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Neuro Flashcards

1
Q

Age-related macular degeneration types and therapies

A

Dry = sub retinal drusen deposits or pigment changes. Wet = abnormal blood vessels w/ sub retinal fluid/hemorrhage, gray subretinal membrane, or neovascularization (acute over days to weeks). Tx of acute = anti-VEGF inhibitors (prevent neovascular membrane formation), laser, photo

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2
Q

1st line drug for partial seizures

A

Carbamazepine; regardless of simple or complex

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3
Q

1st line drug for tonic-clonic sz

A

Phenytoin, carbamazepine, valproate

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4
Q

1st line drug for myoclonic sz

A

Valproic acid

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5
Q

1st line drug for absence sz

A

Ethosuximide, blocks T-type Ca2+ channels that trigger and sustain pulsed discharges in thalamic neurons. (2nd = valproate)

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6
Q

Gene defect in Friedreich’s ataxia?

A

Frataxin gene - mitochondrial protein for respiratory f(x) and Fe homeo. GAA repeat.

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7
Q

Drug after SAH to prevent vascular spasm?

A

Nimodipine

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8
Q

Viral CSF pattern?

A

Lymphocytic pleocytosis, normal glucose, elevated protein.

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9
Q

Bacterial CSF pattern?

A

Neutrophilic predominance, low glucose, high protein.

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10
Q

Early-onset familial Alzheimer’s associated w/ what mutations?

A

APP (21- Down’s!), presenilin 1 (14), and presenilin 2 (1). Apo E4 w/ late.

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11
Q

Path associated with lacunar infarcts?

A

Small vessel lipohyalinosis and atherosclerosis ->fluid-filled cavities

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12
Q

Alzheimer’s path

A

Decreased ACh lvl (deficient choline acetyltransferase) found in basal nucleus. Hippocampus. Neurofibrillary tangles, senile plaques, amyloid angiopathy.

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13
Q

Myasthenia gravis

A

Circulating Ab’s against post-synaptic Ach receptors -> complement-mediated destruction -> weakness (late in day). Associated with thymoma or thymic hyperplasia.

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14
Q

Two types of dopamine agonists

A

Ergot compounds (bromocriptine and pergolide) and nonergot compounds (pramipexole and ropinirole).

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15
Q

Phenytoin mech

A

Blocks Na+ channels and prolongs their rate of recovery. Inhibits high-frequency firing. Tonic-clonic and status.

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16
Q

Triptan mechanism

A

Serotonin 5-HT1b/5-HT1d AGONISTS that counter release of vasoactive peptides

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17
Q

Migraine mech

A

Pain due to activation of trigeminal afferents that innervate meninges -> release of vasoactive neuropeptides (substance P and calcitonin gene-related peptide) -> neurogenic inflammation due to vasodilation and plasma protein extravasation. Neuronal sensitization

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18
Q

How does ketamine block morphine tolerance?

A

NMDA receptor antagonist to block actions of glutamate.

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19
Q

Subfalcine herniation

A

Cingulate gyrus herniates under falx cerebri –> ACA compression

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20
Q

Uncal herniation

A

Ipsi oculomotor, ipsi PCA -> contralateral homonymous hemianopsia w/ macular sparing, compression of contra cerebral peduncle -> ipsilateral hemipareses. brainstem hemorrhages

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21
Q

Dmg to putamen vs. globus pallidus

A

Putamen initiates movt so lesions –> tremor, bradykinesia, and rigidity. GP external dmg = less movt. Internal dmg = excessive motion/movt. Think of damage to globus as the normal pathways through them b/c they are inhibited in their pathways.

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22
Q

Nucleus ceruleus?

A

NE-secreting neurons for flight or fight. Dorsal pons.

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23
Q

Raphe nuclei?

A

Serotonergic neurons. Sleep-wake, lvl of arousal. Lesion -> insomnia and depression. Sir Raphe the sleepy.

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24
Q

Nucleus basalis of Meynert?

A

Cholingergic cells. Decreased amounts in Alzheimer’s disease. Cholling Mr. Meynert?

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25
Q

Red nucleus?

A

In anterior midbrain. Important for motor coordination of upper extremities.

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26
Q

Monocular scotoma?

A

A partial lesion in the retina, optic disk, or optic nerve. etio - macular degeneration and optic neuritis

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27
Q

Homonymous superior quadrantanopia?

A

Lesion or stroke involving temporal lobe (Meyer’s loop)

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28
Q

Homonymous inferior quadrantanopia

A

Lesion or stroke involving PARIETAL lobe (DORSAL optic radiation)

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29
Q

Korsakaoff syndrome damages what particular nuclei?

A

Anterior and dorsomedial thalamic nuclei -> confabulation. Anterograde amnesia (usu. permanent).

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30
Q

Role of the notochord?

A

Induces overlying ectoderm to form the neural plate, which gives rise to the neural tube and neural crest cells (dy 18). Notochord becomes the nucleus puposus of the intervertebral discs.

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31
Q

Forebrain structures

A

Forebrain = prosencephalon = telencephalon + diencephalon = cerebral hemispheres + lateral ventricles + thalamus + third ventricle

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32
Q

Midbrain structures

A

Mesencephalon = midbrain + aqueduct

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33
Q

Hindbrain structures

A

Rhombencephalon = Metencephalon + myeloncephalon = (Pons + Cerebellum + Upper part of 4th ventricle) + (Medulla + lower part of 4th ventricle)

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34
Q

Neuroectoderm gives rise to?

A

CNS neurons, ependymal cells, oligodendroglia, astrocytes

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35
Q

Neural crest cells give rise

A

PNS neurons and Schwann cells. Neural crest is PNS-only!

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36
Q

Mesoderm gives rise

A

Microglia (resident macrophages of the CNS). MESO for MICRO.

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37
Q

Neuropore failing to fuse when? Connects what structures?

A

Wk 4. Pore is FOUR. Connects spinal canal with amniotic cavity. increased alpha-fetoprotein in fluid and serum. Increased AChE in amniotic fluid is confirmatory

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38
Q

Spina bifida occulta vs. meningocele vs. meningomyelocele?

A

Spina bifidia = failure of bony canal to close but NO herniation and intact dura. Associated w/ tuft of hair or skin dimple (lower vertebrae). Meningocele has meningial herniation (normal AFP) whereas meningomyelocele has both meninges and spinal cord herniation.

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39
Q

Anencephaly vs. holoprosencephaly

A

No forebrain and open calvarium vs. failure of hemispheres to separate. Anecephaly findings include increased AFP, polyhdramnios (b/c don’t swallow). Associated with DMT1. Holoprosencephaly has complex multifactorial etio. Mod. form has cleft lip/palate while severe form -> cyclopia

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40
Q

Chiari II vs. Dandy-Walker

A

Significant herniation of cerebellar tonsils and versus w/ aqueductal stenosis and hydrocephalus. Often w/ myelomeningocele. Dandy is AGENESIS of vermis with cystic enlargement of 4th ventricle. Hydrocephalus and spin bifida.

