MS > Environmental + camelids > Flashcards

Environmental + camelids Flashcards

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1
Q

Causes of gangrene?

A

(1) external pressure (e.g., pressure sores, ropes, constricting bands),
(2) internal pressure (e.g., severe edema),
(3) burns (thermal, chemical, frictional, electri- cal, radiational),
(4) frostbite,
(5) envenomation (snake, spider),
(6) vasculitis,
(7) ergotism,
(8) photodermatitis,
(9) various infections (Clostridium, Staphylococcus, Streptococcus, Fusobacterium)

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2
Q

Pododermatitis in llamas and alpacas is caused by?

A
  1. trauma,
  2. bacterial folliculitis
  3. yeast infection
  4. chorioptic mange
  5. sarcoptic mange
  6. contact dermatitis
  7. insect‐bite hypersensitivity and
  8. zinc‐responsive dermatitis
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3
Q

Deep infections in pododermatitis in llamas and alpacas are associated with

A

Staphylococcus spp., Trueperella spp., and Fusobacterium spp

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4
Q

Most common fungal infection in camelids

A

T. verrucosum

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5
Q

What are the predisposition factors for yeast (mostly Malassezia ) dermatitis in camelids?

A
  1. environment (moisture, filth)
  2. poor nutrition
  3. other skin disorders (e.g., chorioptic mange, zinc‐responsive dermatitis)
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6
Q

Where are lesions most commonly seen with yeast deramtitis ?

A

-interdigital area and intertriginous areas (axilla, groin, perineum)

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7
Q

What causes psoropic mange in camelids

A

P. bovis

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8
Q

What causes sarcoptig mange in camelids

A

Sarcoptes scabiei var. auchinae

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9
Q

Has adverse cutaneus drug reactin been reprted in camelids?

A

Yes, ivermectin in alpaca

-Edema and ulcers on the pinnae
- pustular dermatitis on the ventral abdomen, prepuce, perineum, axillary and inguinal regions
-systemic signs:fever, inappetence,depression

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10
Q

Recommended treatment for perivulvar dermatitis

A
  1. Anti-seborrheic (benzoyl peroxide, sulfur): initially shampoo; ointments or gel for maintenance
  2. Glucocorticoids: topical or systemic
  3. Talc
  4. Acetic acid: when Malassezia predominates
  5. Medical honey: no difference from placebo for nasal fold intertrigo
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10
Q

Give most likely diagnosis

A

Aural hematoma and chondritis
-hereditary
-small, fluid‐filled, flat plaques occur on the lateral surface of both pinnae
-no pain no pruritus

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11
Q

Recommend tretament for pyotraumatic dermatitis

A
  1. Clipping, antiseptics
  2. Drying agents: aluminum acetate (Domeboro), aluminum acetate + hydrocortisone, menthol + Hamamelis (Dermacool)
  3. Systemic GC: single injection of dexamethasone 0.1 mg/kg IV
  4. topical GC betamethasone, betamethasone 0.1% + fusidic acid 0.5% gel (Fuciderm, Leo; currently Isaderm, Dechra), prednisolone + neomycin, hydrocortisone aceponate
  5. Systemic antimicrobials- usually not needed
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12
Q

What is pathomechanism of pressure sores

A

occlusion of blood circulation;
-ischemia leads to TXA2 production that causes
a) further vasoconstriction,
b) platelet aggregation leading to vascular occlusion,
c) direct toxicity to the cells

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13
Q

Treatment for callus dermatitis:

A

1) hydrotherapy,
2) magnesium sulfate,
3) topical antibiotics,
4) preparation H

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13
Q

Treatment for callus pyoderma

A

systemic antibiotics (treatment stops 1-2 weeks after negative cytology)

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14
Q

Treatment of calluses

A

balm containing essential oils and essential fatty acids

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15
Q

Possible complications of hygroma

A

1) abscess,
2) granuloma

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15
Q

Pathogenesis of hygromas

A

repeated trauma with necrosis and inflammation

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16
Q

Treatment of hygroma

A

1) bandage,
2) corrective housing,
3) surgery

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17
Q

Simarouba amara wood shavings

A

1.) systemic signs: anorexia, depression, paresis;
2) skin lesions: erosions, ulcers, ulcerated nodules (face, nose, lips, oral cavity, chin, elbows, hocks, scrotum, prepuce, anus);
3) laboratory findings: increased ALT, ALP, AST, hypoalbuminemia

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18
Q

Mycotoxicosis cause

A

1) ergotism (necrosis),
2) NME

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19
Q

Most common arsenic poisoning symptoms

A

swollen muzzle, necrosis of extremities;
Bowen’s disease in Humans

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20
Q

What are most common sources of thallium toxicosis

A

rodenticide, roach poison

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21
Q

Clinical signs of thallium toxicosis

A

Hyperacute toxicity: CNS, circulatory, death
Acute toxicity: sever GI
Chronic toxicity: skin lesions (erythema, alopecia, ulceration, footpad hyperkeratosis) + mucus membrane congestion + GI

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22
Diagnosis of thallium toxicosis
1) histopathology, 2) thallium detection in urine
23
Treatment of thalium toxicosis
supportive + activated charcoal + KCl PO
24
What is pathogenis of arteriovenous fistula
1. Congenital (rare): 2. Acquired (common): 1) penetrating wound, 2) blunt trauma, 3) infection, 4) neoplasia, 5) surgical (declawing), 6) extravascular injection of irritating substances, 7) hyperthyroidism (recurrent arteriovenous fistulas in a C)
25
What are clinical signs of artervenous fistula
Edema, pain, hemorrhage Pulsating vessels, thrills, murmurs Occlusion of the artery: sudden drop of heart rate, disappearance of thrill and murmur
26
Classification of foreign bodies
-exogenous, -endogenous (hair shafts, keratin, free lipids, Ca salts, urate)
27
SUBCUTANEOUS CHYLE causes
1) thoracic duct ligation, 2) lymphangiectasia, 3) lymphangioma
28
What are predisposing factors to frost bite
Ill animal, neonate Recent move from a warm area to a cold area Vasculopathy, cryoglobulinemia Lack of shelter, wind, wet coat
29
Treatment for frost bite
Fast rewarming with warm water Surgery Medication: aspirin, PTX, aloe vera
30
What are the first signs of frost bite
Curling of ear pinnae Leukotrichia
31
Radiation injury , what are the skin lesions
1. Hypotrichosis, scales, moist desquamation (associated with bacterial infection) 2. Depigmentation, leukotrichia (may be permanent) 3. Vascular damage: erythema + swelling up to necrosis
32
Can we use pred for th of radiation injury
NO -prednisolone had no effect in an RCT for acute radiation dermatitis; + prophylactic treatment with cephalexin (starting in the middle of radiation treatment) did not decreased the risk of bacterial infection, increased the risk of MDR staphylococcal infection, resulted in worse scores of radiation injury and is not recommended
33
Name causes of burns:
1. Chemicals 2. Electric currents 3. Radiation: solar (darkly pigmented skin), microwave 3. Heat (e.g. heating pads; garden hoses with hot water due to sun exposure; sun exposure of haired and dark areas of the skin; high core body temperature of 41.7oC) 4. Frictional
33
Name the classification of burns
1. Partial thickness: epidermis + superficial dermis; little or no scar 2. Full thickness: complete destruction of all cutaneous structures; need surgery
34
What is the alternative classification
1st degree: superficial epidermis; no vesicles 2nd degree: entire epidermis; with vesicles 3rd degree: epidermis + dermis + appendages 4th degree: entire skin + SC + muscle, fascia, tendons
35
What is the recommened treatment for burns
1. Bathing (chemical burns) 2. Cooling: water at 3-17oC x 30 min (if examined within 2 h from burn) 3. Surgical debridement; hydrotherapy; bromelanin-based proteolytic enzyme preparation (Nexo-Brid): after 4 hours of occlusive application removed necrotic tissue while preserving healthy dermis 4. Topical antimicrobials: silver sulfadiazine, silver nitrate (wet dressing), mupirocin
36
What is the cause of immersion foot in horses
-standing in cold water 2-3 days -necrosis and sloughing
37
Can we use patch testing in irritant contact dermatitis
NO -unproven efficacy (irritant); -standard diagnostic (allergic); if the allergens used for patch test are at a non-irritant concentration, a positive test result confirms allergic contact dermatitis
38
How can we distingusih irritant contact dermatitis from contact hyeprsensitivity- diagnostic methods
1. Provocative exposure -application onto healthy and diseased skin (irritant); environmental avoidance followed by exposure (allergic) 2. Patch testing
39
UV induced neoplasia UVB>UVA how long do we have to be on sun to get it
SSC: long-term exposure Basal cell carcinoma: episodes of intense exposure-blistering sunburn Melanoma: long term exposure
40
Mechanisms of UV-induced neoplasia
Direct and indirect DNA damage with mutations that have a specific pattern of C to T and CC to TT nucleotide substitutions; mutations of p53: a) formation of pyrimidine dimmers → inhibition of DNA repair; b) production of free radicals; c) production of purine photoproducts; d) stimulation of enzymes that promote tumors; e) inflammation; f) immunosupression; g) stimulation of angiogenesis; h) production of growth factors; i) co-factor with other types of radiation, chemicals or viruses; j) resistance to apoptosis
41
Sun exposure can induce or exacerbate wich autoimmune diseases
1) DLE, SLE, VCLE, PF (?), PE, BP, 2) dermatomyositis
42
What is the prodromal sign of photosensitivity in ovine
-edema of the face and pinnae
43
What are the causes of photosensitivity
a) Primary or type I: 1) plants, 2) medication (systemic, topical) b) Hepatogenous or type III (not in P): 1) plants, 2) other liver diseases c) Aberrant pigment synthesis or type II: porphyria (not reported in C, in O and in P) d) Idiopathic e) Dermatophilosis f) metritis
