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EV ACVD Study > Equine Derm ECVD Video > Flashcards

Equine Derm ECVD Video Flashcards

1
Q

What is the mechanism by which corticosteroids can induce laminitis?

A

Corticosteroids increase insulin level, induce insulin resistance. Long term elevated insulin and can lead laminitis

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2
Q

Risk factors of laminitis (4)

A

1) Equine metabolic syndrome
-Increased baseline insulin levels
2) PPID –> insulin resistance
3) Ponnies
4) Older age

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3
Q

Why would you use an oral glucose tolerance test as a dermatologist

A

Need to r/o EMS before corticosteroids if a horse is obese –> use an oral glucose tolerance test to check insulin, glucose, triglycerides

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4
Q
A
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5
Q

How potent is prednisolone compared to hydrocortisone

A

4x more potent than HC

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6
Q

Does prednisolone have an increased risk of inducing laminitis

A

No

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7
Q

How potent is dexamethasone compared to hydrocortisone

A

25x more potent than HC

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8
Q

Does dexamethasone have an increased risk of inducing laminitis

A

Possibly a small increase

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9
Q

How potent is triamcinolone compared to hydrocortisone

A

5x more potent than HC

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10
Q

How diabetogenic is triamcinolone compared to dexamethasone

A

SAME diabetogenicity, even though LOWER potency

Triamcinolone has a shorter serum half life, BUT binds onto CCR for LONGER –> longer lasting insulin resistance

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11
Q

What allows dexamethasone and triamcinolone to stay in the body for a longer period of time?

A

Dexamethasone and triamcinolone are resistant to inactivation by 11-beta HSD-2

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12
Q

What is 11-beta HSD-2

A

Enzyme to inactivate steroids

Triamcinolone and dexamethasone are more resistant to inactivation by this enzyme

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13
Q

What does active corticosteroid do to the distal limb?

A

Vasoconstriction to hoof, fibroblasts, keratinocytes

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14
Q

How long does prednisolone cause insulin resistance?

A

1 day

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15
Q

How long does triamcinolone cause insulin resistance?

A

7 days

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16
Q

How long does dexamethasone cause insulin resistance?

A

3 days

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17
Q

Is there an increased risk of laminitis with corticosteroids in HEALTHY horses (without risk factors)?

A

No

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18
Q

Which breeds are more prone to pastern dermatitis

A

Cold blooded, heavy horses (draft horses)

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19
Q

Risk factors for pastern dermatitis (6)

A

1) Older age
2) Breed (draft)
3) Heavy feathering
4) Unpigmented skin (pigmentation = protective against photosensitization, photo-aggravated vasculitis)
5) Damage to skin barrier
6) UV light (esp unpigmented skin)

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20
Q

Differentials for pastern dermatitis (15)

A

1) Bacterial (Staph, Strep, E coli, Pseudomonas, others)
2) Chorioptic mange
3) Contact hypersensitivity
4) Dermatophyte
5) Helminths
6) Hepatocutaneous syndrome
7) Localized sarcoidosis
8) MEEEDS (eosinophilic dermatitis and stomatitis- CORONARY BAND)
9) Photodermatitis
10) Pemphigus foliaceus
11) Pemphigus vulgaris
12) Sarcoids
13) Selensiosis
14) Trombiculosis (Chiggers)
15) Yeast infection

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21
Q

Where on the body should you assess a horse with MEEDS (eosinophilic dermatitis)

A

Coronary band + mouth (stomatitis)

Thoroughbreds and standardbreds ONLY affected

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22
Q

Differentials for nodules on pastern (3)

A

1) Chronic progressive lymphedema, verrucous dermatitis
2) Sterile, infectious pyogranulomas (Habronema parasitic!)
3) Neoplasia

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23
Q

What’s your diagnosis: Hair above coronet sticking straight out, thin bead of abnormal horn and tightly backed growth rings below coronet.

A

Coronary Band Dystrophy

Compact parakeratotic hyperkeratosis. Hydropic degeneration

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24
Q

What clinical lesions would you expect to see with a contact reaction?

A

Crusting, erosions, ulcerations

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25
Q

Why are haptens not immunogenic on their own?

