Gen Path - Class 16

Front 1

What is psoriasis?

Back 1

chronic, recurrent, inherited inflammatory condition with well-defined erythematous plaques or papules w/ silvery scales

Front 2

What are the etiology and risk factors of psoriasis?

Back 2

Unknown cause but hereditary (multiple genes involved). Possible immune disorder. Onset or flare-ups triggered by skin irritation (eg. mech, chem, infection, UV, drugs, stress, hormones).

Front 3

What is the pathogenesis of psoriasis?

Back 3

Not fully understood BUT: accelerated proliferation of keratinocytes (4 days vs28 normally) T cell activity (cause or effect role unknown) -- triggers angiogenesis

Front 4

What are five clinical manifestations of psoriasis?

Back 4

(1)erythematous papules or plaques w/ silvery scales, (2)itchy, (3)Scalp, chest, elbows, knees, groin, skin folds, lower back, buttocks (extensor sides), (4)one lesion -- -- numerous patches (Recurrent and persistent), (5)10% develop psoriatic arthritis

Front 5

What is Lupus Erythematosus?

Back 5

chronic, inflammatory connective tissue disorder

Front 6

What are the 2 main classes of Lupus Erythematosus?

Back 6

(1)cutaneous LE, (2)Systemic LE (SLE)

Front 7

What are eight risk factors/etiology of Lupus Erythematosus?

Back 7

(1)Unknown cause, (2)Autoimmune, (3)Genetics, (4)Hormonal, (5)Environmental, (6)immunological, (7)smoking

Front 8

What are four clinical manifestations of Lupus Erythematosus?

Back 8

(1)butterfly (malar) rash w chronic cutaneous LE, (2)discoid lesions (chronic cutaneous lesions w raised edges/central depression) - usually on sun-exposed areas, (3)Rash lasts from hours to days, (4)Precipitated by sun exposure

Front 9

What are Polymyositis & Dermatomyositis?

Back 9

Uncommon disease. Diffuse, recurrent inflammatory myopathies -- systemic weakness esp shoulder & pelvic girdles, neck and pharynx.

Front 10

What is the etiology of Polymyositis & Dermatomyositis?

Back 10

Unknown. Autoimmune with poss T cell attack on muscle cells. May be drug induced. Viral cause?

Front 11

What is the pathogenesis of Polymyositis & Dermatomyositis?

Back 11

Diffuse or focal muscle fiber degeneration (exacerbation)followed by regeneration of new muscle cells (remission)

Front 12

What are seven clinical manifestations of Polymyositis & Dermatomyositis?

Back 12

(1)Symmetrical proximal muscle weakness, (2)Malaise, (3)Weight loss, (4)Fatigue, (5)Aching muscles, (6)Muscle wasting in long standing cases, (7)50% cardiac involvement

Front 13

How does the polymyositis affect dermatomyositis?

Back 13

Dermatomyositisis is diagnosis when rash occurs w Polymyositis

Front 14

What are cold injuries?

Back 14

i.e. Frostbite or hypothermia. Vasoconstriction -- tissue temp dcr'd (-2o C) -- ice crystal formation -- expand extracellular spaces. Compression of cells -- cell and tissue damage. Reperfusion can be significant cause of damage (incr'd capillary permeability and histamine release -- blood clot formation). Rewarm w/ caution-no rubbing or massaging. Can lead to extensive tissue necrosis and gangrene.

Front 15

What are burns?

Back 15

Thermal, chemical, electrical or radiation. Burns occur when energy from a heat source is transferred to tissues of the body

Front 16

What are three factors that influence the severity of burns?

Back 16

(1)burn depth, (2)burn size "rule of nines", (3)location

Front 17

What are two clinical manifestations of burns?

Back 17

(1)Thermal, chemical, electrical or radiation, (2)Burns occur when energy from a heat source is transferred to tissues of the body

Front 18

What are three major phases of burns?

Back 18

(1)emergent phase (injury), (2)acute phase (48 - 72 hours after injury), (3)rehabilitation phase

Front 19

What are eight types of treatments for burns?

Back 19

(1)Cleansing, (2)Removal of damaging agent (i.e. chemical, tar), (3)Removal of dead tissue, (4)Topical antimicrobial creams, (5)Sterile dressing (6)Pain Meds, (7)Skin Grafts, (8)ROM exercises

Front 20

What is a skin ulcer?

Back 20

various causes (diabetes, arterial insufficiency, radiation damage, prolonged pressure, etc)

Front 21

What is a pressure ulcer?

Back 21

aka bed sore / decubitus ulcer. Persistent pressure -- damage of tissues (usually over bony areas). Change in skin temp, consistency or sensation -- loss of superficial layers (e.g. abrasion) -- loss of deep layers -- tissue destruction

Front 22

What are six treatments for pressure ulcers?

