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DERM > DERM > Flashcards

DERM Flashcards

1
Q

what type of epithelium is the epidermis made of

A

stratified cellular (squamous)

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2
Q

what is the dermis made up of

A

connective tissue

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3
Q

from which germ layer does the epidermis arise from

A

the ectoderm

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4
Q

from which germ layer does the dermis arise from

A

the mesoderm

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5
Q

where do melanocytes arise from

A

neural crest

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6
Q

what are the five layers of the skin

A 
keratin layer 
granular layer 
prickle cell layer 
basal layer 
dermis
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7
Q

what structures can be found in the dermis

A

sebaceous glands
arector pilli muscles
hair follicles

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8
Q

where are melanocytes located

A

mainly in the basal layer of the epidermis

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9
Q

what are Blaschko’s lines

A

developmental growth pattern of the skin

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10
Q

which cell is most predominant in the epidermis

A

keratinocytes

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11
Q

other than keratinocytes, which cell types are present in the epidermis

A

melanocytes
langerhans cells
Merkel cells

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12
Q

what mechanism are in control of epidermal turnover

A

growth factors
cell death
hormones

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13
Q

what shape of cells are in the basal layer

A

small cuboidal cells

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14
Q

basal cells are highly metabolically active

true/false

A

true

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15
Q

what shape are cells in the prickle cell layer

A

larger, polyhedral cells

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16
Q

what sort of connections are present in the prickle cell layer

A

desmosomes

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17
Q

how many layers of cells make up the granular layer

A

2-3 layers

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18
Q

where are keratohyalin granules found and what do they contain

A

in the granular layer of the dermis

structural filaggrin and involucrin proteins

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19
Q

are there nuclei present in the granular layer

A

no

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20
Q

what sort of cells are found in the keratin later

A

corneocytes (overlapping non-nucleated cell remnants)

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21
Q

what is the function of the keratin layer?

A

tight waterproof barrier

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22
Q

where are mucosal membranes found

A

eyes, mouth, nose, GU and GI tracts

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23
Q

where are langerhans cells found

A

suprabasally

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24
Q

where are Merkel cells found

A

basal layer

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25
Q

what are melanocytes

A

pigment producing dendritic cells

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26
Q

what organelles are specific to melanocytes

A

melanosomes

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27
Q

what do melanocytes convert to create melanin

A

tyrosine

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28
Q

what are the two different types of melanin

A

eumelanin (brown or black)

phaeomelainin (red/yellow)

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29
Q

how are melanosomes transferred to adjacent keratinocytes

A

dendrites

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30
Q

what is vitiligo

A

an autoimmune disease resulting in loss of melanocytes

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31
Q

what is the function of langerhans cells

A

antigen presenting cells

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32
Q

‘racket organelle’ is associated with which cell type

A

langerhans cell

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33
Q

what is the function of Merkel cells

A

mechanoreceptors

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34
Q

what are the three phases of hair growth

A

anagen - growing
catagen - involuting
telogen - resting/shedding

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35
Q

which hormone influence hair growth

A

thyroxine

androgens

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36
Q

how long does the anagen phase last

A

3-7 years

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37
Q

how long does the catagen phase last

A

3-4 weeks

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38
Q

what is telogen effluvium

A

hair follicles synchronise their telogen phase around 3 months after a stress on the body (infection, childbirth)

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39
Q

what is hirsutism

A

male pattern hair growth in a female

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40
Q

what causes virilisation

A

excess androgen

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41
Q

what is the dermo-epidermal junction

A

the interface between the epidermis and dermis

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42
Q

what are the functions of the derma-epidermal junction

A

support, anchorage, adhesion, growth and differentiation of basal cells
semi-permeable membrane acting as a barrier and filter

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43
Q

what are the three layers of the dermo-epidermal junction

A

lamina lucida
lamina densa
sub lamina dense zone

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44
Q

what types of cells are found in the dermis

A

mainly fibroblasts

macrophages, mast cells, lymphocytes, langerhans cells

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45
Q

what are the special sensory receptors present in the skin and their function

A 
pacinian corpuscles (pressure)
meissners corpuscles (vibration)
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46
Q

how do pacinian corpuscles appear on microscopy

A

lil onions

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47
Q

what causes hair pigmentation

A

melanocytes above the dermal papilla

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48
Q

what types of glands are present in the skin

A

sebaceous
apocrine
eccrine

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49
Q

where are the largest sebaceous glands located?

