Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M3 - Clerkships > Neurology Clerkship > Flashcards

Neurology Clerkship Flashcards

1
Q

What is the workup for potentially reversible causes of cognitive impairment?

A
  1. neuropsychological testing (eg. MOCA)
  2. lab testing (CBC, Vitamin B12, TSH, CMP)
  3. neuroimaging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Huntington Disease
1. Motor features
2. Psychiatric features
3. Cognitive

A
  1. Chorea
  2. depression, irritability, psychosis, obsessive compulsive symptoms
  3. Executive dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Wallenburg Syndrome
1. Location
2. Presentation

A
  1. Lateral medulla
  2. Ipsilateral CN deficits and contralateral deficits of the body.
    – Vestibular nucleus (causes vertigo)
    – Spinal trigeminal nucleus (loss of pain and temp in the face)
    –Spinothalamic tract (loss of sensation on the contralateral side of the body)
    – Descending sympathetic nervous system fibers that travel close to spinothalamic tract (Horner syndrome)
    – Inferior cerebellar peduncle (ataxia)
    – Nucleus ambiguus (diminished gag reflex, dysphagia, dysphonia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cauda Equina Syndrome (CES)
1. What is it?
2. Location in spine
3. Symptoms
4. What is diagnostic?

A
  1. medical emergency caused by compression of >= 2 spinal nerve roots in the lumbar cistern
  2. L2-L5, S1-S5 and the coccygeal nerve
  3. Severe Radicular pain (in one or both legs) PLUS : motor deficits in affected myotome (classically unilateral but sometimes bilateral) with LMN pattern (diminished reflexes); Patchy sensory loss (saddle anesthesia), Rectal sphincter and bladder dysfunction due to compression of S3-S5
  4. MRI - then surgical decompression within 24-48 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Conus Medullaris Syndrome
1. Presentation
2. Vertebral level
3. Physical exam

A
  1. L1-L2
  2. UMN (tracts of lumbosacral cord), severe low back pain, bowel/bladder dysfunction
  3. motor weakness symmetric, Hyperreflexia (UMN), symmetric perianal numbness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the classic triad of Wernicke encephalopathy (WE)
–How is it treated?

A
  1. encephalopathy, ocular dysfunction, and gait ataxia
  2. Give thiamine along or before glucose. Giving glucose before thiamine can precipitate or worsen WE.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Amyotrophic lateral sclerosis (ALS) results form deterioration of what?

A

UMN and LMN
- UMN can be cotricospinal neurons located in primary motor cortex
-LMN can be cranial nerves, anterior horn cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • Early, insidious short-term memory loss
    -Language deficits & spatial disorientation
    -Later personality changes

What Dementia subtype is this?

A

Alzheimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • Stepwise decline
  • Early executive dysfunction
  • Cerebral infarction &/or deep white matter changes on neuroimaging

What Dementia subtype is this?

A

Vascular Dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • Early personality changes
  • Apathy, disinhibition & compulsive behavior
  • Frontotemporal atrophy on neuroimaging

What Dementia subtype is this?

A

Frontotemporal Dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • Visual hallucinations
  • Spontaneous parkinsonism
  • Fluctuating cognition
  • Rapid eye movement behavior disorder

What Dementia subtype is this?

A

Dementia with Lewy Bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Ataxia early in disease
  • Urinary incontinence
  • Dilated ventricles on neuroimaging

What Dementia subtype is this?

A

Normal pressure hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • Behavioral changes
  • Rapid progression
  • Myoclonus with startle &/or seizures

What Dementia subtype is this?

A

Prion Disease

Real time quaking induced conversion testing of CSF is a test for Creutzfeldt-Jakob disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

L2-L4 Radiculopathy
1. reflex affected
2. sensory loss
3. weakness

A
  1. Patellar
  2. Anteromedial thigh, Medial shin
  3. Hip flexion (iliopsoas), Hip adduction, Knee extension (quadriceps)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

L5 Radiculopathy
1. reflex affected
2. sensory loss
3. weakness

A
  1. None
  2. Lateral shin, Dorsum of the foot
  3. Foot dorsiflexion & inversion (tibialis anterior), Foot eversion (peroneus), Toe extension (extensor hallucis & digitorum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

S1 Radiculopathy
1. reflex affected
2. sensory loss
3. weakness

A
  1. Achilles
  2. Posterior Calf, Sole and lateral foot
  3. Hip extension (gluteus maximus), Knee flexion (hamstrings), Foot plantarflexion (gastrocnemius)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

S2-S4 Radiculopathy
1. reflex affected
2. sensory loss
3. weakness

A
  1. Anocutaneous
  2. Perineum
  3. Urinary or fecal incontinence, Sexual dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hemorrhagic stroke
-After assessment of the ABCs what steps are taken to reduce risk of brain herniation

A
  1. blood pressure control (intravenous nicardipine or labetalol)
  2. Reversal of anticoagulation: Vitamin K is given for those on warfarin and protamine sulfate to patients on heparin
  3. Regulation of ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Craniopharyngioma
1. age distribution
2. clinical features

A
  1. bimodal (5-14 and 50-75)
  2. optic chiasm compression (bitemporal hemianopsia), pituitary stalk compression which leads to endocrinopathies (Growth failure in children (↓ TSH or ↓ GH); Pubertal delay in children or sexual dysfunction in adults (↓ LH & FSH); Diabetes insipidus (↓ ADH))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is progressive multifocal leukoencephalopathy?

A

Reactivation of JC virus especially those immunocompromised (CD4 <200). Reactivated virus spreads to the CNS and lyses oligodendrocytes causing white matter demyelination.

Symptoms include altered mental status, motor deficits, ataxia, and vision abnormalities (eg, diplopia). CT of the brain with contrast usually reveals asymmetric, nonenhancing, hypodense white matter lesions with no surrounding edema. Diagnosis requires lumbar puncture with cerebral spinal fluid evidence of JC virus (by polymerase chain reaction); brain biopsy is rarely required. There is no specific treatment for PML, but initiation of antiretroviral therapy (in patients with AIDS) can sometimes prevent progression and death. However, most patients have long-term neurologic sequalae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

-Action tremor
-Bilateral hands &/or head
- Improves with alcohol

What type of tremor is this?

A

Essential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

-increases as hand reaches target
- Associated ataxia, dysmetria, or gait disorder

What type of tremor is this?

A

Cerebellar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  • Action & rest tremor
  • Low amplitude, high frequency (ie, “fine” tremor)
  • Not visible under normal circumstances
  • Enhanced with sympathetic activation (eg, anxiety, caffeine, hyperthyroidism)

What type of tremor is this?

A

Physiologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the difference between tremor due to lithium toxicity and lithium-enhanced physiologic tremor

A

Tremor due to lithium toxicity: an irregular, coarse tremor involving multiple parts of the body (not just the hands) accompanied by gastrointestinal or additional neurologic symptoms. Lithium toxicity requires treatment (eg, hydration, hemodialysis)

Lithium-enhanced physiologic tremor is often managed with watchful waiting and modification of aggravating factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cocaine use can precipitate intracranial hemorrhage and should be suspected when stroke occurs in a subcortical location (like thalamus) and/or young patients.

  1. what indications can tell you cocaine use might be the cause of stroke?
A
  1. young age, absence of typical risk factors, sympathetic activation, subcortical location of strokes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common brain tumor in children?

A
  1. low grade astrocytoma (e.g. pilocytic astrocytoma at cerebellum) - are benign and slow growing causing symptoms to develop over many months.

