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Musculoskeletal and Skin > Rhematologic Disorders of MSK > Flashcards

Rhematologic Disorders of MSK Flashcards

1
Q

What is a rheumatologist disorder? Basic concepts.

A

Rheumatology is the study of inflammatory disorders of the connecAve Assues • ConnecAve Assue – Skin, tendons, ligaments, bones, blood vessels, muscle, joints • Over 140 disorders • Most common presentaAons include disorders of the musculoskeletal system

Joints/bones: Arthralgia, ArthriAs

– Tendons, ligaments: TendoniAs/bursiAs

– Muscle: Myalgia, MyosiAs

Systemic problem

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2
Q

what comprises the MSK system?

A

.

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3
Q

RA definition

A

Definition – symmetric inflammatory peripheral

polyarthriAs characterized by destrucAon of joints

through erosion of carAlage and bone.

• Most common inflammatory arthriAs

– 1% of the populaAon

– 2:1 female to male raAo

– Peak incidence between ages 40 to 60

• Onset usually insidious over months.

Cause is not known

– Complex interacAon between genes and

environment

– Breakdown of immune tolerance and synovial

inflammaAon

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4
Q

How is rheumatoid arthritis treated?

A

Early treatment with a disease modifying drug is

standard of care

• Non-disease modifying

– NSAIDs

– Prednisone

• Disease modifying

– Methotrexate

– Hydroxychloroquine

– Sulfasalazine, leflunomide

– Biological agents: TNF-alpha blockers, abatacept, rituximab,

and tocilizumab.

Goal of treatment is clinical remission if possible

• Control of disease prevents bone erosions and

subsequent deformity and loss of funcAon

• All disease modifying drugs are

immunosuppressive and have side effects

• Joint arthroplasty for end-stage disease

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5
Q

Spondylarthropathies

A

Ankylosing SpondyliAs

  • PsoriaAc ArthriAs
  • Enteropathic ArthriAs and ReacAve ArthriAs
  • UndifferenAated.
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6
Q

How is spondyloarthropathy treated?

A

.

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7
Q

How does crystalline arthropathy present?

A

.

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8
Q

how is crystalline arthropathy treated?

A

.

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9
Q

how to myositis treated?

A

.

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10
Q

How does myositis present?

A

.

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11
Q

How does relapsing polychondritis/PMR/CTD present.

A

.

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12
Q

How is relapsing polycrodritis/PRM/CTD treated

A
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13
Q

Case 1: 60 y/o woman presents for the first time with sudden onset of severe bilateral shoulder pain with difficulty moving her arm. She also complains of bilateral hip pain and sever stiffness. so stiff she cannot get out of bed w/o assistance. Fatigue, tiredness, overall not well. Controlled long term diabetes.

A

Systemic- shoulders and hips, overall fatigue

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14
Q

Case 2: 55 y/o M c/o sever r knee pain. Getting bilateral knee pain intermittently for past 5 yers. stiffness in the morning. lately right knee pain is worse. pain up and down stairs. smoker. hx of HTN.

Systemic or not systemic

A

non systemic

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15
Q

Case 3: 38 y/o F, stiff all over body, thought it was b/c of exercise but hands are especially stiff. takes 1.5 hours before they feel better. swelling in a few of her joints. relatively tired, hard to concentrate and type.

Systemic or not systemic

A

systemic
DD: RA

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16
Q

osteoarthritis most commonly in the …

inflammatory or not inflammatory?

A

Knees

also in hips

non-inflammatory

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16
Q

osteoarthritis most commonly in the …

inflammatory or not inflammatory?

What joints of the hands?

A

Knees

also in hips

non-inflammatory

PIP and first CMC joint

x-ray features: join stays

extra bones - burst

suchondral sclerosis

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17
Q

Osteoarthritis.

A

OA is a progressive disease represenAng the failed

repair of joint damage that, in the preponderance of

cases, has been triggered by abnormal intra-arAcular

stress.

• All of the Assues of the joint are involved, including

the arAcular carAlage, subchondral bone, ligaments,

menisci (when present), periarAcular muscles and

peripheral nerves.

• OA may be iniAated by an abnormality in any of

these Assues. Thus, OA is not a disease merely of

carAlage but is a failure of the synovial joint.

