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PHASE 2A (Mine) > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are the key functions of the skin?

A 
Barrier to infection
Thermoregulation
Protection against trauma
Protection against UV
Vitamin D synthesis
Regulate H2O loss
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2
Q

Where does normal proliferation of the skin ovvur?

A

In the basal layer

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3
Q

What is desquamation?

A

Shedding of mature corneocytes from the skins surface to balance the introduction of new cells.

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4
Q

What is the pH of the skin?

A

5.5

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5
Q

What causes desquamation?

A

Degradation of the extracellular corneo-desmosomes under the action of protease enzymes

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6
Q

What are the 3 main layers of the skin?

A

Epidermis (top layer
Dermis
Hypodermis (Subcutaneous fat)

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7
Q

What does the epidermis consist of?

A

Layers of keratinocytes undergoing terminal maturation.

Non-keratinocyte cells: Melanocytes, Langerhans cells, Merkel cells

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8
Q

What is the stratium corneum and what does it consist of?

A

The outermost part of the epidermis.
Made up of corneo-desmosomes (adhesion molecules) and desmosomes which keep the corneocytes together (brick and iron rod model)

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9
Q

What are corneocytes?

A

Terminally differentiated keratinocytes that compose most of the stratum corneum.

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10
Q

What is the action of melanocytes?

A

Responsible for melanin production and pigment formation

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11
Q

What is the action of Langerhans cells?

A

Antigen-presenting dendritic cells

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12
Q

What is the action of Merkel cells?

A

Sensory mechanoreceptors.

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13
Q

What is cornification?

A

Differentiation of keratinocytes into corneocytes (dead cells) to create a physical barrier for the skin.

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14
Q

What are the layers of the epidermis?

A 
Stratum basale
Stratum spinosum
Stratum granulosum
Stratum lucidum
Stratum corneum
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15
Q

How long does a keratinocyte typically take to travel from the stratum basale to the stratum corneum of the epidermis?

A

30-40 days

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16
Q

What are the layers of the dermis?

A

The superficial papillary layer and the deeper reticular layer

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17
Q

What are the features of the reticular layer of the dermis?

A

Thick with thick bundles of collagen fibres that provide more durability.

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18
Q

What structures are present in the dermis?

A 
Fibroblasts
Mast cells
Blood vessels
Cutaneous sensory cells
Skin appendages
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19
Q

What are the actions of fibroblasts in the dermis?

A

Synthesise the extracellular matrix

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20
Q

What are the different types of skin appendages?

A

Hair follicles
Nails
Sebaceous and sweat glands.

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21
Q

Where are the skin appendages derived from and where do they present?

A

Derived from the epidermis and descend into the dermis during development.

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22
Q

What are holocrine secretions?

A

Mode of secretion by exocrine glands: Secretions are produced in the cytoplasm and released by the rupture of the plasma membrane which destroys the cell and releases the product into the lumen.

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23
Q

What is the hypodermis?

A

The tissue immediately deep to the dermis that is major body store of adipose tissue.

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24
Q

What are Meissner’s corpuscles and where are they?

A

Mechanoreceptors that can sense light touch.

Found in upper dermis

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25
Q

What are Pacinian corpuscles and where are they?

A

Receptors responsible for pressure and vibration found in the deep dermis

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26
Q

What are the most common causes of itch with rash?

A

Urticaria (hives)
Atopic eczema
Psoriasis
Scabies

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27
Q

What are the most common causes of an itch with NO rash?

A 
Renal failure
Jaundice
Iron deficiency
Lymphoma (Hodgkins)
Polycythaemia
Pregnancy
Drugs
Diabetes
Cholestasis
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28
Q

What are pilosebaceous units?

A

Dimples in the skin the contain hair follicles and sebaceous glands.

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29
Q

What do sebaceous glands produce and how?

A

Natural skin oils and sebum via holocrine secretion into the hair follicle shaft.

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30
Q

What causes acne?

