MSS Pathology Flashcards

1
Q

What is Achondroplasia?

A
  • Failure of longiudinal bone growth 9endochonrdal ossification)→ short limbs
  • Membranous ossification is not affected→ large head relative to limbs
  • Common cause of dwarfism
  • Normal life span & fertility
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2
Q

**Growth Factor involved in Achondroplaisa **

A

Constitutive activation of fibroblast GF receptor (FGFR3) acutally inhiits chondrocyte proliferation

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3
Q

Pattern of Inheritance of Achondroplaisa

A
  • AD inheritance
  • 85% occur sporatidaclly & assoc w/ advanced paternal age
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4
Q

What is Osteoporosis?

A

Trabecular (spongy) bone loses mass & interconnections despite normal bone mineralization & lab values ( serum Ca2+ & PO43-)

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5
Q

What are Vertebral Crush Fractures?

A
  • Acute back pain
  • Loss of height
  • Kyphosis
  • Caused by osteoporosis
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6
Q

What is Type I Osteoporosis?

A
  • Postmenopausal: inc bone resportion d/t dec estrogen levels
  • Femoral neck fracture, distal radius (Colles’) fractures
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7
Q

What is Type II Osteoporosis?

A
  • Senile osteoporosis
  • Affects men & women >70 years of age
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8
Q

Prophylaxis for Type II Osteoporosis

A

Regular wt bearing exercise & adequate Ca & Vit D intake throughout adulthood

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9
Q

Tx for Osteoporosis Type II

A
  • Estrogen (SERMs) &/or calcitonin
  • Bisphosphonates or pulsatile PTH for severe cases
  • Glucocorticoids are contraindicated
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10
Q

What is Osteopetrosis?

A

Failure of normal bone resorption d/t defective osteoclasts→ thicekened, dense bones taht are prone to fracture

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11
Q

What does Osteopetrosis look like?

A

Bone fills marrow space, causing pancytopenia, extramedullary hematopoiesis

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12
Q

What do the mutations in Osteopetrosis do?

A

Impair ability of osteoclast to generate acidic environment necessary for resorption (e.g. carbonic anyhydrase II)

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13
Q

Look of Osteopetrosis on X-ray

A

Bone-in-bone appearance

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14
Q

Osteopetrosis can result in:

A
  • Crainial nerve impingement
  • Palsies as a result of narrowed formaina
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15
Q

Tx for Osteopetrosis

A

BM transplant is potentialy curative as osteoclasts are derived from monocytes

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16
Q

What can Vit D deficiency cause?

A
  • Rickets in children
  • Osteomalacia in adults
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17
Q

Pathway of Vit D Deficiency

A
  • dec Vit D→ dec serum Ca→ Inc PTH secretion → dec serum phosphate
  • Hyperactivity of osteoclasts→ inc alk phos
  • defective mineralization/ calcification of osteoid l/t soft bones that bow out
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18
Q

What is Osteitits deformans?

A
  • Pagent’s dz of bone
  • Common, localized disorder of bone remodeling caused by inc both osteoblastic & osteoclastic activity
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19
Q

Lab Values of Osteitis deformans

A

Normal serum Ca, P & PTH levels w/ inc ALP

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20
Q

What does osteitis deformans look like?

A
  • Mosaic (“woven”) bone pattern
  • Long bone chalk-stick fractures
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21
Q

What can Osteitis deformans cause?

A
  • Inc blood flow from inc arteriovenous shunts may cause high-output HF
  • Inc risk of osteogenic sarcoma
  • Hat size can be Inc
  • Hearing loss is common d/t auditory foramen narrowing
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22
Q

What is osteitis fibrosa cystica?

A
  • “Brown tumors” of hyperparathyroidism
  • Inc serum Ca, ALP, PTH & dec P
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23
Q

What is Polyostotic fibrous dysplasia?

A

Bone replaced by fibroblasts, collagem, & irregular bony trabeculae

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24
Q

What is McCune-Albright Syndrome?

