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What areas does the ACA feed? (i.e. lobes and/or structures)
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What areas does the MCA feed? (i.e. lobes and/or structures)
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SCRN-General
General Q's of SCRN
| Question | Answer |
|---|---|
| What areas does the ACA feed? (i.e. lobes and/or structures) | Medial portion of the frontal and parietal lobes ("mohawk"); corpus callosum |
| What areas does the MCA feed? (i.e. lobes and/or structures) | Majority of the frontal, parietal, temporal lobes; the basal ganglia, internal capsule, as well as Broca's and Werneckies Area |
| What areas does the PCA feed?(i.e. lobes and/or structures) | Occipital lobe, midbrain, THALAMUS, pineal gland |
| What are the major S/S of MCA stroke? | Contralateral hemiplegia, contralateral hemianesthesia, Arm weaker than leg, face droopy, eye deviation towards side of lesion, contralateral homonymous hemianopia, if DOMINANT SIDE, global aphasia, if NON-DOMINANT, anogsagnosia |
| What are the major S/S of ACA stroke? | Contralateral motor deficits (some/few sensory), Foot & leg weaker than arm, face and tongue usually spared, abulia (decreased activity and speech), emotionally labile |
| What are the major S/S of PCA stroke? | Depends heavily on portion occluded; on DOMINANT HEMISPHERE: alexia (inability to see words/read) with or without agraphia (inability to write), visual agnosia (inability to interpret sensation or recognize things); NON-DOMINANT HEMISPHERE: neglect on con |
| What are the major S/S of a lateral Thalamic stroke? | Hemiparesthesia, followed by isolated hemisensory deficit in face, arm, & leg, may include trunk, pain may develop resistant to treatment; can also have abnormal movements (inability to stand or walk--thalamic astasia); hyper-reflexive tendons, babinski |
| What are the major S/S of basal ganglia strokes? | Cognition & behavior, memory dysfunction, dysarthria, aphasia, motor abnormalities, if on (L), verbal amnesia, if on (R), visual amnesia |
| Is ASA recommended for a patient in A-Fib already on Warfarin? | Only if history of CAD, especially if they have stents |
| What is the target INR for stroke prevention? | 2.5 |
| What is the target LDL after stroke? (Which would indicate initiation of statin therapy) | 100 |
| What is the target blood pressure AFTER stroke or TIA (secondary prevention)? | 140/90 |
| What cranial nerves originate from the medulla? | Cranial nerves 9-12 |
| What cranial nerves originate from the midbrain? | Cranial nerves 3-4 |
| What crania nerves originate from the pons? | Cranial nerves 5-8 |
| What are the S/S of carotid dissection? | ptosis, myosis (pupillary constriction), and anhidrosis---known as Horner's syndrome |
| What "important feature" does the internal capsule possess? | Nerve tract for the motor cortex |
| What important "pathways" does the thalamus contain? | Nearly ALL sensory pathways coming from the cerebral cortex |
| Regarding LOC, what can a stroke cause if the thalamus is infarcted? | Hyper-somnolence |
| What can a stroke in the hypothalamus disturb? | BODY TEMPERATURE ; also (but less prolific), affect circadian rhythm and body H20/osmo |
| What is Broca's aphasia? | Speech is 'broken,' otherwise, expressive aphasia |
| Where is Broca's area located? | Posterior aspect of frontal lobe |
| What is Werneckies aphasia? | 'What?'; otherwise, receptive aphasia |
| Where is Werneckies area located? | At the temporo-parietal junction |
| If a patient is experiencing hallucinations (but is aware of them not being real), what structure of brain is most likely being infarcted? | Midbrain |
| When is treatment for carotid stenosis considered? | Stenosis >50% and symptomatic |
| Where is the tip of a ventricular drain placed within the skull? | At the Foramen of Monro (a 'channel' that lies between the lateral ventricles and the third ventricle) |
| What is the Cerebral Amyloid Angiopathy (CAA)? | Disorder in which protein deposits in brain damage vessels, causing micro hemorrhages--and important risk factor for ICH!! |
| What medication should be avoided in patients with Cerebral Amyloid Angiopathy? | Statins |
| What is the best diagnostic tool for SAH? | NECT (Non-contrast CT) |
