Alopecia 1 Flashcards
(32 cards)
Classifying spontaneous alopecia
Genetic defect
Hair cycling abnormalities
Inflammation of hair follicles
Ischemia
Genetic defect
Chines crested dog
Mexican hairless dog
Hair cycling abnormalities
Hypothyroidism
Hyperadrenocorticism
Alopecia X
Canine flank alopecia
Color dilute alopecia
Inflammation of hair follicles
Bacterial
Demodicosis
Dermatophytosis
Ischemia
Vaccine- induced
Ischemic dermatopathy
Dermatomyositis
How genetic defect works
Due to defect(s) of the hair shaft or hair follicle
• Diagnosed based on presence of hair loss at birth or shortly after birth
• Most have concurrent dental anomaly (i.e., X-
linked ectodermal dysplasia)
• Several breeds of dogs selected based on their unique appearance
Mechanisms of hair cycling abnormalities
Iatrogenic or stress
Genetic cycling defect
Endocrine disease
Endocrine disease
Hypothyroidism
Hyperadrenocortisism
Primary hypothyroidism
> 95% of cases
Lymphocytic thyroiditis - auto immune
Secondary or tertiary are rare
Dermatological clinical signs of hypothyroidism
Alopecia (frictional areas)
Hyperpigmentation
Excessive scaling (seborrhea)
Recurrent pyoderma
Cutaneous mucinosis
Myxedema
Nondermatological signs of hypothyroidism
Lethargy
Weakness
Obesity
Exercise intolerance
Bradycardia
Cold intolerance
Mechanism of alopecia w hypothyroidism
Result of slowing growing cycle
Due to reduction of thyroid hormones - but will not fall of spontaneously
Rubbed off - friction or folliculitis
Regrowth of hair stunted
Myxedema
Non pitting edema, tragic face
Really severe cases
DX for hypothyroidism
Blood work up
T4, free T4, TSH function tests
Histopath of skin will NOT differentiate from other endocrine diseases = NOT valuable
TX hypothyroidism
Levothyroxine
^ activity, weight loss
Watch derm signs
Recheck 6-8 wks, take samples 4-6 hr post pill
Hyperadrenocorticism
Spontaneous -
Pituitary dependent - most common (80-85%) ^^ACTH by pituitary gland
Adrenal dependent - 15-20% - excessive production of glucocorticoids by adrenal tumor
Iatrogenic - due to chronic admin of GC’s
Dermatological clinical signs of hyperadrenocorticism
Alopecia (bilateral/symmetrical
Comedones
Cutaneous atrophy
Calcinosis cutis
Recurrent pyoderma
No derm signs in hyperadrenocorticism
Polydipsia/polyuria (85%)
Pendulous abdomen (70%)
Hepatomegaly
Polyphagia
Lethargy
Muscle weakness/atrophy
Hyperadrenocorticism Mechanism of alopecia
Due to excess glucocorticoids, hair follicles do not re-enter the anagen phase
Hair follicle eventually undergo atrophy
Hair shafts are expelled spontaneously
Lack of hair shaft leads to formation of comedones (“black head”)
DX hyperADC
Blood work up
ACTH stim test, LDDS test, HDDS test
Abdominal ultrasound - looking for kidney tumor
Hyper ADC DX histopath
Calcinosis cutis - ONLY in dogs that have hyperADC
Can be beneficial DX
TX and monitoring for hyperADC
Pit dependent - Trilostane, mitotane
Adrenal dependent - surgery, trilostane
Clinical response - long recovery, Calcinosis cutis may be permanent
ACTH stimulation test
Alopecia X
Etiology unknown
Proposed pathogenesis: mutation in the signaling pathway of a receptor involved in hair follicle cycle
Prevent hair follicles from entering Anagen phase
- stuck in resting phase
Pomeranians, show, malamute - plush coat
DX for alopecia X
breed, early onset of skin lesion
Distinctive clinical features
Pattern resembles hyperADC (more age specific)
Histopath is NOT useful
