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Sweatman - Antipsychotics and Drug Syndromes Flashcards

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1
Q

What are the names of the typical antipsychotics?

A
  • PHENOTHIAZINES: Chlorpromazine, Fluphenazine, Perphenazine
  • THIOXANTHINES: Thiothixene
  • BUTYROPHENONES (di/phenylbutylpiperidines): Haloperidol
  • NOTE: classified based on structure
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2
Q

What are the names of the atypical antipsychotics?

A
  • Clozapine
  • Risperidone
  • Olanzapine
  • Quetiapine
  • Ziprasidone
  • Aripiprazole
  • Paliperidone
  • NEW: Iliperidone, Asenapine, Lurasidone
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3
Q

How are all drugs that treat psychosis similar?

A
  • All dopamine (D2) antagonists

- NOTE: AC inhibited by D2 and activated by D1 GCPR’s

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4
Q

What are some drugs that can exacerbate psychosis? How?

A
  • Agents associated w/INC dopamine activity
  • Amphetamines, methylphenidate (Ritalin), cocaine
  • NOTE: these drugs may cause psychosis, or make it more severe
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5
Q

What determines the potency of the antipsychotics?

A
  • Clinical potency correlates with in vitro INH of D2 receptor binding
  • NOTE: blocking D2 receptors relieves (+) symptoms
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6
Q

What other receptors (besides D2) do antipsychotics block? What effects does this binding cause?

A
  • To varying degrees (MASH):
    1. Muscarinic - confusion, memory impairment, and protection against EPS
    2. Alpha-1-adrenergic - autonomic side effects like orthostatic hypotension and tachycardia
    3. Serotonin 5-HT2 - relieve (-) symptoms
    4. Histamine (H1) - sedation
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7
Q

What is the key difference between the MOA of the typical and atypical antipsychotics? Why does this matter?

A
  • Relative to typical, 1st-gen, atypical (2nd-gen) show:
    1. Lower affinity for D2 receptors (DEC RISK OF EPS)
    2. Higher affinity for 5-HT2 receptors
  • Typical may produce EPS compared to atypical, which are unlikely to
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8
Q

How do the side effect profiles vary between potent and weak antipsychotics?

A
  • POTENT: INC risk of EPS

- WEAK: additional sedative, hypotensive, and autonomic effects

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9
Q

What are the common features of the typical AP’s?

A
  • Dopamine (D2) blockers
  • Produce EPS
  • Elevate PRL levels
  • Equally effective, but differ in potency and side effects
  • Largely effective for (+) symptoms, e.g., delusions, hallucinations, disorganization of thought and behavior
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10
Q

What are the common features of the atypical AP’s?

A
  • Share D2 and 5HT2A antagonism in common
  • Addition of 5HT2A blockade may:
    1. Reduce EPS
    2. Improve efficacy for (-) symptoms, e.g., withdrawal, flat affect, paucity of thought, avolition (poor initiation of goal-directed behavior)
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11
Q

How do the structures of the typical AP’s affect their potency and side effect profiles?

A
  • PHENOTHIAZINES/THIOXANTHENES:
    1. Chlorpromazine (ALIPHATIC side chain) and Thiothixene (PIPERIDINE ring side chain): low potency -> lower incidence of EPS, but may be associated w/INC anti-muscarinic effects
    2. Fluphenazine, Perphenazine (PIPERAZINE group in side chain) - potent, INC risk of EPS, weak anticholinergic effects
  • BUTYROPHENONES:
    1. Haloperidol - high potency
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12
Q

Describe the pharma profile of Clozapine, Olanzapine, and Quetiapine.

A
  • ATYPICALS
  • Low potency
  • Anti-serotonin effects that may be useful in treating (-) symptoms
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13
Q

Describe the pharma profile of Risperidone. What other 2 agents have similar profiles?

A
  • 5HT2/D2 antagonist
  • Limited EPS at low doses, but acts more like a typical antipsychotic at high doses (INC risk of EPS at high doses)
  • Only approved agent for use in CHILDREN/TEENS
  • Paliperidone (active metabolite of Risperidone) and Ziprasidone (limited EPS) have similar profiles
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14
Q

What is the MOA of Aripiprazole?

