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Dermatology > Autoimmune Dermatoses > Flashcards

Autoimmune Dermatoses Flashcards

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1
Q

Patterns

Pyoderma

A

Ventrum

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2
Q

Patterns

Demodicosis

A

Head
Legs
Paws

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3
Q

Patterns

Scabies/Notoedres

A

Pinnae

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4
Q

Patterns

Endocrine

A

Flanks
Tail tip
Symmetrical

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5
Q

Autoimmune disease is…

A

Implies the body is attacking a self-antigen

Antibodies or activated lymphocytes develop against it-self and causes lesions

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6
Q

Immune-mediated diseases is…

A

Implies a foreign antigen (protein) triggers an immunological reaction

Antigens:
Drugs
Bacteria
Viruses

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7
Q

Auto-immunity development:

Cell type and action

A

Lymphocytes which respond to:
Allergies (cytokines; recruit other cells)
Immune response (antigens)

Reactive lymphocytes:
Cleared in the thymus of normal individuals (tolerance) b/c are too active

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8
Q

Auto-immunity development:

Where do things go wrong?

A

Breakdown in tolerance (reactive lymphocytes stay in circulation) very active lymphocytes

Cross reactivity with self and foreign antigen

Drugs
Infectious agents

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9
Q

Autoimmune Disease

Generalities

A

Skin = target organ

Hypersensitivity reactions:
Type II
Type III (immune complex)

Unknown cause
Commonly seen in middle-aged animals

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10
Q

Pemphigus (KNOW)

What is it?

A

Autoimmune vesicobullous to pustular skin disease characterized by acantholysis (rupturing of kerotinocytes)

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11
Q

Pemphigus (KNOW)

Two main subtypes

A 
Pemphigus foliaceus (more common)
Pustules and crusts
Pemphigus vulgaris (rare)
ulceration of basal cell layer
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12
Q

Keratinocytes are held together by…(2 things)

A

Keratinocytes are held together by adhesions:
Desmosomes (closure to superficial layer)

Hemidesmosomes (attaches keratinocytes to basal cell layer)

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13
Q

Pemphigus foliaceus

Pathogenesis

A

Adhesions of desmosomes mediated by specialized proteins:
Desmogleins
Desmocollins

These are targeted by Pemphigus

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14
Q

Pemphigus foliaceus

Pathogenesis in dogs

A

Autoantibody response primarily involves IgG

Desmocollins 1 glycoprotein in the desmosome is the major autoantigen

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15
Q

Pemphigus foliaceus
Signalment
Dogs

A

Genetic factors may play role in development
Middle age
Akitas
Chows

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16
Q

Pemphigus foliaceus

Cats

A

Median age: 5 but really any age, any breed, any sex can get it

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17
Q 
Pemphigus foliaceus
Triggering Factors (4 main)
A 
UV light
Allergies
Drugs
Medications 
Idiopathic in cats
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18
Q

Pemphigus foliaceus

UV light mechanism

A

Not well understood

Lesions seem to worsen in the summer and improve in the winter

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19
Q

Pemphigus foliaceus

Allergies

A

Potentially triggers due to chronic inflammation

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20
Q

Pemphigus foliaceus

Drug triggers

A

Activation of proteolytic enzymes in skin and autoantibodies against desmosomes

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21
Q

Pemphigus foliaceus

Medications

A

Cephalexin
Clavamox
TMS

Guaranteed and => taken off the market (unsure what exactly was in them that did this)
Promeris
Certifect

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22
Q

Pemphigus foliaceus

Lesions Dogs

A

Skin lesions:
Pustules
Crusts
Erosions

May think pyoderma BUT these dogs have excessive lesions

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23
Q

Pemphigus foliaceus

Location of lesions Dog

A 
Face/muzzle
Bridge of nose
Periocluar skin 
Ears
Paws + Generalized = Rare

Note: do not usually see pyoderma here

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24
Q

Pemphigus foliaceus

Skin Lesions Cat

A

Crusts
Pustules
Erosions
Alopecia

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25
Q

Pemphigus foliaceus

Location of lesions Cat

A

Head
Face
Ears
Claw folds (caseous material, cheese like)
Peri-areolar (crusting around nipple) - unique

