GIT and nutrition

Question 1

How is glucose transported into the cells epithelial cells of the GIT?

Answer 1

by the mechanism of active sodium-glucose cotransport, in which active transport of sodium provides energy for absorbing glucose against a concentration dif- ference.

Question 2

How is glucose transported into cells other than the GIT epithelial cells ?

Answer 2

facilitated diffusion, made possible by the special binding prop- erties of membrane glucose carrier protein.

Question 3

What hormone increases the facilitated diffusion of glucose into the cells?

Answer 3

insulin - when larger amounts are secreted the transport of glucose increases 10 fold

Question 4

Can the cells absorb enough glucose to allow for all essential metabolic functions in the abscence of insulin?

Answer 4

with the exception of liver and brain cells, without insulin too little glucose can enter the cells to supply the required energy for metabolism.

Question 5

What is the cells carbohydrate utilisation rate determined by

Answer 5

insulin

Question 6

What is the first step of glucose metabolism once the sugar enters the cell?

Answer 6

Phsophorilation by glukokinase in the liver and hexokinase in other cells -> glucose combines with a phosphate radical

Question 7

In what tissues is glocose phosphorilation by glukokinase or hexokinase reversible?

Answer 7

iver cells, renal tubular epithelial cells, and intestinal epithelial cells. In thse cells glucose phosphatase can dephosphorylate the glucose

Question 8

Once in the cell, what two pathways can glucose take metabolically?

Answer 8

1) it can be utulised for release of energy
2) can be stored as glycogen

Question 9

Which cells are best at storing glycogen?

Answer 9

All cells can store some glycogen, however, liver (5-8%) and muscle cells (1-3%) can sote lare amounts

Question 10

What is the molecular weight of glycogen and why ?

Answer 10

The glycogen molecules can be polymerized to almost any molecular weight, with the average molecular weight being 5 million or greater. This conversion of monosaccharides into a high- molecular-weight precipitated compound (glycogen) makes it possible to store large quantities of carbohydrates without significantly altering the osmotic pressure of the intracellular fluids. High concentrations of low-molecular- weight soluble monosaccharides would play havoc with the osmotic relations between intracellular and extracel- lular fluids.

Question 11

What is glycogenesis and glycogenolysis?

Answer 11

Glycogenesis - formation of glycogen from excess glucose
Glycogenolysis - breakdown of stored glycogen to reform glucose

Question 12

What is the role of phosphorylase in glycogen metabolism?
How is the function of this enzyme controlled?

Answer 12

The breakdown of glycogen into glucose occurs through severeal phosphorulation steps caused by phosphorylase.

Phosphorylase is usually innactive and has to be activated by cyclic-AMP which is formed by hormones such as glucagon or epinepherine

Question 13

What is the role of epinepherine in energy metabolism?

Answer 13

with increased sympathetic tone, epinepherine is released from the adrenal medulla, where it forms intracellular cyclic-AMP which activated phosphorylase which kicks off glycogenolysis. This is essentiial in the muscle and liver to promote glucose formation which is needed in the flight and fight response

Question 14

What is the role of glucagon in the production of energy ?

Answer 14

When glucose levels drop too low glucagon is released by the alpha-islets of the pancreas. This stimulates cyclic-AMP production intracellularly which activated phosphorylase inducing glycogenolysis

Question 15

How many moles ATP are produced by one mole of glucose

Answer 15

38

Question 16

What is glycolysis ?

Answer 16

The most important mean of releasing energy from glucose. This consists of 10 steps which result in the production of 2 pyruvic acid molecules for each molecule of glucose. Each pyruvic acid molecule will then enter its own Krebs cycle.

Question 17

What is the transition step between glycolysis and Krebs?

Answer 17

The two pyruvate molecuse bind to Coenzyme A to form acetyl-coa which can then enter the citirc acid (aka Krebs) cycle.

Question 18

what is the tricarbxylic acid cycle?

Answer 18

the same things as citric acid or krebs cycle

Question 19

What is the krebs cycle and where does this occur?

Answer 19

The citric acid cycle is a sequence of chemical reactions in which the acetyl portion of acetyl-CoA is degraded to carbon dioxide and hydrogen atoms. These reactions all occur in the matrix of mitochon- dria. The released hydrogen atoms add to the number of these atoms that will subsequently be oxidized through the electron transport chain

Question 20

How much hydrogen is produced in the krebs and glycolysis pathways and what happens to this ?

Answer 20

4 hydrogen atoms during glycolysis, 4 during formation of acetyl-CoA from pyruvic acid, and 16 in the citric acid cycle; thus a total of 24 hydrogen atoms are released for each original molecule of glucose. they are released in packets of two, and in each instance, the release is catalyzed by a specific protein enzyme called a dehydrogenase. Twenty of the 24 hydrogen atoms immediately combine with nicotinamide adenine dinucleotide (NAD+),

Question 21

Why is niacin an essential vitamin ?

Answer 21

because NAD+ is a derivative of this

Question 22

What is the electron transport chain and where is it ?

Answer 22

IT is in the mitocondria and does it do;
(1) split each hydrogen atom into a hydrogen ion and an electron and (2) use the electrons eventually to combine dis- solved oxygen of the fluids with water molecules to form hydroxyl ions. Then the hydrogen and hydroxyl ions combine with each other to form water. During this sequence of oxidative reactions, tremendous quantities of energy are released to form ATP.

Question 23

How is ADP converted to ATP in the ETC?

Answer 23

ATP synthase, which protrudes through the mitocondrial membrane oxidatively phosphorylates the the ADP to ATP

Question 24

What are the main factors that control the quantity of ATP that is produced by the ETC?

Answer 24

1) [ATP and ADP]
- high [ATP] causes phosphofrutokinase inhibition - glycolysis rate reduction. Vice versa for ADP
2) citrate ion in the krebs cycle; an eccess inhibits phosphofrutokinae preventing glycolysis
3) Excess ATP concentration will prevent further formatio until the store is depleted (except with strenous exercise)

Question 25

Why is anaerobic metabolism not preferentially used?

