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Musculoskeletal and skin > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Mucin clot test

  • measures?
  • poor clot formation indicates?
A
  • joint viscosity

- increased inflammation due to DECREASED hyaluronic acid = joint lubricator

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2
Q

3 components of hyline cartilage matrix and fx

A
  1. Proteoglycans - elasticity and reducing friction
  2. Type II collagen - tensile strength
  3. Water - normal distention and friction reduction
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3
Q

2 types of synoviocytes

A

Type A
-phagocytic (macrophage like)

Type B

  • make hyaluronic acid (GAG)
  • make enzymes the degrade cartilage matrix
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4
Q

Pathogenesis of osteoarthritis has it’s origins in what?

A

Chondrocytes

-start releasing inflammatory mediators and proteases that lead to net degradation of cartilage matrix

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5
Q

List the steps of OA pathogenesis

A
  1. chondrocyte injury
  2. cloning
  3. release of inflammatory mediators and proteases
  4. Proteoglycan and collagen degraded -> matrix weakened
  5. fibrillation - superficial clefting + softening
  6. Cracking of matrix and breaking off of fragments
  7. Chondrocyte death
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6
Q

Define:

eburnation

subchondral cysts

Osteophytes

A
  1. smooth bone surfaces due to bone-bone grinding
  2. fluid entry into small fractures
  3. bony growths at margins of articulate surfaces
    - can compress nerves roots
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7
Q

OA more common in males or females?

A

EQUAL

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8
Q

RA - males or females?

A

females 3:1 males

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9
Q

What is rheumatoid factor?

Explain it’s role in RA pathogenesis

A

IgM Ab against Fc portion of IgG

  • Forms immune complex with IgG which leads to Type III hypersensitivity
  • C5a released which attracts inflammatory cells to the joint
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10
Q

Describe pannus formation.

How does it relate to ankylosis?

A

Mass of inflamed, abnormal synovium,
drapes over and causes degradation of cartilage surface

-Pannus may bridge joint surfaces which can lead to tight union = Ankylosis

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11
Q

Inflammatory mediators involved with RA have what pathogenic roles?

A
  1. Upregulate degradative enzymes

2. Activate osteoclasts

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12
Q

JIA - more common in females or males?

A

females 2:1

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13
Q

Define enthesitis

A

Inflammation of insertion sites of tendons and ligaments

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14
Q

List 4 seronegative spondyloarthrpoathies

A
  1. Ankylosing spondylitis
    - SI and intervertebral joints
  2. Reiter syndrome
    - arthritis, urethritis, conjunctivitis
  3. Psoriatic arthritis
  4. Arthritis associated w/ inflammatory bowel disease
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15
Q

Most gout patients have hyperuricemia as a result of

A

decreased excretion

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16
Q

How to tell the difference b/w gout and pseudogout

A

Gout

  • urate crystals
  • negatively birefringent -> yellow when parallel to slow ray

Pseudogout

  • calcium pyrophosphate crystals
  • positively birefringent -> blue when parallel to slow ray
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17
Q

Ganglion cyst

A

small cyst, can be at joint capsule, arises from degeneration of connective tissue there

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18
Q

Synovial cyst

A

from herniation of synovium through joint capsule (or enlargement of bursa
-example Baker Cyst of knee

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19
Q

Tenosynovial giant cell tumor

A

benign, treated by surgical excision

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20
Q

Where does synovial sarcoma arise?

A

in deeper parts of the muscle

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21
Q

Most common cause of inflammatory monoarthritis

A

GOUT

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22
Q

Temporal patterns in polyarthritis

A
  1. Migratory
    - Rheumatic fever
    - gonococcal
    - early phase of lyme disease
  2. Additive
    - RA
    - SLE
    - psoriasis
  3. Intermittent
    - gout
    - reactive arthritis
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23
Q

Tx for viral arthritis?

A

None; self resolving

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24
Q

Parvovirus B-19 associated with?

kids vs adults

classic presentation in adults
-joints involved?

A

5th disease - erythema infectiosum (EI)

kids - slapped cheek

adults - joints more involved

Acute onset symmetric polyarthralgia or
polyarthritis with stiffness in young women exposed to kids with E.I.

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25
Q

Compare the 2 serological tests for RA

A
  1. RF
  2. Anti-CCP
    - Autoantibodies to peptidic antigens containing the amino acid citrulline (generated by posttranslational deamination of arginyl residues)
    - highly specific for RA and present early in the course of the disease
    - marker of bone destructive process
26
Q

NSAIDS for RA

  • MoA
  • what can and can’t they do for patients?
  • side effects?
A

-COX-2 inhibitors

  • Not disease modifying drugs
  • symptomatic relief of joint pain and swelling
  • Do NOT prevent joint damage

-GI bleed is the most concerning risk

27
Q

When should DMARD tx be started? Why?

A

in most patients, erosive disease occurs w/in 2 years of the onset

start DMARDs ASAP

28
Q

Gold standard DMARD?

MoA?

how long does it take to work?

A

methotrexate

immunosuppressant - inhibits DHF reductase -> inhibits lymphocyte proliferation (folate antagonist)

3-8 weeks

29
Q

Leflunomide

  • brand
  • MoA
  • adverse effects
A

-Arava

  • pyrimidine synthesis inhibitor
  • has anti-proliferative and anti-inflammatory activity
  • > blocks T cell clonal expansion
  • highly teratogenic -> must be stopped 2 years before planned pregnancy
30
Q

TNF antagonists

A
  1. Monoclonal antibody
    - sequesters TNF from cells

DRUGS

  1. Inflixamab (Remicade)
  2. Adalimumab (Humira)
  3. Certolizumab
  4. Golimumab
  5. Soluble TNF receptor
    - competes w/ endogenous receptor

DRUGS

  1. Entanercept (enbrel)

Think: “intercepts” TNF before it can bind to real TNF receptor

31
Q

Tocilizumab

  • brand
  • MoA
A

Actemra

IL-6 inhibitor

32
Q

Rituximab

-MoA

A

B cell depleting monoclonal anti-CD20 Ab

33
Q

Abatacept

-brand
MoA

A
  • Orencia

- inhibits co-stimulation of T-cell (selective co-stimulation modulator)

34
Q

Dx of JIA requires:

A
  1. onset < 16 y.o.

2. Requires persistent, objective arthritis for min of 6 weeks

35
Q

JIA w/ highest mortality

A

Systemic JIA

36
Q

Systemic JIA

  • pathology
  • drugs
  • presentation
A
  • autoinflammatory NOT autoimmune
  • disease driven by IL-1 and IL-6

DRUGS

  1. tocilizumab (actemra) -> IL-6 inhibitor
  2. Canakinumab -> IL-1 inhibitor
Presentation 
-fever
-adenopathy
-rash
-arthralgia 
arthritis -> later on
37
Q

Polyarticular JIA

  • definition
  • disease driven by
  • Drugs
A

> 4 joints

Driven by TNF

DRUGS

  1. Methotrexate
  2. Etanercept
38
Q

Which JIA group is at highest risk for uveitis

A

Oligoarticular JIA

39
Q

Management of oligoarticular JIA

A

-intra-articular corticosteroid injection

40
Q

What catalyzes the final conversions to uric acid in the purine degradation pathway?

A

Xanthine oxidase

41
Q

Fx of uricase (uric acid oxidase)

A

Uric acid -> allantoin
-more soluble, readily excretable form

We don’t have this enzyme

42
Q

Most patients with gout have a problem with what?

A

They have issues with excreting uric acid i.e. UNDERSECRETION

43
Q

Which major class of CV drugs interfere with uric acid secretion?

A

Diuretics

44
Q

Drugs for managing acute gout?
Usage guidelines?
Side effects?
Contraindications?

