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EV ACVD Study > Immune mediated dermis dz (ECVD video) > Flashcards

Immune mediated dermis dz (ECVD video) Flashcards

1
Q

Common precursor of DCs and macrophages

A

Blood monocytes (CD18+, CD45+)

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2
Q

Cell surface markers of Interstitial DC (in dermis)

A

CD4+, CD90+

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3
Q

Cell surface markers of LCs

A

CD4-, CD90-

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4
Q

Which type of cell is responsible for reactive histiocytosis?

A

Interstitial DCs

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5
Q

Which cell type is responsible for sterile granulomatous pyogranuloma syndrome; + cell surface markers

A

Macrophages (CD1a, CD11d)

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6
Q

Which of the below DOES express CD4? Interstitial DCs or LCs?

A

Interstitial DCs

LCs do NOT express CD4

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7
Q

CD11d is suggestive of which cell

A

Macrophage

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8
Q

CD18 is suggestive of which cell

A

Blood monocyte

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9
Q

Reactive cutaneous histiocytosis breeds

A

Collie, Shetland sheepdog

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10
Q

Reactive systemic histiocytosis breeds

A

Bernese mountain dogs > Irish wolfhounds, golden retrievers, lab retriever, rottweiler

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11
Q

Age for reactive histiocytosis

A

Cutaneous: 4 yr median
Systemic: 1-9 yr range

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12
Q

Cytokine profile of cutaneous reactive histiocytosis

A

Th1 (IL-6, IL-12, IFNg, TNFa)

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13
Q

Etiology of cutaneous reactive histiocytosis

A

*Persistent antigen stimulation
*Immunologic dysregulation

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14
Q

Cells of cutaneous reactive histiocytosis

A

Dendritic cels
T cells (CD8>CD4)

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15
Q

Clinical lesions of cutaneous histiocytosis

A

Papules, plaques, nodules
Alopecia, erythema, depigmentation, ulcers, crusts

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16
Q

Body region of cutaneous histiocytosis

A

Haired skin
Nasal planum (clown nose)
Foot pads
Linear
Regional LN

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17
Q

Organ systems affected in systemic histiocytosis

A

Everywhere :)

Skin, mucosa
Liver, spleen
LN
BM
Lungs, eyes, kidneys, testes, muscles, nasal cavity

Systemically ill

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18
Q

Labwork findings with systemic histiocytosis

A

Anemia
Monocytosis
Lymphopenia
Hypercalcemia

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19
Q

Cutaneous reactive histiocytosis is DIFFERENT than histiocytoma because ______-

A

Reactive histiocytosis is BOTTOM HEAVY (not affected epidermis

Histiocytoma is TOP HEAVY

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20
Q

Sterile pyogranuloma syndrome breeds

A

Boxer
Collie
Dachshund
Doberman pinscher
English Bulldog
Golden Retriever
Great Dane
Weimeraner

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21
Q

Pathogenesis of sterile pyogranuloma syndrome

A

*Aberrant inflammatory response
*Immune dysfunction
*Infectious agents: low numbers (Leishmania) or incomplete clearance of their antigens –> using PCR may help us find these organisms better!

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22
Q

Body region sterile pyogranuloma syndrome

A

Dog: Head (muzzle, periocular, pinnae), neck, trunk, legs, paws

-Hypercalcemia in dogs!
-Regional lymphadenopathy in 30%

Cat: Muzzle>pinnae, extremities > trunk

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23
Q

Causes of infectious granulomatous diseases

A

*Protozoa
-Leishmania
-Neospora
*Bacteria
-Actinomyces
-Nocardia
-Mycobacteria
-Actinobacillus
*Fungal
-Cryptococcus neoformans
-Coccidiodes immitis
-Histoplasma capsulatum
-Blastomyces dermititidis
-Sporotrixhum schenckii
*Oomyces
-Lagenidium
-Pythium insidiosum
*Pheohyphomycosis
-Alternaria
-Curvularia
*Algae
-Prototheca

