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2nd Year > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is the largest organ in the body?

A

Skin

10% of body mass of average person

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2
Q

Hair Cycle:

What is the anagen stage?

A

Active growing phase

80-90% of hair

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3
Q

Hair Cycle:

What is the Catagen stage?

A

2-3 week phase growth stops/follicle shrinks

1-3% of hair

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4
Q

Hair cycle:

What is the Telogen stage?

A

Resting phase for 1-4 months

up to 10% of hairs in a normal scalp

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5
Q

What are the functions of the Skin?

A
  1. Thermoregulation - insulation, heat transfer
  2. Skin immune system - innate and adaptive functions
  3. Barrier - protects against mechanical, chemical, microorganism, UV light and keeps in water and electrolytes, macromolecules.
  4. Sensation - temp, touch and pain
  5. Vitamin D synthesis - UV light converts 7-dehydrocholesterol to cholecalciferol
  6. Interpersonal Communication - physical appearance, smell, self-identity
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6
Q

What is skin disease important? (5Ds)

A 
Disfigurement 
Discomfort 
Disability 
Depression 
Death
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7
Q

What are the 2 different causes of skin disease?

A
  1. External - temp, UV, chemical (allergen or irritant), infection, trauma
  2. Internal - systemic disease, genetics, drugs, infection
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8
Q

What are the external causes?

A
  1. Photosensitivity - medications.
    Exposed sites affected
    - can be sensitive to UVA, UVB, visible light or a combination.
  2. Cold injury - frostbite, chilblains, skin necrosis, cold urticaria.
  3. Trauma - dermatitis artefacta
  4. Genetic
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9
Q

What are the internal causes?

A
  1. Drug reaction - vary in severity - good history needed. (OTC drugs)
  2. Autoimmune - bullous pemphigoid
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10
Q

How we describe skin lesions: 1. What is a small circumscribed area?

  1. Larger circumscribed area?
  2. Small raised area?
  3. Larger raised area?
A
  1. Macule
  2. Patch
  3. Papule
  4. Plaque
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11
Q

Describing skin lesions:

  1. What is small fluid filled?
  2. Large fluid filled
  3. Small pus filled
  4. Larger pus filled
  5. Loss of epidermis
  6. Loss of epidermis and dermis
A
  1. Vesicle
  2. Bulla
  3. Pustule
  4. Abscess
  5. Erosion
  6. Ulcer
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12
Q

When would someone present with eruptive xanthoma?

A

When hyperlipidaemia is present

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13
Q

When would someone present with Acanthuses nigricans?

A

Insulin resistance
Obesity
Malignancy
(Hyperkeratosis and hyper pigmentation papules - velvety appearance)

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14
Q

What is thyroid skin disease?

A

Pretibial myxoedema
5% of graves disease
Skin chunks filled with mucinosis

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15
Q

What investigations are carried out if bacterial infection is suspected?

A

Charcoal swab

MC&S - microscopy, culture and sensitivities

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16
Q

What investigations are carried out if viral infection is suspected?

A

Viral swab for PCR
Can swab vesicle/bulla if vesicular eruption
If systemic illness, can take throat swab

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17
Q

What investigations are carried out if fungal infection is suspected?

A 
Skin scraping
Nail clipping 
Hair sample 
Fungal cultures
(skin biopsy used for all)
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18
Q

What happens when the technical barrier to infection fails in the skin?

A

Sepsis

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19
Q

What happens when there is failure in temperature regulation of the skin?

A

Hypo and hyper thermia

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20
Q

What happens when the fluid and electrolyte balance of the skin fails?

A

Protein and fluid loss
Renal impairment
Peripheral vasodilation

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21
Q
  1. What is Erythroderma?

2. What causes it?

A
  1. Any inflammatory skin disease affecting over 90% of total skin surface
  2. Psoriasis, Eczema, Drugs, cutaneous lymphoma, hereditary disorders, sometimes unknown
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22
Q

What drug is known to cause “red man syndrome”

A

Vancomycin

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23
Q

What is the management plan for Erythroderma?

