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Pathophysiology > Class #8 > Flashcards

Class #8 Flashcards

1
Q

What protects the brain from external forces?

A
  • rigidity of the skull

- cushioning of the cerebrospinal fluid

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2
Q

What is the difference between Focal cerebral Ischemia and Global Ischemia?

A

FOCAL–> short term low blood flow caused by a stroke, thrombus or embolism that cause cerebral artery occlusion

GLOBAL–> loss of consciousness in cardiac arrest where the blood flow is inadequate to meet the metabolic needs of the entire brain. This causes the inappropriate release of excitatory amino acid neurotransmitters, disrupted CALCIUM balance, free radical formation, and mitochondrial injury, which causes ATP malfunction, and power failure in the brain.

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3
Q

Whats the difference between hypoxia and ischemia?

A

hypoxia is deprivation of oxygen with maintained blood flow
ischemia occurs when there is interrupted or reduced blood flow and glucose, and a disturbance in the removal of metabolic wastes

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4
Q

What conditions may cause hypoxia?

A
  • reduced atmospheric pressure
  • carbon monoxide poisoning
  • severe anemia
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5
Q

What is the zone of penumbra?

A

ischemic but still viable cerebral tissue that lays between the location where the infarction is occurring and healthy, normally perfused tissue

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6
Q

What 4 things occur as a result of global ischemia?

A
  • release of excitatory amino acid neurotransmitters
  • disruption of CALCIUM balance
  • free radical formation
  • mitochondrial injury, causing ATP malfunction and power failure
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7
Q

Where does cell death occur the earliest after global ischemia?

A
  • Purkinje cells of the cerebellum

- Neurons in the Sommer sector of the hippocampus

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8
Q

What are “watershed” areas?

A

Areas if the brain located at the border zones between overlapping territories supplied by the major cerebral arteries that are extremely susceptible to ischemia., resulting in focal defects

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9
Q

What is laminar necrosis?

A

Short segments of necrosis that occur within and parallel to the cerebral cortex

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10
Q

How is global cerebral ischemia treated?

A

depends on the underlying cause, but the goal is to increase oxygen supply to the troubled area of the brain why decreasing the metabolic needs of the brain during the non-flow state.

  • ventilation
  • supplemental O2
  • glycemic management
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11
Q

In global cerebral ischemia, neuron injury causes the release and activation of mediators that overstimulate cell receptors. Why is this a problem? (hint:glutamate)

A

The most common amino acid is glutamate, which attaches to and opens calcium channels, causing excess amounts of CALCIUM to leak into the cells. This causes:

  • protein breakdown
  • free radical formation
  • DNA fragmentation
  • Mitochondrial injury
  • Cell death
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12
Q

Explain the difference between Vasogenic Cerebral Edema and Cytotoxic Cerebral Edema

A

both result in INCREASE intracranial pressure
VASOGENIC
-occurs when the integrity of the blood-brain barrier is disrupted allowing water and proteins to escape into the extracellular fluid (interstitial space) that surrounds brain cells
CYTOTOXIC
-occurs when there is actual swelling of the brain cells themselves due to increased intracellular fluid

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13
Q

What causes Vasogenic edema? And what does it cause?

A

hemorrhage, meningitis, injury, tumors

Causes: herniation, focal defects, increased intracranial pressure, and altered LOC

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14
Q

What causes cytotoxic edema? And what does it cause?

A

water intoxication, impaired Na+/K+ pump

Causes: cell rupture, damage to surrounding tissue, and increased intracranial pressure

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15
Q

Explain the Monro-Kellie hypothesis

A

The cranial cavity contains about 10% blood, 10% cerebrospinal fluid, and 80% brain tissue. It maintains a set intracranial pressure because an increase in one of the 3 components causes a decrease in another, maintaining proper, safe pressure.

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16
Q

What causes an increase in the tissue component of the intracranial space?

