Section 6: Drugs Flashcards

1
Q

6.1 Given an exposure, identify a drug that when ingested in small amounts is potentially life
threatening.

A

6.1 Given an exposure, identify a drug that when ingested in small amounts is potentially life
threatening.

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2
Q
  1. Cyclic antidepressants (amitriptyline; imipramine; desipramine; nortriptyline; doxepin)
A

a. Of note, imipramine is used for childhood enuresis. Comes in 150mg tabs. One tab for a 10kg toddler can be fatal.
b. amoxapine has less cardiotoicity but sz and coma are frequent presenting signs

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3
Q
  1. Phenothiazines (chlorpromazine; thioridazine; thorazine)
A

a. anticholinergic, CNS effects, quinidine like cardiotoxicity, rigidity

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4
Q
  1. Beta blockers (metoprolol; propranolol)
A

a. bradycardia/hypotension generally well tolerated in peds
b. *hypoglycemic coma and sz in peds
c. Propranolol - may cause sz and altered cardiac conductivity
d. Sotalol - may cause QT prolongation/torsades

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5
Q
  1. Calcium channel blockers (amlodipine; diltiazem; nicardipine; nifedipine, verapamil)
A

a. bradycardia and hypotension

b. cardiovascular collapse and sz (verapamil)

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6
Q
  1. Quinidine (antimalarial medication)
A

a. type 1a antiarrhythmic

b. cardiac rhythm disturbances

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7
Q
  1. Clonidine
A

a. coma, miosis, bradycardia, hypotension in children

b. patches have caused critical cardiovascular depression.

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8
Q
  1. Imidazoline eye drops
A

a. Similar to clonidine. SA node arrest

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9
Q
  1. Lomotil (combination formula - diphenoxylate and atropine)
A

a. Diphenoxylate is an opiod. 2 tabs have been fatal. Can have confusing constellation with anticholinergic component, but coma and respiratory depression are most common

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10
Q
  1. Methadone
A

a. CNS and respiratory depression

* QTc prolongation*

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11
Q
  1. Topicals
A

a. Benzocaine
i. Methemoglobinemia (cyanosis)
ii. Sz (common with local anesthetics but uncommon with benzocaine)

b. Camphor
i. CNS, resp depression, sz (usually within an hour)

c. Lindane
i. Organochlorine (chlorinated hydrocarbon)
- topical scabicide
- Sz and CNS depression when ingested
(permethrin - less toxic alternative)

d. Methyl salicylate
i. ASA toxicity

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12
Q
  1. Chloroquine
A

a. Cardiac dysfunction

1 tab/300g - fatal to a 1 y/o

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13
Q
  1. Phenylpropanolamine (amphetamine)
A

a. Common ingredient in OTC decongestants. Narrow therapeutic-toxic margin
b. B-agonist action
c. HTN with compensatory bradycardia
d. Cerebral infarction noted in adults
e. SVT in infant

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14
Q
  1. Quinine
A

a. Used to treat malaria and nocturnal muscle cramps
b. Similar to quinidine but less cardiotoxic
c. Causes direct retinal toxicity
d. Hypersensitivity reactions:
i. Blackwater fever (hemolysis, hemoglobinemia, renal failure)

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15
Q
  1. Sulfonylureas
A

a. Ex glyburide; glipizide; chlorpropamide

b. Hypoglycemia: can be delayed and persistent

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16
Q
  1. Theophylline
A

a. Used to treat asthma, COPD, apnea of prematurity

b. Sz, cardiac arrhythmias
c. Action:
i. Beta 1 and 2 stimulation
ii. Increase heart rate/contractility; bronchodilation; skeletal muscle vasodilation; uterine relaxation
iii. Inhibition of phosphodiesterase and adenosine receptors
iv. Refractory sz with decreased cerebral blood flow in OD

d. Narrow therapeutic window; Toxicity at 80-100mg/kg blood level
e. Chronic toxicity more dangerous than acute
f. Usually sustained release
g. Should draw levels Q2-4 hrs as levels can peak 12-16 hrs post ingestion
h. Caffeine OD has similar s/s and can create false positive on old blood tests

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17
Q

i. S/S of Theophylline

A

i. Mild
1. GI: n/v
2. CNS: anxiety; tremor
3. Labs: Metabolic acidosis; electrolyte abnormalities

ii. Severe
1. GI: vomiting
2. Cardiac: hypotension, dysrhythmias
3. CNS: seizures (often refractory)
4. Labs: metabolic acidosis

iii. Chronic
1. Vomiting occasionally
2. Tachycardia common
3. Hypotension rare

j. Metabolic effects (hypokalemia and hyperglycemia) do occur
k. Seizures with low blood levels

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18
Q

l. Labs (Theophylline):

A

i. LOW: potassium, phosphorus; magnesium

ii. HIGH: calcium, glucose

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19
Q

m. Treatment (Theophylline)

A

i. Supportive
ii. Consider nonselective beta blockers for tachycardia and hypotension (propranolol or esmolol)
iii. Caution for hx of asthma/wheezing
iv. Consider multi-dose activated charcoal (enteroenteric recirculation)
v. Dialysis for severe toxicity (status or level > 200mg/L)

  1. Also consider iron, antidepressants, other cardiovascular drugs, salicylates, anticonvulsants.
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20
Q

6.2 Identify the toxicity and symptoms of exposure to analgesics including over-the-counter or
prescription.

A

Analgesics, Antipyretics, and Anti-inflammatory agents:

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21
Q
  1. Acetaminophen
A

a. Normal max dose
i. 75mg/kg/day or 4g/day for a normal adult

b. Single acute ingestion toxic dose
i. Adult local referral 140 mg/kg local - national is >200mg/kg or 10g, whichever is less.
ii. Child 200mg/kg

c. High risk pts
i. Chronic alcoholics (will have more P450 thus create more NAPQI)
ii. Malnutrition (have less substrate to bind NAPQI thus creates more liver damage)
iii. Pregnant patients (fetal death)
iv. Pts taking CYP2E1/cytochrome P-450 inducers (isoniazid)
[1. This is principal enzyme responsible for breaking acetaminophen into toxic metabolites (thus inducers worsen hepatic injury)]
v. Kids < 5 y/o use sulfation pathway more; so they have less NAPQI production

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22
Q

d. S/S of OD (Acetaminophen)

A

Stage 1; (0-24hrs)
1. Anorexia, n/v

Stage 2; (24-72hrs)
1. Elevated AST/ALT (AST greater); bilirubin and PT; n/v resolve

Stage 3; (72-96hrs)
1. Hepatic necrosis with increasing AST/ALT; coagulopathy; jaundice; hepatic and renal failure; encephalopathy; death or stage 4

Stage 4; (>96hrs)
1. Healing of liver damage with resolution of enzymatic and metabolic abnormalities

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23
Q

e. Labs (Acetaminophen)

A

i. APAP 4 hrs post ingestion (for extended release check 4+6 hour levels)
ii. BUN/Cr
iii. AST/ALT
iv. PT/INR
v. Glucose

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24
Q

f. Four hr treatment level on Rumack/Matthew Nomogram

A

i. Treatment level is 150 mcg/ml
ii. Excludes chronic ingestion
iii. Excludes extended release, diphenhydramine containing, or anticholinergic products
iv. In these cases with elevated LFTs (AST usually > than ALT) start NAC with any positive APAP level

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25
Q

g. Treatment (Acetaminophen)

A

i. Activated Charcoal (<1-2 hrs)
ii. NAC (best started w/i 8 hrs)
iii. Anti-emetics (Zofran preferred)

NOTE: large OD can act as a metabolic poison and cause anion gap metabolic acidosis.

i. Dialysis is effective, but rarely used. May be consideration in later term pregnancy or with significant acidosis in massive ingestion.

