Orthopedic NP Review Course Exam 591 Questions with Verified Answers
Signs of inflammation - CORRECT ANSWER swelling, warmth, erythema, loss of
... [Show More] function, tenderness
Articular inflammation - CORRECT ANSWER Anatomic structure: synovium, cartilage, capsule (whithin the joint)
Painful site: diffuse, deep
Pain on movement: Active/passive, all planes
Swelling: common
Periarticular inflammation - CORRECT ANSWER Anatomic structure: Tendon, bursa, ligament, muscle, bone (outside the joint)
Painful site: focal "point"
Pain on movement: Active, in a few planes
Swelling: uncommon
Inflammatory joint diseases features - CORRECT ANSWER Pain (when?): Yes (AM)
Swelling: soft tissue
Erythema: sometimes
Warmth: sometimes
AM stiffness: prominent
Systemic features: Sometimes
Increased ESR, CRP: Frequent
Synovial fluid WBC: >2000
Ex: Septic, RA, SLE, Gout
Noninflammatory joint disease features - CORRECT ANSWER Pain (when?): Yes (PM)
Swelling: bony
Erythema: absent
Warmth: absent
AM stiffness: minor (<30')
Systemic features: absent
Increased ESR, CRP: uncommon
Synovial fluid WBC: <2000
Ex: OA, AVN
Acute Monoarthritis - CORRECT ANSWER Inflammation (swelling, tenderness, warmth) in one joint
Occasionally polyarticular diseases can present with monoarticular onset: RA, JRA, Reactive and enteropathic arthritis, Sarcoid arthritis, viral arthritis, psoriatic arthritis
Acute Monoarthitis Etiology - CORRECT ANSWER THE MOST CRITICAL DIAGNOSIS TO CONSIDER: INFECTION!
Septic
Crystal deposition (gout, pseudogout)
Traumatic (fracture, internal derangement)
Other (hemarthrosis, osteonecrosis, presentation of polyarticular disorders)
Questions to ask: History helps in Differential Dx - CORRECT ANSWER Pain come suddenly, minutes? - fracture
Over several hours or 1-2 days? - infectious, crystals, inflammatory arthropathy.
History of IV drug abuse or a recent infection? - septic joint.
Previous similar attacks? - crystals or inflammatory arthritis.
Prolonged courses of steroids? - infection or osteonecrosis of the bone.
Indications for arthrocentesis - CORRECT ANSWER The single most useful diagnostic study in initial evaluation of monoarthritis: SYNOVIAL FLUID ANALYSIS
-Suspicion of infection
-Suspicion of crystal-induced arthritis
-Suspicion of hemarthrosis
-Differentiating inflammatory from noninflammatory arthritis
Tests to perform on synovial fluid - CORRECT ANSWER -Low threshold for doing Gram stain and cultures.
-Total leukocyte count/differential: inflammatory vs. non-inflammatory.
-Polarized microscopy to look for crystals
Synovial fluid analysis - CORRECT ANSWER -Less viscous seen with inflammation
-Cloudy - infection, WBC, Crystals
-Reddish = blood
-Glucose - significantly lower w/infection and inflammation
-Protein increased with infection
-LDH - increased with infection, RA, gout
-Uric acid = gout
Septic Joint - CORRECT ANSWER -Most articular infections - a single joint
-15-20% cases polyarticular
-Most common sites: knee, hip, shoulder
-20% patients afebrile
-Joint pain is moderate to severe
-Joints visibly swollen, warm, often red
-Comorbidities: RA, DM, SLE, cancer, etc
Septic Joint - Nongonococcal - CORRECT ANSWER -80-90% monoarticular
-Most develop from hematogenous spread
-Most common: Gram positive aerobes (80%); majority with Staph aureus (60%); gram negative 18%
Septic Joint: Gonococcal - CORRECT ANSWER -Most common cause of septic arthritis
-Often preceded by disseminated gonococcemia
-Sexually active individual, 5-7 days h/o fever, chills, skin lesions, migratory arthralgias and tenosynovitis -> persistent monoarthritis
-Women often menstruating or pregnant
-Genitourinary disease often asymptomatic
Gout - CORRECT ANSWER -Caused by monosodium urate crystals
-Most common type of inflammatory monoarthritis
-Typically: first MTP joint, ankle, midfoot, knee
-Pain very severe; cannot stand bed sheet
-May be with fever and mimic infection
-The cutaneous erythema may extend beyond the joint and resemble bacterial cellulitis
Risk factors for gout - CORRECT ANSWER -Primary gout: obesity, HLD, DM, HTN, atherosclerosis
-Secondary gout: alcoholism, drug therapy (diuretics, cytotoxics), myeloproliferative disorders, chronic renal failure
Gout presenting s/s - CORRECT ANSWER -Systemic: fever rare but may occur, chills and malaise
-MS: Acute onset of monoarticular joint pain. First MTP most common. Usually affected in 90% of patients with gout. Other joints include knees, foot and ankle. Less common in upper extremities (Postulated that decreased solubility of MSU at lower temps of peripheral structures such as toe and ear)
-Skin: warmth, erythema and tenseness of skin overlaying joint. May have pruritis and desquamation.
