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ACVIM General copy > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

The (sympathetic/parasympathetic) nervous system is stimulatory to the GI tract

A

Parasympathetic

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2
Q

What is the primary role for the myenteric plexus

A

Movement

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3
Q

What is the primarily role for the submucosal plexus in the GI tract?

A

Secretion and blood flow

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4
Q

What glands are found in the body of the stomach?

A
  1. Parietal Cells
  2. Enterochromaffin-like Cell
  3. Chief Cells
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5
Q

What glands are found in the antrum of the stomach?

A
  1. G Cell

2. D Cell

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6
Q

What is the source of gastrin?

A
  1. G cells of the gastric antrum
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7
Q

What stimulates gastrin secretion?

A
  1. Stretch
    - Nerves of the gastric mucosa
    - Vagal stimulation → Gastrin-Releasing Peptide
  2. Peptides
  3. Amino Acids → Phenylalanine and Tryptophan are the big players
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8
Q

What cells does gastrin act on?

A
  1. Parietal cell

2. Enterochromaffin-Like Cells

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9
Q

What are the actions of gastrin?

A
  • Endocrine*
    1. Stimulate enterochromaffin like cells to secrete histamine
    2. Stimulate parietal cells to secrete HCl
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10
Q

What are the three secretagogues involved in parietal cell activation?

A
  1. ACh
    - Bind M3 receptors → cause increase in intracellular Ca
  2. Gastrin
    - Bind CCK-B receptors and cause increase in intracellular Ca
  3. Histamine
    - Binds to H2 receptors → increases cAMP
    - Most potent stimulant of parietal cell
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11
Q

What inhibits HCl secretion by parietal cells?

A
  1. Secretin
  2. CCK
  3. Prostaglandins
  4. Dopamine
  5. Somatostatin
  6. GIP
  7. Peptide YY
  8. Enteroglucagon
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12
Q

Where does pepsinogen come from?

A
  1. Chief Cells
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13
Q

What is the stimulus for pepsinogen secretion by Chief Cells?

A
  1. ACh
    - Via the vagus nerve → stimulated by stretch
  2. HCl
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14
Q

What is the function of pepsinogen?

A
  1. Precursor for pepsin → protein digestion
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15
Q

Where does somatostatin come from?

A
  1. D Cells
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16
Q

What is the stimulus for somatostatin secretion?

A
  1. Lipids
  2. Protein
  3. Bile
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17
Q

What are the functions of somatostatin?

A
  • Paracrine*
    1. Decrease gastrin secretion
  • Endocrine*
    2. Decrease parietal cell acid secretion
  • Neurocrine*
    3. Decrease gastric motility
  1. Inhibits CCK release
  2. Inhibits secretin release
  3. Inhibits gallbladder contraction
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18
Q

What are the phases of gastric secretion?

A
  1. Cephalic - 30%
  2. Gastric - 60%
  3. Intestinal - 10%
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19
Q

What are the contributors to the cephalic phase of gastric secretion?

A
  1. Smell/sight of food
  2. ACh → Vagus n.
  3. Gastrin → G cells
  4. Histamine → ECL cells
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20
Q

What are the contributors to the gastric phase of gastric secretion?

A
  1. Gastric digestion and release of peptides
  2. Stretch → vasovagal reflexes, local enteric reflexes
  3. Gastrin → G cells
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21
Q

What are the contributors to the intestinal phase of gastric secretion?

A
  1. Gastric emptying
  2. Decreases intestinal and gastric antral pH
  3. Somatostatin → D cells
  4. Secretin → S cells
  5. CCK - I cells
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22
Q

What are the cells of origin for gastrinomas?

A
  1. Malignant transformation of pancreatic delta cells
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23
Q

What is the underlying reason for the clinical signs seen in gastrinomas?

A

Due to hypergastrinemia

  1. Esophageal and Gastroduodenal erosions and ulcerations
  2. Enzymatic maldigestion
  3. Gastric antral hypertrophy → delayed gastric emptying, gastric outflow obstruction
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24
Q

What are the clinical signs seen with gastrinomas?

A
  1. Vomiting*
  2. Weight loss*
  3. Depression
  4. Lethargy
  5. Anorexia
  6. Diarrhea
  7. Steatorrhea
    * → most common
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25
Q

What changes on a CBC can be found with gastrinomas?

A
  1. Regenerative anemia

2. Leukocytosis → mainly due to stress

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26
Q

What changes on a chemistry can be found with gastrinomas?

A
  1. Hypochloremic, metabolic alkalosis → because the parietal cells are releasing a lot of H, Cl, and K
  2. Mild liver enzyme activity +/- hyperbilirubinemia
    - May be due to metastasis
    - Common bile duct obstruction
  3. +/- alterations in blood glucose due to secretion of other hormones
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27
Q

How can gastrinomas be diagnosed?

A
  1. Fasting serum gastrin → want to see at least >3x the reference range but there are a lot of things that can also increase gastrin levels so its best for it to be >10x
  2. Histopath is the treatment of choice
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28
Q

Gastrin concentrations were found to be significantly (higher/lower) in CKD cats

A

Higher but there was a lack of uremic gastropathy lesions → no indication for gastroprotectants

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29
Q

What is the mechanism of action of Octreotide?

A

Somatostatin Analog

  1. Inhibit gastric acid release from parietal cells
  2. Inhibit gastrin release → reduce 25-50% of pretreatment values
  3. Decrease tumor load (gastrinomas)
  4. Reduce enterochromaffin-like cell hyperplasia
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30
Q

What is the source of Ghrelin?

A

Primarily the stomach (parietal cells)

- Can also come from intestine, pancreas (epsilon cells), and hypothalamus

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31
Q

What is the stimulus for Ghrelin?

A
  1. Fasting
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32
Q

What is the action of Ghrelin?

A
  1. Stimulate growth hormone secretion from the pituitary
  2. Stimulate appetite, body growth, and fat deposition
  3. Anti-inflammatory properties → decreases production of inflammatory cytokines
  4. Increases rate of gastric emptying
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33
Q

What is the MOA of Entyce (Capromorelin)

A
  1. Ghrelin agonist
    * Has also shown that there is a transient increase in growth hormone and sustained increase in IGF-1 concentrations in adult healthy beagles
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34
Q

What are the most common adverse effects of Entyce?

A
  1. Vomiting

2. Diarrhea

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35
Q

What is the source of leptin?

A

Adipocytes

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36
Q

What is the stimulus for leptin secretion?

A

Increased adipose tissue

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37
Q

What are the actions of leptin?

A
  1. Decreased production of appetite stimulators in the hypothalamus
    - Neuropeptide Y
    - Agouti-related protein (AGRP)
  2. Activation of POMC neurons
    - α-melanocyte stimulating hormone
    - Activation of melanocortin receptors
  3. Increase sympathetic activity → increase metabolic rate → increase energy expenditure
  4. Decrease insulin secretion (pancreatic β cells)
  5. Increase TNF-α production and macrophage activation
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38
Q

What is the source of secretin?

A
  1. S cells
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39
Q

What is the stimulus for secretin release?

A
  1. Low duodenal pH
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40
Q

What are the actions of secretin?

A
  1. Inhibit acid secretion by parietal cells
  2. Slow gastric emptying
  3. Secretion of HCO3 rich pancreatic fluid (ductal cells)
  4. Trophic to the exocrine pancreas
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41
Q

What is the source of cholecystokinin?

A

I cells

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42
Q

What is the stimulus of cholecystokinin?

A
  1. Intraduodinal fatty acids, amino acids, H+ ions
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43
Q

What are the actions of cholecystokinin?

A
  • Pancreas*
    1. Potentiates secretin
    2. Pancreatic enzyme secretion (acinar cells)
    3. Stimulation of pancreatic growth
  • Gallbladder*
    1. Gallbladder contraction
    2. Relaxation of the sphincter of oddi
  • Stomach*
    1. Inhibit gastric emptying
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44
Q

What are the functions of the following pancreatic cells?

