Uncovered High-Yield Topics Flashcards

1
Q

What does a normal CSF study look like?

A
  • Opening pressure 5-20 cm water
  • Glucose 50-80 mg/dL (or ~2/3 of serum glucose)
  • Protein 15-40 mg/dL
  • WBC < 3 (<30 in neonates)
  • RBC < 5
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2
Q

AIP vs Wilson’s disease

A

AIP is acute in onset while Wilson’s is gradual

AIP is associated with neuropathic sensations (abdominal pain w/o tenderness, tingling sensations) while Wilson’s is assocaited with movement disorders.

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3
Q

Five P’s of AIP

A
  • Painful abdomen (often confused for acute abdomen, leading to a belly full of scars)
  • Purple urine (urine is colorless initially, but exposure to light causes PBG in urine to oxidize and gives urine its color).
  • Peripheral neuropathy (patchy numbness and paresthesias)
  • Psychological disturbances (anxiety, confusion, psychosis, dementia)
  • Precipitated by drugs or dietary changes (drugs that enhance cytochrome P-450 activity, sulfa drugs, barbiturates, some antipsychotics, alcohol)
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4
Q

Myotonic dystrophy

A
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6
Q

Myotonia

A

Delayed muscle relaxation

Should make you think of myotonic dystrophy

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7
Q

In whom should you use amitryptaline with caution?

A
  1. Patients over age 65 (it has anticholinergic activity)
  2. Patients on multiple other drugs that can cause serotonin syndrome
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8
Q

Steroid psychosis

A

People on high dose steroids can have steroid-induced psychosis!

Little is known about underlying risk factors, but if someone develops new psychosis on high-dose steroids you should trial holding the steroids.

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9
Q

Classic onset of ALS

A
  • Dysphagia
  • Dysarthria
  • Tongue fasciculations
  • Paradoxical breathing (expansion of abdomen on expiration rather than inspiration, caused by diaphragmatic weakness)
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10
Q

Things that mess with anterior horn cells

A
  • Heritable syndromes (spinal muscular atrophy)
  • Lead poisoning
  • Polio myelitis
  • West Nile Virus myelitis
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11
Q

Treatment of PCP intoxication

A
  • Involves treatment of agitation and aggression
  • Benzodiazepines
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12
Q

Really, most parotid gland masses are benign. But, if they grow to involve ___, they are probably malignant.

A

Really, most parotid gland masses are benign. But, if they grow to involve the facial nerve, they are probably malignant.

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13
Q

What diseases does a negative ANA likely exclude?

A
  • SLE
  • Scleroderma
  • MCTD
    • The sensitivity for these diseases is quite high (>90%), but still not entirely perfect. Other diseases you really shouldn’t take a negative ANA into much consideration since it is closer to ~50% positivity
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14
Q

Wilson’s disease pathophysiology

A
  • Autosomal recessive disorder
    • Mutation in ATP7B, a transport protein
    • It is genetic!! Not just copper toxicity
  • Characterized by the reduced excretion of copper into the bile secondary to a transport abnormality, leading to the pathologic accumulation of copper in the liver and other tissues, particularly the brain
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15
Q

Copper chelators

A
  • Penicillamine – pee out copper
  • Trientine – poop out copper
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16
Q

Delayed facial nerve palsy

A

Sometimes occurs after trauma to the head

Basically, the facial palsy does not develop until ~24-48 hours later, when the edema becomes more significant

When this occurs, it will be a complete facial nerve palsy, not an isolated lower facial nerve palsy. The latter should be concerning for epidural hemorrhage.

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17
Q

Connection of the frontal eye field to the cranial nerves

18
Q

Chiari malformation

A

Type I: Cerebellum into the spinal cord

Type II: More cerebellum into the spinal cord, and a myelomeningocele

19
Q

COAT RACK for Wernicke’s and Korsakoff’s

20
Q

A lesion above the red nucleus leads to resting ___.

A lesion below the red nucleus leads to resting ___.

A

A lesion above the red nucleus leads to resting flexion.

A lesion below the red nucleus leads to resting extension.

Basically think of the red nucleus as sending out a default “extend” signal to the body, which is overridden by cortical input.

21
Q

Sign of diffuse axonal injury on CT

A

“Blurring of white-gray junction”

22
Q

Various temporal lobe functions

23
Q

Causes of Kluver-Bucy syndrome

24
Q

Presentation/Features of Kluver-Bucy syndrome

25
Q

What do the superior colliculi regulate?

What commonly damages them?

A

They regulate vertical gaze (superior/inferior)

They are commonly damaged in Parinaud syndrome

26
Quick rule of thumb for HIV infections and CD4s
27
Mnemonic for normal pressure hydrocephalus
"Wet, wild, wacky" Wet -- urinary incontinence Wild -- gait unsteadiness Wacky -- dementia
28
Whipple's disease
* Mostly in males over age 40 * Intracellular gram + bacteria that stains on **PAS** * Clinical features: * Malabsorption + abd pain + **diarrhea** * **Arthritis** * **Movement symptoms** (ataxia, myoclonia, ophthalmoparesis) * Diagnosis: Small intestine biopsy with PAS staining (if GI symptoms present). PCR testing also available for GI or CSF samples. * Treatment: **IV ceftriaxone or penicillin for 2-4 weeks, then batrim for 1 year.**
29
Transient global amnesia
* Presentation: **Abrupt onset, transient memory loss** following **psychological stress or vigorous exercise** * Amnesia is **anterograde, sometimes with partial retrograde** * By definition, takes **\< 24 hours to resolve****, and resolution is complete** * Diagnosis: **Clinical,** but EEG and MRI have associated findings and can rule out other etiologies * EEG: rule out epilepsy/simple partial seizure * **MRI: Shows focal hyperintensities in the hippocampi** * Treatment: None. Self-resolving. Sometimes may monitor for 24 hours if the diagnosis is in question.
30
Two types of infection from Taenia sollium
* If acquired from ingestion of larva in raw pork: **Intestinal taeniasis** * May be asymptomatic * May present with GI upset or malabsorption (similar to trichinellosis or ascariasis) * If acquired from eggs in human faeces (ie, in someone who was infected with intestinal taeniasis): **Cysticercosis** * May manifest in several tissues * **Neurocysticercosis:** Headache, elevated ICP, FNDs, seizures. MRI w/ multiple ring-enhancing lesions (early stage). LP w/ eosinophilia. * **Ocular cysticercosis:** Subretinal cysts on ophthalmologic exam
31
Waterhouse-Friderichsen syndrom
* An **endotoxin-triggered coaguolpathy** that may be induced by **Neisseria meningitidis** * Characterized by the purple, spotty **purpura** of N. meingitidis and **acute adrenal insufficiency** or **adrenal hemorrhage.**
32
Treatment for cryptococcal meningitis
* Induction therapy with **amphotericin B + flucytosine** * Maintenance with **8 weeks of fluconazole**
33
Uncal herniation syndrome (Garret)
Ipsilateral CN 3 palsy Contralateral paralysis Risk of ipsilateral PCA strokes -- The medial temporal lobe is squished against the midbrain
34
Diffuse cerebral edema in cardiac collapse
Due to hypoxic injury
35
Metabolic encephalopathies may precipitate \_\_\_
Metabolic encephalopathies may precipitate **diffuse cerebral edema**
36
ICP ladder
* Head of bed at 30 degrees * Hyperventilation * Hypertonic saline / mannitol * Skull decompression * Therapeutic hypothermia
37
Prophylactic hemicraniectomy
* If you have a patient with a large territory infarct, this may result in cerebral edema that can be life threatening * Hemicraniectomy may be performed to prevent life threatening herniation
38
Right MCA language changes
* Prosody changes * Anomia * Paraphasic errors
39
Treatment for neurocysticercosis
Praziquantel and Albendazole
40
Area postrema syndrome
Subtype of neuromyelitis optica (NMO), hence anti-AQP4 will be present. Characterized by episodes of **intractable nausea, vomiting, and/or hiccups** MRI shows enhancement of *just* the area postrema, which is in the **dorsal medulla** just inferior to the cerebellum.