Diseases of the Alimentary Tract P639-842 Flashcards

1
Q

An abdominocentesis should be performed before laparoscopy because what parameters of the peritoneal fluid changes due to the surgery?

A

The abdominal WBC count and TS will increase

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2
Q

The stomach is located approximately where, by US, in the horse?

A

ICS 9th-13th, on the left side

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3
Q

The stomach should be no greater than how many mm thick?

A) 5
B) 6
C) 7
D) 8

A

C) 7, though when the stomach is completely empty, the wall thickness can extend up to 1 cm

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4
Q

Foals with rota or clostridial diarrhea can become lactose intolerant, due to lose of lactase. This stems from loss of the mucosal brush border along the small intestine. How can lactose tolerance be measured?

A

Administer a 0.5-1 g/kg of 20% soln of D-lactose. The serum glucose levels should double within 60 mins of administration.

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5
Q

What is the most frequently reported oral tumor of the horse?

A) Melanoma
B) SCC
C) Lymphosarcoma
D) Papilloma

A

B) SCC

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6
Q

T/F The esophagus is covered in serosa.

A

F The outer wall of the esophagus is composed of adventitious that is loosely attached to surrounding tissue.

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7
Q

The cranial 2/3rds of the esophageal wall is composed of _____ muscle, whereas the distal 1/3rd of is composed of ____ muscle.

A) skeletal, smooth
B) smooth, skeletal

A

A) The cranial 2/3rds of the esophageal wall is composed of skeletal muscle, whereas the distal 1/3rd of is composed of smooth muscle.

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8
Q

This is a prokinetic drug that may benefit foals with reflux esophagitis. It reduces gastroesophageal reflux by increasing lower esophageal sphincter tone, gastric emptying and gastroduodenal coordination.

A) Cisapride
B) Metaclopramide
C) Erythromycin
D) Lidocaine

A

B) Metaclopramide dosed at 0.02-0.1 mg/kg SC q4-12 hrs

Horses are prone to the extrapyramidal neurologic side effects and CRI of this drug may reduce the risk or severity of the neurologic side effects.

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9
Q

A weanling aged foal presents with dysphagia, drooling of saliva, distention of the cervical esophagus. The foal has an unthrifty hair coat, is smaller than same aged pasture mates and has a poor BCS. There is radiographic evidence of aspiration pneumonia. An endoscopic evaluation of the esophagus reveals dilation of the esophagus and mild evidence of diffuse esophagitis. Radiographs reveal esophageal dilation in the caudocervical region, extending into the thoracic inlet. What is the most likely diagnosis?

A) Foreign body
B) Congenital stenosis
C) Idiopathic megaesophagus
D) Persistent right aortic arch

A

D) Persistent right aortic arch. This formed as a fetus, where the fourth right aortic arch became the definitive aorta instead of the left aortic arch. The ligamentum arteriosum is responsible for constricting the esophagus.

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10
Q

One study has shown that maximal reduction in esophageal lumen occurs ____ days after an esophageal obstruction. The esophagus continues to change and remodel up to ____ days after the obstruction.

A) 15, 30
B) 20, 40
C) 30, 60
D) 40, 80

A

C) 30, 60

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11
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

The epithelium is intact and there is no appearance of hyperkeratosis.

A) Grade 0 ESGUS
B) Grade 0 EGGUS

A

A) Grade 0 for ESGUS

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12
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

The epithelium is intact and there is no hyperemia.

A) Grade 0 ESGUS
B) Grade 0 EGGUS

A

B) Grade 0 EGGUS

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13
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

The mucosa is intact, but there are areas of hyperkeratosis.

A) Grade I ESGUS
B) Grade I EGGUS

A

A) Grade I ESGUS

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14
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

The mucosa is intact, but there are areas of hyperemia.

A) Grade I ESGUS
B) Grade I EGGUS

A

B) Grade I EGGUS

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15
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

Small single or multi focal lesions.

