Toxicology Flashcards
(129 cards)
1
Q
What defines a poison/toxic substance?
A
DOSE
All substances are poisons, but dose separates a poison from a remedy.
2
Q
Acetaminophen intoxication antidote?
A
N-acetylcysteine
3
Q
Anticholinergic intoxication antidote?
A
Physostigmine
4
Q
BNZ’s intoxication antidote?
A
Flumazenil
5
Q
Black widow spider bite antidote?
A
Latrodectus Antivenin
6
Q
Beta Blocker intoxication antidote?
A
Glucagon
Insulin + Glucose
7
Q
CCB intoxication antidote?
A
Calcium
Glucagon
Insulin + Glucose
8
Q
Cyanide intoxication antidote?
A
Hydroxycobalamin
9
Q
Cyanide or Hydrogen Sulfide intoxication antidote?
A
Na Thiosulfate + Nitrate
Hydroxycobalamin
10
Q
Digitalis Glycosides intoxication antidote?
A
Digoxin-specific Fab
11
Q
Ethylene Glycol intoxication antidote?
A
Fomepizole, Thiamine
12
Q
Hydrofluoric acid (HF) intoxication antidote?
A
Calcium gluconate
13
Q
Iron intoxication antidote?
A
Deferoxamine (and Deferasirox)
14
Q
Isoniazid, Hydrazine, + Monomethylhydrazine intoxication antidote?
A
Pyridoxine (Vitamin B6)
15
Q
Lead intoxication antidote?
A
DMSA (Succimer)
EDTA
16
Q
Methanol intoxication antidote?
A
Ethanol, Fomepizole
17
Q
Methemoglobin-forming agents intoxication antidote?
A
Methylene Blue
18
Q
Opioid intoxication antidote?
A
Naloxone, Nalmefene
19
Q
Organophosphates and Carbamates intoxication antidotes?
A
Atropine, Protopam (Pralidoxime)
20
Q
Rattlesnake bite antidote?
A
CroFab Antivenin
21
Q
Serotonin Syndrome antidote?
A
Cyproheptadine
22
Q
Sulfonureas intoxication antidote?
A
Octreotide
23
Q
TCAs intoxication antidote?
A
Na Bicarbonate
24
Q
Valproic acid intoxication antidote?
A
Carnitine
25
Arsenic, Lead, Mercury intoxication antidote?
Dimercaprol
Succimer (DMSA)
d-Penicillamine
26
Toxic substance must show what?
Causal Relationship (Hill Criteria)
27
Effect of toxicant in the body
Look at diagrams on slides 6 and 7
28
Majority of toxin intoxication is _________?
Accidental--> pt misuse, delivery from caregiver, etc
29
What determines which substance are the most frequent etiologies of toxicity?
Accessibility
| reflects accessibility rather than inherent toxicity
30
What are the mc culprits of toxicity in pediatric patients (5)? Why?
Cosmetics & Cleaning Products > Medicines (prescription & OTC) > Art supplies & other household materials
Kids are closer to the ground and try to eat everything.
31
What are the mc culprits of toxicity in adult patients? (6)
Analgesics = Sedative/Hypnotics > Antidepressants = CV Drugs > Alcohol > Pesticides
32
What is the special dose issue of toxins in kids?
Drugs are potentially lethal in small children in small amounts.
Kids have increased water volume & decreased fat, leading to reduced dose required for intoxication.
33
How are pt's suffering from intoxication by a toxin normally managed in the ER?
Decontamination only >> Observation only > No Therapy > Decontamination + Therapy > Therapy only
***No need to treat unnecessarily--> worsen situation--> death
34
General management of intoxicated pt?
```
1. ABCDEFG:
Airway
Breathing
Circulation
Disability-AVPU/Glasgow Coma Scale
DEFG-- Don't Ever Forget Glucose
Get a set of basic observations
```
```
2. Use all your senses to look for clues
Look--track marks, pupil size
Hear--type of breathing (Kussmaul, Hyperventilation)
Feel-- temperature, sweating
Smell-- Alcohol? Fruity?
Dont taste anything
```
35
3 Specific Strategies in the mgmt of intoxicated pt?
1. Decrease absorption (only if toxicant is not already 100% absorbed)
2. Increase elimination (if toxicant is already 100% absorbed)
3. Use a specific antagonist
36
What are some specific antagonists used? What are they used for? (5)
1. Deferoxamin-->Irone
2. Naloxone-->Opiates
3. N-Acetylcysteine--> Acetaminophen
4. Digibind-->Digoxin (digitalis glycosides)
5. Flumazenil-->Benzodiazepines
37
Two treatments used for gastric decontamination?
