MSK/ Derm pathology Flashcards

1
Q
  1. repetitive flexion (forehand shot) causing pain near epicondyle
  2. repetitive extension (backhand shot) causing pain near lateral epicondyle
A
  1. medial epicondylitis
  2. lateral epicondylitis
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2
Q

boxer’s fracture, commonly caused by direct impact with closed fist (punching a wall)

seen in 4th and 5th metacarpals

A

metacarpal neck fracture

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3
Q

entrapment of median nerve in carpal tunnel (between transverse carpal ligament and carpal bones) –> nerve compression–> paresthesia, pain, and numbness in distribution of median nerve

patient comes in with thenar eminence atrophies but sensation spared, because palmar cutaneous branch enters hand external to carpal tunnel

positive tinel sign sign and phalen maneuver

associated with pregnancies (due to edema), RA, hypothyroidism, diabetes, acromegaly, dialysis-related mayloidosis; may be associated with repeitive use

A

carpal tunnel syndrome

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4
Q

compression of ulnar nerve twist. classically seen in cyclist due to pressure from handlebar

A

Guyon canal syndrome (both the ulnar nerve and ulnar artery runs through the Guyon canal)

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5
Q

inflammation of the gluteal tendon and bursa lateral to greater trochanter of femue.

treatment with NSAID, heats, and stretching

A

trochanteric bursitis

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6
Q

common injury in contact sport due to lateral force applied to planted foot. consost of damage to the ACL, MCL, and medial meniscus (attached to the MCL)

however, lateral meniscus involvement is most common than medial meniscus involvement in conjunction with ACL and MCL injury. presents with acute knee pain and signs of joint injury/instability

A

this is the unhappy triad

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7
Q

inflammation of the prepatellar bursa in front of the knee cap due to repeated trauma or pressure from excessive kneeling (housemaid’s knee)

A

prepatellar bursitis

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8
Q

popliteal fluid collection in gastrocnemius-semimembranosus bursa commonly communicating with synovial space and related to chronic joint disease (osteoarthritis and rheumatoid arthritis)

A

baker cyst

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9
Q

non-inflammatory thickening of abductor pollicis longus and extensor pollicis brevis tendons characterized by pain or tenderness at radial styloid.

positive Finkelstein test (pain at radial styloid with active or passive stretch of thumb tendons). risk in new mothers, golfers, racquet sport players

A

De Quervain tenosynovitis

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10
Q

fluid-filled swelling overlying joint or tendon sheath, most commonly at dorsal side of wrist. Arises from herination of dense connective tissue

A

ganglion cyst

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11
Q

overuse injury of lateral knee that occurs primarily in runners. pain develops secondary to friction of iliotibial band against lateral femoral epicondyle

A

iliotibial band syndrome

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12
Q

increase pressure within fascial compartment of limb (defined by pressure different of 30mmHg or less between the tissue compartment pressure and distolic blood pressure)–> venous outflow obstruction and arteriolar collapse–> anoxia and necrosis.

causes include significant long bone fractures, reperfusion injury, animal venoms

present with severe pain and tense, swollen compartments with limb flexion. motor deficits are late sign of irreversible muscle and nerve damage

A

limb compartment syndrome

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13
Q

also called shin splints. common cause of shin pain and diffuse tenderness in runners and military recruits. caused by bone resorption that outpaces bone formation in tibial cortex

A

medial tibial stress syndrome

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14
Q

inflammation of plantar aponeurosis characterized by hell pain (worse with first steps in the morning or after period inactivity) and tenderness.

A

plantar fasciitis

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15
Q

abnormal acetabulum development in newborns. result in hip instability/dislocation. commonly tested with ortolani and barlow maneuvers (reveal “clunk”)

confirmed via ultrasound (x-ray not used until 4-6 months because cartilage is not ossified)

treatment: splint/harness

A

developmental dysplasia of the hip

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16
Q

idiopathic avascular necrosis of femoral head. commonly presents between 5-7 years with insidious onst of hip pain that may cause child to limp. more common in males

initial xray is normal

A

Legg-Calve-Perthes disease

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17
Q

overuse injury casued by reptitive strain and chronic avulsion of secondary ossification center of proximal tibial tubercule. occurs in adolescents after growth spur.

common in running and jumping athletes. presents with progressive anterior knee pain

A
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18
Q

overuse injury that commonly presents in young, female athetes as anterior knee pain.

exaberbated by prologed sitting or weight-bearing on flexed knee.

Tx: NSAIDs, thigh muscle strengthening

A

patellofemoral syndrome

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19
Q

also called nursemaid’s elbow

common elbow injury in children <5 yo. caused by sudden pull on arm–> immature annular ligament slips over head of radius.

injured arm held in extended/slightly flexed and pronated position

A

radial head subluxation

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20
Q

classically present in an obese (12yo) child with hip/knee pain and altered gait. increased axial force on femoral head–> epiphysis displaces relative to femoral neck (like a scoop od ice cream slipping off a cone)

dx with xray and tx with surgery

A

slipped capital femoral epiphysis

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21
Q

incomplete fracture extending partway through width of bone following bending stress; bone fails on tension side; compression side intact (compar to torus fracture). bone is bent like a green twig

A

greenstick fracture

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22
Q

axial force applied to immature bone–> cortex buckles on compression (concave) side and fractures.

