GI / liver - physiology / pathophysiology / Nutrition Flashcards

Question

How severe can pancreatitis be?

Answer 1

From mild and self-limiting to severe fulminant disease with extensive necrosis, systemic inflammation and/or sepsis, multi organ failure and death

Answer 2

May include local complications - acute peri pancreatic fluid collection, acute necrotic collection, pancreatic pseudocyst, or walled-off necrosis

Answer 3

Alcohol exposure or biliary calculi Idiopathic

Answer 4

Involves intrapancreatic activation of digestive enzymes with resultant pancreatic auto digestion: - Initial events within the acing cell -> abnormal fusion of normally segregated lysosomes with zymogen granules (inactive forms of pancreatic enzymes) - That leads to premature activation of trypsinogen to trypsin (may involve changes in signal transduction, intracellular pH and increases in intracellular iCa) - Trypsin in then activates other proenzymes - sets a cascade of local and systemic effects that are responsible for the clinical manifestations of AP. - Local ischemia, phospholipase A2 and ROS -> disrupt cell membranes -> pancreatic hemorrhage and necrosis, increased capillary permeability and initiation of arachidonic acid cascade - Elastase can cause increased vascular permeability -> degrades elastin in vessel walls. - Phospholipase A2 degrades surfactant -> promotes development of pulmonary edema, ALI, ARDS. - Trypsin may activate the complement cascade -> influx of inflammatory cells and production of cytokines and more ROS. - Trypsin can activate the kallikrein-Kinin system -> results in vasodilation, hypotension and possible AKI - Trypsin can activate the coagulation and fibrinolytic pathways -> microvascular thromboses and DIC. - Local inflammation and increased vascular permeability -> may cause massive fluid losses -> compromises perfusion -> further inflammation -> vicious cycle that ends in SIRS and MODS.

Answer 5

Dogs middle age or older Overweight Hx of prior or recurrent GI disturbances Hx of concurrent endocrinopathies (hypothyroidism, Cushing's, DM) Yorkies, Mini Schnauzers and other terrier breeds

Answer 6

Lethargy, anorexia and dehydration. Vomiting and abdominal pain is less common than in dogs. Icterus and pallor often noted.

Answer 7

Hepatic lipidosis IBD Interstitial nephritis or other kidney dz DM Cholangitis / cholangiohepatitis

Answer 8

Dyspnea, bleeding disorders, arrhythmias, oliguria, shock and collapse

Answer 9

Ht and RBCs might be normal Anemia can be seen, especially in cats Increased Ht reflecting hemoconcentration and dehydration - in humans: associated with more severe disease.

Answer 10

May reflect some ischemic and/or toxic hepatocellular injury or concurrent hepatobiliary disease.

Answer 11

- Hypercalcemia has been reported in some dogs with AP - Mild to moderate hypocalcemia and hypomagnesemia are not uncommon - suspected as a result of pancreatic and peri pancreatic fat saponification (multiple mechanisms proposed) - Ionized hypocalcemia appears to be common in cats with AP - associated with poorer outcome.

Answer 12

No. Elevations may occur also from extra pancreatic sources (azotemia, glucocorticoid administration). Often WNL in animals with confirmed pancreatitis, particularly cats.

Answer 13

Elevations in trypsin-like immunoreactivity - may suggest pancreatitis, but can also occur with azotemia and with GI disease in cats. TLI might be normal in some patients with AP. Might have some clinical utility in cats if combined with imaging, but not considered useful in dogs.

Answer 14

- Elevations demonstrated in dogs with AP. - May be useful for dx of SAP, but not for mild AP. - Further evaluation needed

Answer 15

- Data suggests PLI is sensitive and specific for AP in spontaneous cases of AP in both species. - Does not appear to be affected by renal disease or steroids administration. - PLI currently the most useful marker available for dx of AP.

Answer 16

- Increased density and loss of detail in the right cranial abdomen - Displacement of the descending duodenum to the right with widening of the angle between the proximal duodenum and the pylorus - Caudal displacement of transverse colon - Gastric distension and static gas pattern - suggestive of ileum. Cats: nonspecific - decreased peritoneal detail most commonly. Hepatomegaly, mass effect in cranial abdomen and SI dilation have been reported.

Answer 17

- Useful to monitor progression - Pancreas may appear enlarged and hypoechoic - suggestive of edema / necrosis - Pancreatic duct dilation, thromboses and organ infarcts may also be detected. - FNA of pancreatic necrosis done routinely in humans to identify infected pancreatic necrosis.

Answer 18

- In humans contrast enhanced CT is gold standard - Preliminary data suggests not very sensitive for dx of AP in cats.

Answer 19

No. Is more valuable to evaluate local complications, infected necrosis and to monitor disease progression than to diagnose AP per se.

Answer 20

- UA - U culture and susceptibility - Chest xray - Venous / ABG - Lactate and iCa - Coagulation profile - coagulation abnormalities reflecting DIC and thromboses appear to be common in dogs and cats with SAP. - If fluid accumulation (wherever) - fluid analysis, cytology and culture. Serial cytologies might be useful to monitor disease progression. - Recent studies - elevated cPLI and lipase activity in peritoneal fluid may support a diagnosis of AP in dogs.

Answer 21

- Ranson's Criteria - The Glasgow (Imrie) score - Balthazar's CT index - Bedside Index for Severity in AP (BISAP) - Harmless AP Score (HAPS)

Answer 22

- Trypsinogen activation peptides (TAP) - Carboxypeptidase - C-reactive protein (CRP) - IL 6, IL 8 - Neutrophil elastase CRP currently the best established and most widely available marker for predicting severity.

Answer 23

Increases in CRP and urinary TAP-to-creatinine ratio have been demonstrated in dogs with spontaneous AP - further evaluation needed.

Answer 24

- Elimination of any potential underlying cause - Early aggressive intervention against systemic complications - Symptomatic and supportive therapy 1) Resuscitation, fluid therapy and monitoring 2) Pain management 3) Nutrition 4) Additional and supportive therapy 5) +/- antibiotic therapy 6) Surgery?

Answer 25

No. In humans, a study suggested resuscitation with LRS reduced systemic inflammation at 24h when compared with normal saline - no differences in outcomes tho.

Answer 26

- Maintenance fluid requirements might be pretty high due to massive ongoing losses (vomiting, third space into peritoneum, GI tract and interstitial) - Assess lytes - K supplementation usually needed. - Concurrent use of a synthetic colloid is often necessary for patients with SAP

Answer 27

Only if signs of tetany are observed, because of the potential for exacerbation of free radical production and cellular injury

Answer 28

- Patients that are hypotensive despite adequate volume replacement will need pressors. - In experimental feline models of AP - low-dose dopamine (5mcg/kg/min) showed to reduce the degree of pancreatic inflammation by decreasing microvascular permeability - further research.

Answer 29

- Usually advocated as a source of alpha2-macroglobulins (important protease inhibitors that help clear activated circulating proteases) - Studies in human - no improvement in morbidity or outcome with the use of plasma. - Retrospective study in dogs - no benefit. - May be indicated to treat coagulopathies, including DIC.

Answer 30

- Aggressive analgesia indicated in all patients, even the ones that do not show pain. - Will help decrease levels of stress hormones, improve ventilation and improve GI motility if ileus is in part due to pain. - Systemic opioids main therapy. - Can be supplemented with low-dose ketamine or lidocaine. - Low-dose lidocaine - promotility effects - can be beneficial if severe ileum. - Epidural and intraperitoneal analgesia can be used in select patients. - NSAIDs - not recommended unless patient is hemodynamically stable, non azotemic and well perfused.

Answer 31

- Ideally early enteral nutrition - within 24h of hospitalization, especially with MSAP and SAP. - Improves gut mucosal structure and function and decreases bacterial translocation - attenuating stimuli for propagation of SIRS. - Enteral: less complications than parenteral (infection, decreased risk of MODS, decreased mortality rates, less expense, shorter hospitalization) - Jejunostomy tube - bypasses the pancreas - not sure how exocrine pancreatic function is altered (is it beneficial to bypass?), requires general anesthesia - other routes chosen. - Nasogastric / esophagostomy tubes - especially in cats with risk of hepatic lipidosis - If patient has severe ileus or vomiting - tickle feeding - Supplemental total or partial PN should be considered if nutritional requirements cannot be met with enteral nutrition alone. - Ideal composition unknown - recommended supplementation with glutamine. - Cats, especially those with concurrent GI tract dz - Vet B12 supplementation - Avoid overfeeding. - Early enteral nutrition also recommended for mild AP.

