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Toxicology > Lectures 1-5 > Flashcards

Lectures 1-5 Flashcards

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0
Q

Enhanced digestive elimination

A

Osmotic purgatives

SORBITOL 70%, 240 ML
t 1.3h
MAGNESIUM CITRAT 20-30g sol 10%
t 4h
MAGNESIUM SULPHATE sol 10% 15-20g
t 17h
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1
Q

Enterohepatic recirculation compounds

A 
 Chloralhydrat
 Phenotyasines
 Colchicine
 Phenitoyn
 Digitoxin
 Salicylates
 Digoxin
 Isoniaside
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2
Q

Drug removal

A

 Ph modification
 Forced diuresis
 Repetead activated charcoal
 Extracorporeal techniques: haemodyalisis,
haemoperfusion, plasmapheresis, exchange
transfusion
 Hyperoxibarism

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3
Q

ACID DIURESIS

-> phencyclidine, amphetamine overdose

A

optimal urine pH < 5.5

ascorbic acid 0.5-2.0 g iv
NH4Cl 75mg/kg/24 h, po/iv (2%)

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4
Q

ALKALINE DIURESIS

-> salicylate, barbiturate overdose

A

optimal urine pH >7.5

bicarbonate 1-2 mEq/kg
acetazolamide 500 mg

  • Unless managed carefully, potential for fluid overload, electrolyte abnormalities
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5
Q

FORCED DIURESIS

A

Fluids overload

  • Diuretics: furosemide, manitol
  • Urinary flow: 3-5 ml/kg/h
  • Indications: barbiturates, salicylates,
    amphetamines
  • Unless managed carefully, potential for
    fluid overload, electrolyte abnormalities
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6
Q

HEMODIALYSIS

A

Severe poisoning with:

(MW<500, high solubility, low binding plasmatic albumines)

  1. salicylate
  2. lithium
  3. alcohols: methanol, isopropranolol, ethylene glycol
  4. phenobarbitone
  5. chloralhidrat
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7
Q

HEMOPERFUSION

A

Severe poisoning with:

  1. short acting barbiturates
  2. sedatives and hipnothics
  3. phenitoyn
  4. choramphenicol
  5. salicylate
  6. paraquat
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8
Q

