L1: General Toxicology Flashcards

1
Q

Def of Toxicology

A

Science dealing with
- Properties
- Actions
- Toxicity
- Autopsy findings (in case of death, in relation to poisonous substances).
- Fatal dose
- Detection
- Estimation
- Treatment

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2
Q

What is a Toxicant?

A

Specific chemical poisonous.

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3
Q

Categorization of toxic effects

A
  • Toxic effects are categorized according to site of poison effect.
  • In some cases, effect may occur at only one site, This site is referred to as specific target organ.
  • In other cases, toxic effects may occur at multiple sites.
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4
Q

Types of systemic toxicity

A
  • Acute toxicity
  • Subacute toxicity
  • Chronic toxicity
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5
Q

Onset of Acute Toxicity

A
  • occurs almost immediately (hours/days) after an exposure.
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6
Q

Causes of Acute Toxicity

A

usually a single dose or a series of doses received within one day.

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7
Q

Onset of Subacute Toxixity

A

results from repeated exposure for several weeks or months.

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8
Q

Causes of Subacute Toxixity

A

This is a common human exposure pattern for some pharmaceuticals and environmental agents

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9
Q

Onset of Chronic Toxicity

A
  • It represents cumulative damage to specific organ systems
  • takes many months or years to become a recognizable clinical disease.
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10
Q

Causes of Chronic Toxicity

A
  • Damage due to subclinical individual exposures may go unnoticed but with repeated subclinical exposures, cumulative damage slowly builds up until it exceeds threshold for chronic toxicity.
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11
Q

Manners of posining

A

Suicidal (Deliberate): Overdose as self-harm.

Accidental: Most episodes of pediatric poisoning, dosage error or iatrogenic.

Homicidal

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12
Q

what are poisons classified according to?

A
  • According to their mode of action
  • According to the organs affected: (Target Organ Toxicity).
  • According to the chemical nature
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13
Q

Classification of poisons, according to their mode of action

A
  • Poisons with local action
  • Poisons with remote action
  • Poisons with both local and remote actions
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14
Q

what are posions with local action? and are examples for them?

A
  • They act locally producing immediate destruction of tissues with which they come in contact

e.g., corrosives (except organic acids)

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15
Q

Def of poisons with Remote action

A

They act only after absorption without any local effects

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16
Q

Examples of poisons with Remote action

A

plant poisons which act mainly on CNS.

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17
Q

Def of poisons with Local & Remote action

A

which have a local irritant action on tissues, they come in contact for some time and a remote action (on parenchymatous organs) after absorption.

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18
Q

Examples of poisons with Local & Remote action

A

irritant metallic poisons

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19
Q

Classification of poison according to organ affected

A
  • Neurotoxic (Brain)
  • Hepatotoxic (liver)
  • Nephrotoxic (Kidney)
  • Cardiotoxic (Heart)
  • Immunotoxic
  • Respiratory System
  • Reproductive System
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20
Q

Examples of Neurotoxic (brain) toxins

A
  • Alcohol
  • Lead
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21
Q

Examples of Hepatotoxic (Liver) toxins

A
  • Ethanol
  • Acetaminophen
  • Phosphorus
  • Carbon Tetrachloride.
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22
Q

Examples of Nephrotoxic (Kidney) toxins

A

Heavy metals e.g., mercury.

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23
Q

Examples of Cardiotoxic (Heart) toxins

A

Digitalis.

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24
Q

Examples of Immunotoxic toxins

A

Isocyanates.

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25
Q

Examples of Respiratory System toxins

A
  • Tobacco smoke
  • Asbestos
  • Ozone.
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26
Q

Examples of Reproductive system toxins

A

Di-bromochloropropane.

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27
Q

classification of toxins, according to the chemical nature

A
  • Acids
  • Alkalis
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28
Q

Examples of acids

A
  • Sulphuric acid
  • Nitric acid
  • Hydrochloric acid.
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29
Q

Examples of alkalis

A

Caustic soda
Caustic potash
Ammonium hydroxide

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30
Q

What are factors affecting the severity of toxicity?

A
  • Factors related to the person
  • Factors related to the poison
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31
Q

Factors related to the person affecting severity of toxicity

A
  • Age of the person
  • Genetic factors
  • Personal hypersensitivity
  • Tolerance
  • Idiosyncrasy
  • State of health
  • Condition of the stomach
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32
Q

How does age affect the severity of toxicity?