A
  • D2 partial agonist that reduces actions of full agonist
  • 5-HT2A antagonist and 5-HT1A partial agonist
  • Lower incidence of side effects
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15
Q

What is the MOA of Asenapine?

A
  • D1, D2, 5-HT1, 5-HT2, alpha-adrenergic, and histamine receptor antagonist
  • Low affinity for muscarinic receptors
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16
Q

What is neuroleptic syndrome?

A
  • Series of behavioral effects produced by the AP’s (similar effects and therapeutic responses):
    1. Suppression of spontaneous movements and complex behaviors
    2. Reduced initiative and interest in envo
    3. DEC manifestations of emotion or affect
    4. Psychotic symptoms (hallucinations, delusions, disorganized and incoherent thinking) appear to disappear over a period of days
  • NOTE: do not confuse with NMS, which is life-threatening, and involves muscle rigidity, fever, autonomic instability, and cognitive changes such as delirium; associated with elevated plasma creatine phosphokinase
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17
Q

How do AP’s affect the limbic system?

A
  • Thought to be the site of AP effects responsible for reduction of psychosis, esp. the (+) symptoms
  • Dopamine system adapts to long-term therapy: INC synthesis, release, and neuronal activity to overcome receptor blockade
  • Anticholinergics do NOT block therapeutic effect bc they do not affect DA turnover in limbic system
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18
Q

How do AP’s affect the basal ganglia?

A
  • Suggested that DEC dopamine activity associated with EPS and neuro effects
  • AP’s consistently INC dopamine metabolism
  • Initially INC dopamine metabolism, synthesis, and firing rate; diminishes with time due to adaptation to tx
  • Antipsychotic effects not thought to occur here
  • Unlike in limbic system, anticholinergics block AP-induced INC in DA turnover in basal ganglia, and consequently block symptoms of EPS -> this results from restoration of balance between cholinergic and dopamine systems in this region
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19
Q

What are the EPS of the AP’s?

A
  • Acute dystonia
  • Akathesia
  • Parkinsonian syndrome
  • Neuroleptic malignant syndrome (NMS)
  • Perioral tremor (delayed)
  • Tardive dyskinesia (delayed)
  • NOTE: prominent during tx with high potency typical AP’s, but less likely to occur w/low-potency AP’s and atypicals
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20
Q

What are the symptoms and tx for acute dystonia?

A
  • SYMPTOMS: muscle spasms, facial grimacing, torticollis (stiff neck), oculogyeric crisis
    1. Spasms to face and neck that usually occur w/in first 5 DAYS
  • TX: anticholinergic antiparkinsonian agents, i.e., BENZTROPINE
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21
Q

What are the symptoms and tx for akathesia?

A
  • SYMPTOMS: strong subjective feelings of distress or discomfort, often related to legs -> compelling need to be in constant motion
    1. “Ants in the pants”
  • TX: DEC dose, add antiparkinsonian agent, anti-anxiety agent or Propranolol
  • Occurs w/in 5-60 DAYS
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22
Q

What are the symptoms and tx of parkinsonian syndrome?

A
  • SYMPTOMS: akinesia (loss/impairment of voluntary mvmt), mask facies, DEC arm mvmt, rigidity, tremor
    1. Develops gradually during 1ST MONTH
  • TX: anticholinergic antiparkinsonian agents, Amantadine
  • NOTE: may be indistinguishable from idiopathic PD, but use of L-dopa or Bromocriptine will induce agitation, and enhance psychosis -> NOT recommended
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23
Q

What are the features of neuroleptic malignant syndrome (NMS)? Tx?

A
  • Rare; high mortality (10%)
  • SYMPTOMS: fever, severe parkinsonism with catatonia, fluctuations in coarse tremor intensity, autonomic instability (labile pulse, BP, hyperthermia), elevated creatine kinase, myoglobinemia (does not always occur)
  • Usually appears within WEEKS OF ONSET OF THERAPY
  • TX: immediate cessation of antipsychotic, supportive care, Dantrolene (fever) or Bromocriptine (competes for dopa receptors) may help
    1. Specific tx’s are generally unsatisfactory
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24
Q

What are the features of perioral tremor? Tx?