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41
Q

Syringomyelia

A

Cape-like b/l loss of pain and temperature but OK fine touch. Most common at C8-T1. Associated with Chiari I (>3-5 mm tonsillar octopi and asymptomatic till older).

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42
Q

Tongue development overview

A

Anterior 2/3 with 1st and 2nd branchial arches (Sensation V3 and taste VII). Posterior 1/3 from 3-4th branchial arches (sensation and taste IX, X in back). XII is muscle.

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43
Q

Nissl substance located where?

A

Dendrites and cell body. NOT axon.

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44
Q

Astrocyte vs. Microglia

A

Support cell with reactive gliosis derived from NEUROECTODERM VS CNS phagocytes from MESODERM.

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45
Q

Pain and temperature sensory?

A

Free nerve endings found in skin, epidermis, and some viscera. C nerves are slow, unmyelinated. Adelta are fast myelinated.

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46
Q

Meissner corpuscle

A

Dynamic, fine touch, propioception. Glabrous (hairless skin). Large, myelinated, adapt quickly. “A fine hairless adaptable miss.”

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47
Q

Pacinian corpuscle

A

Vibration and pressure. Deep skin, ligaments, joints. Large, myelinated, adapt quickly. “Deeply packed and pressurized Pacinian corpuscle.”

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48
Q

Merkel discs

A

Pressure, deep static touch, propio. Basal epidermal layer, hair follicles. Large, myelinated fibers, adapt slowly.

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49
Q

Name the three parts of peripheral nerve?

A

Endoneurium, Perineurium, Epineurium

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50
Q

Endoneurium

A

SINGLE nerve fiber layer. Infiltrate in Guillan Barre.

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51
Q

Perineurium

A

Surrounds fascicle of nerve fibers. Permability barrier. Rejoined by microsurgery for limb reattachment.

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52
Q

Epineurium

A

Dense CT surrounding entire nerve.

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53
Q

NE change in disease? and location of synthesis?

A

Increased in anxiety and decreased in depression. Locus ceruleus (pons)

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54
Q

DA change in disease? and location of synthesis?

A

Inc. in HD. Dec. in Parkinson’s and depression. Ventral tegmentum and SNc (midbrain)

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55
Q

5-HT change in disease? and location of synthesis?

A

Inc. in Parkinsons. Dec. in depression and anxiety. Raphe nucleus (pons, medulla, midbrain)

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56
Q

ACh change in disease? and location of synthesis?

A

Inc. in Parkinsons. Dec. in Alzheimers and HD. Basal nucleus of Meynert. “Need A/C during Mey?”

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57
Q

GABA change in disease? and location of synthesis?

A

Decreased in HD and anxiety. Nucleus accumbens.

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58
Q

Three major structures for BBB?

A

Tight junctions between NONfenestrated capillary endothelial cells, BM, astrocyte foot processes.

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59
Q

Carrier-mediated transport for BBB?

A

Glucose and amino acids.

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60
Q

Major areas of the hypothalamus

A

Lateral area, ventromedial area, anterior, posterior, suprachiasmatic, OVLT, area postrema, supraoptic nucleus (makes ADH), paraventricular nucleus

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61
Q

Lateral area of hypothalamus?

A

Hunger. Inhibited by LEPTIN = appetite suppressant. Lesion = anorexia/FTT. HUNGRY for LATE’s.

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62
Q

Ventromedial area of hypothalamus?

A

Satiety. Stimulated by leptin. Destruction (e.g. craniopharyngioma -> hyperphagia).

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63
Q

Anterior area of hypothalamus?

A

Cooling and parasympathetics. A for A/C.

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64
Q

Posterior hypothalamus?

A

Heating, sympathetic.

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65
Q

Suprachiastmatic nucleus

A

Circadian rhythm. Need to sleep to be charismatic.

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66
Q

OVLT

A

Organum vasuclosum of the laminal terminals senses changes in osmolarity. NOT protected by BBB.

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67
Q

Area postrema

A

Responds to emetics. NOT protected by BBB. (Toxin sensor). Located on dorsal surface of medulla at caudal end of 4th ventricle

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68
Q

What makes oxytocin and ADH?

A

Paraaventricular = oxytocin. Supraoptic = ADH. “A DH needs super good eyes!” “Vent the room after using Oxy-clean.”

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69
Q

Melatonin production?

A

From pineal gland stimulated by NE made from the suprachiasmatic nucleus.

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70
Q

EEG waveforms phrase

A

BATS Drink Blood.

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71
Q

Theta waves

A

Non-REM 1. Light sleep

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72
Q

Alpha waves

A

Awake with eyes-closed. Alpha: First things first, close your eyes.

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73
Q

Beta waves

A

Awake and alert AND REM sleep (loss of motor tone, dec. oxygen use, variable pulse and pressure, dreaming, tumescence, memory?)

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74
Q

Delta waves

A

Delta = Deepest non-REM sleep (Slow-wave with HIGH amplitude) Stage N3 where night errors, sleepwalking, and bedwetting occur.

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75
Q

Sleep spindles and K complexes?

A

N2 (45% of sleep). N2 is when bruxism occurs.

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76
Q

Neuro vs. adenohypophysis?

A

Neurohypophysis = POSTERIOR. Neuro for ADH and oxytoxcin

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77
Q

Five nuclei of the thalamus

A

VPL, VPM, LGN, MGN, and VL

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78
Q

VPL

A

Ventral posterolateral nucleus - spinothalamic, dorsal column; pain and temperature, pressure, touch, vibration, propioception; headed toward primary somatosensory cortex. P for posterior column (dorsal) and L for anteroLateral system.

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79
Q

VPM

A

Ventral posteromedial nucleus - trigeminal and gustatory pathway; face sensation and taste; primary somatosensory cortex. “Make-up for the face.”

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80
Q

LGN

A

Relay for LIGHT. CN II, vision headed toward Calcarine sulcus.

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81
Q

MGN

A

M for MUSIC. Superior olive and inferir colliculus of tectum, hearing -> auditory cortex of temporal lobe

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82
Q

Limbic system

A

5 F’s - Feeding, Fleeing (autonomics), Fighting (autonomics), Feeling. Emotion, long-term memory, olfaction, behavior modulation, ANS

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83
Q

Input into the cerebellum?

A

Contralateral cortex via the middle cerebellar peduncle. Ipsilateral propioceptive information via inferior cerebellar peduncle (climbing and mossy fibers)

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84
Q

Cerebellar outputs?

A

Contralateral cortex (Purkinje -> deep nuclei -> contralateral cortex via superior cerebellar peduncle)

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85
Q

Cerebellar deep nuclei?

