Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
OCTH 731 exam 3
| Question | Answer |
|---|---|
| UE condition: etiology-chronic, autoimmune, systemic disease; inflammation of synovial tissue over time leads to joint, ligament, and bone concerns | rheumatoid arthritis |
| UE condition: presentation-effects multiple joints, symmetrical presentation, periods of exacerbation/remission, women>men, joint swelling/inflammation, early morning stiffness, fatigue, deformities/joint instability | rheumatoid arthritis |
| UE condition: etiology-non-inflammatory degenerative joint disease; combo of medical, biomedical, biochem, and genetic factors | osteoarthritis |
| UE condition: symptoms-women>men over age of 50, DIP and CMC most common joints involved, joint pain that initially recedes with rest, stiffness and decreased ROM, patient ed on joint protection and activity mod., pain and stiffness | osteoarthritis |
| UE condition: etiology-progressive disease of fascia of palm and digits; northern european descent; associated with chronic alcoholism, diabetes, CPD, hypothyroidism, and HIV | dupuytren's contracture |
| UE condition: symptoms-fascia tightening leading to deformity/contracture of hand/palm, limited grasp and strength | dupuytren's contracture |
| UE condition: etiology-damage caused by trauma, fracture, laceration, etc. to flexor tendons | flexor tendon injury |
| UE condition: symptoms-tendon laceration/damage requiring surgery; zones of injury/structures involved will determine concerns, healing, and rehab (II is no mans land) | flexor tendon injury |
| UE condition: etiology-damage caused by trauma, fracture, laceration, etc. to extensor tendons | extensor tendon injury |
| UE condition: symptoms-injury/laceration to extensor tendon(s) requiring surgical repair which often leads to adhesion on dorsal hand, loss of glide of extensor mechanisms, trauma, decreased grasp patterns, zones of injuries | extensor tendon injury |
| type of fracture: distal radius fractures are most common; mechanism = FOOSH, Colles' fracture = dorsal displacement, Smith's fracture = volar displacement | radius / ulna fractures |
| UE condition: symptoms-clinical presentation before immobilization = pain, edema, deformity of displacement; clinical presentation after immobilization = stiffness, weakness, edema, soft tissue adherence | fractures |
| UE condition: etiology-repetitious awkward postures, static positions, or forceful movement over a duration of time | cumulative trauma disorders |
| UE condition: symptoms-could impact a variety of structures; tingling, inflammation, numbness, clumsiness, persistent pain | cumulative trauma disorders |
| UE condition: acute inflammatory response to tendon injury, overdid something in last weeks or months | tenonitis |
| UE condition: pathologic alternatives seen in tissue, degenerative change of extensor tissue without inflammatory cells | tendonosis |
| UE condition: inflammation of extrinsic extensors of hands and their origins, extensor carpus radialis brevis tendon most common, mechanical overloading/biomechanical strain; symptoms- pain, weakness, inflammation of ECRB tendon | lateral epicondylitis |
| UE condition: inflammation or thickening of EBP or APL tendon preventing gliding; moving thumb and wrist is painful; occurs due to forceful, repetitive, or sustained thumb ABD, thumb ABD with ulnar dev. of wrist, resisted radial dev. | dequarvain's tenosynovitis |
| UE condition: symptoms-pain with thumb motion, swelling, crepitus, positive Finkelstein's test | dequarvain's tenosynovitis |
| UE condition: flexor tenosynovitis at MC neck and A1 pulley; clicking, snapping, catching, or triggering; most common in adulthood with women>men; symptoms-inflammation of flexor tendon=pain and clicking | trigger finger |
| UE condition: median n. impinged beneath transverse carpal ligament; caused by repetitive use environments; symptoms-impaired sensation in median n. distribution and hand weakness, decreased sensation, clumsiness, weakness, pain, numbness | carpal tunnel syndrome |
| UE condition: elbow is the most common site followed by wrist; symptoms-impaired sensation in ulnar n. distribution, pain, claw hand, weak grip/pinch; deformity | ulnar n. compression |
| UE condition: radial n. and posterior interosseous n. compression, symptoms-impaired sensation and weakness in radial n. distribution, impairments-sensory difficulties and weak wrist extensors and digits and thumbs | radial n. palsy |
| UE condition: etiology-misunderstood, CNS/PNS involvement, result of trauma/injury | complex regional pain syndrome |
