Summative Pathologies Flashcards
1
Q
Alternating Hemiplegia
A
Clinical Presentation: contralateral body deficits: spastic paralysis, weakness, loss of touch and proprioception; Ipsilateral facial deficits
MOA: Midline lesions of the brainstem
2
Q
Berry Aneurysm
A
Clinical Presentation: Sudden onset of double vision and severe headache; incomplete adduction and elevation of the eye on affected side
MOA: saccular or intracranial aneurysm
*most common cause of subarachnoid hemorrhage
3
Q
Lateral Medullary Syndrome
A
Clinical Presentation: Ipsilateral - palatal weakness and numbness, facial numbness, Horner’s syndrome and vertigo; Contralateral loss of pain and temperature; ataxia, and dysphagia
MOA: ischemia in the lateral part of the medulla; often due to damage to PICA
4
Q
Bulbar Palsy
A
Clinical Presentation: Dysphagia, difficulty chewing, slurring of speech ,dystonia, dysarthria
MOA: LMN lesion in the medulla or outside the brain stem
*pseudobulbar palsy has the same presentation but is due to UMN damage of corticobulbar tracts in mid pons
5
Q
Abducens Ophthalmoplegia
A
Clinical Presentation: Diplopia; affected eye deviates medially at rest and can’t abduct during lateral gaze
MOA: Paralysis of lateral rectus muscle
6
Q
Trochlear Ophthlamoplegia
A
Clinical Presentation: Affected eye extorts; can’t intort eye; patient tilts head away from lesion
MOA: Trochlear nerve damage
7
Q
Oculomotor Ophthalmoplegia
A
Clinical Presentation: Abduction of affected eye, ptosis, mydriasis
MOA: Oculomotor lesion/damage; disrupts PSYM innervation of pupil
8
Q
Internuclear Ophthalmoplegia
A
Clinical Presentation: Ipsilateral can’t follow contralateral eye when gaze is to contralateral side; nystagmus in the contralateral eye
MOA: Damage to MLF (medial longitudinal fasiculus) which communicates among oculomotor nuclei
Ex: Lesion to L MLF will cause L oculomotor paralysis and L beating nystagmus when looking R
9
Q
Medial Medullary Syndrome
A
Clinical Presentation: Contralateral loss of touch, vibration, and proprioception; contralateral spastic hemiplegia in arm and leg; ipsilateral flaccid paralysis of tongue
MOA: damage to anterior spinal artery which perfuses the medial medulla
10
Q
Medial Pontine Syndrome
A
Clinical Presentation: Contralateral loss of touch, vibration, and proprioception; contralateral spastic hemiplegia in arm and leg; ipsilateral abducens ophthalmoplegia
MOA: Damage to paramedian branches of the basilar artery which perfuses the medial pons
11
Q
Lateral Pontine Syndrome
A
Clinical Presentation: Loss of contralateral pain and temperature sensation; loss of ipsilateral face pain and temperature sensation; ipsilateral Horner’s; ataxia, unsteady gait, fall toward side of lesion; vertigo, nausea, nystagmus, deafness, tinnitus, vomiting; ipsilateral paralysis of masticatory muscles
MOA: Damage to long circumferential branch of basilar artery which perfuses lateral pons
12
Q
Medial Midbrain Syndrome
A
Clinical Presentation: Contralateral loss of touch, vibration, and proprioception; contralateral spastic hemiplegia in arm and leg; UMN paralysis of contralateral lower face and contralateral deviation of tongue protrusion. Ipsilateral ophthalmoplegia with fixed and dilated pupil
MOA: Damage to paramedian branches of the basilar bifurcation and P1 segment of PCA which perfuses the medial midbrain
13
Q
Posterior Cerebral P1 Syndrome
A
Clinical Presentation: Upper alternating hemiplegia, thalamic syndrome
MOA: Damage to P1 segment of PCA
14
Q
Thalamic Syndrome
A
Clinical Presentation: Contralateral hemisensory loss; burning pain in the affected areas, hemiparesis, hemiballismus, choreoathetosis, intention tremor, ataxia
MOA: Damage to thalamogeniculate artery, loss of blood supply to VPM and VPL
15
Q
Werdnig-Hoffman Disease
A
Clinical Presentation: Severe and diffuse weakness, poor feeding, respiratory insufficiency; sparing of facial and oculomotor muscles; reduced or absent deep tendon reflexes
MOA: AR inherited degeneration of the anterior motor horn
*death occurs within a few years after birth; 85% by 17 months
16
Q
Amyotrophic Lateral Sclerosis (ALS)
A
Clinical Presentation:
Lower signs- flaccid paralysis with muscle atrophy, fasciculations, weakness with decreased muscle tone, impaired reflexes, negative Babinski sign
Upper signs - spastic paralysis with hyperreflexia, increased muscle tone, positive Babinski sign
MOA: Degeneration of upper and lower motor neurons of the corticospinal tract; anterior motor horn degeneration leads to lower motor neuron signs; lateral corticospinal tract degeneration leads to upper motor neuron signs
Labs: TDP-43 protein aggregates in motor neurons, corticospinal tract degeneration
*SOD1 (superoxide dismutase) mutation present in some familial cases (leads to free radical injury in neurons); atrophy and weakness of hands is early sign
17
Q
Parkinson Disease
A
Clinical Presentation: TRAP - Tremor at rest, Rigidity in extremities Akinesia/bradykinesia, Postural instability and shuffling gait
MOA: Loss of dopaminergic neurons in the substantia nigra of the basal ganglia; related to aging; unknown etiology
Histo: loss of pigmented neurons in substantia nigra and round eosinophilic inclusions of alpha-synuclein (Lewy bodies)
Tx: L-dopa (administer with carbidopa to minimize peripheral conversion); pallidotomy, deep brain electrical stimulation of GPi and STN
18
Q
Alzheimer’s
A
Clinical Presentation: Slow-onset memory loss, progressive disorientation, loss of learned motor skills and language, behavior and personality changes
MOA: e4 allele of APOE increases risk of sporadic form; beta amyloid plaques from APP processing aggregate; phosphorylated tau aggregate.
