- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
119 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is the mainstay for the treatment of most poisonings?
|
Symptomatic medical care. Immediately check and stabilize all vital functions!
ABCDE's!!! Airway Breathing Circulation Disability (neurologic stabilization) Exposure (limit further exposure to patient as well as health team) |
|
|
What should be done to clear the airway of a patient who comes in unconscious with an acute poisoning?
|
Rapid Sequence Intubation (RSI)
Done to avoid possible aspiration. |
|
|
All patients who come in with acute poisoning should have their breathing monitored with oximetry and be given what to ensure proper ventilation?
|
High flow oxygen
|
|
|
What is a toxidrome?
|
Cluster of signs and symptoms typical of poisoning by certain agents. Can provide important clues to narrow down a differential.
|
|
|
Are the majority of GI overdoses due to acute or chronic exposure/ingestion?
|
Majority are acute toxic ingestions (80%)
|
|
|
When is GI decontamination the most beneficial for a patient suffering from a poisoning?
Will it be beneficial in most cases? |
Within the 1st hour of ingestion, with clinical symptoms occurring.
|
NO, most patients will not present to the ER until at least 3 hours after exposure |
|
What is the preferred method of GI decontamination?
|
Activated Charcoal (AC)
What is the recommended dose? |
1g/kg |
|
What are the major contraindications for using AC?
|
Bowel obstruction/perforation
Unprotected airway (because of tendency to induce vomiting) |
|
|
What are the major complications that can occur when inducing emesis with ipecac syrup in the treatment of acute poisoning?
|
-Aspiration leading to chemical pneumonitis
-Protracted vomiting that will not stop (will interfere with further attempted PO treatment) -Vagal induced bradycardia -Esophageal tearing |
|
|
What substance is used to perform whole bowel irrigation in the setting of acute poisoning?
|
Polyethylene Glycol (PEG) enterally administered.
|
|
|
When should you consider using PEG for whole bowel irrigation?
|
-smugglers with drug packets
-sustained release formula poisoning -Enteric coated preps -Substances that are not well absorbed by AC |
|
|
What is the goal of a cathartic in poisoning treatment?
|
to limit drug absorption by increasing rectal evacuation.
|
|
|
What is the preferred cathartic in acute poisoning treatment?
|
Saccharide cathartics such as sorbitol
|
|
|
Would you use a cathartic as a single agent therapy to treat acute poisoning?
|
NO! Used to prevent constipation and enhance elimination of charcoal-poison complex. Only given if AC has also been administered.
|
|
|
When is urine alkalinization considered a first line treatment?
|
Moderate salicylate poisoning.
Administered ALONGSIDE AC. |
|
|
Would you ever use an agent to cause urine acidification in treating an acute poisoning?
|
NO! Can be associated with serious acidosis
|
|
|
Why are osmotic diuretics no longer recommended to treat acute poisoning?
|
Because of the risk that they may cause volume overload and electrolyte abnormalities.
|
|
|
Why is hemodialysis NOT useful for acute poisonings with substances that have a large Vd?
|
Because hemodialysis will only clear drug that is unbound in the blood. If the majority of the drug is NOT in the circulation system, hemodialysis won't make a dent.
|
|
|
In which types of poisonings is hemodialysis particularly useful?
|
Alcohol, salicylates, ethylene glycol, lithium.
Also, it readily corrects electrolyte imbalances and metabolic acidosis seen in some drug poisonings. |
|
|
What is the antidote for opiate narcotics?
|
Naloxone.
|
|
|
What is the antidote for benzodiazepine toxicity?
|
Flumazenil.
Why can it be dangerous to use on a patient who has chronically used/abused BDZ? |
can cause withdrawal seizures in patients with tolerance to BDZ and these seizures may be resistant to BDZ. |
|
Why do paint removers containing methylene chloride have a risk of causing carbon monoxide poisoning?
|
Methylene chloride is absorbed and metabolized in the body to CO.
|
|
|
What is the major mechanism of toxicity in carbon monoxide poisoning?
|
Anemic hypoxia.
CO has a higher binding affinity than O2 for hb, and thus displaces the O2. COHb also interferes with the release of O2 from any remaining Fe sites on the Hb. This leads to tissues being deprived of O2 because it cannot be transferred from the Hb to the tissue. |
|
|
What mechanism of CO poisoning causes direct toxicity to skeletal and cardiac muscle?
|
CO binding to myoglobin.
|
|
|
What causes the metabolic acidosis associated with CO poisoning?
|
Cytochrome binding --> impairs oxidative metabolism and leads to free-radical formation
|
|
|
In CO poisoning, the CO in the body stimulates guanylate cyclase. What does this lead to?
|
Cerebral vasodilation leading to syncope.
|
|
|
What are the principle signs seen in CO poisoning?
|
Signs associated with hypoxia.
