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MBBS II ERS > L03, 04, 05 - Introduction to Endocrine System, their Physiological Actions, and their Regulation > Flashcards

L03, 04, 05 - Introduction to Endocrine System, their Physiological Actions, and their Regulation Flashcards

1
Q

3 modes of endocrine signalling?

A
  1. Endocrine signaling: acts on distant target cells through bloodstream
  2. Paracrine signaling: secreted into extracellular region, acts on adjacent target cell
  3. Autocrine signaling (e.g. vasopressin): secreted into extracellular region, self- stimulate
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2
Q

what forms the endocrine system?

A

Glands
Hormones
Receptors

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3
Q

Compare the hormones released by adrenal cortex and medulla?

A

Adrenal cortex : mineralcorticoids

  • Aldosterone
  • Cortisol
  • Androgens

Adrenal medulla: Catecholamines

  • Epinephrine
  • Norepinephrin
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4
Q

List the 3 chemical classes of hormones?

A
  1. Amino acid derivatives
  2. Peptide and protein hormones (>3 a.a.)
  3. Steroid hormones
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5
Q

Compare the half-life in blood between 3 chemical classes of hormones?

A
  1. Amino acid derivatives:
    - Insoluble, with carrier protein = days (long)
    - Soluble without carrier = mins (short)
  2. Peptide and protein hormones (>3 a.a.):
    - Soluble, no carrier = mins (short)
  3. Steroid hormones
    - Most bound to carrier protein = hours (long)
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6
Q

Compare the source of amino acid vs peptide vs steroid hormones?

A
  1. Amino acid = Derived mostly from Tyrosine and Tryptophan
  2. Peptide: synthesized in RER as precursor, often need posttranslational processing to activate
  3. Steroid: Derived from cholesterol
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7
Q

Compare the location of hormone receptors based on the chemical calss

A
  1. Water soluble hormones
    • Peptide and protein hormones
    • Repelled by lipid in the cell membrane
    • Bind to a receptor protein on plasma membrane&raquo_space; cytoplasmic or nuclear response
  2. Lipid soluble hormones
    • Steroid hormones
    • Diffuse through the plasma membrane and bind to a receptor protein inside the cell (usually transcription factor)
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8
Q

Describe the intracellular signal transduction mechanism for steroid hormones?

A

1) Steroid hormone bind to receptor = detach repressor* protein
2) Hormone/ receptor complexes dimerize to act as transcription factor
3) Receptor complex decrease in surface hydrophobicity* due to conformational change
4) translocate to nucleus, bind to Hormone Response Element* via DNA binding site of complex
5) Induce or repress gene expression

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9
Q

Compare the MoA of Tamoxifen and Raloxifene on estrogen receptors?

A

Depending on tissue type:

Tamoxifen = suppresses estrogen receptor β activation&raquo_space; recruits corepressor protein to decrease estrogen function

Raloxifene = activates estrogen receptor α = recruits coactivator = more estrogen

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10
Q

Describe the mechanism of GPCRs to generate secondary messengers?

A

GPCR + ligand = undergoing dynamic conformational changes in the Transmembrane domain

> > Allow docking of intracellular signal molecule to activate associated G protein

e.g. allow swapping GDP for GTP to activate G proteins in intracellular domain

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11
Q

Compare the function of 3 types of Gα subunits in GPCRs?

A
  1. Gαs – stimulation leads to increase cAMP
  2. Gαi – stimulation leads to decrease cAMP
  3. Gαq – stimulation leads to activation of phospholipase C (PLC)&raquo_space; calcium signaling pathway
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12
Q

Describe the mechanism of GPCR and G proteins after Vasopressin binding at collecting tubule?

A

Vp binds to extracullar GPCR domain

> > conformational change at transmembrane domain (3rd intracellular loop)

> > Gαs*** stimulation, increase cAMP

> > Increase expression of AQP2 + Increase insertion of AQP2 onto apical membrane

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13
Q

Describe the functional structure of Enzyme-linked receptors?

A

Cytoplasmic domain:

  • Either intrinsic enzyme activity
  • Associated with enyzmes (e.g. Tyrosine kinase, tyrosine phosphatase, serine/threonine kinase)

Transmembrane domain: dimerize and trigger enzyme activity

Extracellular domain: bind ligand

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14
Q

2 downstream signalling pathways of Insulin signalling?

A

PI3K/AKT pathway: controlling metabolic effects of insulin

Ras/ERK pathway: controlling cell growth and differentiation induced by insulin

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15
Q

Explain how insulin receptors cause downstream signalling cascade?

A

insulin receptor = tyrosine kinase transmembrane signaling protein

Insulin binds to α-subunit cause autophosphorylation of β-subunit

> > allow docking of substrates (e.g. insulin receptor substrate 1 (IRS-1)

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16
Q

4 types of hormone-hormone interactions?

A
  1. Redundant effect
  2. Reinforcement effect
  3. Antagonistic effect
  4. Permissive effect
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17
Q

Give example of hormones with redundant effect?

