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Neuro Random facts Flashcards

1
Q

Meissner corpuscles

A

In the glabrous (hairless) skin, for dynamic, fine/light touch, position sense, adapt quickly

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2
Q

Pacinian corpuscles

A

Adapt quickly, in the deep skin layers, ligaments, joints, sense vibration and pressure

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3
Q

Merkel discs

A

Adapt slowly, in the fingertips and superficial skin, sense pressure, deep status touch (e.g., shapes, edges), position sense

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4
Q

Ruffini corpuscles

A

Adapt slowly, in the fingertips and joints, sense pressure, slippage of objects along surface of skin, joint angles change

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5
Q

What are does stress and panic

A

locus ceruleus (where norepi is synthesized)

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6
Q

Vitamin necessary for synthesis and catabolism of GABA

A

B6

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7
Q

How is GABA synthesized?

A

From glutamate by glutamate decarboxylase

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8
Q

Lateral hypothalamus

A

Hunger

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9
Q

Ventromedial hypothalamus

A

Satiety

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10
Q

Anterior hypothalamus

A

Cooling, parasympathetic

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11
Q

Posterior hypothalamus

A

Heating, sympathetic

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12
Q

Suprachiasmatic nucleus

A

Circadian rhythm

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13
Q

What causes the extra ocular eye movements during REM?

A

Paramedian pontine reticular formation/conjugate gaze center

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14
Q

VPL

A

Pain, temp; pressure, touch, vibration, proprioception (from the spinothalamic and DCML pathways)

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15
Q

VPM

A

Face sensation, taste (from the trigeminal and gustatory pathway)

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16
Q

LGN

A

Vision (goes TO the calcarine sulcus)

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17
Q

MGN

A

Hearing

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18
Q

VL

A

Motor

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19
Q

What are the output nerves from the cerebellum?

A

Purkinje cells to the deep nuclei of cerebellum to the contralateral cortex via superior cerebellar peduncle

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20
Q

Characteristic lesion for hemiballismus

A

Contralateral subthalamic nucleus

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21
Q

Which disease do you see Lewy bodies in?

A

PARKINSONS

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22
Q

Neurohormonal changes in Huntington’s disease?

A

Increased dopamine, decreased GABA, decreased ACh

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23
Q

What causes neuronal death in HD?

A

NMDA-R binding and glutamate toxicity

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24
Q

Agraphia, acalculia, finger agnosia, left-right disorientation

A

Lesion to the dominant pariental-temporal cortex, Gerstmann syndrome

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25
Q

Damage to the PPRF

A

Eyes look away from the lesion

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26
Q

Damage to the frontal eye fields

A

Eyes look toward the lesion

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27
Q

What is cerebral perfusion driven by?

A

Pco2 (hypoxemia increases cerebral perfusion only when Po2 is less than 50)

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28
Q

Why do people faint in panic attacks?

A

Hyperventilation leads to decreased cerebral perfusion

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29
Q

Equation for cerebral perfusion pressure

A

CPP=MAP-ICP

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30
Q

Symptoms of lateral medullary syndrome

A

Vomiting, vertigo, nystagmus; decreased pain and temp sensation from ipsilateral face and contralateral body; dysphagia, hoarseness, decreased gag reflex; ipsilateral Horner syndrome; ataxia, dysmetria

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31
Q

What blood vessel is damaged to give Wallenberg syndrome

A

PICA

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32
Q

Symptoms of AICA damage

A

Lateral pontine syndrome. Similar to Wallenberg but PARALYSIS of FACE as well, decreased lacrimation, salivation. (NO dysphagia or hoarseness). “Facial droop means AICA’s pooped”

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33
Q

Lesions where causes allodynia

A

Thalamus

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34
Q

What is an inherited disease that could look like polio?

A

Spinal muscular atrophy (Werdnig-Hoffmann disease), AR

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35
Q

What innervates the salivary glands

A

Facial nerve innervates submandibular and sublingual, glossopharyngeal innervates parotid

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36
Q

What produces aqueous humor?

A

Ciliary epithelium (beta)

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37
Q

What innervates the dilator and sphincter muscle of the eye?

A

Dilator is sympathetic (alpha-1), and spinchter is parasympathetic (M3)

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38
Q

Vision changes in glaucoma

A

Progressive peripheral visual field loss

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39
Q

What is glaucoma?

