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78 Cards in this Set

  • Front
  • Back
What are the components of the skin?
epidermis, dermis, skin appendages, and subcutaneous fat.
Layers of the epidermis from outer to inner?
Stratum corneum

statum granulosum

stratum spinosum

basal layer
Melanocytes. where? what? why are they important?
Melanin producing and they are in the basal layer.

also tumors can arise from these.
Another name for HIves?

Caused by?
Wheat formation from mast cell degranulation which is increased capillary permeability.

Allergic activation of IgE and mast cell degeneration by chemical drugs or insect bites.

When does it normally occur?
Inflammatory dermatoses of unknown cause.

Late adolescence
Psoriasis locations?
Elbows, knees, scalp, lumbosacral areas, interguteal cleft, and HEAD OF THE PENIS!
Psoriasis appearance?
Well-demarcated, pink plaques covered by silver scales. Scaling. Nail changes.

Rarely, Pustular Psoriasis.
Lichen planus?
Chronic skin and mucous membranous disease where lesions resolve in one or two years.
Wickham's striae?
Violaceous papules with white dots or lines.
Acne vulgaris?
Most common.

Chronic inflammatory reaction of the hair follicles.
Black heads?
Open comedomes where keratin was oxidized.
White heads?
Closed comedomes where keratin was trapped under the epithelium.
Pemphigus vulgaris?

Location on the body?
Most common type of autoimmune blistering diease. Affects both mucosa and skin.

Face, axilla, groin, trunk, scalp, and pressure points.
Vesicles and bullae are superficial and rupture easily.
Pemphigus vulgaris location in the skin?
Clefts and intraepithelial blisters.
Pemphigus vulgaris test?
Immunofluorescence testing shows intercellular deposits of IgG.
Bullous Pemphigus?
Affects mainly the elderly people and has tense SUB-epithelial bullea in skin and mucosal surfaces.
Bullous Pemphigus sites?
Thighs, flexor surfaces or forearms, axilla. groin, and lower absomen.

Bullae result from the detachement of epitheilum from underlying CT.
Bullous Pemphigus test?
IF deposits of IgG and complement along the basement membrane.
Dermatitis Herpitiformis?

Looks like Herpes.

IF shows granular deposits of IgA at tips of dermal papillae.
Another word or Warts?
papillomatous epidermal hyperplasia caused by the papilloma virus.
Verruca vulgaris?
Common wart. Anywhere on skin.
Verruca Plana?
Flat wart: smooth slightly elevated papules, often occurs on face.
Verruca plantaris/palmaris?
scaly warts (lesions) on soles and palms, respectively.
Condyloma acuminatum?
Anogenital warts: soft, Tan, cauliflower-like papillomas.

types 6, 11.
What are 4 major staph infections in the skin?
Scalded skin syndrome: Toxic shock.

Impetigo: superficial skin infection due to S. aureus.

Furuncle: "boil" Pus filled nodules in dermis.

Carbuncle: Necrotizing infection of skin and subcutaneous tissue composed of a cluster of furuncules.
Dermatological features of HIV?
Kaposi's sarcoma


molluscum contagiosum




deep mycoses

Seborheic Keratosis?

Common epidermal tumors.

Common in old ppl

Round, flat and "pasted-on"
Three different names for Fibroepithelial polyp?

Squamous papilloma

skin tag
Fibroepithelial polyp?
Appear soft and flesh colored.

Associated with diabetes, intestinal polyposis, and become more numerous during pregnancy.
Epithelial cyst.

filled with keratin and lipid-containing debris.
Rapidly developing neoplasm, clinically and histologically resemble squamous cell carcinoma. heals spontanously.
Actinic keratosis?
Premalignant lesion that occurs on sun-exposed areas in primary light skinned individuals.


High percentage undergo malignant transformation
Squamous cell carcinoma?
Sun-exposed areas in older people. M>F except in lower leg.

Also arise by chronic ulcers, scars, industrial carcinogens, and tobacco.
Micro and Macro appearance of squamous cell carcinoma?
Sharply defined red scaling plaques. Invasive lesions maybe ulcerated and hyperkeratotic.

When mocosa is involved: Leukoplakia.

Cell atypia--> squamous cell carcinoma.
squamous cell carcinoma prognosis?
Mucous membrane lesions have a high rate of metastasis.

Sun-exposed lesions remain localized.
Basal Cell carcinoma?
Very slow-growing tumors that rarely metastasize.

Sun-exposed areas

Associated with basal cell nevus syndrome.
Basal Cell carcinoma appearance?
pearly papules which contain melanin pigment and advanced lesions have ulcerate borders.

Micro: Cell nests by mucinous CT stroma.
Malignant melanoma?
Cutaneous neoplasm from melanocytes.

Most important clinical sign is the changes in color in the pigmented lesion.

Itching, bleeding, ulceration maybe present. Satellite tumors may appear near the primary growth.

Survival depends on early detection. ABCD rules.
What happens to bone resorption ? formation? osteoclast and blast activity in osteoporosis?
Increased resorption and osteoclast activity

Decreased bone formation and osteoblast activity

Bone resorption exceeds that of bone formation.
what happens to bone cortex and mineralization in osteoporosis?
Decreased thickness, trabeculae number and size.

Bone mineralization is the same.
What is the most important factor in osteoporosis?
Age. After 40 or 50. Calcium absorption decreases with age.
Besides age what other factors can cause osteoporosis?
Loss of estrogenic/androgenic activity after menopause and increased age in men.

Immobilization. Helped with exercise.

