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Advanced Patho Exam 4 > Exam 4: Neurocritical > Flashcards

Exam 4: Neurocritical Flashcards

1
Q

describe the Monroe-Kelly Doctrine

A

o Skull is a rigid compartment, contains three structures (1450mL)
* Brain tissue (1300 mL)
* Arterial/venous blood (110mL)
* Cerebrospinal fluid (65mL)
o Normal: Static volumes in balanced state of equilibrium
* Blood and CSF can shift to compensate
o Abnormal: elevations in relative volume of one compartment without compensation = elevated ICP
* There is some injury to the brain that causes one of the three compartments to rise in volume, that causes an increase in ICP

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2
Q

what are causes of elevated ICP

A

o Increase in volume
o Increase in brain tissue
o Increase in blood

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3
Q

Causes of elevated ICP: increase in volume

A
  • Disordered CSF Hydrodynamics
    o CSF overproduction
    o Impaired absorption, unable to drain CSF
     Psuedotumor cerebri, elevated CSF protein/blood, EVD or VPS malfunction
    o Increased Dural pressure (cerebral venous sinus thrombosis)
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4
Q

causes of elevated ICP: increase in brain tissue (3)

A
  • Hydrocephalus
    o ICH, SAH, IVH, tumor, meningitis
    o Compression of the ventricle from edema, tumor, hemorrhage
  • Cerebral edema
    o Osmotic, vasogenic, cytotoxic
  • Mass lesions
    o Tumor (primary or metastatic)
    o Abscess
    o Hematoma
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5
Q

causes of elevated ICP: increase in blood

A
  • Vasodilation from;
    o Increase in CO2 levels
    o Medications that are given
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6
Q

define brain compliance

A
  • Compliance: ability of cranial content to tolerate changes in volume
    o Brain can compensate for a period of time to maintain ICP
    o Small change in volume significantly increases ICP
  • -> Leads to loss of compliance
    o also is a factor in a patient course of tx
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7
Q

what is normal ICP

A

o Normal ICP 0-10 mmHg (or 5-15 mmHg)
* Generally, interventions are >20 (abnormal)

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8
Q

balance of intracranial pressure depends on:

A
  • Balance is critical for normal ICP

o Balance depends on-
* Volume of the cerebral structures
o Brain tissue, CSF, blood

  • Concept of autoregulation
    o Via the cerebral blood vessels
    o Vasodilation/vasoconstriction “protective mechanism”
     [Example- Vessels in brain will dilate if you are hemorrhaging from a trauma, and during HTN crisis the vessels will constrict to decrease the volume in the brain]
  • Cerebral perfusion pressure (CPP)
    o CPP= MAP-ICP
      This is how much blood flow is the brain actually getting
     Normal CPP in normal autoregulator range is 50-150mmHg
     CPP can be reduced by increase in ICP
  • [this is why we want a MAP to be high during an elevated ICP, in order to perfuse the brain]
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9
Q

what is CPP?

A

(cerebral perfusion pressure)
- it is the balance of pressures
(e.g. when someone has an injured brain, we need MAP to perfuse the brain tissue

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10
Q

what are the blood vessels inside the brain going to do if blood flow is dropping?

A

vasodilate

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11
Q

what happens to blood vessels when you’re having really high pressure?

A

vasoconstrict d/c if they do not then it’ll be dumping at high pressure blood into the brain tissue= bad

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12
Q

what values defined as intracranial hypertension

A

> 15-20 mmHg

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13
Q

define stage I of intracranial hypertension

A
  • Vasoconstriction and external compression of the venous system occur in an attempt to further decrease the intracranial pressure
  • ICP may not change because of the effective compensatory mechanisms and there may be few symptoms
  • Small increases in volume cause an increase in pressure, and the pressure may take longer to return to baseline
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13
Q

define stage II of intracranial hypertension and what are the clinical manifestions?

