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[3] Step 1 USMLE > Neurology > Flashcards

Neurology Flashcards

1
Q

Neonatal Abstinence Syndrome

Classic Signs - 5

A

TYT Does Heroin

  1. Tremors
  2. Yawning
  3. Tachypnea
  4. Diarrhea
  5. High Pitched Cry

Caused by maternal opioid (Heroin) use during pregnancy

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2
Q

Which Germ Layer does the ANT Pit come from?

A

Surface Ectoderm

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3
Q

A: Primary CNS Lymphoma is the ___ most common cause of _____ in HIV pts

B: What virus is this associated with?

C: What WBCs would you expect to see in the brain tissue

A

A: 2nd most common cause of ring enhancing lesions in HIV pts (1st = Toxoplasmosis Gondi)

B: EBV

C: B-lymphocytes

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4
Q

A: What function does the iliohypOgastric nerve have (3)

B: What happens when Surgery (Appendectomy) damages it? (2)

A

A:

  1. [Suprapubic Sensation]
  2. [Gluteal Region Sensation]
  3. [Anterolateral Abd Mucle Motor]

B: Loss of the above areas + [Suprapubic Burning]

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5
Q

Dandy Walker Malformation

Clinical Manifestation (2)

A

(Dan - D - Walk - Er = 4 syllables = 4th Vt Dilitation (2/2 → )

+

Can’t walk with NO CEREBELLUM FORMATION!

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6
Q

A: Wilson Disease MOD

B: Wilson Disease Mode of Inheritance and genetic cause

A

A: Damaged Hepatocytes leak free copper and the copper deposits in other tissues (basal ganglia / cornea)

B: [Auto Recessive ATP7B gene mutation]

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7
Q

Wilson Disease Clinical Manifestation (4)

A
  1. Hepatic (Acute Liver Failure - Cirrhosis & Chronic Hepatitis)
  2. Neuro - (Gait Ataxia / Parkinsonism)
  3. Psych - Personality Changes
  4. Cornea - Kayser Fleishcer rings
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8
Q

Wilson Disease

A: Dx (2)

B: Tx

A

A: DEC Ceruloplasmin and [INC Urinary Copper Excretion]

B: D-Penicillamine

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9
Q

Causes of Congenital Hydrocephalus (4)

A
  1. Congenital Obstruction (aqueductal stenosis vs. [Chiari malformation Type 2])
  2. Acquired Obstruction (infection vs. posthemorrhagic)
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10
Q

A: Congenital Hydrocephalus Clinical Manifestations (6)

B: Tx

A

PEDS w/ Mushy Brain

  1. Macrocephaly
  2. Bulging Fontanelle
  3. Enlarged Ventricles
  4. Poor feeding
  5. Developmental Delay
  6. [Spasticity & Hyperreflexia (from periventricular pyramidal tract stretching)]

B: Ventriculoperitoneal Shunt

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11
Q

Most common [1° CNS Tumors] in PEDs (3)

A

PEDs

Pilocytic Astrocytoma = MOST COMMON

Ependymoma

meDulloblastoma (PNET tumor) = 2nd most common

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12
Q

Which 2 Pediatric Brain Tumors occur in the [Cerebellar Vermis]

A

[Pilocytic Astrocytoma] and meDulloblastoma

Cerebellar Vermis = Midline POST fossa

Image shows [Pilocytic Astrocytoma]

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13
Q

A: Histology for [PNET - Primitive NeuroEctodermal Tumors] (MeDulloblastoma)

B: Pgn

A

A: Sheets of [small, primitive blue cells] + [abundant mitotic figures]

B: POOR! (PNET tumors are undifferentiated and aggressive)

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14
Q

A: Histology for [Pilocytic Astrocytoma] (3)

B: Pgn

A

A:

Pilocytic Astrocytes (spindle cells with hair-like glial processes)

+

Rosenthal Fibers

+

[Cerebellar Vermis Cyst]

B: (Better than MeDulloblastoma since it is well-differentiated)

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15
Q

A: Describe Opsoclonus-Myoclonus Syndrome

B: What Childhood tumor is it associated with?

A

A: [Non-Rhythmic Conjugate Eye mvmnts] with myoclonus= “Dancing Eyes and Feet”

B: Neuroblastoma (onset 2 y/o)

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16
Q

Neuroblastoma Histology

A

[Homer Wright Rosettes] made of [small round blue cells w/purple nuclei]

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17
Q

A: Neuroblastoma Genetic cause

B: Neuroblastoma Pgn

A

A: N-myc amplifcation

B: [Better pgn for pts < 1 yo]

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18
Q

Describe the Neuroblastoma metastasis process (6)

A

image

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19
Q

Histology for [Acute Neuronal Injury] (AKA ___ _____) (4)

A

[Acute Neuronal Injury (AKA RED NEURON)]

  • Cell Body Shrinks
  • Nuclei Pyknosis
  • Loss of Nissl substance
  • Eosinophilic Cytoplasm

THIS IS IRREVERSIBLE INJURY that eventually –> Neuronal Degeneration!

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20
Q

What causes [Acute Neuronal Injury] (AKA ___ _____) and When do the changes appear?

A

[Acute Neuronal Injury (RED NEURON)]

12-24 Hrs post [Transient Severe Insult]

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21
Q

Histology for [Chromatolysis Axonal Rxn (Loss of Axon)] (4)

A

[Chromatolysis Axonal Rxn (Loss of Axon)]

  • Cell Body ENLARGES
  • Nucleolus ENLARGES
  • Eccentric nucleus
  • Dispersion of Nissl substance
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22
Q

Histology for [Neuronal Atrophy 2° to Degenerative Dz] (2)

A
  • Neuronal Loss eventually (compensated for by Gliosis)
  • Reactive Gliosis = Astrocyte proliferation in area of neuron degeneration –> Glial Scar (compensates for volume loss)

Can come After [Acute Neuronal Injury (AKA RED NEURON)]

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23
Q

A: What are Craniopharyngiomas

B: What type of tissue do they arise from

A

A: Suprasellar Pediatric tumors

B: Remnants of Rathke’s Pouch (Embryonic Precursor of ANT Pituitary)

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24
Q

A: Craniopharyngiomas Composition

B: What type of tissue do they arise from

A

A: [Brownish Calcified Cyst containing cholesterol and [wet keratin]

B: Remnants of Rathke’s Pouch (Embryonic Precursor of ANT Pituitary)

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25
Q

A: Deep [Intraparenchymal HTN Hemorrhage] is most commonly caused by _____, which results in rupturing of _____

B: This begins as a ______ Aneurysm

A

A: Deep [Intraparenchymal HTN Hemorrhage] is most commonly caused by HTN, which results in rupturing of [lenticulate small penetrating arteries]

B: Charcot Bouchard Aneurysm

Acute [Intraparenchymal HTN Hemorrhage] in image

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26
Q

Where does Charcot Bouchard Aneurysms occur (4)

A

Charcot Bouchard Tears Pink

  • Basal Ganglia
  • Cerebellum
  • Thalamus (shown in image below)
  • Pons

Acute [Intraparenchymal HTN Hemorrhage] in image

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27
Q
  1. What’s the Difference in size between [Charcot Bouchard Aneurysms] and [Berry Saccular Aneurysms]?
  2. Which is associated with Subarachnoid Hemorrhage?
A
  1. [Charcot Bouchard Aneurysm] = < 1 mm

vs.

[Berry Saccular Aneurysm] = 2-25 mm variable

  1. [Berry Saccular Aneurysm] = Subarachnoid Hemorrhage
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28
Q

What conditions are associated with [Berry Saccular Aneurysm]? (5)

A

“Eating AppleBerries Can Sound Heavenly”

  1. ADPKD**
  2. [Ehlers Danlos Syndrome]
  3. HTN
  4. SAH
  5. Coarctation of Aorta (associated w/HTN)
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29
Q

Where do [Berry Saccular Aneurysms] occur?

A

Circle of Willis

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30
Q

Dx for Multiple Sclerosis (3)

A
  • MRI: [Periventricular demyelinating plaques with lipid laden macrophages]
  • CSF Oligoclonal IgG bands
  • Visual Assessment (test conduction velocity)
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31
Q

A: Syringomyelia MOD

  1. How does this manifest (2)
A

Formation of [CSF filled syrinx cavity] in cervical region of spinal cord –> damages [Ventral white commissure (crossing fibers for STT)] –> [Bilateral Pain/Temp Loss in Arms & Hands]

***Eventually Ventral Horns are destroyed also –> LMN signs (FAW) - Fasciculations / Atrophy & Areflexia / Weakness

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32
Q

Destructive Site for Syringomyelia

A

A

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33
Q

What type of Hydrocephalus is shown

A

Normal Pressure Hydrocephalus

CT: Symmetrical Dilation of Ventricles

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34
Q

A; Normal Pressure Hydrocephalus Sx (3)

B: What causes Normal Pressure Hydrocephalus

A

Wacky, Wobbly & Wet!

Wacky (dementia)

Wobbly (ataxia)

Wet (Urinary Incontinence from compressing periventricular cortex white fibers traveling to sacral micturition center)

B: Idiopathic; Episodic; Occurs in Elderly. Does not INC SubArachnoid space volume.

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35
Q

Which vessels are affected by [TUMTL-Transtentorial Uncal Medial Temporal lobe] Herniation? (5) What manifestations result from this?

