Lumps And Bumps Flashcards
What are warts?
- common dermatological condition = HPV infection
- occur anywhere
- cosmetic concern, can become painful/ cancerous
- Pathogenesis = interplay between virus & host immune response
HPV infections
- large group of more than 150 genotypes = infect epithelia of skin/ mucosa
- most commonly = benign papillomas/ warts
- infections = transient subclinical, cleared cellular immune response
150 HPV types
- type might have specific affinity for type of tissues
- mucosal (mouth, resp tract, genitalia)
= moist surface layers - “high-risk”
= 16&18 - premalignant
— low grade abnormalities of mucosal cells
— high grade abnormalities/ pre-cancers in mucosal cells
— various cancers - “low-risk”
= 6&11 - benign
— resp & laryngeal papillomas
— low grade abnormalities of mucosal cells
— genital warts (rarely cancer) - cutaneous
- “common” warts
= hands & feet
Types of cutaneous warts
- common warts (verruca vulgaris)
- plantar warts (myrmecial type) (verruca plantaris) = soles of feet
- plantar warts (mosaic type) = soles
- plane warts (verruca plana) = flat topped plaques
- filiform & digitale warts
- butcher’s wart (similar to common, cuts & abrasions)
- epidermodysplasia verruciforms (rare, autosomal recessive inherited skin disorder = chronic generalized eruption of warts, acquired if immunity compromised)
Condylomata accuminata
- high/ low grade HPV types
- low grade = 6, 11
- high grade = 16, 18
Warts transmission & entry
- skin to skin contact/ contaminated surfaces (towels/ gym equipment)
- HPV enter skin = microscopic breaks/ abrasions in epidermis, viral access to nasal layer of epidermis = active cell division occurs
Warts viral infection & replication
- HPV infects basal keratinocytes in epidermis
- viral DNA is released into host cells nucleus, replicates using host cellular machinery
- virus completes life cycle within keratinocytes = production of new viral particles
- stratum basale is the epidermal cell layer where HPV starts actively dividing
Warts viral persistence & evasion
- HPV developed strategies to evade host immune response & establish long-term persistence
- viral proteins interfere with antigen presentation, reducing recognition of infected cells by immune cells
- HPV modulates cytokine production, inhibiting activation of immune cells
Epidermal hyperplasia & wart formation
- HPV infection leads to abnormal proliferation & differentiation of infected keratinocytes
- infected cells in basal layer exhibit increased mitosis activity, delayed maturation & dyskeratosis (abnormal keratinisation occuring prematurely within cells below stratum granulosum)
- epidermis thickens due to increased cell division & differentiation = clinical appearance of wart
Wart viral particle assembly & release
- infected keratinocytes mature & move toward skin surface, viral particles are assembled
- particles accumulate within cytoplasm & become released into environment
- released viral particles can potentially infect other individuals/ spread to different areas of patient’s own body
Factors influencing wart persistence
- Several factors can influence persistance of warts, patient’s immune status, HPV type, viral load & wart location
- immune compromised individuals, organ transplant recipients/ HIV, experience more persistent/ widespread warts
Cysts
- pathological structures = encapsulated sac/ cavity containing fluid/ semi-sold material
- occur in various organs & tissues throughout body
General characteristics of cutaneous cysts
- cyst wall of basal cells, Supra basal cells & cyst contents
Eg: keratin debris, sebaceous gland, sweat gland/ hair - skin cysts surrounded by layers of dermal cells & basement membrane between dermal cells & basal epidermal cells
- develop as a consequence of epithelial cell dysfunction
Basic micro anatomy of cutaneous cyst
- Dermal cell
- Basement membrane
- Basal cell
- Suprabasal cell
- Keratin debris
Different types of cutaneous cysts
- epidermal cyst = dermal, suprahasal
- steatocystoma multiplex = basement membrane, keratin debris
- dermoid cyst = basal, sebaceous gland
- Trichilemmal cyst = hair follicle
- hidrocystoma = endocrine/ apocrine sweat gland, squamous eddies
Retention cysts
- AKA simple/ non-neoplastic cysts, most common
- develop when normal secretions/ fluids become trapped within closed cavity / duct due to obstruction/impaired drainage
- eg: sebaceous cysts, mucous cysts & renal cysts
Developmental cysts
- arise during embryonic development due to abnormal/ incomplete formation of specific tissues/ structures
- eg: dermoid cysts, branchial cysts & arachnoid cysts
Inflammatory cysts
- occur as a result of chronic inflammation/ infection
- process leads to formation of cavity/ encapsulated collection of inflammatory exudate
- eg: abscesses, pilonidal cysts & cysticercosis
Molluscum contagiosum
- common viral skin infection = Pox virus: MC
- primarily affects children & immunocompromised individuals
- types of pox virus
- multiple small skin nodules = skin-colluded papules with central umbilication
Molluscum contagiosum transmission & entry
- skin to skin contact/ contact with contaminated objects
- virus gains entry into skin through minor breaks in epidermis, scratches/ abrasions
Molluscum contagiosum viral replication & epidermal proliferation
- after entering skin, MCV infects basal layer of epidermis
- virus replicates within cytoplasm of infected keratinocytes = formation of characteristics molluscum bodies
- infected cells = hypertrophy & hyperplasia = formation of raised papules
Molluscum contagiosum immune response & immune evasion
- pox virus possesses mechanisms to evade the host immune response
- encodes viral proteins that interfere with host’s antiviral defenses, evasion of complement- mediated lysis & inhibition of interferon (chemical messengers secreted by immune cells = interfere with viral replication) signaling pathways
- enable virus = chronic infection
Molluscum contagiosum autoinoculation & dissemination
- auto inoculation = virus spread from one area to another on same individual, common in MC
- scratching/ manipulation of lesions = transfer of viral particle to adjacent/ distant sites in skin
Molluscum contagiosum resolution & spontaneous clearance
- immunocompetent individuals, MC lesions typically resolve spontaneously over time
- immune system recognizes presence of virus, immune-mediated clearance process is initiated = regression of lesions