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#separator:tab #html:false Describe a horse's field of vision. large, 350 degrees, narrow blind spots anterior to nose/posterior to tail, can judge depths, rod (light/motion) to cone (color) ratio 9:1 What is epiphora? tearing (pain) What is a blepharospasm? squinting (pain) What are some common sig...

#separator:tab #html:false Describe a horse's field of vision. large, 350 degrees, narrow blind spots anterior to nose/posterior to tail, can judge depths, rod (light/motion) to cone (color) ratio 9:1 What is epiphora? tearing (pain) What is a blepharospasm? squinting (pain) What are some common signs of ocular problems in horses? epiphora, blepharospams, vision loss/loss of night vision, behavior change, conjunctivitis, discharge What are the important aspects of an ophthalmic exam? assessing vision (in ambient and dim light), menace, obstacle course w/ one eye blindfolded, CN 2/3/5/7 What is something important to remember about the menace response in foals? menace response is learned; foals less than 2-3 weeks have not yet developed What tests check which cranial nerves? PLR - 2, 3 Palpebral - 5, 7 Menace - 2, 7, cortex Dazzle - 2, 3, 7 What parts of the eye/head are important to evaluate during an ophthalmic exam? orbit, palpebrae, nictitans (3rd eyelid), conjunctiva, anterior segment (tear, cornea, irdiocorneal, iris, lens, ciliary), posterior (vitreous, retina, choroid, optic nerve) What is the typical sedation/blocking protocol for equine ophthalmic exams? "-Xylazine at 150-250 mg (1000# horse) for 10 mins -Auriculopalpebral block for motor -Supraorbital block for sensory" What diagnostic ophthalmic test should we do on every single horse? Fluorescein stain; adheres to corneal abrasions Describe a Schirmer Tear Test in horses. do prior to any medications and sedation (alpha 2 agonists causes lacrimation), indicated for corneal ulceration or dry cornea What is an abnormal measurement of a Schirmer Tear Test in horses? < 10 mm a minute What do different intraocular pressures of horses tell us? normal 16-30 mmHg high = glaucoma low = inflammation/uveitis When should we get intraocular pressures in horses? performed unsedated w/ normal head position and proparacaine; for chronic eye problems, corneal edema, bupthalmos What is the purpose/use of Rose Bengal staining for horse ophthalmic exams? retentions indicate defect in mucin layer of tear film; helps visualize fungal ulcers, chronic problems (especially w/ deficient Schirmer) What is a Nasolacrimal flush? possibly helpful for blocked channel; max of 20cc per side w/ lidocaine Why do we utilize Tropicamide to cause mydriasis in the eye? mydriasis = dilation; allows thorough retinal examination What are 2 specific diagnostic tests for corneal ulcers? Corneal culture - prior to medication, cotton swab over ulcer, debrides ulcer Corneal scraping - topical anesthesia, back end of scalpel, wipe on slide What is the purpose of using ultrasound on the eye? examines vertical and horizontal view from central axis, examines cornea/lens/retina, can visualize iris/ciliary body, corpra nigra, optic nerve What are 3 common corneal diseases in horses? ulceration/erosion, keratitis, stromal abscesses What is the most commoneye problem encountered in practice? corneal ulceration; simple abrasions to full thickness perforations and prolapse Why should corneal ulcerations be treated aggressively? can lead to globe rupture, phthisis bulbi, and blindness are possible; cornea is only 1-1.5 mm or 8-10 cells thick What is the typical healing time of an uncomplicated corneal ulcer? 7-10 days; considered non-healing if no healing in this time How long do blood vessels take to form with a corneal ulcer? about 3-5 days, growing 1mm per day How do infections interfere with healing of corneal ulcers? MMP and NE from tear film are upregulated causing increased inflammation and degredation of stroma leading to melting ulcers What are good antibiotic choice for corneal ulcers? topicals such as TAO, Ciprofloxacin Cefazolin for Strep How do we treat prevent collagneolysis with corneal ulcers? replace serum every 5 days, Acetylcysteine and EDTA inhibit MMP What medications can we use to decrease inflammation/uveitis with corneal ulcers? Atropine (stabilizes blood-aqueous barrier, stops pain, reduces synchiae), NSAIDS (systemics for reduction of uveal exudation/pain, topical for reduction of degree of uveitits/pain) How do we treat fungal corneal ulcers? caused by Aspergillus, Fusarium, etc.; treat w/ Miconazole and Silver Sulfadiazine What are the purposes of utilizing a sub palpebral lavage line? lavage line utilized for giving medications; can be useful to not have to give meds continuously/touch eye multiple times (Cefazolin, Tobramycin, Serum, Atropine, etc.) What do we do if we encounter a nonhealing corneal ulcer? get a clean cytology to determine infection, keratitis, etc. (Keratectomy is useful); debridement using topical anesthesia (DO NOT CAUTERIZE w/ iodine 3% or 7%) Why is it important that cytology samples are done clean? bacteria and fungi can be dragged deeper into corneal stroma What are the purposes/uses of Conjunctival Grafts? manages deep melting ulcers or descemetoceles, perforated ulcers/iris prolapse; supplies blood and stabilizes eye, permanent scarring inhibits vision When do we use third eyelid flaps for corneal ulcer treatment? for superficial disease or facial nerve paralysis; 2-4 horizontal mattress sutures connecting 3rd eyelid and upper lid near lateral canthus What is Enucleation? How is it done? removal of eye; check other eye before doing procedure; standing procedure, block SO/AP and retrobulbar; suture eye shut (tarsorrhaphy); exenteration includes mucles and is used for neoplasias What are corneal lacerations/perforations? associated w/ iris prolapse, shallow anterior chamber and hyphema; iris plugs hole to save eye What is the purpose of Seidel's Test? large amount of stain can see aqueous humor flowing out of corneal laceration; gentle pressure may be needed to see this How do we treat Corneal