1. Activated Charcoal (SDAC)
| 2. Syrup of Ipecac
38
How does Activated Charcoal work to promote gastric decontamination?
Drug/toxin is absorbed onto the large surface area and then excreted in feces
39
2 key considerations in the use of Activated Charcoal for gastric decontamination?
1. Airway Protection is ESSENTIAL-->w/out airway protection--> vomit charcoal-->aspiration-->death
2. Must be used w/in 1 hour of toxin ingestion (ineffective for drug that is already absorbed)
(3. May be unnecessary depending on drug/dose, routine use is not recommended)
40
What is Syrup of Ipecac and how does it work?
OTC Extract from Cephaelis plant--> alkaloids emetine & cephaeline-->Potent Emetics-->emesis w/in 20 minutes that lasts 30-120 minutes
41
Key considerations in the use of Syrup of Ipecac?
Effects are highly time-dependent--> have to use w/in 30 minutes of ingestion (ineffective for toxin already absorbed)
42
ADEs/Issues w/ Syrup of Ipecac?
1. Acute Use: few ADEs--> drowsiness, abdominal pain, diarrhea
2. Ipecac Abuse--> Anorexic/Bulimic pt's, Moms of children w/ Munchausen syndrome by proxy
3. Persisten/prolonged vomiting-->dehydration, hypochloremia + metabolic alkalosis due to loss of hydrochloric acid
4. Cardiotoxicity w/ chronic systematization--> conduction irregularities, fibrillations, hypotension, possible myocarditis, CHF (these may require the use of cardiac glycosides and pacemakers)
43
Efficacy of gastric decontamination?
No conclusive data support the routine use of gastric decontamination in the poisoned pt.
For asymptomatic pt, the greatest risk is for iatrogenic complications.
GI decontamination should be targeted at pt's who have a potentially LIFE-THREATENING EXPOSURE.
44
2 other methods to decrease the absorption of toxins?
1. Gastric Lavage
| 2. Whole Bowel Irrigation
45
a. What is Gastric Lavage? Where does it work?
b. What is a key consideration w/ GL?
c. Complications of GL? (3)
a. Instill/remove (flush) several liters of H2O via large-bore orogastric tube. Only acts in stomach, not on any toxin that may be in duodenum.
b. Pt's must be able to maintain airways b/c large tube might impair airways and increase aspiration risk
c. Complications: GI perforation, Hypoxia, Aspiration
(No benefit of GL + SDAC in the mgmt of undifferentiated acute poisioning)
46
a. What is Whole Bowel Irrigation?
b. What is it useful for?
c. Key consideration?
d. Contraindications? (5)
e. Adverse Effects?
a. 1-2 L/hr isotonic PEG electrolyte lavage solution
b. Speeds up elimination of sustained-release or enteric-coated drug preparations
c. Not for use w/ unprotected airway
d. CI's: Bowel obstruction of perforation, Hemorrhage, Ileus, Hemodynamic instability, Intractable vomiting
e. Adverse Effects: GI-->N/V, abdominal cramps, bloating
47
2 methods to increase elimination of already absorbed toxins?
1. Hemodialysis
| 2. Hemoperfusion
48
a. For what type of toxins is hemodialysis effective?
b. When is it problematic?
c. For what types of poisonings is it an option? (4)
a. Effective for water-soluble, small (s
| c. Option for poisonings w/: Methanol/Ethylene Glycol, Salicylates, Lithium, Sotalol
49
Hemoperfusion:
a. How does it work?
b. What type of toxin is it useful for?
c. It is an option for intoxication with what? (4)
a. Passage of blood thru absorptive-containing cartridge (usually charcoal)
b. Removes substances w/ high degree of plasma protein binding
c. Option for intoxications w/ Carbamazepine, Phenobarbital, Phenytoin, Theophylline
50
Toxins requiring quantitative levels at a set point for Dx? (7)
ACE-HIMM
| Acetaminophen, Carbon Monoxide (CO), Ethanol/Ethylene Glycol, Heavy Metals (24 hr urine), Iron, Methanol, Methemoglobin
51
Toxins requiring quantitative serial levels for Dx? (7)
Aspirin/Salicylates, Tegretol, Digoxin, Phenobarbital, Phenytoin, Valproic Acid, Theophylline
52
Toxidrome?
