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General - LA 2 > LA /General GI mix > Flashcards

LA /General GI mix Flashcards

1
Q

Cholangioliths found in horses are usually composed of: a. Calcium carbonate b. Struvite c. Calcium bilirubinate d. Magnesium carbonate

A

c. Calcium bilirubinate Biliary stone formation begins with precipitation or aggregation of normally soluble components of bile. Other mechanisms involved in the pathogenesis include ascariasis, ascending biliary infection or inflammation, biliary stasis, changes in bile composition, and presence of a foreign body. Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014.

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2
Q

The prevalence of gastric ulcers in horses is influenced by a range of factors. Which one of the following below does not influence the prevalence of gastric ulcers?

A

a. Type and intensity of training b. Gender and age c. Type of housing d. Feeding practices

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3
Q

A 21-day-old Morgan filly presents for evaluation of loss of suckle, weakness, lethargy and icterus. Evaluation of a serum biochemical profile reveals evidence of hepatic compromise. Of the following options, what is the MOST likely cause? A. Clostridum novyi type B B. Clostridium piliforme C. Equine Herpesvirus D. Hyperammonemia of Morgans

A

B. Clostridium piliforme Ref: Reed, Bayly & Sellon 3rd ed. p. 959.

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4
Q

Which of the following serum biochemical parameters can be markedly above adult reference interval when measured in healthy neonatal foals? A. Albumin B. Bile acids C. Creatine kinase D. Troponin I

A

B. Bile acids Ref: Barton JVIM Volume 21 Issue 3, Pages 508 – 513.

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5
Q

Which of the following stimulates secretion of aqueous components of pancreatic juice? a. Cholecystokinin b. Secretin c. Serotonin d. Motilin

A

b. Secretin

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6
Q

Where and in response to what is secretin secreted?

A

Secreted from the S cells in the duodenal mucosa in response to the prescence of acidic gastric juice

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7
Q

What is the effect of secretin?

A

mild inhibition of most GI motility

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8
Q

Where and in response to what is cholecystokinin secreted?

A

secreted from the I cells in the SI mucosa in response to the presence of fat, fatty acids and monoglycerides.

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9
Q

What is the effect of cholecystokinin?

A

increase gallbladder contraction and inhibit stomach motility

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10
Q

Which of the following statements regarding gastrin is false? a. Stimulates increased lower esophageal pressure to prevent gastric emptying. b. Stimulates proliferation of the gastric mucosa. c. Is produced by Type G cells. d. Inhibits pancreatic bicrbonate production and pancreatic flow

A

d. Inhibits pancreatic bicrbonate production and pancreatic flow Gastrin weakly promotes pancreatic HCO3 production and flow.

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11
Q

Mention the effect and the production site of somatostatin.

A

inhibits gastric activity and is released from duodenal mucosa and pancreatic cells

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12
Q

What are the factors that depolarize the GI smooth muscle cell membrane?

A

Stretching, stimulation of the parasympathetic nervous system (ACH) and stimulation by particular GI hormones.

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13
Q

What are the factors that hyperpolarize the GI smooth muscle cell membrane?

A

Norepinephrine or epinephrine from the adrenals and stimulation of the sympathetic nervous system (NE)

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14
Q

Which of the following substances secreted primarily by the pancreas is requiered for intestinal absorption of Vit B12? a. Intrinsic factor b. Gastrin c. Cholecystokinin d. Pepsin

A

a. Intrinsic factor

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15
Q

Gastrin is secreted by which cell type? a. Enterochromaffin-like cells in the pyloric glands b. G-cells in the pyloric glands c. Parietal cells in the gastric glands of the body of the stomach d. Delta cells in the pancreatic islets of Langerhans

A

b. G-cells in the pyloric glands

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16
Q

Which of the following is a correct statement regarding GI hormone secretion, stimulation and function? a. Cholecystokinin (CCK) is secreted from I cells of the antral mucosa in response to fatty substances and functions in gallbladder contraction. b. GI peptide is secreted from the upper SI in response to mainly fatty substances in chyme and functions in secretion of glucagon by pancreas. c. Motilin is secreted by the upper duodenum during fasting and functions to increase GI motility. d. Gastrin is secreted from G cells located in the pyloric glands of the distal end of the stomach in response to fatty substances in chyme and functions in the stimulation of gastric acid secretion.

A

c. Motilin is secreted by the upper duodenum during fasting and functions to increase GI motility.

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17
Q

Which of the following is correct regarding acid secretion? a. Parietal cells are located deep in pyloric glands and operate in close association with enterochromaffin-like cells. b. The primary function of enterochromaffin-like cells is to secrete gastric acid. c. The most potent mechanism for stimulating histamine secretion is by the hormonal substance secretin. d. The parietal cells are the only cells that secrete gastric acid.

A

d. The parietal cells are the only cells that secrete gastric acid.

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18
Q

Which of the following is primarily responsible for stimulating intestinal motility? a) Enteric nervous system - myenteric plexus b) Sympathetic nervous system c) Enteric nervous system - submucosal plexus d) The hormones gastrin and secretin

A

a) Enteric nervous system - myenteric plexus

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19
Q

Which of the following stimulates secretion of the aqueous component of pancreatic juice? a) Cholecystokinin b) Secretin c) Serotonin d) Motilin

A

b) Secretin

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20
Q

Hemorrhagic diathesis occurring secondary to hepatic failure is due to which of the following mechanisms? a) Decreased production of Factor VIII b) Decreased Vitamin K absorption c) Hypoalbuminemia and decreased oncotic pressure d) Immune-mediated extravascular hemolysis

A

b) Decreased Vitamin K absorption

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21
Q

Which of the following probiotic bacteria has potential as a possible prevention and treatment of Johne’s disease a) Bifidobacterium sp. b) Dietza sp. c) Lactobacillus sp. d) Saccharomyces sp.

A

b) Dietza sp.

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22
Q

Which of the following statement regarding the function of the liver in digestion and metabolism is CORRECT? a) The liver produces bile, which helps to digest fats. b) The liver converts urea to ammonia for excretion by the kidneys. c) The liver is involved in the synthesis of some plasma proteins and amino acids. d) When blood glucose is low, the liver converts glucose to glycogen.

A

c) The liver is involved in the synthesis of some plasma proteins and amino acids.

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23
Q

What are common clinical signs of cholelithiasis?

A

Cholelithiasis should be suspected in horses when a triad of clinical signs exists: recurrent abdominal pain, intermittent pyrexia, and icterus. Hyperammonemic hepatic encephalopathy, photosensitization, and weight loss are other, less common features of cholelithiasis. Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014.

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24
Q

The oxyntic glands of the stomach mucosa secrete all of the following except: A. Hydrochloric acid B. Pepsinogen C. Gastrin D. Mucus

A

C. Gastrin

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25
Q

What are the three basic stimuli that are important in causing pancreatic secretion? A. Acetylcholine, Cholecystokinin, Secretin B. Bicarbonate, Cholecystokinin, Trypsin C. Cholic acid, Cholecystokinin, Gastrin D. Acetylcholine, Gastrin, Histamine

A

A. Acetylcholine, Cholecystokinin, Secretin

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26
Q

Which of the following stimulates the secretion of water solution and sodium bicarbonates by the pancreatic ductal epithelium? A. Acetylcholine B. Cholecystokinin C. Gastrin D. Secretin

A

D. Secretin

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27
Q

Which of these statements is false regarding the regulation of pancreatic secretions? A. Somatostatin is released from the islets of Langerhans and inhibits acinar cell secretions B. Cholecystokinin is released from the upper small intestines and causes release of pancreatic digestive enzymes C. Acetylcholine is released from the parasympathetic nerve endings and stimulates the acinar cells to release pancreatic digestive enzymes D. Secretin is released from the upper small intestines and causes release of a bicarbonate rich water solution from the acinar cells.

A

D. Secretin is released from the upper small intestines and causes release of a bicarbonate rich water solution from the acinar cells.

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28
Q

Which of the following stimulates secretion of a sodium bicarbonate solution by pancreatic ductal epithelium? A. Acetylcholine B. Secretin C. Cholecystokinin D. Somatostatin

A

B. Secretin

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29
Q

Which of the following stimulates secretion of exocrine pancreatic enzymes? A. Secretin B. Cholecystokinin C. Acetylcholamine D. Somatostatin

A

B. Cholecystokinin

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30
Q

Which of the following statements is correct concerning somatostatin? A. Stimulates enterochromaffin-like cells to secrete histamine B. Is secreted into circulation by D cells in the pancreatic islets C. It stimulates contraction of the gallbladder D. Is produced by the S cells in the small intestine.

A

B. Is secreted into circulation by D cells in the pancreatic islets

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31
Q

Which hormone is primarily responsible of relaxation of the sphincter of Oddi and gallbladder contractions? a. Cholecystokinin b. Gastrin c. Secretin d. Motilin

A

a. Cholecystokinin

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32
Q

Which substance is secreted by the parietal cells of the stomach and can lead to pernicious anemia following severe gastritis? a. Vitamin B12 b. Intrinsic factor c. Acetycholine d. Histamine

A

b. Intrinsic factor

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33
Q

What are the causes of ruminal tympany?

A

* Obstruction of eructation (esophageal obstruction, cardia obstruction or failure to clear cardia of fluid or ingesta). * Ruminal motor dysfunction (as trapped in stable foam, failure of smooth muscle contractions, weakened muscle contractions). *Chemical inhibition (abomasal distention, vagus nerve damage, ruminal stasis).

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34
Q

Mention some of the common ulcer invaders in ruminants.

A

Trueperella pyogenes, Fusobacterium necrophorum and several mycotic species.

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35
Q

What are the 2 types of esophageal diverticula?

A

Traction (true) and pulsion diverticula (false)

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36
Q

What is the difference between a traction and a pulsion esophageal diverticula?

A

A traction diverticula results from wounding and subsequent contraction of periesophageal tissues, appear as a dilation with broad neck and have little clinical significance. A pulsion diverticula results from protrusion of esophageal mucosa mucosa through defects in the muscular wall of the esophagus and usually result from trauma or acute changes in intraluminal pressure, it typically has a flask shape with a small neck on an esophagram. Pulsion diverticula may fill with feed material, ultimately leading to esophageal obstruction.

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37
Q

What is the set up of sympathetic NS?

A

Short preganglionic (Ach - N), and long post ganglionic nerve (Adrenergic - NE) onto alpha or beta Some are NANC here too

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38
Q

What is the enteric NS?

A

Nerves within the submucosal and myenteric plexus Secretes lots of different mediators (small molecules, peptides, gases) Acted on sympathetic and parasympathetic NS

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39
Q

What are other inhibitory NTs in enteric NS?