Lacerations/Perforations? small one that seal over may heal medically, large lacerations requires surgery, traumatic perforation w/ extensive extrusion should be enucleated What is Viral Keratitis? Equine Herpesvirus 2; conjunctivitis, punctate corneal opacaities How do we treat Viral Keratitis of the eye? Topical NSAIDs and antivirals (Valcyclovir) What is Eosinophilic Keratoconjunctivits? uncommon, immune mediated/allergens/parasites; corneal granulation tissue w/ eosinophils How do we treat Eosinophilic Keratoconjunctivits? topical steroids and Cetirizine What is a common Dfdx of Eosinophilic Keratoconjunctivits? Squamous cell carcinoma What Immune Mediated Keratitis (IMMK)? chronic corneal opacity w/o ulceration or uveitis; four distinct types (Epithelial, Superficial stromal, Deep stromal, Endothelitis) typically only affecting one eye How do we treat Immune Mediated Keratitis (IMMK)? Cyclosporine, Topical NSAIDs What are stromal abscesses? What are the consequences? abscess of stroma as a sequela to corneal ulcer, can alter vision; extremely painful, usually involve Descemet's membrane How do we treat/heal Stromal Abscesses? need to be vascularized, aggressive medical therapy When are topical corticosteroids for the eye contraindicated? when an ulcer is present due to encouragement of growth of bacteria/fungi and possible increase of proteinase activity in tear film When are topical anesthetics for the eye contraindicated or not warrented? treatment of corneal ulcers as they retard epithelial healing; Proparacain is toxic to it What are some disease of the anterior segment of the eye? Equine Recurrent Uveitis, Glaucoma, Iris Cyst, Iris Hypoplasia, Cataracts What is Equine Recurrent Uveitis? """moon blindness"" that is immune mediated caused by Lepto, Toxoplasma, Brucella, Strep, E. coli, R. equi, Borrelia, etc.; bilateral in 20% of cases" What breeds are overrepresented by Equine Recurrent Uveitis? European Warmbloods and Appaloosas (80% bilateral, TRMP1 gene predisposition) What are the clinical signs of Equine Recurrent Uveitis? epiphora, blepharospasm, photophobia, corneal edema, conjunctival hyperemia; fibrin and iris pigment on lens; cataract formation and corneal vascularization What is the goal of ERU therapy? How do we treat it? goal is to preserve vision, reduce pain, reduce recurrence; lifelong therapy -Corticosteroids like Neopolydex (Hydrocortisone doesn't penetrate cornea) -NSAIDs -Cyclosporine A (2%) What are 2 less common treatments for Equine Reccurent Uveitis? -Vitrectomy: removes fibrin, inflammatory cells and debris to improve vision -Intravitreal gentocin injection What are Cataracts? lens opacities associated w/ blindness occurring congential, secondary to uveitis/trauma, aging; can be progressive or not (cannot be predicted) What is Nuclear Lenticular Sclerosis? cloudiness of lens nucleus starting at 7-8 yrs old, should not interfere w/ vision What is a possible treatment of cataracts? Extracapsular Cataract Surgery, Phacoemulsification (best), Enucleation What are some clinical signs of glaucoma? buphthalmos +/- exposure keratitis, Haab's stria or branching stria (stretch marks in Descemet's membrane), corneal edema, vision loss How do we treat glaucoma? Topical carbonic anhydrase inhibitor (dorzolamide), Topical miotic (pilocarpine), Topical beta blocker, anti-inflammatories What is exophthalmos? normal globe pushed foward by space occupying lesion in orbit (most commonly retrobulbar abscess/cellulitis/neoplasia Compare Buphthalmos and Exophthalmos. Buphthalmos - can be bilateral, eye is stretched in normal position, 3rd eyelid normal, cornea enlarged, normal retropulsion, mouth normal Exophthalmos - unilateral, eye pushed foward, 3rd eyelid elevated, cornea normal, mouth pain, normal IOP What are Iridial Cysts? hallmark of hereditary anterior segment abnormalities of Rocky Mountain Horse; can sometimes inhibit vision What are some diseases of the posterior chamber/tapetum? Night blindness, Chorioretinitis, Cholesterosis bulbi What is Chorioretinitis? inflammation of choroid and reitna; inactive lesions more common than active; caused by infection, immune-mediated uveitis, truama, etc. How do we treat Chorioretinitis? systemic NSAIDs, topical does not reach retinae What is Congenital Stationary Night Blindness? -found in horses w/ two coppies of white spotting pattern mutation known as Leopard spotting; common in Appaloosasa and Minis -visual impairment in dim light w/ normal daylight vision How do we diagnose Congenital Stationary Night Blindness? clinical signs, breed, genetic testing for mutation in calcium ion channel gene known as TRPM1 gene How do we treat and prevent Congenital Stationary Night Blindness? no treatment; do not breed to prevent it What is Dacryocystitis? inflammation of nasolacrimal duct and gland; can be primary or secondary; presents as ocular discharge How do we treat Dacryocystitis? flush w/ saline +/- lidocaine +/- steroids What is Hypopyon? purulent material in anterior chamber What are some unique characteristics of the equine heart? -high resting vagal/parasympathetic tone at rest -predisposition to arrhythmias -slow HR of 26-50 bpm (220-240 max w/ exercise) -extensive Purkinje fibers (simultaneous depolarization) -QRS complex only for rate and rhythm What is one of the more common arrhythmias in horses? 2nd degree AV block What is the normal HR of a horse? 26-50 bpm What is the normal amount of heart sounds ausculted? 2 to 4 What are the components of a complete cardiac workup? auscultation, electrocardiogram, echocardiogram What is the difference between an arrhythmia and murmur? arrhythmias are electrical issues, murmurs are mechanical What is included on a normal ausculation? rate, rhythm, heart sounds -S1 - AV valve closure -S2 - Semilunar Valve closure -S3 - ventricular filling -S4 - atrial systole What categories are used to categorize a murmur? timing, 'shape', point of maximal intensity, intensity level What age group is patent ductus arteriosis common in? newborn foals What age group is aortic regurg common in? older/geriatric horses If a murmur is heard between S1 and S2 where is the problem? during systole at the AV valves If a murmur is heard after S2 where is the problem? during diastole, problem w/ semilunar valves What are the Grades of murmurs? 