Lesson 4: general + tumors Flashcards
Osteomalacia
- CM
- labs
- imaging
- tx
CM Bone pain and muscle weakness Bone tenderness Fractures Difficulty walking and waddling gait
LAB findings
- elev alk phosph
- elev PTH
- low serum Ca and VIt d
Radiographic findings
Vertebral body trabeculae have a distinct appearance due to inadequate mineralization
This is a spine CT scan of a 53 y/o male with osteomalacia.
TX
OSTEOMALACIA
Treatment
Treatment is aimed at the underlying cause
Vitamin D supplementation and calcium supplementation
For patients with severe vitamin D deficiency, they should be given 50,000 IU of Vitamin D2 or D3 PO once a week for 6-8 weeks, then 800 IU of vitamin D3 thereafter.
Osteogenesis Imperfectia
- CM
- PE
- dx
- tx
AUTOSOMAL DOM DZ
CM
Severe, premature osteoporosis - multiple recurrent spontaneous fractures with minimal or no trauma in childhood, leading to limb deformities & shortening.
Deafness can also occur
PE
Blue tinted sclerae is a hallmark
Thin skin
Hyperextensibility of the ligaments
Otosclerosis with significant hearing loss
Brown teeth (hypoplastic and deformed as well). Not to be confused with TETRACYCLINE TEETH.
Intelligence NOT affected
Dx: Clinical & x-rays; Confirmed with genetic/DNA testing
Management:
Bisphosphonates, physical therapy and surgical interventions. Most people are wheelchair bound.
Torticolis
- injury to what muscle
- how does it present
- causes— acute and non acute
- tx
- prognosis
Injury to SCM—during delivery or dz affecting the C-spine in infancy
contracture of SCM causes chin to rotate to SIDE OF OPPOSITE muscle affected—causes head to tilt toward side of contracture
ACUTE=may follow URI or mild trauma in kids
other causes: spinal cord and cerebellar tumors, syringomyelia and RA
TX
- If torticollis in early infancy is left untreated, a striking facial asymmetry can persist.
- Passive stretching is an effective treatment in up to 97% of all cases.
- Surgical release of the muscle origin and insertion if the deformity does not correct with passive stretching during the first year of life
- For acquired torticollis in childhood, traction or a cervical collar usually results in resolution of the symptoms within 1 or 2 days.
Prognosis
- Torticollis is occasionally associated with congenital deformities of the cervical spine.
- Radiographs of the spine are indicated in most cases where such anomalies are suspected. In addition, there is a 15%–20% incidence of associated hip dysplasia
Scoliosis
- cm
- diagnosis– best views on xray
*Scoliosis in adolescents does not typically cause significant pain.
If a patient has significant pain, she/he should be evaluated to rule out the possibility of some other disorder such as infection or tumor.
*Deformity of the rib cage and asymmetry of the waistline are clinically evident for curvatures of 30 degrees or more.
*Lesser curves may be detected through a forward bending test, which is designed to detect early abnormalities of rotation that may not be apparent when the patient is standing erect. Rotation of the spine may be measured with a scoliometer.
*Rotation is associated with a marked rib hump as the lateral curvature increases in severity.
FILMS–PA and lateral best for diagnosis
TX
- Depends on the curve magnitude, skeletal maturity, and risk of progression.
- Specific management is dependent on the Cobb angle, measured on a standing PA x-ray of the spine.
- Curvatures of less than 20 degrees typically do not require treatment unless they show progression.
- Bracing is indicated for curvatures of 20–40 degrees in a skeletally immature child.
- Curvatures greater than 40 degrees are resistant to treatment by bracing.
- Thoracic curvatures greater than 70 degrees have been correlated with poor pulmonary function in adult life, leading treatment algorithms toward preventing progression to this extreme.
- Curvatures reaching a magnitude of 40–60 degrees are indicated for surgical correction as they are highly likely to continue to progress.
- Surgical intervention consists of spinal instrumentation and fusion.
Acute Osteomyelitis
- define
- what is most affected
- who is msot affected
- two main cats
- mc pathogen
- rf
- cm
- dx— most useful imaging?
- tx
- inflammatory destruction of bone due to infection*
- tibia and femur MC affected—ESP IN KIDS
- vertebrae MC in ADULTS
CATEGORIES
- secondary to sepsis–>bacteria is in blood and then infects bone
- direct bacterial infiltration from infected ulcer, trauma or vascular insufficiency
STAPH AUREUS**
**puncture wound thru shoe= psudeomonas aeruginosa
RF
- open fx
- dm
- IVDU
- sepsis
CM
- pain over involved area of bone
- localized erythema, swelling, warmth
- systemic s/s: fever, HA, fatigue
DX
- WBC not helpful
- ESR and CRP not helpful to diagnose but used to elvaluate resp to tx
- needle aspiration of infected bone
- bone biopsy
- XRAY changes not evident for at least 10 days
- MRI generally most effective imaging
TX:
- Prompt antibiotics - for 4-6 weeks. At least two weeks of IV antibiotics.
- Empiric Tx in adults = Nafcillin, Oxacillin, Cefazolin (Vancomycin if PCN allergy)
- Vancomycin if MRSA!**
*If suspecting pseudomonas (IVDU, puncture wound) vanco + cefepime or cipro
Chronic osteomylelitis
- cm
- xrays
- tx
Manifestation = chronic sinus tract drainage is hallmark
X-rays = soft tissue swelling, periosteal reaction, bone destruction
MRI or CT scan is more sensitive
Treatment = surgical debridement and cultures
Osteoarthritis
- define
- mc in wht joints
- rf
- cm
- dx
- tx
- common
- chronic
- non inflamm arthritis of synovial joints
- deterioration of articular cartilage and osteophyte (bony growth) bone formation at joint surfaces
BY agge 65… more than 75% of population has radiographic evidence of osteoarthritis in weight bearing joints— MC in weight beairng joints
RF
MODIFIABLE: obestiy, trauma, heavy labor
NON-MOD: incr age, female, fam hx
CM *JOINT PAIN: often monoarticular *deep dull ache *relieved with rest and worse with activity or later in the day *stiffness in am or after inactivity *late stage=crepitus and LROM NO erythema or warmth*********** *Heberden Nodes (DIP) and/or Bouchard NOdes (PIP)
DX
X-rays show asymmetric joint narrowing, osteophytes, subchondral bone sclerosis, bone cysts.
LABS=lack of inflammatory markers**
TX
- Lifestyle modifications = weight management, exercise
- Analgesia =
* *Acetaminophen is the first choice. NSAIDS also work well, but have more side effects, particularly in the elderly. Topical NSAIDS can be used if one or two joints. - Steroid injections (but more than 3-4 injections per year is not recommended)
- Surgery (joint replacement) if serious disability
Septic Arthritis
- define
- mc joint in adults? kids? IVDU?
- eti
- etiologies
- pathogens—MCC? secod MC? MC in young adults?
- cm
- dx
- tx
MEDICAL EMERGENCY–can rapidly destroy the joint
*infection of joint cavity caused by bacteria— invade joint space— release endotoxins and trigger cytokine release
*knee MC in older kids and adults
*hip MC in younger kids
IVDU=sternoclavicular joint
ETIOLOGIES—bacteria in blood gets into joint space
- abscess
- cellulitis
- traumatic injury to joint
- iatrogenic—arthrocentesis or artrhoscopy
PATHOGENS
*MCC=staph
2nd MC=streptococcal
MC in sexually active young adults=gonococcal arthritis
*pseudomonas in immunocomp—IVDU, older, neonates or with trauma
CM
- warm swollen painful tender joint with decr ROM–active and passive
- constitutional s/s—fever chills malaise
DX
- Arthrocentesis (joint aspiration) and analysis of synovial fluid:
* *WBC count with differential - usually > 50,000 WBCs/mm3 with > 80% PMN (neutrophils)
* *Gram stain of fluid, along with cultures and crystal analysis should also be done. - LABS: Increased ESR, CRP
- Blood cultures are positive in 50% of cases
- If gonococcal arthritis is suspected, should also test patient for gonorrhea
* **X-rays are not helpful unless severe joint damage.
