Exam 2 Flashcards
(142 cards)
1
Q
PCP is used for what?
A
Wood preservative
2
Q
What ways can you get exposed to PCP?
A
dermal, inhalation, GIT
3
Q
MOA PCP
A
uncouples oxidative phosphorylation to decrease ATP
4
Q
Major CS of PCP
A
metabolic acidosis, hyperthermia, weight loss, CNS seizures and hyperkeratosis
5
Q
Dx for PCP
A
rapid rigor mortis, test kidney in dead, urine and blood in live- metabolic acidosis
6
Q
What is 2,4-D
A
phenoxy derivatives of fatty acids- amides and benzoicacids- herbicides
7
Q
How to get toxicosis from 2,4-D
A
from freshly sprayed lawns or pastures- canines and bovines
8
Q
Who has a shorter half life of 2,4-D in? Canine or bovine
A
Canine
9
Q
Increasing pH of urine enhances excretion of 2,4-D, T or F?
A
true
10
Q
MOA 2,4-D
A
uncouples oxidative phosphorylation to decrease ATP
11
Q
CS ruminants and canines fr 2,4-D
A
ruminants- GIT
canines- GIT and neuro
12
Q
Toxicity of paraquat/diquat
A
mod-high toxicity
13
Q
What enhances toxicity of paraquat/diquat?
A
Vit E def, depletion of tissue glutathione and O2 therapy
14
Q
Which is absorbed through GIT? Paraquat or diquat?
A
Paraquat- GIT, skin
Diquat- poorly through GIT
15
Q
paraquat/diquat MOA
A
reduced by NADPH to produce single O causing free radicals and membrane damage
16
Q
paraquat/diquat can have acute, delayed or chronic reactions, T/F?
A
true- acute GI signs
delayed are pulmonary signs
chronic pulmonary fibrosis
17
Q
After 48 hrs post exposure what may be negative to test for paraquat/diquat?
A
Urine
18
Q
What can you NOT give with paraquat/diquat toxicosis?
A
OXYGEN, give antioxidants!
19
Q
T/F alkaline pH (especially in rumen) enhances hydrolysis of urea by urease to ammonia?
A
TRUE
20
Q
What age is the MOST tolerant of NPN?
A
3-6 weeks old
21
Q
MOA NPN
A
NH3 inhibits citric acid cycle -> lack of energy and decrease cellular respiration and tissue damage
22
Q
NPN has a rapid onset of action? T/F
A
true
23
Q
Clinical signs NPN
A
bloat, alkaline rumen, stasis, anorexia, teeth grinding, colic
24
Q
What samples do you use to NPN?
A
feed, and NH3 in blood, freeze specimens immediately except blood
25
Tx of NPN tox?
acetic acid/vinegar with large volume of cold water and NaHCO3 for acidosis
26
Ionophores are used for?
anti-coccidials
27
what species is most sensitive/susceptible to monensin?
equine (and turkeys)
28
Which drugs increase tox of ionophores?
tiamulin, glycosides, fluoroquinolones, chloramphenical, erythromycin and sulfonamindes- inhibit microsomal enzymes
29
MOA ionophores
disrupt transmembrane electrochemical gradients- mitochondria main target. Sequester Ca and decrease ATP and energy made by mito
30
CS for animals with ionophore tox?
eq- heart and some skeletal muscle
bv and av-skm and heart
k9, ov, pc- skm
31
Na enters the brain passively and is actively removed, T/F?
true
32
MOA water deprivation
Na in brain inhibits anaerobic glycolysis -> decrease energy, causes water to come into brain- edema
33
CS water deprivation
circling, pivoting, head-pressing, blindness, inability to drink/eat
Av- depression, ascites, collapse
34
Lesions water deprivation
pinpoint ulcers, GI congestion, edema, eosin meningoencephalitis in porcine
35
Tx water deprivation
small amounts of water GRADUALLY over 2-3 d, antiseizure meds
36
What is included in ethylene glycol that can increase P?