Answer 32

- Might not influence outcome but help with patient comfort - GI protectants - Thermal support - Physical therapy - Antiemetics and prokinetics useful for patients that vomit and with ileus - Dopaminergic antagonists (metoclopramide) may be less effective or should be avoided. - Intermittent NG decompression can help with severe ileus. - Treatment of concurrent dz (DKA, DM)

Answer 33

- Prophylactic not recommended in most cases -> risk of inducing resistant bacterial strains and fungal infections. - In vet medicine incidence of pancreatic / peri pancreatic infection unknown (humans about 30%). - Empiric antibiotic therapy might be reasonable for patients that do not respond to other therapy, or for those that respond but then deteriorate - monitor serial US and FNA of pancreatic areas to look for signs of infection. - Development of infection in urinary tract / respiratory tract can occur.

Answer 34

- Surgery is not indicated in most cases involving sterile pancreatic necrosis - Debridement and/or drainage is indicated in patients with infected necrosis - Surgery also recommended if extra hepatic biliary obstruction is present (EHBO), and those who continue to deteriorate despite aggressive medical therapy.

Answer 35

- Patients that survive might be normal, or continue to have episodic flare-ups. - Those that relapse - monitor for pancreatic pseudocysts, walled-off necrosis or EHBO - Some patients might develop DM, chronic pancreatitis and/or EPI.

Answer 36

Neutrophilic and lymphoplasmacytic, follicular cholecystitis

Answer 37

Any age, breed or sex. Shetland Sheepdogs are predisposed to gallbladder disorders, and mucocele in particular. Cocker Spaniels also. No mention of Terriers¿?

Answer 38

Very nonspecific - anorexia, lethargy, vomiting and diarrhea.

Answer 39

Hematology: inflammatory leukogram - leukocytosis and neutrophilic Biochemistry: Increased ALT, AST, ALP and GGT. If biliary obstruction / cholestasis - increases in cholesterol and bilirubin AUS is recommended based on clinical findings

Answer 40

Infectious - bacteria, parasites Obstruction GB mucocele GB infarction

Answer 41

Typically from enteric origin: E. coli Enterococcus app. Bacteroides spp. Clostridium spp.

Answer 42

- Underlying cause of bacterial infection in the bile is unknown. - Bacterial colonization of bile may occur via reflux of duodenal bacteria or by hematogenous spread through the portal vasculature. - Presence within the bile of bacteria + increased biliary pressure due to obstructive process leads to infection of bile and cholecystitis.

Answer 43

- Hyper or hypo echoic thickening of the GB wall - Distention of the GB and/or cystic duct - Echogenic bile - Presence of gas within the lumen or wall of the GB - emphysematous cholecystitis -> gas producing bacteria - E. coli and Clostridium spp.

Answer 44

3 types: - Type I - areas of necrosis w/o GB rupture - Type II - acute inflammation w/ rupture - Type III - chronic inflammation with adhesions and/or fistulae to adjacent organs. Majority of dogs w/ necrotizing CC have had bacterial infection, although it can occur without infection, secondary to GB mucocele.

Answer 45

- Prompt surgical intervention - Imaging: ff within the GB fossa or generalized through the abdomen, echogenic reaction in the pericholecystic region. Decreased peritoneal detail on abdominal radiographs. - Effusion: bilirubin >2x serum bilirubin - bile peritonitis. - High preoperative mortality, overall long-term survival 61% to 82% for dogs w/ bacterial cholecystitis undergoing surgery.

Answer 46

- Antimicriobial selection based on culture and susceptibility of bile - Empiric - directed at aerobic and anaerobic enteric flora.

Answer 47

- Most common in cats, rarely in dogs - Most common feline parasites - Platynosomum continuum and Amphimerus pseudofelineus - Both similar life cycle: eggs ingested by a land snail -> second intermediate host (fish/arthropod) - cats ingest the second intermediate host. - Adult worms develop in GB or bile ducts - various degrees of illness, from asymptomatic to complete bile duct obstruction. - Tx: praziquantel - Grave prognosis for severe infestations, not reported long-term survival

Answer 48

- Any obstruction to bile flow from the GB will lead to cholecystitis - Complete EHBDO -> dilation of GB and cystic duct within 24h, and dilation of intrahepatic bile ducts within 5 to 7 days.

Answer 49

- Hepatocyte necrosis - Cholangitis - Periportal fibrosis

Answer 50

- Uncommonly associated with cholecystitis in dogs and cats - Can cause cholecystitis by mechanical trauma or duct obstruction. - Can develop secondary to cholecystitis - increased mucus production and decreased GB motility, associated with inflammation, may promote cholelith formation. - Mainly composed of calcium carbonate and bilirubin pigments (vs cholesterol stones in humans). - Radiopaque choleliths - only in 48% of dogs and 83% cats with symptomatic cholecystitis - AUS preferred imaging modality to identify choleliths.

Answer 51

- It might be an incidental finding, but if there is concurrent presence of bile duct dissension and/or clinical signs and clinicopathologic evidence of cholecystitis. - Cholecystectomy is the treatment of choice. - Samples of liver, GB and bile should be obtained for histopathology, cytology and culture (anaerobic and aerobic).

Answer 52

- Depends on the absence or presence of concurrent disease, bacterial infection and/or GB rupture. - Reported long-term survival after surgery: 78% cats, 41% for dogs.

Answer 53

- Accumulation of thick, mucin-laden bile within the GB and bile ducts, leading to different degrees of obstruction to bile flow. - Progressive dissension of the GB can lead to ischemic necrosis of the walk and resultant GB rupture. - It is thought to be the result from a combination of increased mucin production and decreased GB motility.

Answer 54

- Middle age to older (median age of 9 to 11 years) dogs, but younger as 3 years old have been reported. - Shetland Sheepdogs, Cocker Spaniels and Miniature Schnauzers appears to be at increased risk. - Shetland Sheepdogs and other breeds -> insertion mutation on the ABCB4 gene (encodes for a protein that translocates phosphatidylcholine from hepatocyte to biliary canal) has been associated with mucocele formation.

Answer 55

- Dyslipidemias - Glucocorticoids excess - Cushing's dogs significantly increased risk.

Answer 56

- Increased ALT, AST, GGT and ALP - Hypercholesterolemia - Hyperbilirubinemia

Answer 57

- Echogenic, non mobile material fills the distended GB in either a stellate (kiwi) or finely striated pattern, often with a hypo echoic rim along the wall. - Non pathologic bile sludge - moves when changing patient's position - not with a mucocele. - Fluid in GB fossa, generalized or echogenic reaction in the pericholecystic region suggests possible GB rupture.

Answer 58

No. It has been reported in <10% of the cases, with the exception of positive aerobic cultures in 6/9 cases in one study.

Answer 59

- Cholecystectomy. - Cholecystotomy not recommended - underlying cause of mucocele formation is not removed and there might be areas of GB wall necrosis, even in the absence of GB rupture. - Common bile duct must be catheterized to be sure it is patent. - Excised GB has to be sent to histopathology, anaerobic and anaerobic culture.Liver biopsies are recommended to assess underlying disease.

Answer 60

- It can be considered in asymptomatic dogs - Ursodeoxycholic acid (UDCA) - choleresis, immunomodulatory properties, may decrease mucin secretion and may improve GB motility. 10-15mg/kg PO q12-24h. - S-adenosylmethionine (SAMe) - hepatoprotective effects - glutathione precursor and antioxidant, and may have choleretic effects. Given on an empty stomach for better absorption, 20-40mg/kg PO q24h. - Antibiotics - aimed at enteric flora to treat potential cholangitis, although bacterial infection is uncommon. - Medical management assumes a risk of necrotizing cholecystitis and GB rupture, should only be undertaken under close monitoring and client communication.