  1. Acinar Cells
  2. Ductal Cells
A
  1. Secrete digestive enzymes (amylase, lipase, and trypsinogen)
  2. Secrete H20 and HCO3
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45
Q

What converts trypsinogen to trypsin?

A

The brush border enzyme enterokinase

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46
Q

What is the role of ACh in regulation of pancreatic secretions?

A
  1. Secreted by parasympathetic nerve endings in vagus and enteric nerves (stretch)
  2. Digestive enzymes
  3. Small quantities of bicarbonate poor water/electrolyte solution
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47
Q

What is the role of cholecystokinin in pancreatic secretion regulation?

A
  1. Large quantities of digestive enzymes

2. Small quantities of bicarbonate poor water/electrolyte solution

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48
Q

What is the role of secretin in pancreatic secretion regulation?

A
  1. Large quantities of bicarbonate rich water/electrolyte solution → important because it allows for carrying the digestive enzymes to the duodenum
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49
Q

What are the phases of pancreatic secretion?

A
  1. Cephalic - 20%
  2. Gastric - 5-10%
  3. Intestinal - 70-75%
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50
Q

What contributes to the cephalic phase of pancreatic secretion?

A
  • Pavlov*
    1. Sight, smell, taste, or thought of food
    2. Vagal fibers → ACh
    3. Vagal fibers → Gastrin → acinar cells (potency 50-100% of CCK)
    4. Little fluid, so little enzyme makes it to the intestine
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51
Q

What contributes to the gastric phase of pancreatic secretion?

A
  1. Vagal and enteric fibers → ACh
  2. G cells → Gastrin → acinar cells
  3. Little fluid, so little enzyme makes it to the intestine
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52
Q

What contributes to the intestinal phase of pancreatic secretion?

A
  1. HCl acid (pH <4.5-5.0, important for enzyme activity) in small intestine
  2. S cells → Secretin → bicarbonate rich fluid, low chloride
  3. I cells → CCK
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53
Q

What % of bile acids are reabsorbed for recycling? What % are excreted?

A
  1. 95%

2. 5%

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54
Q

What are the most common secondary bile acids?

A
  1. Deoxycholic acid

2. Lithocholic acid

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55
Q

What amino acid are bile acids conjugated to in the liver?

A
  1. Taurine&raquo_space;» glycine

- Cats can only do taurine, dogs can do taurine and glycine

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56
Q

Where are bile acids reabsorbed? How?

A
  1. Ileum

2. Active transport via a Na-K ATPase

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57
Q

What is the source of Gastric inhibitory peptide?

A
  1. K cells
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58
Q

What is the stimulus for gastric inhibitory peptide release?

A
  1. Intraduodenal fatty acids, amino acids&raquo_space; carbohydrates
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59
Q

What are the actions of gastric inhibitory peptide?

A
  1. Inhibition of gastric acid secretion

2. Stimulation of pancreatic insulin release during hyperglycemia

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60
Q

What is the source of glucagon like peptide 1?

A

L cells of the ileum and colon

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61
Q

What is the stimulus for glucagon like peptide 1?

A
  1. Intraluminal glucose and lipid
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62
Q

What are the actions of glucagon like peptide 1?

A
  1. Inhibit gastric acid secretion

2. Pancreatic islet (β) cells → stimulate insulin secretion

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63
Q

What is an incretin?

A

A hormone secreted from the intestine in response to nutrients that potentiate insulin secretion

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64
Q

What are the main incretins?

A
  1. GLP-1 → L cells

2. GIP → K cells

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65
Q

What is the incretin effect?

A

Oral glucose will cause a significantly increased release of insulin compared to IV administration
*responsible for 25-70% of insulin secretion

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66
Q

How do GLP-1 and GIP stimulate insulin secretion?

A
  1. Stimulation of insulin biosynthesis
  2. Stimulation of β-cell proliferation
  3. Promotion of β-cell resistance to apoptosis
  4. Enhanced β-cell survival
  • GLP-1 important for control of fasting hyperglycemia
  • GLP-1 inhibits glucagon secretion by α-cells
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67
Q

What is the source of peptide YY?

A
  1. L Cells in Distal Ileum and Colon
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68
Q

What is the stimulus for peptide YY secretion?

A
  1. Fatty Acids

2. Carbohydrates (lesser degree)

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69
Q

What are the actions of peptide YY?

A
  1. Ileal brake
  2. Inhibition of CCK and secretin
  3. Proliferation of gut mucosa
  4. Slows gastric emptying
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70
Q

What is the MOA of slentrol (dirlotapide)?

A
  1. Microsomal membrane transfer protein inhibitor
    - Block the assembly and release of lipoproteins in the bloodstream → decreases fat absorption
  2. Increases peptide YY (and GLP-1) in rats
    - Increases satiety signals
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71
Q

What is the purpose of using slentrol (dirlotapide)? What are the most common adverse effects?

A
  1. Utilized for weight loss

2. Emesis, loose feces

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72
Q

What is the ileal brake?

A
  1. Lipid and glucose in the ileum → release of Peptide YY

2. Peptide YY → causes stomach relaxation and slow gastric emptying

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73
Q

What is the gastrocolic reflex?

A
  1. Distention of the stomach → causes colon to defecate
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74
Q

What is GI segmentation?

A
  1. Random contraction of circular muscles
  2. Mixes food with digestive enzymes and brings nutrients in contact with absorptive surfaces
  3. Slows transit time
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75
Q

What is GI peristalsis? What controls cranial contraction and caudal relaxation?

A
  1. Short wave of constriction moving aborally over a short segment of intestine
  2. Moves contents aborally
  3. Cranial contraction → ACh, substance P
  4. Caudal relaxation → nitrous oxide, VIP
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76
Q

What is the migrating motility complex?

A
  1. “Housekeeper” that clears the gut of undigested residue and prevents overgrowth of bacteria during the fasting state
    - Occurs every 90 minutes
    - Not present in cats and rabbits → they have a migrating spike complex
  2. Starts in the stomach and propagates to the ICJ (includes the gallbladder)
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77
Q

What are the phases of the migrating motility complex?

A
  1. Phase 1 → quiescence
    - ~1 hour
  2. Phase 2 → Intermittent contractions
    - Similar to that with feeding
    - 15-40 minutes
  3. Phase 3 → Intense propulsive motility
    - 4-8 minutes
    - Motilin
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78
Q

What is the source of Motilin?

A
  1. M cells in the stomach, small intestine, and colon
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79
Q

What is the stimulus of Motilin secretion?

A
  1. H+ and lipid in fed stae
  2. Most important in fasting (inter digestive) state
  3. Episodically released into serum during fasting → causes phase 3 of the migrating motility complex
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80
Q

What are the actions of Motilin?

A
  1. Initiates phase 3 of the migrating motility complex
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81
Q

What are the sources of serotonin in the GI tract?

A
  1. Enterochromaffin like cells

2. Enteric neurons throughout the GI tract

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82
Q

What are the actions of serotonin in the GI tact?

A
  1. Stimulates GI smooth muscle contraction

2. Intestinal electrolyte secretion

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83
Q

What are intestinal carcinoids?

A
  1. Tumors of endocrine cells of the GI tract

2. Contain secretory granules → contain SEROTONIN, secretin, somatostatin, and gastrin

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84
Q

At what point are clinical signs seen in EPI?

A
  1. When 90% of pancreatic function is lost
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85
Q

What is the underlying etiology for EPI? What is the most common in dogs? cats?

A
  1. Pancreatic Acinar Atrophy → most common in dogs
  2. Chronic Pancreatitis → most common ind cats
  3. Pancreatic Hypoplasia
  4. Pancreatic Neoplasia
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86
Q

Describe how B12 is absorbed from the diet

A
  1. B12 from the diet is bound to HAPTOCORRIN (R factor) in the STOMACH
  2. HAPTOCORRIN-B12 enters the DUODENUM and the haptocorrin is digested by pancreatic enzymes
  3. B12 then binds to INTRINSIC FACTOR
  4. INTRINSIC FACTOR-B12 goes to the ILEUM where it is endocytose by epithelial cells
  5. B12 dissociates and binds to TRANSCOBALAMIN
  6. TRANSCOBALAMIN-B12 then exits the epithelial cell and transits to the liver
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87
Q

What kind of anemia is the result of a B12 deficiency?

