Week 1 - Trachte/Kraft Flashcards

(32 cards)

1
Q

What are the two types of cerebral edema?

A
  1. Vasogenic Cerebral Edema

2. Cytotoxic Cerebral Edema

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2
Q

What occurs in Vasogenic Cerebral Edema?

A
  • Increased Vascular Permeability (leaky junctions in vessels –> fill with fluid –> swelling!)
  • Fluid shifts into intracellular spaces in the brain
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3
Q

What causes Vasogenic Cerebral Edema?

A
  • Localized edema due to tumor/abscess

- Generalized edema due to trauma

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4
Q

What causes in Cytotoxic Cerebral Edema?

A

-Cell membrane injury due to hypoxia or metabolic damage

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5
Q

What occurs in Cytotoxic Cerebral Edema?

A
  • Individual cells swell and retain fluid
  • Increased intracellular fluid in endothelial cells of the vessels, but cell junctions are okay
  • Cells swell due to retained fluid
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6
Q

What is the normal pathway of circulation of CSF starting in the lateral ventricles?

A
  1. Made in choroid plexus of lateral ventricles
  2. Circulates through intraventricular foramen –> 3rd ventricle
  3. Passes through cerebral aquaduct –> 4th ventricle
  4. Moves down brainstem via central canal
  5. Travels laterally to venus dural sinus –> arachnoid granules
  6. Enters Superior sagittal sinus –> straight sinus –> confluence of sinuses
  7. Follows Transverse sinus –> sigmoid sinus
  8. Finally enters INTERNAL JUGULAR VEIN
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7
Q

What is the normal pathway of circulation of CSF starting in the fourth ventricle?

A
  1. Made in choroid plexus of fourth ventricle
  2. Circulates through median aperature
  3. Travels around Cerebellum
  4. Empties into occipital sinus –> Confluence of sinuses
  5. Follows Transverse sinus –> sigmoid sinus
  6. Finally enters INTERNAL JUGULAR VEIN
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8
Q

What is Noncommunicating Hydrocephalus?

A
  • Blockage in the ventricular system that does not allow CSF flow in that area
  • Only part of the ventricular system is enlarged
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9
Q

What are the causes of Noncommunicating Hydrocephalus?

A

-Congenital malformation, tumor, abscess, hematoma

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10
Q

What is Communicating Hydrocephalus?

A
  • Blockage in subarachnoid space
  • Enlarges the entire ventricular system
  • Blocks the exit!
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11
Q

What are the causes of Communicating Hydrocephalus?

A
  • Resolving meningitis
  • Subarachnoid hemorrhage
  • Dural sinus thrombosis
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12
Q

What is Hydrocephalus Ex Vacuo?

A
  • Dilation of the ventricular system due to brain atrophy with compensatory increase in CSF volume
  • No blockage in the ventricular system
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13
Q

What are potential causes of Hydrocephalus Ex Vacuo?

A
  • Alzheimer’s disease
  • Pick disease
  • Being on a ventilator for an extended period of time
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14
Q

What is Increased CSF Production Hydrocephalus?

A
  • Dilation of the ventricular system due to increased CSF production
  • Uncommon
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15
Q

What causes Increased CSF Production Hydrocephalus?

A

Choroid plexus papilloma

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16
Q

What is Normal Pressure Hydrocephalus?

A
  • Reversible enlargement of the ventricles
  • May be a form of communicating hydrocephalus
  • No cortical atrophy
17
Q

What are the clinical features of Normal Pressure Hydrocephalus?

A
  • Elderly patient with: gait disturbance, urinary incontinence, and dementia
  • Often misdiagnosed as Alzheimer’s disease
18
Q

What are the causes of increased intracranial pressure?

A
  1. Mass effect
  2. Edema
  3. Tumor
  4. Hematoma
19
Q

What is the problem with increased intracranial pressure?

A

Compromises blood flow to the brain

20
Q

What are the symptoms of increased intracranial pressure?

A

Headache, papilledema, decreased LOC

21
Q

What are the three main types of herniation that can result from increased intracranial pressure?

A
  1. Subfalcine (Cingulate) Herniation
  2. Transtentorial (Uncinate) Herniation
  3. Tonsillar Herniation
22
Q

What are the symptoms of herniation?

A
  • Focal neurologic symptoms
  • Respiratory arrest
  • Cardiac arrest
  • Coma
  • Death
23
Q

What is a Subfalcine (Cingulate) Herniation?

A

-Expansion of one hemisphere displaces the cingulate gyrus under the falx causing compression of the anterior cerebral artery

24
Q

What are the specific symptoms of a Subfalcine (Cingulate) Herniation?

A
  • Weakness of limbs

- Aphasia

25
What is a Transtentorial (Uncinate) Herniation?
- Compression of the Temporal Lobe against the tenorium | - Possibly Affects: CN III, Posterior cerebral artery, brainstem, contralateeral cerebral peduncle
26
What are the specific symptoms of a Transtentorial (Uncinate) Herniation?
1. CN III --> fixed/dilated pupil, impaired ocular movements 2. Posterior cerebral artery --> ischemia in primary cortex of vision 3. Brainstem --> impaired consciousness due to duret hemorrhages (small ripped vessels) 4. Contralateral cerebral peduncle --> Hemiparesis
27
What is a Tonsillar Herniation?
- Cerebellar tonsils get compressed through the foramen magnum. - Compression of medulla can be FATAL if vital respiratory and cardiac centers are compromised.
28
What is the mechanism of action of Acetazolamide?
Carbonic anhydrase inhibitor: - blocks carbonic anhydrase so cell cannot make H+ and HCO3- - Lowers pH --> more acidic plasma - interferes with the sodium pump --> hyperosmolarity in blood thus pulling fluid out of the CSF
29
What is the mechanism of action of Furosemide?
NKCC pump inhibitor: - blocks the NKCC pump on the abluminal side - causes hyperosmolarity in the blood, thus pulling fluid out of the CSF
30
What is the mechanism of action of Mannitol?
- Small sugar that cannot cross BBB | - Blood becomes hyperosmotic and draws water out of neurons & CSF
31
What is the best treatment for Vasogenic Cerebral Edema?
1. Steroids: Dexamethasone reduces water permiability of tight junctions (transcriptional regulator so it takes awhile to work) 2. Mannitol: Osmotic diuretic (osmotic force pulls water across membranes because #particles in blood > #particles in cells or CSF
32
What is the best treatment for Cytotoxic Cerebral Edema?
Agents that suppress CSF production! 1. Acetazolamide 2. Furosemide 3. Mannitol