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PAM Semester 2 > Pharm Neuro Exam > Flashcards

Pharm Neuro Exam Flashcards

1
Q

Headache types

A

Tension

Migraine

Cluster

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2
Q

Treatment for Tension Headaches (General)

A

OTC Pain Meds

Prescription Meds like Tricyclics

Consistent sleep schedule

Regular Exercise and stress relieving activities

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3
Q

Treatment for Migraine Headaches (General)

A

Rescue medication to relieve pain and stop migraine

Preventative medication to avoid future migraines

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4
Q

Treatment for Cluster Headaches (General)

A

Lifestyle changes

Oxygen treatment

Prescription meds such as verapamil, prednisone, or lithium

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5
Q

Tension Headache treatment (acute)

A

NSAIDS vs ASA

APAP (Tylenol)

Trial of Anti-migraine if other failed

Toradol IM (severe)

Local heat, muscle relaxants, PT, Stress reductions

Antidepressants and/or BT for depression and stress

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6
Q

NSAID MOA

A

The primary effect of NSAIDs is to inhibit cyclooxygenase (COX; prostaglandin synthase),

thereby impairing the ultimate transformation of

arachidonic acid
to
prostaglandins, prostacyclin, and thromboxanes

(COX inhibitors)

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7
Q

Migraines Treatment

A

Abortive therapy
ASA, APAP, NSAIDS
(no more than 2 doses/day, no more than 2x per wk

Triptans if OTC med fail

For mild to moderate migraines with no N/V
OTC analgesics are recommended
(rather than migraine specific meds)

For moderate to severe migraines
recommended triptan or combination of sumatriptan/naproxen (Treximet)
(rather than migraine specific meds)

OTC analgesics,(<2xQD/2xQwk) then triptans

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8
Q

Triptan meds for migraines

A 
Sumatriptan (Imitrex)
rizatriptan
eletriptan
almotriptan
zolmitriptan
naratriptan
frovatriptan

All end in -triptan

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9
Q

Sumatriptan Dose

A

Imitrex (Selective 5-HT1B/1Dreceptor agonist.)
For acute migraines

≥18yrs: 25–100mg once, swallow whole with fluids as soon as possible after migraine onset; may repeat dose at intervals of at least 2hrs, max 200mg/day;

25-100, repeat prn Q2hrs, max 200

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10
Q

Sumatriptan (Contraindications)

A

Imitrex (Selective 5-HT1B/1Dreceptor agonist.)
For acute migraines

History, symptoms, or signs of 
ischemic cardiac (eg, MI, angina pectoris, silent myocardial ischemia),

History, symptoms, or signs of cerebrovascular (eg, stroke, TIA)

History, symptoms, or signs of peripheral vascular (eg, ischemic bowel disease) syndromes.

Vasospastic coronary artery disease.

Uncontrolled hypertension.

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11
Q

Sumatriptan (Warnings/Precautions:)

A

Imitrex (Selective 5-HT1B/1Dreceptor agonist.)
For acute migraines

Confirm diagnosis.

Avoid excessive use

Exclude underlying cardiovascular disease

supervise 1stdose

consider monitoring ECG in patients with likelihood of unrecognized coronary artery disease
(eg, postmenopausal women, hypercholesterolemia, men over age 40, hypertension, obesity, diabetes, smokers, strong family history).

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12
Q

Sumatriptan (Interactions)

A

Imitrex (Selective 5-HT1B/1Dreceptor agonist.)
For acute migraines

Ergotamines,

other 5-HT1agonists,

MAOIs: see Contraindications.

Serotonin syndrome with SSRIs (eg, citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline) or SNRIs (eg, duloxetine, venlafaxine).

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13
Q

Selective 5HT 1B/1D Agonist MOA

A

Selective agonist for serotonin (5-HT1B and 5-HT1D receptors) on intracranial blood vessels and sensory nerves of the trigeminal system;

Causes vasoconstriction and reduces neurogenic inflammation associated with antidromic neuronal transmission correlating with relief of migraine

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14
Q

Ergots

A

Both ergotamine and dihydroegotamine (DHE 45) bind to 5HT1b/d receptors,
(Same as triptans)

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15
Q

Ergotamine and caffeine

A

Contras:
PVD, HTN, CVD, Pregnancy Cat X

Adverse:
Vasoconstrictive complications or ergotism

(eg, ischemia, cold extremities, vasospasm, ECG changes, hyper- or hypotension, numbness, gangrene, dizziness),

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16
Q

4 categories of migraine prophylaxis

A

Comorbidities and contras

Amitriptyline
Depression is ok,
but mania contraindicated

Propranolol
HTN is ok,
but depression or asthma contraindicated

Calcium channel blockers
HTN and angina are ok,
but depression contraindicated

Antiepileptics
Epilepsy, anxiety and mania are ok,
but liver disease contraindicated

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17
Q

Topiramate (migraine)

A

Topamax (Sulfamate)
Migraine prophylaxis. Not been studied for use in acute treatment of migraines.

