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ACVIM Generals > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is the definition of an endocrine hormone?

A

Released into the bloodstream and travels to a distant site

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2
Q

What is the definition of a paracrine hormone?

A

Diffuses only short distances through the extracellular space. Acts LOCALLY

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3
Q

What is the definition of an autocrine hormone?

A

Subset of paracrine but acts on same cell that produces it

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4
Q

What is the definition of a neurocrine hormone?

A

Released from nerve endings, diffuses short distances through extracellular space

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5
Q

What are the enteroendocrine cells?

A

“Taste buds” of the gut

Scattered throughout the mucosal layer of the gut

LARGEST endocrine organ in the body

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6
Q

Is the parasympathetic or sympathetic nervous system stimulatory to the GIT for digestion?

A

Parasympathetic stimulates digestion

“rest and digest”

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7
Q

What nerves innervate the upper and lower GIT in the parasympathetic portion of the extrinsic nervous sytem?

A

Vagus nerve - upper GIT

Pelvic nerve - lower GIT

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8
Q

What is the neurotransmitter of the parasympathetic system?

A

Acetylcholine

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9
Q

What neuropeptides are released by the parasympathetic system in the GIT?

A

Substance P
Vasoactive intestinal peptide (VIP)
Neuropeptide Y (NPY)

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10
Q

What percentage of the nerve fibers in the vagus nerve are afferent vs. efferent?

A

75% afferent

25% efferent

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11
Q

Most of the sympathetic action of the GIT in the extrinsic nervous system comes from what nerves?

A

Spinal segments of T1 to L3

50/50 afferent to efferent

Norepinephrine is the neurotransmitter

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12
Q

What are the two main components of the enteric nervous system of the GIT and what are their functions?

A

Myenteric plexus - movements

Submucosal plexus - secretion and local blood flow

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13
Q

What glands are found in the body of the stomach? What cells are found in these glands and what do they secrete?

A

Oxyntic glands - secrete a number of hormones.

Parietal cells - secrete HCl
Enterochromaffin-like cells - secrete histamine
D cells - secrete somatostatin
Chief cells - secrete pepsinogen

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14
Q

What glands are found in the antrum of the stomach? What cells are found in these glands and what do they secrete?

A

Pyloric glands - less hormone secretion than in the body

G cells - secrete gastrin
D cells - secrete somatostatin

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15
Q

What three major stimuli cause release of gastrin?

A

Stretch - causes vagal stimulation which releases bombesin
Peptides
Amino acids

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16
Q

Stretch in the stomach causes stimulation of what nerves and results in what effects?

A

Stretch signal received by nerves of the gastric mucosa which are part of the parasympathetic system –> release ACh which acts on G cells to release gastrin

Stretch signal also stimulates vagus nerve –> release of gastrin-releasing peptide (bombesin) from vagus nerve –> stimulates G cell to release gastrin

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17
Q

What two amino acids are the major stimulators of gastrin release?

A

Phenylalanine
Tryptophan

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18
Q

What cells does gastrin act on?

A

Parietal cells
Enterochromaffin like cells

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19
Q

Does gastrin act in an endocrine, paracrine, or neurocrine manner?

A

endocrine - after release, enters the bloodstream, goes through portal vein, then goes through liver and are circulated back to the body of the stomach

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20
Q

__ is secreted by enterochromaffin like cells (ECLs) and acts in what manner (endocrine, paracrine, or neurocrine manner) and in what cells?

A

Histamine

Paracrine - acts on parietal cells within the oxyntic glands where the ECLs are located

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21
Q

Tubulo-vesicles within parietal cells have what receptors?

A

H/K/ATPases

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22
Q

What three receptors are found on pareital cells and what are the three secretagogues that bind them to activate the parietal cells?

A

M3 receptor: muscarinic receptor that binds ACh (which comes from vagal input)
H2 receptor: binds histamine
CCK-B: gastrin

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23
Q

M3 receptors on parietal cells bind __ which causes increases in __ inside the cell for activation.

A

Bind ACh
Causes increases in calcium

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24
Q

What two secretagogues that bind parietal cell receptors cause increases intracellular calcium levels?

A

ACh
Gastrin

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25
Q

CCK-B receptors on parietal cells bind __ which causes increases in __ inside the cell for activation.

A

Gastrin
Causes increases in calcium

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26
Q

H2 receptors on parietal cells bind __.

A

Histamine

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27
Q

Which receptor is the most potent stimulator of parietal cells?

A

H2 receptor

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28
Q

By what mechanism does histamine binding to H2 receptors activate parietal cells?

A

Causes increases in cAMP

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29
Q

After activation, what happens to the parietal cells?

A

They undergo conformation change. The luminal membranes become highly folded to increase surface area for proton pumps to have more access to the outside of secretion of HCl

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30
Q

Describe the steps of acid production in the proton pumps of parietal cells

A

Water cleaved to OH- and H+

H+ is exchanged for K+ (H+ goes out, K+ comes in) via H/K/ATPase pumps. H+ is secreted into lumen of canaliculus.

On the opposite side (membrane by interstitial fluid), Na/K/ATPase pumps exchange Na+ for K+ (Na+ goes out, K+ goes into cell). This contributes to passive excretion b/c of high intracellular gradient of K+, which allows for exchange with hydrogen.

Na+ will leak into cell from lumen of canaliculus which drives the Na/K/ATPase pump

Carbon dioxide that diffuses into the cell combines with the OH- ion to form bicarb (HCO3-)

BIcarb is exchanged for Cl- from the interstitial fluid. Chloride passively diffuses all the way through the parietal cell to the lumen of canaliculus

Finally, water passes through parietal cell to canaliculus.

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31
Q

What hormones inhibit acid secretion by parietal cells?

A

Secretin
CCK
Prostaglandins
Dopamine
Somatostatin
GIP
Peptide YY
Enteroglucagon

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32
Q

What is pepsinogen and where does it come from?

A

Precursor for pepsin, which is a protein digestive enzyme
Comes from chief cells

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33
Q

What two main stimulus cause release of pepsinogen?

A

ACh binding chief cells (from vagus nerve)

HCl secretion from parietal cells

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34
Q

Pepsin results in how much of total protein digestion?

A

10-20%

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35
Q

What stimulus tells D cells to release somatostatin?

A

Decrease in gastric pH (happens when food starts to leave the stomach –> parietal cells are still secreting acid but food is no longer there to buffer it so it creates a very acidic environment)

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36
Q

What is the paracrine action of somatostatin?

A

Inhibit gastrin secretion by G cells (this leads to decreased activation of ECL cells which in turn decreases activation of parietal cells leading to decreased acid production)

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37
Q

What is the endocrine action of somatostatin?

A

Decrease parietal cell acid secretion

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38
Q

What is the neurocrine action of somatostatin?

A

Decreases gastric motility

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39
Q

What are the phases of gastric secretion?

A

Cephalic phase - 30%
Gastric phase - 60%
Intestinal phase - 10%

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40
Q

What stimulates the cephalic phase of gastric secretion and what happens in this phase?

A

Stimulated by sight/smell of food

ACh release from Vagus n.
Gastrin release from G cell
Histamine release from ECL cells

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41
Q

What stimulates the gastric phase of gastric secretion and what happens in this phase?

A

Stimulated by gastric digestion and release of peptides, as well as stretch of the stomach

Gastrin is released by G cells

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42
Q

What stimulates the intestinal phase of gastric secretion and what happens in this phase?

A

Stimulated by gastric emptying

Causes decrease in intestinal and gastric antral pH –> mediated by release of somatostatin from D cells, release of secretin from S cells, and release of CCK from I cells

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43
Q

What is Zollinger-Ellison Syndrome (ZES) and what tumor type is it associated with?

A

Triad of Non-B-islet cell tumor of pancreas, hypergastrinemia, and refractory peptic ulcer disease

Can be sporadic and a genetically linked form, sporadic more common

Gastrinomas

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44
Q

What is MEN-1?

A

Rare heritable disorder in people characterized by predisposition to tumors of the parathyroid gland, anterior pituitary gland, and pancreatic islet cells

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45
Q

What PANCREATIC cell types transform to form gastrinomas in dogs and cats?

A

Delta cells

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46
Q

Gastrinomas cause excessive release of __.

A

Gastrin

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47
Q

What changes to the GIT result from excessive release of gastrin in cases of gastrinomas?

A

Esophageal and gastroduodenal erosins and ulcerations

Enzymatic maldigestion

Gastric antral hypertrophy (b/c gastrin stimulates growth of these cells) –> results in delayed gastric emptying and possible gastric outflow obstruction

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48
Q

What are the two most common clinical signs associated with gastrinomas?

A

Vomiting
Weight loss

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49
Q

How do we diagnose a gastrinoma in veterinary medicine?

A

Measure fasting serum gastrin

If >3x reference range (often will be at least 10x reference range)

Remember gastrin levels may be transiently normal so you may need to retest

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50
Q

What drugs can be used to treat gastrinomas?

A

Somastostatin analogs

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51
Q

What is an example of a somatostatin analog?

A

Ocretotide

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52
Q

What does ocretoide do?

A

Inhibits gastric acid release form parietal cells

Inhibits gastrin release from G cells

Decreases tumor load in gastrinomas

Reduces ECL cell hyperplasia

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53
Q

What two hormones in the stomach are involved in control of hunger?

A

Grehlin
Leptin

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54
Q

__ increases hunger and __ stimulates satiety/decreases hunger

A

Grehlin increases hunger

Leptin stimulates satiety

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55
Q

Where is the majority of ghrelin produced? What are other minor sites that produce ghrelin?

A

Major source= stomach, specifically from the oxyntic glands

Also intestine, pancreas, hypothalamus

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56
Q

What stimulates ghrelin release?

A

FASTING

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57
Q

What are the actions of ghrelin?

A

Acts on pituitary to stimulate growth hormone secretion

Stimulates appetite, body growth, and fat deposition

Decreases production of pro-inflammatory cytokines (like NFkB) and increases production of anti-inflammatory cytokines (like IL-10)

Increases rate of gastric emptying (which may be helpful in post-op ileus)

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58
Q

What is an example of a ghrelin agonist?

A

Capromorelin (Entyce in dogs/Elura in cats)

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59
Q

Capromorelin is though to help with lean muscle mass due to effects on what two substances?

A

Growth hormone
IGF-1 concentrations

Transient increases in GH and sustained increase in IGF-1 concentrations has been documented in healthy adult beagles. Concern theoretically that it may lead to insulin resistance, so use caution in diabetics

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60
Q

What cells secrete leptin?

A

Adiopocytes

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61
Q

What is the stimulus for leptin scretion?

A

Increased adipose tissue

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62
Q

What are actions of leptin?

A

Decrease production of appetite stimulators in hypothalamus (neuropeptide Y, Agouti-related protein)

Activation of POMC neurons (alpha-melanocyte-stimulating hormone which increases activation of melanocortin receptors)

Increases sympatetic activity which leads to increased metabolic rate and increased energy expenditure

Decreased insulin secretion

Increased TNF-alpha productions and macrophage activation—> makes inflammatory conditions worse

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63
Q

What cells of the duodenum secrete secretin?

A

S cells

S cells are also found in the jejunum

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64
Q

What stimulates release of secretin?

A

Low duodenal pH
Intraduodenal lipid

Aka chyme entering duodenum

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65
Q

Secretin acts in an edocrine/paracrine/autocrine function

A

Endocrine - enters bloodstream and travels to stomach to act on parietal cells

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66
Q

What are the actions of secretion?

A

Inhibit acid secretion by inhibition of parietal cells

Slows gastric emptying

Secretion of HCO3- rich pancreatic fluid

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67
Q

Cholecystokinin (CCK) is released from what cells of the duodenum?

A

I cells

I cells are also found in the jejunal mucosa

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68
Q

What stimulates CCK release?

A

Intraduodenal FAs, amino acids, and H+ ions

Usually driven by amino acids

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69
Q

Does CCK act in an endocrine/paracrine/neurocrine manner?

A

Endocrine

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70
Q

What organs does CCK act on?

A

Pancreas
Gallbladder

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71
Q

What are the actions of CCK in the pancreas?

A

Potentiates secretin

Pancreatic enzyme secretion - acts on acinar cells

Stimulation of pancreatic growth

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72
Q

What are the actions of CCK in the gallbladder?

A

Gall bladder contraction

Relaxation of sphincter of Oddi

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73
Q

What two cell types are found in the exocrine pancreas?

A

Acinar cells
Ductal cells

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74
Q

Which pancreatic digestive enzymes are secreted by acinar cells?

Which are secreted in their active form?

A

Amylase
Lipase
Trypsinogen

Amylase and lipase secreted in active form

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75
Q

What enzyme converts trypsinogen to trypsin?

A

Enterokinase - this is a brush border enzyme

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76
Q

What stimulates acinar cells to secrete digestive enzymes?

A

CCK
ACh

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77
Q

Amylase digests what?

A

Starch

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78
Q

Lipase hydrolyzes what?

A

Triglycerides

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79
Q

What stimulates ductal cells to release bicarb and water?

A

Secretin

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80
Q

What are the three phases of pancreatic secretion?

A

Cephalic - 20%
Gastric - 5-10%
Intestinal - 70-75%

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81
Q

What do bile acids do?

A

Help emulsify large fat particles of food to smaller particles that can be digested by lipase enzymes

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82
Q

In the duodenum, bile acids are ionized to form __, which prevents their reabsorption from the small intestine.

A

Bile salts

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83
Q

In the ileum, bile acids are deconjugated into what?

A

Secondary bile acids

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84
Q

What are the two most common secondary bile acids?

A

Deoxycholic acid
Lithocholic acid

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85
Q

Can secondary bile acids be reabsorbed from the distal ileum?

A

Yes - this is enterohepatic recirculation

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86
Q

What percentage of bile acids are reabsorbed for enterohepatic recirculation and what percentage are excreted?

A

95% reabsorbed
5% secreted

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87
Q

In the liver, what amino acid are bile acids conjugated to?

A

Taurine (main in dogs, only one in cats)
Glycine to a lesser extent in dogs (not in cats)

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88
Q

What is an incretin?

A

A hormone that stimulates pancreatic insulin release

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89
Q

What cells in the duodenum produce GIP?

A

K cells

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90
Q

What stimulates release of GIP?

A

Intraduodenal FA and AAs, and to a lesser degree carbohydrates

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91
Q

Does GIP act in endocrine/paracrine/neurocrine function?

A

Endocrine - travels via blood to act on parietal cells and pancreatic Beta cells)

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92
Q

What are the actions of GIP?

A

Inhibition of gastric acid secretion (acts on parietal cells)

Stimulation of pancreatic insulin release during hyperglycemia

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93
Q

Other than GIP, what is the other main incretin?

A

Enteroglucagon/Glucagon-like peptide-1 (GLP-1)

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94
Q

Where is GLP-1 produced?

A

L cells of the ileum and colon (widely distributed throughout the gut in cats)

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95
Q

What is the stimulus for GLP-1 release?

A

Intraluminal glucose and lipids

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96
Q

What are the actions of GLP-1?

A

Inhibit gastric acid secretion

Acts on pancreatic islet (Beta) cells to stimulate insulin secretion

Acts as the “ileal brake” - when there are FAs in the ileum it will act on the stomach to inhibit gastric emptying

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97
Q

What effects on pancreatic Beta cells do GLP-1 and GIP have?

A
  • Stimulation of insulin biosynthesis –> replenishment of stores
  • Stimulation of Beta cell proliferation
  • Promotion of Beta cell resistance to apoptosis
  • Enhanced Beta cell survival
98
Q

GLP-1 inhibits __ secretion by alpha cells in the pancreas

99
Q

What enzyme inhibits GLP-1?

100
Q

Cats lack what receptor that causes sweet compounds to taste bitter?

101
Q

Where is peptide YY produced?

A

distal ileum and colon

102
Q

What stimulus causes peptide YY release?

A

Fatty acids
To a lesser degree carbohydrates

103
Q

What are the actions of peptide YY?

A

Ileal brake
Inhibition of CCK and secretin
Proliferation of gut mucosa
Slows gastric emptying

Peptide YY is also known as GLP-2

104
Q

What is the MOA of dirlotapide/Slentrol

A

A microsomal membrane transfer protein (MTP) inhibitor –> results in increased peptide YY secretion and GLP-1 secretion in rats

Utilized for weight loss in dogs

105
Q

What is the gastrocolic reflex?

A

Distention of the stomach leads to activation of the colon resulting in defecation

106
Q

What are the two general types of movement that are involved in GI motility?

A

Segmentation

Peristalsis

107
Q

What is segmentation and what does it cause GI contents to do?

A

The random contraction of circular muscles

Mixes food with digestive enzymes and brings nutriends in contact with absorptive surfaces. Also slows transit time

108
Q

What is peristalsis and what does it cause GI contents to do?

A

Short wave of constriction moving abnorally over a short segment of intestine

Moves contents aborally

109
Q

Craniual contraction in peristalsis is regulated by what two things?

A

ACh
Substance P

110
Q

Caudal relaxation in peristalsis is regulated by what two things?

A

Vasoactive intestinal peptide (VIP)
Nitric oxide

111
Q

What are the two periods of motility?

A

Fasting motility (interdigestive period)

Fed motility (digestive period)

112
Q

What part of the gastric nervous system regulates fasting motility?

A

Enteric nervous system

113
Q

What part of the gastric nervous system regulates fed motility?

A

Vagus coordination with enteric nervous system

114
Q

What is the migrating motility complex?

A

“housekeeper” that clears gut of undigested residue and prevents bacterial overgrwoth

Happens every 90 minuts

115
Q

What species DO NOT have the MMC? (but have somthing sijmilar)

A

Cats
Rabbits

116
Q

What do cats and rabbits have in place of MMC?

A

Migrating spike complex

117
Q

Where does the MMC start?

118
Q

T/F: The MMC includes the gallbladder

119
Q

What are the three phases of MMC?

A

Phase 1 - quiescence - slow waves that don’t progress to threshold so no contraction

Phase 2 - Intermittent contractions that gradually increase in frequency and amplitude - similar to that with feeding

Phase 3 - intense propulsive motility - happens every 4-8mins - initiated by motilin

120
Q

Where is motilin produced?

A

M cells in the stomach, small intestine, and colon

121
Q

What stimulates motilin release?

A

H+ and lipid in the fed state

Episodically released into serum during fasting

122
Q

In what state is motilin most important?

A

Fasting (interdigestive) state

123
Q

What is the action of motilin?

A

Initiate phase 3 of the MMC

124
Q

What drug mimics motilin?

A

Erythromycin and other macrolide-like antibiotics

125
Q

5-hydroxytryptamine is also known as what?

126
Q

Where is serotonin produced?

A

Enterochromaffin cells and enteric neurons throughout the GIT

127
Q

What are the actions of serotonin in the GIT?

A

Stimulates gastrointestinal smooth muscle contraction

Intestinal electrolyte secretion

128
Q

5-HT4 agonists include what?

A

Metoclopramide (also a dopaminergic D2 antagonist)
Cisapride
Tegaserod

129
Q

What is the MOA of 5-HT4 receptor agonists?

A

Bind 5-HT4 receptors on enteric cholinergic neurons causing depolarization and contraction of GI smooth muscle

130
Q

Cisapride stimulates distal esophageal peristalsis in what species and why?

A

Cat, human, Guinea pig

NOT DOG

b/c these species have a distal esophageal muscularis composed of smooth muscle

131
Q

What are intestinal carcinoids?

A

Tumors of endocrine cells of the GIT. They contain secretory granules that contain serotonin, secretin, somatostatin, and gastrin

Can also present in tracheobronchial tree, pancreas, and genitourinary system

132
Q

What is the most common form of gastritis in dogs?

A

Mild to moderate lymphoplasmacytic gastritis with lymphoid follicle hyperplasia

133
Q

What parasites are associated with parasitic gastritis in dogs and cats?

A

Ollulanus tricuspis (cats)
Physaloptera
Gnathostoma (cats)
Spirocerca (dogs)

134
Q

What fungal organism causes granulomatous gastritis?

135
Q

What is the treatment and prognosis for pythium?

A

Itraconazole and terbinafine
Poor prognosis

136
Q

Gastric ulcers develop when __ and __ overcome the protective mechanisms of the mucosa

A

gastric acid and pepsin

137
Q

What clin path abnormalities would you expect with gastric ulcers?

A

Microcytic hypochromic minimally regenerative anemia
Thrombocytosis
High BUN

138
Q

What drug can be used to treat gastric ulcers?

A

Misoprostal

139
Q

What is the MOA of misoprostal?

A

PGE2 analog

140
Q

Pyloric perforation has been associated with what drugs?

141
Q

Helicobacter is a gram __, __ shaped bacteria

A

Gram negative
Spiral shaped

142
Q

Helicobacter produce __ which results in production of ammonia and bicarbonate when in contact with __ in gastric juices

A

Urease
Urea

143
Q

True/false: There is correlation between Helicobacter infections and gastritis/ulceration in cats and dogs.

144
Q

How is Helicobacter treated?

A

Triple therapy with amoxicillin, metronidazole, and omeprazole/famoitine

+/- bismuth subsalicylate

145
Q

What is the most common gastric neoplasm in dogs and the most common in cats?

A

Dogs - gastric adenocarcinoma
Cats - lymphoma

146
Q

Where does feline gastrointestinal eosinophilia sclerosing fibroblasia (FGESF) form lesions and in what breed and sex of cats is it most common?

A

Stomach, intestines, and regional LNs
Male rag doll cats

147
Q

What is the treatment for FGESF?

A

Surgical excision
Immunosuppressive steroids, and antibiotics (to prevent translocation)

148
Q

What might you see on histopath with FGESF?

A

Eosinophilic inflammation, large reactive fibroblasts, and dense collagen
+/- intralesional bacteria

149
Q

Are adenomatous gastric polyps typically associated with malignant transformation?

150
Q

What is the definition of the microbiome and metabolome?

A

Microbiome: collective genome of microorganisms inhabiting the body

Metabolome: complete set of metabolites produced by the body’s microbiota

151
Q

What are the roles of the microbiota in the GIT?

A

Energy and nutrient production (synthesis of biotin, folate, vitK; metabolism of bile acids)
Intestinal wall health
Immune system regulation
Protection against pathogenic microbes

152
Q

What happens to serum cobalamine and folate with dysbiosis?

A

Cobalamin decreases
Folate increases

153
Q

What is the dysbiosis index?

A

QPCR based test that reflects the abundances of key bacterial taxa in a fecal sample; can be used to monitor dysbiosis over time and as fecal donor screening

154
Q

What is SIBO?

A

Small intestinal bacterial overgrowth - describes the increased number of anaerobic bacteria in the proximal small intestine

155
Q

What are the “good bacteria” in the GIT?

A

Lactobacillus
Bifidobacterium
Enterococcus
Faecalibacterium

156
Q

What are the “bad bacteria” in the GIT?

A

Clostridium perfringens
Clostridium difficile
Salmonella
Campylobacter

157
Q

Serum cobalamin is most useful to detect trouble where?

A

Distal small intestine

158
Q

What are examples of dysbiosis-associated disease?

A

IBD
Acute gastroenteritis (AHDS)
Intestinal stasis
EPI
Motility disorders (mega colon)
Antibiotic therapy

159
Q

What is a probiotic?

A

A living microorganism that upon ingestion in sufficient numbers impart health benefit beyond basic nutrition

160
Q

What are the mechanisms by which probiotics work?

A

Displacement of pathogenic bacteria
Production of antimicrobial byproducts
Improvement in GIT barrier function
Improvement in micronutrient absorption
Modulation of the metric and innate immune responses

161
Q

What is the definition of a prebiotic?

A

Non-digestible dietary carbohydrates that stimulate the growth and metabolism of endogenous enteric protective bacteria upon consumption

162
Q

What are examples of prebiotics?

A

Psyllium
Insulin
Bran

163
Q

What are the mechanisms by which prebiotics work?

A

Production of short-chain fatty acids (lactate, butyrate)
Reduced cytokine production by intestinal mucosa

164
Q

What are some pathophysiologic mechanisms of intestinal disease?

A

Luminal disturbance
Brush border membrane disease
Micro villas membrane damage
Enterocyte dysfunction
Epithelial barrier disruption
Villus atrophy
Disordered motility
Mucosal inflammation
Hypersensitivity
Neoplasia
Nutrient delivery failure
Congenital abnormalities

165
Q

What is the cardinal sign of SI dysfunction?

A

DIARRHEA - usually osmotic, malabsorptive

166
Q

Borborygmi and flatulence are most commonly caused by

A

Swallowed air and bacterial fermentation

167
Q

What are BIPS?

A

Barium-impregnated polyethylenes - radiopaque markers that provide info on gastric emptying, intestinal transit, and obstructive disorders (particularly partial obstruction)

168
Q

What is AHDS/HGE and what causes it?

A

Acute hemorrhagic diarrhea syndrome/hemorrhagic gastroenteritis

Cause unknown, but thought to be due to Clostridium perfringens enterotoxin production (other considerations: dysbiosis, type I hypersensitivity)

169
Q

What are some viral causes of small intestinal disease?

A

Parvovirus
Panleukopenia
FIP
FIV
FeLV
Distemper

170
Q

What are some bacterial causes of small intestinal disease?

A

Enteroinvasive bacteria - campylobacter, salmonella, Ecoli

171
Q

What GI parasites cause small intestinal disease?

A

Roundworm (Toxocara)
Strongyloides (also cause LI disease)
Hookworms (Ancylostoma)
Tapeworms (Dipylidium caninum)

172
Q

What protozoa can cause small intestinal disease?

A

Isospora
Cryptosporidium
Giardia

173
Q

What are the top 3 causes of a protein losing enteropathy?

A

Lymphangiectasia
IBD
Infiltrative lymphoma

174
Q

What clin path abnormalities might you see with PLE?

A

Hypoproteinemia (usually albumin and globulin, but can see hyperglob in histo, severe IBD, LSA)
Hypocholesterolemia
Lymphopenia
Ionized hypocalcemia
Hypomagnesemia
Loss of fat soluble vitamins (ADEK)

175
Q

Why are dogs with PLE are hypercoagulable?

A

They lose antithrombin

176
Q

What breed is associated with immunoproliferative enteropathy?

177
Q

What breed gets concurrent PLE and PLN?

A

Wheaten terriers

178
Q

What are the goals of nutritional therapy in PLE?

A

High protein/aa (to replace what they are losing)
Low fat (they can’t absorb it)
Low fiber (b/c it impedes with nutritional digestion)

179
Q

What are the different types of IBD and which is most common

A

In order of most common to least common:
Lymphoplasmacytic
Eosinophilic
Neutrophilia
Granulomatous

180
Q

Neutrophilia IBD is associated with what bacteria?

A

Campylobacter
Salmonella

181
Q

Eosinophilic IBD is most commonly associated with what two things?

A

Parasites
Food intolerance

182
Q

IBD is classified clinically as

A

Food responsive
Antibiotic responsive
Steroid responsive

183
Q

What is the pathophysiology of IBD?

A

Complex, but involves an overly aggressive cell-mediated response resulting from the loss of tolerance to antigens of the microbiome in susceptible hosts

184
Q

Polymorphisms in what TLRs have been identified in IBD?

A

TLR 4 and TLR 5

185
Q

Mutation in TLRs in IBD causes what effects?

A

The immune cells identify good commensal bacteria as pathogens and signal “danger” to the host, initiating an inflammatory response

186
Q

What is fecal calprotectin?

A

Calcium binding protein that is highly abundant in neutrophils and has been shown to be increased in humans with IBD

187
Q

What are negative prognostic indicators in IBD?

A

Hypoalbuminemia
Decreased cobalamin
Severe duodenal lesions

188
Q

What is lymphangiectasia?

A

Loss of protein and lymphocytes via ruptured abnormal lacteals

Loss of lymphocytes leads to immunodeficiency, putting these patients at risk for inflammatory or neoplasticism disease

189
Q

What is the difference between primary and secondary lymphangiectasia?

A

Primary - often congenital and limited to the intestines, but can be more widespread (ie chylothorax)

Secondary - caused by intestinal lymphatic obstruction (infiltration/obstruction of lymphatics by inflammation, fibrosis, neoplasia; obstruction of thoracic duct; right CHF)

190
Q

What is sulfasalazine?

A

A pro-drug consisting of 5-amino salicylic acid

NSAID used for treatment of ulcerative colitis in people

191
Q

What is the main adverse effect of sulfasalazine?

192
Q

Granulomatous colitis is associated with what organism?

A

Intracellular E. coli most commonly

Can also be caused by strep, campylobacter, mycobacteria, histo, prototheca

193
Q

What histopath findings might you see with granulomatous colitis?

A

Mucosal infiltration of macrophages with variable infiltrates of neutrophils, lymphocytes, and plasma cells

Used to be called histiocytic ulcerative colitis

194
Q

What breeds of dog are associated with granulomatous colitis? What is the typical age of onset?

A

Boxers
Frenchies

<2y

195
Q

How is granulomatous colitis treated?

A

Enrofloxacin for 12 weeks - although now there is developing resistance

196
Q

What is tritricomonas?

A

A flagellate protozoan that causes persistent diarrhea in cats

Colonizes in the large intestine causing chronic colitis, anal irritation, and fecal incontinence

197
Q

What are the three main types of mega colon in dogs?

A

Idiopathic
Neurologic
Orthopedic

198
Q

What are the 2 pathologic methods through which megacolon can develop?

A

Dilation secondary to electrolyte abnormalities, neuromuscular disorders, or idiopathic

Hypertrophic - develops from obstructive lesions (pelvic fracture male ion, tumor, FB) - this type is reversible

199
Q

What is the most common cause of megacolon in cats?

A

Obstipation

200
Q

What is cricopharyngeal dyssynchrony?

A

A functional/pump problem (oropharyngeal dysphasia) where weak pharyngeal muscles are unable to propel a bonus through the upper esophageal sphincter

201
Q

What is cricopharyngeal achalasia?

A

Structural problem (oropharyngeal dysphagia) where there is an inability of the cricopharyngeal muscle to open during the cricopharyngeal phase of swallowing

202
Q

How is cricopharyngeal achalasia treated?

A

Surgery - myotomy/myectomy
OR
Injection of botulinum toxin into the muscle (weakens contraction of the muscle by blocking release of acetylcholine)

203
Q

PPIs should be tapered over __ if used for __.

A

Tapered over 7-10d if used for >2 weeks

204
Q

What GI condition is thought to maybe contribute to pulmonary fibrosis in Westies?

A

GERD - thought is chronic intermittent micro aspiration may cause pulmonary fibrosis

205
Q

What is the most common cause of esophageal stricture in dogs?

A

Reflux during anesthesia

206
Q

What drugs in cats can cause esophageal stricture?

A

Doxycycline
Clindamycin

207
Q

Where to esophageal foreign bodies tend to lodge?

A

Points of minima distention like thoracic inlet, base of heart, diaphragmatic hiatus

208
Q

What type of hiatal hernia is most common?

A

Sliding - esophagus, LES, and stomach all herniate through hiatus

209
Q

What is a paraesophageal hiatal hernia?

A

When the esophagus and LES stay put while gastric fundus herniates through the hiatus alongside the esophagus

210
Q

What is the most common cause of regurgitation in the dog?

A

Idiopathic megaesophagus

211
Q

What causes primary megaesophagus?

A

A defect in affect vagaries signaling or of esophageal muscle

212
Q

What are some causes for secondary (acquired) megaesophagus?

A

Neuromuscular - myasthenia gravis, dysautonomia, lar par, muscular dystrophy
Esophagitis
Toxicity - lead, organophosphate
Neoplasia - thyme a
Addison’s
Hypothyroidism
Obstruction

213
Q

What are the two types of acquired esophageal diverticula and what causes each?

A

Traction diverticula - caused by periesophageal inflammation and fibrosis

Pulsion diverticula - caused by increased intraluminal pressure secondary to obstruction or altered motility

214
Q

Esophageal fistulas usually communicate with what other structure?

A

Bronchus or trachea

215
Q

What dog breed is predisposed to congenital esophageal strictures?

A

Cairn terries

216
Q

What is Spirocerca lupi?

A

Esophageal worm

217
Q

What does Spirocerca lupi cause

A

Granulomatous nodules in the caudal esophageal submucosa

These can undergo malignant transformation to osteosarcomas or fibrosarcomas

218
Q

How is Spirocercosis treated

A

Macrocyclic lactones (ivermectin)

Non-neoplasticism nodules should regress with treatment

219
Q

What is masticatory muscle myositis?

A

Autoimmune disease affecting temporal, masseter, and pterygoid muscles of the dog

220
Q

Why are the temporal, masseter, and pterygoid muscles of the dog affected by MMM?

A

They possess 2M fibers (different from 2C fibers of other skeletal muscles)

221
Q

How is MMM treated?

A

2M antibodies and/or muscle biopsies

222
Q

What drugs can cause mild induction of ALT and ALP?

A

Phenobarbital
Corticosteroids

These don’t affect ALP in cats

223
Q

Where are ALP and GGT found in the liver (cellular level)?

A

Hepatocyte canalicular membrane
ALP also on the luminal surface of biliary epithelial cells

224
Q

Cells in which zone of hepatic blood supply are most susceptible to toxins?

225
Q

Cells in which zone of hepatic blood supply are most susceptible to hypoxia injury?

226
Q

Where does hepatic biotransformation occur in the liver? (Zone)

A

Zone 3 - closest to venules

227
Q

The liver makes all coagulation factors except __

A

Factor VIII

228
Q

What coagulation inhibitors does the liver produce?

A

Antithrombin
Antiplasmin
Plasminogen
Protein C

229
Q

If you have a fasting hyperammonemia, what should your top ddx be?

230
Q

What causes hepatic encephalopathy?

A

Hyperammonemia

231
Q

Hepatic encephalopathy can occur in cats without shunting as a result of fasting. Why?

A

Cats can’t make arginine which is needed for the urea cycle. Deficiency of arginine causes inadequate detoxification of ammonia

232
Q

What factors affect bile acids in normal animals?

A

Completeness of GB emptying
Rate of gastric emptying
GI transit rate
Efficiency of ideal bile acid reabsorption
Frequency of enterohepatic cycling
Inadequate fat/amino acid content of test meal (failed CCK release)

233
Q

How much functional liver mass must be lost before seeing hypoglycemia?

234
Q

How much functional liver mass must be lost before developing hypoalbuminemia?

235
Q

Bilirubinuria is always abnormal in what species?

A

Cats

Can be normal in dogs

236
Q

What percent of liver FNAs agree diagnostically with biopsies?

237
Q

In cases of liver disease, what form of pred should be used?

A

PrednisOLONE (prednisone is metabolized to prednisolone in the liver)

238
Q

What is the MOA of SAMe?

A

Precursor of glutathione (GSH; primary endogenous cellular antioxidant)

239
Q

What is the MOA of silymarin

A

Strong free radical scavenger

240
Q

What is the MOA of N-acetylcysteine

A

Stimulates GSH production, free radical scavenger, anti-inflammatory

241
Q

What medications are used for copper hepatopathy treatment?

A

D-penicillamine (binds extracellular copper)
Zinc
Antioxidants

242
Q

What is colchicine?

A

Antifibrotic agent that inhibits the microtubular apparatus (aka inhibits collagen deposition)

Also hepatoprotective and anti-inflammatory (inhibits WBC migration)

ACVIM Generals (16 decks)

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