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5 MD > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What is “evidence-based” analysis?

A
  1. to identify at an early stage those who are most at risk of developing serious complications
  2. to identyfy who might potentially benefit from decontamination, elimination techniques
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2
Q

Principles of managing the acutely overdosed patient

A
  1. do not focus on ingredients listed on the container of the product
  2. do not focus on specific antidote
  3. more rational individualized early treatment
  4. treat the patients, not the poison - rapid clinical management plan
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3
Q

Explain the general evaluation protocol in poisoned/overdosed patient

A
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4
Q

The 5 W’s in taking patient history?

A
  1. Who - age, weight, relationship
  2. What - name and dosage of medication(s)
  3. When - the time and date of ingestion
  4. Where - route of poisoning and geographical location
  5. Why - intentional or unintentional
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5
Q

Which drugs are known as “date-rape drugs”?

A
  1. Rohypnol (benzodiazepine)
  2. GHB (γ-hydroxybutyrate)
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6
Q

First thing to do when you get an overdosed patient?

A

Stabilize! Do your ABCDE’s!

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7
Q

Important Rule-Outs in an overdosed patient?

A

ATOMIC

Alcohol: check ethanol lvl

Trauma: consier CT scan

Overdose: drug lvls, other drugs involved?

Metabolic: ABG, Na, K, glucose, Thyroid, creatinine, etc

Infection: consider blood values

Carbonmonoxide: obtain COHb lvl

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8
Q

What is the protocol for empirical treatment of coma patient?

A
  1. Give Oxygen/ventilation if sat% is low
  2. Nolaxone (2.0mg in adults)
  3. Thiamine 100mg (BEFORE glucose)
  4. Glucose 50% IV 50ml (or 1 mg glucagon if you can’t place PVK)
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9
Q

Why do we give thimine before glucose?

A

To prevent risk of Wernicke’s encephalopathy

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10
Q

Nolaxone, when should you consider giving it?

A

When there is a sign of respiratory og CNS depression

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11
Q

How is Nolaxone dosage considered?

A
  1. Adult: 2.0mg (repeated every 2 min, total dose 10mg)
  2. Children > 5 years + respiratory depression: 2.0mg
  3. Children > 5years - respiratory depression: 0.1 - 0.8 mg
  4. Children < 5 years: 0.1mg/kg
  5. Narcotic-dependent patients: 0.1mg, doubled every 2 min, total dose 10mg
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12
Q

Explain the typical toxologic physical exam

A
  1. Mental status: agitation, confusion, coma, reflexes
  2. Pupils: pupils size, nystagmus, reactivity, increased lacrimation
  3. Bowel: sounds, tenderness or rigidity
  4. Muscle: tone, activity, coordination
  5. Skin: dry or diaphoretic, bruising, cyanosis, flushing
  6. Lungs: bronchorrhea or wheezing
  7. Cadriovascular: rhythm, rate, regularity

Based on these consider type of Autonomic Syndromes

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13
Q

What are Autonomic Syndromes?

A

Dysfunctions within the autonomic system with either procholinergic or anticholinergic side effects.

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14
Q

What are toxidromes?

A

Clusters of symptoms that may suggest particular classes of substances bein the cause of poisoning/overdose.

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15
Q

Name the types of toxidromes

A
  1. Sedative-hypnotic toxidrome
  2. Anticholinergic toxidrome
  3. Cholinergic toxidrome (muscarinic)
  4. Cholinergic toxidrome (nicotinic)
  5. Opioid toxidrome
  6. Sympathomimetic
  7. Withdrawl
  8. Thermal
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16
Q

Sedative-hypnotic toxidrome, symptoms and causes?

A
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17
Q

Anticholinergic toxidrome, symptoms and causes?

A
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18
Q

Cholinergic toxidrome (muscarinic), symptoms and causes?

A
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19
Q

Cholinergic toxidrome (nicotinic), symptoms and causes?

A
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20
Q

Opioid toxidrome, symptoms and causes?

A
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21
Q

Sympathomimetic toxidrome, symptoms and causes?

A
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22
Q

Withdrawl toxidrome, symptoms and causes?

A
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23
Q

Thermal toxidrome, causes behind hyper- & hypothermia?

A
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24
Q

Why do certain toxic substances show delayed signs?

A

The delay may occur because only the metabolite is toxic rather than the parent substance (eg, methanol, ethylene glycol, hepatotoxins etc…)

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25
Q

What is the routine lab-test for intoxicated patients?

A
  1. ABGs
  2. complete blood cell count
  3. serum electrolyte
  4. glucose levels
  5. chemical screen with hepatic and renal function studies
  6. serum osmolarity may be helpful if poisoning with methanol, ethylene glycol or isopropanol is suspected.
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26
Q

When should you take chest radiographs?

A

If you suspect:

  1. aspiration
  2. coma
  3. ingestion of substances that may cause non-cardiogenic pulmonary edema
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27
Q

What do you especially need to be conserned about when treating a patient that unintentially overdosed while working as a drug-mule?

A

Monitor blood lvls of the substance and be sure that levels are sustainly decreasing, a sudden increase could be a sign of reexposure (rupture of unremoved hidden drug pouch in the GI)

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28
Q

What is Ipecac and what can it do?

A
  1. A syrup that can induce vomiting by irritating GI mucosae and stimulate chemotrigger zone of the brain
  2. May be used to remove ingested poisons/drugs
  3. 30ml for adults, 15ml for children
  4. Most common side effect is vomiting lasting >60 min

(although prolonged vomiting could also be caused by the toxin)

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29
Q

Contraindications for using Ipecac?

A
  1. ingestions with potential for change in mental status
  2. active or prior vomiting
  3. corrosives and volatile poisons
  4. heart disease patients
  5. pregnant women
  6. toxin with more pulmonary than GI toxicity
  7. ingestion of toxins with potential for seizures (aspiration pneumonia)
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30
Q

According to the AAPCC, at what circumstances should Ipecac be used at all?

A

Only indication for Ipecac use at home is if there would be a delay of 1 h or more before a patient (adult) could get to an Emergency Department (and even then, only if it could be administered within 30-90 min after the ingestion)

Home-use of ipecac in pediatric patients is not recommended!

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31
Q

Indications for Gastric Emptying/Gastric lavage?

A
  • Must be done within 1h of ingestion
  • If the drug contains on of the following:
  1. hydrocarbon
  2. benzene
  3. toluene, camphor
  4. halogenated hydrocarbons
  5. pesticides
  6. heavy metals
  • If the drug is liquid: more than 4ml/kg has to be ingested
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32
Q

What is Gastric Lavage?

A
  • A type of Gastric Emptying procedure
  • Flexible tube is inserted through the nose into the stomach
  • Size: > 36 French for adults or 22-24 French for children
  • Used for retrieving tablet fragments
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33
Q

How is the Gastric Lavage procedure done?

A
  1. Before nose insertion, measure from chin to xiphoid and confirm with air insufflation
  2. Because lavage sometimes forces substances farther into the GI tract, a 25g dose of charcoal is instilled through the tube first
  3. Lavage continues until the withdrawn fluids appear free of the substance (usually 500 - 3000ml), while small aliquits of lavage fluid are repeatadly introduced into the stomach by gravity
  4. After lavage, give a 2nd dose of 25g charcoal
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34
Q

When is gastric lavage contraindicated?

A
  1. no patient’s agreement
  2. large pills
  3. nontoxic ingestion
  4. non-life threatening
  5. most hydrocarbons
  6. airway integrity not secured
  7. drug is more toxic to lung than GI
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35
Q

What is Activated Charcoal?

A
  1. Given when multiple or unknown substances have been ingested
  2. Absorbs most toxins because of its molecular configuration
  3. Given at doses of 1-2g/kg, repeat with 4-6h interval
  4. Given in fluid solution (e.g in a slurry or soft drink)
  5. Given trough gastric tube in unconcious patients
    6.
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36
Q

Which substances do we have to give repeated doses of charcoal (Multi-dose charcoal) for?

A

Substances that undergo enterohepatic recirculation

  1. phenobarbital
  2. carbamazepine SR
  3. aspirin (enterocoated tablets)
  4. theophylline SR
  5. other Sustained-Release products
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37
Q

Which substances is multi-dose charcoal not useful for?

A

The typical substances that we prefer Gastric Lavage for:

  1. cyanide
  2. mineral acids
  3. caustic
  4. organic solvents
  5. iron
  6. ethanol
  7. methanol
  8. lithium
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38
Q

Complications and side effects of active charcoal?

A
  1. decreased O2
  2. nausea/ vomiting
  3. epistaxis
  4. insertion into trachea
  5. aspiration
  6. fluid and elctrolyte abnormalities
  7. small bowel obstruction
  8. pneumonia
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39
Q

What are Cathartics?

A
  1. Substance that accelerates defecation
  2. Consist of either 70% sorbitol 1g/kg or 10 magnesium citrate
  3. Often given with activated charcoal
  4. Typically used in WBI (whole bowel irrigation)
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40
Q

How does WBI work?

A
  • A commercially prepared solution of polyethylene glycol (PEG glycol) (which is nonabsorbable) and electrolytes is given at a rate of 1-2 L/h until the rectal effluent is clear
  • Usually given through gastric tube
  • Benefits of WBI are uncertain, may help for SR drug intox
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41
Q

What is Alkaline Diuresis?

A

A method of eliminating weak acids by giving a solution of Dextrose, NaHCO3 and KCl

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42
Q

What do we mean when we say Extracorporeal Treatment in toxicology?

A

Removing toxin by hemodialysis or hemoperfusion

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43
Q

Absolute indications for Extracorporeal treatment?

A

All of the following must be present:

  1. Exposition to toxic drug
  2. Drug must be readily eliminated by ECT
  3. Evidence of toxicity either (biochemical or clinical sympt)
  4. Lack of alternative life saving treatments (antidote)
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44
Q

Relative indications for Extracorporeal treatment?

A
  1. Deteriorating condition despite optimal therapy
  2. Problems with renal or hepatic metabolism
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45
Q

Common toxins that may require extracorporeal treatment?

A
  1. Ethylene glycol
  2. Lithium
  3. Methanol
  4. Salicylates
  5. Theophylline
  6. VPA
  7. Phenobarbital
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46
Q

In which circumstances is hemodialysis less usefull for removing toxins?

A

If the poison…

  1. Is a large or charged
  2. Has a large volume of distribution
  3. Is stored in fatty tissue
  4. Is extensively bound to protein
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47
Q

When do we use hemofiltration or give plasma exchange?

A

When the liver/kidneys are damaged and need time for recovery/transplantation

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48
Q

A main advantage hemoperfusion has over hemodialysis?

A

It consists of a filter made of activated charcoal in the dialysis circuit (might help in filtrating large or protein-bound toxins)

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49
Q

Antidote for Acetaminophen (paracetamol)?

A

N-Acetylcysteine

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50
Q
A
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51
Q

Antitode for Anticholinergics?

A

Physostigmine

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52
Q

Antidote for benzodiazepines?

A

Flumazenil

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53
Q

Antidote for B-blockers?

A

Glucagon

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54
Q

Antidote for Ca-channel blockers?

A
  1. Ca IV
  2. Insulin with IV glucose
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55
Q

Antidote for Carbametes?

A
  1. Atropine
  2. Pralidoxime
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56
Q

Antidote for Organophosphates?

A
  1. Atropine
  2. Pralidoxime
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57
Q

Antidote for Digitalis glycosides?

A

Specific Fab fragments

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58
Q

Antidote for Ethylene glycol?

A
  1. Ethanol
  2. Fomepizole
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59
Q

Antidote for Methylene?

A
  1. Fomepizole
  2. Ethanol (if fomepizol is unavailable)
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60
Q

Antidote for Heavy metals?

A

Chelating drugs

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61
Q

Antidote for Iron intoxication?

A

Deferoxamine

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62
Q

Antidote for Isoniazid?

