Defense & Barriers 2: Pruritus Flashcards
pruritus
= definition
when it becomes pathologic?
5 common clinical signs & one specific one in cats?
= an UNPLEASANT sensation that PROVOKES DESIRE TO SCRATCH
becomes pathologic when INTERFERES WITH QUALITY OF LIFE and/or causes SKIN INFLAMMATION
5 clinical signs?
1. SCRATCHING
2. LICKING/CHEWING
3. RUBBING (horses)
4. EXCESSIVE GROOMING (symmetrically pulling out hair in CATS)
5. BITING
3 main concepts you should keep in mind when approaching pruritus?
- COMMON DISEASES ARE MOST COMMON!
- treat WHAT YOU CAN SEE FIRST –> skin PARASITES & INFECTIONS are most common, so SEE HOW MUCH ITCH IS REMOVED WHEN YOU TREAT THOSE ALONE
- start with BASICS –> skin SCRAPINGS, CYTOLOGY, TRICHOGRAM & rule out ECTOPARASITES & INFECTIONS
type 1 hypersensitivity reaction…
= what is it BASICS
how quickly does this occur?
why does it happen/how does it lead to itch? (**note about difference in some dogs)
what 4 things can it cause?
= genetic predisposition to produce IgE against “NONSENSE” antigens, or antigens that SHOULD NOT GENERATE IMMUNE RESPONSE (pollen, cat dander)
how quickly?
within MINUTES, but will stop WITHIN AN HOUR if allergen removed
why does it happen/leading to ITCH?
1. allergen CROSS-LINKS to IgE on MAST CELLS or BASOPHILS
2. causes DEGRANULATION and release of INFLAMMATORY MEDIATORS (histamines & proteases)
3. mediators cause SURROUNDING TISSUE TO BECOME INFLAMED –> ITCH
**Some dogs produce IgGd instead of IgE
what 4 things can it cause?
1. URTICARIA (edema) & ANGIOEDEMA, but MOST COMMON IN HORSES
2. ANAPHYLAXIS
3. involved in FLEA BITE ALLERGY
3. DRUG REACTIONS
what type of hypersensivitiy reaction is this?
WHAT IS IT? (dog)
TYPE 1 HYPERSENSITIVITY
WHEALS & FLARES in DOG
urticaria
what basic thing causes urticaria?
rarity in dogs, horses, cats?
2 differentials it can resemble/species?
LEAKY vessels allowing LEAKAGE OF PLASMA INTO INTERSTITIUM
RARE in dogs, NON-EXISTENT IN CATS (elastic skin) and COMMON IN HORSES
2 DDxs?
1. BACTERIAL FOLLICULITIS in SHORT-COATED DOGS/HORSES
2. ERYTHEMA MULTIFORME in HORSES
identify & type of hypersensitivity reaction
URTICARIA
TYPE 1
LATE-phase reactions
= what it is OVERALL, including 2 proteins
timing?
three diseases? (2 are obvious, one is unique)
= occurs when mast cells ALREADY ACTIVATED from TYPE 1 IMMEDIATE & release MORE chemical mediators & EOSINOPHIL CHEMOTACTIC FACTORS
- Chemotactic factors bring eosinophils in, which then cause BYSTANDER TISSUE INJURY by releasing inflammatory mediators…
–> Major Basic Protein
–> Eosinophil Cationic Protein
–> BOTH ARE EXTREMELY NOXIOUS TO SKIN, RESPIRATORY TRACT & GI
timing?
= occurs within 2-4 hours after an immediate hypersensitivity reaction, and may persist for UP TO 24 hours
3 diseases?
1. ATOPIC DISEASES
2. FLEA BITE ALLERGY
3. WELL’S-LIKE Dz, CANINE ACUTE EOSINOPHILIC DERMATITIS
type IV hypersensitivity reaction…
timing? (overall & 2 phases)
provoked by…
3 diseases?
timing? = DELAYED
1. SENSITIZATION PHASE = langerhan cells bind to ANTIGENS & T cells sensitized in REGIONAL LNs upon FIRST EXPOSURE
2. ELICITATION PHASE = RAPID production of T cells after RE-EXPOSURE, usually 24-48 hours later
provoked by…
HAPTENS, or SMALL MOLECULES that ALONE cannot generate allergenic response, but BINDS TO PROTEINS so that they can!
3 diseases?