| UE condition: characterized by a continuing regional pain; symptoms-pain, edema, abnormal hair growth, stiffness, skin discoloration, psychosocial impact, severe limitations in use of extremity for ADLs/IADLs | complex regional pain syndrome |
| factors that influence amount of tissue destruction with burns | temperature and duration |
| types: fire/flame, scald/hot liquid, contact, electrical, chemical, other; locations: home, work, street/highway, recreational/sport, other | burns |
| burn severity: involves only epidermis, redness and pain, dry with no blisters, ex. sunburn or flash from explosion; 3-4 days, no residual scarring | superficial / first degree |
| burn severity: destroys epidermal layer and extends into dermis; superficial-clear blisters, weeping wet skin, burn will blanch, painful to touch, ex. sunburn that peels; deep-white, will not blanch, blisters with bloody fluid, extremely painful; 2-3 wks | partial thickness / second degree |
| burn severity: destroys epidermal and dermal layers of skin and extends to subcutaneous fat, variety of colors, small fragile blisters, dry and leathery hard overall, insensate but sensitive to deep pressure, scarring and contractures very likely | full - thickness / third degree |
| burn severity: destroy all layers and extend into m., tendon, or bone; charred or mummified appearance; can result in partial or total loss of function; amputations may be warranted | deep full - thickness / fourth degree |
| symptoms: can affect all body systems-inhalation injury, hypermetabolism, infection, shock, scars, contractures, cardiac and pulmonary most commonly affected | burns |
| medical management of burns: maintain adequate oxygenation for inhalation injuries, maintain iv volume to ensure profusion and oxygenation of all tissues through IV fluids, nutritional support with sufficient caloric intake | burn / trauma units |
| medical management of burns: surgical debridement of nonviable skin, daily cleansing and debridement is necessary, hydrotherapy, topical dressings | debridement and dressings |
| medical management of burns: skin grafts used to replace skin or for wound coverage, availability of donor sites, after graft is applied body part is immobilized until graft is stable enough to prevent loss | excision and grafting |
| OT's role: depends on phase of healing and includes communication with surgeon and following protocols; positioning, ROM, splinting, exercise, ADLs, contracture prevention and management, scar management | burns |
| injury and disease of bones, joints, and their related structures; leads to pain and dysfunction; severity depends on involvement of supporting structures; some are genetic; may be caused by trauma or disease | orthopedic conditions |
| ortho condition: destruction and loss of articular cartilage which leads to pain and decreased function; etiology-unknown, hereditary components; 1 of leading cause of disability, most common in UE; typically impacts knee, DIP, PIP, and CMC | osteoarthritis |
| ortho condition: symptoms-joint pain and stiffness, crepitation, decreased activity and functional limitations, bony enlargement | osteoarthritis |
| ortho condition: decreased bone density and deterioration of bone; etiology-common in post-menopausal women, increased risk of pathologic fractures; osteopenia is predecessor; irreversible | osteoporosis |
| ortho condition: reversible weakening of bone increasing risk for osteoporosis; no clinical/symptoms; reversible; can progress to osteoporosis | osteopenia |
| ortho condition: abnormal bone formation in extraskeletal soft tissues; associated with burns, SCI, head injuries, and ankylosing spondylitis; etiology unclear; inappropriate formation of fibroblasts causing excessive bone growth | heterotropic ossification |
| ortho condition: symptoms - initially=localized pain/tenderness, joint warmth; later=maturation of both, decreased ROM, palpate bone mass | heterotopic ossification |
| 1 of the most common orthopedic condition; break in continuity of bone caused by trauma or disease; 2 factors involved in determination of a fracture-amount of force applied to bone and strength of bone | fracture |
| type of fracture: caused by bone insufficiency, bone is weak and unable to sustain normal forces experienced during ADLs, OA and osteoporosis are common conditions that may lead to this | pathologic fracture |
| ortho condition: signs and symptoms-localized pain, deformity, edema, injury to surrounding soft tissue, ecchymosis | fractures |
| classification of fracture: no broken skin | closed |
| classification of fracture: 2 or more fragments | comminuted |
| classification of fracture: often seen in kids, bone breaks on 1 side and bends on other | greenstick |
| classification of fracture: break in full continuity of bone | complete |
