SSS 1,2,3,5,6,7,9,11

Myopia

short sightedness

• condition in which an image of a distant object becomes focused in front of retina, either bc eyeball axis is too long or because refractive power of object is too strong

• corrected by concave (minus) lenses

Hyperopia

• far sightedness

• refractive error in which image of a distant object becomes focused behidn retina, either bc eyeball axis is too short or bc refractive power is too weak

• corrected by convex (plus) lenses

Astigmatism

• eye condition that exists when surface of cornea or crystalline lens is irregularly shaped

• corrected by toric lenses (football shaped)

Presbyopia

age-related loss of near vision, typicaly starting around 40, caused by eye’s lens becoming less flexible and losing its ability to focus on close objects

• age related loss of accomodation

• corrected by convex (plus) lenses

Symptoms in an eye exam

1. abnormal vision

2. abnormal sensation eg. discomfort

3. altered appearance

types fo abnormal vision

1. reduced

• central

• peripheral

• impaired night or colour vision

onset

if sudden —> vascular

or gradual

.

2. floaters

• haemorrhage

• inflammation

• vitreous degeneration

• muscae volitantes

.

3. flashers

• irritative stimulation of retinal or visual pathway

can be unilateral —> retinal deatchment?

bilateral —> migraine/basilar artery insufficiency

.

4. haloes - rainbow coloured rings around lights due to corneal oedema or increased intraocular pressure

5. metamorphopsia / micropsia

• apparent distortion of straight lines/minification of objects due to retinal oedema or macular degeneration

6. diplola

binocular 

• resolves when either eye is covered, due to misalignment of visual axes

  

monocular

persists when unaffected eye is covered

• caused by optical/intraocular problems (not alignment)

typical causes

• cataracts, corneal irregularity/scar, refractive error, dry eye, intraocular foreign body

Abnormal sensation types

1. foreign body sensation

• subjective localisation unreliable

• causes include: trichiasis, entropion, conjunctivitis, dry eye

• local anaesthetic relieves

2. photophobia

• iritis

• keratitis

• cycloplegic drops relieves

3. severe deep pain

• acute angle closure glaucoma

• zoster/shingles

4. asthenopia (eye strain)

• occurs after intensive use of eyes

• due to

• inadequately corrected refractive error

• heterophoria

5. watery eyes/ discharge

• overproduction (due to ocular irritation or FB)

• faulty drainage

• instability (dry eyes often blepharitis)

Types of altered appearance

What are the 3 mechanisms of Cellulitis

• spread from local infection like sinusitis

• skin disruption

• haematogenous spread (common under age 2)

GAS/staph/s.pneumo

Periorbital vs orbital cellulitis

Red flags concerning for orbital cellulitis

• painful or restricted eye movements

• visual impairment: reduced acuity, relative afferent pupil defect, diplopia

• proptosis

• severe headache or other features of intracranial involvement

Cellulitis characteristics

Dermatitis vs eczema

terms are used interchangeably but … technically eczema is a type of dermatitis.

Dermatitis refers to any cause of skin inflammation affecting the epidermis

Eczema - oedema within the epidermis (called spongiosis)

Acute vs chronic dermatitis

Acute - red, wet, oozing, even blistering

Chronic - skin thickened, dry, scaly, and fissured (lichenification - secondary lesion)

Subacute - stage between acute and chronic so will show features of both

Seborrhoeic dermatitis

(endogenous)

• red itchy patches (which become scaly or crusted)

• caused by combination of endogenous factors and overgrowth of malassezia furfur yeast

• dermatitis may be aggravated by a combination of endogenous factors - illness, stress, fatigue, change of season, and reduced general health (eg. especially infection with HIV)

1. Infantile seborrhoeic dermatitis

   • characteristic cradle cap ‘greasy’

   • erythematous but non-itchy rash, well defined and covered in greasy scale… (sebaceous glands release a greasy substance that makes old skin cells attach to scalp as they try to dry and fall off)

   • the rash may spread to affect armpit and groin folds (via flexures)

   • possibly due to overactive sebaceous glands in skin of newborn babies due to maternal hormones still in baby’s circulation

   • super-infection with staph and candida albicans is common resulting in weeping and crusting

treatment: for

mild/localised - use gentle emollient or repeated shampooing, remove scales with a soft toothbruhs or comb

extensive/resistent - treat with low-potency topical steroid or antifungal for 1-2 weeks…. topical steroid preferred if significant inflammation

2. Adult seborrheic dermatitis

   • usually appears at any age after puberty

   • exacerbated by emotional and physical stress

clinical features: erythema and fine, greasy scale on cheeks, nose and nasolabial folds

scale and itching of scalp and eyebrows

well defined but non scaly, erythema of axillae, groin, scrotum and perianal skin

management:

scalp:

• anti-dandruff shampoos containing selenium sulphide, ketoconazole, miconazole or zinc pyrithione (which all control malassezia)

• tar containing shampoos are also helpful and combination of a tar and antifungal shampoo gives better control than either alone

non scalp areas:

• topical steroids first and consider adding topical antifungal agent for malassezia

• weak tar creams such as LPC 2% cream may assist (you used this! for something else tho)