A

Pyridoxine (vitamin B6)

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63
Q

Name the Methemoglobin-forming agents

A
  1. Aniline dyes
  2. Some local anesthetics
  3. Nitrates
  4. Nitrites
  5. Phenacetin
  6. Sulfonamides
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64
Q

Antidote for Methemoglobin-forming agents?

A

Methylene blue

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65
Q

Antidote for opioids?

A

Naloxone

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66
Q

Antidote for Tricyclic antidepressants?

A

NaHCO3

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67
Q

Antidote for Cyanide?

A
  1. Hydroxocobalamin
  2. Cyanide antidote kit (includes amyl nitrate, Na nitrite, and Na thiosulfate)
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68
Q

What to do if intoxicated patient shows respiratory depression?

A

First try giving 2mg Naloxone, if it still persists do endotracheal intubation with slow-infusing Naloxone perfusion

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69
Q

What to do if intoxicated patients show altered conciousness?

A
  1. FIRST give 100mg thiamine
  2. Then give 50ml of 50% Dextrose solution
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70
Q

First-choice vasopressor for drug-induced hypotension?

A

Norepinephrine 0.5-1mg/min

(if the hypotension is refractory, consider other vasopressors)

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71
Q

What to do if patient shows refractory arrythmia?

A
  • Cardiac Pacing

For Torsades de Pointes we can give Magnesium Sulfate 1-2g IV

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72
Q

What to give to intoxicated patient with seizures?

A
  1. Benzodiazepines first
  2. Phenobarbital or phenytoin if benzo doesn’t work
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73
Q

How does acetaminophen (paracetamol) hepatotoxicity occur?

A

Ocurrs due to metabolism by p450 (mainly CYP2E1) to the hepatotoxic substance NAPQI –> GSH depletion, oxidative stress and mitochondrial dysfunction

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74
Q

What is the Rumack–Matthew Nomogram used for?

A

Used for estimation of the likelihood of hepatic injury due to acetaminophen toxicity for patients with a single ingestion at a known time

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75
Q

Result of cross reaction between acetaminophen and ACUTE alcohol abuse?

A

Decreased NAPQI due to ethanol being a competitive substrate of CYP2E1

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76
Q

Result of cross reaction between acetaminophen and Chronic alcohol abuse?

A

Increased NAPQI due to long ethanol abuse will over time increase number and action of CYP2E1 enzyme

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77
Q

Acetaminophen overdose:

Clinical manifestations - Stage 1

A
  1. First 24 hours of ingestion
  2. Characterized by the non-specific symptoms of nausea, vomiting, malaise, lethargy and diaphoresis
  3. AST and ALT are usually normal
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78
Q

Acetaminophen overdose:

Clinical manifestations - Stage 2

A
  1. 24 to 72 hours
  2. Characterized by resolution of stage I symptoms
  3. Elevations of AST and ALT typically begin to occur
  4. In severe cases:hepatomegaly (with right-upper quadrant pain), jaundice and coagulopathy
  5. 1∼2% of patients may also experience renal failure
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79
Q

Acetaminophen overdose:

Clinical manifestations - Stage 3

A
  1. 72 to 96 hours after ingestion
  2. Return of stage I symptoms
  3. AST and ALT elevations
  4. Maximal liver injury (jaundice, encephalopathy, coagulopathy and lactic acidosis)
  5. Renal failure, and on rare occasions pancreatitis
  6. Prolonged prothrombin time
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80
Q

Why do we see lactic acidosis in acetaminophen overdose?

A

Increase lactic acid in two ways (two-hit increase):

  1. NAPQI causes hypoxia in hepatic cells –> increased lactic acid
  2. NAPQI-induced hypoxia in hepatic cells –> decreased lactic acid metabolism –> even more lactic acid buildup!
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81
Q

If a patient survives stage 3, what is the recovery time?

A
  • 96 hours after stage 3 (1-2 weeks from time of ingestion)
  • May last longer depen ding on severity
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82
Q

How much acetaminophen is considered to be toxic dose?

A

> 7.5g of acetaminophen is toxic

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83
Q

Alternative antidote for acetaminophen overdose?

A

If acetylcysteine is not accessible, give activated charcoal 1g/kg within 4 hours of poison ingestion

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84
Q

Indications for N-acetylcysteine in acetaminophen overdose?

A
  1. Acetaminophen lvl above “treatment” line on the nomogram chart
  2. Single ingestion of greater than 150 mg/kg (7.5 g total dose regardless of weight)
  3. Unknown time of ingestion and a serum acetaminophen concentration >10 mcg/mL (66 micromole/L)
  4. Patient with a history of acetaminophen ingestion and any evidence of liver injury
  5. Patients with delayed presentation (>24 hours after ingestion) + evidence of liver injury or history of previous acetaminophen overdose
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85
Q

Explain the 20-hour IV acetylcysteine dosing regimen

A
  1. Administer initial loading dose of 150 mg/kg IV for 1 hour
  2. Next, administer a 12.5 mg/kg/h IV for 4 hours
  3. Finally, administer 6.25 mg/kg/h for 16 hours
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86
Q

Explain the 72-hour oral acetylcysteine regimen

A
  1. Loading dose of 140 mg/kg
  2. Then 70 mg/kg every 4 hours (total dose of 17 times)
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87
Q

Side effects of N-acetylcysteine treatment?

A
  • Non-IgE mediated anaphylaxis (when given IV)
  • Vomiting (when given oral)
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88
Q

Protocol for acetaminophen-overdosed patient with hepatic failure?

A
  1. Choose IV acetylcystein regimen (improves hepatic microcirculatory function)
  2. Continued until patient recieves transplant or [encephalopathy is resolved and INR <2]
  3. Additional supportive therapies are also started
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89
Q

Aspirin overdose, mechanism of action?

A
  1. Inhibition of COX 1 and 2 decreased synthesis of prostaglandins, prostacyclin and thromboxanes –> platelet dysfunction and gastric mucosal injury
  2. Stimulation of the chemoreceptor trigger zone in the medulla causes nausea and vomiting
  3. Activation of the respiratory center of the medulla results in hyperventilation and respiratory alkalosis
  4. Interference with cellular metabolism (eg, Krebs cycle, oxidative phosphorylation) leads to metabolic acidosis
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90
Q

Body defense-mechanism against aspirin intoxication include?

A
  1. Binding to protein (90% of normal dose bind to protein)
  2. Hepatic metabolism
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91
Q

What happens to body-defense against aspirin when we overdose?

A

As aspirin lvl rises, the body runs out of enough proteins to bind the aspirin (salisylate) and hepatic metabolism can’t keep up with the large amounts –> elimination becomes dependent upon (slow) renal excretion –> aspirin half-life increase from 2-4h to 30h!

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92
Q

Clinical features of acute aspirin overdose?

A
  1. First symptoms present within 1-2h after ingestion
  2. Early symptoms include hyperpnea (earliest), tinnitus, vertigo, nausea, vomiting and diarrhea
  3. Afterwards if the overdose is severe, another set of symptoms including altered mental status, hyperpyrexia, noncardiac pulmonary edema, and coma
  4. Most patient also have either respiratory-alkalosis or a mix of respiratory-alkalosis and metabolic-acidosis
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93
Q

What is the therapeutic range of aspirin dosage and what is a fatal dose?

A
  • Therapeutic range: 10 to 30 mg/dL
  • Fatal dose: 10-30g/dL

First signs of intoxication appear as early as 40-50mg/dL

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94
Q

Why can aspirin overdose cause altered mental status?

A
  1. Salicylate is directly toxic to the CNS
  2. Overdose may cause neuroglycopenia
  3. Overdose may cause cerebral edema
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95
Q

Important side effect that mainly occur in geriatric aspirin overdose?

A

Salicylate-induced noncardiogenic pulmonary edema

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96
Q

What causes the acid-base abnormalities in aspirin overdose?

A
  • Salicylate directly effects the respiratory center –> hyperpnea –> respiratory alkalosis
  • Cell-damage and glycopnea induced by overdose cause buildup of acids (lactic and ketoacids) –> metabolic-acidosis
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97
Q

What is special about the substance aspirin is made up from?

A
  1. The molecular design of Salisylic Acid consists of a deprotonated (charged) and protonated (uncharged) form
  2. The uncharged form can cross lipid barriers meaning it can cross the blood-brain barrier and epithelium of renal tubule
  3. The lipid soluability means low doses are enough for a cns buildup as it can easyly get reabsorbed in renal collecting tubule and move towards the brain and affect it
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98
Q

How do you treat aspirin overdoes?

A

By giving sodium bicarbonate (NaCOH3 ): Increasing the systemic pH increases the charged/uncharged ratio of salisylic acid, more uncharged means less lipid soluability (less cross blood-brain, and less are reabsorbed in the renals)

  1. Initial dose of NaCOH3 1-2mEq/kg IV
  2. Then: 100-150 mEq NaCOH3 in 1L 5% dextrose solution
  3. Keep going until Serum Salicylate <40mEq/kg
  • Give Potassium even if patient doesn’t have hypokalemia as alkanization will further decrease serum potassium
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99
Q

Diagnostic testing methods for aspirin overdose?

A
  1. Serum Salicylate lvl - >40 mg/dL (2.9 mmol/L)
  2. Serum Creatinine lvl - (aspirin is excreted through kidneys)
  3. Serum potasium - chance of hypokalemia
  4. Prothrombin time - overdose may cause hepatotoxicity –> interfere with Vit K metabolism
  5. Serum Lactate - Salicylates uncouple oxidative phosphorylation –> increased anaerobic metabolism
  6. Anion gap - often elevated with overdose
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100
Q

Further management of aspirin-overdosed patient?

A
  1. ABCDE (stabilize!)
  2. Tracheal intubation ONLY IF NECESSARY (patient has respiratory alkalosis to manage the low pH and we must try to not disturb this natural management)
  3. If hypotensive give fluids, unless patient has cerebral edema or pulmonary edema
  4. Activated Charcoal within two hours of ingestion (1g/kg, 50g total dose)
  5. Give glucose solution despite normal blood glucose (as cerebral glucose lvls are often low)
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101
Q

Aspirin-overdosed patient with respiratory alkalosis, should you treat with bicarbonate?

A

Yes! Respiratory alkalosis is not a contraindication of treatment, just keep serum pH <7.6

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102
Q

Patient with aspirin overdose has low serum pH but large urinary flow, is your treatment working?

A

No, urinary flow is not beneficial to remove salicylate unless the pH is normal or high (when it’s low, most salicylate gets reabsorbed), give more NaHCO3

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103
Q

Indications for hemodialysis in aspirin.overdosed patient?

A

Patient has one or more of the following:

  1. Altered mental status
  2. Pulmonary edema due to respiratory distress
  3. Cerebral edema
  4. Acute or chronic kidney injury
  5. Fluid overload that prevents HCO3 administration
  6. Very high serum salicylate (>90mg/dL)
  7. Severe acidemia (pH <7.2)
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104
Q

How do NSAIDs differ from aspirin in what they inhibit?

A

NSAIDs prevent COX-mediated production of prostaglandins and thromboxanes but not leukotrienes and other eicosanoids (while Aspirin does!)

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105
Q

COX-1 vs COX-2 function?

A

COX-1: Expressed in most tissues and regulates basal cellular homeostasis (platelet function, gastric mucosal integrity, and regulation of renal blood flow)

Cox-2: Regulates inflammatory cytokines and pain

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106
Q

Pharmacokinetics of NSAIDS?

A
  1. They are weak acids
  2. Peak serum lvl within 1-2h, overdose ight cause delay of 3-4h
  3. 99% becomes protein-bound, and 1% is free (ratio changes during overdose, too few proteins to bind it all)
  4. Metabolised in the liver, then excreted through the kidneys
  5. Half life differ based on type (either over or under 8h)
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107
Q

Name the short half-life NSAIDs (<8h)

A
  1. Ibuprofen
  2. Indomethacin
  3. Ketorolac
  4. Diclofenac
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108
Q

Name the long half-life NSAIDs (>8h)

A
  1. Naproxen (shortest of them)
  2. Oxaprozin
  3. Piroxicam)
  4. Phenylbutazone (longest of them)
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109
Q

How much NSAIDs must be ingested for signs of toxicity?

