Tumours (F1) Flashcards
1
Q
LO’s
A
- Describe the pathophysiology, presentation and clinical consequences of tumours of the skin.
- Describe the pathophysiology, presentation and clinical consequences of inflammation of the skin, e.g. eczema and psoriasis.
2
Q
Which cancer is the most common?
A
Skin cancer, so early detection is vital
3
Q
In which layer of the skin are tumours most likely to occur, and why?
A
- The epidermis, because it is in contact with the sun.
4
Q
Name the three major cancers of the skin
A
- Basal Cell Carcinoma
- Squamous Cell Carcinoma of the skin
- Melonoma
- Basal layer cancer = basal cell carcinoma
- The main component of epidermis is stratum spinosum. This can give rise to
- Melanocytes can give rise to melonoma. Normally it produces melanin, to protect DNA from UV radiation.
5
Q
Types of UV light
A
- UVA: can penetrate into the dermis and epidermis. Causes ageing and wrinkling.
- UVB = Can penetrate into the epidermis. Can cause skin to burn.
- UVC= Mostly stopped by the ozone layer.
6
Q
How does UV light damage DNA?
A
- It can directly, and indirectly damage DNA.
- Directly: breaks the bond between A and T. Instead, T and T join together to form a thmyidine dimer.
- Indirectly: it makes free radicals which mediate oxidative DNA damage.
7
Q
What is another name for a benign mole?
A
- Melanocytic nevi
- Can be born with moles = congenital mole
- Normal to aquire moles up to the age of 40 years.
8
Q
How do you clinically differentiate between a benign and malignant mole?
A
- Use the ABCDE criteria:
- Assymetry
- Border: knucke like is irregular
- Colour change
- Diameter: in millimeters
- Evolving: did it grow?
9
Q
Intrinsic risk factors for melanoma?
A
50% of melanomas develop from existing moles and 50% develop from normal skin.
- Fair skin: less melanin made, mans they have less natural sunscreen.
- Increased concentration of melanocytes: people who have more moles, have more opportunities for their moles to mutate.
- Family history of skin cancer: CDKN2A is a gene that codes for p16 protein. This is a tumour suppressor. People with a mutated p16 have uncontrolled cell division.
10
Q
Name and describe the most common melanoma
A
- The most common melanoma is the superficial spreading melanoma.
- It looks like a puddle of brown.
- Normaly it grows horizontal (outwards), but it can invade and spread.
- It occurs in intermittantly sun-exposed areas, like the back and neck.
11
Q
Describe Lentigo Maligna Melanomas
A
- Normally grow horizontally (outwards on skin).
- Also look like a puddle.
- But, unlike the superficial spreading melanoma, the lentigo melanoma appears on always sun exposed areas, like the face and hands.
12
Q
Describe the Nail Melonomas
A
- They can frow both inwards (vertically) and outwards onto the skin (horizontally).
- This means they frequently invade and spread.
- Frequently ignored and misdiagnosed because they look like a nail infection.
13
Q
Describe Amelanotic Melonomas
A
- They have no colour, so are hard to diagnose.
- Also, they grow vertically into the skin.
- This means they frequently invade and spread.
14
Q
Describe the Nodular Melonoma
A
Primarily grow vertically into the skin. It is a burrowing mole.
This means they frequently invade & spread.
15
Q
What are the typical melanoma mimics?
A
- Dysplastic melanocytic nevus: benign moles that just look abnormal.
- Seborrheic Keratosis: waxy, scaly patches on the skin.
- Solar Lentigo: patch of darkened skin.
- Dermatofibroma: a benign, fibrous nodule.
16
Q
Compare the treatment options and survival rate between invasive and non-invasive carcinomas.
A
- Non-invasive melonoma = surgical excision, 98% curative prognosis.
- Invasive melanoma = chemo, 18% 5 year survival.
- B-RAF is mutated to cause cells to always be in the S phase???? see recap
- B-raf inhibitor medication does not work in the long term because the tumour develops aquired.. see RECAP
17
Q
What preventative measures should be taken against skin cancer?
A
- Sunscreen must be be broad spectrum. To protect against UVA, UVB and UVC.
- Use SPF 30 or above.
- Use water resistant sunscreen.
18
Q
What is Atopic Dermatitis?
A
- Allergy mediated/ atopic inflammation of the skin AKA eczema.
- It is a hypersensitivity order, just like allergies and hayfever is.