A

Form of polycystic fibrous dysplasia char by mulitple unilateral bone lesions assoc w/ endocrine ABN (precociou puberty) & café-au-lait spots

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25
Q

What are the 1º benign bone tumors?

A
  • Giant cell tumor (osteoclastoma)
  • Osteochondroma (exostosis)
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26
Q

What age group osteoclastoma occur?

A

20-40yo

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27
Q

What is Ostoclastoma?

A

Locally aggressive benign tumor ofent around the distal femur, proximal tibial region (knee)

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28
Q

Osteoclastoma appearance on X-ray

A

“Double bubble” or “soap bubble”

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29
Q

Histo of osteoclastoma

A

Spindle-shaped cells w/ multinucleated giant cells

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30
Q

What age does Osteochonroma occur?

A

Males <25yo

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31
Q

What is Osteochondroma?

A
  • Most common benign tumor
  • Mature bone w/ cartilagenous cap
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32
Q

Where does Osteochondroma commonly originate?

A

Long metaphysis

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33
Q

What does Osteochondroma transform to?

A

Rare transformation to chondrosarcoma

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34
Q

What are the 1° malignant bone tumors?

A
  • Osteosarcoma (osteogenic sarcoma)
  • Ewing’s sacroma
  • Chondrosarcoma
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35
Q

Who gets Osteosacroma?

A
  • Males> females
  • 10-20 yo
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36
Q

What are the predisposing factors to Osteosarcoma?

A
  • Paget’s dz of bone
  • Bone infarcts
  • Radiation
  • Familial retinoblastoma
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37
Q

Characteristics of Osteosarcoma

A
  • Metaphysis of long bones, often aroudn distal femur, proximal tibial region (knee)
  • Codman’s triangle (from elevation of periosteum or sunburst pattern on X-ray
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38
Q

Tx of Osteosarcoma

A

Aggressive, tx w/ surgical en bloc resection (w/ limb salvage) & chemotherapy

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39
Q

Who gets Ewing’s Sarcoma?

A

Boys <15yo

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40
Q

Where does Ewing’s Sarcoma occur?

A

Commonly appears in diaphysis of long bones, pelvis, scapula & ribs

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41
Q

Histo of Ewing’s Sarcoma

A
  • Anaplastic small blue cell malignant tumor
  • “Onion skin” appearance in bone
  • (Going out for Ewing’s & onion rings)
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42
Q

Prognosis of Ewing’s Sarcoma

A

Extremely aggressive w/ early mets but responsive to chemo

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43
Q

What translocation is Ewing’s Sacroma assoc w/?

A

t(11;22)

(11+22=33 Patrick Ewing’s jersey #)

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44
Q

Who gets Chonrosarcoma?

A

Men 30-60yo

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45
Q

Where is Chondrosarcoma located?

A

Pelvis, spine, scapula, humerus, tibia or femur

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46
Q

What is Chondrosarcoma?

A
  • Malignant cartilaginous tumor
  • May be of 1° origin or from osteochondroma
  • Expansile glistening mass w/in the medullary cavity
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47
Q

Cause of Osteoarthritis

A

Mechanical- joint wear & tear destroys articular cartilage

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48
Q

Joint findings of Osteoarthritis

A
  • Subchondral cysts
  • Sclerosis
  • Osteophytes (bone spurs)
  • Eburnation (polished ivory-like appearance of bone)
  • Bouchard’s nodes (PIP)
  • No MCP involvement
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49
Q

Predisposing factors of Osteoarthritis

A
  • Age
  • Obesity
  • Joint deformity
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50
Q

Clinical Presentation of Osteoarthritis

A
  • Pain in wt-bearing joints after use (at the end of the day) improving w/ rest
  • Knee CT loss begins medially (“bowlegged”)
  • Noninflammatory
  • No systemic sx
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51
Q

Tx of Osteoarthritis

A

NSAIDs & Intra-articular glucocorticoids

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52
Q

Cause of Rheumatoid arthritis

A

Autoimmune- inflammatory destruction of synovial joints. Type III hypersensitivity