A
  • Appropriate setting - ITU or burns.
  • Remove any offending drugs
  • Careful fluid balance
  • Good nutrition
  • Temp regulation
  • Emollients 50:50 liquid paraffin: White soft paraffin
  • Oral and eye care
  • Anticipate and treat infection
  • Manage itch
  • Treat underlying cause
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24
Q

How common are drug reactions?

A

Common - 5% inpatients

  • can occur to any drug
  • commonly 1-2 weeks after drug (72 hours if re-challeged)
25
Q
  1. What are mild drug reactions?

2. What are severe drug reactions?

A
  1. Mild - Morbilliform exanthem

2. Severe - Erythroderma, Stevens Johnson Syndrome/ Toxic epidermal necrolysis, DRESS

26
Q

What is Stevens Johnson syndrome <10% / Toxic epidermal necrolysis 30% of surface epidermal detachment?

A

2 conditions thought to be on same spectrum - RARE.

Secondary to drugs: antibiotics, anticonvulsants, allopurinol, NSAIDs

27
Q

SJS clinical features

A
  • Fever, malaise, arthralgia,
  • Rash - maculopapular, target lesions, blisters, erosions covering <10% of skin surface
  • Mouth ulceration
  • Ulceration of other mucous membranes
28
Q

Toxic Epidermal Necrolysis clinical features

A
  • Often presents with prodromal febrile lines
  • Ulceration of mucous membranes
    Rash - macular, purpuric or blistering.
29
Q

What is the prognosis for 1. SJS and 2. TEN?

A
  1. Mortality up to 10%
  2. Mortality up to 30%
    - SCORTEN used for mortality risk.
30
Q

Long term complications of TENS and SJS

A 
Pigmentary skin changes 
Scarring 
Eye disease and blindness 
Nail and hair loss 
Joint conjectures
31
Q

What is Erythema Multiform?

A

Hypersensitivity reaction usually triggered by infection (most commonly HSV)

  • abrupt onset of up to 100s of lesions over 24hr (distal to proximal)
  • Target looking lesions
  • self limiting and resolves over 2 weeks.
32
Q

What is DRESS?

A

Drug reaction with Eosinophilia and Systemic Symptoms:

Onset 2-8 weeks after drug exposure, fever and widespread rash, eosinophilia and deranged liver function.

33
Q

Management for DRESS

A

Stop causative drug
Symptomatic and supportive
Systemic steroids
(plus and minus immunosuppression or immunoglobulins)

34
Q

Clinical features of Pemphigus

A 
Antibodies targeted at desmosomes
Skin - flaccid blisters, rupture very easily 
Intact blisters may not be seen 
Common sites - face, axillae, groins 
ill defined erosions in mouth 
Can affect eyes, nose and genital areas.
35
Q

Differences between Pemphigus and Pemphigoid

A

Pemphigus:
Uncommon, middle aged, blisters very fragile, mucous membranes usually affected, patients may be very unwell, TREAT with systemic steroids, dress erosions, supportive therapies.

Pemphigoid:
Common, elderly patients, blisters often intact and tense, patients fairly well, topical steroids may be sufficient if localised - systemic usually required if diffuse.

36
Q

What is Eczema Herpeticum?

A

Disseminated herpes virus infection on a background of poorly controlled eczema.

37
Q

Presentation and management for Eczema Herpeticum

A

Monomorphic blisters and “punched out” erosions - generally painful, not itchy., fever, lethargy.
Treatment: Aciclovir (IV or orally) Mild topical steroid if required. Treat secondary infection.

38
Q

What is Staphylococcal Scalded skin syndrome?

Presentation and treatment.

A

Initial Staph. infection.
(Common in children, or immunocompromised adults)
Erythematous rash with skin tenderness, blistering and desquamation, fever, irritability.
Admission fo IV antibiotics initially and supportive care.

39
Q

What is Urticaria?

