Alopecia 1 & 2 Flashcards
Spontaneous alopecia Genetic defects (
1) due to defect(s) of the hair shaft or hair follicle
2) diagnosed based on presence of hair loss at birth or shortly after birth
3) most have a concurrent dental anomaly (x-linked)
Hair Cycling Abnormalities that cause spontaneous alopecia (5)
1) Hypothyroidism**
2) Hyperadrenocorticism (cushing’s)**
3) Alopecia x
4) Canine flank alopecia
5) color dilute alopecia
Primary Hypothyroidism etiology
1) lymphocytic thyroiditis
2) Autoimmune disease
3) autoantibiodes can be detected
Primary Hypothyroidism etiology
1) lymphocytic thyroiditis
2) Autoimmune disease
3) autoantibodies can be detected
Clinical signs of hypothyroidism (6)
1) alopecia (friction areas)
2) hyperpigmentation
3) excessive scaling
4) recurrent pyoderma
5) cutaneous mucinosis
6) myxedema
Hypothyroidism mechanism of alopecia (5)
1) result of slowing of the hair follicle cycle
2) due to reduction of thyroid hormones
3) hair will NOT fall off spontaneously
4) rubbed off (friction) or “expelled” secondary to folliculitis (bacterial)
5) regrowth of hair stunted
Hypothyroidism diagnosis (4)
1) clinical signs
2) BW
3) T4
4) Histopathology does not help differentiate from different diseases
Treatment of hypothyroidism (5)
1) Levothyroxine
2) increases activity & weight loss 1-2 weeks
3) dermatologic signs: months
4) Recheck 6-8 weeks
5) BW 4-6 hours post pill
Hyperadrenocorticism etiology (3)
1) spontaneous: pituitary dependent –> excessive production of ACTH by pituitart tumor
2) spontaneous: adrenal dependent –> excess production of glucocorticoids by adrenal tumor
3) Iatrogenic: chronic admin of steroids
Hyperadrenocorticism clinical signs (5)
1) alopecia (bilateral symmetrical) spares the head and extremities
2) comedones
3) cutaneous atrophy
4) calcinosis cutis * (mineral deposition in the dermis)
5) recurrent pyoderma
Mechanism of alopecia in Cushing’s (4)
1) due to excess glucocorticoids, hair follicles do not re-enter the anagen phase
2) hair follicle eventually undergo atrophy
3) hair shafts are expelled spontaneously
4) lack of hair shaft leads to formation of comedones
Diagnosis of hyperadrenocorticism (5)
1) clinical signs
2) CBC, chem, UA
3) ACTH stimulation test, LDDS test, HDDS test
4) abdominal ultrasound
5) histopathology will NOT differentiate from other alopecia disease
Treating hyperadrenocorticism (3)
1) trilostane/mitotane
2) ACTH stim used to monitor treatment response
3) adjustment based on clinical response and and ACTH stim
Alopecia X * (3)
1) etiology unknown
2) potential mutation in signaling pathway of receptor in hair follicle cycling
3) prevent hair follicles from entering anagen phase stuck in resting phase
Alopecia X skin lesions (4)
1) bilateral symetrical
2) flanks
3) caudomedial thighs
4) neck
Alopecia X diagnosis (4)
1) breed
2) early onset of skin lesion
3) younger
4) Histopathology with NOT differentiate this disease
Alopecia X treatment (4)
1) cosmetic issue
2) melatonin may be effective
3) neutering
4) trilostane, deslorelin or microneedling (triggering trauma of hair follicles to stimulate growth
Canine flank alopecia *
1) etiology unknown
2) suspected to be caused by intermittent hair follicle cycling defect (arrest )
3) skin lesion; alopecia bilaterally on flanks, irregular in shape, hyperpigmented skin
Canine flank alopecia diagnosis (2)
1) breed
2) distinct characteristic clinical features
3) NO HISTOPATHOOOGY
Canine flank alopecia treatment (1)
1) same as alopecia x
Color dilution alopecia * (3)
1) etiology unknown
2) defective transport of pigment-containing vesicle (melanosome)
3) inherited genetic disease
Color dilution alopecia skin lesion (6)
1) alopecia usually starts on trunk and slowly progresses
2) young adult
3)comedones
4) dry brittle hair coat
5) scaling
6) secondary bacterial infection
Color dilution alopecia diagnosis (5)
1) breed & signalment
2) clinical features/skin lesions
3) r/o hypothyroidism and hyperadrenocorticism
4) hair pluck: aggregates of melanin
5) skin biopsy to confirm abnormal melanosome transfer & follicular cycling abnormalities (normal skin and alopecia area)
Telogen effluvium (defluxion) * (1)
1) a response to severe metabolic stress that developes 3-4 weeks after event