A
  1. Colchicine
    - must be used w/in 8 - 12 hours of the gout attack to be effective
    - Diarrhea can be a major issue
    - Can’t used if patient is on dialysis
    - must be cautious if patient has renal or hepatic disease
  2. NSAIDS
    - most commonly used drug for gout
    - contraindications -> renal insufficiency, PUD, concurrent warfarin tx, liver disease
  3. Corticosteroids
    - fast acting
    - use when above 2 are contraindicated
45
Q

Urate lowering drugs

A
  1. Probenecid
    - 1st line for lowering SUA
    - acts on the proximal tubules to increase excretion of uric acid
    - can’t be used if patient has nephrolithiasis, renal insufficiency or if using salicylates
    - adverse effect -> hepatotoxicity
  2. Losartan (Cozaar, Hyzaar) - ACE inhibitor
  3. Fenofibrate (Tricor) - antihyperlipidemic agent
    - 2 birds w/ 1 stone using the above 2 drugs
46
Q

When should Allopurinol (Zyloprim) be used?
MoA?
Adverse effects?

A
  • If probenecid contraindicated -> pt. has kidney stones or renal impairment
  • patient is overproducer
  • xanthine oxidase inhibitor (precursors much more soluble than uric acid)
  • Hypersensitivity rxn can be fatal (1/4000)
47
Q

Febuxostat

  • MoA?
  • indications?
  • benefits over allopurinol?
A
  • non-purine xanthine oxidase inhibitor
  • use w/ renal insufficiency
  • don’t get the hypersensitivity rxn
48
Q

Pegloticase

  • MoA
  • indications
A
  • pegylated uric oxidase

- can be used in patients who fail standard tx

49
Q

How to differentiate b/w SK and Warts on histology?

A

Warts (verucca, condyloma)
Kilocytes with warts due to HPV infection
-Nuclear enlargement (two to three times normal size)
-Irregularity of the nuclear membrane contour
-A darker than normal staining pattern in the nucleus, known as Hyperchromasia
-A clear area around the nucleus, known as a perinuclear halo.

50
Q

The only premalignant epidermal neoplasm?
caused by?
risk for which carcinoma?
features?

A
  • Actinic keratosis
  • 2ndary to sunlight exposure
  • SCC

FEATURES
-early -> basal cells large hyperchromatic and pleomorphic
later -> parakeratotic (nuclei in stratum corneum)

51
Q

Most common type to skin cancer?

A

Basal cell carcinoma

-also most common carcinoma overall

52
Q

Nodular BCC found where in skin?

gross appearance?

A
  • dermis

- smooth red papule

53
Q

Progression of nevi?

Which direction do the melanocytes move?

A

junctional nevus -> compound nevus -> intradermal nevus

-move into the dermis

54
Q

What characteristics describe acute dermatitis?
subacute?
chronic?

A

acute -> spongiosis (edema) and exocytosis

subacute/chronic -> progress towards epidermal hyperplasia and hyperkeratosis; decrease in spongiosis

55
Q

Seborrheic dermatitis

  • occurs where?
  • stimulated by?
A

-areas of greatest sebum production (head, upper trunk)

  • stimulated by androgens
  • increased yeast or inflammatory yeast
56
Q

Histological and gross feature of psoriasis

A

HISTOLOGY

  • diffuse parakeratosis
  • regular epidermal hyperplasia
  • pale papillary dermis because edematous
  • loss of granular layer
  • neutrophils - UNIQUE

GROSS

  • rash on extensor extremities
  • Yellow (neutrophils) elevated scales
  • well demarcated lesions unlike dermatitis
57
Q

How does clostridium perfringens spread through muscle?

A 
Alpha toxin (phospholipase C)
-degrades sphingomyelin and lecithin
58
Q

What’s needed for bacillus anthracis to cause damage?

A

Toxin - 3 parts

  1. PA - protective Ag
  2. LF - lethal factor (metalloprotease)
  3. EF - edema factor (adenylate cyclase)

Need PA + LF or EF for damage

59
Q

Human vaccine for anthrax contains?

A

PA

60
Q

Bacillus anthracis capsule characteristics

A
  1. D-Glutamic acid
  2. anti-phagocytic
  3. Weakly antigenic

Musculoskeletal and skin (11 decks)

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