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tox Flashcards

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1
Q

Uncoupled phophorylation—> blocks or decreases ATP.

increased o2 demand in an effort to produce ATP

oxygen demand is more than o2 supply

resulting in overheating, metabolic acidosis and dehydration–>animal is cooked in its own heat./juices

irritation of the eye, GIT and intact skin

decresased cellular energy may cause neurotoxic and other effects

high exposure–>–>CNS stim/seizures

A

pentachlorophenol

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2
Q

unknown but predominantly is a GIT mucosa irritant

damage skeletal mm

hydrolysis=how its metabolised

A

phenoxyderivative of fatty acids aka: 2,4-D herbicides

aka : phenoxy acetic acid derivative

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3
Q

MOA:

_____ inhibits the TCA/citric acid cycle therefore resulting in lack of energy and decreased cellular respiration and tissue damage.

  • increase in blood ___ , anaerobic glycolysis, blood lactate will icnrease and systemic acidosis will occur, increse glc also d/t no tca (this is what uses glc and no use=accumulation of glc)
  • d/t inhibition of tca: increase in lactate, blood ___, BUN, K+, and P04-, PCV and transaminases

death=cardiac or respiratory failure

A

urea–>–>Ammonia (NH3)

toxicity d/t ammonia, not the urea itsef

answer=ammoniA

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4
Q

urea–> less than what age will be more sensitive d/t rumen condition?

and what age is tolerant?

A

1 year

3-6 weeks d/t underdeverloped rumen

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5
Q

T/F : preconditioned animals are adpated to npn: urea therefore will be more tolerant?

A

true

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6
Q

what increases toxicity of urea? (5)

A
  1. dehydration or low water intake
    2 . fasting: increases concentration of urea in blood
  2. feeds rich in urea
  3. hepatic insufficiency
  4. diet low in energy and protein but high in fiber: MOST IMP!!
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7
Q

T/F: urea is in the NH4 form and tehrefore not absorbed ?

A

True

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8
Q

urea: nonionized or ionized?
nh3=nonionized ionized?

how oes this affect absorption?

A

urea=ionized and nh3=noonionized–>nh3 absorbed and urea isnt itself therefore exaplins why nh3 is the toxic component of this disaes

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9
Q

what is the best lab specimen? for urea

A
  1. rumen fluid
  2. vitreous fluid of eye
  3. feed and urea content
  4. blood chemistry

note: specimes=FROZEN IMMEDIATELY

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10
Q

what kind of disease is urea?

acute or chronic?

A

acute!!

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11
Q

how do u tx urea toxicosis?

A
  1. RELIEVE BLOAT
  2. give icey water to reduce the rxn
  3. give vinegar and acetic acid 5% to make the env acidic
  4. rumenotomy: most effective bc u remove rumen contents incl: urea and ammonia
  5. sodium bicarb=use bc its quicker in its axn then the lactated ringers would be.
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12
Q

whats the most effective treatment for urea toxicosis in cattle?

A

RUMENOTOMY: removes the contents within the rumen

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13
Q

T/F: D+ is NOT hemorhagic with urea toxicosis?

A

TRUE

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14
Q

what is the most common cause of dairy cattle in usa?

A

monensin-ionophore toxicity

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15
Q

what is a anti-coccidial in cattle?

A

monensin: ionophore

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16
Q

what toxin causes a reduction in bloat and reduction of rumen acidosis in ruminants? ie: INHIBITS RUMEN MICROFLORA

A

monensin-ionophore

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17
Q

what spp are affected and in what manor with ionophore/monensin??
and what spp most sensitive?

A

horse=most sensitive=purpose or accident by adding it to their feed

cattle: over error calculation of monensin

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18
Q

t/f: horse and cattle that ingest recommended levels of monensin is going to be poisoned?

A

FALSE: if they eat recommended levels=not poisoned!

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19
Q

sensitivity of monensin spp?

A

horse»cow»poultry/turkey

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20
Q

what is the drug of choice when you have monensin that is ingested and amplification of drugs used to treat intracellular organisms? (mycoplasma)

A
  1. tetracycline for both large and small animal and poultry
  2. if 1 doesnt work then you use floroquinolones for small animals

2 . but large animals/poultry, you use: tiamulin

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21
Q

name the drugs that can be used to tx monensin/ionophore toxicity?