Tension (convex) side remains solid (intact)

A

torus (buckle) fracture

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23
Q

failure of longitudinal bone growth (endochondral ossification)–> short limbs, membransous ossification is not affected–> large head relative to limbs

constitutive activation of fibroblast growth factor (FGFR3) actually inhibits chroncyte proliferation. >85% of mutations occur sporadically; autosomal dominant with full penetrance (homozygosity is lethal)

associated with increase paternal age

most common cause of short limbed dwarfism

A

achondroplasia

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24
Q

trabecular (spongy) and cortical bone lose mass and interconnections despite normal bone mineralization and lab values (serum Ca and PO4)

most commonly due to increase bone resorption related to decreased estrogen and old age,

secondary to drugs (steroids, alcohol, anticonvulsantsm anticoagulant, thyroid replacement therapy)

other condition (hyperparathyroidism, hyperthyroidism, muliple myeloma, malabsorption syndrome)

DEXA at lumbar spine, total hip, femoral neck, with T score of < 2.5 or by fragility fractures. (fall from standing height, minimal trauma) at hip or vertebra.

one time screening recommended in women > 65 yo

Tx: bisphosphonate, teriparatide, SERMs, rarly calcitonin, denosumab (monoclonal antibody against RANKL

A
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25
Q

failure of normal bone resorption due to defective osteoclast–> thickened, dense bones that are prone to fracture, mutation (carbonic anhydrase 2) impair ability of osteoclast to generate acidic environment neccessary bone resorption. overgrowth of cortical bone fills marrow space–> pancytopenia, extramedullary hematopoeisis

can result in cranial nerve impingment and palsies due to narrowed foramina

xray- show diffuse symmeteric sclerosis (bone-in-bone) “stone bone”. bone marrow transplant is potentially curative as osteoclast ferived from monocytes

A

osteopetrosis

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26
Q

defective mineralization of osteoid (osteomalacia) or cartiliaginous growth plates (rickets)

most commonly due to vitamin D deficiency

xray: osteopenia and looser zones (psuedofractures) in osteomalacia. epiphyseal widening and metaphyseal cupping/fraying in rickets

childrens with rickets have pathologic bow legs, bead-like costochondral junctions (rachitic rosary), craniotabes (soft skull)

decrease vit D–> decrease Ca–> increase PTH secretion –> decrease serum PO4

hyperactivity of osteoblast–> increase alkaline phosphotases

A

osteomalacia/rickets

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27
Q

aka Paget disease of bone . common, localized disorder of bone remodeling caused by osteoclastic activity followed by increase osteoblastic activity that form poorly formed bones

serum Ca, phosphorus, and PTH levels are normal.

increase ALP

mosaic pattern of woven and lamellar bone (osteocytes within lacunae in choatic juxtapositions); long bones chalk-stick fractures. increase blood flow from increase arteriovenous shunt may cause high-output heart failure

increase risk of osteosarcoma

hat size can increased (skull thickening), hearing loss is common due to auditory foramen narrowing

stages of Paget disease:

Lytic-osteoclasts

mixed-osteoclast + osteoblast

sclerotic-osteoclast

quiescent-minimal osteoclast/osteoblast activity

tx with bisphosphonates

A

Osteitis deformans

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28
Q

avascular necrosis of bone

femoral head is the most common site of infarction (watershed zone ) due to insufficiency medial circumflex femoral artery)

corticosteroids, alcoholism, sickle cell, trauma, SLE, Legg-Clave-Perhes disease, Gaucher disease, slipped capital femoral epiphysis

A
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29
Q

components

Disorder, serum Ca, PO4, ALP, PTH, comments

Osteoporosis-same in all, decrease bone mass

osteopetrosis-decrease serum Ca or same, rest are the same, dense, brittle bone, Ca decrease in severe case, malignant disease

paget disease of bone- increase ALP, same in rest, abnormal “mosaic” bone architecture”

osteitis fibrosa cystica ( and primary hyperparathyroidism)-PO4 decrease, increase in rest, brown tumors due to fibrous replacement of bone, subperiosteal thinning

secondary hyperparathyroidism-decrease Ca, increase in rest, compensation for CKD (decrease PO4 excretion and production of activated vit D)

Osteomalacia/rickets- decrease in Ca and PO4, increased in rest, soft bones, vitamin D deficiency also causes secondary hyperparathyroidism

Hypervitaminosis D- increase Ca, PO4, decrease PTH, same ALP, caused by oversupplementation or granulomatous disease (sarcoidosis)

A

primary bone tumors (benign)

components in this order

Osteochondroma-most common in male <25yo, located: metaphysis of long bones characterized: lateral bony projection of growth plate (continous with marrow space) covered by cartilaginous cap. rarely transform to chondrosarcoma

Osteoma- middle age, located: surface of facial bones, characterized: associated with Gardner syndrome

Osteoid osteoma-adults <25, male > female located: cortex of long bones, characterized: presents as bone pain (worse at night) that relieved by NSAIDs, bony mass (<2cm) with radiolucent osteoid core

