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ECVECC Board Exam > GI/Pancreas > Flashcards

GI/Pancreas Flashcards

1
Q

What is the difference between dog’s and cat’s esophagus?

A

Dog: 100% striated muscle
Cat: only upper 2/3 are striated muscle, the rest 1/3 is smooth muscle

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2
Q

What can cause the resting membrane potential less negative (more easily excitable) in GI tract? What can cause it to be more negative (harder to depolarize)?

A

Less negative
- stretch of the smooth muscle
- stimulation by acetylcholine released from the endings of parasympathetic nerves
- stimulation by several specific gastrointestinal hormones

More negative
- catecholamines
- stimulation of sympathetic nerves

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3
Q

What are the enteric nerve system composed of? And what are their functions?

A

Myenteric plexus - control the GI movement

Submucosal plexus - control the local blood flow and GI secretion

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4
Q

List 5 different enteric neurotransmitter/hormone substances

A

Substance P
Vasoactive intestinal peptide
Acetylcholine
Dopamine
Cholecystokinin
Somatostatin
Adenosine triphosphate
Norepinephrine
Serotonin
Nitric oxide

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5
Q

Which parts of the GI system dose vagus nerve innervated?

A

esophagus, stomach, small intestines, pancreas, first half of the large intestines

  • The second half of large intestines and anus are innervated by pelvic nerves
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6
Q

Where is cholecystokinin secreted and what are its functions?

A

I cells of the duodenum, jejunum and ileum
It stimulates pancreatic enzymes and bicarb secretion, GB contractions, and inhibits gastric emptying

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7
Q

Where is gastrin secreted and what are its functions?

A

G cells in the gastric antrum
It stimulates gastric acid secretion and growth of the gastric mucosa

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8
Q

Where is motilin secreted and what is its functions?

A

M cells of stomach and upper duodenum during fasting
It increases GI motility

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9
Q

Why are the GI villi vulnerable to ischemia?

A

Because of the countercurrent blood flow of the arterioles and venules in the villi.
Most of the oxygenated blood (~80%) diffused from the arterioles to the venules without reaching the tip of the villi.

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10
Q

Fill out the blank about the gastric secretion.

A
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11
Q

True or False: Pepsinogen in the stomach can only become active in acidic environment.

A

True

Under acidic environment, pepsinogen is activated to form active pepsin and has proteolytic effect.

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12
Q

How does the body control gastric acid secretion?

A

Food goes down to antral end of the stomach → stimulates G cells secrete gastrin → gastrin reach the ECL cells in the oxyntic glands (gastric glands) → stimulates histamine release →histamine stimulate parietal cells secrete HCl

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13
Q

What are the pancreatic enzymes for proteins, carbohydrates and fat digestion?

A

Proteins: trypsin, chymotrypsin, carboxypolypeptidase
Carbohydrates: pancreatic amylase
Fat: pancreatic lipase, cholesterol esterases, phospholipase

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14
Q

What is the enzyme that activates the trypsinogen?

A

Enterokinase (secretes by the intestinal mucosa)

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15
Q

How does pancreas prevent self-digestive under normal condition?

A

The pancreatic cells that secrete proteolytic enzymes also secrete trypsin inhibitor at the same time to prevent activation of trypsin inside the pancreas

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16
Q

What are the three basic stimuli for pancreatic secretion?

A

Acetlycholine
Cholecystokinin
Secretin (make pancreas secretes lots of water and bicarbs by pancreatic duct epithelium)

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17
Q

True or False: only 50% of bile salts undergo enterohepatic circulation.

A

False

94% of bile salts go through enterohepatic circulation.

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18
Q

List the compositions of the bile

A

Water
Bile salt
Bilirubin
Cholesterol
Bicarb
Electrolytes
Fatty acids
Lecithin

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19
Q

What is the precursor of bile salt?

A

Cholesterol

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20
Q

What is the life span of an intestinal epithelial cell?

A

2-5 days

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21
Q

Where does the vomiting center locate?

A

Medulla oblongata of the brainstem

Muscarinic receptors

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22
Q

Where does the chemoreceptor trigger zone locate?

A

Area postrema of the floor of 4th ventricles (no BBB)

D2 receptors
5-HT3 receptors

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23
Q

What is the difference in the pathway of vestibular-induced vomiting between dogs and cats?

A

In dogs, the signal transmits from the vestibular system to the CRTZ zone and then to the vomiting center; in cats, the signal directly transmits from the vestibular system to the vomiting center

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24
Q

How can you determine intestinal dilation via x-rays in dogs and cats?

A

Dogs: diameter of the small intestine should be less than 1.6x of the height of L5 vertebral body at its narrowest point.

Cats: no bigger than 12mm or less than 2x of the height of L4 vertebral body

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25
Q

Where do enterochromaffin cells locate and what do they do?

