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FirstAID > Neurology > Flashcards

Neurology Flashcards

1
Q

In which part of the brain is atrophy most pronounced in Alzheimer’s

A

Hippocampus and frontal lobe

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2
Q

CNS/PNS cells that originate from Neuroectoderm

A
  • CNS neurons
  • ependymal cells (make CSF)
  • Oligodendroglia
  • Astrocytes
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3
Q

CNS/PNS cells that originate from Neural Crest:

A
  • Schwann cells

- PNS neurons

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4
Q

CNS/PNS cells that originate from Mesoderm:

A
  • Microglia

* **note: microglia=macrophages of the brain!

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5
Q

Nissl substance

A

RER in cell body, dendrites of neurons; NOT in axons

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6
Q

GFAP

A

astrocyte marker

–>so, also a marker for astrocyte tumors: glioblastoma and pilocytic astrocytoma

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7
Q

Astrocytes:

  • roles?
  • marker for astrocytes?
A

physical support and repair; maintain BBB; create scar tissue in response to injury

*GFAP = astrocyte marker (elevated in astrocyte tumors: glioblastoma and pilocytic astrocytoma)

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8
Q

macrophages/phagocytes of the CNS?

A
  • ->Microglia
  • mesodermal origin
  • when tissue damage, microglia respond by differentiating into large phagocytic cells
  • HIV-infected microglia fuse to form giant cells in CNS
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9
Q

oligodendrocytes:

A

produce myelin in the CNS

  • one oligodendrocyte can myelinat many CNS axons (up to 30!)
  • destroyed in MS!
  • Look like fried eggs on histology
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10
Q

Schwann cells

A

produce myelin in the PNS

-one Schwann cell only myelinates one PNS axon

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11
Q

Cell types that look like fried eggs on histology (various, not just neuro):

A
  • Oligodendrocytes
  • Koilocytes (HPV)
  • Seminomas
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12
Q

Type of cells that are destroyed in MS?

A

Oligodendrocytes

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13
Q

Type of cells destroyed in Guillain-Barre syndrome?

A

Schwann cells

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14
Q

Acoustic neuroma:

A

type of Schwannoma; usually located in internal acoustic meatus (CN VIII)
–>see bilateral acoustic schwannomas in NF 2)

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15
Q

Endoneurium, Perineurium, Epineurium

A

Endoneurium: surrounds single nerve fibers
Perineurium: surrounds a fascicle of nerve fibers
Epineurium: dense connective tissue that surrounds an entire nerve

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16
Q

Diseases with increased NE?

A
  • ->Anxiety

- ->Mania

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17
Q

Disease with decreased NE?

A

Depression

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18
Q

Disease associated with increased dopamine?

A

Schizophrenia

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19
Q

Diseases with decreased dopamine?

A
  • Parkinson’s

- Depression

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20
Q

Diseases with decreased serotonin (5-HT)?

A
  • Anxiety

- Depression

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21
Q

Diseases with decreased Ach?

A
  • Alzheimer’s

- Huntington’s

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22
Q

Disease with increased ACh?

A
  • Parkinson’s

- Also: increased ACh in REM sleep (b/c ACh is the principal neurotransmitter in REM sleep)

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23
Q

Diseases with decreased GABA?

A
  • Anxiety

- Huntington’s

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24
Q

What is synthesized in Locus ceruleus?

A
  • ->location of NE synthesis

- stress and panic! (elevated NE)

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25
Q

What is synthesized in Raphe nucleus?

A

location of serotonin synthesis

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26
Q

What is synthesized in Nucleus Accumbens?

A
  • GABA

- ->nucelus accumbens and septal nucleus = reward center, pleasure, addiction, fear

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27
Q

What is synthesized in the ventral tegmentum?

A

Dopamine

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28
Q

What is synthesized in the basal nucleus of Meynert?

A

ACh

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29
Q

What vitamin is used in GABA synthesis? What is the precursor to GABA?

A

Glutamate is the precursor to GABA

–>Vitamin B6 = cofactor in GABA synthesis from Glutamate

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30
Q

3 structures that form the blood-brain-barrier:

A
  • tight junctions (b/w endothelial cells)
  • basement membrane
  • astrocyte processes
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31
Q

What types of substances can cross the BBB rapidly via diffusion?

A

Nonpolar/Lipid-soluble substance (lots of anesthetic agents are lipid-soluble!)

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32
Q

What substances can cross the BBB slowly by carrier-mediated transport?

A

glucose and amino acids

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33
Q

How does glucose get across the BBB?

A

glucose crosses the BBB slowly by carrier-mediated transport mechanism

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34
Q

Area postrema of the brain

A

–>area of the brain that has fenestrated capillaries and no BBB; crossing of substances into this area is what results in vomiting post chemo

*Area postrema inputs info into the hypothalamus

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35
Q

OVLT = organum vasculosum of lamina terminalis

A

area of the brain that has fenestrated endothelium and lacks BBB (like the area postrema)
–>can sense osmolarity of the blood and respond (ie by regulating ADH-releasing neurons)….

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36
Q

supraoptic nucleus of the hypothalamus:

A

makes ADH

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37
Q

paraventricular nucleus of the hypothalamus:

A

makes oxytocin

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38
Q

Functions of the Hypothalamus:

A

“Hypothalamus wears TAN HATS”

  • Thirst and water balance
  • Adenohypophysis regulation
  • Neurohypophysis releases hormones from the hypothalamus (ADH, oxytocin)
  • Hunger
  • Autonomic regulation
  • Temperature regulation
  • Sexual urges
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39
Q

Lateral area/nucleus of the hypothalamus:

  • role?
  • if destroyed?
  • inhibited by?
A
  • ->responsible for hunger
  • if destroyed, get anorexia, FTT in infants
  • inhibited by leptin (leptin–>decreased hunger)

“if zap the lateral nucleus, you shrink laterally!”

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40
Q

Ventromedial area/nucleus of the hypothalamus:

  • role?
  • if destroyed?
  • stimulated by?
A
  • involved in satiety
  • if destroyed (ie craniopharyngoma) –> don’t get full, eat more = hyperphagia
  • stimulated by leptin

“if zap ventromedial nucleus, you grow ventrally and medially”

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41
Q

Anterior hypothalamic nucleus:

-Role?

A

Involved in cooling the body

“Anterior Cools like an A/C”

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42
Q

Posterior hypothalamic nucleus:

A

involved in heating the body

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43
Q

Suprachiasmatic nucleus:

-role?

A

involved in the circadian rhythm

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44
Q

Which hypothalamic nuclei send axonal projections to the post pituitary?

A
  • supraoptic nucleus –> ADH

- paraventricular nucleus –> oxytocin

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45
Q

VPL (Ventral Posterolateral) Nucleus of the Thalamus:

-role?

A
  • Roles in:
  • pain and temperature
  • pressure
  • touch
  • vibration
  • proprioception

*where the dorsal column and spinothalamic tracts have their 2nd synapses!

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46
Q

VPM (Ventral Posteromedial) nucleus of the thalamus:

-role?

