A 7-year-old female spayed miniature poodle is presented for hair loss of the trunk. The dog is not pruritic but the owner describes a dramatic increase in water consumption and urination (see Chapter 5). The dog has a ravenous appetite (see Chapter 3).
The vital signs are normal. There is truncal alopecia that spares the head and extremities. The skin is mildly hyperpigmented, very thin, and has poor elasticity. The abdomen is distended but no fluid can be palpated. The liver is enlarged.
Using the problem-oriented medical record approach, identify the problems and write an initial for this case.
Alopecia is the loss or lack of hair in any amount or distribution up to complete baldness. Although alopecia may be a primary disease, it usually occurs secondary to an acquired disorder.
The basic mechanisms that produce alopecia include (1) abnormalities in follicular structure; (2) abnormalities in follicular function (alteration of hair growth cycle); (3) structural abnormalities of the hair shaft; and (4) mechanical removal of hair.
Abnormalities in Follicular Structure
Primary alopecia is caused by inherited abnormalities of follicular structure. These may range from complete absence of hair follicles to absence of hair follicles that produce hair of a particular color.
Secondary (acquired) alopecias may be caused by diseases that disturb the follicular environment, prompting the disruption of hair growth and the dislodgement of hair from the follicles. Bacterial folliculitis, demodectic mange, severe necrotizing processes, and follicular hyperkeratosis are examples of acquired diseases that adversely affect follicular structure.
Abnormalities in Follicular Function
Diseases in this category do not destroy follicular structure per se, but they adversely affect the normal cyclic phases of the hair follicle. The phases of follicular activity are anagen (growth phase), catagen (transitional phase), and telogen (resting phase). The normal follicular cycles in the dog and cat have seasonal variations; however, hair growth is not synchronized but follows a mosaic pattern. The majority of follicles are in anagen, yet a few neighboring follicles may be in catagen or telogen. Certain conditions or diseases cause alopecia by promoting the development of telogen follicles (see Table 13-1). Estrogens, testosterone, and adrenocortical hormones delay the initiation of anagen. Thyroid hormone accelerates follicular activity. Conditions such as severe illness, fever, pregnancy, and lactation may cause the simultaneous precipitation of many follicles into catagen and telogen. The resulting alopecia is called “telogen effluvium.” Certain drugs may also arrest mitotic activity of the follicle, causing alopecia.
The endocrine disorders may also produce follicular hyperkeratosis that results in follicular plugging. Follicular plugging disturbs normal hair growth.
Structural Abnormalities of the Hair Shaft
Certain diseases may weaken the hair shaft so that normal tension on the hair causes it to break. This is a primary mechanism for the alopecia that results from dermatophyte infections. Weakened, brittle hair shafts may be found in certain endocrine disorders such as hypothyroidism.
Mechanical Removal of Hair
This is a common mechanism for the alopecia associated with pruritic dermatoses. Constant self-mutilation mechanically removes or breaks the hair. The underlying inflammatory process may also delay the initiation of anagen.
Alopecia may be classified as to onset (primary vs. secondary) or by its distribution. The distribution pattern of the alopecia may be characteristic of the specific underlying disease. By distribution, alopecias may be classified as diffuse, regional, multifocal, or focal.
The generalized or diffuse alopecias are primarily truncal and tend to spare the head and limbs. Endocrine disorders are the most common cause of nonpruritic diffuse alopecia. Their differentiating features are listed in Table 13-1. Occasionally, allergic, bacterial, fungal, or immune-mediated diseases cause generalized alopecia. Telogen effluvium has been previously described as a cause of diffuse alopecia.