Toxicology

Question 1

What I is the most important aspect in treating intoxications
Patients with depressed mental status should receive what treatment?

Answer 1

Supportive management is the most important aspect of treating most intoxications, although specific antidotes should be considered when indicated.
• Patients with depressed mental status should all receive empiric therapy with oxygen, dextrose, thiamine, and naloxone while evaluation is ongoin

Initial support measures require attention to the “ABCs” (airway, breathing, circulation).
• Administer a combination of thiamine 100 mg IV, dextrose 50 g IV, and naloxone (initial dose of 0.2–04 mg IV) to patients who present with change in mental status.

Question 2

A toxidrome is a cluster of syndromes for a particular patient
You ought to wear protective gloves or decontaminate
How do you do this?

Answer 2

Decontaminate skin by removal of toxin with soap and water. Remove contaminated clothing and store in adequate container to limit ongoing exposure to patient and health care providers.
• Ocular decontamination may require prolonged irrigation with normal saline solution.

Question 3

What is gastric emptying and how is it done

Answer 3

• Large-bore (Ewald) tubes 37–40 F may be needed to remove gastric debris.
Technique: Inspect mouth and clear off foreign material. Have suctioning equipment ready. Insert tube and confirm placement. Immediately withdraw as much of the gastric contents as possible. Instill 200 mL bolus of warmed water and aspirate gastric contents.
Repeat until gastric aspirate is clear.

Question 4

State five contraindications of gastric emptying

Answer 4

Obtunded, comatose, or convulsing patients. Also ingestion of sustained-release or enteric-coated tablets and probably caustic liquids to avoid aspiration-induced lung injury.
This method of tube placement should not be used in patients with depressed level of consciousness unless intubation has been performed, since retching and vomiting is common.

Question 5

What is active charcoal
In what cases is activated charcoal not effective
What are the contraindications of activated charcoal

Answer 5

Activated charcoal is a nontoxic, inert, nonspecific adsorbent that binds intraluminal drugs and decreases systemic absorption.
1 g/kg/every 4 Hour. for at least 3 doses.
It is not effective in iron,lithium,petrochemicals and kerosene poisoning
Contraindications: Patients unable to protect airway or during seizures.

Question 6

When is whole bowel irrigation done and state four contraindications

Answer 6

May be particularly effective in cases of ingestion of sustained-release tablets, drugs where activated charcoal is not effective (iron, lithium)
• Contraindications: ileus, GI hemorrhage, bowel perforation.

Question 7

State three uses of hemodialysis

Answer 7

Effective for removal of certain toxins and drugs (low molecular weight, water soluble, low protein binding, and small volume of distribution).
Early use of hemodialysis (HD) is recommended for intoxication with methanol, ethylene glycol, boric acid, salicylates, and lithium.
• Effective for use in heavy metal intoxication in patients with renal failure.

Question 8

State three uses of hemoperfusion
Which things is it less effective for

Answer 8

Blood is pumped through an adsorbent system (usually a charcoal canister).
Has been effectively used for intoxications with theophylline, phenobarbital, phenytoin, carbamazepine, paraquat, and glutethimide.
• Less effective for lithium, ethanol, methanol, CO, cocaine, and phencyclidine.

Question 9

How does hemofiltration work

Answer 9

Utilizes a highly porous membrane to remove drugs and toxins by convection.
• Potentially useful for removal of toxins that have a large volume of distribution, slow intracompartmental transfer, or extensive tissue binding.
• Specific hemofiltration cartridges can be used to effectively remove digoxin-Fab complexes, deferoxamine-iron complexes, and aluminum.

