Lumps And Bumps

Question 1

What are warts?

Answer 1

• common dermatological condition = HPV infection
• occur anywhere
• cosmetic concern, can become painful/ cancerous
• Pathogenesis = interplay between virus & host immune response

Question 2

HPV infections

Answer 2

• large group of more than 150 genotypes = infect epithelia of skin/ mucosa
• most commonly = benign papillomas/ warts
• infections = transient subclinical, cleared cellular immune response

Question 3

150 HPV types

Answer 3

• 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

Question 4

Types of cutaneous warts

Answer 4

• 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)

Question 5

Condylomata accuminata

Answer 5

• high/ low grade HPV types
• low grade = 6, 11
• high grade = 16, 18

Question 6

Warts transmission & entry

Answer 6

• 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

Question 7

Warts viral infection & replication

Answer 7

• 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

Question 8

Warts viral persistence & evasion

Answer 8

• 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

Question 9

Epidermal hyperplasia & wart formation

Answer 9

• 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

Question 10

Wart viral particle assembly & release

Answer 10

• 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

Question 11

Factors influencing wart persistence

Answer 11

• 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

Question 12

Cysts

Answer 12

• pathological structures = encapsulated sac/ cavity containing fluid/ semi-sold material
• occur in various organs & tissues throughout body

Question 13

General characteristics of cutaneous cysts

Answer 13

• 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

Question 14

Basic micro anatomy of cutaneous cyst

Answer 14

1. Dermal cell
2. Basement membrane
3. Basal cell
4. Suprabasal cell
5. Keratin debris

Question 15

Different types of cutaneous cysts

Answer 15

• 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

Question 16

Retention cysts

Answer 16

• 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

Question 17

Developmental cysts

Answer 17

• arise during embryonic development due to abnormal/ incomplete formation of specific tissues/ structures
• eg: dermoid cysts, branchial cysts & arachnoid cysts

Question 18

Inflammatory cysts

Answer 18

• occur as a result of chronic inflammation/ infection
• process leads to formation of cavity/ encapsulated collection of inflammatory exudate
• eg: abscesses, pilonidal cysts & cysticercosis

Question 19

Molluscum contagiosum

Answer 19

• 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

Question 20

Molluscum contagiosum transmission & entry

Answer 20

• skin to skin contact/ contact with contaminated objects
• virus gains entry into skin through minor breaks in epidermis, scratches/ abrasions

Question 21

Molluscum contagiosum viral replication & epidermal proliferation

Answer 21

• 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

Question 22

Molluscum contagiosum immune response & immune evasion

Answer 22

• 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

Question 23

Molluscum contagiosum autoinoculation & dissemination

Answer 23

• 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

Question 24

Molluscum contagiosum resolution & spontaneous clearance

Answer 24

• immunocompetent individuals, MC lesions typically resolve spontaneously over time
• immune system recognizes presence of virus, immune-mediated clearance process is initiated = regression of lesions

Question 25

Molluscum contagiosum complications & secondary infections

Answer 25

• 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

Question 26

Sporotrichosis

Answer 26

• 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

Question 27

Sporotrichosis transmission

Answer 27

• 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

Question 28

Sporotrichosis factors contributing to disease progression

Answer 28

• 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

Question 29

Erythema Nodosum

Answer 29

• 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

Question 30

Chronic phase erythema nodosum

Answer 30

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

Question 31

Range of precipitating factors in erythema nodosum

Answer 31

• idiopathic = common cause
• infectious causes = especially URTI (Strep & non-strep)
• common causes = drugs, sarcoidosis, inflammatory bowel disease