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MS CVA TBI SCI +
Foundations of Disease SCCC PTA program Final
| Question | Answer |
|---|---|
| Diabetes Mellitus | metabolic syndrome with hyperglycemia and alterations in metabolism of carbs fats and proteins, decondary to absent or reduces production of insulin and or ineffective action of insulin |
| Type 1 | beta cells in islets of langerhans damaged and cannot produce insulin, early onset, patient underweight, lack of effective insulin, ketosis prone, need insulin to live |
| glucose | blood sugar |
| glycogen | stored glucose |
| glucogenolysis | breakdown of glycogen |
| gluconeogenesis | breakdown of fasts and proteins into glucose |
| lipolysis | breakdown of fats |
| pancreas | makes insulin |
| liver | controls glucose levels |
| insulin | hormone produced in pancreas to get glucose from blood stream tot he cell |
| glucogon | gets glucose from cell to bloodstream |
| three purposes of glucose | used as energy stored as glycogen, converted into fatty acids |
| type 2 | cell membrane resistant to glucose leading to hyperglycemia will not progress to ketosis, patient generally overweight, later onset in life |
| retinopathy | eye problems associated withDM |
| neuropathy | nerve damage caused by DM |
| CVD | complication of DM approximately 50% |
| nephropathy | kidney comlications associated with DM, generally kidney failure |
| Macrovascular disease | TIA, Stroke, Angine, Myocardial infarction, cardian failure, PVD |
| Microvascular Disease | diabetic retinopathy, non proliferative, proliferative, macular edema, microalbuminuria, macroalbuminuria, end stasge renal disease, ED, autonomic neuropathy peripheral neuropathyh, osteomyelitis, amputation |
| risk factors for diabetic ulcers | uncontrolable hyperglycemia, durtation of diabetes, PVD, blindness or visual loss, chronic renal disease, older age, peripheral neuropathy, foot deformity, trauma and poorly fitted shoes, callus, Hx of ulcers prolonged elevated pressure, limited jt mob |
| Gangrene | complication of necrosis caused by infection two major types wet and dry and both can lead to an amputation |
| PT education | teach patients to imspect feet and body daily for open wounds that may become infected |
| symptoms of hyperglycemia | excessive thirst polydipsia, urination polyuria, dry skin, hungry polyphagia, blurry vision, drowsy, slow healing wounds, what to do chekc glucose level, call HCP |
| symptoms of hypoglycemia | shaky, increased HR, diaphorisis, dizzy, anxious, hungry, blurry vision, weakness or fatique, headache, irritable, what to do check glucose treat and check again |
| ketoacidosis | is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat proteins in response to a perceived need for respiratory substrate, is a type of metabolic acidosis which is caused by high concentrations of ketone bodies |
| TBI | Truamatic brain injury |
| brain | uses 1/5 of resting cardiac ourput, 1.6 of O2 consumption |
| Major causes | MVA, falls, suicide |
| direct blow injuries | can be closed or open, opne involves penetrating skull, |
| indirect blow injuries | caused by a blow on another part of the body, fall on buttocks or whiplash |
| types of axonal injuries | stretching of axon, twisting of axon, compression of axon, or a reaction of axon to damage |
| primary damage | damage caused by injury nerves and or blood vesels of brain |
| secodnary damage d | death of unaffected cells from bleeing or edema diaschesis |
| associated trauma to other systems | fractures and organ involvment |
| injury mechanisms | compression, hemorhage, hematoma edema: tenion; intracranial pressures: shearing; herniation |
| concussion | transient state of unconcsiousness, associated post traumatic amnesia, closed injury |
| contusion | bleeding and bruising, coup and contrecoup, closed injury |
| laceration, | tearing of tissue, hemorhage and severe edema, open injury |
| grade 1 concussion | mementary confusion, no loss of consciousness, symptoms clear in 15 minutes |
| grade 2 concussion | symptoms last more than 15 minutes |
| grade 3 concussion | you got knocked out, loss of consciousness |
| subarachnoid hematoma | headnache stiff neck, vomitting, photophobia, iritability usually resolves on own |
| subdural hematoma | involves veins, surgical evac required slow healing |
