Acne Vulgaris.ppt - Acne Vulgaris Acne vulgaris-A disease...

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Unformatted text preview: Acne Vulgaris Acne vulgaris -A disease of the pilosebaceous unit. ei“Y (eªY) Zi“Y eq‡m ei“Y (eªY) nq ? A normal pilosebaceous unit A normal sebaceous gland The sebaceous gland is found throughout the skin, except palm and sole and is androgen dependent. The glands predominantly found in scalp, face, neck and trunk (hair bearing area), They occur in association with hair follicles and share a common channel of exit from the skin, known as pilosebaceous duct. A normal sebaceous gland It does not secrete until puberty, apart from temporary activity during infancy, probably caused by adrenal androgen of maternal origin. During the course of evolution, the gland becomes an unnecessary component of skin like the appendix. Main constituents of sebum Constituents of sebum ( oil ); A mixture of lipids: 1. Triglycerides 2. Cholesterol ester 3. Squalene 4. Wax esters ACNE VULGARIS Acne vulgaris is a self-limiting disease of the pilosebaceous unit. The cause is multifactorial. Clinical lesions range from non-inflammatory comedones to inflammatory papules, pustules, nodules and cysts. Incidence of Acne vulgaris Acne vulgaris occurs worldwide, affecting 90% of the people at sometimes in their life. The age of onset is at puberty. Contrary to popular belief, acne is not confined to teenagers. It may continue into 3rd and 4th decades of life. Incidence of Acne vulgaris Acne is commoner and more severe in male than in female, relating to its androgen activity. Heredity also plays a role. If patient’s mother and father had bad acne, the patient may too. Types of acne lesions A. Noninflammatory lesions (comedones ): 1. Closed comedone ( whitehead ) : when a trapped sebum and bacteria stay below the skin surface, a whitehead is formed. 2. Open comedone ( blackhead ) : when a trapped sebum and bacteria open to the surface and turn black due to oxidation of melanin. White head and Black head Types of acne lesions B. Inflammatory lesions: 1. Papules 2. Pustules 3. Nodules 4. Cysts 5. Scar Scars do not occur in all patients; severe inflammation may lead to scar formation. Various types of scar may occur, including atrophic scars, so-called ice-pick scars which are common on the checks & hypertrophic or keloid scars on the chest and back. PATHOGENNESIS OF ACNE Pathogenesis of Acne Vulgaris is multifactorial: Four key factors are responsible for the development of Acne: 1. Follicular epidermal hyperprolifaration. 2. Excess sebum excretion. 3. Presence and activity of Propionibacterium acne. 4. Inflammation. Diagram to show suggested events in the pathogenesis of acne. PATHOGENNESIS OF ACNE 1. Follicular epidermal hyperprolifaration is the first recognized event in the development of Acne. Currently 3 leading hypothesis have been proposed to explain why follicular epithelium is hyperproliferative in individuals with Acne. PATHOGENESIS OF ACNE a. Androgenic hormone is the initial trigger. b. Change in lipid composition have been implicated in the development of AV. c. Inflammation is the 3rd hypothesized factor incriminated in comedone formation. (IL-1 alfa –a proinflammatory cytokine). Pathogenesis of Acne 2. Excess sebum excretion is another key factor for the development of acne and is predominantly androgen dependent: contd--- Pathogenesis of Acne Androgens (from the testes, ovaries, adrenals & sebaceous glands themselves) are main stimulants of sebum excretion, although other hormones (e.g. thyroid hormones & growth hormone) have minor effect too. Increased target organ sensitivity ie sebaceous gland to testosterone. This may be caused by 5 alfa-redctase activity being higher in the target sebaceous gland than in other parts of the body. PATHOGENNESIS OF ACNE 3. Presence and activity of Propionibaterium acne. Proximal to the follicular outlet obstruction, sebum and keratinous debris accumulate. This leads to the formation of the dilated sac of lipid that is called a comedone. This provides an attractive environment for the growth of anaerobic bacteria, specially P. acne. Contd.. Pathogenesis of Acne (contd.) 