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24
Q

Causes of NONinfectious granulomatous diseases

A

*Foreign body
*Endogenous material
-Hair
-Sebum
-Keratin etc
*Sterile granuloma and pyogranuloma syndrome
*Reactive histiocytosis
*Juvenile sterile granulomatous dermatitis and lymphadenitis
*Cutaneous xanthoma
*Canine sarcoidosis

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25
Q

Sarcoidosis gene predisposition (humans)

A

MHC cl II

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26
Q

Sarcoidosis pathogenesis in humans

A

Th1 immune response to infectious agents, allergens
ie: Mycobacterium&raquo_space; minerals (cat litter), chemicals (insecticides)

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27
Q

Other organs affected by sarcoidosis in humans

A

Lungs> skin > eyes, liver > other

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28
Q

Sarcoidosis (human) prognosis)

A

Good

May self-cure.

Tx: GCs +/- 2’ steroid sparing agents

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29
Q

Sarcoidosis, Systemic Granulomatous Disease in horses: age of onset

A

Usually > 3 years old, wide range

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30
Q

Sarcoidosis, Systemic Granulomatous Disease in horses: etiology

A

*Idiopathic
»
*Infectious agents
-Mycobacterium
-Borrelia burgdorferi
-EHV-2
*Toxins
-Hairy vetch

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31
Q

Which infectious agents may cause Sarcoidosis, Systemic Granulomatous Disease in horses

A

*Infectious agents
-Mycobacterium
-Borrelia burgdorferi
-EHV-2
*Toxins
-Hairy vetch

BUT USUALLY IDIOPATHIC

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32
Q

Other organs affected by Sarcoidosis in horses

A

*Skin
*Lungs
»
*Internal LN
*Liver
*GI
*Spleen
*Kidney, bone, CNS, Heart, Adrenal, Thyroid, Thymus, Pancreas, Muscles, BM

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33
Q

3 clinical forms of Sarcoidosis in horses

A

*Localized (focal exfoliative dermatitis, ie lower limb)
*Partially Generalized (Exfoliative dermatitis, nodules that progress from a focal area. LN+ –> generalized)
*Generalized (internal organs +/- cutaneous)

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34
Q

Lab findings with Sarcoidosis in horses

A

*Anemia
*Leukocytosis
-Neutrophilia
*Hyperfibrinogenemia
*Hypoalbuminemia
*Hyperglobulinemia
*Hyperbilirubinemia

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35
Q

Sarcoidosis in horses histopath

A

-Nodular, interstitial granulomatous inflammation with multinucleated giant cells

-Superficial, dermis > panniculus

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36
Q

Prognosis Sarcoidosis in horses

A

*Cutaneous only: RARELY self cure
Variable response

-Relapse with tx discontinued, or seasonal flares, training/competition stress

*Systemic: Often euthanized

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37
Q

Treatment Sarcoidosis in horses

A

*Remove hair vetch from diet
*GC (1-4mg/kg/d prednisolone)
*OFA
*Pentoxifylline

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38
Q

Breed, age for canine Sarcoidosis

A

Shetland sheepdogs

Middle aged

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39
Q

Clinical lesions for canine sarcoidosis

A

Papules, plaques, nodules

*Possibly the same as sterile granuloma/pyogran syndrome

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40
Q

Histopath difference between SGPS and sarcoidosis in dogs

A

*No neutrophils in sarcoidosis
*Sarcoidosis does not affect adnexa or extend to panniculus

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41
Q

Histopath difference between reactive histiocytosis and sarcoidosis in dogs

A

Reactive histiocytosis is bottom heavy

Sarcoidosis is top heavy

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42
Q

T or F: Sarcoidosis in dogs usually progresses to systemic involvement

A

FALSE

Systemic involvement not yet reported in dogs

(It does happen in horses, humans)

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43
Q

Treatment sarcoidosis dogs

A

*GC
*Cyclosporine

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44
Q

Breed predisposed to SNP

A

Dachshunds!!!!

