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CMT > Rheum Pathophys > Flashcards

Rheum Pathophys Flashcards

1
Q

General

underlying pathophys of autoimmune diseases

A

the body’s immune system (T cells) attacks healthy cells (myelin) ; cannot distinguish between healthy and unhealthy cells; leads to an inflammatory state

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2
Q

General

risk factors for autoimmune disease

A
  • environmental (smoking, diet, stress, pollution, infection)
  • genetic
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3
Q

SLE

RASHNIA4

A
  • R: renal disease (proteinuria)
  • A: arthralgias
  • S: serositis (pleuritis, pericarditis)
  • H: heme disorders (anemia, thrombocytopenia)
  • N: neuro disorder (seizure, psychosis)
  • I: immunologic abnormalities
  • A: ANA pos
  • 4: types of malar rashes (butterful, discoid (chronic, scarring), photosensitivity, oral ulcers)

must meet 4/11 criteria above to have SLE

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4
Q

SLE

4 types of lupus

A
  • Systemic: relapsing/remitting multi-systemic disease caused by autoantibodies to a variety of autoantigens
  • Discoid: chronic, scarring skin rash
  • Subacute Cutaneous: rxn to sunlight leading to rash that may last for several wks after brief sun exposure
  • Drug Induced: SLE like rxn but is reversible
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5
Q

Lupus

risk factors for drug induced lupus

DIL CHIPPS

A
  • Carbamazepine
  • Hydralazine
  • Isoniazid
  • Procainamide
  • Penicillamine
  • Sulfasalazine
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6
Q

SLE

Autoantibodies in SLE + frequency of pos result

A
  • ANA: >95%
  • Anti-ds DNA: 55%
  • Anti-Ro/SSA: 30%
  • Anti-U1-RNP: 35%
  • Anti-Smith: 30%
  • Anti-La/SSB: 20%
  • Anti-ribosomal P: 15%
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7
Q

SLE

purpose of different autoantibodies in SLE

A
  • ANA: Useful as an initial screening test; assesses multiple antigens simultaneously
  • Anti-ds DNA: Found in more severe disease, especially kidney disease; antibody levels commonly follow disease activity and are useful to monitor (specific to lupus)
  • Anti-Ro/SSA: Associated with photosensitive rashes, DLE, and neonatal LE; also common when secondary Sjogren syndrome is present; decreased risk of nephritis
  • Anti-U1-RNP:Associated with RP and esophageal dysmotility; also seen in MCTD
  • Anti-Smith: Specific for SLE; often associated with more severe disease
  • Anti-La/SSB: Common in Sjogren syndrome; less common in SLE and neonatal LE
  • Anti-ribosomal P: Can be associated with CNS lupus and lupus hepatitis
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8
Q

SLE

what screening do they need if on hydroxychloroquine?

A

annual eye exams

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9
Q

SLE

components of monitoring lupus

A
  • pregnancy counseling
  • Labs: CBC, UA, BMP, ESR (+/- antibodies), Q6 months
  • screen for hyperlipidema, DM, osteoporosis if on steroids
  • UTD vaccines
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10
Q

Rheumatoid Arthritis

is pt is on biologic what do you need to screen for?

A
  • HBV/HCV
  • TB
  • HIV
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11
Q

Rheumatoid Arthritis

American College of Rheumatology criteria

A
  • morning stiffness of > 1 hr for 6 wks
  • arthritis and soft tissue swelling of > 3 joints for 6 wks
  • arthritis of hand joints for 6 wks
  • symmetric arthritis for 6 wks
  • subQ nodules
  • rheumatoid factor level >95th percentile
  • radiologic changes of joint erosion

have at least 4 to meet criteria

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12
Q

Rheumatoid Arthritis

surgical options for RA

A
  • synovectomy: removes part/all of synovium; provides pain relief only
  • total joint: last step if tx fails
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13
Q

Gout

hyperuricemia overview

A
  • levels of plasma urate > 6.8 mg/dL
  • increased intake, overproduction, and/or unerexcretion of uric acid
  • majority of people w/ hyperuricemia do not have gout, but people with gout have hyperuricemia
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14
Q

Gout

Hyperuricemia- increased intake

A
  • consumption of purine rich foods/drinks
  • Red meat, liver, tuna, scallops, mussels, shrimp, asparagus, mushrooms, carbonated beverages, BEER
  • strict low-purine diet can reduce levels by ~1mg/dL
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15
Q

Gout

hyperuricemia causes of overproduction

A
  • hereditary
  • EtOH
  • heme conditions
  • conditions w/ increased cellular proliferation
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16
Q

Gout

hyperuricemia- causes of underexcretion

A
  • most common cause of hyperuricemia
  • uric acid normally excreted by the kidneys
  • reduced renal excretion: hereditary, diuretics, ASA, high dose cyclosporine, reduced GFR
17
Q

Gout

clinical course

A
  • Flare
  • Intercritical Period (asx, variable duration)
  • Subsequent Flares (become more painful, frequent, and longer)
  • Chronic Gout
18
Q

Gout

what is podagra?

A

gouty attack at the 1st MTP joint

19
Q

Gout

what actually causes pain w/ gout?

A

result of cytokines released from WBCs that enter the joint to remove uric acid

20
Q

Gout

describe use of colchicine

A
  • inhibits WBC migration
  • most effective if given within 12-24 hrs of acute flare
  • contraindicated in severe renal/liver disease
21
Q

Gout

what should be r/o before giving glucocorticoids?

A

septic arthritis

22
Q

Gout

indications for urate-lowering therapies

5

A
  1. tophaceous deposits
  2. > 2 flares annually or disabling flares
  3. urolithiasis
  4. infrequent flares, but levels >9 mg/dL
  5. multiple comorbidities that are contraindications to NSAIDs/corticosteroids

Target level is < 6 mg/dL

23
Q

Gout

urate lowering therapies

A
  • allopurinol
  • febuxostat
  • probenecid
24
Q

Gout

MOA/info on Allopurinol and Febuxostat

A
  • Class: xanthine oxidase inhibitor
  • MOA: inhibits xanthine oxidase which is an enzyme in the purine catabolism pathway
  • Allopurinol: GI discomfort, rash
  • Febuxostat: frequently triggers gout flare, give concurrently with NSAIDs or Colchicine
25
Q

Gout

MOA and info on probenecid

A
  • Class: uricosuric
  • MOA: works by inhibiting active transport sites of hte proximal tubules leading to blocked reuptake of uric acid and increased secretion
  • can trigger acute flares, given concurrently w/ NSAIDs or colchicine
26
Q

GCA

criteria for clinical dx?

A

pt > 50 yrs w:
* new type of HA
* new s/sx compatible w/ ischemia of artery above neck
* jaw muscle pain during chewing
* temporal artery tenderness
* unexplained subacute fever

27
Q

Sjogren Syndrome

primary vs secondary

A
  • Primary: unk etiology, HLA genes, viral connections
  • Secondary: presents in association w/ another autoimmune condition
28
Q

Sjogren Syndrome

pathophys

A
  • EXACT MECHANISM UNKNOWN
  • environmental trigger/genetic predisposition
  • salivary/lacrimal/exocrine glands infiltrated w/ CD4+ T cells and B cells
  • T cells produced inflammatory cytokines (IL-2, interferon gamma)
  • Interferons stimulate B cell activating factor (BAFF) leading to irregular B cell maturation and release of Anti-SSA and Anti-SSB
  • cytokines and autoantibodies cause damage and atrophy of the glandular and ductal epithelium leading to reduced exocrine production
29
Q

Sjogren Syndrome

diagnostic criteria

A

requires 4 of 6 below:
* ocular sx (dry eyes > 3 mo, FB sensation, artificial tear use >3x daily)
* oral sx (dry mouth > 3 mo, swollen salivary glands, dysphagia)
* ocular signs (pos schirmer’s test or dye staining on eye surface)
* oral signs (pos sialography or scintigraphy)
* pos bx
* pos anti-Ro and/or anti-La

(just 1 from each individual category)

30
Q

Psoriatic Arthritis

define:
* enthesitis
* tenosynovitis
* dactylitis
* arthritis multilans

A
  • Enthesitis: inflammation at site of tendon insertion
  • Tenosynovitis: inflammation of fluid filled sheath surrounding a tendon
  • Dactylitis: sausage digits
  • Arthritis Mutilans: severe form that causes destruction of multiple hand joints w/ telescoping
31
Q

Ankylosing Spondylitis

Special Tests PE

A
  • Schober’s Test: reduced lumbar ROM
  • Mennell’s Sign: 3 phase hyperextension test used to differentiate when problem is w/ lumbar spine, SI joint, hip joint (place pressure in different areas which extending leg)
  • Patrick Test: Flexion, ABduction, External Rotation (FABER) making number 4; test is positive if pain in ipsilateral SI joint w/ pressure on abducation
32
Q

Systemic Sclerosis

three classifications of systemic sclerosis

A
  • limited systemic sclerosis (CREST)
  • Generalized systemic sclerosis (w/ diffuse skin involvement)
  • Systemic sclerosis sine scleroderma
33
Q

Systemic Sclerosis

describe limited systemic sclerosis (CREST syndrome)

A
  • Calcinosis cutis
  • Raynaud’s phenomunon
  • Esophageal dysmotility
  • Sclerodactyly (tight over digits)
  • Telangiectasis

Characterized by slow progression, complicated by pulm HTN

34
Q

Systemic Sclerosis

describe generalized systemic sclerosis w/ skin involvement

A
  • Raynaud phenomenon + GI complications
  • evolves rapidly
  • interstitial lung disease + scleroderma renal cirsis are major complications
35
Q

Systemic Sclerosis

describe systemic sclerosis sine scleroderma

A
  • systemic sclerosis related antibodies and visceral manifestations of the disease WITHOUT ANY SKIN MANIFESTATIONS

CMT (72 decks)

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