A
  • Rare
  • Might appear w/in MONTHS TO YEARS of therapy
  • SYMPTOMS: rabbit syndrome
  • TX: anticholinergic agents, STOP antipsychotic
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25
Q

What are the features of tardive dyskinesia? Tx/prevention?

A
  • SYMPTOMS: stereotyped, repetitive, quick choreiform (tic-like) mvmts of face eyelids (blinks or spasms), mouth (grimaces), tongue, extremities, or trunk
  • NO ADEQUATE TX; discontinue antipsychotic
  • Symptoms may fade with time, or be irreversible
  • Cause unknown, but thought to result from compensatory INC in basal ganglia dopa function
  • Neuro side effects may be prevented by using MINIMALLY EFFECTIVE DOSE
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26
Q

What are the effects of AP tx on the cerebral cortex?

A
  • Minimal adaptive changes in dopamine system in cerebral cortex
  • Can lower seizure thresholds: more likely with low potency phenothiazines (Chlorpromazine), and dose-related effect with Clozapine (in epileptic and non-epileptic pts)
    1. Butyrophenones (Haloperidol) unpredictable
    2. More likely in predisposed pts: use low potency agents with caution in epileptic pts
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27
Q

What are the effects of AP tx on the brainstem and CTZ?

A
  • BRAINSTEM: little effect on respiration, but DEC vasomotor reflexes at low doses -> reduced BP not life-threatening
  • CTZ: protect against N/V bc vomiting elicited by activation of dopamine receptors; occurs at low doses
  • NOTE: both of these effects occur at sub-therapeutic doses
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28
Q

How does AP tx affect the hypothalamus? How does this vary by drug?

A
  • INC prolactin secretion (at sub-therapeutic doses) due to interference with dopamine secretion/action
    1. INC: all typical, Risperidone
    2. Little INC: Clozapine, Olanzapine, Ziprasidone
    3. NO INC: Quetiapine, Aripiprazole (DEC?)
  • Little tolerance develops to PRL effects
  • Avoid in pts with established breast carcinoma
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29
Q

What are the clinical consequences of sustained hyperprolactinemia?

A
  • Sexual dysfunction
  • Amenorrhea: absence of menstrual cycle
  • Gynecomastia or enlarge mammary glands in men, and spontaneous milk flow from breast in women
  • Hypoestrogenism/osteopenia
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30
Q

Which AP’s have other (besides PRL) endocrine effects? What are they?

A
  • CHLORPROMAZINE: impairs glucose tolerance and DEC insulin release
  • ATYPICALS: may INC risk for T2D
    1. Clozapine and OLANZEPINE most likely
    2. Risperidone, Paliperidone somewhat likely
    3. Aripiprizole, Zoprasidone, Quetiapine not likely
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31
Q

Which AP’s may affect the CV system? How?

A
  • Low potency typical antipsychotics
  • Prolonged QT: may produce CV mortality via life-threatening ventricular arrhythmias and sudden death
  • Direct effects on heart and vessels
  • Indirect effects via CNS and ANS
  • Mild orthostatic hypotension: more so with Chlorpromazine, Thioridazine and less so with Haloperidol and Risperidone
    1. Tolerance develops
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32
Q

What are some “additional” side effects of the AP’s?

A
  • ANTICHOLINERGIC:
    1. Nasal stuffiness
    2. Dry mouth
    3. Blurred vision
    4. Constipation
    5. CV: orthostatic hypotension
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33
Q

Do the AP’s have a low or high therapeutic index?

A

HIGH

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34
Q

Which antipsychotic may cause jaundice? How can you correct this?

A
  • CHLORPROMAZINE
  • Occurs during 2nd-4th week
  • Hypersensitivity reaction
  • Mild
  • CHANGE AGENTS
35
Q

Which AP may cause blood dyscrasias?

A
  • CLOZAPINE: usually used as a last resort
  • Mild leukocytosis, leukopenia, eosinophilia
  • Leukopenia may be forewarning of impending agranulocytosis -> weekly WBC counts
36
Q

Which AP’s are more likely to cause skin rxns?

A
  • Urticaria or dermatitis - 5% of pts on Chlorpromazine (more common with phenothiazines)
    1. Occur in first 8 weeks
    2. Skin clears with discontinuation
  • Photosensitivity
37
Q

Which AP’s may cause weight gain?

A
  • MORE LIKELY: Clozapine, Olanzapine
  • INTERMEDIATE: Risperidone, Quetiapine
  • LESS LIKELY: Ziprasidone, Aripiprazole, Asenapine
  • INC risk of T2D (impaired glycemic control), HTN, and hyperlipidemia (primarily elevated TG’s)
  • Children/adolescents: atypicals lead to weight gain (REMEMBER: Risperidone only one approved for kids/teens)
  • Produces 2x INC in CV MORTALITY
  • NOTE: avoid using these agents for long-term therapy
    1. Probably the greatest concern for long-term AP use
38
Q

What are the mechanisms of the various AP AE’s?

A
  • D2 blockade: EPS and hyperPRL
  • Alpha-adrenergic blockade: hypotension
  • Histaminergic blockade: sedation
  • Histaminic/serotonergic blockade: weight gain
  • Muscarinic blockade: aanticholinergic (e.g., dry mouth)
  • Serotonergic/muscarinic/NE/D2 (via PRL) blockade: sexual side effects
  • NOTE: binding affinity for various receptor subtypes and thus, side effects, vary by agent
39
Q

Describe the pharmacokinetics of the AP’s.

A
  • Oral absorption erratic; bioavailability INC 4-10x when given IM
  • Highly lipophilic
  • Highly protein- and membrane-bound
  • Accumulate in high blood supply tissues
  • CROSS PLACENTAL barrier and enter breast milk
  • Peak plasma concentration in 2-4 hours after admin
    1. Disappearance from plasma includes: rapid redistribution (t1/2 = 2hr) and slow early elim (t1/2 = 30hr)
    2. Elimination t1/2 = 20-40hrs (plasma concentrations no well correlated with therapeutic effect)
  • Bio effect usually lasts 24 hrs: give entire DAILY DOSE at once
40
Q

Are plasma concentrations well correlated with therapeutic effect of the AP’s? Why or why not?

A
  • NO!
  • Peak plasma concentration in 2-4 hours after admin
    1. Disappearance from plasma includes: rapid redistribution (t1/2 = 2hr) and slow early elim (t1/2 = 30hr)
    2. Elimination t1/2 = 20-40hrs
  • Accumulate in high blood supply tissues (highly lipophilic and protein/membrane-bound)
41
Q

How are the AP’s metabolized?

A
  • OXIDATION main route: hepatic microsomal oxidases and conjugation
  • Most metabolites inactive
  • EXCEPTIONS:
    1. 7-OH-chlorpromazine
    2. Several N-methylated metabolites of phenothiazines
    3. PALIPERIDONE: active metabolite of Risperidone that is available for therapeutic use
    4. Dehydroaripirazole
42
Q

Might pts develop tolerance/physical dependence to the AP’s?

A
  • Not addicting
  • Some physical dependence: malaise, difficulty sleeping if abrupt stoppage
  • Tolerance develops to sedative effects over days to weeks
43
Q

Describe the potential drug interactions of the typical AP’s.

A
  • Metabolized at CYP2D6 and CYP3A4
  • Do NOT induce P450 enzymes, but many INH CYP2D6 (unlikely the result of competition for enzyme site bc AP’s not metabolized by 2D6 like Clozapine also INH enzyme)
    1. Raise levels of many TCA’s and SSRI’s
    2. Raise levels of many other AP’s
  • Theoretically vulnerable to inducers and INH of 2D6 and 3A4, but little known about this in vivo
44
Q

What are the target symptoms of the AP’s?

A
  • TARGET SYMPTOMS: tension, hyperactivity, combativeness, hostility, hallucinations, acute delusions, insomnia, anorexia, poor self care, negativism, withdrawal
  • NOTE: useful for most psychoses, and are equally efficacious as a family
    1. Individual response to drug and potency does vary across drugs, however
45
Q

How do you treat schizophrenia?

A

Antipsychotics

46
Q

How do you tx bipolar disorder with psychotic features?

A

Mood stabilizers and/or antipsychotics

47
Q

How do you treat schizoaffective disorder?

A

Antipsychotics, with mood stabilizers and/or antidepressants

48
Q

How do you tx major depressive disorder with psychotic features?

A

ECT and/or antidepressant meds and/or antipsychotic medication

49
Q

How do you treat psychosis due to substance abuse intoxication/withdrawal?

A
  • Definitive tx of substance abuse condition

- Antipsychotics as adjunct for delirium

50
Q

How do you treat psychosis due to general med condition (e.g., delirium)?

A

Definitive tx of general med condition with antipsychotics as adjunct

51
Q

How do you choose a drug for the tx of psychosis?

A
  • Trial and error
  • Choice based on side effects
  • If pt responded well to a drug in the past, use it again
52
Q

How can you modify drug admin for pts struggling with adherence?

A
  • DEPOT antipsychotics: active drug + fatty acid (decanoic acid) = slow release drug delivered IM and tissue esterase’s remove fatty acids
    1. For pts with relapses who consistently default on oral meds
    2. In pts who have clear-cut compliance problems
    3. When oral absorption poor due to idiosyncratic pharmacokinetic rxns
  • EX: Prolixin Decanoate, Haldol Decanoate, Risperidal Consta
  • NOTE: you would likely not use these preps until it is determined that drug is effective and tolerated by pt
53
Q

What are some of the miscellaneous (effective) uses for AP’s?

A
  • N/V
  • Alcoholic hallucinosis
  • Neuropsychiatric diseases marked by mvmt disorders:
    1. Tourette’s syndrome
    2. Huntington’s disease
    3. Intractable hiccup
54
Q

Why might you administer Benztropine to a pt taking a high potency antipsychotic?

A
  • To achieve better balance between dopamine and Ach in the BASAL GANGLIA
  • Remember that this balance is also key in Parkinson’s Disease
55
Q

How are the low potency AP’s different than the high potency ones?

A
  • Low potency AP’s have MORE anticholinergic and LESS anti-dopa effects
56
Q

Which of these has the greatest anticholinergic effects? Haloperidol
Fluphenazine
Perphenazine
Chlorpromazine

A
  • Chlorpromazine
57
Q
  • What would you use to treat agitation in elderly pt with Alzheimer’s?
A
  • Fluphenazine (according to pharm instructors)
  • Ziprasidone (according to clinician)
  • Try not to use AP’s at all in the elderly
58
Q 
19-y/o woman newly diagnosed with schizophrenia, but concerned about weight gain. What drug might be a good option for her? 
Clozapine
Ziprasidone
Quetiapine
Olanzapine
A
  • Ziprasidone
  • NOTE: drugs like Clozapine and Olanzapine interact with glucose transporter on beta cells in the pancreas
    1. Obesity can also generate non-compliance, esp. in young women
59
Q

What is the incidence of smoking in pt’s on antipsychotics?

A
  • HIGH
60
Q

Which symptoms are atypical antipsychotics most effective in treating?

A
  • Positive symptoms
61
Q

What is the biggest risk factor for pts with psychosis? Implications?

A
  • The period where psychosis goes untreated -> treat as early as possible
  • Typical, then atypical, then Clozapine
  • Try first what works the best to control the psychosis
62
Q

How quickly do these drugs work? How long do you need to wait to see an effect before changing drugs?

A
  • They should work quickly

- If you don’t see a change in 48-96 hours, it might be time to change drugs

63
Q

What AP is very effective in preventing suicide?

A
  • Clozapine
64
Q

Pt recently diagnosed with schizophrenia and develops severe muscle cramps and torticollis a short time after tx began with haloperidol. What should you do?

A
  • Inject BENZTROPINE -> don’t forget to look at the other drugs the pt is taking too
65
Q

What are the features of serotonin syndrome?