*Australian shepherd
*Brittany spaniel
*Chihuahua
*Collie
*Dalmatian
*English bulldog
*Pomeranian
*Poodle

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45
Q

Species w/SNP

A

*Dog
*Cat
*Horse, donkey
*Bovine
*Human

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46
Q

Pseudomonas panniculitis has been reported in which species

A

*Cats
*Ferrets

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47
Q

Causes of panniculitis

A

*Infections (Bartonella, Serratia, Myobacteria, Nocardia, etc
*Physical (trauma, injections, foreign bodies, burns)
*Nutritional (pansteatitis)
*Pancreatic (inflammation, neoplasia)
*alpha1-antitrypsinase deficiency??
*Immune mediated (vasculopathy–ischemic/rabies, KBr, SLE, IMPA, IBD, arthropods)
*Idiopathic

48
Q

Which drug most often causes panniculitis

49
Q

T or F: anti-neutrophil antibodies have been reported in dogs with sterile panniculitis

A

True!! Most!

*Can be perinuclear or cytoplasmic antibodies

*Unknown if this is a cause or a result of SNP

50
Q

In which immune mediated disease has anti-neutrophil cytoplasmic antibodies been reported

A

Sterile nodular panniculitis

51
Q

Septal panniculitis– pyogranulomatous infiltrate among _____ neoplastic cells

A

T cell lymphoma!!

Be cautious not to misdiagnose as SNP

52
Q

Juvenile cellulitis age

A

USUALLY 3w-4mo

BUT case reports of adult onset!!!

53
Q

Sterile granulomatous dermatitis and lymphadenitis other name

A

Juvenile cellulitis

BUT many adult onset cases

54
Q

Sterile granulomatous dermatitis and lymphadenitis clinical signs

A

*Edema of facial MC junctions
*Papules, pustules on face, pinnae
*Nodules, fistulous dracts
*SUBMANDIBULAR lymphadenopathy
*Neuro signs from spinal cord compression or inflammation of CSF

55
Q

Sterile granulomatous dermatitis and lymphadenitis histopath

A

Nodular pyogranulomatous inflammation
Effacement of hair follicles

r/o sterile pyogranuloma granuloma syndrome– looks the same on histopath

56
Q

Sterile granulomatous dermatitis and lymphadenitis treatment

A

May self cure in 1-3 months, but TREAT because might die!!

Usually no relapse if juvenile. May relapse if adult (30%!)

GC +/- cyclosporine
Analgesics

57
Q

Canine pyoderma gangrenosum breed

A

American staffordshire terrier

58
Q

Canine pyoderma gangrenosum: Pathogenesis, Cytokines

A

Autoimmune?

IL-1b, IL-8, IL-17a, TNF-a

59
Q

Canine pyoderma gangrenosum: triggers, concurrent dz

A

Neoplasia
IMPA
Surgery (pathergy)
Idiopathic

60
Q

Canine pyoderma gangrenosum pathomechanism

A

1) Apoptosis of keratinocytes, release DAMPs,PAMPS
2) Innate immune system activated
3) Neutrophils recruited
4) T cells activated
5) Macrophages and neutrophils come to the skin

61
Q

Clinical signs, body distribution: Canine pyoderma gangrenosum

A

Deep pustules, hemorrhagic bullae -> Ulcers (undermined borders), pain

Multiple sites: face, trunk, legs

62
Q

Canine pyoderma gangrenosum: Internal organs

A

*Pancreatitis
*Neutrophilic splenitis
Fever, lameness

*Increased C-reactive protein on labwork

63
Q

Bromodera

A

Drug reaction from contact or systemic bromide administration

-Hemorrhagic bullae, crusted nodules, deep ulcers

Looks similar to Canine pyoderma gangrenosum

-Resolves with KBr discontinued

64
Q

Clinical difference between Sweets and Canine pyoderma gangrenosum

A

Gangrenosum has ulcers
Sweets is more papules/plaques w/o ulcers

Look the same on histopath, so need to differentiate clinically

65
Q

Canine pyoderma gangrenosum Treatment

A

Treat inciting disease (if it exists)
*Pain management
*Prednisolone, cyclosporine vs azathioprine
*CAN do cyclosporine monotherapy

