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N206B

N206B

by trinellipe9, Nov. 2010

Subjects: cushing headaches icp injuries migraines seizures spinal triad

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212 Cards in this Set

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	Headaches Name types of headaches	1) Cluster 2) Migraine 3) Tension
	Headaches Cluster headache 1) site 2) quality 3) frequency 4) specific characteristics	1)Unilateral, radiating from temporal region or around the eye 2) Deep and penetrating, not pulsating 3) 2-3 attacks/day over a period of weeks; Months between attack periods 4) Onset abrupt; Pain peak 10 minutes; Duration 90 minutes; Commonly nocturnal
	Migraines Migraine headache 1) site 2) quality 3) frequency 4) specific characteristics	1) Unilateral and anterior 2) Throbbing and pulsating 3) Periodic- cycles for months to years 4) Combo of neurological, vascular and chemical components; Stress, excitement, bright lights, menstruation, alcohol and/ or foods
	Migraines What's the patho. of a migraine?	Unknown pathophysiology. What is known: triggers stim. the Trigeminal Nerve. Decreased serotonin levels Dilatation and inflammation of the blood vessels feeding the meninges
	Migraines What are the most common stages of migraine headache?	Aura, Headache, Resolution.
	Migraines Describe the aura stage of a migraine. What's is symptom of? S/S are?	Flashing lights in one quad. of the visual field. Patient specific experience. A symptom of reversible brain dysfunction: Dizziness, Confusion Numbness or burning, Motor dysfunction
	Migraines 1) How long does an aura dev. over? 2) What's the duration of an aura? 3) How long will the headache last?	1) over 4 minutes 2) less than 60 minutes 3) within 60 minutes of aura
	Migraines A migraine headache must have 2 of the following characteristics? In addition to either..	Unilateral, Pulsating pain, Moderate to severe intensity, Worsens with activity. Nausea, vomiting, photophobia, or phonophobia.
	Migraines Describe migraine's resolution stage.	Receding headache symptoms, Extreme fatigue, Dizziness, Mild Confusion.
	Migraines Describe how a migraine headache can be managed.	1) Assist the patient to ID and eliminate the trigger: Stress, Dietary, Chemical 2) Pharmacological Assistance: Balancing serotonin levels, Controlling vasodilatation
	Migraines Tension Headaches 1) Site 2) Quality 3) Frequency 4) Triggers	1) Bilateral band like pressure around the head 2) Constant pressure 3) Sporadic, assoc. w/contraction of muscles of neck and skull 4) Neck, shoulder muscle contraction
	Migraines/Cluster headaches Migraine and Cluster headaches patho?	Unknown What is known? Triggers stimulate the Trigeminal Nerve Patient has decreased serotonin levels Serotonin is a vasoconstrictor Dilatation and inflammation of the blood vessels within the meninges create a pain response
	Migraines/Tension Headache What do alpha adrenergic blockers do for migraines or tension headaches? Examples?	Produces vasoconstriction of dilated blood vessels. Ergotamine tartrate (Ergomar) Methysergide (Sansert)
	Migraines/Tension Headaches What do serotonin (5HT 1) receptor agonists do for migraines or tension headaches?	Acts to promote serotonin receptor (5HT 1) site efficiency – in the intracranial blood vessels and the sensory trigeminal nerves Effect is Cranial vessel vasoconstriction which reduces inflammation within the cerebral blood vessels.
	Migraines/Tension Headaches Examples of serotonin (5HT 1) receptor agonists? What's an important nursing consideration for serotonin (5HT 1) receptor agonists?	Almotriptan (Axert), Eletriptan (Relpax), Frovatriptan (Frova), Naratriptan (Amerge), Rizatriptan (Maxalt), Sumatriptan (Imitrex), Zolmitriptan (Zomig). These drugs are “triptans” and they have a pharmacological effect of vasoconstriction
	Migraines Who shouldn't have the “triptan” drug? When would we use a beta blocker in the care of a migraine headache patient?	It's a beta-adrenergic blocker and causes vasodilation. To prevention of migraine headaches. Should not be used in the event of an acute onset of migraine headache
	Migraines Analgesic Combos. What are the most common ones.	Acetaminophen, dichloralphena-zne and isometheptene (Midrine) Butalbital with aspirin (Fiorinal) or acetaminophen (Fioricet) Note Fiorinal/Fioricet are falling out of favor as treatment of choice because they have a strong possibility of dependency
	Migraines Clinical Management of headaches?	Control nutritional triggers of headaches. Monosodium Glutamate (MSG) Found as a preservative in many foods, commercial Chinese food, Aged Cheese, Caffeine, Chocolate, Nitrites, Nitrates, Red Wine. Patient food diary Including the time period where headaches occurred Assessment for list of foods which commonly were ingested prior to onset of headache Food elimination trial Eliminate one identified possible trigger and assess for decrease in number of headaches
	Seizures Seizures D/O vs. Epilepsy	Seizure D/O: Periods of abnormal electrical discharges in the brain that cause involuntary movement, behavior and sensory alterations Epilepsy: chronic disorder characterized by recurrent, unprovoked seizures secondary to a central nervous system disorder; 1 in 100 people have epilepsy
	Seizures Phases of Seizures	1) Prodromal 2) Aural 3) Ictal 4) Post-Ictal
	Seizures Describe Prodromal and Aural stages of a seizure.	1) Prodromal= Signs and activities that precede the seizure event Triggers for seizure activity. Example: flickering of lights “triggers” a seizure 2) Aural (Presence of Aura)= A sensation (visual, auditory, taste or motor) that gives a warning of an impending seizure. Allows the patient to take medications or move to a safe place to avoid injury.
	Seizures Describe Ictal and Post-Ictal stages of a seizure	1) Ictal =Full seizure activity 2) Post-ictal= Period of recovery after the seizure
	Seizures Describe febrile seizure? Is there inc. ICP? What's the usual age? What's peak age? What's chance of future seizures? Why?	Connected with a sudden rise in temperature usually associated with an illness or infection. No evidence of increased ICP. Usual age= 3 months to 5 years Peak age 18-24 months Carries a 30-50% greater chance of having future seizure disorder Indicates child has a lower convulsive threshold
	Seizure What's a generalized seizure? s/s of generalized seizure?	result of diffuse electrical activity in both hemispheres of the brain at the same time, spreading throughout the cerebral cortex and brainstem Symptoms bilateral and symmetrical
	Seizure What's a Partial (focal) seizure? s/s of partial (focal) seizure?	abnormal electrical activity in one hemisphere or specific area of the cerebral cortex Symptoms depend on area of brain affected
	Seizure Types of generalized seizure?	1) Typical Absence Seizure (Petit Mal) 2) Tonic-Clonic (Grand Mal) 3) Akinetic/Astatic/Atonic
	Seizure Describe Tonic-Clonic Seizures. Duration of tonic and clonic stages? Post-ictal stage?	1)Tonic phase: stiffening of the body Clonic phase: subsequent jerking of the extremities 2) Tonic: 10-20 seconds; Clonic: 30-40 seconds following tonic phase 3) Fatigue and no memory of seizure General duration 30-40 seconds following tonic phase Post-ictal fatigue No memory of seizure event
	Seizure Describe Typical Absence seizure (Petit Mal) Seizures.	Occurs rarely in adults Few seconds of staring Often goes un-noticed Can occur 100 times/day
	Seizure Describe Akinestic/Astatic/Atonic Seizures. Risk fo what?	Akinetic: arrest of movement Astatic: loss of balance Atonic: loss of body tone Akinetic, Astatic and Atonic seizures can present as “drop attacks” or “falling spells” Patient regains consciousness before hitting ground in fall Increased risk for head injury in this type of seizure
	Seizures How many types of Partial seizures?	1) simple partial seizures 2) complex partial seizures
	Seizures Describe Simple Partial Seizures: 1) Duration 2) Includes what? 3) Effect on consciousness? 4) AKAs	1) less than one minute 2) simple motor, autonomic or sensory phenomena 3) No loss of consciousness 4) Focal motor seizure, Focal sensory seizure, Jacksonian
	Seizures Describe Partial Seizures: 1) Duration 2) Includes what? 3) Effect on consciousness?	1) longer than one minute 2) Automatisms: repetitive movements that are inappropriate, lipsmacking, Picking at objects 3) impaired consciousness, clouding of it. **Otherwise similar to simple partial seizures.
	Seizures Complications of seizures Status Epilepticus is a? Is? Duration? Cause?	1) medical emergency 2) Continuous seizures or seizures in rapid succession, with regaining consciousness 3) last greater than 30 min. 4) sudden withdrawal of anti-seizure meds
	Seizures What's so dangerous about Status epilepticus?	1) Supplies of glucose and oxygen are dramatically reduced during it. Brains metabolic needs increase during a seizure event.
	Seizure What should the nurse assess before a seizure?	Circumstances which occurred before the seizure, triggers, if there was an aura.
	Seizure What should the nurse assess during a seizure?	Id the 1st motion of the patient, where the movement or stiffness starts gives clue to the location of seizure origin, Movements types, Areas of body in movement, pupil size, eye open or closed? Length of seizure Important because the risk of airway and metabolic complications increases with an extended duration of seizure activity, Presence of automatisms, Incontinence, Duration of each phase, LOC
	Seizure What should the nurse assess after a seizure?	Presence of: Paralysis or weakness Ability to speak Describe movements at the end of the seizure Identify if patient fell asleep after the seizure Describe cognitive state (level of confusion) after the seizure
	Seizure What are the goals of nursing management of seizures?	Accurate assessment/documentation of the event Prevent complications: Safety (injury), Aspiration, Loss of patient’s personal dignity, Metabolic complications
	Seizure How can the nurse ensure accurate assessment/ documentation of the event?	Before: Turn back the bedsheets to expose entire body surface to assessment of body movement. During: Stay focused on assessment of critical areas of concern After: Document your findings Communicate findings to the physician
	Seizure How can the nurse ensure safety of patient before the event?	Before: If aura gives warning, ease patient to the floor if possible. If in bed, remove pillow, raise siderails. Protect the head by placing padding over hard objects in area. Loosen constrictive clothing
	Seizure How can the nurse ensure safety of patient during and after the event?	During: Push furniture out of the area, Do not restrain the patient in any manner. After: Anticipate confusion, anticipate agitation, re-orient patient upon awakening
	Seizure How can the nurse prevent aspiration of patient before and during the event?	Before: Maintain available oxygen, Maintain available suction equipment, Place patient on side with head flexed forward. During: Do not attempt to open airway, Do not attempt to restrain patient in anyway.
	Seizure How can the nurse prevent aspiration of patient after the event?	After: Keep patient on side immediately following seizure, Attain patent airway, Assess need for artificial airway, Assess need for suctioning, Anticipate a short episode of apnea
	Seizure How can the nurse prevent loss of patient's personal dignity before/during/after after the event?	Before, during and after the event: Provide privacy screen for exposed patient Remove onlookers from area
	Seizure How can the nurse prevent metabolic complications before/during/after after the event?	Before: Access pulse ox, oxygen and capillary glucose. After: Immediate assessment of oxygen saturation level, immediate assessment of capillary glucose reading, supplemental oxygen
	Seizure How can seizures be managed non-pharmacologically?	1) Ketogenic diet: Esp. common in treatment of children. High intake of fat, Low intake of protein and carbohydrate. Duration 2-3 years of the diet. Must monitor the urine for ketones. Surgery: Remove a tumor, lesion or portion of the brain which is identified as causing the seizures
	LOC What's the most important indicator of neurological dysfunction?	Altered state of consciousness. Accurate assessment is crucial.
	LOC Consciousness vs. Unconsciousness	Consciousness: Ability of mind to respond to stimuli. Two components Alertness: ability to react to stimuli Cognitive: ability to process stimuli and respond appropriately verbally or physically. Unconscious: Depressed cerebral functioning. Inability of the mind to respond to stimuli.
	LOC What are the types of consciousness?	1) Confusion 2) Delirium 3) Obtunded 4) Stupor 5) Coma
	LOC What are common causes of altered state of consciousness.	Hypoxia Trauma Edema Tumor formation Decrease in blood flow Increase in blood flow Alteration in flow of cerebrospinal fluid
	LOC Describe 1) Confusion 2) Delirium 3) Obtunded	1) Disoriented to time, place or person 2) Expression of confusion accompanied by fear, agitation, hyperactivity or anxiety 3) Expression of confusion accompanied by fear, agitation, hyperactivity or anxiety
	LOC Describe 4) Stupor 5) Coma	4) Response to vigorous stimulation only 5) Severely diminished response Not aroused by painful stimuli Unaware of self or environment for prolonged period of time. Some evidence that auditory ability is intact
	ICP What are the three components of the head? Why's that important?	1) Brain tissue, Blood, Cerebrospinal fluid. 2)The total intracranial volume will not change, so if volume in any one of the three components increases, the volume from another much change because the cranial vault is rigid
	ICP What factors influence ICP? What's the normal ICP?	Arterial pressure, Venous pressure Intra-abdominal and Intra-thoracic pressure, Posture (attitude or position of the body), Temperature, Blood gases (carbon dioxide levels) 0-15 mmHg
	ICP How can the body compensate to maintain normal ICP?	1) Changes CSF volume 2) Displacement CSF into the subarachnoid space 3) Alter intracranial blood volume 4) Collapse of cerebral veins & dural sinuses 5) Cerebral vasoconstriction or vasodilation 6) Change in venous outflow 7) Displacement brain tissue through compression or dispense into dura.
	ICP Assessment findings? card 1 of 3	1) Change in LOC 2) Change in VS d/t increasing pressure on the thalamus, hypothalamus, pons and medulla 3) Cushing Triad (Increasing systolic BP (widening pulse pressure), Bradycardia with bounding pulse, Irregular breathing pattern)
	ICP Assessment findings? card 2 of 3	4)Vomiting 5) Decrease in motor function (hemiparesis or hemiplegia to the side of injury, decreased ability to react to painful stimuli)
	ICP Assessment findings? card 3 of 3	6) Ocular signs: due to compression of ocular motor nerve 7) Dilation of pupil ipsilateral (on the side of the insult) 8) Sluggish or no response to light 9) Inability to move eye upward 10) Ptosis of the eyelid (drooping) 11) Fixed and dilated pupil (neurological emergency) 12) Headache
	ICP Serious complications of increased ICP? Which compartment? Diminished cerebral perfusion pressure and places brain at risk for?	1) Life threatening 2)Increase in any of any the 3 components of ICP 3) Ischemia, Infarction Many injuries which cause increased ICP further complicate it by causing hypoxia or acid/base imbalance
	ICP Describe decorticate posture.	flexion of arms, wrists and fingers with adduction in upper extremities, extension and internal rotation of lower ext.
	ICP Describe decerebrate posture?	more serious brain damage, all four extremities in rigid extension with the hyperpronation of forearms and plantar flexion of feet
	ICP What are the goals of collaborate management of ICP?	1) Identify the causative factor of ICP 2) Support brain function
	ICP How is oxygenation ensured for ICP patient.	Support brain function Endotracheal intubation to maintain adequate ventilation Maintenance of ABG PaO2 at 100 mmHg or greater Maintenance of fluid balance Maintenance of systolic blood pressure between 100-160 mm Hg Reduction of cerebral metabolism Introduction of high dose barbituates
	ICP How should patient be positioned to support brain function?	Elevate head of bed to 30 degrees to allow for gravitational drainage Head in a neutral position
	ICP What drugs are given for ICP?	1) Osmotic diuretics (Mannitol) 2) Loop diuretics (Lasix) 3) Anti-seizure medications (Dilantin) 4) Corticosteroids (Decadron) 5) Histamine H2 receptor antagonists and/or 6) proton pump inhibitors Prevention of peptic stress ulcers due to chronic long term stress
	Brain injury Causes? Damage to? When/where swelling?	1) diffuse axonal injury 2) to axons in the subcortical white matter of the cerebral hemispheres (Basal ganglia, Thalamus, Brainstem) 3) Axonal swelling develops 12-24 hours after the injury
	Brain injury Types of brain injury Commonly associated with closed head injury	1) Cerebral contusions 2) Cerebral lacerations
	Cerebral Contusion What is cerebral contusion? Commonly occurs where? Accompanied by:	1) Bruising of brain tissue with a focual area that maintains the integrity of the pia mater and arachnoid layers 2) in an area of fracture 3) Hemorrhage, Infarction, Necrosis, Edema
	Cerebral Contusion What is Coup-contrcoup? Occurs where?	1) Mass movement of the brain within the skull 2)at the site of direct impact of the brain on the skull (coup) Secondary site of damage on the opposite side of the skull from the original area (contrecoup)
	Cerebral Laceration What's laceration? Associated with what? Repair possible? Accompanied by what?	1) Actual tearing of the brain tissue 2) Fractures and penetrating injuries 3) Tissue damage is severe and surgical repair is impossible 4) Bleeding into the parenchyma Focal and General Neurological deficits
	Cerebral Laceration What are some s/s of cerebral laceration?	1) Decreased LOC 2) Increased ICP 3) Decorticate dysfunction 4) Decerebrate dysfunction 5) Cerebral edema 6) Neuro. deficits r/t impacted brain area by increased pressure
	Brain Injury Complications What are some brain injury complications?	1) Epidural Hematoma 2) Subdural Hematoma 3) Intracerebral Hematoma
	Brain Injury Complications Describe Epidural Hematoma Where's the bleeding? Is it an emergency? Why/why not? Onset of sx? Describe sx?	1) Bleeding between the dura and inner surface of the skull 2) Yes, it's a Neuro. emergency b/c it's usually an arterial bleed and a hematoma develops rapidly. 3) Rapid onset 4) Decreased neuro integrity, Decreased LOC, N/V, Unconsciousness
	Brain Injury Complications Describe Subdural Hematoma Where's the bleeding? Type of bleed? Why/why not? Onset of sx? Describe sx?	1) Bleeding between the dura mater and arachnoid layer of the meningeal covering of the brain 2) Generally a venous bleed, hematoma develops gradually 3) Symptoms occur within 48 hours of injury 5) Drowsiness, Confusion, Pupillary changes, Headache, Decreasing LOC
	Brain Injury Describe Intracerebral Hematoma Where does it occur? What happens? Why/why not? When else might it happen?	1) Injuries involving frontal and/or temporal lobes 2) Rupture of intracerebral vessels A “burst” of vessels feeding the lobes 3) May occur as an extension of a subarachnoid bleed
	Head injury/lesion What's emergent treatment for all head injury/lesion?	1) Ensure patient airway 2) Stabilize cervical spine 3) Admin. O2 via nasal cannula or non-rebreather mask 4) Est. IV access 5) Control external bleeding 6) Assess for nose drainage 7) Assess for ear drainage 8) Remove patient clothing
	Head injury/lesion What's the ongoing treatment for all head injury/lesion?	1) Maintain patient warmth (blanket, warm IV solution, warm humidified oxygen) 2)Assess VS 3) Assess neuro. status 4) Anticipate absent gag reflex 5) Administer fluids cautiously with attention to increased ICP.
	Head injury/lesion What's nursing considerations for all head injury/lesion?	1) Loss of corneal reflex so admin. lubricating eye drops, secure eyes in closed position to prevent abrasion 2) Periorbital ecchymosis so apply cold compresses (first 24 hours) and warm compresses afterwards. 3) Hyperthermia d/t injury or inflammation at the thalamus so Control hyperthermia. Some evidenced based practice results Hypothermia in the first 24 hours following injury may decrease long-term complications
	Cranial Surgery Purpose of cranial surgery?	1) Localized fluid collection 2) Blood collection 3) Lesion 4) Damaged area of brain tissue 5) Relieve increased ICP
	Cranial Surgery Types of cranial surgeries	1) Burr Hole 2) Craniotomy 3) Craniectomy 4) Cranioplasty 5) Stereotaxis 6) Shunt
	Cranial Surgery Describe Burr hole Describe Craniotomy Describe Craniectomy	1) Opening into cranium with a drill Small localized area. 2) Opening into the cranium with removal of a bone flap to provide an opening to the dura. 3) Excision into the cranium to cut away a bone flap
	Cranial Surgery Describe Cranioplasty Describe Stereotaxis	4) Repair of cranial defect resulting from trauma, malformation, or previous surgery. Artificial bone replaces damaged or lost bone mass 5) Precision localization of a specific area of the brain. Uses a frame or frameless aparatus to immobilize head and maintain set coordinates. Utilized for biopsy, radiosurgery or dissection.
	Cranial Surgery When is a craniotomy indicated?	Ultimate required treatment to: remove bone fragments resulting from fracture. Remove blood resulting from hemmorrhage. Visualize bleeding vessels.
	Cranial Surgery When are Burr Holes indicated?	Emergent treatment to reduce ICP Drain placed (several days) post-op. to prevent reaccumulation of blood
	Cranial Surgery What do shunts do?	They create an alternate pathway to redirect CSF from one area to another area using a tube or implanted device
	Cranial Surgery What should the nurse assess for? What are the patient goals?	1) increased ICP 2) Patient will: -- return to normal consciousness -- be free of pain and discomfort -- have maximum neuromuscular functioning -- be rehabilitated to maximum ability
	Cranial Surgery What are some common nursing diagnosis?	1 ) Ineffective airway clearance r/t decreased LOC and immobility. 2) Ineffective tissue perfusion (cerebral) r/t cerebral edema. 3) Impaired skin integrity r/t nutrition and immobility 4) Self-care deficit r/t altered LOC 5) Interrupted family processes r/t comatose family member.
	Cranial Surgery -- Nursing dx Interventions for: Ineffective airway clearance related to decreased level of consciousness immobility	1) Main. patient in side lying position 2) Suction frequently 3) Perform chest PT 4) Monitor for signs of deoxygenation
	Cranial Surgery -- Nursing dx Interventions for: Ineffective tissue perfusion (cerebral) related to cerebral edema	1) Monitor neuro. status 2) Monitor ICP 3) Limit activities that increase ICP 4) Provide comfort measures to decrease agitation 5) Elevate HOB to 30 degrees 6) Monitor reactions to all medications
	Cranial Surgery -- Nursing dx Interventions for: Impaired Skin Integrity related to nutritional deficit, self care deficit and immobility	1) Assess skin frequently 2) Turn and reposition Q 2 hour 3) Use low air loss beds 4) Cleanse all abrasions and lacerations
	Cranial Surgery -- Nursing dx Interventions for: Self care deficit related to altered level of consciousness	1) Assess level of motor and sensory ability 2) Bathe patient daily 3) Perform range of motion 4) Begin bowel program 5) Provide urinary catheter care
	Cranial Surgery -- Nursing dx Interventions for: Interrupted family processes related to comatose family member	1) Assess effect of illness on family 2) Teach and assist family members to provide care 3) Facilitate family communication 4) Facilitate realistic family planning 5) Provide accurate information to family members
	CVA/Stroke/Brain attack What is a a Stroke/ brain attack? What are the two types of stroke?	1) neurological changes which are caused by an interruption of blood supply to a part of the brain 2) Ischemic (83%): caused by a blockage of blood flow to the brain Hemorrhagic (17%): Bleeding into the brain tissue
	CVA/Stroke/Brain attack Patho.: What type of tissue is the brain? What happens in hypoxia?	Brain is sensitive tissue that cannot adapt to low oxygen levels by resorting to anaerobic metabolism. Body will perfuse the brain at the expense of other body organs to preserve cerebral metabolism Hypoxia (low oxygen levels) will cause cerebral ischemia (lack of perfusion).
	CVA/Stroke/Brain attack Patho.: How are TIAs caused? What happens if blood flow isn't restored?	Cerebral ischemia l/t short-term neuro/ deficits (TIAs) and the ischemia will alter brain metabolism. After 3-10 minutes, brain cell death will occur. It's irreversible.
	CVA/Stroke/Brain Attack What's ischemia? What does survival depend upon?	1) Interrupted or totally occluded blood flow to the brain. 2) The amount of brain tissue affected, length of time the brain is deprived of blood supply and the degree of altered brain metabolism
	CVA/Stroke/Brain Attack Large vessel ischemia sites? Small vessel ischemia sites?	1) Major cerebral artery: Internal carotid; anterior, middle, posterior or vertebral cerebral arteries; basilar artery 2)vessels that branch off into the deeper regions of the brain
	Transient Ischemic Attack What is a TIA? Recovery of TIA? Duration of TIA? If left untreated, what could happen?	1) Sudden brief episodes of neurological dysfunction caused by a temporary cerebral ischemia 2) Recovery is complete and within 24 hours. 3) Duration 5-20 minutes 4) Could lead to stroke within 5 years
	Thrombosis Describe how it forms:	1) Starts with damage to the endothelial lining of the cerebrovascular vessel 2) Atherosclerosis allows fatty deposits to form plaque on the damaged vessel wall 3) Plaque enlarges and causes stenosis of the vessel 4) Platelets adhere to the plaque deposit, forming a thrombus 5) Vessel lumen becomes obstructed
	Embolism What's an embolism? Describe how it was formed:	1) Occlusion of the cerebral artery by an embolism 2) Origination of embolus: Forms outside of the brain Then, it detaches and travels through the cerebral circulation until it lodges and occludes a cerebral artery.
	Embolism Common causes of an emboli?	1) Atrial Fibrillation: blood pools in the poorly emptying atria and tiny clots from in the left atrium and travel through heart into cerebral circulation. 2) Mechanical Prosthetic Heart Valves: Have a rougher surface than endocardium and cause increased risk of clot formation 3) Other causes: Detached thrombus, bacteria, tumor, fat and air
	Hemorrhage Results from what? Types of?	1) Bleeding into the brain tissue 2) Two types Intracerebral: caused by rupture of a vessel Subarachnoid (Intraventricular): bleeding into the subarachnoid space
	Intracerbral Hemorrhage Most common when ad with who? Mortaility rate? Quality of life?	1) 50 yo. and having HTN 2) 50 % 3) Decreased 6 months after
	Subarachnoid hemorrhage Is what? Risk factors	1) Bleeding into the space between the arachnoid and pia mater membranes. This space is physiologically for cerebrospinal fluid. 2)Cerebral aneurysm Aneurysm: weakness or ballooning of vessel
	Thrombotic Onset Time of day relationship with consciousness severity	1) gradual 2) during or after sleep 3) uncommon for decreased LOC in first 24 hours 4) Increase in severity over 72 hours as ischemia continues and cerebral edema dev.
	Embolic Stroke Clinical Manifestations of: Onset? When it might resolve? Associated with what? Related to what?	1) Rapid onset with severe neurological clinical deficits 2) may resolve as clot breaks up and blood flow is re-established 3) Often associated with headache 4) May or may not be related to activity
	Subarachnoid Hemorrhage Clinical Manifestations of: Onset? Related to? Warnings? Sx?	1) Sudden 2) R/T activity or trauma 3) May or may not have warnings 4) severe headache, dec. LOC, neuro. deficits, n/v, seizures, stiff neck.
	Intracerebral hemorrhage Clinical Manifestations of: Onset? When? Sx?	1) Sudden onset with progression of deterioration over time (as bleed progresses). 2) During activity 3) Neuro. deficit, headache, n/v, dec. LOC
	CVA/Stroke/Brain Attack Stroke Complications:	Bleeding, cerebral edema, stroke reoccurance, seizure d/o, aspiration
	CVA/Stroke/Brain Attack Stroke Complications When is bleeding a problem? Why is bleeding a problem?	1)When "clot busters" used to manage stroke. 36 hours post-txt is highest risk for intracranial hemorrhage and systemic bleeding 2) Bleed occupies space l/t inc. ICP, shift of intracranial contents, brain stem herniation, and death
	CVA/Stroke/Brain Attack Stroke Complications Since bleeding disrupts blood flow, it does what? How is the risk minimized?	1) increased cerebral ischemia 2) anticoagulants or antiplatelet meds held for 24 hours after administration of clot busters.
	CVA/Stroke/Brain Attack What should be assessed to monitor for bleeding complications?	1) BP and neuro. status
	CVA/Stroke/Brain Attack Stroke Complications When's cerebral edema a complication? Caused by?	1) large vessel strokes and after a hemorrhagic stroke. 2) Increased intracranial pressure due to: Intracerebral hemorrhage Secondary effect of thrombolytic therapy. Reflex HTN.
	CVA/Stroke/Brain Attack Stroke Complications What's the goal for cerebral edema txt? Nursing interventions for it? Surgerical interventions for it?	1) maintain BP low enough to prevent re-occurrence but high enough for optimal cerebral perfusion 2) Bed rest with head of bed elevated 30 degrees to facilitate venous drainage. 3)External ventriculostomy: burr hole placed in the lateral ventricle to allow for controlled drainage of CSF.
	CVA/Stroke/Brain Attack Stroke complications: What's the risk of stroke 4 weeks after? Long term risk?	1) 1st 4 weeks after stroke= 0.6-2.2% per week 2) Long term risk= 4-14%
	CVA/Stroke/Brain Attack How is an ischemic stroke medically txt?	Platelet inhibitors (ASA, Ticlid,Plavix, Persantine) Anticoagulants Initially Heparin IV INR goal= 2.0-3.0 Replaced by Coumadin PO
	CVA/Stroke/Brain Attack How is a hemorrhagic stroke medically txt?	Anticoagulant and platelet inhibitors are CONTRAINDICATED Calcium channel blocker (Nimotop/Nimodipine): to decrease the effect of vasospasm and minimize cerebral damage
	CVA/Stroke/Brain Attack Stroke Complications: How many dev. seizures? When? Why is this bad? How is it prevented	1) 10-15% of all stroke victims will have a seizure disorder as a residual effect 2) For first seizure: within first 24 hours 3) Inc. risk of cell damage d/t hypoxia and inc. glucose metabolism 4) Seizure prophylaxis= Dilantin following intracerebral/ subarach. seizures
	CVA/Stroke/Brain Attack Stroke Complications: Aspiration causes how many deaths? Why?	2) Direct cause of death in 6% of all strokes 2)Most common in early stage of stroke due to: Loss of pharyngeal sensation Loss of oropharyngeal motor control Decrease level of consciousness
	CVA/Stroke/Brain Attack Stroke Complications: How can nurse prevent aspiration?	1) Dysphagia assessment 2) Hold oral food and fluids for 24-48 hours after stroke 3) If residual effects on swallowing after 48 hours, consider alternative feeding route (tube feeds, hyperail).
	Clot Busters When should they be given? Why are they given? How do they work? Effect on patient?	1) Within 3 hours of the stroke 2) Prevent or limit the extent of brain damage experienced during an ischemic stroke. 3) Exogenous plasminogen activators dissolve the clot or emboli. 4) Resolution of the vessel blockage re-establishes cerebral blood flow
	Clot Busters When shouldn't they be given?	1) More than 3 hours from onset of stroke 2) Suspected/confirmed hemorrhagic stroke 3) Rapidly improving neurological status 4) Uncontrolled hypertension
	Clot Busters Shouldn't be given if patient has any of the following medical conditions:	1) Stroke 2) Hemorrhage 3) Trauma 4) Surgery 5) Anticoagulant therapy 6) Gastric bleed
	CVA/Stroke/ Brain Attack How do you prioritize nursing care?	ABCs than Nursing process Airway= promote open airway Breathing= promote breathing Circ.= promote circulation Assessmment Set Expected Outcomes/Goals Interventions Evaluate
	CVA/Stroke/ Brain Attack Stroke Nursing Management: What are nurses goals? how?	1) Identify stroke early 2) Maintain cerebral oxygenation: Turn on affected side (facilitate saliva drainage) Loosen collar of shirt Pulse Ox/O2 supp 3) Restore cerebral blood flow: Thrombolytic agents within 3 hours
	CVA/Stroke/Brain Stroke Monitor for what? Nursing dx:	1) Inc. ICP 2) Altered cerebral perfusion Altered tissue perfusion Impaired physical mobility Hyperthermia (esp. if ischemia in the thermoregulatory section of the brain) Risk for impaired skin integrity Risk for contracture
	CVA/Stroke/Brain Attack What should be assessed on patients with impaired swallowing?	1) weight, facial drooping, drooling, a weak/hoarse voice, swallowing reflex check (feel larynx elevate with thumb and index finger on each side of adam's apple), cough reflex, gag reflex, food trapping, calorie count 2) Have Speech patho. do swallowing study
	CVA/Stroke/Brain Attack How should the patient's environment be assessed if they have impaired swallowing? How do you assess adequate intake?	Want minimal distraction during mealtime (restrict tv,non-immediate family member visits, noise) 2) Food trapping, calorie count
	CVA/Stroke/Brain Attack What some D/C planning for impaired swallowers?	1) Ability to management diet challenges upon discharge to home 2) Ability of support system to safely assist with intake of food 3) Support system knowledge of Heimlich maneuver
	CVA/Stroke/Brain Attack What are the goals for impaired swallowers?	1) Eat meals and fluids without aspiration and maintain/attain his/her usual body weight
	CVA/Stroke/Brain Attack What are the nursing interventions for impaired swallowers?	1) Assess swallowing ability before allowing intake 2) Position patient to facilitate swallowing 3) Should eat all meals sitting up in chair if at all possible 4) Alternative position: sitting straight up in bed 5) Head and neck slightly flexed
	CVA/Stroke/Brain Attack What foods stim. saliva production and should be avoided? Where should food be put?	1) Broth, sweet, sour, salty 2) in back of mouth on unaffected side.
	CVA/Stroke/Brain Attack What are the Long term nursing dx for stroke patients?	1) Self care deficit 2) Risk for injury 3) Altered nutrition 4) Impaired verbal communication 5) Altered thought process 6) Visual/Sensory perceptual alterations 7) Unilateral neglect 8) Ineffective individual coping
	Spinal Cord Complete vs Incomplete?	Complete: Spinal cord severed, damaged in a way that eliminates nerve activity below the level of the injury Incomplete: Spinal cord damage that allows some function or movement below the level of the injury
	Spinal Cord Primary Mech. of Injury? (Types of)	Hyperflexion Hyperextension Axial Loading/Vertical Compression Excessive Rotation Penetrating
	Spinal Cord Hyperflexion vs Hyperextension Similarities	Similarites= Both are cervical spine injuries. Both have tearing/rupturing and fraction/dislocation BUT locations are different. flexion: T/R of post. ligaments; F/D of ant. spine extension; T/R of ant. ligament; F/D of post. spine
	Spinal Cord What type of spinal injury is: Hitting the windshield/steering wheel? Hitting the headrest? Diving in shallow water? Landing on butt? Iceskating twisting injury?	1) Hyperflexion 2) Hyperextension 3) Axial Loading (Compression) 4) Axial Loading (Compression) 5) Rotational
	Spinal Cord Axial Loading (Compression) vs Rotational	Axial= Excessive force to either cervical or lumbar spine. Shatter vertebrae Rotational= Rotational force. Tearing and Rupturing of ligaments.
	Spinal Cord What's a penetrating spinal injury? Examples of?	1) Force that penetrates the spinal column causing damage and trauma to ligaments and/or vertebrae 2) Stabbing, gunshot
	Spinal Cord What worsens the primary injury?	Secondary Mechanisms of injury including: hemorrhage, ischemia(lack of blood flow) , hypovolemia(dec. circ. blood vol.), neurogenic shock (type of hypovol. shock)
	Anterior Cord Syndrome What is it? Cause? What's lost, what's preserved?	1) Damage to the portion of the spinal cord, anterior to the gray/white matter 2) Decreased blood supply (Hyperflexion injury) 3) Lost (below injury)= motor, pain, temp. Preserved= touch, position, vibration
	Posterior Cord Syndrome When does it happen? What is it? Cause? What's lost, what's preserved?	1) Rarely occurs 2) Damage to the portion of the spinal cord, posterior to the gray/white matter 3) Usually due to decreased blood supply 4) Loss (below injury)= vibration, touch, position. Preserved= Motor function
	Central Cord Syndrome Cause of it? What's lost, what's preserved? Effect on motor sensation?	1) Lesions of the central portion of the spinal cord; Compression Injury 2) Varying degrees of and patterns of sensation loss and preservation 3) Incomplete loss of motor sensation
	Brown Sequard Syndrome Caused by? What's lost, what's preserved?	1) Penetrating injuries; hemisection of spinal cord 2) Loss of motor ability, touch, pressure and vibration sensation on the same side as injury Contralateral loss of pain, temperature and light touch
	Spinal Cord Injury Complications of?	1) Spinal shock, spastic activity, pain.
	Spinal Cord Injury Spinal Shock When does it happen? Severity and duration of it? Result of what?	1) immediately after injury 2) Severity and Duration varies (Average of 1 to 6 weeks) 3) Direct result of neuronal injury
	Spinal Cord Injury Sx of spinal shock?	Flaccid paralysis Loss of spinal reflex ability Sensory loss below the level of injury Bradycardia Hypotension Loss of temperature control
	Spinal Cord Injury Spasticy and Pain interventions	Positioning and Exercise ROM Turn q2 Muscle Relaxants
	Spinal Cord Injury Medically managed how?	Medications to suppress inflammation Medications to stabilize vital signs Stabilization and Traction Medications to suppress secondary injury (Methylprednisolone) Medications to support BP and Pulse (Dopamine)
	Spinal Cord Injury What history would a nurse assess?	Mechanism of Injury Position of client Symptoms after injury Changes since initial symptoms Pre-hospital Rescue Personnel Medical History
	Spinal Cord Injury What should the nurse initially assess?	1) Airway, Hemorrhage, and Glascow Coma Scale
	Spinal Cord Injury Terms What do these terms mean: 1) Quadriplegia/Tetraplegia 2) Quadraparesis 3) Paraplegia 4) Paraparesis 5) Hypoesthesia 6) Hyperesthesia	1) Paralysis caused by ill/injuryl/t partial/total loss of all limbs and torso 2)weakness in 4 limbs 3)impairmnt in motor/sens. func. of LEs 4)weakness in LEs 5) reduced sensation/sense of touch 6) inc. sensation/sense of touch
	Spinal Cord Injury What should nurse assess for r/t cardiovascular system?	Bradycardia Hypotension Hypothermia Autonomic Dysreflexia
	Spinal Cord Injury Describe Autonomic Dysreflexia: Caused by what? l/t what?	1) From sustained stimuli at T6 or below (restrictive clothing, pressure areas, full bladder, UTI, fecal impaction) 2) vasodil above: inc BP, flushed face, headache, DNV, bradycardia, diaphoresis vasoconst. below" pale, cool, no sweating.
	Spinal Cord Injury What are causes of resp. problems? Risk for? How should patient be assessed?	1) Immobility or from interruption of spinal innervations. 2) Increased risk for pneumonia, pulmonary emboli, atelectasis 3) Complete respiratory assessment Monitor for impaired gas exchange
	Spinal Cord Injury What MS assessments should be done? What are metabolic/ nutritional concerns?	1) Muscle tone, muscle size, and skin assessment 2) Correct Acid-Base Disturbances Paralytic Ileus, Fluid and Nutritional Maintenance, NG tube, Diet, Daily Weight
	Spinal Cord Injury What are some psychosocial concerns?	Pre-injury Psychosocial Status, Usual Methods of Coping, Level of Independence, Religious/Spirituality, Cultural Background, Sexuality, Grief/Loss, Family
	Spinal Cord Injury Nursing Dx?	Ineffective(breathing pattern, airway clearance, thermoregulation, sex patterns). Dec. cardiac output, Risk for (impaired skin, ineff. ind. coping, constipation), urinary retention, interrupted family processes, impaired phy. mobility, altered nutrition, body image disturbance.
	Spinal Cord Injury Nursing interventions	Maintain Adequate Ventilation Promote Secretion Removal Support Cardiac Output Maintain Stable Body Temperature Prevent Complications from Disuse Protect Skin Establish Pattern of Elimination Promote Elimination Support Sexual Function Support Family Coping
	Spinal Cord Injury New treatments	1) Hypothermia at time of injury 2) Stem cell transplant 3) Riluzole for spinal cord injury, ALS
	Spinal Cord Injury Whats goal of rehab? Focus of rehab?	1) return pt. to highest level of wellness 2) PATIENT, retraining physiological processess, patient/family mgmnt of life changes.
	Spinal Cord Injury C2-C3 injury is: C4 injury is:	1) Fatal (can't breathe), totally dependent for all care 2) quadriplegia, diff. breathing, dependent for all care, vent needed
	Spinal Cord Injury C5 injury is: C6 injury is:	1) Quad. w/shoulder and elbow, can feed self, breathe w/o vent., need other resp. support. 2) Quadriplegia w/shoulder,elbow, wrist func, can propel wc on smooth surface, help feed, groom,dress self. Needs help transferring.
	Spinal Cord Injury C7 injury is: C8 injury is:	1) Quad. w/shoulder, elbow, wrist, hand funct., transfer self, propel wc outsde, drive a care, help with bowel/bladder programs. 2)Quad. w/norm arm func, hand weakness. propel wc outside, transfer self, drive a car, help with bowel/bladder
	Spinal Cord Injury T1-6 is: T6-12 is:	1) Paraplegia w/loss of func. below mid chest, full arm control. Indep. in self care and in wc, employeed full time 2) Para. w/loss of func. below waist, torso control. Good sitting balance, Better at w/c and sports.
	Spinal Cord Injury L1-L5 is:	Para. w/varying degrees of muscle involvement in legs. Maybe could walk short distances w/races and assistive devices
	Eyes What should nurse assess?	Level of impact of visual accuracy How does it impact employment How does it impact family life Any safety risks at home What support mechanisms do they have at home to assist with care deficits? Need for social services What are there feelings about the visual deficit
	Eyes Nursing Dx r/t perm. visual loss?	Disturbed sensory perception r/t visual deficit Risk for injury r/t visual impairment and ability to see potential dangers Self care deficits r/t visual impairment Fear r/t visual impair. and ability to see dangers. Anticipatory grieving r/t loss of func. vision
	Eyes Some expected outcomes?	The patient will: Make a successful adjustment to the impairment Verbalize feelings related to the loss Identify personal strengths and external support systems Use appropriate coping strategies If the patient has been living at a quality of life which is appropriate and acceptable, goal becomes to assist them to maintain that living status
	Eyes What's the nursing management of client with visual problems?	Introduce self to patient, and ack. visual impair. to reduce patient’s anxiety and fear. Do not make unnecessary changes in environment to ensure safety and maintain what the patient has arranged Provide adequate lighting (use natural or halogen) Place meal tray, tissues, water, and call light within patient’s range of vision or reach
	Eyes Nursing management of client with visual problems (card 2)	Com type and degree of impairment to all involved in patient’s care Recommend use of visual aids when appropriate. Visual aids such as magnifying glass, large-type printed books, and magazines encourage reading Place food on tray and plate in same place each meal and explain arrangement of food on tray and plate, using clockwise sequence Encourage use of sense of touch Touch encourages patient to become familiar with unfamiliar objects
	Eyes Nursing management of client with visual problems (card 3)	Explain sounds or other unusual stimuli in environment. Explanations reduce fear Encourage use of radios, tapes, and talking books. Diversional activities should be encouraged. Radio and television increase awareness of day and time Remove environmental barriers to ensure safety If furniture or wastebaskets are moved, notify patient of changes Discourage doors from being left partially open Fully open or closed doors reduce the risk for injury among the vision-impaired Maintain bed in low position with side rails up, if appropriate Side rails help remind patient not to get up without help when needed
	Eyes Nursing management of client with visual problems (card 4)	Keep bed in locked position This prevent falls. Guide patient when ambulating, if appropriate Describe where you are walking; identify obstacles Instruct patient to hold both arms of chair before sitting and to feel for the seat on chairs or sofas without arms These reduce the risk of falls. Consult occupational therapy staff for assistive devices and training in their use Supervise patient when smoking. Supervision prevents accidental fires
	Macular Degeneration Patho. R/t what Contributing factors? What happens?	1) Retinal aging 2) Hereditary, Environmental exposure to ultraviolet light, Dietary intake, History of cigarette smoking 3) Creation of abnormal waste material in the retinal epithelium
	Dry (Atrophic) Macular Degeneration Clinical Manifestations:	Hallmark clinical manifestation- Drusen Drusen: a yellowish exudate Composition of drusen: extracellular waste deposits Location: found on ophthalmology examination in the fundus of the eye
	Wet Macular Degeneration Clinical Manifestations:	Center vision is the visual field that is most commonly effected Blurred vision Scotomas Blind spots in the visual field Metamorphopsia Distortion of vision
	Macular Degeneration What meds are given?	Currently under research High dose vitamin therapy Vitamin C Vitamin E Vitamin B (Carotene) Research continues to verify that this therapy slows the progression of visual loss in patients with macular degeneration
	Macular Degeneration How is it surgically managed?	Laser photocoagulation Treatment of choice Laser coagulation of abnormal blood vessels Complications: laser therapy destroys tissue around the target and creates scar tissue Scar tissue may cause small blind spots
	Cataracts Definition? Cause? How does it mature?	1) opacity of the lens that distorts the image projected onto the retina 2) Lens becomes compacted with new fibers which reduce the water content of the lens 3) Lens proteins begin to precipitate due to decrease water content within lens
	Cataracts Sx	Painless, blurry vision Might see a hazing of the lens of the eye Pupil is white due Color shift Decreased visual acuity Double vision Photophobia Sensitivity to glare: patient’s see better in low light
	Cataracts Why do patients see better in low light?	The opacity of the lens obstructs the reception of light disrupts the transmission of the image to retina In low light, the pupil is dilated and the patient can see around the cataract.
	Cataracts How are cataracts medically mnged?	There isn't medical mngmnt, need surgery.
	Cataract Surgery Explain ECCE (Extracapaular Cataract extraction)	Removing the lens and the anterior portion of the lens capsule, but keeping the posterior side of the lens capsule intact
	Cataract Surgery Explain phacoemulsification (Phaco)	Most common procedure Extracapsular technique Uses ultrasound vibrations to break up old lens material Pieces of lens are removed by suction
	Cataract Surgery Post-op treatment for phaco?	Surgery causes Aphakia: left without a lens Most common corrections Intaocular lens implant Other lenses Eyeglasses Contact Lenses
	Cataract Surgery Complications of cataract surgery	Increased intraocular pressure Sharp pain, with nausea and vomiting Infection Redness in eye Change in visual acuity Tearing Photophobia Hemorrhage into anterior chamber of eye Bleeding or discharge from eye Eyelid swelling Retinal Detachment Sudden loss of full or half vision Sudden flashes of light or floaters
	Cataract Surgery Patient teaching to prevent post-op complications?	May or may not have an eye patch/shield for a few hours Resume normal activity the evening of surgery (reading, walking, eating, watching TV) Eye exam on first postoperative day Heavy lifting is restricted for a few weeks to several months if incision is large Mild discomfort Protect eye from water during showering Administer antibiotic /steroid eye drops as ordered Avoid activities that increase intraocular pressure Sneezing/coughing/blowing nose Straining with bowel movement/vomiting Sexual intercourse
	Glaucoma What's the patho of it? Why's that a problem?	1) Either overabundant amt. of aqueous humor ot inc. intraocular pressure 2) reduce blood flow to optic nerve/retina which can l/t ischemic tissue and blindness.
	Glaucoma Describe open-angle glaucoma	Fluid cannot drain through the trabecular network due to obstruction leading to a back up of aqueous humor pushing the iris forward
	Glaucoma Describe acute angle closure glaucoma	Total blockage of the trabecular mesh work leading to a sudden increase in intraocular pressure
	Glaucoma What's secondary glaucoma? Risk factors?	1) Increase in intraocular pressure secondary to another disease process within the body 2) HTN, DM, Cardiovascular Disease, Obesity, Congenital Defect
	Glaucoma Primary Open Angle Sx?	B/L changes in the eye No symptoms except a gradual almost imperceptible loss of peripheral vision, “Silent Thief of Vision”
	Glaucoma Acute Angle closure sx?	Unilateral changes in the eye Severe eye pain or headache over eye, nausea, vomiting, blurred vision, rainbow colored lights around lights, red eye Pupil is dilated and fixed Medical emergency as blindness will occur very quickly
	Glaucoma Dx assessment	Tonometry: measures intraocular pressure Angle closure= IOP of 30 mm Hg or higher Open-angle= IOP of 22-32 mm Hg Normal IOP= 10-21 mm Hg Ophthalmoscopy: inspect optic nerve Gonioscopy: views the drainage angle in the anterior chamber of the eye Perimetry: assess visual fields
	Glaucoma Management goals	Early detection Promote outflow of aqueous humor Maintain intraocular pressure within a range that prevents further damage to optic nerve Promote independence of the patient
	Glaucoma How's primary open angle managed? How's acute angle closure managed?	1)Pharmacological, Laser Trabeculoplasty used as an adjunct to medical therapy, Surgery. 2) Pharmacological (Miotics Oral or IV hyperosmolar agents) Incisional Iridectomy Laser Iridotomy
	Glaucoma What is: Mydriatic agents: Cycloplegic agents: Miotic agents:	1) causes pupil dilatation 2) paralyzes ciliary body 3) causes pupil constriction
	Glaucoma Nursing concerns for pharmacological management of glaucoma?	Anticipate Photophobia Anticipate decreased vision after drops are administered Anticipate irritation of the conjunctiva
	Glaucoma Management of Open Angle Glaucoma?	1) Promote outflow of aqueous humor 2) Pupil constriction 3) Inhibit aqueous humor production 4) Increase cholinergic activity of the eye
	Prostaglandin Analogs How does it work? What does it do?	1) Inc. outflow of aqeous humor 2) reduce intraocular pressure
	Adrenergic and Alpha 2 Adrenergic agents Action? Beneficial effect? Result?	1) Pupil dilation 2) Improves outflow of aqueous humor, decreased production of aqueous humor 3) decreased intraocular congestion
	Cholinergic Agents Action? Beneficial effect? Result?	1) Strong contraction of the iris and ciliary body 2) Widens filtration angle of eye, permitting aqueous humor outflow 3) Reduces intraocular volume, reduces intraocular pressure
	Beta Blockers Action Beneficial effect?	1) Not known 2) decreased production of aqueous humor
	Carbonic Anhydrase Inhibitors Is what? Beneficial effect? Result?	1) an enzyme necessary for aqueous humor production. 2) reduces volume of aqueous humor 3) reduces intraocular volume and intraocular pressure
	Neuro. Dysfunction Efferent vs. afferent	1) Efferent= Carries impulse from nerve center to the point of action (Away from the brain) 2) Afferent= Carries impulse from point of action to the nerve center (Toward the brain)
	Neuron AKA? Function? Types?	1) Basic unit of the nervous system 2) transmit impulses 3) Motor neurons (Transmit movement impulses ) Sensory neurons (transmit sensation impulses)
	Common Neurotransmitters Inhibitory Excitatory	1) Serotonin, GABA, Dopamine 2) Acetylcholine, glutamate, dopamine
	Glascow Coma Scale	eye: 4 points (spont., verbal command, pain, none) verbal: 5 points (oriented, conf. conv, inapp. response, incomp. speech, none) motor: 6 points (obey, purposeful to pain, withdraw from pain, spastic posture decort., rigid decere., none)
	Alpha Adrenergic Agents Side effects	Headache Restlessness Excitement Insomnia Euphoria Cardiovascular constriction Tachycardia Palpitations
	Beta Adrenergic Agents Side Effects:	Increased heart rate Tremors Headache Nervousness Dizziness Palpitations Blood pressure instability Sweating
	Adrenergic Agents Stimulate what? Name of the receptors? Where are they?	1) SNS 2)Alpha 1, 2 and Beta 1,2 3) Beta 1: Heart, Beta 2: resp., arteriole, visceral organs smooth muscle cells
	Cholinergic Agents Stimulate what? Direct acting vs Indirect acting	1) PSNS 2) bind to cholinergic vs. make more ACH available at receptor site to stim. receptor.

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