Answer 61

- Guarded - With medical management - unknown - With surgery - high perioperative mortality of 20% to 40%. - Dogs surviving the immediate postoperative period appear to have good long-term survival. - Septic bile peritonitis worse prognosis than sterile bile peritonitis.

Answer 62

- Uncommon condition - described in a small group of 12 dogs. - Can mimic cholecystitis and result in GB rupture - Diagnosis confirmed on histopathology post surgery. - Clinical signs and clinicopathological changes same as cholecystitis / GB obst. / rupture. - GB rupture present in 50% of the cases - Bacterial infection documented in 25% of cases - enteric organisms (E. coli and Clostridium). Postoperative survival rate of 67% - Thrombi identified in artery supplying the GB, evidence of distant thrombosis of the spleen - suspected hyper coagulable state - one dog was treated for Cushing's and another one for hypothyroidism.

Answer 63

they act as electrical pacemaker of the smooth muscle cells in the GI. They generate the slow wave activity in the GI.

Answer 64

i. Due to calcium-sodium channels as opposed to the sodium channels of nerves ii. Slower to open-close, accounting for the longer duration of its action potential

Answer 65

1. Stretching of the muscle 2. Stimulation by Ach or the parasympathetic nerves that secrete Ach. 3. Stimulation by various GI hormones

Answer 66

1. NE and epinephrine 2. Stimulation of the sympathetic nerves that secrete these catecholamines

Answer 67

1. Myenteric plexus (Auerbach's plexus)- found between the longitudinal and circular muscle layers and is mostly responsible for GI movements * When stimulated causes: a. Increased tonic contraction of the gut wall b. Increased intensity of the rhythmical contractions c. Increased rate of the rhythm of contraction d. Increased rate of velocity of conduction of excitatory waves along the gut wall, causing more rapid movement of the peristaltic waves * Also releases inhibitory substances that inhibit the sphincter muscles that impede the movement of food (pyloric sphincter, ileocecal valve sphincter, lower esophageal sphicter) 2. Submucosal plexus (Meissner plexus)- lies in the submucosa * control Intestinal secretion, absorption, and local contraction of the submucosa muscle.

Answer 68

Cranial division --> vagus Sacral division --> pelvic nerve

Answer 69

a. Vagus nerve control of gastric motor and secretory function b. Pain reflexes which inhibit the GI tract c. Reflexes that result in muscle contraction to facilitate defecation

Answer 70

a. Release of vasodilator substances i. Cholecystokinin ii. VIP iii. Gastrin iv. Secretin b. Release of kinins from the gut wall i. Bradykinin ii. Kallidin c. Decreased oxygen concentration i. Secondary to an increased metabolic rate and may result in the release of adenosin, a well-known vasodilator

Answer 71

CCK Duodenum and jejunum

Answer 72

secretin and glucagon

Answer 73

Occurs hours after a meal or during the fasting state and recurs approximately every 90 minutes. The migrating complex causes peristaltic waves to “sweep” from the stomach down towards the colon, removing any gastric secretions or chyme

Answer 74

If acting by itself, stimulation usually causes a very mild increase in secretion. However, if parasympathetic stimulation is causing the release of copious amount of secretions, sympathetic stimulation will decrease secretion secondary to the diminished blood flow to the glands

Answer 75

Pepsinogen

Answer 76

HCl and intrinsic factor

Answer 77

1. gastric (oxyntic) acid-forming glands --> 1. Secrete hydrochloric acid, pepsinogen, intrinsic factor, and mucus 2. Pyloric glands --> 1. Secrete mucus, some pepsinogen, and most importantly, gastrin.

Answer 78

1. Secreted by the parietal cells with hydrochloric acid 2. Necessary for the absorption of vitamin B12 in the ileum 3. Failure to secrete intrinsic factor can result in pernicious anemia, failure of RBC maturation in the absence of Vit B12 stimulation of the bone marrow

Answer 79

Ach gastrin histamine

Answer 80

gastrin cells (G cells)

Answer 81

FALSE - they are greatly diminished

Answer 82

<3 1. High acidity stimulates release of somatostatine from delta cells, which in turn, depresses gastrin secretion by G cells 2. Acid causes an inhibitory nervous reflex that inhibits gastrin secretion

Answer 83

Vagus nerve 30%

Answer 84

Inhibits gastric secretion --> Initiated by distention of the small bowel, presence of acid, presence of protein breakdown products, or irritation of the mucosa.

Answer 85

secretin glucose-dependend insulinotropic peptide (GIP) Others --> VIP, somatostatin

Answer 86

Trypsin and chymotrypsin --> split proteins into peptides Carboxypolypeptidase --> splits peptides into AA components Pancreatic amylase --> hydrolyzes starches, glycogen --> forms disaccharides pancreatic Lipase --> digests fats into fatty acids and monoglycerides Phospholipase --> splits fatty acids from phospholipids cholesterol esterase --> hydrolysis of cholesterol esters

Answer 87

Enterokinase

Answer 88

1. Ach- released from the vagus nerve endings and nerve endings of the enteric nervous system 2. Cholecystokinin- secreted by duodenal and upper jejunal mucosa in response to the presence of food 3. Secretin- secreted by the duodenal and jejunal mucosa in response to acidic chyme

Answer 89

*Emulsification of fat so lipases release by pancreas can digest fat * Transport and absorption of digested fat end products to and through the intestinal mucosal membrane * Waste product removal --> mainly billirubim and excess cholesterol synthesized by the liver

Answer 90

Cholecystokinin

Answer 91

Cholesterol

Answer 92

TRUE - they secrete mucus in large amounts in response to secretin, parasympathetic stimulation, and tactile/irritating stiimuli.

Answer 93

Secretion of the intestinal digestive juices

Answer 94

Gobblet cells -->secrete mucus Enterocytes

Answer 95

Saliva - not in SA Pancreatic secretions

Answer 96

TRUE - the disaccharides are: lactose, sucrose, maltose

Answer 97

This means that a hydrogen has been removed from one and a hydroxyl ion from the other. These then combine to form water and the two monosaccharides bind where the hydrogen and hydroxyl ion were removed.

Answer 98

Carbohydrates --> specific enzymes return the hydrogen and the hydroxyl ions to the polysaccharides and thereby separate the monosaccharides from each other. This is the process of hydrolysis Triglycerides --> the fat-digesting enzymes returning molecules of water to the triglyceride molecule and thereby splitting the fatty acid molecules away from the glycerol. In all 3 instances (including proteins), the process of hydrolysis is necessary for digestion, the only difference being the enzymes necessary to promote the reactions of each type of food

Answer 99

FALSE - has to be acidic

Answer 100

Emulsification

Answer 101

TRUE - this effect is specially prominent in the colon

Answer 102

By a sodium co-transport mechanism

Answer 103

c. Goblet cells

Answer 104

c. Increased levels of Ach

Answer 105

Digestive proteins are stored in secretory granules as inactive precursors or zymogens • The secretory granule membrane is impermeable to proteins • Enzyme inhibitors such as pancreatic trypsin inhibitor, co-packaged in the secretory granule, block the activity of trypsin aberrantly activated within the granule

Answer 106

c. If a total gastrectomy is necessary, the patient will have severe protein absorption deficiency and his fecal nitrogen excretion will be considerably elevated (FALSE: Pepsin in the stomach partially digests 10% to 15% of dietary protein Pepsin hydrolysis is not absolutely necessary; patients with either total gastrectomies or pernicious anemia do not have increased fecal nitrogen excretion)

Answer 107

You are suspicious that your patient has a condition know as pernicious anemia, in this condition there is a lack of secretion of _______ and _____(gastric acid and intrinsic factor). The main etiology associated with this condition is _________ (immune-mediated/ abs against parietal cells and IF). The reason why this patient develop anemia is because there is a lack of ___ (IF) that normally is required for _____ (Cobalamin/ vitb12) absorption in the ileum, which is an essential vitamin for the synthesis of RBCs.

