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Pharmacology > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Which drug is one of the more common causes of intentional oversdose because of accessibility?

A

Tylenol

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2
Q

Which drug can lead to acute hepatic failure that needs immediate intervention in an overdose?

A

Tylenol

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3
Q

What is the lethal dose of Tylenol?

A

10 g when acutely ingested

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4
Q

How long does it take for acute hepatic failure to take place in a Tylenol OD?

A

A day or 2

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5
Q

What is the maximum daily recommended dose of Tylenol?

A

3000mg

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6
Q

Tylenol metabolism (OD) in the body and how is this dangerous?

A

90% of the drug gets inactivated and a small percentage gets converted into NAPQI, which is a toxic metabolite that affects the liver.
When you take large amounts of it, your body can’t break it down anymore and you start to accumulate it, which leads to liver failure

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7
Q

What is responsible for APAP (Tylenol) metabolism that prevents toxic acuumulation of NAPQI?

A

Glutathione, this is hepatoprotective

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8
Q

Reasons you can get hepatic depletion of glutathione?

A

Chronic ETOH, APAP use or cirrhosis

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9
Q

How might a chronic APAP use present vs actue?

A

Chronic is more often asymptomatic and may present as a “viral syndrome”

Acute usually starts with emesis with possibly RUQ pain within 48-96 hrs, and can present as hypotensive, encephalopathy, elevations of AST/ALT and coagulopathies

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10
Q

How might labs present in chronic APAP use?

A

could be high-normal, but are mostly normal

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11
Q

What are good liver markers to check for in the lab?

A

AST/ALT, INR, Alkaline phosphatase

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12
Q

What do salicylate levels indicate?

A

ASA use

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13
Q

With acute APAP toxicity, what is a good lab work up?

A

CMP, Acetaminophen level, salicylate level, ETOH level, INR/PT

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14
Q

The Rumack-Matthew Nomogram is used for what?

A

Acute ingestion of alcohol

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15
Q

When can you get a Acetaminophen level?

A

Starting 4 hrs post ingestion

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16
Q

What’s makes diagnoses difficult with overdoses?

A

Many drugs or drug combos are often used

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17
Q

What is the treatment for APAP OD?

A

NAC (N-Acetylcysteine, Acetadote)

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18
Q

What does NAC do?

A

Replenishes glutathiones stores, which helps metabolize NAPQI

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19
Q

Which administration method is prefered for NAC? Why?

A

IV, because PO smells like rotten eggs

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20
Q

What can we give for massive APAP ODs?

A

Hemodialysis

And if it’s within an hour since ingestion, activated charcoal (but it’s not often well tolerated)

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21
Q

APAP OD can also cause what?

A

Cerebral edema, seizures

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22
Q

ASA toxicity can caue you to what?

A

Bleed

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23
Q

Early S/S for ASA OD? (like 1-2 hrs) Which is often the biggest clue for dx?

A

Tinnitus, vertigo, N/V/D, tachypnea

**Tachypnea

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24
Q

What happens, pathophysiologically, in an ASA OD?

A

You ingest a lot of acid, your body compensates via becomine tachypneic to raise CO2 levels. The patient first undergoes respiratory alkalosis. Then, the pH starts to rise and bicarb drops, becoming metabolic acidosis

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25
Q

Fever can occur in which kind of OD?

A

ASA

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26
Q

What ultimately causes the metabolic acidosis disturbance in ASA OD?

A

Anion-gap

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27
Q

The acidity of the metabolic acidosis via ASA OD can cause what?

A

AMS, CV collapse, death

28
Q

Labs for ASA OD?

A

CMP, Lactate, coag panels, Salicylate level, APAP level, ETOH level

29
Q

ASA Treatment?

A

If within 1-2 hrs of ingestion, you can do activated charcoal

Aggressive volume resuscitation, urine alkalinization (sodium bicarb IV bolus and infusion to increase ASA excretion), hemodialysis

30
Q

Which 2 drugs present similarly in OD?

A

CCB and BB

31
Q

Which CCBs cause more AV nodal blockades?

A

Non-DHP

32
Q

AV nodal action can cause what?

A

profound hypotension and bradycardia

33
Q

DHPs can present with what?

A

Profound hypotension (due to peripheral vasodilation) WITHOUT direct myocardial effects

34
Q

In what case could the DHP CCB and the Non-DHP CCB present similar in their OD?

A

With large OD

35
Q

Which meds have a long half life that can make OD treatment difficult?

A

CCB (24 hrs, which means it would take 4-5 days to get out of your system)

36
Q

Main difference in the OD presenting symptoms of CCBs and BBs?

A

HYPERglycemia in CCBs
HYPOglycemia in BBs

CCBs prevent beta islet cells from insulin release
AMS is more common in BBs

37
Q

Presenting symptoms in Non-DHP CCB OD?

A

Hypotension, Bradycardia, CHF symptoms

38
Q

Lab tests for CCB OD

A

EKG, CMP, Glucose, APAP, Salicylate, ETOH levels

39
Q

Treatment for CCB OD?

A

Atropine (for the bradycardic symptoms)

Usually we’ll have to do more, so we add:

IV calcium (helps antagone effects of CCB, but doesn’t alter intracellular dysfunction of calcium)

IV glucagon (assist more with HR) premedicate with anti-emetics for this, though

IV insulin (HIGH dose, 10xs more than what we use for DKA) to help with vasopression and overcome insulin resistance in CCB OD

IV Vasopressors (epinephrine, vasopressin, norepiniphrine)

40
Q

Fun fact? What can you also use to induce vomiting in people who have food stuck in their throat?

A

IV glucagon

41
Q

What do Beta 1 receptors do?

A

They increase RH and contractility

42
Q

What do Beta 2 receptors do?

A

Vasodilation and bronchodilation

43
Q

How long do you see PK changes in BB OD?

A

2-8 hrs

44
Q

Which Beta blockers can cause ventricular arrhythmias?

A

Sotalol, Acebutolol, propranolol

45
Q

Which beta blocker is lipophilic and can easily cross the BBB? What are its side effects?

A

Propranolol

SE: increased CNS SE, seizures

46
Q

Which Beta blockers block alpha receptors?

A

Carvedilol, labetalol

47
Q

Treatment for BB OD?

A

IV atropine, glucagon, insulin with dextrose (watch out for hypoglycemia, need more dextrose infusions), calcium, vasopressors, bensodiazepines, lipids (indicated for refractory seizure, CV collapse due to propranolol OD)

48
Q

What happens in serotonin syndrome?

A

overstimulation of serotonergic receptors in the CNS and periphery

49
Q

What does serotonin do?

A

attention, behavior, thermoregulation

50
Q

What age groups has serotonin syndrome been documented in?

A

All age groups

51
Q

How can serotonin syndrome be diagnosed?

A

NOT by labs, it’s a dx of exclusion

Hunter criteria is used when pt has taken a serotonergic product and has one of:

spontaneous clonus, inducible clonus and agitation/diaphoresis, ocular clonus and agitation/diaphoresis, tremor and hyperreflexia, hyperonia, temp over 100.4F and ocular/inducible clonus

52
Q

Differential dx for serotonin syndrome?

A

MH and NMS, and anticholinergic toxicity

53
Q

What can cause serotonin syndrome?

A

Analgesics (codeine, fentanyl, meperidine, tramadol)
Antibiotics (linezolid)
Antidepressants (SSRIs, SNRIs, TCAs, MAOIs)
Triptans
Herbals (St. John’s Wort, Panax ginseng, tryptophan)
Illicit drugs (Amphetamines, cocaine, ecstasy, LSD)
Dextromethorphan, lithium, methylene blue

54
Q

How do you treate serotonin syndrome?

A

Stop offending agents, stabilize vitals, benzos for agitation

+ cyproheptadine (12 mg inititally PO then 2mg q2hrs until clinical response)

+esmolol/nitroprusside for severe HTN; sedation and paralysis with non-depolarizing agent with intubation

55
Q

What antihistamine has anti-serotonergic activity that is used to treat serotonin syndrome?

A

Cyproheptadine

56
Q

Indications for cyproheptadine?

A

serotonin syndrome, appetite stimulation, spinal cord injury (spasticity)

57
Q

S/S Neuroleptic malignant syndrome

A

AMS (most often the first sign), rigidity, fever, autonomic instability

58
Q

Lab results on NMS

A 
SCK >1000
Leukocytosis
mild elevations in LDH, AlkPhos, AST/ALT
Electrolytes - HypoCa, HypoMg, *HyperK, metabolic acidosis
Elevated SCr (rhabdomyolysis)

*most concerning

59
Q

What drugs can cause NMS?

A

Often with haloperidol, fluphenazine (but really any antipsychotic), metoclopramide, promethazine, withdrawal of carbidopa/levodopa

60
Q

treatment for NMS

A

stop drugs, cooling blankets, anticoagulation, ABCs, fluids

61
Q

Drug of choice for MH?

A

Dantrolene (Ryanodex)

62
Q

What is the mechanism from dantrolene?

A

direct-acting skeletal muscle relaxant that inhibits ryanodine receptors to prevent Ca2+ release from sarcoplasmic reticulum

Reduces temp and muscle rigidity

63
Q

Dantrolene use

A

Max of 10 day therapy (but usually stopped within a couple of days)

64
Q

SE for dantrolene

A

hepatotoxicity

65
Q

What is MH?

A

genetically-linked hypermetabolic state that is life-threatening; usually occurs in those who have taken halothane, isoflurane, enflurane, sevoflurane, or succinylcholine

66
Q

S/S of MH

A

rise in end-tidal CO2 despite increase in minute ventilation, muscle rigidity? (pts are usually sedated, so hard to know), hypertermia (late-stage), sinus tachycardia

67
Q

Post crisis protocol for MH?

A

Dantrolene 1mg/kg q4-6 hrs

OR 0.25mg/kg/hr continusou infustion for at least 24 hrs

Pharmacology (6 decks)

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