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Dermatology Theoretical (no Pic) > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is bullous pemphigoid?

A

Bullous pemphigoid is a rare skin condition that mainly affects older people. It usually lasts a few years, treatment can help manage the condition in most cases.

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2
Q

Available treatments for bullous pemphigoid?

A

Bullous pemphigoid is most commonly treated with corticosteroids. These can be taken by mouth in addition to topically applied creams. Antibiotics or other anti-inflammatory medications may also be useful in mild cases. Severe cases may require the use of immunosuppressant medications

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3
Q

Cause of bullous pemphigoid?

A

Bullous pemphigoid is caused by a problem with the immune system (the body’s defence against infection). Instead of attacking germs, it attacks and damages the skin. It’s not known why this happens. Sometimes it’s been linked to skin damage (such as sunburn) or taking certain medicines.

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4
Q

What is pemphigus vulgaris?

A

Autoimmune skin condition resulting in non-pruritic intra-epidermal bullae. ( vulguare condition / very bad )

Median age onset 40-60 y

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5
Q

Pemphigus vulgaris symptoms and key diagnosis

A
  • Bullae erupt rapidly (may present with erosions)
  • Nikolsky sign present (pressure erupts bullae)
  • Asboe-Hansen sign present (pressure rises Bullae)
  • painful blisters that start in the mouth or skin areas. ( key diagnosis )
  • skin blisters near the surface of the skin that come and go.
  • oozing, crusting, or peeling at the blister site.
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6
Q

Pathophysiology of Pemphigus vulgaris?

A

Production of igG antibodies to superficial (surface proteins) desmoglein -3.
Targets the very superficial skin layer that’s why the outside of the bullae is so weak because it’s already weakens from the IgG antibodies. ( positive signs in symptoms )

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7
Q

Risk factors for developing pemphigus vulgaris

A

1) Genetics (Jewish and Asian population)
2) regular use of medication (Penicillamine, captopril etc….)
3) history of auto immune disorders

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8
Q

Diagnosis of Pemphigus vulgaris.

A
  • Histopathology
  • skin biopsy with direct and indirect immunofluorescence and enzyme-linked immunosorbent assay (ELISA) testing.
  • immunofluorescence (intra epidermal deposition of IgG and C3
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9
Q

Treatment for Pemphigus vulgaris

A

There’s no cure but treatment can help keep symptoms under control.

  • Corticosteroids such as prednisone
    Recommended
  • immunosuppressant such as rituximab
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10
Q

Types of pemphigus

A 
Pemphigus vulgaris.
Pemphigus foliaceus
Pemphigus vegetans
Paraneoplastic pemphigus
Pemphigus erythematosus
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11
Q

What antibodies are present in Pemphigus vulgaris?

A

Desmoglein 3

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12
Q

What antibodies are present in Pemphigus foliaceus?

A

Desmoglein 1

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13
Q

What antibodies are present in Dermatitis herpetiform?

A

Epidermal transglutaminase, gliadin, endomysium

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14
Q

What antibodies are present in bullous Pemphigus?

A

Bp-1 and Bp-2

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15
Q

Is there possibility of biological treatment of bullous disease?

A

Yes

Rituximab

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16
Q

Cutaneous manifestation of coeliac disease is ______________?

A

Dermatitis herpetiforms

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17
Q

Characteristics localisation of skin-lesions in dermatitis herpetiforms?

A

Elbows, knees (joints) and buttocks

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18
Q

Treatment for dermatitis herpetiforms?

A

dapsone (antibiotic) and a gluten free diet

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19
Q

What is the less severe form of Pemphigus?

A

Pemphigus foliaceus

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20
Q

An autoimmune blistering skin disease which occurs during pregnancy is called an a) _____________, which occurs in b)____________ trimester.

A

A) Gestation Pemphigoid

B) 3rd (2nd-3rd)

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21
Q

what is the Raynaud’s phenomenon

A

A phenomenon that causes decreased blood flow to the fingers. This happens due to spasms of blood vessels in those areas
Skin becomes white, then blueish to black in colour.