Answer 108

a. CCK and gastric inhibitory polypeptide (GIP)

Answer 109

c. A, D, E, and K

Answer 110

b. Hypocalcemia (Mg is necessary for proper secretion of parathyroid hormone)

Answer 111

Direct pathway * the vagus nerve innervates parietal cells and stimulates H+ secretion directly. * The neurotransmitter at these synapses is ACh, the receptor on the parietal cells is muscarinic (M3), and the second messengers for M3 and CCK are IP3 and increased intracellular [Ca]. Indirect path * the vagus nerve innervates G cells and stimulates gastrin secretion, which then stimulates H+ secretion by an endocrine action. * The neurotransmitter at these synapses is GRP {notACh). How to block it? * Atropine (cholinergic muscarinic antagonist) --> blocks the direct pathway (which uses ACh). However, does not inhibit the indirect pathway (which uses GRP as a neurotransmitter) * Vagotomy eliminates both direct and indirect pathways.

Answer 112

Prostaglandins inhibit gastric H+ secretion by activating a Gi protein, inhibiting adenylyl cyclase and decreasing cAMP levels. They also maintain the mucosal barrier and stimulate HC03- secretion, thus protecting the gastric mucosa from the damaging effects of H+

Answer 113

(4) same Cl- concentration than plasma. FALSE. Cl is much lower than plasma

Answer 114

* Ductal cells modify the initial pancreatic secretion by secreting HC03- and absorbing Cl via a CI--HCO3- exchange mechanism in the luminal membrane. * secretin acts on the pancreatic ductal cells to increase the HCO3- secretion * Because the pancreatic ducts are permeable to water, H2o moves into the lumen to make the pancreatic secretion isosmotic

Answer 115

Cholic acid and chenodeoxycholic acid

Answer 116

- Cellular adaptations to hypoxia (pH regulation, glucose uptake, erythropoyesis, lipid metabolism) - Beneficial effects for the intestinal barrier function (increases paracellular resistance by upregulating claudin-1, JAM and occludin) which reduces bacterial translocation and associated inflammation - HIF-1 also increases production of mucins - HIF-1 supresses inflammation

Answer 117

Facilitated diffusion Na-dependent cotransport

Answer 118

Liver and brain

Answer 119

Phosphorilation liver, renal tubular epithelium, intestinal epithelial cells Glucose phosphatase

Answer 120

Phosphorilase

Answer 121

38 (2 from glycolysis, 2 from citric acid cycle, 34 from oxidative phosphorilation in mitocondria)

Answer 122

Pyruvate and NADH lactic dehydrogenase lactateand NAD+

Answer 123

Gluconeogenesis

Answer 124

Chylomicrons

Answer 125

addipose tissue and liver tissue lipoprotein lipase fatty acids and glycerol

Answer 126

Lipoproteins

Answer 127

Brain and RBCs

Answer 128

Structural component in cell membranes Convertion of cholesterol into cholic acid that forms part of bile salts --> promotes digestion and absorption of fats Adrenal glands use cholesterol to form adrenal cortical hormones Ovaries use it to form progesterone and estrogen Testes use it to form testosterone

Answer 129

Active transport facilitated diffusion

Answer 130

Deamination

Answer 131

Amino acids deamination in the liver Production by the GI bacteria

Answer 132

Hemolytic: * excretory function of the liver is not impaired * RBC hemolyisis is so rapid that hepatic cells cannot excrete bolirubin as fast as is being formed *free bilirubin in plasma is high Obstructive: * rates of bilirubin formation and conjugation are near normal * conjugated bilirubin cannot pass into the intestines * conjugated bilirubin is high

Answer 133

Uridine diphosphate (UDP) glucuronyl transferase

Answer 134

> 3 mg/dL (and often up to 5 mg/dL) > 0.5-1.0 mg/dL

Answer 135

ALT - Primarily located in the liver with concentrations many times higher than in muscle

Answer 136

ALP novo hepatic synthesis or elution of the enzyme from the cellular membrane

Answer 137

Liver Muscle RBCs

Answer 138

FALSE - is present in the highest quantities, in descending order, in: 1. Intestinal mucosa 2. Renal cortex 3. Placenta 4. Liver 5. Bone

Answer 139

Bone-induced (B-ALP) liver-induced (L-ALP) corticosteroid-induced (C-ALP): Plasma half life • L-ALP and C- ALP: 70 hours in the dog • L- ALP: 6 hours in the cat, cats lack C-ALP Intestinal, renal, and placental isoenzymes contribute little (extremely short half-lives)

Answer 140

Because conjugated bilirubin binds irreversibly covalently with albumin, whose half-life is about 2 weeks

Answer 141

Cholestasis of sepsis hemolysis Artifactual hemolysis or lipemia

Answer 142

Because the liver has a huge reserve capacity for detoxifying ammonia, and 70% reduction in urea cycle function is needed for hyperammonemia to develop.

Answer 143

Von Willebrand subtype of Factor VIII.

Answer 144

Cholestasis can cause malabsorption of fat-soluble vitamins such as vitamin K

Answer 145

o Round or blunted caudoventral liver margins o Extension of liver margins beyond the costal arch o Displacement of the gastric axis -> normal gastric axis: perpendicular to the spine to parallel with the last rib"

Answer 146

o Chronic hepatitis o Lipidosis, Steroid hepatopathy, other vacuolar hepatopathies o Toxic insult o Lymphoma, mast cell disease, histiocytic sarcoma o Phenobarbital administration

Answer 147

Falciform fat spleen

Answer 148

CT- angiography

Answer 149

E. coli, alone or in combination with obligate or facultative anaerobes

Answer 150

a. The majority of dogs reported with necrotizing cholecystitis have had bacterial infection, although it can occur in the absence of infection secondary to gallbladder mucocele b. Parasitic cholecystitis is more commonly seen in dogs when compared to cats and it’s associated with a good prognosis (FALSE. More common in cats and in high loads it has a grave prognosis) --> • Most common in cats: Platynosomum concinnum and Amphimerus pseudofelineus.

Answer 151

• Type I: areas of necrosis without gallbladder rupture • Type II: acute inflammation with rupture • Type III: chronic inflammation with adhesions and/or fistulae to adjacent organs

Answer 152

b. Fluoroquinolones, metronidazole, and chloramphenicol (are commonly used as they achieve high concentrations in bile and have strong anaerobic activity)

Answer 153

Abdominal ultrasounds because radiopaque choleliths are reported in only 48% of dogs and 83% of cats with symptomatic cholelithiasis

Answer 154

Gallbladder mucocele is a major cause of clinical disease, and the presence of inflammation is variable. Gallbladder infarction in dogs is thought to be a vascular disease that is not associated with inflammation of the gallbladder.

Answer 155

TRUE - • Bacterial species isolated typically of enteric origin: o Escherichia coli o Enterococcus spp. o Bacteroides spp. o Clostridium spp

Answer 156

False • Uncommonly is associated with cholecystitis in dogs and cats • Most choleliths are incidental findings • Choleliths also may develop secondary to cholecystitis

Answer 157

FALSE - Calcium- based stones are rare due to the ability of the canine gallbladder to absorb free calcium in bile. Feline choleliths contain cholesterol, bilirubin derivatives, and calcium salts

Answer 158

FALSE - UNCONJUGATED bile acids

Answer 159

Causes choleresis (flow of bile from the liver) Immunomodulatory properties May decrease mucin secretion May improve gallbladder motility ** ursodiol suppresses hepatic synthesis and secretion of cholesterol. Ursodiol also decreases intestinal absorption of cholesterol. By reducing cholesterol saturation in the bile, it is thought that ursodiol allows solubilization of cholesterol-containing gallstones. Ursodiol also increases bile flow and, in patients with chronic liver disease, apparently reduces the hepatocyte toxic effects of bile salts by decreasing their detergent action and may protect hepatic and bile duct epithelial cells from toxic bile acids (eg, lithocholate, deoxycholate, chenodeoxycholate). In patients with chronic hepatitis, ursodiol may also reduce hepatocellular inflammatory changes and fibrosis. 10 to 15 mg/kg PO SID or BID orally once to twice daily"