A

Macrocytic anemia (pernicious anemia)

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88
Q

What are the underlying causes of a B12 deficiency?

A
  1. Increased uptake by intestinal bacteria

2. Decreased intrinsic factor

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89
Q

Cats with EPI are (more/less) often cobalamin deficient than dogs

A

MORE

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90
Q

What produces intrinsic factor?

A
  1. Parietal cells of the stomach (dogs)

2. Pancreatic duct cells (dogs and cats)

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91
Q

Where is folate absorbed?

A

PROXIMAL small intestine

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92
Q

What % of dogs with EPI will have concurrent small intestinal bacterial overgrowth?

A
  1. 70%
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93
Q

Animals with EPI will likely have a (high/low) folate

A

low

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94
Q

Low serum folate suggests malabsorption in ____

A

Proximal small intestine

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95
Q

Low vitamin B12 suggests malabsorption in ____

A

Distal small intestine

Or decreased release of IF

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96
Q

Low or normal vitamin B12 together with a high folate suggests ____

A

Bacterial overgrowth

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97
Q

What are important qualities about serum TLI that need to be kept in mind when performing this test?

A
  1. Species and PANCREAS specific

2. It is eliminated by the kidneys → may be falsely elevated in patients with kidney disease

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98
Q

Serum TLI by radioimmunoassay has (high/low) sens and (high/low) spec for diagnosing EPI

A
  1. High

2. High

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99
Q

Fecal elastase has a (high/low) sens and a (high/low) spec for diagnosing EPI. This means it is good for ruling (in/out) disease.

A
  1. High
  2. Low
  3. Useful for ruling out disease
    * Helpful for ruling out EPI in dogs with chronic diarrhea*
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100
Q

How is EPI treated?

A
  1. Non-enteric coated supplemental enzymes
  2. Antibiotics for SIBO
  3. Dietary modification → highly digestible, low fiber, low to moderate fat
  4. Cobalamine supplements
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101
Q

What kind of diet should be fed to animals with EPI?

A
  1. Highly digestible
  2. Low fiber
  3. Low to moderate fat
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102
Q

What is SIBO?

A
  1. Small intestinal bacterial overgrowth
  2. More of a pathogenic mechanism rather than a diagnosis
  3. When small intestinal bacteria are >10^5 CFU/mL
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103
Q

What is another term for idiopathic SIBO?

A
  1. Antibiotic responsive diarrhea
    * Common in German shepherd dogs
    * Not documented in cats
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104
Q

What are causes for secondary SIBO?

A
  1. Disease that results in excess substrate in the intestinal lumen
    - EPI
    - Motility disorder
    - Blind loop
  2. Disease the affects the clearance of bacteria
    - Partial obstruction
    - Abnormal motility
    - Increased pH in the stomach or proximal SI (ie on PPIs)
  3. Morphologic or functional derangement of the mucosa
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105
Q

What is the pathophysiology of SIBO?

A

Increased bacteria in the small intestine cause malabsorption or diarrhea due to:

  1. Compete for nutrients (bind cobalamin)
  2. Bacterial metabolism of nutrients can create products that promote diarrhea (reduced micelle formation)
  3. Bacteria metabolize undigested lipids due to #2 which produces hydroxylated fatty acids which act as detergents and damage the mucosal surface
  4. Bacterial degradation of carbohydrates → serve as osmotic agents → draw fluid into intestine
  5. Increased intestinal permeability
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106
Q

How is SIBO diagnosed?

A
  1. Aerobic and anaerobic culture of duodenal juice → GOLD STANDARD
  2. Hydrogen breath test
  3. Intestinal permeability assays → increased bacteria unconjugate bile acids which are then readily absorbed
  4. Response to antibiotics
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107
Q

What is the hydrogen breath test?

A
  1. When carbohydrates go to large intestine → fermented → short chain fatty acids → hydrogen goes up
  2. In SIBO → hydrogen levels go up sooner because bacteria are now adding to the fermentation process
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108
Q

How is SIBO treated?

A
  1. Antibiotics
    - Tetracycline
    - Metronidazole (anaerobes only)
    - Tylosin (for chronic cases)
  2. Diet
    - Low fat, highly digestible
  3. Parenteral B12
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109
Q

What are the causes of feline obstipation?

A
  1. Idiopathic megacolon - 62%
  2. Pelvic canal stenosis - 23%
  3. Nerve injury - 6%
  4. Manx sacral SC deformity - 5%
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110
Q

What is believed to be the underlying cause of feline idiopathic megacolon?

A
  1. One study showed a decrease sensitivity to neurotransmitters → dysfunction of smooth muscle
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111
Q

How is feline obstipation treated?

A
  1. Enemas
  2. Rectal suppositories (DSS, glycerin)
  3. Laxatives
    - Hyperosmotics: Lactulose
    - Bulk: Psyllium
    - Lubricant: Mineral oil, petroleum
  4. Prokinetics
    - Cisapride
    - Ranitidine
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112
Q

What is the MOA of cisapride?

A
  1. 5HT2 and 5HT4 AGONIST

2. 5HT1 and 5HT3 ANTAGONIST

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113
Q

What is the MOA of ranitidine?

A
  1. H2 antagonist
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114
Q

What are the diagnostic criteria for abdominal fluid in a uroabdomen?

A

Abdominal fluid creat and K >2x serum

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115
Q

What are the diagnostic criteria for abdominal fluid in a septic abdomen?

A

Abdominal fluid glucose 20 LESS than serum

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116
Q

What metabolic causes should be ruled out prior to an idiopathic megacolon diagnosis in a cat?

A
  1. Hypokalemia
  2. Dehydration
  3. Hypercalcemia
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117
Q

How does the fluid in a septic abdomen hinder a patient?

A
  1. Decreases opsonins and thus phagocytosis
  2. Limits localization and walling off
  3. Intraabdominal hypertension can cause cardiopulmonary issues and urinary issues
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118
Q

What is the most common post-operative electrolyte abnormality in GDVs?

A
  1. Hypokalemia (after correcting for acidosis)

- Can be exacerbated with HYPOMAGNESEMIA

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119
Q

The majority of copper (40-60%) is absorbed where?

A
  1. Proximal small intestine
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120
Q

How is copper taken into the hepatocyte?

A

Copper transporter 1 (CTR 1)

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121
Q

What is the etiology of inherited copper storage disease in Bedlington terriers?

A
  • AUTOSOMAL RECESSIVE*

1. DELETION of MURR1 → accumulation of copper in hepatocytes → chronic hepatitis

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122
Q

How is copper secreted into the bile?

A

MURR1

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123
Q

In what form is copper stored?

A

Metallothrein

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124
Q

What is the role of ceruloplasmin?

A

Converts Fe2+ to Fe3+ for transport

*This is a COPPER DEPENDENT oxidase

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125
Q

Where does copper accumulate in bedlington terriers?

A

Zone 3 (Centrilobular)

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126
Q

Where does copper accumulate in secondary copper accumulation disease? What is the underlying cause of secondary copper accumulation?

A
  1. Zone 1 (Periportal)

2. Cholestasis

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127
Q

When does copper start to accumulate in Bedlington terriers with the MURR1 mutation?

A
  1. 4-5 months

* In heterozygous carriers it will start to rise until 6-9 months where it then goes back to normal

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128
Q

What clinical signs are associated with copper storage disease in Bedlington terriers?

A
  1. Non-specific liver signs

2. HEMOLYSIS → ONLY HAPPENS IN BEDLINGTON TERRIERS

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129
Q

What is the treatment for copper storage disease?

A
  1. Penicillamine
  2. Trientine
  3. Vitamin C → enhances urinary excretion of copper
  4. Zinc
  5. Antioxidants → if hemolytic crisis occurs, in Bedlington’s only
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130
Q

What is the MOA of penicillamine?