1: soft, localized 2: soft, easily heard, consistent over point of max intensity 3: moderate, heard immediately and consistently, small area of radiation 4: loud and audible over wide area 5: loud, palpable thrill 6: loud, palpable thrill, audible w/ stethoscope helo away from chest wall What are some indications for performing an ECG? auscultation of murmur, signs of poor performance/exercise intolerance, syncope, weakness, electrolyte imbalances, unexplained brady/tachycardia Where do we place leads for a 'Base-Apex' ECG? black: left fifth ICS at level of olecranon red: right jugular furrow 2/3 of the way from the mandible to thoracic inlet white: right shoulder Describe a normal horse ECG. -P-waves may be bifid (atrial depolarization w/ S4) -QRS is a negative deflection (ventricular depolarization w/ S1) -T wave may be variable and possible HR dependent (ventricular repolarization w/ S2 and S3) What are some things measured with an echocardiograph? chamber sizes, wall thickness, valves, hemodynamics w/ color flow doppler What are some indications for a cardiac work-up in an athletic horse? -non-physiologic arrhythmia -mumur increasing in intensity -murmur grade 3-6 w/ mitral/aortic regurg -murmur grade 4-6 w/ tricuspid regurg -suspected congenital heart disease (e.g. VSD) -continuous/systolic-diastolic murmur -signs of myocardial disease or congestive heart failure Horses w/ what 3 conditions should NOT be ridden/driven? -signs of congestive heart failure -signs of pulmonary hypertension -complex ventricular arrhythmias What is Atrial Fibrillation? pathologic arrhythmia -can be 'lone' w/o underlying cardiac disease -most often in athletic breeds -only noted on strenuous exercise -likely caused by random re-entry About how much is cardiac output decreased by with A-fib? 20-30% What are 2 common scenarios of reentry? -heart is enlarged, path is longer, by the time impulse returns the refractory period has ended and impulse is transmitted again -HR is slow, impulse travels slowly What are the steps of treatment of a-fib? rule out/in underlying pathology (ECG to confirm rhythm) then perform cardioversion (or not) w/ drugs or transvenous eletrical cardioversion; underlying pathology = poor canidate for conversion What drug is commonly used for cardioversion of a-fib? Quinidine sulfate What is Quinidine sulfate? How does it work? How is it given? -Class 1a antiarrhythmic that blocks Na+ channels to increase duration of action potential and lengthen refractory period -given 22mg/kg q2 hr via NG tube for max of 6 doses; extend dosing to q6 after 48hrs What is Quinidine gluconate? How is it given? may be used for short duration a-fib (< 2wks); 2.2mg/kg IV not to exceed 12 mg/kg total What are some toxic effects of Qunidine? depression, paraphimosis, urticara, URT swelling/obstruction, laminitis, ataxia, convulsions, diarrhea How do we treat a-fib if HR is greater than 60? Digoxin first to slow ventricular rate prior to Quinidine, it is a positive inotrope inhibiting Na+/K+ ATPase increasing Na+ and slowing Ca+ eflux; increases contractility What is Valvular Heart Disease? secondary to infection, inflammation, degenerative disease, trauma (Actinobacillus/Strep) causing vegitative growth on valve What is the most common cause of heart failure in horses? mitral valve disease (chordae tendinae rupture) Where is a left sided systolic murmur most likely originating from? Right sided? left: mitral valve right: tricuspid valve How do ACE Inhibitors work? inhibits conversion of angiotensin I to II; decreases vasoconstriction, retention of water and Na+, arterial pressure What drugs are ACE Inhibitors? Benzepril and Quinapril for treating congestive heart failure What are some causes of Myocardial Disease? infection, toxicities, nutritional deficiencies (Vitamin E or Selenium), bacteria, viruses, rattlesnake venom How do we treat Myocardial Disease? dependent on underlying cause; some examples are gastric lavage, corticosteroids, antibiotics, rest What is Ionophore Toxicity? commonly added to cattle feed, moves ions across membranes to treat/prevent coccida; toxic to horses at 10% of cattle dose; affects cardiac myocytes and decreases systolic function What are some clinical signs of Ionophore Toxicity? How do we treat it? weakness, sweating, colic, tachycardia; often fatal; treat w/ activated charcoal if acute and supportive care What are Cardiac Troponins? molecules of contractile mechanism in skeletal cardiac muscle; normal range 0.47 +/- 0.085 ng.mL; reported to be increased w/ Ventricular arrhythmias, Red Maple Leaf toxicity What can be some causes of Pericardial disease? infectious (Actinobacillus equuli), immune mediated, neoplastic How can we treat Pericardial disease? Pericardiocentesis, Pericardial lavage, antibiotics, supportive care What is Aortic Root Rupture? rupture of aortic root most often resulting in sudden death in older breeding stallions; Friesian horses You are the owner of a successful racetrack practice. Speedy, a 4-year-old Thoroughbred stallion, presents with a history of decreased performance in his last few races. On your initial physical examination you find a temperature of 100.2° F, respiratory rate of 20, heart rate of 52 and a heart rhythm that is irregularly irregular. What is most likely etiology of Speedy’s poor performance? Atrial fibrillation You are called out to do a wellness visit on a 28-year-old Morgan gelding, Tex, who spends his time as a pasture ornament. In the course of your physical exam you note a heart rate of 44 and a Grade 2/6 diastolic, decrescendo murmur at the left fourth intercostal space. Which of the following do you tell the client? it's aortic regurg, recommend a recheck at next visit What are the most common causes of pruritus in horses? ectoparasites (culicoides, horn/stable flies/chorioptes) and allergies (atopic dermatitis) What are the most common pruritic lesions seen in horses? alopecia, papules (parasites, infection), pustules (infection), urticaria (allergies) What are the different common lesion distributions of pruritis and what do they tell us? -ventral midline = culicoides (diffuse), horn/stable flies (focal) -mane and tail = culicoides -pastern = chorioptic mange Describe Culicoides Gnats. biting midges, gnats, sand flies that are blood sucking (attracted to O2, lactic acid); lay eggs in damp marshy areas What is the typical presentation of Culicoides Gnats? prefer to feed from ears, mane, back, and tail (rubbing of mane/tail); bites are painful, cause pruritis, and develop into papules/wheals How do we treat Culicoides Gnats? reduce population (remove manure/standing water), gnat traps (contain octanol), reduce exposure (fans, screens, repellents - permethrin), Prednisolone (0.5-1mg/kg q24 hr) Describe Horn Flies. small blood sucking flies (depending on temp and sun), lay eggs in fresh COW manure; act as vectors for protozoal disease and helminths How do lesions from Horn Flies present? preferred feeding sites depend on temp; prefer ventrum when warm and sunny, topling when rainy or cool; painful, pruritic, papules/wheals, focal ventral midline dermatitis How do we treat for Horn Flies? reduce population (remove manure/access to cattle), reduce exposure (repellents - pyrethroids, fly predators) Describe Stable Flies. Stomoxys calcitrans that are common; blood sucking and big (7-8mm); lay egs in wet straw, bedding, or manure; life cycle temp dependent (4 wks in warm weather) What can Stable Flies be vectors for? viral disease, protozoal disease, helminths What is the presentation of lesions from Stable Flies? feed from neck, back, chest, groin, and legs during the day; painfu, puritic, papules/wheals, insect hypersensitivity How do we treat for Stable Flies? reduce population (destroy breeding sites, moist bedding, sprays), reduce exposure (repellents, fly predators - parasitic wasps) Describe Chorioptes. leg/tail/foot mange tiny 0.3-0.5mm surface mites feeding on epidermal debris live for 3 weeks on host, up to 70 days off (thrive when cold) transmitted through contact How are Stable Flies different from Horn Flies with feeding? Stable flies rest off of host after meal How do lesions from Chorioptes present? most common in draft horses w/ feather fetlocks; distal hind limbs, tail, +/- pruritis How can we diagnose Chorioptes? history, skin scrape, biopsy How can we treat Chorioptes? difficult to treat w/ multi-horse infestations -topicals (lime sulfer, Fipronil - Frontline, Bravecto) -systemic ivermectin, moxidectin, doramectin What is Atopic Dermatitis? How is it spread? allergic reaction to environmental antigen causing Type I hypersensitivity mediated by IgE; spread through percutaneous or respiratory routes What is the mean age of onset of Atopic Dermatitis? 9.6 years What are some of the typical presentations of Atopic Dermatitis? -pruritis, utricaria, face/pina/ventral thorax/legs -bititing at themselves, rubbing, stomp feet, flick tail, shake head -excoriation, self-induced alopecia, lichenification, hyperpigmentation How do we diagnose Atopic Dermatitis? history, clinical signs, rule out (ectoparasites, contact dermatitis, drug, angioedema) How do we treat Atopic Dermatitis? -intradermal allergy testing (desensitization), serology testing, decrease exposure -topicals (shampoos/rinses to remove allergens eliminate dry skin, antipruritic agents - Colloidal oatmeal, Pramoxine, Glucocorticoids) -systemic (Hydroxyzine pamoate, Doxepin, Prednisolone) What are the most common causes of alopecia? infectious (Dermatophytes, Pyoderma - Staph.) follicular (Alopecia areata) What are common dermatophytes in horses? Trichophyton (equinum, mentagrophytes, verrucosum) Microsporum (equinum, gypseum) What are the typical presentations of Dermatophytosis? -alopecia -hoove splitting/weakening -+/- pruritis -lesions on areas of tack, coronary band, face, neck, dorsal lateral thorax How do we diagnose Dermatophytosis? Wood's Lamp, trichogram, Dermatophyte test medium (DTM), bipsy How do we treat Dermatophytosis? -healthy horses spontaneously remiss in 3 months -eliminate imblances, underlying disease, reduce contagion -topicals (miconazole/ketoconazole + chlorhex, lime sulfer) -systemic (Griseofulvin, Fluconazole, Terbinafine) What would be presentation of Staph pyoderma lesions? -folliculitis, furunculosis, circular alopecia, crust/papule, draining tracts, +/- pruritis -on saddle, lumbar, pastern What are some risk factors for spreading MRSA? Ceftiofur/aminoglycosides, large farm, previous colonization/infection, previous admission to hospital (Equine MRSA different strain than human) How can we diagnose Staph Pyodermas? culture/biopsy if no response to antibiotics, draining tracts seen if deep How can we treat Staph Pyodermas? TMS Enrofloxacin Doxycycline Topicals What is Alopecia Areata? follicular disease causing well circumscribes, non-scarring, non-inflammatory alopecia; lymphocytes and antibodies directed against anagen hair follicles What is the typical presentation of Alopecia Areata? -insidious or sudden onset, no pruritis, no pain -focal or diffuse lesions on face, neck, trunk; may spare mane/tail How do we diagnose Alopecia Areata? "-rule out other folliculitides, biopsy -histo showing peribulbar accumulation of lymphocytes, ""swarms or bees""" How do we treat Alopecia Areata? -most regrow hair in 2-3 years (finer, lighter) -no curative treatment, seasonal relapse -corticosteroids possibly What are some Dfdx for scaling and crusting dermatoses? infectious Dermatophilus, immune mediated (Pemphigus foliaceus, Sarcoidosis), keratinization defect (Seborrhea) Describe Dermatophilosis. gram-positive facultative anaerobic, survival dependent on soild type, water, not pH What is the basic pathogenesis of how Dermatophilis causes skin damage? biting flies/arthropods, prickly vegetation, maceration, inflammatory disease; moisture causes release of infective zoospore and increases skin maceration What is the most common bacterial