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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
Compare the 2 serological tests for RA
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
NSAIDS for RA - MoA - what can and can't they do for patients? - side effects?
-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
When should DMARD tx be started? Why?
in most patients, erosive disease occurs w/in 2 years of the onset start DMARDs ASAP
28
Gold standard DMARD? MoA? how long does it take to work?
methotrexate immunosuppressant - inhibits DHF reductase -> inhibits lymphocyte proliferation (folate antagonist) 3-8 weeks
29
Leflunomide - brand - MoA - adverse effects
-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
TNF antagonists
1. Monoclonal antibody - sequesters TNF from cells DRUGS 1. Inflixamab (Remicade) 2. Adalimumab (Humira) 3. Certolizumab 4. Golimumab 2. Soluble TNF receptor - competes w/ endogenous receptor DRUGS 1. Entanercept (enbrel) Think: "intercepts" TNF before it can bind to real TNF receptor
31
Tocilizumab - brand - MoA
Actemra IL-6 inhibitor
32
Rituximab -MoA
B cell depleting monoclonal anti-CD20 Ab
33
Abatacept -brand MoA
- Orencia | - inhibits co-stimulation of T-cell (selective co-stimulation modulator)
34
Dx of JIA requires:
1. onset < 16 y.o. | 2. Requires persistent, objective arthritis for min of 6 weeks
35
JIA w/ highest mortality
Systemic JIA
36
Systemic JIA - pathology - drugs - presentation
- 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
Polyarticular JIA - definition - disease driven by - Drugs
> 4 joints Driven by TNF DRUGS 1. Methotrexate 2. Etanercept
38
Which JIA group is at highest risk for uveitis
Oligoarticular JIA
39
Management of oligoarticular JIA
-intra-articular corticosteroid injection
40
What catalyzes the final conversions to uric acid in the purine degradation pathway?
Xanthine oxidase
41
Fx of uricase (uric acid oxidase)
Uric acid -> allantoin -more soluble, readily excretable form We don't have this enzyme
42
Most patients with gout have a problem with what?
They have issues with excreting uric acid i.e. UNDERSECRETION
43
Which major class of CV drugs interfere with uric acid secretion?
Diuretics
44
Drugs for managing acute gout? Usage guidelines? Side effects? Contraindications?
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
Urate lowering drugs
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
When should Allopurinol (Zyloprim) be used? MoA? Adverse effects?
- 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
Febuxostat - MoA? - indications? - benefits over allopurinol?
- non-purine xanthine oxidase inhibitor - use w/ renal insufficiency - don't get the hypersensitivity rxn
48
Pegloticase - MoA - indications
- pegylated uric oxidase | - can be used in patients who fail standard tx
49
How to differentiate b/w SK and Warts on histology?
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
The only premalignant epidermal neoplasm? caused by? risk for which carcinoma? features?
- Actinic keratosis - 2ndary to sunlight exposure - SCC FEATURES -early -> basal cells large hyperchromatic and pleomorphic later -> parakeratotic (nuclei in stratum corneum)
51
Most common type to skin cancer?
Basal cell carcinoma | -also most common carcinoma overall
52
Nodular BCC found where in skin? | gross appearance?
- dermis | - smooth red papule
53
Progression of nevi? | Which direction do the melanocytes move?
junctional nevus -> compound nevus -> intradermal nevus -move into the dermis
54
What characteristics describe acute dermatitis? subacute? chronic?
acute -> spongiosis (edema) and exocytosis subacute/chronic -> progress towards epidermal hyperplasia and hyperkeratosis; decrease in spongiosis
55
Seborrheic dermatitis - occurs where? - stimulated by?
-areas of greatest sebum production (head, upper trunk) - stimulated by androgens - increased yeast or inflammatory yeast
56
Histological and gross feature of psoriasis
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
How does clostridium perfringens spread through muscle?
``` Alpha toxin (phospholipase C) -degrades sphingomyelin and lecithin ```
58
What's needed for bacillus anthracis to cause damage?
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
Human vaccine for anthrax contains?
PA
60
Bacillus anthracis capsule characteristics
1. D-Glutamic acid 2. anti-phagocytic 3. Weakly antigenic

Musculoskeletal and skin (11 decks)

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