Histo: Cerebral atrophy with gyri narrowing; neuritic plaques of A-beta amyloid derived form amyloid precursor protein; neurofibrillary tau tangles; inflammation, Hirano bodies; hydrocephalus
Tx: Donepezil (Aricept) Memantine (Namenda)
*e2 allele of APOE decreases risk of sporadic form
19
Q
Lewy Body Dementia
A
Clinical Presentation: Dementia, fluctuations in cognition and arousal, and visual hallucinations; Parkinsonism; REM sleep behavior disorder
Histo: Intracellular Lewy bodies in cortex; aggregates of alpha-synucleins
*ApoE4 allele is a risk factor
20
Q
Frontotemporal Lobar Degeneration
A
Clinical Presentation: Progressive language deterioration, personality changes
MOA: Atrophy of frontal and temporal lobes
Histo: Many contain tau deposits
21
Q
Pick Disease (Frontotemporal lobe Dementia)
A
Clinical Presentation: Inappropriate social behavior, lack of empathy, distractibility, loss of insight, repetitive or compulsive behavior, decreased motivation, language disturbance
MOA: Degeneration of frontal and temporal lobe; spares parietal and occipital lobe
22
Q
Dementia
A
Clinical Presentation: Cognitive deficits, acquired after age 18, persistent and multiple areas affected
MOA: Four most prevalent causes: Alzheimer’s, Parkinson’s, Vascular Dementia, Diffuse Lewy body dementia
23
Q
Concussion
A
Clinical Presentation: Confusion, headache, balance problems, dizziness, sluggishness, groggy, foggy, amnesia, difficulty paying attention, nausea, vomiting, double/blurry vision, bothered by light or noise
MOA: Strike to head causes rotation of partially tethered brain putting shearing stress on the brain; get transient stretching of axons WITHOUT transection
24
Q
Diffuse Axonal Injury
A
Clinical Presentation: Slow recovery from concussion symptoms; permanent disability
MOA: Torque from strike to the head causes tearing of the axons; often affects midbrain/diencephalon, corona radiata
25
Epidural Hematoma
Clinical Presentation: Cranial nerve III palsy; 80% are in temporal area; rare in infants and elderly
MOA: Collection of blood between dura and the skull; classically due to fracture of temporal bone with rupture of middle meningeal artery
*lens shaped (biconvex) lesion of CT; not crossing suture lines
*herniation of a lethal complication
26
Subdural Hematoma
Clinical Presentation: progressive neurologic signs
MOA: Blood pooling underneath dura and covers the surface of the brain; due to tearing of bridging veins that lie underneath dura and arachnoid usually b/c of trauma
*crescent-shaped lesion of CT that crosses suture lines
*most are lethal: 30-90% mortality
*herniation is a lethal complication
27
Subarachnoid Hemorrhage
Clinical Presentation: Produces blood in CSF; causes severe headache, stiff neck, loss of consciousness
MOA: typically due to rupture of an aneurysm as arteries pass within subarachnoid space
*acute blood lining cortex in subarachnoid space
*one of the only causes of blood pooling at the bottom/base of the brain
28
Chronic Subdural Hemorrhage
Clinical Presentation: Headache, progressive alteration in mental status, focal neuro signs; common in elderly
MOA: Caused by trauma; common in elderly and the brain shrinks causing stretching/stress of bridging veins
*hyper of isodense area on radiology
29
Brain Herniation
Clinical Presentation:
Central herniation - midsize, bilateral non-reactive pupils
Lateral herniation - unilateral dilated non-reactive pupils
MOA: Edematous brain or hematoma causes compression of brain structures (diencephalon, midbrain, pons, medulla)
30
Athetosis
Clinical Presentation: Slow, writhing movements, especially in fingers
MOA: Lesion to basal ganglia
31
Chorea
Clinical Presentation: Sudden, jerky, purposeless movements
MOA: Lesion to basal ganglia
*dopamine blockers, anticholinergics
32
Dystonia
Clinical Presentation: Sustained, abnormal involuntary movements
MOA: Blapharospasm, torticollis, writer's cramp
33
Essential Tremor
Clinical Presentation: High frequency tremor with sustained posture (i.e. outstretched arms)
Tx: non-selective beta blockers; pts often self medicate with alcohol
*worse when anxious or with movement; often familial
34
Hemiballismus
Clinical Presentation: sudden, wild flailing of one arm; may also have flailing of ipsilateral leg
MOA: lesion to contralateral subthalamic nucleus
35
Intention Tremor
Clinical Presentation: Slow, zig zag motion when pointing/extending towards a target
MOA: Cerebellar dynsfunction