** High grade astrocytomas (eg. glioblastomas) - malignant and much less common. This would cause symptoms over days to weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Medulloblastoma
1. where does it arise
2. symptoms it causes

A
  1. posterior fossa at the cerebellar vermis
  2. ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What drug types can induce symptoms of parkinsonism?

A
  1. antipsychotics (haloperidol, risperidone)
  2. antiemetics (metoclopramide, prochlorperazine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Ankylosing spondylitis
1. age of onset
2. relieved with what?
3. symptoms
4. exam findings and complications
5. associated with what HLA
6. imaging you would want

A
  1. <40
  2. exercise but not rest
  3. noturnal pain, reduced range of motion
  4. Arthritis (sacroiliitis), Reduced chest expansion & spinal mobility, Enthesitis (tenderness at tendon insertion sites), Dactylitis (swelling of fingers & toes), Uveitis
    –complications: Osteoporosis/vertebral fractures, Aortic regurgitation, Cauda equina syndrome
  5. HLA-B27
  6. Xray of sacroiliac joints or MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

saccular aneurysm at the posterior communicating artery induces what type of palsy?

A
  1. Oculomotor N (CN III) palsy - pupillary dilation due to loss of parasympathetic innervation, ptosis and down and out eye positioning due to loss of somatic innervation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

saccular aneurysm at the internal carotid or anterior communicating artery induces what type of palsy?

A
  1. Optic nerve (CN II) palsy - unilateral vision loss and bitemporal hemianopsia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

saccular aneurysm at the superior cerebellar artery induces what type of palsy?

saccular aneurysm at the AICA induces what type of palsy?

A
  1. trochlear nerve (CN IV) palsy
  2. abducens nerve (CN VI) palsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Alcoholic cerebellar degeneration
1. what are the manifestations in this?

A
  1. wide based gait and postural instability (inability to tandem gait, abnormal heel-knee shin testing)
    *relatively preserved limb coordination.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Friedreich Ataxia (FA)
1. inheritance pattern
2. symptoms
3. comorbidities
4. genetic mutation

A
  1. autosomal recessive
  2. progressive ataxia in adolescence, dysarthria, limb weakness, loss of deep tendon reflexes, loss of position and vibratory senses (deterioration of dorsal spinal column)
  3. kyphoscoliosis, pes cavus, hypertrophic cardiomyopathy, increased risk of arrhythmia and heart failure, death by age 40
  4. repeat GAA in frataxin gene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
  1. What is amaurosis fugax?
  2. what is the cause
  3. What testing/imaging should be done?
A
  1. painless, rapid, and transient (<10 minutes) monocular vision loss. Description of a curtain descending over the visual field is highly suggestive of this.
  2. retinal ischemia due to atherosclerotic emboli originating from the ipsilateral carotid artery
  3. duplex ultrasound of the neck
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

When a pt comes in for eval of headache what warning signs should lead to consideration of early imaging?

A
  1. neurologic findings: seizure, changes in consciousness, specific deficits
  2. differences compared to prior headaches
  3. other: new at age >40, sudden onset, trauma, present on awakening.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What vitamin do newborns need to avoid ICH

A

Newborns who do not receive intramuscular vitamin K are at risk of vitamin K deficiency bleeding, which presents with easy bruising or bleeding, including intracranial hemorrhage (ICH). ICH can cause obstructive hydrocephalus, leading to a bulging fontanelle, upward gaze impairment, and signs of increased intracranial pressure (eg, irritability, vomiting, bradycardia, hypertension).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What triad is in normal pressure hydrocephalus?
what is the treatment?

A
  1. urinary incontinence, cognitive impairment, gait abnormalities - all 3 are not required for dx, only gait dysfunction. UMN signs may also occur
  2. high volume lumbar puncture - confirms dx. then shunt can be put in place.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Fluoxetine, paroxetine, sertraline, fluvoxamine, escitalopram and citalopram

  • what drugs are these?
A

SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What can SSRIs be used for?

A
  1. major depression
  2. anxiety
  3. OCD
  4. eating disorders
  5. motor recovery after stroke
  6. premenstrual dysmorphic disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Venlafaxine, desvenlafaxine, duloxetine, milnacipran, and levomilnacipram

  • what drugs are these?
A

SNRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What can SNRIs be used for?

A
  1. Depression
  2. Generalized anxiety disorder
  3. Duloxetine can be used to treat diabetic neuropathy
  4. Venlafaxine can be used for panic disorder and social anxiety disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Lithium clinical uses

A
  1. bipolar disorder
  2. in combination with other meds it can treat schizoaffective disorder, schizophrenia, refractory depression, and other mood disorders with psychotic features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Lithium typical side effects?

A
  1. fine hand tremor
  2. hypothyroidism
  3. nephrogenic diabetes insipidus caused by ADH antagonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are TCAs MOA?

A
  1. block reuptake of NE and 5HT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are clinical uses of TCAs?

A
  1. major depression
  2. panic disorder
  3. enuresis
  4. fibromyalgia
  5. chronic pain disorders
  6. neuropathic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Despiramine, Nortriptyline, imipramine, clomipramine, amitriptyline, amoxapine, and doxepin

What drug type are these?

A

tricyclic anti depressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Tranylcypromine, phenelzine, selegiline, and isocarboxazid

  • what drug type are these?
A

Monoamine Oxidase Inhibitors (MAOIs)

  • to increase seretonin, dopamine, and NE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Clinical uses of MAOIs?

A
  1. Atypical depression
  2. Depression resistant to first and second line medication
  3. specific phobias
  4. panic disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Haloperidol, trifluoperazine, loxapine, perphenazine, pimozide, thiothixene, fluphenazine, chlorpromazine, and thioridazine

  • what drug type are these?
A

1st generation antipsychotics (Typical anti-psychotic agents)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

1st generation antipsychotics (Typical anti-psychotic agents)

  • mechanism of action?
A

Blocking postsynaptic dopamine D2 receptor in the limbic system of brain - to decrease response of postsynaptic membrane to dopamine excitation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

1st generation antipsychotics (Typical anti-psychotic agents)

  • Clinical uses?
A
  1. Used to treat positive symptoms of schizophrenia (e.g. delusions, hallucinations)
  2. bipolar disorder
  3. and tourette syndrome

—Haloperidol is used to delirium and agitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

1st generation antipsychotics (Typical anti-psychotic agents)

  • Side effects?
A
  1. Sedation (due to histamine blockade)
  2. Anti-cholinergic side effects (dry mouth, urinary retention, blurry vision)
  3. Extrapyramidal system side effects (acute dystonia/muscle spasms, akinesia, akathisia/motor restlessness, and tardive dyskinesia/involuntary oral facial movements)
  4. Galactorrhea
  5. Amenorrhea
  6. Hyperprolactinemia

*some patients can develop neuroleptic malignant syndrome - muscle rigidity, change in mental status, elevated temp, and autonomic instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Clozapine, risperidone, olanzapine, ziprasidone, aripiprazole, quetiapine, asenapine, ilioperidone, lurasidone, and paliperidone

  • What drug type is this?
A

2nd generation antipsychotics (Atypical anti-psychotic agents)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

2nd generation antipsychotics (Atypical anti-psychotic agents)

  • mechanism of action?
A

block both 5HT and dopamine receptors but less affinity to dopamine receptors compared to 1st gen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

2nd generation antipsychotics (Atypical anti-psychotic agents)

  • clinical uses?
A
  1. Treat positive and negative symptoms of schizophrenia
  2. Bipolar disorder and other psychotic disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Mirtazapine
-mechanism of action

A

alpha2, 5HT2, and 5HT3 receptor antagonist thereby increasing sympathetic tone and increasing the release of serotonin and norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Mirtazapine
-clinical uses

A
  1. Depressive disorders
  2. Generalized anxiety disorder, especially in underweight patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Trazadone
- mechanism of action?