A

tumor
edema
bleed

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17
Q

What causes an increase in the blood component of the intracranial space?

A

vasodilation, outflow obstruction

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18
Q

What causes an increase in the CSF component of the intracranial space?

A

increased production
decreased absorption
obstruction

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19
Q

Explain the pathophysiology of increased intracranial pressure

A
  • compartment syndrome in the skull
  • intracranial pressure is greater than arterial blood pressure
  • arteries collapse, blood flow to the brain is cut off
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20
Q

What is the formula for “compliance”?

A

C= change in volume
~~~~~~~~~~~~~~~~
change in pressure

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21
Q

Which component of intracranial volume is most restricted in its ability to compensate/undergo change?

A

tissue volume. CSF and blood volume are best able to compensate for changes in ICP

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22
Q

Why is hyperventilation sometimes used as a treatment method for increased ICP?

A

elevated PCO2 in the blood cause compensatory vasodilation of the cerebral blood vessels. Vasodilation would allow the influx of more blood to the brain, thus increasing the ICP even more. A decrease in PCO2 causes vasoconstriction, which will decrease the influx of more fluid to the area, and increase MAP and CPP. This is why hyperventilation (decrease in PCO2) is sometimes used in the treatment of ICP.

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23
Q

Explain the 3 stages of intracranial pressure

A

STAGE 1
-minimal increase in ICP d/t compensatory mechanisms are known as intracranial HTN
STAGE 2
-any change in volume greater than 100-120 mL means a DRASTIC increase in ICP
STAGE 3
- sustained increase in ICP. ICP approaches the MAP, which causes cerebral perfusion to decrease (hypoxia)

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24
Q

What is the body’s natural response to a decrease in cerebral perfusion?

A

raise systemic blood pressure and dilate Cerebral blood vessels, increasing cerebral blood volume, which contributes to further increase in ICP lowering perfusion pressure.

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25
Q

How will my patient with increased intracranial pressure present?

A
  • Decreased LOC
  • headache/vomiting
  • papilledema, pupillary changes
  • posturing (decerebrate, decorticate)
  • decreased motor function
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26
Q

What are the LATE signs of intracranial pressure? How is this treated?

A

CUSHING REFLEX

  • HTN (widened pulse pressure)
  • reflex bradycardia
  • altered respirations

decrease CO2 levels

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27
Q

Explain brain herniation.

A

increased intracranial pressure pushes the brain out of position, which causes brain tissue to be compressed either into the center of the brain, against bone, or against the golds of the dura mater

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28
Q

What is an early sign of brain herniation?

A

compression of the oculomotor nerve

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29
Q

I might think my infant is experiencing increased intracranial pressure when he/she exhibits these signs/symptoms:

A
  • bulging fontanelles
  • cranial suture separation
  • increased head circumference
  • high pitched cry
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30
Q

What is hydrocephalus?

A

When an increase in cerebrospinal fluid enlarges ventricles and compresses brain tissue

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31
Q

What is the difference between non-communicating/obstructive hydrocephalus and communicating hydrocephalus

A

non-communicating/obstructive occurs as a result of CSF blockage by congenital malformations, tumours, inflammation, or hemorrhage.
Communicating occurs as a result of impaired reabsorption of CSD via arachnoid villi d/t infection, scarring, blockage by lysed RBCs post repair of bleed

