SAS/Review Flashcards
Which brain tumors are most likely to arise in young children?
- Pliocytic astrocytoma
- Grade I glioma
- Ependymoma
- Grade II, technically a glimoa but not aways classified that way
- Medulloblastoma
- Grade IV neuronal
- Atypical teratoid/rhabdoid tumor
- Grade IV, neuronal
Retinal vein occlusion leads to [hemorrhage/blanching]
Retinal artery occlusion leads to [hemorrhage/blanching]
Retinal vein occlusion leads to hemorrhage
Retinal artery occlusion leads to blanching
What kind of drug is phentolamine?
What is it used for?
Nonselective alpha-blocker
- Drug of choice for MAO I induced hypertensive crisis
- Hypertensive paroxysms in pheochromocytoma
Basically, out of control hypertension

Which parasympathomimetic is used to treat dry mouth in Sjogren’s?
Cevimeline or pilocarpine
- Stimulate parasympathetic salivation
- Cevimeline is the best one - will also treat other Sjogren symptoms
List 4 locations of demyelinating events characteristic of MS
- Optic neuritis
- Blurred vision, decreased vision, pain with eye movement
- Cerebellar lesion
- Difficulty with balance or coordination
- Spinal cord inflammation
- Bilateral weakness, numbness
- Hemispheric lesion
What kind of tumor is this?
What is the cell of origin?

Meningioma - meningothelial cells
- Dural tails
- Noninfiltrative
- Homogenous enhancing
Describe the symptoms of atropine poisioning (5)
Atropine = anticholinergic
- > decreased parasympathetic activity
- > increased sympathetic activity*
-
Dry as a bone
- Decreased secretions, urinary retention
- **Eccrine sweat gland secretion is inhibitied; only sympathetic action that no longer works
-
Hot as a stove
- **Due to decreased sweating
-
Red as a beet
- Compensates for heat
- Also hitamine is released
-
Blind as a bad
- Pupillary dilation
-
Mad as a hatter
- Delerium, hallucinations, eventual coma
Isolated, bilateral impairment in adduction can result from a lesion in the:
- 6th nerve nucleus
- 3rd nerve fascicle
- 3rd nerve nucleus
- Bilateral orbits
- Bilateral medial longitudinal fasciculus
e. Bilateral Medial longitudinal fasciculus
Indicates demylinating disease or brainstem ischemia
- 6th nerve nucleus -> loss of saccade to one side
- Ex: neither eye can look at an object on the right
- 3rd nerve issue -> Eyes look down and out, pupils dilated
A patient is unable to look left of midline with their left eye. All other eye movements are intact
What is the most likely cause?
CN VI palsy
- If the right eye can look to the left, the saccade signal is intact
- This indicates CN VI palsy, not a problem with the CN VI nucleus
- May be associated with CN V and CN VII palsy
A patient is anesthetized with rocuronium for both intubation and surgery.
When surgery is over, what drug can be given to aid recovery?
How does it work?
Sugammadex
- Like a donut that chelates rocuronium and gets it out of the NMJ
- Works more quickly than neostigmine
What are the signs of transtentorial herniation?
The following appear as the herniation gets worse:
(Ipislateral = the side that is herniating)
- Ipsilateral CN III palsy
- Contralateral weakness
- When the ipsilateral peduncle is compressed
- Ipsilatearl weakness
- When the contralateral peduncle is compressed

A stroke in which artery would result in all of the following symptoms?
- Severe right leg weakness
- Mild right shoulder weakness
- Spastic reflexes on the right side
- Paralysis of the right lower face
Left middle cerebral artery
Describe 4 characteristics of organophosphorous poisoning
Organophosphorous agents = irreversible anticholinesterase
-> tons of parasympathetic action
- Salivation
- Lacrimation (eye watering)
- Urinary frequency (micurition)
- Defecation
Which parasympathomimetic is used to treat GI stasis and urinary retention?
Bethanecol
- Enhances muscle wall contraction and sphincter relaxation
A 22 year old obese women presents with grey outs of her vision when she stands up, headaches, and horizontal binocular diplopia when she looks to the right.
Testing reveals enlarged blindspots, normal color vision and no afferent pupil defect.
What is the most likely pathology?
What do you expect the optic disc to look like?
Papiledema
Bilateral optic nerve swelling, cotton wool spots possible