Back 22

(1)Prevention!!! (2)Ulcer is cleansed thoroughly, (3)Keep ulcer moist, (4)Topical antibiotics, (5)Surgical debridement of necrotic tissue, (6)Skin grafting

Front 23

What are pigmentation disorders?

Back 23

Pigmentation is determined by melanin. Formation of melanin affected by: Heat, Trauma, Radiation, Heavy metals, Carotene

Front 24

What is hyperpigmentation?

Back 24

Increased pigmentation

Front 25

What is the difference between primary and secondary hyperpigmentation?

Back 25

Primary (nevi, freckles, liver spots, café au lait spots). Secondary (eg. phototoxic rxn to drugs; melasma, pregnancy mask).

Front 26

What is Melasma?

Back 26

Melasma is an acquired hypermelanosis of sun-exposed areas. Melasma presents as symmetrically distributed hyperpigmented macules. (Chloasma is a synonymous term sometimes used to describe the occurrence of melasma during pregnancy.) The most important factor in the development of melasma is exposure to sunlight.

Front 27

What is hypopigmentation?

Back 27

decreased pigmentation

Front 28

What is vitiligo?

Back 28

Pathogenesis: melanocytes are destroyed – mechanism unknown. Theories regarding destruction of melanocytes include autoimmune mechanisms, cytotoxic mechanisms, an intrinsic defect of melanocytes, oxidant-antioxidant mechanisms, and neural mechanisms.

Front 29

What is the clinical manifestation of vitiligo?

Back 29

Small or large circumscribed areas of depigmentation

Front 30

What five other pathologies is vitiligo associated with?

Back 30

(1)hypothyroidism, (2)pernicious anemia, (3)DM, (4)Addison’s disease, (5)stomach carcinoma

Front 31

What is alopecia?

Back 31

Loss of hair from the scalp. May be focal (areata) or diffuse. Alopecia areata. Etiology: Autoimmune or fungal/bacterial

Front 32

What is diffuse alopecia?

Back 32

Typically aging males. Idiopathic , though strong hereditary component. In women it is usually a sign of hormonal disorders or nutritional deficiency. Also caused by cytotoxic drugs Ex. Chemotherapy

Front 33

What is skin cancer?

Back 33

MC Cancer/ Cancer with the greatest increase in incidence inUSA. Affecting almost all > 65 yo white. MCC: sun (UVB) – UV protection esp important 0-20y.

Front 34

What are two examples of benign tumours?

Back 34

(1)Seborrheic Keratosis, (2)Nevi

Front 35

What is Seborrheic Keratosis?

Back 35

Hereditary proliferation of epidermal keratinocytes. Often after middle age. Lesions appear following hormone therapy or inflammation. Lesions on chest, back and face. Waxy, smooth/verrucous (wart-like), raised lesions that can be yellow, skin-colored, dark brown or black

Front 36

What is nevi?

Back 36

(Moles) – start in youth. Collection of melanocytes (brown, black, flesh-coloured). Seldom undergoes transition to malignant melanoma –but it can. Note: change in size, colour or texture; bleeding; excessive itching -- REFER

Front 37

What are two precancerous conditions skin conditions?

Back 37

(1)Actinic (aka solar) Keratosis, (2)Bowen’s Disease

Front 38

What is Actinic (aka solar) Keratosis?

Back 38

Common in older population, especially fair complexion. Affects nearly 100% of older Caucasians. ½ of all skin cancers start as Actinic Keratosis most common precursor or lesion for squamous cell carcinoma.

Front 39

What are two clinical manifestations of Actinic (aka solar) Keratosis?

Back 39

(1)Well-defined, crusty, sandpaper-like patch or bump on chronically sun-exposed areas, (2)May itch of prickle.

Front 40

What can cause Actinic (aka solar) Keratosis?

Back 40

Due to many years of UV exposure on sun-exposed parts. Damage caused by overexposure to sunlight results in abnormal cell growth. Cells involved = epidermal keratinocytes.

Front 41

What is Bowen's disease?

Back 41

AKA Squamous cell carcinoma in situ. May progress to SCC. Cells involved : Epidermal keratinocytes. Can occur anywhere on skin or mucous membranes. Less common –associated w/ arsenic exposure.

Front 42

What is a clinical manifestation of Bowen's disease?

Back 42

Brown to reddish brown, scaly plaque with well defined margins

Front 43

What are four malignant neoplasms?

Back 43

(1)Basal Cell Carcinoma, (2)Squamous Cell Carcinoma, (3)Malignant Melanoma, (4)Kaposi’s Sarcoma

Front 44

What is basal cell carcinoma?

Back 44

Most common malignant tumour in Caucasians. From basal cells in epidermis. Slow-growing with no blood vessel invasion. Significant local epidermis/dermis damage. Rarely metastasizes. Pathogenesis unclear. No known precursors

Front 45

What is the etiology and risk factors of basal cell carcinoma?

