NV emergencies and Strokes Flashcards

1
Q

Stroke mimics (6)

A
HYPOglycemia
Electrolyte imbalance, esp. Na+
Epidural/subdural Hematoma
Brain abscess/tumor
post-seizure
migraine
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2
Q

Stroke prevention

A
  1. manage risk factors: high blood pressure, cigarette smoking, atrial fibrillation and physical inactivity.
    meds: antiplatelets, anticoagulants, antihypertensives
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3
Q
Define the terms
 (TIA)
(RIND)
(CVA)
Describe what they mean
A

“transient ischemic attack (TIA)-,” “reversible ischemic neurologic deficit (RIND)(>24 h, but

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4
Q

Describe the classifications of stroke

A

TIA

Ischemic(clots)-persistent blockage of blood vessel due to thrombus or embolism (thrombotic,embolic, lacunar types)

Hemorrhagic (bleeds)- rupture of blood vessel (intracerebral and subarachnoid)

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5
Q

etiology, presentation, evaluation, and management of thrombotic stroke

A
  • caused by a cerebral thrombos that develops gradually in a diseased aa and obstructs it
  • Risk Factor: atherosclerosis, especially carotid aa and MCA)
  • signs/ symptoms develop more gradually than in embolic
  • often occur at night and patient awaken with symptoms
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6
Q

ischemic stroke risk factors

A
HTN
A-fib(embolic)
atherosclerosis (thromb)
sickle cell disease
insulin dependent DM
high cholesterol
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7
Q

Ischemic stroke symptoms, DX and TX

A

Symptoms depend on the effected aa:
Unilateral paralysis (weakness, clumsiness, heaviness; most commonly face and hand; affected body side is opposite to the affected artery
language/speech disturbance
monocular blindness; blurred vision in ONE side of the field of vision; nystagmus; involved visual field is opposite to the side of the affected artery
double vision dur to misalignment of the eyes
unilateral numbness
vertigo; imbalance
loss of consciousness

Dx:
CT scan without contrast (differentiate ischemic(dark areas) from hemorrhagic (white areas)
MRI more sensitive to infarcts and identifies them quicker, but takes longer and not suitable;e for emergency)

Acute Intervention:
reopen blocked aa:
-directly removing clot by surgery (up to 8 h)
-THROMBOLYTIC therapy (IV tPA-fibrinolytic therapy) up to 3 h, or 4.5 h in eligible patients(risk of hemorrhage increases with time from onset)-60-70% are more likely to have favorable outcome if done ASAP: time is brain
-risk: the longer the blockage the stronger the blood flow when the blockage removed-risk of reperfusion hemorrhage).
If NOT on tPA-give ASPIRIN, or other antiplatelets (Plavix, Aggrenox; anticoagulation therapy ISN’t useful in acute stroke

prevention of second injury: decompressive craniectomy for large infarcts due to edema;

control BP up to 220/110 to maintain perfusion to minimize damage to ischemic tissues

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8
Q

Lacunar strokes

A

small vessel strokes, occlusion of arterioles due to small emboli
SUBCORTICAL structures, not cerebral cortex
-symptoms:
focal, contralateral pure motor or pure sensory
-pure motor(internal capsule lesion)
-pure sensory( Thalamus)
ataxic hemiparesis( incoordination ipsilaterally)

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9
Q

Embolic stroke

A
  • VERY RAPID onset
  • caused by solid, liquid or gaseous mass carried to a vessel from another area, most often blood clots
  • Risk factor: A-fib(arrhythmia that can lead to blood clots, stroke, heart failure; the atria beat irregularly instead of beating effectively to move blood into the ventricles. It allows blood to slow down or pool and increases the risk of clotting, and so increases the risk of stroke) + damaged carotid and veretebral aa
  • sudden onset and rarely accompanied by headache
  • anticoag better than antiplatelet
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10
Q

Thrombolytic therapy

A
THROMBOLYTIC therapy (IV tPA-fibrinolytic therapy) up to 3 h, or 4.5 h in eligible patients(risk of hemorrhage increases with time from onset)-60-70% are more likely to have favorable outcome if done ASAP.
contraindications: uncontrolled HTN, bleeding disorder, on anticoagulants, recent trauma or surgery, IRN >1.7
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11
Q

ICH

A

intracerebral (within brain)- ICH, ⅓ will survive, only 20% will gain functional independence
rupture of vessels within brain tissue – outflow of blood into brain tissue, increased ICP that causes damage to the brain tissue, often tears and separates brain tissue

Etiology: hypertension; amyloid angiopathy (proteins called amyloid build up on the walls of the arteries in the brain)anticoag therapy

most common locations for hypertensive ICH: pons, BG, thalamus, cerebellum; CT= acute blood is white; for amyloid: lobar, peripheral)
Symptoms:
SUDDEN Onset
severe HEADACHE;
HTN
altered mental status
high ICP causes nausea, vomiting, headache, somnolensce, syncope
seizure
focus neurological deficits corresponding to the site of bleed

Dx: CT or MRI to differentiate ischemic from ICH; MRI shows HYPOintensity (BLACK) in the area of bleed, CT shows HYPERdensity (WHITE)
supportive care, BP as low as can tolerate

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12
Q

SAH

A

subarachnoid ( fluid filled spaces around blood vessels outside brain, bifurcations of aa in the circle of Willis)
Risk factors: head trauma or congenital abnormalities (HTN and aneurism;polycystic kidney disease; smoking, HTN
blood in subarachnoid space impairs drainage of CSF and causes rise in intracranial pressure- HERNIATION of brain tissue may occur
most disability due to cognitive/emotional problems
symptoms:
asymptomatic until aneurism ruptures
SUDDEN SEVERE headache, neck stiffness
syncope, nausea and vomiting
often no focal neurological findings
DX:
CT head FIRST!= HYPERdense blood in subarachnoid space
Lumbar Puncture: (Blood or xantocromia in CSF= SAH)
Intervention:
clipping/coiling of aneurism
control ICP and BP(low)obstruction of CSF flow can be fatal, so venriculostomy used to divert CSF
late complication: vasospasm, prevented with Ca channel blockers

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13
Q

Brain stem stroke

A

A person may have vertigo, dizziness and severe imbalance without the hallmark of most strokes – weakness on one side of the body. The symptoms of vertigo dizziness or imbalance usually occur together; dizziness alone is not a sign of stroke. Brain stem stroke can also cause double vision, slurred speech and decreased level of consciousness.

Only a half-inch in diameter, the brain stem controls all basic activities of the central nervous system: consciousness, blood pressure, and breathing. All of the motor control for the body flows through it. Brain stem strokes can impair any or all of these functions.

More severe brain stem strokes can cause locked-in syndrome, a condition in which survivors can move only their eyes.

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14
Q

Discuss the indications and contraindications of anticoagulant therapy with heparin or warfarin
(Coumadin) in the treatment of ischemic infarct strokes.

A

Anticoagulants, such as warfarin (Coumadin) and heparin, slow clot formation by competing with Vitamin K. This inhibits the circulation of certain clotting factors with the exotic names of factors II, VII, IX and X.Advantages:
Anticoagulants are considered more aggressive drugs than antiplatelets. They are recommended primarily for people with a high risk of stroke and people with atrial fibrillation. Although anticoagulants tend to be more effective for AF patients, they are generally recommended only for patients with strokes caused by clots originating in the heart. Anticoagulants tend to be more expensive and carry a higher risk of serious side effects, including bruising and skin rash and bleeding in the brain, stomach and intestines.
Disadvantages:.
In comparison to antiplatelets, anticoagulants tend to be affected more by other drugs, vitamins and even certain foods, making anticoagulant therapy somewhat troublesome for stroke survivors. Because warfarin competes with Vitamin K, patients taking it should consult their doctors about possible dietary restrictions, as even some vegetables might cause an imbalance if eaten in excess.. Many prescription drugs make warfarin either stronger or weaker.
Anticoagulant therapy with warfarin also requires regular blood tests to ensure the correct drug dose. A weak dosage increases the risk of stroke and heart attack, but too much puts someone at risk for bleeding. Generic brands may not be the same strength as the one prescribed by your doctor.

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15
Q

Compare and contrast various anti-platelet agents (aspirin, dipyridamole, ticlopidine) for
efficacy as primary or secondary prophylaxis for ischemic infarct strokes stroke.

A

Antiplatelet agents, including aspirin, clopidogrel, dipyridamole and ticlopidine, work by inhibiting the production of thromboxane. Aspirin is highly recommended for preventing a first stroke, but it and other antiplatelets also have an important role in preventing recurrent strokes.

According to a statement by the American Heart Association, taking aspirin within two days of an ischemic stroke reduces the severity of the stroke. In some cases, it prevents death. For long-term (meaning for the rest of your life unless otherwise specified by your physician) prevention, antiplatelet therapy is recommended primarily for people who have had a transient ischemic attack (TIA or “mini” stroke) or acute ischemic stroke.