A

face and chest

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50
Q

what do sebaceous glands produce

A

sebum

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51
Q

what are the functions of sebaceous glands

A

control moisture loss

protection from fungal infection

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52
Q

where are apocrine swear glands found

A

axillae and perineum

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53
Q

what do apocrine glands produce

A

oily fluid

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54
Q

what skin structure are apocrine glands associated with

A

pilosebaceous unit

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55
Q

where are eccrine sweat glands found

A

the whole skin surface

especially the palms, soles and axillae

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56
Q

what is the nerve supply of the eccrine glands

A

sympathetic cholinergic nerve supply

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57
Q

which stimuli stimulate the eccrine glands

A

mental
thermal
gustatory

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58
Q

what are the functions of the eccrine glands

A

cooling by evaporation

moisten palms/soles to aid grip

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59
Q

what are the main functions of skin

A 
barrier protection 
metabolism and detoxification 
thermoregulation 
immune defence 
communication 
sensory functions
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60
Q

how does melanin protect the DNA in the cells’ nucleus

A

it absorbs UV rays

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61
Q

what are some metabolic processes that occur in the skin

A

vitamin D metabolism

thyroid hormone metabolism

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62
Q

what is vitamin D3 metabolised from

A

cholecalciferol (7-dehydrocholesterol)

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63
Q

where is vitamin D3 stored

A

in the liver

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64
Q

in the presence of 290-320 UV light cholecalciferol is metabolised to

A

hydroxycholecalciferol (vitamin D3)

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65
Q

vitamin D3 is converted to what in the kidney

A

1, 25-dihydroxycholecalciferol

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66
Q

thyroxine is converted to which substance in the skin

A

tri-iodothyronine (T3)

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67
Q

how does the skin thermoregulate

A

controls sweating, shivering, blood supply

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68
Q

what sensory functions odes the skin have

A

touch, pressure, vibration
pain and itch
heat and cold

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69
Q

what factors contribute to the skin as an immunological system include

A

structure (keratin layer, stratification)
cell types (immune system cells and keratinocytes)
cytokines, chemokines, eicosanoids, antimoicrobial peptides
genetics

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70
Q

what is the keratin layer also known as

A

the stratum corneum

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71
Q

keratinocytes can be activated by ______ and _______ to cause an immune response

A

UV and sensitisers

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72
Q

what role do keratinocytes play in immunological processes in the epidermis

A
  • sense pathogens via cell surface receptors and help mediate immune response
  • produce antimicrobial peptides that can directly kill pathogens
  • produce cytokines and chemokines
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73
Q

what is the main resident immune cell in the epidermis

A

langerhans cells

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74
Q

which type of cell is characterised by the Birbeck granule

A

langerhans cells

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75
Q

which type of T cell are found in the epidermis

A

CD8+ (cytotoxic)

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76
Q

which T cells are found in the dermis

A

CD4+ and CD8+

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77
Q

plasmacytoid DC are found in healthy skin

true/false

A

false

they are found in diseased skin

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78
Q

what are the main routes of drugs administration involving the skin

A

topical
transdermal
subcutaneous

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79
Q

what is the biggest barrier to drug penetration in the skin

A

the stratum corneum (keratin layer)

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80
Q

what are some examples of skin commensal bacteria

A

staph epidermidis
corynebacterium sp. (diphtheroids)
propionibacterium sp.

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81
Q

staph aureus is coagulase….