36
Akinetic Rigid Syndrome (Parkinsonism)
Clinical Presentation: Bradykinesia/akinesia, rigidity, postural instability
37
Myoclonus
Clinical Presentation: sudden, brief, uncontrolled muscle contraction
38
Resting Tremor
Clinical Presentation: Uncontrolled movement of distal appendages; tremor alleviated by intentional movement
MOA: Parkinson's
39
Rigidity
Clinical Presentation: Sustained muscle contraction at rest (in the absence of any voluntary movement)
40
Spasticity
Clinical Presentation: Little or no contraction at rest
| MOA: Late phase of spinal cord transection; corticospinal lesion
41
Tardive Dyskinesia
Clinical Presentation: Abnormal involuntary movements
| MOA: After the use of dopamine blocking agents
42
Multiple Sclerosis
Clinical Presentation: Neuro deficits with periods of remission; blurred vision in one eye, vertigo, scanning speech, hemiparesis; internuclear ophthalmoplegia; lower extremity loss of sensation or weakness
MOA: Autoimmune destruction of CNS myelin and oligodendrocytes; associated with HLA-DR15
MRI: periventricular plaques (areas of white matter de-myelination); CSF: increased lymphocytes, increased Ig and myelin basic protein; Histo: macrophages, thin myelin
Tx: high dose steroids for acute attacks; interferon beta long term slows progression of disease
43
Acute MS
Clinical Presentation: Affects kids to young adults; mimics a high grade neoplasm
* relatively unresponsive to steroids
* death sometimes in days to weeks
44
Adrenoleukodystrophy
Clinical Presentation: Often occurs in young boys; progressive intellectual and behavioral problems
MOA: Impaired addition of coenzyme A to long chain fatty acids (X-linked mutation of ABCD1 transporter gene); accumulation of fatty acids damages adrenal glands and white matter of brain
Histo: perivascular CD8+ T-lymphocytes; macrophages, adrenal cortical cells, and Leydig cells with trilaminar lipid inclusions; glial scar
45
Acute Disseminated Encephalomyelitis (ADEM)
Clinical Presentation: Rapidly progressive multifocal neuro symptoms; altered mental status; affects children and young adults
MOA: Multifocal periventricular inflammation and demyelination after infection of vaccine; may be auto-immune reaction
Histo: small perivascular foci of myelin loss
Tx: steroids, plasmapheresis, IVIG
46
Progressive Multifocal Leukoencephalopathy
Clinical Presentation: Rapidly progressive neurologic signs (visual loss, weakness, dementia) leading to death
MOA: JC virus infection and destruction of oligodendrocytes (white matter); immune suppression reactivates the latent virus
Histo: Oligodendrocytes with viral inclusions
*typically short course (6-12 months) that leads to death
47
Central Pontine Myelinolysis
Clinical Presentation: Rapid quadriplegia; only eyes move; dysphagia, diplopia, loss of consciousness
MOA: Metabolic demyelination of pons due to rapid osmotic changes (rapid IV correction of hyponatremia, liver transplant, alcoholism)
*occurs in severely malnourished patients (i.e. alcoholics, liver disease)
48
Neuromyelitis Optics (NMO)
Clinical Presentation: Optic neuritis and myelitis; can involve outside the CNS as well
MOA: Autoimmune attack of aquaporin 4 (astrocytic water channel)
MRI: contiguous spinal cord lesion for 3+ segments
Histo: Creutzfeldt cells (macrophages with mitotic figures), thin myelin
49
Acute Hemorrhagic Encephalomyelitis
Clinical Presentation: Abrupt onset of fever, neck stiffness, seizures, cerebral swelling
MOA: Children and young adults after upper respiratory tract infection, vaccine, or drug reaction
*possibly fulminant form of ADEM
50
Alexander Disease
Clinical Presentation:
Young children - seizures, spasticity, megaencephaly, developmental delay
Older patients: brain stem symptoms
MOA: AD inheritance; mutation in GFAP gene
Histo: White matter demyelination, Rosenthal fibers to the max, disorder of astrocytes
51
Conductive Hearing Loss
Impaired conduction of sound through external and middle ear; impacted cerumen, otitis media, otosclerosis
Dx:
Webber test - sound is louder in ear with conductive loss
Rinne test - won't hear when fork is held outside of ear
52
Sensorineural Hearing Loss
Pathology of the inner ear (cochlea, sensory) or CN VIII; Loss of hair cells, perinatal infection, high intensity sounds, ototoxic drugs
Dx:
Webber test - sound quieter in affected ear
53
Presbycusis
Age related; due to the cumulative effect of loud sounds on the ear
