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Dermatology > Posters 2- week 2 derm > Flashcards

Posters 2- week 2 derm Flashcards

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1
Q

What is a cream

A

Semi-solid emulsion of water and oil.

Contain an emulsifier and a preservative

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2
Q

What are creams good for?

A

Higher water content so good for dry skin

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3
Q

What is the risk of creams?

A

Patients can be allergic to the preservative.

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4
Q

What are lotions

A

Liquid formulation

Suspension or solution of medication in water, alcohol or other liquids

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5
Q

What are lotions good for?

A

Scalp and hair bearing areas

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6
Q

What are pastes?

A

Semisolids
Contain finely powdered material
Stiff, greasy and difficult to apply

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7
Q

What are pastes used for?

A

Often used in cooling, drying, soothing bandages.

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8
Q

What are ointments?

A

Semisolids grease/oils with no preservative

Occlusive (meaning not well absorbed)

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9
Q

What are ointments good for?

A

Very good moisturisers

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10
Q

What are gels

A

Thickened aqueous solutions

Semi-solids which contain high molecular weight polymers

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11
Q

Where would gels be used?

A

Scalp, hair bearing areas and face.

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12
Q

What is wet wrap therapy used for? Drawbacks

A

Very dry xerotic skin

However difficult and time consuming to apply

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13
Q

What are emollients used for?

A

Enhance rehydrating of the epidermis- used for all dry/scaly skin conditions such as eczema.

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14
Q

Three ways topical corticosteroids work

A

Vasoconstrictive
Anti-inflammatory
Anti-proliferative

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15
Q

Side effects of topical corticosteroids

A

Thinning of the skin
Purpura
Stretch marks
Steroid rosacea
Perioral dermatitis (raised bumps around the mouth)
Fixed telangiectasia (lots of blood vessels)

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16
Q

Antiseptics

A

Have bacteriostatic or bacteriocidal effects

True to use over antibiotics due to resistance

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17
Q

When are antiseptics clinically used

A

Recurrent infections
Antibiotic resistance
Wound irrigation

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18
Q

Treatment for thrush

A

Nystatin

Clotrimazole

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19
Q

treatment for ringworm

A

Clotrimazole

Terbinafine cream

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20
Q

Antipriuritics

A

Menthol
Capsaicin- depletes substance P at nerve endings
Camphor/phenol

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21
Q

Topical antibiotics used for acne

A

Clindamycin
Erythromycin
Tetracycline

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22
Q

Topical antibiotics used for rosacea

A

Metronidazole

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23
Q

Topical antibiotics used for impetigo

A

Mupirocin

Fusidic acid

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24
Q

What are keritolytics used for?

A

Used to soften keratin in viral warts, hyperkeratotic eczema, corns and calluses, remove keratin plaques.

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25
Q

What virus causes shingles and chicken pox

A

Varicella zoster virus

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26
Q

Symptoms of chickenpox

A

Generalised rash and fever

Macules, to papules to vesicles to recovery to scabs.

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27
Q

Symptoms of shingles

A

Reactivation of latent virus
Occurs in a dermatomal distribution
Tingling pain to erythema to vesicles to crusts

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28
Q

Complications of chicken pox

A

Secondary bacterial infection
Pneumonitis
Scarring
Encaphilitis

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29
Q

When is chickenpox severe

A

Extremes of age

Depressed cell mediated immunity

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30
Q

How is neonatal varicella zoster caused

A

Secondary to chicken pox in the mother in the late stages of pregnancy.

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31
Q

How to prevent neonatal varicella zoster

A

Give Varicella Zoster Immunoglobulin in susceptible women

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32
Q

What is ophthalmic zoster and where does it effect? Management

A

Ophthalmic zoster effects the ophthalmic division of the face (around the eye and on the forehead)
urgent referral

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33
Q

What is maxillary zoster and where does it effect?

A

Maxillary division of the trigeminal nerve affected (around nose and mouth),

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34
Q

What is mandibular zoster and where does it effect?

A

Effects the mandibular division of the trigeminal nerve.

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35
Q

How does herpes simplex virus present?

A

Primary gingivostomatitis- (inflammation of the gingiva and oral mucosa)
Extensive ulceration around the mouth

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36
Q

Who does herpes simplex virus normally affect?

A

Generally preschool children.

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37
Q

What does reoccurring herpes simplex virus present as?