Question 10

What is the toxic dose of acetaminophen or para

Answer 10

Acetaminophen is a ubiquitous analgesic-antipyretic agent that is included in over 600 commercial drug preparations.
It is also a hepatotoxin, and is the leading cause of toxic drug ingestion and acute liver failure in the United States.
toxic dose 7.5–15 grams
or 6-12grams
6g is 12 tablets of 500mg acetaminophen

Question 11

What are the four stages of acetaminophen toxicity and what is the duration for each stage
What is the most sensitive marker of acetaminophen toxicity

Answer 11

The period following acetaminophen overdose is divided into four stages of toxicity.
In the initial stage (the first 24 hours), symptoms are either absent or non-specific (e.g., nausea), and no laboratory evidence of hepatic injury exists.

Second stage (24–72 hours after drug ingestion) occurs where clinical manifestations continue to be minimal or absent, but laboratory evidence of hepatic injury begins to appear. Elevated aspartate aminotranferase (AST) is the most sensitive marker of acetaminophen toxicity; the rise of AST precedes the hepatic dysfunction.

Third stage72–96 hours. In advanced cases of hepatic injury.

Four stage (after 72–96 hours) that is characterized by clinical and laboratory evidence of progressive hepatic injury and hepatic insufficiency (e.g., encephalopathy, oagulopathy) occasionally combined with renal insufficiency. Death from hepatic injury usually occurs within 3 to 5 days. Patients who survive often recover completely, although recovery can be prolonged.

Question 12

What is the antidote for para
If this common antidote isn’t there, what else can you give?

Answer 12

IV N acetyl cysteine

Oral methionine

Question 13

What occurs in benzodiazepine toxicity

Answer 13

Clinical Toxicity: Benzodiazepines produce a dose-dependent depression in the level of consciousness, but there is usually no respiratory or cardiovascular depression. However, there are several factors that predispose to respiratory and cardiovascular depression from benzodiazepines. These include advanced age of the patients, combined therapy with opioid analgesics, and drug accumulation from prolonged drug therapy.

Question 14

What is the antidote for benzodiazepine toxicity

Answer 14

Flumazenil

Flumazenil is a benzodiazepine antagonist that binds to benzodiazepine receptors in the central nervous system.
Flumazenil is given as an intravenous bolus.

Question 15

State ten signs and symptoms of beta blocker toxicity
It may take 24 hours before you see effect of beta blocker and calcium channel blocker overdose. Don’t be in a rush to discharge

Answer 15

Competitive antagonists of beta-receptors found in the heart (β1) and bronchial tree (β2).
Signs and symptoms of toxicity : Include hypotension, bradycardia, atrioventricular blocks, and congestive heart failure (CHF) with or without pulmonary edema.
Other effects include bronchospasm, hypoglycemia, hyperkalemia, lethargy, stupor, coma, and seizures.

Question 16

What is the antidote for beta blocker toxicity

Answer 16

Glucagon as antidote:
Positive inotropic and chronotropic effects mediated via increases in cyclic adenosine monophosphate (cAMP).
Bolus dose of 5–10 mg IV over 1 minute followed by maintenance infusion of 1–10 mg/h.
Cardiovascular manifestations can be treated with IV fluids, vasopressor therapy, transvenous pacing.

Question 17

State ten signs and symptoms ofcalcium channel blocker toxicity

Answer 17

Selectively inhibit calcium flux in cardiac and vascular smooth muscle.
Signs and symptoms of toxicity including hypotension (most common) generally occur within 6 hours. Other effects may include hyperglycemia, lethargy, confusion, and coma. Dizziness or lightheadedness · Weakness · Syncope · Chest pain · Palpitations · Diaphoresis · Flushing ·

At therapeutic doses, CCBs maintain selectivity to certain tissues. However, at toxic doses, CCBs lose their degree of selectivity resulting in potentially life-threatening bradycardia, hypotension, hyperglycemia, and renal insufficiency.30 Aug 2022

Question 18

What is the antidote for calcium channel blocker toxicity

Answer 18

Hypotension is managed with IV fluid.
Refractory hypotension can be treated with 1.calcium gluconate and/or 2.glucagon.