A

Optic disc atrophy with characteristic cupping (thinning of outer rim of optic nerve head) usually with elevated intraocular pressure and progressive peripheral visual field loss

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40
Q

Cause of open angle glaucoma

A

Primary is unclear. Secondary can be from blocked trabecular meshwork from WBCs (e.g., uveitis), RBCs (e.g.. vitreous hemorrhage), retinal elements (e.g., retinal detachment)

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41
Q

Cause of primary closed/narrow angle glaucoma

A

Enlargement or forward movement of lens against central iris causes obstruction of normal aqueous flow through pupil resulting in fluid build up behind the iris, pushing peripheral iris against the cornea and impeding flow through the trabecular meshwork

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42
Q

Secondary causes of closed/narrow angle glaucoma

A

Hypoxia from retinal disease induces vasoproliferation in iris that contracts angle

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43
Q

Painful red eye, sudden vision loss, halos around lights, rock-hard eye

A

Acute angle-closure glaucoma

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44
Q

Distortion and eventual loss of central vision

A

Age-related macular degeneration

45
Q

Diabetic retinopathy

A
  1. Nonproliferative- damaged capillaries leak blood->lipids and fluids seep into retina-> hemorrhages and macular edema. 2. Proliferative- chronic hypoxia results in new blood vessel formation with resultant traction on retina
46
Q

Acute, painless monocular loss of vision

A

Central retinal artery occlusion/retinal detachment (?)

47
Q

Bone spicule-shaped deposits around macula

A

Retinitis pigmentosa

48
Q

What is retinitis pigmentosa

A

An inherited form of retinal degeneration. Painless, progressive vision loss beginning with night blindness (rods affected first)

49
Q

What causes the ptosis in Horner’s syndrome

A

Lack of sympathetic to the superior tarsal muscle

50
Q

Fourth nerve palsy

A

Diplopia when trying to look down (reading or going downstairs) because eye is stuck up, tilt their head toward the opposite side of the affected eye`

51
Q

Right MLF is which one

A

The one that connects the left CN VI nucleus to the right CN III nucleus (Directional term [ie right INO, left INO]) refers to which eye is paralyzed

52
Q

Does ApoE2 increase or decrease the risk for Alzheimer’s

A

Decrease

53
Q

Histology of Alzheimer’s

A

Senile plaques in gray matter (extracellular beta-amyloid core that may causes amyloid angiopathy), and neurofibrillary tangles (intracellular hyperphosphorylated tau protein, number of tangles correlates with degree of dementia)

54
Q

Histology of frontotemporal dementia

A

Pick bodies: silver-staining spherical tau protein aggregates

55
Q

Histology of Lewy body dementia

A

alpha-synuclein defect (Lewy bodies, primarily cortical)

56
Q

Charcot triad of MS

A

Scanning speech, Intention tremor (also incontinency and internuclear ophthalmoplegia, nystagmus)

57
Q

How does baclofen work?

A

GABA-B receptor agonist

58
Q

Tx for neurogenic bladder in MS

A

catheterization, muscarinic antagonists

59
Q

Tx for Guillan barre

A

Respiratory support, plasmapheresis, IV immunoglobulins

60
Q

Charcot-Marie-Tooth disease

A

AD, aka hereditary motor and sensory neuropathy, defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath, associated with scoliosis and foot deformities

61
Q

Krabbe disease

A

AR lysosomal storage disease due to deficiency of galactocerebrosidase. Buildup of galactocerebroside and psychosine destroys myelin sheath. Findings: peripheral neuropathy, developmental delay, optic atrophy, globoid cells

62
Q

Metachromic leukodystrophy

A

AR lysosomal storage disease due to arylsulfatase A deficiency. Build-up of sulfatides causes impaired production and destruction of myelin sheath. Findings: central and peripheral demyelination with ataxia, dementia

63
Q

Adrenoleukodystrophy

A

X-linked, disruption of metabolism of very-long-chain fatty acids causing buildup in the nervous system, adrenal gland, testes. Can lead to long-term coma/death and adrenal gland crisis

64
Q

What can be used for migraine prophylaxis?

A

Propranolol, topiramate, Ca channel blockers, amitriptyline

65
Q

What does positional testing show in peripheral and central vertigo

A

Peripheral-delayed horizontal nystagmus; central- immediate nystagmus in any direction, may change directions

66
Q

Genetics of Sturge-Weber syndrome

A

Congenital, non-inherited (somatic), developmental anomaly of neural crest derivatives dues to an activating mutation of GNAQ gene

67
Q

Sturge-Weber mnemonic

A

STURGE: Sporadic, port-wine Stain, Tram track calcifications, Unilateral, Retardation, Glaucoma, GNAQ gene, Epilepsy

68
Q

Tuberous sclerosis

A

HAMARTOMAS: hamartomas, angiofibromas, mitral regurgitation, ash-leaf spots, cardiac rhabdomyoma, tubers, autosomal dOminant, mental retardation, renal Angiomyolipoma, Seizures, Shagreen patches

69
Q

Features in vHL disease

A

Hemangioblastomas (high vascularity with hyper chromatic nuclei) in retina, brain stem, cerebellum, spine; angiomatosis (e.g., cavernous hemangiomas in skin, mucosa, organs); bilateral renal cell carcinomas; pheochromocytomas

70
Q

What do meningiomas arise from?

