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USMLE First AID > musculoskeletal, skin, connective tissue-1st A > Flashcards

musculoskeletal, skin, connective tissue-1st A Flashcards

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USMLE® Step 1 flashcards
1
Q

Epidermis layers Cali Like Girls in String Bikinis

A

Surface to base 1. Stratum corneum (keratin) 2. Stratum lucidum 3. Stratum granulosum 4. Stratum Spinosum (=desmosomes) 5. Stratum basale (stem cell site)

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2
Q

Epidermal appendages Sebaceous gland

A

Holocrine secretion of sebum. Hair follicle

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3
Q

Epidermal appendages Eccrine gland

A

Secretes sweat. Found throughout body (Eccrine glands are Everywhere)

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4
Q

Epidermal appendages Apocrine gland

A

Secretes milky viscous fluid. Found in axillae, genitalia, atrial. Does not become functional until puberty. Malodorous because of bacteria action

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5
Q

Epithelial cell junctions Tight junction

A

Zonula occludens- prevent paracellular movement of solutes; composed of claudins and occludins.

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6
Q

Epithelial cell junctions Adherens junction

A

Zonula adherens- below tight junction, forms belt connecting actin cytoskeleton of adjacent cells with CADherins (Ca2+ dependent ADhesion proteins). Loss of E-cadherin promotes metastasis.

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7
Q

Epithelial cell junctions Desmosomes

A

Macula adherens- structural support via keratin interactions. Autoantibodies—>pemphigus vulgaris

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8
Q

Epithelial cell junctions Gap junction

A

Channel protein called connexons permit electrical and chemical communication between cells.

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9
Q

Epithelial cell junctions Hemidesmosome

A

Connect keratin in basal cells to underlying basement membrane. Autoantibodies–>BULLOus pemphigoid. (Hemidesmosomes are down BULLOw

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10
Q

Epithelial cell junctions Integrins

A

Membrane proteins that maintain integrity of basement membrane by binding to laminin in BM

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11
Q

Unhappy triad/knee injury Common injury in contact sports

A

Lateral force applied to a planted leg. Triad includes tear: ACL, MCL, Meniscus (classically medial but lateral more common). Requires surgical ACL reconstruction. Anterior & posterior in ACL & PCL= sites of tibial attachment Positive anterior drawer sign=ACL tear Abnormal passive abduction=MCL tear

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12
Q

Clinically important landmarks Pudendal nerve block Appendix Lumbar puncture

A
  1. (Relieve pain of delivery) at ischial spine 2. 2/3 way from umbilicus to anterior superior iliac spine (McBurney’s point) 3. Iliac crest
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13
Q

Rotator cuff muscles in shoulder SItS (small t is for teres minor)

A
  1. Supraspinatus-abducts arm initially (before deltoid); most common rotator cuff injury 2. Infraspinatus-laterally rotates arm; pitching injury 3. Teres minor-adducts & laterally rotates arm 4. Subscapularis-medially rotates & adducts arm Innervates by C5-6
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14
Q

Wrist bones: So Long To Pinky, Here Comes The Thumb. 1. Which is commonly fractured? 2. What causes acute carpal tunnel syndrome? 3. What is carpal tunnel syndrome?

A

Scaphoid Lunate Triquetrium Pisiform Hamate Capitate Trapezoid Trapezium 1.Scaphoid most commonly fractured carpal -prone to avascular necrosis owing to retrograde blood supply. 2.Dislocate of lunate. 3. Entrapment of median nerve in carpal tunnel; nerve compression–> paresthesia, pain, and numbness in distribution of median nerve

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15
Q

Upper extremity innervation routes and common lesions 1.upper trunk 2. Axillary nerve 3. C7 root 4. Lower trunk of brachial plexus 5. Radial nerve in spiral groove 6. Radial nerve 7. Median nerve near elbow 8. Ulnar nerve near elbow 9. Radial nerve (deep branch) 10. Anterior interosseous nerve 11. Median nerve near wrist 12. Ulnar nerve near wrist 13. Recurrent branch of median nerve

A

1.upper trunk-lesioned by trauma 2. Axillary nerve-lesioned by fracture of surgical neck; dislocation of humerus; intramuscular injections 3. C7 root-compressed by cervical disk lesion 4. Lower trunk of brachial plexus-compressed by cervical rib or Pancoast tumor of lung; leads to Klumpke’s palsy 5. Radial nerve in spiral groove- lesioned by midshalft fracture humerus 6. Radial nerve-compressed in axilla by incorrect use of a crutch 7. Median nerve near elbow-compressed by supracondylar fracture of humerus; pronator teres syndrome 8. Ulnar nerve near elbow-lesioned by repeat minor trauma; fracture of medial epicondyle of humerus 9. Radial nerve (deep branch)-stretchde by subluxation of radius 10. Anterior interosseous nerve-compressed in deep forearm 11. Median nerve near wrist-compressed in carpal tunnel syndrome and by dislocated lunate 12. Ulnar nerve near wrist-lesioned by trauma to hell of hand; fracture of hook of hamate 13. Recurrent branch of median nerve-lesioned by superficial laceration

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16
Q

Upper extremity nerves: Axillary C5-C6 1. typical injury 2. motor deficit 3. sensory deficit 4. sign

A
  1. typical injury-fractured surgical neck of humerus, dislocation of humeral head 2. motor deficit- deltoid: arm abduction at shoulder 3. sensory deficit- over deltoid muscle 4. sign- atrophied deltoid consider lesion location; generally muscles innervated by nerve branches distal to lesions will be affected.
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17
Q

Upper extremity nerves: Radial C5-T1 1. typical injury 2. motor deficit 3. sensory deficit 4. sign

A
  1. typical injury- fracture at midshaft of humerus; saturday night palsy (extended compression of acilla by back of chair or crutched) 2. motor deficit- BEST extensor Brachioradialis Extensors of wrist & fingers Supinator Triceps 3. sensory deficit- posterior arm and dorsal hand & thumb 4. sign- wrist drop consider lesion location; generally muscles innervated by nerve branches distal to lesions will be affected.
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18
Q

Upper extremity nerves: Median C5-C8, T1 1. typical injury 2. motor deficit 3. sensory deficit 4. sign

A
  1. typical injury-fracture of supracondylar humerus (proximal lesion) 2. motor deficit- opposition of thumb, lateral finger flexion, wrist flexion 3. sensory deficit- dorsal & palmar aspects of lateral 3.5 fingers, thenar eminence 4. sign- ape hand; Pope’s blessing (hand) consider lesion location; generally muscles innervated by nerve branches distal to lesions will be affected.
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19
Q

Upper extremity nerves: Ulnar C8, T1 1. typical injury 2. motor deficit 3. sensory deficit 4. sign

A
  1. typical injury- fracture of medial epicondyle of humerus, “funny bone” (proximal lesion) 2. motor deficit- medial finger flexion, wrist flexion 3. sensory deficit- medial 1.5 fingers, hypothenar eminence 4. sign- radial deviation of wrist upon wrist flexion consider lesion location; generally muscles innervated by nerve branches distal to lesions will be affected.
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20
Q

Upper extremity nerves: Musculocutaneous C5-C7 1. typical injury 2. motor deficit 3. sensory deficit 4. sign

A
  1. typical injury- upper trunk compression 2. motor deficit- biceps, brachialis, coracobrachialis, flexion of arm at elbow 3. sensory deficit- lateral forearm 4. sign consider lesion location; generally muscles innervated by nerve branches distal to lesions will be affected.
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21
Q

Erb-Duchenne palsy (waiter’s tip appearance of the arm)

A

traction or tear of upper trunk of the brachial plexus (C5-6 roots); seen in infants following trauma during delivery. Findings: -limb hangs by side (paralysis of abductors), -medially rotated (paralysis of lateral rotators), -forearm is protonated (loss of biceps)

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22
Q

Klumpke’s palsy & thoracic outlet syndrome

A

An embryologic or childbirth defect affecting inferior trunk of brachial plexus (C8, T1); A cervical rib can compress subclavian artery & inferior trunk, resulting in thoracic outlet syndrome: -atrophy of the thenar & hypothenar eminences -atrophy of the interosseous muscles -sensory deficits on the medial side of the forearm & hand -disappearance of the radial pulse upon moving the head toward the ipsilateral side

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23
Q

What joints are involve in distortions of the hand (3)

A

Clawing is easily conceptualized as loss of the lumbricals, which flex the MCP joints nad extend both the DIP & PIP joints.

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24
Q

Distortion of hand: Ulnar claw -cause -nerve lesion -Inability

A

1.Can be caused by long-standing injury to ulnar nerve at hook of hamate (falling onto outstretched hand) 2. distal ulnar nerve lesion–>loss of medial lumbrical function–> 3. inability to extend 4th & 5th digits when trying to open hand.

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25
Q

Distortion of hand: median claw -cause -nerve lesion -Inability

A
  1. can be caused by carpal tunnel syndrome or dislocated lunate 2. distal median nerve lesion (after branch containing C5-C7 branches off to feed forearm flexors)–>loss of lateral lumbrical function 3. 2nd & 3rd digits are clawed upon attempted finger extension
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26
Q

Distortion of hand: pope’s blessing -cause -nerve lesion -Inability

A
  1. proximal median nerve lesion causes loss of lateral finger flexion and thumb opposition. When asked to make fist, 2nd & 3rd digit remain extended and thumb ramains unopposed, which looks like the hand of benediction or Pope’s blessing.
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27
Q

Distortion of hand: Ape hand -cause -nerve lesion -Inability

A

Proximal median nerve lesion–>loss of opponens pollicis muscle function–>unopposed thumb (inability to abduct thumb), hence “ape hand”

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28
Q

Distortion of hand: Klumpke’s total claw -cause -nerve lesion -Inability

A

Lesion of lower trunk (C8, T1) of brachial plexus–>loss of function of all lumbricals; forearm finger flexors (fed by part of median nerve with C5-C7) and finger extensors (fed by radial nerve) are unopposed–>clawing of all digits.

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29
Q

Long thoracic nerve (C5-C7) serratus anterior -anchors -functions -injury

A
  1. anchors scapula to thoracic cage 2. used for abduction above horizontal position. 3. injured in mastectomy–>einged scapula and ipsilateral lymphedema
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30
Q

5 Hand muscles

A

1 & #2= both group perform same function Oppose, Abduct, Flex (OAF) 1. Thenar (median-thumb area) -Opponens pollicis -Abductor pollicis brevis -Flexor pollicis brevis 2. Hypothenar (ulnar) -Opponens digiti minimi -Abductor digiti minimi -flexor digiti minimi 3. DAB= dorsals ABduct -Dorsal interosseous muscles (abduct fingers) 4. PAD= Palmars ADduct -Pamar interosseous muscles (adduct the fingers) 5. Lumbrical muscles-flex at the MCP joint, extend PIP & DIP joints

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31
Q

Lower Extremity nerves: -Obturator n. -cause of injury -motor deficit -sensory deficit

A
  1. L2-L4 2. anterior hip dislocation 3. thigh adduction 4. medial thigh
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32
Q

Lower Extremity nerves: -Femoral n. -cause of injury -motor deficit -sensory deficit

A
  1. L2-L4 2. pelvic fracture 3. thigh flexion & leg extension 4. anterior thigh & medial leg
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33
Q

Lower Extremity nerves: -Common peroneal n. -cause of injury -motor deficit -sensory deficit

A

PED= Peroneal Everts & Dorsiflexes; if injured, foor dropPED 1. L4-S2 2. trauma or compression of lateral aspect of leg or fibula neck fracture 3. foor eversion & dorsiflexion; toe extension; foot drop, foot slap, steppage gait 4. anterolateral leg & dorsal aspect of foot

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34
Q

Lower Extremity nerves: -tibial n. -cause of injury -motor deficit -sensory deficit

A

TIP=Tibial Inverts & Plantarflexes; if injured, can’t stand on TIPtoes 1. L4-S3 2. knee trauma 3. foot inversion & plantarflexion; toe flexion 4. sole of foot

