Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Emergency Medicine > Toxicology 1 > Flashcards

Toxicology 1 Flashcards

Toxicology. Study with psychiatry deck, lots of crossover.

You may prefer our related Brainscape-certified flashcards:
Royal College: Emergency Medicine flashcards
1
Q

What are clinical effects of sympathimimetics? (10)

A
  1. CNS excitation - delirium
  2. Dysrhythmias
  3. HTN emergency
    AoD, ACS, CVA, pulmonary edema,
  4. Diaphoresis
  5. Mydriasis
  6. Tachycardia
  7. Tachypnea
  8. Hyperthermia**
  9. Rhabdomyalysis, electrolyte imbalances, renal failure
  10. intestinal infarction, mesenteric ischemia.
  11. retinal vasospasm
  12. Seizures
  13. SAH

cocaine: Inhalational barotrauma: PTX, pneumomediastinum,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

At a pharmacological level, how does cocaine work? (2)

A
  1. Local anesthetic (Na channel blockade)

2. Prevents reuptake of catecholamines (NE and DA) and serotonin from central and peripheral terminals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is speedballing?

A

Mixing of Cocaine and Heroin and injected intravenously.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is one way to distinguish cocaine intoxication with PCP? (hint eyes)

A

PCP may have multidirectional nystagmus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the general approach to management of cocaine intoxication?

A
  1. Delirium:Rapid Sedation! Benzodiazopines! 10 mg diazapam q 5 minutes. titrate to effect.
  2. Hyperthermia: Cool within 20 mins * important if duration longer - can go into DIC and organ failure
  3. Aggressive fluid resuscitation
  4. HTN: benzos, ntiroglycerin, phentolamine (alpha blocker - 1 mg q 3minutes). NO BB (unopposed alpha = worsened HTN, coronary a. vasoconstriction)
  5. Dysrthymias: Benzos, can consider CCB. Check electrolytes, may need NaHCO3! to narrow QRS
  6. Chest Pain: if STE, treat as MI.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Whats the difference between a body pack and a body stuffer?

A

Packer - carefully packs to transport drugs. If a packet breaksdown in GIT then they usually die because of the amount.

Stuffer: smaller amount ingested usu when being pursed by police.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the dose of Activated Charcol for acute cocaine ingestion (may be usu dose too)

A

1g/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What electrolyte AbN is common in MDMA abuse?

A

Hyponatremia - MDMA and its metabolites causes secretion of vasopression = incr reabs of free water.

  • Also get SIADH type syndrome.
  • Concentrated high Na urine.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In MDMA ingestion why would Normal saline or cyrstalloids worsen hyponatremia?

A

Because they will retain more free water than sodium

- If they are seizing then give hypertonic saline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the cholinergic syndrome?

A 
Sludge
Salivation
Lacrimation
Urination
Diarrhea 
GI upset
Emesis 
Miosis- constriction of pupil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the anti-cholinergic syndrome

A 
Hyperthermia
Mydraiasis - large pupils
Dry skin
Urinary retention
No bowel sounds
Hallucinations/agitations
Tachycardia 
Ileus
Red skin- vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the ddx for pinpoint pupils?

A
  1. Cholinergic syndrome (organophosphates)
  2. Opiate OD
  3. Central pontine stroke (hemorrage)
  4. Neurosyphilis apparently..
  5. Pilocarpine drops..
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What symptoms do you get with TCA OD? (early symptoms, electrolye AbN and later sx)

A
  • Early: get anticholinergic syndrome
  • Na Channel blockade (see widened QRS)
  • Block K+ efflux (get QT prolongation)
  • combined effects on various ion channels (aLOC, seizures, hypotension, wide complex tachycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is the ECG prognostic in TCA overdose?

What are ECG findings of TCA OD?

A
  • QRS duration >100ms is predictive of seizures
  • QRS duration >160 ms is predictive of ventricular dysrhythmias
  • Additional ecg findings: R ward axis shift, Interventricular conduction delay — QRS > 100 ms in lead II

Right axis deviation of the terminal QRS:
Terminal R wave > 3 mm in aVR
R/S ratio > 0.7 in aVR
- QT prolongation is less important clinically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Do serum TCA levels correlate with severity of illness?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The constellation of early anticholinergic symptoms, decr.LOC followed by seizures, wide QRS and CV collapse is highly suggestive of which OD?