A) Grade 0
B) Grade I
C) Grade II
D) Grade III
E) Grade IV
A

C) Grade II

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16
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

Large single, or multi focal lesions or extensive superficial lesions.

A) Grade 0
B) Grade I
C) Grade II
D) Grade III
E) Grade IV
A

C) Grade III

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17
Q

Which grade, in the scoring system for Equine Gastric Ulcer Syndrome, does this description match with:

Extensive lesions with areas of apparent deep ulceration.

A) Grade 0
B) Grade I
C) Grade II
D) Grade III
E) Grade IV
A

E) IV

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18
Q

While gastroscopy is the best to diagnose EGUS, what other clinical signs may be present in a horse dealing with this condition?

A

Recurrent colic, poor appetite, weight loss, hair coat and behavioral changes, pain on tightening of the girth, diarrhea

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19
Q

This stomach content contributes largely to squamous ulceration in the horse.

A) Pepsinogen
B) Hydrochloric acid
C) Intrinsic factor
D) Mucin

A

B) Hydrochloric acid

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20
Q

In a horse that is predominantly on a roughage-based diet, the addition of a soluble carbohydrate can contribute to squamous mucosal injury. How does this occur?

A

Fermentation of the carbohydrate to short-chain fatty acids can disrupt the physiological protective effect of the roughage diet.

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21
Q

What is the mechanism of action of omeprazole, to treat EGUS?

A) Impairment of the H+/K+ ATPase pump
B) Blocking the H2 receptor of parietal cells
C) Adherence to ulcerated mucosa
D) Antibacterial

A

A) Impairment of the H+/K+ ATPase pump, which secretes HCl

22
Q

Describe BVDV and related species viruses.

A

BVDV is a RNA Pestivirus, enveloped. Has two subtypes BVDV 1 and BVDV 2

Classical swine fever
Border disease in small ruminants

23
Q

BVDV can be further categorized by types. Describe.

A

BVDV 1 and BVDV 2

Noncytopathic (NCP) and cytopathic (CP)

24
Q

How do persistently infected animals with BVDV occur? What are the survival rates of PIs?

A

PIs begat PIs. These animals are born from dams that acquire BVDV NCP during gestation. PIs can then have mutations that turn them into the cytopathic form. 1-2% prevalence of PIs.

PIs have a less than 50% survival rate.

25
Q

How can BVDV be spread and what other species can be infected?

A

Transmission: vertical and horizontal; nasal secretions, milk, uterine fluids, saliva, tears, semen (can survive cryopreservation)

Sheep, goats, alpacas (25% of herds will be sero(+) and can have 6% PIs) and deer can have BVDV

26
Q

What are the 6 different categories of acute infections that BVDV can cause?

A
Acute-transient 
Severe acute
Acute-immunosuppresion 
Hemorrhagic 
Reproductive 
Respiratory
27
Q

What is the naive cattle incubation period and viremia duration of BVDV?

A

Incubation 5-7 days with viremia of 3-15 days.

28
Q

In what tissues can BVDV be found to replicate?

A

Spleen, thymus, LN, tonsils, Peyers patches

29
Q

How long do maternal Abs last in dairy calves and beef calves?

A

Dairy calves - BVDV1: 117 days BVDV2: 94 days

Beef calves - BVDV1: 185 days BVDV2: 157 days

30
Q

What do severe manifestations of BVDV look like?

A

Diarrhea, pyrexia, decreased milk production, oral ulcerations

31
Q

What are hemorrhagic manifestations of BVDV and what is the likely etiology?

A

Thrombocytopenia, bloody diarrhea, epistaxis, petechia, echymosis, hyphema.

In these animals, bone marrow megakaryocytes are infected by BVDV

32
Q

How does BVDV cause immunosuppression?