A

> 100mg/kg (except mefenamic acid and phenylbutazone)

Most common symptoms include:

  1. Nausea and vomiting
  2. Drowsiness
  3. Blurred Vision
  4. Dizziness

(at this lvl, very few show severe harm or need treatment)

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110
Q

Which other drugs must you always rule out before suspecting NSAID overdose?

A

Aspirin and acetaminophen! People often mistake them for being NSAIDs and initial overdose-symptoms may be similar.

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111
Q

What are more severe clinical signs of NSAID overdose and how much must be ingested for them to show?

A

Severe toxicity at ingestion >400mg/kg

Symptoms:

  1. Anaphylaxis (especially in asthma & urticaria patients)
  2. Increased anion gap
  3. Lactic acidosis and weak-acidic metabolites
  4. Cardiac Dysrythmias (due to acidosis)
  5. Electrolyte disturbance (due to acidosis)
  6. Seizures and mental status change (due to acidosis)
  7. Acute renal failure/necrosis (very rare)
  8. Hypotension/cardiovascular collapse (ibuprofen)
  9. Anemia or agranulocytosis (phenylbutazone and indomethacin)
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112
Q

Which lab-measurments do you want to take for NSAID-overdose patient?

A
  1. Rule out aspirin and acetaminophen ingestion (check blood levels!)
  2. CBC and Hb lvls (in case of NSAID-induced bleeding)
  3. Renal function test in severe cases
  4. Routine ABG if mental status changes (rule out acidosis)

Serum NSAID lvl is of no value, we monitor symptoms rather than NSAID blood lvl, as even high doses might not cause as severe symptoms as mentioned above

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113
Q

Management of NSAID overdosed patient?

A
  1. ABCDE first
  2. Activated Charcoal within 2h of ingestion
  3. Correction of metabolic acidosis
  4. Crystalloid in case of hypotension
  5. Benzodiazepines in case of seizures
  6. External warming in case of hypothermia

*Extracorporeal removal is ineffective due to high protein binding

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114
Q

What are dihydropyridines?

A
  1. Calcium Channel Blockers
  2. Mainly affect smooth muscle
  3. May cause reflex-tachycardia (due to smooth muscle relaxation causing hypotension)
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115
Q

Examples of Dehydropyridines?

A
  1. Amlodipine
  2. Felodipine
  3. Nicardipine
  4. Nifedipine
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116
Q

What are Nondehydropyridines?

A
  1. Calcium Channel Blockers
  2. Affects myocardial muscle and smooth muscle
  3. Cause myocardial depression and decreased electrical activity
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117
Q

Examples of Nondehydropyridines?

A
  1. Diltiazem
  2. Verapamil
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118
Q

Special effects to note about Calcium channel blockers

A
  1. At high doses, can block sodium channels –> QRS prolongation
  2. Often affect pancreas –> decreased insulin release –> hyperglycemia
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119
Q

Signs of Calcium Channel Blocker overdose?

A
  1. Hypotension (the main sign of both types)
  2. Bradycardia (in nondehydropyridines + nifedipine)
  3. Reflex-tachycardia (only in dehydropyridines)
  4. Jugular venous distention and respiratory crackles (and other clinical signs heart failure)
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120
Q

Types of treatment for Calcium channel blocker overdose?

A
  1. Antidotes
  2. Decontamination therapy
  3. Adrenergic agents
  4. High-dose Insulin Euglycemia Therapy (HIET)
  5. Invasive therapy
  6. Intralipid therapy
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121
Q

Antidotes for Calcium channel blockers?

A
  1. Calcium salts:
  • Calcium chloride 10-20ml 10% solution over 10 min
  • Calcium gluconate 30-60ml 10% solution

(both can also be repeated once and given continuously)

  1. Glucagon: 5mg IV (can be repeated twice with 10 min interval)
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122
Q

Explain decontamination therapy for CCB overdose

A

Give a combination of the following:

  1. 50g Activated Charcoal
  2. IV fluids
  3. Atropine 1mg IV (can be repeated until total 3mg)
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123
Q

What do you give if CCB overdose patient still has hypotension after fluids are given?

A

Give vasopressors, especially adrenergic agents (norepinephrine, dopamine etc…)

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124
Q

Explain High-dose Insulin Euglycemia Therapy (HIET) for CCB overdose patients

A

Give the following combination (insulin-glucose):

  1. Insulin bolus 1 U/kg IV. then continuous 0.5–1 U/kg/h
  2. Dextrose 25-50g bolus, then continous 0.5g/kg/h
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125
Q

Invasive methods of managing CCB overdose?

A
  1. Transvenous pacing
  2. Intraaortic balloon pump
  3. Cardiopulmonary bypass
  4. Extracorporeal membrane oxygenation
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126
Q

Explain Intralipid therapy for CCB overdose patients, and how does it help?

A

20% Lipid emulsion is given bolus of 1.5ml/kg, then continous 0.25ml/kg/min

Helps in three ways:

  1. Makes an intravascular fatty compartment that absorbs some of the CCB
  2. The free fatty acids are an alternative energy source for myocardial cells
  3. The triglycerides prolong myocardial calcium channel opening –> increased myocardial Ca2+ concentration
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127
Q

Explain the 3 types of B-receptors

A

B​1: Found in heart muscle, activation causes:

  1. Increased HR and contractility
  2. Increased AV conduction
  3. Decreased Av-node refractory period

B2: Found in heart, but mostly in bronchial and vascular smooth muscle. Activation causes:

  1. Vasodilation
  2. Bronchodilation

B3: Found in the heart and adipose tissue, activation causes:

  1. Reduced cardiac contraction
  2. Catecholamine-induced thermogenesis
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128
Q

Results of non-selective B-receptor blockade?

A
  1. Bronchoconstriction
  2. Decreased gluconeogenesis
  3. Decreased insulin release
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129
Q

Results of B1-receptor blockade?

A
  1. Decreased myocardial contractility
  2. Decreased automaticity in pacemaker cells
  3. Decreased AV-node conduction
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130
Q

Signs of B-blocker overdose?

A

Occur within 2-6h, but can take upto 24h in SR types and sotalol

  1. Bradycardia
  2. Hypotension
  3. Mental status change and seizures (specially in hypotension)
  4. Bronchospasm
  5. Hypoglycemia
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131
Q

ECG changes due to B-blocker intake?

A
  1. PR prolongation (due to decreased AV-node conduction)
  2. RR prolongation (due to bradycardia)
  3. QRS prolongation (due to overall decreased conduction)
  4. Significant QTc prolongation (sotalol antiarrythmatic effect)
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132
Q

Treatment of B-blocker overdose patient?

A

Glucagon IV 5mg over 1min, if no increase in pulse or BP after 10-15min, give 2nd bolus of 2-5mg over 1h

(Atropine and isoprotenerol might also help, but are inconsistent)

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133
Q

Why is Glucagon the chosen B-blocker antidote?

A

Because glucagon receptors activate the same secondary messenger system as B-receptors

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134
Q

Management protocol for B-blocker poisoning?

A
  1. Secure the airways
  2. Give ALS if necessary
  3. Establish IV access and heart monitoring
  4. Isotonic fluid to correct hypotension
  5. Treat bradycardia with Atropine 0.5-1mg IV every 3-5min, total dose of 0.03mg/kg
  6. IV glucagon treatment protocol (main antidote)
  7. NaHCO3 or Magnesium in case of arrythmia
  8. IV calcium salts
  9. Vasopressors
  10. HIET
  11. Lipid Emulsion Therapy
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135
Q

Explain Calcium Salt management of B-blocker overdosed patient

A
  1. Calcium chloride IV 10ml of 10% solution through CVK
  2. Calcium gluconate 30ml of 10% solution through PVK
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136
Q

Benefits of HIET in B-blocker overdose patients?

A

Myocardial cell benefits due to the insulin:

  1. increased glucose and lactate uptake by myocardial cells
  2. improved myocardial function without increased O2 demand
  3. increased pyruvate dehydrogenase activity –> increased myocardial lactate oxidation –> better Ca2+ handling

Myocardial cell benefits due to the glucose:

  1. Increased myocardial SR-ATPase activity
  2. Increased cytoplasmatic Ca2+ concentration
  3. Incrased Ca2+ entrance into mitochondria & sarcolemma
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137
Q

Side effects of High-dose Insulin Euglycaemic Therapy (HIET)?

A
  1. Hypoglycaemia
  2. Hypokalaemia
  3. Hypomagnesaemia
  4. Hypophosphataemia
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138
Q

Effects Digoxin has on the heart?

A

Increases intracellular Ca2 concentration in myocardial cells. Happens due to Digoxin inhibiting Na-K ATPase –> inhibition of Na-Ca symporter –> more intracellular calcium

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139
Q

Which pre-existing conditions might increase overall Digoxin sensitivity?

A
  1. Renal impairment (cause it’s excreted in urine)
  2. Acid–base disturbances
  3. Hypokalaemia
  4. Hypomagnesaemia
  5. Hypercalcaemia
  6. Myocardial ischaemia
  7. Hypoxaemia
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140
Q

Clinical signs of Digoxin overdose?

A
  1. Lethargy
  2. Confusion
  3. GI symptoms
  4. Visual symptoms
  5. Cardiac arrythmias (might be deadly)
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141
Q

The classic ECG sign found in Digoxin-overdosed patients?

A

Reverse ticks: downsloping ST depression

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142
Q

Other conduction abnormalities typical for Digoxin overdose?

A
  1. Premature Ventricular Contractions (PVCs)
  2. Sinus bradycardia
  3. Overall decreased conduction
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143
Q

The main antidote for Digoxin overdose?

A

Digoxin-spesific antibody fragments

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144
Q

Indication for use of Digoxin-spesific antibody fragments in Digoxin-overdose patient?

A
  1. Life-threatening arrhythmia
  2. Cardiac arrest
  3. Potassium >5.0 mmol/L
  4. Acute ingestion of >10 mg in adults or >4 mg in children
  5. Evidence of end-organ dysfunction
  6. Moderate to severe gastrointestinal symptoms
  7. Serum digoxin concentration >12 nanogram/mL
  8. Significant clinical features of digoxin toxicity with serum digoxin concentration >1.6 nanogram/mL.

These indications are needed because the treatment is very expensive, not because of side-effects

145
Q

Dosing protocol of Digoxin-spesific antibody fragments?

A

Different protocols exist, based on what info we have

  1. Known Digoxin concentration: number of ampuoles = (serum digoxin ng/mL x bodyweight (kg)) / 100
  2. Known amount ingested: number of ampuoles = amount ingested x 2 x 0.7
  3. Uknown data about patient: 5 ampuoles if haemodynamically stable, or 10 if unstable
146
Q

Other treatments for Digoxin overdose?

A
  1. Activated Charcoal within 2h of ingestion
  2. Lignocaine for tachyarrythmias
  3. Atropine for bradyarrythmias
  4. Give oral or IV potassium if patient has hypokalemia
  5. In case of cardiac arrest, ALS given for at least 30min after giving digoxin-spesific antibody fragments
147
Q

What types of Hydrocarbons are there?

A
  1. Aliphatic hydrocarbons: carbons connected by a single, double or tripple bond
  2. Aromatic hydrocarbons: cyclic compunds, containing a benzene ring
  3. Halogenated hydrocarbons: containing fluoride, chloride or bromide
  4. Terpenes: derived from isopren (natural gum substance)
148
Q

Types of exposure to hydrocarbons?

A
  1. Nonintentional-nonoccupational (ie. children unintentionally drinking open bottles they find)
  2. Recreational (for getting high)
  3. Occupational exposure (inhaling vapor at work)
  4. Intentional (for suicide)
149
Q

What are the determinants of aspiration hazard when it comes to hydrocarbons?