A

TCA!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Management of TCA OD?

Address: Tachycardia, anticholinergic symptoms, HTN, hypoTN, Dysrythmias, Seizures, Last resort.

A
  • ABC’s intubate if needed.
  • If sinus tach only - supportive, monitor for wide QRS
  • Early Hypertension should NOT be treated
  • Hypotension: crystalloids, if refractory choose direct acting vasopressors (NE,E) NOT dopamine. Some data E better
  • NaHCO3 - only if dysrythmia or wide QRS (>100ms)
    1-2mEq/kg repeated in few minutes until narrowing of QRS. Bicarb infusion can be initiation with goal pH7.5-7.55.
  • If refractory to NaHCO3 (ventricular dysrythmia persists), then 3% hypertonic saline
  • Seizures: Lorazepam, diazepam, phenobarbitol if refractory
  • Intralipids (last resort) 1.5cc/kg 20% lipid solution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some medications that are contraindicated in TCA OD?

A
  • Antidysrhythmics (can worsen cardiac toxicity)

- Physostigmine (cases of asystole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the clinical effects of SSRI overdose? (4)

A
  • Rarely fatal, can ingest 30 times daily dose with no sx
  • GI upset
  • Mild CNS depression
  • Coma/Seizure 1-2%
  • Serotonin syndrome (14%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Of the SSRI’s which one has a higher rate of QT prolongation and seizures?

A

Citalopram

- The QTc prolongation may also be delayed for up to 13 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which electrolyte disturbance is associated with SSRIs?

A

Hyponatremia

- has been assc with SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment of SSRI overdose?

A

Support ABCs
Supportive treatment
Benzos if seizure
Magnesium if QT prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Like TCA’s what time frame of no symptoms after ingestion is safe to discharge home in SSRI or SNRI ingestion.

A

6 hours.
BUT some advocate for 13 hours if they ingest >1000mg Citalopram or escitalopram because of possible delay in QT prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

There is no serum or urine test to detect SNRIs, or SSRIs for that matter. But which SNRI is associated with a false + PCP screen?

A

Venlafaxine (Effexor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are common clinical features of Bupropion ingestion or overdose?

A
  • Sinus Tachycardia
  • Tonic clonic seizures
  • Agitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are symptoms of serotonin syndrome?

A 
'HARMED'
Hyperthermia
Autonomic instability
Rigidity (not as much as NMS)
Myoclonus (clonus more pronounced in lower extremities)
Encephalopathy
Diaphoresis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

There is a Hunter criteria for serotonin syndrome, what does it say?

A

In the setting of exposure to a known serotonin exposure the syndrome can be diagnoised by the presence of any of the following

  1. spontaneous clonus
  2. Inducible clonus and agitation or diaphoresis
  3. Ocular clonus and agitation or diaphoresis
  4. Tremor and hyper-reflexia
  5. Hypertonic with temp >38 and ocular clonus or inducible clonus

i will likely never remember this..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the onset frame of serotonin syndrome and how do you treat it? when does it typically resolve

A

Serotonin Syndrome

  • Onset: within 24 h
  • Neuromuscular findings: Hyperreactivity (tremor, clonus, reflexes)
  • Causative agents: Serotonin agents
  • Treatment: Benzos
  • Resolution: within 24 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which withdrawal syndromes are life threatening?

A

GABA withdrawal from

  1. ETOH
  2. Benzodiazepines
  3. Barbituates (phenobarbital an ex) - act on same place on GABA receptor as ETOH.

Withdrawals from SSRIs, opiods, sympathemimetics are not life threatening but uncomfortable. Require gradual taper for SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What clinical effects do benzodiazepines have by enhancing the inhibitory effects of GABA?

A
  • Sedative
  • Hypnotic
  • Anxiolytic
  • Anti-convulsant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Explain how Benzos work on GABA receptor

A
  • Benzos have specific site that it binds to on the chloride channel at the GABA receptor –>potentiates GABA
  • Leads to intracellular flux of chloride ions and hyperpolarizing the cell
  • Net effect is diminished ability of nerve cell to initiate an action potential, inhibiting neural transmission.

Leads to sedation, Hynotic effects, anxiolysis, anti-convulsant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which benzodiazepines are not metabolized in the liver?

they are water soluble, excreted by the kidney

A

LOT
Lorazepam
Oxapam
Temazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why aren’t urine tests the greatest tool for Benzodiazepines?