| epidural | involves arteries compression of brain herniation surgical evacuation required |
| intracerebral hematoma | hematoma with in the brain generally in the white mater |
| impariments of TBI | level of consciousness, a and O memory, executive functions |
| coma | state of consciousness no arousal or awareness no sleep wake cycle eyes closedm short duration 3-4 weeks |
| vegetative state | sleep wake sycle returns, vegetative functions retunr may be aroused but unaware, reutnr of brainstem reflexes, grimacing, vocalizations to nociceptive stimulus grasp response, tonic reflexes |
| persistant vegetative state | you are not moving out of this state |
| minimally responsive | signs of awareness are present |
| glascow coma scale | measure state of coma |
| ranchos los amigos levels of cognitive function | progess once out of coma |
| decerebrate rigidity | extenor pattern rigidity |
| decorticate rigidity | flexor pattern rigidity in uppers extensor pattern in lowers |
| parkinsons disease | shaking palsy, caused by low levels of dopamine produced by substantia nigra in the basal ganglia, it is idiopathic no known cause |
| parkinsons disease | insidious progressive and degenerative involving the basal ganglia as a result of the substantia nigra which results in a deficiency of the neurotransmitter dopamine |
| Who is PD likely to effect | 50-60s, men over women, whites over blacks, 1.5 million people in the US, 1/1000 people, lower prevalence in africa and china, |
| types of PD | postencephalic, pseudoparkinsonian symptoms due to tumors, and boxers brain or head truama, cna be drug induced from synthetic heroin, MPTP, antipsychotic meds |
| etiology of PD | free radicals, external or internal toxins, genetic factors, aging process is accelerated |
| cause of PD | loss of 80 percfent of the dopamine producing cells in th esubstantia nigra |
| neurotransmitter imbalance | imbalance of dopamine and acetylcholine when dopamine to low acetylcholine takes over and movements become shaky the dopamine and ach work together to produce smooth movement |
| early signs of PD | difficulty dressing, alterations in handwrtiting, stiffness slowness, eating difficulty, voice changes, facial masking, blaance issues, tremors |
| parkinson tetrad | tremor, rigidity, bradykinesia, postural instability |
| tremors | pill rolling, common first symptom, resting, distal, can be exacerbated |
| rigidity | cog wheel lead pipe flexores over extensors, not position dependent |
| brady kinesia | slowing of voluntary movement, secondary to delayed initiation, delayed stopping, decreased reaction time, decreased speed and amplitude |
| akinesia | freezing |
| kinesia paradoxia | may be frozen but you can initiate movement |
| poverty of movment | no blinking, facial expression or arm swing in gait |
| postural instability | loss of righting, and equilibrium reactions, festinating gait, loss of anticipatory postural reflex, stooping posture |
| motor planning | feedback mode instead of feedforward, requires cuing, and triggers |
| sensory | PD is a motor disorder but patient may experience abnormal sensations paresthesias, akathisia- restless moving |
| ANS complications of PD | B and B, thermoregulation, flushing of skin, sialorhea(drooling) seborhea- flaky skin, orthostatic hypertension |
| hypomimia | facial masking |
| hypophonia | low voice |
| micrographia | small writing |
| dysarthria | slowed slurred speech |
| dysphagia | trouble swallowing |
| gait characteristics | decreased BOS, decreased stride length, decreased velocity, loss of pivoting, loss of armswing, stooped posture, short shuffling steps, festination, retropulsion(body leaning back as walking) anteropulsion(body leaning forward in gait using momentum) |
| cognitiv eeffects of PD | affected usually secondary to drugs with psycosis effect |
| treatments of PD | surgical pharmaceutical rehabilitation |
| surgical treatment of PD | cryotherapy, pallidotomy, thalamotomy, neural tissue transplants, tremor control therapy, neurostimulation |
| L dopa | synthetic dopamine |
| carbidopa | slows breakdown of l dopa |
| entacapone | extends time period of l-dope in brain |
| drug complications of treating PD | dyskinesias, depression anxiety, psychotic episodes, halucination, wearing off phenomenon, on/off phenom window of drug use small. |
| stroke | sudden onset of neurological symptoms resulting from a disturbance of the blood supply to the brain |