A
  1. Volatility - the ability to vaporize or to exist in a gaseous form (more votality = easier absorption)
  2. Surface tension – the adherence of molecules along a liquid surface (low surface tension = more spread in the body)
  3. Viscosity – the resistance to flow through an orifice (low viscosity = easier flow into the body)
150
Q

What are the determinants of systemic toxicity when it comes to hydrocarbons?

A

CHAMP

  • C: Camphor
  • H: Halogenated
  • A: Aromatic
  • M: Metal additives
  • P: Pesticides
151
Q

Systemic manifestation of hydrocarbons

A
  • Most commonly seen with aromatic and halogenated
  • When ingested, most toxic types are aliphatic with toxic additives (ie. metals, camphor etc…)
  • When ingested, mainly determined by votality and absorption within the GI
  • Symptoms:
  1. Myocardial sensitization –> arrythmias
  2. CNS depression and seizures
  3. Hepatic and renal tubular necrosis
152
Q

Pulmonary symptoms after inhaling hydrocarbons

A
  1. Pulmonary aspiration (the most common)
  2. Hydrocarbon pneumonitis (type 2 pneumocyte injury)
  3. Histological changes of lung tissue (inflammation, hemorrhage, necrosis etc…)
153
Q

Types of CNS injury due to hydrocarbon toxicity

A
  1. Direct injury to the brain: many HCs are liophilic and cross blood-brain barrier
  2. Indirect injury to the brain: due to hypoxia or asphyxiation after inhaling HCs
154
Q

CNS symptoms from hydrocarbon toxicity

A
  1. Leukoencephalopathy
  2. Peripheral neuropathy
  3. Blurred vision
  4. Sensory impairment
  5. Muscle atrophy
  6. Parkinsonism

+ Hypercarbia: happens in individuals “bagging” HCs for recreational use

155
Q

How are hydrocarbons hepatotoxic

A

Mainly the chlorinated hydrocarbons (halogenated)

  • Hydrocarbon metabolites and free radicals made during hydrocarbon metabolism attach to hepatic structures –> lipid peroxidation response –> hepatic necrosis
  • Example: Methylene chloride is metabolised in the liver into CO (although not as toxic as inhaling CO in the air)
156
Q

Other symptoms of hydrocarbon toxication?

A
  1. Cardiovascular: sensitization to cathecholamines –> tachydysrhytmias –> syncope or death
  2. Hematologic: Aplastic anemia, multiple myeloma, acute myelogenous leukemia, hemolysis
  3. GI: Irritation of GI mucosae –> vomiting, diarrhoea, burning sensation
  4. Renal: Due to repeated aromatic toluene exposure –> renal tubular acidosis
157
Q

Findings during physical examination hydrocarbon intoxicated patient?

A
  1. Respiratory symptoms: cougching, wheezing, tachypnea, dyspnea
  2. Cardiovascular: Arrythmia, hypotension
  3. GI signs: comiting, diarrhoea, burning sensation
  4. Fever (lasting <48h, if >48 suspect bacteria)
  5. Dermal signs: blistering, pain or redness after HC contact
  6. CNS: visual symptoms, metal status change, ataxia, dizziness
  7. Smell: certain hydrocarbon-rich substances have a special smell (ie. petroleum odor, sweed solvent odor, pine etc…)
158
Q

Tests to take for hydrocarbon toxication?

A
  1. Urinalysis: certain HCs have metabolites excreted in urine
  2. Blood lvls: Toluene lvls, Creatinine Kinase lvls
  3. CBC for leukocytosis, leukemia or enmia
  4. Metabolic panel: BUN, vreatinine, glucose, electrolytes (anion gap)
  5. AST and ALT when suspecting hepatotoxicity
  6. Pulse oximetry (especially for inhaled HCs)
  7. ABG (especially for inhaled HCs, and monitors pH changes)
  8. Chest X-ray (if patient has respiratory symptoms)
  9. ECG (in case of arrythmia)
159
Q

Stabilization of hydrocarbon exposed patient

A
  1. Airway management, give O2 or bronchodilators if needed, intubate if necessary, or ECMO if intubatiion doesn’t help
  2. If patient has brionchospasms give B2-agonists
  3. If patient has seizures give benzodiazepines
  4. Give IV fluids if hypotensive
  5. Dermal and eye decontamination if necessary
  6. If HCs are ingested, start GI decontamination
160
Q

Types of GI decontamination for ingested hydrocarbons?

A
  1. Nasogastric lavage: only if CHAMP is high, the amounts ingested are high and symptoms appear within 1h
  2. Activated Charcoal: best for HCs that have toxic additives
161
Q

Reasons for admitting hydrocarbon-exposed patients after stabilizing them?

A

Observe for 6 hours, if you see any of the following during the observation period, admit the patient:

  1. Patient experiences symptoms even though X-ray is normal
  2. Patient experiences symptoms due the toxic additives
  3. Patient has mild symptoms, normal X-ray, but fails to improve
  4. Asymtpomatic patient, normal X-ray, but cannot come back for follow-up

* if the hydrocarbon exposure was intentional, always admit the patient as this is a sign of suicide tendencies

162
Q

Reasons for discharging hydrocarbon-exposed patient after stabilizing him?

A

Observe the patient for 6 hours and if the following is seen, you can discharge them:

  1. Asymptomatic patient with normal >4h old chest X-ray
  2. Asymptomatic patient with mildly abnormal chest X-ray, can come back the next day for outpatient follow-up
163
Q

Extra precaution to consider when dealing with pesticide toxication from trade products

A

Trade products (ie. pesticides in cans and other containers) often are a combination of the pesticide itself and a solvent that often is a hydrocarbon. Therefore pestecide exposure = treat for not only pesticide but also the solvent (HC treatment)

164
Q

What are insecticides made of and what type are there?

A

They are made of organophosphates and are divided into two groups:

  1. Diethyl organophosphates
  2. Dimethyl organophosphates
165
Q

Clinical course of organophosphate poisoning

A
  1. Acute cholinergic crisis
  2. Intermediate syndrome
  3. Delayed polyneuropathy
166
Q

Toxic mechanism of organophosphate exposure

A

They strongly bind to the enzyme Acethylcholinesterase (AChE) –> decreased acethylcholine breakdown –> strong cholinergic effects on peripheral and central nerves

167
Q

Difference between diethyl and dimethyl organophosphates

A

Diethyl organophosphates have a much longer half-life than dimethyl, a wider therapeutic window and a stronger binding affinity to AChE

168
Q

Muscarinic symptoms of organophosphate toxicity

A

SLUDGE:

  • S: Salivation/Sweating/Seizures
  • L: Lacrimation
  • U: Urination
  • D: Defaecation
  • G: Gastrointestinal cramps
  • E: Emesis

+ Miosis and BBB (Bradycardia, Bronchospasm, Bronchorroea)

169
Q

Nicotinic symptoms of organophosphate toxicity

A
  1. Fasciculations
  2. Muscle cramps
  3. Fatigue
  4. Paralysis
  5. Tachycardia
  6. Hypertension
170
Q

CNS symptoms of organophosphate toxicity

A
  1. headache
  2. tremors
  3. restlessness
  4. ataxia
  5. weakness
  6. confusion
  7. slurred speech
  8. coma
  9. seizures
171
Q

What is Intermediate Syndrome?

A
  • Condition that develops in 20-50% of organophosphate intoxications
  • Occurs after cholinergic crisis have subsided, but before polyneuropathy starts (usually within 1-4 days)
  • Symptoms:
  1. Weakness of neck flexion
  2. Respiratory muscle weakness
  3. Cranial nerve palsies (typically III, IV, VI, VII and X)
  4. Proximal muscle weakness of extremities
172
Q
A
173
Q

Delayed effects of organophosphate intoxication?

A
  1. Organophosphate-induced delayed neuropathy (OPIDN)
  2. Psychiatric disorders (schitzo, depression, confusion)
  3. Myonecrosis
  4. Pancreatitis
174
Q

What is Organophosphate-induced delayed neuropathy (OPIDN)?

A
  • Distal ascending neuropathy that occurs 10-21 days after exposure
  • Paraesthesiae and motor weakness are common
175
Q

Lab test for diagnosis of organophosphate toxication?

A
  1. AChE lvl <50% (although symptoms occur at <20%)
  2. Decreased BChE (butyrylcholinesterase) lvl

*Certain organophosphates decrease BChE more than AChE

176
Q

Diseases that may also give low AChE?

A
  1. Sickle cell disease
  2. Thalassaemia
  3. Severe anaemia
177
Q

Main treatment for organophosphate toxication?

A

Atropine IV 1.8-3.0mg (repeat every 3-5min, doubling the dose each time), then continous infusion of 10-20% of the initial dose that was needed to reach atropinization

  • Often given with Glycopyrrolate IV so the atropine amount given can be less
178
Q

Indications for atropine treatment of organophosphate exposed patient?

A
  1. bradycardia (<80/minute)
  2. hypotension (systolic <80 mmHg)
  3. typical cholinergic symptoms
179
Q

What indicators are a sign that enough Atropin has been given to organophosphate-exposed patient?

A

Atropinization is reached when we see the following indicators

  1. dry skin and mucous membranes
  2. heart rate >80 per minute
  3. systolic pressure >80 mmHg
  4. pupil dilation

If you see more severe anticholinergic symptoms, it means you have over-atropinized

180
Q

What are oximes?

A

AChE reactivators (help against organophosphate poisoning)

  1. Mostly benefitial at nicotinic synapses
  2. Mostly beneficial for diethyl poisonings
  3. Example: Pralidoxime, Obidoxime
181
Q

Other treatments for organophosphate poisoning (not main)

A
  1. Glycopyrrolate: often given with the atropine, so we can use less atropine during treatment
182
Q

What are Carbametes?

A
  1. Insecticides with effect similar to organophosphates
  2. Reversibly inhibit AChE and BChE
  3. Doesn’t effect CNS as much as organophosphates due to poor permeability through blood-brain barrier
  4. Also treated with atropine, but not oximes
183
Q

How can organochlorine pesticides enter the body?

A

Can enter transdermally, by ingestion or by inhalation (depending on the solvent)

184
Q

Organochlorine toxicity, mechanism of action?

A
  1. Impair the nervous system by depolirizing nerve membranes
  2. Inhibit the GABA-chloride channel complex –> less inhibition through GABA –> more nerve excitation

Additional cardiological effects:

  • Sensitizes myocardiom to cathecholamines –> arrythmias
  • Cardiovascular dystrophy (mainly due to lindane)
185
Q

Clinical features of organochlorine toxicity?

A

Onset in 30 min after ingestion, mainly epileptic symptoms

  1. Nausea and vomiting
  2. Seizures: myoclonus, opsoclonus, status epilepticus
  3. Dizziness
  4. Tremors
  5. Confusion
  6. Coma
186
Q

Main antidote for organochlorine toxicity?

A

Cholestyramine Resin

  1. Accelerates biliary-faecal excretion of organochlorines
  2. Dosing 4g four times a day
  3. Treatment may take weeks to fully resolve toxicity
187
Q

Organochlorine toxicity management

A
  1. Monitor for seizures
  2. Maintain open airways
  3. Skin and gastric decontamination if necessary
  4. Dopamine for hypotension if severe
  5. Cholestyramine resin (main treatment)
188
Q

What are Pyrethrins and Pyretheroids?

A
  1. Insecticides
  2. Can enter transdermally, by ingestion, or by inhalation
  3. Low dose –> delay of sodium channel closing in nerve fibers –> paraesthesiae
  4. High dose –> conduction block
189
Q

What are type II pyretheroids?

A
  1. Insecticides of pyretheroid kind
  2. Inhibit GABA signaling –> seizures and other organochlorine-like symptoms
190
Q

Symptoms after oral ingestion of pyrethrins and pyrethroids?

