Large Animal Medicine Ii (Up To Midterm 1 Only)

Front 1

The following conditions/ disorders/ diseases all share what common clinical sign?

-Dental disease
-Stomatitis
-Pharyngeal disease
-Esophageal obstruction
-Ruminal disorders
-Neurologic diseases
-Toxicities (slaframine, mercury, iodine, lead, etc)

Back 1

Excessive salivation

+/- Dysphagia

Front 2

T/F It is not required to wear gloves for exploration in the oral cavity in animals with suspected neurologic disease.

Back 2

False. Should always wear gloves for these cases.

Front 3

What main clinical sign does slaframine (legumes) cause in ruminants?

Back 3

Excessive salivation

Front 4

What does necrotic stomatitis or oral necrobacillosis look like (clinical signs, physical appearance) in young mild-fed calves?

What bacteria is usually associated with this condition?

Back 4

-Low grade fever
-Puffy cheeked appearance
-Foul smelling breath

-Fusobacterium necrophorum

Front 5

T/F Actinobacillus lignieresii (NOT normal flora of bovine mouth) is implanted in the tongue by mastication of rough feed.

Back 5

False. Is normal flora, lesion is created from rough feeds.

Front 6

What is the suggestive cytological finding with actinobacillosis (wooden tongue)?

How do you treat it?

Back 6

Sulfur granules or club colonies

Treat by inducing iodism (using IODIDES) and using antimicrobials. Signs of iodism include: tearing, coughing, inappetence, diarrhea, dandruff

Front 7

What is the prognosis of Wooden Tongue (Actinobacillosis) vs Lumpy Jaw (Actinomycosis)?

Back 7

Wooden Tongue - good to excellent

Lumpy Jaw - guarded to poor with extensive involvement of teeth/jaw/etc

Front 8

What species does Actinobacillosis most commonly affect?

Actinomycosis?

Back 8

Wooden tongue - cattle (mainly) and sheep

Lumpy Jaw - cattle (mainly) rarely in sheep and goats

Front 9

T/F Lumpy jaw is most frequently seen in the horizontal ramus of the mandible.

Back 9

True.

Front 10

T/F Iodides is the standard treatment for A. bovis but NOT A. lignieresii.

Back 10

False. Is the standard treatment for both.

Front 11

When hypersalivation occurs in large animals, what metabolic disturbance can occur?

Back 11

Metabolic acidosis & dehydration

Front 12

Mycotic stomatitis in cattle is caused by overzealous use of what type of drug?

Back 12

Antibiotic use
-Usually yeasts or fungi take over

Front 13

Fluoride toxicity can cause what problem in the teeth/mouth of cattle?

Back 13

Exposure to fluorine gas or other flouride substance can cause weaking, chipping, discoloration, and staining of teeth.

Front 14

T/F Bacterial phlegma is a mixed bacterial infection in cattle resulting in lesions in the head and neck regions.

Back 14

True.

Front 15

What are the key features of Bovine Papular Stomatitis when looking at lesions in the nares and mouth?

Should you be wary of spread to yourself when looking in these kinds of mouths?

What general kind of disease is BPS a good DDX for?

Back 15

2-4mm, hyperemic foci in nares and mouth (deep), lesions coalesce.

Are zoonotic, but self-limiting.

Vesicular disease

Front 16

T/F BVD (Bovine Viral Diarrhea) can sometimes produce "red nose" in cattle and proliferative/crusty lesions too.

Back 16

True. But not always present.

Front 17

T/F Foot and Mouth Disease affects cattle, sheep, goats, pigs, and horses.

Back 17

False. Everybody but the horse.

Front 18

In Foot and Mouth Disease, are you more likely to see the vesicular form of the disease or the scooped out round ulcerative form of lesion?

Back 18

Scooped out round ulcerative state of the disease.

Front 19

T/F Vesicular disease is clinically indistinguishable from vesicular stomatitis and vesicular stomatitis will occur in horses.

Back 19

True.

Front 20

If you saw a sheep with crusting, proliferative lesions on the mouth and nose and a client had reported lesions on their hands, what zoonotic disease might you first think of?

Back 20

Contagious ecthyma (Orf)
-Parapoxvirus: sheep, goats, humans
-Is self limiting
-Can make autogenous vx, or give normal vx

Front 21

Older animals affected by contagious ecthyma get their lesions in different locations than younger animals with the same condition. Where are lesions seen in the older animals?

Back 21

Coronary band
Interdigital lesions
Udder/teats

Front 22

What is the difference between primary and secondary reticular-ruminal function?

Back 22

Primary - reticulum->rumen-> reticulum contractions. 3 every 2 min (1-2/min)

Secondary - rumen contraction only (caudal to cranial). 1 every 2 minutes.

Front 23

What are some inhibitory receptors/mechanism that could prevent the process of rumination in the cow?

Back 23

-High tension receptor activation in rumen and/or abomasum
-Rumen epithelial receptors- increased VFA
-Pain- increase sympathetic tone
-Depression of the gastric centers (CNS)
-Defective vagal innervation
-Starvation and/or other diseases

Front 24

What are the common causes of simple indigestion in the bovine?

