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Mammalian Physiology > Slide 3b > Flashcards

Slide 3b Flashcards

1
Q

What are examples of steroid hormones?

A
  • cortisol (adrenals)
  • aldosterone (adrenals)
  • estrogen (ovary and testis)
  • progesterone (ovary-CL)
  • testosterone (testis-leydig cells)
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2
Q

What is the process of steroid hormone synthesis?

A

Steroid hormones are synthesized from cholesterol. They have the 4 ringed structure. Since they are lipid soluble, they pass through the plasma membrane of target cells and travel to the nucleus. They recognize the zinc finger DNA binding domain and bind at the HRE to initiate gene transcription.

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3
Q

What are the different types of non-steroid hormone synthesis?

A
  • from amino acids
    1. some are protein hormones (long folded chains of amino acids) like insulin
    2. glycoprotein hormones are protein hormones with carbohydrate groups attached to the amino chain. eg. hCG (human chorionic hormone for pregnancy recognition.
    3. peptide hormones are smaller than protein hormones, they are short chained amino acids eg. oxytocin and ADH
    4. amino acid derivative hormones are derived form a single amino acid
    eg. modifying a single molecule of tyrosine like epinephrine and norepinephrine (adrenal medulla), thyroxine is synthesized by adding iodine to tyrosine
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4
Q

Describe the general action of hormones.

A
  • signal a cell by binding to target cell’s specific receptor
  • different hormone receptor interactions produces different regulatory changes in target cell like inactivation of enzyme or gene transcription
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5
Q

What are the 3 combined hormone actions? (hormone interactions)

A
  1. synergism: combo of hormones acting together to have a greater summed effect (than each individual hormone acting alone)
  2. permissiveness: a small amount of one hormone permits a second to have a full effect on target cell
    These are precursors to active hormone and are classified as either prohormones or prehormones.
  3. antagonism: one hormone produces the opposite effects of another hormone eg. parathyroid hormone and calcitonin= increase and decrease blood calcium)
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6
Q

How are hormone actions terminated? Give an example.

A

Insulin secretion in blood glucose is high following a meal.

  • the presence of insulin = glucose uptake by cells
  • prolonged action of insulin deprives brain of glucose since all the glucose will be taken up my muscle and fat cells, there is no more for brain
  • regulated by terminating hormone activities
  • hormones have half-life and are degraded into inactive metabolites in liver which are excreted
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7
Q

What is the mechanism of steroid hormone action?

A
  1. diffuse into target cell and bind to their receptor molecule (in cytosol) or
  2. form the mobile receptor model: hormone passes into the nucleus an binds to the mobile receptor to activate gene sequence and begin transcription of mRNA which move into cytosol and associate ribosomes. It begins to synthesized protein molecules to produce effects of hormone
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8
Q

How steroid hormones regulate cells?

A
  • by regulating certain critical proteins
  • amount of steroid hormone present determines the magnitude of target cell response
  • responses of steroid hormones are slow because transcription and protein synthesis take time.
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9
Q

What does the sensitivity of the target cell depend on?

A

the number of receptors the cell has

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10
Q

What allows new receptors to be incorporated and increased transcription of proteins?

A

the process of hormones receptors constantly broken down and replaced.

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11
Q

What is the difference between up-regulation and down-regulation?

A

up regulation: increased number of hormone receptors which increases sensitivity hormones
down-regulation: decreased number of hormone receptors decreases sensitivity

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12
Q

How does it differ from steroid hormone effects? (2 ways)

A
  • effects are amplified by a cascade of reactions which is disproportionally greater compared to the amount of hormone present
  • the second messenger mechanism operates way faster than the steroid mechanism
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13
Q

What is the mechanism of hormone action in hydrophilic-protein and peptide hormones?

A
  • they use a second messenger mechanism: produces target cell effects that differ from steroid hormone effects
  • the non steroid hormone molecule acts as a first messenger to deliver chemical message to the FIXED RECEPTORS in target cell’s plasma membrane
  • the message is relayed via G protein to a second messenger which triggers appropriate cellular changes
    eg. adenylyl cyclase receptor - cAMP and PKA etc.
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14
Q

Explain how calcium acts a second messenger.

