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Small Animal Medicine I > Midterm 3 > Flashcards

Midterm 3 Flashcards

1
Q

Which cell make up the gastric mucosa and what do they secrete?

A
  1. Mucous Cells-lipase and pepsinogen A
  2. Parietal cells-acid, intrinsic factor and pepsinogen A
  3. Chief cells-pepsinogen A
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2
Q

Why is intrinsic factor produced by the parietal cells in stomach mucosa important?

A

Helps digest protein and some fat to produce B12 in dogs ( not cats)

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3
Q

What bacteria are in the gastric flora? What role can these play?

A
  1. Helicobacter spp.
  2. Proteobacteria
  3. Firmicutes

Development of chronic gastritis and neoplasia

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4
Q

What are common clinical signs associated with gastric disease?

A
  1. Vomit
  2. Hematemesis
  3. Melena
  4. Retching/burping
  5. Abdominal dissension/pain
  6. Hypersalivation
  7. Weight loss
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5
Q

What is acute gastritis and how is it caused?

A

The most common gastric disease with acute vomiting due to mucosal irritation. Can be caused by:

  1. Foreign body
  2. Dietary indiscretion
  3. Drugs
  4. Toxins
  5. Systems disease like liver and uremia
  6. Infectious agents
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6
Q

How is chronic gastritis diagnosed?

A

Clinical history with a PE plus CBC and chem panel with abdominal rads

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7
Q

How would you treat an animal with acute gastritis?

A
  1. Fluid therapy
  2. Bland diet for 1-2 days
  3. Acid reducers and Protectants
  4. Possible antiemetic
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8
Q

What two parasites can cause acute gastritis in dogs/cats?

A

In cats, physaloptera spp. And ollulanus tricuspis. IN dogs, physaloptera spp.

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9
Q

A cat has been diagnosed with acute gastritis due to an ollulanus tricuspis parasite, what medication is used to treat?

A

Fenbendazole

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10
Q

A dog presents with acute gastritis including vomiting, retching and was treated with pyrantel pamoate. What was the cause?

A

Physaloptera spp.

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11
Q

What are some causes of gastric ulceration?

A
  1. Metabolic/endocrine disease
  2. Drugs/toxins
  3. Neoplasia
  4. Hypotension
  5. Idiopathic
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12
Q

What is the best way to diagnose a patient with gastric ulcers?

A

Endoscopy

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13
Q

What are the main signs of gastric ulceration?

A
  1. Vomiting
  2. Hematemesis
  3. Melena
  4. Regenerative Anemia
  5. Hypovolemia and dehydration
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14
Q

A dog you suspect as gastric ulcers and the testing reveal low pH and low gastric? What is the likely cause?

A

Mast cell tumor

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15
Q

A dog with a gastrinoma would have what lab values characteristic for the gastric ulcers?

A

Low ph and high gastrin

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16
Q

How are gastric ulcers treated?

A
  1. Fix underlying cause
  2. Fluid therapy
  3. Acid suppression
  4. Barrier protectants
  5. PGE2 analogy like miso pros tall
  6. Antiemetic
  7. Antibiotics if worries about perforation or heliobacter
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17
Q

Which are the two most common prescribed medication for the treatment of gastric ulcers?

Which is preferred?

A
  1. Proton pump inhibitors (omeprazole) to suppress acid production
  2. Histamine-2 receptor antagonists to suppress acid production

Omeprazole

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18
Q

Which species is most likely to suffer from chronic gastritis?

What is the main clinical sign?

A

Dogs

Vomiting

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19
Q

Which cells are found most commonly in the gastric mucosa when chronic gastritis is occurring?

A

Lymphocytes

Plasmocytes

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20
Q

How is chronic gastritis diagnosed?

A

Histopathology Obtained from a biopsy….based on the degree of atrophy, fibrosis or cellular infiltrate in the mucosa along with basal cortisol and TT4 in cats.

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21
Q

Which bacteria is associated with chronic gastritis?

A

Helicobacter spp.

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22
Q

Why is TT4 tested when diagnosing chronic gastritis in cats?

A

To rule out hyperthyroidism due to the similar chronic vomiting and weight loss signs

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23
Q

Why is basal cortisol levels checked when diagnosing chronic gastritis?

A

To rule out Addison’s disease

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24
Q

How is chronic gastritis treated due to helicobacter spp/ treated?

A

Amoxicillin + metronidazole+ famotidine+ bismuth subsalicylate for 2-3 weeks

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25
Q

If a dog is suffering from chronic gastritis and you can’t find a parasitic or helicobacter cause, how do you treat if C/S are mild? What about severe?

A

If mild, treat with a bland diet. If severe, treat with a bland diet and immunosuppressive drugs

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26
Q

How do you know if treatment for heliocbacter spp. Chronic gastritis was successful?

A

60% resolution of C/S and a negative biopsy

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27
Q

If a patient vomits more than 8 hours after eating, what gastric diseases should you think about?

A

Delayed gastric emptying disorders:

  1. Outflow obstruction
  2. Defective propulsion
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28
Q

What are some causes of outflow obstruction of the stomach?

A
  1. Congenital stenosis
  2. Foreign bodies
  3. Hypertrophy of pyloric mucosa
  4. Neoplasia/polyp/granulomas
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29
Q

What are some causes of defective propulsion of the stomach?

A
  1. Gastritis
  2. Ulcers
  3. Neoplasia
  4. Gastroenteritis
  5. Peritonitis
  6. Pancreatitis
  7. Nervous inhibitions
  8. GDV
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30
Q

What gastric motility disorder are brachycephalic breeds predisposed to?

A

Pyloric obstruction from hypertrophic pyloric mucosa

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31
Q

What diagnostic tools are helpful in determining a gastric motility disorder in a patient

A
  1. Rads with a barium series
  2. U/S
  3. Endoscopy with a biopsy
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32
Q

How would you treat a gastric motility disorder?

A
  1. Treat underlying cause
  2. Low fat meals to promote emptying
  3. Prokinetics
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33
Q

Which prokinetics can be used to treat a patient with a gastric motility disorder?

A
  1. Cisapride
  2. Metoclopramide
  3. Erythromycin
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34
Q

How common is gastric neoplasia and what form is most common?

A

Represents less than 1% of tumors with malignant adenocarcinomas the most common

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35
Q

Are malignant or benign gastric neoplasia more common in older dogs and cats?

A

Benign and usually incidental finding at necropsy

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36
Q

How is gastric neoplasia diagnosed?

A
  1. Rads
  2. U/S
  3. Endoscopy and biopsy needed
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37
Q

What are the three forms of gastric adenocarcinomas and which species are these more common?

A
  1. Diffuse
  2. Raised plaque
  3. Polyp

Dogs

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38
Q

In which stomach are gastric adenocarcinomas most likely to be found?

A

The lesser curvature and pyloric region

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39
Q

If there is an gastric adenocarcinomas in a dog’s pyloric region, what may occur?

A

An outflow tract obstruction

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40
Q

Which gastric neoplasia is more common in cats?

A

Lymphoma with metastasis

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41
Q

What disease can predispose a cat to developing gastric lymphoma?

A

Chronic gastritis, SO DONT IGNORE IT !

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42
Q

How is gastric neoplasia treated?

A

Surgical resection unless it is lymphoma. Chemo if it’s lymphoma

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43
Q

How is the prognosis for gastric neoplasia?

A

Poor if malignant and meter with leiomyosarcomas

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44
Q

A mastiff presents with abdominal distention, non productive regurgitation and is in hypovolemic shock. What is he likely suffering from?

A

Gastric dilation and volvulus (GDV)

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45
Q

How is GDV diagnosed?

A

C/S and abdominal radiograph with a displace pyloric on the right side

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46
Q

How is GDV treated?

A
  1. Stabilize patient with fluid therapy, decompression, and drugs to address arrhythmia and VPS
  2. Gastropexy
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47
Q

When working up a GI case, what is included in your minimum database?

A
  1. CBC
  2. Chem penal
  3. Urinalysis
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48
Q

How useful are CBCs in GI disease?

A

Not very unless eosinophilia is detected or anemia

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49
Q

What are the 4 markers of liver dysfunction you want to check on a chem panel when trying to diagnose GI disease?

A
  1. Albumin
  2. Cholesterol
  3. BUN
  4. Glucose
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50
Q

A dog presents with hypoalbuminemia AND hypoglobulinemia…are you suspecting liver dysfunction or GI disease?

A

GI disease manifesting in protein losing enteropathy

Globulin will be normal in kidney and liver disease , but not GI disease/

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51
Q

What is a negative prognostic indicator in chronic enteropathies?

A

Hypoalbuminemia

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52
Q

Which GI disease can show hypocholesterolemia on a chem panel?

A

Lymphangiectasia

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53
Q

When is is common to see secondary mild reactive hepatopathy? In what species?

A

Chronic IBD in cats

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54
Q

How would you rule out pancreatic disease when working up a GI case?

A

Blood chemistry PLI for pancreatitis and TLI for exocrine pancreatic insufficiency

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55
Q

What GI clinical sign can exocrine pancreatic insufficiency cause?

What about pancreatitis?

A

Chronic small bowel diarrhea

Vomiting

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56
Q

Why would you want to test T4 and basal cortisol on blood chemistry when working up a GI case?

A

Hyperthyroidism can cause vomiting and hypoadrenocorticism can cause vomiting, diarrhea, and weight loss

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57
Q

What is the primary manifestation of gastric disease and what will be seen on blood chemistry panel?

A

Vomiting

Hyponatremia
Hypokalemia
Hypochloremia

Loss of hydrochloride acid or bicarbonate

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58
Q

What can blood chemistry values tell you about a patient that has been vomiting?

A

If the patient is in metabolic alkalosis due to the loss of hydrochloric, this is vomit coming from the stomach.

If the patient is in metabolic acidosis , the vomit is coming from the duodenum as chloride and potassium is being lost.

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59
Q

Which diseases can cause a patient to vomit stomach contents versus duodenal and pancreatic fluid contents?

A

Parvoviral enteritis can cause metabolic alkalosis from the loss of stomach fluids.

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60
Q

Which acid base change in more common with a vomiting patient?

