Skin and special senses Flashcards
Auspitz sign
Auspitz sign : Peeling off the surface scale reveals regular areas of pinpoint bleeding (seen in psoriasis) Due to thick adherent scale in psoriasis and proximity of vessels to stratum corneum
Woods light
Woods light: Ultraviolet light : 365nm, Fluorescence in the visible range when applied to certain skin conditions e.g. Erythrasma : coral pink Pseudomonas infection : yellow green Tinea capitis : light blue Pigment : epidermal lighter, dermal darker Porphyrins : red teeth, urine, blister fluid
Diascopy
Diascopy: Diascopy is a test for blanch ability performed by applying pressure with a finger or glass slide and observing color changes. It is used to determine whether a lesion is vascular (inflammatory or congenital), nonvascular (nevus), or hemorrhagic (petechia or purpura). What is the reason? It differentiates telangiectasia from petechia.
Dermographism
Dermographism: Where skin is stroked and the skin responds with a wheal (red swollen skin). This is indicative of a tendency to urticaria (hives). Probably represents Mast cell sensitivity to trauma
Nikolsky sign
Nikolsky sign: Shearing stress on the skin causes separation of the skin along a horizontal plane. This results in a traumatic bulla. Occurs in fragile skin. May occur in epidermolysis bullosa in babies Typically a sign of superficial blistering disorders such as Pemphigus
Dermoscopy
Dermoscopy: Dermoscopy : clinical application. Pigmented lesions : e.g. Melanoma. Non pigmented lesions : e.g. BCC. Vascular lesions. Scabies, bites
Koebner phenomenon
Koebner phenomenon: Also called isomorphic phenomenon. Localisation of a non:infective skin disorder to area of trauma. Many forms of trauma : physical, chemical, thermal, ultraviolet. Examples: Psoriasis, lichen planus, vasculitis, erythema multiforme, vitiligo, atopic dermatitis
Macule
:Macule: flat area of altered colour or texture, less than 0.5cm in diameter
Patch
:Patch: a flat area of altered colour, greater than 0.5cm in diameter
Papule
:Papule: a solid raised lesion, less than 0.5cm in diameter
Nodule
:Nodule: a solid raised lesion, greater than 0.5cm in diameter
Plaque
:Plaque: a palpable flat top raised lesion, greater than 0.5cm in diameter
Vesicle
:Vesicle: raised clear fluid:filled lesion, less than 0.5cm in diameter
Bullae
:Bullae: raised clear fluid:filled lesion, greater than 0.5cm in diameter. Can one of two types; flaccid or tense
Pustule
:Pustule: pus containing lesion, less than 0.5cm in diameter
Abscess
:Abscess: a localised accumulation of pus in the dermis or subcutaneous tissue
Weal/Wheal
:Weal/Wheal: transient raised lesion due to dermal oedema (red middle, white outside)
Comedone
:Comedone: papule due to a blocked sebaceous follicle, occurring in acne. Can be open (blackhead) or closed (whitehead)
Excoriation
:Excoriation: loss of epidermis following trauma (technical word for scratch)
Lichenification
:Lichenification: well:defined thickening of the skin with accentuation of skin markings due to repeated rubbing and scratching
Scale
:Scale: flakes of stratum corneum
Crust
:Crust: rough surface consisting of dried serum, blood, bacteria and cellular debris that have been extruded through an eroded epidermis
Scar
:Scar: new fibrous tissue post wound healing. 3 different types; Atrophic : thinned, Hypertrophic : enlarged within the wound boundary and Keloid : enlargement beyond the wound boundary
Ulcer
:Ulcer: loss of epidermis and dermis (loss of both layers)
Fissure
:Fissure: an epidermal crack due to dryness (more likely to cause scarring)
Erosion
:Erosion: loss of epidermis only
Striae
:Striae: linear, macular or mildly hypertrophic lesion which progress from purple to pink to white, with histopathological appearance of a scar and is associated with excessive steroid use, glucocorticoid production, growth spurts and pregnancy
Telangiectasia
:Telangiectasia: an erythematous, fine linear lesion composed of capillaries. Is a dilated blood vessel within the dermis itself and applying pressure can make them disappear
Discrete
:Discrete: individual (lesion separated from each other)
Confluent
:Confluent: merging together
Linear
:Linear: in a line
Target
:Target: concentric rings
Annular
:Annular: like a circle with central clear
Discoid/nummular
:Discoid/nummular: coin shaped
Generalised/widespread
:Generalised/widespread: all over the body
Localised
:Localised: restricted to one area of the body
Flexural
:Flexural: body folds e.g. groin, neck, behind ears
Extensor
:Extensor: knees, elbow, shins
Pressure areas
:Pressure areas: sacrum, buttocks, ankles, heels
Dermatome
:Dermatome: an area of the skin supplied by a single spinal nerve
Photosensitive
:Photosensitive: sun exposed areas e.g. face, neck, back of hands
Kobner phenomena
:Kobner phenomena: linear eruption arising from trauma
Erythema
:Erythema: redness due to inflammation and vasodilation which blanches on pressure
Hypo:pigmentation
:Hypo:pigmentation: areas of paler skin
Hyper:pigmentation
:Hyper:pigmentation: areas of darker skin due to various causes e.g. post inflammation
De:pigmentation
:De:pigmentation: white skin due to loss of melanin
Petechia
:Petechia: non:blanching, red cell extravasation (pinhead size/pin:point macules)
Purpura
:Purpura: larger red cell extravasation which can be palpable or non:palpable. Red or purple colour due to bleeding into the skin which does not blanch on pressure
HAIR DISTRIBUTION
:Glabrous skin (skin totally devoid of hair) includes the palms, soles and portions of the genitalia
Hair Phases
Anagen, Catagen, Telogen and exogen
Anagen
Is the growing phase. During this phase the follicle penetrates deeply into the hypodermis, before the keratinocytes in the follicular bulb proliferate forming the hair shaft
Catagen
. It is during this phase that melanocytes responsible for giving hair its pigment are dispersed among the keratinocytes
Telogen
Is the programmed cell death phase. After anagen is complete, the keratinocytes and melanocytes undergo programmed cell death to form the characteristic hair structure
Exogen
Shedding phase
Which ducts empty into the hair follicles
Both the sebaceous and apocrine ducts empty into the hair follicles itself
There are 3 general types of hair
Lanugo (fine long hair of foetus and shed 1 month prior to birth), Vellus (which is the fine short hair present all over the body) and Terminal hair (the thick hair on our scalp, beard axillae and genitals)
Pre:pubertal hair function
Do not have terminal hair in the axilla or pubic area and boys have no facial hair
Puberty hair function
Hair growth in axillae and anogenital areas and males may develop more profuse body hair all over
Middle age hair function
Androgen turns frontal scalp hair from terminal to vellus hair. Conversely ongoing exposure of androgens changes vellus to terminal hairs
Females hair function
Particularly after menopause they develop facial hair around the beard area
The nails have a number of different functions, including;
Protect the distal phalanges of fingers and toes , Enhance fine touch discrimination, Help us pick up objects, They are an efficient natural weapon
APOCRINE SWEAT GLANDS
:Discharge from this gland is directly into hair follicles (as opposed to onto the surface). When this is first secreted, no odour is detected, it is actually the bacterial action on the secretion which develops the odour. This gland does produce some pheromones
ECCRINE SWEAT GLANDS
:Are glands that open directly onto the skin. A well acclimatised person can perspire up to several litres per hour. The secretions from this gland start out as isotonic, but end as hypotonic as sodium is reabsorbed
SEBACEOUS GLANDS
? Are found all over the body, typically associated with hair follicles. The largest glands and the greatest density of glands is found on the face and scalp. These glands secrete sebum
? These glands have a number of important functions, such as; Antibacterial agent, Antifungal agent, Contributes to the normal barrier function of the skin
: Sebaceous gland activity is high at birth before declining to almost nothing between 2 and 6 years of age
: From 7, sebum levels increase until the age of 20
: After the 20s, sebum secretion declines
: Men on average have higher rates of sebaceous gland secretions compared with females (why males have worse acne than females)
Where are there no sebaceous glands
The palms and soles, which have no hair follicles are devoid of any sebaceous glands. (except for glabrous skin / skin without hair, for example eyelids, nose, penis, nipples etc.)
NON:CELLULAR COMPONENTS OF SKIN
- Vasculature
- Sensory Receptors: There are few different types of sensory receptors. Free nerve endings, Pacinian corpuscle, Meissner’s corpuscle cells and Peritrichial free nerve endings.