A

Vasoactive intestinal polypeptide (VIP) NO Enkephaline Somatostatin ATP Neuropeptide Y Carbon Monoxide

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40
Q

What are other stimulatory NTs in enteric NS?

A

Ach Serotonin (5-HT) Substance P Neurokinins

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41
Q

Describe the peristaltic reflex?

A

Distension of isolated loop of dog intestine results in forward movement of contents = “Law of intestine” Distension activates cholinergic pathways upstream from bolus and non-adrenergic/non-cholinergic pathways below bolus = Leading to contraction oral to bolus and relaxation in the aboral direction

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42
Q

What is the extrinsic vs intrinsic innervation?

A

Extrinsic: Sympathethetic and Parasympathetic Intrinsic: Enteric NS (hard wired and will continue without innervation)T

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43
Q

What is the pacemaker in gut motility?

A

Activity of smooth muscle is modulated but NOT initiated by extrinsic autonomic nerves Intrinsic pacemarker mechanism in smooth muscle coats sets pace for contraction Exceptions: Ruminant forestomach Avian Gizzard Pacemarkers = Nerve-like cells (Interstitial cells of Cajal) - located btwn intestinal circular and longitudinal smooth muscle layers - Spontaneous rhythmic depolarization

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44
Q

What is a slow wave?

A

Cyclic depolarizations of resting membrane potential arise from pacemarked cells and spread circumferentially and longitudinally down gut from smooth muscle cells to smooth muscle cell Depolarizations are sub-threhold = NOT accompanied by contraction in gut wall

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45
Q

What is a slow wave?

A

Cyclic depolarization of resting membrane potential arise from pacemarker cells and spread circumferentially and longitudinally down gut from smooth muscle cell to smooth muscle cell Depolarization that are sub-threhold (NOT accompanied by contractions)

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46
Q

What is contraction?

A

Results from neuroendocrine stimulation (vagus n) that depolarize slow wave threshold

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47
Q

What determines the maximum rate of contraction?

A

Determined by slow wave frequency and number of waves that exceeding threshold (bear spikes)

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48
Q

What inhibited contractions?

A

Inhibited by neuroendocrine input (sympathetic nerves) that hyperpolarize the slow waves away from threshold

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49
Q

What drives the fasting motility pattern?

A

Driven by slow waves and directed (programmed) by enteric NS (does NOT require extrinsic innervation by vagus n)

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50
Q

Is there a difference in slow wave frequency?

A

Faster slow wave freq in duodenum faster than in distal ileum - Acid is within it and it needs to spread out (start digestion)

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51
Q

T/F. Slow waves = motility.

A

False Slow waves do not mean motility Need actions of enteric NS or extrinsic NS to raise threshold to allow for contraction of GIT

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52
Q

What are the 2 types of digestion?

A
  1. Digestive phase (extrinsic NS - vagus makes the spikes above threshold in the slow waves) 2. Interdigestive (enteric NS) makes spikes above threshold in slow waves
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53
Q

What cells are present in the cardiac mucosa?

A

Cardiac glands secrete mucus and bicarbonate

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54
Q

What cells are present in proper gastric mucosa?

A

Parietal cells - H+ (intrinsic factor) -Chief cells (pepsinogen) -Enterochromaffin-like cells: Histamine D cells (somatostatin)

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55
Q

What cells are present in antral/pyloric mucosa?

A

G cells - Gastrin D cells -Somatostatin

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56
Q

What are the functions of acid in the stomach?

A
  1. Sterilization (pathogens) 2. Activate enzymes (B12, pepsinogen to pepsin)
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57
Q

What are the 3 mediators of gastric HCL secretion?

A

Gastrin (CCK receptor - Ca) Histamine (H2 receptors - cAMP) Acetylocholine (Muscarinic M3 receptors - Ca

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58
Q

How is the barrier maintained in the stratified squamous epithelium?

A

High electrical resistance to strong electrolytes (tight junctions, glycoconjugate secretions) Proximal to distal pH, pepsin, SCFA, bile acid gradients No restitution unknown role of prostaglandins

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59
Q

What are barrier breakers in the stomach?

A
  1. Weak acids (high SCFA - pig and horses) With HCl - diffuse into cells - Intracellular acidification = Cell swelling and death Bile Salts: At low pH unionized and lipid soluble Disruption of gastric stratification (finely ground diet)
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60
Q

What results in the differences in absorption along the villus?

A

As cells move up from crypts they gain and lose transporters

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61
Q

What are the extramural vessels?

A

Celiac artery (stomach and prox duodenum) Cranial mesenteric artery (80% of gut) Caudal mesenteric artery (distal segment of colon) Portal Vein

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62
Q

What are the intramural vessels?

A

Muscle capillaires Submucosal vessels Muscosal capillaries

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63
Q

What is a critical location for ischemic injury and why?

A

Mucosa is the most metabolically active and thus can lead to ischemic injury

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64
Q

What is the blood supply at the villus?

A

central arteriole and peripheral veins Counter current exchange

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65
Q

What is the overall aspect of sympathetic stimulation during hemorrhagic shock?

A

Skeletal: Increase pressure and massive shunting of blood = Autotransfusion Intestine: Decrease pressure and blood pooling - leading to mucosal injury and sloughing

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66
Q

Why does the villus slough from tip down during ischemia?

A

There is lower oxygen tension at the tip of the villus dt counter current exchange results in pathologic hypoxia and the tips will slough off into the lumen

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67
Q

What is the significance of the Gruenhagen’s space?

A

Epithelium still have some transport function and there is extracellular fluid that ends up pooling in this region - Build up of fluid starts to peel off this epithelium and exacerbates the lesion of ischemia

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68
Q

What section of the villus is most resistance to hypoxia?

A

The crypt!! It has its own blood supply

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69
Q

Which neutrophils are important for reperfusion injury?

A

The resident (tissue) neutrophils

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70
Q

What is the model of reperfusion injury?

A
  1. All phosphates are removed from ATP - Leading to hypoxanthine 2. Xanthine Dehydrogenase is converted to xanthine oxidase (by proteases) 3. Xanthine oxidase converts hypoxanthine in the presence of oxygen to superoxide 4. Superoxide leads to lipid membrane peroxidation - leading to leukotriene T4 5. LT4 is a chemoattract for neutrophils 6. Activated resident neutrophils then lead to formation of additional ROS (H2O2 and HOCl) LOTS OF Oxidative Injury
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71
Q

What 2 mechanisms make intestinal mucosa extremely vulnerable to hypoxia?

A
  1. High metabolic demand 2. Villous counter current exchange mechanism (short circuiting of oxygen from central vein to peripheral capillaries) - Pathologic tip hypoxia
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72
Q

What is responsible for the majority of ROS and mucosal injury during reperfusion?

A

Resident (mucosal) neutrophils

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73
Q

Differences btwn Villus and Crypt in: Brush Border hydrolyases Nutrient Transport Net Water/Ion Transport Permeability

A

Brush Border hydrolyases V: Abundant C: Sparse Nutrient Transport V: High C: Low Net Water/Ion Transport V: Absorption C: Secretion (mostly chloride) Permeability V: Low (increased tight junctions) C: High (less tight junctions)

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74
Q

What is the single transporter that drives most transport in cell?

A

Na-K- ATPase 3 Na out and 2 K into cell Sets up electrochemical gradient (more electronegative in the cell)

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75
Q

What regulates the degree of Cl secretion?

A

CFTR - Cystic Fibrosis Transmembrane Conductance Regulator

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76
Q

What is the driving force for Chloride to exit the cell?

A

Electronegative center of the cell, drives chloride out

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77
Q

Describe the structure of the CFTR.

A

The R-domain will block the channel (closed) When Protein kinase A is activated by cAMP - phosphorylates the R-domain heavily making it negatively charged and thus it is repelled and the channel opens to allow Cl out

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78
Q

What also opens K channels?

A

Ca can open basolateral K channels (released from ER - internal store of Ca) K channel opened by Ca - Allows K out faster will allow for cell to be more electrically negative (synergetic effect!)

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79
Q

How is chloride secreted from apical membrane?

A

Multiple Cl- channels Cl (ORCC) CIC-2 Cl (CFTR) - cAMP/PKA Cl (Ca stimulated)

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80
Q

When do you have maximal chloride secretion?

A

When there is cAMP and Ca (through IP - PKC) released here that stimulate the CFTR

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81
Q

How does CFTR impact Na absorption?

A

CFTR communicated with adjacent Na channels to shut them down When Chloride is secreted from CFTR, it will shut down the NHE3 and this is down through NHERF

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82
Q

What are the methods of HCO3 secretion?

A

From the basolateral membrane: Absorbed into cell with Na At apical membrane: AE-1 (HCO3 out and SCFA in) DRA (HCO3 out and Cl into cell) CFTR (HCO3 and Cl out of cell)

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83
Q

In rehydration solutions, what drives Na into the cells?

A

Adding glucose/sugars (But the transporters need to be in place for this to work)!!!

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84
Q

How is glucose transported into cells?

A

Glucose transporter (SGLT-1) on apical membrane in the SI (NOT within colon) Using chemical component of the gradient

  • 2 Na and glucose bind - Conformational change and it flips Na and glucose within the cell
  • GLUT2 - Opens on basolateral membrane when glucose high within the cell and Glucose within the blood
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85
Q

When the Na/glucose transporter is overloaded, how can Na and glucose be absorbed?

A

Na and Glucose activated Myosin light chain kinase (MLCK) • Once MLK phosphorylated the myosin will contract = Leading to opening of tight junctions - Influx of glucose, Na, and water at over the tight junction • Used mannitol (same size as glucose and does not have a transporter) ○ After contraction of tight junction there was an increased in mannitol within the paracellular space (since there are no transporters) • Thought that when Na/glucose transporter is overloaded that then it can contract the tight junction to open to allow • Cytokines can also open the tight junctions and paracellular space

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86
Q

What accounts for 10% of glucose absorption?

A

Na and Glucose activated Myosin light chain kinase (MLCK) • Once MLK phosphorylated the myosin will contract = Leading to opening of tight junctions - Influx of glucose, Na, and water at over the tight junction • Used mannitol (same size as glucose and does not have a transporter) ○ After contraction of tight junction there was an increased in mannitol within the paracellular space (since there are no transporters) • Thought that when Na/glucose transporter is overloaded that then it can contract the tight junction to open to allow Na accumulates in the basolateral area and thus when the tight junction opens that water rushes in and this drags glucose with it • Thought to accounts for 10% of glucose transport

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87
Q

How do bile acids and amino acids get into the cell?

