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Pathology > 10 (part 1) nervous system > Flashcards

10 (part 1) nervous system Flashcards

1
Q

CVA

A

Most common vascular disorder, third leasing cause of death

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2
Q

Risks for CVA

A

Same risks as CAD

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3
Q

CVAs 3 pathos

A

Ischemic thrombus and embolus, hemorrhagic

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4
Q

Ischemic thrombus

A

Thrombi form in intracranial arteries, gradual onset, possibly TIAs first, minimal ICP

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5
Q

TIAs

A

Comparative to angina
Ischemia from partial occlusion (not infarction)
All deficits resolve within 24 hours with no residual dysfunction, USUALLY subside after 1-2 hours

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6
Q

How many thrombosis strokes are preceded by TIA

A

35%

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7
Q

Ischemic embolus

A

From outside brain, usually obstructs at a bifurcation or point of narrowing
Sudden onset, minimal ICP, localized effects

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8
Q

Hemorrhagic Stroke

A

Caused by HTN, aneurysms, bleeding disorders, AV malform
Compresses/displaces brain tissue, with seepage into ventricles, sudden onset (often with activity) ICP present, widespread effects

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9
Q

Patho of CVA

A

Neurons around ischemia area undergo plasma membrane changes resulting in cellular edema resulting in further compression of capillaries, cerebral edema reaches max in 72 hours and takes 2 weeks to subside

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10
Q

Carotid (anterior) CVA

A

Unilateral paralysis
Numbness
Visual disturbances
Monocular blindness

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11
Q

Vertebrobasilar (posterior) CVA

A

Vertigo, visual disturbances, diploplia, paralysis, numbness, dysarthia, ataxia

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12
Q

General S&S of CVA

A

Altered LOC
Walking difficulty
Weakness/numbness on one side of body or in face, arm, grips, legs
Intense headache
Difficulty speaking, comprehending, and/or seeing

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13
Q

ACLS Cincinnati prehospital findings

A

1 of the 3 have 72% chance of ischemic stroke

All 3 85% chance of acute stroke

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14
Q

LAMS

A

Face 1
Grip 1 or 2
Arm strength 1 or 2

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15
Q

Causes of cerebral aneurysms

A

ARteriosclerosis
Congenital abnormality
Embolus
Trauma

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16
Q

Cerebral aneurysms

A

Often at bifurctions in or near circle of willis
Vertebrobasilar arteries
Within carotid system
Often a change in hemodynamics leads to rupture

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17
Q

Saccular (berry) aneurysms

A

Probs due to congenital abnormalities in media of arterial wall, gradually grows over time

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18
Q

Lateral and fusiform aneurysms

A

Diffuse arteriosclerotic changes, most in basilar arteries or terminal portions of internal carotids
Space-occupying lesions, can be due to trauma, rupture causes subarachnoid, intracerebral or combined hemorrhage

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19
Q

S&S of cerebral aneurysm

A 
Severe headache
Vomiting
CNS depression
Meningeal irritation
ICP
CN deficits
Stroke-like manifestations
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20
Q

Warning signs of impending aneurysm rupture

A

Headache, transient unilateral weakness/numbness/speech

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21
Q

AV malmformation

A

Cause of both hemorrhagic and subarachnoid

Congenital that leads to a tangle of thin walled arteries being directly attached to veins

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22
Q

Global ischemia

A

Widespread atherosclerotic narrowing, multiple foci of ishemic necrosis
Over time result in progressive mental deterioration

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23
Q

Bacterial Meningitis infects

A

Primarily pia mater and arachnoid + fluid in subarachnoid space
Involves the ventricles

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24
Q

Causes of bacterial meningitis

A

Meningococcus, pneumococcus, haemophilus influenza
Predisposing factor must be present before bacteria can become blood-borne (prior URT infection)
Method of entering CNS is unclear