-DNS -Myocardial injury -Syncope |
|
|
What is the specific antidote for CO poisoning?
|
100% Oxygen.
In mild poisoning, 5% CO2 may stimulate respiration and intake of O2 |
|
|
What is the treatment sequence for CO poisoning?
|
1. decrease exposure and stabilize vitals
2. keep the patient as still as possible to decrease oxygen demand 3. give 100% O2 (specific antidote) 4. consider hyperbaric chamber 5. if severe, exchange transfusion |
|
|
What intercellular structure is CN specifically toxic to?
|
Mitochondria
|
|
|
What are some things to look out for in history to point you toward CN poisoning?
|
-hx of photography, galvanizing, or metal plating work.
-fumigation on ships -exposure to burning plastics -domestic fire exposure*** MOST COMMON! |
|
|
What should be your first suspicion if a patient presents with severe respiratory distress, but NO cyanosis?
|
Cyanide Poisoning.
|
|
|
What does CN do in the body that causes the primary toxicity?
|
binds to Fe3+, thus preventing reduction to Fe2+ and inhibiting the ox phos pathway and cellular respiration. --> Cells can't make ATP even though O2 is available.
|
|
|
What is the pattern of symptoms seen in cyanide poisoning?
|
Transient CNS stimulation followed by hypoxic seizures
|
|
|
What type of hypoxia does CN poisoning cause?
|
Histotoxic hypoxia (oxygen is available, but cannot be used)
|
|
|
What is the IMMEDIATE treatment given to someone suffering from acute cyanide poisoning?
|
IV Sodium nitrate followed by IV Sodium Thiosulfate.
Positive pressure O2. |
|
|
Why is it important to give Sodium Nitrate first when treating cyanide poisoning?
|
To cause formation of CNmetHb, drawing CN away from mitochondrial cytochrome oxidase.
Helps to facilitate thiosulfate's actions in the mitochondria by decreasing the mitochondrial blockage caused by CN. |
|
|
What treatment for cyanide poisoning has been rather recently approved, and works both within cells and in the intravascular space as an antidote?
|
Hydroxycobalamin. A form of Vit B12 that binds to CN. Forms Vit B12a cyanocobalamin, which is eliminated in the urine
|
|
|
Parathion, Malathion, and Diazinon are all examples of what potential toxin?
|
Organophosphates
|
|
|
What do organophosphates act as in the body that lead to toxic effects?
|
Potent cholinesterase inhibitors
|
|
|
What are the cardinal symptoms of organophosphate poisoning (mnemonic)?
|
SLUDGE!
Salivation Lacrimation Urination Diarrhea GI disturbances Emesis |
|
|
When would you expect to see OPIDN?
|
Usually only in cases where exposure to LARGE doses of organophosphates has occurred, such as suicide, or accidental.
|
|
|
If a patient comes in with organophosphate poisoning, and as you are treating them for their sludge symptoms, they begin to complain of painful pricklings in their hands and feet. What would you be concerned about?
|
That OPIDN is setting in and they were exposed to a large dose of OPs.
|
|
|
What are the specific drugs used to treat organophosphate poisoning?
|
Atropine and 2-PAM
|
|
|
When should 2-PAM be used in the treatment of Organophosphate poisoning?
|
if RBC cholinesterase activity drops by 50%, or if significant nicotinic or CNS effects are seen.
both of the above are signs of significant poisoning. |
|
|
Why is it that carbamate poisoning has similar effects to organophosphate poisoning, but much less severe?
|
Because carbamate poisoning is toxic due to carbamoylation of AChE, and carbamoylation is RAPIDLY reversible.
|
|
|
What is the treatment protocol for carbamate poisoning?
|
Give Atropine.
|
|
|
Would you ever consider using 2-PAM to treat carbamate poisoning?
|
NO!