Question 19

What are the effects of barbiturates toxicity (mild to moderate toxicity then severe overdose)

Answer 19

Mild-to-moderate overdose is characterized by decreased level of consciousness, slurred speech, and ataxia.
• Higher doses cause hypothermia, hypotension, bradycardia, flaccidity, hyporeflexia, coma, and apnea.
• Severe overdose can result in the appearance of brain death with absent electroencephalogram (EEG) activity.
• Cardiovascular and respiratory depression result in a hypotensive, hypercapnic, and hypoxemic state.

Example of barbiturates is phenobarb

Question 20

What is the antidote for barbiturate toxicity

Answer 20

Supportive
No antidote available.
Urinary alkalinization by giving sodium bicarbonate (in phenobarbital overdose only) enhances elimination.
but there’s no antidote

Question 21

What is mainly responsible for methanol toxicity

Answer 21

Metabolized by alcohol dehydrogenase to formaldehyde which is subsequently converted to formic acid by aldehyde dehydrogenase. Formic acid is primarily responsible for metabolic and ocular toxicity.
Ingestion of 100 mL can be lethal with significant toxicity at serum levels of >50 mg/dL.

Question 22

What are the side effects of methanol

Answer 22

Initially: headache, inebriation, dizziness, ataxia, and confusion.
Formic acid accumulates over 6–12 hours, the anion gap increases, visual symptoms become more prominent; other complications include pancreatitis.

Question 23

What is the antidote for methanol toxicity
What is the antidote for ethylene glycol toxicity

Answer 23

Inhibition if alcohol dehydrogenase and dialytic removal is cornerstone of therapy.
Ethanol: Can be given PO or IV to maintain serum levels between 100 and 200 mg/dL.
Indications for HD include level >50 mg/dL, significant and refractory metabolic acidosis, or evidence of end-organ damage.

The antidote is ethanol.

Question 24

How do organophosphate and carbamate insecticide cause toxicity

Answer 24

Exert toxicity by inhibiting cetylcholinesterase.
Reversible (carbamates) or irreversible (organophosphates)
inhibition of acetylcholinesterase causes the accumulation of acetylcholine at parasympathetic synapses leading to the cholinergic syndrome.

Question 25

What are the side effects of organophosphate and carbamate insecticide toxicity State ten

Answer 25

Symptoms are the result of overstimulation of muscarinic, nicotinic, and CNS receptors. Muscarinic: Characterized by SLUDGE (Salivation, Lacrimation, Urination, Diarrhea, GI cramps, and Emesis). Also blurred vision, miosis, bradycardia, and wheezing Nicotinic: Muscle fasciculations and weakness; hypertension, tachycardia, paresis, paralysis, and respiratory failure. CNS: Organophosphates (not carbamates) enter the CNS and induce anxiety, confusion, seizures, psychosis, and ataxia.

Question 26

What is the antidote for organophosphate, ddt, carbamate insecticide toxicity

Answer 26

Atropine: Indicated for all symptomatic patients. Competitively blocks acetylcholine at muscarinic receptors. Initial dose is 2 mg IV (6 mg if life threatening) followed by 2 mg every 15 minutes until atropinization (mydriasis, dry mouth, increased heart rate) Pralidoxime: Initial dose is 1–2 g IV over 10–20 minutes. Continuous infusion (200–500 mg/h). you double atropine dose every 15 minutes until you achieve atropinization If pralidoxime goes beyond 2 hours it’ll cause chemical ageing It works best less than 2 hours after ingestion of chemical

Question 27

What treats insulin overdose? What treats tramadol overdose?

