Exam 3 Flashcards
Lecture 1 Introduction to clinical dermatology
What are the two most essential questions to answer for any dermatology patient of any species?
- What are the infections?
- Why are they there?
How do breakdowns in the normal structure and function of the skin lead to disease?
Physical barrier - Roof house analogy
Stratum corneum
-Major barrier layer
-Keratinocytes: dehydrated “shingles”
-Lipid bilayer: “Glue”
-Brick and mortar model: keratinocytes = brick, lipid bilayer = mortar
What is the Goo?
Epidermal lipid envelope
-Cholesterol, phospholipids
-Free fatty acids, ceramides: Sphingosine - cholesterol complex; triggered dissolution of complex. Antimicrobial, promotes cell growth
-Sebum: triglycerides, wax esters, cholesterol. Squalene, sebaleic acid, linoleic acid
Epidermal turnover
-Stratum corneum 14 days
-Stratum basale 14 days
-Mitosis - basal layer
-Differentiate as cells move up: lose mitotic ability, nucleus and organelles, and aggregate keratin.
Keratinization defects
-Rice paper thin layer, peeling off in pieces
The velcro analogy
-Desmosomes: velcro proteins
-Autoimmune disease: destroys desmosomes = dermis peels away. Pattern non-haired parts, nose footpads.
Dermis
-Support and nourishes epidermis
-Interact with epidermis during embryogenesis
-Wound repair
-Thickness of skin
-Contains cells, fibers, ground substance
-Fibroblast cells: make collagen, elastin, reticulum, ground substance, fibronectin.
- Collagen: Dynamic, constantly being synthesized and degraded. 90% tensile strength
-Elastin: 10% elasticity
-Reticulin: 1% surround appendages, vessels, nerves
-Mast cells: Histiocytes (dermal macrophages), melanocytes (only in some species)
Ehlers-Danlos Syndrome
-Hyperelastosis cutis
-Congenital defect in collagen
Other structures
-Blood vessels ex: post rabies vaccine vasculitis.
-Lymphatics
Sensation
-Thermoreceptors
-Tylotrich pads: Merkel’s cells, mechanoreceptors
-Pacinian corpuscles: vibration and deep pressure
-Meissner or Ruffini corpuscles: velocity of skin movement
-Penicillate nerve endings
Hair - Protection
-UV light protection
-Contact irritants
-Physical damage
-Heat/cold
-Camouflage
-Social interactions
-Appearance
-Pheromones
-Anagen: growing
-Telogen: dormant, non-shedding dog breeds
Glands
-Sebaceous: sebum, oily film, antimicrobial
-Epitrichial: apocrine, chin, feet, rump
-Atrichial: footpads, thermoregulation
Sweat
-Water evaporation
-Salts, ammonia, urea
-Lubricants
-Histamine, prostaglandin, proteases
-Glucose
-Pheromones
Antimicrobial properties, IgA, IgG, Langerhan’s cells
Primary Diseases Alter the Skin
-Temperature: warm = inflammation, bacteria, yeast loves incubator
-Glandular secretions: rancid fat
-Moisture: moist and clammy
-Antibodies: IgE = pruritic due to licking
-Licking: spreads bacteria, increases moisture
-Scratching: excoriations
-Staph binding: more parking for bugs
Examples
-Acne a gland dz: enlargement of sebaceous glands. Vitamin A helps, cats have it
-Sebaceous Adenitis: body attacks glands = dry flaky skin entire body, poodles predisposed
Melanocytes
-Protection from UV light
-Absorbs radiation
-Scavenges free radicals
-Camouflage
-Decorative
-Melanocytes - melanosomes - keratinocytes
-Melanin transferred to keratinocyte required copper. Eumelanin and phenomelanin
Pigmentation
-Pigmentation promoters:
-MSH: synthesis and activation of tyrosinase
-ACTH
-Androgens
-Estrogens
-Progesterone
-UV light
-Inflammation
-Friction
Examples: pyoderma can become darker (black). UVeodermatologic syndrome, albino
How do secondary bacterial pyoderma or yeast infections occur?