A

Metabolic acidosis due to the lost of CL and K from duodenal and pancreatic fluids

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61
Q

If a patient is vomiting and the BUN is elevated, but the creatinine level is not proportional, what is likely occurring?

What if the BUN and creatinine levels are proportional?

A

GI Bleeding

If they are proportional there may be dehydration and/or kidney disease

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62
Q

What is a good way to test for GI bleeding?

A

Fecal occult blood tests, but only helps if the results is negative.

Regenerative anemia leading to micro cystic iron deficiency anemia from chronic blood loss

A high BUN with a creatinine levels that doesn’t match

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63
Q

Is blood chemistry more helpful in cases of gastric disease or enteric disease?

A

Gastric disease…it is less predictable in enteric disease (diarrhea)

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64
Q

What can be seen on a chem panel with a patient with diarrhea?

A
  1. Mild hyperchloremia
  2. Metabolic acidosis
  3. Lactic acidosis if there is hypoperfusion
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65
Q

What are the three things U/S can help us do when working up a GI case?

A
  1. Determine if the GI disease is diffuse or localized.
  2. If the layers are normal? (Is there a loss of layering or thickening of layers)
  3. Where to do a biopsy.
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66
Q

Where is is not possible to use endoscopy to take a biopsy in the GI tract?

A

jejunum

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67
Q

What are the three GI diseases that can be differentiated with U/S?

A
  1. Chronic inflammatory disease
  2. Neoplasia
  3. Infectious diseases
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68
Q

You are performing U/S on the GI system of a cat. There is mild to moderate diffuse transmural thickening of the intestinal wall, but the layering is preserved. What are your differentials?

A
  1. IBD
  2. Lymphoma
  3. Eosinophilia enteritis
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69
Q

No layers are present when you a U/S a dog’s GI tract that has been vomiting. What could cause this to occur?

A
  1. Ulcerative entertitis
  2. Fibrosis
  3. Edema
  4. Severe lymphoplasmacytic infiltration
  5. Adenocarcinoma
  6. Lymphoma
  7. Fungal infection
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70
Q

On U/S, you observe con central loss of layering in the GI tract of cat. What is on your differential list?

A

Lymphoma

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71
Q

What would leiomyosarcoma look like on U/S of the GI tract?

A

Eccentric loss of layering with the wall not uniform any affecting in cross section

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72
Q

Transmural loss With thinking of different layers on GI U/S may indicated which diseases?

A
  1. IBD
  2. Lymphoma
  3. Eosinophilia enteritis
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73
Q

On GI U/S, you see hyperechoic striations that are parallel to each other, but perpendicular to the long axis of the intestine…which GI disease present like this?

A

Lymphangiectasia

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74
Q

What occurs in the intestine in order to create hyperechoic striations on GI U/S?

A
  1. Abdominal effusion
  2. Intestinal thickening
  3. Hyperechoic mucosa
  4. Wall corrugation

Which can all occur with lymphangiectasia

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75
Q

A neoplasitic mass in a dogs GI tract will most likely present as what on U/S?

A

Focal thickening especially if it is greater than 3 mm with a loss of layering

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76
Q

What type of patient is most likely to be diagnosed with GI leiomyosarcoma?

A

OLDER CATS

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77
Q

When performing a fecal exam, what is recommended and why?

A

Centrifugation to decrease false negatives

Not recommended to do fecal smears as there is high false negatives

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78
Q

How could you diagnose giardiasis?

A
  1. ZnSO4 fecal flotatation with 3 samples
  2. Gold standard IFA
    ELISA
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79
Q

Why is an IFA the gold standard for diagnosing giardia over a ELISA or fecal float?

A

Greater than 90% sensitivity and specificity. ELISA only has a high specificity and fecal floats only have a high sensitivity.

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80
Q

What is the best diagnosis technique for cryptosporidium in GI Disease? Why?

A

Enzyme immunoassay

90% sensitivity with one sample

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81
Q

How is tritrichomonas fetus diagnosed?

A

PCR

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82
Q

How is campylobacter diagnosed?

A

Culture/PCR -BEST

Or

Direct smear (doesn’t differentiate between pathogenic and nonpathogenic strains)

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83
Q

How is Clostridium perfringes and C. Difficile diagnosed?

A

ELISA detection of toxins

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84
Q

How is adherent and invasive E. Coli diagnosed?

A

Colonic biopsy with fluorescent in situation hybridization

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85
Q

How is histoplasmosis capsulatum diagnosed?

A
  1. Rectal scraping
  2. Colic mucosal biopsy with imprint cytology
  3. Histopath
  4. Quantitative Antigen EIA
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86
Q

How is Pythium diagnosed?

A

Serology using Immunoblot and ELISA

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87
Q

What tests can be used to determine the function of the small intestine and the bacterial population?

A

Cobalamin and folate

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88
Q

Are cobalamin and folate water or fat soluble?

A

Water

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89
Q

How is cobalamin absorbed?

A

it is complexed to R-proteins in the stomach, intrinsic factor in the duodenum, and then bound to cobalamin receptors in the ileum for absorption into the blood stream where is undergoes enterohepatic cycling

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90
Q

How intrinsic factor made in dogs/cats?

A

Dogs: Parietal cells in stomach along with pancreas
Cats: pancreas only

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91
Q

Low cobalamin may indicate ___________ disease because it can’t be absorbed.

A

Small intestinal disease (Ileum ) or gastric disease if the partial cells are damaged and not producing intrinsic factor or pancreatic disease if it cant produce intrinsic factor.

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92
Q

What can decoupled cobalamin from intrinsic factor and lead to low cobalamin levels?

A

Clostridium and other intestinal bacteria

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93
Q

What part of the GI tract contains more bacteria that compete with cobalamin for intrinsic factor binding?

A

Distal GI tract

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94
Q

Dogs with chronic enteropathies often have _______ __________

A

Low cobalamin

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95
Q

What is folate and where is it found?

A

Vit B9 in offal, leafy vegetables and supplements in animals diets and synthesized by some GI bacteria

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96
Q

How is folate absorbed into the body?

A

It is absorbed in the duodenum, before cobalamin is absorbed. It is in a polyglutamate form in the stomach before deconjugated in the duodenum where receptors absorb the monoglutamate form.

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97
Q

Why can’t folate monoglutamate be absorbed in the ileum or large intestines?

A

There are no receptors

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98
Q

Which bacterial flora is more able to synthesize folate? What does this do?

A

Large intestinal flora and does nothing because it can’t be absorbed there.

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99
Q

What is occurring to diets these days that is making folate levels less diagnostic?

A

Diets are changing to include lactobacilli which is a large intestinal bacteria capable of synthesizing folate which increased folate availability and serum folate numbers. Small intestinal bacterial overgrowth of Large intestinal bacteria used to increase folate levels in abnormal patients, but now normal patients can have high folate levels too.

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100
Q

Is a serum folate test more useful when it is high or low?

A

Low, because new diets contain lactobacilli which can synthesize folate in the small intestine and increased it’s availability.

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101
Q

A dog presents with low serum folate and low cobalamin, what does this suggest?

A

Severe small intestinal disease and justifies a biopsy

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102
Q

What are some examples of severe small intestinal disease that could cause low folate and cobalamin levels?

A

IBD
LSA
Lymphangectasia
Short Bowel syndrome

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103
Q

If a patient has low cobalamin and normal folate levels, what does this suggest?

A
  1. Infiltration or structural Ileum SI disease
  2. Clostridial bacterial overgrowth
  3. Exocrine pancreatic insufficiency (cats)
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104
Q

If a patient has low cobalamin and high folate levels, what does this suggest?

A
  1. SIBO secondary to diffuse SI mucosal disease

2. Ileal disease if cobalamin is extremely low

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105
Q

If a patient has high cobalamin levels and normal folate levels, what does this suggest?

A

Unknown, possibly coprophagia

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106
Q

If a patient has high cobalamin and high folate levels, what may this suggest?

A

Intestinal dysbiosis
Iatrogenic
Coprophagia

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107
Q

What is the hallmark of protein losing enteropathy?

A

Panhypoproteinemia

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108
Q

What can cause hypoalbuminemia?

A
  1. Low production in the liver
  2. Excessive loss at the kidney
  3. Excessive loss in the intestines
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109
Q

Why can’t the protein be measured in the feces?

A

Protein is digested that is lost into the gut and most protein in the feces is from bacteria

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110
Q

How are protein losing enteropathies diagnosed?

A

If before the development of hypoalbuminemia, need to use a1-proteinase inhibitor. If hypoalbuminemia has developed, it s straight forward.

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111
Q

What is a1-proteinase inhibitor?

A

A component of plasma proteins that is the same size/charge as albumin that is resistant to degradation by digestive and bacterial protease in feces and can be detected by immunoassay methods.

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112
Q

What does a high a1-proteinase inhibitor tell us?

A

Suggests protein losing enteropathy in the absence of GI bleeding

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113
Q

When should you consider using a1-proteinase inhibitor immunoassay tests?

A

When you suspect a protein losing enteropathy, there is no GI bleeding, and there the patient is a breed predisposition

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114
Q

Which breeds are predisposed to protein losing enteropathies?

A
  1. Rottweiler
  2. Yorkshire terrier
  3. Wheaten terrier
  4. Norwegian lundehund
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115
Q

What are the four principle of a good oral exam?

A
  1. Sedation/anesthesia
  2. Endotracheal tube
  3. Gentle, but firm manipulation of tissue
  4. Appropriate speculum use
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116
Q

What are contact ulcers?

A

Also called kissing ulcers, they form opposite of severe periodontal disease

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117
Q

How are contact ulcers treated?

A

Dental prophy and extraction with analgesia and antibiotics (Clavamox, clindimyocin)

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118
Q

What is juvenile hyperplastic gingivitis and how is it treated?

A

Occurs in cats and they present with enlarged and inflamed gingiva only. Treatment with a gingivoplasty with hitopath, dental prophy, and brushing with azithromycin toothpaste

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119
Q

This disease may be caused by a herpes or calici virus in cats and involves inflammation of the gingiva with increased immunoglobulins on lab work. What is it?

A

Stomatitis

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120
Q

How is stomatitis in cats treated?

