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PMCOL 303 > Final exam select topics-plant and animal tox > Flashcards

Final exam select topics-plant and animal tox Flashcards

1
Q

what are the 2 delayed onset muschroom toxins

A

amatoxins and orellanine

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2
Q

what are the 3 rapid onset muschroom toxins

A

ibotenic acid, muscimol, muscarine

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3
Q

what is the structure of amatoxins

A

octapeptides

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4
Q

are amatoxins head stable

A

yes

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5
Q

what is the mechanism of amatoxins (general)

A

inhibits protein synthesis

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6
Q

what are the 4 stages of amatoxins

A
  • latent no symptoms (24h)
  • GI
  • apparently recooperation
  • hepative failure, encephalopathy, renal failure
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7
Q

what is a way to help prevent further absorption of amatoxins

A

charcoal

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8
Q

what is the role of charcoal

A

prevent further amatoxins absorption

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9
Q

what does silibinin do

A

prevents toxin uptake by hepatocyte

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10
Q

what compound prevents toxin uptake in liver for amatoxins

A

silibinin

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11
Q

how do amatoxins accumulate in hepatocytes

A

non specific transporters

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12
Q

how does amatoxins cause centrilobar necrosis

A

disrupting P450 synthesis (so toxins can damage hepatocytes)

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13
Q

how is amatoxins dealt with in kidneys

A

filtered by glomerulus and reabsorbed in the tubules - causes acute tubular necrosis

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14
Q

which 3 locations are most hit by amatoxins and why

A

GIT liver and tubules because they need to constantly synthesize new proteins

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15
Q

what specifically does amatoxins target to cause mechanism

A

RNA pol 2 (very potent and specific)

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16
Q

how does amatoxins stop RNA pol 2

A

binds to bridge helix so it prevents polymerase from moving along DNA strand (it goes muchhhhhhhhhhh slower)

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17
Q

how do amatoxins reduce affinity for nucleotide triphosphates

A

it doesnt

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18
Q

what are the 2 phases for orellanine

A 
pre renal (thirst, more urination and headache)
renal (anuria)
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19
Q

where in the body is orellanine toxic to (what does it cause)

A

tubular epithelium - interstitial nephritis, edema, blood cell infiltration

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20
Q

what does orellanine cause the production of

A

orthosemiquinine anion radical and ROS + GSH deplretion

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21
Q

what is the mechanism of coprinus spp

A

inhibits aldehyde dehydrogenase irreversibally

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22
Q

is coprinus spp heat stable

A

yes

23
Q

what happens with alcohol and coprinus spp consumption

A

acetaldehyde build up so feel sick

24
Q

what is the mechanism of amanita muscaria

A

mAChR agonist

25
Q

is amanita muscaria heat stable

A

yes

26
Q

what is antivenin

A

antibody to spider bite

27
Q

what is the main venim in spiders that can hurt us

A

alpha-latrotoxin

28
Q

what does alpha-latrotoxin cause

A

massive NT release (DA, NA, GABA, glu) and maybe reuptake block

29
Q

what is the mechanism of alpha-latrotoxin

A

binds to synaptic terminal proteins (neurexins and latrophilins) to cause NT release

30
Q

what is the role of latrophillins

A

when it binds to alpha-latrotoxin, evoked Ca+ independent NT release

31
Q

how does alpha-latrotoxin cause Ca+ independent NT release

A

when it binds to latrophillins

32
Q

how does alpha-latrotoxin cause Ca+ dependent NT release

A

it can spontaneously insert itself into artificial lipid bilayers to form a cation selective channel (Ca++)

33
Q

what kind of “mer” does alpha-latrotoxin form

A

tetramer

34
Q

what does initial snail sting cause

A

mild local pain progresses into muscle paralysis

35
Q

what happens later with snail sting

A

eyelid droop, blurred vision, speech difficulty, dyspnea, resp arrest, uncounscious

36
Q

what are the 2 main types of venom in conotoxins

A

non-disulfide and disulfide rich peptides

37
Q

what is the diff with non-disulfide and disulfide rich peptides for conotoxins

A

more SH makes them more rigid

38
Q

what are 2 main types of targets with conotoxins

A

NT receptors, ion channels

39
Q

what are the three types of cabals

A

lightning strike cabal, motor cabal and nirvana cabal

40
Q

what is the mechanism of lightning strike cabal

A

inhibiting VG(Na)C from closing and blocking K+ channels - MASSIVE DEPOL

41
Q

what is the results from inhibiting VG(Na)C from closing and blocking K+ channels (lightning strike cabal)

A

massive depol, repetitive firing, receptor desensitization

42
Q

how many types of toxins are at least needed in the lightning strike cabal

A

2 because 1 that inhibits VGSC inactivation and one that blocks VGKC

43
Q

what does motor cabal lead to

A

peptides distributed to circulatory system to inhibit NT transmission

44
Q

does the motor or lightning strike cabal work faster

A

lighting oviB

45
Q

what is the mechanism of motor cabal

A

block nAChR and presynaptive NT release via VGCC inhibition (block NT release and receptors)

46
Q

what is the nirvana cabal

A

makes victims relaxed and sedated

47
Q

what is the mechanism of nirvana cabal

A

NDMA glu R inhibition and Ca++ analgesia

48
Q

what are 4 kinds of peptides that is in snake venom

A

neurotoxins, coagulants, hemorrhagins and hemolytics

49
Q

what is crotamine

A

polypeptide myotoxin from rattlesnakes which induces hind limb paralysis

50
Q

what is the mechanism of crotamine

A

blocks K+

51
Q

how does crotamine enter the cell

A

via clathirin endocytosis

52
Q

where does crotamine go when it enters the cell

A

ends up in lysosomes, nucleus in rapidly dividing cells

53
Q

how does crotamine cause necrosis

A

burst lysosome with hydrolytic enzymes (there is also caspase 3 release)

PMCOL 303 (25 decks)

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