44
What are the chonic changes seen in HF due to solar dermatitis
actinic comedones, follicular cysts, folliculitis, furunculosis
45
What are the chonic changes seen in epidermis due to solar dermatitis
actinic keratosis, SSC
46
What are the chonic changes seen in dermis due to solar dermatitis
fibrosis, elastosis, hemangioma, hemangiosarcoma +vasculopathy
47
What are the recommended treatment fro solar dermatitis
1. Glucocorticoids 2. Sunlight avoidance: indoors, T-shirts (lycra with UPF of 50+) 3. Sunscreens: topical, systemic 4. COX-2 inhibitors: firocoxib (5 mg/kg SID) x 6 months was effective in 4/5 dogs with reduction of macroscopic and histologic (mainly the epidermal) lesions
48
Can we use retinoids in actinic keratosis
-etretinate-acitretin (they may be effective in actinic keratosis but they are not effective in pure solar dermatitis); -isotretinoin was effective in a dog with solar dermatitis and secondary deep pyoderma due to MRSP (the later resolved with only isotretinoin and topical benzoyl peroxide)
49
What are recommened tretament for feline solar dermatitis
1. Sunlight avoidance 2. Sunscreens topical (ear pinnae only; also face) or systemic (b-carotene, canthaxanthine: severe cases may not respond) 3. Cosmetic amputation of ear tip: followed by sunlight avoidance 4. Imiquimod: 2-3/week x at least 6 weeks 5. Actinic keratosis: surgery, vitamin A or etretinate or acitretine, radiation, pinnal amputation
50
Glass effectively filters what part of UV spectrum
UVB and UVC
51
There are 2 kinds of topical sunscreens:
1. physical: zinc oxide, titanium oxide 2. chemical: para-aminobenzoic acid, cinnamates, salicylates, benzophones, octocrylene
52
Do you know any veterinary product for sun protection
Ecran solaire cien chat SPF 30 (Dermoscent) has independent confirmation of the claimed SPF; -4/6 products had no protective activity and 1/6 a lower SPF than the label
53
Name oral sunscreens
1. β-carotene (controversial, does not block UVB; 30 mg/dog BID and then SID), 2. canthaxanthin, 3. chloroquine
54
What are the MOA of sunscreens
quench free radicals and stabilize membranes
55
What are chromatophores
molecules that absorb UV light
56
Classification of photodermatitis
1) phototoxicity, 2) photosensitivity
57
How is solar spectrum divided:
1. Infrared (50%): 760-100,000nm 2. Visible (40%): 400-760nm- penetrates into the dermis and produces thermal energy 3. UV (9%): 100-400nm; does not penetrate into dermis, does not produce substantial amounts of thermal energy
58
How is UV light spectrum divided
1. UVA (320-400nm): deep penetration, photosensitivity; mainly oxidative damage 2. UVB (290-320nm): erythema, phototoxicity; mainly damage to DNA-more carcinogenic than UVA 3. UVC (100-290): cell damage; not on earth surface (absorbed by ozone)
59
What is the pathomechanism of solardermatitis or phototoxicty
1. Keratinocytes: vacuolation; apoptosis (biphasic; at 4h due to direct effect and at 24h due to DNA damage) 2. Vessels: dilatation (erythema), leakage (oedema) 3. LC, mast cells: depletion 4. Mediators: histamine, PG, LT, cytokines, vasoactive compounds, adhesion molecules, reactive O2 species (superoxide radical O2-; hydrogen peroxide-H2O2; hydroxyl radical HO-)
60
Is iritant contact dermatis more common than allergic in hores
Yes, + moisure is an important factor (horses sweat a lot, incerases the contact time)
61
Substances that cause primary contact dermatitis in horses ?
1. body excretions-feces and urine 2. wound secretions, 3. caustic substances (acids and alkalis), 4. crude oil, diesel fuel, turpentine, leather preservatives, mercurials, 5. leg sweats, topical medications 6. improperly used topical parasiticides (sprays, dips, pour-ons, and wipes 7. irritating plants Helenium microcephalum [small-head sneeze- weed], Cleome gynandra [prickly spider flower], Urtica ureus and U. dioica [stinging nettle], and Euphorbia spp. [spurge]), 8. wood preservatives, bedding, and a 9. filthy environment
62
What is thought pathogenesis of immersion foot
-vasoneuropathy -associated with prolonged exposure to moisture, cold temperatures and impaired blood flow -form or irritant contact dermatitis?
63
Signs of mimosine toxicosis
-Mimosa pudica & Leucaena leucocephala -loss of hairs of mane, tail, fetlocks -hoof dysplasia and laminitis
64
DDX for mimosine toxicosis
1. AA, 2. selenosis, 3. mercurialosm, 4. mane and tail dysplasia
65
What toxins of Stachybotrys altra cause
-bone marrow suppression, thrombocytopenia, neutropenia, and hemorrhage -ulceronecrotic lesions- skin and mucous membranes
66
Where does Stachybotrys altra grow and what does it produce
-saprophytic fungus that grows on hay and straw and produces toxins referred to as macrocytic trichothecenes (satratoxins).
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