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Review / Wrong Answers > 5/23 UWorld > Flashcards

5/23 UWorld Flashcards

1
Q

Which is more worrisome and why: unilateral facial paralysis sparing the forehead or unilateral facial paralysis involving the forehead?

A
  • Upper motor neuron lesion - more severe, could mean stroke
    • Destruction of motor cortex or connection between motor cortex and facial nucleus
    • Contralateral paralysis of lower facial muscles (sparing of forehead)
  • Lower motor neuron lesion - Bell’s Palsy
    • Destruction of facial nucleus or facial nerve
    • Ipsilateral paralysis of upper and lower muscles of face
  • Explanation:
    • Facial motor nucleus receives motor fibers for the lower face from the opposite motor cortex and motor fivers for the upper face from both moto cortices
    • So if a lesion occurs in the L motor cortex facial region, there is still sufficient innervation for R upper face from R motor cortex
    • But since L motor cortex is the only innervation of R lower face, there will be paralysis of R lower face
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2
Q

What are the 4 midline structures and associated lesion presentations in the brainstem

A

Motor pathway - contralateral weakness

Medial lemniscus - contralateral proprioception/vibration deficit

Medial longitidinal fasciculus - ipsilateral internuclear ophthalmoplegia

Motor nuclues and nerve - ipsilateral CN motor loss (3, 4, 6, 12)

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3
Q

What are the 4 lateral structures and associated lesion presentations of the brainstem?

A

Spinocerebellar - ipsilateral ataxia

Spinothalamic - contralateral pain and temp

Sensory V - ipsilateral pain and temp of the face

Sympathetic - ipsilateral Horner’s

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4
Q

What are the layers that you go through during a spinal tap?

A

Skin - superficial fascia - supraspinous ligament - interspinous ligament - ligamentum flavum - epidural space - dura mater - subdural space - arachnoid membrane - subarachnoid space (this is where CSF is)

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5
Q

Diseases associated with berry aneurysm

A

Ehlers-Danlos syndrome

Autosomal dominant polycystic kidney disease

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6
Q

Describe the presentation of normal pressure hydrocephalus

A
  • Ventricular dilation with normal ICP
  • Occurs in the elderly
  • Triad - “Wet, wacky, wobbly”
    • Urinary incontinence = wet
    • Dementia = wacky
    • Ataxia = wobbly
      • Magnetic gait – feet appear stuck on floor
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7
Q

Describe cluster HA (duration, location, features, associated sx, treatment)

A

15 min – 3 hours

Repetitive (often occur daily at the same time)

Unilateral, non-throbbing heading

Excruciating pain, usually perioribital

Associated with lacrimation, rhinorrhea, and Horner syndrome (ptosis and miosis, not anhidrosis)

Treatment: 100% O2, sumatriptan

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8
Q

Describe tension HA (duration, location, features, associated sx, treatment)

A

Usually 4 – 6 hours

Bilateral headache with constant, steady pain

Usually in frontal or occipital lobe

No throbbing, no photophobia, no phonophobia, no aura

Treatment: NSAIDs, Acetaminophen

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9
Q

Describe migraine HA (duration, location, features, associated sx, treatment)

A

Usually 4 – 72 hours

Unilateral pulsing, throbbing headache

Associated with nausea, photophobia, phonophobia, and aura

Treatment: Triptans

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10
Q

Describe the MOA of Triptans

A
  • Mechanism of action:
    • Selective agonists of 5HT-1B and 5HT-1D receptors located on meningeal vessels, trigeminal nerve, and brainstem
    • Activation of these receptors on vessels causes vasoconstriction of cerebral and meningeal vessels (this will attenuate inflammation and decrease the stretch at pain receptors)
    • Activation of receptors directly on trigeminal nerve will prevent the release of vasoactive peptides, thus preventing vasodilation in the first place
    • Activation of receptor in brainstem can inhibit pain pathways
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11
Q

Tumors associated with von Hippel-Lindau disease

A

Renal cell carcinoma (bilateral)

Hemangioblastoma

Pheochromocytoma

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12
Q

What is the tumor marker for tumors of astrocytes (glioblastoma multiforme and pilocytic astrocytoma)