Answer 27

Tramadol- naloxone Insulin- glucose, glucagon, octeotide

Question 28

Rumack Mathew scale: The Rumack-Matthew nomogram (the acetaminophen toxicity nomogram or acetaminophen nomogram), is used to interpret serum acetaminophen concentrations in relation to time since ingestion, in order to assess potential hepatotoxicity. diagnosis of acetaminophen toxicity is usually confirmed through diagnostic tests, including an acetaminophen level, electrolytes, kidney function tests, amylase, lipase, liver function tests, complete blood count, and coagulation factors. Use of the scale: Rumack-Matthew nomogram Used to interpret plasma acetaminophen values to assess hepatotoxicity risk after a single, acute ingestion
 Nomogram tracking begins 4 hours after ingestion (time when acetaminophen absorption is likely to be complete) and ends 24 hours after ingestion How many antidotes are there for para :1 Child takes in 4 years old takes 10g of para. Weight is 16kg What is the toxic dose of para expected for this child? do not manifest until 24-48 hours after an acute ingestion. Therefore, to identify a patient who may be at risk of hepatoxicity, the clinician should determine the time(s) of ingestion, the quantity, and the formulation of acetaminophen ingested. Minimum toxic doses of acetaminophen for a single ingestion, posing significant risk of severe hepatotoxicity, are as follows: Adults: 7.5-10 g Children: 150 mg/kg; 200 mg/kg in healthy children aged 1-6 years The clinical course of acetaminophen toxicity generally is divided into four phases. Physical findings may vary, depending on the degree of hepatotoxicity. Phase 1 0.5-24 hours after ingestion Patients may be asymptomatic or report anorexia, nausea or vomiting, and malaise Physical examination may reveal pallor, diaphoresis, malaise, and fatigue Phase 2 18-72 h after ingestion Patients develop right upper quadrant abdominal pain, anorexia, nausea, and vomiting Right upper quadrant tenderness may be present Tachycardia and hypotension may indicate volume losses Some patients may report decreased urinary output (oliguria) Phase 3: Hepatic phase 72-96 h after ingestion Patients have continued nausea and vomiting, abdominal pain, and a tender hepatic edge Hepatic necrosis and dysfunction may manifest as jaundice, coagulopathy, hypoglycemia, and hepatic encephalopathy Acute kidney injury develops in some critically ill patients Death from multiorgan failure may occur Phase 4: Recovery phase 4 d to 3 wk after ingestion Patients who survive critical illness in phase 3 have complete resolution of symptoms and complete resolution of organ failure And check for adults Ask Ellen or charity Read paracetamol poisoning very well Mapping of genotype Classes if antihypertensives ECG basic Airway assessment is over when you Mobilize the C spine in trauma not when patient can talk. Complete chest recoil not chest recoil StAT and SAT triaging Stages of shock Appendicitis Difference between severe asthma and life threatening asthma Treatment goals in hypertensive emergency during first one hour : drop initial bp by 25percent. The goal of therapy for a hypertensive emergency is to lower the mean arterial pressure by no more than 25% within minutes to 1 hour. requires prompt par- enteral treatment with a goal of 25% reduction in mean arterial pressure (MAP) within 30–60 minutes. How will you know if there’s end organ damage 16yearl Old boy has been unwell for two days. CoMplains of fever chills and vague abdominal pain.(4/10) Today while accompanying the mum to the hospital he experienced sudden onset abdominal pain that was generalized and told his mum that everywhere in the abdomen hurts. Pain score Is 10/10. It’s acute abdomen. Because of the sudden onset. Intestinal obstruction,peritonitis,appendicitis(what kind of abdominal pain will be seen here) Put in NG tube Why you’d do which investigations for these disorders in acute abdomen: CT findings of appendicitis (Figure 9.9) include a swollen, fluid-filled appen- dix often with a calcified appendicolith or inflam- matory changes in the periappendiceal mesenteric fat. After perforation, a phlegmon or abscess may be visible. CT is also useful for determining the diagnosis (and in many cases, the clinical severity) of conditions such as renal colic, bowel obstruc- tion, bowel perforation, bowel ischemia, diverti- culitis, pancreatitis, intra-abdominal abscess and AAA. In patients