A
  1. Mobilization of copper from tissues and excretion in urine
  2. May also increase synthesis of metallothionein
    * Teratogenic and crosses placenta
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131
Q

What is the MOA of Trientine?

A
  1. Increases urinary excretion of copper

2. Decreases intestinal absorption of copper

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132
Q

What is the MOA of zinc in copper accumulation disorders?

A
  1. Reduces copper absorption from the diet
  2. Increases Metallothionein in intestinal mucosal cells → prevents absorption into the blood stream
    * Takes 3 months to work
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133
Q

What is the most common form of IBD? Second most common?

A
  1. Lymphocytic/Plasmacytic

2. Eosinophilic enteritis

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134
Q

Which breed has a familial gluten sensitive enteropathy?

A

Irish Setter

*Mucosal permeability precedes development of disease

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135
Q

What is Basenji enteropathy?

A
  1. Severe hereditary form of LPE
  2. Has hyperglobulinemia and is prone to developing LSA
  3. Treatment is usually unsuccessful
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136
Q

Which breed develops familial PLE and PLN?

A

Soft Coated Wheaten Terriers

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137
Q

What are the biochem characeristics of Soft Coated Wheaten Terrier familial PLE and PLN

A

Eventually get both

  1. PLE: Panhypoproteinemia and hypercholesterolemia
  2. PLN: Hypoalbuminea, Hypercholesterolemia, Proteinuria, and Azotemia
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138
Q

What is unique about Boxer ulcerative colitis?

A
  1. PAS Positive

2. Responds to baytril

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139
Q

What is the best negative prognostic indicator for enteritis?

A
  1. Hypoalbuminemia
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140
Q

What are the forms of PLE that cause hypoalbuminemia but HYPERglobulinemia?

A
  1. Basenji enteropathy
  2. Histoplasmosis
  3. Lymphoma
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141
Q

Where does tritrichomonis foetus colonize? What does it cause?

A
  1. Distal ileum in cats

2. Large bowel diarrhea

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142
Q

How is t. foetus diagnosed?

A

Direct fecal smear

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143
Q

How is t. foetus treated?

A
  1. Resistant to metronidazole

2. Will spontaneously resolve in 2 years

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144
Q

What is the most common cause of PLE?

A

Lymphangectasia

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145
Q

What is lymphangectasia?

A

Dilatation and dysfunction of intestinal lymphatics → leak protein rich lymph into intestinal lumen

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146
Q

Which breeds are predisposed to primary lymphangectasia?

A
  1. Small Breeds (Yorkies, Maltese)

2. Norwegian Lundehund

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147
Q

What are secondary causes of lymphangectasia?

A
  1. Intestinal lymphatic obstruction
    - Inflammatory, fibrosing, or neoplastic processes
    - Obstruction of the thoracic duct
    - Right heart failure due to CHF or tamponade, portal vein thrombosis
148
Q

What is the treatment of primary lymphangectasia?

A
  1. Dietary manipulation
    - Low fat
    - Calorie dense
    - Highly digestible
    - Supplement fat soluble vitamins
    - Glutamine
  2. Glucocorticoids
149
Q

What are the underlying causes of chronic colitis?

A
  1. Clostridium, T. foetus, Giardia, T. vulpis
150
Q

How is chronic colitis treated?

A
  1. Diet trial → high in soluble fiber
  2. Sulfasalazine (not in cats)
  3. Steroids
  4. Metronidazole
  5. Tylosin
151
Q

What is short bowel syndrome?

A
  1. > 2/3 of SI missing (either congenital or surgery)
152
Q

What changes are seen with

  1. Jejunum resections
  2. Ileal resections
A
  1. Malabsorption of food, water, and electrolytes
  2. Malabsorption of cobalamin and bile acids → depletes bile acid pool because they cannot be reabsorbed and reclaimed by the liver
  3. All sites cause a change in GI hormonal regulation → HYPERGASTRINEMIA
153
Q

What do the following indicate for patients with short bowel syndrome?

  1. GLP-2
  2. Peptide YY
A
  1. Trophic to intestines → improved prognosis in short bowel patients
  2. Inhibits pancreatic bicarb and gastric acid secretion → diarrhea is minimized in short bowel patients
154
Q

What are treatments for short bowel syndrome?

A
  1. Supplement parenteral B12 if ileum is resected
  2. H2 blockers to counteract hypergastrinemia
  3. Anti-secretory agents (loperamide, diphenoxylate, or octreotide)
  4. Bile salt binding resin (cholestyramine) → may help to reduce colonic secretion caused by the presence of bile salts that were not absorbed in the resected ileum
155
Q

What are causes of feline hepatic lipidosis?

A
  1. Overnutrition → increases hepatic fat accumulation as a result of positive energy balance
  2. Obesity → unrestricted fatty acid release from adipose stores
  3. SAM-e deficiency
  4. Reduced # of peroxisomes
  5. Impaired fatty acid oxidation or VLDL dispersal
  6. Enhanced de novo fatty acid synthesis
156
Q

Where is hormone sensitive lipase located?

A
  1. Intracellular in adipose tissue and liver
157
Q

What are the actions of hormone sensitive lipase?

A
  1. Promote breakdown of triglycerides and secrete into circulation
158
Q

What stimulates hormone sensitive lipase?

A
  1. Norepinephrine/Epinephrine/Stress
  2. Glucocorticoids → inhibits lipoprotein lipase
  3. Growth hormone
  4. Glucagons
  5. Thyroxine
  6. Starvation
159
Q

What inhibits hormone sensitive lipase?

A
  1. Insulin

2. Niacin

160
Q

Where is lipoprotein lipase located?

A
  1. Membrane bound in liver and fat
161
Q

What are the actions of lipoprotein lipase?

A
  1. Promotes breakdown of triglycerides and uptake into adipocytes
162
Q

What stimulate lipoprotein lipase?

A
  1. Insulin

2. Niacin

163
Q

What inhibits lipoprotein lipase

A
  1. Starvation

2. Glucocorticoids

164
Q

Describe triglyceride metabolism

A
  1. Triglycerides are broken down in hepatocytes by hepatic triglyceride lipase → FFAs and glycerol
  2. Glycerol → glycolytic pathway for glucose breakdown → energy
  3. FFA taken on L-CARNITINE to mitochondria for beta-oxidation (degradation of FFAs to acetyl CoA)
    - Enter Kreb’s cycle after combining with oxaloacetate
    - Krebs cycle degrades the Acetyl CoA into CO2 + H
    - CO2 + H enter the chemiosmotic oxidative system of the mitochondria → form ATP → energy
165
Q

Why are the following pathways in SAMe metabolism important?

  1. Transulferation pathway
  2. Methylation pathway
A
  1. Generate glutathione

2. Generate L-carnitine

166
Q

Why is L-carnitine important?

A
  1. Necessary for free acid metabolism

- Responsible for helping transport FFAs into the mitochondria

167
Q

Hepatic lipidosis cats may have a decreased glutathione and B12 concentration - why is this important?

A
  1. May support dysfunction of methionine metabolism → leads to decreased production of SAMe
168
Q

What are changes that can be seen on a CBC with feline hepatic lipidosis?

A
  1. Poikilocytosis
    - Acanthocytes most common
    - >50% of cats with hepatic disease will develop poikilocytosis
169
Q

What are changes on a biochemistry that can be seen in cats with hepatic lipidosis?

A
  1. ALP and ALT go up together
  2. GGT is normal (in the absence of pancreatitis or inflammatory bile disease)
  3. Decreased chloride (vomiting)
  4. Hypophosphatemia (refeeding syndrome)
  5. Hypokalemia (most common)
170
Q

What coag changes can be seen in cats with hepatic lipidosis?

A
  1. Increased PT/PTT/ACT
    - PT will go up first
    - PTT and ACT may be prolonged if the cat is factor 12 deficient
  2. Hypofibrinogenemia → likely due to decreased hepatic production
171
Q

Cats with hepatic lipidosis will have (hyper/hypo)echoic liver parenchyma on AUS

A

Hyper

172
Q

How is feline hepatic lipidosis treated?