Rust remover
37
Ethylene glycol does NOT go through lethal synthesis? T/F
false it does
38
Which part metabolite causes the most problems?
oxalic acid
39
MOA ethylene glycol
direct GI irritation and CNS depression, metabolites cause metabolic acidosis and ARF
40
There are acute or delayed signs from ethylene glycol, T/F?
true
acute- met acid, PU, GI signs, CNS depression, ataxia
delayed- (24-72 hrs) oliguric RF, seizure, coma, anuria, renal pain
41
Ethylene glycol lesions
hem gastroenteritis, pulm edema, tubular necrosis of kidneys, Ca oxalate crystals
42
Lab dx ethylene glycol
increased serum osm and anion gap, low USG, hypocalcemia, hyperglycemia, azotemia, hyperphos, hyperkalemia, increased PCV/TP, CaO crystals
43
Tx of ethylene glycol
1) fomepizole, 2)ethanol
44
Propylene glycol is pleasantly flavored, T/F?
false- it is unpleasant
45
High concentrations of what causes lactic acidosis with propylene glycol?
D-lactic acid
46
T/F propylene glycol is metabolized to toxic metabolites
false
47
what CS does propylene glycol cause?
Heinz body anemia
48
CS of alcohol tox
cns depression, vomiting, metabolic acidosis, irritate MM
| Chronic- L/K damage
49
Tx for methanol tox
ethanol or fomepizole- competitive inhibitors of alcohol dehydrogenase
50
MOA for bleach
with acid, release of chlorine/chloramine gas and hypochlorous acid
51
tx for bleach tox
milk and water
52
three types of detergents (least to most toxic)
non-ionic
53
T/F cationic detergent is contraindicated to use emesis/gastric lavage for tx
true it is contraindicated
54
An animal that smells like lemon/citrus can have a tox of what?
D-limonene
55
D-limonene is used for what?
Topical for fleas/ticks shampoo
56
CS for D-limonene
necrotizing dermatitis, CNS depression
57
Tx for D-limonene
shampoo/mild dish soap to wash off
58
xylitol MOA
insulin release -> hypoglycemia and hypokalemia -> L failure, GI hemorrhage, DIC
59
Tx xylitol
Dex inj and then CRI, oral feeding sugar, antiemetic, fluid therapy, antacids/GI protectants
60
Dermal exposure to phenolic compounds causes what?
coag necrosis, ulcers, white plaques, and later eschar formation
61
Oral exposure to phenolic compounds causes what?
ulceration and necrosis of GIT
62
Which chemical causes green or black urine?
phenolic compounds
63
T/F emetics/gastric lavage contraindicated with phenol compound toxicosis
true
64
methylxanthines are made of what three things?
caffeine, theophylline, and theobromine
65
MOA methylxanthines
inhibit phosphodiesterase and antagonize adenosine receptors
66
CS methylxanthines
theoph: GI
| Caf/theo: clonic convulsions, arrhthymias, seizures, coma, VPCs
67
Tx methyxanthines
AC, fluids, methocarbamol, diaz, B blockers, lidocaine
68
T/F organic Fe> irritant and astringent than inorganic Fe
false, inorganic>organic
69
T/F divalent is less irritating/astringent than trivalent
true
70
T/F iron is absorbed in the SI via an electron dependent carrier
true
71
What is irons electron carrier called?
transferrin extracellular (ferritin intracellular)
72
What is overdose due to, iron is natural in the body right?