A

[TUMTL Hernation–> Compression of [COPPR- [Crus Cerebri CTL] / PCA / [Oculomotor CN3] / Paramedian Pontine vessels/ Reticular Formation] –>

  1. [Crus Cerebri CTL] compression –> CTL Hemiparesis
  2. [PCA compression] –> Occipital lobe infarct –> CTL homonymous hemianopsia w/Macular sparing
  3. Oculomotor CN3 compression –> [Ipsilateral “Down & Out” Eye + Dilated Pupil + Ptosis]
  4. Paramedian Pontine vessel compression –> Duret Hemorrhage
  5. Reticular formation compression–> Altered Mental Status
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36
Q
  1. Clinical Manifestation for [MIOS-MLF Internuclear Ophthalmoplegia Syndrome] (3)
    2: MIOS seen in Younger pts indicates _____
    3: MIOS seen in OLDER pts indicates ______
A

[MIOS-MLF Internuclear Ophthalmoplegia Syndrome]

1.

*[Impaired ADDuction of affected eye]

+

[Normal ADDuction of affected eye during [near reflex convergence]

+

*[Nystagmus of UNaffected eye when attempting to ABduct]

C:

1) Younger pts= Multiple Sclerosis
2) Older pts= Ischemic infarction

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37
Q

Clinical Manifestation of Multiple Sclerosis (9)

A

Charcot classic triad of MS is a [SLUM SiiiN] !

Sensory sx

Lheurmitte sign = pain when chin is touched to chest

Uhthoff phenomenon (heat sensitivity)

Motor sx

Scanning Speech

[Internuclear Ophthalmoplegia (MIOS) w/eye pain] / Intention Tremor / Incontinence

Neuritis Optic - Loss of vision with Marcus Gunn Pupils

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38
Q

Ocular Clinical Presentation for Diabetic Mononeuropathy (3)

A

DM –> Oculomotor CN3 Central Ischemia

  • Ptosis (from Levator Palpebrae paralysis)
  • Down & Out Eye
  • NORMAL PERRL (since Parasympathetic fibers are spared)
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39
Q

Which part of the Cerebellum would cause Truncal and Gait Ataxia? What system is affected?

A

Upper Vermis - Medial Descending System

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40
Q

Which part of the Cerebellum would cause Vertigo/Nystagmus (2)? What system is affected?

A

Flocculonodular Lobe

+

Medial Descending System

Vestibular Nuclei

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41
Q

Which part of the Cerebellum would cause [Limb Dysmetria & Rebound Check Response loss]? What system is affected?

A

Intermediate Hemispheres - [Lateral Descending system]

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42
Q

Which part of the brain demonstrates the most atrophy in Alzheimer’s Dz? (2)

A

Hippocampus and Temporoparietal Lobe

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43
Q

Identify

A

image

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44
Q

Identify

A

image

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45
Q

What 2 brain cells come from Neuroectoderm?

A

Astrocytes and Oligodendrocytes

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46
Q

Embryologically, where does Microglia originate from?

A

[Mesoderm - Bone Marrow Monocytes]

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47
Q

Describe Oligodendrocyte Histology

A

Pale halO surrounding [small / round / dark nuclei] cells

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48
Q

[Creutzfeldt Jakob Dz] MOD

A

PrP (prion protein), normally in neurons as [a-helical structure] converts–> [INFECTIOUS Beta pleated sheets] –> Protease resistance –>

Vacuoles in [Gray Matter Neurons & Neutrophils] develop –> Cyst = [Spongiform Gray Matter]

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49
Q

Microscopic findings for [Creutzfeldt Jakob Dz]

A

Vacuoles in [Gray Matter Neurons & Neutrophils] develop –> Cyst = [Spongiform Gray Matter]

Remember: These PrP are INFECTIOUS!

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50
Q

Facial CN7 Functions (4)

A

FACE

  1. Facial Muscles
  2. Afferents(Somatic) from [Ear Pinna (Pain/Temp)] & [External Auditory Canal (stapedius m.)]
  3. Cry: Parasympathetics to [Lacrimal/Salivary/Sublingual/Submandibular/]
  4. Eat: Taste from ANT 2/3 Tongue
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51
Q

Clinical Manifestations for [Bells Palsy] (4)

A

​Bells Palsy = Facial CN7 paralysis

Loss of F –> Unilateral Paralysis

Loss of A –> Hyperacusis

Loss of C–> DEC Eye lacrimation (tearing)

Loss of E –> Loss of ANT 2/3 Tongue Taste

FACE

  1. Facial Muscles
  2. Afferents(Somatic) from [Ear Pinna (Pain/Temp)] & [External Auditory Canal (stapedius m.)]
  3. Cry: Parasympathetics to [Lacrimal/Salivary/Sublingual/Submandibular/]
  4. Eat: Taste from ANT 2/3 Tongue
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52
Q

What Spinal Columns are affected in [Subacute Combined Degeneration]?-3 ; How does this manifest?-3

A

[SuBACute Combined Degeneration]

[Demyelinating lesions] in 3 Thoracic Spinal Columns:

  1. [Dorsal–> Loss of 2TVP]
  2. [Lateral CST –> UMN Weak MESH + Ataxia]
  3. Spinocerebellar
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53
Q

Causes of [Subacute Combined Degeneration] (3)

A

[SuBACute Combined Degeneration]

1) B12 Deficiency
2) Copper Deficiency
3) AIDS/HIV
* Affects Dorsal / Lateral CST / Spinocerebellar Tracts (Combined)*

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54
Q

Describe SChWannoma Histology (3)

A

SChWannoma

  • Cellularity with Biphasic pattern (Antoni A & B areas)
  • [Verocay Bodies within Antoni A areas]
  • S100 positivity (indicates neural crest origin) - also seen in melanoma

Verocay Bodies = Interspersing nuclear free zones within Antoni A palisading pattern: shown in image

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55
Q

Where does SChWannomas arise from (3)

A

SChWannoma

Peripheral n. vs. Nerve Roots vs. [All CN except 2]

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56
Q

Most common type of Intracranial SChWannoma. Where is it located?

A

SChWannoma

Acoustic Neuroma: located at [CN8 Cerebellopontine Angle]

Verocay Bodies = Interspersing nuclear free zones within Antoni A palisading pattern: shown in image

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57
Q

Identify the arrow AND what Dz it’s associated with

A

SChWannoma

Verocay Bodies = Interspersing nuclear free zones within Antoni A palisading pattern: shown in image

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58
Q

Myotonia Dystrophy Clinical Manifestation (5)

A

My Tonia, My Toupee, My TV Viewers, My Ticker, My Testicles,

Tonia = MyoTonia = [sustained muscle contraction with Weakness & Atrophy]

Toupee = Frontal Balding

TV viewer = Cataracts

Ticker = Arrhythmia

Testicle = Testicular Atrophy

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59
Q

Myotonia Dystrophy MOD

A

My Tonia, My Toupee, My TV Viewer, My Ticker, My Testicles,

Auto Dom [CTG repeat] on [DMPK (Dystrophy Myotonia Protein Kinase) gene] –> Type 1 Dystrophy

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60
Q

Describe Histological finding for [Ischemic Hypoxic Encephalopathy]

A

Bilateral Wedge shaped strips of necrosis over the cerebral convexity, parallel & adjacent to the [longtitudinal cerebral fissure]

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61
Q

List the Location of Watershed infarcts in the Brain (2)

A

Between perfusion Zones of [ANT-Middle] and [Middle-POST] Cerebral a.

Bilateral Wedge shaped strips of necrosis over the cerebral convexity, parallel & adjacent to the [longtitudinal cerebral fissure]: shown in image

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62
Q

Chiari Malformation MOD

A

Congenital Underdevelopment of [POST Fossa] –> [Cerebellar and Medulla herniation] through foramen magnum

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63
Q

Describe Chiari Malformation Type 2

A

Type 2 is TOO BAD:

SEVERE NEONATAL ONSET –> [LUMBAR MYELOMENINGOCELE] & [CONGENITAL HYDROCEPHALUS]

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64
Q

Huntington’s Dz MOD

A

[AUTO DOM [Chromo 4 CAG repeats]] —> Degeneration of (Caudate nc. inside the ((I)ndirect Striatum) –> [DEC GABA]

“Hunting 4 food is way too aggressive & dancey”

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65
Q

Huntington’s Dz Clinical Presentation (2)

A

“Hunting 4​ food is way too aggressive & dancey”

1st: Aggressive Dementia w/ strange behavior
2nd: Dance-like Chorea mvmnts

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66
Q

When does Huntington’s Dz onset

A

30 - 40 y/o

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67
Q

Parkinsonism Clinical signs (7)

A

PARK & ham

[Pill Rolling Resting Tremor]

[Rigidity Cogwheel]

BradyKinesia

[AReflexia posturally] –> Fall

+

  • hypOphonic speech
  • Autonomic Dysfunction (constipation / bladder problems / orthostatic hypOtension)
  • micrographia
  • PARK = primary signs*
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68
Q

Friedreich Ataxia involves Degeneration of the ______, [____ and ____ spinal columns]

A

FriEdreich Ataxia involves Degeneration of the [Dorsal and Spinocerebellar spinal columns]

FriEdrecih is Fratastic! He’s your fav. twisted frat brother, always studdering and falling, but has a sweet, big heart

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69
Q

A: Deficency of what Vitamin mimics Friedreich Ataxia

B: Friedreich Ataxia Mode of Inheritance

A

FriEdreich Ataxia

A: Vitamin E (will also have Hemolytic anemia)

B: [Chromo 9 Auto Recessive]

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70
Q

Describe Friedreich Ataxia (8)

A

FriEdreich is Fratastic! He’s your fav., twisted frat iHouse brother, always studdering and falling, but has a sweet, big heart

FriEdreich = [Vitamin E Deficiency] mimics it

Fratastic has 9 letters = [Chromo 9 Auto Recessive]

twisted = Kyphoscoliosis @ childhood

frat = [frataxin (iron binding protein) defect]

iHouse = [(iron binding protein) defect]

studdering = Dysarthria

falling = [Falls + Gait Ataxia + (Pes Cavus High Foot Arch)]

sweet = DM

big heart = Hypertrophic Cardiomyopathy

Involves Degeneration of [Dorsal, Lateral CST & Spinocerebellar]

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71
Q

Explain the MOD for this Dz process (2)

A

Liquefactive Necrosis

Hypoxic CNS Injury —> Lysosomal complete digestion of necrotic tissue –> cystic cavity formation

vs.