A
  1. inhibits reuptake of seretonin, also blocks 5-HT, alpha1, and H1 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Trazadone
- clinical uses?

A
  1. insomnia
  2. major depressive disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Triazolam, midazolam, lorazepam, temazepam, oxazepam, alprazolam, chlordiazepoxide, diazepam, clonazepam, flurazepam

what type of drugs are these?

A

Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Benzodiazepines

What is the mechanism of action?

A

Enhanced GABA A receptor activation results in increased flow of chloride ion thereby leading to hyperpolarization.

-Decreased activity of the neurons of the limbic, thalamic, and hypothalamic regions of CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Benzodiazepines

What is the clinical use?

A
  1. acute anxiety
  2. seizures
  3. status epilepticus
  4. alcohol withdrawal
  5. Midazolam and diazepam are also used as anesthetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Phenobarbital, thiopental, secobarbital, amobarbital, and pentobarbital

-Type of drug?

A

Barbiturates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Barbiturates
- mechanism of action?

A

Potentiate GABA A receptor activity in the brain, which leads to cell membrane hyperpolarization and decreased activity of CNS neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Barbiturates
- clinical uses?

A
  • sedative (anxiety and insomnia)
  • thiopental has been used for induction of anesthesia
    -phenobarbital is used for management of seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Phenytoin
1. mechanism of action
2. clinical uses

A
  1. decrease flow of sodium and calcium ions - thereby resulting in decreased polarization of the cells of the NS
  2. simple and complex partial seizures
    - generalized tonic-clonic seizures (grand mal)
    -status epilepticus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Phenytoin
1. side effects?

A
  1. Cerebellar dysfunction: Nystagmus (Horizontal), ataxia, dysmetria
  2. slurred speech
  3. n/v
  4. Hyperreflexia
  5. altered mental status, coma, paradoxical seizures, and death
  6. Gingival hyperplasia
  7. Drug induced lupus
  8. Folic acid deficiency - impairs folic acid absorption in the jejunum

Pancytopenia
Arrhythmia
Liver injury
Teratogen
Induce of CYP 450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Lamotrigine
1. Mechanism of action
2. Clinical uses

A
  1. Block fast voltage activated sodium channels at the presynaptic neuron - thereby decreasing the release of glutamate and aspartate at the neuronal synapse
  2. Epilepsy (simple and complex partial seizures and generalized tonic-clonic seizures)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Valproic Acid
1. clinical uses

A
  1. Generalized tonic-clonic seizures
  2. Myoclonic seizures
  3. Absence seizures
  4. Treatment of mania
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Ethosuximide
1. clinical uses

A
  1. treatment of absence seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Carbamazepine
1. Mechanism of action
2. Clinical uses

A
  1. Inhibiting the flow of sodium ions through sodium channels on neural cell membranes - thereby causing hyperpolarization and decreased activity of the neuron
  2. Simple seizures, complex partial seizures, trigeminal neuralgia, and generalized tonic clonic seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Topiramate
1. Mechanism of action
2. Clinical use

A
  1. Block the flow of sodium ions through voltage gated sodium channels - causing hyperpolarization
  2. Epilepsy and prophylaxis for migraine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Tiagabine
1. Mechanism of action
2. clinical uses

A
  1. Inhibit the reuptake of GABA - thereby potentiating effect of GABA (inhibitory)
  2. partial seizures (in combination with other drugs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Vigabatrin
1. clinical uses

A
  1. Infantile spasms in children -
  2. Refractory complex partial seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Levetiracetam
1. clinical uses

A
  1. partial seizures
  2. myoclonic seizures
  3. tonic clonic seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Halothane, isoflurane, desflurane, sevoflurane, enflurane, and methoxyflurane

  • what type of drug?
  • clinical use?
A
  1. General Inhaled Anesthetic Agents
  2. General anesthetic induction and maintenance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Butorphanol
1. mechanism of action
2. clinical use

A
  1. partial agonist at opioid mu receptors and agonist activity at opioid k receptors
  2. pain, especially in management of migraines, labor pain, post op pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Tramadol
1. mechanism of action
2. clinical use

A
  1. weak mu opioid receptor agonist (hyperpolarization and decreased activity of neural cells)
  2. moderate to moderately severe chronic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Dantrolene
1. mechanism of action
2. Clinical use

A
  1. inhibit calcium release for SR of myocytes by binding to ryanodine receptor - leads to muscle relaxation
  2. malignant hyperthermia and neuroleptic malignant syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Tetrabenazine
1. mechanism of action
2. clinical use

A
  1. inhibit uptake of catecholamines (NE, Epi, Dopamine) as well as 5HT into synaptic vesicles
  2. To tx choreiform movements seen in Huntington’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Memantine
1. mechanism of action
2. clinical use

A
  1. NMDA receptor antagonist - thought to decrease neuronal excitation by glutamate
  2. Alzheimers disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Buspirone
1. mechanism of action
2. clinical use

A
  1. partial 5HT(1a) receptor agonist -
  2. generalized anxiety disorder
83
Q

Bupropion
1. Mechanism of action
2. clinical use

A
  1. Inhibit reuptake of NE and Dopamine and also acts as a nicotinic antagonist — all to decrease reward system
  2. Depression and smoking cessation
84
Q

Pregabalin
1. clinical use

A
  1. neuropathic pain
  2. fibromyalgia
85
Q

Heparin
1. Mechanism of action
2. clinical use

A
  1. accelerate the action of antithrombin 3 (responsible for degrading clotting factors like thrombin and factor Xa)
  2. Acute tx of DVTs, PE, acute MI, or other thromboEMBOLIC events

*LMWH has less activity on thrombin

86
Q

Warfarin
1. Mechanism of action
2. clinical use

A
  1. Inhibits K dependent gamma carboxylation of factors 2, 7, 9, 10 and protein C and S
  2. Chronic anti-coagulation in pts at risk for thromboEMBOLIC events or who have had thromboEMBOLIC events
87
Q

Hirudin, bivalirudin, lepirudin, desirudin, argatroban, melagatran, and dabigatran

  1. what drug type are these
A

Direct thrombin inhibitors

88
Q

Direct thrombin inhibitors
1. clinical use

A
  1. Acute and chronic anti-coagulation in patients who have indications for anti-coag. (DVT, Afib, etc)
89
Q

Direct Factora Xa inhibitors (Rivaroxaban, apixaban, betrixaban, edoxaban)

  1. clinical uses
A
  1. Tx and prophylaxis of DVT
  2. Prevent thromboembolism in patients with Afib
90
Q

Abciximab, eptifibatide, and tirofiban

  1. what drug type are these
A
  1. Glycoprotein IIb/IIIa inhibitors
91
Q

Glycoprotein IIb/IIIa inhibitors
1. mechanism of action
2. clinical uses

A
  1. binding to GP IIb/IIIa receptor complex, which is present on the platelet surface, and inhibiting the binding of fibrinogen and von Willebrand factor to the receptor — platelet aggregation is stopped
  2. Tx of coronary artery syndromes
92
Q

Clopidogrel
1. mechanism of action
2. clinical use

A
  1. Irreversibly inhibit the binding of ADP to platelet P2Y(12) receptor thereby blocking ADP-mediated platelet aggregation - platelet plug formation halted
  2. Tx acute coronary syndrome along with aspirin
93
Q

Streptokinase, tenecteplase, alteplase, and reteplase

  1. MOA
  2. clinical uses?
A
  1. Promotion of the conversion form plasminogen to plasmin (which acts to degrade fibrin)
  2. massive PE, stroke, and acute MI
94
Q

What medication for migraine prevention is best to be used during pregnancy?

