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356 Cards in this Set
- Front
- Back
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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”). |
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Gymnast dislocates her shoulder
anteriorly. What nerve is most likely to have been damaged? |
Axillary nerve (C5, C6).
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X-ray shows bilateral hilar
ymphadenopathy. |
Sarcoidosis.
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Child exhibits weakness and
enlarged calves. |
Duchenne’s muscular dystrophy;
X-linked recessive. |
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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.
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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. |
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Epidermis layers From surface to base:
|
Californians Like Girls in
String Bikinis. Stratum corneum Stratum lucidum Stratum granulosum Stratum spinosum Stratum basalis |
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Epithelial cell junctions
surrounds perimeter just below zona occludens |
Zona adherens (intermediate junction)
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Epithelial cell junctions
small, discrete sites of attachment |
Macula adherens (desmosome)
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Epithelial cell junctions
connects cells to underlying extracellular matrix |
Hemidesmosome
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Epithelial cell junctions
maintains integrity of basement membrane |
Integrin
|
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Epithelial cell junctions
prevents diffusion across intracellular space |
Zona occludens (tight junction)
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Epithelial cell junctions
type of protein that forms the Zona adherens (intermediate junction) |
Actin filaments
and E-cadherin |
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Epithelial cell junctions
type of protein that forms the Macula adherens (desmosome) |
Keratin
Desmoplakin |
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Unhappy triad
what |
damage to medial collateral ligament (MCL), medial meniscus, and anterior cruciate ligament (ACL).
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Unhappy triad
when |
lateral hit to the knee
|
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Knee
PCL = LCL = |
PCL = posterior cruciate ligament.
LCL = lateral collateral ligament. |
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“Anterior” and “posterior” in ACL and PCL refer to
|
sites of tibial attachment.
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Knee
Positive anterior drawer sign indicates |
tearing of the
ACL. |
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Knee
Abnormal passive abduction indicates |
a torn MCL.
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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– |
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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. |
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Skeletal muscle contraction
role of ATP |
ATP binds to myosin head and releases actin filament, allowing cross-bridge cycling and shortening to occur.
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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. |
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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.
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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.
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It is the major cellular mediator of calcium-induced calcium release (CICR) in animal cells.
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Ryanodine receptor
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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 |
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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). |
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Skeletal Muscle
what bands change and how |
Contraction results in H and I band shortening, but the A band remains the same length.
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Achondroplasia
geneitcs |
Autosomal-dominant trait
|
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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. |
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Osteoarthritis
mech |
Mechanical––wear and tear of joints leads to destruction of articular cartilage
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Osteoarthritis
predisposing factors |
trauma, age, obesity, joint deformity.
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Osteoarthritis
classic presentation |
pain in weight-bearing joints after use (e.g., at the end of the day),improving with rest. No systemic symptoms.
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Osteoarthritis
different cysts and nodes |
subchondral cysts, sclerosis, osteophytes, eburnation, Heberden’s nodes (DIP), Bouchard’s nodes (PIP).
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Rheumatoid arthritis
mech |
Autoimmune––inflammatory disorder
80% of RA patients have positive rheumatoid factor (anti-IgG antibody). |
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Rheumatoid arthritis
clinical findings |
pannus formation in joints (MCP, PIP), subcutaneous rheumatoid nodules, ulnar deviation, subluxation
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Rheumatoid arthritis
what is RF |
rheumatoid factor (anti-IgG antibody).
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Rheumatoid arthritis
who |
Females > males
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Rheumatoid arthritis
Classic presentation |
Classic presentation: morning stiffness improving with use, symmetric joint involvement, and systemic symptoms (fever, fatigue, pleuritis, pericarditis).
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Osteoporosis
definition |
Reduction of bone mass in spite of normal bone mineralization.
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Osteoporosis
histo |
Sparse trabeculae.
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Osteoporosis
WRT ethnicity |
whites > blacks > Asians.
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Osteoporosis
Type I |
Postmenopausal; ↑ bone resorption due to ↓ estrogen levels. Estrogen replacement is controversial as prophylaxis (side effects).
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Osteoporosis
Type II |
Senile osteoporosis––affects men and women > 70 years.
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Osteoporosis
which type Postmenopausal |
Type I
|
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Osteoporosis
which type affects men and women > 70 years. |
Type II
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Distal radius fractures aka
|
Colles’
|
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Colles’ fractue aka
|
Distal radius fractures
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Vertebral crush fracture
clinical findings |
acute back pain, loss of height, kyphosis.
