UWorld 2 Flashcards

1
Q

Characterize the descending cerebellar pathway for coordination:

A

Info from cerebellar cortex projects to ipsilateral deep grey nuclei of the cerebellum which then project to contralateral red nucleus via superior cerebellar peduncle.

After this the red nucleus gives rise to rubrospinal tract which crosses then travels ipsilaterally to the cerebellar cortex from where the impulse originated.

Red nucleus also gives rise to an ascending projection to the thalamus which synapses primarily in the ventral lateral nucleus.

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2
Q

OF the following meds (metoclopramide, ondansetron,, prochlorperazine, promethazine, and trimethobenxamide) why would you use ondansetron in a Pt with PD who has nausea and not the other drugs?

A

The other ones have dopamine blocking properties.

metoclopramide - Reglan = blocks 5HT chemoreceptor trigger zones in CNS, and dopa R at high [ ], also ^ sensitivity to ACh&raquo_space; ^ GI motility

promethazine - Phenergan = blocks mesolimbic dopa R and alpha A-R. Used for motion sickness.

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3
Q

Based on the following Sx, what is the Dx? Loss of the following: vertical gaze, pupillary light reflex, and lid retraction. Convergence retraction nystagmus triggered by upward gaze.

A

Parinaud syndrome - pineal gland tumor compressing dorsal midbrain.

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4
Q

What are the requirements for a Dx of migraine without aura?

A

Need to have at least 5 episodes of headache lasting 4-72 hrs and assoc with (2) of the following: moderate to severe, worse w/movement, throbbing in nature, and one sided.

Also need (1) of the following: light and noise sensitivity, nausea or vomiting.

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5
Q

If a patient presents with acute onset vertigo, incoordination and L facial numbness, loss of pinprick sensation over L hemiface and R hemibody, L sided dysmetria and rotatory nystagmus, and L sided ptosis and miosis what part of the brainstem should be affected?

A

Lateral medullary Syndrome (Wallenberg syndrome)

Lateral medullary stroke&raquo_space; dysfunction of ipsilateral descending pain and temp, contralaterally ascending pain and temp from body, ipsilateral inferior cerebellar peduncle, and ipsilateral vestibular nuclei.

Ipsilateral horners = interruption of descending sympathetic fibers.

Generally due to vertebral artery or PICA occlusion.

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6
Q

What’s the MOA of dipyridamole in stroke prevention?

A

Dipyridamole has 3 functions:

  1. inhibits RBC uptake of adenosine&raquo_space; inhibition of platelet reactivity.
  2. Phosphodiesterase inhibition increasing cAMP
  3. Inhibition of TXA-2 formation (vasoconstrictor and stimulator of platelet activation)
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7
Q

What’s the MOA of clostridium botulinum toxin (where does it act) and what is the treatment for it?

A

Acts at presynaptic ACh release at NMJ. Rx = equine serum heptavalent botulinum antitoxin.

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8
Q

Describe the general clinical presentation following botulinum toxin ingestion:

A

Sx can develop acutely (within 36 hrs). Prodromal Sx = GI discomfort, dry mouth, and sore throat.

Pt develop bilateral cranial neuropathies (blurred vision from fixed pupil dilation), diplopia, facial weakness, dysarthria&raquo_space; Symmetric descending muscle weakness&raquo_space; Respiratory Failure.

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9
Q

What’s the clinical presenation and genetic mutation assoc with galactosemia?

A

Failure to thrive, bilateral cataracts, jaundice, hypoglycemia, and hepatosplenomegaly. Due to galactose 1 phos uridyltransferase

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10
Q

In what seizure type are automatisms observed?

A

Focal seizures w/impairment of consciousness.

Automatisms = repetitive semi-purposeful movements. (chewing, sucking, swallowing)

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11
Q

What is the management for both cauda equina syndrome and conus medullaris?

A

Emergency MRI&raquo_space; IV glucocorticoids&raquo_space; neurosurg eval

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12
Q

Disruption of the ___ causes Horner syndrome and is characterized by what 3 clinical signs?

A

Oculosympathetic chain. 3 signs are ipsilateral ptosis, miosis, anhidrosis

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13
Q

Oculomotor nerve palsy can be due to nerve compression (uncal herniation) or ischemia (e.g. DM). What sign can help differentiate between the two causes?

A

Mydriasis (pupil dilation) is more common in nerve compression because parasymp fibers are found along the periphery of the nerve.

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14
Q

How does the presentation of tick borne paralysis differ from paralysis caused by botulinum toxin or GBS?

