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Question 1

Congenital hypothyroidism in foals can be secondary to iodine deficiency and /or secondary to excess ______________

Answer 1

Nitrate consumption

Question 2

Mention signs of excess nitrate intake in broodmares.

Answer 2

Broodmares might not display any clinical sign, but it can result in abortion, or dysmature foals after prolonged gestation. Affected neonates have varying degrees of signs including mandibular prognathism, flexural deformities of the forelimbs, secondary rupture of the common digital extensor tendon, poorly ossified cuboidal bones, and poor immune function.

Question 3

How do ergot alkaloids affect ruminants and horses?

Answer 3

Particularly ergovaline, have vasoconstrictive effects (α2 adrenergic agonist) and/or depress secretion of prolactin via effects on lactotropic D2-dopamine receptors in the adenohypophysis of the pituitary. A reduction in steroid genesis is caused including progesterone production by corpora lutea, and relaxin. Thermoregulatory centers are affected by diminutions in prolactin and dopamine receptor perturbation (hyperthermia in extreme temperatures).

Question 4

Why isn’t ergot alkaloid toxicity important in lactation in ruminants as it is in horses?

Answer 4

Because the ruminant placenta can produce a placental lactogen during pregnancy, the suppression of prolactin and hence milk production is minor in comparison with horses.

Question 5

What has high and chronic oxalate consumption been related to in horses?

Answer 5

To secondary nutritional hyperparathyroidism, resulting in deficiency of calcium (Ca binding in the hindgut) and signs of osteodystrophia fibrosa.

Question 6

What is the most important cyanotoxin poisoning in large animals?

Answer 6

Acute hepatotoxicosis subsequent to microcystin exposure. Microcystins are produced by multiple cyanobacteria and have been detected in fresh and coastal waters worldwide.

Question 7

What are the clinical signs of mycrocystin hepatotoxicosis?

Answer 7

Death typically occurs within a few hours.

Severe destruction of the hepatocytes leads to hypovolemia and shock secondary to blood loss into the disintegrated liver lobules and embolism of hepatocytes into the lung.

Acutely poisoning signs include nervousness, reluctance to move, recumbency, diarrhea, and pale mucous membranes. Animals exposed to nonlethal doses may survive and develop hepatogenous photosensitization.

Question 8

What are sulfonylureas?

Answer 8

An oral hypoglycemic agent. It stimulates release of insulin from the beta cells in the pancreas, decreases hepatic glucose output and increases insulin receptor sensitivity

Question 9

Insulin is important to maintain normal glucose levels after and in between meals. Which of the following mechanisms associated with insulin secretion causes glucose uptake and storage in the liver?

a. Suppression of glucokinase
b. Activation of liver phosphorylase
c. Suppression of synthesis of fatty acids
d. Increased glycogen synthase activity

Answer 9

d. Increased glycogen synthase activity

Question 10

Desferoxamine alters iron elimination in foals by chelating iron from:

a. cytochromes and hemoglobin, enhancing urinary excretion
b. transferrin and hemoglobin, enhancing hepatic excretion
c. ferritin and hemosiderin, enhancing urinary excretion
d. ferritin and transferrin, enhancing hepatic excretion

Answer 10

c. ferritin and hemosiderin, enhancing urinary excretion

Question 11

Which of the following will be the best option of treatment for equine sarcoids?

a. Cisplatin
b. 5-fluorouracil
c. Cryosurgery
d. Acyclovir

Answer 11

a. Cisplatin

Question 12

The effects of pentoxifylline on platelet aggregation in horses include:

a. an increase in the onset time of both collagen-induced and ADP-dependent platelet aggregation; no change in the rate of aggregation
b. a decrease in the onset time of collagen-induced platelet aggregation with no effect on the onset-time of ADP dependent platelet aggregation; no change in the rate of aggregation
c. an increase in the onset time of both collagen-induced and ADP-dependent platelet aggregation; decrease in the rate of aggregation
d. no effect on onset time or rate of aggregation for either collagen-induced or ADP-dependent platelet aggregation

Answer 12

b. a decrease in the onset time of collagen-induced platelet aggregation with no effect on the onset-time of ADP dependent platelet aggregation; no change in the rate of aggregation

Question 13

Aspirin has been used to diminish platelet aggregation in horses that may be hypercoagulable.

One potential reason for treatment failure is that aspirin significantly inhibits only:

a. Collagen induced platelet aggregation
b. ADP-induced platelet aggregation
c. Arachadonic acid induced platelet aggregation
d. Arachadonic acid and ADP-induced platelet aggregation, but is ineffective against collagen-induced aggregation

Answer 13

c. Arachadonic acid induced platelet aggregation

Question 14

What is the most appropriate extra label treatment for a cow with mastitis, tachycardia, fever and depression?

a. Intramuscular ceftiofur
b. Intravenous TMS
c. Oral oxytetracycline
d. Sub-cutaneous enrofloxacin

Answer 14

a. Intramuscular ceftiofur

Question 15

What type of placentation is found in horses?

a. Cotyledonary, epitheliochorial
b. Diffuse, epitheliochorial
c. Discoid, hemochorial
d. Zonary, endotheliochorial

Answer 15

b. Diffuse, epitheliochorial

Question 16

What is TK1 (thymidine kinase 1) related to in the cell?