A
  • Children and old people are generally more susceptible to toxic agents
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33
Q

Why are children and people more susceptible to toxic Asians?

A

Due to decrease of detoxification power.

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34
Q

What can children tolerate, and what can’t they?

A

Children can tolerate action of atropine, but not morphine.

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35
Q

Person suffering from G6PD deficiency are susceptible at therapeutic doses to hemolytic effect of some drugs like ……..

A

vitamin K and sulphonamides.

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36
Q

Genetic factors affecting severity of toxicity

A

Persons suffering from glucose-6-phosphate dehydrogenase deficiency are susceptible at therapeutic doses to hemolytic effect of some drugs

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37
Q

How does personal hypersensitivity affect severity of toxicity?

A

Very small harmless doses can produce severe symptoms in sensitive patients

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38
Q

Drugs, which are most commonly associated with personal hypersensitivity

A

Therapeutic dose of penicillin or iodine may produce anaphylaxis in hypersensitive patients.

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39
Q

Describe tolerance

A

where addicts can stand big dose without ill-effect, So, they have to increase the dose to get same effect.

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40
Q

What causes tolerance?

A
  • Repeated intake of substances of abuse leads to development of tolerance
  • So, they have to increase the dose to get same effect.
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41
Q

What is idiosyncrasy?

A
  • Abnormal response to some drugs
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42
Q

Drugs associated with idiosyncrasy

A

Morphine may produce convulsions instead of depression of CNS.

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43
Q

How does state of health affect severity of success?

A

Patients suffering from liver or kidney diseases may show signs of increased toxicity of poisons.

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44
Q

Aspects of condition of the stomach

A
  • Type of food
  • Gastric secretion
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45
Q

How does type of food affect severity of toxicity?

A
  • Fatty foods delay absorption of arsenic
  • while they increase absorption of some poisons as DDT and phosphorus.
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46
Q

How do gastric secretions affect severity of toxicity?

A
  • Poisoning with potassium cyanide may not be fatal
  • In case of achlorhydria: as HCL in stomach is important to form severely toxic hydrocyanic acid.
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47
Q

How does state of the poison affect severity of Toxicity?

A

Poisons in gaseous form are more rapidly absorbed

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48
Q

Factors related to the poison, affecting severity of toxicity

A
  • State of the poison
  • Routes of poison administration
  • Dose of the poison
  • Cumulation
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49
Q

What form of poisons is most Rapidly absorbed?

A
  • Gaseous form are more rapidly absorbed
  • Followed by:
    Liquid
    Fine powder
    Big lumps.
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50
Q

Route of administration causes the quickest toxicity?

A
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51
Q

General scheme for approach of a poisoned patient

A
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52
Q

what questions should history taking in poisoning include?

A
  • Type of toxins (What)
  • Time of toxic exposure (acute versus chronic). (When)
  • Amount of toxin taken (How much)
  • Route of toxin administration (i.e. ingestion, intravenous, inhalation) (How.).
  • Manner of the toxic ingestion or exposure. (Why)
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53
Q

How does Dose of the poison affect severity of Toxicity?

A

The bigger the dose, the more toxic effect

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54
Q

History taking in poisoning

A
  • History of sudden appearance of toxic manifestations in a healthy person or a group of persons after taking certain food or drink (as food poisoning, methanol and carbon monoxide toxicity).
  • History of intake a poison, financial problems, psychiatric troubles, provious altempts at suicide or threatening by somebody.
  • History of presence of bottle.of tablets or insecticide near the victim.
  • History of patients rescued from fire (CO, cyanido).
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55
Q

Diagnosis of poisoning

A
  • History & Circumstantial evidence
  • Clinical Examination: (General & Local)
  • Investigations
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56
Q

Psychiatric information in poisoning history Taking

A
  • History of psychiatric illness or previous suicide attempts.
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57
Q

cumulation of poison & its relation to severity of toxicity, then give examples for some drugs that may be accummilated in this way

A
  • After repeated small doses of certain drugs which are not readily metabolized,
  • The effect of a single large dose is reached leading to poisoning e.g., digitalis.
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58
Q

What information should history in poisoning include?

A
  • Psychiatric Information
  • Drug(s) Information
  • Unavailable Information
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59
Q

Drug information in poisoning history Taking

A
  • Information about all drugs taken, including prescription, over the counter medications, vitamins, and herbal preparations.
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60
Q

Examples of Toxidromes

A
  • Sympathomimetic
  • Anticholinergic
  • Hallucinogenic
  • Opiod
  • Sedative - Hypnotic
  • Cholinergic
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61
Q

What to do if there is unavailable information in poisoning history Taking?

