Class 8 chapter 37 Flashcards Preview

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Flashcards in Class 8 chapter 37 Deck (68)
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1
Q

Hypoxia and Ischemic Injury

A

Focal cerebral ischemia

Global ischemia

2
Q

Focal Cerebral Ischemia

A

Short term
Typical causes - thrombus/embolism
“Zone of penumbra” without infarction

3
Q

Global Ischemia

A

Loss of Consciousness
Release of “excitatory” amino acid neurotransmitters
Disruption of calcium balance
Formation of free radicals
Mitochondrial injury
ATP malfunction = “power failure” = edema

4
Q

Vulnerable Areas in the Brain

A

“Water-shed” areas

  • At limits of cerebral blood flow
  • Fragile, vulnerable
  • Result in focal defects

Segments of short arteries supplying cerebral cortex = Laminar necrosis

5
Q

Excitatory Amino Acid Injury

A

Neuron injury results in release and activation of mediators that overstimulate cell receptors
- Amino acids (glutamate), catecholamines, free radicals etc

Glutamate attaches and opens calcium channels leading to “calcium cascade” into cells

  • Protein breakdown
  • Free radical formation
  • DNA fragmentation
  • Mitochondrial injury
  • Cell death
6
Q

Cerebral Edema

A

Vasogenic (vessel)

Cytotoxic

7
Q

Vasogenic cerebral edema

A

Leaking of water/proteins into ISS (interstitial space)
Causes: hemorrhage, meningitis, injury, tumours
White matter more so (not as dense as gray – more blood vessels)
Result: herniation, focal defects, increased ICP (intracranial pressure), altered LOC

8
Q

Cytotoxic cerebral edema

A
Increased ICF (intracellular fluid)
Causes: water intoxication, impaired K/Na pump
Result: cell rupture with damage to surrounding tissue, increased ICP
9
Q

Monro-Kellie Hypothesis

A
Tissue - 80% (most stable)
Blood - 10% (less stable)
CSF - 10% (less stable)
Compliance!
An increase in one will cause a decrease in the other
10
Q

Increased Intracranial Pressure (ICP)

A

Compartment syndrome in the skull

  • Intracranial pressure greater than arterial blood pressure
  • Arteries collapse; blood flow to brain cut off

Compliance = change in volume (divided by) change in pressure

Tissue: tumour, edema, bleed
Blood: vasodilation, obstruction of outflow
CSF: increased production, decreased absorption, obstruction

Results in hypoperfusion, hypoxia, cell damage = decreased LOC, coma

Cushing Reflex – late signs of ICP

  1. Hypertension
  2. Widening pulse pressure
  3. Reflex bradycardia

Treatment - decreasing CO2 levels (vasodilator)

11
Q

Increased Intracranial Pressure (ICP) manifestations

A
Changes in LOC
Papilledema
Impaired eye movement
Decreased sensory/motor function
Vomiting
Headache
Pupillary changes
Changes in VS (increased BP, decreased P, changes in reap pattern)
Infants - bulging fontanels, cranial suture separation, increased head circumference, high pitched cry
12
Q

Brain Herniation

A

Increased intracranial pressure pushes the brain out of position
Brain tissue is compressed into the center of the brain, against bone or against rigid folds of the dura mater
Compression of the oculomotor nerve is an early sign

13
Q

Hydrocephalus

A

Increased CSF volume enlarges ventricles and compresses brain tissue

Non-communicating/Obstructive
- Congenital malformations, tumors, inflammation, hemorrhage = CSF blockage

Communicating

  • Impaired reabsorption of CSF via arachnoid villi d/t infection, scarring, blockage by lyzed RBCs post repair of bleed
  • Increased production of CSF (rare)

Manifestations

  • Fontanel bulging fetus/newborn
  • Signs of increased ICP in all ages
  • Optic nerve atrophy/blindness
14
Q

Traumatic Brain Injury

A

Primary/Direct injuries

  • D/t impact
  • Microscopic damage: diffuse axonal injury
  • Contusions (coup - brain hits front of skull, countercoup - brain hits back of skull)
Secondary injuries
- D/t:
Ischemia (most common)
Hemorrhage
Infection
Increased intracranial pressure
15
Q

Traumatic Brain Injury types

A
  1. Mild
    Concussion (immediate & possible post-concussion syndrome)
    Limited symptoms to momentary LOC, residual amnesia
  2. Moderate
    Small hemorrhages, edema
    LOC, cognitive/motor deficits, hemiparesis, nerve palsies
  3. Severe
    Shearing, pressure = axon/vessel/tissue damage
    Extensive damage with secondary manifestations (Hemiplegia, signs of elevated ICP, coma)
16
Q

