Hydrocarbon/metal Poisen

Front 1

what are normal household sources of hydrocarbons?

Back 1

kerosene, gasoline, lighter fluid, furniture polish, insecticides.
ii. Used as solvents, fuels, degreasers, pesticides, and as “décor.”

Front 2

what are the two factors that influence hydrocarbon toxicity?

Back 2

a. Related to volatility and viscosity.

Front 3

what is the factors associated with high risk of toxicity in hydrocarbons?

Back 3

b. High volatility and low viscosity increase the risk for toxicity.

Front 4

what are some examples of high risk for toxicity hydrocarbons?

Back 4

i. Kerosene and gasoline are highly volatile and of low viscosity.

Front 5

what issues can result from exposure to kerosend and gasoline?

Back 5

They are capable of causing aspiration pneumonia and acute respiratory distress syndrome.

Front 6

what are low risk toxicity hydrocarbons?

Back 6

ii. Crude oil, petroleum, and mineral oil are of low volatility and high viscosity. These properties impart a decreased risk of injury.

Front 7

what are the hydrocarbons associated with systemic toxicity following ingestion?

Back 7

aromatics
complex hydrocarbons
aromatic and halogenated

Front 8

what are some examples of the aromatics

Back 8

xylene or toluene

Front 9

what are some of the complex hydrocarbons?

Back 9

1. Solvents for other toxic agents, i.e. organophosphates
2. Halogenated hydrocarbons, i.e. carbon tetrachloride
a. Contain chlorine, fluorine, or bromine
b. Not all are toxic

Front 10

what are the effects of aromatic and halogenated hydrocarbons?

Back 10

1. CNS symtoms: CNS depression, sedation, lethargy, coma, confusion, ataxia, headache & seizures
2. Cardiac dysrhythmias

Front 11

what are some less toxic agents of hydrocarbons that usually dont result in systemic effects but can be an issue with aspiration or other complicatinos?

Back 11

1. Kerosene/gasoline
2. Pain thinners, turpentine, charcoal & lighter fluids
3. Mineral seal oil
4. Furniture polish

Front 12

what are the risks factors that affect severity of hydrocarbon tox

Back 12

i. Agent
ii. Route of exposure: aspiration, ingestion, inhalation, presence of voming and/or aspiration, dermal (gasoline vs. organophosphate). It is important to distinguish between ingestion and aspiration.
iii. Amount of exposure
iv. Chemical structure
v. Viscosity and volatility
vi. Age of the patient

Front 13

what are the primary sites of damage in hydrocarbon exposures?

Back 13

contact injury-eye/skin
GI irritation
renal tubular damage
pulmonary adverse effects

Front 14

what is the most common and most critical site of damage in hydrocarbon exposure?

Back 14

pulmonary

Front 15

what types of hydrocarbons most commonly cause renal tubular damage?

Back 15

highly volatile compounds

Front 16

why are hydrocarbons dangerous for the lungs?

Back 16

2. Low surface tension and low viscosity allows a small amount to spread over a large pulmonary surface. Therefore the hydrocarbons with the lowest viscosities produce the greatest lung injury.

1. Pathogenesis is alteration or destruction of surfactant.
2. See an inflammatory reaction.

Front 17

what is normal progression of pulmonary symptoms in hydrocarbon aspriation/inhalation?

Back 17

1. Cough
2. Tachypnea
3. Wheezing
4. Changes in respiration – increased work of breathing with retractions
5. Evidence of pneumonitis clinically and on CXR in 6-12 hours

Front 18

what is a possible additional lung issue that can result from hydrocarbon exposures?

Back 18

iv. Secondary bacterial pneumonia and chronic respiratory disease may occur.

Front 19

what should be done in case of hydrocarbon ingestion?

