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Stefanny Charles - 01071170223

Tutorial 1
Page 1

Mrs Alena, 24-year-old girl was admitted to the hospital because of was found in decrease of consciousness,
had pinpoint pupils and an irregular heartbeat. The girl was sent to the hospital by her neighbor and from the
mouth and clothes was smelt like an insecticide. The neighbor said that she was pregnant but the husband still
jobless and everyday got drunk. They also said 30 minutes before they found the girl unconscious, they talked
with her and she seems very frustrated.

QUESTIONS

1. What are Mrs. Alena problems?


└ decrease of consciousness, had pinpoint pupils and an irregular heartbeat.
└ mouth and clothes was smelt like an insecticide
└ 30 minutes before they found the girl unconscious
└ neighbor said that she was pregnant & seems very frustrated.

2. What is the underlying cause of her problems?


Intoxication dari insecticide

3. What are the possible mechanisms that cause her problems?


Frustrate  ingest insecticide
Stefanny Charles - 01071170223

Tutorial 1
Page 2

The neighbor also found a cup and a can of Baygon. On Physical examination: confusion, temperature was
36.3°C, the pulse was 60 Bpm, and the respirations were 28 X/min. The blood pressure was 90/70 mmHg.
She’s got vomitting, salivation, lacrimation, miosis and muscle fasciculation, tremor, weakness. There is no
sign about anemia or icteric in eye examination. In lung examination was found wheezing and retraction of
intercostals space when inspiration. There is no sign of cardiac abnormalities, and from abdominal
examination the bowel sound was rather increased. Genital area and extremities were in normal condition.

QUESTIONS

1. What are Mrs. Alena problems?


└ Confusion, hyperventilation, hypotension, vomitting, salivation, lacrimation, miosis and muscle
fasciculation, tremor, weakness
└ wheezing and retraction of intercostals space when inspiration.
└ bowel sound was rather increased

2. What is the underlying cause of her problems?


Ingest organo phosphate

3. What are the possible mechanisms that cause her problems?


Ingest oregano phosphate  keracunan zat kimia  hambat asetilkolin esterase inhinitor  over
stimulation acetylcholine  muscarinic over stimulation  increase sympathetic & parasymphatatic
respond

4. What further information do you need?


CBC, SGPT/SGOT, Urine analysis, Arterial blood gas, serum laktat, vit K
Stefanny Charles - 01071170223

Tutorial 2
Page 3

Past medical history, obtained from friends and previous medical record, was noncontributory. There was no
personal history of diabetes, epilepsy, trauma, syncope, cardiac, pulmonary or renal disease. Family history
was also noncontributory.
Laboratory tests were performed
Table 1. Hematologic Laboratory Values
VARIABLE VALUE
Hb (g/dL) 12
Hematocrit (%) 30
White-cell count (per mm3) 12,000
Differential count (%)
Basophils 0
Eosinophils 0
Neutrophils 70
Lymphocytes 30
Monocytes 0
Random blood glucose (mg/dL) 256
SGOT 68
SGPT 74
Platelet count (per mm3) 225.000

QUESTIONS

1. How do you interpret the laboratory finding?


Low hematocrit, leukocytosis, low eosinophil, hyperglycemia, liver dysfunction

2. What does this tell you about the cause of the patient problems?
Ingest many organophosphate  masuk BBB  menyebabkan perubahan reflex batang otak &
penekanan 2/3 batang otak  terjadi unconciousness

3. What other laboratory information do you need?


Urine analysis, ABG, serum lactate
Stefanny Charles - 01071170223

Tutorial 2
Page 4

Next blood laboratory result: Serum pseudocholinesterase concentration was 3 U/mL (normal range 7-
19), RBC cholinesterase was within the normal range, Sodium 130 meq/L (135-145 meq/L), Potasium
33 (35-55 meq/L), Chloride 80 (95-105 meq/L). Blood gas analysis pH : 7.47 , pCO 2 : 40 , pO2 : 75 ,
HCO3- : 28 , BE : +2 , Saturation O2 : 95

QUESTIONS

1. How do you interpret the laboratory finding?


Serum pseudocholinesterase  konfirmasi terjadinya keracunan
Alkalosis respiratory
Low ion: sodium, potassium, chlorine

2. What is the caused of this blood gas change?


Cholinergic toxicity  mepengaruhi muscarinic receptor  symptoms  perubahan ABG
Stefanny Charles - 01071170223

Tutorial 3
Page 5

On arrival at the hospital, an endotracheal tube was inserted and oxygen therapy begun with clearing of
the cyanosis but no change in neurological status.
At the first the patient was treated to prevent of further poison absorption with activated charcoal and be
administrated of antidotes sulfas atropine 0.5-2 mg (2-8 ampul) intravenous and repeated every 5-15
minutes until 40 ampuls of sulfas atropine.

