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CRNA principles
Anesthesia for patients with neuromuscular diseases
| Question | Answer |
|---|---|
| What is the etiology of osteoarthritis (OA)? | Caused by repetitive joint trauma |
| Osteoarthritis is commonly associated with what age groups and conditions? | Advancing age and morbid obesity |
| What does osteoarthritis most commonly effect? | Degenerative disease effecting Articular surface of joints, most commonly hips and knees |
| What is the pathology of of Rheumatoid arthritis (RA)? | RA is a immune mediated joint destruction characterized by chronic, progressive inflammation of synovial membranes. |
| True or false: RA is a systemic disease effecting women 30-50 years old? | True |
| What part of the spine is most effected by RA? | Cervical |
| What cardiovascular abnormalities are seen with RA? | Pericardial thickening/effusion, dilation of aortic root may result in cardiac valve fibrosis. |
| What pulmonary abnormalities are seen with RA? | Pleural effusions are common, restrictive lung changes may result from costochondral involvement |
| What hematopoietic manifestations are seen in RA? | Anemia, plt dysfunction, thrombocytopenia |
| What dermatological conditions are seen in RA? | Thin atrophic skin from disease/immunosuppressive drugs. |
| Treatment for RA/OA for patients who don't respond well to NSAIDS/steroids? | Gold salts/cytotoxic drugs |
| Anesthetic considerations for RA/OA? | Evaluate for cardiac/pulmonary diseases |
| Cervical spine considerations for pt's with RA/OA? | Careful neck positioning due to high frequency of cervical spine involvement |
| Atlantoaxial subluxation risk for pt's with RA include? | Protrusion of odontoid process into the foramen magnum during intubation. |
| During intubation, what does protrusion of the odontoid process into the foramen magnum compress? | blood flow, spinal cord, brain stem |
| What diagnostic test is important for pt's with RA and why? | Lateral XR's because atlantoaxial subluxation can be asymptomatic |
| How many mm of atlantoaxial instability necessitates and awake Fiber optic intubation with neck stabilization? | 5 mm |
| Limits of jaw mobility in pt's with RA/OA include? | TMJ/cricoarytenoid arthritis can complicate intubation |
| What are some complications from cricoarytenoid arthritis and what kind of ETT can you use in these patients? | narrowing of glottic opening, as evidence by hoarseness/inspiratory stridor. Use of a smaller ETT tube. |
| Risks associated with cricoarytenoid arthritis? | Post extubation airway obstruction |
| Pathology associated with Myasthenia Gravis (MG)? | Autoimmune destruction/inactivation of postsynaptic acetylcholine receptors at neuromuscular junction. IgG antibodies against nicotinic act receptors in NMJ are found in pt's with MG. |
| Two Classifications of Myasthenia Gravis? | Two classifications include: (1) only ocular (2)ocular and monocular muscle weakness |
| Other autoimmune disorders associated with MG include? | RA, Hyperthyroid, hypothyroid |
| Ages and genes that MG most commonly effects? | Men in their 60's-70's along with women in their 3rd decade of life |
| Effects of ocular muscles from MG include? | Fluctuating ptosis, diplopia |
| Bulbar involvment causes what complications with MG? | Laryngeal/pharyngeal muscle weakness resulting in dysarthria, difficulty chewing/swallowing, pulmonary aspirations, unable to clear secretions. |
| Severe MG is associated with what two types of muscle weakness? | Respiratory muscles and proximal muscle weakness (neck and shoulders) |
| What conditions have unpredictable effects on MG and often lead to exacerbations? | Infection, stress, surgery, pregnancy |
| Commonly used drugs for MG include? | Anticholinesterase drugs increase the amount of act at the NMJ through inhibition of end plate achE |
| Most common drug used to treat MG? | Pyridostigmine given PO every 2-4 hours. |
| Excessive administration of anticholinesterases may precipitate a cholinergic crisis, these symptoms include: | increased weakness, excessive muscarinic effects, salivation, diarrhea, miosis, decreased HR. |