A

GFAP +

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13
Q

Describe the blood supply of the brainstem (medial and lateral of midbrain, pons, and medulla)

A
  • Midbrain:
    • Medial - posterior cerebral
    • Lateral - posterior cerebral
  • Pons:
    • Medial - Basilar
    • Lateral - Anterior inferior cerebellar artery (AICA)
  • Medullar:
    • Medial - anterior spinal (ASA)
    • Lateral - Posterior inferior cerebellar artery (PICA)
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14
Q

What is the mechanism of Hepcidin sequestering iron

A
  • Hepcidin influences body iron storage through its interaction with ferroportin, a transmembrane protein responsible for transferring intracellular iron to the circulation
  • Upon binding Hepcidin, ferroportin is internalized and degraded, decreased intestinal iron absorption and inhibiting the release of iron by macrophages
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15
Q

Complications of Hereditary spherocytosis

A

Aplastic crisis

Pigmented gallstones - due to increased bilirubin from lysed RBCs

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16
Q

Classic presentation of AML

A

Bleeding in the setting of DIC (characterized by decreased fibrinogen)

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17
Q

Which coagulation factor has the shortes half-life

A

Factor VII

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18
Q

Mechanism of Desmopressin treatment in bleeding disorders

A

Increases release of Factor VIII (treats Hemophilia A) and vWF (treats von Willebrand disease)

19
Q

Enzyme deficient in acute intermittent porphyria

A
  • Deficiency of Porphobilinogen (PBG) deaminase
    • THINK: Acute intermittent = guys hollering “damn” (deam-inase) intermittently at A CUTE pretty big girl (PBG) walking by
20
Q

Presentation and treatment of acute intermittent porphyria

A
  • Symptoms – 5 P’s
    • Painful abdomen, Port wine colored urine (due to increase PGB), Polyneuropathy, Psychological disturbances, Precipitated by drugs (CYP450 inducers), alcohol, and starvation
  • Treatment
    • Glucose + heme = inhibition of ALA synthase
21
Q

MOA of Flutamid

A

Testosterone receptor inhibitor

Inhibits androgen receptor-binding

Used to treat prostate cancer (testosterone-dependent)

22
Q

Name of GP2b3a antagonist drugs

A

Abciximab

Eptifibatide

Tirofiban

23
Q

What causes autosplenectomy in sickle cell patients?

A

Vaso-occlusion

24
Q

Why might you see macrocytic anemia is sickle cell patients

A
  • Hemolytic anemia leads to increased erythrocyte turnover and increased folic acid requirement
    • So patients are prone to developing relative folic acid deficiency
25
Q

What lymphoma has t(14;18) and what gene abnormality will it cause

A

Follicular lymphoma

  • t(14;18) = heavy chain Ig (14) and BCL-2 (18)
    • Overexpression of BCL-2 = decreased apoptosis
      • Recall that BCL2 stabilizes mitochondrial membranes, preventing leakage of cytochrome C, and thus preventing apoptosis
      • Follicle is where B-cells are produced, so lack of apoptosis = malignant B-cell proliferation
26
Q

In what brain bleed do you get a lucid interval

A

Epidural hematoma

Rupture of middle meningial artery

27
Q

Flow of info through the cerebellum

A
  • Inputs (mossy and climbing fibers) - cerebellar cortex - axons of purkinje fibers (always inhibitory signal) - deep nuclei of cerebellum - output targets (usually superior cerebellar peduncle - contralateral ventral lateral nucleus of thalamus)
28
Q
  • Functional units of cerebellum and their corresponding deep nuclei
A
  • Vestibulocerebellum
    • Vermis + flocculonodular (most medial)
    • = Fastigial deep nucleus
  • Spinocerebellum
    • Vermis + paravermis
    • = Interposed (Emboliform + Globose) deep nucleus
  • Cerebrocerebellum
    • Lateral hemisphere
    • = Dentate deep nucleus

REMEMBER:

  • Lateral to medial = Don’t Eat Greasy Foods
    • Dentate
    • Emboliform
      • Emboliform + Globose = Interposed
    • Globose
    • Fastigial
29
Q