A

postive

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82
Q

what effect does coagulase have

A

clots plasma

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83
Q

what antibiotic is used to treat staph aureus infection

A

fluclox fluclox fluclox

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84
Q

some strains of staph aureus produce toxins such as…

A

enterotoxin (food poisoning)
SSSST staphylococcal scalded skin syndrome toxin
PVL Panton Valentine Leucocidin

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85
Q

what antibiotics can be used to treat MRSA

A

doxycycline
co-trimoxazole
clindamycin
vancomycin

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86
Q

coagulase negative staphs may cause infection in associated with…

A

prosthetic material (joints, heart valves, catheters)

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87
Q

beta haemolysis

A

yellow, complete

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88
Q

alpha haemolysis

A

green, partial

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89
Q

gamma haemolysis

A

none

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90
Q

alpha haem. strep includes

A

strep pneumoniae

strep viridans

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91
Q

non-haem strep are found where

A

commensal of the bowel

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92
Q

which antibiotic is used to treat group A strep

A

penicillin

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93
Q

treatment for necrotising fasciitis

A

urgent surgical debridement

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94
Q

what is tinea pedis

A

athletes foot

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95
Q

what virus causes chickenpox and shingles

A

varicella zoster virus

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96
Q

chicken pox is caused by which aspect of VZV

A

varicella

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97
Q

shingles is caused by which aspect of VZV

A

zoster

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98
Q

symptoms of chickenpox

A

generalised rash and fever

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99
Q

distribution of shingles

A

dermatomal

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100
Q

complications of chickenpox

A 
bacterial infection 
pneumonitis 
haemorrhagic rash 
scarring 
encephalitis
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101
Q

what causes neonatal chickenpox

A

VZV infection in mother in late stages of pregnancy

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102
Q

shingels is more common in which patient populations

A

elderly

immunocompromised

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103
Q

presentation of shingles

A

tingling/pain

erythema, vesicles and crusts

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104
Q

pain lasting longer than 4 weeks of shingles is called

A

post herpetic neuralgia

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105
Q

shingles is associated with what type of pain

A

neuralgic

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106
Q

why is ophthalmic shingles more severe than other forms

A

it can affect the eye via the nasociliary branch of CNV1

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107
Q

which dermatome does ophthalmic shingles affect

A

CNV1

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108
Q

how does ramsay-hunt syndrome present

A

shingles causing vesicles and pain in the auditory canal and throat

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109
Q

complications of Ramsay-hunt syndrome

A

facial nerve paralysis

irritation of CNVIII (deafness, tinnitus, vertigo)

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110
Q

recurrence of HSV presents as

A

a blistering rash on the vermillion border

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111
Q

type 1 HSV is the main cause of…

A

oral lesions

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112
Q

treatment for HSV/VZV

A

acyclovir

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113
Q

what is acyclovir

A

anti-viral

analogue of guanosine

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114
Q

how does acyclovir work

A

it is selectively incorporated into viral DNA inhibiting replication

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115
Q

how does erythema multiforme present

A

target lesions

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116
Q

which infections may trigger erythema multiforme

A

HSV

mycoplasma pneumoniae

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117
Q

describe the appearance of molluscum contagiosum

A

fleshy, firm, umbilicate, pearlescent nodules 1-2 mm in diameter

118
Q

treatment of molluscum contagious

A

liquid nitrogen

119
Q

which virus causes warts

A

HPV

120
Q

which types of HPV cause warts

A

types 1-4

121
Q

how can warts be treated

A

salicylic acid

122
Q

how does herpangina present

A

blistering rash at the back of the mouth

123
Q

what causes herpangina

A

enteroviruses (coxsackie/echovirus)

124
Q

how is herpangina diagnosed

A

swab of lesion and stool sample for enterovirus PCR

125
Q

what causes hand foot and mouth disease

A

enteroviruses, mainly coxsackie

126
Q

what is a fatal complication of hand foot and mouth disease

A

pulmonary oedema

127
Q

erythema infectiosum is also known as

A

slapped cheek disease

128
Q

what casues slapped cheek disease

A

erythrovirus (parvovirus) B19

129
Q

presentation of erythema infectiosum

A

rash on the cheeks, followed by lacy, macular appearance

130
Q

erythema infectiosum in adults presents with

A

polyarthritis of small joints

131
Q

complications of parvovirus B19 infection

A

spontaneous abortion
aplastic crises
chronic anaemia

132
Q

diagnosis of erythema infectiosum

A

parovirus B19 IgM test

133
Q

what is orf

A

a sheep virus that affects farmers

134
Q

how does orf present

A

firm fleshy nodule on the hands of farmers

135
Q

what is the presentation of primary infection of syphilis

A

chancre (painless ulcers at the site of infection)

136
Q

presentation of the secondary phase of syphilis

A

red rash over the body, especially the palms and soles

snail track ulcers on mucous membranes

137
Q

tertiary infection of syphilis

A

CNS, CV and gummatous manifestations

138
Q

what bacterium causes syphilis

A

treponema pallidum

139
Q

diagnosis of syphilis

A

blood test or swab of chancre for PCR

140
Q

treatment of syphilis

A

penicillin infections

141
Q

what causes Lyme disease

A

borrelia burgdorferi

142
Q

how long does a tick need to be attached to cause Lyme disease

A

24 hours

143
Q

early presentation of Lyme disease

A

erythema migrans

144
Q

late presentation of Lyme disease

A

heart block
nerve palsies
arthritis

145
Q

treatment of Lyme disease

A

amoxicillin or doxycycline

146
Q

diagnosis of Lyme disease

A

presence of erythema migrans

borrelia burdorferi IgG test

147
Q

Zika presentation

A 
mild fever 
rash (maculopapular)
headaches 
arthralgia 
myalgia 
non-purulent conjunctivas
148
Q

complications of Zika

A

microcephaly

Guillain Barre syndrome

149
Q

what is the ratio of melanocytes of basal cells

A

1:10

150
Q

what types of collagen are present in the dermis

A

types I and III

151
Q

where is the papillary dermis

A

just below the epidermis

152
Q

what is found in the reticular dermis

A

appendage structures eg sweat glands, pilosebaceous units

153
Q

what is the epidermal basement membrane made of

A

laminin and collagen IV

154
Q

what is hyperkeratosis

A

increased thickness of keratin layer

155
Q

what is parakeratosis

A

persistence of nuclei in the keratin layer

156
Q

what is acanthosis

A

increased thickness of epithelium

157
Q

what is papillomatosis

A

irregular epithelial thickening

158
Q

what is spongiosis

A

oedema between shamus cells that appears to increase prominence of intercellular prickles

159
Q

what are the 4 main inflammatory skin disease reaction patterns

A

spongiotic-intraepidermal oedema
psoriasiform
lichenoid-basal layer damage
vesiculobullous-blistering

160
Q

lichenoid disorders are characterised by damage to what skin structure

A

basal epidermis

161
Q

how do lichenoid disorders present

A

itchy flat topped violaceous papules

162
Q

how is lichen planus described histologically

A

irregular sawtooth acanthosis
hypergranulosis and ortohyperkeratosis
band-like upper dermal infiltrate of lymphocytes
basal damage with formation of cymoid bodies

163
Q

what skin disorder has the following histological appearance;
irregular sawtooth acanthosis
hypergranulosis and ortohyperkeratosis
band-like upper dermal infiltrate of lymphocytes
basal damage with formation of cymoid bodies

A

lichen planus

164
Q

examples of immunobullous diseases

A

pemphigus
bullous pemphigoid
dermatitis herpertiformis

165
Q

what age group is most commonly affected by pemphigus

A

middle age

166
Q

how is pemphigus treated

A

steroids

167
Q

what is the most common type of pemphigus

A

pemphigus vulgaris

168
Q

what type of antibodies are associated with pemphigus vulgaris

A

IgG auto-antibodies against desmoglein-3

169
Q

what is the function of desmoglein-3

A

desmosomal attachment

170
Q

what is the pathological process causing pemphigus vulgaris

A 
IgG against desmoglein-3
immune complexes form on cell surfaces 
complement activation and protease release 
disruption of desmosomes
acanothlysis
171
Q

where does pemphigus vulgaris commonly present

A

scalp, face, axillae, groin and trunk

may affect mucosa

172
Q

how does pemphigus vulgaris present

A

fluid filled blisters which rupture to form shallow erosions

173
Q

what is the pathological process causing bullous pemphigoid

A 
circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane
this result complement activation and tissue damage
174
Q

how does bullous pemphigoid present

A

sub epidermal blisters

175
Q

immunofluorescence appearance of bullous pemphigoid

A

linear IgG + complement deposited around BM

176
Q

what autoimmune condition is dermatitis herpetiformis associated with

A

coeliac disease

177
Q

presentation of dermatitis herpetiformis

A

symmetrical, intensely itchy lesions

elbows, knees and buttocks often affected

178
Q

what is the hallmark of dermatitis herpetiformis

A

papillary dermal micro abscesses

179
Q

pathogenesis of acne

A

sebum produced by sebaceous gland plugs pilosebaceous unit
keratin and sebum build up to produce comedones (blackheads/whiteheads)
rupture causes acute inflammation and foreign body granulomas