Osteoblastoma- male> female, located: Vertebrae, characterized: similar histolgy to osteoid osteoma. larger size (>2cm), pain unresponsive to NSAIDs

Chondroma-located in medulla of small bones of hand and feet, characterized by benign cartilage

giant cell tumor- 20-40 yo, located epiphysis of long bones (often in knee region), characterized: locally aggressive benign tumor. Neoplastic mononuclear cells that express RANKL and reactive multinucleated giant (osteoclast-like) cell “osteoclastoma. “soap bubble” apperance on xray

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30
Q

malignant tumors

osteosarcoma (osteogenic sarcoma) <20yo males, less common in elderly, located: metaphysis of long bones (often in knee region), characteristic: pleomorphic osteoid-producing cells (malignant osteoblasts), presnts as painful enlarging mass or pathologic fractures, Coman triangle (from elevated periosteum) or sunburnt pattern on xray.

predisposing factors: paget disease of bone, bone infarcts, radiation, familial retinoblastoma, Li-Fraumeni syndrome

Chondrosarcoma: located: medulla of pelvis, proximal femur and humerus, characterized: tumor of malignant chondrocytes

Ewing sarcoma-most common in caucasians. generally in boy < 15 years, located: diaphysis of long bones (femur), pelvic and flat bones, characterized: anaplastic small blue bells of neuroectodermal origin, t(11;22)-fusion of EWS-FLI1, onion-skin periosteal reaction in bone, aggressive with early metastatases

A

Osteoarthritis-mechanical -wear and tear destroys articular cartilage (degenerative joint disorder)–> inflammation with inadequate repair. Chondrocytes mediate degradation and inadequate repair, presentation: pain in weight-bearing joints after use (end of the day), improved with rest. asymmetrical joint involvement. knee cartilage loss begins medially (bowlegged) no systemic symtpoms, Joint finding: osteophytes (bone spurs) joint space narrowing subcondral sclerosis and cyst. synovial fluid noninflammatory (WBC < 2000) development of Heberden nodes-high, involves DIP, Bouchard nodes (below, involves PIP) and 1st CMC, not MCP, treatment: activity modification, acetaminophen, NSAIDs, intra-artcular glucocorticoids

predisposing: age, female, obesity, joint trauma

Rheumatoid arthritis- autoimmune inflammation induces formation of pannus (proliferative granulation tissue) which erodes articular cartilage and bone, presentation: erosion, juxta-articular osteopenia, soft tissue swelling, subchondra; cyst, joint space narrowing. deformities: cervial subluxation, ulnar finger deviation, swan neck, boutonniere-deformed position of the fingers or toes, in which the joint nearest the knuckle (the proximal interphalangeal joint, or PIP) is permanently bent toward the palm while the farthest joint (the distal interphalangeal joint, or DIP) is bent back away (PIP flexion with DIP hyperextension)., involves PIP, MCP, wrist, not DIP or CMC. synovial fluid inflammatory, Treatment: NSAIDs, steroids, methotrexate, sulfasalazine, hydroxyxhloroquine, leftunomide), biologic agent (TNF-alpha inhibitor)

predisposing: HLA-DR4, positive RF, symetrical joint involvement

extraarticular manifestation: rheumatoid nodules (fibrinoid necrosis with palisading histiocytes) in subcutaneous tissue and lung (positive pneumoconiosis–> Caplan syndrome) interstitial lung disease, pleuritis, pericarditis, anemia of chronic disease, neutropenia + spenomegaly (Felty syndrome) AA amyloidosis, Sjogren syndrome, scleritis, carpal tunnel syndrome

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31
Q

inflammation of monoarthritis caused by precipitation of monosodium urate crystal in joints

  1. underexcretion of uric acid-largely idiopathic, potentiated by renal failurem exacerbated by thiazide and diuretics

2. overproduction of uric acid: lesch-Nyhan syndrome, PRPP excess, increase cell turnover (tumor lysis syndrome, von Gierke disease

crystals are needle shaped and negative birefringent under polarized light (yellow under parallel light, blue under perpendicular light) serum uric acid can be normal in acute gout.

sx: asymmetric joint distribution, joint swollenm red, painful. (MTP of big toe aka podagra), tophus formation (in external ear, olcranon bursa, achilles tendon), attack tends to occur after large meals with food rich in purines (red meat and seafood), dehydration, alcohol consumption (alcohol competes for same excretion site as uric acid.

treatment with NSAIDs (indomethacin) , steroids, colchicine. chronic: preventive: xanthine oxidase inhibitor (allopurinol, febuxostat)

