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ACVIM General Boards - 2022 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Regarding extrinsic innervation to the GI tract, efferent fibers do what?

A

Carry information from brainstem and spinal cord to GI tract

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2
Q

Regarding extrinsic innervation to the GI tract, afferent fibers do what?

A

Carry sensory information (chemoreceptors and mechanoreceptos) from the GI tract to the brainstem and spinal cord

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3
Q

The parasympathetic nervous system is (excitatory/inhibitory) to the GI tract

A

Excitatory

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4
Q

Sympathetic nervous system is (excitatory/inhibitory) to the GI tract?

A

Inhibitory

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5
Q

What is the intrinsic innervation to the GI tract (enteric nervous system)?

A

Coordinates and relays information (parasympathetic and sympathetic) to the GI tract.

Uses local reflexes to relay information within the GI tract

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6
Q

What is the enteric nervous system composed of?

A
  1. Myenteric plexus (Auerback plexus) - Primarily controls the motility of GI smooth muscle
  2. Submucosal plexus (Meissner plexus) - Primarily controls secretion and blood flow
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7
Q

What does the myenteric plexus (Auerbach plexus) control?

A

Motility of GI smooth muscle

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8
Q

What does the submucosal plexus (Meissner plexus) control?

A

Secretion and blood flow

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9
Q

What is the other name for the myenteric plexus?

A

Auerbach plexus

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10
Q

What is the other name for the submucosal plexus?

A

Meissner plexus

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11
Q

What cells secrete gastrin?

A

G cells of pyloric ANTRUM

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12
Q

What are the effects of gastrin? (2)

A

Increased gastric H+ secretion

Stimulates growth of gastric mucosa

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13
Q

What cells release cholecystokinin (CCK)?

A

I cells of duodenum and jejunum

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14
Q

What are the effects of cholecystokinin (CCK)? (4)

A

Stimulates gallbladder contraction and relaxation of sphincter of Oddi

Increased pancreatic enzyme and bicarb production

Increased growth of pancreas/gallbladder

Inhibits gastric emptying

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15
Q

What cells secrete secretin?

A

The S cells of the duodenum

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16
Q

What are the effects of secretin?

A

Increased pancreatic bicarb (HCO3-) secretion

Increased biliary bicarb (HCO3-) secretion

Decreased gastric H+ secretion

Increased bile production

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17
Q

Where is glucose-dependent insulinotropic peptide secreted?

A

K cells of duodenum and jejunum

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18
Q

What does glucose-dependent insulinotropic peptide do?

A

Increased insulin secretion

Decreased gastric acid secretion

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19
Q

What cells secrete motilin?

A

M cells of duodenum and jejunum

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20
Q

What does motilin do?

A

Stimulates gastric and intestinal motility

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21
Q

Which cells secrete acid in the stomach?

A

Parietal cells

(Remember parietal cells also secrete intrinsic factor for B12)

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22
Q

What are stimuli for secretion of gastrin?

A

Small peptides/amino acids in the stomach

Distention of the stomach

Vagal stimulation (mediated by gastrin-releasing peptide)

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23
Q

What is gastrin-releasing peptide?

A

Peptide stimulated by vagal tone. Stimulates gastrin release.

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24
Q

Does atropine block vagally-mediated gastrin release?

A

No - Because vagal gastrin release is mediated by gastrin-releasing peptide and not Ach

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25
Q

What inhibits gastrin release?

A

H+ in the lumen of stomach (negative feedback)

Somatostatin

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26
Q

What is a gastrinoma?

AKA Zollinger-Ellison syndrome

A

Gastrin-secreting PANCREATIC tumor (non-beta cell)

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27
Q

What stimulates CCK secretion?

A

Small peptides and amino acids

Fatty acids and monoglycerides

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28
Q

Can triglycerides stimulate CCK release?

A

NO - triglycerides do not cross intestinal cell membrane

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29
Q

What are stimuli for secretin release?

A

H+ in the lumen of the duodenum

Fatty acids in the lumen of the duodenum

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30
Q

What stimulates glucose-dependent insulinotropic factor?

A

Fatty acids, amino acids, and carbohydrates

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31
Q

What does leptin do to appetite?

A

Decreases appetite

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32
Q

What does ghrelin do to appetite?

A

Increases appetite

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33
Q

What are the GI paracrine hormones?

A

Somatostatin

Histamine

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34
Q

What are the GI endocrine hormones?

A

Gastrin

CCK

Secretin

Glucose-dependent insulinotropic peptide

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35
Q

What are the effects of somatostatin on the GI tract?

A

Inhibits release of all GI hormones

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36
Q

What cells secrete somatostatin in the GI tract?

A

Cells throughout the GI tract in response to H+ in the lumen

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37
Q

What cells secrete histamine in the GI tract?

A

Mast cells in gastric mucosa

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38
Q

What are the effects of histamine in the GI tract?

A

Increases gastric H+ secretion directly and by potentiating the effects of gastrin and vagal stimulation

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39
Q

What are slow waves?

A

Oscillating membrane potentials inherent to GI smooth muscle. Occur spontaneously.

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40
Q

Where do slow waves originate from?

A

Interstitial cells of Cajal (pacemaker cells of GI smooth muscle)

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41
Q

Are slow waves action potentials?

A

NO - but they determine the pattern of action potentials

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42
Q

What is the mechanism for production of slow waves?

A

Cyclic opening of Ca2++ channels (depolarization)

followed by opening of K+ channels (depolarization)

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43
Q

When do spike action potentials occur in the GI?

A

During depolarization of slow waves

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44
Q

Is the frequency of slow waves influenced by neural or hormonal input?

A

No - but the frequency of action potentials is

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45
Q

Which part of the GI tract has the lowest frequency of slow waves?

A

Stomach (3/min)

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46
Q

Where in the GI is the frequency of slow waves the highest?

A

The duodenum (12/min)

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47
Q

What part of the CNS coordinates swallowing?

A

Medulla

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48
Q

What is a primary peristaltic contraction in esophagus?

A

Contraction behind the food bolus - propulsing bolus

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49
Q

What is secondary peristaltic contraction in esophagus?

A

Clears any remaining food

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50
Q

What neurocrine promotes lower esophageal relaxation?

A

vasoactive intestinal peptide

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51
Q

What is achalasia?

A

esophageal sphincter does not relax during swallowing

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52
Q

When is gastric emptying the fastest?

A

When the stomach contents are isotonic

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53
Q

How does fat inhibit gastric emptying?

A

By the production of CCK

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54
Q

What do segmental contractions in the SI do?

A

mix intestinal contents

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55
Q

How are peristaltic contractions controlled in the SI?

A

By the enteric nervous system:

Food in the intestine is sensed by enterochromaffin cells, who release serotonin.

Serotonin binds to afferent neurons, which initiate peristaltic reflex

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56
Q

What is the composition of saliva at the acinus and salivary ducts?

A

Acinus - Produces isotonic saliva

Ducts - Reabsorb Na+ and Cl-, makingit hypotonic. Ducts also secrete K+ and HCO3-

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57
Q

When is saliva most similar to plasma? At low flow rates or high flow rates?

A

At high flow rates (not as much time to remove Na and Cl and excrete bicarb and K+)

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58
Q

What is unique about regulation of saliva production?

A

Saliva production is increased by both sympathetic and parasympathetic activity

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59
Q

What cranial nerves provide parasympathetic stimulation to salivary glands?

A

VII - Facial nerve

IX - Glossopharyngeal

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60
Q

What do the chief cells of the stomach produce?

A

Pepsinogen

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61
Q

What are the parietal cells of the stomach stimulated by?

A

Gastrin secreted by G cells

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62
Q

What do parietal cells of the stomach absorb into the bloodstream?

A

Bicarb (HCO3-) via carbonic anhidrase

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63
Q

How is H+ secreted into the stomach by the parietal cells?

A

Via the H+-K+ ATPase pump

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64
Q

How does omeprazole work?

A

Inhibits H+-K+ ATPase pump

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65
Q

What is the “alkaline tide?”

A

HCO3- produced by parietal cell of stomach is absorbed to venous blood, pH increases

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66
Q

How does cimetidine work?

A

Blocking the effects of histamine on H+ secretion (H2 receptors)

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67
Q

True or false: Pancreatic secretions are always isotonic/

A

True - regardless of flow rate

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68
Q

What does it mean that bile salts are amphipathic?

A

Molecules of bile have both hydrophilic and hydrophobic portions

69
Q

What are the primary bile acids?

A

Cholic acid

Chenodeoxycholic acid

70
Q

What are secondary bile acids?

A

Bacteria in the intestine convert primary bile acids to secondary bile acids:

Deoxycholic acid and lithocholic acid

71
Q

Which amino acids are used to transform bile acids into bile salts?

A

Taurine and glycine

72
Q

What portion of the small intestine absorbs bile acids? Via what cotransporter?

A

Terminal ileum - Na+-bile contransporter

73
Q

Ileal resection results in what?

A

Steatorrhea - decreased absorption of bile acids, depleted bile acid pool and impaired fat absorption

74
Q

Who transforms hemoglobin to bilirubin?

A

Reticuloendothelial system

75
Q

What enzyme conjugates bilirubin?

A

UDP glucuronyl transferase - Conjugates bilirubin with glucuronic acid

76
Q

What happens to bilirubin once it’s conjugated?

A

Some is excreted in urine, and some is secreted into bile

77
Q

What substance is secreted from neurons in the GI to produce smooth muscle relaxation?

A

Vasoactive intestinal peptide

78
Q

Where are the parietal cells located?

A

Gastric FUNDUS

79
Q

Where in the stomach is gastrin secreted?

A

Antrum (G cells)

80
Q

What bacteria has been associated with histiocytic ulcerative colitis (boxer colitis)

A

Enteroinvasive E. coli

81
Q

How is histiocytic ulcerative colitis (boxer colitis) diagnosed?

A

Fluorescence in situ hybridization (FISH) can be performed to detect intramucosal colonization of E. coli.

Culture recommended due to resistance

82
Q

How is Tritrichomonas foetus diagnosed?

A

Fecal smear - low sensitivity

Best sensitivity - PCR on colonic flush or fresh colonic sample

83
Q

Which test offer the best sensitivity for Giaridia

A

ELISA

84
Q

What is heterobilharzia americana? How is it best diagnosed?

A

Trematode that causes schistosomiasis in dogs. Lives in the mesenteric veins. Best diagnosed with PCR of feces

85
Q

What is folate and where is it absorbed?

A

A water soluble B vitamin.

Absorbed in the duodenum

86
Q

How does intestinal dysbiosis cause increased folate?

A

Synthesized by many bacteria- suspected that dysbiosis may lead to increased folate

87
Q

In addition to intrinsic factor, what other proteins are involved in the absorption of B12?

A

Dietary protein

R protein

Intrinsic factor

88
Q

Where is intrinsic factor produced mostly in dogs and cats?

A

Dogs - Exocrine pancreas mostly, parietal cells of stomach (a little)

Cats - Exocrine pancreas only

89
Q

What is used as an estimate of protein loss in the GI tract? Used for diagnosis of PLE

A

Fecal Alpha1-Proteinase Inhibitor Concentration

90
Q

When is fecal alpha-1 proteinase inhibitor concentration indicated?

A

Indicated in dogs without clinical signs of gastrointestinal disease and where an extra-gastrointestinal source of protein loss cannot be identified

91
Q

What is an acute phase reactant that is increased in dogs with IBD?

A

Serum C-Reactive Protein Concentration (CRP)

92
Q

What two medications can cause gingival hyperplasia?

A

Calcium channel blockers

Cyclosporines

93
Q

What infectious agents have been implicated in feline stomatitis?

A

Feline calicivirus

Feline herpesvirus (FHV-1)

94
Q

What are two autoimmune oral conditions?

A

Pemphigus vulgaris - Lesion is suprabasilar (intercellular clefting) with formation of acanthocytes.

Bullous pemphigoid - subepidermal without formation of acanthocytes

95
Q

What are the clinical signs of masticatory muscle myositis?

A

Fever, regional lymphadenopathy, muscle swelling/pain OR atrophy (if chronic), exophthalmos, resistant to opening mouth.

96
Q

What is the pathophysiology behind masticatory muscle myositis?

A

Autoantibodies to myosin component of the type 2M fibers of the temporal, masseter, pterygoid muscles

97
Q

How is masticatory muscle myositis diagnosed?

A

Serum type 2M fiber Ab titer

98
Q

What is sialoadenosis?

A

Non-inflammatory enlargement of a salivary gland. Neurogenic cause.

99
Q

How is sialoadenosis treated?

A

Phenobarbital

(neurogenic mechanism)

100
Q

Can pharyngeal weakness be the only sign in myesthenia gravis?

A

Yes - 1% of dogs with MG

101
Q

How is cricopharyngeal achalasia diagnosed?

A

prominent thickened cricopharyngeus muscle (cricopharyngeal “bar”)

102
Q

How is cricopharyngeal achalasia treated?

A

cricopharyngeal myotomy or myectomy;

less invasive tx = botulinum toxin injection

103
Q

What is the treatment for persistent right aortic arch?

A

surgical ligation of the ligamentum arteriosum

104
Q

Esophageal sarcomas have been associated with what parasite?

A

Spirocerca lupi infection - due to transformation of esophageal granulomas

105
Q

What percentage of cases of myastenia gravis have megaesophagus as the only clincal sign?

A

25-30%

106
Q

Cisapride and metoclopramide work on (striated/smooth) muscle?

A

Smooth

107
Q

(Cisapride/metoclopramide) is better at tightening the lower esophageal sphincter

A

Cisapride

108
Q

What is microbiota?

A

Microbes living in the intestine

109
Q

What is a major source of energy for colonocytes?

A

Butyrate - short chain fatty acid produced by colonic bacteria

110
Q

What are the M cells of the gut?

A

Specialized epithelial cells that overlie lymphoid follicles, sample luminal antigens and deliver producers to dendritic cells and other APCs

111
Q

How do you differentiate between gastrointestinal stromal tumor (GIST) and leiomyosarcoma?

A

Immunohistochemistry (IHC) - GIST expresses c-KIT (CD117) and DOG1

112
Q

What changes are observed with serum cobalamin and folate in patients with small intestinal bacterial overgrowth (SIBO)?

A

Increased folate

Low cobalamin

113
Q

In IBD, what are the cobalamin and folate profiles?

A

Decreased Folate - Proximal inflammation (duodenum)

Cobalamin - Distal inflammation (ileum)

114
Q

What are the fat-soluble vitamins?

A

A, D, E, K

115
Q

What is the ideal diet for PLE?

A

Highly digestible, mod to high protein (20-25%), low fat (<10%), <5% insol fiber

116
Q

What test is used to differentiate feline lymphoma from IBD?

A

PARR

117
Q

What is the gold standard test for exocrine pancreatic insufficiency?

A

Serum Trypsin-Like Immunoreactivity

118
Q

How much of the pancreas’ excretory capacity needs to be lost before symptoms of EPI occur?

A

>90%

119
Q

What type of toxicity predominates in cats with acetaminophen toxicity?

A

hematologic toxicity (methemoglobinemia) predominates over liver toxicity

120
Q

What is the most consistent hepatic biochemical changes in cats with hepatic lipidosis?

A

ALP >>>>>> ALT

GGT usually normal

121
Q

What is a confirmatory test for hepatic lipidosis?

A

FNA of the liver when there is clinical suspicion of HL

122
Q

What are IV fluid considerations for cats with hepatic lipidosis?

A

Dextrose containing fluids CONTRAINDICATED

Impaired lactate metabolism - try to avoid lactate containing fluids

123
Q

What type of diet is ideal for cats with hepatic lipidosis?

A

HIGH protein diet

124
Q

What is the pathophysiology behind coagulopathies in cats with hepatic lipidosis?

A

Decreased absorption of vitamin K1 rather than decreased production of clotting factors (because they respond well to vit K supplementation)

125
Q

How does hypokalemia exacerbate hepatic encephalopathy?

A

Causes hypokalemic alkalosis - Hypokalemia promotes a shift of potassium from the intracellular space to the extracellular space in exchange for hydrogen. The resulting extracellular alkalosis and intracellular acidosis cause ammonia to freely move into cells, including neurons, where it becomes ionized to form NH4+. NH4+ becomes trapped within the cells (e.g. neurons), making them one-way scavengers of ammonia

126
Q

What are precipitating factors for hepatic encephalopathy?

A
  1. GI hemorrhage
  2. Hypokalemia
  3. Hyponatremia
  4. Metabolic alkalosis
  5. Renal failure
127
Q

What drugs should be avoided in hepatic encephalopathy?

A

Benzodiazepines, opioids, other sedatives - Because stimulation of benzo/opiod receptors may be part of pathophys of HE

128
Q

What is the best treatment for acute exacerbation of hepatic encephalopathy?

A

Cleansing enema

129
Q

How does lactulose help in the treatment of encephalopathy?

A

Bacteria transform lactulose to short chain fatty acids - makes environment more acidic, trapping ammonia in the GI

130
Q

How is ALP cleaved from the biliary membrane?

A

Bile acids cleave ALP and releases AL from membranes resulting in increased ALP activity in serum/plasma

131
Q

Gallbladder filling is (active/passive)

A

Passive

132
Q

What are the three types of cholecystitis?

A

Class I - Necrotizing cholecystitis

Class II - Acute necrotizing cholecystitis with rupture

Class III - chronic cholecystitis

133
Q

Patients with extrahepatic biliary obstruction can be (hypocoagulable/hypercoagulable)

A

Hypocoagulable - need vitamin K supplementation

134
Q

When performing mechanical dilation of esophageal strictures, what is more effective?

Balloon dilation

Rigid bougienage

A

Balloon dilation

135
Q

What TLR recognizes LPS?

A

TLR4

136
Q

What TLR recognizes flagellin?

A

TLR5

137
Q

What is the only clotting factor not made by the liver?

A

von Willebrans subtype of Factor VIII

138
Q

What is protein C?

A

Vitamin K activated anticoagulation factor

139
Q

In what liver condition is protein C low? (PSS or microvascular dysplasia)

A

PSS

140
Q

Biacarbonate is exchanged for what in the distal ileum?

A

Cl-

141
Q

What is the most specific indicator of cholestasis?

A

GGT

142
Q

What inhibits glucagon?

A

Somatostatin

143
Q

Where do the hepatic ducts join to secrete produced bile?

A

Common bile duct

144
Q

How much of the bile salts are re-absorbed?

A

94%

145
Q

What are Brunner’s glands?

A

Secrete bicarb in duodenum

146
Q

How is glucose absorbed in the intestine?

A

SGLT-1

147
Q

How is fructose absorbed in the intestine?

A

GLUT-5

148
Q

What emulsifies fats in the small intestine?

A

Bile salts

Lecithin (phospholipid)

149
Q

What is responsable for post prandial hyperlipidemia?

A

Chylomichrons

150
Q

Why do cats lose a large amount of Cobalamin in the intestine as compared to dogs?

A

Cats don’t have transcobalamin

151
Q

What B vitamin can be produced by the intestinal flora?

A

Folate

152
Q

True or false - Most dogs with microvascular dysplasia are asymptomatic.

A

True

153
Q

Can biopsy differentiate between PSS and MVD?

A

No

154
Q

What is more common PSS or MVD?

A

MVD

155
Q

What is different in the morphology of PSS in small vs. large breed dog?

A

Small breed - Single extrahepatic shunt

Large breed - Intrahepatic shunt (patent ductus venosus)

156
Q

What blood test can you use to differentiate between PSS and MVD?

A
  1. Protein C activity:
    1. normal dog= 100%
    2. portal vein hypoplasia>/= 70%
    3. PSS = <70%
157
Q

What is a positive prognostic indicator in PSS?

A

Higher BUN

158
Q

What is the cause of gallbladder mucocele?

A

Likely due to primary disease of the mucous secreting glands of the gallbladder

159
Q

How is copper taken up by the liver?

A

Copper transporter 1 (CTR-1)

160
Q

What is ceruloplasmin?

A

Copper-dependent oxidase - It Fe2+ to Fe3+ for transport

161
Q

How is copper excreted?

A

In the bile by COMMD1 (MURR)

162
Q

Where is copper stored in Bedlinton Terriers?

A

Zone 3 - centrilobular

163
Q

What is the most common chem abnormality in Bedlinton terriers with copper storage disease?

A

Increased ALT = first and most consistent change

164
Q

How are bedlinton terriers diagnosed with Cu hepatopathy?

A

Biopsy

MURR gene test

165
Q

Copper storage secondary to cholestatic hepatopathy happens where?

A

Zone 1 - Periportal

166
Q

What is the major circulating bile acid in dogs and cats?

A

Tauracholate

167
Q

What is the most toxic bile acid?

A

Lithocholic acid

168
Q

Copper is stored as what?

A

metallothionein

169
Q

What is a liver disease in cats that results in ascites?

A

Lymphocytic cholangitis

ACVIM General Boards - 2022 (16 decks)

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