A
  • If history is unavailable from patient, information should be taken from family and friends.
  • Paramedics or emergency medical technicians are also good sources of information, because they may be able to furnish details, such as presence of empty pill bottles.
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62
Q

clinical examination in cases of poisoning

A
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63
Q

Examples of drugs causing Sympathomimetic Toxidrome

A

Cocaine.
Amphetamine.
Pseudo-ephedrine.

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64
Q

Vital signs in Sympathomimetic Toxidrome

A

Hyperthermia.
Tachycardia.
Hypertension.
Tachypnea.

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65
Q

Pupils in Sympathomimetic Toxidrome

A

Mydriasis.

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66
Q

Examples of drugs causing Anticholinergic Toxidrome

A

Atropine.
Tricyclis-antidepressant.
Antibistamine,

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67
Q

Vital Signs in Anticholinergic Toxidrome

A

Hyperthermia.
Tachycardia.
Hypertension.

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68
Q

Pupils in Anticholinergic Toxidrome

A

Mydriasis.

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69
Q

Other findings in Anticholinergic Toxidrome

A

Hot, dry, red.
Blind.
Seizures.

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70
Q

other findings in Sympathomimetic toxidrome

A

Piloerection.
Hyperreflexia.
Diaphoresis.
Tremors.

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71
Q

Examples of Drugs causing Hallucinogenic Toxidrome

A

49-Tetra-Hydrocannabinol.
Phencyclidine.
Lysergic acid diethylamide

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72
Q

Vital Signs in Hallucinogenic Toxidrome

A

Tachycardia.
Hypertension.
Tachypnea.

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73
Q

Pupils in Hallucinogenic Toxidrome

A

Mydriasis.
Nystagmus

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74
Q

Other findings in Hallucinogenic Toxidrome

A

Hallucinations.
Agitation.
Disorientation.

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75
Q

Examples of drugs causing Opiod Toxidrome

A

Opiates.
Heroin.

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76
Q

Pupils in Opiod Toxidrome

A

Hypothermia
Bradycardia.
Hypotension.
Hypopnea

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77
Q

Vital Signs in Opiod Toxidrome

A

Miosis.

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78
Q

Other Findings in Opiod Toxidrome

A

CNS depression.
Coma.
Antidote

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79
Q

Examples of drugs causing Sedative-Hypnotic Toxidrome

A

Benzodiazepines.
Barbiturates.
Alcohol, Anticonvulsant.

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80
Q

Vital Signs in Sedative-Hypnotic Toxidrome

A

Hypothermia
Bradycardia.
Hypotension.
Hypopnea.

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81
Q

Pupils in Sedative-Hypnotic Toxidrome

A

Miosis (usually)

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82
Q

Examples of Drugs Causing Cholinergic Toxidrome

A

Organophosphates.
Carbamates.
Mushrooms.

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83
Q

Other Findings in Sedative-Hypnotic Toxidrome

A

Hyporeflexia.
Confusion.
Stupor.
Coma.
Antidote

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84
Q

Vital signs in Cholinergic Toxidrome

A

Hypothermia
Bradycardia.
Tachypnea.

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85
Q

Pupils in Cholinergic Toxidrome

A

Miosis.

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86
Q

Other Findings in Cholinergic Toxidrome

A

Lacrimation.
Salivation.
Incontinence.
Bronchospasm.
Seizures
DUMBLES

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87
Q

Causes of Coma

A
  • Toxic causes
  • Traumatic causes
  • Pathologic causes
  • Environmental causes
  • Hysterical
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88
Q

toxic causes of Coma

A

Generalized CNS depression:
- (e.g., ethanol, opiates, and sedative-hypnotics).

Post-ictal phenomenon
- after a drug-induced seizure: (e.g. anticholinergics).

Hypoglycemia
- (e.g., insulin, oral hypoglycomic drugs).

Cellular hypoxia:
- (e.g., CO, cyanido).

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89
Q

Pathologic causes of Coma

A
  • Liver and renal failure.
  • Infections as encephalitis or meningitis.
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90
Q

Traumatic causes of Coma

A

Head injuries.

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91
Q

environmental causes of Coma

A

Hypothermia
Hyperthermia.