Antidote for Paracetamol

A

Acetylcysteine

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9
Q

Antidote for ethanol

A

NO antidote ‼️

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10
Q

Antidote for Organophosphates

A

Diazepam, Atropine

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11
Q

Antidote for benzodiazepines

A

Flumazenil

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12
Q

Antidote for Arsenic

A

Dimercaprol

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13
Q

Antidote for iron

A

Deferoxamine

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14
Q

Antidote for beta adrenergic agonists

A

Beta blockers

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15
Q

Antidote for Cyanide

A

Amyl Nitrite

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16
Q

Drug induced hyperthermia

A

Dantrolene

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17
Q

Antidote for HF, fluorides, oxalates

A

Calcium gluconate

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18
Q

Antidote for beta blocker

A

Glucagon

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19
Q

Antidote for ethylene glycol

A

4 methylpyrazole

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20
Q

Antidote for Methaemoglobinemia

A

Methylene blue

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21
Q

Antidote for Opiates

A

Naloxone

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22
Q

Antidote for Organophosphorus insecticides

A

Obidoxime

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23
Q

Antidote for Carbon monoxide, Cyanide

A

Oxygen

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24
Antidote for Organophosphorus compounds
Pralidoxime
25
Antidote for central anticholinergic syndrome
Physostigmine
26
Antidote for Isoniazid, Hydralazine
Pyridoxine
27
Antidote for Copper
Penicillamine
28
Antidote for Cyanide
Sodium nitrite, Sodium Thiosulfate
29
Antidote for Heparin
Protamine Sulfate
30
Antidote for Salicylate, tricyclic antidepressants
Sodium Bicarbonate
31
Emetics
Apomorphine, Ipecacuanha
32
Alkalinize blood and urine
Sodium Bicarbonate
33
Cathartics and sol for whole gut lavage
Sorbitol, Mannitol Magnesium citrate, mag sulfate Bicarbonates, Sodium Sulfates ...
34
Prevents absorbtion in gut:
``` Activated charcoal (for adsorbable poison) Starch (for iodine) ```
35
Prevents skin absorbtion/damage
Calcium gluconate gel - for hydrofluoric acid | Polyethylene glycol - for phenol
36
Anti-foaming agent
Dimethicone (soaps, shampoos)
37
Dystonia
Benztropine
38
Medication for: Psychotic with severe agitation
Chlorpromazine
39
Medication for: Acute allergic reaction, mucosal edema, laryngeal edema, bronhoconstriction
Corticosteroids
40
Medication for: Convulsions, Anxiety, excitation, muscular hypertonia
Diazepam
41
Medication for: myocardial depression
Dobutamine, Dopamine
42
Medication for: Anaphylactic shock, cardiac arrest
Epinephrine
43
Medication for: fluid retention, left ventricular failure
Furosemide
44
Medication for: Hypoglycemia
Glucose
45
Medication for: hallucinations and psychotic states
Haloperidol
46
Medication for: Hypercoagulability
Heparin
47
Medication for cardiac arrhythmia
Magnesium sulfate
48
Medication for Cerebral edema, fluid retention
Mannitol
49
Medication for hypoxia
Oxygen
50
Medication for bronchoconstriction systemic/ inhaled
Salbutamol
51
Medication for acidosis, some cardiac disturbances
Sodium bicarbonate
52
Toxicological screen
Spot urine test, color test Thin layer chromatography - rapid 2 to 4 hours - urine or plasma - not for volatiles, alcohols, metals, cyanide, salicylates Gas and high-pressure chromatography - for any specimen - for confirmation Mass spectrometry -high specific/sensitive but expensive
53
ICU admission criteria
Intubation when: Ventil failure Airway protection Therapy induced hypocapnia/alkalosis CNS: seizures, coma, GCS < 9 CVS: arrhythmia, AV block long QRS, hypotension Large ingested dose: high blood levels = poor outcome
54
Drugs associated with SEIZURES:
P - Pesticides, Propoxyphene L - Lead, Lithium, Lindane, Local anesthetics A - Antidepressant, Anticonvulsants, Antihistamines,Antipsychotics, Abstinence S - Salicylates, Sympatomimetics, Strychnine, Solvents T - Theophylline, Tricyclic antidepressants, Thallium, Tobacco(nicotine) I - Insulin, Insecticides, INH C - Camphor, Cocaine, Cyanide, Chloroquine
55
Odor: Acetone
Acetone, isopropanol,metabolic acidosis
56
Odor: Airplane Glue
Toluene, aromatic hydrocarbon inhalation
57
Odor: alcohol
Ethanol ( no ethylene glycol or vodka)
58
Odor: Ammonia
Ammonia or Uremia
59
Odor: bitter Almonds
Cyanide
60
Odor: Coal gas
Carbon monoxide = odorless but mix with illuminating gas for detection
61
Odor: Disinfectants
Phenol, Creosote
62
Odor: Formaldehyde
Formaldehyde, Methanol
63
Odor: Garlic
Arsenic, Parathion, Yellow Phosphorus, Se, Zn
64
Odor: Pears
Chloral hydrate, Paraldehyde
65
Odor: Rotten Eggs
Disulfiram, Hydrogen Sulfide, hepatic failure
66
Odor: Shoe polish
Nitrobenzene
67
Anticholinergic syndromes
Cause: ``` antihistamines antiparkinsonian atropine antipsychotic agents antidepressant agents mydriatic agents skeletal muscle relaxants Amanita muscaria ``` Common signs: ``` delirium with mumbling speech incoordination and ataxia respiratory failure coma tachycardia hypertension dry, flushed skin dilated pupils myoclonus slightly elevated temperature urinary retention decreased bowel sounds seizures dysrhythmias ```
68
Sympathomimetic Syndromes
Cause: ``` cocaine amphetamine methamphetamine ephedrine pseudoephedrine phenylpropanolamine ``` Common signs: ``` delusions paranoia tachycardia hypertension hyperpyrexia diaphoresis piloerection mydriasis hyperreflexia seizures hypotension dysrhytmias – severe cases ```
69
Cholinergic Syndromes
Cause: organophosphate and carbamate insecticides physostigmine edrophonium some mushrooms Common signs: ``` confusion central nervous system depression weakness salivation lacrimation urinary/fecal incontinence gastrointestinal cramping emesis diaphoresis muscle fasciculations pulmonary edema miosis bradycardia / tachycardia seizures ```