A

They locate in small intestines and secrete serotonin (5-HT) in response to mechanical or chemical stimuli → regulates intestinal secretion and motility

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26
Q

What is the MOA of maropitant?

A

Neurokinin-1 (NK-1) receptor antagonist
It blocks the substance P to the NK-1 receptors in the CNS and GI tract.

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27
Q

What is MOA of ondansetron?

A

Selective 5HT-3 receptor antagonist
It blocks CRTZ and vagal nerve endings in the GI tract.

  • The serotonin receptor in the vomiting center is 5HT-1
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28
Q

What is the MOA of metoclopramide?

A

D2 antagonist (CRTZ zone), 5HT-3 antagonist (mild), 5HT-4 agonist (for the prokinetic effect)

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29
Q

What is the proposed pathophysiology of extrapyramidal effect from metoclopramide?

A

A striatal D2 receptor blockade
Clinical signs: involuntary or uncontrollable movements. tremors. muscle contractions
Treatment: d/c metoclopramide, give antihistamine/anticholinergic drugs

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30
Q

What is the MOA of cisapride?

A

5HT-4 agonist →Increases acetylcholine at the myenteric plexus

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31
Q

What is the MOA of erythromycin for its prokinetic effect?

A

Motilin receptor agonists

Works for canine colon motility but not feline

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32
Q

What is the MOA of omeprazole and pantoprazole?

A

Proton-pump inhibitor (PPI) → irreversibly inhibits the H+/K+ ATP pumps in the gastric gland

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33
Q

What is MOA of sucralfate

A

1) antipeptic effect - absorb pepsin
2) form a barrier at the mucosal surface
3) increases mucus viscosity

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34
Q

For dogs with GDV, which arteries are most commonly lacerated and lead to hemoabdomen?

A

Short gastric arteries

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35
Q

Name the vessels.

A
  1. Splenic artery
  2. Short gastric arteries
  3. Lt. gastroepiploic artery
  4. Lt. gastric artery
  5. Rt. gastric artery
  6. Celiac artery
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36
Q

What are the 5 types of techniques for gastropexy?

A
  1. Incisional
  2. Belt-loop
  3. Circumcostal
  4. G-tube placement
  5. Gastrocolopexy
  6. Endoscopy assisted
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37
Q

What is the key component of successful gastropexy?

A

Make sure the incisions on the gastric serosa and peritoneal wall both reach the muscular surface.

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38
Q

Describe how to perform an incisional gastropexy.

A
  1. Make a midline incision on the ventral abdomen and enter the abdomen.
  2. Identify the gastric antrum and where it is expected to joint on the peritoneum, which should be right lateral or right ventral lateral peritoneum which is 2-3 cm caudal to the last rib.
  3. Make a 4 cm seromuscular incision at the gastric antrum either parallel or perpendicular to the gastric long axis
  4. Make a second 4cm incision on the peritoneum and transversus abdominis muscle.
  5. Appose both incisions with 2-0 monofilament absorbable sutures in a simple continuous suture pattern, beginning with the craniodorsal edge of the incision
  6. Close the abdomen
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39
Q

Describe esophagostomy tube placement.

A
  1. Patient is anesthetized and endotracheally intubated, and positioned in right lateral recumbency.
  2. The left cervical area is clipped and surgically prepped.
  3. The operator measures the esophagostomy tube from the left mid cervical area to the 7-9th intercostal space and make a mark on the tube.
  4. The assistant inserts a Carmalt forceps from oral cavity into the esophagus until the tip reaches the mid cervical esophagus, and the assistant tents skin with the tip of forceps
  5. The operator (with sterile gloves) use a #10 or #11 scalpel blade to make a incision through the skin, connective tissue and esophageal wall so that the tip of the forceps can push through
  6. Place the esophagostomy tube in between the forceps tip and allow the forceps to hold the end of the tube.
  7. Pull the tube back to the oral cavity with the forceps and then re-insert the tube into the esophagus. At the same time gently manipulate the other end of the tube to facilitate the placement.
  8. Once the entire to is in the esophagus, the direction of the part of the tube that exit the left mid cervical esophagus will flip from caudal to cranial. Make sure the tube is inserted to the pre-measured depth
  9. Place a purse-string suture around the tube entrance on the left cervical area.
  10. Place a finger trap suture at the base of the tube at where it enters the skin to secure it.
  11. Take x-rays to confirm tube placement.
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40
Q

Describe the NG tube placement.

A
  1. Apply proparacaine into the nostril 15 min prior to tube placement.
  2. Measure the NG tube from the tip of the nose till the last rib.
  3. flush the NG tube with saline and apply lubricant on the tube
  4. Keep patient’s head in natural position. Insert the NG tube into the nostril at medial-ventral direction. Assist the tube insertion direction by pushing the nose dorsally (piggy-nose).
  5. Once the tube reach the pre-measured mark. Remove the stylet. Secure the tube with suture or tape and staples.
  6. Take x-rays from the nose to the stomach to confirm tube placement.
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41
Q

After a gastrotomy tube is placed, how long should you wait until you can feed the animal and why?