A

Within minutes (local symptoms):

  1. Nausea, vomiting and abdominal pain
  2. Sore throat, salivation and dysphagia

Within hours (neurological):

  1. Headache, dizziness and coma
  2. Blurred vision
  3. Convulsions
191
Q

Symptoms after transdermal or inhalation exposure of pyrethrins and pyrethroids?

A

Transdermal:

  1. Paraesthesiae and stinging sensation
  2. Various forms of dermatitis

Inhalation: Breathlessness and asthma

192
Q

Management of pyretherin and pyrethroid toxication

A

Mainly supportive

  1. O2 and bronchodilators if necessary
  2. Skin decontamination if necessary
  3. If seizures, give benzodiazepines
  4. The paraesthesiae usually resolves by itslef within 12-24h
193
Q

What are Bipyridil compunds?

A
  1. Herbecides
  2. Exposure trough inhalation, ingestion or transdermal
  3. Paraquat and diquat: two special types of bipyridil
194
Q

Bipyridil herbecides, mechanism of toxicity?

A
  1. Oral ingestion: free radical formation –> lipid peroxydation –> hepato-, nephro, and pneumotoxicity
  2. Paraquat: type of bipyridil that builds up in the lungs –> alveolitis –> pulmonary edema and ARDS –> pulmonary fibrosis
195
Q

Symptoms of oral paraquat intoxication?

A
  1. Gastrointestinal corrosive injury
  2. Hepatic failure
  3. Renal failure
  4. Arrythmias and hypotension
  5. CNS depression and seizures
  6. Pulmonary edema –> fibrosis
  7. Rhabdomyolysis

Symptoms and severity depend on amount of dose ingested

196
Q

Symptoms of diquat intoxication?

A
  1. Corrosive effect on the GI tract
  2. CNS symptoms: mental status changes and seizures
  3. Pulmonary symptoms (though not as severe as paraquat)
  4. Mild liver injury
  5. Severe renal injury (tubular necrosis etc…)
  6. Cardiac symptoms: VF and hemmorhage
197
Q

Diagnosis methods of Biperidyl herbecides?

A
  1. Colorimetric urine test (special type of urine chemichal test, where urin turns a certain color, when it contains biperidyls)
  2. Urinary excretion of the biperidyls
  3. Plasma biperidyl concentration
198
Q

Treatment methods for Bipirydil toxicity?

A

Bipitydil has no antidote, treatment is mainly supportive

  1. Nasogastric decontamination
  2. Extracorporeal filtration might help
  3. Imunosuppressive therapy, mainly for paraquat (corticosteroids)
  4. Fluid resuscitation for renal failure
  5. Oxygen therapy: only if patint is very hypoxic, it might increase lung free radicals from paraquat poisoning
  6. Lung transplantation if necessary
199
Q

Chlorophenoxyacetic herbecides, mechanism of toxicity?

A
  1. Dose-dependent cell membrane damage
  2. Disturbing aerobic metabolism
  3. Disturbing acetly-CoA metabolism
200
Q

Symptoms of Chlorophenoxyacetic Herbecide exposure?

A
  1. GI symptoms: nausea, vomit, abdominal pain, diarrhoea
  2. Hypotension
  3. Hypoventilation
  4. Neuromuscular symptoms: ataxia, hypertonia, hyperreflexia, fasciculations and paralysis
  5. Motoric: limb muscle weakness and rhabdomyolysis
  6. Metabolic acidosis and renal failure
201
Q

How to test for Chlorophenoxyacetic Herbecide poisoning?

A

Chromatographic identification test

202
Q

Management of chlorophenoxyacetic herbecide poisoning?

A
  1. Alkaline diuresis (enhances excretion)
  2. Skin or GI decontamination if necessary
  3. Haemodialysis
203
Q

What are Dinitrophenols?

A
  1. Highly toxic hermecides
  2. Can be ingested, inhaled or transported transdermally
  3. Mechanism of toxicity: disrupts mitochondrial metabolism
204
Q

Symptoms of Dinitrophenol intoxication?

A
  1. Symptoms of increased metabolism: hyperpyrexia, tachycardia, tachypnea, hypertension, diaphoresis
  2. Yellow urine and yellow stool
  3. Yellow skin after dermal contact
  4. When severe: hepatic-, renal- and respiratory failure, seizures, bone marrow disruption,
205
Q

Dinitrophenol intoxication management?

A
  1. Skin and GI decontamintion if necessary
  2. Fever reduction - external cooling, no salicylates!
  3. Fluids to prevent dehydration due to hyperthermia
  4. O2 and ventilation if necessary
  5. Benzodiazepines if patient has seizures or is agitated
206
Q

What is Glyphosphate?

A
  1. An herbecide
  2. Is not by itself toxic, but the mixtures it comes commercially in are toxic
207
Q

Symptoms of Glyphosphate intoxication?

A
  1. GI symptoms: nausea, vomiting, diarrhoea
  2. Oral and throat irritation when inhaled
  3. Conjunctivitis and corneal injury when exposed to eyes
  4. Erythema and skin irritation when exposed to skin
  5. In its most potent mixture it can cause GI burns, renal-, hepatic- and respiratory failure, arrythmia and bradycardia, and CNS symptoms like seizures
208
Q

Management of glyphospshate toxication?

A

Mild toxicity:

  • Oral dilution or irrigation, antiemetics, pain medications

Severe toxicity:

  1. Nasogastric aspiration
  2. Gastroscopi to evaluate GI burns
  3. Airway management if necessary
  4. Fluids or vasopressors for hypotension
  5. Correcting electrolyte lvls and metabolic acidosis
  6. Haemodialysis
209
Q

What are Substituted Benzene?

A
  1. They are fungicides
  2. Symptoms based on the 3 types:
  • Chlorothalonil: dermatitis
  • Pentachlorophenol: local irritation, hyperthermia, hepatotoxicity and seizures
  • Hexachlorobenzene: porphyria cutanea tarda

*Treatment is only supportive and based on symptoms

210
Q

What are Dithiocarbamates?

A
  • Fungicides
  • Symptoms include:
  1. Headache, delirium and encephalopathy
  2. Disulfiram-like reaction (red face and neck)
  3. Local irritation of contaminated area
  • Treatment: decontamination if neccesary, O2 or B-agonists if intake is due to inhalation
211
Q

What are Organomercurials?

A
  1. Mercury-containing fungicides
  2. Intake through all three routes
  3. The murcery often builds up in RBCs and CNS
212
Q

Symptoms of organomercurial toxicity?

A

Early:

  1. Numbness and tingling of digits and face
  2. Tremors and mental status change

Severe:

  1. Loff senses (vision, hearing, balnce etc…)
  2. Spasticity and rigidity of muscles
  3. Further mental status change
213
Q

Main treatment of organomercurial toxicity?

A

Chelation, using Succimer (DMSA)

*Extracorporeal treatment might also help

214
Q

What are Organotins?

A
  • Fungicides
  • Interfere with mitochondrial metabolism
  • Symptoms:
  1. Nausea and vomiting
  2. Hepatotoxicity
  3. Dermal irritation
  4. Headache, dizziness, blurred vision
  5. Tremors and weakness

*Treatment is supportive, only treat symptoms

215
Q

Symptoms of Thallium poisoning?

A

Early:

  1. Abdominal pain, nausea, vomiting
  2. Hematochezia
  3. Stomatitis and ileus
  4. Hypotension and arrythmia

CNS (days to >1 week):

  1. Headache, lethargy, weakness
  2. Paraesthesiae, tremor and ataxia
  3. Seizures, delirium, coma

>2 weeks later - alopecia

216
Q

Management of Thallium poisoning?

A
  1. Prussian blue (increases excretion)
  2. Haemodialysis (also helpful)
  3. Electrolyte and fluid correction (decrease seizures)
217
Q

Symptoms of Warfarin intoxication?

A
  1. Prolonged PT and INR (earliest symptom)
  2. Bleeding from nose, gums and lips
  3. Bloody urine, feces and vomit
  4. Hematomis in joints
  5. Cerebral hemorrhage –> paralysis

*all symptoms are bleeding-related

218
Q

Treatment of warfarin toxication?

A

Main treatment:

  1. Vit K1 IV solution
  2. Fresh Frozen Plasma (the next best)

Management:

  1. Activated Charcoal
  2. Gastric lavage
  3. PT and INR monitoring
219
Q

What are Superwarfarins?

A
  1. Inhibit the same as normal warfarin, but has a longer duration of action
  2. Prolongation of PT and INR appears later than in normal warfarin, but lasts can last for months
  3. Same treatment as warfarin (Vit K1 and FFP)
220
Q

What is Aluminium Phosphide?

A
  1. Inhalation rodenticide (becomes phosphine in air)
  2. Toxicity: lipid peroxidation –> various organ damage
  3. When ingested, the liver also metabolises it to phosphine –> delayed/slow toxic effects
221
Q

Symptoms of Aluminium Phosphide inhalation?

A
  1. Mild: local irritation, dizziness, respiratory distress
  2. Moderate: diplopia, ataxia, tremors
  3. Severe: ARDS, arrythmias, liver- and renal failure, seizure
222
Q

Symptoms of Aluminium Phosphide ingestion?

A
  1. GI: epigastric pain, repeated vomiting, diarrhoea
  2. Circulation: hyptension, tachycardia, myocarditis, arrythmia
  3. Respiratory: cough, dyspnoea, cyanosis, ARDS
  4. Metabolic acidosis and hemolysis

+ Benign oesophageal strictures due to local corrosion

223
Q

Aluminium Phosphide management?

A

Mainly supportive

  1. Gastric lavage with potassium permanganate if ingested
  2. Saline in case of shock
  3. Sodium bicarbonate in case of metabolic acidosis
224
Q

What is Zinc Phosphide?

A
  1. Rodenticide powder that releases phosphine gas when in contact with water
  2. Symptoms similar to Aluminium Phosphide, but slower
  3. Treatment: symptom management similar to AP poisoning
225
Q

What are Barium compunds?

A
  • Rodenticides
  • Mechanism: interfere with Na-K pump –> change of cell-membrane permeability –> muscle paralysis
  • Symptoms:
  1. Vomiting and abdominal pain
  2. Muscle ightness and tremors
  3. Convulsions, paresthesiae, ascending quadriparesis –> breathing difficulty
  4. Hypokalemia and arrythmias
226
Q

Management of Barium compunds?

A
  1. Gastric lavage
  2. Eating Magnesium sulphate (precipitates the barium)
  3. Correcting hypokalemia and monitoring arrythmias
227
Q

What is Metaldehyde?

A
  1. Molluscicide similar to acetaldehyde
  2. Intak trough inhalation, GI and skin
  3. Mechanism: decrease effect of GABA –> seizures
    4.
228
Q

Symptoms of Metaldehyde poisoning?

A
  1. Fever and facial flushing
  2. Nausea, vomiting and abdominal cramps
  3. Drowsiness, spasms and tachycardia
  4. Ataxia and increased muscle tone
  5. Seizures, tremor, hyperreflexia
  6. Muscle twiching, coma and death
229
Q

Metaldehyde management?

A
  1. GI decontamination if necessary
  2. N-acetylcysteine might help a little
  3. O2 and ventilation in case of hypoxia
  4. Correction of dehydration and acidosis
  5. Benzodiazepines for seizures
230
Q

What is Diethyltoluamide (DEET)?

A
  • Insect repellent
  • Intake trough inhalation, ingestion and transdermally
  • Symptoms:
  1. Systemic: hypotension and respiratory depression
  2. Dermal: local irritation and bullous eruptions
  3. CNS: mental change, ataxia, seizures, paralysis and areflexia
  • Management: skin decontamination and supportive care
231
Q

What is Ethylene Dibromide?

A

A highly toxic fumigant pestecide (absorbed by all routes)

232
Q

Skin symptoms of Ethylene Dibromide exposure?

A
  1. Ulcerations
  2. Conjunctivitis
  3. Gastrointestinal and mucosal irritation
  4. CNS depression
233
Q

Symptoms of Ethylene Dibromide ingestion?

A
  1. Vomiting, diarrhoea and burning sensation
  2. Tremors and CNS depression
  3. Hypotension
  4. Oliguria
  5. Jaundice
  6. Pulmonary edema

*If death ocurrs within first 24h it’s usually due to respiratory- or circulatory failure, while if it ocurrs after it’s usually due to liver- or renal failure

234
Q

Lab tests for Ethylene Dibromide poisoning?

A
  1. Serum bromide
  2. Urea and creatinine lvl
  3. Level of bilirubin and liver enzymes
  4. Level of protein/blood in urine
235
Q

Management of Ethylene Dibromide toxication?

A
  1. Gastric lavage or activated charcoal (within 2h of ingestion)
  2. Haemodialysis (helpful)
  3. Supportive care of symptoms (ventilation, fluids etc…)
  4. Endoscopy (look for esophageal burns)
236
Q

Other than the CO produced by burning, what other way can one be exposed to CO poisoning?

A

Methylene Chlroide, when ingested 1/3 of it is metabolised in the liver into CO (slow toxicity, longer duration)

237
Q

Carbon monoxide, mechanism of toxicity?

A

It reversibly binds to one of the 4 seats of hemoglobin with high affinity and causes the rest 3 seats to bind oxygen very strongly –> oxygen not released when blood reach the tissues –> hypoxia and necrosis of organs and tissues

*the brain and the heart are especially at risk

238
Q

How to monitor CO intoxication?

A

By monitoring the lvl of HbCO

  • Already at 10% headache start to appear
  • HbCO of 50-70% result inseizure, coma and death
239
Q

Who are especially at risk of CO exposure?

A
  1. COPD patients
  2. Neonates (they have already high O2 affinity)
240
Q

Symptoms of CO poisoning?

A

Although there are MANY symptoms, these are the most important:

  1. Hyperthermia and cherry red skin
  2. Pale sclera (pallor) and bright red retinal veins
  3. Noncardiac pulmonary edema
  4. Flu-like symptoms
  5. Tachycardia and tachypnea
  6. Hypertension or hypotension
241
Q

Neurologic and neuropsychiatric symptoms of CO poisoning

A
  1. Memory disturbance
  2. Emotional disturbance
  3. Gait disturbance
  4. Sensory disturbance
  5. Apraxia and ataxia
  6. Stupor
  7. Long-time exposure = longer time to recover
242
Q

Other ways of monitoring CO poisoning?

A
  1. ABG - acidosis monitoring
  2. ECG: in case of sinus tach or arrythmias
  3. Cardiac ischemia markers: troponin C, CK-MB, myoglobin
  4. CBC: in case of leukocytosis DIC and TTP
  5. Electrolyte lvl
  6. Liver screening panel
  7. Renal screening panel
243
Q

Imaging tests for CO poisoning?

A
  1. Chest X-ray: if severe CO poisoning or if considering using hyperbaric chamber
  2. Head CT: look for edema or focal lesions
  3. MRI: more accurate for focal lesions and white matter demyelination - helsp monitor recovery
    4.
244
Q

Management of CO poisoned patient

A
  1. Cardiac monitor
  2. Venous HbCO lvl (pulsoxymetry is useless here!)
  3. Give 100% O2 (CO half-life goes from 3-4h to 30-90min)
  4. Hyperbaric chamber if HbCO >40% (CO half-life 15-20min)
245
Q

Precautions to take when treating CO poisoned patient

A
  1. Do not agressivly treat acidosis as it may increase effect of CO, oxygen is usually enough
  2. If you consider Cyanide poisoning and wnt to start cyanide treatment aswell, first give sodium thiopental as it prevents the enhancing effect cyanide antidotes have on CO
    3.
246
Q

Indications for hyperbaric chamber treatment for CO poisoning?

A

Although hyperbaric chamber isn’t considered to be in protocol, it is often used when the following is seen:

  1. Loss of conciousness or coma
  2. Ischemic ECG changes
  3. Focal neurological deficits
  4. HbCO lvl >40%
247
Q

Hyperbaric chamber treatment regimen for CO poisoning

A

100% O2 at 2.4-3atm for 90-120 minutes, repeat if necessary

248
Q

What are tropane alkaloids?

A
  1. Natural substances found in plants
  2. Have anticholinergic effects
  3. Example: atropine, scopolamine, hyoscyamine
249
Q

Pathophysiology of Datura-species plants?

A
  1. Contain tropane alkaloids –> anticholinergic symptoms
  2. Found in all parts of these plants, mainly in roots and seeds
  3. Scopolamine is the main tropane alkaloid in these plants, affecting both central and peripheral nerves
  4. Atropine amount varies between species, highly concentrated in the seeds
250
Q

Management of tropane alkaloid poisoning?

A
  1. Physostigmine IV 2mg (antidote)
  2. Activated charcoal - helpful
    3.
251
Q

Precaution to take when treating tropane alkaloid toxicity with physostigmine?

A

Cardiac monitoring to be on a lookout for cholinergic crisis (seizures, respiratory distress, asystole), in that case give atropine IV 1/2 dose of physostigmine given

252
Q

In which states must tropine alkaloid poisoned patient be in for physostigmine to be indicated?

A
  1. unresponsive to supportive treatment
  2. tachydysrhythmias and hemodynamic changes
  3. seizures unresponsive to benzodiazepines
  4. extremely severe agitation or psychosis
253
Q

When is physostigmine contraindicated as an antidote for anticholinergic toxication?

A

Absolute:

  • If the patient takes any medication causing cardiac-rythm abnormalities (e.g TCA’s, quinidine, procainamide etc…)

Relative:

  • Reactive airways
  • Intestinal obstruction
  • Intake of depolarizing paralytic agents
254
Q

Pathophysiology of mushrooms containing Muscimol and Ibotenic acid?

A
  1. Muscimol - GABA agonist (Muscimol-induced GABAergic syndrome)
  2. Ubotenic acid - glutamate agonist (Glutaminergic syndrome)
  3. Becaus these mushrooms contain these two opposite substances, symptoms are both inhibitory and exitatory
  4. CNS symptoms range from agitation to coma
  5. Effects within 30min-1h of ingastion, last up to 8h
255
Q

Symptoms of Muscimol toxicity?

A
  1. lethargy
  2. ataxia
  3. dysarthria
  4. sleep
  5. coma
256
Q

Symptoms of Ibotenic acid toxicity?

A
  1. hallucinations
  2. hyperactivity
  3. ataxia
  4. myoclonic jerks
  5. convulsions
257
Q

Pathophysiology of Amanita Muscaria mushrooms

A
  1. Contain mainly muscimol and ibotenic acid, but also a small amount of muscarinic agonists
  2. Does not contain the deadly amatoxin that is found in certain Amanita species
  3. Symptoms are a mix of excitation, sedation and hallucination
258
Q

Pathophysiology of Inocybe and Clitocybe mushrooms

A
  1. Contain Muscarine (M1, and M2 agonist)
  2. Don’t cross blood-brain barrier, only peripheral symptom
  3. Symptoms: typical cholinergic symptoms (salivation, diaphoresis, bradycardia, bronchoconstriction, increased GI motility etc…)
  4. Mainly supportive treatment, but give atropine or ipratropium if respiratory secretions become severe
259
Q

Pathophysiology of Psilocybin-containing mushrooms

A
  • Contain psilocybin and psilocin (LSD and seretonin analogs)
  • Cause hallucinations and psychosis similar to LSD + some anticholinergic symptoms
  • Treatment:
  1. Mainly supportive of symptoms
  2. Gastric lavage or activated charcoal if necessary
  3. Benzodiazepines if the get too agitated/psychotic or experience seizures
260
Q

What is Phalloidin?

A
  1. A toxin found in several Amanita mushrooms
  2. Causes gastroenteritis-like effects after ingestion
  3. Often ingested alongside amatoxin
261
Q

What is Amatoxin?

A
  1. A toxin found in several Amanita mushrooms
  2. Interferes with DNA and RNA transcription (affects tissues of high protein synthesis)
  3. 60% is excreted into the bile abd then eliminated with urine and GI after 70-90h
  4. Hepatotoxic symptoms are the earliest, then renal
262
Q

Stages of Amanita intoxication?

A

Stage 1: Nausea, vomiting, watery diarrhea, and cramping abdominal pain, 6-12 hours after ingestion

Stage 2: Resolution of symptoms, but hepatic and renal damage is ongoing

Stage 3: if discharged, patients may return to the hospital 2-6 days later with severe coagulopathy, renal failure, and encephalopathy

263
Q

Lab tests for Amarita intoxication?

A
  1. Liver function test
  2. Electrolyte, glucose, BUN and creatinine levels (renal)
  3. Spore analysis in stomach contents and feces’
  4. ELISA test of urine sample for amatoxin
  5. Liver biopsy - histological examination
264
Q

Management of Amanita poisoned patient?

A
  1. Silymarin (Silibinin) IV (main antidote used in EU)
  2. Gastric lavage and activated charcoal might help
  3. Alkaline diuresis (helpfun within 2-4h of ingestion)
  4. Haemodialysis in case of renal failure
  5. Hepatic dialysis system (e.g MARS) until liver transplant is available
265
Q

What is Coprine?

A
  1. A toxin found in Coprinus atramentarius mushrooms
  2. Blocks the enzyme aldehyde dehydrogenase (ALDH) –> acetaldehyde buildup –> disulfiram-like symptoms
  3. Treatment: Fomepizole (blocks alcohol dehydrogenase, decrasing amount of acetaldehyde made after drinking ethanol)
266
Q

What is Monomethylhydrazine (MMH) and how is it made?

A
  • It’s made after gyromitrin and hydrazone react in the stomach after ingestion of Gyromitra mushrooms, this results in the making of MMH
  • MMH is a water-soluble toxin that causes:
  1. Gastroenteritis
  2. Hemolysis Methemoglobinemia
  3. Hepatorenal failure
  4. Seizures and coma
267
Q

MMH, mechanism of toxicity?

A

Neurotoxicity:

Like isoniazid, inhibits pyridoxine kinase –> decreased glutamate synthesis and inhibit GABA production (due to inhibiting GAD enzyme aswell)

Gastrointestinal toxicity:

Inhibition of diamine oxidase in intestinal mucosa ..> several GI symptoms + hepatotoxicity

Hematopoietic toxicity:

Hemolysis and methemoglobinemia –> hematuria –> renal failure

268
Q

Treatment of MMH poisoning?

A
  1. Treat seizures with pyridoxine and benzodiazepines
  2. Treat methemoglobinemia with methylene blue
  3. Blood transfusions for anemia
269
Q

What is Orellanine?

A
  1. Nephrotoxic compund found in cortinarius mushrooms
  2. Affects ATP production in proximal tubule cells –> tubulointerstitial nephritis
  3. Renal failure within the first days of ingestion
  4. Treatment: early hemodialysis and hemoperfusion to prevent renal failure + fluid and electrolyte correction
270
Q

Nerve agents in chemichal warfare, mode of action

A
  1. AChE inhibitors –> overexcitation or paralysis
  2. Main cause of death: respiratory paralysis
  3. Cause muscarinic, nicotinic and CNS effects
  4. Include the following agents:
  • Sarin: EEG changes, arrhythmias, hypoxia, low-grade fever
  • Tabun: peripheral neurotoxicity, CNS and other organ system hypoxic sequelae
271
Q

Nerve agents in chemichal warfare, treatment?

A
  1. Atropine
  2. Oximes (e.g pralidoxime)
  3. HI-6 (oxime alternative, good for sarin poisoning)
  4. Pyridostigmine bromide (prophylactic antidote) - reversibly binds AChE to protect it from strong inhibition
272
Q

What are Blister agents (Vesicants)?

A
  • Gas agents producing skin blistering, upper respiratory damage, and severe eye injuries
  • Include:
  1. Sulfur Mustard
  2. Nitrogen Mustard
  3. Lewisite
273
Q

Pathophysiology of Sulfur and Nitrogen mustards?