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25
Patho of bacterial meningitis
Bacteria irritate and cause vascular changes (congestion and increased perm) so neutrophils migrat to sub arach space, inflamm response mediated in meninges, CSF, and ventricles Purulent exudate is formed and increases rapidly (especially around base of brain and extends to cranial and spinal nerves)
26
Clinical manifestations of bacterial meningitis
Severe general throbbing headache Photophobia, C.N damage, diplopia, tinnitus Neck stiffness, pain and nuchal rigidity (spinal nerve irritation) Projectile vomiting when vomiting center is irritated Fever, confusion, decreased responsiveness
27
Rash of bac meng
Meningococcus septicaemia causes non blanching rash
28
Viral meningitis
Inflamm limited to meninges Caused by mumps, herpes simplex, adenovirus Often undiagnosed Characterized by a lymphocytic exudate in sub arachnoid space
29
Neurosyphilis
Stage 3 of syphilis, can present as chronic meningitis | Meninges infiltrated with lymphocytes and plasma cells, loss of neurons correlates with motor and mental changes
30
Encephalitis
Acute febrile illness of various origins within nervous system involvement Virus - herpes, west nile Bacterial - lyme Parasite - toxoplasmosis (immune suppressed) Can be a complication of systemic viral disease like rabies mono or follow an MMR vaccine
31
Patho of encephalitis
Virus causes widespread nerve degeneration Edema and necrotic areas develop with/without hemorhhage ICP develops and may progress to herniation
32
Clinical manifestations of encephalitis
Fever, delirium, confusion to unconsciousness, ceaser, paresis, paralysis, ICP, involuntary movements
33
Myelitis
Diffuse viral infection of spinal cord
34
Cerebral Abscess
Localized suppurative infection, consists of cavity filled with pus and a capsule composed of glial cells and fibroblasts
35
Gillian-Barre Syndrome AKA
postinfectious polyneuritis Acute idiopathic polyneuropathy Acute infections polyradiculoneuritis
36
Etiology of Gillian-Barre
Precise cause is unknown, autoimmune response precipitated by viral infection or immunization
37
Patho of gillian barre
Periph nerv inflammation Accumulation in periph nerv of lymphocytes Demyelination Axon destruction Mainly efferent fiber effected Usually starts low ext and goes up, spontaenous recovery which goes top down
38
Clinical manifestations of Gillian Barre
Progressive muscle weakness and areflexia in low ext, ascending flaccid paralysis Paresthesia or pain and general muscle aching Speech/vision/resp effected Can be over a few hours or over several days
39
Autonomic nervous impairment from gillian barre
Common Cardiac arrhythmias Labile BP (fast fluctuations of normal to high) Loss of sweating capability
40
Poliomyelitis
Highly contagious polio virus Reproduces in lymphoid tissue (oropharynx and digestive tract) enters CNS, attacks motor nerves of spinal cord and medulla
41
Clinical manifestations of polio
Flu like symptoms | Fever, headache, vomiting, stiff neck, headache, flaccid paralysis
42
Reye's syndrome
Etiology not fully determined, but occurs with viral infection (infleunza) treated with ASA Tylenol OK Pathology occurs within brain and liver
43
Reye's pathology
Noninflamm edema leading to ICP Liver enlargement, fatty changes and progression to failure (without jaundice) Livere enzymes elevated and altered metabolism lead to encephalopathy
44
Reye's syndrome S&S
Manifestation vary in severity | Lethargy, headache, vomiting, diorientation, hyperreflexia, hypervent, ceasers, stupor, coma
45
MS
Progressive CNS demyelination, not involving PNS Degen of previously normal myelin with relative preservation of axons 20-40 years age 2:1 male
46
Patho of MS
Believed to be autoimmune, origins complex with genetic and environmental component Related to dairy intake, climate (sun/temp) epstein-barr virus
47
Theories on patho of MS
T-Cell activity Viral infection creates sensitized T cells to antigen on myelin B lymphocytes trapped in CNS and colonize forming plasma cells which secrete IgG to combat antigens
48
More MS patho
Demyelinating lesions (plaques) form, usually involve white matter, scattered patterns causing variable symptoms Eventually undergo glial scarring with degen of axons (after 20+ years) Axons will transmit slower, progressive loss to permanent disability
49
Clinical manifestations of MS
Initial syndroms followed by remissions and established perm syndromes Most commonly corticospinal, stiffness, slowness, weakness
50
More clinical manifestations of MS
Spastic paraparesis, atxia, bladder dysfunction, paresthesia, CN III - XII dysfunction, eye problems, depression
51
Thiamine (B1) deficiency
B1 essential for neurons energy | Also for acetylcholine
52
Wernicke's is a
B1 deficinecy (wernicke's encephalopathy) goes with korsakoffs pyschocosis
53
Wernicke's
Acute but reversible encephalopathy, Ataxia, eye muscle weakness, mental derangement Korsakoffs (psychosis) in 80% of wernicke's pts, memory disorder
54
Wernicke-korsakoff sydnrome (aka cerebral beriberi)
Triad of ocular function, gait, mental function
55
B12 (isbalamin) has a role in
DNA synthesis RBC maturation facilitation of folate metabolism Erythrocytes
56
B12 deficiency
Uncoordianted movement and sensorimotor peripheral neuropathy with signs of spinal cord disease Demention Depression Pernicious anemia
57
Pellagra
Diarrhea, dermatitis, dementia from niacin (b3) deficiency
58
