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Year 1/2 > Defense & Barriers 2: Pruritus > Flashcards

Defense & Barriers 2: Pruritus Flashcards

1
Q

pruritus
= definition
when it becomes pathologic?
5 common clinical signs & one specific one in cats?

A

= 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

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2
Q

3 main concepts you should keep in mind when approaching pruritus?

A
  1. COMMON DISEASES ARE MOST COMMON!
  2. treat WHAT YOU CAN SEE FIRST –> skin PARASITES & INFECTIONS are most common, so SEE HOW MUCH ITCH IS REMOVED WHEN YOU TREAT THOSE ALONE
  3. start with BASICS –> skin SCRAPINGS, CYTOLOGY, TRICHOGRAM & rule out ECTOPARASITES & INFECTIONS
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3
Q

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?

A

= 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

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4
Q

what type of hypersensivitiy reaction is this?

WHAT IS IT? (dog)

A

TYPE 1 HYPERSENSITIVITY

WHEALS & FLARES in DOG

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5
Q

urticaria
what basic thing causes urticaria?
rarity in dogs, horses, cats?
2 differentials it can resemble/species?

A

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

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6
Q

identify & type of hypersensitivity reaction

A

URTICARIA

TYPE 1

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7
Q

LATE-phase reactions
= what it is OVERALL, including 2 proteins
timing?
three diseases? (2 are obvious, one is unique)

A

= 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

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8
Q

type IV hypersensitivity reaction…
timing? (overall & 2 phases)
provoked by…
3 diseases?

A

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)

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9
Q

PATHOPHYSIOLOGY of pruritus? (**& where they terminate)
what 4 things can bind to cause it?

A

= 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

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10
Q

what 5 differentials should we consider for PRURITUS?
**include one for CATS

what disease is usually NON-PRURITIC?

A

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

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11
Q

3 main diseases that we consider in ALLERGIC PATIENTS?

A
  1. FLEA BITE allergy
  2. atopic dermatitis from ENVIRONMENT or STRESS
  3. FOOD sensitivity
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12
Q

itch threshold
what is it?
what can affect it?

A

POINT ABOVE = ITCHING, POINT BELOW = NOT ITCHING

affected by WHETHER THERE’S ENOUGH ALLERGIC-CAUSING SUBSTANCES IN ENVIRONMENT FOR REACHING THRESHOLD

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13
Q

if ACUTE pruritus… (2)

A
  1. ECTOPARASITIC DISEASES can TAKE TIME TO DEVELOP A CLASSIC DISTRIBUTION PATTERN, so might look like GENERALIZED ITCH in the beginning
  2. Good to RULE OUT INFECTIOUS CAUSES (ectoparasites, staph, Malassezia) before prescribing anti-pruritics and sending dog home!
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14
Q

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)

A

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

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15
Q

FLEA INFESTATION…
what’s the source of annoyance?
when does allergy occur/what is it called?
what is NOT necessary for diagnosis?

A

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!

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16
Q

FLEA ALLERGY DERMATITIS
what FAVORS FAD vs. TOLERANCE?
TIMING? (2)
history?
COMMON CLINICAL SIGN?
what is the flea triangle?

A

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

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17
Q

identify

A

FLEA ALLERGY DERMATITIS, FLEA TRIANGLE

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18
Q

identify

A

FLEA ALLERGY DERMATITIS

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19
Q

identify
**timing? what are the lesions made of?

A

in CHRONIC cases of FLEA ALLERGY DERMATITIS, can cause FIBROPRURITIC NODULES (balls of scar tissue)

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20
Q

what 3 areas does flea bite allergy NOT USUALLY AFFECT IN DOGS? if we find pruritus here, what should we look for?

A

3 areas?
1. FACE
2. EAR CANALS
3. FEET
** should look for CONCURRENT HYPERSENSITIVITIES

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21
Q

identify

A

FELINE flea allergy dermatitis

22
Q

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?

A

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)

23
Q

treatment options for FLEA ALLERGY DERMATITIS for…
flea CONTROL?
flea ALLERGY? (2 examples)
2 others (including taper)
WHAT TREATMENT DOES NOT WORK?

A
  1. Flea CONTROL products like SELAMECTIN & FIPRONIL can help prevent new flea INFESTATION, but NOT QUICK ENOUGH KNOCKDOWN TO PREVENT FLEA ALLERGY REACTIONS
  2. RAPID-KNOCK DOWN PRODUCT to prevent LONG-TERM FLEA FEEDING & injection of salivary antigens
    –> ISOXAZOLINES = ALFOXALANER (nexgard) & FLURALANER (bravecto)
  3. Treat any secondary infections
  4. 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

24
Q

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)

A

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

25
3 big causes of ATOPIC DERMATITIS? describe CASCADE for second!
1. GENE MUTATIONS that cause reduced stratum corneum function so increased penetration of allergens into epidermis 2. 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 3. NEUROENDOCRINE release of SUBSTANCE P and IL-31 from NERVE ENDINGS that cause ITCH
26
3 stages of ATOPIC CASCADE?
1. 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 2. 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 3. 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
27
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
28
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
29
identify
CANINE ATOPIC DERMATITIS
30
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
31
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
32
why are allergen tests NOT tests for atopy?
because most people will have SENSITIVITY TO SOME ALLERGENS, so not ATOPIC
33
3 types of SECONDARY infections common with ATOPIC DERMATITIS? **3rd one involves cats
1. MALASSEZIA (PACHYDERMATITIS) DERMATITIS 2. STAPHYLOCOCCUS PYODERMA 3. BACTERIAL and/or YEAST OTITIS EXTERNA --> not common in CATS
34
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
35
what testing is this?
INTRADERMAL ALLERGY TESTING **GOLD STANDARD OF ALLERGY TESTS
36
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
37
identify
FELINE ATOPIC SYNDROME
38
identify
FELINE ATOPIC SYNDROME
39
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)
40
identify
ALLERGY CONTACT DERMATITIS
41
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!
42
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
43
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
44
identify
CUTANEOUS ADVERSE FOOD REACTIONS
45
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
46
identify
ATOPIC DERMATITIS
47
identify
CUTANEOUS ADVERSE FOOD REACTION, FOOD ALLERGY
48
identify both the DISEASE and what the TERM is for this distribution?
MALASSEZIA PACHYDERMATITIS INTERTRIGO = inflammation caused by skin-to-skin friction
49
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
50
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
51
identify
MALASSEZIA PACHYDERMATITIS
52
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

Year 1/2 (139 decks)

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