Interactions:
Contraindicated with metformin during metabolic acidosis condition.
Concomitant other carbonic anhydrase inhibitors (eg, zonisamide, acetazolamide)

Adverse Reactions:
Paresthesia, anorexia, weight decrease, taste perversion

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18
Q

Cluster headache treatments

A

Oxygen 100% @ 6-12l/min x 15min (non-rebreather)

Triptan medication = Sumatriptan 6mg Sub Q

Verapamil

Lithium

Prophylaxis
Beta blockers (Propranolol 60-320mg QD)

Anticonvulsants (Topiramate 25-100mg QD)

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19
Q

Bacterial meningitis

A

Neonate (<1mo) & Infants (>1mo - <3mo)
Group B Strep

Adults (up to 60 or over 60)
S. pneumoniae

If papilledema, new onset seizure, signs of brain shift
Must perform CT before LP

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20
Q

Essential tremors

A

For patients with mild ET who have situational exacerbations of tremor that cause disability

we suggest treatment as needed withpropranolol

Other monotherapy options include judicious use of a low-dose short-acting benzodiazepine andprimidone.

The usual course of ET is one of slow gradual progression

Propranolol, then benzos and primidone, ET is gradual progression

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21
Q

Primidone

A

Mysoline (barbiturate)
Tonic-clonic, focal and psychomotor seizures

Porphyria (liver disorders), Barbiturate hypersensitivity

Interactions:
Potentiated with alcohol and other CNS depressants. Antagonizes oral anticoagulants and contraceptives,

Adverse Reactions:
Drowsiness, ataxia, dizziness, nystagmus,

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22
Q

Barbiturates MOA

A

CNS depressants

produce sedation by binding to the GABA-receptor via a different receptor from benzodiazepines.

They cause hypotension and may cause cardiovascular and respiratory depression.

As a result, the use of barbiturates should be limited to patients not tolerating or responding to other agents

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23
Q

Parkinson’s Treatment (general)

A

Designed to best restore the balance between dopamine and ACH by blocking the effect of ACH with anticholinergics, administering levodopa (precursor of dopamine) or a combination of both.

The 4 main drugs or classes of drugs that have symptomatic antiparkinson activity as monotherapy are

monoamine oxidase type B (MAO B) inhibitors (rasagiline,safinamide, andselegiline)

amantadine

dopamine agonists (DAs;bromocriptine,pramipexole,ropinirole, androtigotine)

levodopa.

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24
Q

Parkinson Disease Drug MOA

Levodopa MOA

A

Levodopa can get through the blood brain barrier and can mimic dopamine

DDC (carbidopa) inhibits the break down of levodopa to dopamine which cannot get through the BBB
also
COMT inhibits the break down of levodopa to dopamine which cannot get through the BBB

Levodopa goes through the BBB and is converted to dopamine inside the neuron

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25
Q

MOA of medications used to treat Parkinsons

A

COMT
Inhibitors preserve Levodopa

Levodopa
Replaces dopamine

Dopamine
Agonists mimic dopamine

MAO-B
Inhibitors preserve existing dopamine

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26
Q

Type B MAO-B Inhibitors

A

Rasagiline (Azilect)
safinamide (Xadago)
selegiline (Eldepryl or Zelapar)

Inhibitors breakdown dopamine

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27
Q

MAO-B Inhibitors MOA

A

Inhibit degradation of dopamine

Increase efficacy of levodopa by 20%

Reduce “off” time

May increase dyskinesia

May have neuroprotective properties

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28
Q

amantidine

A

Symmetrel

Mild anticholinergic (anticholinergic side effects)

great for younger patients with tremor

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29
Q

levodopa

A

Inbrija (dopamine precursor)
Intermittent treatment of OFF episodes in patients with Parkinson’s disease treated with carbidopa/levodopa.

Contraindications:
During or within 14 days of nonselective MAOIs (eg, phenelzine, tranylcypromine).

Warnings/Precautions:
Sleep disorders: consider discontinuing if significant daytime sleepiness occurs.

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30
Q

Levodopa effects

A

Converted to Dopamine in the body and improved all symptoms of Parkinson’s Disease.

Carbidopa with added to levodopa allows lower dosages of levodopa and reduced side effects.

Prolonged use of levodopa leads to effectiveness to wean. Also dyskinesias can occur. Lowest dose possible.