Acetaldehyde (ETOH) causes
``` HTN Pancreatitis Skeletal muscle regression Liver damage Immune disorders Cerebral atrophy Neuronal cell development in fetus is affected ```
59
ETOH absuers prone to
subdural hematomas
60
Alzheimer characterized by
Atrophy of cortical parts of frontal and temporal parts of brain
61
Patho alzheimer
Protein in cerebral neurons become distorted and twisted forming a neurofibrillary tangle Groups of nerve cells degenerate and coalesce around amyloid core Amyloid deposited in cerebral arteries
62
Possible causes of alzheimers
Loss of neurotransmitter stimulation by choline acetyltrasferase Linked to genetic chromosomal changes Onset usually after 65
63
Clinical manifestations of alzheimers
Forgetfulness, emotional, disoreintation, confusion, decreased concentration abstraction and problem solving Irritability, agitation, restlessness, anxiety, mood swings
64
Parkinson
Disorder of basal ganglia involving dopaminergic nigrostriate, onset after 40 Changes in extrapyramidal motor system of mid brain Dopamine (inhibitory) is decreased in striatum
65
Clinical manifestations of parkinsons
Tremors, rigidity, bradykinesia (slowing) postural instability, tremors/twitching (most prominent in hands), involuntary flexion of head and neck Worsened by emotional stress Short shuffling accelerated steps, 10% have progressive dementia
66
Parkinsons face
Wide-eyed unblinking, staring expression, immobile axial features, drooling from side of mouth
67
Huntington's Disease (chorea)
Rare, genetic, degeneration of basal ganglia and cerebral cortex Onset 40-50 From depletion of GABA which acts inhibitory on dopaminergic neurons
68
Patho of huntington's
Excess of dopaminergic activity in basal ganglial feedback circuit and cerebral cortex (due to lack of GABA) Manifested by hypotonia, hyperkinesia, involuntary, fragmented movements
69
Clinical manifestations of huntington's
Abnormal movements (chorea) progressive dysfunction in intellectual processes (dementia) delusions, depression, impaired memory
70
Amyotrophic Lateral Sclerosis (Lou Gehrigs)
Sporadic motor neuron disease | Occurs between 30-50 years old
71
Amyotrophic definition
"amyotrophic" -progressive wasting (refers to lower motor neuron involvement)
72
Lateral Sclerosis definition
"lateral sclerosis" - scarring of corticospinal tract in lateral spinal column (refers to upper motor neurons)
73
ALS patho
Upper and lower motor neuron degeneration without inflammation Leads to generalized muscle loss and death (from resp function loss)
74
Clinical manifestations of ALS
Weakness (any/all muscles) Paresis (single muscle group, progresses) Not extraocular or heart muscles Progression to paralysis, no remission No mental, sensory or autonomic symptoms present 3-5 years average life Prone to resp problems
75
Types of headaches
Associated with congested sinuses, nasal congestion Temporal headache from TMJ disorder Increased ICP - trauma with edema, TUMAH, meningitis, toxins (ETOH) Migraine Tension Sphenopalatine ganglioneuralgia
76
Migraine
Benign, recurring headache often provoked by trigger | Often prodromal period
77
Migraine triggers
Stress, hunger, weather changes, foods, sunlight and often accompanied by neurologic dysfunction
78
Prodromal period of migrains
Aura, hallucinations, nausea
79
Pain of migraine
Throbbing, severe, ca be incapacitating | Begins in temporal regions and spreads to entire head
80
Symptoms of migraine
Pain, visual disturbances, dizziness, nausea, abdo discomfort, fatigue Last for 24 hours with long recovery periods
81
Patho of migraines
May be due to abnormalities in cerebral blood (constriction then dilation) Have have a reduction in brain and electrical activity, or increase release of serotonin
82
Tension headache
``` Most common Onset in teens Bilat, mild to moderate steady pain Persist for days or weeks Possibly vomiting ```
83
Tension headache etiologies
Hypersensitivity of pain fibers (trigeminal nerve) | Spasms of neck muscles which pulls down scalp
84
Two types of neoplastic disorders (headaches)
Primary - origination from cerebral tissue itself. Rarely metastasize, but may have multiples. Gliomas most common category (from neurolgia or glial cells) Secondary- metastasis from either the breast or lungs
85
Histology neoplastic disorders
Astrocytes, oligodendrolgia, pineal, benign vs malignant
86
Brain stem and cerebellar tumors in young children
Researching focusing on prenatal parental exposure to carcinogens
87
Tumors in mid adult life
Cerebral hemisphere most common | Predisposing factors not established
88
Some risk factors for CNS neoplasms
Genetics, ionizing radiation (10x risk, glial tumors 3-7x) Cell phones, high voltage wires, hair dyes, trauma, dietary n-nitrosourea *all have conflicting evidence
89
Malignant tumors
Have no definitive margins, invasive invaginations
90
Neoplasms patho
Malignant primary tumors have no definitive margins, surrounding tissue becomes inflamed, contributes to pressure Obstruction of CSF production and flow at >5 ICP
91
Clinical manifestations of neoplasms
Depend on location Small tumors of stem or pituitary immediately alter function Large tumors of cortex can grow without symptoms Eventually, headache from minor to severe and more frequent Vomiting Lethargy Irritability Personality/behaviour changes Seizure - focal to generalized Brainstem or cerebral tumors can affect cranial nerves

Pathology (24 decks)

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