Answer 160

S-adenosyl-methionine (SAMe) is an endogenous molecule synthesized by cells throughout the body. --> formed from the amino acid methionine and ATP, in conjunction with SAMe synthetase enzyme SAMe is an essential part of three major biochemical pathways: transmethylation, transsulfuration, and aminopropylation. ** SAMe serves as a methyl donor (necessary for many substances and drugs to be activated and/or eliminated). Transmethylation is essential in phospholipid synthesis important to cell membrane structure, fluidity, and function. ** In aminopropylation, SAMe donates aminopropyl groups and is a source of polyamines. Aminopropylation is important in producing substances that have anti-inflammatory effects, protein and DNA synthesis, and promoting cell replication and liver mass regeneration. ** In transsulfuration, SAMe generates sulfur-containing compounds important for conjugation reactions used in detoxification and as a precursor to glutathione (GSH)

Answer 161

• Neutrophilic cholangitis • Lymphocytic cholangitis

Answer 162

Elevated hepatic copper levels have been identified in dogs with Canine Chronic Hepatitis, but because biliary excretion is the major mechanism of maintaining copper homeostasis, any cause of cholestasis would be expected to increase hepatic copper levels

Answer 163

Corneal edema and anterior uveitis

Answer 164

• Commonly isolated aerobic bacteria: Staphylococcus spp., Streptococcus spp., Enteric gram-negative organisms • Commonly identified anaerobes: Bacteroides spp., Clostridium spp., and Fusobacterium spp.

Answer 165

a. In patients with hepatic failure, hypovolemia and hypotension can diminish renal blood flow and glomerular filtration rate which commonly leads to Acute Kidney Injury in Veterinary Medicine patients. (FALSE, d• hepatorenal syndrome: AKI as a sequela to liver failure described rarely in veterinary patients (common in people) b. In patients with HE, ammonia is associated with a decreased release of glutamate, which inactivates NMDA receptors and causes the typical signs of coma and CNS depression. (FALSE, is excitotoxic and associated with an increased release of glutamate, overactivation of the glutamate receptors (mainly NMDA receptors), has been implicated as one of the causes of HE-induced seizures; with chronicity, inhibitory factors such as GABA and endogenous benzodiazepines surpass the excitatory stimulus, causing signs more suggestive of coma or CNS depression) c. Some dogs with normal ammonia concentrations have obvious HE signs, and many dogs with high ammonia levels appear neurologically normal, suggesting that other suspected neurotoxins are also important in pathophysiology of HE (TRUE)

Answer 166

o Decreased factor synthesis o Increased factor utilization o Decreased factor turnover o Increased fibrinolysis and tissue thromboplastin release o Synthesis of abnormal coagulants (dysfibrinogenemia) o Decreased platelet function and numbers o Vitamin K deficiency (particularly in patients with bile duct obstruction) o Increased production of anticoagulants

Answer 167

a. Albumin is produced only in the liver, representing approximately 80% of all proteins synthesized by the liver. (FALSE, ONLY 25%) b. Altered albumin synthesis is not detected until more than 66% to 80% of liver function is lost c. Because of its short half-life, hypoalbuminemia is a hallmark of acute liver failure (FALSE, Because of its long half-life (8 days in dogs and cats) hypoalbuminemia is a hallmark of chronic liver dysfunction)

Answer 168

c. Propofol (The use of diazepam for the treatment of HE-associated seizures in animals is controversial. GABA and its receptors are implicated in the pathogenesis of HE, and the use of a benzodiazepine antagonist, such as flumazenil, has been proven beneficial in humans with HE-induced comas) ** Levetiracetam has been shown to prevent postanesthetic seizures in dogs with porto- systemic shunts, so prophylactic loading and maintenance therapy now is performed commonly

Answer 169

o PT of greater than 100 seconds o very young or very old animals o viral or idiosyncratic drug reaction as the underlying cause o markedly increased bilirubin

Answer 170

Ammonia (NH3) Urea Urea cycle

Answer 171

FALSE - Dogs and cats with liver failure secondary to congenital portosystemic shunting should not be icteric

Answer 172

o failure of the liver to produce urea, resulting in defective renal medullary concentrating ability, ** decreased release and/or responsiveness of the renal collecting ducts to ADH o Primary polydipsia, resulting from the central effects of hepatotoxins o Increased renal blood flow and increased adrenocorticotropic hormone (ACTH) secretion with associated hypercortisolism

Answer 173

The presence of normal or only mildly elevated liver enzyme activity does not eliminate hepatic failure as a possible diagnosis because animals with end-stage hepatic failure or portal- systemic vascular anomalies may have normal, or near normal, enzyme activities

Answer 174

Ammonium biurate or urate crystals

Answer 175

Spironolactone is the initial diuretic of choice for its aldosterone antagonism and subsequent potassium-sparing effects.

Answer 176

Most common cause --> extrahepatic or intrahepatic portal-to-systemic venous communications Other --> microvascular dysplasia, hepatic lipidosis, hepatic failure, congenital urea cycle enzyme deficiencies

Answer 177

In animals with portosystemic shunting of blood or significant liver disease, high levels of ammonia are present in the systemic circulation. The permeability of the blood-brain barrier to ammonia increases in HE and experimental studies suggest that HE coma is associated with brain ammonia concentrations in the low millimolar range. These concentrations of ammonia decrease excitatory neurotransmission, in part by down-regulating the N-methyl-D-aspartate (NMDA, excitatory) receptors, yet at the same time, also block chloride extrusion from the postsynaptic neuron, decreasing inhibitory neurotransmission. The brain has no urea cycle; consequently, ammonia in the CNS is removed by transamination of glutamate into glutamine in astrocytes. Glutamine concentrations in the cerebrospinal fluid are elevated in dogs with HE and frequently are correlated with the degree of neurologic dysfunction in humans with HE. Glutamine is exchanged across the blood-brain barrier for tryptophan, leading to increased levels of tryptophan and tryptophan metabolites in the central nervous system. The tryptophan metabolites serotonin and quinolinate are important agonists in inhibitory and excitatory neurotransmission, respectively, Glutamine also is transported from astrocytes into neurons, where it is converted to glutamate. Overstimulation of the NMDA receptors by glutamate and ammonia can cause seizures and neurotoxicity, in part because of free radical formation. It is likely that if increased GABA neurotransmission exists in patients with HE, it is due to increased brain concentrations of endogenous GABA ligands, including endogenous benzodiazepines and neurosteroids.

Answer 178

A lactulose enema (1 to 3 ml/10 kg BW diluted 1 : 1 to 1 : 3 with warm water) is administered to minimize ammonia production in, and absorption from, the colon. Lactulose (beta galactosidofructose) is a nonabsorbable disac- charide that exerts an osmotic cathartic action. In addition, intestinal bacteria hydrolyze lactulose-producing organic acids that lower colonic pH. Acidification traps ammonia in its NH4+ form, preventing absorption by nonionic diffusion and also resulting in the net movement of ammonia from the blood into the bowel lumen

Answer 179

Extrahepatic shunts: * complete suture ligation * placement of either an ameroid ring or cellophane band to occlude gradually the shunting vessel. Intrahepatic shunts: * surgically or with interventional radiographic techniques

Answer 180

Glutathione

Answer 181

Azathioprine

Answer 182

Decreased clearance of plasminogen activators by the failing liver

Answer 183

TRUE - important to correct hypokalemia in these patients

Answer 184

FALSE - hypophosphatemia can indicate liver regeneration (due to intracellular shift of P) and might be a positive prognostic indicator, while HYPERphosphatemia is a negative prognostic indicator.

Answer 185

Platelets <80.000 aPTT >1.5 times in cats prolonged PT> upper limit in dogs

Answer 186

Salmonella

Answer 187

Histoplasmosis.

Answer 188

Acute hemorrhagic diarrhea syndrome

Answer 189

severe lymphocytic-plasmacytic, eosinophilic, or granulomatous inflammatory bowel diseases lymphangiectasia diffuse infectious disease * fungal disease (histoplasmosis, pythiosis) * bacterial (salmonella) * viral (CPV-2) *parasites (giardia, ancylostoma) diffuse neoplasia (alimentary lymphoma/lymphosarcoma) GI ulceration structural disease (intussusception)

Answer 190

Abnormal immune responses to bacteria, bacterial endotoxin, or dietary ingredients.