A

Diff. hormones produce same effect = safe-guard physiological functions + synergy

e. g. Glucagon, epinephrine, cortisol act on liver to increase blood glucose level during fasting
* at different time-constants*

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18
Q

Give one example of hormone causing reinforcement effect across whole body.

A

Cortisol: whole body response:

  • Proteolysis at muscles
  • Lipolysis at adipose tissue
  • Glyconeogenesis at liver
  • Desensitize against insulin

> > > Increase blood glucose

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19
Q

Give one example of hormone causing reinforcement effect across one cell?

A

Aldosterone bind to mineralcorticoid receptor:

  • Increase Na/K ATPase expression for Basal membrane
  • Increase ENaC and ROMK expression on apical membrane

> > Na reabsorption + K secretion

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20
Q

Give example of hormones with antagonistic effects?

A

Insulin vs glucagon

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21
Q

Define hormone permissive effect?

A

One hormone control expression of receptor for another hormone

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22
Q

Give example of hormones with permissive effects?

A

Estrogen induce expression of Progesterone receptor in uterus
» proliferate + develop uterus endometrium for implantation

23
Q

3 types of rhythms of hormone secretion?

A
  1. Pulsatile (e.g. insulin, GnRH)
  2. Diurnal (e.g. cortisol and melatonin)
  3. Cyclic (e.g. menstruation)
24
Q

Explain how change in pulsatile secretion of GnRH cause different gonadotrophin release?

A

High frequency release = stimulate LH release from ant. pituitary

Low freq. GnRH = Stimulate FSH release from ant. pit.

25
Q

3 different types of stimuli for controlling hormone secretion?

A
  • Humoral: respond to extracellular fluid change/ blood-bourne chemicals
  • Hormonal: trophic hormone cause release of another hormone
  • Neural: nervous system directly stimulate endocrine glands to release hormones
26
Q

Give one example of hormonal response triggered by change in the extracellular fluid?

A

secrete parathyroid hormone (PTH) in response to Ca2+ level in extracellular fluid:

High [Ca2+]: Ca2+ binds to activate calcium-sensing receptor = inhibits PTH secretion

Low [Ca2+]: Ca2+ not bound to receptor = no inhibition = PTH secretion to increase [Ca2+]

27
Q

Describe how Pancreatic β-cell respond to high blood glucose? think electricity

A

Pancreatic β-cell: ATP-sensitive potassium channels are open at rest

  1. Glucose diffuses into cell through membrane glucose transporter&raquo_space; glycolysis make ATP
  2. ATP-sensitive potassium channels close = no K+ efflux = depolarization
  3. Voltage-dependent Ca2+ channels open = increase intracellular [Ca] = insulin exocytosis
28
Q

Describe how adrenal medulla responds to stress-induced sympathetic activation?

A

sympathetic nervous system

> > AP to chromaffin cells in adrenal medulla

> > neurons secrete Ach to nicotinic receptors of chromaffin cells

> > Trigger Tyrosine hydroxylase converts tyrosine to DOPA to NE

> > Exocytosis of catecholamines (norepinephrine / epinephrine) into capillary

29
Q

Give one example of positive feedback hormonal response?

A

uterine muscle contraction during labor

> > nerve impulse to hypothalamo-pituitary axis

> > posterior pituitary releases oxytocin

> > uterus contracts more vigorously

30
Q

Give one example of negative feedback hormonal response? think glucose

A

Negative feedback of glucose production by glucagon:

After restoring glucose level, glucagon secretion decreases

31
Q

What are the 3 sub-categories of complex multilevel negative feedback systems? use hypothalamo-pituitary system as example

A
  1. Long loop (e.g. target organ to hypothalamus, target organ to anterior pituitary)
  2. Short loop (e.g. anterior pituitary to hypothalamus)
  3. Ultra-short loop (e.g. hypothalamus to itself)
32
Q

Why is there the need for long loop, short loop negative feedback?

A

greater degree of fine-tuning of hormone secretion

Minimizes changes in hormone secretion when one component of the system is dysfunctional

33
Q

Describe the feed-back inhibition of thyroid hormone release?

A

TRH from hypothalamus stimulate Ant. Pituitary to release TSH

TSH stimulate thyroid gland to release thyroid hormones

Increased thyroid hormone conc. = feedback inhibition on TRH and TSH release

34
Q

Set-points in closed negative feedback hormonal control cannot be changed? T or F?

A

False

Set-point can be changed

e.g. Epinephrine can override the pre-determined set-point of blood glucose level

35
Q

What is the function of feed forward hormone response?

A

Anticipatory response in the later stage of the pathway

to prevent large change in variabled

36
Q

Give one example of feed forward control of hormones?

A

E.g. cephalic phase: sight, smell, taste of food

> > anticipate high blood glucose after meal

> > parasympathetic vagus nerve from brain to beta cells of pancreas

> > ACh acts on M3 receptor, signalling insulin release before even eating

37
Q

3 types of control of hormone activity at the hormone/ receptor level?

