Neurology, otology and ophthalmology Flashcards
(192 cards)
1
Q
[EMBRYO]Name 3 primary vesicles of neural tube and their secondary vesicles, and what they become in adults.
A
2
Q
Medications associated with NTD
A
Folate antagonism
3
Q
Name spectrum of caudal NTD
A
4
Q
Name and describe 2 brain malformations incompatible with life
A
- Holoprosencephaly (failure of forebrain - prosencephalon) to divide into 2 cerebral hemispheres.
- Lissencephaly (smooth brain lacking sulci and gyri) - failure of neuronal migration.
5
Q
Dinstinguish between both Chiari malformations
A
Chiari malformations are a group of congenital disorders caused by underdevelopment of the posterior fossa. The small size of the fossa causes parts of the cerebellum and medulla to herniate through the foramen magnum.
6
Q
Dandy-Walker Malformation
A
Patients often present during infancy with developmental delay and progressive skull enlargement. Cerebellar dysfunction can result in unsteadiness and impaired muscle coordination. Non-communicating hydrocephalus may occur due to atresia of the foramina of Luschka and Magendie, resulting in symptoms of elevated intracranial pressure (eg, irritability, vomiting). Other associated features can include agenesis of the corpus callosum and malformations involving the face, heart, or limbs.
7
Q
Explain loss of sensation pattern in syringomyelia
A
8
Q
Neuron markers
A
Synaptophysin, neurofilament protein
9
Q
CNS glial (non-neuronal cells) (4) - Describe and compare.
Bonus - which of the cells is GAFP+?
A
10
Q
Steps (4) of action potential in the CNS
A
11
Q
Neuronal response to axonal injury (3 steps)
A
12
Q
Which part of the nerve sheath is responsible for the blood-nerve permeability barrier?
A
The perineurium
13
Q
A-gamma vs C-fibers of free nerve endings - compare and contrast
A
Sense pain and temperature, C-fibers are slow, unmyelinated whereas A-gamma are fast and myelinated
14
Q
Describe the following neurotransmitters: ACh, Dopamine, GABA, NE, and serotonin in terms of their location of synthesis and the changes we see in various disease processes
A
15
Q
EEG waveforms in order.
Mnemonic: At night, BATS Drink Blood
A
Awake: Beta Alpha
N1: Theta
N2: Sleep spindle
N3: Delta
REM sleep: Beta
16
Q
2 diseases associated with REM sleep behavior disorder
A
Lewy body dementia
Parkinson disease
17
Q
Name all 8 hypothalamic nuclei and their function
A
18
Q
Name all 5 thalamic nuclei and their function(s)
A
19
Q
Function of limbic system + components
A
Emotion, long-term memory, olfaction, behavior modulation and ANS function
- Hippocampus
- Amygdalae
- Mamillary bodies
- Anterior thalamic nuclei
- Cingulate gyrus
- Entorhinal cortex
Famous 5 F’s: feeding, fleeing, fighting, feeling, and sex
20
Q
What is the dopaminergic pathway which is significantly affected by Parkinson’s disease and antipsychotics?
A
The nigrostriatal pathway
Projects from substatia nigra –> dorsal striatum
21
Q
Name functions of 3 cerebellar peduncles
A
Inferior: input from spinal cord (proprioceptive) - balance, posture.
Middle (largest): input from cortex (coordination of voluntary movement and cortical planning)
Superior: output to cortex (motor)
22
Q
Striatum vs lentiform nucleus
A
Striatum = putamen (motor) + caudate nucleus (cognitive)
Lentiform nucleus = putamen + globus pallidus
23
Q
Describe the direct and indirect pathways of dopamine in the basal ganglia
A
Direct - endgoal = increase movement by exciting the thalamus. D1 receptors.
Indirect - endgoal = decrease movement by inhibiting the thalamus. D2 receptors
24
Q
What is Cushing reflex?
A
Triad of hypertension, bradycardia and respiratory depression in response to increased ICP. The goal is to preserve cerebral perfusion.
This is a late and ominous sign of impending brain herniation
25
Does ACA stroke affect legs or upper extremity
Legs!! Humonculus
26
What are watershed zones?
