Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RUSVM LAM I > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What are causes of acute colitis in adult horses?

A 
Salmonella
Clostridum difficile and perfringens
Enterotoxemia
Potomac Horse Fever (late spring to early fall)
Antimicrobial induced diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are causes of acute colitis in foals?

A 
Salmonella
Clostridium difficile and perfringens
Gastric ulcers
Rota virus
Compromised GIT
Antimicrobial induced diarrhea
Foal heat diarrhea
Equine proliferative enterotoxemia (L. intracellularis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are causes of chronic colitis in adult horses?

A

Cyathostomiasis
Sand impaction
IBD**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are causes of chronic colitis in foals?

A 
Villous atrophy (secondary to clostridium)
Lactose intolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are clinical signs of acute colitis?

A 
Explosive watery diarrhea
Malodorous feces
Colic
Dehydration (skin tent, prolonged CRT and jugular refill)
Depression (electrolyte imbalances in the neurons)
Laminitis
Anorexia
Pyrexia
Tachycardia
Dry or toxic mucous membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In what percent of adult colitis cases is a definitive diagnosis reached?

A

Definitive diagnosis is obtained in only about 30-50% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical pathology, biochemistry, and hematology abnormalities with acute colitis (same as for salmonellosis)

A

Leukopenia (left shift, toxic neutrophils, lymphopenia)
Metabolic acidosis (losing bicarb, hyponatremia, hypochloremia, hypokalemia, hypocalcemia)
Increase PCV and lactate
Protein and fibrinogen may be up or down
Azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Salmonella colitis

A

ALWAYS has to be ruled out due to zoonotic potential and risk of hospital outbreak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Associated patient abnormalities with Salmonella

A 
Acute profuse diarrhea
Endotoxemia
CV shock
Vascular leaking
Coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Clinical signs of salmonellosis

A

Febrile
Tachycardic (± tachypnic)
Dehydrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can we test for Salmonella?

A

Multiple culture or PCR as it is shed intermittently, each sample needs to be minimum 5-10g of feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment and prevention of salmonellosis

A 
Aggressive supportive care
Antimicrobials
Endotoxemia therapeutic protocol
High biosecurity
Repeat fecal culture and PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Potomac Horse Fever causative agent

A

Neorickettsia risticii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical signs of Potomac Horse Fever

A

Biphasic fever
Laminitis
Colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnosis of PHF

A

Paired serum titers and IFAT; confirmation with identification of parasite in WBCs in acute phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of PHF

A

IV oxytetracycline
Supportive therapy
Laminitis prevention (ice bandages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T or F: There is a vaccine for PHF.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Etiology of Equine Proliferative Enteritis

A

Lawsonia intracellularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical signs of Equine Proliferative Enteritis

A 
Lethargy
Depression
Peripheral edema
Diarrhea
Colic
Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Typical age for horses affected by Equine Proliferative Enteropathy

A

Young (6 months old)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diagnosis of EPE

A

Clinical signs
Ultrasound showing thickening of SI wall
Hypoproteinemia
Positive serology or molecular detection in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Treatment of EPE

A

Antimicrobial (macrolide + oxytetracycline/chloramphenicol) for 2-3 weeks
Correct hydration, electrolyte derangements, and azotemia if present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Etiology of pyogranulomatous pneumonia

A

Rhodococcus equi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

If Rhodoccus equi is causing enterocolitis, where in the GIT is the lesion?

A

Ulcerative enteritis in the Peyer’s patches of the ileum (may extend to cecum and colon)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Treatment of Rhodoccus equi

A

Macrolides

Supportive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Clostridial colitis (antimicrobial associated enterocolitis) histories

A

Farm outbreak in foals
Horse recently treated with antimicrobials
Mares when foal is being treated for R. equi
Untreated horse with diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clostridial toxin A does what?

A

Induces release of substance P (neurotransmitter) at the dorsal root ganglia
This is cytotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Clostridial toxin B does what?

A

Enterotoxigenic activity and is cytotoxic (necrotizing and hemolytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What might be visible on a radiograph of clostridial colitis?

A

Gas and fluid distended intestine with intramural gas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diagnosis of clostridial colitis

A 
Quantitative culture (normal flora)
PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How can we differentiate C. difficile from other clostridium?

A

Immediate submission of samples
Sending in large samples
Transportation of sample frozen and in air-tight containers
Cytotoxin assay [differentiates from C. perfringens]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Treatment of clostridial colitis

A

Supportive care

Metronidazole (or vancomycin if resistant to metronidazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which two organisms are more commonly associated with neonatal enterocolitis than with adult acute colitis?

A

Cryptosporidium spp

Giardia spp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Inflammatory bowel disease is named based on what?

A

Histopathological findings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Clinical presentation of IBD

A 
Progressive diarrhea
Weight loss
Good appetite
Intermittent colic
Dermatitis
Peripheral edema (hypoproteinemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Treatment of IBD

A

Steroids

Probiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Blister beetle toxicosis is caused by what?

A

Cantharidin absorption consumed in beetle infested alfalfa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the fatality rate of blister beetle toxicosis?

A

> 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does cantharidin cause ulceration?

A

It is an irritant causing cell damage and necrosis on contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What electrolyte derangements associated with cantharidin toxicosis have not been explained?

A

Hypomagnesemia

Hypocalcemia (may be loosely associated with hypoalbuminemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Diagnosis of cantharidin toxicosis via…

A

Beetle ID
History
Concentration of cantharidin in gastric juice, intestinal content, and urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Treatment of cantharidin toxicosis

A 
Supportive care
Electrolyte supplementation
Oral absorbents (mineral oil)
Laminitis prevention
Endotoxemia treatment protocol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Other things that can cause diarrhea

A 
Acorn toxicity
NSAID toxicity
Grain overload
Intestinal LSA
Peritonitis
Heavy metal toxicosis
Sand colic
Enteric pythiosis
Anaphylaxis
Stress (don't we all know it...)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

When treating a colitis patient, after normovolemia has been attained what are two tests that can help us determine adequate fluid delivery?

A

Serial central venous pressure

Serial lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Endoserum (endotoxin neutralizer) is made how?

A

Horses are vaccinated with a recombinant mutant of S. typhimurium and the antibodies are harvested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does Polymyxin B work?

A

Polymyxin B binds to the lipid A region of the endotoxin, thus neutralizing it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the most effective NSAID for preventing endotoxin-induced prostanoid synthesis?

A

Flunixin meglumine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What drug may be beneficial in preventing laminitis?

A

Pentoxifylline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are functions of the liver

A

Process nutrients from food
Store glucose, vitamins, and minerals
Maintain immune function
Remove toxins from the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What percentage of the liver has to be damaged for clinical signs to present?

A

70-80% of the liver being damaged will result in abnormal function or failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Clinical abnormalities associated with liver damage

A 
Icterus
Photosensitization
Hepatoencephalopathy
Coagulopathies
Colic
Pruritus
Ascites
Weight loss
Diarrhea
Rectal prolapse
Fecal color change
Dyspnea (pharyngeal or laryngeal collapse)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Clinical signs of acute liver dysfunction

A 
Depression
Hepatic encephalopathy
Icterus
Colic
Anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What substance can be used to test the excretory function of the liver?

A

Bromsulphalein dye

54
Q

Liver enzymes and how to interpret

A

SDH: elevation may indicate ongoing parenchymal damage
ALP: not liver specific
AST: not liver specific
GGT: elevation my indicate chronic liver disease

55
Q

What coagulation factors are produced in the liver?

A

I, II, V, VII, IX, X

56
Q

What toxicity and disease have been associated with type III photosensitization in horses?

A

Pyrrolizidine alkaloid toxicity

Theiler’s disease

57
Q

Treatment of photosensitization

A

Eliminate photodynamic agent
Provide cover from the sun
Treat as a skin burn (fluids, electrolytes, antibiotics, anti-inflammatories, pain control)

58
Q

Hepatic encephalopathy clinical signs

A 
Frequent yawning
Abnormal behavior
Aimless wandering (apparent blindness) and foot stomping
Head pressing
Circling
Seizures
59
Q

How might aromatic amino acids cause hepatic encephalopathy?

A

Increase inhibitory neurotransmitters (GABA and L-glutamate)
Alter catecholamines
Alter MAOs

60
Q

What drug (and class) improves the neurologic state of hepatic encephalopathy?

A

Flumazenil (benzodiazepine antagonist)

61
Q

Etiologies of Idiopathic Acute Hepatic Disease aka “Serum sickness” aka “Theiler’s Disease”

A

Viral infection with Theiler’s disease
Hypersensitivity type III
Dietary factor (pastured horses)
Pyrrolizidine alkaloid toxicosis

62
Q

Clinical signs of IAHD

A 
6-8 weeks post-vaccination
CNS signs
Icterus
Yawning (early sign)
Photodermatitis
Intravascular hemolysis w/ or w/o hemoglobinuria
Weight loss
Ventral edema
63
Q

What liver enzyme is helpful to monitor in outbreaks of IAHD

A

GGT (increased before onset of clinical signs)

64
Q

Histopathology of IAHD

A

Hepatocellular central and mid-zonal necrosis
Accumulation of mononuclear cells and neutrophils in the portal region
Bile ductule proliferation

65
Q

On necropsy, how is the liver of a patient with IAHD often described?