Back 19

DO NOT INDUCE EMESIS
b. It is not necessary to remove most simple hydrocarbons from the stomach.
c. Aromatic or complex hydrocarbons may necessitate lavage. It is important to protect the airway by placing a cuffed ETT before the lavage tube is passed.
d. Charcoal is not useful for aliphatic and alicyclic hydrocarbons. It may bind significant quantities of some aromatic and substituted hydrocarbons.

Front 20

what is the antidote for carbon tectrachloride?

Back 20

acetylcysteine (Mucomyst)

Front 21

what ist he antidote for methemoglobin formers?

Back 21

methylene blue

Front 22

what is the treatment for leaded hydrocarbons?

Back 22

chelations

Front 23

what do you treat seizures with?

Back 23

benzodiazepams

Front 24

how do you treat hydrocarbon induced pneumonitis?

Back 24

O2 not antibiotics or steroids

Front 25

what is the peak age of inhalation abuse of hydrocarbons?

Back 25

13--16

Front 26

what is the main cause of death in inhalation abuse

Back 26

sudden sniffing death syndrome

Front 27

what are some inhalents of abuse?

Back 27

i. Any hydrocarbon can have mind-altering effects when inhaled in large doses.
ii. Liquids: model glue, adhesives, gasoline, contact cement, laquers, dry-cleaning fluids
iii. Aerosols: compressed air for cleaning computer keyboards, paints, butane fuel, cooking sprays, cosmetics, toiletries, cool whip
iv. Air fresheners
v. Fire extinguishers
vi. The most popular substance used is specific to the region

Front 28

what is the pathophysiology of inhalents?

Back 28

i. Solvent vapors are readily absorbed from the lungs and reach high concentrations in the CNS (high lipid solubility).
ii. Inhalants are depressants and are pharmacologically related to anesthetic gases

Front 29

what is sudden sniffing death syndrome?

Back 29

Sudden sniffing death syndrome” is a result of hydrocarbon induced myocardial sensitivity to epinephrine. There is a sudden surge of epinephrine secondary to the startle reflex with a resultant fatal cardiac dysrhythmia.
1. About 20% of deaths occur with first exposure.
2. Fairly commonly seen with butane.

Front 30

what is most common cause of sudden sniffing death syndrome?

Back 30

butane

Front 31

what are the CNS effects of inhalents?

Back 31

h. CNS Effects: vivid hallucinations, appearance of intoxication, euphoria, feeling of omnipotence, clouding of consciousness, seizures, tinnitus, slurred speech, headache, sedation, coma(rare)

Front 32

what are some clinical findings that may suggest inhalent abuse

Back 32

age13-16
dermal-perioral pyoderma
ii. Chest pain, dysrhythmias
iii. Pulmonary:
1. Laryngospasm
2. Conspicuous odor of the inhalant
3. Asphyxia or pneumonitis

Front 33

what are some organic findings with inhalents?

Back 33

i. CNS damage with dementia and cerebellar damage
1. Loss of cognitive and other higher functions
2. Gait disturbances
3. White matter degeneration and loss of brain mass

Front 34

what is a specific toxicity of toluene?

Back 34

i. Toluene: deafness, metabolic acidosis, decreased visual acuity, toxic hepatitis, embryopathy

Front 35

what is a specific toxicty of hexane?

Back 35

ii. Hexane: peripheral neuropathy

Front 36

what is a specific toxicity of paint pigments

Back 36

lung damage

Front 37

what is a specific tox of benzene

Back 37

aplastic anemia

Front 38

what are some treatments for inhalents?

Back 38

ABCs-airway,breathing,cardiac

oxygen
anticonvulsants
antidysrhythmics
decontamination
prevention through education

Front 39

what are bath salts?

Back 39

a. Definition: relatively new synthetic cathinone
i. It could be purchased legally on the internet, in smoke houses, gas stations, and convenience stores because it was able to evade the illegal status of methamphetamines. In these locations it was marketed as bath salts, plant food, and insect repellants.
ii. The DEA made it illegal in September 2011.

Front 40

what is the CNS penetration of cathinones?