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32
Q

How might someone with hydrocephalus present?

A
  • fontanel bulging in fetus/newborn
  • signs of increased ICP in all ages
  • optic nerve atrophy/blindness
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33
Q

What’s the difference between primary and secondary traumatic brain injuries?

A

primary injuries occur due to direct impact from diffuse axonal injury or contusions

secondary injuries occur due to ischemia, hemorrhage, infection and increased ICP

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34
Q

If my patient has experienced primary impact to the head, what kind of traumatic brain injury is this?

A

coup contusion

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35
Q

What is a contrecoup contusion

A

a traumatic brain injury as a result of secondary impact to the head

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36
Q

How do you explain the difference between a mild, moderate and severe traumatic brain injury?

A

MILD occurs with concussion, exhibiting limited symptoms or mild changes in LOC
MODERATE occurs with small hemorrhage/edema, causing cognitive/motor deficits, hemiparesis and nerve palsies
SEVERE occurs with shearing pressure/tissue damage causing hemiplegia, elevated ICP or coma

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37
Q

What is post concussion syndrome?

A

memory issues, poor concentration, amnesia lasting months

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38
Q

When does an epidural hematoma occur? How would this patient present?

A

It occurs when there is a tear in the meningeal artery.
This patient would exhibit rapid bleeding, unconsciousness followed by a brief lucid period.
-uncal herniation causing:
-ipsilateral pupil dilation &
contralateral hemiparesis
- GOOD PROGNOSIS IF TREATED BEFORE LOSS OF CONSCIOUSNESS

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39
Q

Explain a subdural hematoma

A

venous tear between dura and arachnoid mater, causing slower bleeding
ACUTE
-increased ICP, decerebrate posturing, loss of consciousness, high mortality
SUBACUTE
-some improvement, then rapid deterioration
CHRONIC
-slow bleed, decreased LOC, drowsy, confused, HEADACHE

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40
Q

What are the risk factors for an intracerebral hematoma?

A
  • old age

- alcoholics

41
Q

Where do intracerebral hematomas usually occur?

A

frontal or temporal lobe

42
Q

What is a “dolls eye response”? what does this indicate?

A

normally, eyes move in opposite direction first, THEN goes with head, but dolls move their eyes with the head.

  • brain stem damage
  • tentorial herniation
43
Q

Describe decorticate posturing

A

Arms flexed with legs extended and feet turned inward

occurs when there is damage to one or both corticospinal tracts involving the red nucleus in the midbrain.

44
Q

Describe Decerebrate posturing

A

Upper and lower extremity extension with head arched backwards
indicates brain stem damage below the level of the red nucleus

45
Q

What are Cheyne-Stokes? When might you see them in a patient?

A

progressively faster and deeper breathing interspersed with apnea, seen in diffuse brain injuries

46
Q

3 risk factors associated with ischemic stroke and 3 with hemorrhagic stroke

A

ischemic: age, HTN, obesity
Hemorrhagic: HTN, aneurysm, malformation, head injury

47
Q

What’s the difference between an ischemic stroke and a hemorrhagic stroke?

A 
I= clot blocks blood flow to an area of the brain
H= bleeding occurs inside or around the brain
48
Q

What is a transient ischemic attack?

A

focal cerebral ischemia that is reversed before necrosis occurs

49
Q

How might I know someone is experiencing an acute stroke?

A
  • Unilateral
  • weakness/numbess in face, arm or leg
  • vision loss
  • aphasia
  • ataxia
50
Q

What are the 4 risk factors of an aneurysm?

A
  • arteriovenous malformation of the brain
  • atherosclerosis
  • polycystic kidney disease
  • coarcation of aorta
51
Q

Who is most likely to have an aneurysm that ruptures?

A
  • old
