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Sven's Flashcards > 225 - Malignant Melanoma > Flashcards

225 - Malignant Melanoma Flashcards

1
Q

what is an unraised localise area of skin colour/texture change called?

A

macule

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2
Q

what is an elevation of skin

A

papule

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3
Q

what is an elevation of skin >5mm dia called?

A

nodule

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4
Q

what is a small blister

A

vesicle

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5
Q

what is a large blister >5mm of clear fluid called?

A

bulla

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6
Q

what is a blister with visible collection of free pus called?

A

pustule

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7
Q

what is a nodule consisting of an epithelial lined cavity filled with fluid or semi solid material called?

A

cyst

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8
Q

what is a transitory compressible papule or plaque of dermal oedema called?

A

wheal

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9
Q

what is a palpable plateau like elevation of skin called?

A

plaque

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10
Q

what is a accumulation of thickened horn layer keratin called?

A

scale

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11
Q

what is an area of skin loss extending into the dermis called?

A

ulcer

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12
Q

define eczema and how it presents?

A

skin barrier dysfunction of genetic susceptibility due to an abnormal immune response (IgE raised in 80% of atopics)

Itcy, red, weepy in acute, dry scaly and lichenified in chronic

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13
Q

what therapy is available for eczema?

A

irritant avoidance, emollient, soap substitute, topical steroid, topical calcineurininhibitors, bandages.
In more serious oral ABX/steroids, phototherapy, systemic therapies

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14
Q

what is the difference between irritant contact dermatitis and allergic contact dermatitis?

A

irritant - disruption of skin barrier, irritants damage keratinocytes + inflammatory mediators released
allergic - allergen picked up by APCs and causers immunological memory

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15
Q

what allergy tests exist?

A
  • IGE RAST for tyI (intermediate) hypersensitivity

* Patch testing for TyIV (delayed) hypersensitivity

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16
Q

name topical steroids from weak to very potent

A
  • H - weak - hydrocortisone
  • E - mod potent - Eumovate (clobetasol butyrate)
  • B - potent - Betnovate (betamethasone valerate)
  • D - very potent - Dermovate (clobetasone proprionate)
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17
Q

how can sun exposure cause skin cancers?

A

*IV damages cellular DNA
*Tumour suppressor genes often disabled by UV - TP53 mutation (90% of SCCs), TP16 mutation
can be dysfunctional due to dentics +exoderma pigmentosum and basal cell naevus syndrome

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18
Q

who is at risk from malignant melanoma skin cancer?

A
  • neoplasm of melanocytes or daughter cells
  • middle aged females with white tyI skin
  • sunburn, p16 tumour surpressor protein defects, congenital naevi or high numbers of atypical (irregular colour/shape) naevi
19
Q

how does malignant melanoma develop?

A
  • radial growth phase - outwards

* vertical growth phase - invade dermis and can metastasise

20
Q

what are the signs of malignant melanoma and investigations?

A
  • asymmetry
  • irregular border
  • irregular colour - black or blue
  • diameter >6mm
  • evolving
  • nodular most dangerous - elevated, firm, growing
  • excisional biobsy (Breslow thickness)
  • imaging for mets
21
Q

treatment for malignant melanoma?

A

surgical - increase margins (2-3 cm), sentinel node biopsy, adjuvant IFN-alpha

22
Q

what is small cell carcinoma skin cancer and what causes it?

A
  • invasive neoplasm of keratinocytes - Bowen’s disease (in-situ (not invaded through basal lamina). Affects elderly men with ty1 skin (70y/o)
  • mostly due to sun damage afecting TP53 gene, viruses, heavy metals or immunosupression
  • may develop from existing actinic keratoses
23
Q

how does small cell carcinoma skin cancer present?

A
  • red scaly lesions with endurated base on sun exposed areas. May ulcerate later
  • investigations - biopsy, imaging for mets
24
Q

treatments for small cell carcinoma skin cancer?

A
  • exicisional biopsy with margins
  • radiotherapy
  • cryotherapy
  • chemotherapy 5-fluorouracil cream
  • photodynamic therapy
  • immunotherapy - imiquimod cream
25
Q

describe basal cell carcinoma skin cancer?

A
  • most common tumour in white people
  • locally invasive rarely mets
  • risks - sun exposure, fair skin, age, previous radio, tars and arsenic
  • nodular - cystic lesion or pigmented
  • treatment - excision, radio, cryotherapy if superficial
26
Q

describe squamous carcinoma skin cancer?

A
  • less common than BCC - may arise from AK or bowens
  • lips, mouth, ears, scalp. risks smoking or chew tobacco, sun, alcohol
  • ulcerating lesions or scaly enlarging nodules
  • treatment - surgical or radio if frail
27
Q

name some common skin commensals

A

staph epidermidis
diptheroids (corynebacterias)
micrococci

more dangerous staphylococcus aureas (carried by 20%), streptococcus pyrogenes (carried in 10% in throat)

28
Q

what problems can staphylococcus aureus skin infections cause?

A
  • majority produce B-lactamase and th. resistant to penicillins (eg MRSA). Use Flucloxacillin, Methicillin, Co-Amoxiclav
  • They produce exotoxins - proteases that breakdown dermosomes and superantigens like TSST-1 bind irreversibly to Tcells (massive immune response)
  • produce superficial localised infections with no systemic symptoms - Imetigo and ecthyma, folliculitis/furuncles, abcesses, carbuncles
  • use flucoloxacillin or erythromicin
29
Q

what problems can streptococcus pyrogenes skin infections cause?

A

Deeper, spreading infections with systemic symptoms - Erysipelas, cellulitis, abcesses, necrotising fasciitis
*Use amoxycillin or erythromicin

30
Q

what infections do corynebacterium cause?

A
  • Erythrasma - hyperpigmented macular patches

* pitted keratolysis - pits in superficial skin (on soles of feet) - treat with topical ABX +/- antifungals

31
Q

describe syphilis

A
  • treponema pallidum spirochaete (gram -ve bacteria)
  • solitary red papule at site of infection leading to painless non bleeding ulcer then secondary symmeteric pink/brown macular rash 3-4 months after then necrotic papules (patchy alopecia)
  • treat with penicillin
32
Q

describe lyme disease

A
  • borrelia Burgdoferi spirochaete (gram -ve bacteria) trasmitted by tick bite
  • erythema migrans - growing bulls eye rash around bite then systemic symptoms, facial palsy, arthritis
  • treat with penicillin
33
Q

what skin infections can mycobacteria cause?

A
  • lupus vulgaris - by M.tuberculosis - tuberculous lesions around face
  • fish tank granuloma - by M.Marinum - red scaly plaque on arm
34
Q

what causes thrush (candidaiasis) how how should it be treated?

A

*yeast (unicellular fungi) mainly candida albicans
*risks - moist skin folds, obesity/DM, imunnosupression, poor hygiene
*causes itchiness/soreness, continuous red vesiculopustular rash, maceration and fisuring of skin, white plaques, white discharge from genitals
*treat - oral - amphotericin, nystatin or micronazole
skin - topical imidazoles

35
Q

what skin problems do dermatophytes cause?

A
  • multicellular fungi (3types trichopyton, epidermophyton, microsporum)
  • types tinea - coporis (body), pedis (foot), unguium (nail), cruris (groin), manuum (hand), capotis/kerion (head)
  • treat - topical imidalzoles. systemic Itraconazole, terbinafine, greiseofulvin
36
Q

What is the difference in rashes between DNA and RNA viruses?

A
  • RNA - morbilliform rash like measles eg paramyxoviridae

* DNA - vesicular rash like pox eg herpes viruses, varicella zoster

37
Q

how does measles (rubeola) present?

A
  • transmission via respiratory droplets, URT infection, spreads to lymphatics then organs and skin
  • prodromal phase (fever, malaise,anorexia, cough, conjunctivitis and coryza), koplik’s spots (blue grey) on buccal mucosa, rash 4 days after starts on face the spreads (red macular lesion) and lymphadenopathy
  • treat with abx if 2ry bac. infection
38
Q

how does herpes simplex virus 1 and 2 present?

A
  • passed by direct contact or fluid exchange
  • penetrates skin or mucous membrane then destroys epidermal cells then latent in dorsal root ganglia
  • HSV1 acute herpetic gingivostomatitis or acute herpetic pharyngotonsillitis both with fever and malaise & vesicular lesions. Then recurrent with herpes labialis - prodrome of pain, tingling and burning then paulse>vesicles>pustules/ulcers
  • HSV2 prodrome of pain and burning then eruption of vesicles>ulcers
  • investigations tzanck smear, viral tissue culture, PCR
  • treat - antivirals Penciclovir, aciclovir
39
Q

how does varicella zoster virus present?

A
  • URT infection, then to lymph nodes then whole body via immune cells. stays dormant in one or more dorsal spinal/cranial ganglia
  • varicella (chicken pox) - prodromal phase then rash 3-6 days after staring on trunk/face the spreading. paular>vesicula>pustular>crusted
  • zoster (shingles ) - prodromal phase, pain & paraesthesia, depression, flu. vesicular rash in unilateral dermatomal distribution papules>vesicles>crust
  • investigations tzanck smear, tissue culture, PCR
  • treat - aciclovir
40
Q

what cells are in the epidermis?

A

keratinocytes melanocytes and langerhans cells (dendritic)

41
Q

what are the 5 strata of the epidermis (no blood supply)?

A
  • stratum corneum - dead flattened keratinocytes fused into sheets
  • stratum lucidum - dead keratinocytes undergoing keratinisation
  • stratum Granulosum - keratinocytes undergoing cell death, flattening and keratinisation
  • stratum spinosum - keratinocytes starting keratinisation * langerhan cells
  • statum basale (germinativum) - keratinocyte stem cells and melancytes
42
Q

what makes up the dermis?

A
  • papillary layer - thin layer of colalgen, rich capilary (and shunt vessel) network supplying O2 and nutrients to lower strata of epidermis. Responisble for temp regulation
  • reticular layer - thick later of dense collagen and elastic tissue providing strength and supporting structures (follicles, glands).
  • nerve endings - meissner’s (light touch) and pacinian’s (pain and pressure) corpuscules
43
Q

what does the hypodermis do?

A

fat storage

Sven's Flashcards (32 decks)

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