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Pathophys > CNS > Flashcards

CNS Flashcards

1
Q

What are the most common causes of Brain Injury?

A

Falls, MVC, Moving objects or moving against stationary objects, assault, sports related events, blasts (because of a compressive wave).

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2
Q

What is the hallmark of severe brain injury? What is the most serious of the “not-as-serious” symptoms?

A 
LOC for more than 6 hours.
Memory loss (takes a lot of brain power to create memories)
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3
Q

A traumatic brain injury is an insult to the brain which possibly produces what five changes?

A
  1. Physical
  2. Intellectual
  3. Emotional
  4. Social
  5. Vocational
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4
Q

Who is at-rick for TBI? Name 5 and name whether men or women are more likely to sustain a TBI.

A
  1. Infants 6 months to 2 years
  2. School-Age children
  3. Adolescents and young adults 15-35
  4. People more than 70 years of age
  5. Persons living in high-crime areas

Men are 1.5 times as likely to sustain a TBI.

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5
Q

Focal brain injuries typically result in? Which of these is a huge problem?

A
  1. Observable brain lesion
  2. Cerebral edema (a little bit of edema is a HUGE problem in the brain where the pressure has no where to go).
  3. Coup injury
  4. Contrecoup injury
  5. Contusions.
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6
Q

Contusions can cause?

A
  1. Extradural (epidural hemorrhage or hematoma)
  2. Subdural hematoma (veins communicating to a sinus)
    Subarachnoid (aneurysm)
  3. Intracerebral hematoma
  4. Clinical manifestations of contusions
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7
Q

In an extradural hematoma what % have arterial bleeding? Where is the venous bleeding normally from? Are skull fractures likely? Where is the most common site for an extradural hematoma? Clinically what do we see first?

A
  1. 85% arterial bleeding (middle meningeal)
  2. 15% meningeal vein or dural sinus injury (teaks a lot to tear a sinus because it is essentially a vein lined with dura mater instead of epithelial cells)
  3. 90% have a skull fracture
  4. The temporal fossa is the most common site of extradural hematoma caused by injury to the middle meningeal artery or vein.
  5. Starts with nothing, then progresses to a headache, and then it becomes the worst headache of their life.
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8
Q

What percentage of patient’s with a TBI will have a subdural hematoma? What is the most common cause? What percentage will be associated with skull fractures? What else could cause it?

A
  1. 10-20% of persons with TBI
  2. MVCs are the most common cause
  3. 50% of subdural hematomas are associated with skull fracture.
  4. Falls (older adults, substance abuse)
    Brain gets jerked around. Tears the veins feeding the sinus.
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9
Q

What are the two types of subdural hematomas? What distinguishes them?

A
  1. Acute and Chronic
  2. Acute develops within 48 hours and is often located at the top of the skull. Chronic develops over weeks to months and is more often seen in older adults, alcohol abuse and 80% complain of chrinic headaches and have tenderness at the site of injury. Chronic could actually bleed slow enough that it causes the skull to grow.

(just had to palpate my head for tenderness…the hyperchondriac in me was momentarily convinced that my chronic migraines may have been caused a bleed following many concussions haha)

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10
Q

What are intracerebral hemorrhages(basically a hemorrhagic stroke) associated with? How do they act and what do they cause?

A
  1. Associated with MVC and falls
  2. Intracerebral hemorrhage and resultant hematoma acts as an expanding mass. Increased ICP and compression of the brain tissues with resultant edema.
    Blood pressure shoots up to supply the brain and then because of the increased pressure the veins get compressed. Brain wants the heart to crank up the pressure as high as the heart can. High pressure itself is hurting the situation. Need higher than normal pressure to perfuse the brain 160-180.
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11
Q

Diffuse Axonal Injuries (DAIs) are associated with what kinds of movements? What does this injury result in? What does the severity depend on?

A
  1. Diffuse Axonal Injuries are associated with shaking, inertial effect, acceleration and deceleration (shaken baby)
  2. DAIs are caused from axonal damage such as shearing, tearing or stretching of nerve fibers.
  3. The severity corresponds to the amount of shearing force applied to the brain and brainstem (RASS)…can be mild, mod or severe.
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12
Q

As a result of blunt trauma where the head strikes a hard surface of a rapidly moving object strikes the head, what happens to the dura? What two general types of injuries could this cause?