A
  1. Dental prophy/extractions
  2. Pain meds
  3. Antiinflammatories
  4. Immunosuppressives
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121
Q

A young female cat presents to you with lesions of the oral mucosa, lips and skin. You take a biopsy and there are eosinophilia infiltrates on histopath…what is the likely disease?

A

Eosinophilia granuloma complex

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122
Q

What can cause eosinophilia granuloma complex and how is it treated?

A

Insect bites and environment/food allergies

Treated with prednisone and sometimes surgery

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123
Q

What are common autoimmune oral disease that can affect animals?

A
  1. Lupus erythematosis

2. Pemphigus

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124
Q

How would you diagnose a disease that presents as oral ulceration to the mucocutaneous junction?

A

Biopsy

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125
Q

What causes erythema multiforma of the oral cavity?

A

It is an hypersensitivity reactions involving immune complex deposition secondary to infectious or toxic exposure

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126
Q

What causes toxic epidermal necrolysis of the oral cavity?

A

Severe Hypersensitivity reaction to a drug

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127
Q

How is erythema multiforme and toxic epidermal necrolysis treated?

A

Removed the drug, toxin, or infectious agents, add immune suppressive drugs or anti-inflammatories

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128
Q

What can uremic vasculitis and thrombosis lead to?

A

Uremic ulceration and necrosis of the oral cavity?

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129
Q

How are uremic ulcerations in the oral cavity treated?

A

Resolve the underlying disease, give pain medications, and oral antiseptic rinses

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130
Q

A dog presents with halitosis, decreased appetite, and is pawing at his face. What is your first step?

A
  1. Put the dog under anesthesia and do an oral exam looking for a foreign body
  2. Remove the object
  3. Culture and give antibiotics
  4. Pain medications
  5. Nutritional support
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131
Q

What types oral burns can occur in animals?

A
  1. Electrical
  2. Thermal
  3. Chemical
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132
Q

How are oral burns treated?

A

Treat as wounds with topical therapy, wound debridement and a feeding tube until healed

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133
Q

A dog presents with muscle atrophy of the Massecer, temporalis and pterygoid muscles. What may be going on?

A

Chronic stage of mastication muscle myosin is where the immune system attacks 2M muscle fibers.

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134
Q

How long does the acute stage of masticatory muscle myositis last?

A

2-3 weeks followed by a latent stage where they appear normal..very painful

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135
Q

How is masticatory muscle myositis diagnosed?

A

2M antibody titers > 1:100
And
Muscle biopsy

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136
Q

How is masticatory muscle myositis treated?

A
  1. Corticosteroids
  2. Recheck titers
  3. May relapse
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137
Q

What is a sialocele? how is it treated?

A

Extravasation of saliva into surrounding tissue

Surgery-marsupulization and sialoectomy

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138
Q

What is sialadentitis? Which gland is most commonly affected?

A

Inflammation of the salivary gland caused by sialoliths.

Zygomatic

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139
Q

A older dog presents as febrile, lethargic, dysphasia, and has difficulty opening mouth with a swollen zygomatic salivary gland, what is it?

A

Sialadentitis

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140
Q

How is sialadentitis diagnosed?

A
  1. CT scan
  2. Aspirate with incisional biopsy
  3. Culture/sensitivity
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141
Q

How is sialadentitis treated?

A
  1. Intraoral drainage of mucopurulent discharge
  2. Anti-inflammatories
  3. Pain medications
  4. Antibiotics
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142
Q

What is sialadentitis?

A

Non inflammatory enlargement of salivary gland with no cytological or histopathological abnormalities

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143
Q

What is necrotizing sialometaplasia?

A

Painful enlargement of the salivary gland with squamous metaplasia

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144
Q

What is the signalment for sialadenosis and necrotizing sialometaplasia?

A

Young-middle aged small breed dogs

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145
Q

What causes sialadenosis and necrotizing sialometaplasia?

A

Vagus nerve neurogenic disease and/or concurrent esophageal disease

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146
Q

How is sialadenosis and necrotizing sialometaplasia treated?

A

oral phenobarbital

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147
Q

A dog presents with a decreased ability to open jaw and on radiographs you see boy proliferation in the region of the TMJ, what is at the top of your differential list?

A

Craniomandibular osteopathy

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148
Q

How is craniomandibular osteopathy treated?

A

Anti-inflammatories
Pain medicinal
Nutritional support

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149
Q

List benign oral tumors in small animals:

A
  1. Papilloma
  2. Peripheral odontogenic fibromas
  3. Ameloblastoma
  4. Odontoma
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150
Q

List malignant oral tumors in small animals:

A
  1. Melanoma
  2. Squamous cell carcinoma
  3. Fibrosarcoma
  4. Osteosarcoma
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151
Q

A dog <1 year presents with a nodule in the oral cavity that self resolves in a few month..what was it?

A

Papilloma that was virus induced

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152
Q

In what species are peripheral odontogenic fibromas common? What types are there?

A

Dogs

Ossifying and fibromatous

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153
Q

How are peripheral odontogenic fibromas treated?

A

Surgical resection

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154
Q

This oral tumor arises from the cells that produce enamel, the treatment is surgical excision, and it is locally invasive, but not likely to metastasize…what is it?

A

Ameloblastoma

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155
Q

What is an odontoma?

A

A benign oral tumor that is a conglomeration of normal cells treated with surgical removal

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156
Q

True or False: Oral melanomas can be pigmented or non-pigmented (amelanotic)?

A

True

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157
Q

This oral tumor is malignant, affects older dogs and cats, is highly metastatic and is characterized as proliferative and ulcerative with body invasion common….what is it?

A

Squamous cell carcinoma

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158
Q

What is the second most common oral tumor in cats and third most common in dogs..affecting young large breed dogs and older small breed dogs the most?

A

Fibrosarcoma

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159
Q

What parts of the oral cavity does osteosarcoma invade?

A

Mandible (27%)

Maxilla (22%)

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160
Q

True or false:

Distant metastasis is more common in oral osteosarcoma than with the appendicular form.

A

False: the appendicular form has more distant metastasis involved

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161
Q

How are oral tumors diagnosed?

A
  1. Cytology or histopathology
  2. Thoracic RADs or CT
  3. Lymph node aspirates and biopsy
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162
Q

Why is histopathology needed when diagnosing an oral tumors?

A

For grading

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163
Q

What treatment option is common for all malignant oral tumors?

Which tumors can you not use chemotherapy on?

A

Surgical excision and radiation

Squamous cell carcinoma

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164
Q

Which malignant oral tumor can you use COX-2 inhibitors to treat?

A

Squamous cell carcinoma

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165
Q

Which malignant oral tumor has a vaccine for treatment/prevention?

A

Melanoma

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166
Q

True or false: THe mitosis index in oral melanoma in dogs is highly predictable.

A

True

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167
Q

If the mitosis index for oral melanoma in dogs is less than three, how long can the dog survive?

What bout greater than 3

A

26 months

7 months

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168
Q

Which malignant oral tumor has the highest survival rate? The lowest?

A

Highest is Fibrosarcoma

Lowest is Squamous cell carcinoma

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169
Q

What are the four phases of swallowing?

A
  1. Oral preparatory
  2. Oral
  3. Pharyngeal
  4. Esophageal
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170
Q

Which cranial nerves are located in the pharyngeal area?

A
  1. Trigeminal
  2. Facial
  3. Vagus
  4. Glossopharyngeal
  5. Hypoglossal
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171
Q

What are the species differences with the esophagus?

A

Dog: Striated muscle
Cat: 2/3 striated/ 1/3 smooth muscle

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172
Q

How would you differentiate between oropharyngeal and esophageal disease?

A

OPD: Repetitive swallowing, gagging, retching, and nasopharyngeal reflux

Esophageal: Regurgitation, odynophagia, and excessive salivation

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173
Q

What is the signalment for oralpharngeal disease?

A

Puppies with cleft palates, ciricopharyngeal dysphagia, or muscular dystrophy

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174
Q

What is the signalment for esophageal disease?

A

German Shepard, Great Dane, Labrador, and Siamese cats for congenital megaesophagus

Large breed adult dogs for acquired megaesophagus

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175
Q

What are some good tests to do to determine oral pharyngeal or esophageal disease?

A
  1. Anesthetize oral/laryngeal exam
  2. Neuro exam
  3. Feed and watch patient eat
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176
Q

What is the most helpful parameters when you run cbc, chem and urinalysis to diagnose esophageal or oropharagneal disease?

A
  1. CK

2. Electrolytes

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177
Q

Why would you want to give an acetylcholine antibody titers in a dog that you think has esophageal disease?

A

Acquired myasthenia gravis causing megaesophagus

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178
Q

What laboratory tests other than a cbc, chem and urinalysis should you perform is you suspect oralpharengeal/esophageal disease?

A
  1. Thyroid function
  2. 2M titers
  3. Muscle biopsy
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179
Q

What can cause pharyngitis?

A
  1. Foreign body
  2. Masses
  3. Infectious diseases
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180
Q

How would you diagnose pharyngeal weakness?

A

Look for morphological or neuro causes via lab work, radiographs and a swallow study

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181
Q

What are the two types of cricopharyngeal dysphagia and is this a oropharyngeal disease or esophageal disease?

A
  1. Achalasia
  2. Asynchrony

It is a esophageal disorder

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182
Q

How would you treat the achalasia form of cricopharyngeal dysphagia?

A

Myotomy or myectomy of the cricopharyngeal muscle

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183
Q

What can act as a temporary solution to the treatment of asynchrony cricopharyngeal dysphagia?

A

Botulinum toxin

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184
Q

What is the most common cause of esophagitis?

A

Reflux during anesthesia

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185
Q

What is the best method to diagnose esophagitis?

A

Esophagoscope with a biopsy

Do some thoracic rads to make sure there isn’t aspiration pneumonia

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186
Q

How is esophagitis treated and was an occur if treatment is not successful?

A
  1. Treat underlying cause
  2. If mild, feed low-fat diet to promote gastric emptying
  3. If moderate to severe, give proton pump inhibitors to decrease acid production, sucralfate and prokinetic

Esophageal stricture can occur and may take weeks for C/S to resolve

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187
Q

What is the treatment of choice for a esophageal stricture?

A

Balloon dilation twice 3-5 days apart with triamicinolone injected to reduce inflammation

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188
Q

Where are the most common places for a foreign body to lodge in the esophagus?