A

Beta blockers (eg. propranolol, metoprolol)

95
Q

Complex Regional Pain Syndrome
1. Triggers
2. Clinical Features
3. Dx
4. Management

A

Triggers
- Trauma: fracture, sprain
-Surgery

Clinical features
- Pain: severe, regional (not dermatomal), burning/stinging
-Edema, abnormal sweating
- Vasomotor changes, altered skin temperature
-Trophic skin, hair & nail changes

Diagnosis
-Primarily based on clinical features
-X-ray: patchy demineralization

Management
-PT , OT, exercise
-Medications: NSAIDs, antineuropathic medications (eg, pregabalin, TCAs)

96
Q

Cafe-au-lait macules, axillary and inguinal freckling, Lisch nodules (iris hemartomas), and neurofibromas

  • Autosomal dominant
  • What disease is this?
A

Neurofibromatosis Type 1 (NF1 gene mutation)

  • These pts have increased risk of seizures, learning disabilities, and optic pathway gliomas
97
Q

Bell palsy
1. symptom onset
2. prodrome
3. symptoms

A
  1. acute- maximal weakness occurring within 3 weeks
  2. auricular pain or dysacusis (distortion of sound)
  3. Unilateral facial paralysis (involvement of upper face ! - helps distinguish from stroke)
    –may also have decreased hearing, hyperacusis, reduced sense of taste over anterior 2/3 of the tongue.
98
Q

Main treatment of Bells Palsy

A
  1. high dose oral glucocorticoids (eg prednisone) which should be started within 72 hours from sx onset
99
Q

anterior spinothalamic tract, which transmits (Blank A) and the lateral spinothalamic tract, which conveys (Blank B).

A

anterior spinothalamic tract, which transmits pressure sensations and crude touch; and the lateral spinothalamic tract, which conveys pain and temperature sensations.

100
Q

Where do these tracts decussate?
1. Dorsal Column
2. Spinothalamic column
3. lateral corticospinal

A
  1. decussates in medulla
  2. decussates in spinal cord level
  3. Decussates in the medulla
101
Q
  1. Anterior spinal cord ischemia due to descending aortic dissection (Type B) is greatest at what level of spine?
  2. What symptoms arrive from this?
A
  1. T10-T12 levels - where blood flow is the lowest
  2. bladder paresis, motor paresis of LE, loss of crude touch/pain sensation, and diminished reflexes — all because this affects anterior spinal cord
102
Q

Alcoholic Cerebellar Degeneration
1. degeneration of purkinje cells (cerebellar vermis)

  1. symptoms
  2. diagnosis methods
  3. tx
A
  1. develops over weeks to months, wide based gait, incoordination in legs, truncal ataxia, nystaglmus, pendular knee reflex, postural tremor
  2. Impaired tandem walking/heel-knee shin but preserved finger-nose testing. CT/MRI shows cerebellar atrophy
  3. alcohol cessation, nutritional supplements, ambulatory assistance
103
Q

What disease shows positive 14-3-3 protein titiers and positive RT-QuIC test?

A
  1. Creutzfeldt-Jakob Disease (CJD)

*Elevated 14-3-3 protein titers are a marker for neuronal cell death but not specific for CJD

104
Q

Function of spinocerebellar tract

A

the anterior and posterior spinocerebellar tracts. These are sensory pathways that send unconscious proprioception to the cerebellum, which in turn helps to maintain posture and coordinate voluntary movement.

105
Q

What are some nonpharmacologic and pharmacologic managements of delirium?

A

Nonpharmacologic -

-Environment: noise reduction, intervention grouping
-Sleep facilitation: bright day/dim night lighting
-Personal interaction: reassurance, physical touch
-Constant observation: family, professional sitters
-Mobilization: out of bed, restraint avoidance

Pharmacologic
-Pain management: nonopioid when possible
-Antipsychotics: off-label indication
-Benzodiazepines: antipsychotic failure/withdrawal syndromes

106
Q
  1. Acute headache, nausea, blurry vision, and slugghis/dilated pupil, conjunctival redness – indicate what disease?
  2. What medication can cause this?
A
  1. Acute angle-closure glaucoma (ACG)
  2. Trihexyphenidyl (an anticholinergic used in tx of PD - they cause mydriasis)
    –can also arise spontaneously

*This is a vision threatening condition

107
Q

CN III palsies can happen due to what two things?

A

Non–pupil-sparing CN III palsies are frequently caused by mass effect and should be considered due to an intracranial aneurysm until proved otherwise. Patients should undergo immediate MR or CT angiography of the head for evaluation.

Pupil-sparing CN III palsies are typically caused by microvascular ischemia and are associated with diabetes, hypertension, hyperlipidemia, and advanced age. Observation and supportive care may be appropriate in patients with vasculopathic risk factors (eg, diabetes, hypertension).

108
Q

Classical time course by strokes by etiology
1. embolic
2. thrombotic
3. hemorrhagic

*Max symptoms at onset, progressively worsening, or fluctuating

A
  1. embolic - Max symptoms at onset
  2. thrombotic - fluctuating
  3. hemorrhagic - progressively worsening
109
Q

air conduction [AC] > bone conduction [BC] bilaterally) suggest….

A

bilateral, symmetric sensorineural hearing loss

—most likely diagnosis is presbycusis (age-related hearing loss), which affects >50% of adults by age 75 and initially involves the high frequencies. Presbycusis is likely caused by cochlear hair cell loss and cochlear neuron degeneration.

110
Q

immune-mediated disorder that causes a rapidly progressive myelopathy characterized by motor weakness (with upper and/or lower motor neuron signs), sensory disturbances (characterized by a distinct sensory level), and autonomic dysfunction (including bowel or bladder dysfunction).

A

Transverse Myelitis
- bilateral motor weakness, classically early flaccid (LMN) progressing to late spastic (UMN)

111
Q

(Blank) are contraindicated in patients with migraine with aura due to the increased risk of ischemic stroke.

A

Estrogen-containing contraceptives

112
Q

Autosomal dominant
-tumor growths in various organs (eg. CNS, kidney, adrenal gland, eye)
-Presents most commonly during early adulthood
-CNS and Retinal Hemangioblastomas are most common lesions
-Dx associated: renal cell carcinomas and pheochromocytomas

A

Von Hippel-Lindau (VHL) Disease

-surveillance should be done for malignancies, tumor resection

113
Q

For lumbosacral radiculopathy what is recommended for patient improvement?
1. activity level
2. First 1-2 weeks
3. After 2 weeks
4. After 4-6 weeks

A
  1. activity level - activity modification but not bed rest
  2. First 1-2 weeks - NSAIDs
  3. After 2 weeks - PT, oral glucocorticoids
  4. After 4-6 weeks - obtain MRI and assess for surgical indication
114
Q

3 main clinical manifestations from serotonin syndrome?

A
  1. Mental status changes (anxiety, agitation, delirium)
  2. Autonomic dysfunction (diaphoresis, HTN, tachy)
  3. Neuromuscular hyperactivity (eg. tremor, myoclonus, hyperreflexia)
115
Q

Tranexamic acid -
- what type of drug is it and what is it used for?

A
  1. antifibrinolytic therapy
  2. used for patients who have moderate TBI and are within 3 hours of injury.

