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Physiology > Introduction to endocrine physiology > Flashcards

Introduction to endocrine physiology 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 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

Explain the cell to cell communication molecules

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

For the cellular mechanism of action of hormones, what does it depend on and what does it initiate

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 differe classifcations of hormones

A

Peptide hormones
* Insulin

Steroid hormones
* Cortisol

Amine hormones
* 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 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 nucelus; 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 ves.
  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 sysnthesis
  8. Examples:Thyroxine (T4)
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11
Q

What are Characteristics of peptide hormones

A
  • Watersoluble,Generallydissolveeasilyin extracellular fluid for transport
  • Half- life,Short,e.g.,intherangeofseveralminutes
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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 is cholesterol made?
  • Lipophobic or philic?
  • 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 does steroid hormones do on cytoplasmic or nucelar 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 does steroid hormones do on cell membrane receptors?

A

nongenomic responses

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19
Q

Explain the different pathways that cholesterol can take and hit the major enzymes

A
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20
Q
  • What is aromatase inhibitor?
  • What is it usedd for?
A
  • Anastrozole
  • Used in post-metapausal women who have breat cancer
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21
Q

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

A
  1. Most hydrophobic steriods are bound to plasma protein carriers. only unbound hormones can diffuse into the target cell
  2. Steriod hormone receptors are in the cytoplamsa or nucleus
    2a. some steriod hormones also bind to membrane receptors that use second messenger system to create rapid cellular responses
  3. the receptor hormone complex binds to DNA and activates or represses on or more genes
  4. activated genes create new mRNA that moves back to the cytoplasma
  5. Translation produces new protein for cell processes
22
Q
  • What are the amine hormones?
  • What are they derived from?
A

Tryptophan:
* Melatonin (sleep)

Tyrosine:
* Catecholamines: Epinephrine, Norepineprine, Dopamine
* Thyroid hormones: T3, T4

23
Q
  • How are catecholamines made?
  • How are thyroid hormones made?
A

Cats are made by modifiying the side groups of tyrosine
Thyroid are made from two tyrosines and iodine atoms

24
Q

What are the major neurohormones?

A
  • Adrenal medulla: catecholamines (epi+NE)
  • Hypothalamus
  • Pituitary gland
25
Q

How is pituitary gland structured?

A

Pituitary gland:Two glands fused into one
* Posterior pituitary (neurohypophysis): Neural tissue
* Anterior pituitary (adenohypophysis): Endocrine tissue

26
Q

What does post pit secrete

A

vasopressin (antidiuretic hormone, ADH) & oxytocin

27
Q

What does ant. pit screate?

A

prolactin, thyrotropin, adrenocorticotropin, growth hormone, follicle-stimulating hormone, & luteinizing hormone

28
Q
  • Posterior pituitary is an extension of the _ _
  • Ant. pit is a true _ _ of epithelial origin
A
  • Posterior pituitary is an extension of the neural tissue
  • Ant. pit is a true endocrine gland of epithelial origin
29
Q

SKIP SLIDES 21 and 20
go back

A
30
Q

What controls the secetion of another hormone? give example

A
  • Trophic hormone
  • CRH> ACTH> cortisol
31
Q

What takes hormones from hypothamlus to pituitary

A

Hypothalamic-hypophyseal portal system

32
Q

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

A
  • Hypothalamic stimulation from the CNS
  • Anterior pituitary stimulatio from hypothalamic trophic hormones
  • Endocrine gland stimulation from anterior pituitary trophic hormones (except prolactin), e.g., cortisol
33
Q

Increase dopamine= _ prolactin

A

decrease

34
Q

What does ant pit. hormones control?

A

growth, metabolism and reproduction

35
Q

What are the different types of negative feedback loop?

A
  • Short-loop pathway
    * Parathyroid
  • Long-loop pathway
    * Cortisol
36
Q

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

A

short loop

37
Q

What is another name for growth hormone?

A

Somatropin

38
Q

What is the hypothalmic inhibiting hormone of GH

A

somatostatin

39
Q

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

A
  • go to liver and bind to receptors to release IGFs for bone and soft tissue
  • This is important for growth
40
Q

Explain the pathway for cortisol secretion and their neg feed back loops

A
41
Q

What hormones can have synergism?

A

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

42
Q

What hormone has permissiveness

A

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

43
Q

What hormones are antagonism

A

Glucagonopposesinsulin
– One substance opposes the action of another
– Competitive inhibitors vs. functional antagonism

44
Q
  • What is hypersecrtion?
  • What is caused by?
  • What is an effect of it?
A
  • Excesshormone
  • Caused by tumors or exogenous iatrogenic treatment
  • Negative feedback may lead to gland atrophy
45
Q
  • What is hyposecrtion?
  • What is caused by?
  • What is an effect of it?
A
  • Deficienthormone
  • Caused by decreased synthesis or gland damage
  • Absence of negative feedback leads to overproduction of trophic hormones
46
Q

Skipped slide 30, go back

A
47
Q

What happens when we have too much hormone?

A

Down-regulation
– Hyperinsulinemia → Decreased number of insulin
receptors

48
Q

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

A
  • Androgen insensitivity syndrome: ♂ baby appears ♀
  • Pseudohypoparathyroidism: G protein mutation → ↓ PTH effect
49
Q

What is primary, secondary and tertiary pathology due to?

A

Primary pathology due to issues with last endocrine
gland in pathway

Secondary pathology due to pituitary gland

Tertiary pathology due to hypothalamus
* Hypocortisolism may be due to primary or secondary pathology

50
Q

Explain how primary, secondary and tertiary pathology will play out in hypercorisolism (list out hormone levels)

A

Physiology (22 decks)

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