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22
Q

What are the most common localisation of skin lesions in subacute cutaneous lupus erythematosus?

A

sun-exposed areas such as the face, ears, neck, arms, and legs.

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23
Q

What antibodies are present in systemic lupus erythematosus?

A

SS-A (Ro)

Also know as Anti-Ro/SSA

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24
Q

What antibodies are present in subacute cutaneous lupus? (Discoid Lupus Erythematosus)

A

U1-RNP 100

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25
Q

What is Psoriasis?

A

A chronic non-infectious inflammatory skin condition.

Clearly defined, erythema + silver scaly plaques.

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26
Q

Causes of psoriasis?

A
  • Genetics (having 1 parent = 16% of offspring, 2 parents = 50% of offspring)
  • Weather (especially cold, dry conditions)
  • Injury to the skin, such as a bug bite or severe sunburn.
  • Smoking.
  • Heavy alcohol consumption.
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27
Q

Treatment of psoriasis?

A

There is no cure to psoriasi and topical treatment is used for mild psoriasis

  • coal tar prep (scalp psoriasis)
  • Dithranol
  • Salicylic acid
  • Vitamin D analog
  • Topical corticosteroids
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28
Q

Name the 4 psoriasis autoantigens

A

cathelicidin LL-37
melanocytic ADAMTSL5
lipid antigen PLA2G4D
keratin 17.

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29
Q

Most severe form of psoriasis?

A

Erythrodermic psoriasis

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30
Q

Types of psoriasis?

A
  • Guttate Psoriasis
  • Pustular Psoriasis
  • Plaque Psoriasis
  • Inverse Psoriasis
  • Erythrodermic Psoriasis
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31
Q

Types of lupus erythematosus

A

systemic lupus erythematosus (SLE)
lupus erythematosus induced by drugs (DILE)
discoid lupus erythematosus (DLE)
neonatal lupus erythematosus (NLE)

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32
Q

Skin lesions:

  1. Primary morphology
  2. Flat
  3. <10 mm
A

Macule

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33
Q

Skin lesions:

  1. Primary morphology
  2. Flat
  3. > 10 mm
A

Patch

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34
Q

Skin lesions:

  1. Primary morphology
  2. Flat
  3. > 10 mm
A

Patch

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35
Q

Skin lesions:

  1. Primary morphology
  2. Raised
  3. <5 mm
A

Papule

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36
Q

Skin lesions:

  1. Primary morphology
  2. Raised
  3. > 20 mm
A

Plaque

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37
Q

Skin lesions:

  1. Primary morphology
  2. Raised
  3. Constituency = Liquid filled < 5mm
A

Vesicles

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38
Q

Skin lesions:

  1. Primary morphology
  2. Raised
  3. Constituency = Liquid filled > 5 mm
A

Bulla

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39
Q

Skin lesions:

  1. Primary morphology
  2. Raised
  3. Constituency = Pus filled
A

Pustule

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40
Q

Skin lesions:

  1. Primary morphology
  2. Raised
  3. Constituency = solid
A

Nodule

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41
Q

Skin lesions:

elevated area produced by dermal odema

A

Wheal

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42
Q

Skin lesions:

Localised accumulation of pus in a cavity, > 1cm in diameter

A

Abscess

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43
Q

What do you give along with corticosteroids in psoriasis ?

A

Vitamin D analogs

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44
Q

What is Urticaria (hives, ‘nettle-rash’)

A

Urticaria is a common reaction pattern in which pink, itchy or ‘burning’ swellings (wheals) can occur anywhere on the body. Individual wheals do not last longer than 24 hours, but new ones may continue to appear for days, months or even years.

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45
Q

The various types of urticaria are?

A
  • Ordinary urticaria
  • Physical (Cold, Solar, Heat, Cholinergic etc)
  • Hypersensitivity
  • Autoimmune
  • Pharmacological
  • contact
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46
Q

Cause of urticaria

A

Hyper allergic reaction in your body which causes release of histamines
(Allergic reaction)

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47
Q

Treatment for physical urticaria

A

Eliminate the causes:

  • cold: worm cloths
  • heat: stay away from hot objects and solutions
  • solar: cover yourself from the sun
  • cholinergic: stay in stress and sexual desire free environments
  • Dermograpishm (contact): antihistamine medication (diphenhydramine) and don’t scratch nor rub
  • Pressure: try to not apply pressure to your body
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48
Q

Can you treat physical urticaria with aspirin?

A

NO!!!!!!!!!!!! DONT EVER TREAT IT WITH ASPIRIN

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49
Q

Causes of Erythema Multiforme

A 
Herpes simplex 
Hepatitis A,B,C
Bacterial infections 
Drugs 
Malignancy 
Pregnancy 
Parasitic infestation
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50
Q

Erythema multiform presentation

A
  1. Annular non scaling plaques more purple than urticaria
  2. New lesions often begins on the same place as the original one
  3. Lesions can blister
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51
Q

What is the severe variant of Erythema multiform?

Why is it more severe?

A

Stevens - Johnson’s syndrome

  1. Mucus membrane lesions
  2. Fever and systemic changes
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52
Q

What are Erythema multiforme differential diagnosis?

A
  • urticaria

- other bullous disorders (PV, BP)

53
Q

Treatment of Erythema multiforme?

A
  • minor: antihistamines, topical antibiotics with steroids, Vit C
  • Major: systemic steroids short course, cyclosporine
  • remove the cause
  • good nursing care
54
Q

What is the presentation of Erythema Nodosum?

A
  • Tender red nodule
  • Legs, forearms, rarely face, breasts
  • Painful joints and fever
55
Q

What can Erythema Nodosum cause?

A
  • Inflammation of subcutaneous fat (panniculitis)
  • Immunological reactions:
    Infections (viral, bact, fung)
    Drugs reactions (sulphonamides)
    Systemic disease (sarcoidosis)
56
Q

What are the symptoms of Erythema Nodosum?

A
  • Red, sore bumps on the shins.
  • Fever.
  • Fatigue.
  • Joint pain or swelling.
  • Enlarged lymph nodes in the chest.

Trauma, infection, phlebitis
- biliary lesions: panniculitis from pancreatitis, cold, trauma, injections, lupus erythematosus

57
Q

What is Vasculitis?

A

An inflammation of blood vessels, infection which remains within the vessel wall.

58
Q

Erythema Nodosum treatment

A
  • Eliminate cause
  • Bed rest
  • Drugs: NSAID’s, aspirin, potassium iodide 400-900 mg/d
59
Q

What are the main types of Vasculitis?

A
  • leukocytoclastic vasculitis
  • polyarteritis nodosa (PAN)
  • wegener’a granulomatosis
60
Q

Cause of leukocytoclastic vasculitis?

A
  • PMN leucocytes
  • Activation of complement
  • Immune complexes
61
Q

Presentation of leukocytoclastic vasculitis?

A
  • Painful, palpable purpura (Edema and serum exudation)
  • localisation ( forearms legs buttocks)
  • Henoch Schonlein- Arthritis, abdominal pain, renal disease
  • urticaria Vasculitis - urticaria like lesions which last longer than 24hr leaves bruises and pigmentation
62
Q

Treatment of leukocytoclastic vasculitis

A
  • Eliminate cause
  • Antihistamines
  • Bed rest
  • colchicine, dapsone
  • systemic involvement
  • corticosteroids and immunosuppressive agent
63
Q

What is polyarteritis nodosa? (PAN)

A

Necrotising inflammation of medium sized arteries

64
Q

Presentation of polyarteritis nodosa? (PAN)

A
  • Tender subcutaneous nodules along the lines of the arteries
  • Skin over may ulcerate or develop stellate patches of purpura or necrosis
  • peculiar net like vascular pattern (livedo reticularis)
65
Q

What is the treatment of polyarteritis nodosa? (PAN)

A
  • Systemic steroids

- immunosuppressive agents

66
Q

What are the symptoms of polyarteritis nodosa? (PAN)

A
  • Fever
  • Sweats
  • Weight loss
  • Muscle, joint and abdomen pain
67
Q

What is the cause of Wegener’s granulomatosis?