Telogen effluvium (defluxion) * (1)
1) a response to severe metabolic stress that develops 3-4 weeks after event
Causes of folliculitis (3)
1) Bacterial
2) Demodicosis
3) Dermatophytosis
Demodicosis (2)
1) etiology: mites
2) Normal skin flora, aquired from dam during nursing
Demodicosis pathogenesis (3)
1) proliferation of mites lead to follicular inflammation
2) hair falls out spontaneously
3) predisposes to secondary deep pyoderma
Canine Demodicosis juvenile-onset (5)
1) juvenile or adolescent (first 18 months of life)
2) treatment not required for localized form
3) maybe come generalized & requires treatment
4) distribution on face and front limbs
5) < 4 skin lesions with diameter < 2.5 cm
Canine Demodicosis adult-onset (4)
1) develops spontaneously OR due to underlying condition (immunosuppression)
2) treatment often required
3) distribution on face, feet, dorsal trunk
4) > 5 skin lesions
Canine Demodicosis Demodex injai * (4)
1) long bodies mite species (x2 the size of demodex canis)
2) mites found mainly in the sebaceous ducts & glands
3) terrier & terrier crosses
4) skin lesions similar to D. canis but greasiness of the dorsal trunk
Canine Demodicosis diagnosis * (6)
1) Deep skin scrapings in multiple sires
2) trichogram
3) exudate examination- suppurative lesions
4) tape impression & squeezing skin * (no pain)
5) adult onset- investigate underlying cause
6) in many cases the underlying cause CANNOT be determined
Canine Demodicosis treatment (5)
1)Amitraz the only Rx
2) all else off label
3) Continue treatment until two skin scrapes/plucks one month apart do not yield mites
4) may take up to 6 months
5) secondary bacterial infection must be treated as well
Demodex cati (5)
1) follicular mite
2) associated with underlying condition
3) deep skin scrape or hair pluck
4) older onset
5) oral ivermectin
Feline demodex gatoi * (4)
1) pruritic & contagious mite
2) lives in stratum corneum
3) superficial skin scrape
4) lime sulfur dip, advantage multi
Dermatophytosis *** (8)
1) Microsporim canis (cats)
2) trichophton mentagrophytes (small mammal)
3) Microsporum gypseum (inhabits soil)
4) ZOONOTIC)
5) direct contact with infected host, fomites or environment
6) fungal spores can remain in environement for months
7) young/old/immunosuppressed at higher risk
8) cats may be asymptomatic carries, reservoir for infection
Skin lesions Dermatophytosis (5)
1) patches of alopecia +/- erythema
2) lesion tend to expend centrifugally
3) pruritis: varies
4) mild scaling &/or crusting
5) focal, multifocal or generalized
Dermatophytosis Diagnosis (5)
1) woods lamp (fluoresce green apple) & lack of fluoresce does not rule it out
2) trichophton mentagrophytes & Microsporum gypseum do not fluoresce
3) Trichogram
4) Fungal culture (DTM) color change from yellow to red
5) PCR
Positive PCR does not indicate necessarily an infection. Why?
1) a positive PCR test could reflect either
- true infection
- fomite contamination
- detection of non-viable spores
Why treat the environment? (3)
1) prevents spread of infection to susceptible individuals
2) prevents false positive DTM and PCR
3) wash in chlorine bleach
Ischemic Dermatopathies pathogenesis of lesion (1)
1) disruption of the blood supply results in hypoxia of the cells which then supply to
Skin lesions of Ischemic dermatopathies (1)
1) vary and depends on location, size of the vessel, & degree of disruption
Vaccine associated alopecia* etiology (1
1) vaccine induced (rabies often)
Skin lesions associated with vaccine associated alopecia (2)
1) alopecia at vaccine site
2) hyperpigmentation
Vaccine associated alopecia diagnosis & treatment (3)
1) history
2) biopsy of center of the lesion
3) no treatment, spontaneously resolve
Dermatomyositis (3)
1) etiology: unknown
2) collies & shetland sheepdogs
3) diagnosed via skin biopsies
4) treat via immunosuppression
Dermatomyositis skin lesions & other clinical signs (
1) alopecia, erosion, ulceration, scaring on face, ear, and tail tip
2) megaesophagus
3) muscle atrophy/weakness
Generalized ischemic dermatopathy (4)
1) unknown etiology
2) more generalized but identical to dermatomyositis
3) diagnosed via skin biopsy
4) immunosupression