| incidence of stroke | 700k ppl/yr, 500k first attacks, 200k recurrent |
| morbidity/mortality of stroke | 1/3 recover 1/3 disable, 1/3 die |
| modifiable risk factors of stroke | HTN, smoking, heart disease, diabetes, TIA, high cholesterol, CAD, sleep apnea, birth control pills |
| non modifiable of stroke | age(over 65), gender moremen then women, women die more, ethnicity 2x in AA, family history, prior stroke |
| symptoms of stroke | sudden numbness or weakenss of face, arm or leg, elspecially on one side of the body. trouble speaking, sudden confusion, sudden trouble seeing, in one or both eyes, trouble walking, dizziness LOB, or coordination sudden sever headache with no known cause |
| ischemic attack | embolus blocks area, leading to no blood in area therefore no O2, |
| hemorhaggic attack | blood vessel bursts, secodnary to HTN pin hole in blood vessel |
| aneurysm | weakeing and ballooning of vessel walls |
| symptoms of right CVA | left hemiplegia left hemianopsia, visual sptial skills, motivation, emotional lability, recognition, attention, |
| left CVA | right hemiplegia, right hemianopsia,working memory ,learned skilled movements, brain stem, understaning speech, talking, verbal memory, long term goals, |
| muscle tone | UMN lesion, hypertonia, spasticity, slow disuse atrophy |
| apraxia | association centers inability to do something on command ideational as well as ideomotor |
| synergies | brunstrom, six stages flexors strongers over extensors, six stages moving to normalcy, 6=normal, 5 isolated movement 4 movment in synergy, 3 full synergy, 2 spasticity, 1 flaccidity |
| flexion synergy | shoulder elevators, elbow flaxors, hip flexors |
| extension synergy | , shoulder adductor, and depressors, pronators, hip adductors, hip internal rotators, knee extensors, plantar flexors |
| hemianopsia | half of the visual field is missing, folows plegia of CVA |
| pushers syndrome | pt pushes to affected side |
| neglect | they dont realize there is a side of involvment |
| aphasia | wernickes brocas global depending upon what portion of brain affected wernickes in males, brocas more comon in females |
| pharmacological affects | ticlid reduces risk, selfotel prevents further cell death, tirilazad protects cell from hemorhage, TPA dissolves the clot |
| Best PT timing | early treatment, active treatmenr orient to involved side, bilateral activities, trunk emphasis, proper positioning |
| neurofacilitation techniques | positioning, successive induciton, irradiation, tone inhibition |
| souques phenom | when arm raised over 90 degrees abd or flex fingers fanout |
| successive induction | antagonist facilitates agonist |
| raimistes phenom | overload a strong muscle to get a weak one to fire |
| homolateral limb synkinesis | flex arms legs flex on same side |
| tone inhibition | reciprocal inervation, icing, tapping virbration of opposite muscle, and positioning |
| problems with sling | limit sensory input, place extremetiy into non functional pattern, impairs body image, impairs arm swing in gait can lead to edema of hand |
| assistive devices | encourages asymetry, decreases wlking speed, increase energy expenditure, inhibits WS and WB to weak side, inhibit normal arm swing, may increase hypertonus |
| common gait deviations | slwoer wlking speed, longer cycle, difficulty in singel limb, short stance phase, fast swing phase on stronger side, associated reactions in weak arm, absent trunk rotation, retraction of weak hip during stance phase recurvatum of weak knee, |
| more gait devieation | circumduction hiphiking, extended knee during swing phase, lack of dorsiflexion, +trendelenburg, no push off on weak side |
| diaschesis | flaccid paralysis in muslce bladder and bowel, loss of sensation, areflexia, loss of perspiration, hypotension, bradycardia |
| stretch injury | hyperflexion in c56, hyperextension at c45 |
| falls | severe compression vertebra can shatter, axial loading head c45 feet t10 11 12 |
| complete TSCI | total loss of motos and sensory in the lowest sacral segment s2-4 |
| incompplete TSCI | sacral sparing, partial preservation or complete preservation of motor and sensory function in lowest sacral segment, anal sensation, sphincter function |
| brown sequard | one side of the SC injured common from stab wounds GSW |
| central cord | central part damaged, |