- Glands: Sebaceous glands (empty into hair shaft), Eccrine sweat glands (open directly onto surface), Apocrine sweat glands (empty into hair shaft)
- Hair
- Nails
FUNCTIONS OF SKIN
and chemical barrier (microorganisms and ultraviolent light) and repair
: barrier
: Endocrine organ
: Vitamin D synthesis
: Psychological and communication effect through appearance
: Thermoregulation
: Sensory organ
STRUCTURE OF SKIN
- Epidermis
- Dermis
- Hypodermis
EPIDERMIS
? It is made up of stratified squamous keratinised epithelium and is avascular
? The epidermis primarily functions as a protective barrier, and is continually regenerating
? The main cell type in this layer are Keratinocytes (which produce keratin)
? Other non:keratinocytes in the epidermis include; Melanocytes (pigment cells), Merkel cells (nerve ending associated) and Langerhans cells (antigen presenting cells)
1. Stratum Germinativum / Basale
2. Stratum Spinosum
3. Stratum Granulosum
4. Stratum Lucidum
: Is a thin clear layer of dead skin cells that is only visible in areas of thick skin e.g. hands and soles of the feet
: It is made up of 3 : 4 layers of dead, flattened keratinocytes
5. Stratum Corneum
DESQUAMATION
? Is the migration of cells from the deepest layer of the epidermis (the stratum Basale) superficially to the thick keratinised plug of dead cells before being shed
? This transit time from the deepest layer to the stratum corneum is around 14 days, with the cells remaining on the thick keratinised plug for another 14 days before they are lost
? Thus, the total time from the basal layer to shedding of the skin cells is around 28 days
KERATINOCYTE
? These cells are produced within the Stratum Basale and migrate superficially. As this migration occurs, these cells undergo increased differentiation (e.g. loses its nucleus)
? These cells secrete keratin which are produced and secreted by keratin intermediate filaments in the cytoplasm of the cell
Alopecia
Hair loss, can be scarring or non-scarring (scar tissue does not have hair)
Hair pigmentation
Melanocytes in the cortex of a persons hair shaft cause colour. Hair is only actively pigmented in the anagen phase.
MELANOCYTE
are located in the stratum basale, dermis and in hair follicles. synthesis melanin, and is contained within structures known as melanosomes and which are transferred to keratinocytes via dendritic processes. function of this melanin is to screen out harmful UV radiation and to give pigmentation to skin
Langerhan cells
cells have long dendritic processes which radiate throughout the epidermis. function as antigen presenting cells and are able to migrate through the epidermis and dermis into lymph nodes.
Merkel cells
are located in the stratum basale in areas of thick skin. function as sensory mechanoreceptors, and thus are closely associated with free nerve endings . these cells which facilitate fine touch.
Dermis
deep to the epidermis. made up of a tough, supportive connective tissue matrix. made up of collagen and some elastase tissue. The two layers are papillary(upper thin) and reticular (lower thicker). Cells found in the dermis include fibroblasts, macrophages, mast cells and lymphocytes.
Hypodermis
Layer deep to the dermis, made up of subcutaneous and adipose tissues which effectively insulates the body and provides mobility to the skin.
name all parts
Name all parts
impetigo possible causes and pathogens.
Spreads person to person contact
1. Bullous
- Is a thin walled blister that is full of clear yellow fluid which rupture rapidly leaving exudative
- Is typically caused by Staph Aureus
2. Crusted or Non-Bullous
- Presents with multiple crusts and erosions at one site : face
- May also present as pustular satellite lesions that have a red base and yellow gold crust that is adherent
- Is typically caused by Staphylococcal or Streptococcal bacteria
3. Ulcerated lesions
- Usually caused by Strep Pyogenes
Impetigo
folliculitis causes and pathogens.
characterised by inflamed hair follicles
Signs and symptoms of folliculitis is a tender red papule that is often associated with a surface pustule centred on a hair follicle
CAUSES
1. Infection
- Bacteria that commonly cause it include Staph aureus and Pseudomonas Augerginosa
- Yeasts that cause it include Pityrosporum ovale
- Fungal causes include Tinea capitis from Microsporum canis
- Occlusion: greasy ointments
- Irritation: Waxing, plucking
- Specific skin diseases: acne variants
boils possible causes and pathogens.
Is a deep form of folliculitis that develops from superficial folliculitis
caused by an acute pustular infection of a hair follicle by Staphylococcus Aureus
present ; Tender red nodule which enlarges
- Fever
- Enlarged draining lymph nodes
- People will typically present with
Folliculitis
Who is at risk of developing skin conditions
People who are at risk for developing furunculosis (like all infections) include diabetics, obese patients, malnourished patients, patients with poor skin hygiene and those who are otherwise immunocompromised (e.g. alcoholism)
Boil: deep folliculitis
paronychia: acute and causative pathogens
ACUTE PARONYCHIA
Is an infection of the paronychium (the area surrounding the nail bed) that can develop over a few hours and is typically caused by a Staph infection
Patients that present with acute paronychia will typically have nail folds which are painful, red and swollen (sometimes yellow pus will be evident under the cuticle)
Acute paronychia
paronychia: chronic and causative pathogens
Unlike the acute form of the disease, chronic paronychia is not caused by strep or staph
It presents over a period of weeks and months, and is common in individuals who have their hands wet all the time
It is caused by several different microorganisms (yeasts and bacteria) like candida species and negative bacilli
- It typically starts in one nail fold before spreading to the others
- Affected nails become swollen and are lifted off the nail plate
A key difference between acute and chronic paronychia is the differences in the nails themselves, in acute there is little change to the nails whereas chronic paronychia will show ridges and dystrophic nails
Chronic paronychia
Cellulitis
Nominate General treatment for cellulitis. Be able to give general reasons why it occurs and generalised treatment.
CELLULITIS – TREATMENT (need to know this)
Treatment of cellulitis should follow the following process;
1. Rest and elevation of the area
2. Analgesia
- Pain relief like Panadol
3. Oral or Intravenous antibiotics
- Cephalexin
- Flucloxacillin
- Penicillin
4. Address the original cause
INCLUDING
1. Lymphoedema
2. Tinea of the feet (Causes damage to the skin surface itself allowing the causative bacteria to enter)
3. Chronic dermatitis
4. Poor lower leg circulation (if venous circulation is bad there is a poor nutrient gradient)
5. Wounds
6. Herpes simplex infection
7. Dental caries
8. Chronic sinus infection
9. Chronic venous insufficiency
COMMON WART
- Most commonly arise on the backs of fingers or toes (particularly around the nails where they can distort nail growth) and on knees
- They start out as a smooth skin coloured papule and eventually enlarge into an irregular hyperkeratotic surface (that resembles cauliflower)
- They most commonly occur on the hands but can sometimes arise on the face and genitals
- Plane warts
- Typically occur on the dorsum of the hands, arms and face
- They normally have a flat surface and are skin coloured or pink
- Can be described as a smooth slightly elevated flat-topped papule
- When treating these warts, it is important that you don’t damage the nail bed and other surrounding structures
- Plantar warts (flat wart)
- Occur on the soles of the feet and are characterised by a rough surface that only slightly protrudes above the skin
- They also tend to have a surrounding horny collar
- When the surface is peeled back you tend to see oozing capillaries (which distinguish the wart from corns)
- Filiform warts
- Occur on the face
- Are characteristically long, stalk like warts that look like threads hanging down
- Anogenital warts
- Unlike the others, anogenital warts do cause an issue
- They are papillomatous cauliflower lesions that occur on moist, macerated vascular surfaces
- They can coalesce together to form large lesions
- They also pose a risk of developing into cancer
- These are considered an STI in adults
- It is also important to consider sexual abuse if apparent on children
MOLLUSCUM CONTAGIOSUM
Is a viral skin infection that results in round, firm, painless bumps caused by the Poxvirus
Is a common viral skin infection seen in clinical practice that has two peak periods;
- Children (3 – 9 years of age)
- Young adults (20 – 25 years
The viral infection itself is spread from person to person via direct skin contact (especially in children)
Sexual transmission is possible in adults
- Patients will have clusters of small papules in warm moist areas like the armpit, groin or behind the knee
- They range in size from 1mm – 6mm
- They have a waxy, pinkish look with a white central pit (umbilicated pit) (can be white, pink or brown)
- When they resolve they make become inflamed, crusted or scabby
- They can persist for months (usually 6 to 12 months) or even years
Recount the skin manifestations of herpes simplex virus.
Is the virus that causes cold sores and genital herpes
There are 2 main types of herpes simplex virus (HSV). Type 1 and Type 2
1. Type 1
- Is mainly associated with facial infections and extra genital
- Is common in children and lasts around 2 weeks
- Commonly causes acute gingivostomatitis which is accompanied by malaise, fever, headache and enlarged cervical glands
2. Type 2
- Is mainly associated with genital infections (herpes)
- Is typically sexually acquired
- Causes multiple genital and peri-anal vesicles that rapidly ulcerate
Varcilla
caused by the varicella-zoster virus
It is spread by one of two ways;
1. Inhalation of airborne respiratory droplets from an infected
2. Direct contact with the fluid from the vesicles
It has an incubation time of about 14 days
In terms of the clinical presentation, the following is true;
- Prodromal symptoms: Like high fever, headache, cold like symptoms, vomiting and diarrhoea for 1 – 2 days
- Rash: They will then develop a rash on the trunk that spreads to the face and extremities
- Papules: The lesions will begin as 2 – 4mm red papules before eventually turning into vesicles
- Vesicle: The vesicle will rapidly form a pustule, which will burst (in 8 – 12 hours) and crust over leaving an eroded red base
- New lesions stop appearing after 4 days and crusts fall off within 7 days
- The vesicles are very itchy and uncomfortable
complications are outlined below;
1. Secondary bacterial infection of skin lesions from scratching
2. Dehydration from vomiting and diarrhoea
3. Viral pneumonia
4. Scarring
5. Disseminated primary varicella infection (high morbidity in immunosuppressed)
6. Infection of a pregnant women
MEASLES
measles virus
It has an incubation period of 7 – 14 days
Transmission of the measles virus is facilitated by respiratory droplets from infected persons coughing or sneezing
In terms of the clinical presentation of the disease,
- Initially patients will symptoms typical to an Upper Respiratory Tract Infection with fever, conjunctival irritation and sometimes photophobia
- 3 – 7 days after the onset of the initial symptoms there will be an erythematous macular rash on face
- 2 – 3 prior to the onset of the measle rash there will be Koplik spots on the buccal mucosa (small pinhead sized white spots)
- A non-pruritic rash (not itchy) will begin on the face and behind the ears, and after 24 – 36 hours it will spread to the entire body (lasts for 3 – 4 days)
- rash coincides with a high fever
- The rash will fade 3 – 4 days after it initially appeared (will fade to a purplish colour, then to brown and coppery with fine scales then to nothing)
complications the most common of which are outlined below;
1. Diarrhoea (can be fatal if dehydration occurs)
2. Otitis media (may lead to deafness, almost exclusively occurs in children)
3. Pneumonia (most common cause of death)
RUBELLA
Rubella is of little consequence, unless you are pregnant. Infection of a pregnant women: congenital rubella syndrome and can result in;
1. Miscarriage
2. Stillbirth
3. Major birth abnormalities
It has an incubation period of 12 – 23 days caused by the Rubella Virus
Transmission is facilitated by respiratory droplets from infected persons coughing or sneezing
An infected person is contagious from 7 days prior to the rash appearing and for 7 days after
In terms of the clinical presentation, the following is true;
- Patients may experience slight fever, sore throat, rhinorrhoea (runny nose) and malaise prior to the appearance of the rash
- The rash begins on the face, before spreading to the neck, trunk and extremities
- The may or may not be itchy and usually lasts about 5 days (pink or light red macules about 2 – 3mm in size)
- After the rash passes the skin may shed in flakes (known as desquamation) which assists diagnosis
Pavovirus
Is a common childhood infection that causes a characteristic slapped cheek appearance and rash
It is caused by Parvovirus B19
It rarely causes complications, with 30% of infected individuals presenting with no symptoms
In terms of the clinical progression, the following is true;
- They will first get firm red cheeks which feel burning hot
- This is followed 1 – 4 days later by a network patterned rash on their limbs and then trunk
- May have a slight headache or fever, but usually are quite well
- Usually the rash clears in a few days (some cases can last several weeks)
No treatment is required
ROSEOLA
spread through respiratory droplets from infected individuals
In many cases of roseola, the child appears well with few or no signs or symptoms at all
In terms of the clinical presentation, the following is true;
- High fever for 3- 5 days
- Upper respiratory symptoms like sore throat, cough, runny nose and congestion
- Irritability and tiredness
- A rash appears between days 3 and 5 as the fever stops
- The rash starts on the trunk and can spread to the entire body
- It can be described as a small pink / red maculo-papular rash (2 – 5mm) that blanches (turns white) when touched
- Some macules may be surrounded by a halo of pale skin
- The rash in non-itchy, painless and doesn’t blister
- Can fade in a few hours or persist for as long as 2 – 3 days
No treatment is required
ENTEROVIRUS INFECTIONS
Is commonly referred to as Hand, food and mouth disease
It is a common, highly infectious condition that is caused by the Coxsackie virus A16
It is mild and short lasting and commonly affects children under 5
It has an incubation period of 4 to 6 days
Its clinical progression is as follows;
- Small erosions around 3 – 6mm in size will appear in the oral cavity (can sometimes be painful)
- Patients may have a mild fever
- Within 24 hours of the oral lesions, 66% of cases will develop cutaneous lesions which appear as red macules that evolve into cloudy vesicles around 4 – 7 mm in size (surrounded by an erythematous areola)
- These typically are distributed over palms, soles, dorsal fingers and dorsal toes
- They spontaneously resolve within 10 days (without any crusting or scarring)
HERPES SIMPLEX
Is the virus that causes cold sores and genital herpes
The Herpes Simplex Virus can be spread by the following means;
- Respiratory droplets
- Direct contact with an infection lesion
- Direct contact with infected body fluids
Once transferred, HSV enters the host through abraded skin or through intact mucous membranes
Initially it is the epithelial cells that are targeted by the virus, however as a result of retrograde transport through neural tissue (adjacent to the epithelial cells) into sensory ganglia leads, infected persons often experience lifelong latent infection
T1 and T2
Is a viral disease resulting from the reactivation of the varicella virus
It is typically localised to one or two dermatomes
As is mentioned above, the pathophysiology of the disease is caused by the reactivation of the varicella virus that has lay dormant in its resting phase within a few anterior horn cells of the spinal cord. This reactivation allows it to grow down the nerves to the skin, resulting in shingles
We do not know what causes this reactivation, but we know it is more common in the immunocompromised
Types of tinea
- Tinea barbae (beard)
- Tinea capitis (head)
- Tinea corporis (body)
- Tinea faciei (face)
- Tinea manuum (hand)
- Tinea pedis (foot)
- Tinea unguium (nail)
- Tinea Capitus (scalp)
- Is usually much more subtle, and has no signs of inflammation
- The only sign may be scaling with or without hair loss
- Patches of hair loss in a young person should indicate tinea capitus (if there is no other obvious trauma)
- Differential diagnosis: Psoriasis
- Tinea Corporis (body)
- Asymmetrical presentation
- Is an annular type of lesion with an active edge
- Edge can be raised with a possible pustule
- Will be scaly along the edges
- Will be slowly progressing over weeks and weeks
- Areas of central clearing
- The only manifestation in darker skin may be silvery scale
- Differential diagnosis: Crusted scabies, Leprosy, Systemic Lupus Erythematosus
Know the importance and aietology of Pyoderma and its complications and why it occurs in ATI populations
Is any skin infection that is pyogenic (has pus) caused by some sort of bacteria
This includes superficial bacterial infections like impetigo, ecthyma, folliculitis, furuncle, carbuncle and tropical ulcers
Skin sores are endemic amongst Aboriginal children in Australians northern tropical regions, and are most commonly caused by Group A Streptococcus (GAS)
(worse in the dry season as they experience more minor trauma that allows GAS to penetrate)
Whilst the initial infections can be dealt with, infection by Group A Streptococcus is linked to a number of very serious conditions including;
1. Acute Rheumatic Fever
2. Rheumatic Heart Disease
3. Acute Post Streptococcal Glomerulonephritis
Therefore, if we can reduce GAS infections, we can improve their long-term health
Scabies is also an extremely important cause of these pyoderma skin sore infections
- Oral antibiotics
- Intramuscular Injection of antibiotics
- Topical methods
SCABIES
Is a condition caused by adult mites which burrow through the stratum corneum
Mites are transferred by body to body contacts (cannot live outside of a host for long at all)
Each day, a mite will lay 2-3 eggs a day which take about 2-3 weeks to mature
Scabies results in a generalised erythematous pruritic rash that is caused by an allergic reaction to the faeces and eggs produced by the scabies (not from the burrowing)
The clinical presentation characteristics are outlined below;
- Takes about 4 – 6 weeks for the itch and rash to develop
- The itch is worse at night
- The rash typically presents on the trunk
- Burrows are grey-white slightly scaly tortuous lines up to 1cm long (are often easily missed)
- In Adults: They like between fingers, in finger webbing, the sides of hands and the flexural aspects of the wrists. They also like elbows, ankles, feet, nipples and genitals. They very rarely occur on the face
- In Children: The palms of hands and the soles of feet (not in adults as skin is too thick), and can often occur on the face and neck
Diagnosis of scabies is quite difficult. Confirmation is made with a scrapping under microscopy from a burrow.
1. Scabicide / Permethrin 5% creme - Is first line (due to its efficiency and safety)
- This should be applied from the neck down and left for 8 hours and repeated in a weeks’ time (in case some scabies edge hatch later on)
- Every time you wash your hands the crème should reapplied (if not treatment will fail)
2. Benzyl Benzoate 25% - Is a second choice as it is more irritating then permethrin
- Leave on for 24 hours and repeat in a week
Know Head lice and body lice with treatments
- Head Lice
- Body Lice (Lives on your clothes not your body)
- Pubic Lice (Widest claws)
The main features of all of them are severe itching, following by scratching and eventually a secondary infection
They reproduce by attaching eggs to hairs and clothing, which are small white structures known as nits
HEAD LICE INFESTATION
Head lice infestation are very common and occur in over 10% of children
The peak age of incidence is between 4 – 11 years of age and is typically more common in females
It is spread by person to person head contact (lice cannot fly)
In terms of the clinical presentation, the following is typical of a head lice infestation;
- Itching (may develop over months) caused by a delayed hypercreativity reaction
- Nits
- May see excoriations or local lymphadenopathy
Head lice infestation may result in a secondary bacterial infection
When attempting to diagnose a head lice infestation, apply conditioner (stuns the lice for 20minutes) and wet comb the hair, you should then wipe the comb on paper towel to identify nits and lice
Nits more then 1.5cm away from the skin are unlikely to contain live larvae and instead show an old infestation
Treatment involves repeating the same process described above daily, until there are no more lice (the conditioner suffocates the lice and the combing physically removes the lice). After the nits are gone, the same process should be repeated weekly for several weeks to detect any reoccurrence
Malathion and permethrin preparations are developing resistance. Regardless daily wet combing is still required
Prevention of head lice infestation includes;
- Wash clothes and brushes in hot water
- Don’t share towels
BODY LICE INFESTATION
Infestation by body lice is uncommon except in extreme circumstances of severe poverty poor hygiene (e.g. war, famine)
Basic Mosquito and flea bites presentation
When an insect bites, they often inject a chemical (like an anticoagulant or venom) that causes a painful inflammatory and sometimes allergic reaction
Different people respond differently depending on their own immunological reaction
Continued biting will develop red pruritic papules after 1 – 4 days (can last up to 2 weeks)
Bullous reactions are also common on the legs of children
There is something known as popular urticarial, which is an allergic reaction to bites (more common in children and new visitors who are desensitized)
ACUTE SYSTEMIC LUPUS ERYTHEMATOSUS
Is the most serious type of Lupus Erythematosus that is often fatal in remote aboriginal communities
It effects multiple organ systems and has a high mortality
The clinical features of Acute Systemic Lupus Erythematosus are outlined below;
- Presents typically with a characteristic butterfly rash on the patients’ cheeks, nose and forehead (can sometimes effect the lips, scalp and trunk)
- Hypopigmentation (patches of lighter skin) and scarring
- Erythema on the edge of the hyperpigmented lesion
- There is often lower lip involvement (friable and swollen)
Lupus is aggravated by sunlight
Patients with this disease are at risk of the following complications;
1. SCC development on the areas of hypopigmentation (lips and scarring) as they have lost their natural protection
2. Renal disease
3. Increase risk of infection (which can be fatal)
4. Permanent scarring and discoloration
5. Serious risk to newborn if mother is not treated
Treatment of Acute Systemic Lupus Erythematosus is through sun avoidance, potent topical corticosteroids and systemic immunosuppressive medications
SUBACUTE LUPUS ERYTHEMATOSUS
Is characterised by a non-itchy, dry, well marginated plaque on the upper back and chest that often arises following sun exposure
It is uncommon for this type of lupus to involve significant internal systemic disease
The lesions of this type of lupus can shows the following characteristics;
- Annular or polycyclic (meaning ring shaped)
- Papulosquamous (scaly bumps)
- Vasculitis (purple spots)
- Nodular (lumps)
- Well marginated
- Symmetrical
DISCOID LUPUS ERYTHEMATOSUS
Is the most common form of lupus
It is characterised by unsightly red scaly plaques that develop in areas of sun exposure
Discoid LE predominately effects the cheeks, nose and ears (but can also involve the upper back, V of neck and the backs of hands)
Discoid LE can be localised or widespread, and eventually results in post inflammatory pigmentation and hypopigmented scars
Treatment is with potential topical corticosteroid cream
Is a cause of form of scarring alopecia (hair loss)
Acanthosis Nigricans: INSULIN RESISTANCE DIABETES
There has been a large increase in insulin resistant diabetes in the aboriginal population that is associated with poorer health outcomes
Some important causative factors behind this increase is the social disadvantage they face, the limited economic opportunity they have, the poor-quality diet they eat and rapid weight gain
Insulin resistance results can commonly result in; Blindness, Renal disease and Cardiovascular mortality
Insulin resistance diabetes has a number of important clinical presentations including;
1. Acanthosis Nigricans
- Is a pigmentation and thickening of the skin on the back of the neck, armpit and groin (skin folds)
- It is commonly associated with insulin resistance or diabetes (it is a cutaneous sign of underlying disease)
- Is often the first presentation of insulin resistance (does not necessarily mean they have diabetes)
- It is also associated with an increased risk of cancer
Aware of the possible different perceptions of causes of skin diseases by Aboriginal and Torres Strait Islander People
- Genetic and Racial differences
- Indigenous Australians are more likely to experience keloid scarring (excessive scarring) after trauma
- Because of the darker pigmented / black skin, common skin conditions like atopic dermatitis (eczema) or psoriasis can be quite difficult to diagnose - Geographic
- Whether they live in Cities, rurally or in remote areas - Socioeconomic
- Indigenous Australians typically live in lower socioeconomic places meaning access to health care and living conditions are not ideal - Language, education and hearing
- English is often not their first language
- Education levels are typically lower
- Recurrent ear infections in children can often cause hearing deficits meaning people simple cannot hear what you are saying - Social factors
- A long history of conflict between our indigenous population and the rest of the community has led to distrust forming between Indigenous Australians and non-indigenous doctors, or figures of authority
Aware of the possible different perceptions of causes of skin diseases by Aboriginal and Torres Strait Islander People
- Genetic and Racial differences
- Indigenous Australians are more likely to experience keloid scarring (excessive scarring) after trauma
- Because of the darker pigmented / black skin, common skin conditions like atopic dermatitis (eczema) or psoriasis can be quite difficult to diagnose - Geographic
- Whether they live in Cities, rurally or in remote areas - Socioeconomic
- Indigenous Australians typically live in lower socioeconomic places meaning access to health care and living conditions are not ideal - Language, education and hearing
- English is often not their first language
- Education levels are typically lower
- Recurrent ear infections in children can often cause hearing deficits meaning people simple cannot hear what you are saying - Social factors
- A long history of conflict between our indigenous population and the rest of the community has led to distrust forming between Indigenous Australians and non-indigenous doctors, or figures of authority
Identify the different variants of endogenous eczema.
- Atopic Dermatitis
- Seborrheic Dermatosis
- Asteatotic Dermatitis
- Discoid Dermatitis (also known as nummular dermatitis)
- Stasis Dermatitis (also known as gravitational dermatitis)
- Pompholyx (dyshidrotic dermatitis)
- Otitis Externae
- Is a mixed form of endogenous and exogenous dermatitis
- Is inflammation of the ear canal itself
- Can be caused by endogenous causes (wet ear and bacteria) or seborrheic dermatitis or psoriasis etc.
- Explored more in ENT lectures
Name the diseases that may occur in a patient with atopic eczema.
It is the most common form of dermatitis, and usually occurs in people who have what is known as an atopic tendency, which is a tendency to develop allergic diseases like allergic rhinitis (hay fever), asthma and obviously atopic dermatitis
Identify the immunological abnormalities found in atopic eczema.
- Immune dysregulation
- 80% of patients have increased serum levels of IgE
- It is important to note that the increased IgE is not the cause of the dermatitis, it is a response to the factors which are causing the dermatitis (treating IgE will not treat atopic dermatitis)
Recall the level of the prevalence of atopic eczema in the Australian population.
Atopic dermatitis affects 15 – 20% of children, But only 1 – 2% of adults
The typical age of onset is between 4 months and 2 years of age (can manifest in older people for the first time)
.
ATOPIC DERMATITIS
CAUSE: environmental factors or allergens – such as cold and dry weather, dampness, and more specific things such as house dust mites, pet fur, pollen and moulds.
- Severe itching
- A patchy, erythematous, poorly defined rash (usually in the popliteal and cubital fossa and face, but can happen anywhere on the skin)
- Xeroderma (dry skin)
- Excoriation
- Lichenification
- Crusting (scabbing) and weeping (loss of fluid through the surface of the skin) due to bacterial infection
SEBORRHEIC DERMATITIS – INFANTILE
Usually starts in the first few weeks and continues until around 6 months of age
It is thought to be due to overactive sebaceous glands in the skin of newborn babies as a result of the mothers’ hormones in the baby’s circulation. These glands release a greasy substance that makes old skin cells attach to the top of the scalp as they dry and fall off (known as cradle cap)
Babies will present with an erythematous, non-itchy, well defined rash that is covered in greasy scale over the face, scalp, neck, axillae and nappy area
1/3 of cases are self-limiting and resolve in weeks
Whilst psoriasis and atopic dermatitis can present similarly, they tend to develop a more typical rash over months
A super-infection by Staphylococcus Aureus and Candida albicans is common and will result in weeping and crusting
.
SEBORRHEIC DERMATITIS – ADULT
Usually appears at any age after puberty
It fluctuates in severity and can persist for years
It is exacerbated by emotional and physical stress
It is typically involves the scalp, within the eyebrows, on the edges of eyelids, inside and behind the ears and in the creases behind the nose. It also can involve the chest, flexures and the genital areas
Adult seborrheic dermatitis presents as an erythematous, well defined, fine greasy scale that is well defined on the cheeks, nose and nasolabial folds
- Ille defined dry pink or skin coloured patches
- Yellowish or white bran-like scale
- Can spread to the entire scalp
When it affects the skin folds of the armpits and groin
NUMMULAR DERMATITIS (DISCOID)
The term nummular refers to small round discs, thus nummular dermatitis is characterised by lesions that are;
- Very itchy
- Round plaques
- Have a dry cracked surface
- A very well-defined edge
- They can be between 2mm and 7cm in diameters
- Patches are pink, red or brown
Nummular dermatitis can affect any part of the body, but usually affect the lower leg
Patches can persist for weeks and months
Because these lesions are so itchy, Licehnification often occurs very rapidly
ASTEATOTIC DERMATITIS
Is a very common type of dermatitis that is made worse in winter and by hot showers (remove your natural oils)
It is characterised by a cracked or paving stone like appearance
The most common site is the shins, but also occur on the upper limbs and trunk
Mild cases often go unnoticed, but it can become extremely itchy which often makes it much worse
Its distinctive diamond shaped plates of skin are separated by red bands
Managed: moderate use of hot showers and corticosteroid ointment if needed
STASIS (GRAVITIONAL) DERMATITIS
Is seen in patients with venous insufficiency, who are typically middle aged and older adults
Patients often have varicose veins or Deep Venous Thrombosis (DVT)
The specific clinical signs are outlined below;
- Dry, thick scale and brown hyperpigmentation (as a result of diapedesis of red blood cells into the dermis) on their lower legs and ankles
- Can be on one side as it is caused by venous insufficiency which can be unilateral
- Affected skin is red and scaly and may ooze, crust and crack
- Often associated with venous ulceration
- Affected legs can be swollen and with marked erythema, cellulitis and ‘woody’ oedema
- It is frequently very itchy
POMPHOLYX DERMATITIS
Also known as Dyshidrotic dermatitis, is a type of dermatitis that affects the palms, sides of fingers and the soles of feet
Presents as a vesicular bullous dermatitis
The clinical presentation of pompholyx dermatitis is outlined below;
- The acute stage will present with tiny vesicles deep in the skin of the palms, fingers soles of feet or toes
- These vesicles are often very itchy or have a burning feeling
- These can be mild will only a small amount of peeling, or severe with big blisters and cracks
- The more chronic stages show more peeling, cracking or crusting
- The skin may heal in this time, and the blistering may start again
Severe forms around the nail folds may cause nail dystrophy (irregular ridges and chronic
Identify the precipitating factors in atopic eczema.
- Family history
- The most common are allergic rhinitis, asthma and atopic dermatitis - Immune dysregulation
- 80% of patients have increased serum levels of IgE
- It is important to note that the increased IgE is not the cause of the dermatitis, it is a response to the factors which are causing the dermatitis (treating IgE will not treat atopic dermatitis) - Abnormal epidermal barrier
deficiency in the gene that programs the epidermal protein filaggrin
- This results in an impaired skin barrier that holds water poorly and is more susceptible to irritants and allergens - Susceptibility to infection
- This is caused by a deficiency in a peptide known as defensin which is present in the epidermis
- This results in a reduced immune response to infectious agents - Environmental irritants
- As a result of their impaired epidermal barrier, patients tolerate certain common environmental conditions and substances poorly
- This includes things like soap, sand, woollen and synthetic fabrics and dust
- Many cases are made worse in hot conditions
- Most are improved in humid weather (as it helps hydrate the skin) - Allergy
- Although many patients have raised IgE to specific allergens, dermatitis is not considered to be an allergic disease
Nominate appropriate investigations for patients with atopic eczema.
IgE levels.
skin-prick testing.
patch testing.
skin biopsy.
plus either family history, symptoms in the flex areas.
How to use topical corticosteroids
TOPICAL CORTICOSTEROIDS
As a general rule, the thicker the skin, the more potent the steroid that should be used;
- Face, eyelids, genital, flexures: Hydrocortisone 1% crème (mild)
- Trunk and limbs: Betamethasone valerate 0.02% crème (medium)
- Palms, soles, elbows, knees: Bethamethasone dipropinate 0.01% (potent)
- Thick nodules of lichenification: Bethamethasone dipropinate 0.05% (very potent) or Clobetasol propionate 0.05% (super potent)
For severe cases, a potent topical steroid can be used for up to 2 weeks to achieve remission regardless of age (the potency can then be reduced)
Children normally use mild, but at times you will need stronger (e.g. acute flare ups of dermatitis for a week)
There are 3 types of steroid vehicles;
1. Creams
- Are water based and contain preservatives
- Patients love them as they are easy to spread and aren’t greasy
- Best used for acute dermatitis (moist)
2. Ointments
- Are oil based so very greasy
- Patients do not like them as they are harder to spread
3. Gels and Lotions
- Are alcohol based so may sting when they are applied
- Are commonly used for the scalp
Advise a patient about the risks and benefits of topical corticosteroids.
Some of these side effects and risks include;
- Has the potential to mask infection (particularly tinea)
- Irritation and stinging on application
- Atrophy of skin lead to striae (stretch marks) brushing and visible veins
- Erythema and telangiectasias
- Peri-oral dermatitis (inflammatory rash around the mouth)
- Glaucoma
Recognise common concerns of parents of children with atopic eczema.
- it is important to first explain that whilst the prognosis is good (most cases resolve), the condition is not curable
- You should then discuss lifestyle modifications to avoid exacerbating factors such as;
- Avoid wool and synthetics
- Avoid soaps and shampoos
- Avoid HOT baths
- Avoid cold windy weather as it exacerbates the condition - Understand the psychological issues
- It is a very stressful condition requiring constant time-consuming effort
- not transmissible
How to treat dermatitis
ATOPIC DERMATITIS – TREATMENT
1. it is important to first explain that whilst the prognosis is good (most cases resolve), the condition is not curable
2. You should then discuss lifestyle modifications to avoid exacerbating factors such as;
- Avoid wool and synthetics
- Avoid soaps and shampoos
- Avoid HOT baths
- Avoid cold windy weather as it exacerbates the condition
3. Patients should then be encouraged to use moisturises and bath additives
- Use emollients (any moisturiser) and bath oils (the greasier the better)
- E.g. 50% liquid paraffin and 50% white soft paraffin
- Patients should avoid perfumed emollients
- Warm daily bath helps remove scale and bacteria
4. A patient should be prescribed some topical anti-inflammatory agent
- Is the mainstay of treatment for atopic dermatitis
- Topical corticosteroids (TCS) are used most often however newer topical immunomodulators (TIMS) are also sometimes used but they are not as potent, efficient and are more expensive
5. Understand the use of anti-histamines
- Anti-histamines are used for allergic reactions
- Atopic dermatitis is not caused by the same reaction, meaning an anti-histamine will do anything (except sedate the child)
6. Wet dressings (soaked cotton balls under a dressing) over emollients should be used for acute flare ups to stop itching and nocturnal scratching
7. Discuss possible investigation and treatment of allergy (whilst it is not the cause of the disease, in very very rare cases it may be)
8. Understand the psychological issues
- It is a very stressful condition requiring constant time-consuming effort
- Many patients are fearful of treatment
If after a swab and M/C/S you find an underlying infection, an appropriate antibiotic should be prescribed e.g. Cephalexin against Staph infection
what is the fingerprint unit
FINGERTIP UNIT
One fingertip unit is enough to cover an area of skin twice the size of a flat adult hand with the fingers together
The quantity of cream in a fingertip unit varies with age;
1. Adult Male: 1 fingertip unit provides 0.5g
2. Adult Female: 1 fingertip unit provides 0.4g
The amount of cream that should be used varies with the body part;
- One hand: 1 fingertip unit
- One arm: 3 fingertip units
- One foot: 2 fingertip units
- One leg: 6 fingertip units
- Face and neck: 2.5 fingertip units
- Trunk, front and back: 14 fingertip units
- Entire body: about 40 units
CHRONIC PLAQUE PSORIASIS
Is the most common form of psoriasis (90% of cases)
It is a well-defined, raised, thick plaque with a salmon pink colour covered in a silvery white scale
It is most common on the elbows, knees and lower back
Woronoff’s ring and Auspitz sign (vascular bleeding under scale)
It is persistent and resistant to treatment
Scalp psoriosis
Is one or more scaly plaques in the scalp, most commonly on the back of the head (can affect multiple discrete sites)
It can occur in isolation or with any other form of psoriasis
It is characterised by thick silvery white scale on patches of very red skin
It may extend slightly beyond the hairline but face is sparred
Does not cause hair loss
GUTTATE PSORIASIS
Is characterised by numerous and often widespread small red macules/papules that appear suddenly all over the body (which rapidly become scaly)
PALMOPLANTAR PSORIASIS
Is psoriasis that presents on the palms of hands and the soles of feet
It is usually difficult to recognise as lesions are poorly demarcated and barely erythematous (as the skin is so thick)
It has characteristic scaling, redness and pustules (if you give them large doses of steroids and then suddenly stop them it causes these pustules)
It is often associated with keratoderma (thickening of the skin)
GENITAL PSORIASIS
Is usually well demarcated (unlike dermatitis) but doesn’t typically have the scale.
FLEXURAL PSORIASIS (Inverse)
Is characterised by smooth, well defined plaques that are deep red / salmon pink in colour within body folds
Due to the moist nature of the skin fold it tends not to have silvery scale, but instead is shiny and smooth
There may be a fissure in the depth of the skin crease
Common areas include;
- Armpits
- Groin
- Under breasts
- Buttock cleft
- Umbilicus
PUSTULAR PSORIASIS
Is characterised by scaling, red pustules less than 1cm in size on the palms and soles of the feet (but can involve the whole body)
Is very rare, but very serious
It is often triggered by withdrawal of systemic steroids (never treat psoriasis with systemic steroids)
NAIL PSORIASIS
1. Onycholysis
- Refers to when psoriatic nails become loose and separate from the nail bed
- In severe cases, the nail can crumble
2. Pitting
- is a sign of partial loss of cells from the surface of the nail plate
- It is due to psoriasis in the proximal nail matrix
3. Leukonychia
- Areas of white nail plate caused by parakeratosis in the body of the nail plate and is due to psoriasis of the mid-matrix
4. Oil drop / salmon patch
- Is a translucent yellow-red discolouration in the nail bed proximal to onycholysis
- It reflects inflammation and can be tender
5. Subungual hyperkeratosis
- Scaling under the nail due to excessive proliferation of keratinocytes in the nail bed and hyponychium
6. Ridges
- Due to intermittent inflammation which causes growth arrest followed by hyperproliferation in the proximal nail matrix
7. Psoriatic inflammation
- Causes nail plate crumbling
- Splinter haemorrhages
- Spotted lunula
erythoderma psoriosis
Is a very rare form of psoriasis that is characterised by skin that is universally and uniformly rede (with variable amounts of scaling)
Usually precipitated by systemic steroid withdrawal
Individuals often have a history of unstable psoriasis
It is associated with malaise, shivering and skin feels hot
Complications include thermoregulation (increased heat loss causing hypothermia) and haemodynamic (heart failure due to very high CO)
TINEA BARBAE
Is an infection of the beard and moustache areas with a dermatophyte fungus
It generally only affects adult men and is most commonly seen in agricultural settings in farmers who have direct contact with infected animals (it is rarely passed from one person to another)
The clinical presentation of tinea barbae is as follows;
- Very inflamed with red lumpy areas
- Pustules and crusting forms around hairs (known as a kerion)
- It is not excessively painful or itchy
Diagnosis is confirmed by microscopy and culture of skin scrapings and hair pulled out by the roots
TINEA FACIEI
Is an infection of face (not including the beard and moustache area) with a dermatophyte fungus
It is very uncommon (and is often misdiagnosed)
The clinical presentation is outlined below;
- It resembles ringworm
- Can be acute or chronic in its onset
- Tinea faciei has characteristic round red scaly patches (that are often less red and scaly in the middle or can even been healed in the middle)
TINEA PEDIS
Is an infection of the feet by a dermatophyte fungus
It is the most common type of fungal infection as it is extremely common at swimming pools, in showers and in occlusive foot wear
Tinea pedis has 3 common clinical features;
1. Soggy inter-digital scaling (particularly between the 4th and 5th toes)
2. A diffuse scaling of the soles
TINEA UNGUIUM
Tinea unguium becomes increasingly common with age (it is rarely seen in children)
It can result in complete destruction of the nail, and is often caused by untreated tinea pedis or tinea manuum
Tinea unguium may affect one or more toenails and / or fingernails. It most commonly involves the great toenail or little toenail
In terms of its clinical presentation, tinea unguium can present in several different patterns;
1. Lateral onychomycosis: a white or yellow opaque streak at one side of the nail
2. Subungual hyperkeratosis: scaling occurs under the nail
3. Distal onycholysis: The end of the nail lifts up, and then the free edge typically crumbles
4. Superficial white onychomycosis: Flaky white patches and pits appear on the top of the nail plate
5. Proximal onychomycosis: yellow spots appear in the lunula (half-moon thingo)
FUNGAL FOLLICULITIS
Most common is follicular eruptions from Malassezia
Clinical features:
- Pustular eruption
- Most often on the back
Diagnosis via fungal M/C
- Bacterial culture is negative and thus doesn’t respond to antibiotics
Management includes tropical antifungals but if ineffective oral fluconazole
CUTANEOUS CANDIDIASIS
Candida albicans and species are normal commensals of mouth, vaginal tract & lower GIT
Predisposing factors include warm wet occlusive conditions, macerated skin, immunosuppression (diabetes, drugs, infancy, pregnancy) and fungal folliculitis
Clinical features:
- Red macerated areas with glistering surface and scaling along an advancing border
- Satellite pustules beyond the main border are important
Diagnosis is via fungal M/C
Management includes topical treatment, get inflammation under control, use oral fluconazole if topical treatment failed and address predisposing factors
Recognise the cutaneous changes that may occur in diabetic patients.
- Necrobiosis Lipoidica
- Is fairly uncommon, only 3% of diabetics experience this
- Usually appears on the front of their shins, ulcerates
- These early plaques are violaceous in colour (violet), but atrophy to become brown-red or slightly yellow - Diabetic Dermopathy
- Occurs in 50% of Type 1 diabetics
- Presents as multiple small brownish scars on skin (mostly the shin)
- Requires no treatment - Granuloma Annulare
- Is a skin coloured, slightly pink annular lesion
- It is very common
- The cause of is unknown
- It is only associated with diabetes if there are multiple lesions - Candida infections
- Staphylococcal infection
- Vitiligo
- Is acquired circumscribed depigmentation
- It is caused by complete loss of melanocytes (skin is otherwise normal)
- Is an autoimmune disease
- It is hard to treat, areas of depigmentation are at increased risk of skin cancer (no protective melanocytes) - Eruptive Xanthomas
- Crops of yellow papules with erythematous base in poorly controlled T2D - Neuropathic Foot ulcers
- Acrochordonas (skin tags)
- Pedunculated outgrowths of normal skin on a narrow stalk
- Sign of hyperinsulinemia - Acanthosis Nigricans
- Hyperpigmented, velvety thickening of the skin folds
List the cutaneous changes that may occur in patients with cardiac disease.
CARDIAC DISEASE
- Peripheral and central cyanosis
- Erythema (due to compensatory polycythaemia)
- Finger clubbing
- Splinter haemorrhages (in nail bed)
- Roth Spots (conjunctiva)
- Osler’s nodes (hands)
- Janeway lesions (palms)
- Septic Embolic
These signs are very rare, and do not always indicate endocarditis
Recognise the skin signs of dermatomyositis.
- Dermatomyositis
- Is an acquired inflammatory muscle disease marked by muscle weakness and skin rash
- The cause is unknown, it is probably autoimmune
- Over 30% of adults who have this condition have an underlying malignancy e.g. lung, breast, gastric, ovarian and uterine cancers
- Patients will present with faint Lilac discolouration around the eyes (Heliotrope rash)
- They will have malar erythema (similar to the butterfly rash)
- They will have lilac, slightly atrophic papules over the knuckles
- They will experience photosensitivity
- Their nail cuticles will be ragged
- They will have proximal myopathy (really weak, they will have trouble getting out of chairs etc.)
- Dysphagia and weight loss
HIRSUTISM
Is the term used for increased male pattern hair growth in women
It is a very common condition that is nearly always genetic in origin
Some common hair growths include a moustache and beard, midline of chest or hair growth that is more thick on the limbs
Obviously, what is considered normal is dependent on cultural and race factors
BULLOUS PEMPHIGOID
Is a rare autoimmune skin condition that causes large, fluid filled blisters
It is caused by Ig antibodies targeting the basement membrane causing the separation of the epidermis and the dermis
Patients present with the following clinical features;
- Nonspecific dermatitis or urticarial rash that may remain for months (prior to the bullae beginning)
- Bullae are filled, tense and pruritic
- Have no mucosal involvement
- Nilolsky sign is negative (a positive sign is when you pull skin and it tears away)
Diagnosis is achieved by a skin biopsy and direct immunofluorescence
Treatment involves a potent topical steroid or oral steroids
Describe erythema multiforme (EM).
ERYTHEMA MULTIFORME
Is not usually life-threatening although it can be very severe
It is not a systemic disease and affects only the skin and mucous membranes
Erythema multiforme is characterised by target lesions that are raised, round papules with a darker dusky or blistered centre, surrounded by a pale oedematous ring with a red edge
Lesions are relatively small (up to 3cm in diameter) and occur in crops
The lesions do not migrate (distinguishing them from urticaria)
They last 1 – 2 weeks before resolving
There are 2 types; Erythema Multiforme Minor and Erythema Multiforme Major;
1. EM Minor
- is usually the result of infection with herpes simplex virus and occasionally drugs
- Occur mainly on the extremities with no mucosal involvement
- Only usually 1, 2 or 3 lesions
2. EM Major
- Is usually the result of infection with herpes simplex virus (HSV1 and 2) and Mycoplasma Pneumonia
- It involves mucosal surfaces and large areas of skin
- Can cause erosions and can ulcerate which can be severe and painful
Whilst it can cause significant morbidity it is not life threatening
BOWEN’S DISEASE
Is a form of SCC that is confined to the epidermis, with no invasion into the dermis
They are caused by excessive UV exposure, if there are multiple, they can also be caused by arsenic, radiation or a genetic disorder
They typically present as a single, well defined, erythematous and scaly plaque in sun exposed areas (poorly defined borders, no thick adherent scale and no bilateral distribution like we see in psoriasis)
Diagnosis is made histology, which shows dysplasia in all layers of the epidermis
Treatment is by similar means to BCC
10% will develop into SCC if untreated, they are a slow progressive disease
Differential diagnosis include;
- Early invasive SCC
- Psoriasis
- Dermatitis
- Discoid Lupus Erythematosus
- Tinea Corpis
- Superficial BCC
- Seborrheic keratosis
- Actinic keratosis
SQUAMOUS CELL CARCINOMA
Is the second most common form of skin malignancy after BCC
These can be invasive or non-invasive (Intra-epithelial squamous cell carcinoma)
Unlike BCCs, these have the ability to metastasise. Factors which increase the risk of metastasis include;
- Immunocompromised patients
- SCC on the head and neck, lips, ears and scalp
- Large and/or poor tumour differentiation
They most commonly occur in patients over 40 and with fair skin, in areas of high sun exposure
The incidence of SCC is increasing 4 x faster than BCC due to increased life expectancy and immunosuppression
The clinical presentation of Squamous Cell Carcinomas are highly variable. Some typical clinical features include;
- Any new, enlarging nodule that appears on sun damaged skin
- Firm papule which can be tender and can increase in size
- Crusted surface (that is adherent and difficult to remove)
- Rolled edge and ulceration may develop in an advanced lesion
- No pearly ends or telangiectasia
- Recurrent bleeding from a lesion
Development of Squamous Cell Carcinoma can be caused by 3 different factors;
1. Sun damage
- The vast majority of SCCs are sun induced and develop from actinic damage
- Risk of developing SCCs correlates directly with increased cumulative, life time sun exposure
2. Viral transformation
- Some cases of SCC can be caused by HPV which causes viral transformation of warts
- Immunosuppressed patients are of increased risk of developing SCCs (especially from warts on chronically sun damaged skin)
3. Rare causes
- Radiation sites
- Chronic ulcers, badly burnt skin, cutaneous lupus
- Chronic Arsenic ingestion
NODULAR BCC
Is the most common type of Basal Cell Carcinoma
It most commonly occurs on the face
A nodular BCC has the following classic signs;
- Shiny or pearly rolled edge
- Blood vessels cross its surface (telangiectasia)
- Red / translucent papule or nodule
- Can have a central depression or ulcer
BCC are slow growing (months or years before they cause any real damage)
Differential diagnosis of nodular BCC include;
1. Dermal naevus
2. Keratoacanthoma
3. Pyogenic granuloma
4. Dermatofibroma
There are often multiple, and commonly occur on the trunk and shoulders
A superficial BCC has the following classic signs;
- Flat pink macules / patches
- May have a fine scale
- Under magnification they may have a thin pearly rim around the edge
- Micro-erosions
- Bleed and ulcerate easily
These are slow growing over months or years. They don’t tend to metastasis
Differential diagnosis of superficial BCCs include;
1. Solar keratosis
2. Intraepidermal squamous cell carcinoma (IESCC)
3. Psoriasis
4. Mycosis fungoides
5. Dermatitis
ULCERATIVE BCC
Typically appear as ulcers that are translucent and pearly
They can have a crust or rolled edge
The crust usually separates with gentle pressure
Differential diagnosis for Ulcerative BCCs include;
1. SCC stasis ulcer
2. Melanoma
3. Venous ulcer
4. Extra-genital primary chancre of syphilis
MORPHOEIC BCC
Are also known as sclerosing BCC (as they are sclerotic or scar-like)
They are usually found in mid-facial sites
They clinically present showing;
- Plaque of flat and indurated tissue
- Skin coloured, waxy scar like lesion
- Ill-defined borders
These are prone to recur after treatment as they can infiltrate cutaneous nerves (perineural spread)
Differential diagnosis for this type is a scar
PIGMENTED BCC
Present as papules, nodules or plaques with a foci of pigment
They are a brown, blue or greyish lesion and have smooth glistening surface
They are raised and firm
May resemble melanoma
Differential diagnosis of pigmented BCCs include;
1. Benign Naevus
2. Superficial spreading Melanoma
3. Nodular Melanoma
4. Seborrheic Keratosis
RECURRENT BCC
Is a BCC that has been previously treated but has re-emerged
These occur after previous surgery or treatment
They appear like scars, lumps or ulcers
They often require aggressive surgical intervention e.g. Moh’s Surgery or radiotherapy
KERATOACANTHOMA
Is a well differentiated type of Squamous Cell Carcinoma which resolves spontaneously after three or so months
Keratoacanthomas typically have a volcano shape with a central keratotic plug
They usually start at a site of sun damaged skin, and appear initially as a small papule or boil
These typically develop very quickly
Because it is not always easy to differentiate a keratoacanthoma from a non-resolving SCC (on clinical or histological grounds) they should be treated the same as any other SCC
SUPERFICIAL SPREADING MELANOMA
Is the most common, accounts for 70% of all melanomas. Is a radial growth melanoma
It occurs at a young age (median age of 40)
Superficial spreading Melanoma typically present as a flat, pigmented, asymmetrically macule that is changing in size, shape or colour
They occur on intermittently exposed areas of the body like the trunk and limbs
Risk factors for this type include;
- Intermittent high sun exposure
- Previous melanoma
- Multiple severe sunburns
- Family history
- Fair complexion
- People with multiple moles or dysplastic naevus syndrome
LENTIGOMALIGNA MELANOMA
Account for 10 – 15% of melanomas in Australia, and most commonly affect the elderly (median age is 60 – 70 years old)
Is a radial growth melanoma
Requires a large total dose of sun (why it occurs in the elderly)
Clinical features of this type include;
- Found in sun exposed areas like the head and neck
- Unevenly pigmented, asymmetric facial freckly that is changing in size, shape and colour
- Can remain non-invasive for years in its in-situ phase called lentigomaligna
ACRALLENTIGINOUS MELANOMA
Account for 3% of melanomas
This type is not sun related (as there is the same incidence in light and dark skin races)
This type typically affects the soles of the feet, palms of the hands, toes and fingers, as well as the nail apparatus
If in the nails, it shows a lineal pigmentation pattern which does not clear
On the palms or soles it resembles other radial growth phase melanomas
NODULAR MELANOMAS
Accounts for 15% of melanomas and is most common in older men
Is a vertical growth phase melanoma meaning it metastasises very quickly
Nodular melanomas exist between Superficial and Lentigo melanomas in terms of its relationship to intermittent verses cumulative sun exposure
Incidence of this type is more strongly related to the presence of numerous moles at other sites on the body
The clinical features of this type includes;
- Vertical growth phase melanoma
- Grows rapidly in depth
There is only a small window of opportunity for detection prior to metastasis
DYSPLASTIC NAEVI
Present clinically and histological as intermediates between normal naevi and melanoma
They form a spectrum that begins with normal naevi and finishes with severely dysplastic naevi that merge easily into early melanoma
Clinically they show at least 3 of the following 5 features;
1. Ill-defined border
2. Uneven distribution of pigment
3. Irregular border
4. Diameter > 5mm
5. Erythema
Histologically they show architectural atypia of melanocytes, but only carry a small risk of transformation to melanoma (1 in 1000) and therefore do not warrant excision unless they are suspicious for melanoma
Only severely dysplastic naevi require excision
Individuals with 5 dysplastic naevi are regarded as significantly elevated risk and people with 10 or more are at high risk
COMMON ACQUIRED MELANOCYTIC NAEVI
Also known as moles
They are benign tumours of melanocytes and are completely normal
The average number found on the skin of Australians is close to 100 (>2mm in diameter)
An increased number of naevi is an important risk factor for the development of superficial spreading melanoma (the most common type)
They are typically even in colour and shape, appear in childhood and evolve slowly
New and changing moles are normal in childhood, teenage years and during pregnancy
Classification of these common acquired melanocytic naevi is done according to the presence of epidermal and dermal components;
1. Junctional naevi (left)
- Have an epidermal component only
- Are generally flat and brown in colour
2. Intradermal naevi (right)
- Located in the dermis
- Are raised and not pigmented
3. Compound naevi (middle)
- Is a mixture of junctional and intradermal proliferation
- Are raised and brown to black in colour
SPITZ NAEVI
Are benign lesions, that are variants of intradermal naevus
Can be difficult to differentiate clinically from a normal naevi
They are usually found in the first 2 decades of life