A

Linked to Na, just like glucose All have basolateral transporters to allow them to diffuse out

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88
Q

What happens with NHE3 not working?

A

When NHE3 not working - Na will remain in the lumen meaning that more water is present (overwhelming the colon’s absorptive ability = leading to diarrhea) • Simple colons: Mice, humans, and dogs (changes in SI result in overwhelming colon) ○ Different in pig and horse - Their colons are able to adapt and absorb a very large amount of Na and water to compensate.

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89
Q

How does NHERF work?

A

NHE is inhibited by PKA via interaction with NHERF (NHERF is attached to the cytoskeleton • Unknown if this effects opening of the paracellular space • Coordinated NHE3 with anion exchange and Protein kinase A (PKA) that phosphorylates then it blocks the NHE3 when there is lots of chloride within the lumen)

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90
Q

What is the net effect of cAMP secretion?

A

Secretion of Chloride in to the lumen Stops absorption of Chloride from lumen (linked via NHERF)

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91
Q

What are the mechanisms of SCFA transport in the colon?

A

Short chain fatty acid CANNOT be easily transported (there is a SCFA cotransporter with bicarbonate - but some people to not believe this) - LOW RATE MAJOR mechanism - Production of proton that are pumped out and interacts with SCFA to the protonated form and it is easier to get across the membrane into the cell - HIGH RATE (diffuse directly into the cell)

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92
Q

What happens with K transport in the colon?

A

Proximal colon: Goal is to get rid of K! K channel on luminal side!!! Distal Colon: Can retrieve it (several transporters - K/H exchanger and HKC ATPase)

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93
Q

What are the main ways that Na is absorbed?

A
  1. Nutrient dependent Na Absorption: Linked to Glucose (SGLT-1) and AA 2. Nutrient Independent Na Absorption: Jenjunum: Electroneutral (NHE3) Ileum: Linked NHE3 to Cl/HCO3 exchanger Distal Colon: Electrogeneric Na (requires energy)
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94
Q

What is found in colonic cells as you ascend the crypt?

A

Reduced CFTR and increased NHE and anion exchangers MORE CFTR within the crypt

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95
Q

What is the intestinal mucosa lined by?

A

Single layer of columnar epithelium - Responsible for secretion of fluid, absorption of water, electrolytes, and nutrients

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96
Q

What forms the barrier layer of the intestines?

A

Apical membrane together with interepithelial tight junctions - Continuous seal = BARRIER

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97
Q

What is the role of the Na/K ATPase transporter?

A

Found on basolateral surface, generates electrical potential across cell that provides energy to move other ions in and out of cell (allowing Na to enter the cell)

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98
Q

What drives secretion of chloride?

A

Intracellular environment is electronegative dt the N/K ATPase K channels on basolateral to allow K back in - further increasing electronegative intracellular environment

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99
Q

Can other chloride channels such as CIC2 and Outwardly rectifying Cl channel compensate for defects in CFTR?

A

NO!!

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100
Q

Besides chloride, what also uses CFTR?

A

HCO3 - Important to bugger HCl in SI

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101
Q

What is the consequence of increasing cAMP?

A

increased activation of PKA which will phsophorylate regulatory domain (R domain) of the CFTR - leading to opening of the channel and then Chloride secretion Examples: Pro-inflammatory prostanoids (PGE2) and chlorea toxin and E. coli heat labile (increased cGMP) enterotoxin = All increased cAMP levels

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102
Q

What is the classic mechanism by which Ca is elevated in intestinal cells?

A

It is the secondary messenger system for interaction with Acetylcholine and M3 receptors Increased Ca results in enhanced basolateral K channels = Increasing electronegatively within cell - Leading to synergistic Cl secretion - Open additional apical chloride channels and drives up the electromotive force to drive chloride out of the cells

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103
Q

What is the principal ion involved in absorptive processes?

A

Na - takes advantage of electrochemical gradient of Na (from Na/K ATPase) to enter cell Many linked to other nutrients (glucose, AA, vit B) NHE

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104
Q

Why is the SGLT-1 transporter so important?

A

Most oral rehydration solutions stimulate Na and water absorption by supplying glucose to epithelium (4 fold increase)

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105
Q

What is the solute drag?

A

Debated but thought that Na-glucose transport enchanes absoprtion of Na and water, in which fluid and solutes drawn into the paracellular space based on the osmotic gradient generated by Na and glucose exiting cell Also support that there are SGLT-1 induced alteration in cytoskeletal tone on myosin light chain kinases - opening tight junctions

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106
Q

What drives the NHE transporters?

A

Since they are electroneutral - driven by internal pH of cell, when pH drops in cell from metabolism - NHE2/3 open to expel protons in exchange for Na (linked to Cl/HCO3)

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107
Q

When you absorb NaCl what is it in exchange of?

A

H+ and HCO3 Can be driven by glutamine

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108
Q

How does RAAS affect the intestines?

A

Stimulated ENS to release NE which stimulates NaCL absorption Aldosterone in stimulation of NaCl absorption too (pigs, horse, sheep)

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109
Q

What are the 3 arms of the autonomic nervous system?

A

Parasympathetic

Sympathetic

Enteric

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110
Q

What are the receptors on skeletal muscle?

A

Ach (N)

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111
Q

What is another name for parasympathetic autonomic NS and the transmitters?

A

Cranio-sacral Nerve to medulla to vagus n to Ach (N) to gut smooth muscle (Ach - M)

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112
Q

What is another name for sympathetic autonomic NS and the transmitters?

A

Thoraco-lumbar Nerve to spinal cord to interneuron to prevertebral ganglion (Ach - N) to adrenergic (NE) -

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113
Q

What are the 4 major sensory inputs?

A
  1. Mechanoreceptors 2. Chemoreceptors 3. Thermoreceptors 4. Mediators released from enteroendocrine cells - osmolality, nutrients, drugs, bacterial products (cholecystokinin, secretin, somatostatin, serotonin, CRF, etc)
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114
Q

What are the 2 main nerves for the parasymapthetic NS in GIT?

A

Vagus n (90% gut) Pelvic nerve (distal colon)

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115
Q

What is the set up of the parasympathetic NS?

A

Long pregangloinic and short post-ganglonic nerve Ganglion is within organ (Ach - N) Post ganglionic (Ach-M) - other nonadrenergic/noncholnoergic (NANC) are also located here

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116
Q

What is the role of the parasympathetic NS in the gut?

A

Contraction and stimulation

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117
Q

What is interdigestive motility pattern?

A

Consists of powerful contractions orginate in stomach and propagate along length of intestine to distal small bowel Sweeping retained solids, pooled liquids and bacteria to colon

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118
Q

What are the 3 phases of interdigestive motility?

A

Phase 1: No contractions (but slow waves are in the background) Phase 2: Intermittent contractions Phase 3: Every slow wave results in a contraction

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119
Q

What is another name for interdigestive motility?

A

House keeping = Migrating Myoelectric Complex (MMC) MMC orginate in stomach and LES and propagate through intestine

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120
Q

What happens to motility during feeding?

A

Digestive motility: feeding interrupts MMC cycling dt extrinsic nerve (Vagus) act upon ENS - Different pattern and freq of contractions that is intermittent (Phase 2-like) - To promote mixing and increased digestion/absoprtion

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121
Q

Which animal dose feeding not interrupt the MMC cycline?

A

Ruminants!

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122
Q

What controls the fine tuning of acid secretion?

A

Somatostatin secreting cell (D cell)

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123
Q

What is the most important ligand for stimulation of parietal cell HCl Secretion?

A

Histamine Both gastrin and Ach stimulate histamine release from ECL cells cAMP synergized with either Ca second messenger to stimulate HCl secretion

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124
Q

What are the secondary messenger systems of acid secretion?

A

Histamine - cAMP Ach - Ca Gastrin - Ca When you add cAMP + Ca pathway = Syngery!! When you add Ca + Ca = Additive

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125
Q

What inhibits gastric acid secretion?

A
  1. When the stimulus is not present (vagal n, gastric distension, or protein in stomach) 2. Low intragastric ph (high H=) - D cell secrete somatostatin which inhibits gastrin release from G cells and histamine release from ECL cells = Directly inhibits parietal cells
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126
Q

What effect does gastrin have on gastric mucosa?

A

Proliferative (trophic effects) - Proliferation of ECL cells

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127
Q

What is the rebound secretory response?

A

Concern that increase in gastrin from basic pH in the stomach - lead to proliferation of ECL cells - So when you stop PPI, there is a massive rebound secretory response

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128
Q

What are the differential effects of H. pylori?

A

Helicobacter stimulates inflammation and cytokines that also stimulate these cells Within Antrum: Leads to acid secretion • TNF alpha - Can inhibit D cells • IFN-y - Stimulate G cells to make gastrin = Leads to increased acidity ○ Peptic ulcer formation Within the body: • TNF-alpha - Inhibits parietal cells, ECL cells, and D cells = Decreases acid ○ Bacterial overgrowth and even cancer formation

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129
Q

What are the 6 major ways to prevent back diffusion of H+ with the gastric mucosal barrier?

A
  1. High resistance of epithelial cells membrane and tight junction to H+ movement 2. Thick, unstirred mucus (mucin) layer 3. Trapping of secreted bicarbonate in mucus gel 4. Restitution (migration of uninjured epithelial cells to cover denude basement membrane) 5. Mucosal blood flow 6. Endogenous prostaglandins and nitric oxide (stimulate mucsoal blood flow, inhibit cAMP by parietal cells (less acid secreted), stimulates mucus and bicarbonate secretion, cytoprotective)
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130
Q

What are the mechanisms of endogenous PGs and nitric oxide?

A

Endogenous prostaglandins and nitric oxide (stimulate mucsoal blood flow, inhibit cAMP by parietal cells (less acid secreted), stimulates mucus and bicarbonate secretion, cytoprotective)

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131
Q

What section in the stomach as no protective barrier?

A

Stratified Squamous epithelium!!! No mucus or bicarbonate in this region Epithelium is at risk for acid exposure

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132
Q

What are the divisions within crypt-villus axis?

A

Secretory epithelium = Crypt Absorptive Epithelium = Villus Migrate and mature up from the crypts (replaced every 5 days)

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133
Q

Which portion of the GIT is leaky?

A

Small intestine = Dt loose tight junctions btwn adjacent epithelial cells (move via paracellular route, leading to 95% permeability)

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134
Q

Which portion of the GIT is tightly apposed?

A

Within colon - This reduces the passive movement of solute and fluid across the paracellular space (50% permeability)

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135
Q

What is the role of fluid secretion in the GIT?