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31
Q

carbidopa/levodopa

A

Sinemet (Parkinsonism’s)
Dopa-decarboxylase inhibitor + dopamine precursor

Contraindications:
During or within 14 days of nonselective MAOIs (eg, phenelzine). Narrow-angle glaucoma. Undiagnosed skin lesions. History of melanoma.

Warnings/Precautions:
Severe cardiovascular or pulmonary disease. Asthma. Renal, hepatic, or endocrine disorders. History of peptic ulcer or MI with residual arrhythmias. Suicidal tendencies. Psychosis. Orthostatic hypotension. Chronic wide-angle glaucoma.

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32
Q

COMT inhibitors

A

Cathecholamine-O-methyltransferase inhibitors

Tolcapone (tasmar)
entacapone (Comtan)
Both are adjuncts to Sinemet

Both end in -capone

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33
Q

Tolcapone

A

Tasmar (COMT inhibitor)

Adverse Reactions:
Dyskinesias, nausea, sleep disorders, dystonia, excessive dreaming, anorexia, muscle cramps, orthostatic complaints,

Interactions:
Concomitant non-selective MAOIs (eg, phenelzine, isocarboxazid, tranylcypromine): not recommended.

Warnings: Risk of liver injury

Box Warning: Risk of potentially fatal, acute fulminant liver failure.

Contraindications:
Liver disease (clinical evidence or serum transaminases 2xULN)
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34
Q

Huntington disease (general)

A

Huntington disease (HD) is a condition of relentless progression of motor, cognitive, and psychiatric symptoms.

Treatment is limited to symptom management and optimizing quality of life.

The best care is provided by an interdisciplinary team that addresses the broad physical and psychologic needs of patients and families, and manages new issues as they arise through long-term follow-up

Moderately severe chorea that does not respond to nonpharmacologic intervention, we suggest initial treatment withtetrabenazine (Xenazine)

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35
Q

tetrabenazine

A

Xenazine (Huntington’s chorea)
(Vesicular monoamine transporter 2 (VMAT2) inhibitor)

Contra: Untreated or inadequately treated depression. Suicidal ideation. Hepatic impairment.

Box Warning: Depression and suicide

Interactions:
Avoid concomitant drugs known to prolong QT interval
(eg, chlorpromazine, haloperidol, thioridazine, ziprasidone, moxifloxacin, quinidine, procainamide, amiodarone, sotalol).

VMAT2, Depression/suicide, Liver, Avoid QT meds

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36
Q

VMAT 2 Inhibitor

A

is a mechanism that reduces dopamine stimulation without blocking D2 receptors

Thus, this action reduces the overstimulation of D2 receptors in the indirect pathway,
resulting in lessinhibitionof the stop signal there

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37
Q

Tourette Syndrome

A

A neurological disorder manifested by motor and phonic tics with onset during childhood.

Treatment is guided by the need to treat the most troublesome symptoms,
including both tics and comorbid conditions such as attention deficit hyperactivity disorder (ADHD) and obsessive-compulsive disorder (OCD).

Education is indicated for all.

Comprehensive Behavioral Intervention for Tics (CBIT)

When CBIT is not an option for patients with TS and debilitating tics, we suggest medication treatment withtetrabenazine.

Alternatives includefluphenazineorrisperidone

Medication options that treat both tics and ADHD include the alpha adrenergic agonistsguanfacineorclonidine.

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38
Q

What is the first line treatment for eligible patients with acute ischemic stroke?

A

Intravenous Alteplase Therapy (TPA)

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39
Q

Alteplase Dosage

A

Activase (acute ischemic stroke)
Tissue plasminogen activator (TPA)

Start treatment within 3hrs of symptom onset.

0.9mg/kg (max 90mg total dose) infused over 60min
with 10% of the total dose given as an initial IV bolus over 1 minute.

Monitor frequently and control blood pressure

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40
Q

Alteplase

A

Activase (acute ischemic stroke)
Tissue plasminogen activator (TPA)

Contraindications:
History of recent stroke. Intracranial or subarachnoid hemorrhage.
Active internal bleeding. Intracranial or intraspinal surgery or serious head trauma within 3 months. Intracranial neoplasm, arteriovenous malformation or aneurysm. Bleeding diathesis. Current severe uncontrolled hypertension.

Interactions:
Increased risk of bleeding with anticoagulants, antiplatelets

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41
Q

Alteplase MOA

A

Directly activates plasminogen to form plasmin leading to clot lysis

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42
Q

TIA Treatment

A

ASA
Plavix
ticlopidine
ASA/dipyridamole

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43
Q

Nimodipine

A

Calcium Channel Blocker
(dihydropyridine)

Used after sub-arachnoid hemorrhage to reduce cerebral vascular vasospasm

Adverse:
Decrease blood pressure, GI upset, Headache, Bradycardia, Flushing, Edema

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44
Q

Nimodipine MOA

A

Calcium channel blocker

causes peripheral vasodilation

causes coronary vasodilation

causes slight decrease in SA node automaticity

causes Zero inotropoic effects

causes Zero AV conduction effects

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45
Q

Seizures

A

The management of patients with epilepsy is focused on three main goals: controlling seizures, avoiding treatment side effects, and maintaining or restoring quality of life.

