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P1 Spring Exams > BC Test 2 > Flashcards

BC Test 2 Flashcards

1
Q

Testosterone ->estradiol

A

Aroma taste

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2
Q

DHT development

A

External genitalia

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3
Q

Estradiol development

A

Bone, libido

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4
Q

Testosterone development

A

Wolffish, internal gonads, skeletal muscle

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5
Q

Deficiency of androgen commonly due to (2)

A
  1. Deficiency of Cyp17 hydroxylase
    - would result in entirely female external genitalia, lack of internal & external organ development
  2. Deficiency of 5alpha reductase
    - failure of external genitalia but internal development unaffected, can’t complete puberty
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6
Q

ER-alpha

  1. Affects
  2. Inhibit or activate?
A
  1. Endometrium, ovary, mammary gland, hypothalamus, endothelial cells, vascular smooth muscle
  2. Activate
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7
Q

ER-beta

  1. Affect
  2. Inhibit or activate?
A
  1. Kinsey, intestinal mucosa, lung, bone, brain, prosit state, vasculature
  2. inhibit
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8
Q

Estradiol and receptor binding

A

Equally binds alpha or beta, nonspecific

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9
Q

Estrone and ER binding

A

Alpha favored, present continually

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10
Q

Estriol and ER binding

A

Beta favored, but both very low affinity

-present during pregnancy

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11
Q

Estradiol binding to ligand binding domain steps

A
  1. A large hydrophobic pocket is formed by alpha helix scaffold
  2. Estradiol is sealed within LBD by helix 12
  3. Allows activators to bind in AF2 site

When antagonist present:
Helix 12 is stuck in the spot where coactivators need to bind, therefore no activation

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12
Q

Estrogen synthesis in premenopause

A

Gonadotropins increase cholesterol side-chain cleavage and Aromatase
Ovaries produce estrogen and progesterone

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13
Q

Estrogen synthesis in Postmenopause

A

Synthesized in adipose

Adrenal gland secretes DHEA, an androgen precursor

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14
Q

Estrogen synthesis in males

A

Produced by testes

Circulating estrogens formed from androstenedione and DHEA

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15
Q

5 key points of signal transducing systems

A
  1. Specificity
  2. Amplification
  3. Modularity
  4. Desensitization/adaptation
  5. Integration
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16
Q

Alpha 1 receptors

A

Bind agonists, affect smooth muscle contraction and vasoconstriction of skin

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17
Q

Alpha 2 receptors

A

Bind agonists, inhibit release of NE and contraction of anal sphincter

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18
Q

Beta 1 receptors

A

activation results in increased HR and force of contraction

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19
Q

Beta 2 receptors

A

Activation results in vasodilation and bronchodilation, smooth muscle relaxation

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20
Q

Isoproterenol

A

Mimic Epi, agonist

Treatment for bradycardia or branch block

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21
Q

Propranolol

A

Non-selective B blocker

Antagonist

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22
Q

GPCR Pathway

A
  1. Epi binds receptor
  2. GDP bound GSa replaced by GTp, activating GSa
  3. GSa separates from Gby, moves to adenylyl cyclase and activates it
  4. Adenylyl cyclas catalyzes ATP ->cAMP
  5. cAMP activates PKA
  6. PKA phosphorylates inducing cellular response
  7. cAMP degraded by phosphodiesterase (cAMP -> 5AMP)
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23
Q

Gsa has

A

intrinsic ATPase activity, meaning it can hydrolyze the GTP to GDP, making inactive

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24
Q

Termination of B-adrenergic receptor response

A
  1. [Epi] drops, hormone dissociates from receptor, Gsa inactive
  2. Gsa hydrolyzes GTP, reconnects with Gby
  3. Phosphodiesterase hydrolyzes cAMP
  4. Phosphorprotein phosphatase degrades PKA
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25
Q

Desensitization of B-adrenergic receptor

A

Termination even when conc is high

  1. Gby recruits BARK
  2. BARK phosphorylates receptor, no Barr can bind
  3. Barr causes endocytosis of receptor
26
Q

in low-energy state, PKA activates

A

CREB

27
Q

PGE1

A

Binds to adipose cells to slow mobilization of FA and counteract Epi

28
Q

IP3 pathway

A
  1. Hormone binds GPCR
  2. GTP binds Gq
  3. GTP-Gq binds and activates PLC
  4. PLC cleaves PIP2 to IP3+DAG
  5. IP3 diffuses to ER and binds IP3-gated Ca++ channels, Ca rushes in to cytosol
  6. DAG interacts with Ca to activate PKC
29
Q

Insulin receptor tyrosine kinase

A
  1. Insulin binds 2 extra cellular alpha subunits (homodimer)
  2. Homodimer interacts with 2 beta subunits -> active insulin protein receptor
  3. Autophosphorylation of receptor
  4. INSR phosphorylates IRS-1
  5. IRS-1 goes to Grab 2
  6. Grab 2 binds SOS
  7. SOS binds Ras, causing exchange of GDP for GTP
  8. RAS-GTP activates RAF1
  9. RAF1 phosphorylates MEK
  10. MEK phosphorylates ERK
  11. ERK moves into nucleus
30
Q

IRS-1 interaction with PI3K

A
  1. IRS-1 activates PI3K
  2. PI3k converts PIP2 to PIP3
  3. PIP3 phosphorylates PKB
  4. PKB phosphorylates glycogen synthase 3 kinase GS3K causing INACTIVATION, therefore activating GS
  5. PKB also stimulates Glut4 movement to membrane to increase glucose uptake
31
Q