A

12-24 hours; have to wait for fibrin formation to seal the stoma

  • A permanent stoma will form in 7-14 days
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42
Q

What is Cullen’s sign?

A

Periumbilical ecchymosis → usually associated with peritoneal or retroperitoneal hemorrhage

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43
Q

During abdominocentesis, which patient position is the most ideal position to avoid puncture of the spleen?

A

Left lateral recumbency

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44
Q

Describe diagnostic peritoneal lavage

A
  1. Position the patient in left lateral recumbency.
  2. Surgically clip and clean the midline. Insert a catheter and remove the stylet. Attach a syringe to the catheter
  3. Insert 22ml/kg warm sterile normal saline in a drip set into the abdomen.
  4. Gentle massage and rotate the patient.
  5. Aspirate the fluid back from the syringe
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45
Q

In the study published by Zacher et al in 2010 about lactate measurement in patients with GDV, what kind of changes in lactate were associated with better survival and fewer complications?

A

Initial lactate < 4 mmol/L and/or > 40% reduction after fluid resuscitation

Reference: Zacher LA, Berg J, Shaw SP, Kudej RK. Association between outcome and changes in plasma lactate concentration during presurgical treatment in dogs with gastric dilatation-volvulus: 64 cases (2002-2008).J Am Vet Med Assoc. 2010;236(8):892-897.

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46
Q

What are the examples of protein-losing enteropathy?

A

Eosinophilic bowel disease
Lymphocytic-plasmacytic bowel disease
Lymphangiectasia
Diffuse intestinal fungal disease
Intestinal neoplasia

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47
Q

How do NSAIDs cause GI ulcer & GI bleed?

A

NSAIDs inhibit COX pathway, and therefore inhibit biosynthesis of prostaglandins from AA. Prostaglandins protect upper GI from mucosal damage (by inhibit gastric acid secretion, stimulate mucus and bicarb secretion)

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48
Q

True or False: The canine esophagus is comprised almost exclusively of striated muscle, so metoclopramide and cisapride have no beneficial effect.

A

True

Metoclopramide and cisapride are smooth muscle prokinetic agents

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49
Q

What type of virus is parvovirus (DNA vs RNA; enveloped vs non-enveloped)?

A

non-enveloped DNA virus

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50
Q

True or False: Patients with septic peritonitis and has persistent ionized hypocalcemia during hospitalization was associated with poor prognosis

A

True (CCM textbook)

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51
Q

What are the predictive values for glucose and lactate in the diagnosis of bacterial peritonitis

A

Blood glucose is at least 20 mg/dL higher than abdominal effusion glucose

Blood lactate is at least 2.0 mmol/L lower than abdominal effusion glucose

More recently a cut off of 4.2mmol/L lactate in abdominal fluid and a difference in glucose of >2.06mmol/L have been found to be more sensitive and specific

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52
Q

What are the poor prognosis indicators for septic peritonitis?

A

Refractory hypotension, DIC, respiratory diseases, cardiovascular collapse

Cats: hypothermia and bradycardia

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53
Q

Mortality rates fro bacterial peritonitis in dogs and cats

A

Dogs: 12.5-56%
Cats: 30-60%

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54
Q

When a blind needle paracentesis is performed, what is the minimal amount of fluid required for the result to be positive?

A

5.2 - 6.6 ml/kg

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55
Q

When a peritoneal dialysis catheter is used for abdominocentesis, what is the minimal amount of fluid required for the result to be positive?

A

1.0 - 4.4 ml/kg

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56
Q

Why is BUN less reliable in the diagnosis of uroabdomen?

A

BUN can easily move across between the peritoneum and blood vessels

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57
Q

What are the diagnostic criteria for uroabdomen in dogs and cats?

A

Dogs:
- Abdominal effusion creatinine is 2 times higher than plasma creatinine
- Abdominal effusion K is 1.4 times higher than plasma creatinine

Cats:
- Abdominal effusion creatinine is 2 times higher than plasma creatinine
- Abdominal effusion K is 1.9 times higher than plasma creatinine

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58
Q

Where do H2 blockers work on?

A

Gastric parietal cells

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59
Q

Why H2 antagonist can cause tolerance?

A

Possible compensatory hypertrophy of ECL cells with hyperproduction of histamine and rebound acidity when H2 abruptly discontinued

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60
Q

Why H2 antagonists should not be combined with PPIs?

A

PPIs are weak bases, so they need to be in an acidic environment to dissociate and interact with the cysteine residue of the H/K pump

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61
Q

Why PPIs should not be suddenly discontinued?

A

There is a compensatory hypersynthesis of H/K pumps (as PPIs irreversibly bind)

Drop 50% dose per week, then once a day, then discontinue

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62
Q

Is one PPI better than any other?