| classification of fracture: fracture line is at right angle to longitudinal axis of bone | transverse |
| classification of fracture: twisted fracture line from torsional stress | spiral |
| classification of fracture: bone breaks through skin, aka compound, increased chance for infection | open |
| classification of fracture: involve end of bone and enters joint, may disrupt ligaments | articular |
| classification of fracture: partial break in bone | incomplete |
| classification of fracture: fracture line is diagonal or slanted | oblique |
| type of fracture: most are caused by a FOOSH; cause loss of sensation, strength, movement, and limited functional use of hand | distal radius fracture |
| type of fracture: fracture of proximal femur; intracapsular=femoral neck, extracapsular=trochanter involvement; symptoms-decreased proprioception, inability to bear weight, decreased strength, impaired balance, pain, decreased ADLs | hip fracture |
| type of fracture: may present with humeral displacement and malposition of distal limb, radial n. injury occurs in ~18% of cases, loss of wrist ext. and impaired sensation on dorsal aspect of wrist, recovery of radial n. occurs within 3-4 months | humeral fracture |
| type of fracture: can result in injury to m., n., and tissue; high risk for malunion and Volkmann's deformity; severe damage to tissues and mm. of wrist and fingers caused by increased compartmental pressure | distal humerus fracture |
| type of fracture: most commonly fractured bone in wrist, position of bone makes it more susceptible to injury, sports injuries resulting in wrist hyperext. and radial dev. are a common cause | scaphoid fracture |
| med./surg. management of ortho condition: manual manipulation or traction to align fracture; immobilize through casts, traction, splints, or braces | closed reduction |
| tx. of ortho condition: goal is to align and immobilize fracture site to allow for normal healing | medical / surgical management |
| med./surg. management of ortho condition: surgical opening and reduction of fracture; internal fixation involves securing fractures with pins, rods, plates, and screws; allows for early immobilization | open reduction and internal fixation |
| damage to brain, which occurs after birth and is not related to a congenital or a degenerative disease; impairments may be temporary or permanent and cause partial or functional disability or psychosocial maladjustments | acquired brain injuries |
| includes TBI, brain tumors, anoxic injuries, and stroke | acquired brain injuries |
| type of ABI: alt. in brain function caused by an ext. force; ex. falls, assaults, MVAs, sports and recreation injuries, gunshot wounds, workplace injuries, abusive head trauma, military actions | traumatic ABI |
| type of ABI: alteration in brain function caused by an internal force; ex. stroke, infectious disease, seizure, electric shock, tumors, toxic exposure, metabolic disorders, neurotoxic poisoning, anoxic injury, drug overdose | non - traumatic ABI |
| type of ABI: brain trauma that includes at least 1 of the following-loss of consciousness, posttraumatic amnesia, disorientation and confusion, in more severe cases neurological signs | TBI |
| type of ABI: results in short-term neurological impairment; indicators-confusion immediately following injury, impaired balance within 24 hrs, slowed reaction time, impaired verbal learning and memory within 48 hours | concussion |
| classification of ABI: damage by blunt force, does not penetrate skull; ex. sports injury, MVA | closed BI |
| classification of ABI: damage by foreign object, penetrates skull and enters brain tissue; ex. gunshot wound | penetrating BI |
| classification of ABI: damage caused by energy from explosion; head acceleration, vascular surge, and skull deformation; ex. bomb | blast BI |
| type of BI damage: at time of injury, created by direct impact or intrusion of penetrating object | primary |
| type of BI damage: hours to days post-injury, consequence of physiological response to injury; causes-neuroinflammation, increased intracranial pressure, decreased cerebral blood flow or ischemia | secondary |
| type of BI damage: localized to 1 area of the brain | focal |
| type of BI damage: damage occurs in multiple areas | diffuse |
| type of primary BI damage: occurs under site of impact with an object | coup |
| type of primary BI damage: occur on side opposite of area that was initially impacted | countercoup |
| type of primary BI damage: small lesions and/or shearing of white matter tracts of cortex; sensory and motor cortices, frontal lobe, corpus callosum, brainstem, cerebellum; mechanism is stretching and shearing of brain cell axons | diffuse axonal injuries |