skin disease in large animals? What is the impact? Dermatophilosis; causes damage to hide ($$), contagious, most prevalent in humid climates What are some of the clinical signs? -rump and dorsum ('run off' or 'dribbling') -saddle (under tack, increased skin trauma) -face and neck (under tack, increased skin trauma) -dital legs (pastern, heels, 'grease heel', 'scratches') -crusts -painful -'paintbrush' lesions How do we diagnose Dermatophilosis? histoy, clinical presentation, cytology (gram staining, methylene), culture, 'railroad tracks' How do we treat Dermatophilosis? -often regresses w/ dry weather, limit moisture, crust removal/disposal -topicals: Iodophors, Lime sulfer, Chlorhex -antibiotics: TMS, penicillin What is Pemphigus Foliaceus? most common antibody-mediated auto-immune skin disease in horses and donkeys; antibodies target transmembrane protein antigens What are some of the clinical signs of Pemphigus Foliaceus? distributed lesions on face, trunk, coronary bands edema of legs/ventral abdomen exfoliative, scaling, crusting lesions utricaria exacerbated in warm, sunny, humid weather How do we diagnose Pemphigus Foliaceus? history, clinical signs, cytology (acantholytic keratinocytes), biopsy What is the most common dermatophyte in horses? Trichophyton equinum; can cause acantholytic keratinocytes w/ pemphigus foliaceus How do we treat Pemphigus Foliaceus? What are some adverse effects? Prednisolone, Dex, Azathioprine, Aurothioglucose -Azathioprine can cause bone marrow suppression/increased susceptibility to infection What is Sarcoidosis? -idiopathic, generalized, systemic granulomatous disease -Equine Histiocytic Disease/Dermatitis -rare disorder causing exfoliative dermatitis, severe wasting What are some of the clinical signs of Sarcoidosis? -skin lesions occur first, then internal organ involvement (lungs, GI), emaciation -face, trunk, legs, progression to generalized distribution -scaling, crusting, alopecia, painful +/- pruritus How do we diagnose Sarcoidosis? history, clinical signs, biopsy How do we treat Sarcoidosis? -only skin disease has better prognosis than GI involvement -Prednisolone, Omega 6/3 Fatty Acids, Pentoxifylline What is Equine Pastern Dermatitis? cutaneous reaction pattern NOT disease, has many different prediposing, primary, and perpetuating factors; adult draft horses most represented What are some predisposing factors to Equine Pastern Dermatitis? -genetic: nonpigmented skin, lyphedema, feathers on pastern, keratinization disorder -iatrogenic: topicals, training devices, poor grooming -environmental: climate/moisture, poor pasture, sand (Arabians) What are some primary factors leading to Equine Pastern Dermatitis? -physical/chemical: blistering, motor oil, treated bedding -immune mediated: allergy, photosensitization, vasculitis, pemphigus -infectious: dermatophyte, spirochete -parasitis: Chorioptes, Strongyloides -neoplasia: sarcoids What are some perpetuating factors to Equine Pastern Dermatitis? -secondary infections: Staph, Dermatophytes, Malassezia -pathogenic skin changes: trauma, insect/tick bites -environmental: UV exposure, cold What are the 3 forms of Equine Pastern Dermatitis? 1. mild 2. exudative 3. chronic proliferative What are some clinical signs of the mild form of Equine Pastern Dermatitis? most prevalent, alopecia, dry scale, crust, epidermal hyperplasia What are some clinical signs of the exudative form of Equine Pastern Dermatitis? erythema, erosion, alopecia, serous to purulent crust, epidermolysis, vasculitis What are some clinical signs of the chronic proliferative form of Equine Pastern Dermatitis? excessive granulation tissue, nodular hyperkeratosis, lichenification, fissures, painful lameness How do we diagnose Equine Pastern Dermatitis? -detailed history: age of onset, time of year, topical treament, environmental, lameness, diet, travel history -superficial skin scrape, cytology, trichogram, DTM, bipsy, culture, CBC What is Chronic Progressive Lymphedema? devastating disease of draft horses; defect in dermal and lymphatic elastin fibers What are the clinical signs of Chronic Progressive Lymphedema? all four limbs, swelling/scailing, progressive swelling/thickened skin folds/large firm nodules How do we diagnose Chronic Progressive Lymphedema? history, clinical presentation, cytology, biopsy How do we treat Chronic Progressive Lymphedema? poor response; treat secondary infections, exercise, massage, bandages What are Photosensitivities? increased susceptibility to damaging UVL effects What are Phototoxicities? sunburn reactions, dose-related response to light exposure What UV wavelenghts are associated w/ photosensitivity? UVA 320-400nm What are the three basic features of photosensitivities? photodynamic agent (plants - St. Johns wort, mycotoxins, drugs/chemicals) exposure to sufficient UVL cutaneous absorption in non-pigmented/lightly haired areas What are the classifications of photosensitvities? primary - photodynamic agents hepatogenous - hepatotoxic plants (pyrrolizidine, clover) aberrant pigment synthesis idiopathic What are clinical signs of photosensitivities? white skin, erythema/edema, ulceration, crusts, alopecia, +/- pain How do we diagnose photosensitivity? history, environment (plants), clinical lesions, CBC/chem How do we treat photosensitivity? elimate photodynamic agents, avoid sunlight, symptomatic treatment, glucocorticoids, NSAIDs What are the 2 most common endocrine diseases in horses? Pituitary Pars Intermedia Dysfunction Equine Metabolic Syndrone What is the main cause of PPID? loss of dopaminergic inhibition of pars intermedia What is the normal activity of a healthy pars intermedia in the horse? dopamine from hypothalamus inhibit cells in pituitary pars intermedia; limit release of ACTH into blood stream What is the basic pathogenesis of PPID? hypothalmic dopaminergic neurons undergo oxidative stress; loss of inhibiton of pars intermedia, hyperplasia of adenoma; release of ACTH increase What is the primary product produced by melantocytes of the pars intermedia? pro-opiomelanocortin; can be cleaved into ACTH, beta-endorphin, alpha-melanocytes stimulating hormone (MSH), corticotropin-like intermediate peptide (CLIP) What is most ACTH in the normal pars intermedia cleaved by? prohormone convertase 2 (PC2) What is the epidemiology of PPID? most commonly older horses, all breeds, donkeys What are some common clinical signs of PPID? abnormal hiar coat/shedding (hirsutism)** muscle wasting/weight loss (epaxials) PU/PD chronic laminitis hyperhydrosis immunosuppression (infections, parasites) behavior changes infertility blindness adipositiy/insulin resistance What are some recommended tsts for PPID? early: TRH stim test w/ measuring ATCH** basal ATCH concentration** Dex suppression test MRI What is the basic procedure for baseline ACTH testing? collect into EDTA purple top, keep cool, centrifuge, plasma can be frozen (avoid freeze-thaw cycles) What is the basic procedure for a TRH stim test? not w/in 12 hours after grain (hay only preffered) -give 0.5 mg or 1 mg (> 250kg) IV, collect blood into EDTA at 0 and 10 mins after TRH given Why is season important in testing for PPID? currently no normal for TRH stim between July and December due to shedding of summer and growing of winter coats; negative is likely vaild What is the normal range of ACTH after TRH stim test from Jan-June? 100-200 What is the main treatment of PPID? Pergolide; possible adjunct w/ Cyproheptidine How does Pergolide work? What is the dose? dopamine receptor agonist that restores inhibition of melanocytes to manage PPID; dose at 0.5mg increments of 0.002 mg/kg (~1mg per horse) -possible inappetance What should doses of Pergolide not exceed? 0.01 mg/kg What is Cyproheptidine? What is the purpose? -serotonin antagonist, antihistamine activity, anticholinergic activity -treatment prior to availability of pergolide; adjunct How do we adjust Pergolide doses according to clinical signs? evalutate signs every 1-3 months after starting treatment, then 6-12 months -no improvement = increase dose by 1-2mcg/kg How do we manage PPID? assess for comorbidities/complete wellness exam, periodic quality of life exam What are some clinical pathology findings of PPID? lymphopenia, hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypophosphatemia What is Equine Metabolic Syndrome? an endocrine disorder characterized most uniformly by general/regional adiposity, insulin resistance (hyperinsulinemia), laminitis predisposition What are some breeds that are more respresented in Equine Metabolic Syndrome? Pony, Andalusians, Gaited, Morgans, Mini, Warmbloods What are some conditions/Dfdx that prompt testing for EMS? diabetes mellitus, hyperlipemia, infertility, colic from pendunculated lipoma, mammary gland edema, divergent hoof rings Describe the algorithm for diagnosing EMS. -horse, pony, donkey w/ history/clinical signs -test for insulin dysregulation (ID) + PPID if indicated -negative for ID = PPID -positive for ID + obese = decrease body fat, recheck @ 6mo if resolves -positive for ID + non-obeses = maintain body, recheck @ 6mo if resolves How do we do diagnostic testing for EMS? -resting insulin concentrations: no grain w/in 4 hrs, only hay; > 50uU/L -dynamic insulin testing: oral sugar (0.15 mL/kg corn syrup), measure insulin and glucose T0, T60, T90; > 45 uU/L diagnostic -leptin -triglycerides What is the relation between Leptin and EMS? leptin produced by adipose cells and may be increased w/ obesity; does not necessarily indicate IR, but can help identify source -normal leptin = IP due to PPID -high leptin = IR due to EMS What were horses w/ EMS misdiagnosed with in the past? hypothyroidism What is the first line treatment for EMS? dietary modification and exercise; Metformin may be tried for refractory cases What would be the only undication for use of T4 and Levothyroxine in the horse? only short term for obese IR horse; 3-6mo; helpful if unable to exercise due to laminitis What do T3 and T4 levels in the horse indicate? How do we manage them? -only low T3 = no action required -low T3 and T4 caused by physiologic causes, disease, medication = no action needed -low T3 and T4 or just T4 w/ no explanation = check serum free T4, if low perform TRH stim test, if no response to test, horse is hypothyroid Horses w/ unexplained laminitis should receive...? endocrine workup What is the reference range of ACTH for November to July and July to November? Nov. to July = < 35 pg/mL Jul to Nov. = < 100 pg/mL What is the reference range of glucose in the horse? 71-113 mg/dL What is the reference range of insulin in the horse? 10-40 uIU/mL What is a fecal egg count that should be treated? > 200 About what percentage of horses are geriatric (20+)? 10% What is Immunosenescence? geriatric horse decrease in immune response/function; decreased lymphocytes, increased CD4/CD8, proinflammatory cytokines What is Anhidrosis? loss of ability to sweat; more common in hot/humid climates; often present as 'respiratory' cases from overheating How do Equine sweat glands work? -humoral - adrenergic agonists secrete -nervous** - autonomic adrenergic nerves How do we diagnose Anhidrosis? Terbutaline test -10-fold dilution, saline control, injected ID to observe sweating or not How do we manage Anhidrosis? move to cooler, drier climate diet/electrolytes (K+) One A/C supplement (contains L-tyrosine, ascrobic acid, niacin, cobalt) What is Hyperlipidemia/Hyperlipemia? fat stores mobilized in response to negative energy balance as sequela to illness in mini, pony, donkey breeds -lipidemia = triglycerides 54-500 -lipemia = triglycerides > 500 What are some clinical signs of Hyperlipidemia/Hyperlipemia? lethargy, anorexia, change in attitude; monitor triglycerides in high risk patients How do we treat Hyperlipidemia/Hyperlipemia? enteral feeding if possible (NG tube, small feedings, supplement w/ Dextrose) parenteral nutrition monitor glucose What is a Pheochromocytoma? How is this diagnosed? neoplasia of the adrenal gland, is a Dfdx for hemoabdomen; diagnosed via urinary catecholamines Why would inappropriate lactation occur in horses? most often secondary to PPID, possibly due to phytoestrogens; treat w/ Pergolide and dietary modification What are some Dfdx for increased Ca++? chronic renal failure (creatinine problem also seen) neoplasia (secretion of PTHrP) vitamin D toxicity (ergocalciferol) primary hyperparathyroidism (increased PTH/increased absorption/bone resorption) What are some Dfdx for decreased Ca++? blister beetle toxicosis exercise-induced exhaustion sepsis lactation acute renal failure primary hypothyroidism What are Mules and Hinnys? donkeys Mules = offspring of jack donkey + mare Hinny = offspring of jenny donkey + stallion What are typical PE parameters of donkeys? T = 97.2-100.0 F (102.1F in young donkeyss) P = 36-68 (44) bpm R = 12-20 body condition scored 1-5, more localized fat storage What do we need to remeber when giving vaccines to donkey? avoid intra-fat (IF) injections for IM drugs, especially in neck What is the typical hoof anatomy of donkeys? more upright wall, P3 not aligned w/ dorsal wall like horses, do not elevate heel in laminitic donkeys What are some characteristics of hematology in donkeys? RBC variable, PCV higher in younger, dehydration (12-15%) occurs before increased PCV, different coags What are some characteristics of serum chemistry in donkeys? serum color lighter, creatinine/total bilirubin lower, creatine kinase/GGT higher What are some characteristics of endocrine hormones in donkeys? lower insulin (2.1) ACTH higher (66.7 +/- 20.7) Describe Hyperlipemia in donkeys. What is the pathogenesis? should be on your radar anytime donkey is sick -inciting factors: decreased feed intake (stress, illness, dental, etc.) -triglycerides > 500 mg/dL (normal < 200) -pathogenesis: negative energy balance > release of fatty acids > increased VLDLs in liver What is the most common lesion causing colic in donkeys? large colon impactions (pelvic flexure or cecum) What is the most common neoplasm of horses? equine sarcoids What are Equine Sarcoids? non-metastatic skin tumor most commonly seen on head, ventral abdomen, lims in single lesions or clusters -4 types: flat, verrucous, fibroblastic, mixed What are some gross Dfdx of sarcoids? granulation tissue, habronemiasis, fibroma, fibrosarcoma, neurfibroma How do we diagnose sarcoids histologically? skin needed -capillary poor, fibroblastic proliferation -fibroblasts perpendicular (picket fence) to basement membrane -hyperplastic epidermis (Rete pegs) What kind of biopsy should be used for sarcoid if needed? excisional biopsy How do we treat sarcoids? -surgical excision w/ primary closure (avoid granulation tissue) -lasor vaporization (CO2 resects/evaporates tissue, expensive) -chemo (always) -cryotherapy (2-3 cycles needed, monitor temp w/ thermocouples) -immunotherapy (attenuated M bovis causes complete infiltration) -hyperthermia (heat at 50 C for 30 sec) -radiation What are some common complications of cryotherapy? swelling, hyperemia, destruction of hair follicles, possible nerve damage What are some chemotherapies for sarcoids? -Cisplatin-in-oil injections - does not diffuse, 1yr, 87% relapse free -Cisplatin bead (absorbable) -Fluorouracil creme (topical after lazer) -Mitomycin C What are some differences between Cisplatin injection and beads for chemo? -1 month vs 2 wk intervals -injection must infiltrate entire mass b/c it does not diffuse -beads diffuse 15 mm How does topical Fluorouracil work? inhibits DNA and RNA synthesis (pyrimidine analong) treat daily for 10-14 days What are treatment plans for sarcoids in different locations? -periocular: excision, laser, chemo -trunk, limbs: excision, debulk What are a few antibiotics that we try to avoid/save for people? Vancomycin, Imipenem, Chloramphenicol In what situations do we commonly use antibioitcs? -perioperative to prevent infection -treat an established infection (SAA, Fibrinogen, Globulines) -prevent infection in presdisposed animal What are some considerations to think of when choosing antibiotics? -penetration of drug to infection site -severity -compliance (route, host factors, cost) -food animal withdrawl times, ELDU What are common adverse reactions to many antibiotics? colitis nephrotoxicity cartilage effects teratogenic IMHA What are time dependent antibiotics? need to be above minimum inhibitory concentration for over 50% of the time; dosed more frequently or CRI What are concentration dependent antibiotics? activity best predicted by relationship between peak drug concentration and MIC What are Aminoglycosides? How do they work? move across bacterial cell membranes by O2 dependent interaction w/ LPS of gram-negatives; do not penetrate CNS -dose-dependent -bactericidal -work against gram-negatives -Gentamicin (adults) and Amikacin (foals) What are Penicillins? How do they work? bind penicillin binding proteins in cell membranes preventing cell wall synthesis -work against gram positives and negatives -do not cross CNS -bactericidal and time-dependent What are Aminopenicillins? How do they work? inhibit bacterial cell wall synthesis; amino penetrates gram-negatives better What are Cephalosporins? How do they work? inhibit bacterial cell wall synthesis by binding penicillin binding proteins -first to fourth gen, higher gen more resistant to beta-lactamases Cefazolin (1st), Cefoxatin (2nd), Ceftiofur (3rd), Cefepime (4th) What is Imipenem? How does it work? a carbapenem that inhibits cell wall synthesis by binding penicillin binding proteins How do Potentiated Sulfas work? trimethoprim inhibitds folate production by bidning dihydrofolate reductase, sulfadiazines are mistaken for PABA by bacterial folic acid production -good against aerobic bacteria -bactericidal -time-dependent What are Fluoroquinolones? How do they work? inhibits DNA gyrase and therefore DNA coiling (Enro and Marbofloxacin) -dose-dependent -bactericidal -activity against aerobics What are Tetracyclines? How do they work? inhibit protein syntehsis by binding 30s ribosomes (Doxy, Oxy, Mino) -renally excreted -does not penetrate CNS -works against some anerobes -bacteriostatic -time-dependent What are Macrolides? How do they work? inhibit protein synthesis by binding 50s ribosome (Clarith and Azithromycin) -bacteriostatic for intracellulars -Rhodococcus -can cause extreme deadly diarrhea What are Rifampin? How do they work? inhibits RNA polymerase of bacteria -intracellular bacteria, good lipid solubility -bactericisal -use w/ Clarithromycin What is Chloramphenicol? How do they work? reversibly binds 50s ribosome -gets into abscesses -bacteriostatic, can be bactericidal -causes Aplastic Anemia What is Metronidazole? How do they work? disrupts bacteria w/ nitro reductases and reactive intermediates -distributes into CNS and abscesses -bactericidal -works against protozoa, anaerobes What are Glycopeptides? How do they work? inhibits bacterial cell wall synthesis by binding precursor sites different than b-lactams, inhibit RNA synthesis (Vancomycin) -time-dependent -used w/ MRSA or Enterococcus What is the difference between hemp and marijuana? hemp = 0.3% or less THC marijuana = more than 0.3% THC What are NSAIDs? drugs for pain, reduce PG by inhibiting COX -COX 1 expressed in GI, kidney, platelets -COX 2 expressed in all tissues What are common non-selective COX inhibitors we use? What about COX2? Flunixin (Banamine) Phenylbutazone Acetaminophen Firocoxib (COX2) When can we use steroids and NSAIDs? can be done in horses when disease indicates for a short time; monitor proteins What is a compounded drug? any drug manipulated to produce a dosage form drug; not evaluated by FDA; compounding drugs to mimic FDA-approved drugs is illegal What are Medical Devices? What are some examples we use? instrument for use in diagnosis, treatment, or prevention of disease -Legend and Adequan are FDA for systemic use in horses Cutaneous Squamous Cell Carcinomas make up about what percent of neoplasms? 20% -horses 8.5-14.5 years -lightly pigmented horses (Appaloosas, Pintos, Paints) -UV -common in draft horses What are common locations of cutaneous squamous cell carcinomas? cornea/limbus, 3rd eyelid, lids external genitalial geldings and mares mucocutaneous junctions hoof wall layers secondary to burns How can we treat cutaneous squamous cell carcinomas? laser or sharp resection/vaporization chemo hyperthermia debulking-cryo beta irradition corneal/conjunctival chemo What are the 3 common types of melanomas? -melanocytic nevi: young, subepithelial melanin -dermal melanoma: middle age to older, dermal melanin (gray horses) -anaplastic malignant melanoma: aged horses, pleomorphic cells, metastasis What are some common locations of dermal melanomas? ventral tail perineum external genitalia parotid salivary gland, limb, neck, ears, eyelids lips How do dermal melanomas appear? firm, flat, solitary or multiple, nonulcerated, discrete to coelescing SQ mass overlying skin intact or alopecic, hyperpigmented or amelanotic What is the natural feeding behavior of the healthy horse? forage, water, salt wild - graze about 12-14 hrs a day, domestic horses not managed this way current practices contribute to morbidity (obesity > EMS > laminitis) How do small intestines of horses differe from human, dogs, etc.? less starch digestion, less alpha amylase so more starch reaches cecum What is the physiology of the cecum? fribolytic anaerobes predominate (Clostridium, Fibrobacter) VFA provide 30-60% of caloric requirements starch favors Bacillus, Lactobacillus, Strep (increased lactate, dropped pH, alters production/absorption of SCFAs, disrupts epithelium) In what cases is nutrition especially critical? starves horses, obese laminitis medical conditions (HYPP, PSSM, NPO, liver/renal disease, etc.) What are some general guidelines regarding diet and history of nutrition? -field call patients BCS and weigh -hospitalized should be weighed daily -calorie requirements = 30-36 kcal/kg BW/day, forage 1.5-2% of BW a day -dentition and parasites should be evaluates in unthrifty animals -ask about supplements What are some considerations when deciding on/instituting diets? -history of starved/anorexic -specific disease/disorder -bredd -weight/BCS -loss of 3-5% of initial BW -biochem of indirect bilirubin/triglycerides What is the dietary approach for a starved horse? hydration start w/ 75% maintenance of current BW (30-35 kcal) alfalfa is ideal continue for 3-4 days, small frequent meals slowly increase to 125% maintenance What is refeeding syndrome? severely malnourished individual rapidly begins eating > rapid increase in glucose/insulin > sudden shift in metabolism from catabolic to anabolic > rapid influx of electrolytes like phosphorus, potassium, and magnesium into cells > dangerously low levels of electrolytes in the bloodstream due to depleted stores What is the dietary approach for obese (healthy) horse? restrict/eliminate grain decrease caloric intake to 75% RER or 1.5% BW in forage possible ration balancer exercise How do we use nutritional management to help with HYPP? limit intake of potassium How do we use nutritional management to help with PSSM? forage-based diet, low NSCs, added fat to make up calories (oil, rice bran) How do we use nutritional management to help with Right Dorsal Colitis? low bulk diet (small often feedings of complete feed), psyllium, flax oil (increases SCFA) How do we use nutritional management to help with loss of dentition in geriatric horses? complete feed meals (senior food) How do we use nutritional management to help with renal disease? increase fat to maintain condition, provide protein to maintain BUN/creatinine of 10:1 to 15:1, restrict salt (if edema is an issue) How do we use nutritional management to help with liver disease? adequate protein/calories, add lactulose if hepatic encephalopathy is a concern What are the types supportive feeds? tube feed: assisted enteral, slurries for seniors, critical care meds, small dfeedings parenteral nutrition: suboptimal for starved horses, helpful for anorexia and protracted illness What are the components of parenteral nutrition? dextrose, lipid, amino acids, b-complex vitamins How do we administer parenteral nutrition? dextrose alone for up to 3 days extreme sterility NOT a substitute for IV fluids monitor rate/glucose levels/triglycerides