A

Gout

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32
Q

aka pseudogout. deposition of calcium pyrophosphate crystals within the joint space. occurs in patients > 50 yo; both sex affected equally

associated with hemochromatosis, hyperthhyroidism, joint trauma

pain and swelling with acute inflammation (pseudogout) and chronic degeneration (psuedo-osteoarthritis). knee most commonly affect joint

chondrocalcinosis (cartilage calcification) on xray

crystals are rhomboid and weakly positive birfringent under polarized light (blue when parallel to light)

acute treatment: NSAIDs, colchicine, steroids

prophylaxis: colchicine

A

calcium pyrophosphate deposition

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33
Q

systemic juvenile idiopathic arthritis

systemic arthritis seen in < 12 yo presents with daily feverm salmon-pink macular rashm arthritis (commonly 2+ joints) frequently presents with leukocytosism thrombocytosis, anemia : icnrease ESR, CRP,treatment: NSAIDs, steroids, methotreaxtae, TNF inhibitor

autoimmune disorder characterized by destruction of exocrine glands (especially lacrimal and salivary) by lymphocytic infiltrates

40-60yo

Findings:

ƒ. Inflammatory joint pain

ƒ. Keratoconjunctivitis sicca (tear production

and subsequent corneal damage)

ƒ. Xerostomia ( saliva production B )

ƒ. Presence of antinuclear antibodies,

rheumatoid factor (can be in the absence of

rheumatoid arthritis),

antiribonucleoprotein

antibodies: SS-A (anti-Ro) and/or SS-B (anti-

La)

ƒ. Bilateral parotid enlargement

Anti-SSA and anti-SSB may also be seen in

SLE. ⊕ Anti-SSA in pregnant women with

SLE –> increase risk of congenital heart block in the

newborn.

A common 1’ disorder or a 2’ syndrome

associated with other autoimmune disorders

(eg, rheumatoid arthritis, SLE, systemic sclerosis).

Complications: dental caries; mucosa-associated

lymphoid tissue (MALT) lymphoma (may

present as parotid enlargement).

Focal lymphocytic sialadenitis on labial salivary

gland biopsy can confirm diagnosis.

A

Septic arthritis

picture: A. lymphocytic infiltrates. B) xerostomia (decrease saliva production) –> mucosal atrophy, fissuring of the tongue

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34
Q

S aureus, Streptococcus, and Neisseria gonorrhoeae are common causes. Affected joint is swollen,

red, and painful. Synovial fluid purulent (WBC > 50,000/mm3).

Gonococcal arthritis—STI that presents as either purulent arthritis (eg, knee) or triad of

polyarthralgia, tenosynovitis (eg, hand), dermatitis (eg, pustules).

A

septic arthritis

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35
Q

Arthritis without rheumatoid factor (no anti-IgG antibody). Strong association with HLA-B27

(MHC class I serotype). Subtypes (PAIR ) share variable occurrence of inflammatory back

pain (associated with morning stiffness, improves with exercise), peripheral arthritis, enthesitis

(inflamed insertion sites of tendons, eg, Achilles), dactylitis (“sausage fingers”), uveitis.

  1. Psoriatic arthritis

2. Ankylosing spondylitis

3. Inflammatory bowel disease

4. Reactive arthritis

A

Psoriatic arthritis

Associated with skin psoriasis and nail lesions.

Asymmetric and patchy involvement A .

Dactylitis and “pencil-in-cup” deformity of

DIP on x-ray (C).

Ankylosing spondylitis

Symmetric involvement of spine and sacroiliac

joints –> ankylosis (joint fusion), uveitis, aortic

regurgitation.

Bamboo spine (vertebral fusion) (C) . Can cause restrictive lung disease due to limited chest wall expansion (costovertebral and costosternal ankylosis).

More common in males.

Inflammatory bowel disease

Crohn disease and ulcerative colitis are often

associated with spondyloarthritis.

Reactive arthritis Formerly known as Reiter syndrome.

Classic triad:

ƒ.Conjunctivitis

ƒ.Urethritis

ƒ. Arthritis

Shigella, Yersinia, Chlamydia, Campylobacter,

Salmonella (ShY ChiCS).

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36
Q

Systemic lupus erythematosus

Systemic, remitting, and relapsing autoimmune disease. Organ damage primarily due to a type III

hypersensitivity reaction and, to a lesser degree, a type II hypersensitivity reaction. Associated with

deficiency of early complement proteins (eg, C1q, C4, C2) –> decrease clearance of of immune complexes.

Classic presentation: rash, joint pain, and fever in a female of reproductive age (especially of

African-American or Hispanic descent).

A

Libman-Sacks Endocarditis—nonbacterial, verrucous thrombi usually on mitral or aortic valve and can be present on either surface of the valve (but usually on undersurface). LSE in SLE.

Lupus nephritis (glomerular deposition of DNA-anti-DNA immune complexes) can be nephritic or nephrotic (causing hematuria or

proteinuria). Most common and severe type is diffuse proliferative.

Common causes of death in SLE: Renal disease

(most common)

Rash (malar A or discoid B )

Arthritis (nonerosive)

Serositis (eg, pleuritis, pericarditis)

Hematologic disorders (eg, cytopenias)

Oral/nasopharyngeal ulcers (usually painless)

Renal disease

Photosensitivity

Antinuclear antibodies

Immunologic disorder (anti-dsDNA, anti-Sm,

antiphospholipid)

Neurologic disorders (eg, seizures, psychosis)

pregnancy with positive anti-SSA can have newborn with neonatal lupus (congenital heart block, periorbital/diffusion, rash, transaminitis, cytopenias at birth

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37
Q

1’ or ‘ autoimmune disorder (most commonly in SLE). Diagnose based on clinical criteria including

history of thrombosis (arterial or venous) or spontaneous abortion along with

laboratory findings of lupus anticoagulant,

anticardiolipin, anti-β2 glycoprotein antibodies.

Treat with systemic anticoagulation.

lupus anticoagulant

can cause prolonged PTT that is not corrected

by the addition of normal platelet-free plasma

A

antiphospholipid syndrome

38
Q

SYMPTOMS: Pain and stiffness in proximal muscles (eg, shoulders, hips), often with fever, malaise, weight loss.

Does not cause muscular weakness. More common in women > 50 years old; associated with

giant cell (temporal) arteritis.

FINDINGS : increased ESR, increase CRP, normal CK.

TREATMENT: Rapid response to low-dose corticosteroids

A

Polymyalgia rheumatic

39
Q

Most common in women 20–50 years old. Chronic, widespread musculoskeletal pain associated

with “tender points,” stiffness, paresthesias, poor sleep, fatigue, cognitive disturbance (“fibro

fog”). Treatment: regular exercise, antidepressants (TCAs, SNRIs), neuropathic pain agents (eg,

gabapentin).

A

fibromyalgia

40
Q

increased CK, ⊕ ANA (nonspecific), ⊕ anti-Jo-1 (histidyl-tRNA synthetase) (specific), ⊕ anti-SRP (specific), ⊕ anti-Mi-2 (specific) antibodies.

Both disorders associated with interstitial lung disease.

Treatment: steroids followed by long-term immunosuppressant therapy (eg, methotrexate).

Polymyositis: Progressive symmetric proximal muscle weakness, characterized by endomysial inflammation with CD8+ T cells. Most often involves shoulders.

dermatomyositis: Clinically similar to polymyositis, but also involves malar rash (similar to that in SLE but involves nasolabial folds), Gottron papules A , heliotrope (violaceous periorbital) rash B , “shawl and face” rash C , darkening and thickening of fingertips and sides resulting in irregular, “dirty”-appearing

marks. 

increase risk of occult malignancy. Perimysial inflammation and atrophy with CD4+ T cells.

A

Myastenia gravis- most common NMJ disorder due to autoantibodies to postsynatpic ACh receptor, clinical: ptosis, diplopia, weakness (respiratory muscle involvement–> dyspnea. bulbar muscles–> dysphagia, difficulty chewing), worse with muscle use. treatment: AChE inhbitor: reverse sx

associated with thymoma, thymic hyperplasia

Lambert-Eaton myastenic syndrome-uncommon, autoantibodies to presynaptic Ca channel to lower ACh release, clinical: proximal muscle weakness, autonomic symptoms (dry mouth, impotence) improves with muscle use

AChE inhibitor have miminal effects

associated with small cell lung cancer

41
Q

decreased blood flow to skin due to arteriolar (small vessel) vasospasm in response to cold or stress: color change from white (ischemia) to blue (hypoxia) to red (reperfusion). Most often in the

fingers (A) and toes. Called Raynaud disease when 1’ (idiopathic), Raynaud syndrome when 2’

to a disease process such as mixed connective tissue disease, SLE, or CREST syndrome (limited

form of systemic sclerosis). Digital ulceration (critical ischemia) seen in 2’ Raynaud syndrome.

Treat with Ca2+ channel blockers.

A

Raynaud phenomenon

42
Q

Triad of 1. autoimmunity, 2. noninflammatory vasculopathy, and 3. collagen deposition with fibrosis.

Commonly sclerosis of skin, manifesting as puffy, taut skin (A)without wrinkles, fingertip pitting

(B). Can involve other systems, eg, renal (scleroderma renal crisis; treat with ACE inhibitors),

pulmonary (interstitial fibrosis, pulmonary HTN), GI (esophageal dysmotility and reflux),

cardiovascular. 75% female. 2 major types:

ƒ. Diffuse scleroderma —widespread skin involvement, rapid progression, early visceral

involvement. Associated with anti-Scl-70 antibody (anti-DNA topoisomerase I antibody).

ƒ. Limited scleroderma —limited skin involvement confined to fingers and face. Also with CREST syndrome: Calcinosis cutis (C) , anti-Centromere antibody, Raynaud phenomenon,

Esophageal dysmotility, Sclerodactyly, and Telangiectasia. More benign clinical course.

A

scleroderma

43
Q

Skin has 3 layers: epidermis, dermis, subcutaneous fat (hypodermis, subcutis). Epidermis layers from surface to base A :

ƒ Stratum Corneum (keratin)

ƒ Stratum Lucidum (most prominent in palms and soles)

ƒ Stratum Granulosum

ƒ Stratum Spinosum (desmosomes)

ƒ Stratum Basale (stem cell site)

A

Tight junction (zonula occludens)—prevents paracellular movement of solutes; composed of claudins and occludins.

Adherens junction (belt desmosome, zonula adherens)—below tight junction, forms “belt” connecting actin cytoskeletons of adjacent cells with CADherins (Ca2+-dependent adhesion proteins ). Loss of E-cadherin promotes metastasis.

Desmosome (spot desmosome, macula adherens)—structural support via intermediate filament interactions . Autoantibodies to desmoglein  pemphigus vulgaris.

Gap junction—channel proteins called connexons permit electrical and chemical communication between cells.

Integrins—membrane proteins that maintain integrity of basolateral membrane by binding to collagen, laminin, and fibronectin in basement membrane.

Hemidesmosome—connects keratin in basal cells to underlying basement membrane. Autoantibodies  bullous pemphigoid. (Hemidesmosomes are down “bullow”).

44
Q

macules- flat lestion with well-circumscribed change in skin color <1cm (freckles, labial macule)

patch-macules >1 cm (large birthmark (congenital nevus)

papules- elevatd solid skin lesion < 1 cm (mole (nevus), acne)

plaque - papules > 1 cm (psoriasis)

vesicle - small fluid -caintaining blister < 1 cm (chickenpox (varicella), shingles (zoster)

bulla- large fluid-contain blister > 1 cm (Bullous pemphigoid)

pustule-vesicle containing pus (pustular psoriasis)

wheal- transient smooth papules or plaque (hives (urticaria)

scale- flaking off of stratum corneum (Eczema, psoriasis, SCC)

crust- dry exudate (impetigo)

A

hyperkeratosis- increase thickness of stratum corneum (psoriasis, callus)

parakeratosis- retention of nuclei in stratum corneum (Psoriasis)

hypergranulosis- increased thickness of stratum granulosum (Lichen planus)

spongiosis-epidermal accumulation of edematous fluid in intercellular spacs (Eczematous dermatitis)

achantholysis-separation of epidermal cells (pemphigus vulgaris)

acanthosis- epidermal hyperplasia (increase spinosum) (acanthosis nigricans)

45
Q

Normal melanocyte number with decreased melanin production due to decrease tyrosinase activity or defective tyrosine transport. increase risk of skin cancer.

A

albinism

46
Q

Hyperpigmentation associated with pregnancy (“mask of pregnancy” B ) or OCP use

A

melasma

47
Q

Irregular patches of complete depigmentation (C ). Caused by autoimmune destruction of melanocytes.

A

Vitiligo

48
Q

Erythematous, well-demarcated plaques with greasy yellow scales in areas rich in sebaceous glands, such as scalp, face, and periocular region. Common in both infants and adults, associated with Parkinson disease. Sebaceous glands are not inflamed, but play a role in disease development. Possibly associated with Malassezia spp.

Treat with topical antifungals and corticosteroids.

A

seborrheic dermatitis

49
Q

Multifactorial etiologyincreased sebum/androgen production, abnormal keratinocyte desquamation, Cutibacterium (formerly Propionibacterium) acnes colonization of the pilosebaceous unit (comedones), and inflammation (papules/pustules (A), nodules, cysts).

Treatment includes retinoids, benzoyl peroxide, and antibiotics.

A

Acne

50
Q

Pruritic eruption, commonly on skin flexures. Associated with other atopic diseases (asthma, allergic rhinitis, food allergies); increase serum IgE. Mutations in filaggrin gene predispose (via skin barrier dysfunction). Often appears on face in infancy and then in antecubital fossa in children and adults.

A

atopic dermatitis (eczema)

51
Q

Type IV hypersensitivity reaction that follows exposure to allergen. Lesions occur at site of contact (eg, nickel, poison ivy, neomycin).

A

Allergic contact dermatitis

52
Q

Common mole. Benign, but melanoma can arise in congenital or atypical moles. Intradermal nevi are papular. Junctional nevi are flat macules.

A

melanocytic nevus

53
Q

Foreign body inflammatory facial skin disorder characterized by firm, hyperpigmented papules and pustules that are painful and pruritic. Located on cheeks, jawline, and neck. Commonly occurs as a result of shaving (“razor bumps”), primarily affects African-American males.

A

Pseudofolliculitis barbae

54
Q

Papules and plaques with silvery scaling H, especially on knees and elbows. Acanthosis with parakeratotic scaling (nuclei still in stratum corneum), Munro microabscesses. increase stratum spinosum, decrease stratum granulosum. Auspitz sign ( I )—pinpoint bleeding spots from exposure of dermal papillae when scales are scraped off. Associated with nail pitting and psoriatic arthritis

A

Psoriasis

55
Q

Inflammatory facial skin disorder characterized by erythematous papules and pustules, but no comedones. May be associated with facial flushing in response to external stimuli (eg, alcohol, heat). Phymatous rosacea can cause rhinophyma (bulbous deformation of nose).

A

Rosacea

56
Q

Flat, greasy, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cysts). Looks “stuck on.” Lesions occur on head, trunk, and extremities. Common benign neoplasm of older persons. Leser-Trélat sign (L) —sudden appearance of multiple seborrheic keratoses, indicating an underlying malignancy (eg, GI, lymphoid).

A

Seborrheic keratosis

57
Q

Warts; caused by low-risk HPV strains. Soft, tan-colored, cauliflower-like papules (M). Epidermal hyperplasia, hyperkeratosis, koilocytosis. Condyloma acuminatum on anus or genitals (N).

A

Verrucae

58
Q

Hives. Pruritic wheals that form after mast cell degranulation O. Characterized by superficial dermal edema and lymphatic channel dilation.

A

urticaria

59
Q

Rare blood vessel malignancy typically occurring in the head, neck, and breast areas. Usually in elderly, on sun-exposed areas.

Associated with radiation therapy and chronic postmastectomy lymphedema. Hepatic angiosarcoma associated with vinyl chloride and arsenic exposures. Very aggressive and difficult to resect due to delay in diagnosis.

A

angiosarcoma

60
Q

Benign capillary skin papules found in AIDS patients. Caused by Bartonella infections. Frequently mistaken for Kaposi sarcoma, but has neutrophilic infiltrate.

A

bacillary angiomatosis

61
Q

Benign capillary hemangioma of the elderly . Does not regress. Frequency increase with age

A

cherry hemangioma

62
Q

Cavernous lymphangioma of the neck . Associated with Turner syndrome.

A

Cavernous lymphangioma

63
Q

Benign, painful, red-blue tumor, commonly under fingernails. Arises from modified smooth muscle cells of the thermoregulatory glomus body

A

glomus tumor

64
Q

Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Rarely mistaken for bacillary angiomatosis, but has lymphocytic infiltrate.

A

Kaposi sarcoma

65
Q

Polypoid lobulated capillary hemangioma (E) that can ulcerate and bleed. Associated with trauma and pregnancy.

A

Pyogenic granuloma

66
Q

Very superficial skin infection. Usually from S aureus or S pyogenes. Highly contagious. Honeycolored crusting. Bullous impetigo has bullae and is usually caused by S aureus

A

impetigo

67
Q

Infection involving upper dermis and superficial lymphatics, usually from S pyogenes. Presents with well-defined, raised demarcation between infected and normal skin.

A

Erysipelas

68
Q

Acute, painful, spreading infection of deeper dermis and subcutaneous tissues. Usually from S pyogenes or S aureus. Often starts with a break in skin from trauma or another infection.

A

Abscess

69
Q

Collection of pus from a walled-off infection within deeper layers of skin. Offending organism is almost always S aureus.

A

abscess

70
Q

Deeper tissue injury, usually from anaerobic bacteria or S pyogenes. Pain may be out of proportion to exam findings. Results in crepitus from methane and CO2 production. “Flesh-eating bacteria.” Causes bullae and a purple color to the skin. Surgical emergency

A

Necrotizing fasciitis

71
Q

Exotoxin destroys keratinocyte attachments in stratum granulosum only (vs toxic epidermal necrolysis, which destroys epidermal-dermal junction). Characterized by fever and generalized erythematous rash with sloughing of the upper layers of the epidermis that heals completely. ⊕ Nikolsky sign (separation of epidermis upon manual stroking of skin). Seen in newborns and children, adults with renal insufficiency.

A

Staphylococcal scaled skin syndrome

72
Q

Herpes virus infections (HSV1 and HSV2) of skin can occur anywhere from mucosal surfaces to normal skin. These include herpes labialis, herpes genitalis, herpetic whitlow (H) (finger).

A

Herpes

73
Q

Umbilicated papules single or, more often, multiple, rounded, dome-shaped, pink, waxy papules that are 2-5 mm (rarely up to 1.5 cm in the case of a giant molluscum) in diameter. contain a caseous plug.)(I) caused by a poxvirus. While frequently seen in children, it may be sexually transmitted in adults.

A

molluscum contagiosum

74
Q

Causes varicella (chickenpox) and zoster (shingles). Varicella presents with multiple crops of lesions in various stages from vesicles to crusts. Zoster is a reactivation of the virus in dermatomal distribution (unless it is disseminated).

A

Varicella Zoster virus

75
Q

Irregular, white, painless plaques on lateral tongue that cannot be scraped off (J) EBV mediated. Occurs in HIV-positive patients, organ transplant recipients.

Contrast with thrush (scrapable) and leukoplakia (precancerous).

A

Hairy leukoplakia

76
Q

Potentially fatal autoimmune skin disorder with IgG antibody against desmoglein (component of desmosomes, which connect keratinocytes in the stratum spinosum). Flaccid intraepidermal bullae (A) caused by acantholysis (separation of keratinocytes, resembling a “row of tombstones”); oral mucosa is also involved. Type II hypersensitivity reaction. Immunofluorescence reveals antibodies around epidermal cells in a reticular (net-like) pattern (B). Nikolsky sign ⊕.

A

pemphigus vulgaris

77
Q

Less severe than pemphigus vulgaris. Type II hypersensitivity reaction: involves IgG antibody against hemidesmosomes (epidermal basement membrane; antibodies are “bullow” the epidermis). Tense blisters (C) containing eosinophils affect skin but spare oral mucosa. Immunofluorescence reveals linear pattern at epidermal-dermal junction (D). Nikolsky sign ⊝.

A

Bullous pemphigus

78
Q

Pruritic papules, vesicles, and bullae (often found on elbows) (E). Deposits of IgA at tips of dermal papillae. Associated with celiac disease. Treatment: dapsone, gluten-free diet.