A

Increased production of sebum, trapping keratin (dead skin cells) and causing blockage of the pilosebaceous unit, leading to swelling and inflammation.

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31
Q

What increases the production of sebum?

A

Androgenic hormones (why it is exacerbated by puberty)

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32
Q

What are swollen/ inflamed units of acne called?

A

Comedones.

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33
Q

What bacteria is thought to play a role in acne and how?

A

Propionibacterium acnes bacteria–> colonises the skin and excessive growth is thought to exacerbate acne.

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34
Q

What is the key presentation of acne?

A

Red, inflamed, sore spots on skin, typically across face, upper chest and upper back.
Can vary greatly in severity.

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35
Q

What are

  1. Macules
  2. Papules
  3. Pastules?
A
  1. Macules= flat marks on the skin
  2. Papules= small lumps on the skin
  3. Pastules= small lumps containing yellow pus
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36
Q

What are the steps in acne treatment?

A
  1. No treatment if mild
  2. Topical benzoyl peroxide
  3. Topical retinoids
  4. Topical antibiotics
  5. Oral antibiotics
  6. Oral contraceptive pill
  7. Oral retinoids (e.g. isotretinoin)
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37
Q

What is the action of topical benzoyl peroxide?

A

Reduces inflammation, helps unblock the skin and is toxic to P.acnes bacteria

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38
Q

What is the action of topical retinoids?

A

Slow the production of sebum

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39
Q

Why do women of childbearing age need reliable contraception when taking retinoids?

A

They are highly teratogenic (cause birth defects)

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40
Q

What is the most common variant of acne?

A

Acne vulgaris.

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41
Q

What is eczema?

A

A chronic atopic condition caused by defects in the normal continuity of the skin barrier, causing inflammation of the skin.

42
Q

How and when does eczema usually present?

A

Usually presents in infancy with dry, red, itchy and sore patches of skin over the flexor surfaces (inside of elbows and knees) and on the face and neck. Usually get flares.

43
Q

What is the other name for eczema?

A

Dermatitis

44
Q

What causes eczema?

A

Defects in the skin barrier allow entrance to irritants, microbes and allergens that create an immune response, resulting in inflammation and symptoms.

45
Q

How is eczema managed?

A

Emollients to create artificial skin barrier
Avoid activities that break down skin barrier (e.g. hot water, scrubbing skin, soaps and body washes)
Avoid environemental triggers

46
Q

How can eczema flares be treated?

A

Thicker emollients
Topical steroids
Wet wraps (covering affected areas in emollient and applying wrap to keep moisture locked in overnight)

47
Q

What is the general rule with emollient treatment?

A

Use emollients that are as thick as can be tolerated/

48
Q

What is the general rule with topical steroids to treat eczema?

A

Use the weakest steroid for the shortest period required to get the skin under control.

49
Q

What are the risks with using topical steroids?

A

Can lead to thinning of the skin, which makes it more prone to flares, bruising, tearing, stretch marks and telangiectasia. There may also be systemic absorption of the steroid.

50
Q

What is the steroid ladder from weakest to most potent?

A

Mild: Hydrocortisone
Moderate: Eumovate
Potent: Betnovate
Very potent: Dermovate

51
Q

What are the main complications of eczema?

A 
Opportunistic bacterial infection (e.g. Staph. aureus) 
Eczema herpeticum (viral skin infection caused by herpes simplex virus)
52
Q

What are the two types of eczema?

A

Endogenous–> atopic (due to hypersensitivity)

Exogenous–> Contact dermatitis usually precipitated by chemicals, sweat and abrasives

53
Q

What is psoriasis?

A

Chronic inflammatory autoimmune condition that causes skin lesions due to hyper-proliferation of keratinocytes and inflammatory cell infiltration.

54
Q

What is the appearence of psoriasis?

A

Patches of dry, flaky, scaly, faintly erythematous (red) skin lesions that appear in raised and rough plaques.

55
Q

Where does psoriases typically present?