A

“Make-up goes on the face; vpM”

–>face sensation and taste

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47
Q

LGN (lateral geniculate) nucleus of the thalamus:

A

“L for Light”

–>involved in relaying vision

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48
Q

MGN (medial geniculate nucleus) of the thalamus:

A

“M for Music”

–>involved in relaying Hearing

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49
Q

What is the function of the thalamus?

A

Thalamus is the major relay center for all ascending sensory information, except olfaction
–>relays sensory and motor information to the cerebral cortex

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50
Q

Thalamic syndrome: Vascular lesion to the thalamus (from ischemic or hemorrhagic stroke) - what are the results/symptoms?

A

–>damage to VPL and VPM nuclei; so get complete CONTRALATERAL SENSORY loss. may also have proprioceptive defects. NO motor deficits.

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51
Q

What structures make up the Limbic System?

A
  • Hippocampus
  • Cingulate gyrus
  • Fornix
  • Mammillary bodies
  • Septal nucleus (reward center, pleasure, addiction, fear)
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52
Q

What are the Functions of the Limbic System?

A

5 F’s - all are primitive functions:

  • Feeding
  • Fleeing
  • Fighting
  • Feeling
  • sex
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53
Q

What information does the cerebellum receive contralaterally? ipsilaterally?

A

Cerebellum receives:

  • contralateral cortical input
  • ipsilateral proprioceptive information
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54
Q

Deep nuclei of the cerebellum (from Lateral to Medial):

A

“Dentists Embody Global Fasts”

  • Dentate
  • Emboliform
  • Globose
  • Fastigial

*note: Emboliform and Globose nuclei = “interposed nuclei”

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55
Q

Main function of Basal Ganglia?

A

–>Voluntary movements and making postural adjustments

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56
Q

Depigmentation of substantia nigra pars compacta? What role does the substantia nigra normally play?

A

Parkinson’s syndrome:
–>the substantia nigra is part of the basal ganglia, and normally facilitates movement. But, in Parkinson’s get loss of dopaminergic neurons, so get inhibition of movement from basal ganglia.

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57
Q

Main symptoms of Parkinson’s:

A

“TRAP”

  • Tremor at rest (“pill-rolling tremor”)
  • cogwheel Rigidity
  • Akinesia
  • Postural instability

*have decreased dopamine, increased ACh

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58
Q

Hemiballismus

A
  • sudden, wild flailing of 1 arm +/- leg
  • ->get this with contralateral subthalamic nucleus lesion (like a lacunar stroke in a pt with HTN hx)
  • ->loss of inhibition of thalamus through the globus pallidus (of the basal ganglia)
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59
Q

Neuronal death via NMDA-R binding and glutamate toxicity; and, atrophy of striatal nuclei in what disease?

A

Huntington’s disease

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60
Q

C’s of Huntington’s disease:

A
  • Chorea (b/c atrophy of striatal nuclei, which normally inhibits movement; so, get increased movement)
  • Caudate nucleus degeneration
  • Crazy (dementia)
  • CAG repeats
  • decreased ACh and decreased GABA

“CAG –> Caudate loses ACh and GABA”

(decreased GABA–>increased movement)

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61
Q

Chorea is seen in what types of brain injuries?

A

–>injuries to basal ganglia (like in Huntington’s)

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62
Q

Athetosis:

  • what is it?
  • seen in what types of brain injuries?
A
  • ->slow, writhing movements, especially of fingers (snake-like)
  • ->see in basal ganglia lesions (like Huntington’s)
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63
Q

Myoclonus

A

=sudden, quick muscle contractions; like hiccups, jerks.

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64
Q

Intention Tremor

A

slow, zigzag movement when pointing toward an object; associated with cerebellar dysfxn, MS

(vs essential/postural tremor –> familial, alcohol, beta-blockers; and resting tremor –> Parkinson’s)

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65
Q

Kluver-Bucy syndrome:

  • presentation?
  • d/t lesion in what part of brain?
  • associated with what virus?
A
  • Hyperorality, hypersexuality, disinhibited behavior
  • bilateral lesion of the amygdala
  • associated with HSV-1
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66
Q

Spatial neglect syndrome:

–>d/t lesion to what area of brain?

A

lesion of Right parietal lobe (assuming that Right = NON-dominant lobe)
*don’t recognize/see contralateral side of the world!

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67
Q

Reduced levels of arousal and wakefulness (ie coma) d/t lesion of what area of brain?

A

Reticular Activating System (in midbrain)

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68
Q

What area of the brain is lesioned in Wernicke-Korsakof syndrome?

A

Bilateral lesion to mammillary bodies

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69
Q

Presentation of Wernicke-Korsakoff syndrome?

A
  • Wernicke: confusion, ophthalmoplegia, ataxia

* Korsakoff: memory loss, confabulation, personality changes

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70
Q

Tremor at rest, chorea, athetosis (snake-like mvmnts): what area of brain is lesioned?

A

–>Basal ganglia lesion

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71
Q

Truncal ataxia and dysarthria: what area of brain is lesioned?

A

Cerebellar vermis

*note: lesion to cerebellar hemispheres affects lateral limbs; whereas lesion to cerebellar vermis affects central body.

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72
Q

Contalateral hemiballismus: what area of brain is lesioned?

A

–>lesion to subthalamic nucleus

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73
Q

Anterograde amnesia=can’t make new memories: area of brain lesioned?

A

–>Hippocampus lesion

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74
Q

Eyes look AWAY from side of lesion: area of brain lesioned?

A

–>PPRF lesion (Paramedian Pontine Reticular Formation)

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75
Q

Eyes look TOWARD lesion: area of brain lesioned?

A

Frontal eye fields

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76
Q

Consequence of correcting hyponatremia too rapidly?

A
  • ->Central Pontine Myelinolysis:
  • Acute paralysis
  • Dysarthria (motor inability to speak)
  • Dysphagia
  • Diplopia
  • Loss of consciousness
  • on MRI, see abnormally increased signal in pons
  • IRREVERSIBLE!
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77
Q

Aphasia vs Dysarthria:

A
  • Aphasia = higher-order inability to speak

- Dysarthria = motor inability to speak

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78
Q

Where is Broca’s area?

A

Inferior frontal gyrus

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79
Q

Where is Wernicke’s area?

A

Superior temporal gyrus

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80
Q

Conduction aphasia:

  • presentation?
  • cause?
A

–>No connection between what pt says and what pt understands (comprehension is intact, and have fluent speech, but no connection between comprehension and speech)

*caused by lesion to: Arcuate fasciculus = connects Broca’s and Wernicke’s areas

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81
Q

Arcuate fasciculus

A

connects Broca’s and Wernicke’s areas

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82
Q

Area supplied by the Anterior Cerebral Artery?

A

–>anteromedial surface

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83
Q

Area of brain supplied by Middle Cerebral Artery?

A

–>lateral surface of brain

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84
Q

Area of brain supplied by Posterior Cerebral Artery?

A

–>posterior and inferior surfaces

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85
Q

Which artery supplies Broca’s and Wernicke’s areas?

A

MCA (b/c MCA supplies lateral surface of brain…)

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86
Q

What drives Cerebral Perfusion Pressure, PCO2 or PO2?

A
  • ->PCO2 normally drives the cerebral perfusion pressure
  • But, in severe hypoxia (when PO2 < 50 mmHg) PO2 also drives the cerebral perfusion pressure

**Cerebral Perfusion Pressure is proportional to PCO2 until PCO2 > 90 mmHg, then cerebral perfusion pressure levels off)

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87
Q

Which arteries are responsible for anterior circulation? posterior circulation?

A
  • Anterior circulation–> arteries derived from Internal Carotid: ACA, Lateral striate, MCA
  • Posterior circulation–> arteries derived from Subclavian: AICA, ASA (ant spinal artery), Basilar, PICA, PCA, Vertebral
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88
Q

Most common sites of saccular/berry aneurysms? 2nd most common site?

A 
#1 = AComm (ant communicating artery) 
#2 = PComm (post communicating artery)
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89
Q

What does rupture of a saccular/berry aneurysm lead to?

A

–>hemorrhagic stroke/subarachnoid hemorrhage

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90
Q

3 conditions associated with berry aneurysms?

A
  • ADPKD
  • Marfan’s syndrome
  • Ehlers-Danlos syndrome
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91
Q

CN III palsy:

  • presentation?
  • cause?
A
  • eye is “down and out”

- cause = PCOM aneurysm rupture (saccular/berry aneurysm)

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92
Q

Bitemporal hemianopia/visual field defects:

-cause?

A

–>AComm sacular/berry aneurysm rupture

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93
Q

Contralateral hemianopsia with macular sparing:

–>area of lesion? what artery is stroke in?

A
  • macular sparing = hallmark of occipital lob lesions

* this is an occipital cortex, visual cortex lesion; d/t stroke in PCA

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94
Q

Charcot-Bouchard microaneurysms:

A
  • associated with chronic hypertension

- affects small vessels (ie in basal ganglia, thalamus)

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95
Q

Cause of epidural hematoma?

A

–>rupture of middle meningeal artery (branch of maxillary artery), often secondary to fracture of temporal bone

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96
Q

Cause of subdural hematoma?

A
  • ->rupture of bridging veins
  • Seen in:
  • elderly
  • alcoholics
  • blunt trauma
  • shaken baby
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97
Q

Shaken baby syndrome causes what kind of intracranial hemorrhage?

A

–>subdural hematoma

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98
Q

Cause of subarachnoid hemorrhage?

A

–>rupture of aneurysm (ie berry aneurysm) or AVM (ArterioVenous Malformation –> problem in vein-artery connection)

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99
Q

Time course of a subarachnoid hemorrhage?

A

–>Rapid

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100
Q

Risks 2-3 days after a subarachnoid hemorrhage?

A
  • ->Risk of vasospasm d/t blood breakdown (constriction of blood vessels) –> prevent vasospasm with CCB = Nimodipine
  • ->Risk of rebleed
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101
Q

How to prevent vasospasm following a subarachnoid hemorrhage?

A

–> treat with Nimodipine (a CCB)

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102
Q

Most common sites of Intraparenchymal/Hypertensive Hemorrhage?

A

–>basal ganglia and internal capsule

*usually caused by hypertension, but may also be caused by amyloid angiopathy, vasculitis, and neoplasms.

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103
Q

Ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally); contralateral hemiparesis; pain and temp preserved: what artery is lesioned?

A

ASA = Anterior Spinal Artery

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104
Q

loss of pain and temperature sensation on ipsilateral face, but contralateral body: What artery is lesioned?

A

PICA (posterior inferior cerebellar artery)

  • ->this is Lateral Medullary/Wallenberg’s syndrome
  • **Other findings:
  • dysphagia, hoarseness, decreased gag reflex, ipsilateral Horner’s syndrome, ataxia, etc…
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105
Q

Dysphagia, hoarseness, and decreased gag reflex; ipsilateral Horner’s syndrome: What artery is lesioned?

A

–>PICA (“don’t PICK A (pica) HORSE (hoarseness) that CAN’T EAT (dysphagia)!”

  • ** find this in Lateral medullary / Wallenberg’s syndrome
  • ->Other findings:
  • decreased pain/temp sensation on ipsilateral face, contralateral body
  • ataxia, dysmetria
  • vomiting, vertigo, nystagmus
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106
Q

Lateral Medullary/Wallenberg’s syndrome:

  • what artery is lesioned (where is stroke)?
  • presentation?
A
  • stroke in PICA
  • presentation:
  • decreased pain/temp sensation on ipsilateral face and contralateral body
  • hoarseness, dysphagia, decreased gag reflex
  • ataxia, dysmetria
  • ipsilateral horner’s
  • vomiting, vertigo, nystagmus
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107
Q

Paralysis of face (Facial Drooping); ipsilateral Horner’s; decreased lacrimation, salivation; decreased pain/temp sensation on face; decreased hearing ipsilaterally, vomiting, vertigo, nystagmus: What artery is lesioned/where is stroke?

A

–>AICA (ant inf cerebellar artery)
=Lateral Pontine Syndrome

***Facial nucleus affects = specific to AICA lesions

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108
Q

Contralateral hemiplegia/hemiparesis: What artery is lesioned/where is stroke?

A

–>Lateral striate arteries = “arteries of stroke”; usually secondary to unmanaged HTN (so area lesioned= striatum and internal capsule)

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109
Q

Contralateral paralysis and loss of sensation on UPPER limb and face: what artery is lesioned?

A

–>MCA (Middle Cerebral Artery)

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110
Q

Contralateral paralysis and loss of sensation on LOWER limb: what artery is lesioned/where is stroke?

A

–>ACA = Anterior Cerebral Artery

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111
Q

Areas of the brain that are most vulnerable to ischemia/irreversible injury from ischemia?

A
  • hippocampus
  • neocortex
  • cerebellum
  • watershed areas
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112
Q

Ischemic brain injury - what’s seen at each time after damage:

  • 12-48 hours?
  • 24-72 hours?
  • 3-5 days?
  • 1-2 weeks?
  • after 2 weeks?
A
  • 12-48 hours: red neurons (=neurons that are dying d/t ischemia :()
  • 24-72 hours: necrosis + neutrophils
  • 3-5 days: macrophages
  • 1-2 weeks: reactive gliosis + vascular proliferation
  • after 2 weeks: glial scar (glial cells = fibroblasts of the brain)
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113
Q

Treatment of an ischemic stroke?

A

tPA as long as it’s within 4.5 hours of stroke

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114
Q

Stroke imaging: CT and MRI; hemorrhagic vs ischemic strokes?

A
  • Can see area on MRI within 3-30 minutes, and continue to see for 10 days (can see signs of ischemia on MRI)
  • Can see on CT within 24 hours; but, can only see signs of hemorrhagic stroke, not ischemic…
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115
Q

CSF: produced by? reabsorbed by?

