Neurologic Disorders Flashcards

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1
Q

What are the signs and symptoms of an Acute Ischemic Stroke?

A

Dysarthria, Aphasia, Visual loss (Homonymous hemianopsia), Ataxia and Unilateral weakness

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2
Q

Physical Exam for an Acute Ischemic Stroke:

A

Vitals

Head, Neck, Heart, Skin, Lungs,

NEURO: Level of alertness, Cognition, Cranial nerves, Motor function, Sensory testing, Cerebellar function

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3
Q

Differential Diagnosis

A
  1. Hemorrhagic stroke (SAH vs. intracerebral bleed)
  2. Transient Ischemic Attack
  3. Severe metabolic derangement (Hypoglycemia, Hyperglycemia, Hyponatremia)
  4. Atypical migraine
  5. Intracranial mass
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4
Q

How is an Ischemic Stroke differentiated from a TIA?

A

Differentiated from CVA by TIA resolving on its own (24 hrs), otherwise presents the same!

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5
Q

What goes into the Work Up for an Acute Ischemic Stroke?

A

***Noncontrasted brain CT immediately

CBC, BMP (Glucose by finger stick ASAP), PT/PTT, *ESR, *Tox screen, EKG

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6
Q

What is the Initial Management of an Acute Ischemic Stroke?

A

First need to establish secure Airway. Then BP – don’t over treat!! Get systolic to around 180 if hypertensive. Can cause more ischemia.

Then ASA, Heparin, tPA

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7
Q

IV-tPA Inclusion Criteria

A

Acute ischemic stroke with known time of onset less than 3hrs (Have to know when their symptoms started!!). Upcoming change to 4.5 hours.

Consent if possible, but not absolutely necessary

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8
Q

IV-tPA Exclusion Criteria

A
o	INR > 1.7
o	Recent major surgery
o	History of intracerebral hemorrhage
o	Platelets < 100
o	Uncontrollable blood pressure
o	MI within 3 months
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9
Q

What are the Signs and Symptoms of a Subarachnoid Hemorrhage?

A

Sudden onset of severe headache (“thunder clap”), Neck stiffness, Nausea and vomiting and Altered level of consciousness.

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10
Q

What is the most common etiology of a SAH?

A

Most are caused by a ruptured berry aneurysm. Also caused by AV malformations.

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11
Q

What goes into the work up for a SAH?

A

Non contrasted CT of the brain & Lumbar puncture!

If CT negative and suspicion remains high ->Xanthochromia

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12
Q

How do we treat a SAH?

A

Airway (Often require intubation)

Blood Pressure- Rapidly lower BP 20% then titrate to goal over next hour (SBP < 140).

Clip or Coil (Time to definitive treatment closely linked to outcome).

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13
Q

What are the signs and symptoms of an Intracerebral Hemorrhage?

A

Severe sudden headache presenting symptoms similar to that of ischemic stroke. Patient also can present with seizures and nausea/vomiting.

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14
Q

How is an Intracerebral Hemorrhage Diagnosed?

A

Diagnosed via CT scan

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15
Q

Treatment for an Intracerebral Hemorrhage:

A

BP management is controversial (Systolic >200 should be treated aggressively with IV meds; Systolic >180 should be treated with intermittent meds)

Neurosurgery consult

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16
Q

What is Status Epilepticus?

A

Prolonged seizure lasting 5–15 min. Continuous or multiple seizures w/o intervening periods of consciousnes

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17
Q

Initial Management of Status Epilepticus:

A

Airway management and Rule out hypoglycemia

STOP THE SEIZURES!! and Secure Airway
Ativan (lorazepam) 2 mg IVP, Repeat Ativan 2-4 mg IVP

Load with anticonvulsant: Phenytoin 20 mg/kg IV and/or Fosphenytoin 20mg/kg IV and/or

If all else fails…Propofol & General anesthesia

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18
Q

Myasthenia Gravis

A

Autoimmune disorder in which a patient experiences muscle weakness that is improved with rest. Acute attacks may lead to rapid onset muscle weakness and respiratory failure.

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19
Q

Precipitating factors of MG?

A

Infection or surgery

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20
Q

Symptoms of MG

A

Myasthenia patients that complain of shortness of breath need to be thoroughly evaluated and will require admission

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21
Q

Guillian-Barre

A

Autoimmune disorder with antibodies directed against peripheral myelin. Generally exhibits ascending paralysis (Lower extremities followed by upper extremities and then CNS involvement).

May have rapid onset muscle weakness and respiratory failure which may progress as quickly as 24 hours, and can occur at ANY age.

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22
Q

How is Guillian-Barre diagnosed?

A

It is diagnosed clinically

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23
Q

Precipitating factors of Guillian-Barre?

A

Often preceeded by URI or viral GI illness within ~2 weeks. Other causes include surgery and immunizations

24
Q

What is the first sign of Guillian-Barre?

A

Hyporeflexia often the first sign

25
Q

Guillian-Barre patients will require __________.

A

These patients WILL require intubation. Progress to respiratory distress rapidly

26
Q

Guillian-Barre & Myasthenia Gravis cause ___________.

A

Neuromuscular respiratory failure

27
Q

Neuromuscular Respiratory Failure

A

Weakness of diaphragm and chest wall leads to inability to breathe. The Lungs are unaffected! May occur very abruptly.

Watch patient very carefully. Admit to ICU even if patient looks OK (Patient will look OK until just before crashing).

28
Q

When are symptoms of Myasthenia Gravis worse?

A

Symptoms may get worse at night in MG

29
Q

What is a rule of thumb with intubation in patients with GB and MG?

A

Intubate early so you don’t regret it later

30
Q

Treatment of Myasthenia and Guillain-Barre

A

Intubation then IV Ig and plasmapheresis

31
Q

Rhabdomyolysis:

A

Muscle injury that results ultimately in muscle protein destruction

Ca release into intracellular space triggering a cascade resulting in muscle protein destruction and release of K,PO4, myoglobin, CPK, urate into blood stream

32
Q

Causes of Rhabdomyolysis

A
o	Muscle compression
o	Exercise
o	Status epilepticus
o	DTs
o	Viral infections
o	Drugs
33
Q

How do patients present with Rhabdomyolysis?

A

Vague complaints. Patient will often have pain and proximal muscle weakness, hyporeflexia, dark urine and myalgias

34
Q

How do we diagnose Rhabdo?

A

Elevated CPK (diagnostic indicator), urine abnormalities (may see myoglobin), hyperkalemia, BUN/Cr abnormalities

35
Q

Treatment for Rhabdo:

A

Hydration! – NS is best but can use Sodium Bicarb or LR

36
Q

A 27 y/o patient is brought in by EMS for continuous seizure. His family reports that he was well up until about 30 minutes ago when he began having aura, has been seizing for approximately 20 minutes total. He has a history of epilepsy and is otherwise healthy. He takes phenobarbital. He has NKDA.
Vitals are WNL and the patient is actively having grand mal seizure during your assessment.

Whats your Diagnosis?

A

Status epilepticus

37
Q

A 27 y/o patient is brought in by EMS for continuous seizure. His family reports that he was well up until about 30 minutes ago when he began having aura, has been seizing for approximately 20 minutes total. He has a history of epilepsy and is otherwise healthy. He takes phenobarbital. He has NKDA.
Vitals are WNL and the patient is actively having grand mal seizure during your assessment.

What do you give this patient?

A

Lorazepam IV, if it doesn’t work give it again

38
Q

A 69 y/o female with a history of A-fib is brought in by EMS on stroke alert. She is experiencing right sided weakness with associated garbled speech that started about an hour and a half ago. She takes lopressor, lisinopril and synthroid and has NKDA.
BP is 198/112, HR is 92 and irregular.
Your exam confirms right-sided hemiparesis.

Whats the first test you run?

A

CT the brain

39
Q

A 69 y/o female with a history of A-fib is brought in by EMS on stroke alert. She is experiencing right sided weakness with associated garbled speech that started about an hour and a half ago. She takes lopressor, lisinopril and synthroid and has NKDA.
BP is 198/112, HR is 92 and irregular.
Your exam confirms right-sided hemiparesis.

Is this patient a candidate for tPA?

A

Not until you control the BP below 180

40
Q

Stroke Pathophysiology:

A

Secondary to thrombosis or embolism. Long standing HPT.

41
Q

What are the symptoms of a patient with Meningitis?

A

Fever, Nuchal rigidity (neck stiffness), mental status change, photophobia, HA (continuous, throbbing and is usually over the occiput), CSF findings

42
Q

Meningitis Pathophysiology:

A

Meningitis has changed drastically since Haemophilus influenzae immunizations became available. The incidence of meningitis caused by this agent has decreased by 94%. The average age of a meningitis patient has risen from 15 months to 25 years, and there is an increasing trend for adult meningitis to be nosocomial rather than community acquired (with a corresponding increase in gram-negative organisms). Acute bacterial meningitis is a life-threatening medical emergency.

