CM Flashcards
polymyalgia rheumatica (PMR)
who is it common in? what are the lab tests like? what is commonly associated with this disease? what do you use to treat this disease? how soon can people come off it?
>50, northern european ancestry 2:1 females
abrupt onset of intense morning stiffness of neck, shoulders and hip girdle but muscle strength is normal, fatigure and anorexia also common
elevated ESR >50 mm/hr and CRP
15% can get great cell arteritis/temporal arteritis
low dose steroids 10-20 mg only drug that works, looks to normalize the CRP and ESR
usually self limiting 65% taper of steroids 1 year, 85% in 2 years
what can people develop from Polymyalgia rheumatica (PMR) and what percent of people does this happen in?
giant cell arthritis/temporal areritis
15%
what should you do if the ESR and the CRP values for polymyalgia rheumatica (PMR) don’t normalize with steroid use?
rethink the diagnosis
Giant cell arteritis (GCA)
what age group is this common in and what other disease does this commonly present with? the release of which things cause this? 6 presentations? what can this damage? tests? treatments?
[giant head]
>50, often seen with PMR
involves the medium/large blood vessels of the head and neck including those that supply the optic nerve, involves release of IL1 and IL6
inflammatory cells get into the adventia of the temporal and other arteries and plug the flow
1. scalp tenderness
2. temporal headaches
3. jaw claudication
4. sudden loss of vision
5. bounding or absent temporal pulses
- rare subclavian bruits
higher ESR and CRP than PMR, anemia
high dose steroids 60mg, slowly tabler off 1-2 years, some require low dose chronically <10 mg
what are the four complications that can come from giant cell arteritis?
blindness
scalp necrosis
lingual infarction
aortic dissection/aneurysm
what are the four major complications seen with long term use of high dose steroids?
osteoporosis
cataracts
increased BS
weight gain
Granulomatosis with polyangitis (GWP)
what causes it? what are the 6 presentations? what do you worry about the most? what tests are important for this? what is the treatment and the new drug? where are these patients? what 3 systems do you worry about the most?
potentially fatal, involves small vessels, forms necrotizing granulomas in the upper airways, lungs, and kidneys, multisystem is key, very sick so in the hospital
the antineutrophil cytoplasmic antibodies C-ANCA attack the neutrophil and cause vascular injury and necrosis,
- eyes
- skin (palpable purpura)
- Upper airway ( ottis media, sinusitis, epitaxis, subglottic stenosis)
- kidney (nephrotic syndrome/failure)
- lung (hemmorage, lung failure)
- cardiac (pericarditis)
labs: elevated CRP, ESR, thrombocytosis, creatine, hematuria, casts, and proteinuria (all elevated)
treatment:
- High-dose steroids with cyclophosphamide
- methotrexate (chemo) or azathioprine (transplant drug)
- rituximab=anti CD20 drug targets B cells
what is the survival rate for giant cell arteritis after the invention of immunosuppressants?
90%
polyarteritis nodosa (PAN)
what causes this and what illness is it typically associated with? what are 6 possible presentations on the body? what are four complications we worry about? what is the treatment? what is the special test we do to diagnose this?
[no do web, need a plan B]
50s-60s, medium blood vessels, high adominal involvement, associated with HEP B
abdominal pain due to mesenteric ischemia, pain associated with meal consumption
myalgia
hypertension
skin: livdeo reticularis (lace like rash), palpable purpura, fingertip ulcerations, subcutantous nodules on palms
testicular pain
labs: increased ESR, CRP, increased transaminadases, decreased albumin, HEP B, proteinuria/hematuria without casts
mesenteric/renal angiography where you see beading instead of smooth tubes
treatment:
- high dose steroids with cyclophosphamide
- mexotrexate or azathioprine
- treat Hep B with antiviral acyclovir
- plasma exchange to remove immune complexes
see bowel perforation, renal failure, stroke to HTN, foot/wrist drop since complexes wipe out nerve
ESR inflammation test
what two things effect it? what other 3 factors will it increase in? How long does it take to see result?
sedimentation rate, rate at which RBC fall in a standarized tube in 1 hour
influenced by fibrinogen and immunoglobulins
increases with : age, women, adipose tissue
can take days to increase or decrease
high sed rate means falls faster
CRP inflammation test
synthesized by the liver in response to inflammation or infectious state, rises and falls quickly
what does it mean if the ESR and CRP are both elevated?
infection, inflammation, trauma, cancer
ESR is ELEVATED, CRP is NORMAL
what does this mean? 4 examples?
conditions with elevated immunoglobulins
SLE
myoloma
liver disease
sjogrens
rheumatoid factor test
what is this most commonly seen in? what 4 other diseases can produce a postivite test? what is important to keep in mind when doing this test?
IgM that is directed against IgG that is present in 80% of patients with RA
also seen in: Hep C, Sjogrens, TB, cryoclobulinemia
***may have a low positive result***so must use in relation to clinical picture
anti-CCP antibody
antibody against citrulline-containing peptides
more specific for RA than rheumatoid factor? (95%)
Antinuclear antibody (ANA)
who is it likely to produce a false positive in? percentage? Name 6 patterns
IgG against nuclear antigens
produces titer and pattern with immunofluoresence
higher the titer more clinical significance
false positives in 10-20% of females
diffuse/homogenous
periphreal
speckled
nucleolar
centromere
SCL-70
diffuse homogenous ANA pattern seen in…..
1
SLE
periphreal ANA pattern seen in …..
1
SLE
Speckled ANA patter seen in….
2
SLE, Sjogrens
nucleolar ANA pattern seen in…
1
scheloderma systemic disease
Centromere ANA pattern seen in…
1
CREST syndrome
SCL-70 ANA pattern seen in….
1
schleroderma systemic disease
Antineutrophil cytoplasmic antibody (ANCA)
what are the two types and what do they test for?
autoantibodies that recognize proteins in the neutrophil, associated with vasculitis
P-ANCA- myeloperoxidases (MPO), microscoptic polyangitis
C-ANCA- proteinase 3 (PR3), granulomatosis
fibromyalgia
what is it? how long do you need to have it? what are the requirements? what are the 4 presentations? what are the 4 important things you need to rule out? what testing is ok? which arent? what should you NOT treat with? what are 4 potential medical treatments?
central pain syndrome, pain threshold disorder >3 months 6:1 females
increased activity in somatosensory cortex, posterior insula, and thalamus
allodynia (percieved pain when non, hugging), hyperplasia (aplified pain perception)
aggrevated by stress, lack of sleep, activity
- widespread muskulo pain
- sleep disturbance
- no objective physical findings
-
11/18 trigger points
* important to test deep tendon reflexes and sensation*
testing proceed with caution: NEED TO RULE OUT CELIAC DISEASE, IBS, VIT D DEF, HYPOTHYROIDISM
DO NOT ORDER RA/ANA
can order thyroid, electrolytes, vit D, ESR/CRP, Hep C, CPK
Don’t treat with: NSAIDS, narcotics
Treat with: Tricylic antipressants (help sleep), selective serotonin reuptake inhibitors (SSRIs), dual acting, lyrica neurontin but SO many side effects
what are other therapies important for treating fibromyalgia that aren’t medications?
5 things
- lifestyle modifications
- low impact aerobic exercise
- sleep hygiene/check for sleep apnea
- address depression/stressors
- encourage patients to take control
fibromyalgia
what percent of females have this by age 20? what percent by age 70?
2% have by age 20
8% by age 70
fibromyalgia and depression
- what percent have depression at time of diagnosis?
- what percent have lifttime incidence of depression?
