Derm

Front 1

1.What's the difference between a macule, papule and vesicle?
2.What do they have in common?

Back 1

1.Macule= flat, papule= elevated and solid, vesicle= circumscribed collection of fluid
2. All are under 5mm

Front 2

1. What's the difference between a patch, plaque and bulla?
2. How are they the same?

Back 2

1. patch= flat lesion abnormal in color only, plaque= elevated flat topped lesion, bulla= circumscribed collection of fluid
2. All greater than 5mm

Front 3

1. What's the difference between a nodule and a papule?

Back 3

Nodule= below the epidermis, papule- solid elevated lesion in the epidermis

Front 4

1.What's the difference between a excoriation and lichenification?
2.What's the difference between an erosion and an ulcer ?

Back 4

1.excoriation: an erosion of epidermis 2ndary to scratching lichenification= thickening of epidermis 2ndary to rubbing
2. erosion= focal loss of epidermis that doesn't enter dermis (no scarring)
ulcer= focal loss of epidermis and dermis (scarring)

Front 5

A patient presents to ER with this lesion having suddenly appeared. You tell the patient that the lesion is a result of infiltration of 1. what layer of skin and that it will be resolved in 2. a) 1 week b) 1 day c) 1 month

Back 5

This is a wheal. It is a result of inflamation of the dermis and will resolve in less than 24 hours.

Front 6

Name a disease state in which this abnormality is seen.

Back 6

Psoriasis is a good example. This abnormality is parakeratosis and is a result of rapid turnover of the epidermis without normal maturation (that's why there are nuclei in the stratum corneum)

Hint 6

It is abnormal of nucleated cells to be present in the stratum corneum.

Front 7

1.What is the abnormality in this section?
2.Contrast it with the appearance of a normal section.

Back 7

Hypergranulosis

Granular layer should only be 1-2 cell layers thick.

Front 8

What form of epidermal hyperplasia is this? What cells have proliferated?

Back 8

Acanthosis as a result of proliferation of the cells in the spinous layer.
N.B. acantha is Greek for thorn.

Front 9

What is this condition called? It caused by proliferation of what cell layer?

Back 9

papillomatosis, and it is a subtype of acanthosis (proliferation of spinous layer)

Front 10

What caused this condition?

Back 10

Edema between the spinous cells. Note the widening of the intercellular spaces

Front 11

The section from your patient whom you strongly suspect has IgG antibodies to his cell-cell connection proteins got mixed up on the way to the lab. the tech has it down to these two slides.
1. Which one is it and what condition does your patient have?
2. If you could use this punch biopsy what test would you run to confirm the presence of the antibodies and why?

Back 11

1. The bottom one because it shows evidence of acantholysis. Pts. with anti-self antibodies develop pemphigus vulgaris because of loss of cell-cell cohesion in the epidermis.

2. You would run DIF on the skin biopsy because DIF tests for presence of anitgen on pts. skin, IIF would test for presence in serum.

Front 12

what type of eczematous dermatitishas a different presentation in children and adults and what are they?

Back 12

atopic.
infants: face and head; acute
older children/adults: scaling and lichenification of flexural areas; chronic

Front 13

1.What type of eczematous dermatitis is similar to a burn and requires no prior sensitization?
2. What types of skin are protected from this type of dermatitis?

Back 13

1.irritant contact dermatitis
(more exposure/ worse symptoms)
2. dry and thick (more corneum, more better, so palms of hands)

Front 14

What's the difference between acute spongiotic dermatitis and chronic eczematous dermatitis?

Back 14

acute: no acanthosis, epidermal spongiosis with papillary dermal edema, intraepidermal vesicle formation, the inflammatory infiltrate has lymphocytes with some eosinophils.
chronic: HYKERKERATOSIS, ACANTHOSIS, spongiosis w/o visicles, thickening of dermal collagen

Front 15

What type of eczema can be treated with antihistamines and tacrolimus?

Back 15

atopic (NB all can be treated with topical steroids)

Front 16

1.What type of hypersensitivity reaxn is it if your patient has a itchy wheals that have been reappearing for three weeks after starting penicillin?
2. What is the pathogenesis of this condition?

Back 16

Type I hypersensitivity (urticaria), this is acute onset.
2. This is a vascular reaxn caused by mast cell degranulation.

