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E&E Exam 4 > Large Animal Diseases > Flashcards

Large Animal Diseases Flashcards

1
Q

How can you differentiate between thyroid glands and the retropharyngeal lymph nodes in a horse?

A

Thyroid glands are palpable, movable structures in throat latch area;
Retropharyngeal lymph nodes will not move

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2
Q

What is the most accurate thyroid hormone assay in the horse?

A

Free T4 by dialysis

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3
Q

Foals can have very high/low T3 and T4 at birth, and these levels will increase/decrease in the first 3-4 months.

A

High, decrease

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4
Q

What 2 drugs can falsely lower thyroid hormones in horses?

A

Corticosteroids and phenylbutazone

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5
Q

What effect does fasting, strenuous exercise, and diets high in energy, protein, copper, or zinc have on thyroid hormone levels in horses?

A

Falsely lowers THs

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6
Q

Considering the factors that can falsely lower THs, how long should animals be free of these things prior to testing?

A

At least 2-4 weeks

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7
Q

What test is less affected by nonthyroidal illnesses?

A

Free T4 by equilibrium dialysis

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8
Q

What are 3 general differentials for enlarged thyroid glands in horses?

A

Hypothyroidism, hyperthyroidism, and thyroid tumors

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9
Q

What is congenital hypothyroidism in foals caused by?

A

Too little or too much iodine in dam’s diet or goitrogenic plants (i.e. kelp)

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10
Q

A one-week-old foal that has signs of dysmaturity, an enlarged thyroid gland, poor suckling, hypothermia, flexural deformities, and mandibular prognathism (monkey mouth) is most consistent with what disease?

A

Congenital hypothyroidism

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11
Q

What is the treatment for congenital hypothyroidism in foals?

A

Supportive care, correct mare’s diet, and provide thyroid supplementation if foal is low

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12
Q

What is the prognosis for congenital hypothyroidism in foals?

A

Poor, most foals die within 1-2 weeks of birth but can do well if owners are willing to do aggressive and consistent supportive care

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13
Q

What is the most common cause of hypothyroidism in adult horses?

A

Most due to other disease processes

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14
Q

In addition to misdiagnosed hypothyroidism, name some other reasons why horses may be treated with Levothyroxine (4 answers)

A

Laminitis, anhidrosis, poor fertility, and equine metabolic syndrome

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15
Q

What is the most common cause for a unilaterally enlarged thyroid gland in horses? (Especially in older horses)

A

Thyroid neoplasia; specifically, a thyroid adenoma

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16
Q

What condition in horses is defined as a collection of risk factors (especially obesity/increased adiposity and insulin dysregulation) highly associated with an increased of hyperinsulinemia-associated laminitis and other morbidities?

A

Equine Metabolic Syndrome

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17
Q

In older horses, what condition may co-exist with PPID?

A

Equine Metabolic Syndrome

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18
Q

Horses that are considered to be “easy keepers” or have a “thrifty gene” are predisposed for Equine Metabolic Syndrome. What do these terms mean?

A

These horses have good metabolic efficiency and can maintain their weight with a smaller amount of feed (don’t cost a lot of money to maintain)

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19
Q

T/F: Horses with Equine Metabolic Syndrome can have either regional adiposity or generalized adiposity.

A

T

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20
Q

What common regions on a horse would you see increased adiposity in cases of EMS? 3 answers.

A

Neck, tail head, preputial/mammary swelling

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21
Q

Adipose tissue is an active endocrine organ that secretes _____________, which have local and systemic effects resulting in a(n) chronic/acute inflammatory state.

A

Secretes adipokines, chronic inflammatory state

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22
Q

If a horse has insulin dysregulation, what 3 things may it have?

A

Resting hyperinsulinemia, postprandial hyperinsulinemia, or tissue insulin resistance

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23
Q

What may hyperinsulinemia predispose a horse to?

A

Laminitis

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24
Q

T/F: Insulin dysregulation only occurs when Equine Metabolic Syndrome is present.

A

F, can occur in the absence of EMS and with other cases (such as PPID, systemic illness, stress, pregnancy, and/or starvation)

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25
Q

What is the primary insult of laminitis occurring secondary to equine metabolic syndrome?

A

Alteration in form and function of vasculature; occurs in the absence of recognized inflammatory causes (such as grain overload, colic, metritis, etc.)

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26
Q

Give a common example of a triggering event of laminitis in horses with equine metabolic syndrome

A

High carbohydrate meal; EMS horses are less able to tolerate spikes in BG

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27
Q

What is a tentative diagnosis of Equine Metabolic Syndrome based on?

A

Clinical obesity, predisposed breed/signalment, +/- laminitis, and/or documentation of insulin resistance

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28
Q

What diagnostic test can be used to diagnose insulin resistance in horses?

A

Oral sugar test

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29
Q

What are 3 dietary modifications you would recommend to an owner with a horse that has Equine Metabolic Syndrome?

