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Endo-Repro Midterm > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

How do hydrophilic hormones trigger a cellular response?

A
  • cannot penetrate cell membrane - interact w/ receptor on cell surface
  • activate a second messenger inside the cell to trigger a response
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2
Q

What 2 types of receptors do hydrophilic hormones interact with? Example for each?

A
  • GPCR (Epi)

- RTK (insulin)

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3
Q

What is the half life of hydrophilic hormones?

A

very short (seconds to minutes)

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4
Q

How do hydrophobic hormones trigger a cellular response?

A
  • passively diffuse through plasma membrane
  • bind to a receptor; hormone receptor complex = transcription factor that can bind to HRE (hormone response element) on DNA
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5
Q

What 2 types of receptors do hydrophobic hormones interact with?

A
  • cytoplasmic: bind to hormone in cytoplasm and translocate to nucleus
  • nuclear receptors: already present in nucleus and bound to DNA
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6
Q

What is the half life of hydrophobic hormones?

A

long half lives (hours to days)

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7
Q

What does an inactive GPCR look like?

A

trimeric protein with alpha, beta, and gamma subunits bound together; GDP bound to alpha

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8
Q

What must be done to activate a GPCR? What mediates this?

A
  • GDP -> GTP on alpha subunit; mediated by guanine nucleotide exchange (GEF)
  • alpha subunit breaks off
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9
Q

What must be done to inactivate a GPCR? What mediates this?

A
  • GTP -> GDP via GTPase-activating protein (GAP)

- alpha subunit binds back to beta and gamma

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10
Q

What is the mechanism of each of the following GPCRs: Gs, Gi, Gq, Gt?

A
  • Gs: stimulates adenylate cyclase; increased cAMP
  • Gi: inhibits adenylate cyclase; cAMP not made
  • Gq: stimulates cGMP phosphodiesterase; decreases cGMP
  • Gt: activates phospholipase C; increase in intracellular Ca
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11
Q

Give an example of a hormone that binds to each of the GPCRs (Gs, Gi, Gq, and Gt) and each of their receptors

A
  • Gs: Epi (beta adrenergic); Histamine (H2)
  • Gi: Epi/NE (alpha adrenergic); Dopamine (D2)
  • Gq: ACh (M3)
  • Gt: light (rhodopsin)
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12
Q

Describe the general structure of insulin. Storage form vs active form?

A
  • A and B chains linked by disulfide bridges
  • Storage form: hexamer (w/ zinc in the center)
  • Active form: monomer
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13
Q

Describe the steps of insulin synthesis (3)

A

Preproinsulin mRNA translated to preproinsulin (ribosome) -> forms proinsulin in ER lumen) -> folded and transported to Golgi -> forms insulin

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14
Q

Describe the 2 phases of insulin secretion

A
  • 1st phase: rapid and granules come from readily releasable pool (RRP)
  • 2nd phase: sustained; comes from larger reserve pool
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15
Q

What type of receptor does insulin bind to? What does this cause?

A

binds to RTK (alpha extracellular subunit); causes phosphorylation of tyrosine on beta intracellular subunit

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16
Q

Insulin signaling: what binds to phosphotyrosine in the RAS dependent pathway?

A

insulin receptor substrate 1 (IRS-1) -> becomes phosphorylated

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17
Q

Insulin signaling: what binds to phosphorylated IRS-1 in the RAS dependent pathway? What does this initiate?

A

binds to GRB-2 protein -> activates RAS and MAP kinase

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18
Q

What is the ultimate function of the RAS dependent insulin signaling pathway?

A

increases transcription of glucokinase -> phosphorylates glucose in first step of glycolysis

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19
Q

Insulin signaling: what binds to phosphorylated IRS-1 in the RAS independent pathway? What does this cause?

A

binds to phosphoinositide-3-kinase (PI3 kinase) -> acts as second messenger for protein kinase B (PKB)

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20
Q

What is the ultimate function of the RAS independent insulin signaling pathway?

A

PKB plays a role in movement of GLUT4 into cell membrane and activation of glycogen synthase

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21
Q

Explain the process by which glucose triggers release of insulin into the blood stream

A
  • glucose enters pancreatic B cells through GLUT2 (facilitated diffusion)
  • enters glycolysis -> ATP produced
  • ATP acts on K channel in cell membrane -> depolarization
  • depolarization causes opening of Ca channels -> release of insulin granules
22
Q

What is the MOA of sulfonylurea drugs?

A

treats NIDDM -> targets K channels in pancreatic B cells and causes depolarization w/o presence of glucose

23
Q

What are the 3 domains of nuclear receptors?