Describe the status of the following during a phase I block by a depolarizing neuromuscular blocker:
- Membrane potential:
- ACh receptor:
- Volatage-gated Na+ channels:
Phase I block = block by depolarization
- Membrane potential: near equilibirum potential
- No gradient to drive ion flow
- ACh receptor: Occupied by the blocker
- Volatage-gated Na+ channels: Inactivated
- Due to the initial depolarization
- ONLY at the end plate region (presynaptic Na+ channels are fine
- Note: these are TTX sensitive Na+ channels
What kind of drug is yohimbine?
What is it used for?
- Selective alpha-2 blocker
- -> CNS stimulation, aphrodisiac
- -> Used to treat impotence in diabetics
What method of central sensitization results in the activation of the NMDA receptor?
Wind up
- Activated by constant, repetitive stimulation from C fibers?
How do the presentations of MS, ALS, and MG differ?
- MS
-
Weakness AND numbness (spinal cord inflammation)
- Sensory AND motor deficit
- Visual complaints common (optic neuritis)
-
Weakness AND numbness (spinal cord inflammation)
- ALS
-
Weakness ONLY
- No numbness or tingling
- NO visual complaints
- May begin with difficulty speaking
-
Weakness ONLY
- MG
- Weakness worse with activity and stress
- Classic: Ptosis that worsens with sustained upward gaze
- Visual complaint = diplopia
Inhibition of the mGluR6 receptor inhibits the function of which cells?
What is the effect?
Rod bipolar cells
Decreased night vision
Which “neurotransmitter” is important for generating an erection?
NO
- Parasympathetic stimulation
- -> Increased NO synthase activity
- -> increased NO
- -> NO diffuses into smooth muscle
- -> Activates guanylyl cyclase
- -> cGMP
- -> PKG
- -> Phosphorylation
- -> Relaxation + erection

Which method of central sensitizaton results from A-beta fibers “acting like C-fibers”?
Phenotype switching
Due to actions of CGRP
Which of the following is most likely to produce these results?

A) Magnesium
B) Botulism
C) Myasthenia gravis
D) Hemicholinium-3
E) Myasthenic (Lambert-Eaton) Syndrome
C) Myasthenia gravis
- In MG, you will see EPP, MEPP, and response to ACh decline in proportion to each other
- Due to destruction of ACh receptors
- In LEMS you would see decresased EPP amplitude, but no change in MEPPs or response to ACh
- Due to decreased number of P/Q type Ca2+ channels in the membrane
Describe the management of a patient with a ruptured globe
Put a shield over the eye
Call opthomology immediately - this is an emergency!
In a person with normal NMJ physiology, what kind of drug would produce these results?

Non-depolarizing blocker
- Same EPP, MEPP, as myasthenia gravis
Which one of the following pairs of agents act non-synergistically at the neuromuscular junction?
A) Pyridostigmine and calcium gluconate
B) Botulinum toxin and TTX
C) Pancuronium and vecuronium
D) Neomycin and tubocurarine
E) Magnesium salts and pancuronium
C) Pancuronium and vecuronium
- Pancuronium and vecuronium act by the same mechanism
- Both are non-depolarizing blockers
- This means they cannot act synergistically
What is the best drug to reduce intraocular pressure in patients with glaucoma?
What is a common side effect?
Lananoprost
- Type of drug: Prostaglandin analouge
- Works by increasing AH outflow through the uveal-scleral route
- Side effect = darkening of hazel eyes
A patient is anesthetized with SUX for intubation and then vecuronium during surgery
When some recovery is observed, what drug can be given to aid recovery?
How do you know when recovery is complete?
Neostigmine can accelerate recovery
- Anticholinesterase = more ACh will be in the NMJ = more muscle function
Recovery is complete when a train of 4 produces 4 twitches
What pathology is important to rule out in any patient with suspected AION?
How shoudl you manage this suspected pathology?
Temporal arteritis
- AION = sudden, painless, altitudinal visual field defect
- More likely in older vs. younger patinets
- Treat with steroids until temporal arteritis is ruled out
How does sildenafil work to treat erectile dysfunction?
Sildenafil = PDE inhibitor
- Allows cGMP to hang out longer
- -> PKG activation
- -> Phosphorylation
- -> Cavernosal smooth muscle relaxation
- -> Erection
Remember:
- Parasympathetic stimulation
- -> Increased NO
- -> Diffuses into cavernosal smooth muscle
- -> Activates guanylyl cyclase