A

Remove concentrate from diet, remove high sugar treats, and discourage turnout on pasture (or use grazing muzzle and limit to 1-2 hours/day)

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30
Q

What drug can be used in combination with a restricted diet in horses with EMS that have weight loss resistance or laminitis?

A

Levothyroxine

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31
Q

What drug is indicated in horses with EMS when there is poor owner compliance with diet, persistent hyperinsulinemia, or during the first 2 weeks that horse is put on pasture?

A

Metformin

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32
Q

Ketosis most often occurs in dairy cattle during what period?

A

Transition period between late gestation and early lactation

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33
Q

Late gestational demands of the fetus, combined with the increased energy demand of lactation and possibly decrease in feed intake results in a state of what in early lactation cattle? 2 answers.

A

State of negative energy balance and high glucose demand -> ketosis

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34
Q

What are the 3 common ketone bodies that are produced, leading to ketosis in early lactation dairy cattle?

A

Acetone, Acetoacetic acid, and B-hydroxybutyric acid

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35
Q

Bovine ketosis leads to increased/decreased blood ketones, increased/decreased free fatty acids or NEFAs, and increased/decreased blood glucose. (Choose one for each answer)

A

Increased blood ketones, increased free fatty acids, and decreased blood glucose

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36
Q

T/F: All dairy cows are in negative energy balance during first 8 weeks of lactation, and all develop some degree of ketosis.

A

T

37
Q

What are the clinical signs/history often associated with bovine ketosis? 5 answers, do your best

A
  1. Gradual loss of appetite with decreased milk production
  2. Normal vital signs
  3. Reluctance to move (may be down)
  4. Decreased GI motility
  5. Odor of ketones on breath and milk
38
Q

Are the presence of urine ketones diagnostic for bovine ketosis?

A

No, can be present in urine of normal animals

39
Q

T/F: Milk ketones reflect blood levels accurately.

A

T

40
Q

What are the 2 acceptable screening tests for subclinical ketosis?

A

B-hydroxybutyric acid in milk or ketostix on urine at “small” level

41
Q

What is your primary goal of treatment of bovine ketosis?

A

Treat primary problem if there is one

42
Q

In cases of bovine ketosis, you want to limit mobilization of fat. How can you do that? 5 answers.

A
  1. Bolus of IV dextrose and/or 24 hours of fluids with dextrose
  2. Propylene glycol enterally
  3. Glucocorticoids
  4. Insulin
  5. Transfaunation to get cow eating so rumen will function
43
Q

When should you introduce a lactation ration to ensure cows are eating it at calving (as a means of preventing bovine ketosis)?

A

In late gestation

44
Q

Which lobe of the pituitary produces majority of ACTH?

A

Anterior lobe

45
Q

Cortisol has negative feedback on the breakdown of POMC in the Pars Distalis/Intermedius ONLY. (choose one)

A

Pars distalis

46
Q

Pituitary Pars Intermedia Dysfunction is the result of neurodegeneration of what neurons in the hypothalamus?

A

Dopaminergic neurons

47
Q

What type of neurons in the hypothalamus have an inhibitory effect on breakdown of POMC in the pars intermedia?

A

Dopaminergic neurons

48
Q

With PPID, what does the neurodegeneration of dopaminergic neurons result in?

A

Lack of inhibition of breakdown of POMC in Pars intermedia -> overproduction of ACTH and other products

49
Q

Does PPID occur in young or older horses?

A

Old horses

50
Q

What is a clinical sign that could be an early indicator of PPID in horses?

A

Delayed shedding (Hirsutism) that eventually turns to long, curly hair coat

51
Q

T/F: Almost all horses with hirsutism have abnormal pituitaries but not all horses with abnormal pituitaries will have hirsutism.

A

T

52
Q

What is the appetite/weight like in horses with PPID?

A

Weight loss despite good appetite

53
Q

What is one of the most common presenting complaints of horses with PPID that occurs due to hyperinsulinemia and hypercortisolism?

A

Laminitis

54
Q

T/F: Horses with PPID often have concurrent chronic infections because of the excess alpha-MSH that is produced by the Pars intermedia is immunosuppressive.

A

T

55
Q

If horses with PPID have extension of macroadenoma into the brain, what 3 clinical signs can be associated with it?

A

Ataxia, blindness, and PU/PD

56
Q

What are the 3 endocrine tests used to help diagnose PPID in horses?

A

Basal ACTH, TRH stimulation test, and Dexamethasone suppression test (DST)

57
Q

You suspect an older horse has PPID and decide to measure a basal ACTH. The horse has strong clinical signs associated with PPID, but the results came back in the equivocal range. What is your interpretation?

A

This horse likely has PPID.

58
Q

TRH stimulates/inhibits melanotropes in the Pars Intermedius to produce ACTH, so horses should have an increase/decrease in ACTH after administration of TRH. (choose one for each answer)

A

Stimulates melanotropes, increase in ACTH

59
Q

What is the drug of choice for treating PPID in horses?

A

Pergolide

60
Q

How much of its total body weight does a horse eat in dry feed?

A

1.5-2% of its BW

61
Q

What is an effective test for identifying malabsorption in a horse?

A

Glucose absorption test

62
Q

In addition to performing a physical exam and inspecting factors that influence body weight (i.e. competition), what are 2 other things that should be included in the minimum database for a horse that has chronic weight loss?

A

Dental examination and fecal egg count/inspect feces

63
Q

What is the causative agent of Proliferative Enteropathy in weanling to yearling foals?

A

Lawsonia intracellularis

64
Q

You are presented with a young horse that has a history of adequate access to food but poor weight gain and a poor coat. Bloodwork reveals hypoproteinemia (especially hypoalbuminemia) and ultrasound revealed a thickened small intestine. What is your top differential?

A

Proliferative Enteropathy

65
Q

What is the recommendation for treatment of Proliferative Enteropathy in foals? (Per Dr. Maxwell)

A

Oxytetracycline IV BID for 3-7 days followed by PO Minocycline

66
Q

A 5-month-old foal is presented to you for diarrhea, weight loss, anorexia, and respiratory disease. What is your top differential?

A

Rhodococcus equi enteritis

67
Q

What is the preferred treatment for Rhodococcus equi enteritis in foals?

A

Macrolide for 6 weeks (Erythromycin, Azithromycin, Clarithromycin) +/- Rifampin

68
Q

How can a definitive diagnosis of Lawsonia intracellularis be made in foals?

A

Fecal PCR analysis

69
Q

Do horses usually develop one large bladder stone or multiple small stones?

A

One large bladder stone

70
Q

A male horse presents to you for frequent urination during exercise, pollakiuria, and hematuria after exercise. What is your top differential?

A

Urolithiasis

71
Q

What is the gold standard for diagnosing equine urolithiasis?

A

Endoscopy - usually on referral basis

72
Q

What is the single most common urinary tract disease in small ruminants?

A

Urolithiasis

73
Q

If a small ruminant is showing signs of abdominal pain, distress, or off feed, what urinary disease should be in your top 5 differentials until proven otherwise?

A

Urolithiasis

74
Q

What type of diet is commonly associated with struvite or apatite (calcium phosphate) uroliths in small ruminants?

A

High grain diets/low Ca:P ratio

75
Q

What type of diet is commonly associated with calcium carbonate uroliths in small ruminants?

A

Legume diets

76
Q

Do struvite, apatite (calcium phosphate), and calcium carbonate uroliths typically form in acidic or alkaline pH?

A

Alkaline

77
Q

What is the pathogenesis of uroliths in small ruminants?

A

Precipitates of a supersaturated urine, often due to diet, dehydration, and alkaline pH

78
Q

What are the 4 most common locations for uroliths to form in small ruminants? Name in order of most common.

A
  1. Urethral process
  2. Sigmoid flexure
  3. Ischial arch
  4. Neck of bladder
79
Q

What are 2 possible sequelae of uroliths in small ruminants?

A

Urethral rupture or uroabdomen

80
Q

What is a definitive diagnosis of uroliths in small ruminants based on?

A

Presence of clinical signs and distended bladder on ultrasound or consistently turgid, distended bladder without urinating.

81
Q

Are struvite stones often visible on radiographs of small ruminants?

A

No, they are tiny like sand/grit; if you can see radiopaque stones on radiographs, then it is likely calcium carbonate

82
Q

Why is amputation of the urethral process not a curative procedure in small ruminants with urolithiasis?

A

Most re-obstruct within 36 hours; amputation is only a temporary fix -> could have stones elsewhere in urinary tract

83
Q

Give 2 reasons why catheterization is not useful in small ruminants

A

Urethral diverticulum gets in the way and they have a fibroelastic penis that prevents effective urohydropulsion

84
Q

If clients choose medical therapy to treat uroliths in small ruminants, what is the name of the solution used to dissolve the stones?

A

Walpole’s solution (acidic)

85
Q

What are 2 surgical procedures to remove uroliths in small ruminants that will still preserve the long-term function of urethra so they can still breed and prevents future stricture formation?

A

Tube cystotomy and bladder marsupialization

86
Q

Briefly describe how tube cystotomy in small ruminants allows urine diversion.

A

Reduces urethral spasms, which reduces inflammation and allows the stone to pass.

87
Q

Although castration is a method of prevention for urolith formation in small ruminants, when should it be performed to prevent a smaller diameter urethra?

A

Delay castration until at least 3 months, but 4-6 months is ideal

88
Q

In addition to castration, what are some other prevention methods that can be implemented to prevent urolith formation in small ruminants? 3-4 answers

A

More dilute urine (increase water intake), use ammonium chloride supplements in feed to make urine more acidic, reduce grain in diet or increase dietary roughage to keep Ca:P in diet 2:1

E&E Exam 4 (5 decks)

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