Atopic dermatitis (+aetiological factors* (5), clin features (5), distribution, treatment 9) + pityriasis alba

(endogenous)

• most common form of dermatitis

• atopic eczema also associated with asthma, allergic rhinitis (hayfever), food allergies

aetiological factors

1. family history

2. immune dysregulation - increased IgE due to Th2 immune dysregulation

3. abnormal epidermal barrier - deficiency of fillaggrin (an epidermal protein) which causes impaired skin barrier which holds water poorly and is more susceptible to irritants and allergens

4. susceptibility to infection - epidermis is deficient in peptides known as defensins

5. environmental irritants - bc of the impaired epidermal barrier eg. soap, sand, woollen, synthetic fabrics and dust

clin features

1. a patchy erythematous, poorly defined rash

2. xeroderma - dryness of skin

3. excoriation (de to scratching and itching)

4. lichenification (prurigo may develop)

5. in bacterial infections crusting and weeping

Distribution

infants

• cheeks are often first place

• may have widely distributed small patches of eczema

• napkin area is frequently spared due to mositure retention of nappies

• tends to be vesicular and weeping

• in babies of non-caucasian descent, a micropapular variant is common (instead of vesicular) and temporary hypo/hyperpigmentation may occur

toddlers and pre-schoolers

• as children begin to mvoe around, eczema becomes more localised and lichenified

• flexor aspects of joints (wrists, elbows, ankles, and knees +maybe genitals)

• some individuals have reverse presentation where it affects the extensors

• some develop discoid pattern

adults

• become quite localised involving hands, eyelids, nipples, genital area, lips or face

• in severe: it may involve entire skin (erythroderma)

TREATMENT

1. explanation fo chronicity and overall good prognosis (requires long term management not just reactive care, also need to treat flareups)

2. modification of lifestyle to avoid exacerbating factors

3. use of moisturisers and bath additives (use of emollients and bath oils)

4. investigation and treatment of infection (MCS if flare ups, antibiotics), for recurrent or chronic, add a very dilute chlorine bleach to water

5. discussion, possible investigation and treatment of allergy (allergy testing)

6. use of topical anti-inflammatory agents (MAINSTAY- TOPICAL CORICOSTEROIDS)

7. understanding role of anti-histamines (minimal use as not much benefit)

8. use of wet dressings

9. understanding psychological issues

other options

Pityriasis alba

• low-grade type of atopic dermatitis mainly seen in children

• mild scattered areas of facial eczema complicated by depigmentation on face

• several round or oval slightly scaly pink patches appear, leaving pale marks when redness faded

• regresses spontaneously

• more apparent in summer, especially in dark-skinned children

management: weak topical corticosteroid, emollient and soap avoidance

once dermatitis is controlled, sun exposure will return the pigment

Discoid dermatitis (two forms)

(endogenous)

• affects middle age and elderly

• OFTEN with a previous history of atopic dermatitis

• pink, red, brown and well defined, dry cracked surface and can have blistered or crusty surface

TWO FORMS

• exudative (wet) nummular dermatitis: oozy papules, blisters and plaques

• dry nummular dermatitis: red scaly, very itchy, discrete, round or oval plaques with well defined edge

• may be symmetrical

• lichenification can occur rapidly due to intense scratching

• affects any part of body particularly lower leg

treatment: similar to atopic dermatitis

• moderately potent topical steroids are usually requried

• lichenified lesions may require very potent topical steroids or intralesional steroids

• wet wraps

• antibiotics if bacterial infection

Stasis dermatitis (+complications (8) and management)

• occurs on lower legs due to chronic venous hypertension

• mainly in elderly women

• look for venules, phlebactasia and brown haemosiderin deposition around ankles (early signs)

characteristic dryness, scale and brown hyperpigmentation (due to diapedesis of red blood cells from peripheral circulation into dermis, eczema and ulceration can subsequently develop

• usually associated varicose veins, woody oedema (due to lipodermatosclerosis)

• allergic contact dermatitis may coexist (eg. bandages or leggings for chronic venous hypertension may be an irritant/allergen)

Management

• dryness is managed by avoidance of soap, using a soap substitute and application of a greasy moisturiser at least twice a day

• inflammation treated by moderate topical corticosteroid

• acute attacks are settled by short bursts of potent topical corticosteroids, wet dressings and antibiotics if an infection (like discoid and atopic management)

• In order to treat and prevent you need to treat the cause of the stasis dermatitis by attention to the underlying venous insufficiency. This involves compression bandaging or stockings and elevation of the foot of the bed at night

Pompholyx (dyshidrotic) dermatitis

(endogenous)

• a vesicular or bullous dermatitis

• affects palms, sides of fingers and soles of feet

• cause: unknown, may be precipitated by stress, sweating and overheating

• acute stage: vesicles deep in skin of palms, fingers, instep or toes, the blisters are often intensely itchy or have a burning feeling, the condition may be mild with only a little peeling or very severe with large blisters and cracks

Management

• Management is the similar as for other dermatitis.

• Potent topical corticosteroids should be used initially with wet dressings and antibiotics if secondary bacterial infection.

• Rest is important and because of the location on the hands this can mean time off work for adults.

• After an acute attack, the skin is vulnerable, and patients need to protect their hands from irritating substances including soap for three months.

• Very severe attacks of bullous Pompholyx may require a 2-to-3-week course of oral prednisone.

Asteatotic Dermatitis

(miscellaneous)

hypothyroidism can contribute to condition

Irritant dermatitis

(exogenous)

Cause

• Strong irritant elicit an acute reaction after brief contact

• Sometimes a weak irritant over many years

• Usually, hands and forearms

• E.g. water, detergents, chemicals, oils o Previous Atopic dermatitis increases the risk

Often on backs of hands, between fingers, Napkin area

• Dry "chapped". Later thickened and fissured

• more likely in Cleaners, catering, hairdressing, engineering, health workers

Investigations - patch testing with irritants is not helpful but with common allergens may be

treatment

• avoidance of irritant

• protective gloves and clothing

• barrier cremes more for prevention

• avoid harsh solvents when cleaning hands

• emollients

• corticosteroids

Allergic contact dermatitis

(exogenous)

Functions of the skin

• thermoregulation (evaporation of sweat, in hot or cold weather, cutaneous blood vessels dilate or constrict to give off/conserve heat, arrector pili contraction produces heat (goosebumps))

• protective function and repair

• sensation

• immunological response

• metabolic (vit d synthesis)

• psychological and communication (aesthetic appearance, apocrine gland secretion - odour)

Important notes on epidermis

• stratum corneum - anuclear

• (stratum lucidum)

• stratum granulosum

• stratum spinosum

• stratum basale - melanocytes, keratocytes (where it develops but migrates up) and merkle cells

  +basement membrane zone and then dermis

epidermis is avascular

cells of epidermis

• keratinocytes: develops from basal layer and then migrates upwards to the stratum corneum where it is shed

• langerhan cells - APCs found in epidermis

• melanocytes produce pigment, protect cells of epidermis and dermis from sun damage

• Merkles cells - (sensory mechanoreceptors) transducers associated with fine touch via fine unmyelinated nerve fibres — only present in thick skin

epidermis has an undulating surface with cross-crossing ridges and valleys, with invaginations due to follicles and sweat duct ostia (what we see as fingerprints)

Important notes on dermis (major fibres, major cells)

• fibrous connective tissue in skin

major fibres

• collagen: provide the skin with strength and toughness. Collagen bundles are small in the papillary dermis and form thicker bundles in the reticular dermis (deeper).

• Elastin: provides the properties of elasticity and pliability to the skin.

dermis also contains nerves, blood vessels, lymphatics, epidermal adnexal structures, arrector pili muscle and cells.

major cells

• fibroblasts

• macrophages

• mast cells

• t and b lymphocytes

What are the physiological changes of the skin in aging

• thinning of epidermis

• flattening of dermal-epidermal junction

• hyperpigmentation

• loss of melanocytes

• degradation of collagen and elastin

Hypodermis

Adipocytes organised into lobules (between these lobules are septa) septa contain nerves, larger blood vessels, fibrous tissue and fibroblasts — cna form cellulite

function

• cold insulation

• site of fat and energy storage

• epidermal crosstalk

• immune surveillance

Epidermal appendages - hair types, hair cycle

on all body except glabrous skin (lips, glans penis, labia minora, palms and soles)

• provides protection, sensation and social communication

three types

1. lanugo - fine long hair of fetus that is shed 1 month prior to birth

2. vellus - fine short hair found all over body

3. terminal - thick hair on scalp, beard, axilla and genital area

hirsutism - vellus to terminal

male pattern alopecia - terminal to vellus

hair growth cycle

1. anagen - long growth phase

2. catagen - where active hair growth stops and the follicle begins to regress

3. telogen - ‘resting’ follicle shrinks and atrophies, and new hair follicle begins to grow

4. exogen - hair shed

Epidermal appendages - nails

specialised plates of hard keratin that develop from epidermis overlying small bones at ends of fingers and toes

• stratching

• grooming

• picking up ifne objects

• psycho-sexual communication

• weapon

paronychium - skin around nail

lunula - white area of base of nail

Types of glands - epidermal appendages

1. sebaceous glands

• associated with hair follicles

• secreted onto skin through pilosebaceous canal-discharge into hair follicle ducts

• antibacterial and antifungal action

2. eccrine sweat glands

• all over body

• merocrine

• opening directly into skin

• cholinergic innervation

• watery (hypotonic) secretion

• sweating/thermoregulation

• onset of activity: birth

3. apocrine sweat glands

• axilla, groin, mammary area, umbilicus

• apocrine

• opens into hair follicle (like sebaceous glands)

• adrenergic innervation

• viscous secretion

• body odor

• onset of activity: puberty (androgen dependent)

Macule

flat area of altered colour ≤ 1cm

Patch

flat area of altered colour > 1cm

Papule

elevated, solid, palpable lesion that is ≤ 1cm in diameter.

may be

• acuminate (pointed)

• dome shaped (ronded)

• filiform (thread like)

• flat-topped

• oval or round

• pedunculated

• sessile

• umbilicated

• verrucous

Nodule

elevated, solid, palpable lesion > 1cm

Cyst

papule or nodule that contains fluid or semi-fluid material so is fluctuant

Plaque

circumscribed, palpable lesion > 1cm, most plaques are elevated, with a flat top

Vesicle

raised clear fluid-filled lesion ≤ 0.5cm

Bullae

raised clear fluid-filled lesion > 1cm

Pustule

pus-containing lesion < 0.5cm

Abscess

localised accumulation of pus in dermis or subcutaneous tissue (u can’t rlly see pus that much compared to a pustule)

Wheal

transient-raised lesion due to dermal oedema —> indicates urticaria

Comedone

papule due to blocked sebaceous follicle (occurs in acne) —— open (blackhead) or closed (whitehead)

What is diascopy

test where a clear glass slide is pressed against a skin lesion to assess if it blanches

helps differentiate between telangiectasia and petechiae

Petechiae is caused by blood leaking out from capillaries into surrounding tissue, whereas telangiectasia is the blood is still in the vessel but the capillaries are just dilated which means the blood can be pushed aside in the vessel —> blanching

Auspitz sign

peeling off surface scale to reveal areas of pinpoint bleeding (typical in psoriasis)

Woods light

fluorescence in visible range when applied to certain skin conditions

dermographism

where skin is stroked and a wheal is formed (indicative of tendency to urticaria)

nikolski’s sign

shearing stress of skin causes separation of skin resulting in traumatic bulla

koebner phenomenon

localisation of a non-infective skin disorder to area of trauma eg. psoriasis developing at site of a scar

dariers sign

rubbing of area of mastocytosis causes an intense urticarial reaction

pathergy

penetrating injury to skin causes area of pustulation 72 hours afterwards

bullous diseases types

1. subcorneal —> impetigo (children)

2. intraepidermal —> pemphigus vulgaris (middle aged), herpes zoster (older adults)

3. subepidermal —> bullous pemphigoid (elderly), dermatitis herpetitiformis (adults)

subcorneal - thin roof, not usually intact

intraepidermal - thin roof, rupture easily and leaves oozy denuded surface

subepidermal - thick roof so tending to be tense and intact - may contain blood

Risk factors for bacterial infections

• skin barrier disruption (trauma, insect bites)

• moist, macerated environments (common in warm, occluded areas such as the axilla and groin)

• colonisation with skin flora pathogens

• impaired host defenses

What causes impaired host defenses

Metabolic - diabetes mellitus

Vascular insufficiency - Peripheral arterial disease, chronic venous insufficiency (varicose veins)

Immunodeficiency - HIV/AIDS, malignancy, immunosuppressive therapy eg. glucocorticoids

Impetigo

staph

~ most common in young children (but occurs at any age)

~ less commonly caused by strep pyogenes

~ spreads in warm moist environments with close physical contact and poor hygiene

 

Two presentations

1      Bullous (SUBCORNEAL BULLAE)

~ thin-roofed bullae with clear yellow fluid which rupture quickly leaving exudative and yellow brown crust erosions

~ more likely to have systemic symptoms of malaise, fever, and lymphadenopathy

[staph attacks intracellular adhesion molecules in stratum granulosum, causing bullae formation – explored later]

 

2      crusted or non-bullous (most common)

~ begins with a single erythematous macule which evolves into a pustule or vesicle

~ pustule or vesicle ruptures releasing serous contents which dries leaving honey-coloured crust

~ has satellite lesions due to autoinoculation

what areas of skin are prone to impetigo? broken by insect bites. superficial injury, excoriated eczema

 

complications?

Can trigger post-strep glomerulonephritis and rheumatic heart disease

 

Can grumble on for several weeks and lead to deeper ulcerated and scarring infection called Ecthyma

general measures - TREATMENT

• cover affected areas with watertight dressing to prevent spread

• hand hygiene

• school exclusion (until at least 24 hours after starting appropriate antibiotic treatment)

TOPICAL: for localised non-bullous impetigo, antiseptic recommended for 5-7 days… if ineffective or not appropriate (if around eyes) topical antibiotics can be considered (fusidic acid 1st, mupirocin - reserved for MRSA infection)

SYSTEMIC: fluclox (1st)

alternatives may include trimethoprim and sulfamethoxazole or erythromycin (for MRSA infection or if penicillin allergy)

Ecthyma

Hard crusted sores beneath which ulcers form

~ begins as a vesicle or pustule on inflamed skin

~ removal of crust reveals red, swollen, indurated ulcer oozing with pus

Community-acquired MRSA

mostly occurs

~ in overcrowded places, due to frequent contact of skin and sharing things

~ in people with draining cut or sore or that are carriers of MRSA

 

Management

~ swab for MCS

PCR

Surgical drainage if required

Clindamycin or trimethoprim/sufamethoxazole

For severe infections vancomycin is indicated

 

Clinical features of hospital acquired MRSA

~ present as skin infections (abscesses, furuncles and carbuncles, impetigo and cellultiis) or as wound infections (at trauma and surgical sites)

 

Whereas

Clinical features of community-acquired MRSA mainly presents as bacterial folliculitis, boils, impetigo

Folliculitis

Inflamed hair follicles

 

Presentation

~ tender red papule or pustule centred on a hair follicle

~ more common in hot weater

~ often occurs in macerated areas

~ look at centre of the inflammatory papule for protruding hair shaft

Shaving and waxing common triggers

 

Investigation

MCS

Skin scraping for fungus

Hair pull test (if fungal scalp involvement suspected)

 

Treatment

• Depending on the organism or cause.