A
  1. tetracycline
  2. fluoroquinolone-small animal
  3. large animal-tiamulsin
    other
  4. chloramphenicol
  5. erhythromycin
  6. sulfonamides
  7. cardiac glycosides (DIGITALIS: you can use bc monensin and other ionophores are cardiotoxic, but be aware this can causea wrosening in the toxicity of monensin)
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22
Q

explain why monensin/ionophore toxicity is more toxic in horses?
3 reasons why

A

so, d/t the mannor in which monensin is metabolized by the P450 enzymes in the liver, you are going to get that they are rapidly metabolized by P-450 oxidative demethylation enzymes in the liver and equines lack this demethylation oxidative enzymes and so the most toxic spp is the horse. IN ADDITION, this monensin is excreted in bile and bc horse doesn’t have a gal bladder, you cant get the monensin out!! IN ADDITION, the horse absorb
100% of this monensin!!

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23
Q

MOA: disrupt transmembrane electrochemical gradients and the main target is mitochondria of highly energetic tissues: myocardium, skeletal mm and the kidney. itll hit all tissues but mainly high energetic tissues.

  • influx of a+ ionophore complex increaes intracellular Na and this is accompanied by increaseing intarcellular calcium–>but cells try to gt rid of calclium
  • so sequestering of calcium will lead to by mitochondria and ininhibition of mito and dddecrease ATP energy (mito is the main organelle when it comes to energy and so dmaage=no energy for the cells who need high energy)
  • increase cytoplasmic ca also change pH in cell causing damge
  • cell death d/t disruptig homeostatic mechanisms
  • also, catecholamine release results in oxidaton pdts and free radicals causing sarcolemmal membrane damage (ie: calcium will release catecholamines)
  • finally, disruption of ion concentrations in excitable cells will cause dysfxn
A

monensin

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24
Q

what CS do u see in

  1. horse
  2. cattle
  3. poultry
  4. dogs
A

horse: CARDIAC TOXICITY, tachyA, SUDDEN death (dramatic signs in horses);;ataxia, colic, depression, sweating, hyperventilation
cattle: more skeletall mm signs, shown more than horses

