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Physiology: Exam 2 > Lecture 6: Into to Endocrinology I > Flashcards

Lecture 6: Into to Endocrinology I Flashcards

1
Q

Hormones act on their target cells via control of:

A
  • Rates of enzymatic reactions
  • Transport of ions or molecules across cell membranes (uptake-ex. glucose)
  • Gene expression & protein synthesis
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2
Q

What were the classic steps to identify an endocrine gland and the hormone they produce?

A
  • Remove the suspected gland
  • Replace the hormone
  • Create hormone excess
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3
Q

List the way hormone communicate from cell-to-cell (5)

A
  • Chemical signals
  • Secreted by a cell or group of cells into the blood
  • Transported by blood
  • Distant target tissue receptors
  • Activates physiological response at low concentrations (nanomolar to picomolar)
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4
Q

What is the cellular mechanism of action of hormones?

A
  • Depends on binding to target cell receptors
  • Initiated biochemical responses
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5
Q

What indicates the length of activity of hormone?

A

Half life of the hormone

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6
Q

What are the different classifications of hormones?

A
  • Peptide hormones (e.g. Insulin)
  • Steroid hormones (e.g.Cortisol)
  • Amine hormones (e.g. Epinephrine)
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7
Q

Peptide hormones:

  1. Synthesis and storage:
  2. Release from parent cell:
  3. Transport in blood:
  4. half-life:
  5. location of receptor:
  6. response to receptor-ligand binding:
  7. general target response:
  8. Examples:
A
  1. Synthesis and storage: made in advance; stored in secretory vesicles
  2. Release from parent cell: Exocytosis
  3. Transport in blood: dissolved in plasma
  4. half-life: short (peptidases)
  5. location of receptor: cell membrane
  6. response to receptor-ligand binding: activation of second messenger systems; may activate genes
  7. general target response: modification of existing proteins and induction of new protein synthesis
  8. Examples: insulin, parathyroid hormone
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8
Q

Steroid hormones

  1. Synthesis and storage
  2. Release from a parent cell
  3. Transport in blood:
  4. half-life:
  5. location of receptor:
  6. response to receptor-ligand binding:
  7. general target response
  8. Examples:
A
  1. Synthesis and storage: synthesized on demand from precursors
  2. Release from parent cell: simple diffusion
  3. Transport in blood: bound to carrier proteins
  4. half-life: long
  5. location of receptor: cytoplasm or nucleus; some have membrane receptors also
  6. response to receptor-ligand binding: activation of genes for transcription and translation; may have nongenomic action
  7. general target response: induction of new protein synthesis
  8. Examples: estrogen, androgens, cortisol
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9
Q

Catecholamines:
1. Synthesis and storage:
2. Release from parent cell:
3. Transport in blood:
4. half-life:
5. location of receptor:
6. response to receptor-ligand binding:
7. general target response:
8. Examples:

A
  1. Synthesis and storage: made in advance; stored in secretory vesicles
  2. Release from parent cell: exocytosis
  3. Transport in blood: dissolved in plasma
  4. half-life: short
  5. location of receptor: cell membrane
  6. response to receptor-ligand binding: activation of 2nd messenger systems
  7. general target response: modification of existing proteins
  8. Examples: epi, NE, and dopamine
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10
Q

Thyroid hormones:

  1. Synthesis and storage:
  2. Release from parent cell:
  3. Transport in blood:
  4. half-life:
  5. location of receptor:
  6. response to receptor-ligand binding:
  7. general target response:
  8. Examples:
A
  1. Synthesis and storage: made in advance; precursor stored in secretory vesicles
  2. Release from parent cell: transport protein
  3. Transport in blood: bound to carrier proteins
  4. half-life: long
  5. location of receptor: nucleus
  6. response to receptor-ligand binding: activation of genes for transcription and translation
  7. general target response: induction of new protein synthesis
  8. Examples: Thyroxine (T4)
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11
Q

What are the characteristics of peptide hormones?

A
  • Water soluble = generally dissolves easily in extracellular fluid for transport
  • short half-life ,e.g.,in the range of several minutes
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12
Q

Explain the prohormones process

A

Preproinsulin-> proinsulin-> insulin + C-peptide

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13
Q
  • What is the insulin: C-peptide molar ratio? * What is it used for?
A
  • 1:1
  • Used to determine Hyperinsulinemia (exogenous or endogenous)
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14
Q

Where are steroid hormones derived from?