A
  1. Thoracic inlet
  2. Heart base
  3. Diaphragm
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189
Q

How would a foreign body in the esophagus be diagnosed?

A

Radiography with NO BARIUM

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190
Q

What is the most common cause of a vascular ring anomaly in the esophagus?

A

Persistent right aortic arch with entrapment of esophagus by the ligamentum areriosum

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191
Q

Which breeds of dogs are predisposed to vascular ring anomalies?

A
  1. German Shepards

2. Irish setters

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192
Q

When do clinical signs of a vascular ring anomaly occur?

A

At the time of weaning and can lead to aspiration pneumonia due to regurgitation

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193
Q

How are vascular ring anomalies diagnosed?

A
  1. Radiographs with or w/o contrast

2. Esophagoscope

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194
Q

How are vascular ring anomalies treated?

A
  1. Surgical transaction of ligamentum arteriosum
  2. Management concurrent disease
  3. Balloon dilation of esophagus if needed
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195
Q

A dog has esophageal neoplasia, what type is it most likely to be?

A

Fibrosarcoma or osteosarcoma

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196
Q

A patient present with esophageal neoplasia and after biopsy, you determine is is squamous cell carcinoma…what species is this patient?

A

CAT

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197
Q

What are the types of esophageal neoplasia that can occur?

A
  1. Primary
  2. Peri-esophageal
  3. Metastasis
  4. Granuloma
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198
Q

The clinical signs of esophageal neoplasia are similar to the clinical sign of ________.

A

Esophageal obstruction

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199
Q

How would you treat esophageal neoplasia?

A
  1. Chemo
  2. Radiation
  3. Surgery
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200
Q

How is spirochete lupi treated in the esophagus?

A

Doramectin

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201
Q

A dog presents with a circumscribed sacculation of the esophagus after a foreign body was removed….what is it?

A

An esophageal diverticula

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1
Not at all
2
3
4
5
Perfectly
202
Q

How are esophageal diverticulas diagnosed?

A

Contrast radiographs or endoscopy

203
Q

How are esophageal diverticulas treated?

A
  1. Treat underlying cause
  2. Diverticulectomy
  3. Feeding tube
204
Q

When diagnosing an esophageal fistula, what must you do?

A

An esophageal with non-iodinated contract agents

205
Q

What are the clinical signs of a esophageal fistula?

A
  1. Coughing
  2. Dyspnea
  3. Pneumonia
206
Q

How are esophageal fistula treated?

A

Surgical excision

207
Q

what are the causes of acquired megaesophagus?

A
  1. Idiopathic
  2. Esophagitis
  3. Lead toxicity
  4. Hypoadrenocorticism
  5. Myasthenia gravis
208
Q

What are the clinical signs of megaesophagus?

A
  1. Regurgitation

2. Aspiration pneumonia

209
Q

How is megaesophagus diagnosed?

A
  1. Thoracic radiographs ( possibly with contrast)
  2. Esophagoscopy
  3. Check for myasthenia gravis with a acetylcholine Ab titers, hypoadrenocoriticism with basal cortisol levels, lead levels, and TT4 for hypothyroidism (however, a study showed it was not associated)
210
Q

How is megaesophagus treated if treating the underlying cause doesn’t work?

A

Small, frequent meals in an upright position

Gastrostomy tube

211
Q

What are the clinical signs of a hiatal hernia and how diagnose and treat it?

A

C/S: Regurgitation, vomiting, hypersalivation, esophagitis and dysmotilty

Radiographs with contrast , swallow study, and esophagoscopy

Surgery

212
Q

What is gastroesophageal reflux, how is it caused and what can it result in?

A

Reflux of stomach contents in to the esophagus due to los of tone of the lower esophageal sphincter and can result in chronic esophagitis

213
Q

Why would gastroesophageal reflux occur..what can cause loss of tone to the lower esophageal sphincter?

A
  1. Hiatal hernia
  2. Anesthesia
  3. Chronic vomiting
214
Q

What the clinical signs of gastroesophageal reflux and how is it diagnosed?

A

Regurgitation, odynopagia, excessive salivation

Diagnosed via a good history ( are the C/S occuring more at night?), esophagoscopy and a pH/impedance test

215
Q

How is gastroesophageal reflux treated?

A
  1. Proton pump inhibitors
  2. Sucralfate
  3. Prokinetics
  4. Low fat diet
216
Q

What cells are infected by canine parvovirus?

A

Rapidly dividing cells:

  1. Intestinal epithelial crypt cells
  2. Bone marrow
217
Q

What are the clinical signs of canine parvovirus?

A
  1. Vomit
  2. Diarrhea ( possibly hemorrhagic)
  3. Inappetence
  4. CNS signs
  5. Cardiac signs
218
Q

What age of dog will have the most severe clinical signs from parvovirus?

A

<12 weeks with no prior immunity

219
Q

What is the indication for using sulfasalazine/olsalazine?

A

These are antidiarrheals that inhibit the synthesis of prostaglandin and used in colonic IBD

220
Q

What is loperamide an what is it used for ?

A

It is an opioid agonist antidiarrheal that increases smooth muscle contractions which increases absorption of fluid and used for acute diarrhea

221
Q

What is cisapride used for?

A

It is a oral antiemetic and a prokinetics, used in ileus

222
Q

What is the function of ondansetron/dolasteron?

A

Very effective antiemetics

223
Q

What are the clinical signs of feline panluekopenia virus?

A
  1. Vomiting
  2. Diarrhea
  3. Fever
  4. Depression
  5. Anorexia
  6. Cerebellar signs
  7. Acute death
224
Q

How is feline panleukopenia virus diagnosed?

A

ELISA antigen test for canine parvovirus

225
Q

How is feline panluekopenia infection treatment?

A

Supportive care (similar to canine parvovirus) with fluid therapy, nutritional therapy, antiemetics, and electrolyte supplements..sometimes antibiotics

226
Q

This disease occurs in young puppies, is transmitted fecal-oral, replicates in intestinal epithelial cells, and causes vomiting and small intestinal diarrhea, but more mild compared to canine parvovirus?

A

Canine enteric coronavirus infection

227
Q

How is canine enteric coronavirus diagnosed?

A

Fecal RT-PCR

228
Q

Which disease in cats is characterized by the sequele dry and wet form with pyogranulomatous masses in the ileocecolcolic junction and colon?

A

Feline Enteric coronavirus infection

229
Q

What species and age is affected by tritrichomonas fetus and how is it diagnosed?

A

Young cats in crowded environments and diagnosed via culture or PCR of feces

230
Q

How is tritrichomonas fetus treated?

A

Ronidazole

231
Q

Where does tritrichomonas foetus infect and what clinical signs does it cause?

A

Distal ileum and colon resulting in chronic intermittent large bowel, malodorous diarrhea with blood and mucus

232
Q

What Protozoa infect pigs and non-human primates and causes chronic hemorrhagic colitis?

A

Balantidium coli

233
Q

How is balantidium coli treated and what is it usually coinfected with?

A

Tetracycline and metronidazole

Trichuris spp.

234
Q

Which Protozoa infects puppies and kittens with common spontaneous recovery, but treated with suladimethoxine if not?

A

Isospora spp.

235
Q

What is a common cause of mixed bowel diarrhea in dogs and is diagnosed with zinc sulfate fecal flotations or fecal antigen tests?

A

Giardia spp.

236
Q

How is giardia spp. Treated?

A

Metronidazole

Fenbendazole

237
Q

Where does cryptosporidium spp. Reside and what clinical signs does it cause?

A

In the small intestine of dogs/dats that causes small bowel diarrhea

238
Q

How is cryptosporidium spp. Treated and why is it important to treat?

A
  1. High digestible diets
  2. Macrolides

It is zoonotic

239
Q

What are the signs of acute colitis and how it is treated?

A

Sudden onset of explosive watery diarrhea with signs of large bowel disease

Treated with fluid therapy, metronidazole and a 24 hours fast followed by highly digestible low fat diets for a few days

240
Q

What can cause typhlitis?

A

Inflammatory disease of the ileum or colon associated with IBD

241
Q

What is the best way for diagnoseding typhlitis?

A

Ultrasound and endoscopy

242
Q

How is typhlitis treated?

A

Treat IBD and do surgery if there is an obstruction, neoplasia, abscess, or neoplasia

243
Q

What are the clinical signs of anal sacculitis?

A
  1. Itching/biting perineum
  2. Tail chasing
  3. Scooting
  4. Dyschezia
  5. Tenesmus
244
Q

What is the diagnostic test of choice for anal sacculitis?

A

Digital rectal exam and helps rule out an anal sac tumor

245
Q

What is the treatment of an anal sac impaction?

A
  1. Removal of contents
  2. Topical Glucocorticoid/antibiotic
  3. Frequent fecal evacution for a couple weeks
246
Q

How is anal sacculitis treated?

A
  1. Flush with dilute chlorhexidine
  2. Instill glucocorticoid/ antibiotic
  3. Systemic antibiotics
247
Q

What breed of dog is at higher risk for personal fistulas/anal forunculosis?

A

German Shepards

248
Q

What parts of the body may be affected by a perianal fistula?

A
  1. Anal sac
  2. Circumstances glands
  3. External anal sphincter
249
Q

What may occupancy perianal fistulas?

A

Colitis

250
Q

What are the differentials for perianal fistulas?

A
  1. Anal sacculitis

2. Perineal tumors

251
Q

How are perianal fistulas treated?

A

Cyclosporine and a biopsy is not needed

252
Q

What are the different types of antimicrobial-responsive diarrheas?

A
  1. Small intestinal bacterial overgrowth (SIBO)
  2. Idiopathic antibiotic-responsive diarrhea
  3. Tylosin-responsive diarrhea
  4. Camphylobacter spp.
  5. Clostridium dificile
  6. Clostridium perfringens
  7. Enterohemorrhagic E. Coli
  8. Enteropathogenic E. coli
  9. Salmonella spp.
  10. Yersinia enterocolitica
  11. Brachyspira pilosicoli
253
Q

How does SIBO occur?

A

When there is an increase in total number of bacteria in the small intestinal tract during a fast and usually secondary to other diseases

254
Q

What can SIBO cause in a patient?

