Erosions and Ulcers Flashcards
1
Q
describe physical trauma that can cause erosions and ulcers
A
- abrasions
- scratching!! most common!!
- thermal burns
- chemical burns
- frostbite
- maceration from chronic moisture exposure
2
Q
describe burns
A
- mechanisms: thermal, solar, electric, microwave, chemical
-potential hazard: electric heating pads at vet clinics - wide range from superficial to deep, localized to extensive
-depending on relative strength and length of exposure - the initial symptoms may not be very obvious and may consist only of skin erythema and pain when touched before tissue necrosis becomes more obvious
3
Q
describe the degrees of burns
A
1st degree: erythema and pain (epidermis only)
-heal without complications
2nd degree: erythema, pain, blister formation, moist (epidermis and superficial part of dermis)
-heal with discoloration and scarring
3rd degree: dry, discolored, eschar, loss of sensation (epiderm, derm, and subcutaneous fat = no time to form a blister)
-heal slowly with discoloration, scarring, may need tissue grafts
4th degree: charred, black skin, underlying tissue may be visible, loss of sensation (all the way down to the muscle and/or bone)
-complicated healing; often need grafts, take months to years to heal
4
Q
describe declaration of burns (3)
A
- declaration of burned skin can be fast (48-72 hours) or very slow and take up to 2-3 weeks
- deep burns that cover >20% of body surface are problematic due to fluid and electrolyte imbalances
>50% of body surface coverage = death sentence - burns carry the risk of infection and subsequent sepsis
5
Q
describe burn management basics (6)
A
- cool (not cold/icy) water rinses if burn happened within part 24 hours
- dead skin debridement: often in stages/over time
- hydrotherapy
- topical antiseptics (silver sulfadiazine, mupirocin)
- wound protection if indicated/possible (non-occlusive bandage)
- supportive care: fluids, electrolytes, PAIN MANAGEMENT
the deeper the burn, the slower the healing
no systemic antibiotics because no blood supply in burn to be absorbed!
-NOT prophylactic either because will alter microbiome in a bad way and leave only the bad guys behind
-ONLY indicated in septic patients
6
Q
describe the effects of frostbite/hypothermia (3)
A
- usually affect distant body parts (ear tips, tail tips, paws, scrotum)
- cold wind and moisture amplify skin impact
-can also be caused by contact with frozen metal objects - necrosis and sloughing WITHOUT eschar formation
7
Q
what are 2 infectious external agents causing erosions and ulcers
A
- superficial pyoderma:
-skin fold dermatitis/intertrigo
-hot spots/pyotraumatic dermatitis - feline herpes virus dermatitis
8
Q
describe intertrigo (3)
A
- skin fold dermatitis: associated with inflammation and superficial bacterial infection
- skin fold areas are subject to friction, inflammation, and moisture retention
-environment allows microbes to flourish - commonly on:
-facial/nasal folds
-lip folds
-tail folds (bulldog screw tails)
-vulva folds
-shar pei
9
Q
describe hot spot/pyotraumatic dermatitis (3)
A
- intensely pruritic, often painful, moist, erythematous
- bacterial will complicate the situation if inflammation is not controlled
- if not treated ASAP:
-erosion, then ulceration, then hemorrhage, then deep pyoderma
10
Q
describe treatment basics of intertrigo and pyotraumatic dermatitis (5)
A
- clean and dry
- TOPICAL antiseptics/antibiotics
- +/- topical steroids
- search for possible triggers for pyotraumatic dermatitis (fleas, atopy, etc.)
- surgical fold removal if all else fails or is wiping is impractical
11
Q
describe genetic internal causes of erosions and ulcers (2)
A
- epidermolysis bullosa
- canine familial dermatomyositics
12
Q
describe epidermolysis bullosa (3)
A
- certain adhesion molecules in the basement membrane areas are made in a faulty way due to genetic mutations, leading to construction failure and sloughing of epidermis, resulting in an ulcer!
-will look like autoimmune disease - in Belgian Blue cattle:
-mutation in laminin gene causes extensive epidermal and mucosal sloughing that is present at birth
-in horses (belgian draft horses), sheep, goats, dogs, cats, and humans - no current effective treatment
13
Q
describe familial dermatomyositis (5)
A
- in collies and shetland sheepdogs
-has a genetic background but requires an environmental trigger to develop! - inflammatory disease of the skin and muscles (blood vessels)
- uncommon, underlying cause unknown
- first symptoms often before 6 months of age
-erythema, vesicles, crusts, erosions/ulcers, pigment loss that progresses to alopecia and scarring (heal with scars because lesions are so deep)
-on the face, ear tips, tail tip, bony prominences (areas of mechanical friction)
-other symptoms: myositis (abnormal gait, muscle atrophy, problems chewing), megaesophagus
- diagnosis:
-history and signalment
-skin biopsies
-muscle biopsies
-electromyography
14
Q
describe necrolytic migratory erythema (hepato-cutaneous syndrome), an internal metabolic cause of erosions/ulcers (5)
A
- 80% are linked to cirrhotic/end-stage liver disease
-15% related to phenobarbital-related hepatitis
-5% linked to pancreas neoplasia (glucanomas) - pathogenesis may be linked to amino acid metabolism but remains poorly understood
- erosions/ulcers and crusts over friction areas and pressure points
- diagnosis:
-clinical presentation
-bloodwork/ultrasound
-histopathology of skin lesions - treatment:
-difficult due to underlying disease process (end-stage liver disease = mostly irreversible)
-only exception: surgical removal of pancreatic glucagonoma (full recovery possible)
-IV amino acids help temporarily
-supportive care
15
Q
what are 2 internal neoplastic causes of erosions/ulcers?