Back 24

Dietary indiscretion
Change in feed,
Consuming spoiled feed
Lack of water

Front 25

What key clinical findings would you likely observe in a cow with simple indigestion?

How would you treat it?

Back 25

-Rumenal atony (no contractions)
-Inappetance (decreased feed intake)

-Remove offending feed, could increase fiber, fix bad management practices

Front 26

What conditions should be included on a list of differential diagnoses for diarrhea in a calf younger than 1 week of age?

(a) ETEC E. coli, coronavirus diarrhea, rotavirus diarrhea

(b) Salmonellosis, clostridiosis, primary disaccharidase deficiency

(c) Primary disaccharide deficiency, rotovirus diarrhea, ETEC diarrhea

(d) Coronavirus diarrhea, salmonellosis, coccidiosis

(e) Giardiasis, transmissible gastroenteritis, clostridiosis

Back 26

(a) ETEC E. coli, coronavirus diarrhea, rotavirus diarrhea

Front 27

Which one of the following statements regarding traumatic reticuloperitonitis is correct?

(a) therapy should include antibiotics and confinement

(b) TRP is least common in mature dairy cows

(c) Left paramedian abdominocentesis should be attempted to diagnose peritonitis

(d) Affected animals go off feed abruptly but continue to produce milk at 75% of the normal production level

(e) Affected animals often stand with their hind feet elevated to relieve the acute pain.

Back 27

(a) therapy should include antibiotics and confinement

Front 28

A vet is called to see a 5-year-old Jersey cow. She has been fresh for 2 months and was treated for hardware disease by the owner shortly after calving. She is now milking at a level that is 50% lower than would be anticipated and is selectively inappetent, preferring roughage to her concentrate ration. The owner has been treating her with rumenatorics for 2 weeks, but has seen no response to therapy. Physical examination reveals a distended abdomen with milk gaseous distention of the left paralumbar fossa and succussible fluid in the lower right abdominal quadrant. The cow is passing scant, pasty feces and appears to be thin and mildly dehydrated. The cow exhibits 4 weak rumen rolls per minute but is not chewing her cud. Her heart rate is 30bpm. The most probable diagnosis is:

(a) Chronic bovine viral diarrhea (BVD)

(b) Simple indigestion

(c) Acute localized peritonitis

(d) Vagal indigestion

(e) Johne's disease

Back 28

d) Vagal indigestion

Front 29

(1) In January, a vet is called out to evaluate a herd of Holstein cows that are housed indoors. 80% of the milking cows have developed acute, profuse, diarrhea over the last 12-24 hours. Occasionally, the feces are bloody and mucoid. Milk production in the herd has decreased by 50%. The cows are fed a 18% protein dairy ration and alfalfa-timothy hay. A new source of grain was introduced in the last 3 days. Other animals (virgin heifers and bulls) are normal, although they are fed the same diet. Physical exam reveals that some of the animals are mildly dehydrated. Their vital signs are normal and no other abnormalities are detected. Complete CBC and biochem profiles obtained from several clinically affected cows are essentially normal except for increases in PCV and TP. What is the most likely diagnosis?

(a) Bovine viral diarrhea (BVD)
(b) Salmonellosis
(c) Winter dysentery
(d) Arsenic poisoning
(e) Rotavirus diarrhea

(2) What would you do next?

(a) Treat all affected animals with TMS, flunixin meglumine, and oral or IV fluids

(b) Treat all affected animals with broad spectrum antibiotics and intestinal protectants

(c) Treat all affected animals with oral charcoal and systemic British antilewisite

(d) Run serologic tests to confirm your diagnosis

(e) Wait for the disease to run it's course. Supportive care is indicated for dehydrated animals.

Back 29

1 (c) Winter dysentery
2 (e) Wait for the disease to run it's course. Supportive care is indicated for dehydrated animals.

Front 30

All of the following are true statements regarding grain overload in SHEEP except:

(a) Administration or oral magnesium oxide to sheep not showing signs of shock and dehydration is one correct form of therapy

(b) Absorption of both D and L-lactate occurs, but only the D-lactate causes acidemia

(c) This condition occurs when gram (+) rods overgrow normal rumen flora

(d) Emergency surgery will allow salvage of animals that are convulsing and in shock

(e) The severity of clinical signs depends on the amount and particle size of the ingested grain

Back 30

(d) Emergency surgery will allow salvage of animals that are convulsing and in shock

Front 31

Which one of the following statements is NOT correct regarding calves born to cows 3-9 months after an episode of bovine virus diarrhea (BVD) in a non-immune population?

(a) The calves may be born with mucosal disease that is unresponsive to therapy

(b) The calves may be born with cerebellar disease

(c) The calves are immunotolerant to the BVD virus but they are incapable of mounting an antibody response to it

(d) The calves are chronic shedders of the BVD virus

(e) The calves may appear normal or suffer from ill thrift

Back 31

(a) The calves may be born with mucosal disease that is unresponsive to therapy

-Calves are not born with mucosal disease but develop a fatal mucosal disease sometime later after being exposed to a cytopathic form of the virus.