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92
Q

hysterical causes of Coma

A

No organic cause, normal vital signs, and negative investigations

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93
Q

General lines of treatment of Coma

A
  • Care of Airway & Breathing
  • Coma cocktail
  • Control convulsions
  • Correct electrolyte, or acid-base disturbance
  • CT Scan
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94
Q

When is Dextrose given in cases of Coma?

A
  • It is given to all patients with depressed consciousness & hypoglycemia.
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95
Q

Dose of dextrose in cases of Coma

A
  • Child: 25 % (2 ml/kg) IV.
  • Adolescent/adult: 50 % (1 ml/kg) IV.
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96
Q

When is naloxone given in cases of Coma

A

It is given to all patients with depressed respiration.

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97
Q

Dose of Naloxone in cases of Coma

A
  • Child: 0.1 mg/kg IV.
  • Adolescent/Adult: 0.4 mg IV & 0.1 mg IV “If
    suspected Opioid Abuse”.
  • If no response give up to 2 mg IV.
  • If no response, repeat the dose every 2 min. till a total dose of 10 mg.
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98
Q

when is Thiamine given in cases of Coma?

A
  • It is given to malnourished and chronic alcoholic patients.
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99
Q

Dose are thiamine in cases of Coma

A

100 mg IV or IM (is not given routinely lo children).

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100
Q

Causes of Convulsions

A
  • Toxic causes
  • Metabolic Causes
  • Traumatic causes
  • Pathologic causes
101
Q

Toxic causes of Convulsions

A
  • Poisons acting on cerebrum
  • Poisons acting on brain stem
  • Poisons acting on spinal cord
  • Poisons causing cerebral anoxia
102
Q

Poisons acting on cerebrum

A
  • Causing muscular hyperactivity

e.g., amphetamine, cocaine, caffeine and atropine.

103
Q

Poisons acting on spinal cord

A

Causing tonic convulsions i.e. sustained hypertonia of the muscles

  • e.g., strychnine.
104
Q

Poisons acting on brainstem

A

Causing clonic convulsions** i.o., contraction & relaxation of muscles**

  • o.g., picrotoxin and lead.
105
Q

Poisons causing cerebral anoxia

A

cyanide

106
Q

Metabolic causes of convulsions

A

Hypoglycemia, hyponatremia, hypocalcemia, or hypoxia.

107
Q

Traumatic causes of convulsions

A
  • Head trauma with intracranial injury.
  • Idiopathic epilepsy.
  • Exertional or environmental hyperthermia
108
Q

Pathological causes of convulsions

A
  • CNS infection (meningitis or encephalitis)
  • Febrile seizures in children.
109
Q

General lines of treatment of convulsions

A
  • Maintain an open airway and assist ventilation.
  • Use one or more of the following anticonvulsants
  • Specific measures
  • Consider specific antidotes.
110
Q

Drugs used in cases of convulsions

A
  • Diazepam: 1st Line of therapy:
  • Phenobarbitone 2nd Line of therapy:
  • Phenytoin: It is not indicated in management of toxic seizures.
111
Q

Specific measures in cases of convulsions

A
  • Glucose for hypoglycemia.
  • Cool Immediately for hyperthermia.
  • Fluids for dehydration.
112
Q

Types of Non-Toxic Indigestion

A
113
Q

Def of Non-Toxic Indigestion

A
  • producing little to no toxicity when ingested in small amounts.
  • They are not true poisoning and can be managed by reassurance.
114
Q

Criteria to diagnose non-toxic exposure

A

To diagnose a non-toxic exposure; all of the criteria should be present:

  • Absolute identification of the product.
  • Absolute assurance that only 1 product was ingested.
  • Absence “NO” signal word (Danger, Poison, Warning, Caution) on the container
  • A good approximation of the amount ingested.
  • Assurance that the victim is free of symptoms.
  • Ability to call back at intervals to determine that no symptoms have developed.
115
Q

What causes a patient to be asymptomatic after exposure to toxin?

A

The patient with exposure to toxin may remain asymptomatic due to:

Non-toxic substance: The substance may be nontoxic.

Insufficient amount: An insufficient amount has been ingested

Insufficient absorption: -An sufficient amount has not been absorbed

116
Q

Investigations in toxocology

A

General Investigation “Routine Investigations”:
- ECG
- Lab
- Rad

Specific Investigation “Toxicological Investigations” “Toxicology Screen”

117
Q

General lab investigations in toxicology

A
  • Blood Glucose Level.
  • Arterial blood gases
  • High anion gap metabolic acidosis (MUD PILES)
  • Liver function tests: Clotting profile for paracetamol & anticoagulants toxicities.
  • Renal functions tests: Urine analysis for rhabdomyolysis
  • Complete Blood Picture.
118
Q

High anion gap metabolic acidosis

A

MUD PILES

  • Methanol
  • Uremia
  • Diabetic ketoacidosis
  • Propylene glycol
  • Iron
  • Lactic Acidosis
  • Ethanol
  • Salicylates
119
Q

Radiological Examination in toxicology

A
  • Chest X ray
  • Abdominal X ray
120
Q

When is chest x-ray done in toxicology?