| deficits related to ABI: coma, seizures, post-traumatic hydrocephalus, DVT, persistent vegetative state, dysautonomia | medical deficits |
| deficits related to ABI: decerebrate rigidity (damage to BS, extensor posture of all limbs and/or trunk), decorticate rigidity (cortical damage, flexion of UEs and ext. of LEs), spasticity, reflexes, ataxia, coord., contractures, paresis | sensorimotor deficits |
| deficits related to ABI: vergence, diplopia, homonymous hemianopia, fixation, oculomotor skills, saccades, nystagmus, ptosis, scanning, strabismus, tracking/pursuits, visual acuity, visual fields, visual ROM | visual deficits |
| deficits related to ABI: pattern recognition, form constancy, figure ground perception, visual cognition, visual closure, visual organization, spatial orientation, topographical orientation, unilat. inattention, depth perception, visual agnosia | visual perceptual deficits |
| deficits related to ABI: orientation, attention, processing, memory, anterograde amnesia, retrograde amnesia, working memory, long-term memory, immediate recall/sensory register, EFs, self-awareness | cognitive deficits |
| deficits related to ABI: impulsivity, perseveration, compulsivity, irritability/agitation, aggression, disinhibition, depression, reduced self-esteem, suicide risk, PTSD, substance abuse, personality disorder | psychosocial deficits |
| phase of rehab: focus-preservation of life, management of secondary complications, prev. of secondary damage; ex. maintain airway and circulation, surgical decompression of hematoma, intensive care | acute phase |
| phase of rehab: goals-prevent joint deformity, intro ADL participation as tolerated, provide graded and specific sensory stimulation to improve memory, assess and initiate cognitive intervention, early mobilization | acute phase |
| phase of rehab: requirements-medical stability, need for close medical supervision, need for active and ongoing therapies; goals-max. function, prevent complications, min. additional physical and psychosocial impairments | rehab phase |
| interruption of blood flow to brain leading to inadequate oxygen and nutrient supply to brain; due to blood vessel blockage or rupture; can occur in any part of the brain | cerebrovascular accident |
| type of stroke: most common; following stroke fluid accumulates btw. blood vessel and neuron making it diff. for things to pass through; irreversible cell death w/in 5-10 minutes; 3 subtypes | ischemic stroke |
| subtype of stroke: occurs when a blood clot forms in an a. supplying the brain causing an obstruction, occurs in areas damaged by atherosclerosis, typically occurs overnight, most common subtype | thrombotic ischemic stroke |
| subtype of stroke: 2nd most common subtype, result from occlusion of small branches of larger cerebral aa., minimal symptoms are present, often undetected, small infarcts typically in deep brain structures | lacunar ischemic stroke |
| subtype of stroke: occurs when a clot formed elsewhere, breaks off, travels up bloodstream, and reaches a narrow a.; typically during activity/movement | embolic ischemic stroke |
| type of stroke: caused by a rupture in a blood vessel (aneurysm) with resultant bleeding into or around cerebral tissue, 2 subtypes | hemorrhagic stroke |
| subtype of stroke: bleeding directly into brain, results in high % of deaths; primary-spontaneous rupture; secondary-malformation or other structure/pathology causes; increased pressure on brain | intracerebral hemorrhage |
| subtype of stroke: bleeding occurs around brain, small %, mostly caused by leakage of blood from an aneurysm; symptoms-blood irritates meninges, severe headache, vomiting, altered state of consciousness | subarachnoid hemorrhage |
| etiology: potentially modifiable risk factors-lack of physical activity, diet, apoliproprotein, history of HTN or BP 40/90 or higher, waist-to-hip ratio, psychosocial factors, current smoking, cardiac arrest, alcohol consumption, diabetes | CVA |
| etiology: non modifiable risk factors-ethnicity, age over 55, younger women, genetics/heredity | CVA |
| etiology: modifiable risk factors-hypertension, smoking, obesity and waist-to-hip ratio, diet, activity, diabetes, alcohol and drug use | CVA |
| signs of CVA: face drooping, arm weakness, speech difficulties, time to call 911; balance, eyes and feet | FAST / BE-FAST |
| CVA injury: symptoms-loss of vol. mvmt. and coord. on R face, trunk, extremities; impaired sensation (temp, pain, proprioception) on R side; language deficits; blind spots in R VFs; dysarthria; memory deficits | L - sided cerebral injury to MCA |
| CVA injury: symptoms-hemiparesis on L side; impaired touch, pain, proprioception, temp on L side, spatial and perceptual deficits; unilat. neglect; impulsivity; dressing apraxia; L homonymous hemianopia | R - sided cerebral injury to MCA |