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18
Q

Osteoarthritis findings (epi)

A

Most common type of arthriAs

– OA of the knee, hand, or hip have a similar prevalence of

~20-30% of adults

– More than half of individuals over age 55 have

radiographic evidence, goes up to 90% at age 70

– Slight female predominance in older age, but both sexes

affected

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19
Q

OsteoarthriAs: Classification

A

Idiopathic

– Localized

– Generalized (3 or more sites)

• Secondary

– Trauma, congenital, crystalline arthropathy,

osteonecrosis, inflammatory arthriAs, sepAc

arthriAs, Paget’s disease, Diabetes, Charcot/

neuropathic arthropathy, hypothyroidism,

acromegaly, frostbite

Damage to normal arAcular carAlage by physical forces

(can be single events of macrotrauma or repeated

microtrauma)

– Chondrocytes react to this injury by releasing degradaAve

enzymes

– inadequate repair responses

• Fundamentally defecAve carAlage fails under normal

joint loading, thereby leading to osteoarthriAs.

– type II collagen gene defect

– ochronoAc carAlage that fails because of deleterious

pigment deposiAon

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20
Q

Osteoarthritis: diagnosis

A

History is important – gradual onset of symptoms,

lack of inflammaAon, someAmes history of prior

injury or overuse or other secondary trigger

• Physical exam – crepitance, hypertrophic changes,

lack of erythema or warmth, usually not much

tenderness

• X-ray will confirm diagnosis – asymmetric joint space

narrowing, sclerosis near the joint line, and spurring

are characterisAc

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21
Q

Osteoarthritis nodes - hands

A

Heberden’s nodes - DIP joint bony nodules

  • Bouchard’s nodes - PIP joint bony nodules
  • Both “nodes” are diagnosAc for hand OA

– 10 Ames more common in women than men,

and have a strong geneAc component

Base of thumb :1st CMC

joint

– Very commonly affected

• Treatment

– NSAIDs or Tylenol

– CorAcosteroid injecAons

parAcularly for base of

thumb

– Rarely ever surgery

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22
Q

Genetic factors for RA

A

GeneAc factors clearly important

– HLA “shared epitope” is strongest risk factor

– Non-HLA genes such as PTPN22, STAT4, TNFAIP3

• Environmental factors

– Cigareoe smoking increases both risk of disease

and severity of disease

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23
Q

RA Diagnosis

A

Symmetric pain and swelling in small joints of

hands, wrists, feet, ankles most common,

followed by knees, elbows, shoulders

– Morning sAffness – beoer with acAvity

– ConsAtuAonal symptoms – faAgue, even

weight loss are common, but fever is VERY

RARE

– Steady, progressive, addiAve onset is most

common presentaAon

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24
Q

Rheumatoid ArthriAs

Extra-arAcular features

A

Rheumatoid nodules

  • Pleural effusions
  • Atherosclerosis
  • ScleriAs
  • Rheumatoid vasculiAs (rare)
  • Felty’s syndrome (neutropenia,

splenomegaly, recurrent infecAon)

25
Q

RA presentation

A

High ESR or CRP common but not required

• Rheumatoid factor posiAve in about 50%

– RF usually indicates more severe disease, greater likelihood

of extra-arAcular manifestaAons

• AnA-CCP anAbodies

– Found in about 50% of paAents without much overlap with

rheumatoid factor

– Highly sensiAve – posiAve test almost always indicates

disease (>90% specificity for RA, even in mixed autoimmune

cohorts)

– So can “rule in”, but low sensiAvity prevents “rule out”

Classical findings of inflammatory arthriAs:

– PeriarAcular joint erosions

– PeriarAcular osteopenia

– Symmetric joint space narrowing

• Note that each of these is the opposite of OA!!

– Erosions instead of spurs

– Osteopenia instead of sclerosis

– Symmetric instead of asymmetric joint narrowing

26
Q

Spondyloarthropathy

DefiniAon and Prevalence

A

Group of inflammatory condiAons affecAng the

axial skeleton (spine, pelvis)

– May also demonstrate asymmetric oligoarthriAs and

enthesiAs (inflammaAon of tendon inserAons)

  • Prevalence about 1 per 1000 in US
  • Ankylosing spondyliAs is characterized by a 3:1

male to female raAo

27
Q

Spondylarthropathies

Paoerns of Disease

A

Inflammatory spinal involvement is typical

– differenAates from other arthriAdes

• EnthesiAs or inflammaAon of tendon

inserAons is classical

• Asymmetric oligoarthriAs is typical paoern of

peripheral joint arthriAs

28
Q

Extra-arAcular ManifestaAons- spondylar..

A

Eye involvement (uveiAs) is common

  • AorAAs with valvular insufficiency
  • Apical lung fibrosis
  • IgA nephropathy
  • Secondary Amyloidosis
29
Q

Ankylosing SpondyliAs

A

Symptoms are inflammatory back pain

• Can also affect hips and shoulders, rare to affect more

distal joints

  • HLA-B27 in 90% of European ancestry
  • Diagnosis – SacroiliiAs and anklyosis on X-ray
  • Treatment – NSAIDs for mild disease, TNF-blockers,

IL17A inhibitors, JAKi

30
Q
A

X-ray of sacroiliiAs

31
Q
A

Ankylosing spondyliAs: lumbar vertebrae,

bamboo spine

32
Q
A

PsoriaAc ArthriAs

ACR Image

33
Q

PsoriaAc ArthriAs

A

A subset of paAents with psoriasis (5-7%) have psoriaAc

arthriAs

– Inflammatory spine disease

– Peripheral arthriAs

• Diagnosis

– Underlying psoriasis

– X-rays show erosive joint disease with destrucAve changes

such as “pencil-in-cup”

• Treatment - Steroids may result in flare of skin disease

when tapered, methotrexate and sulfasalazine

common, TNF-blockers, IL17 inhibitors, Il12/23

inhibitors

34
Q

Enteropathic ArthriAs

A

SpondyloarthriAs associated with inflammatory

bowel disease

– Spine

– Peripheral joints: Type 1 and 2 arthriAs

– Therapy for IBD may work for arthriAs

– TNF alpha inhibitors, Il12/23 inhibitors

35
Q

ReacAve ArthriAs

•

A

Spondylarthropathy following GI or GU

infecAon

  • May have associated peripheral arthriAs
  • Onen self-limited

– Can either be recurrent or persistent

– Classic triad: uveiAs, arthriAs, urethriAs

36
Q
A

Reactive Arthritis

37
Q

Crystalline Arthropathies- types

A

Gout

• Calcium pyrophosphate deposiAon disease

38
Q

Gout

A

Gout is a heterogeneous group of diseases resulAng

from monosodium urate (MSU) crystal deposiAon in

Assues or from supersaturaAon of uric acid in

extracellular fluids

The metabolic disorder underlying gout is

hyperuricemia, defined as serum uric acid >2

SD above the mean

(> 7.0 mg/dL for men, > 6.0 for women)

• AsymptomaAc hyperuricemia in the absence

of gout is not a disease

39
Q

Clinical manifestations gout

A

Acute Gout

  1. Chronic tophaceous gout
  2. Uric acid calculi, nephrolithiasis
  3. IntersAAal nephropathy with renal funcAon

impairment, called gouty nephropathy

40
Q

Pathogenesis- gout

A

Uric acid is the normal end product of the

degradaAon of purine compounds:

5-Phosphoribosyl-1-pyrophosphate (PRPP) +

Glutamine to

5-Phosphoribosyl-1- amine

using PRPP synthetase

41
Q

salvage pathway -gout

A
42
Q

pathogenesis gout cont

A
43
Q

Pathoegensis -gout explanation

A

Limit of solubility of MSU in plasma is 6.7 mg/dL

(normal, 5.1 in men; 4.0 in women)

• In humans, hyperuricemia and gout is consequence

of species wide lack of uricase i.e. uric acid is end

product of purine metabolism, rather than allantoin

• Major route of uric acid disposal is renal excreAon

(2/3); bacterial oxidaAon in gut (1/3)

44
Q

Acute gouty arthriAs is triggered

A

Acute gouty arthriAs is triggered by the

supersaturaAon and precipitaAon of MSU crystals in

Assue i.e. joint

• Precise mechanism not known…

– Involves phagocytosis of crystals by neutrophils

– AccumulaAon of chemotacAc factors and cytokines (IL-1,

-6 and TNF), prostaglandins, leukotrienes and oxygen

radicals, acAvaAon of complement and lysosomal enzyme

release

• Why acute aoacks are self-limited also unclear.

45
Q

Clinical ManifestaDons - gout

A

AsymptomaAc hyperuricemia

• Acute gouty arthriAs

-early episodes monarAcular, abrupt onset,

occur at night or early morning

  • exquisite pain, erythema, swelling
  • periarAcular pain, gouty celluliAs
  • 1st MTP = podagra, instep, ankles, heels,

knees, wrists, fingers and elbows

-non-arAcular sites- olecranon bursa, Achilles

46
Q

Chronic tophaceous gout

A

Aner 10 or more years of acute gout

– IntercriAcal periods not pain free

– Persistent pain, swelling deformiAes

– Bony erosions and joint destrucAon

– May be confused with Rh. ArthriAs

47
Q

Diagnosis- gout

A

RecogniAon of Needle-shaped, NegaAvely

birefringent, moNosodium urate crystals present in

leukocytes or tophi

  • Use of compensated polarizing light microscopy
  • Crystals not always idenAfied, parAcularly if late in

aoack

• PresumpAve diagnosis made by signs and locaAon of

aoack, duraAon and presence of hyperuricemia

• N.B. Uric acid levels may be normal during aoackcheck

aner resoluAon of aoack

48
Q

gout microscopy

A
49
Q

Gout -diagnosis

A

Radiographic erosions typical of gout may be

suggesAve i.e. “rat bite”