A
- squamous cell carcinoma (SCC)
- cutaneous lymphoma
16
Q
describe squamous cell carcinoma (4)
A
- usually preceded by chronic solar dermatitis resulting in actinic keratosis
-in white or lightly colored areas - on ears, nose, lips, and eyelids
-erythema, fine scaling, alopecia
-crusting and curling of ear margin
-ulceration, hemorrhage, crusting
-tissue destruction - many species can be affected
- treatment of choice: surgical removal
17
Q
what are 2 internal ischemic causes of ulcers/erosions?
A
- vasculitis
- vasculopathy
18
Q
describe vasculitis (3)
A
- not a disease! is a cutaneous reaction pattern associated with multiple causes
- uncommon in dogs and horses
-rare in cats
-very rare in cattle - can be associated with:
-infection
–strep equi: purpura hemorrhagica
–rickettsia rickettsii: RMSF
-rabies vaccination
-drug reaction
-arthropod reaction
-neoplasia (MCT)
-SLE: systemic lupus erythematosus
-idiopathic: most common, we usually cannot find the trigger
19
Q
describe clinical signs of vasculitis (9)
A
variable depending on size of blood vessels involved
- purpura: purple rash
- uticaria to pitting edema
3, punctate to larger ulcers - acrocyanosis
- necrosis (sloughing)
-lesions do not blanch!
-on: pinnae, lips, oral mucosa, pressure points, scrotum, tail, paws/nails, coronary bands
- +/- fever, anorexia, depression, death
- lesions can be linear or following vascular patterns
-may be focal or widespread - +/- pain
- episodes may be short or carry on for a lifetime
20
Q
describe DANP (6)
A
- dermal arteritis of the nasal planum/nasal arteritis
- ulceration of the nasal philtrum perpendicular to long axis due to local artery inflammation in large breed dogs
- etiology unknown
- acute, severe hemorrhage can be a true dermergency
- biopsy can be tricky and perhaps unnecessary since clinical presentation is unique
-will bleed like a bitch if you do - treatment: topical tacrolimus
-topical version of cyclosporine
-such a focal area = treat topically to keep side effects low
21
Q
describe rostrolateral nasal alar arteriopathy of German Shepherd dogs
A
similar to nasal philtrum arteritis except for different location
treatment: flush lesions with epinephrine to contract vessels to stop profuse bleeding
-ice packs to shrink blood vessels
-hold pressure
-systemic immunosuppression initially then switch to topical
22
Q
describe ischemic dermatopathy (4)
A
- histopathology shows effects of ischemic insult without blood vessel inflammation visible
-also called cell-poor vasculitis - widespread skin lesions after rabies vaccine
-progressive patchy alopecia
-erosions/ulcers
-skin/collagen fibrosis: pale skin areas
-nasal depigmentation and ulceration and tissue loss
-loss of foot pad surface structure, hyperkeratosis, small erosions and ulcers
-loss of multiple nails
-problems walking
-loss of distal pinnae tissue; at ear margin: ulceration, hemorrhage, crusting, and tissue fibrosis - diagnosis:
-history, clinical signs
-histopathology: ulcer ad crusts overlying cartilage - therapy: “correct underlying cause”
-oclacitinib
-glucocorticoids
-cyclosporine
-pentoxyfilline: synthetic xanthine structurally related to caffeine, increases erythrocyte flexibilty and reduces inflammation but no good evidence in vet literature for use in animals currently
23
Q
describe the primary and secondary lesions of pemphigus foliaceus
A
primary: pustule
secondary: crust + erosion
24
Q
describe pemphigus erythematosus (3)
A
- depigmentation and crusting of the nasal planum and adjacent areas
- lesion worsens and improves in the course of a year without treatment
-usually worse in summer and with sun exposure - no other skin lesions or systemic symptoms
25
describe pemphigus vulgaris (4)
1. rare, deep
2. salivation, halitosis, extensive oral ulceration
-may see oral vesicles and ulceration upon rupture
-ulcers and crusts on concave pinna
-ulcers on nasal planum and foot pads
-peripheral depigmentation
-minimal to no crusting
3. fever, anorexia, depression
4. histopathology:
-acantholysis
-suprabasilar clefting
26
compare and contrast pemphigus erythematosus and pemphigus vulgaris
PE:
1. superficial and benign
2. lesions on nose, face, and ears: pustules, crusts, erosion/ulcerations, depigmentation
3 UV light can exacerbate lesions
4. subcorneal and intraepidermal acantholysis (pustule formation) and lichenoid interface dermatitis
5. crossover between PF and discois lupus erythematosus
PV:
1. oral ulcers (from transient vesicles), mucocutaneous junction ulcers, sometime foot pad involvement
-systemic signs: fever, anorexia
2. often poor prognosis
3. suprabasilar (deep) acantholysis (vesicle formation), clefting
4. deep pemphigus form
-if see deep oral ulcers = TROUBLE
27
list the cutaneous lupus variants
1. FDLE: facial (classic) discoid lupus erythematosus
2. MCLE: mucocutaneous lupus
3. ECLE: exfoliative cutaneous
4. VCLE: vesicular cutaneous
all look comparable on histopath!!