A

CSF is produced by choroid plexus
CSF is reabsorbed by venous sinuses via arachnoid granulations; arachnoid granulations drain into the superior sagittal sinus

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116
Q

Pathway of CSF: from lateral ventricle to subarachnoid space:

A
  • Lateral ventricle –> 3rd ventricle via Foramen of Monro
  • 3rd ventricle –> 4th ventricle via Cerebral aqueduct
  • 4th ventricle to subarachnoid space via Foramina of Luschka (laterally) and Foramen of Magendie (medially)
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117
Q

Dementia + Ataxia + Urinary Incontinence:

A

Normal Pressure Hydrocephalus
–>Expansion of ventricles (see really dilated ventricles); No increase in subarachnoid space volume

*this is a cause of reversible dementia in elderly pts; why it’s so important to do a CT in a dementia work-up!!

**“Wet (incontinenc), Wobbly (ataxia), Wacky (dementia)”

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118
Q

Communicating Hydrocephalus:

  • cause?
  • presentation?
A

*decreased absorption of CSF by arachnoid granulations–> increased CSF within ventricles (maybe d/t arachnoid scarring, like after meningitis)

  • presentation/results:
  • increased ICP
  • papilledema
  • herniation

“communicating” –> b/c CSF still flows between ventricles

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119
Q

Obstructive/Non-communicating hydrocephalus:

-cause?

A

Blockage of CSF circulation (like d/t a brain tumor, or stenosis of the cerebral aqueduct (aqueduct of Sylvius)

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120
Q

Hydrocephalus ex vacuo:

A

Have atrophy of brain (like in Alzheimer’s, advanced HIV, Pick’s disease), so it appears like there is increased amount of CSF. But no symptoms, and ICP is normal.

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121
Q

Spinal Nerves:

  • how many total?
  • how many of each type?
  • where do they exit the vertebrae?
A
  • 31 total
  • 8 cervical
  • 12 thoracic
  • 5 lumbar
  • 5 sacral
  • 1 coccygeal

*C1-C7 exit through the intervertebral foramina above the corresponding vertebrae (so, C1 exits above C1 vertebrae; etc). The rest exit below the corresponding vertebrae (So, C8 exits below C8, above T12)

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122
Q

Vertebral disk herniation: between which vertebrae does it usually occur?

A
  • ->usually between L5 and S1

- ->it’s the herniation of the nucleus pulposus through the annulus fibrosus.

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123
Q

Between what vertebrae should an LP be done?

A

–>b/t L3 and L5 (find ASIS and go from there; it marks L4!)

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124
Q

To what vertebrae does the spinal cord extend in adults? subarachnoid space?

A
  • ->spinal cord goes to L1-L2

- ->subarachnoid space to S2 (why do LP b/w L3-L5; want to get CSF, but not damage spinal cord)

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125
Q

Spinothalamic Tract: information?

A

Ascending pain and temperature sensation

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126
Q

Lateral Corticospinal Tract: information?

A

Descending voluntary movement of contralateral limbs

127
Q

Dorsal Column: information transmitted?

A

Ascending pressure, vibration, touch, proprioceptive sensations

128
Q

Fasciculus cuneatus:

A

dorsal column tract nucleus: more lateral, sensations from upper body, extremities

129
Q

Fasciculus gracilis:

A

dorsal column tract nucleus: more medial; sensations from lower body, extremities

130
Q

Polio: where in spinal cord is lesion?

A

–>Destruction of Anterior Horns; get LMN lesion –> flaccid paralysis

131
Q

Werdnig-Hoffmann disease: where in spinal cord is lesion?

A
  • ->Destruction of anterior horns; LMN lesion –> flaccid paralysis
  • **like Polio
132
Q

Where in spinal cord are lesions in MS?

A

–>various locations - random, assymetric; but, mostly in the WHITE matter of cervical region, b/c it’s d/t de-myelination (white matter=composed of myelinated axons and glial cells; gray matter=composed of neurons)

133
Q

Where in spinal cord are lesions in ALS (Amyotrophic Lateral Sclerosis = Lou Gehrig’s)?

A

Both UMN and LMN lesions; no sensory deficit (so, see lesions in lateral corticospinal tract and anterior horn)

134
Q

Tabes dorsalis/tertiary syphilis: what area of spinal cord is lesioned?

A

–>degeneration of dorsal roots and dorsal columns –> impaired proprioception, locomotor ataxia

135
Q

Syringomyelia: what area of spinal cord is lesioned?

A

–>damages anterior white commissure (so, spinothalamic tract cannot deccusate, where 2nd order neurons of spinothalamic tract are) –> get bilateral loss of pain and temperature sensation

–>can expand and thus affect other tracts too

–> see syringomyelia in Chiari I types 1 and 2

136
Q

Vitamin B12 neuropathy: what areas of spinal cord are lesioned?

A

get combined degeneration-demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts
–>ataxic gait (cerebellum), hyperreflexia (corticospinal), impaired position and vibration sense (dorsal column)

137
Q

Vitamin E deficiency: what areas of spinal cord are lesioned?

A

(same as Vit B12 neuropathy):

  • combined degeneration-demyelination of dorsal column, lateral corticospinal tract, spinocerebellar tract
  • ->ataxic gait, hyperreflexia, impaired position and vibration sense
138
Q

Friedrich’s ataxia: what areas of spinal cord are lesioned?

A

(same as Vitamin B12 neuropathy and Vitamin E deficiency):

  • combined degeneration-demyelination of dorsal column, lateral corticospinal tract, spinocerebellar tract
  • ->ataxic gait, hyperreflexia, impaired position and vibration sense
139
Q

signs of both UMN and LMN lesions, but no sensory deficit?

A

–>ALS (lesions to lateral corticospinal tract and anterior horn)

140
Q

Bilateral loss of pain and temperature sensation?

A

–>Syringomyelia –> damage to anterior white commissure, so interferes with spinothalamic tract

*seen with Chiari I types 1 and 2

141
Q

Ataxic gait + hyperreflexia + impaired position and vibration sense?

A
  • Vitamin B12 neuropathy
  • Vitamin E deficience
  • Friedrich’s ataxia
142
Q

LMN signs from anterior horn destruction:

A
  • Polio

- Werdnig-Hoffmann disease

143
Q

“floppy baby” + tongue fasciculations

A

Werdnig-Hoffman disease = “infantile spinal muscular atrophy”

  • ->autosomal recessive
  • ->degeneration of anterior horn of spinal cord; LMN lesion signs.
144
Q

Defect in superoxide dismutase 1 (SOD1) may cause this disease?

145
Q

Riluzole

A

drug that can be used to treat ALS; decreases presynaptic glutamate release; can lengthen survival somewhat

146
Q

Impaired proprioception and locomotor ataxia; Charcot’s joints, pupils that don’t constrict in response to light, absent deep tendon reflexes, and positive Romberg sign?

A

–> Tabes dorsalis (affects dorsal columns and dorsal roots)

*Charcot joints = loss of sensationin a joint; may damage joints without knowing it, because can’t feel it

147
Q

Cause of death in Friedrich’s ataxia?