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35
Q

Lower Extremity nerves: -superior gluteal n. -cause of injury -motor deficit -sensory deficit

A

1.L4-S1 2.posterior hip dislocation or polio 3. thigh abduction (positive Trendelenburg sign-contralateral hip drops when standing on leg ipsilateral to site of lesion)

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36
Q

Lower Extremity nerves: -inferior gluteal n. -cause of injury -motor deficit -sensory deficit

A
  1. L5-S2 2. posterior hip dislocation 3. can’t jump, climb stairs, or rise from seated position; can’t push inferiorly (downward)
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37
Q

Lower Extremity nerve -Sciatic nerve -location -splits into (2 nerves)

A
  1. L4-S3 2. posterior thigh 3. common peroneal & tibial nerve
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38
Q

Muscle contraction steps (6)

A
  1. AP depolarization opens presynaptic voltage-gated Ca2+ channels, inducing neurotransmitter release 2. Postsynaptic ligand binding leads to muscle cell depolarization in motor end plate 3. Depolarization travels along muslce cell and down the T tubule 4. Depolarization of voltage-sensitive dihydropyridine receptor, mechanically coupled to the ryanodine receptor on the sarcoplasmic reticulum, induces a conformational change causing Ca2+ release from sarcoplasmic reticulum. 5. released ca2+ binds to troponin C, causing a conformational change that moves tropomyosin out of the myosin-binding groove on actin filaments 6. Myosin releases bound ADP and is displaced on the actin filament (power stroke). Contraction results in shortening of H and I bands and between Z lines (HIZ shrinkage), but the A band remains the same length (A band is Always the same).
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39
Q

Types of muscle fibers Type 1 m.

A

SLOW twitch; RED fibers resulting from increase mitochondria & myoglobin concentration (increase oxidation phosphorylation)–>sustained contraction think “1 slow red ox”

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40
Q

Types of muscle fibers Type 2 m.

A

Fast twitch; white fibers resulting from decrease mitochondria & myoglobin concentration (increase anaerobic glycolysis); weight training results in hypertrophy of fast-twitch muscle fibers

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41
Q

Bone formation: Endochondral ossification

A

Bones of axial & appendicular skeleton, and base of the skull. Cartilaginous model of bone is first made by chondrocytes. Osteoclasts & osteoblasts later replace with woven bone and then remodel to lamellar bone. IN adults, woven bone occurs after fractures and in Paget’s disease

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42
Q

Bone formation: Membraneous ossification

A

bones of calvarium & facial bones. Womeven bone formed directly without cartilage. Later remodled to lamellar bone.

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43
Q

Cell biology of bone: Osteoblasts

A

build bone by secreting collagen and catalyzing mineralization. Differentiate from mesenchymal stem cells in periosteum.

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44
Q

Cell biology of bone: Osteoclasts

A

Multinucleated cells that dissolve bone by secreting acid and collagenases. Differentiate from monocytes/macrophages

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45
Q

Cell biology of bone: Parathyroid hormone

A

At low, intermittent levels, exerts anabolic effects (building bone) on osteoblasts & osteoclasts (indirect). Chronic high PTH levels (primary hyperparathyroidism) can cause catabolic effects (osteitis fibrosa cystica)

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46
Q

Cell biology of bone: Estrogen

A

Estrogen inhibits apoptosis in bone-forming osteoblasts and induces apoptosis in bone-resorbing osteoclasts. Under estrogen deficiency (surgical or postmenopausal), excess remodeling cylces and bone ressorption lead to osteoporosis.

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47
Q

What is achondroplasia

A

failure of longitudinal bone growth (endochondral ossification)–>short limbs. membraneous ossification is not affected–>large head relative to limbs. constituive activation of fibroblast growth factor receptor (FGFR3) actually inhibits chondrocyte proliferation. >85% of mutation occur sporadically and are associated with advanced paternal age, but the condition also demonstrates autosomal-dominant inheritance. common cause of dwarfism. Normal life span & fertility.

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48
Q

What is osteoporosis?

A

Trabecular (spongy) bone loses mass & interconnections despite normal bone mineralization & lab values (serum Ca2+ & PO4/3-. Can lead to vertebral crush fractures-acute back pain, loss of height, kyphosis

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49
Q

Osteoporosis Type I -postmenopausal -result

A

-Postmenopausal: increase bone resorption due to decrease estrogen levels -femoral neck fracture, distal radius (Colles’) fractures

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50
Q

Osteoporosis Type II -senile osteoporosis -prophylaxis -treatment

A

-senile osteoporosis: affects men & women > 70 yo -prophylaxis: regular weight-bearing exercise & adequate calcium & vit D intake throughtout adulthood -treatment: estrogen (SERMs) &/or calcitonin; biphosphonates or pulsatile PTH for severe cases. Glucocorticoids are contraindicated.

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51
Q

Osteoporosis Marble bone disease

A

-Failure of normal bone resorption due to defective osteoclasts–> kened, dense bones that are prone to fracture. -Bone fills marrow space, causing pancytopenia, extramedullary hematopoiesis -mutation (e.g., carbonic anhydrase II) impair ability of osteoclast to generate acidic environment necessary for bone resorption. -X-rays show bone-in-bone appearance. -Can result in cranial nerve impingement & palsies as a result of narrowed foramina. -Bone marrow transplant is potentially curative as osteoclasts are derived from monocytes

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52
Q

Osteomalacia/rickets

A

-Vit D deficiency -Osteomalacia in adults/ rickets in children -Defective mineralization/calcification of osteoid–>soft bones that bow out -decrease vit D–> decrease serum calcium–>increase PTH secretion–>decreasenserum phosphate. -Hyperactivity osteoblasts–>increase alkaline phosphate (osteoblasts require alkaline environment.