A

Weal, wheal or Hive - central swelling of variable size, surrounded by erythema. Dermal oedema.
Itching, burning, fleeting nature. (1-24hr)
Angiodema - deeper swelling of skin or mucous membranes.

40
Q

Treatment for acute Urticaria

A

Oral antihistamine - 4 x dose
Short course of oral steroid
Avoid opiates and NSAIDs.

41
Q

How does cutaneous lupus present?

A

Butterfly rash
Plaques with clear margins
Photosensitivity
Negative antibodies

42
Q

What is Alopecia?

How is it treated?

A 
1. Alopecia areata - autoimmune. 
T-lympocyte, cytokine rejection of hair. 
- totalis 
- universalis 
Differential dx 
Scarring alopecia 
Androgenic alopecia 
2. topical corticosteroids and patient care with wigs etc.
43
Q

How is Lupus treated?

A

Hydroxychloroquine
non-steroidal anti-inflammatory drug
Corticosteroids
Lifestyle changes

44
Q

What is vitiligo?

How is it treated?

A 
Segmental
Generalised 
Destruction of melanocytes 
Associated with other autoimmune conditions 
2. topical steroids, phototherapy
45
Q

What is acanthosis nigricans?

A

Can precede malignancy (GI adenocarcinoma) products, concern if:
older patient, rapid onset, involves lips and weight loss. (elephants trunk)

46
Q

What is Dermatomyositis?

A

Inflammatory myopathy and rash

  • Periorbital heliotrope rash
  • Gottrons papules: red maculo-papular lesions over bony prominences
  • Shawl sign
  • photosensitive
  • associated with ovarian, breast and lung cancer
47
Q

What is normal body temp and how is it maintained?

A

Core temp = 37

Maintained by balancing heat loss and heat gain

48
Q

What 4 things are involved in thermal balance?

A 
Convection = fluid conduction both ways 
Conduction = heat transfer direct from objects both ways 
Radiation = both ways heat loss and gain 
Evaporation = sweating loss only
49
Q

Where are peripheral thermoreceptors?

Where are central thermoreceptors?

A
  1. Located in skin

2. Located in spinal cord, abdominal organs and hypothalamus

50
Q

How does the body respond to cold street?

A

Heat generated in body is increased by:
General metabolism
Voluntary muscular activity
Shivering thermogenesis.

51
Q

How is heat loss from body reduced?

A

Vasomotor control-
sympathetic arteriolar constriction reduces delivery of blood to the skin
Behavioural responses -
reducing surface area, adding clothing, moving to warmer environment

52
Q

What is hypothermia?

Who is at risk?

A

A fall in deep body temperature to below 35.

Neonates, elderly, cold store workers, outdoor pursuits,vagrants, north sea workers

53
Q

What is the treatment for hypothermia?

A

Dry/insulate to prevent further heat loss
Slow re-warming with bag/blankets
Internal re-warming with hot drinks and warm air
Fast re-warming by immersion in water.

54
Q

What responses do our bodies take to cold stress?

A

Frost bite
Vascular - vasoconstriction - promotes thrombosis - increased blood viscosity
Cellular - ice crystals form in extracellular space - cell dehydration and death

55
Q

Heat production is minimised by what?

A

Decreased physical activity

Decreased food intake

56
Q

What increases heat loss from the body?

A

Vasomotor control - arterial dilation
Sweating - increases evaporation
Behavioural responses - Remove clothing

57
Q

How does our body respond to heat stress?

A

Heat exhaustion
- body temp raised, vasodilation, symptoms including headache, confusion, nausea.
Heat stroke - Raised above 40, control mechanisms fail. = collapse.

58
Q

How do you treat Heat stress?

A 
Move to cool environment 
Remove clothing 
Fan 
Sponge with tepid water 
Give fluids
59
Q

What is a fever?

A

Part of the body’s mechanism for fighting infection
Caused by endogenous pyrogens
Concept of set point controlled by hypothalamus
Analogy of a thermostat that has been reset
Body temp regulates around a higher than normal body temp
Mild fever = beneficial
Severe = dangerous

2nd Year (27 decks)

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