• Synovial fluid is inflammatory i.e. 10-100,000

cells/mm3, but not specific

• Bacterial infecAons can co-exist with gout:

always send fluid for gram stain and culture

50
Q

Treatment- gout

A

AsymptomaAc Hyperuricemia

-Usually not treated

• Acute Gouty ArthriAs

– NSAID’s

– Intra-arAcular steroid for 1-2 joints

– Systemic steroids (prednisone over 10-14 days)

– Colchicine used classically, but a toxic drug

  • Must use early in the aoack
  • Very effecAve as a prophylacAc agent - 0.6mg bid

Chronic (tophaceous) Gout

– frequent aoacks > 2-3 aoacks/year

– chronic gouty arthriAs with erosions

• Xanthine oxidase inhibitors: Allopurinol,

Febuxostat

  • Uricase: PegloAcase (Krystexxa)
  • Colchicine
  • With compliance, and UA <6.0mg/dl, may

prevent aoacks, and tophi should resolve

51
Q

Calcium Pyrophosphate Dihydrate

DeposiDon Disease

A

Calcium salt (Ca2P2O2-2H20) deposited in

carAlage (chondrocalcinosis on radiograph)

• CPPD released into joint, causing acute painful

arthriAs, called pseudogout

• Chondrocalcinosis occurs most commonly in

wrists, knees and shoulders

• Most chondrocalcinosis is asymptomaAc

Acute arthriAs/ pseudogout/ pseudo-rheumatoid

arthriAs can occur without chondrocalcinosis

• Rhomboid-shaped, weakly PosiAvely birefringent

Pyrophosphate crystals

– must rule out sepAc arthriAs

• Hyperparathyroidism, hemochromatosis, familial

form and aging

• NSAID’s, intra-arAcular or systemic steroids,

colchicine (acutely or prophylacAcally)

52
Q

MYALGIA/MYOSITIS

A

Viral infecAons

  • DermatomyosisAs/PolymyosiAs
  • Polymyalgia rheumaAca
53
Q

Inflammatory MyosiAs

•

A

DermatomyosiAs (DM) and polymyosiAs (PM)

are idiopathic inflammatory myopathies

– Proximal skeletal muscle weakness

– Muscle inflammaAon

• Incidence: 2 per 100,000 annually in the general

populaAon

  • F:M raAo of 2:1
  • Peak incidence in adults occurs between the

ages of 40 and 50].

54
Q
A

DermatomyosiAs

Gooren’s Papules

55
Q

Inflammatory MyosiAs

•

A

Proximal muscle weakness

  • Cutaneous manifestaAons in dermatomyosiAs
  • Other manifestaAons:

– IntersAAal pulmonary disease, Dysphagia,

PolyarthriAs, Raynaud’s phenomenon

– May overlap with other systemic rheumaAc disease

• Treatment:

– GlucocorAcoids

– Steroid sparing therapy: Methotrexate/ Azathioprine

56
Q

Polymyalgia RheumaAca

A

Polymyalgia rheumaAca (PMR) is an

inflammatory rheumaAc condiAon characterized

by aching and morning sAffness in the shoulders,

hip girdle, and neck

• May be associated with giant cell (temporal)

arteriAs (GCA)

– The 2 disorders may represent different

manifestaAons of a shared disease process

  • Affects adults > 50 yrs
  • Prevalence increases with age

Cause is unknown

– Environmental and geneAc factors play a role

• Subacute or chronic onset of aching and

morning sAffness in the shoulders, hip girdles,

neck, and torso in paAents over the age of 50

  • The diagnosis is made clinically
  • PaAents will typically have an elevated ESR

>40mmHr

• Treatment: oral steroids

57
Q

Relapsing PolychondriAs

A

Systemic inflammatory disorder

– CarAlage involvement –nose, ear, costal, tracheal

– Eyes, cardiovascular, renal and nervous system

involvement

• GeneAc predisposiAon, exposure of carAlage

(immune privileged Assue)

• Rare disease, can occur in all ages, sexes etc

58
Q
A

Relapsing PolychondriAs

59
Q

Relapsing PolychondriAs- treatment

A

NSAIDS

  • Steroids
  • DMARDs – Methotrexate
  • Cyclophosphamide

Musculoskeletal and Skin (17 decks)

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