If present it usually is related to what diseases?

Answer 16

TK1 is related t DNA replication and cell proliferation.

It is used commonly as a marked for malignancy and has been correlated with high risk of development of neoplasias.

Question 17

Mention what are the 3 contractions during a normal rumino-reticular cycle?

Answer 17

It involves 2 primary contractions followed by a secondary contraction.

Primary cycle occurs approximately once every min (more often during feeding). It is a biphasic contraction of the reticulum followed by a contraction that runs caudally across the dorsal and ventral ruminal sacs.

Secondary contractions only involve the reticulum, it starts on the caudal blinds sacs and runs cranially through the rumen pushing the gas cap into the cardia region.

*A prosecondary contraction has been identified in sheep that helps release pressure when gas production is high

Question 18

What is the difference between septicemia, bacteremia, and sepsis?

Answer 18

Bacteremia is the presence of viable circulating bacteria, can occur without clinical signs.

Septicemia is the systemic disease caused by any circulating microorganisms and/or their products.

Sepsis is the clinical evidence of an infection (documented or suspected) coupled with the presence of a systemic inflammatory response syndrome (SIRS) characterized by alterations in body temperature, heart rate, respiratory rate, and leukogram parameters.

Question 19

What is the difference between LPS and endotoxin?

Describe LPS …

Answer 19

Endotoxin is the activity, and LPS is the molecule, although they currently are used synonymously to refer to that specific gram-negative bacterial membrane component.

Each LPS molecule has three structural domains:

* a polar polysaccharide O-region - projects into the aqueous extracellular environment

* a hydrophobic lipid A-region - is largely buried in the bacterial outer membrane

* a core acidic oligosaccharide region - connects the two

Question 20

Among the horses with acute gastrointestinal disease, how many are estimated to have detctable plasma endotoxin?

Answer 20

Between 12 - 29% would have detectable plasma endotoxin

Question 21

Mention at least 3 criteria that would classify a horse with SIRS, and 3 for organ dysfunction (include criteria for laminitis).

Answer 21

SIRS Criteria (2 or more to qualify):
\* Hypothermia - \<98° F or hyperthermia \>101.5° F

* Leukopenia - <5000/μL or leukocytosis >14,500/μL

* Tachycardia - >50 beats/min

* Tachypnea - >25 breaths/min or PaCO2 < 32 mm Hg

Organ Dysfunction and Laminitis Criteria:
* Neurologic - Severe obtundation (stupor, semicoma, coma)

* Renal - Creatinine >2 mg/dL aſter ≥20 mL/kg IV crystalloid fluids, or increase of ≥0.5 mm Hg since last measurement

* Hemostatic - Platelet count < 100,000/μL or aPTT > 70 sec

* Respiratory - PaO2 < 65 mm Hg, or <75 mm Hg with oxygen supplementation or mechanical ventilation

* Intestinal - Absent gut sounds, or absent motility on ux exam

* Hemodynamic - Mean arterial pressure <65 mm Hg aſter ≥20 mL/kg IV crystalloid fluids

* Hepatic - Bilirubin concentration > 6 mg/dL; GGT > 60 U/L with no other explanation

* Laminitis - Bounding digital pulses, sensitivity to digital
pressure over the coronary band, sensitivity to hoof tester pressure over the sole, Obel grade >1

Question 22

What negative side effects does flunixin have during its use for gastrointestinal disease? How can this effects be ameliorated?

Answer 22

It has shown to slow mucosal healing and increase mucosal permeability to LPS in ischemic-injured equine jejunum (does not appear to occur in the equine colon).
Concurrent administration of misoprostol (a PGE-1 analog) or a lidocaine constant rate infusion has shown to ameliorate these effects.

Question 23

How is hyperimmune plasma produced?

What is the dose when considered to be used in endotoxemia or sepsis?

Answer 23

It is produced by immunization of horses against R-mutant endotoxins.

It is recomended at doses of 10-40ml/kg.

Question 24

What is Polymixin B and at what doses is still considered to have endotoxin binding capacity without the toxic effect?

Answer 24

Is a broad-spectrum cyclic peptide antibiotic with potent endotoxin-binding activity.

At 6000 U/kg Q8H is considered to have continous endotoxic binding capacity wihout the toxic effect, but it can be given intravenously two or three times daily at a dosage rate of 5000 to 6000 U/kg.

Question 25

What does CIRCI stands for? And what is this defined as?

Answer 25

Critical illness related corticosteroid insufiency (CIRCI) and it is defined as an inadequate cellular corticosteroid activity for the severity of a patient’s illness.

Question 26

Where does norepinephrine gets synthesised from?

Answer 26

Tyrosine is the precursor, which then gets converted by tyrosine hydroxylase into DOPA. DOPA is converted into dopamine by DOPA decarboxylase, which is converted into NE by Dopamine-beta-hydroxylase. The last step is by phenylethanolamine-N-methyltransferase to convert NE in epinephrine.