A

If pulmonary edema /aspiration is suspected.

121
Q

What are drugs that causes pneumonitis or pulmonary edema?

A

MOPS

  • Meprobamate & Methadone
  • Opioids
  • Phenobarbital, Propoxyphene, Paraquat & Phosgene
  • Salicylates
122
Q

When is abdominal x-ray done in toxicology?

A

(BETA CHIP).

  • Barium
  • Enteric coated tablets
  • Iricyclic antidepressants
  • Antihistamines
  • Chloral hydrate, Cocaine
  • Calcium
  • Heavy metals
  • lodides
  • Phenothiazines, Potassium
123
Q

Samples for toxicology screen

A

Samples are taken from:
- Blood & Urine “Most Indicated”
- Vomitus, Gastric Lavage & Stool “May Indicated”

124
Q

Value of toxicology screen

A

The most important evidence of poisoning is by chemical analysis.

125
Q

Categories of toxicology screen

A
  • Blood levels
  • Urine screen
  • Specific tests
126
Q

Blood levels of 3A & 3I toxicology screen

A
  • Alcohols “Ethanol & Mothanol”
  • Inotropic “Digoxin & Theophylline”
  • Iron
  • Analgesic “Paracetamol & Salicylates”
  • Anti-Epileptics “Carbamazepine, Phenobarbital”
  • Immunosuppressant “Methotrexate”
127
Q

urine screen

A

In cases of suspected substance of abuse: ABC

  • Amphetamine
  • Benzodiazepines & Barbiturates
  • Cannabis & Cocaine
  • Opioids, Tramadol, Pregabalin, & Synthetic Cannabinoids.
128
Q

Specific tests toxicology screen

A

Carboxyhemoglobin levels “if carbon monoxide poisoning is suspected”

129
Q

General lines of treatment of poison patient

A
130
Q

How to prevent further exposure to the poison?

A
131
Q

Emergency & supportive treatment

A
132
Q

What is the greatest contributor to death from drug overdose and poisoning?

A

Respiratory failure

133
Q

How to maintain Airway opening & clearance?

A
  • Airway opening
  • Airway clearance
  • Maintain airway opened
134
Q

What maneuver is used for airway opening?

A

Triple airway maneuver: (Head tilt, jaw thrust, mouth opening)

135
Q

Airway opening if there is any suspicion of neck injury

A

Place the patient in left lateral position with head downwards which allows tongue to fall forwards and vomitus or secretions to drain out of the mouth.

136
Q

Airway clearance

A
  • Finger sweep technique to remove any F.B. or denture
  • Suctioning of the mouth and oropharynx to remove secretions.
137
Q

How to maintain opened airway?

A

Either by oro or nasopharyngeal airway

138
Q

What are toxic causes of respiratory failure?

A

Central Causes:
- opiates, barbiturates, alcohols.

Peripheral Causes
- Airway obstruction
- Neuromuscular block
- Paralysis of respiratory muscles: BOSP

139
Q

Peripheral causes of toxic respiratory failure

A
  • Airway obstruction
  • Neuromuscular block
  • Paralysis of respiratory muscles: BOSP
140
Q

Central causes of toxic respiratory failure

A

opiates, barbiturates, alcohols.
Peripheral

141
Q

Toxic causes of airway obstruction

A
142
Q

What toxins cause Laryngeal spasm?

A

cyanide poisoning

143
Q

What toxins cause oedema of the airway?

A

irritant fumes or gas such as chlorine inhalation.

144
Q

What toxins cause bronchospasm?

A

organophosphates compounds.

145
Q

What toxins cause excessive secretions?

A

organophosphate or carbamate toxicity.

146
Q

What toxins cause Pneumonia?

A
  • From aspiration of Gastric Contents, or hydrocarbons such as Kerosene.
147
Q

What toxins cause Pulmonary edema?

A

Organophosphates.

148
Q

What are toxins that caused neuromuscular block?

A

Neostigmine and physostigmine.

149
Q

Methods of breathing support

A
  • 02 mask (Face mask) or bag valve mask (Ambu bag) or Endotracheal intubation (ETT)
  • Pulse oximeter to assess 02 saturation:
150
Q

What are toxins that caused paralysis of respiratory muscles?

A

BOSP

  • Botulinum toxins
  • Organophosphates
  • Snake bites
  • Post convulsive muscle exhaustion.
151
Q

What are advantages of endotracheal intubation?

A
  • It protects airway and prevents aspiration and obstruction.
  • It allows for mechanically assisted ventilation.
  • Some emergency drugs can be given through it e.g., naloxone, atropine and opinophrine.
152
Q

Basics of circularatory support

A
153
Q

What to do if there is no pulse?

A

Perform cardiopulmonary resuscitation

154
Q

When to begin continuous ECG monitoring?

A

This is essential for comatose patients and cardiotoxicity.

155
Q

When is a Foley’s catheter introduced?

A
  • It is placed in bladder if patient is seriously ill (shocked, convulsing or comatose).
  • Obtain urine for routine and toxicologic testing and measure hourly urine output.
156
Q

Disability assessment

A
  • Once ABC is addressed, neurological status should be assessed, mainly level of consciousness, Pupil, Random blood sugar (RBS).
157
Q

What is Stupor?

A

It is a grade of unconsciousness in which patient can be aroused (awakened) only by painful stimuli.

158
Q

What is Coma?

A

It is a state of prolonged unconsciousness in which patient cannot be aroused by painful stimuli.

159
Q

Levels of consciousness AVPU Scale

A
160
Q

Reed’s classification of level of consciousness

A
161
Q

Types of decontamination

A
  • Skin decontamination
  • Eye decontamination
  • Lungs decontamination
  • GIT Decontamination
162
Q

indications of skin decontamination

A

Corrosives:
- To prevent skin injury.

Toxins:
That are readily absorbed through the skin:
- To prevent systemic absorption.

As: Organophosphates Insecticides, Paraquat, Phenol & Oxalic Acid.

163
Q

Steps of skin decontamination

A
164
Q

Indications of eye decontamination

A

Corrosive and Hydrocarbon solvents:

  • That can rapidly damage the cornea.

Toxins:
- That are readily skin absorption, can also be absorbed through conjunctiva.

165
Q

Steps of eye decontamination

A
166
Q

Indications of lung decontamination

A

Irritating gases and fumes:
- As chlorine gas.

Toxins:
- That are absorbed through respiratory tract (Inhalation): As CO, Cyanide, Hydrogen Sulphide & Organophosphates Insecticides.

167
Q

Steps of lung decontamination

A
168
Q

Method of GIT decontamination

A
  • Emesis.
  • Cathartics.
  • Gastric Lavage.
  • Whole Bowel Irrigation.
  • Activated Charcoal (Local Antidote).
169
Q

Emesis as a method of decontamination

A

currently abandoned.

170
Q

Def of Cathartics

A

Substances that enhance passage of materials through the GIT, thus decrease time of contact belween poison and absorptive surface of stomach and intestine.

171
Q

Types of Cathartics

A
  • Osmotic Cathartics
  • Irritant cathartics
172
Q

examples of Osmotic cathartics

A

Magnesium Sulfate & Sorbitol.

173
Q

MOI of Osmotic cathartics

A
  • These are substances that increase osmotic pressure in the intestinal lumen
  • Thus causing fluid to be drawn into lumen causing evacuation.
174
Q

Dose of Osmotic cathartics

A

1-2 g/kg “Sorbitol”.

175
Q

Examples of Irritant cathartics

A

Castor oil

176
Q

MOI of Irritant cathartics

A

They act by stimulation of motility

177
Q

Dose of Irritant cathartics

A

60-100ml

178
Q

cautions during using of Irritant cathartics

A
  • In fat soluble toxic substances because they increase their absorption.
  • As yellow phosphorus, CCI4 and chlorinated insecticides.
179
Q

Contraindications of cathartics

A
  • GIT hemorrhage.
  • Recent bowel surgery.
  • Intestinal obstruction and ileus.
  • Renal failure for risk of magnesium load.
180
Q

Complications of cathartics

A
  • Dehydration particularly in children and elderly
  • Electrolyte imbalance.
181
Q

Indications of Gastric Lavage

A
  • A significant amount of Ingested Toxic Substance within. 1.hour.
  • It is usually used for extremoly toxic substances.
  • When patient is unable to protect their own airway, intubate
    before proceeding.
182
Q

Procedure of Gastric Lavage

A
  • Place large boro orogastric or nasogastric tubo.
  • Confirm placement.
  • Warm normal saline is instilled in aliquots until stomach contents are clear.
183
Q

Technique of Whole Bowel Irrigation

A

Using a gastric tube, give a surgical bowel-cleansing solution containing a non absorbable polyethylene glycol until rectal effluent is clear.

