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VTS(ECC) Study > GI/Exocrine Pancreas > Flashcards

GI/Exocrine Pancreas Flashcards

1
Q

How are protons pumped out of parietal cells?

A

Carbonic anhydrase converts H2O & CO2 to HCO3 & H. H secreted through apical H/K ATPase pump. HCO3 exchanges with Cl- in the basolateral membrane

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2
Q

Name the three stimulants for gastric acid production and the associated receptor

A
  1. Histamine - H2 receptor 2. Acetylcholine - M3 receptor 3. Gastrin - CCK2 receptor
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3
Q

Where are stress related mucosal disease (SRMD) lesions found?

A

Stomach with oxyntic glands: fundus & body Contrast: peptic ulcer @ antrum and pylorus

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4
Q

What pH is required for platelet aggregation and fibrin clot formation?

A

>6

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5
Q

What is the function of the extracellular mucus barrier?

A
  1. maintain surface pH 7 2. prevent pepsin infiltration & proteolytic degradation 3. Hydrophobic properties of surfactant repel water soluble agents
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6
Q

What are the most common causes of hemorrhage in dogs with acute abdomen?

A

Splenic rupture (secondary to neoplasia) Hemorrhage from GI ulceration

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7
Q

What is the most common range for glucose in a dog with sepsis?

A

40-60 mg/dL although it can be lower

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8
Q

Where is the most common place to detect free gas in the abdomen on radiographs?

A

Between the stomach or liver and the diaphragm on a lateral projection

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9
Q

Large volumes of free gas in the abdomen are associated with which conditions?

A

Pneumocystography with a ruptured bladder Vaginal rupture Recent surgery Ruptured GDV Pneumoperitoneography Extension of pneumomediastinum

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10
Q

Small volumes of free gas in the abdomen are associated with which conditions?

A

Rupture of the GI tract Infection with a gas-forming organism

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11
Q

What is the normal diameter of the small intestine in the dog? and in the cat?

A

Dog: 2-3x the width of a rib or less than the width of an intercostal space Cat: Should not exceed twice the height of the central portion of the L4 vertebral body, or 12 mm

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12
Q

What difference between blood glucose levels between the periphery and abdominal effusion would you expect in a septic abdomen?

A

BG of periphery should be > 20 mg/dL higher than the abdominal effusion. This has a 100% specificity in dogs and cats, and is 100% sensitive in dogs, 86% sensitive in cats

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13
Q

What difference between lactate levels between the periphery and abdominal effusion would you expect in a septic abdomen?

A

Peritoneal fluid lactate should be > 2.0 mmol/L higher than blood lactate 100% specificity and sensitivity in dogs, not reported in cats

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14
Q

What ratio between potassium levels in abdominal fluid vs blood would you expect in a uroabdomen?

A

Dog 1.4 : 1 Cat 1.9 : 1 100% sensitive in the dog, considered diagnostic for uroabdomen, not reported in the cat

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15
Q

What ratio between creatinine levels in abdominal fluid vs blood would you expect in a uroabdomen?

A

Dog 2 : 1 Cat 2 : 1 86% sensitive, 100% specific in the dog Not reported in the cat

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16
Q

What ratio between bilirubin levels in abdominal fluid vs blood would you expect in a bile peritonitis?

A

> 2 : 1 100% sensitive in dogs

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17
Q

What is the sensitivity and specificity of cPLI?

A

Sensitivity: 82% with severe pancreatitis, 63.6% with less severe pancreatitis Specificity: 96.8%

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18
Q

What is the sensitivity and specificity of fPLI?

A

Sensitivity: 67% in all cats with pancreatitis, 100% in cats with moderate to severe pancreatitis Specificity: 100%

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19
Q

What is the sensitivity and specificity of SNAP cPLI?

A

Sensitivity: 92-94% Specificity: 71-78%

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20
Q

What is the sensitivity and specificity of SNAP fPLI?

A

Sensitivity: 79% Specificity: 80%

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21
Q

What is the ratio of maximal small intestinal diameter to the narrowest width of L5 on the lateral radiograph in dogs?

A

Ratio > 1.6

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22
Q

What is the ratio of maximal small intestinal diameter to the height of the cranial endplate of L2 in the cat?

A

Ratio > 2.0

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23
Q

On abdominal ultrasound in dogs, the jejunum should have a luminal diameter of less than what value?

A

Less than 1.5 cm If greater than 1.5cm with normal wall layering, intestinal obstruction should be investigated

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24
Q

List some breeds predisposed to congenital megaesophagus?

A

wire haired fox terriers, mini schnauzers, g shepherds, great danes, shar peis, irish setters, labs, newfies

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25
Q

Most adult-onset cases of acquired megaesophagus are?

A

idiopathic

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26
Q

Name 4 causes of a small intestinal transit disorder?

A

Enteritis Post-surgical ileus Nematode impaction Intestinal sclerosis Radiation enteritis

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27
Q

True or false: The enteric nervous system can function independently of the central nervous system

A

TRUE The enteric nervous system uses enteroendocrine cells (such as the enterochromaffin cells) as sensory transducers because no nerve fibers actually penetrate the intestinal epithelium

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28
Q

What is the neurotransmitter in the enteric nervous system?

A

5-HT or serotonin

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29
Q

What receptor in the enteric nervous system is responsible for initiating peristaltic and secretory reflexes?

A

5-HT 1p

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30
Q

What receptor in the enteric nervous system is responsible for the sensation of nausea and induction of vomiting?

A

5-HT3

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31
Q

What does stimulation of the 5-HT4 receptor in the enteric nervous system do?

A

It increases the presynaptic release of acetylcholine and calcitonin gene-related peptide, which results in enhanced neurotransmission. This results in enhanced propulsive peristaltic and secretory reflexes

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32
Q

What is the mechanism of action of cisapride?

A

5-HT4 agonist This results in enhanced neurotransmission. however, it depends on natural stimuli to evoke peristaltic and secretory reflexes.

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33
Q

How is cisapride different from metoclopramide?

A

It does not cross the blood-brain barrier or have antidopaminergic effects. It does not have antiemetic effects and it does not cause the extrapyramidal effects seen with metoclopramide It is a more potent prokinetic than metoclopramide and has a wider activity as it increased colonic motility

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34
Q

What is the mechanism of action of metoclopramide?

A

It is a central dopaminergic antagonist and peripheral 5-HT3 receptor agonists. It stimulates and coordinates esophageal, gastric, pyloric, and duodenal motor activity. It also increases lower esophageal sphincter tone and stimulates gastric contractions while relaxing the pylorus and duodenum

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35
Q

What can be done to reverse the extrapyramidal signs (involuntary muscle spasms, motor restlessness, inappropriate aggression) associated with metoclopramide administration?

A

Need to restore an appropriate dopamine to acetylcholine balance with the anticholinergic action of diphenhydramine

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36
Q

What is the mechanism of action of erythromycin as a prokinetic?

A

At microbially ineffective doses, it stimulates migrating motility complexes and antegrade peristalsis in the proximal GI tract. It also stimulates cholinergic and noncholinergic neuronal pathways that increase motility. It also increase gastroesophageal sphincter pressure in dogs and cats

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37
Q

What is the mechanism of action of ranitidine and nizatidine as prokinetics?

A

They are both histamine H2 receptor antagonists. The prokinetic activity is due to acetylcholinesterase inhibition.

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38
Q

What is the postulated mechanism of primary peritonitis?

A

Hematogenous dissemination

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39
Q

What is the most common form of primary peritonitis?

A

Feline infectious peritonitis (FIP)

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40
Q

What percentage of patients that have had an enterotomy or intestinal resection and anastomosis will develop septic peritonitis secondary to surgical site dehiscence?

A

6-16%

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41
Q

What percentage of feline peritonitis patients will exhibit abdominal pain?

A

38-62%

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42
Q

What are the pros and cons of using a Jackson-Pratt drain in a septic abdomen as opposed to the open abdomen technique?

A

Pros: Decreased risk of nosocomial infections Less intensive nursing and bandaging Decreased risk for evisceration Only one surgical procedure Quantitative and qualitative assessment of fluid Cons: Drain may induce fluid production Drain can become occluded

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43
Q

What is the survival rate for canine patients with peritonitis? Feline patients?

A

Canine: 44-71% Feline: Depends on the study, up to 70%

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44
Q

What is the reported mortality rate for patients with septic peritonitis secondary to GI leakage?

A

30-85%

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45
Q

Why should metoclopramide not be used in patients with a pheochromocytoma?

A

Metoclopramide causes release of catecholamines from the tumor. It is better to use cisapride or erythromycin if a prokinetic is needed.

