OnlineMedEd+-Neuro Flashcards
- *Meningitis**
- *Path and Etiology:**
What is the challenge?
S/Sx:
PE: Describe Kernig? Describe Brudinski sign?
Causitive agents: name top 2
Associated conditions leading to infection?
Prevention:
Chemopropylaxis:
Dx: What is the definitive test?
FAILS mnemonic and relationship to LP
CSF information
info on LP and other info
- *Meningitis**
- *Path** Meningitis is inflammation of the meninges, CSF and ventricles caused by any # of etiologies.
The challenge is to identify which organism is most likely, confirm it, then treat it.
S/Sx: FIRST fever plus headache, AMS more likely presentation of nuchal rigidity or positive kernig and brudinski signs
PE:
kernig:
patient lying supine with hip flexed; extion of the knee causes resistance or pain in lower back or back of thigh
brudzinski sign:
passive neck flexion in supine patient causes flexion in knees and hips
papilledema
- = ICP increased*
- 50% Purpura or petechial rash in N. meningitidis*
Causitive: viral, bacterial, fungal, strep. Pneumonia, Neisseria meningitidis (3-4 days incubation), staph species; asymptomatic carriage from throat and nose, extension from otitis media, bacterial rhinosinusitis. congenital problems or trauma.
Prevention:
- PCV13 90% in children 4 dose. 2, 4, 6, 12
- PPV23 50-85% in adults children with heart disease; cochlear implant; asplenia or immunosuppresion. healthy adults > 65
- MCV4 age 11-55 and MPSV4 (A,C, Y and W-135) 2 doses. 11-12; 16. if 2nd dose missed vaccinate prior to college, armed services
- MenB for sero B. MPSV4 for 56 and older
- contact public health for bacterial N. meningitidis
Chemopropylaxis:
oral cipro; IM ceftriaxone; 4 doses rifampin (can induce P450 isoenzyme so check meds); immunization against N. meningitidis
Dx:
The definitive test is the Lumbar Puncture. It gives a wealth of information (glucose, protein, cells) of the CSF as well as a body fluid for Gram Stain andCulture. But sometimes you can’t just jump straight to an LP. A CT must be done first if they have any of the FAILS mnemonic (UNsafe) Hence, two treatment pathways:
- F = FND
- A = AMS
- I = immunocompromised
- L = lesion
- S = seizure
The LP is UNsafe. This treatment plan uses the blood culture as a chance at getting a diagnosis. Antibiotics are given prior to the CT scan and the LP. Cultures are sterilized after 2-4 hours. Then the CT scan is done; if it’s normal the LP follows.
The LP is Safe. This strategy uses the CSF culture as the chance to get a diagnosis (aka the next step is LP). Antibiotics are given immediately after the LP is performed.
The LP gives a wealth of information, but most of it is useless. The only thing you care about is the number of cells and what type they are (lymphocytes or neutrophils). Ignore pH / glucose / protein for most questions.
If there are mega (100s to thousands) neutrophils you can be assured that it’s a bacterial meningitis. Its treatment revolves around Vancomycin or High-Dose Ceftriaxone, PLUS Steroids. In the immunocompromised or elderly, include ampicillin to cover for listeria.
If the LP comes back “no bacterial” then we have a dilemma. It’s “easy” to find what you’re looking for when you know what you’re seeking, but hard to find something if you don’t know what it could be.
Cryptococcal meningitis is found in patients with AIDS and a CD4 count < 200. There may be seizures. Opening pressure is often quite elevated and serial taps may be required to keep the pressure down. Diagnose with a cryptococcal antigen (do NOT use India Ink). Treatment is with induction for 2 weeks with IVLiposomal Amphotericin B and IV Flucytosine, followed by consolidation with PO Fluconazole.
Lyme disease can be suspected if there’s a targetoid lesion and travel to endemic areas such as New England. There’s often NO tick noticed because they’re so small. Use ceftriaxone for Lyme meningitis (not doxycycline as you do for non-invasive disease). Borrelia burgdorferi is the bacteria. Ixodes is the Tick.
RMSF is seen in campers who develop a peripheral rash that moves towards the trunk. Obtain the antibody on the CSF. If positive, treat it with ceftriaxone.
