Week 2 Flashcards

Question

Role of Hypothalamus in Eating Behavior

Answer 1

* Lateral hypothalamus (hunger center) – lesion causes anorexia * Ventromedial hypothalamus (satiety center) – lesion causes obesity

Answer 2

* Arcuate nucleus of hypothalamus – senses systemic hormones via fenestrated capillary → provides input to lateral and ventromedial hypothalamus * Fed: senses leptin (from adipose tissue) and insulin → activates POMC neuron → satiety * Fasting: senses ghrelin (from stomach) and fatty acids → activates AgRP/NPY neurons → hunger

Answer 3

Thirst is a sensation to maintain body fluid homeostasis via ADH release → promote drinking behavior

Answer 4

* Pathway: osmolarity change → osmoreceptor neurons and circumventricular organs (SFO and OVLT) activate → neurons to hypothalamus → * Activates paraventricular nucleus and supraoptic nucleus → release of ADH * Activates median preoptic nucleus → promotes drinking behavior

Answer 5

* Pathway: hypovolemic state → decreased BP → * Activation of RAAS → angiotensin II activates neurons in SFO → neurons to hypothalamus → * Activates paraventricular nucleus and supraoptic nucleus → release of ADH * Activates median preoptic nucleus → promotes drinking behavior * Activation of cardiac and arterial baroreceptors in heart → vagus n. → NTS in medulla → neurons to hypothalamus → median preoptic nucleus → promotes drinking behavior

Answer 6

Sensation via: chemical substances → taste receptors → taste buds (made of taste cells)

Answer 7

* Fungiform papillae (anterior 2/3 of tongue) * Innervation: chorda tympani n. * Circumvallate and foliate papillae (posterior 1/3 of tongue) * Innervation: glossopharyngeal n.

Answer 8

* Innervation: vagus nerve * Types of taste cells: umami, salty, bitter, sour, sweet, fat\*\* * Neural pathway: taste cells → NTS @ medulla → VPM nucleus of thalamus → insular cortex – aka primary gustatory cortex → orbitofrontal cortex (OFC) – aka secondary gustatory cortex

Answer 9

* Functions: enjoying food (flavor), detecting danger (gas leak, spoiled food), recognition (water, alcohol), altering mind/mood (perfume) * \*Olfactory dysfunction is also one of the earliest clinical features in neurodegenerative diseases (i.e. Parkinsons) and depression * Neural pathway: olfactory epithelium → olfactory sensory neuron on olfactory epithelium → olfactory n. → olfactory bulb (ventral brain) → olfactory cortex * Only human sense that bypasses the thalamus

Answer 10

* Geniculate pathway: retinal ganglion cells → optic nerve → optic chiasm → synapse on the lateral geniculate nucleus of thalamus → visual cortex * Info: vision * Extrageniculate pathway: retinal ganglion cells → optic nerve → optic chiasm → superior colliculus * Info: pupillary light reflex, accommodation, sympathetic control of eye

Answer 11

Mainly PCA; MCA has supply to some parts of optic radiations

Answer 12

* Outer nuclear layer: contains nuclei of the photoreceptor * Inner nuclear layer: contains horizontal cells, bipolar cells, and amacrine cells * Ganglion cell layer: contains ganglion cells

Answer 13

Retinal circuit: Light --\> photoreceptor releases glutamate at a slower rate due to hyperpolarization --\> bipolar cell is activated and releases glutamate due to depolarization --\> ganglion cell activated --\> optic nerve --\> optic chiasm --\> visual cortex

Answer 14

* Horizontal cells: connect postganglionic synapses of photoreceptors to modulate signals based on light (gain control – brightness) * Release GABA in order to inhibit activity of photoreceptors and bipolar cells * Amacrine cells: connections between neighboring bipolar cells modulating their actions in inhibitor and excitatory pathways * Release glycine and GABA in order to modulate bipolar and ganglion cell activity

Answer 15

* Cones * Function: provide color vision via 3 types of opsins and function in bright light (photopic) conditions * Red (L – long), Green (M – medium), Blue (S – short) * Cones are concentrated in the fovea (center of retina) and have little convergence (one cone activates one bipolar cell) àlow sensitivity, high acuity (detail) * Fovea: area of highest detail; only contains red and green cones * Rods * Function: provide monochromatic vision and function in low light (scotopic) conditions * Rods are concentrated in the periphery of the retina and have high convergence (many rods activate one bipolar cell) àhigh sensitivity, low acuity

Answer 16

* Pathway: opsin containing cis-rhodopsin + light → trans-rhodopsin transformation → transducin (G-protein) activation → Phosphodiesterase production → decrease in cGMP → closure of Na+ channels and K+ efflux → hyperpolarization of cell → decreased release of glutamate → activation of bipolar cells * Opposite occurs in off-center rods

Answer 17

Description: functions to enhance weak signals by increasing neuronal sensitivity, or it decreases neuronal sensitivity of strong signals to prevent saturating and losing information.

Answer 18

* Contrast (color, edges, etc) is encoded in these ON and OFF pathways. * ON bipolar cells contain mGluR6 receptors and depolarize to light * OFF bipolar cell contain ionotropic (Kainate and AMPA) receptors and hyperpolarize to light * Rod bipolar cells only synapse with rod photoreceptor, and rods signals are sent to ON and OFF pathways in the inner retina through AII amacrine cells

Answer 19

* Parvocellular stream (tonic, high contrast and fine grain, small area, color): Cone driven signals. * Magnocellular Stream (phasic, respond over larger area): Convergence of rod signals

Answer 20

* Genetics: X-linked recessive * Types * Anomalous trichromacy (defective three-color vision) – see all three primary colors, but one is weaker * Protonomaly (L cone defect – red weak), Deteranomaly (M cone defect – green weak), Tritanomaly (S cone defect – blue weak) * Dichromacy (two color vision) – see only two primary color, one is absent * Protanopia (L-cone absent – no red), Deutropanopia (M-cone absent – no green), Tritanopia (S-cone absent – no blue) * Rod monochromacy (no cones at all – no color)

Answer 21

* Epidemiology: elderly * Pathophysiology: progressive loss/death of photoreceptors in macula → loss of fine visual acuity in macula/fovea * Types: * Wet (vascular form) * Tx: Anti-VEGF therapy (block growth of vessels) – ranibizumab, bevacuzimab, aflibercept * Dry (damaged neurons) * Tx: implantable miniature telescope (IMT)

Answer 22

* Genetics: AD, AR, X-linked * Pathophysiology: loss of rod photoreceptors → loss of night vision → eventual blindness * Natural history: presents in childhood, severe disease in adulthood * Dx: ERG

Answer 23

* Open-angle glaucoma (angle where the iris meets the cornea is wide – normal): increased production of vitreous humor or blockage of drainage of vitreous humor at trabecular meshwork → increased pressure in the eye → optic nerve is compressed → blindness * Closed-angle glaucoma: trauma → decreased angle between iris and cornea → inability to drain vitreous humor effectively → increased pressure → optic nerve is compressed → blindness

Answer 24

* Medical: * Alpha adrenergic agonists (reduce aqueous humor production and increases outflow) * Beta blockers (lowers pressure by reducing production of humor) * Carbonic anhydrase inhibitor (eye drops that reduce fluid production in the eye) * Miotics (causes the pupil to constrict and increases drainage) * Prostaglandin analogs (reduces pressure in the eye by increasing outward flow of fluid * Surgery: trabeculoplasty, laser stuff, etc

Answer 25

* Electroretinogram (ERG) * Mechanism: recording of electric potential created by activity of neurons in the retina when light is flashed

Answer 26

* Signs/sx: variable dysfunction of levator palpebrae (drooping eyelid), loss of oculomotor functions (“down and out”) * Etiologies: trauma, infection/inflammation, migraine

Answer 27

* Pupil-involving: * Pathophysiology: aneurysms at PCOM and ICA compress pupillomotor fibers on superficial surface of CNIII * Signs/sx: dilated pupil that responds poorly to light (due to loss of PNS) * Dx: MRA, CTA, angiography (must be performed) * Pupil-sparing: * Pathophysiology: microvascular ischemia of CN3 due to diabetes, HTN, hyperlipidemia * Signs/sx: pain, may resolve within 3 months * Dx: none needed if risk factors align with pathophysiology; pursue if \>3 months

Answer 28

Etiology: congenital, head trauma (CN4 compressed against tentorium cerebelli), microvascular ischemic disease Signs/sx: hypertropia (HT - one eye is higher than the other) that worsens on contralateral gaze and ipsilateral head tilt, patient will present with head tilt contralateral to side of lesion, diplopia with down-gaze

Answer 29

Signs/sx: esotropia (eye pointing more inwards) worse on ipsilateral gaze, unable to abduct ipsilateral to lesion Pathophysiology: microvascular ischemia, elevated ICP, tumor, trauma

Answer 30

* Description: lesion named according to the eye with limited adduction; convergence may be spared * Medial longitudinal fasciculus (MLF) – connects to abducens nucleus to contralateral oculomotor nucleus → conjugate horizontal movement * Description: left lateral eye gaze → contraction of left lateral rectus → firing of left abducens nerve → synapse on right MLF → firing of right CN III nucleus → contraction of right medial rectus → conjugate gaze * Etiology: demyelination, stroke

Answer 31

Etiology: idiopathic Bell’s palsy, infection, tumor, stroke, demyelination, diabetes, trauma Signs/sx: Peripheral: inability to shut affected eye/move forehead; facial droop Central: forehead and orbicularis m. unaffected due to bilateral innervation of forehead; lower-level facial droop

Answer 32

* Etiologies: * Adults: compression (tumor, carotid a. dissection, thyroid mass), trauma, stroke/demyelination * Children: birth trauma, surgical trauma, neruoblastoma * Signs/sx: ptosis (mild), miosis (constriction), anhidrosis (failure of sweat glands) * 1^storder (medullary): ataxia, nystagmus, hemisensory deficit * 2^ndorder (superior sulcus): arm pain, cough, hemoptysis, neck swelling * 3^rdorder: numbness over CN5 distribution and double vision

Answer 33

* Topical cocaine drops: * MOA: inhibits reuptake of norepi in synaptic cleft → dilation of pupils → pupil that does not dilate is deemed to be affected by Horner’s syndrome * Apraclonidine: * MOA: weak alpha1 agonist → * Normal eyes: no effect * Horner’s syndrome eyes: dilation of affected eye more than other eye → reversal of aniscoria (unequal pupils) * Hydroxyamphetamine: * MOA: enhances release of presynaptic norepi from intact 3^rdorder neuron → dilation * In Horner’s syndrome: * If no effect → lesion of 3^rdorder neuron * If pupil dilates → lesion is more proximal (1^stor 2^nd)

Answer 34

Etiologies: traumatic optic neuropathy, ischemic optic neuropathy, glaucoma, retinal detachment (crinkling of retinal tissue), central retinal artery occlusion (cherry red spot) Dx: Swinging flashlight test

Answer 35

* Relative Afferent Pupillary Defect: * MOA: affected eye does not process light at all and remains dilated → unable to send consensual response to the contralateral eye → contralateral eye also remains dilated * Relative Efferent Pupillary Defect: * MOA: affected eye processes light, but is unable to constrict itself → sends consensual response to contralateral eye → contralateral eye successfully constricts

Answer 36

* Imaging: blurred border of optic disc, dilation of capillaries and nerve fibers, hemorrhage * Causes: ischemic optic neuropathy, optic neuritis, papilledema * Papilledema: mass effect → increased ICP → optic disc edema * Etiology: intracranial mass, hydrocephalus, encephalitis, intracranial HTN

Answer 37

* Subdivisions * Sympathetic (thoracolumbar) * Postganglionic NT: norepinephrine * Exception: sweat glands are mediated by ACH * Parasympathetic (craniosacral) * Postganglionic NT: Acetylcholine (ACH) * Enteric NS * Functions * Regulates/coordinates: BP, HR, RR, Temp, sweating, lacrimation, nasal secretion, pupil size, GI motility, bladder contraction * Disorders: Sjogren’s Syndrome, Guillain-Barre Syndrome

Answer 38

* Description: a form of multi-system atrophy * Epidemiology: men in late 50s to early 60s * Sx: autonomic dysfunction (ED, bladder dysfunction, abnormal sweating, constipation, sleep disorder), ataxia, parkinsonism * Signs: orthostatic hypotension, minimal facial expression * Tx: Fludrocortisone (mineralcorticoid àincreases BP), midodrine (stimulant àvasoconstriction), salt tablets, compression stockings * L-dopa does not work

Answer 39

* Description: autonomic failure resulting in orthostatic hypotension and tachycardia when upright * Sx: autonomic dysfunction (GI problems), anxiety (increased levels of epi/norepi), hypotension, tachycardia, hypoperfusion (decresed cerebral flow) * Complications: vasovagal syncope (fainting due to decreased BP) * Rule of B12 deficiency due to similar presentation * Tx: lifestyle changes (fluid, no alcohol, salt, caffeine), Fludrocortisone, beta blockers (lowers HR), miodrine, SSRIs/SNRIs, Methylphenidate/Adderall (increase norepi and dopamine)

Answer 40

* Sudomotor * QSART (Quantitative sudomotor axon reflex test): put dye on patient àwatch for color change as they sweat * TST (thermoregulatory sweat test): put patient in sauna àmeasure sweat * Tests of cardiovagal function * Heart rate response to deep breathing (HRDB) * Vasalva maneuver (pinching nose shut & forcing exhalation against closed airway) * Adrenergic function * BP and HR response to head-up tilt * Beat to beat BP response to Vasalva and DB

Answer 41

* Genetics: autosomal dominant * Mutation: due to repeat expansion of CAG in HTT gene (4p16.3) * Severity based on number of CAG repeats: \>39 (complete penetrance), \<36 (normal) * Pathophysiology: mutant HTT is unable to be cleaved by capsase 2 àtoxic levels of CAG remain àclump together * Testing: PCR (more repeats àbigger fragments àtravel slower) * Symptoms: * Early: irritable/depressed, subtle loss of intellectual ability, balance issues * Late: chorea, seizures, dementia, death (within 18 years of onset)

Answer 42

* Description: a group of 3 distinct genetic disorders (NF1, NF2, Schwanomatosis) that cause tumors to grow in the nervous system * Genetics: autosomal dominant * Mutation: NF1 (tumor suppressor gene – negative regulator of RAS) mutation on 17q11.2 * Pathophysiology: loss of NF1 àunregulated growth of Schwann cells àneurofibroma or Scwannoma (benign) àmalignant progression * Signs: Café au lait spots, neurofibromas, Lisch nodules (in iris of eye), optic nerve tumors, freckling in armpit and groin, epilepsy, bowing of legs * Testing: genetic tests, prenatal testing via amniocentesis or chorionic villus sample

Answer 43

* Description: neurogenetic disease that results in loss of memory * Genetics * Amyloid precursor protein (APP) on chromosome 21 * Presenilin-1, Presenilin-2, ApoLipoprotein E * Epidemiology * Early onset (age 30-60) is rare: autosomal dominant * Late onset (\>60) is common: autosomal recessive

Answer 44

Normal: APP lodges in plasma membrane → secretase-alpha cleaves A-alpha part of cytoplasmic domain → A-alpha becomes important in vital gene transcription Abnormal: APP lodges in plasma membrane → secretase-beta cleaves A-beta part of cytoplasmic domain → A-beta 42 leaves cells → sticks together

Answer 45

* Definition: a sudden onset neurologic deficit from a vascular cause * Risk Factors: * Non-modifiable: age, gender, race, heredity * Modfiable: HTN, atrial fibrillation, dyslipidemia, diabetes, tobacco, carotid stenosis

Answer 46

* Hemorrhagic: vessel rupture leading to intracranial bleeding with progressive onset of deficits accompanies with headaches, nausea, and vomiting * Intracranial hemorrhage (ICH) * Etiologies: HTN, cerebral amyloid angiopathy, tumors, vascular malformations, traumas * Sx: abrupt onset of headache, N/V, neuro sx (based on location) * Subarachnoid hemorrhage (SAH) * Etiologies: trauma, aneurysm, spontaneous * Sx: abrupt onset of worse headache, impaired consciousness, neuro sx (based on location) * Subdural hemorrhage is NOT a type of stroke

Answer 47

* Ischemic: embolism/thrombosis of a vessel that leads to impaired blood supply of the brain with maximal symptoms at onset * Presentation: no pain, neuro sx (based on location of ischemia) * Anterior circulation * Cortical stroke: aphasia, neglect, gaze preference + subcortical sx (arm \>\> leg) * Subcortical stroke (i.e. internal capsule stroke): weakness, sensory loss, dysarthria, visual loss (face = arm = leg) * Posterior circulation: * Symptoms: ataxia, vertigo, cranial nerve findings, impaired consciousness, severe dysarthria, visual loss/diplopia * Presentation: may be crossed findings due to decussations * i.e. Left facial weakness and right arm/leg weakness

Answer 48

* Thrombotic: due to atherosclerotic plaques forming on vessel walls * Risk factors: HTN, DM, dyslipidemia, smoking * Small vessel disease: lacunar arteries near internal capsule * Large vessel disease * Embolic: due to atrial fibrillation, DVT with associated patent foramen ovale, valvular disease, prosthetic valves * Hypoxia: due to hypoperfusion or hypoxia secondary to cardiac surgeries → affects watershed areas (areas most distal to where two major arteries meet) * Other/undetermined * Other: dissection, hypercoagulable states, vasospasms, vasculitis, paradoxical venous embolism, MoyaMoya, hematological disorders * Undetermined: more than two reasons or unknown

Answer 49

* Imaging: * Initial: non-contrast CT scan (ischemic vs hemorrhagic), echocardiogram * CT scan does not show an ischemic stroke early * Later: CT/MRI brain, brain/neck angiogram * Labs: * Initial: blood glucose (stroke presents similarly to hyper/hypoglycemia), pulse ox * Later: HgbA1C, lipid panel, CBC, coagulation studies

Answer 50

* Tissue plasminogen activator (tPA) – administer within first 3-4.5 hours to avoid hemorrhagic risk * MOA: tPA activates plasminogen → plasminogen cleaved to plasmin → plasmin breaks down fibrin to dissolve clots * Contraindications: active bleeding, high risk of bleeding, clotting issues * Intra-arterial devices * Solitatire stent-retriever, penumbra suction catheter, merci retrieveal device

Answer 51

* Prevention strategies (ABCDE): **A**nti-coagulants (aspirin, warfarin, clopidogrel, -xaban drugs, thrombin inhibitors), **B**P meds, **C**holesterol meds (statins), **D**iabetes meds, **E**xercise, **F**umar (stop smoking) * Also: a-fib meds (heparin) if applicable

Answer 52

* Includes: speech therapy (swallowing, language, cognitive function), OT (fine motor and upper extremity coordination), PT (balance and gait, lower extremity coordination) * Types * Inpatient rehab: * Inpatient acute rehab: daily care with services like such as speech therapy, OT, PT (\>3 hours) * Subacute rehab: nursing facility rehab (\<3 hours) * Outpatient rehab: * Traditional outpatient: a single type of therapy * Day program: intense therapy daily until not needed anymore * In-home program: must be home-bound to qualify * Stroke recovery: everyone recovers to a certain degree, but this is patient-dependent * Hyperbolic curve with a plateau * Neurological recovery: * These conditions benefit from rehab: MS, GBS, MG, TBI * Use drugs to complement rehab (i.e. fluoxetine, ACHase inhibitors, dopamine)