Which channels are affected by succinylcholine during a phase I block by depolarizaiton?
- Ligand-gated nonspecific cation channel at the motor end plate
- Binds SUX
- Channels opens and remains open -> depolarizing block
- Voltage-gated Na+ channels (TTX sensitive) at the motor end plate
- Incactivated by depolarization
When a high dose of intracardiac epinephrine is given..
What is the immediate effect on HR and BP?
What happens as the dose begins to wear off?
- Immediate
- HR increases at first due to direct beta-1 effect on the SA node. This also increases contractile strength
- BP increases at first due to the effect of EPI on the SA node
- Later
- BP stays high due to an alpha-1 effect on blood vessels
- HR decreases as a result of reflex bradycardia
- Eventually
- BP returns to normal as the dose wears off completely

Which one of the following direct effects of sympathethetic nerve stimulation would be blocked by atropine at the end organ?
- decrease in heart rate
- decrease in airway resistance
- prostate gland contraction
- eccrine sweat gland secretion
- dilation of the pupil
D. eccrine sweat gland secretion
- Atropine is an anticholinergic
- Most sypathetic effects are due to adrenergics/catecholamines
- Eccrine sweat gland secretion is mediated by sympathetic cholinergics
What is the difference between a floater and a scotoma?
A floater lags behing eye movement
A scotoma is fixed; it doesn’t drift in the field of vision
What is this visual field deficit called?
Where does it localize?

Right homonymous superior quadrantopia
Left temporal lobe lesion
- Pie in the sky = contralateral temporal lesion
- Pizza on the floor = contralateral parietal lesion
Which fibers contribute most to “constant burning pain”?
C fibers
- A-delta fibers also transmit pain, but they are more for “fast pain”
Which two drugs are used to manage pheochromocytoma?
- Phenoxybenzamine = management
- Phentolamine = hypertensive paroxysms
Both are nonselective alpha blockers
A patient presents with a dilated right pupil after head trauma.
Their right eye cannot look up or left of midline.
What is the most important diagnosis to exclude?
Posterior communicating aneurysm
- Look for this in anyone with CN III palsy
- Can lead to subarachnoid hemorrhage if missed
What kind of drug is mirabegron?
What is it used for?
Beta-3 receptor agonist
Treat overactive bladder
An optic disc that is “swollen with splinter hemorrhages” indicates what pathology?
What visual field defect do you expect?
Anterior ischemic optic neuritis (AION)
Expect inferior altitudinal defect

A - MS
What would you expect the histopathology of an infarct to look like at the following time points?
- 1 day:
- 5 days:
- 2 weeks:
- 2 months:
- 1 day:
- Red neurons
- 5 days:
- Lipid laden macrophages
- Gliosis
- 2 weeks:
- More lipid laden macrophages in sheets
- Gliosis
- Cavitation
- 2 months:
- CSF-filled cavity
- Sub-pial tissue kind of supporting the structure
Describe the status of the following during a phase II block by a depolarizing neuromuscular blocker:
- Membrane potential:
- ACh receptor:
- Volatage-gated Na+ channels:
Phase II block = block by desensitization
- Membrane potential: Recovered
- Back to physiologic normal
- ACh receptor: Occupied by the blocker AND desensitized
- Volatage-gated Na+ channels: Can be activated by depolarization
What method of central sensitiztion results in A-beta fibers innervating the parts of the dorsal horn that A-delta and C fibers usually innervate?
Neuronal sprouting
Which brain tumor is most likely to arise in the cerebellum?
Pliocytic astrocytoma
A patient presents with complete loss of somatic senses on the right side of their body (no sensation of pain, temperature, touch, pressure, vibration, or proprioception)
They are not experiencing any motor or cranial nerve deficits.
What is the most likely location of the legion?
Left thalamus
- No crossed symptoms or cranial nerve symptoms
- => Not the brainstem
- Entire right body affected
- => Not the cortex; one legion is unlikely to affect the entire sensory homuncluus
- Legion of the posterior capsule is possible, but unlikely
- Would have to be very, very small to have this effect
In a patient with MS, what do you expect to see on…
- MRI:
- CSF:
- MRI
- Demyelination
- Findings in gray and white matter, but more visible in white
- CSF
- Oligoclonal bands
How would propranolol affect the action of low doses of epinephrine
Normally, epinephrine would increase HR via Beta-1 activation
However, propranolol is a beta blocker
Propanolol would prevent HR increase due to epinephrine
What is the effect of increased cGMP or cAMP on smooth muscle?
Relaxation
Which drugs to treat BPH are best for patinets with orthostatic hypotension?
-osin drugs: Selective alpha-1a inhibitors
- Tamsulosin
- Silodosin
NOT -azosins; these block alpha-1a and alpha-1b, and can cause orthostatic hypotension
Occlusion of which artery leads to lateral medullary syndrome?
PICA
What symptmoms would indicate acute closed angle glaucoma, rather than retinal artery occlusion?
Both are acute-onset
- Glaucoma
- Increased sensitivity to light
- Extreme pain
- Peripherla vision loss/blurred vision
- Retinal artery occlusion
- Painless
- Sudden loss of vision
What kind of drug is an -oprost?
What is it used for?
Prostaglandin analouge
- Increases AH outflow via uveal-scleral route (thorugh ciliary muscle)
- This is the best drug to reduce intraocular pressure
- Used to treat glaucoma
- May result in irreversible darkening of iris in hazel-eyed patients!
What is the relevant fact about drug metabolism that we should remember for beta blockers?
CYP2D6 required for metabolism
Variation -> beta blocker not metabolized as well
- May result in super slow HR, bronchiole constriction
May need to use lower dose or other drug?