A

They use calcium instead of cAMP where there is still binding of G protein but instead of adenylyl cyclase it is phospholipase C that is activated, splits phospholipid (PIP2) into IP3 + DAG, IP3 increases intracell calcium (via SR)and cytosolic calcium which activates calmodulin

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15
Q

How are hormone secretin regulated?

A
  • negative feedback loop: when output of system counteracts change in input
  • simplest mechanism: when endocrine gland is sensitive to the physiological changes produced by the target cell
  • can be regulated by secretion of hormone from another gland
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16
Q

Give an example of a negative feedback control. (thyroid hormone)

A
  1. plasma concentration of thyroid hormone falls = low t3/t4
  2. anterior pituitary secretes TSH
  3. thyroid in turn secretes TH
  4. Thyroid hormone (TH) inhibits further secretion of TSH due to negative feedback to pituitary gland
17
Q

Give an example of a negative feedback control. (plasma calcium)

A
  1. lactation causes low blood calcium
  2. Parathyroid senses and responds by increasing secretion of PTH. (parathyroid hormone)
  3. PTH stiulates osteoclasts in bone to release more calcium from storage in bone tissue
  4. maternal blood calcium is raised back to set point level
    This is a short feedback loop.
18
Q

Where is the pituitary gland and describe its division and connection to the hypothalamus?

A

-well protected area of the brain on the ventral surface of the brain within the skull.
-infundibulum: stem-like stalk that connects the pituitary to the hypothalamus
-made of 2 separate glands: anterior (bigger half) and posterior pituitary glands
remember it looks like 2 testicles

19
Q

How is the anterior pituitary signalled?

A

from the hypothalamus, the neurons synthesizing trophic hormones release the tropic hormones into capillaries of portal system

  • portal vessels carry trophic hormones DIRECTLY to the anterior pituitary
  • endocrine cells release their hormones into the second set of capillaries for distribution to the rest of the body (target organs: prolactin- mammary glands, GH-musculoskeletal system, TSH- thyroid gland, ACTH-adrenal cortex, LH&FSH - ovary & testis)
    (posterior: ADH - kidney tubules and OT oxytocin - mammary glands and uterus smooth muscle)
20
Q

What is the difference tropic and non-tropic hormones?

A

tropic: act on other glands
-it tends to stimulate the synthesis and secretion of target hormone
non-tropic: directly stimulate target cells to induce effects

21
Q

Describe the anterior pituitary gland (adenohypophysis) anatomically.

A
  • divided into two parts: pars anterior - major portion of adenohypophysis & pars intermedia
  • composed of irregular clumps of secretory tissue with fine connective tissue fibers and a rich vascular network
22
Q

What are the 5 functional types of secretory cells in the adenohypophysis?

A
  1. somatotrophs : GH
  2. gonadotrophs : FSH & LH
  3. lactotrophs: PRL
  4. corticotrophs: ACTH (regulate levels of steroid hormone cortisol) & MSH (melanin)
  5. thyrotrophs: TSH
23
Q

What does GH do and how does it do it?

A
  • promotes growth by stimulating liver to produce more growth factors which accelerates amino acid transport into cells
  • promotes growth of bone, muscle and other tissues by making amino acid transport into cells faster (involves protein anabolism)
  • stimulates lipid metabolism: accelerates mobilization of lipids from cells and speeds up lipid catabolism shifting the cell use of nutrients from glucose to lipid catabolism (hyperglycemic affect)
24
Q

What is the agonist of GH?

A

insulin! it promotes glucose entry into cell

25
Q

How does GH affect metabolism directly? (3 ways)

A
  1. promotes protein anabolism
  2. promotes lipid mobilization and catabolization
  3. indirectly inhibits glucose metabolism by shifting energy use to lipid catabolism (increasing blood glucose)
26
Q

What is the function of PRL?

A
  • produced by lactotrophs (acidophils) in adenopypophysis
  • promotes development of breasts during preg and
  • milk secretion after baby is born
  • stimulates mother’s mammary glands to produce milk
27
Q

What are the four main tropic hormones produced and secreted by the basophils of the pars anterior?