A

cholesterol

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15
Q
  • Where are steroid hormones made?
  • Lipophobic or lipophilic?
  • When it is made?
A
  • Made only in a few organs: adrenal glands & gonads (testes+ovaries)
  • Lipophilic & easily cross membranes
  • Made as needed, not stored
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16
Q

What can steroid hormone do to have a longer half life

A

Bind to carrier protein in blood

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17
Q

What effect do steroid hormones have on cytoplasmic and nuclear receptors?

A
  • Genomic effect to activate or repress genes for protein synthesis
  • Slower acting but longer effect than non-genomic
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18
Q

What response do steroid hormones have on cell membrane receptors?

A

nongenomic responses

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19
Q

What is Anastrozole? What is it used for?

A
  • Used in post-menopausal women who have breast cancer = decreases estrogen levels
  • Nonsteroidal aromatase inhibitor
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20
Q

Explain the two pathways that a steroid hormone can take to get to a receptor

A
  1. Most hydrophobic steroids are bound to plasma protein carriers. only unbound hormones can diffuse into the target cell
  2. Steroid hormone receptors are in the cytoplasm or nucleus
    2a. some steroid hormones also bind to membrane receptors that use a second messenger system to create rapid cellular responses
  3. the receptor hormone complex binds to DNA and activates or represses one or more genes
  4. activated genes create new mRNA that moves back to the cytoplasm
  5. Translation produces new proteins for cell processes
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21
Q
  • What are the amine hormones?
  • What are they derived from?
A
  • Tryptophan: Melatonin (sleep)
  • Tyrosine: Catecholamines: Epinephrine, Norepinephrine, Dopamine
    Thyroid hormones: T3, T4
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22
Q
  • How are catecholamines made?
  • How are thyroid hormones made?
A
  • Catecholamines are made by modifying the side groups of tyrosine
  • Thyroid are made from two tyrosines and iodine atoms
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23
Q

What are the major neurohormones? (3)

A
  • Adrenal medulla: catecholamines (D.E.N.)
  • Hypothalamus
  • Pituitary gland
24
Q

How is the pituitary gland structured?

A

Pituitary gland: Two glands fused into one

  • Posterior pituitary (neurohypophysis): Neural tissue
  • Anterior pituitary (adenohypophysis): Endocrine tissue
25
Q

What does the posterior pituitary secrete?

A

vasopressin (antidiuretic hormone, ADH) & oxytocin

26
Q

What does the anterior pituitary secrete? (6)

A
  • Prolactin
  • Thyrotropin
  • Adrenocorticotropin
  • Growth hormone
  • Follicle-stimulating hormone
  • Luteinizing hormone
27
Q
  • Posterior pituitary is an extension of the _ _
  • Anterior pituitary is a true _ _ of epithelial origin
A
  • Posterior pituitary is an extension of the neural tissue
  • Anterior pituitary is a true endocrine gland of epithelial origin
28
Q

What controls the secretion of another hormone? give example

A
  • Trophic hormone
  • CRH> ACTH> cortisol
29
Q

What takes hormones from hypothamlus to pituitary

A

Hypothalamic-hypophyseal portal system

30
Q

What are the three integrating centers? and where they are from

A
  • Hypothalamic stimulation from the CNS
  • Anterior pituitary stimulation from hypothalamic trophic hormones
  • Endocrine gland stimulation from anterior pituitary trophic hormones (except prolactin), e.g., cortisol
31
Q

Increase dopamine= _ prolactin

A

decrease

32
Q

What does ant pit. hormones control?

A

growth, metabolism and reproduction

33
Q

What are the different types of negative feedback loops?

A
  • Short-loop pathway
    -Parathyroid
  • Long-loop pathway
    -Cortisol
34
Q

What type of loop is the homeostasis of calcium levels? Explain the loop

A

Short loop

  • If Ca2+ levels rise
    1. Thyroid gland releases calcitonin
    2. Blood Ca2+ levels fall
  • If Ca2+ levels fall
    1. Parathyroid glands release parathyroid hormone (PTH)
    2. Blood Ca2+ levels rises
35
Q

What is another name for growth hormone?

A

Somatropin

36
Q

What is the hypothalmic inhibiting hormone of GH

A

somatostatin

37
Q

After GH cells are released from the ant pit where do they go and what do they do?

