Or me to go
back
Rheumatology
Dan Cushman
2007
Note: Hit me
to advance
to the next
slide
Joints
What type of
Articular (hyaline)
cartilage are
cartilage
bones covered by?
What’s special
It secretes
about the synovial
synovial fluid!
membrane?
Which parts of the
joint
Cartilage
are not
&
covered
intraarticular
by the
fibrocartilage
synovial
membrane (2)?
How long does it
take for the
It never fully
articular cartilage
regenerates
to fully
regenerate?
Synovial Fluid
Is there a high or a
What types of
Synovial
low proteinCan
cells secrete
What
It provides
is the point
Low protein
fibroblasts
be
contentarthrocenteses
in synovial
hyaluronic
acid?
viscosityacid?
Yep, if you’re good of hyaluronic
performed on
fluid (SF)?
at it
patients with
coagulopathies?
What’s the main
A vasovagal
risk of
Immuneepisode
What are arthrocentesis?
the main
surveillance,
three purposes of
supply nutrients,
SF?
remove wastes
It is happens
digestedtoby
What
the
enzymesacid

hyaluronic
content
during
a Why
Real
menbranes
is the
decreased
Because it lacks a
pathological
process?
synovial
cry when
viscosity don’t
true basement
membrane
you bump your
not a
membrane
real membrane?
knee
Culture!
What else should
When is it “NonWhatWBC
would
<= fat
you test for?inflammatory?”
globules2000
suggest?
Synovial Fluid
Cloudy
Yellow
Red
Low
>>
20,000
= Periph
blood
None
Oh
yeah
None
Septic
>20,000
>50,000
Normal
Cloudy
Yellow
Cloudy
Yellow
None
• RBC
<200
per uL
• WBC
High
• Viscosity
Clear
Yellow
• Color
A
fracture
Inflamm
Bloody
Gouty
Acute Phase Reactants
What causes them
What are the main toInflammatory
increase in the
ESR and CRP
states
two tests?
blood?
Which
They’re
disease
not are
APRsspecific
specific for?
Plasma proteins
What
created
arebythey?
the
liver
Fever,
neuroendocrine
What can they
effects,
cause?
behavioral
changes, etc.
Cytokines
What molecules
(IL-6, IL1, TNF-α,
cause the
IFN-β,
TGF-β,
increase?
etc.)
C-Reactive Protein
What is the main
Bind to
(presumed)
phosphocholine?
C-Reactive Protein
function of CRP?
C-Reactive Protein
Run
Is CRP considered
Because it could
Why would youpart of the innate
be a way to
want to bind to or Innate
humoral
recognize foreign
phosphocholine?
pathogens immune system?
To recognize the
phospholipid
Activates the
Why else?
constituents
of
When
complement
bound,
damaged cells
what
system
does
and/or
CRP
Is it rapid
Rapid
or slow?
bind to do?
phagocytic
cells
Erythrocyte Sedimentation Rate
What molecule
largely is
Fibrinogen
responsible for
the ESR?
Which changes
moreThe
quickly
CRP– the
ESR or the CRP?
Is it a direct or
indirect measure
of theIndirect
acute phase
protein
concentrations?
How can the red
By their shape,
cells affect the
size, and number
ESR?
Rheumatoid Factor
Yes – it’s a known
Is it
marker;
even related
RF+
to
patients
rheumatoid
have
more
arthritis?
aggressive
RA
Which isotype is
most commonly
IgM
identified by
testing?
An auto-antibody
to the
What’s
Fc portion
RF?
of IgG
What is its role in
the
immunopathology
Unknown
of rheumatoid
arthritis?
CCP Antibodies
It’sWhich
seen inisthe
early
important…
stages of
why?
RA
Antibodies to
Cyclic
What’re
Citrullinated
those?
Peptide
It’s seen almost
Which is
exclusively in RA
important… why?
patients
AWhat’s
form of
citrulline?
arginine
At what level is
someone
Serum urate
considered to
above 6.8mg/dL
have
hyperuricemia?
What type of
nucleic acid can
Purines
lead to increased
uric acid levels?
What
Inflammatory
would the
(>2000)
WBC count
– usually
be in
between
in the synovial
20,000
Is there
andfluid?
100,000
inflammation
Yep
present?
Gout
Which
Adenosine
onesand
are
purines
guanine
again?
Which
The joint
first is
most
metatarsal
commonly
phalangeal
affected?
(MTP)
What
Negatively
would the
crystals
birefringent
look like?
What type of
crystals
Monosodium
deposit
into urate
tissues in
gout?
Xanthine
Oxidase
What is the
final enzyme
in purine
degradation?
Dietary
purines
Tissue
nucleic acids
Endogenous
purine synthesis
Urate
Overproduction
Underexcretion
Proximal
tubules
The Hyperuricemia Cascade
Where does
most of the
urate
reabsorption
occur in the
kidney?
