parathyroid Hormone Negative feedback

Rising Ca2+ in the blood inhibits PTH release

Hyperparathyroidism causes severe osteoporosis

Normal bone Osteoporotic bone

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Parathyroid Hormone Negative feedback

Rising Ca2+ in the blood inhibits PTH release

Hyperparathyroidism causes severe osteoporosis

Figure 16.12

Intestine

Kidney

Bloodstream

Hypocalcemia (low blood Ca2+) stimulatesparathyroid glands to release PTH.

1

2

3

Bone

Ca2+ ions

PTH Molecules

Figure 16.12

Intestine

Kidney

Bloodstream


1 PTH activatesosteoclasts: Ca2+

and PO43S released

into blood.2

3

Bone

Ca2+ ions

PTH Molecules

Figure 16.12

Intestine

Kidney

Bloodstream



and PO43S released

into blood.2 PTH increasesCa2+ reabsorption

in kidneytubules.

3

Bone

Ca2+ ions

PTH Molecules

Figure 16.12

Intestine

Kidney

Bloodstream



and PO43S released


in kidneytubules.

3 PTH promoteskidney’s activation of vitamin D,which increases Ca2+ absorptionfrom food.

Bone

Ca2+ ions

PTH Molecules

Figure 16.12

Intestine

Kidney

Bloodstream


Rising Ca2+ inblood inhibitsPTH release.


and PO43S released


in kidneytubules.

3 PTH promoteskidney’s activation of vitamin D,which increases Ca2+ absorptionfrom food.

Bone

Ca2+ ions

PTH Molecules

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Adrenal Glands

Paired, pyramid-shaped glands atop the kidneys Essentially two glands in oneAdrenal medulla Nervous tissue: part of the sympathetic nervous system NE and Epinephrine

Adrenal cortex Three layers of glandular tissue Synthesize and secrete steroid hormones

Figure 16.1

Pineal glandHypothalamusPituitary gland


Thyroid gland

Adrenal glands

Pancreas

Ovary (female)

Testis (male)

Adrenal Cortex

Three layers that produce corticosteroids Outer layer = mineralocorticoids (ex. aldosterone) Middle layer = glucocorticoids (ex. cortisol) Inner layer = sex hormones or gonadocorticoids (ex. androgens)

Figure 16.13a

• Cortex

Kidney

• Medulla

Adrenal gland

CapsuleZona

glomerulosa

Zonafasciculata

Zonareticularis

Adrenalmedulla

(a) Drawing of the histology of theadrenal cortex and a portion ofthe adrenal medulla

Med

ulla

Cor

tex

Mineralocorticoids

Regulate extracellular Na+ and K+

Na+: affects ECF volume, blood volume, blood pressure K+: sets resting membrane potential of cells

Aldosterone is most important Stimulates Na+ reabsorption (and water retention) by kidneys Stimulates K+ secretion Effect on blood pressure? Consequences of overproduction?

Figure 16.14

Primary regulators Other factors

Blood volumeand/or blood

pressure

Angiotensin II

Blood pressureand/or blood

volume

K+ in blood

DirectstimulatingeffectRenin

Initiatescascadethatproduces

Kidney

Hypo-thalamus

Heart

CRH

Anteriorpituitary

Zona glomerulosaof adrenal cortex

Enhancedsecretionof aldosterone

Targetskidney tubules

Absorption of Na+ andwater; increased K+ excretion

Blood volumeand/or blood pressure

Inhibitoryeffect

Stress

ACTH Atrial natriureticpeptide (ANP)

Secretion mainlycontrolled by

blood pressure andpotassium levels

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Figure 16.14

Primary regulators Other factors

Blood volumeand/or blood

pressure

Angiotensin II

Blood pressureand/or blood

volume

K+ in blood

DirectstimulatingeffectRenin

Initiatescascadethatproduces

Kidney

Hypo-thalamus

Heart

CRH

Anteriorpituitary

Zona glomerulosaof adrenal cortex

Enhancedsecretionof aldosterone

Targetskidney tubules

Absorption of Na+ andwater; increased K+ excretion

Blood volumeand/or blood pressure

Inhibitoryeffect

Stress

ACTH Atrial natriureticpeptide (ANP)