| CVA injury: symptoms-visual disturbances, impaired temp sensation, localized numbness, vertigo, dizziness, coord. when walking or standing, paralysis of face and limbs, clumsy mvmt. of hands, dysmetria, dysphagia, loss of memory | vertebrobasilar / posterior stroke |
| CVA injury: rare; symptoms-paralysis of LE contralat. to occluded vessel, lack of spont. with emotion or loss of comm., loss of sensation of contralat. foot and leg, balance probs., memory impairment, loss of bowel and bladder control | anterior cerebral a. stroke |
| CVA injury: results in coma because of damage to centers involved with alertness and wakefulness, rare and usually fatal, those who survive often have good recovery | Wallenburg's syndrome |
| CVA injury: symptoms-contralat. pain and temp loss, ipsilat. Horner's syndrome, ataxia, facial sensory loss, dysphagia, hoarseness, vertigo | Wallenburg's syndrome |
| type of CVA: result from temporary blockage of blood supply to brain, stroke warning signs, lasts <24 hours, signs dep. on part of brain affected, lack of permanent damage, urgent eval and tx. needed | transient ischemic attach (TIA) |
| leading cause is MVA followed by falls and violence, sports-related injuries account for majority remaining, non-traumatic causes - developmental or acquired | SCI |
| classification of SCI: full transection of cord, all pathways interrupted, UMN injury if reflexes are still present, LMN injury if below conus medullaris, total loss of motor and sensory function below level of injury | complete SCI |
| classification of SCI: damage does not cause total transection, some degree of voluntary movement or sensation will be present below level of injury, categorized by which part of cord was damaged | incomplete SCI |
| SCI: damage to ant. spinal a. or indirect damage to ant. SC tissue; signs-loss of motor function below level of injury and loss of thermal, pain, and tactile sensation below level of injury; light touch and proprioception unaffected | Anterior Cord Syndrome |
| SCI: 1 side of SC is damaged typically because of a penetrating wound; signs-ipsilat. loss of motor function below level of injury, ipsilat. reduction of deep touch and proprioception, contralat. loss of pain, temp, and touch | Brown - Sequard Syndrome |
| SCI: neural fibers serving UEs are more impaired due to injury to central part of cord, commonly due to hyperext. of neck with spinal canal narrowing | Central Cervical Cord Syndrome |
| SCI: signs-motor and sensory function in LEs less involved than UEs, potential for flaccid paralysis of UEs, intrinsic hand function recovers last if at all | Central Cervical Cord Syndrome |
| SCI: damage to spinal nn. that extend below end of cord, usually incomplete, chance for n. regeneration and recovery of function, result of direct trauma from fracture dislocations of lower thoracic or upper lumbar vertebrae | cauda equina injuries |
| SCI: signs-loss of motor function and sensation below level of injury, absence of reflex arc, motor paralysis with flaccidity and m. atrophy below level of injury | cauda equina injuries |
| complication after SCI: posttraumatic; period of altered reflex activity, lasts 1 week to 3 months post-injury, flaccid paralysis below level of injury and absence of reflexes, increased spasticity | spinal shock |
| complication after SCI: posttraumatic; injuries above T12, most common cause of death post-SCI, above C4 may need a respirator; symptoms-shallow breathing, weak cough production; need for deep breathing and assisted cough techs. | respiratory complications |
| complication after SCI: posttraumatic complication; exaggerated response of ANS caused by irritation of nn. below injury; above T6; signs-sudden pounding headache, diaphoresis, flushing, goosebumps, tachycardia followed by bradycardia | autonomic dysreflexia |
| complication after SCI: posttraumatic; cervical or thoracic SCI; blood pools dist. in LEs be. of decreased trunk/LE tone; signs-light headedness, pallor, unresponsiveness, dizziness, sudden weakness | postural (orthostatic) hypotension |
| complication after SCI: posttraumatic; med. screenings needed; occur with SCI due to reduced circulation, prolonged bed rest, direct trauma to legs; signs-swelling of LEs, localized redness, low-grade fever; undetected could lead to embolism or death | deep vein thrombosis |
| complication after SCI: posttraumatic; difficulty maintaining appropriate body temp; above T6; body assumes temp of ext. environment after injury | thermal regulation |