A
  1. TSH: promotes and maintain growth and development of thyroid- causes thyroid to secrete hormones t3+t4
  2. adrenocrticotropic hormone (ACTH) or adrenocrticotropin: promotes and maintains normal growth and development of the cortex in the adrenal gland (on the kidneys), stimulates adrenal cortex to secrete hormones : cortisol and aldosterone
  3. Follicle stimulating hormone (FSH):
    -females: stimulate graffian follicles to grow to maturity
    - acts on ovary
    -stimulates follicle cells to secrete estrogen
    -males: stimulate development of seminiferous tubules of testes and maintains spermatogenesis
    -acts on sertoli cells4. Luteinizing hormone (LH)
    females: stimulate formation of corpus luteum of ovary
    -corpus luteum: secretes progesterone and estrogen when stimulated by LH
    - LH also supports FSH to stimulate maturation of follicles
    males: LH stimulates interstitial cells (leydig cells) in testes to develop and secrete testosterone
    both are gonadotropins because they stimulate growth and maintain the gonads
28
Q

How is the anterioir pituitary controlled by the hypothalamus (hormones wise)

A
  • inhibiting hormones- influence secretion of basophils and acidophils in the adenohyphosis via negative feedback=hypothalamus adjusts the secretions to anterior pituitary, adjusting target glands and the activity of their target tissues
  • minute by minute variation sin hormone secretion can exhibit occasional large peaks due to the pulse in releasing hormone secretion by hypothalamus
29
Q

What happens to FSH levels during menopause? Why?

A

It rises.
FSH stimulates follicles to release eggs for ovulation, which secretes estrogen reaching peak where continued maturation causes the formation of the corpus luteum.
However, since at menopause, there are no more eggs, FSH tries to stimulate follicles but there is no response of ovulation. Since FSH wants to respond to the high estrogen level produced by dominant follicle (during ovulation) it keeps sending FSH to get a response for the negative feedback. (however no more eggs so wont get the response.)

30
Q

How is the hypothalamic hypophyseal portal system inhibited?

A

Since it is the capillary to capillary connection (direct), target gland hormones inhibit this via negative feedback.
eg. a rise in cortisol from the adrenal cortex feeds back to reduce CRH secretion by the hypothalamus and sensitivity of the ACTH secreting cells (in anterior pituitary) to CRH.

31
Q

What is a portal system?

A

Makes a direct link from one organ to another via the direct connection of capillaries which can carry the blood directly without bypassing other tissues.

32
Q

What is the relationship between the posterior pituitary and the hypothalamus?

A

-neurosecretory cells have bodies directly on the hypothalamus and the corresponding axon terminal on the posterior pituitary.

33
Q

What are alternate names for posterior pituitary and anterior pituitary?

A

posterior: neurohypophysis
anterior: adenohypophysis

34
Q

How does the hypothalamus signal the posterioir pituitary to release hormones?

A
  • hormone is made and packed in neuron cell body (hypothalamus)
  • vesicle transport down cell
  • vesicles store the hormone in the posterioir pituitary
  • hormones are released in the blood (veins)
35
Q

What are 3 hormone pathologies?

A
  1. hormone excess
  2. hormone deficiency
  3. abnormal responsiveness of target tissues
36
Q

What is the case of Cushing’s disease?

A

-hormone excess
Normal cortisol action:
-protein breakdown, glucose formation, lipoylysis, anti-inflammatory effect, depression of immune responses
Cushing’s disease: adrenal cortex tumour hypersecretion of cortisol
- breakdown of muscle proteins, redistribute fat, spindly arms/legs, moon face,flushed

37
Q

What is a case of hormone deficiency?

A

Normal thyroid hormones:
-increased metabolic rate (use of O2 to ATP), stimulate Na/K ATPase
-protein synthesis and use of glucose and fatty acids for ATP production, catecholamines, body growth
Deficiency: swelling (puffiness), slow heart rate, low body temperature, etc.

38
Q

What is an abnormal responsiveness of target tissue?

A

Type 2 diabetes mellitys (loss of tissue sensitivity to insulin- not taken up by cells)
caused by diabtese
Type 1: autoimmune, no secretion of insulin which means cells do not have the signal to uptake in cells.

39
Q

What balances calcium ion use?

A

calcitonin, parathyroid hormone and vitamin D

Mammalian Physiology (17 decks)

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