70
Opiate, Sedative or Ethanol Intoxication
Cause: ``` narcotics barbiturates benzodiazepines ethchlorvynol glutethimide methyprylon meprobamate ethanol clonidine ``` Common signs: ``` coma respiratory depression miosis hypotension bradycardia hypothermia pulmonary edema decreased bowel sounds hyporeflexia seizures may occur (propoxyphene) ```
71
Normal Anion Gap
3-11
72
High Anion Gap induced by:
- metabolic acidosis - dehydration / loss of fluid - infusions of salts of organic acids (lactate, acetate, citrate) - reduced unmeasured cations (K, Ca, Mg) - alkalemia - systematic underestimation of serum chloride - laboratory error
73
Low Anion Gap induced by:
- volume expansion with free water - systematic underestimation of serum sodium (hyperNa, hyperviscosity) - systematic overestimation of serum chloride - raised unmeasured cations - acidemia from a respiratory or hyperchloremic metabolic acidosis - laboratory error
74
Osmolal Gap
M – C > 10 mOsm/kg H2O laboratory error decreased serum water content ↓M subst not used in equation M normal and C ↓ decrease in serum water associated with hyperproteinemias and hyperlipidemias M↑ and C normal/↓ gap= unmeasured osmoles ``` sorbitol ethanol mannitol methanol glycerin ethylene glycol isoniazid ether diatrizoate sodium acetone ```
75
Specific Antidote in (~5% acute poisonings):
NALOXONE + GLUCOSE 5% | Patients having CNS
76
First priority:
Airways, Breathing - ventilation - oxygenation Obstruction: mucosa edema, secretions, foreign body, defectuos position of tongue Symptoms: cyanosis, tahipneea, dyspnea, diaphoresis, altered mental status
77
Second Priority:
CIRCULATION ``` Shock: ↓level of consciousness ↓BP peripheral vasoconstriction metabolic acidosis oliguria ``` Mechanism: ↓contractility hypovolemia preload, afterload
78
Third priority:
DISABILITY CNS - pupils - coma  IV Decontamination
79
REED classification
``` Conscious level Pain response Reflex response Respiration Circulation __________ ``` ``` 0 asleep arousable intact normal normal I comatose withdraws intact normal normal II comatose none intact normal normal III comatose none absent normal normal IV comatose none absent cyanosis shock ```
80
Absorbtion prevention
Internal decontamination Dilution: caustics, corrosive -> 300ml milk or water CI: neutralization reactions
81
Emetics
 Ipecac syrup 10-30 ml, apomorphine, pharyngeal stimulation  Must have: awake patient with gag reflex __________ Absolute contraindications: 1. unprotected airway (altered mental status) 2. strong acids/alkalis 3. petroleum derivates 4. children<6m 5. seizures 6. hematemesis
82
Gastric lavage
 Saline solutions: 200-250 ml, 1min, drainage  Useful early after ingestion 4-6h  Doubtful efficacy after this but may be useful for slow absorbed agents ``` Indications: ___________ CI emesis analgesics antidepressants alcohols: meth, EG others: digoxin, theophilline ``` ``` Contraindications: ____________ strong acid/alkalis petroleum derivates bleeding ```
83
Activated charcoal
 50-100 g immediately following lavage , then 50g q4h Mechanism: adsorbtion !!!! ``` Repeted dose effctive for: ______________ benzo, barbiturates narcotics tricyclics phenothiazines salicylates digoxin digitoxin atropine ``` ``` Inefective for: ____________ most heavy metals pesticides cyanide alcohol strong acid/alkalis ``` ``` Contraindications: ____________ unprotected airway strong acid/alkali petroleum derivates ```
84
Barbiturates
* Hypnotic and sedative agents * Induction of anesthesia * Treatm of epilepsy  Mechanism of toxic: depression of neuronal activity GABA mediated synaptic inhibition depression of central sympathetic tone ↓ cardiac contractility  Toxic dose: (drug, route, rate, individual tolerance) toxicity= 5-10 x hypnotic dose  Clinical presentation: A. lethargy, slurred speech, nystagmus, ataxia hypotension, coma, resp arrest B. Hypothermia - deep coma + hypotension/bradycardia
85
Barbiturates Diagnosis
Diagnosis : history of ingestion epileptic patient with stupor or coma skin bullae –no specific serum level: 60-80 mg/l -> coma electrolytes, glucose, ABG, BUN, creatinine
86
Barbiturates Treatment
Treatment: A. airway, assist ventilation coma, hypotermia, hypotension B. no specific antidote C. Decontamination: prehospital: activated charcoal, ipeca (min) hospital: activated charcoal, gastric lavage D. Enhanced elimination: 1. alkalinization of the urine 2. repeat-dose activated charcoal 3. hemoperfusion
87
Benzodiazepines Mechanism of Toxicity:
GABA med synaptic inhibition Inhib other neuronal syst -> depression of spinal reflexes / RAS
88
Benzodiazepines Toxic dose:
Oral overdose: Diazepam 15-20 x therap dose Rapid iv - Respiratory arrest
89
Benzodiazepines Clinical:
lethargy, slurred speech, ataxia, coma, resp arrest hyporeflexia, midposition or small pupils hypothermia complications ! short acting/other depressant
90
Benzodiazepines Diagnosis
History ingestion or injection Dif Diagnosis Reverse with Flumazenil
91
Benzodiazepines Treatment
A. Emergency and supportive measures: airway, assist ventilation coma, hypotermia, hypotension B. Specific drugs and antidotes: FLUMAZENIL iv 0,1 – 0,2 mg, repetead as needed < 3mg C. Decontamination: prehospital: activated charcoal, ipeca (min) hospital: activated charcoal, gastric lavage D. Enhanced elimination: no role for diuresis, dialysis, etc.
92
Cyclic Antidepressants Mechanism of toxicity
CV mechanism: 1. anticholinergic effects => tachycardia , mild hypertension 2. peripheral α adrenergic blockade =>vasodilation 3. effect quinidinelike => myocardial depression, conduction disturbances CNS mechanism: 1. anticholinergic toxicity 2. inh reuptake of norepinephrine/serotonin - relevant pharmacokinetics 1. slow absorbtion 2. active metabolites 3. binding to body tissues and plasma proteins
93
Cyclic Antidepressants Toxic dose
Toxic dose: narrow therapeutic index: intoxication 10-20 mg/kg potentially life-threatening
94
Cyclic Antidepressants Clinical
3 major syndromes: A. Anticholinergic: sedation, delirium, coma, dilated pupils, dry skin, ↓sweating, tachycardia, ↓ bowel sounds, urinary retention B. Cardiovascular: abnormal cardiac conduction, arrhythmias, hipotension C. Seizures: recurrent/ persistent hyperthermia, rhabdomyolysis, brain damage,multisystem failure, death D. Death: ventricular fibrillation, intractable, cardiogenic shock, status epilepticus with hyperthermia
95
Cyclic Antidepressants Diagnosis
Diagnosis any patient with lethargy, coma, seizures, QRS ↑ QRS ↑> 0,12 = severe poisoning A. specific levels: ______ terapeutic c% = 300 ng/ml serious poisoning = 1000 ng/ml or greater B. other useful lab studies: electrolytes, glucose, BUN, creatinine, cont EKG monitoring, x-ray, ABG
96
CYCLIC ANTIDEPRESSANTS Treatment
A. Emergency and supportive measures: 1. airway and assist ventilation; 2. coma, seizures, hyperthermia, hypotension, arrhythmias 3. neuromuscular blocker 4. continuos monitor Temperature, vital signs, ECG B. Specific drugs and antidotes: sodium bicarbonate 1-2 mEq/kg iv -> pH 7.45-7.55 C. Decontamination 1. prehospital : activated charcoal ! not emesis 2. hospital : activated charcoal gastric lavage D. Enhanced elimination : dialysis/ hemoperfusion not efective
97
PHENOTHIAZINES Mechanism of toxicity
CV mechanism: 1. anticholinergic effects => tachycardia, mild hypertension 2. peripheral α adrenergic blockade => vasodilation => hypotension 3. effect quinidinelike => myocardial depression, conduction disturbances CNS mechanism: 1. anticholinergic toxicity => CNS depression 2. α adrenergic blockade => miosis 3. central dopamine receptor blockade => extrapyramidal dystonic reactions 4. distrubances of temperature regulation => poikilothermy 5. low seizure threshold => mech unknown
98
PHENOTHIAZINES Toxic Dose
high toxic-therapeutic index extrapiramidal reactions, anticholinergic side effects, orthostatic hypotension => therapeutic doses
99
PHENOTHIAZINES Clinical
A. Mild intoxication: sedation, small pupils, orthostatic hypotension. Aach manifestions:dry mouth, absence of sweating, tachycardia, urinary retention B. Severe intoxication: coma, seizures, respiratory arrest, QT ↑, hypo/hyperthermia C. Extrapyramidal distonic effects: torticollis, jaw muscle spasm, rigidity, bradykinesia D. Chronic => neuroleptic malignant syndrom: rigidity, hyperthermia, sweating, lactic acidosis, rhabdomyolysis
100
PHENOTHIAZINES Diagnosis
History of ingestion sedation, small pupils, hBP, QT ↑ A. specific levels: Q not available, only qualitative B. other useful lab studies: electrolytes, glucose, BUN, creatinine, CPK, cont EKG monitoring, chest and abdominal x-ray, ABG
101
PHENOTHIAZINES Treatment
A. Emergency and supportive measures: 1. airway and assist ventilation; supplemental O2 2. coma, seizures, hyperthermia, hypotension, arrhythmias 3. continuos monitor Temp, vital signs, ECG B. Specific drugs and antidotes: no specific antidote C. Decontamination 1. prehospital : activated charcoal 2. hospital : activated charcoal, gastric lavage ? D. Enhanced elimination : dialysis/ hemoperfusion not efective
102
OPIOIDS Mechanism of toxicity
*stimulates specific opiate receptors in CNS => sedation, => respiratory depression -> resp.failure -> apneea -> death * noncardiogenic pulmonary edema
103
OPIOIDS Toxic dose
Depend on: compound, route, tolerance, rate of adm
104
OPIOIDS Clinical
A. mild/moderate overdose: lethargy, small pupils (pinpoint size), TA↓, flaccid muscles, bowel sounds ↓ B. higher dose: respiratory depression, apnea, pulmonary edema C. seizures: not common
105
OPIOIDS Diagnosis
pinponts pupils, respiratory and CNS depression -> quickly awakens after adm of Naloxone signs of iv drug abuse Screening Lab: electrolytes, glucose, ABG, x-ray
106
Which iv injected drug can induce non-cardiogenic pulmonary edema and resp distress?
iv injected HEROIN | also salicylates and cocaine
107
OPIOIDS Complications
``` ARDS Aspiration pneumonia Lezional APE Postinject venous thrombosis Necrosis after inject paravenous Hepatitis B, C HIV Abcess Rabdomiolisis Renal insuf ```
108
Sindrom de intrerupere - OPIOIDS
INTENTIONALE (pentru obtinerea drogului) la 6 – 8 ore DUPA INTRERUPERE maxim : 36 – 72 ORE NEINTENTIONALE la 8-12 ORE: ↑ 24 ORE ULTERIOR STABILE LACRIMATIE, RINOREE, CASCAT, PERSPIRATIE SOMN AGITAT, TREZIRE DEZAGREABILA MIDRIAZA, ANOREXIE, AGITATIE, IRITABILITATE, TREMOR Pentru MORFINA, HEROINA: max 36 – 48 ore -> 72 ore ↓ 5 – 10 ZILE MAXIM: INSOMNIE, ANOREXIE INTENSA, AGITATIE EXTREMA, ANXIETATE, LACRIMATIE, RINOREE, DEPRESIE, GREATA, VOMA, SPASM INTESTINAL, DIAREE, TAHICARDIE, HTA, DURERI SI CRAMPE MUSCULARE, SCADERE IN GREUTATE, DESHIDRATARE, CETOZA, TULB. ACIDO-BAZICE
109
Sindrom de intrerupere Tratament
INSOMNIA: NITRAZEPAM, FLURAZEPAM, CLORALHIDRAT ANXIETATEA: CLORDIAZEPOXID 10 mg x 4 / zi CRAMPE DIGESTIVE: PROPANTELINA PREPARAT DE BELLADONA GREATA: PROCLORPERAZINA (METOCLOPRAMID) PREVENIREA SINDR. DE ABSTINENTA: CLONIDINA 0,1 mg x 3/zi PREFERABIL INTRASPITALICESC
110
ACETAMINOPHEN Toxic dose
Toxic dose acute ingestion: children > 140 mg/kg adults > 6g; lethal 13-25 g Rapid absorbtion: 1-4 h ; T1/2: 2-3 h
111
ACETAMINOPHEN Mechanism of toxicity
Mechanism of toxicity: acetaminophen -P-450- toxic metabolit (hepatotoxic) NAPQI -glutathione- detoxified =liver injury
112
ACETAMINOPHEN Clinical
Clinical presentation (depend upon the time after ingestion) A. Early (0-24 h) - anorexia, nausea, vomiting , diaphoresis B. After 24-48 h (latent) -transaminase level ↑ - PT ↑ C. Hepatic phase - acute hepatic failure -> encephalopathy -> death D. Recovery phase: normalise hepatic tests (after 5 days)
113
Acetaminophen Diagnosis
Diagnosis - serum acetaminophen level - history A. Specific levels : 4 h postingestion B. Other useful lab studies: electrolytes, glucose, BUN, crea, transaminases, PT
114
Acetaminophen Treatment
Decontamination 1. prehospital : activated charcoal emesis (4-6 h) 2. hospital : activated charcoal Enhanced elimination : hemoperfusion Specific drugs and antidotes: N-acetylcysteine 140 mg/kg orally 70 mg/kg q4 h 17 doses - replates glutathion - adverse effects: vomiting
115
SALICYLATES Mechanism of toxicity
Mechanism of toxic: ► central stimulation of the respiratory center-> hyperventilation => respiratory alkalosis ► intracellular effects: Inhib of Krebs enzymes & uncoupling of oxidative phosphorylation => metabolic acidosis ► alteration in capillary integrity ► alteration of platelet function ► increase in glycolysis => hypoglycemia
116
SALICYLATES Toxic dose
Toxic dose: therapeutic single dose 10 mg/kg * acute ingestion: 150-200 mg/kg mild intoxication 300-500 mg/kg severe intoxication * chronic intoxication: 100mg/kg/d for 2 or more days
117
SALICYLATES Clinical
Clinical presentation A. Acute ingestion: vomiting, epigastric pain, hyperventilation, tinnitus, lethargy, respiratory alkalosis + metabolic acidosis coma, seizures, hypoglycemia, hyperthermia, dehydration, arrhythmias (K ↓) pulmonary edema, CV collapse B. Chronic intoxication: confusion, dehydration, metabolic acidosis mortality rates > acute ingestion cerebral and pulmonary edema
118
SALICYLATES Diagnosis
history of acute ingestion typical signs and symptoms qualitative: colorimetric; lab studies: anion gap calculation, glucose, BUN, PT, ABG, chest X-ray
119
SALICYLATES Treatment
A. Emergency and supportive measures: airway, assist ventilation, supplemental oxygen , X ray coma, seizures, pulmonary edema, hyperthermia metabolic acidosis: sodium bicarbonate 1-2 mEq replace fluid and electrolyte deficits monitoring B. Specific drugs and antidotes: no antidote C. Decontamination: prehospital: activated charcoal, ipeca induced emesis (30 min) hospital: activated charcoal, gastric lavage ``` D. enhanced elimination: 1. urinary alkalinization : sodium bicarbonate -> pH 7.5 alkalemia is not a CI 2. hemodialysis, hemoperfusion 3. repeat dose activated charcoal ```
120
IZONIAZID Mechanism of toxicity
Mechanism of toxicity: PYRIDOXINKINASE PYRIDOXINE PYRIDOXALPHOSPHAT  Acute overdose: competition with pyridoxal 5-phosphate ↓ GABA inh lactat>piruvat => lactic acidosis  Peripheral neuritis
121
IZONIAZID Toxic dose
Toxic dose acute: min 1.5g 6g = severe toxicity => death 3mg/kg epileptics => status epilepticus
122
IZONIAZID Clinical
Clinical presentation ```  slurred speech, ataxia, coma, seizures (30-60 min), metabolic acidosis, hemolysis  tahicardia, cianosis, hTA, colaps  oliguria -> anuria  midriasis, nistagmus,  toxic psihosis, hyperpirexia ```
123
IZONIAZID Diagnosis
Diagnosis : history of ingestion clinical presentation ! Acute onset seizures + acidosis
124
IZONIAZID Treatment
Treatment A. Emergency and supportive measures: airway, assist ventilation coma, seizures, metabolic acidosis (NAHCO B. Specific drugs and antidotes: pyridoxine eq INH C. Decontamination: prehospital: activated charcoal, -> ! Not emesis hospital: activated charcoal, gastric lavage D. Enhanced elimination: forced diuresis, dialysis
125
IZONIAZID Intoxication Outcome -> End Result
Blocking pyridoxinkinaza. Hepatic necrosis Tubular necrosis Inh GABA => Metabolic Acidosis
126
Classes of Pesticides
``` Insecticides (kill insects) • Organochlorines • Organophosphates • Carbamates • Synthetic Pyrethroids Herbicides (kill plants) Rodenticides (kill rodents) Fungicides (kill fungus) Fumigants (kill whatever) ```
127
ORGANOPHOSPHATES Mechanism of toxicity
A.inhibit acetylcholinesterase -> accumulation of acetylcholine muscarinic R – cholinergic effector cells nicotinic R – skeletal NM junctions, autonomic ganglia CNS B. Absorbtion: inhalation ingestion skin contact - highly lipophilic
128
ORGANOPHOSPHATES Clinical
Toxic dose: wide spectrum, rate, metabolism Clinical presentation: 1-2 h after exposure M: vomiting, diarrhea, abd cramping, bronhospasm, miosis, bradycardia, salivation, sweating -> dehydration -> shock N: muscle fasciculations, tremor, weakness, resp muscle paralysis CNS: agitation, seizures, coma, tremor delayed peripheral neuropathy
129
ORGANOPHOSPHATES Diagnosis
Diagnosis: history of exposure characteristic sign solvent odor  Specific levels: ↓PChE, ↓AChE (more reliable)
130
ORGANOPHOSPHATES Classification
a. Latent poisoning: Plasma chol activity >50% No clinical manifestations ``` b. Mild poisoning: Fatigue, headache, dizziness N,V,D, abd cramps Sweating, salivation Plasma chol activity 20-50% ``` -> Atropine 1mg sc, good prognosis !!! c. Moderate poisoning: Miosis, fasciculations Generalized weakness, unable to walk, difficulty speaking Plasma chol activity 20-50% -> Atropine 1-5mg iv q5min d. Severe poisoning: Miosis, fasciculations, coma, flaccid paralysis, no light reflex, profuse sweating, salivation, bronchorrhea, Plasma chol activitity Atropine 1-5 mg iv q5min fatal if untreated !!!!!!
131
ORGANOPHOSPHATES Treatment
A. Emergency and supportive measures: airway, assist ventilation, ! sudden resp arrest coma, seizures, 6-8 h observation B. Specific drugs and antidotes: ATROPINE, PRALIDOXIME atropine: 0.5-2 mg iv, repeated (persistent wheezing, bronchorrhea) , HR>60 bpm pralidoxime: regenerate enzyme activity 1-2 g iv bolus, cont infusion, most effective first 24 h ``` C. Decontamination: skin: remove, wash exposed areas ingestion: preH: activated charcoal, ipeca H: activated charcoal, cathartic , gastric lavage ``` D. Enhanced elimination: dialysis/ hemoperfusion not generally indicated
132
ETHANOL Mechanism of toxicity
A. CNS depression additive effect B. hypoglycemia C. predisposition to trauma, hypothermia, metab derangements
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ETHANOL Toxic dose
Toxic dose: 5-8 g/kg Individual degree of tolerance: 300 mg/dl coma for novice drinkers 500 – 600 mg/dl awakeness – chronic alcoholics Absorbtion: 20% stomach; 80% intestin usual 30-60 min (80-90%) food delayed abs 4-6 h
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ETHANOL Clinical
Clinical presentation: sensitivity: frontal> occipital> cerebellum *moderate intoxication: euphoria, mild incoordination, ataxia, nystagmus, impaired judgment and reflexes, aggressive behavior, hypoglycemia * deep intoxication: coma, respiratory depression, pulmonary aspiration, TA↓, small pupils , HR↓ - alcohol withdrawal * tremulousness, anxiety, SNS overactivity, convulsions -> delirium - other problems * substitutes ingestion
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ETHANOL Diagnosis
history of ingestion smell nistagmus, ataxia, altered mental status, hypoglicemia may acompany : head trauma, meningitis, hypothermia other drug intoxication rough correlation blood levels – clinical presentation other lab studies
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ETHANOL Treatment
A. Emergency and supportive measures: airway (prevent aspiration), intubate, assist ventilation glucose, thiamine, treat coma, seizures, corect hypothermia with gradual rewarming B. Specific drugs and antidotes: no antidote C. Decontamination: ipeca, gastric lavage not indicated prehospital: ipeca (min) hospital: gastric lavage (30 min), activated charcoal if + other toxin D. enhanced elimination: hemodialysis (rarely needed) hemoperfusion, forced diuresis not effective
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ETHANOL Antidote for poisoning by:
Methanol Ethylene glycol Diethylene glycol ``` - Inhibits metabolic activation by alcohol dehydrogenase (ADH) ```
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Alcohol withdrawal effects
* Tremor * Nausea * Irritability * Agitation * Tachycardia * Hypertension * Seizures * Hallucinations
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METHANOL Mechanism of toxicity & Toxic dose
Mechanism of toxicity: methanol -> formaldehyde -> formic acid (systemic acidosis) formate -> blindness Toxic dose: fatal min oral dose: 30 ml 40% 10 ml sol 40% - blindness
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METHANOL Clinical
A. first few hours: inebriation, gastritis, not acidosis, ↑OG B. after a latent period (up to 30h): severe metabolic acidosis, visual disturbances, blindness, seizures, coma, death visual disturbances: “ like standing in a snowfield” fundoscopic exam: optic disk hyperemia, venous engorgement, papilledema
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METHANOL Diagnosis
history of ingestion symptoms lab findings, AG, OG a. Specific levels: serum methanol > 20 mg/dl =toxic latent period Elevated serum formate: better measure of toxicity b. Other useful lab studies: electrolytes, glucose, BUN, creatinine, serum osmolality, osmolar gap, ABG, lactate level
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METHANOL Treatment
A. Emergency and supportive measures: airway , intubate, assist ventilation treat coma, seizures metabolic acidosis : SODIUM BICARBONATE B. Specific drugs and antidotes: ETHANOL history of significant methanol ingestion, OG>5mosm/l metabolic acidosis, methanol c% >20 mg/dl -> c% ethanol 100-150 mg% FOLIC ACID enhance formate -> CO2 + water ; 50mg iv q4h 4-METHYLPYRAZOLE – INH adh, experimental C. Decontamination: preH: ipeca, H: gastric lavage , activated charcoal = not efficiently D. enhanced elimination: hemodialysis , τ↓ 3-6 h ind: methanol poisoning with significant metabolic acidosis OG>10mosm/l
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ETHYLENE GLYCOL Mechanism of toxicity & toxic dose
Ethylene glycol -> glycoaldehyde glycolic / glyoxylic / oxalic acids -> metab acidosis Oxalate + Ca -> calcium oxalate crystals (insoluble) -> tissue injury Toxic dose: 100 ml
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ETHYLENE GLYCOL Clinical
1. first 3-4 h: ≈ethanol, OG↑, no acidosis; gastritis with vomiting 2. after 4-12 h: anion gap acidosis, hyperventilation, convulsions, coma, cardiac conduction disturbances, arrhythmias, renal failure (reversible), pulmonary /cerebral edema, hCa
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ETHYLENE GLYCOL Diagnosis
history of antifreeze ingestion typical symptoms, OG ↑, AG ↑ oxalate crystals (urine) ethylene glycol level 50 mg/dl -> serious intoxications Other lab studies: electrolytes, glucose, BUN, creatinine, calcium, transaminases,osmolality, ABG, ECG
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ETHYLENE GLYCOL Treatment
A. Emergency and supportive measures: airway ,intubate, assist ventilation treat coma, seizures, cardiac arrhytmias, metabolic acidosis -> treat hypocalcemia: CALCIUM GLUCONATE iv B. Specific drugs and antidotes: ETHANOL (prevent metabolism of EG to its toxic metabolites: pyridoxine, folate, thiamine) C. Decontamination: ipeca, gastric lavage not indicated prehospital: ipeca (min) hospital: gastric lavage (30 min), activated charcoal not efficiently D. enhanced elimination: hemodialysis ind: OG>10 mosm/l, intoxication+renal failure c%>20 – 50 mg/dl
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HYDROCARBONS Mechanism of toxicity & toxic dose
Used: petroleum, plastic, agricultural chemical industries as solvents, degreasers, fuels, pesticides Mechanism of toxic: - pulmonary aspiration - sistemic intox: ingestion, inhalation, skin absorbtion * simple petroleum distillates: poorly absorbed * aromatic / halogenated HC, alcohols, ethers,ketones: serious systemic toxicity Toxic dose: pulmonary aspiration: few ml -> chemical pneumonitis ingestion: 10-20 ml (camphor, CCl4)
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HYDROCARBONS Clinical
A. pulmonary aspiration: coughing, choking, gagging, tachipneea, wheezing, severe chemical pneumonitis, sec bacterial infection, respiratory complications B. ingestion: abrupt nausea, vomiting, hemorrhagic gastroenteritis C. systemic toxicity: confusion, ataxia, lethargy, headache, syncope, coma, respiratory arrest, cardiac arrhythmias D. skin/eye contact: irritation, burns, corneal injury
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HYDROCARBONS Diagnosis
A. aspiration : history of exposure, respiratory symptoms ,<4-6h chest X-ray, ABG B. systemic intoxication: history of ingestions/inhalation systemic clinical manifestation Specific level: not available
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HYDROCARBONS Treatment
``` A. Emergency and supportive measures: 1. general: BLS for all symptomatic patients airway , supplemental O2, assist ventilation monitor ABG, chest X-ray, ECG ``` 2. pulm aspiration: observation 4-6 h coughing on arrival= aspiration ! Do not use steroids ! 3. ingestion: 5-10 ml – systemic toxicity rare B. Specific drugs and antidotes: no specific antidote (acetylcysteine –CCl4,) C. Decontamination: Inh: move the victim to fresh air, O2 Skin /eyes: remove, wash Ingestions: do not induse emesis, activated charcoal, cathartic D. Enhanced elimination: no role
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HYDROGEN SULFIDE Mechanism of toxicity & toxic dose
= Highly toxic, flammable, colorless gas, heavier than air • industrial processes, petroleum, mines, carbon disulfide production, hot asphalt Mechanism of toxic: inh cytocrom oxidase system -> cellular asphyxia rapidly absorbed -> symptoms immediately = mucous membrane irritant ``` Toxic dose: •rotten egg odor=0.025ppm •recomm workplace limit=10ppm •resp tract irritation, olfactory nerve paralysis =50-100 ppm •dangerous for life =300 ppm •fatal= 600-800 ppm ```
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HYDROGEN SULFIDE Clinical
A. irritant effect: upper airway irritation, burning eyes, blepharospasm; skin exposure: painful dermatitis, pneumonitis, noncardiogenic pulmonary edema B. Acute systemic effect: headache, nausea, vomiting, dizziness, confusion, seizures, coma -> massive exposure: immediate CV collapse, respiratory arrest, death
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HYDROGEN SULFIDE Diagnosis
Diagnostic: hystory of exposure progressive airway irritation and cellular asphyxia smell: rotten eggs ‼️ N. olfact. Paralysis serum levels : not available
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HYDROGEN SULFIDE Treatment
A. Emergency and supportive measures: airway , high-flow humidified O2, assist ventilation treat coma, seizures, hypotension corect hypothermia with gradual rewarming B. Specific drugs and antidotes: nitrites -> methemoglobinemia: sulfide ion -> sulfhemoglobin (less toxic) C. Decontamination: remove from exposure, supplem O2 D. enhanced elimination: no role hyperbaric oxigen therapy: no scientific evidence
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CARBON MONOXIDE Mechanism of toxicity + Toxic dose & Sources
SOURCES: - smoke inhalation in fires - auto exhaust fumes - poorly or faulty ventilated charcoal - kerosene, cigarette smoke • Mechanism of toxic: cellular hypoxia and ischemia ► CO affinity= 250 x O2 curve ► inhibit cytochrom oxidase SaO2↓ • T1/2 COHb = 3 – 4 h IN ATMOSPERIC air = 30 – 40 min ATMOSFERA O2 100% = 15 – 20 min O2 HIPERBARR (2,5 ATM) ► sensitivity of the brain ► Hb F fetal=2 x maternal levels • Toxic dose: limit accepted = 25ppm dangerous = 1500 ppm (0.15%) mins 1000 ppm SaCO 50%
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CARBON MONOXIDE Clinical
Clinical presentation: brain and heart A. Headache, dizziness, nausea / angina, myocardial infarction, impaired thinking, syncope, coma, convulsions, cardiac arrhythmias, hipotension, => death Concentration | COHb | Symptoms ppm % : ``` < 35 | 5 none, mild headache 50 | 10 slight headache, dyspnea on vigorous exertion 100 | 20 throbbing headache, dyspnea with moderate exertion 200 | 30 severe headache, irritability, fatigue 300-500 | 40-50 headache, tachycardia, confusion, lethargy, collapse 800-1200 | 60-70 coma, convulsion 1900 | 80 rapidly fatal ``` B. Neurologic sequelae : parkinson, persistent vegetative state, personality and memory disorders C. Pregnancy -> fetal death
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CARBON MONOXIDE Diagnosis
``` Diagnosis – history of exposure, - no specific findings - cherry red skin coloration + bright red venous blood - ABG, pulse oximetry ``` A. Specific levels: CoHb B. lab studies: electrolytes, glucose, BUN, creatinine, ECG
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CARBON MONOXIDE Treatment
• Treatment A. Emergency and supportive measures: airway, assist ventilation, early intubation if smoke inhalation coma, seizures monitoring EKG B. Specific drugs and antidotes: OXIGEN (100%) ↓τ C C. Decontamination: remove from exposure / suppl O2 D. Enhanced elimination: HYPERBARIC OXYGEN 100% -> 2-3 atm ‼️
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CYANIDE Source & Toxic dose
``` • Sources: -industry, chemical lab, plants - burns: polyurethane, polyacrylonitryl, silk, wool - drugs: nitroprusside ``` ``` • Toxic dose: – INHALED: 100 ppm (in 1 hour) 300 ppm MINUTE – INGESTED: 50 mg LETAL (HCN) 200- 300 mg KCN ``` * ABSORBTION : rapidly * ELIMINATION : metabolic
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CYANIDE Mechanism of toxicity
• Mechanism: CN-(+ Fe3+) blocks cytochrome oxidase -> impairing oxidative phosphorylation, anaerobic metabolism, lactic acid generation -> metabolic acidosis
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CYANIDE Clinical
CLINIC: – coma, convulsions -> metabolic acidosis -> shock -> respiratory failure -> DEATH (few min) – Early effects: cellular hypoxia -> headache,anxiety, tachycardia, hyperpnea, mild HTA, palpitations – Later effects: nausea, vomiting,tachi/bradi, hTA, seizures, coma, apneea, mydriasis, cardiac dysrhytmias, heart blocks, asystole ! Absence of cyanosis sugests CN-
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CYANIDE Diagnosis
DIAGNOSTIC: ``` severe metabolic acidosis red venous blood bitter almond odor ‼️ <- typical coma with rapidly onset, ‼️ absence of Cyanosis tachypnea ```
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CYANIDE Treatment
• SUPPORTIVE TREATM: - assisted ventilation, OXYGEN 100% - correct acidosis • DECONTAMINATION: - AFTER ANTIDOTE ADM ! - < 2h: Lavage, ACTIVATED CHARCOAL • ENHANCE ELIM - HEMODIALYSIS, HEMOPERFUSION – NO ❌ - HYPERBARIC O2 ANTIDOTES: ‼️NITRITES →Methaemoglobinemia MeHb-Fe3+ +CN-CITOCROMOXIDAZA →MeHb-CN + CITOCROMOXIDAZA METHEMOGLOBINE →40% ___________ * AMYL NITRITE - FIRST EMERGENCY‼️‼️ * SODIUM NITRITE 3% 10 ml i.v. SLOW (~ 20% MeHb) • THIOSULFATE: sol. 25% 50 ml i.v. SLOW; Repeted cca. 1 h NITRITE + THIOSULFATE - half doses * HYDROXYCOBALAMIN * CoEDTA (KELOCYANOR) - monitoring 2 – 3 days - MeHb 40% - TREAT ACIDOSIS !!!