Answer 25

This process is extremely wasteful of glucose because only 24,000 calories of energy are used to form ATP for each molecule of glucose metabolized, which represents only a little over 3 percent of the total energy in the glucose molecule.

Question 26

Which of the following 3 can function in an anaerobic environement? 1) glycolysis 2) Krebs 3) ETC

Answer 26

Glycolysisas the formation of 2 pyruvate does not need O2

Question 27

What are the essential products needed for aerobic energy production

Answer 27

Krebs and ETC cannot work without O2. At the end of glycolysis you end up with 2x pyruvate + 2 H+. These build up in concentration and can rate limit glycolisis through phosphofructokinase. When their concentration accumlates excessively the end products react with each other forming lactic acid

Question 28

What is the benefit of lactic acid?

Answer 28

Lactic acid diffuses readily out of the cells into the extracellular fluids and even into the intracellular fluids of other less active cells. Therefore, lactic acid represents a type of “sinkhole” into which the glycolytic end products can disappear, thus allowing glycolysis to proceed far longer than would oth- erwise be possible. Heart muscle is especially capable of converting lactic acid to pyruvic acid and then using the pyruvic acid for energy. This is beneficial in heavy exercise as large volumes of lactic acid are produced which can be used by th e heart for energy and is a salvage mechanisms during infactation When a person begins to breathe oxygen again after a period of anaerobic metabo- lism, the lactic acid is rapidly reconverted to pyruvic acid and NADH plus H+. Large portions of these substances are immediately oxidized to form large quantities of ATP. This excess ATP then causes as much as three fourths of the remaining excess pyruvic acid to be converted back into glucose.

Question 29

Other than glycolysis which other important first step pathway exists for energy metabolism;

Answer 29

Pentose phosphate patheway (phosphocluconate pathwy) which is responsibe for 30% of the glucose breakdon in the live and even more in the fat cells

Question 30

why does the pentose pathway exist?

Answer 30

This pathway is especially important because it can provide energy independently of all the enzymes of the citric acid cycle and therefore is an alternative pathway for energy metabolism when certain enzymatic abnormalities occur in cells. It has a special capacity for providing energy to multiple cellular synthetic processes.

Question 31

What key differece exists in hydrogen untilisation in the pentose phosphate pathway compared to glycolysis?

Answer 31

The hydrogen released during the pentose phosphate cycle does not combine with NAD+ as in the glycolytic pathway but combines with nicotinamide adenine dinucleotide phosphate (NADP+), which is almost identical to NAD+ except for an extra phosphate radical, P. This difference is extremely significant because only hydrogen bound with NADP+ in the form of NADPH can be used for the synthe- sis of fats from carbohydrates - hence why this pathway is common in fat cells

Question 32

What happens to the pentose pathway when glycolysis is downregulated due to cellular innactivity ?

Answer 32

he pentose phosphate pathway remains operative (mainly in the liver) to break down any excess glucose that continues to be transported into the cells, and NADPH becomes abundant to help convert acetyl-CoA, also derived from glucose, into long fatty acid chains. This is another way in which energy in the glucose molecule is used other than for the formation of ATP—in this instance, for the formation and storage of fat in the body.

Question 33

What is excess glucose stored as?

Answer 33

Glucose is prefer- entially stored as glycogen until the cells have stored as much glycogen as they can—an amount sufficient to supply the energy needs of the body for only 12 to 24 hours. When the glycogen-storing cells (primarily liver and muscle cells) approach saturation with glycogen, the addi- tional glucose is converted into fat in liver and fat cells and is stored as fat in the fat cells.

Question 34

what is gluconeogensis ?

Answer 34

When the body’s stores of carbohydrates decrease below normal, moderate quantities of glucose can be formed from amino acids and the glycerol portion of fat. This process is called gluconeogenesis.

Question 35

During prolonged fasting which processes mantain glucose levels?

Answer 35

Gluconeogenesis breaks down fats. kidneys also synthesize considerable amounts of glucose from amino acids and other precursors. About 60 percent of the amino acids in the body proteins can be converted easily into carbohydrates; the remaining 40 percent have chemical configurations that make this conversion difficult or impossible.

Question 36

What is the role of corticotropin and glucocorticoids on gluconeogenesis?

Answer 36

When normal quantities of carbohydrates are not available to the cells, the adenohypophysis, for reasons not completely understood, secretes increased quantities of the hormone corticotropin. This secretion stimulates the adrenal cortex to produce large quantities of glucocorticoid hormones, especially cortisol. In turn, cortisol mobilizes proteins from essentially all cells of the body, making these proteins available in the form of amino acids in the body fluids. A high proportion of these amino acids immediately become deaminated in the liver and provide ideal sub- strates for conversion into glucose. Thus, one of the most important means by which gluconeogenesis is promoted is through the release of glucocorticoids from the adrenal cortex.

Question 37

What is the normal Bg of a person?

Answer 37

90mg/dl during fasting, 140mg/dl after a large meal.

Question 38

what are the layers of the GIT ? what do these look like on US?

Answer 38

Same throughout; - Mucosa (hypoechoic) - Submucosa (hyperechoic) - Muscularis (Hypoechoic) - Serosa (hyperechoic)

Question 39

what are the 4 major activities of the GIT?

Answer 39

1) motility = moving food from mouth to rectum - mixes and reduces size of food - rate is regulated to optimize digestion and absorbtion 2) secretions = juices from dalivary gland, pancreas and liver added to GI tract - enzymes, electrolytes, fluid and mucus 3) Digestion -= food digested into absorbable molecues 4) absorbtion - nutrients, electrolytes, H20 are absobed from the lumen to the blood stream

Question 40

What are the main regulators of function?

Answer 40

- innervation - hormones - autocrine secretions - neurocrine secretions

Question 41

What nerves innervate the GIT

Answer 41

1) Autnomic - extrinsic 2) extrinsic component - sympathetic - parasympathetic 3) intrinsic - enteric nervous system

Question 42

what is the 2 key parasympathetic nerves of the git. Are these efferent or afferent? What stilmutea these nerves ? What do they do? What types of postganglionic neurons do they have ?