| complication after SCI: MSK; UMN=increased spasticity below injury; triggered by infection, positioning, pressure sores, UTIs, heightened emotional states; spasms can be used functionally; excessive can lead to pain, contractures, and reduced partic. | spasticity |
| complication after SCI: MSK; abnormal formation of bone on mm., joints, and tendons; signs-heat, pain, swelling, decreased ROM | heterotropic ossification |
| complication after SCI: UTI due to residual urine; signs-cloudy, dark, foul-smelling urine, fever/chills, increase in spasticity; reflex or spastic bladder; nonreflex or flaccid bladder | genitourinary complications |
| complication after SCI: reflex bowel, flaccid bowel (can't be stimulated to empty reflexively); implications-constipation with injuries above T6, diarrhea/invol. bowel movements | bowel complications |
| complication after SCI: damage to nn. in genital area; impacts men much greater than women | sexual complications |
| complication after SCI: no/impaired sensation; pressure sores; 4 stages | dermal complications |
| complication after SCI: high rate of depression; symptoms-disinterest, feelings of worthlessness, fatigue, changes in weight/appetite, suicidal ideation | mental health challenges |
| debilitating immunological and degenerative disease; person's own immune system attacks myelin sheaths which reduces axon's ability to conduct impulses | multiple sclerosis |
| etiology: unknown but thought to be multifactorial most common being genetics, infections, and smoking; familial recurrence rate of 20-30% with 1st degree relatives | MS |
| specific symptoms: visual, sensory disturbances, urinary incontinence/retention, ED, m. weakness, GM and FM incoord., pain, spasticity, fatigue, ataxia, dysphagia, dysarthria, vestibular dysfunction, cog. or emotional disturbances | MS |
| clinical course has 4 types/patterns: benign, relapsing-remitting-nonprogressive, relapsing-remitting-progressive, primary progressive | MS |
| type of MS: 1 or 2 episodes of neurological deficits with no residual impairments | benign |
| type of MS: person returns to previous level of function after each exacerbation with no residual deficits | relapsing - remitting - nonprogressive |
| type of MS: some residual impairment with each remission, unpredictable course with varied patterns of exacerbation/remission | relapsing - remitting - progressive |
| type of MS: steady decline in function without remissions and exacerbations | primary progressive |
| medical management: medications to reduce relapse rates, reduce brain lesions, reduce disability progression, and manage symptoms; non-pharm. interventions; lifestyle changes; bone marrow transplants; low-impact exercise | MS |
| characterized by death of dopaminergic neurons in substantia nigra and presence of Lewy bodies; deficits in speed and quality of motor movements, postural stability, cog. skills, affective expression due to lack of dopamine; 2 subtypes | Parkinson's Disease |
| subtype of PD: tremors and few other motor symptoms | tremor - dominant |
| subtype of PD: more akinesia and rigidity, more gait instability | non - tremor - dominant |
| etiology: cause is unclear but evidence implies genetic and environmental factors; familial or sporadic typically | PD |
| motor symptoms: primary-resting tremor, m. rigidity, bradykinesia, shuffling gait; other-postural instability, reduced facial expression, micrographia, reduced bowel and bladder function | PD |
| non-motor symptoms: cog. impairments, visual perceptual deficits, sleep disturbances, fatigue and excessive daytime sleepiness, emotional disorders, ANS dysfunction, muffled speech | PD |
| 1st diagnosed older than 50; progression varies with each person, generally a slow progressive disorder; 3 phases-preclinical period, prodromal period, symptomatic period; life expectancy not significantly impacted | PD |
| med. management: meds-none that inhibit disease progression, tx. motor symptoms and increase concentration of dopamine intake; surgery-deep brain stim., continuous device-aided drug delivery; gene therapy; growth factors; rehab | PD |
| fatal, progressive, degenerative motor neuron disease; scars form on UMNs in corticospinal pathways and functionally-linked LMNs in motor nuclei of BS and ant. horn cells of SC; 2 types | Amyotrophic Lateral Sclerosis |
| etiology: no known cause but speculated that several disorders with several causes lead to it; familial type caused by genetic mutation; sporadic unknown but presumed to be acquired | ALS |
| initial symptoms: weakness in small mm. of hand, asymm. foot drop, night cramps in calf | ALS |
| common symptoms: progressive loss of m. movement -> weakness -> atrophy; spasticity; difficulty speaking and swallowing; loss of emotional control; reduced body temp regulation; distal to proximal pattern; cog. deficits | ALS |