53
Q

Paget’s disease of bone Osteitis deformans

A

Common, localized disorder of bone remodleing caused by increase in both osteoblastic & osteoclastic activity. -serum calcium, phosphorus, PTH levels normal -increase ALP -Mosaic (woven) bone pattern; long chalk stick fractures -increase blood flow from increase arteriovenous shunts may cause high-output heart failure. -increase risk of osteogenic sarcoma -hat size can be increase; hearing loss is common due to auditory foramen narrowing

54
Q

Lab values in bone disorders: Serum Ca2+/ Phosphate/ ALP/ PTH/ Comments Osteoporosis Osteopetrosis Osteomalacia/ rickets Osteitis fibrosa cystica Paget’s disease

A

Serum Ca2+/ Phosphate/ ALP/ PTH/ Comment Osteoporosis - / - / - / -/ de bone mass Osteopetrosis de/ - / in/ - / thickened, dense bone Osteomalacia/ de/ de/ in/ in/ soft bones rickets Osteitis fibrosa in/ de/ in/ in/ brown tumors of hyperparathyroidism cystica Paget’s disease -/ - /in/ - / abnormal bone architecture

55
Q

Polyostotic fibrous dysplasia

A

-Bone is replaced by fibroplasts, collagen, irregular bony trabeculae. -McCune-Albright syndrome is a form of polyostotic fibrous dysplasia characterized by multiple unilateral bone lesions associated with endocrine abnormalities (precocius puberty) and cafe-au-lait spots

56
Q

Primary bone tumors: Giant cell tumor (osteoclastoma) -epidemiology/location -characteristics -benign/malignant

A
  1. 20-40 yo. Epiphyseal end of long bones 2. - locally aggressive benign tumor often around the distal femur, proximal tibial region (knee). - “Double bubble” or “soap bubble” appearance on x-ray. -spindle-shaped cells with multinucleated giant cells 3. benign
57
Q

Primary bone tumors: Osteochondroma (exostosis) -epidemiology/location -characteristics -benign/malignant

A
  1. males <25 yo. most common benign tumor. 2. mature bone with cartilaginous cap. Commonly originates from long metaphysis. Malignant transformation to chondrosarcoma is rare. 3. benign
58
Q

Primary bone tumors: Osteosarcoma (osteogenic sarcoma) -epidemiology/location -characteristics -benign/malignant

A
  1. 2nd most common primary malignant bone tumor (after multiple myeloma) -male>female, 10-20 yo for primary -predisposing factors: Paget’s disease of bone, bone infarcts, radiation, familial retinoblastoma -metaphysis of long bones, often around distal femur, proximal tibial region (knee) 2. Codman’s triangle (from elevation of periosteum) or sunburst pattern on x-ray. Aggressive. Treat with surgical en bloc resection (with limb salvage) and chemotherapy. 3. malignant
59
Q

Primary bone tumors: Ewing’s sarcoma -epidemiology/location -characteristics -benign/malignant

A
  1. Boys s jersey number) 3. malignant
60
Q

Primary bone tumors: Chondrosarcoma -epidemiology/location -characteristics -benign/malignant

A
  1. men 30-60 yo. usually located in pelvis, spine, scapula, humerus, tibia, femur 2. malignant cartilaginous tumor. -May be of primary origin or from osteochondroma -expansile glistening mass within the medullary cavity 3. malignant
61
Q

Osteoarthritis & rheumatoid arthritis Osteoarthritis -etiology -joint findings -predisposing factors -classic presentation -treatment

A

-etiology: mechanical-joint wear & tear destroys articular cartilage -joint findings: subchondral cysts, - sclerosis, -osteophytes (bone spurs) -eburnation (polished, ivory-like appearance of bone -Heberden’s nodes (DIP) -Bouchard’s nodes (PIP) -no MCP involvement -predisposing factors: age, obesity, joint deformity -classic presentation: pain in weight bearing joints after use (eg. at the end of the day), improving with rest. Knee cartilage loss begins medially (bowlegged). Noninflammatory. NO systemic symptoms -treatment: NSAIDS, intra-articular glucocorticoids

62
Q

Osteoarthritis & rheumatoid arthritis Rheumatoid arthritis -etiology -joint findings -predisposing factors -classic presentation -treatment

A

-etiology: autoimmune-inflammatory destruction of synovial joints. Type III hypersensitivity -joint findings: pannus formation in joints (MCP, PIP) -subcutaneous rheumatoid nodules (fibrinoid necrosis) -ulnar deviation of fingers -subluxation -Baker’s cyst (in popliteal fossa) -NO DIP involvement -predisposing factors: xx>xy. 80% have positive rheumatoid factor (anti-IgG antibody); anti-cyclic citrullinated peptide antibody is more specific. Strong association with HLA-DR4 -classic presentation: -morning stiffness lasting > 30 min and improving with use, symmetric joint involvement, systematic symptoms (fever, fatigue, pleuritis, pericarditis) -treatment: NSAIDS, glucocorticoids, disease-modifying agents (methotrexate, sulfasalazine, TNF,-alpha inhibitors)

63
Q

Lab values in bone disorders: Serum Ca2+/ Phosphate/ ALP/ PTH/ Comments Osteoporosis Osteopetrosis Osteomalacia/ rickets Osteitis fibrosa cystica Paget’s disease

A

Serum Ca2+/ Phosphate/ ALP/ PTH/ Comment Osteoporosis - / - / - / -/ de bone mass Osteopetrosis de/ - / in/ - / thickened, dense bone Osteomalacia/ de/ de/ in/ in/ soft bones rickets Osteitis fibrosa in/ de/ in/ in/ brown tumors of hyperparathyroidism cystica Paget’s disease -/ - /in/ - / abnormal bone architecture

64
Q

Polyostotic fibrous dysplasia

A

-Bone is replaced by fibroplasts, collagen, irregular bony trabeculae. -McCune-Albright syndrome is a form of polyostotic fibrous dysplasia characterized by multiple unilateral bone lesions associated with endocrine abnormalities (precocius puberty) and cafe-au-lait spots

65
Q

Primary bone tumors: Giant cell tumor (osteoclastoma) -epidemiology/location -characteristics -benign/malignant

A
  1. 20-40 yo. Epiphyseal end of long bones 2. - locally aggressive benign tumor often around the distal femur, proximal tibial region (knee). - “Double bubble” or “soap bubble” appearance on x-ray. -spindle-shaped cells with multinucleated giant cells 3. benign
66
Q

Primary bone tumors: Osteochondroma (exostosis) -epidemiology/location -characteristics -benign/malignant

A
  1. males <25 yo. most common benign tumor. 2. mature bone with cartilaginous cap. Commonly originates from long metaphysis. Malignant transformation to chondrosarcoma is rare.
67
Q

Primary bone tumors: Osteosarcoma (osteogenic sarcoma) -epidemiology/location -characteristics -benign/malignant

A
  1. 2nd most common primary malignant bone tumor (after multiple myeloma) -male>female, 10-20 yo for primary -predisposing factors: Paget’s disease of bone, bone infarcts, radiation, familial retinoblastoma -metaphysis of long bones, often around distal femur, proximal tibial region (knee) 2. Codman’s triangle (from elevation of periosteum) or sunburst pattern on x-ray. Aggressive. Treat with surgical en bloc resection (with limb salvage) and chemotherapy. 3. malignant
68
Q

Primary bone tumors: Ewing’s sarcoma -epidemiology/location -characteristics -benign/malignant

A
  1. Boys s jersey number) 3. malignant
69
Q

Primary bone tumors: Chondrosarcoma -epidemiology/location -characteristics -benign/malignant

A
  1. men 30-60 yo. usually located in pelvis, spine, scapula, humerus, tibia, femur 2. malignant cartilaginous tumor. -May be of primary origin or from osteochondroma -expansile glistening mass within the medullary cavity 3. malignant
70
Q

Osteoarthritis & rheumatoid arthritis Rheumatoid arthritis -etiology -joint findings -predisposing factors -classic presentation -treatment

A

-etiology: autoimmune-inflammatory destruction of synovial joints. Type III hypersensitivity -joint findings: pannus formation in joints (MCP, PIP) -subcutaneous rheumatoid nodules (fibrinoid necrosis) -ulnar deviation of fingers -subluxation -Baker’s cyst (in popliteal fossa) -NO DIP involvement -predisposing factors: xx>xy. 80% have positive rheumatoid factor (anti-IgG antibody); anti-cyclic citrullinated peptide antibody is more specific. Strong association with HLA-DR4 -classic presentation: -morning stiffness lasting > 30 min and improving with use, symmetric joint involvement, systematic symptoms (fever, fatigue, pleuritis, pericarditis) -treatment: NSAIDS, glucocorticoids, disease-modifying agents (methotrexate, sulfasalazine, TNF,-alpha inhibitors)

71
Q

Sjogren’s syndrome

A

-lymphocutic infiltration of exocrine glands, especially lacrimal & salivary -classic triad: -xerophthalmia (dry eye, conjunctivitis, “sand in eyes” -xerostomia (dry mouth, dysphagia) -Arthritis -Paratid enlargement, increase risk of B cell lymphoma, dental caries. -Autoantibodies to ribonucleoprotein antigens: SS-A (Ro), SS-B (La) -predominantly affects females btw 40-60 yo -associated with rheumatoid arthritis

72
Q

Gouts: 1. findings: 2. symptoms: 3. treatments:

A
  1. findings: -precipitation of monosodium urate crystals into joints due to hyperuricemia, which can be caused by Lesch-Nyhan syndrome -PRPP excess -decrease excretion of uric acid (eg. thiazide diuretics) -increae cell turnover or von Gierke’s disease -90% due to underexcretion -10% due to overproduction -crystals are needle shaped and negatively birefringent=yellow crystals under parallel light. -more common in men 2. symptoms: -asymmetric joint distribution -joint swollen, red, painful -classic manifestation is painful MTP joint of big toe (podagra) -Tophus formation (often on external ear, olecranon bursa/Achilles tendon) -acute attack tends to occur after a large meal or alcohol consumption (alcohol metabolites compete for same excretion sites in kidney as uric acid, causing decrease uric acid secretion and subsequent buildup in blood. 3. Treatment: -Acute: NSAODS (indomethacin); glucocorticoids -chonric: xanthine oxidase inhibitors (allopurinol, febuxostat)
73
Q

Pseudogout

A

-Caused by deposition of calcium pyrophosphate crystals within the joint space. -forms basophilic rhomboid crystals that are weakly positively birefringent. 0usually affects large joints (classically the knee) ->50 yo, both sexes equally -treatment: NSAIDS for sudden severe attacks; steroids, colchicine -Gout: crystals are yellow when parallel to light -pseudogout: crystals are blue when parallel to light

74
Q

Infectious arthritis

A

S. aureus, Streptococcus, Neisseria gonorrhoeae are common causes -goncoccal srthritis is an STD that presents as a migratory arthritis with anasymmetric pattern -affected joint is swollen, red, painful *STD= Synovitis (knee), Tenosynovitis (hand), Dermatitis (pustules)

75
Q

Osteonecrosis (avascular necrosis)

A

infarction of bone & marrow. Pain associated with activity. -Caused by trauma, high-dose corticosteroids, alcoholism, sickle cell. -most common site is femoral head

76
Q

seronegative spondyloarthropathies: P.A.I.R.

A

-arthritis w/o rheumatoid factor (no anti-IgG antibody) -strong association with HLA-B27 (gene that codes for HLA MHC class I) -occurs more often in males

77
Q

seronegative spondyloarthropathies: Psoriatic arthritis:

A

-joint pain & stiffness associated with psoriasis -asymmetric & patchy involvement -dactylitis (sauge gingers) -pencil in cup deformity on x-ray. seen in fewer than 1/3 of patients with psoriasis

78
Q

seronegative spondyloarthropathies: Ankylosing spondylitis

A

-chronic inflammatory disease of spine & sacroiliac joints–>ankylosis (stiff spine due to fusion of joints), uveitis, aortic regurgitation -bamboo spine (vertebral fusion)

79
Q

Inflammatory Bowel Disease

A

Crohn’s disease & ulcerative colitis are often accompanied by anklyosing spondylitis or peripheral arthritis.

80
Q

Reactive arthritis (Reiter’s syndrome)

A

Classic triad: -Conjunctivitis & anterior uveitis -Urethritis -arthritis * Can’t see, can’t pee, can’t climb a tree post-GI or chlamydia infection

81
Q

Systemic Lupus erthematosus “I’M DAMN SHARP”

A

-90% XX; 14-45 yo -most common & severe in black females -presentation can include fever, fatigue, weight loss, Libman-Sacks endocarditis (verrucous, wart-like, sterile vegetation on both sides of valve), hilar adenopahty, Raynaud’s phenomenon -Nephritis common cause of death in SLE. Difficult proliferative glomerulonephritis (if nephretic); membranous glomerulonephritis (if nephrotic) -False positives on syphilis tests (RPR/VDRL) due to antiphospholipid antibodies, which cross-react with cardiolipin used in tests. -lab tests detect presence of: -antinuclear antibodies (ANA)-sensitive (primary screening) but not specific for SLE -antibodies to double-stranded DNA (anti-dsDNA)-very specific, poor prognosis -anti-Smoth antibodies (anti-Sm)-very specific, but not prognostic -antihistone antibodies-more sensitive for drug-induced lupus -Immunoglobulin (anti-dsDNA, anti-Sm, antiphospholipid -Malar rash -Discoid rash -Antinuclear antibody -Mucositis (oropharyngeal ulcers) -Neurologic disorders -Serositis (pleuritis, pericarditis) -Hematologic disorders -Arthritis -Renal disorders -Photosensitivity

82
Q

Sarcoidosis

A

-characterized by immune-mediated, widespread noncaseating granulomas and elevated serum ACE levels -common in black females -often asymptomatic except for enlarged lymph node -incidental finding on CXR of bilateral hilar adenopathy or reticular opacities -associated with restrictive lung disease (interstitial fibrosis), erythema nodosum, Bell’s palsy, epithial granuloma containing microscopic Schaumann & asteroid bodies, uvetitis, hypercalceia (due to elevated 1alpha-hydroxylase-mediated vit D activation in epitheloid macrophages -treatment: steroids

83
Q

Polymyalgia rheumatica 1. Symptoms: 2. Findings: 3. Treatment:

A
  1. Symptoms: -Does not cause muscular weakness. -Pain & stiffness in shoulders & hips, often with fever, malaise, weight loss. -more common in XX>50 yo -associated with temporal (giant cell) arteritis 2. Findings: -increase ESR -normal CK 3. Treatment: -Rapid response to low-dose corticosteroids
84
Q

Firbomyalgia

A

Most commonly seen in women 20-50 yo chronic, widespread musculoskeletal pain associated with stiffness, paresthesia, poor sleep, fatigue

85
Q

Polymyositis/dermatomyositis: 1. Symptoms 2. Findings: 3. treatments:

A
  1. Symptoms -Polymyositis-progressive symmetric proximal muscle weakness, characterized by endomysial inflammation with CD8+ T cells. most often involve shoulders -Dermatomyositis-similar to polymyositis, but also involves malar rash (similar to SLE), Gottron’s papules, heliotrope rash, “shawl & face rash” mechanic’s hands, increase rish of occult malignancy. Perimysial inflammation and atrophy with CD4+ T cells 2. Findings: -increase CK -positive ANA -positive anti-Jo-1 antibodies 3. treatments: -steroids
86
Q

Neuromuscluar junction disease: Myasthenia gravis 1. frequency 2. pathophysiology 3. clinical 4. associated with 5. AChE inhibitor administration

A
  1. frequency: most common NMJ disorder 2. pathophysiology: autoantibodies to postsynaptic ACh receptor 3. clinical: Ptosis, diplopia, weakness; worsens with muscle use 4. associated with: thymoma, thymic hyperplasia 5. AChE inhibitor administration: reversal of symptoms
87
Q

Neuromuscluar junction disease: Lambert-Eaton Myasthenia syndrome 1. frequency 2. pathophysiology 3. clinical 4. associated with 5. AChE inhibitor administration

A
  1. frequency: uncommon 2. pathophysiology: autoantibodies to presynaptic Ca2+ channel leading to ACh release 3. clinical: proximal muscle weakness; improves with muscle use 4. associated with: small cell lung cancer 5. AChE inhibitor administration: no effect
88
Q

myositis ossificans

A

-metaplasia of skeletal muscle to bone following muscular trauma. -most often seen in upper or lower extremity -may present as suspicious “mass” at site of known trauama or as incidental finding on radiography

89
Q

Scleroderma (systemic sclerosis)

A

-excessive fibrosis & collagen deposition throughout body. Commonly sclerosis of ksin, manifesting as puffy & taut skin with absence wrinkles. Sclerosis of renal, pulmonary (most likely cause of death), cardiovascular, GI systems, 75% xx -2 major types: -Diffuse scleroderma: widespread skin involvement, rapid progression, early visceral involvement. Associated with anti-Scle-70 antibody (anti-DNA topoisomerase I antibody) -CREST syndrome: Calcinosis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia -limited skin involvement, often confined to fingers & face. More benign clniical course. Associated with antiCentromere antibody C for CREST

90
Q

Dermatologic macroscopic terms (morphology) characteristics & examples 1.macule 2. patch 3. papule 4.plaque 5. vesicle 6. bulla 7. pustule 8. wheal 9. scale 10. crust

A

1.macule- flat lesion with well circumscribed change in skin color 5mm; large birthmark (congenital nevus) 3. papule- elevated solid skin lesion 5mm; psoriasis 5. vesicle:- small fluid containing blister 5mm; bullous pemphigoid 7. pustule- vesicle containing pus; pustular psoriasis 8. wheal- transient smooth papule/plague; hives (urticaria) 9. scale- flaking off of stratum corneum; eczema, psoriasis, SCC 10. crust- dry exudate; impetigo

91
Q

Dermatologic microscopic terms Characteristics & examples 1. hyperkeratosis 2. parakeratosis 3. acantholysis 4. acanthosis 5. dermatitis

