Diseases Week 1 Flashcards
Spitz Nevi
Bright red dome-shaped nodule. Unpredicatable behavior that can become melanoma –> Excise all.
Necrotizing Fascitis
trauma allows for deep seated infection–> release of exotoxin B (protease) –> rapid necrosis along fascial planes w/ no damage to muscles. Treat aggressively and fast. IV AB’s and debridement/amputation.
Aquired localized increase in sebaceous glands. Larger than normal glands. Yellow papules
Sebaceous hyperplasia
Common (acquired) and Congenital Nevi
Most common pigmented lesion. Higher risk for melanoma.
Nephrogenic Systemic Fibrosis (NFS)
Rare condition caused by gadolinium based contrast agents. Causes multisystem fibrosis esp in skin and subcutaneous tissues. Risk factors include: chronic renal insufficiency, chronic hemodialysis, and multiples exposures to contrast. Screen for renal dysfunciton.
Skin tag/ Fibroepithelial polyp/ Acrochordon
Very common cutaneous lesion, not neoplastic. Soft flesh colored bag-like tumor with stalk.
Bullous pemphigloid
Autoimmune blistering disorder of dermis-endodermis (hemidesmosome) juction. Blister in lamina lucida region.
Most common human malignancy –> pearly papule with telangiectasia (defined blood vessels in papule) Slow growing. Rarely metastasize Risk factors: sun exposure, light pigment, XP
Basal Cell Carcinoma
Impetigo
Lesions look like peeling skin, crusty and flaky scabs, or honey-colored crusts. Usually around mouth face and extremeitis. Same for SA and SP. Treat both bacteria.
Nevus of Ota/Ito
Ota: Peri-Ocular, intraocular dermal melanocytic nevus Ito: Mongolian spot, same type of lesion, different site.
Hemangioma
Well formed benign vascular spaces in dermis. Clinically must seperate from malignant vascular neoplasms
Benign fibrous histocytoma or Dermatofibroma
Very common dermal proliferation of histiocytes and fibroblasts. Tan brown firm papules. Use pinch test (squeeze edges of lesion and dimple will appear in middle of lesion most of the time)
Very aggressive epithelial neoplasm mostly caused by polyomavirus. Presumed to differentiate as Merkel cells (touch cells). Microscopicall mimics small cell lung carcinoma and lymphoma.
Merkel cell carcinoma
Hyper pigmentation of basal epidermis due to excess melanin production
Solar Lentigo
Common epithelial neoplasm. Brown and velvety papules/plaques. Related with age and normally benign. Due to increased melanin not melanocytes. Leser-Trelat Sign- paraneoplastic, rapid growth of numerous seborrheic keratoses.
Sebhorrheic Keratosis
Benign lobular circumscribed neoplasm of sebocytes and peripheral basaloid epithelial cells
Sebaceous Adenoma
Very common dermal proliferation of histiocytes and fibroblasts. Tan brown firm papules. Use pinch test (squeeze edges of lesion and dimple will appear in middle of lesion most of the time)
Benign fibrous histocytoma or Dermatofibroma
Psudomonas Aeruginosa
Burn wound infection (cellulitis) and folliculitus (hot tub foliculitis) Infection arises by breach of host defense barriers.
skin infection (cellulitis) –> systemic release of pyrogenic exotoxins A (superantigen) or TSS1 –> polyclonal T cell activation –> acute fever, shock, multiorgan failure
Toxic Shock Syndrome
Staphylococcal Scalded Skin Syndrome (SSSS)
dermolytic condition caused by SA. Affects mostly newborns and babies. Like impetigo it is an exotoxin-mediated disease (systemic form) ET-A and ET-B. Breaks connection of dermis and epidermis.
Malignant neoplasm. Most are periocular (inner/outer lid) Extraocular forms are more likely in Muir Torre Syndrome Metastasis common, death in 20%
Sebaceous Carcinoma
Sebaceous Adenoma
Benign lobular circumscribed neoplasm of sebocytes and peripheral basaloid epithelial cells
Dysplastic Nevi (DPN)
Irregular shaped nevi that can be familial or sporadic. Multiple DPN = increased risk of melanoma. Excise moderate and severe atypia (mild can go either way).
