Endocrine System Flashcards

1
Q

Compare and contrast the general control of body functions by the nervous and
endocrine systems.

A

Nervous System - Regulates the activity of muscles and glands via electrochemical impulses delivered by neurons.
- initiates responses rapidly
- short duration responses in milliseconds
- acts vis AP’s and neurotransmitters
- acts on SPECIFIC LOCATIONS determined by axon pathways
- act over SHORT distances

Endocrine System- Influences metabolic activity by means of hormones released into the blood
- initiates responses slowly
- long duration responses (minutes, hours, days)
- Acts at DIFFUSE LOCATIONS (any location) targets can be anywhere blood reaches
- act over LONG distances

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2
Q

Distinguish between endocrine and exocrine glands.

A

Endocrine glands (ductless glands) - produce hormones and lack ducts. They released their hormones into the surrounding (interstitial) tissue fluid

Exocrine glands - secrete product into ducts that travel to the surface of the skin. ex: sweat and saliva

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3
Q

What is a hormone? a target cell?

A

Hormones- long distance chemical signals that were produces at one site and cause an effect on a different side of the body

Target cell - tissues/cells which have a receptor that is specifically able to recognize and bind to a particular hormone

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4
Q

Distinguish between classical endocrine signaling, paracrine signaling, and autocrine
signaling.

A

The classical endocrine signaling glands - anterior pituitary, thyroid, parathyroid, adrenal & pineal glands

classical endocrine signaling - circulating hormones are extreted into the blood and travel to DISTANT target cells

paracrine signaling - short-distance chemical signals that act within the same tissue, but affect different cell types other than those releasing the chemicals

autocrine signaling - short distance chemical signals that exert their effects on the same cells that secrete them.

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5
Q

In terms of their general chemistry, hormones can be broadly classified as amino acid-
based (this category includes biogenic amines, peptides, and protein hormones) and
steroid hormones. Explain the basic difference between each of these classes and list
several examples of each class of hormone.

A

amino acid base - water soluble
-cant travel through the plasma membrane
- have to bind to target cells embedded in the plasma membrane

steroid- lipid soluble
- can diffuse through the plasma membrane
- binds to intracellular receptors (within the cell)

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6
Q

Which class of chemical messenger is derived from cholesterol? from amino acids?

A

(most hormones are based on) amino acids: biogenic amines (ex: epinephrine and thyroxine) , peptides, proteins

cholesterol : steroid hormones . of the major endocrine organs, only gonadal and adrenocortical hormones are steroids.

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7
Q

Hormones in the biogenic amine class are all derived from a single amino acid. From
what amino acid are the catecholamines (i.e., epinephrine and norepinephrine) and
thyroid hormones derived?

A

tyrosine

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8
Q

Name the individual steroid hormones presented in this chapter. Identify the site of
secretion for each of the steroid hormones.

A

gonadal hormone - pituitary gland , triggers the gonads to secrete sex hormones called gondatropins : LH & FSH

adrenocortical - pituitary gland , triggers adrenal gland

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9
Q

Where are the receptors for most amino acid derived hormones located?

A

on the surface of target cells because hormones cannot pass through plasma membranes of cells

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10
Q

Describe the 5-stepped process of G protein activation (in your explanation include the role of the
hormone, its receptor, GDP, GTP, the alpha subunit and the beta-gamma dimmer).

A

hormones are the first messengers : it binds to the receptor

THEN

G proteins: involved in hormone-receptor binding (signal transduction)

step 1) Inactive G protein = GDP + alpha subunit + beta + gamma

step 2) ligand-receptor binding – when the G protein binds to the receptor protein, GDP is released for GTP instead

step 3) GTP binds and activates the G protein, which causes the alpha to dissociate. now the GTP is bound to the alpha subunit and beta+ gamma dimmer is there.

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11
Q

Describe the specific steps in the activation of the cAMP second messenger system.

A

step 1) the hormone-receptor binding activates the G-protein

step 2) G-stimulatory alpha subunit binds to and activates adenylate cyclase

step 3) adenylate cyclase generates cAMP from ATP
- cAMP phosphorylates (adds a phosphate) to protein kinase A, which activates it
- protein kinase A phosphorylates proteins that produce a physiologic effect (triggers the responses of target cells: activates enzymes, stimulates cellular secretion, opens ion channels etc)

step 4) cAMP is degraded by phosphodiesterase (PDE)

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12
Q

Why is cAMP called a “second messenger”?