The “classic”ketogenic dietis a special high-fat, low-carbohydratedietthat helps to controlseizuresin some people with epilepsy.

In general, enzyme-inducing anti-seizure drugs are the most problematic for interactions with drugs such aswarfarin
(eg,phenytoin,carbamazepine,phenobarbital,oxcarbazepine)

Control seizures, Quality of life, avoid side effects, keto diet, interacts with warfarin

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46
Q

Lamotrigine

A

Lamictal
Adjunct in partial seizures

Box warning: Sever skin rashes

Adverse: Stevens-Johnson syndrome

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47
Q

Carbamazepine

A

Tegretol
Generalized tonic-clonic partial or mixed seizures

Contra:
History of bone marrow depression. Sensitivity to tricyclic antidepressants. During or within 14 days of MAOIs

Adverse Reactions:
Drowsiness, dizziness, unsteadiness, nausea, vomiting

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48
Q

Phenytoin

A

Dilantin
Tonic-clonic, psychomotor and neurosurgically induced seizures.

Interactions:
Potentiated by acute alcohol ingestion

Warnings/Precautions:
Suicidal tendencies (monitor). Diabetes. Discontinue if acute hepatotoxicity occurs;
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49
Q

Phenytoin Dosage

A

Dilantin

100mg 3 times daily. Increase weekly if needed; max 200mg 3 times daily

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50
Q

topriamate (seizures)

A

Topamax
Initial monotherapy and adjunct in partial-onset or primary generalized tonic-clonic seizures

Interactions:
Contraindicated with metformin during metabolic acidosis condition.

Adverse Reactions:
Paresthesia, anorexia, weight decrease,

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51
Q

phenobarbital

A

Clinically useful as an anti-seizure drug
(phenobarbital, mephobarbital, metharbital)

MOA:
Elevate seizure threshold
Limits the spread of seizure discharge in brain
Binds to a regulatory site on GABA receptor, prolonging the opening of Cl- Channels
Blocks excitatory responses induced by glutamate

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52
Q

ethosuxmide

A

Zarontin

Absent seizures

53
Q

Gabapentin

A

Neurontin
Adjunct in partial seizures.

Renal dysfunction. Suicidal behavior and ideation (monitor).

Interactions:
Potentiates CNS depression with alcohol, morphine, other CNS depressants. Give 2 hrs after antacids

Adverse Reactions:
Somnolence, dizziness, ataxia, fatigue, nystagmus;

54
Q

Gabapentin Dosage

A

Neurontin
Adjunct in partial seizures.

Initially 300mg three times daily. Usual range: 900–1800mg/day in 3 divided doses;

55
Q

pregabalin

A

Lyrica
Adjunct in partial onset seizures

Warnings/Precautions:
Avoid abrupt cessation (taper over ≥1 week).

Interactions:
Potentiates CNS depression with alcohol, other CNS depressants

Adverse Reactions:
Dizziness, somnolence, dry mouth, edema, blurred vision, weight gain,

It is a Controlled Category V drug

Unknown MOA

56
Q

MOA Carbamazepine

A

Na+ channel blocker
binds inactive Na channel
extend inactivation

Main side effect = Hyponatremia

57
Q

MOA Phenytoin

A

Na+ channel blocker
complex actions

Main side effect = Bone demineralization

58
Q

MOA Lamotrigine

A

Na+ channel blocker
selective for excitatory neuron NT like glutamate

Main side effect = Stevens-Johnson Syndrome

59
Q

MOA Ethosuximide

A

Ca2+ Channel blocker
a subunit
T type
Thalamic

60
Q

MOA Phenobarbital

A

GABA antagonist
augments GABA receptor
Cl- Channel

Main side effect = Hyperactivity, addiction, sedation

61
Q

MOA Valproate

A

Many,
Blocks Na+
Enhances GABA
Blocks CA2+

Main side effect = Fetal malformation

62
Q

MOA Topiramate

A

Many,
Blocks Na+
Enhances GABA
Blocks Glutamate NDMA receptor

Main side effect = Cognitive impairment, weight loss, kidney stones

63
Q

MOA Gabapentin

A

Unknown or partially known mechanism

Main side effect = Ankle edema & weight gain

64
Q

MOA Pregabalin

A

Unknown or partially known mechanism

Main side effect = Ankle edema & weight gain

65
Q

fosphenytoin

A

Cerebyx
Control of generalized tonic-clonic status epilepticus.