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53
Q

Joint findings in RA

A
  • Pannus formation in joints (MCP, PIP)
  • SQ rheumatoid nodules (fibrinoid necrosis)
  • Ulnar deviation of fingers subluxation
  • Baker’s cysts (in politeal fossa)
  • No DIP involvement
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54
Q

Predisposing Factors of RA

A
  • Females> males
  • 80% have + Rheumatoid factors (anti-IgG Ab)
  • Anti-cyclic citrullinated peptide Ab is more specific
  • Strong assoc w/ HLA-DR4
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55
Q

Clinical Presentation of RA

A
  • Morning stiffness lasting >30 min & improving w/ use
  • Symmetric joint involvement
  • Systemic sx- fever, fatigue, pleuritis, pericarditis
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56
Q

Tx of RA

A
  • NSAIDs
  • Glucocorticoids
  • Dz-modifying agents (methotrexate, sulfasalazine, TNF-alpha inhibitors)
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57
Q

What is Sjögren’s Syndrome?

A

Lymphocytic infiltration of exocrine glands, especially lacrimal & salivary

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58
Q

Classic Triad of Sjögren’s Syndrome

A
  • Xerophthalamia- dry eyes, conjuctivitis, “sand in my eyes”
  • Xerostomia- dry mouth, dysphagia
  • Arthritis
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59
Q

Characteristics of Sjögren’s Syndrome

A
  • Parotid enlargement
  • inc risk of B-cell lymphoma
  • Dental Caries
  • Auto-Ab to ribonucleoprotein Ag: SS-A (Ro), SS-B (La)
  • Assoc w/ rehumatoid arthritis
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60
Q

What is Gout?

A
  • Precipitation of monosodium urate crystals into joints d/t hyperuricemia which can be caused by Lesch-Nyhan synd
  • PRPP excess, dec excetion of uric acid (d/t thyazide diruetics)
  • Inc cell turnover or von Gierke’s dz
  • 90% d/t underexcretion
  • 10% d/t overproduction
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61
Q

What does Gout look like?

A

Crystals are needle shaped & negatively birefringemant= yellow crystals under parallel light

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62
Q

Sx of Gout

A
  • Asymmetric join distribution
  • Joint is swollen, red & painful
  • Classic manifestation is painful MTP joint of the big toe (podagra)
  • Tophus formation (often on external ear, olecranon bursa or Achilles tendon)
  • Acute attack tends to occur after a large meal or alcohol consumption (alcohol metabolites compete for same excretion sites in kindney as uric acid, causing dec uric acid sec & subsequent bulidup in blood)
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63
Q

Tx of Gout

A
  • Acute: NSAIDs (indomethacin), glucocorticoids
  • Chronic: xanthine oxidase inhibitors (allopurinol, febuxostat)
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64
Q

Cause of Pseudogout

A
  • Depostions of Ca pyrophosphate crystals w/in the joint space
  • Usuallly affects large joints (classically the knee)
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65
Q

What does Pseudogout look like?

A
  • Forms basophilic, rhomoid crystals that are weakly + birefringement
  • Crystals are blue when parallel to the light
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66
Q

Who gets Pseudogout?

A
  • >50yo
  • Effects both sexes equally
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67
Q

Tx of Pseudogout

A
  • NSAIDs for sudden severe attacks
  • Steroids
  • Colchicine
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68
Q

Causes of Infectious Arthritis

A
  • S. aureus
  • Streptococcus
  • Niesseria gonorrheaoeae
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69
Q

What is Infectious Arthritis?

A

Gonococcal arthritis is an STD that presents as a migratory arthritis w/ an asymmetric pattern

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70
Q

Sx of Infectious Arthritis

A
  • Affected joint is swollen, red & painful
  • Synovitis (knee)
  • Tenosynovitis (hand)
  • Dermatitis (pustules)
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71
Q

What is Osteonecrosis?

A
  • Avascular necrosis
  • Infarction of bone & marrow
  • Pain assoc w/ activity
  • MC site is femoral head
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72
Q

Causes of Osteonecrosis

A
  • Trauma
  • High-dose corticosteroids
  • Alcoholism
  • Sickle cell
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73
Q

What are Seronegative spondyloarthropathies?