A

because it translates the presence of the first messenger-the water soluble hormone into a response inside the cell

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13
Q

What is the function of phosphodiesterase (PDE)? How is PDE activated?

A

PDE degrades cAMP, lowering its cellular activity and thus reducing the enzyme activity

Activation process:

step 1) hormones bind to receptors associated with inhibitory G proteins (ligand-receptor binding)
- this activates an inhibitory alpha-subunit, which activates PDE

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14
Q

Explain why second messenger systems are said to have an “amplifying effect” on the
initial hormone signal.

A

because hormones can act through second messengers even in low concentrations since they cause a ripple effect that just amplify

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15
Q

Describe the specific steps in the activation of the PIP2-calcium signal mechanism.

A

step 1) hormone-receptor binding leads to activation of the G protein

step 2) activated G protein dissociates an alpha-subunit which activates phospholipase C (PLC)

step 3) phospholipase C catalyzes hydrolysis of a membrane phospholipid named PIPI2. and splits it into DAG and IP3 (second messengers)
DAG: Activates protein kinase C
IP3: Causes a release of calcium from the ER and the mitochondria

*Calcium acts kind of like a third messenger and binds to intracellular proteins (like calmodulin) to activate enzymes that amplify the cellular responses.

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16
Q

Name and identify the location of the second messengers of the PIP2-calcium signal
mechanism.

A

DAG and IP3 ?

dag - stays in plasma membrane
ip3- moves into cytoplasm to er and mitochondria

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17
Q

Identify several chemical messengers that induce signal transduction via
autophosphorylation of their receptor.

A

Insulin, growth factors and cytokines

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18
Q

Describe the structure of receptor tyrosine kinase (RTK).

A

two identical subunits

the ligand binding site is extracellular (outside the cell)

the intracellular portion of the molecule has a region with tyrosine kinase activity (meaning it is able to add a phosphate group to tyrosine residues in inside the cell)

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19
Q

Describe the process of signal transduction by the RTK (I suggest you use insulin as the
ligand).

A

1.) ligand-binding initiates dimerization (when two subunits become one) of the RTK (the tyrosine kinase receptor)

  • when insulin binds to the tyrosine kinase enzyme, it adds phosphates to several of its own tyrosines.

2.) the dimerization activates tyrosine kinase activity in both monomers

3.) autophosphorylation (the addition of a phosphate to the receptor) occurs

4.) effector proteins are activated by attaching to the phosphotyrosines residues

  • the activated insulin receptor provides docking sites for intracellular relay proteins
    that, in turn, initiate a series of protein phosphorylation that trigger specific cell responses
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20
Q

Which hormones affect their target cells by binding to an intracellular receptor?

A

thyroid and steroid hormones

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21
Q

What is the general mechanism through which the thyroid and steroid hormones
induce changes in their target cell’s metabolism.

A

direct gene activation

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22
Q

Describe the specific steps in direct gene activation by a lipid-soluble hormone (note
that thyroid hormone also exerts its effect via direct gene activation).

A

They diffuse through he plasma membrane into their target cells.

There, they bind and activate intracellular receptors.

The activated receptor-hormone complex makes its way to the nuclear chromatin and binds to a specific region of DNA.
*(However, thyroid hormone receptors are always bound to DNA, even in the absence of thyroid hormones)

This alters the rate of transcription or specific genres which leads to the altered rate of translation
- helps modify the structure and or function of the cell

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23
Q

Identify the three types of stimuli that regulate endocrine gland secretion.

A

humoral stimuli- changes in blood levels (critical ions and nutrients) causes secretion
ex: rise in glucose triggers release of insulin

hormonal stimuli- the release of a hormone in response to another hormone

neural stimuli- a neural stimulus triggers the release of a hormone
ex: Here, neuronal signaling from the sympathetic nervous system directly stimulates the adrenal medulla to release the hormones epinephrine and norepinephrine in response to stress.

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24
Q

Give an example of negative feedback control of hormone secretion.