3. Presence and activity of Propionibaterium acne. These bacteria produce lipase that hydrolyze the sebaceous lipids, resulting in the release of free fatty acids, which defuse through the follicular wall & create dermal inflammation that we call a ‘spot’ or ‘zit’. Pathogenesis of Acne 4. Inflammation may be a primary or a secondary phenomenon. Most of the evidence to date suggests a secondary inflammatory response to p. acne. However, IL-1-alfa expression have been identified in microcomedone, and it may play a role in the development of acne. Acne Vulgaris moderately severe Closed comedones, inflammatory papules on the checks, chin and forehead. Inflammatory papules, papulo-pustules, irregular depressed on the checks and forehead Papulo-pusturar and cystic lesions on the checks. Large cystic lesions and several closed comedones on the check with irregular scars. Irregular shaped pitted scars on the check caused by acne Acne vulgaris. Note comedones, papules and pustules. Acne vulgaris. Note the closed (white) comedones and open (black) comedones. Acne vulgaris. Nodular and nodulo-cystic acne. Acne vulgaris. Scaring occurs in some individuals and it is permanent. Acne keloids. Acne may result in scarring and occasionally keloids, especially on the shoulders and front of the chest. Nodulocystic acne. Large, inflamed nodules, cysts and scarring occur. Isotretinoin has revolutionized treatment. Treatment of acne with isotretinoin. Treatment of acne. Dryness of the mucous membranes is a universal side effect of isotretinoin, but teratogenicity is the most serious hazard. Infantile acne (milk spots). Transplacental maternal adrenal androgens stimulate the infantile sebaceous glands and produce acne. It disappears spontaneously within 3 to 6 months. Post adolescent female acne. Papules and pustules occur, particularly on the chin, cheeks and jaw, which may be deep and painful and worse premenstrually. Pomade acne. Greases used for the hair may spread onto the forehead and occlude the pilosebaceous orifices. This is common in blacks. Steroid Acne Monomorphic lesions on the back of a young man on systemic corticosteroids. Note the absence of comedones and scars. Steroid Acne Steroid Acne with hypertrichosis Acne Myths Versus Facts Myths: Blackheads are caused by dirt. Fact: They (open comedones) are black because of oxidation of melanin. Myths: Frequent facials are beneficial. Fact: Professional facial (a form of facial beauty treatment) or at-home scrubs are not generally recommended because they tend to aggravate acne. Acne Myths Versus Facts Myths: Cosmetics, particularly oil-based preparations, ‘clog pores’ and cause acne. Fact: Their use very rarely cause adult acne. More commonly, cosmetics can be irritants and may cause contact dermatitis. Myths: Acne should disappear by the end of adolescence. Fact: Some women have acne that persist well past adolescence. Acne Myths Versus Facts Myths: Acne is caused or worsened by certain foods such as chocolates, sweets, and greasy food. Fact: Acne is not significantly influenced by diet. Myths: A dirty face exacerbates acne; so, scrubbing the face daily will help to clear it up. Fact: Scrubbing the face with acne will irritate and redden the already inflamed area. Acne Myths Versus Facts Myths: Acne is due to ‘hormonal imbalance’. Fact: Hormones are normal in vast majority. In acne, sebaceous glands are unusually sensitive to androgens due to an enhanced target organ sensitivity. This is due to increased activity of an enzyme 5alfa-reductase present in the sebaceous gland. The enzyme converts testosterone to more potent 5alfadihydrotestosterone. This binds to specific receptors in the sebaceous glands, increasing sebum excretion. Acne Myths Versus Facts Myths: Acne is related to sexual behavior. Fact: Neither too little nor too much sex makes any difference. Masturbation do not cause acne. ( Thank goodness ! ) A.V treatment is multipronged-attacking four mechanisms which lead to acne. 1 3 3 3 2 4 Topical Acne Medications 1. Retinoids (comedolytic & anti-inflammatory) (Tretinoin, Isotretinoin, Adapalene, Tazarotane) 2. Antibiotics (anti-bacterial & anti-inflammatory) (Clindamycin, Erythromycin, Benzoyl peroxide) 3. Azelaic acid (20% cream) (antibacterial, anti-inflammatory & reduce proliferation of Keratinocytes >inhibits formation of comedones) Oral Acne