In Class

Question 1

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

Answer 1

Anticipatory N/V would be tx with something like benzodiazepines

Question 2

NSAIDs do cause some hearing loss (reversible)

Peripheral neuropathy: cisplatin (accumulate in DRG), vincristine, vinblastine, taxanes

4: All are sedating, with anticholinergic effects

Answer 2

Setrons are good prophylaxis for chemotherapy

Question 3

“Nocibo” effect; anticipatory of bad outcome

Answer 3

Question 4

Question 5

Stroke doesnt affect the vestibular apparatus (it just is- dont know why)

Answer 5

Dont tx forever! You will damper central compensation

Question 6

B. Only

If you get a CT might as well get a CT angiogram too for large vessel disease

Answer 6

Notice the basillar artery thrombosis

Question 7

Note that a right beating nystagmus (the direction of the catch-up saccade) would indicate either left vestibular neuritis or right cerebellar disfunction/stroke

1. Right

Answer 7

Menieres

Question 8

2. Low salt diet and diuretics

Answer 8

2. Immediate but temporary relief

Lesion would be on the right

Question 9

2. No

Answer 9

4. Acute vesticular neuritis

Question 10

Menieres causes vertigo via rupture of Reissner’s membrane which seperates endolymph and perilymph

Answer 10

Question 11

Higher decibels needed at all frequencies

Answer 11

Sensorineural= hgher frequencies lost more

Question 12

Ex. cant understand men but can understand women’s voices

Answer 12

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

Question 13

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)

Answer 13

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!

Question 14

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)

Answer 14

Ice water calorics will inhibit the vestibular apparatus

Question 15

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)

Question 16

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

Answer 16

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

Question 17

Classic vestibular neuritis- present all the time (continuous- not BPPV)

Answer 17

Question 18

C. LP (subarachnoid until proven otherwise)

MRI is not as good as CT in detecting hemorrhage

Answer 18

F.

Question 19

Right: Cant really see the sulci (occluded by blood) and the ventricles has red cells

Answer 19

Question 20

WNL= within normal limits

No hx of confusion limits subdural hematoma

5. GCA (consider age, temporal tenderness, muscle aches)

Answer 20

5.

ESR could be elevated in infection, inflammation, or cancer

Temporal artery ultrasound needs to be proved with biopsy

Question 21

3. Prednisone

Answer 21

4. Vision loss can occur rapidly

Question 22

May see anisecoria

B. nasal oxygen (CCB is good for prophylaxis)

Meperidine causes rebound (opiates)

Answer 22

Question 23

A: Subdural

B: Subarachnoid

C: Contusion

D: Epidural

Answer 23

Question 24

7. Broca’s Aphasia

Answer 24

Question 25

4. Better at picking up blood

Answer 25

5. Notice the ptosis and pinpoint pupil (loss of sympathetics)

Question 26

2. Give IV tPA within an hour or two and need a CT angiogram to ID which vessel clots are too big for only tPA

Answer 26

6. All of the above

Question 27

Answer 27

4.

Question 28

4.

Answer 28

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.

Question 29

Question 30

1. head CT scan

Answer 30

2. Look for the lucid interval

Question 31

4. Forced vital capacity Fundoscopic exam would be normal

Answer 31

3. Guillain-Barre Syn.

Question 32

3.

Question 33

3.

Answer 33

Question 34

NSAIDs good until 3rd trimester

Answer 34

4.

Question 35

Ergots tend to last much longer than triptans!!

Answer 35

C.

Question 36

E.

Answer 36

2. Worried about serotonin syndrome

Question 37

3. Cat X= ergots

Answer 37

C.

Question 38

C.

Answer 38

B.

Question 39

Answer 39

2.

Question 40

4.

Answer 40

Question 41

Answer 41

Question 42

Answer 42

Anticoag= worry about subdural hematoma

Question 43

Question 44

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.

Answer 44

B.

Question 45

C.

Answer 45

A.

Question 46

B. Not seen with premedication (with a benzo commonly) but this is the body fighting the anesthetic and short lived

Answer 46

C.

Question 47

A.

Answer 47

C.

Question 48

B.

Answer 48

B.

Question 49

B.

Answer 49

E. Sevoflurane

Question 50

B. Thiopental will only last about 10-15 minutes

Answer 50

D.

Question 51

B.

Answer 51

A. Benzos have a ceiling

Question 52

B.

Answer 52

E. Etomidate

Question 53

C. Increases neuronal activity

Answer 53

E. Etomidate

Question 54

C. Ketamine

Question 55

Answer 55

D. Malignant Hyperthermia

Question 56

D. Lidocaine

Answer 56

C.

Question 57

B.

Answer 57

B. Ionized forms of the drugs actually block the channel

Question 58

Answer 58

D. Lidocaine

Question 59

D. Hygoglycemia

Answer 59

C.

Question 60

Answer 60

Question 61

Answer 61

Question 62

2. CN III (may even cause CN III on the opposite side-10%)

Answer 62

3.

Question 63

5.

Answer 63

5.

Question 64

5.

Answer 64

5.

Question 65

4. 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)

Answer 65

1.

Question 66

4.

Question 67

Answer 67

Question 68

1.

Answer 68

2.

Question 69

4. B12 deficiency

Answer 69

3.

Question 70

3.

Answer 70

5.

Question 71

Hu Abs