A

1) Conversion of prohormone to active form
2) Regulation of hormone receptors: up-regulate/priming or down-regulate/ desensitization
3) Hormonal clearance by degradation

38
Q

Describe the role of the renin-angiotensin system in regulating fluid levels?

A
  1. Liver releases angiotensinogen (= precursor) into blood
  2. Macula densa of kidney sense low [Na]&raquo_space; juxtaglomerular cells secrete renin
  3. Renin convert angiotensinogen to angiotensin I
  4. ACE in pulmonary blood convert angiotensin I to angiotensin II
  5. Angiotensin II cause vasocontriction + release aldosterone from adrenal cortex to uptake Na in DCT
39
Q

Describe the role of Deiodinase subtypes on T4 hormone function?

A

Different subtypes of Deiodinase are present at diff. tissue

Control of which subtype of deiodinase is released = control whether to activate or deactivate T4

40
Q

Hormone-receptor interactions are limited by the number of receptors. T or F?

A

True

Biological effect is proportional to the amount of complex that forms

41
Q

Give one example of hormone priming effect?

A

High frequency GnRH pulse can increase the sensitivity of its target cell (anterior pituitary cells) to further stimulation

42
Q

Describe the mechanism of growth hormone receptor down-regulation?

A

After prolonged exposure to GH:
internalize/endocytose its own receptor-hormone complex for degradation

Decrease cell surface receptors = decrease sensitivity of cell

43
Q

3 routes for hormone breakdown and elimination?

A
  1. Liver enzyme degradation, bile excretion
  2. Kidney enzyme degradation, urine excretion
  3. Breakdown inside target cell, endolysosomal degradation
44
Q

List the degradation reactions for protein and steroid hormones?

A

Peptide hormones: proteolysis

Steroid hormones:reduction, hydroxylation, oxidation, decarboxylation,or esterification

45
Q

Formula for metabolic clearance rate for any substance?

A

𝒓𝒂𝒕𝒆 𝒐𝒇 𝒅𝒊𝒔𝒂𝒑𝒑𝒆𝒂𝒓𝒂𝒏𝒄𝒆 𝒐𝒇 𝒂 𝒉𝒐𝒓𝒎𝒐𝒏𝒆 𝒇𝒓𝒐𝒎 𝒕𝒉𝒆 𝒑𝒍𝒂𝒔𝒎𝒂
÷ 𝒄𝒐𝒏𝒄𝒆𝒏𝒕𝒓𝒂𝒕𝒊𝒐𝒏 𝒐𝒇 𝒉𝒐𝒓𝒎𝒐𝒏𝒆 𝒊𝒏 𝒆𝒂𝒄𝒉 𝒎𝑳 𝒐𝒇 𝒑𝒍𝒂𝒔𝒎𝒂

(𝑢𝑟𝑖𝑛𝑒 𝑝𝑟𝑜𝑑𝑢𝑐𝑡𝑖𝑜𝑛 × 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑖𝑛 𝑢𝑟𝑖𝑛𝑒) ÷ 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑖𝑛 𝑝𝑙𝑎𝑠𝑚𝑎

46
Q

Define primary, secondary and tertiary endocrine disorders?

A

Primary = Secretory gland problem e.g. tumors, infection

Secondary and tertiary = Endocrine feedback error (mostly hypothalamic-pituitary axis)

47
Q

Principle of testing for endocrine disorders?

A

Stimulation / suppression testing

Excess hormone suspected = suppression test

Deficiency suspected = Stimulation test

48
Q

Describe the dexamethasone suppression test at low or high dose? think primary or secondary endocrine disorder

A

Measure cortisol level next morning
- Low dose = Present or absent cushing syndrome

  • High dose = -ve feedback on ACTH producing cells but not ectopic or adenoma making ACTH
    » distinguish Cushing disease from cushing syndrome
49
Q

Describe the captopril suppression test?

A
  • Captopril suppress ACE = suppress aldosterone level

Test for primary aldosteronism (hypersecretion of aldosterone)

50
Q

Describe the ACTH stimulation test and what it tests for?

A

Adrenal insufficiency = not increase cortisol after ACTH stim

ACTH stimulate cortisol production

51
Q

If Pituitary hormone level is high, but target hormone is low. What is defective?

A

Primary disorder (target organ fails to produce / secrete hormone)

52
Q

If Pituitary hormone level is low and Target hormone level is low. What is defective?

A

Secondary disorder (pituitary failure)

53
Q

If Pituitary hormone level is high and target hormone level is abnormally high. What is defective?

A

Autonomous secretion of pituitary hormone (e.g. pituitary tumor); or

Resistance to negative feedback from target hormone

54
Q

If pituitary hormone level is low but target hormone level is high. WHat is defective?

A

Autonomous secretion by target organ (e.g. tumor, primary hyperthyroidism)

MBBS II ERS (37 decks)

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