• Physical factors such as occlusive clothing, grease or massage oils or in a child case nappies need to be managed.

Furuncles and carbuncles

deep form of bacterial folliculitis

~ furuncles (boils) present as single or multiple tender, red, firm or fluctuant nodules or walled-off abscesses which eventually point and discharge pus from a central core

 

~ carbuncles are when multiple furuncles coalesce and extend to the subcutis

~ carbuncles often have systemic signs (malaise, chills, fever)

 

Treatment

~ apply topical antiseptic like povidone iodine or chlorhexidine cream

Then cover with gauze

 

~ oral antibiotics: fluclox, cephalexin

 

~ incision and drainage

Acute vs chronic paronychia

Acute paronychia

~ common in nail biters and those with chronically wet hands

 

Presentation

~ nail fold becomes painful, red and swollen, sometimes yellow pus under cuticle

 

Treatment

~ drainage with sterile needle, application of a topical antibiotic, sometimes oral

 

Acute herpetic paronychia

~ caused by HSV

 

Chronic paronychia

~ chronic irritant dermatitis and C.albicans superinfection

~ may start on one and spreads to several others

~ affected nail fold is swollen and lifted off nail plate

~ becomes distorted and ridged as it grows. May become yellow or green and brittle

 

~ common in people with chronically wet hands, such as bar tenders and housewives

SSSS

~ characterised by erythematous painful blistering

~ skin looks like a burn or ‘scald’

~usually from a local infection eg. impetigo

 

Treatment: systemic antibiotics

 

Mechanism of Staph to cause SSSS

~ release of epidermolytic toxins A and B from staph

~ toxins target desmoglein-1 (a cell adhesion protein) in the stratum granulosum

~ leads to intraepidermal splitting

~ results in blistering, skin peeling and positive nikolsky sign

What is Nikolsky’s sign?

shearing stress of skin causes separation of skin, results in traumatic bulla

Toxic shock syndrome

~ caused by release of exotoxins from staph and can also be caused by s.pyogenes

~ presents with sudden high fever, widespread erythematous rash, and multi-organ involvement

~ may lead to circulatory collapse

~ classically linked to tampon use but can arise from skin or wound infections

Cellulitis vs erysipelas

Cellulitis

~ acute diffuse spreading skin infection (what ur brother had)

 

Erysipelas

~ skin infection involving upper dermis with clearly delineated borders, eg. butterfly rash

 

Both present with localised redness, pain, swelling and +/- systemic symptoms (fever)

~ usually caused by s.pyogenes (GAS)

~ if around a wound, consider staph

~ periorbital cellulitis can occur in children (like ur bro) usually S.pyogenes. his was HSV, Hib is now rare due to vaccination

 

Cellulitis presentation

~ more raised n swollen, less marginated, favours lower legs in adults, and for children, limbs and periorbital region

 

Predisposition for cellulitis

On legs (lymphoedema, tinea of feet, chronic dermatitis, poor lower leg circulation arterial and venous, wounds)

 

On face: Herpes simplex infection, dental caries, chronic sinus infection, more common in diabetics, immunosuppression)

 

Treatment:

rest and elevation of area

analgesia

oral or IV antibiotics eg. cephalexin, fluclox, penicillin-dependent on sensitivities

 

Presentation for erysipelas

~ may see lymphatic streaking

~ blisters may develop on red plaques

~ most commonly affects lower limbs

 

Treatment:

Oral antibiotics or IV if severe, usually penicillin

Necrotising fasciitis

~ infection of soft tissue and fascia

~ presents as a dusky cellulitis which progresses to extensive necrosis

~ bacteria multiplies and releases toxins and enzymes that results in thrombosis in blood vessels  destruction of soft tissues and fascia

~ due to mixture of staph, strep and anaerobes?

Erythrasma

~ in skin folds, axilla or groin or between the toes

~ macular wrinkled, slightly scaly, pink, brown or macerated

~ WOODS LIGHT: CORAL PINK

 

Treatment:

Fusidic acid cream, whitfield ointment, clindamycin solution

 

 

Trichomycosis Axillaris

Infection of underarm hair

 

~ characterised by yellow, black or red granular nodules or concretions that stick to hair shaft

~ caused by overgrowth of corynebacterium

 

~ topical antibiotics and shaving

Pitted keratolysis

~ combination of unusually sweaty feet and occlusive shoes encourages growth of microorganisms that digest keratin

~ results in honeycomb like pits in webs and toe pulps, forefott and heel

~ often with offensive odour

 

Treatment

~ keep feet dry

~ topical clindamycin, erythromycin, fuscidic acid

~ oral macrolides

Herpes Simplex Virus infection (types, recurrence, complications, diagnosis, treatment