| What are the nursing considerations before/after cerebral angiography? | Before: NPO 4-6hrs, PT/INR, allergies to shellfish/iodine, consent After: Bedrest 6hrs, HOB only to 30 degrees, assess for bleeding/circulation, avoid flexing & hyper flexing affected extremity for 12-24hrs, liberal fluid intake |
| What is the gold standard for diagnosing vascular deformities? (such as AVM's, aneurysms, fistulas, dissections) | Cerebral Angiography |
| What is the advantage of MRI's? | More sensitive than NECT for ischemic strokes |
| What is digital subtraction angiography (DSA) used for? Particularly, what is it "best" at detecting? | DSA helps visualize vascular lesions and atherosclerotic disease; it is #1 to detect hight grade STENOSIS |
| What is TCD used for? | Identifies intracranial vessel abnormalities, occlusions, and stenosis; Effective to determine VASOSPASM! |
| What is the gold standard diagnostic for vasculitis? | biopsy |
| What would be the characteristics of CSF after an LP that would indicate SAH? | rusty appearance (related to xanthrocrome, a by-product of Hgb breakdown, which is seen 4-6hrs after bleed, and up yo 3-6 days after) |
| In an echocardiogram, what does a bubble study help detect? | PFO (patent foramen ovale) |
| What is the target SpO2 in stroke patients? | Above 94% |
| What is desired EMS arrival time to possible stroke patient? | Under 8 minutes, an to ER in 15min |
| What are the three structures of the brain stem (in order)? | Midbrain, Pons, Medulla (descending order) |
| What are the structures of the basal ganglia? | Caudate nucleus, Putamen, Globus pallidus |
| What are the structures of the diencephalon? | -Thalamus (sensory pathways), -Hypothalamus (visual pathways, body temp, H20/Osmo control) -Pituitary gland (multiple hormone) -Pineal gland (sleep wake cycles) |
| What are the structures of the limbic system? | -Hypothalamus (h20 and body temp) -Amygdala (stress & emotion control, "enhancer") -Cingulate Gyrus (emotions & ecoding memory) -Hippocampus (memory & learning--short term) |
| Are strokes more prevalent in men or women? | More prevalent in males, except for ages 35-44 (related to OC use), and greater than 85 (women live longer) |
| Does family history of stroke affect one's risk? | Increases risk by approximately 30% |
| What is the #1 modifiable risk factor for preventing both ischemic and hemorrhagic stroke? | Hypertension |
| How much does smoking increase stroke risk? | Doubles risk |
| Having D.M increases stroke risk by how much? | 2-6x times risk (varies greatly in studies) |
| What is the target A1c for stroke patients? | Less than 7 |
| Having A-Fib increasing stroke risk by how much? | 4-5x times risk; strokes usually larger |
| What are ICH risk factors? | HTN (#1), race (hispanic, black), sex (male), age |
| Are D.M are smoking risk factors for ICH? | Yes, but very weak, in comparison to ischemic |
| What are SAH risk factors? | Smoking (#1), ETOH, HTN, family history, sex (women, men only after 50 more prevalent), race (blacks) |
| Approximately how many neurons are lost every minute in large strokes? | 1.9million! |
| What is the most important 'patient history' information for EMC crews to attain from a suspected stroke patient? | Last time seen normal |
| What is the goal time for stroke patient to see MD? | 10min |
| What is the goal time for stroke patient to see stroke team? | 15min |
| What is the goal time for stroke patient to get to CT scan? | 25min |
| What is the goal time for stroke patient to get CT scan interpreted/read? | 45min |
| What is the goal time for patient to get TpA? | 60min |
| What will appear white (hyperdense) in a CT scan? | Bone, calcium deposits, blood (acute) |
| What will appear dark gray (hypodense) in CT scan? | CSF, edema, fat, infarcted tissue, blood (chronic) |
| What will appear black in CT scan? | Air |
| How long does it take for infarcted tissue to appear on a CT scan? | Approximately 6-8hrs |
| Is CT or MRI better for diagnosis of SAH? | CT scan |
| How long does it take for blood to appear on a CT scan? | Immediately |
| What is considered the acute phase of an ischemic stroke? | 24-72hrs |
| What is considered the acute phase of ICH an SAH? | Admit through discharge |
| What is one of the drawbacks of the NIH? | It does not account for posterior circulation stroke symptoms |