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46
Q

Describe the differences between osmotic diarrhea, secretory diarrhea, diarrhea from altered permeability, and deranged motility

A

Osmotic- excess luminal osmoles drawing fluid into the intestinal lumen; this is common in diarrhea Secretory- net increase in intestinal fluid secretion; can be caused by an absolute increase in secretion vs decreased intestinal absorption Altered permeability- microscopic and macroscopic damage to epithelial cells and/or junctions can lead to abnormal permeability; vital substances can be lost into the intestinal lumen Deranged motility- least understood cause; increased peristaltic contractions vs decreased segmental contractions

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47
Q

Describe the characteristics of large vs small bowel diarrhea

A

Large: mucus common, +/- hematochezia, normal to decreased stool volume, absent melena, increased frequency, increased urgency/tenesmus Small: stool volume increased to normal, melena may be present, frequency increased to normal, no urgency/tenesmus

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48
Q

When is it indicated to start symptomatic tx for diarrhea?

A

Pt quality of life is decreased, possibility IVC/u cath infection, fecal scald

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49
Q

Name some medications commonly associated with diarrhea

A

PPI, H2 antagonists, chemotherapeutic drugs, digoxin, procainamide, ACE inhibitors, azathioprine, cyclophosphamide, cyclosporine, NSAIDs, mitotane, methimazole, parasiticides, amitriptyline

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50
Q

How does R sided CHF potentially cause diarrhea?

A

Congestion of the splanchnic vasculature can cause alterations in the absorptive capacities of the SI

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51
Q

How does hypoadrenocorticism potentially cause diarrhea?

A

cortisol is vital for maintenance of normal GI fxn, motility and integrity and vascular tone/perfusion

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52
Q

Name some common bacterial causes of diarrhea

A

Salmonella, Campylobacter, E coli, Clostridium difficile, Clostridium perfringens

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53
Q

Viral infections commonly causing diarrhea?

A

parvo, feline panleukopenia

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54
Q

What is one of the most common causes of chronic diarrhea in cats and dogs?

A

IBD

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55
Q

What are the different types of IBD?

A

Lymphocytic-plasmacytic Eosinophilic Granulomatous

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56
Q

What test is useful for testing for exocrine pancreatic insufficiency? For small intestinal bacterial overgrowth?

A

Trypsin-like immunoreactivity; cobalamin and folate

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57
Q

What other medications besides steroids can be used for IBD?

A

locally actie steroid budesonide, azathioprine, chlorambucil, metronidazole for abx and anti-inflammatory effects

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58
Q

T/F: a recent study in HGE (aseptic) in dogs showed an improvement in clinical signs and outcome with administration of clavamox?

A

False- no change in outcome

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59
Q

T/F: one one veterinary report, probiotics have been shown to shorten the duration of clinical signs in dogs with acute gastroenteritis?

A

true

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60
Q

How does hyperthyroidism lead to diarrhea?

A

increased food intake, increased intestinal hypermotility

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61
Q

which type of IBD is the most common?

A

Lymphocytic-plasmacytic

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62
Q

List vasoconstrictors of the GI mucosa

A

Leukotriene C4, thromboxane A2, endothelin-1

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63
Q

How does H2S modulate inflammation of the GI mucosa?

A

Inhibition of leukocyte adherence to the vascular endothelium and diminishes tissue injury induced by neutrophils

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64
Q

List 4 bacterial causes of gastroenteritis

A

Campylobacter, clostridium, escherichia coli, Salmonella, Helicobacter

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65
Q

List 5 out of 7 viral causes of gastroenteritis

A

Parvovirus (CVP2), rotavirus, enteric coronavirus, FIP, distemper, FeLV, FIV, Feline panleukopenia

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66
Q

What are 3 fungal/algal causes of gastroenteritis?

A

Histoplasmosis, pythiosis, protothecosis

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67
Q

List 5 parasitic causes of gastroenteritis

A

Ascarids, hookworms, strongyloides stercoralis, whipworms, isospora canis/felis, toxoplasma, cryptosporidium parvum, giardia, tritrichomonas, balantidium coli

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68
Q

What rickettsial disease is a possible cause of gastroenteritis?

A

Neorickettsia helminthoeca (salmon poisoning)

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69
Q

List the three cell types of the glandular portion of the stomach and their chief secretion

A

Parietal cell - HClChief cell - pepsinogenMucous producing cells - mucous and bicarbonate

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70
Q

What is the approximate life span of an enterocyte?

A

2-5 days

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71
Q

E.coli is thought to be the causative organism for what disease process?

A

Histiocytic ulcerative colitis (in boxer dogs)

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72
Q

How is HUS treated and the diagnosis of organisms confirmed?

A

Fluoroquinolones; FISH (fluorescent in situ hybridization) to confirm

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73
Q

What is the suggested pathogenesis of HGE?

A

Abnormal immune responses to bacteria, bacterial endotoxins, or dietary indiscretion/ingredients. C. Perfringens have been isolated from HGE dogs but exact role is not known.

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74
Q

Why is the PCV elevated in HGE?

A

Splenic contraction and/or hemoconcentration

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75
Q

Why are the total solids normal to decreased in HGE?

A

GI loss of proteins or redistribution of body water into the vascular space

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76
Q

What are 4 causes of PLE?

A

Severe lymphoplasmacytic IBD, eosinophilic IBD, granulomatous IBD, lymphangectasia, diffuse GI fungal disease, diffuse neoplasia (ie lymphoma)

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77
Q

List 4 extra GI causes of gastroenteritis

A

Addison’s, liver disease, kidney disease, acute pancreatitis, peritonitis, DKA, vestibular disease, pyometra, prostatitis

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78
Q

What are 3 possible drugs to treat Camphylobacter

A

Erythromycin, enrofloxacin, cefoxitin

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79
Q

What are the 3 proposed mechanisms through which probiotics may provide benefits in GI disease in vet med?

A

May compete with pathogenic organisms for nutrition, may produce anti microbial substances, and may stimulate the immune system

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80
Q

Congenital megaesophagus is found in what breeds?

A

Wire-haired fox terriers, mini schnauzers, GSD, GD, Irish Setters, Labs, Newfies, and Chinese Shar-Peis

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81
Q

What are 4 causes of secondary megaesophagus?

A

Myasthenia gravis, generalized neuromuscular disease, Addison’s, lead toxicity, hypothyroidism, dysautonomia

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82
Q

List 4 mechanical obstruction causes of regurgitation

A

Esophageal stricture, foreign body, neoplasia, vascular ring anomalies, extra luminal compression (ie mediastinal mass), hiatal hernia, gastroesophageal intussussception

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83
Q

Most cases of drug induced esophagitis are related to the administration of what?

A

Doxycycline

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84
Q

Why are metoclopramide and cisapride potentially not useful in regurgitating canine patients?

A

The canine esophagus is almost exclusively striated muscle, those drugs work on smooth muscle; these drugs may also decrease transit of food to the stomach by increasing lower esophageal tone

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85
Q

What is the parasympathomimetic that may be a useful prokinetic in dogs with megaesophagus?

A

Bethanechol

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86
Q

T/F: regarding animals with congenital idiopathic megaesophagus, with appropriate care many animals develop improved esophageal motility over several months

A

T

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87
Q

What are the 3 CNS sites that provide input to the vomiting center?

A

Vestibular system, cerebrum, CRTZ

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88
Q

What is the most common acid/base finding in patients with GI foreign bodies?

A

Hypochloremic metabolic alkalosis

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89
Q

What is the most common electrolyte abnormality in vomiting patients?

A

Hypokalemia

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90
Q

List 5 risk factors for developing GDV

A

First degree relatives that have had GDV, higher thoracic depth to width ratio, lean body condition, advancing age, stressful events, fearful, nervous, or aggressive temperament, raised food bowl, eating only dry food, single meal/day

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91
Q

What cause of GDV in children has been proposed as a cause of GDV in dogs?

A

Laxity or agenesis of the peri gastric ligaments

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92
Q

T/F: Stretching or transection of peri gastric ligaments (as with splenic torsion or splenectomy) were suggested in early studies to increase the risk for GDV

A

T

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93
Q

T/F Gastric dilitation always occurs before volvulus

A

F - it is unknown - isolated cases of both gastric dilatation and gastric volvulus have been reported

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94
Q

Decreased venous return and increased venous pressure result in what 2 abnormalities that can contribute to interstitial edema and loss of intravascular volume?

A

Splanchnic pooling and portal hypertension

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95
Q

List 2 physiological side effects of compression of intra abdominal veins secondary to significant gastric distention

A

Decreased caudal vena cava flow rate, decreased venous return, subsequently decreased cardiac output and MAP

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96
Q

Describe 2 respiratory complications secondary to gastric distention and increased abdominal pressure associated with GDV.

A

decrease total thoracic volume, prevent normal caudal diaphragmatic excursion, may result in partial lung lobe collapse resulting in decreased tidal volume and V/Q mismatch. RR and RE increase to compensate though efforts may not be enough

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97
Q

What might be a mechanism for aspiration pneumonia specifically suggested for GDV patients?