Hematoma - Epidural

A

Meningeal artery tear

  • Rapid bleeding; unconsciousness may be followed by brief lucid period
  • Ipsilateral pupil dilation, contralateral hemiparesis d/t uncal herniation (push down to brain stem)
  • Treatment prior to LOC has good prognosis
17
Q

Hematoma - Subdural

A

Venous tear between dura & arachnoid
Slower bleeding
1. Acute (within 24 hours)
Increased ICP, decerebrate posturing, LOC, high mortality rate
2. Subacute (2-10 days)
Periods of improvement prior to rapid deterioration
3. Chronic (weeks)
Slow bleed, decreased LOC, drowsiness, confusion, apathy, headache

18
Q

Hematoma – Intracerebral (Traumatic)

A
Usually frontal or temporal lobes 
Risk: age, alcoholism
Symptoms dependent on size and location
Increased ICP
Herniation
19
Q

Diffuse Brain Injury Signs

A
  1. Doll’s eye response (vestibulo-ocular reflex)
    - Indicates brain stem damage
    - Possible tentorial herniation

Abnormal posturing

  1. Decorticate posturing
    - Damage to one or both corticospinal tracts involving the “red nucleus” (motor movement) in midbrain
    - Arms flexed
    - Legs extend with feet turned inward
  2. Decerebrate posturing
    - Indicates brain stem damage bwloe level of red nucleus
    - Upper and lower extremity extension
    - Head arched back
    - Can be one side or both or just arms
  3. Cheyne-Stokes
20
Q

Brain Attack (CVS/Stroke) Risk Factors

A
  1. Ischemic Stroke (interruption in blood flow)
    - Age, gender, race, familial, HTN, smoking, DM, sickle cell disease, atrial fibrillation, CAD
    - Obesity, physical inactivity, alcohol, drug use, hypercoagulability disorders, oral contraceptives, hormone replacement therapy
  2. Hemorrhagic Stroke (bleed into brain tissue)
    - Htn, aneurysms, AV malformations, head injury, blood dyscrasias
21
Q

Transient Ischemic Attack (TIA)

A
Focal cerebral ischemia
“zone of penumbra” without infarction
Reverses prior to ischemia
Similar risk factors and symptoms as stroke but symptoms last < 1 hour with fully recovery
Increases risk of stroke
22
Q

Manifestations of Acute Stroke

A
Usually unilateral and focal
Always sudden
Weakness/numbness (face, arm, leg)
Vision loss
Aphasia (language disorder)
Dysarthria (motor speech disorder)
Ataxia (muscle coordination disorder)
23
Q

Aneurysmal Subarachnoid Hemorrhage

A
  1. Pre-rupture
    - Sudden-onset headache with nausea and vomiting, dizziness
  2. Hemorrhage
    - Sudden severe headache, N/V, nuchal rigidity (neck), photophobia, vision and motor problems, LOC
  3. Complications post-op
    - Rebleeding, vasospasm, hydrocephalus
24
Q

Risk factors of rupture

A
Age
Smoking
HTN
Alcoholism
Size of aneurysm
Conditions that increase ICP
25
Q

Arteriovenous Malformations

A

Tangle of abnormal arteries and veins linked by fistulas

  • Possibly due to lack of capillary formation
  • Structurally unstable with high pressure flow from arteries to veins
  • Ischemic symptoms

Symptoms may not show until > 40 years of age
Hemorrhage usually slower process
Surgical removal

26
Q

Acute Bacterial Meningitis

A

Inflammation of pia, arachnoid and subarachnoid
Contagious (direct contact – blood/mucous)
Carriers
10% permanent damage (ear, sight)
10% fatal

Neisseria meningitidis or Streptococcus pneumoniae
Group B streptococci (neonates)

27
Q

Acute Bacterial Meningitis risk factors

A
Basilar skull fracture
Otitis media
Sinusitis/mastoiditis
Neurosurgery
Sepsis
Living in close quarters/aged/infants
28
Q

Acute Bacterial Meningitis patho

A

Bacteria replicate and lyze in CSF
Endotoxins/debris result in inflammatory process
Neutrophils/albumin allowed in CSF
Thrombi, scarring, blockage