They have a rapid growth phase which may cause alarm, and they have a characteristic histopathology which resembles melanomas
They are frequently red but can be brown to black
CONGENITAL NAEVI
Are present at the time of birth
These naevi grow with the child. Generally they become proportionally smaller and less obvious with time, however sometimes they can become darker (especially at puberty), and develop a bumpy or hairy surface. Some fade, some disappear altogether
They are classified as either;
1. Small (less than 1.5cm)
2. Medium (1.5 – 20cm)
3. Giant (over 20cm, are rare)
These have a low malignant potential (giant have a 3% lifetime risk of melanoma) and are generally removed due to cosmetic reasons
After puberty their malignant potential increases slightly
HALO NAEVI
Are benign naevi that tend to occur in children and adolescents
Once the halo appears, it is uncommon for the naevus to regress
It is considered an autoimmune process
They present clinically as;
- Naevi surrounded by a de-pigmented halo of normal skin
- Does not increase in size
- The halo is symmetrical
SOLAR LENTIGINES
Is a benign patches of darkened skin from exposure to sun damage
They are extremely common in middle aged to elderly, fair skinned people
They are often found in association with sun damage
The clinical features are as follows;
- Brown, well defined macule
- Occur on sun exposed skin
Pathology shows an increase in benign melanocytes in the basal layer of epidermis
These can be easily treated with cryotherapy, but patients should follow this up with sun protection or they tend to recur
FRECKLES
The fancy name is Ephelides
They are small, pale brown macules on the face and other sun exposed areas
Red headed infidels almost always have numerous freckles on sun exposed skin
Freckles are normal in fair skinned people and appear for the first time in childhood
The clinical features include;
- Small, pale brown macules
- Occur on the face or other sun exposed areas
- They darken on sun-exposure and lighten if the skin is sun protected
Babies are born without freckles, they usually appear for the first time around 2 – 3 years of age
Freckles are caused by an increase in melanin in the epidermis (biopsy shows no abnormality)
BLUE NAEVI
Are benign naevi occurring entirely in the dermis. They contain collections of benign dermal melanocytes (hence the blue colour)
Clinically they appear as very dark blue-black papules with a smooth regular surface and ovoid shape (poorly defined border as they are deep)
The majority of these lesions are harmless and can be left alone
Very rarely, they undergo malignant changes (When this happens, normal ABCDES rules of melanoma still applies)
They tend to appear from puberty onwards
SEBORRHEIC KERATOSES
Are very common benign lesions that occur commonly after the age of 40
They are often referred to as old age warts because they look very similar to common warts
Clinically they present as;
- Slightly raised, skin coloured or light brown macules/plaques
- They gradually thicken and take on a rough warty surface
- They slowly darken and can turn black
- They stick on to the skin like barnacles
Can appear on both covered and uncovered parts of the body
Do not require treatment on medical grounds
Some patients may wish to have them removed for cosmetic reasons (which is easily achieved with cryotherapy or light curettage and cautery)
SKIN TAGS
Are harmless lesions also known as acrochrocordons
They are very common in middle aged patients
They tend to be more numerous in obese patients and in those with T2DM
The clinical features include;
- Pedunculated and have a narrow pedicle
- Skin colour to brown
- Commonly occur in the axilla and groin and on the neck
They are easily removed with a simple snip excision
DERMATOFIBROMAS
Is a harmless and common lesion found in adults and children
There can be multiple of them
They are often confused with pigmented naevi, but rarely with melanoma as they are symmetrical and usually only one colour is evident
Clinical features include;
- Skin colour to light brown firm papule
- Asymptomatic
- When the skin either side is squeezed, the lesion tends to invaginate slightly (pinch test which is a very characteristic feature)
SEBACEOUS CYSTS
Are common benign lesions commonly seen in adults (rarely in children)
They are smooth raised dome shaped lesions in the dermis of the skin, that are tethered to the epidermis
There is usually a central punctum from which it may express sebaceous material
They are most commonly found on the head, neck and upper trunk (also can be found on the scrotum or labia majora)
They can become infected which cause them to become tender and inflamed, causing them to rapidly increase in size
If a patient wishes to have them removed, they have to be removed surgically as if they are drained, they simply recur
SEBACEOUS HYPERPLASIA
Is common in middle aged adults
They clinically present with multiple small, yellow umbilicated papules across the face (usually the forehead)
Close inspection shows a central hair follicle surrounded by yellowish lobules
Patients with this condition frequently have oily skin types
CAMPBELL de MORGAN SPOTS
Also known as Cherry angioma
Are commonly seen in patients over 40 years of age
They typically present as;
- Bright, asymptomatic red papules (rarely bleed)
- Can be numerous
- Most commonly occur on the back
- They can be red, blue, purple, or black (the deeper they are the darker they are)
Other angiomas in adults include;
- Spider angioma (spider naevus on the left)
- Venous lake (middle)
- Cherry angioma (right)
LESIONS IN OPTIC PATHWAY
If a patient incurs damage to the above described visual pathway, it will usually result in some sort of visual deficit
As is outlined above, the visual pathway consists of 3 main nerve pathways; the optic nerve, optic chiasm, optic tract and the geniculocalcarine tract
If anyone of these pathways is affected by a lesion, the following will happen;
1. Optic nerve
- A lesion here will cause blindness in the ipsilateral eye
- This is because all sensory information coming from that eye is lost
2. Optic chiasm
- A lesion here will cause bitemporal hemianopia
- Bitemporal (both temporal visual fields) hemianopia (loss of vision in half the visual field)
- Loss of temporal field in both eyes
- Common in pituitary adenoma
3. Optic tract
- A lesion here will cause homonymous hemianopia
- Homonymous men’s vision loss on the same visual field in both eyes
- This is loss of the same opposite visual field in both eyes (e.g. nasal in left and right eye)
4. Higher order neurons
- The further back you go, the more visual sparing you get (due to magnification of nerve fibres)
ACUTE OTITIS MEDIA
Is a painful type of ear infection that occurs when the middle ear becomes inflamed and infected
It is a common problem in early childhood, 2/3 children have at least one episode by age 3, and 90% have at least one episode by school entry (peak age prevalence is 6 – 18 months)
A patient with Acute Otitis Media will typically present with;
- Fever
- Ear pain (which presents as irritability in pre-verbal children)
- Vomiting
- Lethargy
- +/- Anorexia
The following characteristic signs will be apparent in an examination of a case with of Acute Otitis Media;
- Usual middle ear landmarks are not well seen (e.g. handle of malleus, incus and light reflex)
- The tympanic membrane is dull and opaque, and may be bulging
- There can also be dilated blood vessels
- Associated signs of URTI (e.g. coryza, red tonsillopharynx, cough etc.)
- Pneumatic otoscopy will show reduced tympanic membrane mobility
OTITIS MEDIA WITH EFFUSION
Symptoms usually involve hearing loss or aural fullness and does not typically involve pain or fever
This eustachian tube dysfunction is caused by a failure of the clearance mechanisms which include ciliary dysfunction, mucosal oedema, hyper viscosity of the effusion and an unfavourable pressure gradient. Some predisposing factors of this dysfunction include;
Otitis media with effusion is the leading cause of hearing loss in children.
- Conductive hearing loss is caused by the build up of fluid in the middle ear which reduces the ability of the ossicles to mechanically transmit sound waves
- Sensorineural hearing loss is caused by increased exposure to prostaglandins and leukotrienes (metabolites of arachidonic acid) causes temporary and sometimes permanent sensorineural hearing loss
Otitis Media with Effusion (OME) “glue ear”
TM is retracted with prominence of the handle of the malleus, which is also drawn in/more horizontal
TM may be bulging or have an air-fluid level behind the TM
Yellow/amber appearance is consistent with fluid
Light reflex on otoscopic examination
How does Granuloma annulare (GA) present?
Granuloma annulare usually presents as an annular plaque with a raised, red edge and a paler centre.
The backs of the hands and dorsal aspects of the feet are the most common sites. The skin surface is
never scaly or eroded and lesions are not symptomatic.
Granuloma annulare can sometimes appear as a flat, red macule or a subcutaneous nodule. Lesions can
be few or very numerous.
There is a rare papular form which is most closely associated with diabetes
How do Eruptive Xanthomas present and with what illnesses are they associated
with?
In patients with poorly controlled diabetes, high levels of triglycerides or familial hyperlipidaemia and
occasional inflammatory or neoplastic conditions may result in the appearance of numerous small
xanthomas. These present as red-orange papules, usually occurring on the lower back and buttocks.
What are the clinical features of atopic dermatitis?
Dry, cracked skin.
Itchiness (pruritus)
Rash on swollen skin that varies in color depending on your skin color.
Small, raised bumps, on brown or Black skin.
Oozing and crusting.
Thickened skin.
Darkening of the skin around the eyes.
Raw, sensitive skin from scratching.
A poorly defined approximately 10
macule with variable red-brown
pigmentation and poorly defined
borders on the back. There is a 4
mm pigmented areas of tan
coloured macule with poorly
defined margins at 11-12o’clock.
There appears to be a further area
of ill-defined tan pigmentation at
2o’clock in the photo. The inferior
area has ill defined pink to red
macule with poorly defined border
and areas of whitening in the center
urticaria
