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Physiology Flashcards

1
Q

Where is the pituitary gland located? What is directly in front of and behind the hypothalamus?

A

Sella Turcica (fossa in the sphenoid bone)

Front: optic chiasm

Behind: mammillary body

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2
Q

What influences pituitary function? What does it regulate?

A

Brain: sleep/wakefulness, pain, emotion, smell, fear, light and thought

Hypothalamus-pituitary regulates activities of the adrenal, thyroid, and reproductive glands: Water balance, milk secretion, body growth, reproduction, body fluid homeostasis

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3
Q

How does the hypothalamic-hypophyseal blood supply help control the release of hormones?

A

Neurosecretory cells (neurons) in the hypothalamus make and secrete stimulatory or inhibitory hormones that enter capillaries in the median eminence and travel to the anterior pituitary via hypothalamic-hypophyseal portal veins where they then leave fenestrated capillaries to act upon hormone secreting cells.

In the posterior pituitary, the hormones released are actually neuroendocrine hormones because they are made by neurons that originate in the hypothalamus. They are released from axon terminals into a mostly separate capillary system.

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4
Q

What is the main role of the hypothalamus?

A

Maintain homeostasis

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5
Q

What are the cell types of the anterior pituitary? What are their relative proportions? What do they secrete and where does the effect take place?

A

Somatotrophs (40-50%)— somatotropin, growth hormone (all tissues)

Mammotrophs (10-25%)— prolactin (breasts, gonads)

Corticotrophs (15-20%)— ACTH; B-lipotropin (Adrenal gland; Adipose tissue/melanocytes)

Gonadotrophs (10-15%)— FSH and LH (Gonads)

Thyrotrophs (3-5%)— TSH (thyroid)

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6
Q

Where are hypothalamic releasing/inhibiting neurohormones released from?

A

Paraventricular nucleus

Medial Preoptic nucleus

Arcuate nucleus

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7
Q

GnRH

A

Gonadotropin releasing hormone— stimulates release of FSH and LH

Hypothalamus

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8
Q

GHRH

A

Growth hormone releasing hormone

Hypothalamus

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9
Q

TRH

A

Thyrotropin releasing hormone— stimulates TSH

Hypothalamus

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10
Q

CRH

A

Corticotropin releasing hormone— stimulates ACTH release

Hypothalamus

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11
Q

Somatostatin

A

Inhibits release of GH

Hypothalamus

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12
Q

Dopamine

A

Inhibits release of Prolactin

Hypothalamus

Only hypophysiotropic hormone that is a catecholamine (others are all peptides)

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13
Q

Why is the pulsatile secretion of the anterior pituitary important? When is it altered?

A

Important for the effective and efficient signaling of tissues because it allows change in signal strength as well as metabolic clearance of the hormone.

Altered in Cushing’s disease or with acromegaly when GH remains detectable throughout the day time.

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14
Q

How does negative feedback work in the hypothalamic-hypophyseal hormone system? What is ultra short loop, short loop, and long loop?

A

Hypothalamus releases XRH which inhibits release of too much XRH (ultra short loop)

XRH causes release of XTH from pituitary which feeds back to inhibit XRH release (short loop)

XTH causes release of X from the tissues which feeds back to inhibit release of XTH in pituitary and release of XRH from hypothalamus. Also stimulates release of XIH from hypothalamus which inhibits XTH release (long loop)

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15
Q

What is POMC? Where is it made? What does it become? What is MSH activity?

A

ACTH family

Pro-opiomelanocortin is a single gene precursor that is cleaved first into ACTH intermediate and B-lipotropin

ACTH intermediate is cleaved into ACTH and N-terminal peptide which both also have MSH activity (melanocyte stimulating hormone)

B-lipotropin is cleaved into B-endorphin and y-Lipotropin (which has MSH activity)

In Addison’s disease, the abnormally high levels of POMC and ACTH can cause pigmentation of the skin as a symptom.

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16
Q

Describe the regulation of CRH and ACTH. Describe the negative feedback loop. Which receptors do they act on? What happens in Addison’s disease?

A

Stimulators: CRH and ADH; NE, ACh (stress) and 5-HT are positive modulators

Inhibitors: Brain Natriuretic Peptide (BNP), Endorphins, ACTH, and GABA are all inhibitors or negative modulators.

CRH binds CRH-R1 receptor on corticotroph and causes PKA cascade to stimulate POMC expression and ACTH release

ACTH binds MC2R receptor on adrenal cortex and causes PKA cascade to stimulate steroidogenesis (cortisol)

Cortisol increases blood glucose, decreases inflammatory response. Also inhibits ACTH and CRH through neg feedback

Addison’s causes abnormally high levels of ACTH which bind low affinity MC1R receptors in skin and increase POMC levels and thus MSH activity

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17
Q

What does GH do? How is it regulated?

A

Stimulates postnatal growth and development by causing liver and other cells to secrete IGF and protein synthesis and carb/fat metabolism in other tissues. In adults, it continues to modulate metabolism but at much lower levels

Hypothalamus secretes GHRH which has an inhibitory effect on itself

GHRH stimulates GH release from pituitary (through cAMP and IP3/Ca2+). GH also has a stimulatory effect on somatostatin which inhibits GH by blocking cAMP and blocking GHRH

GH stimulates release of IGF from tissues which inhibit GH release from pituitary and stimulate somatostatin release from hypothalamus

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18
Q

What do Growth Hormone, Prolactin, and Human Placental Lactogen (hCS) have in common?

A

They share homologies and likely have a common origin. Have common structural homologies

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19
Q

What are some other inhibitors and stimulators of growth hormone?

A

Hypoglycemia and starvation are stimulators of growth hormone as well as exercise and stage III and IV sleep

Obesity, senescence, increased glucose and fat concentration all inhibit it

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20
Q

What does prolactin do? What factors affect prolactin release? Feedback mechanism?

A

Stimulates milk secretion and breast development

Stimulators: TRH (increases transcription of gene), pregnancy, breast feeding, sleep, stress, dopamine antagonists

Inhibitors: Dopamine, Bromocriptine (dopamine agonist), Somatostatin, Prolactin (neg feedback)

Prolactin stimulates release of Dopamine which inhibits more prolactin release

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21
Q

What do FSH, LH, and TSH all have in common? (Glycoprotein family)

A

All are made up of a and B subunits

All the a subunits are the same but the B subunits are unique to each

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22
Q

How are TRH and TSH regulated?

