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ABOMS Medicine (Psychiatric, ADHD, Addict, Neurologic, MSK)
Terms in this set (98)
Attention deficit hyperactivity disorder is manifested with signs/symptoms of?
Inattention, hyperactivity (restlessness in adults), disruptive behavior, and impulsivity
What drugs are used to treat ADHD?
medications are the pharmaceutical treatment of choice
medications, such as atomoxetine, bupropion, guanfacine, and clonidine
MOA of methylphenidate?
primarily acts as a dopamine-norepinephrine reuptake inhibitor (NDRI).
MOA of atomoxetine?
norepinephrine reuptake inhibitor
Chronic administration of methyphenidate can result in?
depletion of norepinephrine and dopamine storage.
This decreased reserve of endogenous catecholamine can contribute to a blunted sympathetic response which can lead to
Severe bradycardia and hypotension in patients taking Amphetamines can be managed by?
Careful titration of cardiac depressor anaesthetic drugs (propofol)
Direct acting vasopressors such as epinephrine or phenylephrine are preferable because of possible cross-tolerance to other indirect vasopressors such as ephedrine
Use of atropine (pre-operatively) can help blunt bradycardia
Post-operative nausea/vomiting in patients taking amphetamines may be exacerbated by what meds?
Central dopamine is increased in patients taking amphetamines.
Perioperative concerns for patients receiving psychotropic drugs are grouped into the following categories
Drug class physiologic effects
Drug-drug interactions involve
• Lowered seizure threshold
• Altered response to vasoconstrictors
• Exaggerated CNS depression
• Anticholinergic effects
Drug-disease interactions involve
• Drug induced EKG changes
• Hepatic and renal impairment leading to accumulation of parent drug and
Drug class physiologic effects involve what syndromes?
• Serotonins syndrome
• Neuroleptic malignant syndrome
How do you diagnose depression?
Anhedonia: inability to feel pleasure
Dysphoria: unease or generalized dissatisfaction with life.
What medications are used to treatment depression?
MOA of TCAs?
Blocks Ach, Serotonin, NE, histamine
Side effects of TCAs?
Atropine like side affects: dry mouth, dry nose, blurry vision, lowered gastrointestinal motility or constipation, urinary retention, cognitive and/or memory impairment, and increased body temperature
Alpha1 blocker: postural hypotension & arrhythmias
H1 blocker: sedation, confusion
What drugs are cautioned with TCA's?
May see exaggerated effects of sympathomimetics (ephedrine, epi, phenylephrine)
Management of anaesthesia for a patient on TCA?
What drugs should be avoided?
Chronic therapy with TCA drugs depletes cardiac catecholamines, potentiating the cardiac depressant effects of anaesthetic agents. During anaesthesia and surgery, it is important to avoid stimulating the sympathetic nervous system. If hypotension occurs and vasopressors are needed, direct acting drugs such as
are recommended. The dose should probably be decreased to minimize the likelihood of an exaggerated hypertensive response.
Pancuronium (releases stored noradrenaline), ketamine, meperidine and epinephrine containing solutions should be AVOIDED.
MOA of MAOIs?
There are two isoforms of monoamine oxidase, MAO-A and MAO-B.
MAO-A deaminates serotonin, melatonin, epinephrine, and norepinephrine and tyramine
MAO-B deaminates phenethylamine and certain other trace amines
MAO-A inhibition (irreversible and unselective inhibitors) reduces the breakdown of primarily
What are some examples?
endogenous (5-HT, NE, and DA) and exogenous (tyramine) monoamines
(Nardil), isocarboxazid (Marplan), and tranylcypromine (Parnate)
Selective (reversible) inhibition of MAO-A allows for breakdown of
tyramine = metabolised via MAO-B (thus not having to restrict the diet)
Selegeline is a selective MAO-B inhibitor
MAO-B inhibition reduces the breakdown mainly of
dopamine and phenethylamine so there are no dietary restrictions associated with this.
Taking MAOIs with wine and cheese results in?
Taking MAOIs with foods with substantial amount of tyramine will = a
Hypertensive responses can also be associated particularly with OTC sympathomimetic drugs such as ephedrine, pseudoephedrine and phenylpropanolamine, which are present in several decongestants and cough medicines.
What are the signs/symptoms of hypertensive crisis?
confusion, fever, diaphoresis, shivering, ataxia, myoclonus, hyperreflexia, and death
What other drugs will cause a hypertensive crisis with MAOIs and should be avoided?
