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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
Q

Patho of bacterial meningitis

A

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)

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26
Q

Clinical manifestations of bacterial meningitis

A

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

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27
Q

Rash of bac meng

A

Meningococcus septicaemia causes non blanching rash

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28
Q

Viral meningitis

A

Inflamm limited to meninges
Caused by mumps, herpes simplex, adenovirus
Often undiagnosed
Characterized by a lymphocytic exudate in sub arachnoid space

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29
Q

Neurosyphilis

A

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

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30
Q

Encephalitis

A

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

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31
Q

Patho of encephalitis

A

Virus causes widespread nerve degeneration
Edema and necrotic areas develop with/without hemorhhage
ICP develops and may progress to herniation

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32
Q

Clinical manifestations of encephalitis

A

Fever, delirium, confusion to unconsciousness, ceaser, paresis, paralysis, ICP, involuntary movements

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33
Q

Myelitis

A

Diffuse viral infection of spinal cord

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34
Q

Cerebral Abscess

A

Localized suppurative infection, consists of cavity filled with pus and a capsule composed of glial cells and fibroblasts

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35
Q

Gillian-Barre Syndrome AKA

A

postinfectious polyneuritis
Acute idiopathic polyneuropathy
Acute infections polyradiculoneuritis

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36
Q

Etiology of Gillian-Barre

A

Precise cause is unknown, autoimmune response precipitated by viral infection or immunization

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37
Q

Patho of gillian barre

A

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
Q

Clinical manifestations of Gillian Barre

A

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
Q

Autonomic nervous impairment from gillian barre

A

Common
Cardiac arrhythmias
Labile BP (fast fluctuations of normal to high)
Loss of sweating capability

40
Q

Poliomyelitis

A

Highly contagious polio virus
Reproduces in lymphoid tissue (oropharynx and digestive tract)
enters CNS, attacks motor nerves of spinal cord and medulla

41
Q

Clinical manifestations of polio

A

Flu like symptoms

Fever, headache, vomiting, stiff neck, headache, flaccid paralysis

42
Q

Reye’s syndrome

A

Etiology not fully determined, but occurs with viral infection (infleunza) treated with ASA
Tylenol OK
Pathology occurs within brain and liver

43
Q

Reye’s pathology

A

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
Q

Reye’s syndrome S&S

A

Manifestation vary in severity

Lethargy, headache, vomiting, diorientation, hyperreflexia, hypervent, ceasers, stupor, coma

45
Q

MS

A

Progressive CNS demyelination, not involving PNS
Degen of previously normal myelin with relative preservation of axons
20-40 years age
2:1 male

46
Q

Patho of MS

A

Believed to be autoimmune, origins complex with genetic and environmental component
Related to dairy intake, climate (sun/temp) epstein-barr virus

47
Q

Theories on patho of MS

A

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
Q

More MS patho

A

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
Q

Clinical manifestations of MS

A

Initial syndroms followed by remissions and established perm syndromes
Most commonly corticospinal, stiffness, slowness, weakness

50
Q

More clinical manifestations of MS

A

Spastic paraparesis, atxia, bladder dysfunction, paresthesia, CN III - XII dysfunction, eye problems, depression

51
Q

Thiamine (B1) deficiency

A

B1 essential for neurons energy

Also for acetylcholine

52
Q

Wernicke’s is a

A

B1 deficinecy (wernicke’s encephalopathy) goes with korsakoffs pyschocosis

53
Q

Wernicke’s

A

Acute but reversible encephalopathy,
Ataxia, eye muscle weakness, mental derangement
Korsakoffs (psychosis) in 80% of wernicke’s pts, memory disorder

54
Q

Wernicke-korsakoff sydnrome (aka cerebral beriberi)

A

Triad of ocular function, gait, mental function

55
Q

B12 (isbalamin) has a role in

A

DNA synthesis
RBC maturation
facilitation of folate metabolism
Erythrocytes

56
Q

B12 deficiency

A

Uncoordianted movement and sensorimotor peripheral neuropathy with signs of spinal cord disease
Demention
Depression
Pernicious anemia

