Pharm Neuro Exam Flashcards
(128 cards)
1
Q
Headache types
A
Tension
Migraine
Cluster
2
Q
Treatment for Tension Headaches (General)
A
OTC Pain Meds
Prescription Meds like Tricyclics
Consistent sleep schedule
Regular Exercise and stress relieving activities
3
Q
Treatment for Migraine Headaches (General)
A
Rescue medication to relieve pain and stop migraine
Preventative medication to avoid future migraines
4
Q
Treatment for Cluster Headaches (General)
A
Lifestyle changes
Oxygen treatment
Prescription meds such as verapamil, prednisone, or lithium
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
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)
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
8
Q
Triptan meds for migraines
A
Sumatriptan (Imitrex) rizatriptan eletriptan almotriptan zolmitriptan naratriptan frovatriptan
All end in -triptan
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
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.
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).
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).
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
14
Q
Ergots
A
Both ergotamine and dihydroegotamine (DHE 45) bind to 5HT1b/d receptors,
(Same as triptans)
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),
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
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
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)
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
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
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,
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
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.
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
25
MOA of medications used to treat Parkinsons
COMT
Inhibitors preserve Levodopa
Levodopa
Replaces dopamine
Dopamine
Agonists mimic dopamine
MAO-B
Inhibitors preserve existing dopamine
26
Type B MAO-B Inhibitors
Rasagiline (Azilect)
safinamide (Xadago)
selegiline (Eldepryl or Zelapar)
Inhibitors breakdown dopamine
27
MAO-B Inhibitors MOA
Inhibit degradation of dopamine
Increase efficacy of levodopa by 20%
Reduce "off" time
May increase dyskinesia
May have neuroprotective properties
28
amantidine
Symmetrel
Mild anticholinergic (anticholinergic side effects)
great for younger patients with tremor
29
levodopa
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.
30
Levodopa effects
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.
31
carbidopa/levodopa
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.
32
COMT inhibitors
Cathecholamine-O-methyltransferase inhibitors
Tolcapone (tasmar)
entacapone (Comtan)
Both are adjuncts to Sinemet
Both end in -capone
33
Tolcapone
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)
```
34
Huntington disease (general)
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 with tetrabenazine (Xenazine)
35
tetrabenazine
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
36
VMAT 2 Inhibitor
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 less inhibition of the stop signal there
37
Tourette Syndrome
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 with tetrabenazine.
Alternatives include fluphenazine or risperidone
Medication options that treat both tics and ADHD include the alpha adrenergic agonists guanfacine or clonidine.
38
What is the first line treatment for eligible patients with acute ischemic stroke?
Intravenous Alteplase Therapy (TPA)
39
Alteplase Dosage
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
40
Alteplase
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
41
Alteplase MOA
Directly activates plasminogen to form plasmin leading to clot lysis
42
TIA Treatment
ASA
Plavix
ticlopidine
ASA/dipyridamole
43
Nimodipine
Calcium Channel Blocker
(dihydropyridine)
Used after sub-arachnoid hemorrhage to reduce cerebral vascular vasospasm
Adverse:
Decrease blood pressure, GI upset, Headache, Bradycardia, Flushing, Edema
44
Nimodipine MOA
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
45
Seizures
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 diet is a special high-fat, low-carbohydrate diet that helps to control seizures in some people with epilepsy.
In general, enzyme-inducing anti-seizure drugs are the most problematic for interactions with drugs such as warfarin
(eg, phenytoin, carbamazepine, phenobarbital, oxcarbazepine)
Control seizures, Quality of life, avoid side effects, keto diet, interacts with warfarin
46
Lamotrigine
Lamictal
Adjunct in partial seizures
Box warning: Sever skin rashes
Adverse: Stevens-Johnson syndrome
47
Carbamazepine
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
48
Phenytoin
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;
```
49
Phenytoin Dosage
Dilantin
100mg 3 times daily. Increase weekly if needed; max 200mg 3 times daily
50
topriamate (seizures)
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,
51
phenobarbital
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
52
ethosuxmide
Zarontin
Absent seizures
53
Gabapentin
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
Gabapentin Dosage
Neurontin
Adjunct in partial seizures.