Zones between major cerebral arteries, that are most affected when there is a general decrease in cerebral perfusion (as opposed to a stroke)
27
Draw out the cerebral arteries
28
Describe the direction of CSF flow
1. Production in choroid plexus (specialized epydenmal cells in lateral ventricles)
2. Lateral ventricles
3. Interventricular foramina of Monro
4. Third ventricle
5. Cerebral aqueduct of Sylvius
6. Fourth ventricle
7. Foramina of Luschka (lateral) + Foramen of Magendie (medial)
8. Central canal of spinal cord
29
Where do all CNs exit the brain?
4 CN above pons (I, II, III, IV)
4 CN exit pons (V, VI, VII, VIII)
4 CN exit medulla (IX, X, XI, XII)
4 CN are medial (III, IV, VI, VII) - Factors of 12 except 1 and 2
30
Describe function of the colliculi
They are structures of the midbrain
**Superior colliculi - visual stimuli** processing, coordinate eye and head movements primarily to visual stimuli
**Inferior colliculi - auditory processing**, coordonate eye moevments to auditory stimuli
Mnemonic: Eyes above ears
31
What is a vagal nucleus? Can you name all 3 and the CNs that make them up?
Vagal nuclei are clusters of neurons in the brainstem associated with the vagus nerve (cranial nerve X). They are responsible for the motor, sensory, and parasympathetic functions of the vagus nerve.
1. Nucleus tractus solitarus: visceral sensory information (tase, baroreceptors, gut distension). **CN VII, IX, V**.
2. Nucleus ambiguus: motor innervation of pharynx, larynx and upper esophagus (e.g. swallowing, palate elevation). **CN IX, X**
3. Dorsal motor nucleus: autonomic PS fibers to heart, lungs, upper GI. **CN X**.
32
Draw a cross-section of the midbrain
33
Draw a cross-section of the pons
34
Draw a cross-section of the medulla
35
3 muscles of mastications
Masseter
Temporalis
Medial pterygoid
(My teeth much)
36
Dorsal columns organization in the spinal cord
Thoracic and cervical spinal cord:
Arms outside
Legs inside
Lumbar cord: only legs (1 dorsal column)
37
Describe the position of the following dermatomes (remember the mnemonics!):
C2
C3
C4
C6
T4
T7
T10
L1
L4
S2-S4
38
Symptoms of a lesion in the prefrontal cortex
E.g. frontotemporal dementia
Dishinhibtion, hyperphagia, impulsivity, loss of empathy, impaired executive function, akinetic mutism (like locked-in syndrome)
39
How does a PPRF lesion manifest?
The eyes look **away from brain lesion** and towards side of hemiplegia
40
Does INO involve the PPRF?
No, the INO involves the MLF
41
Contrast manifestations of a lesion in the dominant vs non-dominant parietal cortex
42
What is hemiballismus and where does a lesion need to arise in order for it to manifest?
Lesion in the subthalamic nucleus
= lage amplitude involuntary movements
43
What is Wernicke-Kosakoff syndrome?
Bilateral lesion of the mamillary bodies due to **thiamine deficiency** (vitamin B1) - acute confusion, ophthalmoplegia, ataxia, memory loss
Thiamine sources: whole grains, legumes, meats
44
How do bilateral lesions of the amygdalae manifest?
Kluver-Bucy syndrome: disinhibition (hyperphagia, hypersexuality, herporality). Seen in HSV-1 encephalitis
45
How do bilateral lesions of the hippocampi manifest?
Anterograde amnesia - seen in Alzheimer's
46
Most common cause of Parinaud syndrome, and what is Parinaud syndrome
Pineal gland tumors
Parinaud syndrome (also called dorsal midbrain syndrome) is a neurological condition caused by lesions in the dorsal midbrain, particularly around the superior colliculi.
47
Compare and contrast decorticate and decerebrate posturing. Which has the worst prognosis?
48
Describe histologic features of ischemic stroke with time away from stroke
49
Vasogenic vs cytotoxic edema - which is the early and which is the late consequence of ischemic stroke?
Cytotoxic - early, due to osmotic shift (e.g. stroke, Na+/K+ATPase dysfunction, SIADH, hyperammonemia, etc)
Vasogenic - late, due to disruption of the BBB (increased permeability). Other causes = trauma, hemorrhage, inflammation, tumors
50
Which arteries supply Wernicke and Broca areas respectively?
MCA in both cases!