1. CONTACT ALLERGY
**Poison ivy/sumac NOT ALLERGENIC TO PETS
2. INSECT reactions (flea bites in dogs/cats, flies in horses)
3. MYCOBACTERIA (TB, leprosy)
PATHOPHYSIOLOGY of pruritus? (**& where they terminate)
what 4 things can bind to cause it?
= PRURITUS is sensed by FREE-ENDINGS OF UMYELINATED C-FIBERS that TERMINATE AT EPIDERMAL-DERMAL JUNCTION (in epidermis) INFLAMMATORY MEDIATORS bind, such as…
1. HISTAMINES
2. PROSTAGLANDINS/LEUKOTRIENES released by MAST CELLS
3. CYTOKINES, particularly IL-31
4. SUBSTANCE P = NEUROENDOCRINE, released in STRESS
what 5 differentials should we consider for PRURITUS?
**include one for CATS
what disease is usually NON-PRURITIC?
5 differentials?
1. ALLERGIC DISEASES
2. PRIMARY INFECTIONS (ex = ringworm)
2. SECONDARY INFECTIONS (ex = malassezia, bacterial infection, pyoderma)
4. PARASITIC DISEASES
5. DRUG REACTIONS –> cats get FACIAL pruritus on TAPEZOLE for thyroid
URTICARIA is usually NON-PRURITIC
3 main diseases that we consider in ALLERGIC PATIENTS?
- FLEA BITE allergy
- atopic dermatitis from ENVIRONMENT or STRESS
- FOOD sensitivity
itch threshold
what is it?
what can affect it?
POINT ABOVE = ITCHING, POINT BELOW = NOT ITCHING
affected by WHETHER THERE’S ENOUGH ALLERGIC-CAUSING SUBSTANCES IN ENVIRONMENT FOR REACHING THRESHOLD
if ACUTE pruritus… (2)
- ECTOPARASITIC DISEASES can TAKE TIME TO DEVELOP A CLASSIC DISTRIBUTION PATTERN, so might look like GENERALIZED ITCH in the beginning
- Good to RULE OUT INFECTIOUS CAUSES (ectoparasites, staph, Malassezia) before prescribing anti-pruritics and sending dog home!
if CHRONIC pruritus…
MULTI-YEAR HX w/ SEASONALITY? (3, give two diseases it could be and what we still need to rule out)
NON-SEASONAL cases? (2 diseases)
muti-year history WITH seasonality?
1. ATOPIC dermatitis when SENSITIZED TO POLLEN or INSECT HYPERSENSITIVITY
2. CONTACT ALLERGY to plants in SOUTHEAST USA
3. Must STILL RULE OUT SECONDARY INFECTIONS/ECTOPARASITES
NON-SEASONAL cases?
1. ADVERSE FOOD REACTION can develop at any time
2. In OLD DOGS = CUTANEOUS T CELL LYMPHOMA can mimic allergy
FLEA INFESTATION…
what’s the source of annoyance?
when does allergy occur/what is it called?
what is NOT necessary for diagnosis?
annoyance?
MECHANICAL MOVEMENT of fleas CRAWLING ACROSS SKIN & TAKING BLOOD MEALS
allergy/name?
called FLEA ALLERGY DERMATITIS when the FLEA SALIVARY ANTIGENS get DEPOSITED INTO SKIN AFTER BLOOD MEAL cause HYPERSENSITIVITY REACTION (Type I –> Late phase, or Type IV)
DO NOT NEED TO FIND FLEA DIRT because it MIGHT’VE BEEN REMOVED BY FASTIDIOUS GROOMING ANIMALS!
FLEA ALLERGY DERMATITIS
what FAVORS FAD vs. TOLERANCE?
TIMING? (2)
history?
COMMON CLINICAL SIGN?
what is the flea triangle?
favoring?
–> INTERMITTENT, MASSIVE exposures = FAD
–> CHRONIC LOW-GRADE INFESTATIONS = TOLERANCE
timing?
1. can get FLEAS AT ANY TIME OF YEAR
2. in TROPICAL REGIONS, usually NON-SEASONAL, but CAN BE SEASONAL IN SOME PLACES
history?
= no age, sex or breed predilections
clinical sign?
= PRURITUS AND PAPULAR RASH over the CAUDAL 1/3 OF BODY
flea triangle?
= SELF-INDUCED alopecia due to PRURITUS on…
1. RUMP/TAILHEAD
2. CAUDAL THIGHS
3. GROIN
identify
FLEA ALLERGY DERMATITIS, FLEA TRIANGLE
identify
FLEA ALLERGY DERMATITIS
identify
**timing? what are the lesions made of?
in CHRONIC cases of FLEA ALLERGY DERMATITIS, can cause FIBROPRURITIC NODULES (balls of scar tissue)
what 3 areas does flea bite allergy NOT USUALLY AFFECT IN DOGS? if we find pruritus here, what should we look for?
3 areas?
1. FACE
2. EAR CANALS
3. FEET
** should look for CONCURRENT HYPERSENSITIVITIES
identify
FELINE flea allergy dermatitis
FELINE flea bite allergy dermatitis…
what kind of rash is present? (**+ rule out)
where are the 2 locations it can be found?
what disease can be PROVOKED by flea bite allergy?
what 4 things should we do to DIAGNOSE?
what 2 things are UNHELPFUL for diagnosis?
what kind of rash?
MILIARY (papular & crusted), should ALWAYS ASSUME MILIARY DERMATITIS = FLEA BITE ALLERGY IN CATS UNTIL PROVEN OTHERWISE
what 2 locations can it be found?
1. CAUDAL 1/3 OF BODY
2. DORSAL NECK
what disease can be PROVOKED by this?
FELINE EOSINOPHILIC REACTION PATTERNS
4 things to diagnose?
1. history
2. physical exam
3. flea combing
4. RESPONSE TO THERAPY IS THE GOLD STANDARD
2 unhelpful?
1. INTRADERMAL ALLERGY TESTING
2. HISTOPATHOLOGY (too general)
treatment options for FLEA ALLERGY DERMATITIS for…
flea CONTROL?
flea ALLERGY? (2 examples)
2 others (including taper)
WHAT TREATMENT DOES NOT WORK?
- Flea CONTROL products like SELAMECTIN & FIPRONIL can help prevent new flea INFESTATION, but NOT QUICK ENOUGH KNOCKDOWN TO PREVENT FLEA ALLERGY REACTIONS
- RAPID-KNOCK DOWN PRODUCT to prevent LONG-TERM FLEA FEEDING & injection of salivary antigens
–> ISOXAZOLINES = ALFOXALANER (nexgard) & FLURALANER (bravecto) - Treat any secondary infections
- STEROIDAL THERAPY TO BREAK CYCLE OF PATHOLOGIC ITCH, but WE STILL NEED ADEQUATE FLEA CONTROL
–> Steroid taper over 2-4 weeks depending on severity
HYPOSENSITIZATION VIA ALLERGY SHOTS DOESN’T WORK
flea biology…
for EVERY FLEA you see on a pet… (3)
how are fleas TRANSMITTED?
heat/desiccation? (2)
what does NO stage of flea survive?
outdoor sources of fleas? (2)
for EVERY FLEA on a pet…
1. 2X the PUPAE developing in the CARPET
2. 7X the LARVAE JUST HATCHED
3. 10X the EGGS WAITING TO HATCH
transmission?
via EGGS ROLLING OFF OF PETS and ACCUMULATING IN ENVIRONMENT (hatching in carpet)
heat/dessication?
1. LARVAE are SUSCEPTIBLE to HEAT/DESSICATION
2. PUPAE are RESISTANT!! need to treat CARPET WITH ADULTICIDE
NO stage survives GREATER THAN 10 DAYS OF FREEZING TEMPS
outdoor sources?
1. urban wildlife
2. outdoor cats
3 big causes of ATOPIC DERMATITIS?
describe CASCADE for second!
- GENE MUTATIONS that cause reduced stratum corneum function so increased penetration of allergens into epidermis
- GENETIC PREDISPOSITION for IgE-MEDIATED ALLERGIC CASCADE and release of MAST-CELL DERIVED MEDIATORS/EOSINOPHIL PRODUCTS; DYSREGULATED T-cell response shifting from Th1 to Th2
–> ALLERGY uses the same pathway as anti-parasitic response (Th2), so when dominated by Th2 lymphocyte response –> cytokine release from T cells/mast cells/eosinophils/keratinocytes –> ITCH - NEUROENDOCRINE release of SUBSTANCE P and IL-31 from NERVE ENDINGS that cause ITCH
3 stages of ATOPIC CASCADE?