Front 32

All of the following statements concerning bovine malignant catarrhal fever are true EXCEPT:

(a) BMCF occurs sporadically and is usually spread from cow to cow

(b) BMCF causes a vasculitis and atypical proliferation of lymphocytes

(c) BMCF causes lymph node enlargement

(d) BMCF causes a panophthalmitis. Corneal opacity usually begins peripherally and spreads centrally.

(e) BMCF is frequently accompanied by CNS signs.

Back 32

(a) BMCF occurs sporadically and is usually spread from cow to cow

-spread from sheep to cow in North America, does not spread from cow-to-cow. Rhinderpest spreads by direct contact, through contaminated water, and aerosol.

Front 33

All of the following are suspected pathophysiologies of left displacement of the abomasum (LDA) EXCEPT:

(a) Reduction in abomasal motility due to hypocalcemia

(b) Reduction in abomasal tone through stabling and lack of exercise

(c) Reduction in abomasal motiliy from toxins released during concurrent disease

(d) Reduction in abomasal motility due to a decrease in volatile fatty acid (VFA) production

(e) Reduction in abomasal motility due to an increased dietary concentrate: roughage ratio.

Back 33

(d) Reduction in abomasal motility due to a decrease in volatile fatty acid (VFA) production

-High dietary concentrate:roughage ratio INCREASES the production of volatile fatty acids.

Front 34

T/F In simple indigestion in cattle, all clinical and lab values will be normal.

Back 34

True.

Front 35

T/F The extent to which cattle will be affected by grain overload depends upon previous diet, quantity, particulate size, type of carbohydrate consumed and time lag from engorgement.

Back 35

True.
-This also affects the degree to which you will treat the individual animal.

Front 36

What does the feces look like from a bovine with acute rumen acidosis?

Back 36

Watery, may be sweet smelling, can have pieces of undigested feed present

Front 37

Acute rumen acidosis will (RAISE/LOWER) rumen pH and (ENHANCE/DESTROY) rumen protozoa.

Back 37

Lower pH
Destroy rumen protozoa

-Checking the rumenal contents can be a very useful test in this condition

Front 38

What are two important sequelae of acute rumenitis?

Back 38

Laminitis
Liver abscesses

Front 39

What is the difference (quick version) between primary and secondary bloat (rumen distention)?

Back 39

Primary bloat - Frothy bloat, caused by animal eating lush legumes

Secondary bloat - bloat caused by excessive gas production and inability to release the gas

Front 40

T/F Bloat in the cow is one of the few true emergencies in bovine medicine.

Back 40

True.

Front 41

(1) In rumen distention (bloat) which side (paralumbar fossa) distends first?

(2) What does it mean if both sides are distended?

(3) How can you differentiate between primary and secondary bloat?

Back 41

(1) Left paralumbar fossa distends first

(2) If both are distended, you better act fast before respiratory compromise and death soon follow

(3) Passage of a stomach tube (primary bloat won't be fixed with a stomach tube - need mineral oil or DSS, rumenotomy)

Front 42

You are presented with an adult diary cow that is completely anorexic, has dropped to 1/3 of her normal milk production, and is dull/depressed (w/ mild to moderate increase in TPR).

You try a withers pinch test and xyphoid compression test and they both come up positive. You pull blood to run a CBC and see an increase in fibrinogen and total protein.

(1) What is your tentative diagnosis?
(2) How would you treat this cow?

Back 42

(1) Traumatic reticuloperitonitis
(2) Rumen magnet - if there isn't one already, Antibiotics if there is peritonitis, confinement and hay, raise the FRONT end (keep rumen from pressing on offending material)

Front 43

T/F The clinical signs of chronic traumatic reticular peritonitis in cattle are more subtle than an acute case of TRP.

Back 43

True. Inflammation and fibrous reaction attempts to wall-off the infection and is usually successful, minimizing the clinical signs.

Front 44

What are the 4 recommended conservative therapy measures for traumatic reticular peritonitis in a cow?

What is the best way to prevent TRP?

Back 44

-Rumen magnet (if one is not already present)
-Parenteral antibiotics (Penn, oxytet)
-Confinement (raise up front end slightly to take pressure of the rumen off of the area)
-Hay diet

Prevent: magnets (to all heifers >8months old) and secure feedsource free of any metal

Front 45

T/F If no improvement after 3-4 days of conservative treatment for traumatic reticular peritonitis in a cow, surgery is indicated and the prognosis becomes guarded.

Back 45

True.
The prognosis is good if there is response to conservative therapy. If peritonitis develops and is severe/diffuse the prognosis is poor.

Front 46

T/F Congestive heart failure, fatal hemorrhage, and diaphragmatic hernia are all possible sequelae or alternate outcomes of traumatic reticular peritonitis in a cow.

Back 46

True. Also:
-Traumatic splenitis or hepatitis
-Pericarditis, pleuritis, or pneumonia
-Chronic peritonitis
-VAGAL INDIGESTION
-Acute, diffuse, septic peritonitis

Front 47

What is the connection between vagal indigestion and traumatic reticular peritonitis?

Back 47

Adhesions from TRP cause failure of ingesta passage through upper GIT (VAGAL NERVE INJURY and/or physical effects of adhesions) and alters normal rumen cycle.

Front 48

What is the main clinical pathology finding in a cow with vagal indigestion?

Back 48

Hypochloremic metabolic alkalosis, increased rumen chloride

Front 49

T/F Abomasal ulcers occur primarily in cattle and range from type 1 (non-perforating erosive ulcers) to type 4 (perforating with diffuse peritonitis).

Back 49

True. Rarely sheep and goats

Front 50

T/F Abomasal ulcers are not a sequelae of LDA and lymphosarcoma.

Back 50

False.

Front 51

Where would you ping to confirm an LDA diagnosis?

Back 51

Ping is best heard in the area of the 9th to 13th rib. Draw a line from the tuber coxae to the elbow and ping along that line in area first described.

Front 52

What 4 things are displaced abomasums in cattle associated with?

Back 52

-Early postpartum
-High carb. diets (increased VFAs)
-hypocalcemia
-genetics

Front 53

T/F Salmonella dublin and S. newport are host adapted strains of Salmonellosis in cattle.

Back 53

False.
S. dublin is main host adapted strain

S. typhimurium, S. newport, S. montivideo, S. anatum are all NON-HOST ADAPTED strains

Front 54

What is the main mode of infection of cattle with host adapted Salmonella?

What risk factors contribute to the increased likelihood of this occuring?

Back 54

Fecal/oral transmission

-Confinement
-Overcrowding
-Poor sanitation
-Constant new admissions

Also:
-Transplacental and milk (up to 4 weeks post parturition) transmission are possible

Front 55

What are 6 ways that cattle get infected with non-host adapted Salmonella?

Back 55

-Shedders
-Rodents and wild birds
-Feeds containing animal biproducts
-Recycled water
-Humans
-Pets

Front 56

What is the range of age in which calves will most likely get infected with Salmonella?

Back 56

2-6 weeks of age (30 day cut off, if calf is greater than 30 days old then it is not salmonella)

Front 57

T/F Infection of cattle with Salmonella by itself is sufficient to cause clinical disease.

Back 57

False. There has to be a trigger for clinical disease to appear which could be:
-Feed change
-Parturition
-Concurrent disease
-Calving
-Movement
-Malnutrition
-Young (no immunity)

Front 58

List the 3 clinical syndromes of Salmonella commonly seen in calves.

Back 58

-Septicemia (meningitis, omphlophlebitis, etc.)
-Pneumonia
-Severe diarrhea/acute enteritis

Front 59

A cow presents to you with severe diarrhea with blood, mucous, and fibrin/mucosal shreds (fibrin casts) in the stool. She is dull in appearance, dehydrated, has a fever, and decreased milk production.

What is your tentative diagnosis?

Back 59

Salmonella (acute enteritis)

Front 60

How many serial fecal cultures are necessary to diagnose Salmonella in adult cattle? What do you culture in calves?

Back 60

5
Blood culture in calves

Front 61

What are 6 DDX for Salmonella in CALVES?

Back 61

-Septicemia
-Pneumonia (S. dublin)
-Rota/Corona Virus
-Cryptosporidia spp
-C. perfringens C & D
-BVD

Front 62

What are 6 DDX for Salmonella in adult cattle?

Back 62

-BVD
-Winter dysentery
-MCF
-Peritonitis (abo ulcer)
-Endotoxemia (mastitis
metritis)
-Oak toxicity

Front 63

How would you treat an adult cow with salmonella? 5 things

Back 63

Fluid therapy
NSAIDs
Change in diet (grass hay)
Clean up the environment (reduce fecal-oral transmission)
Quarantine clinical cases

Front 64

What are the only 2 situations in which antibiotic use is justified in a Salmonella infection?

Back 64

In young calves with sepsis
Severely ill adults

*Resistance is high for Salmonella

Front 65

Where is the best location on a cow to assess hydration status?

What percent dehydration can you reliably detect?

Back 65

Eyelid
5-8% dehydration is the status you can reliably detect

Front 66

T/F Vaccination against Salmonella is generally successful.

Back 66

False. Killed bacterins have limited value and type specific vaccines have variable results. Prevention is the most important aspect of this disease.

Front 67

You are called out to a dairy farm in February with the following history:
-Entire barn has become affected with diarrhea over the span of a 1-2 week period
-Explosive, profuse, watery diarrhea is observed lasting 2-4 days.
-Occasionally fresh blood flecks are observed in the stool
-There is no odor, no mucus, and no evidence of necrosis in the stool
-A few of the cows are observed coughing

What is your tentative diagnosis?

Back 67

Winter dysentery

Front 68

How is winter dysentery (in cattle) spread?

Do you treat winter dysentery or not?

Back 68

Fecal-oral route; vets, AI techs, milk trucks, etc. can all aid in spread of disease.

Most cases recover without treatment in 4 days, may last 2 weeks in the herd. Supportive care may be necessary if fluid loss is severe.