A

Hypertrophic cardiomyopathy

148
Q

Frataxin

A

protein that is mutated in Friedrich’s ataxia

–>leads to impairment in mitochondrial functioning

149
Q

Brown-Sequard syndrome:

  • what is it?
  • presentation?
A
  • ->hemisection of spinal cord
  • presentation:
  • ipsilateral UMN signs below lesion (corticospinal tract)
  • ipsilateral dorsal column lesion signs below lesion (loss of touch, vibration, proprioception sensations)
  • loss of contralateral pain and temp sensation below lesion (spinothalamic tract)
  • ipsilateral loss of all sensation at level of lesion
  • LMN lesion signs (ie flaccid paralysis) at level of lesion

*If lesion occurs above T1 –> presents with Horner’s syndrome

150
Q

Horner’s syndrome:

A
  • Ptosis (droopy eyelid)
  • Miosis (pupil constriction)
  • Anhidrosis (no sweating; flushed face on side that’s affected)

*d/t loss of sympathetic innervation of face

151
Q

What 3 conditions may be associated with Horner’s syndrome?

A
  • Any lesion of the spinal cord above T1
  • Pancoast tumor
  • Brown-Sequard syndrome
  • Syringomyelia (late stage, if it expands)
152
Q

Gallbladder and diaphragm pain referred to right shoulder via which nerve?

A

Phrenic nerve

153
Q

Where is the T4 dermatome?

A

Nipple level

154
Q

Where is the L1 dermatome?

A

level of inguinal ligament

155
Q

Where is the T10 dermatome?

A

level of umbilicus

156
Q

Which dermatomes are involved in erection and sensation of penile and anal zones?

A

S2, S3, S4 “keep the penis off the floor”

157
Q

Where is the L4 dermatome?

A

Includes the kneecaps

158
Q

What is a positive Babinski sign?

A
  • ->dorsiflexion of big toe and fanning of other toes (so big toe extends up, other toes just fan out)
  • UMN lesion sign
  • NORMAL in 1st year of life!
159
Q

Moro reflex

A

infant reflex –> “hang on for life”; when startled, abduct/extend limbs, and then draw them together

160
Q

Rooting reflex

A

=nipple-seeking reflex; if stroke one cheek, move head towards that cheek

161
Q

Sucking reflex

A

sucking when roof of mouth is touched

162
Q

Palmar and Plantar reflexes

A

curl fingers/toes if palms of hands/feet are stroked

163
Q

Pineal body

A
  • secretes melatonin

- involved in circadian rhythm

164
Q

Superior colliculi

A

vision –> conjugate vertical gaze center

165
Q

Inferior colliculi

166
Q

Parinaud syndrome

A

–>lesion in superior colliculi (like from a pinealoma); get paralysis of conjugate vertical gaze

167
Q

Which cranial nerves are sensory? motor? both?

A

“Some Say Money Matters But My Brother Says Big Brains Matter More”

CN I --> sensory
CN II --> sensory
CN III --> motor
CN IV --> motor
CN V --> both
CN VI --> motor
CN VII --> both
CN VIII --> sensory
CN IX --> both
CN X --> both
CN XI --> motor
CN XII --> motor
168
Q

Only cranial nerve without thalamic relay to cortex?

A

–> CN I (olfactory)

169
Q

Taste from anterior 2/3 of tongue?

A

Facial Nerve (CN VII)

170
Q

Taste from posterior 1/3 of tongue?

A

Glossopharyngeal (CN IX)

171
Q

Taste from epiglottic area (base of tongue)?

A

Vagus nerve (CN X)

172
Q

Which CNs have nuclei in the midbrain?

A

CN III, IV

173
Q

Which CNs have nuclei in the pons?

A

CN V, VI, VII, VIII

174
Q

Which CNs have nuclei in the medulla?

A

CN IX, X, XI, XII

175
Q

Sensation from anterior 2/3 of tongue?

A

CN V3 = Mandibular division of Trigeminal nerve

176
Q

Sensation from posterior 1/3 of tongue?

A

Glossopharyngeal (CN IX)

177
Q

Nucleus Solitarius

A

vagal nucleus –> involved in visceral sensory information (ie taste, baroreceptors, gut distention)

178
Q

Nucleus Ambiguus

A

vagal nucleus –> involved in Motor innervation of pharynx, larynx, upper esophagus (swallowing, palate elevation…)

179
Q

Dorsal Motor Nucleus

A

vagal nucleus –> sends Autonomic (Parasympathetic) fibers to heart, lungs, upper GI

180
Q

What CN passes through the cribriform plate?

A

–>CN I = olfactory

181
Q

What passes through the cavernous sinus?

A

CN III, IV, V1, V2, VI and postganglionic sympathetic fibers; also, internal carotid artery

182
Q

Cavernous sinus syndrome:

A

Ophthalmoplegia + Ophthalmic (V1) and maxillary (V2) sensory loss

183
Q

Tongue deviates TOWARD side of lesion: Cause?

A

lesion to CN XII (Hypoglossal)

–>b/c have weakened tongue muscles on affected side

184
Q

Jaw deviates TOWARD side of lesion: cause?

A 
CN V (trigeminal) motor lesion
-->b/c unopposed force from opposite pterygoid muscle (weakened muscle on affected side)
185
Q

Uvula deviates AWAY from side of lesion: cause?

A 
CN X (Vagus) lesion
-->weak side collapses, so uvula points away
186
Q

In an accessory nerve (CN XI) lesion: what is the presentation?

A
  • shoulder drop on side of lesion (trapezius)

- can’t turn head to side opposite lesion (SCM)

187
Q

Facial paralysis d/t UMN or LMN lesions:

A
  • UMN lesion: contralateral paralysis of lower face only (b/c upper face gets bilateral innervation)
  • LMN lesion: ipsilateral paralysis of both upper and lower parts of face (like what see with Bell’s palsy)
188
Q

Bell’s palsy:

  • Cause?
  • Presentation?
  • Complication of what conditions?
A
  • destruction of the facial nucleus
  • ->ipsilateral paralysis of upper and lower face (like LMN lesion)
  • Complication of: “ALexander graHam bell with STD”
  • AIDS
  • Lyme disease
  • HSV
  • Sarcoidosis
  • Tumors
  • Diabetes
189
Q

Which 3 muscles close the jaw? Which 1 opens it?

A
  • muscles that close the jaw:
  • Masseter
  • Temporalis
  • Medial pterygoid
  • muscle that closes jaw:
  • lateral pterygoid
190
Q

Cherry red spot on macula of eye: DD?

A
  • Occlusion of central retinal artery
  • Tay-Sachs
  • Niemann-Pick disease
191
Q

Clouding of cornea: DD?

A
  • Hurler’s disease (a mucopolysaccharidosis; not Hunter’s though)
  • I-cell disease
192
Q

Subluxation of lens: DD

A
  • Marfan’s

- Homocysteinuria

193
Q

Anterior Uveitis = inflammation of iris and ciliary body: DD?

A

Reactive Arthritis (and other PAIR and inflammatory diseases)

194
Q

Obstruction of Canal of Schlemm?

