Integration & Consolidation II COPY > WebCAI - Toxicology > Flashcards

WebCAI - Toxicology Flashcards

(100 cards)

Study These Flashcards
1
Q

what is the first thing you should do when a patient comes to you with obvious signs of toxicity?

A

ABCDT

A: airway should be clear; an airway or endotracheal tube inserted

B: breathing assessed by observation, measurements, pulse-oximetry

C: circulation; monitor pulse, BP and urine output; start IV and draw blood for glucose

D: drugs - dextrose for every patient with altered mental status, 100mg thiamine to alcholic and malnourished patients, naloxone, flumazenil, IV lorazepam/diazepam

T: temperature…should cool patient down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the contraindications to the induction of emesis?

A
  1. patient is unconcious
  2. caustic substance was ingested (ie drain cleaner - will cause damage to the esophagus and oral tissue)
  3. hydrocarbons - will cause chemical pneumonia
  4. seizures present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

when would you induce emesis

A

no later than 4 hours after ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when would you use gastric lavage? contraindications?

A

aka pumping the stomach

use: patients are hysterical, comatose
contraindication: caustic agents (risk of puncturing esophagus) or seizure producing agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the benefit of using activated charcoal?

A

most drugs are adsorbed by activated charcoal

charcoal is inert, nontoxic and there are no contraindications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the most appropriate agent for inducing emesis in children in the home where they consumed a potential toxin?

A

syrup of ipecac - local irritant effect on the enteric tract and effects chemoreceptor trigger zone in the area postrema of the medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what group of individuals is most susceptible to accidental poisoning? and with what substance?

A

children under the age of 5 years old with analgesics (aspirin and acetaminophen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the best definition for the conditions that cuase chronic toxic effects form poison exposure?

A

rate of poison input exceeds the excretion rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the most reliable method of identifying any toxic agent?

A

chemical identifiation of toxin in blood or tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

the addition of 5% CO2 to O2 for resuscitation in respiratory failure does what?

A

stimulates chemoreceptors, leading to increased ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

characteritic toxic effect of benzene

A

bone marrow toxicity: aplastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

carbon tetrachloride characteristic toxic effects?

A

acute: CNS manifestations, stupor convulsions, coma
delayed: cardiac arrhythmias, kidney injury, liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

toxic effect of narcotics

A

depression of respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what drugs can you give for narcotic overdose?

A

naloxone - short half life; pure narcotic antagonist; induce withdrawal syndrome

nalmefene - long acting (48 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

symptoms of opioid intoxication

A

Triad: coma, pinpoint pupils and respiratory depression

  1. unconsciousness
  2. pin-point pupils
  3. slow, shallow respiration
  4. cyanosis
  5. hypotension
  6. spasms of GI tract
  7. spasticity and twitching of the muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F: oxygen therapy in acute morphine poisoning must be used with caution because the main respiratory drive in morphine poisoning is hypoxic stimulation of the carotid chemoreceptors.

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

toxic effect of barbiturates?

A

CNS depression of respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what should you do if you suspect a patient has barbiturate poisoning and there is CNS depression?

A
  1. endotracheal tube should be used to maintain the airway
  2. gastric lavage should be performed
  3. do not administer pure oxygen

NO antidote - supportive therapy only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the symptoms of aspirin poisoning? why?

A

aspirin directly stimulates the respiratory center -> increase in breathing -> respiratory alkalosis -> eventually will be replaced by metabolic acidosis

other symtpoms: fever, roaring in the ears, blurred vision, vomiting, sweating

can also get prolongation of bleeding time….aspirin inhibits platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the treatment of aspirin poisoning?

A

induce emesis or gastric lavage

elimination of absorbed drug can be hastened by giving sodium bicarbonate to alkalinize the urine (also helps correct the metabolic acidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

if aspirin toxicity is suspected, what tests can you run?

A

urine analysis for salicylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can you do if a patient has overdosed on phenobarbital?