A

Esomeprazole in one study showed better pH control than traditional PPIs but not enough evidence to universally recommend.

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63
Q

Which drugs can be impaired in their absorbtion by concurrent use of PPIs?

A
  • azole antifungals
  • iron
  • mycophenolate
  • clopidogrel (P450 in humans only)
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64
Q

Rank the potency of the following H2 blockers from the most the least:
cimentidine, ranitidine, nizatidine, famotidine

A

Famotidine > Nizatidine > Ranitidine = Cimentidine

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65
Q

Which of the following H2 blocker does not go through first-pass hepatic metabolism?
cimentidine, ranitidine, nizatidine, famotidine

A

Nizatidine

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66
Q

Which of the following H2 blocker absorption is delayed by food?
cimentidine, ranitidine, nizatidine, famotidine

A

Cimentidine

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67
Q

True or False: Ranitidine is excreted in the urine and famotidine is metabolized by liver.

A

False

Ranitidine is metabolized by liver and famotidine is excreted in the urine

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68
Q

Which of the following H2 blocker is shown to inhibit hepatic P-450 enzyme and can be used to lessen the severity of acetaminophen toxicity?
cimentidine, ranitidine, nizatidine, famotidine

A

Cimentidine

69
Q

What is the special instruction for omeprazole administration to maximize its effect? What is the reason behind that?

A

Give it on an empty stomach
Maximize the acidity of the gastric parietal cell so more omeprazole can be sequestrated there

70
Q

Which PPI inhibits hepatic P-450 enzymes?
Pantoprazole, omeprazole, lansoprazole, esomeprazole

A

Omeprazole

71
Q

What is the MOA of misoprostol? What does it do?

A

Prostaglandin E1 analog (Gi mediated decrease H/K activity)
Antacid, GI mucosal protectant (it stimulates secretion of mucus and bicarbonate and increases gastric mucosal blood flow)

Evidence for treating high dose aspirin intoxication

72
Q

How is metoclopramide being metabolized?

A

Excreted via kidneys

73
Q

How does promazine derivatives exhibit their antiemetic effect?

A

Antidopaminergic, alpha adrenergic antagonist, antihistaminic, anticholinergic, antispasmodic

74
Q

What is the MOA of bethanechol?

A

Cholinomimetic drug
Acts on the M1 parasympathetic receptors of the gastric parietal cells inciting gastric motility and increasing gastric tone.

75
Q

In a recent study published by Grange et al., how many percentage of patients with GDV has concurrent aspiration pneumonia?

A

14%

Reference: Grange AM, Clough W, Casale SA: Evaluation of splenectomy as a risk
factor for gastric dilatation-volvulus, J Am Vet Med Assoc 241(4):461-466,
2012.

76
Q

Which part of the stomach is most likely to develop gastric necrosis in GDV?

A

Gastric fundus

77
Q

What is the definition and common causes of transudate, modified transudate, and exudate?

A

Transudate
- TP < 2.5 g/dL
- cell count < 500 cells/uL
- cause: hypoalbuminemia, low oncotic pressure

Modified transudate
- TP > 2.5 g/dL but < 5.0 g/dL
- cell count > 300 but < 5500 cells/uL
- causes: passive congestion of the liver (e.g. right-sided CHF), lymphatic drainage obstruction

Exudate
- TP > 5.0 g/dL
- cell count > 5000-7000 cells/uL
- causes: any kind of peritonitis

78
Q

How do you diagnose Giardia spp?

A

Zinc fecal flotation

79
Q

What are the predominant parvovirus strains in the USA?

A

CPV 2b & CPV 2c

80
Q

What does IDEXX Canine Parvo SNAP kit test for (antigen/antibody)?

A

ELISA, test for parvovirus antigen

81
Q

In parvoviral enteritis, what kind of findings on the CBC are associated with better survival?

A

Degenerative left shift, lymphocytosis, monocytosis

  • monitoring the monocyte count in the blood is beneficial in evaluating the recovery from a leukopenic state in patients suffering from CPV enteritis (it takes shorter time to produce monocytes than neutrophils; 3 days vs 6 days)

Reference: Goddard, A et al. “Prognostic usefulness of blood leukocyte changes in canine parvoviral enteritis.”Journal of veterinary internal medicinevol. 22,2 (2008): 309-16.

82
Q

In a recent study published by Chalifaux, what are the negative prognostic indicators for parvoviral enteritis?

A

Lower BG, higher total Mg, lower HCT on presentation

  • Leukopenia, number of band cells are not associated with outcome in this study

Reference: Chalifoux, Nolan V et al. “Prognostic indicators at presentation for canine parvoviral enteritis: 322 cases (2001-2018).”Journal of veterinary emergency and critical care (San Antonio, Tex. : 2001)vol. 31,3 (2021): 402-413.