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IRON Mechanism of toxicity & toxic dose
• Mechanism of toxicity: 1. direct corrosive effect -> hemorrhagic necrosis /perforation 2. absorbed iron => cellular dysfunction -> lactic acidosis and necrosis • Toxic dose: acute lethal dose 150-200 mg/kg ❗️ lowest LD 600 mg 20-30 mg/kg -> vomiting, abd pain, diarrhea > 60 mg/kg = potentially lethal
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IRON
• Clinical presentation: A. shortly after ingestion: vomiting, diarrhea (bloody) massive fluid loss -> shock, renal failure, -> death B. apparent improvement over 12 hours C. coma, shock, seizures, coagulophaty, hepatic failure, YE sepsis, death D. pyloric stricture, other intestinal obstruction ``` • Diagnosis: history of exposure vomiting diarrhea hTA L↑ Gluc↑>150 mg/dl ```
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IRON Treatment
A. Emergency and supportive measures: airway, assist ventilation, hypovolemia, shock coma, seizures, metabolic acidosis B. Specific drugs and antidotes: DEFEROXAMINE ‼️ pink red color = chelated deferoxamine-iron complex C. Decontamination: prehospital: ipeca –emesis hospital: emesis, gastric lavage, x-ray ❌activated charcoal does NOT adsorb iron‼️ D. Enhanced elimination: hemodyalisis, hemoperfusion not effective
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ARSENIC Mechanism of toxicity & Toxic dose
Mechanism of toxic: interacting with sulfhydryl groups (trivalent) substituting for phosphate (pentavalent) A. soluble comp. – greatest risk B. inorganic dusts – skin, mucous memb., resp and GIT C. human carcinogen • Toxic dose: ``` A.inorganic acute 100-300 mg As+3 chronic 20-60 μg/kg/d B. organic less toxic - marine organisms ```
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ARSENIC Clinical
Clinical presentation A. acute exposure: 1. GIT effects: nausea, vomiting, abd pain, watery diarrhea 2. cardiopulm effects: congestive cardiomyopathy, pulm edema, ↑QT 3. neurologic effects: delirium, encephalopathy, coma 4. others: Aldrich-Mees lines, hair loss, leukopenia B. chronic intoxication: fatigue, gastroenteritis, anemia, leukopenia 1. skin lesions 2. cancer – chronic inhalation -> lung cancer - chronic ingestion ->lung, liver, kidney, bladder
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ARSENIC Diagnosis
Diagnosis: history of exposure + typical presentation garlic odor ‼️ X-ray specific levels : n <1 ppm
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ARSENIC Treatment
A. Emergency and supportive measures: airway, assist ventilation coma, shock, arrythmias, hypotension B. Specific drugs and antidotes: BAL (DIMERCAPROL‼️) 3-5 mg/kg/im 4-6 h C. Decontamination: prehospital: activated charcoal, ipeca (min) hospital: activated charcoal, gastric lavage D. enhanced elimination: hemodialysis
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LEAD What is it ?
Lead acetate (Pb (C2H3 O2)2· 3H2O) • White, crystalline substance • Sugar of lead has a sweet taste • Paint Lead tetraethyl (Pb(C2H 5)4) • antiknock compound added to gasoline • air pollution
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LEAD Mechanism of toxicity
Mechanisms Of Lead Toxicity * Inhibition of enzymatic processes * Lead-Calcium Interactions * Lead-Protein Interactions * Lead-Dopamine Interactions * Lead-Opioid Interactions
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LEAD Health effects
Health Effects * Encephalopathy * Colic * Frank Anemia * Hemoglobin Synthesis * Peripheral Neuropathies * Infertility (MEN) * Systolic Blood Pressure (MEN) * Nerve Conduction Velocity * Erythrocyte Protoporphyrin * DEVELOPMENTAL TOXICITY❗️ * IQ, Memory, Learning * Growth
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LEAD Half life
* 25 DAYS -- BLOOD * 40 DAYS -- SOFT TISSUE * 20 YEARS -- BONE
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LEAD Clinical
A.acute ingestion: abdominal pain, anemia, toxic hepatitis B.chronic intox: fatigue, irritability, anorexia, insomnia, weight loss, arthralgias, myalgias, hypertension -GI: nausea, constipation/diarrhea, crampy abd pain (lead colic) -CNS: impaired concentration, headache, ↓ visual-motor coordination, ataxia, delirium, convulsion, coma, ↓ intelligence, decreased growth - peripheral motor neuropathy: upper extremities, extensor muscle weakness - hematologic: anemia (normochromic,microcytic), hemolysis -nephrotoxic: acute tubular dysfunction, (Fanconi-like aminoaciduria), chronic interstitial fibrosis, hyperuricemia -adverse reproductive outcomes: aberrant sperm production, decreased gestational age
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LEAD Diagnosis
Diagnosis: symtomatology – multisystem findings: abd pain, headache, anemia – child with: delirium, convulsions, neurobehevioral deficits – whole blood level – Urinary lead excretion; n<50 microg/d
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LEAD Treatment
A. Emergency and supportive measures: treat seizures, coma, adequate fluids (avoid overhydration) increased ICP -> corticosteroids B. Specific drugs and antidotes: CHELATORS encephalopathy: CALCIUM EDTA C. Decontamination: ipeca (min) ,gastric lavage , activated charcoal, cathartics D. enhanced elimination: no role
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ETHANOL METABOLISM Which enzyme transforms Ethanol in Acetaldehyde?
ADH – Alcohol Dehydrogenase
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ETHANOL METABOLISM Which Enzyme transforms Acetaldehyde in Acetate?
ALDH – Acetaldehyde Dehydrogenase
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Antidote for Methanol, Ethylene Glycol
Ethanol
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Antidote for LEAD
Edetate calcium disodium CaNa2-EDTA

Toxicology (1 decks)

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