Secondary infection triggered by allergy or hormones (endocrine disease)
What are the infections?
1. Folliculitis major ddx:
-Pyoderma: staphylococcus
-Demodex
-Dermatophyte
Major cause: allergy, endocrinology, cornification disorder or defect.
- Pododermatitis
-Bacterial
-Yeast - Otitis
-Bacterial
-Yeast
Why are they there?
1. Allergies
-Atopy
-Food allergy
-Scabies
- Endocrinopathy
-Hypothyroidism
-Cushingn’s
Why are they there?
-Pruritus leads to licking, damage on skin barrier, adding moisture, bacterial and yeast love the incubator. Loss of adequate antimicrobial defenses on the skin.
How do autoimmune skin diseases cause blisters or ulcers?
Pattern
-Face, pinnae, nasal planum
-Oral cavity
-Pads
Damage to the skin barrier by destruction of the desmosomes, which are the “velcro” proteins maintaining the stratum corneum and stratum granulosum together.
The outermost barrier peels away from the dermis leaving it exposed and damaged
How do T helper cells benefit or cause disease in the skin?
Why are mast cells and eosinophils especially important in dermatology?
What are the 10 core patterns in dermatology?
Secondary
1. Folliculitis
2. Pododermatitis
3. Yeast dermatitis
4. Otitis
Primary
5. Pruritus - allergy
6. Auto immune skin disease
7. Non pruritic alopecia
8. Keratinization defects
9. Lumps, bumps, and draining tracts
10. Weirdopathies
Secondary infections
-Pyoderma
-Demodex
-Dermatophyte
-Yeast dermatitis
-Pododermatitis
-Otitis
Primary Disease
-Allergies: atopy feet, food rears + ears, scabies PP reflex, flea/insects back/hotspots
-Endocrine: hypothyroid big dogs, Hyperthyroid small dogs.
Lecture 2
Folliculitis (bacterial pyoderma, demodicosis, dermatphytosis)
What are the 3 most common causes of folliculitis in the dog and cat?
Folliculitis: infection of the hair follicle
Furunculosis (when severe enough to cause cellulitis, pus oozing out of the skin)
-Lesions: They all look alike
- Staphylococcus
- Demodex
- Dermatophyte
Furunculosis
-Min 21-30 days treatment, likely 6-12 weeks
-Deeper infection
Bacterial infections are always secondary to an underlying disorder, why?
What are common organisms that cause superficial vs. deep infections and cellulitis (fungal, bacterial, and parasitic)?
Superficial Pyoderma
Cause underlying allergy or endocrine disease
C/S
-Infection of hair follicle that spreads outward under stratum corneum
-Single follicle = papular rash > papule > pustule > crust > epidermal collarette
-Alopecia, papules, crusts
Staphylococcus schleiferi
-Staphylococcus aureus
-Potential zoonosis
-Papular dermatatis coalescing lesions, erythematous plaque.
-Early epidermal collarettes
Superficial Pyodermas
Pyotraumatic dermatitis - Hotspot
-Thick-coated dogs
-Alopecia, erythema, exudation, ulceration
-Pruritic and painful
90% triggered by insect bites
Tx
-Clip and clean
-Atringents
-Antipruritics topical or sytemic
-Topical antibacterials, usually do not need systemic antibiotics
Correct predisposing cause = insects
Skin fold dermatitis
-Anatomic defect!
-Erythema, exudation within folds
-Must differentiate from folliculitis/furunculosis, malassezia dermatitis.
Tx
-Like diaper rash
Treatment - Pyoderma
-Topical shampoos
-Chlorhexidine
-Colloidal silver
-Antibiotics: minimum 21 days
-Cefpodoxime, Ceohalexin, Clavamox, Clindamycin, TMS or PRIMOR.