Secretion mainlycontrolled by

blood pressure andpotassium levels

HPA axis (more on this later)

Glucocorticoids Regulate carbohydrate metabolism Keep blood sugar levels relatively constant

Stimulates gluconeogenesis during fasting

Suppress inflammation ↑ Vasoconstriction ↓ Vessel permeability Stabilizing lysosomes

Imbalances of Glucocorticoids

Cushing’s diseaseOver-production of cortisolUsually due to pituitary adenomaWeight gain (“moon face,” stretch marks)High blood pressure Poor short-term memory Excess hair growth Poor immune system

Figure 16.15


Addison’s disease Deficiency of glucocorticoids and mineralocorticoids Hyperpigmentation of skin and mucous membranes Weight loss Fatigue Lightheadedness Muscle weakness Fever Anxiety Vomiting and diarrhea


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Gonadocorticoids (Sex Hormones) Most are androgens (male sex hormones)

Converted to testosterone in tissue cells or estrogens

Supplement hormones secreted by gonads May contribute to

Onset of puberty Secondary sex characteristics Sex drive

Adrenal Medulla - Catecholamines

Epinephrine Affects the metabolic rate of all cells Bronchial dilation Increased blood flow to skeletal muscles and heart

Norepinephrine Increased blood pressure Increased heart rate Increased stroke volume

Figure 16.16

Short-term stress More prolonged stress

Stress

Hypothalamus

CRH (corticotropin-releasing hormone)

Corticotroph cellsof anterior pituitary

To target in blood

Adrenal cortex(secretes steroidhormones)

GlucocorticoidsMineralocorticoids

ACTH

Catecholamines(epinephrine andnorepinephrine)

Short-term stress response1. Increased heart rate2. Increased blood pressure3. Liver converts glycogen to glucose and releases

glucose to blood4. Dilation of bronchioles5. Changes in blood flow patterns leading to decreased

digestive system activity and reduced urine output6. Increased metabolic rate

Long-term stress response1. Retention of sodium

and water by kidneys2. Increased blood volume

and blood pressure

1. Proteins and fats convertedto glucose or broken downfor energy

2. Increased blood glucose3. Suppression of immune

system

Adrenal medulla(secretes amino acid-based hormones)


Spinal cord

Nerve impulses

HPA axis (more on this later; really, I

promise)

Imbalances in Adrenal Medulla

Adrenal medullary hormones not essential for life Pheochromocytoma

Neuroendocrine tumor of adrenal medulla Secretes high levels of catecholamines What symptoms do you think would present?

Imbalances in Adrenal Medulla

Adrenal medullary hormones not essential for life Pheochromocytoma

Neuroendocrine tumor of adrenal medulla Secretes high levels of catecholamines High BP and heart rate, palpitations Anxiety/panic attacks Headaches Excessive sweating High blood glucose

Pancreas

Long, flat gland near stomach Exocrine function

Produces enzyme rich juice for digestion

Endocrine function Pancreatic islets (islets of Langerhans) Alpha () cells = glucagon

Hyperglycemic hormone Beta () cells = insulin

Hypoglycemic hormone

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Figure 16.1

Pineal glandHypothalamusPituitary gland


Thyroid gland

Adrenal glands

Pancreas

Ovary (female)

Testis (male)

Exocrine Pancreas

Pancreatic juices excreted into pancreatic duct Enzymes for digestion

Trypsinogen, pancreatic lipase, amylase, nuclease, others

Bicarbonate for neutralizing stomach acid

Required for optimal enzyme activity

Joins common bile duct at ampulla of Vater Drains into duodenum Blocking the pancreatic duct may lead to pancreatitis

Most commonly due to gallstones

Common bile duct

Pancreatic duct

Ampulla of Vater

Exocrine PancreasEndocrine Pancreas - Glucagon

Major target is the liver Initiates breakdown of glycogen into glucose (glycogenolysis) Causes increase in blood glucose Opposite action of insulin

For severe diabetic hypoglycemia (seizures, unconsciousness)

Endocrine Pancreas - Insulin Effects

Lowers blood glucose levels Enhances membrane transport of glucose Inhibits glycogenolysis and gluconeogenesis

Figure 16.18

Liver

Liver

Tissue cells

Stimulates glucose uptake by cells

StimulatesglycogenformationPancreas

Pancreas

Insulin

Bloodglucosefalls tonormalrange.

