Kristine's Neuro

Front 1

What is MS?

Back 1

The mylein is destroyed by plaques. Autoimmune dz w/ environmental exposure. Genetic. Diagnosed by MEPs. These pts have relapsing resp insufficiency. More common in women. Can be triggered by dz, infections, viral...

Front 2

MS symps

Back 2

Muscle weakness, paralysis, resp insufficiency. Demyleination of the brain stem causes nystagmus. Optic nerve usully 1st (visual disturbances). Treatment:steroids

Front 3

MS anesthetic management

Back 3

on steroids, on methotrexate.
Pts often have autonomic dysfct. and keep them normothermic! Careful to titrate muscle relaxants. Avoid Sch. Extent of resp insuffiency.

Front 4

MS avoid...

Back 4

Sch...because of muscle atrophy. Neurotoxic effects of LAs...spinal no, epidural OK. Avoid hyperthermia which can further destroy the mylein sheath.

Front 5

Most common motor neuron dz

Back 5

ALS
-muscle atrophy, increased Ach receptors, and sch contraindicated.

Front 6

Charcot Marie Tooth dz

Back 6

Demyelinating dz. Both motor and sensory demyleinating polyneuropathy. Can be autonomic dys fct, muscle atrophy. May have association b/t this dz and MH.

Front 7

Other motor neuron dz (3)

Back 7

1) ALS
2) Spinal muscular atrophy
3) Friedrichs Ataxia

Sch contraindicated b/c increased receptors.

Front 8

What is ALS?

Back 8

NOT associated with autonomic dysfct.
Progressive muscle weakness, atrophy, resp failure. Symptoms do not stabilize, no treatment and death is w/in 2-5 yrs.

Front 9

What are the two things in assessing ALS?

Back 9

Degree of muscle atrophy and resp insufficiency.

Front 10

What is Friedrich's Ataxia?

Back 10

Like ALS (has both UMN and LMN are affected), muscle atrophy. There is degen of spino cellabellar tract as well as the pyramidal tract. Specific to this dz: cardiomyopathy is present in 10-50% of pts. Kyphoscolosis is present in 80% of these pts, which negatively affects pulmonary fct.

Front 11

Spinal Muscular Atrophy

Back 11

Only the LMN are affected.

Front 12

Other LMN diseases other than Spinal muscular atrophy

Back 12

Syringomyelia
Syringobulbia
- The spinal cord degenerates leading to cavitation. Obstruction of outflow of CSF from 4th ventricle.

Front 13

GBS

Back 13

Polyneuritis, denervation( tempeorary)

axonal degeneration (one you have axon invol, this is permanent). Problem is with the LMN, so paralysis is flaccid. Unknown cause.

Front 14

GBS anesthetic considerations

Back 14

Autonomic dysfct common. Can have bulbar involvment (phyarngeal weakness=full stomach). Resp muscle weakness, ventilation should be controlled. NO SCH b/c of the muscle atrophy.

Front 15

Porphyria- what it is and what to avoid

Back 15

Not a NMD. They have neuritis. Heme synthesis dz. Avoid barbs and etomidate.

Front 16

Myasthenia Gravis- what is it?

Back 16

Decreased regulation of Ach receptors (Ach receptors degenerate). Autoimmune dz. There are fewer fct Ach receptors b/c they are destroyed by the antibodies.

Front 17

MG treatment

Back 17

1) Neostigmine/pyridostigmine=
which increases Ach at the jct (the few ones that you have)
2)corticosteroids=to decrease the # of antibodies.
3) Removal of the thymus gland-b/c this gland produces antibodies that destroy the Ach receptors.

Front 18

MG symptoms

Back 18

Muscle weakness/fct
post-op respiratory weakness, Aspiration risk.

Front 19

MG anesthesia considerations

Back 19

-NO SCH, b/c would have to give a lot of sch in order to work. But pt wouldn't be able to break it down.
-Sensitive to NDMB. Small amt of NDMB will block the few receptors they have. 80% fewer receptors.
-All muscle relaxants should be avoided. If can't, careful titrate and monitor TOF.
-Aminoglyoside can aggrevate skeletal muscle weakness-in ALL of these NMD.

Front 20

Myastemic Syndrome

Back 20

MG like dz. Skeletal muscle weakness. Associated with small cell lung CA.

Front 21

Up regulation with Sch admin

Back 21

Hyperkalemia happens when you have muscle atrophy. They have MORE Ach receptors.

Front 22

Muscular Dystrophy- what is it.

Back 22

LMN Muscle disease. Mutation of the dystrophan gene on the X chromosome. Sex linked recessive trait. Females carriers, males get it.

Front 23

S/sx of Muscular Dystrophy

Back 23

Progressive muscle weakness and atrophy. Intact sensation. Muscles become abnormally perm to Ca+. and the muscle cells necrosis. Then there is muscle atrophy predisposes to bone fx. Degeneration of cardiac muscle.

Front 24

Muscular dystrophy anesthetic considerations.

Back 24

-Kyphoscolosis (b/c of muscle weakness)=abnormal lung fct.
-HyperK+, high CPK and cardiac arrest after Sch b/c muscle membrane is abnormal.
-Linked to post-mortum diag of MD b/c thought to be MH. Now restricted used of Sch in pedi.

Front 25

Central core Dz

Back 25

Myopathy which is susceptible to MH.

Front 26

Steinert's Dz-what is it?

Back 26

Myotonic dystrophy, a disorder of the skeletal muscle which is persistent contracture of the skeletal muscle after the volunatry contracture of muscle ceases. Abnormal Ca+ metabolism. Example: pt shakes your hand and can't let go.

Front 27

Steinert's Anesthetic management

Back 27

Pt's are suseptible to MH. NO SCH or volatile agents.
-anti-cholinesterase drugs, cold temp, surgical manip and electrocautery can precip myotonia. Progressive deteroriation of the cardiac conduction system.

Front 28

Parkinson's Dz-what is it?

Back 28

dz of the basal ganglia. Insufficient dopamine and too much Ach. Movement disorder. Eventually have AKINESIA.

Front 29

What is the goal of parkinsonan treatment?

Back 29

Increase dopaminergic activity and decrease cholinergic activity.

Front 30

L-dopa

Back 30

Most common med to treat parkinsons. Increases the amt of dopamine in the basal ganglia. Levo-dopa becomes dopamine, but has a short 1/2 life.

Front 31

Parkinson's anesthetic considerations

Back 31

Have autonomic dysfct. At risk during induction and maintence for hypotension b/c of hypovolemia and venous pooling.
-Drugs to use: propofol, benedryl, scopalamine.
-Drugs to avoid: Reglan
-Drugs to be careful: muscle relaxants

Front 32

What types of chemicals are dopamine and Ach?

Back 32

Dopamine are inhibitory
Ach-excitatory

Front 33

Name the Basal Ganlia Dz (3)

Back 33

1) parkinsons
2) Huntingtons Correa
3) Halloverdan Spatz

Front 34

What is huntingtons correa
-correa=abnormal movement

Back 34

High dopamine and low ach (opposite of parkinsons).
Have pharyngeal muscle weakness
Reglan may help!
May have prolonged response to Sch b/c of decreased Ach amt and thus decreased plasmacholinesterase.

Front 35

What is halloverdan Spatz?

Back 35

-Basal Ganglia dz. Causes torticolis.
-Pts can have bony prominences on TM joint & the c-spine which may make intubation difficult.
-severe cases cause progressive resp insuf. and death in about 10 yrs. onset late childhood.

Front 36

What is Charcot Marie Tooth?

Back 36

-Motor and sensory demyelinating polyneuropathy.
-Can have autonomic dysfct, muscle atrophy.
-May have association b/t this dz and MH.

Front 37

What is Multiple Sclerosis?

Back 37

Inflammation, demylineation and axonal damage in the CNS. Mylein destroyed by plaques. Autoimmune dz that is genetic, triggered by enviromental factors. More common in females. Diaganosed by MEPs.

Front 38

Preanesthesia assessment in MS

Back 38

Muscle atrophhy (extent)
Avoid Sch
Resp muscle weakness at baseline
Avoid hyperthermia

Front 39

Anesthetic management in MS

Back 39

Pts are usually on sterioids, give stress dose.
Have autonomic dysfct.
Keep normothermic b/c increased temp causes deterioration of NMJ

Front 40

Brain weighs

Back 40

1500 grams

Front 41

Brain consums

Back 41

20% of whole body uptake

Front 42

Brain cardiac output

Back 42

is 5L/min

Front 43

What is the total cerebral blood flow?

Back 43

50ml/100g of brain tissue per min

Front 44

How much oxygen the brain consumes each minute (CMRO2)

Back 44

0.04ml/g/min OR
4ml/100g/min
Brain's oxygen consumption
AKA CMRO2

Front 45

Amount of oxygen consumed equation

Back 45

arterial O2 content-jugular venous 02 content=amt of O2 consumed.
Can also be quantified by an MRI

Front 46

Brain is dependent on 2 substrates

Back 46

glucose
oxygen

Front 47

Metabolism is coupled to flow, therefore...

Back 47

the brain has a high metabolism and cerebral blood flow is high. When blood flow is high, metabolism is high.

Front 48

If you increase the CO2 from 40 to 80, the CBF...

Back 48

doubles

Front 49

The relationship b/t CO2 and CBF is...

Back 49

linear

Front 50

Total Body oxygen consumption

Back 50

250ml-300ml

Front 51

Brains oxygen consumption is divided into areas of....(2)

Back 51

1) low metabolism (white matter)
2) high metabolism (grey matter)

Front 52

What is intracerebral Steal syndrome?

Back 52

If there is an increase in CO2 and therefore an increase in CBF. CO2 is high and therefore everything is dilated and not able to redirect flow to the needed area (the ischemic area).

Front 53

What is the Robin-hood phenomenon?

Back 53

AKA reverse steal.
Purposefully lowering the CO2 so that you have overall vasocontriction and therefore have a greater ability to redirect flow to an ischemic area.

Front 54

Autoregulation of CBF happens between...

Back 54

50-150mmHg

Front 55

Autoregulation can be abolished by...

Back 55

trauma or hypoxia.

Front 56

Autoregulation if you are HTN

Back 56

70-170mmHg. Curve shifts to the right.

Front 57

If >150mmHg...then CBF

Back 57

goes up.

Front 58

If <50mmHg....then CBF

Back 58

goes down.

Front 59

As CO2 rises by 1mmHg

Back 59

CBF rises by 1-2ml/per min.

Front 60

Does Oxygen have an affect on CBF?

Back 60

Only when your pt becomes hypoxic...below a PaO2 of 50, then your CBF increases.

Front 61

What can't get through the BBB?

Back 61

Large substances, Ions

Front 62

What CAN get through the BBB?

Back 62

lipid soluble, volatile agents

Front 63

What mediates things across the BBB?

Back 63

Glucose

Front 64

Cranium is a fixed volume of ...(3)

Back 64

1) CSF/ECF
2) Brain tissue
3) Blood

This is a fixed space in the cranial valut. If any of these components increase/chagne, you have problems (increased ICPs).

Front 65

What is the equation for CPP?

Back 65

MAP-ICP=CPP

Front 66

What is normal ICP?

Back 66

5-15mmgHg

Front 67

What value is considered intercranial HTN?

Back 67

>20mmHg

Front 68

What can the BBB be distrupted by?

Back 68

Infection, trauma, acute HTN, tumors, ischemia.

Front 69

What is the Blood CSF barrier?

Back 69

similar to the BBB. Allows free movement of H20, gases and lipid soluble compounds, but doesn't allow large molecules and ions to cross over.

Front 70

What happends when ATP levels fall in brain damage?

Back 70

Lactic acid occurs. Ca+ rush INTO cell and K+ rushes OUT of cell (blood hyperK+). This causes cells to depolarize releasing GLUTAMATE (excitatory a.a.). Glutamate further depolarizes neuron. High intracellular Ca+ triggers ischemia causing damage.

Front 71

name the 3 intercranial compartments

Back 71

1) cells
2) Fluid: ECF/ICF/CSF
3) Blood

Front 72

How to treat the intercranial cellular compartment when volume is altered.

Back 72

Surgical removal

Front 73

How to treat the intercranial Fluid compartment when volume is altered.

Back 73

Diuretics
Steroids (tumors, to decrease swell)
Drainage- w/ a bolt

Front 74

How to treat the intercranial Blood (arterial and venous sides) compartment when volume is altered.

Back 74

Arterial: want to decrease CBF. Avoid Vasodilators, sevo/iso which increase CBF. Avoid hypoxemia, hypercapnia

Veous: Improve cerebral veouns drainage. HOB up. Avoid coughing, straining of ETT which raises jugular venous pressure.

Front 75

Why is BP high in a head injury patient?

Back 75

B/c whenever ICP is high, you have compensatory increase in mean arterial pressure. Almost all brain injury pts come in with HTN to compensate for change in CPP which needs to be atleast 70mmHg.

Front 76

What does hypotension in brain injury pts mean?

Back 76

Delatarious and concomitent injury.

Front 77

What is cushings triad?

Back 77

decreased HR
HTN
Irreg. resp

These are signs of increased ICP, >20mmHg

Front 78

Epidural hematomas s/sx

Back 78

have "lucid interval"
Head trauma-> LOC->vessel seals up (wake up)->then opens up again

Front 79

Subdural AKA sub arachnoid, hematomas s/sx

Back 79

Under the dura mater, lac of venous sinus. Bleeds develop slowly. Progressive LOC.

Front 80

Intracerebral hematomas s/sx

Back 80

Can be large or small. Collecting of blood in the brain. Deep in the brain, medically managed.

Front 81

Epidural treatment

Back 81

Inner surface of the skull and dura.
Needs to be drained.
Can clot or vasospasm and then rebleed.
Best prognosis

Front 82

Subdural treatment

Back 82

b/t the dura and the arachnoid. Develop slowly. Manage by intubation, use NDMB b/c Sch can increase ICP, no ketamine, no NG tubes. Hyperventilate (selectively) bc only lasts 6-8 hours.

Front 83

What is MINOR injury range on the GCS?

Back 83

13-15

Front 84

What is MODERATE injury range on the GCS

Back 84

9-12

Front 85

What is SEVERE injury range on the GCS?

Back 85

<9

Front 86

What are the goals in treating acute head injury?

Back 86

-Decrease ICP
-Maintain CPP 70mmHg
-Keeping MAP of 90 if beneficial bc ICP is high and need to keep CPP at 70

Front 87

What are the s/sx of increased ICP?

Back 87

Cushings triad
Pupil dilation
dizzy, double vision
papel edema (eyes, optic disc)
N/V
Change MS
Coma

Front 88

Down regulation of Sch

Back 88

-Have to give a lot of sch to do the job, but pt can't break it down b/c they have LESS Ach receptors.
-No hyperK+.
-Sensitive to NDMB.
-Example: MG