Alopecia Flashcards
how do you differentiate between spontaneous and self induced alopecia in a clinical case? (LO)
spontaneous:
-well-demarcated/sharp margins
-usually less or no inflammation
-hair epilated easily
-intact hair tips
self-induced:
-not well-demarcated
-usually more inflammation
-hair does not epilate easily
-broken hair tips
describe systemic and cutaneous signs in hypothyroidism (LO)
cutaneous:
1. friction alopecia or failure/delay of hair growth
-alopecia on dorsal muzzle, neck (collar area), and lateral aspects of pressure points and tail
- lack of hair production = comedome/blackhead formation
- skin may be thickened (mucinosis = myxedema), cool to the touch, hyperpigmented
-scaling +/- greasy coat
-thickening possibly due to accumulation of glycosaminoglycans in dermis due to low avail of thyroid hormones = slower metabolism of GAGs - predisposition to secondary bacterial skin infections, otitis infections, demodicosis
systemic:
1. lethargy
2. weight gain or obesity
3. exercise intolerance
4. bradycardia
5. neurological signs
6. dermatological signs: most common! not the first signs, but the other signs are very nonspecific so can help with diagnosis
describe systemic and cutaneous signs in hyperadrenocorticism (LO)
cutaneous:
1. alopecia not always present!
- when present, bilateral symmetrical truncal alopecia that normally spares head and extremities
- skin is thin (atrophic), esp on abdomen and medial thighs with chronic disease
-skin may tear if dermal collagen fiber production is severely altered (esp in cats = skin fragility syndrome)
-when potent topical glucocorticoids used: atrophy at site of application - hyperpigmentation and scaling NOT common
- calcinosis cutis: well-demarcated thick pink small to large hard superficial cutaneous erythematous plaques with gritty surface
-skin cannot be folded over these lesions
-histopath: diffuse mineral deposition extending from the superficial to mid-dermis
-can progress to bone formation (irreversible at that point) - secondary bacterial skin infections +/- demodicosis +/- superficial pyoderma
- comedones: very common
systemic:
1. PU/PD/PP
2. abdominal distension
3. lethargy
4. muscle wasting/weakness
describe Cushing’s/PPID in horses
- degeneration of neurons that produce dopamine leads to inability to control middle lobe of pituitary gland (pars media) and secreted hormones
- long and often curly hair coat that fails to shed
-excessive or decreased sweating and recurrent pyoderma - excessive hairgrowth (hypertrichosis) in PPID-affected horses is due to persistence of hair follicles in anagen
describe alopecia due to genetic hair follicle or hair defects
- hairless X-linked ectodermal dysplasia in chinese crested and mexican hairless dogs
-monogenic autosomal semi-dominant trait with ID’d mutation in forkhead box I3 gene (FOXI3), so homozygosity is lethal
-hairless dogs are heterozygotes
-3 phenotypes: true hairless, semicoated, and powderpuff (haired phenotype)
-lots of comedomes (blackheads) that can develop into secondary bacterial infections like bacterial folliculitis - X-linked anhydrotic ectodermal dysplasia
-recessive mutation of EDA (ectodysplasin A gene)
-abnormalities in sweat glands, sebaceous glands, hair, and teeth
-symmetrical alopecia on frontotemporal area, sacral region, ventral region of neck and trunk, and proximal halves of the 4 limbs
-respiratory infections common due to lack of respiratory tract glands
-hairless breeds (+ dental abnormalities) = follicular ectodermal dysplasias
describe the mechanism of lesion formation of hypothyroidism and general treatment
due to slowing of the hair follicle cycle following a reduction of thyroid hormones
-predominance of telogen phase without atrophy, slow hair growth leads to friction alopecia
-hair will NOT fall off spontaneously unless rubbed off or expelled during folliculitis
-histopath: (no need to biopsy for diagnosis though)
1. primary hair follicles are of normal size and in anagen
2. secondary hair follicles are in telogen
3. infundibula are dilated and filled with a large amount of keratin
general treatment: oral levothyroxine (T4)
-takes 3-6 months before significant hair regrowth
describe the mechanism of lesion formation of hyperadrenocorticism/Cushing’s
- due to excess of endogenous or exogenous systemic or topical glucocorticoids, hair follicles do not re-enter the anagen (growth) phase after the resting (telogen) period/anagen is terminated
-as follicles undergo atrophy, hair shafts are expelled spontaneously, leading to prominent alopecia
- histopath:
-hair follicles severely atrophic
-no anagen
-comedone formation
-collagen production stops = skin gets thinner
describe hair cycle arrest (HCA, alopecia X) of nordic breeds
mechanism of lesion formation: unknown; something causes follicles to be stuck in the resting phase
characteristics:
1. signalment:
-breed: Nordic plush coats: poms, samoyeds, chows
-age: young adults
-both genders
- lesions: bilaterally symmetrical alopecia on caudomedial thighs, abdomen, flanks, neck, caudal ears
-spares the head, distal extremities, and tail
-histopath: hair follicles in telogen, infundibula are dilated and filled with keratin, flame follicles with trichilemmal keratin
-secondary hair may still be present, but primary fluffy hair may be alopecic - other signs:
-no systemic signs - dx:
-r/o hypothyroid and cushing’s
-skin biopsies NO HELP
-no lab changes - tx: purely cosmetic, none necessary
-nonspecific stimulation of hair follicles with oral melatonin (variable clinical responses, more secondary regrowth than primary regrowth)
describe cyclic recurrent flank alopecia (LO)
mechanism of lesion formation: unknown, intermitted hair follicle cycling defect
characteristics:
1. signalment:
-breed: boxers, EBD, airedale terriers, mini schnauzers
-age: adults
-both genders
- lesions:
-hyeprpigmented irregular alopecic patches, usually bilateral and symmetrical on the flanks and may extend dorsal
-no systemic signs
-histopath: hair follicle infundibula dilated, elongated, and plugged with keratin
–witches foot: lower follicular segments are short, atrophic, and distorted - dx:
-r/o cushing and hypothyroid
-skin biopies no help and no lab changes - tx: cosmetic only, none needed
-melatonin or microneedling if you must
describe color dilution alopecia (CDA) and black hair follicular dysplasia (BHFD)
CDA = LO
mechanism of formation: unknown; suspected to be hair follicle cycling defect transmitted concurrently with a genetic disease of pigment vesicle (melanosome) transfer, clumping makes hair shaft more predisposed to rupture and resulting in alopecia
characteristics:
1. signalment:
-CDA: dilute coat colors
-BHFD: any multicolored breed
- lesions:
-CDA: partial to incomplete alopecia of dilute colored areas, with or without scaling, with or without hair breakage
–histopath: large, irregularly sized melanin aggregates in infundibulum, outer root sheath of hair follicles and bulb (similar for BHFD)
-BHFD: alopecia restricted to black colored coat areas, usually no associated scaling
- other signs:
-sometimes hair follicle inflammation and secondary infections
-no systemic signs - dx:
-r/o cushing’s and hypothyroid
-skin biopsies confirm melanosome transfer and cycling follicular anomalies
-no lab changes - treatment: nonspecific stimulation of hair follicles with oral melatonin
-outcome: poor, hair loss usually permanent
describe telogen effluvium
mechanism of lesion formation: high fever, severe illness, surgery, anesthesia, pregnancy, or other stress results in cessation of hair follicle anagen activity and synch most follicles in telogen; when follicle cycling restarts, most synch in growth phase and growing shafts push old ones out leading to massive shedding and transient hair loss
characteristics:
1. signalment: anyone, more common in LA possibly
- lesions: hair loss without inflammation or any other lesions weeks after a stressful event has resolved
-trichogram: hair shafts in telogen (spear like endings) - dx:
-no ddx
-skin biopsies no help, no lab changes - tx: none, outcome is excellent
describe anagen defluxion
mechanism of lesion formation: chemo leads to transient cessation of hair bulb function bc keratinocytes of hair bulbs divide often so are sensitive to cytoxic drug effects
characteristics:
1. signalment:
-anagen predominant coat (long hair that needs haircuts): yorkies, maltese, poodles, bichons
-dogs seem to be more resistant than humans
- lesions: hair loss rapidly following chemo
- no ddx or dx or tx needed
-outcome good
describe the different syndromes of canine demodicosis and give the prognoses (LO)
sudden overgrowth in hair follicles causes folliculitis and furunculosis and results in alopecia and comedones; draining tracts open up with severe inflammation
- juvenile onset demodicosis:
-3-6 months when puppy vx
-most lesions resolve without treatment
-thought to be due to mites from mom during nursing
-clin signs: one or more patches of spontaneous alopecia with erythema and gray-ish hyperpigmentation, comedones, localize to front limbs and face
-will occasionally generalize: if so = genetic mutation so don’t breed!
-juvenile = better prognosis than adult onset - adult onset demodicosis:
-alopecia with or without secondary pyoderma
-lesions: truncal, dorsal, face, and feet
-severe cases: furuncles (boils), draining tracts, lymphadenopathy, fever, anorexia
-not normally pruritic but can depending on host reaction
-pododemodicosis: non-resolving pododermatitis, no response to abx courses (interdigital skin affected), check for demodicosis and treat appropriately if find
what 4 underlying conditions predipose adult dogs to develop demodicosis without having suffered from it at a young age?
- long term glucocorticoid therapy
- spontaneous hyperadrencorticism
- hypothyroidism
- chemotherapy
if none of these = idiopathic
describe diagnosis of demodicosis
- skin scrapes
-deep, in the center of alopecic patches
-most sensitive for localized
-gold standard - hair plucks/trichograms: from center of lesions
-equally as sensitive as scrapes for generalized - exudate examination/tape cytology: collect material from draining tract of deeply infected lesions
-most sensitive for supperative demodicosis
describe the available treatments for canine demodicosis and the side effects (LO)
FIRST AND FOREMOST: treat any deep bacterial infection with antibiotics if present and discontinue previously administered glucocorticoids
4 drugs:
- amitraz:
-only FDA-licensed for treatment
-applied as a dip left on the hair coat (topical)
-alpha 2 agonist: will cause sedation, lower BP and HR, hypothermia in small dogs, transient hyperglycemia
-clip coat short to enhance treatment
-bathe whole dog even if localized disease
-avermectins-
2. oral ivermectin/milbemycin: dose dependent toxicity, so start low and work up to dose; NO use is collies
-side effect: white feet, don’t treat! (MDA1 mutation)
-if see ataxia, lethargy, hypersalivation, DISCONTINUE
- topical combo of imidacloprin/moxidectin might have some efficacy to prevent recurrence of signs once remission obtained
- isoxazoline drugs: oral systemic
-off label use currently but showing promise and efficacy
-fluraner (Bravecto), afoxolaner, sarolaner, lotilaner
-continue until 2 monthly negative samples (skin scrapes)
describe feline demodicosis
- D. cati: rare, alopecic patches with erythema and crusting or ceruminous otitis externa
-underlying condition must be considered if see infection - diagnosis like dogs
- treatment:
-caution with amitraz due to toxic effects
-ivermectins: effective but possibility of neurotoxicity
-oral and topical isoxazalines seem to be well tolerated and safe - D. gatoi: short bodied, predom in stratum corneum
-pruritis, overgrooming, self-induced alopecia
-dx like dog but small so also consider fecal for undigested groomed mites
-isoxazaline to treat
describe bacterial pyoderma of short-coated breeds
exfoliative and follicular pyodermas may manifest as well-demarcated patches of hair loss with erythema and scattered papules
describe bacterial follicular pyoderma in horses
- most commonly caused by coagulase positive staph spp.
-S. aureus and MRSA most common - rapid development of small painful papules that develop into typical inflamed, exudative and edematous areas
-lesions circular and exudative in early stages
-some develop into isolate pusutles while others coalesce into abscesses or furunculosis
describe lesion formation in dermatophytoses
- arthrospores attach to hair shaft
- fungal extrapilar hyphae of surface of hair shafts
- typical ectotrix spores
- dermatophytes degrade keratin: epidermis, hair shafts, nails
-initially: erythema, scaling, alopecia
-in rare cases: nodular dermatophytosis (kerion); granuloma or pyogranuloma formation with fragments of hair shafts containing fungal spores
give 3 methods for diagnosing dermatophytosis and explain the limitations of each (LO)
- Wood’s lamp:
-M. canis is only species that will fluoresce! green apple color at base
-lack of fluorescence does NOT rule out
-valuable screening test! cheap and easy and is positive, can confirm by trichogram - trichogram exam:
-fungal spores and hyphae - culture: gold standard!
-send to a diagnostic lab
-DTM medium
-color change does not always mean dermatophyte, just means you need to look closer! (pathogens and contaminants can cause color change to red!)
-suggestive of dermatophytosis: pale/buff colonies with red ring around and change the whole media red, if see then evaluate microscopically (when colony is 10-14d old, use clear sticky tape and lay on slide with a drop of methylene blue) - PCR: false positives possible and could just indicate exposure
-be careful with negative results as well, esp if history and clinical signs suggest dermatophytosis - if no hair may have to biopsy and use special stains:
-hematoxylin and eosin
-periodic acid schiff fungal stain
-small round lightly basophilic arthrospores encircling hair shafts
describe the 3 most common dermatophytes causing disease and explain why speciation of the dermatophyte is important in a treatment plan (LO)
- microsporum canis
-cat is definitive host, may be infected without clinical signs
-50% of infections worlwide - trichophyton metagrophytes:
-host: small mammals - microsporum gypseum
clinical signs: ZOONOTIC
-alopecic patches with variable erythema and scaling present of previously haired areas
-lesions expand centrifugally, so SAMPLE THE LEADING EDGE FOR DIAGNOSIS
describe treatment of dermatophytosis
- self limiting and will resolve in 1-4 months in most healthy animals
-treat to shorten infection and limit spread to others (ZOONOTIC) - topical therapy for all species:
-normally safe, limits spread to environment, preferred!
-miconazole and ketoconazole: dogs and cats
-emilconazole: canine
-lime sulfur dips: effective but smelly
-terbinafine cream: available OTC
-horses: limited info about safety and efficacy of systemics in horses so topical therapy alone in horses! - systemic therapy:
-griseofulvin: dogs, cats, and horses; teratogenic so not in <6 weeks, may cause bone marrow suppression (esp in FIV+), best absorbed with fatty meal
-ketoconazole or itraconazole (fewer side effects than keto, NO use compounded, generic okay)
-terbinafine: GI upset side effect
-lufenuron: inhibition of chitin synth; but not used anymore
treat until remission of signs or at least 6 weeks until 2 negative cultures and decontaminate environment with 1:1 chlorine bleach!
describe alopecia ariata
- immunological folliculitis
- histopath:
-intra and peribulbar dermatitis
-only anagen bulb of hair follicles are affected - focal, multifocal, or diffuse noninflammatory alopecia
-can be localized or generalized
-tends to be bilterally symmetric but apre the head so rule out endocrine causes - dx tests:
-biopsies of the center of alopecia lesions and marginal skin between lesional and normal skin - treatments:
-initially thought spontaneous remission and regrowing nonpigmented (leukotrichia, melanocytes got killed in first wave of destruction)
-but now spont remission is rare so need to treat with oclacitinib (off label) or cyclosporine - in horses: mane and tail affected in many horses
-treat with oclacitinib (apoquel)