A

Glaucoma (impaired outflow of aqueous humor); seen in open/wide-angle glaucoma

195
Q

Open/Wide Angle vs Closed/Narrow Angle Glaucoma:

A
  • Open/Wide Angle: d/t obstructed outflow of aqueous humore (like obstruction of Canal of Schlemm) –>increased introaocular pressure…
  • ->more common, painless, insidious onset
  • Closed/Narrow Angle: obstruction of aqueous humor flow between iris and lens –> pressure builds up behind iris
  • ->really painful, decreased vision, frontal headache
  • ->emergency!
  • ->don’t treat with epinephrine, b/c can lead to mydriasis (pupil dilation)
196
Q

Cataracts:

  • what is it/presentation?
  • risk factors?
A
  • Painless, bilateral opacification of lens; get decreased vision
  • Risk factors:
  • Diabetes (sorbitol)
  • Galactokinase deficiency and Classic Galactosemia
  • trauma, infection, age, smoking, alcohol, sunlight…
197
Q

innervation of extraocular muscles:

A

SO4 LR6 R3

  • CN IV = Trochlear nerve –> innervates Superior Oblique m.
  • CN VI = Abducens nerve –> innervates Lateral Rectus m.
  • CN III = Oculomotor nerve –> innervates all the other muscles!
198
Q

Vertical diplopia - eye drifts upward (like when reading newspaper, going down stairs) –> cause?

A

CN IV (Trochlear N) damage

199
Q

Medially-directed eye: cause?

A

CN VI (Abducens n) damage

200
Q

eye looks down and out, ptosis, pupillary dilation, loss of accomodation: cause?

A

CN III (oculomotor nerve) damage

201
Q

Cause of Right Anopia (visual defect in right eye)?

A

Injury to right optic nerve

202
Q

Cause of bitemporal hemianopia (visual defect in both eyes when looking laterally/toward temples)?

A

injury to optic chiasm

203
Q

Cause of left homonymous hemianopia (can’t look to left with either eye)?

A

–>lesion to right optic tract

204
Q

Cause of Left upper quadrant anopia (can’t see upper left/lateral)?

A

Right temporal lesion, MCA

205
Q

Cause of left lower quadrant anopia (can’t see lower left/lateral)?

A

Right parietal lesion, MCA

206
Q

Cause of Left hemianopia with macular sparing (can’t see left side of either eye, but CAN see through center of eye)?

A

PCA lesion

207
Q

Only can’t see out center of eye?

A

Macular degeneration = Central scotoma

208
Q

MLF syndrome = Internuclear Ophthalmoplegia:

  • Presentation?
  • Associated with what disease?
A
  • Presentation:
  • when look straight ahead, both eyes look straight ahead
  • Right MLF lesion: when try to look to left: left eye moves, but right eye continuous to look straight, cannot adduct (or visa versa). Left eye (which moved), has nystagmus when looking to left

*Seen in MS

209
Q

Genes associated with:

  • early onset Alzheimers?
  • late onset Alzheimers?
  • Protective against Alzheimers?
A
  • Early Onset:
  • APP (chrom 21–>why down’s pts have increased risk of AD)
  • Presenilin-1
  • Presenilin-2
  • Late-onset: ApoE4
  • Protective: ApoE2
210
Q

Senile plaques

A

Beta-amyloid cortical deposits; seen in Alzheimer’s

211
Q

Neurofibrillary tangles:

A

cortical, intracellular, abnormally phosphorylated tau protein
–>seen in Alzheimer’s

212
Q

Aphasia + Dementia + Personality changes:

A
  • ->Pick’s disease = Frontotemporal dementia

- have Pick bodies = intracellular, aggregated tau protein

213
Q

alpha-synuclein defect

A

Lewy body dementia

214
Q

Parkinsonian symptoms + dementia + visual hallucinations?

A

Lewy body dementia

215
Q

Rapidly progressive dementia with myoclonus (brief, involuntary twitching of muscles):

A

Creutzfeldt-Jakob disease (CJD)

216
Q

Diagnostic findings in MS:

A
  • increased IgG protein in CSF
  • oliclonal bands (from Igs) = diagnostic
  • MRI = gold-standard
  • Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis)
217
Q

Charcot’s triad of symptoms in MS (not really a triad…):

A

“SIIIN”

  • Scanning speech
  • Incontinence
  • Intention tremor (make zig-zag line when reach for things)
  • Internuclear Ophthalmoplegia = MLF syndrome
  • Nystagmus
218
Q

CSF findings in Guillain-Barre syndrome:

A
  • increased protein
  • normal cell count

*get papilledema d/t increased protein

219
Q

Cause of Guillan-Barre (after an infection)?

A

–>autoimmune attack of peripheral myeline d/t molecular mimicry

220
Q

Treatment/Therapy for Guillan-Barre?

A
  • Respiratory support = must until recovery (b/c have ascending demyelination, so want to prevent weakening of diaphragm, respi failure!)
  • Plasmpharesis
  • IV Ig’s
221
Q

PML = Progressive Multifocal Leukoencephalopathy:

A
  • associated with JC virus; seen in AIDS pts
  • demyelination of CNS d/t destruction of oligodendrocytes (similar to MS)
  • ->rapidly progressive; usually fatal
222
Q

Charcot-Marie-Tooth Disease

A

Group of progressive hereditary nerve disorders; has to do with defective production of proteins involved in structure and function of peripheral nerves and myelin sheath–> so lack of myelination

223
Q

In which part of brain do partial seizures usually originate?

A

Temporal lobe

224
Q

Acute and Prophylactic treatment for migraines:

A
  • Acute –> Triptans (serotonin agonists)

* Prophylactic –> Propranolol and NSAIDs

225
Q

Bilateral headache; steady pain for >30 minutes; not effected by light, noise; no aura

A

Tension headache (like a band around head)

226
Q

Unilateral headache; brief, repetitive headaches; periorbital pain, ipsilateral lacrimation, rhinorrhea, Horner’s syndrome:

A

Cluster headache

227
Q

Treatment for cluster headaches:

A

Oxygen = 1st line treatment

–>can also treat with triptans (serotonin agonists)

228
Q

Meniere’s disease:

A

Peripheral Vertigo + Tinnitus + Hearing loss

229
Q

port-wine stains, seizures, early-onset glaucoma, hemiparesis, mental retardation:

A

Sturge-Weber syndrome (a congenital vasculitis)

230
Q

Possible presentations of Tuberous Sclerosis: “HEMARTOMAS”

A
  • Hemartomas in CNS and skin (benign growths, resemble tissue of origin)
  • Adenoma sebaceum (cutaneous angiofibromas–> looks like a whole bunch of bad acne on face; kind of malar area)
  • Mitral regurgitation
  • Ash-leaf spots
  • cardiac Rhabdomyoma (primary cardiac tumor, usually seen in children)
  • Tuberous sclerosis
  • autOsomal dominant
  • Mental retardation
  • renal Angiomyolipoma (benign kidney tumor)
  • Seizures
231
Q

Cardiac Rhabdomyoma

A

most common primary cardiac tumor in children; associated with tuberous sclerosis

232
Q

Renal Angiomyolipomas

A

Benign tumors in kidney; highly associated with Tuberous Sclerosis

233
Q

cafe au lait vs ash leaf spots:

A

-cafe au lait –> NF1; darker skin pigmentation

ash leaf spots–> tuberous sclerosis; lighter; depigmented

234
Q

Presentations of Neurofibromatosis type 1:

A
  • ->autosomal dominant
  • Cafe-au-lait spots
  • Lisch nodules (pigmented iris hamartomas)
  • Pheochromocytoma
  • optic gliomas (tumor of optic nerve; may cause vision loss)
  • neurofibromas in skin
235
Q

Presentations of von Hippel-Lindau disease:

A
  • Bilateral renal cell carcinoma
  • pheochromocytomas
  • hemangioblastomas (tumors) in retina, brain stem, cerebellum
  • autosomal dominant
236
Q

Bitemporal Hemianopsia from brain tumor in adult? child?

A
  • Adult –> pituitary adenoma/prolactinoma
  • Kid –> Craniopharyngioma (benign)

***both may arise from Rathke’s pouch

237
Q

GFAP positive brain tumors:

A
  • Glioblastoma multiforme (adults)
  • Pilocytic astrocytoma (kids)

–>both are astrocyte tumors

238
Q

Brain tumor with psammoma bodies and spindle cells concentrically arranged in a whorled pattern:

A

Meningioma (adult brain tumor)

239
Q

Adult brain tumor that is S-100 positive?

A

Schwannoma (ie an acoustic schwannoma)

240
Q

List the 4 most common Adult brain tumors:

A

“MGM Studios”

  • Metastasis
  • Glioblastoma
  • Meningioma
  • Schwannoma

*also: Oligodendroglioma, Pituitary adenoma

241
Q

slow-growing adult primary brain tumor with “fried egg” cells and chicken-wire capillary pattern.

A

Oligodendroglioma

242
Q

Glioblastoma multioforme

A
  • most common primary adult brain tumor
  • astrocyte origin –> GFAP positive
  • bad prognosis
  • found in cerebral hemispheres; may cross the corpus callosum
243
Q

Meningioma:

A
  • 2nd most common primary adult brain tumor
  • psammoma bodies and spindle cells arranged in a whorled pattern
  • arises from arachnoid cells external to brain (like cells from arachnoid granulations)
  • resectable!
244
Q

Psammoma bodies - DD? (various, not just neuro)

A
  • PSaMMoma:
  • Papillary thyroid cancer
  • Serous carcinoma of ovaries
  • Meningiomas
  • Malignant mesothelioma

***psammoma bodies look kind of like a rose! or rings on a tree!

245
Q

Schwannoma:

A
  • 3rd most common adult primary brain tumor
  • S-100 positive
  • Schwann cell origin
  • Resectable
  • often acoustic schwannoma (localized to CN VIII) in cerebellopontine angle
  • ->bilateral schwannomas are associated with NF2
246
Q

Oligodendroglioma:

A
  • Rare, slow growing adult primary brain tumor
  • “fried egg” cells and chicken-wire capillary pattern on microscopy
  • originate from oligodendrocytes
247
Q

Pituitary adenoma

A
  • usually prolactinoma
  • have bilateral hemianopsia (from compressing the optic chiasm)
  • symptoms of hyper- an hypo-pituitarism
  • ->amenorrhea, hypogonadism, galactorrhea….
248
Q

Homer-Wright Pseduorosettes:

A
  • found in 2 childhood tumors:
  • Medulloblastoma (primary brain tumor)
  • Neuroblastoma (adrenal tumor; like a pheochromocytoma, but in kids)
249
Q

2 primary brain tumors that may cause hydrocephalus in kids:

A
  • Medulloblastoma –> may compress 4th ventricle, causing hydrocephalus
  • Ependymoma –> most commonly found in 4th ventricle, causing hydrocephalus
250
Q

Primary brain tumor with Rosenthal fibers = eosinophilic, corkscrew fibers

A

Pilocytic astrocytoma (benign, good prognosis)

251
Q

Highly malignant childhood cerebellar tumor:

A
  • ->Medulloblastoma
  • may compress 4th ventricle–>hydrocephalus
  • Homer-wright pseudorosettes
  • small blue cells
  • gait instability and limb ataxia, b/c it’s cerebellar
  • a PNET = primitive neuroectodermal tumor
252
Q

Perivascular pseudorosettes, hydrocephalus, tumor within 4th ventricle:

A

Ependymoma

253
Q

Hemangioblastoma:

A

childhood primary brain tumor

  • ->associated with von-Hippel Lindau syndrome (get retinal angiomas)
  • may also have increased production of EPO (perhaps secondary to VHL syndrome)–> polycythemia
254
Q

Craniopharyngioma

A
  • benign childhood tumor; derived from remnants of Rathke pouch
  • can cause bilateral hemianopsia, and thus look like a pituitary adenoma
255
Q

Medulloblastoma:

A
  • childhood primary brain tumor
  • really malignant, cerebellar tumor (so may have cerebellar defects–>ataxia, gait instability…)
  • may compress 4th ventricle, causing hydrocephalus
256
Q

Ring-enhancing lesion - DD:

A
  • Abscesses
  • Toxoplasma
  • Metastases (from lung > breast > melanoma > kidney > GI)
  • primary CNS lymphoma (from AIDS, EBV)
257
Q

5 classes of medications that can be used to treat glaucoma:

A
  • alpha-agonists (epinephrine, brimonidine)
  • beta-blockers (timolol, betaxolol, carteolol)

-diuretics (Acetazolamide for long-term;
Mannitol for acute/emergency cases)

  • Cholinergic agonists (direct–>pilocarpine, carbachol; indirect–>physostigmine, echothiphate)
  • Prostaglandins (Latanoprost –>PGF-2-alpha)
258
Q

Of the glaucoma drugs, which should NOT be used in closed-angle glaucoma?

A

–>Epinephrine

259
Q

Dextromethorphan

A

=DXM, DM (in robitussin, nyquil, etc)

  • opiod analgesic
  • used for cough suppression
260
Q

Loperamide

A

opioid analgesic; used to treat diarrhea

261
Q

Diphenoxylate

A

opioid analgesic; used to treat diarrhea

262
Q

drug given to opioid addicts in maintenance programs?

A

–>methadone

263
Q

Naloxone or Naltrexone

A
  • ->opioid receptor antagonists

- treat opioid toxicity

264
Q

Fentanyl

A

opioid analgesic

265
Q

Mechanism of Opioid analgesic drugs

A

*Opioid anelgesics: Morphine, Codeine, Fentanyl, Diphenoxylate, Dextromethorphan, heroin, methadone, meperidine

  • Mechanim:
  • ->act as agonists at opiod receptors (mu, delta, kappa), modulating synaptic transmission: open K+ channels, close Ca2+ channels –> decrease synaptic transmission
  • ->inhibit release of ACh, NE, Serotonin, Glutamate, substance P (normally causes pain, so decreased substance P–>decreased pain)
266
Q

Codeine

A

opioid analgesic

267
Q

morphine

A

opioid analgesic

268
Q

meperidine

A

opioid analgesic

269
Q

heroin

A

opioid analgesic

270
Q

Main toxicities of opiods?