A
  • The resulting increase in ICP may exceed the brain’s compensatory capacity to adjust
  • The pressure begins to compromise neuronal oxygenation, and systemic arterial vasoconstriction occurs in an attempt to elevate the systemic blood pressure sufficiently to overcome the ICP
  • Clinical manifestations at this stage-
    o usually subtle and transient, including episodes of confusion, restlessness, and drowsiness, and slight pupillary and breathing changes
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14
Q

define stage III of intracranial hypertension and what are the clinical manifestations

A
  • The ICP begins to approach arterial pressure, the brain tissue begins to experience hypoxia and hypercapnia, and the individuals’ condition rapidly deteriorates
  • Clinical manifestations include-
    o decreasing levels of arousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia, and pupil’s that become small and sluggish
  • Autoregulation no longer working
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15
Q

define stage IV intracranial hypertension

A
  • Brian tissue shifts (herniates) from the compartment of greater pressure to a compartment of lower pressure
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16
Q

Explain consequences of impaired autoregulation: intracranial hypotension

A

o Major cause is loss of CSF volume
o Effects on decrease of CSF volume-
* Sagging of cerebral tissue away from the skull
* Pulling and breaking of bridging veins and dura
* Which leads to Hemorrhage

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17
Q

Explain consequences of impaired autoregulation: intracranial hypertension

A

o Sustained values >15-20 mmHg
* ICP >20 warrants treatment
* ICP >40 is life threatening

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18
Q

Two factors that MATTER and are important to determine severity of ICP

A
  • Onset (timing)
    o Slow growing lesion versus acute cause of elevated ICP
     Acute vs chronic, such as a tumor there for years which slowly increased the ICP.
  • Location
    o ICP levels vary according to compartment of the brain and may not always be reflected by neuromonitoring
    o Acute lesion in the temporal area may cause herniation at ICP levels 15-20 mmHg
     [for example- increase in volume, 100ml of blood, closer to the surface of the brain will have a different exam pictured vs if it were found in the base or deeper of the brain]
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19
Q

what happens to autoregulation with increased ICP

A
  • Autoregulation the compensatory alteration in the diameter of the intracranial blood vessels designed to maintain a constant blood flow during changes in cerebral perfusion pressure, is lost with progressively increased ICP
  • Increase in ICP can break down–>
    o Autoregulation system and blood brain barrier
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20
Q

Autoregulation vs Lack of autoregulation: Normal

A
  • Cerebral blood vessels vasodilate and/or constrict to maintain constant blood flow to cerebral tissue
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21
Q

Autoregulation vs Lack of autoregulation: Semi-normal (danger zone)

A
  • Acute increase in one structure volume may be compensated by a decrease in another tissue (CSF shifting or decreased blood flow)
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22
Q

Autoregulation vs Lack of autoregulation: Abnormal

A
  • Either end of the autoregulatory curve
  • Neurologic injury
    o Impaired or loss of cerebral autoregulation
  • Vasodilatory cascade
    o Increased ICP leads to decreased CPP leads to vasodilation to address decreased CPP leads to increased ICP
    o Increased CCP results in vasoconstriction and may reduce ICP
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23
Q

what is cerebral edema?

A
  • an increase in the fluid content of brain tissue
  • it is key cause of increased brain tissue volume
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24
Q

what is the result of cerebral edema?

A

increased extracellular or intracellular tissue volume

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25
Q

when does cerebral edema occur?

A

o occurs after brain insult from trauma, infection, toxicity, hemorrhage, tumor, ischemia, infarction, or hypoxia.

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26
Q

what are the harmful effects of cerebral edema caused by?

A

caused by the distortion of blood vessels, the displacement of brain tissues, increase in ICP, and the eventual herniation of brain tissue from one brain compartment to another.

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27
Q

what are the types of cerebral edema?

A
  • osmotic
  • vasogenic
  • cytotoxic
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28
Q

cerebral edema: Osmotic (interstitial)

A

due to hypo-osmolar state
* Change in oncotic pull
o i.e., Acute hyponatremia or Rapid hemodialysis
* [abnormal shifts in substrates in blood and fluid shifting to brain tissue]

*have fluid shifting into brain tissue b/c there’s not enough substrates in the blood to keep the osmotic pull inside the blood vessels

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29
Q

cerebral edema: vasogenic

A

due to altered capillary permeability
* Allows the fluid to leak into the brain and manifests as swelling
* Disruption in the brain-blood barrier
* Plasma proteins leak into the extracellular spaces, drawing water to them, and the water content of the brain parenchyma increases
o i.e., Hypertensive encephalopathy or Tumor-related edema
* [this is happening at the capillary level causing abnormal leakage of capillaries, such as a brain tumor- the edema around the tumor- the edema causes the symptoms, not the tumor itself]
o Clinical manifestations-
 Focal neurologic deficits, disturbances of consciousness, and a severe increase in intracranial pressure