A

Flush mucus from crypts into the lumen Provide fluid in lumen to aid in digestion

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136
Q

What is the principal ion secreted that results in fluid movement?

A

Chloride (numerous apical Cl channels)

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137
Q

Why are Na and water drawn across the paracellular space?

A

Dt secretion of chloride - in response to electrical and osmotic gradients

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138
Q

How does Cl enter the cell?

A

NKCC1 or Na-K-2Cl channel (basolateral) - Which is driven by electrochemical gradient of Na set up by Na/K ATPase

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139
Q

How are SCFA transported?

A

Acetate, butyrate, and propionate - Formed in ionized molecule and transported unionized once linked to H+ (driven by NHE or carbonic anhydrase)

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140
Q

Explain how cholera results in secretory diarrhea?

A

Best example of secretory diarrhea • Epithelial layer is intact but the organism attaches and results in intense secretion • Receptor on epithelium (brush border - microvilli) - • Toxin is translocated within the cell • Toxin binds to adenylate cyclase (increased cAMP - continuously production uncontrolled) • cAMP = Protein kinase A stimulated and major ion secretion is through the CFTR (releases chloride) - Pouring chloride into the lumen (secretory diarrhea) ○ Death dt dehydration • Neutral NaCl (NHE) - Blocked (phosphorylation of NHE) • Involvement of enteric nerves

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141
Q

How does inflammation result in diarrhea?

A
  1. Stimulated secretion and inhibits absorption 2. Stimulation of enteric nerves = Propulsive contractions and stimulate secretion 3. Mucosal destruction and increased permeability - neutrophils squeeze through tight junctions (eventually blow them apart) 4. Nutrient maldigestion and malabsoprtion
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142
Q

What are the 2 general categories of diarrhea?

A

Toxin induced (secretory) Damage and mucosal inflammation (crypto, salmonellosis)

143
Q

How do you get secretion with mucosal inflammation?

A

Reduced absorption (loss of epithelium) Increased ion secretion (via secondary messengers ) Enteric nerves exacerbate secondary messengers Increased osmotic load in the lumen

144
Q

What results in water absorption with oral rehydration solutions?

A

Osmotic gradient from Na and glucose being transported into cell = Draws Cl and water across tight junctions via paracellular space

145
Q

The major and minor duodenal papilla are the openings for what?

A

Major: Bile and pancreatic ducts Minor: Accessory pancreatic duct

146
Q

What provides the blood supply to the ileum? a) Cecocolic artery b) Ileocecal artery c) Caudal mesenteric artery d) Cranial mesenteric artery

A

b) Ileocecal artery NB. It is a branch of the cranial mesenteric artery

147
Q

Which cell type makes up the majority of small intestinal epithelium? a) Paneth cells b) Goblet cells c) Columnar absorptive cells/enterocytes d) Enteroendocrine cells

A

c) Columnar absorptive cells/enterocytes

148
Q

What cells are the pacemakers of the intestine?

A

Interstitial cells of Cajal (ICCs)

149
Q

Which option correctly matches the phase of activity with the type of activity of small intestinal motility? a) I: NSA, II: ISA, III: RSA b) I: ISA, II: NSA, III: RSA c) I: RSA, II: ISA, III: NSA d) I: RSA, II: NSA, III, ISA

A

a) I: NSA, II: ISA, III: RSA

?????

150
Q

What are the borders of the epiploic foramen

A

Visceral surface of caudate process of liver (dorsal and craniodorsal) Portal vein (cranioventral) Gastropancreatic fold (ventral)

?????

151
Q

List the grades of rectal tear and describe them. Also give the prognosis for each (based on the two papers mentioned in Auer)

A

I - mucosa and submucosa only 93% (medical) 100% (medical) II - muscular only (mucosa intact) 100% (medical) IIIa - mucosa, submucosa, muscular (serosa remaining) 70% (medical) 38% (medical) 81% (suturing) IIIb - tear into mesorectum or retroperitoneal tissues 69% (medical) IV - everything (communicates with abdomen) 6% (medical) 2% (medical) 50% (suturing)

152
Q

Name the methods for repairing chronic incising hernias

A

Subperitoneal Mesh Placement with Fascial Overlay Subperitoneal Meach Placement with Hernial Ring Apposition Subcutaneous Mesh Placement with Hernial Ring Apposition Laparoscopic Intraperitoneal Mesh Onlay

153
Q

What mesh materials are available for repairing incisional hernias

A

Knit polypropylene mesh (Marlex): Strong, elastic, inert, resists infection Coated polyester (Mersilene) Polyglactin 910 Absorbable mesh; may not need to be removed, even if infection

154
Q

What suture size, type and patterns would be used to close umbilical hernias in foals

A

Simple continuous appositional pattern recommended using appropriate size (USP 1,2,3) absorbable, monofilament suture

155
Q

What are the predisposing factors for prepubic tendon rupture

A

Hydrops allantois Hydrops amnions Trauma Twins Fetal gaints Normal pregnancy Draft breeds Older mares

156
Q

What material, patter, bite size, etc is used to repair acute total dehiscence of an abdominal incision

A

Monofilament stainless steel wire Through and through interrupted vertical mattress pattern Sutures 2-3cm apart Suture through skin, fascia, rectum abdominal muscle 5cm from wound edge Hard rubber tubing used as stents Second bite 2.5cm from wound edge Preplace sutures and close by applying tension on all sutures Wires twisted Cut ends bent back into lumen of tubing Leave skin unsutured if infected

157
Q

Name 2 drugs, their function and their doses that can be used to treat gastric ulcers

A

Histamine (H2) antagonists:

Ranitidine (6.6mg/kg PO q8hrs or 1.5-2mg/kg IV q6-8hrs)

Proton pump inhibitors:

Omeprazole (2-4mg/kg PO q24hrs)

158
Q

What is the fancy term for migration of epithelium across gastric ulcers

A

Epithelial restitution

159
Q

What methods can be used to treat gastric impactions

A

Medical:Nasogastric intubation:

Water

Reflux contents

Carbonated cola

Surgery:Infusion/Massage

Massage

Infuse impaction via insertion of needle adjacent to greater curvature

Infusion of balanced polytonic fluid

Gastronomy:

Pack of abdomen with towels

Incision parallel and caudal to attachment of omentum on greater curvature

Evacuate contents

Double layer inverting closure

Rarely necessary to open stomach

160
Q

How do you treat a laceration of the parotid duct

A

Most close spontaneously in 1-3 weeks

Anastomosis techniques:

Suture over intraluminal tube

Three sutures opposing two cut ends as a triangle and suturing between apices

(Size 2 nylon threaded normograde through distal laceration; guide tubing over nylon to cannulate duct before suturing)

Use 4-0 to 7-0 absorbable or non-absorbable suture in simple interrupted pattern

Leave tube in place while duct heals

If only one side lacerated, do not need to leave tube in place after closing defect

If anastomosis not possible, interposition polytetrafluoroethylene tube graft may restore duct continuity

Can create fistula from duct to oral cavity proximal to injury

Duct translocation

Surgical removal of gland, duct ligation or chemical ablation of gland

161
Q

What are the normal peritoneal fluid values day 6 post-op?

A

40,000 WBC/ml; 6g/dL TP

162
Q

What are the normal peritoneal fluid values day 4 post-op?

A

200,000WBC/ml

163
Q

What are the most common organisms found in septic peritonitis?

A

Streptococcus

Rhodococcus equi

Esherichia coli

Staphylococcus

Bacteriodes (anerobic)

Clostridium (anerobic)

Fusobacterium (anerobic)

164
Q

In what percentage of cases does recurrences of a right dorsal displacement of the large colon occur?

A

15%

165
Q

What are the predisposing and protective factors for incisional complication?

A

Predisposing factors:

Repeat laparotomy

Increased duration of surgery

Use of near-far-far-near

Chromic catgut

Leukopenia

Incisional edema

Post-operative pain

>300kg weight

>1 year age

Staple

Closure by less experienced surgeons

Protective factors:

Abdominal bandage

Short surgery time

Adequate draping

Isolating enterotomy incision

Minimize trauma to incision during exploration

Minimally reactive suture material

Do not take overly large bites

Avoid excessive force when tightening sutures

166
Q

List the uses of buscopan

A

Anti-spasmodic for colic

Choke

Rectal exam

Uterine movement during pregnancy

167
Q

What side effect of buscopan may affect monitoring for colic/pain

A

Increases heart rate

168
Q

Which laxative is anionic?

A

DSS

169
Q

Which laxative can form an oil embolus when administered with mineral oil?

A

DSS

170
Q

Mesenteric rents can be congenital in origin but what structure is the cause

A

Mesodiierticular band

171
Q

The prognosis for mesenteric rents is lower than for other strangulating lesions. What are the reasons for this

A
  1. Inability to reduce hernia 2. Long segments of bowel involved 3. Haemorrhage from mesentery 4. Failure to close entire mesenteric defect
172
Q

What is the difference between direct and indirect hernias

A

Indirect: Small intestine passes through naturally occurring ring (eg. vaginal ring) Direct: Small intestine passes through acquired defect in musculature

173
Q

What are the risk factors for enteroliths

A

1.California, Florida, 2.Arabians, Morgans, American Saddlebreds, donkey and Minis 3. feeding alfalfa hay 4.