A

Arachnoid cells

71
Q

Histology of meningioma?

A

Spindle cells concentrically arranged in a whorled pattern; psammoma bodies (laminated calcifications)

72
Q

What can hemangioblastomas produce?

A

Erythropoietin (so can cause secondary polycythemia)

73
Q

What do Scwannomas stain positive for?

A

S-100

74
Q

Histology of schwannoma

A

Spindle cells with palisading nuclei arranged around Verocay bodies and composed of eosinophilic cores (Antoni A pattern) and mixed regions of low cellularity (Antoni B)

75
Q

Round nuclei with clear cytoplasm

A

“Fried egg” cells of an oligodendroglioma. May also see calcifications and “chicken wire” capillary pattern

76
Q

Rosenthal fibers

A

Pilocytic astrocytoma (in children), optic glioma in an adult

77
Q

Perivascular rosettes

A

Ependymoma

78
Q

Rod-shaed blepharoplasts found near nucleus

A

Ependymoma. Blepharoplasts=basal ciliary bodies

79
Q

Which alpha agonists can be used in glaucoma?

A

Epinephrine and brimonidine, both decrease aqueous humor synthesis. Do not use epic in closed-angle glaucoma because it causes mydriasis

80
Q

Which beta-blockers are used in glaucoma?

A

Timolol, betaxolol, carteolol

81
Q

MOA of pilocarpine, carbachol, physostigmine, and echothiphate in glaucoma

A

Increased outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

82
Q

What do you use for glaucoma in an emergency

A

Pilocarpine

83
Q

Which prostaglandins can you use in glaucoma and what are their side effects?

A

Latanoprost and travoprost, SE: darkens color of iris

84
Q

How do opioid analgesics work?

A

Act at opioid G-protein coupled receptors. Open K channels and close Ca channels, decreasing synaptic transmission. Inhibit the release of Ach, norepi, 5-HT, glutamate, and substance P.

85
Q

MOA of tramadol

A

Very weak opioid agonist, also inhibits 5-HT and norepi reuptake

86
Q

MOA of ethosuximide

A

Blocks thalamic T-type Ca channels

87
Q

MOA of phenytoin

A

Increases sodium channel activation; zero-order kinetics

88
Q

MOA of gabapentin

A

Primarily inhibits high-voltage-activated Ca channels; designed as a GABA analog

89
Q

First line for seizures in neonates

A

Phenobarbital

90
Q

Which anti-epileptic causes kidney stones?

A

Topiramate

91
Q

What is vigabatrin used for?

A

Infantile spasms (West syndrome), but ACTH is a better treatment

92
Q

First line for simple and complex partial seizures

A

Carbamazepine

93
Q

Drugs with low solubility in the blood have what type of induction

A

Rapid

94
Q

Drugs with high solubility in lipids have what type of potency

A

high

95
Q

Cause of malignant hyperthermia

A

Due to abnormal ryanodine receptors on the surface of the sarcoplasmic reticulum releasing large amounts of calcium after exposure to an anesthetic

96
Q

Why is thiopental so short acting?

A

Rapid redistribution into tissue

97
Q

MOA of arylcyclohexylamines

A

(Ketamine) PCP analogs that act as dissociative anesthetics. Block NMDA receptors.

98
Q

MOA of propofol

A

Potentiates GABA-A

99
Q

Order of nerve blockades from local anesthetics

A

Small myelinated -> small unmyelinated -> large myelinated -> large unmyelinated. Order of loss: pain, temp, touch, pressure

100
Q

MOA of local anesthetics

A

Block Na channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na channels, so most effective in rapidly firing neurons

101
Q

Reversal of blockade for non-depolarizing neuromuscular agents

A

Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia)

102
Q

Drugs for Parkinsons

A

BALSA: bromocriptine, amantadine, levodopa (with carbidopa), selegiline (and COMT inhibitors), antimuscarinics

103
Q

MOA of pramipexole, ropinirole

A

Dopamine agonist

104
Q

MOA of amantadine in Parkinsons

A

Increases dopamine release and decreases dopamine reuptake

105
Q

Toxicity of amantadine

A

Ataxia, livedo reticularis

106
Q

Use of benztropine in Parkinsons

A

Antimuscarinis, improves tremor and rigidity but has little effect on bradykinesia

107
Q

Drugs used for Alzheimers

A

Memantine (NMDA receptor antagonist); helps prevent excitotoxicity (mediated by Ca); AChE inhibitores- donepezil, galantine, rivastigmine, tacrine

108
Q

MOA of sumatriptans

A

5-HT-1B/1D agonists. Inhibit trigeminal nerve activation; prevent vasoactive peptide release; induce vasoconstriction

109
Q

Treatment for RLS

A

Dopamine agonists (eg, pramiprexole)

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