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26
Q

Pemphigus foliaceus

Clinical Signs

A

Fever
Lethargy
Anorexia
Lymphadenopathy

Pruritus; up to 50% of the dog cases and 80% of cat cases

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27
Q

Pemphigus foliaceus

DfDx

A

Superficial pustular dermatophytosis

Bacterial (Staph.); produces toxins that target desmosomes and mimic PF

Demodex
Scabies/Notoedres

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28
Q

Pemphigus foliaceus

Diagnosis (broad)

A 
History
PE
Dermatologic exam
Cytology (rule out dermatophytosis)
Negative skin scrapings (demodex, scabies, notoedres)

Histopathology; a MUST because treatment requires steroids and must confirm prior to steroid treatment

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29
Q

Pemphigus foliaceus

Cytology Results

A

Take 1-5 samples; slightly lift crust and dab area

Acantholytic keratinocytes (immature keratinocytes)
Non-degenerative neutrophils
Absence of organism

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30
Q

Pemphigus foliaceus

Biopsy

A

Subcorneal/intracorneal
Acantholytic keratinocytes
Pustules
Absence of organisms

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31
Q

Pemphigus foliaceus

Prior to biopsy…

A

Must have been off steroids for 2-3 weeks; steroids will suppress the acantholytic keratinocytes

Treat secondary infection(s); bacteria can cause acantholysis

Sample less active lesions; pustules are the best but undisturbed crusts will work

Take multiple samples of only lesioned tissue

Do NOT prep site

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32
Q

Pemphigus Erythematosus

Characteristics

A

Uncommon

Benign variant of pemphigus foliaceus

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33
Q

Pemphigus Erythematosus

Clinical Lesions

A

Facial distribution (usually bridge of nose)

Pustules
Crust
Alopecia
Erosions
Oozing
34
Q

Pemphigus Vulgaris

Background

A

Vulgar = BAD

Rare

Most severe form of the pemphigus complex

Poor prognosis; decline quickly

35
Q

Pemphigus Vulgaris

Clinical lesions

A

Vesicles
Bullae
Ulcers
Crust

36
Q

Pemphigus Vulgaris

Distribution of lesions

A

Ears
Foot pads
Mucocutaneous junctions
Oral cavity (80%)

37
Q

Pemphigus

Treatment

A

Suppress immune system

Induce remission

Taper to lowest dose (anti-inflammatory) and frequency

Note: if no biopsy confirmation was done and it is ringworm the lesions will get worse

38
Q

Pemphigus

Treatment Rx Regimen

A

Glucocorticoids:
Primary choice
Immune-suppressive (2 mg/kg) for 14 days

Recheck; if improving start tappering

Goal: Life-long treatment on anti-inflammatory dose every other day (trying to avoid negative side effects of steroids)

39
Q

Pemphigus

Glucocorticoids help with…

A 
Decrease arachidonic acid
Inhibits inflammatory cytokines
Decrease chemotactic factors and inflammatory cells
Suppress T-cell function
Induce apoptosis of T cells 
Suppress B-cell antibody production
40
Q

Mycophenolate

What is it?

A

Immune-Modulatory Drug

If glucocorticoids did not work this is next best thing; can also use it in combination with steroids to lower steroid dose

41
Q

Mycophenolate

MOA

A

Immune-Modulatory Drug

Inhibits DNA synthesis 
Inhibits macrophages, T, and B cell profliferation
Induces apoptosis of T cells
Suppresses B-cell antibody production
Rapid onset of action (2-4 hours)
42
Q

Azathioprine

What is it?

A

Immune-Modulatory Drug

Pro-drug; gets transformed into active form

Purine analogue that interferes with nucleic acid synthesis

CANNOT USE IN CATS

43
Q

Azathioprine

MOA

A

Immune-Modulatory Drug

Cytotoxic to T cells
Slow onset of action (1-2 weeks)
Side effects:
Fulminant hepatic necrosis with increase of ALT
Bone marrow suppression
Increased risk of infections
DO NOT USE IN CATS because cannot inactivate it

44
Q

Cyclosporine

MOA

A

Immune-Modulatory Drug

Calcineurin inhibitor

Prevents activation of T lymphocytes

Blocks pro-inflammatory cytokines and pro-inflammatory pathways

Might be better in maintaining remission opposed to inducing remission

45
Q

Three other auto-immune diseases

A

Discoid lupus Erythematosus

Systemic Lupus Erythematosus (not common)

Uveodermatologic Syndrome

46
Q

Discoid Lupus Erythematosus

Background

A

Second most common auto-immune disease

Lesions limited to nose
Benign disease

Pet feels good

Can be aggravated and/or induced by UV light

47
Q

Discoid Lupus Erythematosus

Clinical Lesions

A 
Depigmentation of nose
Gray/bluish color
Loss of cobblestone appearance
Erosions
Ulcers
Crusting
48
Q

Discoid Lupus Erythematosus

Lesions

A

Nose

Can extend to:
Bridge of nose
Eyes
Ears

Note: Pemphigus does NOT affect the dose itself!

49
Q

Discoid Lupus Erythematosus

Diagnosis

A

Rule out: mucocutaneous pyoderma

Cytology

Biopsy

First treat for pyoderma if no results do a biopsy

50
Q

Discoid Lupus Erythematosus

Treatment (3)

A

Tacrolimus:
Very effective topical
Cousin of cyclosporine; too large of molecule to be a topical

Avoid direct sunlight; sunscreen on nose!

Doxycycline/niacinamide

51
Q

Doxycycline/niacinamide

A

Inhibit matrix metalloproteases

Anti-inflammatory properties

Can take 6-8 weeks to work

52
Q

Immune-Mediated Diseases
Skin changes…
What is important to do at the beginning of the appointment

A

Skin changes are severe!

Thorough history is key:
Travel 
Tick-borne
Drug history
Vaccines
53
Q

Vasculitis

What is it?

A

Seen with immune-mediated disease

Inflammation and destruction of blood vessels which results in ischemic necrosis
=>
Poor blood supply to skin leads to ischemic dermatopathy

54
Q

Vasculitis

Triggers (4)

A

Idiopathic
Infectious
Drugs
Immune-mediated

55
Q

Vasculitis

Idiopathic Triggers

A

Up to 50% of cases

Especially seen in Jack Russell Terriers

56
Q

Vasculitis

Infectious Triggers

A 
Bacterial
Viral (Parvo, Coronavirus)
Protozoal (Leishmania, Sarcocystis) 
Rickettsial (RMSF, Ehrlichia, Babesia)
Fungal
57
Q

Vasculitis

Drug Triggers

A 
Injection of foreign protein (vaccines; rabies)
Antibiotics
Ivermectin 
Itraconazole
Fenbendazole
58
Q

Vasculitis

Immune-mediated

A

RARE

Systemic lupus erythematosus
Rheumatoid arthritis

59
Q

Vaculitis
Rabies Vaccine Induced
Breeds

A

Detected in blood vessels and epithelium of hair follicles
Unsure why this occurs

Breeds: 
Poodles
Silky Terrier
Pekingese
Bichon Frise
Maltese
60
Q

Vasculitis
Rabies Vaccine Induced
Lesions

A

Circular area of alopecia at site of vaccine

Signs can be seen 2-8 months after vaccination

NO inflammation, papules, or crusts

Note: always important to note where you give injections

61
Q

Vasculitis
Rabies Vaccine Induced
DfDx

A

Dermatophytosis

Folliculitis

62
Q

Vasculitis
Ear Tip
DfDx

A

Rabies Vaccine Induced
Pemphigus (usually on nose though)
Ectoparasites (scabies, notoedres and will be very pruritic)

See notches in ear tip
Painful

63
Q

Vasculitis

Diagnosis

A

Clinical signs
History (vaccination times and drug administration)

Rule out: tick borne diseases

Biopsy: rare to see active vasculitis but can see atrophy of hair follicles which is supportive

64
Q

Vasculitis
Rabies Vaccine Induced
Treatment

A

If rabies vaccine is trigger do not vaccinate; check titers and consult state vet for what to do if titers low

65
Q

Vasculitis

What type of hypersensitivity?