- what percent have lifetime incidence of anxiety?
depression at diagnosis: 30%
lifetime depression incidence: 74%
lifetime anxiety incidence: 60%
chronic fatigue syndrome
what ususally comes before this? what type of people are usually effected? what percentage of people have despression before? how many of the symptoms do you need to have? list some of the 8 possible symptoms? what should you NOT treat with? what should you treat with??
affects previously active people, often preceeded by flu like symptoms
25-45 years old, can happen in clusters, maybe “immune system temper tantrum”
2/3 of people are depressed
need to have 4/6 of the following for 6 months
- short term memory impairment
- sore throat
- tender cervical/axillary nodes
- muscle pain
- multijoint pain
- headaches
- unrefreshing sleep
- postexertional malaise lasting longer than 24 hrs
DONT USE ANTIVIRALS, CORTICOSTEROIDS, IV Ig
USE: NSAIDS, antihistamines, antidepressants, EDUCATE
what is a strang symptom associated with chronic fatigue syndrome?
unusual sensitivity to sustained upright tilting resulting in hyptension and syncope
Systemic Lupus Erythematosis (SLE)
who is this common in? what happens? what are the four main body systems you worry about? what are the 11 presentations and how many do they need to have?
womens disease, 16-55, african american 15:1
debris from abnormal cell apoptosis promotes polyclonal B cels and autoantibodies, complexes deposit everywhere causing the symptoms
1. renal (nepthritis, nephrotic syndrome, tubulointerstitial disease)
2. neuro (seizures, psychosis)
3. hematologic (hemolytic anemia, leukopenia, lymphopenia ALL GO DOWN)
4. Immunological (vascular thrombosis) (antiophospholipid syndrome)
malar rash, arthritis without erosion just deformity, alopecia, raynauds, photosensitivity, positive ANA arthritis
must have 4/11 symptoms ANA is the only one that MUST be there
what are 8 lab tests seen in SLE?
- CBC (anemia/cytopenias)
- BUN/Cr (kidney involvment)
- UA (proteinuria/ casts)
- C3/C4 (decreased)
4. ESR ELEVATED, CRP NORMAL
5. positive ANA with all patterns EXCEPT centromere and SCL70
- dsDNA that is more specific than ANA, speckled or nucleolar
SLE treatment
- skin
- renal
- other
Skin/fatigue: hydroxychloroquine
renal: high dose corticosteroids and cyclophosphamadine (immunosuppressant)
other immuno:
azathioprine
mycophenalate
methotrexate
the drugs used to treat SLE puts the patients at increased risk for two things? you should treat the side effects of these when treating SLE patients
atherosclerosis
osteoporosis
what is an important thing you want to discuss with women who have SLE?
birthcontrol and family planning, Pregnancy is VERY risky!!!
what interesting false positive test resulte can SLE create?
false positive syphilis
drug induced SLE
what is it? what are 3 drugs that commonly cause it? what pattern does it have?
acts and looks like SLE but is reversible when the drug is discontinued
minocycline: most common derm drug for acne
hydralazine: for BP
procainamide
histone pattern ANA
discoid lupus
what is it and where is it located? how do you confirm it?
limited to the skin “limited SLE”
confirmed by biopsy
scarring rash
don’t need to have 4/11 since subset
what do most SLE patients die from?
thromboembolitic disease from long term steroid use
systemic scleroderma
who is it common in? what is it? what are the 6 unique physical findings? what do you worry most about? what do you see on the test restults? what is the treatment?
[scler scler..eating]
hardening and thickening of the collagen in the skin, females 4:1 30-50
1. raynauds
2. thickening of the skin and vascular changes in the nailbeds
3. lung disease and fibrosis
4. GI dysmotility “watermelon stomach”
5. renal failure with HTN
6. cardiac complications
7. arthalgias puffy hands think they have carpal tunnel but when it leaves left with thickened skin, same thing with fixed face
most worried about thickening of the lungs!!
positive ANA with nuceolar/SCL-70 pattern
treatment aimed at the organs it involves or affects
renal=ace inhibitors
raynauds=calcium channel blockers
GI=promotility agents
lung=cyclophosphamide
what do you never want to use in a patient with systemic scleroderma?
high dose steroids…can lead to renal crisis
CREST scleroderma
What does the acronym stand for? what do you worry about in these patients? what should you reccomend them to do and how often?
“limited scleroderma”
C-calcinosis of joints and fingers, bone growths off it
R-raynauds
E-esophageal dysmotility
S- sclerodactyly of fingers and MCPs
T-telangiectasia (dilation of blood vessels)
worry about pulmonary hypertension so encourage these patients to get ANNUAL PFT/DLCO (diffusing capability of lungs for CO), pulmonary function tests
polymyositis/dermatomyositis
what is this? what is it strongly associated with? what are 6 presentations? what will you find for tests and what imaging can be done? what do you treat with?
autoimmune myopathy of striated muscles of proximal limbs
pts have hard time getting out of chairs, climbing stairs, curling hair
usually associated with underlying malignancy
PAINLESS MUSCLE WEAKNESS
- heliotrope (lavander around eyes)
- gottren’s papules (rashes over joints)
- shawl sign
4. mechanic’s hands
- periungal erythema
- calcinosis cutis
+/- ANA, elevated CPK (creatine phosphokinase) aldoase
EMG, MRI, muscle biopsy
treat: high dose corticosteroids
methotrexate or azathiorine
IV Ig for severe cases
if there is a maligancy, DM will resolve once malignancy is cleared
sjogren’s syndrome
what is it? what are 3 main things you see? what are two things it can transition into? what is 1 important tests and what are the other 4 tests you want to do? what do you do to treat it?
extremely female dominant 20:1, 30-40
often seen with SLE and RA
autoimmune effecting exocrine glands
xerostomia (dry mouth) and xeropthalmia (dry eyes), parotid swelling
B cells produce autoantibodies, over time transitions to malignant expansion or lymphoma
POSITIVE RHEUMATOID (70) AND ANA (60), elevated ESR normal CRP
shirmer’s test
treatment: hydration, artificial tears, lacriminal duct plugs, restasis eye drops
Shirmer’s test
what disease do you use it for and what is the test?
use for sjogren’s
tests exocrine glands in eye, put a strip of paper in the eye <5mm is positive for decreased production
>10 mm is normal
what is important to reccomend to patients with sjogrens for good health precautions?
3-4 dental visits per year since they have decreased salivary secretions the enzymes to fight bacteria aren’t there
what are 5 complications you should worry about from sjogrens?
- lymphoma
- primary biliary cirrohosis
- accelerated dental caries
- cornreal atrophy/ulcerations
- oral candidiasis
inpingement/bursitis/tendonitis
what happens in this? what three things ilicit pain? what degrees do you catch at? what are the movement limitations? what two movement tests should the patient do? what tests do you want to order? what are the five treatment considerations?
repetitive overhead work, gradual progression
impingement: subacromial bursa, rotator cuff compressed between humeral head and acromion
inflammation: subacromial bursa, rotator cuff tendons (as it gets more inflammed the space gets smaller and pinches the tendons more)
pain: lifting or reaching, night
catch at 80-120*
DECREASED AROM BUT FULL PROM
tests: Neers inpingment sign, hawkins manuver (elbow bent out in front and push down)
xray: A/P/axillary/lateral, MRI rarely indicated
REST, NSAIDS, naprosen, PT, corisone injection, surgery
what two exam tests are important for impingement/bursitis/tendonitis of the shoulder?
hawkins
Neers (impingement sign)
what type of surgery do you do for impingment, bursitis, or tendonitis of the shoulder?
arthroscopic subacromial decompression
(scrapping off the bursa)
rotator cuff tear
what four muscles are included as part of the rotator cuff? which is the most common culpriate? what types of pain will you find? what 5 tests do you want to do? what are the three types of images you can use and why are they helpful?
can be complete or partial tear of musculotendonous complex, +/- muscle atrophy/tendernous/crepitus
includes:
1. supraspinatus (most common)
2. infraspinatous
3. teres minor
4. subscapularis
pain/weakness with elevation and rotation, @ night, radiates to mid humerous AROM>>PROM PAIN
testing:
1. drop arm test
2. empty can test (supraspinatus)
3. lift off test (subscapularis)
- hawkins (think it looks like a bird wing)
- Neer impingement sign
imaging:
- xrays (subacromial spur, calcified tendonosis, head of humerus may migrate forward
- MRI-helpful but expensive
- arthrogram
when is a arthrogram used for a patient with a rotator cuff tear?
when pt has an implant and can’t have MRI, dye is injected into the joint and you wait to see if the dye leaves the joint
what does a “global” tear mean for a rotator cuff tear?
all the four muscle tendons are torn
can be acute (trauma) or gradual (fraying over time)
what are the conservative vs aggressive treatment options for someone with a rotator cuff tear? what is important fun fact to know here?
conservative:
- PT
- Cortisone Injections (good for elderly)
- NSAIDS
Surgical:
- arthroscoptic repair
Fun fact: want to have it repaired in healthy individual because it can lead to rotator cuff arthritis and arthropathy which leads to total shoulder replacement
should seperation
what happens? what does the patient report? what are the 3 important tests to do? what do you want for imaging? how are they classified?