43
Q

Meningitis Evaluation and Management:

A

Lumbar puncture, serum glucose, gram staining of CSF. Treat with Empiric antimicrobial therapy.

For acute-begin IV antimicrobial within 30min.

Subacute-tx based on gram stain of CSF and other tests.

44
Q

Altered mental state Presentation:

A

Basically you need to rule everything else out

45
Q

How do we diagnose meningitis?

A

CSF gram staining and leukocytes > 10000, PMNs at least 85% of WBC or if CSF glucose is <50% of serum glucose

46
Q

What is the role of corticosteroids in meningitis treatment?

A

Both a decrease in neurologic sequela and mortality in adults with bacterial meningitis given dexamethasone. The effect was most dramatic in those with Staphylococcus pneumonia as the causative organism.

Dexamethasone should preferably be given prior to antibiotic therapy.

47
Q

What CN is most commonly affected in Guillian-Barre?

A

CN VII Facial

48
Q

How are seizures diagnosed?

A

Clinically, seizures are diagnosed by episodes of LOC or depressed consciousness and period of confusion or disorientation (postictal state) following it. Firm diagnosis of subtler types of seizures like absence or complex partial may require an ECG.

49
Q

What is the most common type of seizure?

A

Most common type of seizure is generalized tonic–clonic seizure.

50
Q

How do we diagnose and manage a Postural HA?

A

Follows LP, HA exacerbated by upright position, HA relieved by lying down.

TX: recumbency for 18-24 hours. Hydration and analgesics

51
Q

What are the types of subacute headaches and how are they diagnosed/treated?

A
  1. Posttraumatic HA: may have associated dizziness, vertigo, insomnia. May be immediate or wks after trauma
  2. Trigeminal neuralgia: excruciating, stabbing facial pain, pain in distribution of facial nerve; TX: Phenytoin, Carbamazepine, Baclofen, Lamotrigine
  3. Intracranial Mass: mild to moderate HA increasing in frequency or duration, associated with focal neuro deficit; CT contrast/MRI; TX: neuro consult
52
Q

How do we diagnose and treat Idiopathic Intracranial HTN (Pseudotumor Cerebri)?

A

Papilledema, increased ICP (250mm H2O), nonspecific brain imaging w/ normal/small sized ventricles. Most common in females, obese, 30’s
– SS: diffuse headache, diplopia, blurred vision, transient visual obscuration

TX: hospitalize for eval; repetitive LPs, Acetazolamide, Thiazide diuretics, optic nerve sheath decompression

53
Q

How do we diagnose and treat Temporal Arteritis (Giant Cell Arteritis)?

A

Older than 50, unilateral HA, usually tender over temporal artery, elevated ESR, unilateral vision loss. More common in females.

SS: Malaise, myalgia, weight loss, arthralgia, fever; rapid onset HA, unremitting, localized over temporal arteries, unilateral, jaw claudication

DX: suspect with ESR over 50; biopsy with vasculitis
TX: admit, corticosteroid (prednisone 40-60 mg/d)

54
Q

Types of Chronic Headaches:

A

– Tension HA
– Migraine
– Cluster

55
Q

How do we diagnose and treat a Tension HA?

A

Gradual onset, bilateral pressure/tightening. W>M; 25-30 yo; a/w emotional stress, constant/nonthrobbing, hours-days, photophobia

TX: NSAIDs with caffeine, Amitryptiline

56
Q

How do we diagnose and treat a Migraine?

A

Throbbing pain, NV, photophobia, neuro symptoms; FH; aura or without; precipitated by food, fasting, emotion, menses, drugs, bright lights.

TX: aspirin, NSAIDs, caffeine, analgesics, sedative, dopamine antagonists (prochlorperazine/metoclopramide), Triptans, Ergot derivatives

57
Q

How do we diagnose and treat a Cluster HA?

A

Daily attacks, severe unilateral HA, lacrimation, miosis, conjunctival injection, nasal congestion, rhinorrhea, ptosis; M>F

TX: O2 by face mask, Sumatriptan, Dihydroergotamine/ Ergotamine, Lidocaine, CS, Naratriptan