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Neuro Day 1/5
Francis: Anat/Phys, Imaging, Headache
| Question | Answer |
|---|---|
| Bone that encloses and supports brain | Cranium |
| What are the Meninges | Dura mater, arachnoid, pia mater |
| Controls sensory impulses, initiation of voluntary movement, site of reasoning ability and emotional function | Cerebrum |
| Site of coordination of skeletal muscles | Cerebellum |
| What portion of the brain contains nuclei for cranial nerves and vital autonomic functions | Medulla Oblongata |
| This is the portion of the CNS that extends beyond the head. It controls reflexes and impulses | Spinal cord |
| This is a layer of gray matter that covers the surface of each cerebral hemisphere | Cortex |
| Known as the "gatekeeper" this feature of the brain is made up of a wall of capillaries, connective tissue and nerve cells (astrocytes) | Blood Brain Barrier |
| What is the function of the Blood Brain Barrier | Determines which substances can move from plasma to extracellular fluid of the brain. |
| This imaging study may or may not require the use of contrast dye | CT |
| This imaging study is most helpful in evaluating the brain, lung, mediastinum, and liver | CT |
| Procedure of choice for imaging of the brain and spinal cord | CT |
| Used in cases of spinal trauma or stroke to differentiate between infarct or hemorrhage | CT |
| ____is superior to ____ for imaging of the brain and spinal cord | MRI; CT |
| This study has an excellent display of vascular anatomy | MRI |
| This study has better visualization of linear structures | MRI |
| This study is based on 3D reconstruction of the brain sections | PET (Positron Emission Tomography) |
| Shows alterations in blood flow, blood volume, O2 metabolism...useful in epilepsy | PET |
| Records exlectrical activity of the brain with electrodes placed on the scalp | EEG |
| MOST useful in evaluating patients with suspected epilepsy and coma | EEG (Electroencephalography) |
| Records pattern of electroactivity in muscle, both at rest and during activity. Needle is inserted into muscle | EMG (Electromyography) |
| Used to obtain sample of CSF from subarachnoid space between L4 and l5 | LP (Lumbar Puncture) |
| Name a contraindication to LP | Increased ICP (papilledema, mass lesion), infection near puncture site, coagulation disorder |
| Rapid series of films obtained after a bolus of contrast via percutaneous catheter, used to image major arteries | Angiography |
| The 3 portions of the history she emphasized for questioning about Headaches | Quality, Location, Timing |
| Common causes of Headache | Umm. there's a lot LOL! they're on the slide at the top left corner of page 7-first packet :) |
| Benign recurring HA with pain-free periods that is often provoked by stereotyped stimuli | Migraine Headache |
| What is the pathophysiology behind a migraine HA | INTRAcranial vasoSPASM followed by EXTRAcranial vasoDILATION |
| What are the three classes of Migraine? | Classic, Common, Complicated |
| This type of migraine presents with an aura | Classic Migraine |
| This type of migraine is most frequent, and does not present with an aura | Common Migraine |
| This type of migraine presents with focal neruological features | Complicated Migraine |
| Name 3 triggers for migraines | Alcohol, lack of sleep, OCP, stress, missed meals, chocolate, cheese, caffeine, nitrites(lunch meat) |
| How does a migraine present? How is the pain distributed? (Quality) | UNILATERALIZED, or generalized DULL, THROBBING headache, frontal-temporal |
| Common associated symptoms of migraines | Nausea, vomiting, PHOTOPHOBIA, PHONOPHOBIA, blurred vision. |
| Describe the onset of a migraine headache | builds gradually |
| How long does the typical migraine last? What makes the pain worse? | 4-72 hours; physical activity |
| Nonpharmacologic management of migraines | avoid triggers, rest in a dark quiet room |
| Prophylactic treatment for migraines | ASA, Amitriptyline, Propanolol, Imipramine |
| What subQ autoinjection is available for migraine headache patients? | Sumatriptan |
| Treatment for mild attacks of migraine HA pain | Acetaminophen, NSAIDS |
| Treatment for moderate pain of migraine HA | Butalbital with caffeine and ASA, Ergotamine, Sumatriptain (Except in HTN and CAD) |
| Treatment for severe pain of migraine HA | Dihydroergotamine, Merperidine |
| This HA is usually bilateral, occipital-nuchal, generalized; MC type of primary HA | Tension HA |
| This headache is described as "fullness, tightness, tight band, waves of aching pain" | Tension HA |
| How long does a tension HA last | minutes to days |
| Tension HA treatment | acetaminophen & NSAIDS, anti-migraine agents, and reduce stress. May require TCA's if chronic |