Cushing's syndrome and pregnancy as well as hormone problems,
T/F Osteopenia "little bone" is only seen in osteoporosis?
False It's also seen in other diseases of the bone.
Rickets and Osteomalacia is caused by what? What is the difference b/w them?
Vit. D deficiency

Rickets is in children

Osteomalacia is in adults.
What happens to mineralization in Rickets and Osteomalacia?
Defective and leads to decreased calcified bone.
What can cause Vit. D deficiency
no sunlight


Phosphate depletion: Fanconi syndrome, heavy metal poisoning, and idiopathic leak.
Clinical signs of Rickets and Osteomalacia?
Bone deformities: Rachitic rosary (swollen costochondral junctions of ribs), Pigeon chest from the sternum, deformed limbs.

Compression fractures and decreased bone thickness.
Osteomyelitis is caused by what?
Staph, E. coli, N. gonorrhea, H. influenza, and Salmonella species (most common in in children with sickle cell anemia.
Organisms are introduced in Osteomyelitis by?
Hematogenous route: long bones usually 5-15. Starts in medullary and spreads.

Extension of adjacent infection

Direct introduction of organisms into bone penetrating wounds, fractures, or surgery-most common cause of osteomyelitis in US.
Necrosis of bone fragments is called?
Sequestrum. Dead bone no osteocytes and empty lacunae.
What is an Involucrum?
Subperiosteal new bone formation (sheath of new bone which encloses inflammatory focus).
Garre's sclerosing osteomyelitis?
Dense sclerotic bone causing enlargement of shaft.
Brodie's abscess?
When the bone infection becomes walled off.
Complications of Osteomyelitis
Septicemia, acute bacteria arthritis, pathologic fractures, squamous cell carcinoma, and amyloidosis (abnormal protein growth).
Tuberculous Spondylitis (Pott disease) main points?
Affect thoracic vertebrae especially T11.

Necroses leads to collapse and kyphosis and scoliosis.

Exudate produce a psoas abscess which is present as a cold fluctuating abscess.

Systemic amyloidosis may develop in protracted cases.
Osteoarthritis (OA)?
Degenerative process of articular cartilage mainly in wt bearing joints.

Wear and tear. cell death and reactive proliferation of chondrocytes death and cartilage degeneration.

Age related.
Primary OA and Secondary OA?
Occurs de novo; males in midlife; females later.

Any age in previously damaged joints
OA appearance?
Thinning of cartilage.

Flaking and cleft formation in cartilage.

Ulceration can lead to eburnation (ivory-like appearance)

"join mice" osteophytes (bone spurs) may erode and loose pieces of bone go into the joint.
What joints are effected in OA?
Hips, knees and vertebrae.
Heberden's nodes?
Distal joints of fingers at the base of terminal phalanges.
Rheumatoid arthritis (RA)?
Systemic chronic inflammatory CT disease that involves the joints.

Autoimmune disease Rheumatoid arthritis RA antibody against IgG present in 80% of patents.

Immune complex formation leads to joint inflammation and lytic enzymatic destruction of joint.
Rheumatoid arthritis (RA) Appearance?
Mostly small joints of fingers, wrists, but large joints may also be involved.

Painful, swollen, tender joints.

Pannus destroys cartilage and fills joint space and results in fibrous and bony ankylosis.

Neutrophils can be present in synovial fluid.
Rheumatoid arthritis (RA) clinical findings and lab tests?
Systemic disease effecting many organs.

Lab: Hypergammaglobulinemia which contains Rheumatoid factor which is an antibody against IgG. Titers depend on severity of disease.
Disease characterized by increased uric acid levels.
Primary gout?

Secondary gout?
No other intercurrent disease is present. Increased urate production, decreased urate excretion or both.

Hyperuricemia is caused by an intercurrent condition associated with increased cell lysis and release of nucleic acids. Chronic hemolysis, polycythemia, leukemia and lymphoma. Maybe drugs. Also congenital effects which lead to hypercalcemia.
Gout appearance?
Uric acid crystals in the joints have birefringent with polarized light,

Marked inflammation reaction composed of macrophages, lymphocytes, fibroblasts and foreign-body giant cells: tophus which is pathognomoic of gout.
What is the most important complication of gout?
Renal disease: Acute uric acid nephropathy, nephrolithiasis or chronic urate nephropathy. 90% of pts with chronic arthritis have renal impairment.
Clinical presentation of gout?
sudden around 30years/old. Almost never female. Usually big toe first.
Highly malignant tumor characterized by production of osteoid and bone.

ages 10-20 with males more then females.

Etiology is unknown: predisposing factors maybe radiation, Paget's disease and genetic.
Osteosarcoma appearance and spread?
80-90% arise in medullary cavity.

Stroma consist of bizarre pleomorphic cells with hyperchromatic, irregular nuclei, and abundant mitoses. Necrosis, hemorrhage, islands of cartilage and foci of multinucleated giant cells are also present.

Metastasis to lungs 90% are fatal.
Malignant cartilaginous tumor which occurs half as often as Osteosarcoma.

Arise in Central skeleton and about the knee (rarely in ankles or wrists).
Chondrosarcoma appearance?
Lobulated, gray-white, translucent mass with areas of necrosis and calcification.

Immature cartilage showing anaplasia within lacunar cells, hyperchromatic nuclei, and two or cells within a single lacuna.
Metastatic tumors?
More common then primary tumors. Often first sign.

carcinomas at various sites.

Most frequent sites:
Brochus + prostate in males (osteoblastic)

Breast in females (osteolytic).
Myathenia Gravis effects males or females more? age?

Thymic hyperplasia? Thymoma?
Myathenia Gravis associated.

The Thymus plays an important role in the autoimmunity in MG.
Duchenne muscular dystrophy?
aka progressive muscular dystrophy.

Most common. sex-linked recessive (boys) Gene deletion (dystrophin) on the short arm of X-chromosome

Weakness in pelvic and shoulder girdles.

Death before 20 (respiratory insufficiency and cardiac arrhythmia)