What class of drugs are used to treat benign prostatic hypertrophy?
Alpha-1A blockers
-osin drugs
- Afuzosin
- Silodosin
- Tamsulosin
Note: the nonselective alpha-1 blockers (-azosins) can treat BPH, but not used becuase they can cause orthostatic hypotension
Where is the legion?
What is this syndrome called?

Ventral Midbrain Syndrome aka Weber’s Syndrome in the right midbrain
- Ipsilateral CN III palsy
- Ipsilateral facial weakness
- Contralateral motor deficits
What are the possible causes of amblyopia?
- Strabismus
- Unequal refractive error
- Media opacity
Basically, anything that causes vision in one eye to be worse than the other
Treatment is to occlude the good eye
Which parasympathomimetic is used to treat glaucoma?
Pilocarpine
- Narrow angle: Pilocarpine leads to…
- Contraction of pupillary sphincter and ciliary muscle
- -> Uncrowds the filtration angle, allows AH to drain
- Wide angle: Pilocarpine leads to…
- Contraction of pupillary sphincter and ciliary muscle
- -> Improved trabecular tone
- -> Opening of pores, allowing AH to flow out
The inner retina is…
- Closest to the inside of the eye
- Deepest in the skull
a. Closest to the inside of the eye

What adrenergic agonist can be used to treat overactive bladder?
What receptors does it act on?
Mirabegron
Beta-3 agonist
- Sympathetic effects on the bladder:
- Relax muscle wall
- Constrict sphincter
- -> hold the pee in so you can run away from a bear/scary monster
Which drugs are selective alpha-1 agonists?
Selective alpha-1 agonists = vasoconstriction without inhibition of cellular functions
- Phenylephrine
- Imidazolines
- Oxymetazoline
- Xylometazoline
- Midodrine

C. Emboli
- Drusen are unlikely to cause vision loss
- Cotton wool spots are whiter and more spott-y
Describe the features of central cord syndrome?
- Loss of pain/temperature sensation in a “slice” of the body
- Ex: shoulders and arms, bilaterally
- Weakenss in a “slice
- Ex: hands, finger flexors and extensors, shoulders bilaterally
What would you expect the gross pathology of an infarct to look like at the following time points?
- 1 day:
- 5 days:
- 2 weeks:
- 2 months:
- 1 day:
- Swelling/edema, not a lot of change
- 5 days:
- Edema, gelatinous, blurring of border between white/gray matter
- 2 weeks:
- Liquifactive necrosis
- 2 months:
- CSF-filled cavity
What deficits would be present in a patinet with an MLF lesion?
Isolated ipsilateral adduction impairment
A lesion in the right MLF = the right eye can’t look left
- Convergence is intact
- => Eye can adduct, but there is no signal telling them to adduct when there is an object on the contralateral side