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Toxicology > Lectures 1-5 > Flashcards

Lectures 1-5 Flashcards

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
Q

Antidote for Organophosphorus compounds

A

Pralidoxime

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25
Q

Antidote for central anticholinergic syndrome

A

Physostigmine

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26
Q

Antidote for Isoniazid, Hydralazine

A

Pyridoxine

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27
Q

Antidote for Copper

A

Penicillamine

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28
Q

Antidote for Cyanide

A

Sodium nitrite, Sodium Thiosulfate

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29
Q

Antidote for Heparin

A

Protamine Sulfate

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30
Q

Antidote for Salicylate, tricyclic antidepressants

A

Sodium Bicarbonate

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31
Q

Emetics

A

Apomorphine, Ipecacuanha

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32
Q

Alkalinize blood and urine

A

Sodium Bicarbonate

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33
Q

Cathartics and sol for whole gut lavage

A

Sorbitol, Mannitol
Magnesium citrate, mag sulfate
Bicarbonates, Sodium Sulfates
…

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34
Q

Prevents absorbtion in gut:

A 
Activated charcoal (for adsorbable poison)
Starch (for iodine)
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35
Q

Prevents skin absorbtion/damage

A

Calcium gluconate gel - for hydrofluoric acid

Polyethylene glycol - for phenol

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36
Q

Anti-foaming agent

A

Dimethicone (soaps, shampoos)

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37
Q

Dystonia

A

Benztropine

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38
Q

Medication for: Psychotic with severe agitation

A

Chlorpromazine

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39
Q

Medication for: Acute allergic reaction, mucosal edema, laryngeal edema, bronhoconstriction

A

Corticosteroids

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40
Q

Medication for: Convulsions, Anxiety, excitation, muscular hypertonia

A

Diazepam

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41
Q

Medication for: myocardial depression

A

Dobutamine, Dopamine

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42
Q

Medication for: Anaphylactic shock, cardiac arrest

A

Epinephrine

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43
Q

Medication for: fluid retention, left ventricular failure

A

Furosemide

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44
Q

Medication for: Hypoglycemia

A

Glucose

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45
Q

Medication for: hallucinations and psychotic states

A

Haloperidol

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46
Q

Medication for: Hypercoagulability

A

Heparin

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47
Q

Medication for cardiac arrhythmia

A

Magnesium sulfate

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48
Q

Medication for Cerebral edema, fluid retention

A

Mannitol

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49
Q

Medication for hypoxia

A

Oxygen

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50
Q

Medication for bronchoconstriction systemic/ inhaled

A

Salbutamol

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51
Q

Medication for acidosis, some cardiac disturbances

A

Sodium bicarbonate

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52
Q

Toxicological screen

A

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

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53
Q

ICU admission criteria

A

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

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54
Q

Drugs associated with SEIZURES:

A

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

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55
Q

Odor: Acetone

A

Acetone, isopropanol,metabolic acidosis

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56
Q

Odor: Airplane Glue

A

Toluene, aromatic hydrocarbon inhalation

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57
Q

Odor: alcohol

A

Ethanol ( no ethylene glycol or vodka)

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58
Q

Odor: Ammonia

A

Ammonia or Uremia

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59
Q

Odor: bitter Almonds

A

Cyanide

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60
Q

Odor: Coal gas

A

Carbon monoxide = odorless but mix with illuminating gas for detection

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61
Q

Odor: Disinfectants

A

Phenol, Creosote

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62
Q

Odor: Formaldehyde

A

Formaldehyde, Methanol

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63
Q

Odor: Garlic

A

Arsenic, Parathion, Yellow Phosphorus, Se, Zn

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64
Q

Odor: Pears

A

Chloral hydrate, Paraldehyde

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65
Q

Odor: Rotten Eggs

A

Disulfiram, Hydrogen Sulfide, hepatic failure

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66
Q

Odor: Shoe polish

A

Nitrobenzene

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67
Q

Anticholinergic syndromes

A

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
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68
Q

Sympathomimetic Syndromes

A

Cause:

cocaine
amphetamine
methamphetamine
ephedrine
pseudoephedrine
phenylpropanolamine

Common signs:

delusions
paranoia
tachycardia
hypertension
hyperpyrexia
diaphoresis
piloerection
mydriasis
hyperreflexia
seizures
hypotension
dysrhytmias – severe cases
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69
Q

Cholinergic Syndromes

A

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
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70
Q

Opiate, Sedative or Ethanol Intoxication

A

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)
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71
Q

Normal Anion Gap

A

3-11

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72
Q

High Anion Gap induced by:

A
  • 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
Q

Low Anion Gap induced by:

A
  • 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
Q

Osmolal Gap

A

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
Q

Specific Antidote in (~5% acute poisonings):

A

NALOXONE + GLUCOSE 5%

Patients having CNS

76
Q

First priority:

A

Airways, Breathing

  • ventilation
  • oxygenation

Obstruction:
mucosa edema, secretions, foreign body,
defectuos position of tongue

Symptoms:
cyanosis, tahipneea, dyspnea, diaphoresis,
altered mental status

77
Q

Second Priority:

A

CIRCULATION

Shock: 
↓level of consciousness
↓BP
peripheral vasoconstriction
metabolic acidosis
oliguria

Mechanism:
↓contractility
hypovolemia
preload, afterload

78
Q

Third priority:

A

DISABILITY

CNS

  • pupils
  • coma

 IV Decontamination

79
Q

REED classification

A 
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
Q

Absorbtion prevention

A

Internal decontamination

Dilution: caustics, corrosive
-> 300ml milk or water

CI: neutralization reactions

81
Q

Emetics

A

 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
Q

Gastric lavage

A

 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
Q

Activated charcoal

A

 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
Q

Barbiturates

A
  • 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
Q

Barbiturates Diagnosis

A

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
Q

Barbiturates Treatment

A

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
Q

Benzodiazepines

Mechanism of Toxicity:

A

GABA med synaptic inhibition

Inhib other neuronal syst
-> depression of spinal reflexes / RAS

88
Q

Benzodiazepines

Toxic dose:

A

Oral overdose:
Diazepam 15-20 x therap dose

Rapid iv - Respiratory arrest

89
Q

Benzodiazepines

Clinical:

A

lethargy, slurred speech, ataxia, coma, resp arrest
hyporeflexia, midposition or small pupils
hypothermia
complications ! short acting/other depressant

90
Q

Benzodiazepines

Diagnosis

A

History ingestion or injection
Dif Diagnosis
Reverse with Flumazenil

91
Q

Benzodiazepines

Treatment

A

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
Q

Cyclic Antidepressants

Mechanism of toxicity

A

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
Q

Cyclic Antidepressants

Toxic dose

A

Toxic dose:
narrow therapeutic index: intoxication

10-20 mg/kg potentially life-threatening

94
Q

Cyclic Antidepressants

Clinical

A

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
Q

Cyclic Antidepressants

Diagnosis

A

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
Q

CYCLIC ANTIDEPRESSANTS

Treatment

A

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
Q

PHENOTHIAZINES

Mechanism of toxicity

A

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
Q

PHENOTHIAZINES

Toxic Dose

A

high toxic-therapeutic index

extrapiramidal reactions, anticholinergic side effects, orthostatic hypotension =>
therapeutic doses

99
Q

PHENOTHIAZINES

Clinical

A

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
Q

PHENOTHIAZINES

Diagnosis

A

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
Q

PHENOTHIAZINES

Treatment

A

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
Q

OPIOIDS

Mechanism of toxicity

A

*stimulates specific opiate receptors in CNS
=> sedation,
=> respiratory depression -> resp.failure -> apneea -> death

  • noncardiogenic pulmonary edema
103
Q

OPIOIDS

Toxic dose

A

Depend on:

compound, route, tolerance, rate of adm

104
Q

OPIOIDS

Clinical

A

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
Q

OPIOIDS

Diagnosis

A

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
Q

Which iv injected drug can induce non-cardiogenic pulmonary edema and resp distress?