Despite the potential benefits, antiplatelet therapy is not for everyone. People with a history of liver or kidney disease, gastrointestinal disease or peptic ulcers, high blood pressure, bleeding disorders or asthma may not be able to take aspirin or may require special dosage adjustments.

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16
Q

Explain how to decide between anti-platelet agents and warfarin (Coumadin) as secondary
prophylaxis for ischemic infarct strokes.

A

Warfarin has been shown in multiple trials to be superior to aspirin for patients with atrial fibrillation, and is clearly indicated in patients with stroke caused by atrial fibrillation if they have no contraindications to therapy. Recent trials, however, have failed to show a significant benefit for warfarin over aspirin for other ischemic stroke subtypes.The American College of Cardiology has recommended antiplatelet agents over oral anticoagulation for most patients with noncardioembolic stroke. For the subset of patients with noncardioembolic stroke with well-documented prothrombotic disorders, they suggest oral anticoagulation over antiplatelet agents.7

17
Q

Compare and contrast various anti-platelet agents (aspirin, dipyridamole, ticlopidine) for
efficacy as primary or secondary prophylaxis for ischemic infarct strokes stroke.

A

aspirin-optimal dose not yet established
dipyridamole- with aspirin benefits pts with prior cerebral ischemia
ticlopidine-not better than aspirin, but more expensive

18
Q

high ICP

A
Review signs and symptoms for increased ICP- 
Cushings Triad is hallmark:
1) Hypertension 
2)Change in respirations(rate, regularity, and depth) 
3) bradycardia
	Also
  headache
  nausea
  vomiting
  increased blood pressure
  decreased mental abilities
  confusion about time, then location and people as pressure worsens
  double vision
  pupils that do not respond to changes in light
  shallow breathing
  seizures
  loss of consciousness
  coma
19
Q

Describe the Glasgow coma scale and demonstrate how to evaluate the results

A

The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. Cannot be below 3 or above 15.
Eye opening, best verbal, best motor response

20
Q

Discuss the correlation between ICP levels, cerebral perfusion and the effects of brain
edema.

A

One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.

In lecture, hyperventilation was mentioned as a treatment for increased ICP. This is done to blow off CO2 since CO2 is a vasodilator. If the ruptured vessel is dilated from increased CO2 levels, bleeding can occur faster and the blood around the brain causes an even higher increase in pressure. Edema can trap the blood around the brain, so since it is not being circulated that leads to lower oxygen levels and even higher co2 levels, perpetuating the increase in pressure and decrease in oxygen. hyperventilation is called ‘relative hyperventilation’ because it is done relative to CO2 levels.

21
Q

Subdural Hemmorhage

A

An acute subdural hematoma (SDH) is a clot of blood that develops between the surface of the brain and the dura mater, the brain’s tough outer covering, usually due to stretching and tearing of veins on the brain’s surface. Common in the elderly and alcoholics. These veins rupture when a head injury suddenly jolts or shakes the brain.Traumatic acute SDHs are among the most lethal of all head injuries. SDHs are best diagnosed by computed tomography (CT) scan. They appear as a dense, crescent-shaped mass over a portion of the brain’s surface. Most patients with acute SDHs have low Glasgow Coma Scale (GCS) scores on admission to the hospital.Treatment: surgical evacuation of the clot, reversal of INR by Vit K if applicable. High mortality. Consider risk factor prior to surgery (elderly prone to recurrence, high risk in surgery)

22
Q

Epidural hemmorhage

A

An epidural hematoma (EDH) occurs when blood accumulates between the skull and the dura mater. They typically occur when a skull fracture tears an underlying blood vessel. EDHs are about half as common as a subdural hematomas and usually occur in young adults. Classic symptoms of EDH involve “LUCID InTERVAL” brief loss of consciousness followed by a period of awareness that may last several hours before brain function deteriorates, sometimes leaving the patient in a coma.If untreated, the condition can cause increased blood pressure, difficulty breathing, damage to brain function and death. Other symptoms include headache, vomiting and seizure.Medical personnel typically use computed tomography (CT) brain scans to diagnose an EDH, which appears as a dense mass that pushes the brain away from the skull- convex shape. A magnetic resonance imaging (MRI) scan can also diagnose an EDH, although CT is faster and more commonly used for evaluating trauma patients. A small EDH with no pressure on the brain can be treated without surgery. Severe headache and deterioration of brain function, or an EDH larger than 1 cm at its thickest point, generally indicates surgery is necessary. Mortality lowered if pt awake on presentation