Bacteria or Fungal Abscess formation also –> Liquefactive Necrosis

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72
Q

What causes Coagulative Necrosis

A

Irreversible Ischemic Injury (every organ EXCEPT BRAIN)

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73
Q

What causes FAT Necrosis

A

Acute Pancreatitis

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74
Q

What causes Caseous Necrosis (5)

A

TB vs. Histoplasma vs. Cryptococcus vs. Coccidioides vs. Nocardia

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75
Q

Morphology for Coagulative Necrosis (2)

A
  1. Preserved Tissue Architecture (since lytic enzymes denature b4 they have a chance to break dwn)
  2. Anucleated Cells with eosinophilic cytoplasm
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76
Q

Morphology for FAT Necrosis

A

Release of Lipase allows fatty acids to combine with Ca+ –> [Chalky White Saponification]

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77
Q

Morphology for Caseous Necrosis (2)

A
  1. Cheesy Tan-White Appearance
  2. Granuloma
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78
Q

What structures does the lenticulostriate vessels perfuse (5)

A

lenticulostriate vessels perfuse everything in [Be TIPC] EXCEPT PONS!

Basal Ganglia

Thalamus = pure sensory stroke

[Internal Capsule / / Corona Radiata] = pure motor stroke

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79
Q

Lacunar Stroke MOD

A

lenticulostriate vessels perfuse [Be TIPC]

Lacunar Stroke= [HTN Arteriolosclerosis] of lenticulostriate vessels –> [cystic infarcts < 15 mm] –> Lacunar Syndrome

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80
Q

Describe the Lacunar Syndrome

A

lenticulostriate vessels perfuse [Be TIPC]

Lacunar Stroke= [HTN Arteriolosclerosis] of lenticulostriate vessels –> [cystic infarcts Lacunar Syndrome (listed below)

1A: [Internal Capsule/Pons/Corona Radiata] Stroke–> pure Motor stroke (ataxia vs. clumsy hand)

1B: ThalamuS Stroke –> pure Sensory stroke

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81
Q

Most common [1° CNS Tumors] in Adults (3)

A

GMS

Glioblastoma (GRADE 4 - MALIGNANT - MOST COMMON)

MeninGioma

SChWannoma

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82
Q

Glioblastoma Radiographic Findings (2)

A
  1. Midline shift from Lateral Vt. Compression (Red arrow)
  2. Butterfly lesion from crossing Corpus Collosum
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83
Q

Glioblastoma Histological Findings (5)

A

CREEPY

  • Cystic Change
  • Reddish brown hemorrhage
  • Endothelial Cell Hyperplasia on Histo
  • Pseudopalisading Necrosis on Histo - image
  • Yellow necrosis
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84
Q

What’s the marker for Glioblastoma?

A

GFAP

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85
Q

A: [LEMS - Lambert Eaton Myasthenic Syndrome] MOD

B: Clinical Presentation (2)

A

A: [Autoimmune attack against (Presynpatic Ca+ channel)–> No ACh release]

B:

  • Fatigable Weakness of [Proximal limbs and trunk] mimicking myopathy
  • Autonomic sx (Dry mouth /Orthostasis / Impotence)
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86
Q

What other condition is [LEMS​ - Lambert Eaton Myasthenic Syndrome] associated with?

A

“LEMS has a good SOLC(soul)”

SOLC-Small Oat cell Lung Carcinoma

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87
Q

Name 3 Differentiating Factors for Myasthenia Gravis vs. [Lambert Eaton Myasthenic Syndrome]

A
  1. [LEMS] improves with exercise/exertion during the day!
  2. [LEMS] will show no imprvmnt with [Tensilon Edrophonium] injection
  3. [LEMS] nerve testing shows INC muscle responses
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88
Q

What other condition is [Myasthenia Gravis] associated with?

A

May cause Thymoma(thymic hyperplasia)

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89
Q

[Myasthenia Gravis] MOD

A

Autoantibodies block and degrade [postsynpatic nicotinic ACh Receptors]] –> [DEC motor end plate potential]

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90
Q

[Myasthenia Gravis] Clinical Presentation (6)

A

Generalized= P DDD WF

[Ptosis

[Diplopia from Disconjugate gaze]

Dysarthria

Dysphagia

[Weakness(Respiratory / limbs / Extraocular m.)

[Fatigue that worsens throughout day]

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91
Q

Violent Infant Shaking —> ________. This is characterized by what 3 things?

B: How is this differentiated from similar conditions?

A

Violent Infant Shaking –> [AHT- Abusive Head Trauma]! =

  1. Subdural Hemorrhage (from tearing bridging veins between Dura and Arachnoid)
  2. Retinal Hemorrhages Bilaterally (from congested retinal vein ruptures)
  3. POST rib fractures

B: Accidental Fall is not sufficient for Subdural Hemorrhage OR Retinal Hemorrhage

AHT is formely known as Shaken Baby Syndrome

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92
Q

[Von Hippel Lindau Dz] Clinical Presentation (3)

A

[Cerebellar Hemangioblastoma]

+

[Cyst of Kidney vs. Liver vs. Pancreas]

+

Pheochromocytoma

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93
Q

[Von Hippel Lindau Dz] MOD

A

[Tumor cells lose [Chromo 3 VHL Tumor suppressor gene] –> [INC VEGF from Hypoxia Inducible Factor]

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94
Q

Tuberous Sclerosis MOD

A

([Hamartin C1 9q] and [Tuberin C2 16p])–> HAMARTOMASSS

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95
Q

Tuberous Sclerosis Clinical Presentation (12)

A

HAMARTOMASSS

[Hamartomas benign]

[Angiofibroma on Face-triad] - image

Mitral Regurgitation

[Ash Leaf Macules]

[Rhabdomyoma Cardiac –> Valvular Obstruction]

Tuberous Sclerosis

AUTO DOM

Mental Retard-triad

[AngioMyoLipoma Kidney]

Seizures-triad

SEGA (SubEpendymal Giantcell Astrocytoma)

[Shagreen forehead patches]

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96
Q

Genetic Cause of Neurofibromatosis Type 1

A

[chromo 17 mutation]–> [NeurofibroMin loss]. NeurofibroMin tumor suppresses (RAS GTPase activating protein

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97
Q

Characteristics of Neurofibromatosis Type 1 (6)

A

CLAP ON type 1!”

  1. Neurofibroma PLEXIFORM
  2. Acoustic Schwannoma-Unilateral (HA/Tinnitus/Vertigo)
  3. [Optic n. Glioma]
  4. Lisch nodules
  5. [Cafe Au Lait Spots]
  6. Pheochromocytoma
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98
Q

Neurofibromatosis Type 2 Genetic Cause

A

[chromo 22 tumor suppresor gene mutation–> (Merlin cytoskeletal protein)]

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99
Q

Neurofibromatosis Type 2

Clinical Manifestation (2)

A
  • [Bilateral Acoustic Schwannomas] (HA/Tinnitus/Vertigo)
  • Multiple Meningiomas

Bilateral Acoustic Schwannomas @ Cerebellopontine angle

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100
Q

A: [HIV Encephalopathy] Histology

B: [HIV Encephalopathy] PGN

A

A: Microglial Nodules (microglial formed around necrotic areas) –> fuse & form [multinucleated Giant Cells]

B: [Subcortical Dementia from HIV attacking gray matter] –> Progressive cognitive decline

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101
Q

Describe Decerebrate Posturing

A

[dEcErEbrate ExtEnsor posturing]

Rigid ExtEnsion of UE and LE

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102
Q

Describe Decorticate Posturing

A

[Decorticate Flexion Posturing] “Flex toward ur Core”

Rigid Flexion of UE

but

LE Extension

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103
Q

Describe [Cavernous Hemangiomas] and list the 2 things they put pts at risk of developing

A

Vascular malformations in the brain parenchyma –> INC risk of [intracerebral hemorrhage & Seizures]

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104
Q

This Mass is a Vascular Malformation that INC pt risk for Intracerebral hemorrhage and Seizures

What is this lesion and where does it occur?