51
Wernicke aphasia is associated with ______________________ due to temporal lobe involvement
Right superior quadrant visual field defect
52
Most common cause of lenticulostriate artery stroke, and its manifestations
Lacunar infarcts due to microatheroma and hyaline arteriosclerosis secondary to unmanaged hypertension
Affects striatum (putamen + caudate nucleus) and internal capsule - contralateral paralysis with absence of cortical signs (neglect, aphasia, visual field loss)
53
What is locked-in syndome and what causes it?
Basilar artery stroke of the pons, medulla and lower midbrain. Mnemonic = locked-in the **bas**ement
54
Distinguish UMN vs LMN lesion of the 7th CN
UMN: sparing of the forehead
LMN: no forehead sparing
55
Lateral medullary vs medial medullary syndromes
56
Compare Caput succedaneum and cephalhematoma
Vs subgaleal hemorrhage
Caput succedaneum: caused by prolonged fetal birth, resolves spontaneously
Cephalhematoma: forceps delivery, may lead to indirect hyperbilirubinemia
Subgaleal hemorrhage = serious and life-threatening. Blood accumulation between periosteum and gala aponeuosis (above cephalhematoma).
57
4 main types of intracranial hemorrhages + locations
58
Tell me about this kind of hemorrhage and most typical presentation
59
Tell me about this kind of hemorrhage and most typical presentation
60
Tell me about this kind of hemorrhage and most typical presentation
60
Diffuse axonal injury - definition + mechanism
60
Broca vs wernicke lesion in dominant hemisphere
Broca = intact speech comprehension but inability to speak
Wernicke = intact ability to speak but does not make any sense
60
Tell me about this kind of hemorrhage and most typical presentation
61
Saccular aneurysms vs Charcot-Bouchard aneurysms
62
Classification of seizures
63
Explain the phenomenon of ischemic neuronal death that extends beyond the isolated location of the ischemic infarct
64
Management of TIA
Anti-platelets
Statins
Lifestyle modifications
65
2 most susceptible parts of the brain to ischemic injury
The hippocampus is the most succeptible part of the brain to ischemic injury (3-5 minutes of hypoxia). Results in inability to make new memories. Then, it's the Purkinje cells and neocortex pyramidal neurons (5-10 minutes).
66
What is the pterion?
Pterion region: where the frontal, parietal, temporal and sphenoid bones meet. This is where the middle meningeal artery passes, which is a branch of the maxillary artery.
Associated with epidural hemorrhages
67
Nerve injured with transtentorial/uncal herniation
CN III
68
Tell me about brain herniation from epidural hematoma (order, symptoms)
When imminent, Cushing triad
69
Describe subfalcine, uncal, central and tonsillar herniations and symptoms
70
Tell me about IVH in the newborn
IVH almost always manifests within the first 5 postnatal days in infants born before 32 weeks gestation and/or with birth weight <1,500 g (3 lb 5 oz). IVH in a newborn can be clinically silent or present with altered level of consciousness, hypotonia, and decreased spontaneous movements. If the bleeding is severe, catastrophic deterioration can occur with a bulging anterior fontanelle, hypotension, tonic-clonic seizures, irregular respirations, and coma.
IVH in preterm infants usually originates from the germinal matrix, a highly cellular and vascularized layer in the subventricular zone (source of neurons and glial cells during brain development).
71
Most common cause of lobar hemorrhage (subtype of intraparenchymal hemorrhage)
Amyloid angiopathy
72
Treatment modalities for seizures (focal vs generalized vs absence)
73
Which anticonvulsant medication has the worst teratogenic effect?
Valproate
74
Status epillepticus management
Lorazepam (benzodiazepene) = treatment of choice for status epilepticus. Potentiates GABA action (inhibitory).
Phenytoin is administered concurrently to prevent recurrence of seizure.
75
Name anticonvulsant therapies according to where they act
76
MoA of benzodiazepines
Increased GABAA action by increasing the frequency of activation of Cl- channel opening
77
Tell me about temporal lobe epilepsy
most common type of focal epilepsy
78
Tell me about febrile seizure
79
Describe 3 main types of primary headaches
80
Describe treatment modalities for migraines
81
Management of trigeminal neuralgia
Carbamazepine
82
Carbamazepine major SFX
-Carbamazepine can cause bone marrow suppression: leading to aplastic anemia, agranulocytosis and thrombocytopenia. CBC should be monitored regularly.