A

Type III

Antigen-Complex:
Triggers neutrophils, mast cell degranulation, platelet aggregation

66
Q

Vasculitis

Repeat exposure can lead to…

A

Worsening of lesions

Glomerular nephritis due to accumulation of antigen-antibody complex

67
Q

Vasculitis

Pentoxifylline

A

Methylxanthine (caffine) derivative

Potent hemorheologic and anti-inflammatory properties:
Helps RBCs to become more deformable which allows for better circualation

Improves mirocirculation

Inhibits:
Cytokines
Leukocyte and platelet adhesion to endothelial cells

Takes 6-8 weeks to be effective

68
Q

Vasculitis

Doxycycline/Niacinamide

A

If patient does not respond to Pentoxifylline

Inhibits matrix metalloproteases (anti-inflammatory)

Takes 6-8 weeks to be effective

Usually on this for the rest of their life

69
Q

Symmetrical Lupoid Onychodystrophy (SLO)

What is it?

A

Uncommon claw disease

Unknown etiology

Suspected to have a “vasculitic” immune-mediated component (Type III Hypersensitivity)

70
Q

Symmetrical Lupoid Onychodystrophy (SLO)

Clinical Signs

A

Acute onset of nail loss (nails literally falling off); onycholysis -separation of nails from quick
onychoschizia -splitting of claws

May affect only a few but will progress

Painful

+/- liking of paws

May get secondary infections (mal-odor, swollen digit)

71
Q

Symmetrical Lupoid Onychodystrophy (SLO)

Diagnosis

A

Consider causes of vasculitis:
Rabies or other vaccines?
Tick borne disease?
Drugs?

Biopsy is NOT recommended

72
Q

Symmetrical Lupoid Onychodystrophy (SLO)

Treatment (3 aspects)

A

Treat Secondary infections: Deep infection that will have to be treated for 6-8 weeks. Also do Chlorhexidine foot soaks

Pentoxifylline:
6-8 weeks to work
Long term treatment
No improvement add Doxy

Trim nails; keep them short

Nails will never be normal again

73
Q 
Erythema Multiforme (KNOW)
What is it?
A

NOT a diagnosis

A reaction pattern described by pathologists on histopathology:
Epidermal/keratinocyte apoptosis with lymphocytic satellitosis

74
Q

Erythema Multiforme

Pathogenesis

A

Unknown

T lymphocytes infiltration and activation -> keratinocyte apoptosis

Many triggers

75
Q

Erythema Multiforme

Triggers (5)

A 
Drug reactions 
Food Allergies
Neoplasia
Infectious (parvo)
Idiopathic (old dog EM)
76
Q

Erythema Multiforme

Drug Triggers

A

Antibiotics:
Sulfa, cephalosporines

Phenobarbital (hard to discontinue)
Levothyroxine

Many more but these are the common ones

77
Q

Erythema Multiforme

Clinical Signs

A 
Acute onset
May affect skin and mucus membranes
Erythematous 
Target lesions
Bullae/vesicles
Crust; plaque-like
78
Q

Erythema Multiforme

DfDx

A

Pemphigus vulgaris (rare and patient would be systemically ill)

Cutaneous lymphoma

Thermal burn

79
Q

Erythema Multiforme

Diagnosis

A

Biopsy (multiple):
Mark where you take it from

Epidermal/keratinocyte apoptosis with lymphocytic satellitosis

Lymphocytes surrounding keratinocytes

80
Q

Erythema Multiforme

Treatment

A 
Address underlying cause:
Drugs
Food allergy
Screen for neoplasia
Cyclosporine?
Prednisone?

Dermatology (13 decks)

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