A

Unknown cause

68
Q

Symptoms of Wegener’s granulomatosis?

A 
fever
weight loss
rhinitis
hearing loss
sinusitis - 50% skin lesions
69
Q

Treatment of Wegener’s granulomatosis?

A

Steroids

Cyclophosphamide

70
Q

What are the clinical characteristics of Drug eruptions

A
  • types of primary lesions
  • distribution and number of lesions
  • mucus membrane Involvement
  • associated signs and symptoms: fever, pruritus, lymph node enlargement
71
Q

What is the main cause of drug eruption?

A

For different drugs there will be different types of eruptions but the cause is:

Immediate reactions occur within an hour of exposure to the drug and are mediated by IgE antibodies this causes clinical symptoms of urticaria and anaphylaxis

72
Q

What drugs are the cause of urticaria and anaphylaxis?

A
  • Penicillins
  • Cephalosporin
  • NSAID’s
  • Monoclonal antibodies
  • Contrast media
73
Q

what is scleroderma?

A

Hardening of skin due to extra collagen production in extremitis

74
Q

What is Morphea?

A

Morphea is a rare autoimmune skin disorder of the connective tissue which can be described as a less severe form of scleroderma, without internal problems.

75
Q

What is the treatment morphea?

A
  • PUVA therapy
  • Clobetasol propionate (corticosteroids)
  • Intradermal mesodermal therapy
  • Calcineurin inhibitors
  • Methatrezane (more severe cases)
76
Q

Is morphea more common in men or women?

A

Women (auto immune disorder which is more common in women)

77
Q

What is treatment of “keratosis pilaris“ ?

A
  • Topical keratolytics (salicylic acid, lactic acid)
  • Retinoids
  • Mechanical peeling
78
Q

Where does keratosis pilaris occur?

A

Located on :

  • buttocks
  • lateral upper arms
  • thighs
  • on perfollicular areola ( which may be pink - red or violet in colour )
79
Q

What is Ichtyosis vulgaris?

A

The most common disorder of keratinization.
Is characterized by mild generalized hyperkeratosis with xerosis in lower extremities and perifollicular hyperkeratosis

Inherited autosomal semidominant disorder

https://www.youtube.com/watch?v=q3BqAmpKx3s&ab_channel=JJMedicine

80
Q

What is ichtyosis vulgaris connected with?

A

With a defect of filaggrin/a component of keratohyalin granules

81
Q

What are the 2 forms of ichtyosis vulgaris?

A

Lack of filaggrin- severe form

Heterozygous filaggrin mutation (filaggrin insufficient) - mild form

82
Q

What are the ichtyoses?

A

The heterogeneous group of disorders characterized by an excess accumulation of cutaneous scale, whose serverity varies from very mild and asymptotic to life threatening

83
Q

Where is keratosis pilaris often present?

A

It is often present on the limbs

84
Q

How does the skin look with ichtyosis vulgaris?

A

Skin is dry and covered by small, brainy scales.

85
Q

Where is ichtyosis vulgaris localized?

A

It is localized on the trunk, limbs. Major flexures may be spared. The skin creases of the palms may be accentuated.
Xerosis and pruritus worsen in winter months

86
Q

When does ichtyosis vulgaris condition improve?

A

Improvement during the summer and in adolescence

87
Q

Where is X linked recessive ichtyosis localized?

A

Trunk
extremities
occasionally flexures
Palms and soles are spared

88
Q

When does x linked recessive ichtyosis occur in humans?

A

It usually appears at birth and persists throughout life.

89
Q

Describe the scales in X linked recessive ichtyosis?

A

The scales are larger and become brownish in first weeks of life in 75% of patients, “dirty neck - effect”

In 25% the scales remain bright

90
Q

What is x linked recessive ichtyosis?

A

It is a rare type of ichtyosis, associated with steroid sulphatase deficiency, an enzyme responsible for conversion of cholesterol sulphate to cholesterol in the granular cell layer.

91
Q

Who does x linked recessive ichytosis affect?

A

Affects only males with the frequency 1 in 2000-6000 males

92
Q

What are associated conditions of X linked recessive ichtyosis?

