Derm2- Non-Pruritic Alopecia

  1. What are causes of acquired canine alopecia? (8)
    pattern baldness, color dilution alopecia, black hair follicular dysplasia, seasonal flank alopecia, sertoli cell tumor, hypothyroidism, hyperadrenocorticism, and alopecia X
  2. What are the 3 phases of the hair cycle?
    • Anagen: active growth
    • Catagen: transitional phase
    • Telogen: resting phase
  3. Contrast the microscopic appearance of anagen-phase versus telogen-phase hairs.
    • Anagen: comma-shaped, pigmented
    • Telogen: arrow-shaped, non-pigmented
  4. What factors influences the duration of the hair cycle? (9)
    age, body region, breed, sex, photoperiod, ambient temperature, hormones (esp. cortisol), general state of health, growth factors/cytokines
  5. Potential causes of acquired alopecia. (5)
    auto-inflicted, infectious, inflammatory reactions, follicular dysplasia, endocrinopathies, other
  6. What are auto-inflicted causes of acquired alopecia? (2)
    hypersensitivities, parasites
  7. What are infectious causes of acquired alopecia? (4)
    bacterial folliculitis, demodex, dermatophytosis, leishamniasis
  8. What are inflammatory reaction causes of acquired alopecia? (4)
    rabies vaccine reaction, dermatophytosis, alopecia areata, sebaceous adenitis
  9. What are endocrinopathic causes of acquired alopecia? (4)
    hypothyroidism, hyperadrenocorticism, sex hormone imbalances, alopecia X
  10. What are follicular dysplasia causes of acquired alopecia? (3)
    color dilution alopecia, black hair follicular dysplasia, recurrent flank alopecia
  11. What are miscellaneous causes of acquired alopecia? (3)
    telogen and anagen defluxion, canine pattern alopecia, paraneoplastic alopecia
  12. Describe telogen/anagen defluxion.
    stressful situation (sx, illness, cortisol)—> hair follicles simultaneous enter telogen—> when a new hair cycle starts 3mo later—> all telogen hairs shed simultaneous—> transient alopecia
  13. What should you rule out when approaching an alopecic patient?
    pruritus and systemic diseases
  14. If pruritus is absent, what is you diagnostic approach? (6)
    pattern of hair loss, presence of inflammation, presence of lesions, skin scraping (r/o demodex), skin cytology (r/o bacterial folliculitis), dermatophyte culture (r/o ringworm)
  15. In what breeds (generally) is alopecia due to chemotherapy most likely to occur?
    breeds with anagen-driven hair cycle
  16. Why do some dogs need hair cuts frequently (constantly growing hair) and some have short hair that does not need to be cut?
    Some breed have an anagen-driven hair cycle (like humans) and need frequent grooming and hair cuts; some breeds have a telogen-driven hair cycle (if you pluck hair from a lab and most of the hairs are telogen hairs, this is probably contrast to a yorkie)
  17. What can potentially cause failure to regrow after clipping? (5)
    hypothyroidism, hyperadrenocorticism, alopecia X, post-clipping alopecia (unknown pathogenesis), normal (you shaved when most of the hairs were in telogen....wait for hair cycle to restart in ~3 months)
  18. How can sexual status shed light on the cause of alopecia? (3)
    intact: sertoli cell tumor, ovarian cyst, not cycling? consider endocrinopathy
  19. What is the assumed pathophysiology of pattern baldness?
    miniaturization of the hair follicle with age, and they no longer produce a hair shaft