Prognosis: Good

66
Q

Triggers for Sweets-like

A

*Carprofen
*Firocoxib
*Plant-oil containing flea preventative in cats
*IMPA

(In humans, infections, vaccines, immune-mediated dz, neoplasia, pathergy, pregnancy)

67
Q

Immune response to Sweets-like Syndrome

A

*Th1 OR Th17 in different patients

*Aberrant neutrophil proliferation, maturation, and dermal infiltration. Increased G-CSF to promote neutrophils

*IL-1b, IL-8, IL-33, IFNg, TNFa, CCL2, CXCL10

68
Q

Clinical signs Sweets-like syndrome

A

*Edema, erythema
*Macules, papules, plaques
*Vesicles
*PAIN

*Generalized. Haired skin and MM

69
Q

Lab findings with Sweets-like syndrome

A

*IMHA
*IMTP
*Decreased albumin
*Neutrophilia
*Increased c-reactive protein

70
Q

Which special stain can help determine CAEDE vs Sweets-like?

A

Luna stain (eosinophilic infiltration amount)

71
Q

Treatment Sweets-like syndrome

A

*Drug withdrawal
*Pain management
*GC, cyclosporine, azathioprine, MMP

72
Q

Which species have CAEDE

A

*Dogs
*Horses

73
Q

What other organ system is affected in CAEDE

A

GI in 80% of cases

Usually before skin lesions (60%), but can be concurrent (15%)

74
Q

Pathogenesis of CAEDE

A

*GI dz
*Drugs
*Insects

75
Q

Clinical signs of CAEDE

A

*Erythema (macular, diffuse)
*Wheals
*Edema (pitting, face/legs).
*Pruritus in 30%

Face, pinnae, ventrum > extremities

76
Q

Lab findings CAEDE

A

RARE to have peripheral eosinophilia

*Low TP
*Low Cholesterol

77
Q

Difference between Pattern 1, 2, 3 of CAEDE

A

1: Superficial
3: Diffuse eos inflammation with flame figures, edema, ulcers

78
Q

Treatment for CAEDE

A

*Hospitalized for severe GI signs
*Skin disease may wax/wane
*Rare for skin signs to relapse once treatment discontinued. BUT GI signs often do relapse

GLUCOCORTICOIDS + CETIRIZINE!!!

79
Q

Species with Hypereosinophilic syndrome

A

*Dogs (no skin involvement)
*Cat
*Horse
*Ferret
*Human

80
Q

Pathogenesis Hypereosinophilic syndrome

A

*Idiopathic
*Paraneoplastic (lymphoma in a cat!)

81
Q

Clinical signs Hypereosinophilic syndrome

A

*Macules, papules, plaques, edema-wheals, pruritus

*Oral cavity, LN, BM, liver, spleen, GI heart, lung involvement possible

*Eosinophilia on labwork!!!

82
Q

Prognosis Hypereosinophilic syndrome

A

Usually fatal if systemic involvement

Cats with skin only: live 2-4 years

83
Q

Hypereosinophilic syndrome Treatment

A

Glucocorticoids– only temporary response

Hydroxyurea (block bone marrow production of eos, but general BM suppression)
Cyclosporine

84
Q

Perianal fistula breed

A

MI GSD > MN GSD

GSD (80%), but other large/medium breeds possible.

85
Q

Perianal fistula genetics predisposition

A

MHC cl II

Potentially also intestinal bacterial dysbiosis

86
Q

Which type of T cell is more common in Perianal fistula

A

CD4+ cells

B cells, plasma cells, macrophages

(Cells that respond to MHC cl II)

87
Q

Cytokines upregulated in Perianal fistula

A

Mostly Th1 cytokines (IL-2, IFNg&raquo_space;»)

