Derm Flashcards

1
Q

What are the four layers of epidermis?

A
  • Keratin layer
  • Granular layer
  • Prickle cell layer
  • Basal layer
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2
Q

components of keratin layer

A
  • Corneocytes (80% keratin and filaggrin)

- lamellar granules (secrete lipids)

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3
Q

components of granular layer

A
  • keratohyalin granules

- odland bodies (contain secretory organelles)

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4
Q

What is the origin of the cornified envelope

A

Granular layer

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5
Q

Components of prickle cell layer

A
  • desmosomes (connections)
  • keratin filiaments
  • langerhans cells
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6
Q

Components of basal layer

A
  • keratin filaments
  • Merkel cells (mechanoreceptors)

highly metabolically active: keratinocytes created here and migrate upwards (takes 28 days)

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7
Q

Key feature of langerhans cells

A
  • birbeck granules

- look like tennis rackets

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8
Q

What is in the dermis?

A
  • connective tissue
  • fibroblasts
  • macrophages, mast cells, lymphocytes, langerhans cells
  • collagen and elastin fibres
  • blood vessels
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9
Q

Pacinian corpuscules sense what?

A

pressure

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10
Q

Meissner’s corpuscules sense what?

A

Vibration

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11
Q

Which enzyme effected in Erythropoetic protoporphyria ?

A
  • ferrochelatase

- genetic ->dysfunctional protein

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12
Q

Which enzyme affected in porphyria cutanea tarda?

A
  • uroporphyrinogen

- lack or enzyme due to it being used or break down e.g. excessive alcohol, haemochromatosis, hepatitis

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13
Q

what enzyme is affected in acute intermittent porphyria

A
  • PBG deaminase

- genetic -> dysfunctional protein

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14
Q

Bacteria which may be responsible for necrotising fasciitis

A
  • mixed anaerobes/coliforms (post abdominal surgery)

- group A strep (pyrogenes)

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15
Q

Investigation for Tinea

A
  • florescence under woods lamp
  • microscopy
  • take scrapings from edge of lesions
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16
Q

Treatment for tinea/ candida

A

-clotrimazole cream

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17
Q

Herpes responsible for oral lesions

A

-HSV type 1

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18
Q

Herpes responsible for genital lesions

A
  • HSV type 1

- HSV type 2

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19
Q

What is Aciclovir?

A

-analogue of guanosine

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20
Q

Types of HPV which cause cervical cancer

A

16 and 18

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21
Q

Types of HPV which cause genital warts

A

6 and 11

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22
Q

What causes erythema infectiosum/ slapped cheek disease?

A

erythrovirus B19

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23
Q

symptoms of primary phase of syphilis

A
  • painless chancres

- occur at site of entry

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24
Q

symptoms of secondary phase of syphilis

A
  • red rash all over body
  • prominent on soles, palms and mucous membranes
  • ‘snail track ulcers’
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25
Q

Symptoms of tertiary phase syphilis

A
  • CNS
  • gummatous
  • CVS

-widespread effects

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26
Q

Bacteria which causes lyme disease

A

Berrelia burgdorferi

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27
Q

late complications of lyme disease

A

heart block, nerve palsies, arthritis

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28
Q

Treatment for lyme disease

A

doxycycline or amoxicillin

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29
Q

Pathological appearance of psoriasis

A
  • epidermal hyperplasia
  • parakeratosis
  • absent granular layer
  • elongated and clubbed ret ridges
  • neutrophilic and lymph histocytic infiltrate
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30
Q

example of vitamin D3 drugs

A
  • calcipotriol

- tacalcitol

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31
Q

What is pathological appearance of lichen planus?

A
  • hyperkeratosis
  • dense T cell infiltration in dermo-epidermal junction
  • liquefactive degeneration of basal layer
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32
Q

Which areas are commonly involved in lichen planus?

A
  • flexors
  • lower legs
  • wrists
  • mouth
  • anogenital region
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33
Q

Which populations is pemphigus vulgaris more common in?

A
  • indian

- jewish

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34
Q

Pathophysiology of pemphigus vulgaris

A

-IgG auto-antibodies against desmoglein 3

35
Q

Where is the split in pemphigus vulgaris

A
  • superficial intra-epidermal split

- just above basal layer

36
Q

Pathophysiology of bullous pemphigoid

A

-antibodies agains haemosdesmosomes

37
Q

Where is the split in bullous pemphigoid?

A

between basal cells and basement membrane

38
Q

investigation for bullous pemphigoid

A
  • immunofluorescence

- will show IgG and complement deposition around basement membrane

39
Q

Who is likely to present with dermatitis herpatiformis?

A
  • young adult males

- with coeliac disease

40
Q

possible causes of rosacea

A
  • skin mite dermodex

- vasmotor instability of blood vessels

41
Q

treatment of rosacea

A
  • oral tetracyclines

- topical metronidazole

42
Q

possible cause of atopic dermatitis

A
  • loss of function of filaggrin protein

- is responsible for maintaining the epidermal barrier

43
Q

What is lichen simplex?

A

-chronic scratching/rubbing without an underlying cause

44
Q

Cause of seborrheic dermatitis

A
  • overgrowth of pityrosporum ovale fungus

- cutaneous immune response to the yeast it produces

45
Q

proteins affected in tuberous sclerosis

A
  • tuberin and hemartin

- both are tumour regulating genes

46
Q

is tuberous sclerosis dominant or recessive?

A

autosomal dominant

47
Q

cutaneous sign which could indicate tuberous sclerosis

A

ash leaf macules

48
Q

What is epidermolysis bullosa

A
  • group of genetic skin fragility diseases

- mutations in genes responsible for skin structure/adhesion e.g. keratin, integrins, collagen

49
Q

Cutaneous sign of neurofibromatosis type 1

A

greater than 5 cafe au lait macules

50
Q

What is seborrheic keratosis?

A
  • benign proliferation of epidermal keratinocytes

- gives ‘stuck on’ appearance

51
Q

pathological appearance of BCC

A
  • desmoplastic fibrous stroma
  • peripheral palisading
  • lots of apoptosis and mitosis
52
Q

common mutations involved in BCC

A
  • PTCH1
  • key component of hedgehog signalling pathway
  • which is important in cell proliferation and angiogenesis
53
Q

SCC precursor lesions

A
  • acitinic keratosis

- bowen’s disease

54
Q

Common presentation of Bowen’s disease

A
  • older women

- scaly patch/ plaque with irregular border on lower legs

55
Q

Common mutations involved in malignant melanoma

A
  • Ras
  • Raf
  • MAPK

-CDKN2A (familial)

56
Q

what is breslow thickness?

A
  • prognostic tool

- measurement of how far a lesion extends below the granular layer

57
Q

what does a breslow thickness less than 1mm indicate?

A
  • good prognosis

- 50-100% 5y survival

58
Q

if breslow thickness greater than 4mm what is the 5y percentage survival?

A

50%

59
Q

What is xeroderma pigmentosum

A

-inability to repair DNA damage from UV light

60
Q

example of spongiotic intra-epidermal oedema

A

eczema

61
Q

example of psoriasiform-elongation of the rete ridges

A

psoriasis

62
Q

example of lichenoid basal layer damage

A
  • lichen planus

- lupus

63
Q

example of vesiculobullous blistering

A
  • pemphigoid
  • pemphigus
  • dermatitis herpatiformis
64
Q

hyperkeratosis defintion

A

increased thickness of keratin layer

65
Q

parakeratosis definition

A

persistance of nuclei within the keratin layer

66
Q

acanthosis definition

A

increased thickness of the epidermis

67
Q

How does UVB cause skin damage?

A
  • energy causes covalent bonding between adjacent pyrimidines (T and C) on same DNA strand
  • this interferes with base pairing when DNA replicates
  • can be difficult to repair correctly leading to insertion of wrong base
68
Q

How does UVA cause skin damage

A
  • energy causes oxidation of bases especially deoxy guanosine
  • deoxy guanosisn then might misspair with deoxy adenosine
  • leads to GC -> AT point mutations
69
Q

Which UV penetrates more deeply into skin

A

UVA

70
Q

Mutations involved in familial melanoma

A
  • CDKN2A
  • codes for p16 and p14
  • prevent cells form activating when they contain damaged DNA
71
Q

Which gene controls skin and hair pigment

A
  • MC1R

- turns pheomelanin (red/freckles) into eumelanin

72
Q

Tinea capitis treatment

A

-oral terbinafine or itraconazole

73
Q

scabies treatment

A
  • malathion lotion

- benzyle benzoate (but not for kids)

74
Q

what is Ramsay hunt syndrome?

A
  • shingles affecting facial nerve/ geniculate ganglion

- can cause facial paralysis/ hearing loss in affected ear

75
Q

what is herpangina?

A
  • blistering rash at back of mouth

- caused by enteroviruses e.g. coxsackie

76
Q

which antibody tends to appear early in the course of infection?

A

-IgM

77
Q

treatment of acne

A
  • bensoyl peroxide (keratinolytic)

- isotretinoin (retinoid)

78
Q

SCC risk factors

A
  • viral lesions e.g. HPV 16
  • precursor lesions e.g. actinic keratosis, bowen’s
  • areas exposed to lots of sun in particular ear, lip, scalp
  • sites of chronic inflammation e.g. ulcers, burns, sinuses (osteomyelitis)
79
Q

primary intention definition

A
  • healing of clean wound without tissue loss
  • wound edges brought together with stitches
  • works for laceration type injuries
80
Q

secondary intention definition

A
  • loss of tissue or damage prevents closure by primary intention
  • wound is left and allowed to granulate
  • may be packed with gauze or have drainage
  • must be cleaned regularly
81
Q

tertiary intention definition

A
  • wound is debrided, left open and observed

- closure can then be achieved by primary intention or tissue grafts

82
Q

mild steroid cream

A

hydrocortisone 1-2%

83
Q

moderate steroid cream

A

eumovate

84
Q

potent steroid cream

A

betnovate