with acute cholecystitis, ultrasound may detect gallstones, gallbladder wall thickening, perichole- cystic fluid or a sonographic Murphy’s sign. Ultrasound is also commonly used to make the diagnosis of acute appendicitis, particularly in children, thin adults, women of reproductive age and pregnant patients. The primary sonographic criterion of appendicitis is demonstration of a swollen, noncompressible appendix 􏰀7 mm in diameter with a target configuration Electrocardiograms (ECGs) should be considered for all patients with unexplained epigastric or abdominal pain. They are particularly essential in the evaluation of elderly patients with vague, poorly localized abdominal complaints. An acute coronary syndrome (ACS) or inferior MI can present with epigastric pain, diaphoresis and vomiting. Though a normal ECG in the setting of abdominal pain does not exclude an MI, it makes it less likely. FBC: complete blood count (CBC) is frequently ordered in patients with abdominal pain. Despite the association of an elevated white blood cell (WBC) count with many infectious and inflamma- tory processes, Urinalysis : Findings suggestive of UTI include pyuria, positive leuko- cyte esterase, positive nitrites and the presence of bacteria. However, up to 30% of patients with appendicitis may present with blood, leukocytes or even bacteria in their urine. A mild degree of pyuria may be present in elderly patients at base- line. Be wary of ascribing abdominal pain to a UTI when the clinical picture does not fit. Red blood cells (RBCs) in the urine are consistent with infec- tion, trauma, tumors and stones. The patient with acute flank pain and hematuria suggests renal colic but also may represent a leaking or ruptured AAA. LFTs: Liver function tests may be elevated in patients with biliary or hepatic disease. Serum electrolytes may be abnormal in patients with significant vomiting or diarrhea, symptoms 􏰀24 hours dura- tion, diuretic use, or a history of kidney or liver disease. Serum phosphate and serum lactate may be elevated in cases of bowel ischemia. Amylase/lipase Though a serum amylase is commonly ordered when looking for pancreatitis, it may be normal in as many as a third of patients with pancreatitis. The serum amylase may also be elevated in other conditions including peptic ulcer or liver disease, SBO, common duct stones, bowel infarction, ectopic pregnancy, ethanol intoxication and dia- betic ketoacidosis (DKA). Serum lipase has a higher sensitivity and specificity for pancreatitis than total amylase, and is therefore the most use- ful test in a patient with suspected pancreatitis. Burns : know when to refer your patient (Burn injuries that should be referred to a burn center include: Partial thickness burns greater than 10% total body surface area (TBSA). Burns that involve the face, hands, feet, genitalia, perineum, or major joints. Third degree burns in any age group.) ,or how to estimate percentage burns :rule of nines(what else can you use to estimate percentage burns-The Lund-Browder chart (only thing to remember) Progressive worsening breathlessness with fever and cough: pneumonia What you’ll see to show there’s end organ damage Pulmonary edema in emergency and none in urgency How will you diagnose someone of DKA,HHS,hypo,diabetes Difference in therapy in hypertensive emergency and hypertensive urgency Target bp dropping in both scenarios Are you dropping MAP or pressure Drop MAP What’s the formula for calculating MAP :1/3rd systolic of something Left ventricular failure from the hypertension that’s why patient is having difficulty breathing Unresponsiveness,absent carotid Pulse ,not breathing or agonal breathing or gasping breath. If patient collapses it doesn’t mean patient is in cardiac arrest Brain dies after 5 minutes Bag when there’s no carotid pulse for ten seconds How to bag: Triangle should be on nose Balloon Not supposed to be too full or too empty Make sure seal doesn’t leak ECE technique to make sure it’s fitted properly on the face or nose (airway maneuvers at the same time pressing down and making the seal )

Question 29

Antidote for cyanide poisoning

Answer 29

Hydroxocobalamin (HCO, vitamin B12) is the first-line therapy for cyanide toxicity. It functions by binding cyanide to its cobalt ion to form cyanocobalamin, which is essentially nontoxic and is cleared by the kidneys. HCO can be combined with sodium thiosulfate for accelerated detoxification.