  • smokers
  • HTN
  • alcoholism
  • larger aneurysms
  • increased ICP
52
Q

What are the symptoms of a pre-ruptured aneruysmal subarachnoid hemorrhage?

A

sudden onset headache with nausea and vomiting and dizziness

53
Q

What might indicate that my patient’s aneurysm is hemorrhaging?

A

sudden severe headache, N&V,
nuchal rigidity,
photophobia,
vision and motor problems, loss of consciousness

54
Q

What is nuchal rigidity?

A

neck stiffness d/t meningeal irritation

55
Q

Why can brain aneurysms cause hydrocephalus?

A

If there is a bleed in the arachnoid area of the brain, the villi are unable to properly absorb CSF, causing an accumulation of the CSF

56
Q

What are arteriovenous Malformations?

A

tangle of abnormal arteries and veins linked by fistulas, possibly due to lack of capillary formation in vitro. These areas are structurally unstable with high pressure flow from arteries to veins.

57
Q

Explain the pathophysiology of acute bacterial meningitis

A

bacteria (streptococcus pneumoniae, neisseria meningitides, group b stretococci) replicate and lyze in CSF

  • endotoxins/debris stimulate the inflammatory process causing inflammation of the pia, arachnid and subarachnoid space
  • neutrophils/albumin allowed into the CSF
  • This causes thrombi, scarring and blockage
58
Q

What are the risk factors for acute bacterial meningitis?

A
  • basilar skull fracture
  • otitis media
  • sinusitis
  • neurosurgery
  • sepsis
  • living in close quarters
59
Q

How would someone with acute bacterial meningitis present?

A
  • headache, fever, nuchal rigidity
  • N&V, photophobia, altered LOC
  • PETECHIAL RASH, palpable purpura
  • siezures, creanial nerve palsies
60
Q

How can you diagnose acute bacterial meningitis?

A
  • lumbar puncture is cloudy and or purulent
  • Kernig sign
  • bruzinski sign
61
Q

What is the Kernig sign?

A
  • Used to diagnose acute bacterial meningitis

- resistance to extension of knee while lying with hip flexed

62
Q

What is the brudzinski sign?

A
  • used to diagnose acute bacterial meningitis

- flexion of neck induces flexion of hip and knees

63
Q

What viruses are associated with viral meningitis?

A 
enterovirus
epstein-barr
mumps
Herpes simplex
West nile
64
Q

What does the cerebrospinal fluid contain in viral meningitis?

A

lymphocytes
protein
normal glucose

65
Q

How is viral meningitis treated?

A

rest, self-limiting

*UNLESS HERPES, which requires Acyclovir

66
Q

What is encephalitis?

A

parenchymal infection of the brain or spinal cord, usually caused by Herpes or west nile virus

67
Q

How might someone with encephalitis present to me?

A
  • lethargy/disorientation
  • fever, headache, nuchal rigidity
  • seizures, paralysis, delirium, coma
68
Q

What is the diagnostic process for encephalitis?

A
  • lumbar puncture

- cerebrospinal fluid investigation

69
Q

Are primary brain tumours more common in children or adults?

A

children with a mortality rate of 45%

70
Q

What puts people at increased risk for brain tumours?

A

genetics

radiation

71
Q

Why are benign brain tumours still dangerous?

A
  • increased ICP

- difficult to excise

72
Q

What type of brain tumor is most common in adults? Kids?

A

adults: neurogliomas of astrocytic origin
kids: medulloblastomas

73
Q

LOOK AT BRAIN TUMORS SHEET

A

LOOK AT BRAIN TUMORS SHEET

74
Q

What 4 things can provoke a seizure?

A
  • fever (children)
  • metabolic condition (adult)
  • structural changes
  • cellular changes
75
Q

What is the “Jacksonian March” a symptom of?

A

simple partial/elementary seizure, when seizure activity starts central and ends distal

76
Q

What is a simple partial or Elementary seizure? How might this patient present?

A

a seizure that only affects one hemisphere

  • jacksonian march
  • prodrome/aura
  • tachycardia, hypo/hypertension, diaphoresis, pupil changes
77
Q

What kind of seizures often occur in the temporal lobe?

A

Complex partial seizures

78
Q

What would someone with a complex partial seizure experience?

A
  • altered consciousness
  • hallucinations, déjà vu, idea flood
  • automatisms (repetitive, non-purposeful movements like tapping, scratching)