Back 45

Etiology: sun, UV tanning

Risk Factors: blond/fair skin, Burns, Immunosuppression, Genetic predisposition

Front 46

What are five clinical manifestations of basal cell carcinoma?

Back 46

(1)MC sites head, neck, trunk, (2)starts as a small, shiny papule on sun exposed area, (3)after several months -- pearly quality, raised border, telangectasia, (4)Painless, (5)can invade deeper tissues/ulcerate if not detected

Front 47

What is Squamous Cell Carcinoma?

Back 47

2nd most common skin cancer in Caucasians. Tumour of epidermal keratinocytes –predominantly sun-exposed areas (ears, lips, mouth, backs of hands)

Front 48

What are the etiology and risk factors of squamous cell carcinoma?

Back 48

Etiology: sun, UV tanning, burns, radiation therapy, arsenic,c arcinogens

Risk Factors: blond/fair skin, pre-malignant lesions, chronic irritation or inflammation

Front 49

What is the pathogenesis of squamous cell carcinoma?

Back 49

UV radiation -- epithelial cell DNA damage -- damaged cells have deficient repair mechanisms -- malignancy

Front 50

What are four clinical manifestations of squamous cell carcinoma?

Back 50

(1)Red papule w/ scaly, crusted appearance, (2)poorly defined margins, (3)may appear lumpy or nodular (like a wart), (4)may ulcerate, can be invasive and can metastasize

Front 51

What is Malignant Melanoma?

Back 51

neoplasm of melanocytes

Front 52

What are the four types of malignant melanoma?

Back 52

(1)Superficial spreading melanoma, (2)Nodular melanoma, (3)Lentigo Maligna melanoma, (4)Acral Lentigo melanoma

Front 53

What is superficial spreading melanoma?

Back 53

Most common (70%). Can occur from pre-existing mole (50%) or normal skin (50%). Spreads superficially for years. Asymptomatic

Front 54

What is nodular melanoma?

Back 54

>men. Blue, black nodule on the skin. Appears suddenly and spreads into dermis quickly

Front 55

What is lentigo maligna melanoma?

Back 55

Less common. Comes from pre-existing lentigo. Large flat freckle (3-6cm).

Front 56

What is Acral Lentigo melanoma?

Back 56

Uncommon. But is the most common melanoma in dark-skinned people. Typically appears on the palms, soles, or under the nails

Front 57

What is the etiology of malignant neoplasms?

Back 57

holiday sun exposure/work indoors. Chronic irritation.

Front 58

What are five risk factors for malignant neoplasms?

Back 58

(1)red/blond hair, green/blue eyes, (2)North European ancestry, (3)Atypical Mole Syndrome (genetic-large # irregular moles), (4)UV/tanning exposure, (5)Pilots/flight crews exposed to ionizing radiation of Cosmic origin

Front 59

What is the pathogenesis of malignant neoplasms?

Back 59

intense UV exposure. Pre-existing mole -- similar to Squamous cell (but different cell type)

Front 60

What are six clinical manifestations of malignant neoplasms?

Back 60

(1)anywhere on the body, (2)~70% arise from pigmented nevi and 50% from normal skin, (3)maculopapular rash or lesion, (4)gradually develops irregular, raised borders, (5)within borders -- coloured spots (red, blue, white, black) or little nodules, (6)Increased risk for metastasis -- clues are bleeding or ulceration

Front 61

What are the ABCD's of moles?

Back 61

A: Asymmetry

B: Border (irregular edges, scalloped or indefinite edges)

C: Colour (funky: black, browns, red, white, and occ blue)

D: Diameter (> pencil eraser)

Front 62

What is Kaposi’s Sarcoma?

Back 62

vascular tissue malignancy (ie. not actually skin tumour, but manifests in the skin, mucous membranes + other organs)

Front 63

What is the etiology of Kaposi's Sarcoma?

Back 63

HHV-8 (5-10% gen pop’n, up to 70% homosexual males; increase with increased number of partners)

Front 64

What are the two types of Kaposi's Sarcoma?

Back 64

Classic KS (older Mediterranean men)-Genetic predisposition

Epidemic KS (immunodeficient, AIDs or transplant, etc)

Front 65

What is the pathogenesis of Kaposi's Sarcoma?

Back 65

HHV-8 mechanism of trasmission unknown. KS is an angioproliferative tumour. Cell origin is unclear – thought to be pluripotentmesenchymal progenitor

Front 66

What are six clinical manifestations of Kaposi's Sarcoma?

Back 66

(1)Epidemic KS commonly on upper body involving LN, lungs, GI, (2)Classic KS occurs on lower extremities, (3)raised papules/thickened plaques, oval-shaped, red to brown, (4)Itching, (5)Pain, (6)Fever, chills, night sweats, anorexia, diarrhea, dyspnea, cough chest pain