-Hyponatremia due to increased sensitivity to ADH
-Carbamazepine is a P450 inducer that increases the metabolism of many other medications, thereby decreasing their effectiveness.
83
When are the following dyskenesias typically seen?
- Chorea
- Dystonia
- Essential tremor
- Intention tremor
- Hemiballismus
- Resting tremor
- Myoclonus
84
Tell me about Parkinson disease
85
Tell me about Huntington disease
86
Name 5 reversible causes of dementia
Depression (pseudodementia)
Hypothyroidism
Vitamin B12 deficiency
Neurosyphilis
Normal pressure hydrocephalus
87
Pathogenesis of Alzheimer's disease
**Beta-amyloid plaque deposition** causes increased excitotoxicity (glutamate NMDA receptor overactivity) = neuronal degeneration = **diffuse cortical atrophy**. Leads to loss of **cholinergic neurons**.
88
Proteins and association with Alzheimer's disease
89
Management principles of Alzheimer's disease
90
Early vs late findings in Alzheimer's disease
91
Pathophysiology of neurofibrillary tangles
Hyperphosphorylated tau protein which is normally associated with neuronal microtubules. Leads to disrupted axonal transport.
Associated with AD and FTD
92
Wernicke encephalopathy causes, triad and management
93
Frontotemporal dementia two proteins that are deficient
A. Tau, a protein associated with neuronal microtubules that normally takes part in microtubule stabilization. In patients with FTD, tau becomes hyperphosphorylated and disassociates from the microtubules --> neurofibrillary tangles.
B. TDP-43 (transactive response DNA-binding protein 43), a protein that normally functions as a transcription inhibitor or a DNA repair protein.
94
Lewy body dementia presentation and differences with Parkinson's
95
Vascular dementia presentation
96
Creutzfeltd-Jacob disease presentation and characteristics
- Prion disease (beta-pleated sheet resistant to proteases)
- Rapidly progressive (weeks-months)
- Myoclonus and ataxia
- Sporadic, but may be transmitted by contaminated materials (e.g. corneal transplant, neurosurgery equipment)
On microscopy, there is spongiform degeneration of the gray matter, which is characterized by formation of microscopic vacuoles within the neuronal processes. Cerebrum and cerebellum affected
*Mad cow disease
97
HIV associated dementia
Advanced HIV infection
Cognitive deficits, gait disturbance, irritability, depressed mood. Microglial nodules with multinucleated giant cells.
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Triad of normal pressure hydrocephalus
Wobbly, wacky and wet: gait apraxia (magnetic gait), cognitive dysfunction, urinary incontinence.
Dilated ventricles on neuroimaging, but does not result in increased subarachnoid space volume.
ICP normal.
99
Is NPH triad seen in ex vacuo ventriculomegaly?
No!! Because due to decreased brain tissue and neuronal atrophy as opposed to increased CSF.
ICP normal.
100
What are classic manifestations of relapsing-remitting Multiple Sclerosis?
Vitamin D deficiency
Female
20-50y
101
What is osmotic demyelination syndrome and when does it occur?
Massive axonal demyelination in the **pontine white matter**.
Secondary to osmotic changes, e.g. **iatrogenic correction of hyponatremia**. Causes acute paralysis, dysarthria, dysphagia, diplopia, LOC.
102
Correcting hyper- vs hypo-natremia too fast...
Hypo: "from low to high, your pons will die" (osmotic demyelination syndrome)
Hyper: "from high to low, your brains will blow" (cerebral edema/herniation
103
CSF and MRI findings of MS
CSF: oligoclonal bands, increased IgG and myelin basic protein
MRI: periventricular plaques, multiple white matter lesions disseminated in space and time
104
Management of MS
Disease-modifying therapies: beta-interferon, rituximab (anti-CD20 - B cells)
Acute flares: IV steroids
Sympathetic treatment for neurogenic bladder (muscarinic antagonists, botulinum injctions)
105
Guillain-Barré Syndrome
Most common subtype of acute inflammatory demyelinating polyneuropathy.
Autoimmune destruction of Schwann cells. Likely due to **molecular mimicry** associated with infections (CMV, Campylobacter jejuni).