Back 40

i. Contain a ketone group on the beta carbon which causes decreased CNS penetration and less potency.
1. May lead to overdose or increased adverse effects.

Front 41

what are the main components of most cathinones?

Back 41

ii. The product usually contains either methyelnedioxypyrovalerone (MDPV) or 4-methylmethcathinon (Mephedrone)

Front 42

what does MDPV or mephedrone do?

Back 42

release and inhibit the reuptake of serotonin, dopamine, and norepinephrine.

Front 43

what are cathiones similar to?

Back 43

iv. They produce a sympathomimetic toxidrome, meaning that the clinical effects mimic drugs that are structurally similar to methamphetamines.

Front 44

what are symptoms of cathiones?

Back 44

v. Symptoms include euphoria, empathy, bruxism, agitation, tachycardia, delusions, increased sexual desire, panic, and hallucinations.

Front 45

what is iron suppliments used for

Back 45

b. Used to treat anemia, as prenatal supplementation, or in combination with other daily vitamin supplements.

Front 46

how much iron usually in a multivitamin?

Back 46

ii. Multivitamins usually contain 15-18 mg elemental iron/tablet.

Front 47

how much iron is in a prenatal vitamin

Back 47

iii. Prenatal vitamins contain 65 mg elemental iron/tablet.
1. If children ingest mom’s prenatal vitamins, they get a large dose of elemental iron.

Front 48

what is the minimum dose of iron that will cause mild symptoms?

Back 48

20mg

Front 49

what dose of iron can be moderate to severe symptoms?

Back 49

60-100

Front 50

what dose is life threatening and what is considered lethal dose?

Back 50

greater than 100 life threatening
lethal over 180

Front 51

what is the absorption order for iron?

Back 51

first order

Front 52

how is iron transported?

Back 52

transported to RES bound to transferrin

Front 53

how is iron excreted by the body?

Back 53

iii. Excretion is via desquamation of the skin, blood loss, and excretion into bile.
1. Fixed daily loss is 1 mg, but can increase to 2 mg/day in iron overload

Front 54

what is the pathologic effect of iron overload on the stomach and small intestine?

Back 54

a. Stomach and small intestine
i. Corrosive mucosal damage initially.
1. Hydrogen ion production
2. Generation of vasoactive substances such as histamine, serotonin, and ferritin. The end result is vasodilation with subsequent venous pooling, low CO, and shock. This may cause hemorrhagic necrosis and perforation

Front 55

what is the pathologic issue with circulatieng free iron?

Back 55

b. Circulating free iron
i. Disrupts mitochondrial function and cellular metabolism by uncoupling oxidative phosphorylation and interfering with the electron transport chain.
ii. Free radical formation can damage membranes via peroxidation. This is due to iron’s capacity for oxidation/reduction reactions.
iii. Lactic acidosis may develop

Front 56

what is irons effects on the CNS

Back 56

direct CNS depression

Front 57

what is a late complication in the stomach with iron poisening?

Back 57

d. Pyloric stenosis is a late finding as a result of scarring. It may subsequently lead to gastric outlet obstruction.

Front 58

what occurs in phase 1 of iron poisening(0-6hours)

Back 58

b. Phase I (0-6 hours after ingestion)
i. Early symptoms
1. GI – avdominal pain, nausea and vomiting, hematemesis, hemorrhagic diarrhea, melena
2. CV – tachycardia, hypotension
3. Other – pallor, fever, hyperglycemia, leukocytosis, acidosis
ii. Massive fluid loss leading to shock, renal failure, and death.
iii. Poor prognostic signs include shock, coma, or hypotension during this period.

Front 59

what occurs in phase 2(6-24H) of iron poisen

Back 59

c. Phase II (6-24 hours after ingestion)
i. Temporary recovery for 2-24 hours
ii. Metabolic acidosis
iii. Lethargy
iv. There is debate about the existence of this latency phase

Front 60

what does it mean if there are no symptoms within 6 hours of iron poisening?