| If a patient has a NIH score of 14 or more, where can you anticipate he or she will be discharged to? | SNF |
| If a patient has a NIH of 6-13, where can you anticipate he or she will be discharged to? | Inpatient rehab |
| If a patient has a NIH of 5 or less, where can you anticipate he or she will be discharged to? | Home |
| What percentage of stroke patients will deteriorate in the fist 1-2days? | 25% |
| What is the ideal blood glucose for an ischemic stroke patient? | It is of DEBATE, yet current consensus is a GOAL of 140-180mg/dL |
| What is the ideal blood glucose for an ICH stroke patient? | It is of DEBATE, yet current consensus is a GOAL of 140-180mg/dL |
| What is the ideal blood glucose for a SAH stroke patient? | NO ideal glucose set; yet, research has shown glucose greater than 105mg/dL in first 10 days is associated with multi-organ dysfunction |
| What is one of the leading causes of epilepsy in the older population? | Ischemic stroke |
| Is prophylactic seizure medication recommended for strokes? | ONLY for SAH and for a short term (3-7days) |
| Seizure is more likely if a patient suffers a stroke in what areas of the brain? | temporal lobe or cerebral cortex |
| What percentage of stroke patients will get a UTI within 1month? | 25% |
| What percentage of stroke patients will get PNA (pneumonia)? | 50% in ICU and stroke unit, and up to 11% in post-acute rehab |
| What is the rate of urinary incontinence in stoke patients? | 60% |
| When can heparin safely be started as DVT prophylaxis of ICH and SAH patient? | After 24-48hrs, given hemorrhage is stable |
| What is considered ideal for chemical DVT prophylaxis--Lovenox or heparin? | Controversial, currently no 'ideal' |
| When can warfarin be safely restarted in a stroke patient? | Of debate, current practice is 10-14 DAYS, longer in larger strokes |
| What are the major functions of the parietal lobe? | Cortex for sensation in front; speech and language (Werneckies area there) |
| What are the major functions of the occipital lobe? | vision; visual cortex |
| What are the major functions of the temporal lobe? | visual memory, language comprehension, auditory processing |
| Strokes in what area can leave deficits on both 'sides' of the body? | Brain stem strokes (cerebellar strokes can have ipsilateral deficits too) |
| What are the major signs/symptoms of a lateral medulla (medullary) stroke? | Wallenberg syndrom, N/V, dysphagia, sensory loss (contralateral limbs and body, ipsilateral face), Horner's syndrome |
| What are the major signs/symptoms of a medial medulla (medullary) stroke? | Contralateral hemiparesis sparing face, ataxia, diplopia, H/A, vertigo |
| What are the major signs/symptoms of a cerebellar stroke? | Vertigo, vomiting, tinnitus, dysarthria, can have facial palsy, auditory loss, ataxia, Horner's syndrome |
| What are the major signs/symptoms of a pons (pontine) stroke? | Hemiparesis, cerebellar symptoms; Lacunar syndromes --> pure motor hemiparesis, transient dizziness, diplopia, nystagmus, dysarthria, dysphagia, ataxic hemiparesis |
| What are the major functions of the frontal lobe? | Behavior/emotions, contains motor cortex in posterior aspect; Broca's area (expressive aphasia) |
| What are major signs/symptoms of midbrain strokes? | 3rd nerve palsies (Weber's, Claude's, Benedikts); locked in syndrome, Ataxia, Upward and/or downward gaze palsies, pendicular hallucinosis (hallucinations depiste pt. knowing they are not real) |
| What is the only FDA approved Rx for acute stroke? | TPA; approved for up to 3hrs, yet endorsed for up to 4.5hrs (yet more restrictive) |
| What is the usual TpA dose? | 0.9mg/kg to a max dose of 90mg |
| At what rate is tPA administered? | 10% as a bolus over a minute, remainder over 60min |
| What should you do/anticipate if a patient has a decline in neurological status during an TPA infusion? | Stop TPA, notify MD, anticipate STAT CT--there are no standardized measures to treat patient if they have indeed bled post TPA--cryoprecipitate and/or platelets can be considered |
| What are the major S/S of a medial thalamic stroke? | CLASSIC TRIAD: Acute decreased LOC (abulia, apathy, hyper-somnolence), Neuropsychological Amnesia (disoriented, aphasia if on [L], Neglect if on [R], difficulty with new memories), Vertical Up-gaze palsies |
| What can carotid bruit indicate? | Carotid dissection |
| What can Olser nodes and Janeway lesions indicate? | Osler nodes and Janeway lesions are nodes/ulcerations on hands and feet (osler nodes are painful) that indicate INFECTIVE ENDOCARDITIS--a big risk factor for stroke |
| What is the mainstay treatment for vasculitis? | STEROIDS mainline, can consider immunosuppressants |
| What is normal CPP (Cerebral Perfusion Pressure)? | 70-90mm/hg (some say up to 150mm/hg) |
| What is the treatment for cocaine induced hypertension? | Cardene |
| What is the best position to 'place' a patient? | On the affected side |
| What is normal ICP (intracranial pressure)? | 5-15mmHg (greater than 20 is considered 'increased') |
| What is the first line treatment to reduce ICP (intracranial pressure)? | MANNITOL to reduce cerebral edema (can also consider hypertonic saline, ventricular drains, decompresive surgery, mild hypocarbbia [hyperventilation to reduce CO2, which vasodilates]) |
| What is normal CO2? | 30-35mmHg |
| Are steroids recommended to reduce ICP (intracranial pressure)? | NO, not recommended |
| What is the duration of aspirin in human body? | 5-7 days, which is the same as the life of platelets themselves (therefore, considered irreversible) |
| What is the duration of Plavix in human body? | 5-7 days, which is the same as the life of platelets themselves (therefore, considered irreversible) |
| Are Brilanta and Effient ideal for secondary stroke prevention? | NO, considered only if Plavix is ineffective as demonstrated by PY12 tests |
| What is the half-life of Warfarin? What is the onset? | Onset = 48-120hrs, Half Life = 20-60 hours |
| Are novel anticoagulants (Pradaxa, Eliquids, Xarelto) indicated for A-FIB CAUSED by a HEART VALVE ISSUE? | No! Can actually increase risk of stroke |
| Orolingual angiodema is a potential side effect of what drug? | tPA administration, ESPECIALLY if on an ACE-inhibitor |
| What should BP be BEFORE starting tPA? What about DURING & AFTER tPA? | BEFORE = 185/110 DURING & AFTER = 180/105 |
| How often should vitals be checked during tPA infusion? | q15min for 2hrs q30min for 6hrs q60min for 16hrs |
| How long does TPA remain in body? | 80% of TPA is eliminated in 10min, the remainder is eliminated in about 24hrs |
| What are exclusion criteria for patients with stroke in the 3 - 4.5 hr window? (note, not 3hr exclusion, but the 'extended' window exclusions) | -Over 80yrs old -Pt. on anticoagulant therapy (regardless of INR) -NIH greater than 25 -Patients with history of stroke AND diabetes |
| What are the most common sites of ICH (intracerebral hemorrhage)? | #1 BASAL GANGLIA, #2 is thalamus |
| A stroke in what area can cause ipsilateral 'drunk-like' motor dysfunction? | Stroke in the cerebellum |
| Basilar artery syndrome is also known as what? | Locked-in syndrome |
| What is the most easily modifiable risk factor for stroke? | Atrial fibrillation |
| What is the 'threshold' GCS score that would indicate a need for intubation? | GCS of 8 or less |
| If a patient is not a candidate for tPA, what are the BP goals? | Only treat if higher than 220/120; after 24hr period, we can begin to decrease BP by 10-15% |
| What is the "goal" of TPA and all other interventions? | Re-establish blood flow and save the penumbra |
| When and for how long should nimodopine be started on a SAH patient? | Day 1-21 |
| What is the usual dose of nimodopine to prevent vasospasm? | 60mg q4h for 21 days (may do 30mg q2h if patient becomes hypotensive) |
| What does nimodopine do? | DECREASES INCIDENCE/prevents vasospasm, DOES NOT TREAT IT |
| Besides testing for vasospasm, what does TCD help identify? | Lets us know if a stroke was cardioembolic (from heart) or thrombotic (from cranial arteries) |
| What is the gold standard for recognizing cavernous malformations? | MRI/MRA with gradient echo |
| When should LP be considered for SAH diagnosis? | ONLY when SAH cannot be diagnosed wit CT |
| What is constraint-induced movement therapy (CIMT)? | Retraining the 'good' arm of the patient to "force them" to use the affected (weaker) side. ONLY USE WITH ARMS--IF USED IN LOWER EXT, CAN CAUSE FALLS! |
| What does a patient need to 'have' to qualify for an Acute In-Patiet Rehab? | Tolerate 3hrs of therapy 5 days a week, need two or more disciplines (OT/ST/PT), be medically stable |