| 3 areas of symptoms related to different tracts being involved: LMN-weakness, atrophy, cramping, fasciculation; corticobulbar tract-dysphagia, dysarthria; corticospinal tract-spasticity, hyperreflexia, dysphagia, dysarthria | ALS |
| typically diagnosed between 40-70 years; progressive and rapid; duration of survival after diagnosis is usually 1-5 years, 50% die within 30 months; life expectancy dependent on type, rate of progression, early respiratory failure, nutritional status | ALS |
| medical management: txs. do little to alter fatal course; meds to tx. symptoms and keep people at milder stages for longer; other txs.-gastronomy, noninvasive ventilation, nebulizers, low-dose radiation and Botox | ALS |
| vital sign: number of heart beats per minute; normal-60 to 100 bpm, bradycardia-below 60, tachycardia-above 100, irregular heart beat | pulse / heart rate |
| vital sign: number of breaths per minute; normal-12 to 20 breaths/min, abnormal-less than 12 or over 25 | respiratory rate |
| vital sign: combo of systolic and diastolic forces; average-120/80 mmHg; systolic pressure-blood pushed out of heart, diastolic pressure-heart rests between beats, hypertension-above 120/80, hypotension-less than 90/60 | blood pressure |
| vital sign: amount of hemoglobin in blood that's saturated with oxygen; normal-96 to 100%, hypoxemia-<90%, depends upon oxygen breathed in, hemoglobin, concentration, and gas exchange in lungs | oxygen saturation |
| cardiopulm. disorder: increase in amount of force that is pushing against a. walls as heart pumps, systolic consistently higher than 140 mmHg and/or diastolic consistently over 90 mmHg | hypertension |
| cardiopulm. disorder: etiology-primary has no identifiable cause but is tied to age, family hx., obesity, or lifestyle factors, gradual; secondary caused by underlying conditions, sudden onset | hypertension |
| cardiopulm. disorder: symptoms-often asymptomatic, "silent killer", if untreated can damage heart and other structures, could go undiagnosed/untreated for years; when symptoms are severe could experience headaches, shortness of breath, nose bleeds | hypertension |
| cardiopulm. disorder: coronary aa. are damaged, most commonly due to atherosclerosis, chronic inflammation of disease leads to narrowing of coronary aa. supplying heart, overtime leads to weakened heart musculature and risk for health concerns | coronary a. disease |
| cardiopulm. disorder: build up of fatty, fibrous plaque on walls of blood vessels, particularly in medium or large vessels in body | atherosclerosis |
| cardiopulm. disorder: etiology-combo of lifestyle choices and genetics; high cholesterol, diabetes, limited physical activity, smoking, excess alcohol consumption, HTN, exposure to stress and/or inability to manage stress | coronary a. disease |
| cardiopulm. disorder: symptoms-no initial symptoms; complete blockage leads to MI; plaque build-up can cause angina, symptoms with increased activity and stress, shortness of breath, nausea, rapid or irregular heart beat, diaphoresis | coronary a. disease |
| cardiopulm. disorder: chronic, progressive, impacts heart's ability to pump blood to body and organs, results from impaired ventricle structure and/or function, manifestation of other health conditions | congestive heart failure |
| cardiopulm. disorder: etiology-CAD is most common cause, HTN is another cause; other risk factors-arrythmias, heart infection, diabetes, thyroid problems, obesity, unhealthy lifestyle choices | congestive heart failure |
| cardiopulm. disorder: symptoms-dyspnea with exertion, wheezing and bronchospasms, R-sided heart failure, depression, decreased alertness, decline in cognition | congestive heart failure |
| cardiopulm. disorder: group of progressive lung disorders (ex. emphysema and bronchitis); irreversible airflow obstruction (ex. dyspnea and decreased lung capacity); preventable yet progressive and life-threatening | chronic obstructive pulmonary disease |
| cardiopulm. disorder: type of COPD-damaged/destroyed walls between air sacs -> alveoli lose shape or fewer/larger air sacs -> poor gas exchange; caused by long-term exposure | emphysema |
| cardiopulm. disorder: type of COPD-inflammation of lining of airways -> increased mucus production and thickening/narrowing of airways -> breathing difficulty | bronchitis |
| cardiopulm. disorder: etiology-cigarette smoking leading cause as well as long-term exposure to environmental pollution and a history of asthma | chronic obstructive pulmonary disease |
| cardiopulm. disorder: symptoms-dyspnea with minimal expulsion, persistent cough with increased mucus production, wheezing, fatigue; severe - edema in LEs, weight loss, cyanosis | chronic obstructive pulmonary disease |