All phenylpiperidine opioids (meperidine, methadone, tramadol)
Benzodiazepines, inhalational anaesthetic agents, anticholinergic drugs and non-steroidal anti-inflammatory drugs can be used safely in patients taking MAOIs
MOA of SSRIs and SNRIs?
More favorable profile with limited adverse effects (with regard to sedation, orthostasis, and cardiovascular risks)
Serotonin syndrome occurs SSRI's are used with?
Occurs when SSRIs are used in combination with agents that increase serotonin concentrations (MAOIs, TCA's, tramadol,
, amphetamines, Cyclobenzaprine, and St. John's Wort)
Do not discontinue SSRI's in the perioperative period (Discontinuation syndrome)
Signs and symptoms of serotonin syndrome are?
●Slow, continuous, horizontal eye movements (referred to as ocular clonus)
●Deep tendon hyperreflexia (common)
●Inducible or spontaneous muscle clonus (common)
●Dry mucus membranes
●Flushed skin and diaphoresis
Discontinuation syndrome signs/symptoms?
♦ dizziness, nausea, lethargy, and headache
♦ resume therapy shortly after surgery
Management of serotonin syndrome?
●Discontinuation of all serotonergic agents
●Supportive care aimed at normalization of vital signs
●Sedation with benzodiazepines (lorazepam 2 to 4 mg IV)
●Management of hypertension (Esmolol 1mg/kg)
●Managment of hypotension (phenylephrine, epinephrine)
●Administration of serotonin antagonists (Cyproheptadine 4mg PO q4hours = only PO)
●Management of hyperthermia
●Intubation if needed (succinylcholine (1.5 to 2 mg/kg IV)
SSRI's and bleeding?
When combined with NSAIDs (not much of a concern but just be aware)
blockade of the serotonin transporter by an SSRI leads to a decreased concentration of serotonin within the platelet, along with a slight inhibition of platelet aggregation, which could account for any observed impairment in hemostasis
Bipolar disorder is characterized by
mood swings from depressive episodes to manic episodes with normal behaviour in between these episodes.
Mainstay medical treatment of bipolar disorder is
Lithium and valproate
Side effects of lithium?
Should lithium be stopped prior to major surgery?
Lithium can be stopped at once because no withdrawal symptoms occur. Taking a half-life of 24-36 h into account, lithium should be discontinued 72 h before surgery.
Minor surgery with local anesthesia - no need to stop
What medications should be avoided with lithium?
NSAIDs (40% increase in lithium concentration)
Depolarizing and non-depolarizing muscle relaxants may be prolonged
Lithium toxicity signs/symptoms?
Predominately gastrointestinal (GI), including nausea, vomiting, cramping, and sometimes diarrhea.
Progression of acute toxicity can involve neuromuscular signs such as tremulousness, dystonia, hyperreflexia, and ataxia.
Cardiac dysrhythmias have been reported but rarely occur. The most common electrocardiographic finding is T-wave flattening.
Schizophrenia signs and symptoms involve?
Positive and Negative symptoms
Medications used for the treatment of Schizophrenia?
Typical antipsychotics (chlorpromazine, haloperidol, trifluoperazine) cause extrapyramidal side-effects like acute dystonia, akathisia, Parkinsonism and tardive dyskinesia.
Atypical antipsychotics (clozapine, olanzapine, risperidone, amisulpiride, quetiapine and aripiprazole), which do not have a tendency to cause extrapyramidal side-effects.
Difference between Typical and Atypical?
seizures and neutropenia.
Weight gain, postural hypotension and gynaecomastia are also very common with antipsychotic drugs.
Antipsychotics can produce glucose intolerance by decreasing insulin action
Perioperative concerns regarding the use of anesthetics?
hypotension, cardiac conduction effects (prolongation of the QT and PR intervals), sedation, lowered seizure threshold (avoid Ketamine)
Describe Neuroleptic Malignant Syndrome (NMS), treatment involves what?
Acute hyperthermia, muscular rigidity, altered mental status, elevated creatinine phosphokinase and autonomic dysfunction (hours to days to occur vs MH)
ICU admission, Dantrolene 2.5mg/kg IV prn up to 30mg/kg
MOA of Dantrolene?
inhibiting Ca2+ ions release from sarcoplasmic reticulum stores by antagonizing ryanodine receptors.
In a drug addicted patient, what is tolerance vs dependence vs abuse?
Tolerance refers to a physiological state where the effectiveness of a drug has decreased due to chronic administration.
Physical dependence refers to how the body experiences physiological adaptation in response to chronic use of a drug (withdrawal symptoms)
Abuse is best defined as an individual who continues to use a drug despite social, interpersonal, and legal consequences.
Patients with miosis vs mydriasis in regards to drugs?