TB meningitis is simply extrapulmonary TB. Consider this in someone who has Pulmonary TB risk factors. Treat with RIPE.
Lumbar Puncture Findings
Brain inflammation
Presentation:
What are the 3 categories:
Any brain inflammation will present with a backbone of fever + a headache. This is nonspecific for a particular diagnosis, but antennae should go up for “problem in the brain.” Other signs and symptoms that help (photophobia, N/V, and seizures) may be present but are likewise nonspecific.
There are 3 categories of disease - each with their own unique findings:
- Meningitis will have a stiff neck (Kernig and Brudzinski’s Signs),
- Abscesses will present with Focal Neurological Deficits, and
- Encephalitis will present with encephalopathy (aka confusion)
MS
Define:
S/sx:
dx:
Tx for relapse:
Tx of disease modifying: i
mitoantrone;
natalizumab
fingolimod:
glatiramer -
teriflunomide -
symptomatic managment based on pat needs
Get expert opinions and assistance.
MS
Define: relapsing, remitting chronic demylinating disorder of the central nervous system. RRMS or Primary progressive MS
S/sx: episodes of FND. weakness, numbness, visual loss, diplopia; vertigo, facial weakness, numbness, spincnter disturbances.
dx: LP + for pleocytosis (monocytes); abnormal protein, increase in gamma globulin; presence of oligoclonal band. Evoked potential test: detect lesions or nerve damage
Tx for relapse:high dose steroids
Tx of disease modifying: interferon beta 1b
- mitoantrone; immunosuppresive*
- natalizumab (leukoenchepalopathy)*
- fingolimod: bradycardia - monitor heart rate*
- glatiramer - block attack on myelin*
- teriflunomide - monitor liver function*
symptomatic managment
Parkinson’s
Path:
S/sx:
PE: 6 symptoms:
Diagnosis
Treatment:
Meds < 70.
Meds >70
Adjuvant medications: .
The COMT-inhibitors
MAO-B-inhibitors
Apomorphine:
Med for tremor:
Med for dyskenesias:
Advanced treatments:
Deep brain stimulation:
SE of Tx:
Parkinson’s
Path:
Loss of Dopaminergic Neurons within the substantia nigra. This essentially eliminates the “go” signal, preventing the initiation of movement.
The classic symptoms of Parkinson’s stems from bradykinesia (difficulty initiating movement). This will manifest itself in slow- movements in general and even cognitive slowing.
6 symptoms:
tremor at rest (pill-rolling)
cogwheel rigidity
bradykinesia (shuffling steps)
flexed posture
- gait/loss of postural reflexes*
- mask like facies*
Logo for the classic cog-wheel rigidity, a resting pill-rolling tremor, andgait disturbances / postural instability (the little muscles that keep you straight up don’t correct for position, so these patients are high risk for falls). The patient will have difficulty with theget-up-and-go test, and will walk with shuffling steps. A board buzz word is a mask-like expressionless face.
Diagnosis is clinical. While brain imaging might be attempted to rule out something else (CT for a bleed, MRI for stroke), said imaging is not needed.
Treatment: is about the go signal. The go signal is dopamine. The stop signal is Acetylcholine. The focus of therapy is supplying the go signal.
Meds < 70. Dopamine Agonists agonists are the mainstay of therapy for young, functional people (<70, maintained function). Bromocriptine is an older, dirtier dopamine agonist, so the newer ones should be used instead. Ropinirole (requip) = Pramipexole.(mirapex)
Meds >70 Levodopa-Carbidopa is the mainstay of therapy for everyone else (>70 or nonfunctioning). Levodopa CAN cross the blood brain barrier, carbidopa cannot. Carbidopa prevents the conversion of L-Dopa into dopamine. This means more levodopa gets into the brain, and more dopamine is created from more levodopa. Long term use (5-10 yrs) of levodopa causes dyskinesias (uncontrolled writhing motion)
Adjuvant medications: levodopa-carbidopabegins to wear off. are brought in as levodopa-carbidopa begins to fail. There’s no way to determine how to add them.