A

Tick borne = rapidly progressing ascending paralysis (probably asymmetric).

Botulinum = descending paralysis w/early CN involvement

GBS = slowly progressive ascending symmetric paralysis. Sensation is typically normal and autonomic Sx may be present.

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15
Q

What Dz should be suspected if you have bilateral trigeminal neuralgia?

A

MS

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16
Q

What 3 general neurological findings occur in basal ganglia hemorrhage?

A
  1. Contralateral hemiparesis and hemisensory loss (because putamen is adjacent to internal capsule).
  2. Homonymous hemaniopia
  3. Gaze palsy (towards side of lesion) - due to damaged frontal eye field efferents in anterior limb
17
Q

How would an ischemic stroke of the midbrain present?

A

Typically presents as ipsilateral oculomotor nerve palsy, ataxia (due to damaged superior cerebellar peduncle), and contralateral hemiparesis

18
Q

Why is it that patients with CN III palsy typically have a down and out gaze with ptosis but still have pupillary response?

A

MCC of CN III palsy = ischemic neuropathy due to DM.

Two components of CN III (inner somatic fiber and superficial parasymp fibers on the outside). Since the inner somatic fibers are farther away from blood supply they are affected first.

** Note that in cases of CN III compression the parasymp fibers are typically affected&raquo_space; abnormal pupillary response (mydriasis)

19
Q

What are the treatment options for restless leg syndrome?

A

First line = dopamine agonists (pramipexole)

Second line = alpha 2 delta Ca2+ channel ligands (gabapentin)

20
Q

What’s the most common cause of lobar hemorrhage in older adults?

A

Cerebral amyloid angiopathy. Beta amyloid deposition in the walls of the arteries&raquo_space; vessel wall weakening and predisposition to rupture.

Occipital and parietal lobes are most often affected.

21
Q

If a patient presents with new onset loss of pain and temp over R face and L body, R bulbar muscle weakness (dysphagia, dysarthria), R sided horner’s syndrome, and vesitbulocerebellar impairment then what is the most likely Dx?

A

R sided lateral medullary infarct (Wallenberg syndrome) due to PICA or vertebral artery occlusion. Bulbar weakness is due to involvement of the nucleus ambiguus on that side.

22
Q

What clinical signs would help localize an infarction to the lateral pons vs the medulla?

A

All about pattern of CN involvement.

Mid pons lesions would affect the sensory and motor nuclei of CN V&raquo_space; impaired mastication, decreased jaw reflex, and impaired tactile sense of the face.

Lateral Medullary lesions would present with dysphagia, hoarseness, and diminished gag reflex due to CN IX and X involvement.

23
Q

What are first line treatment options for Alzheimers?

A

Cholinesterase inhibitors = donepezil (Aricept), galantamine (Razadyne), rivastigmine (Exelon).

Can also use memantine (NMDA R antag) for moderate to severe dementia.

24
Q

What is benztropine?

A

Anticholinergic used for PD

25
Q

What is pramipexole?

A

Dopamine agonist for PD

26
Q

What are the presenting Sx of drug induced parkinsonism and how do you treat it?

A

Sx = extrapyramidal symptoms, tremor, rigidity, bradykinesia and gait abnormalities. (NO fever or autonomic instability).

Rx = benztropine + diphenhydramine

27
Q

If an 63 year old woman presents with rapid onset eye pain and complains of seeing halos, and has tearing and headache with nausea and vomiting then what should be on the differential?

A

Acute Angle Closure glaucoma

- Nausea and vomiting happens as ICP ^

28
Q

Why do patients with central cord syndrome have weakness more pronounced in upper extremities vs the legs?

A

motor fibers serving the arms are closer to the central part of the corticospinal tract.

Pt may also experience occasional loss of pain an temp in the arms due to spinothalamic tract damage.

29
Q

Why does diffuse axonal injury happen mostly at grey white matter junction?

A

Diffuse axonal injury is the MCC of morbidity in Pt with TBI. Frequently due to deceleration injuries and can cause a vegetative state. Sudden accel-decel impact can create rotational forces (affects areas where there is greatest difference in density between the tissues)

Evidenced on CT scan by punctate hemorrhages and blurring of grey white interface.

30
Q

How do berry aneurysms in anterior vs posterior communicating arteries differ in presentation?

A

Anterior communicating = compresses central optic chiasm&raquo_space; bitemporal hemaniopia

Posterior communicating = CN III palsy&raquo_space; mydriasis, ptosis and down+out pupil

31
Q

What’s gold standard of Rx for GBS?

A

IV Ig and plasmapheresis