A

Cavernous Hemangioma occur in [Brain Parenchyma above Cerebellar Tentorium]

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105
Q

Which Fish bind to Na+ channels (Brain & Heart) and inhibit Na+ influx –> prevents action potential conduction? (2)

A
  1. [Tetrodotoxin Puffer Fish]
  2. [Saxitoxin Red Tide Dinoflagellates]

will have DEC Deep Tendon Reflexes

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106
Q

Which Fish bind to Na+ channels (Brain & Heart) and KEEP IT OPEN –> PERSISTENT depolarization? (2)

A
  1. [Ciguatoxin Exotic Fish vs. Moray eel]
  2. [Batrachotoxin South Amr. frog]
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107
Q

Name the Major UMN signs (5)

A

UMN signs = Weak MESH

Weakness

[Spastic Paralysis]

[Exaggerated Reflexes (Babinski)]

Mental Status change

HemipLegia

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108
Q

A: What 2 microbes is [1° CNS Lymphoma] associated with?

B: Which lymphocytes are involved and what’s pgn?

A
  1. EBV
  2. HIV/AIDS

B: B-cell lymphoma that’s a high-grade tumor = POOR PGN!

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109
Q

Alzheimer’s Dz MOD (3)

A

Alzheimers MOD = CHA

**Cleavage, Hemorrhage, ACh **

  1. Cleavage of [transmembrane amyloid precursor glycoprotein] –> Beta-amyloid which accumulates–> [Neuritic Senile plaques] in temporal lobe early on.
  2. Eventually Beta-amyloid starts to deposit in cerebral vessels –> [Spontaneous Occipital/Parietal hemorrhages]
  3. Beta-amyloid accumulation causes defective [Choline acetyltransferase] in the [Basal nc. of Meynert] & Hippocampus –> DEC ACh in those areas –> Alzheimer Sx
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110
Q

How do you diagnose Alzheimer’s Dz? (2)

A
  1. Apple Green Birefringence when stained with Congo red under polarized light
  2. [Hyperphosphorylated Tau Neurofibrillary Tangles]
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111
Q

[Amyotrophic Lateral Sclerosis] (Lu Garret’s) MOD

A

[Superoxide Dismutase gene mutation] –> copper-zinc dysfunction —>[Upper AND Lower Motor Neuron Disease!]

UMN Dz includes loss of neurons in motor nc. 5/9/10/12

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112
Q

A: Tx for ALS

B: What do pts with ALS end up dying from?

A

ALS (AKA Lu Garrets Dz)

A: RiLuzole (DEC Glutamate release since Glutamate over excites neurons)

B: Respiratory Complications (PNA vs. failure)

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113
Q

[Carpal Tunnel Syndrome] MOD

A

BILATERAL Median n. Compression from the [Flexor Retinacular Transverse carpal ligament] –> Peripheral mononeuropathy

[Flexor Retinacular Transverse Carpal ligament] can be surgically incised for relief

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114
Q

[Carpal Tunnel Syndrome] Clinical Manifestation (4)

A
  1. Paresthesia vs. Pain with Median n. Distribution (worst at night)
  2. Thenar Atrophy from motor weakness (flexion/ABduction/Opposition impairment)
  3. Tinel Sign (tapping over flexor surface DEC sx)
  4. Phalen Sign (flexing Wrist INC sx)

CARPEL TUNNEL IS BILATERAL

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115
Q

Which parts of the brain are the most susceptible to injury post [Global Cerebral Ischemia] (3)

A
  1. Hippocampus (pyramidal cells) <—AFFECTED FIRST!
  2. [Cortex pyramidal - layers 3/5/6]
  3. Cerebellar Purkinje Cells
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116
Q

What [mini mental state exam] do you use to test for: Concentration & Attention?

A

Reciting months of the year backwards

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117
Q

What [mini mental state exam] do you use to test for: Comprehension?

A

Following multistep commands

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118
Q

[Wernicke Korsakoff Syndrome] Clinical Presentation (3)

A

Wernicke problems come in a CAN of beer!

[Confusion & Confabulation]

Ataxia (Gait & Postural)

[Nystagmus + Oculomotor Dyf] (Opthalmoplegia)

beer = chronic alcoholism is most common cause

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119
Q

What serious finding is most likely to occur despite treatment in [Wernicke Korsakoff Syndrome]?

A

Memory Loss is permanent!

Antero and Retrograde

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120
Q

Causes of [Wernicke Korsakoff Syndrome] (2)

A

Wernicke Problems come in a CAN of beer!

[Thiamine B1 Deficiency] from:

  1. Chronic Alcoholism = MOST COMMON
  2. Giving [Glucose that doesn’t have B1] to a B1-deficient pt (i.e. homeless malnutrition pt)
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121
Q

Tx for [Wernicke Korsakoff Syndrome] (2)

A
  1. IV [Thiamine B1]
  2. Glucose administration
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122
Q

A: Parkinson’s Disease Histology

B: What other Dz shares this Histology and how do you tell the diff. clinically?

A

A: Lewy Bodies = [intracell eosinophilic inclusions] made of a-synuclein

B: [Lewy Body Dementia] (will aso have visual hallucinations and attention deficit clinically)

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123
Q

Describe the Prodromal phase of [Measles RubeOla Paramyxovirus] (4)

A

1st: Fever
2nd: 3 C’s of Measles= [Cough / Coryza / Conjunctivitis]
3rd: Koplik spots
4th: Maculopapular Rash starting from head then down

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124
Q

What are the dangerous potential sequelae of [Measles RubeOla Paramyxovirus] (3)

A
  • Encephalitis (days later)
  • [Acute Disseminated Encephalomyelitis] (weeks later)
  • [SSPE- Subacute Sclerosing PanEncephalitis] (years later)
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125
Q

Identify the Finding & Dz associated

A

Koplik spots found in [Measles RubeOla Paramyxovirus]

Prodromal phase:

1st: Fever
2nd: 3 C’s of Measles= [Cough / Coryza / Conjunctivitis]
3rd: Koplik spots
4th: Maculopapular Rash starting from head then down

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126
Q

Why does [Chromatolysis Axonal Reaction (Loss of Axon)] changes occur?

A

Cell body attempts to repair/regain Axon by INC protein synthesis –> Enlargement of Cell Body

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127
Q

What syndrome occurs from rapidly correcting Na+ levels from low to High ?

A

“Rapid Na+ From low to HIGH, your pons will DIE” =

[Osmotic Central Pontine Demyelination]

Osmotic demyelination of pons white matter

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128
Q

What syndrome occurs from rapidly correcting Na+ levels from High to low ?

A

“Rapid Na+ From HIGH to low, your brain will blow” =

Cerebral Edema & Herniation

129
Q

Clinical Manifestation of [Osmotic Central Pontine Demyelination] (

A

“Rapid Na+ From low to HIGH, your pons will DIE” =

[Osmotic Central Pontine Demyelination]

Osmotic demyelination of pons white matter

130
Q

What vascular Dz is Polymyalgia Rheumatica associated with and does this affect vision?

A

Temporal Arteritis (Med. and Large vessel vasculitis) often —> Monocular Vision loss!

131
Q

Clinical Presentation for [Polymyalgia Rheumatica] (4)

A

PolyMyalgia Rheumatica

Painful Stiff Shoulder & Hips

Malaise & Morning Stiffness

Really Hot (Fever)

Associated w/Giant Cell Temporal Arteritis–>Monocular Vision loss

132
Q

[Paraneoplastic Cerebellar Degeneration] MOD

A

“Anti Yo/PQ & Hu get crazy when Seeing B/O & U”

[Antibodies Yo, PQ and Hu] initially target tumor cells but cross react with [Cerebellar Purkinje] by mistake—> [RAPID Autoimmune Cerebellum Degeneration]

133
Q

Which CA are associated with [Paraneoplastic Cerebellar Degeneration]? (4)

A

“Anti Yo/PQ & Hu get crazy when ​Seeing B/O & U”

  1. SOLC
  2. Breast
  3. Ovarian
  4. Uterine
134
Q

Etx of [Frontotemporal Pick’s Dementia] and manifestation-2

A

Prounouced Frontal & Temporal lobe atrophy –> [Socially inappropriate Behavior] + aphasia

135
Q

A: When does [Frontotemporal Pick’s Dementia] onset?

B: Mode Of Inheritance

A

A: 50-60 (Alzheimer = 60+)

B: Auto Dominant

136
Q

[Frontotemporal Pick’s Dementia] Histology (2)

A
  • Neuron loss in Frontotemporal lobes
  • Pick Bodies = [microtubule tau protein] in cytoplasm of neurons
137
Q

What is [Hydrocephalus Ex Vacuo] and which pts do you see it in?

A

Ventricular Enlargement only because of cortical atrophy, typically found in HIV pts (cortical atrophy is normal sequelae in HIV)

True Hydrocephalus is actual build up of CSF (obstruction vs. hyperproduction**)

138
Q

What type of tumor stains positive for Synaptophysin?

A

[Neuronal CNS Tumors]

Also includes neuroendocrine and neuroectodermal CNS tumors

139
Q

Name the CNS Neoplasms that are of Glial Origin (i.e. Glioma) (4)

A

AGE comes from Glia

  1. [Glioblastoma & OligodendroGlioma]
  2. Astrocytoma
  3. Ependymoma

These stain positive for GFAP

140
Q

[Creutzfeldt Jakob Dz] Clinical Presentation (2)

A

[RAPIDLY Progressive Dementia] + [Myoclonic Jerks] –> DEATH

Can be Acquired vs. Inherited

141
Q

Identify the Pathology and List the causes (3)

A

A: SubDural Hemorrhage = CRESCENT SHAPED!