Front 17

1. What are the LM pathological signs of urticaria?

2. What is the treatment for urticaria?

Back 17

normal epidermis, dermal edema, perivascular inflammatory cell infiltrate, ** also eosinophil hanging out in tissue is typical

2. avoid irritant, antihistamines

Front 18

1. describe the key features of a target lesion

2. If your patient presented with target lesions on hands and feet what syndrome would you be thinking of?

3. Of the three diseases in the Em like illness group, which are associated more with infections, and which are associated more with drugs?

Back 18

1.Central dusky purpura/vesicle
elevated edematous pale ring
peripheral ring of macular erythema

2. Erythema Multiforme

3. EM-infection related
SJS/TEN drug related

Front 19

Your patient had a HSV infection a month ago. They show up with target lesions after feeling tired for a week. They probably have ______?

2. If a patient with target lesions had been taking sulfa antibiotics for a sinus infection and NSAIDS for headache/fever like symptom, what other derm syndromes would be in your differential?

Back 19

1.EM, EM also associated with mycoplasma

2. SJS and TEN (antiepileptics and allopurinol can trigger also)

Front 20

Name 4 ways to differentiate Em from SJS/TEn

Back 20

1. trigger (infectious)/drug
2. prodrome (febrile/ mild-absent)
3. aytpical or confluent lesions/ typicl target lesion
4. prominent mucosal involvement/ no mucosal involvment

Front 21

1.Where would you look for blister formation on histologic sections for EM or SJS/TEN?

2.In these diseases what is the cause of the blister formation?

3. T/F You would expect to see necrotic keratinocyted in SJS extending from the basal layer of the epidermis upward

Back 21

1.At the dermal/epidermal junction.

2. damage to basal cells-> vacuolization ->(blister) + inflammatory infiltrate at junction

3. True.

Front 22

1. T/F: EM is self limited and is treated by avoiding the trigger or treating the viral/infectious cause.

2. T/F: The role of oral steroids early in treatment of SJS/TEN is standard of care.

Back 22

1. True

2. False, controversial. IVIG is established for TEN. It is standard of care to treat as burn patient.

Front 23

What is the Koebner phenomenon? Name a skin condition that it's associated with.

Back 23

appearance of lesion at the site of trauma (aka isomorphic response)
psoriasis

Front 24

1.This patient is a 14 yo male with hx of acute sore throat. After treatment with antibiotics, he had abrupt onset of these itchy papules. What's the diagnosis?
2. What test could confirm the diagnosis?

Back 24

1.Guttate psoriasis (2-5 mm red papules, also demonstrates Koebnner/ isomorphic response

2. ASO titer (antistreptolysin). Why? b/c Streptococcal inf. (pharyngitis)is typical cause. N.B. usually seen in younger individuals.

Front 25

What is the most common arthritic presentation of psoriasis?

Back 25

aymmentric oligoarthritis hand joints, most commonly DIP and PIP

Front 26

What is the pathologic name for nuetrophils in the stratum corneum and what skin condition is it associated with?

Back 26

Munro's microabscesses

psoriasis

Front 27

What is the manifestation of epidermal thinning of the dermal papillary tips and dilated vessels in the dermal papillae?

Back 27

Aupitz' sign.

Pinpoint bleeding when scale is forcibly removed from psoriasis plaque.

Front 28

1.How do you treat guttate psoriasis?

2. How do you treat conventional psoriasis?

Back 28

1.Antibiotics

2. Topical therapy: vit d, retinoids; light: PUVA, UVB;

Front 29

What psoriasis therapy can cause "iaotrogenic HIV" and what is its mechanism of action?

Back 29

1. Alefacept

It targets Th cells for destruction. (it binds Cd2 on memory T Cells)

Front 30

What psoriasis drug inhibits t cell adhesion to endothelium and what are its side effects?

Back 30

Efalizumab

Thrombocytopenia, rebond phenomenon in 5%

Front 31

1.How do is the demographics of Lichen Planus different for men and women?

2. What is the etiology of L.P.?

3. What disease is L.P. associated with?

Back 31

1.incidence in men stays the same, it increases in women until age 60.

2. Unkown, but involves helper T cells acting at basal layer.

3. Hep C. (increased incidence in Japan bc Hep C is more common in Japan)

Front 32

T/F The course of Lichen Planus generally follows regular, predictable stages.

T/F If you have LP with mucouse membrane involvement you are less likely to have recurrences.

Back 32

False

2/3 have it less than 1 year, 50% of people recurrences, course is unpredictable.

2. False, you are more likely to have Chronic LP with mucouse membrane involvement.

Front 33

1. What is the most common form of Lichen Planus?

2. What form of LP is associated with increased risk of squamous cell cancer?

Back 33

1. reticulate N.B. - these demonstrate Wickham's striae.

