cell bio > nocat probs > Flashcards

nocat probs Flashcards

(39 cards)

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1
Q

histamine production

A

in vivo:
- less HDC means less histamine is produced

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2
Q

histamine packaging

A

in vivo:
- less VMAT or ATPase = less histamine granulated

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3
Q

histamine release

A

in vivo:
- botulinium and tetanus cleave SNARE proteins

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4
Q

histamine response

A

in-vivo:
- inverse agonist present = decrease in H1 expression
- diff H receptor that causes physiological antagonism

ex-vivo:
- different quantities of H1 receptors = altered response
- receptors in one tissue may have decreased affinity for histamine due to genetic differences

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5
Q

histamine termination

A

in vivo:
- less DAO = response keeps going
- less HNMT = response keeps going

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6
Q

H1 overstimulation causes

A
  • asthma, respiratory discomfort (contraction)
  • contraction of smooth muscles (involuntary)
  • vasodilation/flushing
  • typical allergy/inflammation
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7
Q

H2 overstimulation causes

A
  • ulcers, too much gastric acid
  • GERD
  • vasodilation/increased heart rate
  • smooth muscle relaxation
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8
Q

H3 overstimulation causes

A
  • reduced release of neurotransmitters
  • dizziness/motion sickness
  • narcolepsy
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9
Q

H4 receptor overstimulation causes

A
  • chemotaxis of eosinophils/mast cells
  • itchy skin (pruritis), more chronic
  • immune-cell driven inflammation
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10
Q

what’s histamine intolerance caused by?

A
  • intolerance of histamine ingested as food
  • DAO deficiency OR DAO inhibited by another drugw
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11
Q

what can inhibit DAO?

A
  • wine
  • green tea
  • cimetidine
  • NSAIDS
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12
Q

alpha 1 receptor overstimulation causes

A
  • constriction
  • vasoconstriction = high blood pressure
  • difficulty urinating/constipation
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13
Q

alpha 2 receptor overstimulation causes

A
  • constriction
  • decreased NE release (feedback inhibition)
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14
Q

beta 1 receptor overstimulation causes

A
  • cardiac muscle constriction
  • increased heart rate
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15
Q

beta 2 receptor overstimulation causes

A
  • relaxation
  • drop in blood pressure
  • warm/flushed skin
  • broncho/vaso dilation
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16
Q

beta 3 receptor overstimulation causes

17
Q

what inhibits neuronal reuptake?

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A
  • cocaine
  • antidepressants
  • amphetamines
18
Q

what inhibits non-neuronal reuptake?

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A

steroids (mainly glucocorticoids)
- endogenous: cortisol increased by cushing’s
- exogenous: prednisone, dexamethasone, hydrocortisone

19
Q

catecholamine production/packaging

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A

in vivo
- less phenylalanine in blood
- less prod’n enzymes (decarboxylases/hydroxylases/methyltransferases)
- VMAT doesn’t work

20
Q

catecholamine release

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A

in vivo
- SNARE proteins inhibited (genetically or by botulinium/tetanus)

21
Q

catecholamine termination

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A

in vivo:
- receptor desensitization/downregulation = reduced response
- inhibition of MAO by tyramine in cheese or antidepressants = increased dopamine/NE
- inhibition of reuptake (NET) by cocaine = increased response

22
Q

acetylcholine production

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A

in vivo/ex vivo:
- less CHaT = less prod’n
- less choline/acetyl CoA = less prod’n
- uptake of choline by Na dependent carrier reduced = less prod’n

23
Q

acetylcholine packaging

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A

in vivo/ex vivo
- VAT altered in conformation/problems with transcription = ACh doesn’t go into vesicles

24
Q

acetylcholine release

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A

in vivo
- botulinium/tetanus inhibits SNARE proteins

ex vivo
- low extracellular calcium = depolarization can’t trigger translocation of vesicle

25
acetylcholine response
in vivo: - tubocuranine antagonizes NMJ receptors - hexamethonium antagonizes neuronal type receptors in vivo/ex vivo - receptor desensitization
26
acetylcholine termination
in vivo - organophosphate insecticides inhibit acetylcholinesterase = increased ACh ex vivo - decreased acetylcholinesterase (AChE) = increased ACh - reuptake of ACh inhibited = too much ACh/response
27
steroid production
in vivo: - not enough of the specific CYP enzyme tht creates the steroid = less of that steroid
28
steroid release
in vivo - not enough globulins = steroids can't get to receptors - too much binding proteins = not enough free steroids = reduced response
29
steroid response
in vivo - inhibition of heat shock proteins = steroid can't enter nucleus and cause transcriptional changes = reduced response - glucocorticoid receptors: have many isoforms due to folding/alternative splicing/post-translational modification. as such, same corticosteroid can have different impacts on receptor variants. the exact same corticosteroid can increase transcription of one gene but decrease it for another - SHBGs can allosterically modulate receptors - mutations can impair corticosteroid receptors - chronic stress can cause resistance in cortisol receptors
30
steroid termination
in vivo/ex vivo - not enough CYP = steroid not broken down and activity doesn't get reduced
31
how do CYP enzymes interact w/ medicines?
- can activate drugs like codeine into morphine - can terminate some drugs - if we eat food that inhibits CYP (like grapefruit), it can't breakdown drugs = overdose
32
NO production
in vivo/ex vivo - not enough extracellular ACh = nitric oxide synthase not activated - L-NMMA is a competitive inhibitor of NOS = less NO byproduct made - molecule X binds causes competitive antagonism on NOS = reduced prod'n of NO - NOS also inhibited by L-NAME and 7-nitroindazole
33
NO response
in vivo - methylene blue inhibits guanylyl cyclase from converting GTP to cGMP = less response
34
NO termination
in vivo/ex vivo - less PDEs = cGMP not terminated enough and muscles keep relaxing
35
prostaglandin production
in vivo/ex vivo - COX2 mutation = reduced PGG2 prod'n even when stimulated - phospholipase A2 inhibited = decreased arachidonic acid - NSAIDs inhibit COX1/COX2 = less PGG2 - glucocorticoids/steroids inhibit phospholipase A2
36
prostaglandin response
in vivo/ex vivo - receptor desensitization from tm PGs = downregulation, less PGs - mutations in GPCRs = increase/decrease of sensitivity - aspirin: inhibits COXs but allows for lipoxin (anti-inflammatory) prod'n = less response in everything except anti-inflammation - prostaglandin analogues (like bimaprost) can induce favourable effects, can target many receptors/pathways
37
prostaglandin termination
- not a good source of error - not enough termination enzymes = inflammation/buildup of PGs - too many termination enzymes = ulcers
38
what if there aren't enough PGs?
- stomach ulcers can happen - PGs maintin gastric lining (NSAIDs can cause ulcers)
39
wht happens if partial and full agonists present?
- partial acts as antagonist - blocking receptors, not giving full response
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