*All patients who sustain significant trauma, including patients with TBI, are at risk of secondary injury from acute traumatic coagulopathy. Acute traumatic coagulopathy is characterized by increased activation of the coagulation pathway (due to severe tissue injury), leading to uncontrolled coagulation and consumption of coagulation factors. This results in the following:

Hypocoagulability from secondary coagulation factor deficiency (ie, consumptive coagulopathy)
Hyperfibrinolysis, which may break down necessary clots

116
Q

Management of traumatic brain injury
1. What main two things are managed
2. How are these managed?

A
  1. Mantain CPP (=MAP-ICP) + Prevent ICH
    2.Maintain CPP(= MAP − ICP)
    –Maintain MAP: isotonic fluids, vasopressor therapy
    –Reduce ICP: head elevation, sedation, osmotic therapy (eg, hypertonic saline, mannitol), decompressive interventions (eg, CSF removal, craniectomy)

Prevent ICH
–Antifibrinolytic therapy (ie, tranexamic acid) within first 3 hr
–Reversal of preexisting anticoagulation

Other measures
–Prevent seizures (eg, levetiracetam, phenytoin)
–Control blood glucose (eg, insulin to target 140-180 mg/dL glucose)
–Maintain normothermia (eg, antipyretics, surface-cooling devices)

117
Q

How is carpal tunnel syndrome and Dialysis related?

A

CTS is the most common mononeuropathy in patients on hemodialysis, with up to a third reporting symptoms. The etiology in this population is multifactorial. The most common cause is likely

—> dialysis-related amyloidosis, in which inflammation stimulates the formation of beta-2 microglobulin. This is inadequately cleared and deposited as amyloid within the carpal tunnel.

—> Other contributing factors include increased venous pressure during hemodialysis, blood tracking (through fascial planes) from the fistula into the carpal tunnel during vascular access, and deposition of calcium phosphate in the tunnel, all of which worsen extrinsic compression of the nerve. In addition, vascular steal through the fistula may lead to ischemic neuropathy.

118
Q

Pyridostigmine
-MOA
-used for what

A
  1. AChE inhibitor
  2. Myasthenia gravis
119
Q

common causes of vertigo
-Recurrent episodes lasting 20 min to several hours
-Sensorineural hearing loss
-Tinnitus &/or feeling of fullness in the ear

A

Meniere disease

120
Q

common causes of vertigo
-Brief episodes triggered by head movement
-Dix-Hallpike maneuver causes nystagmus

A

BPPV

121
Q

common causes of vertigo
-Acute, single episode that can last days
-Often follows viral syndrome
-Abnormal head thrust test

A

Vestibular neuritis

122
Q

common causes of vertigo
-Sudden-onset, persistent vertigo
-Usually other neurologic symptoms (posterior headache, unilateral dysmetria)

A

Brainstem/cerebellar stroke

123
Q

Guillain-Barre Syndrome
1. Symptoms
2. LP findings
3. Treatment

A
  1. ascending muscle weakness, absent deep tendon reflexes after recent infections, bulbar symptoms (eg. dysarthria), respiratory compromise, parasthesias and sensory ataxia (eg. fingertip numbness), dysautonomia
  2. elevated CSF protein with normal white blood cell count
  3. supportive care, IV immunoglobulin or plasmapheresis
124
Q

Chiari I malformation - what is displaced vs Chiari II malformation?

A
  1. Chiari I malformation - cerebellar tonsils
  2. Chiari II malformation - herniation of cerebellar tonsils and vermis + inferior displacement of medulla
125
Q
  1. What are some symptoms associated with Chiari I malformation
  2. complication
A
  1. Frequently asymptomatic in childhood
    - occipital headache and/or neck pain
    - dizziness and worsening pain with physical activity or Valsalva
    - increased ICP
    - Cranial neuropathies from brainstem compression
    - Cerebellar dysfunction

2 . Complication can be syringomyelia - when a cyst (syrinx) forms in the spinal cord (in about 30% of CM-I)

126
Q
  1. Inflammation of spinal cord - leading to motor, sensory, and autonomic dysfunction below level of the spinal cord
  2. symptoms include
    -weakness or paralysis
    -sensory disturbances (pins and needles, tingling, numbness)
    -pain
    -bladder and bowel problems
    -coordination and balance issues
    -fatigue
A

Transverse myelitis -
This is a demyelinating disease

127
Q

Cryptococcus neoformans type meningitis (fungus)

  1. cell count
  2. cell type
  3. glucose levels
  4. Protein levels
  5. onset
  6. patient type at risk
A
  1. slightly elevated
  2. lymphocytes
  3. low
  4. slightly elevated
  5. slowly progressive symptoms
  6. immunocompromised can develop infection after inhalation

*PLUS elevated opening pressure

128
Q

Bacterial meningitis

  1. cell count
  2. cell type
  3. glucose levels
  4. Protein levels
  5. onset
A
  1. very elevated
  2. neutrophils
  3. low
  4. very elevated
  5. very quick onset (hours or days)
129
Q

Viral meningitis

  1. cell count
  2. cell type
  3. glucose levels
  4. Protein levels
A
  1. slightly elevated
  2. lymphocytes
  3. normal
  4. normal or slightly elevated
130
Q

Herpes encephalitis

  1. cell count
  2. cell type
  3. glucose levels
  4. Protein levels
A
  1. slightly elevated
  2. lymphocytes and erythrocytes
  3. Normal
  4. slightly elevated
131
Q

Guillain Barre Syndrome
1. cell count
2. cell type
3. glucose levels
4. Protein levels

A
  1. Normal
  2. Normal
  3. Normal
  4. slightly elevated
132
Q

Dermatologic

  • Ash-leaf spots
  • Angiofibromas of the malar region
  • Shagreen patches
    *periungual fibromas

Neurologic
* CNS lesions (eg, subependymal tumors)
* Epilepsy (eg, infantile spasms)
* Intellectual disability
* Autism & behavioral disorders (eg, hyperactivity)

Cardiovascular: rhabdomyomas

Renal: angiomyolipomas

-what is this?

A

Tuberous Sclerosis Complex
- mutation in TSC1 or TSC2 gene and autosomal dominant
- an inherited or de novo mutation in the TSC genes leads to benign tumors (hamartomas) of the brain, skin, and other organs

133
Q

Physiologic vs Functional (psychogenic) Tremors

A
  1. Physiologic - physiologic tremor is typically a fine, fast, symmetric action tremor of the hands that increases with sympathetic activity
  2. Functional Tremors - Functional tremor typically occurs with rest, posture, and action. Any body part may be involved, but hand tremor, leg tremor, and whole-body tremor are common sites. Often improve with distraction.
134
Q

Forceful abduction and external rotation at the glenohumeral joint suggests an anterior shoulder dislocation - what nerve does this injure?

A

Axillary nerve - innervates teres major and deltoid muscles. Leads to weakened shoulder abduction and decreased sensation over the lateral shoulder

135
Q

Alcohol withdrawal with alcohol reduction/cessation
1. when do manifestations begin
2. what is primary treatment

A
  1. 6-24 hours
  2. benzos
136
Q

What are the two major components of CN III

A
  1. Inner somatic fibers - innervate the levator muscle of the eyelid, 4 of extraocular muscles
  2. superficial parasympathetic fibers - innervate sphincter of the iris and the ciliary muscles (controlling pupil CONSTRICTION)
  • dilation is controlled by sympathetic innervation
137
Q
  1. No pupillary involvement, irregular respiration, or coma. Consciousness often preserved
  2. Contralateral leg weakness (ipsilateral ACA compression)

-What type of herniation is this?