A

Flaccid liver or “Dishrag liver”

66
Q

Signalment for cholelithiasis

A

Middle age to older

No sex or breed predilection

67
Q

Define choledocholithiasis

A

Stone found in the common bile duct (most common biliary obstruction in equine patients)

68
Q

Composition of choleliths includes…

A 
Bilirubin
Bile pigment
Cholesterol esters
Ester of cholic and carboxylic acid
Calcium phosphate
Sodim taurodeoxycholate
69
Q

Pathogenic mechanisms proposed for cholelithiasis

A 
Ascending biliary infection (cholangitis)
Parasitism (ascarid)
Biliary stasis
Change in bile composition
Foreign body
70
Q

Clinical signs of cholelithiasis

A

Colic with pyrexia and icterus ongoing for 2 weeks

71
Q

Diagnosis of cholelithiasis

A

Ultrasound (75% diagnosed via this method) of the R 14-16 ICS
Hepatomegaly
Increased hepatic echogenicity

72
Q

What bacteria can be cultured in cases of cholelithiasis?

A

Bacterioides vulgatus

E. coli

73
Q

Histopathology with cholelithiasis

A

Periportal fibrosis
Bile duct hyperplasia
(Suppurative cholangitis)

74
Q

Treating cholelithiasis

A 
Medical:
-broad spectrum abx
-fluids
-NSAIDs
-DMSO
-Diet
Surgical:
-choledocholithotomy
-choledocholithotripsy
75
Q

With which liver disease can we see moist exfoliative dermatitis and necrotic leathery skin along the coronary band?

A

Chronic active hepatitis

Moist exfoliative dermatitis: aseptic vasculitis

76
Q

Treatment of chronic active hepatitis

A

Supportive care
Corticosteroids (if LPC infiltrate seen on biopsy)
Antimicrobials
Anti-inflammatories
Colchine (inhibit collagen production and reduce inflammation caused by macrophages/cytokines)

77
Q

Etiology of Tyzzer’s disease

A

Clostridium piliformis (gram - anaerobic spore forming intracellular rod shaped)

78
Q

Who is most commonly affected by Tyzzer’s disease

A

Foals (7-14 d old) ESPECIALLY foals born in the spring

Rapidly fatal

79
Q

Hematology abnormalities with Tyzzer’s disease

A 
Elevated liver enzymes
Severe hypoglycemia (<20mg/dL)
80
Q

Diagnosis of Tyzzer’s disease

A

PCR

Necropsy (Warthin-starry stain)

81
Q

What medications can decrease blood ammonia?

A 
Mineral oil
Oral neomycin
Oral lactulose
Metronidazole
Low protein diet and small meals
82
Q

Atopic dermatitis type of reaction and clinical signs

A 
Type I (IgE)
Pruritus, alopecia, erythema, urticaria, papules
83
Q

Erythema multiforme is death of what type of cells?

A

Keratinocytes

84
Q

Where does leukocytoclastic vasculitis occur and what is the age of the patient?

A

Lower extremities (pasterns) lacking pigment, mature horses

85
Q

Pemphigus foleaceus definition

A

Intra-epidermal acantholysis and intracellular deposition of immunoglobulins

86
Q

With pemphigus foleaceus, what are type of antibodies are involved and what do they target?

A

Autoantibodies targeting transmembrane proteins (releases proteolytic enzymes which destroy cell attachments causing vesicles and intraepidermal clefts)

87
Q

How is pemphigus treated?

A

Immunosuppressives

88
Q

Pemphigus vulagaris, what immunoglobulin and what is is directed against?

A

IgG against epidermal transmembrane proteins (same as pemphigus foliaceous)

89
Q

What is the common name of dermatophytosis?

A

Ringworm

90
Q

What is the causative agent of ringworm in horses?

A

Microsporum equine and Trichophyton verrucosum

91
Q

How is ringworm spread and what is the incubation period?

A 
Direct contact (or grooming equipment)
Incubation period is 1-6 weeks
92
Q

What is the prognosis of dermatophytosis?

A

It is a self-limiting infection, lasting 1-4 months

93
Q

What is the treatment for dermatophytosis?