A

For example, the hypothalamus produces hormones that stimulate the anterior portion of the pituitary gland. The anterior pituitary
1164 Chapter 37 | The Endocrine System
in turn releases hormones that regulate hormone production by other endocrine glands. The anterior pituitary releases the thyroid-stimulating hormone, which then stimulates the thyroid gland to produce the hormones T3 and T4. As blood concentrations of T3 and T4 rise, they inhibit both the pituitary and the hypothalamus in a negative feedback loop.

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25
Q

How are hormones transported in the blood? Explain the importance of transport
proteins in circulating lipid-soluble hormones.

A

Water soluble hormones travel through the blood freely because blood is water-based, while lipid-soluble hormones have to be bound to plasma proteins in order to travel faster through the blood (lipids are not attracted to water and move slower)

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26
Q

List the ways in which the hypothalamus contributes to homeostasis of body systems.

A

-control the ANS
- regulates temperature, hunger, body fluids etc

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27
Q

Name the two active lobes of the adult pituitary gland. Describe the general histology
and identify the embryologic origins of each.

A

anterior pituitary or adenophypohysis -
- the larger lobe
- develops from an out pocketing of ectodermal cells from roof of mouth
- forms glandular part of the pituitary

posterior pituitary or neurohypophysis -
- forms from an out pocketing of ectodermal cells in embryonic hypothalamus
- consists primarily of neurological cells called pituicytes
- contains axons and axon terminals of neurons whose cell bodies are located in the supraoptic& paraventricular nuclei of the hypothalamus

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28
Q

Describe the hypophyseal portal system, noting the general location of each of the three
main components of the system –i.e., the primary capillary, the hypophyseal portal
veins, and the secondary capillary plexus.

A

How the hypothalamus communicates with the anterior pituitary

  • hypothalamic neurons synthesize and release inhibiting and releasing hormones into the primary capillary plexus
  • blood flows from the the primary capillary plexus to the hypophyseal portal veins to the secondary capillary plexus into the anterior pituitary
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29
Q

What is the functional significance of each of the structures noted above (#28)?

A

primary capillary-
the hypophyseal portal veins-
the secondary capillary plexus-

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30
Q

What cells create the structural and functional relationship between the hypothalamus
and the posterior lobe of the pituitary?

A

Bundle of axons called hypothalamic - hypophyseal tract running through infundibulum
Neurosecretory cells - when they fire, the release stored hormones into a capillary bed for distribution

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31
Q

What are the hormones associated with the posterior pituitary?

A

ADH and OT

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32
Q

Where are the posterior pituitary hormones synthesized? where are they stored?

A

in large neurons of supraoptic and paraventricular nuclei (which synthesize ADH and OT)

They’re stored into the capillary beds of the posterior pituitary

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33
Q

Describe the process through which posterior pituitary hormones are secreted.

A

1) tract arises in large neurons of supraoptic & paraventricular nuclei - which synthesize/ release ADH & OT

2) hormones pass down the axons of the large neurosensory cells into the posterior pituitary

  1. the hormones released from axon terminals ( as an NT) fo into the capillary beds of the posterior pituitary
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34
Q

Describe the effects of antidiuretic hormone (ADH) on its target cells and tell how its
secretion is regulated.

A

when plasma osmolarity increases (meaning its hypertonic, more solutes in the blood) or BP is low, it triggers the osmoreceptors on the hypothalamus to release ADH.

ADH is what brings more water from the kidney collecting ducts that secrete urine, into the blood (which eventually causes the capillaries to expand, increase BP), which decreases the amount of water in your pee

so this explain why when youre dehydrated (and have a lot of solutes in your blood), your pee is concentrated because it is signaling to bring the water out of the urine into the blood

and when youre over hydrated, your osmolarity (amount of solutes) can fall as low as 50-100mOsm because theres not enough of a gradient to signal the release of ADH to bring more water into the blood so it goes out with your urine

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35
Q

Describe the effects of oxytocin (OT) on its target cells and tell how its secretion is
regulated.

A

Stretching of cervix of the uterus as birth nears dispatches afferent impulses to the hypothalamus which synthesizes oxytocin and releases from posterior pituitary. Also triggered by suckling of babies on nursing women

Causes uterine contraction and ejection of breast milk

Acts via PIP2-CA2+ second messenger system to mobilize Ca 2+ allowing stronger contractions
Positive feedback mechanism

Also promotes nurturing, sexual, affectionate behavior in brain

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36
Q

What is a tropic hormone?