A

Their sequence is too simple to bind to MHC cl II, so not presented to T cells

BUT when they bind to another peptide, the COMBINATION can be immunogenic

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26
Q

What topical product is a hapten that induces contact hypersensitivity

A

Chlorhexidine

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27
Q

What is your top differential diagnosis when a horse has pastern dermatitis with crusting and pruritus in the fall/winter

A

Chorioptic mange

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28
Q

What is your top differential diagnosis when a horse has pastern dermatitis with crusting and pruritus in the summer/early fall

A

Trombiculosis (chiggers)

**This is in Europe
*Chiggers usually live in decaying plant matter, but need to feed on blood for larval life stage

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29
Q

3 chemicals that cause percutaneous photosensitization

A

1) Plants
2) PABA (used in sunscreen? UVB filter)
3) Hexachlorophene (disinfectant)

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30
Q

Distribution of pastern vasculitis

A

Hind limbs > front limbs
Lateral/medial > cranial/caudal

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31
Q

In 1 study, which sex was more predisposed to vasculitis

A

Mares
(but not repeatable in a different study)

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32
Q

Which clinical sign was present in most horses with vasculitis?

A

SQ edema

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33
Q

Which infection can cause vasculitis in horses?

A

Purpura hemorrhagica 2’
-Streptococcus equi (strangles)
-Corynebacterium pseudotuberculosis

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34
Q

What is the prognosis for vasculitis in horses

A

Guarded. 63% survival rate

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35
Q

What is a negative prognostic indicator in horses with vasculitis?

A

Fever

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36
Q

Which bacteria is associated with vasculitis

A

Staphylococcus intermedius

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37
Q

While photoaggrevated vasculitis causes crusts/erosions/ulcers, what clinical signs are seen with pigmented vasculitis?

A

Scale, alopecia

38
Q

Thickened nodules, corrugated skin of distal limb in a draft horse. Diagnosis?

A

Chronic progressive lymphedema

39
Q

Labwork values indicative of hepatocellular injury

A

AST, SDH, GLDH

40
Q

Labwork values indicative of biliary disease

A

GGT, ALP, Bile acids

41
Q

Labwork values indicative of inflammation

A

Fibrinogen, SAA, TP, Albumin

42
Q

Risk factors for chronic progressive lymphedema (7)

A

1) Older age
2) Larger cannon circumference
3) Poor hoof grooming
4) Fetlock feathers
5) Larger ergots, chestnuts
6) Pastern bulges
7) Poor hygienic conditions

43
Q

Type of inflammatory cell seen in chronic progressive lymphedema

A

T cell perivascular inflammation with lymph edema and dermal fibrosis

44
Q

What is the primary tissue affected with progressive lymphedema

A

Altered ELASTIN metabolism –>

impaired lymphatic drainage in distal extremities. Inflammatory changes are 2’ to lymph issues

45
Q

Differentials for alopecia and scaling of distal limbs (4)

A

1) Dermatophyte
2) Bacteria
3) Vasculitis of pigmented skin
4) Localized sarcoidosis (localized lympho-histiocytic granulomatous dermatitis); unknown trigger for this inflammatory reaction

46
Q

Is localized sarcoidosis the same as generalized sarcoidosis?

A

NO. Unknown trigger for localized; not associated with BPV. Better prognosis than generalized sarcoidosis (which is also not BPV associated)

47
Q

Coronary band differentials (7)

A

1) Infections
DRY/FISSURES
2) Coronary band dystrophy
3) Selenosis
EROSIVE/ULCERATIVE/CRUSTED
4) Pemphigus
5) Multisystemic Equine Eosinophilic Epitheliotrophic Dermatitis and Stomatitis (MEEEDS)
6) Sarcoidosis (Multisystemic granulomatous disease)
7) Hepatocutaneous syndrome

48
Q

Seleniosis signs

A

Dry, fissures of coronary bands

49
Q

MEEDS prognosis

A

Grave

50
Q

T or F: Horses can have hepatocutaneous syndrome

A

True

51
Q

Differentials for spontaneous, nonpruritic noninflammatory, alopecia (5)

A

Multifocal:
1) Alopecia areata
2) Demodicosis

Generalized:
3) Alopecia areata (rare to be generalized)
4) Telogen/anagen effluvium
5) Selenium toxicosis

52
Q

Differentials for sontaneous, nonpruritic alopecia WITH crusting (4)

A

1) Bacterial folliculitis
2) Occult sarcoid
3) Dermatophilosis
4) Dermatophytosis

53
Q

If you are suspicious of Staphylococcal folliculitis, what other differentials should you think of (look similar)?

A

Dermatophilosis
Dermatophytosis

54
Q

Linear keratosis (crusting, alopecia). Most common body sites

A

Rump, shoulder, neck, lateral chest

55
Q

Age with linear keratosis

A

Young, persists lifelong

56
Q

Does linear keratosis track nerves, vessels, dermatomes?