174
Q

For how long should feed be withheld following a jejunocolostomy

A

36-48 hours

175
Q

What is the mortality rate for large colon volvulus (according to Auer)

A

56-65% (although one study reported 84%

176
Q

List the complications associated with large colon resection

A
  1. Perstent endotoxemia 2. Peritonitis (contamination or bowel) 3. Continued bowel devitalisation 4. Post-op pain 5. Post- op diarrhoea 6. Weight loss 7. Colon ileus 8. Haemorrhage
177
Q

How should small colon enterotomy incisions be closed

A

2 layers Full thickness simple continuous Seromuscular inverting pattern 2-0 polyglactin 910 Careful not to invert too much

178
Q

Describe the post-op care following esophagotomy

A

Withheld feed 48 hours (can be immediate if incision closed and separate esophagostomy tube placed) Small quantities pelleted feed over next 8 days Parenteral electrolytes - can as deficiencies can happen Attention to hydration status Will heal by first intention and intraluminal suture will slough within 60 days

179
Q

List the options for fixing rectal tears

A

Indwelling rectal liner Loop Colostomy: Single incision - high flank/low flank/ventral midline. Double incision - high flank/ventral midline End Colostomy Direct suturing Medical treatment

180
Q

Describe the mechanism of action of the following prokinetics: a. metoclopramide b. lidocaine c. erythromycin d. neostigmine

A

a. metoclopramide dopamine 1 (DA1) and 2 (DA2) receptor antagonism and through 5-HT 4-receptor (5-HT4) agonism and 5-HT3 receptor antagonism b. lidocaine - Basically a sodium channel blocker but Auer has a bunch of info: reducing the level of circulating catecholamines through inhibition of the sympathoadrenal response, (2) suppressing activity in the primary afferent neurons involved in re ex inhi- bition of gut motility, (3) stimulating smooth muscles directly, and (4) decreasing in ammation in the bowel wall through inhibition of prostaglandin synthesis, inhibition of granulocyte migration and their release of lysosomal enzymes and cyokines, and inhibition of free radical production. c. erythromycin motilin agonist that in u- ences motility partly by acting on motilin receptors on GI smooth muscles and motilin and/or 5-HT3 receptors to stimulate the release of acetylcholine. d. neostigmine cholinesterase inhibitor

181
Q

Describe the arterial supply and venous drainage of the spleen

A

Arterial supply:

Splenic artery (branch of celiac artery)

Within hilus

Branches to supply spleen and greater curvature of stomach

Venous drainage:

Affluent of portal vein

182
Q

List the possible approaches for splenectomy

A

Left side. Standing or right lateral recumbency

Incision caudal to 18th rib in left paralumbar fossa:

Difficult to assess primary vessels

Between ribs 17-18

Resection of 18th/17th/16th rib

Removal of distal aspect of last 3 ribs

Removal of 17th and transecting of 16th and 18th ribs

Laparoscopic-assisted

183
Q

Describe the ventrolateral approach to the oesophagus

A

GA, right lateral or dorsal recumbency or standing

Place feeding tube

5cm skin incision just ventral to jugular vein

Sternocephalicus and brachiocephalicus muscles separated

Deep cervical fascia incised to expose oesophagus

May be necessary to incise cutaneous colli muscles in distal cervical area

184
Q

List the methods of treating oesophageal stricture

A

First 60 days:

Bougienage - not useful

Pneumostatic/hydrostatic dilators - no useful

Balloon dilation

Initially low-bulk diet, NSAIDs and antibiotics for first 60 days

Then surgical options:

Esophagomyotomy

Partial or complete resection and anastomosis

Patch grafting

185
Q

What suture material/patterns should be used in an oesophageal resection and anastomosis

A

Submucosal layers apposed with 3-0 simple interrupted monofilament non absorbable polypropylene placed 3cm from cut edge, 2-3mm apart, with knots tied in lumen

Oesophageal muscle apposed with interrupted horizontal mattress sutures, 2-0 polydioxanone or monofilament non absorbable suture material (relief incision - circular myotome 4-5cm proximal or distal to anastomosis may help)

186
Q

List the complications of oesophageal surgery

A

Dehiscence and stricture

Acid-base electrolyte alterations

Laryngeal hemiplegia

Carotid artery rupture

187
Q

What are the 4 layers of the oesophagus

A

Tunica adventitia (fibrous layer)

Tunic muscular (muscular layers)

Tela submucosa (submucosal layer)

Tunica mucosa (mucous membrane)

188
Q

How can you treat diastemata

A

Cleaning out periodontal pockets with diastema forceps, dental picks, long forceps or high pressure-pneumatic or water instruments and filling periodontal defects with antibiotics in plastic impression material

Use diastema burr to wide to 4-6mm (clear periodontal pockets and diastema for feed first). Stop burr at 5 second intervals. Spray water continuously. Remove more from rostral aspect of caudal tooth as pulp horns located towards caudal aspect of tooth

May require extraction of a displaced cheer tooth

Do not widen diastema in young horses

189
Q

Name lots of methods of removing cheek teeth and which teeth they are appropriate for

A

Oral (anything)

Minimally invasive transbuccal (anything but more difficult caudally as may not be able to get sufficient angle)

Repulsion (any)

Lateral buccotomy (Upper 6,7,8; can also be used for lower 6,7,8)

190
Q

How do you close a partial (decent size that needs repair but not needing partial glossecomy) thickness tongue laceration

A

GA/Standing and local

Debride

Lavage

Multi layer closure

Vertical mattress sutures replaced deep in muscular body of tongue with absorbable or non-absorbable size 0 or 1 monofilament suture

Buried rows of simple interrupted 2-0 to 0 monofilamter absorbable suture subsequently used to appose muscles, obliterating dead space

Vertical mattress sutures tied and lingual mucosa apposed with simple continuous or interrupted vertical matters sutures

191
Q

What are sialoliths made of

A

Calcium carbonate and organic matter that develops within salivary duct (or a gland)

192
Q

On incision, the oesophagus separates into 2 layers, what is in each layer?

A

Mucosa and submucosa:

Inner

Elastic

Muscular layer and adventitia:

Outer

Inelastic

193
Q

Describe the arterial blood supply to the oesophagus

A

Cervial part:

Carotid arteries

Thoracic/abdominal part:

Bronchoesophageal and gastric arteries

Vascular pattern arcuate but segmental

Minimal collateral circulation (preservation of vessels important)

194
Q

Describe the ventral approach to the oesophagus

A

GA, dorsal recumbency

10cm skin incision exposes 6cm esophagus

Skin and subQ fascia divided used scalpel blade

Paired steronothyroid, sternohyoid and omohyoid muscles are separated along midline to expose trachea

Blunt separation of fascia on left side of trachea permits identification of esophagus containing NG tube

Retract trachea to right

Gentle sharp dissection of overlying loose adnentitia to expose ventral wall of esophagus

195
Q

List the possible diagnostic tests for choke (even the funky tests)

A

Clinical exam

Palpation

Ultrasound

Radiography

Contrast radiography

Negative/double positive contrast radiography

Bloodwork: WBC, electrolytes, hydration

Cineradiogrpahy

Electromyography

Manometric evaluation

Functionally distinct regions:

Cranial esophageal sphincter

Caudal esophageal sphincter

Fast (cranial 2/3)

Slow (caudal 1/3)

196
Q

What drugs does Auer like to use for choke?

A

Atropinization (0.02mg/kg)

Acepromazine

Oxytocin (0.11 and 0.2IU/kg)

Xylazine

197
Q

The left carotid sheath is super close to the oesophagus - what structures does it contain?

A

Carotid artery, vagus and recurrent largngeal nerves

198
Q

Describe the procedure for a cervical esophagostomy

A

Lateral recumbency and GA or standing and local anesthesia

Pass NG tube

Skin over left jugular furrow prepped (can occasioanlly be right)

5cm skin incision ventral to jugular vein

Esophagus sharply incised lonitudinally for 3cm down to indwelling NG tube

NG tube removed and polyethylene NG tube (outer diameter 14-24mm) placed into stomach (make sure placed through both layers of esophagus)

Place sutures in mucosa to form a seal around tube (likely unncessary as saliva will still leak)

Secure tube firmly with butterfly tape bandages sutured to skin, then elastic tape bandages

Large diameter tubes preferred

Cap tube between feedings; flush with water at end of each feeding

Tube should remain in place for minimum of 7-10 days to allow stoma to form (longer if in area of rupture or perforation)

Can feed normally when tube removed

Large portion of swallowed feed lost through stoma when fed from ground (feed a withers height)

Stoma heals spontaneously

Fistula formation rare

Complications:Fatal infection:

Drain and infection early

ABs for 7-10 days, until mature stoma develops

199
Q

What do I cells release and what does it do?

A

Cholecystokinin (CCK): Released in response to protein and fat in duodenum. Stimulates pancreas to secrete amylase, lipase, trypsin, chymotrypsin, carboxypeptidase, elastase and colipase.

200
Q

What is the effect of high Mg on Ca absorption?

A

Decreases Ca absorption

201
Q

Describe the neural stimulation of motility of the small intestine

A

Vagus nerve, components of sympathetic NS, enteric NS

Enteric NS: ganglia in myenteric (Auerbach) plexus and submucosal (Meissner) plexus - independent of CNS

Myenteric neurone: innervate longitudinal muscle and outer lamella of circular muscle

Submucosal neurons innervate inner lamella of circular muscle

202
Q

Apart from WBC and TP, which 6 factors in peritoneal fluid have a strong correlation with a strangulating lesion?

A

Gross appearance

Peritoneal chloride

pH

Lactate (peritoneal better than blood; also good for prognosis)

Myeloperoxidase (MPO) - potentially useful to indicate neutrophil activation

D-dimer concentration - potentially for fibrinolytic activity

203
Q

What 4 issues in the GI tract can Parascaris equorum lead to?

A

Obstruction

Intussusception

Abscesation

Rupture

204
Q

What is a Littre hernia?

A

Protrusion of a Meckel diverticulum through a potential abdominal opening

205
Q

What is a Richter hernia?

A

Antimesenteric wall of intestine protrudes through defect in abdominal wall

206
Q

Between which bands (for the cecum and colon) do you perform a cecocolic anastomosis

A

CCA between dorsal and lateral bands of cecum and lateral and medial free bands of RVC

207
Q

List the causes of cecocecal or cecocolic intussusception

A

Dietary changes, Cecal wall abscess, Salmonella, Eimeria leuckarti, Strongulus vulgaris arteritis, Organophosphate exposure, Parasympathomimetic drugs and/ or Tapeworms.

  • Eimeria leuckarti - In general, infection is more prevalent in foals than in adults. Reports on adults in isolated cases.
  • Parasympathomimetic drugs - also called cholinomimetic drugs such as neostigmine or caffeine.
  • Organophosphates - block neurotransmission by inhibiting acetylcholinesterase. Various formulations available for treating GI nematodiasis such as haloxon, coumaphos, trichlorfon, and dichlorvos.

Nelson, B., & Brounts, S. (2012). Intussusception in horses. Compendium (Yardley, PA), 34(7), E4.

Dubey, & Bauer. (2018). A review of Eimeria infections in horses and other equids. Veterinary Parasitology, 256, 58-70

Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014. page 1515

208
Q

What type of laxative is Polyethylene glycol 3350?

A

Osmotic laxative

209
Q

What is DCAB? What is the equation to calculate it and what is the target in horses?