2. Ulcerative

Front 34

What is the pathologic name for nuetrophils in the stratum corneum and what skin condition is it associated with?

Back 34

Munro's microabscesses

psoriasis

Front 35

What is the manifestation of epidermal thinning of the dermal papillary tips and dilated vessels in the dermal papillae?

Back 35

Aupitz' sign.

Pinpoint bleeding when scale is forcibly removed from psoriasis plaque.

Front 36

1.How do you treat guttate psoriasis?

2. How do you treat conventional psoriasis?

Back 36

1.Antibiotics

2. Topical therapy: vit d, retinoids; light: PUVA, UVB;

Front 37

What psoriasis therapy can cause "iaotrogenic HIV" and what is its mechanism of action?

Back 37

1. Alefacept

It targets Th cells for destruction. (it binds Cd2 on memory T Cells)

Front 38

What psoriasis drug inhibits t cell adhesion to endothelium and what are its side effects?

Back 38

Efalizumab

Thrombocytopenia, rebond phenomenon in 5%

Front 39

What are 5 histologic feature of lichen planus?

Back 39

1.hyperkeratosis
2.saw tooth epidermal hyperplasia
3.lymphocytes at dermal-epidermal junction
4.vacuolation at basal level
5. civatte bodies

Front 40

What type of immunoflourcence is more specific?

Back 40

Direct, it uses the pts tissues.

Front 41

What are two ways to test for Pemphigus Vulgaris in a physical exam?

Back 41

Nikolsky- apply slight pressure at edge of blister and see if epidermis sloughs off
asboe-hansen- gentle pressure on intact blister pushes fluid away into adjacent skin

Front 42

1.What are the two antigens culpable for Pemphigus Vulgaris and what are the immunoglobins that mediate the immune response?

2.What is the result of the immune response against these antigens?

Back 42

1.Desmoglein-1 and Desmoglein-3; IgG mediated

2. Loss of intercellular adhesion: flaccid blishter

Front 43

1.What is the presenting sign of Pemphigus Vulgaris most of the time?

2. If fatal, what do pemphigus vulgaris pts die of?

Back 43

1.oral lesions

2. sepsis 5-10% of the time

Front 44

1.What findings do you note on these slides?

2. What blistering disease is it associated with?

3. What test could you run to confirm your diagnosis and what positive finding would you expect to see?

Back 44

1. intrapepidermal blister, suprabasal acantholysis, "row of tombstones"

2. pemphigus vulgaris

3. punch bipsy with DIF, "chickenwire" intercellular staining

Front 45

1.What are example of 1st line Pemphigus treatments?

2. What treatment is reserved for refractory cases?

Back 45

1.predinsone, azothioprine, mycophenolate mofetil, methotrexate, cyclosporine and IVIG
2. Retuximab (shuts done antibodies

2.

Front 46

What is the etiology of this skin disease?

Back 46

IgG antibodies to basement membrane antigens, the hemidesmosomal proteins. Causes subepidermal blistering and large tense bullae that rupture and heal spontaneously.

Front 47

1.T/F: Bullous pemphigoid pts. usually present with oral mucosal involvement.

2. T/F There are no clear age associations with BP.

Back 47

1. False, the mucosa is rarely involved in BP.

2. False, 65-75 and young children are the age groups.

Front 48

What conclusions can you draw from high levels of circulating IgG antibasement membrane Abs in a bullous pemphigoid pt.?

Back 48

not very many as they do not parallel disease activity.

Front 49

What features are evident from path sections of B.P.?

Back 49

1. subepidermal blistering, lack af acantholysis, perivascular inflammation with eosinophils**, nuetrophils and lymphocytes.

Front 50

What features are evident on DIF taken from the edge of a skin lesion of a pt. with antibodies to his basement membrane proteins?

Back 50

No staining in epidermis. Its a linear staining along the basement membrane.

Front 51

what pathological findings are responsible for the staining of basement membrane in bullous pemphigoid?

Back 51

IgG and C3

Front 52

Which condition is more responsive to low doses of steroids, pemphigoid or vulgaris?

Back 52

pemphigoid

Front 53

What are the immunoflourescence findings of Dermatitis herpeteformis?

Back 53

IIF negative (igA antibodies)
DIF postive for IgA in the tips of dermal papillae

Front 54

What is the mainstay treatment for the skin disorder that is present in people with gluten senstive enteropathies?

Back 54

Dapsone (g6pd level must be monitored)
sulfapyradie = secondary