A
  1. Diet → 60 kcal/kg/day
  2. Fluids (avoid LRS)
  3. Lactulose (reduce contact with endotoxic feces)
  4. Supplement water soluble vitamins (B12, B1)
    - B12 deficiency limits methylation reaction and SAMe production
  5. Supplement fat soluble vitamins (Vit K, Factor 12)
  6. L-carnitine
  7. Choline
    - Methyl donor required for synthesis of phosphatidyl choline → essential for packaging VLDLs and exporting TGs out of the liver
  8. Taurine → needed for bile acid conjugation
173
Q

What treatments should be avoided in hepatic lipidosis cats?

A
  1. Cimetidine (inhibitor of p450)
  2. Tetracyclines (affect hepatocellular metabolism → disturb mitochondrial fatty acid beta oxidation)
  3. Appetite stimulants → many are hepatically metabolized
  4. Propylene glycol → oxidative damage
  5. Prolonged vitamin K → oxidative damage/heinz bodies
174
Q

What is the most common underlying cause for feline neutrophilic (acute/chronic) cholangitis?

A

Typically ascending from the GI tract (E. coli)

*These patients may also have pancreatitis

175
Q

How is feline neutrophilic cholangitis treated?

A
  1. Use antibiotics against gram NEGATIVE AEROBES for 4 weeks
  2. Pain meds
  3. Vit E, SAMe, Vit C, Silbyn
176
Q

What are the histopath characteristics of feline lymphocytic cholangitis?

A
  1. Lymphocytic infiltration in portal areas with variable fibrosis and biliary proliferation
177
Q

What is a unique finding associated with feline lymphocytic cholangitis?

A
  1. ASCITES → one of the few feline liver diseases that will cause ascites
178
Q

How is feline lymphocytic cholangitis treated?

A
  1. Anti-inflammatories

2. Supportive care

179
Q

What are the histopath characteristics of lymphocytic portal hepatitis?

A
  1. SMALL numbers of lymphocytes in portal areas
  2. LACKS bile duct involvement
  3. Slowly progress
  4. Likely a reactive change reflecting extra hepatic disease
180
Q

What is the pathophysiology for chronic/acute pancreatitis?

A
  1. An initial decrease in secretion of pancreatic enzymes followed by formation of abnormal cytoplasmic vacuoles in which the contents of lysosomes and zymogen granules colocalize → inappropriate intracellular activation of trypsin and subsequently other digestive zymogens
  2. Local effects: inflammation, hemorrhage, acinar cell necrosis, and peripancreatic fat necrosis
  3. Systemic release: Systemic inflammatory changes, systemic vasodilation, pulmonary edema, DIC, CNS signs, renal failure, MODS
181
Q

Serum lipase: Sens/Spec

A
  1. VERY Sensitive → too sensitive, lots of false +

2. 50% spec

182
Q

cTLI has a ____ sens

A

30-60%

183
Q

What is the most sensitive and specific test for pancreatitis?

A

cPLI

184
Q

What are some causes of chronic pancreatitis?

A
  1. Traumatic (secondary to pancreatic ischemia)
  2. Infectious (Toxo gondii)
  3. Drug induced (humans and dogs; NOT CATS)
  4. MOST IDIOPATHIC
185
Q

Which is better? fTLI or fPLI? Why?

A
  1. fPLI

2. fPLI is elevated for 7-10 days whereas fTLI is only elevated for 2-3 days

186
Q

Acute pancreatitis is more common in (dogs/cats) and chronic pancreatitis is more common in (dogs/cats)

A
  1. Dogs

2. Cats

187
Q

What are complications associated with chronic pancreatitis?

A
  1. Pseudocyst → collection of sterile pancreatic juice enclosed by fibrosis or granulation tissue → surgical correction needed
  2. Pancreatic abscess
  3. Pancreatic parasites → EURYTREMA PROCYONIC → FENBENDAZOLE
  4. Hepatic fluke → AMPHIMERUS PSEUDOFELINUS → PRAZIQUANTEL
188
Q

What is the treatment for chronic pancreatitis?

A
  1. Remove inciting cause
  2. Aggressive fluids
  3. FFP for α-2 macroglobulin replenishments
  4. ABX if concurrent cholangiohepatitis
  5. Corticosteroids
  6. Dopamine → improve splanchnic blood flow
  7. Cobalamin supplementation for life
  8. Vitamin E +/- Vitamin K
189
Q

What is exposed in true peptic ulcers?

A

Muscularis

190
Q

What does Cox 1 inhibition cause in the context of gastric ulcers?

A
  1. Decreased HCO3 secretion
  2. Decreased mucus production
  3. Increased vascular damage
191
Q

What causes inhibition of Gastrin secretion?

A
  1. CCK
  2. Secretin
  3. Somatostatin
  4. VIP/GIP
  5. Decreased pH
  6. Peptide YY
  7. GLP1
192
Q

What is the gastroileal reflex?

A
  1. New meal stimulates ileal peristalsis
193
Q

What is the enterogastric reflex?

A
  1. Acid in the duodenum <4.5 inhibits gastrin secretion

2. Inhibits gastric motility and release of HCl

194
Q

How does Ghrelin increase appetite?

A

Stimulates neurons in the brain that secrete AGRP/NPY in the feeding center

195
Q

Which breeds are reported to have congenital megaesophagus?

A
  1. Wire-haired fox terrier (autosomal recessive)

2. Miniature schnauzer (autosomal dominant/autosomal recessive)

196
Q

What is the underlying defect in type II glycogen storage disease?

A
  1. Deficiency in α-glucosidase
    * May have evidence of megaesophagus in these patients
    * Spitz → die by 2 years
197
Q

What is the underlying defection type III glycogen storage disease?

A

Deficiency in glycogen debranching enzyme (amylo-1,6-glucosidase)

  • Rapidly fatal
  • German shepherds
198
Q

What is the underlying defect in type IV glycogen storage disease?

A

Deficiency in phosphofructokinase

  • Can exhibit hemolytic anemia
  • Springer Spaniels
199
Q

What is the most common cause of acquired megaesophagus?

A
  1. Myasthenia gravis
200
Q

What is group 1 myasthenia gravis?

A
  1. Focal → esophagus, pharynx, facial muscles

* Often misdiagnosed as “idiopathic megaesophagus”

201
Q

What is group 2 myasthenia gravis?

A
  1. Generalized

2. Muscle weakness + megaesophagus

202
Q

What is group 3 myasthenia gravis?

A
  1. Acute fulminant
203
Q

What is group 4 myasthenia gravis?

A
  1. Paraneoplastic (thymoma)

* Cats with MG more likely to have a mediastinal mass (25.7%) compared to dogs (3.4%)

204
Q

What is the gold standard diagnostic for myasthenia gravis?

A

ACh receptor antibody test by immunoprecipitation radioimmunoassay

205
Q

False positives are (common/rare) in the ACh receptor antibody test

A
  1. Rare
206
Q

What is the treatment for myasthenia gravis?

A
  1. AChase inhibitors → pyridostigmine and neostigmine

2. Elevated feedings

207
Q

What is unique about myasthenia gravis in dogs compared to humans?

A
  1. Dogs can go into spontaneous remission → if not paraneoplastic
    * Recurrence is RARE once remission is achieved
208
Q

What is the pathway for bile secretion?

A
  1. Hepatocytes → bile caniculi → interlobular septa → terminal bile ducts → hepatic duct → common bile duct → then either:
    a. Enters the duodenum
    b. Diverts up into the cystic duct into the gall bladder for storage
209
Q

Bilirubin is primarily conjugated to _____ after RBC breakdown

A
  1. Glucaronic acid
210
Q

What is the main bile acid?

A
  1. Taurocholic acid
211
Q

Why might hepatic microvascular disease be more common than we think/is reported?

A

Most dogs are asymptomatic

212
Q

What is the anatomical site associated with microvascular dysplasia?

A
  1. Terminal portal veins
213
Q

Which breed is reported to have inherited microvascular dysplasia?

A
  1. Cairn terriers
214
Q

What are some differences in diagnostic findings in hepatic microvascular dysplasia compared to portosystemic shunts?