Hyperuricemia
Silent
tissue
deposition
Gout
Renal
manifestations
Associated
cardiovascular events
and mortality
Gout
Which
Too high;
is a obesity
worse –
a is
BMI
a comorbid
that is too
highcondition
or too low?
>3 attacks/year,
tophaceous gout,
Who should get
urate
What shape are allopurinol?
Needle-shaped nephropathy,
the urate crystals?
More males or
urate > 12 mg/dL
Males
females?
What three
Lose weight, eat
lifestyle
less
modifications
meat/seafood,
should be
NSAIDs,
canlow-dose
be done
drink less alcoholWhich What
type
recommended?
prophylactically?
oralofcolchicine
alcohol
Beeris the
Which
three drugs
Cyclosporines,
lowdoseincrease
aspirin, and
worst?
can
the
diuretics
risk?
Gout
Where is gout
present?
You can be sure that
this guy is gout-free,
though.
Where is the pig who
ate roast beef?
That is a direct
contradiction, because
roast beef should
cause gout (increased
purine intake).
What are
Asymptomatic
intervals
between
“intercritical
acute flares
segments”
Gout
Where do
Joints
monosodium
and soft
How
Decreased
can diuretics
urate
crystals
tissues
tend to
What
food should
cause
excretion
gout?
What’s the most
accumulate?
is
lead 
LeadHow

bekidneys
avoided
if you
Alcohol  lapseUnderexcretion
of
common
general
of
Meat.
decreased
associated
urate
with
don’t
want to
I mean,  mechanism
judgement
urate for
How can alcohol
excretion
gout?
have gout?
underexcretion
of
promiscuity 
contracting
gout?
cause gout?
STGurate
(sexually
No, there is hidden
transmitted gout)
Are
intercritical
damage
that can
What are two
occur
duringsafe?
those
Increased
ATP
sgements
mechanisms that
periods
Who
told
I did.
you so?
LowerHow
pH, lower
↓ solubility,
joint/soft
could
tissue
degradation

How can
could
cause
temperature
tissue disturbances,
underperfusion
increased
precipitation of
decreased
reabsorption of water
exacerbate
adenosinegout?

crystals
occur (3)?
solubility?
 supersaturation
increased urate
Pseudogout – six causes
1.
2.
3.
4.
5.
6.
Hemochromatosis
Hyperparathyroidism
Hypophosphatemia/-magnesemia
Familial Hypocalciuria/-emia
Aging
Thyroid Disease
Calcium oxalate,
What other types
calcium
are possible?
hydroxyapatite
Pseudogout
Inflammation
What type of
Yep
present?
birefringence
Positive do
crystals have?
Whatthe
is chronic
NSAIDs,
Calcium
Pseudo-What
type of
polyarticular
Colchicine,
Pyrophosphate
rheumatoid
What’s
the
arthritisDihydrate
alsocrystals?
steroids,
(CPPD) treatment
arthritis
(4)?
called?
underlying
disease
Is the ROM of
It’s painful
treatment
preserved?
Where does it
most
Wristcommonly
and knee
Is the
Negative,
synovial
butcell
What is the WBC
occur?
culture
there can
usually
be a
count
>2000
in the
concurrent
positive or
synovial fluid?
negative?
infection
Osteomyelitis
What
are 
two
Trauma
contamination;
other routes of
contiguous
infection?
spread
What are the most What is commonly
common
Staph aureus
bacteria
and
apparent before
Bacteremia
Strep
involved
pyogenes
in
acute
osteomyelitis?
What is the most
osteomyelitis?
common
Hematologic
route of
infection?
Why should
children be
They harbor
treated differently
different bacteria
with
osteomyelitis?
Osteomyelitis
IV antibiotics,
surgical
How is it treated?
What is the
debridement &
Where do children
Whatstabilization
are two
Bone
definitive
biopsy &
Long
most
bones
often
of the diagnostic
diseases that can
culture
test for Pott’s
disease, TB
present
extremities
with
cause spinal
ostemyelitis?
osteomyelitis?
osteomyelitis?
Where do adults
most commonly
The vertebrae
present with
osteomyelitis?
Fever, chills,
Back pain, spine
What symptoms
malaise,
How do
localized
they
tenderness, loware present?
pain,
present?
erythema,
grade fever
warmth, edema
Where do adults
usually get
The knee
infectious
arthritis?
Infectious Arthritis
Rapid – it’s a
Rapid
medical
or slow?
emergency!
Previous damage,
prosthetics, IV drug
What
are the main
use,
4 risk factors?
immunocompromised
patients
Most common
Hematogenous
route of infection?