83
Q

Does modified live parvo vaccine interfere with the Parvo SNAP test result?

A

No

Reference: Schultz RD, Larson LJ and Lorentzen LP. Effects of Modified Live Canine Parvovirus Vaccine on the SNAP ELISA Antigen Assay. Veterinary Emergency and Critical Care Society 2008.

84
Q

How do you disinfect the surface that is exposed with parvo?

A

Diluted bleach (1:30) and leave it at the surface for at least 10 minutes

85
Q

What kind of bacteria is Clostridium perfringens?

A

Gram (+), anaerobic bacillus

86
Q

What is the difference in cholesterol level between PLE and PLN?

A

Cholesterol level is high in PLN but low in PLE

87
Q

In dogs with PLE, what is the proposed cause for ionized hypocalcemia?

A

Decreased GI vitamin D absorption

88
Q

What is the predisposed breed for mesenteric torsion?

A

German shepherd (usually young, like 2-4 yrs)

89
Q

What is the difference of the pancreatic duct anatomy between the dogs and cats?

A

Dogs: pancreatic duct usually doesn’t join the common bile duct before entering the duodenum, there is a second small pancreatic duct entering the duodenum separately

Cats: pancreatic duct usually join the common bile duct before entering the duodenum

90
Q

What is the major biotype of Clostridium perfringens?

A

Type A

most commonly with necrotizing enteritis (68% AHDS)

91
Q

What kind of bacteria is Samonella spp (e.g. gram positive/negative, aerobic/anaerobic, spore-forming or not)?

A

Gram negative, motile, non-spore forming, facultative anaerobic bacilli

family Enterobacteriaceae

92
Q

What kind of bacteria is Campylobacter spp (e.g. gram positive/negative, aerobic/anaerobic, spore-forming or not)?

A

Gram negative, microaerophilic, motile, curved rods

High resistance to fluoroquinolones, treat with macrolides

93
Q

Is Escherichia coli a normal GI flora in dogs and cats?

A

Yes

94
Q

What are the 7 pathotypes of E coli?

A

Enteropathogenic E. coli (EPEC)
Enterotoxigenic E. coli (ETEC)
Enterohemorrhagic E. coli (EHEC)
Necrotoxi- genic E. coli (NTEC)
Enteroinvasive E. coli (EIEC)
Enteroaggregrative E. coli (EAEC)
Adherent-invasive E. coli (AIEC) strains

Reference: Marks SL, Rankin SC, Byrne BA, Weese JS. Enteropathogenic bacteria in dogs and cats: Diagnosis, epidemiology, treatment, and control. J Vet Intern Med 2011; 25:1195-1208.

95
Q

What is the recommended treatment for boxer granulomatous colitis?

A

Enrofloxacin 10 mg/kg q24h for 8 weeks

96
Q

According to the ACVIM consensus statement of pancreatitis in cats, what are the proposed mechanism of spontaneous pancreahtits?

A

1)co-localization of lysosomal proteases and zymogen granules (because of an apical block of zymogen granule secretion)
2) activation of trypsinogen by cathepsin B
3) activation of zymogens by thrombin during bacterial toxemia, ischemia, or hypoxia
4) Auto-activation of trypsinogen (when pH>5)
4) enterokinase entering the portal circulation after a meal in conjunction with biliary-pancreatic reflux

97
Q

True or False: Hypertriglyceride is a common finding in feline pancreatitis.

A

False

It’s actually rare in feline pancreatitis

Reference: ACVIM consensus statement of feline pancreatitis

98
Q

Which electrolyte abnormality has been associated with poor outcome in feline acute pancreatitis?

A

ionized hypocalcemia

  • Other poor prognostic indicators include hypoglycemia and azotemia
99
Q

What does 5-HT stand for?

A

5-Hydroxytryptamine, also known as serotonin

100
Q

Where does the majority of the serotonin locate in the body?

A

GI tract (> 95%; more than 90% in the enterochromaffin cells)

101
Q

What are the different 5-HT receptors in the GI tract and what are their function and drugs work on them?

A

5-HT1p: initiate peristalsis and secretory reflexes
- mirtazipine (agonist) –> risk of serotonin syndrome

5-HT2a and c: anorexygenic
- cyproheptadine and mirtazipine (antagonists)

5-HT3: activates sensory nerves and is responsible for nausea or vomiting from GI irritation/mechanical force
- 5-HT3 antagonist: metoclopramide, ondansetron

5-HT4: increases pre-synaptic release of acetycholine and facilitates propulsive peristaltic and secretory reflexes.
- 5-HT4 agonist: metoclopramide, cisapride (does not cross BBB)

102
Q

How does ranitidine work as prokinetics?

A

It is an H2 blocker. It can also inhibit acetylcholinesterase → more acetylcholine to bind to smooth muscle muscarinic receptors
*greatest activity at upper GI tract

103
Q

What is the definition of intra-abdominal hypertension?