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30
Q

cerebral edema: cytotoxic

A

due to loss of cell membrane ionic pumps and/or buildup of osmotic particles intracellular
* Directly affect the cellular elements if the brain parenchyma causing failure of the active transport systems
* –>The cells lose their potassium and gain larger amounts of sodium
* –>Water follows the sodium into the cell
* –>The cell can no longer make ATP
o The cell can’t fuel the sodium potassium pump
 cell will swell causing a hyperosmolar state inside the cell
* [brain tissue dies “Cell dies” causes an inflammatory response causes edema in the area] this can cause –>
o Acute ischemic stroke
 Intracellular accumulation of sodium which leads to a hyperosmolar state
o Fulminant hepatic failure

31
Q

describe abnormal blood-brain barrier

A
  • Can be caused by cerebral edema
    o Unpredictable transit of drugs and other metabolites into the brain
  • Normally
    o Endothelium of capillaries contains tight junctions between endothelium cells which minimizes movement of crystalloids and proteins (drugs, bacteria, etc.)
    o Ionic pumps maintain strict gradient between intracellular and extracellular spaces
32
Q

describe herniation

A

o Shift in brain tissue from one compartment to another caused by pressure difference between compartments
o ICP is rising and at some point, it exceeds what brain can handle
* Increase in ICP pressing out against skull, because there is nowhere to go, it presses down
o All types of herniation lead to central herniation which is attributed to brain death

33
Q

what are s/s of herniation

A

o Different types have diff s/s but most:
- decreased level of consciousness
- ipsilateral pupil dilation/constriction
- ptosis
- contralateral/ipsilateral hemiparesis –>coma, respiratory arrest, extensor posturing

34
Q

describe uncal herniation and the s/s

A

o lateral displacement and herniation of temporal lobe tissue causing midbrain compression
* [Moves down and around/into tentorium]
o Significant changes in neuro exam

s/s:
* decreased level of consciousness, ipsilateral pupil dilation (then contralateral pupils), ptosis, contralateral hemiparesis, Cheyne-Stokes respirations (which later shift to central neurogenic hyperventilation),
o If uncorrected  Coma, impaired breathing, loss of oculocephalic reflex, extensor posturing (appearance of decorticate and then decerebrate posturing)

35
Q

define central herniation and the s/s

A

o Frontal or parietal pressure exerts downward force and compress midbrain
* [moves down the center of brain, leading to no blood flow to the brain= brain death]
o S/S-
* confusion progresses to decreased level of consciousness, small pupils
o individual rapidly becomes unconscious; moves from Cheyne-Stokes respirations to apnea; develops small, reactive pupils and then dilated, fixed pupils; and passes from decorticate to decerebrate
* If uncorrected  pupils dilate, loss of brainstem reflexes via transtentorial herniation

36
Q

describe Subfalcine (cingulate) Herniation

A

o Lateral displacement of frontal or parietal lobe across the Falx
* [pressure growing out from surface of brain pushing down and around falx]
o There is change in neuro status, but no brain death
o S/S-
* contralateral or ipsilateral leg weakness

37
Q

describe Cerebellar Herniation “Tonsillar herniation” and the s/s

A

o Dislocation of the cerebellum downward through the cerebellar tonsils
* [cerebellum pulls out the back of the skull, pushes tonsils up or down- is more dangerous if it is moving downward]
o S/S-
* sudden respiratory arrest
* arched stiff neck, paresthesia in the shoulder area

38
Q

describe Transtentorial Herniation

A

o Central, uncal, and cerebellar herniation may all progress to transtentorial herniation
o Progression to brain death if unchecked

39
Q

define meningitis

A
  • Meningitis
    o Infection/inflammation of meninges layer covering brain and spinal cord
    o Meninges- flow in the subarachnoid space
40
Q

Identify common causative organisms for meningitis in adults and neonates: bacterial

A

o H. Influenza
 Children, adolescents, young adults
o Meningococcus (Neisseria meningitides)
 Predominantly affecting children and adolescents
 Less incidence d/t vaccine
o Pneumococcus (Streptococcus pneumonia)
 Young people and those more than 40 years of age