Histo: affects higher frequency hair cells first
54
Meniere's Disease
Clinical Presentation: Fluctuating hearing loss, rotational vertigo, tinnitus, aural fullness
Tx: low salt diet and diuretics
55
Tinnitus
Clinical Presentation: Perception of phantom sound that occurs in the absence of actual sound
MOA: Often seems to be of CNS origin; often accompanies cochlear hair cell loss
56
Hollywood Amnesia
Clinical Presentation: Severe long term memory deficit; preserved short term memory
MOA: Is due to psychogenic issue; NOT caused by a neurogenic problem
57
Isolate Amnestic Syndrome
Clinical Presentation: Short term memory loss
MOA: Often idiopathic; can be due to thalamic damage, basilar occlusion, thiamine deficiency, anoxia, or trauma
*usually goes away on its own fairly quickly
58
Korsakoff's Psychosis
Clinical Presentation: Little to no acquisition of new information; impaired retrieval of old memories, confabulation
59
Anophthalmia/Microphthalmia
Clinical Presentation: Absence of an eye or presence of a small eye
MOA: SOX2 and PAX6 gene dysfunction
60
Coloboma
Clinical Presentation: Missing part of the iris
| MOA: Failure of closure of the choroidal fissure; PAX2 mutations in 50%
61
Congenital Cataracts
Clinical Presentation: Clouding of the lens
| MOA: Due to incomplete differentiation of the lens during development
62
Treacher Collins Syndrome (TCS)
Clinical Presentation: Maral hypoplasia (underdevelopment of zygomatic bones): under developed mandible malformed or missing ears, downslanting palpebral fissures
MOA: AD inheritance; due to not enough neural crest cells proliferating and migrating to branchial arches.
63
Pierre Robin Sequence (PRS)
Clinical Presentation: Micrognathia of mandible, cleft palate, glossoptosis (posterior displaced tongue)
MOA: Defect in neural crest cell affecting mandible development; environmental and genetic factos
Tx: Palatoplasty mandibular distraction; avoid respiratory distress
64
DiGeorge Anomaly
Clinical Presentation: CATCH-22. Cardiac outflow tract abnormalities, Abnormal facies, Thymic aplasia, Cleft palate, Hypoparathyroidism, Chromosome 22
MOA: Deletion of long arm of chromosome 22 (22q11) causing errors in the development of the branchial arches
65
Hemifacial Microsomia
Clinical Presentation: Malformed auricle (microtia/anotia);ossicluar malformation, facial muscle asymmetry, hyoid malformation
MOA: Anomaly of development of the second branchial arch
66
First Pouch Anomaly
Clinical Presentation: Eustachian tube dysfunction, recurrent ear infection, absent tympanic cavity, absent mastoid cavity
MOA: Anomaly of development of the first branchial pouch
67
Thyroglossal Duct Cyts
Clinical Presentation: Asymptomatic midline neck mass that may move/elevate with protrusion of the tongue
MOA: Anomaly of development of the 3rd/4th branchial pouch; failure of complete obliteration of the thyroglossal duct
Tx: Remove surgically
*found in 7% of the population
68
Lingual Thyroid
Clinical Presentation: Reddish mass at the base of the tongue
MOA: Complete failure of thyroid descent (anomaly of 3rd/4th branchial pouch development)
Tx: Remove thyroid tissue surgically and use thyroid replacement hormone
69
Type 1 First Cleft Anomaly
Clinical Presentation: Sinus or cyst anterior to ear canal, ends blindly at ear canal, enters ear canal, or middle ear space; lateral to CN VII
MOA: Anomaly of first branchial cleft development
70
Type 2 First Cleft Anomaly
Clinical Presentation: Sinus or cyst at angle of mandible, ends in ear canal, lateral or medial to CN VII
MOA: Anomaly of first branchial cleft development
*more common
71
Second Cleft Anomaly
Clinical Presentation: Painless, fluctuant cyst, sinus, or fistula in anterior triangle
MOA: Anomaly in 2nd branchial cleft development
72
Third/Fourth Cleft Anomaly
Clinical Presentation: Sinus/fistula in lower third of anterior neck that ends in piriform sinus; associated with thyroid gland
MOA: Anomaly in 3rd/4th branchial cleft development
Tx: Hemithyroidectomy, direct laryngoscopy, endoscopic cauterization
73
Broca's Aphasia
Clinical Presentation: Non-fluent speech, comprehension is normal, difficulty repeating words
MOA: Damage to Broca's area (in anterior multi-modal association area), such as due to an MCA stroke/hemorrhage
74
Wernicke's Aphasia
Clinical Presentation: Speech is fluent but nonsensical, distorted comprehension, cannot repeat words
MOA: Damage to Wernicke's area (in posterior multi-modal association area)
75
Conduction Aphasia
Clinical Presentation: Fluent speech, normal comprehension, cannot repeat words
MOA: Damage to the tract connecting Broca's and Wernicke's area
76
Trans-cortical Sensory Aphasia
Clinical Presentation: Fluent speech, poor comprehension, can repeat words
MOA: Disconnection of Wernicke's area from the rest of the multi-modal association area
77
Trans-cortical Motor Aphasia
Clinical Presentation: Non-fluent speech, normal comprehension, can repeat words
MOA: Disconnection of Broca's area from the rest of the multi-modal association area
78
Paranoid Personality Disorder
Group A
| Pattern of irrational suspicion and mistrust of others; interpreting motivations as malevolent
79
Schizoid Personality Disorder
Group A
| Lack of interest and detachment from social relationships; restricted emotional expression
80
Schizotypal Personality Disorder
Group A
Extreme discomfort interacting socially, distorted cognitions and perceptions, behavioral eccentricities, magical thinking
Gross: see compromise of temporal lobe and basal striatothalamic structures
81
Antisocial Personality Disorder
Group B
Pervasive pattern of disregard for violation of the rights of others, lack of empathy
MOA: must first have history of conduct disorder in childhood
*childhood physical, parental marital abuse, poverty, and foster care are associated
82
Borderline Personality Disorder
Group B
Instability in relationships, self-image, identity, behavior, and affect; often leads to self harm and impulsivity
*40-70% have had childhood sexual abuse; see lower volume of hippocampus, LPFC, and cingulate
83
Histrionic Personality Disorder
Group B
| Attention seeking behavior and excessive emotions; seduction/manipulation of others
84
Narcissistic Personality Disorder
Group B
| Pattern of grandiosity, need for admiration, lack of empathy
85
Avoidant Personality Disorder
Group C
| Feelings of social inhibition and inadequacy, extreme sensitivity to negative evaluation, strong social anxiety
86
Dependent Personality Disorder
Group C
| Psychological need to be care for by other people
87
Obsessive Compulsive Personality Disorder
Group C
| Rigid conformity to rules, perfectionism, and control
88
Superior Division of MCA Stroke
Clinical Presentation: Contralateral hemiparesis of face, hand, and arm; contralateral hemisensory deficit of face, hand, and arm; ipsilateral deviation of head/eyes
MOA: Affects the precentral and postcentral gyrus; affects from the waist up
89
Inferior Division of MCA Stroke
Clinical Presentation:
Dominant Hemisphere - Wernicke's aphasia
Non-Dominant Hemisphere - visual field neglect, agitated and confused state; superior quadrantanopsia
MOA: Loss of blood supply to lateral surface of temporal lobe below the lateral sulcus
90
Anterior Cerebral Artery Stroke
Clinical Presentation: Paraplegia of lower extremities; frontal lobe syndrome (abuilia - loss of will power, inability to make decisions, personality change); urinary incontinence
MOA: Motor and sensory cortices lesion affecting lower limb
91
Lenticulostriate Artery Stroke
Clinical Presentation: Contralateral hemiparesis and sensory deficit; contralateral ataxia; contralateral lower face hemiparesis
MOA: Loss of blood to basal ganglia structures; part of head and body of caudate, globus pallidus, putamen, and internal capsule
92
Anterior Spinal Artery Stroke
Clinical Presentation: Medial medullary syndrome
MOA: stroke causes damage to the lateral corticospinal tract, medial lemniscus, and hypoglossal nerve/nucleus in medial medulla
93
Posterior Inferior Cerebellar Artery Stroke
Clinical Presentation: Lateral medullary syndrome (Wallenberg's Syndrome)
MOA: PICA stroke damaging AL fibers, spinal trigeminal tract and nucleus, nucleus ambiguous, descending hypothalamic fibers, vestibular nuclei, inferior cerebellar peduncle, and spinocerebellar fibers in lateral medulla
94
Paramedian Branch of the Basilar Artery Stroke
Clinical Presentation: Medial pontine syndrome
| MOA: Leads to damage to ML, corticospinal fibers, abducens nerve/nucleus found in medial pons
95
Long Circumferential Branch of Basilar Artery Stroke
Clinical Presentation: Lateral pontine syndrome
MOA: Damage to AL fibers, spinal trigeminal tract and nucleus, descending hypothalamic fibers, middle and superior cerebellar peduncles, vestibular and cochlear nerve/nucleus, facial motor nucleus, trigeminal motor/sensory nucleus
96
Paramedian Branch of Basilar Bifurcation Stroke
Clinical Presentation: Medial midbrain syndrome
| MOA: Damage to ML, corticospinal fibers, oculomotor nerve, and corticobulbar fibers
97
Posterior Cerebral Artery Stroke
Clinical Presentation: Contralateral hemianopia with macular sparing
MOA: Occipital cortex or visual cortex lesion
98
Ophthalmic Artery
Painless, ipsilateral blindness (often transient)
99
Internal Carotid Artery
Altered conscious level, contralateral homonymous hemianopia, hemiplegia, hemisensory disturbance; gaze towards side of lesion; ipsilateral Horner's Syndrome
100
Acute Alcoholic Gastritis
Clinical Presentation: Anorexia, epigastric pain, vomiting
| MOA: Alcoholism
101
Acute Alcoholic Pancreatitis
Constant epigastric pain, pain worse after eating, low grade fever, epigastric tenderness
102
Alcoholic Fatty Liver
Clinical Presentation: Tender, enlarged liver, GGTP, AST, and ALT elevated
*reversible in several weeks with abstinence
103
Alcoholic Hepatitis
Jaundice, low grade fever, enlarged, tender liver; persistently elevated AST, ALT, and alkaline phosphate
104
Alcoholic Cirrhosis
Clinical Presentation: Jaundice, elevated AST, ALT, billirubin; ascites, peripheral edema, nodular liver
MOA: Scarring of the liver due to chronic alcohol use
105
Alcoholic Polyneuropathy
Clinical Presentation: Lower, distal extremities affected; sensory and motor deficits; dysesthesia ("burning feet")
MOA: May be due to vitamin B complex deficiency (decreased intake and decreased absorption in small intestines)
Tx: Slow improvement (months to years) with abstinence and vitamins
106
Alcoholic Optic Neuropathy
Clinical Presentation: Bilateral central scotoma and blurred vision
MOA: May be due to vitamin B complex deficiency (decreased intake and decreased absorption in small intestines)
Tx: Reversible with cessation of alcohol and treatment with vitamin B complex
107
Wernicke's Encephalopathy
Clinical Presentation: CN VI paralysis/palsy; truncal ataxia, confusion
MOA: Thiamine deficiency which can cause cerebellar degeneration
108
Karsakoff's Syndrome
Clinical Presentation: Inability to retain new information
Tx: usually irreversible
*often occurs with Wernicke's
109
Marchiafava-Bignami Syndrome
Clinical Presentation: Coma, seizures, quadriparesis
MOA: Demyelination of anterior and posterior corpus callosum
*very rare
*associated with red wine
110
Migraine
Clinical Presentation: Severe pain; unilateral, throbbing quality, nausea, photophobia and phonophobia
MOA: Usually idiopathic; can be neurogenic, vascular or trigeminal
Tx: Analgesics, caffeines, sedatives, anti-emetics, ergotamine, triptans; prophylactic therapy
111
Cluster Headache
Severe, uni-lateral peri-orbital 15-180 in untreated headache; associated with conjunctival injection, lacrimation, rhinorrhea, miosis, ptosis, and eyelid edema
112
Tension Headache
Mild to moderate pain
| Tx: TCAs, SSRIs, SNRIs, analgesics, stress management, exercise
113
Syndrome of Neglect
Clinical Presentation: Inability to respond to stimuli on the contralateral side of the body or the contralateral visual field
MOA: Parietal cortex lesion
114
Apraxia
Clinical Presentation: Difficulty manipulating objects with the contralateral hand
MOA: Parietal cortex lesion
115
Astereognosis
Clinical Presentation: Failure to recognize objects placed in contralateral hand
MOA: Parietal cortex lesion
116
Myasthenia Gravis
Clinical Presentation: Fluctuating weakness with abnormal fatiguability that improves with rest; diplopia and ptosis, dysarthria, dysphagia, dyspnea
MOA: Antibody mediated attach on nicotinic acetylcholine receptors preventing Ach from binding and exciting muscle; inhibits NMJ transmission
Tests: Edroponium test, AchR antibody test (most specific), single fiber EMG (most sensitive)
Tx: Cholinesterase inhibitors, immunosuppression, plasmapheresis, IVIG, thymectomy
117
Vestibular Nerve Lesions
Clinical Presentation: Subject tends to fall towards the side of the lesion; nystagmus to the contralateral side
MOA: Sets up an imbalance in favor of the opposite side
118
Adiadochokinesis (dysdiadochokinesis)
Clinical Presentation: Inability to make rapid, alternating movements
MOA: Lesion to the cerebrocerebellum
119
Acute Cerebellar Ataxia
Clinical Presentation: Inability to walk (severe ataxia), headache
MOA: Can develop in children after an illness, often a viral illness
*considered benign; symptoms often diminish within several weeks
120
Pseudo-tumor Cerebri
Clinical Presentation: Headache developing over weeks or months; episodic blurred or double vision, papilledema
MOA: Increased flow resistance in arachnoid villi or increased dural sinus pressure; poor absorption of CSF in arachnoid granulations
*normal head imaging
121
Giant Cell Arteritis (Temporal Arteritis)
Clinical Presentation: New onset of headaches, temporal artery tenderness, ESR elevated
Histo: Necrotizing arteritis
*can cause blindness
122
Intraparenchymal Hemorrhage
Clinical Presentation: Most often at putamen, thalamus, pons, and cerebellum
MOA: Most often caused by HTN; also by accelerated atherosclerosis, hyaline arteriosclerosis, and Charcot-Bouchard aneurysms
123
Subfalcine Herniation
Central herniation; anterior cerebral artery compression
124
Transtentorial (Uncal) Herniation
CN III compression, PCA compression
125
Schizophrenia
Clinical Presentation: Two or more of the following for at least 6 months: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, negative symptoms
Histo: Enlarged lateral and 3rd ventricle, reduced hippocampus, amygdala, and parahippocampal gyrus, hypoactive frontal lobe, thalamic disorder
Tx: atypical anti-psychotics
126
Schizophreniform Disorder
Same symptoms as schizophrenia but duration is greater than one month and less than 6 months
127
Schizoaffective Disorder
Major depressive, manic, or mixed episode occurring simultaneously with characteristic criterion A symptoms of schizophrenia
128
Delusional Disorder
Non-bizarre delusion of at least one month; without hallucinations, disorganized speech, catatonic behavior, negative symptoms, or bizarre behavior
129
Brief Psychotic Disorder
Delusions, hallucinations, or disorganized speech/behavior for less than a month
Tx: return to full pre-morbid functioning after this brief period
130
Metabolic Coma
Clinical Presentation: Small and reactive pupils, absent fast ocular movements, localized motor response
MOA: Toxic metabolic process causing cortical dysfunction
131
Diencephalic Coma
Clinical Presentation: Small, reactive pupils, intact slow ocular movements, decorticate motor response
MOA: reticular activating system dysfunction or cortical dysfunction
132
Supratentorial Coma
Clinical Presentation:
Early - small reactive pupils, intact slow ocular movements, decorticate motor response
Late - midrange unreactive pupils, abnormal slow ocular movements, decerberate motor response
MOA: Reticular activating system dysfunction or cortical dysfunction
133
Subtentorial Coma
Clinical Presentation: Mid-range unreactive pupils, abnormal slow ocular movements, decerberate motor response
MOA: Reticular activating system dysfunction or cortical dysfunction
134
Psychogenic Coma
Clinical Presentation: Midrange reactive pupils, intact slow and fast ocular movements, localized motor response
135
Creutzfeldt-Jakob Disease
Clinical Presentation: Rapidly progressive dementia with ataxia and startle myoclonus, visual decline, pyramidal dysfunction, akinetic mutism
MOA: Protease resistant prion protein converted to beta Tests: Periodic sharp waves seen on EEG; CSF elevated 14-3-3 protein; MRI increased signal in deep nuclei
Histo: Neuronal loss, gliosis, spongiform change, florid plaques
Tx: no therapies. Results in death
136
Meningitis
Clinical Presentation: Headache, nuchal rigidity, fever; photophobia, vomiting, altered mental status, nausea
MOA: Inflammation of leptomeninges (pia and arachnoid layers) most commonly due to group B strep, E. coli, Listeria monocytogenes, N. meningitidis, Strep pneumonia, H. Influenza, Coxsackievirus, Fungi
CSF: Cloudy, neutrophils, increased pressure, increased protein content, decreased glucose
Dx: made by LP
*complications usually seen with bacterial meningitis
137
Brain abscess
MOA: Can be caused by staph or strep from endocarditis, congenital heart disease, lung infection, or local sinus infection
Histo: Ring enhancing lesion with white matter expansion, gliosis of white matter
*can look like glioblastoma
138
Toxoplasmosis
MOA: T. Gondii protozoan; transferred from cats and their poop
Tests: Necrotic abscesses, free organisms, organisms in cysts; ring enhancing lesion on imaging
*AIDS, organ transplant, malignancy, and those with connective tissue disease are more at risk
139
Cryptococcus Neoformans
Clinical Presentation: Subacute or chronic meningitis; hydrocephalus
MOA: Yeast invades the parenchyma, thickening leptomeninges and hydrocephalus
Histo: Mucoid encapsulated yeasts with India ink or PAS stain
Tx: Fluconazole
*85% of sufferers have debilitating illness
140
Herpes Simplex Encephalitis
Clinical Presentation: Seen in teens and young adults in temporal and inferior frontal lobes
MOA: Usually caused by HSV-1
Histo: chronic inflammatory cells present
Dx: via CSF PCR
141
Poliomyelitis
Clinical Presentation: Flaccid paralysis with muscle atrophy, fasciculations, weakness with decreased muscle tone, impaired reflexes, negative Babinski sign
MOA: Damage to anterior motor horn due to poliovirus infection (an enterovirus)
Histo: Inflammation, neuronophagia of anterior horn cells, no inclusion bodies
142
HIV Encephalitis
Clinical Presentation: Diffuse encephalopathy in subset of late stage AIDS
Histo: Microglial nodules, muti-nucleated giant cells
143
Subacute Sclerosing Panencephalitis
Clinical Presentation: Cognitive decline, spasticity of limbs, seizures
MOA: Persistent infection by altered measles virus; occurs years after infection
Histo: Gliosis, sclerosis, myelin degeneration, viral inclusions, chronic encephalitis, neurofibrillary tangles
144
Bipolar I
Clinical Presentation: Period of abnormally and persistently elevated, expansive or irritable mood lasting one week and 3 or more of the following - inflated self esteem/grandiosity, decreased need for sleep, more talkative, flights of ideas, distractibility, increased goal directed activity
MOA: Glutamate and NE elevation with HPA activation during mania; NE deficiency in depression
Tx: Anticonvulsants, mood stabilizers, lithium, valproic acid, carbamazepine, lamotrigine
145
Bipolar II
Clinical Presentation: Period of abnormally and persistently elevated, expansive or irritable mood lasting 4 days and 3 or more of the following - inflated self esteem/grandiosity, decreased need for sleep, more talkative, flights of ideas, distractibility, increased goal directed activity
MOA: Glutamate and NE elevation with HPA activation during mania; NE deficiency in depression
Tx: Anticonvulsants, mood stabilizers, lithium, valproic acid, carbamazepine, lamotrigine
146
Cyclothymic Disorder
Clinical Presentation: 2 years of numerous hypomanic episodes and depressive episodes; not without symptoms for more than 2 months at a time
Tx: Anticonvulsants, mood stabilizers, lithium, valproic acid, carbamazepine, lamotrigine
147
Major Depressive Disorder
```
5 or more of the following for 2 weeks or more:
- sad/irritable mood
- loss of interest
- change in appetite or body weight
- difficulty sleeping or oversleeping
- loss of energy
- worthlessness
- difficulty concentrating
Tx: Tricyclics, MAOIs, SSRIs, SNRIs
```
148
Persistent Depressive Disorder
2 year duration of depression, more chronic but less severe; poor appetite or oversleeping, insomnia, hypersomnia, low energy or fatigue, low self-esteem, hopelessness
Tx: Tricyclics, MAOIs, SSRIs, SNRIs
149
Rabies
Clinical Presentation: Acute neurological symptoms; brain edema, inflammation
MOA: Virus transported to CNS via intra-axonal transport
Histo: Negri bodies (intra-cytoplasmic inclusions) in Purkinje cells and hippocampus
*fatal in non-immunized hosts
150
Thalamic Pain Syndrome
Clinical Presentation: Initial sensory loss followed by excruciating, intractable pain
MOA: Occlusion of the thalamogeniculate artery which supplies latero-posterior half of the thalamus
151
Prosopagnosia
Inability to recognize faces, still have measurable emotional response to familiar faces
152
Capgrass Syndrome
Consciously able to recognize faces, but no unconscious emotional response to familiar faces
153
Cerebral Amyloid Angiopathy
Collection of amyloid protein leads to alteration of vessel wall structure
Histo: Concentric rings of tissue; stain positive with Congo red stain
154
Arteriovenous Malformation
Vascular malformation
Histo: Tangle of arteries and veins. Have brain tissue in between the vessels
*not resectable
155
Cavernous Angioma
Vascular malformation
Histo: Back to back hyalinized vessels. No brain tissue in between. See hemosiderin deposits.
*resectable
156
Capillary Telangiectasia
Dilated thin walled vessels separated by normal brain
157
Cholesteatoma
Clinical Presentation: Can present with hearing loss or repeated middle ear infections
MOA: Abnormal skin growth in the middle ear behind the eardrum from repeated infections and/or a tear or pulling inward of the eardrum
Tx: Antibiotics and/or surgery