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26
Q

Kings College Criteria

A

Ph < 7.3 or

INR >6.5, Cr > 3.4, and grade 3-4 encephalopathy

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27
Q
  1. Aspirin
A

a. Analgesia, anti-inflammatory, antipyretic
iii. Common forms ASA: Oil of Wintergreen (ACF - 1.39/Sp.G - 1.18), Bismuth salicylate (ACF - 0.49)
b. Delayed absorption in OD (bezoar formation)
c. Is an UNcoupler

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28
Q

d. S/S (Aspirin)

A

i. Respiratory alkalosis (protective as alkalotic environment prevents crossing into CNS)
ii. Possible metabolic alkalosis from emesis
iii. Final Metabolic acidosis from mitochondrial uncoupling
iv. GI upset, tinnitus/auditory changes, tachypnea followed by
v. Coma, seizures, hyperthermia, muscle rigidity
vi. Chronic OD more toxic

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29
Q

e. Treatment (Aspirin)

A

i. Bicarb for acidosis (Goal pH 7.5) and/or ASA > 40mg/dL (national ASA > 30 and rising)

ii. Dialysis for severe OD (level >100 mg/dL, coma, seizures).
1. dialysis for inability to tolerate fluids/bicarb treatment (renal failure or pulmonary edema)

iii. Monitor ASA; BMP level Q2H

iv. May need glucose with ASA associated AMS
1. Decreased BS in brain even when BS is normal in blood

v. Standard hydration changing to LR
1. NS could create some anion gap acidosis and increase distribution across blood/brain barrier

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30
Q
  1. Colchicine
A

a. General cellular poison, inhibits dividing cells, rapidly absorbed, extensively distributed to body tissues

b. Multiorgan effects can occur from days to weeks
i. s/s delayed 2-12 hrs in acute OD
ii. severe gastritis: abd pain, n/v/bloody diarrhea
iii. shock, sz, coma, lactic acidosis
iv. rhabdo, kidney failure, DIC
v. Late: bone marrow suppression, alopecia, myopathy, neuropathy

c. Renal insufficiency, erythromycin, cimetidine and cyclosporine inhibit colchicine clearance
d. Treatment: supportive care, AC, dialysis not effective

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31
Q
  1. Nonsteroidal anti-inflammatory drugs
A

a. Act by prostaglandin inhibition (COX inhibitors); inflammatory mediators

b. Five kinds of NSAIDS
i. Propionic acids (ibuprofen)
ii. Acetic acids (toradol)
iii. Fenamic acid (can cause seizures; requires aggressive management)
[1. Ex mefenamic acid/Ponstel]
iv. Oxicams (piroxicam)
v. Pyrazolines (require aggressive management)

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32
Q

c. S/S (Nonsteroidal anti-inflammatory drugs)

A

i. GI c/o
ii. Mild CNS disturbances (drowsiness, h/a)
iii. Massive OD
1. Sz, hypotension, metabolic acidosis, renal and hepatic dysfunction
iv. S/S may occur in children after OD >100mg/kg

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33
Q

d. Treatment (Nonsteroidal anti-inflammatory drugs)

A

i. Symptomatic
ii. Charcoal
iii. Dialysis not useful

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34
Q
  1. Opioids
A

a. Slang terms: China white, brown, superbuick, black tar, hot shot, bird’s eye, homicide
b. Use: snorted, smoked, injected, oral
c. Three receptors: Delta, Kappa, Mu
d. S/S
i. CNS and respiratory depression
ii. Miosis
iii. Noncardiogenic pulmonary edema (complication)

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35
Q

e. Atypical Opioids

A

i. Have serotonergic properties:
1. Meperidine

ii. Do not cause miosis/may cause seizures:
1. Meperidine/Demerol (sz from metabolite which accumulates with renal
insufficiency as well as from serotonergic effect)
2. Propoxyphene/Darvon (sz)
3. Tramadol (sz)

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36
Q

f. Treatment (opioids)

A

i. Supportive
ii. Narcan
1. Monitor 4-6 hrs s/p last dose of narcan. Increase time with renal insufficiency as narcan is renally eliminated.

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37
Q

g. Withdrawal (opioids)

A

i. CNS excitation (restless)
ii. GI (n/v/d/abd pain)
iii. Piloerection, lacrimation, rhinorrhea, diaphoresis
iv. ***FEVER and AMS are not associated with opioid withdrawal

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38
Q

h. Meds for opioid withdrawal (Methadone, Clonidine, Buprenorphine)

A

i. Methadone (causes QT prolongation)
ii. Clonidine (causes sleepiness/HTN followed by apnea, coma, bradycardia, hypotension)
iii. Buprenorphine (Suboxone). Has opioid antagonist and agonist in the same medication. Can trigger a mild withdrawal in an opioid using patient.

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39
Q
  1. Serotonin receptor agonists (i.e. sumatriptan)
A

a. In therapeutic use cause cerebral vasoconstriction, theoretically antagonizing cerebral vasodilation that causes migraines.
b. In overdose lose cerebral selectivity and cause excessive vasoconstriction. This causes HTN and end organ ischemia. Can cause serotonin syndrome.
c. Treatment: supportive care. Treat HTN with nitroprusside or nitroglycerin. Labetalol and dihydropyridine calcium channel blockers may be effective.
d. AC okay. Hemodialysis not effective

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40
Q
  1. Tramadol
A

a. Opioid analgesic, also inhibits norepi and serotonin reuptake

S/S:
Euphoria, CNS depression, n/v, serotonergic, sz, no miosis

Treatment:
i. Narcan, charcoal with caution d/t CNS depression, hemodialysis not effective

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41
Q

6.3 Identify the toxicity and symptoms of exposure to anticonvulsants.

A

6.3 Identify the toxicity and symptoms of exposure to anticonvulsants.

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42
Q
  1. General s/s of anticonvulsant OD
A

a. AMS (anxiety, confusion, irritability, lethargy, somnolence)
b. Ataxia
c. N/V
d. Coma, resp depression, hypotension (LARGE OD)
Anticonvulsant Hypersensitivity Syndrome
i. Seen with drugs with an aromatic amine or sulfonamides (Phenobarbital, Primidone)
ii. S/S:
- Skin eruption (SJS); eosinophilia, hepatitis, interstitial nephritis, hypothyroid

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43
Q

Carbamazepine/Oxcarbazepine (Tegratol/Trileptal)

A

a. Nystagmus, ataxia, hyperreflexia, CNS depression, dystonia, mild anticholinergic s/s

b. Can progress to coma, seizures, rhabdo, renal failure, cardiac interval changes
i. Sz potential close to therapeutic dose
ii. hyponatremia (trileptal)

c. AHS (anticonvulsant hypersensitivity syndrome)

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44
Q

Lamotrigine (Lamictal)

A

a. Sz, Rash (SJS), AHS (anticonvulsant hypersensitivity syndrome)
b. CNS depression, dizziness, ataxia, nystagmus, hypertonia, QRS prolongation, n/v, hypokalemia, fever, hepatitis, renal failure

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45
Q

Levetiracetam (Keppra)

A

a. drowsiness

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46
Q

Gabapentin

A

a. Somnolence, ataxia, dizziness, mild tremor, slurred speech, diplopia

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47
Q

Phenytoin (Dilantin)

A

a. Rash (DRESS), IV formulation causes cardiotoxicity, AHS (anticonvulsant hypersensitivity syndrome)
b. IV use: bradycardia, hypotension, dysrhythmias. Cardiotoxicity believed from diluent propylene glycol/Na channel blockade
c. Oral: n/v, *NYSTAGMUS, ataxia, CNS depression
d. Chronic use risk of DRESS (resembles viral infection with multiorgan/system involvement)

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48
Q

Pregabalin (Lyrica)

A

a. Limited data. Large ingestions minimal symptoms. CNS depression to coma.