180
Q

presentation of rosacea

A

recurrent facial flushing
visible blood vessels
pustules
thickening of skin (rhinophyma)

181
Q

factors that aggravate rosacea

A

sunlight
alcohol
spicy foods
stress

182
Q

chemical mediators of itch

A

histamine, PGE2, acetylcholine, serotonin, kvllikrein, interleukin 2

183
Q

what are the 4 causes of itch

A

pruritoceptive
neuropathic
neurogenic
psychogenic

184
Q

what causes pruritoceptive itch

A

something (usually associated with inflammation or dryness) in the skin causes itch

185
Q

what causes neuropathic itch

A

damage of any sort to central or peripheral nerves

186
Q

define neurogenic itch

A

no evident damage in CNS but itch is caused by something acting on CNS receptors (eg opiates)

187
Q

what causes psychogenic itch

A

psychological causes with no CNS damage (eg itch with delusions of infestation)

188
Q

what is dermographism

A

stroking the skin causes excessive mast cell degranulation and release of histamine and other within-skin mediators resulting in a raised white mark, with surrounding erythema

189
Q

examples of pruritoceptive itch

A

lichen planus, eczema, insect bites, psoriasis,

190
Q

what types of systemic diseases are associated with itch

A 
haematological 
paraneoplastic 
liver and bile duct 
psychogenic 
kidney disease 
thyroid disease
191
Q

what is the commonest form of psoriasis

A

chronic plaque psoriasis (psoriasis vulgaris)

192
Q

what is Koebner phenomenon

A

psoriasis developing in an area of trauma

193
Q

what is Auspitz sign and what is it is sign of

A

removal of scale surface reveals tiny bleeding point (dilated capillaries in elongated dermal papillae)
psoriasis

194
Q

what are the 4 types of psoriasis

A

chronic plaque (psoriasis vulgaris)
guttate
palmoplantar pustular
erythrodermic/widespread pustular

195
Q

nail signs of psoriasis

A

onycholysis (separation of nail from nail bed)
nail pitting
dystrophy
subungual hyperkeratosis

196
Q

why do people with severe psoriasis have a life expectancy reduced by about 4 years

A

increased CV risk

197
Q

topical therapies for psoriasis

A 
vitamin D analogues (calcipotriol, calcitriol)
coal tar 
dithranol
steroid ointments 
emollients
198
Q

specialist treatments for psoriasis

A 
phototherapy (narrow band UVB and PUVA)
systemic treatments (immunosuppression eg methotrexate, immune modulation eg biologic agents
199
Q

initial management of acne

A 
oral antibiotic (doxycycline)
topical retinoid
200
Q

second line acne management

A

oral isoretinoin (systemic retinoid)

201
Q

side effects of isoretinoin

A

causes initial flare of acne for 2-3 weeks

congenital defects

202
Q

what is acne vulgaris

A

chronic inflammatory disease of the pilosebasceous unit

203
Q

what sites are most affected by acne vulgaris

A

face, upper back, anterior chest

204
Q

morphological description of acne vulgaris may include

A

comedones (open = blackhead, closed = whitehead)
pustules and papules
cysts
erythema

205
Q

how does rosacea differ from acne

A

no comedones as there is no involvement of the pilosebaceous unit

206
Q

what is rhinophyma

A

enlarged/unshapely nose

associated with rosacea

207
Q

topical therapy for rosacea

A

metronidazole

ivermectin (reduce demodex mite)

208
Q

oral therapy for rosacea

A

tetracycline long term

isoretinoin low dose if severe

209
Q

sites commonly affected by lichen planus

A

volar triste/forearms, shins and ankles

210
Q

what is Wickham’s striae and what is it a sign of

A

fine lace-like pattern on the surface of papules and buccal mucosa
lichen planus

211
Q

how long does lichen planus normally last

A

12-18 months

212
Q

treatment of lichen planus

A

topical steroids (oral steroid is extensive)

