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Pathophysiology > Nervous system Part II > Flashcards

Nervous system Part II Flashcards

1
Q

intracranial pressure

A
  • normal 8-12 mmHg
  • measured in lateral ventricles
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2
Q

cranial vault fixed volume

A
  • brain (cellular and ICF) = 80%
    • fixed, can’t manipulate the brain
  • Blood (arterial and venous) = 12%
    • we can manipulate this
  • CSF = 8% (100-150 ml)
    • can also manipulate (ventric, lumbar drains)
    • don’t do this in OR very often
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3
Q

ICP curve

A
  • once compensation abilities is maxed out, ICP will increase significantly
    • high ICP decreases CPP
    • herniation
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5
Q

Intracranial Elastance (compliance)

A
  • determined by the change in ICP after a change in intracranial volume
  • compensatory mechanisms are:
    • displacement of CSF from cranial to spinal compartment
    • Increased CSF absorption
    • Decreased CSF production
    • Decreased CBV (mostly venous)
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6
Q

CPP

How do you calculate it?

What is normal?

How does CPP compare to what you will see on EEG?

A
  • CPP = MAP-ICP (or CVP, whichever is greater)
  • normal is 80-100
  • CPP < 50 mmHg- slowing seen on EEG
  • CPP < 25-40 mmHg - flat EEG
  • CPP < 25 mmHg sustained - irreversible brain damage
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7
Q

What are the 4 types of herniation?

A
  • Subfalcine
    • expansion of cerebral hemisphere pushes cingulate gyrus under the falx cerebri
  • Transtentorial
    • supratentorial contents compressed against the tenorium cerebelli
  • Tonsillar
    • displacement of cerebellar tonsils through the foramen magnum
  • Herniation through traumatic defect
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8
Q

how does the falx cerebri partition the brain?

A

separates the right and left cerebral hemispheres

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9
Q

How does the tentorium cerebelli partition the brain?

A
  • Separates the occipital lobes of the cerebral hemispheres from the cerebellum
  • divides the cranial cavity into supratentorial and infratentorial compartments
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10
Q

How does the Falx cerebelli partition the prain?

A

partially separates the cerebellar hemispheres

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11
Q

How does the diaphragma sellae partition the brain?

A

circular extension that forms a partial roof over the hypophyseal fossa

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12
Q

CSF

Capacity?

What rate is it made and reabsorbed?

What pressure gradient is important for CSF to be reabsorbed?

A
  • Cavity enclosing brain and cpinal cord is about 1600-1700 ml; about 100-150 is CSF
  • CSF is made and reabsorbed at about 21 ml/hr for a total of about 500 ml/day
  • CSF will be reabsorbed if CSF pressure is 1.5 mmhg > than venous pressure
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13
Q

How should increased ICP be managed?

A
  • Goal to maintain CPP and cerebral blood flow
    • ICP < 20 mmgh and increase BP
  • Mannitol/hypertonic saline
  • furosemide
  • vasopressors
  • PaCO2 low/normal = 30 mmHg
  • maintain normothermia
  • barbituate/propofol coma (decrease O2 need)
  • CSF drainage if available (ventric)
  • HOB 30 degreessurgical decompression or cranie (trauma)
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14
Q

What dose of Mannitol would you administer?

Hypertonic Saline?

A
  • Mannitol- 0.25 -0.5 g/kg
  • Hypertonic saline- 1-2 ml/kg over 5 min
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15
Q

Which patients with increased ICP would you corticosteroids to?

A
  • Pts with brain tumor
    • steroids help fix the BBB that is weak because of the vasculature to the tumor
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16
Q

What is hydrocephalus and what are the different causes?

A
  • Excessive CSF within the cerebral ventricles which increases ICP
  • Communicating= free flow through ventricles
  • Non-communicating= flow out of one or more ventricles is blocked
    • brain tumor blocks flow to arachnoid villi
  • hemmorrhage or infection (excessive RBC& WBC in csf cause blockage of small channels in arachnoid villi
  • too few villi or non absorptive enough (dx as infants)
  • choroid plexus tumor- too much CSF produced
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17
Q

What are the two major types of edema?

A
  • Vasogenic
    • capillaries are more porous than usual and BBB is disruptive
    • corticosteroids or hyperosmolar infusion to treat
  • Cytotoxic
    • Ion transport failure (from metabolic failure)
    • inadequate ATP, pumps dont work, water accumulates
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18
Q

What are the 3 types of traumatic head injuries?

A
  • Closed head
    • rapid acceleration/deceleration causes the soft brain to hit the rigid skull and ricochet
  • Blunt trauma
    • direct impact to the head (MVA, falls, assault)
  • penetrating trauma
    • bullets, foreign objects
  • **leading cause of death and disability among young ppl in us; often associated with other injuries to cervical spine, thorax, abdomen
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19
Q

What is the difference between primary and secondary injury?

