Derm1- MicroLab

  1. Degeneration occurs in response to... (4)
    physical damage, infection, inflammation, or metabolic disorders.
  2. Proliferative responses always indicate ___________.
    chronic disease
  3. What is hyperkeratosis?
    increased thickness of the stratum corneum, in which the cells have no nuclei
  4. Hyperkeratosis is aka __________.
    orthokeratotic hyperkeratosis
  5. What is parakeratosis?
    increased thickness of the stratum corneum with retention of nuclei
  6. Parakeratosis is aka _____________.
    parakeratotoic hyperkeratosis
  7. Hyperkeratosis and parakeratosis are common features of ____________, producing the clinical manifestations of... (4)
    chronic dermatoses; scale, crusts, scabs, and lichenification.
  8. What dermatological manifestation arises from Vit A or Zinc deficiencies?
    diffuse perakeratosis
  9. What is acanthosis? (2)
    increased thickness of the stratum spinosum, hyperplasia of the epidermis
  10. How do rete ridges form?
    acanthosis--> path of least resistance is down--> hyperplastic epidermis forms downward projections that extend into the dermis but are still attached to the epidermis (not invading dermis)
  11. The "wavy border" b/w the epidermis and dermis that is caused by acanthosis/rete ridges.
    psoriasiform (psoriasis) hyperplasia
  12. When does pesudoepitheliomatous hyperplasia occur?
    when hyperplasia and acanthosis become extreme due to intense chronic irritation, causing rete ridges to become very long and form cross-bridges
  13. What is epidermal atrophy associated with?
    metabolic disorders/endocrine dermatoses
  14. Abnormal growth of keratinocytes in which the cells lose normal relationship b/w one another, forming atypical growth patterns is called ____________ and is usually found in association with ____________.
    epidermal dysplasia; neoplasms or preneoplastic syndrome
  15. Apoptosis (premature death or accelerated keratinization) was previously known as __________ and is a feature of __(2)__.
    dyskeratosis; metabolic disorders or immune-mediated diseases.
  16. What is a Civatte body?
    a degenerate or apoptotic keratinocyte confined to the stratum basale
  17. What are Civatte bodies associated with?
    feature of lichenoid or interface dermatitis
  18. Describe hydropic degeneration.
    swollen cells with expanded cytoplasm and clear vacuoles or perinuclear space
  19. Hydropic degeneration represents ____________.
    intracellular edema
  20. What is edema associated with?
    pathologic processes promoting vascular leakage or damage (such as inflammation, vasculitis)
  21. What is koilocytosis?
    type of hydropic degeneration in which the cell cytoplasm is swollen but does not contain a discrete vacuole- indicative of viral infection
  22. Describe spongiosis.
    separation or pulling apart of keratinocytes with clear spaces b/w them caused by intercellular edema
  23. The migration of inflammatory cells into and through the epidermis, contributing to scab and crust formation.
    exocytosis
  24. How do vesicles and clefts form?
    if spongiosis becomes severe enough, creating a fluid filled cavity or pocket in or beneath the epidermis [clefts are vesicles beneath the epidermis]
  25. What are pustules?
    vesicles filled with inflammatory cells or degenerate keratinocytes
  26. What is acantholysis?
    loss of cohesion b/w keratinocytes due to degeneration of the intercellular cement and desmosomes, resulting in the formation of intraepidermal clefts and pustules
  27. Describe what acantholytic cells look like on histology.
    keratinocytes that lose their polygonal shape and become rounded spheres floating in the edema fluid
  28. What are potential causes of melanosis/hyperpigmentation? (3)
    increased melanin synthesis, increased transfer of melanin to keratinocytes, decrease in melanin degradation
  29. Focal spots of hypopigmentation.
    vitiligo
  30. What is the pathology of furunculosis?
    keratin leaks into the dermis, which stimulates an intense and irritating inflammatory response
  31. What is pigmentary incontinence associated with?
    interface dermatitis--> discoid lupus
  32. What does mucinous degeneration of dermal collagen look like on histopathology?
    amorphous, stringy to granular basophilic material that separates the collagen bundles
  33. How does calcinosis cutis occur?
    mineralization of dermal collagen fibers during degeneration- Cushing's disease
  34. Collagen fiber degeneration associated with eosinophils, which occurs b/c eosinophils contain major basic protein, which mediates degeneration- as seen on histopathology.
    "flame figures"
  35. An inappropriate increase in the amount of dermal collagen may be called... (3)
    fibrosis, sclerosis, or fibroplasia.
  36. When dermal proliferation is stimulated by fibroblast growth factors secreted by neoplastic cells, it is termed _____(2)_____.
    desmoplasia or reactive fibrosis
  37. Fibroblastic connective tissue that is rich in sprouting capillaries.
    granulation tissue
  38. What is a unique characteristic of granulation tissue on histopathology?
    capillaries are oriented perpendicular to the fibroblasts and collagen bundles
  39. An abnormal decrease in the amount of dermal collagen, often with collagen looking normal on histo but only thinner.
    atrophy
  40. Dermal atrophy is a feature of __________.
    metabolic/endocrine disorders
  41. How does dermal dysplasia appear on histopathology?
    disorganization of poorly defined collagen bundles
  42. What does vasculitis look like histologically?
    numerous neutrophils within the capillary wall and migrating out of the capillary into the dermis
  43. When does pigmentary incontinence occur?
    when basal epithelium is damaged and cells cannot hold melanin granules, causing them to "leak" into the superficial dermis, where they are phagocytized by macrophages
  44. Severe damage to follicles results in loss of the hair is seen clinically as __________.
    alopecia
  45. What characterizes telogen phase hairs?
    "club hairs"- have a jagged zone of keratin near the base b/c they are separating from the outer root sheath--> alopecia
  46. Common causes of folliculitis. (3)
    mites (Demodex), dermatophytes (ringworm), bacteria (Staph)
  47. Hypertrophy and hyperplasia of sebaceous glands is usually secondary to __________.
    chronic dermatitis
  48. Hypoplasia and atrophy of sebaceous glands is usually a sign of ___________.
    metabolic/endocrine disorders
  49. Describe the histological appearance of superficial perivascular dermatitis.
    acute inflammatory cells accumulate around superficial and mid-ermal vessels, often with dermal edema
  50. What are some causes of superficial perivascular dermatitis? (3)
    hypersensitivities, ectoparasites, infections
  51. Describe the histological appearance of interface/lichenoid dermatitis.
    form of superficial perivascular dermatitis in which the inflammation is concentrated right at the dermal-epidermal junction
  52. What causes interface/lichenoid dermatitis?
    autoimmune diseases
  53. What causes periadnexal/nodular dermatitis?
    bacterial, fungal, or parasitic infections of the hair follicles/adnexal structures
  54. What is ulcerative dermatitis, and what usually causes it?
    epithelium is removed, usually by self-inflicted trauma, usually secondary to pruritic skin disorders
  55. What is vesicular or pustular dermatitis?
    vesicles or pustules form at different layers of the epidermis- symmetrical distribution on the body
  56. What manifests as vesicular or pustular dermatitis?
    immune-mediated skin disorders, such a pemphigus
  57. Describe the histological appearance of endocrine dermatosis.
    characterized by atrophy of the epidermis, follicles, adnexae, and sometimes a thin dermis
Author
Mawad
ID
314189
Card Set
Derm1- MicroLab
Description
vetmed derm1
Updated