Back 60

iv. If there are no symptoms within 6 hours of ingestion, it is very unlikely that the patient will develop symptoms.

Front 61

what occurs in the third phase of iron poisening (8-48H)

Back 61

i. Abrupt relapse of symptoms
1. GI - persistent GI symptoms, hepatic necrosis
2. CNS – obtundation, coma, seizures
3. Pulmonary edema/hemorrhage
4. Shock
5. Metabolic – refractory metabolic acidosis, hypoglycemia
6. Renal tubular dysfunction
7. Clotting abnormalities – depress activity of factors V, VII, IX, and X

Front 62

what occurs in phase 4 of iron poisening(2days-3weeks)

Back 62

e. Phase IV (2 days to 3 weeks after ingestion)
i. Late symptoms
1. ARDS
2. Cirrhosis
3. Sepsis (Y. enterocolitica): damage to mucosa allows bacteria to move from the intestine to the bloodstream
4. Gastric scarring with pyloric stenosis

Front 63

how is iron poisoning diagnosed?

Back 63

i. Serum iron obtained 4-6 hours after ingestion can predict the severity of the poisoning. A repeat serum iron level in 8-12 hours after initial level should be done to determine if there is delayed absorption.

Front 64

what are the iron levels at the various phases of iron poisoning?

Back 64

1. Iron levels do not correlate with phases of toxicity.

Front 65

what is not a reliable measure of iron during overdose?

Back 65

TIBC

Front 66

what are the serum iron concentrations assciated with the different levels of toxicity?

Back 66

less than 350 -not toxic
350-500 mildly toxic
500-1000 moderately toxic
greater than 1000 life threatening

Front 67

at what serum iron level should patients be treated?

Back 67

Treat if serum level is 500 or above, or at a lower serum level if symptoms are present

Front 68

what are some other diagnostic tests that can be useful in a case of iron poisoning?

Back 68

CBC,hepatic and renal function test, coagulation studies, abdominal Xray, barium swallow.

Front 69

what will be seen on CBC and MP for iron poisoning?

Back 69

1. Metabolic acidosis with high anion gap
2. Blood glucose > 150 mg/dl
3. WBC > 15,000/mm

Front 70

what will be seen on abdominal xray in iron poisoning?

Back 70

1. Radiopaque pills/fragments will be seen only if pure iron tablets are ingested.

Front 71

who should followup with barium swallow

Back 71

iv. Follow-up barium swallow – late in course
1. Patients with significant GI symptoms
2. Patients with prolonged GI exposure to iron

Front 72

how is iron poison decontaminated?

Back 72

i. Decontamination
1. Emesis or lavage is not usually indicated.
2. Cathartic or GI lavage (WBI) may be of value, especially in large ingestions to expel undissolved tablets. (Risk of bezoar.)

Front 73

what is the antidote for iron poisoning?

Back 73

ii. Chelation with Deferoxamine

Front 74

how does chelation with deferoxamine work?

Back 74

3. It works by pulling iron out of mitochondria and cells by mass action and forming water-soluble ferrioxamine which is renally excreted.

Front 75

when should chelation be stopped?

Back 75

4. Discontinue use when the urine color is back to normal and serum iron is <100-150 mcg/dl.

Front 76

what are some adverse effects of chelation with deferoxamine?

Back 76

5. Adverse effects:
a. Hypotension if infused too rapidly
b. Allergic reactions

Front 77

what are the main inhalents that are abused?

Back 77

propellants

Front 78

what organism is most common for late phase 4 sepsis in iron overdose?

Back 78

y. enterocolitica

coming to blood by invasion from GI tract due to mucosal damage

Front 79

what is an issue with basing treatment of iron overdose on serum iron?

Back 79

intracellular iron burden produces systemic tox not the iron in the blood.

we can't measure the intracellular iron so we exptrapolate based on what is in the serum.