A

SUBFALCINE

138
Q

Central vertigo
1. what are nystagmus characteristics compared to peripheral vertigo?
2. hearing changes
3. walking changes?
4. Other CNS symptoms

A

Central
1. nystagmus is not fatigable (>1 min), no latency period, not inhibited by fixation of gaze, may have any trajectory.
2. Hearing loss/tinnitus ABSENT
3. postural instability
4. Other CNS symptoms - HA, diplopia, weakness/numbness of face, etc
———————————-

Peripheral
1. nystagmus is never purely vertical, inhibited by fixation, fatigable, latency period (2-40 sec)
2. Hearing loss/tinnitus may occur
3. walking preserved
4. No other CNS symptoms

139
Q

How to differentiate between Herpes meningitis and Tuberculous meningitis?

  1. onset
  2. symptoms
  3. imaging
A

Herpes meningitis
1. onset is rapid
2. fever, HA, AMS, and/or seizure
3. unilateral temporal lobe enhancement

TB
1. onset is subacute (over weeks)
2. fever, nuchal rigidity, vomiting, HA, CN palsy, and stroke
3. basilar meningeal enhancement, hydrocephalus, vasculitis due to cerebral artery inflammation

140
Q

– ipsilateral fixed and dilated pupil due to compression of ipsilateral oculomotor n. and accompanying parasympathetic fibers
– EARLY: contralateral hemiparesis: d/t compression of ipsilateral cerebral peduncles of midbrain, damaging descending corticospinal tracts
-LATE: ipsilateral hemiparesis (contralateral cerebral peduncle compression)
–contralateral homonymous hemianopsia d/t compression of ipsilateral PCA

-What type of herniation is this?

A

UNCAL

141
Q

–Typically fixed, midposition pupils due to disruption of both sympathetic and parasympathetic innervation
– coma
– loss of CN reflexes
– flaccid paralysis
–respiratory arrest (brainstem compression)

What type of herniation is this?

A

Tonsillar

142
Q

-Rupture of paramedian basilar artery branches
-Bilateral midposition and fixed pupils
-Decorticate (flexor) –> decerebrate (extensor) posturing

A

-Central herniation

begins with decorticate (flexor) posturing with damage above the level of the midbrain (ie, red nucleus) but often changes to decerebrate (extensor) posturing as brainstem injury progresses caudally.

143
Q
  • Gait dysfunction
    -extremity weakness and numbness
    -LMN signs (arms)
    -UMN signs (legs)
  • decreased proprioception/vibration/pain sensation
    -at times positive Lhermitte sign

what is this?

A

Cervical myelopathy

144
Q

Cervical myelopathy
1. age
2. what is it
3. dx methods
4. tx?

A
  1. > 55 years old
  2. degenerative cervical spine/discs lead to canal stenosis and cord compression
  3. MRI of cervical spine, CT myelogram
  4. Nonsurgical tx is immobilizaiton;;; surgical would be decompression
145
Q

BIND (bilirubin induced neurologic dysfunction)
1. what is it
2. what symptoms (acute and chronic)

A
  1. when bilirubin concn dramatically rises (>= 30 mg/dL) and exceeds binding capacity of albumin. Unbound bilirubin crosses BBB and deposits in the basal ganglia and brainstem nuclei (oculomotor, auditory) causing neuronal damage
  2. Acute: lethargy, tone abnormalities, high pitched crying
  3. Hyperkinetic movements, sensorineural hearing loss, abnormal eye movements (upward gaze palsy), developmental delay
146
Q

Internuclear ophthalmoplegia
1. what does it look like
2. What are the issues that cause this?

A
  1. affected eye (ipsilateral to lesion) is unable to abduct and contralateral abducts with nystagmus. Convergence and pupillary light reflex are preserved.
  2. damage to medial longitudinal fasciculus (MLF). MLF mediates communication between CN III and CN VI allowing for coordinated horizontal eye movements.

*bilateral Internuclear ophthalmoplegia is classically seen in MS patients

147
Q

Neurosyphilis happens with untreated infection - typically takes weeks or months

Describe manifestations
- Meningovascular
- Ocular
- Otologic

A
  1. Meningeal - HA, N/V, neck stiffness, dizziness followed by ischemic stroke signs (sudden onset unilateral weakness, hyperreflexia). Imaging will show vasculitis (focal segmental arterial narrowing)
  2. Ocular: uveitis and optic neuritis
  3. Otologic: hearing loss and tinitus

Late manifestations: general paresis, tabes dorsalis

148
Q

What is the management of migraines in pregnancy
5 step algorithm

A
  1. Nonpharm: rest, hydrate, heat
  2. acetaminophen
  3. Antiemetics (e.g. promethazine, codeine, caffeine/bultalbital)
  4. NSAIDs (naproxen)
  5. Opioids (oxycodone)
149
Q

B12 deficiency symptoms

A

-this is subacute (over weeks to months) combined degeneration of the spinal cord

  • progressive symmetric sensory loss/parasthesia
  • sensory ataxia
  • spastic muscle weakness
150
Q

Transverse myelitis, optic neuritis, internuclear ophthalmoplegia, and cerebellar dysfunction are all common initial presentations of what disorder?

A

Multiple sclerosis

151
Q

A single episode of delirium can increase risk of (blank)

A

further cognitive decline

152
Q

*psychiatric symptoms (anxiety, psychosis, insomnia)
* autonomic instability
* cognitive impairment
*rigidity, hyperreflexia, dystonia
*Focal seizure after a flu like prodrome

–> this is strongly indicative of?

A

anti-NMDA receptor encephalitis

*median age of onset is 21
*more common in women of whom >50% have an associated ovarian teratoma
*tx : immunosuppressive tx

153
Q

Acute dystonia (sudden, sustained contraction of the neck, mouth, tongue, and eye movements)

-what pharmacotherapy is used to improve?

A
  1. Benzotropine
  2. Diphenyhydramine
154
Q

Akathisia (subjective restlessness, inability to sit still)

what pharmacotherapy is used to improve?

A
  1. Beta blocker (propranolol)
  2. Benzodiazepine (lorazepam)
  3. Benztropine
155
Q

Parkinsonism
what pharmacotherapy is used to improve?

A
  1. Benztropine
  2. Amantadine
156
Q

Tardive dyskinesia (gradual onset after prolonged therapy (>6 months), dyskinesia of the mouth, face, trunk, and extremities)

what pharmacotherapy is used to improve?

A
  1. Valbenazine
  2. Deutetrabenazine
157
Q

CMV retinitis presentation
1. symptoms
2. fundoscopic exam

A
  1. blurred vision, floaters, and photopsia (sensation of flashing lights) - complications are vision loss and retinal detachment
  2. yellow-white, fluffy, hemorrhagic lesions adjacent to the fovea and retinal vessels
158
Q

Generalized convulsive status epilepticus (GCSE) is defined as what?

-what are the next steps if patient has this

A
  1. a single seizure lasting >= 5 min or >=2 seizures in which the pt does not fully regain consciousness
  2. IV access and fingerstick glucose
    —-concurrently, IV benzos (lorazepam, diazepam) for seizure termination
    —–Give longer acting nonbenzo antiepileptic meds to prevent seizures like levetiracetam
159
Q

Huntington’s Dx
1. what neuron types are lost
2. Where is atrophy found
3. symptoms/clinical features

A
  1. GABA-ergic neurons
  2. Caudate nucleus & Putamen Atrophy
  3. chorea, delayed saccade, depression, irritability, psychosis, OCD, executive dysfunction
160
Q

Lithium toxicity
1. symptoms
2. serum level indicating toxicity

A
  1. lethargy, confusion, slurred speech, tremor, ataxia, seizures. Cardiac abnormalities can also occur mainly in form of QT interval prolongation and bradycardia.
  2. > 1.5 mEq/L
161
Q

Restless leg syndrome
-what medications can help?