Front 69

For the following pathogens, match the age of onset of diarrhea (seen in calves) with the pathogen causing the diarrhea.

(1) E. coli
(2) Rotavirus, C. perfringens type C
(3) Coronavirus, Cryptosporidium
(4) Coccidia, C. perfringens type D
(5) Salmonella, BVD

(A) 7-21 days
(B) >14 days
(C) Anytime
(D) 1-3 days
(E) 4-14 days

Back 69

(1) D
(2) E
(3) A
(4) B
(5) C

Front 70

Describe the two strains of Bovine Viral Diarrhea virus.

Back 70

Type 1: mild or subclinical disease seen
Type 2: high morbidity/mortality in improperly vaccinated herds

Front 71

What are the three most common viral agents causing diarrhea in calves?

Back 71

Rotavirus
Coronavirus
BVD

Front 72

T/F Malignant Cattahral Fever is an uncommon disease in cattle that often live in close proximity of sheep.

Back 72

True. Is fatal in cattle, deer, bison, buffalo, and other ruminants. No treatment, ~100% mortality. Besides sheep, wildebeest are also a reservoir host.

Front 73

You are presented with a cow with diarrhea, mucopurulent nasal discharge, generalized severe lymphadopathy, and severe oral erosions (looks scalded).

What is your tentative diagnosis?

What are two other DDX?

Back 73

Malignant Cattahral Fever
DDX: BVD, Rinderpest

Front 74

What is the best way(s) to diagnose a rotavirus/coronavirus infection in a calf?

Back 74

EM or FA of feces, Elisa and fecal latex agglutination

Front 75

You are presented with a lamb that is 3.5 weeks of age. This animal has severe diarrhea that has become chronic in nature. The diarrhea has a foul odor, mucous, and frank blood in it. The lamb strains when defecating and appears dehydrated.

You perform a fecal float and see oocytes in the feces.

What is your tentative diagnosis?

Back 75

Coccidiosis - is a self-limiting disease. Can treat a group of animals with coccidiostats when clinical cases are present.

Front 76

What are the GI effects of Oak toxicity in ruminants?

Back 76

Direct damage to the GI mucosal epithelium resulting in ULCERS with hemorrhagic diarrhea.

Front 77

T/F Johne's Disease causes diarrhea in cattle, sheep, and goats.

Back 77

False. Only in cattle.

Front 78

When do the clinical signs of Johne's Disease manifest themselves in cattle?

Back 78

Usually between 2-6 years of age.

Front 79

What are the characteristic lesions/clinical signs of Johne's Disease in cattle?

Back 79

Granulomatous enteritis (esp in the ileum)
Malabsorptive diarrhea
Protein losing enteropathy
Bottle jaw and other edema

Front 80

What is the most significant GI parasite in cattle? What problems and lesions does it cause?

Back 80

Ostertagia
-Destruction of abomasal mucosa, protein loss, diarrhea, maldigestion, bottle jaw

Front 81

What do you use to treat Ostertagia in cattle?

Back 81

Fenbendazole, Ivermectin/Eprinomectin

Front 82

What is the main parasitic agent causing diarrhea in calves?

Back 82

Cryptosporidium parvum

Front 83

What are the two main goals of therapy in treating diarrhea in calves?

Back 83

Rehydration
Correct acid/base and electrolyte abnormalities (often metabolic acidosis)

Front 84

T/F You should take a calf off feed when treating for diarrhea as to not interfere with the action of antibiotics.

Back 84

False. Caloric intake should be maintained during diarrhea. Access to free water should also be maintained. Antibiotic use is only warranted in severe cases (sepsis).

Front 85

What are the three broad mechanisms of anemia?

Back 85

(1) Loss (eg trauma w/ blood loss)
(2) Destruction (intravascular or extravascular)
(3) Decreased production (bone marrow)

-could be one or more of these occurring at the same time

Front 86

A racehorse presents to you with the following signs:
-weakness
-exercise intolerance
-pallor
-icterus
-heart mermur
-melana

What is your tentative diagnosis?

Back 86

These are all clinical signs of anemia.

Front 87

What two easy tests can you run to confirm a diagnosis of anemia?

Back 87

PCV
CBC (red blood cell parameters)

Front 88

T/F Dehydration will increase the PCV level artificially in large animals.

Back 88

True.

Front 89

In what two types of horses (broad categories of breed) does PCV values tend to be lower?

Back 89

Draft horse breeds
Mini breeds

Front 90

Do neonates or geriatrics have lower PCV values in horses?

Back 90

Neonates

Front 91

T/F Goats are capable of plasma trapping which will cause a falsely elevated PCV reading.

Back 91

True.

Front 92

What two mechanisms of anemia is regenerative anemia associated with?

Back 92

Red cell loss
Increased red cell descruction

Front 93

What clinical condition is the most potent stimulator of erythropoiesis?

Back 93

Hypoxia**

Front 94

T/F There are no reliable indicators of regeneration in the horse when measuring peripheral blood parameters.

Back 94

True.

Front 95

What is the only reliable parameter used in horses that will indicate regenerative anemia?

