Acne vulgaris- pathology & treatment!!!!

Acne vulgaris:- skin disorder

3. What is it?
0Disorder of pilosebaceouscomplex which
predominantly affects the peripubertalpopulation
and manifest as
comedones, papules, nodules, pustules and cysts and
heals with scars.

4. ETIOLOGY
0Increased sebum secretion.
0Follicular duct hypercornification.
0Increased colonization with Propionibacterium.
0Inflammation.

5. PATHOGENESIS
0Occlusion of
pilosebaceousorifice.
0Increased sebum
secretion.
0Microbial colonization.
0Release of
inflammatory
mediators.

6. OCCLUSION OF PILOSEBACEOUS
ORIFICE
Occluded by keratinous plug induced by chemicals and
reduced level of linoleic acid in sebum
Retention of sebum encouraging growth of microbes.
Distended follicle rupture, releasing proinflammatory
chemicals into dermis
Stimulate inflammation.

7. INCREASED SEBUM
SECRETION
0Occurs due to end organ sensitivity to androgens.
Increased activity of 5αreductasein sebaceous
gland.
Converts testosterone to 5αtestosterone
Binds to receptors in sebaceous gland
Increase sebaceous secetion.

8. Microbalcolonization
0Organisms involved-Propionibacterium, Malassezia
furfur,Staphepidermidis
Bacteria thrive
Inflammation results
Chemotactic factors attract neutrophils
Depending on conditions
Non-inflammatory
open/closed comedones
Inflammatory papule/
pustule/nodule

10. EPIDEMIOLOGY
0PREVELANCE-affects all adolescents.
0AGE-
Onset-12-14 years.
0GENDER-
Both sexes equally but nodulocysticacne common in
males.

11. FACTORS
1.GENETIC PREDISPOSITION
Found to be familial
Identical twins shows greater concordance of severity of acne.
2)DIET
High glycemic diet.
3.COSMETICS
Seen in women using oil based cosmetics for long time.
Follows facial massage.
4.MENSTRUAL CYCLE
Premenstrual edema of pilosebaceousduct.
5.PSYCHOLOGICAL FACTORS

12. MORPHOLOGY
0Polymorphic eruption consisting of
papules, pustules, nodules, cysts, and pathognomic
open and closed comedoneson a background of
oilness.

13. COMEDONES
0Hyperkeratoticplug made of sebum and keratin in
follicular canal.
0Pathognomiclesions of acne vulgaris.
02 types:
1.Open comedones.
2.Closed comedones.

14. OPEN COMEDONES
0Also known as Black head.
0Due to plugging of pilosebaceousorifice by keratin
and sebum on the skin surface.

15. CLOSED COMEDONES
0Due to keratin and sebum accretions plugging the
pilosebaceousducts below the skin surface.
0SUBMARINE COMEDONES-deep seated and seen by
stretching the skin.

17. Grades of Acne (Pillsburry’s
classification)
Grade I: Comedones(open or closed), occasionally
pustules or papules; no scarring.
Grade II: papules, comedones, few pustules; mild scarring.
Grade III: predominant pustules, nodules, abscesses;
moderate scarring.
Grade IV: mainly cysts, abscesses, scars; severe scarring.

18. SCARS
0Acne scars can be:
Depressed scars
1.Ice pick scars-deep pits.
2.Box car scars-superficial/deep
3.Rolling scars
Hypertrophic and keloidalscars.

19. VARIANTS

20. ACNE CONGLOBATA
0Severe form of acne characterisedby
intercommunicating abscess, cysts, and sinuses
loaded with serosanguinousfluid or pus.
0Multiporouscomedones.
0Lesions take months to heal and on healing leave
behind deep pitted or hypertrophic scars.

22. OCCUPATIONAL ACNE
0Caused by exposure to industrial chemicals
(tar, chlorinated hydrocarbons) and cutting oils.
0Predominantly comedones

23. COSMETIC ACNE
0Seen in women using cosmetics(oil based ones)
0Comedones
0Frequently on the chin

24. DRUG INDUCED ACNE
0Steroids, androgens, oral
contraceptives, antitubercular
drugs, iodides, bromides and anticonvulsants.
0Lesions are monomorphic, consisting of papules and
pustules
0Site-trunk especially back.