Deep Pyoderma
- Pus, Cellulitis, Swiss cheese, draining tracts
-Organisms: Nocardia, Actinomyces, Blasto/Crypto
What is the best way to determine the cause of deep infections and cellulitis?
General Dx
-Cytology
-Skin Impression smear
-Culture
-Tape preps
Best
-Biopsy
-Culture bacteria + fungal
-DNA PCR testing
Staph, demodex, dermatophyte, nocardia, actinomyces, balsto/crypto
How and why is Malassezia such a common secondary infection and what are the unique clinical lesions?
Unique lesions: interdigital bullae, lesions, rash, abscess.
Malassezia Dermatitis = Linchenification = Elephant skin
-Malassezia pachydermatis: Hypersensitivity reaction, IgE serology test, allergy skin testing
-Takes 6-12 weeks to tone down and normalize, up to several months
-Football-shape yeast, purple diff-quick solution
Tx
-First try: Vinegar + water (1:1) TID
-Degreasing shampoos: bezoyl peroxide, selenium sulfide.
-Systemic fungals
-Ketoconazole, Terbinafine, Fluconazole, Itraconazole. 30 days
Pododermatitis - Interdigial Bullae
Secondary infection
-Bacteria or Malassezia
Primary disease
-Allergies or endocrine
-Environment: moist and dirt, plant awns.
-Traumatic folliculitis: ingrown hairs, micro-abscess
Antibiotic Resistance
Staphylococcus Resistant
-Penicillin
-Ampicillin
-Amoxicillin
-Tetracycline
-Doxycycline
Methicillin Resistance - Use
-mecA gene: inducible, transferable
-Oxacillin
-Cephalexin
-Clavamox
Three ways we get into trouble
1. Steroids
2. Apoquel
3. MARSA continuous use of fluoroquinolones
Culture & min 21-30 d Tx
Good systemic skin drugs - Staphy mecA
-Cephalexin
-Clavulanic acid - amoxicillin
-clindamycin
-Cefpodoxime
-Trimethoprim sulfa
-Ormetoprim sulfa (Primor)
Dermatophytosis - Microsporum canis = Cats
Microsporum gypseum = dogs
-Cutaneous fungal infection
-Invades keratinized structures
-Self-limiting disease
-May take months to resolve
-Depends on host immune status
Zoonosis
-Immune compromised humans
-Folliculitis
-Common cats from shelters
Dx
-Fungal culture 8-% accurate but slow
-Skin scrape
Tx
-Topical therapy &
-Systemic therapy
Ringworm - Dermatophytosis - Fungal
Tx
-Topical: Terbinafine - Lamisil
-Systemic: Terbinafine, ketoconazole, itraconazole/fluconazole
Demodex - Folliculitis, furunculosis
-Demodex mites should be easy to find except in cats
Tx
-Bravecto, simparica, Credelio monthly preventatives
Do not use high dose avermectins
-Collies, Australian sheperds, Old english sheepdogs, shelties.
“White feet do not treat” Genetic test
Lecture 3 Otitis
The healthy External Ear Canal
-Microflora: low numbers of yeast (Malassezia) and Gram (+)
What are the very few causes of primary otitis?
What causes secondary otitis?
How should recurrent secondary otitis be treated and controlled?
Otitis Externa
-Inflammation of the ear canal
-Rise in temperature, humidity, pH
-The three Ps
-Predisposing causes
-Primary causes
-Perpetuating causes: secondary
Predisposing factors
1. Conformation
-Pendulous pinnae
-Increased ceruminous glands: Cockers
-Stenotic ear canals: Shar Pei, Chow
-Hair: Poodles
- Excessive moisture
-Swimming
-Overzealous cleaning - Systemic disease
-Immune suppression
Primary Causes
1. Parasites
-Otobius megnini (spinous ear tick)
-Demodex mites
-Chiggers
-Sarcoptes scabiei
-Poultry mites
- Hypersensitivity disorders - allergies
-Atopy (pollen/grass)
-60% have otitis
-3-5% only clinical sign
-Food allergies Ears and rears 80% otitis, 25% only clinical signs - Foreign bodies
-Grass, awns, seeds
-Dirt, sand, dead insects
-Concentrations of medications - Neoplasm
- Endocrinopathy -Hypothyroidism, hyperthryroidism
- Auto immune diseases
Secondary Infections
-Yeast: Malassezia pachydermatis
-Bacteria - cocci Staph
Stage 1 or 2: Wax 99% of otitis (sterile?), Staph and Malassezia.