Differentiate toward hair follicle, eccrine, sebacious, eccrine, and apocrine glands. Benign and malignant types. Too many to learn. Can be a clue to internal pathology (Cowden’s and Muir Torre)
Adenexal Proliferations/Neoplasms
Papules and nodules of skin in infants/children. Dendritic cells arise in bone marrow and travel to skin. Skin has dense dermal infiltrate of LCs.
Langerhans cell histiocytosis
Muir-Torre Syndrome
Germline mutations in DNA mismatch repair proteins: MLH1, MLH2, MSH6, PMS2. Skin: sebaceous adenoma and carcinoma, keratoacanthomas. Internal carcinomas: Colon/Rectal, endometrial, ovarian Rerpresents subset of HNPCC (hereditary non-polyposis colorectal carcinoma syndrome) Young Aduld w/ sebaceous adenoma or carcinoma –> test for MTS
Basal Cell Carcinoma
Most common human malignancy –> pearly papule with telangiectasia (defined blood vessels in papule) Slow growing. Rarely metastasize Risk factors: sun exposure, light pigment, XP
Most likely to occur in line with pedicles. Most likely causes problems with inferior spinal cord(s)
Herniated disc
Lentigo Simplex
Localized hyperplasia of melanocytes that is not sun related. Small brown macules with uniform coloration.
Toxic Shock Syndrome
skin infection (cellulitis) –> systemic release of pyrogenic exotoxins A (superantigen) or TSS1 –> polyclonal T cell activation –> acute fever, shock, multiorgan failure
Most common pigmented lesion. Higher risk for melanoma.
Common (acquired) and Congenital Nevi
Sebhorrheic Keratosis
Common epithelial neoplasm. Brown and velvety papules/plaques. Related with age and normally benign. Due to increased melanin not melanocytes. Leser-Trelat Sign- paraneoplastic, rapid growth of numerous seborrheic keratoses.
Most common type of cutaneous T cell lymphoma. Neoplastic cell is CD4+
Mycosis Fungoides
Common neoplasm on sun exposed skin in older people. Largest risk factor is sun exposure. Also XP In situ: contained above basement membrane Invasive: invades basement membrane and dermis Less than 5% will metastasize.
Squamous Cell Carcinoma
Rocky Mountain Spotted Fever
Causative agent- Rickettsia rickettsii (obligate intracellular and palm and sole rash big indicators) Clinical Presentation: Rash, fever, headache Pathology: Dermacentor wood or dog tick –>inflamation of endothelial cells of small blood vessels –> macopopular rash on palms and soles spreading to the trunk –> headache and CNS changes, renal damage –> death if untreated (mortality = 30%) Treatment - Doxycycline
Breslow Depth test
Depth of invasion of melanoma is the best predictor for the probability to metastasize. >1mm = do sentinel node biopsy. Other important indicators are ulceration and mitotic rate.
Well formed benign vascular spaces in dermis. Clinically must seperate from malignant vascular neoplasms
Hemangioma
Dermatofibrosarcoma Protuberans (DFSP)
Well differentiated fibrosarcoma of skin. Rarely metastasize/locally aggressive. Protuberant nodule within a firm plaque.
Germline mutations in DNA mismatch repair proteins: MLH1, MLH2, MSH6, PMS2. Skin: sebaceous adenoma and carcinoma, keratoacanthomas. Internal carcinomas: Colon/Rectal, endometrial, ovarian Rerpresents subset of HNPCC (hereditary non-polyposis colorectal carcinoma syndrome) Young Aduld w/ sebaceous adenoma or carcinoma –> test for MTS
Muir-Torre Syndrome
Solar Lentigo
Hyper pigmentation of basal epidermis due to excess melanin production
trauma allows for deep seated infection–> release of exotoxin B (protease) –> rapid necrosis along fascial planes w/ no damage to muscles. Treat aggressively and fast. IV AB’s and debridement/amputation.
Necrotizing Fascitis
Melasma
Butterfly mask like facial hyperpigmentation. Can be brought on by pregnancy or OCPs (reversible)
dermolytic condition caused by SA. Affects mostly newborns and babies. Like impetigo it is an exotoxin-mediated disease (systemic form) ET-A and ET-B. Breaks connection of dermis and epidermis.
Staphylococcal Scalded Skin Syndrome (SSSS)
Albinism
No melanin produced (or decreased) due to inherited defect in tyrosinase
Rare condition caused by gadolinium based contrast agents. Causes multisystem fibrosis esp in skin and subcutaneous tissues. Risk factors include: chronic renal insufficiency, chronic hemodialysis, and multiples exposures to contrast. Screen for renal dysfunciton.
Nephrogenic Systemic Fibrosis (NFS)
Mycosis Fungoides
Most common type of cutaneous T cell lymphoma. Neoplastic cell is CD4+
Benign blue/brown papules. Often clinically concerning for melanoma. Excise.
Blue Nevi
Cellulitis
Fast spreading infection in the dermis and subcutaneous tissues. Pain, tenderness, warmth and swelling. In healthy individuals think SA and SP. Many causes in immunocomprimised. Treat with something that kills SA and SP. Surgical debridement is warranted in extensive damaged tissues.
Causative agent: B. burgdorferi (spirochete) Clinical presentation: Stage 1 (10 days after bite): Erythema chronicum migrans Stage 2 (weeks later): CNS involvement - Bell’s palsy, aseptic meningitis, peripheral neuropathy CV - carditis, AV nodal block Skin - secondary annular lesions Joints- migratory myalgias, transient arthritis Stage 3 (month to years) - chronic arthritis, encepalopathy, acrodermatitis chronicum atrophicans Treatment- Doxycycline
Lyme Disease
Pemphigous vulgaris
Autoimmune blistering disorder caused by disruption of desmosomes linking keratinocytes. Antibodies made against desmogleins.
Well differentiated fibrosarcoma of skin. Rarely metastasize/locally aggressive. Protuberant nodule within a firm plaque.
Dermatofibrosarcoma Protuberans (DFSP)
Leukemia Cutis
Spread of leukemia cells to the skin.
BCC at early age with abnormalities of bone, nervous system, eyes, and reproductive organs. Tumor suppressor gene is mutated.
Basal Cell Nevus Syndrome (Gorlin Syndrome)
Adenexal Proliferations/Neoplasms
Differentiate toward hair follicle, eccrine, sebacious, eccrine, and apocrine glands. Benign and malignant types. Too many to learn. Can be a clue to internal pathology (Cowden’s and Muir Torre)
Butterfly mask like facial hyperpigmentation. Can be brought on by pregnancy or OCPs (reversible)
Melasma
Mastocytosis
Mast cells originate in marrow and travel to skin. Uticaria pigmentosa: localized to skin –> Darier’s sign (histamine) Systemic mastocytosis: organ involvement
Down growth of epidermis which becomes cystic leading to subcutaneous or dermal nodule.
Epithelial Cyst
Sebaceous hyperplasia
Aquired localized increase in sebaceous glands. Larger than normal glands. Yellow papules
Fast spreading infection in the dermis and subcutaneous tissues. Pain, tenderness, warmth and swelling. In healthy individuals think SA and SP. Many causes in immunocomprimised. Treat with something that kills SA and SP. Surgical debridement is warranted in extensive damaged tissues.
Cellulitis
Cowden’s Syndrome
Hereditary condition prone to multiple hamartomas and malignancy. Skin: multiple trichilemmomas (face) –> benign neoplasm growing towards hair, benign keratoses of acral skin. Internal: breast, endometrial, and thyroid carcinoma Mutation in PTEN (tumor suppressor gene)
Basal Cell Nevus Syndrome (Gorlin Syndrome)
BCC at early age with abnormalities of bone, nervous system, eyes, and reproductive organs. Tumor suppressor gene is mutated.
Benign proliferation of hair follicle epithelium. Important epithelial marker for internal problems of Cowden’s Syndrome
Trichilmmoma
Sebaceous Carcinoma
Malignant neoplasm. Most are periocular (inner/outer lid) Extraocular forms are more likely in Muir Torre Syndrome Metastasis common, death in 20%
Langerhans cell histiocytosis
Papules and nodules of skin in infants/children. Dendritic cells arise in bone marrow and travel to skin. Skin has dense dermal infiltrate of LCs.
Depth of invasion of melanoma is the best predictor for the probability to metastasize. >1mm = do sentinel node biopsy. Other important indicators are ulceration and mitotic rate.