It is NOT effective, and may actually make things worse! |
|
|
Which herbicide acts as a specific pulmonary toxicant in cases of poisoning?
|
Paraquat
|
|
|
How does paraquat cause damage to lung tissue?
|
accumulates in the lungs due to preferential transporter regardless of exposure route. Once there, it begins to create reactive oxygen species, leading to significant lung tissue damage
|
|
|
If you ingest paraquat poisoning rather than inhale it, will you be safe from its pulmonary effects?
|
NO. No matter where ingestion occurs, preferential transport takes the poison to the lungs!
|
|
|
What are the early and late symptoms seen after oral exposure to paraquat?
|
Early: GI irritation (hemetemesis, bloody stools) due to corrosive properties
Later (may take WEEKS): Respiratory distress, progressive lung fibrosis Note: fatal pulmonary fibrosis may occur even in patients who recover from initial toxic effects. |
|
|
What is the treatment for paraquat poisoning?
|
There is NO specific antidote.
use Activated Charcoal or Fuller's Earth, which are effective if given IN TIME. Irrigate skin with soap and water, but DO NOT SCRUB! |
|
|
Why is it so important to treat oral ingestion of paraquat as soon as possible?
|
Because once absorption has occured, the treatments are less than 50% successful.
|
|
|
Would you ever induce emesis in paraquat poisoning?
|
NO. concentrated solutions are corrosive.
|
|
|
Would you use gastric lavage in paraquat poisoning?
|
YES! May be life-saving if used alongside AC.
|
|
|
What is warfarin used in that may lead to exposure causing poisoning?
|
Rodenticides.
|
|
|
What is the MOA for toxicity in warfarin poisoning?
|
Antagonizes the action of Vitamin K in activating clotting factors. This induces bleeding, which may be hemorrhagic at higher doses.
|
|
|
What is the treatment protocol for warfarin poisoning?
|
MASSIVE doses of Vitamin K (50-800mg/day) for several months.
|
|
|
What potential toxin is used as a fumigant to kill insects, nematodes, weed seeds, and fungi in soil and silo-stored foods?
|
Methyl bromide
What is often added to the formulation of methyl bromide as a precaution since the chemical is odorless? |
Lachrymator |
|
Where do the major toxic effects occur in methyl bromide poisoning?
|
CNS: headache, visual disturbances, seizures, CNS depression and coma
What toxic effect is produced if respiratory exposure occurs? |
Pulmonary edema |
|
Is there a specific antidote or treatment protocol available for methyl bromide?
|
NO. Treatment is symptomatic.
|
|
|
Exposure to what chemical can cause Opisthotonus?
|
Strychnine.
What IS opisthotonus? |
a spasm where the head and heels arch backward in extreme hyperextension |
|
How does death occur in cases of strychnine toxicity?
|
Respiratory paralysis.
how does tha paralysis occur? |
strychnine acts at the postsynaptic receptor in motor neurons of the spinal cord's neural horn to antagonize inhibitory tone. This leads to powerful and uncontrollable muscle contractions (spastic paralysis) |
|
It is essential to treat strychnine poisoning immediately by...?
|
Minimizing external stimulation and supporting respiration with diazepam
|
|
|
Gasoline, kerosene, turpentine, mineral oil are all examples of what?
|
Petroleum hydrocarbons.
What is the major toxic effect of these chemicals? |
CNS depression |
|
In cases of acute gasoline inhalation, what are the toxic effects at low doses, vs high doses?
|
Low dose: dizziness and coordination problems
High dose: CNS depression, convulsion, coma, death What are the 2 reasons death can occur? |
Asphyxia. Gasoline sensitizing the myocardium to epinephrine causeing ventricular fibrillation (fatal arrythmia) |
|
What is the most common route of exposure that physicians see when it comes to petroleum hydrocarbon poisoning?
|
Oral ingestion, usually of charcoal lighter fluid
What is one of the concerns with vital functions to consider with lighter fluid ingestion? |
Pulmonary aspiration. Monitor the airway! |
|
How often do you see significant CNS symptoms in cases of petroleum hydrocarbon oral ingestion?
|
Rarely, usually need LARGE volumes to produce significant systemic effects.
Major concern is pulmonary aspiration, since patient may vomit. |
|
|
What is the treatment protocol for oral exposure of petroleum hydrocarbons.
|
No specific antidote. Mostly symptomatic treatment (supplemental oxygen, antibiotics, steroids)
DO NOT lavage unless poisoning is severe. DO NOT induce emesis to avoid aspiration and chemical pneumonitis |
|
|
What does CHAMP stand for?
|
Camphor
Halogenated Hydrocarbons Aromatic Hydrocarbons Metal additives (arsenic, mercury) Pesticide Additives (organophosphates) |
|
|
What systemic toxic effect should you be worried about if a patient comes in with an acute poisoning after working in an organic chemistry lab full of BENZENES?
|
Cardiac arrythmias secondary to myocardial sensitization and CNS depression.
|
|
|
Both petroleum hydrocarbons and halogenated/aromatic hydrocarbons can cause cardiac arrythmias. But what is the major difference in their absorption qualities?
|
Petroleum hydocarbons are not readily absorbed in the GI tract.