A

a hormone that regulates the release of hormones by other endocrine glands

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37
Q

Name the hormones secreted by the anterior lobe of the pituitary and tell which of the
secretions are tropic hormones.

A

GH - not tropic ; growth hormone - somatrope
PRL- not tropic ; prolactin - lactotrope
TSH - thyroid-stimulating hormones - thyrotrope
ACTH - adrenocorticotropic hormone - corticotrope
LH - luteinizing hormone. - gondatrope
FSH - follicle-stimulating hormone - gondatope

38
Q

How does the hypothalamus regulate the secretory activity of the anterior pituitary?

A

Hypothalamus stimulates the anterior pituitary to secrete a specific hormone based on the specific releasing hormone from the hypothalamus

39
Q

Describe the effects of thyroid-stimulating hormone (thyrotropin) and tell how its
secretion is regulated.

A

Stimulation: by TrH and in infants indirectly by cold temperatures

Target/Goal: Stimulates the thyroid gland to release thyroid hormones

Inhibition: By feedback inhibition exerted by thyroid hormones on anterior pituitary and the hypothalamus by GIHH

Hypo secretion: Hypothyroidism

Hypersecretion: Hyperthyroidism

40
Q

Describe the effects of adrenocorticotropic hormone (ACTH) and tell how its secretion
is regulated.

A

Stimulation: Things like fever, hypoglycemia and other stressors stimulate CRH to release ACTH.

Target organs: Adrenal cortex

Goal: Promotes release of glucocorticoids and androgens

Inhibited by feedback inhibition exerted by glucocorticoids

Hyposecretion is rare, Hypersecretion leads to Cushings disease

CRH stimulates your anterior pituitary lobe to release ACTH. ACTH then triggers your adrenal glands, specifically your adrenal cortex, to release cortisol and androgens. The resulting increase in cortisol then signals your hypothalamus to decrease CRH levels, thus completing the feedback loop

41
Q

Describe the diurnal rhythm of corticotrophin-releasing hormone (CRH) release.

A

it triggers the release of ACTH and it has a daily rhythm, with levels peaking in the morning, shortly after awakening.
Things that mess up the rhythm: fever, hypoglycemia, and stress of all types

Rising levels of glucocorticoids feed back and block the secretion of CRH to release ACTH.

42
Q

Describe the effects of growth hormone/ GH (somatotropin) on its target cells and tell how
its secretion is regulated.

A

somatotropin cells of the anterior lob produce GH

It is an anabolic (tissue building) hormone that have both metabolic and growth-promoting actions

Direct actions:
-increases blood glucose and has other anti-insulin effects
-increases fat breakdown and release

Indirect actions:
Liver and other tissues that produce insulin like growth factors
- increases skeletal growth
- increase cartilage growth
- at extraskeletal tissues, promotes protein synthesis and cell growth and proliferation

43
Q

What is the normal biologic role of the insulin-like growth factors (IGFs)?

A

Liver and other tissues that produce insulin like growth factors
- increases skeletal growth
- increase cartilage growth
- at extraskeletal tissues, promotes protein synthesis and cell growth and proliferation

44
Q

What conditions result from over-secretion of GH in children? in under-secretion of
GH in children? What condition results from over-secretion of GH in adults?

A

hypo secretion in children: pituitary dwarfism

hyper secretion:
children - gigantism
adults - acromegaly (abnormal growth of the hands, feet, and face, caused by overproduction of growth hormone by the pituitary gland)

45
Q

Why is growth hormone said to exert a diabetogenic (i.e., an anti-insulin) effect?

A

GH encourages glycogen breakdown and release of glucose to the blood in the liver - glucose-sparing action - raises blood glucose levels
-Called anti-insulin effect because its effects oppose those of insulin

46
Q

What is the primary function (in males vs. females) of each of the gonadotropins?