| Cluster Headache | Recurrent episodes of frequent HA separated by pain free periods |
| This HA is characterized by 1-3 short lived attacks per day of PERIORBITAL, SUPRAORBITAL, or TEMPORAL pain over a 4-8 week period. | Cluster HA |
| How long do Cluster HA last? | 15min-3hours |
| Cluster HA are typically ___-lateral | uni- |
| This HA has no warning and the pain crescendos within 5 min | Cluster |
| This HA tends to recur at about the SAME HOUR EACH DAY for the duration of a bout and may be nocturnal and AWAKE PATIENT | Cluster |
| Management of cluster HA includes | High flow O2, ergotamine, and SQ sumatriptan or tartrate aerosol or lithium carbonate |
| This condition is common in elderly people age 50-85, but the average onset is 70. | Giant Cell Arteritis |
| This is an inflammatory process of the cranial arteries | Giant Cell Arteritis |
| If GCA isn't treated with _______, 50% of patients will go blind | high dose glucocorticoids |
| GCA is diagnosed via a ________ biopsy | Temporal artery biopsy |
| This condition frequently coexists with GCA but does not cause blindness on it's own. | Polymyalgia rheumatica |
| What condition is described as a progressive impairment of intellectual functioning with compromise in multiple cognitive domains, 1 of which is memory? | Dementia |
| What are the two D's that are usually associated with Dementia? | Depression and delirium |
| What are the four subtypes of dementia? | 1. DAT (dementia of Alzheimer's) 2. MID (Multi-Infarct Dementia) 3. Subcortical Dementia 4. Secondary Dementia |
| What is the most common type of dementia? | DAT |
| DAT is a relentless deterioration of __________ __________ functioning (language, perception, calculation) at a variable rate | higher cortical |
| What is MID usually due to? | Cerebral infarcts secondary to atherosclerosis |
| Movement and gait disoders and disturbance of motivation, mood and arousal are usu associated with what type of dementia? | Subcortical dementia; Parkinsonism, Huntington's for example |
| Which type of dementia is reversible if you treat the underlying dz? | Secondary dementia: Ex. hypothyroidism, Vit B def., normal pressure hydrocephalus, AIDS, syphillus, neoplasms, meds |
| What are some risk factors associated with dementia? | Inc. age, family hx, head injury, CNS infection, HTN, cholesterol, low education, female, smoking, DM |
| What is the simplistic pathophys behind dementia? | Widespread neuonal degenerations or multifocal disorders |
| What is the historical hallmark of DAT? | Prescence of numerous NEUROFIBILLARY TANGLES and SENILE PLAQUES, microvascular amyloid |
| When can the historical hallmark of DAT be seen? | Autopsy/Post-death |
| What happens to the brain in DAT (cortical tissue, gyri, and ventricles)? | There is a loss of cortical tissue and inc. space between gyri enlargement of the ventricles |
| What are the four A's associated with dementia? | Aphasia (imparied ability to comprehend or use language), apraxia (imparied ability to do previously learned motor skills despite intact motor function), agnosia (cant identify objects despite intact sensory function), anomia (inability to name objects) |
| What are some other clinical manifestations of Dementia? | *Imparied short therm/long term memory, abstract thinking and judegement *personality change, emotional outbursts, wandering, restlessness, hyper *sleep and mood disturbances *urinary/fecal incontinance *ridgidity, tremor *hallucinations, delusions, |
| What are some pathological findings of DAT? | Granuloveicular degeneration, neurofibrillary tangles, senile neuritic plaques, microvascular amyloid |
| What are some pathological findings of MID | Old infarcts, atheroscelrotic dz |
| What are some patho findings for cortical dementia | Degeneration of NIGROSTRIATAL neurons |
| How is dementia diagnosed? | Usu clinically (Hx and phys very important) |
| What other tests can we use for dementia? | EEG- for altered conciousness or seizures: CT of head to rule out mass: MRI- detects small infarcts, mass lesions, atrophy: |
| When is the diagnosis of dementia confirmed? | During autopsy |
| Which drugs may make the dementia patient more confused? | Psychotropic drugs |
| What are the RX treatments for sundowning/aggressive behavior? | Haldol or Risperidol |
| What are the RX treatments for Depression? | Nortirptyline, Sertaline, Fluoxeine, Paroxetine |
| What are the rx treatments for sleep disturbane | Zolpidem |
| What are the Rx treatments for Mild-Moderate DAT | Donepezil |
| Mecanical destruction of brainstem or cerebral cortex describes a _____________ coma | anatomic |
| Global disruption of brain metabolic processes describe a ________________ coma | metabolic |
| What are some causes of a metabolic coma? | Hypoxia, ischemia, hypoglycemia, drug/ ETOH induced intoxication, epilepsy |