A

Aspiration of pharyngeal contents preoperatively resulting in sub clinical pneumonia preoperatively but contributing to post op morbidity and mortality

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98
Q

List 3 reasons for decreased gastric blood flow in a patient with GDV

A

Compression, thrombosis, avulsion of the splenic and/or short gastric arteries, elevated intragastric pressures, and reduced cardiac output

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99
Q

What is the expected pattern of gastric necrosis in GDV?

A

Fundus most commonly affected followed by progression to the body of the stomach.

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100
Q

How is necrosis of the cardia potentially different from other gastric necrosis in GDV?

A

Cardia necrosis is likely related to direct vascular occlusion

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101
Q

Why is intestinal blood flow compromised in dogs with GDV?

A

Direct compression of the portal vein and decreased cardiac output

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102
Q

T/F splenic compromise is not uncommon in dogs with GDV and is associated with a worse outcome

A

T

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103
Q

List 3 splenic complications reported in dogs with GDV

A

Splenic vascular avulsion, intravascular thrombosis, splenic torsion, and splenic infarction.

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104
Q

List 3 possible causes of ventricular arrhythmias associated with GDV

A

Decreased coronary blood flow, myocardial ischemia which may lead to ectopic foci of electrical activity, circulating epinephrine and proinflammatory cytokines

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105
Q

Describe 2 possible acid/base disorders associated with GDV and their causes

A

High anion gap (lactate), metabolic acidosis (decreased DO2), hypochloremic metabolic alkalosis (from sequestration of gastric HCL), respiratory acidosis (from Hypoventilation and hypercapnia)

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106
Q

List 4 possible causes of hypokalemia in a patient with GDV

A

Administration of low K fluids, sequestration of K in the stomach or lost through vomiting or lavage, hyperchloremic metabolic alkalosis with transcellular shifting, activation of the RAAS, and catecholamine induced intracellular shifting of K.

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107
Q

In a dog with GDV, where is the pylorus located on the DV view?

A

To the left of midline

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108
Q

Why is VD positioning potentially contraindicated in GDV?

A

May lead to further cardiovascular compromise, and may predispose to aspiration if the dog regurgitates/vomits

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109
Q

T/F the presence of 2 or more abnormal hemostatic parameters consistent with DIC has been shown to correlate with gastric necrosis

A

F…3 or more

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110
Q

What are 2 possible complications associated with attempted trocharization?

A

Splenic laceration, gastric perforation

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111
Q

T/F - dogs with GD and no V do not require surgical intervention

A

False- recommend explore if are unresponsive to medical treatment; also pexy is recommended In the future to prevent GDV

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112
Q

What is the most common degree of pyloric rotation in a GDV?

A

180-270 degrees

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113
Q

What are the 3 markers to assess gastric wall viability?

A

Serosal color, palpation of gastric wall thickness, and evidence of arterial bleeding if incised

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114
Q

List 3 possible consequences associated with gastric wall necrosis

A

Peritonitis, DIC, sepsis, and arrhythmias

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115
Q

Why is tube gastropexy associated with higher morbidity?

A

Due to premature tube removal and peristomal cellulitis

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116
Q

List 4 gastropexy techniques

A

Tube, incisional, muscular flap, circumcostal, belt loop

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117
Q

List 4 risk factors associated with death before suture removal

A

Hypotension during hospitalization, combined splenectomy and partial gastropexy, peritonitis, sepsis, and DIC

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118
Q

What are the two plexuses of the enteric nervous system and where are they located?

A

Myenteric (or Auerbachs) which is between the longitudinal and circular muscular layers, and the submucosal (or Meissners) which is in the submucosa

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119
Q

What does the myenteric plexus control? and the submucosal plexus?

A

myenteric controls gastrointestinal movements, the submucosal controls gastrointestinal secretion and local blood flow

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120
Q

When the myenteric plexus is stimulated, what are its effects?

A

1 - increased tonic contraction of tone of the gut wall 2- increased intensity of rhythmic contractions 3- slightly increased rate of the rhythm of contraction 4- increased velocity of conduction of excitatory waves along the gut wall

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121
Q

Name 6 neurotransmitters secreted by enteric neurons

A

acetylcholine norepinephrine adenosine triphosphate serotonin dopamine cholecystokinin substance P vasoactive intestinal polypeptide somatostatin leu-enkephalin met-enkephalin bombesin

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122
Q

In the enteric nervous system which is the main excitatory and which is the main inhibitory neurotransmitter?

A

excitatory is acetylcholine inhibitory is norepinephrine

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123
Q

What is the gastrocolic reflex?

A

Signal from the stomach to cause evacuation of the colon (reflex from the gut to the prevertebral sympathetic ganglia and then back to the GI tract)

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124
Q

what are the two types of electrical waves that cause excitation of the GI tract?

A

slow waves, spike potentials

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125
Q

What is the colonoileal reflex?

A

reflex from the colon to inhibit emptying of the ileal contents into the colon (reflex from the gut to the prevertebral sympathetic ganglia and then back to the GI tract)

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126
Q

What gastrointestinal reflexes travel from the gut to the spinal cord or brain stem and then back to the GI tract?

A

1- reflexes to control gastric motor and secretory activity 2- pain reflexes that cause general inhibition of the GI tract 3- defecation reflexes that travel from the colon and rectum to the spinal cord and back to produce contractions required for defecation

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127
Q

List the layers of the intestinal wall from outer surface inwards

A

serosa, longitudinal smooth muscle, circular smooth muscle, submucosa, mucosa

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128
Q

how are spike potentials involved in smooth muscle contraction of GIT?

A

occur automatically when resting membrane potential of GI smooth muscle is more positive than -40 mV; appear on peaks of slow waves

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129
Q

compare the types of channels used for action potentials in GI smooth muscle vs nerve fibers

A

nerve fibers- action potential caused by rapid entry of Na through sodium channel to interior (Na channels); more rapid open/close GI smooth muscle- large numbers of Ca enter alone with smaller # of Na ions (Ca-Na channels); slower to open/close; results in longer duration of action potential

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130
Q

What cells secrete cholecystokinin (CCK)?

A

I cells in the mucosa of the duodenum and jejunum

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131
Q

what are the two types of electrical waves that cause excitation of the GI tract?

A

slow waves, spike potentials

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132
Q

list factors that may cause hyperpolarization (more negative) of membrane potential

A

effect of epi or norepi on fiber membrane, stimulation of sympathetic nerves that secrete norepi at their endings

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133
Q

What cells secrete secretin?

A

S cells of the duodenum, jejunum, and ileum

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134
Q

Name stimuli for secretin secretion

A

Acid Fat

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135
Q

What are the actions of secretin?

A

Stimulates pepsin secretion, pancreatic bicarbonate secretion, biliary bicarbonate secretion, growth of exocrine pancreas Inhibits gastric acid secretion

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136
Q

what are the two plexuses that compose the enteric nervous system

A

myenterix/Auerbach’s; submucosal/Meissner’s

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137
Q

What are the actions of cholecystokinin?

A

Stimulates pancreatic enzyme secretion, pancreatic bicarbonate secretion, gallbladder contraction, growth of the exocrine pancreas Inhibits gastric emptying

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138
Q

What cells secrete secretin?

A

S cells of the duodenum, jejunum, and ileum

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139
Q

Name stimuli for secretin secretion

A

acid fat

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140
Q

What are the actions of secretin?

A

Stimulates pepsin secretion, pancreatic bicarbonate secretion, biliary bicarbonate secretion

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141
Q

describe slow waves and how they cause electrical excitation in the GIT

A

slow, undulating changes in the resting membrane potential that may be caused by interactions between smooth muscle cells and specialized cells such as interstitial cells of cajal

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142
Q

what is the proposed role of interstitial cells of cajal?

A

act as an electrical pacemaker for smooth muscle cells

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143
Q

in what part of the GIT can slow waves cause muscle contraction by themselves (i.e. not along with intermittent spikes)

A

stomach

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144
Q

compare the types of channels used for action potentials in GI smooth muscle vs nerve fibers

A

nerve fibers- action potential caused by rapid entry of Na through sodium channel to interior (Na channels); more rapid open/close GI smooth muscle- large numbers of Ca enter alone with smaller # of Na ions (Ca-Na channels); slower to open/close; results in longer duration of action potential

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145
Q

what is the average resting member potential in the GI?

A

-56 mV

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146
Q

list factors that may cause depolarization (less negative) of membrane potential

A

stretching of muscle, stimulation by Ach released from parasympathetic nerves, stimulation by GI hormones

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147
Q

list factors that may cause hyperpolarization (more negative) of membrane potential

A

effect of epi or norepi on fiber membrane, stimulation of sympathetic nerves that secrete norepi at their endings

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148
Q

t/f- slow waves cause calcium ions to enter the smooth muscle fiber

A

false- only Na ions enter

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149
Q

t/f- spike waves cause significant amts of Ca ions to enter smooth muscle fiber

A

true; this is why they more often cause action potential and muscle contraction

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150
Q

where is the enteric nervous system located

A

wall of gut from esophagus to anus

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151
Q

what are the two plexuses that compose the enteric nervous system

A

myenterix/Auerbach’s & submucosal/Meissner’s

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152
Q

what does the myenteric plexus mainly control?

A

GI movements

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153
Q

what does the submucosal plexus mainly control?

A

GI secretion and local blood flow

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154
Q

What cells secrete gastric inhibitory peptide?

A

K cells of the duodenum and jejunum

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155
Q

Name stimuli for gastric inhibitory peptide secretion

A

Protein Fat Carbohydrate

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156
Q

What are the actions of gastric inhibitory peptide?

A

Stimulates insulin release Inhibits gastric acid secretion decreases motor activity of stomach

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157
Q

What cells secrete motilin?

A

M cells of the duodenum and jejunum

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158
Q

Name stimuli for motilin secretion

A

Fat Acid Nerve

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159
Q

What are the actions of motilin?

A

Stimulates gastric motility and intestinal motility

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160
Q

Give the 3 motor functions of the stomach: (Guyton)

A
  • Storage of food - Mixing of food with gastric secretions (formation of chyme) - Emptying of the chime at a rate suitable for proper digestion
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161
Q

How is the reflex triggered by a bolus of food and allowing the stomach to distend called? (Guyton)

A

Vagovagal reflex (from the stomach (stretching) to the brain stem to the stomach)

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162
Q

Are the gastric glands present in the entire wall of the body of the stomach? (Guyton)

A

No, almost except along a narrow strip on the lesser curvature of the stomach

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163
Q

What are the 2 types of gastric contractions (presence of food or not)? (Guyton)

A
  • Peristaltic contractions (when food is present) - Hunger contractions (when the stomach has been empty for several hours)
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164
Q

What is the ratio between weak peristaltic contractions (mixing) and strong ringlike peristaltic contractions? What is the pressure generated by strong peristaltism? (Guyton)

A

20% of ringlike contractions, 50-70 cmH2O

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165
Q

T or F: Peristaltic constrictor waves increase in intensity as they progress from the body of the stomach to the antrum (Guyton)

A

True

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166
Q

What is the frequency of the gastric peristaltic constrictor waves when food is present in the stomach? (Guyton)

A

One every 15-20 seconds

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167
Q

What are the 2 roles of the gastric peristaltic constrictor waves? (Guyton)

A
  • Propulsion of food - Mixing (by retropulsion: peristaltic wave while the pylorus is contracted, squeezing the antral content)
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168
Q

How is called the mixture of food with gastric acid? (Guyton)

A

Chyme

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169
Q

What parts of the GI tract regulate the stomach emptying? (Guyton)

A

Duodenum >> Stomach

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170
Q

What are the main gastric factors promoting stomach emptying and name the reflexes elicited when needed? (Guyton)

A
  • Increased gastric food volume resulting in gastric wall stretching (and not increased storage pressure) -> local myenteric reflexes -> accentuate the activity of the pyloric pump, inhibit the pylorus - Gastrin
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171
Q

What are the main duodenal factors inhibiting stomach emptying? Name the reflexes elicited and their pathways, or hormones released. (Guyton)

A
  • Distention of the duodenum / Irritation of the duodenal mucosa / Osmolality of the chyme (hypertonic > hypotonic) / Presence of certain breakdown products in the chyme (breakdown of proteins > fat) -> Enterogastric nervous reflexes - From the duodenum to the stomach through the enteric nervous system in the gut wall - Through extrinsic nerves that go to the prevertebral sympathetic ganglia and then back through inhibitory sympathetic nerve fibers to the stomach - Through the vagus nerves all the way to the brain stem, where they inhibit the normal excitatory signals transmitted to the stomach through the vagi - Fatty substances in the chyme -> Hormones from the duodenal and jejunal epithelium (cholecystokinin, +/- secretin +/- gastric inhibitory peptide)
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172
Q

most of the chewing muscles are innervated by which cranial nerve?

A

the motor branch of the 5th CN (trigeminal)

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173
Q

the nuclei in control of the chewing process are located in which area of the CNS?

A

brain stem

174
Q

what is the chewing reflex?

A

presence of a bolus of food in the mouth at first initiates reflex inhibition of the muscles of mastication, which causes the lower jaw to drop

175
Q

what is rebound contraction in regards to chewing?

A

raising of the jaw to cause closure of the teeth to allow chewing

176
Q

why is chewing especially important for fruits and raw veggies?

A

they have indigestible cellulose membranes around the nutrient portions that must be broken down before digestion can occur

177
Q

the rate of digestion is absolutely dependent on what?

A

the total surface area of the food exposed to the digestive secretions

178
Q

what are two benefits of the GI tract that occur when food is ground into a very fine particulate consistency in the mouth?

A

prevents excoriation of GI tract and increases the ease with which food is emptied from stomach to SI

179
Q

what are the 3 general stages of swallowing

A

voluntary stage, pharyngeal stage, esophageal stage

180
Q

describe the voluntary stage of swallowing

A

the tongue voluntarily moves food to the pharynx and backward against the palate

181
Q

briefly describe the pharyngeal stage of swallowing

A

the food in the posterior mouth/pharynx stimulates epithelial swallowing receptor areas, then brain stem initiates automatic pharyngeal muscle contractions

182
Q

There are 5 steps to the pharyngeal stage of swallowing. Describe.

A
  1. Soft palate is pulled upward to closer posterior nares 2. palatopharyngeal folds on each side of pharynx are pulled medially to form a slit for masticated food to pass 3. vocal cords are approximated and larynx is pulled upward and rostrally, causing epiglottis to cover opening of larynx 4. upward mvmt of larynx pulls up and enlarges the opening to the esophagus; upper esophageal sphincter relaxes 5. entire muscular wall of the pharynx contracts, which propels food into esophagus
183
Q

where is the swallowing center located in the brain?

A

medulla and lower pons

184
Q

which cranial nerves control motor impulses from swallowing center to to pharynx/upper esophagus?

A

V, IX, X, XII trigeminal, glassopharyngeal, vagus, hypoglossal

185
Q

how does swallowing center affect the respiratory center?

A

it inhibits respiratory center of medulla during pharyngeal stage of swallowing, which only takes about 6 sec

186
Q

list and describe the 2 types of esophageal peristaltic movements

A
  1. Primary peristalsis- continuation of the peristaltic wave that begins in the pharynx and spreads into the esophagus 2. secondary peristalsis- results from distension of esophagus itself by retained food when primary peristalsis fails to move food into stomach; they continue until all food has reached stomach
187
Q

how long does it take for food to pass from pharynx into stomach in normal adults?

A

8-10 seconds; 5-8 seconds if person is upright

188
Q

what type of muscle makes up the pharyngeal wall and upper 1/3 of esophagus? what controls the muscle?

A

striated muscle- controlled by skeletal nerve impulses from glossopharyngeal and vagus nerves

189
Q

what type of muscle makes up the distal 2/3 of the esophagus? what nerves control the muscle?

A

smooth muscle; controlled by vagus nerves or myenteric nerve plexus

190
Q

t/f: the stomach and duodenum become relaxed as the esophageal peristaltic wave approaches the stomach?

A

true

191
Q

where is the LES located in esophagus?

A

about 3 cm above esophageal juncture with stomach

192
Q

what ist he normal intraluminal pressure at the LES?

A

30 mm Hg

193
Q

t/f: the esophageal mucosa is capable of resisting the digestive actions of gastric secretions for long periods of time?

A

false- only the distal 1/8 can resist for long

194
Q

what are two mechanisms that help prevent reflux of stomach contents into esophagus?

A

Lower esophageal sphincter being contracted Valvelike mechanism of esophagus that extends into the stomach- caves the esophagus inward with increased intra-abdominal pressure

195
Q

What cells mostly contain the pyloric glands? What is mainly secreted by the pyloric glands on top of gastrin and pepsinogen?

A
  • Mucous cells (+ few peptic cells and almost no parietal cells) - Thin mucus to help lubricating food movement
196
Q

How are called the type of mucous cells covering the entire surface of the stomach mucosa? What do they secrete? Give 3 roles for this secretion?

A
  • Surface mucous cells - Large quantity of viscid mucus - Shell of protection for the stomach wall / Lubrification of food transport / Alkaline protection (wall not directly exposed to the highly acidic, proteolytic stomach secretion)
197
Q

What are the only cells secreting hydrochloric acid?

A

Parietal cells of the oxyntic glands of the main body of the stomach

198
Q

What type of cells operate in close association with the parietal cells of the oxyntic glands?

A
  • Enterochromaffin-like cells (ECL)
199
Q

Describe the association between gastrin, histamine and hydrochloric acid

A
  • Gastrin secreted by the G cells in the pyloric glands in response to proteins being digested - Stimulation of histamine secretion by the ECL - Stimulation of hydrochloric acid release by the parietal cells of the oxyntic glands
200
Q

What are the 2 stimuli for pepsinogen secretion by the peptic cells in the oxyntic glands?