A
  1. Malabsorption
  2. Decreased water absorption
  3. Increased membrane permeability
  4. Deconjugation of bile acids
  5. Enzyme dysfunction
  6. Increased secretion of colonocytes
255
Q

T/F: A high folate level and low cobalamin may support the presence of SIBO

A

True

256
Q

What breed of dog is at risk for idiopathic antibiotic-responsive diarrhea?

A

Young German Shepards

257
Q

What are common clinical signs of idiopathic antibiotic-responsive diarrhea?

A
  1. Small bowel diarrhea
  2. Weight loss
  3. Vomiting
  4. Polyphagia
  5. Gas and abdominal discomfort
258
Q

How is idiopathic antibiotic-responsive diarrhea treated?

A

Doxycycline
Metronidazole
Highly digestible diets

259
Q

What antimicrobial-responsive diarrhea is treated with macrolides due to it being a gram 1 bacteria and is characterized by mild to blood diarrhea with fever, inappetance, and vomiting?

A

Camphylobacter spp.

260
Q

What gram positive bacteria infects the GI tract of dogs and cats and causes diarrhea from the toxins it creates?

A

Clostridium dificile

261
Q

How is clostridium dificile antibiotic responsive diarrhea treated compared to clostridium perfringens?

A

Metronidazole for C. Dificile

Aminopenicillins, macrolides and metronidazole for C. Perfringens

262
Q

Which bacteria are found in normal GI flora of dogs/ cats, but can cause disease if the right conditions are met?

A
  1. Camphylobacter spp.
  2. C. Dificile
  3. C. Perfringens
  4. Salmonella spp.
  5. Yersinia enterocolitica
263
Q

Which GI bacteria is found in greater numbers in greyhounds and causes bloodying diarrhea with a hemolytic-uremic syndrome from infecting the kidney?

A

Enterohemorrhagic E. coli

264
Q

What toxin is released by enterohemorrhagic E. coli in the GI tract that causes bloody diarrhea?

A

Shiga-like toxin

265
Q

Which bacteria attaches to the intestinal epithelial cells and injects bacterial products causing diarrhea that is not shiva-like toxin?

A

Enteropathogenic E. Coli

266
Q

What its the difference in treatment between enterohemorrhagic E. Coli an enteropathogenic E. Coli infections in the GI tract?

A

Both require supportive care, but you can use antibiotics with enteropathogenic E. Coli infections

267
Q

This gram - bacteria causes disease through th ingestion of raw or undercooked meat and is characterized by neutrophil influx into the intestinal tract leading to leukopenia…what is it?

A

Salmonella spp.

268
Q

What are the clinical signs of salmonella spp. Antimicrobial-responsive diarrhea?

A
  1. Mixed small/large bowel diarrhea

2. Systemic illness with shock and even death

269
Q

How is salmonella spp. Antimicrobial-responsive diarrhea diagnosed and treated?

A

Fecal or extraintestinal site culture
PCR

Treat with supportive care and antibiotics

270
Q

What type of diarrhea is caused by yersinia enterocolitica?

A

Bloody

271
Q

What bacteria is a spirochete that attaches to cecal and colonic epithelial cells and found in the diarrhea of dogs?

A

Brachyspira pilosicoli

272
Q

What is the blood supply to the intestines?

A

Artery: Cranial and caudal mesenteric branches of the celiac artery

Vein: Portal vein via the cranial and caudal mesenteric veins

273
Q

Where does the small intestine begins and end?

A

Begin: Pyloric antrum
End: Ileocecocolic junction

274
Q

Where do the common bile duct and major pancreatic duct enter?

A

The proximal duodenum at the duodenal papilla

275
Q

Where do the lacteals of the small intestinal vill drain?

A
  1. Mesenteric lymphatic and nodes
  2. Cisterns chyli
  3. Thoracic duct
276
Q

Where does lymph rom the colon drain?

A
  1. Colic nodes
  2. Cisterna chyli
  3. Thoracic duct
277
Q

How does parasympathetic inner action reach the enteric nervous system?

A

Vagus nerve: small intestine and proximal colon

Pelvic nerve: Distal colon

278
Q

How does sympathetic innervation reach the GI tract?

A

Sympathetic trunk

279
Q

Hw long does it take for a crypt cell i the GI tract to reach death and exfoliation?

A

3-5 days

280
Q

When should you recommend more diagnostics in the form of imaging and biopsies in animals with GI disease instead of a diet/treatment trials?

A
  1. Severe vomiting
  2. Weight loss
  3. Severe PLE
  4. Severe malabsorption
281
Q

What type of diet should be fed in acute, self-limiting GI diseases like pancreatitis, dietary indiscretion and parvovirus?

A

Highly digestible low fat

282
Q

What type of diet should be fed animals with lymphangiectasia?

A

Low fat

283
Q

What are the characteristics of gastrointestinal diets?

A
  1. High digestibility
  2. Moderate protein level
  3. Low fat
284
Q

Which cell of the pancreas secrete digestive enzymes, intrinsic factor, and pancreatic secretory trypsin inhibitor?

A

Acinar cells

285
Q

What do the ductal cells of the exocrine pancreas secrete?

A

Bicarbonate and fluid

286
Q

What is the purpose the the bicarbonate and fluid release from the pancreas?

A

To neutralize gastric acid in duodenum and provide an optimum pH for digestive enzymes

287
Q

Wha is the function of trypsinogen?

A

Precursor to trypsin, a major proteolytic enzyme from the pancreas

288
Q

What is the precursor to cymotrypsin, a proteolytic enzyme?

A

Chymotrypsinogen

289
Q

What is the function of elastase?

A

It is a pancreatic enzyme secreted by acinar cells that degrades elastin

290
Q

What pancreatic digestive enzyme hydrolyzes starch molecules to di and trisaccharides and small branch polysacccharides?

A

Amylase

291
Q

What is the function of lipase?

A

It is a pancreatic digestive enzyme that hydrolysis triglycerides to FFA and monoglycerides

292
Q

What is the function of gelatinase?

A

It is a pancreatic digestive enzyme that degrades collagen and gelatin

293
Q

What is a zymogen?

A

The inactive pecursor of proteolytic enzymes trypsinogen and chymotrypsinogen that protect the pancreas against autodigestion

294
Q

Other than zymogens, how else does the pancreas protect itself from autodigestion my proteolytic enzymes?

A
  1. Pancreatic secretory Trypsin inhibitor

2. Serine proteinase Inhibitors (SERPIN)

295
Q

What is the function of pancreatic secretory trypsin inhibitor?

A

It inhibits any trypsinogen that becomes activated within the cell

296
Q

What substance targets neutrophil elastase and inhibits trypsin released into the interstitium of the pancreas preventing local damage?

A

a1-proteinase inhibitor, a serine proteinase inhibitor

297
Q

What is Cholecystokinin?

A

Substance that is stimulated by fat and protein in the stomach and secreted in the duodenal mucosa where it increases the release of digestive enzymes from the pancreas.

298
Q

What substance is synthesized from the duodenal mucosa in response to low pH in the stomach and increases bicarbonate and fluid production from the pancreas?

A

Secretin

299
Q

What is gastrin?

A

A substance released from the gastric mucosa in response to distension which increases the release of pancreatic digestive enzymes.

300
Q

How are pancreatic enzyme secretion increased by the nervous system?

A

Parasympathetic stimulation of the vagus nerve stimulates cholinergic fibers which increase enzyme secretion

301
Q

How are pancreatic enzyme seretions down regulated?

A
  1. Somatostatin

2. Small Intestinal negative feedback

302
Q

How does somatostatin down regulate pancreatic enzymes?

A

It inhibits CCK and secretin effects

303
Q

What are the phases of pancreatic enzyme secretion?

A
  1. Cephalic phase: vagal cholinergic input from sight/smell of food
  2. Gastric phase: gastrin stimulates enzyme secretion
  3. Intestinal phase: food enters sm. intestines and secretin and CCK is secreted
304
Q

What are the four main pancreatic diseases that affect small animals?

A
  1. Acute pancreatitis
  2. Chronic pancreatitis
  3. Pancreatic adenocarcinoma
  4. Exocrine Pancreatic insufficiency
305
Q

What tests can be used to determine if there is pancreatitis?

A
  1. Pancreatic lipase assays

2. Serum trypsin/trypsinogen

306
Q

Why is using the traditional method of diagnosing pancreatitis not the best way to do it anymore?

A

Measuring serum amylase and lipase activity has poor sensitivity and specificity as it is dependent on renal clearance and lipase can originate from many cells throughout the body

307
Q

What test is considered the indirect index of pancreatic function and the test of choice for diagnosis of exocrine pancreatic insufficiency?

A

Trypsin-like immunoassay (TLI)

308
Q

What is the spec cPL and the spec fPL?

A

A diagnostic assay for pancreatitis; specific pancreatic lipase quantitative ELISA test that you must send out to the lab, but has high sensitivity and specificity

309
Q

What is the SNAP cPL/fPL?

A

A semiquantitative immunonassay for pancreatitis that is point of care and has a high sensitivity.

310
Q

What is the VetScan cPl Rapid test?

A

A dog only semiquantitative immunoassay for pancreatitis that is point of care with a sensitivity/specificity of 80%

311
Q

What is precision PSL?

A

It is a colorimetric lipase assay for pancreatitis that must be sent out and has a high sensitivity and and lower specificity.

312
Q

What are some causes of low specificities or false positives on pancreatic lipase assays?

A
  1. Hyperadrenocorticism
  2. GI foreign body obstruction
  3. Pancreatic inflammation due to septic peritonitis
  4. Pancreatic hypoprofusion
313
Q

How can radiography help determine if a patient has pancreatitis?

A

Pancreatitis can cause local peritonitis which can be seen on radiographs in the form of loss of detail/contrast and increased density in the right cranial abdomen. May also see increased angle of the pyloro-duodenal angle, evidence of abdominal effusion and ileus

314
Q

What can be seen on ultrasound that can help diagnose pancreatitis?

A
  1. Pancreatic enlargement
  2. Mixed echogenicity
  3. Peritoneal effusion
  4. Peripancreatic fat/ mesentery that is hyperechoic
315
Q

Is ultrasound for pancreatitis diagnosis highly specific or sensitive?