• Miosis - opiods
• Mydriasis - hallucinogens and stimulants
In alcoholic patients, what Electrolyte disturbances are seen?
due to dehydration and malnourishment
Alcohol is a CYP450 inducer (CRAP GPS)
In alcoholic patients, what ECG anomalies are seen?
• AV Block
• Bundle branch block
• Prolonged QT interval
The "CAGE" questionnaire is a simple means of
screening for alcohol abuse and potential dependency. What does it stand for?
Have you ever felt the need to cut down?
Have you ever felt angry at someone's criticism of your drinking?
Have you ever felt guilty about your drinking?
Have you ever had an eye opener?
>2 positive answers correlates with a high likelihood of alcohol abuse
Alcohol withdrawal involves what signs and symptoms?
Early (1st 24-48 hrs): tremors, nausea, mild diaphoresis, tachycardia, insomnia, headache (autonomic hyperactivity)
Late: hallucinations, seizures. Late withdrawal can lead to DT (delirium tremens)
Explain Wernicke-Korsakoff Syndrome
Wernicke's encephalopathy - 6th nerve palsy (diplopia / ophthalmoplegia), gait ataxia, mental confusion, nystagmus.
Korsakoff's Syndrome - anterograde & retrograde amnesia, abstract & conceptual reasoning impairment, confabulation
Treatment of DTs, AWS
thiamine 100 mg PO/IV qd x 1week ( Co enzyme in Kreb's cycle, depleted with chronic ETOH use)
folate 1 mg IV or PO x 3 days
MVI x 3 days
Mg Sulfate 1 gm IM / IV x 3 days
Chlordiazepoxide (Librium®) 25-50 mg IM/IV/PO q6-8 h
Lorazepam (Ativan®) 1-2 mg IM / IV / PO q 8-12 h
In an opiod addict on agonist/antagonists (Subutex) can be given what meds for IV sedation?
- Benzodiazepines may be used in doses/frequencies similar to use in any patient NOT on opioids.
- Nitrous Oxide, Propofol, or other non-opioid medications (Ketamine) are NOT affected by buprenorphine or Suboxone.
- You may hold agonist/antagonist for 3 days prior to procedure and use opioids or you can use opioids but expect higher doses because of tolerance.
Anesthetic concerns for a cocaine user.
- Anesthetic management is directed toward optimization of cardiopulmonary parameters
- Increased risk of cardiac dysrhythmias
- Avoid dopaminergic agonists (haloperidol, droperidol and promethazine) which may cause delayed awakening
- No treatment within 24 hours of last use
- Local anesthetics with AND without vasoconstrictors have additive dysrhythmic effects
-Propofol, benzos are safe
- Greater incidence of CVA, malignant HTN, and MI
MOA of cocaine
Cause vasocontriction, ischemia, tachycardia
Cocaine abuse patient with hypotension or hypertension is treated with?
Hypotension = phenylephrine (100mcg IV q10mins); ephedrine (indirect) will not work
Hypertension = Labetalol (40mg IV q10mins) has been another medication recommended, but its use is also controversial. Its non- selective b- and a-adrenergic blockade which acts fast and restores blood pressure without changes in heart rate, seems useful in cardiovascular changes resulting from cocaine toxicity
b-Blockers, such as propanolol, are
in these patients because of the potential for unopposed a-adrenergic stimulation
What anesthetic precautions are taken in a stimulant abuser (amphetamines, ephedrine, nicotine, caffeine)?
- Chronic users will demonstrate labile BP secondary to catecholamine depletion
- Careful use of epinephrine and bupivacaine due to dysrhythmia potential
- Avoid ketamine
- MDMA causes a massive release of serotonin (serotonin syndrome)
Epilepsy is a disorder of the brain defined by ANY of the following conditions:
1. At least 2 unprovoked (or reflex) seizures occurring >24 hours apart
2. 1 unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after 2 unprovoked seizures, occurring over the next 10 years
3. Diagnosis of an epilepsy syndrome
Seizures can be classified as
partial and generalized seizures
Generalized vs partial seizures
Generalized - sudden
♦ Convulsive - muscle contractions
♦ Myoclonic - contract and relax continuously
♦ Tonic-clonic (grand mal) - LOC, fall to ground, and jerking movements
♦ Absence - brief LOC with minimal activity
♦ Complex - aura followed by
♦ Simple - no LOC, but isolated tonic-clonic activity
If a seizure lasts longer than
or if there are more than 2 seizures in an hour without a return to a normal level of consciousness between them, it is considered a medical emergency known as
Treatment for Status epilepticus
- Control airway/O2
- Activate EMS
- Midazolam 2mg IV then 1mg/min IV (0.05mg/kg, or 0.025mg/kg in children; Lorazepam 4 mg/dose slow IV at 2 mg/min
- Glucose check
- Glucose and thiamine prn
- Monitors and possible respiratory support in postictal period
- Phenytoin and fosphenytoin
Other causes of seizures
• Vasovagal syncope - most common cause in OMS office
• Lidocaine overdose
Anesthetic agents that increase electrical activity
♦ Methohexital (Brevital)
♦ Ketamine (Ketalar)
♦ Enflurane. sevoflurane
♦ Flumazenil, Demerol
In spinal cord injured patients, ACUTE transection results in what kind of issues?
