Toxicology-final Flashcards

1
Q

What are the normals you should assess in an adult pt?

A

Blood Pressure (90-140/90-50mmHg), Pulse (60-100 beats/min), Respiratory Rate (8-14 breaths/min), Temperature (98-100.4 F)

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2
Q

What drugs cause mydriasis?

A

Adrenergic agonists

Anticholinergics

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3
Q

What drugs cause miosis?

A

Sympatholytics

Cholinergics

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4
Q

What hx should you get when assessing a poisoned pt?

A

Substance ingested, amount ingested, time since ingestion, symptoms, prior therapies, prior medical conditions

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5
Q

What poisons have antidotes?

A

APAP, carboxyhemoglobin, methemoglobin, digoxin, heavy metals, iron

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6
Q

What qualitative labs are run to assess poisoning?

A
Urinary Toxicology Screen
        •Test for presence of toxin in urine 
        •Expressed as present or absent
         •Many false positives
Radiograph for radioopaque compounds
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7
Q

What are management strategies for poisoning?

A
  • Supportive Care
  • Prevent Further Absorption
  • Enhance Elimination
  • Provide Antidote
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8
Q

What is the supportive care?

A

•Stabilize the Patient
ABC’s, Altered mental status •Monitor for complications as they arise
Assess and treat for shock

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9
Q

What is hypovolemia shock and what is used to tx it?

A
  • Loss of fluid, Decreased CO due to decreased preload

* Fluids, inotropes/vasopressors

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10
Q

What is cardiogenic shock and what can cause it?

A

Decreased CO due to decreased stroke volume, typically due to a decrease in myocardial contractility
iron, CCB, BB, Cyclic antidepressants

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11
Q

What is distributed shock?

A

Redistribution of blood from central compartment to peripheral vasculature

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12
Q

How can you prevent further absorption depending on the route?

A

Inhalation: Fresh air, oxygen
Dermal: Irrigation with water, Removal of contaminated clothing
Ocular: Eye irrigation
Ingestion: Emetic, lavage, activated charcoal, WBI

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13
Q

What is the benefit of GI decontamination?

A

Evidence shows gastrointestinal decontamination reduces poison bioavailabilty
Also shows NO evidence of improvement in morbidity or mortality

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14
Q

What are the general indications for GI contamination?

A

Substantial risk of serious toxicity
Recent ingestion
Can be performed safely and will work
No alternative is available

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15
Q

What are general contraindications to GI contamination?

A

Rapid onset of seizures
Rapid onset of CNS depression
Alkaline corrosives (acids controversial)
Loss of gag reflex

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16
Q

What are the general indications and CI for emesis?

A

The same at GI contamination

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17
Q

When is emesis typically used in tox?

A

Typically used in rural settings where there will be a delay of > 1 hour before patient will arrive to ER

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18
Q

What is the emesis used?

A

Syrup of Ipecac

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19
Q

What is the onset of syrup of ipecac?

A

15-20 min

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20
Q

What are the side effects of ipecac?

A
  • Acute: Diarrhea, Drowsiness

* Chronic: Cardiac arrhythmias, neuropathy, muscle weakness

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21
Q

What is lavage?

A

Orogastric retrieval of a substance

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22
Q

What are CI to lavage?

A

Same as the above ones except….
Can lavage patients with CNS Depression if intubated and cuffed with endotracheal tray.
If seizures are controlled and patient is intubated
DO NOT lavage patients with underlying pathology of esophagus or stomach

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23
Q

What are the ADRs of lavaging?

A

Aspiration, esophageal/gastric bruising, fluid/electrolyte imbalance, EKG changes, hypoxia, esophageal rupture

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24
Q

What is the dosing for absorbents charcoal?

A

1gm/kg

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25
Q

What will charcoal not bind to?

A

Low molecular weight, charged compounds; cyanide, bromide, potassium, ethanol, methanol, iron, lithium, alkaline corrosives, mineral acids
Highly concentrated solutions; gasoline, kerosene, alcohols

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26
Q

What do carthartics do?

A

Promote movement of AC bound drug through GI tract

May cause hypovolemia and electrolyte imbalance

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27
Q

What are ADRs of activated charcoal?

A

Vomiting, constipation, aspiration, GI obstruction, charcoal empyema, GI perforation

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28
Q

What is whole bowel irrigation reserved for?

A
Substances not adsorbed to AC
Very large ingestions
Significant GI hemorrhage
Intestinal obstruction
Unprotected airway
Hemodynamic instability
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29
Q

What is he endpoint of whole bowel irrigation?

A

clearing of rectal effluent

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30
Q

What solution is most commonly used for whole bowel irrigation?

A

Golytely

31
Q

When are enhancing elimination indicated?

A

Impaired normal route of elimination
Severe presentation
Progressive deterioration despite full supportive care
Significant toxicity expected

32
Q

What are the methods for enhancing elimination?

A
Multiple Dose Activated Charcoal
Ion trapping
Hemodialysis
Forced Diuresis
Exchange transfusions
33
Q

What does multiple dose activated charcoal do?

A

Interrupts entero-enteric and entero-hepatic recirculation of poison and or poison metabolite

34
Q

What are the indications for multiple dose activated charcoal?

A

Theophylline, carbamazepine, phenobarbital overdose

35
Q

What are CI of multiple dose activated charcoal?

A

Ileus, intestinal obstruction, unprotected airway

36
Q

What are the ADRs of multiple dose activated charcoal?

A

Pulmonary aspiration, constipation, fluid and electrolyte imbalance

37
Q

What is ion trapping?

A

Change pH of urine to ionize poison preventing reabsorption

38
Q

What weak acid can be given in ion trapping?

A

sodium bicarb to achieve a urine pH of > 7

39
Q

What are the properties of a good antidote?

A

Completely reverses or neutralizes the effects of the poison
No action of its own
Easy to administer
No unpleasant side effects

40
Q

What chelator can be used for As, Hg, Pb, and Cd and has HTN and tachycardia as a result of toxicities?

A

Dimercaprol

41
Q

What chelator can be used for Cu, Pb, Hg, and As and has allergic rxn toxicity?

A

Penicillamine

42
Q

What chelator is used for PS, As, and Hg and has gas and abdominal pain as toxicity?

A

DMSA ( succimer)

43
Q

What chelator is used for Pb and has nephrottoxicity?

A

Edetate calium disodium ( EDTA)

44
Q

What chelator is used for Fe and has Hypotension, anaphylactoid rxn, and ARDS?

A

Deferoxamine

45
Q

What agent is used for rattlesnake envenomation?

A

Crotalidae antivenin

46
Q

What agent is used for black widow spider envenomation?

A

Lactrodectus antivenin

47
Q

What agent is used for eastern and texas coral snake envenomation?

A

Elapidae antivenin

48
Q

What agent is used for botulism types A, B, and E?

A

Trivalent botulinum

49
Q

What agent is used for digoxin and digitoxin?

A

Digoxin immune fab

50
Q

What agent is used for acetaminphen poisoning and what is the mechanism?

A

N-acetylcysteine and is prevents NAPQI binding at hepatocyte

51
Q

What agent Is used for opioids and what is the MOA?

A

Naloxone, an it is an opioid receptor antagonist

52
Q

What agent is used for benzo poisoning and what is the MOA?

A

Flumazenil and benzo receptor antagonist

53
Q

What is the agent for organophosphate and pesticide poisoning?

A

Atropine-muscarinic receptor antagonist

54
Q

What is the agent for methanol and ethylene glycol poisoning and what is the MOA?

A

Fomepizole and blocks metabolite formation

55
Q

What are the 4 ADR categories?

A

1) ADR’s resulting from drug binding to intended receptor but at inappropriate concentration, with suboptimal kinetics, or in incorrect tissue
2) ADR’s resulting from drug binding to a target or receptor not intended
3) ADR’s mediated by the immune system
4) Idiosyncratic responses (mech is unknown)

56
Q

What is type I hypersensitivity rxn?

A

Immediate hypersensitivity; results from production of IgE after exposure to an antigen
Antigen may be a foreign protein or an endogenous protein modified by a hapten to become immunogenic

57
Q

What is type II hypersensitivity rxn?

A

Antibody-dependent cytotoxic hypersensitivity

Occurs when a drug binds to cells and is then recognized by immune system usually IgG

58
Q

What are type III hypersensitivity rxn?

A

Immune-complex mediated hypersensitivity
Antibodies formed against soluble antigens
Antigen-antibody complex deposited in tissues initiating serum sickness (inflammatory response in tissues)

59
Q

What are type IV hypersensitivity rxn?

A

Delayed-type hypersensitivity

Activation of cytotoxic T-cells

60
Q

What drugs can initiate autoimmune rxn?

A

Methyldopa
-Hemolytic anemia
Hydralazine, Isoniazid, Procainamide
-Lupus Like syndrome

61
Q

What skin rashed can be caused by meds?

A

Stevens-Johnson syndrome

Reported with barbituates, sulfonamides, phenytoin, carbamazepine, allopurinal, NSAID’s, Penicillins

62
Q

What do cytotoxic agents do?

A

damage proliferating normal cells

Cytotoxic to WBC –increased risk of infection

63
Q

What therapies target specific cells and are associated with increased risk of infection?

A

Immunotherapy

64
Q

What is the most frequent reason for drug withdrawals?

A

Hepatotoxicity

65
Q

What are many cases of fulminant hepatitis caused by?

A

Idiosyncratic

66
Q

What is an example of a metabolite that can cause liver damage?

A

Acetaminophen oxidation to N-acetyl-p-benzoquinoneimine ..results in hepatotoxicity

67
Q

What might renal toxicity manifest as?

A

Alterations in renal hemodynamics, tubular damage and obstruction, glomerular nephropathy, and interstitial nephritis

68
Q

What drugs lead to progressive renal failure ( or contribute to)?

A

NSAID’s, ACEI, some antibiotics, antineoplastic agents, immunomodulators

Gentamicin- renal tubular injury reversible upon cessation

Amphotericin B- High frequency of injury because mechanism for efficacy is shared by the mechanism responsible for toxicity

Contrast-Media- Dose related nephrotoxicity

69
Q

What are the 3 major mechanisms of cardiovascular toxicity?

A

Drug interacts with cardiac potassium channels to cause QTc prolongation, delayed repolarization, and cardiac arrythmia

70
Q

What is directly cytotoxic to myocytes?

A

Doxorubicin leads to production of reactive oxygen species

71
Q

What drugs cause pulmonary toxicity?

A

Bleomycin and amiodarone

72
Q

What are teratogens?

A

Substance that can induce defects in the developing fetus

73
Q

What are specific time frames that relate to teratogenicity?

A

Prior to week 3 usually result in death to embryo
Week 3-8 organogenesis occurs so very profound effects on developing organs
After organogenesis drugs may affect growth and maturation of organ but not the developmental plan

74
Q

What are tx for drug toxicity?

A

Reduce or eliminate exposure to drug
Provide supportive measures
Provide an antidote