A

TRH binds TRH receptor and causes release of TSH through Ca2+ and PKC cascade.

TSH binds a TSH receptor on follicular cell and causes T3/T4 production and secretion (through PKA cascade)

T3 has an inhibitory effect on both TRH and TSH secretion.

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23
Q

What happens to FSH and LH levels during menstruation? After menopause?

A

The secretion of these hormones varies and their concentration in the gonadotroph changes dramatically

They increase

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24
Q

What do LH and FSH do?

A

FSH— stimulates spermatogenesis in Sertoli cells and follicular development and estrogen synthesis in ovaries

LH— stimulates testosterone synthesis in Leydig cells and ovulation, formation of corpus luteum, estrogen and progesterone synthesis in ovaries

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25
Q

How are LH and FSH regulated? What is the mechanism of GnRH? What are Activin, Inhibin, and Follistatin? Any other regulators?

A

Release of both are stimulated by GnRH (LHRH) from the hypothalamus.

Pulsatile secretion of 1 GnRH pulse per hour or faster stimulates LH release. Slower (1 in 3 hours) stimulates FSH release. More frequent pulses increase LH concentration. (You must remember though that frequency isn’t the only factor here. If magnitude increases, then both FSH and LH secretion goes up).

The gonadal steroids, Testosterone and Estrogen, block GnRH at the pituitary and inhibit GnRH release from the hypothalamus. However, if estrogen reaches a certain threshold, it exhibits positive feedback on FSH and LH

GnRH mechanism not clear but probably increased Ca2+ and PKC activity

Activin is a gonadal protein product that stimulates FSH release
Inhibin is a protein that inhibits FSH and LH and inhibits GnRH release
Follistatin inhibits FSH and LH release

Dopamine and Endorphins block GnRH release while NE stimulates it.

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26
Q

What is neurophysin I and II?

A

Pre prohormones (precursors for ADH and OTC) are also cleaved into neurophysins which help carry the hormones down the axon for secretion. Other than that their role is still under investigation

Neurophysin I (for OTC) and II (for ADH) are identical.

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27
Q

What do ADH and Oxytocin have in common? What makes them different?

A

Both are cleaved from Pre prohormones and only two of their nine amino acids differ (both have same disulfide bond)

Both are made in neurons in both the paraventricular and supraoptic nuclei, but they are made in separate neurons.

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28
Q

Describe the function of ADH (or Arginine Vasopressin AVP)

A

Conserves water and regulates plasma tonicity through V1 and V2 receptors

Binds to V1a receptors to cause vasoconstriction (V2 receptors counterbalance this effect)

Increases ACTH secretion which increases cortisol secretion

Binds to V2 renal receptors to conserve water in 3 ways:

1) Stimulates Na+/K+ 2Cl- co-transport in the thick ascending limb
2) increases the permeability of the collecting duct to urea
3) increases the permeability of the collecting ducts to water

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29
Q

What are the four major factors that regulate the secretion of ADH? Describe their mechanisms

A

Osmolarity— osmolarity receptors are located in the anterior hypothalamus, mainly on the OVLT; sense as little as 1% increase in osmolarity and increase their firing rate to stimulate ADH producing neurons in the PVN and SON (also stimulates thirst)

Hypovolemia (body fluid volume)— greater effect; volume receptors in right atrium sense 10% changes in volume and activate volume receptors which increase activity of ADH neurons (drinking water decreases volume loss)

CSF Na+ concentration— increase in Na+ concentration increases ADH via Na+ sensors located in the circumventricular organs.

Body temperature increase

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30
Q

What are some other factors that affect ADH secretion?

A

Stimulators: Nausea, Ang II, Nicotine, Bradykinin and Histamine (lower BP), stress, hypoglycemia

Inhibitors: ANP, alcohol, NE (increases BP)

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31
Q

What is Diabetes Insipidus? What can cause it? (Central vs. Nephrogenic)

A

Polyuria (with hypoosmotic urine and increased serum osmolality)

Polydipsia (muscle weakness due to lack of water)

Central: destruction of hypothalamic nuclei, pituitary stalk, or posterior pituitary due to tumor, trauma, or surgery. Leads to deficiency of ADH and thus inability to concentrate the urine.

Nephrogenic: Inability to concentrate urine despite sufficient ADH due to chronic kidney disease, drugs (lithium), ADH receptor deficiency, decreased AQP2

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32
Q

How to diagnose Diabetes Insipidus

A

Must be distinguished from Diabetes Mellitus (hyperosmotic urine, glucose) and psychogenic polydipsia/polyuria (hypotonic urine, but serum ADH is fine)

Water deprivation test- increases serum osmolality, and sodium, but urine osmolality doesn’t change— central diabetes Insipidus
No change in serum osmolality and sodium— psychogenic

Desmopressin test— increases urine osmolality 50%— Diabetes Insipidus
No change in psychomotor version.

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33
Q

SIADH

A

Syndrome of Inappropriate ADH secretion

Most patients have no symptoms (no edema, or dehydration) despite hyponatremia below 110 mmol/L. Lethargy leading to coma

Caused by excess ADH despite low plasma osmolality due to: synthesis of ADH by malignant tumors, secretion of ADH in non-neoplastic lung tissue in chronic lung disorders, excessive release of ADH from hypothalamus in brain disorders

Therapy: limit fluid intake; block V2 receptors

Should be suspected in patients that have hyponatremia and hyperosmolal urine despite no clinical symptoms

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34
Q

What does Oxytocin do? How is it regulated?

A

Let down reflex— ejects milk from alveoli into ducts via myoepithelial contractions

Stimulation of smooth muscle contractions in the uterus

Stops postpartum bleeding

Suckling of an infant is an immediate and major stimulus of oxytocin
Uterine and genital stimulation cause OTC release
Actions of OTC are augmented by estrogen and inhibited by catecholamines
Opioids inhibit OTC release

Exhibits POSITIVE feedback for both uterine contraction and mammary lactation

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35
Q

What is the structure of GH? What is it similar to?

A

Single large polypeptide of 191 amino acids and two disulfide bonds. Helical tertiary structure.

Prolactin is homologous to GH. 198 amino acids with 3 disulfide bonds

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36
Q

What is glycosylated prolactin?

A

Prolactin is synthesized as a preprohormone and is temporarily N-glycosylated in the ER (deglycosylated in Golgi)

In non pregnant women, glycosylated form is secreted and is much less biologically active.

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37
Q

How does growth hormone secretion change over time?

A

Stable in childhood

In puberty, there is an enormous burst (increased frequency and magnitude) stimulated by estrogen in females and testosterone in males— growth spurt

Declines to stable level after puberty

Drops to lowest levels in senescence.

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38
Q

What is the prognosis of Acromegaly patients or those given excessive amounts of pituitary or recombinant GH?

A

Higher mortality rate and increased risk of cancer in acromegaly

Higher risk of tumors (3 times likelihood of brain tumors) and cardiovascular hemorrhage.

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39
Q

What effect does GHRH have on GH (dual effect)?

A

Binds GHRH receptor on somatotrophs and increases cAMP, Ca2+, and IP3 to increase secretion of GH (short term increase)

Activates pituitary transcription factor (Pit1) to increase transcription/production of GH

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40
Q

Besides GHRH, what else up-regulates GH?

A

Thyroid hormone and cortisol synergistically enhance transcription and synthesis of GH

Estrogen and testosterone also mildly increase GH transcription and synthesis

Fasting, stress, sleep, and amino-acid rich meals increase GHRH secretion

GHRP increases GHRH and GH secretion

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41
Q

How does down-regulation of GH work? What increases somatostatin? What decreases GHRH?

A

Somatostatin binds Gi receptors on somatotrophs to block cAMP synthesis thus decreasing the secretion of GH

GH secretion stimulates somatostatin, thus inhibiting itself

Somatomedins (IGFs from peripheral tissues) stimulate somatostatin and inhibit GH secretion by somatotrophs (by blocking GHRH effects)

GHRH exhibits negative feedback on itself; high levels of glucose and fFAs also inhibit GHRH release

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42
Q

What effect does obesity have on GH secretion?

A

Obesity reduces GH responses to all stimuli including GHRH

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43
Q

How does sleep effect GH secretion?

A

Nocturnal surge of GH occurs 1-2 hours after onset of deep sleep

Light sleep associated with rapid eye movements, inhibits GH release

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44
Q

What are the biological effects of GH? Does it deliver all of its effects directly?

A

GH is predominantly an anabolic hormone and is partially diabetogenic (because it partially blocks insulin mediated glucose uptake in order to mobilize fat stores)

Some GH effects are direct while others are mediated by IGFs released from the liver or IGFs in specific tissues such as linear growth, organ size, and lean body mass

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45
Q

What effect does protein intake have on GH, insulin, and somatomedin?

A

Increases GH, increases Somatomedin, increases insulin

Leads to increased protein synthesis and growth with no change in caloric storage

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46
Q

What effect does carbohydrate intake have on GH, somatomedin, and Insulin?

A

Decrease in GH, no change in Somatomedin, and increase in insulin

Leads to no change in protein synthesis or growth

Increased caloric storage

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47
Q

What effect does fasting have on GH, somatomedin, and insulin?

A

Increased GH, decreased somatomedin, and decreased insulin

Decreased protein synthesis and growth

Increased caloric mobilization

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48
Q

What effects does GH have on the liver? How does GH increase linear growth, organ size, and muscle mass? What effect does GH have on adipose tissue?

A

Increases RNA synthesis, protein synthesis, and gluconeogenesis. Causes liver to release IGFs which help with the other tasks

GH and IGF increase DNA, RNA, and protein synthesis in organs to increase size.

GH and IGF increase DNA, RNA and protein synthesis plus AA uptake, collagen synthesis, proteoglycan chondroitin, and cell proliferation in bones and chondrocytes to increase linear growth

GH and IGF decrease glucose uptake and increase AA uptake and protein synthesis to increase muscle mass

GH decreases glucose uptake and increases lipolysis to decrease adiposity.

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49
Q

Who has higher serum GH levels: premature infants or full-term babies?

A

Premature infants

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50
Q

What effect does GH administration have on GH deficient children?

A

Enhanced positive nitrogen balance
Decrease urea production
Redistribute fats
Reduce carb utilization but without increasing the incidence of diabetes mellitus

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51
Q

What is the mechanism of GH action at the cellular level?

A

One GH molecule binds two plasma membrane GH receptors causing them to come together

Two Janus Kinases (JAK) bind the dimer and cause tyrosine phosphorylation of STAT molecules which then come together to either induce or repress transcription of target molecules (IGFs for example)

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52
Q

What happens in individuals who lack the ability to produce IGFs?

A

They experience retarded growth despite high levels of GH

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53
Q

Is GH the only regulator of IGF?

A

No. Hence why IGF levels decrease during fasting while GH levels are high

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54
Q

What is the dual reflector theory of long bone growth?

A

GH stimulates differentiation of prechondrocytes into early chondrocytes which secrete IGF-1

IGF stimulates clonal expansion and maturation of chondrocytes leading to longitudinal growth.

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55
Q

Which IGF is greatly reduced in GH deficient individuals? What effect does IGF administration have on these individuals?

A

IGF-1

Decreases plasma AAs due to increased protein synthesis

Lean body mass increases while fat mass decreases and bone formation is enhanced

As well, resting metabolic rate, exercise capacity, and sense of well-being all increase

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56
Q

How does GH oppose insulin? What happens to patients with acromegaly

A

GH actually increases expression of insulin, but GH blocks uptake of glucose into muscle and adipose cells in order to increase fat mobilization and protein synthesis (blood glucose rises)

Also antagonizes insulin activated lipogenesis; blood levels of fFAs and ketoacids increase

Those with acromegaly exhibit all the effects described above due to a slow growing GH secreting tumor

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57
Q

GH and insulin together augment the level of IGFs

A

Okay

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58
Q

What are some causes of Acromegaly? When is it diagnosed?

A

Excessive secretion of GH after puberty. Can be due to pituitary tumor or hyperpituitism.

Progression is gradual so usually takes 15-20 years to diagnose

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59
Q

What are the regulators of prolactin release?

A

Prolactin inhibiting factors (PIFs): Dopamine, Somatostatin, GnRH

TRH is a major stimulator of prolactin synthesis and release

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60
Q

What are the biological effects of prolactin? What happens to prolactin if there is a disruption in hypothalamic-pituitary connection? What can excess Prolactin cause?

A

Breast development and milk production in women. May play a role in reproductive function in both sexes. Stimulates parental protective behaviors as well.

Prolactin levels greatly increase (because no dopamine to inhibit)

Inhibits GnRH release which can lead to lack of ovulation and infertility in women and decreased sperm production in men.

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61
Q

What do T4 and T3 do?

A

Thyroxine (T4) and triiodothyronine (T3) increase the rate of O2 consumption and metabolism in response to changes in heat production, energy demand, caloric supply, and environmental temperature

They are critical for normal development of fetus and child.

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62
Q

What happens to iodine uptake and TH production when follicular cells are stimulated by TSH?

A

Both increase

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63
Q

What is the structure of T4 and T3? Which is the major product? What is unique about these molecules? What does the unique structure require?

A

3,5 3,5 tetraiodothyronine (T4)— prohormone but major product of thyroid

3,5,3 triiodothyronine— much lower quantity

Called iodothyronines because they incorporate inorganic iodide onto two organic tyrosine residues. However, the tyrosines must be part of the thyroglobulin colloid in the follicles.

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64
Q

What is the structure of TSH? What is its mechanism of action?

A

TSH is a glycoprotein composed of an a and B subunit.

The two subunits each bind active sites on a receptor that triggers an increase in cAMP, Ca2+, phosphoinositol, and growth factors (second messenger system).

It causes rapid follicular cell growth (DNA, RNA, protein synth) and proliferation while also increasing the synthesis of T3/T4 hormone (increased iodide trapping, iodination, endocytosis of colloid, ATP production, etc.)

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65
Q

What is the structure of TRH? What is its mechanism of action?

A

Tripeptide hormone (glutamine, histidine, proline) that stimulates release of TSH from thyrotrophs.

Binds to receptor and causes increase in Ca2+ and IP3

TRH down-regulates the sensitivity of its own receptor

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66
Q

How are TRH and TSH regulated by the release of T3/T4? What else inhibits or stimulates TRH and TSH?

A

TRH stimulates TSH release which stimulates T3/T4 synthesis and release

Most T4 is converted to T3 in peripheral tissues; T3 has a desensitizing effect on TRH receptors in thyrotrophs which inhibits secretion of TSH. It also represses TSH gene expression and down-regulates TSH receptors.

T3/T4 also exhibit negative feedback on TRH release from the hypothalamus

TSH secretion is also inhibited by dopamine, somatostatin, cortisol, and growth hormone

TRH is upregulated by thermal and caloric signals

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67
Q

What would happen to TSH levels if there were an impairment of thyroid hormone synthesis? What can this cause?

A

TSH levels increase by negative feedback

TSH hypersecretion can cause enlargement of the thyroid gland known as Goiter

They may also have an enlarged pituitary gland due to an increased number of thyrotrophs

68
Q

What would excessive thyroid hormone secretion cause?

A

Low levels of plasma TSH (neg feedback) and possible atrophy of thyrotrophs

69
Q

Which of the thyroid hormones is the predominant active form in the tissues?

A

T4 serves as a prohormone for T3 which is the real actor in the tissues. T4 does have some intrinsic intracellular action of its own however.

70
Q

How do T3/T4 circulate in the blood?

A

Bound to one of three proteins:

  • Thyroxin binding globulin (TBG)— glycoprotein synthesized in the liver; 20%
  • Transthyretin (thyroxin binding parvalbulmin)— other 80%
  • Albumin
71
Q

How do TBG and Transthyretin protect against acute changes in thyroid gland function?

A

They create a circulating reservoir of T4 which acts as a buffer against acute changes

72
Q

How much T4 and T3 are found unbound in the blood? What is the purpose of these molecules?

A

.03% of T4 and .3% of T3

They are responsible for the pituitary feedback

73
Q

What is the equilibrium equation for determining the levels of free T4 in the blood?

A

Free T4/Bound T4 = [T4]/[T4TBG] = 1/Keq [TBG]

So [T4] = [T4TBG]/Keq [TBG]

74
Q

Sustained increases/decreases in daily T4 supply due to thyroid disease or a change in TBG concentration itself can lead to disruption of which important ratio?

A

Free T4/ Bound T4

Hepatic disease, pregnancy, estrogen therapy, or kidney disease can all change levels of serum TBG

75
Q

What is the enzyme that catalyzes the conversion of T4 to T3? Which hormone is used in hormone replacement therapy?

A

5 monodeiodinase

T4 is always used in hormone replacement therapy for thyroid deficient patients (probably because straight T3 would have a more drastic effect)

T4 is 25% as hormonally active as T3

76
Q

What are the major target tissues of thyroid hormone?

A

Liver, kidney, and skeletal muscle

77
Q

What is the mechanism by which T3 and T4 increase O2 consumption and metabolism in the peripheral tissues? Why might hormone replacement therapy take a couple of weeks in patients? What’s the interplay between hypothyroidism and thyroid receptors?

A

T3 and T4 enter target cells via energy dependent transport mechanisms where most of the T4 is then turned into T3. Both T3 and T4 are then transported to the nucleus where they bind thyroid receptors (T3 greater affinity than T4).

The T3/receptor complex interact with DNA to stimulate or inhibit transcription of certain genes and thus protein synthesis. This part may take 12-48 hrs which is why enzyme replacement therapy may take weeks.

Patients with hypothyroidism may have mutant receptors that cannot transduce the hormone signal effectively or simply can’t even bind T3

78
Q

What are the hypothyroid, euthyroid, and hyperthyroid levels of full body O2 consumption?

A

Hypo- 150 ml/min

Eu- 250 ml/min

Hyper- 400 ml/min

These are all without increasing level of work being done

79
Q

What are the ‘important actions’ of thyroid hormone?

A
  • increases O2 utilization and maintains normal O2 supply to the tissues
  • overall effect of TH is accelerating the metabolic response to starvation
  • TH modulates skeletal growth and CNS development
  • TH contributes to the regulation of reproductive function in both sexes
80
Q

What effect does TH have on BMR (basal metabolic rate) and thermogenesis? What are the secondary effects of this?

A

Increases BMR and thermogenesis

Secondary effects are increased body temperature which increases blood flow, sweating, and ventilation

81
Q

How does TH affect Na+/K+ ATPase activity? Does it affect mitochondrial movement of ATP? What is a non-genomic effect of T3?

A

Increases Na+/K+ ATPase activity which increases ADP concentration and also increases mitochondrial O2 uptake

T3 also stimulates adenine nucleotide translocase in the inner mitochondrial membrane which increases exchange of ADP in and ATP out. This is a non-genomic effect because it does not alter gene expression

82
Q

What effect does TH have on drug metabolism, vitamin turnover, and steroid hormone metabolism?

A

Increases them all due to increased catabolic state

83
Q

What effect does TH have on the kidneys?

A

Increases RPF and GFR while also increasing tubule transport (i.e. reabsorption of glucose and amino acids, etc.)

84
Q

What effects does TH have on the heart?

A

Increases stroke volume, heart rate, increases systolic BP while decreasing diastolic BP

Increased sarcolemma uptake of Ca2+ which allows for faster diastole and thus higher heart rate

85
Q

What are the clinical manifestations of hyperthyroidism? What can help ameliorate those symptoms?

A

High metabolic rate which leads to weight loss and increased food intake

Excessive generation of heat which causes discomfort in warm environments, excessive sweating, thirst, and increased ventilation (gotta get that O2 doe)

Muscle weakness/atrophy and possible osteoporosis due to excessive protein metabolism

High cardiac output, heart rate, and emotional liability

B adrenergic antagonists can help ameliorate symptoms

86
Q

What are the causes of hyperthyroidism?

A

Graves’ disease: autoimmune disorder where antibodies bind TSH receptors incessantly and mimick their stimulation

Benign neoplasm of thyroid that is unregulated by TSH

Inflammation of thyroid, excessive TSH, ingestion of excess T3 and T4, and high iodide intake

87
Q

Treatments of hyperthyroidism?

A

Short-term iodide excess (paradoxical)

Thiouracil (blocks thyroid hormone synthesis)

Ablation of thyroid material using radioactive iodide or surgery

88
Q

Clinical manifestations of hypothyroidism?

A

Decreased development and mental retardation

Lethargy, growth retardation, poor performance

Decreased metabolic rate leads to cold intolerance, decreased sweating, dry skin, low cardiac output and weight gain

89
Q

Hormones help to initiate, mediate, and regulate….

A

the growth, development, maturation, reproduction, and senescence.

90
Q

What are hormones?

A

Chemical substances produced by cells that travel in the blood to act on distant target cells

The target cells act to oppose the changes that induced the hormone release in the first place (neg feedback)

91
Q

What is homeostasis? What is included?

A

Maintenance of cellular and whole body metabolic conditions at optimum levels

Body temp, O2 supply to cells, BP, blood glucose levels, cell division/differentiation, growth, maturation, reproduction, behaviors, senescence

92
Q

What are the hormones of the pancreas?

A

Insulin, glucagon, and somatostatin

93
Q

What are the non-classic endocrine hormones secreted by the following tissues: hypothalamus, heart, kidney, liver, platelets, macrophages, and GI tract?

A

Hypothalamus— GHRH, LHRH (GnRH), TRH, CRH

Heart— ANP, BNP (brain natriuretic peptide)

Kidney— EPO, renin

Liver— Insulin like growth factor (IGF)

Platelets— platelet derived growth factor (PDGF), Transforming growth factor-B (TGF-B)

Macrophages— various cytokines

GI tract— Gastrin, secretin, vasoactive intestinal peptide (VIP)

94
Q

What is the process of synthesis, storage, and secretion of peptide hormones? How do peptide hormones travel?

A

Gene transcription-> mRNA-> pre-prohormone synthesized on ER ribosomes-> signal sequence cleavage in ER membrane-> prohormone-> Golgi apparatus for packaging into granules and post-translational mods-> secretion

Peptide hormones are water soluble so they travel freely in the blood plasma but they cannot cross cell membranes without a receptor

95
Q

Name some common steroid hormones and their precursor. How are they usually stored?

A

Cortisol, aldosterone, androgen, estrogens, progestins, Vitamin D

Cholesterol is common precursor.

They aren’t really stored within their gland of origin. Instead, when needed the entire biosynthetic pathway from cholesterol to hormone is upregulated

96
Q

What type of defect in a hormone-receptor system might cause a hormone-dependent genetic disease?

A

In a peptide hormone, a defect causing abnormal synthesis of peptide hormone is rare and usually involves point mutations in the hormone and/or receptor genes (causing mal-coupling)

In a steroid hormone, the defect is usually in a gene coding the enzyme that catalyzes a specific reaction in the biosynthetic pathway from cholesterol to hormone

97
Q

How does exocytosis of peptide hormones work?

A

A stimulus (maybe another hormone) causes secondary messenger rxn. Intracellular cAMP and Ca2+ increases which stimulates protein kinases to phosphorylate cellular components (like tubulin) which ultimately activates microtubules and microfilaments to move granules out of the cell

Ca2+/calmodulin also activates myosin light chain kinase which allows granule movement along actin filaments

98
Q

What is the initial determinant of the rate of hormone action in a cell? Is hormone binding like an puzzle piece?

A

Rxn between hormone and receptor is the determinant of rate

No; some hormones may look like others and thus bind weakly to receptors, but they won’t have the same efficacy as the true hormone.

99
Q

The physiologic conditions that require the action of a hormone also stimulate…

The conditions or products resulting from hormone action…

A

Hormonal release

Suppresses hormone release

100
Q

Positive and negative feedback are exhibited at which levels of cellular function? The feedback loop is also regulated by which exogenous factors?

A

Transcription, translation, AND release of hormones

Circadian rhythms, stage of sleep, seasonal variation, stage of development, and immune response

101
Q

Metabolic clearance rate

A

Mass of hormones removed per unit of time divided by its plasma concentration

MCR=(mg/min (removed))/(mg/min (plasma)) = ml plasma (cleared)/min

102
Q

What are the major sites of the metabolic degradation of hormones? How do they do it?

A

Kidneys and liver

Proteolysis
Oxidation
Reduction
Hydroxylated
Decarboxylation
Methylation
103
Q

What is Kassoc? What about initial receptor capacity?

A

Affinity constant

[HR]/[H] = Kassoc * R

Where H is free hormone, R is unoccupied receptors, and HR is occupied receptors

Initial receptor capacity (Ro) is [HR] + R

104
Q

Scatchard plot

A

Really weird way of showing what happens to [HR] if you increase free H (in other words, decrease the [HR]/[H] ratio).

Theoretically should be a straight line that crosses HR axis at Ro with a slope of of Kd (1/Kassoc).

However, an exponential plot (see slides for picture) results when the hormone occupancy of one receptor affects the affinity of a second receptor for the hormone. NEGATIVE COOPERATIVITY

105
Q

What is the protective effect of negative cooperativity on peptide hormone receptors? What is the difference between full biological effect of peptide hormones vs. steroid hormones

A

Negative cooperativity defends against massive excess of hormone concentration with quantitatively changing the hormone effect

Peptide hormones show full biological effect at small occupancy (i.e. there are spare receptors). This is partly due to the signal amplification of cAMP and Ca2+

Steroid hormones full biological effect is determined by number of receptors (i.e. exhibits full occupancy).

106
Q

What terminates the hormone signal at the cellular level?

A

Receptor down-regulation and desensitization

107
Q

What are the five classes of peptide hormone second messagers?

A 
Cyclic AMP
Cyclic GMP
Ca2+
Inositol 1,4,5 triphosphate (IP3)
Diacylglycerol (DG)
108
Q

What tests can be done to determine the amount of hormone secreted?

A

Radioimmuno Assay (RIA) and Enzyme linked immunosensitive assay (ELISA) of plasma and urine samples

109
Q

Radioimmuno Assay (RIA) vs. ELISA

A

RIA: One of the most sensitive methods of measure small quantities of circulating tissue hormone levels (can measure a trillionth of a gram of material per milliliter of plasma)

Problem: detects antigenic amounts of hormone all of which might not be biologically active

ELISA is equally as sensitive without the issue of radioactivity. Same antigenic problem though

110
Q

Describe the hormonal function of NO (and its synthesis)

A

Released by endothelial cells as a paracrine vasodilator (it doesn’t go very far) of vascular smooth muscle

Produced by NO synthase which is a Ca2+/calmodulin dependent enzyme that accelerates conversion of arginine to Citrulline plus NO

NO stimulates cytosolic guanalyl cyclase in the target cells and produces cGMP which activates GMP dependent protein kinases

111
Q

What do ANP and BNP do? What is the structure of guanalyl cyclase?

A

Released by the heart in response to elevated blood/arterial pressure

Stimulate excretion of salt and water by kidneys and vasodilation of vasculature to lower BP

ANP and BNP bind guanalyl cyclase to cause cGMP cascade

Guanalyl cyclase has extracellular domain, transmembrane linking domain, and intracellular domain. Natriuretic peptides bind the extracellular domain which causes conformation change of intracellular domain to increase cGMP production and cause vasodilation

112
Q

What are catecholamines made from?

A

Catecholamines (Epinephrine, NE, dopamine) are tyrosine derivatives

113
Q

Give the mechanism of various hormones at the cellular level

A

Adenylyl cyclase (cAMP): ACTH, LH, FSH, TSH, ADH (V1 receptor), HCG, MSH, CRH, calcitonin, PTH, glucagon, B1 and B2 receptors

Phospholipase C (IP3/Ca2+): GnRH, TRH, GHRH, Ang II, ADH (V2 receptor), Oxytocin, a1 receptor

Steroid hormone mechanism: Glucocorticoids, estrogen, progesterone, testosterone, aldosterone, 1,2,5-dihydroxycholecalciferol, thyroid hormones

Tyrosine Kinase mechanism: Insulin, IGF-1, GH, Prolactin

Guanylyl Cyclase (cGMP): ANP, NO

114
Q

Which hormones exhibit up regulation of their own receptors in their target tissues?

A

Prolactin— increases prolactin receptors in the breasts

GH— increases GH receptors in skeletal muscle and liver

Estrogen— increases the number of its receptors in the uterus

115
Q

What is the role of insulin and glucagon?

A

Maintain optimum blood glucose levels (homeostasis)

Glucagon— catabolic state
Insulin— anabolic state

116
Q

Describe the structure of insulin. What is it’s precursor?

A

Two polypeptide chains weighing 6000 Da (A and B) connected by two disulfide rings

A chain= 21 amino acids
B chain= 30 amino acids

Insulin gene has 3 Exons and 2 introns. Gene directs synthesis of Preproinsulin which contains 4 sequential peptides and an N-terminal signal peptide which is cleaved in the Golgi to become Proinsulin (A,B, and C chains). C chain is cleaved before release from the cell

117
Q

Why is there always a low rate of constitutive insulin secretion?

A

1% of proinsulin escapes storage granules and is slowly secreted by the cells all the time

118
Q

What is the most important factor that influences the secretion of insulin? Which is more effective, oral or intravenous glucose? What are other factors that stimulate or inhibit insulin release?

A

GLUCOSE

Oral is more important because it stimulates Glucose-dependent insulinotropic polypeptide (GIP) from the GI tract which has an independent stimulatory effect on insulin

Stimulants: increased AAs, incr. fFAs, glucagon, cortisol, K+, vagal stimulation, obesity, etc.

Inhibitors: decr. blood glucose, fasting, EXERCISE (think about it), somatostatin, a-adrenergic agonists, Diazoxide

119
Q

What does it mean that the relationship between insulin and glucose is sigmoidal?

A
  • No insulin secreted below blood glucose levels of 50 mg/dL
  • Half maximal insulin response occurs at glucose of 150 mg/dL
  • Maximal response occurs at 300 mg/dL
120
Q

What must happen before ATP/K+ channel induced depolarization can cause insulin release from B cells?

A

GLUT2 must take up glucose and convert it to ATP via glycolysis.

121
Q

How does biphasic insulin secretion work? When does insulin secretion peak?

A

Within seconds of glucose exposure, there is a release of insulin

Then, it takes about 10 min of sustained exposure to trigger another release. This time slowly increases and then sustained for a few hours

Peak 30-60 minutes after eating is initiated

122
Q

What happens in the early stages of type 2 diabetes?

A

Hyperinsulinemia

Complete loss of recognition of glucose as a stimulus for insulin secretion.

123
Q

What is the half-life of insulin? Why is it so short?

A

5-8 minutes

It travels unbound in the blood

124
Q

A tumor of B cells can lead to which condition?

A

Hypoglycemia (due to hyperinsulinemia)

125
Q

What are the most important tissues for insulin induced glucose uptake?

A

Adipose, liver, and muscle tissues

126
Q

Describe the structure of an insulin receptor. How does signal transduction work?

A

Two extracellular a subunits disulfide bonded to two B subunits (both transmembranal)

Insulin binds the two a subunits which causes autophosphorylation of tyrosine residues on the B subunit. The receptor then uses tyrosine kinase activity to phosphorylate tyrosine residues of Insulin Receptor Substrates (IRS)

IRS proteins serve as docking and activating site for other protein kinases, phosphatases, phospholipases, ion channels, and activating G-proteins. Many of these subsidiary steps involve serine and threonine phosphorylation.

127
Q

Where are IRS-1, IRS-2, and IRS-3 expressed? What are the main roles of IRSs?

A

1 and 2– muscle, adipose, and liver

3- brain

1) They translocations glucose transporters to the membrane via this path: IRS—>PI-3 kinase—> PIP2 —> PIP3 (independent from IP3) —> synthesis and translocation of glucose transporter via Akt/PKB and PKC
2) Also activate and deactivate enzymes in glucose and fatty acid metabolism
3) transcribe or repress genes in target cells

128
Q

Insulin cause a ….. in plasma levels of glucose, free fatty acids, and amino acids

A

Decrease

Promotes glycogen storage and glycolysis in the liver. Decreases hepatic glucose output by decreasing hepatic glycogenolysis

129
Q

What effect does insulin have on hormone-sensitive lipase?

A

Insulin profoundly inhibits hormone sensitive lipase activity in adipose tissues. Insulin is the major and most likely ONLY anti ketogenic hormone

Instead, it turns glucose and free fatty acids into triglycerides

130
Q

What is the structure of glucagon? What inhibits its release? What stimulates it?

A

Starts life as preproglucagon in a-islet cells; 29 amino acids; single chain; first 6 amino acids are really important

Insulin and glucose inhibit transcription of glucagon gene— decr. synthesis and release

Stimulatants: Hypoglycemia causes 2-4 fold increase in plasma glucagon (hyperglycemia decr. by 50%); intense exercise; fasting; stress (infections, burns, surgery)

Excess glucagon can lead to hyperglycemia

131
Q

What are the hormonal actions of glucagon? Mechanism?

A

Exact opposite of insulin

Increases mobilization of energy stores; increases plasma glucose, fFAs, and amino acids

Increases glycogenolysis and gluconeogenesis by liver; glycolysis slowed down

Increased lipolysis of adipose tissues—> ketone formation in the liver

Mechanism: binds to seven transmembrane G protein coupled receptors to increase cAMP levels

132
Q

How does the insulin/glucagon ratio fluctuate? Difference between consuming high glucose meal vs. high protein meal?

A

Normal state, post meal the ratio is close to 2.0

In fasted state or after prolonged exercise, ratio drops to 0.5

Pure carbohydrate meals can spike the ratio to 10 promoting nutrient uptake and decreasing proteolysis and lipolysis

High protein meal (with little carbs) will increase both insulin and glucagon. The insulin increases AA uptake and decreases proteolysis while the glucagon increases hepatic glucose output and inhibits glucose uptake to prevent hypoglycemia

133
Q

Somatostatin structure and regulation

A

Prosomatostatin yields either a 14 AA or 28 AA (intestines); both have same action

Synthesized in D cells of pancreatic islets and by intestinal cells

Stimulants: glucose, amino acids, fFAs, GLUCAGONS, various GI hormones

Inhibitors: INSULIN

134
Q

What are the jobs of somatostatin?

A

Profound inhibitor of both insulin and glucagon secretion

Inhibits uptake of all nutrients from GI tract by inhibiting motility and secretion of most other GI hormones

135
Q

What effect does glucagon have on somatostatin and insulin? What about insulin on glucagon and somatostatin?

A

Glucagon— stimulates insulin release; stimulates somatostatin

Insulin— inhibits somatostatin and glucagon

136
Q

What metabolite does insulin increase the uptake of?

A

K+ (by increasing Na+/K+ ATPase activity)

137
Q

What makes up 80-90% of the adrenal gland?

A

Adrenal Cortex— secretes corticosteroids

138
Q

Which adrenal hormone regulates extracellular fluid volume and Na+ retention?

A

Aldosterone

139
Q

Which adrenal androgen is most abundantly produced? Which others are produced? How biologically active are they?

A

Dehydroepiandrosterone sulfate (DHEA-S)

DHEA and androstenedione are also produced

These are required for survival and life

Even lower amounts of Aldosterone are still physiologically more active than these weak androgens

140
Q

Why does the adrenal medulla produce 80% epinephrine and 20% NE?

A

The blood supply received by the chromaffin cells is:
80-90% from the short arteries that pass through the cortex and pick up PNMT which converts NE to Epi
10-20% goes straight to the medulla and doesn’t have those enzymes

141
Q

What is the rate-limiting step for the synthesis of all adrenal cortex hormones?

A

The availability of cholesterol in cytosolic lipid droplets to be converted into pregnenolone by P 450scc in the inner mitochondrial membrane

142
Q

What cofactors are required in the cytochrome P450 rxns that hydroxylate steroid intermediates?