A
  • ligand binding domain (LBD)
  • activation function 1 domain (AF1) - aka transcription activating domain
  • DNA binding domain (DBD)
24
Q

Which domain on NRs remains the same throughout all NRs?

A

DNA binding domain -> binds to HRE

25
Q

What are 2 types of estrogen receptors (ERs)?

A
  • ERa: mostly in female reproductive tract

- ERb: mostly in ovaries and prostate

26
Q

What is the MOA of ERs?

A

promotes histone acetyl transferase (HAT) to loosen chromatin structure and enhance transcription

27
Q

What is the MOA of Tamoxifen? What is it used to treat?

A
  • antagonist of ERs
  • recruits proteins like histone deacetylase (HDAC) which is the opposite of HAT -> stabilizes nucleosome structure and prevents transcription
  • used to treat breast cancer
28
Q

What controls the short term and long term stress response by the adrenal glands?

A
  • short term: nerve impulses -> release of catecholamines

- long term: steroid hormone signaling -> release of mineralocorticoids and glucocorticoids

29
Q

What enzyme catalyzes conversion of cholesterol to pregnenolone?

A

desmolase - rate limiting step of steroid hormone synthesis

30
Q

What is the precursor to corticosteroids and androgens?

A

progesterone

31
Q

What positively regulates desmolase?

A

ACTH

32
Q

How is cancer related to ACTH?

A

tumor cells can activate ACTH receptor w/o the presence of ACTh and turn on massive cortisol production and cell proliferation

33
Q

What helps convert prenenolone to progesterone?

A

hydroxysteroid dehydrogenase (HSD)

34
Q

What is the general function of glucocorticoids?

A

mediates stress response by increasing protein catabolism, gluconeogenesis, and reducing inflammation; increases BP and Na uptake by kidneys

35
Q

What is an example of a glucocorticoid and what receptor does it bind to?

A

Cortisol: binds to glucocorticoid receptor (GR)

36
Q

Explain the importance of glucocorticoids in infants

A
  • there is a burst of glucocorticoids during delivery that stimulates production of surfactant (allows lung expansion)
  • premature infants may not have burst -> leads to infant respiratory distress syndrome
37
Q

What is the general function of mineralocorticoids?

A

increase Na/H2O retention, K excretion, and BP

38
Q

What is an example of a mineralocorticoid and what receptor does it bind to?

A

Aldosterone: binds to mineralcorticoid receptor (MR)

39
Q

What is an example of an androgen and what receptor does it bind to?

A

testosterone: binds to androgen receptor (AR)

40
Q

How do women generally present w/ congenital adrenal hyperplasia (CAH)?

A
  • hirsutism: excessive body hair in men and women on body parts usually absent of hair
  • also present w/ general oligomenorrhea and infertility
41
Q

Which enzyme is defective in 95% of cases of CAH?

A

21-hydroxylase (pathways to aldosterone and cortisol

42
Q

Which enzyme is defective in 5% of cases of CAH?

A

11B-hydroxylase (pathways to aldosterone and cortisol)

43
Q

What happens to ACTH and androgen levels when production of glucocorticoids and mineralocorticoid can’t occur?

A
  • Excessive androgen production (only route it can take)

- increased ACTH (can’t stimulate cortisone/aldosterone production)

44
Q

CAH: Why does 17-a-hydroxyprogesterone accumulate?

A

fork in the road between androgens and cortisol (can’t make cortisol)

45
Q

CAH: How does accumulation of 11-deoxycorticosterone lead to HTN?

A

it is an MR agonist -> leads to disregulated salt and water balance (promotes Na and water retention and lower plasma K)

46
Q

CAH: how does 21-a-hydroxylase deficiency lead to salt wasting?

A
  • lack of aldosterone being produced -> high rate of Na loss in urine
47
Q

What are 2 steroid hormone blood transport proteins and where are the made?

A

corticosteroid-binding globulin (CBG) and sex steroid binding globulin (SHBG) - both made in the liver

48
Q

What is 17,20-lyase? What does deficiency (ILD) lead to?

A
  • gateway enzyme from progesterone to all sex steroids

- impaired production of androgen and estrogen sex steroids

49
Q

How will ILD present in males and in both sexes?

A
  • Males: psuedohermaphroditism

- Both sexes: reduced/absent puberty, child like appearance in adulthood

50
Q

Does ILD result in adrenal hyperplasia or HTN?

A

No - doesn’t affect glucocorticoids or mineralcorticoids

51
Q

What is the function of aromatase in females?

A

FSH stimulates aromatase to produce estrone; also converts testosterone -> estradiol (requires FSH and aromatase)

Endo-Repro Midterm (3 decks)

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