• clinical sign: grouped vesicles on an erythematous base

• spread via resp droplets or direct contact with an infected lesion or bodily fluids

• HSV enters host through abraded skin or intact mucous membranes

• targets epithelial cells initially but retrograde transport through adjacent neural tissue to sensory ganglia leads to lifelong latent infection

two types: HSV1 and HSV2

HSV1 is more associated with oral n facial infections (cold sores)

• often initial episode has no symptoms but can be severe if have systemic symptoms

• vesicles turn quickly into ulcers (red based)

HSV2 more associated with anogenital herpes

• presents after onset of sexual activity

• painful vesicles, ulcers, redness and swelling last for 2-3 weeks, often accompanied by fever and tender inguinal lymphadenopathy

minor injury helps inoculate HSV into skin

How can HSV recur

• can either be local or systemic stimuli

• UV light

• fever

• trauma

• mensturation

• sexual intercourse

• stress

• immunodeficiency

recurrence is often less severe 

Complications

• eye infection: dendritic ulcer

• throat infection

• eczema herpeticum (in patients with history of atopic dermatitis or darier disease)

• erythema multiforme (target lesions, symmetrical plaques on hands, forearms, feet and lower legs)

• cranial/facial nerve infections by HSV (bells palsy)

• widespread infection —> disseminated infection (eg. can occur in a HIV patient)

Diagnosis

• clinical diagnosis, culture and PCR

treatment

• mild uncomplicated eruptions of herpes simplex require no treatment

• sunscreen and other sun protection measures are crucial as sun exposure often triggers facial herpes simplex

for mild oral lesions: topical acyclovir

severe infection may require treatment with an oral antiviral agent

• acyclovir

• valaciclovir

• famciclovir

theyre suppressive not curative

How can HSV recur

can either be local or systemic stimuli

• UV light

• fever

• trauma

• mensturation

• sexual intercourse

• stress

• immunodeficiency

recurrence is often less severe 

Diagnosis for HSV

Clinical diagnosis, culture, PCR

Treatment for HSV

• mild uncomplicated eruptions of herpes simplex require no treatment

• sunscreen and other sun protection measures are crucial as sun exposure often triggers facial herpes simplex

for mild oral lesions: topical acyclovir

severe infection may require treatment with an oral antiviral agent

• acyclovir

• valaciclovir

• famciclovir

theyre suppressive not curative

Varicella (chickenpox) (rash, lesion characteristics, diagnosis, complications, treatment, vax?)

• caused by varicella-zoster virus

• remains in dorsal ganglia of the spinal cord —> can reappear later as shingles or herpes zoster infection

spread via inhalation of resp droplets or direct contact with the vesicles’ fluid.

RASH: begins on trunk and spreads to face and extremities (the opposite of rubella and measles)

LESIONS are: 2-4mm red papules —> become vesicular and umbilicated —> breaks and crusts over leaving an eroded red base 

diagnosis

• made clinically in typical cases

• can be confirmed by PCR on a viral swab from base of vesicle 

complications

• secondary bacterial infection from scratching

• dehydration from vomiting and diarrhoea

• systemic: 

~ viral pneumonia

~ encephalitis

~ thrombocytopenia

~ hepatitis 

~ scarring

pregnancy complications

• If a non-immune pregnant woman is infected:

◦ Maternal varicella pneumonia (serious).

◦ Congenital varicella syndrome (limb hypoplasia, eye/brain defects, skin scarring in fetus).

◦ Severe neonatal varicella if infection occurs just before or after delivery.

treatment

symptomatic eg. antipruritis lotions, antihistamines?

• antiviral therapy is indicated for patients with complications or who are immunocompromised 

antiviral agents include acyclovir, valacyclovir, famciclovir (same as HSV)

varicella-zoster immune globulin (VZIG) is indicated for immunocompromised and neonates exposed to varicella (must be given within 96 hours of exposure)

vaccination

• immunisation schedule in australia for infants aged 18 months and children 10-13 years who have not been previously immunised or previously had varicella infection

• zoster vax has also been introduced for patients over 60 and who are most at risk of this condition

Herpes Zoster (shingles) +diagnosis, clinical features, treatment

• reactivation of varicella virus localised to one or two dermatomes (what ur auntie had)

• virus remains in selected ?anterior? horn cells of spinal cord before it is reactivated and grows down the nerves to the skin

• predisposing factors apart from age are immunocompromised individuals eg. HIV

Diagnosis

• clinical

• viral PCR for herpes zoster virus

clinical features

• unitlateral

• dermatome (one or several)

first sign of shingles is usually pain, which may be severe, in areas of one or more sensory nerves. the patient may appear quite unwell with fever and headache, lymph nodes draining the affected area are often enlarged and tender

pain —> closely grouped lesions start as erythematous papules or plaques —> turn vesicular and become crusted —>over a course of 2-3 weeks clear vesicles appear in the affected dermatome

complications

• post-herpetic neuralgia (can last for years)