poultry: same
dog: same

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25
what type of disease is monensin?: chronic or acute?
acute
26
what are ddx for cattle of monensin tox?
vit E/selenium def or Coffee Senna =dx is going to have chocolate urine color
27
what are the ddx for horse for monensin tox?
colic or blister beetle ingestion
28
wha are the clin path findings for monensin? 1. elevated ezymes 2. pcv? 3. ion changes?
1. CK, AST, ALP, LDH 2. decrease blood Ca, K no change in Na 3. increase PCV
29
how to tx monensin tox? 3 and one speciifc to horses
1. mineral oil can decrease irriation and keep things moving quicker 2. FLUIDS d/t high PCV 3. vit E and selenium: give but make sure to give before and not after ie: dont reverse existing damage but can prevent further damge in the furture if this monensin toxicity were to occur 4. horse shouldnt be stressed/ridden for many months
30
what animals are more susceptible to Na ion toxicosis?what animal isnt?
cow, pig, chickens NOT DOGS
31
moa : - restricted water intake will increase the amount that is within the blood/csf-->and high na in the brain will cause cerebral edema and then it also inhibits glycolysis tehrefore lacking energy for the transport of na out of the brain - in addn: Na in the brain is going to attract water -->-->EDEMA
Na ion toxicosis
32
what are main CS seen with na tox?: most animals chickens: ?
seizures!! and edema in brain chickens: depression, ascites, collapse
33
what is a histopath pathopneumonic finding in pigs of na deprevation toxicicty?
eosinophilic menginoencephalitis
34
inorganic arsenic source?
- wood preservative - roach and ant bait - insecticide, herbicide, fungicide and rodenticides - milk from poisoned cows may be toxic to calves, humans
35
types of toxicity of the inorganic arsenic?
peracute acute subacute NO CHRONIC
36
whats the most toxic version of the inorganic arsenic?whats its axn?
trivalent: arsenite - it will bind to SH group on an enzyme and inhibit the axn of the enzyem therefore we need a chelator to break this bond
37
what spp is most susceptible to inorganic arsenic toxicity?
herbivores
38
inorganic arsenic is found highly concentrated in what tissues?
kidney and liver d/t the high blood flow to these areas.
39
T/F : inorganic arsenic does not cross BBB
true
40
how is inorganic arsenic excreted?
urine, rapidly within 24 hours
41
MOA: the trivalent ___: binds to 2 SH groups of lipoic (thioctic acid) and the trivalent will inhibit the lipoic (thioctic) acid inhibition of lipodic acid inhibtis/ slows down glycolysis==>lower energy , TCA, and oxidative enzymes (places like the GIT has tons of oxidative enzymes therefore we know this is a more senstive area that is affected by this toxin) and in kidney!!! (endothelial cap cell =leak=edema=hemorhage) pentavalent: - uncouples oxPhos (no fever) and may interfere with vit B1 and B6 metabolism outcome: local corrosive effect, it isnt only mechanical but its also d/t inhibition of the oxidative enzymes: lack energy and that damages the GI mucosa in addn: ause hypovolemia and electrolyte imbalance-->shock and -->death
inorganic arsenic
42
source of urea tox?
1. salt licks 2. drink water with salt 3. ice melts: dog 4. dog on beach drink water from sea 5. over crowding 6. frozen water 7. unpalatable water
43
signs of inorganic aresenic toxicity? peracute: CS and time? acute?: CS and time? :
peracute: sudden death d/t hypovolemic shock: sec-min acute: rapid onset, colic, salivation, vomit, thrist, WATERY D+ which may be hemorhagic=mintes -hrs subacute: D+ with blood/mucosal shreds, depression, anorexia, colic, etc. : hrs-days: less severe in the git, but also include paralysis of hind limbs typical GI signs, anorexia, V+, hemorhagic D+, hypovolemia and can get corrosive perforation
44
what is the MOST IMP ANTEMORTEM AND POSTMORTEM specimens to collect for inorganic arsenic?
AM: urine PM: kidney and liver see increase PCV, and increased BUN
45
how do u tx inorganic arsenic poisoning?
1. tx hypovolemia and shock: fluids and electrolytes 2. tx acidosis 3. activated charcoal
46
what is contraindicated in the tx of inorganic arsenic poisoning?
1. gastric lavage 2. emetics and 3 strong cathartics 4 peptobismal aka: has salicylic acid in it
47
what is chelation options for inorganic acid?: ie: what is the chelator of choice and which of the two chelators is going to be less harmful?
dimercaprol: BAL, british antilewisiste - chelator of choice - not 100% effective - may increase toxicity by mobilization of aresenic (bind to metal) dimercaptosuccinic acid: DMSA, succimer, chemet : less effective and less toxic bc less lipidsoluble -causes peripheral neural toxicity
48
moa of organic arsenic?
peripheral nn damage, axonal damage very simialr to animals with vitamin B deficiency
49
list the CS of organic arsenic tox of pigs and chickens?
...nts
50
what are common lesions of organic arsenic poisoning?
-peripheral nn and optic nn degeneration, gliodsis and demylination
51
what are the ddx for an animal with subacute selenium toxicosis (paralysis w/o blindness) in pigs? or vitamin B deficiency
ARSANILIC ACID
52
what is source of excess copper? aka : chronic Cu toxicicty
1. feed additives: =GRAS: generally recognized as safe 2. natural cu in soils and plants 3. mining 4. metals in soil and water and can get absorbed into plants and eating these plants lead to toxicosis 5. IMP: crap of chickens and pigs=eaten by sheep=toxicosis bc the chickens and pigs arent susceptible to tox by Cu
53
whats the normal Cu to molybdenum ratio?
6:1
54
how is Cu excreted?
URINE: its going to bind to molybdate (molybdenum form) and then binds and forms copper molybdate and this is excreted out urine
55
accumulation of cu in the liver is d/t imbalanced ratio of what compounds?
imbalanced btwn cu, molybdenum and sulfate
56
how is Cu excreted?
bile
57
what is a factor that induces Cu to come out of liver and cause toxicosis to sheep?
STRESS
58