B: Cortical Bridging Veins between Dura & Arachnoid are stretched by:

  1. [Age related Cortical Atrophy which stretches Bridging Veins in Elderly]
  2. Trauma
  3. [Abusive Head Trauma] in infants
142
Q

Identify this Dz if it was preceded by TB meningitis

A

Bilateral Symmetrical Dilation of Ventricles = [Communicating vs. Normal Pressure Hydrocephalus]

Communicating = CSF can’t communicate with [Arachnoid granulation villi] –> DEC absorption –> INC ICP

This is Communicating Hydrocephalus

(only since it was preceded by [Meningitis vs. SubArachnoid/Intraventricular Hemorrhage)

143
Q

[Communicating Hydrocephalus] cause

A

[Meningitis vs. SAH/Intraventricular Hemorrhage] –>Disrupts communication of CSF with [Arachnoid Granulation Villi] ReAbsorption

144
Q

What’s the major complication of [SubArachnoid Hemorrhage] during recovery? How do you tx this?

A

Severe Cerebral Vasospasm 4-12 days post SAH onset –> morbidity vs. mortality. Prevent with [Nimodipine CCB].

145
Q

Describe the Demographic for the HA:

Migraine

Tension

Cluster

A

Migraine = Female

Tension = Female

Cluster = Male

146
Q

Describe the Onset for the HA:

Migraine

Cluster

Tension

A

Migraine = Variable

Cluster = During Sleep

Tension = When Stressed “think tense”

147
Q

Describe the Location for the HA:

Migraine

Cluster

Tension

A

Migraine = POUND = [Pulsating/One-3 Day Duration /Unilateral/Nausea/Disabling] + photo vs. phonophobia & aura

Cluster = Behind 1 eye

Tension = [Bilateral & Band-like around the head]

148
Q

Describe the Character for the HA:

Migraine

Cluster (3)

Tension (2)

A

Migraine = POUND = [Pulsating/One Day-3 day Duration/Unilateral/Nausea/Disabling] + photo vs. phonophobia & aura

Cluster = [Excruciating, sharp & steady]

Tension = Dull & tight

149
Q

Describe the Duration for the HA:

Migraine

Cluster

Tension

A

Migraine = POUND = [Pulsating/One-3 Day Duration /Unilateral/Nausea/Disabling] + photo vs. phonophobia & aura

Cluster = 15 - 90 MINUTES

Tension = 30 min to 7 DAYS!!!! (Tammy’s Entire Work Week)

150
Q

Describe the Associated Sx for the HA:

Migraine

Cluster (4)

Tension

A

Migraine = POUND = [Pulsating/One-3 Day Duration /Unilateral/Nausea/Disabling] + photo vs. phonophobia & aura

Cluster = [Sweating/Nasal Congestion/Lacrimation/Pupil changes]

Tension = [Muscle “Tension” in Head, Neck or Shoulders]

151
Q

Identify the pathology and Describe the corresponding Histology (2)

A

Liquefactive Necrosis (occurs 1 wk.-1 mo. post ischemia)

Reactive Gliosis + [Vascular proliferation around necrotic area]

152
Q

When does Liquefactive Necrosis appear?

A

[1 week to 1 mo.] post ischemic injury ( >2 week Glial Scar will appear)

153
Q

Identify the pathology and Describe the Clinical Presentation

A

SubArachnoid Hemorrhages will presents as “the worst HA of my life!”

Typically caused by [Berry Saccular Aneurysm] vs. AVM

154
Q

Most common cause of [Lobar hemorrhages]

A

[Beta-Amyloid Angiopathy]

(pt>60 w/Alzheimers & within Occipital/Parietal regions)

155
Q

Identify the [CNS Tumor] and describe its Histology

A

Meningioma (Men are Whorls(whores))

Whorled arachnoid cells that form NEST (RED arrow), and then calcify into eosinophilic Psammoma Bodies (Black arrow)

156
Q

Where does this [CNS Tumor] typically occur (3)

A

Meningioma (Men are Whorls (whores))

Dural Reflection *(Attached to Dura & Extra-Parenchyma) at the:

  1. [Falx Cerebri vs. Tentorium Cerebelli]
  2. Lateral Convexity
  3. Parasagittal
157
Q

What’s the Clinical Manifestation of this [CNS Tumor] (2)

A

Meningioma (Men are Whorls(whores))

  1. Seizures (from compression of cerebral cortex)
  2. LE Sensory Loss (+ possible hemineglect if in non-dominant hemisphere: as shown in image)
158
Q

Trigeminal Neuralgia Tx

A

Carbamazepine

Can cause aplastic anemia so monitor carefully

159
Q

Describe Trigeminal Neuralgia and what triggers it

A

Brief episodes of [Sudden / Severe / Shock like Stabbing Pain] with [Trigeminal CN5 -B2 & B3 distribution]

Triggered by CN5 stimulation (chewing, teeth brushing, shaving)

160
Q

Carbamazepine MOA

A

Blocks Voltage-gated Na+ channels in neuronal membranes

161
Q

Carbamazpine SE (5)

A
  1. Aplastic Anemia (bone marrow suppression)
  2. Agranulocytosis
  3. CYP450 inducer
  4. SIADH
  5. Steven Johnson rash
162
Q

Carbamazpine Indications (2)

A
  1. Seizures (simple partial vs. complex partial vs. [GTC-Generalized Tonic Clonic])
  2. Trigeminal Neuralgia
163
Q

Serotonin Syndrome Clinical Presentation (8)

A

“Serotonin gave me the SHIVERS!”

Shivering

[Hyperreflexia & Myoclonus]

INC Temp

[Vital sign instability] (tachycardia vs. tachypnea vs. HTN)

Encephalopathy (Confusion vs. Agitation)

Restlessness

Sweating

Italicized = Triad Sx

164
Q

How do you treat Refractory Serotonin Syndrome

A

Cyproheptadine

(antihistamine with anti-serotonergic properties)

165
Q

Baclofen MOA

A

GABA-B Agonist

166
Q

A: Baclofen Indication

B: Alternative med

A

[Spasticity 2° to Brain & Spinal Cord Dz (MS vs. low back pain)]

B: Alternative = Tizanidine

167
Q

Physostigmine MOA

How well does it cross BBB

A

Reversible AChE inhibitor

READILY crosses BBB due to tertiary amine structure

168
Q

Physostigmine Indication (2)

A
  1. Delirium from anticholinergic drugs
  2. Glaucoma
169
Q

Difference between Physostigmine and [Neostigmine & Edrophonium]

A

ALL HAVE SAME MOA (AChE inhibitor)!

but Physostigmine = tertiary amine = readily crosses BBB

[Neostigmine & Edrophonium] = quaternary ammonium = limits BBB penetration

170
Q

Donepezil MOA

How well does it cross BBB

A

Reversible AChE inhibitor

READILY crosses BBB

171
Q

Tx for Alzheimer’s (3)

A

Dementia is Very Malevolent

  1. Donepezil (Reversible AChE inhibitor)
  2. Vitamin E antioxidant
  3. Memantine (NMDA Blocker)
172
Q

SE of [Inhaled Anesthetics] (5)

A
  1. INC Cerebral blood flow –> INC ICP :-(
  2. Myocardial Depression
  3. Respiratory Depression
  4. hypOtension
  5. DEC Renal function
173
Q

Parkinson’s Dz Tx (5)

A

“Eat a SALAD after you Park”

  1. [Levodopa (Dopamine Precursor)]
  2. Amantidine
  3. Anticholinergics
  4. [Dopamine Agonist Post synaptic] (NonErgot: Ropinirole vs. Pramipexole) & (Ergot:Bromocriptine)
  5. Surgical tx vs. Selegiline
    - Pallidotomy: Destructive of [Globus Pallidus:internal]
    - SubThalamic nuc. inhibition with electrode
174
Q

EThosuximide MOA

A

EThosuximide

[Thalamus T-type Ca+ Channel BLOCKER]

Sux to have Silent Seizures

175
Q

A: What is the cause of Neonatal Abstinence Syndrome

B: Tx

A

A: Withdrawal from opiates

B: [Opiate Replacement Therapy]

176
Q

Ethosuximide Indication

A

Sux to have Silent Seizures

Silent (Absent) Seizures

177
Q

Anesthetics that have [LARGE Arteriovenous concentrations] says what about their [Tissue Solubility] and [Onset of Action]

A

[LARGE Arteriovenous concentrations] of an Anesthetic will indicates:

[High Tissue (And blood) Solubility]

and thus

[Slow Onset of Action (since it’ll take longer to get to brain if other peripheral tissues are Absorping so much of it)]

178
Q

Triptans MOA

A

[PostSynpatic 5HT1B&1D Receptor Agnoist]

–> vasoconstriction

179
Q

Triptans indication

A

Abortive therapy for Acute Migraines

180
Q

List the Drugs used for Migraine Px (5)

A

“Prevent Migraines with a TAB of VV”

  • Topiramate
  • Amitriptyline
  • Beta blcokers
  • Venlafaxine
  • Valproate
181
Q

Primary Purpose of NE in the Autonomic Systems

A

Released from [PostGanglionic Sympathetic neurons] on alpha & beta receptors for most [organ/smooth m.gland stimulation] (i.e. Bladder)

182
Q

Jimson Weed Poisoning MOD

and what other condition does it resemble?