A
  • Stimulation by acetylcholine released from the vagus nerves or from the gastric enteric nervous plexus - Stimulation in response to acid in the stomach (which acts indirectly by eliciting additional enteric nervous reflexes)
201
Q

T-F: Intestinal chyme always inhibits gastric secretion

A

F: Intestinal chyme can stimulate gastric secretion during the early intestinal phase

202
Q

How is called the reflex responsible for stomach secretion inhibition? Give 5 triggers for this reflex.

A

Reverse enterogastric reflex, initiated by: - Presence of food in the small intestines, transmitted through the myenteric nervous system and extrinsic sympathetic and vagus nerves - Distension of the small bowel - Presence of acid in the upper intestine - Presence of protein breakdown products - Irritation of the mucosa

203
Q

T-F: Secretin stimulates gastric and pancreatic secretion.

A

F: Secretin opposes gastric secretion and stimulates pancreatic secretion

204
Q

What is the composition of the gastric secretion during the ‘interdigestive phase’?

A

(nonoxyntic type) Composed mainly of mucus with little pepsin and almost no acid

205
Q

Give 2 causes for increased peptic and acidic phases of the interdigestive gastric secretion.

A
  • Emotional stimuli - Cephalic phase (idea/visualization of a meal)
206
Q

What are the 2 (3) main compounds of the pancreatic juice and where are they secreted from?

A
  • Pancreatic digestive enzymes secreted by pancreatic acini - Large volumes of sodium bicarbonate solution secreted by the epithelial cells of small ductules and larger ducts from the acini (- Water secreted by the epithelial cells of small ductules and larger ducts from the acini)
207
Q

What is the main stimulus for pancreatic juice secretion?

A

Presence of chyme in the upper portions of the small intestine

208
Q

T-F: The pancreatic juice also contains insulin secreted by the islets of Langerhans

A

F: insulin is secreted directly into the blood

209
Q

What are the 3 most important pancreatic enzymes for digesting proteins? Which one of those splits some peptids into individual amino acids?

A
  • Trypsin > chymotrypsin, carboxypolypeptidase (secreted in their inactivated form -> activated by enterokinase and trypsin) - Carboxypolypeptidase
210
Q

What are the pancreatic enzymes responsible for digesting carbohydrate? fat?

A
  • Pancreatic amylase - Pancreatic lipase, cholesterol esterase, phospholipase
211
Q

What is the mechanism to prevent pancreatic autodigestion by the pancreatic enzymes?

A

Concurrent secretion of trypsin inhibitor by the cells into the acini (overwhelmed if large quantities of pancreatic secretion are pooled in damaged area of the pancreas)

212
Q

What are the basic steps in the cellular mechanism for secreting sodium bicarbonate solution and water into the pancreatic ducts?

A
  • CO2 diffuses into the cell -> carbonic anhydrase -> carbonic acid (H2CO3) -> dissociation into bicarbonate ions and hydrogen ions (HCO3- and H+) - Active symport transport with sodium through the luminal border of the cell - Formed hydrogen ion exchanged for sodium ion through the blood border of the cell - Overall movement of bicarbonate and sodium creates an osmotic pressure gradient -> osmosis of water into the pancreatic duct
213
Q

What are the 3 basic stimuli for pancreatic secretion?

A
  • Acetylcholine released from the parasympathetic vagus nerve (mainly pancreatic enzymes) - Cholecystokinin in response to food entering the small intestine (mainly pancreatic enzymes) - Secretin in response to acidic food entering the small intestine (mainly water and sodium bicarbonate solution to ‘flush’ the accumulated pancreatic enzymes)
214
Q

What are the 3 phases of pancreatic secretion?

A
  • Cephalic phase (acetylcholine release by the vagal nerve endings in the pancreas -> 20% of total secretion of pancreatic enzymes) - Gastric phase (same nervous stimulation -> 10%) - Intestinal phase (After chyme leaves the stomach and enters the small intestine, pancreatic secretion becomes copious, mainly in response to the CCK (70-80% of total pancreatic enzymes) and secretin (mainly H2O and NaHCO3))
215
Q

What is the pH below which secretin begins to be released from the mucosa of the small intestines? What is the optimal pH for the pancreatic enzymes to be effective?

A
  • 4.5 / 5 (increases greatly as the pH falls to 3) - 7.0-8.0
216
Q

What are the 2 most important functions of the bile?

A
  • Fat digestion and absorption - Excretion of waste products
217
Q

What is the most abundant fat in a diet?

A

Neutral fat = triglycerides

218
Q

Which one of those is considered a fat (similar characteristics and metabolites) but does not contain fatty acids? Phospholipids, cholesterol, cholesterol ester

A

Cholesterol

219
Q

Which enzyme is responsible for 10% of triglycerides digestion in the stomach?

A

Lingual lipase

220
Q

what is hydrolysis?

A

return of hydrogen and hydroxyl ions from water to the polysaccharides, which separates the monosaccharides from each other; it occurs when carbs are digested

221
Q

t/f: almost all of the carbs in the diet are either large polysaccharides or disaccharides?

A

true

222
Q

What is emulsification? Under which influence?

A

Breaking down of the fat globules into small sizes so that water-soluble lipase enzymes can act on the globule surfaces under the influence of bile salts, lecithin (decreasing interfacial tension of the globules) and agitation

223
Q

What is the most important enzyme for digestion of triglycerides? What are the products?

A
  • Pancreatic lipase - Free fatty acid and 2-monoglyceride
224
Q

How are called the small intestinal mucosa folds? Where are they

A

Valvulae conniventes or folds of Kerckring

225
Q

What are the 2 enzymes to hydrolyze cholesterol esters and phospholipids? Where are they produce?

A
  • Cholesterol ester hydrolase and phospholipase A2 - Pancreas
226
Q

How are caled the small intestinal mucosa folds? Where are they

A

Valvulae conniventes or folds of Kerckring

227
Q

Why is the stomach a poor absorptive area? (2 reasons)

A
  • Lack of villus type of absorptive membrane - Tight epithelial cells junction
228
Q

By how many folds the presence of villi on the mucosal surface enhance the total absorptive area? By how many folds the presence of a brush border (microvilli) on each villus enhance the total absorptive area? By how many folds the presence of the folds of Kerckring, villi and microvilli enhance the total absorptive area?

A
  • 10-fold - 20-fold - 1000-fold
229
Q

How does the distribution of the villi on the mucosal surface differ between the upper and distal small intestine?

A

The villi lie very close to each other and touch in most areas of the upper small intestine.Their distribution is less profuse on the distal small intestine

230
Q

What is the motive power for sodium absorption by the epithelial intestinal cells (necessay to create a gradient) between the sodium concentration inside the cell and the chyme)?

A

Active Na-K-ATPase pump on the basolateral membrane (+ passive absorption along with a negatively charged chloride on the basolateral membrane)

231
Q

Which portion of all the sodium present in the body is absorbed everyday to prevent net loss of sodium into the feces?

A

About one seventh

232
Q

What is the motive power for sodium absorption by the epithelial intestinal cells?

A

Active Na-K-ATPase pump on the basolateral membrane (+ passive absorption along with a negatively charged chloride on the basolateral membrane)

233
Q

Give 3 transporters for sodium present on the intestinal brush border membrane?

A
  • Na-amino acid cotransporter - Na-glucose cotransporter - Na-H exchanger
234
Q

t/f- the chemistry of digestion with all 3 major types of food (proteins, fats, and carbs) is due to hydrolysis?

A

true

235
Q

what is ptyalin?

A

a digestive enzyme that is secreted by the parotid glands to mix up the food with saliva; it hydrolyzes starch into maltose and other small glucose polymers

236
Q

the carbs are almost totally converted into maltose and/or other small glucose polymers before passing what part of the SI?

A

duodenum or upper jejunum

237
Q

at what stomach pH is pepsin most active?

A

2-3

238
Q

above what stomach pH is pepsin inactive?

A

>5

239
Q

list the four major proteolytic pancreatic enzymes

A

trypsin, chymotrypsin, carboxypolypeptidase, proelastase

240
Q

Green, JVECC, 2011, Eval initial lactate and gastric necrosis and subsequent lactate survival. What were main findings?

A
  1. NO * sig relationship b/t survival and presence of macroscopic gastric necrosis with initial lacate > 62. * sig relationship b/t initial lactate > 2.9 mmol/L for predicting necrosis and 50% reduction in lactate 12h after tx (of the 40 that had repeat lactate)4. The other 3/40 that had repeat lactates that were not more than 50% lower, all died
241
Q

Beal, JVECC, 2011. Regarding fluoroscopically placed NJT, which of the following is true?a) Most common primary diagnosis was adenocarcinomab) Ability to achieve transpyloric passage was 92.3%c) Ability to achieve jejunal access was 58.2%d) Median duration of feeding was 6.5 days

A

bpanc most common primary dz, jejunal access in 78.2%, medial duration feeding 3.3 d

242
Q

What is stress related injury?