41
Q

Identify common causative organisms for meningitis in adults and neonates: viral

A
  • Viral
    o Enteroviral 90%
    o Arboviruses
     Mosquito born, west nile
    o Herpes
    o Mumps
    o Cytomegalovirus (CMV)
42
Q

viral meningitis

A
  • develops over days and patient may not be sick enough to come into hospital
  • much less common to die from viral meningitis than bacterial meningitis
  • patient doesnt look toxic compared to bacterial meningitis
  • virus can be dormant and have flare-ups once in a while
43
Q

bacterial meningitis

A
  • quick onset and rapid progression of the disease
  • replicates very quickly–>causes endotoxin and inflammatory mediators, the immune system and inflammatory system goes into overdrive to try to fight bacteria
44
Q

why shouldnt you do LP on someone with high ICP

A

b/c risk of downward herniation

45
Q

Identify the common organisms involved in bacterial meningitis by age group: Newborns

A

o Group B Streptococcus
o E coli
o Listeria monocytogenes

46
Q

Identify the common organisms involved in bacterial meningitis by age group: Infants and children

A

o Haemophilus Influenza B
o Streptococcus pneumoniae
o Neisseria meningitidis

47
Q

Identify the common organisms involved in bacterial meningitis by age group: Adolescents and young (2)

A

o Neisseria meningitidis
o Pneumococcal

48
Q

bacterial meningitis pathophysiology

A

o Bacteria penetrate the blood-brain barrier
o Endotoxin and inflammatory mediators instate a CSF inflammatory response (overreaction of the immune system is what causes the problems)
 Edema formation
 Cerebral vascular thrombosis
* Increase in intracranial pressure
* Reduction in cerebral perfusion, cerebral infarction and/or brain death
o Rapid, quick replication!

49
Q

clinical manifestations of bacterial meningitis

A

 Inflammation and irritation
* Generalized meningeal signs, throbbing headache that becomes more severe, photophobia that becomes more severe, nuchal rigidity, positive Kernig and Brudzinski signs
 Local tissue dysfunction
* Cranial nerve palsies, focal neurologic deficits (such as hemiparesis/hemiplegia, ataxia)
* Seizures
 Mass effect
* Decreased level of consciousness, nausea, vomiting, and increased intracranial pressure
 Vascular compromise
 Stiff neck and pain
 Low grade fever at onset, progresses to HIGH fevers
 Sensitivity to light and sound
 As infection progresses, may find s/s of increased ICP
 Progression to coma
 These patients look very ill looking, toxic look, sleepy look!
 Signs of meningeal irritation

50
Q

what are signs of meningeal irritation

A
  • Nuchal rigidity-
    • pain and resistance to the neck flexion
  • Brudzinski sign-
    • flexion of the knees and hips when the neck is flexed forward rapidly
  • Kernig sign-
    • resistance to knee extension in the supine position with the hips and knees flexed against the body
51
Q

viral (aseptic) meningitis pathophysiology

A

o Penetration of virus into CNS via blood (hematogenous) or traveling along the nerve root (particularly with herpes virus)
o Virus replicates within the body (any organ system) and gains access of the blood stream (primary viremia)
 Replication continues despite immunological response (secondary viremia) with seeding in CNS
o Slow replication- development over days!
o These patients have diffuse s/s and recent viral infection is key

52
Q

viral meningitis clinical manifestation

A

 Mild compared to bacterial
 Mild generalized headache, mild photophobia, mild neck pain, stiffness, fever, and malaise
 Signs of viral infection (rash, pharyngitis, lymphadenopathy)

53
Q

describe pathogen migration

A

o Migration of pathogens from external site to the brain (i.e., gut, inner ear, neuronal ganglia)
* Blood stream dissemination
* Tissue planes –i.e., posterior fossa, ENT, upper respiratory tract
* Temporal bone fractures
* Membranes of labrinths
o Meningeal – blood brain barrier disruption
* Once isolated in the CNS, difficult immune reach
o Inflammatory response including leaky capillaries and blood brain barrier perpetuates problem
o Development of interstitial edema
* Vasogenic and cytotoxic as process progresses
* Vasogenic and pro-inflammatory mediator in CSF
* Secondary mediators exacerbate inflammatory response
* Perpetuates blood brain barrier breakdown and CSF permeability

54
Q

Risk Factors to meningeal disease

A

o Overcrowding
o Lower socioeconomic status
o New school/ residence
o Smoking
o Steroid use
o Recent viral or bacterial infection
o Immunocompromised
o Alcoholism
o Recent neurosurgical event, procedure, trauma

55
Q

Identify two types of primary epilepsy.