- SENSITIZATION
–> Atopic dog has REDUCED STRATUM CORNEUM FUNCTION
–> Langerhan cells CAPTURE ALLERGENS and TRANSFER THEM TO LOCAL LNs where they then SENSITIZE/PRESENT IT TO T-HELPER CELLS - IgE PRODUCTION
–> Allergen-specific Th2 lymphocytes ACTIVATE ALLERGEN-SPECIFIC B-cells via IL-4, then T and B cells migrate from lymph nodes to DERMIS
–> B cells MATURE into allergen-specific IgE-secreting PLASMA CELLS - RE-EXPOSURE to allergen & elicitation
–> Next time allergen penetrates into skin, cross-links to allergen-specific IgE receptors on MAST CELLS and triggers DEGRANULATION to dump…
* CYTOKINES
* Lipid mediators
* PGs
* Histamines
CYTOKINES…
IL-2 (produced by what? what drug can inhibit it?)
IL-5
IL-4
IL-31 (what drug can inhibit it?)
IL-2?
–> produced by ACTIVATED Th2 cells when activated by LANGERHAN CELLS
–> can be inhibited by CYCLOSPORIN
IL-4 = promotes B cells to class-switch to IgE
IL-5 = enhances EOSINOPHIL PRODUCTION, encourages themto participate in LATE-PHASE RESPONSE
IL-31 can be INHIBITED BY CYTOPOINT
HISTORY/SIGNALMENT of atopic dermatitis…
5 predisposed breeds? what percent of all dogs?
age of onset average and range?
majority of cases are ____, but if they’re ___-___, then likely due to….
5 breeds?
1. FRENCH bulldogs
2. ENGLISH bulldogs
3. LABS
4. GOLDENS
5. PIT CROSSES
**10% OF ALL DOGS
age of onset = MAJORITY 1-3 years, range 6 MOS –> 7 YEARS
SEASONAL, NON-SEASONAL, INDOOR ALLERGENS
identify
CANINE ATOPIC DERMATITIS
CLINICAL SIGNS of CANINE ATOPIC DERMATITIS
primary lesion?
visible lesions are due to WHAT 2 things?
hair coat?
rare reactions? (2)
types of areas lesions are found in? (2)
DISTRIBUTION of lesions (11, including 2 SURFACES of limbs)
primary lesion?
primary lesion = PRURITUS +/- ERYTHEMA
visible lesions due to…
1. SELF-TRAUMA
2. SECONDARY INFECTIONS
hair coat?
can have SEBHORREIC OLEOSA (greasy coat) from SEBACEOUS GLAND HYPERTROPHY/HYPERSECRETION
rare reactions?
1. ALLERGIC BRONCHITIS
2. ASTHMA
types of areas lesions are found in?
1. hair is SPARSE
2. skin is MOIST
DISTRIBUTION of lesions?
1. axilla
2. periocular region
3. muzzle/perioral
4. external ear canals
5. ventrum
6. inguinal
7. perineum
8. conjunctiva
9. feet/interdigital
10. EXTENSOR surfaces of FORELIMBS
11. FLEXURAL surfaces of HINDLIMBS
DIAGNOSIS of ATOPIC DERMATITIS?
overall, it’s… (3)
2 MAIN things that can contribute to diagnosis?
FIRST-TIME scratchers must rule out WHAT THREE THINGS?
LONG-TERM scratchers? (hint: seasonality and if not 2 rule-outs)
allergy testing?
skin biopsy?
= DIAGNOSIS OF EXCLUSION based on history, signalment and clinical signs
2 MAIN things?
1. AGE OF ONSET LESS THAN 3 YEARS
2. CORTICOSTEROID-RESPONSIVE PRURITUS
FIRST-TIME SCRATCHERS, rule these out BEFORE treating with allergy control medication…
1. FLEAS
2. MITES
3. SECONDARY INFECTIONS
LONG-TERM SCRATCHERS, determine HISTORY OF SEASONALITY
–> If NON-SEASONAL, then RULE OUT…
1. FOOD SENSITIVITY
2. SCABIES/PARSITES
ALLERGY TEST ONLY IF ALLERGY-SPECIFIC IMMUNOTHERAPY
SKIN BIOPSY NOT HELPFUL, TOO NON-SPECIFIC
why are allergen tests NOT tests for atopy?
because most people will have SENSITIVITY TO SOME ALLERGENS, so not ATOPIC
3 types of SECONDARY infections common with ATOPIC DERMATITIS?
**3rd one involves cats
- MALASSEZIA (PACHYDERMATITIS) DERMATITIS
- STAPHYLOCOCCUS PYODERMA
- BACTERIAL and/or YEAST OTITIS EXTERNA
–> not common in CATS
INTRADERMAL allergen testing..
2 big testing risks?
withdrawal times & medications? (2)
procedure? (2)
it’s widely considered the ____ ____ of allergen tests
risks? –> HIGH LIKELIHOOD OF
1. FALSE NEGATIVES
2. FALSE POSITIVES
withdrawal times?
1. 30-days for ORAL steroids
2. 14 days for ANTIHISTAMINES/FATTY ACIDS
procedure?
1. done under SEDATION for REPRODUCIBLE RESULTS & PATIENT COMFORT
2. inject small amounts of allergen UNDER THE SKIN
GOLD STANDARD
what testing is this?
INTRADERMAL ALLERGY TESTING
**GOLD STANDARD OF ALLERGY TESTS
SEROLOGIC allergen testing…
ALL of them use what?
what specifically do they measure?
testing risks?
use ELISAs!
measure serum concentration of allergen-specific IgE in circulation
still prone to FALSE POSITIVES & FALSE NEGATIVES
identify
FELINE ATOPIC SYNDROME
identify
FELINE ATOPIC SYNDROME
FELINE ATOPIC SYNDROME
why is it called a syndrome?
how common?
age of onset?
any concurrent diseases? (2)
2 main clinical signs? (1st is broad and has 6 subs)
one common clinical sign that can be mistaken for another?
diagnosis based on what 2 things?
what other 4 DDxs must you rule out?
SYNDROME because it can INVOLVE RESPIRATORY COMPONENT
it’s LESS COMMON in cats than AD is in DOGS
age of onset = 6 to 24 months
25% of cats have CONCURRENT FOOD or FLEA BITE ALLERGY
2 main CLINICAL signs?
1. PRURITUS (perioral/muzzle, periocular, ears, perineum, abodmen/groin,
2. RESPIRATORY DZ (asthma/bronchitis)
EXCESSIVE GROOMING can be mistaken for PRURITUS
diagnosis based on…
1. history
2. signalment
RULING OUT DDxs –> parasites, dermatophytes, food allergy, psychogenic/stress (RARE)
identify
ALLERGY CONTACT DERMATITIS
ALLERGIC CONTACT DERMATITIS…
common WHAT parts of the US? why?
type of HYPERSENSITIVITY reaction?
easily confused with ___ ___ due to distribution over ___ & ____ ____
2 main DDxs?
best way to diagnose?
common in SOUTHERN US usually from ORNAMENTAL COMMELINACAE FAMILY plant contact
TYPE IV (DELAYED) hypersensitivity (haptens, 24-48 hours later)
fill in the blanks?
atopic dermatitis, venture, foot pads
2 DDxs?
1. ATOPIC DERMATITIS
2. IRRITANT CONTACT DERMATITIS –> from CONTACT with CAUSTIC chemicals
diagnosis?
–> via RESPONSE TO TREATMENT, usually through PENTOXIFYLLINE that can ELIMINATE/CONTROL allergic contact dermatitis!
CUTANEOUS ADVERSE FOOD REACTIONS…
= definition
2 hypotheses?
evidence for TYPE I, IV, and III reactions?
= any ADVERSE REACTION TO FOOD that causes HYPERSENSITIVITY REACTION
2 hypotheses?
1. IMMATURE or DAMAGED gut epithelium is permissive to ABSORPTION OF PROTEINS MORE THAN THEY SHOULD
2. Presentation of INCOMPLETELY DIGESTED FOOD ANTIGENS to GUT-ASSOCIATED LYMPHOID tissue causes DESENSITIZATION
Evidence for TYPE 1 reactions?
–> Occurs ALONG WITH ENVIRONMENTAL ATOPIC DERMATITIS
–> Some cases exhibit IMMEDIATE REACTIONS (1-2 hours) TO FOOD CHALLENGES
–> Some dogs present with URTICARIA (IgE-mediated)
Evidence for TYPE IV (delayed) reactions?
–> GREATER than 24-48 hours after exposure, up to 10-14 days!
**Tell owners to feed food challenge for at least 2 weeks to ALLOW ENOUGH TIME FOR HYPERSENSITIVITY before moving on to next food
Evidence for TYPE III (vasculitis) reactions?
–> ARTHRUS reaction occurs in vessel walls
–> URTICARIAL VASCULITIS & PINNAL MARGIN VASCULOPATHY can be EXACERBATED BY FOODS
continued CUTANEOUS ADVERSE FOOD REACTIONS…
age of onset in DOGS & CATS (range & averages)?
what particular ages will INDICATE food allergy?
TWO MAIN things in history? (one has 4 subs)
response to steroid therapy?
how long have animals been on diet before developing hypersensitivity?
4 CLINICAL signs?
GOLD STANDARD DIAGNOSTIC?
age of onset?
DOGS = 2 MOS –> 13 YEARS, 2-4 years on AVERAGE
CATS = 3 MOS –> 11 YEARS, 4-5 years on AVERAGE
IN VERY YOUNG (<6 MOS) or OLD (> 7 YEARS) animals with NON-SEASONAL PRURITUS, FOOD ALLERGY!
history?
1. NON-SEASONAL pruritus
2. GI signs (vomiting, diarrhea, flatulence, loose stools)
good INITIAL response to steroid therapy
animals have been on diet for MONTHS to YEARS BEFORE DEVELOPING SENSITIVITY
4 clinical signs?
1. pruritus
2. recurrent urticaria
3. distribution SIMILAR TO ATOPY
4. SECONDARY INFECTIONS ARE COMMON (staph pyoderma, malassezia dermatitis, yeast/bacterial otitis)
GOLD STANDARD = DIET TRIAL for 8 WEEKS with at least 2 WEEKS HEALTHY SKIN
identify
CUTANEOUS ADVERSE FOOD REACTIONS
DIETARY ELIMINATION TRIAL
how to prove it at the end?
how long must trial run? what happens to have it extended?
might require WHAT intervention? (more common in one species)
how do we know how it’s over?
how to prove it at the end?
can re-expose them to FORMER food to prove it at the end!
trial length?
Trial must run for MINIMUM OF 8 WEEKS
–> If relapse in trial MUST EXTEND
WHAT intervention?
–> Might require GLUCOCORTICOID THERAPY may be required during the first month to REDUCE INFLAMMATION & stop itch-scratch-itch cycle; ESPECIALLY IN CATS
when is it over?
Patient should maintain healthy skin for AT LEAST 2 WEEKS off of medications ONLY with test diet to SUGGEST CAUSATION
identify
ATOPIC DERMATITIS
identify
CUTANEOUS ADVERSE FOOD REACTION, FOOD ALLERGY
identify both the DISEASE and what the TERM is for this distribution?
MALASSEZIA PACHYDERMATITIS
INTERTRIGO = inflammation caused by skin-to-skin friction
STAPHYLOCOCCUS PYODERMA…
commonly caused by WHAT?
it’s the most common cause of….
= caused by OVERGROWTH of normal bacterial flora (Staph pyoderma) and cause FOLLICULITIS, usually due to ATOPIC patients that have IMPAIRED IMMUNE RESPONSE to STAPH
MOST COMMON SECONDARY INFECTION IN PATIENTS WITH ALLERGIC SKIN DISEASE
MALASSEZIA PACHYDERMATITIS…
commonality?
what 3 things can cause overgrowth?
3 common presentations?
4 things that occur if undiagnosed/chronic? (1 main one)
how is it best diagnosed/using what 2 tools?
SECOND most common cause of secondary infection to allergic skin disease
3 things that cause overgrowth?
1. increased MOISTURE on skin
2. increased LIPID PRODUCTION from sebaceous glands –> YEAST EAT FATTY ACIDS
3. disruption of STRATUM CORNEUM function in ALLERGIC SKIN DZ (INFLAMMATION)
3 presentations?
1. PARONCHYNIA = inflammation of the CLAW FOLD
2. INTERDIGITAL PODODERMATITIS
3. INTERTRIGO = skin-to-skin friction that causes INFLAMMATION, often SKIN FOLDS
chronic/undiagnosed?
–> SEVERE PRURITUS, leading to SELF-INJURY and therefore…
1. alopecia
2. lichenification
3. hyperpigmentation
4. excoriations
diagnosed via CYTOLOGY via ACETATE TAPE or IMPRESSION SMEAR
identify
MALASSEZIA PACHYDERMATITIS
TREATMENT for MALASSEZIA DERMATITIS
overall course?
TOPICAL options?
3 oral drugs in DOGS?
1 alternative oral drug in CATS?
overall course?
use both ORAL & TOPICAL ANTI-FUNGALS for 21-30 days
topicals?
CHLORHEXIDINE & AZOLES (ketoconazole or miconazole) in SHAMPOOS, WIPES, SPRAYS
DOG oral drugs?
1. FLUCONAZOLE or KETOCONAZOLE
2. TERBINAFINE
CATS oral drugs
** all the same except can use ITRACONAZOLE instead of KETOCONAZOLE due to HEPATOTOXICITY risk