Answer 191

Idiopathic

Answer 192

FALSE - Myasthenia gravis accounts for the majority of cases with a known cause

Answer 193

Idiopathic myastenia gravis Esophagitis Addison's disease Esophageal neoplasia Inflammatory myopathies Lead and thallium poisoning Lupus

Answer 194

The GI tract, mostly in the enterochromaffin cells (90%) and a small portion in the ENS where 5HT acts as a neurotransmitter

Answer 195

5-HT3 antagonists --> this receptor activates extrinsic sensory nerves and is responsible for the sensation of nausea and induction of vomiting from visceral hypersensitivity.

Answer 196

5-HT4 agonists --> this receptor increases the presynaptic release of ACH and calcitonin gene-related peptide, thereby enhancing neurotransmission. --> This enhancement promotes propulsive peristaltic and secretory reflexes. * enhances gastric emptying while simultaneously increasing gastroesophageal sphincter pressure

Answer 197

Gastric stasis idiopathic constipation gastroesophageal reflux postoperative ileus cats with megacolon

Answer 198

Is a central dopaminergic antagonist / peripheral 5-HT3 receptor antagonist / 5-HT4 receptor agonist with GI and CNS effects * Stimulates and coordinates esophageal, gastric, pyloric, and duodenal motor activity. * increases lower esophageal sphincter tone and stimulates gastric contractions, while relaxing the pylorus and duodenum * dopamine antagonism at the chemoreceptor trigger zone produces an antiemetic effect

Answer 199

Dopamine antagonism in the striatum causes adverse effects known collectively as extrapyramidal signs, which include involuntary muscle spasms, motor restlessness, and inappropriate aggression.

Answer 200

By restoring an appropriate dopamine to ACH balance with the anticholinergic action of diphenhydramine (1mg/kg IV)

Answer 201

Metclopramide (dopamine and 5HT3 antagonist and 5HT4 agonist) Cisapride (5HT-4 agonist) Macrolide antibiotics --> erythromycin, clarithromycin --> (Motilin receptor agonist) Rikkunshito (Ghrelin mimetic) Ranitidine and nizatidine (H2 antagonists)

Answer 202

Migrating motor complex

Answer 203

Hypersecretion of gastric acid in response to histamine release from mast cell tumors and gastrin from gastrinomas are clear causes of gastroduodenal ulceration and esophagitis in dogs and cats Mast cell tumors are thought to cause vomiting via the central effects of histamine on the chemoreceptor trigger zone (CRTZ) and the peripheral effects of histamine on gastric acid secretion, with resultant hyperacidity and ulceration. • Neoplasia is a common cause of GI ulceration in cats o systemic mastocytosis, gastrinoma, intestinal lymphosarcoma, and adenocarcinoma are the most commonly reported tumors

Answer 204

Omeprazole

Answer 205

At higher dosages (1.1 mg/kg PO q 12 h) omeprazole has been associated with significant hypergastrinemia and gastric dysbiosis.

Answer 206

Indicated in cases of severe GI ulceration and hemorrhage refractory to medical treatment * injecting epinephrine or 98% alcohol through an endoscope sclerotomy needle into the base of an ulcer.

Answer 207

Idiopathic megaesophagus

Answer 208

E (Ptyalism is commonly seen secondary to nausea in vomiting patients or as a result of pooling and/or inability to swallow saliva effectively in animals with regurgitation)

Answer 209

Decreased transit to the stomach due to increased lower esophageal sphincter tone Metoclopramide and Cisapride have no beneficial effect = smooth muscle prokinetics and the canine esophagus is comprised almost exclusively of striated muscle

Answer 210

C - Acetylcholine receptor antibody assay (Myasthenia gravis = most common cause of secondary megaesophagus = 20% to 30% of all cases.

Answer 211

Hypokalemia

Answer 212

FALSE - Animals with esophagitis show signs of apparent esophageal discomfort (a diferencia de los pacientes con megaesofago), such as pain on swallowing (odynophagia), repeated swallowing attempts, lip smacking, and arching of the neck

Answer 213

Specialized region (area postrema) located on the floor of the fourth ventricle in the medulla Stimulated by: - Vagal and sympathetic afferent pathways from the GI tract --> by inflammation or overdistention - Vestibular system, cerebrum * chemoreceptor trigger zone

Answer 214

IBD Lymphocytic-plasmacytic

Answer 215

Lymphangiectasia

Answer 216

a. Osmotic diarrhea ** presence of excess luminal osmoles, drawing fluid into the intestinal lumen. ** Most causes of a diarrhea have an osmotic component. b. Secretory diarrhea o Absolute increase in intestinal secretion o Or a relative increase caused by a decrease in intestinal absorption c. Altered permeability o microscopic and macroscopic damage to either the epithelial cells or epithelial cell junctions d. Deranged motility o Increased peristaltic contractions o Or decreased segmental contractions

Answer 217

Visceral pain Unmyelinated C fibers

Answer 218

Somatic (paretal) pain

Answer 219

Pancreatic nodular hyperplasia

Answer 220

o Supplementation with glutamine currently is recommended o Cats (particularly with concurrent GI disease) may require cobalamin supplementation

Answer 221

• Infected pancreatic necrosis • Extrahepatic biliary obstruction (EHBO) • Deterioration despite aggressive medical therapy

Answer 222

In general, acute pancreatitis is characterized by inflammation that is completely reversible after removal of the inciting cause, whereas chronic pancreatitis results in irreversible histopathologic changes.

Answer 223

Hypotension associated with anesthesia may be more important than pancreatic manipulation *Although pancreatitis has been observed in cats with various infections, including certain parasites (eg, Toxoplasma gondii, Eurytrema procyonis, Amphimerus pseudofelineus) and viruses (eg, coronavirus, parvovirus, herpesvirus, calicivirus), these infections represent rare causes of pancreatitis in cats * Although pancreatic injury is possible with manipulation, an increased risk for the development of pancreatitis has not been noted in studies involving pancreatic sampling

Answer 224

* autoactivation of cationic trypsinogen (more likely when pH ≥5.0) * activation of zymogens by thrombin during bacterial toxemia, ischemia, or hypoxia * activation of trypsinogen by cathepsin B * enterokinase entering the portal circulation after a meal in conjunction with biliary-pancreatic reflux, which may cause zymogen activation * Recent hypotheses postulate that abnormalities in calcium signaling lead to the colocalization of lysosomes and zymogen granules and trypsinogen activation, causing acinar cell death and early activation of the nuclear factor kappa B (NFκB) pathway. * cholecystokinin and oxidative stress synergistically sensitize pancreatic acinar cells to injury and necrosis, independent of trypsin activation The local and systemic inflammation that ensues in acute pancreatitis is independent of trypsin activation, but dependent on ongoing stimulation of the NFκB pathway. (proved in rodents and people only)

Answer 225

FALSE - The local and systemic inflammation that ensues in acute pancreatitis is independent of trypsin activation, but dependent on ongoing stimulation of the NFκB pathway.

Answer 226

accesory pancreatic duct minor dueodenal papilla

Answer 227

Because of the shared entry of the common bile duct and the pancreatic duct into the duodenum

Answer 228

Pancreatic stellate cells (PSC)

Answer 229

Pancreatic lipase why --> Various substrates are utilized for lipase activity assays, but, despite choosing favorable conditions for measurement of pancreatic lipase, none have shown to be specific for the measurement of pancreatic lipase to date.

Answer 230

Neurokinin1 receptor (NK1R) antagonist, which acts both centrally and peripherally by inhibiting the binding of substance P to the NK1R located in the vomiting center, chemoreceptor trigger zone, and the gastrointestinal tract. may have additional benefits, such as visceral analgesia and antiinflammatory activity

Answer 231

Initiates peptic hydrolysis of dietary proteins Liberates vitamin B12 from dietary protein Facilitates duodenal absorption of inorganic iron and calcium Stimulates pancreatic HCO3− secretion via secretin release suppresses antral gastrin release Modulates the intestinal microbiome by killing microorganisms and preventing bacterial overgrowth

Answer 232

It is unlikely that they increase gastric pH (or only temporary), because these agents do not exhibit strong enough buffering capacity.