Symmetric ascending muscle weakness/paralysis. Autonomic dysregulation.
106
GBS CSF findings
Increased CSF protein with normal cell count
107
Do steroids aid management of GBS
No. Respiratory support is critical until recovery. Plasma exchange of IVIg is treatment.
108
Charcot-Marie-Tooth. Tell me everything you know.
Hereditary (AD), due to lack of proteins involved in peripheral nerve and myelin sheath production.
Foot deformities: pes cavus, hammer toe.
Manifests as lower extremity weakness and sensory deficits.
109
Progressive multifocal leukoencephalopathy
110
What disease is this?
Neurofibromatosis type I.
AD, 100% penetrance.
NF1 tumor suppressor gene mutation on chromosome 17.
Increased risk of developing CNS neoplasms
111
Neurofibromatosis type II.
Autosomal dominant mutation in NF2 tumor suppressor gene on Chromosome 22.
112
What are cutaneous neurofibromas made of (type of tissue) in neurofibromatosis type I?
Cutaneous neurofibromas usually manifest during early adolescence as multiple, raised, fleshy tumors (<2 cm) that often increase in size and number with age. **These are benign nerve sheath neoplasms predominantly comprised of Schwann cells, which are embryologically derived from the neural crest.**
113
Von-Hippel-Lindau disease
114
What is detected on amniocentesis for the diagnosis of NTD?
Amniotic fluid consists primarily of fetal urine; therefore, it can contain fetal serum proteins such as alpha-fetoprotein (AFP). Amniotic fluid does not usually contain acetylcholinesterase (AChE), an enzyme normally concentrated in the cerebrospinal fluid (CSF). Therefore, elevated AChE on amniocentesis suggests a leak of fetal CSF into the amniotic cavity known as an open neural tube defect (NTD).
115
What disease is this and what can you tell me about it?
Tuberous sclerosis complex.
116
What are the 6 most common primary adult brain tumors?
GOMe HiPS
Glioblastoma
Oligodendroglioma
Meningioma
Hemangioblastoma
Pituitary adenoma
Schwannoma
117
What is this adult primary brain tumor and what can you tell me about it?
Glioblastoma.
118
What is this adult primary brain tumor and what can you tell me about it?
Oligodendroglioma.
Frontal lobes, calcified.
Rare.
119
What is this adult primary brain tumor and what can you tell me about it?
120
What is this adult primary brain tumor and what can you tell me about it?
Cerebellar commonly
Associated with Von-Hippel-Lindau disease when found with retinal angiomas
Can produce erythropoietin --> secondary polychythemia
121
What is this adult primary brain tumor and what can you tell me about it?
122
What is this adult primary brain tumor and what can you tell me about it?
Classically at cerebello-pontine angle
Benign
commonly arise from the vestibular branch of cranial nerve VIII
123
What is the most common primary brain tumor in childhood and what can you tell me about it?
Pilocytic astrocytoma
124
What is the most common **malignant** brain tumor in childhood and what can you tell me about it?
125
What is this common pediatric tumor and what can you tell me about it?
Craniopharyngioma.
126
What is the most common extragonadal germ cell tumor and what can you tell me about it?
Pineal gland tumor.
127
Are fasciculations seen with UMN or LMN lesions?
LMN
128
What is polio?
Poliomyelitis, caused by polio virus.
Asymmetic destruction of anterior horn cells = LMN acute signs and symptoms of viral meningitis (fever, headache, neck stiffness).
CSF shows increased WBC and slight increase in proteins with no change in glucose.
Now largely eradicated thanks to vaccines
129
Name the diseases associated with the following spinal cord lesions
130
Tell me about SMA (spinal muscular atrophy).
Congenital degeneration of AHC.
Autosomal recessive SMN1 mutations
LMN apoptosis
Symmetric weakness, with LMN signs only.
Classic presentation- floppy baby: hypotonia (flaccid paralysis) and tongue fasciculations
131
Tell me about ALS (amyotrophic lateral sclerosis)
UMN + LMN degeneration
Usually idiopathic
**No sensory or bowel/bladder deficits**
Fatal most often due to respiratory decline
132
What spinal cord disease does T pallidum cause?
Tabes dorsalis
= tertiary syphilis
Degeneration and demyelination of dorsal columns. Causes progressive **sensory ataxia**. Positive Romberg sign.