| Some evident causes of a coma include: | Trauma, cardiac arrest, known drug ingestion |
| What are some other causes of coma? | Seizures, hypothermia, metabolic disturbances, structural lesions, mass lesion |
| For physical exam of a comatose patient what are the steps? | 1. Observe without intereferece 2. Arouse with stimulus 3. Check for brain stem reflexes |
| What are some brain stem reflex tests? | Pupillary light response (fixed and dilated poor prog): Eye movements (deviation could mean a lesion): Respiratory pattern (irregular or hyperventilation could mean lesion |
| What are the four most important Labs and/or imaging techniques | Urine/Blood Chem tox: (for exogenous drugs) CT/MRI: (anatomic lesions, infarcts, CHI, encephalitis, subdural hematoma) EEG: (more prognostic than diagnostic) CSF exam (for infection or hge) |
| What is an alpha coma? | Determined from EEG which notes poor prognosis in Comatose pt |
| What is important in coma management? | 1. Prevention of further CNS damage 2. Correct metabolic abnormalities 3. Maintain airway, inubate/ventilate if necessary; 4. LP to rule out meningitis |
| What medication do you give to prevent herniation in a comatose patient? | Mannitol |
| what IV meds do we give to comatose patients who may have had a narcotic overdose? | Naloxone |
| If the comatose pt is hypoglycemic what do we give them? | Dextrose |
| What scale do we use to determine coma prognosis? | Glascow Coma Scale |
| The glascow scale measures three areas: __________, ____ ________ _______, and ______ ______ _________ | eyes, best motor response, best verbal response |
| Is cerebral palsy progressive or non progressive? | Non-progressive |
| A motor function disorder caused by a permanent nonprogressive brain defect or lesion present at _____ or during the first _____ years of life | birth, 3 |
| In cerebral palsy, there is a chronic impairment of ________ ________, strength, __________ or movements | muscle tone, coordination |
| Since 70% of causes are idiopathic (of cerebral palsy), what are some causes that we do know? | Intrauteral INFECTION, malformations, chromosomal abnormalities, strokes. 20% OB mishaps |
| What are some risk factors of cerebral palsy? | Premature birth, birth asphysia, intrauterine growth retardation, infection, trauma |
| What are some other risk factors for cerebral palsy? | Hypoxic ischemia, encephalopathy in perinatal period, seizures in perinatl period, interventricular hge in perinatal period, meningitis/encephalitis postnatal, child abuse |
| What are the 4 subtypes of cerebral palsy? | Spastic, Athetoic, Ataxic, Spastic Diplegia |
| What is the most common type of cerebral palsy? | Spastic Diplegia |
| What are some clinical features of Spastic cerebral palsy? | Diplegia, Quadriplegia, Hemiplegia, Bilateral Hemiplegia, Involuntary muscle contraction of sudden onset., hyperreflexia, mental retardation, aphonia, seizures |
| What is another name for spastic cerebral palsy? | Pyramidal |
| What are some clinical features of Atheotic CP | Slow writhing continuous and involuntary movement of EXTREMITIES, Usu normal intelligence; Choreiform movement (like a dance) |
| what are the clinical features of Ataxic CP? | Clumsy disposition, normal intelligence, highly talkative |
| What are some clinical features of Spastic Diplegia CP? | Affecting legs but spares upper extremities, SCISSOR gait, Normal intelligence |
| What are some symptoms babies/ toddlers may have with CP? | Abnormalities in breathing, sucking, swallowing, and responsiveness, walking delayed |
| In CP, deep tendon reflexes are usually ___________ | Exaggerated |
| What is Quadraplegia usually caused by in CP? | Cysts, tumors, malformations. (usu produced in infants by fractures-dislocation of cervical spine during breech delivery) |
| What are some diagnostic studies for CP? | CT & MRI: may show cyst, cerebral atrophy, calcifications, tumors, malformations, stroke |
| What are the Labs that should be run for Cp? | Urine screening, IgG, IgM, Blood amino acids, lactate, pyruvate, amonia |
| What is another test that also be run for CP? | EEG |
| How is CP diagnosed? | Clinically |
| PT, OT, speech therapy and braces are all some techniques in managing ______- | cerebral palsy |
| Are oral meds successful for managing CP? | No, Side effects occur before benefits |
| Injection of _______ ______ into abnormal muscles decreases spacicity | botulism toxin |
| What is a rhizotomy? | Surgical resection of dorsal root of spinal nerve (management for CP) |
| What is intrathecal baclofen? | An Antispasmatic agent |
| What are some medications that may be cnsidereed in CP management? | Diazepam, Dantolene sodium, muscle relaxers |
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