TX Management: 1. PROMPT IV ABX TREATMENT! 2. Joint drainage as needed 3. Debridement as needed
ABX choice:
1. Empiric = Ceftriaxone & Vancomycin
If KNOWN to be gonococcal = Ceftriaxone alone is sufficient
Compartment syndrome
- two main causes
- seen after what? MC injury?
- CM
- PE–earliest exam finding?
MEDICAL EMERGENCY
TWO MAIN CAUSES
1. blood and swelling of muscle— incr contents of compartment
2. Cast or bandage is too tight– decrs in volume of compartment
***MC seen after trauma—- long bone fx (75%)
OTHER: Trauma, fracture, crush injury, contusion, gunshot wounds, thermal injury, burn eschar, extravasation of IV infusion
CM
pain out of proportion to injury
paresthesia + pain early symps
SIX/SEVEN P’s:
1. PAIN=out of proportion to inj despite analgesia… this is indicate ischemia pain
2. PARESTHESIA= pins, needles, pirckling, burning
3. PALLOR=white shiny skin
4. POIKILOTHERMIA=feels cooler than surrouding areas
5. PULSELESSNESS=dim or absent pulses—LATE + OMINOUS findings** (yes pulse does not r/o comp syndrome)
6. PARALYSIS=cannot move muscle in that compartment–LATE SIGN
7. PALPATION=of compartment becomes hard and tense– compare to opp side
PE
- 6-7 Ps
- pain with passive stretching of affected muscle is most sensitive earliest exam finding
DX=clinical suscpicion is KEY
*Incr intracompartmental prssure >30 mm Hg
TX
- Emergent fasciotomy to decompress the compartment
- While waiting for surgery: place limb at level of heart, remove constrictive clothing or casts, etc., IV fluids and O2.
Avasc Necrosis
- etiologies
- CM
- dx
ETIOLOGIES
- Direct bone damage (fracture, dislocation) that impedes blood supply to the bone
- Bone marrow damage (radiation treatment, genetic disorders)
- Long term corticosteroid use (most common)
- Sickle cell anemia
- Alcohol use
- Lupus
- Bisphosphonates (mandible)
CM
- pain–>groin pain is MC in PT with femoral head dz— then pain in thigh–>buttock
- weight bearing or motion-induced pain that progresses into pain at rest
dx
-gold stand=MRI w/o contrast
TX
- Non operative management with bed rest, non-weight bearing, and medications including bisphosphonates and pain medication.
- Joint-preserving procedures aimed at halting or slowing the progression:
* *Core decompression (taking out the dead tissue and sometimes filling the cored area with grafts
* *Grafting - creating a structural support for the bone from fibular grafts - Total joint replacement
RHABDO
-define
ACUTE b/d and necrosis of skel muscle–leads to release of muscle fiber contents (MYOGLOBIN) into bloodstream—>myoglobin is toxic to kidneys–>leads to AKI
ETIOLOGIES
- trauma
- strenous activity
- prolonged immobility
- crush inj
- seizures
- cocaine
- ***STATIN TX
- viral infections
- snake bites
CM
- *TRAID**
1. muscle pain
2. muscle weakness
3. myoglobinuria— shows as dark, tea colored urine
DX WORK UP
- EKG—– most imp initial test— want to r/o hyperK–life threatening
- urine dipstick and UA—->dipstick will be (+) for heme (-) for RBCs
- LABS: muscle enzymes—> INCR creatine phosphokinase >20,000, incr ALT/AST, incr LDH, HYPERK, HYPOcalcemia, HYPERuricemia
TX
- IVF=1st line and mainstay tx
- IV Mannitol (osmotic diuretic)
- IV Bicarb–for some pts
- If patient shows EKG changes of HYPERK–> calcium gluconate IV— stabilizes cardiac membranes
WHY HYPERK WITH THIS DZ???
-bc muscles contain potassium— and when they b/d and necrotize… release K+ into blood
compartment syndrome
- what is it
- what happ if not corrected
**anything that increases pressure in the compartment separating the muscles–>leads to inadequate perfusion of tissues
- if not fixed–>soft tissue death
- leads to disability or loss of a limb
- MEDICAL EMERGENCY*
GOUT
- MC in what joint
- whats caused inflammation
- hallmark ?
- MC in?
- list the four stages
- diagnosis —toc?
- TX– acute? prophylaxis?
- **crystallization of monosodium urate in joints
- Hallmark=hyperuricemia
- MC in men over 30
- JOINTS:
- mc in first MTP joint of great toe (Podagra)
STAGE 1–>asympto hyperuricemia— incr serum uric acid but no s/s– no tx
STAGE 2–>acute gouty arthritis
STAGE 3–>intercritical gout
STAGE 4–>chronic tophaceous gout
DIAGNOSIS
- TOC= arthrocentesis: joint aspiration and synovial fluid analysis
* **negatively birefringent crystals–>needle shaped crystals and WBC in fluid is a (+) test (WBC count <50,000) - serum uric acid is not helpful bc it can be normal
- xrays– punched out erosions w/ overhanging rims aka RAT BITE LESIONS
TX
- ***ACUTE:
1. NSAIDS (not asa)—superior to cholchicine
2. corticosteroids– if refractory to NSAIDS or NSAIDS contra–injected into joint or oral
3. Colchicine– if NSAIDs and steroids dont work - **PROPHYLAXIS
1. avoid purine rich foods
2. allopurinol–>decrs uric acid production
3. Uricosuric drugs (probenecid)–>incrs urine excretion of uric acid
4. Colchicine (lower doses)
how to differentiate b/w gout and pseudogout
CLINICALLY— pain, erythema, warmth, swelling, tenderness–BOTH
Arthrocentesis of synovial fluid—> POSITIVE birefringent for pseudogout and NEGATIVE in gout
Crystal shape:
- needle shape in GOUT
- rhomboid shape in pseudo
what is gout
- MC population
- two main etiologies
- inflammatory monoarticular arthritis
- caused by crystalization of monosodium urate in joint
- hyperuricemia is hallmark of dz but does NOT itself indicate gout
- MC=men >30 YO
- ETIOLOGY=incr production of uric acid OR decreased excretion of uric acid (90%)
- inflamm in joint occurs when uric acid crystals collect in synovial fluid as extracellular fluid becomes saturated with uric acid
Triggers for gout
- etoh
- purine rich foods: etoh, liver, seafood, yeast
- MEDS: thiazide and loop diuretics, ACEI, Pyrazinamide, Ethamnutol, ASA, ARBs (except losartan)
stage 2 of gout
- what is it
- whose affected
- triggerrs
- cm
Peak age=40-60–MEN
TRIGGERS:
-purine rich foods: etoh, liver, seafood, yeast
-MEDS: thiazide and loop diuretics, ACEI, Pyrazinamide, Ethamnutol, ASA, ARBs (except losartan)
*most often affected big toe–but can also affect elbows, knees and ankles
*CM=pain, erythema, swelling, tenderness, warmth
+/- fever
stage 3 of gout
- name it
- where is the attack
INTERCRITICAL GOUT
- asympto period after initial attack
- patient may not have another attack for years or ever–only 10% never have anotehr
- 60% of PT have recurrence wihtin 1 year
- attacks tend to become polyarticular with increased severity over time
stage 4 of gout
- name
- what develops and wheere
CHRONIC TOPHACEOUS GOUT
*ppl who have had poorly controlled fout for >10 yrs
TOPHI=aggregation of urate crystals–surrounded by giant cells in infalmmatory reaction
- causes deformity and destruction of hard and soft tissues
- in joints it leads to arthritis
- can be extra-articular
- locations for tophi: extensor surface of forearms, elbows, knees, Achilles tendon, pinna of external ear
Pseudogout
- define
- RF
- joints MC
- CM
- Dx
*calcium pyrophosphate dihydrate deposition in joints + soft tissue–leads to inflammation and bone destruction
RF: hemochromatosis, hyperparathyroidism, hypomagnesemia
MC joints: knees + wrists
other joints: hand
CM
- majority are asympto
- acute CPP= clinically indistinguishable from gout—- severe joint pain, erythema, warmth, swelling and tenderness
DX–how to differentiate b/w this and gout
- Arthrocentesis TOC–> (+) birefringenet rhomboid shaped ca crystals and incr WBC 2,000-50,000
- xray=linear calcification of cartilage— chondrocalcinosis
TX
- first lne= NSAIDS (if 2+ joints invovled)
- corticos inj (if 1 or 2) or PO (2+ joints)
- colchicine—-can be used acutely or prohylaxtically in PT with 3+ pseudogout attacks/yr
Osteoporosis
- define
- basic etiology
- precursor dz?
- primary vs secondary
- CM
Loss of bone density (mineral and matrix)–imbalance of incr bone resoprtion>formation of new bone (decrs)
**PRECURSOR=osteopenia
ETIOLOGY:
1. failure to atttain optimal bone mass before age 30
OR
2. rate of bone resoprtion exceedds rate of bone formation after peak bone mass is attained
PRIMARY
- postmenopausal and senile MC for women
- RF=white, female, estrogen depletion, low BMI, corticosteroid use, smoking, CA and/or Vit D deficiency, lack of exericse
SECONDARY–caused by a dz or medication
- hypogonadism
- hyperthyroid
- DM
- low estorgen
- CA
- DRUGS=heparin, phenytoin, lithium, levothyroxine, steroids (cushings syndrome)
CM
- usually asympto
- MC=vertebral body compression fx—>causes pain, deformity, kyphosis, severe back pain after minor trauma, restricted spinal movement, loss of height
- colles fx
- hip fx
DX for osteoporosis
-give T scores and what they mean
DEXA SCAN
DEXA= dual energy x-ray absorpitometry=gold stand
T-score is used— calc by comparing bone density of PT with a healthy 30 YO
- NORMAL= 1.0 or greater— equal to a healthy 30 YO
- OSTEOPENIA= -1.0–> -2.5
- OSTEOPOROSIS= -2.5 or less
ALSO want to order labs to r/o secondary causes of osteoporosis
–CA, phosphorus, alk phosph, Vit D, Free PTH, creatinine and CBC levels
inds for dexa scan
- all women over 65
* postmenopausal women <65 with one or more RFs
TX for osteoporosis
LIFE STYLE MODS:
- CA 1,500 mg/day and Vit D 800 mg/IU supplementations per day
- weight bearing exercises
- smoking cessation
PHARMACO TX—indicated for pts with T score of -1.5–> -2.5 OR under -2.5
- Bisphosphonates are 1st line for prevention and management
*PO: Alendronate and Risedronate are preferred–>if cannot tolerate PO, IV can be done
MOA: inhibit bone reabsorption and decrease osteoclastic activity, which decrease the risk of fractures - Denosumab–>Monoclonal antibody prevents osteoclasts from developing
* good for high risk PT or PT who failed bisphosphonates - Teriparatide–>PTH therapy— incrs bone mineral density– SEVERE osteoporosis ( t-score < -3.5)
- Raloxifene–> selecive estrogen receptor modifer–>inhibs bone resoprtion and reduces risk of vertebral fx—- also used for BCA prophylaxis
list the benign tumors
- osteochondroma
- paget disease (ostitis deformans)
- Osteoid osteoma
list the malignant tumors
- chondrosarcoma
- ewing’s sarcoma
- osteosarcoma
where is ewing sarcoma on the bone
diaphysis
where is osteosarcoma on the bone
metaphysis
where is osteochondroma on the bone
Metaphysis
Osteochondroma
- what is it
- looks like?
- MC tumor in?
- CM
- diagnosis—- definitive?
- tx—asymp and sympto and prognosis
- benign chondrogenic lesion— derived from cartilage
- looks like cartialge-capped bony overgrowth on surface of bone
- MC bone tumor in kids
Seen MC in males 10-20YO
CM
- pain-free mass (when present, pain is from bursitis or tendinitis due to irritation by tumor)
- palpable mass
DX=xray with pedunculated stalk that grows away from growth plate
—-Definitive dx=biopsy
Management = observation if asymptomatic
Symptomatic = surgical resection of lesion
-> should be excised if it interferes with function, is frequently traumatized, or is large enough to be deforming. The prognosis is excellent. Malignant transformation is very rare.
Paget’s disease of Bone
- aka?
- define
- ares it affects
- MC areas it affects
- M or W?
- first line tx
aka Osteitis Deformans
- interfers with normal bone recycling–new bone is generated faster than normal bone
- but the new bone is softer and weaker than normal bone–leads to bone pain, deformity and fractures
AFFECTS
*one or two areas OR can be widepsread
MC=pelvis, skulls, spine and legs
MEN»women
FIRST LINE TX=bisphosphonates
Osteoid osteoma
- define
- MC age group and gender
- MC location
- patho
- cn
- dx
- tx and prognosis
*benign bone tumor characterized by small, radiolucent nidus—- produces high levels of prostaglandins
MC in 20s and MALES
MC location=prox femur
CM
*progressively incring pain that is worse at night and unrelated to activity
*pain relieved within 20-30 mins of taking NSAIDs— since NSAIDs block prostaglandins
*tender over the lesion
+/- referred pain to knee
DX=xray with small round lucency (nidus)
Ct/MRI are more sensitive
TX
- NSAIDs with serial exmas/xrays every 6 MO–most resolve spontaneously over years
- SYMPTO=surgical resection
* PROGNOSIS=excellecent.. no known cases of malignant transformation
* but does have tendency to recur if incompletely excised
Chondrosarcoma
- define
- mc age group
- mc body locations
- cm
- dx
- tx
CA of bone cartilage
MC in adults 40-50
MC locations= central portion of skeleton— prox femur, prox humerus, pelvic bones, ribs
CM
- localized pain and swelling
- pathologic fxs
DX
XRAY–mineralized chondroid matrix with punctate or ring and arc apperance calcifications
TX
- if not mets=surgical resection
- mets=chemo
Ewing's sarcoma -etiology -mc age group race and gender -common sites for mets -MC location forthe tumor -CM -main DDX? dx -tx
etiology=translocation b/w chromosomes 11 and 22
-destroys the cortex— frequently diaphyseal region
MC in white males 5-15 YO
Bone, bone marrow and lung=common mets
LUNG mets=common cause of death
MC location= (50%) on diaphysis of long bones-- femur MC -pelvis -tib -fib -
CM *localized bone pain and swelling *systemic s/s sometimes *Osteomyelitis is the main DDX PE: palpable mass--local tenderness and joint swelling
DX: xrays
-periosteal reaction… “onion skin”, lytic lesions with “moth eaten” apperance
LABS=incr ESR
TX = chemotherapy followed by limb sparing resection when possible. If excision not possible, radiation.
Osteosarcoma
- define
- MC location for tumor
- MC mets
MC primary bone malig in kids and young adults
- malig tumor of osteoblastic proliferation
- very aggressive
- 90% occur in metaphysis of long bones— distal femur MC
- LUNGS mc site for mets— mcc of death
CM
- localized bone pain worse at night
- presenting complaint=pain in a long bone–loss of function, mass or limp
DX
- xrays: “hair on end” or “sunburst” apperance due to tumor spicules of calcified bone radiation at right angles
- CT OF CHEST TO r/o METS TO LUNG**
- mri
TX
- surgery to remove tumor
- chemo
- surgical exicion– limb salavge– or amputation dep on severty of tumor
DEATH usually occurs due to lung mets– poor prognosis