Back 95

Bone marrow evaluation or rising sequential PCVs over time**

Front 96

T/F Blood loss anemias are regenerative anemias.

Back 96

True.

Front 97

How long does it take for RBC and protein redistribution to occur after blood loss in the horse?

Back 97

24 hours

Front 98

T/F Horses are capable of self (blood) transfusion and would have to lose 6-9L of blood in order for anemia to be evident.

Back 98

True.

Front 99

What happens in cattle that experience severe, rapid blood loss? Horses?

Back 99

Cattle - hypoxic dementia, they go crazy. So be careful when taking blood from bovine blood donors.

Horses - blindness

Front 100

What is the number one cause of blood loss anemia in the horse?

Back 100

Trauma

Front 101

What are 3 causes of blood loss anemia in the horse besides trauma?

Back 101

-Parasitism

-Epistaxis/hemoptysis (Caval syndroma in cattle, ethmoid hematoma, EIPH, guttural pouch mycosis in horses)

-GI ulcers (abomasal in cattle, right dorsal colitis in horses)

Front 102

What is a common cause of blood loss anemia in older brood mares?

Back 102

Post parturient uterine artery rupture

Front 103

T/F Immune mediated thrombocytopenia is as common in the horse as it is in dogs.

Back 103

False. Not common in equines.

Front 104

What is the danger of using phenylephrine to treat nephrosplenic entrapment in horses?

Back 104

Pulmonary hemorrhage
Abdominal artery rupture
Transient hematuria
Fatal hemorrhage

Front 105

(1) What is the mechanism of action of Sweet Clover toxicity (Melilotus spp.)?

(2) Does it usually present as individual cases or groups of animals?

Back 105

(1) Coumarin is transformed to dicoumarol by molds growing on the sweet clover (Melilotus spp.).

Dicoumarol interferes with vit. K dependent coagulation factors: II, VII, IX, X (2, 7, 9, 10). This is the same mechanism of action as Warfarin toxicity.

(2) Usually seen in groups of animals grazing on the same pasture

Front 106

In which species will you see bleeding abnormalities after ingestion of Bracken fern and which species shows neurological signs?

(Horses and Ruminants)

Back 106

Ruminants - coagulopathy, bleeding, bone marrow suppression.

Horses - neurological signs due to thiamine inhibition***

Front 107

You are presented with a high producing dairy cow that has melena, and anemia. What class of abomasal ulcer would you assign to it?

Back 107

These are signs of a class II abomasal ulcer. They are usually secondary to other diseases.

Front 108

What signs are seen in a high producing diary cow with a class III abomasal ulcer? Describe a class III ulcer.

Back 108

Fever, lethargy, poor doing cow. Class III ulcers are perforating, cause localized peritonitis.

Front 109

Describe a class IV abomasal ulcer in a high producing dairy cow.

Back 109

Perforating ulcer, diffuse peritonitis.

Front 110

What is the rule of thumb concerning abomasal ulcers in cattle?

Back 110

Bleeding ulcers tend not to perforate and perforating ulcers tend not to bleed.

Front 111

T/F Fecal occult blood test is more reliable in horses than in ruminants.

Back 111

False. More reliable in ruminants.

Front 112

What are the 4 therapeutic objectives in treating blood loss anemia in the horse?

Back 112

(1) Correct/find the underlying cause
(2) Give fluids: hypertonic or isotonic fluids
(3) Decide whether or not to give a blood transfusion. If the horse collapses due to blood loss, may strongly consider it.
(4) Supplement lost iron

Front 113

Which of the following two products should you NOT give to horses to supplement iron?

Iron dextran
Ferrous sulfate

Back 113

Iron dextran

Front 114

Hemoglobinemia and hemoglobinuria, icterus (jaundice) are characteristic of which of the two types of hemolysis?
-Intravascular hemolysis
-Extravascular hemolysis

Back 114

Intravascular hemolysis (but can also be extravascular)

Front 115

T/F Total bilirubin can be elevated in a horse that hasn't eaten for a while.

Back 115

True.

Front 116

What are the main 9 DDX for hemolytic anemia in ruminants?

Back 116

1) Bovine leptospira septicemia
2) Cold water hemoglobinuria
3) Hypophosphatemia
4) Neonatal isoerythrolysis
5) Bacillary hemoglobinuria (Clostridial disease)
6) Babesiosis
7) Anaplasmosis (A. marginale) - SE Unites States especially
8) Copper toxicity
9) Phenothiazine, onions, Brassica

Front 117

What are the main 6 DDX for hemolytic anemia in horses (no toxins)?

Back 117

1) Neonatal isoerythrolysis
2) IMHA
3) Babesia equi, B. cabilli (emerging disease in north america)
4) Anaplasma phagocytophilium
5) terminal liver failure
6) Undiluted DMSO IV

Front 118

What are the 5 DDX for hemolytic anemia in horses with a red cell toxicity involved?

What might you see with these toxicities on a RBC smear?

Back 118

1) Red maple
2) Onion (garlic + other similar plants also)
3) Phenothiazine (not as common anymore)
4) Snake venom
5) Heavy metals

Heinz body formation

Front 119

Summarize the etiology/pathogenesis of neonatal isoerythrolysis in foals.