A

Dietary cation anion balance (DCAB)

Target DCAB +200-300 mEq/kg

Grass hay/cereal grains ok

Not alfalfa - important in enterolith formation

210
Q

List the Ddx for meconium impaction

A

Bladder rupture

Atresia colic

Ileocolonic aganglionosis

Enteritis

211
Q

List the factors that predispose to post-op ileus

A

Intestinal ischemia

Distention

Peritonitis

Electrolyte imbalances

Endotoxemia

Traumatic handling of intestine

R&A

Anesthesia

>10yrs

Arabian

PCV>45%

High serum protein and albumin

Elevated serum glucose

>8L reflux at admission

Anesthesia >2.5hrs

Surgery >2yrs

High pulse rate

Strangulating lesions of SI and ascending colon

Length of SI resection

Obstruciton of SI

Ischemic SI

212
Q

List 2 factors that protect against post-op ileus (presuming the horse had SI surgery)

A

Pelvic flexure enterotomy

Intra-operative lidocaine

213
Q

What is the mechanism of action of bethanecol

A

Muscarinic cholinergic agonist

Stimulate Ach (M3 and M2) recetors at level of myenteric plexus

Affects duodenum, jejunum, cecum emptying, pelvic flexure, gastric emptying

214
Q

List the complications that can occur with abdominal drain placement

A

Partial obstruction of drain (26%)

Leakage of fluid around drain (16%)

Subcutaneous fluid accumulation (12%)

I guess peritonitis too but not listed in Auer

215
Q

What is cricopharyngeal achalasia?

A

Rare form of dysphagia → Inadequate relaxation of cricopharyngeal muscle

*In very young animals, tx with myotomy

216
Q

What test should be performed to assess for myasthenia gravis?

A

Ach Receptor Antibody Titer

217
Q

What are the 2 techniques commonly used to treat esophageal strictures?

A

Ballooning and Bougienage (similar results)

218
Q

What are the steps in primary peristalsis in the esophagus?

A

o Afferent vagal receptors (pharynx and proximal esophagus) stimulated by presence of food (solids more effective than liquids in stimulating swallowing reflex) → initiates efferent response via somatic nerve fibers of vagus (ends at myoneural junction) → coordinated contraction of UES and propagation of peristaltic wave aborally along esophagus through LES into stomach

219
Q

What is dysautonomia?

A

Idiopathic condition - Failure of sympathetic and parasympathetic NS = Motility issues Mydriasis with absent PLRs, decreased tear production, dry mucous membranes

220
Q

What are the 3 main secretagogues to stimulate acid production in parietal cells?

A

acetylcholine (M3), gastrin (CCKB) and/or histamine (H2) receptors on basolateral membrane via secondary messengers

221
Q

What are the 3 lines of defense against injury from acid/pepsin?

A
  1. Pre-epithelial - Mucus and bicarbonate barrier
  2. Epithelial - Barrier function of apical plasma membrane, intrinsic cell defense
  3. Subepithelial - Blood flow mediated removal of back diffused H+ and supply of energy
222
Q

How do prostaglandins play a KEY role in protecting gastric mucosa against injury?

A

§ Inhibition of acid secretion and enhancement of mucosal resistance to injury by mechanisms independent of acid secretion inhibitor called cytoprotection

223
Q

How do NSAIDs result in mucosal injury?

A

Impairing prostanglandin-dependent mucosal protective mechanisms by nonselective inhibitor of 2 isoforms of cyclooxygenase (COX) = COX-1 and COX-2 Cox-1 inhibitor can lead to reduced bicarbonate levels Direct topical effect of NSAID on gastric mucosa

224
Q

How does sucralfate work?

A

Suiplhated disaccharide-aluminium hydroxide complex that adheres to ulcerate tissue and provide barrier to acid and pepsin penetration Effective at acidic to neutral pH

225
Q

What are the 2 most common types of inflammation in IBD?

A

Lymphoplasmocytic and eosinophilic

226
Q

What are the major gases in the intestine?

A

Nitrogen, oxygen, hydrogen, carbon dioxide, methane

227
Q

What are the 3 components of innervation to the anus?

A

○ PSNS – controls defecation (contraction of rectum, relaxation of internal anal sphincter)

○ SNS – control storage of feces (relaxation of rectum, contraction of internal anal sphincter)

○ Pudendal n. – striated muscle of external anal sphincter

228
Q

What is GGT (location, half life)?

A

γ-glutamyl transferase (GGT) Hepatocyte canalicular membrane · Dogs: lower sensitivity (50%) but higher specificity (87%) for hepatobiliary dz · If concurrent ↑ ALP: specificity for liver dz ↑ to 94% · Cats: Higher sensitivity (86%) but lower specificity (67%) for hepatobiliary dz than T-ALP Largest ↑: Dz of biliary epithelium → bile duct obstruction, cholangiohepatitis, and cholecystitis Moderate ↑: Primary hepatic neoplasia Mild ↑: Hepatic necrosis Cats: GGT>ALP: cirrhosis, extrahepatic bile duct obstruction (EHBDO), or cholangitis Feline Idiopathic Hepatic Lipidosis: GGT only MILDLY elevated

229
Q

What is cholestasis of sepsis?

A

Cholestasis of sepsis: Cytokines that inhibit expression of hepatocyte transported necessary for bilirubin transport (+/- liver dz) – Esp common in cats

230
Q

What are the two genes for ALP synthesis?

A

Tissue nonspecific and intestinal → two isoenzyme proteins with different polypeptide sequences but similar enzymatic function o Tissue Nonspecific: ALP in kidney, liver, bone, placenta (differ only in degree of glycosylation) o Intestinal: ALP in intestine and corticosteroid ALP (C-ALP) Corticosteroid ALP (C-ALP): UNIQUE, only found in dogs

231
Q

What are the 3 isoenzymes of ALP that are measured in the blood?

A

o Liver (L-ALP) § Predominant isoenzyme in dogs > 1 yrs o Bone (B-ALP) § Dogs < 1 yrs = 96% of total ALP, declines to 25% in dogs >8yrs o Corticosteroid (C-ALP) § 0-30% in normal dogs (higher in older dogs)

232
Q

What is bone ALP related to?

A

· Attached to external cellular membrane of osteoblasts · Function of enzyme unknown (plays role in bone formation) Increased levels related to increased osteoblastic activity = Bone growth in young animals, fracture healing, osteosarcoma (mild, <4x normal, but correlated with POOR survival, found in tumors with increased osteoblastic acitvity), nutritional osteopathies (less common), renal secondary hyperparathyroidism

233
Q

What transport is responsible for hepatocellular uptake of copper?

A

Copper transporter (CTR1)

234
Q

What is copper bound to in the blood?

A

Ceruloplasmin

235
Q

How are bile acids made?

A

· Primary bile acids synthesized from cholesterol (liver) → chenodeoxycholic acid and cholic acid · Conjugated in liver by glycine or taurine

236
Q

Discuss the anatomy of a portosystemic shunt.

A

• Ductus venosus (Carries blood oxygenated placenta blood to fetal systemic circulation bypassing hepatic circulation) normally closes in 10 days of birth = abnormal patency leads to congenital shunts

237
Q

What can be found on CBC, Chemistry, urinalysis of animals with PSS?

A

CBC: Microcytosis, leukocytosis, anemia Chemistry: Low BUN, cholesterol. Protein. Albumin, glucose with increased ALT and ALP (bone) UA: Low USG and ammonium biurate crystals

238
Q

What is considered normal for gastric emptying?

A

?

239
Q

What are the 3 major components of acid secretion?

A

Histamine, Gastrin, ACh

240
Q

How can diuretics exacerbate HE?

A

Alkalosis and HypoK!!!

241
Q

What are the target organs of cyanobacteria?

A

Microcystins: Liver, Kidney (prox tub) and Neuro (anabaena)

242
Q

What is the toxin with aflatoxin?

A

Aspergillus = Aflatoxin B1 converted to AFB1 8,9 epoxide (esp dogs and poultry)

243
Q

What are the target tissues of aflatoxin?

A

Liver Kidney (prox tubules) - CASTS before azotemia

244
Q

How do you make a definitive diagnosis of aflatoxin?

A

ELISA, HPLC, LC/MS for toxin AFB1 in food source (>60 ppb) Serum, liver, urine = Alfatoxin M1

245
Q

What are the prognostic indicators for aflatoxin?

A

100% predictive of death = CASTS Longer PT/PTT, decreased AT, decreased protein C, increased bili, decreased albumin and cholesterol = Risk factors for mortality

246
Q

What are the 3 defensive lines to prevent epithelial damage?

A
  1. Mucus and Bicarbonate Barrier 2. Epithelial cell mechanisms; barrier function of apical plasma membrane, intrinsic cell defenses 3. Blood flow mediated removal of back diffused H and energy supply If all FAIL = Epithelial Cell Injury!!
247
Q

An increase in which TRL is seen with IBD?

A

TLR2 Also 4, 9

248
Q

What is zone 3 necroinflammatory hepatitis?

A

Associated with IBD and see in Maltese ASCITES!!! Portal Hypertension Inflammation veno-occlusive dz (lymphs and eosins around hepatic v.)

249
Q

How does portal hypertesion lead to ascites?

A

Progressive splanchnic dilation - Peripheral vasodilation Compensatory hyperdynamic changes (increased CO), compensatory failure, increased circulating volume RAAS activation and ADH release = Na and Water retenion = Ascites

250
Q

What is hepatic lipidosis?

A

Enhanced mobilization of peripheral fat to lover and impaired dissemination of lipid from hepatocytes = Severe hepatic dysfunction

251
Q

Why is the esophagus so easily damaged by gastric acid?

A

The mucosa has NO mucus-bicarbonate pre-epithelial barrier!!! NOT protected

252
Q

What is a proton pump inhibitor?

A

Noncompetitive inhibitor of gastric acid secretion (omeprazole)

253
Q

Which technique for esophageal strictures allows you to apply more force?

A

Bougienage

254
Q

What is a common complication of megaesophagus?

A

Aspiration pneumonia

255
Q

Which nerves controls the upper esophageal sphincter?

A

Glossopharyngeal, pharyngeal , recurrent laryngeal branches of vagus n.

256
Q

What is acquired megaesophagus?

A

· Caused by any disorder that inhibits esophageal peristalsis either by disrupting esophageal neural pathways or by causing esophageal muscular dysfunction

257
Q

What is the diagnostic test for myasthenia gravis?

A

Increased antibody titer to ACh receptors

258
Q

What is the MOA of prokinetic drugs like metoclopramide and cisapride?

A

Increased motility by bindings to 5-HT4 (serotonin) receptors on enetric cholinergic neurons

259
Q

Which bone disorder has been seen in humans with achalasia?

A

Hypertrophic osteoarthropathy (seen in 1 GSD)

260
Q

What is a carminitive?

A

Used to relieve flatulence activated charcoal, bismuth subsalicylate, alpha-galactosidase, pancreatic enzyme supplements, probiotic

261
Q

What is atresia ani?

A

congenital anal agenesis - grave prognosis

○ May develop recto-vaginal, recto-urethral or recto-vestibular fistulae

262
Q

Why can you see mild thrombocytopenia in heptobliary disease?