When the free iron concentration saturates transferrin causing there to be free Fe circulating
73
MOA Fe
circulating free Fe causes free radical lipid peroxidation and damage to membranes- vasculitis
74
CS Fe parenteral and orl prep
parenteral- anaphylactoid rxn, shock, death
oral- stage 1: nausea, vom, diarrhea
Stage 2: "apparent" recovery
Stage 3: most serious (12-96 hrs) severe metabolic effects- V, D, hemorrhage, CV collapse
Stage 4: GI obstruction
75
Tx Fe tox
w/in 4 hrs emetics/gastric lavage (not AC), milk of magnesia, sucralfate, chelation therapy- deferoxamine**
76
Toxicity of inorganic arsenic
Tri > pent > organic
77
How toxic is inorganic arsenic?
highly toxic
78
Which species is most susceptible to inorganic arsenic
herbivores
79
MOA inorganic arsenic
inhibition of lipoic acid inhibits or slows glycolysis and citric acid cycle -> inhibits oxidative enzymes and inactivates glutathione, capillary endo cells are most sensitive
80
CS inorganic arsenic
GI and cardio collapse, colic**
81
Tx inorganic arsenic
chelation- Dimercaprol (BAL) or demercaptosuccinic acid (Succimer)- safer but less effective than BAL
82
Name the two names for organic acid and species they go with
porcine-arsanilic acid
| poultry- roxarsone
83
CS arsanilic acid
porcine- incoord, ataxia, partial paralysis, peripheral neurologic but GOOD APPETITE, possible blindness
poultry-CNS depression, ANOREXIA, coma and death (no peripheral neurotox)
84
CS roxarsone
porcine- hyperexcitability, tremors, collapse, NO blindness
| poultry- incoord and ataxia, PERIPHERAL neurotox
85
T/F puppies are most susceptible to lead tox because they eat everything and have increased absorption
true
86
T/F lead is easily degraded in environment
false it is not
87
T/F acid environmenet decreases absorption of lead
false, it increases it
88
MOA lead
dysfunction of enzyme receptors and structural proteins, disurpt heme synthesis causing premature release of nRBCs
89
CS lead
GIT (SA), CNS (LA)- roaring, megaesophagus, anemia; hematopoietic
90
Lesions for lead
cerebral cortical necrosis and poliomalacia in bovine, inclusion bodies, BASOPHILIC STIPPLING
91
T/F 99% of lead is attached to RBCs
true
92
T/F serum is the best sample to test for lead
FALSE whole blood**
93
Tx for lead toxicosis
Ca EDTA for chelation
can also use succimer, DMSA or BAL
fluids, mannitol, propofol/phenobarb, cathartic
ALSO SURGERY IF FOREIGN BODY
94
Which crosses the BBB?
Ca EDTA
Succimer
BAL
BAL crosses the BBB, use when CNS signs
95
Which is more hydrophilic, succimer or BAL?
succimer
96
Uses of zinc
part of many enzymes and proteins, for growth, cell proliferation, collagen formation, skin etc
97
T/F acid environment increases Zn release and absorption
true
98
What does zinc bind to?
2/3 to albumin and 1/3 to B-macroglobulin
99
MOA zinc
unknown but excess zinc interferes with absorption and utilization of copper and iron -> hemolytic anemia
100
hematologic lesions of zinc
regenerative HA, icterus, hemoglobinuria
also prerenal azotemia
can cause PANCREATITIS
101
what type of tube do you use to sample blood for zinc?
dark/navy blue tube for trace elements (no Zn stearate)
102
Tx for zinc toxicosis
first try to decontaminate then try surgery, make sure to stabilize patient
can chelate with Ca EDTA
103
T/F increased [Cu] in liver is due to imbalances between Cu, molybdenum and sulfate
true
| increased sulfate decreases Cu absorption
104
Which species are resistant to Cu tox?
swine and poultry
105
MOA/CS copper
accum in liver > necrosis, RBCs get metHb and can't carry O2 -> liver, kidney, organ damage
106
Which form of Cu tox is more common, chronic or acute?
chronic!! acute NOT common
107
Lesions with copper tox
icterus, hemolysis, methemoglobinuria, liver is enlarged/yellow/friable, "gunmetal" kidney, "black berry jam" spleen with "portwine" urine
108
Dx copper tox
see increased liver enzymes 3-6 weeks before hemolytic crisis (when liver fails), also hemoglobinuria and HA
109
how to PREVENT cu tox
easier to prevent than treat, add Mo to sheep feed make sure enough sulfur
to treat can use a chelator- D-penicillimine to increase Mo
110
T/F decreased Mo causes a Cu deficieny
false- INCREASED Mo causes a Cu deficieny
111
Which states have Mo rich soil?
