Neuro Flashcards
Shock
cellular and tissue hypoxia due to reduced oxygen delivery or increased oxygen consumption or inadequate oxygen utilization
4 types of shock
Distributive, Cardiogenic, Hypovolemic, Obstructive
Distributive shock
has many causes including septic, SIRS, neurogenic shock, anaphylactic, toxic and endocrine like through addisons disease. A reduced systemic vascular resistence leads to a compensatory increase in cardiac output. All other forms of shock have an increased SVR and decrease cardiac output.
Cardiogenic shock
cardiomyopathic through MI, arrythmia like sustained VTach, or mechanical abnormality like valvular rupture
Hypovolemic shock
hemorrhagic from trauma or nonhemorrhagic fluid loss from vomiting
Obstructive shock
Pulmonary embolism or pulmonary vascular related, due to mechanical causes like tension pneumo, pericardial tamponade (obstructing oxygen flow –> shock)
Anaphylaxis
serious allergic or hypersensitivity reaction that is rapid in onset and may cause death
Criteria for anaphylaxis
acute onset of illness involving the skin or mucosal tissue and at least one of the following: resp compromise (wheeze, stridor) or reduced BP or s/s end organ malperfusion (hypotonia, syncope) can be after a likely allergen with two of the following: skin issue, resp compromise, reduced BP, GI symptoms. Known allergen: reduced bp systolic
Children and those with food induced anaphylaxis do not usually have this symptom
hypotension
Anaphylaxis results from this
igE mediated allergic reaction from foods, insects, medications or anything really including allergen immunotherapy, chemotherapy, vaccines, food additives, spices, cat dander, human seminal fluid, latex
Anaphylaxis blood work
within 15 minutes to 3 hours obtain total tryptase in serum or plasma or plasma histamine in excluding other disorders which do not involve mast cells. Histamine between 2 and 15 minutes no vacuum tube manually pul blood both on ice
Symptoms of anaphylaxis
Warm, flushing, itching, urticaria, angioedema, hair standing on end, tingling lips, edema of lips, tongue, metallic taste, congestion, sneezing, sob, tightness, cough, nausea, abd pain, diarrhea, syncope, ams, incontinence, anxious, headaches, sudden behavior change, tearing, eye itching, uterine cramps
Increased risk for stroke with those who have this type of migraine
migraine with aura
Stroke risk most increased in women with these risk factors
child bearing age, migraine with aura, smoking, taking the pill
migraine with aura causing strokes describes as
silent infarct-like lesions in posterior circulation of the white matter or cerebellum
patho of migraine leading to stroke
vasospams and changes in blood flow
patients with vascular disease are not allowed to take these medications
vasoconstrictive meds that treat migraines including triptans and ergots and seratonin agonists
women with migraine with aura who are smoking need to do these two things to control their risk factor of stroke
control blood pressure, use another form of birth control other than the pill
Biggest priorities in managing a patient with a traumatic brain injury
prevent hypoxia (Pa02
First thing to order with a TBI
CT Head
Treatment for impending herniation following a TBI from increased ICP
Head of bed elevation and IV Mannitol osmotic therapy
Treatment with a severe TBI causing mass hamatoma, contusions and swelling
ventriculostomy placement with ICP monitoring
target ICP pressure number
20 mmHg
prevention og early seizures post TBI
only one week of antiepileptic drugs (valproic acid,m phenytoin)
exacerbates secondary neurological injury
fever and hyperglycemia both need to be avoided
glasgow coma scale meaures
eye opening, verbal response, motor response. 3-15. 3 is the worst.
do not use this to manage TBI as it will lead to increased mortality
glucocorticoids
symptoms of elevated ICP
Headache from the pain fibers of CN 5, depressed global consciousness, vomiting
papilledema
intracranial hypertension leading to a blurred optic disc margin, loss of physiological cupping and fullness in the veins
TIA
transient episode of neurological dysfunction by focal brain, spinal cord, or retinal ischemia without an acute infarction. Absent end organ injury. The defined end point is tissue injury and not timed 24 hours
TIA timing
Was less than 24 hours caused by decreased blood supply but this is inadequate as even relatively brief ischemia can cause a permanent brain injury so the new TIA definition is absent end organ injury
Antithrombotic treatment of TIA
4.5 hours after symptom onset for yPa and 6 hours for a mechanical thrombectomy
Acute ischemic stroke antithrombotic treatment
no urgent anticoagulation, instead do early aspirin therapy 160 or 325 daily, ideally start within 48 hours of stroke onset. beyond the acute phase it should continue with asa plus plavix
Antithrombolytic for symptomatic large artery disease
aspirin plus plavix for 90 days
Options to prevent stroke with large artery disease
revascularization with carotid endarterectomy/stenting and multifactoral risk reduction with antiplatelets, antihypertensive drugs, and statins
treatment for symptomatic carotid atherosclerosis
carotid endarterectomy
When is surgical revascularization a viable option
when residual flow can be demonstrated in the internal carotid artery. If completely occluded, medical mgmt is the only practical option
Aortic arch disease mgmt
antiplatelet and statin therapy
AF is associated with these types of strokes
worsened ischemic strokes and longer TIAs due to embolization of larger particles
Confirm absence of intracranial hemorrhage before starting anti-thrombotic therapy by
cranial CT and MRI
When to initiate TPA (alteplase)
4.5 hours, preferably 3, from the onset on symptoms with acute ischemic stroke to reduce long term disability
Most effective long term therapy for prevention of recurrent stroke
Warfarin. Target INR 2-3
Mild versus moderate versus severe TBI
13 > mild. 9-12 moderate. less than 8 is severe.q
Primary TBI
intra- and extra=parenchymal hemorrhages and diffuse axonal injury from shearing mechanisms showed as white matter tracks
Secondary TBI
Cascade of molecular injury mechanisms that are initiated at the time of initial trauma and continue for hours or days. This can be exaccerbated by hypotension, hypoxia, fever and seizures
Leading cause of TBI
Falls. Second leading cause is MVA
Subdural hematoma
between the dura and the arachnoid membrane caused by bleeding. Most commonly caused by tearing of the brdiging veins that drain from the surface of the brain to the dural sinus.
