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IPT: CC > Block 3 Neuro > Flashcards

Block 3 Neuro Flashcards

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
Q

What are the main excitatory and inhibitory NT? What receptors?

A

Excitatory - glutamate on NMDA

Inhibitory - GABA

26
Q

Epilepsy + Glutamate

Causes opening of (calcium/potassium/sodium/magnesium/chloride) channels leading to (depolarization/hyperpolarization/repolarization)

A

Calcium + sodium

Depolarization

27
Q

Epilepsy + GABA

Causes opening of (calcium/potassium/sodium/magnesium/chloride) channels leading to (depolarization/hyperpolarization/repolarization)

A

Chloride

Hyperpolarization

The reason it goes away is GABA receptors experience endocytosis, decreasing their concentrations in prolonged seizures

28
Q

Seizure patho Part 1

during the first ________ of seizure

A

30 minutes

Phase 2 is immediately after

29
Q

What is happening in your body during part 1 of seizures?

A

Epinephrine, norepinephrine, and steroid concentrations increase significantly

Glycogenolysis

Lactic acid buildup

Airway obstruction, increase in secretions

30
Q

What is happening in your body during part 2 of seizures?

A

Patients may stop convulsing but seizures may still be evident on EEG
Converted to NCSE

Everything in part 1 is basically depleted

31
Q

________ is a big marker of a true seizure

A

Incontinence

32
Q

Prehospital Care of SE?

A

PR diazepam if available; otherwise:

IN midazolam or IM midazolam

33
Q

Initial Hospital Care of SE

A

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
Q

GSCE (0-30 min) Treatment?

A

IV lorazepam

Consider IN midazolam or IM midazolam

35
Q

GSCE (30-60 min) Treatment?

A

First line
Phenytoin (IV) or fosphenytoin (IV or IM)

Second line
Phenobarbital (IV)
Valproate (IV)

Third line
Lacosamide (IV)
Levetiracetam (IV)

36
Q

GSCE (>120 min) Treatment?

A

Midazolam, propofol, or pentobarbital infusions
If on propofol, continuous ECG monitoring

Assure cerebral perfusion pressure is > 70 mmHg

Achieve MAP > 120 mmHg

37
Q

GSCE (>24 hours) Treatment?

A

Ketamine, lidocaine, topiramate
Hypothermia
Inhaled anesthetics
Immunomodulating therapies

Assure cerebral perfusion pressure is > 70 mmHg

Achieve MAP > 120 mmHg

38
Q

Dose and rate of phenytoin and fosphenytoin for SE?

A

Phenytoin 15-20 mg/kg IVPB (rate < 50 mg/min)

Fosphenytoin 15-20 mg PE/kg IVPB (rate < 150 mg PE/min)

39
Q

(Phenytoin/Fosphenytoin) is mixed in diluent (propylene glycol) that can cause hypotension and cardiac arrhythmias

A

Phenytoin

40
Q

How do you check the free level of phenytoin?

A

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
Q

Phenobarbital dosing and AE?

A

Phenobarbital (IV) 15-20 mg/kg

Hypotension, respiratory and CNS depression
Contains propylene glycol

42
Q

Goal levels of valproate?

A

50-100

43
Q

If valproate + phenytoin are given together, what do you do?

A

Increase valproate dose

44
Q

What happens if valproate + aspirin are given together?

A

Valproate concentrations go up

45
Q

Valproate AE?

A

LFT elevation + edema

46
Q

Lacosamide AE?

A

Dizziness, loss of balance, memory problems

47
Q

Keppra AE?

A

Somnolence, headache, mood swings

48
Q

How are meds for refractory GCSE given?

A

Bolus, then drip

49
Q

alpha 1 antagonism
muscarinic antagonism
sodium blockade
potassium blockade

QRS widening - myocardial depression
QT widening - torsades
hypotension
anticholinergic effects

Match antipysch effects!

A

alpha - hypotension

muscarinic - anticholinergic

sodium - QRS widening - myocardial depression

potassium - QT widening - torsades

50
Q

NMS general signs?

A

Rigidity, fever

51
Q

NMS treatment?

A

BZD
Bromocriptine
Dantrolene

52
Q

Antipsych + hypotension or QRS widening, what do you do?

A

Hypotension - fluids with vasopressors

QRS widening - sodium bicarb

53
Q

Acute and chronic lithium toxicity symptoms? How do you treat it?

A

Acute - N/V, dizziness

Chronic - tremors, more kidney damage, diabetes

Fluid resuscitation
Avoid enhancing elimination with loop diuretics

Hemodialysis if poor eGFR

54
Q

MAOI overdose symptoms and treatment?

A

Hyperthermia - cooling bath/blankets

Hyperreflexia - BZD

HTN - Titratable calcium channel blocker (nicardipine, clevidipine), sodium nitroprusside

CNS effects (seizures) - BZD

55
Q

TCA overdose symptoms and treatment?

A

Arrhythmia - sodium bicarb

Hypotension - fluids + vasopressors

Seizure - BZD, barbiturates

Refractory sx - IV fat emulsion

56
Q

Serotonin syndrome general signs?

A

Hyperreflexia

Hot + sweaty

Confusion, tremors

57
Q

Serotonin syndrome treatment?

A
  1. BZD

If refractory, give Cyproheptadine (serotonin antagonist)

58
Q

What is the concern of taking flumazenil for chronic and acute BZD users?

A

Chronic - Causes abrupt withdrawal from BZD which could result in neuronal hyperexcitation

Acute - withdrawal should not happen, so no issues

IPT: CC (7 decks)

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