A
  1. The dura remains intact; brain tissue is NOT exposed to the environment.
  2. Causes focal (local) or diffuse (general) brain injuries.
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13
Q

In an extradural hematoma what % have arterial bleeding? Where is the venous bleeding normally from? Are skull fractures likely? Where is the most common site for an extradural hematoma? Clinically what do we see first?

A
  1. 85% arterial bleeding (middle meningeal)
  2. 15% meningeal vein or dural sinus injury (teaks a lot to tear a sinus because it is essentially a vein lined with dura mater instead of epithelial cells)
  3. 90% have a skull fracture
  4. The temporal fossa is the most common site of extradural hematoma caused by injury to the middle meningeal artery or vein.
  5. Starts with nothing, then progresses to a headache, and then it becomes the worst headache of their life.
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14
Q

Which type of brain injury accounts for more than 2/3 of head injury deaths?

A

Focal brain injury.

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15
Q

Which type of brain injury accounts for the greatest number of severely disabled survivors?

A

Diffuse axonal injury (DAI)

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16
Q

An injury directly below the point of impact is referred to as?

A

Coup-injury

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17
Q

An injury on the pole opposite of the site of impact is referred to as?

A

Contrecoup injury.

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18
Q

Temporary axonal distrubances causing attention and memory deficits but no LOC are termed? What branch of brain injuries are these under?

A
  1. Mild concussion

2. Diffuse brain Injury

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19
Q

How many grades of a mild concussion are there? Describe the differences,

A

1, 3
2. I: confusion, disorientation and momentary amnesia. II: momentary confusion and RETROgrade amnesia (lost memories that formed before the accident). III confusion with retrograde and ANTEROgrade (before and after) amnesia

Lower the number the less the prblem.

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20
Q

What is a Grade IV concussion termed?

A

Classic Cerebral Concussion.

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21
Q

Describe a classic cerebral concussion (4). What is the difference between a complicated and an uncomplicated classic cerebral concussion?

A
  1. Disconnection of cerebral systems from the brainstem and RAS.
  2. Physiologic and neurologic dysfunction w/o substantial anatomic disruption
  3. LOC under 6 hours
  4. Anterograde (can’t form new memories after the incident) and retrograde amnesia

Uncomplicated means no focal injury, complicated means focal injury.

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22
Q

Headache, cognitive impairments, psychologic and somatic complaints, CN signs & symptoms describe what syndrome? What is it’s treatment?

A
  1. Postconcussive syndrome
  2. Treatment includes reassurance and symptomatic relief as well as close observation fr 24 hours by a reliable individual so immediate intervention can be obtained if delayed effects become severe.
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23
Q

SC trauma commonly occurs from? As a result of? Most common locations are? How do we classify injury?

A
  1. Commonly occurs from vertebral injuries (simple fracture, compressed fracture and comminuted fracture).
  2. As a result of traumatic injury of vertebral and neural tissues due to compressing, pulling or shearing forces.
  3. Most common locations Cervical (1, 2, 4-7) and T1-L2 because they are the most mobile portions of vertebral column and the locations where the SC occupies most of the vertebral canal.
  4. Primary vs. secondary injury.
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24
Q

In spinal shock what happens to the normal activity below the level of injury? why? what does this include?

A
  1. normal activity below the level of injury ceases.
  2. Because the sites lack continuous nervous discharges from the brain
  3. Complete loss of reflex function (skeletal, bladder, bowel, sexual, thermal control, autonomic)

Neurogenic shock. Need the SNS to oppose the PSNS.

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25
Q

Loss of what is associated with neurogenic shock? Causing what four complications?

A
  1. Loss of sympathetic outflow

2. Vasodilation, hypotension, bradycardia and hypothermia

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26
Q

Autonomic hyperreflexia is stimulated by? And causes what?

A
  1. Stimulation of the sensory receptors below the level of the cord lesion
  2. Massive, uncompensated CV response to stimulation of the SNS.

Too much reflexes.

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27
Q

We can regrow injured axons at what rate? Considerations?