A

they only detect benzos that are metabolized to oxazepam glucuronide. So many will not detect Clonazepam, lorazepam, midazolam..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the general management of Benzo OD?

A

ABCs, supportive
Generally expectant
NO routine flumazenil - can precipitate seizures, and dsyrythmias. Esp in presence of TCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is Flumazenil?

A

Nonspecific competitive antagonist of benzodiazepine receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are indications for Flumazenil? (only 2)

A
  1. Isolated benzodiazepine overdose in non habituated user (ex accidental peds OD)
  2. Reversal of conscious sedation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are Absolute contraindications to Flumazenil? name 4

Name 2 relative CI

A
  1. Suspected co ingestion that lowers sz threshold (TCA, cocaine, lithium, methylxanthines, isoniazide, MAOIs).
  2. Patient taking benzo for control of seizures
  3. Concurrent sedative hypnotic withdrawal
  4. Seizure activity or myoclonus
  5. Patient with neuromuscular blockade
  6. Hypersenitivity

Relative CI

  1. Chronic Benzo use, not taking for life threatening
  2. known sz d/o not treated with benzos
  3. Head injury
  4. Panic attacks
  5. Chronic alcoholism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the 3 types of opiod receptors?

A

mu, kappa, delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the time frame that people abusing heroine and methodone start to get withdrawal symptoms? What is the typical duration of withdrawal symptoms?

A

heroine: 30 minutes
methadone:24-48 hours
Duration of symptoms for 1-2 weeks.!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why do you get miosis in opiod overdoses?

A

Stimulation of mu receptors in the Edingerwestphal nuclei of the 3rd nerve results in pin point pupils..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Why do you get the N/V s/e with opiods?

A
  • opiod induced delayed gastric emptying
  • direct stimulation of the chemoreceptor trigger zone
  • Vestibular stimulation
42
Q

During opiod withdrawal pts get N/V, diaphoreis, abdominal cramps, piloerection, yawning, lacrimation. Is it life threatening?

A

No.

ETOH and sedative/benzodiapine withdrawal are the only life threatening withdrawal syndromes.

43
Q

Which are the Dializable Betablockers?

A 
AANTS
Atenolol
Acebutolol
Nadolol
Timolol
Sotolol
44
Q

In a patient that presents with severe hypotension and bradydysrthmias what overdoses are on the ddx?

A 
Betablockers
Calcium channel blockers
Digoxin
Clonidine
Cholinergic agents (will have 'sludge' symptoms also tho)
Hypothyroid (Myxedema coma)
Shock - cardiogenic, Neurogenic 
Acute MI
Sepsis
ENdocrine disorder
Sedative hypnotic drugs
Hypothermia
Hyperkalemia
Neurogenic shock
Na Channel blockeres
Incr ICP
Sick sinus syndrome
Opiods!
45
Q

What is the treatment for betablocker overdose?

A
  1. ABC’s secure airway - careful with induction agents!
  2. IV fluids
  3. Atropine 0.5-1 mg q 2-5 minutes. max 0.04mg/kg
  4. NaHCO3 (1-2 amps) or Mg(2g IV bolus) if arrhythmia
  5. IV glucagon (5mg over 1 minute IV) - effect in 3 mins
  6. IV Calcium (1g CaCl 10%, or Ca Gluconate)
    ‘10cc of 10% calcium over 10 minutes’
  7. IV High dose insulin/glucose (1u/kg bolus then infus)
  8. Vasopressors (Epi 1mcg/min titrate MAP 60)
  9. Intralipids
  10. Dialysis for AANTS
46
Q

Which betablocker is notorious for causing seizures?

A

Propanolol - is ++ lipophilic

47
Q

Which betablocker is more likely to cause dysrythmias?

A

Propanolol and Acetbutolol (both have membrane stabilizing activity, inhibiting myocardial fast Na channels resulting in widened QRS

Sotalol blocks K channels and prolongs QT. It also has a long 1/2 life.

48
Q

What is the antidote for Sulfonylurea ingestion?

A

Can give glucagon (doesnt usu work), glucose (temporizing)

*Octreotide IV, IM, SQ
Adult: 50-150 mcg q 6 hours
Peds: 1-1.5mcg/kg q 6 hours

49
Q

Whats the difference in calcium content CaCl vs Ca gluconate?

A

CaCl- can only give thru central line, more risk of extravasation dose 1 g 10% solution. 10cc of 10% over 10 minutes.

Risk: hyperca, Hypophosphatemia.

Ca gluconate has 1/3rd Calcium as CaCl so a 10% solution need to give 3 times more (30mL/ 3 amps) to get same amount of Calcium

50
Q

Repeat card: Management of BB OD?

A

Management
1. Atropine 0.5-1mg (0.01mg/kg peds)
2. Glucagon bolus 5-10mg IV x 3 q 3-5 minutes
3. Glucagon infusion start at total dose given/hr (2-10mg/hr)
works by incr cAMP independent B receptor –> incr Ca and incr ionotropy. Zofran - glucagon causes ++ N/V,
4. High Dose insulin/Dextrose
1 unit/kg IV bolus
if glucose 11 start infusion, add dextrose
Works by incr glucose uptake in heart –> gives more NRG
5. Calcium - gives iontropy
Contraindicated in digoxin OD - stone heart risk, ?prob ok in chronic dig tox
6. Intralipids
works well esp in really sick
works by drawing out BB from toxic sites (heart etc)
Risk of fat embolism, lab error
7. Pressors
Norepi 0.1 mcg/kg/h? starting
8. Pacing
Last resort, doesnt work well
9. ECMO, intra-arterior balloon pump.

51
Q

What are the 2 types of CCB?

A

Dihydropyridines - block vasculature L-type calcium channels
- potent vasodilators, little negative effect on contractility or conduction

Non-dihydropyridines - block L-type calcium channels in myocardium (verapamil, diltiazem)
- weak vasodilator but depressive effects on cardiac conduction and contractility

52
Q

How do dihydropyridine and Non-dihydropyridines differ in presentation in context of overdose?

A

Dihydropyridines (DHP) typically present with reflex tachycardia and arterial vasodilation where the Non-DHP (verapamil, diltiazem) present with peripheral vasodilation, decr cardiac ionotropy, bradycardia

However with increasing doses the selectivity is LOST and they come in hypotensive and bradycardic, and decr contractility leading to heart failure

53
Q

In CCB overdose what is the glucose usually? how is this different than BB OD?

A

Usu hyperglycemia (more for the Non-DHP - verapamil, diltiazem) (due to inhibition of calcium mediated insulin release and myocardial uptake) where in BB OD they are more likely hypoglycemic.

54
Q

What is the Treatment for CCB OD?

A
  1. ABCDEF

If presents 1-2 hours post ingestion and no contraindicated give Activated charcoal 1g/kg or 50g and consider whole bowel irrigation even if no sx.

  1. Fluids first line for hypotension
  2. Atropine 0.5-1mg first line (3mg max)
  3. IV Calcium (CaCl (1 amp) or Cagluc (3amp) over 10 min), can give Ca infusion
  4. IV glucagon (5-10 mg IV bolus q 10 min), give zofran
    if effective give infusion
  5. High insulin/glucose 1u/kg bolus, then infusion 0.5u/kg/h
  6. Vasopressors (NE 2mcg/min)
  7. Intralipids
  8. Pacer

Last ditch: pacing (doesnt work), ECMO, intra-aortic balloon pump

55
Q

What are some complications of intralipid emulsion therapy?

A 
Hypertriglyceridemia
Fat embolism
Infection 
Hypersensitivity reaction
Lab reading error for few hours. Doesn't effect potassium
56
Q

Can you use hemodialysis in CCB OD?

A

No. Most are protein bound. not effective

57
Q

What what overdose is calcium contraindicated?

A

Digoxin toxicity due to concern for stone heart. Incr calcium will cause sustained contraction of heart - this is more for acute toxicity, it may be okay in chronic toxicity but I would avoid.

58
Q

How does digoxin work?

A

1) Blocks Na/K ATPase
- This increases intra-cellular Na
- The Na/Ca anti-porter then is not as active and more calcium accumulates in the cell
- This leads to incr inotropy and contractility

2) increases vagal tone which results in decr conduction thru SA and AV nodes

59
Q

can you clear digoxin by dialysis?

A

No, its ineffective due to the large size/molecular weight.

60
Q

Which electrolyte abnormality in acute digoxin toxicity is also a predictor or mortality?

A

Hyperkalemia.

Digoxin recall blocks the Na/K ATPase so there is an increase in extracellular K.

61
Q

In chronic digoxin toxicity which electrolyte abnromalities are of concern and more common?

A

Hypokalemia
Hypomagnesemia
HypERcalcemia

Renal dysfunction is also commonly encountered in the setting of chronic digoxin toxicity and is often what precipitates the rise in the digoxin level

62
Q

Do serum digoxin levels correlate with degree of clinical toxicity?

A

No they may not correlate with clinical manifestations of toxicity. They are still used for Fab fragment dosing tho

63
Q

How does glucagon work in CCB and BB OD?

A

activates adenylate cyclase independent of beta receptor –> incr cAMP intracellularly resulting in iontropy.

Doesnt typically work with CCB OD, more effective in BB

64
Q

In an acute unknown ingestion of digoxin how much Fab Fragment should you use?

How much digoxin does 1 vial bind?
What is the formula to calculate the amount to use?

A

10-20 vials

1 vial binds 0.5mg of digoxin

Number vials = mg ingested x 0.8(bioavailability) /0.5 (mg/vial)

65
Q

In suspected digoxin toxicity and cardiac arrest how much Fab fragment vials should u administer?

A

20 vials

66
Q

What is the ddx for drug induced hyperthermia? (5)

A
  1. Malignant hyperthermia
  2. Neuroleptic malignant syndrome
  3. Psychostimulants (cocaine)
  4. Anticholinergic toxicity
  5. Serotonin Syndrome
67
Q

Describe normal acetaminophen (tylenol) metabolism

A
  • 90% of acetaminophen is conjugated with glucuronide and sulfate into non-toxic metabolites excreted in the urine. Some of it is excreted in urine unchanged (as APAP)
  • ~5% is oxidized by the hepatic cytochrome p450 (CYP2E1) into NAPQI which is hepatotoxic. In normal circumstances NAPQI combines with glutathione (or other thiol containing compounds) to make non-toxic metabolites excreted in the urine.
  • In overdose circumstances glutathione becomes saturated and NAPQI increases and causes heptaocellular necrosis (centrolobular).
68
Q

When is peak plasma concentration of acetominophen? when is absorption complete?

A

Peak plasma concentration occurs 30-60 minutes post ingestion and complete absorption occurs at 4 hours.

69
Q

What is the treatmetn of acetaminophen or APAP overdose?

A

NAC (N-acetyl cystine)

70
Q

How does NAC work in Acetaminophen overdose? (name 2 mechanisms)

A

1) NAC serves as a glutathione precursor
2) Is a sulfur-containing glutathione substitute binding to and thereby detoxifying NAPQI and avoiding subsequent hepatotoxicity.
3) In addition, NAC may decrease NAPQI formation by enhancing acetaminophen conjugation with sulfate to nontoxic metabolites.

71
Q

In acetaminophen overdose, at what time frame does the patient experienced RUQ pain, jaundice, and rise in liver enzymes?

A

8-36 hours

72
Q

In acetaminophen overdose at what time does the risk of hepatotoxicity increase if left untreated (another way ideally when should we treat)

A

Within 6 hours post ingestion (no significant risk of heptotoxicity) ideally before 8 hours (that is when risk increases)

73
Q

Can the Rumack-Matthew treatment nomogram be used for Chronic APAP overdose?

A

No.

also, the value of serum APAP level is less. if they are symptomatic and have evidence of liver damage (AST, ALT) treat.

74
Q

What features would make someone at risk for chronic APAP toxicity?

A
  • Increased activity CYP2E1 (ETOH, drugs like isonizade, carbamazapine, phenytoin)
  • Malnourished (less glutathione stores)

There is some controversy surrounding. Elderly and cirrhosis were not shown to have an incr’d risk..

75
Q

In APAP toxicity and there is an indication to treat, PO or IV?

A
  • PO and IV are equal in effectiveness in OD presenting 8-24 hours.
  • In pts with liver failure (encephalopathy, coagulopathy) IV has been studied and decr death.
  • IV NAC h/e is assc with anaphylactoid rxns (2-6%) more than PO
  • PO NAC is nasty and alot of pts throw it up.
76
Q

How does salicyclate OD cause hyperthermia?

A

Salicyclates uncouple oxidative phosphorylation in the mitochondria leading to the generation of heat.

The cells become dependent on anerobic metabolism and which also results in the accumulation of lactate.

77
Q

What are at least 4 main cellular and systemic effects of Salicyclate OD?

A
  1. Inhibition of cyclooxygenase results in decreased synthesis of prostaglandins, prostacyclin, and thromboxanes. This contributes to platelet dysfunction and gastric mucosal injury.
  2. Stimulation of the chemoreceptor trigger zone in the medulla causes nausea and vomiting.
  3. Activation of the respiratory center of the medulla results in hyperventilation and respiratory alkalosis.
  4. Interference with cellular metabolism (eg, Krebs cycle, oxidative phosphorylation) leads to metabolic acidosis +/- hyperthermia.
  5. Hypoglycemia - they can have neuroglycopenia despite normal serum glucose levels because it effects CNS glucose..
78
Q

In respect to airway management in ASA toxicity why do you need to be careful with the decision to intubate?

A

ASA directly stimulates the respiratory centre in the medulla causing incr RR and Tidal volume resulting in a respiratory alkalosis.

This helps ‘trap’ salicyclate anions in the blood and preventing them from diffusing into tissues and CNS. With intubation cessation of such a rapid RR and Vt will lead to a respiratory acidosis, worsening acidemia and salicyclate anions become protonated to uncharged salicyclate acid worsening CNS toxicity. This can lead to death.

It is also difficult to replicate the patients RR and Vt to maintain the degree to resp alk with a ventilator.

79
Q

In ASA OD what is the management for hypotension?

A

Hypotension is usu due to fluid losses (tachypnea, emesis, fever).

  1. Give fluids
  2. Watch for signs of cerebral edema or pulmonary edema
  3. If unresponsive to fluids –>pressor (Norepi)
80
Q

ASA OD: What is a possible method for decontamination?

A

Activated charcol absorbs ASA
Its 1g/kg or 50 g PO
Give if within 2 hours ingestion
Patient must be alert, risk of aspiration. or intubated

81
Q

In ASA OD when should you give glucose?

A

Always, esp in somewhat altered, causes neuroglycopenia despite possible normal serum levels.

82
Q

In ASA OD what is the vital and mainstay treatment?

A

Alkalinization of the urine and serum with NaHCO3

83
Q

ASA OD: what is the dose sodium bicarb and what is the infusion?

A

1-2 mmol/kg IV bolus

This is followed by a sodium bicarbonate infusion of 100 to 150 mEq (or mmol) in one liter of sterile water with 5 percent dextrose.

The rate of the infusion is titrated to a urine pH of 7.5 to 8, but is usually 1.5 to 2 times the maintenance dose for intravenous fluids.
goal u/o 1-2cc/kg/hr.

Hypokalemia must be corrected or prevented for alkalinization to be effective. Monitor hourly.

84
Q

What are at least 5 indications for dialysis in ASA OD?

A
  1. Altered mental status
  2. Cerebral edema
  3. Non cardiogenic pulmonary edema – limits use of bicarb for alkinalization
  4. Fluid overload that prevents administration of fluids
  5. Levels above 7.2 mmol/L
  6. Renal failure – ASA is excreted almost exclusively by the kidneys. Mild renal impairment is a relative indication of dialysis
  7. Clinical deterioration despite aggressive and appropriate care
85
Q

What acid base disturbance accompanies ASA OD?

A

Most adults have either a

primary respiratory alkalosis or a mixed primary respiratory alkalosis-primary metabolic acidosis

86
Q

Common: tachypnea, tinnitus, nausea, vomiting, acid-base abnormalities
Severe cases: hyperthermia, altered mental status, pulmonary edema

What is the diagnosis?

A

ASA OD

87
Q

Why is azetazolamide contraindicated in ASA toxicity?

A

Acetazolamide is a carbonic anhydrase inhibitor that alkalinizes the urine by reducing bicarbonate reabsorption. While this does enhance salicylate excretion, the bicarbonate loss from plasma lowers the arterial pH, which promotes salicylate movement into the brain, potentially worsening salicylate neurotoxicity

88
Q

What are the 4 main pharmacological properties of TCAs that make them toxic?

A
  1. Inhibition of norepinephrine reuptake at
    nerve terminals.
  2. Direct alpha adrenergic block.
  3. A membrane stabilising or quinidine-like
    effect on the myocardium. - Na channel blockade at myocardium and conducting tissue
    - delays propagation and depolarization = widened QRS
  4. Anticholinergic action
89
Q

A patient is exposed to an inhaled toxin of chlorine or hydrogen chloride gas, what can be used for symptomatic relief?

