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Module 1: Mali Rheum/MSK > CM > Flashcards

Flashcards in CM Deck (224)

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



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

6. 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?


scalp necrosis

lingual infarction

aortic dissection/aneurysm


what are the four major complications seen with long term use of high dose steroids?



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,

1. eyes

1.5. skin (palpable purpura)

2. Upper airway ( ottis media, sinusitis, epitaxis, subglottic stenosis)

3. kidney (nephrotic syndrome/failure)

4. lung (hemmorage, lung failure)

5. cardiac (pericarditis)


labs: elevated CRP, ESR, thrombocytosis, creatine, hematuria, casts, and proteinuria (all elevated)


1. High-dose steroids with cyclophosphamide

2. methotrexate (chemo) or azathioprine (transplant drug)

3. rituximab=anti CD20 drug targets B cells


what is the survival rate for giant cell arteritis after the invention of immunosuppressants?




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



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



1. high dose steroids with cyclophosphamide

2. mexotrexate or azathioprine

3. treat Hep B with antiviral acyclovir

4. 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




what does this mean? 4 examples?

conditions with elevated immunoglobulins



liver disease



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 ANA pattern seen in.....




periphreal ANA pattern seen in .....





Speckled ANA patter seen in....


SLE, Sjogrens


nucleolar ANA pattern seen in...



scheloderma systemic disease


Centromere ANA pattern seen in...


CREST syndrome


SCL-70 ANA pattern seen in....


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



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

1. widespread muskulo pain

2. sleep disturbance

3. no objective physical findings

4. 11/18 trigger points

important to test deep tendon reflexes and sensation




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

1. lifestyle modifications

2. low impact aerobic exercise

3. sleep hygiene/check for sleep apnea

4. address depression/stressors

5. encourage patients to take control



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

1. what percent have depression at time of diagnosis?

2. what percent have lifttime incidence of depression?

3. 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

1.short term memory impairment

2. sore throat

3. tender cervical/axillary nodes

4. muscle pain

5. multijoint pain

6.  headaches

7. unrefreshing sleep

8. postexertional malaise lasting longer than 24 hrs



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?

1. CBC (anemia/cytopenias)

2. BUN/Cr (kidney involvment)

3. UA (proteinuria/ casts)

4. C3/C4 (decreased)


5. positive ANA with all patterns EXCEPT centromere and SCL70

6. dsDNA that is more specific than ANA, speckled or nucleolar


SLE treatment

1. skin

2. renal

3. other

Skin/fatigue: hydroxychloroquine

renal: high dose corticosteroids and cyclophosphamadine (immunosuppressant)


other immuno:





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




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


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



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


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



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


1. heliotrope (lavander around eyes)

2. gottren's papules (rashes over joints)

3.shawl sign

4. mechanic's hands

5. periungal erythema

6. 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?

1. lymphoma

2. primary biliary cirrohosis

3. accelerated dental caries

4. cornreal atrophy/ulcerations

5. oral candidiasis



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*


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?


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


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


1. drop arm test

2. empty can test (supraspinatus)

3. lift off test (subscapularis)

4. hawkins (think it looks like a bird wing)

5. Neer impingement sign



1. xrays (subacromial spur, calcified tendonosis, head of humerus may migrate forward

2. MRI-helpful but expensive

3. 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?


1. PT

2. Cortisone Injections (good for elderly)




1. 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


1. cross arm test

2. pain with restricted horizontal abduction

3. 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?

1. AC lig injury

2. AC lig torn

3. AC and CC lig torn

4. AC and CC lig torn, avulsion (pulling away), displacement through skin or muscle

5. AC and CC lig torn with deltoid and trapezius fascia stripped off acromion and clavicle

6. 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)

1. immobolization for pain, get out quickly to avoid pain for 1-3 weeks


3. PT

Grade 3-6 surgical aggressive treatment (any displacement or fascia stripping)

needed if unstable or cosmetic




*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?


1. sling for 3-4 weeks

2. reassurance!! almost always heal w/o surgery, may still have deformity but 100% functional

3. 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!****


1. used for unstable fractures (aka bone is puncture skin or injurying something below)

2. tricky and dangerous since next to Brachial plexus and subclavian a

3. 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




what imaging should you do for something with shoulder insability/dislocation?


1. A/P, Y view

2. always get xray with first time dislocators




1. 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?


NSAIDS, sling

PT after 3 weeks for <40 yr olds

PT after 1 week for >40 yr olds

**don't want them to stiffen**



1. Bankhard (labral) repair for labrum tear

2. 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!



1. reduction

2. 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



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


involves the tendonous insertion of extensor carpi radialis brevis


tennis, golf, weight lifting

pain with repetitive extension and flexion


1. radiate down the arm

2. passive wrist flexion

3. active and resisted wrist extension


1. eliminate aggrevating factors


3. tennis elbow strap

4. cortisone injection, DONT INJECT TENDON

5. 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:

1. padding/compression wrap, NSAIDS, heat, ice

2. cortisone injection ***need to make sure 100% not infected if so***


treatment for infectious:

1. treat cultured pathogens

2. 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



1. NSAIDS, splint, cortisone injection, symptoms resolve in about a year

2. 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....



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



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.



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


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


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?



genetics FR2B, GDF-5, DIO2

-endochondryl ossification, skeletal malformations, chondrocyte self destruction



primary osteoarthritis is.....

idiopathic, arises spontaneously


secondary osteoarthritis can come from....


1. posttraumatic

2. congentiral deformation

3. endocrinopathy

4. neuropathic arthropathy

5.padgets disease

6. avascular necrosis

7. skeletal hyperostosis DISH


characteristics of erosive osteoarthritis


more agressive


persistent symptoms

inflammatory findings


what puts a person for increased risk for stomach ulcers when using NSAIDS?

>60 years old


past ulcers


long term NAID use


what is the most common joint disorder in the US?



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)


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?



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*)


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

1. thickest hyaline cartilage

2. protects tibiofemoral joint

3. provides mechanical advantage for extension mechanism

4. decreases friction in extension mechanism

5. 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


hemarthrosis develops quickly within 3 to 4 hours

Lachman's test is sensitive for diagnostic


what imaging should you do for knee ligament tears?


1. associated fractures

2. medial femoral condyle avulsion

3. lateral tibial fracture



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


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?



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



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?


2. medications fluoroquinolones

3. 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?

1. stretch

2. partial tear

3. 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



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?



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?

1. distended joint

2. increased density

3. debris production

4. dislocation

5. disorganization

6. 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



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



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)

1. synovitis

2. enthesitis: inflammation of the tendon and lig insertions to bone don't have in RA

3. spinal AND periphreal involvement


what is the gene associated with general arthrospondloarthropathies?



what are two things that can increase someones risk for general spondyarthapies?

genetics predisposition

infectious influence


are there any diagnositc tests for general spondyarthropathies?




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:

1. 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


9:1 Men


what are the 4 bacteria you should worry about in reactive arthritis that you should worry about in the gastroenteritis pathway?






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. 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?



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


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?




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?


3:1 male to female


what would you commonly see sacroilliacitis with?

ankylosing spondylitis


and bamboo spine



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?






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?



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)



1. 2 days with pillow under legs and NSAIDS

2. Mckenzie exercises for disk herniations

3. if not better in 6 weeks move on to imaging unless indicated by red flags

4. if nothing, continue with conservative





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?


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



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)


1. bisphosphonates: inhibits osteoclasts (jaw necrosis)

2. HRT, estrogen, or progesterone (stroke, breast cancer)

3. 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?


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?

1. TNF and IL cause catabolic effect on chondrocytes, attracts macrophages, weakens it

2. introduction of metalloproteinases, stromolysin, and collagenase

3. 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!!


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?

1. denial

2. anger/sadness

3. acceptance

but people still worry about it regardless


what two inflammatory contributors will you find remarkedly elevated in RA?



if you add a biologic agent to methotrexate, how much do you increase remission by?



why don't you prescribe two biologic agents?

increase infection rates by 30%




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

1. methotrexate

2. in partial or non responders frm 4-8 weeks, get them on biologic DMARD ETANERCEPT combined with Methotrexate!!

3. 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?



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


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...



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?



if adams forward bending test is positive...what is it likely the patient has?



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