Contraindications:
Sinus bradycardia, sinoatrial block, or 2ndand 3rddegree A-V block

Boxed Warning:
Cardiovascular risk associated with rapid infusion rates

Interactions:
Potentiated by acute alcohol intake

66
Q

MMSE Scores

A 
Orientation = 5 and 5 = 10
Registration = 3
Attention and calculation = 5
Recall = 3
Language = 9

Total
Mild = 21 or above
Moderate = 10-21
Severe = 9 or less

Alzheimer’s patient expect a 2-4 decrease in points each year

67
Q

For patients with newly diagnosed Alzheimer disease (AD) dementia
(Initial trial treatment)

A

For patients with newly diagnosed Alzheimer disease (AD) dementia, we suggest a trial of a cholinesterase inhibitor.

We also suggest a cholinesterase inhibitor in most patients with newly diagnosed dementia with Lewy bodies (DLB), vascular dementia (VaD), and Parkinson disease (PD) dementia.

The choice is donepezil (Aricept)

68
Q

In patients with moderate to advanced dementia (eg, Mini-Mental State Examination [MMSE] ≤18)
Treatment

A

In patients with moderate to advanced dementia (eg, Mini-Mental State Examination [MMSE] ≤18)

We suggest addingmemantine (10 mg twice daily) to a cholinesterase inhibitor
or
using memantine alone in patients who do not tolerate or benefit from a cholinesterase inhibitor.

69
Q

In patients with severe dementia (MMSE <10)

Treatment

A

In patients with severe dementia (MMSE <10)

We suggest continuingmemantine, given the possibility that memantine may be disease modifying.

However, in some patients with advanced dementia, it may make sense to discontinue administration of medications to maximize quality of life and patient comfort.

70
Q

donepezil

A

Aricept

Warnings/Precautions:
Cardiac conduction conditions

Pharmacologic Class:
Reversible acetylcholinesterase inhibitor (piperidine deriv).

71
Q

donepezil doasge

A

Aricept

Mild-to-moderate: Initially 5mg daily at bedtime, may increase to max 10mg daily after 4–6 weeks; usual dose: 5mg or 10mg once daily.

72
Q

memantine

A

Namenda
Moderate-to-severe dementia of the Alzheimer’s type.

Pharmacologic Class:
NMDA receptor antagonist. N-methyl-D-Aspartic acid receptor antagonist

Interactions:
Caution with other NMDA antagonists (eg, amantadine,

73
Q

Thiamine supplementation should be considered in all patients with??

A

delirium

74
Q

Delirium Treatment

A

Treatment of severe agitation or psychosis with the potential for harm.

In this setting, we suggest using low-dosehaloperidol(0.5 to 1 mg orally [PO] or intramuscularly [IM]).

Other antipsychotic agents (quetiapine,risperidone,ziprasidone,olanzapine) are reasonable alternatives

75
Q

Cerebral Palsy Treatment

A

Management focuses on maximizing the child’s independence in daily functional activities and reducing the extent of disability.

Assessment of the child’s functional status guides treatment selection and allows for monitoring of change over time.

Physical and occupational therapy (PT/OT) are established and vital parts of treatment programs for CP.

PT has an important role in promoting range of motion, positioning, stamina, and coordination, all of which can directly impact mobility and, with more severe forms of CP, transfers

76
Q

Cerebral Palsy Treatment

in Children

A

For children with generalized spasticity, we suggest oral antispasticity drugs as first-line therapy.
(eg,baclofenor benzodiazepines)

77
Q

Baclofen

A 
Pharmacologic Class:
Muscle relaxant (central).

Interactions:
Alcohol and other CNS depressants potentiated.

Adverse Reactions:
Transient drowsiness, confusion, dizziness, weakness, fatigue

78
Q

Baclofen MOA

A

Baclofen (beta-[4-chlorophenyl]-GABA) is an agonist at the beta subunit of gamma-aminobutyric acid on mono and polysynaptic neurons at the spinal cord level and brain.

The thinking is that baclofen reduces the release of excitatory neurotransmitters in the pre-synaptic neurons and stimulates inhibitory neuronal signals in the post-synaptic neurons with resultant relief of spasticity

It is a GABA agonist, and its primary site of action is the spinal cord, where it reduces the release of excitatory neurotransmitters and substance P by binding to the GABA-B receptor.

79
Q

Relapsing-remitting multiple sclerosis (RRMS)

Treatment

A

recommended initial therapy

Intramuscular interferon beta-1a
Subcutaneous interferon beta-1a

80
Q

Interferon beta

A

Avonex
Relapsing forms of multiple sclerosis (MS), to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease.