Syndrome of characteristic signs and symptoms resulting from a given poison
53
Physical findings of Andrenergic intoxication?
a. Vitals: RR, HR, BP, Temp all increased
b. Mental Status: Alert, Agitated
c. Pupils: Dilated
d. Mucus Membranes: Wet
e. Skin: Diaphoretic
f. Reflexes: Increased
g. Bowel Sounds: Increased
h. Urine Output: Increased
i. Other: Possible Seizures
54
Physical findings of Anticholinergic intoxication?
a. Vitals: HR & Temp increased, BP no change (NC) or slight increase, RR NC
b. Mental Status: Depressed, Confused, Hallucinating
c. Pupils: Dilated
d. Mucus Membranes: Dry
e. Skin: Dry
f. Reflexes: Normal
g. Bowel Sounds: decreased
h. Urine Output: decreased
i. Other: Possible seizures
55
Physical findings of Cholinergic intoxication?
a. Vitals: Increased/NC RR, decreased HR, NC/decreased BP, NC Temp
b. Mental Status: Depressed, Confused
c. Pupils: Constricted
d. Mucus Membranes: wet
e. Skin: diaphoretic
f. Reflexes: Normal/decreased
g. Bowel Sounds: increased
h. Urine Output: increased
i. Other: Muscle fasciculations, possible seziures, vomiting
56
Physical findings of Opioid intoxication?
a. Vitals: decreased RR; HR/BP/Temp are NC/decreased
b. Mental Status: Depresses
c. Pupils: Pinpoint (constricted)
d. Mucus Membranes: Normal
e. Skin: Normal
f. Reflexes: Normal/decreased
g. Bowel Sounds: decreased
h. Urine Output: decreased
57
Physical findings of Sedative-Hypnotic intoxication?
a. Vitals: RR NC/decreased; HR/BP/Temp are NC
b. Mental Status: depressed
c. Pupils: normal
d. Mucus Membranes: normal
e. Skin: normal
f. Reflexes: normal/decreased
g. Bowel Sounds: normal
h. Urine Output: normal
58
Physical findings of Serotonin Syndrome (serotonergic intoxication)?
a. Vitals: RR, HR, BP, Temp all increased
b. Mental Status: Agitated, Euphoric, Hypomanic
c. Pupils: Dilated
d. Mucus Membranes: dry
e. Skin: diaphoretic
f. Reflexes: increased
g. Bowel Sounds: increased
h. Urine Output: increased/decreased
i. Other: Muscle rigidity, tremor, ataxia/loss of coordination, nystagmus
59
Sympathomimetic Intoxicants? (8)
Agents: Cocaine, Amphetamine, Methamphetamine, OTC Decongestants (Phenylpropanolamine, Ephedrine, Pseudoephedrine) Caffeine, Theophylline
60
Rx of Sympathomimetic Intoxication?
Treatment is primarily Supportive:
a. Vasodilators such as Phentolamine, Nitrates, or CCBs for HTN
b. BNZs for Agitation
c. BB + alpha-blocker to decrease cardiac stimulation/HR--> BB w/out alpha-blocker is contraindicated (unopposed alpha stimulation)
61
3 toxicities associated w/ sympathomimetic intoxication? (Im not sure if this is right or not)
Arrhythmias + Hypotension + Blunt Force Trauma
62
a. 4 Agents causing arrhythmias?
| b. Treatment? (
a) 1. Ephedrine, Amphetamines, Cocaine
2. TCAs 3. Digitalis 4. Theophylline
b) 1. BNZ + BB/vasodilatory; muscle blocker
2. Bicarb displaces drug from Na channels--> increase inward Na+
2. Vasopressor (NE) + IV fluids
3. Digibind
4. BBs/muscarinic antagonists for hypotension/tachycardia
63
a. Causes of Hypotension toxicity?
| b. Treatment? (2)
a. Reduced cardiac contractility, hypovolemia; vomiting, diarrhea, fluid sequestration, peripheral vascular collapse; alpha-R blockade; hyper or hypothermia
b. Rx: Fluid replacement, Vasopressors (like NE)
64
a. Agents increasing risk of blunt force trauma? (2)
| b. Treatment?
