Lumps And Bumps Flashcards
1
Q
What are warts?
A
- common dermatological condition = HPV infection
- occur anywhere
- cosmetic concern, can become painful/ cancerous
- Pathogenesis = interplay between virus & host immune response
2
Q
HPV infections
A
- large group of more than 150 genotypes = infect epithelia of skin/ mucosa
- most commonly = benign papillomas/ warts
- infections = transient subclinical, cleared cellular immune response
3
Q
150 HPV types
A
- 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
4
Q
Types of cutaneous warts
A
- 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)
5
Q
Condylomata accuminata
A
- high/ low grade HPV types
- low grade = 6, 11
- high grade = 16, 18
6
Q
Warts transmission & entry
A
- 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
7
Q
Warts viral infection & replication
A
- 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
8
Q
Warts viral persistence & evasion
A
- 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
9
Q
Epidermal hyperplasia & wart formation
A
- 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
10
Q
Wart viral particle assembly & release
A
- 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
11
Q
Factors influencing wart persistence
A
- 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
12
Q
Cysts
A
- pathological structures = encapsulated sac/ cavity containing fluid/ semi-sold material
- occur in various organs & tissues throughout body
13
Q
General characteristics of cutaneous cysts
A
- 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
14
Q
Basic micro anatomy of cutaneous cyst
A
- Dermal cell
- Basement membrane
- Basal cell
- Suprabasal cell
- Keratin debris
15
Q
Different types of cutaneous cysts
A
- 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
16
Q
Retention cysts
A
- 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
17
Q
Developmental cysts
A
- arise during embryonic development due to abnormal/ incomplete formation of specific tissues/ structures
- eg: dermoid cysts, branchial cysts & arachnoid cysts
18
Q
Inflammatory cysts
A
- occur as a result of chronic inflammation/ infection
- process leads to formation of cavity/ encapsulated collection of inflammatory exudate
- eg: abscesses, pilonidal cysts & cysticercosis
19
Q
Molluscum contagiosum
A
- 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
20
Q
Molluscum contagiosum transmission & entry
A
- skin to skin contact/ contact with contaminated objects
- virus gains entry into skin through minor breaks in epidermis, scratches/ abrasions
21
Q
Molluscum contagiosum viral replication & epidermal proliferation
A
- 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
22
Q
Molluscum contagiosum immune response & immune evasion
A
- 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
23
Q
Molluscum contagiosum autoinoculation & dissemination
A
- 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
24
Q
Molluscum contagiosum resolution & spontaneous clearance
A
- immunocompetent individuals, MC lesions typically resolve spontaneously over time
- immune system recognizes presence of virus, immune-mediated clearance process is initiated = regression of lesions
25
Q
Molluscum contagiosum complications & secondary infections
A
- self-limited infection, complications = impaired immune function
- secondary bacterial infections (scratching) eg: impetigo, occur due to scratching & breaks in skin integrity = lesions
- secondary infections further contribute to persistence & spread
- conjunctivitis (infected eyelid)
- large widespread MCV larger than normal = uncontrolled HIV/ immunosuppressing drugs
- spontaneous scarring
- scarring = surgical treatment
26
Q
Sporotrichosis
A
- chronic subcutaneous mycosis = fungus sporothrix schenckii
- primarily transmitted through traumatic implantation of fungal conidia into skin from plant materials
- Sporothrix spp. = thermodimorphic fungi, presenting filamentous form (saprophytic phase) in nature/ in vitro at 25 degrees & developing yeast-like cells (parasitic phase) in mammal host/ in vitro at 35-37
27
Q
Sporotrichosis transmission
A
- fungus is found in soil, decaying organic matter & vegetation
- nursery workers, florists & gardeners acquire the disease from roses, sphagnum moss & other plants
- infection limited to site of infection (plaque sprorotrichosis) / extend along proximal lymphatic channels (lymphangitic sprorotrichosis)
- contact with skin leads to entry of fungal conidia
28
Q
Sporotrichosis factors contributing to disease progression
A
- factors influencing disease progression include size of fungal inoculum, strain virulence, host immune status & anatomical site of infection
- immunocompromised individuals = more susceptible to severe forms of Sporotrichosis
29
Q
Erythema Nodosum
A
- multifactorial
- delayed hypersensitivity response to variety of antigenic stimuli = bacteria, viruses & chemical agents
- complex series of intermediate steps is involved in development of lesions
- adhesion molecules & inflammatory mediators associated
— lesions = vascular cell adhesion molecule, platelet endothelial cell adhesion molecule-1, HLA-DR & E-selectin = endothelial cells
— intracellular adhesion molecule-1, very late antigen-4, L-selectin & HLA-DR = expressed by inflammatory cells - neutrophils are numerous in early lesions
— higher % circulating = production of reactive oxygen intermediates
— provoke inflammation & tissue damage - support pathogenic role for these cells & molecules = effects colchicine
— inhibitor of neutrophil chemotaxis diminishes L-selectin expression ICAM-1 on endothelium
30
Q
Chronic phase erythema nodosum
A
Granuloma formation
- TNF is known to play role
- link between deregulation of TNF alpha production & granuloma formation = strong correlation of polymorphism in promoter region of gene that encodes TNF alpha & development of sarcoidosis associated
31
Q
Range of precipitating factors in erythema nodosum
A
- idiopathic = common cause
- infectious causes = especially URTI (Strep & non-strep)
- common causes = drugs, sarcoidosis, inflammatory bowel disease