| When is the peak incidence of vasospasm after SAH? | Day 7-10 are peak incidence (but lasts up to 21days) |
| What is Moyamoya disease? | A chronic, vaso-occlusive disease that leads to narrowing and eventual occlusion of the internal carotids and branching vessels. It is very prominent in YOUNG ASIAN WOMEN. |
| How is Moyamoya disease treated? | Generally supportive treatment, such as anticoagulation/anti-platelet, surgical revascularization procedures if needed |
| What is central venous thrombosis (CVT)? How is it treated? | CVT is a rare type of stroke in which a clot forms in the dural sinuses or the cerebral veins. It is treated with acute anticoagulation, start with hep. drip, then oral for a few months; closely monitored |
| What is the standard treatment for arterial dissections? | Anticoagulation!!! Consider stenting |
| What is the standard treatment for AVM's? | BP management, surgical resection, embolization |
| How many stroke core measures are there? | 8! VTE prophylaxis, d/c on antithrombotic, anticoagulation for Afib, TPA, antithrombotic by end of hospital day 2, d/c on statin, stroke education, assess for rehab) |
| What causes non-obstructive (communicating) hydrocephalus? | lack of CSF absorption |
| What causes obstructive (non-communicating) hydrocephalus? | Narrowing of canals that carry CSF, leading to obstruction |
| What is the penumbra? | Brain cells next to the 'core,' which are damaged but not infarcted. Silent but metabolically active |
| Cell death (after hypoxia) occurs via what two mechanisms? | NECROTIC pathway (cells die due to lack of O2 and sugar) and APOPTOTIC pathway (cells die due to 'programmed' death since the one's around them are dying) |
| What causes secondary injury to brain cells (apart from initial insult of lack of O2)? | Release of thrombin at site, vasogenic edema, blood-brain barrier disruption, inflammatory response |
| What are the two types of aneurysms? | Saccular (also known as berry aneurysms) [which are the most common], and fusiform |
| What is amaurosis fugax, and what can cause it? | Transient blindness in one eye; common with internal carotid (ICA) strokes [because the ophthalmic artery branches from the ICA] |
| What is Marcus Gunn pupil and what can cause it? | After shining a light to test patient's pupil reaction. the pupil continues to dilate and constrict for short period of time; it is caused by central retinal artery occlusion (CRAO) |
| What are watershed strokes? What generally causes them? | Small strokes in area between major arterial territories (for example, areas between ACA and MCA territories); usually caused by HYPOTENSION or shower emboli from cardiac or vascular surgery |
| What is reperfusion syndrome and what can cause it? | Defined as ipsilateral cerebral blood flow above brain tissue needs; can occur after revascularization (carotid stent or endarterectomy, TPA) |
| What are s/s of reperfusion syndrome? | ipsilateral headache, contralateral neurological deficits, and seizure if cortical areas involved |
| What is the treatment for reperfusion syndrome? | BP control, and ONLY IF SYMPTOMATIC. If BP greater than 180, IV Rx preferred; if less than 180, oral preferred. Goal is less than 140 |
| A thunderclap headache and neck pain (nuchal rigidity) would be indicative of...? | aSAH |
| If a patient is being considered for TPA (in 3hr window) and is taking anticoagulants, what must his INR be in order to not be 'excluded?' | INR 1.7 or less (PT of 15 or less) |
| Angioedema is a common side effect of what medication? | tPA, ESPECIALLY if the are on an ace-inhibitor! |
| What is the treatment of choice for patients with SYMPTOMATIC carotid stenosis and greater than 70% occlusion? | Carotid Endarterectomy |
| In patients with a patent foramen ovale (PFO), what is the ideal treatment? | Anti-platelet and/or Anticoagulation! Surgical closure has NOT shown to be more effective. |
| What is the mainline treatment for spasticity? | Exercise and ROM stretching |
| What is the goal of rehabilitation for a stroke patient? | Teaching a patient to be self-sufficient, decrease dependence on others, and achieve the highest functional level realistically possible |
| What is a common side effect of Coumadin (aside from bleeding)? | Osteoporosis |
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