A
  • Go to the liver and bind to receptors to release IGFs for bone and soft tissue
  • This is important for growth
38
Q

What hormones can have synergism?

A

Glucagon,epinephrine,cortisol– Combined effect is greater than the sum of individualeffects

39
Q

What hormone has permissiveness

A

*T3 +GH (tissue and bone growth)
* Need second hormone to get the full effect

40
Q

What hormones are antagonism

A
  • Glucagon opposes insulin– One substance opposes the action of another
  • Competitive inhibitors vs. functional antagonism
41
Q
  • What is hypersecretion?
  • What is caused by?
  • What is the effect of it?
A
  • Excess hormone
  • Caused by tumors or exogenous iatrogenic treatment
  • Negative feedback may lead to gland atrophy
42
Q
  • What is hyposecretion?
  • What is caused by?
  • What is the effect of it?
A
  • Deficient hormone
  • Caused by decreased synthesis or gland damage
  • Absence of negative feedback leads to overproduction of trophic hormones
43
Q

What happens when we have too much hormone?

A

Down-regulation– Hyperinsulinemia → Decreased number of insulinreceptors

44
Q

What are some pathologies when there is a missing or nonfunctional receptor?

A
  • Androgen insensitivity syndrome: ♂ baby appears ♀
  • Pseudohypoparathyroidism: G protein mutation → ↓ PTH effect
45
Q

What are primary, secondary and tertiary pathology due to?

A
  • Primary pathology due to issues with the last endocrine gland in the pathway
  • Secondary pathology due to pituitary gland
  • Tertiary pathology due to hypothalamus
46
Q

What causes Hypercortisolism (Cushing’s Syndrome)?

A

Hypocortisolism may be due to primary or secondary pathology

47
Q

When their is pathology in the Adrenal Cortex (1° pathology) what are the levels of:

  • CRH
  • ACTH
  • Cortisol
A
  • CRH: low
  • ACTH: low
  • Cortisol: high (excess amount d/t 1° pathology)
48
Q

When their is pathology in the Anterior Pituitary (2° pathology) what are the levels of:

  • CRH
  • ACTH
  • Cortisol
A
  • CRH: low
  • ACTH: high (excess amount d/t 2° patholgy)
  • Cortisol: high (excess d/t excess ACTH)
49
Q

When their is pathology in the Hypothalamus (3° pathology) what are the levels of:

  • CRH
  • ACTH
  • Cortisol

Very RARE

A
  • CRH: high (excess amount d/t 3° pathology)
  • ACTH: high
  • Cortisol: high
50
Q

Which of the following pituitary hormones controls cell growth and metabolism in many tissues?
A) Dopamine
B) Somatotropin
C) Prolactin
D) Insulin

A

B) Somatotropin (also called GH)

51
Q

Which of the following pituitary hormones stimulates milk production in the mammary glands?
A) TSH
B) ACTH
C) Growth hormone
D) Prolactin

A

D) Prolactin

52
Q

All of the following are produced in the adrenal cortex except:
a. Cortisol
b. Dopamine
c. Aldosterone
d. Estradiol

A

b. Dopamine

53
Q

Which of the following hormones is synthesized on demand?
a. Insulin
b. T3
c. Epinephrine
d. Aldosterone

A

d, Aldosterone

54
Q

Key characteristics of the posterior pituitary include:
I. Cell body within the hypothalamus
II. Portal vein system
III. Production of its own hormones

a. I only
b.II and III
c. I, II, and III
d. None of the above

A

a. I only

55
Q

Cortisol secretion is controlled through short and long negative feedback loops. Which of the following describes the short feedback loop?
A. Excess cortisol inhibits CRH release
B. Excess cortisol inhibits ACTH release
C. Excess ACTH inhibits the anterior pituitary
D. Excess ACTH inhibits the hypothalamus

A

D. Excess ACTH inhibits the hypothalamus

56
Q

Which of the following statements is true?
a. Synergism is the combined effect of more than one hormone is less than the sum of the individual effects
b. Down regulation of insulin receptors leads to hypoinsulinemia
c. A tertiary hypersecretion causes can increase in target hormone levels, but a decrease in releasing hormone and tropic hormone levels
d. Hydrophobic hormones have a longer half-life than hydrophilic hormones

A

d. Hydrophobic hormones have a longer half-life than hydrophilic hormones

Physiology: Exam 2 (9 decks)

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