Back 119

-Occurs when the SIRE and FOAL share a blood group antigen that is NOT present in the MARE. Aa and Qa blood group antigens are strongly immunogenic and responsible for most cases.

-The MARE is exposed to these blood group antigens and forms antibodies against them.

-These antibodies (along with all the other normal ones) collect in the colostrum.

-When the foal suckles the colostrum, the antibodies against the blood group antigens attach to the foal's RBCs and cause RBC destruction.

Front 120

T/F The milk and colostrum of a mare known to have autoantibodies against Aa and Qa blood group antigens should not be given to a foal with Aa and Qa blood group antigens.

Back 120

False. The milk is fine to give, just not the colostrum.

Front 121

What is the usual treatment regime for neonatal isoerythrolysis in foals?

Back 121

-Supportive care, RBCs will regenerate on their own over time
-O2 supplementation may be necessary if collapse
-Blood transfusion

Front 122

What vaccine is associated with neonatal isoerythrolysis in calves?

Back 122

Anaplasmosis vaccine

Front 123

T/F Red maple toxicity (Acer rubrum) is likely to be seen in only the boss horse (in a group of horses).

Back 123

True. Horses love to eat it so the boss horse will hog all of the leaves.

Front 124

T/F Ruminants are 10X more sensitive to nitrate toxicity than monogastrics.

Back 124

True.

Front 125

What is the treatment protocol for hemolysis due to oxidative injury after ingestion of toxic plants in horses?

Back 125

-Identify and remove the source of toxin
-Supportive care
-IV ascorbic acid (Vitamin C) at a high dose

Front 126

What is the antidote for nitrate toxicity in horses?

Back 126

Methylene blue - 5-15mL of 1% solution

Front 127

What is the "flagship species" for copper toxicity?

Back 127

Most important in sheep. But can be seen in calves.

Front 128

What two elements put into feed are protective against copper toxicosis?

Back 128

Molybdenum and sulfur
-if these are in low levels then copper toxicosis incidence will increase

Front 129

Where in the animal's body does copper like to accumulate?

Back 129

Hepatocytes

Front 130

What are 4 specific treatment options for treatment of copper toxicosis?

Back 130

-Ammonium molybdate (fed daily)
-Na thiosulfate (daily for 3 weeks)
-Ammonium tetrathiomolybdate (IV or SC on alternate days for 3 weeks)
-Cupramine AKA D-penicillamine (daily for 6 wks - chilates copper)

Front 131

What type of hemolysis (INTRA or EXTRAvascular) does Anaplasma marginale cause in cattle? Does it cause hemoglobinuria?

Back 131

**Extravascular hemolysis, therefore hemoglobinuria is NOT a feature of this disease.**

Front 132

T/F Fever, anemia, and jaundice are the most obvious clinical signs associated with Anaplasmosis.

Back 132

True.

Front 133

What type of hemolysis (INTRA or EXTRAvascular) does Equine Infectious Anemia cause in horses? How is it transmitted?

Back 133

Extravascular hemolysis + bone marrow suppression (so can be intracellular)

Transmitted by Tabanids (horse and deer flies) and fomites

Front 134

What are the three clinical syndromes possible with Equine Infectious Anemia?

Back 134

(1) Acute fever, thrombocytopenia, anemia
(2) Recurrent, cyclic, ventral edema, weight loss, depression, anemia, thrombocytopenia
(3) Asymptomatic - infectious for life, shedders (spooky)

Front 135

What is the main method of screening horses for Equine Infectious Anemia?

Back 135

"Coggins testing" via ELISA test (mainly) and Agar gel immunodiffusion (classic Coggins test)

Front 136

T/F There is a vaccine available for treatment and prevention of Equine Infectious Anemia.

Back 136

False. There is NO treatment or vaccine available for prevention of this disease.

Front 137

What is the etiological agent causing Bacillary Hemoglobinuria (Red Water Disease) of ruminants?

Back 137

Clostridium hemolyticum, C. novyi type D toxemia

Front 138

What is the pathogenesis of Bacillary Hemoglobinuria (Red Water Disease) of ruminants?

Is there a vaccine available to prevent this disease?

Back 138

Clostriduim hemolyticum or C. novyi type D (or both) are harbored in the liver where they release necrotizing and hemolyzing toxins which cause the majority of the damage.

Yes, there is a vaccine.

Front 139

In what two large animal species is Leptospirosis most common?

What is/are the etiological agent(s)?

Back 139

Calves and lambs

L. pomona and L. icterohemorrhagica

Front 140

T/F Leptospirosis is potentially zoonotic and is an occupational hazard of veterinarians.

Back 140

True. Is also a hazard to animal owners, especially if they are assisting with parturition.

Front 141

Is IMHA in horses usually a primary disease or secondary to a concurrent disease?

Back 141

Secondary to other disease or drugs (human recombinant erythropoietin in athletic horses)

Front 142

Name 4 secondary diseases that can cause IMHA in horses.