Fl, Ca, Or, Nv
112
Which species are resistant to Mo tox?
equine and porcine (bovine MOST susceptible)
113
CS Mo tox?
green diarrhea after 8-10 days, rough hair coat and depigmentation (ESPECIALLY around eyes), anemia, osteoporosis and exostosis, lameness
114
Tx for Mo tox?
Cu glycinate subQ or Cu sulfate in diet
115
Se def diseases are?
white muscle/nutritional muscle dystrophy (lambs/calves/foals)
hepatosis dietetica in pigs
exudative diathesis in chicks
nutritional pancreatic atrophy in chickens
porcine stress syndrome in pigs
116
3 types of accumulators (plants) in Se tox
obligate, faculatative, passive
117
Name the 9 Se rich states
N and S Dakota, Wy, Montana, Ne, Ks, Ut, Co, NM
118
T/F selenium toxicity most to least
| Organic Se > selanate = selenite > selenide > synthetic Se compounds
true
119
What type of environment increases formation of selanate?
arid alkaline
120
Is elemental Se absorbed easily in water?
No it is INSOLUBLE- not absorbed
121
Where does Se accumulate?
hair and hoof (chronic exposures)
122
MOA Se
Se replaces S in AA, cause malformed proteins- decrease tissue glutathione
123
Acute, subacute and chronic Se tox CS
Acute- GI, resp (edema) when PO; neuro signs when parenteral
Subacute- "blind staggers"
1- aimless walking, circling, normal resp/temp
2-incoordination, walking on knees, anorexia
3-colic, hypothermia, emaciation, blindness, paresis, coma
In pigs "porcine focal symmetrical poliomyelomalacia"
Chronic- "alkali disease", rough hair coat, loss of hair, hoof deformities, stiff joints, partial blindness
124
Se prevention
Easier- take animals away from high Se rich soil, add Cu to diet, high protein diet, increase sulfur containing compounds
125
T/F only crude oils are highly irritant to MM and skin, not refined petroleum products
False- BOTH are
126
Are more or less volatile compounds more toxic because of increased absorption?
More volatile (low BP), MORE pneumotoxic potential
127
T/F sweet crude more toxic than sour crude
true
128
Aromatic hydrocarbons cause what?
bone marrow suppression
129
Can the oily substance aspirated into the lungs of petroleum products be eliminated by cough or ciliary activity?
no
130
MOA petroleum products
aspiration pneumonia or chemical pneumonitis -> inhalation, swelling, inflammation, edema, bronchoconstriction and necrosis -> hypoxia and bacterial pneumonia
131
CS petroleum products
aspiration pneumonia, bovine hyperkeratosis, smell like oil/kerosene, CNS signs (hydrocarbons), ulceration of trachea
132
Lab dx petroleum products
panleukopenia, x ray asp pneumonia
133
T/F emetic/gastric lavage and steroids contraindicated in petroleum product toxicosis?
true
134
Fluoride has a high affinity for what elements?
Ca, Al, and Fe
135
Whats more common, acute or chronic toxicity with Fl?
chronic
136
Which species is most susceptible to Fl tox?
dairy cattle
137
T/F CaF2 > tox than NaF
FALSE- NaF. CaF2
138
Where is Fl stored?
teeth (especially in young)
139
MoA chronic Fl tox?
brown/black tooth discoloration, altered and decaying bone/teeth
140
CS chronic Fl tox?
lame, painful gait, bony extoses, fractures, brown teeth, emaciation, lesions on mandible, metacarpals, ribs, spine and joints
141
Specimen for Fl tox?
BONE
142
Tx Fl tox
Al salts, Cacarbonate, defluorinated phosphate PO to form insoluble compounds