A

Sulfur Mustard:

Yellow, mustard-smelling compund that passes into cells –>irreversible alkylation of DNA, RNA and proteins –> cell death

Nitrogen Mustard:

Colorless, garlic-smelling polyfunctional alkylating agent of DNA –> cell death

274
Q

Symptoms of Mustard poisoning?

A

Skin: spreading erythaema and blister formation

Inhalation:

  1. Burning respiratory passages and bronchitis
  2. Dyspnoea and hypoxia –> respiratory acidosis
  3. Erythaema, oedema, and ulceration of affected mucosa

Ocular: lacrimation, photphobia, eyelid blisters, corneal ulceration

Systemic: Fever, bone marrow disturbance, seizure, shock

275
Q

Management of Mustard poisoning?

A
  1. No spesific antidote once mustard reach the cells
  2. Decontaminate eyes and skin
  3. 100% humidified supplemental O2 and ventilation
  4. Tracheotomy in case of airway obstruction due to irritation
  5. Atropine into eyes for relief of pain (decrease ciliary spasms)
  6. Surgical debridement ans skin grafts if necessary
  7. Colony stimulating factor (CSF) in granulocytopenic patients
276
Q

What is Lewisite?

A
  1. Arsenic compund that prevent acetyl-CoA formation –> blistering
  2. Also increase capillary permeability –> haemoconcentration and hypotension (lewisite shock)
277
Q

Symptoms of Lewisite poisoning?

A
  • Skin: Blisters
  • Eyes: burning, spasms and loss of vision within 1 min
  • Systemic:
  1. Pylmonary edema
  2. Hypothermia and hypotension (lewisite shock)
  3. Haemolytic anaemia
  4. Liver and gallbladder necrosis
  5. Kidney damage

Sequela: Bowen’s Disease (cause lewisite is teratogenic)

278
Q

Management of Lewisite poisoning?

A
  1. BAL (dimercaprol) injected IM + skin ointment version (antidote)
  2. Decontaminate with an alkaline agent (soap)
  3. Supportive treatment of symptoms
279
Q

What are Blood Agents, and what do they do?

A
  • Cyanide-containing gases or liquids used in chemichal warfare to cause asphyxia
  • Mechanism of action: CN binds to cyt C oxidase i mitochondria –> inhibition of respiratory chain –> depression of CNS, respiration and myocardial activity –> hypoxemic-cytotoxic hypoxia
280
Q

Symptoms of Blood Agent poisoning?

A
  1. Almond odour in breath
  2. CNS: Headache, lighdheadedness, vertigo, agitation, seizures and coma
  3. Respiratory: tachypnea and hyperpnea followed by dyspnea and then apnea
  4. Cardiac: Hypertension and tachycardia followed by hypotension and bradycardia, arrythmia

Cyanosis is not common due to detah occuring within minutes

281
Q

Treatment of blood agent poisoning?

A
  1. Hydroxocobalamine/sodium thiosulfate
  2. Cyanide antidote kit
  3. Sodium nitrite
  4. Dicobalt-EDTA
  5. Symptomatic support
282
Q

Pathophysiology of Chlorine?

A
  • Greenish-yellow gas with strong, pungent odour
  • React with moist tissue and causes oxidization –> damage
  • Reaction also causes production of certain acids like HCL –> more damage
  • Symptoms:
  1. Airway burning and irritation –> feeling of suffocation
  2. Pulmonary edema and respiratory arrest
  • Treatment: symptomatic treatment + humidified NaHCO3 might help
283
Q

What is Chloropicrin?

A
  • Alkylating choking agent that causes inhibition of several enzymes and interferes with oxygen transportation by Hb
  • No antidote, only supportive care
284
Q

Symptoms of Chloropicrin exposure?

A
  1. Irritation of all body surfaces in contact
  2. Lacrimation and eye pain
  3. Pharyngeal or pulmonary edema
  4. Rhinorrhea
  5. Erythema
285
Q

Pathophysiology of Phosgene?

A
  1. Choking agent that produce HCL when in contact with moist tissue
  2. AlsoI increases pulmonary vascular permeability –> pulmonary edema
  3. Also causes bronchial epithelial damage –> local emphysema and partial atelectasis
286
Q

Symptoms of Phosgene toxication?

A
  1. Lacrimation
  2. Nausea and vomiting
  3. Dyspnea and pulmonary edema
  4. Bloody or foaming white sputum
  5. Cyanosis
  6. Nephrotoxicity
  7. Polycythemia

* Mainly supportive/symptomatic treatment, maybe aminophylline for the pulmonary edema

287
Q

Management of Phosgene toxication?

A
  1. Mainly supportive/symptomatic treatment
288
Q

Pathophysiology of Lacrimators (tear gas agents?)

A

Inactivate SH-containing enzymes and activate TRPA1 receptors (noxious/irritation receptors)

289
Q

Symptoms of exposure to Lacrimators (tear gas)? Treatment?

A

*Treatment is mainly symptomatic/supportive

290
Q

What is Quinuclidinyl Benzilate?

A
  1. Non-selective anticholinergic gas used as psychomimetic/incapacitating agent
  2. Much stronger than atropine
  3. Anticholinergic symptoms
  4. Treated with physostigmine
291
Q

Symtoms of Botulinum Toxin ingestion?

A

Mechanism: Prevents presynaptic release of ACh

Ocular: ptosis, blurred or double vision, strabismus, nystagmus

GI: constipation, dysphagia

Respiration: respiratory failure

Nurological: descending paralysis, weakness

292
Q

Treatment of Botulinum Toxin intoxication?

A

Spesific antitoxin therapy: antitoxin binds circulating toxin and prevents progression

293
Q

What is T-2 toxin?

A
  1. Mycotoxic compund that is cytotoxic to rapid-dividing tissue (e.g spleen, bone marrow, GI, thymus etc…)
  2. Its toxic effects resemble damage done by radiation
294
Q

Pathophysiology of Ricin?

A

Four ways of effecting the body:

  1. Binding to ribosomal subunit –> inhibition of protein synthesis
  2. Aactivation of apoptic pathways
  3. Direct cell membrane damage
  4. Stimulate release of inflammatory cytokines
295
Q

Symptoms of Ricin poisoning?

A
  1. Early fever
  2. Nausea, vomiting and diarrhoea
  3. Irritation of GI mucosae –> GI hemorrhage
  4. Hepatic and renal damage
  5. Adrenal insufficiency
  6. CNS depression

If it is injected instead of ingested, the above symptoms occurr very fast and patient dies within 3 days!

296
Q

Treatment of Ricin poisoning?

A
  1. No antidote yet
  2. Gastric lavage and activated charcoal
  3. Whole-bowel irrigation with polyethylene glycol
  4. Supportive treatment of symptoms
297
Q

Theophylline, medical function and toxicity?

A
  • Taken for Asthma and COPD
  • Therapeutic lvls 10-20 mcg/mL
  • Toxic lvl >20 mcg/mL
  • Mainly metabolised in the liver
  • Half-life varies (somwehere around 5-8h)
298
Q

Theophylline, mechanism of action?

A
  1. Phosphodiesterase inhibition –> increased cAMP –> adrenergic simulation –> B1 and B2 stimuli –>vasodilation and vasoconstriction
  2. A2 receptor antagonist –> increased HR and contraction
299
Q

Symptoms of theophylline overdose?

A
  1. Metabolic: Hyperglycemia, Hypercalcemia, Hypophosphatemia and Hypokalemia
  2. CNS: Tremors, agitation, hallucination, seizures
  3. Cardiac: Dysrythmias, Supraventricular tachycardia –> ventricular tachycardia –> VF –> PEA
  4. Pulmonary: Acute lung injury and respiratory alkalosis –> respiratory failure
300
Q

Tests for a Theophylline overdose patient?

A
  1. Serum Theophylline lvl
  2. Serum lvl of other medications to check for cross-reaction (common cause of chronic theophylline injury)
  3. Electrolyte lvl (monitor metabolic symptoms)
  4. ABG - monitor metabolic acidosis
  5. ECG - monitor cardiac symptoms
301
Q

Management of Theophylline overdose?

A
  1. Multidose Activated Charcoal (main treatment)
  2. Cathartics (with first dose of MDAC)
  3. Gastric lavage - often helpful
  4. Whole Bowel Irrigation - for Theophylline SR
  5. Benzodiazepines in case of seizures
  6. Fluids for hypotension, a1 agonists or B-antagonists (Esmolol) also helpful
  7. Antiemetics in case of vomiting
  8. Extracorporeal treatment
302
Q

Indications for hemoperfusion of Theophylline overdosed patient

A
  1. Symptomatic patients > 90 mcg/mL
  2. Long-time theophylline concentrations > 40 mcg/mL
  3. Life-threatening toxicity
  4. Persistent seizures
  5. Hypotension that is not responding to IV fluids
  6. Ventricular dysrhythmia
303
Q

How is ethanol metabolised?

A

80%: Ethanol –> Acetaldehyde –> H2O and CO2

304
Q

Pathophysiology of ethanol?

A
  1. Downregultes GABA in CNS –> sedation
  2. Disrupt motor cortex in cerebellum –> ataxia
  3. Inhibits NDMA receptors –> memory disturbances, slurred speech and black out
  4. Increase endogenous opioid release –> Euphoria and analgesics
  5. Seretonin analog –> antidepressive
  6. Dopamine analog –> Dependance
  7. Inhibit ADH release –> dehydration
  8. Loss of thermoregulation –> Hypothermia
305
Q

Symptoms of acute ethanol intoxication?

A

Common:

  1. Many metabolic dearrangement (Everything is hypo)
  2. Behavioural effects
  3. Children suffer more from hypoglycemia (less glycogen stores)

Severe:

  1. CNS- and respiratory depression
  2. Arrhythmias hypogylcemia
  3. Hypotension
  4. Hypothermia
  5. Lactic acidosis
306
Q

Test and diagnosis of ethanol intoxication?

A
  1. Clinical features and Breathalyzer (main way of diagnosis)
  2. ABG and blood sample
  3. Exclude all ATOMIC criteria
  4. Osmolar gap >10 (osmolar gap: 2xNa + glucose + urea)
  5. Anion gap > 20 (anion gap: Na + K - (Cl + HCO3))
    6.
307
Q

Symptoms of alcohol withdrawl?

A
  1. Mild: Autonomic hyperactivity, tremor, weakness, anxiety, headache sweating
  2. Hyperreflexia and GI sympotoms. < 6h
  3. Tonic-Clonic seizures <48 h
  4. Alcoholic hallucinations: Conciousness remains
  5. Delirium tremens: 48-72h: Anxiety attacks, increasing confusion, poor sleep (scared), profuse sweating, tachycardia, hyperpyrexia and severe depression
308
Q

What is Isopropanol?

A
  1. Rubbing alcohol
  2. Metabolised to Acetone and excreted through the kidneys
  3. Intoxication produces KETOSIS (not acidosis)
  4. Diagnosis similar to ethanol, but look for ketosis
  5. Treatment: supportive
309
Q

What is Ethylene glycol, and what is its mechanism of action?

A
  1. Found in antifreeze (ask about fluid color)
  2. Mechanism: Ethylene glycol → Glycoaldehyde (nephrotoxic) → Glycolic acid (Acidosis)→glyoxylic acid→ Glycine, OXALATE (nephrotoxic) and a-hydroxy-b-ketodiapate

*Thiamine and pyridoxime deficiencies will further increase oxalate metabolite, because they are needed as co-factors when glycine and a-hydroxy-b-ketoadipate are made

310
Q

Phases of Ethylene Glycol toxicity?

A
  • Phase 1: Neurological/drunk <12h
  • Phase 2: Cardiopulmonary phase 12-24h
    • Hypocalcaemia with QT elongation → arrhythmias
    • High metabolic acidosis with kussmaul breathing
  • Phase 3: Renal toxicity
311
Q

Diagnosis and treatment of Ethylene Glycol intoxication?