A
  1. supplemental iron if ferritin <75 ng/mL
  2. with mild intermittent symptoms: carbidopa-levodopa as needed
  3. Frequent/daily symptoms: gabapentin, pregabalin –> this is an alpha2delta calcium channel ligand

Other: Ropinirole (dopamine agonist) - careful because it can increase risk for impulse control problems, manic, or depressive episodes

162
Q

Retinitis Pigmentosa
1. pathology
2. symptoms
3. Fundoscopic findings

A
  1. genetic mutation causing loss of photoreceptors and progressive retinal degeneration
  2. night blindness, clumsiness due to progressive peripheral vision loss, decreased visual acuity
  3. retinal vessel attenuation (narrower vessels due to decreased retinal metabolic demand), waxy/pale optic disc (due to nerve gliosis and atrophy), degeneration of retinal pigment epithelium
163
Q

What are some signs that surgery is needed for intracerebral hemorrhage?

A
  1. signs of neurologic deterioration
  2. radiologic evidence of a bleed >3 cm, brainstem compression, or obstructive hydrocephalus
164
Q
  1. Right hemiparesis - loss of vibration and proprioception in weak extremities (contralateral to lesion)
  2. CN XII palsy - tongue deviates ipsilateral to lesion

-where is this stroke localization?

A

Medulla (consistent with left medullary syndrome - often caused by occlusion of the paramedian bulbar arteries)

165
Q

What are some lifestyle modifications for Meniere disease

A

Dietary salt restriction (2-3 g maximum per day): Sodium restriction may reduce endolymphatic fluid, thereby helping reduce endolymphatic hydrops

Limitation of caffeine and nicotine: Vasoconstrictors may reduce blood flow to the inner ear.

Limitation of alcohol: Alcohol may cause fluid shifts that impact the inner ear.

Avoidance of allergy triggers: Both food and environmental allergies seem to trigger attacks in some patients, perhaps due to allergies leading to increased fluid extravasation into the endolymphatic sac.

166
Q

-Sensory disturbances, motor weakness, bowel/bladder dysfunction
-Ocular manifestations: optic neuritis (painful eye movement), internuclear ophthalmoplegia (impaired adduction on lateral gaze)
-Lhermitte sign: electrical sensation in limbs or back
-Uhthoff phenomenon: symptom worsening with increased body temperature

what disease is this?

A

MS

Risk factors include
Female, HLA-DRB1
Environmental factors (United States, Europe, Australia)
Low vitamin D levels
Epstein-Barr infection

167
Q

What imaging is done to dx cerebral vein and venous sinus thrombosis?

what are some risk factors for this type of thrombosis?

what are symptoms?

A
  1. MR venography of the brain
  2. Thrombophilia (eg, factor V Leiden)
    Pregnancy & postpartum
    Oral contraceptive pills
    Malignancy
    Infection
  3. Headache, ↑ ICP (eg, vomiting, papilledema)
    Focal neurologic symptoms, seizures
    Encephalopathy
168
Q

How many ft/m can a child <2 fall before its considered a risk factor for pediatric traumatic brain injury

-what about >= 2-18 year old

A
  1. 3 ft/0.9 m
  2. 5 ft/1.5 m

management is Head CT without contrast

169
Q

*Immobility or excessive purposeless activity
*Mutism, stupor (decreased alertness & response to stimuli)
*Negativism (resistance to instructions & movement)
*Posturing (assuming positions against gravity)
*Waxy flexibility (initial resistance, then maintenance of new posture)
*Echolalia, echopraxia (mimicking speech & movements)

-often develops in context of mood disorders but may also occur in psychotic disorders

-what is this?

A

Catatonia

170
Q

What is catatonia treated with?

A
  1. Benzos
  2. severe cases can require electroconvulsive therapy
171
Q
  1. What lobe is brocas area in
  2. What lobe is wernickes area in
A
  1. Fronta
  2. Temporal
172
Q

When wernickes/brocas aphasia is being presented - what side of brain is being affected?

  • if right handed what lobe (L or R) is this typically
A
  1. dominant lobe
  2. L lobe
173
Q

Euphoria
Depressed mental status
Respiratory depression
Miosis
Constipation

-what is drug of abuse here?

A

opioids

174
Q

What is treatment for Tourette syndrome

A
  1. Education/watchful waiting if mild & nondisabling
  2. Behavioral therapy (habit reversal training)
  3. Antidopaminergic agents
    —–Tetrabenazine (VMAT2 inhibitor) (preferred as initial tx)
    —–Antipsychotics (receptor blockers)
  4. Alpha-2 adrenergic receptor agonists
175
Q

Onset: age 2-3
1. proximal muscle weakness + calf pseudohypertrophy
2. cardiomyopathy, arrhythmias, and scoliosis are assoc. findings
3. pts are wheelchair dependent in teens, death by 20-30 due to respiratory heart failure

-What dx is this?

A

Duchenne muscular dystrophy

-x linked recessive with deletion of dystrophin gene

176
Q

Onset: 5-15
1. milder proximal weakness
2. cardiomyopathy, arrhythmias are assoc. findings
3. death by age 40-50 d/t heart failure

-What dx is this?

A

Becker muscular dystrophy
1.-x linked recessive with deletion of dystrophin gene

177
Q

Onset: 12-30
1. Facial and distal muscle weakness (ptosis and temporal wasting and delayed ability to open eyes after closing them tightly) + grip hand myotonia (delayed muscle relaxation) + sleep disturbances (excessive daytime sleepiness)
2. Cardiomyopathy, arrhythmias, dysphagia, cataracts, testicular atrophy
3. Death at age 45-55 from respiratory or heart failure

-What dx is this?

A

Classic myotonic muscular dystrophy
1. Autosomal dominant
Trinucleotide repeat of CTG in DMPK gene

178
Q

What antiepileptic drugs are good for childbearing women

A
  1. lamotrigine
  2. levetiracetam (kepra)
179
Q

Dopamine activity in the tuberoinfundibular pathway (BLANK) prolactin release.

A

inhibits

180
Q

*Progression of dx >8 weeks
*Motor dysfunction is more often&raquo_space; sensory
—when sensory is affected its usually vibration and position sense
*Symmetric proximal & distal muscle weakness
*LMN signs (eg, hyporeflexia, atrophy)

  1. What dx is this?
A

Chronic inflammatory demyelinating polyneuropathy

  • Immune-mediated demyelination of peripheral nerves and nerve roots
    -Non–length dependent which is why it affects both proximal and distal muscles
181
Q

What is bell’s palsy thought to be caused by?

A
  1. Bell palsy is thought to be due to reactivation of a neurotrophic virus, most commonly herpes simplex virus. Viral infection causes inflammation and edema of the facial nerve, resulting in nerve compression and degeneration of the myelin sheath. Treatment involves glucocorticoids; because of the association with herpes simplex virus, some experts also recommend the addition of valacyclovir.
182
Q
  1. ipsilateral hemiparesis
  2. ipsilateral diminished proprioception, vibration, and light touch
  3. Contralateral diminished pain and temp - these symptoms occur 1-2 levels distal to the cord injury
  • what disease is this?
A

Brown-Sequard syndrome

183
Q

Carotid artery dissection
1. clinical presentation

A
  1. unilateral head and neck pain
  2. transient vision loss
  3. ipsiilateral horner syndrome (ptosis and miosis)
  4. signs of cerebral ischemia like focal weakness
184
Q
  1. RAPIDLY progressive bilateral motor weakness (early flaccid LMN progressing to late spastic UMN)
  2. Bilateral sensory dysfunction
  3. Distinct sensory level (like sensation is decreased below this point)
  4. autonomic dysfunction (bowel and/or bladder)

+immune mediated destruction of spinal cord and often post infectious

-what is this?