A

No!

57
Q

Would you expect orthokeratosis or parakeratosis with linear keratosis?

A

Orthokeratotic

(as opposed to Coronary Band Dystrophy, which is parakeratotic)

58
Q

What is the most common cause of generalized crusting?

A

Pemphigus foliaceus

59
Q

Generalized granulomatous disease (sarcoidosis) prognosis

A

Grave

Eventually get “wasting syndrome” with internal organ involvement –> die

60
Q

Diagnosis?

A

MEEDS

61
Q

Differentials for generalized crusting/scaling in the horse? (6)

A

1) Pemphigus foliaceus
2) Generalized granulomatous disease (sarcoidosis)
3) MEEEDS
4) Lupus
5) Cutaneous lymphoma
6) Toxicosis (selenium, arsenic, mercury, iodine)

62
Q

Most common cutaneous neoplasms in the horse

A

*Sarcoids
*Melanoma
*SCC
*MCT

63
Q

Incubation time for equine viral papilloma on the muzzle

A

60-70d

64
Q

VIrus that causes equine papilloma virus on muzzle

A

EcPV1

65
Q

Vector for EPV on muzzle

A

Insects

66
Q

Age for equine viral papillomas (muzzle)

A

Young (<2 yr old)

Spontaneously regresses in 3-4 months usually (1-9 months)

67
Q

Body regions affected by equine viral papilloma

A

Muzzle, eyelid, genitalia, legs

68
Q

Equine ear papillomas, aural plaque: viruses

A

EcPV 1,3,4,5,6
Coinfection in 59%

69
Q

Vector for Equine ear papillomas, aural plaque

A

Black fly

70
Q

Age for Equine ear papillomas, aural plaque

A

> 1 yr old

Require treatment

71
Q

Black flies can spread EcPV. Which form is usually spread by this fly?

A

Equine ear papillomas, aural plaque

72
Q

What other sites of the body should you check in a horse with Equine ear papillomas?

A

Concave pinnae
Genitalia
Mammaries

73
Q

Most common location of SCC

A

Eyelids, external genitalia

74
Q

Type of skin affected by SCC

A

Unpigmented

75
Q

Risk factors for SCC

A

UV light
EcPV2 (the ONLY papilloma not indicated in aural plaques)

76
Q

Differential for nodules near frictional areas (2), ie saddle frictional areas

A

-Eosinophilic granulomas!!!

-Infectious granulomas

77
Q

Most common tumor on ventral tail/perianal area in grey horses

A

Dermal melanoma

(also, lips, eyelid, sheath, muzzle)

78
Q

Gene associated with grey horse phenotype, dermal melanoma progression

A

STX17 (and agouti-signaling protein, ASIP)

(Risk of metastasis, look at soft palate, gutteral pouch)

79
Q

What can equine papilloma transform into?

A

SCC
EcPV2

80
Q

Where on the body are sarcoids found?

A

Anywhere!

More common where skin is thin (ie frictional areas, face)

81
Q

Most common skin tumor in horses

A

Sarcoid

82
Q

Viruses associated with sarcoids

A

BPV 1 & 2

83
Q

What type (greek letter) papillomavirus is BPV 1?

A

DELTA papilloma virus

This means not only does it infect keratinocytes, but ALSO dermal fibroblasts

84
Q

Oncogenes associated with sarcoids from BPV 1, 2

A

E5, E6, E7

Maintenance of infection + neoplastic transformation of fibroblasts

Degrade p53 , so can’t regulate cell cycle

Affect chromosome stability

85
Q

What genetic mutation is a potential predisposition for development of Sarcoids?

A

MHC class II

86
Q

Breed that get sarcoids LESS frequently

A

Standard bred horses

87
Q

Most common nodular skin disease in horses

A

Collagenolytic granulomas (eosinophilic granuloma w/collagen degeneration) –> Calcify

2’ insect bites > trauma, atopy

Often seasonal

88
Q

Treatment of choice for Sporotrichosis schneckii in horses

A

Ethylene diamine dihydroiodide (EDDI)

89
Q

Breed of horse predisposed to panniculitis

A

Shetland ponies

Steatitis of weaning foals

90
Q

Genetic predisposition for equine sarcoids

A

Certain Equine Leukocyte Antigen (ELA) alleles increase risk: A3, W13

EV ACVD Study (52 decks)

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