A

-Follicle-stimulating hormone - stimulates production of gametes (sperm or eggs
-Luteinizing hormone - promotes production of gonadal hormones;
–females - works with FSH to cause an egg-containing ovarian follicle to mature; triggers ovulation and promotes synthesis and release of ovarian hormones;
–LH: males - stimulates the interstitial cells of the testes to produce testosterone

47
Q

At what stage of development does GnRH (gonadotropin- releasing hormone) begin to circulate in measurable quantities in
the blood?

A

During puberty, gonadotropic cells of anterior pituitary are activated and gonadotropin levels rise, causing gonads to mature
GnRH - produced by hypothalamus - prompts gonadotropin release - gonadal hormones are produced which feed back to suppress FSH and LH release

48
Q

Describe the effects of prolactin on its target cells and tell how its secretion is regulated (reminder that its not tropic)

A

Produced by prolactin cells; stimulates milk production by the breasts
-role of prolactin in males is not understood
-Release is controlled mostly by an inhibitory hormone (prolactin-inhibiting hormone) or dopamine which prevents prolactin secretion
-Decreased PIH secretion leads to a surge of prolactin release
-there are a number of prolactin-releasing factors
Females - prolactin levels rise and fall in rhythm with estrogen blood levels
-Rise in prolactin levels just before menstruation causes breast swelling
-suckling of breasts stimulates release of prolactin-releasing factors to produce milk

49
Q

Name the two types of endocrine cell of the thyroid gland, and identify the secretory
product of each.

A

Follicular cells - form the walls of each follicle; cuboidal or squamous epithelial cells - produce the glycoprotein thyroglobulin
Parafollicular cells - produce calcitonin; lie in follicular epithelium but protrude into soft connective tissue that separates and surrounds the thyroid follicles

50
Q

Name the two hormones that are collectively referred to as “thyroid hormone”. Which
of the two is the main hormone secretion of the follicular cells?

A

T3 and T4
Two iodine-containing amine hormones - thyroxine (T4) and triiodothyronine (T3)
T4 is main hormone secretion

51
Q

Describe the process of thyroid hormone synthesis and release.

A

TSH from anterior pituitary binds to receptors on follicular cells - first response is to secrete stored thyroid hormone; second response is to begin synthesizing more colloid to “restock” the follicle lumen
1. Thyroglobulin is synthesized on the ribosomes of the follicular cell’s rough ER - transported to golgi apparatus and packed in vesicles; discharged into follicle lumen to become part of stored colloid
2. Follicular cells accumulate iodides from the blood; iodide moves into follicle lumen by facilitated diffusion
3. Iodide is oxidized to iodine
4. Iodine is attached to tyrosine amino acids that are part of the thyroglobulin molecule - one iodine to tyrosine (monoiodotyrosine - MIT), two ioidines to tyrosine (diiodotyrosine - DIT)
5. Iodinated tyrosines are linked together to form T3 and T4
6. Thyroglobulin colloid is endocytosed in a vesicle and combined with lysosomes
7. Lysosomal enzymes split T3 and T4 from thyroglobulin and the hormones diffuse from follicular cell into bloodstream.

52
Q

Where is thyroglobulin synthesized? From what amino acid is thyroid hormone
derived?

A

Thyroglobulin is synthesized on the ribosomes of the follicular cell’s rough ER - transported to golgi apparatus where sugar molecules are attached; packed in transport vesicles

Thyroid hormone is derived from amino acid tyrosine

53
Q

What is the role of thyroid peroxidase?

A

catalyzes iodine oxidation to have thyroglobulin iodination - key enzyme in thyroid hormone biosynthesis

54
Q

Where does thyroglobulin become iodinated?

A

Occurs at the junction of the follicular cell and the colloid

55
Q

How is thyroid hormone secretion regulated?

A

Falling TH blood levels trigger release of TSH and ultimately of more TH
-Rising TH levels feed back to inhibit the hypothalamic-anterior pituitary axis, temporarily shutting off stimulus for TSH release
-GHIH (growth hormone inhibiting hormone), dopamine, rising levels of glucocorticoids inhibit TSH release
-excessively high blood iodide concentrations inhibit TH release

56
Q

What effects does thyroid hormone have on metabolism?

A

Increases basal metabolic rate and body heat production - calorigenic effect

57
Q

What is the role of thyroid-binding globulin?