A

Diffuse, superficial mucosal erosions that are unlikely to result in GI bleeding associated with hemodynamic compromise.

243
Q

What is stress related mucosal disease?

A

Stress ulcers extend deeper into submucosa and are more focal. Increased risk for bleeding necessitating pRBC transfusion and intervention to control bleeding

244
Q

Difference in mortality in humans with SRMD?

A

48.5% with bleeding vs. 9.1% w/o bleeding

245
Q

Alaskan sled dogs SRMD incidence?

A

48.5%

246
Q

Pathogenesis for SRMD involves…

A

Splanchnic ischemiaLoss of host defensesAssault by gastric acid

247
Q

What is the GMDS?

A

gastric mucosal defense system that protects against gastric acid, pepsin, and bile acids

248
Q

What makes up the GMDS?

A
  1. Extracellular mucus barrier2. Cellular membrane properties3. Rapid epithelial cell restitution4. Mucosal HCO3 secretion5. High mucosal blood flow rate6. Neurohormonal factors7. Prostaglandins
249
Q

What is the extracellular mucus barrier?

A

unstirred layer of mucus gel, bicarb, and surfactant phospholipids

250
Q

What is fxn of extracellular mucus barrier?

A
  1. maintain surface pH 72. prevent pepsin infiltration and proteolytic degredation3. hydrophopic properties of surfactant phospholipids to repel water soluble agents
251
Q

Mucus gel is…

A

95% water, 5% mucin glycoproteins

252
Q

What are trefoil factor family proteins?

A

peptides co-secreted with mucus gel - fxn in intracellular assembly and packing of mucins and increase mucus viscosity

253
Q

What influences gastric mucus secretion?

A

ACTH, corticosteroids, NSAIDS

254
Q

What prevents back diffusion of acid and pepsin in stomach?

A

cellular tight jxns and correct functioning of membrane pumps and exchanges

255
Q

What do gastric epithelial cells secrete?

A

prostaglandins, TFFs, heat shock proteins, cathelicidins, defensins

256
Q

What do cathelicidin and defensins do?

A

participate in innate immunity, preventing bacterial colonization

257
Q

What is epithelial restitution?

A

rapidly sealing epithelial compromise

258
Q

pH requirement for epithelial restitution?

A

>3.0

259
Q

What is survivin?

A

protein expressed by progenitor cells that prevents apoptosis and promotes mitosis. Takes 3-7 days for epithelial restitution.

260
Q

What do parietal cells do?

A

secrete acid from apical membrane and bicarb from basolateral membrane (alkaline tide). The interstitial bicarb transported paracellularly to GI epithelial surface to be trapped in mucus.

261
Q

What vasodilators do endothelial cells produce?

A

NO, prostacyclin (PGI2)protects from vasoconstrictors

262
Q

What are vasoconstrictors?

A

leukotriene C4, thromboxane A2, endothelin-1

263
Q

How does H2S help maintain mucosal blood flow?

A

mucosal protectant, modulates inflammation via inhibiting leukocyte adherence to vascular endotheliam

264
Q

Vagal stimulation does what in GMDS?

A

increases mucus secretion and intracellular bicarb concentration

265
Q

When vagal afferents detect noxious stimulus or acid at gastric epitheliam, nerve endings release..

A

calcitonin gene-related peptidesubstance PResult: NO mediated vasodilation

266
Q

What other peptides enhance mucosal blood flow?

A

gastrincholecystokininthyrotropin-releasing hormonecorticotropin releasing factorepidermal growth factor

267
Q

What does ghrelin do?

A

stimulates appetite and increases acid secretionMaybe: enhance mucosal blood flow thru NO and CGRP, and inhibit IL-1B, IL-6, TNF-alpha

268
Q

What prostaglandins are cytoprotective in the gastric mucosa?

A

PGE2 and PGI2Fxn: stimulation of mucus, bicarb, and phospholipid secretion AND inhibit acid secretion, tissue mast cell degranulation, leukocyte and plt adhesion

269
Q

ROS

A

superoxide anion, hydrogen peroxide, hydroxyl radical

270
Q

Where are parietal cells found?

A

oxyntic glands

271
Q

What happens in parietal cells?

A

carbonic anhydrase converts water and CO2 to H and HCO3. H secreted thru apical H-K-ATPase pump and HCO3 secreted thru basolateral membrane in exchange for Cl-

272
Q

Secretion of gastric acid is mediated by…

A

gastrin (paracrine) acetylcholine (neurocrine)histamine (endocrine)

273
Q

What is the most potent secretogogue?

A

histamine

274
Q

How do gastrin, ACh, and histamine increase acid secretion?

A

Bind their receptors, activates second messenger that increases intracellular calcium (gastrin, ACh) of increases cAMP (histamine). The second messengers then activate protein kinase, increasing cytosolic phosphoproteins, which ultimately activate proton pump

275
Q

Risk factors for SRMD

A

PPV and coagulopathy (HIGHEST)sepsisshock/hypotensionrenal failurehepatic failureneuro trauma and sxMOFtraumaaspiration pneumoniaileusmajor sxburns >35% BSAorgan transplanthigh dose corticosteroidprolonged ICU stay

276
Q

Where are SRMD lesions found?

A

stomach with oxyntic glands - fundus, bodycontrast peptic ulcer dz is antrum and pylorus

277
Q

Pepsin inhibited and fibrinogen halted at pH over…

A

>4

278
Q

pH over ___ required for plt aggregation and fibrin clot formation

A

>6

279
Q

Histamine released from…

A

tissue mast cells and enterochromaffin cells

280
Q

Where is the H2 receptor?

A

basolateral membrane of parietal cells

281
Q

List H2 receptor antagonists

A

cimetidinenizatidineranitidinefamotidinemetabolized in liversecreted in kidneys

282
Q

Which H2 receptor antagonists have prokinetic actions?

A

ranitidinenizatidine

283
Q

Which H2 receptor antagonist impairs P450 liver?

A

cimetidine

284
Q

Adverse effects of H2RAs

A

diarrhea, headache, drowsiness, fatigue, muscle pain, constipation, leukopenia, thrombocytopenia, anemia

285
Q

What reaction has IV famotidine caused in cats? Speculated reason?

A

hemolysis, maybe due to benzyl alcohol preservative

286
Q

How do PPIs work?

A

Substituted benzimidazoles that bind to the proton pump, inhibiting the final step in gastric acid secretion in a dose dependent mannerweak base, accumulates in canaliculi where converted to sulfenamide form which irreversibly binds to proton pump

287
Q

List PPIs

A

omeprazolelansoprazolepantoprazoleesomeprazolerabeprazole

288
Q

Bases behind why PPIs provide more potent acid suppression than H2RAs?

A

Irreversible proton pump inhibition, progressive intracellular acidification, drug accumulation

289
Q

What drug has decreased bioactivation via CYP 450 when administered with omeprazole?

A

clopidogrel

290
Q

What drugs have prolonged eliminates when administered with PPIs?

A

cyclosporinediazepamphenytoinwarfarintheophyllinepropanololP450 pathway

291
Q

Reported adverse effects of PPIs in people?

A

Abd pain, nausea, vomiting, diarrhea, pancreatitis, hepatic necrosis/failure, pancytopenia, agranulocytosis, hypergastrinemia with chronic use

292
Q

What is sucralfate?

A

Complex salt of sucrose sulfate and aluminum hydroxideAluminum negative and will bind everything

293
Q

What are benefits of sucralfate?

A
  1. Coat mucosa2. Inhibit pepsin molecules3. Stimulate prostaglandin release4. Increase mucosal blood flow5. Increase HCO3 and mucus secretion6. Stimulates epidermal growth factor for cell renewal
294
Q

What are potential benefits of EN?

A
  1. Acid buffering2. Mucosal energy source3. Enhance mucosal immunity4. Induction of prostaglandin secretion5. Improve mucosal blood flow
295
Q

Gastric layers.

A

Serosa, longitudinal SM, circular SM, submucosa, mucosa

296
Q

When myenteric plexus is stimulated, what happens?

A
  1. Increased tonic contraction2. Increase intensity of rhythmical contractions3. Increase rate of rhythm of contraction4. Increase velocity of conduction of excitatory waves along the gut wall
297
Q

Some of the neurons of the myenteric plexus secrete what inhibitory NT?

A

vasoactive intestinal polypeptide

298
Q

Where is gastrin released from?

A

G cells of antrum, duodenum, and jejenum

299
Q

What stimulates release of gastrin?

A

protein, distension, vagal stimulation (ACh)

300
Q

What inhibits release of gastrin?

A

acid

301
Q

What does gastrin do?