28
describe the pathogenesis of lupus
1. lymphocyte-mediated death of basal keratinocytes in the epidermis cause progressive loss of structural integrity leading to depigmentation, erosions, and ulcers
2. on histopath:
-lichenoid interface dermatitis (lymphocytes)
-apoptosis of basal keratinocytes
29
describe canine DLE (5)
1. facial/classic form and generalized form
2. GSD, shetland sheepdog, collies
3. facial:
-planum nasale lesions
-depigmentation
-loss of cobblestone structure, ulceration, crusting, scarring
4. aggravation by UV light
5. usually no systemic signs
30
describe VCLE (3)
1. in rough collies, shetland sheepdogs, border collie mixes
2. figurate erythema, vesicles, erosions
-on the VENTRUM, axillae, and medial thighs
3. no systemic signs usually
31
describe ECLE (4)
1. german shorthaired pointers
2. erythema, scaling, follicular casts, alopecia (sometimes scarring)
-on the muzzle, pinnae, trunk, and abdomen
3. systemic signs!
-lameness, progressive lethargy, lymphopenia, thrombocytopenia, infertility
4. poor prognosis
32
describe MCLE (3)
1. 50% GSDs
2. erosions, ulcers, and peripheral hyperpigmentation
-locations: anal, perianal, perigenital, perioral, periocular
3. usually no systemic signs
33
describe general treatment for ALL forms of lupus (2)
1. topical tacrolimus
2. UV avoidance
the treatment side effects should NOT be worse than the disease!!
34
describe uveodermatological syndrome/VKH (4)
1. lymphocyte-mediated death of melanocytes of the skin and eye
2. in samoyeds, akitas, huskies, malamutes
3. perimucosal skin depigmentation, erosions, ulcers of the face
AND
uveitis
-risk of blindness
4. eye treatment is priority!!
-response to immunosuppressive treatment is variable
35
describe MMP, an autoimmune subepidermal blistering disease (AISBD) (4)
blister = clear fluid collection underneath the epidermis with resulting ulceration
1. MMP: mucous membrane pemphigoid
-autoantibodies against multiple components of the basement membrane causes subepidermal vesicle formation and ulceration
2. in dogs and cats (GSDs overrepresented) but rare
3. lesions in ORAL CAVITY, nose, ears
-vesicles, bullae, ulceration
-nose can look like PE or DLE but will have ULCERS in the MOUTH (the other two will not)
4. variable response to immunosuppressive treatment
36
describe erythema multiforme/Steven-Johnson Syndrome/Toxic Epidermal Necrolysis (3)
1. death of keratinocytes in ALL layers of the epidermis with increasing severity and variable clinical presentations
2. EM: uncommon in dogs and rare in cats and horses
-pathogenesis unknown
-epidermis still mostly sturdy and intact, dead keratinocytes spread throughout
-single keratinocyte death/apoptosis in all layers of epidermis + interface dermatitis
3. SJS (less severe), TEN (very severe)
-rare in dogs and cats, horses, cattle, and goats
-predominantly due to drug reactions
-high risk drugs in dogs: TMS, cephalosporins, penicillins, NSAIDs
-ALL keratinocytes are dead, epidermis lifts off = giant ulcer but minimal inflammation
37
describe EM lesions
humans:
-classic papules which spread peripherally and clear centrally = target lesion
-can be triggered by herpesvirus
animals:
-often atypical targetoid lesions, erosions, ulcers
-mucosal lesions may be present
-animals often develop a chronic form
38
describe SJS/TEN lesions (4)
1. widespread erythematous macules/patches on body and multiple mucosal surfaces that lead to bullae formation and extensive ulceration/epidermal detachment
2. moderate to severe skin pain
3. acute onset +/- rapid progression to life-threatening situation possible
-skin sloughing
4 SJS when less than 10% of body surface affected
-TEN when >30% of body surface affected
-if over 50% affected, likely fatal
-TRUE EMERGENCY
39
compare prognosis and treatment of EM to SJS/TEN
1. EM:
-often good prognosis, but varies
-treatment: immunosuppression
2. SJS/TEN:
-prognosis guarded to poor in dogs and cats
-massive fluid and electrolyte loss via skin and sepsis risk
-treatment: stop any suspected drug, fluid and electrolyte replacement, wound management (infection/sepsis prevention), pain management