A

BVDV immunosuppresion causes are speculative:

  • Leukopenia is present, decreases in CD8+, CD4+ and gamma/delta T cells, B lymphocytes and neutrophils
  • System removal of BVDV infected cells
  • BVDV destruction of immune cells
  • Trafficking of immune cells into areas of viral replication
  • NCP BVDV is lymphotrophic, leading to cytolysis and lymphoid depletion
  • Infection into Ag-presenting cells
33
Q

When BVDV is seen in conjunction with BRDC, what other viruses have been commonly isolated?

A

Bovine herpes virus-1 and Bovine respiratory syncytial virus

34
Q

Can BVDV last in semen?

A

BVDV has been seen in sero(+), non viremia bulls planned for AI, resulting in infection and seroconversion of inseminated heifers

Has also been seen in 12.5 months post BVDV exposure

35
Q

If a dam is affected in the first 45 days of gestation with BVDV, what can happen to fetus? How can embryonic cells be protected?

A

Animals will have lower conception rates if animal becomes viremia between conception and 1st 3 weeks of pregnancy. During first 18 days, the zona pellucida can be seen protecting embryonic cells (there are no cotelydons!).

36
Q

If a dam is affected with BVDV during d45-125 of gestation, what can occur? During the last trimester?

A

Abortions are seen generally among 1st trimester, can be expelled, mummified or resorbed.

45-125 d = fetal immunotolerance leading to NCP strains
100-150 d = organogenesis is occurring so infection at this time can lead to microencephaly, cerebellar hypoplasia, and growth retardation

Last trimester - animals could be clinically normal, but also have severe illness during the 1st 10 months of age

37
Q

How does mucosal disease occur? What are the clinical forms and how do they occur? Clinical manifestations of each?

A

Mucosal disease occurs when immunotolerant PIs with NCP BVDV get infected with CP BVDV.

Acute mucosal disease - fatal, chronic, chronic with recovery and delayed onset; this is usually due to a mutation event
- pyrexia, depression, anorexia, and decreased milk production, diarrhea, ptyalism, discharge and oral erosions

Chronic - generally due to external infection with CP form
- lameness, skin and mucosal lesions, anorexia, weight loss, diarrhea, bloat, alopecia, CAN RECOVER if immune response is made

38
Q

What are diagnostics for BVDV? Gold standards?*

A

Immunohistochemistry - post mortem Ag
Virus isolation on live tissues *
Whole blood - acute infections *
Ag capture in blood/milk, or skin

39
Q
Define each of the following: 
Endotoxemia 
Bacteremia 
Septicemia 
Sepsis
SIRS
Severe sepsis 
Septic shock 
MODS
A

Endotoxemia - literally the presence of endotoxins in the blood; when used clinically, implies the presence of clinical signs typically caused by the inflammatory response to circulating endotoxins

Bacteremia - the presence of bacteria in the bloodstream; can occur without clinical signs

Septicemia - systemic disease caused by any circulating microorganisms and/or their products

Sepsis - related to septicemia, clinical evidence of an infection, coupled with its presence of SIRS

SIRS - systemic inflammatory response syndrome which is characterized by alterations in heart rate, respiratory rate, leukogram and body temperature

Severe sepsis - infection + SIRS and evidence of organ dysfunction

Septic shock - the above + acute circulatory failure despite supportive measures

Multiple organ dysfunction syndrome - dysfunction of two or more organs

40
Q

In what ways is the immune system in animals able to recognize patters on molecules that signal potential danger?

A

Damage-associated molecular patterns (DAMPs) which include pathogen-associated molecular patterns (PAMPs) and alarmins (released from damaged tissues)

41
Q

What are some examples of pathogen-associated molecular patterns?

A

LPS, lipoprotein, peptidoglycan, flagellum, lipoteichoic acid, zymosan, viral double-stranded RNA, N-acetyl glucosamine

42
Q

Once LPS enters the bloodstream, it encounters LBP (plasma acute-phase protein), which facilitates binding to the soluble or cell-assoc. co-receptor CD14. This this recruits and activates TLR4 and MD-2, in preparation for LPS signaling. What is the ultimate culmination of this pathway?