A

From lateral to medial: Dentate, Emboliform, Globose, Fastigial (DEGF)

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86
Q

Lateral cerebellar vs. medial cerebellar lesions?

A

Lateral lesions -> fall ipsilaterally. Medial lesions -> truncal ataxia, nystagmus, head tilting, b/l motor deficits.

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87
Q

Basal ganglia structures

A

Striatum = putamen and caudate. Lentiform = putamen and globus pallidus.

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88
Q

Excitatory pathway of basal ganglia

A

Cortex stimulates striatum (GABAerg) which inhibits the GPi/SNr to disinhibits the thalamus (VA/VL).

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89
Q

Inhibitory pathway of basal ganglia

A

Cortex stimulates striatum to inhibit the GPe, which disinhibits the sub-thalamic nucleus, which activates the GPi/SNr to inhibit the VA/VL thalamus.

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90
Q

Substantia nigra pars compacta’s role in Parkinson’s

A

Acts via D1 on excitatory pathway to reinforce and acts via D2 on inhibitory pathway to oppose. These neurons degenerate in Parkinson’s

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91
Q

GPe vs. GPi/SNr

A

GPi/SNr tonically inhibits the VA/VL. GPe tonically inhibits the sub-thalamic nucleus (which activates the GPi/SNr). Globus = globally tonically active in inhibiting. Internal segment INHIBITS movt. External = EXTRA and inhibits STN, which normally inhibits GPi)

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92
Q

Chorea vs. athetosis?

A

Sudden jerky movts vs. slow writhing movts (esp. fingers). Both seen in basal ganglia lesions (HD).

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93
Q

Essential vs. resting vs. intention tremor?

A

Action tremor exacerbated by holding posture/limb vs. alleviation by movt (Parkinson’s) vs. poor finger2nose (cerebellar)

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94
Q

General homunculus

A

Medial to lateral = Toes to hand to face to tongue and swallowing

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95
Q

Amygdala lesions

A

B/l - Kluver-Bucy = hyperorality, hypersexuality, disinhibied behavior. Associated with HSV-1

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96
Q

Mammillary body lesion?

A

B/l lesions in Wernicke-Korsakoff syndrome (confusion, opthalmoplegia, ataxia, memory, confab, personality)

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97
Q

STN lesion?

A

STN activates GPi to inhibit movt. So lesion = contralateral hemiballismus.

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98
Q

Hippocampus lesion?

A

B/l lesions lead to anterograde amnesia.

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99
Q

Central pontine myelinolysis

A

Massive axonal demyelination in pontine white matter 2/2 osmotic forces and edema (Na+ from low to high correction). Acute paralysis, dyarthria, dysphagia, dipolopia, LOC. (Pseudobulbar symptoms)

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100
Q

Where do the ICA’s come from?

A

Right one from the brachiocephalic artery. Left one straight from the aortic arch.

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101
Q

Basilar artery into Circle of Willis anatomy?

A

Superior cerebellar arteries come off 1st, THEN the posterior cerebral arteries!

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102
Q

Where do the vertebral arteries come from?

A

Right one from braciocephalic artery (after R ICA). Left one from the subclavian artery.

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103
Q

AICA vs. PICA?

A

PICA’s off the vertebral arteries. AICA’s at junction with basilar artery.

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104
Q

A1 vs. A2 ACA?

A

A1 between MCA and ACom. A2 after Acom.

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105
Q

P1 vs. P2 PCA?

A

P2 after PCom. P1 between Pom and Basilar before Superior cerebellar arteries.

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106
Q

Two numbers to know for cerebral blood flow.

A

PO2 < 50 mmHg —> increased cerebral perfusion pressure. PCO2 > 90 mmHg is LIMIT to increasing cerebral blood flow (via vasodilation) in proportion to PCO2.

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107
Q

Therapeutic hyperventilation?

A

By decreasing PCo2, we decreased cerebral blood flow and therefore intracranial pressure. Used for stroke, trauma.

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108
Q

MCA stroke

A

Contralateral paralysis of upper limb and face. Contralateral loss of sensation in upper and lower limbs, and face. Aphasia if dominant or hemineglect if non-dominant.

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109
Q

ACA stroke

A

Contralateral paralysis and loss of sensation in the LOWER limb. (B/c ACA perfuses in the middle-inside portion of brain.

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110
Q

Common location of lacunar stroke?

A

Internal capsule of the striatum supplied by lenticulotriate artery.

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111
Q

ASA (anterior spinal artery) stroke

A

Complete motor paralysis. Loss of pain and temp b/l. Retained propioception.

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112
Q

PICA stroke

A

Lateral Medullary syndrome - dec. pain and temp from ipsilateral face and contralateral body, dysphagia, hoarseness, dec. gag, ipsilateral Horner, ataxia

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113
Q

AICA stroke

A

Lateral pontine syndrome - vertigo, vomiting, nystagmus, falling over to side, ipsi facial paralysis and loss of sensation

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114
Q

PCA stroke

A

Contralateral hemianopia w/ macular sparing

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115
Q

Basilar artery stroke

A

Locked-in syndrome.

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116
Q

ACom lesion

A

Most commonly from aneurysm. Visual field deficits.

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117
Q

PCom lesion

A

Saccular aneurysm. CN III palsy.

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118
Q

Berry aneurysm

A

Occurs at bifurcations in Circle of Willis. e.g. Acom and ACA. Rupture to SAH. Associated with ADPKD, Ehlers-Danlos, Marfan. Age, HTN, smoking.

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119
Q

Charcot-Bouchard microaneurysm

A

Associated with chronic HTN, affecting small vessels

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120
Q

Crossing hematomas. Epidural vs. subdural?

A

Epidural will cross Falx and tentorium but NOT sutures. Subdural is exact opposite.

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121
Q

Most vulnerable areas of the brain for hypoxia?

A

Hippocampus, neocortex, cerebellum, watershed.

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122
Q

Histologic features of ischemia in brain.

A

NOTHING from 3-6h. Red neurons 12-48 hrs. Necrosis + neutrophils from 24-72h. Macrophages from 3-5 days. Reactive gliosis + vascular proliferation from 1-2 weeks. >2 weeks is a glial scar.

123
Q

TIA definition?

A

Brief, reversible focal neurologic dysfunction lasting <24 hrs with NEG MRI findings of infarction.

124
Q

Superior sagittal sinus vs. inferior saggital sinus

A

Superior on top. Inferior is inside off of the straight sinus as a branch (other being Great cerebral vein of Galen)

125
Q

Phenytoin vs. phenobarbital SE’s?

A

Generalized lymphadenopathy w/ hirsuitsm, coarsened features, gingival hyperplasia vs. acute intermittent porphyria, sedation

126
Q

Neurofibromatosis-1

A

AD (Chromosome 17). Cafe-au-lait. Neurofibromas. Lisch nodules (hamartomas of iris). Pseudoarthrosis.

127
Q

CN’s in medulla

A

CN IX-XII

128
Q

CN’s in Pons

A

CN V-VIII

129
Q

CN’s above the Pons

A

CN I-IV

130
Q

Restless legs syndrome treatment

A

First nonpharm (limit aggravating factors), Fe supplement, Dopamine agonists (pramipexole, ropinirole)

131
Q

Valproic acid pregnancy risk?

A

NEURAL tube defects. 1-3%

132
Q

By what age should a child be able to play cooperatively?

A

Age 4

133
Q

By what age able to copy circle and use utensils?

A

Age 3

134
Q

By what age have friends?

A

Age 5

135
Q

Steps for hearing from TM

A

Stapes to TM -> oval window (amplification) -> fluid displacement of endolymph of scala media -> bending of cilia of hair cells (basilar vs. tectorial membranes) -> inc. OR dec. K+ conductance = dpol. or repol. -> dpol to Ca2+ release of repol to no Ca2 -< release of neurotransmitter or not -> CN VIII; Higher frequency closer to stapes (stiff) while lower frequency at compliant near apex.

136
Q

Purpose of the foramina of Luschka and Magendie?

A

Connect 4th ventricle to the subarachnoid space. Luschka = Lateral. Magendie = Medial.

137
Q

NPH

A

Expansion fo ventricles distorts fibers of the CORONA RADIATA -> urinary incontinence, ataxia, cognitive dysfunction

138
Q

Communicating hydrocephalus

A

Decreased CSF absorption by arachnoid graduation lead to inc. ICP, papilledema, herniation

139
Q

Hydrocephalus ex vacuo

A

Apparent increase of CSF 2/2 atrophy. ICP is normal. (e.g. Alzheimer’s, adv. HIV, Pick)

140
Q

Noncommunicating hydrocephalus

A

Due to a structural blockage within the CSF system

141
Q

How many spinal nerves are there?

A

31 spinal nerves. “Have the spine of a man walking outside on January 31st.”

142
Q

Which nerves exit above their corresponding vertebra?

A

C1-C7.

143
Q

To what vertebrae does the spinal cord extend to? And where do you do a LP?

A

Lower border of L1-L2. LP usu. between L3-L4 or L4-L5. Subarachnoid space down to S2.

144
Q

Dorsal column body organization

A

Fasciculus gracilis (lower body and legs) are inside. Fasciculus ceunatus (upper body, and arms)

145
Q

Anterolateral system body organization

A

Lateral spinothalamic tract. Sacral outside to cervical inside.

146
Q

Corticospinal tract body organization

A

Sacral lateral. Cervical medial.

147
Q

Anterolateral system pathway

A

Free nerve endings synapse in ipsilateral gray matter and decussates within 2-3 levels in anterior white commisure, ascending CONTRlaterally, synapsing at VPL -> sensory cortex

148
Q

Dorsal column pathway

A

Fine touch, vibration, pressure, propioception enter spinal cord and ascend ipsilaterally until it synapses at the nucleus cuneatus (lateral) or gracilis (medial) -> decussates at the MEDULLA and ascends contralaterally up the medial lemniscus -> synapses at VPL -> sensory cortex

149
Q

Spastic paralysis vs. flaccid paralysis

A

UMN vs. LMN signs

150
Q

ALS

A

Combined UMN and LMN w/ NO sensory, cognitive, or oucular motor deficits. Some etio = defective superoxide dismutase I. Riluozole tx modest (dec. presynaptic glutamate release).

151
Q

Tabes dorsalis

A

Tertiary syphilis -> demyelination of dorsal columns and roots -> impaired sensation, propioception, coordination. Charcot joints, Argyll Robertson pupils (small pupils that accommodate but do not react to light). Absent DTRs and POS romberg

152
Q

Syringomyelia

A

Syrinx damages anterior white commisure -> b/l loss of pain and temperature

153
Q

Poliomyelitis

A

Poliovirus (oropharynx and SI replication before spreading hematogenously to CNS). Destruction of anterior horn cells -> LMN death. Weakness, hypotonia, flaccid paralysis, fasciculations. CSF shows inc. WBCS and slight increased protein w/ NO CSF glucose change.

154
Q

Spinal muscular atrophy (Werdnig-Hoffmann disease)

A

Congenital degeneration of anterior horn cells. AR.

155
Q

Friedreich ataxia

A

AR GAA on Chromosome 9 (frataxin) -> mt dysf(x). Muscle weakness and loss of DTRs. Staggering, frequent falls,nystagmus, pes caves, hypertrophic cardiomyopathy

156
Q

Brown-Sequard syndrome

A

Hemisection. Ipsilateral UMN signs (corticospinal). Ipsilateral dorsal column. Contralateral anterolateral. (pain and temperature). At the level of lesion, loss of all sensation. Above T1, could have Horner’s syndrome

157
Q

Horner syndrome and its pathway.

A

Ptosis (superior tarsal m.), Anhidrosis and flushin, Miosis. Hypothalamus to synapse in lateral horn of intermediolateral column of spinal cord (T1) -> superior cervical (sympathetic) ganglion (which is near bifurcate of common carotid) synapse -> sweat glands of face, opthalmic division of trigeminal nerve for pupillary dilator, sweat glands of forehead + smooth muscle of eyelid

158
Q

C2 vs. C3

A

Posterior part of skull cap vs. high turtleneck

159
Q

Spinal cord lvls that would affect erection

A

S2,3,4

160
Q

Biceps reflex

A

C5,6

161
Q

Triceps reflex

A

C7,8

162
Q

Patellar reflex

A

L3,4

163
Q

Achilles reflex

A

S1,2

164
Q

Cremaster reflex

A

L1,L2

165
Q

Anal wink reflex

A

S3,S4

166
Q

When are primitive reflexes exhibited?

A

Before age 1. Or “frontal release” (adult with frontal lobe lesions)

167
Q

Galant reflex

A

Stroking one side of spine while ventral suspension causes lateral flexion of lower body toward stimulated side

168
Q

Parinaud syndrome

A

Paralysis of conjugate VERTICAL gaze 2/2 lesion in superior colliculi (e.g. pinealoma)

169
Q

Inferior colliculi

A

auditory

170
Q

What are the cranial nerves that have both sensory and motor nerves?

A

CN V, VII, IX, X. “Some say marry money, but my brother says big brains matter most.”

171
Q

Midbrain vs. Pons vs. Medulla CN nuclei

A

Midbrain = CN III, IV. Pons = V, VI, VII, VIII. Medulla = IX, X, XII. Pons 5-8. Generally, lateral nuclei are sensory while medial nuclei are motor.

172
Q

Corneal reflex?

A

Afferent V1, efferent VII (orbicularis oculi)

173
Q

Lacrimation reflex

A

Afferent V1, efferent VII.

174
Q

Jaw jerk reflex

A

Afferent V3 (masster spindle), efferent V3 (masseter)

175
Q

The vagal nuclei

A

Nucleus solitarius, nucleus ambiguus, dorsal motor nucleus

176
Q

Nucleus solitarius

A

S for Sensory. Visceral sensory (taste, baro, gut distenstion. CN VII, IX, X.

177
Q

Nucleus ambiguus

A

M for MOTOR - pharynx, larynx, upper esophagus. IX, X, XI.

178
Q

Dorsal motor nucleus

A

Parasympathetics of heart, lungs, upper GI. CN X

179
Q

Parotid, submandibular, and sublingual gland innervation?

A

Parotid = CN IX. Other two are CN VII.

180
Q

Superior orbital fissure

A

CN III, IV, V1, VI, opthalmic vein, sympathetic fibers. Standing room only, but the spinster is meningeal.

181
Q

Foramen rotundum

A

CN V2 = Standing room only, but the spinster is meningeal.

182
Q

Foramen ovale

A

V3. CN V = Standing Room Only, but the spinster is meningeal.

183
Q

Foramen spinosum

A

Middle meningeal artery

184
Q

Internal auditory meatus

A

CN VII, VIII

185
Q

Jugular foramen

A

CN IX, X, XI, jugular vein

186
Q

Hypoglossal canal

A

CN XII

187
Q

What’s in the cavernous sinus?

A

CN III, IV, V1, V2, VI, post-ganglionic sympathetics.

188
Q

Cavernous sinus syndrome

A

Opathlmoplegia , decreased corneal and maxillary sensation with NORMAL VISUAL acuity. CN VI common.

189
Q

Middle ear ossicles

A

Malleus, incus, stapes

190
Q

Rinne test

A

Abnormal in conductive hearing loss (Bone > air) but normal in sensorineural (air > bone).

191
Q

Weber test

A

Localizes to affected ear in conductive hearing loss. Localizes to unaffected ear in sensorineural hearing loss.

192
Q

Muscles of Mastication

A

Masseter, Temporalis, Medial pterygoid CLOSE. Only opener is lateral pterygoid. M’s munch. Lateral lowers.

193
Q

Uveitis

A

Inflamation of anterior urea and iris. Sterile pus, conjuctival redness. Associated with sarcoid, RA, JIA, TB, HLA-B27

194
Q

Hyperopia vs. myopia vs. presbyopia?

A

Myopia = short-sighted b/c eye is too long (football!). Hyperopia = far-sighted b/c eye is too compressed. Presbyopia = decreased focusing ability during accommodation 2/2 sclerosis and decreased elasticity

195
Q

Retinitis

A

Retinal edema and necrosis that can lead to a scar. Often viral and associated with immunosuppresion.

196
Q

Central retinal artery occlusion

A

Acute, PAINless, monocular vision loss. Cloud retina and cherry-red spot at the fovea.

197
Q

Retinal vein occlusion

A

Retinal hemorrhage and edema

198
Q

Diabetic retinopathy

A

Non-proliferative type is due to leakage of of blood, lipids, and fluid (tx w/ blood sugar control and macular laser). Proliferative type is due to angiogenesis b/c of chronic hypoxia (tx w/ peripheral retinal photocoagulation, anti-VEGF injections)

199
Q

Aqueous humor pathway

A

Ciliary epithelium produces aqueous humor (Beta stimulation). Aqueous soln moves through posterior chamber in the space between the iris and the lens, then moves into the anterior chamber where it is collected via trabecular meshwork into the Canal of Schlemm.

200
Q

Glaucoma

A

Optic disc atrophy and progressive PERIPHERAL visual field loss associated w/ increased IOP

201
Q

Open angle glaucoma

A

Associated with in creased age, AA, family. Painless. Primary - unknown. Secondary - blocked trabecular meshwork b/c of WBC’s (uveitis), RBCs (vitreous hemorrhage), retinal elements (retinal detachment)

202
Q

Closed/narrow angle glaucoma

A

Primary - enlargement or forward movt of lens against the central iris leads to OBSTRUCTION of aqueous flow. Fluid build-up behind iris also pushes peripheral iris against cornea to impede trabecular meshwork flow. Secondary - hypoxia from retinal disease induces a vasoproliferation in the iris that contracts the angle. Acute closure from increased IOP is PAINFUL, frontal headache. No Epi b/c mydriatic.

203
Q

Cataract

A

Painless often b/l opacification of the lesion. RF include age, smoking EtOH, excessive sunlight, cortico, classic galatosemia, galactokinase deficiency, DM, trauma, infection

204
Q

How does miosis happen?

A

Edinger-Wetphal nucleus to ciliary ganglion piggy-backing CN III. After synapse, short ciliary nerves to pupillary sphincter

205
Q

How does mydriasis happen?

A

From hypothalamus to ciliospinal center of Budge (C8-T2!). Exit T1 to superior cervical ganglion. Then move through plexus on internal carotid, through cavernous sinus, through long ciliary nerve to pupillary dilators

206
Q

Pupillary light reflex

A

From retina to CN II to pretectal nuclei - activates b/l Edinger-Westphal -> miosis.

207
Q

Marcus Gunn pupil

A

Afferent pupillary defect

208
Q

Cranial nerve III anatomy

A

Is fed from outside in. Motor components INSIDE are vulnerable to DM. Parasympathetic output (outside) are vulnerable to compression (blown pupil)

209
Q

Internuclear opthalmoplegia

A

lesion in MLF leads to lack of coordination between eyes.. CN III talking to opposite CN VI. So, when Left eye moves left and right eye does not, the R oculo III isn’t syncing with L abducens, so it is the Right MLF that is NOT working. (III is priority) for a Right INO (refers to eye that is paralyzed)

210
Q

Ciliary muscle, pupillary dilator, pupillary sphincter, ciliary epithelium innervation?

A

Cholinergic (parasympathetic) M3’s for sphinter and ciliary muscle. Alpha-1 for dilator. Beta for ciliary epithelium

211
Q

Entacapone

A

A Catechol-O-methyl-transferase (COMT) inhibitor that helps increase the bioavailability of levodopa by inhibition PERIPHERAL methylation. Tolcapone does both peripheral and central but associated with hepatotoxicity.

212
Q

Carbamazepine mech and SE’s?

A

Blocks voltage-gated Na+ channels in cortical neurons. Bone marrow suppression, hepatotoxic, SIADH.

213
Q

Two major mechs of diabetic neuropathy?

A

Glycoslyation leads to thickness, hyalinization, and narrowing of arterial walls -> ischemic damage. Accumulating glucose as sorbital -> inc. cell osmolarity -> osmotic dmg to axons and Schwann cells. Retina, renal papilla, and scwhann cells have DEC. activity of sorbitol dehydrogenase, which prevents clearance of sorbitol into fructose.

214
Q

Genetics affecting course of Alzheimers?

A

Early onset associated with APP (21), presenilin-1 (14), and preseinili-2 (1). Late onset with ApoE4 (19). ApoE2 (19) appears to be protective

215
Q

Senile plaques vs. neurofibrillary tangles

A

Senile plaques are extracellular Beta-amyloid core. amyloid-Beta comes from cleavage of amyloid precursor protein (APP). Neurofibrillary tangles are INTRAcellular, hyperphosphorylated TAU protein = insoluble. Tangles correlate to degree of dementia.

216
Q

Frontotemporal dementia vs. Lewy body dementia

A

Personality and parkinsonian vs. Visual hallucination -> parkinsonian. Pick bodies (spherical tau protein aggregates) + fonrtotemporal atrophy vs. alpha-synuclein defect.

217
Q

Acute inflammatory demyelinating polyradiculopathy

A

Most common Guillan-Barre variant. Autoimmune condition associated w/ infection (Campy and CMV) -> destruction of Schwann cells leading to a simmering ascending muscle weakness/paralysis starting from lower extremities. Autonomic findings! Tx - respiratory support, plasmapheresis, IVIG. LP shows increased protein with NORMAL cell count and increased protein.

218
Q

PML

A

Progressive multifocal leukoencephalopathy. Destruction of OLIGO’s associated with JC. Found in AID’s and inc. risk with natalizumab (MS drug). Usu. fatal.

219
Q

ADEM

A

Acute disseminated encephalomyelitis. After infection (measles, VZV) or vaccination (rabies, smallpox), multifocal perivenular inflammation and demyelination

220
Q

Metachromatic leukodystrophy

A

AR, arylsulfatase A deficiency -> buildup of sulfatides -> impaired myelin sheet production -> central and peripheral demyelintation with ATAXIA and dementia. Many-colored Arya becomes ataxic in the sulfur pits.

221
Q

Charcot-Marie-Tooth

A

Progressive hereditary nerve disorder 2/2 defective protein production for structure or function of peripheral nerves or myelin. Typically AD, scoliosis, high or flat arches

222
Q

Krabbe disease

A

Galactocerebrosidase (Gaucher is glucocerebrosidase) -> buildup of galactocerebroside and pyschosine -> myelin destruction -> peripheral neuropathy, dvpt delay, optic atrophy, globoid cells. Krabs are delayed.

223
Q

Adrenoleukodystrophy

A

X-linked! Metabolism of VLCFA’s -> buildup in nervous, adrenals (crisis), testes. ADRENO! luekodystrophy.

224
Q

Status epilepticus

A

Continuous seizure for > 30 minutes or recurrent sz without regaining consciousness between sz. Emergency

225
Q

Myoclonic vs. tonic-clonic vs. tonic vs. atonic sz.

A

Myoclonic are quick, repetitive jerks while tonic-clonic are grand mal alternating stiffening and movement. Tonic sz = stiffening. Atonic sz = “drop” sz.

226
Q

Etios of sz for children?

A

Genetic, infection (febrile), trauma, congenital, metabolic

227
Q

Cluster vs. Tension vs. Migraine HA’s regarding DURATION

A

Cluster - 15min-3 hrs repetitive. Tension HA > 30 min and constant. Migraines are 4-72 hours.

228
Q

Cluster HA vs. trigeminal neuraglia

A

TN produces repetitive shooting pain in distribution of CN V typically lasting < 1 min. Cluster HA pain is > 15 min.

229
Q

Tx for cluster headaches?

A

Inhaled oxygen and sumatriptan vs. analgesics or amitriptyline for chronic pain

230
Q

Peripheral vs. central vertigo

A

Peripheral is more common (inner ear etio). Positional testing leads to a delayed horizontal nystagmus. Central is brain stem or cerebellar with directional change of nystagmus, dipolopia, dymetria, immediate nystagmus with positional testing

231
Q

Sturge-Weber

A

Sporadic, port-wine Stain, Tram track, Unilateral, Retardation, Glaucoma, GNAQ, Epilepsy. (SSTURGGE). Activating mut -> dvpt anomaly of neural crest derivatives. Port-winte in V1/V2 distribution. Ispsi leptomeningeal angioma -> sz/epilepsy. Congenital NON-inherited. GNAQ sporadic.

232
Q

Tuberous sclerosis

A

HAMARTOMAS = Hamartomas in CNS/skin, Angiofibromas, MR, Ash-leaf spots, cardiac Rhabdomyoma, TS, autosomal dOminant, Mental retardation, renal Angiomyolipomas, Sz, Shagreen patches. Increased subependymal astrocytomas.

233
Q

NF-1

A

Cafe-au-lait, Lisch nodules, NF’s in skin, optic gliomas, pheochromocytomas. NF1 is a tumor suppressor gene (Ras regulator) on chromosome 17.

234
Q

VHL

A

Cavernous hemangiomas in skin, mucosa, organs, b/l RCC, hemangioblastoma in retina, brainstem, cerebeullum, and pheochromocytomas. AD. VHL is tumor suppressor on chromsome 3 -> constitutive HIF (transcription factor) expression -> angiogenic growth factors

235
Q

Gliobastoma multiforme

A

Hemispheres, “Butterfly glioma,” Astrocytes stain’d for GFAP, pseudopalisading pleomorphic tumor cells with central areas of necrosis

236
Q

Meningioma

A

Arachnoid cells, EXTRA-exial. Dural-tail. Often asymptomatic with sz or focal neuro. Path w/ spindle cells concentrically and Psammoma bodies

237
Q

Hemangioblastoma

A

VHL associated when w/ retinal angiomas. Cerebellar. Often produce EPO => secondary polycythemia. Path - closely arranged, thin-walled caps with minimal parenchyma

238
Q

Schwannomas

A

Cerebellopontine angle. Schwann cell. S100 POS. B/l acoustic schwannomas found in NF-2.

239
Q

Oligodendoglioma

A

Rarer, slower growing. Frontal lobe. Path - fried egg cells (oligo’s) and chicken-wire capillary pattern. Often calcified.

240
Q

Pilocytic astrocytoma

A

In children, often found in posterior fossa. Well-circumscribed. Benign w/ good prognosis. Path - GFAP POS, Rosenthal fibers (corkscrew, eosinophilic), cystic on gross.

241
Q

Medulloblastoma

A

PNET. Highly malignant cerebellar. Compress 4th ventricle; Drop metastases into spinal cord. Path - Homer-Wright rosettes. Solid, small blue cells.

242
Q

Ependymoma

A

Usu. FOURTH ventricle. Hydrocephalus. Poor prognosis. Path - perivascular rosettes. Rod-shaped blepharoplasts (basal ciliary bodies) near nucleus.

243
Q

Craniopharyngioma

A

Most common childhood supratentorial tumor derived from Rathke’s pouch (evagination of ectoderm that lines fetal oral cavity -> adenohypophysis; neurohypophysis from neuroectoderm). Often calcified. CYSTS filled with yellow, viscous fluid rich in cholesterol crystals.

244
Q

Uncal herniation

A

Ipsilateral CN III (blown and down and out), ipso PCA (contralateral homonymous hemianopsia), contralateral crus cerebra (ipsi paralysis)

245
Q

Adrenergic glaucoma drugs

A

Epinephrine decreases aqueous humor synthesis via vasoconstriction (se of mydriasis so don’t use in closed-angle). Brimonidine (alpha-2, decreases synthesis) w/ se of blurry vision, hyperemia, foreign body sensation, allergy, ocular. The beta-blockers are timlol, betaxolol, and carteolol.

246
Q

Cholinomimetics used for glaucoma

A

Direct (pilocarpine, carbachol) and indirect (physostigmine, echotiophate). Contract ciliary muscle and open trabecular meshwork to increase outflow. SE include miosis and cyclospasm.

247
Q

Prostaglandin used for glaucoma

A

Latanoprost (PDG2alpha) increases aqueous humor outflow and browns the iris.

248
Q

Mechanism of opioid analgesics

A

Opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to open K+ channels, close Ca2+ channels -> DECREASED synaptic transmission. Inhibit release of ACh, NE, 5-HT, glutamate, and substance P.

249
Q

Butorphanol

A

PARTIAL mu-opioid receptor agonist and kappa-opioid receptor agonist. Used for severe pain (migraine and labor) with LESS reparatory depression. H/e, withdrawal symptoms if patient on full opioid agonist. Overdose hard to reverse with naloxone.

250
Q

Tramadol

A

VERY weak opioid agonist that also inhibits 5-HT and NE reuptake. Chronic pain. Similar tox profile as opioids, decreases sz threshold, serotonin syndrome.

251
Q

Ethosuximide

A

Absence sz. Blocks t-type Ca2+ channels in thalamic neurons. SE’s fatigue, GI, HA, Itching, Stevens-Johnson

252
Q

1st line acute tx for status vs. 1st line ppx for status?

A

Benzos (diazepam, lorazepam) vs. Phenytoin

253
Q

Phenytoin

A

1st line tonic-clonic and ppx for status. Na+ channel inactivation. 0-order kinetics. Induces P450. Lots of SE (nystagmus, dipolpia, gingival hyperplasia, teraogeneis w/ fetal hydantoin syndrome, ale-like). Fosphenytoin is IV.

254
Q

Carbamazepine

A

1st line for simple, complex, tonic-clonic sz, and trigeminal neuralgia. Na+ channel inactivation. SE diplopia, ataxia, blood dyscrasia, liver, teratogenesis, induces P-450, SIADH, Stevens

255
Q

Valproic acid

A

1st line for tonic clonic. Used for partial sz and absence. Na+ channel inactivation and inhibition of GABA transaminase to increase GABA. GI, hepatotoxicity (rare but fatal, Neural tube defects, tremor, wt gain. Myoclonic sz and bipolar.

256
Q

Gabapentin

A

Partial and tonic-clonic, peripheral neuropathy, postherpetic neuralgia, migraine ppx, bipolar. Inhibits high-voltage activated Ca2+ channels. SE - sedation and ataxia

257
Q

Phenobarbital

A

Partial, tonic-clonic. Increases GABA action. 1st-line for neonates! sedation, tolerance, induce P-450, CV dep.

258
Q

Topiramate

A

Partial and tonic-clonic. Blocks Na+ channels and increases GABA. Migraine prevention. Sedation, mental dulling, kidney stones, wt loss.

259
Q

Lamotrigine

A

Partial, tonic-clonic, absence. Blocks voltage-gated Na+. Stevens-Johnson syndrome.

260
Q

Levetiracetam (Keppra)

A

Partial, tonic-clonic. Unknown mech. No SE’s noted.

261
Q

Barbiturates - Mech and Tox

A

Increase DURATION of Cl- channel opening (GABA), decrease neuron firing. Contra’d in porphyria. Used for anxiety, sz, insomnia, induction of anesthesia (thiopental). Tox - CV depression, dependence, induces P450. Overdose tx is supportive. “Barbies are durable.”

262
Q

Benzos - Mech and Tox

A

Increase FREQUENCY of Cl- channel opening. Decreases REM sleep. Tox - dependence, CNS depression with alcohol, but less resp depression than barbiturates. Tx overdose w/ flumazenil. “Ppl that buy Benz’s (and do benzos) are flippant.”

263
Q

Nonbenzo hypnotics - mech and tox

A

Zolpidem, Zaleplon, Eszopiclone. Act on BZ1 subtype of GABA receptor. Tox - ataxia,HA, confusion. Short duration b/c rapidly metabolized by LIVER. dec. dependence

264
Q

What properties of anesthetics do we care about?

A

Solubility in lipids and blood. MAC - minimal alveolar concentration req. to prevent 50% from moving in response to noxious stimuli. Inc. solubility in lipids = greater potency (lower MAC). Inc. solubility to blood = slower cross to CNS = slower induction and recovery

265
Q

Toxicities of inhaled anesthetics

A

Heptotoxicity (halothane), nephrotoxicity (methoxyflurance), proconvulsant (enflurane), expansion of trapped gas in body cavity (NO). All of these except NO and the addition of succinylcholine can cause malignant hyperthermia which is life-threatening HEREDITARY condition with fever and severe muscle contractions. Tx = dantrolene

266
Q

IV anesthetics

A

Barbiturates, Benzos, Ketamine, Opioids, Propofol

267
Q

Propofol

A

Sedation in ICU, rapid anethesia induction, short procedures. Less postop nausea than thiopental. Potentiates GABA.

268
Q

Thiopental

A

IV barbiturate of high potency and rapid entry into brain. Induction and short surgical procedures. Rapid redistribution into skeletal muscle and fat (recovery quick). Decreased cerebral blood flow

269
Q

IV midazolam

A

Commonly used for endoscopy. Used w/ gaseous anesthetics and narcotics. May cause severe post-op respiratory depression, decreased pressure, and anterograde amnesia

270
Q

Ketamine

A

PCP analog that blocks NMDA (dissociative anesthetic). CV stimulant. Disorientation, hallucination, bad dreams. Inc. cerebral blood flow.

271
Q

Local anesthetics

A

Amides are lidocaine, mepivacaine, bupivacaine. Esters are procain, cocaine, tetracaine.

272
Q

Mech of local anesthetics

A

Block Na+ channels (inner portion) and preferentially bind to activated ones. Tertiary amines penetrate membrane uncharged, then after charge, bind ions.