Initially 300mg three times daily. Usual range: 900–1800mg/day in 3 divided doses;
55
pregabalin
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
MOA Carbamazepine
Na+ channel blocker
binds inactive Na channel
extend inactivation
Main side effect = Hyponatremia
57
MOA Phenytoin
Na+ channel blocker
complex actions
Main side effect = Bone demineralization
58
MOA Lamotrigine
Na+ channel blocker
selective for excitatory neuron NT like glutamate
Main side effect = Stevens-Johnson Syndrome
59
MOA Ethosuximide
Ca2+ Channel blocker
a subunit
T type
Thalamic
60
MOA Phenobarbital
GABA antagonist
augments GABA receptor
Cl- Channel
Main side effect = Hyperactivity, addiction, sedation
61
MOA Valproate
Many,
Blocks Na+
Enhances GABA
Blocks CA2+
Main side effect = Fetal malformation
62
MOA Topiramate
Many,
Blocks Na+
Enhances GABA
Blocks Glutamate NDMA receptor
Main side effect = Cognitive impairment, weight loss, kidney stones
63
MOA Gabapentin
Unknown or partially known mechanism
Main side effect = Ankle edema & weight gain
64
MOA Pregabalin
Unknown or partially known mechanism
Main side effect = Ankle edema & weight gain
65
fosphenytoin
Cerebyx
Control of generalized tonic-clonic status epilepticus.
Contraindications:
Sinus bradycardia, sinoatrial block, or 2nd and 3rd degree A-V block
Boxed Warning:
Cardiovascular risk associated with rapid infusion rates
Interactions:
Potentiated by acute alcohol intake
66
MMSE Scores
```
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
For patients with newly diagnosed Alzheimer disease (AD) dementia
(Initial trial treatment)
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
In patients with moderate to advanced dementia (eg, Mini-Mental State Examination [MMSE] ≤18)
Treatment
In patients with moderate to advanced dementia (eg, Mini-Mental State Examination [MMSE] ≤18)
We suggest adding memantine (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
In patients with severe dementia (MMSE <10)
| Treatment
In patients with severe dementia (MMSE <10)
We suggest continuing memantine, 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
donepezil
Aricept
Warnings/Precautions:
Cardiac conduction conditions
Pharmacologic Class:
Reversible acetylcholinesterase inhibitor (piperidine deriv).
71
donepezil doasge
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
memantine
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
Thiamine supplementation should be considered in all patients with??
delirium
74
Delirium Treatment
Treatment of severe agitation or psychosis with the potential for harm.
In this setting, we suggest using low-dose haloperidol (0.5 to 1 mg orally [PO] or intramuscularly [IM]).
Other antipsychotic agents (quetiapine, risperidone, ziprasidone, olanzapine) are reasonable alternatives
75
Cerebral Palsy Treatment
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
Cerebral Palsy Treatment
| in Children
For children with generalized spasticity, we suggest oral antispasticity drugs as first-line therapy.
(eg, baclofen or benzodiazepines)
77
Baclofen
```
Pharmacologic Class:
Muscle relaxant (central).
```
Interactions:
Alcohol and other CNS depressants potentiated.
Adverse Reactions:
Transient drowsiness, confusion, dizziness, weakness, fatigue
78
Baclofen MOA
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
Relapsing-remitting multiple sclerosis (RRMS)
| Treatment
recommended initial therapy
Intramuscular interferon beta-1a
Subcutaneous interferon beta-1a
80
Interferon beta
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
Interferon beta (Avonex) MOA
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
Seizures associated with MS
Seizures associated with MS are generally benign and transient, and respond well to antiepileptic drug therapy or require no therapy.
83
For patients with MS who have clinically significant spasticity, we suggest initial treatment with??
oral baclofen
84
dalfampridine
Ampyra (Potassium channel blocker.)
To improve walking in patients with multiple sclerosis (demonstrated by an increase in walking speed).
Contraindications:
History of seizures.
85
Myasthenia Gravis Treatment
Symptomatic therapy with an acetylcholinesterase inhibitor (pyridostigmine)
Initial symptomatic therapy in patients with MG consists of an acetylcholinesterase inhibitor.
Oral pyridostigmine is 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
pyridostigmine
Mestinon (Cholinesterase inhibitor)
Myasthenia Gravis
Contraindications:
Intestinal or urinary obstruction.
Warnings/Precautions:
Bronchial asthma.
87
Syncope
| Major cardiovascular cause of syncope
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
Traumatic brain injury
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
When impending herniation due to elevated ICP is suspected in a patient with severe TBI, we recommend??
Empiric interventions including endotracheal intubation
head of bed (HOB) elevation
hyperventilation
and a bolus dose of 23.4 percent sodium chloride or mannitol
pending the results of the CT and measurement of ICP.
90
For patients with moderate TBI (GCS greater than 8 and less than 13) presenting to the ED within three hours of injury, we recommend?
Immediate administration of tranexamic 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
mannitol
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
mannitol dosage
0.25 g/kg IV times one infused over 30-60 minutes; may repeat q6-8hr
93
Tranexamic acid
cyklokapron
Plasminogen activation inhibitor.
Contraindications:
Acquired defective color vision. Subarachnoid hemorrhage. Active intravascular clotting.
94
Bells Palsy / Facial Palsy
(idiopathic or viral etiology)
Treatment
Early treatment with oral glucocorticoids.
Treatment should preferably begin within three days of symptom onset.