A

A carrier protein that T3 and T4 binds to while circulating in the blood

58
Q

What is the result of severe hypothyroidism in infants? Describe the abnormalities
associated with the condition.

A

Congenital hypothyroidism - usually caused by poor development of the thyroid gland
-First weeks of life - no symptoms
-Requires lifelong TH replacement
-Normal growth patterns will be inhibited

59
Q

What hormone prevents high blood calcium levels?

A

calcitonin - polypeptide hormone released by the parafollicular cells

60
Q

Describe the effects of calcitonin (CT) and tell how its secretion is regulated.

A

increases calcium excretion by the kidneys

-does not have a known physiological role
-At pharmacological doses (doses higher than normally found in body), calcitonin has a bone-sparing effect and is given therapeutically to patients to treat Paget’s disease and sometimes osteoporosis

-At high concentrations - calcitonin targets the skeleton where is inhibits osteoclast activity, inhibiting release of calcium ions from bony matrix, and it stimulates Calcium ion uptake

your thyroid will decrease the amount of calcitonin released

61
Q

What hormone prevents low blood calcium levels?

A

parathyroid hormone PTH

62
Q

Normally, how many parathyroid glands does each human have? Where are they
located?

A

four, posterior to the thyroid gland

63
Q

Describe the effects of PTH on its target cells and tell how its secretion is regulated.

A

Falling blood calcium ion levels trigger PTH release; rising blood calcium levels inhibit its release
PTH increases calcium ion levels in blood by stimulating 3 target organs: the skeleton, kidneys, and intestine
PTH release:
-Stimulates osteoclasts (bone-resorbing cells) to digest some of the calcium-rich bony matrix and release ionic calcium and phosphates to the blood
-Enhances kidney’s reabsorption of calcium ions from the forming urine into the blood
-promotes activation of vitamin D - increases absorption of Calcium ions by intestinal mucosal cells; stimulates transformation of vitamin D to its active form calcitriol

64
Q

What are the potential deleterious effects of hypercalcemia (abnormally high blood
calcium levels)? of hypocalcemia (abnormally low blood calcium levels)?

A

Hypercalcemia - depresses the nervous system which leads to abnormal reflexes and weak skeletal muscles; excess calcium salts precipitate in the kidney tubules forming kidney stones; calcium deposits may also form in soft tissues throughout the body and severely impair vital organ functioning

Hypocalcemia - makes neurons more excitable and accounts for signs and symptoms of tingling sensations (tetany) and convulsions; symptoms may progress to respiratory paralysis and death

65
Q

Where are the adrenal glands located?

A

on top of the kidneys

66
Q

Identify and locate the 2 major structural and functional regions of each adrenal gland.

A
  1. Adrenal medulla - part of sympathetic nervous system; inner layer of adrenal gland
  2. Adrenal cortex - outer layer; encapsulates the medulla and forms bulk of the gland; glandular tissue derived from embryonic mesoderm
67
Q

Identify and locate the 3 secretory zones of the adrenal cortex.

A

Outside –> Inside
-Zona glomerulosa
-Zona fasciculata - largest layer
-Zona reticularis

68
Q

What is the main secretory product of each of the zones identified above (#67)?

A

-Zona glomerulosa - secretes mineralocorticoids; hormones that help control the balance of minerals and water in the blood (ex: aldosterone)
-Zona fasciculata - secretes glucocorticoids; metabolic hormones
-Zona reticularis - secrete small amounts of adrenal sex hormones - gonadocorticoids

69
Q

What is the principle mineralocorticoid secreted by the adrenal cortex? Describe the
effects of this hormone on its target cells and tell how its secretion is regulated.

A

primary one is aldosterone - it enhances sodium reabsorption and potassium excretion (urine) in the kidney to allow us to maintain the sodium ion content in the blood

sodium reabsorption enhanced water reabsorption

indirectly: increases blood pressure

70
Q

Describe the steps in the renin-angiotensin-aldosterone cascade.

A
  1. When BP/blood volume falls, specialized cells of the juxtaglomerular complex in the kidneys are excited
  2. These cells respond by releasing renin into the blood
  3. Renin splits off part of the plasma protein angiotensinogen, triggering an enzymatic cascade that forms angiotensin II, which stimulates the glomerulosa cells to release aldosterone
71
Q

How does angiotensin II (AT II) contribute to homeostasis of blood volume and blood
pressure?