A
  • Hippocampal sclerosis (HS)
    o Loss of neurons in Ammon’s horn of the hippocampus
    o Unclear cause of HS
    • Cause versus result of disease
    • May be related to birth or early childhood trauma
    • May be result of multiple seizures
      o Mechanism of damage
    • Elevated glutamate
      o Type of excitatory neurotransmitter
  • Temporal lobe epilepsy (TLE)
    o Epileptogenic focus in medial temporal portion of the temporal lobe
    o Stubborn to treatment
    o Causes-
    • HS, tumor, cortical dysplasia, vascular malformation or unable to determine pathology–these patient have multiple seizures a day their entire life
56
Q

define partial seizures (focal origin)

A
  • Partial Seizures (FOCAL ORIGIN)
    o Seizures originating in one hemisphere
  • [Specific origin to brain with an aura – tremor to the arm, and only the arm]
    o Simple
  • Consciousness is NOT impaired
  • Motor (Jacksonian)-
    o Movement of body part, repetitive jerking
  • Sensory-
    o visual, auditory, olfactory, gustatory, vertiginous
    o Sensory experience is subjective
     If sensory seizure begins on the hand area of the sensory cortex, the person experiences numbness, tingling, or “pins and needles” phenomena
    o Complex
  • Impaired consciousness!
  • Localized to the Temporal lobe
  • The person is able to interact with the environment with purposeful, although inappropriate movements
  • Automatism-
    o Lip smacking, chewing, facial grimaces, swallowing movements, and patting, picking, or rubbing oneself or one’s clothing
    o Secondary Generalization
  • Simple or complex that leads to a generalized seizure
57
Q

define Generalized Seizures (SYMMETRICAL, BILATERAL, NO FOCAL ONSET)

A

o Seizures originating on both sides of brain, spreading across mult. areas of cortex

o Tonic Clonic (grand mal)
* Abrupt loss of consciousness, body stiffening (tonic) and then shaking (clonic) abnormal posture for seconds or 2 minutes
* sometimes loss of bladder control or biting of tongue
* followed by a period of confusion, agitation, and fatigue
* headaches and soreness are common afterwards without losing consciousness and brief flexion

o Absence (petit mal)
* Characterized by lapses of consciousness that rarely last longer than 10 seconds and Immediate return to normal consciousness
o small periods of drawing blankness, vague/dreamlike state]
* Can be induced by hyperventilation for typical

o Myoclonic
* sudden brief shocklike jerks or twitches of the arms and/or legs
* may drop things
* no impairment of consciousness
* frequently occurs shortly after awakening

o Infantile spasm

o Atonic
* Drop attacks
* Sudden loss of postural muscle tone; the tone loss may be mild, resulting in a head nod, or more dramatic, including falls
* No loss of consciousness

58
Q

define status epilepticus

A
  • Continues seizure for >3-5min OR 2 or more seizures without recovery to baseline consciousness
    o There is no post ictal state- “sleepy, lethargic state, there is lack of interaction with environment during this time this is due to the neurons are exhausted after that excitatory period!”
59
Q

define convulsive seizure

A
  • Motor symptoms- literally you can see this seizure
60
Q

define nonconvulsive seizure

A
  • Decreased LOC- you CANNOT see any physical s/s of them having a seizure, so let’s say they got a CT and it was normal and they are so lethargic or sleepy all day, possibly think patient has been having a seizure
61
Q

Explain how partial seizures can generalize.

A
  • Secondary Generalization
    o Starts with seizure only in the arm then becomes generalized seizure
    o Unconsciousness appears
  • Consciousness may be maintained as long as the seizure activity is limited to one hemisphere in simple partial seizures but partial seizures may become generalized to involve neurons of the other hemispheres and the deeper brain nuclei
    o Consciousness is lost at the point of generalization
    o General symptoms are produced
62
Q

define seizures

A

o Abnormal excitatory of series of neurons in cerebral cortex
* Occurs when there is a disruption in the balance of excitation and inhibition of electrical impulses
o Excessive excitation and loss of inhibition

63
Q

what anatomical structures are involved in seizures? (3)

A
  • Cerebral cortex, neuronal synapses, ion channels at synapse axons or dendrites
64
Q

what is epilepsy

A
  • Multiple seizures, a disorder
65
Q

what can seizures result from?