Back 142

EIA
Lymphosarcoma
Anaplasmosis
Ehrlichiosis

Front 143

What are three tests used to diagnose IMHA in horses?

Back 143

(1) Autoagglutination test
(2) Coombs test (before steroids...important)
(3) Looking for spherocytes on a blood smear

Front 144

Which immune suppressant is used to treat IMHA in horses?

Back 144

Dexamethasone - starting at 20-40 mg per day and tapering off over time

Front 145

What is the most common cause of anemia in LA species?

Back 145

****Anemia of chronic disease

Front 146

T/F You should supplement a horse with iron if you suspect they have anemia related to chronic disease.

Back 146

False. The body is likely hiding the iron away to prevent the infectious agent from using it.

Front 147

What are 5 causes of non-regenerative anemia due to decreased RBC production in the horse?

Back 147

(1) Iron deficiency anemia
(2) Chronic renal disease
(3) Toxicity
(4) Bone marrow aplasia
(5) Inherited bone marrow dysfunction

Front 148

**If the cause of anemia is due to IRON DEFICIENCY, what will be the status of the following parameters:

-FERRITIN (increase/decreased/stay same)
-SERUM IRON (increase/decreased/stay same)
-BONE MARROW (functional or non-functional)
-IRON BINDING CAPACITY (increase/decreased/stay same)
-SUPPLEMENTATION (needed or not needed)

Back 148

-FERRITIN (decreased)
-SERUM IRON (decreased)
-BONE MARROW (non-functional)
-IRON BINDING CAPACITY (increased)
-SUPPLEMENTATION (needed)

Front 149

**If the cause of anemia is due to ANEMIA OF CHRONIC DISEASE, what will be the status of the following parameters:

-FERRITIN (increase/decreased/stay same)
-SERUM IRON (increase/decreased/stay same)
-BONE MARROW (functional or non-functional)
-IRON BINDING CAPACITY (increase/decreased/stay same)
-SUPPLEMENTATION (needed or not needed)

Back 149

-FERRITIN (increased)
-SERUM IRON (decreased)
-BONE MARROW (functional)
-IRON BINDING CAPACITY (decreased)
-SUPPLEMENTATION (not needed)

Front 150

What is the classic RBC description seen on a blood smear for iron deficiency anemia in the horse?

Back 150

Microcytic, hypochronic anemia

Front 151

T/F Relative erythrocytosis is VERY rare.

Back 151

False. Is VERY common.

Front 152

What are two causes of relative erythrocytosis in LAs?

Back 152

Dehydration (causes transient erythrocytosis)
Hemoconcentration

Front 153

T/F Absolute erythrocytosis is VERY rare.

Back 153

True.

Front 154

T/F Absolute erythrocytosis in LAs will respond to fluid administration.

Back 154

False. No response.

Front 155

A horse is presented to you with the following clinical signs:

-Muddy heperemic mucous membranes
-Sludgy blood (when you took a blood sample for analysis)
-Low oxygenation status

What is your tentative diagnosis?

Back 155

Absolute erythrocytosis

Front 156

What are three causes of Secondary Absolute Erythrocytosis in the horse?

Back 156

(1) Increased erythropoietin due to chronic hypoxia
(2) Pulmonary disease
(3) High altitude disease

Front 157

What are two causes of Primary Absolute Erythrocytosis in the horse?

Back 157

(1) Myeloproliferative disease
(2) Idiopathic

Front 158

A positive Coombs' test would NOT be likely for which one of the following causes of anemia in large animals?

(a) Neonatal isoerythrolysis
(b) Red maple toxicosis
(c) Penicillin-induced, immune mediated hemolytic anemia
(d) Equine infectious anemia
(e) Equine lymphosarcoma

Back 158

(b) Red maple toxicosis

Front 159

Which one of the following morphological descriptions is NOT true?

(a) Babesia equi - Maltese cross in erythrocytes

(b) Anaplasma centrale - small bodies near the center of erythrocytes

(c) Eperythrozoon ovis - ring form in erythrocytes

(d) Anaplsama marginale - free organisms in plasma

(e) Ehrlichia equi - small bodies in neutrophils

Back 159

(d) Anaplsama marginale - free organisms in plasma (only Eperythrozoon organism are found free in the plasma)

Front 160

Which one of the following vector-pathogen associations is NOT correct?

(a) Biting flies - leptospirosis
(b) Biting flies - bovine leukosis virus
(c) Ticks - anaplasmosis
(d) Biting flies - equine infectious anemia virus
(e) Keds - eperythrozoonosis

Back 160

(a) Biting flies - leptospirosis

Front 161

Which one of the following signs is NOT typical of the regenerative response to anemia?

(a) Basophilic strippling in cattle
(b) Polychromasia in cattle
(c) Macrocytosis in pigs
(d) Reticulocytosis in horses
(e) Marrow erythroid stem cell hyperplasia in horses

Back 161

(d) Reticulocytosis in horses (horses do not get reticulocytes)

Front 162

What etiological agents cause malabsorptive diarrhea in calves?

Back 162

viruses
Cryptosporidia
C.perfringens
Salmonella
BVD
Coccidia