133
What type of spinal cord degeneration can Vitamin B12 cause?
Subacute combined degeneration: demyelination of spinocerebellar tracts, lateral corticospinal tracts, and dorsal columns.
134
What does spinal artery occlusion cause?
Spares dorsal horns and dorsal columns. Can be caused by AAA repaired.
UMN signs below the lesion, LMN at the level of the lesion and loss of pain and temperature below the lesion.
135
Describe Brown-Séquard Syndrome
136
Describe Friedreich ataxia
137
What kind of vitamin deficiency can mimic Friedreich ataxia?
Vitamin E
138
Replace the sentences with "toward" and "away".
139
3 bones in the middle ear
Malleus, incus, stapes
140
What is the middle ear bone that we can see through the tympanic membrane?
Malleus
141
Otitis externa pathogen and presentation and complication
Pseudomonas
Water exposure (swimmer's ear), ear canal trauma/occlusion (hearing aids).
Presents with otalgia that worsens with ear manipulations.
Complication: malignant necrotizing otitis externa. Invasive infection causes osteomyelitis.
142
Otitis media pathogens and presentation and complication
Strep pneumo, Haemophilus influenzae, Moraxella catarrhalis.
Fever, otalgia, hearing loss
Bulging, erythematous tympanic membane that may rupture.
Complication = mastoiditis, which may lead to brain abscess.
143
Describe Weber and Rinne test for differentiating between conductive and sensorineural hearing loss + findings in each
144
tell me 3 refractive errors and how to correct them.
145
Compare open-angle and close-angle glaucome
OAG: Anterior chamber angle is open, increased IOP due to increased resistance to aqueous humor drainage through trabecular meshwork.
CAG: angle is closed or narrowed. Associated with anatomical anomalies (e.g. lens displacement). When accute,
146
Signs and symptoms of acute angle-closure glaucoma
Severe eye pain
Conjunctival erythema
Sudden vision loss
Halos aronud lights
Headaches
Fixed and mid-dilated pupil
Nausea and vomiting
147
How does age-related macular degeneration present?
Elderly, scotomas.
If wet: **metamorphopsia**
148
Two types of ARMD
Dry (most common) - gradual, subretinal deposits (drusen)
Wet - rapid, secondary to bleeding due to choroidal neovascularization.
149
Two types of diabetic retinopathy
Non-proliferative (most common): microaneurysms, hemorrhages
Proliferative: retinal neovascularization due to chronic hypoxia. Abnormal new vessels may cause vitreous hemorrhage and tractional retinal detachment
150
Retinal artery occlusion presentation
Acute, painless monocular vision loss
151
Triad of retinitis pigmentosa
Optic disc pallor
Retinal vessel attenuation
Retinal pigmentation with bone spicular-shaped deposits
152
Retinopathy of prematurity pathophysiology
In utero: hypoxic conditions
Prematurity: hyperoxia due to O2 management for RDS
Stage 1. Hyperoxia suppresses VGEF, so less blood vessels for a growing eye. This causes hypoxia of the avascular retina.
Stage 2. Hypoxia of the retina induces eventual retinal neovascularization which in turn may lead to tractional retinal detachment and hemorrhage (those vessels are unstable).
153
What is the most common intraocular malignancy in children? What mutation causes it?
Retinoblastoma.
RB1 tumor suppressor genes on Chr13
154
ID the following retinal disorders:
155
DDx leukocoria in newborn
Congenital cataracts
Retinoblastoma
156
Which is which between miosis and mydriasis and which type of ciliary nerves are responsible for each?
Miosis - constriction (PS) - short ciliary nerves
Mydriasis - dilation (sympathetic) - long ciliary nerves
157
Triad of Horner Syndrome
Miosis
Ptosis
Anhidrosis
158
Causes of Horner syndrome along 3 neurons involved in this sympathetic chain
- 1st neuron (from hypothalamus to cervical spinal cord): pontine hemorrhage, spinal cord lesion above T1 (e.g. Brown-Sequard syndrome, late-stage syringomyelia), lateral medullary syndrome
- 2nd neuron (from spinal cord to superior cervical ganglion): stellate ganglion compression by pancoast tumor. Stellate ganglion is the "from".
-3rd neuron (from SCG to destination): carotid dissection (painful)
159
Which CN innervate which EOM?