Warnings/Precautions:
Depression. Suicidal ideation. Pre-existing psychiatric disorders (eg, psychosis). Seizure disorders.

Interactions:
Risk of hepatic injury with concomitant hepatotoxic drugs or alcohol.

Adverse Reactions:
Flu-like symptoms,

81
Q

Interferon beta (Avonex) MOA

A

Unknown
but
this drug does bind to type 1 interferon receptors and activating tyrosine kinase producing antiviral, antiproliferative and immunomodulatory effects

Thought to inhibit T cell activation,
Thought to Prevent T cell proliferation
Thought to block T cell migration across Blood brain barrier
Thought to Reduce CNS inflammation

82
Q

Seizures associated with MS

A

Seizures associated with MS are generally benign and transient, and respond well to antiepileptic drug therapy or require no therapy.

83
Q

For patients with MS who have clinically significant spasticity, we suggest initial treatment with??

A

oralbaclofen

84
Q

dalfampridine

A

Ampyra (Potassium channel blocker.)
To improve walking in patients with multiple sclerosis (demonstrated by an increase in walking speed).

Contraindications:
History of seizures.

85
Q

Myasthenia Gravis Treatment

A

Symptomatic therapy with an acetylcholinesterase inhibitor (pyridostigmine)

Initial symptomatic therapy in patients with MG consists of an acetylcholinesterase inhibitor.

Oralpyridostigmineis the most widely used choice.

Pyridostigmine provides marked improvement in some patients and little or none in others.

In some patients, pyridostigmine is the only therapy ever needed for good control.

86
Q

pyridostigmine

A

Mestinon (Cholinesterase inhibitor)
Myasthenia Gravis

Contraindications:
Intestinal or urinary obstruction.

Warnings/Precautions:
Bronchial asthma.

87
Q

Syncope

Major cardiovascular cause of syncope

A

Autonomic failure

Primary: pure autonomic failure
Parkinson’s, Multiple system atrophy, Lewy Body dementia

Secondary: Diabetes, amyloidosis, spinal cord injuries, auto immune neuropathy, Guillen barre, paraneoplastic neuropathy

88
Q

Traumatic brain injury

A

Patients with severe traumatic brain injury (TBI),

defined by a Glasgow Coma Scale (GCS) score <9,

are most optimally managed in a specialized neurotrauma center

with neurosurgical and neurocritical care support

and the use of guidelines-based standardized protocols.

ED evaluation should include frequent clinical neurologic assessments and a computed tomography (CT) scan of the head.

89
Q

When impending herniation due to elevated ICP is suspected in a patient with severe TBI, we recommend??

A

Empiric interventions including endotracheal intubation

head of bed (HOB) elevation

hyperventilation

and a bolus dose of 23.4 percent sodium chloride ormannitol

pending the results of the CT and measurement of ICP.

90
Q

For patients with moderate TBI (GCS greater than 8 and less than 13) presenting to the ED within three hours of injury, we recommend?

A

Immediate administration oftranexamic acid.

Tranexamic acid (1g infused over 10 minutes,

followed by an intravenous infusion of 1g over eight hours)

is associated with reduced mortality in patients with moderate TBI.

91
Q

mannitol

A

Osmitrol

Contraindications:
Anuria, Severe hypovolemia via dehydration, Pre-existing severe pulmonary vascular congestion or pulmonary edema, Active intracranial bleeding, except during craniotomy; uncorrected electrolyte abnormalities.

92
Q

mannitol dosage

A

0.25 g/kg IV times one infused over 30-60 minutes; may repeat q6-8hr

93
Q

Tranexamic acid

A

cyklokapron
Plasminogen activation inhibitor.

Contraindications:
Acquired defective color vision. Subarachnoid hemorrhage. Active intravascular clotting.

94
Q

Bells Palsy / Facial Palsy
(idiopathic or viral etiology)
Treatment

A

Early treatment with oral glucocorticoids.

Treatment should preferably begin within three days of symptom onset.

Our suggested regimen isprednisone (60 to 80 mg/day) for one week.

For the subgroup of patients with severe facial palsy at presentation, defined as House-Brackmann grade IV or higher. we suggest early combined therapy withprednisone(60 to 80 mg per day) plusvalacyclovir(1000 mg three times daily) for one week rather than glucocorticoids alone.

Acyclovir(400 mg five times daily for 10 days) is an alternative to valacyclovir but is less convenient and has inferior bioavailability.

