Block 3 Neuro Flashcards

(58 cards)

1
Q

Sx of HTN ICH? Diagnosis?

A

Patients usually have focal deficits

Headache and vomiting common

Diagnosis confirmed with head CT w/o contrast or MRI

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2
Q

RF for SAH?

A

Cigarette smoking and hypertension are the largest risk factors

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3
Q

Hallmark Sx of SAH?

A

Almost always caused by saccular aneurysm
“Worst headache of my life”/thunderclap headache

Sentinel headache 6-20 days prior

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4
Q

What is Cushing’s Reflex? What condition is it found in?

A

Found in Herniation

Cushing’s Reflex:

Increased pulse pressure (elevated SBP)
Bradycardia
Irregular breathing

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5
Q

Normal CPP and how do you calculate it?

A

60-70

𝑪𝑷𝑷=𝑴𝑨𝑷−𝑰𝑪𝑷

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6
Q

SBP goal of Hypertensive ICH + Aneurysmal SAH?

A

HTN ICH <140

Aneurysmal SAH <160

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7
Q

What are the agents used for acute BP reduction?

A

Hydralazine
Labetalol
Nicardipine
Clevidipine

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8
Q

Pearls of:

Hydralazine
Labetalol
Nicardipine
Clevidipine

A

Nicardipine = titratable, but large amounts of fluid/hr

Clevidipine = titratable (fastest), but solution is in a lipid emulsion

Hydralazine = unpredictable onset

Labetalol = caution in patients with bradycardia or history of reactive airway disease

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9
Q

If antifibrinolytic therapy is started, how long should you use it for aneurysmal SAH?

A

Dont go beyond 72hrs, but typically its not recommended to use at all

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10
Q

_________ is a major contributor to death and complications related to aneurysmal SAH

A

Vasospams

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11
Q

Vasospasms can be detected using ________ or directly with endovascular approaches

A

Transcranial dopplers

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12
Q

What is the only FDA-approved medication to reduce DCI associated with aSAH?

A

Nimodipine

Dosing: 60 mg orally or per tube every 4 hours for 21 days

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13
Q

When is VTE prophylaxis started after HTN ICH or Aneurysmal SAH is stable?

A

After 24 hrs

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14
Q

What are the 2 types of TBI injury?

A

Focal
Caused by penetrating or closed impact
Evidenced by hematomas and contusions on CT scan

Diffuse
Caused by rapid acceleration/deceleration
No impact required for this type of injury (MRI works better)

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15
Q

What does the Glasgow Coma Scale (GCS) look at?

A

Eyes

Motor Response

Verbal Response

3-8 = severe

13-15 = minor

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16
Q

Complications of TBI?

A

Nosocomial Infection

Deep Vein Thrombosis

Post-traumatic seizures (PTS)

Post-traumatic epilepsy (PTE)

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17
Q

SBP goal of TBI?

A

Age 50-69 → SBP > 100 mmHg

Age 15-49, 70+ → SBP > 110 mmHg

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18
Q

IC Pressure goal of TBI?

A

<20

Tx if >22

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19
Q

Non pharm Tx for TBI?

A

Craniectomy

Therapeutic or prophylactic hypothermia (not recommended)

CSF drainage

Ventilation therapies

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20
Q

What rx are used for TBI?

A

Mannitol (diuretic) careful in AKI pt

Hypertonic saline; anything above 900 osmolarity (3%NaCl) needs to be given in central line

Analgesics, anesthetics, and Sedatives; they dont lower ICP pressure except propofol

Seizure prophylaxis; phenytoin or keppra can be used for EARLY post-traumatic seizure

Dont give steroids

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21
Q
Albuterol
Theophylline
Pseudoephedrine
Midodrine
Fludrocortisone

Which ones increase HR/BP?

A

HR only:
Albuterol
Theophylline

BP only:
Midodrine
Fludrocortisone

Both:
Pseudoephedrine

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22
Q
Albuterol
Theophylline
Pseudoephedrine
Midodrine
Fludrocortisone

Which one has a narrow concentration level?

A

Theophylline

10-20

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23
Q

What kind of diet works well with fludrocortisone to increase BP?

A

High salt diet

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24
Q

What are the different GSCE stages?

A

1 - 0 to 30 min (impeding)

2 - 30 to 60 min (established)

3 - >120 min (refractory); continuous after 2-3 Tx

4 - >24 hrs (super refractory)

25
What are the main excitatory and inhibitory NT? What receptors?
Excitatory - glutamate on NMDA Inhibitory - GABA
26
Epilepsy + Glutamate Causes opening of (calcium/potassium/sodium/magnesium/chloride) channels leading to (depolarization/hyperpolarization/repolarization)
Calcium + sodium Depolarization
27
Epilepsy + GABA Causes opening of (calcium/potassium/sodium/magnesium/chloride) channels leading to (depolarization/hyperpolarization/repolarization)
Chloride Hyperpolarization The reason it goes away is GABA receptors experience endocytosis, decreasing their concentrations in prolonged seizures
28
Seizure patho Part 1 during the first ________ of seizure
30 minutes Phase 2 is immediately after
29
What is happening in your body during part 1 of seizures?
Epinephrine, norepinephrine, and steroid concentrations increase significantly Glycogenolysis Lactic acid buildup Airway obstruction, increase in secretions
30
What is happening in your body during part 2 of seizures?
Patients may stop convulsing but seizures may still be evident on EEG Converted to NCSE Everything in part 1 is basically depleted
31
________ is a big marker of a true seizure
Incontinence
32
Prehospital Care of SE?
PR diazepam if available; otherwise: IN midazolam or IM midazolam
33
Initial Hospital Care of SE
Consider thiamine 100 mg (adult), pyridoxine 50-100 mg (infants) Glucose (D50W or D10W) if hypoglycemic Naloxone for suspected narcotic overdose Antibiotics if infection suspected Treatment of hyperthermia
34
GSCE (0-30 min) Treatment?
IV lorazepam Consider IN midazolam or IM midazolam
35
GSCE (30-60 min) Treatment?
First line Phenytoin (IV) or fosphenytoin (IV or IM) Second line Phenobarbital (IV) Valproate (IV) Third line Lacosamide (IV) Levetiracetam (IV)
36
GSCE (>120 min) Treatment?
Midazolam, propofol, or pentobarbital infusions If on propofol, continuous ECG monitoring Assure cerebral perfusion pressure is > 70 mmHg Achieve MAP > 120 mmHg
37
GSCE (>24 hours) Treatment?
Ketamine, lidocaine, topiramate Hypothermia Inhaled anesthetics Immunomodulating therapies Assure cerebral perfusion pressure is > 70 mmHg Achieve MAP > 120 mmHg
38
Dose and rate of phenytoin and fosphenytoin for SE?
Phenytoin 15-20 mg/kg IVPB (rate < 50 mg/min) Fosphenytoin 15-20 mg PE/kg IVPB (rate < 150 mg PE/min)
39
(Phenytoin/Fosphenytoin) is mixed in diluent (propylene glycol) that can cause hypotension and cardiac arrhythmias
Phenytoin
40
How do you check the free level of phenytoin?
If no lab exists use equation: PHT level / (0.2 or 0.1 if CrCl<20 x albumin + 0.1) Should be 10-20
41
Phenobarbital dosing and AE?
Phenobarbital (IV) 15-20 mg/kg Hypotension, respiratory and CNS depression Contains propylene glycol
42
Goal levels of valproate?
50-100
43
If valproate + phenytoin are given together, what do you do?
Increase valproate dose
44
What happens if valproate + aspirin are given together?
Valproate concentrations go up
45
Valproate AE?
LFT elevation + edema
46
Lacosamide AE?
Dizziness, loss of balance, memory problems
47
Keppra AE?
Somnolence, headache, mood swings
48
How are meds for refractory GCSE given?
Bolus, then drip
49
alpha 1 antagonism muscarinic antagonism sodium blockade potassium blockade QRS widening - myocardial depression QT widening - torsades hypotension anticholinergic effects Match antipysch effects!
alpha - hypotension muscarinic - anticholinergic sodium - QRS widening - myocardial depression potassium - QT widening - torsades
50
NMS general signs?
Rigidity, fever
51
NMS treatment?
BZD Bromocriptine Dantrolene
52
Antipsych + hypotension or QRS widening, what do you do?
Hypotension - fluids with vasopressors QRS widening - sodium bicarb
53
Acute and chronic lithium toxicity symptoms? How do you treat it?
Acute - N/V, dizziness Chronic - tremors, more kidney damage, diabetes Fluid resuscitation Avoid enhancing elimination with loop diuretics Hemodialysis if poor eGFR
54
MAOI overdose symptoms and treatment?
Hyperthermia - cooling bath/blankets Hyperreflexia - BZD HTN - Titratable calcium channel blocker (nicardipine, clevidipine), sodium nitroprusside CNS effects (seizures) - BZD
55
TCA overdose symptoms and treatment?
Arrhythmia - sodium bicarb Hypotension - fluids + vasopressors Seizure - BZD, barbiturates Refractory sx - IV fat emulsion
56
Serotonin syndrome general signs?
Hyperreflexia Hot + sweaty Confusion, tremors
57
Serotonin syndrome treatment?
1. BZD If refractory, give Cyproheptadine (serotonin antagonist)
58
What is the concern of taking flumazenil for chronic and acute BZD users?
Chronic - Causes abrupt withdrawal from BZD which could result in neuronal hyperexcitation Acute - withdrawal should not happen, so no issues