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Week 5 Flashcards

1
Q

what are the general clinical feature of CNS tumors

A

Clinical features: focal neurological deficit (usually due to compression), seizures (usually with cerebral cortex), general neuro sx (HA, AMS), increased ICP

Increased ICP tends to be due to: growth of neoplasms, peritumoral edema, secondary changes to neoplasm (cysts, hemorrhage), or obstruction of CSF pathway àbrain herniation

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2
Q

Primary vs Metastatic

regarding CNS tumors

A
  • Metastatic (poor prognosis)
    • Etiology: Metastatic tumors present as multiple, well-circumscribed lesions usually from lung, breast, or kidney tumors
    • Site: cerebellum, cerebrum, vertebral bodies with compression of spinal cord
    • Micro: resembles original tissue
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3
Q

Adult vs Children

CNS tumors

A

Adults usually get supratentorial tumors while children get infratentorial tumors

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4
Q

Craniopharyngioma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: children, but can also be seen in adults
  • Location: suprasellar (origin from Rathke’s pouch) –> can cause bitemporal hemianopsia
  • Micro: crystals found in “motor oil” and calcifications (see pic)
  • Gross: well-defined cystic mass; may be calcified
  • Prognosis: benign; high ten-year survival if small and excised
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5
Q

Neurofibroma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Etiology: genetic (NF1 mutation) or sporadic mutations
  • Location: cutaneous/visceral nerves, spinal roots
  • Micro: S100 positive Schwann cells, NFP-positive axons present; spindle cells with wavy collagen (see pic)
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6
Q

Schwannoma (malignant tumor of Schwann cells)

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: adult
  • Location: anywhere Schwann cells are present; classically at the cerebellar-pontine angle, peripheral nerves, CN VIII (vestibular Schwannoma)
  • Micro: S100 positive, contain compact areas (Antoni A – see star) and loose areas (Antoni B – see arrow), palisading growth pattern (Verocray bodies) is typical of Antoni A
  • Gross: well-defined, compressing surrounding tissue; if bilateral –> NF-2
  • Prognosis: good, treated with surgery
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7
Q

Meningioma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: very common tumor in adults
  • Location: anywhere where arachnoid cells are found (meninges)
  • Micro: proliferation of arachnoid cells; whorling growth (see pic), psammoma bodies
  • Gross: well-defined tan-fibrous mass attached to dura –> compressing adjacent CNS tissue
  • Prognosis: good prognosis; benign; can be excised
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8
Q

Pinealoma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: children
  • Sx: can cause parinaud syndrome (compression of tectum –> vertical gaze palsy), hydrocephalus, precocious puberty in males (beta-HCG production)
  • Micro: looks like testicular seminoma/germ cell tumor
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9
Q

Hemangioblastoma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: adult; associated with von-Hippel-Lindau syndrome with retinal angiomas
  • Location: cerebellum
  • Micro: closely arranged thin-walled capillaries; produces EPO –> secondary polycythemia
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10
Q

Medulloblastoma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: children (common tumor in children)
  • Location: cerebellum (esp. vermis)
  • Micro: Homer Wright rosettes (see pic - cells surrounding vessel), small blue cells, synapthophysin (yellow) IHC
  • Gross: well-defined; may extend into 4thventricle/aqueduct/CSF foramina àhydrocephalus
  • Prognosis: highly malignant, but 5 to 10 year survival possible with treatment (surgery/chemo); drop metastasis via CSF to spinal cord possible
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11
Q

Ependymoma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: children or young adults
  • Location: 4thventricle (in children) and caudal end of spinal cord (in young adults)
  • Pathophysiology: due to location, may block CSF flow and spread along CSF pathways àhydrocephalus
  • Micro: perivascular pseduorosettes (see pic - cells surrounding a vessel), rod-shaped blepharoplasts (basal ciliary bodies), ependymal canal seen
  • Gross: well-defined (note location)
  • Prognosis: poor if in ventricle; good if caudal end of spinal cord
  • Treatment: gross total resection with possible radiotherapy
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12
Q

Oligodendroglioma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: adult
  • Etiology: deletions of 1p and 19q chromosomes
  • Location: frontal lobes
  • Micro: round nuclei, clearing of cytoplasm (see pic – fried egg)
  • Gross: calcified circumscribed tumor of white matter
  • Prognosis: favorable if treated (mean survival: ten years)
  • Treatment: surgical excision with or without temozolomide and PCV (procarbazine, lomustine, vinicristine)
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13
Q

Glioblastoma Astrocytoma (Grade IV)

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: 50s to 70s
  • Location: cerebral hemispheres
  • Micro: pseudo-palisading pleomoprhic tumor cells, mitotic figures prevalent, poorly differentiated, GFAP-positive, vascular proliferation (see pic)
  • Gross: ill-defined borders; necrosis, hemorrhage; not homogenous, crosses corpus callousàbutterfly lesion
  • Prognosis: poor (12-month survival); if progression from lower grade àbetter prognosis
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14
Q

Anaplastic Astrocytoma (Grade III)

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: 40s to 60s
  • Location: cerebral hemispheres
  • Micro: highly infiltrative, poorly differentiated, increased mitotic activity (see pic), no vascular proliferation
  • Gross: ill-defined edges on MRI
  • Prognosis: mean survival about 3 years
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15
Q

Diffuse Astrocytoma (Grade II)

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: 30s to 40s

Location: cerebral hemispheres

Micro highly infiltrative astrocytic cells (see pic - small dark cells diffusely), no mitotic activity, no vascular proliferation/necrosis

Gross: ill-defined edges on MRI

Prognosis: usually progress to anaplastic astrocytoma or glioblastoma, 6-8 year survival

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16
Q

Pilocytic Astrocytoma

epidemiology, locations, micro, gross, prognosis, tx

A
  • Epidemiology: most common glial neoplasm in children
  • Location: cerebellum and optic nerve pathway/hypothalamus
  • Micro: Rosenthal fibers (see pic - red corkscrew fibers), biphasic pattern of density, GFAP-positive, eosinophilic (granular bodies found)
  • Gross: on imaging, cystic lesion with mural nodule (white dot with black around it)
  • Prognosis: benign; excellent prognosis with total excision
  • Treatment: surgical excision
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17
Q
A

Pilocytic Astrocytoma (Grade I)

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18
Q
A

Diffuse Astrocytoma (Grade II)

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19
Q
A

Anaplastic Astrocytoma (Grade III)

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20
Q
A

Glioblastoma Astrocytoma

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21
Q
A

Oligodendroglioma

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22
Q
A

Ependymoma

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23
Q
A

Medulloblastoma

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24
Q
A

Meningioma

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25
Q
A

Schwannoma

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26
Q
A

Neurofibroma

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27
Q
A

Craniopharyngioma

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28
Q

Myasthenia gravis

epidemiology, pathophys

A
  • Epidemiology: women (more common: 20s to 40s), men (40s to 60s); first degree relatives have a higher incidence
  • Pathophysiology: auto-antibodies to post-synaptic Ach receptors → destruction of Ach receptors → weakness of muscles
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29
Q

Myasthenia gravis
sx, dx, tx

A
  • Signs/sx: ptosis → frontalis sign (wrinkling of forehead), diplopia, dysarthria, dysphagia, weakness (improves with rest; worsens with activity), fatigability, nasal (weakness of soft palate), slurred speech (weakness of tongue, lips, and faces; dropped head appearance
    • Associated with thymoma and thymic hyperplasia; ocular involvement is a must
    • NO pupillary dysfunction, cognition, autonomics, or sensory deficits
  • Diagnosis: Ice test (improves ptosis), lab studies (for Ab), Edrophonium/Tensilon (acetylcholinesterase inhibitor), electrodiagnostic study, imaging to exclude thymoma due to hyperthyroidism (can cause ptosis)
  • Treatment: pyridostigmine (AchE inhibitor), prednisone, IVIG, plasmapharesis
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30
Q

Lambert-Eaton Myasthenic Syndrome (LEMS)

A
  • Pathophysiology: autoantibodies to presynaptic Ca channels → decreased Ach release
    • Associated with: paraneoplastic syndrome (i.e. small cell lung cancer)
  • Signs/sx: proximal muscle weakness (improves with use → increased availability of ACh), autonomic sx (dry mouth, impotence)
    • Eyes are spared
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31
Q

Botulism

A
  • Etiology: Clostridium botulinum
  • Pathophysiology: Toxin cleaves SNARE proteins → prevents release of Ach → paralysis
  • Signs/sx: dilated pupils, muscle weakness
  • Diagnosis: EMG (nerve stimulation → increase in muscle fiber contraction)
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32
Q

Polymyositis

sx,dx,tx

A
  • Signs/sx: proximal muscle weakness, speech and swallowing dysfunction
    • NO sensory loss, skin involvement
  • Diagnosis (autoimmune): increased CK, EMG shows myopathic features, + ANA, +anti-Jo-1, +anti-SRP, +anti-MI-2 antibodies
    • Pathology (see pic): endomysial inflammation with CD8+ T-cells;
  • Treatment: steroids (prednisone) with chronic immunosuppressant therapy (methotrexate)
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33
Q

Dermatomyositis

sx, dx, tx

A
  • Signs/sx: proximal muscle weakness, rash on upper eyelids (heliotrope rash), malar rash, red papules on elbows/knuckles/knees (Gottron papules)
  • Diagnosis (autoimmune): increased CK, + ANA, +anti-Jo-1, +anti-SRP, +anti-MI-2 ABs
    • Pathology (see pic): perimysial inflammation (CD4+ T-cells) with perifasicular atrophy
  • Treatment: steroids (prednisone) with chronic immunosuppressant therapy (methotrexate)
34
Q

Inclusion Body Myositis

pathology

A

Pathology: rimmed vacuoles

35
Q

Duchenne Dystrophy

epidemiology, etiology, pathophys

A
  • Epidemiology: males (at birth)
  • Etiology:X-linked frameshift mutation of dystrophin
  • Pathophysiology: deficient dystrophin → lack of binding of intracellular cytoskeleton to transmembrane proteins (alpha-beta dystroglycan) in plasma membrane of muscle → weak connections to extracellular matrix → myonecrosis → muscle weakness
36
Q

Duchenne Dystrophy

sx,dx,tx

A
  • Signs/sx: delayed milestones, waddling gait, enlarged muscles (pseudohypertrophy: fatty depositions), proximal LE weakness weaker than UE, enlarged tongue, scoliosis
    • Other systems: EKG abnormalities/CHF, gastric dilation, intellectual dysfunction
  • Diagnosis: Gower’s sign (standing up from kneed position using arms)
    • Labs: increased CK (50-100x), aldolase increased
    • Electromyography
    • Muscle biopsy: shows type I predominance, fibro-fatty replacement
    • Dystrophin analysis via western blot
  • Treatment: Eteplirsen (Exondys 51) injection, Steroids
37
Q

Becker Dystrophy

etiology,sx,dx

A
  • Etiology: x-linked non-frameshift mutations of dystrophin → truncated protein → see above
  • Signs/sx: similar to DMD, but less severe; survival into 40s to 50s
  • Diagnosis: same as DMD
38
Q

Myotonic Dystrophy

etiology,pathophys

A
  • Etiology: AD inheritance of CTG trinucleotide expansion of DMPK gene on 19q13
    • More repeats = worse disease (anticipation=increased CTG repeats in successive generations)
  • Pathophysiology: Mutation of DMPK gene → abnormal expression of myotonin protein kinase → myotonia (delayed muscle relaxation after contraction)
39
Q

Myotonic Dystrophy

sx,dx,tx

A
  • Signs/sx: myotonia, muscle wasting/weakness, cataracts, cardiac arrhythmias, dysarthria, swallowing difficulty
    • Facial features: long face, temporo-mandibular wasting, ptosis, frontal balding, atrophy of SCM
    • Endocrine abnormalities: diabetes, gynecomastia, testicular atrophy
  • Diagnosis:increased CK, EMG (myotonic discharges – dive bomber), muscle biopsy (type 1 fiber atrophy, increased inernal nuclei – see pic)
  • Treatment
40
Q
A

Polymyositis

41
Q
A

Dermatomyositis

42
Q
A

Inclusion Body Myositis

43
Q
A

Myotonic Dystrophy (most common dystrophy)

44
Q

Peripheral Nerve Disease – General

mononeuropathy, mononeuropathy multiplex, polyneuropathy

A

Mononeuropathy: carpal tunnel syndrome, ulnar nerve neuropathy, peroneal neuropathy,

Mononeuropathy multiplex: at least two different regions with asymmetric nerve deficits

Polyneuropathy: distal, symmetric involvement of nerves in feet>hand in a gradual manner (i.e. diabetes, alcohol, etc)

45
Q

Carpal Tunnel Syndrome

etiology, sx

A
  • Etiology: entrapment of the median nerve at the wrist
    • Associated with: repetitive use of wrist (keyboard/cellphone), RA, pregnancy
  • Signs/sx: numbness/sensory loss in median distribution (distal to thenar region, but not thenar region itself – thumb/index finger), atrophy of thenar eminence, weakness/atrophy of abductor pollicis brevis (abducts thumb)
    • Sensory loss spared in thenar region due to it being innervated by palmar cutaneous branch of the median nerve (branches before carpal tunnel)
    • LOAF muscles: Lumbricals 1 and 2, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis
46
Q

Carpal Tunnel Syndrome

dx,tx

A
  • Diagnosis: Tinel’s sign (percussion to reproduce tingling), Phalen’s (praying stance), EMG/NCV
    • EMG/NCV: indicated prolonged sensory and motor latency (decreased conduction velocity seen in median nerve)
  • Treatment: splints at nighttime (avoid flexion of wrist), steroid injection (outside of tunnel), surgery to open tunnel
47
Q

Ulnar Neuropathy

etiology,sx

A
  • Etiology: entrapment across the cubital tunnel or at the Guyon canal (wrist)
  • Signs/sx: numbness/sensory loss in ulnar distribution (medial two fingers), and weakness of hand intrinsic muscles (interossei muscles, hypothenar eminence, lumbricals 3 and 4), elbow pain
    • In Guyon canal entrapment: sensory loss spared in dorsal surface of medial hand due to it being innervated by dorsal ulnar cutaneous nerve (branches at forearm)
    • In cubital tunnel entrapment: both dorsal and palmar surfaces are lost
48
Q

Ulnar Neuropathy

dx,tx

A
  • Diagnosis: subluxation of nerve across elbow segment (risk factor), Tinnel at elbow, EMG/NCV
    • Measures conductance at wrist, below elbow, and above elbow → determines if Guyon or cubital issue
  • Treatment: splinting to avoid pressure on elbow, steroid injection, surgery (outcomes are less favorable)
49
Q

Peroneal Neuropathy

etiology,sx

A
  • Etiology: crossing legs, excessive weight loss (loss of fat pad cushion at fibular head), fibular neck fracture
  • Signs/sx: footdrop (lesion of deep fibular n → weakness of tibialis anterior), weak eversion (lesion of superficial fibular n → weakness of peroneus longus)
    • Superficial fibular n: dorsum (top) of foot
    • Deep fibular n: between first two toes
50
Q

Guillain-Barre Syndrome (AIDP/GBS)

etiology, pathophys, presentation

A
  • Etiology: demyelinating disease that often occurs post viral illness (campylobacter jejuni)
  • Pathophysiology: autoimmune destruction of Schwann cells → demyelination of peripheral nerves and motor fibers
  • General presentation: acute or subacute weakness developing over hours to weeks
51
Q

Guillain-Barre Syndrome (AIDP/GBS)

sx,dx,tx

A
  • Signs/sx: facial/bulbar weakness (very common), peripheral muscle weakness, respiratory involvement, LMN signs (areflexia, hypotonia, no atrophy), +/- sensory loss, cardiac irregularities, hypotension/hypertension
    • Bell’s phenomenon: tendency of eyes to roll up to show sclera when eyes are shut → can help determine if patient is truly trying to close eyes
  • Diagnosis:
    • CSF: protein increased (may cause papilledema), no increase in WBC (albuminocytologic dissociation)
    • EMG (reveals multifocal demyelination): slowing of conduction velocities, absent/prolonged F response
  • Treatment: supportive, mechanical ventilation if needed, plasmapheresis/IVIG (attacks ABs), NO steroids
52
Q

Root Disease/Radiculopathy

description,sx,dx

A
  • Description: compression of nerve roots leading to motor and/or sensory loss
  • Signs/sx: pain in root distribution, weakness of muscles in associated myotome, sensory loss/numbness (pinprick and light touch) in associated dermatome, hyporeflexia/areflexia
  • Diagnosis: MRI of spine
53
Q

Poliomyelitis

etiology, pathophys,sx,dx

A
  • Etiology: polio virus via feco-oral transmission
  • Pathophysiology: virus replicates in oropharynx → small intestines → bloodstream → CNS → destruction of cells in anterior horn → LMN deficits
    • Werdnig-Hoffman Disease/Spinal Muscular atrophy (autosomal recessive) – “floppy baby”
      • Similar destruction of cells of anterior horn → symmetric weakness
  • Signs: LMN signs (asymmetric weakness, hypotonia, areflexia, fasciculations), respiratory weakness, signs of infection (fever, malaise, HA)
  • Dx: CSF shows increased WBC, slight increase in protein, no change in glucose
54
Q

Amyotrophic Lateral Sclerosis (ALS)

etiology, epidemiologyy, sx,dx,tx

A
  • Etiology: defect in superoxide-dismutase-1 enzyme (some may have genetic incidence)
  • Epidemiology: 40s to 60s; often fatal
  • Signs/sx: UMN and LMN lesions, asymmetric weakness (tends to present with bulbar weakness), dysarthria, dysphagia, fasiculations of limbs/tongue, atrophy of intrinsic hand muscles
    • NO sensory, bladder/bowel, or cognitive deficits
  • Diagnosis: EMG (active and chronic denervation changes in 3 or more muscles)
  • Treatment: Riluzone, Edavarone
55
Q

Parkinson’s Disease

description, etiology,

A
  • Description: loss of dopaminergic neurons in the substantia nigra of the basal ganglia
    • Affects the nigrostriatal pathway of basal ganglia pathway; normally uses dopamine to initiate movement
  • Etiology: unknown, MPTP (contaminant in illict drugs causes Parkinsonian sx)
56
Q

Parkinson’s Disease

sx,dx,complications

A
  • Signs/sx (TRAPS): Tremor (resting), Rigidity (cogwheel), Akinesia (bradykinesia/ expressionless face), Postural instability, Shuffling gait
  • Diagnosis
    • Histology: Lewy bodies
  • Complications: early-onset dementia (Lewy-body dementia – dementia w/ hallucinations)
    • Lewy-body dementia: Lewy-bodies are found in the cortex
57
Q

Huntington’s Disease

descritpion,etiology,pathphys

A
  • Description: degeneration of GABAnergic neurons in the nucleus of the basal ganglia
  • Etiology: AD trinucleotide (CAG) repeat disorder (> 36 repeats) on chromosome 4 of huntingtin gene
    • Anticipation: repeats increase thru generations → disease worsens
  • Pathophysiology: increased CAG repeats → increased glutamine in cells → production of glutamate → Glutamate binding to NMAD-r → Glutamate excitotoxicity in neurons → neuronal death in caudate and putamen (increased lateral ventricle) → excess movement
58
Q

Huntington’s Disease

epidemiology, sx,labs,complications

A
  • Epidemiology: ages 20-50
  • Signs/sx: chorea, athetosis (slow chorea), dementia
  • Labs: increased dopamine, decreased GABA, decreased Ach
  • Complications: death within 10 – 20 years
59
Q

Alzheimer’s Disease

descritption,etiology,risk factors, pathophys

A
  • Description: degenerative disease of cortex, common cause of dementia
  • Etiology:
    • Sporadic form (elderly): ApoE4 (ApoE2 assoc. w/ decreased risk of Alzheimers)
    • Early-onset form (younger): assoc. with APP (chromosome 21), presenilin 1/2
  • Risk Factors: Down Syndrome
  • Pathophysiology: genetic mutation of APP protein → beta cleavage of APP protein → amyloid-beta → forms plaques → disrupts cortical structures
    • Alpha cleavage results in normal amyloid protein → no plaque formation
60
Q

Alzheimer’s Disease

sx,complications,dx

A
  • Signs/sx: slow-onset memory loss (short term → long term), loss of motor skills, language deficits, changes in behavior, neurological deficits not til late, hyperreflexia
  • Complication: mute and bedridden late in disease, infection, intracranial hemorrhage (Amyloid angiopathy: amyloid deposition onto vessels)
  • Diagnosis
    • Gross: narrowing of gyri, widening of sulci, big ventricles (aka cerebral atrophy)
    • Histology:
      • Senile plaques in neurons
      • Neurofibrillary tangles (intracellular hyperphosphorylated tau cytoskeleton proteins → correlated with degree of dementia)
      • Loss of cholinergic neurons → decreased Ach
61
Q

Pick Disease

description,sx,patho

A
  • Description: degenerative disease of the frontal and temporal and frontal cortex
  • Sign/sx: behavioral (behavioral variant) or language (primary progressive aphasia) sx → progressive dementia
    • Associated with parkinsonism/ALS
  • Pathology: hyperphosphorylated tau protein (Pick bodies) in neurons or ubiquitinated TDP43
62
Q

Vascular Dementia

description,etiology,sx,dx

A
  • Description: multi-focal infarctions → dementia (second most common cause)
  • Etiology: HTN, atherosclerosis, vasculitis
  • Signs/sx: stepwise decline in cognitive ability with late onset impairment
  • Dx: MRI/CT shows cortical/subcortical infarcts
63
Q

Normal Pressure Hydrocephalus

pathophys, etiology,sx,tx

A
  • Pathophysiology: increased CSF → dilated ventricles → dementia
  • Etiology: idiopathic
  • Signs/sx: triad of urinary incontinence, gait instability, and dementia (wet, wobbly, and wacky)
  • Treatment: LP, ventriculoperitoneal shunting
64
Q

Idiopathic Intracranial Hypertension (pseudotumor cerebri)

description, risk factors,sx,dx,tx

A
  • Description: increased ICP with no apparent cause on imaging
  • Risk factors: Vit A excess, female, obese, tetracyclines, danazol
  • Signs/sx: HA, CN 6 palsy, papilledema, no AMS
  • Dx: LP (increased opening pressure, relief of HA)
  • Treatment: weight loss, acetazolamide, topiramate, repeat LPs, CSF shunt placement
65
Q

spongiform encephalopathy

description, etiology, pathophys, sx, patho

A
  • Description: rapidly progressive degenerative disease due to prion protein
    • Prion protein normally expressed in CNS neurons in an alpha helical configuration
  • Etiology: disease can be sporadic, inherited, or transmitted
  • Pathophysiology: Prion converted from alpha-helix configuration to beta-pleated formation → pathological proteins convert normal proteins to diseased proteins → cycle of damage to neurons and glial cells → spongy degeneration
  • Signs/sx: cortical signs (speech changes, gait changes, memory loss, personality changes, hyperreflexia)
  • Pathology: sponginess of cortex sparing white matter (bottom part)
66
Q

explain Crueutzfeldt-Jakob Disease (CJD) and Fetal Familial Insomnia

A
  • Crueutzfeldt-Jakob Disease (CJD)
    • Etiology: sporadic
      • Variant CJD: related to bovine spongiform encephalopathy (aka Mad Cow Disease)
    • Signs/sx: rapidly-progressive dementia with ataxia and startle myoclonus
    • Dx: spike wave complexes are found on EEG
    • Complications: death within a year
  • Fetal Familial Insomnia
    • Etiology: inherited
    • Signs/sx: insomnia with exaggerated startle response
67
Q
A

Gray matter in cerebral cortex

Large purple polygonal shaped cells are neuron cell bodies

68
Q
A

White matter in cerebral cortex

  • No neuronal cell bodies found

Many oligodendrocytes (fried-eggs) and astrocytes (spider-appearance)

69
Q
A

Normal anterior horn cell:

Motor neurons are large multipolar cells with abundant Nissi substance (granular substance around nucleus)

70
Q

which is normal? what process is going on?

A

Axonal Reaction

Characterized by central chromatolysis: nucleus of cell body neuron expands and is displaced peripherally, dispersion of Nissi substance, destruction of axon cord àaxonal sprouting

71
Q

which is normal? what happened?

A

Neuronal Degeneration

Reduction in size of neuron due to progressive or degenerative disease (i.e. Alzheimer’s, ALS)

72
Q

whats going on here?

A

Transsynaptic “transneuronal” atrophy: lesion to presynaptic terminal –> postsynaptic cell atrophies

73
Q

what is going on this picture?

A

Eosinophilic neuronal change (acute neuronal injury)

Red staining of neuronal cytoplasm in H&E stain due to hypoxia or ischemia

74
Q

Intraneuronal Accumulations

what is it?

name soe examples?

A

Intraneuronal accumulations: accumulation of material within the nucleus or cytoplasm of neurons due to:

  • Storage diseases (i.e. Tay-Sachs disease)
  • Degenerative disease (Lewy bodies in Parkinson’s disease, neurofibrillary tangles and senile plaques in Alzheimer’s)

Viral inclusions (i.e. Negri bodies in rabies, inclusion bodies in CMV/HSV)

75
Q

name what disease for each pic

A

a. taysachs
b. parkinsons
c. alzheimers
d. rabies
e. alzheimers again…

76
Q

WHAT PROCESS IS GOING ON HERE?

A

Astrogliosis: pathological lesion or old infarct àincreased astrocyte deposition àcyst or cavity formation

  • Ex: Old infract or MS plaques
77
Q

what process is going on here? examples of dieases

A

Oligodendrocytes/Myelin Alterations: destruction of ologiodendrocytes (loss of fried egg appearance with cytoplasmic extensions) àdestruction of myelin

Examples: MS, PML (pink intranuclear inclusions)

78
Q

disease?

A

PML

79
Q

what process is going on here?

A

Microgliosis during acute injury: inflammation and immune response –> phagocytosis of dead cells and cellular debris by macrophages

Microglia will appear elongated and many macrophages will be seen

80
Q

what process is going on here?

A

Ependymal alterations: inflammation or infection of the ventricle –> loss of ependymal cells –> aqueductal stenosis –> congenital hydrocephalus

NBS (8 decks)

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