-GU: Renal colic with renal calculi formation in patients with hyperuricemia
Gout Dx - CORRECT ANSWER Uric Acid (limited value as majority of hyperuricemic pts will never develop gout; levels may be normal during acute attack)
CBC (mild leukocytosis in acute attacks, but may be higher than 25,000/mm)
ESR (mild elevation or may be 2-3 x normal)
24 hr urine uric acid (only useful in pts being considered for uricosuric therapy or if cause of marked hyperuricemia needs investigation)
Trial of colchicine (Positive response may occur in other types of arthritis to include pseudogout
Gout treatment goals - CORRECT ANSWER -Gout can be treated without complications
-Therapeutic goals include: terminating attacks; providing control of pain and inflammation; preventing future attacks; preventing complications such as renal stones, tophi, and destructive arthropathy
Acute gout attack treatment - CORRECT ANSWER -NSAIDS most commonly used, all work the same, Indocin most commonly used, remember to use with caution with CAD, GI bleed, RF
-Indocin 50 mg PO BID-TID for 2-3 days and then taper
-Ibuprofen 400mg PO q4-6hr max 3.2g/day
-Ketorolac 60 mg IM or 30mg IV x1 dose in pts <65 (30mg IM or 15mg IV in single dose in pts >65 yo, or w pts who are renally impaired
-Continue meds until pain and inflammation have resolved for 48 hr
Colchicine for acute gout - CORRECT ANSWER -Inhibits microtubule aggregation which disrupts chemotaxis and phagocytosis
-Inhibits crystal-induced production of chemotatic factors
-Administered orally in hourly doses of 0.5 to 0.6 mg until pain and inflammation have resolved or until GI side effects (diarrhea) prevent further use. Max dose 6mg/24hr
-2mg IV then 0.5mg q6hr until cumulative dose of 4mg over 24hr
Corticosteroids for acute gout - CORRECT ANSWER Used for pts who cannot tolerate NSAIDs, or failed NSAID/colchicine therapy. Daily doses of prednisone 40-60 mg a day for 3-5 days then taper 1-2 weeks. Improvement seen in 12-24 hr.
ACTH (Adrenocorticotropic hormone) for acute gout - CORRECT ANSWER Peripheral anti-inflammatory effects and induction of adrenal glucocorticoid release. 40-80 IU IM followed by second dose if necessary
Intra-articular injection with steroids for acute gout - CORRECT ANSWER Beneficial in pt with 1-2 large joints affected. Good option for elderly pt with renal or PUD (peptic ulcer disease) or other illness.
Triamcinolone 10-40mg or Dexamethasone 2-10mg alone or in combination with Lidocaine
Non-Pharm Tx for acute gout - CORRECT ANSWER Immobilization of joint.
Ice packs.
Abstinence of ETOH (consumption can increase serum urate levels by increasing uric acid production. When used in excess it can be converted to lactic acid which inhibits uric acid excretion in the kidney).
Dietary modification (low carb, increase protein and unsaturated fats, decrease in dietary purine-meat and seafood. Dairy and vegetables do not seem to affect uric acid - bing cherries and vitamin C)
Gout prophylaxis - CORRECT ANSWER Frequent attacks >3/year, tophi development or urate overproduction. Avoid use of meds that contribute to hyperuricemia: Thiazide and loop diuretics, low-dose salicylates, niacin, cyclopsorine, ethambutol (Losartan promotes urate diuresis and may even normalize urate levels. This action does not extend to other members of the ARB class. Useful in elderly with HTN + gout). Colchine 0.6 mg daily-BID. Use alone or in combination with urate lowering drugs. Prophylaxis w/o urate lowering drugs may allow tophi to develop.
Gout prophylaxis: Urate lowering drugs - CORRECT ANSWER Used for documented urate overproduction. Goal is for serum urate concentartion to 6mg/dL or less. Start of therapy can precipitate acute attack; therefore, may need to use colchicine as long as six months.
-Xanthine oxidase inhibitors: Allopurinol. Blocks conversion of xanthine to uric acid. Works for underexrectors and overproducers. Start typically 300mg/day and titrate weekly 100mg/day until optimal urate levels achieved. Start lower doses with renally impaired pts.
-Uricosuric drugs: Probeneicd or Sulfinpyrazone. Increased renal clearance of uric acid by inhibiting tubular absorption. SE may prohibit use (GI and renal). Need measurement of 24hr urine in anyone for whom Probenecid therapy is initiated.
New therapies for gout management - CORRECT ANSWER -Uricase (enzyme that oxidized uric acid to a more soluble form. Natural Uricase from Aspergillus flavus and Candida utilis under investigation)
-Febuxostat (new class of Xanthine Oxidase inhibitor. More selective than allopurinol. Little dependence on renal excretion)
-Losartan (ARB given as 50mg/dL can be urisuric. When given with HCTZ, it can blunt the effect of the diuretic and potentiate its antihypertensive action
-Fenofibrate (studies note when used in combo with Allopurinol produced additional lowering of the urate)
Gout Complications - CORRECT ANSWER Renal failure (ARF can be caused by hyperuricemia, chronic urate nephropathy
Nephrolitiasis
Joint deformity
Recurrent Gout
Calcium pyrophosphate deposition disease (CPPD) - CORRECT ANSWER Can cause monarthritis clinically indistinguishable from gout - Pseudogout. Often precipitated by illness or surgery. Pseudogout is most common in the knee (50%) and wrist. Reported in any joint (including MTP -metatarsophalangeal). CPPD disease may be asymptomatic (deposition of CPP in cartilage).
Associated conditions for CPPD - CORRECT ANSWER Hyperparathyroidism
Hypercalcemia
Hypocalciuria
Hemochromatosis
Hypothyroidism
Gout
Aging
Polyarthritis - CORRECT ANSWER Definite inflammation (swelling, tenderness, warmth of >5 joints)
A patient with 2-4 joints is said to have paucior oligoarticular arthritis
Acute Polyarthritis - CORRECT ANSWER Infection: gonococcal; meingococcal; lyme disease; rheumatic fever; bacterial endocarditis; viral (rubella, parvovirus, Hep B)
Inflammatory: RA; JRA; SLE; reactive arthritis; psoriatic arthritis; polyarticular gout; sarcoid arthritis
Inflammatory Arthritis features - CORRECT ANSWER Morning stiffness >1 hr
Fatigue: profound
Activity: improves symptoms
Rest: worsens symptoms
Systemic: Yes
Corticosteroid: yes
Noninflammatory arthritis features - CORRECT ANSWER Morning stiffness: < 30 min
Fatigue: minimal
Activity: worsens symptoms
Rest: improves symptoms
Systemic: no
Corticosteroid: no
Temporal patterns in polyarthritis - CORRECT ANSWER Migratory pattern: Rheumatic fever, gonococcal (disseminated gonococcemia), early phase of Lyme disease
Additive pattern: RA, SLE, psoriasis
Intermittent: gout, reactive arthritis
Patterns of joint involvement - CORRECT ANSWER Symmetric polyarthritis involving small and large joints: viral, RA, SLE, one type of psoriatic (the RA-like)
Asymmetric, oligo- and polyarthritis involving mainly large joints, preferably lower extremities, esp knee and ankle: reactive arthritis, one type of psoriatic, enteropathic arthritis.
DIP (distal interphalageal joint, the first knuckle from the top of the finger) joints: Psoriatic
Viral arthritis - CORRECT ANSWER Younger patients
Usually presents with prodrome, rash
History of sick contact
Polyarthritis similar to acute RA
Prognosis good; self-limiting
Ex: Parvovirus B-19, Rubella, Hep B & C, acute HIV, Epstein-Barr virus, mumps
Parvovirus B-19 - CORRECT ANSWER The virus of "fifth disease", erythema infectiosum (EI).
Children "slapped cheek"; adults flu-like illness, maculopapular rash on extremeties.
Joint involved more in adults (20% of cases).
Abrupt onset symmetric polyarthralgia/polyarhtritis with stiffness in young women exposed to kid with E.I.
May persist for a few weeks to months.
Acute Sarcoid Arthritis - CORRECT ANSWER Chronic inflammatory disorder - noncaseating granulomas at involved sites.
15-20% arthritis; symmetrical: wrists, PIPs (proximal interphalangeal), ankles, knees.
Common with hilar adenopathy.
Erythema nodosum.
Lodgren's syndrome: acute arthritis, erythema nodosum, bilateral hilar adenopathy
Psoriatic Arthritis - CORRECT ANSWER Prevalence of arthritis in Psoriasis 5-7%
Dactilytis ("sausage fingers"), nail changes.
Subtypes: asymmetric, oligoarticular associated dactylitis; predominant DIP (distal interphalangeal) involvement - nail changes; polyarthritis "RA-like" - lacks RF (rheumatoid factor) or nodules; arthritis mutilans - destructive erosive hands/feet; axial involvement - spondylitis - 50% HLAB 27 (+); HIV-associated - more severe
HLA-B27 - CORRECT ANSWER HLA-B27 is a blood test to look for a protein that is found on the surface of white blood cells. The protein is called human leukocyte antigen B27 (HLA-B27). Human leukocyte antigens (HLAs) are proteins that help the body's immune system tell the difference between its own cells and foreign, harmful substances.
Reactive arthritis - CORRECT ANSWER Infection-induced systemic disease with inflammatory synovitis from which viable organisms cannot be cultured.
Associated with HLA B27
Asymmetric, oligoarticular, knees, ankles, feet.
40% have axial disease (spondyloarthropathy).
Enthesitis: inflammation of tendon-bone junction (Achilles tendon, dactylitis).
Extraarticular: rash, nails, eye involvement
Spondyloarthropathy - CORRECT ANSWER Spondyloarthropathy or spondyloarthrosis refers to any joint disease of the vertebral column. As such, it is a class or category of diseases rather than a single, specific entity. It differs from spondylopathy, which is a disease of the vertebra itself.
Rheumatoid Arthritis - CORRECT ANSWER Symmetric, inflammatory polyarthritis, involving large and small joints.
Acute, severe onset 10-15%; subacute 20%.
Hand characteristically involved.
Acute hand deformity: fusiform (tapering at both ends, spindle shaped) swelling of fingers due to synovitis of PIPs.
RF may be negative at onset and may remain negative in 15-20%.
RA is a clinical diagnosis, no lab test is diagnostic, just supportive.
ACR (American College of Rhuematology) criteria for RA diagnosis - CORRECT ANSWER Must have 4 out of 7:
Early morning stiffness > 1 hr;
> 3 joint arthritis;
Symmetrical arthritis;
Wrist, MCP, PCP arthritis;
RA nodules;
Rheumatoid factor +;
X-ray changes: periarticular osteopenia/marginal erosions
Rheumatoid factor - CORRECT ANSWER RF, an IgM antibody is seen in the serum of 75% of pts with RA. High titers of RF are associated with severe disease. RF is also found in other diseases like syphilis, sarcoidosis, infective endocarditis, TB, leprosy, parasitic infections; in advanced age and in asymptomatic relative of pts with rheumatoid disease.
Antinuclear antibody are seen in 20% of pts with RA, though their titer is lower than in SLE.
DMARDS - CORRECT ANSWER Biologics: Non-TNF (Abatacept, Rituximab, Tocilizumab, Tofacitinib, Anakinra) & Anti-TNF (Adalimumab, Certolizumab, Etanercept, Golimumab, Infliximab)
Non-Biologics: Hydroxychoroqine, Leflunomide, Methotrexate, Minocycline, Sulfasalazine
DMARDs (disease modifying anti-rheumatic drugs) - CORRECT ANSWER These drugs need frequent monitoring: blood, liver, lung and kidney are frequent sites of adverse effects. Interval of lab testing varies with the drug - 4-8 wk intervals are common. Most pts need to be seen 3-6 times/yr
Prognosis of RA - CORRECT ANSWER 2 divergent course: 50-75% experience remission in 2 years (these pts are negative for rheumatoid factor and have goof functional status even during disease activity). Conservative therapy is advised for this group. Pt who have severe disease have a worse prognosis, and on an average die 10-15 yrs earlier than people e/o RA. Since most of the joint damage occurs in the first 2 yrs, these patients should be started on a disease modifying agent early
)You are doing a preop physical for a routine THA on a 43 yo F w RA since age 20. PMH b/l TKA. No other medical problems. Current mes: NSAID, low-dose prednisone, MTX (methotrexate), and HCQ (Hydroxychloroquine, sold under the brand name Plaquenil). General PE normal. MS exam, extensive deformities, mild synovitis. In addition to routine tests, what test should be ordered before surgery? - CORRECT ANSWER Cervical spine films AP&Lateral, NOT flexion and extension. We don't want to miss a C1-C2 sublaxation. RA can cause asymptomatic instability of the neck - manipulation under anesthesia can cause spinal cord injury!
Clues to look for C1-C2 sublaxation - CORRECT ANSWER Long-standing RA or JRA. May have NO symptoms. C2-C3 radicular pain in the neck and occiput. Spinal cord compression: quadriparesis or paraparesis, sphincter dysfunction, sensory deficits, TIAs secondary to compromise of the vertebral arteries
Pre-Op exam of RA patient - CORRECT ANSWER C1-C2 sublaxation
Cricoaryternoid arthritis w adductor spasm of the vocal cords and a narrow airway.
Pulmonary fibrosis.
Risk for GI bleeding.
Need for stress steroid coverage.
Discontinue NSAIDs several days preop.
Discontinue methotrexate 1-2 weeks preop** (coverage with analgesic meds or if necessary short-term, low dose steroid if RA flares)
68 yo F w 3 yr ho RA new pt. Presents w 4 wks increasing fatigue, dizziness, dyspnea, and anorexia. Joint pain and stiffness are mild and unchanged. Managed with ibuprofen and hydroxychloroquine until 4 mo ago, when a flare cause a switch to piroxicam and prednisone. PMH: peptic ulcer 10 yrs ago, mild HTN. Exam shows a thin, pale, apathetic woman w T 98.4F, BP 110/65, HR 110. Symmetrical 1+ synovitis of the wrist, MCP, PIP and MTP joints. Exam of heart, lungs, and abdomen is unremarkable. What system much you inquire more about today? - CORRECT ANSWER GI** NSAID gastropathy is sneaky and can be fatal!
Clues of impending disaster: high risk for NSAID gastropahty; presentation suggestive of blood loss (pale, dizzy, weak, tachycardia w low BP); no evidence of flare in RA to explain recent symptoms of increased fatigue
Synovitis - CORRECT ANSWER Synovitis is the medical term for inflammation of the synovial membrane. This membrane lines joints that possess cavities, known as synovial joints. The condition is usually painful, particularly when the joint is moved. The joint usually swells due to synovial fluid collection.
NSAID gastropathy - CORRECT ANSWER gastric ulcers are more common than duodenal ulcers. No reliable warming signs. 80% of serious events occur w/o prior symptoms. Risk of hospitalization for NSAID ulcers in RA in 2.5 to 5.5 X higher than general pop. 107,000 pts are hospitalized and 16,000 death occur annually in US because of NSAID-induced GI complications
Risk factors for NSAID ulcers - CORRECT ANSWER older age.
Prior h/o peptic ulcer or GI symptoms w NSAIDs.
Concomitant use of prednisone.
NSAID dose: more prostaglandin suppression = greater risk fo serious events.
Disability level: the sicker the pt the higher the risk
Treatment of NSAID gastropathy - CORRECT ANSWER Acute bleed or perforation: Stop NSAID, endoscopy or surgery, start omeprazole.
Ulcer w/o bleed or perforation, and needs or wants continued NSAID: omeprazole 20 mg qd - 76% healed; OR misoprostol 200 uq qid - 71% healed
Prevention of NSAID gastropathy - CORRECT ANSWER Avoid the problem: stop the NSAID and use alternative treatment: low-dose prednisone, Tylenol, Nonacetylated salicylates.
Use a selective cyclooxygenase-2 inhibitor.
Antacids and H2 blockers are not the answer! May mask symptoms but DO NOT prevent serious events
52 yo M w destructive RA treated w NSAID and low-dose prednisone. MTX (methotrexate) started 4 mo ago, now 15mg/wk. Presents w 3-wk h/o fever, dry cough, and increasing SOB. Exam: low grade fever, fine rales in both lungs, normal CBC and liver enzymes, low albumin, diffuse interstitial infiltrates on CXR. What next? - CORRECT ANSWER Give oral steroid for hypersensitivity pneumonitis and stop methotrexate.
DMARDs have a dark side.
Methotrexate may cause serious problems: lung, liver, bone marrow. Be on the look out for toxicity w all the DMARDs
Erythematosis, Lupus - CORRECT ANSWER Lupus is an autoimmune disease in which the body creates antigens that attack different body tissues.
3 types of lupus: Discoid, Systemic, and Drug-induced
SLE (systemic lupus erythematosus) symptoms - CORRECT ANSWER Skin rash
Arthritis
Fever
Anemia
Joint pain
Photosensitivity
Hair loss
Ulcers in the mouth
Kidney damage
Arthritis of SLE - CORRECT ANSWER Musculoskeletal manifestation 90%
Most have arthralgia
May have acute inflammatory synovitis RA-like.
Do not develop erosion.
Other clinical features help with DD: malar rash, photosensitivity, rashes, alopecia, oral ulceration
SLE diagnostic tests - CORRECT ANSWER LE cell; ANA titer; Anti-DNA; Complement fixation; ESR/CRP.
Criteria to DX: Malar, discoid rash; photosensitivity; arthritis; renal disorder; immunological disorder; DNA, ANA
Lupus Criteria - CORRECT ANSWER Need 4 of 11:
M - malar rash
D - discoid rash
S - serositis
O - oral ulcers
A - arthritis
P - photosensivity
B - blood abnormalities
R - renal
A - ANA antibiodies
I - immune abnormalitis
N - neurologic
Fibromyalgia ACR criteria - CORRECT ANSWER Heightened myodenia (pain to touch).
History of chronic widespread pain >3 mo.
Exhibit >11 of 18 tender points.
ACR criteria are both sensitive (88.4%) and specific (81.1%)
Fibromyalgia treatment - CORRECT ANSWER Aerobic exercise; Cog behavioral tx; pt education; strength training; acupuncture; biofeedback; hypnotherapy; antidepressants; analgesics; anticonvulsants (pregabalin - Lyrica); SNRI (duloxitine - Cymbalta)
In early June a 15 yo boy comes to your practice w his mother. He had been fine until about 5 days ago when he developed a fever. He has a stiff neck and a rash on his back. He and his family live in Connecticut near the New York State border. His mother reports he was playing in the woods recently. He has a bulls-eye rash on his arm. What is the diagnosis? - CORRECT ANSWER Lyme disease.
Erythema migranes rash, along with fever and stiff neck, along with the geographic local of the patient suggests Lyme disease.
Other s/s: fatigue, headache, muscle and joint pain.
Borrelia burgdorferi is the causative agent of Lyme disease (spirocete, same family as syphillis).
Treat with amoxicillin or doxycycline for 3-4 weeks.
Lyme Disease - CORRECT ANSWER Epidemiology: tick borne disease (Borrelia burgdorferi in deer tick); Multi-system, inflammatory; in 2010, 94% of cases from Northeast with cases noted in MN & WI.
Early presentation: distinct skin rash - local lesion; recent h/o pt walking in wooded areas.
Later stages: cardiac/neurologic/arthritis complications
Stages of Lyme disese - CORRECT ANSWER 1st: erythema migrans (bulls eye) rash 7-10 days; headache/fever/malaise; treated w antibiotics.
2nd: days to mo later, early disseminated w a hematogenous spread (spread in the blood).
Later stage: If untreated 10% develop chronic arthritis; bells palsy/myopericarditis/poor memory
Lyme Disease - CORRECT ANSWER Pt hx: exposure to tick bite - wooded areas.
Dx test: ELISA test screen for antibodies (once positive, will always be positive even after treatment).
Tx: Antibiotics - PCN/Rocephin; NSAIDs; intra-articular corticosteroids for Lyme arthritis; medical specialist monitoring for systemic conditions.
Patient education for Lyme disease - CORRECT ANSWER Walk in the center of path in the woods in high risk areas; wear light colored clothing so ticks are easier to see; wear long pants tucked into socks; check for ticks; use repellant; PROMPT eval for suspicious symptoms
A 21 yo M presented w acute pain and swelling of 1 knee. On exam, the joint is tender and restricted in movement. Xray of the knee showed periarticular OA. On investigation, he had a raised ESR of 102, and mild anemia (Hb 10.6) but no detectable serum RA factor. The knee effusion was aspirated; the fluid contained a polymorphonuclear leucocytosis but no organisms or RA factor. No diagnosis was made at this stage but he was treated empirically with indomethacin; his arthritis improved. What was his diagnosis? - CORRECT ANSWER Possibly Ankylosing spondylitis.
Our 21 yo M presented w acute pain and swelling of 1 knee returns 15 mo later and now has developed an iritis in his left eye, low back pain and stiffness. His peripheral joints were normal but pain could be elicited in both sacroilian joints. X-rays of his pelvis showed the classic changes of ankyosing spondylitis and tissue typing revealed that he was HLA-B27 positive. He has intermittent backache over the last 5 years, although daily exercises have limited the stiffness. He has developed bony ankylosis between the lumbar vertebrae.
anylosing spondylitis - CORRECT ANSWER Etiology: unknown - link to HLA-B27 gene; chronic inflammatory disease; axial skeleton; Synovial inflammation -> fibroblast response -> dense fibrous scars -> vertebrae fuse.
Epidemiology: onset age 25-34 yo; occurs in males 5X greater than females.
Clinical presentation: long h/o dull achiness w stiff back or neck, ascending stiffness of spine, fatigue and impaired sleep.
Diagnostic testing: radiographs show bamboo spine (later stages, calcification formation between vertebra); elevated ESR, decreased PFT (pulmonary function test) if there is thoracic involvement.
Pharamcologic tx: NSAIDs/DMARDS/AntiTNF blockers; non-narcotic analgesics prn; muscle relaxants prn.
Non-Pharmacologic tx: balance activity and rest periods; PT; daily stretching exercises; assistive devices - canes
Systemic Sclerosis - CORRECT ANSWER AKA scleroderma
Etiology: autoimmune disorder; multi-system (microvascular and connective tissue).
Vasculopathy and fibrosis.
Alterations in skin and internal organs.
Limited (CREST syndrome) and diffuse types.
Incidence: est 100,000 in US. Usually age 30-50. Women > men. All races and ethnic groups.
Pulmonary fibrosis is the leading cause of death for this disease.
Limited scleroderma (CREST syndrome) - CORRECT ANSWER C- Calcinosis (CA deposits under skin)
R - Raynaud's phenomenon
E - esophageal dysfunction
S - sclerodactyly (tightening of the skin)
T - telangiectasia (dilated blood vessels)
2 out of 5 symptoms confirm the disese
Anticentromere antibodies + < 90%
Clinical presentation of diffuse scleroderma - CORRECT ANSWER Edema of hands.
Thickened skin w loss of skin folds.
Stiff joints.
Decreased thoracic excursion.
H/O of Raynaud's.
GI issue/esophageal dysfunction.
Causes changes to internal organs.
Anti topoisimerase-I or Anti-Scl-70 antibodies + in < 40%.
CXR, PFTs may show changes.
treatment of systemic sclerosis - CORRECT ANSWER No cure.
Avoid cold.
Cease smoking.
Skin care.
Good dental care (Sjorn's syndrome common).
PT - maintain ROM, facial mobility.
GI management.
Meds: modify disease/symptomatic treatment. ACEI for renal crisis. Vasodilators to increase blood flow to fingers, prevent/tx pulm HTN. Immunosupressants.
Sometimes requires dialysis, kidney transplant.
Progression and complications of systemic sclerosis - CORRECT ANSWER Once in remission - relapse is uncommon.
Lung impairment - leading cause of death.
Loss of hand grips.
GI: hypomotility -> malabsorption/constipation; esophageal fibrosis -> dysphagia.
Dermatomyositis/Polymyositis - CORRECT ANSWER Inflammatory myopathy of skeletal muscles.
S/S: fatigue; fall unrelated to balance; heliotrope rash; shawl sign; V-sign.
Dx test: elevated CK (muscle damage); EMG - inflammation; biopsy - necrosis.
Tx: Corticosteroids; immunosuppressives; IV IgG; topicals for rash; bed rest - slow return; ROM activities.
Differential diagnosis in inflammatory arthritis - CORRECT ANSWER Eye involvement: conjunctivitis in reactive arthritis, uveitis in enteropathic and sarcoidosis, episcleritis in RA.
Oral ulcerations: painful in reactive arthritis and enteropathic, not painful in SLE.
Nail lesions: pitting (psoriasis), onycholysis (reactive arthritis).
Alopecia (SLE)
Onycholysis - CORRECT ANSWER Onycholysis is when a person's nail or nails detach from the skin underneath. Although not a serious health condition by itself, onycholysis can be a symptom of a potentially serious illness.
Anatomy of the spine - CORRECT ANSWER 7 cervical vertebra
12 thoracic
5 lumbar
5 sacral fused vertebra (Sacrum and Coccyx).
THe vertebral column i sthe part of the axial skeleton that surrounds and protects the spinal cord, while bearing the weight of the head, neck, and trunk. The vertebral column is not straight; its curves accomodate the thoracic and abdominopelvic viscera and also balance the weight of the trunk and head over the lower limbs. Cervical is concave on the posterior surface, thoracic is convex on the posterior surface, lumbar is concave, and the sacrum is convex.
T4 = nipple line
T10 = umbilicus
L4 = iliac crest
The adult human vertebral column consists of 26 bones total. Generally, 1 spinal nerve emerges at each vertebrae, save in the cervical spine where there are 7 vertebrae but 8 cervical nerves.
Scoliosis - CORRECT ANSWER Scoliosis is a sideways curvature of the spine that occurs most often during the growth spurt just before puberty. While scoliosis can be caused by conditions such as cerebral palsy and muscular dystrophy, the cause of most scoliosis is unknown.
kyphosis - CORRECT ANSWER excessive outward curvature of the spine, causing hunching of the back.
Cervical spine - CORRECT ANSWER 7 vertebrae
8 cervical nerve root
Atlas C1
Axis C2 has the odontoid process which fits inside C1.
The 1st cervical vertebrae is called the atlas; its superior articular processes have facets that articulate with the occipital condyles of the skull in a type of joint that permits forward-backward motion of the head. The body of the 2nd cervical vertebrae, the axis, has a prominent odontoid process that extends superiorly and articulates with a facet on the atlas, providing a pivot point to allow rotational movement of the head. The facet of the superior articular process of the axis articulates with a similar flat surface on an inferior articular process of the atlas. Like other individual vertebrae, the axis has a prominent dorsal spinous process, which is notched as it is in cervical vertebrae 3-6 and is referred to as bifid; the atlas has a smaller dorsal process known as the posterior tubercle. Laterally, a transverse process provides attachment sites for muscle, while the transverse foramen allows passage of vertebral arteries and veins.
Vertebrae - CORRECT ANSWER Each individual vertebrae consists of a vertebral body or centrum that transfers weight to the next lower vertebrae, a vertrebral arch forming the posterior margin of the vertebral canal, and variable types of processes that either provide attachment points for muscles or articulate with ribs. The 5 sacral vertebrae begin fusing after puberty and are usually completely fused by age 25-30. The coccyx is not completely fused until late in adulthood.
Recommended preop testing - CORRECT ANSWER Hgb for major surgery w significant expected blood loss or CBC count if the cost is not substantially increased; Serum Cr level for people older than 40; EKG in pts older than 40; CXR in pts older than 60; no labs must be repeated if results were normal
Preop cardiac considerations - CORRECT ANSWER For emergency noncardiac surgery, preop heart testing should not be done; rather, the pt should immediately undergo the emergency procedure. Pts w severe or symptomatic cardiovascular disease and/or active cardiac conditions should undergo eval & tx before noncardiac surgery. These conditions include unstable CAD, blockage of 2 or more coronary vessels, decompensated HF, significant cardiac arrhythmias, or severe valvular disease.
Geriatric considerations - CORRECT ANSWER Careful PE; malnutrition suspected - CBC, albumin, cholesterol; UA, CBC, Chem panel, coag studies; lytes if on diuretic; EKG & CXR
Geriatric guidelines - CORRECT ANSWER Complete H&P; cog assessment; depression screening; risk factors for postop delirium; substance abuse/dependence screening, ETOH; cardiac eval following American College of Cardiology/AHA algorithm for pts underdoing noncardiac surgery; risk factors for postop pulmonary complications and implementing suitable prevention strategies; functional status and fall history documented; calculate frailty at baseline; assessing nutritional status and considering implementation of preoperative interventions for high-risk patients; complete Rx hx, preop adjustments, monitoring for polypharm; identify patient's treatment goals and expectations; assess family and social support system; performing suitable diagnostic tests prn.
Functional Capacity Evaluation (FCE) - CORRECT ANSWER 1-4 metabolic equivalents (METs) include eating, dressing, using the bathroom, walking indoors, walking 1-2 blocks on level ground, and doing light housework.
4-10 METs include climbing stairs or walking up a hill; running a short distance; scrubbing floors or moving furniture; and recreational activities, such as golf, bowling, dancing, and playing tennis.
ASA Physical Status Classification System - CORRECT ANSWER ASA 1 Normal healthy patient
ASA 2 Patients with mild systemic disease
ASA 3 Patients with sever systemic disease
ASA 4 Patients with severe systemic disease that is a constant threat to life
ASA 5 Moribund patients who are not expected to survive w/o the operation
ASA 6 A declared brain-dead patient whos organs are being removed for donor purposes
Malignant hyperthermia - CORRECT ANSWER An inherited disorder of skeletal muscle triggered in humans or animals in most stances by inhalation agents and/or succinylcholine, resulting in hypermetabolism, skeletal muscle damage, hyperthermia, and death if untreated. Underlying physiologic mechanism - abnormal handling of intracellular Ca+ levels.
Triggering agents: potent volatile anesthetics (e.g. Halothan, Sevoflurane, desflurane).
Non-triggering: IV agents, opioids, non-depolarizing agents succinylcholine, ketamine, propofol, anxiolytics
Clinical signs of malignant hyperthermia - CORRECT ANSWER specific signs: muscle rigidity; increased CO2 production; rhabdomyolysis; marker temperature elevation.
Non-specific signs: tachycardia; tachypnea; acidosis (respiratory/metabolic); hyperkalemia
Immediate tx of malignant hyperthermia - CORRECT ANSWER DC INH agents, succinylcholine; hyperventilate w 100% O2; bicarb 1-2 mg/kg prn; get additional help; dantrolene 2.5 mg/kg IV push, repeat prn; cool patient: gastric lavage, surface, wound; tx arrhythmias; do NOT use Ca+ channel blockers
Continued tx of malignant hyperthermia after initial phase - CORRECT ANSWER Give dantrolene 1 mg/kg every 4-6 hrs for 24-48 hrs; monitor for recrudescence - rate is 25%; follow lyte panel, blood gases, CK, core temp, urine output & color; coag studies.
Biochemical markers: blood gases esp p CO2, pH; myoglobin levels in serum and urine; PT, PTT, INR, fibrin split products, liver enzymes, BUN; monitor for signs of myoglobin and rhabdomyolysis and institute therapy to prevent renal failure.
Malignant hyperthermia (MH) prevention - CORRECT ANSWER Avoid MH trigger agents in MH susceptible or those suspected of being susceptible. Preop personal/family hx of anesthetic problems, neuromuscular disorders to identify those who may be MH-susceptible. Temp/end tidal CO2 monitoring during general anesthesia. Recognition of masseter muscle rigidity. Prompt investigation of unexplained tachycardia, herpcarbia, hyperthermia. Availability of Dantrolene. ORs should perform regular MH drills to be prepared. [Show Less]