JAK-STAT pathway

A
  1. Epo binds Epo receptor
  2. JAK is recruited and phosphorylates receptor
  3. STAT5 attracted to receptor and comes in close proximity to JAK, and becomes phosphorylated
  4. 2 phosphorylated STAT5s form a dimer
  5. Dimer can enter nucleus as transcription factor to regulate expression of genes for RBC synthesis
32
Q

conversion of GTP->cGMP

A

Guanylyl cyclase

33
Q

cGMP activates

A

PKG

34
Q

Membrane bound guanylyl cyclase

A

Homodimer

Responds to atrial naturetic factor

35
Q

Soluble guanylyl cyclase

A

Heme containing enzyme
Response to intracellular NO concentration
Present in smooth muscle of heart and blood vessels and leads to smooth muscle contraction

36
Q

Pathway when atrial naturetic factor released

A
  1. When blood volume too high, atrium released ANF
  2. ANF binds to ANF receptors in collecting ducts of kidneys and vascular smooth muscle
  3. [cGMP] increases in collecting ducts
  4. Triggers release of Na and renal excretion of H20 -> blood volume decreases
37
Q

Nitric oxide production

A

Arginine -> citrulline by nitric oxide synthase

-needs Ca++, NADPH and O2

38
Q

Viagara

A

Inhibits phosphodiesterase, therefor keeps cGMP high

39
Q

Acetylcholine presence?

A
  • All preganglionic autonomic
  • Most postganglionic parasympathetic
  • Some postganglionic sympathetic
40
Q

ACh synthesis, storage, breakdown

A
  1. Choline taken up in diet
  2. transported to nerve terminal via choline transporter
  3. Choline + acetyl Coa acted on by choline acetyltransferase
  4. ACh stored in vesicles by VATs
  5. VAT fuses SNAP with SNARE and releases ACh to cleft
  6. Acetylcholinesterase degrades in synaptic cleft
41
Q

Butylcholinesterase

A

Degrades ACh and opiates

Not as fast as acetylcholinesterase (pseudocholinesterase)

42
Q

Botulinum toxin

A

Blocks ACh release by preventing SNARE from binding

43
Q

Catecholamine synthesis pathway

A
  1. Phe to L-tyrosine by Phe hydroxylase, tetrahydrobiopterin
  2. L-tyrosine to L-DOPA by L-tyrosine tyrosine hydroxylase, tetrahydrobiopterin
  3. L-DOPA to Dopamine by DOPA decarboxylase
  4. Dopamine to NE by dopamine B-hydroxylase
  5. NE to Epi by PNMT, SAM in chromaffin granules of adrenal gland
44
Q

Glucocorticoid affect on Catecholamine synthesis

A

Upregulate PNMT, therefor favor Epi production

Also induce TH and DBH

45
Q

Catecholamine transporters (3)

A
  1. NET - takes NE from cleft to nerve terminal
  2. VMAT2 - takes from cytoplasm to storage vesicle
  3. ENT - uptake into extra neuronal cells
46
Q

Dopamine degradation

A
  1. Dopamine to DOPAL by MAO
  2. DOPAL to DOPAC by aldehyde DH
  3. Into blood
  4. DOPAC to HVA by COMT
47
Q

NE degradation

A
  1. NE to DOPEGAL by MAO
  2. DOPEGAL to DHPG by aldehyde reductase
  3. Into blood
  4. DHPG to VMA by COMT
48
Q

Epi degradation

A
  1. (In blood) Epi to metanephrine by COMT
  2. Metanephrine to MHPG by MAO
  3. MHPG to VMA by aldehyde DH
49
Q

Monocarboxylic acids

A

Commonly cause inhibition

Include GABA, glycine, taurine and B-alanine

50
Q

Dicarboxylic acids

A

Commonly cause activation

Glutamine and Aspartate

51
Q

GABA shunt pathway

A
  1. aKG transaminase from Krebs to L-glutamate by aKG, PLP
  2. L-Glu to GABA by GAD
  3. GAD to succinic semialdehyde by aKG transaminase, PLP
  4. Succinic semialdehyde to succinic acid by succinic semialdehyde DH
52
Q

Serotonin synthesis and degradation

A
  1. Typ to 5-hydroxytrptophan by tryptophan hydroxylase, tetrahydropterine
  2. 5-hydroxytrptophan to 5-hydroxytrptamine by AADC, vitB6
  3. 5-HT to 50HIAA by MAO
53
Q

Ionotropic receptors have ______ effect and metabotropic have ______ effect

A

Ionic - immediate

Metabotropic - long-acting

54
Q

Nucleobases attach pentose at ________ with ______ bond

Purines attach at
Pyrimidines attach at

A

Anomeric C
B-N-glycosidic

Purines attach at N9
Pyrimidines attach at N1

55
Q

Purines include

A

Adenine (amino group in top left)

Guanine (carbonyl top left, amino bottom left)

56
Q

Pyrimidines include

A

Cytosine (carbonyl bottom left, amino at top)
Uracil (2 carbonyls)
Thymine (2 carbonyls and a methyl)

57
Q

Mycophenolate mofetil

A

Inhibits inosine monophosphate dehydrogenase, therefor stopping B-cells from making inosine

58
Q

DNA - 1 turn is how many residues and Angstroms

A

10 residues

36 Angstroms

59
Q

Hogsteen base pairing

A

H bonds b/t 3 or 4 nucleotides

Common near prontooncogenes

60
Q

IMP construction (half - only what we need to know for this test)

A
  1. PRPP to 5-phospho-B-D-robosylamine by glutamine-PRPP amino transferase and Gln
  2. 5-PBDRA to GAR by GAR synthetase and gly, ATP
  3. GAR to FGAM, FGAM to AIR by AIR synthetase and ATP (cyclyzes)
  4. AIR to CAIR by AIR carboxylate (direct methylation w/out biotin)
61
Q

Testosterone -> DHT

A

5alpha reductase

P1 Spring Exams (1 decks)

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