Epidural hematoma
space between the dura and the skull
Subdural hematoma s/s
can be from a loss of consciousness to a coma.
Acute subdural hematoma
coma is usually present at the time of injury,some may have a lucid interval followed by a progressive neurological decline. Headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nucal rigidity On CT it is a high dense crescent collection
Chronic subdural hematoma
insidious onset of headache, light headedness, cognitive impairment, somnolence and occasional seizures, on CT it is a hypodense crescent shaped lesion
Refer to a neurologist if a child has these symptoms of concussion
symptoms > 10 days, those with multiple concussions occuring with progressively less force and or are associated with more intense symptoms, uncertain dx of concussion
concussion s/s
headache, dizzy, nausea, difficulting concentrating, vision changes, drowsiness, amnesia, sensitivity to noise, tinnitus, irritability, loss of consciousness, hyperexcitability
Most SAH caused by
ruptured saccular aneurysms
s/s SAH
sudden, severe headache, worst headache of my life may be a/w LOC, seizures, n/v.
dx SAH
CT. If negative and still suspicious then do a lumbar puncture which will show elevated RBCs. After CT do an angiography.
Migraine s/s
unilateral, throbbing, pulsating, nausea, vomiting, photophobia, phonophobia, crescendo pattern, aggravated by activity duration 4-72 hours
Migraine triggers
stress, menstruation, visual stimuli, weather changes, nitrates, fasting, wine, sleep disturbances, aspartame
Tension headache
mild to moderate, bilateral, nonthrobbing, no other features, 30min to 7 days, pressure and tightness will wax and wane no other symptoms
Cluster headache
idiopathic, unilateral, severe with autonomic symptoms. orbital, supraorbital or temporal pain, lacrimation, conjunctival injection, rhinorrhea, nasal congestion
Physical exam done with headache complaint
blood pressure, pulse, bruit at neck, palpate head, neck and shoulders, check temporal and neck arteries, examine spine and neck muscles. Mental status, cranial nerves, gait
Danger signs
SNOOP. Systemic symptoms (fever, weight loss, cancer) Neuro symptoms (confusion, papilledema, seizures) Onset is new or sudden (after 40 or thunderclap) Other symptoms (head trauma, drug use, worse with valsalva) Previous headache history with a progression or change in attack.
giant cell arteritis
chronic vasculitis of large and medium sized vessels. Older than 50. Temporal or frontal. Fever, fatigue, weight loss, visual changes, polymyalgia rheumatica
trigeminal neuralgia
sudden, unilateral severe brief stabbing pain across trigeminal nerve older than 50 years of age
chronic subdural hematoma
insidious onset of headaches, light headed, dizzy, apathy, cognitive impairment, tired, possible seizures
new onset seizure older than 50 worry about
brain tumor
anaphylaxis
acute, potentially lethal, multi system syndrome resulting from a sudden release of mast cell, basophil and macrophage derived mediators into circulation
immunologic anaphylaxis
igE and igG mediated reaction with immune complex mediated mechanisms
nonimmunologic anaphylaxis
caused by agent or event that induces a sudden, massive mast cell or basal cell degranulation without antibodies
anaphylaxis is a/w these cardiac issues
MI and arrhythmias, due to cardiac hx, exogenous epinephrine and hemodynamic stress
anaphylaxis resp s/s
bronchospasm, mucus plugging, larygeal edema and asphixiation esp w those w hx asthma
meds that make anaphylaxis worse
opiods, nsaids, ethanol, beta blockers, ACE inhibitors
level that supports diagnosis of anaphy.
serum tryptase 15 min to 3 hours after diagnosis
diagnosing anaphylaxis
acute onset of illness with skin, mucosal tissue (swollen lips/tongue…hives) with at least 1) resp compromise OR 2) decreased BP
Exposure to known allergen dx
bp less than 90 or a 30 percent decrease from baseline, infants and children are age specific
