DIT review - MSK 2 Flashcards

1
Q

Why does meat consumption exacerbate gout?

A

excess DNA and RNA consumption

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2
Q

Why does alcohol consumption exacerbate gout?

A

alcohol competes with uric acid for renal excretion

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3
Q

What is the deficient enzyme in Lesch-Nyhan syndrome, and why does it cause gout?

A

Deficiency in HGPRT (hypoxanthine and guanine –> IMP/GMP) in the purine salvage pathway

Results in excess uric acid production and de novo purine synthesis

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4
Q

What is the MOA of colchicine

A
  • Colchicine – stabilizes tubulin to impair leukocyte chemotaxis
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5
Q

MOA of Probenecid

A
  • Probenecid – inhibits reabsorption of uric acid in PCT
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6
Q

MOA of Allopurinol

A
  • Allopurinol – inhibits xanthine oxidase, thus inhibiting uric acid synthesis
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7
Q

What are the seronegative spondyloarthropathies

A

PAIR:

Psoriatic arthritis, ankylosing spondyltitis, inflammatory bowel disease, reiter syndrome

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8
Q

What HLA is associated with seronegative spondyloarthropatheis

A

HLA-B27

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9
Q

What seronegative spondyloarthropathy is associated with “pencil-in-cup” x-ray?

A

Psoriatic arthritis

Deformity of the DIP

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10
Q

What are the 3 main clinical features of ankylosing spondylitis

A
  • (1) Fusion of vertebrae (ankyloses) = bamboo spine
  • (2) Uveitis
  • (3) Aortitis (weakened walls may lead to dilation and aortic regurgitation)
  • Think: Pandas:
    • They eat bamboo = bamboo spine
    • Raccoon eyes = uveitis
    • Clumsy climbing up trees causes branches to bend = aortitis
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11
Q

Most common pathogens involved in septic arthritis

A

Neisseria, Staph aureus, Strep

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12
Q

Which arthritis is associated with osteophyte (bone spurs)?

A

Osteoarthritis

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13
Q

What type of HSR is lupus?

A

Type III

Due to antibody-antigen complex deposition

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14
Q

Describe symptoms associated with lupus

A
  • RASH OR PAIN
    • R – Rash (malar or discoid)
    • A – Arthritis (non-erosive, 2 joints)
    • S – Serositis (e.g. pleuritic, pericarditis)
    • H – Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia)
    • O – Oral/nasopharyngeal ulcers (painless)
    • R – Renal disease
    • P – Photosensitivity
    • A – Antinuclear antibodies (+ANA)
    • I – Immunologic disorder (anti-dsDNA, anti-Smith, anti-histone, or anti-phospholipid/anti-cardiolipin)
    • N – Neurologic disorders (seizures, psychosis)
  • Other findings:
    • Fever, weight loss, fatigue
    • Raynaud phenomenon
    • Libman-Sacks endocarditis – vegetations on both sides of mitral valve
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15
Q

What renal diseases are associated with lupus

A

diffuse proliferative glomerulonephritis

membranous glomerulonephritis

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16
Q

What are common antibodies found in lupus

A

anti-nuclear (ANA), anti-dsDNA, anti-Smith, anti-histone, or anti-phospholipid/anti-cardiolipin

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17
Q

What antibody is present in drug-induced lupus?

A
  • Will have (+) anti-histone antibodies
18
Q

What are the drugs that cause drug-induced lupus?

A
  • SHIPP-E
    • S – sulfa drugs
    • H – Hydralazine
    • I – Isoniazid
    • P – Procainamide
    • P – Phenytoin
    • E – Etanercept
19
Q

What disorder is associated with anti-phospholipid antibodies?

A

Hypercoagulable state

20
Q

What is the antibody in diffuse and limited scleroderma

A

Diffuse = anti-Scl-70 aka anti-DNA topoisomerase

Limited = anti-centromere

21
Q

What are the features of CREST syndrome

A

· Calcinosis (calcium deposition) / anti-centromere antibody

· Raynoud

· Esophageal dysmotility

· Sclerodactyly (tightening of skin with loss of wrinkles)

· Telangiectasias

22
Q

What is the triad in Sjogren syndrome

A

§ Dry eyes (xerophthalmia)

· Dryness, conjunctivitis, sand in eyes

§ Dry mouth (xerostomia)

· Dysphagia, difficulty swallowing

§ Arthritis

23
Q

What are the antibodies associated with Sjogren?