A

It stimulates aldosterone secretion which causes BP increase

72
Q

Name the glucocorticoid hormone secreted by the adrenal cortex. Describe the effects
of this hormone on its target cells and tell how its secretion is regulated.

A

glucocorticoids

cortisol (main one) , cortisone, corticosterone

functions: major effects on fuel metabolism (has a glucose-sparing, diabetogenic effect , enhance epinephrines effects on BP

Cortisol (hydrocortisone)
-Negative feedback regulates it
-cortisol release is promoted by ACTH - ACTH release is triggered in turn by hypothalamic releasing CRH
-Rising cortisol levels feed back to act on both the hypothalamus and the anterior pituitary, preventing CRH release and shutting off ACTH and cortisol secretion
-cortisol provokes a marked rise in blood levels of glucose, fatty acids, and amino acids
-main metabolic effect: provoke gluconeogenesis - formation of glucose from fats and proteins; saves glucose for the brain and encourages use of fatty acids for energy
-other function: enhance sympathetic nervous system’s vasoconstrictive effects, helping to maintain BP

73
Q

What are the potential negative side-effects of abnormally high and/or prolonged
glucocorticoid exposure?

A
  • inhibits collagen synthesis
  • depresses the immune system
  • have a strong anti-inflammatory effect
74
Q

What are the principle gonadocorticoids secreted by the adrenal cortex? What seems to
be the biological role of the adrenal sex hormones?

A

Androgens - male sex hormones
-most are converted in tissue cells to more potent male hormones like testosterone and some are converted to estrogens
-no exact role
-contributes to axillary and pubic hair development
-females - may contribute to libido/sex drive; account for estrogens produced after menopause

75
Q

Describe the relationship between the adrenal medulla and the autonomic nervous
system.

A

embryologically, these cells arise from the same tissue as sympathetic ganglia

chromaffin cells receive direct innervation from preganglionic fibers of the sympathetic division of the ANS

76
Q

Identify the hormone-producing cells of the adrenal medulla.

A

Medullary chromaffin cells - synthesize catecholamines (epinephrine and norepinephrine)

77
Q

Identify the major secretions of the adrenal medulla. Which of the hormones accounts
for the greatest proportion of the medullary secretions?

A

catecholamines, epinephrine and norepinephrine

80% epinephrine and 20% norepinephrine

78
Q

Describe the effects of the catecholamines (epinephrine and norepinephrine) and tell how their secretion is
regulated.

A

catecholamines - increase in BP and contractility and (+) vasoconstriction, increased respiration rate and bronchodilator, decrease in digestive activity, increase in blood glucose levels and increase in FA mobilization from adipose tissue

Both - increase HR and contractility; increase vasoconstriction; increase respiration rate and cause bronchodilation; stimulate glycogenolysis in the liver and lipolysis in adipose tissue - helps maintain normal blood glucose level; re-routing of blood flow to essential organs and decreased digestive activity

Epinephrine - more potent stimulator of metabolic activities and dilator of small airways; binds to both alpha and beta receptors

Norepinephrine - greater influence on peripheral vasoconstriction and BP, only binds to alpha receptors

79
Q

There are two general receptor types for the catecholamines (i.e., alpha and beta) and
subclasses of each type. Review the major locations of each of these receptors (see
chapter 14, page 544,in the Marieb textbook) and know the general effect of the
hormones on their target cells.

A

Beta 1 - located in heart, but also in kidneys and adipose tissue; increases heart rate and force of contraction; stimulates kidneys to release renin
-Beta 2 - lungs and most other sympathetic target organs; abundant on blood vessels serving heart, liver, skeletal muscle; mostly inhibitory effects; dilates blood vessels and bronchioles; relaxes smooth muscle walls of digestive and urinary visceral organs
-Beta 3 - Located in adipose tissue; stimulates lipolysis by fat cells
-Alpha 1 - Located in almost all sympathetic target organs; constricts blood vessels and visceral organ sphincters; dilates pupils
-Alpha 2 - Located in membrane of adrenergic axon terminals and pancreas; inhibits release of norepinephrine from adrenergic terminals; inhibits insulin secretion

80
Q

Describe how the hypothalamus/pituitary gland/adrenal glands (i.e., the HPA axis)
work together to mediate the body’s response to stress.