A

systemic infectious disorder or synthetic failure from decreased hepatic thrombopoietin production

263
Q

What is ALT (location, half life)?

A

Alanine aminotransferase (ALT) LEAKAGE

Liver-specific cytosolic enzyme · ↑ with severe muscle necrosis (dog)

Half Life: 2.5 days (dog); Cats? - 6hrs Large ↑: Acute hepatocellular necrosis/ inflammation Mild-to-moderate ↑: Hepatic neoplasia

264
Q

What is AST (location, half life)?

A

Aspartate aminotransferase (AST) LEAKAGE Cytosol and mitochondria ·

More sensitive, LESS liver specific

Half Life: 22 hours (dog); 77 mins (cat) ↑ Parallel ALT (smaller magnitude) · If opposite consider muscle source or release of mitochondrial AST(severe irreversible hepatocellular injury)

265
Q

What is ALP (location, half life)?

A

Alkaline phosphatase (ALP) Membrane-bound enzyme ·

Dogs: high sensitivity (80%) but low specificity (51%) for liver dz L-ALP: Luminal surface of biliary epithelial cells and hepatocyte canalicular membrane C-ALP: Hepatocyte canalicular membrane Half Life L-ALP: 70 hrs (dog); 6 hrs (cat) Isoenzymes (dog) · Bone (B-ALP): 1/3 · Osteoblastic activity (bone growth, osteomyelitis, osteosarcoma, and secondary renal hyperparathyroidism) · Liver (L-ALP) · Largest ↑: Focal or diffuse cholestatic disorders and primary hepatic neoplasms · Less ↑: chronic hepatitis, hepatic necrosis, and canine nodular hyperplasia · Corticosteroid (C-ALP) · ↑ exogenous or endogenous steroids (dog ONLY) · Chronic illness (endogenous steroids) Drug induction Feline hepatocytes have less ALP Cats lack C-ALP: T-ALP less sensitive (50%) but more specific (93%) for liver dz

266
Q

Which antioxidant should not be use in patients with liver disease if there is evidence of vitamin K deficiency?

A

Vitamin E

267
Q

Which cells in the liver are responsible for hepatic fibrogenesis?

A

Hepatic stellate cells (Ito cells, lipocytes, perisinusoidal cells)

268
Q

Which vitamin K dependent coagulation factors are made by the liver?

A

factors II, VII, IX, and X § From lack of dietary vitamin K uptake, poor vitamin K absorption by cholestatsis, altered bacterial flora associated with abx use, hepatic dysfunction–associated impairment of the vitamin K epoxide cycle □ Identified and monitored with prothrombin time (PT) or proteins induced by vitamin K absence or antagonism (PIVKA)

269
Q

Where is copper absorbed?

A

40-60% from small intestine

270
Q

What is a poor prognostic indicator in humans with drug assoicated liver disease?

A

Progressive elevation in bilirubin

271
Q

What is a potential complication with chronic Vitamin K administration?

A

Oxidation injury to organs and RBCs

272
Q

What is the MOA of metoclopramide?

A

Dopaminergic (D2) antagonist

273
Q

What is the MOA of erythromycin?

A

Motilin agonist (cats), 5-HT3 antagonist (dogs) - Stomach and intestines

274
Q

What is the MOA of ranitidine?

A

Acetylcholinesterase inhibitors, M3 muscarinic cholinergic agonist = Stomach, intestine, colon

275
Q

Which cell in the stomach makes intrinsic factor?

A

Parietal cells

276
Q

Which hormone is responsible for decreasing gastrin, histamine, and acid secretion when stomach pH

A

Somatostatin

277
Q

What factors slow emptying of stomach?

A

Carbs, AA, fats Release of CCK in response to FA and AA

278
Q

What gastric tumors are found in these locations? Pyloric antrum, cardia, diffuse

A

§ Pyloric antrum · Adenocarcinoma (lesser curvature also) § Cardia · Leiomyoma § Diffuse · LSA

279
Q

Which coag factor is NOT made by the liver?

A

Factor VIII

280
Q

What is the MOA in cyanobacteria toxin?

A

Microcystins: Inhibit serine-threonine phosphatases = Build up of phosphorylated proteins = Necrosis = Apoptosis = Massive HEMORRHAGE

281
Q

What is the histopath finding for cyanobacteria?

A

Hepatic necrosis - MASSIVE hemorrhage Acute renal tubular necrosis

282
Q

What is the MOA of aflatoxin?

A

P450 converts to AFB1 8,9 epoxide Inhibits RNA polymerase Bind to mitochondrial DNA Depletes GSH

283
Q

What is a treatment for round worms?

A

Fenbendazole

284
Q

What is a tx for hookworms?

A

Pyrantel

285
Q

What is a tx for tapeworms?

A

Praziquantel and flea control

286
Q

Where is copper located if you have secondary copper accumulation?

A

Periportal

287
Q

Why do PSS get microcytosis?

A

iron transport defect

288
Q

What are H2 blockers?

A

Competitive inhibitors of gastric acid secretion (famotidine, cimetidine, ranitidine)

289
Q

What is the pathogenesis of myasthesia gravis?

A

§ Acquired auto-immune dz: Interferes with neuromuscular transmission, production of autoantibodies against nicotinic ACh receptors →Decreased receptors = skeletal muscle weakness

290
Q

What are the 2 forms of myasthenia gravis?

A
  1. Generalized (exercise-related generalized muscle weakness, worsens with exercise)
  2. Focal (muscle weakness affecting esophagus, pharyngeal, facial muscles
291
Q

What type of gastric acid suppressor results in suppression from hsitamine, acetylcholine, and gastrin induced gastric acid secretion?

A

PPIs (inhibit that final step in acid secretion = gastric pump)

292
Q

How does the colon play a role in digestion and metabolism?

A

Colonic bacteria ferment undigested carbs from dietary fibers

293
Q

What is the suspected pathogenesis of pancreatitis?

A

· Exocrine pancreas respond to noxious stimuli by decrease in secretion of pancreatic enzymes, followed by formation of giant cytoplasmic vacuoles within pancreatic acinar cells (seen with EM)

o Vacuoles: Colocalization of zymogens of digestive enzymes and lysosomal enzymes (which are normally strictly segregated)

o Decreased pH and/or presence of lysosomal enzymes (cathepsinB) lead to premature activation of trypsinogen

o Trypsin activates other zymogens = Local effects (inflammation, pancreatic edema, hemorrhage, pancreatic necrosis, parapancreatic fat necrosis) = CS of abdominal pain and vomiting

o Systemic CS are thought to be related to circulating pancreatic enzymes

294
Q

How much of the liver needs to be lost in order to result in synthetic failure?

A

□ Synthetic failure occurs only when 70% of hepatic functional mass has been lost

295
Q

What is the sensitivity and specificity of ALP in detecting liver disease?

A

· High sensitivity (86%) for detecting liver disease BUT poor specificity (49%) due to lots of disease outside the liver, drugs, steroids = induced production of enzyme

296
Q

How is copper excreted from liver cells?

A

· Golgi apparatus the ATPases ATP7A (Menkes disease protein) and ATP7B (Wilson’s disease protein) are responsible for preparation of copper excretion o Excretion into bloodstream copper bound to ceruloplasmin o Also if excessive copper excretion within bile via interactions with copper metabolism murr1 domain-containing protein 1 (COMMD1)

297
Q

What are the 2 main goals of diagnosis in feline hepatic lipidosis?

A

to identify lipidosis in the liver and rule in/out an underlying disease process

298
Q

What are 3 electrolyte abnormalities that can occur with refeeding syndrome?

A

Hypokalemia, Hypomagnesium, hypophosphatemia

299
Q

What was developed to provide a more accurate diagnosis of liver dysfunction?

A

Ammonia tolerance test

300
Q

How is metoclopramide an antiemetic?

A

Dopaminergic (D2) antagonist = CRTZ

301
Q

How is B12 absorbed?

A

• CBL homeostasis = Complex, multisteps (within stomach, pancreas, intestines, and liver) ○ CBL is released from food in stomach ○ Bound to nonspecific CBL-binding protein (Haptocorrin) - Salivary and gastric origin ○ Intrinsic factor (IF) - CBL binding protein that promotes CBL absorption in ileum § Produced by pancreas (NOT stomach in cats!) § Humans = Only gastric production (def from atrophic gastritis ○ High affinity of CBL for haptocorrin in acid pH (binds in stomach) ○ Duodenum: Haptocorrin is degraded by pancreatic proteases → CBL transferred from haptocorrin to IF § Facilitated by high affinity of IF for CBL at neutral pH ○ Cobalamin-IF complexes then bind to specific receptors (intrinsic factor cobalamin receptor, aka cubilin) - Located in microvillus pits of apical brush border membrane of ileal enterocytes ○ CBL transcytose to portal bloodstream bound to transcoablamin 2 (TC II) = mediated CBL absorption by target cells ○ Portion of CBL taken up by hepatocytes = Re-excreted rapidly in bile bound to haptocorrin § CBL of hepatobiliary origin and dietary derived CBL thought to undergo transfer to IF and receptor mediated absoprtion →ENTEROHEPATIC RECIRCULATION

302
Q

What are the 3 major digestive enzymes in the stomach?

A

Pepsin (releases as pepsinogen in response to ACh and histamine)Gastric lipase (in response to pentagastrin, histamine, PGE2, and secretin, active in SI)Intrinsic factor (dogs)

303
Q

What are the 3 major digestive enzymes in the stomach?

A

Pepsin (releases as pepsinogen in response to ACh and histamine) Gastric lipase (in response to pentagastrin, histamine, PGE2, and secretin, active in SI) Intrinsic factor (dogs)

304
Q

What are causes of metabolic alkalosis?

A

· Metabolic alkalosis o Associated with pyloric/duodenal outflow obstruction o Associated with parvo and pancreatitis o Gastrinomas § Also associated with aciduria § hypoCl/K due to gastric acid hypersecretion Conservation of volume at expense of pH (renal reabsorb HCO3 and exchange Na for H+ = promotes acidic urine (paradoxical aciduria)

305
Q

What is the most toxic bile acid?

A

Lithocholic acid

306
Q

What tropic factors are important for hepatic growth?

A

Insulin and Glucagon (from portal blood)

307
Q

What is the toxin in cyanobacteria?

A

Microcysts aeruginosa (blue green algae) = Microcystins

308
Q

What is the presentations of cyanobacteria?

A

Microcystins: ACUTE (hours) - GI, respiratory, liver, tremors, seizures, comas

309
Q

How is a definitive diagnosis of cyanobacteria made?