A

Pathologic elevation of IAP of more than 12 mmHg

104
Q

Main causes of IAH

A
  • decreased abdominal wall compliance
  • increased abdominal fluid
  • increased abdominal organ size
  • oedema formation
105
Q

What is abdominal perfusion pressure (APP)?

A

APP = MAP - IAP

should always be >60mmHg

106
Q

What is the definition of abdominal compartment syndrome?

A

Sustained increase in IAP of more than 20 mmHg that is associated with newly developing organ failure or dysfunction (i.e. GI ischemia)
However IAP 15mmHg can already cause oliguria (anuria occurs at 30mmHg)

107
Q

What is the grading cutoff and recommended therapy for IAP?

A
108
Q

According to the World Society of the Abdominal Compartment Syndrome, which way of intra-abdominal pressure measurement is considered gold standard?

A

Placing the probe in the urinary bladder

109
Q

Describe how to measure IAP with urinary bladder method

A

1) Place a foley urinary catheter sterilely and inflate the foley. Empty the bladder. Place the patient in lateral recumbency.
2) Attach the urinary catheter to the proximal port of the three-way stopcock. Attach a water manometer to the upright port of the three-way stopcock. Attach a bag of normal saline with IV set to the distal port of the three-way stopcock.
3) Fill the bladder with 0.5-1 ml/kg of normal saline (max is 25ml per patient).
4) Zero the system at the patient’s midline at the symphysis pubis.
4) Turn the three-way stopcock away from the patient end and fill the water manometer with normal saline.
5) Turn the three-way stopcock away from the fluid bag and allow the water manometer and the urinary bladder equilibrate.
6) The difference between the reading at the meniscus and the zero point at the end of expiration is the IAP.

110
Q

What is normal IAP in dogs? What about cats?

A

Dogs: 0-4 mmHg
Cats: 3-6 mmHg

111
Q

What is the relationship between glomerular filtration gradient, MAP and IAP?

A

Filtration gradient = glomerular filtration pressure - proximal tubular pressure = MAP - IAP - IAP = MAP - 2IAP

112
Q

Corrected Pplat when increased IAP

A

Pplat = (Pplat - 7) + (IAP x 0.7)

113
Q

What are the three antioxidant systems and their examples?

A

1) Antioxidant proteins: albumin, haptoglobin, ceruloplasmin

2) Enzymatic antioxidants: superoxide dismutase, glutathoine peroxidase, catalase

3) Non-emzymatic or small molecules antioxidants: vitamin C, vitamin E, glutathione, selenium

114
Q

Arginine is contraindicated in patients with what diseases? Why?

A

Severe sepsis

Arginine supplementation will increase nitric oxide production and potentially worsen the cardiovascular tone and tissue perfusion

115
Q

What is the normal enteral protein intake for dogs and cats?

A

Dogs: 4-6g/Kg (15-25% of total energy)

Cats: 6g+/Kg (25-35% of total energy)

116
Q

What are the common electrolytes derangement in refeeding syndrome?

A

Hypophosphatemia
Hypokalemia
Hypomagnesemia
Hypocalcemia
Hyponatremia

Others: hyperglycemia, thiamine deficiency, vitamin deficiency

117
Q

What is the pathophysiology of refeeding syndrome?

A

During prolonged starvation/anorexia or certain catabolic state, the intracellular electrolytes are depleted. When the enteral nutritions introduced, the cells start to switch to metabolic states and certain electrolytes (e.g. phosphorus and magnesium) are heavily required as the source or co-factors for the metabolic pathways, which leads to rapid depletion of those extracellular electrolytes.

118
Q

When do clinical signs of refeeding syndrome commonly seen after initiating feeding?

A

2-5 days
(can range from within hours to up to 10 days)

119
Q

What are the clinical signs for refeeding syndromes?

A

Muscle weakness, tachyarrhythmias, hemolytic anemia, neurological signs, peripheral edema, respiratory failure

120
Q

True or False: EPA is Omega-6 fatty acid.

A

False

EPA (eicosapentaenoic acid) is one of the Omega-3 fatty acids. An example of Omega-6 fatty acid is AA (arachidonic acid).

121
Q

What is the kcal/ml of 50% dextrose? What about its osmolality?

A

1.7 kcal/ml, 2500 mOsm/L

122
Q

How much percentage of calories can be given via lipid in parental nutrition?

A

50-70% (of the non-protein calories)

123
Q

What is the kcal/ml of 20% lipid emulsion?

A

2 kcal/ml

124
Q

How many kcals does one gram of protein provide?

A

4 kcal/g

125
Q

What are the recommended dosage for Vitamin B com, Mg, Zinc and potassium?

A
126
Q

What are the electrolytes changes can cause constipation?