QUESTIONS

1. What is an important procedure do you need to do?


ABC, TTV, cardiac monitoring, supportive, privent toxic absorption,
Atropine (muscarinic receptor) + plaridoksin (buat nikotinikreceptor)
2. What is a specific antidote for this condition?
Stefanny Charles - 01071170223

LO:
1. To know the general principles of treatment in poisoning and drug overdose
 1st goal  prevent absorption & increasing elimination
 2nd goal  menetralkan toxicological effect
Treatment:
 Treat dengan tepat
 Supportive therapy
 Maintain respiratory & circulation  primary
 Judge progress intoxication  measuring vital sign & reflex

Other treatment:

 Supportive care
 Activated charcoal for serious oral poisonings
 Occasional use of specific antidotes or dialysis
 Only rare use of gastric emptying

2. To know the supportive care and prevention of poison absorption


SUPPORTIVE CARE
- ABC
└ AIRWAY  endotracheal tube of need, watch fluid accumulation
└ BREATHING  supplemental oxygen, bag valve mask & respiratory
└ CIRCULATION  monitor ECG (arrththmias, cardiac arrest & shock)
a. Vasogenic shock  fault vasomotor tone, increase capillary permeability
b. Cardiogenic shock  inadequate cardiac output, krn cardiac dilation
- Treatment symptoms
└ Arrhythmias  cardiac
└ Torsade de pointes  sulfate 2 to 4 g IV, overdrive pacing, or a titrated isoproterenol infusion.
└ Seizure  benzodiazepine (large dose  sedative/ inductuin paralysis & mechanical ventilation
rewuired), phenobarbital/ phenytoin
└ Hyperthermia  aggressive sedation physical cooling measurement
- DRUGS:
└ IV NALOXONE
 2 mg in adults; 0.1 mg/kg in children; doses as high as 10 mg
 tried in patients with apnea or severe respiratory depression while maintaining airway
support.  kl hilang monitor  kl ada lagi treated with another bolus of IV naloxone or
endotracheal intubation and mechanical ventilation
 If respiratory depression persists despite use of naloxone  endotracheal intubation and
continuous mechanical ventilation
└ IV DEXTROSE
 50 mL of a 50% solution for adults; 2 to 4 mL/kg of a 25% solution for children
 altered consciousness or CNS depression, hypoglycemia ruled out
└ THIAMINE (100 mg IV)
 given with or before glucose to adults with suspected thiamine deficiency (eg, alcoholics,
undernourished patients).
└ IV FLUID
 For hypotension
 Ineffective invasive hemodynamic monitoring
 first-choice vasopressor for most poison-induced hypotension is norepinephrine 0.5 to 1
mg/min IV
- Antidote use in comatose patient at hospital  glucose, insulin, naloxone, vit K, atropine
Stefanny Charles - 01071170223

PREVENTION
Other preventive measures include

 Clearly labeling household products and prescription drugs


 Storing drugs and toxic substances in cabinets that are locked and inaccessible to children
 Promptly disposing of expired drugs by mixing them in cat litter or some other nontempting substance and
putting them in a trash container that is inaccessible to children
 Using carbon monoxide detectors
 Refraining from prescribing opioids and using nonopioid treatments whenever possible

3. To know the enhancement of poison elimination and prevention of exposure


- REMOVAL DRUG (emesis)
 Emesis inducer  mechanical (stroking posterior pharynx); apomorphine parenteral;
Syrup of ipecac 30 ml (1 oz) followed by one glass of water (150-200 ml)
 Contraindication:
• Caustic acid or alkali agent -- rupture of upper GIT
• Petroleum hydrocarbon solvent -- aspiration
• Seizing Patient
• Comatose Patient
Removal drug treatment:

└ TOPICAL DECONTAMINATION
 Untuk surface exposed toxin  pk water/ saline
└ ACTIVE CHARCOAL
 Dikasih kl ada multiple/ unknown substance ingest
 Give as soon as possible
 Active charcoal absorb toxin because molecular configuration & large surfave area
 Multiple dose active charcoal  buat substance yg enterohepatic recirculation (eg, phenobarbital,
theophylline) and for sustained-release preparations
 given at 4- to 6-h intervals for serious poisoning, dose 5-10 times (suspect toxin ingested)
 usual dose is 1 to 2 g/kg, which is about 10 to 25 g for children < 5 yr and 50 to 100 g for older
children and adults.
 Charcoal is given as a slurry in water or soft drinks.
  ineffective for caustics, alcohols, and simple ions (eg, cyanide, iron, other metals, lithium).
└ GASTRIC EMPTYING
 considered if it can be done within 1 h of a life-threatening ingestion.
 Gastric lavage may cause complications such as epistaxis, aspiration, or, rarely, oropharyngeal or
esophageal injury. 
 syrup of ipecac has unpredictable effects, often causes prolonged vomiting, and may not remove
substantial amounts of poison from the stomach.
 gastric lavage, tap water is instilled and withdrawn from the stomach via a tube.
 If patients have altered consciousness or a weak gag reflex, endotracheal intubation should be done
before lavage to prevent aspiration.
└ WHOLE BOWEL IRRIGATION
 flushes the GI tract
 prepared solution of polyethylene glycol (which is nonabsorbable) and electrolytes is given at a rate
of 1 to 2 L/h for adults or at 25 to 40 mL/kg/h for children until the rectal effluent is clear; (hours or
even days)
 caranya: give gastric tube  motibated patient drink large volume

Irrigation is indicated for any of the following:

 Some serious poisonings due to sustained-release preparations or substances that are not adsorbed by charcoal
(eg, heavy metals)
 Drug packets (eg, latex-coated packets of heroin or cocaine ingested by body packers)
 A suspected bezoar
└ ALKALINE DIURESIS
 elimination of weak acids (eg, salicylates, phenobarbital). 
Stefanny Charles - 01071170223

 solution made by combining 1 L of 5% D/W with 3 50-mEq ampules of NaHCO 3 and 20 to 40 mEq
of K can be given at a rate of 250 mL/h in adults and 2 to 3 mL/kg/h in children.
 Bisa terjadi  Hypernatremia, alkalemia, and fluid overload
 Contraindicated  renal insufficiency.
└ DIALYSIS

Common toxins that may require dialysis or hemoperfusion include

 Ethylene glycol
 Lithium
 Methanol
 Salicylates
 Theophylline

└ SPECIFIC ANTIDOTE

Prevent exposure  labeling, self protection, jauhi barang dari anak- anak
Stefanny Charles - 01071170223

4. To know specific poison and approach for organophosphate and carbamate


Examples of organophosphates include the following:
 Insecticides – Malathion, parathion, diazinon, fenthion, dichlorvos, chlorpyrifos, ethion
 Nerve gases – Soman, sarin, tabun, VX
 Ophthalmic agents – Echothiophate, isoflurophate
 Antihelmintics – Trichlorfon
 Herbicides – Tribufos (DEF), merphos
 Industrial chemical (plasticizer) – Tricresyl phosphate

5. Effect & mechanism organophosphate and carbamate

CARBAMATE:
-  Carbamates are N-methyl Carbamates derived from a carbamic acid and cause
carbamylation of acetylcholinesterase at neuronal synapses and neuromuscular
junctions.
- irreversible phosphorylation of acetylcholinesterase by organophosphates,
carbamates bind to acetylcholinesterase reversibly.
- poisonings with a duration of toxicity that is typically less than 24 hour
- carbamate bonds are hydrolyzed from acetylcholine spontaneously and rarely
cause symptoms after 24 to 48 hours. 
Stefanny Charles - 01071170223

- Common agents resulting in toxic exposure are aldicarb, carbofuran, carbaryl,


ethinenocarb, fenobucarb, oxamyl, methomyl, pirimicarb, propoxur, and
trimethacarb.
- Carbamate poisoning cases are most often related to intentional oral ingestion
or dermal occupational exposure.
- Acetylcholinesterase (AChE) normally hydrolyzes acetylcholine to acetic acid
and choline, leading to the cessation of neurotransmitter signaling. 
- cause reversible inhibition of the acetylcholinesterase enzyme, which is
present at parasympathetic and sympathetic ganglia, parasympathetic
muscarinic terminal junctions, sympathetic fibers located in sweat glands, and
nicotinic receptors at the skeletal neuromuscular junction
- Central nervous system symptoms from increased acetylcholine include
confusion, delirium, hallucinations, tremor, and seizures. Increased
acetylcholine levels in the autonomic nervous system increase sympathetic and
parasympathetic activity.
- "DUMBBELS" stands for defecation, urination, miosis, bronchospasm or
bronchorrhea, emesis, lacrimation, salivation.
- TOXICOKINETIC
chronic or acute and absorbed from the skin, lungs, conjunctiva, mucous
membranes, lungs, and GI tract. 
Dermal absorption appears to be low with increasing absorption in cases of
disruption in the skin and exposure to highly toxic carbamates.
- HISTORY PHYSICAL

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