A

stimulates gastric acid secretion and mucosal growth

302
Q

Where is cholecystokinin released from?

A

I cells of dudenum, jejunum, and ileum

303
Q

What stimulates release of CCK?

A

protein, fat, acid

304
Q

What does CCK do?

A

Stimulates pancreatic enzyme and bicarb secretion, stimulate GB contraction and growth of exocrine pancInhibits gastric emptying

305
Q

Where is secretin released from?

A

S cells of duodenum, jejunum, ileum

306
Q

What stimulates release of secretin?

A

acid!!!!!! and fat

307
Q

What are the actions of secretin?

A

Stimulates: pepsin secretion, pancreatic bicarb secretion!!!!, biliary bicarb secretion, growth of exocrine pancInhibits: gastric acid secretion

308
Q

Where is gastric inhibitory peptide (GIP) released from?

A

K cells of duodenum and jejunum

309
Q

What stimulates release of GIP?

A

protein, fat, carbs

310
Q

Fxns of GIP

A

Stimulates insulin release and inhibits gastric acid secretion

311
Q

GIP also known as

A

glucose-dependent insulinotropic peptide

312
Q

Where is motilin secreted from

A

M cells of duodenum and jejunum

313
Q

Motilin secretion stimulated by?

A

fat, acid, nerve

314
Q

What does motilin do?

A

Stimulates gastric and intestinal motility

315
Q

Oxyntic glands (acid forming) secrete…

A

hydrochloric acid and intrinsic factor (from parietal cells), pepsinogen (from chief or peptic cells)mucus (from mucous neck cells)

316
Q

Pyloric glands secrete…

A

mucus and gastrin

317
Q

Ach stimulates what in the stomach

A

pepsinogen by peptic/chief cells, HCl by oxyntic/parietal cells, and mucus by mucous cells

318
Q

Gastrin and histamine stimulate what…

A

strongly stimulate acid by parietal/oxyntic cells

319
Q

Pyloric glands secrete…

A

mucus and gastrin

320
Q

What activates pepsinogen to pepsin?

A

hydrochloric acid

321
Q

Fxn of pepsin.

A

proteolytic enzyme, optimal pH 1.8-3.5

322
Q

What are the 3 phases of gastric secretion?

A

cephalic, gastric, intestinal

323
Q

Basic stimuli that cause pancreatic secretion.

A

ACh, CCK, secretin

324
Q

Young GSDs with EPI predisposed to what severe cause of acute abdominal pain?

A

mesenteric torsion

325
Q

Severe vomiting and GI FBs have what typically on blood gas?

A

hypochloremia metabolic alkalosis with hypokalemia and hyponatremia

326
Q

Where is free peritoneal gas usually seen on radiographs?

A

B/t stomach or liver and diaphragm on lateral viewOr, can increase sensitivity with pet in LEFT lateral recumbency and horizontal beam focused on least dependent area

327
Q

Most common causes of pure transudate in abdomen?

A

hypoalbuminemiaportal vein obstruction

328
Q

Most common causes of modified transudate in abdomen?

A

R-CHF, HWD, cancer, liver dz

329
Q

What is a poor prognostic indicator in cats with acute panc?

A

ionized hypocalcemia

330
Q

Radiographic signs of acute panc?

A

increased density and loss of detail right cranial abdomenwidening of angle b/t prox duodenum and pylorusdisplacement of descending duodenum to rightcaudal displacement of transverse colon

331
Q

What is the rational for using FFP for pancreatitis?

A

provide a source of alpha-2 macroglobulins (protease inhibitors to help clear activated circulating proteases)

332
Q

In experiimental feline panc, what pressor has shown ability to reduce panc inflammation by decreasing microvascular permeability?

A

dopamine

333
Q

What is feline triaditis?

A

pancreatitis, cholangitis, IBD

334
Q

Obstructive biliary dz in dogs most commonly…

A

pancreatitis

335
Q

What makes up bile?

A

water, conjugated bile acids, bile pigments, cholesterol, inorganic salts

336
Q

Obstructive biliary dz in cats most commonly d/t…

A

cancer

337
Q

Sensitivity of US to detect GB rupture with mucocele?

A

86%

338
Q

What percent of dogs with GB mucocele had rupture intraop?

A

50%

339
Q

Liver fluke in cats?

A

Platynosomum fastosum

340
Q

What is Caroli’s syndrome?

A

congenital malformation of the bile ducts

341
Q

What are the most common causes of bile peritonitis?

A

necrotizing cholecytitis, trauma, cholelithiasis

342
Q

MOA of ursodeoxycholic acid

A

Hydrophilic bile acid that increases water content of biliary secretions, encourages choleresis, decreases inflammation and immune-mediated reactions, and lessens hepatotoxic nature of bile acis

343
Q

Mortality with biliary surgery if…

A

septic bile peritonitis, prolonged PTT, post op hypotension

344
Q

MOA chlorpromazine

A

alpha-2 adrenergic antagonistD2 dopaminergic antagonistH1 histaminergic antagonistM1 muscarinic cholinergic antagonist

345
Q

MOA cisapride

A

5-HT4 serotinergic agonist

346
Q

MOA dimenhydrinate

A

H1 histaminergic antagonist

347
Q

MOA diphenhydramine

A

H1 histaminergic antagonist

348
Q

MOA dolasetron

A

5-HT3 serotonergic antagonist

349
Q

MOA domperidone

A

D2 dopaminergic antagoistincreased gastroesophageal sphincter tone and antiemetic

350
Q

MOA erythromycin

A

motilin agonist

351
Q

MOA famotidine

A

H2R antagonist

352
Q

MOA maropitant

A

NK1 receptor antagonist

353
Q

MOA metoclopramide

A

D2 dopaminergic antagonist5HT3 serotinergic antagonist5HT4 serotonergic agonist

354
Q

MOA nizatidine

A

cholinesterase inhibitorH2RA antagonist

355
Q

MOA omeprazole

A

PPI

356
Q

MOA ondansetron

A

5HT3 serotonergic antagonist

357
Q

MOA pantoprazole

A

PPI

358
Q

MOA prochlorperazine

A

alpha2 adrenergic antagonistD2 dopaminergic antagonistH1 histaminergic antagonistM1 muscarinic cholinergic antagonist

359
Q

MOA ranitidine

A

H2R antagonist

360
Q

MOA scopolamine

A

M1 muscarinic cholinergic antagonist

361
Q

MOA sucralfate

A

sucrose sulfate aluminum complex cytoprotective

362
Q

MOA yohimine

A

alpha-2 adrenergic antagonist

363
Q

Enterocyte life span

A

2-5 days

364
Q

Rotavirus and coronovirus affect the intestinal crypts. T/F

A

F - affect the tips of villi (parvo affects crypts)

365
Q

Bacterial causes of gastrointeritis.

A

Clostridium (perfringens and difficle), Campylobacter, Escherichia, Salmonella, Heliocobacter

366
Q

Where does serotonin come from in GI tract?

A

Enterochromaffin cells (95% of body’s serotonin in GI tract) - released and secreted into lamina propria in high concentrations which overflows into portal circulation and intestinal lumen

367
Q

5HT^1P

A

Initiates perstaltic and secretory reflexes (no drugs for this receptor)

368
Q

5HT3

A

activates extrinsic sensory nerves and is responsible for the feeling of nausea and induction of vomiting from visceral hypersensitivity5HT3 antagonist = ondansetron, dolasetron, granisetron, metoclopramide

369
Q

5HT4

A

Increases presynaptic release of AcH and calcitonin gene-related peptide, enhancing neurotransmission5HT4 agonist = cisapride, tegaserod, metoclopramide

370
Q

Why does metoclopramide cause extrapyramidal signs?

A

It crosses the BBB to antagonize D2 receptors in CRTZExtrapyramidal signs: involuntary muscle spasms, motor restlessness, inappropriate aggression (can reverse with diphenhydramine)

371
Q

How do ranitidine and nizatidine increase GI motility?

A

Acetylcholinesterase inhibition - so increase amt of acetylcholine available to bind smooth muscle muscarinic cholinergic receptors

372
Q

If severe GI bleed and underlying cause not found on diagnostics, not responding to medical mgmt, options are:

A
  1. Exploratory sx2. Scintigraphy with technetium-labeled red blood cells3. arteriography
373
Q

Causes of secondary megaesophagus.

A

MG, NM dz, hypoadrenocorticism, lead toxicity, hypothyroidism

374
Q

What is odynophagia?

A

pain on swallowing

375
Q

What drug may stimulate esophageal contractions in some dogs?

A

bethanechol - parasympathomimetc that stimulates muscarinic receptors, not nicotinic

376
Q

Where is the chemoreceptor trigger zone?

A

floor of 4th ventricle, lacks complete BBB

377
Q

What receptors make up the CRTZ?

A

D2, H1, alpha2, 5HT3, M1, NK1, ENKudelta

378
Q

What receptors make up the vestibular system?