Stage 3: Pus - pain - ulcers 1% of otitis: pseudomonas + mixed rods. Corynebacterium, E. coli.
C/S
Acute
-Head shaking
-Inflammation
-Abnormal ear carriage
-Pain/pruritus
-Wet - pus or Wax
-No infection does not mean normal Sterile allergy vs. infectious
Dx
-Cytology should be done every time
-Technique: swab junction of horizontal and vertical canal. Roll swab on slide = L + R
-Stain with Diff Quick for cytology, mineral oil for mites
-Examine at 100x (oil) 4-10x for mites
Severe Otitis Externa
-Culture and sensitivity
-Radiographs/CT scan: bullae osteomyelitis suspicion, many weeks of treatment
-CBC/Chem TT4/TSH
-Bacterial cultures are based on oral dosing. Pseudomonas are always predictable
Otitis Media
-Inflammation of the middle ear
-Temporomandibular, bulla, auditory tube, and ossicles
-Eustachian tube, facial nerves affected
-Parasympathetic and sympathetic nerve pass through middle ear = Horner’s syndrome
C/S
-Chronic otitis externa
+/- pain when opening the mouth
+/- ruptured tympanic membrane
+/- facial paralysis
+/- Horner’s syndrome
+/- Head tilt
Sedation required for examination
Tx
-Control primary disease
-Resolve secondary infection
Otitis Steps
Pick only one product for each spot
- Cleaning Stage 1
-EpiOtic advanced 4oz
-No acids no alcohols, herbals
-Fill ear canal - let shake dry - repeat until clean
-Alchohol flush for swimmers - Otitis Stage 2
-EasOtic short acting 1ml pump
-Claro (florfenicol, terbinafine, mometasone furoate) long acting. Need dry ear cannal
-Oti-pak long acting
-Allergy or endocrine disorder as the trigger
-Mild non infected will become infected
-Multimodal ointment: Antibacterial, anti-yeast with steroid
-Long acting vs. short acting: do not stop long acting bc resistance develops, so 1-4 weeks - Severe purulent ulcerated and painful Stage 3
-Usually mixed bacteria, pseudomonas
-TrisEDTA 4 oz with 1200 mg enrofloxacin and 40 mg Dexmethasone
Pseudomonas
-Tris EDTA chalates ions, perforates cell wall/coat, allows antibiotic to penetrate
-Lowers mic levels
-Clean ear canal SID 10-14 days treatment
Prevention
-Use whichever ear product at longer intervals
-Multimodal: use every 3-7 days
-Long-term Ear pack use every 2-3-4 weeks
Ear Miticides
-Simparica
-Bravecto
-Credelio
Lecture 4 - Allergies
What are the unique patterns associated with each type of allergy? Food, Atopy, Insects
Food, Atopy & Insects = Pruritus
Itchy dog
-Face, feet, axilla, flanks
-Excoriated mosquito bite
Atopy = feet
Food = ears and rears
Scabies = PP reflex
Flea/insects = back/hotspots
Describe the immune response that causes allergies
Type 1
-Immediate hypersensitivity
-Late phase IgE
-Injured keratinocytes - Leukotrines - IL4 - PG - Substance P - Mast cell - IgE - from Th2 B-lymphocyte and Langerhan’s cells.
Type IV
-Cell mediated
Basophilic reactions