25. INFANTILE ACNE
0Due to presence of maternal hormones in child.
0Common in males.

26. LATE ONSET ACNE
0Onset after 25 years of age.
0Predominantly women.
0Deep seated persistent lesions on lower half of face.

27. ACNE EXCORIEE
0Seen in young girls, who obsessively pick their mild
acne.
0Results in discrete excoriations on face, while
comedones, and papules are few and far between.

28. ACNE FULMINANS
0Acute onset.
0Crusted ulcerated lesions.
0Associated with fever, myalgia and arthralgia.

29. ACNE AFTER FACIAL
MASSAGE
03-6 weeks later as acneiformeruption.
0Indolent deep seated nodules with vey few
comedones.
0Predominantly on cheeks along the mandible.

30. DIFFERENTIAL DIAGNOSIS
0Rosacea
0Folliculitis
0Acne scarring may be mistaken for acne
keloidalis, varioliform, atrophy and porphyria cutanea
tarda

31. TREATMENT
0General measures
0Topical therapy
0Systemic therapy
0Physical therapy

32. GENERAL MEASURES
1.Local hygiene
Regular cleansing with soap and water and avoiding
use of oil based cosmetics.
2.Diet
Avoid use of high glycemic diet.
3.Stress

33. TOPICAL THERAPY
0Retinoids
Most frequently used agent in acne.
Effective against comedonesand inflammatory acne.
Reduces formation of microcomedo.
Side effects include irritation and photosensitivity.

34. 0Benzoyl peroxide
Powerful antimicrobial which decrease population of
Propionibacteriumacnes.
Used in both inflammatory acne and non inflammatory
acne.
Side effects include irritation and bleaching of hair.

35. 0Topical antibiotics
Clindamycin(1-2%) and erythromycin(2-4%)
Used in inflammatory acne since it suppress P.acnes.
Side effect: antibiotic resistance. So should be
combined with retinoidsor benzoyl peroxide.

36. Systemic treatment
0Antibiotics
Mostly Doxycycline and minocycline; Erythromycin and
azithromycin.
Inhibit growth of P.acnesand has direct anti
inflammatory effect.

37. ADVERSE EFFECTS
Doxycycline -onycholysis, oesophagitiswith
ulceration, fixed drug eruptions, photosensitivity etc.
Minocycline -benign intracranial hypertension,
pappiloedema, blue-black pigmentation and rarely
hypersensitivity reactions
Macrolide group -gastritis, diarrhoea.

38. HORMONES
0Act by decreasing sebum secretion rate.
0Used only in females with late onset acne and
menstrual irregularities.

39. Adverse effects of hormonal
therapy
Weight gain
Menstrual irregularity
Occasional fluid retention
Melasma
Hypertension
Thrombophlebitis
Pulmonary embolism

40. ISORETINOIN
13-cis-retinoic acid (Vitamin A derivative )
Mechanism of action:
◦Inhibiting sebum secretion.
◦Alters the composition of sebum
◦Lowers P.acnesconcentration and has anti-
inflammatory activity

41. Indicated for :
◦Nodulocystic/ severe Acne
◦Pyodermafaciale
◦Excessive seborrhoea
◦Depression / Dysmorphophobia
◦Acne conglobata/ other unusual variants
◦Scarring

42. Dose: 0.5 –1 mg/ kg per day is given after meals.
Cumulative dose: 120-150 mgs/kg
Side effects
◦Teratogenicity
◦Mucocutaneousside effects, dryness
◦Elevation of serum lipids
◦Neurological : pseudotumorcerebri
Optic Neuritis, depression, mood swing
◦Arthritis, myalgia
◦Acne flares

43. PHYSICAL MODALITIES
0Intralesionalcorticosteroids
0Cryotherapy
0Laser therapy
0Photodynamic treatment
0Dermabrasion
0Fillers

44. Thank You…..