A
  1. Corneal opacities
  2. Hypogonadism
  3. Anosmia
  4. Neurological defects
93
Q

What is the treatment of x linked recessive ichtyosis?

A

Regular use of emollients, emulsifying ointments, creams or lotions with urea or lactic acid.
Avoidance of degreasing agents.

94
Q

What is lammelar ichtyosis?

A

It is a rare condition inherited as an autosomal recessive disorder (2 types) and as an autosomal dominant disorder (1 type)

95
Q

What is Impetigo?

A

Impetigo is a common and highly contagious skin infection that mainly affects children and young adults.

96
Q

what are the different impetigo types?

A
  • Nonbullous impetigo (honey crust)
  • Bullous Impetigo (Vesicle->Bullae)
  • Ecthyma (More serious, aka ulcerative impetigo)
97
Q

What is the treatment for Impetigo?

A

topical antibiotics such as fusidic acid or mupirocin are prefered, in more serious cases use oral antibiotics such as flucloxacillin, erythromycin or cefalexin (not Penicillin)

98
Q

What is the etiology of Impetigo?

A
  • Bullus Staphylococcus aureus.
  • Nonbullous Impetigo; Group A B - Hemolyticss (s pyogenes) or S. aureus
  • Echtyma is usally a mixture of both.
99
Q

What is Echtyma?

A

Echtyma is a deeper form of impetigo, also known as ulcerative impetigo.

100
Q

what are the characteristics of impetigo?

A
  • Reddish sores often around mouth and nose.
  • Honey-coloured crust erosion
  • Pustules
  • Itchiness and soreness is usually mild
101
Q

what are the characteristics of Echtyma?

A

full thickness ulcers forming under the crusted surface infection and heals with scaring.

102
Q

What are the available treatments for Ecthyma?

A

Antibiotics; e.g. Dicloxacillin or flucloxacillin

103
Q

what is furunculosis?

A

an acute pustular infection of a hair follicle by s.aureus

104
Q

What are the available treatments for Furunculosis?

A
  • Incision and drainage
  • Systemic Antibiotics
  • Improved hygiene
  • Daily baths in antiseptic soap
105
Q

what is Staphylococcal scaled skin syndrome? (SSSS)

A

Staphylococcal scalded skin syndrome (SSSS) is a serious skin infection. The infection causes peeling skin over large parts of the body. It looks like the skin has been scalded or burned by hot liquid.

106
Q

What are the available treatments for Staphylococcal scaled skin syndrome? (SSSS)

A

Systemic antibiotics e.g. flucloxacillin

107
Q

presentation of Staphylococcal scaled skin syndrome? (SSSS)

A

Resembles a scaled burn, horny cell layer shed.

108
Q

What is the etiology of Staphylococcal scaled skin syndrome? (SSSS)

A

s. aureus, this bacterium produces exfoliative toxin.

109
Q

What is erysipelas?

A

Erysipelas is an infection of the upper layers of the skin (superficial). The most common cause is group A streptococcal bacteria, especially Streptococcus pyogenes.

110
Q

What are the available treatments for Erysipelas?

A

Antibiotics, Penicillin administered orally or intramuscularly is sufficient for most cases of classic erysipelas and should be given for 5 days
lincomycin may also be used.

111
Q

What are the different variants of erysipelas?

A
  • Bullosum
  • Haemorrhagicum
  • Gangrenosum
  • Migrans
  • Recivians ( May be followed by elephantiasis)
112
Q

Symptoms and presentation of Erysipelas?

A
  • Abrupt in onset
  • Geral illness, in the form of fevers, chills and shivering.
  • Usually effects lower limb
  • When affects face it can have a butterfly distribution on cheeks and bridge of nose
113
Q

Does psoriasis have a peak of onset?

A

Yes, while it can begin at any age, psoriasis has 2 peaks of onset, the first at age 20 to 30 years and the second at age 50 to 60 years.

114
Q

what is the treatment for Guttate Psoriasis?

A
  • Systemic antibiotic

- Emollients while erupting; then UVB

115
Q

what is the treatment for stable plaque Psoriasis?