29
Q

Acute Bacterial Meningitis manifestations

A

Headache, fever, nuchal rigidity
N/V, photophobia, altered mentation
Petechial rash/palpable purpura (N. meningitides)

30
Q

Acute Bacterial Meningitis manifestations

A

Headache, fever, nuchal rigidity
N/V, photophobia, altered mentation
Petechial rash/palpable purpura (N. meningitides)
Seizures, cranial nerve palsies, focal cerebral signs

31
Q

Acute Bacterial Meningitis diagnosis

A

Lumbar puncture - cloudy, purulent
Kernig sign
- Resistance to extension of knee while lying with hip flexed
Brudzinski sign
- Flexion of neck induces flex of hip/knees

32
Q

Acute Bacterial Meningitis treatment

A

Antibiotics

33
Q

Viral Meningitis

A

Acute lymphocytic
Enteroviruses, Epstein-Barr virus, mumps virus, HSV, West Nile

Similar to bacterial but less severe

CSF has lymphocytes and small amounts of protein only, normal sugar

Self-limiting unless herpes simplex virus type 2 (HSV-2) which requires acyclovir

34
Q

Encephalitis

A

Parenchymal infection of brain or spinal cord
Usually viral
- HSV
- West Nile

35
Q

Encephalitis manifestations

A

Lethargy, disorientation
Fever, headache, nuchal rigidity
Seizures, paralysis, delirium, coma

36
Q

Encephalitis diagnosis

A

Lumbar puncture

CSF investigation

37
Q

Brain Tumors

A

Most often secondary site of metastasis
Primary more common in children (mortality rate 45%)
Risks:
Rarely benign, but if so, still dangerous
- Pressure
- Attachment = difficult to excise

Neurogliomas of astrocytic origin most common in adults
Medulloblastomas most common in children

38
Q

Neuroglial Tumors

A

Most common primary tumor
Graded I to IV
Astrocytes: protective neurons, supply nutrients/oxygen
Oligodendrocytes: supportive cells in brain, ex form myelin
Ependyomal: line ventricles & spinal cord

39
Q

Astrocyte

A
  1. Infiltrating (middle adult)
    Usually cerebral hemispheres
    Focal deficits, headache, seizures
  2. Non-infiltrating (children)
    Usually cerebellum, 3rd ventricle
    Slow growth, minimal symptoms, easily resected
40
Q

Oligodendroglioma

A

Middle adult
Usually cerebral hemispheres white matter
Unpredictable, prone to hemorrhage

41
Q

Ependymoma

A

Young adult
Epithelial lining of 4th ventricle/spinal canal
Hydrocephalus, increased ICP

42
Q

Medulloblastoma

A

Originates in neurons of cerebullum, posterior fossa
Fast growing, spreads via CSF to brain/spine
Appears in infants, young children
Manifestations include signs of increased ICP
Highly malignant, but radiosensitive and excisable

43
Q

Meningiomas

A

Outside brain, grows slowly
Older adult
Usually benign and excisable

44
Q

Primary central nervous system lymphomas

A

Increased incidence of late
Common in immunocompromised
B-cell origin (lymphocytic)
Invasive, diffuse, aggressive

45
Q

Metastatic tumors

A

Melanomas to frontal & temporal lobes
Breast cancer to cerebellum and basal ganglia
NSC (non small cell) lung cancer to occipital lobe

46
Q

Brain Tumor Manifestations

A
Dependent on location and size
Vasogenic edema/papilledema/increased ICP
Headache - distinctive characteristics 
- In morning
- Improves with elevation of head
- Worse with sudden head movements
- Doesn’t respond to usual medications
- Accompanied by N/V
47
Q

Diagnosis of Brain Tumors

A

MRI as CT unreliable
EEG
Cerebral angiogram

48
Q

Treatment of brain tumours

A

Surgery
Irradiation
Chemotherapy

49
Q

Seizure Disorders

A

Temporary alterations in cerebral activity
Causes are numerous

1. Provoked = seizure
Fever (children)
Metabolic condition (adults)
Structural changes
Cellular changes
  1. Unprovoked/idiopathic = epilepsy
    Genetic
50
Q

Partial Seizures

A

Simple Partial/Elementary
Complex Partial
Secondarily Generalized Partial

51
Q

Simple Partial/Elementary seizures

A
One hemisphere only
No LOC
Symptoms dependent on area involved
May cause “Jacksonian march”
 Sensory symptoms may be only sign
No observable symptoms
Prodrome/aura is not just a warning!
ANS involvement (tachycardia, diaphoresis, hypo/hypertension, pupil changes)
52
Q

