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NHarvey PATH2220 Pimples and Boils!! · PDF file Pimples and Boils!! Dr Nathan Harvey...

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  • Pimples and Boils!!

    Dr Nathan Harvey Anatomical Pathology, PathWest

  • Overview & Learning Objectives

    • Review the cardinal signs/symptoms of acute inflammation

    • Review the histological features of acute inflammation • Overview of the possible outcomes of acute inflammation • Understand the clinical signs/symptoms, pathological

    mechanisms and histological features of common acute inflammatory disorders of the skin: – Impetigo – Acne vulgaris – Folliculitis – Furuncle – Erysipelas/cellulitis

  • Neutrophils

  • What is Pus?

    • A protein-rich fluid produced as a product of inflammation

    • It comprises: – Leukocytes (white blood cells) – Debris from dead cells – Tissue elements which have been liquified

    by the action of neutrophil enzymes

    • Bacteria that cause pus formation are called suppurative, pyogenic or purulent

  • www.siumed.edu

  • Microscopic Structure of the Skin

    Stratum Corneum

  • Epidermis

    Dermis

    Subcutaneous adipose tissue

    Hair follicle

    Arrector pili muscle

    Eccrine sweat gland

  • Papillary dermis (note the solar elastosis : not technically normal, but almost ubiquitous in WA!)

    Reticular dermis

    Hair follicle

    Arrector pili muscle

    Eccrine sweat gland

    Sebaceous gland

    Blood vessels

  • Cornified layer

    (stratum corneum)

    Solar elastosis

    Melanin pigment Melanocyte

    Granular layer

    (stratum granulosum)

    Prickle layer

    (stratum spinosum)

    Basal layer

    (stratum basalis)

  • Cutaneous Bacterial Infections

    • Pyogenic infections – Staphylococcus aureus – Streptococcus

    • Corynebacteria • Neisseria • Mycobacteria • Chlamydia • Rickettsia

  • Impetigo

    • Acute superficial infection of the skin • Most common bacterial skin infection of

    childhood • Adults can also be affected

    – Athletes – Military – Institutions

    • Predisposing factors – Minor trauma – Poor hygiene – Warm, humid climate

  • Impetigo

    • Organism is often Staphylococcus aureus (esp in bullous subtype)

    • Also Streptococcus, anaerobes • Staphylococcus aureus may produce

    exfoliative toxins

  • Impetigo • Common Impetigo

    – “School sores” – Thin walled vesicles or pustules – Rupture to form a thick golden crust – Solitary or clustered, face or extremities

    • Bullous Impetigo – Erosions and flaccid bullae – Caused by an exotoxin which results in

    keratinocytes falling apart and blister formation

  • Histopathology

    • Subcorneal (ie under the stratum corneum) collection of neutrophils

    • Can see more neutrophils migrating upwards through the epidermis

    • Surface crust of serum and dying neutrophils

    • May see bacterial colonies

  • Neutrophils

    www.Derm101.com

  • Staphylococcal Scalded Skin Syndrome

    • Another blistering disorder caused by Staphylococcus aureus, but with a different mechanism

    • Occurs in infants • Widespread blisters that rupture easily • No bacteria in the blisters • Caused by an endotoxin that is made by

    the bacteria elsewhere and is transported via the bloodstream

  • Acne Vulgaris – Pimples! • An inflammatory

    disorder of the pilosebaceous unit – ie the hair follicle and

    attached sebaceous gland

    • Common • Affects a large

    proportion of teenagers

    • Usually improves spontaneously after adolescence

  • Clinical Appearances • The lesions that make up acne are

    variable and include: – Comedones – Papules – Pustules – Cysts – Sinuses – Scars

  • Clinical Appearances

    • Comedones are widened hair follicles which are filled with keratin, other debris, bacteria and sebum – Closed : “whiteheads” – Open: “blackheads”

  • www.Derm101.com www.Derm101.com

  • Open comedones

    Inflamed papule

    Scars

    www.Derm101.com

  • Pathogenesis • Four inter-related factors

    – Abnormal follicular keratinisation, with retention of keratin within the follicle

    • This process is the precursor to comedone formation

    • May be aided by a bacterial ‘biofilm’

    – Increased sebum production • Androgens

    – Presence of bacteria: Propionibacterium acnes

    – Inflammation

  • Pathogenesis • Ongoing dilation of comedo leads to the wall of the

    follicle becoming very thin • Eventually it ruptures • The keratin, sebum and bacteria incite an acute

    inflammatory response • Predominantly neutrophils at first – pustule

    formation • Followed by granulomatous inflammation and

    fibrosis (scarring) • The acute inflammatory focus can enlarge into an

    abscess. Sinus tracts result when the epidermis grows down in an attempt to ‘wall off’ the inflammation

  • Plugged and dilated follicle

    Neutrophils

  • Superficial Folliculitis • Typically affects the superficial part of the hair

    follicle, called the ‘infundibulum’ – Thus, perhaps more correctly should be called

    ‘infundibulitis’ • May be related to bacterial infection (eg

    Staphylococcus aureus) • Neutrophils under the statum corneum and

    around the infundibulum • ‘pseudofolliculitis’ is a term used to describe a

    foreign body response to hair shafts that have ruptured out of the follicle into the surrounding dermis

  • Small pustules around hair follicles

    www.Derm101.com

  • Neutrophils

    www.Derm101.com

  • Furuncle – “Boils” • A deeper infectious inflammatory process

    centred on the pilosebaceous unit • Typical locations include the back of the neck,

    buttocks and thighs – Sites of friction with clothing

    • Begins as a painful papule with surrounding erythema (redness) and swelling

    • The centre becomes soft, yellow and may discharge pus

    • A ‘carbuncle’ is a coalescence of several furuncles

  • Histological features

    • A deep dermal abscess (ie neutrophils again!) centred around a hair follicle

    • The follicle may be destroyed although residual hair shafts may be seen

    • The surrounding inflammation may extend into the deeper tissues

    • The surface oftens shows a ‘crust’ of serum and dying neutrophils

  • www.Derm101.com

  • Acute inflammation (ie neutrophils) in the deeper parts of the follicle

  • Furuncle - Causes • Often bacterial, usually

    Staphyloccocus aureus • Pseudomonas

    aeruginosa is associated with ‘hot tub folliculitis’ – Develops 8-48 hours

    after recreational exposure to the organisms, which is found in contaminated spas

    • Viral eg herpes simplex • Fungal

  • Erysipelas/Cellulitis • Erysipelas is an acute inflammatory

    process within the dermis which is usually caused by Streptococcus pyogenes

    • Oedematous, tender, hot, well demarcated red plaques

    • Often accompanied by a fever • Face, feet, hands and lower limbs are

    most affected

  • Erysipelas/Cellulitis

    • Cellulitis is a similar processs which involves slightly deeper tissues

    • More often occurs on the legs • Expanding area of erythema • S pyogenes is again usually the

    causative organism

  • Predisposing Factors

    • Minor trauma • Peripheral vascular disease • Diabetes • Lymphoedema • Alcohol abuse

  • Histology

    • Dermal oedema and lymphatic dilatation • Diffuse infiltrate of neutrophils

  • Erysipelas

    www.Derm101.com

    www.Derm101.com

  • www.Derm101.com

    Oedema

    Neutrophils

  • Summary

    • Remember: – the cardinal signs & symptoms of acute inflammation – The histological features – The possible sequelae

    • By applying the above to different anatomical components of the skin: – Impetigo – Acne vulgaris – Folliculitis – Furuncle – Erysipelas/cellulitis

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