Lecture 14 3/25/25 Flashcards

1
Q

What is the pathomechanism of uveodermatological syndrome?

A

specific destruction of melanocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which lesions are seen in uveodermatological syndrome?

A

-depigmentation
-leukotrichia/white hair
-deep erosion/ulcer
-loss of cobblestone appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which breed commonly presents with uveodermatological syndrome?

A

akitas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What ocular syndrome is seen in uveodermatological syndrome?

A

acute onset of bilateral granulomatous uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the presence/absence of pigmentation and cobblestone appearance help to differentiate conditions?

A

-normal: pigmentation and cobblestone both present
-uveodermatological syndrome: pigmentation and cobblestone both absent
-vitiligo: pigmentation absent, cobblestone present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is uveodermatological syndrome diagnosed?

A

-histopathology showing lichenoid dermatitis and pigmentary incontinence
-ophthalmic exam showing bilateral uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the treatment for uveodermatological syndrome?

A

immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the three main immune-mediated dermatoses?

A

-erythema multiforme
-stevens-johnson syndrome
-toxic epidermal necrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mortality rate for toxic epidermal necrolysis in animals?

A

around 100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the pathomechanism of erythema multiforme/stevens-johnson syndrome/toxic epidermal necrolysis?

A

cytotoxic lymphocyte responses against altered keratinocytes, triggered by infectious agents or drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the causes of erythema multiforme minor/major?

A

-significant number is idiopathic
-drug reactions account for 19% of minor cases and 59% of major cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of stevens-johnson syndrome and toxic epidermal necrolysis?

A

-mostly triggered by drugs; NSAIDs and antibiotics
-occasionally triggered by infectious agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical signs of EM minor?

A

-less than 10% of body surface affected
-raised targetoid lesions
-0 or 1 mucosal surfaces involved
-no systemic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical signs of EM major?

A

-less than 10% of body surface affected
-flat or raised targetoid lesions
-more than 1 mucosal surface involved
-systemic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical signs of SJS?

A

-less than 10% of body surface affected
-flat erosions/ulcers
-more than 1 mucosal surface involved
-systemic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical signs of TEN?

A

-greater than 30% of body surface affected
-flat erosions/ulcers
-more than 1 mucosal surface involved
-systemic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does the clinical presentation of EM differ from SJS/TEN?

A

EM:
-targetoid lesion
-well-circumscribed ulceration
SJS/TEN:
-coalescing macules and patches
-widespread ulceration
-multiple mucosal surfaces involved

18
Q

What is the Pseudo-Nikolsky sign?

A

indication of epidermal detachment; touching the skin is enough to cause erosion

19
Q

What findings on histopath allow for EM diagnosis?

A

individual keratinocyte apoptosis at the multiple epidermal levels

20
Q

What findings on histopath allow for SJS/TEN diagnosis?

A

full thickness coagulation necrosis

21
Q

How else are EM, SJS, and TEN differentiated for diagnosis?

A

clinical presentation

22
Q

What is the treatment for EM, SJS, and TEN?

A

-drug withdrawal
-immunosuppression for EM; controversial for SJS/TEN due to sepsis risk
-advanced supportive therapy for SJS/TEN

23
Q

What is the pathomechanism of cutaneous vasculitis?

A

blood vessel walls become targets of an inflammatory response (type III hypersensitivity)

24
Q

What are the potential causes of cutaneous vasculitis?

A

-vaccines
-vector-borne infection
-drugs
-SLE
-idiopathic

25
Q

What are the lesions seen in cutaneous vasculitis?

A

-ulcer
-scarring
-urticaria
-purpura

26
Q

Which lesions are associated with acute phase cutaneous vasculitis?

A

-erythematous urticaria (diascopy +)
-petechia
-purpura
-edema

27
Q

Which lesions are associated with chronic phase cutaneous vasculitis?

A

-“wedge-shaped” necrotic ulcer
-crust
-alopecia
-scarring/ischemic dermatopathy

28
Q

What is diascopy?

A

pressing a slide to the skin to look for blanching

29
Q

What are potential diagnoses based on diascopy result?

A

-positive diascopy/blanching: vascular inflammation
negative diascopy/no blanching: hemorrhage or non-vascular inflammation

30
Q

What is the distribution of lesions in cutaneous vasculitis?

A

-at extremities
-ear tips
-tail tip
-center of paw pads
-claws

31
Q

How is cutaneous vasculitis diagnosed?

A

-typical clinical presentation
-history
-histopath. taken from CENTER showing vasculitis (acute) or ischemic dermatopathy (chronic)

32
Q

How is cutaneous vasculitis treated?

A

-avoidance of trigger
-elimination of infectious triggers
-immunosuppression

33
Q

What is the use of primary immunosuppressant agents?

A

initial therapy for a short course

34
Q

Which drug class is used as a primary immunosuppressant agent?

A

glucocorticoids

35
Q

What is the use of secondary immunosuppressant agents?

A

maintenance therapy for a long course

36
Q

Which drugs are used as secondary immunosuppressant agents?

A

-cyclosporine
-oclacitinib/apoquel
-azathioprine
-mycophenolate mofetil

37
Q

How do glucocorticoids work?

A

-regulation of multiple mediators
-prevent arachidonic acid cascade
-increase anti-inflammatory cytokine production
-decrease inflammatory cytokine production

38
Q

How does cyclosporine work?

A

inhibition of T cells

39
Q

How does oclacitinib/apoquel work?

A

inhibition of JAKs

40
Q

How do azathioprine and mycophenolate mofetil work?

A

inhibition of lymphocytes