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Movments D/O
Clinical Medicine II-Spring 2012
| Question | Answer |
|---|---|
| How do we diagnose movement disorders | after r/o other causes such as drugs, lesions, systemic illnesses |
| Overall tx of a movement d/o | symptomatic |
| Three classifications of abnl movement | Impaired voluntary: paralysis, ataxia, impaired motor planning, abnl muscle tone: spasticity, rigidity, involuntary movements: tremor, chorea/athetosis/dystonia, tics/myoclonus |
| Dance like movement uncontrolled | chorea |
| Twisting, rotational involuntary movement | athetosis |
| Myoclonic movement | falling asleep in class and jolting awake: nl, not nl is involuntary happening frequently |
| Where is the parkinson’s belt | upper Midwest, most per capita is in ND |
| Pathology of Parkinson’s | sustantia nigra: dopamine producing cells→by product is melonin linked to parkinson’s movements? |
| With someone is having parkinson’s movements, what should we look for | skin cancer: melanoma |
| Cause of parkinson’s | both environmental and possibly genetic, not set and stone pathology |
| At dx, how much damage is happening | ~70 at start of of sxs, slow onset, hard to dx sometimes |
| Core motor features of Parkinson’s | resting tremor, bradykinesia, rigidity, posture/balance changes |
| Pt’s with simultaneous PD, dementia, and hallucinations | lewy body dz |
| Sxs with rididity of trunk, falling, unable to look up/down | supranuclear palsy-no tremor |
| How do we test for PD | can’t actually test for it, just r/o other causes, r/I by clinical sxs: give them a PD drug see if +result |
| What is the tx for PD | no tx just treat the symptoms, MC levodopa (dopamine), or dopamine agonists, |
| SE’s of levodopa | nausea, postural hypotension, dyskinesia, motor fluctuations |
| As dz progresses, what happens to sxs | need more meds, cells die, need more dopamine, sxs: tremors/can’t move, take pills, control, dyskinesia,then can’t move again |
| When do the motor complications of PD start | 3-10yrs post start of levodopa: dyskinesias |
| What does deep brain stimulation do | high frequency pulsatile, to “ablate” the overactive nerves, targets the nucleus (subthalamic) |
| When do we do the DBS to the brain | middle dz when drugs aren’t nearly as effective, but before in nursing home |
| What are some sxs that will precede the motor sxs of parkinsons | REM, constipation, loss of smell |
| Cause of death in pt’s w/ PD | pulmonary infx/aspiration, UTI, PE, complications w/ falls and fxs |
| Classification of Essential tremor | Action or postural tremor or kinetic with tasks, can move to rest post action |
| Two most common places to see E.T. | Hands and voice, usually bilaterally |
| Secondary criteria for identifying E.T | long duration to dx, Fhx, beneficial response to EtOH |
| What can a “neck tremor” be | contraction of sternocleidomastoid muscle: torticollis |
| Cause of E.T and Dx | Genetic, Fhx, Dx: clinical hx, movement tremor, |
| Tx for E.T. | none, life modifications, wrist weights, biofeedback, BB’s primidone, benzodiazepines, thalamic DBS |
| Desire to move in association w/ paresthesias/dysethesias of the limbs | Restless legs syndrome |
| Is jerking while sleeping at night RLS? | no it is most likely nocturnal myoclonus |
| Two types of RLS | idiopathic, or secondary RLS d/t renal failure, DB neuropathy, RA, radiculopathy, preggo, iron def, |
| Pathophysiology of RLS | CNS abnormality, dopamine dysfx, endogenous opiate system |
| Why does iron deficiency cause RLS | iron a cofactor for dopamine production |
| Tx RLS | tx underlying dz, remove potential aggravators, ↑sleep hygiene, relaxation techniques, Dopamine agonists 1st line drug |
| Problem with shorter length drugs | Levodopa: sxs will start occurring more and more throughout the day |
| When would we use opioids for RLS tx | usually only when there are other sxs with pain |
| Neurologic movement d/o w/ sustained muscle contractions that cause twisting or repetitive movements w/abnl sometimes painful, postures or positions | Dystonia |
| What is primary dystonia | only sign, no specific pathology, DYT1 mutation inheritation |
| What is secondary dystonia | from drugs, w/ parkinsonism, psychogenic causes |
| 5 types of dystonia | focal, segmental, multifocal, generalized, hemidystonia |
| MC types of focal dystonia | laryngeal dystonia |
| Tx of dystonia | botox, inject while in a flexed position, just enough to relax/paralysis the muscle good for focal |
| How do we dx dystonia | r/o other causes |
| Dry eye syndrome or tics | blepharospasm |
| Subtypes of dystonia | Blepharospasm, cervical dystonia, writer’s cramp |
| What is a sign associated with problems in Upper motor neurons | Babinski sign + for spasticity |
| What signs are associated w/ spasticity | muscle shortening, motor weakness, + Babinski, muscle overactivity |
| Tx of spasticity | oral meds, muscle relaxants: careful d/t weakness in muscles can turn into jelly, PT, Denervation, intrathecal drug delivery, botox, |
| What is poor coordination, examples? | ataxia, dysmetria of eye movements, nystagmus, dysarthria, limb dysmetria, gait ataxia |
| Trouble forming words | dysarthria |
| When does ataxia occur | anytime from many causes |
| Workup of ataxia | look for underlying causes and treatable conditions, Brain MRI: detect cerebellar atropy and lesions |
| DDx of Ataxia | toxins, paraneoplastic cerebellar syndrome, sporadic cerebellar degeneration or hereditary |
| Tx of ataxia | supportive, assistive devices |
| What diz has chorea or involuntary movements, later dystonia, and voluntary motor dyscontrol, cognitive, and emotional d/o | Huntinton’s disease |
| Dx and patho of HD | gene test, autosomal dominant, attacks the caudate nucleus and putamen, and secondary atrophy in the brain |
| When does HD set in | age 30-40, survival about 15-20yo |
| Tx HD | none, tx sxs: antipsycotic or dopamine antagonists, therapy: PT, OT, speech, nutrition, social services |
| What is the genetic testing for HD | repeated CAG (poly Q) in the HD gene, blood test |
Created by:
streetsmarts
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