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Health Assessment > Neurological diaseases exam 3 > Flashcards

Neurological diaseases exam 3 Flashcards

1
Q

Cerebral blood flow is modulated by: (5)

A

CMR
CPP (MAP- ICP)
PaCO2
PaO2
drugs, intracranial pathologies

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2
Q

What is normal CBF?

A

50 mL/100g brain tissue per minute
750 mL/min
15% of CO

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3
Q

What does the intracranial and spinal vault contain?

How much volume does brain tissue, intracranial blood and CSF have combined?

A

IC and spinal vault contains neural tissue (brain + spinal cord) blood and CSF. Is enclosed by dura matter and bone

-1200-1500 mL (ICP 5-15 mmHg)

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4
Q

What is the monro kellie hypothesis?

A

Any increase in one component of intracranial volume must be offset by a decrease in an other component to prevent an elevated ICP

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5
Q

How do homeostatic mechanisms support CCP?

A

Homeostatic mechanisms can increase MAP to support CPP despite increases in ICP, but eventually these compensatory mechanisms fail, result in cerebral ischemia

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6
Q

What do meningeal barriers separate?

A

Meningeal barriers separate the falx cerebri and tentorium cerebelli

Intracranial vault is compartmentalized

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7
Q

What is the falx cerebri?

What is the tentorium cerebelli?

A

falx cerebri- dura that ceperates 2 cerebral hemispheres
tentorium cerebelli: dura that lies the rostral to the cerebellum and marks the border between the supratentorial and infratentorial spaces

increases in the contents of one region causes increase in ICP and contents can herniate

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8
Q

What is subfalcine herniation?

A

Herniation of hemispheric contents under the falx cerebri; typically, compressing branches of the anterior cerebral artery, creating a midline shift

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9
Q

What is transtentorial herniation?

A

Herniation of the supratentorial contents past the tentorium cerebelli, causing brainstem compression in a rostral to caudal direction. This leads to AMS, defects in gaze and ocular reflexes, hemodynamic and respiratory compromise, and death

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10
Q

What is uncal herniation?

A

a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli. This results in ipsilateral oculomotor nerve dysfunction
Sx: pupillary dilatation, ptosis, and lateral deviation of the affected eye, brainstem compression and death

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11
Q

What causes herniation of the cerebellar tonsils?
What are the s/s?

A

Elevated infratentorial pressure, causes the cerebellar structures to herniate through foramen magnum
Sx: medullary dysfunction, cardiorespiratory instability and subsequently death

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12
Q

Label the herniation

A
  1. subfalcine:
  2. transtentorial
  3. cerebellar contents thru foramen magnum
  4. traumatic event causing herniation out of cranial cavity–> displacement of bone tissue
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13
Q

What are some causes of ICP

A

Tumors bc of their size and cause edema in surrounding tissue. They also can obstruct CSF flow (tumors in third ventricle)
-intracranial hematomas
-blood in CSF–> leads to obstruction of CSF reabsorbtion
-infections (meningitis, encephalitis)

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14
Q

What are some methods (8) to decrease ICP?
How do they work?

A
  • Elevation of the head: encourages jugular venous outflow
  • Hyperventilation: lowers PaC02
  • CSF drainage: external ventricular drain (EVD)
  • Hyperosmotic drugs: increase osmolarity, drawing fluid across BBB
  • Diuretics: induce systemic hypovolemia
  • Corticosteroids: decrease swelling and enhance the integrity of the BBB
  • Cerebral vasoconstricting anesthetics (propofol): decrease CMR02 and CBF
  • Surgical decompression
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15
Q

What to do during neurological assessment?

A
  • Look at patients’ history, symptoms, and baseline neuro-deficits
  • Review imaging and available neurological testing results
  • Review the patients’ current drugs and treatments
  • Evaluate the potential risks/benefits of various anesthetic options to determine the most appropriate plan of care
  • Implement pre-op measures that may help optimize the patients’ condition prior to anesthesia
  • Provide clear pre-op documentation of the factors above, and have a rational for chosen anesthetic plan
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16
Q

What is multiple sclerosis and who’s at risk?

A
  • Progressive, autoimmune demyelination of central nerve fibers
  • Rx factors: Female, 1st deg relative, epstein barr-V, other autoimmune disorders, smoking
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17
Q

What triggers MS? (3)

What are the s/s

A

stress, elevated temps and postpartum period

s/s: motor weakness, sensory disorders, visual impairment and autonomic instability.
Symtoms vary based on site of demyelination

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18
Q

What are some preanesthetic considerations for MS?

A

-consider PFT if respiratory compromise
-CBC, BMP, +/- liver function tests (LFT if on dantrolene and azathioprine)
-pre op steroids (pay attention to glucose and electrolytes)
-temp managment (trigger for MS)

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19
Q

How is MS managed?

A

There is no cure. Managed w corticosteroids, immune modulaters and targeted antibodies (IgG)

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20
Q

What med to avoid during MS?

A

Avoid succ! may induce hyperkalemia (upregulated N-ach receptors)
GA, RA, and peripheral nerve blocks are acceptable

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21
Q

What is myasenthia gravis?

Which nerves are susceptible?

A

-autoimmune, antibodies are gerenated against N-Ach receptors at skeletal motor endplate.

-cranial nerves are susceptible

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22
Q

S/S of myasenthia gravis

A

ocular symptoms are common (diplopia, ptosis) and there is bulbar involvement (laryngreal and pharyngeal weakness) aspiration risk!)
-thymic-hyperplasia is common! 90% improve after thymectomy

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23
Q

What exacebate MG?
What is treatment of MG?

A

-exarcabated by exercise, pain, insomnia, infection and surgery

-Ach-E inhibitors (Pyridostigmine), immunosuppressive agents, steroids, plasmapheresis, IVIG

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24
Q

Preanesthetic considerations for MG

A

-PFT, optimize respiratory function
-reduce paralytic dosage to avoid weakness
-caution w opoids to avoid respiratory compromise
-AchE inhibitors may prolong succ and ester LA
-Pre op steroids

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25
Q

Labs for MG patients?

What are MG patients increased risk of post op?

A

-* Labs: CBC, BMP, +/-LFT (LFT if on Azathioprine)
-pay attention to glucose and electrolytes d/t steroids
-counsel pts on increased risk for post op resp support and ventilation until fully recovered from anesthesia

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26
Q

What is Eaton-Lambert Syndrome?

A

-disorder causing the development of autoantibodies against VG calcium channels.
-Reduced Ca++ influx into presypnaptic Ca+ channels causes reduced Ach release at NMJ

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27
Q

What are the s/s for ELS?

A

-s/s progressive limb girdle weakness, dysautonomia, oculobulbar palsy

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28
Q

What is the treatment for Eaton Lambert?
What are 60% cases associated with?

A

Treatment: selective K+ channel blocker “3-4 diaminopyridine”, Ach-E inhibtors, immunologics (azathioprine), steroids, plasmapheresis, IVIG
-60% cases related to small cell carcinoma

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29
Q

What to caution with ELS patients?

A

-Caution with paralytic and opioid dosing
-they are very sensitive to nondepolarizing NMB (more than MG patients) and depolarizing NMB
Caution with opioid dosing
Regional > GA

Might also need post op vent!

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30
Q

What is muscular dystrophy?

A
  • Hereditary disorder of muscle fiber degeneration caused by breakdown of the dystrophin-glycoprotein complex, leads to myonecrosis, fibrosis, and skeletal muscle membrane permeability. 6 types of MD.
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31
Q

What is the most common and severe form of muscular dystrophy?

A

Duchenne MD, occurs only in boys 2-5 y/o. wheelchar bound 8-10 y/o. Lifespan 25 y/o dt pulm complications

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32
Q

S/S of muscular dystrophy
Common lab finding?

A
  • Sx: progressive muscle wasting without motor/sensory abnormalities, kyphoscoliosis, long bone fragility, respiratory weakness, frequent pneumonia, EKG changes
    -elevated serum creatine kinase seen caused by muscle wasting
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33
Q

What should you obtain prior to surgery for muscular dystrophy?

A

CBC, BMP, PFT, CK and preop EKG and echocardiogram (evaluate for cardiomyopathy)

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34
Q

What meds to avoid in muscular dystrophy and why?

A

Avoid succ and volatile anesthetics! They can lead to hypermetabolic syndrome (can lead to rhabdo, hyperkalemia, vfib and cardiac arrest

35
Q

What meds are acceptable to use during surgery for muscular dystrophy?

A

-consider low dose rocuronium and TIVA for GA
-RA> GA

Have MH cart ready w dantrolene!

36
Q

What is myotonia?

A

prolonged contraction after muscle stimulation; seen in several disorders

37
Q

Myotonic dystrophy is the most common type of myotonia.
What are the s/s?
What heart condition is common?

onset 20-30’s

A

-s/s: wasting in face, masseter, pretibial muscles. Can also affect pharyngeal, laryngea and diaphgramatic muscles.
-20% have mitral valve prolapse

38
Q

What is myotonia congenita?

A
  • milder form of myotonia; involves the skeletal muscles.
39
Q

What is central core disease?
What are the symptoms?

A

-Central core muscles lack mitochondrial enzymes.
Proximal muscle weakness & scoliosis

rare

40
Q

What triggers myotonias and what is the treatment?

A

Myotonias are triggered by stress & cold temps
Tx: No cure. Sx managed w/Quinine, Procainamide, Steroids

41
Q

What to assess for in myotonia?
What are they at risk for?

A

-Assess breath and heart sounds
-Risk for aspiration and high risk for endocrine abnormalities (thyroid and glyucose levels)
-Risk for risk for post op respiratory weakness and also high aspiration risk

42
Q

What to avoid in myotonia patients?
Caution with what meds?
What to do to avoid flareups during surgery?

A

-Avoid succ d/t fasciculations (can trigger myotonia)
-Caution w opioids to avoid respiratory depression
-Keep them warm to avoid flareups

43
Q

What are the 3 major dementia syndromes?
What meds are they usually on?

A
  • Alzhemiers (70%), vascular dementia (25%), parkinsons 5%
  • AchE-I, MAOI’s, psych meds; meds may affect anesthetic
44
Q

What are dementia patients at risk for post op?

A

High risk for post op delirium (consider TIVA); RA preferred (dt low opoid requirment)

45
Q

What meds to avoid for parkinsons’ patients? (4)

What med do you continue?

A

-Avoid reglan, phenothiazine butyrophenones
-Avoid demerol if on MAIO

-continue PO levodopa to avoid unstable extrapyramidal effect such as chest wall rigidity

46
Q

What is parkinsons disease?

A

Degeneration of dopaminergic fibers of basal ganglia; extrapyramidal motor neurons are overstimulated

Dopamine regulates the extrapyramidal motor system, which is stimulated by Ach

47
Q

Parkinsons triad of symptoms

A

skeletal muscle tremor, rigidity, akinesia

other: pill rolling,” facial rigidity, slurred speech, difficulty swallowing, respiratory difficulty, depression & dementia

48
Q

What to disable before surgery in Parkinsons pateints?
What settings are recommended for cautery?

A

***** Deep brain stimulators may need to be disabled to avoid interaction w/cautery
* If cautery used, bipolar recommended as it reduces scattering of electro-currant

49
Q

What are common s/s for brain tumors?

A

high ICP, papilledema, headache, AMS, mobility impairment, vomiting, autonomic dysfunction, seizures

50
Q

Types of tumors

Whare are gliomas?

A

-gliomas: primary tumor, least agressive astrocytoma (found in young adults and new onset sezires)

51
Q

What are pilocytic astrocytomas?

A

-pilocytic astrocytoma: common in children and young adults, mostly benign

52
Q

What do anaplastic astrocytoma evolve to?

A

Anaplastic astrocytoma are poorly differentiated and usually evolve into gliobllastoma multiforme– these have a high mortality; require surgery and chemo and are very deadly

53
Q

Where do meningiomas arise from?

A

-Meningiomas are usually benign and arise from sura or arachnoid tissue.
-Good prognosis w surgical resection!

54
Q

What are pituatary adenomas; what is the treatment?

A

Pituatary adenomas are noncancerous; transsphenoidal or open crani is usually curative

55
Q

What are acoustic neuromas?

A

Acoustic neuromas are usually benign schwannomas involving the vestibular component of CN VIII within auditory canal. Good prognosis w resection & radiation

56
Q

What does radiation damage cause?

What do patients with brain tumors present with in regards to vital signs

A

radiation damage may cause lethargy and AMS

-Present w autonomic dysfunction; which may manifest on EKG, labile HR and BP

57
Q

What meds are brain tumor patients on?

A

-Pt are often on steroids to minimze cerebral edema (monitor glucose levels)
-Also on anticonvulsants (especially w supratentorial lesions; closer to motor cortex)

58
Q

What meds are usually used with brain tumor patients?

A

-preop steroids and antiseizure meds per surgeon
-Mannitol used to reduce ICP and volume

59
Q

What are clinical features for occluded ACA?
What are clinical features for occluded MCA?

A

ACA: contralateral leg weakness

MCA: contralateral hemiparesis and hemisensory deficit, aphasia in the dominant hemisphere and contralateral visual field defect

60
Q

What are clinical features for occluded PCA?

What are clinical features for occluded penetrating arteries?

A

PCA: contralateral visual field defect, contralateral hemiparesis.

Penetrating arteries: contralateral hemiparesis, contralateral hemisensory deficits

61
Q

What are clinical features for occluded basiliar artery?

What are the clinical features for occluded vertebral artery

A

BA: oculomotor deficits and or ataxia w crossed sensory and motor deficits

VA: lower cranial nerve deficits and or ataxia w crossed sensory deficits

62
Q

What are 5 causes of ischemic strokes?

A
  1. Large artery atherosclerosis (carotid stenosis)
  2. Small vessel occlusion (lacunar stroke)
  3. Cardioaortic embolic ( emboli from atrial fibrillation)
  4. Other etiology (stroke due to hypercoagulable states or vasculopathies)
  5. Undetermined etiology
63
Q

What is ischemic CVA treatment?

A

-PO aspirin
-IV or IA TPA (when specific criteria is met; <4.5 hr from symptoms)
-thrombectomy
-revascularization

64
Q

2 most reliable predictors of outcomes for hemorrhagic stroke?
Treartment depends on ____

A

blood volume and change in LOC
Tx depends on severity

65
Q

What is conservative treatment for hemorrhagic stroke?
Surgical treatment involves what

A

-Conservative tx is centered on the reduction of ICP, BP control, seizure precations, and vigilant monitoring
-surgical tx involves hematoma evacuation

66
Q

If someone is on a new anticoagulant, they can’t have elective cases for how long?

A

3 months

67
Q

High risk patients for CVA that pause ____ will need _____ to bridge the gap.

A

Pause **long acting AC ** (warfarin) will need short acting AC (LMWH, IV heparin)

68
Q

What do you assess preop for cerebrovascular disease patients?

A

Assess orientation, bilateral grip strenght and LE strenght
Ask for h/a, tinnitus, vision/memory issues and bathroom issues

69
Q

Why are majority of cerebral aneurysms undiagnosed?

What are risk factors ?

A

-Most cerebral aneurysms are not diagnosed before rupture bc only 1/3 patients show symptoms.

Risk factors: HTN, smoking, female, oral contraceptives, cocaine

70
Q

S/S for cerebral aneurysm?

A

H/A, photophobia, confusion, hemiparesis, coma

71
Q

Intervention should be performed within _____ of rupture for best outcomes

Preanesthesia considerations for cerebral aneurysms include:

A

within 72 h!

preanesthesia considerations include CT angio, EKG, Echo, CBC,BMP, Type and cross w blood on hold, BP control and mannitol

72
Q

What are post SAH patients at risk for?

What is the triple H therapy?

A

Risk for vasospasm 3-15 days post SAH

Hypertension, Hypervolemia, Hemodilution

Free Hgb triggers inflammatory mediators which reduce NO and inc endothelin 1, leads to vasoconstriction

73
Q

Intervention treatments for post SAH vasospams are?

A

balloon dilation and direct injection of vasodilators relieve the spasm

74
Q

What is arteriovenous malformation

A

Arterial to venous connection w/o intervening capillaries
Creates an area of high flow, low resistance shunting
Majority are supratentorial
sx: mass effects to hemorrhage

75
Q

What is the treatment for AVM ?

A

Tx: radiation, angio-guided embolization, surgical resection (higher mortality)

76
Q

Chiari Malformation: cerebellum displacement

Type 1 is downward displacement of _____.

Type 2 is downward displacement of _____ _____ and is associated w/ myelomeningocele

A

cerebellum

cerebellar vermis

77
Q

Chiari

Type 3 is rare; occipital _____ with downward cerebellar displacement

Type 4: cerebellar hypoplasia w/o displacement of _____ _____ contents. (Not compatible w life)

A

encephalocele

posterior fossa

78
Q

What is tuberous sclerosis aka bourneville disease

A

Autosomal dominant disease causing benign hematomas, angiofibromas, and other malformations that can occur anywhere in the body

Often involves co-existing tumors of face,oropharnyx, heart, lungs, liver &kidneys
And cortical tumors and giant cell astrocytoma in brain

79
Q

What is von hippel lindau disease?
What disorder do they present with

A

Benign tumors of the CNS, eyes, adrenals, pancreas and kidneys
May present w/ pheochromocytoma

80
Q

Anesthesia considerations for Neurofibromatosis

A

Anesthesia considerations account for increased ICP, airway issues, scoliosis, possibility of pheochromocytoma

-avoid neuroaxial d/t tumors

tumors on nerves! no cure

81
Q

Hydrocephalus treatment

A

VP shunt: drain placed in ventricle of the brain andempties into peritoneum, high failure rate

ETV: catheter placed into the lateral ventricle that drains into the peritoneal space, right atrium, or more rarely the pleural space

82
Q

Surgical treatment for cerebral aneurysm include ? (3)

A

Coiling, steering and trapping/bypass (for large aneurysm)
Neurosurgeon on standby in case of rupture

83
Q

What is the aneurysm grading scale for prognosis

A

Hunt and Hess

84
Q

Phenytoin, tegretol and barbs are ______ _____

A

Enzyme inducers; likely required higher dose of hepatic cleared medications

Health Assessment (30 decks)

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