184
Q

Contraindications of Gastric Lavage

A

In cases of:

  • Corrosives
  • Sharp objects
  • Large pills.
185
Q

Indications of Whole Bowel Irrigation

A
  • Ingestion of large dose of iron or lithium or “Other drugs poorly adsorbed to activated charcoal”.
  • Ingestion of Large amount of sustained release or enteric coated tablets.
  • Ingestion of foreign bodies or drug filled packets or condoms.
186
Q

Contraindications of Whole Bowel Irrigation

A
  • lleus or intestinal obstruction.
  • Comatose or convulsing patient unless airway is protected by endotracheal tube.
187
Q

AE of Whole Bowel Irrigation

A

Nausea, regurgitation and pulmonary aspiration.

188
Q

MOI of Activated Charcoal

A
  • Almost irreversibly adsorbs drugs and chemicals, preventing absorption
189
Q

Indications of Activated Charcoal

A
  • Consider for all significant toxic ingestions except poorly binds substances “PGAIS”
190
Q

Dose of Activated Charcoal

A
  • Give 50 g (adults) or 1 g/kg (children) as a singlo oral doso placed in a cup for self-administration.
  • Prepared with a ratio 1:4 charcoal to water
    “Goal is to have a charcoal to toxin ratio > 10:1”.
  • Mixing with ice cream improves palatability for children.
  • In intubated patient, AC may be given via oro- or nasogastric tube.
191
Q

Contraindications of Activated Charcoal

A
192
Q

Principle of Enhanced Elimination

A
  • It is used in drug intoxication when renal route is a main route to its total clearance.
  • Forced diuresis may increase glomerular filtration rato and ion trapping by urinary pH manipulation may enhance elimination of polar drugs.
  • It is used in case of healthy kidney,
193
Q

Types of Enhanced Elimination

A
  • Urinary Manipulation
  • Hemodialysis
  • Hemoperfusion
  • Hemofiltration
  • Peritoneal Dialysis
  • Repeated Dose Activated Charcoal (Gut Dialysis)
194
Q

Types of Urinary Manipulation

A
  • Urinary alkalization
  • Urinary acidification
195
Q

Uses of Urinary alkalization

A
196
Q

Uses of Urinary acidification

A
197
Q

What characters should a toxin have to undergo Hemodialysis?

A
198
Q

Indications of Hemodialysis

A
199
Q

Why are Drug size, water solubility and protein binding not important limiting factors in cases of hemoperfusion procedure?

A

Because drug or toxin is in direct contact with adsorbent material

200
Q

Advantages of Hemoperfusion

A

For most drugs, hemoperfusion can achieve greater clearance rates than hemodialysis.

201
Q

Disadvantages of Hemoperfusion

A

Systemic anticoagulation is required, often in higher doses than for hemodialysis and thrombocytopenia is a common complication.

202
Q

Indications of Hemoperfusion

A
203
Q

Principle of Hemofiltration

A

It can remove compounds with large molecular weight through porous membrane.

204
Q

Indications of Hemofiltration

A
205
Q

Advantages of Peritoneal Dialysis

A

It is easier to perform than hemodialysis or hemoperfusion and does not require anticoagulant.

206
Q

Substances not amenable to significant extracorporeal removal include ……

A
207
Q

Disadvantages of Peritoneal Dialysis

A
  • However, it can be performed continuously, 24 hours a day,
  • 24-hour peritoneal dialysis with dialysate exchange every 1-2 hours is approximately equal to four hours of hemodialysis.
208
Q

Indications of Repeated Dose Activated Charcoal (Gut Dialysis)

A
209
Q

Dose of Repeated Dose Activated Charcoal (Gut Dialysis)

A
210
Q

Route of adminstration of Repeated Dose Activated Charcoal (Gut Dialysis)

A

It is given orally or via gastric tube

211
Q

Types of Antidotes

A
  • Antagonists
  • Competitors
  • Chelators
  • Inactivators
212
Q

Principle of action of Antagonist

A
  • Substance which antagonizes action of the poison
213
Q

Examples of Antagonists

A

Atropine
- antagonizes muscarinic action of organophosphate’s insecticides.

Pilocarpine
- antagonizes the peripheral action of atropine.

214
Q

Principle of Competitors

A
  • A substance which competes with poisons at sites of their action preventing them from exerting their effects.
  • They are characterized by having similar chemical formula to poison.
215
Q

Examples of Narcotic antidotes

A
  • Naloxone (Narcan, N-ally) oxymorphine)
  • Nalmefene (Revex)
  • Nallorphine (N-allyl morphine, lethidrone)
216
Q

Examples of Competitors

A
  • Narcotic analgesics
  • Ethyl Alcohol
217
Q

Characters of Naloxone (Narcan, N-ally) oxymorphine)

A
  • It acts as a pure antagonist.
  • It is potent with no depressant action on CNS.
  • It provides both a therapeutic & diagnostic modality for opioid poisonings.
218
Q

Characters of Nalmefene (Revex)

A
  • It acts as a pure antagonist.
219
Q

Characters of Nallorphine (N-allyl morphine, lethidrone)

A
  • It acts as agonist-antagonist
220
Q

Characters of Ethyl alcohol as an antidote

A
  • It is the antidote for methanol poisoning.
  • It competes with the enzyme alcohol dehydrogenase, → so methanol doses do not change into toxic formaldehyde and formic acid.
221
Q

Principle of Chelators

A

A substance which unites with the absorbed poison forming soluble less toxic and easily excreted complex.

222
Q

Examples of Chelators

A
  • All antidotes of heavy metals are chelators
223
Q

Principle of Inactivators

A

A substance which unites with poison to form non-toxic complex

224
Q

Examples of Inactivators

A

Hydroxocobalamin (Vil. B.12a): It unites with cyanide forming cyanocobalamin (Vit. B12).

225
Q

Antidote of acetaminophen

A

N-Acetylcystoine (Mucomyst).

226
Q

Antidote of anticholinergics

A

Physostigmine

Caution: may cause seizures, asystole, cholinergic crisis”.

227
Q

Antidote of OCP (Anticholinestrases) & Carbamates

A

OCP
- Atropine
- Pralidoxime

Carbamates
- Atropine

228
Q

Antidote of benzodiazepines

A

Flumazenil

229
Q

Antidote of Beta-adrenergic blockers

A

Glucagon

230
Q

Antidote of CO toxicity

A
  • Oxygen.
  • Hyperbaric O2 in severe cases.
231
Q

Antidote of CCBs

A

Calcium chloride
Glucagon

232
Q

Antidote of Digitalis

A

Fab antibodies (Digi-bind).

233
Q

Antidote of Heavy metals

A
  • BAL (dimercaprol), EDTA, Penicillamine, DMSA, Unithiol & DMPS
234
Q

Antidote of Iron

A

Deferoxamine.

235
Q

Antidote of Methemoglobinemia agents

A

Methylene blue.

236
Q

Antidote of Methanol & Ethylene glycol

A
  • Ethanol, Folate.
  • Fomepizole.
237
Q

Antidote of opiods

A

Naloxone.

238
Q

```

Antidote of warfarin & Super warfarin

A

Vit. K.

239
Q

Def of the principle One pill can kill in children

A
  • Drugs with potential for severe toxicity if one or two tablets ingested by a 10-kg toddler
240
Q

Types of One pill can kill in children

A
241
Q

Cardiac Indications for ICU Admission

A
  • Cardiac arrhythmias.
  • QRS duration > 0.12 s.
  • Systolic BP < 80 mm Hg.
  • Second or third degree atrioventricular block.
  • Anticholinergic cardiac toxicity.
242
Q

Indications for ICU Admission

A

For All Patients Who Present with Poisoning or Potential Exposure to A Toxic Substance

  • Neurological
  • Cardiac
  • RESP
  • Metabolic & Electrolytes
243
Q

Neurological Indications for ICU Admission

A
  • Toxin-induced seizures
  • Unresponsiveness to verbal stimuli or Glasgow coma scale score ≤12.
244
Q

Respiratory

Respiartory Indications for ICU Admission

A
  • PaCO2 > 45 mm Hg.
  • Need for endotracheal intubation
245
Q

Metabolic & Electrolytic Indications for ICU Admission

A
246
Q

Disposition of intoxicated patients

A
247
Q

When to transfer the patient

A
248
Q

we are DONE ✅

A

🫡