A

Topical ketoconazole shampoo
Anti-inflammatory agents
Systemic griseofulvin
Equipment disinfection

94
Q

What is the common name for dermatophilosis?

A

Rain rot

95
Q

What is the causative agent of rain rot in horses?

A

Dermatophilus congolensis, a gram +, branching, filamentous anaerobic bacteria

96
Q

What are the three conditions required for development of rain rot?

A
  1. Carrier animal
  2. Moisture
  3. Skin abrasion
97
Q

When is dermatophilosis seen most commonly?

A

Fall and winter months

98
Q

Where are dermatophilosis lesions located on the patient?

A

Dorsal aspect

99
Q

What is the treatment for dermatophilosis?

A

Remove from wet environment
Remove all crusts
Wash patient with ionophores or lime sulfur
Prescribe antimicrobials

100
Q

What part of the body is affected by equine staphylococcal cellulitis?

A

Usually the hind limbs, one limb at a time

101
Q

Clinical signs of equine staphylococcal cellulitis

A 
Prominent limb swelling, warm and painful to the touch, ± pitting edema
Lameness
Pyrexia
(Lethargy)
(Anorexia)
102
Q

What leads to equine staphylococcal cellulitis?

A

Injury or trauma (including procedures)

103
Q

Treatment of staphylococcal cellulitis

A

Eliminate infection (broad spectrum abx)
NSAIDs (pain modulation)
Hydrotherapy

104
Q

T or F: surgical debridement is necessary for the treatment of equine staphylococcal cellulitis

A

If medical management fails, surgical debridement and drainage is necessary

105
Q

Who is affected by chronic progressive lymphedema most commonly

A

Draft horses

106
Q

Where on the patient is chronic progressive lymphedema noted?

A

Distal limb

107
Q

What is the causative agent of Pigeon fever?

A

Corynebacterium pseudotuberculosis (gram +)

108
Q

Where on the patient are Pigeon fever lesions found?

A

Pectoral region (rupture in 1-4 weeks)

109
Q

What is the common name for Pythium infection?

A

Swamp cancer/Florida horse leech/Kunker

Casused by Pythium insidiosum (protozoa)

110
Q

Cutaneous habronemiasis lesions are found where

A

Wound sites

111
Q

When there is a cutaneous habronemia lesion at the medial canthus of the eye, what is it called?

A

Dracocystitis

112
Q

Papillomatosis affects what age group and what is the etiology

A

Young animals most affected

BPV 1-10

113
Q

What causes aural plaques

A

Possibly viral papilloma

114
Q

T or F: aural plaques resolve spontaneously

A

F

115
Q

How are aural plaques treated?

A

Imiquimod topical

Cryosurgery

116
Q

How is SCC treated in the equine patient

A

Surgical excision
5-FU (5-flurouracil)
Intralesional cisplatin

117
Q

What is the most common tumor in horses?

A

Equine sarcoids

118
Q

What organism is associated with pathogenesis of equine sarcoids?

A

Bovine papilloma virus

119
Q

What is equine sarcoids?

A

Fibroblastic tumor, slow growing, no metastasis; NOT a benign tumor

120
Q

What are the types of equine sarcoids and what do the lesions look like?

A

Occult (circular alopecia)
Verrucous (sessile or pedunculate)
Nodular (invasive, destroying adjacent tissue)

121
Q

Treatment of equine sarcoids

A 
PCR for BPV 5-6 on margin after surgical excision
Topical caustic ointment
5-FU
Intralesional chemo
Radiation
122
Q

Equine melanoma is associated with what horses

A

Gray horses

123
Q

Where are melanoma lesions commonly found

A

Ventral tail, perineum, external genitalia, lip, udder, periocular

124
Q

Treatment of melanoma

A

Excise dermal tumors
Cimetidine PO for 16wk
Cisplatin intralesional

125
Q

How is eosinophilic granuloma diagnosed?

A

Biopsy histopath reveals collagen surrounded by granulomatous inflammation (eosinophils, lymphocytes, histiocytes)

126
Q

Who is affected by hereditary equine regional asthenia

A

QH and related breeds

127
Q

What is the cause of HERDA

A

mutation in the pro collagen I N-proteinase (cyclophilin B–PPIB defect)

128
Q

What is a clinical sign of HERDA?

A

Skin on back/neck easily torn or stretched (seroma, hematoma)

129
Q

Equine B cell LSA has been demonstrated to be caused by what?

A

Estrogen secreting ovarian tumor

130
Q

What scale is used to body condition score horses?

A

Henneke (1-9)

RUSVM LAM I (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions