1.
Physiological Antidote
-act on different sites/receptor to produce opposite
effect of poison
-e.g. anaphylaxis (Epinephrine)
Organophosphate (Atropine)
Atropipne (Physostigmine)
2. Chemical Antidote
-changing the chemical nature/structure of the poison
3. Mechanical Antidote
-preventing the absorption of the toxin
-e.g.
 Gastric lavage
 Emesis (IPECAC or syrup of EPICAC)
 Catharsis (Normal Saline Cathartics;
Magnesium Citrate and Magnesium Sulfate,
and Castore oil)
 Whole Bowel Irrigation
 Alteration of pH
 Adsorption (Activated Charcoal but not
effective with alcohol poisoning)
4. Poison Present Systematically
-force diuresis with urine pH manipulation
-e.g. Phenobarbital and Salicylates (Urinary
Alkalinization e.g. NaHCO3)
-e.g. Phencyclidine and Amphetamine (Urinary
Acidification e.g. Ascorbic Acid and NH4CL)
5. Extracorporeal Method
-a treatment modality promoting removal of
endogenous or exogenous poison
-e.g. Dialysis (Peritoneal dialysis; hemodialysis)
Hemodialysis – susbtances that are removed are
WATER soluble, have a small VD (<0.5 L/kg), have
a low molecular weight and are NOT significantly
bound to plasma proteins
-for life-threatening ingestions of ethylene glycol,
methanol, or paraquat
-used to enhance the elimination of ethanol,
theophylline, lithium, salicylates, and long-acting
barbiturates
Peritoneal Dialysis
-10% - 15% as effective
-easier to perform, NO NEED for anti-coagulant
Hemoperfusion
-is a technique in which anti-coagulated blood is
passed through (perfused) a column containing
activated charcoal or resin particles
-more rapid than hemodialysis
-more effective in removing phenobarbital,
phenytoin, carbamazepine, methotrexate, and
theophylline
-less effective in removing ethanol or methanol
Complications:
 Thrombocytopenia (normal low level of
platelets of blood)
 Leukopenia (lack of white blood cells)
 Hypokalemia (low potassium)
 Hypocalcemia (low calcium)
 Hypoglycemia (low glucose)
 Hypotension (low blood)
6. Patient with Decrease Mental Satus
 Hypoglycemia
-Adult - 50ml 50% Dextrose
-Children 1ml/kg Dextrose
 Wernicke-Korsakoff (lack of thiamine nga
naga result lack of muscle coordination, lack
of posture (imbalance), tremor, vision
problem na usually gakatabo sa alcohol
poisoning)
-Thiamine 100mg IV push
 Opioid Ingestion (decreased mental status)
-Naloxone 0.4 – 20mg IV push
COMMON MECHANISM OF TOXICITY
 Interfere with tissue utilization of Oxygen
 Depression or Stinulation of CNS
 Affect ANS
 Affect Vasculature and Heart
 Affect Lungs
 Local Damage
1. Interfere with tissue utilization of Oxygen
a. Carbon Monoxide
-product of incomplete combustion of organic matter
-cars, exhaust (gasoline powered machines)
Mechanism of Toxicity
-CO combine with Hgb  Carbohemoglobin (O2
cannot bind to Hbg)  Hypoxia (ow oxygen sa
tissues and cells
s/sx: Headache and cherry skin
tx: Hyperbaric oxygen therapy – increase atm
pressure of 100% O2 (in order to eliminate faster the
carbon monoxide)
B. Hydrogen Sulfide (H2S)
Source: crude, petroleum, natural gas, and volcanic
gases
-rotten egg odor, highly toxic colorless gas
Mechanism of Toxicity
-occurs by inhalation
-arrest of cellular respiration (ginapatigil niya ang
imo pag ginhawa)
-forms a complex bond to the ferric moiety (ga bind
sa iron) causing inhibition of mitochondrial
cytochrome oxidase (iron-containing protein),
thereby arresting aerobic metabolism
-decrease or low oxygen utilization (tungod sa
mitochondrial cytooxygenase)
CHA kyutieee
S/sx: irritation of mucous membrane and respiratory -white, odourless, bitter crystalline power
depression -persticide for killing rat/rodent
Tx: Amyl Nitrite (inhalation) and Sodium Nitrite Mechanism of Toxicity
(IV) -antagonist of post synaptic glycine receptor which
 NITRITE induce Methemoglobin acts as a is present in spinal cord (dominant on receptor and
scavenger with strong affinity to hydrogen can cause involuntary painful skeletal muscle
sulphide contraction)
NaNO2 + Hgb = Methemoglobin  bind to H2S -antagonist of acetylcholine (can cause excitation of
(Sulfhemoglobin)  serlf resolving all parts of the CNS)
-sinasabayang ng Hyperbaric O2 B. Muscle Relaxant
C. Cyanide -Panuronium Br. And Succinylcholine
-available forms: industrial and some nail polish s/sx:
removers  Muscle Weakness
-Prunus sp (bitter almond (raw), apricot, cherry,  Convulsion
cassava, and silver jewelry cleaner  Seizure
Mechanism of Toxicity  Malignant Hyperthermia (Grabe nga init sa
-Inhibition of Cytochrome oxidase  low cellular lawas)
respiration 3. Affect ANS
s/sx: A. Organophosphates
 Headache -e.g. Malathion (insecticide) and Carbamates
 Dyspnea (low breathing) (baygon)
 Nausea Mechanism of Toxicity
 Vomiting -inhibition of acetylcholinesterase (AchE) 
 Ataxia (uncontrollable muscle movements) accumulater Ach
 COMA s/sx DUMBBELLS
 Seizures  Diarreha
 Death (not a s/sx but can lead to death)  Urination
Tx:  Miosis
Cyanide antidote kit  Bronchorrhea
 Amyl Nitrite (inhaled)  Bronchospasms (constriction of airway)
 Sodium Nitrite (10ml IV push)  Emesis
 Sodium Thiosulfate (50ml of a 25% solution  Lacrimation
IV push)  Laxation
Hbg  methemoglobin  bind to CN  Sweating
(cyanomethemoglobin)  readily excretable
 Oxygen
 Sodium Bicarbonate (if may sever acidosis)
IMPORTANT
 Hydroxocobalamin S/SX – Signs and
-5g IV over 15 mins (ADULT) and repeated Symptoms
for a total dose of 10g
TX – Treatment
BAWAL SA BATA kay maapektohan and
heart or cardiovascular embarrassment HGB - Hemoglobin
D. Nitrates
 Inorganic Nitrates (preservatives)
KNO3 – salt peter
NaNO3 – chili salt peter
 Organic Nitrates
Glyceryl Trinitrates
Isosorbide Dinitrite
 Inorganic Nitrites
Na Nitrite
Amyl Nitrite
2. Depression or stimulation of CNS that may
cause either COMA or CONVULSION
A. Strychnine

CHA kyutieee