Acne,Roasea,p Gangr

8/3/2019 Acne,Roasea,p Gangr

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Acne vulgaris

THIS IS THE MOST COMMON SKINDISORDER SEEN IN CLININICS

THIS IS SAID TO BE THE DISEASEOF TEEN AGE WHICH IS PARTIALYTRUE.

THERE IS A COMMON WRONG

BELIEF THAT IT WILL GET BETTERAFTER MARRIAGE

THIS HAS THE POTENTIAL TO MAKETHE FACE COSMETICALLY BAD

THUS PRODUCING LIFE LONGPYCHOLOGICAL DISABILITY


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Epidemiology

Onset? Males 10-17 yrs Females

14-19 yrs

May persist through 4th decade orolder

Prevalence? Asians 10%

African-American 25%

Caucasians 29%


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Causes?

Majority of patients have a familyhistory of acne

Emotional stress

Androgens Dioxins, lithium

Occlusion and pressure acne

mechanica NOT DUE TO CHOCOLATE OR

FATTY FOODS!


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Pathogenesis:

Acne vulgaris is a disease ofpilosebaceous follicles.

Factors:

Retentionhyperkeratosis.

Increased sebumproduction.

Propionibacterium acnes

within the follicle.

Inflammation


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Initial pathogenesis (reason unknown):

follicular hyperkeratinization

proliferation +decreased desquamation of keratinocytes

hyperkeratotic plug(microcomedone)


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Pathogenesis

Sebaceous glands enlarge

Sebum production increases

Growth medium forP. Acnes

plugs provide anaerobicLipid-rich environment


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Pathogenesis

Bacteria thrive

Inflammation results

Chemotactic factors attract neutrophils

Depending on conditions

Non-inflammatory

open/closed comedones

Inflammatory papule/

pustule/nodule


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Terms/Definitions Microcomedone:

hyperkeratotic plug made of sebum and keratin in

follicular canal


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Whitehead and blackheads


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Open comedo (blackhead)

open comedo

(a blackhead):

when follicularorifice is opened +

distended.

Melanin + packedkeratinocytes +

oxidized

lipids dark colour


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Pustular


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Cysts papules,pustules, nodules

Cysts:

when folliclesrupture into

surrounding

tissues, resulting in

papule/pustule/nod

ule.


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Cysts


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How to arrive at

diagnosis When was the onset? Adolescence

Where? Face, neck, trunk

& buttocks

Does it itch or hurt? Pustulespainful

How have the individual lesions

changed?

Triggers?

Milk,chocalates,corbohydrates,stres

s,cosmetics use,working envirnoment?

Hirsutism? Oligomenorrhea?


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Differential Diagnosis

Face Staph aureusfolliculitis

Rosacea

Perioral dermatitis Trunk

Pityrosporumfolliculitis

Hot Tub folliculitis Acne Aestivalis

Appears after sun exposure


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Types of Acne

Comedonal Papulopustular

Nodulocystic

Why is this important?

Directs treatment options


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Comedonal Acne

Closed comedones

(whiteheads)

Sebum accumulation results in

a white papule visible at the

skin surface

Open comedones

(blackheads)

Plug protrudes from canal and

turns dark

Non-inflammatory

Usually responds to topical

keratolytic


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Papulopustular Acne

Papules/Pustules Follicular wall

ruptures

Releases sebum and

bacteria into dermis

Topical agents alone

usually insufficient

Consider topical

retinoidsplussystemic antibiotics


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Diagnosis

Complete history

Pay attention to endocrine function

- Rapid appearance withvirilization/menstrual irregularityPCOS

and other syndromes

Complete medication list

Physical exam:- Location - scarring

- Lesion type - keloid

- pigmentation


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Medications that can cause acne

ACTH

Azathioprine

Barbiturates Isoniazid

Lithium

phenytoin

Disulfiram

Halogens

Iodides Steroids

Cyclosporine

VitaminsB2,6,12


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TREATMENT OPTIONS

SYSTEMIC DRUGS

-Tetracycline - erythromycin

- minocycline - TMP-SMX

- doxycycline - clindamycin

SYNTHETIC VITAMIN A DERIVATIVESISOTRETINOIN

ANTIANDROGENS

aldactone,diane 35,cimetidine,ketaconazole

TOPICAL DRUGS ANTIBIOTICS,BENZYLE PEROXIDE,TRETINOIN,ADAPALENE.

AZELOIC ACID

SULPHUR,SALICYLIC ACID,GLYCOLIC ACID


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RECENT ADVANCES IN ACNE

TREATMENT INCLUDES BLUE LIGHT

THERAPY,LASER THERAPY ALL YETEXPERIMENTAL.

ACNE SCARRING CAN BE MANAGED

BY VARIOUS METHODS

LASER THERAPY,CHEMICALPEELING,DERMAROLERS.


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Rosacea

Chronic inflammatory facial

dermatoses characterised by

erythema and pustules Cause unknown

Middle aged

Flushing

Erythema, telangiectasia, papules,

pustules, occasional lymphoedema :

rhinophyma


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Rosacea

Eye involvementblepharitis,

conjunctivitis

No comedones Treatment

Topicalmetronidazole

Systemicantibiotics, retinoids, Rhinophymalaser, plastic surgery

Avoid topical steroids


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PYODERMA

GANGRENOSUM ACQUIRED

INFLAMMATORY

IDIOPATHIC

AUTOIMMUNE?

NEUTROPHILICINFILTRATE IN

DERMIS WITHDESTRUCTIONOF TISSUES


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Clinical features

Non healing ulcers

painful

Bullous lesions

Vegetative lesions Dirty looking deep

ulcers withoverhanging borders

Atrophic scars seen

after healing.


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ASS0CIATIONS

BLOOD

DYSCRASIAS

INFLAMMATORYBOWEL DISEASES

ARTHRITIS

SLE

MALIGNANCIES

CHRONIC ACTIVE

HEPATITIS


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Different clinical

presentations


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TREATMENT

SYSTEMIC

STEROIDS

CYCLOSPORIN AZATHIOPRINE CYCLOPHOSPHAMIDE

DAPSONE

CLOFAZAMINE

NURSING CARE


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Fever,pruritus,polymorp

hic vesicular rash

P iti d t


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Pruritis,good response to

steroids but the rash

persists

Acne,Roasea,p Gangr

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