A

Translocation to the nucleus of inductively transcription factors including nuclear factor kappa B and activator protein 1. This binds to a promoter or enhancer region on an array of genes whose products are involved in the inflammatory response.

43
Q

What cells are TLR4 found?

A

On cells of both the innate and adaptive immune system: mononuclear phagocytes (of importance pulmonary intravascular macs and Kupffer cells), neutrophils, endothelial cells and dendritic cells

44
Q

Endotoxin-induced NF-kappa B activation in peripheral blood and tissue leukocytes acts via multiple signaling pathways to induce the expression of more than 200 genes. What are some of the things produced?

A
Cytokines: TNF-alpha, IL-1beta, IL-6, IL-8, IL-12 and IL-18 (stimulate IFN-gamma synthesis and secretion from natural killer cells)
Chemokines: IL-8, MIP
Type I IFNs
Procoagulation factors
Adhesion molecules 
Immunoreceptors
Acute phase proteins (fibrinogen)
45
Q

What is a cause for the neutropenia often found in endotoxemia?

A

Neutrophils are sequestered on activated endothelium and aggregate.

46
Q

During sepsis, what is a cellular reason for compromise of microvascular perfusion?

A

Sepsis-associated increase in “stiffness” of both RBCs and WBCs, rendering cells less able to deform and squeeze through narrow capillaries.

47
Q

During sepsis, various hemodynamics combinations may create a systemic imbalance between tissue oxygen supply and demand. What are these?

(5)

A
  1. Hypovolemia - early endotoxemia can see low cardiac output, from arterial vasoconstriction and left ventricular dysfunction related to hypovolemia
  2. Maldistribution perfusion - regional hypoperfusion in the face of rehydration can occur, due to loss of vasoregulatory control to certain vascular beds
  3. Myocardial depression - damage and death of cardiomyocytes can occur due to inflammatory mediators; this is a large reason for death in cases of sepsis
  4. Increased metabolic demand - during SIRS, there is an increased splanchnic and total body oxygen consumption
  5. Impaired oxygen use - mitochondrial dysfunction causes abnormal bioenergetics of cellular extraction and use or respiration
48
Q

Early sepsis shows the development of a self-perpetuating imbalance in the systemic redox state resulting in oxidative stress that is believed to be at the root of SIRS and resultant organ dysfunction in sepsis. How does mitochondrial dysfunction perpetuate this?

A

Mitochondrial dysfunction and oxidative stress can result in tissue dysoxia and organ failure, as well as further stimulate inflammatory response and NF-kappa beta activation = vicious cycle characteristics of SIRS and MODS.

49
Q

What are the three primary mechanisms that contribute to sepsis-associated immunosuppression?

A
  1. Widespread apoptosis death of lymphocytes (particularly B cells and CD4-positive T-helper cells) secondary to activation of intracellular caspases
  2. Dendritic cell loss and dysfunction, leading to inefficient or impaired Ag presentation
  3. Impaired phagocyte chemotaxis and killing responses
50
Q

A prioritized strategy for management of sepsis or endotoxemia has 5 main steps. List and discuss.

A
  1. Cardiovascular resuscitation - expansion of blood volume
  2. Laminitis prevention - (bundle: fluid resuscitation, cryotherapy, Flunixin, pentoxifylline, plasma)
  3. Removal of the cause of sepsis - (mechanical removal of endotoxin source, abx, sequestration of diarrhea, etc)
  4. Neutralization of circulating endotoxins or other PAMPs - (Hyperimmune plasma and serum, polymyxin B)
  5. Inhibition of PAMP-induced inflammation - (NSAIDs, methylxanthine, corticosteroids, heparin, ROS scavengers)