A
  • Primary injury- direct injury from the force applied to the skull and brain
    • contusions, lacerations, diffuse axonal injury
    • can’t really do much about primary injury
  • Secondary injury- caused by the ischemia, brain swelling, edema, hemmorrhage, increased ICP, herniation in the minutes to hours following primary injury
    • aggravating factors are hypoxia, hypercarbia, hypotension, anemia, hyperglycemia, sz, infection
    • lots of glutamate, increases calcium to cells–>apoptosis
    • goal to prevent
20
Q

What can cause parenchymal injury?

A
  • diffuse axonal injury
    • sudden deceleration or acceleration causes stretching or tearing of nerve cell in white matter
  • contusions
    • hemorrhages in the superficial brain parechyma caused by blunt trauma, resulting in coup/contrecoup contusions (shaken baby)
  • traumatic intracerebral hemorrhages
    • usually multiple deep in brain
  • brain swelling
    • may be isolated or found with something above; may be local or global
21
Q

What is an epidural hematoma?

How is it diagnosed?

treatment?

A
  • AN EMERGENCY!
  • arterial bleeding between the skull and dura
    • usually meningeal artery rupture secondary to skull fracture
  • diagnosed by CT and signs and symptoms
    • LOC fllowed by lucid honeymoon then sudden decompensation (liam Neeson’s wife)
    • honeymoon period caused by artery spasming enough to stop bleeding for a minute
  • Promt burr holes at fracture site
22
Q

What is a subdural hematoma?

symptoms?

treatment?

A
  • lacerated or torn veins that bleed between the dura and arachnoid–slow beed
  • Chronic- spontaneous or follows minor head trauma in the elderly, hemodialysis, or anticoagulated pt
  • Acute- whip-lash, shaken baby
  • symptoms develop over 48 hrs
    • HA, drowsiness, obtundation, hemiparesis, difficulties with language, dementia
    • diagnosis varified by CT scan
  • Conservative medical management or surgical removal of clot if symptoms worsen
23
Q

How are head injuries treated?

A
  • immobilization of cervical spine
  • GCS< 8; intubate
  • protect lungs from aspiration
  • CT to rule out epidural or subdural hematoma
  • frequent neuro checks to rule out hematoma formation/ cerebral edema/ secondary injury
  • Craniotomies for depressed skull fx and evacuation of hematomas
    • if break in skull, but be to OR within 24 hours or increases infection
24
Q

What is the incidence of brain tumors?

Where do they usually arise from?

A
  • Intracranial incidence 10-17:100,000
  • 20% of all pediatric cancers
  • May arise from:
    • meningeal layers
    • CNS cells
      • glial, neurons, choroid plexus)
    • cells housed in the skull
      • primary CNS lymphoma
    • metastasis
25
Q

Where are pediatric tumors most common?

adult?

A
  • infratentorial most common for peds
  • supratentorial more common for adults
26
Q

What is a glioma?

What types of gliomas (4) were discussed and what are their outcomes?

A
  • Glioma is a type of tumor that starts as a glial cell
  • Low grade astrocytoma- most common; good outcomes
  • Grade IV glioblastoma- devastating
    • very aggressive, grows diffusely
    • difficult to remove, always reoccurs
    • releases lots of glutamate; good for tumor, bad for us
  • Oligodendroglioma- relatively good prognosis
  • Ependymoma- formed out of cells that line ventricles
27
Q

What are the other (non glioma) intracranial tumors?

(4)

A
  • Meningiomas- typically the arachnoid layer, pretty benign, good outcomes
  • Pituitary adenomas- influence pituitary fuction, can affect optic nerve
  • Acoustic neuromas- Acoustic nerve, good outcomes
  • Metastatic tumors
28
Q

What is the only agent known to increase the incidence of intracranial tumors?

How does it affect the different types of tumors?

A
  • Ionizing radiation
  • Glial = 10x more likely
  • meningeal = 3-7x more likely
  • **manifest 10-20 years after exposure
29
Q

How are intracranial tumors diagnosed?

A
  • symptoms related to ICP
  • HA
  • N/V
  • neurological changes
  • seizures
  • increased BP and decreased HR
  • Symptoms appear when compensatory mechanisms exhausted
    • small changes in BP = big changes in CBF/ICP
30
Q

Where does the pituitary gland lie?

What are the parts of the pituitary?

A
  • Pituitary gland lies in the sella turcica
  • Anterior (adenohypophysis)
    • regulated by hypophyseal portal system
    • releases growth hormone, TSH, FSH, etc
  • Posterior (neurohypophysis)
    • connected to hypothalamus by infundibular stalk
    • releases ADH and Oxytocin
31
Q

What are some non-functioning pituitary tumors?

A
  • chromophobe adenomas
  • craniopharyngiomas
  • meningiomas
  • these are diagnosed when they are large and cause symptoms by impinging on nearby structures
    • loss of one or more pituitary functions
    • loss of all pituitary functions = panhypopituitarianism
32
Q

What are some functioning pituitary tumors?

A
  • These tumors release hormones
  • prolactinomas- females: amnorhhea, males: impotence
  • GH tumor-
    • before puberty: giantism
    • after puberyt: agromegaly (overgrowth of bones in face), tong, and organs–>big airway problem
  • ACTH- too much cortisol
33
Q

How are intracranial tumors treated?

A
  • Manage ICP
  • surgery- for diagnosis and removal
  • radiation therapy- useful with malignant tumors
  • corticosteroids- for cerebral edema
  • Brachytherapy- stereotactic implantation of radiation for 4-6 days (for glioblastomas)
  • chemotherapy, immunotherapy, oncolytic virotherapy
34
Q

What are the statistics related to stroks?

ischemic vs hemorrhagic

men vs women

most common in caucasians?

most common in African americans?

A
  • 88% are ischemic, 12% hemorrhagic
  • leading cause of disability and 4th leading cause of death in US
  • Men have higher incidence
  • More likely over 75 yrs
  • Caucasians- Extracranial carotid artery disease and cardioembolism
  • African Americans- Intracranial thromboembolic disease more common
35
Q

What are the most common causes of ischemic stroke?

What determines the extent of the infarct?

A
  • Causes:
    • cerebral athersclerosis (DM, HTN, smoking)
    • emboli and loose atherosclerotic plaques
  • Extent of infarct
    • site of occlusion
    • collateral circulation
    • perfusion pressure
    • time course of occlusive event
36
Q

What are the subtypes of stroke?

A
  • systemic hypoperfusion- cardiac arrest, hypotension
  • embolism- fat, air, blood clot
  • thrombosis- often preceded by TIA
  • subarachnoid hemorrhage- trauma, hypertension, coagulopathy, aneurysm
  • Intracerebral/brain parenchymal hemorrhage- trauma, HTN, coagulopathy, open heart surgery
37
Q

What are the causes of acute ischemic stroke?

A
  • Cardioembolism- afib, ventricular dysfunction following MI, dilated cardiomyopathy, valvular disease
  • large vessel atherosclerotic narrowing- carotid bifurcation in the neck
  • small vessel occlusive disease (DM, HTN)
  • Hypercoagulable state
38
Q

What are the risk factors for acute ischemic stroke?

A
  • systemic hypertension
  • smoking
  • hyperlipidemia
  • DM
  • ETOH > 6 drinks/day
  • increased homocysteine level
39
Q

What are treatments for acute ischemic stroke?

A
  • Carotid endarterectomy- preventative measure when the carotid artery is >70% stenotic
  • supportive therapy- airway, oxygenation, ventilation, systemic BP, bood glucose, temperature, heparin prophylaxis
  • Aspirin initial treatment
  • IV recombinant tissue plasminogen activator- within 3 hours
    • may also directly infuse TPA into occluded blood vessel with angiography
  • ICP, CPP, and cerebral edema management
40
Q

What is malignant middle cerebral artery syndrome?

What else are acute ischemic stroke patients at risk for?

A

edematous infarcted tissue that compresses other cerebral arteries causing secondary injury

  • also at risk for infarction of the cerebellum with basillar artery compression and brain stem ischemia
    • caused by swelling
41
Q

Random information about intracerebral hemorrhagic stroke.

(good luck)

A
  • 4x the risk of death compared to ischemic stroke
    • high incidence among african americans
  • noncontrast CT needed to diagnose
  • volume of blood + LOC determine prognosis
  • pts often decompensate 24-48 hrs after the bleed secondary to edema formation
  • surgical decompression of blood unclear in effectiveness
  • ICP control is important (a second bleed is often fatal)
  • Supportive therapy- ETT, ICP monitor, MAP < 130 mmHg
42
Q

What is the pathophysiology of subarachnoid hemorrhagic stroke?

A
  • usually caused by aneurysms at the circle of will involving the anterior and posterior communicating arteries
  • systemic HTN, DM, and cigarette smoking increase risk
  • size of aneurism is important in determining risk of rupture
    • 6-10 mm at greatest risk
    • >25mm 6% risk of rupture increase per year
43
Q

How are hemorrhagic strokes diagnosed?

A
  • “worst HA of my life”
  • photophobia
  • stiff neck
  • decreased LOC
  • focal neurologic changes
  • ECG changes- catecholamine rush
    • CT scan
  • *prompt diagnosis and clipping can decrease M&M
44
Q

What is the treatment for hemorrhagic stroke?

A
  • Ideally to OR within 72 hours
  • pre-op kept sedated on stool softeners to prevent re-bleed and anticonvulsants
  • systemic BP kept normal
    • Goal CPP 61-80
  • Ventricular drainage if hydrocephalus seen on CT after clinical deterioration
  • Vasospasm prevention
45
Q

How is vasospasm prevented?

A
  • Daily transcranial doppler examinations
  • Nimodipine (Ca channel blocker)
  • Triple H therapy after clinical signs begin
    • HTN
    • Hypervolemia
    • hemodilution
    • *not clear if triple H works–goal to get the blood through that spasming vessel

Pathophysiology (26 decks)

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