A

NADPH and an iron-containing protein called adrenoxin

143
Q

What is the most common cause of excess cortisol or adrenal androgen secretion?

A

Hypersecretion of ACTH

Secondary is adrenal tumor or blockade in another pathway that causes build up in this pathway

144
Q

How is cortisol produced? What is the last step?

A

Pregnenolone—>progesterone—> 17a-hydroxyprogesterone—> 11-deoxycortisol

11-deoxycortisol gets hydroxylated at the 11 position to become cortisol

145
Q

What are the significant steps in aldosterone production? What precursors can act similarly to aldosterone?

A

11-deoxycorticosterone—> corticosterone—> 18-hydroxycorticosterone—> C18 methyl oxidized to aldosterone

11-deoxycorticosterone and 18-hydroxycorticosterone both have some mineralocorticoid activity

146
Q

Are estrogen and testosterone secreted by the adrenal cortex?

A

Only in trace amounts

They really specialize in weak androgens

147
Q

The secretion of adrenal hormones serves a wide variety of physiologic functions:

A
  • Na+, K+, and Ca2+ balance
  • blood glucose regulation
  • protein turnover and fat metabolism
  • maintenance of cardiovascular tone
  • tissue response to injury and infection
  • survival as a result of stress
148
Q

How does cortisol exhibit negative feedback on ACTH and CRH? What happens if cortisol production is blocked?

A
  • can rapidly inhibit ACTH secretion by blocking CRH receptors on corticotrophs
  • can slowly inhibit ACTH secretion by blocking its synthesis at a nuclear level
  • can inhibit hypothalamic release of CRH
  • if cortisol is blocked, corticosterone can act as an alternative
149
Q

What other stimuli increase the secretion of CRH? What about ACTH?

A

Stress:

  • physical: surgery, trauma, infection
  • emotional: anxiety, depression
  • chemical: hypoglycemia
  • ACh, NE

Inhitors: GABA, Cortisol, Endorphins, etc.

ADH has a weak stimulatory effect on ACTH secretion

150
Q

What effect does a 21 or 11-hydroxylase enzyme deficiency have on infants?

A

Neither cortisol nor aldosterone can be made; overproduction of androgens leads to masculinization of female fetuses and early secondary sexual changes in male infants

151
Q

Deficiency of 11-hydroxylase can lead to overproduction of which mineralocorticoid? What secondary symptoms?

A

11-deoxycorticosterone

hypertension and hypokalemia

152
Q

Which physiological processes does cortisol facilitate?

A
  • sustained glucose production from protein (muscles)
  • vascular responsiveness and muscle function to catecholamines
  • skeletal turnover
  • modulation of CNS
  • hematopoeisis
  • renal function
  • immune response
153
Q

By what mechanism does ACTH increase steroid hormone production?

A

Binds a G protein linked plasma receptor which increases cAMP causing:
-increased steroidogenesis activator peptide
-sterol transfer protein
-steroidogenic acute regulatory protein
(All these to increase cholesterol esterase and increase mobilization of cholesterol)

-steroid-hormone producing protein
(To increase gene transcription of cytochrome P450 enzymes)

-growth factor (to increase cell size and number of cells)

154
Q

Why is cortisol so important? What is the most important overall effect of cortisol? What does it inhibit? Why is it called a “permissive” hormone?

A

You will DIE without it

Stimulate conversion of protein to glucose via gluconeogenesis and storage of glucose as glycogen in the liver. Also increases lipolysis to provide glycerol for gluconeogensis. Therefore, Cortisol is both CATABOLIC and DIABETOGENIC

Cortisol blocks insulin stimulated glucose uptake in order to drive glucose mobilization and storage in the liver. Can cause diabetes mellitus or make it worse if already occurring.

Cortisol is a permissive hormone because it does not stimulate gluconeogensis or protein metabolism by itself (glucagon does that), it simply enhances the process or allows it to occur

155
Q

When is ACTH secretion the highest? Lowest?

A

ACTH secretion is always pulsatile. Highest right before waking. Lowest at night during sleep

156
Q

What are the anti-inflammatory effects of cortisol? What secondary effect does this have?

A

1) induces synthesis of lipocortin which inhibits phospholipase A2 so prostaglandins and leukotrienes can’t be made
2) inhibits IL-2 production and proliferation of T lymphocytes
3) inhibits release of histamine and serotonin from mast cells and platelets

This suppresses the immune system as well

157
Q

How does cortisol inhibit bone formation?

A

Inhibits synthesis of type I collagen and formation of new bone by osteoblasts

also inhibits intestinal absorption of Ca2+

158
Q

What effect does cortisol have on GFR?

A

Increases it by causing vasodilation of afferent arterioles

159
Q

What is the interplay between cortisol, GH, and Epinephrine?

A

Cortisol permits maximum growth hormone and epinephrine stimulated lipolysis

Thus prolonged increase in cortisol can lead to obesity of abdomen, face, and trunk

160
Q

Cortisol levels increase sharply in response to…

A

Acute Hypoglycemia

161
Q

What effect does cortisol have on cardiac output, arterial tone, and endothelial permeability?

A

Maintains cardiac output, increases arterial tone, and decreases endothelial permeability by increasing a1-adrenergic receptors.

Hypercortisolism—> hypertension

Hypocortisolism—> hypotension

162
Q

What effect does cortisol have on the CNS?

A

Cortisol decreases REM sleep, increases awake time

163
Q

Long-term glucocorticoids increases a patient’s susceptibility to…

A

Infection

164
Q

Cushing Syndrome

A

Caused by excessive production of cortisol due to adrenal/pituitary dysfunction

Skin becomes very thin due to loss of connective tissue; blood vessels rupture easily; muscle weakness, atrophy, and osteoporosis

Obesity around the face, midsection, neck, etc.

165
Q

What stimulates aldosterone secretion?

A

Decreased ECFV, increased K+, Ang II

Ang II binds AT1 receptors in zona glomerulosa and cause IP3/Ca2+ increase

Increased K+ depolarizes aldosterone secreting cell; Ca2+ flows in and causes secretion of aldosterone

Endo/Repro (4 decks)

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