Answer 42

Two key nerves; 1) vagus 2) pelvic VAGUS Mainly afferent - take sensory info from mechano/chemo receptors to CNS Some efferent = take motro info from CNS to muscle/secretory/endocrine cells Two types of postganglionic neurons 1) peptodergic - release peptides like substance P or VIP 2) cholinerci = relese ACh

Question 43

where do parasympathetic nerves in the GIT synapse?

Answer 43

Long preganglionic nerve fibers which synapse on ganglia in the GI walls. Remeber parasympathetic is a longer word than sympathetic hence long ganglia

Question 44

what are the 2 types of parasympathetic post ganglionic neurons

Answer 44

Two types of postganglionic neurons 1) peptodergic - release peptides like substance P or VIP 2) cholinerci = relese ACh

Question 45

what is the sympathetic innervation of the GIT What are the 4 sympathetic ganglia? Is this afferent or efferent ?

Answer 45

short preganglionic neurons which synapse on ganglia outside of the GIT (sympathetic is shorter than parasympathetic, hence, shorter ganglia. The 4 sympathetic ganglia are; Celiac, superior mesenteric, inferior mesenteric, hypogastric The postganglionic fibers (release NE) then synapse on the plexus or directly on smooth muscle, endocrine or secretory cells Sympathetic innervation is 50:50 efferent:afferent

Question 46

what are the 4 sympathetic ganglia?

Answer 46

Celiac, superior mesenteric, inferior mesenteric, hypogastric

Question 47

what proportion of the Sympathetic innervtion of the GI tract is afferent or efferent

Answer 47

it is 50:50

Question 48

draw a diagram of the GIT extrensic nervous system, what it secretes and where ?

Answer 48

Question 49

What is the enteric nervous system?

Answer 49

this is the intrinsic NS. Can direct all functions of the GI tract in abscence of the extrensic. It is modulated by para and sympathetic innervation It is enterely in plexuses.

Question 50

Tabulate all of the GIT neurocrines, the source of the these and what their actions are?

Answer 50

Question 51

what are the 3 main categories of GI peptides

Answer 51

1) hormones -> endocrine cells of GIT - substances secred into the portal system, picked up by the liver and then go and work on cells elsewhere 2) pacrines -> endocrine cells of GIT but their target cell is close and they reach this by diffusion 3) neurocrines -> nerve cells that are transported by an action potential

Question 52

what are the 4 main GI hormones ?

Answer 52

1) gastrin 2) cholicystokinin 3) secretin 4) glucose dependent insulinotropic peptid (also known as gastric inhibitory peptide or GIP)

Question 53

what is a candidate hormone and what are examples (less important question)

Answer 53

Molecules that don't met all of the criteria of what a hormone is; - Motalin, pancreatic polypeptide, serotonin, somatostatin, ghrelin, leptin, GLP-1, GLP-2, enteroglucgon, peptide YY

Question 54

tabulate the GI hormones, what family they belong to, site of secretion, stimulus of secretion and action

Answer 54

Question 55

Describe the key features of gastrin; Cells secreted from? Stimuli for production? Actions?

Answer 55

secreted by G cells in the stomach. when a meal is eaten. - Stimuli for production are; are products of protein digestion (as), stomach distension, vagal stimulation, neuroen docrine-releasing peptide (bombesin) - Stimuli for decreased production are; low pH, hastric contents, somatostatin Actions 1) stimulates H+ secretion by gastric parietal cells (makes stomach more acidic) 2) stimulates growth of gastric mycosa

Question 56

what is a gastrinoma? What are the symptoms of this

Answer 56

gastrin secreting tumour usually in non-B cell pancrease -> results in increased H+ secretion by parietal cels, get ulcer, antral hypertrophy and statorrhea/diarrhoea (excessive gastrin inactivates lipase)

Question 57

why is low pH an inhibitor of gastrin ?

Answer 57

hastrin secretes H+ so once the stomach is acidic enough it will inhibit the production of more acid as its not needed

Question 58

if you suspect a gastrinoma what test could you run and what are the limitations ?

Answer 58

Texas A&M can measure gastin. 0.5 ml fasting (12-18 hours) non-hemolyzed serum The reference interval for serum gastrin concentration in dogs using this assay was established as <28 ng/L, but most normal dogs will have undetectable serum gastrin concentrations. The test is recommended in chronic vomiting where there is suspicion of a gastrinoma. Until a more precise cut-off value for the diagnosis of a gastrinoma can be determined, recommend using the traditional cut-off value of 10 times the upper limit of the reference range, or >280 ng/L.

Question 59

Can proton pump inhibitors affect gastrin secretion and testing though the Texas A&M test?

Answer 59

Giving PPI results in hypergastrinemia in chronic enteropathies, but the levels do not reach those where you may get a false positive result for a gastrinoma on the texas A&M test (ie recomended cut off is 10x the reference interval for gastrinoma)

Question 60

what is the role and stimuli of secretion for cholcystokinin (CCK)? What cells secrete this? And where? What receptors does this bind to? Stimuli of secretion?

Answer 60

Essential for fat digestion and absorbtion. It looks like gastrin and will have some gastrin activity. 2 receptors; - CCKa--only recognises CCK - CCKb- recognizes CCK and gastrin Secreted by I cells of the duodenum and jejunal mucosa Stimuli of secretion; monoglycerides and fatty acids, small peptides and AAs (aka fats and proteins) End goal = make sure that the right pancreatic enzymes + bile salts are secreted to aid in digestion and absorbtion

Question 61

what are 5 main actions of CCK ?

Answer 61

1) contract the gallbatter and relaxation of the sphincter of Odi -> ejection of bile - > essential for emulsification of fat 2) Secretion of pancreatic enxymes (lipase, protesase and amylase) 3) Secretio fo bicarb from pancreas 4) growth of exocrine pancreas and GB 5) inhibit gastric emptying (fat takes a LONG TIME to be digested)

Question 62

what are amylases, proteases and lipases

Answer 62

Amylase -> break down varbs Protease -> break down protein Lipase -> break down fat

Question 63

What is the secretin ?