Answer 233

Constipation In renal failure, magnesium and aluminum accumulation may be a problem Aluminum toxicity after administration of aluminum hydroxide has been documented in dogs with advanced renal failure interfere with the PO absorption of other drugs

Answer 234

Tolerance may be caused by gastrin-induced up-regulation of enterochromaffin-like cell (ECL) synthesis of histamine, which in turn competes with the antagonist at the parietal cell. Because of this tolerance, abrupt discontinuation of H2RAs causes rebound acid hypersecretion in humans ** within 13 days, may be noticed within 3 days

Answer 235

Enterochromaffin-like (ECL)

Answer 236

TRUE * That's why plasma concentration of PPIs do not necessarily predict their efficacy * that's why PPI's are most effective when taken shortly before a meal (30 - 45 min) or with a meal * That’s why effectiveness of omeprazole is amrkedly compromised in dogs if administered while acid secretion was inhibited by co-administration of H2RAs

Answer 237

* When administered in an acid environment, the acid-labile drug may be degraded before it reaches the intestine where it is absorbed systemically --> After repeated administration, acid secretion gradually diminishes to maximize intestinal drug absorption * Initial treatment with IV formulations, administering an enteric-coated delayed-release formulation, or combining PO formulations with bicarbonate will decrease the lag-time for achieving maximal effect --> Breaking or crushing an enteric-coated form, or using a compounded formulation may diminish this protective effect

Answer 238

weak parietal alpha subunit of H+-K+- ATPases

Answer 239

Dormant parietal cells are activated after initial PPI administration. Thus, inhibition of acid secretion is approximately 30% of maximal on day 1 of administration because of incomplete binding to all H+-K+-ATPases * Maximal inhibitory effect is achieved within approximately 2-4 days

Answer 240

TRUE Drug interactions with proton pump inhibitors Antifungal drugs * ketoconazole, itraconazole, voriconazole, and posaconazole Exceptions: * Itraconazole - it is formulated in a cyclodextrin complex to maintain solubility in solution. * Fluconazole - it is more water soluble Clopidogrel * In humans, the CYP enzymes are responsible for conversion to the active metabolite, but whether or not dogs and cats metabolize clopidogrel with the same enzymes is unknown

Answer 241

Twice daily >3-4 weeks rebound gastric acid hypersecretion (RAH).

Answer 242

Iron --> Hydrochloric acid in the stomach promotes iron absorption because it reduces the ferric acid (Fe3+) form to the more soluble ferrous form (Fe2+). (This has not been studied in VM) Mycophenolate mofetil --> requires acidic pH for dissolution of the medication and for hydrolysis to mycophenolic acid.

Answer 243

Small intestinal bacterial overgrowth due to *decreased intestinal peristalsis *decreased gastric emptying *changes in epithelial mucus composition *increased pH, and increased bacterial translocation **This may increase the risk of aspiration pneumonia When used in conjunction with NSAIDs: * Intestinal dysbiosis arising from PPI administration increases the risk of NSAID-induced intestinal injury. * Antibiotics or probiotics may mitigate injuries caused by this drug combination Diarrhea is the most common adverse effect reported in association with PPI administration in dogs

Answer 244

Synthetic PGE1 analogue * specificity for parietal cell receptors and decreases histamine, penta-gastrin, and meal-stimulated gastric acid secretion. * binds to prostaglandin receptors and inhibits histamine-stimulated cAMP formation Cytoprotective effects: increased bicarbonate secretion decreased pepsin content of gastric secretion preservation of tight junctions among epithelial cells increased mucus layer increased mucosal blood flow improvement of mucosal regenerative capacity.

Answer 245

Misoprostol

Answer 246

FALSE - this is true for NSAIDS not for corticosteroids * No evidence supports the use of misoprostol for preventing corticosteroid-induced GUE in dogs.

Answer 247

* Forms stable complexes with protein in damaged mucosa where there is a high concentration of protein, either from fibrinogen, albumin, or globulins from the exudate of an ulcer or from damaged cells * In an acidic environment, it partially dissociates into sucrose sulfate and aluminum hydroxide *** Sucrose sulfate moiety --> binds electrostatically with the positively charged proteins in the damaged mucosa *** the protection afforded by sucralfate against esophageal acid injury is mediated by intraluminal pH buffering via aluminum hydroxide and protection against H+ entry and injury via sucrose octasulfate * Sucralfate also stimulates prostaglandin production in the gastric epithelium * anecdotal evidence indicates drug's analgesic properties in people with esophagitis.

Answer 248

Gastrointestinal and pancreatic neoplasia NSAIDs hepatic disease Inflammatory bowel disease

Answer 249

Altered mucosal blood flow because of portal hypertension (most common cause in humans) Decreased hepatic degradation of gastrin and subsequent stimulation of acid hypersecretion may occur in dogs.

Answer 250

If there is concurrent GI bleeding Consensus: there is weak evidence to support the prophylactic use of acid suppressant therapy in dogs and cats with hepatic disease that is not associated with GI bleeding.

Answer 251

1. If evidence of gastroduodenal ulceration/erosion 2. If critically ill and concurrent NSAIDs administration (if PPI + NSAID --> increased risk of intestinal disbiosis and NSAID-induced intestinal injury --> consider antibiotics or probiotics) 3. If critically ill and evidence of GI hemorrhage 4. Prophylactic PPI administration in animals competing in strenuous, competitive events might decrease 5. Stress Related Mucosal Damage (SRMD) and improve overall performance 6. For prevention of esophagitis secondary to Gastroesophageal Reflux (GER), particularly in animals when it is associated with an anesthetic procedure (PPIs does not decrease gastric reflux, but may prevent injury by increasing the pH of the refluxate) 7. +/- could be considered in thrombocytopenia-induced bleeding since platelet aggregation and clot formation are optimal at pH >6.8, however --> there is insufficient evidence to support the use of standard dosages of acid suppressant treatment for prevention or management of thrombocytopenia-induced bleeding.

Answer 252

FALSE - Gastrointestinal complications associated with spinal cord disease and spinal surgery are more likely caused by the administration of high doses of glucocorticoids than other factors. In these cases, there is no convincing evidence that gastroprotectant drugs are beneficial.

Answer 253

Nizatidine and ranitidine reportedly have some gastric prokinetic activity, probably via antiacetylcholinesterase activity.

Answer 254

Cimetidine

Answer 255

FALSE - it is an antagonist and acts in the CTZ

Answer 256

FALSE - it is the opposite

Answer 257

Maropitant often causes pain when injected and is reported to cause bone marrow hypoplasia when administered to puppies younger than 11 weeks old.

Answer 258

Maropitant

Answer 259

Cats are thought to have a paucity of dopamine receptors.

Answer 260

Centrally acting antiemetics * antidopaminergic and antihistaminic effects that block the CTZ and at higher doses the MVC * These drugs also have anticholinergic, antispasmodic and alpha-adrenergic blocking effects

Answer 261

TRUE - Aminopentamide has been used as antiemetic in dogs. (not as effective as the others)

Answer 262

TRUE - Binds to muscarinic receptors and affects motility throughout the GI tract

Answer 263

Objective measures of body composition

Answer 264

10% to 15%

Answer 265

70 x Kg^0.75

Answer 266

Patients that are anorexic for more than 3 to 5 days Hyporexic for more than 1 week Have lost 10% of their body weight involuntarily Have a low BCS or moderate to severe muscle atrophy

Answer 267

The cyclooxygenase, 5-lipoxygenase, and cytochrome P450 pathways arachidonic acid (AA), eicosapentaenoic acid (EPA) and γ-linolenic acid (GLA)

Answer 268

ALI: acute hepatocellular damage and necrosis with retained hepatic function ALF: once hepatocellular damage is so extensive that compromises hepatic synthetic, excretory and regulatory functions.