| blood flow to heart is severely reduced or blocked, causes heart m. tissue to be without oxygen->damage or death to that tissue; caused by atherosclerosis, coronary a. spasm, or spont. coronary a. dissection/tear | myocardial infarction |
| cardiopulm. disorder: etiology-atherosclerosis is leading cause of blockages, blood clot can occlude blood flow to coronary a. | myocardial infarction |
| cardiopulm. disorder: symptoms-chest pain or discomfort, pressure, aching, fullness, squeezing sensation; dyspnea; diaphoresis; nausea/vomiting; syncope or near syncope; impaired cognition | myocardial infarction |
| cardiopulm. disorder: disruption in normal cardiac rhythm; types-tachycardia (extra beats) and bradycardia (slow beats) | arrhythmias |
| group of metabolic conditions, malfunction in body's ability to make and/or use insulin which regulates metabolism; without insulin glucose builds up in bloodstream, death may occur, organs and tissues have to break down own fats or lipids for energy | diabetes |
| type of diabetes: complete insulin deficiency requiring insulin replacement for survival, 5-10% of diabetes, occurs more frequently in kids, symptoms develop in weeks or months but can be severe | type I |
| type of diabetes: body does not produce insulin properly, includes insulin deficiency and resistance, increased age and obesity, 90-95% of diabetes, gradual onset | type II |
| type of diabetes: transient DM that appears during 2nd or 3rd trimesters of pregnancy, 2-10% of pregnancies, 50% will develop into type II, due to hormones blocking action of insulin | gestational |
| type of diabetes: blood glucose levels normal too high and meet other criteria for diabetes, associated with obesity and HTN -> increased risk for CV disease, prevent with lifestyle mods. | prediabetes |
| type of diabetes: etiology-autoimmune response that destroys insulin-producing cells, multifactorial cause with unknown aspects, genetic susceptibility coupled with environmental factors | type I |
| type of diabetes: beta cell formation; genetics, age, ethnicity, and lifestyle factors | type II |
| type of diabetes: low blood sugar; symptoms - mild to moderate-jittery, irritable, dizzy, weak, nauseous, blurred vision; severe-inability to eat/drink, seizures, unconsciousness | hypoglycemia |
| type of diabetes: high blood sugar; symptoms-polydipsia, polyuria, polyphagia, fatigue, blurred vision, slow healing, weight loss, ketoneuria | hyperglycemia |
| management of DM type: lifelong with significant management; daily routines include insulin replacement, blood glucose monitoring, glycemic control; insulin replacement-self administered, surgical options | type I |
| management of DM type: lifestyle changes-nutritional strategies, regular exercise, prevent and/or tx. of complications, glycemic control; pt. ed.; pharmacological management-when diet and exercise are not effective, oral or injectable insulin | type II |
| surgical removal of all or part of a limb or extremity resulting in absence of a limb, not all absence is due to acquired loss | amputation |
| levels of amputation: partial hand, wrist disarticulation, transradial (below elbow), transhumeral (above elbow), shoulder disarticulation, forequarter (entire arm into clavicle) | UE |
| level of amputation: above knee, below knee | LE |
| etiology: LE - vascular disease such as DM and PAD; UE - trauma, cancer, infections, burns, congenital abnormality | amputation |
| symptoms: kids - lack of full UE ext., acquisition of milestones and functional skill dev., pain from overgrowth or prosthesis fit; acquired - phantom pain, pain, isolation and depression due to social stigma, discomfort with prosthesis | amputation |
| course varies from person to person based on individual needs and nature of limb loss; specialized and collab interprofessional team needed to optimize outcomes | amputation |
| congenital - impact to parents and families in addition to kid; potential impact on physical, social, functional, and emotional dev.; focus of intervention-restore limb function and appearance, facilitate skill acquisition, early fitting of prosthetic | amputation |
| acquired - impact on clients and families whether planned or sudden; focus of intervention-wound healing, addressing functional deficits, prep for and provide prosthesis, training, acceptance, vocational counseling, peer support, ed. | amputation |
| how to choose a prosthesis: residual limb, cosmesis and/or function, hand dominance, prior level of function and activity level, desired activities, patient goals, attitude, motivation, financial coverage, cognitive abilities | amputation |
Created by:
emma.scarmon-coyotes
Popular Occupational Therapy sets