Breslow Depth test
Small tan red macules arising in childhood that fade and reapper in cycle.
Freckle (Ephilis, Ephelides)
Benign vs. Malignant
Benign: Not penetrated BM, no ability to metastasize. -Melanocytic - Nevi -Eptihelial - Actinic Keratosis, Adenomas -Stromal - Leiomyoma, hemanioma Malignant: Penetrated BM and has the ability to metastasize. -Melanocytic - Melanoma - Epithelial - SCC, BCC -Stromal - Dermatofibrosarcoma Protuberans (DFSP), leiomyosarcoma, angiosarcoma.
Results from an increase in the number of proliferating cells in stratum basale and spinosum. Also increase in cell turnover. Results in greater epi thickness and continual turnover.
Psoriasis
Trichilmmoma
Benign proliferation of hair follicle epithelium. Important epithelial marker for internal problems of Cowden’s Syndrome
Very common cutaneous lesion, not neoplastic. Soft flesh colored bag-like tumor with stalk.
Skin tag/ Fibroepithelial polyp/ Acrochordon
Nevus (mole)
Benign neoplasms of melanocytes. Congenital or acquired Most have mutations (BRAF)
Benign: Not penetrated BM, no ability to metastasize. -Melanocytic - Nevi -Eptihelial - Actinic Keratosis, Adenomas -Stromal - Leiomyoma, hemanioma Malignant: Penetrated BM and has the ability to metastasize. -Melanocytic - Melanoma - Epithelial - SCC, BCC -Stromal - Dermatofibrosarcoma Protuberans (DFSP), leiomyosarcoma, angiosarcoma.
Benign vs. Malignant
Autoimmune blistering disorder caused by disruption of desmosomes linking keratinocytes. Antibodies made against desmogleins.
Pemphigous vulgaris
Squamous Cell Carcinoma
Common neoplasm on sun exposed skin in older people. Largest risk factor is sun exposure. Also XP In situ: contained above basement membrane Invasive: invades basement membrane and dermis Less than 5% will metastasize.
Herniated disc
Most likely to occur in line with pedicles. Most likely causes problems with inferior spinal cord(s)
Less common than CTCL. Solitary of few nodules rather than patches/plaques. Good prognosis. Must exclude secondary cutaneous involvement by nodal lymphoma
Cutaneous B cell Lymphomas
Cutaneous T cell Lymphoma
T cells arise in marrow and travel to skin. Usually a very slowly progressive disease in adults >40. Looks like psoriasis, excema etc. early on. Nodules later. If cells seed blood: Sezary syndrome
Localized hyperplasia of melanocytes that is not sun related. Small brown macules with uniform coloration.
Lentigo Simplex
Psoriasis
Results from an increase in the number of proliferating cells in stratum basale and spinosum. Also increase in cell turnover. Results in greater epi thickness and continual turnover.
Vitiligo
Partial or complete loss of melanocytes due to lymphocyte mediated autoimmunity. Well demarcated macules/patches. Associated with other autoimmune disorders.
Actinic Keratosis (AK)
Benign neoplasm of epidermis (may precede squamous cell carcinoma. Induced by sunlight. Rough spots on skin less than 1 cm. Treated with liquid nitrogen, curettage, topical chemotherapy.
Benign neoplasms of melanocytes. Congenital or acquired Most have mutations (BRAF)
Nevus (mole)
Epithelial Cyst
Down growth of epidermis which becomes cystic leading to subcutaneous or dermal nodule.
Freckle (Ephilis, Ephelides)
Small tan red macules arising in childhood that fade and reapper in cycle.
Blue Nevi
Benign blue/brown papules. Often clinically concerning for melanoma. Excise.
