Brain Injury: Final Exam Flashcards

1
Q

Define Focal Injury.

A

A focal traumatic injury results from direct mechanical forces (such as occur when the head strikes a windshield in a vehicle accident)

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2
Q

Define Global Injury.

A

Yielding a larger deficit from the injury. (Such as altered consciousness, coma, loss of reflexes)

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3
Q

What is the Reticular Activating System?

A

RAS is the brain stem’s reticular activation system (which is responsible for our wakefulness, and our ability to focus, fight-flight responses)
Low RAS activity means lower awareness/wakefulness

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4
Q

What Happens When the RAS Becomes Damaged?

A

Damage can cause an overall decrease in awareness and activity which will lead to:

  • Decreased Perfusion
  • Altered metabolic State (Metabolic acidosis)
  • Altered Consciousness
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5
Q

Define Brain Death.

A

Brain death is used to define a state where there is no motor control, no response to stimuli, no brain stem reflexes and apnea when the patient is removed from the oxygen machine.

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6
Q

Define Vegetative State.

A

The brainstem functions to maintain adequate hypothalamic function to meet basic metabolic needs. However, there is no awareness of self or surroundings, and an inability to voluntarily interact and reproduce behavioural responses.

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7
Q

Define Cerebral Edema.

A

Cerebral edema is the swelling of the brain bowling a primary brain injury! Caused by an increase in fluid within the extravascular space and increased ICP.

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8
Q

What is the Monro- Kellie Hypothesis?

A

It deals with how ICP is affected by CSF, the brain’s blood, and tissue and how these structures work to maintain cerebral perfusion pressure (CPP). If the volume of one of these structures increases, the others must decrease their volume to help alleviate pressure.

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9
Q

What are the Main Types of Edema?

A

Vasogenic: this occurs when the blood-brain barrier is compromised. Mainly a result of head injury, hemorrhage OR CNS infection which leads to inflammation. The blood flow is increased in the brain which causes Edema.

Cytotoxic: Increased Intracellular fluid shift into the cells, causing an increased ICP. Extracellular Na+ and other cations enter into neurons and astrocytes and accumulate intracellularly causing fluids to accumulate.

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10
Q

What Happens When the Intracranial Pressure Increases?

A

There is limited cerebral flow, due to the decreased cerebral perfusion from the building pressure in the brain. The brain cells will be starved from oxygen, blood and nutrients causing cellular dysfunction.

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11
Q

What is the Normal ICP?

A

Normal ICP= 0- 15 mmHg

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12
Q

Define Cranial Perfusion Pressure (CPP).

A

CPP= pressure gradient between the internal carotid artery and subarachnoid veins
(this tells us how much blood pressure is required to perfuse the brain)

The minimum CPP is 45 mmHg

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13
Q

Signs and Symptoms of Increased ICP.

A
  1. Mental Status Changes
  2. Irregular breathing
  3. Nerve changes to the optic and oculomotor nerve: double vision, swelling of the optic nerve (papilledema), pupil changes (decreased, increased, or unequal size)
  4. Cushing’s Triad: Increased systolic blood pressure (widening pulse pressure: increase in SBP and decrease in DBP), decreased heart rate, and abnormal breathing
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14
Q

Treatment for Cerebral Edema.

A
  1. Administer hypertonic normal saline solution
  2. Administer Osmotic Diuretics
  3. Drainage of CPF (if necessary)
  4. Treat the cause (Administer antibiotics, reperfuse, clot lysis)
  5. Maintain Vitals
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15
Q

Define Cerebrovascular Accident.

A

Also known as a STROKE. When blood flow to a part of your brain is stopped either by a blockage or the rupture of a blood vessel.

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16
Q

Two Types of CVAs

A
  1. Thrombotic/Ischemic Stroke
  2. Hemorrhagic Stroke
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17
Q

Define Thrombotic/ Ischemic Stroke.

