Apex Neuro Flashcards
(180 cards)
1
Q
What are the four types of glial cells?
A
Astrocytes
Ependymal cells
Oligodendrocytes
Microglia
2
Q
What are Astrocytes?
A
Most Abundant type of glial cell
Regulates metabolic environment
Repair neuron after neuronal injury
3
Q
Which glial cell produces CSF? Where?
A
Ependymal cells
3rd and 4th ventricles of spinal canal
Choroid Plexus
4
Q
What cells form the myelin sheath in the CNS?
A
Oligodendrocytes
5
Q
What cells from the myelin Sheath in the PNS?
A
Schwann
6
Q
What cells phagocytize neuronal debris?
A
Microglia
7
Q
What are the 4 lobes of the cerebral cortex?
A
Frontal
Parietal
Occipital
Temporal
8
Q
Which lobe contains motor cortex?
A
Frontal
9
Q
Which lobe contains somatic sensory ?
A
Parietal
10
Q
Which lobe contains vision cortex?
A
Occipital
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
12
Q
Name the 12 cranial nerves mnemonic?
A
O
O
O
To
Touch
And
Feel
Very
Good
Velvet
A
H
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
14
Q
Which CN adducts the eye?
A
CN - 3
15
Q
Which CN abducts the eye?
A
CN - 6
16
Q
Which CN elevates the eye?
A
CN - 3
17
Q
Which CN depresses the eye?
A
CN - 4
18
Q
Which system do all cranial nerves reside in?
A
PNS
19
Q
What is the only nerve that resides in the CNS?
A
CN2 (optic)
20
Q
What is the tic douloureux?
A
Trigeminal neuralgia
(CN5)
21
Q
What is Bells Palsy? What CN contributes to this problem?
A
Injury to the facial nerve (CN7)
Causes ipsilateral facial paralysis
22
Q
What is the function of the CSF?
A
CSF -
- Cushions the brain
- Provides buoyancy
3.Delievres optimal neurologic function
23
Q
Where is CSF located?
A
-Ventricles
-Cisterns around the brain
-Subarachnoid space in the brain and spinal cord
24
Q
Which regions of the brain are not protected by the BBB?
A
CTZ
Posterior pituitary
Pineal
Choroid plexus
Hypothalamus
25
Why are most parts of the brain protected by the BBB?
- Has tight junctions
26
What is the normal CSF volume and specific gravity?
Volume - 150mL
Gravity - 1.002 - 1.009
27
Which cells produce CSF? how much is made per hour?
Ependymal cells of the choroid plexus
30ml/hr
28
CSF circulation mnemonic ?
Love
My
3
Silly
4
Lorn
Magpies
29
Which area reabsorbs CSF?
Venous circulation via the arachnoid villi in the superior sagittal sinus
30
What is the formula for Cerebral Blood Flow?
Cerebral perfusion pressure/ cerebral vascular pressure
31
Normal values for global, cortical, and, subcortical flow?
Global - 50mL/100g tissue or 15% of CO
Cortical - 75mL/100g tissue
Subcortical - 25ml/100g tissue
32
What are 5 determinants of CBF?
1. CMRO2
2. CPP
3. Venous pressure
4. PaCO2
5. PaO2
33
Normal CMRO2?
3mL/O2
34
What increases CMRO2?
Hyperthermia
Seizures
Ketamine
Nitrous
35
What decreases CMRO2
Hypothermia
Halogenated anesthetics
Propofol
Etomidate
Barbiturates
36
A one degree drop in temperature, decreases CMRO2 by how much?
7%
37
Equation for CPP?
MAP - CVP or ICP (Whichever is higher)
38
What are the parameters for cerebral autoregulation?
50-150
39
What conditions impair venous drainage ?
1. Jugular compression from improper head positioning
2. Increased thoracic pressure (Coughing or PEEP)
3. Vena cava thrombosis
4. Vena cava syndrome
40
What is the relationship between PaCO2 and CBF?
pH of the CSF around the arterioles controls cerebral vascular resistance
PaCO2 of 40, CBF is 50mL/100g brain tissue
41
At what PaCO2 does maximal vasoconstriction occur?
PaCO2 25
42
At what PaCO2 does maximal vasodilation occur?
PaCO2 80-100
43
For every 1 mmHg increase or decrease in PaCO2, how much will CBF change?
1-2mL/100g/min
44
As a general rule, what is the relationship between CMRO2 and CBF? Exception?
As CMRO2 goes up, CBF goes up
As CMRO2 go down, CBF goes up
Anesthetic gases decouple this.
45
How does acidosis and alkalosis affect CBF?
Respiratory acidosis increases CBF
Respiratory alkalosis decreases CBF
*Metabolic conditions do not affect it
46
Does PaO2 affect CBF?
PaO2 below 60 causes cerebral vasodilation and increases CBF
PaO2 above 60 has NO affect
47
What is a normal ICP? When does cerebral HTN occur?
Normal 5-15
HTN > 20
48
When is ICP indicated? What is the gold standard?
Glasgow score < 7
Intraventricular catheter
49
Where can ICP be measured with bolt placement?
Over the convexity of the cerebral cortex
50
S&S of intracranial HTN
-Headache
-N/V
-Decreased LOC
-Seizure
-Coma
-Focal deficit
-Papilledema (Swelling of optic nerve)
51
What is the Monroe-Kellie hypothesis?
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)
52
What is Cushing triad?
Intracranial HTN
Bradycardia
HTN
Irregular respirations
53
What are the four locations where the brain can herniate?
-Cingulate gyrus under the falx
-Surgery site or trauma
-Tentorium cerebelli
-Cerebellar tonsils through the foramen magnum
54
How does hyperventilation affect CBF? Ideal PaCO2?
Decreases PaCO2
Causes vasoconstriction - decreased CBF and ICP
Ideal 30-35
55
How does Co2 affect cerebral vessels?
Co2 dilates them which increases CBF and ICP
56
How does nitro and nipride affect ICP?
Vasodilates, increases ICP and CBF
57
What can happen if mannitol given with a disrupted BBB?
Can cause cerebral edema by increasing blood volume
58
Where do the anterior and posterior circulation of the brain converge?
Circle of Willis
59
What is the anterior circulation of the brain ?
Internal carotid arteries supply anterior circulation
1. Aorta
2. Carotid arteries
3. Internal carotid
4. Circle of Willis
5. Cerebral hemispheres
60
Where does the anterior circulation enter through?
Enter the skull through the foramen lacerum
61
Where does the posterior circulation enter the skull through?
Foramen magnum
62
What is the posterior circulation of the brain?
1. Aorta
2. Subclavian arteries
3. Vertebral arteries
4. Basilar arteries
5. Posterior fossa structures and cervical spinal cord
63
What is the role of the circle of Willis, what happens if one side is occluded?
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
64
What is the timeline for tPA? Who should this be given to? Test to decide? Alternative to tPA?
Administered <4.5 hours after onset of symptoms
NEED CT
DO NOT GIVE TO hemorrhagic stroke
Aspirin is the alternative
65
Relationship between hyperglycemia and cerebral hypoxia?
During cerebral hypoxia, glucose is converted to lactic acid which destroys brain tissue
****CAUTION WITH IV FLUIDS THAT CONTAIN DEXTROSE
66
How is transmural pressure calculated?
MAP-ICP
MAP is the pressure pushing out on the blood vessel
ICP is the pressure pushing in on the blood vessel
67
Most common symptom of a Subarachnoid hemorrhage? Other symptoms?
Most common - Headache
50% lose consciousness
N/V
Meningismus (signs of meningitis)
68
What is the most significant source of morbidity and mortality in patients with a subarachnoid hemorrhage?
Cerebral vasospasm
More blood increases incidence of vasospasm
69
What is the incident of cerebral vasospasm ? When is it most likely to occur?
25%
Most like 4-9 days following SAH
70
What is the treatment for cerebral vasospasm?
Triple H therapy
Hypervolemia
HTN
Hemodilution to HCT of 30%
71
Which drug can be given to reduce mortality with a cerebral vasospasm?
Nimodipine
DOES NOT RELIEVE THE SPASM
but
it increases collateral flow
72
During a coiling procedure the aneurysm ruptures, what is the best treatment?
Give protamine to reverse heparin
Can give adenosine to arrest the heart so bleeding can be controlled
73
Calculate the Glasgow Coma Scale
74
What GCS is consistent with a TBI?
<8
75
How do you treat a patient with a intracerebral bleed who is on warfarin? What treatment is not the best option ?
Reverse Warfarin with FFP, Prothrombin concentrate or factor VIIa
Vitamin K is not the best option for acute reversal
76
How do you treat a patient with a intracerebral bleed who is on Plavix? Aspirin?
**Give Platelets
Also may use VIIa
77
What are the two common ways of reducing ICP that should be avoided in patients with a TBI?
Avoid hyperventilation because it can cause brain ischemia
Avoid steroids
78
Is nitrous safe with a TBI?
No
79
Key concepts to grand mal seizures
Generalized tonic-clonic
Tonic - whole body rigidity
Clonic - repetitive jerking
Respiratory arrest is common
Give propofol, diazepam or thiopental
80
Key concepts to Focal Cortical seizures
Localized to cortical
Can be motor or sensory
Usually no LOC
81
Key concepts to Absence seizures
Loss of awareness but stays awake
Common in children
82
Key concepts of Akinetic seizures
Loss of LOC and results in falling and head injury
More common in children
83
Key concepts of status elipepticus
Seizure > 30 minutes or 2 grand mal seizures without regaining consciousness
Respiratory arrest
84
Relationship between etomidate and seizures
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
What is the pathophysiology of Alzheimer's?
Diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain
*Disrupts nicotinic Ach neurons
and cause apoptosis
86
What drugs are used to treat Alzheimer's? How does this effect anesthesia?
**Tries to restore Ach
Cholinesterase inhibitors
*****Causes increased duration action of Succ
87
Pathophysiology of Parkinsons?
Dopaminergic neurons are destroyed
Causes an imbalance and increased Ach
88
What drugs cause an increase of extrapyramidal effects with Parkinsons?
Reglan
Butyrophenones like haloperidol and droperidol
Phenothiazines like promethazine
89
Most common eye complication during the perioperative period?
Most common cause of vision loss?
Corneal abrasion
Ischemic optic neuropathy
90
Pathophysiology of ischemic optic neuropathy?
Venous congestion which reduces perfusion pressure
91
Formula for ocular perfusion pressure?
MAP-Intraocular pressure
92
What can increase intraocular pressure?
Increased abdominal pressure
Increased thoracic pressure
93
What ocular arteries are at the highest risk?
Central retinal and posterior ciliary arteries
They are "watershed" areas which mean they lack anastomoses with other arteries
94
Which surgical procedures have the highest risk of ION?
Prone
Wilson frame
Long duration
Large blood loss
Low ratio of colloid to crystalloid
Hypotension
95
Which patient risk factors have the highest risk of ION?
Male sex
Obesity
Diabetes
Smoking
HTN
Old age
Atherosclerosis
96
How is the spinal cord perfused?
1 Anterior spinal artery
2 Posterior spinal arteries
6-8 Radicular arteries
97
What is the most important radicular artery? Which spinal segment does it typically enter?
Artery of Adamkiewicz
Supplies the anterior cord in the thoracolumbar region
T11-T12
98
Where do sensory neurons enter the spinal cord?
Via the dorsal root
99
Where do motor and autonomic neurons exit ?
Via the Ventral root
100
What is the three neuron pathway of the spinal tracts?
First order - Periphery to spinal cord
Second order - Spinal cord to subcortical
Third order - Subcortical to Cerebral cortex
101
**** Describe the Dorsal Column Medial Lemniscal System
Transmits mechanoreceptor sensations:
-fine touch, proprioception, vibration, pressure
Capable of two point discrimination
Large, myelinated fibers
Transmits fast
More evolved system
102
**** Describe the anterolateral Spinothalamic tract
Transmits - pain, temperature, crude touch, tickle, itch, and sex
No Two point
Smaller, slow conducting fibers
Primitive system
103
**What bedside exam assesses the corticospinal tract?
**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
How does an upper motor neuron injury present?
Hyperreflexia and spastic paralysis
105
How does a lower motor neuron injury present ?
Impaired reflex and flaccid paralysis
106
Pathophysiology of neurogenic shock?
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
Difference between neurogenic shock and hypovolemic shock?
Neurogenic - bradycardia, hypotension, hypothermia with pink and warm extremities
Hypovolemic - Tachycardia, hypotension, cool and clammy
108
How long should succ be avoided in a spinal cord injury?
Okay for the first 24 hours
Then after 24 hours, do not use for 6 months - 1 year
109
When does a patient with spinal cord injury become at risk for autonomic hyperreflexia? What factors contribute to this risk?
After 1-3 weeks
The higher the injury the more intense the response
85% will develop with injury above T6
110
List 6 situations that can precipitate autonomic hyperreflexia? (AH)
Stimulation of hollow organs such as bladder, bowel, uterus
Bladder catherization
Surgery- especially cysto or colonoscopy
Bowel Movement
Cutaneous stimulation
Childbirth
111
Classic presentation of autonomic hyperreflexia?
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
Anesthetic management for patients with AH?
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
Pathophysiology of ALS?
Degeneration of motor neurons in the corticospinal tract
Astrocyclic gliosis replaces affected motor neurons
114
Management of ALS?
Consider post op mechanical ventilation
Avoid Succ
Chest weakness
Increased risk of pulmonary aspiration
115
Describe Myasthenia Gravis
Autoimmune
IgG antibodies destroy post junctional, nicotinic acetylcholine receptors.
There is enough Ach but the receptors are destroyed
Muscle weakness
116
What surgical procedure is performed to reduce Myasthenia gravis symptoms?
Removal of thymus gland which reduces circulating Anti-AchR IgG
117
How does MG affect pregnancy?
1/3 of women have symptoms intensify
Crosses the placenta and causes weakness in 20% of neonates for up to 4 weeks
118
**Difference in cholinergic crisis and myasthenic crisis? What test?
Tensilon test
119
What is the first line treatment for MG?
Pyridostigmine (anticholinesterase)
120
What can an overdose of anticholinesterase cause?
Cholinergic crisis
121
What is the tensilon test?
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
**How do patients with MG respond to neuromuscular blockers?
-reduction in nicotinic receptors
Depolarizers - need less
Non depolarizers - need more
123
Why are patients with MG prone to aspiration?
Bulbar muscle weakness - difficulty handling oral secretions
124
What is Eaton Lambert syndrome?
Caused by IgG mediated destruction of the presynaptic voltage gated calcium channel at the presynaptic terminal
125
Does Eaton-Lambert affect pre or post synaptic nerve terminals?
Pre (EAT the pre first)
Post synaptic are NOT affected
126
Compare and contrast Eaton-Lambert and MG. Region affected?
EL - Presynaptic Ca channel
MG - Post Nm receptor
127
Compare and contrast Eaton-Lambert and MG. Defect?
EL - Decreased Ach release
MG - Decreased response to Ach
128
Compare and contrast Eaton-Lambert and MG. Common co-morbidities ?
EL - Small cell lung carcinoma
MG - Thymoma
129
Compare and contrast Eaton-Lambert and MG. Response to Succ?
EL - sensitive
MG- Resistant - need more
130
Compare and contrast Eaton-Lambert and MG. Response to non depolarizers?
EL - Sensitive
MG - Sensitive
131
Compare and contrast Eaton-Lambert and MG. Effectiveness of AchE Inhibitors?
EL - Poor
MG - Adequate
132
What is Guillain-Barre syndrome?
Acute idiopathic polyneuritis
An immunologic assault on myelin in the peripheral nerves.
Action potential can not be conducted
Usually last 4 weeks
133
How does GB present?
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
What is familial periodic paralysis and how can you tell the difference between the two variants?
-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
Drugs to avoid with familial hypokalemic periodic paralysis?
Glucose
Beta 2
Succ
Potassium wasting diuretics
136
What drug treats both types of familial periodic paralysis?
Acetazolamide - creates a non-anion gap acidosis
137
Drugs to avoid with familial hyperkalemic periodic paralysis?
Succ
Potassium solutions like LR
138
What condition needs to be avoided with familial periodic paralysis?
Hypo and hyperthermia
139
Steps in MH?
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
6. When all ATP is gone, the cell membrane breaks down and myoglobin and potassium are released into the systemic circulation
140
Consequences of too much Ca inside skeletal myocyte. (8)
-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
Early S+S of MH?
Tachycardia
Tachypnea
Masseter spasm
Warm soda lime
Irregular heart rhythm
142
Three conditions linked to MH?
King Denborough syndrome
Central core disease
Multiminicore disease
143
What conditions are NOT linked to MH?
Deschene
Becker
Neuroleptic malignant syndrome
Myotonia congentia
Myotonic dystrophy
Osteogenesis imperfecta
144
Intermediate S+S of MH?
Cyanosis
Irregular HR
Patient is warm to touch
145
Late S+S of MH?
Muscle rigidity
Cola colored urine
Coagulopathy
Irregular HR
Overt hyperthermia
146
Difference between trismus and MH? How to proceed?
Trismus - tight jaw that can be opened
MH- Tight jaw that cannot be opened
Trismus - normal and can proceed
147
Will neuromuscular blockers treat MH?
NO
148
Masseter spasm and jaw cannot be opened ? What is this?
Treat as MH
149
What is the definitive test for MH?
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
How does dantrolene treat MH?
Halts Ca release from RYR1 receptor
Prevents Ca from entering the myocyte
151
Most common side effects of dantrolene?
Muscle weakness and venous irritation
152
How is dantrolene formulated? Prepared?
Each vial contains 20mg of Dantrolene and 3 g of mannitol
Need to be reconstituted with preservative free water
153
Steps for treating MH?
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
What drug class should not be given with Dantrolene?
CCB because of the hyperkalemia
155
What is Duchenne's Muscular Dystrophy
Absence of dystrophin which is critical in anchoring actin and myosin
Allows extra junctional receptors to populate
156
How does Duchenne's affect pulmonary function?
Kyphoscoliosis (restrictive lung disease)
Decrease reserve
Increased sections
Respiratory muscle weakness
157
How does Duchenne's affect cardiac? What EKG findings are seen?
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
What is the gold standard for cardiac evaluation?
Echocardiogram
159
What is Cobbs Angle?
Describes the magnitude of the spinal curvature
160
What degree of Cobbs angle is an indication for surgery?
40-50
161
What degree of Cobbs angle causes a decreased pulmonary reserve?
60
162
What degree of Cobbs angle will the patient have pulmonary symptoms?
70
163
What degree of Cobbs angle has significant impaired gas exchange? and high risk for pulmonary complications?
100
164
With early respiratory complications from scoliosis, what PFTs are reduced? Which ones are normal?
FEV1 and FRC are reduced
FEV1/FVC ratio is normal
Will have decreased VC, TLC, FRC, and RV
165
With late respiratory complications from scoliosis, what will be seen?
V/Q mismatch
Hypoxemia
Hypercarbia
Pulmonary HTN
Reduced response to hypercapnia
Cor pulmonale
Respiratory failure
166
How does RA affect the airway?
Temporomandibular joint mobility (Hard to open the mouth)
Cricoarytenoid joints (Decreased glottic opening)
Cervical Spine - Atlanto-occipital subluxation with flexion
(Limited extension)
167
What is the most common airway complication with RA? Why does this matter?
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
What is RA? Pathophysiology?
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
List complications of RA on each system -
170
What is lupus?
Systemic autoimmune by the proliferation of antinuclear antibodies
Affects every organ except the spine through vasculitis and tissue destruction
171
What is the most common consequence or lupus?
Polyarthritis and dermatitis
172
What percent of patients with lupus have a butterfly rash?
30-50%
173
Affects on the body's systems from lupus?
174
What drugs exacerbate lupus?
PISSED CHIMP
Pregnancy
Infection
Surgery
Stress
Enalapril
D-penicillamine
Captopril
Hydralazine
Isoniazid
Methyldopa
Procainamide
175
What condition can be developed from Lupus?
Antiphospholipid syndrome
aPTT is prolonged but patients are prone to thrombus
Risk for stroke, DVT, and PE
176
What is myotonic dystrophy?
Prolonged contracture after a voluntary contraction resulting from dysfunctional calcium
**Can affect airway
177
What three things can contribute to myotonic dystrophy?
Succ
Reversals
Hypothermia
178
Pathophysiology of Marfan?
Connective tissue disorder through autosomal dominant trait
179
What are people with Marfan at risk for?
Aortic dissection
Mitral valve prolapse
MR
Aortic regurgitation
Cardiac Tamponade
Spontaneous pneumothorax
180
What is Ehlers-Danlos syndrome? What is important ?
Disorder of procollagen and collagen
Risk of bleeding due to vessel integrity
Avoid regional, IM, and line placement
Pneumothorax is also common