Aromatic/Halogenic hydrocarbons ARE readily absorbed in the GI |
|
|
Would you be more likely to induce gastric emptying in a patient suffering from benzene poisoning or from gasoline poisoning?
|
More likely to consider Gastric Emptying for Benzene poisoning, since it is an aromatic hydrocarbon. Aromatic/halogenated hydrocarbons are readily absorbed in the GI tract.
|
|
|
In lead poisoning cases, is the problem usually acute or chronic exposure?
|
Chronic.
Why? |
Long half life enables the metal to slowly accumulate to toxic concentrations, making it difficult to determine the source of exposure |
|
What do you need to be particularly concerned about in a child suffering from lead poisoning?
|
CNS effects. They tend to be more sensitive because the Pb can cause the BBB.
|
|
|
Where does Pb initially bind in the body?
What about later? |
to hemoglobin on RBCs
Later it redistributes to bone, teeth and hair where it's half life is about 25 years |
|
|
What is the most serious manifestation of lead poisoning (CNS)?
|
Lead encephalopathy.
What are the early signs of toxicity? |
clumsiness, vertigo, ataxia, headache, restlessness, irritability progressive central neuropathy may involve vomiting, seizures, delirium |
|
major GI symptoms of Pb poisoning?
|
loss of appetite, constipation.
lead colic (severe abdominal pain) Gingival lead lines (especially if poor dental hygeine. Are GI problems more common in adults or children? |
Adults |
|
What are the major neuromuscular symptoms of lead poisoning?
|
Lead Palsy:
wrist drop!!! muscle weakness, quick muscle fatigue in active muscle groups: extensors of forearm, wrist, fingers, extraocular muscles. |
|
|
What are some hematological effects of lead poisoning that are diagnostically helpful?
|
-Inhibits delta ALA dehydratase --> elevated ALA levels in urine.
-Inhibits ferrochelatase --> zinc-protoporphyrin is fluorescent -hypochromic microcytic anemia with possible basophilic stippling |
|
|
Renal effects of Pb poisoning?
|
nephropathy, interstitial fibrosis.
hyperuricemia with gout |
|
|
What is the most useful screening and diagnostic tool to determine lead poisoning?
|
Blood Lead Level (BLL). Level also determines what actions need to be taken in treatment
|
|
|
What type of treatment needs to be administered in severe lead poisoning cases?
|
Removal from exposure/lead abatement.
chelation therapy: EDTA is preferred (in combo with BAL if severe poisoning). Succimer may be useful in kids without encephalopathy Penicillamine. |
|
|
Will BLL be useful if the patient is suffering from organic lead poisoning rather than inorganic?
|
NO! The BLL remains nearly normal in organic poisoning.
What are the major symptoms of acute organic lead poisoning? |
rapidly progressive CNS symptoms: insomnia, nightmares, anorexia, NV, diarrhea, muscular weakness, emotionally volatile |
|
Which type of lead poisoning tends to be acute and which tends to be chronic?
|
acute: organic lead poisoning
chronic: inorganic lead poisoning |
|
|
Name some sources of inorganic arsenic.
|
coal, metal ores, herbicides, seafood, drinking water, pressure-treated wood.
|
|
|
Where is the highest content of inorganic arsenic distribution?
|
hair and nails (may see Mee's lines in chronic poisoning)
|
|
|
Which form of inorganic arsenic has higher toxicity? Trivalent or Pentavalent?
|
Trivalent (arsenites) > Pentavalent (arsenates)
|
|
|
Which type of inorganic arsenic (trivalent or pentavalent) causes uncoupling of mitochondrial ox phos?
|
Pentavalent (arsenates)
|
|
|
A person presents with severe nausea and projectile vomiting and recent history of rice-water stools with some blood. While in your care, they start to convulse and you note pulmonary edema has begun to develop. What type of poisoning do you suspect?
|
Acute inorganic arsenic poisoning.
If your patient survives, what might they still suffer from after recovery? |
Bone marrow depression, severe neuropathy, encephalopathy |
|
What are the common symptoms of chronic arsenic poisoning?
|
weight loss
hair loss muscle weakness and aching garlic odor to breath and sweat sensorimotor peripheral neuropathy (stocking and glove pins and needles) GI is less prominent than in acute poisoning. Usually non-specific |
|
|
What skin changes tend to be hallmark of chronic arsenic poisoning?
|
Hyperpigmented palms and soles, and mee's lines in nails (hyperkeratosis)
|
|
|
If a patient's lab work shows pancytopenia, what does it indicate, and what poisoning may cause it?
|
Indicates BM suppression.