A

[Belladonna Alkaloid Toxin] has strong ANTI-cholinergic properties and thus resembles atropine poisoning

Jimson Weed Poisoning is AKA Gardener’s Mydriasis

183
Q

[Jimson Weed Poisoning] Clinical Manifestation (7)

A

“Blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel & bladder lose their tone, and the heart runs alone…..”

  1. Blind as a bat = [Mydriasis and [cycloplegia (blurry vision especially when focusing on near objects)]
  2. Mad as a hatter= Agitation & Hallucinations
  3. Red as a Beet = Cutaneous flushing despite vasoconstriction
  4. Hot as a hare = Hyperthermia from DEC ability to sweat
  5. Dry as a bone= DEC Secretions (including sweat)
  6. Bladder & Bowel lose tone
  7. Heart runs alone = No vagal tone at SA –> Tachycardia
184
Q

How do you treat [Jimson Weed Poisoning]

A

Same as Atropine poisoning …

Physostigmine (AChE inhibitor)

185
Q

What is [MAC-Minimal Alveolar Concentration] in relation to anesthetics, and what does it measure?

A

MAC = Minimal concentration of anesthetic in alveoli to render 50% of pts unresponsive to pain (ED50). This measures the potency of inhaled anesthetics

186
Q

Benzodiazepine MOA

A

INC frequency of [GABA-A Chloride channel] opening

187
Q

Tx for Febrile Seizures

A

APAP (improves fever) but not the seizure

188
Q

Febrile Seizures MOD

A

Most common neurologic DO in children. Comes after Fever. These kids are at risk of recurrence but rarely epilepsy development

189
Q

Describe Neuroleptic Malignant Syndrome

A

RARE SE of Any Dopamine Blocker (Antipsychotics vs. GI meds) that –> FEVER

  • [Fever > 40C]
  • Encephalopathy (Confusion)
  • Vitals unstable (INC HR / RR / BP from autonomic dysfunction)
  • Enzymes INC (CPK)
  • Rigitidy INC (Tremor)
190
Q

What’s the best way to approach treatment for [Neuroleptic Malignant Syndrome]

A

Treat Rigiditiy with Dantrolene (inhibits Ca+ release from sk. muscle sarcoplasmic reticulum)

+

supportive care

191
Q

[Entacapone & Tolcapone] MOA

A

COMT inhibitor

INC Levodopa availability to brain by preventing Levodopa COMT conversion –> 3OMD in periphery

192
Q

[Entacapone & Tolcapone] Indication

A

Parkinson Dz

193
Q

Malignant Hyperthermia MOD. Which pts are susceptible?

A

After giving [inhaled anesthestics and/or succinylcholine] (to genetically predisposed pts (AUTO DOM)) –> [Fever & Muscle Rigidity soon after surgery with Unstable Vitals]

Malignant = Muscle Rigiditiy

Malignant = Unstable Vitals

Hyperthermia = Fever

194
Q

Malignant Hyperthermia Tx

A

Dantrolene

TREAT PROMPTLY! AS THIS IS LIFE THREATENING CONDITION!

195
Q

Describe what each letter representsfor [Neuron Action Potential]

A

A: Resting Potential

B: Depolarization (from Na+ influx)

C: Overshoot (+35 mV)

D: Repolarization (from [Na+ channel closure] and K+ efflux)

E: Hyperpolarization (K+ efflux remains open too long even after repolarization is done)

196
Q

Phenytoin MOA

A

Disrupts [propagation & generation] of Action potentials by blocking [Voltage gated Na+ channels] at [axon hillock & proper]

197
Q

Carbamazepine MOA

A

Disrupts [propagation & generation] of Action potentials by blocking [Voltage gated Na+ channels] at [axon hillock & proper]

198
Q

Function of [Arcute hypothalamic nuclei] (3)

A

Secretion of

  • Dopamine (inhibits prolactin)
  • GHRH (growth hormone releasing hormone)
  • GnRH (Gonadotropin-releasing Hormone)
199
Q

Where would you inject Lidocaine to anesthetize [Skin & Muscles of ANT Thigh (Quadriceps, femur, knee)

A

[Inguinal Crease @ lateral border of femoral artery] (Femoral N. Block)

200
Q

Injury to the ____ n. is most common in Shoulder Trauma. What is the Clinical Manifestation of this? (2)

A

Injury to Axillary n. is most common in Shoulder Trauma –>

  • Lateral Shoulder Sensory Loss
  • Weak ABduction from (deltoid & teres minor m. denervation)
201
Q

List perfusion areas and Clinical Manifestation of [ACA-ANT Cerebral Artery] occlusion (3)

A

ACA perfuses [Medial Frontal & Parietal Lobe]. If occluded –>

  1. CTL Motor and Sensory Deficits of LE
  2. Behavioral change
  3. Urinary Incontinence

would have hard time climbing stairs

202
Q

In regards to Carpal Tunnel, the ______ n. courses between the _____ and ____ muscles before crossing _____ inside carpal tunnel

A

In regards to Carpal Tunnel, the Median n. courses between the [Flexor Digitorum superficialis] and [Flexor Digitorum Profundus] before crossing [Flexor Retinaculum] inside carpal tunnel

203
Q

What is the Function and Dz associated with the [MesocorticalLimbic dopaminergic system]

A

Regulates Behavior ; Schizophrenia

204
Q

What is the Function and Dz associated with the [Nigrostriatal dopaminergic system]

A

Voluntary mvmnt coordination ; Parkinsonism

205
Q

What is the Function and Dz associated with the [Tuberoinfundibular dopaminergic system]

A

Prolactin Secretion ; Hyperprolactinemia

206
Q

Identify

A

A: Basilar A. (formed by 2 vertebral arteries)

B: R PCA

C: L PCA

D: SCA (SUP cerebellar a.)

E: parapontine perforating a.

F: AICA (ANT inferior cerebellar a.)

207
Q

What would a [R Partial Retinal lesion] manifest as

A

R Monocular scotoma

208
Q

Lesion at which letter would result in [R Nasal Hemianopia]

209
Q

Lesion at which letter would result in [L Pie on the Floor (Homonymous INF quadrantanopia)] lesion

210
Q

Describe Hemiballismus

A

Wild, involuntary, large-amplitude flinging mvmnts of arms vs. legs on 1 side of body

211
Q

What causes Hemiballismus

A

Damage (i.e. lacunar stroke) to Subthalamic nc., important in modulating basal ganglia output

212
Q

Identify

A

image

Remember: Caudate + Putamen = Striatum

213
Q

Where is Wernicke’s Area located?

A

Auditory association cortex: POST portion of [SUP temporal gyrus] within dominant temporal lobe

214
Q

What neural structure is affected in [Wernicke Korsakoff Encephalopathy]?

Refer to image

A

B

Mamillary Bodies!

215
Q

Damage to what nerve would cause absent Corneal Reflex (2)

A

[Sensory limb Corneal Reflex = CN5B1: nasociliary branch]

vs.

[Motor Limb Corneal Reflex = Facial CN7: temporal branch]

216
Q

What all vessels & nerve enter the orbit via [SUP Orbital Fissure] (6)

A
  1. CN3
  2. CN4
  3. CN5B1
  4. CN6
  5. [SUP Opthalmic Vein]
  6. Sympathetics
217
Q

Identify

218
Q

Identify C in image and list its functions (3)

A

Insula

  1. Emotions (limbic system)
  2. Autonomic control
  3. Visceral sensation consciousness
219
Q

Describe Asociated Features of Brocas Aphasia (2)

A

Right Hemiparesis (weakness) + Impaired Repititon

In addition to nonfluent/sparse speech

220
Q

Describe Asociated Features of Wernickes Aphasia (2)

A

[R SUP Visual field defect] + Impaired Repetition

This is in addition to Comprehension problems

221
Q

Describe Asociated Features of CONDUCTION Aphasia

A

VERY POOR Repetition

This is in addition to Fluent but many phonemic errors

222
Q

Which nerve is damaged from trauma to axilla (i.e. long term crutches) and what are the findings? (4)

A

Radial Nerve

  1. Wrist Drop (No Wrist extension)
  2. Absent Triceps Reflex (spared if lesions is distal)
  3. Sensory loss of POST arm/forearm
  4. Sensory loss of dorsal hand/thumb
223
Q

A: [MSUD- Maple Syrup Urine Dz] MOD

B: What does the defective enzyme need to work (5)

A

Defective Breakdown of [isoLeucine / Leucine / Valine] due to DEC transamination to their a-ketoacids by defective [a-ketoacid dehydrogenase].

B: [a-ketoacid dehydrogenase] requires “Tender Loving Care For Nancy” to work

[(Thiamine B1)/Lipoate/CoenzymeA/FAD/NAD]

224
Q

[MSUD- Maple Syrup Urine Dz] tx

A

[a-ketoacid dehydrogenase] requires “Tender Loving Care For Nancy” to work

[Thiamine/Lipoate/CoenzymeA/FAD/NAD]

Tx = Thiamine B1

+

[Lifelone restriction of isoLeucine/Leucine/Valine]

225
Q

[MSUD- Maple Syrup Urine Dz] Clinical Presentaiton (2)

A
  1. Burned Caramel Urine odor (isoleucine)
  2. Neurotoxicity (Leucine accumulation)
226
Q

Conversion Disorder

A

Loss of sensory/motor function after acute
stressor; patient may be aware but sometimes indifferent (“la belle indifférence”)

227
Q

Malingering

A

Falsifying/Exaggerating Sx in order to obtain external incentives

228
Q

Somatic Sx Disorder

A

Excessive Anxiety & PreOcupation with ≥ 1 unexplained sx

229
Q

Factitious Disorder

A

Falsifying or Inducing sx to assume the sick role

230
Q

DSM5 Criteria For Narcolepsy (2)

A

[Recurrent lapses into sleep at least (3 x/week) x 3 mo.]