| How do you differentiate a cholinergic vs myasthenic crisis? | Edrophonium test: Increased weakness after a max of 10mg of IV edrophonium indicates cholinergic crisis. Increased strength post edrophonium implies myasthenic crisis. |
| Treatments for MG include? | Thymectomy if less than 55 years old, plasmapheresis for pt's with dysphagia/respiratory failure, anticholinesterase drugs, corticosteriods, cyclosporine, immunogloblin therapy |
| Potential problems with continuing MG therapy prior to anesthesia include? | Increased vagal reflexes, can prolong duration of ester LA/sch |
| MG pt's with bulbar involvement are at risk for? | Pulmonary aspiration |
| MG pt's may be sensitive to what medications pre-op? | Respiratory depressants such as Opiods & Benzodiazepines. This can be seen with smaller than normal doses |
| Effects of NMBA on MG ? | Increased sensitivity, if necessary give cisatracurium or mivacurium, make sure you carefully evaluate pulmonary status prior to extubation. |
| Effects of Succinylcholine (Sch) on MG? | Unpredictable, prolonged effect, can cause phase II block |
| Most preferred drug for MG? | Propofol due to its short DOA |
| What volatile agents are most desired for MG? | Desflurane or Sevoflurane |
| Whats the greatest anesthesia risk to be concerned with MG? | Post op respiratory failure |
| MG and pregnancy, increased weakness is common in what trimester? What type of anesthesia is preferred? | 3rd trimester epidural anesthesia |
| Lambert eaton myasthenic syndrome manifestations? | Paraneoplastic syndrome characterized by proximal muscle weakness that typically begins in the lower extremities. May spread to the upper limbs, bulbar, and respiratory muscles. |
| CA associated with Lambert eaton syndrome? | Small cell CA of lung |
| Common manifestations of Lambert eaton syndrome include | Autonomic dysfuction, dry mouth, male impotence. |
| Lambert eaton pathology | Presynaptic defects of neuromuscular transmission. Antibodies to voltage gaited calcium channels on the nerve terminal reduce release of act at the motor end plate. |
| Lambert eaton syndrome muscle weakness is improved by? | Muscle weakness improves with repeated effort and is improved less with anticholinesterase drugs. |
| Treatment for Lambert eaton syndrome? | Guanidine HCL & 3,4 diaminopyridine: Increase release of ach producing improvement. |
| Guanidine HCL causes? | Hepatotoxicity |
| What anesthetics are pt's with Lambert eaton syndrome sensitive to? | Depolarizing and Non-depolarizing NMBA. If absolutely necessary give small doses of NMBA with careful neuromuscular monitoring. |
| True or false? Volatile agents are usually sufficient to provide muscle relaxation in pt's with lambert eaton syndrome. | True |
| Duchanne's muscular dystrophy (DMD) pathology/symptoms? | Abnormal dystrophin is produced, a protein found on the sarcolemma of muscle fibers. This develops muscle weakness and gait disturbance. |
| Age/Gender of DMD include? | Children 3-5 years old, most commonly male from X-linked recessive disorder. Most are WC bound by age 12 |
| Complications associated with DMD? | Fatty infiltration causes psedohypertrophy of muscles, mostly calves. Progressive weakness/contractures eventually result in kyphoscoliosis, this causes retention of secretions and frequent pulmonary infections. Pulmonary HTN |
| How to delay disease progression of DMD? | Glucocorticoid therapy |
| Cardiovascular complications of DMD? | Atrial arrithmias, degeneration of cardiac muscle. Death occurs from respiratory or cardiac complications. |
| Differences between DMD and Beckers Muscular dystrophy (BMD)? | Less common, presents later in life and progresses more slowly. Mental retardation is less common, usually reach 40-50 years old. Death=Resp complications |
| Anesthetic considerations for DMD and BMD? | Association with MH suggested but not proven. Sch used safely, but best to avoid. Avoid pre-meds due to aspiration precautions. |
| Risk of using Sch in pt's with DMD or BMD include? | Hyperkalemia triggering MH |
| True or False? Pt's with DMD or BMD can be sensitive to non-depolarizing NMBA? | True |
| Myotonic dystrophy physiology? | Slowing of relaxation after muscle contraction in response to electrical/percussive stimuli. |
| Principle manifestation of myotonic dystrophy ? | Myotonia, muscle weakness. atrophy. Usually effects cranial muscles, distal muscles involved more than proximal. |
| Myotonic dystrophy multiple organ systems involved? | Cataracts, premature frontal blindness. Hypersomnolence with sleep apnea. Endocrine dysfunction leading to pancreatic, adrenal, thyroid, and gonadal insufficiency. |
| Respiratory involvement of myotonic dystrophy leads to what pulmonary complications? | Alveolar hypoventilatoin and decreased Vital capacity |
| GI involvement of myotonic dystrophy lead to what GI complications? | GI hypo motility which can predispose to pulmonary aspiration |
| Cardiac manifestations of myotonic dystrophy? | Atrial arrithmias, heart block, depressed ventricular function |
| How do you best describe myotonia? | "stiffness" that may ease with continued activity. Patients report stiffness with cold temps. |
| Should Sch be given to pt's with myotonic dystrophy? | No, ssh should not be given, it may precipitate intense myotonic contractions. |
| Should non-depolarizers be given to pt's with myotonic dystrophy? | the response to Non-depolarizers is reported to be normal. May not prevent/relieve myotonic contractions. Reversal drugs aggregate myotonia. |
| Effects of opiods, sedatives, inhalational agents on pt's with myotonic dystrophy? | Can cause sudden/prolonged apnea |
| Postop pulmonary complications of myotonic dystrophy? | Prolonged hypoventilation, atelectasis, pneumonia. Use aspiration prophylaxis, agressive pulmonary hygiene with pt, incentive spirometry, careful postop monitoring. |
| Periodic paralysis disorders are characterized by? | sudden attacks of transient muscle weakness/paralysis. Attacks can last for a few hours for up to 2 days. |
| What causes these attacks with periodic paralysis? | Attacks/weakness are due to loss of muscle fiber excitability due to partial depolarization of the resting potential. Depolarization prevents the generation of action potentials, precipitating weakness |
| Sporadic episodes of weakness can worsen with what condition in patients with periodic paralysis? | Hypothermia |
| Hypokalemic periodic paralysis is associated with what disorder? | Hyperthyroidism |
| Hypokalemic periodic paralysis is associated with what channel? | Calcium channelopathy |
| What precipitates hypokalemic periodic paralysis? | Strenuous exertion, high carb meals |
| What part of they day is common for a patient with hypokalemic periodic paralysis to have symptoms? | Early in the AM |
| What happens during a hypokalmeic periodic paralysis attack? | Potasium/phosphorus levels are normal or slightly decreased, kidneys retain sodium, potassium, Chloride, and H20. |
| What happens during a hypokalmeic periodic paralysis attack to the ICF and ECF? | Increased ICF volume and decreased ECF volume. |
| How do you treat an attack of hypokalemic periodic paralysis? | 2-10g of K+, also encourage exercise |
| What should be avoided in patients with Hypokalemic periodic paralysis? | Glucose solution, due to the uptake of glucose into cells, with changes in serum potassium can worsen the hypokalemia/weakness. |
| Hyperkalemic Periodic paralysis effects what channels | Sodium channelopathy |
| Hypokalemic periodic paralysis can last how long? | 3-4 hours to days! |
| Hyperkalemic periodic paralysis can last how long? | Shorter more frequent attacks lasting 1-2 hours |
| What occurs at a cellular level with hyperkalemic periodic paralysis? | Paralysis triggered by abnormal inactivation of sodium channels by a mild increase in potassium. |
| What happens with depolarization in pt's with hyperkalemic periodic paralysis? | Sodium/water flows into cells with prolonged depolarization resulting in hyponatremia/hemoconcentration. |
| Conditions aggravated by hyperkalemic periodic paralysis? | Hypothermia, pregnancy, glucocorticoids, potassium. |
| What happens during an attack of hyperkalemic periodic paralysis? | Potassium levels can increase to >6 MEq/L but remain normal between attacks |
| Anesthesia considerations for hyperkalmeic periodic paralysis? | Frequent K+ levels, avoid Sch!, monitor neuromuscular function, maintain core temperature and prevent shivering considering hypothermia can trigger these attacks. Careful ECG monitoring. |
Created by:
evanrn1983
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