  • ->what are 2 opioid toxicities that one does NOT develop tolerance to?
  • ->treatment for opioid toxicity?
A
  • Main toxicities:
  • Respiratory depression
  • Addiction
  • Constipation
  • Miosis = pinpoint pupils
  • CNS depression is additive with other drugs
  • Don’t develop tolerance to: Miosis and Constipation
  • Treat toxicity with: Naloxone or Naltrexone (opioid receptor antagonists)
271
Q

Tramadol

A
  • ->weak opioid agonist; inhibits serotonin and NE reuptake, too (works on many NTs–> “tram-it-all in!”
  • used to treat chronic pain

***decreases seizure threshold!

272
Q

Butorphanol

A

partial agonist at opioid mu receptors; full agonist at opioid kappa receptors

-used to treat pain; causes less respiratory distress than full opioid agonists

273
Q

3 1st line treatments for tonic-clonic seizures?

A

–>Valproic Acid, Phenytoin, Carbamezapine

274
Q

1st line for prophylaxis against status epilepticus?

275
Q

1st line treatment for partial seizures (simple and complex)?

A

Carbamezapine

276
Q

1st line treatment for absent seizures?

A

Ethosuximide

277
Q

1st line treatment for acute status epilepticus?

A

–>Benzos! (Diazepam or Lorazepam)

278
Q

1st line treatment for trigeminal neuralgia?

A

Carbamezapine

279
Q

1st line treatment of seizures in pregnant women and children?

A

Phenobarbital

280
Q

Epilepsy drug that can be used for seizures of Eclampsia? What is 1st line in treating seizures of eclampsia?

A
  • ->can treat eclampsia seizures with Benzodiazepines (Diazepam or Lorazepam)
  • 1st line treatment for eclampsia seizures is MgSO4, though
281
Q

phenytoin and carbamezapine mechanism?

A

Inactivate Na-channels

282
Q

Gabapentin mechanism?

A

–>GABA analog; but, main mechanism = inhibits Ca channels

283
Q

Phenobarbital mechanism?

A

–>stimulates GABA

284
Q

Valproic acid mechanism?

A

inactivates Na channels, and increases GABA concentration

285
Q

Ethosuximide mechanism?

A

blocks Calcium channels

286
Q

Tigabine

A 
epilepsy drug (for partial seizures)
-->inhibits GABA reuptake
287
Q

Vigabatrin

A 
epilepsy drug (for partial seizures)
-->increases amount of GABA
288
Q

Levetiracetam

A 
epilepsy drug (for partial seizures and tonic clonic seizures)
-->unknown mechanism; may increase GABA...
289
Q

anti-epileptic drugs that may lead to Steven-Johnson syndrome?

Presentation of SJS?

Drugs (all categories) that causes SJS?

A
  • Ethosuxamide, Phenytoin, Lamotrigine, Carbamezapine, Phenobarbital
  • first malaise and fever, then rapid onset of erythematous/purpuric macules (oral, ocular, genital)… eventually skin lesions become necrotic and slough
  • **SJS from
  • cillins
  • sulfas
  • seizures
290
Q

3 anti-epileptic drugs that are contraindicated in pregnancy:

A
  • Phenytoin–>can lead to fetal hydantoin syndrome
  • Valproic acid
  • Carbamezapine

***both valproic acid and carbamezapine decrease folate absorption, similarly to folate-antagonists. So, if use during pregnancy, must increase folate supplementation.

291
Q

Which anti-epileptic drugs are Cytochrome P-450 Inducers?

A
  • phenobarbital
  • phenytoin
  • carbamezapine
292
Q

Infant with IUGR, microcephaly, dysmorphic craniofacial features, mental retardation, hypoplastic nails and distal phalanges, cardiac defects: Which anti-epileptic was mother taking during pregnancy?

293
Q

Infant with neural tube defects: which anti-epileptic taken during pregnancy can cause this?

A

Valproic Acid

Carbamezapine

294
Q

Agranulocytosis and Aplastic Anemia: Caused by which anti-epileptic?

A

Carbamezapine

295
Q

Carbamezapine side effects:

A
  • cytochrome P-450 inducer
  • liver toxicity
  • agranulocytosis
  • aplastic anemia
  • teratogenic (neural tube defects, b/c decreases folate absorption)
  • SIADH
  • diplopia
  • ataxia
296
Q

Which anti-epileptic drug may cause SIADH?

A

Carbamezapine

297
Q

Which anti-epileptic drug may cause drug-induced lupus?

298
Q

Phenytoin side effects:

A
  • Megaloblastic anemia
  • Teratogenic (fetal hydantoin syndrome)
  • cytochrome P-450 inducer
  • hirsutism
  • drug-induced lupus
  • gingivial hyperplasia
299
Q

Gingivial hyperplasia is a side effect of which anti-epileptic drug?

300
Q

Thiopental

A

babiturate

-can be used to induce anesthesia

301
Q

Why can phenobarbital be used to treat Crigler-Najjar syndrome?

A

Phenobarbital increases liver enzyme synthesis, so can get increased synthesis of UDP-glucorynl transferase, and thus convert more indirect bilirubin to direct in the liver

(barbiturates are cytochrome P-450 inducers…not sure if that has anything to do with it, but I imagine it does…)

302
Q

Short-acting benzos:

A

“TOM”

  • Triazolam
  • Oxazepam
  • Midazolam

–>short-acting benzos have highest addictive potential

303
Q

Chlordiazepoxide

304
Q

Which 2 benzos can be used to treat status epilepticus?

A
  • Lorazepam

- Diazepam

305
Q

Treat benzo overdose with? mechanism?

A

Flumazenil

–>competitive antagonist at GABA benzo receptor

306
Q

Zolpidem:

mechanism?

A

=Ambien

  • ->also acts on GABA and enhances inhibitor properties of GABA
  • ->metabolized by cytochrome P-450, so short duration
  • ->less tolerance, addiction, withdrawal symptoms than benzos
307
Q

Zaleplon

A

non-benzo hypnotic (for insomnia); similar to zolpidem

308
Q

Eszopiclone

A

non-benzo hypnotic (for insomnia); similar to zolpidem

309
Q

MAC (Minimal Alveolar Concentration): how is it related to potency?

A

Lower MAC–> Higher potency
(potency = 1/MAC)

*Low MAC = high potency = high lipid solubility = Low Km

  • ->has to do with anesthetics…
  • ->varies with age!
  • ->it’s literally a measurement at which 50% of the population is anesthetized.
310
Q

Solubility of a drug in blood vs lipids: How is it related to potency? induction time?

A
  • Drugs that have low solubility in blood–> rapidly induced and rapid recovery times
  • Drugs that have high solubility in lipids –> increased potency

***So, a drug that has low blood and low lipid solubility: fast induction, low potency (ie Nitrous oxide)

***Drug that has high blood and lipid solubility: slow induction, high potency (ie Halothane)

311
Q

Potency and induction times of a drug with: low blood and lipid solubility?

A

–>example = Nitrous Oxide

Fast induction, low potency

312
Q

Potency and induction of a drug with high blood and lipid solubility?

A

–>example = Halothane

Slow induction, high potency

313
Q

Inhaled anesthetic that can cause hepatotoxicity?

A

–>Halothane

FirstAID (24 decks)

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