+

1 of the following:

a. Cataplexy
b. [Low CSF hypOcretin1 orexin A]
c. [REM latency ≤ 15 min]
* Cataplexy = Brief Muscle tone loss during Positive emotion*

231
Q

Clinical Manifestations of Narcolepsy (3)

A
  1. hypnagogic vs. Hypnopompic hallucinations
  2. Sleep paralysis (excessive daytime sleepiness)
  3. Cataplexy
232
Q

Name the 3 components of EPS-ExtraPyramidalSymptoms

A

EPS = DAD

[Drug-induced Parkinsonism]

Akithisia (restlessness)

Dystonia (Abnormal twisted posture exacerbated with activity)

233
Q

What is EPS caused by, and which drugs are the most likely to cause it?

A

EPS (DAD) comes from [Nigrostriatal D2 Blocking], usually from [1st generation Antipsychotics (Haloperidol/Fluphenazine)]

234
Q

What is Hypocretin 1 and 2 also known as, and what is their function?

A

[Hypocretin 1 (Orexin A)[and [Hypocretin 2 (Orexin B)] are [Lateral hypothalamus neuropeptides] that promote wakefullness & inhibit [REM sleep-related phenomena]

These are deficient in Narcolepsy

235
Q

Clinical Presentation for [Ataxia Telangiectasia] (5)

A

[Ataxia TelAngiectasia] = ATM gene defect

  • Ataxia (cerebellar defect)
  • TelAngiectasia
  • IgA deficiency (recurrent sinopulmonary infections)

Labs = INC AFP

236
Q

Lab Dx for [Ataxia Telangiectasia]

A

[Ataxia Telangiectasia] = ATM gene defect

INC AFP (Alpha fetal protein)

237
Q

[Ataxia Telangiectasia] MOD

A

[Ataxia Telangiectasia] = ATM gene defect –> Inability to repair DNA double stranded breaks –> cell cycle arrest. These pts are highly susceptible to radiation-induced mutations!

238
Q

Describe Telangiectasia

A

Superficial blancing nest of distended capillaries on sun-exposed sites

239
Q

Name the most common pineal gland tumor and how it clinically manifest (3)

A

Germinoma

  • Obstructive Hydrocephalus
  • [Parinaud Dorsal Midbrain syndrome]
  • [Pituitaryhypothalamic dysfunction (if in suprasellar region)
240
Q

Parinaud Syndrome MOD and Clinical Manifestation (3)

A

“Parinaud loved his PUP”

Direct Compresion of [Midbrain Pretectum SUP Colliculi] (possibly from Gemrinoma) –>

  1. Ptosis
  2. Upward Gaze paralysis
  3. Pupil abnormalities
241
Q

Identify

242
Q

Describe the MOD of [TMD- TemporoMandibular Disorder] (3)

A

Problems involving:

  • Temporomandibular joint
  • Mastication m. (contracting too much)
  • [Trigeminal CN5B3: mandibular branch] –> Otologic sx since this also supplies mid ear
243
Q

Clinical Manifestations of Ulnar n. Injury (2)

A
  1. Sensory loss in medial 1.5 digits of hand
  2. Ulnar claw = DEC [Wrist Flexion/ADDuction] / [4th & 5th digit flexion] and [Finger ABduction/ADDuction]
244
Q

Which nerve enters pelvis through [Obturator Foramen]? Clinical Manifestation if this n. is compressed? (2)

A

Obturator nerve when compressed (surgery vs. trauma vs. tumor) –>

[Weak Thigh ADDuction] + [Sensory loss of Distal Medial thigh]

245
Q

Radial n. damage during its passage thru the supinator canal may be from _____(3) and —> _______

A

Radial. n. damage during its passage thru supinator canal may be from [forearm alternating pronation/supination (screwdriver)] vs. trauma vs. [radius subluxation] –> [DEC Finger & Thumb Extension only]

246
Q

Where would you inject anesthesia to Nerve block Brachial Plexus, and what m. will be affected by this?

A

Between [ANT Scalene] and [Middle Scalene].

This –> [transient ipsilateral diaphragm paralysis] since phrenic n. roots pass through interscalene sheath

247
Q

Identify Cerebral Blood Perfusion

in image

248
Q

Sciatica MOD and Clinical Manifestation (3)

A

“Having Sciatica is like breaking LAWS”

  • [Lower Back pain w/radiation down POST thigh –> lateral foot]
  • Ankle jerk reflex ABSENT
  • Weak Hip Extension
  • [S1 n. posterolateral compression at L4-5 vs. L5-S1]
249
Q

[Cauda Equina Syndrome] Clinical Manifestation (2)

A

(Damage to S2 through S4 n. roots) –>

  • Saddle Anesthesia
  • Anocutaneous Reflex LOSS (perianal pinpoint does NOT cause anal sphincter contraction)
250
Q

Which vessels (nerves & vasculature) go through Jugular Foramen

A

“9, 10, 11 goes through Jugular Foramen”

CN9, CN10, CN11 & Jugular Vein

Lesion of Jugular Foramen –> Vernet Syndrome

251
Q

Which vessels (nerves & vasculature) go through Foramen Magnum

A
  • CN11 spinal rooots
  • Brain Stem
  • Vertebral a.
252
Q

Loss of POST 1/3 Tongue Taste indicates what n. damage

253
Q

Loss of Gag Reflex indicates what n. damage (2)

A

CN9 and 10

254
Q

Dysphagia indicates what n. damage (2)

A

CN9 and 10

255
Q

Dysphonia/Hoarseness indicates what n. damage

256
Q

Fill in the Blank regarding Myotomes and Reflexes

in image

257
Q

Which vessels (nerves & vasculature) go through Foramen Ovale

A

[Trigeminal CN5B3: mandibular branch]

258
Q

Which vessels (nerves & vasculature) go through Foramen Rotundum

A

[Trigeminal CN5B2: maxillary branch]

259
Q

Which vessels (nerves & vasculature) go through Foramen Spinosum (2)

A

[Middle meningeal Artery & Vein]

260
Q

[Common Peroneal n.] injury is common and results from _______. What are the 2 hallmark signs?

A

Trauma to Fibular head region –>

foot dropPED (Peroneal n. Everts & Dorsiflexes) –> Steppage Gait

261
Q

Intraventricular Hemorrhage occurs often in ____ Infants, originating from the ______. Why is this?

A

IVH occurs often in Preterm Infants, originating from Germinal Matrix.

Germinal Matrix contain thin-walled vessels which contribute to hemorrhage risk.

These thin -walled vessels eventually migrate out, but in preterm infants, they’re still there.

262
Q

Classic Presentation for a pt with [Trochlear CN4 Palsy]

A

Vertical Diplopia worst when looking down and toward nose (i.e. walking downstairs vs. up close reading)

SUP Oblique is responsible for moving eye Down & In

263
Q

Musculocutaneous n. covers sensory to what part of the body

A

Lateral Forearm

264
Q

What innervates [General Sensation of Tongue]

A

[Trigeminal CN5B3: mandibular branch]

265
Q

What type of neurological predispositions do Down syndrome pts have? (2)

A
  1. Intellectual disability
  2. Early Alzheimer Dz
266
Q

Organophosphate poisoning MOD

A

AChE inhibitor –> TOO MUCH ACh in cleft

Organophospahtes are used in Agricultural Pesticides

267
Q

Describe the [On Off Phenomenon] in Parkinson Disease Tx

A

Long-term tx of Parkinson Dz can sometimes –> [UNPREDICTABLE MOTOR FUNCTION FLUCTUATIONS] mostly from levodopa-induced nigrostriatal neurodegeneration –> DEC therapeutic window for Levodopa

off = bradykinesia/rigidity vs. on=normal motor

268
Q

Phenytoin SE (3)

A
  1. Gingival Hyperplasia (reversible with withdraw)

Gingival macrophage exposure to INC PDGF stimulate [gingival cell and alveolar bone proliferation]

  1. Ataxia (cerebellar)
  2. Nystagmus (vestibular)
269
Q

Capsaicin MOA (2)

A

Topical Capsaicin [defunctionalizes afferent pain fibers] and [depletes Substance P]—>initial stinging but w/chronic exposure –> DEC pain

270
Q

Clinical Manifestation of DRESS Syndrome (6)

A

Dysfunctional Internal organs

Really Hot (Fever)

Eosinophilia w/LAD

Skin Rash

Swollen Face

271
Q

What drugs (6) causes [DRESS Syndrome] and when does this happen

A

2-8 weeks after taking…

“Summer CAMPS –> bad DRESS game”

Carbamazepine

Allopurinol

[Minocycline & Vanc]

Phenytoin

Sulfonamides

272
Q

Isoniazid is structrually similar to Vitamin ___ and as a result causes what DO?