273
Q

Factors affecting the effectiveness of local anesthetics?

A

It’s hard for charged, alkaline anesthetics to get into infected (acidic) tissue. Order of nerve blockade small diameter > large diameter. Then myelinated > unmyelinated. Lose pain, temp, touch, then pressure. Can give with vasoconstrictors like epi to enhance local action via dec bleeding and dec. systemic conc.

274
Q

Local anesthetic toxicity

A

CNS excitation, CV tox (bupivacaine), HTN, hypotension, arrhythmias (cocaine)

275
Q

Basic overview of paralytics

A

Used for surgery or mech ventilation. Selective for motor nicotinic receptors. Depolarizing vs. nondepolarizing = agonist vs. competetive antagonist

276
Q

Succinylcholine

A

Strong ACh receptor agonist -> sustained depolarization and prevents muscle ctx. Complications - hyperCa, hyperK, malignant hyperthermia. Phase 1 block is prolonged depol. w/ no antidote. Phase 2 block is repolarized but AChR desensitized and req. cholinesterase inhibitors. Patients with hyperK (crush/burn, denervating injuries, myopathies) -> depolarizing agents

277
Q

Dantrolene

A

Ryanodine receptor. Prevents release of Ca2+ from SR in skeletal muscle. Used for malignant hyperthermia and NMS.

278
Q

Parkinsons drugs

A

BALSA = Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics.

279
Q

Selegeline

A

MAO-B inhibitor that prevents DA breakdown (MAO-B prefers to breakdown DA > NE and 5-HT). Other DA breakdown inhibitors are COMT inhibitors (entacapone and tolcapone)

280
Q

Benztropine

A

Curbs excess cholinergic activity in Parkinsons as an antimuscarinic.

281
Q

Memantine

A

Alzheimer’s drug. NMDA receptor antagonist. Tox includes dizziness, confusion, hallucinations

282
Q

AChE inhibitors for Alzheimer’s

A

Donepezil, galantamine, rivastigmine.

283
Q

HD drugs

A

Haloperidol (DA receptor antagonist). Inhibitors of vesicular monoamine transporter (VMAT) - tetrabenazine and reserpine.

284
Q

Sumatriptan

A

5-Ht1b/1d agonist. Inhibits treigeminal n. activation and prevents vasoactive peptide release. t1/2 <2hrs. Used for acute migraines and cluster headaches. Tox = coronary vasospasm CONTRA = CAD or Prinzmetal angina

285
Q

Myotonic muscular dystrophy

A

Myotonia = slow relaxation of muscles. Difficulty loosening one’s grip. AD. CTG (myotonia-protein kinase). Anticipation. Cataracts. Atrophy of type 1> type 2.

286
Q

Meniere’s disease

A

Increased volume of endolymph. Tinnitus, vertigo, hearing loss is sensorineural (Weber will lateralize to HEALTHY side)

287
Q

Fluorinated anesthetics effect on CV, Resp, Cerebral blood flow, Kidney, hepatic blood flow?

A

Myocardial depression leads to decreased CO. Hypotension. Respiratory depressant (dec. TV and minute ventilation -> hypercapnea and dec. mucociliary clearance). Halothane and sevolurane have bronchodilation prop’s - asthma. Decreased vascular resistance -> increased cerebral blood flow -> ICP. Dec. GFR, increased renal vascular resistance, and decreased RPF. Decreased hepatic blood flow.

288
Q

How does solubility of anesthetic in peripheral tissues effect anesthetic concentration?

A

If peripheral tissue solubility is high (AV gradient high), then it takes more anesthesia to saturate the blood and the brain.

289
Q

How does pulmonary ventilation rate affect anesthetic concentration?

A

Rise of gas tension in alveoli is proportional to the rate AND depth of respiration.

290
Q

How does the blood/gas partition coefficient affect the action of anesthetics?

A

Higher blood/gas partition coefficient means highly SOLUBLE –> blood saturates slowly leading to delayed rise in partial pressure -> increasing onset of time. (e.g. halothane)

291
Q

MS path

A

Plaques. Demyelination w/ relative preservation of axons. Accumulation of lipid-laden macrophages. Astrocytosis. Infiltration by lymphocytes and mononuclear cells.

292
Q

Pheochromocytoma

A

PNET tumor of chromatin cells of sympathetic nervous system (90% from adrenal medulla).

293
Q

HD location

A

AD 100% penetrance. Loss of neurons in caudate nucleus and putamen (striatum). STN lesion = hemiballismus.

294
Q

Side effects for 1st gen antipsychotics?

A

Generally, low-potency (Chlorpromazine and thioridazine) have more non-neuro SE’s (sedation, Antichol, orthostatic hypotension). High-potency (haloperidol, fluphenazine) will have EPS - acute dystonia, akathisia, parkinsonism.

295
Q

Congenital torticollis

A

Etio - birth trauma or malposition of head in utero -> SCM injury and fibrosis. Develops by wk 2-4. Head tilted toward AFFECTED side with CHIN pointed AWAY. Good prognosis. Tx = conservative and stretching

296
Q

Alcoholic cerebellar degeneration

A

Chronic thiamine deficiency. Gait ataxia, truncal instability, intention tremor. Atrophy of anterior lobes and cerebellar vermis.

297
Q

Two ways that tumors increase ICP?

A

Blockage. Breakdown of the BBB.

298
Q

How does NPH lead to urinary incontinence?

A

Disrupts paraventricular fibers from cortex which normally inhibit the SACRAL micturition center (responsible for bladder contraction and found in S2-S4 level)

299
Q

Causes of exacerbations of myasthenia gravis?

A

(1) Myasthenic crisis 2/2 not enough Ach in cleft (e.g. not enough drug). Dx with edrophonium improvement. (2) Cholinergic crisis 2/2 TOO much Ach -> refractory muslce. Dx with no improvement with edrophonium.

300
Q

Neuroblastoma

A

Most common extra cranial cancer of children. Found in any neural crest deviated. Associated with N-myc. Paraneoplastic syndrome includes opsoclonus and myoclonus. Often see increased excretion of catecholamines in urine.

301
Q

Protein 14-3-3

A

CSF protein helpful in diagnosing Cretuzfeldt-Jakob

302
Q

Narcolepsy CSF findings?

A

Decreased hypocretin-1 (orexin-A) and hypocretin-2 (orexin-B)

303
Q

Arachnoid granulations vs. choroid plexus?

A

Choroid plexi MAKE CSF. Arachnoid granulations ABSORB CSF. Communicating hydrocephalus 2/2 dysfunction of subarachnoid villi (e.g. meningeal infection or SAH)

304
Q

Length constant vs. time constant?

A

Length constant = how far down an axon an AP can go. Time constant = how quickly it takes for a membrane to reset. Myelination increases length constant and decreases time constant.

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