a. Hallucinogens, EtOH
| b. Protect airways. supportive care usually enough
65
a. What is the most toxic BB?
| b. Effects of BB toxicity?
a. Propanolol (lipophilic)
| b. Cardiodepression (decreased HR & CO) + increased/wide QRS interval--> Persisent BRADYCARDIA + HYPOTENSION
66
Rx of BB Toxicity? (4)
1. Activated charcoal only for severe cases (w/in 1hr & maintain airways or aspiration death)
2. For bradycardia/hypotensions--> IV Glucagon followed by high dose Insulin+Glucose (dextrose) infusion
3. Na Bicarbonate boluses (displace drug from Na channel-->increase inward Na+) for membrane-depressant effects (wide QRS interval)
4. IV Lipid Emulsion for severe propanolol OD--> attracts toxic drug--> excreted hepatically
67
CCB toxicity?
Hypotension + Bradycardia
68
Rx of CCB toxicity?
1. Activated charcoal
2. IV Calcium Chloride or Calcium Gluconate for bradycardia/hypotension (increased serum Ca2+ to 2x normal). Ca2+ is most effective for rx of negative inotropic effects, less effective for AV node blockade & bradycardia
3. Epinephrine + Glucagon
4. High dose Insulin + Dextrose (to maintain euglycemia)
5. Intralipid Emulsion to improve hemodynamics
69
How do CCBs and BBs affect insulin levels?
```
CCBS decrease insulin secretion via inhibition of pancreatic L-type CCs.
BBs decrease insulin secretion via inhibition of pancreatic B2-R's.
Decreased insulin (hypoinsulinemia)--> hyperglycemia
```
70
How does Insulin + Dextrose (hyperinsulinemia-euglycemia, HIE) work in Rx of BB/CCB toxicities?
1. Insulin promotes glc uptake into skel & cardiac muscle and adipose tissue
2. Shifts K+ into cells
3. HIE improves inotropy & increases PVR (unknown mech)
4. Insulin may reverse hyperglycemia, hypoinsulinemia, and acidosis due to CCB poisoning
5. Insulin increases myocardial metabolism and decreases FFA metabolism
6. Insulin may increase glc uptake by cardiac myocytes
71
a. Isoniazid (INH) Toxicity? (2)
| b. Antidote?
Toxicity:
1. Decreased brain Pyridoxal-5-Phosphate (active vitamin B6)
Decreased P5P/B6-->decreased CNS GABA--> Seizures
2. Exacerbates lactic acidosis from seizures via inhibition of hepatic conversion of lactate to pyruvate
Antidote: Pyridoxine (Vitamine B6) terminates seizures and hastens resolution of metabolic acidosis
BNZs can also help w/ seizures.
72
Acetaminophen (APAP) Poisioning Phases? (4)
Generally symptoms diminish & then get worse
a. Phase 1 (30min-4hrs): may appear NORMAL; can have anorexia, pallor, N/V, diaphoresis, malaise
b. Phase 2 (24-48hrs): Sx less severe, but RUQ Pain + Decreased Renal Function
RUQ Pain=hepatic damage--> abnormal enzyme-->increased PT
c. Phase 3 (3-5days): Hepatic Encephalopathy (Centrilobular Necrosis, Jaundice, Coagulation Defects) + Renal Failure + N/V
Death due to hepatic failure
d. Phase 4 (4days-2weeks): resolution or death
73
What is the Rumack-Matthew Nomogram for Acetaminophen Toxicity? Use?
Draw blood at set points and measure acetaminophen concentration vs time since ingestion.
Use: predicts rate of drug elimination and estimates hepatic damage w/out antidote Rx
74
Essential Points of Management of Acetaminophen intoxication?
1. Administer NAC if [acetaminophen] > "Risk Line" (~150ug/ml at 4hrs = "Treat Level")
* *Do NOT stop NAC once started** (1 loading dose + 17 maintenance doses)
2. Metoclopramide for N/V
3. APAP is present in many poly-drug OD's
4. Pt may appear normal (no sx)--> screen pt
75
2 Effects of Salicylate (Aspirin) Poisoning?
Metabolic Acidosis + Respiratory Alkalosis
1. Metab Acidosis: uncouples cellular oxidative phosphorylation--> anaerobic metabolism & excessive production of lactic acid & heat; interferes w/ several Krebs Cycle enzymes
2. Respiratory Alkalosis: stimulates brainstem causing tachypnea
76
What is unique about aspirin metabolism?