A
  1. idiopathic transverse myelitis
    — MRI of spine shows no compression but does show T2 hyperintensity

–Tx is glucocorticoids

185
Q

First line treatments for postherpetic neuralgia

A
  1. gabapentin
  2. TCA (amitriptyline)
186
Q

Niemann-Pick
1. deficiency in what enzyme?
2. clinical features

A
  1. sphingomyelinase deficiency
  2. Loss of motor milestones
    Hypotonia
    Feeding difficulties
    Cherry-red macula
    Hepatosplenomegaly (Diff from tay-sachs)
    Areflexia (Diff from tay-sachs)

*Autosomal recessive
*Ashkenazi Jewish Inheritance

187
Q

Tay-Sachs Disease
1. deficiency in what enzyme?
2. clinical features

A
  1. Beta-hexosaminidase A deficiency
  2. Loss of motor milestones
    Hypotonia
    Feeding difficulties
    Cherry-red macula
    Hyperreflexia (diff from Niemann)

*Autosomal recessive
*Ashkenazi Jewish Inheritance

188
Q

Parkinson-plus (atypical parkinsonism) syndromes*
–which one is this?

*Early autonomic failure (eg, severe orthostasis, urinary incontinence)
*Early postural instability (eg, falls)
*Cerebellar findings (eg, gait ataxia)

A

Multiple system atrophy

189
Q

Parkinson-plus (atypical parkinsonism) syndromes*
–which one is this?

*Vertical gaze palsy
*Early postural instability (eg, falls)
*Akinesia (eg, early gait freezing)
*Progressive aphasia

A

Progressive supranuclear palsy

190
Q

Parkinson-plus (atypical parkinsonism) syndromes*
–which one is this?

*Relatively rare
*Myoclonus, dystonia
*Alien limb phenomenon (ie, has a will of its own)
*Cortical sensory loss

A

Corticobasal degeneration

191
Q
  1. First line tx for Alzheimers dx
  2. Tx for mild to moderate AD
  3. TX for moderate to severe Dementia
A
  1. The first-line treatment for cognitive symptoms of AD is a cholinesterase inhibitor, which may improve quality of life and cognitive function (eg, memory, language, thought, reasoning), although drugs in this class have not been shown to alter the disease course in any type of dementia.
  2. Donepezil, galantamine, and rivastigmine are effective in patients with mild to moderate AD.
  3. Memantine, an NMDA receptor antagonist, is approved for moderate to severe dementia.
192
Q

What treatment is given to someone with organophosphate poisoning?

A
  1. Atropine reverses muscarinic sx
  2. Pralidoxime reverses nicotinic and muscarinic sx (give after atropine)

*Muscarinic sx
Diarrhea/diaphoresis
Urination
Miosis
Bronchospasms, bronchorrhea, bradycardia
Emesis
Lacrimation
Salivation

*Nicotinic sx: muscle weakness, paralysis, fasciculations

193
Q
  1. flashes of light (photopsia)
  2. Dark spots or webs
  3. Peripheral visual field defect

-what is this?

A

Retinal detachment

194
Q

Trihexyphenidyl
-what is this often used for?

A
  1. resting tremor seen in Parkinson’s - limited to younger patients <55 due to risk of side effects in older patients
195
Q

What are the most common used meds for reducing muscle tone and painful muscle spasms like those seen in MS?

A
  1. Baclofen (agonist at GABA-B)
  2. Tizanidine (alpha 2 adrenergic agonist)
196
Q
  • a thrombotic event (deep venous thrombus or arterial thrombus) or pregnancy morbidity (fetal loss, severe preeclampsia, placental insufficiency)

*plus a positive serology for 1 of 3 antiphospholipid antibodies: anticardiolipin antibody, anti-beta2-glycoprotein-I antibody, or lupus anticoagulant.

—> what is this?

A

Antiphospholipid antibody syndrome

The biggest risk factor for APS is SLE; APS occurs in up to 40% of these patients.

197
Q

*Paresthesia, neuropathic pain
*Symmetric, ascending weakness
*Decreased/absent deep tendon reflexes
*Autonomic dysfunction (eg, arrhythmia, ileus)
*Respiratory compromise

A

Guillan Barre syndrome
**Radicular pain, is due to nerve root inflammation and commonly accompanies the initial presentation.

198
Q

What is tonometry used for?

A

Tonometry is a test to measure the pressure inside your eyes. The test is used to screen for glaucoma. It is also used to measure how well glaucoma treatment is working

199
Q

Severe sensitivity to antipsychotics is seen with what dementia subtype?

A

Dementia with lewy bodies
* Adverse effects to antipsychotics are not dose related and include worsening of parkinsonian symptoms, confusion, and autonomic dysfunction. Reactions are more common with high-potency first-generation antipsychotics (eg, haloperidol) but may also be seen with second-generation antipsychotics.

200
Q

Early signs
—Symmetric extremity weakness
—↓ Deep tendon reflexes

Late signs
—↓ Rectal tone
—↑ Deep tendon reflexes, bilateral Babinski reflex
—Paralysis

-What is this?
-what is the initial tx?
-what are concerns of causes of this?

A
  1. Epidural spinal cord compression
  2. IV glucocorticoids (eg. malignancy) or antibiotics (eg. infection)
  3. Mechanical (disc herniation, spinal stenosis), Malignancy, Infection

Glucocorticoids decrease vasogenic edema (caused by obstructed epidural venous plexus), help alleviate pain, and may restore neurologic function

201
Q

Pronator drift is a relatively sensitive and specific sign for (BLANK)

A
  • upper motor neuron or pyramidal (corticospinal) tract disease affecting the upper extremities.
202
Q

Common etiologies of pediatric stroke

A

**Sickle cell disease
*Prothrombotic disorders
*Congenital cardiac disease
*Bacterial meningitis
*Vasculitis
*Focal cerebral arteriopathy
*Head/neck trauma

203
Q

*Limited upward gaze
*Upper eyelid retraction (Collier sign)
*Pupillary abnormalities (ie, reactive to accommodation but not to light)

—> What syndrome does this indicate?

A
  1. Parinaud Syndrome - results from pressure on the pretectal region of the midbrain near the superior colliculus and the oculomotor nerve (CN III).

***Pineal gland masses often block cerebrospinal fluid flow in the aqueduct of Sylvius, causing obstructive hydrocephalus. Papilledema, headache, and vomiting can occur due to increased intracranial pressure. Progressive hydrocephalus may also lead to ataxia.

204
Q

Trigeminal neuralgia - how is the nerve compressed?

A

compressed by an abnormal vessel loop (vascular)

205
Q

*Acute, peaks at 2 weeks
*Monocular vision loss
*Eye pain with movement
*“Washed-out” color vision
*Afferent pupillary defect
*Central scotoma

-What is this?
-Dx with?
-Tx with?

A

Optic neuritis
* primarily in young women and assoc. with MS
*DX with MRI of orbits and brain
*Tx with IV corticosteroids bc its an immune mediated demyelination

M3 - Clerkships (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions