UNIT 7 Neuro Flashcards

Question

When is ICP measurement indicated? What is the gold standard for measurement?

Answer 1

when GCS <7 intraventricular catheter is the gold standard other ways: - subdural bolt - catheter placed over the convexity of the cerebral cortex

Answer 2

``` HA N/V papilledema (swelling of the optic nerve) focal neurologic deficit decreased LOC seizures coma ```

Answer 3

- if one component increases in volume, another component must decrease in order to maintain constant pressure - remember intracranial compliance curve

Answer 4

**indicates intracranial hypertension** - HTN - bradycardia - irregular respirations increased ICP --> decreased CPP w/ compensatory HTN --> baroreceptor reflex activation compression of medulla --> irregular respirations

Answer 5

1. of the cingulate gyrus under the falx 2. transtenotorial 3. cerebellar tonsils via the foramen magnum 4. via a site of surgery or trauma

Answer 6

- CO2 dilates vessels = decreased CVR = increases CBF = increases ICP - **hyperventilation causes vasoconstriction and decreases CBF = decreases ICP** - **lowering PaCO2 <30 increases the risk of cerebral ischemia d/t vasoconstriction & L shift of the oxyHgb dissociation curve** - Don’t hyperventilate the PaCO2 below 30!

Answer 7

cerebral vasodilators = increases CBF = increase ICP

Answer 8

head elevation >30 degrees facilitates venous drainage away from the brain neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP head down positions increase CBV & ICP

Answer 9

0.25-1g/kg increases serum osm & "pulls" water across the BBB towards the bloodstream for excretion - **if BBB is disrupted, mannitol enters the brain & promotes = cerebral edema** - **mannitol transiently increases blood volume, which can increase ICP & stress the failing heart** bad for low EF patients!!!!!!

Answer 10

converge at the circle of willis anterior ICA enter skull via foramen lacerum aorta --> carotid --> ICA --> circle of willis --> cerebral hemispheres posterior vertebral a enter skull via foramen magnum aorta --> SC --> vertebral --> basilar --> posterior fossa structures & cervical SC

Answer 11

primary function of the circle of willis is to provide redundancy of blood flow in the brain. If one side of the circle becomes occluded, the other side should theoretically be able to perfuse the affected areas of the brain ``` - Basilar artery - Posterior cerebral artery - Posterior communicating artery - Middle cerebral artery - Anterior cerebral artery - Anterior cerebral communicating artery ```

Answer 12

CVA d/t thrombosis diagnosis must be made by emergent head CT prior to administration if tx can begin <3hrs after onset of symptoms, the pt should receive tPA - aspirin is acceptable if tPA cannot be administered

Answer 13

During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue & is associated w/ worse outcomes monitor serum glucose, treat hyperglycemia, be careful administering dextrose containing IVF

Answer 14

an increased transmural pressure predisposes the aneurysm to rupture. transmural pressure = MAP - ICP MAP = pressure pushing outward against the aneurysmal sac ICP = counterpressure that pushes against it. --> creates a tamponade effect risk of rupture is increased by HTN and/or acute reduction in ICP

Answer 15

WHOL (worst HA of life) others - LOC (50%) - neurologic deficits - N/V - photophobia - fever

Answer 16

**cerebral vasospasm- due to delayed contraction of the cerebral arteries** can lead to cerebral infarction Free Hgb that is in contact w/ the outer surface of the cerebral arteries increases the risk there is a correlation b/n amount of blood observed on CT & vasospasm incidence

Answer 17

25% of patients | most likely 4-9days after SAH!!!!!!!!!!!!!!!

Answer 18

triple H therapy (hypervolemia, HTN, permissive hemodilution to Hct 27-32%) nimodipine (CCB) reduces M&M associated w/ vasospasm --> doesn't actual reduce the spasm, but increases the collateral blood flow

Answer 19

- **Give them protamine 1mg/100U heparin** - **low/normal MAP** - **adenosine to temporarily arrest the heart to see where the bleeding is**

Answer 20

eyes (1-4) motor (1-6) verbal (1-5)

Answer 21

- FFP - prothrombin complex concentrate - recombinant factor 7a vitamin K isn't the best option for acute warfarin reversal

Answer 22

We need to reverse clopidogrel with a **platelet transfusion (aspirin can be reversed this way too)** there is also evidence of reversal w/ recombinant factor VIIa

Answer 23

**hyperventilation**- can worsen cerebral ischemia + it's only indicated as a temp measure **steroids- worsen neurologic outcome in traumatic brain injury**

Answer 24

No | other injuries, such as pneumothorax, may only become evident after anesthetic induction & PPV

Answer 25

grand mal - generalized tonic/clonic activity - **apnea, respiratory arrest --> hypoxia** - tx: propofol, diazepam - surgical: vagal nerve stim or rsxn of foci focal cortical - localized to a particular cortical region - can be motor or sensory - usually no LOC absence (petit mal) - **temporary loss of awareness** staring into space and blinking - more common in children akinetic - **temporary lost of consciousness and loss of postural tone** (can result in fall & TBI) - more common in children status epilepticus - seizure activity >30min or 2 grand mal w/out regaining consciousness in between - resp arrest --> hypoxia - tx: phenobarb, phenytoin, benzos, propofol, and even GA

Answer 26

etomidate commonly causes myoclonus. **This is not associated w/ increased EEG activity in those that do not have epilepsy** In those w/ sz disorders, etomidate (or methohexital or alfentanil) increases EEG activity and can be used to help determine location of seizure foci during cortical mapping

Answer 27

diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain consequences: - dysfunctional synaptic transmission (most notable at nACh neurons) - apoptosis (programmed cell death)

Answer 28

tx is palliative & aims to restore the [ACh]; cholinesterase inhibitors (tacrine, donepezil, rivastigmine, galantamine) cholinesterase inhibitors increase the DOA of succ, although the clinical significance is debatable

Answer 29

dopaminergic neurons in the basal ganglia are destroyed ---> imbalance of DA & ACh (relative ACh increase) this leads to suppression of corticospinal motor system + overactivity of extrapyramidal motor system -skeletal muscle tremor - akinesia- inability to initiate purposeful movement - rigidity-limited movement

Answer 30

- reglan - butyrophenones (haldol, droperidol) - phenothiazines (promethazine)

Answer 31

corneal abrasion ischemic optic neuropathy = most common cause of vision loss

Answer 32

ischemia of the optic nerve. Most likely explanation is that venous congestion in the optic canal reduces perfusion pressure ocular PP = MAP - intraocular pressure central retinal & posterior ciliary arteries are at highest risk b/c they are "watershed" areas -- they lack anastomoses w/ other arteries

Answer 33

spinal surgery in the prone position = most significant risk other factors: - prone - use of Wilson frame = BAD. - long duration of anesthesia - large EBL - low colloid:crystalloid resus - hypotension - male - obesity - DM - HTN - smoking - old age - atherosclerosis CRAE: the other eye injury is from occlusion like eyeball is squished on horseshoe frame

Answer 34

SC is perfused by: 1) 1 anterior spinal artery (anterior 2/3 of SC) 2) 2 posterior spinal arteries (posterior 1/3 of SC) 3) 6-8 radicular arteries

Answer 35

artery of Adamkiewicz along w/ the anterior spinal artery, the artery of adamkiewicz supplies the anterior cord in the thoracolumbar region. Most commonly originates b/n T11-T12

Answer 36

sensory neurons from the periphery via the dorsal nerve root motor & autonomic neurons exit via the ventral nerve root

Answer 37

dorsal column (medial lemniscal system) - **transmits mechanoreceptor sensations (fine touch, proprioception, vibration, pressure)** - capable of 2 point discrimination (high degree of localization) - large, myelinated, faster fibers anterolateral system (spinothalamic tract) - **transmits pain, temp, crude touch, tickle, itch, sexual sensation** - no 2 point discrimination - smaller, myelinated, slower fibers

Answer 38

most important motor pathway (often referred to as the pyramidal tract, all others are collectively the extrapyramidal tract) Babinski test (firm stimulus to underside of foot) yields: - normal: downward motion of all the toes - upper motor neuron injury: upward extension of big toe + fanning of the others = abnormal, positive test - lower motor neuron injury: no response

Answer 39

upper motor neurons begin in the cerebral cortex & end in the ventral horn of the SC, while the lower motor neurons begin in the ventral horn & end at the NMJ upper motor neuron injury presents w/ hyperreflexia & spastic paralysis lower motor neuron injury presents w/ impaired reflexes & flaccid paralysis

Answer 40

impairment of cardioaccelerator fibers (T1-T4) --> unopposed cardiac vagal tone --> bradycardia & decreased inotropy decreased SNS tone --> vasodilation --> venous pooling --> decreased CO & BP impairment of sympathetic pathways from hypothalamus to blood vessels --> inability to vasoconstrict or shiver --> hypothermia

Answer 41

neurogenic: **bradycardia, hypotension, hypothermia w/ pink, warm extremities d/t cutaneous vasodilation** hypovolemia: **tachycardia**, hypotension, cool, clammy extremities

Answer 42

avoid if >24hrs post injury | do not use for at least 6months thereafter, some books say 1yr

Answer 43

It occurs after the neurogenic shock phase ends (1-3 weeks), the body begins to mend itself in a pathologic and disorganized way, putting the pt at risk for autonomic hyperreflexia. up to 85% of patients w/ injury >T6 will develop

Answer 44

``` sitmulation of the hollow organs (bladder, bowel, or uterus) bladder catheterization surgery (esp cysto, colonoscopy) bowel movement cutaneous stimulation childbirth ```

Answer 45

classic presentation = HTN & bradycardia! So choose meds that treat hypertension. stimulation below the level of SCI triggers sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury --> baroreceptor activation in carotid bodies (bradycardia) --> body attempts to reduce afterload w/ vasodilation above the level of the injury. other s/s: - reflex vasodilation above level of SC injury --> **nasal stuffiness** - HTN --> HA/blurred vision - malignant HTN --> CVA, sz, LV failure, dysrhythmias, pulmonary edema, and/or MI, seizure, or stroke

Answer 46

prevent stimulation to the area below level of injury to prevent AH! - GA or spinal = best - epidural not as good for laboring mother b/c doesn't inhibit sacral nerve roots as much - tx HTN w/ removal of stim, deepen IA, + rapid vasodilator (SNP) - tx bradycardia w/ atropine/glyco - **avoid meds that increase HR & vasoconstrict** - avoid sux x6months - monitor for AH closely in the immediate post-op period, when anesthesia is wearing off.

Answer 47

**Progressive degeneration of motor neurons in the corticospinal tract** Astrocytic gliosis replaces the affected motor neurons. Both the upper & the lower motor neurons are affected. Etiology is unknown - Avoid sux due to risk of hyperkalemia - They have increased sensitivity to nondepolarizers, so decrease the dose - upper motor produces hyperreactive responses - ortho hypotension - bulbar atrophy

Answer 48

- no clear evidence that supports one technique over another - avoid sux (hyperK+) - increased sensitivity to NDMR: so decrease the dose - bulbar m dysfunction increases risk of aspiration - chest weakness decreases VC & MMV - consider post-op mechanical ventilation

Answer 49

autoimmune disease **IgG Ab destroy post-junctional nAChR at the NMJ** (ACh is present in sufficient quantity, the receptors just aren't there) --> skeletal m weakness. Key feature is **skeletal m weakness that becomes worse later in the day or that develops w/ exercise** & can recover some w/ rest. Early signs: diplopia and ptsosis Other signs: bulbar muscle weakness of mouth and throat, dysphagia, dysarthria, difficulty handling saliva, proximal weakness Things that make it worse: - **pregnancy** - infection - electrolyte imbalance - stress - **aminoglycoside antibiotics- so avoid this bc it makes them more weaker** Treat: **First line treatment with oral pyridostigmine AchE.** But if you overdose is it cholinergic crisis or if they’re feeling better was it myasthenia crisis? Test with Tensilon test with Edrophonium 1-2mg IV

Answer 50

the thymus gland plays a key role in MG, and thymectomy - it reduces circulating anti-AChR IgG in most patients - surgical approach may be via median sternotomy or by the transcervical approach Other treatments: - Immunosuppresants like steroids cylosporine, azathioprine, mycophenolate - Plasmapharesis- temp relief during crisis

Answer 51

in 1/3 of women, pregnancy intensifies the symptoms of MG. Anti-AChR IgG Antibodies cross the placenta and cause weakness in 15-20% of neonates. This can persist x2-4 weeks, which is consistent w/ the half-life of these antibioties in the neonates circulation Neonate may require airway management.

Answer 52

**Pyridostigmine (anticholinesterase) is the first line tx for MG.** An OD can cause cholinergic crisis, which can include skeletal m weakness (makes differentiation difficult) diagnosis is made by administering 1-2mg IV edrophonium ("Tensilon test") because it has the FAST onset - if weakness is made worse, then the pt has cholinergic crisis (tx = anticholinergic) - if weakness improves, then it was an MG exacerbation Treat with = anticholinesterase, immunosuppression, plasmapheresis

Answer 53

There less nicotinic type m receptors at the neuromuscular junction. - They’re more resistant to Sux. give 1.5-2mg/kg. **Remember pyridostigmine impairs efficacy of pseudocholinesterase and can also prolong sux** - More sensitive to nondepolarizers. If roc was used there’s a higher risk of residual blockade. REDUCE THE DOSE **Volatile anesthetics cause skeletal m relaxation by acting in the ventral horn of the SC - in many cases this eliminates the need for NMB.**

Answer 54

**bulbar weakness (mouth and throat)** manifests as difficulty handling oral secretions --> increased risk of aspiration just like in ALS!

Answer 55

**IgG mediated destruction of the v-gated Ca++ channel at the presynaptic nerve terminal.** presynaptic!!! When the AP depolarizes the nerve terminal, Ca++ entry into the presynaptic neuron is limited, **reducing the amount of ACh that is released into the synaptic cleft.** Postsynaptic nAChR is normal - **they’re sensitive to both depolarizers and non depolarizers** - Volatile anesthetics also provide enough muscle relaxation for most surgical procedures like in MG - **association with small cell lung carcinoma** - **Treatment: 3,4-diaminopyridine (DAP) increases ACh release from the presynaptic nerve terminal and improves the strength of contraction.** - resistant to neostigmine reversal

Answer 56

eaton-lambert - Destroyed v-gated Ca++ channels (pre-synaptic) - decreased ACh release - presynaptic neuron of NMJ - comorb: small cell lung CA - sensitive to NMB (both) - **AChE inhibitors doesn't improve symptoms** MG - Fewer Nm receptor (post-synaptic) - **decreased ACh response** - comorb: thymoma - resistant to sux, sensitive to NDMR - AChE inhibitors improve symptoms

Answer 57

common etiologies: campylobacter jejuni bacteria, Epstein Barr virus, and cytomegalovirus starts like flu-like illness **Starts in distal extremities and ascends up** Muscle weakness: impairs ventilation and difficulty swallowing **Immunologic assault on the myelin in the peripheral nerves** Persists for 2 weeks and ends w/ full recovery in approx 4 weeks. **Treatment: plasmapheresis like in MG, and you also give IgG. Steroids do NOT help** **Avoid sux and decrease dose of nondepolarizers like in ALS!** Sensory deficits are common: parathesias, numbness, and pain **Autonomic dysfunction is common: tachy or Brady, htn or hypotension, orthostatic hypotension, diaphoresis or anhidrosis** There is an exaggerated response to indirect acting sympathomimetics due to upregulation of postjunctioanl adrenergic receptors. So avoid ephedrine Regional is not preffered over GA

Answer 58

flu-like illness usually precedes paralysis by 1-3 weeks s/s: - flaccid paralysis begins in the distal extremities and ascends bilat toward proximal extremities, trunk, face - intercostal m weakness impairs ventilation - facial, pharyngeal weakness causes dysphagia - sensory deficits: paresthesias, numbness, +/- pain - autonomic dysfunction is common: HR, BP, sweating abnormalities, orthostatic hypotension Avoid sux and use less Roc!

Answer 59

two distinct disease processes that are characterized by acute episodes of skeletal m weakness that is accompanied by hypo or hyperkalemia hypokalemia: diagnosed if skeletal m weakness follows a glucose-insulin infusion hyperkalemia: diagnosed if skeletal m weakness follows oral K+ administration

Answer 60

Familial periodic paralysis is acute episodes of skeletal muscle weakness with changes in potassium. It is not a disease with the neuromuscular junction. It’s a disorder of the skeletal muscle membrane: reduced excitability With hypokalemic avoid: - **glucose containing solutions! AVOID D5LR** because it usually follows an insulin infusion - K+ wasting diuretics - **B2 agonists like Terbutaline** - avoid succinylcholine because this condition might be associated with MH - **it is associated with a calcium channelopathy** With hyperkalemia avoid: - succinylcholine - K+ containing slns (LR) - **it’s associated with a sodium channelopathy** **acetazolamide is the tx for both forms bc it creates a nonanion gap acidosis, which protects against hypokalemia. It also facilitates renal K+ excretion which guards against hyperkalemia** Shorter acting nondepolarizers are best! **Avoid hypothermia for both types at all costs**

Answer 61

when T-tubule is depolarized, extracellular Ca++ enters the myocyte via the dihydropyridine receptor at the T-tubule this activates the **ryanodine receptor (RYR1) and it’s dysfunctional**, which instructs the SR to release massive Ca++ into the cell. In the case of MH, it releases WAY TOO MUCH (consumes ATP, O2, produces CO2) cell attempts to return some Ca++ into the SR via the SERCA2 pump (in MH, this pump becomes overworked) (consumes ATP, O2, produces CO2) when the skeletal m consumes all of its ATP, cell membrane integrity is no longer maintained & intracellular components (myoglobin & K+) are released into the systemic circulation MH inherited disease: disordered calcium homeostasis

Answer 62

- sustained muscular contraction - accelerated metabolic rate & rapid ATP depletion - increased O2 consumption - increased CO2 & heat production - **mixed respiratory and lactic acidosis** - sarcolemma breaks down - K+ & myoglobin leak into the systemic circulation - rigidity from sustained contraction **MH is inherited disease of skeletal muscle. Exposure of halogenated activates the defective ryanodine receptor RYR1 and stimulates SR to release too calcium**

Answer 63

1. King-Denborough syndrome 2. central core disease 3. multiminicore disease

Answer 64

- Duchenne muscular dystrophy- **due to rhabdomylolysis** - Becker muscular dystrophy - neuroleptic malignant syndrome - myotonia congenita or dystrophy - osteogenesis imperfecta

Answer 65

MH can occur as late as 6hrs after exposure to a triggering agent. most sensitive indicator of MH: EtCO2 rises out of proportion to MV early: - tachycardia - tachypnea - **masseter spasm**- jaw can’t be opened - warm soda lime - irregular heart rhythm intermediate: - cyanosis - pt warm to touch - irregular heart rhythm late: - muscle rigidity - cola-colored urine - coagulopathy - irregular heart rhythm

Answer 66

trismus & masseter m rigidity exist on a continuum - trismus: tight jaw can still be opened, normal response to sux - **masseter muscle rigidity: cannot open jaw** trismus is a normal response to succinylcholine - ok to proceed w/ surgery if occurring in isolation, but may want to avoid other triggering agents. if the pt has masseter m rigidity, assume MH until proven otherwise - **NMB will not help this since it's occurring distal to the NMJ** spasm is due to increase calcium in the myoplasm

Answer 67

Caffeine halothane contracture test- live muscle biopsy Gold standard High sensitivity but low specificity

Answer 68

classified as a muscle relaxant. two mechanisms of action: - halts Ca++ release from the RyR1 receptor - prevents Ca++ entry into the myocyte which reduces the stimulus for calcium induced calcium release. **the most common side effects are muscle weakness & venous irritation**

Answer 69

each vial contains 20mg dantrolene + 3g mannitol & **must be reconstituted w/ preservative free H2O 60 ml** Initial dose 2.5mg/kg IV NaCl introduces additional solute which prolongs the time required for dantrolene to dissolve into the dilutent enlist help early!! Dantrolene can irritate the vein, also a muscle relaxant and can cause muscle weakness

Answer 70

#1 d/c triggering agent #2 call for help 100% FiO2 >10L/min **dantrolene 2.5mg/kg IV, repeat Q5-10mins** - hyperventilate - correct lactic acidosis w/ bicarb - treat hyperK+ - CaCl 5-10mg IV - insulin 0.15U/kg + D50 1mL/kg protect against dysrhythmias - charcoal filter to inspiratory and expiratory limb of the circuit if you have time. **Vapor- clean filter needs to be changed every hour during MH crisis** - class I agents (lido, procaine) - **avoid CCB like Verapamil w/ dantro to avoid hyperK+** - maintain UOP - IV hydration - 0.25mg/kg mannitol - 1mg/kg - **cool the pt until temp <38C** - cold IVF - cold fluid lavage - ice packs monitor coags, avoid DIC If at risk of MH: monitor in PACU 1-4 hours **If they actually had MH: need to go to the ICU, MH can reoccur up to 36 hours!!!!!!**

Answer 71

dystrophin is a critical structural component of the cytoskeleton of skeletal and cardiac muscle cells. DMD- skeletal muscle myopathy with **absence of dystrophin protein from X linked recessive disease, affects many males** Absence of it destabilizes the sarcolemma during muscular contraction & increases membrane permeability. **creatine kinase and myoglobin to leak through the membrane and results in elevated plasma concentration** elevated labs **Calcium also freely enters the cell = inflammation, fibrous, cell death** extrajunctional receptors populate --> avoid succinylcholine At risk for MH-like symptoms with hyperkalemia and rhabdomyolysis not true MH. Best to use TIVA and avoid sux and volatile agents however, there is no denervation of skeletal tissue, meaning that **sensation and reflexes are intact**

Answer 72

**kyphoscholiosis (restrictive lung disease) --> decreased vital capacity and residual volume --> increased secretions & risk of PNA** respiratory muscle weakness also occurs They have impaired airway reflexes and GI hypo motility - increased risk of aspiration

Answer 73

cardiac considerations: - degeneration of cardiac m --> **decreased contractility, pap m dysfunction, mitral regurgitation, cardiomyopathy, CHF** - **signs of cardiomyopathy = resting tachycardia, JVD, S3/S4 gallop** - gold standard = echo EKG changes - **ST + short PR** - scarring of posterobasal aspect of LV manifests as **increased R wave amplitude in lead 1 & deep Q waves in the limb leads**

Answer 74

describes the magnitude of the spinal curvature **40-50 degrees = indication for surgery** **60 degrees = decreased pulmonary reserve** 70 degrees = pulmonary symptoms present 100 degrees = gas exchange significantly impaired, higher risk of post-op pulmonary complications

Answer 75

alters thoracic geometry, which compresses the lungs & creates a restrictive ventilatory defect. One side of the thorax becomes smaller than the other early: - restrictive ventilatory defect (same lung volume, capacity decreases as any) - decreased chest wall compliance late: - VQ mismatching - hypoxemia - hypercarbia (sign of impending failure) - pHTN - reduced response to hypercapnia - cor pulmonale - cardiorespiratory failure CV changes: RV hypertrophy and **mitral prolapse (most common), mitral regurgitation, and coarctation of the aorta**

Answer 76

TMJ, cricoarytenoid joints, cervical spine are affected 1. TMJ: limited mouth opening 2. cricoarytenoid joints: decreased diameter of glottic opening 3. cervical spine: A-O subluxation w/ flexion + limited extension Common complication is Atlantoaxial subluxation and seperation of the antlanto-odontoid articulation

Answer 77

RA: vasculitis **AO subluxation is the most common airway complication of RA** This is d/t the weakening of the transverse axial ligament, which allows the odontoid to directly compress the SC at the level of the foramen magnum. - puts the pt at risk for quadriparesis or paralysis - side note: pts w/ Down syndrome are also at risk for AO subluxation Other complications: - **cricoarytenoiditis**- painful swallowing airway obstruction or stridor - **restrictive lung disease** - pleural effusion/ fibrosis - **aortic regurgitation**!!!!!!! - anemia - **renal insufficiency from NSAID use**

Answer 78

autoimmune disease that targets the synovial joints. There is also widespread systemic involvement d/t infiltration of immune complexes in the small & medium arteries --> **vasculitis** cytokines (TNF & interleukin-1) play a central role in the pathogenesis. Hallmark of RA: morning stiffness that improves w/ activity joints are painful, swollen, and warm other symptoms: - weakness - fatigue - anorexia - lymph node enlargement

Answer 79

Rheumatoid arthritis is characterized by symmetric polyarthropathy that affects weight-bearing joints and proximal interphalangeal and metacarpophalangeal joints. It is typically worse in the morning. **In the most severe forms, every joint can be affected except for the lumbar and thoracic spine.** airway: - TMJ synovitis - cricoarytenoid arthritis - AO instability pulmonary - **pleural effusion** - restrictive pattern d/t diffuse interstitial fibrosis + costochondral involvement that limits chest wall expansion cardiac - **pericardial effusion/tamponade** - **restrictive pericarditis** - **aortic regurgitation** - valvular fibrosis - coronary artery arteritis hematologic - **anemia** - platelet dysfunction d/t NSAIDs renal - renal insufficiency d/t vasculitis, NSAIds endocrine - adrenal insufficiency & infections d/t steroids GI - gastric ulcerations d/t NSAIDs, steroids Eyes - Sjogren's syndrome - risk of corneal abrasion PNS - peripheral neuropathy d/t nerve entrapment

Answer 80

SLE is an autoimmune disease characterized by the proliferation of antinuclear antibodies SLE affects nearly every organ system & most consequences are the direct result of Ab-induced vasculitis and tissue destruction - Can cause **cricoarythenoiditis: hoarseness/stridor/airway obstruction, recurrent laryngeal nerve palsy is a complication, hypercoagulability**

Answer 81

targets young women most common problems are **polyarthritis** (generally not the spine) & **dermatitis** only 33-50% develop the "butterfly rash" airway: - **cricoarytenoiditis: hoarseness, stridor, a/w obstruction** - RLN palsy pulmonary - restrictive - pHTN - interstitial lung dz w/ impaired diffusing capacity - pleural effusion - recurrent PE CV - pericarditis - Raynaud's - HTN - conduction defects - endocarditis hematologic - **antiphospholipid antibodies** - **hypercoagulability** = risk of DVT - anemia - thrombocytopenia - leukopenia renal: nephritis w/ proteinuria CNS: stroke

Answer 82

occurs d/t stress or drug exposure drug induced usually persists for several weeks-months & presents w/ mild symptoms ``` most common offenders (PISSED CHIMP) Pregancy Infection Surgery Stress Enalapril D-penicillamine Captopril Hydralazine- can cause tachycardia Isoniazid Methyldopa Procainamide ```

Answer 83

**those w/ SLE are prone to developing antiphospholipid antibodies** Although aPTT is prolonged, these pts are prone to a state of hypercoagulability & thrombosis - **risk for stroke, DVT, PE** - pregnant pts are at higher risk - Cyclophosphamide- immunosuppressent can prolong sux

Answer 84

characterized by prolonged contracture after a voluntary contraction. **This is the result of dysfunctional Ca++ sequestration by the SR** Contractions can be so severe that they interfere w/ ventilation & intubation **3 things increase risk of contractures** 1) sux 2) NMB reversal so consider Sugammadex 3) hypothermia = sustained contractions

Answer 85

Prolonged contracture after voluntary contraction, from dysfunctional calcium sequestration by the SR. 1. succinylcholine 2. reversal of NMB w/ anticholinesterases (theoretical) like neostigmine 3. hypothermia (shivering --> sustained contractions) Other risks include: - aspiration, respiratory muscle weakness, cardiomyopathy

Answer 86

It is an autosomal dominant trait. It is a connective tissue disorder that's associated w/ an elevated **risk of aortic dissection, MV prolapse, mitral regurg, aortic regurgitation** Aortic dissection of the ascending aorta can extend into the pericardium, and this increases the risk of **cardiac tamponade!** **Becks' triad: JVG, hypotension, muffled heart tones** **spontaneous pneumo** is a common complication in these patients.

Answer 87

inherited disorder of procollagen and collagen. There are several types, but only type IV is associated w/ vascular rupture **(i.e. AAA)** **increased bleeding tendency d/t lack of blood vessel integrity+ coagulopathy** - **avoid regional anesthesia** = hematoma is a risk - **avoid IM injections** - be careful during airway management & line placement. **Pneumothorax is also a common complication; avoid high PIP!!!!!**

Answer 88

A! Intrathecal opioids act centrally by diffusion into the spinal cord and interact with mu receptors in the substantia gelatinosa in the dorsal horn. Opioid receptors (mu receptors) are present in the substantia gelatinosa (A) of the dorsal horn in the spinal cord. The substantia gelatinosa comprises the cell bodies of the second-order projection neurons that ascend from the spinothalamic tract to the thalamus. These cells are densely populated with mu receptors and form the primary immediate site of action of intrathecal opioids that diffuse from the cerebrospinal fluid into the spinal cord.

Answer 89

Common etiology: campylobacteri jejuni, Epstein Barr virus, cytomegalovirus Weakness begins in lower extremities and ascends, autonomic dysfunction is common: hypotension/htn, bradycardia/tachycardia Avoid sux, decrease Rocuronium dose Tx: with plasmaparesis and IVgG

Answer 90

- **Demyelination disease of Central Nervous System** diagnose with an MRI - can be exacerbated by increase in temp by 1 degree - **epidural is safe, but spinal can worsen it** - Occurs after 35 years old - Avoid SUX! - Pregnancy is associated with a reduced incidence of exacerbation, while the **postpartum period is associated with an increased risk of relapse**

Answer 91

MG, MS, ALS You want to avoid sux bc they have extrajunctional Ach receptors. The body tries to maintain communication between muscle and nerves. This is seen in immobile patients. They have an abnormal configuration and when depolarized, they have a **longer time in the open channel** and releases abnormal amounts of K+. = risk of hyperkalemia. Since there are more receptors to bind to, non-depolarizers can bind to more receptors and cause profound paralysis at lower doses. But in MG patients: - Their functional receptors are destroyed so they need a higher dose of Sux for it to bind to. But the higher dose of sux can also cause a longer duration of action. - Lower dose is required due to fewer functional receptors and Non depolarizers are more potent. They’re more sensitive to non depolarizers

Answer 92

Two Zebras Bit My Cat Temporal, zygomatic, buccal, Mandibular, cervical

Answer 93

Cranial nerve 7

Answer 94

Cranial nerves 3, 7, 9, 10

Answer 95

Some Say Marrying Money. But My Brother Says Marrying Money Brings Bad Business Marrying Money 12 Cranial nerves

Answer 96

PEB: Propofol, etomidate, barbituates Elevating HOB Hyperventilation Neo can help increase cerebral perfusion pressure

Answer 97

4.5 hours from symptom onset

Answer 98

6 hours!!!!

Answer 99

Glucose -> lactic acid and worsens ischemia

Answer 100

Which one is continuous touch? Which one is reading braille? Which one is vibration? Which one is proprioception? Ruffini

Answer 101

Nociceptors and free nerve endings transmit pain signals to the brain via the spinothalamic tracts (anterolateral system).

Answer 102

Volume expansion and neo infusion

Answer 103

- Anterior- internal carotid arteries - Posterior- vertebral arteries

Answer 104

The SNS releases acetylcholine at ganglionic receptors. And it releases epinephrine, norepinephrine, or dopamine at target receptors - has short preganglionic fibers - **have a postganglionic to preganglionic ratio of 30:1** post > pre - Originates from T1-T12 and L1-L3.

Answer 105

Anterolateral system (Spinothalamic tract)

Answer 106

- fine touch - proprioception - vibration - pressure

Answer 107

It relaxes sensory input to the spinal cord

Answer 108

**The posterior blood supply.** This is why touch and proprioception are preserved if the aortic cross clamp is placed above the artery of the Adamkiewicz **The tracts that are perfused by the anterior blood supply**: - The Corticospinal tract- that’s why will have flaccid paralysis of lower extremities - Autonomic motor fibers- explains why bowel and bladder dysfunction - Spinothalamic tract- explains why pt will lose some pain and temperature sensation

Answer 109

Dorsal column

Answer 110

Laminae 1-6 in the dorsal grey matter are sensory Laminae 7-9 in the ventral grey matter are motor

Answer 111

Axon- this makes up the white matter

Answer 112

- first order neuron enters spinal cord via the dorsal root ganglia - second order neuron decussates in the medulla - it transmits sensory information faster than the anterolateral system

Answer 113

- **transmits mechanoreceptive sensations: fine touch, proprioception, vibration, pressure (fine degree of intensity)** - capable of 2 point discrimination- high degree of localizing the stimulus - large, myelinated, rapid conducting fibers - transmits sensory faster than the anterolateral system 1) First order- usually A beta, enters spinal cord through dorsal root ganglion, relays sensory info from dorsal column to the medulla 2) **Second order- crosses contralateral side in the medulla** 3) Third order- fibers pass through internal capsule and go in the postcentral gyrus in the parietal lobe in the cerebral cortex

Answer 114

- Meissner’s corpuscles- 2 point discriminative touch and vibration. READING BRAILLE - Merkel’s discs- continuous touch - Ruffini’s endings- proprioception, prolonged touch and pressure - Pacinian corpuscles- vibration

Answer 115

Anterolateral system (Spinothalamic tract) - pain - temperature - crude touch - itch - tickle - sexual sensation Smaller, myelinated and NON myelinated, slower fibers Does not have 2 point discrimination

Answer 116

**Transmits: pain, temperature, crude touch, tickle, itch, and sexual sensation** Has smaller myelinated and nonmyelinated slower conducting fibers There is NO 2-point discrimination 1) First order: there is 2 nerve fibers types: **Alpha-delta fast pain, glutamate is the neurotransmitter.** **C fibers slow pain, substance P is the neurotransmitter** (Where as in the DCL tract, the first fiber is alpha-beta fibers) Pain neurons synapses with the 2nd order neuron in the substantia gelatinosa Rexed Lamina 2. Primary pain neurons can also synapse in the 2nd order neuron in the dorsal horn Laminae 1,4,5, 6. 2) **Second order neuron: crosses contralateral side of the spinal cord and ascends in 2 pathways** - 1) Lateral Spinothalamic tract- pain and temperature - 2) Anterior spinothalaic tract- crude touch and pressure **Second-order neurons synapse with third-order in the reticular activating system and thalamus** 3) Third order neuron: fibers pass through internal capsule in the post central gyrus in the parietal lobe in the cerebral cortex. **Many pain fibers synapse with the third order neuron in the reticular activating system and thalamus**

Answer 117

**Dorsal column:** - pressure - 2 point discrimination - proprioception - transmits vibrations -large myelinated fibers **Anterolateral system:** - small unmyelinated fibers - transmits pain - transmits sexual sensations - transmits temperature

Answer 118

1. A-delta first pain mechanoreceptors 2. C fibers slow pain polymodal nociceptors

Answer 119

Substantia gelatinosa of the dorsal horn lamina 2 They can also synapse in Laminae 1,4,5,6

Answer 120

Reticular activating system and the thalamus

Answer 121

**Injury above the decussation= spastic paralysis on the contralateral side** **Injury below the decussation= flaccid paralysis on the ipsilateral side** Corticospinal tract is also called the pyramidal tract it is the motor pathway to control limbs and posture Motor neurons exit the pre central gyrus of the frontal lobe and travel through the pyramids of the medulla

Answer 122

**Upper motor begins in the cerebral cortex and ends in the ventral horn of the spinal cord** Upper motor neuron injury - contralateral spastic paralysis + hyperreflexia Ex: cerebral palsy and ALS Can do babinski test to assess corticopinal tract: toes fanning out is abnormal

Answer 123

Begins in ventral horn and ends in neuromuscular junction

Answer 124

Monitor dorsal column medial leminiscus Loss of SSEPs during spinal fusion is most likely due to interruption of posterior spinal artery

Answer 125

Neurogenic shock triad: Bradycardia, hypotension, **hypothermia- with pink and warm extremities** Hypovolemia shock: tachycardia, hypotension, cool and clammy. No hypothermia! C7 is most common site of SCI. Can last 1-3 weeks. Initially leads to flaccid paralysis, loss of sensation below the level of injury, loss of bowel and bladder function occurs After acute phase, spinal reflexes return which leads to **spastic paralysis after 6 weeks** **Treatments: Levo gtt to restore SVR and give volume** sux is ok first 24 hours but switch to non depolarizer

Answer 126

Nitroprusside works faster than hydralazine and we need to quickly treat pressure. They’re at risk of intracerebral hemorrhage Autonomic hyperreflexia- they will Vasodilate above the level of injury and vasoconstrict below the injury Hypertension produces bradycardia via the baroceptor reflex. You can give anticholinergics

Answer 127

Hypertension needs to be treated ASAP or it can cause stroke, LV failure, and pulmonary edema, seizures Other signs: nasal stuffiness, headache or blurred vision FIRST REMOVE STIMULUS! Then deepen anesthesia, and give sodium nitroprusside, avoid sux in chronic SCI Adding lube to the foley doesn’t prevent AH Things that can elicit AH: stimulation of hollow organs like bladder bowel uterus, bladder catherization, surgery like cystoscopy to colonoscopy, bowel movement, childbirth

Answer 128

Progressive degeneration of motor neurons in the corticospinal tract in the upper and lower motor. Sensory remains intact - upper neurons: spasticity, hyperreflexia, loss of coordination - lower motor neuron: muscle weakness, fasciculations, and atrophy - **it begins in the hands and spreads** - Respiratory failure is the common cause of death - Bulbar muscle weakness increases risk of aspiration - Extrajunctional receptors at the NMJ can cause life threatening hyperkalemia - **More sensitivity to non depolarizing neuromuscular blockers** so try to avoid all of them - **Riluzole is an NMDA antagonist and is the only drug that reduces mortality** - Chest weakness reduces vital capacity. Consider postoperative mechanical ventilation

Answer 129

Spinothalamic tracts (anterolateral system): nociceptors and free nerve endings transmit pain signals to the brain via this tract

Answer 130

1) 2 posterior spinal arteries perfuse the posterior 1/3 of the spinal cord - Medial lemniscal system dorsal column 2) 1 anterior spinal artery that perfuses 2/3 of the spinal cord perfuses: - Spinothalamic - corticospinal - autonomic fibers

Answer 131

**initial treatment for spinal cord injury = Levo gtt and intravascular volume expansion** Deep hypothermic circ arrest is for neuroprotection for pts undergoing aortic arch surgery and not SCI You want to avoid sux for pts with SCI and risk of severe Hyperkalemia 24 hours after the injury

Answer 132

Meissner’s corpuscles. Reading braille requires highly sensitive mechanoreptors in the fingertips that are capable of 2-point discrimination

Answer 133

- SSEPs- monitor posterior spinal cord- dorsal column (proprioception) - MEPs- monitor anterior spinal cord (motor) **Wake up test complications: Venous air embolism, awareness, tracheal extubation, pain, damage to surgical instruments. YOU WILL NOT GET ISCHEMIC OPTIC NEUROPATHY!**

Answer 134

Dens also called odontoid process= superior boney projection off the axis C2, provides pivot point that helps with head rotation

Answer 135

Marfan’s syndrome- aortic insufficiency Ehlers-Danlos syndrome- bleeding into joints Osteogenesis imperfecta- **blue sclera eyes is a unique finding**, connective tissue disorder, weak bones, risk of fractures! **Serum thyroxine is increased and increase basal metabolic rate = hyperthermia**

Answer 136

M.S = sensitivity to hyperthermia Myotonic dystrophy = sustained contracture with Sux Paget’s diease = risk of bone fracture. Excess osteoblastic osteoclastic but it causes thick, weak, bone deposits. Caused by excess parathyroid hormone or calcitonin deficiency. Scleroderma = CREST syndrome. Excessive fibrosis in organs. Calcinosis, Raynaud’s, Esophageal hypo motility, Sclerodactyly, Telangiectasis spider veins) which increase risk of mucosal bleeding. They also have limited mouth opening from the skin fibrosis

Answer 137

D5W, glucose causes insulin spike and it shifts K+ into the cells and leads to exacerbation of skeletal muscle weakness

Answer 138

Scleroderma- risk of mucosal bleeding

Answer 139

Every hour

Answer 140

Arachnoid and pia mater

Answer 141

CNS neurons: bipolar, pseudounipolar, multipolar

Answer 142

The pH of the CSF!

Answer 143

Posterior circulation: 1. Subclavian artery 2. Vertebral artery enter through the foreman magnum 3. Basilar artery 4. Posterior cerebral artery Anterior circulation: 1. Carotid artery enter through the foramen lacerum 2. Internal carotid artery 3. Middle cerebral artery

Answer 144

Hypothermia reduces both, it reduces CMRO2 by 7% for every 1 degree decrease Propofol and barbs: potent vasoconstrictors. They reduce CMRO2 and reduce CBF Ketamine and nitrous: increase CMRO2 and increase CBF Precedex doesn’t affect CMRO2 but it does reduce CBF

Answer 145

Cranial nerves Peripheral nervous system made up of cranial and spinal nerves

Answer 146

Movement and bowel control

Answer 147

Edrophonium 1-2mg IV: increases amount of Ach - Myasthenia gravis pt becomes stronger - pt with cholinergic crisis becomes weaker, they have too much Ach and will need an anticholinergic

Answer 148

CREST syndrome: 1) Calcinosis 2) Raynaud’s 3) Esophageal hypomotility 4) Sclerodactyly 5) Telangiectasis (T- spider veins and bleeding in mucosa) Excessive fibrosis, and micro vascular involvement in organs: **think pulmonary hypertension, blood pressure hypertension membrane bleeding, and kidney issues** - **pulmonary fibrosis and pulmonary hypertension** - Dysrhythmias and CHF - Hypertension - **Renal failure/stenosis** - neuropathy - eye dryness - **mouth/nose bleeds**

Answer 149

Disease of connective tissue = brittle bones - Fractures during positioning or during NIBP cuff or even following Sux fasciculations! - They have kyphoscoliosis and pectus excavatum (sunken chest) which reduces chest wall compliance and vital capacity and V/Q mismatching = **Arterial hypoxemia** - **Serum thyroxine is increased. It increases O2 consumption and can lead to hyperthermia.** The risk of MH is not increased. - Blue Sclerae eyes

Answer 150

Remember! This is also known as Guillan-Barre! Immunologic **assault on myelin in the peripheral nerves** Sux should be avoided = Hyperkalemia risk **Exaggerated response to ephedrine, so avoid it. = due to upregulation of postjunctioal adrenergic receptors** Epstein Barr is a common etiology Steroids don’t help Paralysis begins in the distal extremities

Answer 151

50 degrees- indication for surgery 60 degrees- decreased pulmonary reserve 70 degrees- pulmonary symptoms begin 100 degrees- significant gas exchange impairment

Answer 152

1) Rheumatoid arthritis: targets synovial joints and arteries - Atalantoaxial subluxation - **cricoarytenoiditis**- painful swallowing airway obstruction or stridor - **restrictive lung disease** - pleural effusion/ fibrosis - **aortic regurgitation** - anemia - **renal insufficiency from NSAID use** 2) Systemic Lupus Erythematosus: proliferation of antinuclear antibodies and damage nearly every organ

Answer 153

Most common arthritis. Degenerative disease affecting cartilage of joints, there is NO VASCULAR INVOLVEMENT (Unlike Rheumatoid arthritis!)

Answer 154

** Firstline treatment with oral pyridostigmine AchE.** Other treatments include: plasmapheresis, immunosuppressive therapy (steroids, cyclosporine, mycophenolate, azathioprine)

Answer 155

Calcium! Hyperkalemic paralysis- sodium channelopathy Familial periodic paralysis is acute episodes of skeletal muscle weakness, it is a disorder of the skeletal muscle membrane with reduced excitability. It is not a diease of the neuromuscular junction

Answer 156

Rhabdomyolysis with hyperkalemia followed by Dysrhythmias and cardiac arrest

Answer 157

Anterior spinal artery: 1. Corticospinal tract 2. Autonomic motor fibers 3. Spinothalamic tract Posterior spinal artery: 1. Dorsal column

Answer 158

Part of the Dorsal column: - Merkel’s discs- continuous touch - **Ruffini’s endings- proprioception, prolonged touch and pressure** - Meissner’s corpuscles - 2 point touch

Answer 159

**In the spinal cord! In the substantia gelatinosa of the dorsal horn in lamina 2** They can also synapse in lamina 1, 4, 5, 6

Answer 160

Desflurane - most potent cerebral dilator it decreases CBF. It preserves CO2 responsiveness. **But it does not preserve cerebral autoregulatation at a MAC > 1** It can cause blood vessels in the brain to dilate too much or too little, making it harder for the brain to adjust to changes in blood pressure or CO₂ levels. - Opioids and IV anesthetics usually preserve both cerebral autoregulation and vascular responsiveness to CO2. - Ketamine- increases CMRO2, CBF, autoregulation, and CO2 responsiveness is preserved.

Answer 161

Auto regulatory responses are abolished Blood flow becomes pressure-dependent

Answer 162

Venous blood flow obstruction can develop with increase Intrathoracic pressure following obstruction, cough, or straining

Answer 163

Middle cerebral and anterior cerebral arteries (Posterior cerebral arteries branch from the basilar artery)

Answer 164

- hypernatremia - hyponatremia - hypomagnesemia - **hypophastemia** < 1mg/dl - **hypocalcemia**

Answer 165

**Increases in CBF = Vasodilates = increases ICP which is bad!** - respiratory acidosis- hypoventilating and PaCO2 dilates - seizure activity- increases CBF and CMRO2 - PO2 50 torr. PO2 below 60 increases CBF - temperature 37- 42C increase CBF

Answer 166

- Complete immobility of pt - Assess ACT - gold standard of monitoring is cerebral angiography

Answer 167

- **recommended lithium levels 0.8-1.2 meg/L** - **decreases MAC requirement** - impaired parathyroid hormone secretion- **leading to hypocalcemia** - decreased tubular response to ADH - **thiazide diuretics increase reabsorption and increase toxicity NOT loop diuretics.** Loop diuretics are preferred - NSAIDS and ACEI can also increase toxicity

Answer 168

Muscle atrophy avoid Sux due to hyperkalemia

Answer 169

C. Shivering D. Vasoconstriction GA inhibits thermoregulation

Answer 170

- Rising peak pressure - Abrupt onset of tachycardia and hypertension

Answer 171

Charcot- Marie- Tooth: slow distal muscle weakness and **loss of sensation of lower extremities.** Mutations in genes responsible for myelin destruction

Answer 172

Choreiform jerking writhing movements CAG test Dysfunction in basal ganglia Haloperidol can be used to treat exacerbations of choreiform movements and emotional lability in these patients They can still receive SUX

Answer 173

Mitral valve prolapse

Answer 174

Duchenne’s. The most common causes of death in patients with kyphoscoliosis are restrictive lung disease and pulmonary hypertension.

Answer 175

Pulmonary function tests should be performed in patients with severe scoliosis as a **vital capacity < 40%** of predicted is associated with the likelihood of postoperative ventilatory support.

Answer 176

Risk for postoperative ventilation: - **Disease > 6 years** - **Daily pyridostigmine > 750 mg/day** - **Vital capacity < 2.9L** - COPD - If they did a thymectomy and chose the median sternotomy approach - a negative inspiratory pressure less than -25 cm H2O

Answer 177

Multiple sclerosis Postpartum exacerbates it, epidural is safe

Answer 178

Duchenne muscular dystrophy- X-linked disorder and rarely cause symptoms in females. Death is most often attributed to pneumonia, respiratory failure, or cardiac failure and usually occurs between the ages of 20 and 25.