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49
Q

Tiagabine

A

a. Somnolence, confusion, agitation, dizziness, ataxia, tremor, clonus, sz

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50
Q

Topiramate (Topamax)

A

a. Sz, non AG acidosis, hyperkalemia

b. Sedation, confusion, slurred speech, ataxia, tremor, anxiety, sz

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51
Q

Valproic Acid (Depakote)

A

a. Hyperammonemia, cerebral edema
b. CNS depression, emesis, tachycardia, QTc prolongation, resp depression, sz, cerebral edema, hyperammonemia, high sodium, low calcium

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52
Q

Zonisamide

A

a. Na channel blockade. Somnolence, ataxia, agitation, bradycardia, hypotension, resp depression, sz

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53
Q

6.4 Identify the toxicity and symptoms of exposure to non-cyclic antidepressants.

A
  1. General s/s expected to cause ataxia, sedation, coma. Noncyclic or tetracyclic antidepressants less toxic than tricyclic or MAOIs.
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54
Q
  1. Bupropion (Wellbutrin)
A

a. Stimulant that can cause sz. Acts more like amphetamine than serotonergic
b. Tachycardia and mild HTN, agitation/lethargy, hallucinations, sz, tremors, clonus, hyperreflexia
c. In larger ingestions may see status, hyperthermia, hypotension, coma, cardiac interval prolongation.
d. *increased sz risk for 24 hrs with >600mg of ER product

  • UDS false + for amphetamines
  • sometimes prescribed for smoking cessation
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55
Q
  1. Desvenlafaxine/Venlafaxine (SNRI)
A

a. Serotonergic effects in mild toxicity
b. Serotonin syndrome, QRS and QT prolongation. Rhabdo. Sz.
c. Somnolence in mild toxicity progressing to delirium in more severe toxicity
d. Exacerbation of CHF

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56
Q
  1. Duloxetine (Cymbalta) - (SNRI)
A

a. OD rare.
b. Mild to moderate: sleepy, GI upset, tachy, diaphoresis, agitation, confusion, HTN
c. Severe toxicity: serotonin syndrome, sz, hypotension, coma

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57
Q
  1. Escitalopram (Lexapro) - (SSRI)
A

a. Serotonergic s/s mild to severe. Citalopram causes delayed QT prolongation. Sz

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58
Q
  1. Lithium
A

Acute or Chronic (chronic worse)

S/S OD ACUTE

i. n/v
ii. delayed neuro effects

S/S OD CHRONIC

i. Tremor, confusion, ataxia, slurred speech, myoclonus, hyperreflexia
ii. **severe** agitated delirium, coma, hyperthermia, convulsions, cerebellar effects, Parkinson like, Diabetes Insipidus

ECG changes

i. T wave flattening
ii. Prolonged QT

Labs

i. Obtain serial blood levels Q2H 1. Lithium and BMP
ii. Goal Na+ 145-150 for max renal lithium excretion
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59
Q

f. Treatment (Lithium)

A

i. NO ACTIVATED CHARCOAL
ii. IVF (watch for hypernatremia)
iii. Dialysis for severe cases (Sz or AMS)

Interactions
i. Lithium with SSRIs can precipitate serotonin syndrome

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60
Q
  1. Monoamine Oxidase Inhibitors
A

a. Mechanism of action
i. Makes dopamine, norepi and serotonin more available

b. Food interactions
i. Tyramine containing products (beer, fava beans, aged cheese, aged meats, pickled foods, red wine, yeast extract and pepperoni)
ii. MAO-A found in the liver and intestinal wall; metabolizes tyramine (tyramine releases catecholamines from neurons)

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61
Q

MAOI Types

A

c. 1 st generation Ex: Marplan, Nardil, Parnate are nonselective for MAO-A/MAO-B

d. Newer MAOI have selectivity for MAO-B)
i. Ex selegiline will not interact with foods
ii. Note: selectivity is lost in overdose
iii. Metabolized to amphetamines: causes + amphetamine on UDS

e. Other products with MAO effect: linezolid (abx for MRSA), PMA (mistaken for MDMA), St John’s Wort

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62
Q

f. Associated syndromes (MAOI)

A

i. Sympathomimetic syndrome
1. When MAOIs used with amphetamines, cocaine, phentermine, PCP

ii. Serotonin syndrome
1. Can result from MAOI use with other serotonergic meds [SSRIs, LSD, dextromethorphan, meperidine, and tramadol]

iii. Use with foods high in tyramine can cause hyperthermic/hypertensive crisis

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63
Q

g. S/S of OD (MAOI):

A

i. Tachycardia, HTN, flushing, headache in mild toxicity
ii. Hyperadrenergic, hypertensive crisis in severe toxicity (hypertension, hyperthermia, delirium, seizures, cardiovascular collapse, multi-organ failure)

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64
Q

h. Treatment (MAOI)

A

i. Supportive care
ii. Short acting anti-hypertensives (NO BETA BLOCKERS)
iii. Benzos for seizures
iv. Cyproheptadine for oral serotonergic antidote

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65
Q
  1. Selective Serotonin Reuptake Inhibitors (antidepressants)
A

a. Ex fluoxetine (Prozac), citalopram (Celexa), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine, venlafaxine (Effexor), trazodone (Desyrel)
b. May interact with one another or MAOIs to produce serotonin syndrome (The classic clinical triad is altered mental status, neuromuscular abnormalities (tremors, clonus, hyperreflexia, rigidity), and autonomic instability (eg, hypertension, tachycardia, hyperthermia). Mydriasis

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66
Q
  1. Trazodone (Desyrel)
A

a. Peripheral alpha-adrenergic blockade causing hypotension (and orthostatic hypotension) w/ reflex tachycardia. May see bradycardia
b. Serotonin syndrome, CNS depression, sz, QT prolongation, priapism, tremors, clonus, hyperreflexia

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67
Q

6.5 Identify the toxicity and symptoms of exposure to tricyclic antidepressants.

A
6.5 Identify the toxicity and symptoms of exposure to tricyclic antidepressants.
Amitriptyline.
Amoxapine.
Desipramine (Norpramin)
Doxepin.
Imipramine (Tofranil)
Nortriptyline
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68
Q
  1. Signs and symptoms of tricyclic antidepressants.
A

a. s/s generally appear within 1 hr but may be delayed if mixed ingestion or delayed gastric emptying
b. initial s/s are often anticholinergic (dry mouth, blurred vision, urinary retention, dizziness, n/v)

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69
Q

c. Cardiac (tricyclic antidepressants)

A

i. Tachycardia
1. Biogenic amine reuptake inhibitor (serotonin and norepi) causes initial hypertension/tachycardia

ii. Initial hypertension then hypotension

iii. QRS prolongation (Na channel blockade)
1. Treat with Bicarb
2. 50 mEq IVP. If QRS narrows, assume drug related and start drip
3. Drip = 3 amps bicarb in 1L D5W w/ 40meq KCl
4. Rate = 2cc/kg/hr or 2x maintenance

iv. QTc prolongation (K channel blockade)
1. Treat with 2g Mag Q6H

*Note: do not use procainamide or other type 1a or 1c antiarrhythmic agents for vtach as may aggravate cardiotoxicity

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70
Q

d. Neuro (tricyclic antidepressants)

A

i. Seizures
1. From GABA inhibition or antihistamine effect
2. Treat with Benzos

ii. CNS depression & coma
1. resembles brain death. May last 3-4 d
2. Do not withdraw care

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71
Q

e. Hypotension (tricyclic antidepressants)

A
i. Alpha blockade causes vasodilation
Treat with
    1. IVF
    2. norepi (alpha 1&amp;2 agonist)
    3. phenylephrine (alpha 1 agonist)

**no dopamine (beta agonist) as it relies on body’s release of catecholamines which may be depleted

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72
Q

6.6 Identify the toxicity and symptoms of exposure to antimicrobials and antimalarials.

A

6.6 Identify the toxicity and symptoms of exposure to antimicrobials and antimalarials.

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73
Q
  1. Severe toxicity in acute ingestion of antibiotics is rare.
A

a. Some IV preparations may contain preservatives such as benzyl alcohol or large amounts of potassium or sodium.

b. Quinolones (ciprofloxacin/Cipro;
levofloxacin/Levaquin) and macrolides (azithromycin and erythromycin) cause prolonged QT/torsades.

c. Sulfonamides can cause sulfhemoglobenemia.
d. Linazolid (Zyvox) is MAOI and serotonergic.

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74
Q

Aminoglycosides (gentamicin, tobramycin, amikacin, plazomicin, streptomycin, neomycin)

A

a. Toxicity more closely associated with trough levels of drug.
b. Renal damage (acute tubular necrosis), ototoxicity (irreversible), and vestibular toxicity (irreversible).
i. Renal injury may go unnoticed until significant.
c. Crosses placenta and some may cause fetal ototoxicity.

Examples:
gentamicin, amikacin, tobramycin, neomycin, and streptomycin

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75
Q

Cephalosporins

A

a. Expect GI upset in oral ingestion
b. Sz have occurred after parenternal OD
c. Ceftriaxone has caused pseudoithiasis (gall bladder sludge) when administered rapidly
d. Some have caused coagulopathy

Examples:
    Ancef and Kefazol (cefazolin)
    Ceclor and Cefaclor (cefaclor)
    Cefdinir.
    Ceftin and Zinacef (cefuroxime)
    Duricef (cefadroxil)
    Keflex and Keftabs (cephalexin)
    Maxipime (cefepime)
    Rocephin (ceftriaxone)
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76
Q

Chloroquine and related drugs

A

Treatment of malaria, parasitic diseases, lupus, and rheumatoid arthritis

Examples:
Chloroquine (more potent), hydroxychloroquine/ Plaquenil, Primaquine

 ii. Mild to moderate ingestion may see GI upset, dizziness, headache, visual disturbances (can cause blindness), and auditory disturbances (can cause deafness) .    iii. Severe ingestion may see coma, sz, shock, cardiac interval changes, respiratory and cardiac arrest.
  • Extremely long half life
    1. Primaquine causes GI upset and may cause methemoblobinemia & hemolysis.
  1. Findings of gastritis, visual disturbances and neuromuscular excitability especially if accompanied by hypotension, QRS /QT prolongation, or ventricular
    arrhythmias, should suggest chloroquine.
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77
Q

Fluoroquinolones

A

a. Cipro associated with crysatalluria. Inhibits cytochrome P450 1A2, GI upset
* Severe SE: tendon ruptures, extreme fatigue, joint and muscle pains, nerve pains, nervous system disturbances

Examples:
ciprofloxacin (Cipro), gemifloxacin (Factive), levofloxacin (Levaquin), moxifloxacin (Avelox), norfloxacin (Noroxin), and ofloxacin (Floxin)

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78
Q

Isoniazid (treatment for TB)

A

Seizures, metabolic acidosis

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79
Q

Oxazolidinones

A

MAOI, serotonergic, thrombocytopenia, anemia, peripheral neuropathy.

*Give pyridoxine for seizures

Examples:
linezolid (Zyvox), tedizolid (Sivextro)

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80
Q

Penicillins

A

a. Seizures in pts with renal dysfunction, kidney problems, leukopenia, neutropenia, bleeding disorder, hypokalemia. Risk of toxicity higher in pts with renal insufficiency

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81
Q

Metronidazole (Flagyl) and Septra

A

Can cause Antabuse (disulfiram) type reactions

*When ingested with alcohol. The disulfiram reaction is a very uncomfortable reaction characterized by severe flushing, and may be accompanied by tachycardia and hypotension.

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82
Q

6.7 Identify the toxicity and symptoms of exposure to antipsychotic agents (neuroleptics).

A

6.7 Identify the toxicity and symptoms of exposure to antipsychotic agents (neuroleptics).

aripiprazole (Abilify)
asenapine (Saphris)
cariprazine (Vraylar)
clozapine (Clozaril)
lurasidone (Latuda)
olanzapine (Zyprexa)
quetiapine (Seroquel)
risperidone (Risperdal)
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83
Q
  1. S/S of antipsychotic agents (neuroleptics)
A

a. Anticholinergic
i. tachycardia, dry mouth, dry skin, urinary retention

b. CNS depression/sedation

c. Alpha-adrenergic blockers
i. hypotension and miosis

d. QT prolongation (occasional QRS prolongation)

e. Extrapyramidal symptoms
i. torticollis, jaw muscle spasm, oculogyric crisis, rigidity, bradykinesia, pill rolling tremor
ii. Often caused by dopamine receptor blockade.

f. Disturbed temperature regulation
i. hypo or hyperthermia

g. Neuroleptic malignant syndrome
i. Rigidity, hyperthermia, sweating, lactic acidosis, rhabdomyolysis

  • Dystonias in children should always suggest the possibility of antipsychotic exposure
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84
Q

Labs and Treatment (antipsychotic agents (neuroleptics)

A

Labs:
a. Electrolytes, Glucose, BUN, Cr, CK, ABG

Treatment:

a. Benadryl for dystonic reactions (consider Haldol)
b. Bicarb for QRS prolongation
c. IVF and norepi or phenyl for hypotension
* Drugs with beta 2 activity may worsen hypotension (vasodilation)
d. Mag or pacing for QT prolongation
e. Charcoal for decontamination
f. Dialysis NOT recommended

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85
Q

First generation antipsychotics (“typical”)

A

b. D2 antagonist
c. Produce psychomotor slowing, emotional quieting, and affective indifference
d. Side effects: EPS, dystonia, tardive dyskinesia, rigidity

  • phenothiazines are occasionally visible on plain abd xrays

Examples:
haldol, chlorpromazine, fluphenazine, loxapine

86
Q

Atypical antipsychotics (2nd generation)

A

b. 5HT2a/D2 antagonists
c. Are “newer” and differ from other antipsychotics in their dopamine receptor binding
d. Dopamine/serotonin antagonist
e. Have less EPS side effect
f. Higher risk of metabolic side effects
- ex: hyperglycemia, weight gain, dyslipidemia.

  • Clozapine can cause hypersalivation, prolonged confusion, cardiac toxicity

Examples:
Fazaclo (clozapine), Zyprexa (olanzapine), Invega (paliperidone), Seroquel (quetiapine), Risperdal (risperidone), Geodon (ziprasidone), Abilify (aripiprazole)

87
Q

3rd generation antipsychotics

A

Dopamine antagonist

Example:
Abilify aripiprazole

88
Q

6.8 Identify the toxicity and symptoms of exposure to common antihypertensives.

A

6.8 Identify the toxicity and symptoms of exposure to common antihypertensives.

89
Q
  1. Angiotensin Converting Enzyme (ACE) Inhibitors and Angiotensin II Receptor Antagonists
A

a. Hypotension. Generally responsive to fluid therapy. Vasopressors not generally needed
b. Bradycardia has been reported
c. Hyperkalemia (may occur with therapeutic use). Esp in renal insufficiency and co-
ingestion of NSAIDS
d. Bradykinin mediated effects: dry cough and angioedema

90
Q

Examples:

ACE Inhibitors

A
Benazepril (Lotensin)
  Captopril.
  Enalapril (Vasotec)
  Fosinopril.
  Lisinopril (Prinivil, Zestril)
  Moexipril.
  Perindopril.
  Quinapril (Accupril)
91
Q

Examples:

Angiotensin II Receptor Antagonists

A
Azilsartan (Edarbi)
    Candesartan (Atacand)
    Eprosartan.
    Irbesartan (Avapro)
    Losartan (Cozaar)
    Olmesartan (Benicar)
    Telmisartan (Micardis)
    Valsartan (Diovan)
92
Q
  1. Alpha-2 Adrenergic Receptor Agonists
A

b. Decrease sympathetic outflow. s/s: sedation, miosis, early hypertension followed by bradycardia and hypotension

Examples:
gunabenz, guanfacine, clonidine, tizanidine

93
Q
  1. Diuretics
A

a. n/v, dehydration, electrolyte abnormalities
i. Hypokalemia, hypomagnesemia, hyponatremia, hypochloremic alkalosis
ii. Electrolyte imbalance may cause arrhythmias and enhance digitalis toxicity

b. Treat with hydration and electrolyte repletion as needed
c. OD generally benign

d. Spironolactone & Triamterene
i. may cause hyperkalemia (K sparing)
ii. spironolactone slow onset

e. Furosemide and Ethacrynic acid
i. high dose/rapid IV admin (esp to pts in renal failure) may be ototoxic

f. Thiazides
i. may cause hyperglycemia, hypercalcemia, hyperuremia

g. Carbonic anhydrase inhibitors
i. may cause metabolic acidosis
ii. acetazolamide, dichlorphenamide, methazolamide

94
Q
  1. Peripheral Vasodilators
A

b. Dilate peripheral arterioles to lower BP.
c. Reflex tachycardia and occasionally cardiac arrhythmias may or may not occur

*OD may cause headache, nausea, dizziness, weakness, syncope, orthostatic hypotension, warm flushed skin, palpitations. Lethargy and ataxia may occur in children.

Examples:
Minoxidil, hydralazine, diazoxide, Alpha Adrenergic Blockers, phentolamine, prazosin, doxazosin, terazosin, tamsulosin

95
Q

6.9 Identify the toxicity and symptoms of exposure to beta blockers and calcium channel antagonists.
Given an exposure to a beta blocker or calcium channel blocker, identify the appropriate treatment.

A

6.9 Identify the toxicity and symptoms of exposure to beta blockers and calcium channel antagonists.
Given an exposure to a beta blocker or calcium channel blocker, identify the appropriate treatment.

96
Q
  1. Beta Adrenergic Blockers
A

Action: Type II antiarrhythmic

S/S:

i. Cardiac: 1 st degree AV block; hypotension; bradycardia most common
ii. CNS depression/sz
iii. Bronchospasm
iv. Hypoglycemia/Hyperkalemia

Treatment:

i. Monitor BS Q2H unless severely symptomatic
ii. Glucagon followed by Epinephrine (bradycardia/hypotension)
iii. High dose insulin with glucose infusion (bradycardia/hypotension)
iv. Isoproterenol (bradycardia/hypotension)
v. Bicarb (wide QRS)
vi. Isoproteranol, Magnesium, Overdrive pacing (torsades)
97
Q

Examples of Beta Blockers

A

Examples:
Acebutolol (Sectral), Atenolol (Tenormin), Bisoprolol (Zebeta), Metoprolol (Lopressor, Toprol XL), Nadolol (Corgard), Nebivolol (Bystolic), Propranolol (Inderal, InnoPran XL)

98
Q
  1. Calcium Channel Blockers
A

Action: decrease Ca entry into cells, primarily acts on cardiac and vascular smooth muscle

 i. Coronary and peripheral vasodilation
 ii. Reduced cardiac contractility
 iii. Slowed AV conduction
 iv. Depressed sinus node activity
* *Create increased need for heart to use carbohydrate metabolism but inhibit pancreas from releasing insulin

S/S:

 i. Hypotension
 ii. Bradycardia, sinus arrest with junctional, or AV blocks
 iii. Prolonged PR or QT (normal QRS)
 iv. Depressed mental status
 v. Metabolic acidosis (from hypotension)
 vi. Hyperglycemia (blockade of insulin release), hypokalemia

Treatment:

 i. Check blood sugar
 ii. IVF for volume expansion (NS or LR)
 iii. Calcium reverses depression of cardiac contractility
 iv. Insulin/Glucose (HIE therapy)
 v. Lipids
 vi. Epi drip (or dopamine/norepinephrine)
 vii. Glucagon drip
 viii. Charcoal
 ix. Dialysis not effective
99
Q

Examples of Calcium Channel Blockers

A
Norvasc (amlodipine)
Plendil (felodipine)
DynaCirc (isradipine)
Cardene (nicardipine)
Procardia XL, Adalat (nifedipine)
Cardizem, Dilacor, Tiazac, Diltia XL (diltiazem)
Sular (Nisoldipine)
Isoptin, Calan, Verelan, Covera-HS (verapamil)
100
Q

6.10 Identify the toxicity and symptoms of exposure to cardiac glycosides.

A
  • Ex Digoxin

Act by inhibition of sodium-potassium-ATPase pump

a. Hyperkalemia *
b. Vagal tone (slowed rate and conduction)

Toxic interactions

a. Amiodarone
b. Verapamil
c. Quinidine
d. Macrolide antibiotics
S/S:
Acute
     i. GI s/s
     ii. Hyperkalemia *
     iii. Cardiac arrhythmias (brady and tachy). Almost any rhythm possible, but NOT likely to see afib.

Chronic

 i. GI
 ii. Visual disturbances (flashing lights, halos, green-yellow perceptual impairment)
 iii. Neuro (weakness)
 iv. Cardiac arrhythmias (classic bidirectional vtach)

**low K+ and Mag+ from diuretics worsen arrhythmias

Treatment:

i. Digifab
ii. Ca+, bicarb, insulin, etc for hyperkalemia
iii. Correct mag
iv. Atropine or pacing for brady
v. Charcoal
vi. Dialysis is NOT useful

101
Q

6.11 Identify the toxicity and symptoms of exposure to over-the-counter stimulants and weight-loss
preparations.

A

6.11 Identify the toxicity and symptoms of exposure to over-the-counter stimulants and weight-loss
preparations.

102
Q
  1. DXM (dextromethorphan)
A

a. Psychoactive effects in OD; mildly stimulating, euphoric or hallucinogenic properties

b. Described as depressant and sometimes hallucinogenic effect in large doses similar to
ketamine and PCP
i. When taken mixed with soda for flavor is called robo-tripping or skittling
ii. Can also be injected

103
Q
  1. Ephedrine
A

a. Was used in diet pills. Used by athletes to enhance performance. Similar to amphetamine. Use as fat burner. Can be used as a substitute for ecstasy.
b. Adverse effects: n/v, dizziness, palpitations, hyperthermia, psychosis, stroke, sz, MI.

104
Q
  1. Caffeine
A

a. Coffee, energy drinks, pills, energy boosters

105
Q
  1. Laxatives
A

a. For weight loss

106
Q
  1. Immodium/Loperamide
A

a. For opioid effect, esp when used with tonic water to cross blood brain barrier

107
Q
  1. Pseudoephedrine
A

a. Active ingredient in decongestants. Used for euphoria & stimulant effect
b. Used for production of methamphetamine

108
Q
  1. Motion sickness pills (ex Dramamine/meclizine)
A

a. Antihistamine in higher doses produce mild euphoria, relaxation, hallucinations similar to those from LSD and mushrooms

109
Q
  1. Diphenhydramine
A

a. For euphoric high and potentially hallucinations

110
Q
  1. Ephedrine/Pseudoephedrine (from Ma Huang)
A

Act as a sympathomimetic

i. Stimulates central alpha (inhibition of norepi and decrease sympathetic outflow)
ii. Used for decongestants
iii. Should not be used with buproprion, MAOIs, other NDRIs.

S/S:

i. Vomiting, mydriasis, HTN, tachycardia, agitation/ anxiety, reflex brady.
1. Severe dysrhythmias can occur.
2. Hypertension
a. Can cause ICH, MI
b. May see reflex bradycardia or AV block in attempt to regulate HTN

Labs:
i. Electrolytes, glucose, BUN, Cr, CK, troponin

d. Treat HTN
Use a vasodilator such as phentolamine or nitroprusside
ii. Do not use beta blockers alone to treat hypertension unless first using a vasodilator. Paradoxic worsening of the hypertension may result
iii. Treat tachyarrhythmias with esmolol or metoprolol
iv. Do not treat reflex bradycardia or AV block except indirectly by lowering blood pressure.
v. May use charcoal
vi. Dialysis not effective

111
Q
  1. Imidazoline and propylhexedrine also used as decongestants
A

a. Imidazole toxicity with miosis, bradycardia, hypotension, resp depression, CNS depression

112
Q
  1. Chromium picolinate (dietary supplement)
A

a. supratherapeutic use can cause hepatic/renal toxicity

113
Q
  1. SIbutramine (Meridia) (rx drug)
A

a. Nonamphetamine appetite suppressant also has antidepressant effects d/t blockade of
norepi, serotonin & dopamine reuptake

114
Q

Others over-the-counter stimulants and weight-loss

preparations

A
  1. Diethylproprion HCl (Tenuate Dospan) is amphetamine like anorectant agent
  2. Orlistat (Xenical) limits absorption of dietary fat. It may cause diarrhea in OD.
115
Q

6.12 Identify the toxicity and symptoms of exposure to antidiabetic agents. Given a patient with an overdose of an antidiabetic medication, identify the appropriate treatment.

A

6.12 Identify the toxicity and symptoms of exposure to antidiabetic agents. Given a patient with an overdose of an antidiabetic medication, identify the appropriate treatment.

116
Q
  1. Alpha-glucosidase Inhibitors
A

a. Slow the absorption of starches you eat
b. GI s/s (bloating, flatulence, abd pain, diarrhea); possible electrolyte abnormalities
c. Contraindicated in bowel problems

Examples:
acarbose (Precose), miglitol (Glyset), Voglibose

117
Q
  1. Dipeptidyl Peptidase-4 Enzyme (DDP-4) Inhibitorss
A

a. Inhibits insulin degradation48
b. No significant hypoglycemia

Examples:
Vildagliptin, Sitagliptin, Saxagliptin

118
Q
  1. Insulin
A

Insulin

119
Q

a. Rapid acting: Lispro (Humalog), Aspart (Novolog), Glulisine (Apidra)

A

i. Onset < 15 min
ii. Peak 30-90 min
iii. Duration 3-5 hrs

120
Q

b. Short acting: Regular (Novolin R or Humalin R)

A

i. Onset 30-60 min
ii. Peak 2-4 hrs
iii. Duration 4-8 hrs

121
Q

c. Intermediate acting: NPH (Novolin N or Humalin N)

A

i. Onset 1-2 hrs
ii. Peak 4-10 hrs
iii. Duration 10-18 hrs

122
Q

d. Long acing: Glargine (lantus),Detemir (levemir)

A

i. Onset: 1-2 hrs
ii. Peak: none
iii. Duration 20-24 hrs

123
Q

e. Combinations:

A

i. Onset: <15 min-1 hr
ii. Peak: 1-10 hrs
iii. Duration: 10-18 hrs

124
Q
  1. Metformin
A

a. Is a Biguanide antidiabetic medication
i. Decrease the amount of glucose made by the liver. Generally does not cause hypoglycemia
ii. May have lactic acidosis
iii. Dialysis for lactic acidosis and to clear metformin

Examples:
Glucophage, Glumetza

125
Q
  1. Other hypoglycemic agents (i.e. nateglinide, repaglinide)
A

a. Meglitinides
i. Stimulates insulin secretion
ii. Can cause hypoglycemia.
iii. Treat with dextrose

126
Q
  1. Sodium-Glucose Cotransporter 2 Inhibitors
A

a. Increases urinary glucose excretion.
b. Not expected to cause hypoglycemia alone, but may when combined with insulin or
insulin secretagogues

Examples:
scanagliflozin (Invokana), dapagliflozin (Farxiga), empagliflozin (Jardiance)

127
Q
  1. Sulfonylureas
A

a. Increase insulin secretion. Can cause prolonged and delayed hypoglycemia.
b. Tx Octreotide or Diazoxide for OD (inhibit insulin secretion)
c. Watch for hyponatremia d/t induction of SIADH

128
Q

Examples of Sulfonylureas

A

Examples: DiaBeta, Glynase, or Micronase (glyburide or glibenclamide) Amaryl (glimepiride) Diabinese (chlorpropamide) Glucotrol (glipizide) Tolinase (tolazamide) Tolbutamide.

129
Q
  1. Glitazones/thiazolidindiones
A

a. Make you more sensitive to insulin
b. No significant hypoglycemia
c. May cause fluid retention; peripheral edema; possible hepatotoxicity

Examples:
Rosiglitazone (serious cardiac adverse effects)
Pioglitazone
Troglitazone (off market d/t liver failure)

130
Q

6.13 Identify the toxicity and symptoms of exposure to thyroid drugs.

A
  1. T3: triiodothyronine
    a. dose 0.75mg considered toxic.
    b. SE may be manifest within first 6 hrs.
  2. T4: levothyroxine
    a. dose 5mg considered toxic.
    b. SE may be delayed 2-5 d for T4 to be metabolized to T3
  3. Watch for adrenergic activity in GI, cardio, neuro.
    * Ex: tachycardia, hyperthermia, flushing,
    diarrhea, vomiting, headache, anxiety. Severe toxicity may see sz/hypotension.
  4. In massive T4 ingestion may use propylthiouracil or iopanoic acid to inhibit change into T3
  5. Treat tachyarrythmias with propranolol or esmolol.
  6. Charcoal is appropriate; Dialysis not useful.
131
Q

6.14 Identify the toxicity and symptoms of exposure to iron.

A
  1. Total amount iron ingested per unit of body weight

[total # tablets] [weight (mg) per tablet] [% elemental Fe per tablet] / [pt weight (kg)]

  1. Elemental iron in formulations
    a. Ferrous gluconate 12% (11% - “911”)
    b. Ferrous sulfate 20% (22% - “backwards 2”)
    c. Ferrous fumarate 33% (33% -“full”)
  2. Toxic dose
    a. >= 10mg/kg GI effects
    b. >= 40mg/kg systemic effects
    c. >=60mg/kg potentially lethal
132
Q
  1. Stages of poisoning (iron)
A

The clinical course of iron toxicity is divided into five stages. The progression from stage to stage may be very rapid, and not every patient goes through every stage.

  1. During the first stage (0.5 to 6 hours), the patient mainly exhibits gastrointestinal (GI) symptoms including abdominal pain, vomiting, diarrhea, hematemesis, and hematochezia.
  2. The second stage (6 to 24 hours) represents an apparent recovery phase, as the patient’s GI symptoms may resolve despite toxic amounts of iron absorption.
  3. The third stage (6 to 72 hours) is characterized by the recurrence of GI symptoms, shock, and metabolic acidosis. Iron-induced coagulopathy, hepatic dysfunction, cardiomyopathy, and renal failure are also observed in this stage.
  4. The fourth stage (12 to 96 hours) is characterized by an elevation of aminotransferase levels and possible progression to hepatic failure.
  5. The fifth stage (2 to 8 weeks) represents the consequences of the healing of the injured GI mucosa including pyloric or proximal bowel scarring and obstruction.
    * A patient may present in or skip any of the five stages. Determination of the iron toxicity stage should be based on symptoms and clinical manifestations and not on time of ingestion.
133
Q
  1. Diagnosis (iron)
A

a. May have elevated WBC (>15k); hyperglycemia (>150mg/dL); radiopaque material on abd xr. Symptomatic presentation and history.

Labs:

a. Initial iron level (ideally 4-6 hrs after ingestion)
b. Repeat iron level (8-12 hrs after ingestion to ensure not rising from ER or bezoar)

134
Q
  1. Treatment (iron)
A

a. Deferoxamine (IV preferred over IM)
i. Use for shock, severe acidosis, or iron level >500mcg/dL
ii. Watch for vin rose color or urine (does not always occur)
iii. Stop infusion when UOP color returns to normal OR when iron level return to normal range
iv. **deferoxamine longer than 36-72hrs associated with Yersenia sepsis

b. Gastric lavage only if liquid ingested or chewed tablets
c. Do NOT use phosphate containing or sodium bicarb solutions for lavage!!!!
d. Consider whole bowel for tablet ingestion
e. No charcoal
f. No dialysis for iron (may use dialysis to remove deferoxime/iron complex with renal failure

135
Q

6.15 Identify the toxicity and symptoms of exposure to sedative, hypnotics, antianxiety agents

A
  1. major toxic effect is CNS depression
136
Q
  1. Barbiturates
A

a. Sedative-hypnotic
i. Used for anesthesia induction, sz, and pain. High abuse potential
ii. Varying length of action (ultra-short to long acting)
iii. Increase GABA

b. S/S
i. CNS depression
ii. Barbiturate burns

c. Treatment
i. Supportive care
ii. Charcoal
iii. Alkalization of urine for phenobarbital OD
iv. Dialysis increases elimination of long acting agents but rarely used

  • Barbiturate coma resembles brain death*
    1. Cannot withdraw care until documenting nontoxic barbiturate levels
137
Q
  1. Benzodiazepines
A

a. Sedative-hypnotic
i. Used for sedation, anxiolysis, and seizure management
ii. Increase GABA

b. S/S
i. CNS depression. Increased when combined with other drugs such as barbiturates and ethanol
ii. Hypotension, hypothermia, memory impairment, lethargy, ataxia

c. Treatment
i. Flumazenil for benzo naïve or to prevent difficult/dangerous procedure

138
Q

Buspirone (Buspar) - anxiety

A

a. May cause n/v, drowsiness, miosis

b. serotonergic

139
Q

Chloral hydrate - (sedative and hypnotic)

A

a. Metabolized to trichloroethanol, also has CNS depressant activity
b. May sensitize myocardium to catecholamines (arrhythmias)

140
Q

Zolpidem (used to treat insomnia)

A

a. CNS depression. Is not a benzo but has similar effects.

141
Q

Zopiclone/Eszopiclone

A

a. CNS depression. GABA agonist. Have seen methemoglobinemia in very large OD.

142
Q

6.16 Identify the toxicity and symptoms of exposure to skeletal muscle relaxants.

A
  1. Skeletal muscle relaxant (sedative-hypnotic that affects muscle indirectly)
143
Q

a. Chlorzoxazone and Methocarbamol, Carisoprodol listed as central acting skeletal muscle relaxants.

A

a. Expect CNS depression, n/v, hypotension, etc

144
Q

b. Metaxoalone/Methaqualone

A

a. may cause muscular hypertonicity, clonus, hyperreflexia

145
Q

c. Carisoprodol/Meprobamate

A

a. Anticholinergic/serotonergic s/s from carisoprodol

b. Large OD may cause concretions. May cause hypotension.

146
Q

d. Cyclobenzaprine (Flexeril) and orphenadrine (Norgesic)

A

a. Anticholinergic (tachy, mydriasis, delirium); hypotension

b. Orphenadrine only: status epilepticus, Vtach, asystole

147
Q

e. Baclofen (Lioresal)

A

a. Coma, resp depression, bradycardia, paradoxical seizure like activity, delirium,
AV dysfunction

Baclofen can mimic brain death

148
Q

f. Tizanidine (Zanaflex)

A

a. Similar to clonidine

b. Coma, profound hypotension, bradycardia, SA and AV node dysfunction

149
Q
  1. Treatment: symptomatic
A

a. Flumazenil may work for chlorzoxazone and carisoprodol
b. Physostigmine may reverse anticholinergic s/s with cyclobenzaprine and orphenadrine (may cause seizures)
c. Dialysis: possibly for symptomatic baclofen with impaired renal function

150
Q

6.17 Identify the toxicity and symptoms of exposure to amphetamines and related compounds.

A
  1. Ex MDMA, meth, dextroamphetamine (Dexedrine), methylphenidate (Ritalin)
    a. Schedule II drug

b. Toxidrome
i. Sympathomimetic
ii. Serotonergic

c. Treatment
i. Benzos (agitation, seizures); may add antipsychotic
ii. Phentolamine or nitroprusside for HTN if not treated with benzo
iii. Propranolol or esmolol for tachyarrhythmias (paradoxical HTN may occur requiring a vasodilator)
iv. Charcoal
v. Dialysis not effective

151
Q

6.18 Identify the toxicity and symptoms of exposure to cocaine.

A
  1. Slang:
    a. Speedball (cocaine and heroin)
    b. Crack (free base). Most addictive form
  2. Use: snorted, smoked, injected, oral
    a. May be adulterated with lidocaine, benzocaine, stimulants, or levamisole (causes
    agranulocytosis)
  3. MOA
    a. Blocks reuptake of norepi, dopamine, and serotonin
    b. Na+ channel blockade (neuronal and cardiac)
    c. Metabolized plasma/liver
152
Q
  1. S/S (cocaine)
A

a. Stroke (ischemic/embolic/ICH)
b. MI
c. Arrhythmias
i. QRS and QTc prolongation
d. Sz (usually brief)
i. Status reflects continued absorption of drug (ruptured packing) or hyperthermia
e. Anxiety/agitation
f. HTN/tachycardia
g. Muscle rigidity
h. Hyperthermia

153
Q
  1. Labs (cocaine)
A

a. Electrolytes, glucose, BUN, Creatinine, CK, urinalysis and urine myoglobin, Trop, ECG, CT,
abd x-ray (body packing)

154
Q
  1. Treatment (cocaine)
A

a. Benzodiazepines for anxiety, hypertension, tachycardia
* DO NOT USE BETA BLOCKERS*

  1. If HR/BP refractory to benzos and IVF, consider cardioselective BB such as esmolol or metoprolol. May be used with vasodilator such as phentolamine for HTNii. Bicarb for QRS prolongation
    iii. Lidocaine for wide complex tach
155
Q

6.19 Identify the toxicity and symptoms of exposure to street drugs.

A

6.19 Identify the toxicity and symptoms of exposure to street drugs.

156
Q
  1. Stimulants, Hallucinogens, Street drugs
A
  1. Stimulants, Hallucinogens, Street drugs
157
Q

a. Amyl and Butyl Nitrates

A

i. methemoglobinemia

158
Q

b. Caffeine

A

i. S/S OD (Caffeine)
1. Tremor
2. Vomiting
3. Tachycardia
4. Seizures (can be refractory)
5. Hypokalemia
6. Hyperglycemia

ii. Labs
1. May draw a theophylline level (it is a metabolite of caffeine)

iii. Treatment
1. Benzos for seizures
2. Beta blockers (propranolol or esmolol) for tachyarrhythmias and hypotension
3. Vasopressin/phenylephrine for hypotension
4. Charcoal
5. Dialysis

159
Q

c. Gamma Hydroxybutyric Acid and Related Compounds (GHB)

A

i. Abrupt onset of sleep, enuresis, myoclonic movements, bracycardia, coma

160
Q

d. Heroin, Fentanyl, and Related Compounds

A

i. CNS/resp depression. Miosis. Pulmonary edema

ii. Reverse with narcan

161
Q

e. LSD and Other Hallucinogens

A

i. Hallucinogen/Enactogen
1. Examples: LSD, MDA, MDMA

ii. Use: snorted, smoked, injected

iii. S/S
1. Cardiac:
a. HTN, tachycardia
2. Neuro
a. Anxiety, psychosis, hallucinations, dilated pupils, tremor, hyperreflexia
3. Metabolic
a. Hyperthermia & Sweating

iv. Labs
1. Include PT (untreated hyperthermia can result in coagulopathy)
2. CK and urine blood/myoglobin (rhabdomyolysis)

v. Treatment
1. Supportive care
2. Diazepam, midazolam, Haldol for severe agitation
3. No charcoal or dialysis

162
Q

Marijuana and THC Analogs

A

i. Slang terms: Hashish, Kief, Bhang, Budder
ii. Use: oral or smoked

iii. S/S
1. Cardiac
a. Tachycardia and orthostatic hypotension
2. Neuro
a. Slurred speech and ataxia
3. Other
a. Conjunctival erythema
b. Decreased IOP

iv. Treatment
1. Supportive care
2. s/s requiring treatment generally due to co-ingestions

163
Q

g. Phencyclidine (PCP) and Derivatives

A

i. S/S
1. Cardiac
a. Tachycardia, HTN,
2. Neuro
a. Hallucinations, euphoria, disinhibition.
3. Other
a. Nystagmus often prominent
4. Severe toxicity may cause psychosis, hyperthermia, rhabdo, organ failure, acidosis, sz.

164
Q

h. Sympathomimetics

A

i. Sympathomimetic toxidrome.

ii. This is a general class and includes amphetamines, cathinones, cocaine, ephedrine, etc.

165
Q

i. Synthetic Cathinones (“bath salts”)

A

i. Sympathomimetic toxidrome.

ii. May see paranoia, delirium, aggressive behavior, hallucinations, hyperthermia,
hypotension, rhabdo, dysrhythmias.

166
Q

6.20 Identify the toxicity and symptoms of exposure to over-the-counter topicals.

A

6.20 Identify the toxicity and symptoms of exposure to over-the-counter topicals.

167
Q
  1. Antiseptics (i.e. mercurochrome, iodine)
A
  1. Antiseptics (i.e. mercurochrome, iodine)
168
Q

a. Mercurochrome: organic mercury

A

i. No significant absorption if applied topically; ingestion poses risk

169
Q

b. Iodine

A

i. Can be corrosive

ii. Antidote for ingestion is starch (cornstarch, potatoes)

170
Q

c. Chlorhexidine

A

i. Corrosive in higher concentration

171
Q

d. Glutaraldehyde (ph 3-4)

A

i. Irritating to skin and resp tract. May cause dermatitis/ocular damage

172
Q

e. Hexylresorcinol

A

i. Related to phenol but less toxic. Found in anthelmintics and throat lozenges. Has vesicant properties

173
Q

f. Hydrogen peroxide

A

i. may cause gastric distention, perforation, air emboli. More commonly in industrial concentrations.

174
Q

g. potassium permanganate

A

i. (sometimes found in antiseptic mouth wash)

corrosive burns, methemoglobinemia

175
Q

h. hypochlorite

A

i. corrosive

176
Q

i. isopropyl alcohol

A

i. GI irritation/bleeding

177
Q

j. Phenol

air fresheners, aftershave, bronchial mists, chloroseptic throat spray, deodorants, feminine powders & sprays, hair spray, decongestants, mouthwash, aspirin, solvents, acne medications, antiseptics, calamine lotions, cleaning products, detergents, furniture polish, hair setting lotions, lice shampoo, polishes, cold capsules, all-purpose cleaners, aerosol disinfectants, anti-itching lotions , carnex , cosmetics, disinfectant cleaners, hand lotions, lip balms,

A

i. Multiple sources: clove oil has eugenol; Lysol has bisphenol; creosote, etc.
ii. Well absorbed via multiple routes
iii. Denatures protein, disrupts cell wall, causes coagulative tissue necrosis, corrosive injury to eyes, skin and resp tract. Some may cause methemoglobinemia, CNS stimulation, cardiac arrhythmias
iv. Dx based on history of exposure, presence of characteristic odor (sickeningly sweet and tarry); painless skin burns with white discoloration

178
Q

k. Pine oil

A

i. oral irritation, CNS depression, bradycardia, hypotension

179
Q
  1. Camphor, Methyl Salicylate, and Other Essential Oils
A
  1. Camphor, Methyl Salicylate, and Other Essential Oils
180
Q

a. Birch oil

A

i. 98% methyl salicylate or 1.4g ASA/ml

ii. Aspirin toxicity

181
Q

b. Camphor

A

i. CNS stimulant. Oral irritation, n/v, sz 20-30 min s/p ingestion.

182
Q

c. Cinnamon oil

A

i. Stomatitis and skin burns. Smoked as hallucinogen

183
Q

d. Clove oil

A

i. 80-90% eugenol. Metabolic acidosis, CNS depression, sz, coagulopathy, hepatotoxicity. May treat with NAC

184
Q

e. Eucalyptus oil

A

i. Acidosis, multi organ system failure

185
Q

f. Guaiacol

A

i. Nontoxic

186
Q

g. Lavender oil

A

i. CNS depression; May cause photosensitization

187
Q

h. Melaleuca oil

A

i. Tea tree oil. Toxic peds dose is 10ml. sedation, confusion, ataxia, coma. Onset 30-60min.

188
Q

i. Menthol

A

i. Is an alcohol; may cause oral irritation, emesis, tremor, ataxia, CNS depression

189
Q

j. Nutmeg

A

i. Hallucinogen and amphetamine like effect/psychogenic effects

190
Q

k. Pennyroyal oil

A

i. Moderate to severe toxicity with >10ml. coma, hepatotoxicity. Abortifacient. May treat with NAC

191
Q

l. Peppermint oil

A

i. 50% menthol. Oral irritation, emesis, tremor, CNS depression, bradycardia, metabolic acidosis

192
Q

m. Thymol

A

i. Allergic dermatitis (used as antiseptic)

193
Q

n. Wintergreen oil

A

i. 98% methyl salicylate or 1.4g ASA/ml

ii. Aspirin toxicity

194
Q

6.21 Identify the toxicity and symptoms of exposure to vitamins.

A
  1. Minerals and Electrolytes
    a. Iron-see above

b. Fluoride
i. Hypocalcemia, n/v
c. Other Minerals
i. GI upset

195
Q

6.22 Identify the toxicity and symptoms of exposure to other drugs.

A

6.22 Identify the toxicity and symptoms of exposure to other drugs.

196
Q
  1. Anticholinergics-see toxidrome
A
  1. Anticholinergics-see toxidrome
197
Q
  1. Anticoagulants
A

a. Heparin
b. Newer anticoagulants (i.e. dabigatran and rivaroxaban)
c. Warfarin/Rodenticides/Super Coumadins

198
Q

a. Heparin

A

i. Check PTT

ii. Protamine sulfate is reversal agent

199
Q

b. Newer anticoagulants (i.e. dabigatran and rivaroxaban)

A

i. Thrombin inhibitor (dabigatran)
1. Reverse with Idarucizumab
a. Humanized, monoclonal antibody fragment

ii. Xa inhibitor (Rivaroxaban, apixaban, endoxaban)
1. Reverse with Andexa

200
Q

c. Warfarin/Rodenticides/Super Coumadins

A

i. Check INR
ii. Vitamin K is reversal agent,
iii. FFP or whole blood for clotting factors; recombinant factors

201
Q
  1. Antihistamines
A

a. Action

i. H1 blockers have two types:
1. 1 st generation more lipid soluble and cross blood-brain barrier
a. Sedating
b. Ex benadryl, promethazine, meclizine, chlorpheniramine

  1. 2nd generation less lipid soluble and do not cross BBB
    a. Nonsedating
    b. Ex loratadine (Claritin), desloratadine (Clarinex), cetirizine (Zyrtec), fexofenadine (Allegra)

ii. H2 blockers delay gastric emptying; do not share other effects and do not produce significant intoxication (cimetidine, famotidine, nizatidine and ranitidine)

202
Q

b. S/S (Antihistamines)

A

i. Anticholinergic effects (antimuscarinic) and Na channel blockade
ii. May have rhabdo
iii. QRS and QT prolongation with some

203
Q

c. Labs and Treatment (Antihistamines)

A

c. Labs
i. Electrolytes, glucose, CPK

d. Treatment
i. Benzos for sz, hyperthermia, agitation
ii. Aggressive cooling
iii. Bicarb for QRS
iv. Physostigmine with caution (for anticholinergic)
v. Take care with antiarrhythmic use (some will worsen s/s)
vi. Charcoal
vii. Dialysis not effective

204
Q
  1. Gastrointestinal Agents
A
  1. Gastrointestinal Agents
205
Q

a. Diphenoxylate/atropine (Lomotil)

A

i. Antidiarrheal agent

ii. Onset of s/s d/t atropine may be delayed 6-8 hrs or longer. Coma/resp depression may be delayed up to 30 hrs

206
Q

b. Loperamide (Imodium)

A

i. Antidiarrheal agent
ii. Popular drug of abuse
iii. Drowsiness, n/v, abd pain, headache. Miosis is common. Bradycardia/resp depression can occur. Cardiac dysrhythmias have been reported in large doses of med abuse.

207
Q

c. Metoclopramide (Reglan)

A

i. Antiemetic/prokinetic agent. Blocks dopamine and serotonin receptors.
ii. Inadvertent OD in infants has caused methemoglobinemia and opisthotonic posturing
iii. Dystonic reactions more common in children and young adults
iv. NMS may occur
v. Common toxic effects are restlessness, drowsiness, insomnia, headache, confusion, dizziness, and dystonic reactions

208
Q

Genitourinary Agents

A

a. Erectile Dysfunction Agents
i. Sildenafil (Viagra); Tadalafil (Cialis); Vardenafil (Levitra)
ii. PDE5 inhibitor
iii. Headache, flushing, dizziness, weakness, priapism, vertigo, hypotension, tachycardia, weakness

b. Phenazopyridine (Pyridium)
i. Urinary anesthetic
ii. Methemoglobinemia/hemolytic anemia

c. Urinary Antispasmodics
i. Oxybutyin (Ditropan), Hyoscyamine, Solifenacin
1. Anticholinergic s/s

209
Q

Hormone and Hormone Antagonists

A

a. Steroids
i. Acute ingestion unlikely to cause toxicity
ii. Chronic exposure to high doses may result in adverse effects

210
Q

Local Anesthetics

A

a. Methemoglobinemia

b. Cardiac toxicity

211
Q

Methotrexate

A

a. Antineoplastic agent, used for RA or psoriasis

b. GI upset, pancytopenia, ALI, resp failure, sepsis

212
Q

Veterinary Medications

A

a. Antihelmenthics (i.e. heartworm products)

b. Vaccines (live vaccines can cause a problem ex brucellosis)