- The COMT-inhibitors (tolcapone and entacapone increase the half life of levodopa)*
- MAO-B-inhibitors(selegiline or rasagiline) increase levodopa 1/2 life by reducing metabolism.*
- Apomorphine: injectable dopamine agonist rescue therapy for hypomobility or “off” periods.*
Med for tremor: Acetylcholine-R-antagonists like Benztropine (cogentin) could theoretically work, but the anti-acetylcholine side effects are not worth it for the elderly; the effect is also weak. Use this on young people who have a tremor only.
Med for dyskenesias: amantadine. only @ 1yr. DONT
Advanced treatments: pallidotomy for tremor, rigidity, bradykinesia and dyskinesias uncontrolled writhing motion)
Deep brain stimulation: off state more like movement in the on state
SE of Tx:While you DO want dopamine in the substantia nigra, the cost of “putting dopamine in the brain” is overstimulation of other dopamine tracts. In particular, it can induce psychosis with overstimulation of dopamine, causing schizophrenic symptoms and hallucinations. Remember, you use anti-dopamine drugs (antipsychotics) to treat schizophrenia. We haven’t figured out how to target one tract over another just yet.
Seizures: (this can be improved)
Path:
What makes seizures difficult in presentation?
Is it a seizure or something else?.
What is a seizure emergency?:
TX if pt currently Seizing: (just for fun–not for FNP)
TX first time with no current seizure:
Tx Epilepsy:
Seizure mnemonic/Vitamins
Types of Seizures:
General vs Partial?
Complex or simple? (
Absence;
Myoclonic:
Tonic-Clonic (Grand mal seizure):
Simple Partial:
Complex partial:
Atonic:
Nonconvulsive Status
Epilepsy
What are the broad based seizure drugs
What are some AED drugs?
What is NTI and some NTI AE drugs?
Explain protein binding concerns with NTI drugs:
Explain CYP 450 concerns with NTI drugs:
Phenytoin + theophylline =
Carbamezine + OCP =
What are the broad specturm first-line AEDs?
Seizures: (this can be improved)
Path: Seizures are uncontrolled synchronous firing of neurons in the brain when awake.
Considerations: There are many different types of seizures with many different presentations. As such, they should be considered a symptom of an underlying disease. For the disease and appropriate intervention consider epilepsy (usually only with a history of this disease) and the VITAMINS mnemonic. “Seizure/Vitamins” for a 1st time seizure, section marked “Epilepsy” for repeat offenders.
Is it a seizure? + LOC can be many things, jerking, bowel/bladder incontinence, tongue biting **** post-ictal state (groggy, slow to return to full) post-ictal confusion separates a seizure from alternative causes of loss of consciousness.
What is a seizure emergency?: patients are actively seizing, are post-ictal, or have entered Status Epilepticus, they need to be treated as a medical emergency.
TX if pt currently Seizing: > 5 mins or failure to return to baseline in 20 mins (status epilepticus) BENZO (BZD) then EEG (best during the seizure) and MRI and then vitamins (fix it). #1 priority is to control ABCs (Intubation, oxygenation, ventilation, IVF). Before drawing labs to investigate VITAMINS the seizure must be aborted. Do so by following this cascade until seizure stops: (1) IV/IM Benzos(lorazepam / diazepam) à (2) FosPhenytoin à (3) Midazolam and Propofol à (4) Phenobarbital. Then draw labs and reverse any underlying defects.
TX first time with no current seizure: A patient who has a seizure but is now normal requires observation, VITAMINS workup, and an EEG. send for treatment!
Tx Epilepsy: Check drug levels, increase, change or add a drug; consider vitamins; still consider VITAMINs
Seizure mnemonic/Vitamins
V - vascular; stroke
I = infection (meningitis)
T = trauma. (TBI -
- A = autoimmune. (lupus)*
- M = metabolic. (very general)*
I = ingestion or withdrawal (benzo or alcohol)
N = neoplasm
S = Psych
Types of Seizures:
General vs Partial? total brain involvement or specific complaint
Complex or simple? (loss of conscious vs no loss)
Absence; negative for loss of tone, positive loss of consciousness
Myoclonic: no loss conscious +abnormal tone jerky
Tonic-Clonic (Grand mal seizure): presents with tonic clonic convulsions, bowel/bladder incontinence, and tongue biting. post-ictal confusions
Simple Partial: awake with abnormal motor, sensory, autonomic or psychic behavior (seeing spiders)
Complex partial: Aura of smell or taste; visual or auditory hallucinations, stomach upset; followed by stare and facial movements; muscle contraction and autonomic signs.
Atonic: no loss of conscious; loss of tone = valproate
Nonconvulsive Status
The altered person, intubated, but no seizure activity. Get an EEG.-
Epilepsy
A patient with epilepsy (any history of seizure, repeat seizure in an idiopathic cause, etc) is treated a little different. an epileptic also requires chronic therapy to decrease the risk of another seizure. What to give is dependent on the type of seizure.
What are the general AED drugs
lamotrigine, valproic acid; Don’t use in pregnancy
levciteram.
What are some AED drugs and SE/concerns? All AED increase the risk for suicide
phenytoin,: Skin rash; screen bones (decrease Vit D); induces hepatic enzymes
carbamzaepine: skin (SJS) LOTS!! CYP34A
clonazepam; sedation; dependence
ethosuximide,; change dose slowly, blood dyscrasias; DRESS;
gabapentin: SJS; Taper
toperamate,
What is NTI and some NTI AE drugs? Narrow therapeutic index - a specifc amount has a therapeutic effect; just a little over therapeutic level and its is toxic. carbamazepine/ phenytoin;
Explain protein binding concerns with NTI drugs: highly protien bound drugs taken with other highly protein bound drugs increase nonbound medication and therefore can create toxic levels
Explain CYP 450 concerns with NTI drugs: increase use of hepatic enzymes (inducers); more rapid metabolism so lower blood levels of the drug.
Phenytoin + theophylline = reduced blood levels
Carbamezine + OCP = reduced estrogen = contraceptive failure.
Valproate, lamotrigine, and levetiracetam are broad spectrum and generally considered first line. As you dose patients it’s important to reach therapeutic levels and switch if they seize while therapeutic. Diagnose the seizure and the location of origination with EEG by looking for spike and waves indicative of organized neuronal firing (abnormal for an awake adult). 24hr video monitoring + EEG may be required to catch the seizure and its manifestations.
For the test, you’ll need to be able to identify certain types of seizure and link them with their treatment. See to the right
Stroke, Acute (Cerebrovascular Accident [CVA])
What is a stroke:
What are the two broad categories?
What is the Predominant age and sex?
What is the Etiology and Pathophysiology?
What are the uncontrollable Risk Factors?
Controllable?
What is the General Prevention?
S/Sx What are big 5 and the others
What are the basic Diagnostic Tests & Interpretation
Treatment at discharge?
What is the secondary prevention?
Patient Monitoring?
bonus: What are the Exclusion criteria for thrombolysis within 3 hours of onset include
Stroke, Acute (Cerebrovascular Accident [CVA])
What is a stroke: the sudden onset of a focal neurologic deficit(s) resulting from either infarction or hemorrhage within the brain
What are the two broad categories?
Two broad categories: ischemic (thrombotic or embolic) (87%) and hemorrhagic (13%)
What is the Predominant age and sex?
Risk increases >45 years of age and is highest during the 7th and 8th decades.
Predominant sex: male > female at younger age but higher incidence in women with age ≥75 years
What is the Etiology and Pathophysiology?
87% of strokes are ischemic,
What are the Risk Factors?
Uncontrollable: age, gender, race, family history/genetics, prior stroke or TIA
Controllable/modifiable/treatable
Metabolic: diabetes, dyslipidemia
Lifestyle: smoking, cocaine and amphetamine use
Cardiovascular: hypertension, atrial fibrillation, valvular heart disease, endocarditis, recent MI, severe carotid artery stenosis, hypercoagulable states, and patent foramen ovale (1)
What is the General Prevention?
Smoking cessation, regular exercise, weight control to maintain nonobese BMI and prevent type 2 diabetes, moderate alcohol use; control BP; manage hyperlipidemia; use antiplatelet agent (e.g., aspirin) in high-risk persons; treat nonvalvular atrial fibrillation with dose-adjusted warfarin or dabigatran, apixaban, and rivaroxaban
S/sx
- Altered consciousness, diminished consciousness.