Medications 1. Antibiotics (Tetracycline, Doxycycline, Clindamycin Erythromycin, Azithromycin) 2. Hormonal agents a. Spironolactone b. Prednisolone c. Birth control pills (2mg cyproterone acetate & 0.035 mg ethinylestradiol) 3. Isotretinoin Principle of treatment of acne vulgaris Type of acne Topical Agents Mild acne Retinoids or Benzoyl peroxide Moderately severe acne Retinoids and (Predominantly comedonic) Benzoyl peroxide Systemic Agents Not necessary Not necessary Principle of treatment of acne vulgaris Type of acne Topical Agents Moderately severe acne Retinoids or Benzoyl peroxide and Antibiotics + Antibiotics Retinoids or Benzoyl peroxide + Antibiotics and Antiandrogens (in females) or Retinoids (Predominantly inflammatory) Severe acne Systemic Agents Surgical / physical agents Treatment of comedones: Comedo extraction Electrocautery Chemical peels *Cryotherapy Treatment of inflammatory nodules: *Intralesional corticosteroids(2.5mg/ml) Treatment of inflammatory lesions: Photodynamic Blue light 1450-nm laser Surgical/physical agents Treatment of scarring: Chemical peels *Dermabresion Excisions *Laser resurfacing *Filler substances Ref. Goodheart”s photoguide of Common Skin Disorders. Ref. Goodheart”s photoguide of Common Skin Disorders. (Patient education) The most important aspect of a successful acne treatment programme is patient compliance. At the initial visit, instructions should be given verbally and on a written sheet that reinforces what was said. The patients are best able to comply if medications are used twice daily so that medications schedule can be centered on an already established daily habit such as tooth brushing. (Patient education) Patients with acne are often depressed and needs sympathetic counseling and support. They will eventually improve as the treatment continues -need to be stressed. They may be informed that dramatic improvement may not occur overnight and they may experience 40% improvement after 4 months and 80% improvement after 8 months. (Patient education) Patient should not have inappropriate expectations. Acne, in most cases, can be controlled but not cured. Acne remits spontaneously with time. For individual patient, there is no way to predict in advance when they will ‘outgrow’ their acne. Patient may express concern over the long –term use of oral antibiotics, but they should be reassured that this is a safe practice. (Patient Handout) Acne can be aggravated by a number of things: Emotional stress may worsen. Hair pomades and greasy cosmetics tend to clog pores and may worsen acne. Pricking or squeezing of pimples is harmful and may led to scars. Hard scrubbing of the skin, too much exposure to the sun often make acne worse. Acne usually runs in families. (Patient Handout) Sweating Sweating appears to worsen acne in 15% of acne sufferers. Humidity may also worsen the condition. Contraceptive pills Estrogen is usually helpful for acne control but Progesterone may make acne worse. It is common for all women to have an acne flare up days before their periods. ( Progesterone) (Patient Handout) Use only your bare hands to wash. Washcloth is irritating. Washing itself does not clear breakout since dirt does not cause acne, so there is absolutely no need to scrub. Washing with worm water, rinse with cold. Gently pad dry. Rubbing the skin is irritating. Further Acne Facts Because acne is a visible disease, patients may suffer from anxiety, impaired self-image, depression, employment insecurities, social withdrawal, self-destructive behavior and suicidal ideation. Acne tends to improve temporarily during summer. Fall and winter acne flare-ups are quite common often influenced by mood swings. (Patient Handout) A gentle cleansing must precede treatment in order to prevent irritation. Look for the terms ‘oil-free’ and ‘non-comedogenic’ when selecting a facial cleanser. You are on a right tract when references to ‘mild’, ‘non-irritating’ and ‘non-overdrying’ are mentioned as well. Wash your face twice daily, morning and evening. Excess washing can cause irritation. Further Acne Facts Acne, Hirsuitism and irregular menstruation may be associated with hyperandrogenism and/or polycystic ovaries. Adult acne is often more persistent than teenage acne. The two Hs – hormones & heredity- underlie teenage acne and not the proverbial -bad diet and dirty face- the two Ds. Further Acne Facts Severe, unremitting, scaring acne is more prevalent among men. Skin care should be kept simple and gentle with the use of mild soaps and harsh soaps are to be avoided. The treatment of acne is suppressive, not curative ! Be patient………and don’t expect results overnight ! Types of Acne 1. Infantile acne Infants below the age of three months may develop facial acne. They have elevated plasma adrenal androgens of maternal origin. 