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Apex Neuro Flashcards

1
Q

What are the four types of glial cells?

A

Astrocytes

Ependymal cells

Oligodendrocytes

Microglia

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2
Q

What are Astrocytes?

A

Most Abundant type of glial cell

Regulates metabolic environment

Repair neuron after neuronal injury

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3
Q

Which glial cell produces CSF? Where?

A

Ependymal cells

3rd and 4th ventricles of spinal canal

Choroid Plexus

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4
Q

What cells form the myelin sheath in the CNS?

A

Oligodendrocytes

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5
Q

What cells from the myelin Sheath in the PNS?

A

Schwann

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6
Q

What cells phagocytize neuronal debris?

A

Microglia

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7
Q

What are the 4 lobes of the cerebral cortex?

A

Frontal

Parietal

Occipital

Temporal

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8
Q

Which lobe contains motor cortex?

A

Frontal

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9
Q

Which lobe contains somatic sensory ?

A

Parietal

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10
Q

Which lobe contains vision cortex?

A

Occipital

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11
Q

Which lobe contains auditory and speech centers? Which is understanding of speech? Which is motor control of speech?

A

Temporal

Wernicke’s - understanding

Broca’s - motor control

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12
Q

Name the 12 cranial nerves mnemonic?

A

O
O
O
To
Touch
And
Feel
Very
Good
Velvet
A
H

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13
Q

Name the 12 cranial nerves?

A

Olfactory - smell
Optic - vision
Oculomotor - eye movement
Trochlear - eye movement
Trigeminal -
Abducens - eye movement
Facial - movement, eyelid, taste anterior 2/3 tongue
Vestibulocochlear- hearing and balance
Glossopharyngeal - posterior 1/3 tongue
Vagus - Swallowing
Accessory - Shoulder shrug
Hypoglossal - Tongue movement

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14
Q

Which CN adducts the eye?

A

CN - 3

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15
Q

Which CN abducts the eye?

A

CN - 6

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16
Q

Which CN elevates the eye?

A

CN - 3

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17
Q

Which CN depresses the eye?

A

CN - 4

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18
Q

Which system do all cranial nerves reside in?

A

PNS

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19
Q

What is the only nerve that resides in the CNS?

A

CN2 (optic)

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20
Q

What is the tic douloureux?

A

Trigeminal neuralgia

(CN5)

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21
Q

What is Bells Palsy? What CN contributes to this problem?

A

Injury to the facial nerve (CN7)

Causes ipsilateral facial paralysis

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22
Q

What is the function of the CSF?

A

CSF -

  1. Cushions the brain
  2. Provides buoyancy
    3.Delievres optimal neurologic function
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23
Q

Where is CSF located?

A

-Ventricles
-Cisterns around the brain
-Subarachnoid space in the brain and spinal cord

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24
Q

Which regions of the brain are not protected by the BBB?

A

CTZ
Posterior pituitary
Pineal
Choroid plexus
Hypothalamus

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25
Q

Why are most parts of the brain protected by the BBB?

A
  • Has tight junctions
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26
Q

What is the normal CSF volume and specific gravity?

A

Volume - 150mL
Gravity - 1.002 - 1.009

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27
Q

Which cells produce CSF? how much is made per hour?

A

Ependymal cells of the choroid plexus

30ml/hr

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28
Q

CSF circulation mnemonic ?

A

Love
My
3
Silly
4
Lorn
Magpies

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29
Q

Which area reabsorbs CSF?

A

Venous circulation via the arachnoid villi in the superior sagittal sinus

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30
Q

What is the formula for Cerebral Blood Flow?

A

Cerebral perfusion pressure/ cerebral vascular pressure

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31
Q

Normal values for global, cortical, and, subcortical flow?

A

Global - 50mL/100g tissue or 15% of CO

Cortical - 75mL/100g tissue

Subcortical - 25ml/100g tissue

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32
Q

What are 5 determinants of CBF?

A
  1. CMRO2
  2. CPP
  3. Venous pressure
  4. PaCO2
  5. PaO2
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33
Q

Normal CMRO2?

A

3mL/O2

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34
Q

What increases CMRO2?

A

Hyperthermia
Seizures
Ketamine
Nitrous

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35
Q

What decreases CMRO2

A

Hypothermia
Halogenated anesthetics
Propofol
Etomidate
Barbiturates

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36
Q

A one degree drop in temperature, decreases CMRO2 by how much?

A

7%

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37
Q

Equation for CPP?

A

MAP - CVP or ICP (Whichever is higher)

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38
Q

What are the parameters for cerebral autoregulation?

A

50-150

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39
Q

What conditions impair venous drainage ?

A
  1. Jugular compression from improper head positioning
  2. Increased thoracic pressure (Coughing or PEEP)
  3. Vena cava thrombosis
  4. Vena cava syndrome
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40
Q

What is the relationship between PaCO2 and CBF?

A

pH of the CSF around the arterioles controls cerebral vascular resistance

PaCO2 of 40, CBF is 50mL/100g brain tissue

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41
Q

At what PaCO2 does maximal vasoconstriction occur?

A

PaCO2 25

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42
Q

At what PaCO2 does maximal vasodilation occur?

A

PaCO2 80-100

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43
Q

For every 1 mmHg increase or decrease in PaCO2, how much will CBF change?

A

1-2mL/100g/min

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44
Q

As a general rule, what is the relationship between CMRO2 and CBF? Exception?

A

As CMRO2 goes up, CBF goes up

As CMRO2 go down, CBF goes up

Anesthetic gases decouple this.

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45
Q

How does acidosis and alkalosis affect CBF?

A

Respiratory acidosis increases CBF

Respiratory alkalosis decreases CBF

*Metabolic conditions do not affect it

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46
Q

Does PaO2 affect CBF?

A

PaO2 below 60 causes cerebral vasodilation and increases CBF

PaO2 above 60 has NO affect

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47
Q

What is a normal ICP? When does cerebral HTN occur?

A

Normal 5-15

HTN > 20

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48
Q

When is ICP indicated? What is the gold standard?

A

Glasgow score < 7

Intraventricular catheter

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49
Q

Where can ICP be measured with bolt placement?

A

Over the convexity of the cerebral cortex

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50
Q

S&S of intracranial HTN

A

-Headache
-N/V
-Decreased LOC
-Seizure
-Coma
-Focal deficit
-Papilledema (Swelling of optic nerve)

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51
Q

What is the Monroe-Kellie hypothesis?

A

Pressure and volume equilibrium between the brain, blood, and csf.

If one increases the others must decrease or else the pressure increases

Brain, Blood, and CSF are all contained in a bony box (skull)

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52
Q

What is Cushing triad?

A

Intracranial HTN

Bradycardia
HTN
Irregular respirations

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53
Q

What are the four locations where the brain can herniate?

A

-Cingulate gyrus under the falx

-Surgery site or trauma

-Tentorium cerebelli

-Cerebellar tonsils through the foramen magnum

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54
Q

How does hyperventilation affect CBF? Ideal PaCO2?

A

Decreases PaCO2

Causes vasoconstriction - decreased CBF and ICP

Ideal 30-35

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55
Q

How does Co2 affect cerebral vessels?

A

Co2 dilates them which increases CBF and ICP

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56
Q

How does nitro and nipride affect ICP?

A

Vasodilates, increases ICP and CBF

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57
Q

What can happen if mannitol given with a disrupted BBB?

A

Can cause cerebral edema by increasing blood volume

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58
Q

Where do the anterior and posterior circulation of the brain converge?

A

Circle of Willis

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59
Q

What is the anterior circulation of the brain ?

A

Internal carotid arteries supply anterior circulation

  1. Aorta
  2. Carotid arteries
  3. Internal carotid
  4. Circle of Willis
  5. Cerebral hemispheres
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60
Q

Where does the anterior circulation enter through?

A

Enter the skull through the foramen lacerum

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61
Q

Where does the posterior circulation enter the skull through?

A

Foramen magnum

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62
Q

What is the posterior circulation of the brain?

A
  1. Aorta
  2. Subclavian arteries
  3. Vertebral arteries
  4. Basilar arteries
  5. Posterior fossa structures and cervical spinal cord
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63
Q

What is the role of the circle of Willis, what happens if one side is occluded?

A

Provide redundancy of blood flow to the brain

If one side becomes occluded, then the other side should be able to perfuse the affected areas

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64
Q

What is the timeline for tPA? Who should this be given to? Test to decide? Alternative to tPA?

A

Administered <4.5 hours after onset of symptoms

NEED CT

DO NOT GIVE TO hemorrhagic stroke

Aspirin is the alternative

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65
Q

Relationship between hyperglycemia and cerebral hypoxia?

A

During cerebral hypoxia, glucose is converted to lactic acid which destroys brain tissue

**CAUTION WITH IV FLUIDS THAT CONTAIN DEXTROSE

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66
Q

How is transmural pressure calculated?

A

MAP-ICP

MAP is the pressure pushing out on the blood vessel

ICP is the pressure pushing in on the blood vessel

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67
Q

Most common symptom of a Subarachnoid hemorrhage? Other symptoms?

A

Most common - Headache

50% lose consciousness

N/V

Meningismus (signs of meningitis)

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68
Q

What is the most significant source of morbidity and mortality in patients with a subarachnoid hemorrhage?

A

Cerebral vasospasm

More blood increases incidence of vasospasm

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69
Q

What is the incident of cerebral vasospasm ? When is it most likely to occur?

A

25%

Most like 4-9 days following SAH

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70
Q

What is the treatment for cerebral vasospasm?

A

Triple H therapy

Hypervolemia
HTN
Hemodilution to HCT of 30%

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71
Q

Which drug can be given to reduce mortality with a cerebral vasospasm?

A

Nimodipine

DOES NOT RELIEVE THE SPASM

but

it increases collateral flow

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72
Q

During a coiling procedure the aneurysm ruptures, what is the best treatment?

A

Give protamine to reverse heparin

Can give adenosine to arrest the heart so bleeding can be controlled

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73
Q

Calculate the Glasgow Coma Scale

A
74
Q

What GCS is consistent with a TBI?

A

<8

75
Q

How do you treat a patient with a intracerebral bleed who is on warfarin? What treatment is not the best option ?

A

Reverse Warfarin with FFP, Prothrombin concentrate or factor VIIa

Vitamin K is not the best option for acute reversal

76
Q

How do you treat a patient with a intracerebral bleed who is on Plavix? Aspirin?

A

**Give Platelets

Also may use VIIa

77
Q

What are the two common ways of reducing ICP that should be avoided in patients with a TBI?

A

Avoid hyperventilation because it can cause brain ischemia

Avoid steroids

78
Q

Is nitrous safe with a TBI?

A

No

79
Q

Key concepts to grand mal seizures

A

Generalized tonic-clonic

Tonic - whole body rigidity
Clonic - repetitive jerking

Respiratory arrest is common

Give propofol, diazepam or thiopental

80
Q

Key concepts to Focal Cortical seizures

A

Localized to cortical

Can be motor or sensory

Usually no LOC

81
Q

Key concepts to Absence seizures

A

Loss of awareness but stays awake

Common in children

82
Q

Key concepts of Akinetic seizures

A

Loss of LOC and results in falling and head injury

More common in children

83
Q

Key concepts of status elipepticus

A

Seizure > 30 minutes or 2 grand mal seizures without regaining consciousness

Respiratory arrest

84
Q

Relationship between etomidate and seizures

A

Can cause seizures in patients with a seizure history

Can cause myoclonus but not associated with increased EEG activity with patients that do not have a history

85
Q

What is the pathophysiology of Alzheimer’s?

A

Diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain

*Disrupts nicotinic Ach neurons

and cause apoptosis

86
Q

What drugs are used to treat Alzheimer’s? How does this effect anesthesia?

A

**Tries to restore Ach

Cholinesterase inhibitors

*****Causes increased duration action of Succ

87
Q

Pathophysiology of Parkinsons?

A

Dopaminergic neurons are destroyed

Causes an imbalance and increased Ach

88
Q

What drugs cause an increase of extrapyramidal effects with Parkinsons?

A

Reglan

Butyrophenones like haloperidol and droperidol

Phenothiazines like promethazine

89
Q

Most common eye complication during the perioperative period?

Most common cause of vision loss?

A

Corneal abrasion

Ischemic optic neuropathy

90
Q

Pathophysiology of ischemic optic neuropathy?

A

Venous congestion which reduces perfusion pressure

91
Q

Formula for ocular perfusion pressure?

A

MAP-Intraocular pressure

92
Q

What can increase intraocular pressure?

A

Increased abdominal pressure

Increased thoracic pressure

93
Q

What ocular arteries are at the highest risk?

A

Central retinal and posterior ciliary arteries

They are “watershed” areas which mean they lack anastomoses with other arteries

94
Q

Which surgical procedures have the highest risk of ION?

A

Prone
Wilson frame
Long duration
Large blood loss
Low ratio of colloid to crystalloid
Hypotension

95
Q

Which patient risk factors have the highest risk of ION?

A

Male sex
Obesity
Diabetes
Smoking
HTN
Old age
Atherosclerosis

96
Q

How is the spinal cord perfused?

A

1 Anterior spinal artery

2 Posterior spinal arteries

6-8 Radicular arteries

97
Q

What is the most important radicular artery? Which spinal segment does it typically enter?

A

Artery of Adamkiewicz

Supplies the anterior cord in the thoracolumbar region

T11-T12

98
Q

Where do sensory neurons enter the spinal cord?

A

Via the dorsal root

99
Q

Where do motor and autonomic neurons exit ?

A

Via the Ventral root

100
Q

What is the three neuron pathway of the spinal tracts?

A

First order - Periphery to spinal cord

Second order - Spinal cord to subcortical

Third order - Subcortical to Cerebral cortex

101
Q

** Describe the Dorsal Column Medial Lemniscal System

A

Transmits mechanoreceptor sensations:
-fine touch, proprioception, vibration, pressure

Capable of two point discrimination

Large, myelinated fibers

Transmits fast

More evolved system

102
Q

** Describe the anterolateral Spinothalamic tract

A

Transmits - pain, temperature, crude touch, tickle, itch, and sex

No Two point

Smaller, slow conducting fibers

Primitive system

103
Q

**What bedside exam assesses the corticospinal tract?

A

**Most important motor tract

Babinski Test

Normal response - Downward motion of all toes

Upper motor injury - Upward extension of big toe

Lower motor injury - No response

104
Q

How does an upper motor neuron injury present?

A

Hyperreflexia and spastic paralysis

105
Q

How does a lower motor neuron injury present ?

A

Impaired reflex and flaccid paralysis

106
Q

Pathophysiology of neurogenic shock?

A
  1. Impairment of cardioaccelerator fibers — unopposed cardiac vagal tone - bradycardia and reduced vagal tone
  2. Decreased SNS - vasodilation, venous pooling, decreased CO and BP
  3. Hypothermia - inability to shiver
  4. Hypothermia allows blood to flow towards periphery thus allowing more heat to escape
107
Q

Difference between neurogenic shock and hypovolemic shock?

A

Neurogenic - bradycardia, hypotension, hypothermia with pink and warm extremities

Hypovolemic - Tachycardia, hypotension, cool and clammy

108
Q

How long should succ be avoided in a spinal cord injury?

A

Okay for the first 24 hours

Then after 24 hours, do not use for 6 months - 1 year

109
Q

When does a patient with spinal cord injury become at risk for autonomic hyperreflexia? What factors contribute to this risk?

A

After 1-3 weeks

The higher the injury the more intense the response

85% will develop with injury above T6

110
Q

List 6 situations that can precipitate autonomic hyperreflexia? (AH)

A

Stimulation of hollow organs such as bladder, bowel, uterus

Bladder catherization

Surgery- especially cysto or colonoscopy

Bowel Movement

Cutaneous stimulation

Childbirth

111
Q

Classic presentation of autonomic hyperreflexia?

A

Hypertension and bradycardia

Also - nasal congestion, headache, blurred vision, MH

**This is because stimulation below the level of SCI triggers an SNS response that creates vasoconstriction that activates the baroreceptors

Body tries to fix this with vasodilation above the level of injury

112
Q

Anesthetic management for patients with AH?

A
  1. General or spinal
  2. Spinal is preferred over epidural
  3. Best treatment is to remove the stimulation causing the HTN
  4. Treat bradycardia with atropine or glyco
  5. Positive chronotrope will worsen HTN
  6. Lidocaine does not prevent AH
  7. Avoid succ
  8. May present in PACU
113
Q

Pathophysiology of ALS?

A

Degeneration of motor neurons in the corticospinal tract

Astrocyclic gliosis replaces affected motor neurons

114
Q

Management of ALS?

A

Consider post op mechanical ventilation

Avoid Succ

Chest weakness

Increased risk of pulmonary aspiration

115
Q

Describe Myasthenia Gravis

A

Autoimmune

IgG antibodies destroy post junctional, nicotinic acetylcholine receptors.

There is enough Ach but the receptors are destroyed

Muscle weakness

116
Q

What surgical procedure is performed to reduce Myasthenia gravis symptoms?

A

Removal of thymus gland which reduces circulating Anti-AchR IgG

117
Q

How does MG affect pregnancy?

A

1/3 of women have symptoms intensify

Crosses the placenta and causes weakness in 20% of neonates for up to 4 weeks

118
Q

**Difference in cholinergic crisis and myasthenic crisis? What test?

A

Tensilon test

119
Q

What is the first line treatment for MG?

A

Pyridostigmine (anticholinesterase)

120
Q

What can an overdose of anticholinesterase cause?

A

Cholinergic crisis

121
Q

What is the tensilon test?

A

Give 1-2mg of edrophonium

If symptoms improve then the patient had an exacerbation of myasthenic symptoms

If muscle weakness worsens then the patient is in cholinergic crisis - give anticholinergic

122
Q

**How do patients with MG respond to neuromuscular blockers?

A

-reduction in nicotinic receptors

Depolarizers - need less

Non depolarizers - need more

123
Q

Why are patients with MG prone to aspiration?

A

Bulbar muscle weakness - difficulty handling oral secretions

124
Q

What is Eaton Lambert syndrome?

A

Caused by IgG mediated destruction of the presynaptic voltage gated calcium channel at the presynaptic terminal

125
Q

Does Eaton-Lambert affect pre or post synaptic nerve terminals?

A

Pre (EAT the pre first)

Post synaptic are NOT affected

126
Q

Compare and contrast Eaton-Lambert and MG. Region affected?

A

EL - Presynaptic Ca channel

MG - Post Nm receptor

127
Q

Compare and contrast Eaton-Lambert and MG. Defect?

A

EL - Decreased Ach release

MG - Decreased response to Ach

128
Q

Compare and contrast Eaton-Lambert and MG. Common co-morbidities ?

A

EL - Small cell lung carcinoma

MG - Thymoma

129
Q

Compare and contrast Eaton-Lambert and MG. Response to Succ?

A

EL - sensitive

MG- Resistant - need more

130
Q

Compare and contrast Eaton-Lambert and MG. Response to non depolarizers?

A

EL - Sensitive

MG - Sensitive

131
Q

Compare and contrast Eaton-Lambert and MG. Effectiveness of AchE Inhibitors?

A

EL - Poor

MG - Adequate

132
Q

What is Guillain-Barre syndrome?

A

Acute idiopathic polyneuritis

An immunologic assault on myelin in the peripheral nerves.

Action potential can not be conducted

Usually last 4 weeks

133
Q

How does GB present?

A

Flu like illness for 1-3 weeks

Flaccid paralysis begins in distal extremities

Intercostal muscle weakness impairs ventilation

Facial and pharyngeal weakness

Sensory deficits like numbness/tingling

Autonomic dysfunction - tachycardia or bradycardia, hypotension or hypertension, diaphoresis

134
Q

What is familial periodic paralysis and how can you tell the difference between the two variants?

A

-Acute episodes of skeletal muscle weakness accompanied by hyper or hypokalemia

Hypokalemia - muscle weakness following glucose-insulin infusion

Hyperkalemia - muscle weakness after PO potassium is given

135
Q

Drugs to avoid with familial hypokalemic periodic paralysis?

A

Glucose
Beta 2
Succ
Potassium wasting diuretics

136
Q

What drug treats both types of familial periodic paralysis?

A

Acetazolamide - creates a non-anion gap acidosis

137
Q

Drugs to avoid with familial hyperkalemic periodic paralysis?

A

Succ
Potassium solutions like LR

138
Q

What condition needs to be avoided with familial periodic paralysis?

A

Hypo and hyperthermia

139
Q

Steps in MH?

A
  1. T tubule depolarized
  2. Ca enters myocyte through the dihydropyridine receptor
  3. Activates the ryanodine receptor (RYR1)
    4.RYR1 instructs the SR to release Ca but can’t be turned off
    5.SERCA2 pump tries to restore balance but uses ATP and O2 which increases CO2 production
  4. When all ATP is gone, the cell membrane breaks down and myoglobin and potassium are released into the systemic circulation
140
Q

Consequences of too much Ca inside skeletal myocyte. (8)

A

-Sustained muscle contraction
-Accelerated metabolic rate and depletion of ATP
-Increased O2 consumption
-Increased CO2 and heat production
-Mixed acidosis
-Sarcolemma breaks down
-K and myoglobin leak into systemic circulation
-Muscle rigidity

141
Q

Early S+S of MH?

A

Tachycardia
Tachypnea
Masseter spasm
Warm soda lime
Irregular heart rhythm

142
Q

Three conditions linked to MH?

A

King Denborough syndrome

Central core disease

Multiminicore disease

143
Q

What conditions are NOT linked to MH?

A

Deschene
Becker
Neuroleptic malignant syndrome
Myotonia congentia
Myotonic dystrophy
Osteogenesis imperfecta

144
Q

Intermediate S+S of MH?

A

Cyanosis
Irregular HR
Patient is warm to touch

145
Q

Late S+S of MH?

A

Muscle rigidity
Cola colored urine
Coagulopathy
Irregular HR
Overt hyperthermia

146
Q

Difference between trismus and MH? How to proceed?

A

Trismus - tight jaw that can be opened

MH- Tight jaw that cannot be opened

Trismus - normal and can proceed

147
Q

Will neuromuscular blockers treat MH?

A

NO

148
Q

Masseter spasm and jaw cannot be opened ? What is this?

A

Treat as MH

149
Q

What is the definitive test for MH?

A

Caffiene-Halothane contracture test

Need muscle biopsy

Anyone that has a masseter spasm should have this done

Risk for false negative since only 80% specificity

150
Q

How does dantrolene treat MH?

A

Halts Ca release from RYR1 receptor

Prevents Ca from entering the myocyte

151
Q

Most common side effects of dantrolene?

A

Muscle weakness and venous irritation

152
Q

How is dantrolene formulated? Prepared?

A

Each vial contains 20mg of Dantrolene and 3 g of mannitol

Need to be reconstituted with preservative free water

153
Q

Steps for treating MH?

A

D/C agent

Call for help

100% FiO2 >10L

Administer Dantrolene 2.5mg/kg and repeat every 5 minutes

Hyperventilate

Sodium Bicarb to correct lactic acidosis

Treat Hyperkalemia with CaCl and Insulin

Give Lidocaine 2mg/kg

IV hydration + diuretics

Cool patient to <38

Monitor coag and correct

154
Q

What drug class should not be given with Dantrolene?

A

CCB because of the hyperkalemia

155
Q

What is Duchenne’s Muscular Dystrophy

A

Absence of dystrophin which is critical in anchoring actin and myosin

Allows extra junctional receptors to populate

156
Q

How does Duchenne’s affect pulmonary function?

A

Kyphoscoliosis (restrictive lung disease)

Decrease reserve

Increased sections

Respiratory muscle weakness

157
Q

How does Duchenne’s affect cardiac? What EKG findings are seen?

A

Degeneration of cardiac muscle

Reduced contractility, papillary dysfunction, mitral regurg, cardiomyopathy, and CHF

Impaired conduction - ST and short PR interval

Increased R wave in lead 1 and deep Q waves in limb leads

158
Q

What is the gold standard for cardiac evaluation?

A

Echocardiogram

159
Q

What is Cobbs Angle?

A

Describes the magnitude of the spinal curvature

160
Q

What degree of Cobbs angle is an indication for surgery?

A

40-50

161
Q

What degree of Cobbs angle causes a decreased pulmonary reserve?

A

60

162
Q

What degree of Cobbs angle will the patient have pulmonary symptoms?

A

70

163
Q

What degree of Cobbs angle has significant impaired gas exchange? and high risk for pulmonary complications?

A

100

164
Q

With early respiratory complications from scoliosis, what PFTs are reduced? Which ones are normal?

A

FEV1 and FRC are reduced

FEV1/FVC ratio is normal

Will have decreased VC, TLC, FRC, and RV

165
Q

With late respiratory complications from scoliosis, what will be seen?

A

V/Q mismatch
Hypoxemia
Hypercarbia
Pulmonary HTN
Reduced response to hypercapnia
Cor pulmonale
Respiratory failure

166
Q

How does RA affect the airway?

A

Temporomandibular joint mobility (Hard to open the mouth)

Cricoarytenoid joints (Decreased glottic opening)

Cervical Spine - Atlanto-occipital subluxation with flexion
(Limited extension)

167
Q

What is the most common airway complication with RA? Why does this matter?

A

Atlantoaxial subluxation

Weaking of the transverse axial joint which can directly compress the spinal cord at the level of the foramen magnum - causing paralysis

168
Q

What is RA? Pathophysiology?

A

Autoimmune that attacks synovial joints

Cytokines - TNF and interleukin 1

Systemic inflammation in small and medium arteries

Stiff in the morning and feel better throughout the day

Fatigue

More common in women

169
Q

List complications of RA on each system -

A
170
Q

What is lupus?

A

Systemic autoimmune by the proliferation of antinuclear antibodies

Affects every organ except the spine through vasculitis and tissue destruction

171
Q

What is the most common consequence or lupus?

A

Polyarthritis and dermatitis

172
Q

What percent of patients with lupus have a butterfly rash?

A

30-50%

173
Q

Affects on the body’s systems from lupus?

A
174
Q

What drugs exacerbate lupus?

A

PISSED CHIMP
Pregnancy
Infection
Surgery
Stress
Enalapril
D-penicillamine
Captopril
Hydralazine
Isoniazid
Methyldopa
Procainamide

175
Q

What condition can be developed from Lupus?

A

Antiphospholipid syndrome

aPTT is prolonged but patients are prone to thrombus

Risk for stroke, DVT, and PE

176
Q

What is myotonic dystrophy?

A

Prolonged contracture after a voluntary contraction resulting from dysfunctional calcium

**Can affect airway

177
Q

What three things can contribute to myotonic dystrophy?

A

Succ
Reversals
Hypothermia

178
Q

Pathophysiology of Marfan?

A

Connective tissue disorder through autosomal dominant trait

179
Q

What are people with Marfan at risk for?

A

Aortic dissection
Mitral valve prolapse
MR
Aortic regurgitation
Cardiac Tamponade

Spontaneous pneumothorax

180
Q

What is Ehlers-Danlos syndrome? What is important ?

A

Disorder of procollagen and collagen

Risk of bleeding due to vessel integrity

Avoid regional, IM, and line placement

Pneumothorax is also common

Neuro (7 decks)

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