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acute back pain, loss of height, kyphosis.
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Vertebral crush fracture
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Osteopetrosis aka
|
marble bone disease
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marble bone disease aka
|
Osteopetrosis
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Osteopetrosis
clinical and lab findings |
thickened, dense bones. Serum calcium, phosphate, and alkaline phosphatase are normal. Decreased marrow space leads to anemia, thrombocytopenia, infection.
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Osteopetrosis
mech |
Bone defect is due to
abnormal function of osteoclasts. |
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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. |
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Osteomalacia/rickets
Tx |
Reversible when vitamin D is replaced. Vitamin D deficiency in childhood causes rickets.
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Osteitis fibrosa cystica aka
|
Von Recklinghausen's disease of bone
|
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Von Recklinghausen's disease of bone aka
|
Osteitis fibrosa cystica
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Osteitis fibrosa cystica
caused by |
Caused by hyperparathyroidism
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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).
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Osteitis fibrosa cystica
lab findings |
High serum calcium,
low serum phosphorus, and high alkaline phosphatase. |
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Paget’s disease aka
|
osteitis deformans
|
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osteitis deformans aka
|
Paget’s disease
|
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Paget’s disease
what is it |
Abnormal bone architecture caused by ↑ in both osteoblastic and osteoclastic activity.
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Paget’s disease
lab values |
Serum calcium, phosphorus, and PTH levels are normal. Serum alkaline phosphatase is elevated.
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Paget’s disease
clinical findings |
Long bone chalkstick (transverse to the long axis) fractures. Increased blood flow may
cause high output CHF. |
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Polyostotic fibrous dysplasia
what is it |
Bone is replaced by fibroblasts, collagen, and irregular bony trabeculae.
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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. |
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multiple unilateral bone lesions associated with endocrine abnormalities
(precocious puberty) and unilateral pigmented skin lesions. |
Albright’s syndrome (a form of polyostotic fibrous dysplasia)
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Polymyalgia rheumatica
what is it |
Pain and stiffness in shoulders and hips, often with fever, malaise, and weight loss.Does not cause muscular weakness.
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Polymyalgia rheumatica
wrt strength |
Does not cause muscular weakness.
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Pain and stiffness in shoulders and hips, often with fever, malaise, and weight loss.
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Polymyalgia rheumatica
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Polymyalgia rheumatica
wrt labs |
↑ ESR
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Polymyalgia rheumatica
who and associations |
Occurs in patients > 50 years of age; associatedwith temporal (giant cell) arteritis.
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Polymyalgia rheumatica
Tx |
prednisone.
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Polymyositis
describe |
progressive symmetric proximal muscle weakness caused by CD8 T-cell-induced injury to myofibers.
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Polymyositis
Dx |
Muscle biopsy with evidence of inflammation is diagnostic.
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progressive symmetric proximal muscle weakness caused by CD8 T-cell-induced injury to myofibers.
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Polymyositis
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Dermatomyositis
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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.
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similar to polymyositis but also involves "shawl and face" skin rash and ↑ risk of malignancy.
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Dermatomyositis
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polymyositis/dermatomyositis
wrt labs |
↑ CK, ↑ aldolase, and positive ANA, anti-Jo-1.
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↑ CK, ↑ aldolase, and positive ANA, anti-Jo-1.
|
polymyositis/dermatomyositis
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Mixed connective tissue disease
clinical findings |
Raynaud’s phenomenon, arthralgias, myalgias, fatigue, and esophageal hypomotility.
|
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Mixed connective tissue disease
what type of antibodies |
Antibodies to U1RNP.
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Mixed connective tissue disease
Tx |
Responds to steroids.
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Antibodies to U1RNP
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Mixed connective tissue disease
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Raynaud’s phenomenon, arthralgias, myalgias, fatigue, and esophageal hypomotility.
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Mixed connective tissue disease
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similar to polymyositis but also involves "shawl and face" skin rash and ↑ risk of malignancy.
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dermatomyositis
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Sjögren’s syndrome
clinical findings |
-xerophthalmia
-xerostomia -arthritis. -dental caries -Parotid enlargment |
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Sjögren’s syndrome
wrt cancer |
↑ risk of B-cell lymphoma
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Sjögren’s syndrome
antibodies |
Autoantibodies to ribonucleoprotein antigens, SS-A (Ro), SS-B (La).