A

§ Autoantibodies: Anti-SSA (Anti-Ro) and Anti-SSB (Anti-La)

24
Q

What is the difference in gene defect between Duchenne and Becker MD?

A

Duchenne = frameshift mutation leading to absent or truncated dystrophin gene

Becker = non-frameshift mutation with partially functional dystrophin gene

25
Q

Clinical features and common cause of death in Duchenne?

A
  • Weakness begins in pelvic girdle and progresses superiorly
  • Pseudohypertrophy of calf muscles due to fibrofatty replacement of muscle
  • Waddling gait
  • Gower sign
  • Onset before 5 y/o
  • Dilated cardiomyopathy is common cause of death
26
Q

What are the clinical features of polymyalgia rheumatica

A

This is a problem of joints, not muscles (even though it has myalgia in name)

  • § Pain and stiffness in proximal joints (shoulders and hips)
  • § No muscle weakness
  • § Fever, malaise, weight loss
27
Q

Describe lab values in polymyalgia rheumatica (ESR and CK)

A

§ Elevated ESR and CRP

§ Normal CK (this is not a muscle problem!)

28
Q

What other disorder is associated with polymyalgia rheumatica?

A

o Associated with Giant cell (temporal) arteritis

29
Q

What are the antibodies associated with polymyositis/dermatomyositis?

A
  • (+) ANA
  • (+) anti-Jo-1 antibodies
30
Q

How do you differentiate between polymyositis and polymyalgia rheumatica

A

Polymyositis =

  • Bilateral proximal muscle weakness (shoulders and pelvic girdle)
    • Vs. Polymyalgia rheumatica which is a disorder of proximal joints, not muscles
  • Elevated CK
    • vs. polymyalgia rheumatica which has normal CK
31
Q

What are common derm findings in dermatomyositis

A
  • Rash of upper eyelids (heliotrope rash)
  • Malar rash (butterfly rash)
  • Gottron papules – red papules on elbows, knuckles, and knees
  • “Shawl sign”
  • “Mechanic’s hands” – hands or feet rough and cracked
32
Q

Differentiate between muscle inflammation in dermatomyositis and polymyositis

A
  • Polymyositis
    • Endomysial inflammation with CD8+ T cells
  • Dermatomyositis
    • Perimysial (THINK: periphery b/c of muscle + skin involvement) inflammation with CD4+ T cells
33
Q

What is fibromyalgia?

A
  • Chronic, widespread musculoskeletal pain in 11/18 particular sites
  • Also associated with:
    • Stiffness, Paresthesias, Poor sleep, Fatigue, Cognitive disturbances (“fibro fog”)
34
Q

Treatment of fibromyalgi

A

o Treatment = exercise, anti-depressants, anticonvulsants

35
Q

What are the layers of the epidermis

A
  • Stratum corneum lucidum, granulosum, spinosum, basale
    • THINK: Californians Like Girls in String Bikinis
36
Q

What type of junction acts as a paracellular barrier, preventing things from passing between cells

A

Tight junctions

37
Q

Protein components of tight junctions?

A

Claudins and occludins

38
Q

What are the two type of junctions that act as cell anchors between adjacent cells, and what is their protein component?

A

Adherens (intermediate) junctions and desmosomes

Connects actin skeleton of adjacent cells via cadherins

39
Q

What junction allows signalling between adjacent cells, and what is the protein component?

A

Gap junctions

Made up of connexons

40
Q

What type of junction attaches cell to basement membrane, and what is the protein component?

A

Hemidesmosomes

Integrins

41
Q

What are the 4 main pathologic features of acne?

A
  • (1) Hyperkeratosis – increased keratin
  • (2) Sebum overproduction
  • (3) Propionibacterium acnes proliferation
  • (4) Inflammation
42
Q

What is the pathophysiology behind freckles?

A
  • Increased number of melanosomes (melanocytes NOT increased)