160
What is the difference between strabismus and amblyopia?
Amblyopia may be due to strabismus.
161
Draw out CN III in cross-section. What type of fiber is central vs peripheral?
162
Draw out the visual defects of the following affections
163
What structures go through the cavernous sinus?
I, TOMATO
ICA
Trigeminal nerve
Ophtalmic division
Maxillary division
Abducens nerve
Trochlear nerve
Oculomotor nerve
164
What is the MLF (ophthalmology)
Medial longitudinal fasciculus
Pair of tracts that interconnect CN VI and CN III nuclei.
165
Explain how a right INO (internuclear ophthalmoplegia) lesion would manifest
Right INO = Right MLF legion
Right MLF = pathway communicating **from left CN VI** to **right CN III**.
Therefore, right gaze OK
Left gaze impaired with nystagmus towards the center
166
What benzodiazepines can be used in heavy alcohol consumers?
Lorazepam, Ozaxepam and Temazepam [can be used for those with liver disease who drink a LOT] due to minimal first pass metabolism
167
What are the 3 categories of insomnia therapies and mechanisms of action?
168
What is the clinical indication and the mechanism of action of triptans + give an example
E.g. Sumatriptan
MoA: 5-HT agonists - inhibit trigeminal nerve activation, prevent vasoactive peptide release, induce vasoconstriction.
Use: acute migraine and cluster headache attacks
169
Parkinson disease therapy in young vs old patients
Young: non-ergot dopamine agonists
Old: levodopa/carbidopa
170
Why do we give carbidopa with L-DOPA for Parkinson's?
inhibit peripheral conversion to dopamine by inhibiting the dopa decarboxylase inhibitor
Increases bioavailability of L-DOPA in the brain and limits its peripheral adverse effects of fopamine
171
Name the drug for Parkinson's that increases dopamine availability by increasing its release and decreasing its reuptake
Amantadine
172
Name the strategies for Parkinson's disease management (pharmacological)
173
Treatment principles of Alzheimer's disease pharmacology
1. AChE inhibitors (first-line)
2. NMDA receptor antagonist to prevent excitotoxicity mediated by Ca2+
174
ALS principle of treatment phamacology
Riluzole
Decrease neuron glutamate excitotoxicity
Improves survival
175
Huntington disease management principle pharmacology
Inhibits VMAT = decreased dopamine vesicle packaging and release
176
Sensory order of loss with local anesthetics
Pain
Temperature
Touch
Pressure
177
Categories of local anesthetics and name a few in each
Esters and amides
178
MoA of local anesthetics
Binding to voltage-gated Na+ channels on inner portion of the channel along nerve fibers.
179
In infected tissue, do we need more or less local anesthetic for maximal use and why
More because infection is acidic whereas local anesthetics are alkaline and therefore penetrate the membrane more difficultly
180
Is a gas with low solubility in blood more or less potent
Less potent but **acts faster**.
E.g. N2O = rapid induction and recovery times, but MAC = 105% so not potent at all.
181
Compare blood and lipid solubility of anesthetics and what they affect and if it makes them more or less potent
182
Compare high vs low blood-gas partition coefficient
183
Compare two classes of neuromuscular blocking drugs. Name their Moa, some drugs in each category, antidotes. Which one carries the risk of malignant hyperthermia?
184
What are atropine and glycopyrrolate and why would you give them in junction with AChE inhibitors
They are muscarinic receptor blockers meant to prevent the adverse parasympathetic activation that occurs when we increase ACh in the synaptic cleft (e.g. in reversal of nondepolarizing neuromuscular blocking agents)
185
What is the hypermetabolic condition that can arise when inhaled anesthetics or succinylcholine are administered? Tell me about the etiology of this condition.
Malignant Hyperthermia.
De novo or inherited AD mutations in the ryanodine receptors = increased Ca2+ release from sarcoplasmic reticulum = sustained muscle contraction.
This manifests as hypercapnia, tachycardia, generalized muscle rigidity (seen in the masseter muscle of mastication), rhabdomyolisis, hypertermia.
186
What is the pharmacological treatment principle of malignant hyperthermia?
Dantrolene - ryanodine receptor antagonist
187
What is capsaicin and when is it used?
188
Glaucoma therapy agents
BAD humor may not be Politically Correct
189