A
  • Diagnosis: calcium oxalate crystals in urine
  • Treatment: Fomepizol (antidote) + kidney transplant if necessary
312
Q

Explain Methanol metabolism

A

Methanol → formaldehyde → Formate (Accumulates, can cross BBB) → C02 and H20

  • Metabolism is VERY slow, which means formic acid has time to accumulate and cause systemic acidosis
  • It also inhibits mitochondrial activity, causing tissue hypoxia and lactic acidosis
313
Q

Symptoms of Methanol intoxication?

A
  1. CNS: Coma and convulsions + basal ganglia necrosis = parkinsonism
  2. Retinal: Mydriasis, Optic nerve hyperaemia, photophobia (toxicity due to formic acid buildup in optic disc and nerve)
  3. Cardiac: Tachycardia, hypertension –> hypotension
  4. Respiratory: Tachypnea
314
Q

Treatment of Methanol intoxication?

A
  1. Fomepizole
  2. Ethanol
  3. Hemodialisys (if acidosis is severe or there’s renal failure)
315
Q

What test can you take if you’re not sure if patient is intoxicated with methanol or ethylene glycol?

A

ABG (acidosis does not occur in ethylene glycol toxication)

316
Q

What is Methcathinone?

A
  • Psychoactive stimulant
  • Can be snorted or injected
  • Dopamine reuptake inhibitor
  • Effect:
  1. Spontanous motor activity
  2. Appetite and drink suppression
  3. Euphoria
317
Q

What is MDPV?

A
  • An aphrodisiac stimulant
  • Norepinephrine-reuptake inhibitor
318
Q

Effects of MPDV?

A

Short-term:

  1. Tachycardia and hypertension
  2. Increased alertness, anxiety and arousal

Severe: Panic attacks and psychosis from sleep withdrawl

Long-term: Comedown syndrome (lethargy, headache, depression)

319
Q

What differs synthetic cannabinoids from natural?

A

Same psychoactive effect as natural but:

  1. THC lvl cannot be measured in patients using them
  2. Much more addictive
  3. Effect last much longer

*Symptomatic treatment + benzo or SSRI’s in case of psychotic agitation

320
Q

What are Sedative-hypnotics?

A
  • Group of drugs causing CNS depression
  • Include Barbiturates and non-barbiturates (Benzo,carbamates, GHB etc…)
321
Q

What are GHB and GHL?

A
  • Non-barbiturate that increase GABA B receptor activity and dopamine levels in the CNS
  • Date-rape drugs (cause loss of conciousness)
  • Symptoms:
  1. Slurred speech
  2. CNS- and mild respiratory depression
  3. Seizures
  4. Coma
322
Q

What are Benzodiazepines?

A
  • Non-barbiturates used for many medical conditions
  • Bind to allosteric site of GABA receptors –> increased receptor stimulation –> depression of spinal reflexes and RAS
  • Addictive and cause withdrawl syptoms similar to ethanol withdrawl
323
Q

Symptoms of benzodiazepine exposure?

A

Mild:

  1. Sedation
  2. Slurred speech
  3. Ataxia

Severe:

  1. Hypotension and hypothermia
  2. Respiratory depression
  3. Coma
  4. Rhabdomiolysis
324
Q

Management of benzodiazepine overdose?

A
  1. Flumazenil (main antidote)
  2. Gastric lavage and activated charcoal
  3. Supportive treatment of symptoms (e.g ventilation)
325
Q

What can flumazenil cross-react with and are contraindications of its use?

A
  1. TCA’s
  2. Cocaine
326
Q

What are short-acting Barbiturates?

A
  • Sedative hypnotics used for sedation and treatment of epilepsy, including status epilepticus
  • Increase stimulation of GABA receptors
  • Symptoms:
  1. CNS depression: somnolescense, ataxia, coma
  2. Myocardial depression –> hypotension, collapse
  3. Respiratory depression (cause of death)
  4. Blisters
327
Q

Management of short-acting barbiturate toxication?

A
  1. No antidote!
  2. Activated Charcoal - might help
  3. Monitor heart and kidneys
  4. Intubate in case of hypoxia
  5. Correct hypothermia and hypotension
  6. Hemodialisys - if nothing else helps
328
Q

What differs Long-acting barbiturates from short-acting?

A
  1. Includes phenobarbital
  2. They have longer effect and severe symptoms come early
  3. Can be monitored (at least serum phenobarbital lvl)
  4. Urine alkalinization works for long-acting, but not short-acting!
329
Q

What is Carbamezipine?

A
  1. An antiepileptic drug with large destribution
  2. Lipid soluable, easily enters the brain
  3. Selectivily inhibit overactive epileptic foci by blocking Na-K pump, while normal-firing neurons are not affected
  4. Has an active metabolite (carbamezipine epoxide) that can buildup
330
Q

Symptoms of Carbamezipine intoxication?

A
  1. Nystagmus
  2. Tachycardia and hypotension
  3. Ataxia
  4. Variation between CNS agitation and depression –> coma
  5. Respiratory depression and apnea
  6. Urinary retention
  7. Toxic Epidermal Necrolysis (TEN), blisters
  8. DRESS syndrome
  9. Stevens-Johnson syndrome
331
Q

Tests for Carbamezipine toxicity?

A
  1. Serum Carbamezipine lvl
  2. Glucose and electrolytes for differentials
  3. Abdominal radiograph (might see pill buildup)
  4. ECG: Sinus tach, AV-block, long WRS and QTc
332
Q

Management of Carbamezipine intoxication

A
  1. Multiple Doses of Activated Charcoal
  2. Gastric lavage
  3. WBI
  4. Symptomatic treatment
333
Q

Valproic Acid, mechanisms of action?

A
  1. Prolongs recovery period of inactiva Na channels –> less nerve firing (similar effect as carbamezipine)
  2. Increase amount of GABA release at synapses
  3. Interfere with urea cycle –> hyperammonemia
  4. Interfere with fatty acid metabolism and deplete carnitine lvls –> fatty liver
  5. Metabolised to active metabolites –> prolonged action

*Used for seizures, as mood stabilizers and bipolar disease

334
Q

Symptoms of Valpric Acid toxication?

A
  1. Nusea and vomiting (most common)
  2. Lethargy, cerebral edema and coma
  3. Fever
  4. Hypotension
335
Q

Tests for Valproic acid toxicity?

A
  1. Serum Valproic Acid lvl
  2. Liver panel
  3. Anion gap
  4. CT head: cerebral edema
336
Q

Treatment of Valproic Acid toxication?

A
  1. Hemodialisys (main treatment)
  2. L-carnitine supplementation (may resolve some symptoms)
  3. GI decontamination
  4. Supportive treatment
337
Q

What are Neuroleptics mainly used for?

A
  1. Reduse delisions, confusion and agitation in psych-patients
  2. Used as sedatives and tranquilizers
  3. Used as anitemetics
338
Q
A
339
Q

Neuroleptics, mechanism of action?

A

Antagonise the following:

  1. Central D2 receptor)
  2. Muscarinic receptors
  3. Serotonin receptors
  4. a1-receptors
  5. H1-receptors

Pathophysiology include anticholinergic and extrapyramidal symptoms

340
Q

What is Neuroleptic Malignant Syndrome (NMS)?

A
  1. A special reaction to neuroleptic drugs
  2. Often linked with haloperidol use
  3. Linked to D2-receptor inhibitory effect of neuroleptics
341
Q

Symptoms of NMS?

A
  1. Hyperthermia
  2. Autonomic dysfunction: tachycardia, BP instability, arrythmia
  3. Lead-pipe rigidity
  4. Altered mental status
  5. Hypotension and seizures might also occur

The first 4 clinical findings are enough for diagnosis +also look for high CK lvls in urine

342
Q

Diagnosis criteria for NMS?

A
  1. The 4 main symptoms are enough for diagnosis
    2.
343
Q

Treatment of NMS?

A
  1. Dantrolene (main antidote)
  2. Dopamine agonists - Bromocriptine and Amantadine
  3. Supportive treatment
344
Q

What is Biperiden hydrochloride (Akineton) used for?

A

For treating the dystonia caused by Neuroleptics and other antipsychotic drugs

345
Q

Most common SSRI’s?

A
  1. Sertraline
  2. Fluoxetine
  3. Paroxetine
  4. Fluvoxamine
346
Q

What does Seretonine regulate?

A

CNS:

  1. Mood and personality
  2. Temperature
  3. Wakefulness

Systemic:

  1. Vascular tone
  2. Platelet activation
  3. Peristalisis
347
Q

What is Seretonin Syndrome?

A
  • A series of severe side effects of SSRI’s
  • Charcterized by:
  1. Mental status changes
  2. Neuromuscular dysfunction
  3. Autonomic instability
348
Q

Sternbach Criteria for the diagnosis of serotonin syndrome?

A
  1. Symptoms increase with increased SRRI intake
  2. Three of the following is seen: altered mental status, agitation, tremor, shivering, diarrhea, hyperreflexia, myoclonus, ataxia, or hyperthermia
  3. Other causes are excluded
  4. Patient has not taken neuroleptics before symptoms occur
349
Q

Main difference between NMS and Seretonin syndrome?

A
350
Q

Treatment of Seretonin Syndrome?

A
  1. No antidote!
  2. WBI
  3. Activated Charcoal
  4. Airway management and benzo for seizures
  5. Supportive treatment
351
Q

What is Malignant Hyperthermia?

A
  1. A drug-induced or stress-induced hypermetabolic syndrome
  2. Characterized by hyperthermia, muscle contractions, and cardiovascular instability
  3. Linked to genetic Ca-transport defect of skeletal muscles
  4. Several drugs like Halothane and Succinylcholine are triggers of this syndrome
352
Q

Clinical manifestation of malignant hyperthermia?

A
  1. May occur within 30 min of anesthesia
  2. Begins with muscle rigidity of the chest, then spreads
  3. Following tachycardia
  4. And finally hypertension
353
Q

Treatment of mailgnant hyperthermia?

A

Dantrolene (main treatment) - stops muscular overactivity by stopping release of Ca from the sarcoplasmatic reticulum in muscles

*CC-blockers are useless for malignant hyperthermia

354
Q

Tricyclic antidepressives, mechanism of action?

A
  1. Inhibit reuptake of seretonin and norepinephrine
  2. In chronic use may inhibit alpha-, Beta, and seretonin receptors
355
Q

Pathophysiology of TCA’s?

A
  1. Cholinolityk properties –> anticholinergic symptoms
  2. Cardiotoxic: Long QRS and QT, Torsades, myocardial depression and a-antagonism –> hypotension
  3. Cross BBB –> delirium and seizures
  4. Discontinuation –> withdrawl symptoms

* Diagnose by tox analysis and ECG

356
Q

Causes of Rhabdomyolysis?

A
  1. Exercise induced
  2. Traumatic (blunt force trauma etc…)
  3. Toxicologic
  4. Metabolic disorders
  5. Genetic disorders
  6. Infections
357
Q

Clinical sequelae of rhabdomyolysis?

A
  1. Hypovolemia (water goes into injured myocites)
  2. Hyperkalemia (release of cellular K into blood)
  3. Metabolic acidosis (release of cellular phosphate and sulfate)
  4. Acute renal failure (nephrotoxic effects of myocyte components)
  5. Disseminated intravascular coagulation (DIC)
    6.
358
Q

Lab test results typical of rhabdomyolysis?

A
  1. Increased serum CK (most useful)
  2. Positive urine dipstic for hemoglobin/myoglobin
  3. High serum creatinine
  4. Increased LDH
  5. Hyperkalemia
  6. Hypocalcemia
  7. Hyperuricemia

+ ECG abnormalities might also be seen

359
Q

Management of rhabdomyolysis?

A

Mainly supportive treatment to prevent end-organ damage, especially kidneys, monitor CK while you do this:

  1. Crystalloid fluid to keep urinary output
  2. Urinary alkanization + consider osmotic- or loop diuretics
  3. Treat electrolyte abnormalities and DIC

5 MD (7 decks)

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