- Headache: sudden, intense and severe
- Aphasia, facial weakness or asymmetry, difficulty with speech or swallowing,
- Altered coordination: Acute onset of focal arm/leg weakness, ,
- Visual loss, visual disturbances, dipl
- Misc. vertigo, diploplia, unilateral hearing loss, Nausea/vomiting, photophobia, phonophobia
- Vomiting and severe headache favor hemorrhagic stroke
What are the basic Diagnostic Tests & Interpretation
CT for acute cerebral hemorrhage
MRI for ischemic stroke
What is the secondary prevention?
aggressive management of controllable risk factors:
HTN: Thiazide, CCB, ACE and ARBs
Platelet inhibition using aspirin, clopidogrel, or aspirin plus extended-release dipyridamole(Aggrenox) based on physician and patient preference
Patient Monitoring
Follow-up every 3 months for 1st year and then annually
Exclusion criteria for thrombolysis within 3 hours of onset include:
Any history of ICH or new symptoms suggestive of ICH (3)[B]
Head trauma or prior stroke within 3 months
MI within 3 months
GI malignancy or bleed within 21 days (3)[C]
Major surgery within 14 days
Arterial puncture at noncompressible site within 7 days
Elevated BP (systolic >185 mm Hg and diastolic >110 mm Hg)
Active bleeding or evidence of acute trauma on examination
Taking anticoagulant and INR ≥1.7
If low-molecular-weight heparin received during previous 24 hours (3)[B]; platelet count <100,000 mm3 (3)[C]
Blood glucose concentration <50 mg/dL
Seizure with postictal residual neurologic impairment
Multilobar infarction on CT (hypodensity >1/3 cerebral hemisphere)
Patient or family members not able to provide input and understand potential harms and benefits of treatment
Extended AHA/ASA exclusion criteria for thrombolysis within 4.5 hours include:
Age >80 years
All patients taking oral anticoagulants regardless of INR
National Institutes of Health (NIH) Stroke Scale >25
History of stroke and diabetes
What is a TIA? Why does it matter?
Most common patient? (epidemiology)
Pathophysiology:
What are the risk factors for a TIA
What is general prevention?
Geriatric, Pediatric and Pregnancy considerations?
What are s/sx of a TIA f?
Primary Care first step in outpatient?
Treatment? Contraindications and precautions?
A transient episode of neurologic dysfunction due to focal brain, retinal, or spinal cord ischemia without acute infarction
Most important predictor of stroke: 15% of patients with stroke report previous TIA.
Predominant age: Risk increases >60 years; highest in 7th and 8th decades
Predominant sex: male > female (3:1)
Predominant race/ethnicity: African Americans > Hispanics > Caucasians. The difference in African Americans is exaggerated at younger ages.
Etiology and Pathophysiology
Temporary reduction/cessation of cerebral blood flow adversely affecting neuronal function
Embolism secondary to the following:
- Valvular (mitral valve) pathology
- Mural hypokinesias/akinesias with thrombosis (acute anterior MI/congestive cardiomyopathies)
- Cardiac arrhythmia (atrial fibrillation accounts for 5–20% incidence)
- Hypercoagulable states
- Increased estrogen (e.g., oral contraceptives)
- Pregnancy and parturition
- Arteritis
- Noninfectious necrotizing vasculitis
- Drugs
- Irradiation
- Local trauma
- Sympathomimetic drugs (e.g., cocaine)
- Other causes: spontaneous and posttraumatic (e.g., chiropractic manipulation) arterial dissection
Risk Factors
- HTN
- Cardiac diseases (atrial fibrillation, MI, valvular disease)
- Diabetes
- Hyperlipidemia
- Atherosclerotic disease (carotid/vertebral stenosis)
- Cigarette smoking
- Thrombophilias (hypercoagulable)
- combined OCP
General Prevention
Lifestyle changes: smoking cessation, diet modification, weight loss, regular aerobic exercise, and limited alcohol intake
Strict control of medical risk factors: diabetes (glycemic control), HTN (thiazide and/or ACE/ARB), hyperlipidemia (statins), anticoagulation when high risk of cardioembolism (e.g., atrial fibrillation, mechanical valves)
Geriatric Considerations
Older patients have a higher mortality rate than younger patients—highest in 7th and 8th decades.
Atrial fibrillation is a frequent cause among the elderly.
Pediatric Considerations
Congenital heart disease is a common cause among pediatric patients.
Pregnancy:
Preeclampsia, eclampsia, and HELLP
weakness, flaccidity, visual changes, ataxia or dysarthria that resolve in minutes to 24 hours. Considered a stroke warning.
Treatment
TIA is a neurologic emergency. Immediate medical attention should be sought within 24 hours of symptom onset due to increased stroke risk.
Current evidence suggests that patients with high-risk TIAs require rapid referral and 24-hour admission
First Line
Enteric-coated aspirin: 160 to 325 mg/day
Antiplatelet therapy: Aspirin 81 to 325 mg/day (5)[A]
Contraindications: active peptic ulcer disease and hypersensitivity to ASA or NSAIDs
Precautions: may aggravate preexisting PUD; or worsen symptoms of asthma
Significant possible interactions: may potentiate effects of anticoagulants and sulfonylurea analogues
ER dipyridamole ASA (Aggrenox): 25/200 mg BID (5)[B]
Clopidogrel 75 mg/day (5)[B]
Can be used in patients who are allergic to ASA (5)[B]
Precautions: Thrombotic thrombocytopenic purpura (TTP) can occur and increases risk of bleeding when combined with aspirin.
Giant Cell Temporal Arteritis
What is the etiology/pathology?
Why is it a medical emergency?
What is the Epidemiology?
What are the Risk Factors
What is a Commonly Associated Conditions
What are the S/sx
What is needed for Dx:
What is first line Tx:
3 Adjuvants and rationale
bonus: What might be seen on Physical Exam
Giant Cell Temporal Arteritis
What is the etiology/pathology?
A chronic, generalized, cellular, and humoral immune-mediated vasculitis of large- and medium-sized vessels, predominantly affecting the cranial arteries originating from the aortic arch. Giant cell arteritis (TA) is a chronic, systemic vasculitis of large vessels. Primarily external carotids, ophthalmic and temporal.
Why is it a medical emergency?
Considered medical emergency due to risk of permanent vision loss if not treated
What is the Epidemiology?
- Most common form of systemic vasculitis affecting persons ≥ 50 years old*
- Typically occurs ages 70 to 80 years (80% of cases)*
Women are affected about 2 times as often as men.
- Most common vasculitis in individuals of Northern European descent (Scandinavian countries)*
- Rare in Asians and African Americans*
What are the Risk Factors
Increasing age >70 years is the greatest risk factor.
Early menopause (<43 years) and lower BMI at menopause in women 50 to 69 years old
Female gender
Northern European and Scandinavian
What is a Commonly Associated Conditions
PMR
What are the S/sx
Most common presenting symptom is
unilateral headache (2/3 of patients) in front, vertex or occipital region but not in the temporal area
Jaw claudication (presence of symptom significantly increases likelihood of a positive biopsy)
Acute reduction or change in vision
Temporal tenderness
Other symptoms:
Respiratory symptoms: cough, sore throat, hoarseness. (older)
Mental status changes (older)
Constitutional symptoms (fever, fatigue, weight loss)
Any visual disturbances (amaurosis fugax, diplopia)
Vision loss (20% of patients); unilateral is most common, often proceeds to bilateral if untreated.
Scalp tenderness or sensitivity
Claudication of upper extremities or tongue
Symptoms of PMR (shoulder and hip girdle pain and stiffness)
Distal extremity swelling/edema
fatigue, headaches, jaw claudication, loss of vision, scalp tenderness, polymyalgia rheumatica (PMR), and aortic arch syndrome (decreased or absent peripheral pulses, discrepancies of blood pressure, arterial bruits).
What is needed for Dx:
artery bx. CRP and ESR. Biopsy multiple sites because disease skips portions of the vessal
What is first line Tx:
Steroids prednisone 1-2 mg/kg/day.
- Have GI protection from extended steroid use with PPI
- bone protection with calcium and Vit D; from extended steroid use
- aspirin for stroke
bonus: What might be seen on Physical Exam
Temporal artery abnormalities (beading, prominence, tenderness)
Typically appear “ill”
Decreased peripheral pulses in the presence of large vessel diseases
Funduscopic exam shows pale and edema of the optic disc, scattered cotton wool patches, and small hemorrhages.
Bruits supraclavicular, axillary, supra-orbital