A

iv injected HEROIN

also salicylates and cocaine

107
Q

OPIOIDS

Complications

A 
ARDS 
Aspiration pneumonia 
Lezional APE
Postinject venous thrombosis 
Necrosis after inject paravenous
Hepatitis B, C 
HIV
Abcess
Rabdomiolisis
Renal insuf
108
Q

Sindrom de intrerupere - OPIOIDS

A

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
Q

Sindrom de intrerupere

Tratament

A

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
Q

ACETAMINOPHEN

Toxic dose

A

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
Q

ACETAMINOPHEN

Mechanism of toxicity

A

Mechanism of toxicity:

acetaminophen -P-450- toxic metabolit (hepatotoxic) NAPQI
-glutathione- detoxified
=liver injury

112
Q

ACETAMINOPHEN

Clinical

A

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
Q

Acetaminophen

Diagnosis

A

Diagnosis

  • serum acetaminophen level
  • history

A. Specific levels : 4 h postingestion

B. Other useful lab studies: electrolytes, glucose, BUN, crea, transaminases, PT

114
Q

Acetaminophen

Treatment

A

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
Q

SALICYLATES

Mechanism of toxicity

A

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
Q

SALICYLATES

Toxic dose

A

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
Q

SALICYLATES

Clinical

A

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
Q

SALICYLATES

Diagnosis

A

history of acute ingestion
typical signs and symptoms

qualitative: colorimetric;

lab studies:
anion gap calculation, glucose, BUN, PT, ABG, chest X-ray

119
Q

SALICYLATES

Treatment

A

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
Q

IZONIAZID

Mechanism of toxicity

A

Mechanism of toxicity:
PYRIDOXINKINASE
PYRIDOXINE PYRIDOXALPHOSPHAT

 Acute overdose: competition with pyridoxal 5-phosphate
↓ GABA
inh lactat>piruvat => lactic acidosis

 Peripheral neuritis

121
Q

IZONIAZID

Toxic dose

A

Toxic dose acute: min 1.5g

6g = severe toxicity => death

3mg/kg epileptics => status epilepticus

122
Q

IZONIAZID

Clinical

A

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
Q

IZONIAZID

Diagnosis

A

Diagnosis :

history of ingestion
clinical presentation

! Acute onset seizures + acidosis

124
Q

IZONIAZID

Treatment

A

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
Q

IZONIAZID

Intoxication Outcome -> End Result

A

Blocking pyridoxinkinaza.

Hepatic necrosis

Tubular necrosis

Inh GABA => Metabolic Acidosis

126
Q

Classes of Pesticides

A 
Insecticides (kill insects)
• Organochlorines
• Organophosphates
• Carbamates
• Synthetic Pyrethroids
Herbicides (kill plants)
Rodenticides (kill rodents)
Fungicides (kill fungus)
Fumigants (kill whatever)
127
Q

ORGANOPHOSPHATES

Mechanism of toxicity

A

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
Q

ORGANOPHOSPHATES

Clinical

A

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
Q

ORGANOPHOSPHATES

Diagnosis

A

Diagnosis:
history of exposure
characteristic sign
solvent odor

 Specific levels: ↓PChE, ↓AChE (more reliable)

130
Q

ORGANOPHOSPHATES

Classification

A

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
Q

ORGANOPHOSPHATES

Treatment

A

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
Q

ETHANOL

Mechanism of toxicity

A

A. CNS depression
additive effect
B. hypoglycemia
C. predisposition to trauma, hypothermia, metab derangements

133
Q

ETHANOL

Toxic dose

A

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

134
Q

ETHANOL

Clinical

A

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
135
Q

ETHANOL

Diagnosis

A

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

136
Q

ETHANOL

Treatment

A

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

137
Q

ETHANOL

Antidote for poisoning by:

A

Methanol
Ethylene glycol
Diethylene glycol

- Inhibits metabolic activation by 
alcohol dehydrogenase (ADH)
138
Q

Alcohol withdrawal effects

A
  • Tremor
  • Nausea
  • Irritability
  • Agitation
  • Tachycardia
  • Hypertension
  • Seizures
  • Hallucinations
139
Q

METHANOL

Mechanism of toxicity & Toxic dose

A

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

140
Q

METHANOL

Clinical

A

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

141
Q

METHANOL

Diagnosis

A

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

142
Q

METHANOL

Treatment

A

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

143
Q

ETHYLENE GLYCOL

Mechanism of toxicity & toxic dose

A

Ethylene glycol -> glycoaldehyde
glycolic / glyoxylic / oxalic acids -> metab acidosis

Oxalate + Ca -> calcium oxalate crystals (insoluble) -> tissue injury

Toxic dose: 100 ml

144
Q

ETHYLENE GLYCOL

Clinical

A
  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
145
Q

ETHYLENE GLYCOL

Diagnosis

A

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

146
Q

ETHYLENE GLYCOL

Treatment

A

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

147
Q

HYDROCARBONS

Mechanism of toxicity & toxic dose

A

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)

148
Q

HYDROCARBONS

Clinical

A

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

149
Q

HYDROCARBONS

Diagnosis

A

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

150
Q

HYDROCARBONS

Treatment

A 
A. Emergency and supportive measures:
1. general: 
BLS for all symptomatic patients
airway , supplemental O2, assist ventilation
monitor ABG, chest X-ray, ECG
  1. pulm aspiration:
    observation 4-6 h
    coughing on arrival= aspiration
    ! Do not use steroids !
  2. 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

151
Q

HYDROGEN SULFIDE

Mechanism of toxicity & toxic dose

A

= 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
152
Q

HYDROGEN SULFIDE

Clinical

A

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

153
Q

HYDROGEN SULFIDE

Diagnosis

A

Diagnostic:

hystory of exposure
progressive airway irritation and cellular asphyxia

smell: rotten eggs ‼️

N. olfact. Paralysis
serum levels : not available

154
Q

HYDROGEN SULFIDE

Treatment

A

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

155
Q

CARBON MONOXIDE

Mechanism of toxicity + Toxic dose & Sources

A

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%

156
Q

CARBON MONOXIDE

Clinical

A

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

157
Q

CARBON MONOXIDE

Diagnosis

A 
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

158
Q

CARBON MONOXIDE

Treatment

A

• 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 ‼️

159
Q

CYANIDE

Source & Toxic dose

A 
• 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
160
Q

CYANIDE

Mechanism of toxicity

A

• Mechanism:

CN-(+ Fe3+) blocks cytochrome oxidase -> impairing oxidative phosphorylation, anaerobic metabolism, lactic acid generation -> metabolic acidosis

161
Q

CYANIDE

Clinical

A

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-

162
Q

CYANIDE

Diagnosis

A

DIAGNOSTIC:

severe metabolic acidosis
red venous blood
bitter almond odor ‼️ <- typical
coma with rapidly onset, 
‼️ absence of Cyanosis
tachypnea
163
Q

CYANIDE

Treatment

A

• 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 !!!
164
Q

IRON

Mechanism of toxicity & toxic dose

A

• 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

165
Q

IRON

A

• 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
166
Q

IRON

Treatment

A

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

167
Q

ARSENIC

Mechanism of toxicity & Toxic dose

A

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
168
Q

ARSENIC

Clinical

A

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
169
Q

ARSENIC

Diagnosis

A

Diagnosis:

history of exposure + typical presentation

garlic odor ‼️

X-ray
specific levels : n <1 ppm

170
Q

ARSENIC

Treatment

A

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

171
Q

LEAD

What is it ?

A

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

172
Q

LEAD

Mechanism of toxicity

A

Mechanisms Of Lead Toxicity

  • Inhibition of enzymatic processes
  • Lead-Calcium Interactions
  • Lead-Protein Interactions
  • Lead-Dopamine Interactions
  • Lead-Opioid Interactions
173
Q

LEAD

Health effects

A

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
174
Q

LEAD

Half life

A
  • 25 DAYS – BLOOD
  • 40 DAYS – SOFT TISSUE
  • 20 YEARS – BONE
175
Q

LEAD

Clinical

A

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

176
Q

LEAD

Diagnosis

A

Diagnosis: symtomatology

– multisystem findings: abd pain, headache,
anemia
– child with: delirium, convulsions, neurobehevioral deficits
– whole blood level
– Urinary lead excretion; n<50 microg/d

177
Q

LEAD

Treatment

A

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

178
Q

ETHANOL METABOLISM

Which enzyme transforms Ethanol in Acetaldehyde?

A

ADH – Alcohol Dehydrogenase

179
Q

ETHANOL METABOLISM

Which Enzyme transforms Acetaldehyde in Acetate?

A

ALDH – Acetaldehyde Dehydrogenase

180
Q

Antidote for Methanol, Ethylene Glycol

A

Ethanol

181
Q

Antidote for LEAD

A

Edetate calcium disodium CaNa2-EDTA

Toxicology (1 decks)

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