Our suggested regimen is prednisone (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 with prednisone (60 to 80 mg per day) plus valacyclovir (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
Meds for mild - moderate
| Bells palsy
House Brackman scale 1-3
Early treatment with Oral glucocorticoids
Prednisone 60-80mg QD x 7 D
96
Meds for Moderate - severe
| Bells palsy
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
Carpal Tunnel Syndrome
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 use prednisone 20 mg daily for 10 to 14 days.
No NSAIDS for treatment of CTS
98
Complex regional pain syndrome (CRPS)
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:
* Ibuprofen 400 to 800 mg three times a day or naproxen 250 to 500 mg twice daily
* An adjunctive medication for neuropathic pain, such as gabapentin, amitriptyline or nortriptyline
* A short-term bisphosphonate course for patients with early CRPS who have pain and abnormal uptake on bone scan
99
Guillain-Barré syndrome
The main modalities of disease modifying therapy for GBS are plasma exchange and intravenous immune 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 recommend not treating 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
Peripheral neuropathy-Most commonly diabetic neuropathy
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 discuss capsaicin cream, lidocaine patch, alpha-lipoic acid (ALA), and transcutaneous electrical nerve stimulation (TENS).
101
Which of the following migraine medications is a 5-HT agonist?
Sumatriptan (Imitrex)
Aspirin (ASA)
Acetaminophen (Tylenol)
Propranolol (Inderal)
Sumatriptan (Imitrex)
102
Which of the following is a contraindication for the drug sumatriptan (Imitrex)?
Severe renal impairment
History of MI
History of seizures
History of pneumonia
History of MI
103
Which of the following is the best treatment for a patient with cluster headaches?
Sumatriptan (Imitrex)
Aspirin (ASA)
Verapamil (Calan)
High-flow Oxygen
High-flow Oxygen
104
Which of the following dementia medication is a NDMA receptor antagonist?
Donepezil (Aricept)
Memantine (Namenda)
Rasagiline (Azilect)
Bromocriptine (Parlodel)
Memantine (Namenda)
105
Which of the following is the best medication for absence seizures?
Carbemazepine (Tegretol)
Gabapentin (Dilantin)
Ethosuximide (Zarontin)
Pregabalin (Lyrica)
Ethosuximide (Zarontin)
106
Which class of controlled substance is pregabalin (Lyrica)?
Class 2
Class 3
Class 4
Class 5
Class 5
107
Which medication is considered a GABA antagonist?
Carbemazepine (Tegretol)
Gabapentin (Dilantin)
Phenobarbital (No trade name)
Pregabalin (Lyrica)
Phenobarbital (No trade name)
108
Which of the following is a contraindication for the drug, mannitol (Osmitrol)?
Anuria
Hematuria
Dysuria
UTI
Anuria
109
Which medication is least likely to help in the treatment for diabetic neuropathy?
Paroxetine (Paxil)
Amitriptyline (Elavil)
Gabapentin (Neurontin)
Duloxetine (Cymbalta)
Paroxetine (Paxil)
110
TXA MOA
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
Mannitol MOA
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
Mestinon MOA
Mestinon (pyridostigmine) inhibits the destruction of acetylcholine by cholinesterase and thereby permits freer transmission of nerve impulses across the neuromuscular junction
113
Namenda MOA
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
TPA Alteplase MOA
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
MAO-B Inhibitor MOA
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
MAO-B Inhibitor MOA
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
Dopamine agonists MOA
Bromocriptine (ergot)
Pramipexole (non-ergot)
Ropinirole (non-ergot)
All mimic dopamine and can activate dopamine receptors
118
Acetylcholine
Main neurotransmitter in neuromuscular junctions
Responsible for muscle contractions
119
Cluster headache prophylaxis
Beta blockers (Propranolol 60-320mg QD)
Anticonvulsants (Topiramate 25-100mg QD)
120
Broad spectrum anti seizure meds
Lamotrigine
Depakote
Topamax
121
Narrow spectrum anti seizure meds
```
Carbamazepine
phenytoin
gabapentin
pregabalin (Cat 5)
phenobarbital
primidone (barb)
```
122
Med for status epilepticus
fosphenytoin
123
Absent seizures med
Ethosuximide
124
Enzyme inducing anti seizure meds
Carbamazepine
Phenobarbital
Phenytoin
Oxcarbamazepine
125
Memantine plus Donepezil
```
Namzaric
inhibits ACH breakdown
NMDA antagonist (binds NMDA, blocks glutamate)
```
126
Barbiturates Side effects
CNS depressants
hypotension, cardiovascular and respiratory depression.
should be limited to patients not tolerating other meds
127
Na+ blockers
```
Carbamazepine
Phenytoin
Topiramate
Depakote
lamotrigine
```
128
Ca+ blockers
ethosuximide
Depakote
nimodipine