A

Hypokalemia
Ionized hypomagnesemia
Ionized hypercalcemia
Ionized hypocalcemia

127
Q

What are the drugs that can cause constipation?

A

Opioids
Sucralfate
Anticholinergics
Diuretics
Barium
Phenothiazines
Antihistamins
Iron

128
Q

What are the drugs that can work as colonic prokinetics and what are their MOAs?

A

Cisapride - 5-HT4 agonist
Ranitidine - Acetylcholinesterase inhibitor
Erythromycin - Motilin agonist (in vitro)

129
Q

What is the maximal gastric capacity in dogs and cats?

A

45-90 ml/kg

130
Q

What is the MOA of capromorelin?

A

ghrelin receptor agonist

Ghrelin is roduced by the parietal cells of the gastric mucosa as an endogenous ligand for growth hormone.

131
Q

What is MOA of mirtazapine as an appetite stimulant in cats?

A

5-HT2c antagonist

132
Q

What are the osmolality limitation for peripheral route and central route of parenteral nutrition administration?

A

Peripheral: < 750 mOsm/L
Central: < 1400 mOsm/L

133
Q

What are the substances that excite the GI motor neurons and what inhibit the GI motor neurons?

A

Excites: acetylcholine, serotonin, substance P

Inhibits: norepinephrine, GABA, NO, vasoactive intestinal peptides (VIP), somatostatin

134
Q

Where is somatostatin produced and what stimulates its production?

A

Produced by antral D cells.
Decreased pH - feedback to stop the production of gastrin by G cells (paracrine action)

135
Q

True or False: Both cats and dogs can generate migrating motor complexes (MMC) during the interdigestive phase.

A

False.

Only dogs generate MMC and it’s about 15-20 sec/min. Cats generate giant migrating complex.

136
Q

Describe enterogastric reflex.

A

When the duodenum detects low PH, high lipid content or high osmolality, it will inhibit the vagus nucleus and activate the sympathetic nerves to inhibit the gastric peristalsis, tighten the pyloric sphincter and delay gastric emptying.

137
Q

What are the three gastrointestinal reflexes?

A

Enterogastric reflexes
Gastrocolic reflexes
Gastroileal reflexes

138
Q

What are the 5 main contraction patterns for small intestines?

A

Peristaltic waves
Mixing patters:
* Stationary segmenting contractions
* Stationary or migrating clusters of contractions
Giant contractions (aboral)
MMCs

139
Q

What are the two main motility patterns in the large intestine?

A
  • haustral (mixing) movements (teniae)
  • Mass movements (only transversal and descending colon) driven by gastro-colic reflex
140
Q

What are the average small intestinal transit time in dogs and cats?

A

Dogs: 3-5 hours

Cats: 2-3 hours

141
Q

What are the two main theories for gastroparesis in critically ill patients?

A

1) Primary gastric pump failure
2) Excessive feedback theory: nutrients release excessive CCK and serotonin which cause disproportional inhibitory effect from the intestines to the stomach

142
Q

How does inflammation cause intestinal ileus?

A

The inflammatory mediators can damage the intestinal muscular layer by releasing proteolytic enzymes and cytokines. They can also cause NO release and paralyze the muscular layer which leads to ileus

143
Q

How does opioid cause decreased GI motility?

A

Opioid binds to the peripheral mu-receptor in the GI system and lead to decreased GI motility. It also inhibits the release of Ach.

144
Q

What are the treatment strategies for GI dismotility?

A

Early nutrition intervention
Early ambulation
Pain management
Maintain euhydration status
Maintain normothermia
Prokinetics
Address the underlying diseases (e.g. correct electrolyte imbalances)

145
Q

Which serotonin receptors in the GI tract is mainly responsible for peristalsis?

A

5-HT4

146
Q

Where do the following prokinetics work for the colon?
Metoclopramide
Cisapride
Ranitidine/Nizatidine
Erythromycin/Azithromycin
Ondansetron
Maropitant

A

Cisapride, Ranitidine/Nizatidine

147
Q

What are the suggested drugs that may be reported to be associated with acute pancreatitis in dogs?

A

L-asparaginase
Phenobarbital
KBr
Azathioprine
Potentiated sulfonamides
Organophosphates
Corticosteroids
Furosemide
Atovaquone/proguanil (Malarone)
N-methyl-glucamine (Meglumine)
Clomipramine
Zinc

148
Q

What are the endocrinopathies that have been reported as risk factors for AP in dogs?

A

Hyperadrenorcorticism, hypothyroidism, DM

149
Q

What are the two major pathways for AP pathogenesis?

A

Premature trypsinogen activation
Activation of nuclear factor- kappa beta (NF-κB)

150
Q

What are the proposed mechanisms for activation of trypsinogen and NF-κB in dogs with AP?