A 
Clinical signs/breeds will be similar
MVD will NEVER have
1. Microcytosis
2. Urate crystalluria
3. Hyperammonia
215
Q

What is the hallmark diagnostic finding in hepatic microvascular dysplasia?

A
  1. Elevated bile acids with no macroscopic vascular anomaly
216
Q

Liver biopsy (can/can not) distinguish hepatic microvascular dysplasia from portosystemic shunts

A
  1. Does not

- Histopath changes are the same

217
Q

What will be seen on a mesenteric portogram in hepatic microvascular dysplasia patients?

A
  1. Prolonged tissue “contrast blush”

- Due to deranged portal venous or sinusoidal perfusion

218
Q

What is the treatment for hepatic microvascular dysplasia?

A
  1. > 95% require no treatment other than pharmacologic caution for consequences of delayed metabolism or plasma clearance
  2. If treatment is necessary → diet adjustments are usually all that is needed
219
Q

Portosystemic shunts are 30x (more/less) common than microvascular dysplasia based on genotyping data

A

Less

220
Q

Which breed has a 59x increased risk for portosystemic shunts?

A
  1. Yorkies

* Himalayan cats are also at an increased risk

221
Q

Large, purebred dogs are more likely to acquire what type of portosystemic shunt?

A
  1. Intrahepatic
222
Q

Abdominal ultrasound is more sensitive for (intrahepatic/extrahepatic) shunts

A
  1. Intrahepatic (100% sensitive)

* Only 80-98% sens for extrahepatic

223
Q

When will ascites be seen in a patient with a portosystemic shunt?

A
  1. If they have severe hypoalbuminemia
    * High portal pressure is not a feature of vein to vein vascular anomalies so ascites does not usually form in PSS patients
224
Q

What are diagnostic findings commonly found in patients with portosystemic shunts?

A
  1. Small liver
  2. Increased bile acids
  3. Decreased liver function tests
  4. Increased ammonia
  5. Decreased portal vein:aorta ratio
  6. Bilateral RENOMEGALY → kidneys are doing the job of gluconeogenesis
  7. Copper colored irises (most cats, some dogs)
  8. MICROCYTOSIS
225
Q

What protein C activity results can be used to differentiate portal vein hypoplasia from portosystemic shunts?

A
  1. Normal dogs = 100%
  2. Portal vein hypoplasia >= 70%
  3. PSS <= 70%
226
Q

Cholestasis (is/is not) an issue with portosystemic shunts

A

Is not

*An increased ALP in these patient is usually from bone growth in young animals

227
Q

What kind of crystalluria has been associated with portosystemic shunts?

A
  1. Ammonium biruate crystals
228
Q

What is the treatment for portosystemic shunts?

A
  1. Surgery → Suture, cellophane, ameroid constrictor
  2. Low protein diet
  3. Lactulose → decrease intestinal transit, acidify colon contents, and reduce production/absorption of ammonia
  4. PPI
  5. Oral antibiotics against urease producing bacteria → neomycin/metronidazole
  6. Liver support (milk thistle)
229
Q

What % of dogs with portosystemic shunts will do well with medical management? What are some positive prognostic factors in these patients?

A
  1. 1/3

2. Older at time of initial clinical signs and high BUN

230
Q

What additional diagnosis should you consider in a patient with a portosystemic shunt that has an increased bile acid that does not normalize after therapy?

A

Microvascular dysplasia

231
Q

What two diseases are grouped into the diagnosis of idiopathic non cirrhotic portal hypertension?

A
  1. Hepatoportal fibrosis

2. Primary hypoplasia of the portal vein

232
Q

What is the underlying cause of idiopathic non cirrhotic portal hypertension

A

Severe diffuse or multifocal intrahepatic portovascular dysplasia

233
Q

Gall bladder mucoceles are likely related to

A

Primary disease of the mucous secreting glands in the gallbladder

  • Hydrophobic bile salts when exposed to epithelium → promote mucus secretion
  • Underlying liver disease, pancreatitis
  • One study showed a significant association with Cushing’s disease
234
Q

What is the diagnostic of choice for gallbladder mucoceles?

A

Abdominal ultrasound → kiwi appearance

235
Q

What is the treatment for gallbladder mucoceles?

A
  1. Surgery
236
Q

What is the peri-operative mortality rate for gallbladder mucoceles? What is a negative prognostic indicator?

A
  1. 20-25%

2. If you need to reconstruct the common bile duct

237
Q

Feline gingivitis and caudal stomatitis patients have what kind of immunoglobulin changes?

A
  1. Decreased SALIVARY IgA

2. Increased SERUM IgM, IgG, and IgA

238
Q

What is the treatment for feline gingivitis and caudal stomatitis?

A
  1. Pull ALL TEETH (usually except canines)

2. Steroids (usually depo) → will rarely work by itself, need to use with extractions

239
Q

Why is the esophagus more susceptible to acid damage?

A
  1. The esophageal mucosa does not have a mucus-bicarb barrier and does not heal by epithelial restitution like the gastric mucosa
  2. Endogenous prostaglandins are not as effective at protecting the esophageal mucosa
  3. Do not produce a mucus cap
240
Q

What are some causes for esophagitis?

A
  1. Gastro-esophageal reflux
  2. Doxycycline
  3. Trauma
  4. Hiatal hernia
241
Q

What is the treatment for esophagitis?

A
  1. Decrease acid → H2 receptor antagnosts, PPI
  2. Increase motility
  3. Maintain nutrition (g-tube)
  4. Sucralfate → questionable efficacy
  5. Bouginage or ballooning
242
Q

Helicobacter (is/is not) zoonotic

A

Is!

243
Q

How is helicobacter diagnosed?

A
  1. Bruch cytology via endoscopy and then smeared on slide and stained → 100X
    * MOST SENSITIVE
  2. Rapid urease test of gastric mucosa
  3. Histopath evaluation (90% sens, 100% spec)
244
Q

What kind of association has been found between helicobacter and vomiting dogs?

A

No true association has been found
- There have been some studies where no other cause of vomiting could be found and the patients were positive on brush cytology. Treatment of the helicobacter improved their signs

245
Q

How is helicobacter treated?

A
  • Only treat if you cant find any other reason for vomiting and the patient is positive on brush cytology*
    1. Amoxicillin, metronidazole, + Pepto
246
Q

Slow waves are always present in the GI tract and (cause/do not cause) muscle contraction

A

Do not cause

247
Q

Why are the action potentials in the GI tract smooth muscle different than in other muscle fibers?

A
  1. Ca/Na channels allow large numbers of Ca ions to enter cells but only a small amount of Na
248
Q

Duodenal effects have a (stronger/weaker) effect on gastric motility and emptying than do gastric factors

A

Stronger

249
Q

What is the most potent inhibitor of gastric emptying?

A

CCK

250
Q

Which is the only GI hormone that will respond to the presence of carbohydrate, fat, AND protein

A

Gastric Inhibitory Peptide (GIP)

251
Q

____ in the duodenum is the major stimulus for release of hormones that inhibit gastric emptying

A

Fat

252
Q

What are the components of saliva? What do they do?

A
  1. Ptyalin (amylase) → digest starch

2. Mucus → contains bicarbonate and potassium

253
Q

What is the primary stimulator for saliva secretion?

A

Parasympathetic influence

254
Q

Saliva is (hypertonic/hypotonic) compared to plasma

A

Hypotonic

255
Q

Pepsin is only active at what pH?

A

<5

256
Q

What is essential for the activation of pepsinogen?

A

HCl

257
Q

What is the mechanism for HCl secretion by parietal cells?

A
  1. H secreted into gastric lumen in exchange for K via a H/K ATPase countertransporter
  2. HCO3 absorbed into circulation in exchange for Cl
258
Q

When are parietal cells maximally activated for HCl secretion?

A
  1. When all of the receptor types are occupied (Histamine receptors, ACh receptors, and gastrin receptors)
259
Q

What is the most potent stimulus for pancreatic juice secretion?

