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PMHNP > Serotonin Syndrome > Flashcards

Serotonin Syndrome Flashcards

1
Q

Serotonin Syndrome incidence and epidemiology

A

incidence unknown due to lack of data

some evidence for mild cases being self limiting

Occurs across all age groups

Of those overdosing on SSRI, SS is in 15% of those cases

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2
Q

Serotonin Syndrome Symptomatology triad

A
  • Altered mental status

Maybe presenting as anxiety, agitation, confusion

  • Neuromuscular abnormalities

Muscle rigidity, hyperkinesis, hyper reflexivity

  • Autonomic hyperactivity

Diaphoresis, tachycardia, HTN, N/V/D

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3
Q

Serotonin Syndrome clinical findings spectrum

A

Akathisia to hyperthermia

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4
Q

most common ddx (2)

A

anticholinergic toxicity

malignant hyperthermia

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5
Q

Serotonin Syndrome sx and distinguishing factors

A

Clonus
Hyperreflexia
Mydriasis
Diaphoresis
Tachycardia
Tachypnea
Agitation, delirium

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6
Q

Anticholinergic Toxicity sx and distinguishing factors

A

Dry mouth
Urinary retention, decreased bowel sounds
Mydriasis, blurry vision
Fever
Agitation, delirium, hallucinations

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7
Q

Malignant Hyperthermia sx and distinguishing factors

A

from a volatile anesthetic

During or after surgery
Hyperthermia
Tachycardia
Acidosis
Muscle rigidity
Rhabdomyolysis

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8
Q

DDX differences between SS AND
-anticholinergic toxicity
-malignant hyperthermia
-NMS

A
  • Anticholinergic toxicity
    No neuromuscular abnormalities or diaphoresis
  • Malignant hyperthermia
    Anesthetic agents primarily
    Does not have HYPER reflexia
  • NMS
    Dopaminergic agent
    Days to wk vs SS which is abrupt
    Prolonged vs SS which is rapidly resolved
    Vitals similar
    NMS would have lab results like ELEVATED CK, LFT, WBC, Low Fe while SS does not
    NMS is hyporeflexia vs SS which is hyper
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9
Q

Hunter serotonin toxicity criteria

A

MOST ACCURATE

Presence of a serotonergic agent AND

spontaneous clonus
then
inducible clonus + agitation OR diaphoresis
then
ocular clonus + agitation OR diaphoresis
then
tremor + hyperreflexia
then
hypertonic + temp >38 + ocular clonus or inducible clonus

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10
Q

sternbach criteria for SS

A

addition or inc of a serotonergic agent and 3 or more features on a list and told to r/o other etiologies listed

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11
Q

serotonin syndrome patho

A

5HT effects CNS and PNS

  • In CNS it modulates behavior and thermoregulation
  • In PNS it modulates GI motility, broncho, uterine
  • Mult families of 5HT receptors that mediate
    -Stimulation of 1a and 2a associated with SS but no 1 receptor is associated
    -Can be antag or agonist
  • Mult mechanisms
    -Inc L tryptophan means inc 5HT
    -MAOI causes inc presynaptic 5HT which leads to inc 5HT
    -Inc 5HT release
    -Direct or indirect 5HT receptor agonist
     1A
    -Direct or indirect 5HT receptor antagonist
     2A
  • How does it play out
    o Inc 5HT means inc NE
    -Mult responses from that in chart listed
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12
Q

inc in 5HT synthesis causes

A

tryptophan

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13
Q

inhibition of 5HT metabolism causes

A

MAOI
NDRI
St johns wort

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14
Q

inc 5HT release causes

A

amphetamines
dextromethorphan
NMDA/cocaine

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15
Q

5HT1 receptor activation causes

A

triptans
opiates
mirtazapine/trazodone
lithium
ergot derivatives
NDRI
LSD

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16
Q

5HT2A receptor antagonism rx class

A

SGA

17
Q

5HT Synaptic cleft uptake inhibition causes

A

SSRI
SNRI
TCA
NMDA/cocaine

18
Q

inc in 5HT receptor activation leads to

A

inc NE release

19
Q

inc NE release leads to

A

uncoupling of oxidative phosphorylation
—-inc thermogenesis

inc skeletal muscle activity
—-inc thermogenesis, muscle rigidity, clonus, hyperreflexia, tremor

vasoconstriction
—-inc heat dissipation
—-inc BP

autonomic instability
—-diaphoresis, inc HR, inc BP, N/V/D

20
Q

What feature distinguishes SS and NMS?

  1. NMS has an abrupt time to onset.
  2. Patients with SS will likely demonstrate deviation in lab values, including CK, LFTs, and WBC.
  3. Patients with SS exhibit hyperreflexia and lower extremity rigidity, a contrast to the hyporeflexia seen in NMS.
  4. Tachycardia and hyperthermia are more common with SS.
A

3

21
Q

The increased 5-HT receptor activation seen with serotonin syndrome leads to

  1. An increase in norepinephrine and vasodilation.
  2. Vasoconstriction and autonomic instability.
  3. A decrease in norepinephrine and uncoupling of oxidative phosphorylation.
  4. Autonomic instability and decreased skeletal muscle activity.
A

2

22
Q

How do antidepressants cause SS

A

Mechanism: overstimulation of serotonin receptors; dose-related

Risk Factors: concomitant serotonergic agents

most cited and implicative agents

23
Q

triptans and SS warning

A

d/c

24
Q

linezolid and SS warning

A

monitor
use only if no other therapies available

25
Q

Which of the following correctly pairs the agent with its mechanism in serotonin syndrome?

  1. Tryptophan inhibits 5-HT uptake from the synaptic cleft.
  2. SSRIs increase 5-HT synthesis.
  3. Opiates inhibit 5-HT metabolism.
  4. Triptans activate 5HT-1B and 5HT-1D receptors.
A

4

26
Q

Tx of SS MILD

A

d/c offending agent
supportive care
BZD

27
Q

Tx of SS Moderate

A

Consider 5HT2A ANTAG

Aggressively correct cardiorespiratory and thermal abnormalities

28
Q

Tx of SS severe

A

Sedation

Neuromuscular paralysis

Intubation

29
Q

supportive care for SS

A

SpO2 >94
volume resuscitation
vital sign correction
continuous cardiac monitoring

30
Q

BZD and SS

A

essential regardless of severity

controls agitation and blunts adrenergic response

Diazepam 5-10mg IV q8-10 min
Lorazepam 2-4mg IV q8-10 min

31
Q

Cyproheptadine and SS

A

5HT-2A receptor antagonist

initial: 12mg once then 2mg every 2 hrs until clinical response

PRN : 4-8mg q 6hrs

32
Q

Key components of the treatment of serotonin syndrome include?

  1. Benzodiazepine administration for agitation.
  2. Supportive measures to maintain vital signs.
  3. Cyptoheptadine should be considered for patients with cardiac, respiratory, or thermal abnormalities.
  4. All of the above.
A

4

PMHNP (26 decks)

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