A

Rebuild it from the injured site to the end. However we only make proteins in the cell body in the dorsal root ganglion so the cell body has to send the proteins down that are carried by little motor molecules at 4mm/day. If anything gets in the way of it’s path then you can’t regrow it.
Myelinated axons are more likely to grow back.
It almost never happens in spinal cord trauma because of scar tissue (glial cells) that result in inflammation/necrotic tissue.

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28
Q

Necrosis consumes 40% of cross sectional cord within how many hours of trauma? and 70% within how many hours.

A
  1. 4

2. 24

29
Q

What kind of effect does cord swelling have on the degree of dysfunction?

A

Increases

30
Q

The increased degree of dysfunction related to cord swelling makes distinguishing what difficult? Where is swelling life threatening?

A
  1. Distinguishing functions to be lost permanently from those that are impaired temporarily becomes difficult
  2. In the cervical region
31
Q

Name some of the risk factors for strokes.

A

Familial history, people over 65-70, African American more than Caucasian, HTN, cardiac disease, A-fib, DM, smoking, increased lipoprotein a and homosystein, certain pneumonias.

32
Q

Intracranial aneurysms include which four types?

A

1, Saccular (berry) aneurysms

  1. Fusiform (giant) aneurysms
  2. Mycotic aneurysms-bacterial arthritis
  3. Traumatic (dissecting) aneursyms
33
Q

Which is more severe normally coup or contrecoup?

A

Coup but contrecoup is more severe then we think

34
Q

If we lose an old memory is there anything wrong with your memory forming system? What about if you can’t form new memories? What isn’t working correctly?

A

If you lose an old memory it doesn’t mean that there is anything wrong with your memory forming system. If you can’t form a new memory it means that the hippocampus and it’s friends aren’t working correctly.

35
Q

In spinal stenosis the pain and loss of function is what compared to the extent of the injury? why doesn’t this show up on MRIs?

A

Way out of proportion.

Doesn’t show up on MRIs because the MRIs are in 1cm intervals and the contact area could be 1mm.

36
Q

Many strokes is usually which artery? Survivable? Where is a popular place for hemorrhagic strokes?

A

Middle cerebral artery.
Yes
Blood vessels feeding the basal ganglia (lenticulostraiate arteries)

37
Q

What is an AVM? Where are we supposed to have them? What happens if we have them in the brain?

A

AVM is when arterioles run into venuoles and the only place this is supposed to be is our skin. Greater chance of rupture in the brain leading a patient to a hemorrhagic stroke.

38
Q

Can we have cancer of the neurons? Why or why not?

A

Cancer has to happen in cells that are mitotic and divide. Neurons do not divide (except ones in the olfactory bulb and hippocampus but not anywhere else)

39
Q

What type of cells do we have in the brain that can divide?

A

Glial cells (specialized epithelial cells that divide) except microglia (macrophage).

40
Q

Are cancers of the brain deadly because they metastasize?

A

No, they don’t actually invade of metastasize but they are deadly because they are growing in a closed space.

41
Q

First symptom of a brain cancer is? Other symptoms include?

A

First symptom is constant HA all the time.
Vision problems- compression of the optic nerve. Papilledema (enlargement of the blind spot, blurry vision, loss of vision in a particular area). Increased blood pressure in the eyes.
Speech and walking: any impaired brain function and it’s easy to lose the naturalness of these too and end up with slurred speech and unsteady gait.

42
Q

Why is aseptic meningitis names aseptic?

A

Because it’s not bacterial, however it is viral.

43
Q

What is the first indication of meningitis?

A

Neck is rigid. If they move their neck it hurts like hell.

44
Q

After an infection in the brain will axons grow back?

A

No, the infection blocks the route.

45
Q

What kind of memory loss do we see in dementia?

A

Anteriograde. They may forget where they put their keys but they remember what keys are for.

46
Q

What kind of memory loss do we see in Alzheimers?

A

Anteriograde and retrograde memory loss. They forgot where they put their keys and what their keys are for.

47
Q

In early onset Alzheimers what kind of predisposition is there? Can we predict late onset?

A

Genetic.

It is hard to predict for late onset.

48
Q

Is there more or less blood flow in Alzheimers?

A

Less.

49
Q

What have we lost in Parkinsons Disease? When is this made?

A
  1. Loss of the substancia nigra (neuro melanin) which is made during the production of dopamine. When the cells die they stop making dopamine and then become pale.
50
Q

Is the basal ganglia usually excitatory or inhibitory? If we lose one? What is it responsible for in PD?

A

Bunch of connections that are usually inhibitory.

If we lose one then everything goes widely off. Responsible for starting and stopping actions.

51
Q

What controls midcourse movements? Is this damaged in PD? Meaning?

A

Cerebellum
No
Movement if smooth (fine) mid-course

52
Q

Dopamine is a precursor to? Meaning if we lose it we’re going to have problems with?

A

Epi and nor epi

SNS

53
Q

What transports does El-dopa get into the brain using? When is this problematic?

A

Tyrosine, phenylalanine and tryptophan.

This is problematic after a protein rich meal.

54
Q

Can cells store El-dopa?

A

In initial PD yes they can. Later on in the disease the patients are going to need a constant supply.

55
Q

Do PD patient’s lose their sphincter control?

A

No just voluntary muscles.

56
Q

What disease is the exact opposite of PD? What is degenerated in this disease?

A

Huntington chorea.
The basal ganglia is also degenerated and we are depleted of GABA which is inhibitory so now we have too much output and have excessive starting and stopping. Muscles are always going.

57
Q

When parts of the brain (caudate and putamen) degenerate in Huntingtons what gets bigger?

A

Ventricles to fill up the rest of the space.

58
Q

What kind of disorder is MS? How does it present? Triggers?

A

Autoimmune, where the immune system attacks the myelin of the CNS. Any myelinated axon can be affected. Can show up as a vast range of problems. Normally the easiest to diagnose are clear cut effects on sense or motor when there is weakness in ONE specific muscle because of demyelination of axons controlling that spot.
No idea what the triggers are but it is thought to be part genetic and part environmental

59
Q

The progressive weakness of ALS leads to? What kind of effect does it have on cognition? Which motor neurons are affected?

A

Respiratory failure and death.
No effect on cognition
Upper and lower motor neurons.

60
Q

Why am I worried about Guillain-Barre syndrome? What kind of weakness do we see? Resolution rate? What causes this?

A

Because it normally shows up two weeks after an intestinal infection trigger.
Ascending motor weakness
Fairly decent resolution rate
Autoimmune.

61
Q

What is the trigger for Myasthenia gravis? What kind of disease is this? Explain. When does this regress? When does it get worse? Where does it normally start?

A

No idea what the trigger is. It is a chronic autoimmune disease where an IgG antibody is produced against the ACh receptors. No depolarization, muscle weakness. Regresses in the morning when axons have built up a ton of ACh vesicles and then as we go through this ACh they can no longer activate the receptors that are left.
Usually starts in the face most common is droppy eye (pitosis), trouble talking and swallowing. Progressive.

62
Q

Where is the big problem in myasthenia crisis?

A

When the muscles of respiration are lost. End up needed vent support.

63
Q

Why are the pupils really diagnostic?

A

Because they are controlled by a ton of places and can essentially indicate where the brain damage is.

64
Q

Can you survive cerebral death?

A

Yes but you just have your brainstem so you remain a vegetable in a coma.

65
Q

Does the brain use more or less energy in a seizure?

A

More, 250% increase in ATP usage, 60% increase in oxygen consumption. 250% increase in cerebral blood flow.

66
Q

Are the majority of our neurons excitatory or inhibitory?

A

Inhibitory

67
Q

What kind of intelligence do people with hydrocephalus have? What is the most common cause in children? How is it corrected? What is the most common cause in the older adult? Which is communicating and which is non communicating

A

Normal.
Obstruction in the cerebral aqueduct. Skull is malleable so it grows. NONcommunicating
Stick in a shunt.
Decreased re-absorption because of damaged arachnoid granulations (usually because of blood that has gotten into the CSF. Communicating.

68
Q

What is a normal pressure hydrocephalus?

A

If someone loses brain material that volume gets made up by an increase in the ventricles because of the atrophy of the brain.

69
Q

If a stroke progresses to the internal capsule what happens?

A

The internal capsule holds all of the information from the body to the cortex and vice versa. If you damage even a small section in this area you can be completely paralyzed or lose sensation from one side of your body.

Pathophys (5 decks)

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