A

H1, M1, NMDA

379
Q

What receptors are in teh vomiting center?

A

alpha2, 5HT^1a

380
Q

What receptor does apomorphine work on?

A

D2 - CRTZ

381
Q

What increases risk of post op peritonitis?

A

preop peritonitis, intestinal FB, alb < 2.5 g/dL

382
Q

Single paracentesis (blind) successful in ….

A

20% patients with low volume (10 ml/kg)

383
Q

DPL technique

A

Clip, scrub, use peritoneal dialysis catheter or 14/16 g cath, insert caudal to umbilicus, influse 22 ml/kg warm isotonic crystalloid and remove

384
Q

Uroperitoneum if fluid:serum creatinine and K>

A

>2:1 (creat) or >1.4.1 (K)

385
Q

Presence of bicavitary effusion increases mortaliy by…

A

3.3 fold

386
Q

What are gastropexy options?

A

tubeincisionalmuscular flapcircumcostal belt loop

387
Q

Post op GDV arrhythmia source?

A

poor myocardial perfusionelectrolyte disturbanceacidosisDICpainmyocardial depressant factor

388
Q

Perioperative risk factors significantly associated with death before suture removal GDV.

A

hypotension at any point during hospitalizationcombined splenectomy and partial gastrectomyperitonitissepsisDIC

389
Q

In the cat, mean serum:abd fluid creatinine and K for diagnosis of uroabd.

A

creat 1:2K 1:1.9

390
Q

In the dog, serum:abd fluid creatinine and K for diagnosis of uroabd.

A

creat 1:2 (86% sensitive, 100% specific)K 1:1.4 (100% sensitive and specific)

391
Q

Bilirubin serum:abd fluid for diagnosis of bile peritonitis?

A

> 1:2

392
Q

What is hypotensive resuscitaiton?

A

Mean 60, SBP 80 are goals to prevent excessive bleeding or diruption of clot fxn or formation

393
Q

Most common cause of uroperitoneum in cat?

A

blunt trauma (60%) due to ruptured bladder (85%)

394
Q

What is most common cause of bile peritonitis after blunt trauma?

A

Ductal rupture just distal to the last hepatic duct

395
Q

Blind needle paracentesis may yield peritoneal fluid when _____ fluid present.

A

5.2-6.6 ml/kg

396
Q

A peritoneal dialysis catheter used for abdominocentesis may detect presence of _____ abd fluid.

A

1-4.4 ml/kg

397
Q

Indications for abdominocentesis.

A
  1. loss of serosal detail on rads2. abd injury w/o obvious peritoneal entry wound3. shock, multiple injuries, signs of abd injury blunt trauma4. head or spinal injury precluding abd exam5. persistent abd pain or fluid distension of unknown cause6. postop complications
398
Q

What is a Cullen sign?

A

periumbilical ecchymosis (abd or retroperit bleeding)

399
Q

Significant hemorrhage is present if the PCV of peritoneal fluid exceeds _____ from a DPL.

A

5%

400
Q

Indications for peritoneal drainage.

A

Septic peritonitisBile peritonitisUroperitoneumPancreatitis-associated peritonitisPeritoneal dialysisIncreased IAHAbdominal pressure compromising ventilation or causing pain

401
Q

What two H2RAs have gastric prokinetic effects?

A

ranitidine and nizatidineMOA: anticholinesterase activity

402
Q

What’s special about cimetidine?

A

Inhibits hepatic P450 so can be used therapeutically (acetaminophen tox) or can delay metabolism of drugs

403
Q

H2RA MOA

A

block H1 receptor on parietal cellscompetitive inhibitors

404
Q

Rank potentcy of nizatidine, famotidine, ranitidine, cimetidine

A

famotidine > nizatidine > cimetidine = ranitidine

405
Q

Which H2RA absorption is delayed by food?

A

cimetidine

406
Q

Which H2RA has longest duration of action?

A

famotidine

407
Q

Which H2RA does NOT undergo substantial first pass metabolism in liver?

A

nizatidine

408
Q

Which H2RA is most bioavailable? least bioavailable?

A

MOST - nizatidineLEAST - famotidine

409
Q

Which two H2RAs undergo extensive liver metabolism? Which two excreted unchanged in urine?

A

extensive metabolism: cimetidine, ranitidineexcreted unchanged in pee: famotidine, nizatidine

410
Q

In what toxicity should cimetidine be considered for?

A

acetominophen - b/c cimetidine inhibits P450 markedly can lessen severity of acetominophen toxicityAlso decreases metabolism of other drugs (theophylline, lidocaine, metronidazole) - potentiating toxic effects of these meds

411
Q

Cimetidine decreases hepatic blood flow by 40%. T/F

A

F - 20%

412
Q

Side effects of H2RAs

A

CNS and cytopenias (only reported in humans)hemolytic anemia with famotidine (CATS)

413
Q

PPI MOA

A

irreversibly inhibit H-K-ATPase on luminal side of parietal cell, thus stopping secretion of hydrogen ions into the gastric lumen

414
Q

Why should omeprazole be given 1 h before feeding?

A

undergoes 1st pass metabolism and remainder sequestered in acidic environment of parietal cells, so if give after feeding, maximize acidity of parietal cell and therefore increasing amt omeprazole sequestered in cell

415
Q

Side effects of PPIs

A

diarrhea (dogs), inhibits P450, elevations in liver enzymes, increased gastric pH can affect absorption of other meds (ketozonazole and digoxin)

416
Q

Sulcralfate MOA

A

octasulfate of sucrose combined with Al-OH; in acidic environment binds to epithelial cells for 6 h, stimulates local production of prostaglandins and pinding to epidermal growth factor

417
Q

Misoprostal MOA

A

PGE1 analog; antacid and mucosal protective properties (stimulates bicarb and mucus and increases gastric mucosal blood flow)Acts directly on parietal cells to inhibit both nocturnal acid secretion and secretions in response to food, histamine, pentagastrinfood delays absorption, short half life

418
Q

Misoprostal side effects

A

diarrhea, uterine contractions

419
Q

What are 3 promazine derivatives used for antiemetics?

A

chlorpromazine, prochlorpromazine, acepromazinemay cause hypotension d/t alpha1 adrenergic antagonism

420
Q

Maropitant MOA

A

NK1 antagonist that blocks action of substance P in CNS and peripheral NK1 receptors in GI tract

421
Q

What is aminopentamide? Who should not take this?

A

anticholinergic antiemetic, not very good, maybe acts on muscarinic receptorsContraindications with glaucoma, cardiomyopathy, tachycardia, hypertenion, MG, gastroesophageal reflux

422
Q

Consequences of IAH

A

increased CVP, PAP, RAP, PCWP, MAP, SVRDecreased CO and urine outputIncreased lactateDecreased pulmonary complianceIncreased ICPDecreased hepatic, portal, intestinal and gastric blood flowIncreased ADH, renin, aldosterone (reverse when reduce pressure)

423
Q

Renal effects of IAH

A

10-20 cm H20 decreases GFRoliguria and anuria at > 25 cm H20

424
Q

Bacterial translocation to mesenteric LN reported with ACS pressures at…

A

34 cm H20

425
Q

IAH assessment

A

0-10 = normal10-20 = mild increase, ensure p normovolemic and press on20-30 = moderate to severe IAH, volume resuscitation, diagnostics, consider decompression>35 = severe IAH, decompression necessary to reverse organ damage and prevent further deterioration, explore or tap

426
Q

Enteropeptidase synthesized by…

A

duodenal enterocytes

427
Q

Where do salmonella organisms colonize?

A

ileum, invade M cells w/i Peyer’s patches

428
Q

What was always associated with failure to tolerate complete surgical attentuation of a CPSS, JAVMA, 2011, Lamb?

A

Ductular reaction w/o identifiable intrahepatic portal veins

429
Q

Breeds with benign familiarl hyperphosphatemia

A

Siberian huskyScottish terrier

430
Q

McCord, JVIM, 2012. Spec cPLI vs. SNAP cPL in dogs suspected of having acute panc. Findings?

A

SNAP: SN 90%, SP 70%Spec (>200): SN 90%, SP 75%Spec (>400): SN 75%, SP 85%Amylase: SN 55%, SP 75%Lipase: SN 50%, SP: 90%Negative result very likely to be accurate. Used to rule out panc.

431
Q

Israeli, JVIM, 2012. Serum pepsinogen-A, canine PLI, CRP as prognostic markers in dogs with GDV. Findings:

A

cPG-A * higher in GDV dogs compared to controls. Median cPB-A higher in nonsurvivors, compared to survivors. cPG-A increased with gastric wall damage. cPG-A as predictor of death: AUC 0.75 (lactate AUC 0.66), SN 53%, SP 88%CRP increased 75%, cPLI 40%, but no assc’n with outcome

VTS(ECC) Study (30 decks)

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