A

Blistering rash at vermillion border.

Can spread.

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38
Q

Herpes simplex virus can be categorised into?

A

Type 1 and type 2

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39
Q

Effects of type 1 herpes simplex

A

Main cause of oral lesions
Accounts for half of genital lesions
Can cause encephalitis (inflammation of the brain)

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40
Q

Effects of type 2 herpes simplex virus

A

Rare cause of oral lesions
Accounts for half of genital lesions.
Also can cause encephalitis.

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41
Q

How would you confirm it was herpes simplex virus?

A

Lab confirmation with viral transport medium.

Antibody tests.

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42
Q

Therapy for herpes simplex virus and varicella zoster virus?

A

Aciclovir (analogue of guanosine)- selectively incorporated into viral DNA to inhibit replication.

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43
Q

What is erythema multiforme?

A

Well defined ‘target’ lesions with erythema.

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44
Q

What can trigger erythema multiforme?

A

Drug reactions and injections.

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45
Q

What is molluscum contagiosum?

A

Fleshy, firm depressed nodules.

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46
Q

Treatment for molluscum contagiosum?

A

Self limiting however can take months to clear.

Could use liquid nitrogen

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47
Q

How is molluscum contagiosum acquired and who does it infect?

A

Common in children.

Can be transmitted sexually.

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48
Q

What virus causes warts?

A

Human papilloma virus

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49
Q

When is a wart called a verruca?

A

If it is on the feet.

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50
Q

Treatment of warts?

A 
Self-limiting. 
Could use keratinolytics (to thin the keratin layer)
Formaldehyde
Glutaraldehyde
Cryotherapy (usually liquid nitrogen)
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51
Q

Who gets warts?

A

Most commonly children.

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52
Q

Other diseases caused by human papilloma virus

A 
Genital warts (types 6 and 11)
Cervical cancer (types 16 and 18)
Warts (types 1-4)
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53
Q

What vaccines are available for HPV

A

Gardasil- protects against types 6,11, 16 and 18.

Cervarix- protects against types 16 and 18

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54
Q

What treatment can you use for genital warts?

A

Imiquimod- has antiviral and anti tumour effect.

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55
Q

Treatment of psoriasis

A 
Emollients AND
coal tar (however messy and smelly)
Vitamin D analogue
Keratolytic
Topical steroids
Dithranol
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56
Q

How would treatment of psoriasis differ if it was axillary psoriasis?

A

Steroids need to be more dilute because the skin is more prone to thinning.

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57
Q

How would treatment of psoriasis differ if it was scalp psoriasis

A

Greasy ointments to soften scalp.
Tar shampoo
Steroids in the shampoo
Vitamin D analogues (calcipotriol- Daivonex trade name)

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58
Q

What does hyperkeratosis mean?

A

Increased thickness of the keratin layer

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59
Q

What does parakeratosis mean?

A

Persistence of nuclei in the keratin layer.

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60
Q

What is aconthosis?

A

Increased thickness of the epithelium.

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61
Q

What is papillomatosis?

A

Irregular epithelial thickening

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62
Q

What is spongiosis?

A

Oedema fluid increasing in prominence of intercellular prickles.

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63
Q

Name the 4 main classifications of pathological skin disease?

A

Psorisiform
Spongiotic intraepidermal oedema
Vesiculobullous
Lichenoid-

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64
Q

What does lichenoid mean?

A

Basal layer damage. Most common condition is lichen planus

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65
Q

An example of spongiotic intraepidermal oedema?

A

Eczema.

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66
Q

Pathology of psoriasis

A

Remains relatively unknown- could be due to
Epidermal hyperplasia
Hereditary factors
Sites of trauma
Complement mediated attack on keratin layer (due to neutrophils gathering in surface layer of the epidermis)

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67
Q

Signs and symptoms of psoriasis

A

Blood vessels come very close to the surface- Ausfitz sign (when you pick the scab it bleeds a lot)
Dystrophic nails
Nuclei persist in the keratin layer.

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68
Q

What is lichen planus?

A

Itchy, flat topped, violet coloured papules.

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69
Q

Histological appearance of lichen planus

A

Irregular, saw tooth, aconthosis.
Hypergranulosis (increased thickness of granular layer)
Band like upper dermal infiltrate of lymphocytes.
Basal damage with formation of cymoid bodies.

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70
Q

What resembles lichen planus?

A

Discoid lupus

Drug reactions

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71
Q

Vacuolar interface change

A

Change at the DEJ.

72
Q

What are immunobullous disorders?

A

Blisters are the primary feature (in lots of other conditions they are secondary)

73
Q

What is pemphigus?

A

Rare autoimmune condition where you get loss of epidermal cell adhesion.

74
Q

Immunological explanation of pemphigus

A

Autoantibodies made against desmoglien 3 (the bit that holds the epidermal cells together). Therefore causes immune complexes to form on the cell surface activating complement and protease release.

75
Q

Treatment of pemphigus

A

Responds to steroids.

76
Q

Pemphigus can be divided into

A

4 distinct subtypes. Most common (80%) pemphigus vulgaris.

77
Q

Symptoms of pemphigus vulgaris

A

Fluid filled blisters that rupture to form shallow erosions.
May affect the mucosa
Involves skin especially on the scalp, face, axillae and groin.

78
Q

What is bullous pemphigoid?

A

Circulating IgG antibodies react with hemidesmosomes which anchor the basal cells to the basement membrane.

79
Q

Symptoms of bullous pemphigoid?

A

Fluid filled blisters- that don’t easily rupture when touched.
Itchy and red skin

80
Q

Investigations into bullous pemphigoid and what they will show

A

Immunoflourescence- will show linear IgG and complement deposited around the basement membrane.

81
Q

What is dermatitis herpetiformis?

A

Relatively rare condition where IgA antibodies target gliadin in gluten but cross react with connective tissue matrix proteins.

82
Q

What is dermatitis herpetiformis associated with?

A

HLA DQ2

Gluten sensitive enteropathy (coeliac disease)

83
Q

Symptoms of dermatitis herpetiformis

A 
Extreme itch (priuritis)
Eruption classically seen on the buttocks and extensor surfaces of the arms and legs. 
Papillary dermal micro-abscesses.
84
Q

Pathogenesis of acne

A

In puberty- increased androgens are produced
Androgen sensitivity in sebaceous glands also increases meaning they make more keratin
The keratin and sebum plug the pilosebaceous unit
The build up can be infected with bacteria.

85
Q

Presentation of rosacea

A

Rhinophyma
Red flushed cheeks
Visible blood vessels
Pustules.

86
Q

What triggers rosacea

A

Sunlight
Alcohol
Stress
Spicy food

87
Q

Pathology of rosacea

A 
Vascular ectasia (blockage). Patchy inflammation therefore occurs with plasma cells. Pustules form. Perifollicular granulomas. 
Follicular dermodex mites often noted.
88
Q

The two phases of eczema

A

Acute and chronic

89
Q

Acute phase of eczema

A

Papillovesicular
Red erythematous lesions
Oedema (spongiosis)
Ooze or scaling and crusting

90
Q

Chronic phase of eczema

A

Thickening (lichenification)
Elevated plaques
Increased scaling.

91
Q

Name all 7 types of dermatitis

A 
Contact allergic dermatitis
Contact irritant dermatitis
Atopic
Drug induced
Photosensitive or photoinduced
Lichen simplex
Stasis dermatitis
92
Q

What is contact allergic dermatitis?

A

Delayed type 4 hypersensitivity reaction- in response to chemicals, topical therapies etc.

93
Q

Immunopathology of contact allergic dermatitis

A

Langerhan cells in the epidermis process the antigen
This is then presented to naive T cells
Sensitised T cells then migrate to lymph nodes and the presentation becomes amplified
On the next appearance of the antigen- sensitised T cells proliferate and migrate to the skin

94
Q

How would you identify the substance triggering the contact allergic dermatitis

A

Patch testing.

95
Q

What is irritate contact dermatitis

A

Non-immunological process where damage is caused directly to the skin through trauma/abrasion.

96
Q

What thing is key in the history to find out whether it is irritant contact dermatitis?

A

Occupation

97
Q

What is atopic eczema?

A

Genetic and environment factors resulting in inflammation.

98
Q

Which age group are likely to be effected by atopic eczema?

A

School aged children.

99
Q

Why does itch have an effect on neurological development?

A

Priuritis leads to sleep disturbance which causes neurocognitive impairment.

100
Q

Symptoms of atopic eczema?

A

Itch
Ill defined erythema and scaling
Generalised dry skin
Flexural distribution (involving skin folds)
Associated with other atopic diseases (asthma)

101
Q

Complications of atopic eczema?

A

Staph aureus is a common secondary infection.

Eczema herpeticum- eczema infected with herpes

102
Q

Presentation of eczema herpeticum

A

Monomorphic punched out lesions

103
Q

Sign of staph aureus infected eczema

A

Crusting.

104
Q

Diagnostic criteria for atopic eczema

A

Itching plus 3 or more of:

  • flexural rash
  • previous flexural rash
  • History of atopy
  • Generally dry skin
  • Onset before 2.
105
Q

Treatment of atopic eczema

A 
Plenty of emollients
Avoidance of irritants
Topical steroids
Treat any infections
Phototherapy- mainly UVB
Systemic immunosuppressants
106
Q

Discoid eczema

A

Well defined erythema and scale

Patients often atopic too

107
Q

Photosensitive eczema

A

Contact eczema to airborne allergens and UV light.

108
Q

Stasis eczema

A

Skin under pressure secondary to hydrostatic pressure. Oedema and red cell extravasation.

109
Q

Seborrhoeic dermatitis

A

Combination of atopic eczema and pittosporum on skin

110
Q

Pompholyx eczema

A

Spongiotic vesicles characteristically down lateral aspects of digits.

111
Q

What virus causes herpangina?

A

Enterovirus e.g. cocksackie virus or echo virus.

112
Q

What is herpangina?

A

Blistering rash at the back of the mouth.

113
Q

Treatment of herpangina

A

self limiting.

114
Q

Investigations into herpangina?

A

Swab lesion

Stool sample for enterovirus PCR.

115
Q

What is hand foot and mouth disease

A

Wart like blisters on the back of the mouth, typically occurring in children and has some family outbreaks.

116
Q

What is erythema infectiosum?

A

Slapped cheek disease- caused by parovirus B19. As the rash on the face fades- a lacy macular rash on the body appears.

117
Q

Erythema infectiosum presentation in adults

A

In adults the rash may be absent and acute poly arthritis of the small joints may be more prominent.

118
Q

Lab confirmation of erythema infectiosum

A

Antibody testing

Parovirus B19 IgM

119
Q

Complications of erythema infectiosum

A

Spontaneous abortion
Aplastic crises (sudden drop in Hb seen in patients with short RBC life span)
Chronic anaemia.

120
Q

What is Orf?

A

Virus of sheep “scabby mouth”

121
Q

Presentation of Orf?

A

Firm, fleshy nodule on farmers hand.

122
Q

Treatment and diagnosis of orf

A

Self limiting and diagnosed clinically.

123
Q

How does syphilis progress?

A

Through three phases, primary, secondary and tertiary.

124
Q

Primary phase of syphilis

A

Chancre- painless ulcer on the genitals

125
Q

Secondary phase of syphilis

A

Red rash over the body. Particularly prominent on the soles of the feet and palms of the hands.
Mucous membranes have small track ulcers.

126
Q

Tertiary phase of syphilis

A

CNS, cardiovascular, gummatous.

127
Q

What causes syphilis?

A

STD with bacterium treponema pallidum

128
Q

Lab confirmation of syphilis

A

Blood test

Swab of chancre for PCR

129
Q

Treatment of syphilis

A

Penicillin injections

130
Q

What causes Lyme disease?

A

Caused by ticks

Borrelia burgdorferi

131
Q

Presentation of Lyme disease?

A

Early- erythema migrans

Late- heart block, nerve palsies, arthritis.

132
Q

Lab confirmation of Lyme disease

A

Blood test for antibodies for the organism.

133
Q

Treatment of Lyme disease

A

Docycline or amoxicillin

134
Q

How is Zika virus spread?

A

Mosquitos

Can be transmitted sexually.

135
Q

Symptoms of zika virus

A 
Mild fever
Rash
Headaches
Arthralgia
Myalgia
Non-purulent conjunctivitis
136
Q

Complications of Zika virus

A

Guillian Barre Syndrome

Microcephaly

137
Q

Name for ringworm

A

Tinea

138
Q

Ringworm on the scalp

A

Tinea capititis

139
Q

Ringworm on the beard

A

Tinea barbae

140
Q

Ringworm on the body

A

Tinea corporis

141
Q

Ringworm on the hand

A

Tinea manuum

142
Q

Ringworm on the nails

A

Tinea unguium

143
Q

Ringworm in the groin

A

Tinea cruris

144
Q

Ringworm on the foot

A

Tinea pedis

145
Q

What is the source of a ringworm infection?

A

Other infected people
Animals
Soil

146
Q

Pathogenesis of ringworm

A

Fungus enters abraded or soggy skin.
Hyphae spread in stratum corneum.
Infects keratinised tissues only.
Increased epidermal turnover causes scaling. Inflammatory response provoked.
Hair follicles and shafts invaded.
Lesions grows outwards and heals in the centre.

147
Q

Organisms that can cause ringworm

A

Trichophytom rubrum- 70% from human to human
Trichophytom mentagraphytes- 20% human to human
Microsporium canis- from cats and dogs to humans

148
Q

How is the diagnosis of ringworm made?

A

Clinical appearance
Wood lamps
Skin scrapings/nail clippings

149
Q

Treatment of ringworm

A

Small areas of infected skin/nails- clotrimazole

Extensive infections, nail infections or scalp infections- terbinafine orally

150
Q

Candida infection

A

Causes thrush

Infection within the skin folds (e.g. under breasts)

151
Q

How to diagnose candida infection

A

Swab for culture.

152
Q

Treatment of candida infection

A

Clotrimazole cream.

153
Q

2 types of staphylococcus

A

Staph aureus

Coagulase negative staph

154
Q

What colour does staph aureus show on coagulase?

A

Golden yellow

155
Q

What colour does coagulase negative staph show on coagulase?

A

White

156
Q

What does staph aureus cause?

A

Wound, skin and joint infections

157
Q

What antibiotic can be used against staph aureus

A

Flucloxicillin

158
Q

Which strains of staph aureus produce toxins?

A

Enterotoxin- food poisoning
SSSST- staph scalded skin syndrome toxin
PVL- panton valentine leukocidin.

159
Q

Where are coagulase negative staph usually found?

A

It is a skin commensal

160
Q

When would coagulase negative staph cause infection?

A

On artificial implanted material e.g. heart valves.

161
Q

Which coagulase negative staph causes UTI’s in women of child bearing age

A

Staph saprophylicus

162
Q

Describe staphylococcal bacteria

A

Gram positive circular aerobic bacteria arranged in clumps

163
Q

Describe streptococcus bacteria

A

Gram positive circular aerobic bacteria arranged in chains.

164
Q

How can streptococcal species be classified?

A

Haemolysis- either alpha haemolysis- partial
Beta haemolysis- complete
or gamma haemolytic which is none.

165
Q

Describe beta haemolytic strep

A

Pathogenic organisms
Produce haemolysin as a toxin (among others)
Further classified by antigenic structure into group A and group B

166
Q

What does group A beta haemolytic strep commonly cause?

A

Throat and severe skin infections

167
Q

What does group B haemolytic strep commonly cause?

A

Meningitis in neonates.

168
Q

What are the two important categories in alpha haemolytic strep

A

Strep pneumoniae

Strep viridian’s- commensals of throat, vagina (rarely cause infection)

169
Q

Where would you find/ what are non-haemolytic strep

A

Enterococcus species
Commensals of the bowel
Common cause of UTI’s

170
Q

When does staph aureus cause skin infection?

A 
In boils and carbuncles
Cellulitis
Infected eczema
Impetigo
Wound infection
SSSST
171
Q

When does strep pyogenes (group A strep) cause skin infection?

A

Infected eczema
Impetigo
Cellulitis
Necrotising fasciitis

172
Q

How to diagnose strep pyogenes

A

Swab of lesion if surface has broken
Pus or tissue if deeper lesion
+/- blood cultures

173
Q

Treatment of strep pyogenes

A

Penicillin or flucloxicillin

174
Q

What is necrotising fasciitis?

A

Bacterial infection spreading along fascial planes below the skin surface causing rapid tissue destruction. Causes severe pain

175
Q

Causative organism for necrotising fasciitis

A

Either group A streptococcal (type 2) or mixed anaerobes and coliforms (type 1)

176
Q

Treatment of necrotising fasciitis

A

Life threatening- EMERGENCY SURGICAL DEBRIDEMENT.

Dermatology (21 decks)

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