• corneal damage if CN V involved

• encephalitis

• myelitis causing contralateral hemiplegia

*Hutchinson’s sign - vesicle on side or tip of nose in ophthalmic zoster (WHAT UR AUNTIE HAD)

treatment 

• antiviral medication within 72 hours

• analgesia

• vaccination for patients over 60 

Viral exanthem

rash due to a virus

can be divided into

1. classic eg. measles rubella

2. non-specific (in children usually enteroviridae (coxsackie or echovirus))

whereas there are specific presentations with varicella, measles, rubella, hand, foot and mouth disease, parvovirus (slapped cheek), roseola, pityriasis rosea

What are the two non-specific presentations of viral exanthem in children

1. generalised, bilaterally symmetrical maculopapular rashes, often with confluence on the face

2. peripheral papular eruptions mainly on arms and leg

Measles (clinical presentation, diagnosis, complications)

• spread via resp droplets

clin presentation

• initially URTI symptoms of fever, malaise, cough and conjunctivitis

• characteristic KOPLIK spots (pinhead size white spots on buccal mucosa) in prodromal stage —> a widespread morbilliform (macular) rash appears HEAD then spreads to TRUNK and limbs

• non-pruritis rash

• macules may coalesce, esp on face

• when it fades —> purplish hue —> brown/coppery coloured lesions with fine scales

diagnosis

clinical n confirm with serology

complications (Did this in GH)

• diarrhoea

• otitis media

• pneumonia

• encephalitis

vax at 12 months of age

*notifiable disease

Rubella (german measles) = presentation, diagnosis, complications

• mild pink maculopapular rash and lymphadenopathy

• begins on FACE and spread to TRUNK and limbs (less widespread than measles)

• mild fever, sore throat and rhinitis

• adults have arthralgia and arthritis

• infected by direct contact with nasal or throat secretions of infected individuals, infected personcontagious 7 days prior to rash, until 7 days after

diagnosis

• clin and confirm with serology (same as measles)

complications

• first trimester of pregnancy has 50% risk of congenital rubella syndrome (sensorineural deafness, CNS dysfunction, cataracts, cardiac defects)

*notifiable disease (like measles)

rubella vax is on national schedule

Hand, foot and mouth disease (clin presentation + DDx + diagnosis)

most often affecting young children under 5

• due to coxsackie virus A16

children present with small red macules that rapidly evolve into cloud vesicles and surrounded by erythematous areola in the oral cavity

• there may be lesions distributed over plams and soles, and dorsal fingers or toes

• 20% of cases have submandibular / cervical lymphadenopathy

DDx for hand, foot and mouth disease

• enterovirus 71 infection

• herpetic stomatitis

• aphthous ulceration

• herpangina

• erythema multiforme

• scabies

(see the ppt for explanation on ddx)

diagnosis

clin and serology (same as measles and german measles (rubella))

DDx for hand, foot and mouth disease

• enterovirus 71 infection

• herpetic stomatitis

• aphthous ulceration

• herpangina

• erythema multiforme

• scabies

(see the ppt for explanation on ddx)

Parvovirus infection - slapped cheek - fifth disease (clin features, treatment, complications, DDx)

• parvovirus B19

transmitted via resp droplets

clin features

• firm red burning-hot cheeks

• rash follows with lace or network pattern on limbs and then trunk

treatment - supportive

complications

• in pregnant women may cause foetal anemia and cardiac failure and fetal loss

• arthralgia in adults

DDx

• enterovirus exanthemata

• rubella

• scarlet fever

Roseola (clin presentation and treatment?)

transmitted via resp droplets

• HHV-6B, HHV-7

clinical presentation

• high fever and upper resp symptoms

• rash appears as fever subsides (days 3-5)

• rash: small pink or red maculopapular rash that blanch when touched, may be surrounded by lighter halo of pale skin

• begins on TRUNK and may spread to neck, face, arms and legs (sort of like varicella)

• non-itchy, painless and does not blister

no treatment required

Pityriasis Rosea (presentation)

• rash of unknown cause (possible reactivation of Herpes 7 or 8 virus)

• most commonly affects teenagers or young adults

PRESENTATION

• single inner circlet of scaling, oval red or pink plaque (the HERALD patch) appears before general rash

• few days later, smaller plaques appear on chest n back, uncommon on face

• these lesions follow the relaxed skin tension lines (LANGER’S LINES) on both sides of upper trunk (so it looks like a fir tree?)

• can be very itchy and sometimes not at all. on darker skin they appear more pigmented or white due to scales

Monkey pox (MPox) - presentation, transmission, prevention, diagnosis, treatment and vax

• viral zoonotic disease

presentation

• general symptoms (fever, chills, headache, muscle aches, back aches, fatigue, swollen lymph nodes)

• USUAL symptoms: rashes, pimple-like lesions or sores, particularly in areas like genitals, anus or buttocks…. ulcers, lesions or sores in mouth… rectal pain (with or without rash)

• all lesions go crusted and fall off to reveal a fresh layer of skin

most people with MPox get better within a few weeks without needing any specific treatment

Mpox spread via

• direct contact w rashes, blisters or sores, or contact w bodily fluids also

• TOUCHING contaminated objects

who is at risk: men who have sex w men

prevention

• isolation

• hand hygiene

• keeping lesions covered and wear a face mask

diagnosis

• by lab testing

treatment

• supportive care —> pain relief

• antivirals for more severe disease

vaccine for at risk population!

Molluscum contagiosum - presentation, DDx, control spread, treatment

• poxvirus

• two peaks: in children (3-9) and young adults

spread from direct contact

the papules form a row —> known as pseudokoebnerised molluscum

presents as clusters of small pearly papules with a central umbilication, core can be expressed by firm pressure, occurs in warm moist areas like armpits, groin or behind knees in kids, in adults in groin

DDx

• verrucae (but have no central umbilication)

• herpes (rapid onset and vesicles)

treatment

• in children leave alone

• cryotherapy

• can use tape occlusion

• immune techniques such as imiquimod creme, topical retinoids

Viral warts - transmission, presentation, DDx, treatment

• common benign growths

• usually on hands, feet and extensor surfaces

• HPV

transmission

• direct contact w infected skin or contaminated surfaces (breaks in skin increase transmission)

presentation

• comon warts (verruca vulgaris)

• plane warts

• plantar warts

• digitate/filiform warts

• characterised by papillomatous surace, loss of skin lines and papillary capillaries

DDx

• Bowen’s disease

• seborrheic keratosis

• corns and callous

• penile pearly papules and equivalent papillomatosis of vulva

treatment

• spontaneous resolution usually 2 years

• topical salicylic acid, podophyllin or cryotherapy

• imiquimod topical treatment

• specialist referral if conservative fail

• HV vax 

reason we see viral warts as doctors

• cosmetic

• teasing from school mates

• exclusion from sport

• increasing number of warts

• pain in weight bearing

• distortion of structure

• concern of diagnosis

Scabies * presentation, diagnosis, complications, treatment

• scarcoptes sscabiei hominus

transmitted by body-to-body contact

• burrow through strateum corneum, produce 2-3 eggs a day which mature in 2-3 weeks 

presentation

• variable due to allergic reaction which is dependent on individual 

• generalised eruption and itchiness is thought to be caused by sensitisation to their products eg. faeces and eggs 

• pruritic excoriated nonspecific rash on trunk with scaly burrows on fingers and wrists

• papular or nodular lesions are often seen on genitals and nipples in adults and major flexor surfaces of children

in infancy, rash on face

diagnosis

• confirm with scrapping from burror and examine under microscope

• dermoscopy sometimes helps

• pracical method is positive response to anti-scabicide

complications

• secondary bacterial infection, rarely glomerulonepritis or RHD

• crusted scabies —> more on this

treatment

What are crusted scabies

• severe variant of scabies

• often seen in immunosuppressed

• numerous more mites

• widespread, scaly and hyperkeratotic rash

Head lice (transmission, presentation, complication, diagnosis, treatment, prevention)

head-to head contact

presentation

• itching

• may see excoriations or local lymphadenopathy

complication

secondary bacterial infection

Insect bites (presentation, treatment)

• bites present as persistent itchy, oedematous papules

• bullous reactions are common on legs of children

treatment

• preventative measures like with insect sprays

• treat fleas if present

• treat infection if present

• calamine lotion

• local potent topical steroids

• wet dressings for severe cases

Body and public lice

so yeah

Give me 4 resp causes of nail clubbing

• TB

• lung cancer

• interstitial lung disease

• sarcoidosis

Give 4 cardio causes of nail clubbing

• CHD

• tetralogy of fallot

• subacute bacterial endocarditis

• AA

Characteristics of nail clubbing

• loss of small diamond window when index fingers are brought together

• thickening of fingers

• softening of nail beds

• increased nail convexity

4 GI causes of nail clubbing

• Crohns and UC

• hepatocellular

• Celiac disease

• Liver cirrhosis

Treatment of nail clubbing

Treat underlying disease

Alopecia areata

• Discrete annular areas of hair loss anywhere on body

• sudden onset of hair loss, increasing area will have a smooth surface, completely devoid of hair or with scattered ‘exclamation mark’ hairs

Trichotillomania (+ddx)

condition where patients compulsively pull out their hair

can be a sign of stress relief habit, impulse control disorder, depression

DDx

• alopecia areata 

• tinea capitis 

NORMAL HAIR GROWTH IN THE BALDING AREAS

Telogen effluvium

when anagen stops prematurely and hair then enters telogen phase. anagen then recommences and telogen hairs are released from follicles after the shock

THIS OcCURS DUE TO A SHOCK OF THE SYSTEM

like acute telogen effluvium occurs folllowing childbirth or stopping OCP, any acute illness or major surgery and severe dieting

chronic may be primary and idiopathic or secondary to hypo/hyperthyroidism, malnutrition, cancer, TB, or iron deficiency anemia

CONFIRM by examining lost hair which is mostly in telogen stage (white bulb or club-shaped tip)

Anagen effluvium

drugs, toxins or inflammation cause interruption of active or anagen hair growth

Hypertrichosis vs hirsutism

widespread overgrowth of non–androgen-dependent hair, occasionally

seen with drugs such as cyclosporin and phenytoin.

• In hypertrichosis, areas like the forehead and forearms have increased hair growth— rather than the lower face and midline of the trunk that are preferentially affected by androgens