A

It is highly specific, the sensitivity is variable

316
Q

A more hypoechoic pancreas on ultrasound suggest ________ and a more hyperechoic pancreas suggests ________.

A

Necrosis due to acute pancreatitis

Fibrosis due to chronic pancreatitis

317
Q

What would be seen on CT when diagnosing pancreatitis?

A

Enlarged, homogenously to heterogeneously attenuating and contrast enhancing pancreas with ill defined borders

318
Q

When should you not take a pancreatic biopsy?

A

When there is necrotizing, liquefying pancreatitis

319
Q

Why is taking a FNA of the pancreas helpful?

A

It has little risk and if there is pancreatic acinar cells with inflammatory cells, it can bolster a diagnosis of pancreatitis…however, the lack of inflammatory cells doesn’t rule out pancreatitis

320
Q

What are the differences seen on histology with acute versus chronic pancreatitis?

A

There will be edema, necrosis and neutrophilic infiltrate in acute, but chronic will have lymphocytic inflammation and fibrosis

321
Q

Dogs are more likely to suffer from _______ pancreatitis and cats are more likely to suffer from ________pancreatitis.

A

Acute

Chronic

322
Q

What re the clinical signs of acute pancreatitis?

A
  1. Acute vomiting
  2. Abdominal pain
  3. Anorexia
  4. Lethargy
  5. Dehydration
  6. Fever
323
Q

What are differential diagnosis for pancreatitis?

A
  1. Gastroenteritis
  2. GI foreign body causing obstruction or perforation and sepsis
  3. GI neoplasia
  4. Renal failure
  5. Biliary mucocele
  6. Uncontrolled diabetes/diabetic ketoacidosis
324
Q

What are the key factors initiating pancreatic inflammation?

A
  1. Blockage of acinar cells secretion in pancreatic duct leading to activation of trypsinogen
  2. Oxidative stress
    3, Hypotension
325
Q

What is the end result of pancreatic inflammation?

A

Zymogens are activated causing autodigestion of the pancreas and the pancreatic specific trypsin inhibitor is overwhelmed.

326
Q

What is the cascade of inflammation and destruction of the pancreatitis during pancreatitis?

A

Trypsin activates inactive proenzymes in zymogen granules causing locale inflammation while neutrophils migrate to the pancreatitis leading to reactive oxygen species and nitric oxide release and more inflammation. Lastly, cytokines increase vascular permeability that lead to edema and necrosis.

327
Q

What are the more severe sequele to acute pancreatitis?

A

SIRS and MODS

328
Q

What are the breed signalments for acute pancreatitis

A

Miniature schnauzer and yorkshire terrier

329
Q

Which endocrinopathies can increase an animal’s risk for developing pancreatitis?

A
  1. Diabetes mellitus
  2. Hypothyroidism
  3. Hyperadrenocorticism
    4 Idiopathic hyperlipidemia of miniature schnauzers
330
Q

What are some risk factors other than breed, drugs/toxinss and concurrent endocrinopathies for acute pancreatitis?

A
  1. Hypertriglyceridemia
  2. Dietary indiscretion
  3. Hypotension
  4. Pancreatic duct obstruction
331
Q

Which toxins can increase the risk of developing acute pancreatitis?

A
  1. Organophosphates

2. Zinc

332
Q

Which chemotherapy drugs can increase the risk of developing acute pancreatitis?

A
  1. L-asparginase

2. Doxorubicin

333
Q

Which immunosuppressive drugs can increase the risk of developing acute pancreatitis?

A
  1. Corticosteroids

2. Azathioprine

334
Q

Which antibiotics can increase the risk of developing acute pancreatitis?

A
  1. TMS

2. Doxycycline

335
Q

Which anti-epileptic drugs can increase the risk of developing acute pancreatitis?

A
  1. Phenobarbital

2. Potassium bromide

336
Q

Which tests are preferred for diagnosing acute pancreatitis?

A
  1. Spec cPL

2. use SNAP cPLI to rule it out ( high sensitivity)

337
Q

What is seen on a CBC with acute pancreatitis?

A
  1. Neutrophilia with left shift
  2. Hemoconcentration
  3. DIC
338
Q

What is seen on a chem panel with acute pancreatitis?

A
  1. Azotemia

2. Elevated liver enzymes and bilirubin

339
Q

How can abdominal radiographs help in the diagnosis of acute pancreatitis?

A

It can rule out obstructions as a differential diagnosis

340
Q

How can abdominal u/s help with the diagnosis of acute pancreatitis?

A

Used to rule out other differentials

341
Q

Why is acute pancreatitis frustrating to diagnose?

A

The underlying cause is usually never identified ( medication, diets, concurrent endocrinopathy)

342
Q

What fluid therapy should be given in the case of acute pancreatitis?

A

Crystalloids for IV volume replacement and to correct metabolic alkalosis from excess vomiting

343
Q

What treatment is essential when dealing with acute pancreatitis cases? Why?

A

Nutritional support with a nasogastric or esophagostomy tube to provide enteral nutrition to prevent intestinal translocation secondary to sepsis, SIRS and MODS.

344
Q

Which pain medications are best to use when treating acute pancreatitis?

A

Cats: Buprenorphine
Dogs: Fentanyl CRI or methadone

345
Q

Which pain medications should be avoided in the treatment of acute pancreatitis?

A
  1. Hydromorphone
  2. Morphine
  3. Butorphanol
346
Q

Which antiemetics should be used when treating acute pancreatitis?

A
  1. Maropitant (1st choice)

2. Ondansetron/dolasetron

347
Q

Why would you use Trasylol when treating a patient for acute pancreatitis?

A

In experimentally induced dogs, they responded well the the proteinase inhibitor, but no studies have shown strong evidence of efficacy in dogs with spontaneous pancreatitis.

348
Q

Why would you possibly give fresh frozen plasma to a dog with acute pancreatitis?

A

To add anticoagulant and coagulation factors plus antithrombin for DIC treatment

349
Q

Would you give antibiotics to a patient with acute pancreatitis? why or why not?

A

No as the fever and neutrophilia associated is due to inflammation, not infection…there is no evidence for bacteria’s role in causing pancreatitis.

350
Q

How is acute pancreatitis prevented?

A
  1. Controlling and testing for hypertiglycerididemia
  2. Ultra low fat diets with less thn 20g/1000 kcals
  3. Avoid predisposing medications
  4. Address endocrinopathies
351
Q

What are the clinical signs of chronic pancreatitis?

A
  1. Chronic vomiting
  2. Decreased appetite
  3. Lethargy
352
Q

What are the risk factors/causes in cats for chronic pancreatitis?

A
  1. Cholangiohepatitis
  2. Inflammatory bowel disease
  3. Diabetes mellitus
  4. Hepatic lipidosis
353
Q

What are the risk factors/causes in dogs for chronic pancreatitis?

A

Being a english cocker spaniel, cavalier, boxer, collie, or miniature schnauzer

354
Q

How is chronic pancreatitis treated?

A
  1. Treat like acute pancreatitis
  2. Diet change to ultra low fat in dogs and novel protein or hypoallergenic in cats
  3. Treat concurrent diseases
355
Q

Which breeds of dogs/cats are more at risk to developing IBD?

A 
Boxers
GSD
Dobermans
Basenji and 
SCWT

Siamese

356
Q

What clinical sign is the most common with IBD in dogs?

A

Diarrrhea

357
Q

What clinical sign is the most common with IBD in cats?

A

Vomiting

358
Q

Which form of IBD involves hematemesis and melena as clinical signs?

A

Eosinophilic form

359
Q

What age patient does IBD most commonly affect?

A

Middle aged

360
Q

What are the different types of IBD?

A
  1. Lymphocytic-plasmacytic
  2. Eosinophliic
  3. Granulomatous
  4. Neutrophilic
  5. Regional enteritis
  6. Basenji enteropahty
  7. PLE/PLN of soft coated wheaten terriers (SCWT)
361
Q

What is CIBDAI?

A

The canine inflammatory bowel disease activity index which takes into account:

  1. Attitude
  2. Appetite
  3. Vomiting
  4. Stool consistency
  5. Stool frequency
  6. Weight Loss
362
Q

What is the CCEAI?

A

The Canine chronic enteropathy activity index which takes into account all the same perameters as theCIBDAI, except adds:

  1. Albumin
  2. Ascites/edema
  3. Pruritis
363
Q

What can the CIBDAI and CCEAI scores be used for?

A

Therapy, but not in themselves diagnostic

364
Q

Which IBD scoring system corelates better with prognosis?

A

CCEAI

365
Q

How is IBD diagnosed?

A

Clinical signs along with histology

366
Q

On CBC, what may be seen with IBD?

A
  1. Iron deficiency anemia

2. Eosinophilia

367
Q

On blood chem, what may be seen with IBD?

A
  1. hypoalbuminemia ( protein-losing enteropathy)
  2. Panhypoproteinemia
  3. hypocholesterolemia
  4. hypokalemia
  5. Reactive hepatopathy in dogs
368
Q

How can a fecal evaluation be helpful in supporting a protein losing enteropathy diagnosis?

A

a1 protease inhibitor

369
Q

What is the most common form of IBD?

A

Lymphocytic-plasmacytic enteritits

370
Q

Which disease is part of triaditis in cats?

A

Lymphocytic-plasmacytic enteritis

371
Q

Why do full thickness surgical biopsies need to be taken in cats suspected with IBD?

A

To differentiate small cell lymphoma from lympho-plasmacytic enteritis IBD

372
Q

Why is immunohistochemistry done in cats with lymphocytic-plasmacytic entertitis IBD?

A

To determine if lymphocyte populations are B or T and if they are monoclonal or polyclonal

373
Q

Which dog breed is prone to developing severe lymphocytic-plasmacytic enteritis IBD along with protein losing enteropathy? How is it treated?

A

Basenji

Treatment not successful and die within months

374
Q

Which form of IBD is associated with erosions and ulcerations of the GI tracts?

A

Eosinophilic enteritis

375
Q

Which form of IBD is characterized by infiltration of macrophages and localized enteritis to to ileum?

A

Granulomatous enteritis

376
Q

How is neutrophilic enteritis treated and how common is is?

A

It is rare and treated with antibiotics

377
Q

Which form of IBD is the rarest and is characterized by wall thickening of the GI tract on U/S?

A

Segmental enteritis

378
Q

What can cause protein-losing enteropathy?

A
  1. lymphatic obstruction/damage
  2. Increased mucosal permeability from cell infiltrates
  3. Mechanical distruptions to the mucosa
379
Q

Which diseases can include protein-losing enteropathy?

A
  1. IBD
  2. Lymphangiectasia
  3. Infiltrative lymphoma
  4. Infiltrative fungal disease
  5. Intussusception
  6. Ulceration/erosion
  7. Adverse food reactions
  8. GI parasites
  9. Splanchnic vascular congestion from portal hypertension
380
Q

This is primarily a disease of dogs that is characterized by dilation of lacteals in the GI tracts resulting in ballooning and rupture leading to edema and loss of lymphatic fluid in the intestinal lumen. What is it?

A

Lymphangiectasia

381
Q

What are the main clinical abnormalities found with cbc/blood chem with lymphangiectasa?

A
  1. Panhypoproteinemia

2. Hypocholesterolemia

382
Q

What is seen on U/S with lymphangiectasia?

A

Hyperechoic striations in mucosa

383
Q

What is required in order to make a diagnosis of lymphangiectasia?

A

Biopsy with histopath

384
Q

How is lymphangiectasia most likely to form and in what type of patient?

A

Due to inflammatory/neoplastic infiltrates in the intestinal wall. Acquired in dogs and sometimes congenital in young dogs

385
Q

How can an animal develop immunologic reactions to food (food allergy)?

A

Dietary antigens are recognized by the immune cells in peyers patches of the small intestine, then deliver to naive T and B lymphocytes which activate.

386
Q

How does oral tolerance of food antigens occur?

A

When there is balance between IgA induction, T cell deletion, anergy and immunosuppression vs. the ability to have lymphocytes ready to produce antibodies and cytokines needed to destroy pathogens.

387
Q

What can cause a loss of oral tolerance of food and lead to a food allergy?

A
  1. Increased mucosal permeability
  2. Substances that activate and change phenotypes of intestinal dendritic cells
  3. Parasites
  4. Altered intestinal microflora
388
Q

What is the results of the loss of oral tolerance of food?

A
  1. Localized cell-mediated inflammation
  2. Local production of IgE
  3. Mast cell response and degranulation
  4. Systemic antibody production
389
Q

What does the mast cell response require in order to cause clinical food allergy size?

A

A minimum food particle size, the antigen must be at least 10 kDA to be absorbed intact and elicit a response

390
Q

What are the most common clinical signs of adverse reactions to food?

A

Vomiting
Diarrhea
Pruritis

391
Q

What is the difference between a food intolerance and a food allergy?

A

A food intolerance is non-immunologic and usually due to food additives

392
Q

What can cause food induced dysbiosis?

A

An abrupt diet change

393
Q

What can cause a food-induced dysmotility?

A
  1. High fat diet
  2. Large dietary volume
  3. Increased dry matter
394
Q

What can cause a food toxicity?

A
  1. E. coli
  2. S. pseudintermedius
  3. C. clostridium spp.
395
Q

What can cause maldigestions/malabsorption?

A
  1. Lactose infolerance

2. High fiber diets leading to increased gas production

396
Q

Which breed of dog is affected by gluten enteropathy?

A

Irish setters

397
Q

What is the best way to diagnose and treat adverse food reactions?

A

Diet trials in stable patients involving:

  1. Changing brand
  2. Eliminating additives
  3. New bag of food
  4. Raw/home-cooked with vet nutritionist balancing
  5. Slower introduction of new diets
  6. Not feeding fat or poorly fermentable fiberous food
  7. Feed only dry food
398
Q

What is the ideal elimination diet and what is is used for?

A

It is used for food allergies and

  1. Contains intact or hydrolyzed protein sources novel to the patient
  2. One or two protein sources
  3. High digestibility
  4. Lower in fat and protein
  5. Moderate fermentable fiber content
399
Q

What is a hydrolyzed diet?

A

Use hydrolysis of proteins to help prevent the immune system from recognizing the intact version of proteins..the proteins can evade immune responses

400
Q

Why should a novel protein be selected along with the hydrolyzed diet?

A

Hydrolysis does not completely eliminate immune recognition of food antigens

401
Q

How long should a elimination diet be give to a patient?

A

3 weeks before rendering diet ineffective and if a successful diet found, add an old ingredient one by one every two weeks

402
Q

What disease includes a type 1 hypersensitivity reaction to food or a bacterial endotoxin/enterotoxigenic clostridial strain reaction with acute vomiting, hematemesis, hemorrhagic diarrhea, anorexia, and lethargy?

A

Acute Hemorrhagic Diarrhea syndrome

403
Q

How is acute hemorrhagic diarrhea syndrome diagnosed?

A

Exclusion of other causes of signs

404
Q

How is acute hemorrhagic diarrhea syndrome treated?

A
  1. Fluid therapy
  2. Maropitant
  3. Proton pump inhibitors
  4. Feeding digestible diets
  5. Antibiotics if bacterial cause
405
Q

What is the AHDS?

A

The canine acute hemorrhagic diarrhea syndrome index with scores of 0-18 with 0-3 being insignificant and over 9 being severe. It takes into acount:

  1. Activity
  2. Appetite
  3. Vomiting
  4. Fecal consistency
  5. Frequency of defecation
  6. Dehydration
406
Q

What is the typical signalment for a patient diagnosed with acute hemorrhagic diarrhea syndrome?

A

Young and small like Yorkies, miniature pinschers, maltese and miniature schnauzers and tend to occur in the winter

407
Q

An older dog presents with diarrhea, straining to defecate, and decreased appetite…what type of neoplasia is most likely?

A

Large intestinal tumors like

408
Q

What are the common clinical signs in an older cat that has a tumor of the small intestine or stomach?

A
  1. Anorexia
  2. Weight loss
  3. Vomiting
409
Q

How is GI neoplasia usually diagnosed?

A

With abdominal ultrasound and cytology or histopathology

410
Q

When is chemotherapy used with GI neoplasia?

A

Lymphoma
Mast cell tumors
Other systemic tumors

411
Q

A dog presents with abdominal discomfort, tenesmus, and mucus and blood in large bowl diarrhea. The dog responds well to a highly digestible diet supplemented with psyllium ( a soluble fiber). What disease is this?

A

Irritable Bowel Syndrome

412
Q

What medication can be used as an antidiarrheal and restore smooth muscle segmentation, prolong transit time and improve fecal consistency in a dog with the diarrheal form of IBS?

A

Loperamide, an opiod

413
Q

Other than giving a dog with IBS loperamide, what other medications will you consider?

A
  1. Ondansetron for vomiting/diarrhea
  2. Tylosin/metronidazole or dozycyline for SIBO
  3. Probiotics
414
Q

What is the treatment of choice for IBS?

A

A highly digestible diet supplemented with a soluble fiber

415
Q

What medication may be helpful in a dog with costipation stemming from IBS?

A
  1. Laxatives

2. Aminopentimide that is a antispasmodic

416
Q

What can cause short bowel syndrome?

A
  1. Massive small bowel surgical resection
  2. Malabsorption
  3. Protein-calorie malnutrition
417
Q

What occurs to the intestinal bacterial flora in short bowl syndrome?

A

The small intestinal flora will start to resemble large intestinal flora

418
Q

What can occur if the ileocecal sphincer is removed?

A

Short bowel syndrome with reflux of colonic contents into the small intestine

419
Q

What are the clinical signs of short bowel syndrome?

A
  1. Thin with continual weight loss

2. Severe diarrhea

420
Q

How is short bowel syndrome treated?

A
  1. Aggressive supplementations with elemental diets using TPN and enteral nutrition (at first)
  2. Highly digestible diet in small, frequent feeding with elemental diets supplementation
  3. Proton pump inhibitors
421
Q

Why would you possibly use proton pump inhibitors in a dog with short bowel syndrome?

A

Decrease damage to the small intestine from gastric acid and antibiotics to control dysbiosis that may worsen malabsorption and diarrhea

422
Q

What supplements are typically given to short bowel syndrome patients?

A
  1. Colbalamin
  2. Fat soluble vitamins
  3. Ursodiol to help with fat absorption
423
Q

What type of diseases are more commonly the cause of fecal incontinenece?

A

Neurogenic like diseases of the sacral spinal cord and peripheral nerves

424
Q

What endocrinopathy can lead to fecal incontinence?

A

Hypothyroidism

425
Q

What are the two forms of megacolon?

A
  1. Hypertrophic

2. Dilated

426
Q

Which form of megacolon is end stage, permanent, and requires a colectomy once medical management eventually fails?

A

Dilated

427
Q

What is a common signalment for idiopathic megacolon?

A

Male DSH cats

428
Q

When would you use a laxatives and prokinetics with megacolon?

A

After evacuation of feces

429
Q

If you susptect a patient with megacolon, what tests should you do?

A
  1. Do a rectal exam to check for foreign bodies, strictures, diverticulums and masses and rule them out
  2. Do a neuro exam
  3. CBC to rule out other constipation causes
  4. Radiographs/U/S and endoscopy
430
Q

What conditions can cause constipation other than megacolon and must be ruled out?

A
  1. Hypokalemia
  2. Hypocalcemia
  3. Hypothyroidism
431
Q

What type of diet is best to feed a patient with early

megacolon? End stage or after a colonectomy?

A

Increased fiber diets ( more or less fermentable)

After a colonectomy, give a low residue diet as the colon will be gone and can’t hold feces….diets needs to be highly digestible.

432
Q

What medications can be used to treat megacolon?

A
  1. Oral laxatives like DSS and laxatone with switching to lactulose later
  2. Cisapride
433
Q

If medical management fails for megacolon, what must be done next?

A

Manual removal of feces with water/saline enema followed by abdominal manipulation of colon. Sponge forceps to help with removal and sedation may be needed.

434
Q

Approximatly how long can a patient have hypertrophic megacolon before it is going to turn into dilated megacolon and be irreversible?

A

6 months

435
Q

How long can diarrhea last after a colectomy?

A

4-6 weeks

436
Q

What is the difference between constipation and obstipation?

A

Obstipation is constipation that is unresponsive to treatment and implies permanent dysfunction

437
Q

What is ileus?

A

Inhibition of propulsive bowel activity

438
Q

What types of intestinal obstructions are most likely to be partial?

A

Gastric obstructions

439
Q

What is the difference in onset of clinical signs between a complete and partial GI obstruction?

A

During a complete obstruction, the C/S are likely to be more acute and severe than with partial obstructions, which are more chronic, intermittent and less severe.

440
Q

What is the most common cause of acute intestinal obstruction?

A

Foreign body

441
Q

How is motility and secretion/absorption affected in the GI tract when there is a foreign body obstruction?

A

It will be hypermotile and hypersecretional proximal and hypomotile with hypoabsorption distal to the obstruction

442
Q

What are some consequences of a GI foreign body that is not removed?

A
  1. Vascular compromise
  2. Inflammation
  3. Bacterial toxins
  4. Mechanical stimulation
  5. Dysbiosis
  6. Bacterial translocation
  7. Abdominal pain
  8. Peritonitis
443
Q

What are some clues on radiographs that there is a GI foreign body present?

A
  1. Distended loops of bowel
  2. Loss of serosal detail
  3. Free abdominal gas
  4. Mass effect
  5. Sedimentation of material proximal to the obstruction
444
Q

What is the first choice imaging technique with GI foreign bodies?

A

U/S

445
Q

What is the most common type of intussusception?

A

Enterocolic (cecocoli, ileocecal, ileocolic)

446
Q

What is the cause of most intussuceptoins?

A

Idiopathic, but can be caused by parasites, viruses, foreign bodies and masses

447
Q

What are the clinical signs of an intussusception?

A
  1. Intermittent vomiting
  2. Inappetence
  3. Mucoid bloody diarrhea
  4. Palpable abdominal mass
448
Q

How is an intussusception diagnosed and treated?

A

Barium contract rads and ultrasound with surgery as a treatment

449
Q

In what part of the GI tract is a stricture most likely to form? Why?

A

Esophagus

TRAUMA or neoplasia

450
Q

How are rectal or colonic neoplastic strictures treated?

A

Stents

451
Q

What is the treatment for a prototheca zopfi infection in a animal? How successful is it?

A

Prototheca zopfi is an fungal algae that is best treated with amphotericin B and itraconazole. This slows progression, but animals will die from the disease…prognosis is grave.

452
Q

What are the clinical signs of a prototheca zopfi infection in a cat?

A

Cutaneous lesions

453
Q

What are the clinical signs of a prototheca zopfi infection in a dog?

A

Disseminated disease through the colonic wall, blood, lymphatics, and into the kidney, liver, heart, brain and eye. It causes granulomatous and pyogranulomatous lesions leading to bloody large bowl diarrhea.

454
Q

A dog presents with acute kidney injury, central vestibular disease, uveitis and bloody large bowel diarrhea. The dog was playing near raw sewage earlier in the week. What is causing these clinical signs?

A

Prototheca zopfi algae

455
Q

How is prototheca zopfi diagnosed?

A

Rectal scrapping and urine cytology

456
Q

Why does pythium insidiosum infection have a guarded prognosis?

A

Eosinolphilic, pyogranulomatous and necrotic lesions form in the GI tract which cuases segmental thickening in the gastroduodenal and ileocolic regions that can not be fully surgically resected.

457
Q

How is pythium insidiosum diagnosed?

A

HIstopathology or
PCR on cultures and histopathology
ELISA for serum

458
Q

What clinical signs are you most likely to see in a dog that skin was penetrated by pythium insidiosum?

A

Skin or GI lesions that can lead to diffuse GI disease

459
Q

Wha tis the treatment for pythium insidiosum?

A

Surgical resection with itraconazole and terbinafine post-operative

460
Q

What is the fungus that disseminates through vessels and lymphatics after being digested or inhaled causing fever, signs that look like protein losing enteropathy, and respiratory disease?

A

Histoplasma capsulatum

461
Q

What is the bacteria though to be responsible for the clinical signs associated with Histiocytic Ulcerative Colitis?

A

Adhesive and invasive E. coli

462
Q

Why does histiocytic ulcerative colitis occur?

A

There is a defect in neutrophils leading to impaired clearance of E. coli in macrophages. This causes an aberrant immune response to the E. coli that results in a severe inflammatory response.

463
Q

What age and breeds of dogs have a higher risk of developing histiocytic ulcerative colitis?

A

YOUNG ( less than 2 years)

  1. Boxer
  2. French/english bulldogs
  3. Mastiff
  4. Malamute
464
Q

What are the clinical signs associated with histiocytic ulcerative colitis?

A

Weight loss
Anorexia
Diarrhea

465
Q

How is histiocytic ulcerative colitis diagnosed?

A
  1. Histopathology that consists of mixed inflammatory infiltrate in the lamina propria
  2. Endoscopy to reveal ulcers and hemorrhage
  3. Fluorescent in-situ hybridization to identify E. coli
466
Q

How is histiocytic ulcerative colitis treated?

A

Enrofloxacin

467
Q

What is the most common prebiotics used?

A

Dietary fiber and fructooligosaccharides

468
Q

What diseases are treated with fructooligosaccharide prebiotics?

A
  1. Colonic diseases like IBD and dyspiosis

2. SI dysbiosis

469
Q

What prokinetics are the most clinically effective?

A
  1. Cisapride

2. Erythromycin

470
Q

When would you treat an animal with a prokinetic?

A
  1. Ileus

2. Constipation

471
Q

What is exocrine pancreatic insufficiency?

A

Syndrome characterized by insufficient synthesis of digestive enzymes form the exocrine pancreas

472
Q

What percent of the exocrine pancreas must be lost for exocrine pancreatic insufficiency to become clinical?

A

More than 90%

473
Q

What is the cause of exocrine pancreatic insufficiency in cats?

A

Chronic pancreatitis

474
Q

What is the most common cause of exocrine pancreatic insufficiency in dogs?

A

Pancreatic acinar atrophy (PAA)

475
Q

What is a congenital cause for exocrine pancreatic insufficiency?

A

Pancreatic hypoplasia

476
Q

Which dog breed is susceptible to pancreatic acinar atrophy leading to EPI?

A

German Shepards

477
Q

When do signs of maldigestions appear in dogs that develop pancreatic acinar atrophy?

A

Before the age of 4 in 93% of dogs

478
Q

Why does pancreatic acinar atrophy lead to maldigestion of fat and protein?

A

Decreased secretion of pancreatic digestive enzymes

479
Q

Why does cobalamin absorption decrease with EPI?

A

Intrinsic factor is not produced from parietal cells in the gastric mucosa it is required for the synthesis of cobalamine

480
Q

What are the clinical signs of exocrine pancreatic insufficiency?

A
  1. Weight loss
  2. Steatorrhea
  3. Greasy hair coat
  4. Flatulence
  5. Polyphagia/copraphagea
  6. Pain
481
Q

What is the diagnostic test of choice for exocrine pancreatic insufficiency?

A

Serum TLI

482
Q

What vitamin will be low in all cats and most dogs with exocrine pancreatic insufficiency?

A

Cobalamin

483
Q

What are the treatments for exocrine pancreatic insufficiency?

A
  1. Enzyme replacement therapy
  2. Vitamine supplementation
  3. Diet
484
Q

What is the best enzyme replacement therapy for patients with exocrine pancreatic insufficiency? What is the worst?

A

Best: Powder pancreatic extract from a pork pancreas

Worst (aka, don’t use): Plant derived

485
Q

Where should maximal pancreatic enzyme activity occur and why?

A

Proximal duodenum because the pH Is above 3.5 where amylase and lipase wont be destroyed..however trypssin is tolerant to acidic pH

486
Q

What is the most important vitamin that needs to be supplemented to exocrine pancreatic insufficiency patients?

A

Cobalamin

487
Q

What is the treatment diet for exocrine pancreatic insufficiency?

A

High quality maintenance that is not a high in fiber. Only use a low fat diet as a last resort.

488
Q

What are common concurrent diseases an animal may have that is suffering from exocrine pancreatic insufficiency?

A
  1. IBD
  2. Diabetes Mellitus
  3. GI parasites
  4. Small intestinal dysbiosis
489
Q

What treatment is used for small intestinal dysbiosis?

A

Tylosin

490
Q

What treatment is used for decreasing gastric pH in animals with EPI?

A

Omeprazole, a proton pump inhibitor

491
Q

What factor is associate with a poor prognosis in dogs with EPI?

A

Hypocobalaminemia

492
Q

What is the most ccommon type of pancreatic neoplasia?

A

Benign nodular hyperplasia

493
Q

What is the most common malignant pancreatic neoplaisa in dogs?

A

Carcinoma from acinar cells

494
Q

What dogs are at the greatest risk for developing pancreating carcinoma?

A

Older female dogs and spaniels

495
Q

How is pancreatic neoplasia diagnosed?

A
  1. U/S and CT with >2cm masses suggesting malignancy
  2. FNA and cytology of lymph nodes
  3. Exploratory laparotomy
496
Q

How is pancreatic neoplasia treated?

A

Pancreatectomy, but complicated if pancreatic duct involved

497
Q

What is the prognosis for pancreatic neoplasia?

A

Guarded despite aggressive treatment

498
Q

Which diet is more palatable and less expensive than hydrolyzed diets and used for food allergies?

A

Novel protein diets

499
Q

How can the bacteria in the colon produced more short chain fatty acids?

A

A highly fermentable diet

500
Q

What are some examples of moderately fermentable fibers that could be in diets used to GI disease?

A
  1. Beet pulp
  2. Rice bran
  3. Gum Arabic
  4. xanthin gum
  5. Inulin
  6. Psyllium
501
Q

What are examples of low fiber ingredients that can be in diets in order to add bulk to the feces?

A
  1. Cellulose

2. Methycellulose

502
Q

Why do we not want to feed small animals high fiber diets?

A

It cause more gas production and diarrhea and the short chain fatty acids produced are not important for an energy source in small animals ( it is in ruminants)

503
Q

Which two prokinetics are the most clinically effective?

When are they used?

A

Cisapride
Erythromycin

Ileus or constipation

Small Animal Medicine I (2 decks)

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