A

Caused by a thrombus (blood clot) in a blood vessel that belongs to the brain. The clot affects the tissues surrounding it by restricting oxygen supply causing the neural tissue and cells to die unless the circulation is quickly returned.

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18
Q

Define Hemorrhagic Stroke.

A

Caused by a rupture of a cerebral vessel with associated bleeding into the neural tissue. A hemorrhagic stroke is when bleeding interferes with the brain’s ability to function. Hemorrhagic strokes have a sudden onset!

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19
Q

Treatment for Hemorrhagic Stroke.

A

Osmotic Directs and Hypertonic NS

(Diuretics help remove excess fluids, hypertonic NS shifts fluids OUT of the cells)

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20
Q

What Factors Increase the Risk of CVAs?

A
  • Hypertension
  • Coronary Artery Disease
  • Smoking
  • Artherosclerosis
  • Dyslipidemia
  • TIA (transient ischemic attack)
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21
Q

What is a Transient Ischemic Attack (TIA)?

A

A ‘mini stroke’. TIAs result when a cerebral artery is temporarily blocked, decreasing blood flow to the brain. Although the blockage is temporary it is a warning sign to indicate that an individual is at risk for a stroke.

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22
Q

Treatment for Ischemic Cerebral Vascular Accidents.

A
  • THROMBOLYTICS (Tissue plasminogen activator).
    • Thrombolytics allow for plasminogen to be converted into plasmin. The plasmin will cause the thrombus to degrade!
  • Carotid Endeterecormy (a.k.a Angioplasty)
    • Antiplatelets, anticoagulants
  • Treat hypertension, dyslipidemia addresses risk factors
23
Q

Define Dysarthria.

A

Weak muscle control (slurred speech)

24
Q

Define Dysphagia.

A

Difficulty Swallowing including; problems with coughing or choking when eating or drinking.

25
Q

Define Aphasia.

A

Impaired speech.

  • including speaking any words or saying the correct word(expressive aphasia)
  • comprehension of speech (receptive aphasia)
26
Q

Define Apraxia.

A

the inability to perform learned (familiar) movements on command, even though the command is understood and there is a willingness to perform the movement.

27
Q

Define Dyslexia.

A

a learning disorder that involves difficulty reading due to problems identifying speech sounds and learning how they relate to letters and words (decoding).

28
Q

Define Agnosia.

A

Inability to recognize and identify objects or persons.

29
Q

Define Meningitis.

A

Meningitis is an inflammation (swelling) of the protective membranes covering the brain and spinal cord. Specifically the inflammation of the pia mater, arachnoid, subarachnoid space (cerebrospinal fluid).

30
Q

What are the Two Ways of Infections for Meningitis?

A
  1. Bacterial (Purulent)
  2. Viral (Lymphocyte)
31
Q

Pathophysiology for Meningitis.

A
  1. Severe inflammation
  2. The blood-brain barrier is compromised
  3. Inflammation causes ‘capillary leaking’
    1. Release of Cytokines and Prostaglandins
  4. The accumulation of fluid causes cerebral edema
    1. Cerebral edema will result in increased ICP
    2. Increased ICP leads to a decreased CPP
  5. Vascular Congestion: obstruction of the normal flux of blood within the blood vessels of the brain
    1. The increased pressure decreased perfusion and accumulation of fluid impair circulation
  6. Cellular death: due to lack of oxygen, nutrient and perfusion
  7. Meningeal Thickening: the inflammatory response thickens the meninges
  8. The CSF will be trapped within due to limited space of flow which is called (hydrocephalus)
32
Q

Signs and Symptoms of Meningitis.

A
  • Fever
  • Headache
  • Stiff Neck
  • Seizures
  • Petechial rash (emergency signs of sepsis)
33
Q

Treatment for Meningitis.

A
  • Cephalosporins
  • Penicilins
  • Vancomycin
  • Glucocorticosteroids
34
Q

Sequelae of Treatment for Meningitis.

A
  1. Immediate administration of Broad-spectrum antibiotics
  2. Glucocorticosteroids
35
Q

How do Glucocorticosteroids Work?

A

They have the ability to suppress histamine release and inhibit the synthesis of prostaglandins and COX-2! They also suppress phagocytes and lymphocytes (two major mediations of an immune reaction). This inhibition of the immune system reduces inflammation!

36
Q

Define Seizures.

A

Spontaneous, abnormally synchronous electrical discharges from neurons in the cerebral cortex. It can cause changes in behaviour, movements or feelings, and in levels of consciousness.

37
Q

What are the Three Classifications of Seizure?

A
  1. Focal Seizures (Partial Seizures)
  2. Generalized Seizure
  3. Febrile Seizure
38
Q

Define Focal (Partial) Seizures.

A

When a seizure begins in just one area. In partial seizures, the excess neuronal discharge occurs in one cerebral cortex

39
Q

Define Global Seizures.

A

The aberrant electrical discharge involves the entire cortex of both hemispheres. Separated into two sections: petit mal and grand mal seizures

40
Q

Absence Seizures.

A

An absence seizure causes you to blank out or stare into space for a few seconds. They can also be called petit mal seizures.

41
Q

Tonic-Clonic Seizures.

A

The tonic-clonic seizure allows the muscles and joints to stiffen and subsequently the body will start to rhythmically jerk. Also known as grand mal seizures.

42
Q

Febrile Seizures.

A

Febrile seizures are convulsions that can happen when a young child has a fever above 100.4°F (38°C). (Febrile means “feverish.”)

43
Q

Life-Threatening Symptoms of Seizures.

A
  • Tonic convulsions cause muscular constriction which includes constriction of the airways!
    • Loss of consciousness impairs respiratory rate and depth
  • Large convulsions cause falls
    • Prevent injury and keep the patient in a secure position
  • Stimulation of ANS causes severe VS change
    • Monitor patient for tachycardia, hypertension, reflex hypotension, hyperventilation
44
Q

How are Seizures Treated?

A
  • Benzodiazepines
  • Barbituates
  • Anticonvulsants
45
Q

How Do Benzodiazepines Treat Seizures?

A

Benzodiazepines (sometimes called “benzos”) work to calm or sedate a person, by raising the level of the inhibitory neurotransmitter GABA in the brain. Benzodiazepines= ‘sedativ-hypnotic” drugs. Benzodiazepines open GABA-activated chloride channels and allow chloride ions to enter the neuron. This action allows the neuron to become negatively charged and resistant to excitation. (Cl- agonists)

46
Q

Benzodiazepine (Medications).

A
  • Lorazepam (Ativan)
  • Alprazolam (Xanax)
  • Diazepam (Valium)
47
Q

Benzo Overdose Treatment.

A

Flumazentil (Romazicon)

48
Q

Kinetics of Benzos.

(How is it metabolized and excreted?)

A
  • Hepatic metabolism (metabolized by the liver)
  • Excreted through urine (Renal Excretion)
  • Crosses placenta and breastmilk
49
Q

How do Barbituates Treat Seizures?

A

Barbiturates amplify the effects of the neurotransmitter GABA (gamma-aminobutyric acid) by influencing GABA receptors.

50
Q

Barbituates (Medications)

A
  • Phenobarbital
  • Pentobarbital
  • Secobarbital
  • Butalbital
51
Q

Side Effects of Benzos and Barbituates.

A
  • Respiratory Depression
  • Altered LOC and CNS activity
  • Very high risk of overdose
  • Highly addictive
52
Q

How do Anti-Convulsant Treat Seizures?

A

Alter electrolyte movement – delay action potential, decrease neuronal activity. These medications decrease the flow of Calcium and Sodium ions across the neuronal membranes.

53
Q

Anti-Convulsant (Medications)

A
  • Phenytoin (Dilantin)
  • Carbamazepine (Tegredol)
  • Valproic Acid (Valporate)
54
Q
A