How It
long
canuntil
be the
joint
permanent
regains its
function?
damage!
Damage can occur
How fast?
within a few hours
The
Where
knee;dobut
kids
the
hip
usually
is more
get
Yes, but most
common
infectious
than inCan
it be chronic?
commonly acute
arthritis?
adults
Contiguous,
How else can
direct
it
inoculation
spread?
Infectious Arthritis
Are the symptoms
localized
Both or
systemic?
What is the most
common
Gonococcal
cause of
arthritis
arthritis
in sexually
active adults?
What are the
three most
Knee, wrist, hand
common sites
affected?
Is it considered
autoimmune
Both or
infectious?
What
Staph
areaureus,
the main
Strep
three
pyogenes,
bacteria H.
responsible?
influenzae
What would the
WBC > 10,000;
fluid
Is it more commonsynovial
>80%
polys
Women
in men or women? show?
Skeletal
What
homeostasis,
are the
three
mineral
main
functions
homeostasis,
ofphysis
bone?
Is the
hematopoiesis
metabolically
Active
Bone
YesCan
– without
bone
Is the physis
regenerate
scars itself?
stronger or
Weaker
weaker than
When can a
regular bone?
active or inactive? fracture
Neoplasm,
be a
result
endocrinopathy
of another
inherent process?
Infection,
What
complications
compartment
can
When does bone
occur
syndrome,
with a In which part of
calcification
In utero
The
bone
physis
does
fracture
thrombosis
(3)? the
begin?
growth occur?
Bone
Comminuted
1
2
3
2
Simple
Open
Growing Bone
3
4
1
5
2
6
7
8
9
Fractures – identify location
Type I
Type II
Type III
Type IV
Type V
The tissue is
Then…?
calcified
What
Precise
are the
reapproximation
physician’s two
of goals
the fracture
of the &
primary
rigid
stage of
immobilization
bone healing?
Inflammation
&
Then…?
angiogenesis
Bone
What happens
Hematoma
first in secondary
forms
fracture healing?
Deposition
What is of
thenew
boneprimary
across the
physiology
fracture byof
bone
osteoblasts
healing?
Blood vessels
invade  A primitive scar is
Then…?
Then…?
formation of
formed  scar
normal bone!
Bone healing – Steps
Early Fracture
Inflammation
Repair
Remodelling
Bone Healing – Three Processes
1. Inflammatory
2. Reparative
3. Remodelling
When does
each stage
occur?
Bone Healing – Six Stages
1.
2.
3.
4.
5.
6.
Hematoma
Inflammatory
Formation of granulation tissue
Soft callus formation
Hard callus formation
Remodelling
Hours – days
Begins < 48 hours
2-12 days
1 week – months
1 week – months
Several months
Ewing sarcoma
DIAPHYSIS
Name
the
tumor!
Chondrosarcoma
Chondroma
Osteochondroma
METAPHYSIS
EPIPHYSEAL
PLATE
EPIPHYSIS
Osteosarcoma
Giant cell tumor
What
Myeloma,
are the
lymphoma,
three most
common
metastatic
bone
carcinoma
tumors?
Bone Tumors
What’s the capital
of theLome
country of
Togo?
What’s the most
common
Osteosarcoma
type of
sarcoma?
Malignant
neoplasm
What is aof
mesenchymal
sarcoma?
tissue
What do the
lesions
Multiple
of multiple
lytic
myeloma
lesionslook
like?
Bone Tumors
Tumor
Origin
Osteo(-sarcoma, …)
Bone
?
Chondro(-sarcoma, …)
Cartilage
?
Chordoma
Notochord
?
Ewing sarcoma
Unknown
?
Giant Cell Fibroma
Bone
?
?
Osteosarcoma
10-20
Age?
BodyKnee
location?
Bone
Metaphysis
location?
LevelHigh-grade
of malignancy?
Sunburst, Codman
Radiologic findings?
Triangle
Produces?
Osteoid
Osteoma
Age?
60
?
Skull
Body
andlocation?
facial bones
Level ofBenign
malignancy?
Osteoid Osteoma
?
Body
Longlocation?
bones
Bone
Cortex,
location?
<2cm
Aspirin
Treatment
at night
Osteoblastoma
BodySpine
location?
>2cm in
Size?
diameter
Chondrosarcoma
?
50-70
Age?
Pelvis, proximal femur,
Body location?
shoulder, ribs
LevelLow-grade
of malignancy?
Dedifferentiation
Notable finding?
Chondroma
30-50
Age?
Hands/feet, humerus,
Body location?
femur
?
Level ofBenign
malignancy?
X-rays
Radiologic
mustimportance?
be reviewed
?
Osteochondroma
10-30
Age?
Femur, humerus, tibia,
Body location?
fibula
Bone
Metaphysis
location?