A

while for all other barbiturates in an acute setting you can only give supportive therapy, you can alkalinize the urine with sodium bicarbonate if the patient overdoses on phenobarbital.

phenobarbital has a low protein binding, relatively low pKa, relatively slow reabsorption and are detoxified by renal excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

organic phosphate insecticides are…

A

irreversible inhibitors of cholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

symptoms of organophosphate poisoning?

A
  1. constricted pupils
  2. excessive salivation
  3. sweating
  4. fasciculations of eyelids, tongue, face and neck muscles
  5. weakness
  6. confusion
  7. convulsions
  8. nausea
  9. cramps
  10. diarrhea
  11. blurred vision
  12. respiratory failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
treatment of organophosphate poisoning
atropine + pralidoxime (2-PAM) atropine: blocks peripheral and central muscarinic actions of ACh (does not block nicotinic actions of ACh) pralidoxime: weak inhibitor of cholinesterases
26
name four organocarbamate insecticides
aminocarb, carbaryl, carbofuran, aldicarb
27
what will improve skeletal muscle function in a patient poisoned with an organophosphate nsecticide?
pralidoxime - reactivates the phosphorylated acetylcholinesterase atropine only blocks M effects, not nicotinic effects
28
treatment for cyanide intoxication?
amyl nitrate by inhalation followed by IV sodium nitrite and then sodium thiosulfate and/or methylene blue
29
MOA of cyanide
blocks respiration at the cellular level by preveting the tissues from utilizing oxygen (aka interfering with the ETC in the mitochondria); specifically it blocks cytochrome oxidase and has a high affinity for Fe+3 (ferric state) does not affect the ability of blood to transport oxygen to the tissues
30
symptoms of cyanide poisoning?
dizziness, headache, fall in BP, unconciousness, convulsions, respiratory arrest
31
what is cyanocobalamin
in the presence of cyanide, each hydroxocobalamin molecule can bind one cyanide ion by displacing it for the hydroxo ligand linked to the trivalent cobalt ion
32
how is cyanide excreted from the body?
first, nitrite produces methemoglobin, which is capable of removing the cyanide from the mitochondria. then, the thiosulfate is a source of sulfur, which is requried by the liver for the conversion of cyanide to thiocyanate (which is non toxic and excreted; enzyme = rhodanese)
33
moa of methemoglobin in cyanide poisoning treatment
The ferric form of iron in methemoglobin has even a greater affinity for cyanide than does the ferric form of iron in cytochrome oxidase; thus, there is a shift of cyanide from mitochondria to methemoglobin and cellular respiration is restored.
34
metabolites of methanol?
formaldehyde and formic acid
35
what causes less severe CNS depression than any other CNS depressant?
methanol
36
how do you treat methanol toxicity? why?
you treat methanol toxicity by blocking the metabolism of methanol. this is because the toxicity of methanol is due to its metabolites give 50% ethanol IV to block metabolism OR can give fomepizole (synthetic alcohol dehydrogenase inhibitor) since one of the metabolites is formic acid, which causes acidosis, must give sodium bicarbonate to neutralize this acid
37
toxicity of ethylene glycol?
CNS depression and kidney damage
38
how does the kidney get damaged when ethylene glycol is ingested?
ethylene glycol is metabolized to oxalic acid, which chelates with Ca+2. this complex damages the kidneys! "calcium oxalate crystals"
39
treatment of ethylene glycol toxicity?
give calcium gluconate IV, oxygen, artificial respiration and immediate kidney dialysis can block metabolism of ethylene glycol by using the same methods as methanol toxicity - ethanol IV or fomepizole
40
what "glycol" is not toxic and is used as a vehicle for drugs?
propylene glycol
41
what other serious toxicity does methanol cause?
neurotoxicity, including blindness from retinal damage
42
what glycol directly inhibitos vasopressin?
ethanol
43
describe the moa behind hypothermia during acute ethanol intoxication
peripheral vasodilation -\> warm, flushed skin -\> interfere with normal homeostatic mechanisms for maintaining constant core body temperature -\> hypothermia in cold environments
44
if someone, who has ingested ethanol, is slurring their words, what level of intoxication are they at?
moderate poisoning - blood alcohol = 150-300 mg %
45
what blood level of ethanol is necessary in order for someone to be in a coma?
greater than 500 mg %
46
what blood level of ethanol would someone need to be considered to have severe poisoning? what special characteristics would you see?
300-500 mg % approaching stupor, severe hypoglycemia, convulsions, fatalities
47
when do you begin hemodialysis for someone who has alcohol poisoning?
when their blood levels are \> 500 mg %
48
what drug is NOT useful for alochol withdrawal seizures unless there is a preexisting seizure disorder?
phenytoin
49
moa acamprostate
analog of homotaurine and GABA
50
death from methanol intoxication is primarily due to
acidosis and respiratory failure
51
A 23-year-old man is brought to the emergency department after attempting suicide with ink remover (oxalic acid). What should you treat him with?
calcium gluconate - same treatment as ethelyne glycol
52
poisoning from methanol is more serious than that from ethanol because?
methanol poisoning produces blindness and acidosis due to production of formic acid
53
symptoms of carbon monoxide poisoning?
typically the patient is unconsciousness if conscious, will complain of: headache, dizziness, confusion, loss of visual acuity signs and symptoms of anoxia begin to occur as COHb exceeds 15%
54
what does CO do in the body (ie what are its toxic effects)
binds to hemoglobin therefore forming carboxyhemoglobin carboxyhemoglobin = COHb; cannot carry O2 and impairs the ability of oxyhemoglobin to give up its oxygen to peripheral tissues (therefore there is a left-shift in the O2 dissociation curve) COHb has a cherry red color and cyanosis may not be present
55
treatment of CO poisoning?
give O2 - carboxyhemoglobin can be converted to oxyhemoglobin in the presence of high tensions of oxygen
56
affinity of CO for Hb is ZZZ times greater than the affinity of O2 for Hb
220
57
what is the difference between CO toxicity and cyanide poisoning?
CO: reduces blood O2 carrying capacity Cyanide: reduces O2 utilization by mitochondrial cytochrome oxidase
58
what do nitrites do in the body
cause the conversion of Fe from 2+ -\> 3+ (ferrous to ferric) Hb containing Fe in the ferric state is known as methemoglobin
59
what are the characteristics of methemoglobin?
form of Hb where the iron atom is oxidized from the ferrous (Fe+2) to the ferric (Fe+3) state cannot bind with O2 -\> chocolate brown color person will become cyanotic in color
60
treatment of nitrite poisoning? MOA?
only necessary when 35% or more of Hb is in the oxidized form low concentrations of methylene blue: will convert Fe+3 -\> Fe+2 through its catalyzing effect on an intraerythrocytic enzymatic reducing mechanism (NADPH dependent)
61
Explain why you would give a patient with cyanide posioning sodium nitrate to help them get better.
Cyanide has a very high affinity for iron in the ferric (Fe3+ state) and thus interacts with cytochrome oxidase in the mitochondria to inhibit cellular respiration. Recall that nitrates convert Hb to methemoglobin (where iron is in the ferric state). Therefore, the methemoglobin can compete with the cytochrome oxidase ferric iron to get the attention of cyanide. Thus, when cyanide binds to methemoglobin, cyanmethemoglobin is formed and cytochromie oxidase activity is restored.
62
what types of metals does EDTA bind with/
Ca, Ba and Sr (Class A metals)
63
what types of metals do BAL (dimercaprol) bind to?
Hb, As and Au (Class B)
64
what is the specific chelating agent for iron?
deferoxamine
65
what is the specific chelating agent for lead?
well lead binds to all four atoms: O, N, S and P but CaNa2EDTA = drug of choice for severe lead poisoning succimer (DMSA) = newer chelating agent that is the preferred agent for less severe lead intoxication
66
MOA of arsenic in the body
inhibits enzymes which contain sulfhydryl groups and increases the permeability of capillaries As5+: substitutes for inorganic phosphate inproduction of ATP As3+ binds sulfhydryls especially in lipoic acid, thus interfering with energy production
67
clinical presentation of arsenic poisoning?
The 3 D's: Diarrhea, dermatitis (Mees' lines on finger and toe nails), dementia