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Autoantibodies to ribonucleoprotein antigens, SS-A (Ro), SS-B (La).
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Sjögren’s syndrome
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Sjögren’s syndrome
who |
Predominantly affects females between 40 and
60 years of age. |
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Sjögren’s syndrome
associated conditions |
rheumatoid arthritis.
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Sicca syndrome
|
dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis.
|
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dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis.
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Sicca syndrome
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SLE
who |
90% are female and between ages 14 and 45. Most common and severe in black females.
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SLE
cause of death |
death from renal failure and
infections. |
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SLE
False positives |
False positives on syphilis tests
(RPR/VDRL) due to antiphospholipid antibodies. |
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SLE Lab tests
Antinuclear antibodies (ANA) |
sensitive, but not specific for SLE
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SLE Lab tests
Antibodies to double-stranded DNA |
very specific, poor prognosis
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SLE Lab tests
Anti-Smith antibodies (anti-Sm) |
very specific, but not prognostic
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SLE Lab tests
Antihistone antibodies |
drug-induced lupus
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SLE Lab tests
sensitive, but not specific |
Antinuclear antibodies (ANA)
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SLE Lab tests
very specific, poor prognosis |
Antibodies to double-stranded DNA
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SLE Lab tests
drug-induced lupus |
Antihistone antibodies
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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 |
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Gout
what is it |
Precipitation of monosodium urate crystals into joints due to hyperuricemia,
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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.
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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). |
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Gout
lab |
Crystals are needle shaped and negatively birefringent.
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Gout
who and when |
birefringent. More common in men. Acute attack tends to occur after alcohol consumption or a large meal
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Gout
Tx |
allopurinol, probenecid, colchicine, and NSAIDs.
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Pseudogout
cause |
Caused by deposition of calcium pyrophosphate crystals within the joint space.
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Pseudogout
labs |
Caused by deposition of calcium pyrophosphate crystals within the joint space. Forms
basophilic, rhomboid crystals that are weakly positively birefringent |
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Pseudogout
joints |
Usually affects large joints
(classically the knee). |
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Pseudogout
who |
> 50 years old; both sexes affected equally.
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Pseudogout
Tx |
No treatment.
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Sarcoidosis
histo and lab |
Characterized by immune-mediated, widespread
noncaseating granulomas and elevated serum ACE levels. |
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Sarcoidosis
who |
Common in black females.
|
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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 |
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Associated with restrictive lung disease, erythema nodosum, Bell’s palsy, epithelial granulomas containing microscopic Schaumann and asteroid bodies, uveoparotitis, and hypercalcemia
|
Sarcoidosis
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Sarcoidosis
mech of hypercalcemia |
elevated conversion of vitamin D to its active form in epithelioid macrophages
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Sarcoidosis
mnemonic |
GRAIN:
Gammaglobulinemia Rheumatoid arthritis ACE increase Interstitial fibrosis Noncaseating granulomas |
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Seronegative
spondyloarthropathies name them |
Ankylosing spondylitis
Reiter’s syndrome |
|
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Seronegative
spondyloarthropathies lab findings |
Arthritis without rheumatoid factor (no anti-IgG antibody). Strong association with HLA-
B27 |
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Seronegative
spondyloarthropathies who |
more often in males.
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Ankylosing spondylitis
Lab findings |
RF negative
HLA-B27 positive |
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Reiter’s syndrome
Lab findings |
RF negative
HLA-B27 positive |
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Ankylosing spondylitis
clinical findings |
Chronic inflammatory disease of spine and sacroiliac joints → ankylosis (stiff spine), uveitis, and aortic regurgitation.
Bamboo spine. |
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Reiter’s syndrome
clinical findings |
Classic triad:
1. Urethritis 2. Conjunctivitis and anterior uveitis 3. Arthritis |
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Reiter’s syndrome
who |
Post-GI or chlamydia infections.
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Scleroderma aka
|
progressive systemic sclerosis
|
|
|
progressive systemic sclerosis aka
|
Scleroderma
|
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Scleroderma
mech |
Excessive fibrosis and collagen deposition throughout the body
|
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Scleroderma
2 main types |
1. Diffuse scleroderma
2. CREST syndrome |
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Scleroderma
who |
75% female
|
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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
|
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|
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 |
|
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Associated with anticentromere
antibody |
CREST syndrome
|
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|
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
|
|
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Verrucae aka
|
warts
|
|
|
warts aka
|
Verrucae
|
|
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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 |