T cells arise in marrow and travel to skin. Usually a very slowly progressive disease in adults >40. Looks like psoriasis, excema etc. early on. Nodules later. If cells seed blood: Sezary syndrome
Cutaneous T cell Lymphoma
Causative agent- Rickettsia rickettsii (obligate intracellular and palm and sole rash big indicators) Clinical Presentation: Rash, fever, headache Pathology: Dermacentor wood or dog tick –>inflamation of endothelial cells of small blood vessels –> macopopular rash on palms and soles spreading to the trunk –> headache and CNS changes, renal damage –> death if untreated (mortality = 30%) Treatment - Doxycycline
Rocky Mountain Spotted Fever
Malignant neoplasm of melanocytes. Risk Factors: fair skin, sun exposure, many DPN Usually asymptomatic, may itch. Change in color or size of pre-existing lesion –> remember ABCD’s (Asymmetry, Border, Color, Diameter -6mm, or pencil eraser, or bigger)
Malignant Melanoma
Lesions look like peeling skin, crusty and flaky scabs, or honey-colored crusts. Usually around mouth face and extremeitis. Same for SA and SP. Treat both bacteria.
Impetigo
Merkel cell carcinoma
Very aggressive epithelial neoplasm mostly caused by polyomavirus. Presumed to differentiate as Merkel cells (touch cells). Microscopicall mimics small cell lung carcinoma and lymphoma.
Burn wound infection (cellulitis) and folliculitus (hot tub foliculitis) Infection arises by breach of host defense barriers.
Psudomonas Aeruginosa
Gas Gangrene
Cauative agent: Clostridium perfingens. Pathology: clostridia are not very invasive, infection requires damaged or dead tissue and anaerobic environoment. Produce several exotoxins, the most potent of which is alpha toxin, causes rbc rupture, edema, and tissue destruction.
Ota: Peri-Ocular, intraocular dermal melanocytic nevus Ito: Mongolian spot, same type of lesion, different site.
Nevus of Ota/Ito
Bright red dome-shaped nodule. Unpredicatable behavior that can become melanoma –> Excise all.
Spitz Nevi
Mast cells originate in marrow and travel to skin. Uticaria pigmentosa: localized to skin –> Darier’s sign (histamine) Systemic mastocytosis: organ involvement
Mastocytosis
No melanin produced (or decreased) due to inherited defect in tyrosinase
Albinism
Irregular shaped nevi that can be familial or sporadic. Multiple DPN = increased risk of melanoma. Excise moderate and severe atypia (mild can go either way).
Dysplastic Nevi (DPN)
Benign neoplasm of epidermis (may precede squamous cell carcinoma. Induced by sunlight. Rough spots on skin less than 1 cm. Treated with liquid nitrogen, curettage, topical chemotherapy.
Actinic Keratosis (AK)
Autoimmune blistering disorder of dermis-endodermis (hemidesmosome) juction. Blister in lamina lucida region.
Bullous pemphigloid
Lyme Disease
Causative agent: B. burgdorferi (spirochete) Clinical presentation: Stage 1 (10 days after bite): Erythema chronicum migrans Stage 2 (weeks later): CNS involvement - Bell’s palsy, aseptic meningitis, peripheral neuropathy CV - carditis, AV nodal block Skin - secondary annular lesions Joints- migratory myalgias, transient arthritis Stage 3 (month to years) - chronic arthritis, encepalopathy, acrodermatitis chronicum atrophicans Treatment- Doxycycline
Spread of leukemia cells to the skin.
Leukemia Cutis
Cauative agent: Clostridium perfingens. Pathology: clostridia are not very invasive, infection requires damaged or dead tissue and anaerobic environoment. Produce several exotoxins, the most potent of which is alpha toxin, causes rbc rupture, edema, and tissue destruction.
Gas Gangrene
Partial or complete loss of melanocytes due to lymphocyte mediated autoimmunity. Well demarcated macules/patches. Associated with other autoimmune disorders.
Vitiligo
Hereditary condition prone to multiple hamartomas and malignancy. Skin: multiple trichilemmomas (face) –> benign neoplasm growing towards hair, benign keratoses of acral skin. Internal: breast, endometrial, and thyroid carcinoma Mutation in PTEN (tumor suppressor gene)
Cowden’s Syndrome
Malignant Melanoma
Malignant neoplasm of melanocytes. Risk Factors: fair skin, sun exposure, many DPN Usually asymptomatic, may itch. Change in color or size of pre-existing lesion –> remember ABCD’s (Asymmetry, Border, Color, Diameter -6mm, or pencil eraser, or bigger)
Cutaneous B cell Lymphomas
Less common than CTCL. Solitary of few nodules rather than patches/plaques. Good prognosis. Must exclude secondary cutaneous involvement by nodal lymphoma