68
treatment of arsenic poisoning
acute: BAL given IM chronic: oral succimer
69
iron poisoning: moa
causes hemorrhaging due to damage to the cells of the GI tract
70
early and late symptoms of iron poisoning?
early: GI disturbance late: matabolic acidosis (main cause of death)
71
treatment of iron poisoning
deferoxamine given IV or IM (chelator)
72
clinical presentation of chronic mercury poisoning compared to acute mercury poisoning
chronic: salivation, **swollen and bleeding gums**, **emotional instability (Mad as a Hatter)**, tremors, loss of memory, hallucination acute: irritation and superficial corrosion, abdominal pain, vomiting
73
toxic form of mercury
Hg+2
74
acute and chronic mercury poisoning treatment
acute: BAL parenterally (never given orally due to increased absorption) chronic: succimer
75
what two metal toxicities are nevery treated with a chelator? why?
cadmium (released from chelator in kidney causing renal damage) and manganese (Parkinson's like syndrome)
76
chelator fo choice for severe lead poisoning?
calcium disodium edetate (CaNa2EDTA)
77
what chelating can reactivate sulfhydryl enzymes and can protect sulfhydryl enzymes from further inactiation?
dimercaprol
78
what chelator produces hypocalcemia unless given in the calcium-chelate form?
EDTA
79
what is most likely to be helpful in confirming the diagnosis of iron poisoning in a child who ingested ferrous ulfate tablets?
abdominal x-ray film
80
what does burtonian (blue) line on gums typically suggest?
chronic lead poisoning
81
CaNa2EDTA is superior to dimercaprol in the treatment of chronic intoxication from what chemical?
lead
82
a black line on the gums, tremors of the extremities and progressive anuria suggest chronic poisoning by what metal?
mercury black line on the gums is more characteristic of lead poisoning but can also be seen with mercury poisoning
83
what is the initial disturbance of the body's acid-base balance that is observed when a 3-year-old child ingests a large dose of aspirin?
respiratory alkalosis - hyperventilation resulting from direct respiratory center stimulation
84
what poison can produce CNS excitation when a 4 year old child is exposed to toxic levels?
isoniazid
85
dimercaprol protexts against the toxic actions of mercury because?
forms a complex with the metal
86
what is the moa of etoposide?
programmed cell death (apoptosis) due to inhibiting topoisomerase II
87
what will you see in a child that has overdosed on benadryl?
cycling between coma and seizures
88
An infant girl developed nitrite poisoning because her parents made her formula with contaminated well water. Since they lived in a rural area where excessive fertilizers are used for agricultural crops, the well water was highly contaminated with nitrates. The bacterial flora of infants produce nitrate reductases that convert nitrates to nitrites. What do you treat her with?
methylene blue
89
chronic exposure to which toxin is most likely responsible for aplastic anemia in a 58-year-old man who recently arrived in the US after working several years in an industrial factory in a foreign country?
benzene
90
you can treat phenobarbital overdose with....?
IV sodium biarbonate - helps facilitate excretion of the toxin
91
Most appropriate treatment for a 3 year old poisoned with oxalates from consuming dish washer detergent?
oral calcium antacids to precipitate oxalates
92
what toxin can cause fatal lung injury produced by the formation of oxygen free radicals?
paraquat
93
what pesticide is pralidoxime (2-PAM) contraindicated?
carbaryl
94
treatment for a child who accidetally ingested sodium hypochlorite from bleach?
give her milk
95
True or false: OP insecticides (parathion) have to be bioactivated to be toxic
true
96
treatment of overdose of beta-blockers?
glucagon
97
findings of acute arsine gas exposure?
hemolysis and hemoglobinurea
98
what is a characteristic finding of acute exposure to metallic mercury?
acute chemical pneumonitis
99
effects of pentachlorophenol in the body
uncoupling of oxidative phosphorylation - causes hypothermia
100
what chelating agent can be given orally in the treatment of mild lead poisoning?
succimer
Integration & Consolidation II COPY
flashcards
Decks in class (36)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions