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356 Cards in this Set

  • Front
  • Back
Soccer player who was kicked in
the leg suffered a damaged
medial meniscus. What else is likely to have been damaged?
Anterior cruciate ligament
(remember the “unhappy triad”).
Gymnast dislocates her shoulder
anteriorly. What nerve is most
likely to have been
damaged?
Axillary nerve (C5, C6).
X-ray shows bilateral hilar
ymphadenopathy.
Sarcoidosis.
Child exhibits weakness and
enlarged calves.
Duchenne’s muscular dystrophy;
X-linked recessive.
25-year-old woman presents with
a low-grade fever, a rash across
her nose that gets worse when
she is out in the sun, and
widespread edema.
SLE.
85-year-old man presents with
acute knee pain and swelling.
X-ray shows joint space without erosion. What is the diagnosis, and what would you find on aspiration?
Pseudogout; rhomboid calcium
pyrophosphate crystals.
Epidermis layers From surface to base:
Californians Like Girls in
String Bikinis.

Stratum corneum
Stratum lucidum
Stratum granulosum
Stratum spinosum
Stratum basalis
Epithelial cell junctions

surrounds perimeter just below
zona occludens
Zona adherens (intermediate junction)
Epithelial cell junctions

small, discrete sites of attachment
Macula adherens (desmosome)
Epithelial cell junctions

connects cells to underlying extracellular matrix
Hemidesmosome
Epithelial cell junctions

maintains integrity of basement
membrane
Integrin
Epithelial cell junctions

prevents diffusion across intracellular space
Zona occludens (tight junction)
Epithelial cell junctions
type of protein that forms the

Zona adherens (intermediate junction)
Actin filaments

and

E-cadherin
Epithelial cell junctions
type of protein that forms the

Macula adherens (desmosome)
Keratin

Desmoplakin
Unhappy triad

what
damage to medial collateral ligament (MCL), medial meniscus, and anterior cruciate ligament (ACL).
Unhappy triad

when
lateral hit to the knee
Knee
PCL =
LCL =
PCL = posterior cruciate ligament.

LCL = lateral
collateral ligament.
“Anterior” and “posterior” in ACL and PCL refer to
sites of tibial attachment.
Knee

Positive anterior drawer sign indicates
tearing of the
ACL.
Knee

Abnormal passive abduction indicates
a torn MCL.
Shoulder muscles that form the rotator cuff:

just name them
S I t S (small t is for teres
minor).

Supraspinatus
Infraspinatus–
Teres minor––
Subscapularis–
Shoulder muscles that form the rotator cuff:

names and functions
Supraspinatus––helps deltoid abduct arm.
Infraspinatus––laterally rotates arm.
Teres minor––adducts and laterally rotates arm.
Subscapularis––medially rotates and adducts arm.
Skeletal muscle contraction

role of ATP
ATP binds to myosin head and releases actin filament, allowing cross-bridge cycling and shortening to occur.
Skeletal muscle contraction

role of Ca2+
Ca2+ binds to troponin C,
causing conformational change. This causes tropomyosin to move out of the way to allow actin/myosin cycling.
Muscle conduction to contraction

Ryanodine receptor
Ryanodine receptors (RyRs) form a class of intracellular calcium channels (on SR) It is the major cellular mediator of calcium-induced calcium release (CICR) in animal cells.
Muscle conduction to contraction

Dihydropyridine receptor
is a voltage-dependent calcium channel found in the transverse tubule of muscles. In skeletal muscle it associates with the ryanodine receptors of the sarcoplasmic reticulum to induce calcium release and thus muscle contraction.
It is the major cellular mediator of calcium-induced calcium release (CICR) in animal cells.
Ryanodine receptor
Skeletal Muscle

Action potential steps up to Ca2+ release
1.depolarization opens voltage-gated Ca2+ channel
2.muscle cell depolarization in the motor end plate
3. impulse travels along muscle cell down the T tubule.
4. Ryanodine receptor and
Dihydropyridine receptor cause Ca2+ release
Skeletal Muscle

Action potential steps after Ca2+ release
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).
Skeletal Muscle

what bands change and how
Contraction results in H and I band shortening, but the A band remains the same length.
Achondroplasia

geneitcs
Autosomal-dominant trait
Achondroplasia

mech and clinical features
Failure of longitudinal bone growth → short limbs.
Membranous ossification is not affected (skull, facial bones, and axial skeleton are
normal). Impaired cartilage maturation in growth plate caused by fibroblast growth
factor receptor mutation.
Osteoarthritis

mech
Mechanical––wear and tear of joints leads to destruction of articular cartilage
Osteoarthritis

predisposing factors
trauma, age, obesity, joint deformity.
Osteoarthritis

classic presentation
pain in weight-bearing joints after use (e.g., at the end of the day),improving with rest. No systemic symptoms.
Osteoarthritis

different cysts and nodes
subchondral cysts, sclerosis, osteophytes, eburnation, Heberden’s nodes (DIP), Bouchard’s nodes (PIP).
Rheumatoid arthritis

mech
Autoimmune––inflammatory disorder
80% of RA patients have positive rheumatoid factor (anti-IgG antibody).
Rheumatoid arthritis

clinical findings
pannus formation in joints (MCP, PIP), subcutaneous rheumatoid nodules, ulnar deviation, subluxation
Rheumatoid arthritis

what is RF
rheumatoid factor (anti-IgG antibody).
Rheumatoid arthritis

who
Females > males
Rheumatoid arthritis

Classic presentation
Classic presentation: morning stiffness improving with use, symmetric joint involvement, and systemic symptoms (fever, fatigue, pleuritis, pericarditis).
Osteoporosis

definition
Reduction of bone mass in spite of normal bone mineralization.
Osteoporosis

histo
Sparse trabeculae.
Osteoporosis

WRT ethnicity
whites > blacks > Asians.
Osteoporosis

Type I
Postmenopausal; ↑ bone resorption due to ↓ estrogen levels. Estrogen replacement is controversial as prophylaxis (side effects).
Osteoporosis

Type II
Senile osteoporosis––affects men and women > 70 years.
Osteoporosis

which type Postmenopausal
Type I
Osteoporosis

which type affects men and women > 70 years.
Type II
Distal radius fractures aka
Colles’
Colles’ fractue aka
Distal radius fractures
Vertebral crush fracture

clinical findings
acute back pain, loss of height, kyphosis.
acute back pain, loss of height, kyphosis.
Vertebral crush fracture
Osteopetrosis aka
marble bone disease
marble bone disease aka
Osteopetrosis
Osteopetrosis

clinical and lab findings
thickened, dense bones. Serum calcium, phosphate, and alkaline phosphatase are normal. Decreased marrow space leads to anemia, thrombocytopenia, infection.
Osteopetrosis

mech
Bone defect is due to
abnormal function of osteoclasts.
Osteomalacia/rickets

mech and lab findings
Defective mineralization of osteoid → soft bones. Vitamin D deficiency in adults →
↓ calcium levels →↑ secretion of PTH, ↓ in serum phosphate.
Osteomalacia/rickets

Tx
Reversible when vitamin D is replaced. Vitamin D deficiency in childhood causes rickets.
Osteitis fibrosa cystica aka
Von Recklinghausen's disease of bone
Von Recklinghausen's disease of bone aka
Osteitis fibrosa cystica
Osteitis fibrosa cystica

caused by
Caused by hyperparathyroidism
Osteitis fibrosa cystica

characteristic finding and what are they
Caused by hyperparathyroidism. Characterized by “brown tumors” (cystic spaces linedby osteoclasts, filled with fibrous stroma and sometimes blood).
Osteitis fibrosa cystica

lab findings
High serum calcium,
low serum phosphorus, and high alkaline phosphatase.
Paget’s disease aka
osteitis deformans
osteitis deformans aka
Paget’s disease
Paget’s disease

what is it
Abnormal bone architecture caused by ↑ in both osteoblastic and osteoclastic activity.
Paget’s disease

lab values
Serum calcium, phosphorus, and PTH levels are normal. Serum alkaline phosphatase is elevated.
Paget’s disease

clinical findings
Long bone chalkstick (transverse to the long axis) fractures. Increased blood flow may
cause high output CHF.
Polyostotic fibrous dysplasia

what is it
Bone is replaced by fibroblasts, collagen, and irregular bony trabeculae.
Albright’s syndrome
a form of polyostotic fibrous dysplasia in which there
are multiple unilateral bone lesions associated with endocrine abnormalities
(precocious puberty) and unilateral pigmented skin lesions.
multiple unilateral bone lesions associated with endocrine abnormalities
(precocious puberty) and unilateral pigmented skin lesions.
Albright’s syndrome (a form of polyostotic fibrous dysplasia)
Polymyalgia rheumatica

what is it
Pain and stiffness in shoulders and hips, often with fever, malaise, and weight loss.Does not cause muscular weakness.
Polymyalgia rheumatica

wrt strength
Does not cause muscular weakness.
Pain and stiffness in shoulders and hips, often with fever, malaise, and weight loss.
Polymyalgia rheumatica
Polymyalgia rheumatica

wrt labs
↑ ESR
Polymyalgia rheumatica

who and associations
Occurs in patients > 50 years of age; associatedwith temporal (giant cell) arteritis.
Polymyalgia rheumatica

Tx
prednisone.
Polymyositis

describe
progressive symmetric proximal muscle weakness caused by CD8 T-cell-induced injury to myofibers.
Polymyositis

Dx
Muscle biopsy with evidence of inflammation is diagnostic.
progressive symmetric proximal muscle weakness caused by CD8 T-cell-induced injury to myofibers.
Polymyositis
Dermatomyositis
similar to polymyositis but also involves "shawl and face" (diffuse, flat, erythematous lesion over the chest and shoulders or in a "V" over the anterior neck and chest) skin rash and ↑ risk of malignancy.
similar to polymyositis but also involves "shawl and face" skin rash and ↑ risk of malignancy.
Dermatomyositis
polymyositis/dermatomyositis

wrt labs
↑ CK, ↑ aldolase, and positive ANA, anti-Jo-1.
↑ CK, ↑ aldolase, and positive ANA, anti-Jo-1.
polymyositis/dermatomyositis
Mixed connective tissue disease

clinical findings
Raynaud’s phenomenon, arthralgias, myalgias, fatigue, and esophageal hypomotility.
Mixed connective tissue disease

what type of antibodies
Antibodies to U1RNP.
Mixed connective tissue disease

Tx
Responds to steroids.
Antibodies to U1RNP
Mixed connective tissue disease
Raynaud’s phenomenon, arthralgias, myalgias, fatigue, and esophageal hypomotility.
Mixed connective tissue disease
similar to polymyositis but also involves "shawl and face" skin rash and ↑ risk of malignancy.
dermatomyositis
Sjögren’s syndrome

clinical findings
-xerophthalmia
-xerostomia
-arthritis.
-dental caries
-Parotid enlargment
Sjögren’s syndrome

wrt cancer
↑ risk of B-cell lymphoma
Sjögren’s syndrome

antibodies
Autoantibodies to ribonucleoprotein antigens, SS-A (Ro), SS-B (La).
Autoantibodies to ribonucleoprotein antigens, SS-A (Ro), SS-B (La).
Sjögren’s syndrome
Sjögren’s syndrome

who
Predominantly affects females between 40 and
60 years of age.
Sjögren’s syndrome

associated conditions
rheumatoid arthritis.
Sicca syndrome
dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis.
dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis.
Sicca syndrome
SLE

who
90% are female and between ages 14 and 45. Most common and severe in black females.
SLE

cause of death
death from renal failure and
infections.
SLE

False positives
False positives on syphilis tests
(RPR/VDRL)
due to antiphospholipid antibodies.
SLE Lab tests

Antinuclear antibodies (ANA)
sensitive, but not specific for SLE
SLE Lab tests

Antibodies to double-stranded DNA
very specific, poor prognosis
SLE Lab tests

Anti-Smith antibodies (anti-Sm)
very specific, but not prognostic
SLE Lab tests

Antihistone antibodies
drug-induced lupus
SLE Lab tests

sensitive, but not specific
Antinuclear antibodies (ANA)
SLE Lab tests

very specific, poor prognosis
Antibodies to double-stranded DNA
SLE Lab tests

drug-induced lupus
Antihistone antibodies
SLE mnemonic
I’M DAMN SHARP:
Immunoglobulins (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
Gout

what is it
Precipitation of monosodium urate crystals into joints due to hyperuricemia,
Gout

causes
caused by Lesch-Nyhan syndrome, PRPP excess, ↓ excretion of uric acid, or glucose-6-phosphatase deficiency. Also associated with the use of thiazide diuretics, which competitively inhibit the secretion of uric acid.
Gout

joint pattern and presentation
Asymmetric joint distribution. Classic
manifestation is painful MTP joint in the big toe (podagra). Tophus formation (often on external ear or Achilles tendon).
Gout

lab
Crystals are needle shaped and negatively birefringent.
Gout

who and when
birefringent. More common in men. Acute attack tends to occur after alcohol consumption or a large meal
Gout

Tx
allopurinol, probenecid, colchicine, and NSAIDs.
Pseudogout

cause
Caused by deposition of calcium pyrophosphate crystals within the joint space.
Pseudogout

labs
Caused by deposition of calcium pyrophosphate crystals within the joint space. Forms
basophilic, rhomboid crystals that are weakly positively birefringent
Pseudogout

joints
Usually affects large joints
(classically the knee).
Pseudogout

who
> 50 years old; both sexes affected equally.
Pseudogout

Tx
No treatment.
Sarcoidosis

histo and lab
Characterized by immune-mediated, widespread
noncaseating granulomas and elevated serum ACE levels.
Sarcoidosis

who
Common in black females.
Sarcoidosis

associated with
Associated with restrictive lung disease, bilateral
hilar lymphadenopathy, erythema nodosum,
Bell’s palsy, epithelial granulomas containing
microscopic Schaumann and asteroid bodies, uveoparotitis, and hypercalcemia (due to
Associated with restrictive lung disease, erythema nodosum, Bell’s palsy, epithelial granulomas containing microscopic Schaumann and asteroid bodies, uveoparotitis, and hypercalcemia
Sarcoidosis
Sarcoidosis

mech of hypercalcemia
elevated conversion of vitamin D to its active form in epithelioid macrophages
Sarcoidosis

mnemonic
GRAIN:
Gammaglobulinemia
Rheumatoid arthritis
ACE increase
Interstitial fibrosis
Noncaseating granulomas
Seronegative
spondyloarthropathies

name them
Ankylosing spondylitis


Reiter’s syndrome
Seronegative
spondyloarthropathies

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

who
more often in males.
Ankylosing spondylitis

Lab findings
RF negative
HLA-B27 positive
Reiter’s syndrome

Lab findings
RF negative
HLA-B27 positive
Ankylosing spondylitis

clinical findings
Chronic inflammatory disease of spine and sacroiliac joints → ankylosis (stiff spine), uveitis, and aortic regurgitation.

Bamboo spine.
Reiter’s syndrome

clinical findings
Classic triad:
1. Urethritis
2. Conjunctivitis and anterior uveitis
3. Arthritis
Reiter’s syndrome

who
Post-GI or chlamydia infections.
Scleroderma aka
progressive systemic sclerosis
progressive systemic sclerosis aka
Scleroderma
Scleroderma

mech
Excessive fibrosis and collagen deposition throughout the body
Scleroderma

2 main types
1. Diffuse scleroderma


2. CREST syndrome
Scleroderma

who
75% female
Diffuse scleroderma

describe
widespread skin involvement, rapid progression, early visceral
involvement. Associated with anti-Scl-70 antibody.
Associated with anti-Scl-70 antibody
Diffuse scleroderma
CREST syndrome

describe
Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. Limited skin involvement, often confined to fingers and face. More benign clinical course. Associated with anticentromere
antibody
Associated with anticentromere
antibody
CREST syndrome
describe the skin disorder

Impetigo
Superficial skin infection. Honey crusting. Highly contagious.
describe the skin disorder

Dermatitis
A group of inflammatory pruritic skin disorders. Etiology: allergy (usually type IV
hypersensitivity), chemical injury, or infection.
describe the skin disorder

Atopic dermatitis
Pruritic eruption, commonly on flexor surfaces. Often associated with other atopic diseases (asthma, allergic rhinitis).
describe the skin disorder

Psoriasis
Epidermal hyperplasia (acanthosis) with parakeratotic scaling (nuclei still in stratum corneum) especially on knees and elbows.
describe the skin disorder

Allergic contact dermatitis
Type IV hypersensitivity reaction that follows exposure to allergen (poison ivy, poison oak,
nickel, rubber, chemicals). Lesions occur at site of contact.
describe the skin disorder

Dermatitis herpetiformis
Pruritic papules and vesicles. Deposits of IgA at the tips of dermal papillae. Associated
with celiac disease.
describe the skin disorder

Lichen planus
Pruritic, purple, polygonal papules; infiltrate of lymphocytes at dermoepidermal junction.
describe the skin disorder

Erythema multiforme
multiple types of lesions, including macules, papules, vesicles, and target lesions (red
papules with a pale central area).
describe the skin disorder

Seborrheic keratosis
Flat, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cysts).
Benign.
describe the skin disorder

Actinic keratosis
Caused by sun exposure. Small, rough erythematous or brownish papules. Premalignant
lesion. Risk of carcinoma is proportional to epithelial dysplasia.
describe the skin disorder

Keloid
Tumor of connective tissue elements of dermis that causes raised, thickened scars.
Follows trauma to skin,
describe the skin disorder

Bullous pemphigoid
Autoimmune disorder with IgG antibody against epidermal basement membrane
hemidesmosomes (linear immunofluorescence). Similar to but less severe than
pemphigus vulgaris––affects skin but spares oral mucosa
describe the skin disorder

Pemphigus vulgaris
Potentially fatal autoimmune skin disorder. Intraepidermal bullae involving the oral
mucosa and skin. Findings: acantholysis (breakdown of epithelial cell-to-cell
junctions), IgG antibody against epidermal cell surface desmosomes
describe the skin disorder

Verrucae
Soft, tan-colored, cauliflowerlike lesions. Epidermal hyperplasia, hyperkeratosis,
koilocytosis.
Atopic dermatitis aka
eczema
eczema aka
Atopic dermatitis
Verrucae aka
warts
warts aka
Verrucae
Psoriasis wrt different skin layers
↑ stratum spinosum, ↓ stratum granulosum
parakeratotic scaling what is it and when do you see it
nuclei still in stratum
corneum

Psoriasis
nuclei still in stratum
corneum aka
parakeratotic scaling
Atopic dermatitis aka
eczema
eczema aka
Atopic dermatitis
Verrucae aka
warts
warts aka
Verrucae
Psoriasis wrt different skin layers
↑ stratum spinosum, ↓ stratum granulosum
parakeratotic scaling what is it and when do you see it
nuclei still in stratum
corneum

Psoriasis
nuclei still in stratum
corneum aka
parakeratotic scaling
Superficial skin infection. Honey crusting. Highly contagious.
Impetigo
A group of inflammatory pruritic skin disorders. Etiology: allergy (usually type IV
hypersensitivity), chemical injury, or infection.
Dermatitis
Pruritic eruption, commonly on flexor surfaces. Often associated with other atopic
diseases (asthma, allergic rhinitis).
Atopic dermatitis
(eczema)
Type IV hypersensitivity reaction that follows exposure to allergen (poison ivy, poison oak,
nickel, rubber, chemicals). Lesions occur at site of contact.
Allergic contact
dermatitis
Epidermal hyperplasia (acanthosis) with parakeratotic scaling (nuclei still in stratum
corneum) especially on knees and elbows. ↑ stratum spinosum, ↓ stratum granulosum
(see Color Image 65). Auspitz sign.
Psoriasis
Pruritic papules and vesicles. Deposits of IgA at the tips of dermal papillae. Associated
with celiac disease.
Dermatitis
herpetiformis
Pruritic, purple, polygonal papules; infiltrate of lymphocytes at dermoepidermal junction.
Lichen planus
Flat, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cysts).
Benign.
Seborrheic keratosis
Caused by sun exposure. Small, rough erythematous or brownish papules. Premalignant
lesion. Risk of carcinoma is proportional to epithelial dysplasia.
Actinic keratosis
Tumor of connective tissue elements of dermis that causes raised, thickened scars.
Follows trauma to skin, especially in African-Americans.
Keloid
Autoimmune disorder with IgG antibody against epidermal basement membrane
Bullous pemphigoid
Potentially fatal autoimmune skin disorder. Intraepidermal bullae involving
mucosa and skin. Findings: acantholysis (breakdown of epithelial cell-to-c
junctions), IgG antibody against epidermal cell surface desmosomes
Pemphigus vulgaris
Soft, tan-colored, cauliflowerlike lesions. Epidermal hyperplasia, hyperkeratosis,
koilocytosis.
Verrucae (warts)
Auspitz sign.
appearance of punctate bleeding spots when psoriasis scales are scraped off
appearance of punctate bleeding spots when psoriasis scales are scraped off
Auspitz sign.
target lesions
Erythema multiforme
Actinic keratosis wrt cancer
Risk of carcinoma is proportional to epithelial dysplasia.
Keloid

who
African-Americans.
Autoimmune disorder with IgG antibody against epidermal basement membrane
hemidesmosomes (linear immunofluorescence).
Bullous pemphigoid
acantholysis
breakdown of epithelial cell-to-cell junction
breakdown of epithelial cell-to-cell junction
acantholysis
warts on hands versus on genitals
Verruca vulgaris on hands, condyloma acuminatum on genitals.
Skin cancer
Squamous cell carcinoma

associations
excessive exposure to
sunlight
and arsenic exposure.
Skin cancer
Squamous cell carcinoma

where and spread
Commonly appear
on hands and face. Locally invasive, but rarely
metastasizes.
Skin cancer
Squamous cell carcinoma

histo
keratin “pearls”
Skin cancer
Basal cell carcinoma

where and spread
Most common in sun-exposed areas of body. Locally invasive, but almost never metastasizes.
Skin cancer
Basal cell carcinoma

histo
“palisading” nuclei.
Skin cancer
Basal cell carcinoma

gross
pearly papules- characteristic "pearly white" translucent quality on the periphery
Skin cancer
melanoma

where and spread
Common tumor with significant risk of metastasis
Skin cancer
melanoma

who
Associated with sunlight exposure; fair-skinned
persons are at ↑ risk.
Skin cancer
melanoma

prognosis factors
Depth of tumor correlates with risk of metastasis
Skin cancer
melanoma

precursor
Dysplastic nevus is a precursor
to melanoma.
Dysplastic nevus is a precursor
to
melanoma.
name the benign Primary bone tumors
-Osteoid osteoma
-Osteoblastoma
-Giant cell tumor
-Osteochondroma (exostosis)
-Enchondroma
name the Malignant Primary bone tumors
-Osteosarcoma (osteogenic
carcinoma)
-Ewing’s sarcoma
-Chondrosarcoma
Describe

Osteoid osteoma
Interlacing trabeculae of woven bone surrounded by osteoblasts. < 2 cm and found in
proximal tibia and femur.
Describe

Osteoblastoma
Same morphologically as osteoid osteoma, but larger and found in vertebral column.
Describe

Giant cell tumor
old. Locally aggressive benign tumor often around the distal femur, proximal tibia
region. Characteristic “double bubble” or “soap bubble” appearance on x-ray.
Describe

Osteochondroma
Mature bone with cartilaginous
Commonly originates from long metaphysis.
Describe

Enchondroma
Benign cartilaginous neoplasm found in intramedullary bone. Usually distal extremities
Describe

Osteosarcoma
Commonly found in the metaphysis of long bones.
Codman’s triangle (from elevation of periosteum) on x-ray.
Describe

Ewing’s sarcoma
Anaplastic small blue cell malignant tumor
Describe

Chondrosarcoma
Malignant cartilaginous tumor. Usually located
pelvis, spine, scapula, humerus, tibia, or femur. Expansile glistening mass within the medullary cavity.
Interlacing trabeculae of woven bone surrounded by osteoblasts. < 2 cm and found in
proximal tibia and femur.
Osteoid osteoma
Same morphologically as osteoid osteoma, but larger and found in vertebral column.
Osteoblastoma
Characteristic “double bubble” or “soap bubble” appearance on x-ray. Spindle-shaped cells with multinucleated giant cells.
Giant cell tumor
Most common benign bone tumor
Osteochondroma
(exostosis)
Benign cartilaginous neoplasm found in intramedullary bone. Usually distal extremities
Enchondroma
Most common 1° malignant tumor of bone.
Osteosarcoma
(osteogenic carcinoma)
Osteosarcoma

who
Peak incidence in men 10–20 years old.
Osteosarcoma

where
Commonly found in the metaphysis of long bones
Osteosarcoma

Gene involved
familial retinoblastoma. Rb
Rb and bone cancer
Osteosarcoma
(osteogenic carcinoma)
Osteosarcoma and predisposing factors
Paget’s disease of bone, bone infarcts, radiation, and familial retinoblastoma.
Ewing’s sarcoma

who
Most common in boys < 15
Ewing’s sarcoma

prognosis
Extremely aggressive with early mets, but responsive to chemotherapy.
Ewing’s sarcoma

mnemonic
“onion-skin” appearance in bone
11:22
(“going out for Ewings and onion rings at 11:22”)
Expansile glistening mass within the medullary cavity.
Chondrosarcoma
May be of 1° origin or from
osteochondroma.
Chondrosarcoma
Chondrosarcoma

who
Most common in men aged 30–60
Buerger’s disease aka
thromboangiitis obliterans
thromboangiitis obliterans aka
Buerger’s disease
Buerger’s disease

Findings
Intermittent claudication, superficial nodular phlebitis, cold sensitivity
(Raynaud’s phenomenon), severe pain in affected part; may lead to gangrene.
Buerger’s disease

Treatment
Quit smoking.
Buerger’s disease

mech and who
idiopathic, segmental, thrombosing vasculitis
of intermediate and small peripheral arteries and veins. Seen in heavy smokers.
Takayasu’s arteritis aka
“pulseless disease”
“pulseless disease” aka
Takayasu’s arteritis
Takayasu’s arteritis

clinical findings
FAN MY SKIN On Wednesday.

Fever, Arthritis, Night sweats, MYalgia, SKIN
nodules,
Ocular disturbances,
Weak pulses in
upper extremities.
Takayasu’s arteritis

mech
granulomatous thickening of aortic arch and/or proximal great
vessels.
Takayasu’s arteritis

labs
Associated with an elevated ESR.
Temporal arteritis aka
giant cell arteritis
giant cell arteritis aka
Temporal arteritis
Most common vasculitis that affects medium and small arteries
Temporal arteritis
Temporal arteritis

which arteries
branches of carotid artery.
Temporal arteritis

lab values
ESR is markedly elevated
Temporal arteritis

who
elderly females.
Temporal arteritis

findings
unilateral headache, jaw claudication, impaired vision
(occlusion of ophthalmic artery, which can lead
to blindness). Half of patients have systemic
involvement and polymyalgia rheumatica
Temporal arteritis

mech
Focal, granulomatous
Temporal arteritis

Tx
steroids.
Polyarteritis nodosa

Characterized by
necrotizing immune complex
inflammation of medium-sized muscular arteries typically involving renal and visceral vessels.
Polyarteritis nodosa

Symptoms
Fever, weight loss, malaise, abdominal pain, melena,
headache, myalgia, hypertension, neurologic dysfunction, cutaneous eruptions.
Polyarteritis nodosa

Findings
Hepatitis B seropositivity in 30% of patients. Multiple
aneurysms and constrictions on arteriogram. Typically not associated with ANCA.
Polyarteritis nodosa

Treatment
Corticosteroids, cyclophosphamide.
Wegener’s granulomatosis

mech
Characterized by triad of focal necrotizing vasculitis, necrotizing granulomas in the
lung and upper airway, and necrotizing glomerulonephritis.
Wegener’s granulomatosis

Symptoms
hemoptysis, hematuria, and upper respiratory symps
Wegener’s granulomatosis

Findings
C-ANCA
chest x-ray may reveal large nodular densities;
hematuria and red cell casts.
Wegener’s granulomatosis

Treatment
Cyclophosphamide and corticosteroids.
ANCA-positive vasculitides
Wegener’s C-ANCA

Microscopic polyangiitis P-ANCA.

1° pauciimmune crescentic
glomerulonephritis p-ANCA

Churg-Strauss syndrome P-anca
p-ANCA target
neutrophil (myeloperoxidase )
c-ANCA target
proteinase 3
describe Churg-Strauss syndrome
p-ANCA
Granulomatous vasculitis with eosinophilia. Involves lung, heart, skin, kidneys, nerves.
Often seen in atopic patients.
Kawasaki disease

what/who/mech
Acute, self-limiting disease of infants/kids. Acute necrotizing vasculitis of small/medium-sized vessels.
Kawasaki disease

clinical findings
Fever, congested conjunctiva, changes in lips/oral mucosa,
lymphadenitis.

can develop coronary aneurysms.
Fever, congested conjunctiva, changes in lips/oral mucosa,
lymphadenitis.

can develop coronary aneurysms.
Kawasaki disease
Most common form of childhood systemic vasculitis
Henoch-Schönlein purpura
Henoch-Schönlein purpura

clinical findings
Skin rash (palpable purpura),
arthralgia, intestinal hemorrhage, abdominal pain, and melena.
Lesion age in

Polyarteritis nodosa
Lesions are of different ages.
Lesion age in

Henoch-Schönlein purpura
Multiple lesions of the same age.
Telangiectasia

what and look
Arteriovenous malformation in small vessels. Looks like dilated capillary.
Hereditary hemorrhagic telangiectasia

genetics
autosomal dominant inheritance.
Hereditary hemorrhagic telangiectasia

presentation
nosebleeds and skin discolorations.
autosomal dominant inheritance. Presents with nosebleeds and skin discolorations.
Hereditary hemorrhagic telangiectasia
Opioid

Mechanism
Act as agonists at opioid receptors to modulate synaptic transmission.
Opioid

Clinical use
Pain,
cough suppression (dextromethorphan),
diarrhea (loperamide and diphenoxylate),
acute pulmonary edema, maintenance programs for addicts (methadone).
Opioid

Toxicity
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS
depression with other drugs.
Opioid

names
Morphine,
fentanyl,
codeine,
heroin,
methadone,
meperidine,
dextromethorphan.
Opioid

Tolerance does not develop to
miosis and constipation.
Opioid

Toxicity treated with
naloxone or naltrexone (opioid receptor antagonist)
Opioid

what contraindicated if morphine overdose
Oxygen
(might contribute to respiratory failure)
Opioid

specific receptors
(mu = morphine,
delta = enkephalin,
kappa = dynorphin)
Arachidonic acid products

Lipoxygenase pathway yields
L for Lipoxygenase and
Leukotriene.

Leukotrienes.
Arachidonic acid products

LTB4 function
neutrophil chemotactic agent.
Arachidonic acid products

LTC4 , D4 , and E4 function
bronchoconstriction,
vasoconstriction, contraction of smooth muscle,
and ↑ vascular permeability.
Arachidonic acid products

which mediate bronchoconstriction,
vasoconstriction, contraction of smooth muscle,
and ↑ vascular permeability.
LTC4 , D4 , and E4
Arachidonic acid products

neutrophil chemotactic agent
LTB4
Arachidonic acid products

PGI2 function
"Platelet-Gathering Inhibitor."

inhibits platelet aggregation and promotes vasodilation.
Arachidonic acid products

inhibits platelet aggregation and promotes vasodilation.
"Platelet-Gathering Inhibitor."
PGI2
non specific NSAIDs

names
asa, Ibuprofen, naproxen, indomethacin, ketorolac.
non specific NSAIDs

Mechanism
Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block prostaglandin
synthesis.
non specific NSAIDs

Clinical use
Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
non specific NSAIDs

Toxicity
Renal damage,
aplastic anemia,
GI distress,
ulcers.
COX-2 inhibitors

Names
celecoxib, valdecoxib
COX-2 inhibitors

Mechanism
Reversibly inhibit specifically the cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and mediates inflammation and pain; spares COX-1
COX-2 inhibitors

Clinical use
Rheumatoid and osteoarthritis.
COX-2 inhibitors

Toxicity
Increased risk of thrombosis. Less toxicity to GI mucosa (lower incidence of ulcers, bleeding).
Acetaminophen

Mechanism
Reversibly inhibits cyclooxygenase 3, mostly in CNS. Inactivated peripherally.
Acetaminophen

Clinical use
Antipyretic,
analgesic,
Acetaminophen

Toxicity
hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver.
Acetaminophen

Toxicity Tx
N-acetylcysteine is antidote––regenerates
glutathione.
Gout drugs

names
Colchicine and indomethacin
Probenecid
Allopurinol
Colchicine

mechanism
Depolymerizes microtubules,
impairing leukocyte chemotaxis and degranulation.
Colchicine

clinical use
Acute gout.
Colchicine

Toxicity
GI side effects, especially if
given orally. (Note: indomethacin is less toxic, more commonly used.)
more commonly used for acute gout
indomethacin is less toxic, more commonly used than colchicine
Probenecid

mechanism
Chronic gout. Inhibits reabsorption of uric
acid (also inhibits secretion of penicillin).
Probenecid

clinical use
Chronic gout due to under excretion
Allopurinol

mech
↓ conversion of xanthine to uric acid.
Allopurinol

Clinical use
Chronic gout due to overproduction

Also used in lymphoma and leukemia to prevent tumor lysis –associated urate nephropathy.
Etanercept

Mechanism
Recombinant form of human TNF receptor that binds TNF-α.
Etanercept

Clinical use
Rheumatoid arthritis, psoriasis, ankylosing spondylitis.
Infliximab

Mechanism
TNF-α antibody.
Infliximab

Clinical use
Crohn’s disease, rheumatoid arthritis, ankylosing spondylitis.
Infliximab

Toxicity
Predisposes to infections (reactivation of latent TB).
Recombinant form of human TNF receptor that binds TNF-α.
Etanercept
TNF-α antibody.
Infliximab
which Immunosuppressive agents act at the proliferation stage
this is stage 2

All except Rh3(D) immune
globulin
which Immunosuppressive agents act at the Antigen recognition
(B and T cells) stage
This is stage 1

Only
-Antilymphocytic
globulin
-monoclonal anti-
T-cell antibodies
-Rh3(D) immune
globulin
which Immunosuppressive agents act at the Differentiation
synthesis stage
This is stage 3

-Cyclosporine
-Dactinomycin
-Antilymphocytic globulin and
monoclonal anti-T-cell antibodies
-Tacrolimus
which Immunosuppressive agents act at the Cytokine secretion stage
This is stage 4

only Tacrolimus
which Immunosuppressive agents act at the Tissue injury stage
This is stage 5

only Prednisone
Cyclosporine

Mechanism
Binds to cyclophilins. Complex blocks the differentiation and activation of T cellsby inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.
Cyclosporine

Clinical use
Suppresses organ rejection after transplantation; selected autoimmune disorders.
Cyclosporine

Toxicity
Predisposes patients to viral infections and lymphoma; nephrotoxic (preventable with
mannitol diuresis).
Cyclosporine

Toxicity Tx
nephrotoxic (preventable with
mannitol diuresis).
Tacrolimus aka
FK506
FK506 aka
Tacrolimus
Tacrolimus

Mechanism
Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and
other cytokines.
Tacrolimus

Clinical use
Potent immunosuppressive used in organ transplant recipients.
Tacrolimus

Toxicity
Significant––nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion,
hyperglycemia.
Azathioprine

Mechanism
Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and
synthesis of nucleic acids. Toxic to proliferating lymphocytes.
Azathioprine

Clinical use
Kidney transplantation, autoimmune disorders (including glomerulonephritis and hemolytic anemia).
Azathioprine

Toxicity
Bone marrow suppression. Active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be ↑ by allopurinol.
Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and
other cytokines.
Tacrolimus (FK506)
Binds to cyclophilins. Complex blocks the differentiation and activation of T cells
by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.
Cyclosporine
Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and
synthesis of nucleic acids. Toxic to proliferating lymphocytes.
Azathioprine
Recombinant cytokines

Clinical use for Aldesleukin (interleukin-2)
Renal cell carcinoma, metastatic melanoma
Recombinant cytokines

Clinical use for epoetin
Anemias (especially in renal failure)
Recombinant cytokines

Clinical use for Filgrastim
Recovery of bone marrow
Recombinant cytokines

Clinical use for Sargramostim
Recovery of bone marrow
Recombinant cytokines

Clinical use for α-interferon
Hepatitis B and C, Kaposi’s sarcoma, leukemias, malignant melanoma
Recombinant cytokines

Clinical use for β-interferon
Multiple sclerosis
Recombinant cytokines

Clinical use for gamma-interferon
Chronic granulomatous disease
Recombinant cytokines

Clinical use for Oprelvekin
Thrombocytopenia
Recombinant cytokines

Clinical use for Thrombopoietin
Thrombocytopenia
Which Recombinant cytokine is used for

Renal cell carcinoma
Aldesleukin (interleukin-2
Which Recombinant cytokine is used for

metastatic melanoma
Aldesleukin (interleukin-2)
Which Recombinant cytokine is used for

Anemias (especially in renal failure)
Erythropoietin (epoetin)
Which Recombinant cytokine is used for

Recovery of bone marrow
Filgrastim (granulocyte
colony-stimulating factor)

Sargramostim (granulocyte-
macrophage colony-
stimulating factor)
Which Recombinant cytokine is used for

Hepatitis B and C
α-interferon
Which Recombinant cytokine is used for

Kaposi's sarcoma
α-interferon
Which Recombinant cytokine is used for

leukemias
α-interferon
Which Recombinant cytokine is used for

malignant melanoma without mets
α-interferon
Which Recombinant cytokine is used for

Multiple sclerosis
β-interferon
Which Recombinant cytokine is used for

Chronic granulomatous disease
gamma-interferon
Which Recombinant cytokine is used for

Thrombocytopenia
Oprelvekin (interleukin-11)

Thrombopoietin