Steve Nash's Neuro Assists

Question 1

Where does Herpes labialis go dormant

Answer 1

Trigeminal ganglia

HSV-1

Question 2

Where does Herpes genitalis go dormant

Answer 2

sacral ganglia

HSV-2

Question 3

Where does Herpes zoster go dormant

Answer 3

Dorsal root or trigeminal ganglia

Question 4

Which elements of the neural cytoskeleton form neurofibrillary tangles in alzheimer’s disease

Answer 4

Microtubules

Question 5

Notochord induces what

Answer 5

Induces overlying ectoderm to differentiate into neuroectoderm and form the neural plate

Question 6

Neural plate gives rise to the

Answer 6

neural tube and neural crest cells;

Question 7

Notochord becomes what

Answer 7

Notochord becomes nucleus pulposus of the intervertebral disc in adults;

Question 8

Alar plate

Answer 8

Dorsal spinal cord;

gives to sensory

Question 9

Basal plate

Answer 9

Ventral spinal cord;

Gives rise to motor

Question 10

Prosencephalon develops into

Answer 10

Telencephalon and diencephalon;

Question 11

Mesencephalon develops into

Answer 11

Mesencephalon;

Question 12

Rhombencephalon develops into

Answer 12

Metencephalon and myelencephalon;

Question 13

Telencephalon gives rise to

Answer 13

Cerebral hemispheres;

Lateral ventricles

Question 14

Diencephalon gives rise to

Answer 14

Thalamus;

Third ventricles

Question 15

Mesencephalon gives rise to

Answer 15

Midbrain;

Aqueduct

Question 16

Metencephalon gives rise to

Answer 16

Pons and cerebellum;

Upper part of fourth ventricle

Question 17

Myelencehalon gives rise to

Answer 17

Medulla;

Lower part of fourth ventricle

Question 18

In the brain, what does the neuroectoderm give rise to

Answer 18

CNS neurons;
ependymal cells (inner lining of ventricles, make CSF);
oligodendroglia;
astrocytes

Question 19

In the nervous system, what does the neural crest give rise to

Answer 19

PNS neurons;

Schwann cells

Question 20

In the nervous system, what does the mesoderm give rise to

Answer 20

Microglia (like macrophages, originate from mesoderm)

Question 21

Neural tube defects: when do they happen, what are the findings

Answer 21

neuropores fail to fuse (4th week);
Elevated alpha fetoprotein (AFP) in amniotic and maternal serum;
increased AChE in amniotic fluid confirms (fetal AChE in CSF transudates across defect into amniotic fluid)

Question 22

Spina bifida occulta

Answer 22

Failure of bony spinal canal to close, but no structural herniation;
Dura is intact;
associated with tuft of hair or skin dimple at level of bony defect

Question 23

Meningocele

Answer 23

Meninges (but not the spinal cord) herniate through spinal canal;
normal AFP

Question 24

Meningomyelocele

Answer 24

Meninges and spinal cord herniate through spinal canal defect

Question 25

Spina bifida with myeloschisis

Answer 25

Spinal cord visibly seen; | increased AFP

Question 26

Anencephaly

Answer 26

Malformation of the anterior neural tube resulting in no forebrain, open calvarium (frog like appearance); Findings: increased AFP, polyhydramnios (no swallowing); associated with maternal diabetes type I; maternal folate intake decreases chances

Question 27

Holoprosencephaly

Answer 27

Failure of left and right hemispheres to separate; Usually occurs during weeks 5 and 6; complex multifactorial etiology that may be related to mutations in sonic hedgehog signaling pathway; Moderate form has cleft lip/palate, most sever form results in cyclopia; Associated with Patau

Question 28

Lissencephaly

Answer 28

smooth brain with no gyri; lack of hemisphere sulci; severe neurologic impairment

Question 29

Chiari II (arnold chiari malformation)

Answer 29

Significant herniation of cerebellar tonsils and vermis through foramen magnum with aquaductal stenosis and hydrocephalus; Often presents with lumbrosacral myelomeningiocele and paralysis below the defect

Question 30

Dandy Walker

Answer 30

Agenesis of cerebellar vermis and cystic enlargement of 4th ventricle (fills the enlarged posterior fossa); Associated with hydrocephalus and spina bifida;

Question 31

Chiari I malformation

Answer 31

Usually seen in adults; less significant herniation of cerebellar tonsils into magnum foramen; Valsalva makes worse; Usually asymptomatic

Question 32

Syringomyelia

Answer 32

Cystic cavity (syrinx) within the spinal cord (if central then it is called hydromyelia); Crossing anterior spinal commissural fibers are typically damaged first leading to cape like bilateral loss of pain and temperature sensation in upper extremities; Mostly at C8 T1 level; Associated with Chiari 1 malformation;

Question 33

Tongue development

Answer 33

1st and 2nd branchial arches form the anterior 2/3 (taste is CN 7 and sensation is CN V3); 3rd and 4th give rise to posterior 1/3 (taste and sensation is CN 9, very posterior taste is 10); motor is CN12; Muscles of the tongue are derived from occipital myotomes

Question 34

Stain used for neurons

Answer 34

Nissl Substance (Stains RER, which is only present in dendrites and cell bodies, NOT axons)

Question 35

If an axon is injured it undergoes what

Answer 35

Wallerian degeneration; degeneration distal to injury and axonal retraction proximally; allows for potential regeneration of axon if in PNS (CNS will never regenerate unless it is the olfactory nerve)

Question 36

Astrocyte

Answer 36

Physical support, repair, K metabolism, removal of excess neurotransmitter, foot process are component of the BBB, glycogen fuel reserve buffer; Reactive gliosis in response to neural injury; Astrocyte marker is GFAP; Derived from neuroectoderm

Question 37

Microglia

Answer 37

CNS phagocytes; derived from bone marrow bone monocytes (mesodermal origin); not readily seen in Nissl stains; Have small irregular nuclei and relatively little cytoplasm; Scavenger cells of CNS; respond to tissue damage by differentiating into large phagocytic cells; Is an Antigen presenting cell; Secretes free radicals; HIV infected microglia fuse to form multi-nucleated giant cells

Question 38

Oligodendroglia

Answer 38

Myelinates neurons of the CNS; 1 oligodendroglia can myleniated around 30 to 50 nerves; Derived from neuroectoderm; fried egg appearance; MS, progeressive multifocal leukoencephalopathy, and leukodystrophies attacks this cell type;

Question 39

Glial cells

Answer 39

Supporting cells of the CNS; | capable of cell division

Question 40

Schwann cells

Answer 40

myelinates PNS in a 1:1 ratio; promotes axonal regeneration; Derived from neural crest; destroyed in Guillain-Barre;

Question 41

Acoustic neuroma

Answer 41

type of schwannoma; Typically located in internal acoustic meatus (CN 8); If bilateral think NF2 (on gene 22, affecting 2 ears)

Question 42

Sensory: Free nerve endings

Answer 42

C fibers: slow unmyelinated fibers; A delta fibers: fast, myelinated fibers; Located on all skin; conveys pain and temperature

Question 43

Sensory: Meissner corpuscles

Answer 43

Large, myelinated, and adapt quickly; Found in glabrous (hairless) skin; Senses dynamic, fine/light touch and position sense

Question 44

Sensory: Pacinian corpuscles

Answer 44

Large, myelinated and adapt quickly; Found in Deep skin layers, ligaments, and joints; Senses vibration and pressure sensation

Question 45

Sensory Merkel discs

Answer 45

Large, myelinated and adapt slowly; Found in the basal epidermal layer and in hair follicles; Sense pressure, deep static touch (e.g. shapes, edges), and position sense

Question 46

What are the different layers/parts to a peripheral nerve and important info about them

Answer 46

Endoneurium- invests single nerve fiber layers (inflammatory infiltrate in guillain Barre syndrome); Perineurium (permeability barrier)- surrounds a fascicle of nerve fibers, must be rejoined in microsurgery for limb reattachment; Epineurium- dense connective tissue that surrounds entire nerve (fascicle and bleed vessels)

Question 47

Ependymal cells

Answer 47

Line ventricles of brain; some differentiate into choroid epithelial cells; cilia assist in CSF circulation

Question 48

Tanycytes

Answer 48

Specialized type of ependymal cells; basal cytoplasmic processes contact CNS blood; thought to aid in blood-CSF transport

Question 49

NE: where is it made, what disorders alter its levels

Answer 49

Made in Locus Ceruleus in pons; increased in anxiety; decreased in depression

Question 50

Dopamine: where is it made, what disorders alter its levels

Answer 50

Made in ventral tegmentum and SNc (midbrain); increased in Huntington; decreased in Parkinson; Decreased in Depression

Question 51

5-HT: where is it made, what disorders alter its levels

Answer 51

Made in Raphe nucleus (pons, medulla, midbrain); Increased in parkinson; decreased in anxiety; decreased in depression

Question 52

ACh: where is it made, what disorders alter its levels

Answer 52

Made in basal nucleus of Meynert; Increased in Parkinson; decreased in Alzheimer; Decreased in Huntingtons

Question 53

GABA: where is it made, what disorders alter its levels

Answer 53

Decreased in Anxiety; Decreased in Huntington; Made in nucleus Accumbens

Question 54

Locus ceruleus is activated by what emotion

Answer 54

stress and panic

Question 55

Nucleus Accumbens and septal nucleus are know for being what

Answer 55

the reward center, pleasure, addiction, and fear

Question 56

Blood-Brain Barrier: made from

Answer 56

Foot process of astrocytes, tight junctions in non fenestrated capillary endothelial cells, and a Basement membrane;

Question 57

Blood-Brain Barrier: what crosses it

Answer 57

Glucose and amino acids cross slowly via carrier mediated transport; Nonpolar/lipid soluble cross rapidly via diffusion; Area postrema has no BBB (vomiting center, OVLT-osmotic sensing);

Question 58

Function of Hypothalamus

Answer 58

``` Hypothalamus wears TAN HATS; Thirst and water balance; Adenohypophysis control (regulates anterior pituitary), Neurohypophysis releases hormones produced in the hypothalamus; Hunger; Autonomic Regulation; Temperature Control; Sexual urges ```

Question 59

what is the OVLT

Answer 59

Part of hypothalamus; not covered by BBB; Organum vasculosum of the lamina terminalis-senses change in osmolarity)

Question 60

Area postrema responds to

Answer 60

responds to emetics

Question 61

What nucleus makes ADH

Answer 61

Supraoptic nucleus

Question 62

What nucleus makes oxytocin

Answer 62

Paraventricular nucleus

Question 63

Lateral area of the hypothalamus

Answer 63

Hunger; Destruction leads to anorexia and failure to thrive in kids; Inhibited by leptin; If you zap you lateral nucleus you shrink laterally

Question 64

Ventromedial area of the hypothalamus

Answer 64

Satiety; Destruction (e.g. craniopharyngioma) leads to hyperphagia; stimulated by leptin; If you zap your ventromedial nucleus, you grow ventrally and medially

Question 65

Anterior hypothalamus

Answer 65

Cooling and parasympathetics; | Anterior Nucleus=Cooling off (A/C=anterior cooling)

Question 66

Posterior hypothalamus

Answer 66

Heating, sympathetics; | Posterior nucleus=get fired up (heating and parasympathetics)

Question 67

Suprachiasmatic nucleus of the hypothalamus

Answer 67

Circadian rhythm; SCN releases NE on the pineal gland leading to melatonin; SCN responds to light (or lack there of)

Question 68

Rapid Eye movement in REM sleep is caused by the

Answer 68

PPRF paramedian Pontine Reticular Formation

Question 69

Drugs that decrease REM

Answer 69

Alcohol, Benzodiazepines, and barbiturates all decrease REM and delta wave sleep as well; NE also decreases REM

Question 70

How do you treat enuresis

Answer 70

bedwetting treated with oral desmopressin acetate (DDAVP), which mimics ADH; Preferred over imipramine due to side effects

Question 71

What can treat night terrors and sleep walking

Answer 71

Benzodiazepines

Question 72

Awake (eyes open) what is the EEG look like

Answer 72

Beta waves (highest frequency, lowest amplitude)

Question 73

What is the EEG look like in Awake stage with eyes closed

Answer 73

Alpha waves

Question 74

Stage N1 of sleep

Answer 74

light sleep, theta wave

Question 75

Stage N2 of sleep

Answer 75

Deeper sleep; when bruxism occurs; Sleep spindles and K complexes

Question 76

Stage N3 of sleep

Answer 76

Deepest sleep that is non-REM; sleepwalking, night terrors, and bedwetting occur; delta waves (lowest frequency, highest amplitude)

Question 77

REM sleep

Answer 77

``` Loss of motor tone, increased Brain O2 usage, increase and variable pulse and blood pressure; When dreaming and penile/clitoral tumescence occur; may serve a memory processing function; Beta waves (live awake with eyes open stage) ```

Question 78

Posterior pituitary

Answer 78

Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei;

Question 79

input, information, destination of the VPL of the thalamus

Answer 79

Input is the spinothalamic and dorsal column/medial lemniscus; Info is pain and temp, pressure, touch, vibration and proprioception; destination is the primary somatosensory cortex

Question 80

input, information, destination of the VPM

Answer 80

Trigeminal and gustatory pathway; info is Face sensation and taste; destination is the primary somatosensory cortex; Makeup goes on the FACE (vpM)

Question 81

input, information, destination of the LGN

Answer 81

Input is CNII; Info is vision; destination is the Calcarine sulcus; Lateral=Light

Question 82

input, information, destination of the MGN

Answer 82

input is the Superior olive and inferior colliculus of tectum; info is hearing; Destination is the auditory cortex of the temporal lobe; Medial=music

Question 83

input, information, destination of the VL

Answer 83

Input is the basal ganglia and cerebellum; Info is motor; Destination is the Motor Cortex

Question 84

Limbic system

Answer 84

Involved in emotion, long-term memory, olfaction, behavior modification, and autonomic nervous system function; Structures include hippocampus, amygdala, fornix, mammillary bodies, and cingulate gyrus; 5 F's-Feeding, Fleeing, Fighting, Feeling, Sex

Question 85

Cerebellum

Answer 85

Aids in coordination and balance; Control ipsilateral side (outputs go to contralateral motor cortex, then that crosses when going down the corticospinal tract)

Question 86

Inputs into the Cerebellum

Answer 86

Contralateral cortex via the middle cerebellar peduncle; Ipsilateral proprioceptive information via inferior cerebellar peduncle from the spinal cord (inputs nerves=climbing and mossy fibers)

Question 87

Outputs from the Cerebellum

Answer 87

Sends info to contralateral vortex to modulate movement; Output is the purkinje cells to the deep nuclei of the cerebellum to the contralateral cortex via the superior cerebellar peduncle;

Question 88

What are the deep nuclei of the Cerebellum

Answer 88

Lateral to medial they are the Dentate, Emboliform, Globose, Fastigial (don't eat greasy foods);

Question 89

Lateral lesions in the Cerebellum

Answer 89

Voluntary movement of the extremities; | when injured, you tend to fall toward injured (ipsilateral) side

Question 90

Medial lesions in the cerebellum

Answer 90

Lesions involve midline structures (vermal cortex, fastigial nuclei) and/or the flocculonodular lobe result in truncal ataxia, nystagmus, and head tilting; These patients also may have a wide-based gait and deficits in truncal coordination; Usually midline lesions result in bilateral motor deficits in axial and proximal limb muscles

Question 91

What does dopamine do in the basal ganglia

Answer 91

Binds D1 in the excitatory pathway, and to D2 in the inhibitory pathway which leads to increased motion

Question 92

Parkinson Disease

Answer 92

Degenerative disorder of CNS associated with Lewy Bodies (composed of alpha-synuclein- intracellular eosinophilic inclusion) and loss of dopaminergic neurons (i.e. depigmentation) of the substantia nigra pars compacta

Question 93

Huntington Disease

Answer 93

Autosomal dominant trinucleotide repeat (CAG) disorder on chromosome 4; symptoms manifest between 20 and 40; Choreiform movements, aggression, depression, dementia; Decreased levels of GABA and ACh in the brain; Neuronal death via NMDA-R binding and glutamate toxicity; Atrophy of the caudate nuclie can be seen on imaging; CAG=Caudate loses Ach and Gaba

Question 94

Hemiballismus

Answer 94

Sudden, wild flailing of 1 arm with or without leg; | Contralateral subthalamic nucleus injury (e.g. lacunar infarct);

Question 95

Chorea

Answer 95

Sudden, jerky, purposeless movements; | Lesion in the basal ganglia (think Huntington)

Question 96

Athetosis

Answer 96

Slow, writhing movements, especially seen in fingers; | lesion to the basal ganglia (think Huntington)

Question 97

Myoclonus

Answer 97

Sudden, brief, uncontrolled muscle contraction; Jerks, hiccups; Common in metabolic abnormalities such as renal and liver failure

Question 98

Dystonia

Answer 98

Sustained, involuntary muscle contractions; Writer's cramp; blepharospasm (sustained eyelid twitch)

Question 99

Essential tremor

Answer 99

Action tremor; exacerbated by holding posture/limb position; Genetic predisposition; Patients often self-medicated with EtOH, which decreases tremor amplitude; Treat using beta blockers, primidone

Question 100

Resting tremor

Answer 100

Uncontrolled movement of distal appendages (most noticeable in hands); tremor goes away with purposeful movement; Think Parkinson disease;

Question 101

Intention tremor

Answer 101

Slow, zigzag motion when pointing/extending arm towards target; Cerebellar dysfunction

Question 102

Internal Capsule: what are the 3 areas and what 3 tracts go through each

Answer 102

Anterior Limb that carries the Frontopontine and thalamicortico fibers; Genu which carries the Corticobulbar fibers; Posterior limb which carries the Corticospinal and some corticobulbar tracts

Question 103

Lesion to the amygdala

Answer 103

Kluver-Bucy Syndrome (hyperorality, hypersexuality, disinhibited behavior); Associated with HSV-1 infection

Question 104

Lesion to the Frontal lobe

Answer 104

Disinhibition and deficits in concentration, orientation, and judgment; May have reemergence of primitive reflexes

Question 105

Lesion to the Right parietal-temporal cortex

Answer 105

Spatial neglect syndrome (agnosia of the contralateral side of the world); This is the non-dominant side in most people

Question 106

Lesion to the left parietal-temporal cortex

Answer 106

Agraphia, acalculia, finger agnosia, and left-right disorientation; Called Gerstmann syndrome

Question 107

Lesion to the Reticular activating system

Answer 107

found in the midbrain; | Reduced levels of arousal and wakefullness (e.g. coma)

Question 108

Lesion to the Mammilary bodies

Answer 108

Wernicke-Korsakoff syndrome; Confusion, opthalmoplegia, ataxia; memory loss (anterograde and retrograde amnesia), confabulation, personality changes; associated with thiamine B1 deficiency, EtOH abuse; can be precipitated by giving glucose to a B1 deficient patient; Wernicke likes a CAN of beer (Confusion, Ataxia, Nystagmus)

Question 109

Lesion to the basal ganglia

Answer 109

May result in tremor at rest, chorea, or athetosis; | Think Parkinson

Question 110

Lesion to the Cerebellar hemispheres

Answer 110

Intention tremor, limb ataxia, and loss of balance; damage to the cerebellum leads to ipsilateral deficits; Fall toward side of lesion; Cerebellar hemispheres are lateral and affect lateral limbs

Question 111

Lesion to the cerebellar vermis

Answer 111

Truncal ataxia; Dysarthria; Vermis is medial so it affects medial structures

Question 112

Lesion to the Subthalamic nucleus

Answer 112

Get a contralateral hemiballismus

Question 113

Lesion to the bilateral hippocampus

Answer 113

Anterograde amnesia-inability to make new memories

Question 114

Lesion to the Paramedian Pontine Reticular Formation

Answer 114

Eyes look away from side of lesion

Question 115

Lesion to the Frontal Eye Fields

Answer 115

Eyes look toward the side of lesion

Question 116

Lesion to the temporo-occipital association cortex

Answer 116

Get visual agnosia (see an object, but you can't recognize it)

Question 117

Central Pontine Myelinolysis

Answer 117

A variant of osmotic demyelination syndrome; Acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness; Can cause locked in syndrome; Massive axonal demyelination in pontine white matter tracts secondary to osmotic forces and edema; Usually caused by overly rapid correction of hyponatremia; From low to high you pons will die, from high to low your brain will blow (cerebellar edema/herniation)

Question 118

Aphasia

Answer 118

Higher order inability to speak

Question 119

Dysarthria

Answer 119

motor inability to speak

Question 120

Broca aphasia

Answer 120

non-fluent aphasia with intact comprehension; broca area is in the inferior frontal gyrus of frontal lobe; Broca Broken Boca (mouth in spanish)

Question 121

Wernicke aphasia

Answer 121

Fluent aphasia with impaired comprehension and repetition; Wernicke area is in the superior temporal gyrus of temporal lobe; Wernicke is Wordy by makes no sense

Question 122

Global aphasia

Answer 122

Non-fluent with impaired comprehension; | both broca and wernicke areas affected

Question 123

Conduction aphasia

Answer 123

Poor repetition but fluent speech and intact comprehension; Can be caused by damage to the superior temporal gyrus and/or left supramarginal gyrus; Can't repeat phrases

Question 124

Transcortical motor aphasia

Answer 124

Non-fluent aphasia with good comprehension and repetition

Question 125

Transcortical sensory aphasia

Answer 125

Poor comprehension with fluent speech and repetition

Question 126

Mixed transcortical aphasia

Answer 126

non-fluent speech, poor comprehension, good repetition

Question 127

Middle Cerebral Artery lesions can affect what areas

Answer 127

``` Motor cortex (contralateral upper limb and face paralysis); Sensory cortex (contralateral loss of sensation of upper and lower limbs and face); Temporal lobe (Wernicke and Broca; See aphasia if dominant side (left), See hemineglect if lesion is nondominant (right) side) ```

Question 128

Anterior Cerebral Artery lesion can affect what areas

Answer 128

``` Motor cortex (lower limb contralateral paralysis); Sensory Cortex (Contralateral lower limb loss of sensation) ```

Question 129

Lenticulo-Striate Artery lesion can affect what areas

Answer 129

Striatum and internal capsule (contralateral hemiparesis/hemiplegia)

Question 130

Anterior spinal artery lesion can affect what areas

Answer 130

``` Lateral corticospinal tract (contralateral hemiparesis of upper and lower limbs; Medial lemniscus (decreased contralateral proprioception); Caudal medulla/hypoglossal nerve (ipsilateral hypoglossal dysfunction and tongue deviates ipsilaterally) ```

Question 131

Medial Medullary Syndrome

Answer 131

Caused by infarct of paramedian branches of the ASA and vertebral arteries;

Question 132

Posterior Inferior Cerebellar Artery lesion affects what areas

Answer 132

Lateral Medullary (Wallenberg) syndrome Lateral medulla; Vestibular nuclei (vomiting, vertigo, nystagmus); Lateral spinothalamic and spinal trigeminal nucleus (decreased pain and temp from ipsilateral face and contralateral body); Nucleus ambiguus (dysphagia, hoarsenss, decreased gag reflex); Sympathetic fibers (ipsilateral horners syndrome); Inferior cerebellar peduncle (ataxia, dysmetria)

Question 133

Anterior inferior Cerebellar artery lesion affects what areas

Answer 133

Lateral pontine syndrome; Facial nucleus are specific to AICA; Lateral pons, cranial nerve nuclei, vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers; Symptoms are vomiting, vertigo, nystagmus, Paralysis of the face, decreased lacrimation and salvation, decreased taste from ant. 2/3 tongue, decreased corneal reflex, decreased facial pain and temp, ipsilateral decreased hearing, ipsilateral horners ,ataxia and dysmetria

Question 134

Posterior Cerebral Artery lesion affects what

Answer 134

Occipital cortex and visual cortex; | contralateral hemianopia with macular sparing (visual acuity is fine, but decreased visual field)

Question 135

Basilar artery lesion affects what areas

Answer 135

Pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve nuclei, PPRF; Symptoms are preserved consciousness and blinking with quadraplegia, loss of voluntary facial, mouth, and tongue movements (locked in syndrome where you can do vertical eye movements and blink)

Question 136

Anterior Communicating artery lesion

Answer 136

Most common lesion in aneurysm; can lead to stroke; Saccular (berry) aneurysm can impinge cranial nerves; Symptoms are visual field defects; Lesions are typically aneurysms not strokes!

Question 137

Posterior Communicating artery lesions

Answer 137

Common site for saccular aneurysms; CN III palsy where eye is down and out with ptosis and pupil dilation; Lesions are typically aneurysms not strokes!

Question 138

Berry Aneurysms

Answer 138

Occur at bifurcations in the circle of willis; Mostly at the junction of the Acom and ACA; Rupture leads to subarachnoid hemorrhage (worst headache ever) or hemorrhagic stroke; can compress optic chiasm; Associated with ADPKD, Ehlers-Danlos, Marfan; Risk factors are old age, HTN, smoking, being black

Question 139

Charcot-Bouchard microaneurysm

Answer 139

Associated with chronic HTN; | affects small vessels (mostly basal ganglia and thalamus)

Question 140

Central post stroke pain syndrome

Answer 140

Neuropathic pain due to thalamic lesions; Initial sensation of numbness and tingling followed by weeks to months of allodynia (normal stimuli cause pain) and dysaesthesia; occurs in 10% of stroke patients

Question 141

Epidural Hematoma

Answer 141

Rupture of the middle meningeal artery (branch of the maxillary artery), often secondary to fracture of the temporal bone; Lucid Interval; Rapid expansion of blood since it is arterial leading to transtentorial herniation and CN III palsy; CT shows lens like lesions, hyperdense blood collection that does NOT cross suture lines (Can cross falx, tentorium)

Question 142

Subdural Hematoma

Answer 142

Snaking Subdural; Rupture of bridging veins; slow venous bleeding so it takes longer; seen in elderly individuals, alcoholics, blunt trauma, shaken baby; Can cross suture lines but cannot cross falx or tentorium

Question 143

Subarachnoid hemorrhage

Answer 143

Rupture of an aneurysm or an AVM; rapid time course; Patient complains of worst headache of my life; bloody or yellow (xanthochromic) spinal tap; 2-3 days afterward, risk of vasospasm due to blood breakdown (not visible on CT, treat with nimodipine) and rebleeding (seen on CT)

Question 144

Intraparenchymal hemorrhage

Answer 144

AKA Hypertensive hemorrhage; Most commonly caused by systemic HTN; Also seen with amyloid angiopathy, vasculitis, and neoplasm; Typically occurs in the basal ganglia and internal capsule (charcot-bouchard aneurysm of lenticulostriate vessels), but can be lobar

Question 145

What is the time table of histologic events after a ischemic stroke

Answer 145

12-48 hours you get Red neurons; 24-72 hours you get necrosis + neutrophils; 3-5 days you get macrophages; 1-2 weeks you get reactive gliosis + vascular proliferation; >2 weeks you get glial scars

Question 146

Ischemic stroke: what areas are susceptible to damage

Answer 146

irreversible damage starts at 5 minutes; | most vulnerable areas are the hippocampus, neocortex, cerebellum, watershed areas;

Question 147

Hemorrhagic stroke

Answer 147

Intracerebral bleeding, often due to HTN, anticoagulation, and cancer (abnormal vessels can bleed); may be secondary to ischemic stroke followed by reperfusion (increased vessel fragility); Basal ganglia are most common site of intracerebral hemorrhage

Question 148

Ischemic Stroke: what is it

Answer 148

Acute blockage of vessels leading to disruption of blood flow causing ischemia; results in liquefactive necrosis;

Question 149

How do you treat ischemic strokes

Answer 149

Treatment- tPA (if within 3 to 4.5 hr of onset and no hemorrhage/risk of hemorrhage). Reduced risk with medical therapy (e.g. aspirin, clopidogrel)

Question 150

What are the types of ischemic strokes

Answer 150

1) Thrombotic-due to a clot forming directly at the site of infarct (commonly at MCA); 2) Embolic-an embolus from another part of the body obstructs a vessel, can affect multiple vascular territories, often cardioembolic; 3) Hypoxic-due to hypoperfusion or hypoxemia, common during cardiovascular surgery, tends to affect watershed areas;

Question 151

Transient ischemic attacks

Answer 151

Brief, reversible episode of focal neurologic dysfunction

Question 152

Ventricular system: the flow of CSF

Answer 152

Lateral ventricle dumps into the 3rd ventricle via right and left interventricular foramina of Monro; 3rd vent. dumps into 4th vent via cerebral aqueduct of Sylvius; 4th dumps in to subarachnoid space via 2 foramina of Luschka (Lateral) and 1 foramen of Magendie=Medial;

Question 153

How is CSF made and reabsorbed

Answer 153

Made by the ependymal cells of the choroid plexus; | reabsorbed by arachnoid granulations in the superior sagittal sinus

Question 154

Communicating Hydrocephalus

Answer 154

decreased CSF absorption by arachnoid granulations, which can lead to increased intracranial pressure, papilledema, and herniation (e.g. arachnoid scarring post meningitis)

Question 155

Normal pressure hydrocephalus

Answer 155

Does not result in increased subarachnoid space volume; Expansion of ventricles distorts the fibers of the corona radiata and leads to clinical triad of urinary incontinence, ataxia, and cognitive dysfunction (wet, wobbly, and wacky); treat with ventricle shunt

Question 156

Hydrocephalus ex vacuo

Answer 156

Appearance of increased CSF in atrophy (Alz, advanced HIV, Huntington, Pick disease); Intracranial pressure is normal; triad not seen; Apparent increase in CSF observed in imaging is actually result of decreased neural tissue due to atrophy

Question 157

Noncommunicating hydrocephalus

Answer 157

Caused by structural blockage of CSF circulating within the ventricular system (e.g. stenosis of the aqueduct of Sylvius) leading to increased intracranial pressure leading to bilateral papilladema, nausea/vomiting, nuchal rigidity, mental status change

Question 158

How many spinal nerves do we have

Answer 158

31 spinal nerves; 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal; C1-C7 exit at corresponding vertebra, all others go out one vertebra below

Question 159

Vertebral disc herniation

Answer 159

``` Nucleus pulposus (soft central disc) herniates though the annulus fibrosus (outer ring); usually occurs posterolaterally at L4-L5 or L5-S1 ```

Question 160

Dorsal column sense what

Answer 160

sends ascending pressure, vibration, fine touch, and proprioception;

Question 161

Dorsal column first order neurons

Answer 161

1st order neurons: sensory nerve endings to the cell bodies in the dorsal root ganglia, enters the spinal cord, ascends ipsilaterally in dorsal column; 1st synapse: ipsilateral cuneatus (upper body, arms) or gracilis (lower body, legs) in medulla

Question 162

Dorsal column second and third order neurons

Answer 162

from ipsilateral cuneatus (upper body, arms) or gracilis (lower body, legs) it decussates in medulla then ascends contralaterally in medial lemniscus; second synapse is in the VPL of the thalamus; 3rd order neuron goes to sensory cortex

Question 163

Spinothalamic tract: senses what

Answer 163

Sends ascending-lateral: pain, tempurature and medial: crude touch and pressure;

Question 164

Spinothalamic tract: 1st order neurons

Answer 164

1st order neurons are sensory nerve endings (Adelta and C fibers) to the cell body in dorsal root ganglia where it enters the spinal cord; 1 synapse is in the ipsilateral gray matter of the spinal cord (dorsal horn)

Question 165

Spinothalamic tract: 2nd order neurons

Answer 165

from the synapse in the ipsilateral dorsal horn the 2nd order neuron decussates at the anterior white commissure and ascends contralaterally to the VPL thalamus where it synapses and a 3rd order neuron goes to the sensory cortex

Question 166

Lateral corticospinal tract: sends what

Answer 166

Sends descending voluntary movement of contralateral limbs

Question 167

Lateral corticospinal tract: first order neurons

Answer 167

UMN: cell body in primary motor cortex where it descends ipsilaterally (through internal capsule), most fibers decussate at caudal medulla (pyramidal decussation) where it descends contralaterally; First synapse is in the cell body of the anterior horn in the spinal cord

Question 168

Lateral corticospinal tract: second order neurons

Answer 168

from the anterior horn the LMN (2nd order) leaves the spinal cord and goes to the NMJ

Question 169

Romberg test looks at what

Answer 169

unconscious proprioception; | tests the spinocerebellar and dorsal column pathways

Question 170

Multiple sclerosis is destruction of what in the spinal cord

Answer 170

Due to demyelination; mostly white matter of cervical region; random and asymmetric lesions, due to demyelination; scanning speech, intention tremor, nystagmus

Question 171

Amyotrophic lateral sclerosis: is damage to what

Answer 171

Combined UMN and LMN deficits with NO sensory, cognitive, or oculomotor deficits; Can be caused by defect in superoxide dismutase 1; Commonly presents as fasciculations with eventual atrophy and weakness of hands; fatal; RiLUzole (Lou Gerhrig) is given to decrease presynaptic glutamate release;

Question 172

Complete occlusion of the anterior spinal artery damages what parts of the spinal cord

Answer 172

Spares the dorsal columns and lissauer tract; Every other tract is lesioned at and below the area of the occlusion; The upper thoracic ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below T8

Question 173

Tabes dorsalis affects what

Answer 173

Caused by tertiary syphilis; Results from degeneration (demyelination) of dorsal columns and roots leading to impaired sensation and proprioception and progressive sensory ataxia leading to poor coordination; associated with Charcot joints, shooting pain, Argyll Robertson pupils; See absent DTRs and + romberg

Question 174

Syringomyelia

Answer 174

Syrinx expands and damages anterior white commissure of spinothalamic tract (2nd order neurons) leading to bilateral loss of pain and temp sensation (usually C8 to T1); Seen with Chiari 1 malformations; can expand and affect other tracts

Question 175

Vitamin B12 or Vitamin E deficiency leads to problems with what parts of the spinal cord

Answer 175

Get subacute combined degeneration which is demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts; see ataxic gate, paresthesia, impaired position and vibration sense

Question 176

Poliomyelitis;

Answer 176

Cause by polio virus (Fecal-oral); replicates in the oropharynx and small intestine before spreading via blood to the CNS; Infection causes destruction of cells in the anterior horn of the spinal cord (death of LMNs); Symptoms are LMN signs and general infection signs; Findings: CSF with increased WBCs and slight increase of protein (no glucose change); Virus can be found in stool or throat;

Question 177

Werdnig Hoffmann Disease

Answer 177

AKA spinal muscular atrophy; Congenital degeneration of the anterior horns of the spinal cord leading to LMN lesions; Floppy baby with marked hypotonia and tongue fasciculations, starts eating then gets tired; infantile type has median age of death of 7 months (corticobulbar tract damage leads to respiratory failure); Autosomal recessive

Question 178

Friedreich Ataxia

Answer 178

Autosomal recessive trinucleotide repeat disorder (GAA) on chromosome 9 in gene that encodes frataxin (iron binding protein); leads to impairment in mitochondrial function; degeneration of multiple spinal tracts leads to muscle weakness and loss of DTRs, vibratory sense, proprioception; Friedreich is Fratastic (frataxin): he is your favorite FRAT brother, always STUMBLING, STAGGERING, and FALLING, but has a big heart (hypertrophic cardiomyopathy cause of death); Present in child with kyphoscoliosis

Question 179

Brown Sequard syndrome

Answer 179

Hemisection of spinal cord; Ipsilateral UMN signs below level of the lesion (corticospinal damage); Ipsilateral loss of tactile, vibration, proprioception sense 1-2 levels below lesion (dorsal column damage); Contralateral pain and temp loss below level of lesion (spinothalamic damage); Ipsilateral loss of all sensation at level of lesion; Ipsilateral LMN at level of lesion; If at level T1 will get Horners due to damage of the oculosympathetic pathway

Question 180

Horner Syndrome

Answer 180

Sympathectomy of face; Ptosis (slightly drooping eyelid; superior tarsal muscle); Anhidrosis (absent sweating) and flushing of affected side; Miosis (pupil constriction); Associated with lesion at T1; PAM is horny

Question 181

Track the oculosympathetic pathway

Answer 181

starts in hypothalamus descends with 1st neuron to the lateral horn in T1 where it synapses on 2nd order; 2nd order leaves spinal cord and goes to sympathetic chain where it rises to C2 (at bifercation of common carotid) and synapses on 3rd order; Exits at C2 and innervation of sweat tracts with the external carotid and innervation of eye tracts the internal carotid

Question 182

Notable Dermatomes

Answer 182

C2 is back of head (skull cap) but not face; C3 is the turtleneck; C4 is the low collar shirt; T4 is nipples; T7 is the xiphoid process; T10 is the umbilicus; L1 is inguinal ligament; L4 wraps lateral thigh and covers knee cap; S2, 3, 4; erection and sensation of penile and anal zones

Question 183

Clinical Reflexes

Answer 183

``` Biceps=C5; Triceps=C7; Patella=L4; Achilles=S1; Cremaster reflex=L1, L2; Anal wink=S3, S4 ```

Question 184

Moro reflex

Answer 184

Hang on for life reflex; | abduct/extend limbs when startled, and then draw together

Question 185

Rooting reflex

Answer 185

Movement of head toward one side if cheek or mouth is stroked; nipple seeking

Question 186

Sucking reflex

Answer 186

sucking response when roof of mouth is touched

Question 187

Palmar reflex

Answer 187

Curling of fingers if palm is stroked

Question 188

Galant reflex

Answer 188

Stroking along one side of the spine while newborn is face down; causes lateral flexion of lower body toward stimulated side

Question 189

Pineal gland function

Answer 189

Melatonin release; | Circadian rhythms

Question 190

Superior colliculi

Answer 190

Conjugate vertical gaze center; | Remember that your eyes are SUPERIOR to your ears

Question 191

Inferior Colliculi

Answer 191

Auditory; | Remember that your eyes are SUPERIOR to your ears

Question 192

Parinaud syndrome

Answer 192

Paralysis of conjugate vertical gaze due to lesion in superior colliculi (e.g. pinealoma)

Question 193

CN III does what

Answer 193

``` Oculomotor nerve; Eye movement; pupillary constriction (sphincter pupillae: Edinger-Westphal nucleus, muscarinic receptors); Accommodation, Eyelid opening (levator palpebrae) ```

Question 194

Cranial nerve reflexes: Corneal reflex

Answer 194

Afferent: V1 ophthalmic (nasociliary branch); Efferent: VII (temporal branch: orbicularis oculi)

Question 195

Cranial nerve reflexes: Lacrimation

Answer 195

Afferent is the V1 (loss of reflex does not preclude emotional tears); Efferent: VII

Question 196

Cranial nerve reflexes: Jaw Jerk

Answer 196

Afferent is V3 (sensory- muscle spindle from masseter); | Efferent is V3 (motor-masseter)

Question 197

Cranial nerve reflexes: Pupillary

Answer 197

Afferent is II; | Efferent is III

Question 198

Cranial nerve reflexes: Gag

Answer 198

Afferent is IX (ipsilateral); | Efferent is X (bilateral)

Question 199

CN VII innervates what muscles

Answer 199

Facial movement; Orbicularis oculi (eye closing); Stapedius of ear

Question 200

What muscles doe CN IX innervate

Answer 200

Swallowing, Stylopharyngeus (elevates pharynx, larynx)

Question 201

Nucleus Solitaris

Answer 201

Visceral Sensory information which is taste, baroreceptors and gut distention; Sensory=Solitaris CN VII, IX, and X

Question 202

Nucleus Ambiguus

Answer 202

Motor innervation of pharynx, larynx, and upper esophagus (e.g. swallowing, palate elevation); CN IX, X, XI (cranial portion); aMbiguus=Motor

Question 203

Dorsal motor nucleus

Answer 203

``` Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI; CN X ```

Question 204

How does this structure exit the Skull: CN I

Answer 204

cribiform plate

Question 205

How does this structure exit the Skull: CN II

Answer 205

Through sphenoid bone (optic canal)

Question 206

How does this structure exit the Skull: ophthalmic artery

Answer 206

Through sphenoid bone (optic canal)

Question 207

How does this structure exit the Skull: Central retinal vein

Answer 207

Through sphenoid bone (optic canal)

Question 208

How does this structure exit the Skull: CN III

Answer 208

Superior Orbital fissure of the sphenoid bone

Question 209

How does this structure exit the Skull: CN IV

Answer 209

Superior Orbital fissure of the sphenoid bone

Question 210

How does this structure exit the Skull: V1

Answer 210

Superior Orbital fissure of the sphenoid bone

Question 211

How does this structure exit the Skull: VI

Answer 211

Superior Orbital fissure of the sphenoid bone

Question 212

How does this structure exit the Skull: ophthalamic vein

Answer 212

Superior Orbital fissure of the sphenoid bone

Question 213

How does this structure exit the Skull: parasympathetic fibers

Answer 213

Superior Orbital fissure of the sphenoid bone

Question 214

How does this structure exit the Skull: CN V2

Answer 214

Foramen Rotundum in the sphenoid bone

Question 215

How does this structure exit the Skull: CN V3

Answer 215

Foramen Ovale in the sphenoid bone

Question 216

How does this structure exit the Skull: Middle Meningeal Artery

Answer 216

Foramen spinosum in the sphenoid bone

Question 217

How does this structure exit the Skull: CN VII

Answer 217

Internal acoustic meatus

Question 218

How does this structure exit the Skull: CN VIII

Answer 218

Internal acoustic meatus

Question 219

How does this structure exit the Skull: CN IX

Answer 219

Jugular Foramen

Question 220

How does this structure exit the Skull: CN X

Answer 220

Jugular Foramen

Question 221

How does this structure exit the Skull: CN XI

Answer 221

Jugular Foramen

Question 222

How does this structure exit the Skull: Jugular Vein

Answer 222

Jugular Foramen

Question 223

How does this structure exit the Skull: CN XII

Answer 223

Hypoglossal Canal

Question 224

How does this structure exit the Skull: Spinal roots of XI

Answer 224

Foramen magnum

Question 225

How does this structure exit the Skull: Vertebral Arteries

Answer 225

Foramen Magnum

Question 226

What Passes through this structure: Optic Canal

Answer 226

CN II, ophthalamic artery, central retinal vein

Question 227

What Passes through this structure: Superior Orbital Fissure

Answer 227

CN III, CN IV, V1, VI, ophthalmic vein, sympathetic fibers

Question 228

What Passes through this structure: Foramen Rotundum

Answer 228

CN V2

Question 229

What Passes through this structure: Foramen Ovale

Answer 229

CN V3

Question 230

What Passes through this structure: Foramen spinosum

Answer 230

Middle Meningeal artery

Question 231

What Passes through this structure: Internal Auditory Meatus

Answer 231

CN VII, VIII

Question 232

What Passes through this structure: Jugular Foramen

Answer 232

CN IX, X, XI, Jugular Vein

Question 233

What Passes through this structure: Hypoglossal Canal

Answer 233

CN XII

Question 234

What Passes through this structure: Foramen Magnum

Answer 234

Spinal roots of CN XI, Brain stem, vertebral arteries

Question 235

Cavernous Sinus

Answer 235

A collection of venous sinuses on either side of the pituitary; blood from eye and superficial cortex drains to the cavernous sinus and then into the internal jugular vein

Question 236

Cavernous Sinus: what is it in

Answer 236

CN III, IV, V1, V2 and VI and postganglionic sympathetic fibers en route to the orbit all pass through the cavernous sinus; Cavernous portion of internal carotid artery is also here; Think of it as the nerves of eye movement plus V1 and V2

Question 237

Cavernous sinus syndrome

Answer 237

Due to mass effect, fistula, thrombosis; ophthalmoplegia and decreased corneal and maxillary sensation with normal visual acuity; CN VI commonly affected

Question 238

CN V motor lesion

Answer 238

Jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle

Question 239

CN X lesion

Answer 239

Uvula deviates away from side of lesion; | weak side collapses and uvula points away

Question 240

CN IX lesion

Answer 240

Weakness turning head to contralateral side of lesion (SCM); Shoulder droop on side of lesion (trapezius); The left SCM contracts to help turn the head to the right

Question 241

CN XII lesion (LMN)

Answer 241

Tongue deviates toward side of lesion ("lick your wounds") due to weakened tongue muscles on the affected side

Question 242

Bones of middle ear

Answer 242

Malleus, incus, and stapes

Question 243

Inner ear

Answer 243

Snail shaped, fluid filled cochlea; contains basilar membrane that vibrates secondary to sound waves; Vibration transduced via specialized hair cells to the auditory nerve signaling to the brainstem; low frequency is heard at apex near helicotrema (wide, flexible); High frequency heard best at base of cochlea (thin, rigid)

Question 244

Rinne and Weber test for Conductive hearing loss

Answer 244

Rinne test is abnormal (bone > air); | Weber Test localized to the affected side

Question 245

Rinne and Weber test for Sensorineural hearing loss

Answer 245

Normal Rinne test (Air > Bone); | Weber test localizes to unaffected ear

Question 246

Noise-induced hearing loss

Answer 246

Damage to sterocilliated cells in organ of Corti; Loss of high frequency hearing 1st; Sudden extremely loud noises can produce hearing loss die to tympanic membrane rupture

Question 247

Facial Lesions: UMN lesion

Answer 247

Lesion of motor cortex or connection between cortex and facial nucleus; Contralateral paralysis of lower face; Forehead spared due to bilateral UMN innervation

Question 248

Facial Lesions: LMN lesion

Answer 248

Ipsilateral paralysis of upper and lower face

Question 249

Facial Lesions: Facial nerve palsy

Answer 249

Complete destruction of the facial nucleus itself or its branchial efferent fibers (facial nerve proper); Peripheral ipsilateral facial paralysis (drooping smile) with inability to close eye on affected side; Can occur idiopathically, or with lyme disease, herpes simplex, herpes zoster, sarcoidosis, tumors and diabetes; Treatment includes corticosteroids

Question 250

Mastication muscles

Answer 250

3 muscles Masseter, teMporals, Medial pterygoid; 1 opens the mouth-Lateral Pterygoid; All innervated by V3; M's Munch and Lateral Lowers

Question 251

Hyperopia

Answer 251

Eye too short for refractive power of cornea; Light focused behind the retina; Farsightedness

Question 252

Myopia

Answer 252

Eye too long for refractive power of cornea and lens leading to the light focusing in front of retina; Nearsightedness

Question 253

Astigmatism

Answer 253

Abnormal curvature of cornea resulting in different refractive power at different axes;

Question 254

Presbyopia

Answer 254

Decrease in focusing ability during accommodation due to sclerosis and decreased elasticity

Question 255

Uveitis

Answer 255

Inflammation of anterior uvea and iris, with hypopyon (sterile pus), accompanied by conjuctival redness; Often associated with systemic inflammatory disorders (sarcoid, RA, Juvenile idiopathic arthritis, TB, HLA-B27 PAIR disorders)

Question 256

Retinitis

Answer 256

Retinal edema and necrosis leading to scar; often viral (CMV, HSC, HZV); associated with immunosuppression

Question 257

Central retinal artery occlusion

Answer 257

Acute, painless, monocular vision loss; | Retina cloudy with attenuated vessels and cherry-red spot at fovea

Question 258

Retinal vein occlusion

Answer 258

Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis; Retinal hemorrhage and edema in affected area

Question 259

Diabetic retinopathy: pathophysiology

Answer 259

Non-proliferative: damaged capillaries leak blood so lipids and fluid seep into retina and you see hemorrhages and macular edema (treat with macular laser and better glucose control); Proliferative is chronic hypoxia results in new blood vessel formation with resultant traction on retina (treat with anti-VEGF injections)

Question 260

Glaucoma

Answer 260

Optic disc atrophy with characteristic cupping, usually with increased intraocular pressure and progressive peripheral visual field loss

Question 261

Open angle glaucoma

Answer 261

Associated with increased age, African American race, family history; Painless, more common in U.S.; Primary- Cause unclear; Secondary- Blocked trabecular meshwork from WBC (e.g. uveitis), RBCs (vitreous hemorrhage), retinal elements (e.g. retinal detachment

Question 262

Closed/Narrow angle glaucoma

Answer 262

Primary- enlargement or forward movement of lens against central iris (pupil margin) leads to obstruction of normal aqueous flow through pupil so fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork; Secondary- hypoxia from retinal disease (e.g., diabetes, vein occlusion) induces vasoproliferation in iris that contracts angle;

Question 263

Chronic closure of glaucoma

Answer 263

often asypmtomatic with damage to optic nerve and peripheral vision

Question 264

Acute angle closure of glaucoma

Answer 264

true ophthalmic emergency; increased IOP pushes iris forward causing angle to close abruptly; very painful, sudden vision loss, halos around lights, rock hard eye, frontal headache; do not give epinephrine because of its mydriatic effect

Question 265

Cataract

Answer 265

Painless, often bilateral, opacification of lens leading to decreased vision; Risk factors are increased age, smoking, EtOH, excessive sunlight, prolonged corticosteroid use, classic galactosemia, galactokinase deficiency, diabetes (sorbital), trauma, and infections

Question 266

Papilledema

Answer 266

optic disc swelling (usually bilateral) due to increased ICP; enlarged blind spot and elevated optic disc with blurred margins seen on fundoscopic exam

Question 267

CN IV damage

Answer 267

motor to superior oblique; patient's eye moves upward, particularly with contralateral gaze and head tilt toward the side of the lesion (problems going down stairs, may present with compensatory head tilt in the opposite direction)

Question 268

Miosis

Answer 268

constriction, parasympathetic; 1st neuron: Edinger Westphal nucleus to ciliary ganglion via CN III; 2nd Neuron: short ciliary nerves to pupillary sphincter muscles;

Question 269

Mydriasis

Answer 269

Dilation, sympathetic; 1st neuron: hypothalamus to ciliospinal center of Budge (C8-T2); 2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels; 3rd neuron: plexus along internal carotid, through cavernous sinus: enters orbit as long ciliary nerve to pupillary dilator muscles

Question 270

Pupillary light reflex

Answer 270

Light in either retina travels via CN II to pretectal nucleus in midbrain that activates bilaterally the Edinger-Westphal nuclei; Pupils contract bilaterally; So light in one eye causes both eyes to constrict

Question 271

Marcus Gunn Pupil

Answer 271

Afferent pupillary defect due to optic nerve damage or severe retinal injury; decreased bilateral pupillary constriction when light is shone in affected eye relative to unaffected eye; Tested via swinging light reflex

Question 272

Damage to CN III: what areas are affected first

Answer 272

outer layer of CN III is parasympathetic; Inner layer is Motor; so vascular disease that cuts off oxygen affects motor, and compression first hurts parasympathetic (think aneurysm, uncal herniation)

Question 273

Retinal detachment

Answer 273

separation of neurosensory layer of retina (photoreceptors layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina) leading to degeneration of photoreceptors leading to vision loss; May be secondary to retinal breaks, diabetic traction, inflammatory effusions; Often Preceded by posterior vitreous detachment (flashes and floaters) and eventual monocular loss of vision

Question 274

Age related macular degeneration

Answer 274

Degeneration of macula (central area of retina); causes distortion (metamorphopsia) and eventual loss of central vision; Dry (nonexudative, 80%)- deposition of yellowish extracellular material in and beneath Bruch membrane and retinal pigment epithelium (drusen) with gradual decrease in vision, give antioxidants and multivitamin; Wet (exudative, 15%)- rapid loss of central vision due to bleeding secondary to choroidal neovascularization, Treat with anti-VEGF or laser

Question 275

internuclear ophthalmoplegia (INO)

Answer 275

MLF is pair of tracts that allow for crosstalk between CN VI and CN III nuclei; coordinates both eyes to move in same horizontal direction; Highly myelinated; Lesions seen in demyelination; Lesions cause medial rectus on ipsilateral side to not tract, but eyes can converge (medial rectus is working)

Question 276

Alzheimer disease: genetics

Answer 276

old folks and increased risk in down syndrome; Genetics: early onset in APP (Chr 21), Presenilin-1 (Chr 14), presenilin-2 (Chr 1), late onset ApoE4 (Chr 19); ApoE2 (Chr 19) is protective;

Question 277

Histology of Alzheimer disease

Answer 277

Decreased ACh; Extracellular beta amyloid core; Amyloid beta synthesized by cleaving amyloid precursor protein (APP on Chr 21); Neurofibrillary tangles are intracellular hyperphosphorylated tau protein = insoluble cytoskeletal elements, and amount correlates to degree of dementia (worst in hippocampus)' May see amyloid angiopathy which leads to intracranial hemorrhages (parietal lobe is most common)

Question 278

Frontotemporal dementia

Answer 278

Picks disease; dementia, aphasia, parkinsonian aspects; change in personality; Spares parietal lobe and posterior 2/3 of superior temporal gyrus; Pick bodies are spherical tau protein aggregates; Frontotemporal atrophy leading to disinhibition, impaired judgement and personality changes

Question 279

Lewy body dementia

Answer 279

Initially dementia and visual hallucinatinos followed by parkinsonian features; Alpha-Synuclein defect; increased ubiquitin is also present

Question 280

Creutzfeldt-Jakob Disease

Answer 280

Rapidly progressive (weeks to months) dementia with myoclonus ("startle myoclonus"); ataxia; Spongiform cortex; Prions (PrPc transform into PrPsc sheet (beta pleated sheets that are resistant to proteases) AKA 14-3-3 protein; EEG shows recurrent bursts of biphasic and triphasic periodic sharp wave complexes

Question 281

Multiple Sclerosis

Answer 281

Autoimmune inflammation and demyelination of CNS (brain and spinal cord); Patients can present with optic neuritis (sudden loss of vision resulting in Marcus Gunn pupils) internuclear ophthalmoplegia, hemiparesis, hemisensory symptoms, or bladder/bowel incontinence; Relapsing and remitting course; mostly women in their 20s and 30s, most white;

Question 282

Classic triad of MS

Answer 282

Charcot classic triad of MS; 1) Scanning speech; 2) Intention tremor; 3) Nystagmus

Question 283

Multiple Sclerosis: Findings

Answer 283

Increased protein (IgG) in CSF; oligoclonal bands are diagnostic; MRI is gold standard; Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis) with destruction of axons; Multiple white matter lesions separated in space and time

Question 284

Multiple Sclerosis: Treatment

Answer 284

beta-interferon, immunosuppresion, natalizumab; Symptomatic treatment for neurogenic bladder (catheterization, muscarinic antagonists), spasticity (baclofen, GABA receptor agonist), pain (opioids)

Question 285

Acute inflammatory demyelinating polyradiculopathy

Answer 285

most common variant of Guillain-Barre syndrome; autoimmune condition that destroys Schwann cells leading to inflammation and demyelination of peripheral nerves and motor fibers; Results in symmetric ascending muscle weakness/paralysis beginning in lower extremities; Facial paralysis in 50% of cases; Autonomic function may be severely affected (e.g. cardiac irregularities, HTN, or hypotension); Almost all patients survive; the majority recover completely after weeks to months;

Question 286

Acute inflammatory demyelinating polyradiculopathy Findings:

Answer 286

increased CSF protein with normal cell count (albuminocytologic dissociation); increased protein leads to papilledema

Question 287

Acute inflammatory demyelinating polyradiculopathy: associated with what

Answer 287

Associated with infections (campylobacter jejuni and CMV) leads to autoimmune attack of peripheral myelin due to molecular mimicry, inoculations, and stress, but no definitive link to pathogens;

Question 288

Acute inflammatory demyelinating polyradiculopathy: treatment

Answer 288

Treatments are respiratory support, plasmapheresis, IV immune globulins

Question 289

Progressive multifocal leukoencephalopathy

Answer 289

demyelination of CNS due due to destruction of oligodendrocytes; associated with HC virus; seen in 2-4% of AIDS patients (reactivation of latent viral infection); Rapidly progressive, usually fatal; increased risk associated with natalizumab

Question 290

Acute disseminated (postinfectious) encephalomyelitis

Answer 290

Multifocal perivenular inflammation and demyelination after infection (commonly measles or VZV) or certain vaccinations (e.g. rabies, smallpox); MRI shows inflamed white matter of CNS; treat with high dose IV corticosteroids

Question 291

Metachromatic leukodystrophy

Answer 291

autosomal recessive lysosomal storage disease, most common due to arylsulfatase A deficiency; buildup of sulfatides leads to impaired production of myelin sheath; findings are central and peripheral demyelinatino with ataxia, dementia; no treatment

Question 292

Charcot-Marie-Tooth disease

Answer 292

also known as hereditary motor and sensory neuropathy (HMSN); group of progressive hereditary nerve disorders related to the defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath; typically autosomal dominant inheritance pattern and associated with scoliosis and foot deformities (high or flat arches)

Question 293

Krabbe disease

Answer 293

autosomal recessive lysosomal storage disease due to deficiency of galactocerebrosidase; Buildup of galactocerebroside and psychosine destroys myelin sheath; findings are peripheral neuropathy, developmental delay, optic atrophy, globoid cells

Question 294

Adrenoleukodystrophy

Answer 294

X-linked genetic disorder typically affecting males; Disrupts metabolism of very-long fatty acids leading to excessive buildup in nervous system, adrenal gland, and testes; progressive disease that can lead to long-term coma/death and adrenal gland crisis

Question 295

Partial (focal) seizures

Answer 295

Affect 1 area of the brain; most commonly originate in medial temporal lobe; often preceded by seizure aura; can secondarily generalize; Types: 1) simple partial (consciousness intact)-motor, sensory, autonomic, psychic 2) complex partial (impaired consciousness)

Question 296

Generalized seizures

Answer 296

Diffuse; Absence (petit mal)- 3Hz, no postictal confusion, blank stare, no muscle tone loss; Myoclonic-quick, repetitive jerks; Tonic-clonic (grand mal)-alternating stiffening and movement; Atonic-"drop" seizures (falls to floor) and mistaken fainting

Question 297

Cluster headaches

Answer 297

Unilateral; last 15 minutes to 3 hrs; Repetitive brief headaches, excruciating periorbital pain with lacrimation and rhinorrhea, may induce Horner syndrome, more common in males; Treat with inhaled O2 and sumatriptan

Question 298

Tension headache

Answer 298

bilateral and constant; >30 min (4-6 hour); Steady pain, no photophobia, or phonophobia, no aura; treat with analgesics, NSAIDs, acetaminophen, amitriptyline for chronic pain

Question 299

Migraine

Answer 299

Unilateral; lasts 4-72 hrs; Pulsating pain with nausea, photophobia, or phonophobia, may have aura, due to irritation of CN V, meninges, or blood vessels (release of substance P, CGRP, vasoactive peptides); Treat active migraine with triptans, NSAIDs, and prophylactic with propranolol, topiramate, Ca channel blockers, amitriptyline

Question 300

Peripheral Vertigo

Answer 300

more common; inner ear etiology (e.g. semicircular canal debris, vestibular nerve infection, Meniere disease); positional testing leads to delayed horizontal nystagmus

Question 301

Central vertigo

Answer 301

Brain stem or cerebellar lesion (e.g. stroke affecting vestibular nuclei or posterior fossa tumor); Findings with directional change of nystagmus, skew deviation, diplopia, dysmetria; Positional testing leading to immediate nystagmus in any direction; may change directions; focal neurological findings

Question 302

Sturge-Weber Syndrome

Answer 302

Congenital, non-inherited (somatic), developmental anomaly of neural crest derivatives (mesoderm/ectoderm) due to activating mutation of GNAQ gene; Affects small (capillary-sized) blood vessels leading to port-wine stain of the face (non-neoplastic "birthmark" in CN V1/V2 distribution); ipsilateral leptomeningeal angioma leads to seizures/epilepsy; intellectual disability; and episcleral hemangioma leading to increased IOP leading to early onset glaucoma;

Question 303

Tuberous Sclerosis:

Answer 303

``` HAMARTOMAS: Hamartomas in CNS and skin; Angiofibromas; Mitral regurgitation; Ash-leaf spots; cardiac Rhabdomyoma; Tuberous sclerosis; autosomal dOminant; Mental retardation; renal Angiomyolipoma; Seizures and Shagreen patches; increased incidence of subependymal astrocytomas and ungual fibromas ```

Question 304

Neurofibromatosis type 1 (von Recklinghausen disease)

Answer 304

Cafe-au-lait spots, Lisch nodules (pigmented iris hamartomas), neurofibromas in skin, optic gliomas, pheochromocytomas; mutated NF1 tumor suppressor gene (neurofibromas, a negative regulator of Ras) on chromosome 17; skin tumors of NF-1 are derived from neural crest cells

Question 305

von-hippel-Lindau disease

Answer 305

VHL= chromosome 3; Cavernous hemangiomas in skin, mucosa, organs; bilateral renall cell carcinomas; hemangioblastoma (high vascularity with hyperchromatic nuclei) in retina, brain stem, cerbellum, and pheochromocytomas; autosomal dominant; mutated VHL tumor suppressor gene on chromosome 3, which results in constitutive expression of HIF (transcription factor) and activation of angiogenic growth factors

Question 306

Astrocytoma or gliobastoma multiforme

Answer 306

Adult tumor; Common in adult, highly malignant primary brain tumor ~1 year median survival; found in cerebral hemispheres; can cross corpus callosum (butterfly glioma); stain astrocytes for GFAP; Pseudopalisading pleomorphic tumor cells-border central areas of necrosis and hemorrhage

Question 307

Meningioma

Answer 307

Adult tumor; Most common benign, second most common brain tumor; most often occurs in convexities of hemispheres (near surface of brain) and parasagittal region; arises from arachnoid cells, is extra-axial (external to brain parenchyma), and may have a dural attachment (tail); often asymptomatic; may present with seizures or focal neurological signs; resection and/or radiosurgery; spindle cells concentrically arranged in a whorled pattern; psammoma bodies (laminated calcifications); has estrogen receptors and can grow during pregnancy;

Question 308

Hemangiobalstoma

Answer 308

adult tumor; most often cerebellar; associated with von hippel-lindau syndrome when found with retinal angiomas; can produce erythropoietin leading to secondary polycythemia; Closely arranged, thin-walled capillaries with minimal interleaving parenchyma

Question 309

Schwannoma

Answer 309

Adult tumor; usually found at cerebellopontine angle; schwann cell origin; s-100 positive; often localized to CN VIII leading to acoustic schwannoma (aka acoustic neuroma); resectable or treated with stereotactic radiosurgery; bilateral acoustic schwannomas found in NF-2;

Question 310

Oligodendroglioma

Answer 310

``` Adult, relatively rare, slow growing; most often in frontal lobes; chicken-wire capillary pattern; oligodendrocytes=fried egg cells (round nuclei with clear cytoplasm); often calcified in oligodendroglioma; surgically remove but may return ```

Question 311

Pituitary adenoma

Answer 311

Adult cancer most commonly prolactinoma; bitemporal hemianopia due to pressure on optic chiasm; hyper or hypo pituitarism are sequelae;

Question 312

Pilocytic astrocytoma

Answer 312

usually well circumscribed; Children, most often found in posterior fossa (e.g. cerebellum); Cystic and solid on gross exam; may be supratentorial; Rosenthal fibers-eosinophilic, corkscrew fibers; GFAP +; benign, good prognosis

Question 313

Medulloblastoma

Answer 313

highly malignant childhood cerbellar tumor; a form of primitive neuroectodermal tumor; can compress 4th ventricle, causing hydrocephalus; can send "drop metastases" to spinal cord; Homer-Wright rosettes; solid on gross exam; small blue cells on histology

Question 314

Ependymoma

Answer 314

Childhood Ependymal cell tumors most commonly found in 4th ventricle; can cause hydrocephalus; poor prognosis; characteristic perivascular rosettes; rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus

Question 315

Craniopharyngioma

Answer 315

Benign childhood tumor, may be confused with pituitary adenoma (both can cause bitemporal hemianopia); most common childhood supratentorial tumor; derived from remnants of Rathke pouch; Calcification is common (tooth enamel like)

Question 316

Effect on glaucoma: epinephrine

Answer 316

alpha agonist; decrease aqueous humor synthesis via vasoconstriction; Side effects are mydriasis, do not use in closed angle glaucoma

Question 317

Effect on glaucoma: Brimonidine

Answer 317

Alpha 2 agonist; decrease aqueous humor synthesis; side effects are blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

Question 318

Effect on glaucoma: timolog, betaxolol, carteolol

Answer 318

beta blockers; decrease aqueous humor synthesis; side effects are no pupillary or vision changes

Question 319

Effect on glaucoma: acetazolamide

Answer 319

Decrease aqueous humor synthesis via inhibition of carbonic anhydrase; Side effects are no pupillary or vision changes

Question 320

Effect on glaucoma: direct and indirect cholinomimetics

Answer 320

direct-pilocarpine, carbachol; indirect-physostigmine and echothiophate; increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork; Use pilocarpine in emergencies-very effective at opening meshwork into canal of Schlemm; Side effects are miosis and cyclospasm (contraction of ciliary muscles)

Question 321

Effect on glaucoma: Latanoprost (PGF2alpha)

Answer 321

Increased outflow of aqueous humor; | Side effect of darkening color of iris (browning)

Question 322

Opioid analgesics: drug names

Answer 322

morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate;

Question 323

Opioid analgesics: mechanism

Answer 323

act as agonists at opioid receptors (mu= morphine, delta= enkephalin, kappa= dynorphin) to modulate synaptic transmission- open K+ channels, close Ca2+ channels leading to decrease synaptic transmission; Inhibit release of ACh, NE, 5-HT, glutamate, substance P

Question 324

Opioid analgesics: Clinical use

Answer 324

Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone)

Question 325

Opioid analgesics: Toxicity

Answer 325

Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs; Tolerance does not develop to miosis and constipation; toxicity treated with naloxone or naltrexone (opioid receptor antagonist)

Question 326

Butorphanol

Answer 326

Mechanism: Mu-opioid receptor partial agonist and kappa-opioid receptor agonist, produces analgesia; Clinical use: severe pain (migraine, labor, etc.), causes less respiratory depression than full opioid agonists; Toxicity: can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors), overdose not easily reversed with naloxone

Question 327

Tramadol

Answer 327

Mechanism: very weak opioid agonist, also inhibits serotonin and NE reuptake (works on multiple neurotransmitters- "tram-it all" in with tramadol); Used in chronic pain; Toxicity: similar to opioids, decreases seizure threshold, serotonin syndrome

Question 328

Ethosuxamide

Answer 328

Used for generalized absence seizures; mechanism- blocks thalamic T type Ca2+ channels; side effects of GI, fatigue, headache, urticaria, steven-johnson, EFGHIJ (ethosuximide causes Fatigue, Gi distress, Headache, Itching, and steven Johnson); SUX to have Silent Seizures

Question 329

Benzodiazepines

Answer 329

Names: diazepam, lorazepam; used for status epilepticus; mechanism: increased GABA-a action (increases frequency of Cl- channel opening); Side effects: sedation, tolerance, dependence, respiratory depression; also used for eclampsia seizure after MgSO4

Question 330

Phenytoin

Answer 330

Used for simple, complex, tonic-clonic, status epilepticus; increased Na+ channel inactivation; zero-order kinetics; Side effects of nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome) SLE-like syndrome, induction of cyp P-450, lymphadenopathy, Steven Johnson, osteopenia

Question 331

Carbamazepine

Answer 331

Used for simple, complex, and tonic-clonic; increased Na+ channel inactivation; Side effects-Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cyp P450, SIADH, steven johnson; 1st line for trigeminal neuralgia

Question 332

Valproic acid

Answer 332

Used for simple, complex, tonic-clonic, and absence seizures; Increased Na+ channel inactivation, increased GABA concentration by inhibiting GABA transaminase; Side effects are GI, distress, rare but fatal, hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy; Also used for myoclonic seizures, bipolar disorder

Question 333

Gabapentin

Answer 333

Simple, Complex, tonic-clonic seizures; Primarily inhibits high voltage-activated Ca2+ channels, designed as GABA analog; side effects sedation and ataxia; Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

Question 334

Phenobarbital

Answer 334

used for simple, complex, tonic-clonic seizures; | increased GABAa action (increases the duration of opening Cl channel)

Question 335

Topiramate

Answer 335

For simple, complex and tonic clonic; blocks Na+ channels, increased Gaba action; Side effects are Sedation, mental dulling, kidney stones, weight loss; Also used for migraine prevention

Question 336

Lamotrigine

Answer 336

For simple, complex, tonic-clonic, absence; blocks voltage-gated Na channels; Side effects are steven johnson (titrate slowly)

Question 337

Levetiracetam

Answer 337

For simple, complex, and tonic clonic; | Mechanism is unknown, may modulate GABA and glutamate release

Question 338

Tiagabine

Answer 338

for simple, complex seizures; | increases GABA by inhibiting re-uptake

Question 339

Vigabatrin

Answer 339

Simple and complex seizures; | Increase GABA by irreversibly inhibiting GABA transaminase

Question 340

barbiturates

Answer 340

Names: phenobarbital, pentobarbital, thiopental, secobarbital; Mechanism: facilitate GABAa action by increasing duration of Cl- channel opening, thus decrease neuron firing; Contraindicated in porphyria; Used for: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental); Toxicity: respiratory and cardiovascular depression (Can be fatal); CNS depression (can be exacerbated by EtOH use), dependence, drug interactions (induces cyp P-450), overdose treatment is supportive (assist respiration and maintain BP)

Question 341

Benzodiazepines: names

Answer 341

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam

Question 342

Benzodiazepines: mechanism

Answer 342

Facilitate GABAa action by increased frequency of Cl- channel opening; decrease REM sleep; most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting leading to higher addictive potential)

Question 343

Benzodiazepines: Uses

Answer 343

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

Question 344

Benzodiazepines: toxicity

Answer 344

Dependence, additive CNS depression effects with alcohol; less risk of respiratory depression and coma than with barbiturates; treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

Question 345

Benzo, barbs, and EtOH all bind what

Answer 345

bind the GABAa receptor, which is a ligand-gated Cl- channel

Question 346

Nonbenzodiazepine hypnotics: names

Answer 346

Zolpidem (ambien), Zaleplon, esZopiclone (ZZZs put you to sleep);

Question 347

Nonbenzodiazepine hypnotics: mechanism

Answer 347

act via the BZ1 subtype of the GABA receptor

Question 348

Nonbenzodiazepine hypnotics: Clinical use

Answer 348

insomnia

Question 349

Nonbenzodiazepine hypnotics: Toxicity

Answer 349

ataxia, headaches, confusion; short duration because of rapid metabolism by liver enzymes; unlike older sedative-hypnotics, cause only modest day after psychomotor depression and few amnestic effecs; decreased dependence risk compared to benzodiazepines

Question 350

Nonbenzodiazepine hypnotics: treat toxicity with

Answer 350

Effects reversed by flumazenil

Question 351

Anesthetics-general principles

Answer 351

CNS drugs must be lipid soluble (cross BBB) or be actively transported; Drugs with decreased solubility in blood=rapid induction and recovery times; drugs with increase solubility= increased potency= 1/MAC;

Question 352

what is the minimal alveolar concentration

Answer 352

(of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision)

Question 353

inhaled anesthetics: names

Answer 353

halothane, enflurance, isoflurane, sevoflurane, methoxyflurane, nitrous oxide

Question 354

inhaled anesthetics: effects

Answer 354

Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decrease cerebral metabolic demand)

Question 355

inhaled anesthetics: toxicity

Answer 355

Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (nitrous oxide); can cause malignant hyperthermia

Question 356

Malignant hyperthermia

Answer 356

rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions; treat with dantrolene

Question 357

Barbiturates: intravenous anesthetics

Answer 357

Thiopental-high potency, high lipid solubility, rapid entry into brain; used for induction of anesthesia and short surgical procedures; effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat; decreased cerebral blood flow

Question 358

Benzodiazepines: intravenous anesthetics

Answer 358

Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics; may cause severe postoperative respiratory depression, decreased BP, and anterograde amnesia; treat overdose with flumazenil

Question 359

Arylcyclohexylamines (ketamine)

Answer 359

PCP analogs that act as dissociative anesthetics; block NMDA receptors; cardiovascular stimulants; cause disorietnation, hallucinations, and bad dreams; increase cerebral blood flow;

Question 360

Opioids: intravenous anesthetics

Answer 360

Morphine, fentanyl used with other CNS depressants during general anesthesia

Question 361

Propofol: intravenous anesthetics

Answer 361

Used for sedation in ICU, rapid anesthesia induction, and short procedures; less postoperative nausea than thiopental; potentiates GABAa

Question 362

Local anesthetics: names

Answer 362

Esters (procaine, cocaine, tetracaine); | Amides (Lidocaine, mepivacaine, bupivacaine, (amides have 2 I's))

Question 363

Local anesthetics: mechanism

Answer 363

Block Na channels by binding to specific receptors on inner portion of channel; preferentially bind to activated Na channels, so most effective in rapidly firing neuorns; Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form

Question 364

Local anesthetics: order of nerves they block

Answer 364

small diameter blocked before big; myelinated fibers blocked before unmyelinated fibers; overall, size matters more than myelination; Lose 1)pain then 2) temperature then 3) touch 4) pressure

Question 365

Local anesthetics: Toxicity

Answer 365

CNS excitation, severe cardiovascular toxicity (bupivacaine), HTN, hypotension, and arrhythmias (cocaine)

Question 366

Neuromuscular blocking drugs: depolarizing

Answer 366

Succinylcholine- strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction; reversal of blockade: Phase 1- (prolonged depolarization)-no antidote. Block potentiated by cholinesterase inhibitors; Phase 2- (repolarized but blocked, ACh receptors are available, but desensitized)-antidote consists of cholinesterase inhibitors; Complication include hypercalcemia, hyperkalemia, and malignant hyperthermia

Question 367

Neuromuscular blocking drugs: Nondepolarizing

Answer 367

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium- competitive antagonists-compete with ACh for receptors; Reversal of blockade-neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors

Question 368

Dantrolene

Answer 368

Prevents the release of Calcium from the sarcoplasmic reticulum of skeletal muscle; Uses: used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

Question 369

Parkinson disease drugs: dopamine agonists

Answer 369

Bromocriptine (ergot), pramipexole, ropinirole (non-ergot); | non-ergots are preferred;

Question 370

Parkinson disease drugs: increased dopamine

Answer 370

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity=ataxia; L-dopa/Carbidopa (converted to dopamine in CNS)

Question 371

Parkinson disease drugs: Prevent dopamine breakdown

Answer 371

Selegiline (selective MAO type B inhibitor); | entacapone, tolcapone (COMT inhibitors- prevent L-dopa degradation leading to increased dopamine availability)

Question 372

Parkinson disease drugs: curb excess cholinergic activity

Answer 372

Benztropine (antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia); Park your Benz

Question 373

L-dopa(levodopa)/carbidopa: Mechanism

Answer 373

increased level of dopamine in brain; unlike dopamine, L-dopa can cross BBB and is converted by dope decarboxylase in the CNS to dopamine; carbidopa, an peripheral decarboxylase inhibitor, is given with L-dopa to increased the bioavailability of L-dopa in the brain and to limit peripheral side effects;

Question 374

L-dopa(levodopa)/carbidopa: Clinical use

Answer 374

Parkinson disease

Question 375

L-dopa(levodopa)/carbidopa: toxicity

Answer 375

Arrhythmias form increased peripheral formation of catecholamines; long-term use can lead to dyskinesia following administration ("on/off" phenomenon), akinesia between doses

Question 376

Selegiline

Answer 376

Mechanism: selectively inhibits MAO-B, which preferentially metabolized dopamine over NE and 5-HT, thereby increased the availability of dopamine; Clinic use: adjunctive agent to L-Dopa in treatment of Parkinson disease; Toxicity: may enhance adverse effects of L-dopa

Question 377

Memantine

Answer 377

Alzheimer drug; Mechanism: NMDA receptor antagonists, helps prevents excitotoxicity (mediated by Ca2+); Toxicity: dizziness, confusion, hallucinations

Question 378

Donepexil, galantamine, rivastigmine

Answer 378

Alzheimer drugs; Mechanism: AChE inhibitors; Toxicity: nausea, dizziness, insomnia

Question 379

Neurotransmitter changes in Huntington disease

Answer 379

decreased GABA, Decreased ACh, increased dopamine

Question 380

Medications for Huntington disease

Answer 380

Tetrabenazine and reserpine- inhibit vesicular monoamine transporter (VMAT), limit dopamine vesicle packaging and release; Haloperidol- dopamine receptor antagonist

Question 381

Sumatriptan

Answer 381

Mechanism: 5-HT(1B/1D) agonist; inhibits trigeminal nerve activation, prevents vasoactive peptide release, induces vasoconstriction; half life