95
Q

Meds for mild - moderate

Bells palsy

A

House Brackman scale 1-3

Early treatment with Oral glucocorticoids

Prednisone 60-80mg QD x 7 D

96
Q

Meds for Moderate - severe

Bells palsy

A

House Brackman scale 4-6

Early treatment with oral glucocorticoids

Prednisone 60-80mg QD x 7 D

Adjunct treatment with

Valacyclovir 1000mg TiD x 7 D

97
Q

Carpal Tunnel Syndrome

A

For patients with mild to moderate CTS,

effective nonsurgical treatment options for short-term improvement include

splinting, glucocorticoids injected into the carpal tunnel, and oral glucocorticoids.

For patients with CTS who do not have surgery, we suggest either nocturnal wrist splinting in the neutral position or a single glucocorticoid injection as initial therapy.

For nonsurgical patients who fail or decline injection therapy and fail wrist splinting, we suggest treatment with oral glucocorticoids. We useprednisone 20 mg daily for 10 to 14 days.

No NSAIDS for treatment of CTS

98
Q

Complex regional pain syndrome (CRPS)

A

Complex regional pain syndrome (CRPS) is defined as a disorder of the extremities characterized by regional pain that is disproportionate in time or degree to the usual course of any known trauma or other lesion.

Treatment:

  • Ibuprofen400 to 800 mg three times a day ornaproxen250 to 500 mg twice daily
  • An adjunctive medication for neuropathic pain, such asgabapentin,amitriptyline ornortriptyline
  • A short-term bisphosphonate course for patients with early CRPS who have pain and abnormal uptake on bone scan
99
Q

Guillain-Barré syndrome

A

The main modalities of disease modifying therapy for GBS are plasma exchange and intravenousimmune globulin(IVIG).

The treatments are equivalent and improve outcome.

Treatment shortens the time to walking independently by 40 to 50 percent.

For adult patients with GBS, we recommendnottreating with glucocorticoids.

Most patients with GBS have continued progression (ie, worsening) for up to two weeks, followed by a plateau phase of two to four weeks, and then gradual recovery of function

100
Q

Peripheral neuropathy-Most commonly diabetic neuropathy

A

Effective pharmacotherapy options for patients with painful diabetic neuropathy include

serotonin-norepinephrine reuptake inhibitors (SNRIs;duloxetine,venlafaxine),

tricyclic antidepressants (TCAs;amitriptyline,desipramine,nortriptyline)

gabapentinoid antiepileptic drugs (pregabalin,gabapentin).

All have been shown to be more effective than placebo in randomized trials, and limited comparative data suggest that efficacy is similar across agents.

For patients who do not tolerate any of the first-line medications or who prefer nonpharmacologic therapies, we discusscapsaicincream,lidocainepatch, alpha-lipoic acid (ALA), and transcutaneous electrical nerve stimulation (TENS).

101
Q

Which of the following migraine medications is a 5-HT agonist?

Sumatriptan (Imitrex)
Aspirin (ASA)
Acetaminophen (Tylenol)
Propranolol (Inderal)

A

Sumatriptan (Imitrex)

102
Q

Which of the following is a contraindication for the drug sumatriptan (Imitrex)?

Severe renal impairment
History of MI
History of seizures
History of pneumonia

A

History of MI

103
Q

Which of the following is the best treatment for a patient with cluster headaches?

Sumatriptan (Imitrex)
Aspirin (ASA)
Verapamil (Calan)
High-flow Oxygen

A

High-flow Oxygen

104
Q

Which of the following dementia medication is a NDMA receptor antagonist?

Donepezil (Aricept)
Memantine (Namenda)
Rasagiline (Azilect)
Bromocriptine (Parlodel)

A

Memantine (Namenda)

105
Q

Which of the following is the best medication for absence seizures?

Carbemazepine (Tegretol)
Gabapentin (Dilantin)
Ethosuximide (Zarontin)
Pregabalin (Lyrica)

A

Ethosuximide (Zarontin)

106
Q

Which class of controlled substance is pregabalin (Lyrica)?

Class 2
Class 3
Class 4
Class 5

A

Class 5

107
Q

Which medication is considered a GABA antagonist?

Carbemazepine (Tegretol)
Gabapentin (Dilantin)
Phenobarbital (No trade name)
Pregabalin (Lyrica)

A

Phenobarbital (No trade name)

108
Q

Which of the following is a contraindication for the drug, mannitol (Osmitrol)?

Anuria
Hematuria
Dysuria
UTI

A

Anuria

109
Q

Which medication is least likely to help in the treatment for diabetic neuropathy?

Paroxetine (Paxil)
Amitriptyline (Elavil)
Gabapentin (Neurontin)
Duloxetine (Cymbalta)

A

Paroxetine (Paxil)

110
Q

TXA MOA

A

TXA is a synthetic reversible competitive inhibitor to the Lysine receptor found on plasminogen.