Benign (may convert to
Level of malignancy?
malignant)
MRI shows medullary
Radiologic importance?
connection
Ewing sarcoma
?
10-20
Age?
LongBody
bones,
location?
ribs, pelvis
Metaphysis
Bone location?
or diaphysis
Level
Highly
of malignancy?
aggressive
Notable
CD99 finding?
stain
Chordoma
?
27-80
Age?
Sacrum,
Body
clivus,
location?
vertebrae
Notochord
Origin?
Level
Slow-growing
of malignancy?
Giant Cell
Tumor
?
25-40
Age?
Body
Distal
location?
femur
Bone
Epiphysis
location?
Level ofBenign
malignancy?
Easily confused with
Notable finding?
tendon sheath tumor
Tumor
Age
Bones
affected
Location on
bone
Malignancy
Special
points
Osteosarcoma
10-20
Knee
Metaphysis
High
Sunburst, Codman
Triangle, osteoid
Osteochondroma
10-30
Tibia, fibula,
humerus
Metaphysis
Ben.
Medullary connection
Ewing Sarcoma
10-20
Long bones,
ribs, pelvis
Dia./meta.
High
CD99 stain
Giant Cell Tumor
25-40
Femur
Epiphysis
Ben.
Chondroma
30-50
Hands, feet,
arms, legs
Cortex, surface
Ben.
Osteoma
60
Skull
Chondrosarcoma
50-70
Pelvis, ribs,
femur
Cortex
Low
Dedifferentiation
Osteoid Osteoma
Long bone
Cortex
Ben.
<2cm
Osteoblastoma
Spine
Ben.
>2cm
Chordoma
Sacrum,
vertebrae
Low
Ben.
Joint Hypermobility
Age,Joint
gender,
hypermobility
family
depends
background,
on which
ethnic
fourbackground
factors?
Why are AfricanA failed war on
Americans much
By the
drugs unfairly
How is joint
likely to be
extensibility of the more
our
mobility limited, segregates
jailed
for
joint
joint capsule,
society
generally
hypermobility?
ligaments, and
speaking?
tendons
Name three
Skin striae, lax
extraarticular
upper eyelids,
features involved
weakness of pelvic
in hypermobility
floorIs it determined by
syndrome.genetics
Bothor the
environment?
Is the genetic trait
Polygenic, of
mono- or
course
polygenic?
Ehlers Danlos Syndrome
Does
musculoskeletal
pain present
Early early
or late in the
syndrome?
What is the main
Theskeletal
X-rays are
abnormality
normal on XWhich joints are
ray?
Shoulder, patella,
particularly
TMJ
susceptible?
What’s the most
Hypermobility
Is this chronic or
A heterogenous
prevalent
form
of
Chronic, of Bruising,
course scarring,type
acute?What other
group of heritable
four EDS?
What is EDS?
tissue fragility,
connective tissue
presentations can
What generally
How
can
EDS
skin
Joint sublaxations occur?
Pes planus (flat disorders
happens withhyperextensibility
this
present in the
& dislocations
foot)
type of EDS?
lower extremities?
Vascular EDS
What’s the most
common cause of
Arterial rupture
sudden death for
vascular EDS?
Where can
The
adipose
face and
limbs,
deposition
particularly
be
limited?
What’s the genetic
Autosomal
inheritance in this
dominant
disorder?
Arterial,
What internal
intestinal,
damage
and uterine
can
fragility/rupture
occur?
What facial
characteristics
Large eyes, thin
can
nose,
be seen
lobeless
in this
ears
type of EDS?
Marfan Syndrome
What is the
Fibrillin-1
mutation?
Dilation of the
aorta, involving
…due to?
the sinuses of
Valsalva
What cardiac
Aortic
symptom can be
regurgitation
associated?
What’s the genetic
What is the most
Autosomal
inheritance in this
severe associated
dominant
Aortic dissection
disorder?
cardiovascular
complication?
Which is longer for
Marfan patients –
Arm span
arm span or body
height?
What is another
Ectopia
associated
lentis
It’s a major
symptom?
What does fibrillin
protein building
do?
block
Arthritis
Osteoarthritis
Is local
inflammation
It can be
present?
Is joint effusion
It can be
present?
More common in
Women
men or women?
Are systemic What’s the most
No
Osteoarthritis!
form of
Radiographic effects present? prevalent
arthritis?
Why
findings
shouldn’t
are far
the
hands
more common
be X-rayed
in
the
for screening?
hands than
symptoms
Osteoarthritis
It gets worse
When is pain the
throughout the
worst?
What is the
day
Very
pattern
irregular
of
What happens to
cartilage loss?
metabolic
It’s increased
activity
in the joint?
Is chondrocyte
Can joint
proliferation
instability
Sure be
What happens to
It’s increased
increased or
present? What is the level
the
It’sjoint
decreased
space in
of stiffness
Low in the
What can happen
decreased?
an X-ray?
Subchondral cysts
morning?
below the
and/or sclerosis
cartilage?
What happens to
It’s
proteoglycan
decreased
concentration?
Osteoarthritis
Deep groin pain
Radiographic
How
can hip OA
Typically, should
What’s the
radiating into
evidence appears
present?
the pain be
problem
with this?
medial thigh
Yes
late in the disease
recreated with
How
MTPdoes
joints
diabetic
with
What is the gold
passive motion?
neuropathy
excessive
standard
Radiograph
for
usually
destruction
present
seen
on
diagnosis?
inX-ray?
X-ray Is OA associated
Previous trauma,
with
Short-term
short- or
NM
What
disease
are three
(e.g.
long-term
stiffness (<1
stiffness
hr)
secondary
diabetes),
causes
How good are ESR
Which five joints (>What
Pain
or < 1are
relief,
hour)?
the
metabolic
of OA? MCP,
wrist, elbow,
and
Not CRP
useful
as disorders are typically
not exercise
three main
regiment,
points
ankle,
or
shoulder
markers for OA?
involved?
patient
of treatment?
education
Osteoarthritis Risk Factors
•
•
•
•
•
•
•
H ereditary
A ge
Metabolic disorders
S ex (female)
N euromuscular disease
O besity
T rauma
Osteoarthritis – Joints Involved
Neck
Hip
Spine
PIP, DIP,
CMC
Knee
1st MTP
Spondyloarthropathies
Which parts of the
Can it be
Vertebrae &
Yup
1.is Ankylosing spondylitis
body
are generally
What
are
the
5
peripheral too? If it’s peripheral,
Usually 2. Reactive arthritis sacroiliac joints
affected?
it symmetric or3. IBD-associated
arthritis
spondyloasymmetric
4.
Psoriatic arthritis
What
age
group
is
asymmetric?
5. arthropathies?
Undifferentiated
No,
Is nor
HLA-B27
does it
Genetically, what
generally
Younger
rulescreening
in or rule out
HLA-B27
Is
it
genetic
or
is the main cause?
affected?
recommended?
a disease
environmentally
Both
ANA+
Negative
or ANA-?
determined?
Are these
Inflammatory or
conditions more
WhatInflammatory
doesnonMales
What is common
the main
in males
Probably
a
inflammatory?
spondylosis
The
vertebrae
refer
What
does
RF+
Negative
or RF-?
environmental
Fusion/crooked
or females?
bacterial infection
to?
ankylosis mean?
cause?
Ankylosing Spondylitis
Are big joints or
“Ankylosing spondylitis”
small joints
isDid
Catherine
Crawford’s
you know…?
affected
Big joints
more
Age?
<40
favorite medical term?
When is the pain
often
At night
Which
Vertebrae
joints&are the
worst?
peripherally?
Movement,
affected?
sacroiliac
NSAIDs,
What’s
Anti-TNF,
the
What test is used
osteoporosis
treatment?
toSchober’s
monitor spinal
test
prophylaxis
mobility?
Is the pain better
Acute or
More men or
Progressive
or worse
Worsewith
Men
progressive onset?
women?
rest?
Extraarticular AS
•
•
•
•
•
•
•
•
A ortic insufficiency
N eurological symptoms
K idneys: amyloidosis
S pinal fracture, stenosis
P ulmonary fibrosis
O cular: anterior uveitis
N ephropathy (IgA)
D iscitis
Reactive Arthritis
Symmetrical or
Asymmetric
asymmetric?
When are women
Approximately
likely to get
WhatEnteric
two types
or ofmost
overreactive
per month
1-3When
weeksdoes
afterit an
infection
urogenital
usually once
arthritis? infection
appear?
(chlamydia)
cause RA?
NSAIDs – it’s
Treatment?
usually self-limited
Conjunctivitis,
arthritis,
Triad?
non-GC
urethritis
Mono-, oligo-, or
Oligoarticular
polyarticular?
What type of
bacteria is usually
None; it’s sterile
found in the
synovial fluid?
How can RA be
differentiated
AS is bilateral
from SA in
sacroiliac arthritis?
Psoriatic Arthritis
Inflammatory or
Inflammatory
noninflammatory?
Erosive bone
What can be seen
disease in DIP
radiographically?
joints
What is the severe
Arthritis mutilans
form of PA called?
Chronic
Chronic
or acute?
Which comes first
– skin
Skindisease
diseaseor
joint disease?
What
Theage
under-50
group is
affected?
crew
Anti-TNF
Treatment?
agents
IBD-Associated Arthritis
What
Erythema
about from
nodosum
Crohn’s?
How do you treat
Steroids
those?
Which causes
deformity – the
Axial form (fusion
peripheral or axial
& disability)
form of the
disease?
can show on
What’s
Treat
the
the
main What
Pyoderma
the skin from
underlying
treatment?
disease
gangrenosum
ulcerative colitis?
Should X-rays be
No – they areBilateral sciatica, saddle
Watchful
How is mechanical
waiting +
used for anesthesia,
Onlybowel/bladder
1 out of 2500
more often I incontinence
don’t believe you Cauda EquinaLBP
treated?
mechanical back patients under When is acute LBPexercise
misleading
– give
me
a to muscles,
syndrome,
Does
carryvariable
a 60yo
Injury
What
does
painhas
pattern,
pain?itBruits,
an
a medical
statistic
abdominal
mass
abdominal
aortic
Good
goodprognosis
or poor
“mechanical”
ligaments,
refer
unexpected
X-ray bones,
emergency (3
aneurysm,
prognosis?
disks
to? conditions)?
neurologic deficit
Yes! Those who
Fifth-most
Should
remain
activity
activebe
How common a
common reason
despite
advised
acute
during
pain
complaint is it?
for how
an office
visit
How long until
For
long
acute
have pain
less future
phase?
90% resolve
most cases have
2-3
should
days rest
at most
be
chronic pain
within 8 weeks
resolved?
advised?
Which type of
exercises should
How much acute
What’s the main
Mechanical
be performed
Both
back
–
pain
<5% turns
type of LBP?
strength or
chronic?
endurance?
Lower Back Pain
Low Back Pain – Red Flags
What am I?
Low back
Lowpain
back
pain
• Fever, weight loss
• Intractable pain—no improvement in 4 to 6
weeks
• Nocturnal pain or increasing pain severity
• Morning back stiffness with pain onset before
age 40
• Neurologic deficits
What is the main
What is the main
Resuming activity
presenting
goal for acute
Sudden back pain.
What
Pain
at
are
night,
the
main
local
as soon as
symptom of an
compression
Duh.
symptoms
tenderness,
of
a
possible
acute compression
fractures?
elevated
spinalESR,Hormone
Epidural
LegWhat
pain/tingling
is thefracture?
How is it
weight lossreplacement
What’s
the severe
corticosteroids, malignancy?
with
presentation
less
of or
a
managed?
therapy,
treatment
thiazides,
of pain
exercise, surgery Non-improving
herniated
no
back
disk?
osteoporosis?
Ca/Vit D, Fever, rigors, focal
What are the
pain, increasing
bisphosphonates
Surgery tends to
What
tenderness
are thewith
main
symptoms
of
Why not do
lower neurological
have no better
muscle
symptoms
spasm;
of
spinal
stenosis?
surgery?
symptoms
pain reliefAnd don’t forget
spinal
needle
infections?
tracks
Yeah!
the exercise!
present
What labs should
How
is a herniated
When is surgery
What
surgical
Symptomatic What
Neurologicbe
deficits
Mildcan
anemia,
be seen
taken for the
disk treated?
indicated?
option exists
for
Vertebroplasty
in
elevated
the labsESR
of
initial
Hb,evaluation
ESR, Ca
compression
spinal
and/or
infections?
CRP
of osteoporosis
fractures?
(3)?
Back pain
Low Back Pain
Tolerance,
What are the four
Ignorance,
consequences of
Activation-death,
Ag encounter with
Activationlymphocytes?
proliferation
What’s
Defectsthe
in
Immunology apoptosis
relationship
may
between
lead to
autoimmunity
autoimmuneand
The
What
periphery
about B&
apoptosis?
conditions
What
type
of
bonecells?
marrow
They
How encounter
do B cells
autoimmune
Repetitive
becomehigh
anergic in
condition
ITPinvolvesWhat
stimulation,
is AICD?
concentrations
the peripheralof
platelets as acausing apoptosis
lymphoid
antigens
tissue?
target?
Where does
“anergy”
Tolerance
fall into What two general
What two types of
those
four?
Co-stimulator
are
What
type of Ag +signals
cells are largely
Where
The periphery
does T-cell
& autoimmune (e.g.
required
B7/CD28)
for Treg and Tsuppressor
anemia
responsible for
tolerance
the thymus
occur? Hemolytic
activation?
condition involves
cells
peripheral T-cell
RBC’s as a target?
tolerance?
Immunopathogenic Mechanisms
Condition
Immunological disease type
SLE
II, III, IV
ITP
II
Hemolytic anemia
II
RA
III & IV
Type I Diabetes Mellitus
IV
Cryoglobulinemia
III
Goodpasture’s
II
Explain
SLE’s
type
•Malar
rash
Anti-snRNP T cells
IV •Discoid
involvement
rash
SLE
Which immune
mechanisms (type
II, III, & IV
I-IV) are involved
in SLE?
•Photosensitivity
•Oral ulcers
Azathioprine,
Four symptoms
What are•Arthritis
the main
methotrexate,
•Serositis
from
Howthe
is SLE
SLE
drugs used
in the
cyclo•Renal disorder
Classification
diagnosed?
What’s
Overall
the
treatment?
What test isdisorder
phosphamide
•Neurologic
Criteria
Nothing
like that suppression
general
focus
of
the
of
pathognomonic
•Hematologic
disorder
exists
treatment
disease
for SLE?
for
SLE?
•Immunologic disorder
What are the main
•ANA
Explain SLE’s type
Arthralgia
two initial
(53%),
Explain SLE’s type
IC nephritis
Anti-RBC
III involvement
presentations
Rash (19%) of
II involvement
SLE?
Rheumatoid Arthritis
They’re the
minority of
Inflammatory or
What are type B Prevalence
0.5-1% of in
the
the
synoviocytes &
Inflammatory
nonsynoviocytes?
population
US?
can
damage
the
inflammatory?
joint
1:3 (more
M:F?
women)
What are the main
RA patients are at
concerns for RA
a higher risk to
Increased risk of
Lymphoma
patients with
contract which
stroke & MI
respect to sudden
type of cancer?
death?
Mono-, oligo-, or
Polyarticular
polyarticular?
Local orBoth
systemic?
Age 25-50
of onset?
Rheumatoid Arthritis
What are the
Cervical
Does RA cause
Swan-neck,
How can the spine
three main hand
subluxation
(C1
on
Which
two
general
bone
Erosion
erosion
or
Boutonniere,
MCP
be
affected?
Where do
deformities from
C2)
Joint
radiographic
narrowing,
formation?
subuxation
rheumatoid
HLA-DR4
(which
RA?
Olecranon
process
findings
erosion
are most
Which
HLA
nodules
usually
stands
for type
HLA-is
Serpositive RA
prominent in RA?
associated
with
appear?
Develops
with
What’s
splenomegaly
Felty’s Is there a
RA?
Rheumatoid 4)*
necrotic
correlation Central
&
*Not syndrome?
really
What is in a
zone
with sharp
between
YupRA titer rheumatoid
granulocytopenia
border of
and disease
nodule?
What
are
the
What’s
the
most
With
which
palisading
cells
Is exercise good
severity?DMARDs,
NSAIDS,
Of course
main pharm
important aspect
treatment isthree
early
for
RA? stiffness
Morning
Stiffness
– a little
biologics (antiEarly intervention
Any of them
treatments
of successful
>or1ahour
lot? intervention most TNF) for
RA? treatment of RA?
effective?
RA – Extraarticular Manifestions
• P ulmonary
• H ematologic
• Ocular
• N eurologic
• V asculitis
Interstitial fibrosis,
pulmonary nodules,
pleuritis
Anemia, thrombocytosis
Scleritis, episcleritis
Entrapment syndromes,
peripheral nephropathy
Subcu nodules,
leukocytoclastic vasculitis
Psoriatic Arthritis
What’s the
relationship
Does PsA affect
How
3-5%
common
of the is
between
No relationship
PsA and
men or
M=F
women
population
psoriasis?
the severity of the
more?
What other
psoriasis?
component
Tendonsof
– the
What is the worst
Pencil-in-cup
What does the
joint
What are the
Arthritis mutilans
>
joint
enthesitis
can be How many ofcase of PsA?Using handsradiology
show?
three main erosions
5-39%
have
Standing >
inflamed? those
activities affected
psoriatic
arthritis?
Sleeping
What type of
byoccurs
PsA? first
Which
edematous NSAIDs, Symmetric or – arthritis
Dactylitis What is the
A- Usually structural
Age 30-50
of onset?
pattern occurs
in
asymmetric?
corticosteroids,
symptoms or
treatment?
damage
the fingers?
DMARDs, Biologics
structural
damage?
Psoriatic Arthritis – 5 subgroups
•
•
•
•
•
Spondylitis
Polyarticular, symmetric
Oligoarticular, asymmetric
Mutilans
DIP synovitis
Vasculitis
Disease?
Disease?
Disease?
Disease?
Intima, internal
elastic lamina,
media, adventitia
Aorta +
major
branches
“Medium?”
“Large?”
Which half of the
Blindness,
body
The is
lower
most
What are the main
headache, jaw
extremities
affected by
complications of
How is temporal
pain, neurological
vasculitis?
temporal arteritis?
Possibly because arteritis
Biopsy
disturbances Why
do differenteach size has a diagnosed?
sized vessels have
Due to the skipdifferent antigen
What is the
What is a common
different diseases?