A
  1. Nebulized 2% Na bicarbonate
90
Q

A patient has had smoke inhalation from a fire and has a lactate over 10 mmol/L, what condition are you most concerned about?

A

The patient has a metabolic lactic acidosis. Cyanide toxicity is highly likely.

91
Q

What toxin has been described to have the odor of bitter almonds?

A

Hydrogen Cyanide.

92
Q

What toxin has been described to have the odor of rotten eggs?

A

Hydrogen Sulfide.

- Been used for suicide, classic case of rescue workers trying to save person and ends up dead.

93
Q

What is the pathophysiology of Hydrogen cyanide toxicity?

A
  • CN is absorbed systemically and inhibits oxidative metabolism by binding to complex IV on the electron transport chain in mitochondria.
  • The tissue depletes its ATP reserves and the cell can no longer function.
  • Cell switches to anerobic metabolism producing lactate but substrates run out.
  • Metabolic acidosis results
  • Tissue hypoxia and cellular death results
94
Q

What is the pathophysiology of Hydrogen Sulfide toxicity

A

Is exactly the same as CN

  • it is absorbed systemically
  • Binds complex 4 of the electron transport chain ceasing cellular metabolism
  • Tissue quickly depletes its ATP stores and cannot make more so dies.
  • Only difference is that hydrogen sulfide can spontaneously dissociate from the complex IV and patients can survive after a brief exposure

Patients with hydrogen sulfide poisoning generally respond to removal from exposure and ventilatory support.

95
Q

What is the treatment for Cyanide Toxicity?

A

The Cyanide kit. Provide source of Fe3+ for cyanide to bind to

  1. Amyl Nitrate (inhaled, use only if no IV)
  2. Sodium Nitrite (IV solution, can cause hypotension)
    - Both induce methemoglobiemia - CN has a higher affinity for this forming cyanmethemoglobin
  3. Sodium Thiosulfate - allows conversion of cyanide and cyanmethemoglobin into thiocyante which is renally excreated
  4. Hydroxocobalamin - colbalt has high affinity for CN. binding CN forms cyanocobalamin or Vitamin B12
    (this messes with blood tests requiring spectrophotometry)
  5. Hyperbaric oxygen has no proven benefit and is not routinely indicated in CN tox unless CO as well. but potential benefit is ability to superoxygenate thus permitting higher levels of methemoglobinemia
96
Q

What is an contraindication for Amyl Nitrate or Sodium Nitrite?

A

If suspected CO poisoning. as methemoglobinemia causes tissue hypoxia as well and these treatments would worsen this.
- In case of CN and CO give sodium thiosulfate and hydroxocobalamin

97
Q

Describe the Mechanisms/pathophysiology of CO poisoning? (2)

A
  1. CO binding to Hb to create carboxyHb leading to tissue hypoxia
  2. CO, like CN inhibits complex IV of the electron transport chain involved in mitochondrial oxidative phosphorylation. Halts ATP production, anerobic cellular metabolism only occurs for so long but results in cellular death.
98
Q

What is the half life of COHb? (carboxyhemoglobin)

A

5 hours on room air
1 hour on 100% FiO2
Hyperbaric O2 reduces 1/2 life to 30 minutes

99
Q

What is the indication of Hyperbaric Oxygenation?

A
  • Asymptomatic patient >25% COHb
  • Pregnant patient COHb>15% (prevent fetal hypoxia)
  • The primary indication for HBO is not to prevent mortality but rather to prevent delayed neurologic sequelae.
  • there is controversy with HBO because the effect is not immediate
  • HBO can decrease delayed neurologic sequelae from 12% to <1%
100
Q

A fire victim arrives in the Emergency department, aside from burn injuries what are 2 other life threatening conditions that can be present?

A
  1. Trauma

2. Cyanide and/ or Carbon monoxide Toxicity.

101
Q

What is the progression of acid-base status in ASA toxicity?

A
  1. Metabolic alkalosis secondary to N/V (triggers chemoreceptor zone in medulla)
  2. Respiratory alkalosis – due to trigger in resp. centre in medulla
  3. Metabolic acidosis – interferes with oxidative phosphorylation - incr. lactate, etc
  4. Respiratory acidosis as pt becomes more obtunded..

Emergency Medicine (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions