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32 Cards in this Set
- Front
- Back
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Basilar Skull Fractures |
- Periorbitaledema and ecchymosis (raccoon eyes) = orbital fracture - Postauricularecchymosis (Battle’ssign) and otorrhea= temporal bone fracture - Rhinorrhea = fracture of ethmoidbone/cribriform plate, posterior frontal sinus, and sphenoid bone (CSF rhinorrhea indicates a 10-foldincreased risk for meningitis) |
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Concussion (general) |
- Transient and reversible, loss of consciousness for 5 minutes or less - However, may not lose consciousness - Amnesia is present - No damage seen on CT/MRI |
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Concussion (adults) |
- Headachesor neck pain that won’t goaway - Troublewith mental tasks such as remembering, concentrating, or decision-making - Gettinglost or easily confused - Feelingtired all the time, having no energy or motivation - Moodchanges (feeling sad or angry for no reason) - Changesin sleep patterns (sleeping a lot more or having a hard time sleeping) - Feelinglight-headed or dizzy, or losing balance - Nauseaand vomiting - ↑dsensitivity to lights, sounds, or distractions - Blurredvision - Ringingin the ears |
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Concussion (children) |
- Feelingtired or listless - Beingcranky (will not stop crying or cannot be consoled) - Changesin eating habits (will not eat) - Changesin sleep patterns - Changesin the way the child plays—lack of interest in favorite toys or activities - Changesin performance at school - Lossof new skills, such as toilet training - Lossof balance, unsteady walking - Vomiting |
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Postconcussion Syndrome |
(2weeks to 2 months) - Persistentheadache - Shortattention span - Lethargy - Personality & behavior changes |
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Cerebral Contusion (Parietal) |
Affected: - sense of touch - awareness of spatial relationships & academic functions (reading, etc.) |
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Cerebral Contusion (Occipital) |
Affected: -Vision |
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Cerebral Contusion (Cerebellum) |
Affected: - Balance - Coordination - Skilled motor activity |
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Cerebral Contusion (Brainstem) |
Affected: - Breathing ---Respirations may be normal, periodic, rapid, ataxic (irregular, muscle movement) - HR - Arousal and consciousness ---Pupils are usually small, equal, reactive:damage to upper brain stem --> loss of normal eye movement - Sleep and wake cycles - Mayrespond with purposeful or non-purposeful movements, or may not respond at all - Mayexhibit posturing with or without stimuli - Hightemp, rapid pulse and respirations, diaphoresis.
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Cerebral Contusion (Frontal) |
Affected: - Emotional control - Self awareness - Motivation - Judgment - Problem Solving - Talking - Movement and initiation |
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Cerebral Contusion (Temporal) |
Affected: - Memory - Hearing - Understanding - Language - Processing Information |
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Diffuse Axonal Injury |
- decreased LOC - increased ICP - Decerebrationor decortication - Globalcerebral edema |
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Myasthenia Gravis (general) |
- Fluctuatingweakness of skeletal muscle: muscular weakness and fatigue worsen w/ exercise/activity; Strength restored after rest periods Areas most often affected:Muscles moving eyes andeyelids; Jaws—chewing; Muscles for speech/swallowing; Intercostal muscles and muscles for breathing; Impaired facial expression. - Periodsof exacerbation/remission - Musclesof the eyes, face, mouth, throat, & neck affected first - Extraocular muscles and levator muscles are most affected |
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Myasthenia Gravis (face) |
- Muscles of the eyes, face, mouth, throat, & neck affected first - pt has diplopia, ptosis, and ocular palsies (unable to move eyes normally). Muscles of facial expression, mastication, swallowing and speech are next most involved: pt. has weight loss, episodes of choking and aspiration Dysphagia and a nasal, low-volume monotonous quality to speech occur; Voice fades after long conversation. - May see difficulty in maintaining head position. |
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Myasthenia Gravis (thoracic/respiratory) |
- Muscles of the shoulders/hips are affected less frequently. - When respiratory muscles of the diaphragm and chest wall become fatigued and weak, ventilation is impaired. - Impairment in deep breathing and coughing predisposes the individual to atelectasis and chest congestion. - Patient may require intubation and mechanical ventilation. |
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Myasthenia Crisis (Undermedication) Nicotinic Response |
Undermedication= acetylcholinesterase isallowed to continue breaking-down acetylcholine and eventually eliminate it. So,without acetylcholine: (musclesdon’t contract ) - severe muscle weakness - respiratory distress/failure - paralysis - absentcough - difficulty swallowing, chewing, speaking - restlessness,fear |
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Myasthenia Crisis (Undermedication) Muscarinic Response |
Undermedication = acetylcholinesterase is allowed to continue breaking-down acetylcholine and eventually eliminate it. So, without acetylcholine: (instead of slowing HR & decreasing contraction strength, it is enhanced. (highBP, tachycardia); Smooth muscle of lungs stops contracting (respiratorydistress/failure)) - sudden rise in BP - tachycardia |
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CholinergicCrisis (Overmedication) Nicotinic Toxicity |
Overmedication= acetylcholinesterase istotally blocked—therefore acetylcholineis left unopposed.So, with too much acetylcholine: (involuntarymuscle contraction and twitching) - muscle fasciculation - severe muscle weakness - respiratory distress/failure - difficultyswallowing, chewing, speaking - restlessness,fear |
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Cholinergic Crisis (Overmedication) Muscarinic Toxicity |
Overmedication = acetylcholinesterase is totally blocked—therefore acetylcholine is left unopposed. So, with too much acetylcholine: (excessgland secretion (saliva, sweat, pulmonary secretions); excess smoothmuscle contraction in GI tract (vomiting/diarrhea); excessbronchoconstriction (respiratory distress/failure); In heart: excessacetylcholine = very low BP and HR (remember PNS isstimulated) - ↑d secretions: pulmonary, tears, sweat, oral (salivation) - ↓dB/P & bradycardia - ↑d GI motility: n/v, abdominal cramps, diarrhea - urinaryincontinence |
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Multiple Sclerosis (head/neuro) |
- visual disturbances (blurred vision, color distortion, loss of vision in one eye, eye pain) - loss of sensation (speech impediment, tremors,dizziness, numbness, tingling, dysarthria, dysphagia) - mental changes (↓d concentration, attention deficit, memory loss) - tinnitus, hearing impairment - depression, paranoia, uncontrollable laughter/weeping (Cognitive/emotionalproblems—intellectual functioning remains intact; patient has anger, depression, euphoria, etc.) |
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Multiple Sclerosis (muscular) |
- limb weakness ( loss of coordination/balance) - paralysis of limbs - muscle spasms (fatigue: generalized worse with fever & hot weather; numbness; prickling pain) (Insidious onset withearly symptoms of leg weakness or paralysis of the limbs, trunk, or head;diplopia and speech problems.May see progressive deterioration or remissions and exacerbations.) |
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Multiple Sclerosis (GI/GU) |
Bladder & Bowel Dysfunction |
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Guillain Barre’Syndrome |
1. Ascending symmetrical muscleweakness: starts in legs, moves to upper extremities, moves toswallowing (dysphagia) 2. Loss of deep tendon reflexes (areflexia); Hypotonia (↓d muscle tone); Deep, muscle aches & cramps—worse at night; hyperesthesias (hypersensitive to stimuli) 3. ANS dysfunction—both SNS and PSNS affected: respiratory muscle paralysis; labile B/P: hypotension to hypertension, orthostatic hypotension; abnormal vagal responses: bradycardia, heart block, asystole - facial flushing & diaphoresis - loss of bowel & bladder control - Withprogression to the lower brainstem—cranial nerves VII, VI, III, XII, V, and Xmay become involved (facial weakness, extraocular eyemovement difficulties, diplopia, dysphagia, difficulty speaking, and paresthesias ofthe face) |
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Parkinson's |
Dopamine—neurotransmitter essential for normal functioning of the extrapyramidal motor system. Withoutit: - slow, shuffling gait, difficulty in the initiation & execution of movement, ↑dmuscle tone/rigidity, tremor at rest, impaired postural reflexes -TRAPS: Tremor-”pill-rolling”/restingtremor; aggravated by emotional stress or ↑d concentration; Rigidity; Akinesia/bradykinesia; Postural disturbance (forward tile to posture); Secondary manifestations: monotoneface (blank expression), mask-like facies, depression, weakness, slow/monotonous/slurred speech |
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Central Cord Syndrome |
Damageto the central spinal cord with compression on anterior horn cells: - Motorweakness and sensory loss in all extremities, but upper extremitiesare worse - Usually results from hyperextension of osteoarthritic spine (common in older people) |
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Anterior Cord Syndrome |
Acute compression of the anteriorportion of thecord—usually after flexion injury.Bloodflow to the anterior spinal cord is compromised due to damage to the anterior spinalartery: - Immediate,complete motor paralysis from site of injury down: ↓sensation (no pain), loss of temperature control - BUT,touch, position, vibration, and motion remain intact (posterior tracts are notinvolved) |
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Brown-SequardSyndrome |
- Transection or lesion of one-half of thecord; caused by penetrating injury. - Loss of motor function (paralysis), position, and vibratory sense, aswell as vasomotor paralysis on the same side. - On the contralateral side—loss of pain and temperature sensation. |
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Posterior Cord Syndrome |
Associated with cervical hyperextensiontrauma: compression or damage to the posterior part of the spinal cordcontaining sensory neurons and position-sense capabilities. Blood flow is compromised due todamage to posterior spinal artery. - Lossof proprioception. -Pain, temperature and motor function are intact. |
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Cauda EquinaSyndrome |
Damage to the lowest portion of thespinal cord and the LS nerve roots: - Flaccid paralysis of the lower limbs with areflexic (flaccid) bladder and bowel |
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Spinal Shock |
- temporary loss of motor, sensory, and reflex functions below the level of theinjury - Ptmay present with flaccid paralysis, areflexia to both deep tendon and cutaneousstimuli, and bowel and bladder dysfunction—below site of injury - Returnof sacral reflexes indicates the resolution of spinal shock (99% ofpatients w/in 24 hours): sacral nerves S-3 to S-5 supply the perianal muscles (control voluntary contraction of external bladder sphincter & external anal sphincter) - highrisk for autonomic dysreflexia (notreally a "type of shock," bc usually doesn't compromisetissue profusion throughout body (except for perfusion at the sight ofinjury)) |
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Neurogenic Shock |
SCinjuries at the level of T-6 or above - Impairmentof descending sympathetic pathways in the spinal cord (loss ofvasomotor tone and sympathetic innervation to the heart) - loss of sympathetic activity leads tovasodilation, maldistribution of blood volume, and cardiacdeceleration, Massivevasodilation results in ↓ preload, ↓ cardiac filling, ↓stroke volume, and hypotension despite a normal blood volume. - hypotension and bradycardia - T-1 through T-6 injury leads toparaplegia with loss of function below mid-chest (function ofthe hands, arms, neck, and breathing are usually not affected) - If injury is higher, thepatient may be a quadriplegic (problems with heart, breathing, arm and chestmovement, etc.) (is a type of "shock" because there is inadequate tissue perfusion throughout the body due to massive vasodilation (perfusion to kidneys, brain, GI tract, etc. are compromised)) |
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Autonomic Dysreflexia |
- SevereHTN (up to 300 mmHg systolic) - Bradycardia (30 – 40 bpm) - Poundingheadache - Diaphoresisand skin flushing above the level of injury - Bronchospasm - Nasalcongestion - Chillswithout fever—goose bumps above level of injury - Seizures Most common precipitating factors: Distended bladder; Fecal impaction; Stimulation of skin or pain receptors |