Mostly unknown
lesion nature,
concentration
a
causative agent?
mistake made in
single biopsy may
temporal arteritis
result in a false
biopsy? The
temporal
is affected
and
negative What
What age group is
by
ophthalmic
giant cell
Middle-age and
usually
affected by
arteritis?
arteries
What
size
of
elderly
Systemic, with
What lab test is
temporal arteritis?
Are vasculites
vessels
does
localized
useful
ESR >in50
the
Smaller
systemic or
rheumatoid
symptoms (e.g.
diagnosis?
localized?
arthritis affect?
ischemia)
Vasculitis
Polyarthralgia Rheumatica
Pain/stiffness in
What are the main
neck, shoulder, &
clinical symptoms?
pelvic girdles
When is the
After rest (it’s hard
stiffness usually
to get out of bed)
the worst?
Are the peripheral
Usually
symptoms
bilateral
and
symmetric
symmetric
or
asymmetric?
What disease can
Temporal arteritis
be associated with
(GCA)
PR?
Fibromyalgia
What is the cause
Unknown
of fibromyalgia?
What 30-50
age group?
Is the onset slow
It can be either
or fast?
Which lab test
Are symptoms helpsNone
diagnose
constant
Varyingor
fibromyalgia?
varying? FMWhat
patients
is the
have
anrelationship
abnormalitytoin
deep
sleep?
sleep
What kind of pain
Diffuse, amplified
is felt?
Which organbased disease
IBD
is it
associated with?
How 5%
many
of all
people
Chronic,
does
Americans
it affect?
widespread
What are pain
the +
cardinal
tender points
features?
on
exam
Joint surgeries
Which result in
What is the gold
more
Who
should
get
a
Cemented
total
Cemented
Who
is
more
likely
Younger,
more
standard in hip
radiolucencies
–nerve is noncemented hip
What
hip–prosthesis
How
Debridement,
do
you
treat
to
get
Younger;
osteolysis
it’s
active
prostheses?
cemented
or
non?
replacement?
The
mostsciatic
commonly
nerve
a drainage,
superficial
related
youngertoor
activity
older
What
are the
DM,
affected?
antibiotics
infection?
patients?
three main risk
Immunosuppressi
What causes the
factors for
on,
prior surgery
Soft-tissue
majoritylaxity
of
infection?
What
treatments
Are
they
likely
to
Two-stage
type of
dislocations?
Antigoagulation, Most do not recur Which
are suggested
recur?
reconstruction
antibiotics
post-op?
(92%
works
success)
best?
What’s the main
Observation,
What’s the main
How
do you
treat
bacteria
Staph. aureus
involved
The
What
is the
it’sradiolucency
Are they usually
problem
Osteolysis
with non-unless
that?
in infection?
outcome
of the cement,
defined
progressing
anterior
Posterior
or
cemented?
post-op
by?
posterior?
Bursitis & Tendonitis
The abductor Which part of the
What is affected hand is involved in
pollicis
longus and The palmar fascia
Obstruction at A1
with de Quervain’s Dupuytren’s
pulley
What in
is involved
proximal extensor pollicis
tenosynovitis?
Contracture?
brevis tendons
in
portion
triggeroffinger?
flexor
Where
tendon
do sheath
most
ganglion
Dorsal wrist
cysts
What test helps
occur?
Finkelstein’s test
diagnose this?
What can be a
A compressive
complication of a
neuropathy
Inflammation of
Which age group
ganglion cyst?
Is proliferative Which sheathisisaffected with
theWhat
synovium
is
Many
Older males
Chronic
tenosynovitis?
surrounding a tenosynovitis
affected? Dupuytren’s
tendon chronic or acute?
Contracture?
What is the main
Leg
cause
length
of a
trochanteric
discrepancy
bursitis?
Which fingers are
Bursitis & Tendonitis
What is affected
with
The median
carpal tunnel
nerve
Manual pressure
McMurthry’s sign?
syndrome?
innervated
The first by
3 ½the
of median nerve
Which three
Are the symptoms median nerve?
They’re worse at
rheumatoid
or better
Scleroderma, RA, worsenight
conditions can
during the day?
and gout
lead to olecranon
What are the main
Which muscleWhat
is does Cubital
bursitis?
The extensor carpi
tunnel
Ulnarsyndrome
nerve
Swelling
clinicaland
affected by lateral
radialis brevis
affect?
presentations
numbness of
What test epicondylitis?
involves
How
can you
carpal tunnel?
percussion
at
the
Flexion of the
What about
Point tenderness What’s
Phalen’s
Pronator teres or
differentiate
it
Tinel’s
wrist
that
signtrochanterichands at the wrist
medial
in the
test?
flexor carpi radialis recreates the
from
for one minute
epicondylitis?
bursa
osteoarthritis?
paresthesia?