what does stress do to sheep with Cu accumulated within the liver?
causes hemolysis -->hemolytic anemia
59
moa of cu?
Cu in liver causes liver degeneration and necorsis. release from the liver by stress causes oxidation of RBC membranes and this increases fragility of membrane and therefore causes a hemolytic crisis bc its easily stressed out. in addn, Cu will oxidize the hb to methb-emia: CHOCOLATE BLOOD!!
60
cs of Cu toxicosis?
-shock, pale mm, icterus, sudden weakness, anorexia, resp signs bc hb cant carry o2 d/t metjbemia
61
what specimens do u collect from a sheep : Cu toxicosis, if alive or dead?
alive: serum and whole blood dead: elevated liver enzymes: LIVER -AST and LDH - kidney also
62
what is the chelator of choice for Cu tox?
D-penicillamine: expensive for sheep and sometimes used in dogs
63
whats the Cu difference in dogs from sheep?
it only causes liver necrosis and not hemolytic crisis
64
how to tx / pv Cu toxicossi in sheep? 5
1. D-penecillamine 2. Supplemental Zn 3. molybendum: ADD ASAP!! wont help if given later on 4. ammonium tetrathiomolybate 5. ammonium molybdate: given once per day
65
EQ: ddx for Cu toxicosis?
1. hemolytic agents: zinc, napthelene, DMSO, guaifenesin, phenolics, 2. poisonous plants: onion, gossypol, red maple, mustard 3. certain snake venoms 4. infectious dz: lepto, babesia, anaplasmosis, bacillary hemoglobinuria
66
what conditions favor Pb absorption?
acidic
67
source of pb?
aeriel emmision from conbustion of pb fuel, battery waste, insecticide, herbicide, Pb based paints most common source of toxicosis in homes built before 1960s , pet toys, pet dish, ceramics, etc. OCEANS!! a thumbnail sized chip of pb based paint may contain 50-200 mg of Pb
68
which is more toxic organic or inorganic Pb?
organic!! more readily absorbed
69
which metal has an effect of plumbism? what is it?
Pb --> its one of te most common toxicoses of acute-chronic toxicities. its where you get the pb2+ repalceing the ca 2+ and ZINC 2+ in the body. young>>old patients d/t immature BBB and GIT absorption dog>>=DEATH of puppies birds=avian plumbism, avian saturism goat , pig, chicken=more resistant than dogs
70
MOA: interferes with the cel and can replace Ca, Zn, Mg, Fe 2+ competes in the bone with Ca and alters the movement of Ca across the membranes. XBBB,PLACENTA, GIT (better absorbed in stomach: acidic env) breakdown of BBB throguh toxic effect on the blood vessel endocthelim cells and alteration of microvascular systems will make the BV weak and induce leakage-->edema in that area forms complexes SH also binds to methallothioninE: this is a livEr enzyme that will be a chelating protein involved in cellular detox and bc this ___ is bound to it, we are then going to get that there will be sequestered pb ions that are elevated in concentration bc they are just sitting on it. bound to rbc for 60-90% of the RBC and this will induce damage.
pb
71
what are the cs of pb? GIT RBC CNS
GIT: caustic, anorexia, salivate, vomit, Pb colic, rumenatomy RBC: anemia, basophilic stippling* cns: spontaneous release of gaba=block neuroTs =hyperstimulation and cns depression: increase gaba and ach and cause mixed effects: hyperstim: ach and gaba: depression of cns
72
target tissues of toxicity of the pb?
cns, git,rbc
73
what specimens do we check for AM and PM of pb?
AM: whole blood and PM: kidney, liver and git
74
most common pb chelator?
1. calcium disodium edta
75
sources of zinc?
1. pennies (post 1982) 2galvinized metals 3. zinc oxide in shampoos and stuff 4. OD on zinc supplementation
76
which heavy metal undergoes enterohepatic recirculation?
ZINC
77
how does zinc circulate?
*plasma proteins: albumin and globulins
78
moa of zinc?
1. unknown but most consistent is intravascular hemolysis-->hemolytic anemia and lead to hemoglobinuria and hemoglobinemia 2. injury to RBC, liver, kidney, pancreas 3. Zn mediated hemolysis 4. zinc mediated kidney damge: secondary to hemolysis
79
IMP: how is zinc excreted?
1. liver is a major organ of excretion and metabolism.. - metallothionein: sequester metal and excretes - glutathione: sequester free radicals and associated with zinc toxicity
80
what are the CS of zinc?
acute, chronic, peracute 1. GIT: caustic-->anorxia, v+, lethargic, d+, pica 2. hematologic /rbc damage: hemolytic anemia, jaundice, etc. 3. renal (cell damge): azotemia: elevated BUN, hyperP
81
what to use for analysis of zinc?
royal/dark blue top-->trace element tubes
82
chelating agent for zinc?
calcium di-sodium edta or d-penecillamine * note: chelation may increase absorption and distribution from the intesteins and cause further damage to kidneys * guarded to poor outcome if patient experience
83
what are common routes of iron?
PO, IV IV>>IM>>>PO=toxicity IV: piglets!!!! most toxic
84
state of iron and how are they transported?
1. ferrous: 2+ 2. ferric : 3+ *hemosiderin, ferritin and transferrin =iron brinding protein that transport it
85
how is iron toxic? ie: whats its use of changing states and how does that affect organs
Fe is very unstable in that it changes quite quickly from Fe2+ to Fe3+ and this will induce free radicals to be released (ROS, glutathione) and this will in turn--> cellular damage-->tissue death-->organ failure
86
what is chelator of choice for Fe?
deferoxamine (desferal)
87
CS of Fe, that is unique? and general organs affected?
1. GIT 2. heart 3. liver *unique=follows 4 stages of toxicity
88
acute toxicosis of Fe will bind to which protein? but in general for TK binds to which one?
ferretin transferrin
89
moa: involved in copper deficiency!!! -Cu involved in hematopoiesis, CT metabolism, myelin formation, pigmentation, none Cu imp for absorption of Fe and tehrefore you get microcytic anemia(iie: Fe deficiency anemia) in addn: Cu imp for cytochrome oxidase and metabolizing enzymes in addn: copper containing prt in most aerobic cells have superoxide dismutase activity
Molybdenum
90
best specimen : whole bloood for molybdenum: T/F
True
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