| posterior chord | sensory involvment |
| anterior cord | motor involvment |
| cauda equina | horses tail involvement compression of cauda equina |
| UMN lesion | PMC to AHC, causing spasticity |
| LMN lesion | flaccid areflexia, @ level of lesion |
| motor level of injury | last nerve root that innervates key muscles at F strength |
| sensory level of injury | last nerve root in which sensation is normal, light touch and pin prick |
| zone of partial preservation | neurological levels below injury that may still exhibit some function |
| impairments TSCI | across all body systems, NM, pulmonary, CV ANS, genitourinary, Musculoskeletal, integumentary |
| breathing complications | phrenic nerve c3-5 primary muscle of inspiration, intercostals, t1-12 inspiration and expiration functions, cervical c2-4 acccessory to resp. abd. t6-t12, forced expiration and cough |
| pulmonary impairments of SCI | no independent respiratory function with lesions above c4, respiratory fatique, sleep apnea with high cervical lesions, difficulty clearing secretions, atelectasis(collapsed lung), bronchial obstruction, pneumonia, pneumothorax |
| CV impairments SCI | bradycardia, hypotension, disruption of sympathetic nervous system decreased BP, |
| ANS impairments SCI | thermoreg, orthostatic hypotension, apnea bradyarrythmia, syndrome, autonomic dysreflexia, neurogenic bladded/bowel, sexual dysfunction |
| GI impairments SCI | paralytic iteus, motility stops, stress ulcers-ans not working |
| Musculo skeletal SCI | osteoporosis, heterotropic ossificans, contractures, paraplegia dystonia, spasticity, pain |
| integumentary SCI | decubiti, complications infection abscess, sepsis, osteomelitis, death |
| PT goals of SCI treatment | maintain and improve function |
| c3 | face and neck motion none to litlediaphram, portable ventilation, totally dependent in self care, sip n puff wc, able to use environmental contorl unit |
| c4, | diaphragm trap, dependent on personal care, independent pressure relief with poer tilt in space wc |
| c5 | delt some biceps low respiratory reserve, light grooming and feeding with hand device,sassistance for bathing dressing and transferes with sleiding board |
| c6 | rotator cuff biceps wrist extensors, may acheis ind in perosnal care, assist in transfers, rolling in bed with side rails, manual propulsion in wc, pressure relief, skin inspection, cough with abdominal pressure |
| c7-8 | triceps, writs flexors, finger flex and extends, upper limb except hand intrinsics, may totally independent in personal care, can roll over, sit up in bed, mover in sitting positioning, transfers with and without sliding board wheelchair smooth surface |
| t1-5 | hand intrinsics, and some intercostals, full inervation of UE at t1, can function independent form WC, lacks trunk, trnasfers between floor and WC |
| t6-12 | intercostals and abd, enhanced respiration, may ambulate with bracing and swing thru |
| l1-3 | hipflexors some quads may ambulate with short leg bracing |
| l4-s1 | hamstrings some ankle and foot, ambulation with minimal aids |
| CV impairments | bradycardia, hypotension, disruption of sympathetic nervous system decreased BP, |
| ANS impairments | thermoreg, orthostatic hypotension, apnea bradyarrythmia, syndrome, autonomic dysreflexia, neurogenic bladded/bowel, sexual dysfunction |
| GI impairments | paralytic iteus, motility stops, stress ulcers-ans not working |
| Musculo skeletal | osteoporosis, heterotropic ossificans, contractures, paraplegia dystonia, spasticity, pain |
| integumentary | decubiti, complications infection abscess, sepsis, osteomelitis, death |
| PT goals | maintain and improve function |
| c3 | face and neck motion none to litlediaphram, portable ventilation, totally dependent in self care, sip n puff wc, able to use environmental contorl unit |
| c4, | diaphragm trap, dependent on personal care, independent pressure relief with poer tilt in space wc |
| c5 | delt some biceps low respiratory reserve, light grooming and feeding with hand device,sassistance for bathing dressing and transferes with sleiding board |
| c6 | rotator cuff biceps wrist extensors, may acheis ind in perosnal care, assist in transfers, rolling in bed with side rails, manual propulsion in wc, pressure relief, skin inspection, cough with abdominal pressure |