A

General Adaption Response (GAS)
alarm, resistance, exhaustion

81
Q

Identify the physiologic changes that occur during a stress response (short-term and
long-term).

A

Short-term:
1. APs triggered by hypothalamus in response to stressors activate the sympathetic nervous system
2. APs travel along preganglionic sympathetic axons to the adrenal medulla
3. adrenal medulla secretes amino acid-based hormones (epinephrine and norepinephrine)
4. Epinephrine and norepinephrine reinforce other sympathetic responses to ready the body for exertion (fight or flight)

Long-term:
1. Stressors cause hypothalamic neurons to release corticotropin-releasing hormone (CRH)
2. CRH travels via the portal system of blood vessels to anterior pituitary
3. anterior pituitary cells (corticotrophs) release adrenocorticotropic hormone (ACTH)
4. ACTH travels in blood to adrenal cortex
5. adrenal cortex synthesizes and releases glucocorticoids

82
Q

What are the insulin-secreting cells of the pancreatic islets? What cells of the pancreatic
islets secrete glucagon?

A

Beta cells - release insulin and are more numerous
Alpha cells - release glucagon and are fewer in number

83
Q

Describe the effects of each of alpha and beta cells and tell how their secretion is
regulated.

A

Alpha cells - falling blood glucose levels prompt the cells to secrete glucagon;

sympathetic nervous system stimulation and rising amino acid levels are stimulatory;

suppressed by rising blood glucose levels, insulin, and somatostatin

Beta cells - secrete insulin when stimulated by elevated blood glucose levels, rising blood levels of amino acids and fatty acids, acetylcholine released by parasympathetic nerve fibers, hyperglycemic hormones;

somatostatin and sympathetic nervous system activation depress insulin release

84
Q

Why are insulin and glucagon described as antagonists?

A

Insulin - hypoglycemic hormone (decreases blood glucose)
Glucagon - hyperglycemic hormone (increases blood glucose)

85
Q

What are the 3 cardinal signs of type 1 diabetes mellitus? Physiologically speaking, why
do these 3 cardinal signs occur?

A
  1. Poly–uria - excessive glucose in blood leads to excessive glucose in kidney filtrate where it acts as an osmotic diuretic - end result is polyuria (huge urine output that decreases blood volume and causes dehydration)
  2. Poly–dipsia - dehydration stimulates hypothalamic thirst centers, causing polydipsia (excessive thirst)
  3. Poly–phagia - excessive hunger and food consumption
86
Q

Compare and contrast diabetes type 1 and type 2.

A

Diabetes type 1:
-insulin-dependent diabetes mellitus
-immune system destroys the pancreas’s beta cells
-lack insulin
-autoimmune disease

Diabetes type 2:
-non-insulin-dependent diabetes mellitus
-insulin receptors are unable to respond to insulin - insulin resistance
-grows more common with age
-caused more by lifestyle factors

87
Q

Name the male and female sex hormones.

A

Male: testosterone
Female: estrogen; progesterone

88
Q

What are the general effects (in males vs. females) of the sex hormones?

A

The sex hormone for the male is testosterone. The sex hormone for the female is estrogen. Testosterone is needed for development of the sperm, as well as the secondary sex characteristics. Male secondary sex characteristics include body hair, increased muscle mass, a deeper voice, and thicker bones. Estrogen thickens the endometrium of the uterus, as well as the secondary sex characteristics. Female secondary sex characteristics include development of the breasts, the accumulation of adipose tissue in specific locations of the body, and the skin becoming more vascularized.

89
Q

Identify the hormone secreted by the pineal gland.

A

melatonin

90
Q

Describe the general effects of melatonin and tell how its secretion is
regulated.

A

controls the production of protective antioxidants and detoxification molecules within cells , may affect the timing of puberty and inhibit too early sexual maturation , change in levels may influence rhythmic variations in physiological processes such as body temp, sleep and appetite.

Melatonin conc, in the blood rise and fall in a daily cycle. Peal levels occur during the night and make us drowsy, lower levels happen about noon. The pineal gland receives input from visual pathways on daytime and the length of it.