A
  • Arthritis w/o rheumatoids factor (no IgG Ab)
  • Psoriatic arthritis
  • Ankylosing spondylitis
  • IBS
  • Reactive arthritis (Reiter’s synd)
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74
Q

What seronegative spondyloarthropathies asoc w/?

A
  • HLA-B27 (gene that codes for HLA- MHC class I)
  • Occurs more often in males
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75
Q

What is Psoriatic arthritis?

A
  • Joint pain & stiffness seen in <1/2 of pts w/ psoriasis
  • Asymmetric & patchy involvement
  • Dactylitis “sausage fingers”
  • Pencil-in-cup deformity on X-ray
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76
Q

What is Ankylosing spondylitis?

A

Chronic inflam dz of spine & sacroiliac joints→ ankylosis (stiff spine d/t fusion of joints), uveitis & aoritic regurg. Bamboo spine (vertebral fusion)

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77
Q

What is IBS?

A

Chron’s dz & UC are often accompanied by ankylosing spondylitis or peripheral arthritis

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78
Q

Reactive arthritis (Reiter’s Synd) Triad

A
  • Conjunctivitis & anterior uveitis
  • Urethritis
  • Arthritis
  • “Can’t see, can’t pee, can’t climb a tree”
  • Post GI or chlamydia infections
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79
Q

Who gets SLE?

A
  • 90% are female
  • 14-45yo
  • MC & severe in black females
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80
Q

Clinical presentation of SLE

A
  • Fever, fatigue, wt loss
  • Libman-sacks endocarditis (verrucous war-likem sterile vegetations on both sides of valve)
  • Hilar adenopathy
  • Raynaoud’s phenomenon
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81
Q

What is the common COD in SLE?

A

Nephritis-Diffuse proliferative glomerulonephritis (if nephrotic)

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82
Q

What causes false + on the syphillis test (RPR/VDRL)?

A

Antiphospolipid Ab’s which cross-react w/ cardiolipin used in tests

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83
Q

What do SLE lab tests detect?

A
  • Antinuclear Ab’s (ANA)- sensitive, (1° screening) but not specific for SLE
  • Ab’s to ds-DNA (anti-dsDSA)- very specific, poor prognosis,
  • Anti-Smith Ab’s (anti-Sm)- very specific, but not prognostic
  • Antihistone Ab’s- more sensitive for drug-induced lupus
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84
Q

I’M DAMN SHARP

(SLE characteristics)

A
  • Ig’s (anti-dsDNA, anti-Sm, antiphospholipid)
  • Malar rash
  • Discoid rash
  • Antinuclear Ab
  • Mucositis (oropharyngeal ulcers)
  • Neurologic disorders
  • Serositis (pleuritis, pericarditis)
  • Hematologic disorders
  • Arthritis
  • Renal disorders
  • Photosensitivity
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85
Q

Characteristics of Sacroidosis

A
  • Immune-mediated, widesspread noncaseating granulomas & elevated serum ACE levels
  • Often asx except for enlarged LN
  • Common in black females
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86
Q

What is Sarcoidosis assoc w/?

A
  • Restrictive lung dz (interstitial fibrosis)
  • Erythema nodosum
  • Bell’s palsy
  • Epi granulomas containing microscopic Schaumann & asteroid bodies
  • Uveitis
  • Hyper-Ca (d/t elevated 1-alpha-med vit D activation in epitheloid macro)
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87
Q

Tx of Sarcoidosis

A

Steroids

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88
Q

Sx of Polymyalgia rheumatica

A
  • Pain & stiffness in shoulds & hips
  • Fever
  • Malaise
  • Wt loss
  • Does not cause muscle weakness
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89
Q

Who gets Polymyalgia rheumatica?

A

MC in women >50yo

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90
Q

What is Polymyalgia rheumatica?

A

Temporal (giant cell) arteritis

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91
Q

Findings in Polymyalgia rheumatica

A

Inc ESR & normal CK

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92
Q

Tx of Polymyalgia rheumatica

A

Rapid response to low-dose corticosteroids

93
Q

Who gets Fibromyalgia?

A

MC seen in women 20-50yo

94
Q

What is Fibromyalgia?

A

Chronic, widespread MSS pain assoc w/ stiffness, paresthesia, poor sleep & fatigue

95
Q

What is Polymyositis?

A

Progressive symmetric proximal muscle weakness, characteristized by endomysial inflam w/ CD8+ T cells. Most often involves shoulders

96
Q

What are the characteristics of Dermatomyositis?

A
  • Similar to polymyositis
  • Malar rash (similar to SLE)
  • Gottron’s papules
  • Heliotrope rash
  • “Shoulder & face rash
  • “Mechanic hands”
97
Q

What is dermatomyositis?

A

Perimysial inflam & atrophy w/ CD4+ T cells

98
Q

What does Dermatomyositis inc the risk of?

A

Occult Malignancy

99
Q

Findings in Polymyositis/Dermatomyositis

A
  • Inc CK
    • ANA
    • anti-Jo-1 Ab’s
100
Q

Tx of Polymyositis/dermatomyositis

A

Steroids

101
Q

What is the freq of Myasthenia gravis?

A

MC NMJ disorder

102
Q

What is the pathophysiology of Myasthenia gravis?

A

Auto-Ab’s to postsynaptic ACh receptors

103
Q

What does AChE inhibitor admin do in Myasthenia gravis?

A

Reversal of sx

104
Q

Clinical characterisitics of Myastenia gravis

A
  • Ptosis
  • Diplopia
  • Weakness
  • Worsens w/ muscle use
105
Q

What is Myasthenia gravis assoc w/?

A

Thymoma & thymic hyperplasia

106
Q

Freq of Lmabert-Eaton myasthenic synd

A

Uncommon

107
Q

Pathophysiology of Lamber-Eaton myasthenic synd

A

Auto-Ab’s to presynaptic Ca2+ channel→ dec ACh release

108
Q

Clinical sx of Lamber-Eaton Synd

A

Proximal muscle weakness that improves w/ muscle use

109
Q

What is Lamber-Eaton synd assoc w/?

A

Small cell lung cancer

110
Q

What does AChE inhibitor admin in Lamber-Eaton Synd do?

A

No effect

111
Q

What is Myositis ossificans?

A

Metaplasia of skm to bone following muscular trauma

112
Q

Where is Myositis ossificans most often seen?

A

Upper or lower extremity

113
Q

How does Myositis ossificans present?

A

Suspicous “mass” at site of known trauma or as incidental finding on radiography

114
Q

What is Scleroderma (systemic sclerosis)?

A

Excessive fibrosis & collagen deposition throughout the body

115
Q

How does Scleroderma of skin commonly present?

A

Sclerosis of skin, manifesting as puffy & taut skin w/ absence of wrinkles

116
Q

What organ systems does slceroderma affect?

A
  • Renal
  • Pulmonary (most likely COD)
  • CV
  • GI system
117
Q

Who gets scleroderma?

A

75% female

118
Q

What is Diffuse scleroderma?

A

Widespread skin involvement, rapid progression, early visceral involvement

119
Q

What is Diffuse scleroderma assoc w/?

A

anti-Scl-70 Ab (anti-DNA topoisomerase I Ab)

120
Q

Clinical sx of CREST synd

A
  • Calcinosis
  • Reaynaud’s phenomenon
  • Esophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
  • Limited skin involvement often confined to fingers & face
121
Q

What is the clincial course of CREST synd?

A

More benign clinical course

122
Q

What is CREST synd assoc w/?

A

Anti-Centromere Ab ( C fo CREST)

123
Q

What is a macule?

A

Flat lesion w/ well-circumscried change in skin color <5mm. Ex) freckle, labial macule

124
Q

What is a Patch?

A

macule >5mm Ex) large brithmark (congenital nevus)

125
Q

What is a papule?

A

Elevated solid skin lesion < 5mm

Ex) Mole (nevus), acne

126
Q

What is a Plaque?

A

Papule >5mm

ex) psoriasis

127
Q

What is a vesicle?

A

Small fluid-containing blister <5mm

ex) Chickenpox (varicella), shingles (zoster)

128
Q

What is Bulla?

A

Large fluid-containing blister >5mm

ex) Bullous pemphigoid

129
Q

What is a pustule?

A

Vesicle containing pus

ex) Pustular psoriasis

130
Q

What is a Wheal?

A

Transient smooth papule or plaque

ex) Hives (urticaria)

131
Q

What is a Scale?

A

Flaking off of stratum corenum

ex) eczema, psoriasis, SCC

132
Q

What is a Crust?

A

Dry exudate

ex) Impetigo

133
Q

What is Hyperkaratosis?

A

Inc thickness of stratum corneum

ex) psoriasis

134
Q

What is parakeratosis?

A

Hyperkaratosis w/ retention of nuclei in stratum corneum

ex) psoriasis

135
Q

What is Acantholysis?

A

Separation of epidermal cells

ex) Pemphigus vulgaris

136
Q

What is Acanthosis?

A

Epidermal hyperplasia (inc spinosum)

ex) Acanthosis nigricans

137
Q

What is Dermatitis?

A

Inflam of the skin

ex) Atopic dermatitis

138
Q

What is Albinism

A

Normal melanocyte # w/ dec melanin production d/t dec tyrosine activity. Can also be caused by failure of neural cress cell migration during dev

139
Q

What is Melasma (chloasma)?

A

Hyperpigmentation assoc w/ pregnancy (“mask of preg”) or OCP use

140
Q

What is Vitiligo?

A

Irreg areas of complete depigmentation

141
Q

What causes Vitiligo?

A

Dec in melanocytes

142
Q

What are Verrucae?

A

Warts, Condyloma acuminatum on genitals

143
Q

What causes Verrucae?

A

HPV

144
Q

What do Verrucae look like?

A

Soft, tan-colored, cauliflower-like papules

145
Q

Histo of verrucae

A

Epidermal hyperplasia, hyperkartosis, koilocytes

146
Q

What are Melanoctic nevus?

A

Common mole

147
Q

Prognosis of Melanocytic nevus

A

Benign, but mealonoma can arise in congenital or atypical moles

148
Q

What does Intradermal nevi look like?

A

Papular

149
Q

What do Junctional nevi look like?

A

Flat macules

150
Q

What is Urticaria?

A

Hives; pruritic wheals that form after mast cell degranulation

151
Q

What is Ephelis?

A
  • Freckle
  • Normal # of melanocytes
  • Inc melanin pigment
152
Q

What is Atopic dermatitis (eczema)?

A

Pruritic eruption, commonly on skin flexures. Us. on the face in infancy & antecubital fossae therafter

153
Q

What is Atopic dermatitis assoc w/?

A

Other atopic dz- asthma & allergic rhinitis

154
Q

What is allergic contact dermatitis?

A

Type IV hypersensitivity reaction that follows exposure to allergen. Lesions occur at contact site (nickle, poision ivy, neomyocin)

155
Q

What is Psoriasis?

A

Papules & plaques w/ silvery scaling, esp on knees & elbows

156
Q

Histo of Psoriasis

A

Acanthosis w/ perakeratotic scaling (nuclei still in stratum corneum). Inc stratum spinousm & dec stratum granulosum

157
Q

What is Auspitz sign?

A

Pinpoint bleeding spots from exposure of dermal papillae when scales are scraped off

158
Q

What is Psoriasis assoc w/?

A

Nail pitting & psoriatic arthritis

159
Q

What is Seborrheic keratosis?

A

Flat, greasy pigmented squamous epi prolif w/ keratin-filled cysts (horn cyts). Looks “stuck on”

160
Q

Where do Seborrheic keratosis lesions occur?

A

Head, trunk & extremities

161
Q

Who gets Seborrheic keratosis?

A

Common benign neoplasm of older persons

162
Q

What is Leser-Trélat sign?

A

Sudden appearance of multiple seborrheic keratoses, indicating an underlying malignancy (GI, lymphoid)

163
Q

What is Pemphigus vlugaris?

A

Potentially fatal autoimmune skin disorder w/ IgG Ab against desmoglein 3 (1 &/or 3), a part of desmosomes (needed for cell adhesion)

164
Q

What does immunofluorescense of Pemphigus vulgaris reveal?

A

Ab’s around epidermal cells in a reticular or netlike pattern

165
Q

What is Acantholysis in Pemphigus vulgaris look like?

A

Intraepidermal bullae causing flaccid blister involving the skin & oral mucosa

166
Q

What is Nikolsky’s sign?

A

Separation of epidermis upon manual stroking of skin. + in Pemphigus vulgaris

167
Q

What is bullous pemphigoid?

A

Autoimmune disorder w/ IgG ab against hemidesmosomes (epi BM; Ab’s are “bullow” the epidermis)

168
Q

What does Bullous pemphigoid show on immunoflurorescence?

A

Linear immunofluorescence

169
Q

What are the clinical characteristics of Bullous pemphigoid?

A
  • Eosinophils w/in the tense blisters.
  • Similar to but less severe than pemphigus vulgaris- affects skin but spares oral mucosa.
  • Negative nikolsky’s sign
170
Q

What is Dermatis herpetiformis?

A

Pruritic papules, vesicles & bullae. Deposits of IgA at the tips of dermal papillae

171
Q

What is Dermatitis herpetiformis assoc w/?

A

Celica dz

172
Q

What is Erythema mutliforme assoc w/?

A

Infections (Mycoplasma pneumonia, HSV), cancers & autoimmune dz

173
Q

How does erythema muliforme present?

A

Multiple types of lesions- macules, papules, vesicles & target lesions

174
Q

What does a target ring look like?

A

Targets w/ muliple rings & a dusky center showing epi disruption

175
Q

What is Stevens-Johnson synd characterized by?

A
  • Fever
  • Bulla formation
  • Necrosis
  • Sloughing of skin
  • High mortality rate
176
Q

What does Stevens-Johnson synd look like?

A

Typicaly 2 mucous mem involved & skin lesions maybe appear liek targets as seen in erythema multiforme

177
Q

What is Stevens-Johnson synd assoc w/?

A

Adverse drug reaction

178
Q

What is Toxic epidermal necrolysis?

A

A more severe form of Stevens-Johnson synd w/ >30% of the body surface area involved. Destroys the epidermal-dermal junction.

179
Q

What is acanthosis nigricans?

A

Epidermal hyperplasia cuasing symmetrical, hyperpigmented, velvety thickening of skin, esp on neck or in axilla

180
Q

What is aconathosis nigricans assoc w/?

A

Hyperinsulinemia (DM, obesity, Cushing’s synd) & visceral malignancy

181
Q

What is actinic keratosis?

A

premalignant lesions caused by sun exposure

182
Q

What does actinic keratosis look like?

A

Small, rough, erythematous or brownish papules or plaques

183
Q

What is actinic keratosis a risk for?

A

Risk of SCC is proportional to degree of epi dysplasia

184
Q

What is erythema nodosum?

A

Inflam lesions of SQ fat, usually on anterior shins

185
Q

What is erythema nodosum assoc w/?

A

Sarcoidosis, coccidioidomyocosis, histoplasmosis, TB, strep infections, leprosy & Chron’s dz

186
Q

What are the 6 P’s of Lichen Planus?

A

Pruritic, Purple, Polygonal Planar Paules & Plaques

187
Q

Histo of Lichen Planus

A

Sawtooth infilitrate of lymphocytes at dermal-epidermal junction

188
Q

What is Lichen Planus assoc w/?

A

Hepatitis C

189
Q

What is Pitryiasis rosea?

A

“Herald patch” followed days later by “Christams tree” distribution. Multiple plaques w/ collarette scale.

190
Q

What is the clinical courseof Pityriasis rosea?