A
  • Vitamin D analogue (long term)
  • Local corticosteroid (short term)
  • Corticosteroid–calcipotriol combination
    (short term)
116
Q

what is the treatment for Acute erythrodermic, unstable

or generalized pustular Psoriasis?

A

Inpatient treatment with ichthammol paste
Local steroid may be used initially with or
without wet compresses

117
Q

what is the function of the skin?

A
  • Provides a protective barrier against mechanical, thermal and physical injury and hazardous substances.
  • Prevents loss of moisture
  • Reduces harmful effects of UV radiation
  • Acts as a sensory organ (Touch, detects temperature)
  • Helps regulate temperature
  • An immune organ (SALT)
  • Production of vitamin D
118
Q

Skin as an immunological organ

A

The skin has an immune system that protects the body from infection, cancer, toxins, and attempts to prevent autoimmunity, in addition to being a physical barrier against the external environment.
The skin immune system is sometimes called skin-associated lymphoid tissue (SALT), which includes peripheral lymphoid organs like the spleen and the lymph nodes.
Cellular components of SIS (Skin immune system): Keratinocytes, Langerhans cells, dermal dendritic cells, T lymphocytes, natural killer cells and mast cells.

119
Q

what is the function of hai?

A 
Function:
•	Conservation of heat
•	Protection against UV radiation
•	Protection against minor injury
•	Sexual attraction
•	Cosmetic

Types:
• Terminal/long hairs – thicker and darker found on the scalp, eyebrows, eyelashes, pubic, axillar and beard areas.
• Lanugo hairs – fine and long, are formed in the fetus at 20 weeks gestation. They are normally shed before birth but may be seen in premature babies.
• Vellus hairs – short, light-coloured hairs that cover most body surface

120
Q

What is the function of nails?

A
  • Protection of fingertip
  • Facilitation of grasping and tractile sensitivity in the finger pulp
  • Cosmetic
121
Q

What is the Nikolsky sign?

A

Nikolsky sign is a skin finding in which the top layers of the skin slip away from the lower layers when rubbed. basically the superficial layer of the skin tears away when rubbed.

122
Q

what is Raynaud’s phenomenon?

A

Raynaud phenomenon (RP) is characterized by recurrent spasms of small digital arterioles/arteries at fingers and toes, usually triggered by cold and emotional stress. Clinically a sudden pallor of individual digits is followed by reactive hyperaemia, in severe cases also by cyanosis.

123
Q

what is Koebner phenomenon?

A

The Koebner phenomenon describes the appearance of new skin lesions of a pre-existing dermatosis on areas of cutaneous injury in otherwise healthy skin. It is also known as the Köbner phenomenon and isomorphic response.

The Koebner phenomenon (KP) is basically the appearance of new skin lesions on previously unaffected skin secondary to trauma.

124
Q

Syphilis etiology

A

Treponema pallidum

125
Q

Syphilis transmission

A

(1) intimate contact with a sexual partner or an infectious lesion (most common)
(2) blood transfusion
(3) during delivery of a baby he/she may contract syphilis from the birth canal.

126
Q

Syphilis treatment

A

Penicillin is still the treatment of choice. Procaine penicillin is given parenterally for 10 days in early syphilis and 17 days in late stage disease or in early syphilis with neurological involvement.
Benzithine penicillin can be given as a single intramuscular dose in primary or secondary syphilis.

127
Q

Syphilis stages

A

Inoculation
Primary stage - Button-like ulcerated chancre. Localized lymphadenopathy.

Secondary syphilis - Malaise, Generalized lymphadenopathy, Patchy hair loss, Mucosal patches, Skin eruptions, Condyloma lata

Late syphilis - Neurosyphilis (general paralysis of the insane, tabes dorsalis), Cardiovascular syphilis, Circinate arrangement of skin nodules, Gummata

128
Q

What are the two major causes of Acanthosis nigricans?

A 
Insulin resistance (DM, Cushing's)
Gastric adenocarcinoma
129
Q

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A

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Dermatology Theoretical (no Pic) (1 decks)

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