Acne and Other Disorders of the Glands



Acne and Other Disorders of the Glands


Sarah W. Matthews

Noreen Heer Nicol






I. OVERVIEW

A. The pilosebaceous unit comprises the hair follicle and one or more sebaceous glands attached to it. Sebaceous glands are found in greater numbers on the face, scalp, chest, and anogenital regions. Sebaceous glands are small at birth, enlarge between 8 and 10 years of age with maturation continuing through adolescence, and remain unchanged until later years. They decrease in menopause in females and after the 70th decade in males. As people age, sebum secretion decreases even though the size of sebaceous glands increases. Development of sebaceous glands and sebogenesis are hormone dependent (testosterone, androstenedione, dehydroepiandrosterone).

B. Apocrine gland ducts usually open into the hair follicle above the entrance of the sebaceous glands, but some ducts open directly upon the surface of the skin. Apocrine glands are found in the axillae; around the areolae; the periumbilical, perineal, and circumanal areas; prepuce; scrotum; mons pubis; labia minora; external ear canal; and eyelids. Like sebaceous glands, the activity of the apocrine glands is hormone dependent, but also stimulated by epinephrine and norepinephrine. The apocrine gland secretion is modified by the action of bacteria in the follicular infundibulum causing production of short-chain fatty acids, ammonia, and other odoriferous substances.

C. Eccrine sweat glands are not associated with hair follicles and are found everywhere on the body except for mucocutaneous junctions. They are found in greatest concentration on the palms, soles, axillae, and forehead. Eccrine sweat glands function to help regulate the body’s temperature. This is accomplished by the production of eccrine sweat that flows to the skin surface and cools by evaporation. Eccrine sweat is an odorless, colorless, hypotonic solution and is excreted during periods of stress and heat. Axillary eccrine sweat glands contribute to the odor-producing secretion of the apocrine glands by providing a moist environment that is conducive to bacterial proliferation.


SEBACEOUS GLAND DISORDERS: ACNE VULGARIS


I. OVERVIEW

A. Definition: a disease of the pilosebaceous (hair follicle/sebaceous gland) unit where abnormally adherent keratinocytes cause plugging of the follicular duct followed by accumulation of sebum and keratinous debris (Figure 10-1). This results in the formation of microcomedones followed by open and/or closed comedones and/or pustules. In severe acne, cysts or nodules may develop.







FIGURE 10-1. Acne closed comedone (whitehead). (From Anatomical Chart Company, Wolters Kluwer, 2004.)

B. Epidemiology

1. Age: affects all ages, with higher incidence (approximately 85%) between ages of 12 and 25.

2. Sex: more severe in males than in females. In males, usually subsides by mid-20s. In females, may occur at any age.

3. Race: lower incidence in Asians and darkly pigmented individuals.

4. Genetic aspects: genetic influence of sebum excretion.

5. Neonatal acne is a response to maternal androgens. Persistence of neonatal acne beyond 12 months of age may be associated with endocrine abnormalities.

6. Other factors (Box 10-1):

a. Emotional stress exacerbates.

b. There is good evidence that acne negatively affects quality of life, self-esteem, and mood in adolescents. Acne is also associated with an increased risk of anxiety, depression, and suicidal ideation, highlighting the importance of asking patients with acne directly about psychological issues in order to identify those who might benefit from early psychiatric support.

c. Occlusion with pressure and friction on skin from headbands, football helmets, hats, tight bras, etc., can exacerbate.

d. Oil-based cosmetics and hair products can also be responsible for predominantly comedonal acne.

e. Drugs (such as androgens, ACTH, glucocorticoids, phenytoin, lithium, and isoniazid) and hyperandrogenism may also induce acne.


f. Science still does not know whether diet and acne are related, and dietary research needs to be read with critical review. Based on the clinical research, it seems prudent to eat a relatively low-glycemic diet rich in colorful fruits and vegetables and omega-3 fats. Some weak evidence has emerged that suggests a possible link between dairy and acne, which warrants further research.

g. Systemic steroids exacerbate.

C. Etiology and pathogenesis. Basic cause thought to be multifactorial, complex interaction between androgen hormone and bacteria colonization in pilosebaceous units. There are at least four primary contributing factors.

1. Increased sebum production secondary to stimulation by androgenic hormones

2. Abnormal follicular keratinization with the development of a keratin plug at the sebaceous follicle opening

3. Proliferation or bacterial colonization with Propionibacterium acnes, an anaerobic bacterium

4. Inflammation

D. Diagnostic hallmarks

1. Distribution: face (which is usually oily), forehead and chin (first areas to be noticed), neck, upper arms, trunk, and buttocks

2. Lesions: comedones (pathognomonic lesions), papules, pustules (Figure 10-2), and inflammatory nodules and cysts

E. Course and prognosis

1. Hormonal factors greatly affect development and course of acne; use of anabolic steroids likely to worsen.







FIGURE 10-2. Acne. A: Comedones. B: Papular and pustular acne. (From Goodheart, H. P. (2008). Goodheart’s photoguide of common skin disorders (3rd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.)