213
Q

how to differentiate between pemphigus vulgaris and bullous pemphigoid

A

bullous pemphigoiD - the split is Deeper, through the DEJ

pemphiguS - split is more Superficial, intra-epidermal

214
Q

what is Nikolsky’s sign and what is it associated with

A

the top layers of the skin slip away from the lower layers with slightly rubbed
pemphigus

215
Q

is bullous pemphigoid associated with blisters

A

yah, blisters burst to leave erosions

216
Q

Nikolsky’s sign is positive in bullous pemphigoid

true/false

A

false - the split in BP is not intra-epithelial

217
Q

bullous diseases may initially present with urticated itchy plaques
true/false

A

true

218
Q

is mucosal involvement common in bullous pemphigoid, pemphigus vulgaris or both

A

pemphigus

219
Q

tense bullae are associated with…

flaccid bullae are associated with…

A 
tense = bullous pemphigoid 
flaccid = pemphigus
220
Q

which bullous disorder has the worse prognosis

A

pemphigus

221
Q

signs of acute phase eczema

A

papulovesicular rash
erythema
oedema (spongiosis)
ooze or scaling and crusting

222
Q

signs of chronic phase eczema

A

thickening (lichenification)
elevated plaques
increased scaling

223
Q

how is contact allergic dermatitis investigated

A

patch testing

224
Q

what is the typical distribution of atopic eczema

A

flexural distribution

225
Q

what causes eczema herpeticum

A

HSV

226
Q

morphology of eczema herpeticum

A

monomorphic punched-out lesions

227
Q

diagnostic criteria fro atopic eczema

A 
itching + 3 or more of;
visible flexural rash**
history of flexural rash**
history of atopy 
dry skin
onset before 2 yo
**cheeks and extensor surfaces in infants
228
Q

which gene is most significant in the development of atopic eczema

A

filaggrin

229
Q

stasis eczema is secondary to

A

hydrostatic pressure
oedema
red cell extravasation

230
Q

what is ash-leaf macule a sign of

A

tuberous sclerosis

231
Q

what tumours are associated with tuberous sclerosis

A

periungual fibromas (around nails)
facial angiofibromas
hamartomas (angiomyolipomas - heart, lung, kidneys)
bone cysts

232
Q

why is tuberous sclerosis associated with seizures

A

cortical tubers and/or calcification of falx cerebri

233
Q

presentation of epidermolysis bullosa

A

blistering at birth

234
Q

type of epidermolysis bullosa

A

simplex
junctional
dystrophic

235
Q

result of haploinsufficiency

A

only one copy of working - reduced protein production

236
Q

result of dominant negative mutation

A

expression of abnormal protein interferes with normal protein

237
Q

result of gain of function mutation

A

mutant protein gains new function, affecting cell processes

238
Q

result of autosomal recessive mutations

A

2 faulty copies of gene produce no protein

239
Q

cafe au lait macules

A

neurofibromatosis type 1

240
Q

presentation of NF1

A 
cafe au lait
neurofibromas
plexiform neuroma 
axillary or inguinal freckling 
optic glioma 
lisch nodules 
bony lesions
241
Q

ichthyosis vulgaris is caused by a mutation in which gene

A

filaggrin

242
Q

ABCDE melanoma

A 
asymmetry
borders
colour 
diameter 
evolution
243
Q

what is the ugly duckling sign

A

a mole that looks different from all the others on a patients skin is more likely to be melanoma

244
Q

describe appearance of BCC

A 
pearly/translucent 
slow growing lump or non-healing ulcer 
visible blood vessels 
central ulceration 
scaly plaque
245
Q

what is a morphoeic BCC

A

infiltrative

246
Q

SCC presentation

A

hyperkeratotic (crusted lump or ulcer
fast growing
painful, bleeding

247
Q

precursor lesions for SCC

A

actinic keratoses

Bowen’s disease (carcinoma-in-situ)

