EIM 15-18 Haem/Endo/Skin

Question 1

The most common cause of thrombocytopenia in hospitalized horses

Answer 1

increased utilization or destruction of platelets secondary to a primary infectious, inflammatory, or neoplastic disease process.

Thrombocytopenia is also common in strangulating/ischemic gastrointestinal disorders.​

Question 2

An association between thrombocytopenia and a poor prognosis has been demonstrated in

Answer 2

hospitalized horses in general and in horses with colon torsion.​

Question 3

Thrombocytopenia occurs in cases of EIA due to ?

Answer 3

combined effect of immune-mediated destruction and decreased platelet production

Question 4

A foal presents with ulcerative dermatitis, thrombocytopenia and neutropenia. Based on the most likely suspected diagnosis, what treatment would be indicated?

Answer 4

DEXAMETHASONE

Neonatal Alloimmune Thrombocytopenia. Immune-mediated destruction of platelets following ingestion of preformed antiplatelet antibodies with the colostrum has been reported in horse and mule foals and is suspected to be more common in the latter.​

responsive to corticosteroid administration, suggesting an immune-mediated component. ​

Question 5

The most common clinical sign of Glanzmann’s thrombasthenia is

Answer 5

epistaxis

Question 6

Glanzmann’s thrombasthenia

Answer 6

Prolonged or recurrent epistaxis appears to be the most common clinical sign whereas the presence of petechiae or ecchymosis is more variable. ​
​
Definitive diagnosis: demonstration of reduced CD41/61 expression on the platelet surface using flow cytometry. ​
​
Glanzmann’s thrombasthenia is a quantitative deficiency or a qualitative defect of the platelet fibrinogen receptor (also referred to as GP IIb/ IIIa, αIIbβ3 integrin, or CD41/61). It is an autosomal recessive disorder, and the genetic defect has been localized to the gene encoding GP IIb (also referred to as αIIb).​
Breeds: QH, TB, SB, WB, Peruvian Paso ​
​
NOTE: distinct from ‘Atypical Equine Thrombasthenia’ = Reduced fibrinogen binding, only occurs in TBs, normal number of CD41/61 expression ​

Question 7

Von Willebrand’s Disease

Answer 7

Is rare in horses, only congenital
​
Diagnosis achieved by measuring plasma von Willebrand antigen levels using an ELISA​
​

​

Question 8

Hemophilia A in horses

Answer 8

Reported in Thoroughbreds, Standardbreds, Quarter Horses and an Arabian ​
​
Typically factor VIII deficiency, but also can occur with factor IX and X and to a lesser degree factor VII and prothrombin (F 2) deficiencies. ​
​
Transmitted via an X-linked recessive trait, colts affected ​
​

Question 9

Iron deficiency anemia

Answer 9

is characterized by low serum ferritin concentration, decreased stainable iron stores in the bone marrow, decreased plasma transferrin saturation, normal or increased total iron binding capacity (TIBC), hypochromic erythrocytes (decreased MCHC), and microcytosis (decreased MCV)​

Question 10

hemangiosarcoma

Answer 10

Present as a disseminated malignancy involving the spleen, heart, lung, liver, and soft tissues of the trunk and extremities​

Question 11

hemangioma

Answer 11

Typically benign, solitary, deep, dermal tumors

Question 12

What are two well documented causes of IMHA in horses?

Answer 12

NI - primary IMHA

penicillin

Question 13

EIA

Answer 13

Reverse transcriptase and integrase are utilised by the virus to generate and integrate viral DNA into the host cell genome​

Replication occurs in monocytes, dendritic cells, tissue macrophages, and endothelial cells ​

Fever and thrombocytopenia considered to be the most reliable clinical indicators​

One of the ELISA kits detects gp45​

Time from infection to seroconversion may take up to 180 days​

“ELISA is a sensitive gal”​

Question 14

Babesia caballi

Answer 14

Carrier: can be cleared

Invasion site: erythrocyte

Severity: milder

Incubation period following infection by tick: 10-30days

cELISA target: Apical merozoite protein rhoptry (RAP) 1

TX: Imidocarb, quarantine, or euthanasia

Question 15

Theileria equi

Answer 15

Carrier: lifelong

Invasion site: leukocyte

Severity: severe; colic, resp, neuro signs also possible

Incubation period following infection by tick: 12-19 days

cELISA target: Equi merozoite antigens (EMA) 1 and 2

TX: Imidocarb, quarantine, or euthanasia

Question 16

Red Maple Leaf toxicity

Answer 16

Wilted/dried leaves of silver and sugar maple also potentially toxic​

Signs of haemolysis predominate before mid-September, whereas signs of methaemoglobinaemia predominate after mid-September​

Oxidising agents include gallic acid, and pyrogallol (formed from the metabolism of gallic acid and gallotenins by Klebsiella pneumoniae and Enterobacter clocae in the ileum​

Factors associated with mortality include lack of pyrexia on admission and corticosteroid administration​

Question 17

Immune Mediated Vasculitis

Answer 17

Deposition of complexes of antigen and immunoglobulins in the walls of the capillaries and other small blood vessels leads to a type III hypersensitivity reaction​

Microscopically, lesions are characterised by a leukocytoclastic vasculitis​

Secondary complications such as laminitis and thrombophlebitis are not uncommon ​

Question 18

Anaplasmosis

Answer 18

Obligate intracellular bacterium infecting neutrophils​

Transmitted by Ixodes ticks​

Worldwide distribution​

Incubation period of ~10 days​

Signs vary from subclinical to high fever (100 – 106.9 F)​

Question 19

how can you diagnose IMHA

Answer 19

Coomb’s test​
Presence of autoagglutination​
Osmotic fragility testing of RBC’s

Question 20

Reported causes of equine hypothyroidism are

Answer 20

Iodine deficiency​
Iodine excess​
Neoplasia ​

Hypothyroidism in adults is rare and usually non life threatening

Question 21

In equine primary hypothyroidism, what will be increased/decreased?

Answer 21

Horses with primary hypothyroidism have decreased T4 and T3 concentrations and increased TSH concentrations​

Question 22

The major cause of neonatal hypothyroidism in foals is

Answer 22

nutritional, resulting in congenital goiter (thyroid enlargement at birth). Possibly due to Iodine deficiency in utero (inadequate intake by the dam)​ OR Iodine excess in utero (excessive intake by the dam) ​

Question 23

CHD: congenital hypothyroidism and dysmaturity

Answer 23

First recognized 1970s​
Prolonged gestation + signs of dysmaturity​
-Musculoskeletal abnormalities (weakness, delayed ossification carpal and tarsal bones, OCD, prognathia) ​
-Thyroid enlargement rare (different to neonatal hypothyroidism)​
–Still have thyroid gland hyperplasia on biopsy though ​​
Etiology unknown ​
-Nitrates? Combo with low iodine forage​
Typically disease of western Canada and north-western USA​

Usually die a few days after birth, or suffer many complications

Question 24

CS: Neonatal Hypothyroidism

Answer 24

Enlarged thyroid or normal thyroid size ​
Stillbirths, prematurity​
Weakness, lethargy, depression, weak suckle​
Long haircoat, rough hair coat, silky if premature/dysmature​
Respiratory insufficiency and distress​
Incoordination​
Cold intolerance and hypothermia ​
Physeal dysgenesis, defective ossification ​
Carpal and tarsal bone collapse, hypoplastic carpal bones​
Common digital extensor tendon rupture​
Forelimb contracture​
Prognathism, delayed incisor eruption​
Growth retardation and death​
Or born apparently normal but develop skeletal lesions weeks later ​

Question 25

diseases that may have low TH levels but not truly hypothyroid

Answer 25

Nonthyroidal illness syndrome (e.g. septic / SIRS horses)​
Obesity, laminitis, insulin resistance, EMS ​
Infertility, agalactia​
Poor performance​
Rhabdomyolysis ​
Dermatopathies, alopecia ​
Anhidrosis​
​
TH therapy to euthyroid horses may be harmful, inhibiting the HPTA, and suppressing endogenous TH synthesis and secretion. ​

Question 26

Thyroid Tumors

Answer 26

Thyroid adenoma ​
-Age related phenomenon, > 16yo​
-Benign, usually unilateral ​
-Not associated with thyroid dysfunction ​
​
Thyroid adenocarcinoma​
-Malignant, euthyroid, hypothyroid, and hyperthyroid​
​
Thyroid medullary carcinoma ​
-Parafollicular cell (C-cells) tumor ​
​
Multiple endocrine neoplasia (MEN)​

Question 27

Adrenal insufficiency (AI) - reduced capacity of the adrenal gland to secrete adrenocortical steroids in sufficient amounts to meet physiologic needs, thus resulting in clinical and laboratory disturbances – typically occurs in acutely ill horses/foals. ​
At which level of the HPAA does this usually occur in horses/foals?​

Answer 27

Steroid deficiency of the adrenal cortex

inadequate production of cortisol in relation to an increased demand during periods of severe illness and stress, and it is characterized by high ACTH/cortisol ratios.​

Question 28

Pheochromcytoma

Answer 28

Tumors that arise from the chromaffin cells of the adrenal medulla​
Rare in horses, most non-functional (thus undiagnosed)​
In horses, these tumors have low incidence of malignancy, usually unilateral​
Median age 17yo (13 – 38), poor prognosis​
If functional – acute onset CS ​
Diagnosis - measurement of blood catecholamines / metabolites in urine​

Question 29

acute onset CS seen with functional phaeochromcytomas in horses

Answer 29

COLIC: abdominal pain from large hematomas/hemoperitoneum  or gastrointestinal distention secondary to ileus​
Anxiety​
Tachycardia, tachypnea​
Profuse sweating​
Muscle tremors, ataxia​
Hyperthermia​
Dry and pale mucous membranes, increased capillary refill time​
Mydriasis​
Abortion has been documented. ​

Question 30

Hematologic abnormalities of functional pheochromocytomas

Answer 30

A: hemoconcentration (due to splenic contraction)​
B: stress leukogram ​
C: hyperglycemia​
D: hyperlactatemia ​
E: Electrolyte changes - hyponatremia, hypochloremia, hyperkalemia, hypocalcemia, hypophosphatemia

Question 31

pathogenesis of ppid: which of the three neuroendocrine dopaminergic tracts are most critical in regulating cell proliferation and hormone production and release in the pars intermedia?

Answer 31

Periventricular dopaminergic neurons​

The periventricular neurons originate in the periventricular nucleus, adjacent to the third ventricle, and project through the infundibular stalk, terminating in the pars intermedia. In the pars intermedia, the periventricular neurons directly innervate melanotropes, where they release dopamine that interacts with dopaminergic D2-type receptors on melanotropes ​

Question 32

proposed mechanisms of equine anhidrosis

Answer 32

Poor sweat gland response to β2-adrenergic stimulation​

Deficiency in β2-adrenoceptor agonists​

Inflammation

Question 33

what is the most consistent early lab finding in horses with vitamin d intoxication?

Answer 33

hyper-phosphatemia

Question 34

What drugs should you chose to lower calcium?

Answer 34

furosemide - inhibits the Na+/K+/2Cl− cotransporter in the distal nephron, increasing urinary excretion of calcium

glucocorticoids

Thiazide diuretics are contraindicated because they stimulate calcium reabsorption

Question 35

what is the main cause of hypophosphatemia in critically ill patients?​

Answer 35

Redistribution (intracellular shift of PO4)

Question 36

What is the pathophysiologic mechanism behind muscle fasiculation/tetany of hypocalcemia?​

Answer 36

fast Na+ channels open with small changes in membrane potential​

extracellular Ca2+ binds to Na+ channels to reduce Na+ entry, increasing depolarization threshold (mechanism by which Ca2+ antagonizes the effects of hyperkalemia)​

Question 37

Which clotting factor is Ca2+

Answer 37

IV

Question 38

Which clotting factor is Ca2+ a co-factor for?

Answer 38

II, VII, IX, X, XI, XII, XIII

2, 7, 9, 10, 11, 12, 13

Question 39

How does oxalate affect dietary calcium absorption?

Answer 39

decreases it

Question 40

What are the clinical signs associated with chronic dietary phosphorus excess?

Answer 40

A) Clinical signs of calcium deficiency - lameness, abnormal cartilage and bone development, fracture, osteodystrophis fibrosa (nutritional secondary hyperparathyroidism)​
B) Weight loss, weakness, depraved appetite (pica), lameness, DOD​

Question 41

The target organ for PTH is

Answer 41

the kidney

promotes 1,25(OH)2D3 synthesis

Question 42

Blood concentration of 1,25(OH)2D are regulated by

Answer 42

Increased by:
low PO4​
low PTH

Decreased by:
high PO4​
high Ca​
high 1,25(OH)2D​
high FGF23​

Question 43

Calcitonin

Answer 43

Inhibits osteoclast function​
Post-prandial increases in serum levels mediated by gastrin​
Secreted in response to hypercalcemia​
Secreted by parafollicular (C cells) of thyroid​
Decreases plasma Ca2+ and PO4 concentrations​
Important for protection against extreme hypercalcemia not really day-to-day​
Most important – prevents bone resorption during lactation​

Question 44

The diagnosis of food allergy is most accurately made by

Answer 44

eliminating the causative feed from the diet of affected horses through a food elimination trial. A complete dietary history is essential, and all components of the diet (concentrate, forage, and supplements) should be considered. ​
A practical approach to a food elimination trial is to begin by eliminating any supplements and concentrates from the diet for 4 to 6 weeks. The offending substance is identified by reintroducing one dietary item at a time each week and observing the horse for recurrence of clinical signs, usually within 24 to 72 hours. ​
​
Note: Food allergy in horses can occur not just by ingestion, but also inhalation and contact.​

Question 45

True contact allergies in horses are what type of hypersensitivity reaction: ​
​

Answer 45

Type IV

Potential allergens are usually small molecules that penetrate the skin, bind to dermal collagen or carrier proteins, and are taken up by antigen-presenting cells (Langerhans cells) in the dermis. ​

On re-exposure, an inflammatory response occurs that results in skin disease. ​

Development of allergic contact reactions can takes months to years; a horse may suddenly develop clinical signs of a hypersensitivity reaction to a substance to which it has been exposed for years without prior incident. ​

Question 46

ASIT

Answer 46

Theory of hyposensitization is to redirect the immune response to an allergen, shifting the IgE dominated to IgG dominated response​

Question 47

Pemphigus foliaceus

Answer 47

autoimmune disease of the skin
autoantibodies against desmoglein-1&3 (DSG1,3) destroy the bonds that maintain cell-to-cell adhesion.​

YOUNGER horses are more likely to respond to therapy, less likely to have relapses, have potential for spontaneous regression

Systemic signs = fever, depression, lethargy, anorexia, weight loss​
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definitive dx = histologic examination of a skin biopsy specimen​
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Treatment options = CCS / chrysotherapy (aurothiomalate) / azathioprine​

acute death can occur​

Question 48

systemic lupus erythematous

Answer 48

Rare; Dx on skin biopsy
Tx: immunosuppressive doses of glucocorticoids

CS: Weight loss, bilaterally symmetric alopecia, seborrhea, oral ulceration, and lymphadenopathy

Some horses have concurrent Coombs test-positive hemolytic anemia

Poor prognosis

Question 49

discoid lupus erythematous

Answer 49

Rare; Dx on skin biopsy
Tx: immunosuppressive doses of glucocorticoids

CS: Areas of patchy erythema, crusting alopecia, and scaling on the face, ears, and neck. + / - coronary band lesions +/- chestnuts/ergots

Aggravated by sunlight

Usually can be managed - prognosis not as bad as SLE

Question 50

Which is the most practical therapy for large, full-thickness burns in horses:

Answer 50

Continuous wet dressings (semi-open technique)

Question 51

What type of photosensitivity does St John’s Wart (Hypericum perforatum) cause when ingested? ​

Answer 51

Type 1: primary photosensitivity ​

photodynamic agent is ingested, systemically administered (certain drugs) or absorbed through the skin​

Question 52

What type of photosensitivity does phylloerythrin cause when ingested? ​

Answer 52

Type 2: hepatogenous photosensitivity (phylloerythrin > 8.0 μg/dL)​

Question 53

Which is the most common toxic cause of hepatogenous photosensitization?​

Answer 53

Pyrrolizidine alkaloids ​

E.g. Crotalaria spp., Amsinckia spp. (fiddleneck), Senecio spp. (tansy ragwort, groundsels), common heliotrope, Patterson curse​

Question 54

Sarcoids

Answer 54

Are the most common neoplasm in horses worldwide
​
Consist of cutaneous accumulations of transformed fibroblasts

Can stay dormant for extended periods of time before spontaneously enlarging or converting to more aggressive types

Question 55

STACHYBOTRYOTOXICOSIS

Answer 55

Mycotoxicosis caused by toxins of the fungus Stachybotrys atra​

This fungus grows on hay and straw and produces toxins referred to as macrocytic trichothecenes​

These toxins cause bone marrow suppression, profound neutropenia, thrombocytopenia, and necrotic-ulcerative lesions of the skin and mucous membranes​

Lesions commonly begin at mucocutaneous junction as focal areas of necrosis and ulceration. Petechiae, ulcers, large areas of necrosis, catarrhal rhinitis, and laryngitis follow

Skin lesions as early as 24 h after toxin ingestion. Systemic signs incl lethargy, anorexia, weight loss, hyperactivity, proprioceptive deficits, colic, muscular stiffness, and 2nd degree AV block ​

Affected animals develop haemorrhagic diathesis, haemorrhagic enteritis, septicaemia, and die

Dx based on hx, csx, finding toxin in feed. If toxicosis recognised early in course of dz, withdrawal of affected feed has resulted in resolution.

Animals with extensive lesions and chronic exposure = poor px

Question 56

Lice

Answer 56

Highly host-specific, obligate parasites that spend entire life cycle (20-40 days) on host​

In ideal environvment, can live 2 to 3 weeks off host, however less than 7 d more typical ​

Transmission by direct or indirect contact ​

Biting lice – Damilinia equi - feed on epidermal debris and prefer dorsolateral trunk​

Sucking lice – Haematopinus asini - feed on blood and tissue fluid, most commonly infest mane, tail and fetlock region​

When managing lice infestation, goal is to treat all animals on the premises​

Ivermectin 0.2 mg/kg PO q 2 weeks for three txs – gen effective for sucking lice​

Biting lice – topical eprinomectin (Eprinex) 0.5 mg/kg SIW for 4 tx​

Both biting and sucking respond to insecticidal or 1% selenium sulphide shampoos – kill adult lice, but hatchling nits will require a second shampooing in 2 weeks. Two applications of insecticidal sprays or powders containing pyrethrins and pyrethroids at 14-day intervals also efficacious

Presence of lice in the nearby env should be addressed by cleaning and decontaminating all tack and grooming supplies and decontaminating the stabling area using a commercial flea premise spray

Question 57

Chorioptes Equi

Answer 57

Spend entire 3 week lifecycle on host, but can live off the horse for 70 days​

Tends to be more common in winter months​

Feed on epidermal debris at preferred sites, which incl distal limbs and perineum​

Infested horses exhibit intense pruritis with chewing, licking, stomping of the feet, and rubbing of the tail and perineal area​

Skin lesions incl papules, alopecia, erythema, scabs and crusting o the pasterns, fetlocks, or perineum​

Dx can sometimes be made by deep skin scraping​ - burrow deep

Draft breed horses or other horses w feathered fetlocks are predisposed to C equi where they may contribute to the lesions of chronic progressive lymphedema (CPL)​

Incl in list of ddx for pastern dermatitis​

If dx, treat all horses on property​

Tx w topical eprinomectin solution (Eprinex) at the manufacturer’s recommended therapeutic dose for cattle of 500 ug/kg bwt weekly once for four administrations is recommended – administer along back line, from withers to proximal tail ​

Resistance to ivermectin and moxidectin may be developing ​

Question 58

ONCHOCERCIASIS

Answer 58

Lesions of onchocerca cervicalis infection begin as simple thinning of the hair coat, oft around the eyes, muzzle, neck, chest and ventral abdomen​

As dx progresses, lesions vary from focal to generalised areas of alopecia, scales, crusts and plaques and may become severely excoriated, ulcerated, oozing and lichenified​

Ocular diseases associated with O cervicalis include ERU, sclerosing keratitis, vitiligo of the bulbar conjunctiva, and conjunctival nodules ​

Nematode lives in the ligamentum nuchae and produces microfilariae that migrate through the skin and are ingested by the intermediate host, the Culicoides species​

Microfilarial populations vary seasonally and are highest in the spring and summer, which are also peak season for the Culicoides vector ​

Csx of onchocerciasis believed to be caused by an idiosyncratic hypersensitivity rxn to one or more microfilarial antigens because many horses that have circulating microfilariae do not have lesions ​

Important disease of horses worldwide, no breed or gender predilection, usu horses 4 years of age and older​

Dx most reliably made with a mince preparation or via histologic examination of skin from a biopsy specimen​

Mince prep req 4-mm or 6-mm punch specimen – mince and incubate room temp 30 – 60 min – look under microscope for rapid motion of microfilariae​
Skin biopsies: perivascular eosinophilic dermatitis ​

Tx w either ivermectin or moxidectin at standard dosage effective against microfilariae – may require two monthly treatments before csx resolve​

~25% horses w severe disease have adverse rxn, such as ventral midline oedema or pruritis, which occurs 1 – 10 d after tx – tis rxn believed to be caused by dead and dying microfilariae​

None of the currently available anthelmintics kills adult parasites in the ligamentum nuchae, and affected individulas require periodic retreatment w ivermec when csx recur​
The more recent use of deqorming by FECs appears to have increased the incidence of Onchocerca-related dermatitis ​

Question 59

Habronemiasis: house fly is the intermediate host for what species?

Answer 59

Habronema muscae

Draschia megastoma

Question 60

Habronemiasis: stable fly is the intermediate host for what species?

Answer 60

Habronema majus

Question 61

Habronemiasis

Answer 61

Adult nematodes live in stomach and produce larvae, which are passed in the faeces and ingested by maggots of the previously mentioned intermediate hosts​

The intermediate host deposits infective larvae near horse’s mouth – which the horse then swallows to complete the cycle​

Cutaneous habronemiasis occurs when the intermediate host deposits infective larvae on skin, open wounds, or chronically moist areas ​

Horses with cutaneous habronemiasis have ulcerative nodules in the spring and summer that partially or completely regress in the winter​
​

Question 62

Pin worms

Answer 62

A diagnosis of pinworm is based on clinical signs and identification of pinworm eggs on cellophane tape preparations​

Eggs develop to the infective stage within a 2- to 3- day period. At this time the cement substance cracks and dries and then detaches from the skin as it flakes. The flakes contain are large number of eggs that adhere to walls, buckets, and other objects in the environment​

Adult pinworms are found in the colon​

The female worm deposits eggs around the anus​

In ideal conditions, pinworm eggs can survive in the environment for up to 1 month​

Reports of resistance to ivermectin and pyrantel dewormers - can use FBZ

Question 63

Selenium concentrated plants often grow

Answer 63

in the Great Plains and Rocky Mountain areas of the US​

Question 64

Selenium Toxicity

Answer 64

At toxic levels, selenium is substituted for sulphur in sulphur-containing amino acids and alters keratinisation of the hoof and hair​

Selenium in excess of 1-4 ppm from blood, 11-45 ppm for hair, and 8-20 ppm for hoof indicate chronic toxicity​

The hair coat becomes rough, and there is a dramatic loss of mane and tail hairs​

Generalised alopecia may also be visible​

Lameness can be severe as the coronary band and hoof develop cracks and separate, and some hooves eventually slough ​

Question 65

TX of Selenium Toxicity

Answer 65

Horses should be moved from the selenium source as quickly as possible, but recovery often prolonged and prognosis for severely affected animals poor. ​

A high-protein diet rich in sulfa-containing amino acids and 2 to 3 mg PO SID of DL-methionine may be beneficial.

Question 66

CHRONIC ARSENIC TOXICITY

Answer 66

Clinical signs of chronic arsenic toxicity include a long hair coat, thinning of the mane and tail, and severe dry seborrhea. Horses may also develop poor body condition and weight loss. ​

Once upon a time, heaps of wankers though that it was a good idea to use arsenic to improve hair coat and body condition. This practice probably still exists in Oklahoma. ​

Definitive diagnosis is by measurement of arsenic levels in the kidney or liver (>10 ppm)​

Reported treatments for chronic arsenic toxicity include sodium thiosulphate and dimercaprol

Question 67

Atopic Dermatitis

Answer 67

Second most common form of skin allergy in horse​

Inherited hyperreactivity to environmental allergens that produce skin disease, and less, commonly, respiratory disease ​

The skin barrier of atopic horses is different to that of normal horses, likely allowing absorption of allergenic proteins, which are then carried to the lymph node​

Cytokines involved include IL-4, IL-5, IL-6, IL-13, and IL-31​

Question 68

Characterized by uniform hairs with no shaft abnormalities and a nonpigmented root end lacking a root sheath​

Answer 68

Telogen Defluxion

Question 69

Characterized by dysplastic hairs; the hair shaft may be weak or narrow, and the root end contains a root sheath

Answer 69

Anagen Defluxion

Question 70

Hair loss occurs within days of the insult or drug – high fever, systemic illness, or malnutrition.​

Answer 70

Anagen Defluxion

Question 71

Sudden shedding of hair and a new wave of growth occurs 2-3 months after a stressful situation.

Answer 71

Telogen Defluxion

Question 72

what is an important ddx to rule out for primary seborrhea?​

Answer 72

Pemphigus foliaceus

all other ddx’s are idiopathic and untreatable

Question 73

HERDA

Answer 73

Hereditary Equine Regional Dermal Asthenia​

• cutting horses
• autosomal recessive
• is caused by a missense mutation of the peptidyl-prolyl cis-trans isomerase B gene, which encodes cyclophilin B and is important in the formation of collagen’s triple helical molecule

Question 74

Warmblood Fragile Foal Syndrome

Answer 74

is autosomal recessive​

most commonly causes lesions on pressure points

is caused by a point mutation in the equine pro-collagen-lysine, 2-oxoglutarate 5-dioxygenase 1 (lysyl hydroxylase1) gene

Question 75

DERMATOPHILUS CONGOLENSIS TREATMENTS

Answer 75

A) sedating the horse, soaking and removing the crusts​

C) shampooing the area with chlorhexidine​
D) keeping the horse dry​
E) applying topical antibiotics​

G) PPG IM for 5-7 days​
H) TMS PO for 5-7 days

Question 76

Common cause of superficial pyoderma

Answer 76

staphs

Question 77

The incubations period for VS is

Answer 77

24-72 hours

Question 78

the most common fungal disease in the horse​

Answer 78

Dermatophytosis - Trichophyton equinum, T. mentagrophytes, Microsporum​
gypseum, and M. canis​

Question 79

superficial fungal disease of horses that causes nodules on the hair shaft – black or white filamentous nodules consisting of tightly packed hyphae on the mane and tail​

Answer 79

piedra

Question 80

Fungal dz causing hard subcutaneous nodules develop along the lymphatics​

Answer 80

Sporotrichosis

a zoonotic mycosis caused by Sporothrix schenckii ​

Question 81

Mycetomata

Answer 81

Single or multiple nodules of varying size can occur almost anywhere on the body of the horse – often pigmented and ulcerated and may discharge tissue grains​

chronic pyogranulomatous infections of the skin and subcutaneous tissues caused by actinomycetes (actinomycetoma) or fungi (eumycotic mycetoma​)

Question 82

Typical location for culicoides hypersensitivity

Answer 82

mane
tail
ventral abdomen
face

Question 83

Which is the typical location for pruritus due to Black flies?

Answer 83

ears

Question 84

How long should topical and systemic antimicrobials be discontinued before sampling for skin fungal and bacteriologic culture?​

Answer 84

at least 36 hours

Question 85

Blue-black circumbscribed nodules or dark hyperkeratotic/verrucous lesions​

Answer 85

hemangioma

Question 86

Subcutaneous nodules which ulcerate and drain honey-colored material​

Answer 86

glanders

Question 87

Severe seborrhea, ulcer, nonhealing wounds, hypertrichosis​

Answer 87

arsenic poisoning

Question 88

Swelling of coronary band, necrosis of feet, sloughing of ears/tail/feet​

Answer 88

ergotism

Question 89

Lymphedema, panniculitis, alopecia, leukoderma, scaling of face/neck/trunk​

Answer 89

SLE

Question 90

Vitiligo of Arabian horses

Answer 90

also called Arabian fading syndrome or pinky syndrome

waxing and waning, symmetric leukoderma with lesions 1mm-3cm in size on the muzzle, face, lips, and periocular areas

May also occur at the mucocutaneous junctions of the genital and anal area. The skin may repigment within 1-2 years (rare). Considered heritable; limited success with topical glucocorticoids or vitamin-mineral supplementation. ​

Question 91

sarcoid development

Answer 91

A) Often occurs in areas that have experienced trauma​
B) Have been associated with BPV-1 and 2 and potentially BR-UEL-4​
C) Genetically susceptibility is thought to play a role in which horses exposed to BPV develop sarcoids​
D) Biting flies may be route of transmission

Question 92

How are fibroblastic sarcoids different from pythiosis?​

Answer 92

Sarcoids are generally neither painful nor pruritic and grow more slowly​

Question 93

Do sarcoids metastasize?

Answer 93

Malignant/malevolent sarcoids are locally malignant but don’t metastasize to other areas​

Question 94

Sarcoid Treatment

Answer 94

A) 0.5-1 cm margin of normal tissue is recommended for surgical excision​

B) new scalpel blades, instruments, and gloves should minimize tumor spread after excision​

C) CO2 laser treatment may have some benefit over conventional surgical excision​

D) With cisplatin adjunctive treatment, 96.4% resolution rate after 4 years in 573 horses

E) Intratumoral hyperthermia can be combined with chemotherapy to boost the delivery of oxygen to the lesion, improves the distribution of chemotherapy inside the tumor and significantly increases the uptake of the chemotherapeutic agent

Question 95

What breed is genetically susceptible to ocular SCC?

Answer 95

Halflingers - 5.5X more likely if they are R/R than R/N or N/N

there is a commercially available genetic test

Question 96

___ has been implicated as a positive etiologic agent in equine SCC

Answer 96

EcPV2

equine papillomavirus

Question 97

Mast Cell Tumors

Answer 97

A) Arabians are predisposed
B) Tumors are usually single and located on head or lower extremity​
C) Radiographs show soft tissue mineralization​
D) surgical excision is usually curative​
E) Tumors respond well to triamcinolone treatment​

Question 98

Which form of cutaneous lymphoma has a poorer prognosis?

Answer 98

epitheliotropic lymphoma has a worse prognosis than non-epitheliotropic​

Question 99

Pseudolymphoma

Answer 99

excellent prognosis - often spontaneously regresses

Question 100

Panniculitis

Answer 100

Show deep-seated nodules and plaques. Lesions may be single or multiple and vary in size. They may be hard and well defined or soft and ill defined. Initially, lesions are not fixed to the overlying skin, but as the disease progresses, nodules become cystic and rupture onto the skin surface. The ulcerating nodules drain a yellow to brown to bloody oily material. Pain varies. Healed lesions may leave depressed scars. Affected animals may be febrile, depressed, lethargic, and anorectic​

Question 101

Equine Axillary Nodular Necrosis​

Answer 101

The condition has no known age, gender, or breed predilection. Clinically, single or multiple nodules develop unilaterally in the axillae. The nodules are painless, nonpruritic, haired, well-circumscribed firm masses that vary in size from 0.5 to 4.0 cm or greater in diameter. Multiple lesions tend to be arranged in a row

Question 102

Eosinophilic granuloma

Answer 102

Probably the most common nodular skin disease of the horse ​
Firm dermal nodules that are associated with degenerative collagen.​
No breed, gender, or age predisposition has been identified for this disease. Nodules usually arise in the warmer months of the year.​
Sites most commonly affected are the withers, back, and sides of the neck

Question 103

Treatment of eosinophilic granuloma

Answer 103

surgical excision, intralesional corticosteroids, or systemic corticosteroids ​

Question 104

MEEDs

Answer 104

Rare idiopathic disease
—nodules or masses in numerous organs, ulcerative stomatitis, severe wasting, significant exfoliation, and eosinophil infiltration of the skin
—hypoalbuminemia, hypoproteinemia, impaired small intestinal carbohydrate absorption, and increased GGT, ALP, and bile duct isoenzymes​

Question 105

Treatment of MEEDs

Answer 105

symptomatic and includes anthelmintics, antibiotics, azathioprine, and corticosteroids ​

Question 106

Sarcoidosis

Answer 106

can occur as a localized, partially generalized, or generalized condition ​
The skin disease begins as scaling, crusting, and alopecia on the face, limbs, and/or trunk. ​
Clinical signs may progress rapidly or slowly. Peripheral lymphadenopathy may develop concurrently with weight loss, muscle wasting, anorexia, exercise intolerance, and fever​

Question 107

SeM-specific antibody titres > _____? are strongly suggestive of vasculitis secondary to strangles vaccination or exposure​

Answer 107

(>1:12,800)

Question 108

Anaplasma marginale causes ____ hemolysis

Answer 108

Extravascular

Question 109

Extravascular hemolysis results in ____ colored urine

Answer 109

Normal

Question 110

Copper and lepto result in ______

Answer 110

Intravascular hemolysis

Red urine

Question 111

Anaplasma affects adults or calves more

Answer 111

Adults - less able to regenerate RBCs