Answer 63

Secreted by S cells of the duodenum (S for Secretin) Funciton to promote secetion of pancreatic and billiary HCO3 -> which neutralises H+ in the SI (don't want all the stomach acid produced by a gastrin to break down food in the SI). Secretin is inhibited by the effects of Gastrin on parietal cells (turns off H= secretion and tissue growth)

Question 64

why is secetin essential for fat digestion when fat requires a lot of digestion to be broken down?

Answer 64

Bicarb is needed for fat digestion as pancreatic lipase works best between pH of 6-8, and lipases do NOT work if pH<3. Without this the pH would be too low from gastrin. also increases secretion of pancreatic lipases.

Question 65

what are parietal cells;

Answer 65

Parietal cells, also known as oxyntic cells, are specialized epithelial cells found in the stomach lining. They play a crucial role in gastric acid secretion, which is essential for digestion

Question 66

what is the role of glucose-dependent insulinotropic peptide (GIP)? What are its functions? Where is it secreted from?

Answer 66

One of the 4 fondamental GIT hormones Secreded by K cells of the duodenum and jejunum. Secreted in response to glucose, AA, and FA. Functions; 1) stimulation of insulin secretion by B-cells (referred to as an incretin because it stimulates insulin secretion) 2) inhibition of gastic H+ secretion 3) inhibition of gastric emptying

Question 67

Why is PO glucose better utilised than IV ?

Answer 67

when you injest glucose, you have release of glucose-depndent insulinotropic peptide (GIP). This promotes insulin secretion from the ß cells allowing the glucose to be uptaken by the cells. Iv glucose will only result in insulin seretion when this directly binds ß-cells in the pancreas

Question 68

What is role of motilin?

Answer 68

this is a cadidate hormone secreted by the duodenum during fasting and increases GII motility and initiates interdigestive myoelectric complexes

Question 69

What are the two main GI paracrins?

Answer 69

1) somatostatin 2) histamine

Question 70

From secretion, how do paracrins reach the target tissue;

Answer 70

via capillaries and act locally. They travel short distances and do NOT enter the systemic circulation

Question 71

What is the role of somatostatin?

Answer 71

SOMATOSTATIN SHUTS IT DOWN - key buzz phrase to remember Inhibits hormone release, especially insulin, glucagon, growth hormone, tsh. It also reduces GIT motility and secretion SECRETED by D (down) cells of the GI mucosa in response to decreased lumen pH. Also (less important) by the hypothalamus and by delta endoctine pancreatic cells INHIBITED by; secretion of other GI hormones and inhibits gastric H+ secretion

Question 72

what is the role of histamine? What cells secrete this?

Answer 72

sereted by enterochromaffin like cells (H+ secreting region of the stomach) Histamine (along with gastrin) stimulates H+ secretion by gastric parietal cells (bind H2 receptor)

Question 73

where are enterochomaffin like cells found?

Answer 73

in the acid secreting region of the stomach

Question 74

What are the main GI neurocrines?

Answer 74

Acetylcholine and norepinepherin

Question 75

What is the major area of the body responsible for the regulation of satiety?

Answer 75

Hypothalamus - satiety center -> inhibits appetite even in the presence of food - Feeding center -> increases appetite - Arcuate nucleous of the hypothalamus gives info to these centers via anorexigenic and oregigenic neurons

Question 76

What are the main neuropeptides involved in signaling of appetite ?

Answer 76

- POMC (proopiomelanocortin) -> decreases appetite -> released by anorexigenic neurons - Neuropeptide Y -> increases appetite ->relesed by orexigenic neurons

Question 77

What substances influence apetite:

Answer 77

KEY ONES YOU MUST KNOW FIRST 1) Leptin -> DECREASE appetite and INCREASES energy expenditure (Leptin-LEss of an aPeTIte Now, and LiPid cells secrete leptin in proportion to the amount of fat stored in adipose) 2) Insulin -> similar to leptin -> DECREASES eppetite 3) Ghrelin -> INCREASES apetite and food intake LESS IMPORTANT AND SECONDARY GLP-1; DECREASES appeite Peptide YY (PYY): DECREASES appetite

Question 78

Why would insulin decrease appetite?

Answer 78

insulin is secreted when there are plenty of available nutrients, and as a result more is not needed, hence its role in supressing appetite

Question 79

Ghrelin secretin occurs when and how? What is a key stimulator of Ghrelin?

Answer 79

secreted by gastic cells BEFORE ingestion of a meal. It stimulates orexigenic neurons and inhibits the anorexigenic neurons. It is stimulated by weight loss and starvation

Question 80

what is a stimulus for leptin secretion and where does it act?

Answer 80

Sensed fat level -> leptin secreted by fat cells -> crosses BBB -> acts on arcuate nucleous of hypothalamus -> stimualtes anorexigenic neurons and inhibits orexigenic neurons

Question 81

Of the 5 appetite influencing substances, which decrease appetite and which ones increases it?

Answer 81

Ghrelin is the ONLY INCREASOR Leptin, insulin, GLP-1 and Peptide YY ALL DECREASE `

Question 82

How can we stimulate hunger in patients and what pathway does this take?

Answer 82

Entice is a ghrellin receptor agonist which stimulates hunger and food intake in patients

Question 83

What is the role of kidney disease in hunger control;

Answer 83

recent study has shown an increase in adoponectin and leptin in dogs with non proteinuric kidney disease which may exacerbate weight loss through reduced food intake

Question 84

The GIT tract is made of what muscle type?