The binding of this receptor prevents plasmin (activated form of plasminogen) from binding to and ultimately stabilizing the fibrin matrix

Inhibits Plasmin so clots aren’t broken down as quickly

111
Q

Mannitol MOA

A

Mannitol then constitutes a new solute in the plasma, which increases the tonicity of the plasma.

Since mannitol cannot cross the intact blood-brain barrier, the increased tonicity from the mannitol draws water out of the brain parenchyma and into the intravascular space.

The water then travels with the mannitol to the kidneys, where it gets excreted in the urine.

The mannitol causes the cells in the brain to dehydrate mildly.

The water inside the brain cells (intracellular water) leaves the cells and enters the bloodstream as the mannitol draws it out of the cells and into the bloodstream.

Once in the bloodstream, the extra water is whisked out of the skull.

When the mannitol gets to the kidneys, the kidneys filter the mannitol into the urine.

The mannitol again draws the water with it, and diuresis (increased urination) ensues.

112
Q

Mestinon MOA

A

Mestinon (pyridostigmine) inhibits the destruction of acetylcholine by cholinesterase and thereby permits freer transmission of nerve impulses across the neuromuscular junction

113
Q

Namenda MOA

A

Memantine is an uncompetitive antagonist of the NMDA subtype of glutamate receptors in the CNS.

Alzheimer disease is believed to be caused by overstimulation of glutamate, the primary excitatory amino acid in the CNS, resulting in excitotoxicity and neuronal degeneration.

The NMDA receptor is a voltage-gated cation channel that in the physiologic unstimulated state is blocked by magnesium ions.

Stimulated magnesium is displaced allowing calcium influx and activation.

In Alzheimer disease, there is pathologic overstimulation of the receptor causing it to be in a chronically active state.

Memantine helps to counteract the excessive stimulation.[1]

It has no activity at the GABA, benzodiazepine, dopamine, adrenergic, histamine, or glycine receptors

114
Q

TPA Alteplase MOA

A

Alteplase is a fibrinolytic agent;

it also is referred to as tissue plasminogen activator (tPA).

Alteplase converts plasminogen to the proteolytic enzyme plasmin,
which lyses fibrin as well as fibrinogen

tPA is a thrombolytic (i.e., it breaks up blood clots) formed by aggregation of activated platelets into fibrin meshes by activating plasminogen

115
Q

MAO-B Inhibitor MOA

A

Monoamine oxidase B (MAOB) is an enzyme involved in the metabolism of dopamine.

It converts dopamine to its corresponding carboxylic acid via an aldehyde intermediate.

MAOB regulates both the free intraneuronal concentration of dopamine and the releasable stores.

MAOB inhibitors bind to and inhibit MAOB, preventing dopamine degradation.

This results in greater stores of dopamine available for release.

MAOB inhibitors are used in the treatment of depression.

People with depression have higher levels of the brain protein MAOB than people without depression.

116
Q

MAO-B Inhibitor MOA

A

MAOB inhibitors bind to and inhibit MAOB, preventing dopamine degradation. breakdown
This results in greater stores of dopamine available for release.

MAOB inhibitors are used in the treatment of depression.

People with depression have higher levels of the brain protein MAOB than people without depression.

Stops Dopamine breakdown and reuptake

117
Q

Dopamine agonists MOA

A

Bromocriptine (ergot)
Pramipexole (non-ergot)
Ropinirole (non-ergot)

All mimic dopamine and can activate dopamine receptors

118
Q

Acetylcholine

A

Main neurotransmitter in neuromuscular junctions

Responsible for muscle contractions

119
Q

Cluster headache prophylaxis

A

Beta blockers (Propranolol 60-320mg QD)

Anticonvulsants (Topiramate 25-100mg QD)

120
Q

Broad spectrum anti seizure meds

A

Lamotrigine
Depakote
Topamax

121
Q

Narrow spectrum anti seizure meds

A 
Carbamazepine
phenytoin
gabapentin
pregabalin (Cat 5)
phenobarbital
primidone (barb)
122
Q

Med for status epilepticus

A

fosphenytoin

123
Q

Absent seizures med

A

Ethosuximide

124
Q

Enzyme inducing anti seizure meds

A

Carbamazepine
Phenobarbital
Phenytoin
Oxcarbamazepine

125
Q

Memantine plus Donepezil

A 
Namzaric
inhibits ACH breakdown 
NMDA antagonist (binds NMDA, blocks glutamate)
126
Q

Barbiturates Side effects

A

CNS depressants

hypotension, cardiovascular and respiratory depression.

should be limited to patients not tolerating other meds

127
Q

Na+ blockers

A 
Carbamazepine
Phenytoin
Topiramate
Depakote
lamotrigine
128
Q

Ca+ blockers

A

ethosuximide
Depakote
nimodipine

PAM Semester 2 (22 decks)

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