AC joint stress or disruption, fall on the point of shoulder, obvious deformity
sudden onset of pain (trauma), patient reports “pop”, “arm went dead”, depressed affected shoulder
pain with or WITHOUT motion
tests:
- cross arm test
- pain with restricted horizontal abduction
- spring test (push down on clavicle)
xray: A/P, no need for weighted views
6 grads of shoulder seperation
what are the 6 grades of shoulder seperation?
- AC lig injury
- AC lig torn
- AC and CC lig torn
- AC and CC lig torn, avulsion (pulling away), displacement through skin or muscle
- AC and CC lig torn with deltoid and trapezius fascia stripped off acromion and clavicle
- AC and CC lig torn with inferior dislocation with many other injuries
AC-acromioclavicular lig CC-coracoclavicular lig
what is the treatment plan for shoulder seperation? what is it dependent on?
depends on the grade
Grade 1-3: conservative approach (only ligs are torn)
- immobolization for pain, get out quickly to avoid pain for 1-3 weeks
- NSAIDS
- PT
Grade 3-6 surgical aggressive treatment (any displacement or fascia stripping)
needed if unstable or cosmetic
AC DJD
*denegenerative joint disease*
who is it common in? when/where is the pain? presentation? what motion tests and imaging should you do? what might you see on these images? what is conservative vs aggresive treatment?
middle aged men, esp in manual laborers, weighlifters, and athletes with a lot of horizontal adduction
pain with pushing, horizontal adduction, resisted abduction
may see AC hypertrophy, so larger on one side
+/- crepitus
tests: cross arm test
Imaging: A/P, axillary, lateral xray, this will show the degenerative changes
changes possibly seen: hypertrophy, spurring, joint space narrowing
conservative treatment: rest, NSAIDS, cortisone injection but is hard to get it in
surgical: excision of distal clavicle mumford procedure
***no cure for arthritis, can only cut it out***
conservative treatment: rest, NSAIDS, cortisone injection but difficult to get it in
what is the most common fracture in children and adolescents?
clavicular fracture
what can sometimes occure as a result of live birth trauma?
clavicular fracture
clavicular fracture
what part of the clavicle does this usually happen on? how does it present? what causes pain? what is it always nessacary to check???? what imaging do you need to do
fall on outstretched arm, sometimes in live births
breaks between middle and lateral 1/3 of clavicle, always “looks bad”, feel crepitus and pain at fraction site
obvious visual deformity, pain with AROM, PROM, and rest “I broke my collar bone”
Xray: A/P only, bone fragments usually overlap
always want to check for reflexes, sensory, and weakness of extremity since right next to major blood vessels and brachial plexus, need to know if these are damaged
what imaging shouldn’t you do for a clavicle fracture?
MRI and CT
what are the conservative and aggressive treatments for clavicle fracture?
conservative
- sling for 3-4 weeks
- reassurance!! almost always heal w/o surgery, may still have deformity but 100% functional
- gradual return
****even though it looks bad on a xray, the body can heal it!! a callus will form and the body can reabsorb the bone!****
surgical
- used for unstable fractures (aka bone is puncture skin or injurying something below)
- tricky and dangerous since next to Brachial plexus and subclavian a
- sometimes can still fail because of tension on the clavicle
adhesive capsulitis
what are 4 risk factors? what causes this? what imaging do you want to do? what is the reccomended treatment and how long can this take to be effective? what is last resort treatment? how do you make the diagnosis?
sedentary people, decreaed volume of the joint capsule and capsular contraction
“frozen shoulder”, insidious onset, gradual progression, pain at night
increased risk with: age, obesity, diabetic, middle aged women
there is a physical “block” preventing motion
xray: rule out other bony deformities
diagnosis is based on history and PE
treatment: NSAIDS and stretching, GH cortisone injection, takes patience since it can take up to a year to heal, manipulation under anesthesia as last chance
should instability/dislocation
who is this common in? what falling position is most common? what are the two types? what type is the most common? if dislocated what will it look like? what interesting thing should you look for on a xray?
overhead, younger athletes
95% are anterior dislocations, 90% will reoccur
most common cause is falling on abducted extended arm
dislocation: full disarticulation of GH joint
subluxation: partial disarticulation, pops out and then back in
“dead arm”, can relocate spontaneously, sense of instability, may sense clicking in GH joint, patient usually holding affected arm with the other
if dislocated: flattened deltoid (not held up by head of humerus), prominent acromion, arm held in splitting position, dramatically reduced ROM
ON XRAY LOOK FOR HILLS SACHS, DENT IN HEAD OF THE HUMERUS
what imaging should you do for something with shoulder insability/dislocation?
X-ray
- A/P, Y view
2. always get xray with first time dislocators
3. MUST ALWAYS GET A POST REDUCTION XRAY, 2 FILMS!!!!
MRI
- helpful to access for Bankart lesion tear of the anterior glenoid labrum (lining) during shoulder location
what is a interesting thing you should look for on a xray of someone who has dislocated their shoulder?
Hill-Sach lesion
-labrum catches on the head of humerus during dislocation and puts a dent in the head of the humerus
what is the treatment conservative vs aggresive treatment for dislocation?
conservative
NSAIDS, sling
PT after 3 weeks for <40 yr olds
PT after 1 week for >40 yr olds
**don’t want them to stiffen**
surgical
- Bankhard (labral) repair for labrum tear
- capsulorrhaphy: tightens the capsule
what does a capsulorraphy do? what do you use it in/
surgical intervention to tighten the capsule and prevent against future dislocations
elbow dislocation
who is it common in? how does it happen? what must you access for? what do you treat with? what is important to do after reduction?
most common in children, 50% happen from sports
fall on outstrectched hand, 98% are posterior
arm held at side in splinted position, unwillingness to move elbow
obvious deformity, olecranon swelling
MUST access neurovascular structures, MUST perform POST reduction xray!!! two films!
treatment:
- reduction
- spint/cast 1-3 weeks
elbow gets very stiff very fast esp in kids, so want to initiate early ROM exercises to prevent flexion contracture
NSAIDS
lateral epicondylitis
what is a nickname for this condition? what muscles specifically does it effect? what does this person have a difficult time doing? what happens with pain and ROM? what are 5 treatment options? what is the last resort treatment and why?
“TENNIS ELBOW”, dengeneration/inflammation of the wrist extensor mechanism
LATERAL EPICONDYLE, DIFFICULTY LIFTING THINGS WHEN HAND IS PRONATED
involves the tendonous insertion of extensor carpi radialis brevis
tennis, golf, weight lifting
pain with repetitive extension and flexion
pain:
- radiate down the arm
- passive wrist flexion
3. active and resisted wrist extension
Treatment:
- eliminate aggrevating factors
- NSAIDS, ICE, HEAT
- tennis elbow strap
- cortisone injection, DONT INJECT TENDON
- surgical release/faciotomy if all else fails. only successful in 50% of people and longer than 6 months
olecranon bursitis
what are the two different causes? what is the difference in treatment between the two? what is the most common organism to cause it? what should you test? and for what two things?
inflammation of olecranon bursitis, can be from resting on the elbows a lot
usually quick onset
can be from infection: septic bursa
suspect infection if erythema and intense pain on palpation
send joint fluid for analysis: culture and crystal analysis
treatment for non infectious:
- padding/compression wrap, NSAIDS, heat, ice
- cortisone injection ***need to make sure 100% not infected if so***
treatment for infectious:
- treat cultured pathogens
- incision and drainage
most common organism is S. aureus
carpal tunnel syndrome
what happens? what causes the symptoms? what 4 special tests can you when diagnosing? what is the gold standard of care? what should you do first and for how long? describe the numbness pattern
most common nerve entrapement syndrome, median nerve under transverse carpal lig
pain and numbness in media distribution (pic), pain at night, weakness in thumb grip strength
tendernous and tingling at wrist and palmar area
Special tests:
Phalens test w/tingling after 1 min (I think of “flailing hands)
Tinel’s sign-taping over transverse lig produces tingling (I think tinel=tingle)
decreased 2 point sensation
electromyography/nerve conduction
gold standard: surgery, releases transverse lig, but first try night splint, NSAIDS for 4-6 weeks before surgery consult
DeQuervain’s disease
what is this caused by? who is it more common in? where do you see the localized pain, between what two things? what is 1 special test you want to do? what are the two treatment options?
extensor pollicus brevis and abductor pollicus longus act to abduct the thumb away from the hand in the radial plane, more common in women and diabetics
synovial/tendon sheath becomes inflammed from OVERUSE
pain over the CMP joint of first digit, trapezium and metacarpal of thumb
special test: finkelstein’s test (place thumbs inside of fist and ulnar deviate which causes pain!!)
tests: xray to rule out other things, labs for gout
treatment:
- NSAIDS, splint, cortisone injection, symptoms resolve in about a year
- fasciotomy of 1st dorsal compartment (not as common) but releases overlying lig
scaphoid fracture
why are scaphoid fractures important not to miss? what is unique about this bone? where does pain present? what two images do you do? what is really interesting about the treatment plan for this? what happens at the second xray?
most common fracture carpal bone, most common in men 20-40
caution: poor blood supply to this bone so can be easily comprimised by fractures and lead to necrosis
blood enters through distal 1/3 of bone
high rate of non-unions
fall on outstretched hand, PAIN IN ANATOMICAL SNUFF BOX
xray: scaphoid views must repeat xrays 2 weeks after injury to look for healing or signs of injury, sometimes fractures don’t show up immediately or seen easily
can do a bone scan which will show metabolic activity
interesitng plan of action: CAST with or without fracture after first xray, then reacess at second xray
at second xray if
healing-recast 4 weeks
no fracture-splint two weeks
displaced fracture-surgical intervention
what is one interesting thing about a scaphoid fracture that you don’t see with other breaks?
if you suspect a scaphoid fracture and the xray is negative YOU STILL CAST IT!!! breaks are hard to see here so you need to be really cautious since the bone has poor blood supply it can become necrotic easily so cast!!
reacess at 2nd xray in two weeks and if still no evidence YOU STILL SPLINT FOR 2 WEEKS!!
how strange.
mallet finger
what happens here? what can’t this person do? How do you treat?
most common extensor injury
rupture of the extensor tendon at distal phalynx
hyper-flexion injury, if you flex too far forward it pops off
cant extend finger tip
swelling and ecchymosis at DIP, DIP held in slight flexion since nothing counterbalancing it
xray: A/P and lateral, look for avulsion (bony fracture from tendon ripping off)
treatment: splint DIP in FULL EXTENSION, 4 weeks
jersey finger
what tendon is effected? what can’t this person do? how do you treat this?
rupture of the flexor digitorum profundus
inability to flex fingertip
swelling and ecchymosis of DIP
xray: A/P, lateral, may show avulsion
treat: split initially but refer ASAP to surgery
***all flexor tendon injuries require surigcal repair***
All flexor tendon injuries require….
SURGICAL REPAIR!!!
boutinere deformity
what happens here? what is the presentation? what can’t this pt do? how do you treat?
tear of the central slip (median band) of the extensor tendon at PIP level
fingers are slightly flexed since nothing is opposing it
DIP joints extend due to pull of intact lateral bands
Classic boutinere look seen in pic
Xray: A/P abd lateral, rule out fracture
treatment: splint PIP in complete EXTENSION, can leave DIP free for movement, splint 6 WEEKS
Explain the grading for muscles
5/5: complete ROM, maximal resistance
4/5: complete ROM, moderate resistance
3/5: complete ROM, against gravity
2/5: complete ROM, gravity eliminated
1/5: no ROM, isometric muscle contraction
0/5: no muscle contraction
osteoarthritis
what is this? where is it most common? what are the two types? what would you expect to see on a xray?
joint disease with protective cartilage on the ends of your bones wears down over time and subchondral bone wears down over time >40 yrs olds THINK ELDERLY, slow developing joint pain
early onset and late onset OA, erosive
hands, hips and knees most common
primary or secondary causes
joint enlargement, red swollen PIP, DIP, weakness and wasting of muscles around joint, deformities
xray: see narrowed asymetric joint space, with osteophyte formation, bony sclerosis
what is a osteophyte? what disease is this commonly seen in?
a bony outgrowth associated with the degeneration of cartilage at joints.
osteoarthritis
what are the characteristics associated with early osteoarthrits? (4 things)
1-2 years
morning stiffness lasting <1 hour
they’re ok, they say they just keep going
red, prominent PIP, DIP joints with normal radiographs
what are the characteristics associated with late osteoarthritis?
AM stiffness lasting <30 mins
mechanical stiffness that gets worse with movement, more pain the more they do
claim not to have the same strength they used to (opening jars/doors etc)
little evidence of inflammation
ABNORMAL RADIOGRAPHS
get less symptomatic in non-weight bearing joints AKA many patients have extreme hand deformities but are asymptomatic (once they are deformed they don’t hurt anymore)
what is the treatment options for osteoarthritis? (7 things)
joint conservation
exercise
weight loss
NSAIDs (caution with ulcers)
COX-2 inhibitor (safer for people with history of ulcers, but still need to watch for cardiac complications)
cartilage replacement (15-55)
total joint replacement
why are patients who take COX-2 inhibitors for osteoarthritis at increased risk for heart complications?
use these instead of tNSAIDs beacuse they reduce the risk for stomache ulcers
but they also increase thromboxane levels making platelets stickier
cause vascular remodeling after 18 months which causes hypertension
these patients are 2.5 more likely to get a MI or CVA
what are the genes associated with osteoporosis?
weight
trauma
genetics FR2B, GDF-5, DIO2
-endochondryl ossification, skeletal malformations, chondrocyte self destruction
primary osteoarthritis is…..
idiopathic, arises spontaneously
secondary osteoarthritis can come from….
- posttraumatic
- congentiral deformation
- endocrinopathy
- neuropathic arthropathy
- padgets disease
- avascular necrosis
- skeletal hyperostosis DISH
characteristics of erosive osteoarthritis
more agressive
destruction
persistent symptoms
inflammatory findings
what puts a person for increased risk for stomach ulcers when using NSAIDS?
>60 years old
coumadin
past ulcers
prednisone
long term NAID use
what is the most common joint disorder in the US?
osteoarthritis
Osteoarthritis of the hip
what is this? what will you see on the xray? what is the “definitive cure”? what other surgical interventions can you do in younger patients?
degredation of articular cartilage, thickening of the subcondral bone
progressive hip pain that often complain of groin pain, “crunching” noises aka crepitus
xray osteophyte formation, decreased joint space, sunchondryl sclerosis and cysts
conservative: same as always
definitive cure: total hip arthroplasty THA (replace joint)
surgical: arthroscopic debridement, femoral head resurfacing in younger patients
avascular necrosis
what causes the necrosis? how long can the cells survive? what is a unique sign that you will see? where does the pain present and what happens when the person rests? what are four surgical interventions you can do?
bone death from disruption of blood supply
osteocytes, blasts and clasts, die withing 24-48 hours of oxygen deprivation
reprofusion may regenerate bone growth
cresent sign: collapse of sunchondral bone
often seen pain in groin, thigh, buttock
pain typically decreases with rest
Treatment: NSAIDS, anticoagulants (heparin, coumadin etc) since can thin blood and help it get to the site if there is a clot!!
Surgical intervention: hip resurfacing, core depression, fibular bone graft, total hip arthroplasty
greater trochanteric bursitis
what does the bursa do? what 5 potential causes? when do you get pain (KEY!)? what do you do for treatment and what won’t help you with diagnosis?
inflammation of the greater trochanteric bursa
bursa function: acts as a pad for the greater trochanter
causes: overuse, trauma, weak abductors, prior sugery, unequal leg length
pain with: repetitive motions (running, cycling, etc)
pain with RESISTED ABDUCTION, PASSIVE ADDUCTION KEY!! POINT TENDER OVER GT
xrays will be normal.
NSAIDS, ice/heat, PT, activity modification or surgical removal
what is the difference between a strain and a sprain?
strain: injury to the bone-tendon unit at the myotendinous junction or the muscle itself
sprain: involves collagenous tissue, such as tendons or ligaments
quadriceps/hamstring strain
what motions can cause a strain in both the quads and hamstrings? what do you use to classify the amount of damage done? what do you NEED to make a diagnosis? when do you do a MRI? what might you feel or see? what is the treatment?
quadriceps strain: cause forced hip extension or knee flexion
hamstring strain: forced hip flexion, knee extension
excessive force causing excessive muscular contraction, causes musculotendous unit stretch or tear
grading system for type,
palpable hematoma in muscle belly, possible defect in muscle or tendon
HX and PE all that are needed to make DX
mri may be helpful if complete tear is suspected
TX: conservative usuals surigcal: hematoma evacuation, repair COMPLETE TEAR tendom/muscle , fasciotomy
what are 4 predisposing factors for a strain?
inflexibility
overtraining
poor body mechanics
muscle imbalance
Extensor Mechanism Rupture
what are the four structures included in this mechanism? what trauma causes this (1) or atraumatic events (3)? what might this patient say? what can’t they do? what do you always want to do with this patient unless they don’t qualify? what are the two sites this can occur at and what are their funny names?
middle aged men most common
includes: quadriceps, quadriceps tendon, patella, patella tendon (ligament actually)
caused by hyperflexion of the knee (traumatic)
or inflammation, degredation, cortisone injections around patella, tendon weakening
inability to bear weigh, “I tore my knee, I felt a pop”
always want to do surgery unless they don’t qualify
otherwise they will most likely loose extensor function, tendon repaired with sutures, otherwise they will be in a boot 6-8 weeks. after surgery can WBAT in immobalizer
patella alta: patella tendon rupture
patella baja: quad tend rupture
osteoarthritis of the knee
what is this? what are four presentations you see with this? what is a possible muscle presentation? what is the gold standard for diagnosis? what are the conservative vs surgical treatment options?
degredation of the hyaline cartilage of the knee
pain is worse in AM, giving away or locking
joint hypertrophy, and tendernous at the joint line, possivle quadricept atrophy
gold standard: xray…see osteophyte formation, decreased joint space so bone on bone, sunchondral sclerosis
treatment: conservative normals plus cortisone injections and hyaluronic acid injections
surgical: knee arthroscopy, tibial/femoral osteotomy, total knee arthroplasty
patellofemoral pain syndrome/anterior knee pain syndrome
who is it common in? what are the four main categories of causes? what do these pts have pain doing? what are 5 things specific to the knee area you might find? what might you see on a xray (2)? what is the difference between the conservative (2) and surgical (3) options?
one of most frequence complaint in teens!
can be caused by 4 things: biomechanical, muscular, trauma, overuse
anterior knee pain with difficulty squatting, kneeling, down stairs, sitting for long periods of time (car, movie theater)
quadriceps weakness, peripatellar pain, patella apprehension, “J” sign, pain with resisted knee extension
shows shallow femoral sulcus, tilted patella
conservative: normal, quad strengthening, patellar support brace, foot orthotics
surgical: medial patellofemoral ligament reconstruction, lateral release, tibial tubercle osteotomy
patellofemoral pain syndrome
biomechanical cause explaination (6)
increased Q angle (normal is 10-22*)
pronation
tibial internal rotation
patell instability
shape of patella or femoral sulcus
angle of flexed knee
patelloafemoral pain syndrome
muscular explaination
aka, where is their weakness and tightness?
weakness in: quadriceps, hip flexors
tightness in: hamstrings, iliotibial band, gastrocs
what is the function of the patella? (5)
specifically as part of the extensor mechanism
- thickest hyaline cartilage
- protects tibiofemoral joint
- provides mechanical advantage for extension mechanism
- decreases friction in extension mechanism
- acts to guide/direct forces in extension mechanism
Medial collateral ligament (MCL)
what is this the most common of? what else is often injured if this is injured? what stress does this prevent against? where is the stability? where do you specifically find tenderness? what is the degree range of extension with valgus force?
most commonly injured lig in the knee
prone to injury because of long lever arms of tibia and femur
provides medial stability against lateral force, prevents against valgus force
variable laxity with valgus force (0-30* extension)
medial meniscus tear association, medial femoral condyle tenderness
loose knee, giving way
lateral collateral ligament (LCL)
where is the stability? what force can cause it? it is associated with what other 2 injuries? where are the two point tender locations?
provides lateral stability, varus deformity
associated with fibular head fracture and posterolateral corner injuries
“loose knee” sense of instability
point tender over LCL/fibular head
laxity with varus force
posterior cruciate ligament (PCL)
where is the stability? what is it assocaited with? what does it feel like and where is the pain? what two tests should you do?
provides posterior and rotational stability
dashboard injury/total knee dislocation
associated with multiple ligament injuries so always check for others
“knee is un-hinged”, posterior/popliteal pain
posterior drawer sign, sag sign (lay on back with hips and knees 90*)
anterior cruciate ligament (ACL)
what other two things are commonly injured with this and what is this called when they’re all injured? what type of stability does this provide? who and how does this typically happen? what do patients hear? what develops quickly? what test is diagnostic?
terrible triad! UH OH: included MCL and medial meniscus tears
provides anterior and rotational stability
MOI: medial tibial rotation and anterior tibial translation
very common in younger athletes, from cutting, pivoting, sudden stop while running
1/3 of patients hear “pop”, large effusion
women>men
hemarthrosis develops quickly within 3 to 4 hours
Lachman’s test is sensitive for diagnostic
what imaging should you do for knee ligament tears?
Xrays:
- associated fractures
- medial femoral condyle avulsion
- lateral tibial fracture
MRI:
definitive test for ligament damage/meniscus
what are the treatment options for knee ligament tears?
what are the two big branches? who are they appropriate for? what options must be considered for surigcal repair? who do you always repair in?
conservative: bracing, ice, appropriate in patients who do not do competitive activities or do not report instability with desired activities
-all grade I and II sprains, some III
-can be MCL if isolated injury
surgical: those who report instability, compete in competitive activities,
-MCL/PCL reconstruction if associated with multiple lig injury
-LCL reconstruction if posterolateral corner injury
-ACL reconstruction always repair in young people, age, activity, demands, allograph vs. auto (<40)
Meniscal tear
what two common pt populations does this happen in? how do injuries in these two groups occur? which one is more commonly injured? when does the patient have pain? what are 3 things they may report as feelings? what are the two tests that are important? what are the two next steps after conservative treatment fails? what must be considered?
older patients: associated with OA, degenerative tear, chronic complaints
younger patients: associated with rotational injury from femur on tibia or trauma
W>M, medial more commonly torn
pain with rotation/squatting, fullness behind knee, and giving way or locking (can’t extend knee)
joint-line tenderness biggests key
mcMurray’s test is the gold standard
appleys compression tests
tears rarely heal on their own, symptoms may get better but they will return
repair vs. menisectomy
(dependent on type of tear, zone red vs white, activity demands)
what is the difference between the white and red zones on the meniscus?
white: inner avascular portion of meniscus
red: outter vascularized portion of the meniscus
what are the functions of the meniscus?
5 things
lubrication of the joint
nuitrition
diffuses forces from femor onto the tibia
decreases hyaline cartilage wear
shock absorption
what does the medial meniscus look like? how much motion is allowed? what does it attach to?
Medial Meniscus
“C” shaped
attaches to tibia and MCL
2mm of motion
what is the shape of the lateral meniscus? how is it attached? how many mm of motion does it have?
Lateral meniscus
“o” shaped
loosely attached, decreasing risk for for injury
10 mm of motion as knee flexes
Pre-patella bursitis
what else is this known as? what do patients get it from? what is the organism that can cause it if infection? what do you want to do for imaging/testing? what do you do for treatment?
roofers, floorers, people who are kneeling down all the time, feels like water on the knee
“housemaids knee”
inflammation of prepatellar bursa, between patella and skin
trauma or repetitive kneeling
can become infected by micropenetrating trauma S. aureus
xray to rule out bony injury, or foreign body in bursa
joint aspiration if question of infection, analyze for organism
conservative approach plus knee pad or cortisone if 100% no infection
shin splints/tibial stress fractures
who is this more common in? where does the pain present for shin splints? what makes it worse? what do stress fractures disrupt? what causes them? where will this patient be tender? what two movements will illicit pain in these patients?
what might you see on a xray? what is conservative treatment? what are the two surgical options?
women>>men
3x
15% of runners biggest complaint, dull ache in middle 1/3 of tibia, gets worse with longer activity
tibial stress fracture disrupts tibial cortex from repetitive stress, point tender at posteromedial border of tibia, pain with dorsiflexion and toe extension
xray: may be able to see periosteal thickening
bone scan: show early stages of stress reaction, compartment pressure measurement
conservative+footwear/orthotics, crutches for stress fracture
surgical: release deep posterior fascia for exercise induced compartment syndrome, prophylatic intramedullary rodding for stress fx
how many more times is a achilles tendon rupture common in men than women?
20x more common in men than women
WHAT?!
achillnes tendon rupture
what two ways can this happen? what do you see? what exam test can you do? what imaging? what are the two treatment options and which is preferred? what does the achilles connect?
complete or partial tear of achillnes tendon
strongest, thickest tendon in body
connects gastrocnemius and soleus to calcaneous, can’t walk if completely torn, feel a big hole if torn
plantar flexion at ankle, pain posterior calf 2-6 cm above insertion
causes: acute dorsiflexion, chronic degredation
thompson test, squeezing calves
those who refuse or don’t qualify for surgery: cast up to 12 weeks, change cast every 2 weeks, progressively increase dorsiflexion to neutral, 3 months no WB
surgical is best: decreases risk for retears, cast 8 weeks, progressively increase dorsiflexion to neutral by recasting, 6 months full recovery
what are 2 medical risk factors for achilles tendon tear?
- medications fluoroquinolones
- corticosteroid injections
also prolonged immoalization, causes it to be weak
ankle sprain
what are the three types that can cause this and which ligaments are included in which types? what are the presents? what exam tests are important to do? what rule do you use to determine if a xray is needed? what is the treatment and what is one exception and how long do these patients need to be immobalized?
inversion injuries (90%), anterior talofibular (#1), calcaneofibular, posterior talofibular
eversion (10%), deltoid lig
lateral rotation (high ankle sprain): syndesmotic ligs, anterior tibiofibular joint, high ligs connect the tibia and fibula, pain with external rotation, pain just above the ankle squeeze test of tibia/fibula
point tender over lig, hypermobility with stress testing
anterior drawer tests
ottowa ankle rule to determine if xray is needed
Tx: conservative even if grade III, surgical repairs but is reserved for chronic instability, crutches 48-72 hours and brace, with syndesmotic sprain longer immobalization for 4-6 weeks
what is the grading for ligament sprain?
- stretch
- partial tear
- complete disruption
what are 5 risk factors for ankle sprains?
- joint instability
- muscle weakness
- poor shoe selection
- decreased flexibility
- prior sprains/injuries
plantar fascititis
what are 3 risk factors for this? where does this attach and insert? what happens here? what arch does this support? where might there be palpable pain and how does the pt describe the pain? what isn’t present that you would think would be? what might you see on a xray?
what are some unique conservative treatment options? what is the last resort?
RF: overweight, poor footwear, weight-bearing activities
inflammation of plantar fascia, calcaneous to metatarsal head
supports transverse longitudal arches
pain in AM, “stepping on knife”, first steps very painful and heel pain at night, pain over medial calcaneus, tight fascia on palpation and inflexible achilles w/o swelling
Xray: can show heel spur at fascia origin
conservative: stretching, arch support, orthotics, night splints, reccomended for 6-12 months
surgical: release fascia, ABSOLUTE last resort, not that effective in relieving pain
Metatarsalgia/stress fracture
what are 3 risk factors? where is the most common site for pain? where is the most common site for fracture? what MUST you differentiate this from? what is the pain like? what is a better choice than a xray? why? what are the conservative choices for treatment? what about a stress fracture?
RF: running, ballet, pes cavus foot, excessive arch
mid-foot pain from metatarsals, head of 1st metatarsal or 1st cuneiform/metarsal joint
need to differentiate from seamoiditis (fracture of semoids that rest under big toe)
stress fractures common at 2nd/3rds metatarsal shafts
“dull ache”, relieved with rest
bone scan better than xray since fracture can take 2-4 weeks to appear
Tx: conservative, metatarsal pad, stiff soled shoes
stress factor: cast or brace for 4weeks
how long may a metatarsal fracture take to show up on xray? therefor what should you do instead?
2-4 weeks, therefore, do a bone scan
gout
what happens here? what do the crystal depositions look like? what is effected commonly as a strange presentation in most cases? what are the two ways these crystals accumulate and what are the percentages? what hardened structure can be found within joints of chronic gout? what labs do you do? what is diagnostic? what is the difference between the treatment for acute and chronic treatment?
most common form of inflammatory arthritis in m/w over 40
acute arthritis (usually at night) by sudden increase and deposition of uric acid crystals in the joint
great toe effected in 50% of cases, but can effect any joint in the body: ankles, knee, hands, wrists
cause: hyperuricemia, too much in circulation and in 90% of cases there isn’t enough secreted from the kidneys instead of overproduction (10%)
joints contain tophi, hardened nodules (chronic)
Labs: uric acid levels, may have elevated WBC, uric acid crystals in joints are diagnostic, xray to access joint damage
Acute TX: NSAIDS, colchicine
Chronic: Xanthine oxidase inhibitor, allopurinol (blocks production) or probenecid (increases uric acid excretion)
what do the crystals in gout look like?
needle like WITHOUT birefringence
when does the ratio of men>women, switch to women>men who are effected by gout?
after menopause, then it is more common in women
what is the name when the big toe is effected by gout?
podogra
what is the most common cause of gout in people?
metabolic syndrome 75%
what are three interesting things that increase risk of gout?
alcohol, meat, seafoods
metabolic conditions
charcots foot
what two joints are most commonly effected with this? what are the 3 characteristics associated with this? what are the two man theories about what this happens? what can the foot look like? what are 3 presentations you would see with this? who is this really common in? what will you see on the xray for this think Candy? what will you ALWAYs do for treatment forthis and what do you try to avoid with this?
degeneration of the WB joints, tarsal-metatarsal (TMT) 60%, and metatarsal-phalange joints (MTP) 30%
joint dislocations, fractures, anatomic deformities
diabetics pretty common
50% relate to traumatic mode of injury
foot may look like it is flattening out (deformed), increased skin temp, possible skin ulcers, decreased sensation depending on neuropathy
Two theories: neurotraumatic and neurovascular
total contact cast doesnt allow any motion, prevents further destruction 6-9 months for stability
surgery rarely indicated, causes lots of problems
Xray: atrophic changes, distal metatarsal thinning “Licking candy stick”, hypertrophic changes “the 6 d’s”
what are the 6 “D’s” hypertrophic changes associated with charcots foot?
- distended joint
- increased density
- debris production
- dislocation
- disorganization
- destruction
what is the neurotraumatic theory of charcots foot?
decreased periphreal sensation leads to repeated micro trauma of joints
micro trauma tiggers inflammation
causes bone reabsorption and decreased density
less bone density makes them more likely to continue to get injured
what is the neurovasculature theory associated with charcots foot?
neuropathy causes densensitized joint to have increased blood flow
blood stimulates increases osteoclast activity more than osteoblast
decreases density, creating more chance for injury
what is a major population that is effected by charcots foot?
diabetics, esp with neuropathy
pseudogout
what is this caused by? what joint is the most commonly effected? what isn’t present that is seen in regular gout? where do you see the deposits? what do the crystals look like under the microscope?
acute inflammatory disease caused by calcium pyrophospate crystals
calcium pyrophosphate dihydrate disease
knees most commonly effected
*****no tophi present that differentiates from gout****
see calium deposits in the cartilage
aspiration see rod shapped crystals with blunt ends and befringement unlike gout
conservative and excision of chondrocalcinosis
osteomyelitis
what is this and how does it present? what is the most common organism in this and what are the different potential organisms from adults to children? what can a xray show you? MRI? Labs? How long does this person need to be on antibiotics? what is commonly needed? what needs to be removed?
infection of the bone, bacterial, fungal
symtoms come from inflammatory response, pus inhibits blood flow, causing necrosis, if bacteria gets into the bone itself it can be difficult to eradicate
S. aureus most common in children and adult
Adults: S. pyogenes, Pseudomonas, E. coli
Children: Group B strep, E. coli, Streptococcus pyogenes, haemophilis influenzae
fever, chills, malaise, may have ulcer over effected area
xray:done destruction/hetertrophic bone formation
Labs: soft tissue involvement
6 weeks of antibiotic therapy required, can do hyperbaric chamber if not healing, debridement required in most cases and hardware removal, also amputation
where are the 3 most common locations for osteomyelitis in children?
femur, tibia, and humerus
aka the long bones
where are the three most common locations for osteomyelitis in adults?
vertebrae, maxilla, pelvis
what are two things you can see on a xray in osteomyleitis?
late sequestra: dead bone surround granulation tissue
involucrum: (periseal new bone) make take several weeks to months to appeare
but careful when looking at xray…..visible changes on cray lag behind symptoms by 10 days
when it comes to osteomyelitis, sickel cell patients are at risk for…
salmonella osteomyelitis
infectious (septic) arthritis
how many joints does this involve? what joint is the most common? what is the most common agent? what are the four agents in children? what active people does this often effect and percent? what should you treat with until the cultures come back?
involves a single joint, most commonly the knee 90%
then hip, shoulder, anklet
Adults: S. aureus, streptococcus
children: Haemophilis influenzae, E. coli, pseudomonas, borrelia burgdoferi
- sexually activite individuals have increased risk from Neisseria gonnoreah 50%*
xray: may see gas in the joint space, arthrotomy and culture - treat until culture comes back: ceftrixaone, followed by 4 weeks of antibiotic after organism identified*
in infectious (septic) arthritis….what must you always do if the hip is involved?
arthrotomy….test it and see what it is!!
what is a exciting new drug that is being used for Giant Cell Arteritis? What does it do?
tocilizumab: promising anti-IL6 drug
what are 3 characteristics of general spondyloarthroapies? (3)
- synovitis
- enthesitis: inflammation of the tendon and lig insertions to bone don’t have in RA
- spinal AND periphreal involvement
what is the gene associated with general arthrospondloarthropathies?
HLA-B27
what are two things that can increase someones risk for general spondyarthapies?
genetics predisposition
infectious influence
are there any diagnositc tests for general spondyarthropathies?
no
where do you typically see the periphreal arthritis for general spondyloarthropathies?
assymetric lower limb and random
EXCEPT psoriatic arthritis which is upper limbs
Ankylosing spondylitis
what age group does this happen in? what joint does it often effect first and then where does it go? what does the spine classically look like? Fast or slow? what else can it effect which you wouldn’t normally think of? what are 4 other things this can commoly present with? what test do you want to do? what do you see?
leads to fusion of the vertebrae in 20s-30s
effects the sacroiliac joint symmetricaly and then the rest of the spine in ascending matter bamboo spine, plantar fascia, achilles tendon, patellar tendon involvement
commonly also see: uveitis, aortic valve, cauda equine sundrome, interstitial lung disease
strong association with HLA-B27
gradual onset, morning stiffness that improves with activity for >3 months
schober test: lumbar flexion is abnormal
can’t do anything about it except NSAIDS then try DMARDS, try to restore function
Reactive Arthritis (Reiter Syndrome)
what is this join infection caused by? what are the two most common routes a person can contract this? what are the 4 symtoms that are included as a part of this tetrad? what do you want to make sure you do? and what test will be negative? what do you treat with?
joint inflammation that presents after PREVIOUS INFECTIONs commonly from sexually transmitted or gastroenteritis
chlamydia urethritis most common pathogen
Tetrad presentation:
- urethritis (difficulty urinating,
2. conjunctivitis (eye inflammation)
3. olioarthritis (1-4 joints)
4. mucosal ulcers (oral, balantitis*peeling of skin on penis*, stomatitis *inflammation of the mouth)
5. keratoderma blennhoragicum rash/ulcers on bottom of feet
want to do a culture, will be RF NEGATIVE!
Treatment: NSAIDS, DMARDS antibiotics not really helpfuly even though infection!
what are te two bacteria seen in reactive arthritis in the sexually transmitted pathway?
chlamydia urethritis
ureaplasma
9:1 Men
what are the 4 bacteria you should worry about in reactive arthritis that you should worry about in the gastroenteritis pathway?
Yersina
Salmonella
Shigella
Campylobacter
psoriatic arthritis
what is this associated with? what is a classic sign of this? what are 2 other things you commonly see? which 2 joints are most commonly effected? what will you never have with this? what is the worst case presentation of this called? what is the treatment?
inflammatory arthritis with skin involvement of psoriasis usually preceeding joint disease
spinal and DIP joints
1. spondyloarthritis
2. DIP arthritis “PENCIL IN CUP” (pic, see psoriasis in joints)
3. NO OSTEOPENIA
4. EROSION NEXT TO ANKYLOSIS (FORMATION OF NEW BONE)…interesting see both
3. in extreme cases can be in arthritis mutilans where all joints fuse!! can’t move (see in pics, here all tendons are gone, could stretch out finger and move it all around) fingers collapse down
sausage digits (dactylitisi) , nail pitting or onycolysis, tendon swelling
treatment: NSAIDS, DMARDS
what condition is this called and what is it a classic sign of?
PENCIL IN A CUP, seen with psoratic arthritis
Seen in this picture is spine involvement, with the weird little outcrops, doesn’t look like ankylosing spondylitits spine!
Explain the ranking of DMARDS for spondyarthropathyies…when do you use each of these?
sulfasalazine
Methotrexate
Anti-TNF etanercept
sulfasalazine: mild not for skin
methotrexate: moderate to severe disease
Anti-TNF Etanercept: used in Methotrexate non responders!
Cool table about the differences between RA and spondyloarthropathys
cauda equina syndrome
large midline disk herniation that compresses the nerves at L4-L5
#1 SPINE EMERGENCY–BY WALL
concerning triad: saddle anastesia, loss of bowel and urinary function, bilateral weakness
requires surgical emergency!!! diagnose with CT/MRI
Burning prodrome of pain into dermatome followed by a vesicular rash…what is this bacteria?
Herpes Zoster…SHINGLES
what plane are the abnormalites in scoliosis found?
coronal
scoliosis
what are the two general shapes of the spine you can see? what age group is this in and what gender? what are two unique indicators you can see? what do you see with the shoulder, iliac, scapula and flank? how do you describe the curve? what vertebrae is this most common in? what type of curvature is really rare?
lateral curvature of the spine in C or S shape, 3-18 years old!
cafe au lait spots and tufts of hair present=indicators
asymmetric in shoulder and iliac height, asymmetric scapula, flank decrease flexion
more common in girls during puberty growth spurt and cessation of spinal growth rate at are the greatest risk!
to measure the curvatue you look at the vertebrare at the apex of the curve and then describe relative to that
most common at T7-T8, left curvatures is rare!
what is the most common spinal deformity evaluated by a clinician?
idiopathic adolescent scoliosis
explain the 2 divisions of patients for scoliosis and what the treatment reccomendations are?
>20* curvatures: back brace and surgery consult
in scoliosis patients, when are increased xrays indicated? what is considered clinically significant for a curvature change using scolimeter?
>5* curvature change: increased xray
curve changes: >15% is signficant!!
herniated nucleus pulposus
what happens in a herniation? where does this most commonly occur in the vertebrae and in the spinal cord? what will the 3 main symptoms be and what are 3 things a patient will get pain with that are normal things? what do you do for treatment?
this is when the nucleus pulposus, the soft gelatinous center is herniated posteriorally since this is where the annulus fibrosis is the weakest!!!
usually occurs in lumbar spine since takes the most load
see motor and sensory manifestation
- tingling, numbness, or burning pain (seen in sagital and axial MRI images)
- pain with coughing, sneezing, and laughing
RICE, NSAIDs, surgery
what test should you do for herniated disk pulposa?
straight leg test
pain at <60* is positive test
spinal stenosis
what is this caused by? what two conditions for the risk of stenosis increase with? what unique thing makes this better, and what makes this worse? what can you see the in the lumbar region? what will you see on the MRI? what can you do for treatments for this?
compression of nerves of spinal cord caused by narrowing of the spinal cord and foramen
commonly seen in spondylosis and degenerative arthritis
pain increases with walking or axial loading (leaning back), and decreases with leaning forward, flexion!
back and leg pain, soft tissue and thecal narrowing, can see loss of lumbar lordosis
TX: acetaminophen, weight reduction, pelvic tilt, abdominal exercises….last choice decompressive surgery
MRI with gadalidium allows you to see…
see the nerves better!
if you suspect ankylosing spondylitis what should you test for? what is the ratio of males to females?
CHECK FOR HLA-B27
3:1 male to female
what would you commonly see sacroilliacitis with?
ankylosing spondylitis
and bamboo spine
kyphosis
what vertebrae do you see this in? what other curvature typically accompanies this in the spine? what is the difference in treatments based on the degress of curvature in the spine?
increased curvature of thoracic vertebrae, commonly associated with scoliosis
rounded back appearance, usually accompanied by excessive lordosis
if 45-60* of curvature: PT and bending
if >60*: milwakee brace
surgery as last resort
what is one interesting illness that can subsequently cause kyphosis??
tuberculosis!! weird! POTT DISEASE
what is the name of kyphosis seen in children?
scheurermanns idiopathic osteochondrosis
what are four things that can cause kyphosos?
- dengeneration
- osteoporosis
- trauma
- spondylolisthe
what are the two most common causes of low back pain?
prolapsed intervertebral disk
low back strain
what percent of americans have low back pain?
90%
what are 7 red flags you should look for when someone presents with low back pain?
>50 or <20
histroy of cancer
night sweats/weight loss
urinary or bowel incontinence
recent bacterial infection
pain worse when supine
Hx of trauma
what are the three general rule of thumb for treatment of someone with lower back pain?
(3 options)
WITHOUT RED FLAGS
- 2 days with pillow under legs and NSAIDS
- Mckenzie exercises for disk herniations
- if not better in 6 weeks move on to imaging unless indicated by red flags
- if nothing, continue with conservative
SURGERY IS NOT COMMON WITH BACK PAIN!!
what percent of people with lower back pain actually recieve surgical intervention?
ONLY 5% so it is not very comon at all!!!
osteoarthris…explain what happens in this…
normal bone programming
“cartilage scenescence”–we outlive our chondrocytes around 25-30 years old, it frays and falls apart and the chondrocytes become hypertrophic and grow larger, however they produce enzymes MMP and aggrecanases that break down the cartilage and act like growth plate cells where THEY MAKE MORE collagen 1 and 9, BONE THAN BREAK IT DOWN…CARTILAGE CAN’T REGROW SO YOU JUST GET INCREASED BONE GROWTH!!
“progressive loss of articular cartilage and reactive changes at the joint margins from bone rubbing on sunchondral bone rubbing on bone “behaves like a fracture” and stimulates chondrocyte hypertrophy and increased bone growth
what are the Early osteoarthritis presentations? (4)
1-2 years
morning stiffness lasting <1 hour!!! “they’re ok, they just keep going!”
red, prominent DIP and PIP joint involvement
normal radiographs
what are the common presentations of late osteoarthritis? (5)
morning stiffness lasting <30 mins/1 hour
mechnical stiffness, gets worse with movement, more pain the more they do
not the same strength they used to (opening jars, turning handles)
abnormal radiographs! deformities obviously present, bone hypertrophies
get LESS symtomatic in non weight bearing joints, asymatic once they are deformed because they aren’t able to move them
what is neuropathic arthropathy nicknamed? what are 3 risk factors for this?
CHARCOT foot!! this is a type of osteoarthritis
diabetes, alcoholism, tabes dorsalis!
what is an osteophyte?
bone outgrowth seen in osteoarthritis, increase in bone production
what joints are most commonly effected by osteoarthritis?
PIP, DIP, hips, knees
what are the treatment options for someone with osteoporosis?
Not much…its a natural bone programming
Its “supposed” to happen
- joint conservation
- exercise low impact
- weight loss to relieve load on joints
NSAIDS and COX-2, total joint replacement, autologous cartilage implantation (not many people qualify)
what are the genes associated with osteoarthritis? (3) what do they do?
FR2B, GDF-5, DIO2
endochondral ossification, skeletal malformations, and hypertrophic chondrocyte activity
secondary cause of osteoporosis: Padget’s disease
ribbed or holey bones which throws the angles off and causes you to get bone on bone running
osteoporosis
what is this? who is it most common in? what is the nickname for this disease? what imaging type do you want to preform? what 3 presentations might you find on physical exam?
abnormal bone remodeling, decrease in the total volume of bone making it less dense, since less strong it leads to increased fractures!
imbalance between bone formation and reabsorption
most common in menopausal women
“silent disease”
presentation: height loss, kyphosis, severe cervical lordosis dowagers hump
Dexxa scan of spine and hip
what is an abnormal DEXA scan result that can indicate osteoporosis?
-2.5 and below
what are the treatment options for osteoporosis? (3)
- bisphosphonates: inhibits osteoclasts (jaw necrosis)
- HRT, estrogen, or progesterone (stroke, breast cancer)
- selective estrogen receptor modulator (serms)
rheumatoid arthritis
what are the four criteria for diagnosis?
1. morning stiffness >1 hour, usually don’t feel better till 10-11 am
2. arthritis of >3 joints and soft tissue, immune system is activated!
3. symmetrical!!
4. >6 weeks!
explain what happens in rheumatoid arthritis?
affects the lining of multiple joints synovitis, causing a painful swelling that can eventually result in bone erosion and joint deformity, autoimmune (not wear and tear like osteoarthritis)
hyperplastic synovial tissue called pannus erodes the cartilage, subchondral bone, tendons, and ligs “like a line of soldier marching to battle and destroying everything in their pathway. joint erosion
what two tests do you want to run for someone with rheumatoid arthritis? which is more specific?
RF: 65-70% positive
A-CCP: POSITIVE 70, more specific
what is the a specific indicator for Rheumatoid arthritis that isn’t seen in ANY OTHER DISEASE!!!!!!
cyclic citrullinated protein
when is the most critical point to catch Rheumatoid arthritis? what is the difference in the timeframe for progression? when are you likely to see radiologic changes?
ASAP
will see radiographic changes <2 years
rapid during first year compared to second and thurs
“at first its a fire and an entire war so need to get treatment asap, the second wave is just the reserve and the damage and action has already taken place”
explain the 3 phases of rheumatoid arthritis?
- TNF and IL cause catabolic effect on chondrocytes, attracts macrophages, weakens it
- introduction of metalloproteinases, stromolysin, and collagenase
- phagocytosis of cartilage and bone by pannus
why is it important to always look at the feet of a rheumatoid arthritis pt? if suspicious they have it what is important to do?
see it on the feet before the hands so really important to get xrays of both the hands and feet!!
ALWAYS DO BOTH!!
if suspicious on physical exam, must feel joints because you will feel the difference between individual joints!
what three joints does RA commonly effect?
MCP, PIP, wrist
also feet fyi
what is rheumatoid arthritis an independent predictor of?
cardiovascular disease 2.5
what are the 3 stages to accepting a chronic illness?
- denial
- anger/sadness
- acceptance
but people still worry about it regardless
what two inflammatory contributors will you find remarkedly elevated in RA?
TNF, IL-1
if you add a biologic agent to methotrexate, how much do you increase remission by?
20%
why don’t you prescribe two biologic agents?
increase infection rates by 30%
NEW RA DRUG
xeljanz does what?
blocks phosphorylation of janus kinase inhibitor
only had for 1.5 years
if a RA patient isn’t responding to the biologic agent what should you do?
try a different one!! 70% will respond to a medication switch with biologic meds!
explain the medication treatment rational for rheumatoid arthritis!!
3 conditions
- methotrexate
- in partial or non responders frm 4-8 weeks, get them on biologic DMARD ETANERCEPT combined with Methotrexate!!
- if erosions at time of xray, then go straight to Etanercept or biologic dmards!
how many of the characteristics do you need to have to qualify for rheumatoid arthritis?
6/10
juvenile rheumatoid arthritis
what common general age is this found in? what age range is most common for females? what age range is most common for males? what are 3 types that you can see and what are associated with each?
chronic synovitis in
females: 1-3 years old
males: 8-12
see spiking fever, pink macropapular rash, warm, red joints
Systemic: fevers, rash, hepatosplenomegaly, leukocytosis, myocarditis
pauciarticular:
poly articular: like adult RA, five or mor small joints, nodules
Bilateral LBP- Diffuse, Non-Radiating, worse with sitting, stationary positions
pain associated with?
degenerative disc disease
Unilateral Right LBP, posterior buttock, radiating into right leg typical for
lumbar disk herniation
LBP at night, persistent, unrelieved by rest or laying supine common in…
malignancy
when would you see cafe au lait spots and missing tufts of hair and edema?
neurofibromatosis, scoliosis
most lower back pain/strain will result in…
1-4 weeks with conservative treatment
guidelines reccomend conservative treatment for 4-7 weeks
30% of asymptomatic individuals may display abnormal MRI changes consistent with disc degeneration in the absence of clinical symptoms.
fun fact!
what type of imaging is the gold standard for tumors, disk herniation, nerve impingement? when would you use the next step down?
Magnetic Resonance Imaging MRI
if they have a pacemaker or internal metal and can’t get one
what can you see with a CT (computed tomography)? what about when you add contrast? what type of patient would have to use this if they couldn’t use MRI?
3D image, bone, facet joints
with contrast look at nerves or intradural lesions
use with a patient if they have a placemake and can’t use MRI
Bone scan (scintigraphy)
what do you use this for?
vertebral body osteomyelitis or osteoblastic lesion
what is always important to test for someone who presents with back pain?
LYME TITERS
if adams forward bending test is positive…what is it likely the patient has?
scoliosis
where is a common site for stress fractures? what makes these fractures worse?
pars interarticularis region, spondylolysis
full extension and rotation to the effected side
if postivie, need to brace for at least 3 months