What is the presentation and cause of hemiballismus

A

Sudden, wild flailing of half of body (1 arm +/- ipsilateral leg)

Seen in lesion of contralateral subthalamic nucleus

30
Q

Define athetosis and it’s cause

A

Slow, writhing movements, especially seen in the fingers

Due to lesion of basal ganglia (Huntington’s)

31
Q

Define chorea and its cause

A

Sudden, jerky, purposeless movements

Seen in lesion of basal ganglia (e.g. Huntington’s)

32
Q

Define dystonia

A

Sustained, involuntary muscle contractions

Due to Writer’s cramp, blepharospasm, torticollis

33
Q

Define akathisia and its cause

A
  • Dancing in place (voluntary) / Restlessness
  • Compulsion to move
  • Seen with neuroleptic use or in Parkinson’s
34
Q

Define asterixis and its cause

A
  • Extension of wrists causes “flapping” motion
  • Associated with hepatic encephalopathy, Wilson disease, and other metabolic derangements
35
Q

Identify the location of the following in the spinal cord:

Dorsal column

Spinothalamic tract

Corticospinal tract (lateral and anterior)

A
36
Q

What part of the spinal cord is damaged in Werdnig-Hoffman disease

A

Anterior motor horn - LMN deficit with SYMMETRIC weakness

(vs. poliomyelitis which is LMN deficit with ASYMMETRIC weakness)

37
Q

What part of the spinal cord is affected/presentation of complete occlusion of the anterior spinal artery

A
  • Damage to everything except dorsal column
    • Spinothalamic damage = loss of bilateral pain and temperature below the lesion
    • Corticospinal damage = UMN below the lesion
    • Anterior horn damage = LMN deficit at the level of the lesion
38
Q

What part of the spinal cord is damaged/presentation of ALS

A
  • Aka Lou Gehrig disease
  • Damage to anterior motor horn and lateral corticospinal tract
  • Presents with both UMN and LMN deficits
  • Lack of sensory impairment distinguishes from syringomyelia
  • Caused by defect in superoxide dismutase (O2- to H2O2)
39
Q

What part of the spinal cord is damaged/presentation of Tabes dorsalis

A

Due to tertiary syphilis

Damage to dorsal column

Impaired propriocepton

Absence of DTRs and (+) Romberg

Argyll Robertson pupils (accommodation but no reaction to light)

40
Q

Findings in Brown-Sequard syndrome

A

Ipsilateral UMN signs below level of lesion (corticospinal tract damage)

Ipsilateral loss of tactile, vibration, proprioception sense below level of lesion (dorsal column)

Contralateral pain and temp loss 2-3 segments below level of lesion (spinothalamic tract)

2-3 segments below because remember info travelled up 2-3 segments via Lissaur’s tract

Ipsilateral pain and temp loss at level of lesion

Ipsilateral LMN signs at level of lesion

41
Q

What is the Charcot triad and what disease is it for?

A
  • Multiple sclerosis
    • Charcot triad of symptoms - SIN:
      • Scanning speech
      • Intention tremor, Incontinence, Internuclear ophthalmoplegia
      • Nystagmus
42
Q

Describe MRI and lumbar puncture of MS

A
  • MRI (gold standard)
    • Periventricular plaques (areas of oligodendrocyte loss secondary to demyelination and reactive gliosis)
  • Lumbar puncture
    • Increased protein
    • Oligoclonal IgG bands
43
Q

\Describe cause/presentation of Friedrich ataxia

A
  • Autosomal recessive trinucleotide repeat disorder - GAA
  • Frataxin gene of chromosome 9
  • Leads to impairment in mitochondrial function
  • Degeneration of cerebellum and spinal cord
    • Ataxia, muscle weakness, loss of vibratory sense and proprioception, diabetes mellitus, hypertrophic cardiomyopathy
    • Presents in childood with kyphoscoliosis
  • THINK: Friedreich is fratastic (frataxin): he’s your favorite frat brother, always staggering and falling but has a sweet, big heart

Review / Wrong Answers (140 decks)

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