Zero-order (aspirin, phenytoin, ethanol)-->increase dose-->increase time to eliminate a constant amount
77
3 Levels of Salicylate toxicity?
1. Acute Ingestion: N/V +/- Gastritis
2. Moderate Intoxication: hyperpnea (tachypnea), tachycardia, tinnitus
3. Severe Intoxication: agitation, confusion, seizures, CV collapse, pulmonary edema, hyperthermia--> death
78
Causes of high Anion Gap Acidosis?
```
MUDPILES CAT
Methanol or Metformin
Uremia
DKA
Iron, INH, Ibuprofen
Lactic Acidosis
Ethylene Glycol
Salicylates
Cyanide
Alcohol or Acids (Valproate)
Toluene or Theophylline
```
79
Dx of/when to treat Salicylate Poisoning?
Anion Gap + Positive Stat Salicylate Test--> 100mg/dL after acute OD (more likely to have severe poisoning)
80
Rx of Salicylate Poisoning?
1. Activated Charcoal (decrease absorption)
2. Glucose-containing fluids to decrease risk of cerebral hypoglycemia
3. Na Bicarbonate for metabolic acidosis--> alkalinization of urine traps salicylate anion (and other weak acids: MTX, phenobarbital, TCA, aspirin) and enhances renal salicylate excretion.
Administer Potassium Chloride w/ Na bicarb to avoid depletion
4. Hemodialysis in severe cases with severe metabolic acidosis or altered mental status
81
a. Antidote for Serotonin Syndrome?
| b. MoA?
a. Cyproheptadine
| b. H1 antagonist (antihistamine) w/ anti-5HT activity in GI smooth muscle and CNS
82
What else is used in Rx of Serotonin Syndrome? (4)
In addition to Cyproheptadine, depending on Sx, pt may also require:
1. Diazepam/lorazepam to control agitation, seizures, muscle stiffness
2. O2 + Fluids
3. Esmolol or Nitroprusside for tachycardia or HTN
4. Phenylephrine or Epinephrine for hypotension
83
Poisonous Gases? (7)
```
1. Carbon Monoxide (CO)
2-4. Irritants: Chlorine, Ammonia, Sulfur Dioxide
5. Cyanide
6. Hydrogen Sulfide
7. Nitrogen Oxides (oxidizing agents)
```
84
Carbon Monoxide (CO):
a. Mechanism of Toxicity?
b. Clinical Features?
c. Treatment?
a. Mechanism: Binds Hb (carboxyhemoglobin), reducing O2 carrying capacity-->hypoxia
b. Features: HA, dizziness, N/V, seizures, coma
c. Rx: 100% O2
85
Irritants--> Chlorine, Ammonia, Sulfur Dioxide
a. Mechanism of Toxicity?
b. Clinical Features?
c. Treatment?
a. Mechanism: Corrosive effects on upper and lower airways
b. Features: Cough, stridor, wheezing, pneumonia
c. Rx: Humidified O2 + Bronchodilators
86
Cyanide (CN):
a. Mechanism of Toxicity?
b. Clinical Features?
c. Treatment?
a. Mechanism: Blocks O2 binding to Cytochrome C
b. Features: HA, N/V, syncope, seizures, coma
c. Rx: CN Antidote Kit
87
Hydrogen Sulfide:
a. Mechanism of Toxicity?
b. Clinical Features?
c. Treatment?
a. Mechanism: similar to cyanide
b. Features: similar to cyanide + Smell of Rotten Eggs
c. Rx: No specific antidote
88
Nitrogen Oxides (oxidizing agents):
a. Mechanism of Toxicity?
b. Clinical Features?
c. Treatment?
a. Mechanism: cause Methemoglobinemia (nitrogen oxide binds Hb-> Fe2+ to 3+ ->methemoglobin)
b. Features: Dyspnea, cyanosis, syncope, seizures, coma
c. Rx: Methylene Blue
89
Components of Cyanide (CN) Kit? (3)
Sodium Nitrite + Sodium Thiosulfate + Amyl Nitrite
90
How does Cyanide Kit work?
Inhaled Amyl Nitrite, followed by IV Na Nitrite converts a portion of Hb to methemoglobin (ferrous to ferric).
Cyanide is more strongly drawn to methemoglobin than to Cytochrome oxidase in cells. It binds to methemoglobin forming Cyanmethemoglobin.
Na Thiosulfate + Cyanmethemoglobin--> become Thiocyanate releasing Hb, and renal elimination of Thiocyanate
91
Effects of Hydrocarbon solvent intoxication?
Occurs via Skin Contact or Inhalation of volatile fumes. Hydrocarbons are typical of light industrial premises.
1. Coughing/gagging/choking w/in 30min (can be delayed several hrs)
2. HA, lethargy (weakness, fatigue), decreased mental status
3. Dyspnea or Syncope
4. Myocardial sensitization to catecholamines
5. Hepato & Renal Toxicity
6. Local Rxns (burning sensation in mouth, pruritis, perioral rash) (not uncommon, usually mild)
92
Mgmt of Hydrocarbon solvent intoxication?
1. Decontaminate + ABCs, keep calm (ID toxin if possible)
2. Supportive care
3. Intubation if resp failure occurs
4. Magnesium and K+ for arrhythmias
5. Lidocain or BBs for V-fib
93
Why is GI decontamination controversial in mgmt of pt w/ hydrocarbon solvent intoxication?
Activated Charcoal does NOT work for hydrocarbons.
Gastric Lavage may be indicated in rare situations, in a pt who is highly symptomatic from a few selected hydrocarbons, which are associated w/ severe systemic toxicity.
94
Key point in mgmt of pt w/ hydrocarbon solvent intoxication?
Decontaminate pt BEFORE transportation or else expose yourself and others.
95
Insecticides that cause toxicity?
1. Organophosphates (Malathion)
2. Carbamates (Carbofuran)
3. Nerve Gases-> Phosphates + Sarin, Soman, VX
96
Routes of intoxication by insecticides? (3)
Topical, Respiratory, and GI absorption
97
Mech of Toxicity of Insecticides? Effects? Which types have shorter effect?
a. Inhibits Acetylcholinesterase (AchE) via phosphorylation (more irreversible) or carbamoylation--> SLUDGE-BBB (salivation, lacrimation, urination, defecation, GI sx, emesis, bronchorrhea, bronchospasms, bradycardia)
b. Some phosphates target neuronal esterases--> Neurotoxicity + Paralysis
c. Carbamates have shorter effect w/ spontaneous recovery of AchE function
98
Rx of Insecticide intoxication?
1. Supportive + Atropine
| 2. Pralidoxime (Protopam/2-PAM) via slow infusion for nerve gases
99
3 Botanical Insecticides?
1. Nicotine
2. Pyrethrum
3. Rotenone
100
Nicotine botanical insecticide:
a. Routes of intoxication?
b. Mechanism?
c. Rx?
a. Route: via skin or oral absorption
b. Mech: Stimulation then depolarizing blockade of post-synaptic nicotinic receptor--> seizures
c. Rx: Symptomatic support + seizure control
101
Pyrethrum:
a. Routes of intoxication?
b. Mechansim/Toxicity? (2)
c. Rx?
a. Route: inhalation or ingestion
b. 1) CNS Toxicity: Acts on voltage-sensitive Na/Ca/Cl- channels-->excitation, convulsions, tetanic paralysis
2) Contact Dermatitis
c) Symptomatic support + seizure control
102
Rotenone:
a. Routes of intoxication?
b. Toxicity? (4)
c. Rx?
a. Route: Skin or Oral ingestions
b. Toxicity: GI irritation, rhinitis, pharyngitis, dermatitis
c. Rx: Symptomatic support
103
2 Herbicide intoxicants?
a. 2,4-Dichlorophenoxyacetic Acid (2,4-D)
| b. Paraquat
104
2,4-Dichlorophenoxyacetic Acid (2,4-D):
a. Routes of absorption?
b. Effects?
c. Rx?
a. GI>>Pulmonary; minimal cutaneous absorption
b. Breath odor, vomiting/diarrhea, HA, confusion, bizarre or aggressive behavior; progresion to coma in severe cases.
Metabolic acidosis, elevated CK, Myoglobinuria
c. Rx:
1. Symptomatic support;
2. IV fluids + forced alkaline diuresis via Na Bicarb (accelerates urinary excretion; maintain urine pH b/t 7.6 & 7.8); control for electrolyte (K+, Ca2+) loss
105
Mech of Paraquat toxicity?
slowly evolving free-radical tissue damage
106
1. Effects of Paraquat toxicity?
| 2. Rx?
1. a. Acutey: Pain/Swelling of mouth/throat + N/V, abdominal pain, bloody diarrhea
b. Slower onset (speed depends on dose): Liver/Kidney/Heart/Lung failure + Lung scarring (over several weeks) w/ pulm edema/resp failure + CNS toxicity (confusion, coma, seizures)
2. Prolonged supportive care, no antidote!
107
Caustic Acid Toxicity:
a. Mech of tissue injury?
b. mc organ affected? 2nd mc?
c. Least common organs affected?
d. Effects of toxicity?
a. Coagulation Necrosis--> eschar/coagulum sloughs in 3-4 days->replaced by granulation tissue
b. MC involved organ = STOMACH--> Emesis secondary to pyloric/antral spasm
Small bowel affected in 20%
c. Pharynx & Esophagus are relatively resistant
d. Effects: a. GI/intestinal perforation/hemorrhage b. Metabolic acidosis + Hemolysis + Acute renal failure--> Death
108
Common sources of caustic acids? (7)
Toilet bowl cleaner, Car battery liquid, Rust remover, Metal cleaner, Cement cleaners, Drain cleaners, Solder flux
109
Caustic Alkalis Toxicity:
a. Mech of Tissue injury?
b. Organs involved?
c. Effects?
a. Liquefactive Necrosis: emulsification and disruption of cell membranes
b. Epithelium of oropharynx, hypopharynx, & Esophagus (mc organ involved)
c. Effects: Airway Obstruction + Strictures
Tissue edema immediately (persists up to 48hrs)-->progresses to Airway Obstruction; granulation tissue replaces necrotic tissue-->scar tissue thickens and forms Strictures (2-4 weeks), severity depends on burn depth (perforation in extreme cases)
110
Common sources of caustic alkalis? (9)
Drain cleaner, Ammonia containing brands, Oven cleaner, Swimming pool cleaner, Dishwashing detergent, Hair relaxers, Clinitest tablets, Bleaches, Cement
111
Emergency care for Acid/Alkali toxicity?
Do nots:
a. No emetics (if it burnt going down, it will burn coming uo)
b. No Dilution of acids w/ H2O-->excessive heat
c. No Neutralization--> excessive heat & emesis
d. Activated charcoal ineffective--> causes endoscopic interference
Do's:
a. Fiberoptic-assisted Intubation
b. Gastric Lavage using large bore orogastric tube
c. Nasogastric tube (NGT) suction of liquid products
d. Dilution of solid/granular alkalines w/in 30 min
112
Sources of Lead?
a. Industrial Pollution, Vehicle exhaust, Soil & dust, paint chips, water
b. Odd exposures: Chinese tea, spices, Mexican/asian remedies, Ceramics, trinkets/candy, pool-cue chalk (yellow), fishing weights
c. Secondary exposure to kids via close contact w/ exposed caregivers
113
Mechanism of Lead toxicity/damage?
Inhibits heme synthesis (ALA Dehydratase + Ferrochelatase)--> increased erythrocyte protoporphyrin
114
Effects of Lead intoxication on organs?
L-E-A-D
1. Lines: Burton's lines + bones
2. Encephalopathy (CNS): interferes w/ PKC and nt's--> ion flux, membrane permeability, edema
3a. Anemia: micro- or normo-cytic anemia w/ reticulocytosis. Complexes sulfhydryl groups in active sites of ALA, coproporphyrinogen, and ferrochelatase.
3b. Acute GI: decreased Ach release + NKA inhibition--> decreased mobility + water flux abnormalities--> Colic + Constipation
3c. Acute Kidney damage: PT impairment--> Aminoaciduria + Glycosuria + Hyperphosphaturia
4. "Drop:" Peripheral neuropathy--> schwann cell destruction + axonal demyelination/degeneration--> slowed nerve conduction
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Rx of Lead Poisoning?
Chelation Therapy:
- Effectively lowers blood level, but unable to reverse existing damage
- NOT indicated for levels < 45ug/dL
- Rapid fall in lead blood levels, then rebound as lead is mobilized from tissue
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3 Agents used for Chelation Therapy in lead poisoning? Use/issues w/ each?
1. Succimer (DMSA) for mild/asymptomatic cases
2. Dimercaprol (BAL) for severe sx & encephalopathy
3. Calcium EDTA: ONLY used in conjunction w/ dimercaprol bc it can increase CNS lead levels; renal toxicity so maintain adequate hydration
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How can you monitor/quantify Arsenic Poisoning?
Hair (also blood and urine)
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Effects of Arsenic Poisoning?
Accumulates in liver, kidneys, heart, and lungs.
a. Chronic Exposure: derm changes--> hyperpigmentation + palmar & solar keratoses
b. Malignant change in almost all organs (most serious effect)
c. Increased risk of CV dz, PVD, respiratory dz, DM, neutropenia
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Rx of Arsenic Poisoning? Adverse effects of each?
1. Dimercaprol (BAL in peanut oil)--> 1st line;
- Issues include: Hypersensitivity, G6PD deficiency,concurrent iron supplementation
- ADEs: Nephrotoxic, sterile abscesses at injection site, fever, tachycardia, N/V, urticaria, burning sensation around mouth, diaphoresis
2. Succimer (DMSA): bead-filled oral capsule
- Problems: Hypersensitivity; hydration important bc renally excreted
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Effects of Mercury Poisoning?
1. Interstitial pneumonitis (vapor exposure)
2. Intention tremor, Inflammation of gums w/ excessive salivation, Pyschiatric sx (excitability, insomnia, irritation, shyness)
3. Acrodynia (desquamative rash) in small kids
4. Paresthesias ( esp around mouth), malaise, constriction of visual field, deafness, ataxia
5. Dose-related Nephrotoxicity--> tubular injury leading to excretion of smaller proteins that are normally filtered and then reabsorbed; ATN w/ severe exposure
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Rx of Mercury Poisoning?
1. Supportive care
2. Chelation: Dimercaprol, Succimer (chelation not effective for neuro sx)
Placebo responses (pt's w/ amalgam fillings)
3. Last resort = Exchange Transfusion
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Penicillamine uses?
1. DOC for Wilson's Dz (copper deposition)
2. Rheumatoid arthritis
3. Rarely used for iron, lead, mercury as well
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Penicillamine toxicities? (5 types)
a. Fatal thrombocytopenia, agranulocytosis, aplastic anemia, pancytopenia, sideroblastic anemia
b. Exertional dyspnea, cough, wheezing
c. Renal failure
d. Neuro deficits-->Tinnitus, neuropathy, optic neuritis, agitation, anxiety, dystonia
e. N/V, anorexia, abdominal pain, diarrhea
f. Hypersensitivity--> Erythematous or maculopapular rash
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Who typically overdoses on iron? Why?
Children overdose on iron supplements they mistake for candy
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Mechanism & Effects of Iron Intoxication? Mech
Mitochondrial toxicity-->decreased oxidative phosphorylation/dysfunction-->cell death
a. Corrosive effects on mucosa-->Hematemesis + Hemorrhagic Diarrhea--> hypovolemic shock
b. Liver damage and eventual failure (also heart, renal, lungs, hematologic toxicity)
GI toxicity w/ > 20 but < 40mg/kg ingestion
Moderate/Severe toxicity w/ > 40mg/kg
>60mg/kg may be lethal
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Stages of iron intoxication?
a. Nausea + Hemorrhagic diarrhea w/ abd pain--> hypovolemia/shock
b. At 6-12hrs: resolution of GI sx and apparent recovery-->hypotension, metabolic acidosis, coagulopathy
c. > 24hrs: metabolic acidosis (possible heart/renal failure. Venous pooling & third spacing of fluids. Increased liver enzymes and bilirubin and coagulopathy. Hypoglycemia
d. Long term: GI tract scarring w/ obstruction
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Rx of Iron intoxication? (2)
1. Deferoxamine
| 2. Deferasirox
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Deferoxamine
- IV infusion
- Does not chelate other trace metals
- Excreted in urine and bile--> red urine discoloration
- Tachycardia, Hypotension, Shock--> could add to CV collapse caused by iron toxicity
- N/V, diarrhea, abd discomfort
- Flushing, fever
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Deferasirox
- Oral suspension in water, OJ, apple juice (do not swallow tablet whole, do not chew/crush)
- Approved to Rx chronic Fe overload due to multiple transfusions
- ADEs: a. Diarrhea, nausea, abd pain, HA, pyrexia, cough
b. Increased serum Creatinine and LFTs
c. Auditory and visual disturbances