• Respiratory insufficiency
• Exaggerated hyperkalemic response to succinylcholine administration for
first 6 months
• Orthostatic hypotension - due to lack of regulatory control -> peripheral vasodilation
In spinal cord injured patients, CHRONIC transection results in what kind of issues?
• Autonomic hyperreflexia due to sympathetic spinal reflex activity (no inhibition)
• Bradycardia and HYPERtension (T6 or higher)
• Cervical spinal cord injury is associate with increased vagal tone
• Cardiovascular/hemodynamic instability
Autonomic hypereflexia is ?
Effects of vertebral fractures at different levels
What is multiple sclerosis? 3 main characteristics?
Demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged by an autoimmune process = inflammatory process is caused by T cells.
The 3 main characteristics of MS are the formation of lesions in the central nervous system (also called plaques), inflammation, and the destruction of myelin sheaths of neurons.
How is MS diagnosed?
Multiple sclerosis is typically diagnosed based on the presenting signs and symptoms, in combination with supporting medical imaging and laboratory testing. Neuroimaging (Lesions in time/space), analysis of CSF (IgG) and evoked potentials
What are the clinical manifestations of MS?
almost any neurological symptom or sign, with autonomic, visual, motor, and sensory problems being the most common
What are the 4 disease or clinical patterns seen in MS?
1. relapsing-remitting (RRMS)
2. primary progressive (PPMS)
3. secondary progressive (SPMS)
4. progressive relapsing
OMS concerns when treating patients with MS?
-Stress reduction (anxiolysis)
-Temperature management (do not overheat)
-Adrenal insufficiency (stress dose steroids at hydrocortisone 100mg IV q8h)
-Treatment with INTERFERON (get CBC to rule out thrombocytopenia, neutropenia, anemia)
Undiagnosed MS = may present as bilateral trigeminal neuralgia (refer to neurologist)
What is cerebral palsy?
Permanent movement disorder that appears in early childhood.
Signs and symptoms include poor coordination, stiff muscles, weak muscles, and tremors.
Cerebral palsy is caused by abnormal development or damage to
parts of the brain that control movement, balance, and posture
Most often thru pregnancy, delivery or shortly after birth. (pre-term birth, difficult delivery, genetics)
Classification for CP
Spastic (70%) - can be quadraplegic, Diplegia, hemi, etc.
Ataxic (intention tremor and head tremor)
Clinical problems/comorbidities in CP?
Cardiovascular (vascular access 2/2 contractures)
Respiratory (pulmonary aspiration, recurrent respiratory infections and chronic lung disease, poor cough with retention of secretions)
GI (Gastro-oesophageal reflux is common due to esophageal dysmotility and spasm, abnormal
lower esophageal sphincter function and spinal deformity)
Common medications patients with CP are on?
Anticonvulsants (Carbamazepine - check CBC)
Antispasmodics (Baclofen, Benzos, Botox)
Prokinetic (Cisapride - Prolongs QT interval, increased risk of Torsades de Pointe) = get ECG
Anesthesia concerns for patient with CP?
Vulnerable to hypothermia (keep warm)
Positioning may be difficult due to fixed contractures
MAC is reduced
Excessive secretions and reflux (RSI)
can be used (resistant non-depolorizing agents)
What medications do you want to avoid in patients with CP?
Myasthenia gravis is described as?
An autoimmune disorder characterized by weakness and fatigability of skeletal muscles caused by autoantibodies directed against acetylcholine receptors of the neuromuscular junction.
What muscle groups are impacted with Myasthenia gravis?
• Lid muscles (
• Extraocular muscles - resulting in
• Masticatory muscle weakness and fatigue
• Oropharyngeal weakness -
dysarthria and dysaphagia
• Weakness can lead to
• Can lead to "myasthenic crisis" which can occur spontaneously or in response to infections, surgery, medications, or tapering immunosuppression.