A

ELISA (confirmed with LC/MS) or MMPB method to detect all forms of toxin) Best in vomit!!!, can check water source too Liver (toxin level)

310
Q

What is the prognosis for cyanobacteria?

A

GRAVE

311
Q

What is the prognosis for aflatoxin?

A

Guarded, 60% mortality

312
Q

What are precipitating factors of HE?

A

Increased production of ammonia in GIT (high protein meal, GI bleeding) Increased systemic generation of ammonia (blood transfusion, poor quality protein) Factors affecting uptake and metabolism of ammonia in CNS (metabolic alkalosis, hypoK, hypoglycemia, inflammation, infections, sedation/anesthesia)

313
Q

What is the progression with complete occlusion of the CBD?

A

24 hrs = GB distension 48-72 hrs = Extrahepatic bile duct distension 5-7 days = Intrahepatic ductal dilation

314
Q

What was associated with worse survival in Hepatic lipidosis?

A

HypoK Advanced age Decreased PCV

315
Q

Name the 5 nerves that can involved with swallowing.

A
  1. Sensory and motor of trigeminal n.
  2. Facial n.
  3. Glossopharyngeal n.
  4. Vagus n.
  5. Hypoglossal n.
316
Q

Mention the 3 types of dysphagias

A
  1. Oropharyngeal dysphagia
  2. Esophageal dysphagia
  3. Gastroesophageal dysphagia
317
Q

What are the 3 stages of oropharyngeal dysphagia?

A
  1. Oral Stage - Prehending, tranporting food to oropharynx
  2. Pharyngeal Stage
  3. Cricopharyngeal Stage - Relaxation of cricopharyngeal muscles (upper esophageal sphincter)
318
Q

What can occur with chronic gastroesophageal reflux?

A

Severe histology changes in distal esophagus (metaplasic changes) = Barrett’s esophagus in humans

319
Q

When does sucralfate need to be administered in order to work?

A

Needs to be administer when high acid production, otherwise neutral esophagus will not allow sucralfate to function Minimal to no benefit in humans

320
Q

What is the most common form of IBD (diffuce infiltration of cells into lamina propria of intestinal mucosa?

A

Lymphoplasmocytic

321
Q

What are the 4 primary sources of gas in the intestines?

A

○ Aerophagia (O2 and N2) § This contributes the most!

○ Gastric acid interacting with food, saliva or pancreatic HCO3- (CO2)

○ Diffusion from blood (CO2, O2, N2)

○ Large amount of gas comes from bacterial fermentation in the colon § Foods with large amounts of oligosaccharides produce gas § High fiber and fructose diets also create gas § Foods with sulfates are converted by sulfate reducing bacteria to H2S and others § High protein foods may also contribute

322
Q

Name 2 enzymes that result from leakage from damage hepatobiliar cells?

A

ALT and AST

323
Q

Name 2 enzymes that results from elution from damage membranes

A

ALP and GGT

324
Q

Name 1 enzymes that can have increased synthesis in hepatobiliary disease?

A

ALP

325
Q

What enzymes can be elevated with steriod use? How long does this take to get to normal after stopping the steroids?

A

Steroids: ↑ L-ALP, C-ALP, ALT (less) and GGT secondary to induction ◊ Stopping them results in gradual normalization of values (2-3 months)

326
Q

When would you expect to see hypoglycemia with hepatobiliary disease?

A

ONLY if 75% of hepatic mass is nonfunctional

Decreased gluconeogenesis and clearance of insulin

327
Q

What is the basis behind using total serum bile acids for hepatobiliary disease?

A

§ Bile acids are synthesized from cholesterol exclusively in the liver § Conjugated to glycine or taurine → secreted into bile → stored/concentrated within gallbladder § Meal = cholecystokinin (CCK) release → GB contraction § Bile acids transported in intestines = Aid in emulsification and digestion of fats § Terminal ileum bile acids resorbed and return to liver (enterohepatic circulation) – Re-extracted by hepatocytes □ Normally enterohepatic circulation of bile acids = 95-98% efficiency □ Disruption of circulation = ↑ TSBAs (acquired or congenital PSVA or cholestatic hepatobiliary disease)

328
Q

What are 2 nuclear methods that can be used to diagnosis liver shunts?

A

· Transcolonic pertechnate scintigraphy (TCPS) = Detection of PSVA o Absorbed by portal venous system = Detected in liver PRIOR to heart (normal) o PSAV = heart BEFORE liver o Dogs: High PPV for PSVA: Discriminates macroscopic PSVA (abnormal) from primary hypoplasia of portal vein (normal) · Transplenic portal scintigraphy (TSPS) = Detect PSVA o US guided, reduced radiation exposure (smaller dose) o NOTE: misses cases when shunt originates distal to splenic vein

329
Q

Name 5 tissues that membrane bound ALP is found.

A

Kidney, liver, bone, placenta, intestine

330
Q

Name 2 situations that liver ALP can be induced.

A

§ Cholestasis: Accumulation of bile from impaired bile flow = Induced L-ALP production □ Accumulate on hepatic membranes and solubilization of membrane-bound enzymes occurs by glycosylphosphatidylinositol (GPI) phospholipase (found in plasma and on cell membranes) ® Bile salts also increase activity of GPI phospholipase → release L-ALP into circulation § Drugs: Phenobarbital, endogenous/exogenous glucocorticoids □ Poorly understood

331
Q

Name 3 conditions where only ALP is increased?

A

Benign nodular hyperplasia, idiopathic vacuolar hepatopathy, and breed-related conditions

332
Q

What are the 7 general principles of treating hepatic disease?

A

· Address the underlying cause, if known (withdrawal of hepatotoxic drug). · Reduce and prevent inflammation. · Reduce and prevent copper accumulation, if applicable. · Reduce and prevent oxidative damage. · Reduce and prevent fibrosis. · Provide adequate nutrition. · Treat complications as needed (e.g., hepatic encephalopathy, coagulopathy, gastric ulceration, fluid/electrolyte disturbances, ascites, and infection/endotoxemia)

333
Q

What is the most biologically active form of Vitamin E?

A

α-Tocopherol

334
Q

What is the most common antifibrotic?

A

Colchicine = Plant alkaloid · Inhibit fibrosis by binding selectively/reversibly to microtubules, inhibiting their polymerization and thus collagen secretion Does not decreased fibrosis

335
Q

Name several other antifibrotics.

A

· Interferon-γ, milk thistle, penicillamine, prednisone, ursodeoxycholic acid, and zinc § Not evaluated in dogs and cats with fibrosis but many used for other liver dz (coincidental benefit)

336
Q

Once copper is within liver cells what happens?

A

· In liver cells copper is immediately bound to transport proteins: COX17, ATOX1, CCS → deliver copper to their target destination in cell o Targets: Superoxide dismutase, mitochondrial enzymes

337
Q

If liver injury occurs randomly when a medication is given, it is known as….

A

Idiosyncratic hepatotoxin

338
Q

Name 4 mechanisms that can occur with drug associated liver disease.

A
  1. Cytopathic change on hepatocytes (lysis, necrosis) 2. Induction of cholestasis and metabolic dysfunction 3. Induction of immune system activity against hepatocytes 4. Production of proinflammatory response to liver
339
Q

Where does metoclopramide result in prokinetics effects?

A

Stomach - Agonism of serotongeric 5-HT4

340
Q

What are the components of the gastric mucosal barrier?

A

§ Tightly opposed epithelial cells § Bicarbonate rich mucous § Abundant mucosal blood supply § Prostaglandins (PGE2) are important in modulating · Blood flow · Bicarbonate secretion · Epithelial cell renewal

341
Q

What defines DIC?

A

Prolonged PT/PTT Decreases fibrinogen thrombocytopenia increased FDPs (all of which can be seen with liver dz too)

342
Q

What are the clin path findings with cyanobacteria?

A

Increased ALP, GGT, bili Marked increased in ALT (can be less if microcystoin inhibits tansminase synthesis??)

343
Q

What is the antidote for cyanobacteria?

A

NONE Rifampin in mice/rats can inhibit uptake

344
Q

What is the CS onset of aflatoxin?

A

Highly variable, most are chronic (>1 month of eating food)

345
Q

What are the clin path findings with aflatoxin?

A

Increased LEs, icterus, low cholesterol, decreased AT and protein C

346
Q

What are the histopath findings with aflatoxin?

A

Acute: Centrilobular necrosis ****Diffuse hepatocyte lipid vacuolization**** Chronic: MIXED

347
Q

What is the antidote for aflatoxin?

A

Replenish GSH (N-acetylcysteine or SAMe) Sulfhydryl groups may bind AFB1 8,9 epoxide too

348
Q

What are the effects of NSAIDs on mucosa?

A
  1. Direct effect (uncoupling mitochondria) 2. COX 1 inhibition: Neutrophil activation and ROS 3. COX 2 inhibition: Neutrophil activation and ROS; Also inhibits GF production and impairs repair
349
Q

What are the 5 steps of cobalamin absorption?

A
  1. Cobalamin released from food in stomach 2. Binds to cobalamin binding protein (Haptocorrin - from salivary and gastric source) 3. In duodenum: Haptocorrin degraded (by pancreatic proteases) and Cobalamin binds to intrinsic factor (pancreas and stomach in dog and ONLY pancreas in cats) 4. Cobalamin-IF binds to receptors (cubilin) in microvillus 5. Cobalamin transcytose portal blood bound to tanscobalamin 2 - mediated absoprtion by target cells Can undergo enterohepatic recirculation with haptocorrin in bile
350
Q

Name several compounds that are associated with hepatic encephalopathy?

A

Ammonia Tryptophan Glutamine Aromatic AA/Branch Chained AA SCFA GABA Endogenous benzodiazepines Bile Acids Phenol Flase neutrotransmitters

351
Q

What is noncirrhotic portal hypertension?

A

Portal v hypoplasia with portal hypertension Seen in Dobies, Rotties, and Cockers Have abdominal effusion with acquired shunts

352
Q

What is portal v. hypoplasia?

A

MIcroscopic malformation in hepatic microvascular Thought to nonprogressive Can be asymptomatic increased bile acids with normal Protein C, CBC, chem, AUS, scinitgraphy Can be seen with macroscopic PSS too

353
Q

What are the mainstays in Tx of hepatic lipidosis?

A
  1. Feeding!!! High quality protein!!!
  2. B vitamins (B1 and B12)
  3. Fat soluble vits (E and K1)
  4. Amino Acids = L-carnitine and taurine
  5. Antioxidants = SAME and ursodiol
  6. electrolytes: HypoK and HypoMg

General - LA 2 (10 decks)

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