57
Q

Pellagra

A

Diarrhea, dermatitis, dementia from niacin (b3) deficiency

58
Q

Acetaldehyde (ETOH) causes

A 
HTN
Pancreatitis
Skeletal muscle regression
Liver damage
Immune disorders
Cerebral atrophy
Neuronal cell development in fetus is affected
59
Q

ETOH absuers prone to

A

subdural hematomas

60
Q

Alzheimer characterized by

A

Atrophy of cortical parts of frontal and temporal parts of brain

61
Q

Patho alzheimer

A

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
Q

Possible causes of alzheimers

A

Loss of neurotransmitter stimulation by choline acetyltrasferase
Linked to genetic chromosomal changes
Onset usually after 65

63
Q

Clinical manifestations of alzheimers

A

Forgetfulness, emotional, disoreintation, confusion, decreased concentration abstraction and problem solving
Irritability, agitation, restlessness, anxiety, mood swings

64
Q

Parkinson

A

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
Q

Clinical manifestations of parkinsons

A

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
Q

Parkinsons face

A

Wide-eyed unblinking, staring expression, immobile axial features, drooling from side of mouth

67
Q

Huntington’s Disease (chorea)

A

Rare, genetic, degeneration of basal ganglia and cerebral cortex
Onset 40-50
From depletion of GABA which acts inhibitory on dopaminergic neurons

68
Q

Patho of huntington’s

A

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
Q

Clinical manifestations of huntington’s

A

Abnormal movements (chorea) progressive dysfunction in intellectual processes (dementia) delusions, depression, impaired memory

70
Q

Amyotrophic Lateral Sclerosis (Lou Gehrigs)

A

Sporadic motor neuron disease

Occurs between 30-50 years old

71
Q

Amyotrophic definition

A

“amyotrophic” -progressive wasting (refers to lower motor neuron involvement)

72
Q

Lateral Sclerosis definition

A

“lateral sclerosis” - scarring of corticospinal tract in lateral spinal column (refers to upper motor neurons)

73
Q

ALS patho

A

Upper and lower motor neuron degeneration without inflammation
Leads to generalized muscle loss and death (from resp function loss)

74
Q

Clinical manifestations of ALS

A

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
Q

Types of headaches

A

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
Q

Migraine

A

Benign, recurring headache often provoked by trigger

Often prodromal period

77
Q

Migraine triggers

A

Stress, hunger, weather changes, foods, sunlight and often accompanied by neurologic dysfunction

78
Q

Prodromal period of migrains

A

Aura, hallucinations, nausea

79
Q

Pain of migraine

A

Throbbing, severe, ca be incapacitating

Begins in temporal regions and spreads to entire head

80
Q

Symptoms of migraine

A

Pain, visual disturbances, dizziness, nausea, abdo discomfort, fatigue
Last for 24 hours with long recovery periods

81
Q

Patho of migraines

A

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
Q

Tension headache

A 
Most common
Onset in teens
Bilat, mild to moderate steady pain
Persist for days or weeks
Possibly vomiting
83
Q

Tension headache etiologies

A

Hypersensitivity of pain fibers (trigeminal nerve)

Spasms of neck muscles which pulls down scalp

84
Q

Two types of neoplastic disorders (headaches)

A

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
Q

Histology neoplastic disorders

A

Astrocytes, oligodendrolgia, pineal, benign vs malignant

86
Q

Brain stem and cerebellar tumors in young children

A

Researching focusing on prenatal parental exposure to carcinogens

87
Q

Tumors in mid adult life

A

Cerebral hemisphere most common

Predisposing factors not established

88
Q

Some risk factors for CNS neoplasms

A

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
Q

Malignant tumors

A

Have no definitive margins, invasive invaginations

90
Q

Neoplasms patho

A

Malignant primary tumors have no definitive margins, surrounding tissue becomes inflamed, contributes to pressure
Obstruction of CSF production and flow at >5 ICP

91
Q

Clinical manifestations of neoplasms

A

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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