A
  1. Chyme in the upper SI
260
Q

What are the pancreatic enzyme secreted for digestion of the following:

  1. Protein
  2. Carbohydrate
  3. Fat
A
  1. Trypsin, Chymotrypsin, and Procarboxypolypeptidase
  2. Pancreatic Amylase
  3. Pancreatic Lipase, Cholesterol Esterase, and Phospholipase
261
Q

Where are trypsin, chymotrypsin, and procarboxypolypeptidase activated? How?

A
  1. In the small intestine
    2a. Trypsinogen → Enterokinase, Trypsin
    2b. Chymotrypsinogen → Trypsin
    2c. Procarboxypolypeptidase → Trypsin
262
Q

What are the functions of bile salts?

A
  1. Emulsify fats in the small intestine → allows digestion by pancreatic lipases
  2. Allow for absorption of digested fat end products via the formation of MICELLES
  3. Excretion for degradation products → bilirubin and cholesterol excesses
263
Q

Where are bile salts synthesized?

A

Hepatocytes

264
Q

How is bile concentrated in the gallbladder?

A
  1. Active transport of Na (followed by passive absorption of water)
265
Q

Where are Brunner’s glands located? What is their function?

A
  1. First part of the duodenum

2. Secrete large amounts of bicarb in response to → secretin, duodenal irritants, vagal stimulation

266
Q

Where are the Crypts of Lieberkuhn? What is their function?

A
  1. Lie between intestinal villi
  2. Have two types of cells
    - Goblet cells → secrete mucus
    - Enterocytes → secrete water/electrolytes to aid in absorption
267
Q

What are the three main sources of carbohydrates?

A
  1. Sucrose
  2. Lactose
  3. Starches
268
Q

Where does initial carbohydrate digestion begin?

A

In the mouth with amylase

269
Q

What is the main result of carbohydrate digestion in the mouth, stomach, and duodenum?

A

Convert most starches to MALTOSE

270
Q

Enterocytes in the duodenum and jejunum contain which enzymes to help with carbohydrate digestion?

A
  1. Maltase (maltose → glucose)
  2. Sucrase (sucrose → fructose + glucose)
  3. Lactase (lactose → galactose + glucose)
271
Q

Glucose constitutes what % of the final products of carbohydrate digestion?

A

~80%

272
Q

Absorption of glucose and galactose occurs via what mechanism?

A
  1. Secondary active transport with Na via SGLT-1 receptors
273
Q

Absorption of fructose occurs via what mechanism?

A
  1. Facilitated diffusion via GLUT-5 receptors

* Cannot be transported UP a concentration gradient, there is NO active transport

274
Q

Where does initial digestion of protein occur?

A
  1. Stomach via pepsin to proteoses and peptones
275
Q

Where does major digestion of protein occur?

A

Duodenum/Jejunum via pancreatic enzymes to di and tripeptides

276
Q

What happens in enterocytes in the context of protein digestion?

A
  1. Peptidases break down di/tripeptides into amino acids
277
Q

How are amino acids absorbed? Di/Tripeptides?

A
  1. Na-dependent cotransport

2. H-dependent cotransport

278
Q

Where does most fat digestion take place?

A
  1. Duodenum
279
Q

What is the process of fat digestion?

A
  1. Break down fat globules via emulsification with bile salts and lecithen
  2. Allow pancreatic lipase, phospholipase, and cholesterol ester hydrolase to digest fats to glycerol, free fatty acids, and monoglycerides
  3. Enclose digestion products in micelles to ferry them into the enterocytes to allow for passive absorption
  4. Bile acids are taken up in the ileum by secondary active transport coupled with Na
280
Q

What is the gold standard for quantifying gastric emptying?

A

Scintigraphy

281
Q

What are the forms of idiopathic hepatic fibrosis? Which has the worst prognosis?

A
  1. Diffuse pericellular → worst prognosis
  2. Central perivenous
  3. Periportal
282
Q

What is the treatment for idiopathic hepatic fibrosis?

A
  1. Steroids → inhibits Prolyl hydroxylase (plays a role in collagen stability), anti-inflammatory
  2. D-Penacillamin → inhibit collagen synthesis and disrupt cross-linking of collaged by interfering with Lysyl oxidase
  3. Zinc → inhibits Prolyl oxidase
  4. Colchicine → activates collagenase, inhibits Prolyl hydroxylase
283
Q

What are medications that inhibit Prolyl hydroxylase?

A
  1. Steroids
  2. Zinc
  3. Colchicine
284
Q

What are medications that inhibit lysyl oxidase?

A
  1. D-penacillamine
285
Q

What is the gold standard for documenting intestinal protein loss?

A
  1. Quantitate radio labeled albumin in the feces after IV administration
286
Q

What is the pathognomonic finding for histiocytic ulcerative colitis?

A
  1. Period acid-Schiff positive macrophages
287
Q

What are the two most common causes of chronic colitis in dogs?

A
  1. Whipworms and Diet responsive diarrhea
288
Q

How is ulcerative colitis treated?

A

Baytril

289
Q

What are the characteristics for the best diet for small intestinal diarrhea?

A
  1. Single protein source, not high content
  2. Single carbohydrate source
  3. No gluten, no lactose
  4. Low fat
  5. Highly digestible
  6. Isotonic
290
Q

What is epithelial restitution?

A
  1. Epithelial cells adjacent to a defect will flatten and migrate over the exposed basement membrane
  2. Dose not involve proliferation of these epithelial cells
  3. Results in an area that is protected but is not physiologically functional
291
Q

What is the pacemaker of the GI tract?

A

The interstitial cells of Cajal

292
Q

What is the most important secretagogue for stimulation of gastric acid secretion?

A

Histamine

293
Q

What is the MOA of proton pump inhibitors?

A
  1. Blocks parietal cell H/K ATPase
  2. Inhibits gastric acid secretion irrespective of the stimulus
  3. Inhibit p450
294
Q

What frequency of administration of PPIs is needed for dogs with ulcerative disease?

A

Twice daily

295
Q

Why are PPIs and H2 receptor agonists not recommended to be given together?

A
  1. PPIs get trapped in parietal cells if they are acidic
  2. When H2 receptor agonists are given, the acidity of the parietal cells is decreased and the ability of the PPI to get protonated and trapped in the cell is decreased
296
Q

Why are H2 receptor agonists less effective than PPIs?

A
  1. They work really well on days 1 and 2
  2. Tolerance is induced in dogs with famotidine by day 12-13 → tolerance for H2 agonists occurs in people at all types and doses
  3. Better for short term use or low level acid suppression
297
Q

What are the adverse effects of PPIs in animals?

A
  1. Diarrhea → changes in fecal microbiota
  2. Hypergastrinemia
  3. p450 inhibitor and pH dependent drug reactions
  4. Cats - rebound gastric hyperacidity
298
Q

What inhibits gastrin secretion?

A
  1. Decreased stomach pH

2. Somatostatin

299
Q

What inhibits CCK secretion?

A
  1. Somatostatin
300
Q

What inhibits secretin secretion?

A
  1. Somatostatin
301
Q

What is the source of GLP-1?

A

L cells in the ileum and colon

302
Q

What stimulates GLP-1 secretion?

A
  1. Lipids

2. Glucose

303
Q

What are the actions of glucagon-like peptide 1 (GLP-1)?

A
  1. β cells → insulin release

2. Stomach → INHIBITS gastric emptying

304
Q

What is the source of gastric inhibitory peptide (GIP)?

A
  1. K cells of the duodenum and jejunum
305
Q

What is the stimulus for gastric inhibitory peptide (GIP) secretion?

A
  1. Fatty Acids
  2. Glucose
  3. Amino acids
306
Q

What are the actions of gastric inhibitory peptide (GIP)?

A
  1. INHIBITS intestinal motility and gastric emptying → acts on Myenteric (Aurbach) plexus
  2. Decrease H secretion in the stomach
  3. Stimulates insulin secretion
307
Q

What is the source of histamine?

A
  1. Enterochromaffin like cells (ECL)
308
Q

What is the stimulus for histamine release?

A

Gastrin

309
Q

What inhibits histamine release?

A
  1. Somatostatin
310
Q

What is the action of histamine in the GI tract?

A
  1. Increase H+ secretion
311
Q

What is the source of vasoactive intestinal peptide (VIP)

A

Neurons in teh mucosa and smooth muscle of the GI tract

312
Q

What are the actions of vasoactive intestinal peptide (VIP)?

A
  1. Produces GI smooth muscle relaxation
  2. Stimulates HCO3 secretion
  3. Inhibits H secretion by the stomach
313
Q

What is the source of intrinsic factor?

A
  1. Parietal cells of the gastric antrum
314
Q

What is the stimulus for intrinsic factor release?

A
  1. Gastrin
  2. Histamine
  3. ACh
315
Q

What inhibits intrinsic factor release?

A
  1. Somatostatin
316
Q

What is the action of intrinsic factor?

A

Allows for absorption of vitamin B12 in the ileum

317
Q

Where are G cells located?

A
  1. Gastric Antrum
318
Q

Where are chief cells located?

A
  1. Gastric Body
319
Q

Where are I cells located?

A
  1. Duodenum

2. Jejunum

320
Q

Where are S cells located?

A
  1. Duodenum

2. Jejunum

321
Q

Where are L cells located?

A
  1. Ileum

2. Colon

322
Q

Where are K cells located?

A
  1. Duodenum

2. Jejunum

323
Q

Where are the D cells located?

A

Pancreas

*Some scattered in the stomach and duodenum

324
Q

Where are M cells located?

A
  1. Duodenum

2. Jejunum

325
Q

Where are epsilon cells?

A

Pancreas

326
Q

Where are parietal cells located?

A

Gastric body

327
Q

Where are enterochromaffin like cells located?

A

Gastric body

328
Q

True/False

The in-house ELISA for CPV-2 detects antigen in feces for parvovirus in dogs?

A

True

329
Q

Fecal Alpha-1 Proteinase Inhibitor serves as a marker for what?

A
  1. Intestinal protein loss
330
Q

Bacterial flagellin is recognized by which TLR?

A

TLR5

331
Q

Which breed is predisposed to congenital esophageal fistulae?

A

Cairn Terriers

332
Q

What is the treatment for Spirocerca lupi esophageal granulomas?

A

Doramectin

333
Q

Which enzyme that is important for maintaining cobalamin levels is lacking in the cat?

A

Transcobalamin I

334
Q

Why does hyperthyroidism cause diarrhea in cats?

A

Hypermotility

335
Q

When is campylobacter infection most pathogenic in the dog?

A

When it is combined with infection of a viral organism

336
Q

What is the primary immunoglobulin produced in healthy intestinal mucosa?

A

1gA

337
Q

3-Bromotyrosine is a stable product of which cell?

A

Eosinophils

338
Q

What is the most common colonic tumor?

A

Adenocarcinomas

339
Q

Cats have a (lower/higher) rate of metastasis for colorectal adenocarcinomas compared to dogs

A

Higher

340
Q

Which GI hormones show neurocrine activity?

A
  1. Gastrin
  2. CCK
  3. Somatostatin
  4. VIP
341
Q

Which GI hormones show paracrine activity?

A
  1. Somatostatin

2. Peptide YY

342
Q

Which GI hormones show solocrine activity?

A
  1. Pepsinogen
343
Q

Which GI hormones show endocrine activity?

A
  1. Gastrin
  2. CCK
  3. Secretin
  4. GLP-1
  5. GIP
  6. Somatostatin
  7. Motilin
  8. Ghrelin
  9. Peptide YY
344
Q

What clinical signs can be seen with thiamine deficiency in cats?

A

CNS signs and neck ventroflexion

345
Q

Where are the following located? What stimulates them?

  1. Satiety Center
  2. Feeding Center
A
  1. Ventromedial aspect of the hypothalamus → POMC

2. Lateral hypothalamus → Neuropeptide Y

346
Q

How does the composition of saliva change

  1. With low flow rates
  2. With high flow rates
A
  1. Lowest osmolarity and lowest Na, Cl, and HCO3; Highest K → has more time for the resorption and secretion process to occur
  2. Closest to that of plasma
347
Q

How is stimulation of saliva production unique?

A
  1. It is stimulated by both the parasympathetic and sympathetic nervous systems
348
Q

What inhibits gastric H secretion?

A
  1. Low stomach pH (<3.0)
  2. Somatostatin
  3. Prostaglandins
349
Q

Salivary ducts reabsorb ____ and secrete _____. Aldosterone acts on the salivary ducts to ____.

A
  1. Na and Cl
  2. K and HCO3
  3. Increase Na reabsorption and K secretion
350
Q

How does somatostatin inhibit gastric H secretion?

A
  1. Directly → binds to receptors on parietal cells

2. Indirectly → inhibits release of histamine and gastrin

351
Q

What is the alkaline tide?

A

When a large amount of HCO3 is absorbed into the bloodstream from parietal cells after a meal → this HCO3 is eventually used in pancreatic secretions to neutralize H in the intestine

352
Q

How is bile formed?

A
  1. Primary bile acids (cholic acid and chenodeoxycholic acid) are synthesized from CHOLESTEROL in hepatocytes
  2. In the INTESTINE, bacteria convert primary bile acids into secondary bile acids (deoxycholic acid and lithocholic acid)
  3. Bile acids are then conjugated to either taurine or glycine to form bile salts
  4. Electrolytes and H20 are added to the bile
  5. During the inter digestive period, the gallbladder is relaxed and the sphincter of Oddi is closed → the gallbladder fills with bile
  6. In the gallbladder, bile then becomes concentrated as a result of isosmotic absorption of solutes and H2O
353
Q

What would be caused by a lack of apoprotein B?

A

The inability to transport chylomicrons out of the intestinal cells

354
Q

What are the fat soluble vitamins?

A

Vitamins A, D, E, and K

355
Q

What is calcium absorption in the small intestine dependent on?

A
  1. The active form of vitamin D (1,25-dihydroxycholecalciferol)
    - Induces the synthesis of an intestinal Ca binding protein → calbindin D-28K
356
Q

How is iron absorbed in the GI tract?

A
  1. Either has heme iron or as free Fe2+
  2. In intestinal cells → heme iron is degraded to free Fe2+
  3. The free Fe2+ binds to apoferritin and is transported into the blood
  4. Free Fe2+ circulates in blood bound to transferrin which transports it from SI to storage sites in the liver or from the liver to the BM for the synthesis of hemoglobin
357
Q

How is bilirubin produced and excreted?

A
  1. Hgb is degraded to bilirubin
  2. Bilirubin is carried in the blood bound to albumin
  3. In liver, bilirubin is conjugated to glucuronic acid by UDP glucoronyl transferase and becomes conjugated bilirubin
  4. A portion is excreted in the urine and some is in the bile
  5. In the intestine, conjugated bilirubin is converted to urobilinogen
    - Urobilinogen is returned to the liver via enterohepatic circulation
    - Urobilin and stercobilin are excreted in feces
358
Q

What is considered the main nutrient for enterocytes?

A
  1. Glutamine
359
Q

What is the most ammoniagenic protein?

A

Blood

360
Q

What is the most common cause of hepatic encephalopathy?

A
  1. PSS
361
Q

What is the most common cause of hyperlipidemia?

A
  1. Post-prandial
362
Q

What is secreted in the bile that aids in iron absorption?

A
  1. Apotransferrin
    * Called transferrin when bound to iron
    * Ferritin is the storage form
363
Q

What is the enzyme that breaks down triglycerides in chylomicrons?

A
  1. Lipoprotein lipase
364
Q

What do the following cells of the pancreas secrete?

  1. Alpha
  2. Beta
  3. Delta
A
  1. Glucagon
  2. Insulin
  3. Somatostatin
365
Q

Basenji enteritis is characterized by what immunoglobulin?

A

IgA

366
Q

Sucralfate stimulates the increase of what?

A
  1. Prostaglandin E2
  2. Epidermal growth factors
  3. bFGF
  4. Gastric Mucus

ACVIM General copy (15 decks)

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