In Class Flashcards
Hearing loss seen only in phase IV trials
Platin cells are taken up via copper transporters and produce apoptosis (irreversible death of cells, not disfunction)
Vestibular system drugs like antihistamines/anticholinergic would apply to motion sickness and dizziness associated with movement
Anticipatory N/V would be tx with something like benzodiazepines
NSAIDs do cause some hearing loss (reversible)
Peripheral neuropathy: cisplatin (accumulate in DRG), vincristine, vinblastine, taxanes
4: All are sedating, with anticholinergic effects
Setrons are good prophylaxis for chemotherapy
“Nocibo” effect; anticipatory of bad outcome
Stroke doesnt affect the vestibular apparatus (it just is- dont know why)
Dont tx forever! You will damper central compensation
B. Only
If you get a CT might as well get a CT angiogram too for large vessel disease
Notice the basillar artery thrombosis
Note that a right beating nystagmus (the direction of the catch-up saccade) would indicate either left vestibular neuritis or right cerebellar disfunction/stroke
- Right
Menieres
- Low salt diet and diuretics
- Immediate but temporary relief
Lesion would be on the right
- No
- Acute vesticular neuritis
Menieres causes vertigo via rupture of Reissner’s membrane which seperates endolymph and perilymph
Higher decibels needed at all frequencies
Sensorineural= hgher frequencies lost more
Ex. cant understand men but can understand women’s voices
Hearing loss seen with these commonly but no complaints of vestibular dysfunction/vertigo because of central compensation (remember that antinausea drugs will blunt this compensation and delay recovery)
ataxia can be seen
Remember that turning your head to the right will cause the right vestibular apparatus to PUSH the eyes to the left to maintain central vision (i.e. Doll’s Eye maneuver)- i.e. loss of one side will push the eyes toward the weak side (ie. infection, cold water calorics)
peripheral vertigo pts can typically be sent home and central compensation will kick in
Visual fixation can mask nystagmus! (basis of frenzel glasses)
“central” vertigo will present with other signs like ataxia, hemiparesis, CN dysfunction, etc.
Basilar migraine- cortical spreading depression can affect the brainstem as well!
vestibular neuritis (consistent vertigo!) can present like a cerebellar stroke or basillar artery thrombosis (these can present with pure vertigo without anything else initially)- Need to do a head thrust maneuver to differentiate (CT scan will be too early to see anything) (head thrust is normal with cerebellar stroke and abnormal with neuritis)
NOTE: The cerebellum ipsilaterally inhibits the vestibular apparatus (thus stroke of the cerebellum increases the firing pushes the eyes to the other side). Thus if you had a left cerebellar stroke, it would be present like a right vestibular neuritis (catch up saccades needed when turning head to right)
Ice water calorics will inhibit the vestibular apparatus
Vertigo
With ototoxcity (from i.e. aminoglycosides) there is no vertigo because both sides are affected equally but it ill manifest when the pt walks or reads because they cant balance (cant move head and read something stationary)
Classic BPPV eyes on Dix-Hallpike Maneuver= vertical nystagmus when looking medial and torsional when looking lateral and mixed when looking forward
Alexander Law= nystagmus becomes more pronounced with increased gaze distance
Note that there are central etiologies of POSITIONAL (not constant) vertigo like BPPV
BPPV wont produce symptoms in the horizontal plane (side to side)- only when the psoterio canal is stimulated
Classic vestibular neuritis- present all the time (continuous- not BPPV)
C. LP (subarachnoid until proven otherwise)
MRI is not as good as CT in detecting hemorrhage
F.
Right: Cant really see the sulci (occluded by blood) and the ventricles has red cells
WNL= within normal limits
No hx of confusion limits subdural hematoma
5. GCA (consider age, temporal tenderness, muscle aches)
5.
ESR could be elevated in infection, inflammation, or cancer
Temporal artery ultrasound needs to be proved with biopsy
- Prednisone
- Vision loss can occur rapidly
May see anisecoria
B. nasal oxygen (CCB is good for prophylaxis)
Meperidine causes rebound (opiates)
A: Subdural
B: Subarachnoid
C: Contusion
D: Epidural
- Broca’s Aphasia
- Better at picking up blood
- Notice the ptosis and pinpoint pupil (loss of sympathetics)
- Give IV tPA within an hour or two and need a CT angiogram to ID which vessel clots are too big for only tPA
- All of the above
4.
4.
- Congophilic angiopathy
Lumbar hemorrhages (those of a single love) dont typically occur with HTN. HTN hemorrhage cause destruction of deep grey structures like basal ganglia, thalamus, etc.
- head CT scan
- Look for the lucid interval
- Forced vital capacity
Fundoscopic exam would be normal
- Guillain-Barre Syn.
3.
3.
NSAIDs good until 3rd trimester
4.
Ergots tend to last much longer than triptans!!
C.
E.
- Worried about serotonin syndrome
- Cat X= ergots
C.
C.
B.
2.
4.
Anticoag= worry about subdural hematoma
Note that with inhaled anesthetics, the more lipid they are, the more they are sequestered in lipids in the body and the slower the onset of unconsciousness
C.
B.
C.
A.
B. Not seen with premedication (with a benzo commonly) but this is the body fighting the anesthetic and short lived
C.
A.
C.
B.
B.
B.
E. Sevoflurane
B. Thiopental will only last about 10-15 minutes
D.
B.
A. Benzos have a ceiling
B.
E. Etomidate
C. Increases neuronal activity
E. Etomidate
C. Ketamine
D. Malignant Hyperthermia
D. Lidocaine
C.
B.
B. Ionized forms of the drugs actually block the channel
D. Lidocaine
D. Hygoglycemia
C.
- CN III (may even cause CN III on the opposite side-10%)
3.
5.
5.
5.
5.
- Intubation and hyperventilation- she is herniating. Hyperventilate to reduce ICP to give 30 min to get to OR (mannitol will take about 15 minutes to kick in so give that after)
1.
4.
1.
2.
- B12 deficiency
3.
3.
5.
Hu Abs