How is myasthenia gravis diagnosed?
Anticholinesterase test (Tensilon test) - produces a marked improvement of strength
A test dose of 2 mg IV is given; if no reaction occurs after 45 seconds, an additional 3 mg is injected. If no reaction occurs after 45 seconds, the remaining 5 mg is given, for a total dose of 10 mg.
EMG (demonstrative progressive weakness)
Antibodies to Ach
Get a CXR to rule out thymoma
How is myasthenia gravis treated?
Anticholinesterase drugs (Pyridostigmine should be started at 30-60 mg po tid-qid)
Immunosuppressive drugs (prednisone 60-80mg/day)
Plasmapheresis is used in the treatment of acute exacerbations, impending crisis, disabling MG refractory to other therapies or prior to surgery.
What is a myasthenic crisis?
Paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life.
Crises may be triggered by various biological stressors such as infection, fever, an adverse reaction to medication, or emotional stress
Preoperative considerations for patients with myasthenia gravis are?
= ever been on ventilator?
Use of anticholinesterase medication (Pyridostigmine), IVIG and plasmapharesis
Medications to avoid in myasthenia gravis patients?
Anticholinesterases, used for treatment for patients with MG, may theoretically impair the hydrolysis of ester local anesthetics and result in prolonged block.
Avoidance of the use of neuromuscular blocking agents (NMBAs)
Patients with MG are
to depolarizing NMBAs (eg, succinylcholine)
Patients with MG are extremely
to nondepolarizing NMBAs (eg, rocuronium, vecuronium, cisatracurium).
Drugs that may unmask or worsen myasthenia gravis
Drugs usually well-tolerated in myasthenia gravis but occasionally associated with an exacerbation*
Inhalation anesthetics - eg, isoflurane, halothane
Local anesthetics - eg, bupivacaine, lidocaine, procaine
Tetracyclines - eg, doxycycline, tetracycline
Macrolides - eg, azithromycin, clarithromycin, erythromycin
Antipsychotics and other psychiatric drugs
Butyrophenones - eg, haloperidol
Phenothiazines - eg, chlorpromazine, prochlorpromazine
Calcium channel blockers - eg, verapamil
Duchenne muscular dystrophy (DMD) involves the mutation of what gene?
recessive X-linked form
mutation in the gene
, located on the human X chromosome, which codes for the protein dystrophin.
Dystrophin is an important component within muscle tissue that provides structural stability to the dystroglycan complex (DGC) of the cell membrane. While both sexes can carry the mutation, females are rarely affected.
What is the main symptoms of DMD?
a progressive neuromuscular disorder, = muscle weakness associated with muscle wasting with the voluntary muscles
A positive Gowers' sign
What ventilatory issues do DMD patients have?
Vertebral and rib contractures that lead to kyphoscoliosis and RESTRICTIVE ventilatory defect
Anesthesia concerns for DMD?
- No depolarizing muscle blockers (SUCC→ hyperkalemia)
- Can USE non-depolarizing steroidal muscle relaxants
- ↑ incidence of MH (may be triggered by NDNM blockers, volatile anesthetics)
- AVOID volatile anesthetics
Marfan's Disease is characterized by what mutations?
Autosomal dominant; abnormal chemical makeup of connective tissue
- 2° mutations in
* which plays an important role as scaffolding for elastic tissue
- Disruption of scaffolding causes changes in elastic tissue (aorta, eye, skin)
What are the clinical findings of Marfan's disease?
- skeletal defects - long, lanky frame, spider-like fingers (
), chest abnorm (pectus excavatum or pectus carinatum), scoliosis, joint laxity
- facial features - highly arched palate, micrognathia, crowded teeth
- eye problems - nearsightedness,
dislocation of lens
- Cardiovascular abnormalities- dilatation of base of aorta (aortic root), aortic regurg,
, Dissceting aortic aneurysm
Anesthetic concerns regarding Marfan's disease?
- Use Beta-blockers = decrease HR, help prevent stress on aorta (discourage athletics/contact sports)
- annual echo to assess the aortic root and regurgitation
Ehlers-Danlos syndrome (EDS) is characterized by what mutation?
inherited connective tissue disorder
defect in the structure, production, or processing of
or proteins that interact with collagen, such as mutations in the COL5A or COL3A genes
Classification of EDS?
Clinical manifestations of EDS?
Musculoskeletal - Hyper-flexible joints
Skin - Fragile skin that tears easily
Cardiovascular - Arterial rupture, Valvular heart disease
Other manifestations or complications - Platelet aggregation failure, Insensitivity to local anesthetics
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