*IL-1b
*IL-2
*IL-6
*IL-8
*IL-10
*IFNg
*TNFa
*TGFb

88
Q

What human disease is potentially related to Perianal fistula

89
Q

Which MMPs are upregulated in Perianal fistula

A

MMP 9, MMP 13

*Implicates macrophages in pathogenesis
*Explains extensive tissue destruction

90
Q

What non-skin clinical sign is present in 42-100% of dogs with Perianal fistula

91
Q

What comorbidities can accompany Perianal fistula

A

CAFR
Metatarsal sinuses
Chronic superficial keratitis

92
Q

Which MMPs are upregulated in Perianal fistula

A

MMP 9, MMP 13

*Implicates macrophages in pathogenesis
*Explains extensive tissue destruction

93
Q

Treatment for Perianal fistula

A

Cyclosporine + topical tacrolimus (96% of dogs respond)
*Higher dose SID is best to achieve remission

-Prednisone
-Aza
-MMP
-Apoquel (2 cases)
-Stem cell injection
-Phovia
-Elimination diet?
-Sx?
-Tx 2’ infections

Some people use metronidazole too

94
Q

Metatarsal fistula breed

95
Q

Metatarsal fistula sex

96
Q

Metatarsal fistula age of onset

A

Middle-aged

97
Q

Metatarsal fistula pathogenesis

A

Focal panniculitis

-Mechanical stress?
-Anticollagen antibodies?

98
Q

Are front or hind limbs more often affected in Metatarsal fistula

A

Metatarsus > Metacarpus

99
Q

Is Metatarsal fistula usually bilateral or unilateral

100
Q

Non-GSD breed w/ reported Metatarsal fistula

A

Grey hound

Cleared with topical tacrolimus

101
Q

Treatment Metatarsal fistula

A

-GC (topical, oral)
- Cyclosporine
-Tacrolimus (use for maintenance once in remission)
-Vitamin E
- Doxy/niacinamide

May self cure, with recurrences common

102
Q

Metatarsal fistula histopath

A

Pyogranulomatous inflammation of panniculus, deep dermis

Sinus formation

Fibrosis in necrotic areas

103
Q

Feline plasma cell pododermatitis: Sex

A

Males (esp neutered)

104
Q

Feline plasma cell pododermatitis: Age, breed

A

None reported

105
Q

Feline plasma cell pododermatitis: pathogenesis

A

Immune mediated
*plasma cells *increased g-globulins in serum
*response to immunosuppression tx

Allergic
Contact (perfumed litter)
Structural (localization, response to sx)
Infection (FIV/FeLV)

106
Q

Are plasma cells monoclonal in Feline plasma cell pododermatitis?

A

NO. They are polyclonal

107
Q

Which Ig are the plasma cells secreting in Feline plasma cell pododermatitis

A

IgG mostly

A little IgA

108
Q

Does Bartonella cause Feline plasma cell pododermatitis

A

No

But study was used on formalin-fixed tissue.

Was studied because cats respond to doxycycline

109
Q

What viruses implicated in Feline plasma cell pododermatitis

A

FIV (60% are +)
FeLV less common, but reported in 2 cats

110
Q

Feline plasma cell pododermatitis: Sex

A

Males (esp neutered)

111
Q

Lab findings from Feline plasma cell pododermatitis

A

Increased g-globulins, thrombocytopenia

112
Q

Feline plasma cell pododermatitis: other body sites

A

*Stomatitis
*Bridge of nose

*Glomerulonephritis
*Amyloidosis
-from hyperactive plasma cells

113
Q

Plasma cell special stain

A

Methyl Green-Pyronin (MGP)

-Nucleus: dark blue
-Cytoplasm: pink (stains mRNA for Ig synthesis)

114
Q

Feline plasma cell pododermatitis: treatment

A

Mild: allow to self-cure. Change litter, doxycycline x3-10w

Severe: glucocorticoids, cyclosporine

Very severe (nodules, ulcers, hemorrhages): surgery

115
Q

Clinical course of cutaneous histiocytosis

A

Waxes/wanes

Consider maintenance therapy to minimize recurrence

116
Q

Body location with more aggressive cutaneous histiocytosis

A

Nasal planum lesions

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