2. Cystic lesions and severe acne more common in men.

3. In women, activity may peak during a week prior to menses; may clear up or substantially worsen during pregnancy.

4. Presence of cysts and family history of scarring acne are prognostic signs for predicting future severity.

5. Postinflammatory hyperpigmentation or hypopigmentation may persist for months.

6. Cystic acne frequently leads to permanent scarring.


II. ASSESSMENT

A. History

1. Duration of lesions: weeks to years

2. Season: may be worse in the fall and winter and better in the summer

3. Symptoms: lesions may be painful, especially nodulocystic type.

B. Clinical presentation

1. Open comedones (blackheads)—incompletely blocked pores and no scarring

2. Closed comedones (skin colored)—completely blocked pores and no scarring.

3. Pustules—plugged duct ruptures with extrusion of keratin plug into surrounding dermis causing inflammatory response and no scarring

4. Nodules—plugged duct ruptures at the level too deep to result in a visible pustule and no scarring

5. Cysts—plugged duct ruptures at the level of the sebaceous gland itself and heals with scar formation

C. Clinical manifestations

1. Neonatal acne

a. Appears at 2 to 4 weeks of age and lasts until 4 to 6 months.

b. Lesions are seen primarily on the face, particularly the cheeks, and occasionally on the upper chest and back.

c. An oily face or scalp may be observed.

d. Individual lesions are similar to the adolescent acne lesions.

2. Adolescent acne

a. May first appear at the age of 8 to 10 years, peaks in late adolescence, and may continue until the late 20s or early 30s.

b. Distribution occurs in areas of high sebaceous activity, such as the face (Figure 10-3), upper chest, and back.

c. Types of lesions

(1) Noninflammatory microcomedones

(2) Noninflammatory comedones

(a) Closed comedones

(b) Open comedones

(3) Inflammatory papules

(4) Inflammatory pustules

(5) Inflammatory nodules

d. Classification of inflammatory acne

(1) Mild—consists of few to several inflammatory papules or pustules and no nodules

(2) Moderate—several to many inflammatory papules, pustules, and a few nodules






FIGURE 10-3. Papulopustular acne on the face. (From Rosedahl, C. B. (2011). Textbook of basic nursing. Philadelphia, PA: Wolters Kluwer.)


(3) Severe—numerous extensive inflammatory papules, pustules, and many nodules

e. Scarring is common in inflammatory nodulocystic acne and with frequent manipulation of the acne lesions.

D. Atypical findings

1. Acne conglobata—scarring severe cystic acne with more involvement of the trunk rather than the face (genetically malformed sebaceous follicles present or rarely seen in XYY genotype of tall males who are slightly mentally retarded with aggressive behavior or in polycystic ovary syndrome)

2. Acne excoriee—individuals neurotically pick at their lesions

3. Drug-induced acne—acne-like folliculitis without comedones or cysts

E. Differential diagnosis

1. Folliculitis

2. Pseudofolliculitis barbae

3. Acne rosacea

4. Perioral dermatitis.

F. Laboratory and special tests

1. No diagnostic testing is generally required, and diagnosis is based on the clinical appearance of the lesions.

2. Hormonal workup, if needed, for detecting polycystic ovary syndrome.

3. Hyperandrogenism is evaluated by obtaining blood levels of free testosterone, DHEA, and androstenedione.

4. Patients being prescribed isotretinoin require the following lab tests before starting treatment and monthly during treatment: complete blood count, platelets, liver function studies, fasting lipid profile, BUN, and creatinine.

5. Females being prescribed isotretinoin need two negative pregnancy tests prior to initiation of treatment, monthly pregnancy tests during treatment, and a pregnancy test 1 month after the treatment is complete.


III. COMMON THERAPEUTIC MODALITIES

A. Topical therapy which includes products delivered as cleansers and medications

1. Gentle skin cleansing techniques that use mild soap and water twice a day. Avoid abrasive soaps and cleansers as well as astringents and toners, unless directed. If cleansers with medications are used, caution should be taken to avoid side effects, which include drying and therapy intolerance.

2. Benzoyl peroxide (2.5% up to 10%): apply once to twice daily for mixed comedones and inflammatory acne as wash, lotion, cream, foam, pads, or gel; side effects include skin irritation, allergic contact dermatitis, and bleaching of clothes. Combining benzoyl peroxide with antibiotics dramatically decreases the incidence of bacterial resistance.

a. Benzoyl peroxide plus erythromycin—pregnancy (category C)

b. Benzoyl peroxide plus clindamycin—pregnancy (category C)

3. Topical antibiotics for inflammatory acne apply once to twice daily as a solution, gel, lotion, or pads; side effects include excessive drying, depending upon vehicle, and emerging bacterial resistance with long-term use.

a. Erythromycin 2%—pregnancy (category B)

b. Clindamycin 1%—pregnancy (category B)

4. Salicylic acid/glycolic acid for mild comedonal acne apply once to twice daily as a cleanser, gel, lotion, or solution to unplug follicles; side effects include mild local irritation.