A

Isoniazid is structurally similar to [Pyridoxine B6] and as a result –> [INC Urinary excretion of Vitamin B6 pyridoxine] + competetition to [B6 GABA binding sites]

Presents as Peripheral Neuropathy + [Potential Sideroblastic Anemia]

273
Q

How does Vitamin [Pyridoxine B6] deficiency present (2)

A

Peripheral Neuropathy + [Sideroblastic Anemia]

274
Q

Selegiline MOA

A

[MAO-B inhibitior]

275
Q

Thiopental Indication

A

Lipid soluble barbituate used in Anesthesia for minor surgery

276
Q

Why does Thiopental (and other lipid soluble barbituates) have rapid plasma decay?

A

Rapid plasma decay is due to redistribution to lean tissues and clearance from brain–> allows use in minor surgery

277
Q

Buprenorphine MOA

A

[partial opioid R agonist] that binds with HIGH AFFINITY but has low intrinsic activity–> displaces other opioids

278
Q

Why is Buprenorphine contraindicated with other opioids?

A

displaces other opioids which may –> Withdrawal!

279
Q

Sx of Opioid Withdrawal. When does this happen?

A

Dilated Pupils

Tachycardia

Diaphoresis

1-2 days post cessation

280
Q

How can you differentiate between pediatric [Pilocytic Astrocytoma] and MeDulloblastoma?

A

Pilocytic Astrocytoma will have BOTH Solid AND Cystic componenents

MeDulloblastoma only has Solid

Image shows [Pilocytic Astrocytoma]

281
Q

Describe the __x__ of Delirum in Elderly

A: onset

B: Consciousness

C: Course

D: Pgn

E: Memory impairment

282
Q

Describe the __x__ of Dementia in Elderly

A: onset

B: Consciousness

C: Course

D: Pgn

E: Memory impairment

283
Q

Describe the __x__ of Depression in Elderly

A: onset

B: Consciousness

C: Course

D: Pgn

E: Memory impairment

284
Q

Early-onset Alzheimer’s is associated with 3 gene mutations. Name them

A
  1. Down Syndrome
  2. Presenilin 1
  3. Presenilin 2
285
Q

LATE-onset Alzheimer’s is associated with 1 gene mutations. What is it?

A

[ApoLipoprotein E4]

Onset After 60 yo

286
Q

Failure of neural tube closure at __ weeks gestation –> Neural Tube Defects. What INC risk? What DEC Risk?

A

Failure of neural tube closure at 4 weeks gestation –> NTD.

**[Valproate/Carbamazepine/Maternal DM] INC Risk of non-closure

** [Folate B9] DEC Risk of non-closure :-)

287
Q

Anterior [Neural Tube Defects] manifest how (2)

A

Anencephaly (absence of brain)

and

Encephalocele (protrusion of neural tissue thru cranial defect)

288
Q

Posterior [Neural Tube Defects] manifest how (2)

A
  1. Spina Bifida Occulta
  2. Meningocele
  3. MeningoMyelocele

2 and 3 both with cystic mass @ lower spine and tuft of hair on pt

289
Q

Prenatal Dx for [Neural Tube Defects] (2)

A

Increased…..

  1. [Amniotic AFP]
  2. [Maternal AChE (from amnion)]

NTD occurs when NT fails to fuse/close by 4 week gestation

290
Q

What Musculoskeletal structures derive from [1st Pharyngeal Arch] (6)

A
  1. Incus
  2. Malleus
  3. Maxilla
  4. Mandible
  5. Mastication m.
  6. Temporalis m.
291
Q

What Musculoskeletal structures derive from [2nd Pharyngeal Arch] (3)

A
  1. Stapes
  2. Styloid Process
  3. Lesser Horn of Hyoid
292
Q

What Musculoskeletal structures derive from [4th & 6th Pharyngeal Arch] (2)

A
  1. [Cricoid & Thyroid Cartilage]
  2. [Pharyngeal & Laryngeal m.]
293
Q

[Treacher Collins Syndrome] MOD

A

Genetic disruption of [Pharyngeal Arch 1 and 2] –> hypOplasia of mandible & Zygomatic bones

294
Q

In [Neurofibromatosis Type 1], Fleshy cutaneous neurofibromas are made of ______ which embryologically come from _____. These pts may also have hyperpigmented spots known as ____

A

In NF1, Fleshy cutaneous neurofibromas are made of Schwann cells, which are embryologically from Neural Crest. May also have [Cafe Au Lait Spots (image)]

Image: Cutaneous Neurofibromas & Cafe Au Lait Spots

295
Q

How does CO2 affect Cerebral vasculature and when is this clinically helpful?

A

Since pCO2 is a vasoDilator of cerebral vessels, DEC pCO2 –> vasoconstriction –> Helps pts with cerebral edema

296
Q

Morphine MOA

A

Binds to [Mu GPCR] –> K+ Efflux –> hyperpolarization

297
Q

VitB12 deficiency presents with ____ anemia from ____. How can this be dx (2)

A

VitB12 deficiency presents with Megaloblastic Anemia from Impaired DNA synthesis.

Dx = Elevated Methylmalonic acid & Homocysteine

298
Q

How does [Tricyclic Antidepressent] OD Manifest

A

Anti-Cholinergic Activity but with no effect on NeuroMuscular Junction (normal CMAP)

299
Q

Name the 3 enzymes that use [Thiamine VitB1] as a cofactor and how they’re associated with [Wernicke Encephalopathy Syndrome]

A
  • [Pyruvate Dehydrogenase]
  • [A-ketoglutarate Dehydrogenase]
  • [Transketolase]

Without [Thiamine VitB1] –> No CNS Glucose Utilization with these enzymes –> [WES]

300
Q

[PKU - PhenylKetonUria] MOD

A

[Phenylalanine Hydroxylase] or its [TetrahydrobioPterin cofactor] –> Phe CNS accumulation –> DEC 50 IQ pts in 1st year of life vs. Seizures

301
Q

Bacterial Meningitis Sx Triad

A

FAN

  1. Fever
  2. [Aches (HA) + photophobia]
  3. Nuchal Rigiditiy
302
Q

Define [Length Constant]. What Dz Directly affects this?

A

How far along the axon an electrical impulse can travel before dissipating. DEC in Multiple Sclerosis

303
Q

Define [Time Constant]

A

Time it takes for a change in membrane potential to achieve 63% of the new value

MS INC Time Constant

304
Q

[Orbital Floor] Fracture manifestations (2)

A
  1. Paresthesia (Upper cheek, Lip, Gingiva)-from infraorbital n. damage
  2. [Entrapment of Inferior Rectus m. –> limited Superior Gaze]
305
Q

Which n. is commonly stretched/injured during labor?

A

Pudendal n.

Stretch injury from stress placed on pelvic floor during labor–> Pudendal n. damage

306
Q

[Pudendal n. damage] manifestation (3)

A
  1. Incontinence from perineal m. weakness
  2. Perineal Pain
  3. Sex Dysfunction
307
Q

Where, in CNS, is the [APCTZ - Area Postrema Chemoreceptor Trigger Zone]?

A

Dorsal Medulla near 4th Ventricle

D on image

308
Q

Identify

A

A: Thalamus

B: Dorsal Midbrain

C: Pons

D: Dorsal Medulla

E: Cerebellum

309
Q

Causes of L5 Radiculopathy (2)

A

Compression of L5 n. root from…

Verebral Disc Herniation

Spinal Foraminal Stenosis

310
Q

L5 Radiculopathy Sx (4)

A
  • [Back pain + radiation down leg]
  • Sensory loss over Butt / lateral thigh / dorsal foot
  • Weak Dorsiflexion
  • Weak Toe extension
312
Q

What’s an easy way to damage the [lower trunk Brachial Plexus] (2) and how will this manifest (2)

A
  1. Thoracic Outlet Syndrome (Extra Cervical Rib)
  2. Sudden upward arm stretching at shoulder

[Klumpke Claw Hand] + Finger Clumsiness

313
Q

How does [Subactue Combined Degeneration] manifest? (2)

A

[SuBACute Combined Degeneration]

[Demyelinating lesions] in 3 Thoracic Spinal Columns:

  1. [Dorsal–> Loss of 2TVP]
  2. [Lateral CST –> UMN Weak MESH]
  3. Spinocerebellar
314
Q

Describe Chiari Malformation Type 1 (2)

A

Benign = adult onset occipital HA + cerebellar dysfunction

315
Q

[Von Hippel Lindau Dz] Mode of Inheritance

316
Q

What lesion causes Decerebrate Posturing

A

[dEcErEbrate ExtEnsor posturing]

Rigid ExtEnsion of UE and LE

[Lesion of rubrospinal tract] at or below Red Nucleus:

Pons

vs.

Midbrain-accompanied w/ vertical gaze palsy & light dissociation (pupils constrict only with accomodation)

317
Q

What lesions cause Decorticate Posturing

A

[Decorticate Flexion Posturing] “Flex toward ur Core”

Rigid Flexion of UE and LE

Lesion between Cerebral Cortex and Red Nucleus

318
Q

Manifestation of [Oculomotor CN3 palsy] (2)

A

DOP

[Down & Out eye]

+

Ptosis

pupil dilation is determined by parasympathetic fiber involvement

319
Q

Which Germ Layer does the POST Pit come from?

A

NeuroEctoderm

[3] Step 1 USMLE (8 decks)

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