2. Senile acne Occurs in individuals over the age of 50 years. Comedones localized to the temples and forehead. 3. Acne Cosmetica Cosmetics were considered to be a major cause of adult acne in women. With the exception of very greasy, occlusive products, cosmetics are infrequent etiologic agents for acne. Types of Acne 4. Steroid acne (STAR- MON) Sudden onset (usually within 2 weeks of starting high-dose systemic or potent topical corticosteroid therapy). Occurrence at any age. Trunk is more commonly affected than face. Not necessarily limited to the sebaceous gland rich areas. Monomorphic presentation. Rarity of cyst formation. Absence of true comedones. Types of Acne 5. Pomade acne. 6. Acne Mechanica. 7. Occupational acne. 8. Tropical acne 9. Acne with facial edema. Acne uncommonly associated with a peculiar inflammatory edema of mid-third of face. 10. Acne aestivalis. Monomorphous, papular lesion occur after sun exposure, mostly in women. Types of Acne 11. Acne fulminans ( acute febrile ulcerative acne ) 12. Excoriated acne Common in females. The patient excoriates, scratches and plays with skin of acne lesions so that even the smallest lesion may be aggravated. There is some associated mental stress or personality disorder. Types of Acne 13. Acne Conglobata Characterized by comedones, papules, pustules, nodules, cysts and burrowing intercommunicating abscesses. Healing results in an admixture of depressed and keloidal scars. Occurrence at a latter age and chronic unremitting course. Prolonged antibiotic therapy guided by c/s. The use of isotretinoin produces dramatic results and is now the treatment of choice in dose of 2 mg/ kg/ day for 20 weeks. A combination of systemic steroid and isotretinoin produces a better response. 1. ( May-2005) Define acne vulgaris. Write down the pathogenesis (Jan-2008) and treatment (Jan-12; Sep-2008; Jan-2008) of acne vulgaris. 2. Name 6 skin lesions found in Acne vulgaris (Jan2009). 6. A 23-year-old girl had few scattered small papules like closed comedones (whiteheads) and pustules for last 3 years on face. During last 3 month she developed small papules, monomorphic in nature. She had history of applying topical steroid on face for last 4 months. Q. What is the (1) diagnosis and (2) management? 5. A 19-year-old girl had inflammatory papules, pustules with open and closed comedones on both the cheek and forehead for last two years. Q. What is the (1) diagnosis and (2) management? 1. A 20 years old college girl presented with comedones and papulo-pustular lesions on her face and forehead about 6 months ( July-2008). a. What is your clinical diagnosis? b. Name 3 topical preparations for the patient. c. Name 3 systemic drugs with doses and duration. d. Give 2 advices. 8. Acne Vulgaris is disease: __a) of sweet gland. __b) Commensales of epidermis is related. __c) Black head and yellow head comedon are present. __d) Clinically comedon,papule,nodule and cyst are present in all patients. __e) Tetracycline is the safest and cheapest drug of choice. 62. ‘Steroid acne’ differs from acne vulgaris: a. By absence of comedones b. By absence of pustules c. In its distribution d. In its outcome e. In no way at all 144. The following factors are operative in the causation of acne: a. Excessive secretion of the sebaceous glands b. Bacterial infection c. Abnormal hormones d. Emotional tension E. Over-work 13. Clinical features of acne vulgaris includes ___a) White head. ___b) Hardening of skin ___c) Papules. ___d) Black heads. ___e) Herald patch. 145. The following drugs given systemically can also control acne vulgaris: a. Antibiotics b. Androgens c. Oestrogens d. Corticosteroids e. Chlorquine THANK YOU ...
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