A

Over extensor surfaces of elbows and knees and on scalp.

56
Q

What causes the skin changes in psoriasis?

A

Rapid generation of new skin cells, resulting in an abnormal buildup and thickening of the skin in those areas

57
Q

What are the different types of psoriasis?

A

Plaque psoriasis–> Thickened erythematous plaques with silver scales commonly seen on extensor surfaces and scalp. (most common type)
Guttate psoriasis–> Second most common type that commonly occurs in children. Presents with many small raised papules across trunk and limbs.
Pustular psoriasis–> Rare severe form where pastules form under areas of erythematous skin.
Erythrodermic psoriasis–> Rare severe form with extensive erythematous inflamed areas covering most of the skins surface.

58
Q

What are the specific signs suggestive of psoriasis?

A 
Auspitz sign (small points of bleeding when plaques are scraped off)
Koebner phenomenon (development of psoriatic lesions to areas of skin affected by trauma) 
Residual pigmentation after lesions resolve
59
Q

How is psoriasis managed?

A 
Topical steroids
Topical vitamin D analogues
Topical dithranol
Topical calcineurin inhibitors
Phototherapy 
It can be difficult to treat and psychosocial support is important
60
Q

What are the key psoriarisis complications/ associations?

A

Nail psoriasis
Psoriatic arthritis
Psychosocial implications
Other co-morbidities

61
Q

What causes arterial ulcers?

A

Poor blood supple to the skin due to peripheral arterial disease

62
Q

What causes venous ulcers?

A

Pooling of blood and waste products in the skin secondary to venous deficiency (varicose veins, DVT e.t.c.)

63
Q

What causes ulcers?

A

When small wounds (e.g. tiny cut or pressure sore) cannot heal properly due to poor blood supply. It progressively gets larger and more difficult to heal and can potentially cause complications such as infection.

64
Q

What distinguidhes an arterial ulcer?

A 
Absent pule
Pallor
Tend to be smaller
More regular border
Grey colour (poor blood supply)
Less likely to bleed
More painful 
Pain at night when legs elevated
Pain worse when elevated
65
Q

What distinguishes a venous ulcer?

A 
Oedematous flushed skin
Hyperpigmentation to skin
Varicose eczema
Tend to be larger
Irregular border
More likely to bleed
Pain relieved by elevation and worse on hanging.
66
Q

What is an ulcer?

A

Loss of skin below the knee on the leg or foot that takes 2 or more weeks to heal.

67
Q

How are ulcers managed?

A

Treat underlying cause (arterial or venous disease)
Good wound care (debridement, cleaning, dressing, antibiotics)
Plastic surgery if severe.

68
Q

What causes the majority (80%) of ulcers?

A

Venous pathology

69
Q

What causes ulcers?

A 
Venous insufficiency
Arterial insufficiency 
Pressure ulcers
Diabetic neuropathy. 
Infection
Trauma
Vasculitis
Malignancy
70
Q

Where are venous ulcers typically found?

A

Gaiter region of leg (just above ankle to below knee)

71
Q

Where are arterial ulcers typically found?

A

Distally at sites of trauma and in pressure areas (e.g. heel) or higher up the leg.

72
Q

How can venous/ arterial ulcers be diagnosed?

A

Clinically

Doppler ultrasound

73
Q

What are neuropathic ulcers like?

A

Painless ulcers that form on pressure points on the limb. Typically punched out appearance.

74
Q

What are the main types of skin cancer?

A

Basal cell carcinoma
Melanoma
Squamous cell carcinoma
Breast cancer

75
Q

What is squamous cell carcinoma?

A

Locally invasive malignant tumour of the squamal keratinocytes (outermost keratinocytesin the epidermis).

76
Q

How does squamous cell carcinoma typically present?

A

On sun-exposed sites later in life.

Keratotic ill-defined nodules that may ulcerate and can grow rapidly.

77
Q

How is squamous cell carcinoma treated?

