Unit 5: Chapter 6 Flashcards

(40 cards)

1
Q

Manifestations of Brain Injury

A

By changes in the LOC and alterations on cognitive, motor and sensory funtion

Cerebral hemisphere are the most susceptible to damage .

As structures in the diencephalon, midbrain, pons, and medulla are affected, signs related to pupillary and eye movement reflexes, motor function, and respiration become evident.
Hemodynamic and respiratory instability are the last signs to occur because their regulatory centers are low in the medulla.

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2
Q

LOC

A

Is caused by brain injury and disease.
Consciousness is the state of awareness of self and environment and of being able to orient to new stimuli
It is divided into:
(1)Arousal and wakefulness and (2) content and cognition.
Arousal and wakefulness require function of both cerebral hemispheres and an intact reticular activating system (RAS).
The content and cognition aspects of consciousness are determined by a functioning cerebral cortex.

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3
Q

Full Consciousness

A

Wakes alert and oiented x 3.

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4
Q

Confusion

A

Disoriented to time, place, or person; memory difficulty; difficulty following commands

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5
Q

Lethargy

A

Oriented to time, place, and person; very slow in mental processes, motor activity, and speech; responds to pain appropriately.

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6
Q

Obtundation

A

Responds verbally with a word; arousable with stimulation; responds appropriately to painful stimuli; follows simple commands; appears very drowsy.

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7
Q

Stupor

A

Unresponsive except to vigorous and repeated stimuli; responds appropriately to painful stimuli; lies quiet with minimal spontaneous movement; may have incomprehensible sounds and/or eye opening.

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8
Q

Coma

A

Does not respond appropriately to stimuli; sleeplike state with eyes closed; does not make any verbal sounds

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9
Q

Brain Death

A

The irreversible loss of function of hte brain including the brain stem.
Some conditions such as drug and metabolic intoxication can cause cessation of brain functions that is completely reversible, even when they produce clinical cessation of brain functions and electroencephalogram (EEG) silence. This needs to be excluded before declaring a person brain dead.

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10
Q

Vegetive State

A

Need nonoral feeding and full nursing care

Diagnosis of vegetative state includes absence of awareness of self and environment and inability to interact with others; absence of sustained or reproducible voluntary behavioral responses; lack of language comprehension; sufficiently preserved hypothalamic and brain stem function; bowel and bladder incontinence; and variably preserved cranial nerve and spinal cord reflexes.
The diagnosis requires that the condition has continued for at least 1 month.

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11
Q

Mechanism of Brain Injury

A

Injury to brain tissue can be due to trauma, tumors, stroke, metabolic derangements, and degenerative disorders.
Brain damage involves several common pathways, including the effects of ischemia, excitatory amino acid injury, cerebral edema, and injury because of ICP.
The mechanisms of injury are often interrelated.

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12
Q

Cerebral Edema

A

occurs with an increase in water and sodium content, causing an increase in brain volume.
Vasogenic edema occurs when fluid escapes into the extracellular fluid that surrounds brain cells, whereas cytotoxic edema involves the swelling of brain cells themselves.
The impact of brain edema depends on the compensatory mechanisms and extent of swelling.

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13
Q

Brain Energy

A

Mainly by ATP. As it is essential that cerebral circulation deliver O2 in high concentrations to facilitate metabolism of glucose and generate ATP.

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14
Q

Primary Injuries

A

Damage caused by impact

injuries include focal (e.g., contusion, laceration, hemorrhage) and diffuse (e.g., concussion, diffuse axonal injury) injuries. Secondary brain injuries are diffuse or multifocal, including edema, infection, and hypoxic brain damage.

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15
Q

Coup Injury

A

Direct contusion of the brain at the site of external force

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16
Q

Contrecoup Injury

A

The rebound injury on the opposite side of the brain

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17
Q

Hematomas

A

Rsult from vascular injury and bleeding.
Occurs as the brain strikes the rough surface of the cranial vault, brain tissue, blood vessles, nerve tracts and other structures are brushed and torn.
Bleeding occurs in several compartments: epidural, subdural, intracerebral and sunarachnoid spaces.

18
Q

Secondary Brain Injuries

A

which damage results from the subsequent brain swelling, infection, or cerebral hypoxia.
Most common : ischemia (result from hypoxia and hypotension)
Depends on the extent of damage caused by the primary injury.

19
Q

Epidural Hematoma

A

usually are caused by head injury in which the temporal area of the skull is fractured.
Develops between the inner table of the bones of the skull and the dura.
results from a tear in an artery, most often the middle meningeal, usually in association with a skull.
bleeding is arterial in origin, rapid expansion of the hematoma compresses the brain.
Occurs in younger ages as dura is less firmly attached to the to the skull.

20
Q

Subdural Hematoma

A

develops in the area between the dura and the arachnoid and usually is the result of a tear in the small bridging veins that connect veins on the surface of the cortex to dural sinuses.
The bridging veins pass from the pial vessels through the CSF-filled subarachnoid space, penetrate the arachnoid and the dura, and empty into the intradural sinuses. These veins are readily snapped when the brain moves suddenly in relation to the skull

21
Q

Traumatic Intracerebral Hematomas

A

May be single or multiple
Can occur in any lobe of the brain but most common in frontal or temporal related to the bony prominences on the inner skull surface
Occurs from severe motion that the brain undergoes during a head injury

22
Q

Stroke

A

Acute focal neurologic deficit from a vascular disorder that injures the brain.
80% are ischemic strokes caused by an interruption of blood flow in a cerebral vessel.
Hemorrhagic stoke is from blood vessel rupture caused by hypertension, aneurysm or ateriovenous malformation.

23
Q

ischemic Stoke

A

Cause by cerebrovascualr obstruction by thrombosis or emboli.

24
Q

Transient Ischemic Attacks (TIA)

A

eflects a temporary disturbance in focal cerebral blood flow that reverses before infarction occurs.
Causes of TIAs are similar to ischemic stroke and include atherosclerotic disease of cerebral vessels and emboli. TIAs may provide warning of impending stroke.

25
Arterivenous Malformations
are a tangle of abnormal arteries and veins linked by fistula(s). These networks lack a capillary bed, and the small arteries have a deficient muscularis layer. Thought to arise from failure in development of the capillary network in the embryonic brain. As the brain grows, the malformation forms a tangled collection of thin-walled vessels that shunt blood directly from arterial to venous circulation.
26
Arteriovenous Malformations Manifestations
are intracerebral hemorrhage and SAH, seizures, headache, and progressive neurologic deficits. Headaches often are severe, described as throbbing and synchronous with their heartbeat. Other, focal symptoms depend on the location of the lesion and include visual symptoms, hemiparesis, mental deterioration, and speech deficits.
27
Arteriovenous Malformations Patho
There are two major hemodynamic effects of arteriovenous malformations: 1. blood goes from a high-pressure arterial system to a low-pressure venous system without the buffering of the capillary network, predisposing venous channels to rupture and hemorrhage. 2. elevated arterial and venous pressures divert blood from surrounding tissue, impairing tissue perfusion.
28
Meningitis
inflammation of the pia mater, the arachnoid, and the CSF-filled subarachnoid space. Inflammation spreads rapidly because of CSF circulation around the brain and spinal cord. Inflammation usually is caused by an infection, but chemical meningitis can occur. Two types: acute purulent meningitis (usually bacterial) and acute lymphocytic (usually viral) meningitis.
29
Bacterial Meningitis
Most are caused by Streptococcus pneumoniae (pneumococcus) or Neisseria meningitidis (meningococcus), except in neonates (usually group B streptococci). Other pathogens that cause infection are gram-negative bacilli and Listeria monocytogenes. Bacteria replicate and undergo lysis in the CSF releasing endotoxins or fell wall fragments.
30
Bacterial Meningitis Manifestations
are fever and chills; headache; stiff neck; back, abdominal, and extremity pain; and nausea and vomiting. Other signs include seizures, cranial nerve palsies, and focal cerebral signs. Meningeal signs are also present: photophobia and nuchal rigidity
31
Viral Meningitis
course is less severe than BM and CSF findings are markedly different. There are lymphocytes in the fluid, the protein content is only moderately elevated, and the sugar content usually is normal. The acute viral meningitides are self-limited and usually require only symptomatic treatment, except for herpes simplex virus (HSV) type 2, which responds to intravenous acyclovir. caused by many viruses, most often enteroviruses, including coxsackievirus, poliovirus, and echovirus. Others include Epstein–Barr virus, mumps virus, HSV, and West Nile virus.
32
Focal Seizure
Begin in a spefic if area of the cerebral hemisphere Are without impairment of consciousness or with impaired consciousness \with observable motor or automobile components Involve sensory or psychic phenomena
33
Generalized Seizures
Most common type are classified when clinical signs, symptoms, and supporting EEG changes indicate involvement of both hemispheres at onset. The symptoms include unconsciousness and involve varying bilateral degrees of symmetric motor responses.
34
Motor: Tonic Clonic Seizure
formerly called grand mal seizures, are the most common major motor seizure. Frequently, a person has a vague warning and experiences a sharp tonic contraction of muscles with extension of extremities and immediate loss of consciousness. Incontinence is common. Cyanosis may occur from contraction of airway and respiratory muscles. The tonic phase is followed by the clonic phase, involving rhythmic bilateral contraction and relaxation of extremities. At the end of the clonic phase, the person remains unconscious until the RAS begins to function again (postictal phase). The tonic–clonic phases last approximately 60 to 90 seconds.
35
Motor: Myoclonic Seizure
Myoclonic seizures involve brief involuntary muscle contractions induced by stimuli of cerebral origin. It involves bilateral jerking of muscles generalized or confined to the face, trunk, or extremity.
36
Clonic Seizures
begin with a loss of consciousness and sudden hypotonia. This is followed by limb jerking that may or may not be symmetrical.
37
Tonic Seizures
There is a sudden onset of increased tone, which is maintained in the extensor muscles. It is often associated with falling.
38
Atonic Seizure
There is a sudden loss of muscle tone leading to slackening of the jaw, drooping of the limbs, or falling to the ground. These seizures also are known as drop attacks.
39
Nonmotor: Absense Seizures
are generalized, nonconvulsive epileptic events and are expressed mainly as disturbances in consciousness. Formerly referred to as petit mal seizures, absence seizures typically occur in children and cease in adulthood or evolve to generalized motor seizures.
40
ICP
Cranial Cavity contains 10% blood, 80% brain tissue and 10% CSF that all contribute to ICP. Maintained between 0 and 15 mm Hg when measured in the later ventricles. Resp alkalosis : Hyperventilation decreased PCO2 which can treat increase ICP.