A
  • Pts of all ages: newborn - elderly -> about 14-16% of ppl who OD on SSRI’s
  • Clinicians and pts may dismiss symptoms as inconsequential, or due to pt’s mental state
  • SINGLE SSRI DOSE can produce the syndrome
  • Concurrent CYP2D6 and 3A4 INH can precipitate syndrome, as can withdrawal of concurrent drug tx
66
Q

Where are the serotonergic neurons/receptors in the body?

A
  • Midline RAPHE nuclei: brainstem from midbrain -> medulla
    1. Rostral end assists in regulation of WAKEFULNESS, affective behavior, food intake, thermoregulation, migraine, emesis, and sexual behavior
    2. Raphe in lower pons and medulla participate in regulation of nociception and MOTOR TONE
  • Peripherally, serotonin assists in regulation of vascular tone and GI motility
  • Agonism of 5-HT2a receptors contributes substantially to serotonin syndrome -> impact a wide range of brain functions that lead to dysregulation of autonomic function
67
Q

What is the spectrum of clinical findings found in pts with serotonin syndrome?

A
  • Akathisia -> tremor -> altered mental status -> clonus (inducible) -> clonus (sustained) -> muscular hypertonicity -> hyperthermia -> life-threatening toxicity
  • NOTE: not all findings may be evident in all pts bc some signs can be masked by presence of the others -> range from mild inconvenience issues to life-threatening
68
Q

What are the important features of the algorithm for dx of serotonin syndrome?

A
  • 1) Has serotonergic agent been administered in the last 5 weeks?
  • 2) Are any of the following symptoms present?
    a. Tremor and hyperreflexia
    b. Spontaneous clonus (repeated, rhythmic contractions)
    c. MM rigidity, temp >38 degrees C, and either ocular or inducible clonus
    d. Ocular clonus and either agitation or diaphoresis
    e. Inducible clonus and either agitation or diaphoresis
  • NOTE: clonus and hyperreflexia are highly dx; muscle rigidity can overwhelm these NM findings
69
Q

What is the mgmt for serotonin syndrome?

A
  • Discontinue use of all potential precipitating drugs
  • Provide supportive mgmt
  • Control agitation
  • Administer serotonin antagonists -> CYPROHEPTADINE
  • Control autonomic instability (pharmacologically)
  • Control hyperthermia (cooling)
  • Reassess need to resume use of serotonergic agent once symptoms have resolved
70
Q

What drugs are associated with serotonin syndrome?

A
  • SSRI’s: Sertraline, Fluoxetine, Fluvoxamine, Paroxetine, Citalopram
  • Anti-depressants: SARI’s, Venlafaxine (SNRI), Clomipramine (TCA: prevent serotonin reuptake), Buspirone (anxiolytic)
  • MAOI’s: Phenelzine and Isocarboxazid -> INH serotonin breakdown
  • AED’s: Valproate
  • Analgesics: Meperidine, Fentanyl, Tramadol, Pentazocine (have serotonergic properties)
  • Antiemetics: Ondansetron, Granisetron, Metoclopramide
  • Antimigraine drugs: Sumatriptan
  • Dietary supplements/herbal products: Tryptophan, SJW (hypericum perforatum), ginseng
  • Other: LITHIUM -> reported to INC serotonin metabolites in CSF, and may interact pharmacodynamically with SSRI’s in serotonin syndrome
71
Q

What are the features of neuroleptic malignant syndrome (NMS)?

A
  • Blockade of D2 receptors in hypothalamus -> hyperthermia
  • Blockade of INH actions of dopamine on SYM NS -> autonomic dysfunction
  • Blockade of nigrostriatal dopamine results in INC mm rigidity/tremor via EPS pathways
    1. Possible direct mm toxicity via INC in Ca release from sarcoplasmic reticulum
72
Q

What are the classical symptoms of NMS?

A
  • Hyperthermia
  • Autonomic dysfunction
  • Mm rigidity
  • Extrapyramidal tremor
  • Possibility of direct effect on skeletal mm
73
Q

What are the risk factors for NMS?

A
  • High antipsychotic dosage or use of high-potency agents, i.e., Haloperidol, Fluphenazine
  • Rapid escalation of AP dose
  • Use of depot IM preps (Haloperidol&raquo_space;> Clozapine)
  • Concomitant use of predisposing drugs, like anti-depressants, anticholinergic agents, and Lithium
  • Withdrawal of anti-parkinsonian agents
  • Previous history of NMS
  • INC ambient temp or dehydration
  • Catatonia or agitation
  • Hx of affective disorders or physical disorders of brain that cause DEC in mental function
74
Q

What is the mgmt for NMS?

A
  • WITHDRAW CAUSATIVE DRUG and institute supportive care
    1. Treat acute symptoms: fever, rigidity, altered mental status
    2. Aid recovery by preventing complications: rhabdomyolysis, renal and respiratory failure, prevent recurrence
  • Common drug approaches include:
    1. Dopamine agonists: Bromocriptine&raquo_space;> Amantadine
    2. Dantrolene: skeletal mm relaxant also used to treat malignant hyperthermia
    3. Lorazepam: reduce psychosis, agitation and anxiety, where present, and as anticonvulsant
75
Q

What drugs are associated with NMS?

A
  • Most commonly high-potency antipsychotics like Haloperidol
  • Can occur with ANY ANTIPSYCHOTIC AGENT
76
Q

How do you manage malignant hyperthermia? What is it most commonly associated with?

A
  • Administer Dantrolene IV to restore IC mgmt of Ca levels
  • Correct METABOLIC ACIDOSIS
  • Monitor serum POTASSIUM
    1. Admin insulin and glucose
    2. Admin calcium chloride or gluconate
    3. IV Lidocaine for arrhythmia
  • Cool body to 38 degrees C
  • Maintain urinary output: cold fluids, Furosemide and Mannitol, if needed
  • Most commonly associated with use of VOLATILE ANESTHETICS (Halothane, Enflurane, Isoflurane, Desflurane, Sevoflurane), and short-acting NM blocking drug, Succinylcholine
77
Q

What is the mechanism of malignant hyperthermia?

A
  • Uncontrolled release of Ca from sarcoplasmic reticulum, leading to skeletal mm contraction and stimulation of intermediary metabolism, resulting in METABOLIC ACIDOSIS
78
Q

What is the mgmt for anticholinergic poisoning?

A
  • Hyperthermia and agitation (due to unimpeded SYM stimulation) should be treated with cooling and BNZ’s
  • Physostigmine (anti-cholinesterase) has intrinsic toxicity, and is not necessary in most cases of anticholinergic poisoning
    1. Admin in rare instances when pt has severe “self-harming” psychosis or hemodynamic dysfunction secondary to tachydysrhythmias
    2. CONTRA with TCA OD bc of seizures
    3. This drug can also give rise to bradyasystole: ventricular rate below 60 beats per minute in adults, periods of absent heart rhythm (asystole), or both (can also occur with admin after TCA OD)
79
Q

How does the timing to devo vary by syndrome?

A
  • MH: 30m-24h after admin or inhalation

- SS and AC:

80
Q

How do pupils/mucosa/skin vary by syndrome?

A
  • PUPILS:
    1. SS, AC: mydriasis
    2. NMS, MH: normal
  • MUCOSA:
    1. SS, NMS: sialorrhea
    2. MH: normal
    3. AC: dry erythema
  • SKIN:
    1. NMS, SS, MH: diaphoresis (NMS - pallor, MH - mottled)
    2. AC: hot and dry
81
Q

How do bowel sounds vary by syndrome?

A
  • SS: hyperactive
  • AC: DEC or absent
  • NMS: normal or DEC
  • MH: DEC
82
Q

How do NM tone and reflexes vary by syndrome?

A
  • SS: INC tone (esp. lower extremities), hyperreflexia, clonus
  • AC: normal, normal
  • NMS: lead-pipe rigidity in all mm, bradyreflexia
  • MH: rigor-mortis-like rigidity, hyporeflexia
83
Q

How does mental status vary by syndrome?

A
  • SS: agitation, coma
  • NMS: stupor, alert mutism, coma
  • AC: agitated delirium
  • MH: agitation

Psych (11 decks)

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