A

Dermatitis herpetiformis

79
Q

Associated with infections (eg, Mycoplasma pneumoniae, HSV), drugs (eg, sulfa drugs, β-lactams, phenytoin), cancers, autoimmune disease. Presents with multiple types of lesions—macules, papules, vesicles, target lesions (look like targets with multiple rings and dusky center showing epithelial disruption) (F).

A

Erythema multiforme

80
Q

Characterized by fever, bullae formation and necrosis, sloughing of skin at dermal-epidermal junction, high mortality rate. Typically 2 mucous membranes are involved, and targetoid skin lesions may appear, as seen in erythema multiforme.

Usually associated with adverse drug reaction. A more severe form of Stevens-Johnson syndrome (SJS) with > 30% of the body surface area involved is toxic epidermal necrolysis (I J) (TEN). 10–30% involvement denotes SJS-TEN

A

Steven Johnson syndrome

81
Q

Epidermal hyperplasia causing symmetric, hyperpigmented thickening of skin, especially in axilla or on neck. Associated with insulin resistance (eg, diabetes, obesity, Cushing syndrome), visceral malignancy (eg, gastric adenocarcinoma).

A

Acanthosis nigricans

82
Q

Premalignant lesions caused by sun exposure. Small, rough, erythematous or brownish papules or plaques (C D). Risk of squamous cell carcinoma is proportional to degree of epithelial dysplasia.

A

Actinic keratosis

83
Q

Painful, raised inflammatory lesions ofErythema Nodosum usually on anterior shin. Often idiopathic, but can be associated with sarcoidosis, coccidioidomycosis, histoplasmosis, TB, streptococcal infections (E) , leprosy (F) , inflammatory bowel disease.

A

Erythema Nodosum

84
Q

Pruritic, Purple, Polygonal Planar Papules and Plaques are the 6 P’s of lichen Planus (G H). Mucosal involvement manifests as Wickham striae (reticular white lines) and hypergranulosis. Sawtooth infiltrate of lymphocytes at dermal-epidermal junction. Associated with hepatitis C.

A

Lichen planus

85
Q

Herald patch” I followed days later by other scaly erythematous plaques, often in a “Christmas tree” distribution on trunk (J). Multiple pink plaques with collarette scale. Self-resolving in 6–8 weeks.

collarette scale-Fine scaling and central wrinkling, with a cigarette paper aspect, is usually present. A characteristic feature is the collarette appearance of the scale, with edges peripherally attached and lifted up near the center of the lesion.

A

Pityriasis

86
Q

Acute cutaneous inflammatory reaction due to excessive UV irradiation. Causes DNA mutations, inducing apoptosis of keratinocytes. UVB is dominant in sunBurn, UVA in tAnning and photoAging. Exposure to UVA and UVB

increase risk of skin cancer. Can also lead to impetigo.

A

sunburn

87
Q

1. -superficial, through epidermis (common sunburn) (painful, erythematous, blanching)

2. (partial-thickness burn through epidermis and dermis). skin is blistered and usually heals without scarring (painful, erythematous, blanching)

3. full-thickness burn through epidermis, dermis, and hypodermis , skin scars with woud healing (painless, waxy or leathery appearance nonblanching

A

first degree burn

second degree burn

third degree burn

88
Q

Most common skin cancer. Found in sun-exposed areas of body (eg, face). Locally invasive, but rarely metastasizes. Waxy, pink, pearly nodules, commonly with telangiectasias, rolled borders, central crusting or ulceration (A). BCCs also appear as nonhealing ulcers with infiltrating growth (B) or as a scaling plaque (superficial BCC) (C). Basal cell tumors have “palisading” nuclei (D.)

A

basal cell carcinoma

89
Q

Second most common skin cancer. Associated with excessive exposure to sunlight, immunosuppression, chronically draining sinuses, and occasionally arsenic exposure.

Commonly appears on face (E) , lower lip (F) , ears, hands. Locally invasive, may spread to lymph nodes, and will rarely metastasize. Ulcerative red lesions with frequent scale.

Histopathology: keratin “pearls” (G).

Actinic keratosis, a scaly plaque, is a precursor to squamous cell carcinoma. Keratoacanthoma is a variant that grows rapidly (4–6 weeks) and may regress spontaneously over

A

squamous cell carcinoma

90
Q

Common tumor with significant risk of metastasis. S-100 tumor marker. Associated with sunlight exposure and dysplastic nevi; fair-skinned persons are at increase risk.

Depth of tumor (Breslow thickness) correlates with risk of metastasis.

Look for the ABCDEs: Asymmetry, Border irregularity, Color variation, Diameter > 6 mm, and Evolution over time.

At least 4 different types of melanoma, including superficial

  1. spreading (I)
  2. nodular (J)
  3. lentigo maligna (K)
  4. acral lentiginous (highest prevalence in African-Americans and Asians) (L)

Often driven by activating mutation in BRAF kinase.

Primary treatment is excision with appropriately wide margins. Metastatic or unresectable melanoma in patients with BRAF V600E mutation may benefit from vemurafenib, a BRAF kinase inhibitor

A

melanoma