A
  1. hyperkeratosis- increased thickness of stratum corneum; psoriasis 2. parakeratosis- hyperkeratosis with retention of nuclei in stratum corneum; psoriasis 3. acantholysis- separation of epidermal cells; pemphigus vulgaris 4. acanthosis- epidermal hyperplasia (increase spinosum); acanthosis nigricans 5. dermatitis- inflammation of the skin; atopic dermatitis 5. dermatitis
92
Q

Albinism

A

Pigmented skin disorder -normal melanocyte number with decrease melanin production due to decrease tyrosinase activity. -can also be caused by failure of neural crest cell migration during development

93
Q

Melasma (chloasma)

A

pigmented skin disorder -hyperpigmentation assocaited with pregancy (mask of pregnancy) or OCP use

94
Q

Vitiligo

A

irregular areas of complete depigmentation caused by decrease in melancocytes

95
Q

Common skin disorders: Verrucae

A

-warts; caued by HPV. Soft, tan colored, cauliflower-like papules. -Epidermal hyperplasia, hyperkeratosis, koilocytosis -condyloma acuminatum on genitals

96
Q

Common skin disorders: Melanocytic nevus

A

-common mole -Benign, but melanoma can arise in congenital or atypical moles -intradermal nevi are papular -junctional nevi are flat muscles

97
Q

Common skin disorders: Urticaria

A

-hives. Pruritic wheals that form after mast cell degranulation

98
Q

Common skin disorders: Ephelis

A

Freckles. Normal number of melanocytes -increase melanin pigment

99
Q

Common skin disorders: Atopic dermatitis (eczema)

A

pruritic eruption, commonly on skin flexures. Often associated with other atopic diseases (asthma, allergic rhinitis). usually starts on the face in infancy and often appears in the antecubital fossae thereafter

100
Q

Common skin disorders: allergic contact dermititis

A

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

101
Q

Common skin disorders: Psoriasis

A

Papules & plague with silvery scaling, especailly on knee and elbows. Acanthosis with parakeratotic scaling (nuclei still in stratum corneum). -increase stratumspinosum -decrease stratum granulosum -auspitz sign-pinpoint bleeding spots from exposure of dermal papillae when scales are scraped off. Can be associated with nail pitting & psoriatic arthritis

102
Q

Common skin disorders: Seborrheic keratosis

A

flat, greasy, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cyst) -looks stuck on -lesions occur on head, trunk, extremities -common benign neoplasm of older persons -Leser-Trelat sign: sudden appearance of multiple seborrheic keratoses, indicating an underlying malignancy (GI, lymphoid)

103
Q

Blistering skin disorders: Pemphigus Vulgaris

A

-potentially fatal autoimmune skin disorder with IgG antibody against desmoglein 3 (1 and /or 3), a part of the desmosomes (needed for cell adhesion). -immunofluorescence reveals antibodies around epidermal cells in a reticular or netlike pattern. -acantholysis-intraepidermal bullae causing flaccid blister involving the skin and oral mucosa. -positive Nikolsky’s sign (separation of epidermis upon manual stroking of skin)

104
Q

Blistering skin disorders: BULLOus pemphigoid

A

-autoimmune disorder of IgG antibody against hemidesmosomes (epidermal basement membrane; antibodies are BULLOw the epidermis) - shows linear immunofluorescence. -Eosinophils within tense blisters. -similar to but less severe than pemphigus vulgaris-affects skin but spares oral mucosa -negative Nikolsky’s sign

105
Q

Blistering skin disorders: Dermatitis herpetiformis

A

-pruritic papules, vesciles, bullae -deposits IgA at tips of dermal papillae -associated with celiac disease

106
Q

Blistering skin disorders: Erythema multiforme

A

-associated with infection (Mycoplasma pneumoniae, HSV), drugs (sulfa drugs, beta-lactams, phenytoin), cancers and autoimme disease. -presents with multiple types of lesions-macules, papules, vesicles, target lesions (look like targets with multiple rings and a dusky center showing epithelial disruption

107
Q

Blistering skin disorders: Stevens-Johnson syndrome

A

-characterized by fever, bulla formation, necrosis, sloughing of skin, high mortality rate -typically 2 mucus membranes and skin lesions may appear like targets as seen in erythema multiforme. -usually associated with adverse drug reaction -more severe form >30% of body surface aread involved in toxic epidermal necrolysis

108
Q

Miscellaneous skin disorders: Acanthosis nigricans

A

-epidermal hyperplasia causing symetrical hyperpigmented, velvety thickening of skin, especially on neck or in axilla -associated with hyperinsulinemia (diabetes, obesity, Cushing’s syndrome) nad visceral malignancy.

109
Q

Miscellaneous skin disorders: Actinic keratosis

A

-premalignant lesions caused by sun exposure -small rough erythematous or brownish papules or plaques -risk of squamous cell carcinoma is proportional to degree of epithelial dysplasia

110
Q

Miscellaneous skin disorders: Erythema nodosum

A

-inflammatory lesions of subcutaneous fat, usually on anterior shins -associated with sarcoidosis, coccidiodomycosis, histoplasmosis, TB, streptococcal infections, leprosy, Crohn’s disease

111
Q

Miscellaneous skin disorders: LIchen Planus

A

-Pruritic, Purple, Polygonal Planar Papules and Plaques are the 6Ps -sawtooth infiltrate of lymphocytes at dermal-epidermal junction. -associated with hepatitis C

112
Q

Miscellaneous skin disorders: Pityriasis rosea

A

Herald patch followed days later by Christmas tree distribution -multiple plaques with collarette scale -self-resolving in 6-8 weeks

113
Q

Miscellaneous skin disorders: Sunburn

A

-UV irradiation causes DNA mutation inducing spoptosis of keratinocytes -UVA is dominant in tanning and photoagining -UVB in sunburn -can lead to impetigo and skin cancers (basal cell carcinoma, squamous cells carcinoma, nad melanoma

114
Q

Infectious skin disorders Impetigo

A

-very superficial infection. -usually from S. aureus or S. pyogenes -highly contagious -honey-colored crusting -bullous impetigo has bullae and is usually caused by S. aureus

115
Q

Infectious skin disorders: Cellulitis

A

-acute, painful, spreading infection of dermis and subcutaneous tissues. -usually from S pyogenes or S. aureus -often starts with break in skin from trauma or another infection

116
Q

Infectious skin disorders necrotizing fasciitis

A

-deeper tissue injury, usualy from anaerobic bacteria or S. pyogenes. -results in crepitus from methane and CO2 production -flesh eating bacteria -causes bullae and purple color to the skin

117
Q

Infectious skin disorders Staphylococcal scalded skin syndrome (SSSS)

A

-exotoxin destroys keratinocytes attachments in the stratum granulosum only (vs. toxic epidermal necrolysis, which destroys the epidermal-dermal junction) -characterized by fever and generalized erythematous rash with sloughing of the upper layers of the epidermis taht heals completely -seen in newborns and children

118
Q

Infectious skin disorders Hairy leukoplakia

A

-white, painless, plaques on tongue that cannot be scraped off. -EBV mediated, -occurs in HIV-positive patients

119
Q

Skin cancer: Basal cell carcinoma

A

-most common skin cancer -found in sun-exposed area -locally invasive, but almost never metastasizes -pink, pearly nodules, -commonly with telangiectasis, rolled borders, central crusting or ulceration -BCC also appears as nonhealing ulcers with infiltrating growth or as a scaling plaque (superficial BCC) -basal cell tumors have palisading nuclei

120
Q

Skin cancer: squamous cell carcinoma

A

-second most common -associated with excessive exposure to sunlight, immunosuppression, and occasionally arsenic exposure -commonly appears on face, lower lip, ears, hands -locally invasive, but may spread to lymph nodes and wlll rarely metastasize -ulcertaive red lesions with frequent scale -associated with chronic draining sinuses -histopathology: keratin pearls -actinic keratosis: scaly plaque is a precursor to SCC -keratoacanthoma: variant that grows rapidly (4-6 wks) and may regress spontaneoulsy over months

121
Q

Skin cancer: melanoma

A

-common tumor with significant risk of metastasis -S-100 tumor marker -associated with sunlight exposure; fair skinned persons are at increase risk -depth of tumor correlates with risk of metastasis -look for the ABCDE: -Asymmetry -Border irregularity -Color variation -Diameter >6mm -Evolution over time -at least 4 different types of melanoma -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

122
Q

Pharmacology: Aspirin: 1. mechanism 2. clinical use 3. toxicity

A
  1. mechanism- irreversibly inhibit cyclooxygenase (both COX1 & COX 2) by acetylation which decrease synthesis of both thromboxane A2 (TXA2) adn prostaglandins. INcrease bleeding time. No effect on PT, PTT. A type of NSAID 2. clinical use: low dose (s syndrome in children treated with aspirin for viral infection. Also stimulates respiratory centers, causing hyperventilation and respiratory alkalosis
123
Q

Pharmacology: NSAIDS: Ibuprofen, naproxen, indomethacin, ketorolac, diclofenae 1. mechanism 2. clinical use 3. toxicity

A
  1. mechanism-reversibly inhibit cycooxygenase (both COX-1 COX2). block prostaglandin (PG) synthesis, 2. clinical use: antypyretic, analgesic, anti-inflammatory. Indomethacin used to close a PDA 3. toxicity: interstitial nephritis, gastric ulcer (PGs protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole
124
Q

Pharmacology: COX-3 inhibitors (celecoxib): 1. mechanism 2. clinical use 3. toxicity

A
  1. mechanism- reversibily inhibit specifically COX isoform 2 which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX 1 which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on COX-1 2. clinical use: rheumatoid arthritis & osteoarthritis; patients with gastritis or ulcers 3. toxicity: increase risk of thrombosis. Sulfa allergy
125
Q

Pharmacology: Acetaminophen: 1. mechanism 2. clinical use 3. toxicity

A
  1. mechanism- reversibily inhibit cycooxygenase mostly in CNS. INactivated peripherally 2. clinical use- antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye’s syndrome in children with viral infection 3. toxicity- overdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver. N-acetylcysteine is antidote-regenerate glutathione
126
Q

Pharmacology: Bisphosphonates (alendronate, other -dronates) 1. mechanism 2. clinical use 3. toxicity

A
  1. mechanism- pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclasts activity 2. clinical use- osteoporosis, hypercalcemia, Paget’s disease of the bone 3. toxicity- corrosive esophagitis, osteonecrosis of the jaw
127
Q

1.TNF-alpha inhibitors characteristics 2. Etanercept 3. Infliximab, Adalimumab

A
  1. all TNF alpha inhibitors predispose to infection including reactivation of latent TB since TNF blockade prevents activation of macrophages and destruction of phagocytoses microbes 2. Etanercept mechanism: fusion protein (receptor for TNF alpha + IgG1 Fe) produced by recombinant DNA. Etanercept is a TNF decoy receptor Clinical use: rheumatoid arthritis, psoriasis, ankylosing spondylitis 3. Infleximab/adalimumab- mechanism: anti-TNF alpha- monoclonal antibody Clinical use: Crohn’s disease, rheumatoid arthritis, ankylosing spondylitis, psoriasis
128
Q

Gout drugs: A. Chronic 1. allopurinol 2. fexbuxostat 3. probenecid 4. colchicine B. Acute 1. NSAIDs 2. Glucocorticoids

A

A. Chronic 1. allopurinol-inhibits xanthine oxidase, decrease conversion of xanthine to uric acid. Also used in lymphoma & leukemia to prevent tumor lysis-associated urate nephropathy. Increased concentrations of azathioprine and 6MP (both normally metabolized by xanthine oxidase). Do not give salicyclates; all but the highest doses depress uric acid clearance. Even high doses (5-6g/day) have only minor uricosuric activity. 2. fexbuxostat- inhibit xanthine oxidase 3. probenecid- inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin) 4. colchicine- binds & stabilizes tubulin to inhibit polymerization, impairing leukocytes chemotaxis and degranulation. GI side effects, especially if given orally B. Acute 1. NSAIDs- naproxen, indomethacin 2. Glucocorticoids- oral or intraarticular

129
Q
A

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