NUR2063 Final Exam module 7,8,9 Focused Review graded A+

NUR 2063 Module 7, 8, 9 Focused Review

 Brain abscess s/s (infection, pus)

Signs of infectious etiology, localized collection of pus

-Stiff neck, headache, intracranial pressure, change in LOC, vision/speech/behavior

changes

 Priority assessments

ABC’s (airway, breathing/respiratory, circulation/cardiovascular), level of consciousness

 Glascow coma scale

Used to assess LOC in acutely brain-injured patients, eye opening/arousal-directed

responses/motor reactions, under 8 is severe, over 12 is mild

 Mechanisms of spinal cord injuries

Hyperflexion (forward), hyperextension (backward), compression

 Decorticate vs decerebrate posturing

Decorticate=abnormal flexor (arms/hands up on chest), decerebrate=abnormal extension

(arms/hands at sides)

 Meningitis (S.P. bacteria in CNS)

-Bacteria usually reach the CNS via the bloodstream or extension from cranial structures

like sinuses or ears.

-Most common bacteria are Streptococcus pneumoniae.

-Bacteria invade leptomeninges; accumulation of inflammatory exudate can result in

obstructive hydrocephalus (excess fluid in head).

-Classic presentations: headache, fever, stiff neck (meningismus), and signs of cerebral

dysfunction (confusion, delirium)

 Types of traumatic brain injuries

LOCATION: Primary=focal (coup), polar (coup countercoup)(acceleration/deceleration,

injury to polar sides), diffuse (widespread)

MECHANISM: Concussion, contusion, intracranial hematomas=epidural, subdural,

subarachnoid

SEVERITY: Secondary Injury=ischemia (decreased blood flow), hypoxic events

(decreased blood oxygenation), vasogenic/neurogenic edema

 Focal (coup) brain injuries

-Localized to site of impact

-Decreased LOC, muscle weakness, cranial nerve dysfunction

 Difference between hemorrhagic stroke and thrombotic/embolic stroke (ischemic) as

well as diagnosis

-Ischemic strokes result from sudden occlusion of a cerebral artery secondary to

thrombus formation or embolization

-Thrombotic strokes associated with atherosclerosis and coagulopathies- clot traveled to

brain

-Hemorrhage within the brain parenchyma , usually occurs secondary to severe, chronic

hypertension (secondary injury, morbidity much higher)

-CT, MRI, LOC

 Increased intracranial pressure s/s

-Headache, vomiting, and altered level of consciousness (drowsiness)

-Blurry vision and edema of the optic disk (papilledema)

-As ICP rises to higher levels, LOC decreases, pupil responsiveness to light becomes

impaired; altered respiratory patterns and unresponsive to stimulation; unable to move,

verbalize, or open the eyes

 Activities that cause traumatic brain injuries

Transportation-related accidents, falls, firearms, sports-related accidents

 Differences between subarachnoid hemorrhage, epidural hematoma, subdural

hematoma

Subarachnoid: (berry aneurysm/circle of willis/thunderclap)

-Collection of blood between arachnoid membrane and the pia mater

-Caused by rupture of bridging veins that pass through the subarachnoid space

-More commonly associated with rupture of cerebral aneurysms or arteriovenous

malformations; arterial in origin

-Blood spreads throughout CSF, causing meningeal irritation, hydrocephalus, headache,

vasospasms, ischemia

Epidural: (lens/arteries/trauma/lucid interval before rapid deterioration)

-Collection of blood between dura and skull, outside brain tissue

-Typically involves arterial injury thus rapid onset of symptoms

-Brief period of disturbed consciousness followed by a period of normal cognition (lucid

interval), then consciousness rapidly deteriorates

Subdural: (crescent/veins/older/alcohol/rebleeding risk/increased ICP)

-Collection of blood between dura and outer layer of arachnoid membrane

-Typically involves bridging veins; symptom onset may be slower

-Acute: symptoms within 24 hours of injury

-Subacute: increased ICP (headache, vomiting, blurred vision) 2 to 10 days later

-Chronic: prone to rebleeding

 Diagnosis of seizures

-Clinical symptoms

-Electroencephalograms: assess electrical patterns of brain regions

-Laboratory studies: identify metabolic/nutritional deficits, infections, and exposure to

toxins

-Lumbar puncture: for CNS infections

-CT, MRI: for structural causes

 Cerebral aneurysm (dilation/ballooning of an artery, circle of willis)

-Lesion of an artery that results in dilation and ballooning of a segment of the vessel

-High blood pressure, acute alcohol intoxication, and recreational drug use (especially

cocaine) implicated

-Congenital defect of the medial layer of the artery weakens, allowing dilated portion to

fill with blood and eventually burst causing hemorrhage; most found in circle of Willis.

-Clinical manifestations: typical presentation is severe headache with meningismus;

photophobia (visual sensitivity to light), n/v

 Reperfusion injury

- Once blood supply is re-established, injury is caused by free radicals