  • confusion after
79
Q

What is a secondarily generalized partial seizure?

A

a seizure with a focal onset that is actual generalized in nature.

  • tonic/clonic activity
  • may have aura
80
Q

When someone gives you a blank stare while standing motionless, or exhibiting automatisms for a a few seconds, what could be occurring?

A

absence or “petit mal” generalized seizures

81
Q

Sudden loss of muscle tone suggests…

A

Atonic generalized seizure or “drop attack”

82
Q

Describe a myoclonic seizure

A

brief, bilateral muscle contractions in your face, trunk or one or more extremities

83
Q

What is the difference between a tonic seizure and a clonic seizure?

A

Tonic shows rigid, violent contractions and clonic has repetitive contraction and relaxation
*Neither one affect LOC

84
Q

What occurs in a Tonic-Clonic seizure?

A

TONIC
-extension of extremities, loss of consciousness, incontinence, cyanosis
CLONIC
-rhythmic contraction/relaxation
-return to consciousness after reticular activating system starts to function
POSTICTAL
-come out of seizure

85
Q

If someone has a seizure that will not cease on its own or occurs successively, what is this called?

A

Status epilepticus

  • High mortality rate
  • must treat cause
86
Q

What 3 pathophysiological processes contribute to the development of alzheimers disease?

A
  1. Neuritic plaques
    - accumulation of amyloid peptide cause degenerative nerve terminals
  2. Neurofibrillary Tangles
    - Helical fibrous proteins
  3. Decreased enzyme that synthesizes acetylcholine
    - neurotransmitter associated with memory
87
Q

What are the manifestations of the initial stage of alzheimers?

A
  • denial
  • loss of memory
  • mild personality changes (withdrawal, loss of sense of humour)
88
Q

What does the moderate stage of alzheimers present with?

A
  • loss of problem solving
  • depression
  • hostility
  • SUNDOWN SYNDROME
89
Q

What is sundown syndrome?

A

a symptom of the moderate stage of alzheimers disease. Individuals exhibit confusion, agitation around sunset

90
Q

What are the hallmark signs of late stage alzheimers disease?

A
  • loss of ability to respond to family/environment

- incontinence

91
Q

Dementia that occurs secondary to other co-morbidities is called….

A

Vascular Dementia
as a result of damage from MI, arrhythmias, DM, PVD, infection, smoking
-causes slow psychomotor functioning
DEPRESSION COMMON

92
Q

Your patient has just undergone neuroimaging and been diagnosed with frontotemporal dementia. How can you explain this to the family?

A

it is a progressive syndrome that occurs secondary to atrophy of the frontal and temporal lobes of the brain.
-often become impulsive, exhibit inappropriate social behaviour, and become apathetic.

93
Q

What is the biggest concern with individuals diagnosed with frontotemporal dementia?

A

most die from INFECTION within 2-10 years

94
Q

What is Creutzfeldt Jakob Disease?

A

disease caused by the infective protein “prion” that causes bovine spongiform encephalopathy. These patients get dementia within 6 months of the infection because of the degeneration of pyramidal and extrapyramidal systems

95
Q

If I have a patient with Creutzfeldt Jakob disease, how will they present to me?

A
  • personality changes
  • visual/spacial coordination issues
  • impaired memory and judgement
  • insomnia
  • ataxia
  • death in months
96
Q

Who is at risk for Wernicke-Korsakoff Syndrome?

A

chronic alcoholics du to a thiamine deficiency

97
Q

How will my patient with Wernicke-Korsakoff Syndrome present to me?

A
  • weakness of eye muscles
  • Delirium, confusion, hallucinations
  • memory loss
  • POLYNEURITIS
  • Physical symptoms are reversible, but psychosis is NOT
98
Q

What is huntington disease?

A

hereditary disease that emerges in 40s-50s

that causes cell death in basal ganglia motor control

99
Q

What are the manifestations of huntington disease?

A

CHOREA–abnormal involuntary movement disorder of the feet and hands comparable to dancing
-cognitive decline

Pathophysiology (10 decks)

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