  20. What are the 4 clinical syndromes of pattern baldness?
    • [most common] alopecia on pinnae, ventral neck, ventrum, caudomedial thighs- restricted to these areas
    • pinnal alopecia of dachshunds
    • caudal thigh alopecia of greyhounds
    • follicular dysplasia in american water spaniels (not true pattern baldness....needs more research)
  21. Breeds with a predisposition for pattern baldness. (7)
    dachshunds, boston terriers, chihuahuas, whippets, manchester terriers, greyhounds, italian greyhounds
  22. What are rule outs to diagnose pattern baldness? (5)
    hair follicle dysplasia, sex hormone dermatoses, hypothyroidism, hyperadrenocorticism, alopecia areata [need biopsy to confirm]
  23. What might you give to a dog with pattern baldness?
    cosmetic problem so probably nothing, but if the client wants something, try oral melatonin
  24. What is the cause of color dilution alopecia?
    inherited autosomal recessive disorder in dogs with color-diluted coats (blue or fawn)
  25. What are clinical signs of color dilution alopecia? (4)
    hypotrichosis to alopecia affecting hair follicles in the diluted areas of fur, clinical signs start b/w 6m-3y old, prone to bacterial folliculitis, white macules (leukoderma)
  26. How do you diagnose color dilution alopecia? (3)
    breed/coat color suggestive, trichogram (hairs with large melanin clumps, causing distortion and fracture of hair shaft), histopathology to confirm
  27. In what animals does black hair follicular dysplasia occur? (3)
    black dogs, coat changes seen as young as 4 weeks, progressive alopecia until all black hair is lost
  28. How do you diagnose black hair follicular dysplasia? (3)
    only black hair affected (suggestive), r/o demodex and ringworm, histopath to confirm
  29. What is the treatment for black hair follicular dysplasia? (3)
    no effective treatment, treat secondary infections, do not use harsh shampoos/be gentle when grooming
  30. What is suggestive of seasonal flank alopecia? (2)
    episodes of recurrent truncal hair loss, Boxers and English Bulldogs predisposed (assumed genetic influence- pathogenesis not understood)
  31. How do you diagnose seasonal flank alopecia? (3)
    characteristic clinical signs, r/o hypothyroidism/demodex/sex hormone imbalance/alopecia X [biopsy and blood work]
  32. How do you manage seasonal flank alopecia?
    difficult to evaluate response b/c the hair regrows anyway, suggested to try oral melatonin (cosmetic problem)
  33. Male feminization syndrome is associated with __________, which are more common in ____________.
    sertoli cell tumors; cryptorchids
  34. What breeds are predisposed to sertoli cell tumors? (5)
    boxers, shelties, collies, weims, cairn terriers, pekingeses
  35. What are clinical signs of sertoli cell tumors? (6)
    linear preputial dermatosis, pendulous prepuce, gynecomastia, enlarged nipples, cryptorchids or mass in scrotum, prostate often enlarged/infected
  36. How do you treat male feminization syndrome? (3)
    castration, clinical response seen in 3 months, remission followed by relapse indicated mets
  37. What are causes of hypothyroidism? (3)
    congenital dwarfism (uncommon), primary acquired hypothyriodism (most common), secondary hypothyroidism (inadequate TSH production in pituitary)
  38. What are the etiologies of primary hypothyroidism? (2)
    lymphocytic thyroiditis, idiopathic thyroid atrophy
  39. What are the possible dermatologic manifestations of hypothyroidism? (8)
    thinning hair coat, symmetrical non-inflammatory alopecia, don't regrow hair after shaving, hyperpigmentation, generalized seborrhea, rat tail, secondary infections, myxedema
  40. Why does hypothyroidism cause alopecia?
    thyroid hormones promote the initiation of the anagen phase of the hair cycle
  41. How does hypothyroidism lead to secondary infections?
    the normal barrier function of the epidermis is likely impaired, impaired neutrophil and lymphocyte function--> recurrent pyoderma and otitis externa
  42. What blood work abnormalities may lead you to test for hypothyroidism? (5)
    hypercholesterolemia, hypertriglyceridemia, +/- mild non-regenerative anemia, hyponatremia, +/- elevated ALP/CK
  43. How do you diagnose primary hypothyroidism?
    low T4 or fT4 and elevated TSH
  44. How is hypothyroidism managed?
  45. How long does it take for signs of hypothyroidism to resolve?
    activity/alertness within 1 week, weight loss within a month, neuro signs improve in 1-2m, derm signs within 3 months
  46. When do you re-check for levothyroxine therapy?
    recheck 6-8 weeks after starting, 4-6hr post-pill tT4
  47. What are possible etiologies of Cushing's? (3)
    pituitary adenomas (increased ACTH), adrenal tumors (increased cortisol without increased ACTH), iatrogenic
  48. Atypical Cushing's can be due to increased... (4)
    androgens, estradiol, progesterone, dehydroepiandrosterone
  49. Systemic effects of excess glucocorticoids. (7)
    increased hepatic gluconeogenesis, increased glycogen deposition, increased protein catabolism, affects fat metabolism (redistribution and deposition), increased BP, increased sodium retention and potassium loss, lymphocyte inhibition
  50. Dermatologic effects of glucocorticoids. (6)
    thin skin/hyperkeratosis, atrophic hair follicles and sebaceous glands, fragile blood vessels, delayed wound healing, increased susceptibility to infections, calcinosis cutis
  51. Common clinical signs associated with Cushing's disease. (5)
    PU/PD, polyphagia, abdominal distention, muscle wasting, skin lesions
  52. Cutaneous signs of Cushing's. (8)
    dull haircoat, bilaterally symmetrical truncal alopecia, failure to regrow hair after clipping, think skin, comedones, poor healing, hyperpigmentation, secondary infections
  53. What diseases can often be secondary to Cushing's)? (3)
    pyoderma, yeast dermatitis, demodicosis
  54. Comedones are seen with... (2)
    Cushing's and demodex (rule out demodex)
  55. __________ is a common underlying cause of adult onset demodicosis.
  56. When __________ is present with Cushing's, prognosis is poor.
    calcinosis cutis
  57. Blood work abnormalities common with Cushing's disease. (7)
    increased ALP/ALT/cholesterol, decreased BUN/Cre, hyperglycemia,stress leukogram, low USG, glucosuria, proteinuria
  58. How do you diagnose Cushing's? (4)
    • if you have low level of suspicion, may be able to rule out with urine cortisol:creatinine ratio
    • LDDST- screening test
    • HDDST- differentiating test
    • if suspect iatrogenic, ACTH stimulation test
  59. Describe potential treatments of cushing's disease. (4)
    mitotane, trilostane, surgery, radiation
  60. Alopecia X is aka __________.
    hair cycle arrest
  61. What breeds are predisposed to alopecia X? (5)
    Pomeranians, Keeshon, Chows, Samoyed, miniature poodles
  62. What age dogs usually present with alopecia X?
    middle-aged to older
  63. What are clinical signs of alopecia X?
    bilaterally symmetrical alopecia originating in frictional areas, primary hairs lost first then variable loss of secondary hairs (puppy coat)
  64. What initially affected areas are common with alopecia X? (5)
    rump, perineum, caudal thighs, neck, tail
  65. What body areas are usually spared with alopecia X, even in late/severe disease?
    head and distal legs
  66. How do you diagnose alopecia X? (7)
    • rule out hypothyroidism/cushing's/testicular tumors(if intact), rule out follicular dysplasia (biopsy), diagnosis of exclusion based on signalement
    • ACTH stim??
    • urine C:C ratio measured daily for 10 days?
  67. What test used to be used for alopecia X that is no longer used because non-clinical dogs were positive?
    17-hydroxypregesterone levels on adrenal panel
  68. How is alopecia X managed?
    • melatonin (variable response- give at least 3 months)
    • Trilostane- block excessive production of cortisol by blocking 3-beta hydroxysteroid dehydrogenase (can be tapered down after hair regrowth)
    • Microneedling
Card Set
Derm2- Non-Pruritic Alopecia
vetmed derm2