A

Surgical excision

Radiotherapy

78
Q

What is the most common malignant skin cancer?

A

Basal cell carcinoma

79
Q

Why does BCC occur?

A

UV radiation triggers changes in the basal cells in the epidermis, resulting in uncontrolled growth

80
Q

What can BCC look like?

A
  • Open sore that doesnt heal
  • Shiny bump/ nodule
  • Reddish patch/ irritated area
  • Scar-like area
  • Small pink growth with slightly raised, rolled edged and crusted indentation
81
Q

How is BCC treated?

A

Surgically excised with wide borders and histology to ensure clear and adequate tumour margins.
Cyrotherapy
Photodynamic therapy

82
Q

When does SCC occur?

A

When DNA damage from exposure to UV radiation of other damaging agents trigger abnormal cheanges in the squamous cells of the epidermis.

83
Q

What does SCC look like?

A
  • Scaly red patches with irregular borders
  • Open sore that bleeds or crusts
  • Elevated growth with central depression
  • Wart- like growth that crusts
84
Q

Why is melanoma more dangerous than BCC and SCC?

A

Because of its ability to spread to other organs more rapidly if not treated early. (Most malignant skin cancer)

85
Q

Why does melanoma occur?

A

When DNA damage due to UV radiation causes mutations in melanocytes, resulting in uncontrolled cellular growth.

86
Q

What are the two types of melanin and what is the difference?

A

Eumelanin and pheomelanin. Only eumelanin attempts to protect the skin by releasing melanin causing it to tan (Darker skinned people have more eumelanin and so are at less risk of melanoma)

87
Q

What does melanoma look like?

A

Can present in many different shapes, sizes and coulours. >95% show very dark colour/ black in part of lesion

88
Q

ABCE symptoms to diagnose melanoma?

A 
Asymmetrical shape
Border irregularity
Colour irregularity
Diameter
Elevation/ evolution
89
Q

What are the different types of melanoma?

A
  1. Superficial spreading (most common form that usually arises in a mole)
  2. Lentigo maligna
  3. Acral lentiginous (most common in people of colour)
  4. Nodular melanoma (most aggressive type)
90
Q

How is melanoma treated?

A 
Surgical excision (only curative in early cases) 
For metastatic disease--> Removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemotherapy.
91
Q

What is cellulitis?

A

An infection of the skin and soft tissue underneath

92
Q

What causes cellulitis?

A

A breach in the skin barrier allowing a point of entry for bacteria. (e.g. trauma, eczema, fungal nail infection, ulcers)

93
Q

How does cellulitis present?

A 
Erythema
Warm to touch
Tense/ thickened
Oedematous
Bullae (fluid filled blisters)
Golden-yellow crust (indicates staph. aureus infection)
94
Q

What are the most common causes of cellulitis?

A

Staph. aureus
Group A and Group C Streptococcus
MRSA

95
Q

How is cellulitis treated?

A

Flucloxacillin. (antibiotic that is very effective against staph and gram positive infections)

96
Q

What is necrotising fasciitis?

A

A rare but serious bacterial infection that affects the fascia (sub-cutaneous tissue)

97
Q

What does necrotising fasciitis cause?

A

Bacteria release toxins that cause necrosis of the fascia, fat and eventually skin

98
Q

What are the main symptoms of necrotising fasciitis?

A

Intense pain that is out of proportion to skin damage
Flu-like symptoms (fever)
Small but painful cut/ scratch
May develop swelling and redness, diarrhoea/ vomiting, dark blotches.

99
Q

How is necrotising fasciitis treated?

A

Surgery to remove infected tissue
Antibiotics
Supportive treatment

100
Q

What is the outlook for necrotising fasciitis?

A

1-2 in every 5 cases is fatal.

Can progress very quickly

101
Q

What causes necrotising fasciitis?

A

When bacteria get into deep tissue, either through the bloodstream or an injury or wound.

PHASE 2A (Mine) (15 decks)

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