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ER 1 > Pharm - Salicylate and TCA OD Tx > Flashcards

Pharm - Salicylate and TCA OD Tx Flashcards

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1
Q

Clinical features of acute salicylate OD

A
  • onset of sx: 1-2 hrs after acute ingestion
  • vital signs: increased RR and depth, increased body temperature, tachycardia
  • tinnitus: very common even at therapeutic concentrations
  • n/v
  • acid base abnormalities
  • altered mental status: agitation, confusion, restlessness, seizures
  • pulmonary edema
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2
Q

pathophysiology of the vital sign changes in a salicylate overdose

A

Increased repiratory rate and depth
• Salicylates stimulate respiratory center in the medulla
• Pts become tachypnic and hyperventilate

Increased body temp
• Salicylates uncouple mitochondrial oxidative phosphorylation
• Heat generated – body temp increases

Increased HR – tachycardia
• May be d/t agitation, distress, hypovolemia

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3
Q

pathophysiology of n/v in a salicylate overdose

A

o Direct irritation of the gastric mucosa
o Decreased production of prostaglandins
o Direct stimulation of the chemoreceptor trigger zone in the medulla
o Vomiting can be severe and lead to volume loss
o Hemorrhagic gastritis, though uncommon, can also occur

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4
Q

pathophysiology of acid-base abnormality in a salicylate overdose

A

o Increased respiration can lead to decrease in PaCO2 leading to a respiratory alkalosis
o Anion gap metabolic acidosis occurs d/t accumulation of organic acids

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5
Q

pathophysiology of altered mental status in a salicylate overdose

A
  • Direct toxicity to the CNS:
    • Salicylic acid is a weak acid
    • Exists as charged and uncharged forms
    • Uncharged form can enter the CNS
    • The acidosis increases the uncharged form
  • Neuroglycopenia: salicylates lower CNS glucose concentrations (can occur even if serum glucose concentration is nl)
  • Cerebral edema
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6
Q

early symptoms associated with a salicylate overdose

A

i. Tinnitus
ii. Vertigo
iii. N/v/d

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7
Q

late symptoms associated with a salicylate overdose

A

i. Altered mental status
ii. Increased temp
iii. Pulmonary edema
iv. Coma

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8
Q

serum salicylate concentration associated with toxicity

A
  • Values above 40 mg/dL associated w/ toxicity
  • Measure every 2 hrs until 2 consecutive levels show a decline from the peak concentration also monitoring other sx and RR
  • Levels above 100 mg/dL are an absolute indication for hemodialysis
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9
Q

lab values and imaging studies that should be obtained in a salicylate overdose

A
  • creatinine
  • K
  • coag studies
  • lactate
  • anion gap
  • imaging: CXR; head CT
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10
Q

Creatinine in salicylate OD

A
  • ASA is eliminated by kidneys so check to assess rnal statue
  • Renal failure is an indication for hemodialysis
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11
Q

K in salicylate OD

A
  • If hypokalemic, tx aggressively
  • In metabolic acidosis, K moves from intra to extracellular space and is removed by the kidneys so: a low serum K in light of a metabolic acidosis represents a significant reduction in total body K
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12
Q

Coag studies in salicylate OD

A
  • Large salicylate OD can cause hepatoxicity, interfere w/ vit. K metabolism and cause a coagulopathy
  • May see increase in PT
  • Clinically significant bleeding is unusual
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13
Q

lactate in salicylate OD

A
  • Uncoupling of oxidative metabolism lead to increase in anaerobic metabolism
  • Lactate accumulates
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14
Q

anion gap in salicylate OD

A

usu elevated

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15
Q

imaging in salicylate OD

A
  • CXR – pulmonary edema

- Head CT – altered mental status not contributable to noncerebral causes

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16
Q

role of activated charcoal in a salicylate overdose

A

GI decontamination w/ activated charcoal – some experts recommend multi-dose activated charcoal for management after ABCs

17
Q

State the reasons for administering supplemental glucose in a salicylate overdose

A
  • Administer supplemental glucose if patient has altered mental status even if serum glucose is WNL
  • Salicylates decrease glucose concentrations in the brain
18
Q

State the reasons for alkalinizing the serum in a salicylate overdose

A
  • Salicylic acid (HSal) is a weak acid
  • Increasing the serum pH by adding sodium bicarbonate moves the equation to the left
  • Higher serum pH will cause plasma levels to fall which will cause [ HSal] to fall in the CNS as salicylate moves from brain to plasma. This will decrease the toxic effects of salicylate on the brain

H+ + Sal- HSal

19
Q

State the reasons for alkalinizing the urine in a salicylate overdose

A
  • Moves the equation to the left
  • Urinary HSal is converted to Sal- preventing back diffusion of HSal, trapping it in the urine and enhancing elimination
20
Q

indications for hemodialysis in a salicylate overdose

A
  • Altered mental status
  • Pulmonary edema
  • c. Cerebral edema
  • Serum creatinine 2 mg/dL or GFR < 45 mL/min
  • Inability to administer sodium bicarb
  • Markedly elevated serum salicylate levels (depend on renal function) > 100 but can use dialysis at lower levels
  • Severe academia pH < or = to 7.2
  • Pt continues to deteriorate clinically despite supportive care
21
Q

pharmacologic effects of tricyclic antidepressants in an overdose

A
  • Blockage of cardiac fast sodium channels
  • Antagonism of:
    1. Central and peripheral muscarinic Ach receptors
    2. Alpha-1 adrenergic receptors
    3. H1 receptors
    4. CNS GABA A receptors
  • And therefore:
    1. Delayed absorption d/t anticholinergic effects
    2. Bioavailability may be increased
    3. Decreased rate of metabolism
    4. Increased amount of free drug
    5. Delayed excretion
22
Q

Identify the cardiac toxicity associated with a TCA overdose

A
  • Conduction abnormalities d/t inhibition of fast Na channels in the His-Purkinje system and myocardium
  • Conduction velocity decreases, duration of repolarization increases, and absolute refractory period increases
  • Ventricular tachycardia and v. fib – more common in severe poisonings and when there is extreme QRS prolongation
  • Hypotension: decreased contractility and peripheral hypotension d/t blockade of alpha 1 adrenergic receptor; can be refractory and a cause of mortality
  • Sinus tachycardia: anticholinergic effect and compensatory mechanism d/t peripheral hypotension
23
Q

Identify the CNS toxicity associated with a TCA overdose

A

i. Decreased level of consciousness (antihistamine properties)
ii. Delirium (anticholinergic)
iii. Seizures (GABA-A antagonism) – can be associated w/ arrhythmias and/or hypotension

24
Q

Identify the anticholinergic effects associated with a TCA overdose

A

i. Elevated temp
ii. Flushing
iii. Dilated pupils
iv. Delirium
v. Intestinal ileum
vi. Urinary retention

25
Q

Identify EKG changes associated with cardiotoxicity due to TCA overdose

A
  • Arrhythmias are common and can develop quickly
  • Signs of cardiotoxicity:
    QRS prolongation > 100 ms
    Most prominent ECG manifestation
    Increases risk of seizures and/or ventricular arrhythmia
  • Indication for bicarb treatment
    1. Abnl morphology of the QRS (deep, slurred S waves in lead I and AVL): associated w/ an increased risk of seizures and/or ventricular arrhythmia
    2. Abnl size and ratio of the R and S wave in lead AVR
26
Q

indications for sodium bicarbonate in a TCA OD

A
  • Sodium bicarb is the standard initial therapy for hypotension or arrhythmia d/t TCA toxicity
  • Indicated in pts w/ TCA poisoning who develop widening of QRS interval > 100 ms or a ventricular arrhythmia
27
Q

the expected response to sodium bicarb in a TCA overdose

A
  • QRS narrows

- Decrease in R wave

28
Q

What is used to treated seizure secondary to TCA overdose

A

-Benzos: IV diazepam or lorazepam

29
Q

interventions used to treated hypotension refractory to traditional treatments in a TCA overdose

A
  • Vasopressors: indicated when BP doesn’t respond to sodium bicarb. Use IV NE or phenylephrine to counteract alpha adrenergic antagonist effect
  • Hypertonic saline (3%): Used when pt has be unresponsive to other interventions to increase blood pressure

ER 1 (18 decks)

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