Final--New Material Flashcards

1
Q

Name 4 conditions that are required in order for a mold to grow

A

1) aerobic conditions
2) feed moisture >14%
3) relative humidity >70%
4) temperature–warm

+/- plant damage

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2
Q

Definitive diagnosis of mycotoxicosis comes from identification of ______

A

the toxin

NOT the mold

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3
Q

Of the many toxin types, ___ is the most toxic and oncogenic of the aflatoxins

A

B1

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4
Q

What are the 3 outcomes of aflatoxin binding to cellular components?

A

1) oncogenesis (most potent natural hepatocarcinogen)
2) altered anabolic/catabolic processes (i.e. protein synthesis, inhibited lipid transport, and decreased glycogen)
3) immunosuppression

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5
Q

What are the two toxin types assoc. with Tricothecens? Which is more toxic?

A

1) DON (vomitoxin)

2) DAS (T-2) **more toxic

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6
Q

Which body system(s) are primarily impacted by Fumonisin and in which spp.?

A

Hepatic and neuro

Horses

**Equine leukoencephalomalacia (Moldy corn dz)

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7
Q

Fumonisin is assoc. with which type of food/feedstuffs?

A

corn, corn-based feeds

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8
Q

Citrinin & Ochratoxins primarily affect which body system? How? In which TYPES of animals does this most commonly occur?

A

Citrinin & Ochratoxins= KIDNEYS

Degeneration of proximal tubules–alters reabsorption

**MONOGASTRICS

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9
Q

Which toxin can cause early development of mammary tissue and red, swollen vulvas in Gilts? Also describe it’s MOA

A

Zearalenone–binds to estradiol 17-beta receptor and causes hyperestrogenism

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10
Q

Describe Fescue’s interactions at the following receptors and the response/outcome

1) D1 dopaminergic receptor
2) D2 dopaminergic recepot

A

1) Inhibition–> vasoconstriction

2) stimulation –> decreases prolactin secretion

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11
Q

4 clinical syndromes assoc. with fescue ingestion?

A

Summer slump
Fescue foot
Fat necrosis
Repro Disorders

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12
Q

Though they cause many of the same types of syndromes, what’s the primary difference between Ergotism and fescue?

A

Ergotism does NOT cause fat necrosis like fescue

Ergot= Claviceps spp.

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13
Q

A horse showing excessive salivation may have ingested which mycotoxin?

A

Slaframine

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14
Q

Describe the mechanism whereby NSAIDs can cause renal disease?

A

NSAIDs inhibit prostaglandins that are important for vasodilation–> decreased perfusion pressure to kidney –> ischemia

**NOT directly nephrotoxic

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15
Q

NSAIDs primarily cause coagulopathy via inhibition of?

A

Thromboxane A2 (TXA2) which comes from platelets and normally causes vasoconstriction and platelet aggregation

**remember the function of PGI2

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16
Q

For how long must you treat NSAID toxicity? Which NSAID has the longest tx time?

A

At least THREE HALF-LIVES

Naproxen (Aleve)–> 72hr half-life

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17
Q

Salicylates (Aspirin) primarily cause their clinical effect through which mechanism?

A

Uncoupling of oxidative phosphorylation

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18
Q

Most the clinical effects of Amphetamines are due to?

A

Stimulation of CNS and Sympathetic nervous system

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19
Q

Cocaine causes its clinical signs via which TWO mechanisms?

A

1) reuptake inhibitor (serotonin, dopamine, NE)

2) Blockage of voltage-gated Na channels

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20
Q

What is the main MOA of Tricyclic antidepressants (TCAs) and how do the CV signs differ from cociane or amphetamines

A
reuptake inhibitor (5-HT & NE) 
*also blocks alpha-1 and muscarinic*

causes tachycardia with HYPOTENSION due to alpha-blockade

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21
Q

The primary clinical sign assoc. with serotonin elevations in dogs? (Serotonin syndrome)

A

Tremors

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22
Q

Death from TCAs primarily occurs due to?

A

Cardiac failure

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23
Q

Which drug may be helpful in treating serotonin syndrome and why?

A

Cyproheptadine; serotonin antagonist

24
Q

Which pathway of metabolism of acetaminophen is assoc. with formation of toxic metabolite? What’s the name of the metabolite?

A

Metabolism by cytochrome P450 creates NAPQI

25
Q

Normally, the toxic effect of NAPQI are mediated by?

A

Glutathione conjugation

26
Q

Primary system affected by acetaminophen

1) dogs
2) cats

A

1) liver

2) hematologic (RBCs)

27
Q

How does interpretation of an elevated ALT differ between dogs and cats

A

It’s more significant in cats bc it has a short half-life…so elevations typically mean ongoing damage

28
Q

A specific antidote for acetaminophen toxicity and it’s MOA?

A

N-acetylcysteine (NAC)

replenishes glutathione & binds NAPQI

29
Q

How can Glucagon and Insulin be used for treatment of Ca channel blocker intoxication

A

Both of these work to increases cAMP levels which stimulates release of intracellular Ca from the SR

30
Q

What are the main cardio effects seen with Ca channel blockers? (2)

What do you expect to happen to serum Ca levels?

A

1) bradycardia
2) AV block (2nd & 3rd degree)

**Ca level remains normal

31
Q

Baclofen is a ______ and is most life-threatening when it affects which body system?

A

Muscle relaxant

Respiratory (paralysis= death..need ventilator)

32
Q

What two hematologic changes might you expect to see on a blood smear with lead toxicity

A

Basophilic stippling (disrupted heme synthesis)

Nucleated RBCs

33
Q

Oral administration of what can help to decontaminate the GI tract of lead by inhibiting its absorption

A

Magnesium sulfate (MGSO4)

34
Q

Concerning chelation therapy for lead toxicity

1) name the 3 chelation drug options
2) which drug is potentially nephrotoxic
3) which drugs would be good to give in combination…describe the MOA

A

1) Ca-EDTA, Succimer DMSA, Dimercaprol
2) Ca-EDTA
3) Ca-EDTA + Dimercaprol–> CaEDTA pulls it out of bone and dimercaprol enhances it’s excretion

35
Q

The main disease seen with zinc toxicity is?

A

Hemolytic anemia

36
Q

Which form of iron is assoc. with the greatest risk of toxicity

A

soluble salt forms

37
Q

Free iron in systemic circulation is normally bound by _______ but this can become overwhlemed, leading to clinical signs

A

Transferrin

38
Q

What chelation agent can be used for iron toxicity? What’s a unique side effect of this drug you should warn owners about?

A

Deferoxamine

Can turn urine bright red (normal)

39
Q

Amanits phalloides mushrooms primarily impact which body system? What are the two principle toxins it produces?

A

Hepatic

1) amatoxins
2) Phallotoxins

40
Q

The neuro signs caused by Hydrazine-containing mushrooms is primarily due to inhibition of?

A

GABA

41
Q

With neuro toxic Amanita spp. why do clinical signs fluctuate between neuro depression and stimulation?

A

Because there a 2 principles toxins

1 toxin is glutamate agonist (excitation)–Ibotenic acid

the other toxin is GABA agonist (depression)–Muscimol

42
Q

Muscarine containing mushrooms cause development of which type of clinical signs? A specific antidote for these?

A

muscarinic signs(SLUDDE)

**ATROPINE

43
Q

Which spp. of mushroom is assoc. with the development of AKI (nephrotoxic)

A

Cortinaria spp.

44
Q

Are grapes or raisins more likely to be assoc. with adverse effects?

A

Raisins (dried form)

45
Q

Grapes/raisins primarily impact which body system?

A

Renal (nephrotoxic)

46
Q

T/F: Dogs who ingest Macadamia nuts are unlikely to die and owners can probably offer supportive care at home

A

true!!

These dogs typically just get weak/depressed

47
Q

What are the two methylxanthines we care about?

A

Caffeine

Theobromine (chocolate)

48
Q

Treatment of _______ toxicity should include a urinary catheter. Why?

A

Thebromine (chocolate)

Metabolites can be reabsorbed from bladder

49
Q

How does Xylitol causes most of it’s clinical signs

A

strong promoter of insulin release –> hypoglycemia

50
Q

Spp. most susceptible to onions/garlic toxicity have low _____ ______ activity

A

erythrocyte catalase

51
Q

What body system is primarily effected by onions/garlic?

A

Hematologic–oxidative injury (heinz bodies) and methemoglobinemia

Hemolysis later on

52
Q

What are the two risks assoc. with ingestion of bread dough

A

1) ethanol toxicity

2) obstruction/GDV/rupture

53
Q

Though sago palms initially cause GI upset, eventually clinical signs can progress and affect which two other systems?

A

neuro and hepatic

54
Q

Cardiac glycosides primarily affect which system and by what mechanism?

A

Cardiovascular

disrupts function of Na/K ATPase pump

55
Q

How do insoluble Ca oxalates cause clinical signs?

A

They are sharp and released during biting/chewing –> pain in mouth and edema of lips/tongue

56
Q

The soluble Ca oxalata primarily affect which types of animals? Clinical signs are related to….

A

Large animals

hypocalcemia (oxalates bind systemic Ca)

*stones/renal failure less common

57
Q

Two toxin types assoc. with Blue-green algae and the system they each affect. Which is more common?

A

1) Microcystins–liver (more common)

2) Anatoxin–neuro