Can be caused by both acute and chronic arsenic poisoning. |
|
|
A patient with chronic arsenic poisoning is at an increased risk for what?
|
Several cancers: lung, skin, bladder
|
|
|
Treatment protocol for ingestion arsenic poisoning:
|
Key is to limit exposure and empty stomach:
gastric lavage in hospital activated charcoal supportive treatment chelation therapy: BAL, Penecillamine, Succimer in children |
|
|
What poisoning produces rapid, severe hemolysis and is often fatal?
|
Arsine gas (organic arsenical)
what is the prognosis for patients who survive the rapid hemolysis and extensive hemolytic anemia? |
Poor. Surviving patients often have renal failure, which can be fatal. |
|
Are chelating agents helpful to treat arsine gas poisoning?
|
Nope.
What about dialysis? |
Nope. arsine complexes with Hb and can't be dialyzed. |
|
Mercury has primary effects on:
|
CNS
Kidneys |
|
|
Are chelating agents helpful to treat arsine gas poisoning?
|
Nope.
What about dialysis? |
Nope. arsine complexes with Hb and can't be dialyzed. |
|
Which form of mercury readily crosses the BBB?
|
Elemental (vapors enter via lungs and cross BBB). Inorganic does NOT.
|
|
|
Classic Triad of effects in chronic mercury vapor poisoning?
|
Neuropsychiatric disorders, tremors, gingivostomatitis.
|
|
|
Describe Erethism:
|
bizarre behavioral symptoms associated with chronic mercury poisoning.
-shyness, withdrawal, depression, explosive anger |
|
|
What is the treatment protocol for mercury vapor poisoning?
|
Remove from exposure
Monitor pulmonary function Chelation with: succimer (preferred) penecillamine dimercaprol (BAL) |
|
|
What is the most common and most concerning effect of acute inorganic mercury ingestion?
|
Renal toxicity. Acute tubular necrosis.
|
|
|
What is the treatment for acute inorganic mercury poisoning?
|
Supportive therapy
NO lavage or emesis unless ingestion is VERY recent. Chelation therapy: Succimer is preferred |
|
|
What problems do you tend to see in a patient who has chronic inorganic mercury poisoning?
|
Renal damage (predominant problem)
Acrodynia (pink disease): erythema of extremities, severe leg cramps, paresthesias, and painful pink fingers. Young children mostly Tachycardia GI problems CNS problems as seen with mercury vapor |
|
|
What effects are seen with chronic exposure to organic mercurials?
|
CNS effects predominate
|
|
|
What are the first symptoms of acute iron poisoning?
|
Within 30 minutes:
GI damage (necrotizing gastroenteritis) Abdominal pain, Diarrhea, vomiting, cyanosis, acidosis, CV collapse, DEATH |
|
|
If patient survives the first 6 hours of acute iron poisoning, what follows?
|
apparent recovery in 12-24 hours followed by death. Rarely survival... but still, a few weeks later: hepatic damage, GI damage and obstruction
|
|
|
Treatment for Acute Iron Poisoning?
|
Empty the stomach: lavage or emesis if shortly after ingestion
Xrays to see how many pills are in the GI tract Deferoxamine chelation Supportive measures |
|
|
What is EDTA primarily used to treat?
|
Lead poisoning
Is it useful in Hg, As, or Fe poisoning? |
NO |
|
What is the major side effect to worry about in EDTA?
|
Nephrotoxic at high doses.
Also, given in disodium Ca form, to prevent hypocalcemia from occuring |
|
|
What is Dimercaprol (BAL) used to treat?
|
arsenic, mercury or lead poisoning.
|
|
|
What are the side effects of BAL (dimercaprol)?
|
hypertension, tachycardia
NV, fever, headache anxiety |
|
|
What is succimer used to treat?
|
useful in lead, arsenic and mercury poisoning.
Orally effective |
|
|
What is penicillamine used to treat?
|
copper, mercury poisoning
adjunct in lead and arsenic poisoning. Treatment of Wilson's Disease |
|
|
Adverse effects of Penicillamine?
|
Allergic
Hematological tox: may be fatal renal toxicity |
|
|
Deferoxamine use:
|
Iron chelation.
Adverse effects? |
Red urine, allergic neuro/nephrotox (rare) |
