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2019/2020 Alcohol CLASP and Derm > Pathology > Flashcards

Pathology Flashcards

Pathology of dermatological diseases

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

What are the functions of the skin?

A 
Barrier
Thermoregulation
Fluid and electrolyte balance
Endocrine function
Melanin pigment
Immune function
Sensory function
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2
Q

Describe the papillary dermis

A

Thin, lies just beneath the epidermis

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3
Q

Describe the reticular dermis

A

Thicker bundles of type 1 collagen and contains appendage structures

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4
Q

Define hyperkeratosis

A

Increased thickness of the keratin layer

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5
Q

Define parakeratosis

A

Persistence of nuclei in the keratin layer

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6
Q

Define acanthosis

A

Increased thickness of the epithelium

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7
Q

Define spongiosis

A

Oedema in the epidermis

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8
Q

What are the 4 main reaction patterns for inflammatory skin disease

A

Spongiotic-intraepidermal oedema
Psoriaform elongation of the rete ridges
Lichenoid basal layer damage
Vesiculobullous blistering

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9
Q

Describe the Koebner phenomenon

A

New psoriasis lesions arising at sites of trauma

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10
Q

What are lichenoid disorders characterised by?

A

Damage to the basal epidermis

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11
Q

Histology of lichen planus

A

Irregular sawtooth acanthosis
Band like upper dermal infiltrate of lymphocytes
Basal damage with formation of cytoid bodyes

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12
Q

What is irregular sawtooth acanthosis?

A

Jagged appearance of the rete ridges of the epidermis

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13
Q

What is the presentation of immunobullous disorders?

A

Vesicles and bullae occur as secondary phenomena in many skin diseases

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14
Q

What happens to form bullae in pemphigus?

A

Loss of integrity of epidermal cell adhesions

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15
Q

Describe the mechanism of pemphigus vulgaris

A

IgG auto-antibodies made against desmoglein 3
Desmoglein 3 maintains desmosomal attachments
Immune complexes form on the cell surface
Complement activations and protein release
Disruption of desmosomes
Acantholysis

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16
Q

What happens to form bullae in bullous pemphigoid

A

Sub-epidermal blister without evidence of acantholysis

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17
Q

What is dermatitis herpetiforms strongly associated with

A

Coeliac disease

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18
Q

What are the hallmarks of dermatitis herpetiforms?

A

Papillary dermal micro-abcesses

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19
Q

What is the mechanism of dermatitis herpetiforms?

A

Direct immunoflouresence shows deposits of IgA in the dermal papilla
Targets the gliadin component of gluten but cross react with connective tissue matrix proteins
Immune complexes form in dermal papilla and activate complement

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20
Q

What is acne a disorder of?

A

The sebaceous glands

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21
Q

What is the mechanism of acne?

A

Keratin plugging of pilosebaceous units

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22
Q

What is the prevalence of rosacea in caucasian adults?

A

~10%

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23
Q

How does rosacea present?

A

Recurrent facial flushing

Leading to eventual thickening of the skin

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24
Q

What is often noted in rosacea?

A

Follicular demodex mites

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25
Q

What is an oncogene?

A

An overactive form of a gene that positively regulates cell division

26
Q

What is a tumour suppressor

A

A gene that down regulates cell division

27
Q

What are the two forms of melanin and which is more efficient?

A

Eumelanin and pheomelanin

Eumelanin is more efficient

28
Q

What are the 5 types of DNA damage?

A 
Altered or missing base
Incorrect base
Insertion/deletion
Strand break
Crosslinking
29
Q

What are the two major types of UVB-induced DNA lesions?

A

Cyclobutane pyrimidine dimers

Pyrimidine-pyrimidone (6-4) photo-products

30
Q

What repairs UVB induced lesions

A

DNA polymerase

31
Q

How does UVA cause damage to DNA

A

Via the oxidation of DNA bases

32
Q

Outline excision repair of DNA

A

Repair of oxidised bases

  1. Recognition of chemically altered base causing slight helix distortion
  2. Cleavage of altered base from the deoxy-ribose by DNA glycosylase
  3. Base-free deoxyribose cleaved away endonuclease
  4. Single nucleotide gap filled by DNA polymerase beta
  5. DNA ligase seals the end
33
Q

How do UV rays induce immunosuppression?

A

Depletion of langerhans cells
UV induced regulatory T cells with immune supressive activity
Secretion of anti-inflammatory cytokines by macrophages and keratinocyes

34
Q

What mutations are important in BCC?

A

Mutations in PTCH1

Key component of hedgehog signalling pathway

35
Q

What does hedgehog signalling do?

A

Activates transcription factors Gli 1/2, leading to induction of cell proliferation genes and angiogenesis factors

36
Q

What drug can be used in the case of mutation in PTCH1?

A

Vismodeglib

37
Q

What genes have been linked to familial melanoma?

A

CDKN2A

CDK4

38
Q

What does CDKN2A do?

A

Prevents cells from replicating when they contain damaged DNA by activating G1/S

39
Q

What does CDK4 do?

A

Permits cell cycle progression by phosphorylation of retinoblastoma protein

40
Q

What are the important mutations in melanoma?

A

Ras/Raf/MAPK signalling pathways

~50% of melanomas have activating BRAF mutations

41
Q

Which drugs target the mutated form of BRAF?

A

Vemurafenib and dabrafenib

42
Q

Apart from verumafenib and dabrafenib what type of drugs are starting to be used in melanoma?

A

Target MEK

Trametinib

43
Q

What gene determines how pigmented we are?

A

MCR1 gene
1 defective = freckles
2 defective = freckles + red hair

44
Q

What are actinic lentigines?

A

Age or liver spots, related to UV exposure

45
Q

What are junctional naevi?

A

Melanocyte nests develop along the dermal epidermal junction

46
Q

What are compound naevi?

A

Juntional clusters and dermis involvement

47
Q

Junctional naevi, compoun naevi, and _______ naevi

A

Intradermal naevi

48
Q

What are the two clinical settings of dysplastic naevi?

A

Sporadic

Familial (lifetime MM risk 100%)

49
Q

What are the rarer naevi?

A

Halo naevi
Blue naevi
Spitz naevi

50
Q

Is malignant melanoma entirely dependant on UV exposure?

A

No, it is mostly dependant on UV exposure but it is multi factorial and genetics also plays a role

51
Q

What are the 4 main types of melanoma?

A

Superficial spreading
Acral/mucosal letigo
Letigo maligna
Nodular

52
Q

What is melanoma prognosis largely related to?

A

Breslow thickness

53
Q

Define breslow thickness

A

The distance between the upper layer of the epidermis and the deepest layer of the cancer
In ulcerated cancers measurement is from the base of the ulcer

54
Q

What is seborrhoeic keratosis?

A

Benign profliferation of the epidermal keratinocytes

55
Q

What are the 3 main types of basal cell carcinoma?

A

Nodular
Superficial
Infiltrative

56
Q

How are BCCs described?

A

Slow growing
Locally destructive
Poorly defined margins

57
Q

What is Bowen’s disease?

A

A precursor of SCC

Scaly patch, irregular border, no dermal invasion

58
Q

What is actinic keratosis?

A

A precursor of SCC
Sun exposed skin
several atypical bowenoid lesions

59
Q

Where do SCCs occasionally arise?

A

Chronic leg ulcers

Sites of burn

60
Q

Adverse prognostic features of SCC

A

> 4mm
Vessel invation
Perineural spread

2019/2020 Alcohol CLASP and Derm (4 decks)

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