A
  • Increased excitatory synaptic neurotransmitters
    o Increase in glutamine aspartate
    o Ionic excitation with inflow of Na, Ca
  • Decreased inhibitory neurotransmitters
    o GABA
    o Ionic inflow of Cl, outflow of K
  • Alterations in voltage-gated ion channels
  • Changes in intra/extracellular ion concentrations- favoring membrane depolarization
  • Activation of secondary- messenger systems
    o [think of these like the expressways in Chicago highways]
66
Q

Identify risk factors for ischemic and hemorrhagic strokes

A
  • Poorly or uncontrolled arterial hypertension
  • Smoking, which increases the risk of stroke by 50%
  • Insulin resistance and diabetes mellitus
  • Polycythemia and thrombocythemia
  • High total cholesterol or low high-density lipoprotein (HDL) cholesterol
  • elevated lipoprotein-a
  • Congestive heart disease and peripheral vascular disease
    -Hyperhomocysteinemia
  • Atrial fibrillation
  • Physical inactivity
    -Family history and genetics
  • Sleep apnea
  • Chlamydia pneumoniae infection
  • Sickle cell disease
  • Postmenopausal hormone therapy
  • High sodium intake, >2300 mg; low potassium intake, <4700 mg
  • Obesity
  • Depression
67
Q

Determine stroke etiology based on the area of brain affected: ischemic stroke

A

a clot on an artery forms, causing a decrease in blood flow in the artery, causing a decrease in O2 to brain tissue

  • As blood flow is starts to drop, there is a threshold.
  • Varying levels of ischemia
  • Zone of penumbra- damaged tissue but NOT YET dead
  • Infarct- dead tissue
  • Collateral Circulation-
    o Begins to form immediately
    o Capillaries begin to develop to compensate a decrease in blood flow
68
Q

Determine stroke etiology based on the area of brain affected: cryptogenic stroke

A

unknown cause

69
Q

Determine stroke etiology based on the area of brain affected: cardiogenic embolic stroke

A

 Emboli fragments breaking off from the heart
 Can be air, fat, tumor, bacterial clumps, foreign bodies
* Afib, aflutter, MI, prosthetic valve, endocarditis

“#1 a.fib, endocarditis, anything that puts debris in the heart.
bacterial infection that causes debris that valves can easily flick off and go towards the brain
- artificial valves->prone to developing clots and patients who had a MI: develops a clot in the ventricle of the heart”

70
Q

Determine stroke etiology based on the area of brain affected: small penetrating artery thrombosis (lacunar stroke)

A

 small artery thrombosis close to a bigger artery caused by uncontrolled risk factors
* i.e., uncontrolled htn, dm, uncontrolled obesity–their small vessels become very susceptible to the development of clots

“a small vessel stroke–>a little penetrating artery off of one of the big arteries that has developed a blood clot”

71
Q

Determine stroke etiology based on the area of brain affected: Large Artery Thrombosis-

A

 Anything atherosclerotic from the brain to heart
 Artery to artery AND/OR large artery thrombosis
“main vessels to worry about carotids, aorta, the aortic arch, vertebral arteries”

72
Q

describe causes hemorrhagic strokes

A

o Subarachnoid Hemorrhage
o Intracerebral hemorrhage (ICH)- a bruise in the brain
 *HTN #1 cause
 Amyloid angiopathy-
* protein gets into blood vessels, make them hard and prone to bleed
 Vascular malformation-
* artery-venous formation (AVM), dural fistula, ruptured aneurysm, cavernoma
 Other causes-
* Tumor related (because they become sooo vascular)
* Toxic/drug abuse
* Arteritis, angiitis, endocarditis, dissection

73
Q

describe primary injury of hemorrhagic stroke

A

Mechanical disruption “the actual trauma”

74
Q

describe secondary injury of hemorrhagic strokes? (6)

A
  • “The irritation happens, the bruise is breaking down”
  • Oligemia (reduction of blood volume)
  • Release of excitatory neurotransmitters
  • Membrane depolarization
  • Edema formation
  • Increased pressure
  • Cell necrosis
75
Q

Discuss factors that influence the development, growth, and rupture of aneurysms: Subarachnoid Hemorrhage (SAH)

A

o Release blood into the CSF circulating in the subarachnoid space
o Symptoms-
 Meningeal irritation- pain, photophobia, nuchal rigidity
 Increased Pressure
o Causes-
 Aneurysm* most common!
* The aneurysm itself is NOT the emergency, the spilling of blood into the subarachnoid space is the actual emergency!
 With dissection, Trauma (not in nature, this is traumatic), Neoplastic (melanoma)

Advanced Patho Exam 4 (4 decks)

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