Stimulatesglycogenbreakdown

Bloodglucoserises tonormalrange.

Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

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Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

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Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

Figure 16.18

Liver

Liver

Tissue cells



Pancreas

Insulin




Glucagon

StimulusBlood

glucose level

StimulusBlood

glucose level

GlycogenGlucose

GlycogenGlucose

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Imbalances of Insulin

Diabetes mellitus (DM)Due to hyposecretion or hypoactivity of insulinGlucose comes through in the urine and takes water

with it Three cardinal signs of DM Polyuria = copious urine output Polydipsia = excessive thirst Polyphagia = excessive hunger and food consumption

Diabetes Mellitus Type I Type II Gestational

Insulin cont.

Other hormones affecting insulin levels Growth hormone (GH) raises blood glucose Adrenocorticotropic hormone (ACTH) increases

glucocorticoid production, which raises blood glucose Effect on insulin release?

Insulin cont.

Other hormones affecting insulin levels Growth hormone (GH) raises blood glucose Adrenocorticotropic hormone (ACTH) increases

glucocorticoid production, which raises blood glucose Stimulates insulin release

Minor Endocrine Glands

Thymus Pineal gland

Thymus

2 lobed organ high in chest Thymosins Small proteins Stimulate lymphocyte production

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Thymus

Hugely important in immune system developmentActive during fetal development and for first two

years after birthBlood-thymic barrier strongest blood barrier in the

body

Pineal Gland

Small gland hanging from the roof of the third ventricle Melatonin Timing of sexual maturation and puberty Photoperiod Physiological processes that show rhythmic variations

Body temperature, sleep, appetite

Not well understood in humans

Stress

Physical

Psychological Real

Perceived

Strong emotional reactionsIndividual reactions vary

HPA Axis

Hypothalamic-pituitary-adrenal axis Regulates many body processes

Digestion, mood, immune system, metabolism

Most significantly: body’s response to long-term stress

Figure 16.16


Stress

Hypothalamus



To target in blood



ACTH







and blood pressure



system



Spinal cord

Nerve impulses

HPA axis (finally)

Stress

Short-term stress Sympathetic

Hypothalamus

Spinal cord

Adrenal medulla

EpinephrineNorepinephrine

“Sympathomimetic”

Long-term stress• Endocrine

Hypothalamus

Anterior pituitary

Adrenal Cortex

Glucocorticoids

(Cortisol)

Mineralcorticoids

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Increased cortisol = negative feedback to hypothalamus

High cortisol baseline = reduced sensitivity to

negative feedback

Low cortisol baseline = increased sensitivity to

negative feedback

The Stress Response

Changes largely mediated by hypothalamus, with the effector being the adrenals

Three stages Alarm (acute, sympathetic) Resistance (chronic, endocrine) Exhaustion

Temporary change in homeostasis = General Adaptation Syndrome (GAS)

Alarm Reaction

Immediate Hypothalamus Sympathetic nervous system Adrenal medulla

Increased serum glucose Increased circulation

Resistance Reaction

Long-term modification Hypothalamus Pituitary gland

Many effects… Increases energy availability Produces new proteins Improves circulation

Figure 16.16


Stress

Hypothalamus



To target in blood



ACTH







and blood pressure



system



Spinal cord

Nerve impulsesFight or Flight Resistance Exhaustion

Stressor too strong K+ loss = cell death Glucocorticoid depletion = cell starvation Immune system failure

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General Adaptation Syndrome (or Stress Response)

Video

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Lecture 13 Endocrine System - Linn–Benton Community Collegecf.linnbenton.edu/mathsci/bio/waitea/upload/Lecture_13... · 2017-03-08 · )ljxuh p51$ 1hz surwhlq '1$ +ruprqh uhvsrqvh