5. Azelaic acid 20%—pregnancy (category B). For comedonal and inflammatory acne, apply once to twice daily as an antibacterial of P. acnes, to normalize keratinization and for postinflammatory hyperpigmentation; side effects include mild local irritation.

6. Topical retinoids: apply once daily for comedonal acne to decrease cohesiveness of follicular epithelial cells; side effects include erythema, desquamation, hypo-/hyperpigmentation, and sensitization of skin to sunlight.

a. Tretinoin (0.025%, 0.05%, 0.1% cream; 0.01%, 0.025% gel; Retin-A Micro 0.04% and 0.1% gel)—pregnancy (category C): not recommended during pregnancy. Unstable in sunlight. Apply at night.

b. Adapalene (0.1% and 0.3% gel, 0.1% cream, solution, or pledgets)—pregnancy (category C): not recommended during pregnancy. Less irritating than tretinoin or tazarotene and stable in sunlight.

c. Tazarotene (0.05% and 0.1% gel or cream)—pregnancy (category X). Women of childbearing potential: obtain reliable negative pregnancy test within 2 weeks before starting therapy, use effective contraception during therapy, and begin therapy during normal menses. Stable in sunlight.

7. Combination therapy

a. The combination of benzoyl peroxide every morning and a topical retinoid (tretinoin, adapalene, tazarotene) every evening is often effective.

b. Frequently systemic antibiotics are combined with topical medications.

c. Combination of topical benzoyl peroxide with both topical and systemic antibiotics is recommended to reduce the development of antibiotic-resistant organisms.

B. Systemic therapy

1. Antibiotics for inflammatory acne; take one pill or capsule two times per day for a bactericidal effect; side effects include emerging resistance. Pregnancy and nursing mothers: not recommended.

a. Tetracycline (category D), 250 to 500 mg bid, inexpensive; side effects include photosensitivity, gastrointestinal (GI) upset, candidiasis, tooth discoloration, and enamel hypoplasia (use only in patients >8 years old).

b. Doxycycline (category D), 50 to 100 mg bid, may be taken with food; side effects similar to tetracycline but with greater photosensitivity.


c. Minocycline (category D), 50 to 100 mg bid, rare photosensitivity or GI upset; side effects include blue pigmentation, serum sickness-like reactions, and drug-induced lupus.

d. Erythromycin (category B), 250 to 500 mg bid, may be taken during pregnancy; side effects include GI upset.

2. Isotretinoin (category X) 0.5 to 2.0 mg/kg/d for nodulocystic acne and inflammatory acne recalcitrant to other modes of treatment to normalize keratinization, decrease sebum production, and deplete P. acnes; multiple side effects include teratogenicity, cheilitis, conjunctivitis, dry eyes and mouth, pruritus, musculoskeletal pain, and alopecia (Figure 10-4). Strict adherence to pregnancy prevention measures is required as well as monthly pregnancy tests for all women regardless of sexual activity.

3. Oral contraceptives as an adjunct treatment in women for moderate-to-severe inflammatory acne decrease sebum production; side effects include suppressing growth in patients less than 16 years old; contraindicated in males.

4. Spironolactone 50 to 200 mg once daily. Pregnancy (category C). The antiandrogen effects have been shown to cause feminization of the male fetus in animal studies. Used off-label for female acne. Indicated when there are signs of a strong hormonal component such as worsening around menses, acne concentrated in the lower part of the face and upper neck, and/or acne that is recalcitrant to other treatments. Check potassium and creatinine at 1 week after initiation and 1 week after each dose increase. If potassium increases to >5.5 mEq/L or renal function worsens, hold dose until potassium is normal again, then consider restarting at lower dose.






FIGURE 10-4. Severe cystic acne. This patient was subsequently treated with isotretinoin. (From Goodheart, H. P. (2003). Goodheart’s photoguide of common skin disorders. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins.)

C. Follow-up visits

1. Every 4 to 6 weeks until control is obtained.

2. Then every 1 to 3 months particularly if being treated with systemic medication.

3. Patients on isotretinoin are seen monthly during the course of treatment.



ACNE ROSACEA


I. OVERVIEW

A. Definition: rosacea is a chronic inflammatory disorder involving the flush area of the face associated with diffuse sebaceous gland abnormality and increased reactivity of capillaries that develops over time and is characterized by persistent erythema, papules, tiny pustules, and telangiectasia. There are no blackheads (comedones).

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Mar 9, 2021 | Posted by in NURSING | Comments Off on Acne and Other Disorders of the Glands
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