A

Self resolving in 6-8 weeks

191
Q

How does a sunburn occur?

A

UV irradiation causes DNA mut, inducing apoptosis of keratinocytes

192
Q

Which UV irradiation is dominant in tanning & photoaging?

A

UVA

193
Q

Which UV irradiation is involved in sunburns?

A

UVB

194
Q

What can sunburns lead to?

A

Impetigo & skin cancers (basal cell CA, SCC & melanoma)

195
Q

What is Impetigo?

A

Very superficial skin infection. Highly contagious

196
Q

What causes Impetigo?

A

S. aureus or S. pyogenes

197
Q

What does Impetigo look like?

A

Honey-colored crusting

198
Q

What is Bullous impetigo?

A

hass bullae & is caused by S. aureus

199
Q

What is Cellulitis?

A

Acute, painful, spreading infection of dermis & SQ tissues

200
Q

What causes cellulitis

A

S. pyogenes or S. aureus of starts w/ a break in skin from trauma or another infection

201
Q

What is Necrotizing fascitis?

A

Deeper tissue injury, usually from anaerobic bacteria or S. pyogenes. “Flesh-eating bacteria”

202
Q

What does Necrotizing fasciitis cause?

A

Results in crepitus from methane & CO2 production. Causes bullae & a purple color to the skin

203
Q

What is Staphylococcal scalded skin synd (SSSS)?

A

Exotoxin destroys keratinocyte attachments in stratum granulosum only

204
Q

What is Staph scalded skin synd (SSSS) characterized by?

A

Fever & gen erythematous rash w/ sloughing of upper layers of the epidermis that heals completely

205
Q

Who is SSSS seen in?

A

Newborns & children

206
Q

What is hairy leukoplakia?

A

White painless plaques on the tongue that cannot be scraped off

207
Q

What is hairy leukoplakia mediated by?

A

EBV

208
Q

Who gets hairy leukoplakia?

A

HIV + pts

209
Q

What is the MC skin cancer?

A

Basal cell CA

210
Q

Where is Basal cell CA found?

A

Sun-exposed areas of body

211
Q

What is the clinical course of Basal Cell CA?

A

locally invasive but almost never mets

212
Q

What does Basal Cell CA look like?

A

Pink, pearly nodules*, commonly w/ telangiectasias, rolled borders, & central crusting or ulceration. Also appear as nonhealing ulcers w/ infiltrating growth or as a scaling plaque (superficial BCC)

213
Q

What is the histo of Basal Cell tumors?

A

Palisading peripheral nuclei*

214
Q

What is the 2nd MC skin cancer?

A

SCC

215
Q

What is SCC assoc w/?

A

Excessive exposure to sunlight, immunosuppression, & occasionaly arsenic exposure

216
Q

Where does SCC occur?

A

Appears on face, lower lip, ears & hands

217
Q

What is the clincial course of SCC?

A

Locally invasive, but may spread to LN & will rarely mets. assoc w/ chronic draining sinuses

218
Q

What do SCC lesions look like?

A

Ulcerative red lesions w/ freq scale

219
Q

What is the histopathology of SCC?

A

keratin pearls

220
Q

What is Keratoacanthoma

A

Variant that grows rapidly (4-6 weeks) & may regress spon over months

221
Q

What is Melanoma?

A

Common tumor w/ significant risk of mets

222
Q

What is the tumor marker for Melanoma?

A

S-100

223
Q

What is melanoma assoc w/?

A

Sunlight exposure; fair-skinned persons are at high risk

224
Q

What does the depth of melanoma correlate w/?

A

risk of mets

225
Q

What are the ABCDEs of melanoma?

A
  • Asymmetry
  • Border irreg
  • Color variation
  • Diameter >6mm
  • Evolution over time
226
Q

What mut is melanoma driven by?

A

Activating mut in BRAF kinase

227
Q

What is the 1º tx of melanoma?

A

Excision w/ appropriately wide margins

228
Q

What can pts w/ melanoma w/ BRAF V600E mut be tx w/?

A

May benefit from vemurafenib, a BRAF kinase inhibitor