| c7-8 | triceps, writs flexors, finger flex and extends, upper limb except hand intrinsics, may totally independent in personal care, can roll over, sit up in bed, mover in sitting positioning, transfers with and without sliding board wheelchair smooth surface |
| t1-5 | hand intrinsics, and some intercostals, full inervation of UE at t1, can function independent form WC, lacks trunk, trnasfers between floor and WC |
| t6-12 | intercostals and abd, enhanced respiration, may ambulate with bracing and swing thru |
| l1-3 | hipflexors some quads may ambulate with short leg bracing |
| l4-s1 | hamstrings some ankle and foot, ambulation with minimal aids |
| MS | chronis progressive demyelinating inflammatory disease involving the CNA |
| demelinating | myelin erodes from the axon decrease NCV and more energy to conduct impulses |
| etiology MS | viral autoimmune or combination, first sixteen years determines risk |
| autoimmune response | system attacks itself |
| plaques | slcerosis and scarring of CNS, around spinal cord |
| incidence of MS | white temperate climate, young adult women folk |
| diagnosis MS | made upon evidence of lesions in CNS demonstrated onCT or MRI, or two seperate attacks lasting at least 24 hrs at least one month apart, and involving 2 areas of CNS, progression of symptoms for at least 6 month |
| course MS | unpredictable exacerbations remissions classical coursed, subclinical, benign, relapsing remitting, secondary crhonic progressive, primary progrressive which has no remissions |
| common attacks | corticospinal tract, optic nerve pathways, brainstem and cerebellar pathways, posterior column tracts |
| somatosensory impariment | 5-70 percent or patients, usually first symptom, one limb, one side, all limbs, parethesias, loss of vibration and proprioception, loss of tactile discrimination, l'hermittes sign |
| l'hermittes sign | neck bends forward electircal shock down back |
| somato motor | first noted in gait, corticospinal tract, fluctuating muscle tone, heaviness of limbs, weakness, spastic paresis, spasms, UMN symptoms, cerebellar symptoms + babinski |
| Visual | early symptom, 8% of patients, optic neruitis, decreased visual acuity, photophobia, nystagmus, ptosis, strabismus, pain, dimmin, oscillopsia |
| ANS complications | neurogenic bladder, detrusor internal sphincter dysynergia, bowl problems, abnormal sweating, intolerance to heat, sexual difficulties |
| cognitive impairments | 50% of patients, more prominnetn as disease progresses, mood swings, euphoria, lability, memory problems, reasoning difficulties, |
| related difficulties | central fatigue, paroxsymal symptoms(sudden outburt of symptoms and sudden remisison) |
| charcot triad | is the combination of nystagmus, intention tremor, and scanning or staccato speech |
| best prognosis | acute before 35, monosymtomatis, sensory over motor, complete remission after first attack |
| worst prognosis | early cerebellar signs, early spasticity or trmor |
| pharmacy | ACTH replacement, steroids, immuno suppressant, antiviral mood elevators, antispasmotics(valium baclophen dantrium) |
| disease modifiers | betaseron interferon avonex, copaxone |
| other treatments | dorsal stimulators, snake venom bee venom |
| arthritis | inflamation of joints cna be reumatoid or osteo |
| RA | systemic disease affecting the synovial sac, invovles joints, organ including heart eyes skin vascular, systemic response, malaise, weakness, fatigue, depression ,exacerbations and remissions |
| three major courses of RA | flareups and remissions, long clinical remissions, progressive unremitting |
| RA | affects all structures of join increaes join pressure and joint effusion |
| granulation tissue | in joint pannus, describes the granulation tissues that is formed with the synovium by proliferating fibroblasts and inflammatory cells |
| joint bones | characterized by pitted carilage and bone |
| joints affected | cervical spine, shoulders, finger (ulnar deviation) knees, ankles, toes,wrist general morning stiffness lasting 1-3 hrs, knockkneed, peripheral involvment progressing proximal |
| deformities | hammertoes rhematoid nodule, ulnar drift, vallets of weakend muscles |
| swan neck | hyperextension of PIP, flexion of DIP RA |
| bouteniere | flexion of PIP, extension of DIP, RA |
| Ankylosing Spondylitis | fusing of vertebrae as well as kyphosis |
| Osteoarthritis | Trophis degeneration not inflmmation |
| Etiology of OA | abnormal physical forces, OBesity, orthpedic problems, trauma,, altered biocheimical processes of cartilage, aging hormones and drugs |
| SYmptoms of OA | pain with exercise, gel phenomenon, osteophyte, hypertrophy of bone, squaring off of bone, enlarged bony jt, crepitus, deformity and loss of ROM ,muslce weakness, and dusue atrophy, aching with cold, |
| Joints affected, | spine, hips, fingers, knees big toes bow legged |
| bouchards node | huge PIP |
| heberdens node | huge DIP |
| Arthritic Gait pattern | slow antalgic, decreased stance, asymmetrical step length, less motion in involved jts, decreased forward and alteral smoothness, + trendellenberg |
| PT GOals of OA | releive paint, analgesis and anti inflammatory, maintain mobility, ROM and exercise, reduce disability, protective splinting adaptice devices, prevent progression with surgery and drugs |
| pharmacology of Arthritis | nsaids corticosteroids, disease modifiers |
| surgeries for Arthritis | synovectomy, tenosynovectomy, tendon surgery, athrodesis, athroplasty the last two are for OA |
| athrodeissi and atrhoplasty | relieve pain provide stability correct or reduce deformity improve function |
| total hip contraindications | hip flex past 90, hip add, and IR |
| patient education | remove things that promote ulnar drift jar opening, stirring spoon, lifitn pots |
| Glascow COma Scale | numbered scale that measures the level of consciousness of a person |
| exacerbation | an increase in symptoms when speaking of MS or RA |
| remission | when a symptom disapears |
| euphoria | an emotional and mental state defined as a sense of great (usually exaggerated) elation and well being |
| uthoff symptom | diplopia or blurred vision in people with MS |
| dyskinesia | decreas of voluntary movement |
| dysphagie | difficulty swallowing |
| wearing off phenomenon | drug wears off |
| hypokinesia | slow movements |
| hypomimia | facial masking |
| micrographia | small handwriting |
| on/off phenomenon | drug on and off |
| sialhorrhea | drooling |
| seborhea | flaky skin |
| hypophonia | weak voice |
| akinesia | no voluntary movements |
| akathersia | reslessness |
| brsdykinesia | extreme slowness |
| autonomic dysreflexiA | HYPERREFLEXIA` |
| postural hypotension | othrostatic hypotension |
| DVT | deep vein thrombosis, clot |
| heterotropic ossification | bone formation within soft tissue |
| spinal cord dysethesias | pain or abnormal sensations |
| post traumatic seizures | seizures after the trauma occurs |
| multipodus boot | boot used for wounds lots of padding |
| tilt in space wheelchair | gives the TBI patient ability to move |
| status epilepticus | refers to a life-threatening condition in which the brain is in a state of persistent seizure |
| seizure trigger | stiumulus that forces a seizure |
| ansence seizure | the person may appear to be staring into space with or without jerking or twitching movements of the eye muscles. These periods last for seconds, or even tens of seconds. |
| prodromal sign | first symptoms |
| focal seizure | seizure occurs in one spot |
| jacksonian seizure | grand mall seizure |
| aura | prodromal sign of seizure episode |
| anomia | trouble recalling words |
| paraphasia | is a notable feature of aphasia in which one loses the ability of speaking correctly, substitutes one word for another, and changes words and sentences in an inappropriate way. The patient's speech is fluent but is error-prone |
| abulia | lack of initiative |
| disinhibition | no inhibitions |
| emotional labiltiy | INABILITY TO CONTROL EMOTION |
| PERSEVERATION | is the uncontrollable repetition of a particular response, such as a word, phrase, or gesture, despite the absence or cessation of a stimulus, usually caused by brain injury or other organic disorder |
| emotional dysregulation syndrome | uncontrollable lauching crying, pseudobulbar affect |
| learned nonuse | they dont use affected side |
| unilateral neglect | they negelct a side dont realizxe they even have it |
| ideomotor apraxia | inability to perform a task on command and to imitate gestures even though the person understands the concept of the task |
| ideoational apraxia | an inability to perform a purposeful act automatically or upon command an inability to retain the idea of the task and to formulate the necessary motor pattern |
Created by:
dels322
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