248
Q

where does SCC tend to present

A

sun-damaged skin

249
Q

what are actinic keratoses

A

precancerous skin lesions

250
Q

risk factors for skin cancer

A 
sun exposure 
genetic predisposition 
immunosuppression
(HPV infection)
environmental carcinogen
251
Q

what is Gorlin’s syndrome

A

nevoid basal cell carcinoma syndrome

presents with early onset/multiple BCCs, palmar pits, jaw cysts and ectopic calcification falx

252
Q

what are melanocyte precursor cells called

A

melanoblasts

253
Q

when do melanblasts become melanocytes

A

when they settle in the skin

254
Q

what sort of melanin causes red hair

A

phaeomelanin

255
Q

which gene determines skin pigment and hair colour

A

melanocortin 1 receptor gene

256
Q

what is the function of the MC1R gene

A

turns phaeomelanin into eumelanin

257
Q

what is the science name for freckles

A

ephilides

258
Q

what are actinic/solar lentigenes

A

liver/age spots

259
Q

what causes actinic lentigenes

A

increased melanin and basal melanocytes

epidermis elongated rete ridges

260
Q

what are the two types of dysplastic naevi

A

sporadic

familial

261
Q

presentation of sporadic dysplastic naevi

A

one to several atypical naevi

262
Q

presentation of familial dysplastic naevi

A

strong FH of melanoma

lots of atypical naevi

263
Q

how does familial dysplastic naevi affect risk of MM

A

lifetime risk of melanoma up to 100%

264
Q

what are halo naevi

A

naevi with a peripheral halo of depigmentation

265
Q

what are blue naevi made up of

A

pigment rich dendritic spindle cells

266
Q

where are blue naevi found

A

dermis

267
Q

what colour are spitz naevi

A

pink

due to prominent vasculature

268
Q

what are the four main types of malignant melanoma

A

superficial spreading
acral/mucosal lentiginous
lentigo maligna
nodular

269
Q

melanomas in which growth phase can metastasise

A

vertical growth phase

270
Q

how does the growth of nodular melanoma differ from the other types

A

there is no evidence of radial growth phase

271
Q

how is melanoma prognosis measured

A

Breslow depth

272
Q

melanoma poor prognostic factors

A 
ulceration 
high mitotic rate 
lymphovascular invasion 
satellites 
sentinel lymph node involvement
273
Q

treatment of melanoma

A

primary excision to give clear margins

274
Q

treatment if melanoma with positive sentinel nodes

A

primary excision + regional lymphadenectomy

275
Q

treatment of melanoma with mets

A

chemo, immunotherapy, genetic therapies

276
Q

what is seborrhoeic keratosis

A

benign proliferation of epidermal keratinocytes

277
Q

were are seborrhoeic keratoses most common

A

on the face and trunk

278
Q

what is Leser-Trelat sign

A

eruptive appearance of many seborrhoeic keratoses that may indicate internal malignancy

279
Q

presentation of Bowen’s disease

A

scaly patch/plaque
irregular border
no dermal invasion

280
Q

atypical presentations of SCC

A

chronic leg ulcers (stasis ulcers)
sites of burns
chronic lupus vulgaris

281
Q

specific sites of poor prognosis for SCC

A

scalp, ear, nose

282
Q

definition of chronic leg ulcer

A

a open lesion between the knee and ankle joint that remains unheralded for at least 4 weeks

283
Q

swab a leg ulcer?

A

only if there are signs of infection - increasing pain/exudate/smell/enlarging

284
Q

treatment of venous ulcer

A

4 layer compression bandaging

leg elevation

285
Q

indications for surgery: rash

A

assist in diagnosis

286
Q

indications for surgery: tumours

A

assist in diagnosis
remove malignancy
remove unwanted skin growth (cosmesis)

287
Q

types of skin disease caused by adverse reaction to amoxicillin

A 
morbilliform (measles like) eruption 
urticaria 
angiodema 
fixed drug eruption 
generalised pustulosis
288
Q

what is imiquimod cream used to treat?

A

actinic keratoses

superficial BCC

289
Q

treatment of precancerous skin lesions

A 
cryotherapy 
solaraze 
5 FU
PDT
imiquimod 
resurfacing
290
Q

what are the 5 layers of the scalp

A 
skin
connective tissue 
aponeurosis 
loose connective tissue 
periosteum

DERM (5 decks)

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