- Eczema presents on exposed skin and flexor surfaces (where skin bends).
19
Q
Describe the pathophysiology of eczema
A
- Allergen absorbed into the skin.
- Taken up by antigen presenting cell.
- Allergen presented to a naive T cell.
- Naive T cell activates a helper T cell.
- Helper T cell causes a B cell to produce the allergen specific antibody.
- The antibodies sit on mast and basophils. This is sensitisation.
- When the allergen is next come to contact with, the mast cell degranulates to release histamine and leukotrienes.
- This causes the skin to be more leaky, so more water escapes the skin, and more allergen can enter too. This makes it dry and itchy. Itching skin damages it, allowing bacteria to enter and cause infection.
20
Q
What other clinical efffects can eczema and psorasis have?
A
- Eczema allows recurrant skin infections. For example cellulitis, which can lead to sepsis, organ failure and death.
- Sleep disturbance and weight gain.
- Painful movement, so cardiovascular issues and weight gain.
- Anxiety and depression
21
Q
What is psoriasis?
A
- Red plaque with silver sheen
- Red, flaky, crusty patches covered by silvery scales
22
Q
Describe the pathiophysiology of psoriosis
A
see diagram
23
Q
How is psoriasis treated?
A
- Cortiocosteriods: to reduce inflammation, but can cause tissue atrophy.
- Phototherapy: offered sunbed, kills hyperactivated lymphocytes, skin cancer keratinocytes???? see recap
24
Q
Non Melanoma Skin Cancer (NMSC)
A
- Apart from melonoma, people can develop other skin cancers:
- Basal Cell Carcinoma
- Actinic Keratosis
- Squamous Cell Carcinoma
25
Describe Actinic Keratosis Skin Cancer
* Characterised by red, scaly patches that develop in the skin.
* Takes a while to form, so seen in older patients.
* RF: Chronic sun exposure. Found on scalp, face, lips, ears, back of hands,
* Precursor to squamous cell carcinoma.
* But even without treatment, only 0.5% of actinic keratosis will become squamous cell carcinoma.
* Excellant prognosis: 99% cured, using a cream called Imiquimod.
* Imiquimod activated the immune system to recognise the actinic keratosis as cancerous cells that the body needs to get rid of. Makes the cancer cells undergo necrosis.
*
26
How common is each type of skin cancer?
1. Basal cell skin cancer is the most common (75%)
2. Squamous cell skin cancer and Actinic Keratosis (15%)
3. Other skin cancers, like malignant melanoma are rarer.
27
Describe Squamous Cell Carcinoma
* The 2nd most common skin cancer, after BCC.
* Two RFs:
* Long term sun exposure
* Immuno-compromised patients (patients who are elderly, having chemo, or have HIV)
* Elevated growth with a central depression. Looks like a wart.
* Are vascularised (have blood vessels supplying them) so can bleed.
* If non ivasive, then do sugical excision (cut a rugby ball shape out of skin). This has 98% curative prognosis.
* If non-invasive SCC 0.5% of patients progress to invasive SCC.
* Invasive SCC is treated with chemotherapy. Only have 15% 5 year survival.
28
Basal cell carcinoma
* The most common type of skin cancer. (75% of all skin cancers).
* RFS: intermittent sun exposure.
* There are three types of BCC:
* Nodular BCC
* Superficial BCC
* Infiltrative BCC
29
Nodular BCC
* A single nodular growth, that is either pink or flesh coloured.
* Has a pearly/translucent quality.
* Can easily rupture.
* Contained mass that doesn't invade downward.
* Ecxellant prognosis: surgical excision = football shape.
* 99% curative rate after excision.
* Invasion is extremely rare.
30
Superficial BCC
* Grows horizontally, not downwards.
* Can be missdiagnosed as eczema or psoriasis.
* Red scaly plaque.
* Not itchy.
* Ecxellant prognosis: surgical excision = football shape.
* 99% curative rate after excision.
* Invasion is extremely rare.
31
Infiltrative BCC
* Most severe type of BCC.
* Difficult to remove, as they spread over a large area.
* Looks like a tissue injury, like a scar. So is hard to diagnose.
* Is slightly depressed.
* If specialised surgical excision is done has 95% curative rate.
* Invasion only happens 0.5% of the time
* Can be offered drugs/cream if IBCC is on the face, called Sonic Hedgehog Inhibitor.