Answer 269

o Absence of preexisting liver disease o Presence of HE within 8 weeks after onset of hyperbilirrubinemia, defined as plasma bilirubin > 2.9mg/dL o Presence of coagulopathy, defined by an INR.

Answer 270

Toxic Drug-related Infectious Idiosyncratic

Answer 271

o Direct (destruction of liver tissue) * Cycad-palms * Blue-green algae * Amanita phalloides * Aflatoxins * Xylitol o Indirect (disruptive) * Xylitol * Carprofen * Acetaminophen * Phenazopyridine * Sulfonamides * Lomustine * Zonisamide * Stanozalol * Benzodiazepines

Answer 272

Carprofen Acetaminophen Sulfonamides Zonisamide Lomustine Phenazopyridine

Answer 273

Leptospirosis Canine Adenovirus 1 Trematodes

Answer 274

Hepatic lipidosis in cats Hypoglycemia, increased AST, ALT, GGT, ALP, bilirubin, bile acids Possible bilirrubinuria AXRAY - enlarged liver and large amount of abdominal fat AUS - Hyperechoic liver FNA - lipid-filled hepatocytes

Answer 275

Icterus Coagulopathy Hepatic encephalopathy Hypoglycemia Sepsis

Answer 276

Hyperfibrinolysis -> decreased clearance of plasminogen activators by the failing liver

Answer 277

Regurgitation is the passive ejection of food, water, or saliva associ- ated with esophageal or, less commonly, pharyngeal disease.

Answer 278

Aspiration pneumonia

Answer 279

TRUE It can be sometimes a manifestation of systemic disease.

Answer 280

FALSE - in dogs

Answer 281

Idiopathic megaesophagus

Answer 282

Pain when swallowing

Answer 283

o Thoracic radiography is the most important and useful imaging modality for evaluating patients with regurgitation. o Plain radiographs are diagnostic in most cases of megaesophagus resulting from a foreign body obstruction. o Plain radiographs also may show evidence of secondary aspiration pneumonia, mediastinal masses, or congenital abnormalities (e.g., vascular ring anomaly). o Two lateral radiographs and an orthogonal view should be obtained to evaluate all lung fields. If plain radiographs do not show any abnormalities, contrast studies or endoscopy may be indicated.

Answer 284

Abdominal ultrasonography rarely provides useful information in animals with regurgitation.

Answer 285

o Serum should be submitted for acetylcholine receptor antibody assay on all patients with megaesophagus. o Additional tests to consider based on clinical suspicion include an adrenocorticotropic hormone stimulation test, serology for antinuclear antibody, serum creatine phosphokinase activity, lead levels in the blood, electromyography and nerve conduction velocity, and muscle and nerve biopsy. o Evidence for an association with hypothyroidism is lacking, but thyroid function (thyroid stimulating hormone assay, thyroid stimulating hormone stimulation, free and total thyroid hormone levels) testing may be warranted in individual patients with other suspicious signs. o Most patients with megaesophagus secondary to hypoadrenocorticism have electrolyte changes and other systemic signs.

Answer 286

o Most animals with regurgitation are stable and well hydrated and do not require emergent therapy before a definitive diagnosis is made. o Empiric treatment with a histamine-2 receptor antagonist or proton pump inhibitor is indicated to reduce the risk of secondary esophagitis. o The addition of sucralfate may be warranted in patients with suspected active esophageal ulceration. o The canine esophagus is comprised almost exclusively of striated muscle, so smooth muscle prokinetic agents such as metoclopramide and cisapride have no beneficial effect. o Moreover, these agents could decrease the transit of ingesta to the stomach by increasing lower esophageal sphincter tone. o Anecdotal reports show that the parasympathomimetic agent, bethanechol, is a useful prokinetic agent in dogs with megaesophagus, but data are lacking. o The caudal third of the feline esophagus comprises smooth muscle. However, although prokinetics such as cisapride theoretically may be more useful in this species, primary esophageal dysmotility is uncommon in the cat.

Answer 287

o If regurgitating animals require hospitalization, the priority should be to prevent aspiration pneumonia by feeding a high-calorie diet in small, frequent meals from an elevated or upright position, and dietary consistency should be tailored to the animal. o Although intuitively a firm diet would appear to reduce the risk of aspiration, many patients have less frequent regurgitation when fed a more liquid ration. o Animals that cannot maintain adequate nutritional balance with oral intake should be fed using a temporary or permanent gastrostomy tube. o Esophagostomy and nasoesophageal tube placement is contraindicated.

Answer 288

Vomiting is the forceful ejection of upper GI tract contents and may occur as a result of gastric, intestinal, or systemic disease.

Answer 289

o The vomiting reflex is mediated by the vomiting center in the medulla. o Vagal and sympathetic afferent pathways from the GI tract transmit impulses to the vomiting center when stimulated by inflammation or overdistention. o The vomiting center also receives stimulation from within the brain: the vestibular system, cerebrum, and chemoreceptor trigger zone provide input to the vomiting center. o The latter is a specialized region (area postrema) that is located on the floor of the fourth ventricle and lacks an intact blood-brain barrier. o The chemoreceptor trigger zone is sensitive to several common drugs and toxins. o Sufficient stimulation of the vomiting center results in the initiation of vomiting. o A period of intestinal antiperistalsis is followed by a highly coordinated sequence of events, beginning with a deep inspiration and ending with a strong simultaneous contraction of the diaphragm and abdominal wall musculature and relaxation of the lower esophageal sphincter.

Answer 290

GI foreign bodies, regardless of their location.

Answer 291

More prone to developing metabolic acidosis as a result of dehydration, and mixed acid-base disorders may be seen

Answer 292

o Because reflex closure of the glottis occurs during emesis. o It is a greater risk in animals with impaired laryngeal function, typically a result of primary laryngeal disease or a decreased level of consciousness.

Answer 293

o In the acutely vomiting patient, the priority is to establish whether medical or surgical management is indicated (i.e., rule out a GI obstruction). o Abdominal radiographs have reasonable specificity in identifying the presence of obstruction and the wide availability of abdominal radiography makes them an acceptable first line test. o However, in the hands of an experienced operator, abdominal ultrasonography has been shown to have greater accuracy for identifying small intestinal obstruction than radiographs and is indicated in patients with equivocal radiographs or persistent vomiting. o Abdominal ultrasound also may assist in the identification of neoplastic obstructions and allows evaluation of the other abdominal organs to help exclude extra-GI cause of the vomiting. o If ultrasonography is not available, administration of barium and sequential abdominal radiographs may be helpful.

Answer 294

o Patients with chronic vomiting are less likely to suffer from intestinal obstruction than those that are vomiting acutely, and abdominal radiography therefore has a lower diagnostic yield. o Abdominal ultrasonography generally is preferred in these patients. It allows an evaluation of the intestinal wall thickness and layering along with a thorough evaluation of the extraintestinal structures. o It therefore proves useful in helping to decide whether medical management, endoscopy, or surgery would be the most appropriate management strategy.

Answer 295

o They may show evidence of esophageal disease if the history has led to an incorrect identification of the primary problem. o They aid in the detection of neoplastic involvement in the thorax and allow for assessment of the heart and pulmonary vasculature. o And they may show evidence of pulmonary disease such as aspiration pneumonia.

Answer 296

o Treatment of the underlying cause o Treatment and prevention of electrolyte and acid-base disturbances o Symptomatic control of further vomiting, when appropriate.

Answer 297

o The general recommendation for stable animals with recent onset of vomiting is to withhold food for 24 to 48 hours. o The rationale behind this recommendation is to avoid stimulating further vomiting and let the GI tract rest, to prevent the development of food aversions in nauseated patients, and to reduce the risk of aspiration pneumonia. o Food always should be withheld from patients with suspected GI obstruction or any patient whose signs worsen after feeding. o However, some vomiting patients may have a significantly quicker recovery when early enteral nutrition is instigated, and dogmatic enforcement of starvation may be unnecessary for some canine and feline patients. o Animals with persistent vomiting may not be good candidates for feeding tubes, and parenteral nutrition may be necessary.

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