Complex Partial

A
Often temporal lobe
Altered consciousness
Hallucinations, déjà vu, idea flood, fear, etc.
Automatisms
Repetitive non-purposeful movements 
Confusion after is common
53
Q

Secondarily Generalized Partial

A

Focal onset but generalized

Tonic/clonic activity, may have aura

54
Q

Generalized Seizures

A
Absence (“petit mal”)
Atonic (“drop attacks”)
Myoclonic
Tonic-Clonic (“grand mal”)
Status Epilepticus
55
Q

Absence seizure

A

Generalized disturbance of consciousness
Blank stare, often motionless or automatisms
Lasts only seconds so can be overlooked
“Atypical” type has slow onset/end

56
Q

Atonic seizures

A

Sudden loss of muscle tone

57
Q

Myoclonic seizures

A
Brief muscle contractions bilaterally
Face, trunk or one or more extremities
Tonic  
- Rigid, violent contractions or 
Clonic  
- Repeated contraction/relaxation
58
Q

Tonic-Clonic seizures

A
  1. Tonic Phase
    - Extension of extremities, LOC, incontinence, cyanosis
  2. Clonic Phase
    - Rhythmic contraction/relaxation
  3. Postictal Phase
    - Return to consciousness once RAS (wake/sleep center) function
59
Q

Status Epilepticus

A

Seizure activity that doesn’t cease on own or occurs successively
High mortality rate
Must treat cause

60
Q

Dementia

A
Permanent brain damage resulting in impaired memory and cognition
- Short and long-term memory
- Abstract thinking
- Judgement
- Personality changes
Alzheimer Disease
Vascular Dementia
Frontotemporal Dementia
Creutzfeldt Jakob Disease
Wenicke-Korsakoff Syndreom
Huntington Disease
61
Q

Alzheimer Disease

A
40% of 85 year olds
Genetic, familial or sporadic
Death in 8 years (average)
Diffuse degeneration/atrophy of cerebral cortex
Enlargement of ventricles
62
Q

Alzheimer Disease – pathological processes

A
  1. Neuritic (senile) plaques
    - Accumulation of amyloid peptide
    - Degenerative nerve terminals with an amyloid core
  2. Neurofibrillary tangles
    - Helical fibrous proteins
  3. Decreased enzyme that synthesizes acetylcholine
    - Neurotransmitter associated with memory
63
Q

Manifestations of Alzheimer’s

A
  1. Initial: subtle
    Loss of memory and denial of shame
    Mild personality change – withdrawal/loss of sense of humour
2. Moderate stage
Loss of higher cortical functions (problem solving)
Depression if aware of changes
Hostility
Sundown syndrome
  1. Late stage
    Loss of ability to respond to environment/family
    Incontinence
64
Q

Vascular Dementia

A

Ischemic or hemorrhagic damage (MI, arrhythymias, DM, PVD, infection, smoking)
Slow psychomotor functioning
Depression is common

65
Q

Frontotemporal Dementia (Pick)

A

Atrophy of frontal and temporal lobes
- Progressive syndrome
Behavioral changes common
- Impulsiveness, loss of inhibitions (social behaviour), apathy
Language/understanding issues are less common but do happen
Death d/t infection in 2-10 years

Diagnosis: Neuroimaging

66
Q

Creutzfeldt Jakob Disease (mad cow)

A

Rapid, infective protein “prion” (protein)
Bovine spongiform encephalopathy (BSE)
- “Mad cow disease”
Dementia within 6 months of infection
Results in degeneration of pyramidal and extrapyramidal systems

Personality changes
Visual/spatial coordination issues
Impaired memory and judgement 
Extreme dementia 
Insomnia
Ataxia
Death in months
67
Q

Wernicke-Korsakoff Syndrome

A
Cause is typically thiamine deficiency as a result of chronic alcoholism
Manifestations:
- Weakness of eye muscles
- Delirium, confusion, hallucinations
- Memory loss with confabulation
- Polyneuritis 

Physical symptoms are somewhat reversible with nutrition, thiamine, but not “psychosis”

68
Q

Huntington Disease

A

Cause is hereditary
Emerges in 40-50’s
Cell death in basal ganglia motor control

Manifestations

  • Chronic progressive chorea (rhythmic movement)/ dyskinesia (inability to control movement)
  • Psychological changes
  • Cognitive decline, dementia