A
  1. Deranged **calcium **signaling
  2. **Colocalization **of zymogens and lysosomes
  3. Impared autophagy (lysosomal instability LAMP-1 and LAMP2)
  4. Endoplasmicreticulum stress (maladaptive/overwhelmed unfolded protein system)
  5. Oxidative stress
  6. Mitochrodrial dysfunction (mediated by NEFA)
151
Q

Where in the GI tract is bile acid reabsorbed?

A

Distal ileum by apical Na dependent bile acid transporter (ASBT)

152
Q

Describe how to perform gastrotomy.

A

1) Make a midline incision and achieve hemostasis with cauterization
2) Isolate the stomach from the remainder of abdomen with moistened laparotomy sponges
3) Place two stay sutures
4) Make an incision at the ventral surface of the stomach between the lesser and greater curvatures (find the area with least vascularity)
5) place the **suction tip **into the stomach to remove all the gastric fluid
6) Close the stomach with continuous double-layer inverting closure patterns with monofilament absorbable sutures. The first layer incorporates full thickness of stomach wall. The second layer incorporates serosa and muscular layers.

153
Q

In general, inflation pressures higher than _______ are not recommended during laparoscopy

A

15 mmHg
This is because >15mmHg causes a favorable gradient for gas to enter the venous side of the vasculature

154
Q

How do parietal cell produce HCl?

A

Parietal cells are very rich in mitochondria –> CO2 production –> carbonic anhydrase –> H+ produced and exchanged for K+ (apical membrane) while HCO3- exhanged for Cl- (baso-lateral membrane)

Alkaline tide after meal due to reabsorbtion of HCO3

155
Q

Where is secretin produced? what stimulates its production? what effects does it have?

A

S cell in duodenum
Increase in fatty acid and decreased pH
Reduce gastrin production, induce production of bile in liver cells, increase bicarbonate in pancreas and increase pepsinogen release by chief cells

156
Q

Where is GIP released? stimulated by? effects?

A

K cells in duodenum, oligosaccarides and FFA
Decrease HCl production and release of insulin

157
Q

Following peritoneal lavage how to estimate amount of blood in abdomen?

A

Volume blood = (PCV in lavage x Volume lavage) / (PCV blood - PCV lavage)

158
Q

Which two toxins by Clostridium perfrigens are thought to contribute to AHDS?

A
  • CPE
  • NetF (pores in enterocytes)
159
Q

What is the optimal pH for healing esophagitis and duodenal ulcers?

A

pH>4 for 16h/day
pH>3 for 18h/day

160
Q

In which conditions PPIs should be considered?

A
  • hepatic disease
  • possibly stage IV CKD
  • esophagitis
161
Q

Etological classification of peritonitis

A
  • primary (idiopathic): high prevalence in cats (14-23%, FIP)
  • secondary (septic or sterile)
  • tertiary (recurrent or persistent intra-abdominal infection despite interventions): high mortality (56% in dogs)
162
Q

Three main factor supporting repair of the injured intestinal barrier

A
  • Hypoxia Inducible Factor (HIF): bridges healthy thight junction, immunomodulatory and anti-inflammatory
  • CIC-2: chloride channel regulated endocytocis and recycling of tight junction proteins
  • NHE: ion exchanger associated with tight junction recovery
163
Q

According to ENOVAT guidelines for antimicrobial use in canine acute diarrhoea - which cathergories of patients warrant antimicrobial use?

A

Patients with hemorrhagic or non-hemorrhagic diarrhoea and severe disease (signs of systemic disease despite IVFT) –> amoxycillin-clavulanic acid or TMPS
Critically ill patients –> combination of co-amox/clynda + fluoroquinolones

164
Q

Define gastrointestinal pneumatosis

A

GP is a diagnostic imaging diagnosis (not clinical) and refers to the accumulation of gas within the GI walls.

There are three recognised types:
- gastric pneumatosis
- pneumatosis intestinalis
- pneumatosis coli

165
Q

What are the two theories for GI pneumatosis formation?

A
  1. mechanical: gas enters the wall due to mucosal tearing secondary to trauma or increased intraluminal pressure (i.e. GDV)
  2. bacterial: gas-producing bacteria (i.e. Clostridium difficile, Klebsiella and Sarcina) invade the GI wall due to a defective immune or mucosal barrier
166
Q

What is the most common location of GI pneumatosis in dogs and cats?

A

Stomach followed by colon and then SI

167
Q

Most common causes of GI pneumatosis in dogs and cats

A
  1. GI disease (i.e. GDV, IBD, AHDS, etc.)
  2. GI endoscopy
  3. feeding tube placement
  4. corticosteroids and chemotherapeutics (not NSAIDs)
168
Q

Medical vs surgical management of GI pneumatosis

A

No longer considered an exclusively surgical condition

Medical management indicated if patient not pyrexic, hypotensive or with severe abdominal pain.

Medical management survival 54% vs 20% with surgical intervention

ECVECC Board Exam (24 decks)

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