Answer 84

All is smooth muscle except the larync, cranial esophageal sphincter and parts of the oesephagous and external anal sphincter

Question 85

Glucose and galactose are transported from the intestinal epithelial cells to the blood by facilitated diffusion through what transporter? a) GLUT 2 b) GLUT5 c) SGLT1 d) SGLT2

Answer 85

a) glut 2

Question 86

Trypsin is made into active trypsin by what important brush border enzyme? Enterokinase Lipase Pepsinogen Phospholipase A2

Answer 86

enterokinase

Question 87

Pancreatic lipase is secreted as an active enzyme and hydrolyzes _________ to ___________ and ____________. 1 triglyceride molecule; 1 monoglyceride molecule; 2 fatty acid molecules 1 amino acid; 1 cholesterol; 1 fatty acid molecule 1 phospholipid molecule; lysolecithin; 2 fatty acid molecules 1 chylomicron molecule; 1 phospholipid molecule; 1 apoprotein molecule

Answer 87

1 triglyceride molecule; 1 monoglyceride molecule; 2 fatty acid molecules

Question 88

what is the orientation of the muscle fibers in the GIT and why?

Answer 88

External layer is longitiudinal while internal is circular -> this allows for peristalsis to occur as the tissue milks the food aborally. The longitudinal layer crunches the intestine togeter while the circular propels the chyme forward.

Question 89

what are the two types of muscle contraction ?

Answer 89

1) phasic (tension goes up and then relaxes in a wave like form) -> this occurs in the oesophagous, gastric antrum - aka places than need to mix and propel food forward 2) Tonic contraction (constant contra`ction without relaxation) -> occurs in orad stomach, LES, illeocolic sphincter, internal anal sphincter (ie sphincters should be closed until they are told to relax)

Question 90

How do sphincters stay closed?

Answer 90

Specialised circular muscle - at rest they maintain a higher pressure than the adjacent regions thereby staying closed and preventing flow. For something to move past, the sphincter must relax

Question 91

What are slow waves in the muscles of the GIT?

Answer 91

These are oscillating depolarization and representations of t›he smooth muscle cells. These are not true depolarization though. These are sub-threshold depolarization which allow the muscle to maintain its rigidity in a closed position, ie tonic contraction. Waves that meet/exceed threshold result in phasic contraction

Question 92

where do slow waves originate from ?

Answer 92

Interstitial celss of Cajal

Question 93

what is the intrinsic rate of slow action potentials?

Answer 93

Depends on the location. for example they are low in the stomach (3 waves per min) but high in the illeum (12 slow waves) sets the frequency of AP's thus contractions

Question 94

other than the git where are slow waves found?

Answer 94

Nowhere else

Question 95

what ion channels are involved in slow wave depolarisation and repolarisation ?

Answer 95

Depolarisation -> opening of Ca channels which causes Ca to enter and depolarise the membrane Repolarisation -> opening of K channels and outward K current

Question 96

if there is a slow wave, can depolarisation happen?

Answer 96

yes, depolarisation happens when the slow wave hits the membrane potential

Question 97

What are the 3 phases of pharyngeal motility?

Answer 97

1) prehension -> with teeth and tongue 2) Mastication -> breaking food down and coating with saliva 3) Deglutition -> rostral to caudal pharyngeal contractions propel food bolus to the base of the tongue to cricopharyngeal/cranial esophageal sphincter opening a) sphincter relaxes b) bolus pases into cranial esophageal body c) cranial esophageal sphincter contract and pharyngral muscles relax

Question 98

what are the major nervous system structures involved in Oropharyngeal motility?

Answer 98

Medulla, vagus and glossopharyngeal

Question 99

Is swallowing voluntary or involuntary

Answer 99

initially voluntary but once in the oropharyngeal area it is involuntary

Question 100

abnormalities in the oropharyngeal phases results in what clinical findings ? What are the two mechanisms of disease for oropharyngeal disease ?

Answer 100

Two main clinical signs are dysphagia and hypersalivation. Two mechanisms can be; 1) functional -> mainly neuromuscular 2) Morphological -> strictures, FBs, neoplasia, trauma, inflammation of the oral cavity and pharynx

Question 101

fill in the clinical signs and disease location table

Answer 101

Question 102

what type of muscle makes up the oesophageal sphincters and oesophagous

Answer 102

UES (upper es sphinc) = crycopharyngeal is striated esophageal body in dog is all striated. In cat 1/3 to 1/2 distal is smooth. Lower oesophageal sphincter = gastroesophageal is smooth

Question 103

What is the name for the upper and lower esophageal sphincter?

Answer 103

UES= crocopharyngeus LES= Gastroesophageal

Question 104

(VI) what nerve innervates the oesophagous and the sphincters ?

Answer 104

vagus Somatic branches -> glossopharungeal, pharyngeal and recurrent laryngeal (these innervate striated muscle) Autonomic branches -> innervate smooth muscle

Question 105

what is primary and secondary peristalsis ?

Answer 105

swallowing triggers primary which moves the food back and that kicks off sec

Question 106

What is esophageal dismotility

Answer 106

This is when there is lack of synchronization between swallowing, primary and secondary peristalsis, and sphincter opening

Question 107

Hallmark of esophageal dysmotility ?

Answer 107

Regurgitation!! Also, painful swallowing, dysphagia, multiple swallowing attempts, excessive salivation, changes in appetite

Question 108

What are the 5 distinct anatomical compartments of the stomach ?

Answer 108

1) cardia 2) fundis, 3) body 4) antrum 5) pylorus

Question 109

How many layers of muscle are there in the stomach, what is their thickeneses, and what is the origtantion and name

Answer 109

1) Outer longitudial 2) Middle circular 3) Inner oblique Thickness of the muscle increases from proximal to distal

Question 110

what are the regions of the stomach on the image ?

Answer 110

Question 111

How many and what are the physiological stomachs? What are the roles of these section ? What anatomical parts of the stomach make up these physiological sections and what are distinguishing features

Answer 111

there are 2 1) Proximal (orad) - cardia, fundus and first 1/3 of body - has TONIC contractions (contracts until told to relax) - thin wall - Responsible for receptive relaxation which allows food to accumulate -> mediated by vagus and VIP 2) Distal (Caudad)- antrum, pylorus and second 2/3rd of the body - has PHASIC contraction - Thick wall - Responsible for mixing and digestion of food - Contractions push food into the SI

Question 112

1)why does the distal physiologic stomach have phasic contraction? 2) why does proximal have tonic contractions

Answer 112

1) so that it can milk food into the SI. 2) it goes through waves of contraction to mix the food. It also needs to relax so that it can accomodate food

Question 113

what are the 3 components of gastric motility?

Answer 113

1) relaxation of orad stomach - to receive food 2) contraction - help mix food 3) gastric emptying

Question 114

(VI) the orad stomach relaxes in response to what nerve?

Answer 114

the vagus nerve and VIP

Question 115

contraction phase of the stomach is determined by what? how often does it contract? what hormones and neurons effect this?

Answer 115

Slow waves affect this. They are not affected by neurons or hormones. They contract at 3-5 waves/min=3/5 contractions per minute

Question 116

during contraction of the stomach, why is all of the food not extruded into the intestine in one go? what allows for trickling of food out into the SI

Answer 116

The slow waves (3-5min) cause contractions, but each wave also causes the pyloric sphincter to contract. As a result, the waves of peristalsis and food bolus are interrupted by the sphincter being forced shut

Question 117

(VI) How does neural input and hormonal input impact gastric contraction action potential frequency and force?

Answer 117

- Parasympathetic stimulation, gastrin, motalin = increase the frequency of action potentials and force of gastric contraction(i.e. when you are RESTING and DIGESTING) - Sympatheric stimulation, secretin and GIP =DECREASE the frequency of action potentials and force of contraction (when fighting you are not digesting

Question 118

why are secretin and GIP upregulated in sympathetic stimulation ?

Answer 118

Secretin and GIP are important for digestion that occurs in the SI, and thus they don't want more gastric material until thats occurred

Question 119

what are migrating myelotric comprexes (MMC)?

Answer 119

These are sfasting periodic contractions mediated by motalin. The role of these is to clear the stomach of any residual material. They are only found in dogs

Question 120

what are myoelectric spike complexes?

Answer 120

These are weaker versions of MMC's, and consist of weaker migrating complexes found in cats and rabbits.

Question 121

what steps have to occur during gastric emptying?

Answer 121

1) need to allow for neutralisation of gastric H+ in the duodenum 2) Neetd to allow time for adequate digestion and absorbtion

Question 122

how is the rate of gastric emptying vary based on the type of nutrient, density of the nutrient, and acidity ? List from fast to slow

Answer 122

Liquids > solids >indigestible solids Carbohydrates >proteins > lipids Neutral pH>acidic/alkaline (rare for it to be alkaline due to the acid in the stomach)

Question 123

how does temperature affect gsastric emptying?

Answer 123

Hot and cold are slower than body temp

Question 124

What are the 2 MAJOR factors that slow gastric emptying? What physiological responses are there in response to this?

Answer 124

1) FAT - it takes time to digest fat. CCK is involved in digesting fat, and when there is a lot of fat, CCK is upregulated. CCK will then slow down gastric emptying 2) low pH (lot of H+); this has to be neutralised as low pH deactivates enzymes. Receptors in the duodenum sense low pH -> allows pancreatic HCO3 to neutralize which is essential for pancreatic enzyme function

Question 125

what are the 3 main roles of the SI?

Answer 125

1) mix enzymes and bicarb with chyme 2) expose nutrients to the mucosa for absorbtion 3) move unabsorbed material to the LI

Question 126

Where do slow waves occur?

Answer 126

stomack SI - > these are a bit faster

Question 127

What hormone regulates slow waves and MMC?

Answer 127

No hormones regulated slow waves MMC are regulated by motalin

Question 128

what drugs are used for increasing interstinal motility and how does these work ?

Answer 128

Erythromycin and azithromycin are motilin analogues which increase migrating myelogenic complexes (MMC).

Question 129

What is the nervous control of SI motility

Answer 129

Parasympathetic -> vagus Sympathetic-> from ganglia Enteric nervous system - > regulates the pattern of contraction

Question 130

what is segmented vs peristaltic contraction?

Answer 130

Segmented- > acts to mix chyme and enxymes and does not move food forward (crashes and relaxes) Peristaltic -> wave moves oral->aboral moving food forward

Question 131

(VI) what causes the segmented and peristaltic contractions to initiate and what transmitters are involved? When a bolous is moving through the intestine, what neurotransmitters work aborally and orally to the bolus?

Answer 131

1) ECL (enterochromaphin like cells) in the intestinal mucosa sense bolus 2) 5-HT (serotonin) is released -> peristaltic reflex starts 3) behind the bolus; excitatory neurotransmitters ( ACh, Substance P, neuropeptide Y) cause contraction 4) in front of bolus: inhibitory signals (VIP, NO) cause relaxation

Question 132

why does maropitant have visceral analgesic properties?

Answer 132

It is a substance P inhibitor. When there is a bolus of food, we have exitatory neurotransmittor release (substance P, neuropeptide Y, ACh) which cause contraction -> the stronger the contraction the more pain

Question 133

where is the vomiting center?

Answer 133

medulla of the brain - collects info from a lot of places whcih can cause vomiting like medulla, stomach, SI, chemoreceptor trigger zone etc.

Question 134

what physiological differences are there in vomiting and wretching?

Answer 134

Both coordinated by the medulla; Vomiting = LES and UES are open Wretching= LES open but UES CLOSED -> the contents as a result cannot pass past the UES hence nothing is vomited out

Question 135

what is the role of the large intestine ? What segments is this divided into ? What are the distinguishing charachteristics of the waves of peristalsis in this region?

Answer 135

1) extract water and electrolytes - proximal colon -> slow and weak contractions to allow for absorbtion 2) controls defecation - descending colon -> fast and strong contractions to push faeces out

Question 136

what are haustration contractions in the proximal colon? Do they happen in the distal colon ?

Answer 136

These are segmental contractions. They break up the bolus so that it is exposed to the mucosa of the ascending colon so that water can be absorbed. These can happen in the distal colon but this is mostly to break up the bolus so that it does not arrive all at once

Question 137

what are the steps that occur in defecation ?

Answer 137

1) rectum fills with faecal material -> smooth muscle contracts and internal anal sphincter relaxes (rectosphincter reflex) -> this is a true sphincter 2) External anal sphincter still contracted (is striated muscle and under voluntary control) this no defecation until time permits -> this is under voluntary control (pudendal nerve)!

Question 138

What is the gastrocolic reflex?

Answer 138

distension of the stomach increases motility of the colon. Mediated by CCK and gastrin

Question 139

what is the rectosphincter reflex?

Answer 139

it is a reflex where dilation of the smooth muscle of the recutm contracts and the internal anal sphincter relaxes. This will not allow defecation as the external anal sphincter is under voluntary control

Question 140

(VI) n the gastrointestinal tract, slow waves are a unique characteristic that provides tonic contraction of the smooth muscle. At the peak of the slow wave, if the membrane potential is maximally depolarized and meets threshold, an action potential occurs. Depolarization is caused by opening of what channels? A) Calcium channels B) Chloride channels C) Potassium channels D) Sodium channels

Answer 140

a

Question 141

(VI) During peristaltic contractions in the small intestine, what substance contributes to relaxation of the intestinal smooth muscle in front of (aborad) the food bolus? A) Acetylcholine B) Neuropeptide Y C) Substance P D) VIP

Answer 141

VIP

Question 142

(VI) Pick if the below substances increase or decrease appetite. A) Leptin: DECREASES/INCREASES appetite B) Insulin: DECREASES /INCREASES appetite C) GLP-1: DECREASES/INCREASES appetite D) Ghrelin: DECREASES/INCREASES appetite a E) Peptide YY (PYY): DECREASES/INCREASES appetite

Answer 142

A) Decrease B) Decrease C) Decrease D) Increase E) Decrease ONLY GHRELLIN INCREASES

Question 143

(VI) Pick the correct neurotransmitter. Postganglionic neurons of the parasympathetic NS within the GI tract release peptides or (ACETYLCHOLINE / NOREPINEPHRINE) Postganglionic neurons of the sympathetic NS within the GI tract release (ACETYLCHOLINE / NOREPINEPHRINE)

Answer 143

1) ACETYLCHOLINE 2) NOREPINEPHRINE

Question 144

Main secretion organs of the GIT?

Answer 144

Salivary glands Gastric mucosa Exocrine pancreas Liver

Question 145

Fill in the secretion table

Answer 145

Question 146

2 major types of salivary secretion

Answer 146

Serous = alpha-amylase to start digestion of starches, water, ions, electrolytes Mucous = lubrication

Question 147

name the 3 salivary glands ? What type of saliva do they secrete

Answer 147

Parotid = serous secretion only Submandibular = mixed → serous and mucous Sublingual = mixed → serous and mucous

Question 148

What is the innervation of the salivary system and what determines secretions?

Answer 148

Salivary glands have BOTH parasympathetic and sympathetic control! Parasympathetic dominates but saliva production is stimulated by BOTH

Question 149

Parasympathetic innervation of the salivary glands is performed by which nerves and what effect does this have ?

Answer 149

When parasympathetic in control = increased flow rate - Facial and glossopharyngeal CNs - Postganglionic parasympathetic neurons release ACh which interacts on muscarinic receptors

Question 150

Sympathetic innervation of the salivary glands occurs due to which nerves and what effect does this have?

Answer 150

When sympathetic in control = more viscous (thicker), high in protein Innervation from T1-T3 segments Postganglionic sympathetic neurons release NE which talks to B-adrenergic receptors

Question 151

draw a schematic of the regulation of saliva secretion

Answer 151

Question 152

Describe the cellular structure of the salivary gland and what each cell type does;

Answer 152

Acinar cells: make initial saliva which is water, ions, enzymes, mucus Intercalated duct (just a tunnel) Striated duct: lined with ductal cells which MODIFY the saliva (Na and Cl removed, K and HCO3 added) Myoepithelial cells = eject the saliva

Question 153

(VI) describe the formation of saliva;

Answer 153

1) Acinus makes initial isotonic fluid -- has approximately the same lytes as plasma 2)Ductal cells modify initial saliva a) 3 transporters in lumen: Na-H exchange, Cl-HCO3 exchange, and H-K exchange (HCO3, K, and H out, while Cl, Na, H in) b) 2 channels in basolateral membrane i) Na-K ATPase ii) Cl channel 3) NET EFFECT = NaCl absorption and secretion of K+ and HCO3- (NaCl greater) 4) Final product = hypotonic b/c ductal cells are impermeable to water

Question 154

(VI) How does flow rate affect the composition of saliva?

Answer 154

High flow rates - no time to alter saliva so it looks like it did when the acinar cells made it; - higher concentration of NaCl (less time to reabsorb it!) - lower concentration of K (less time to secrete it!) Low flow rate - lots of time to modify the saliva - lower concentration of NaCl (more time to reabsorb it!) - higher concentration of K+ (more time to secrete i!) **Bicarb doesn’t listen to this! Remember it’s secreted by ductal cells thus you’d think its concentration should be high at low flow rates...but it’s concentration is lowest at low flow rates and highest at high flow rates b/c secretion of bicarb is selectively stimulated when saliva production is stimulated. So more flow rate = more HCO3 - secretion $

Question 155

(VI) Describe the two gland types involved in gastric secretions and what cells make up each section?

Answer 155

Oxyntic glands = in body of stomach - Parietal cells = Secrete HCl and intrinsic factor - Chief cells = Secrete pepsinogen Pyloric glands = in antrum of stomach - G cells = Secrete gastrin into circulation - Mucous neck cells =Make Mucus, HCO3-, and pepsinogen

Question 156

Draw a table and diagram of the location of the cell gastric secretion cell types, location and secretion

Answer 156

Question 157

(VI) what cells secrete HCL

Answer 157

Parietal cells

Question 158

(VI) what is the role of HCL in the GIT?

Answer 158

make very acidic environment so pepsinogen (made by chief cells) can become pepsin (starts protein digestion)

Question 159

(VI) what cells produce and what is the role of pepsinogen?

Answer 159

Pesinogen is made by chief cells and with exposure to acid it can become pepsin which starts protein digestion

Question 160

(VI) what is the mechanism of HCL secretion by parietal cells?

Answer 160

1) H+ secreted into lumen via H+K+ ATPase 2) HCO3- is absorbed into the blood NET EFFECT = secretion of HCl (into stomach lumen) and absorption of HCO3- into blood

Question 161

(VI) How do proton pump inhibitors work?

Answer 161

PPIs block H+K+ATPase in the parietal cells. This proton pump is what secretes HCL into the stomach

Question 162

What is an alkaline tide?

Answer 162

Post eating a meal, the blood pH becomes more alcaline as HCO3 is secreted into the blood stream. HCO3 is secreted by the HCO3-Cl pump on the capillary side of gastric parietal cells, and is essential in giving Cl to the cell which will be secreted into the lumen so that it can bind to H+, also secteted by parietal cells (carbonic anyhydrase pathway) to form HCL

Question 163

(VI) Parietal cells secrete HCO3 into the circulation when acidifying the stomach. where is this HCO3 produced

Answer 163

HCO3 is a byproduct of H+ production by the parietal cells. The parietal cells have carbonic anyhydrase which produces H2HCO3 from CO2+H2O, after which one hydrogen ion is cleaved off, secreted into the lumen of the stomach, leaving HCO3 behind that is then secreted into the blood via the HCO3-Cl cotransporter

Question 164

(VI) What increases HCl secretion by PARIETAL cells? KNOW THIS. What medications blocks these

Answer 164

1) Histamine - INCREASES HCl secretion a) Released from Enterochromafin life (ECL) cells and mast cells b) Binds to H2 receptors on parietal cells i) Blocked by cimetidine / famotidine 2) ACh - INCREASES HCl secretion a) Released by vagus nerve b) Binds muscarinic (M3 receptors) on parietal cells i) Blocked by atropine c) Indirect stimulation-- stimulates ECL cells to make histamine 3) Gastrin - INCREASES HCl secretion a) Released into circulation by G cells b) Binds CCK-b receptors on parietal cells c) Indirect stimulation - stimulates ECL cells to make histamine

Question 165

What are the sites of action of PPI, Famotidine, cimetidine and atropine

Answer 165

PPI; H+K+ ATPase in the parietal cells Famotidine/cimetidine; H2 receptors on parietal cells reducing histmine release Atropine; binds to muscarinic M3 receptors on parietal cells preventing ACh from binding thus reducing acid secretion

Question 166

draw a diagram showing the main pathways of acid decretion and the inhibition of these

Answer 166

Question 167

(VI) how is HCL secretion regulated

Answer 167

Vagus nerve stimulates parietal cells (via ACh) and G cells (via GRP) Parietal cells make HCl, G cells make gastrin Gastrin further stimulates HCl production by acting on parietal cells

Question 168

(VI) what are the phases of HCL secretion ?

Answer 168

1) Basal phase -> occurs in abscence of all gastric/intestinal stimulation 2) Cephalic phase -> 30% of HCL in reponse to smell/tast/chew/swallowing/conditioned antivipation of food Vagus- > ACh->parietal-> HCL 3) Gastric phase -> 60% of HCL Stimuli= stomach distension, peptides, AA Direct path; Distension -> vagus-> parietal/G-cells Indirect path; AAs -> G cells ->Gastrin 4) Insteinal ->10% HCL stimuli = proteins, distension

Question 169

How do we have the inhibiton of HCL secretion ?

Answer 169

1) Major inhibitory control = decrease pH of gastric contents 2) somatostatin (secreted by D cells) - Direct; binds to parietal cells - indirect; inhibits histamine and gastrin release 3) Prostaglandins (prostaglandin E2) - antagonizes histamine

Question 170

(VI) How does the stomach protect its self from all of the acid? 5 steps

Answer 170

1) Mucus - secreted by mucous neck glands 2) HCO3- - secreted by gastric epithelial cells a) Helps neutralize H+ and any pepsin that accidentally gets activated 3) Prostaglandin E2 a) Maintains mucosal barrier and stimulates bicarb secretion 4) Mucosal cell renewal 5) Mucosal blood flow

Question 171

(VI) decribe pepsinogen secretion and activation

Answer 171

1) Inactive precursor to pepsin 2) secreted by chief cells and mucous cells 3) Parietal cells secrete HCl→ lowers pH→ inactive pepsinogen made into pepsin→ starts protein digestion 4) Major stimulus = VAGUS a) also stimulated by H+ Know chief cells esp

Question 172

What is the intrinsic factor, and where is it secreted?

Answer 172

This is needed for B12 absorbtion in the ileum - humans secrete it from Parietal cells - Dogs and cats, most is secreted by the pancreas

Question 173

How much of the pancreas is exocrine?

Answer 173

90%

Question 174

what anatomical differences are there between dog and cat pancreases?

Answer 174

dogs’ pancreatic duct does not empty into the common bile duct; cats’ pancreatic duct merges with the common bile duct

Question 175

(VI) what are the two main cell families of the exocrine pancreas?

Answer 175

Acinar cells = secrete digestive enzymes Ductal cells = secrete water and bicarbonate

Question 176

(VI) what is the innervation of the pancreas? what does nerve stimulation result in?

Answer 176

Innervation -sympathetic = inhibits secretion -parasympathetic = VAGUS = stimulates secretion

Question 177

(VI) 3 major functions of pancreatic juice

Answer 177

1) Neutralize the material in the duodenum 2) Provide enzymes for digestion of food 3) Secrete intrinsic factor (mediates B12 absorption in distal GI)

Question 178

(VI) in what area of the pancreas is the endocrine component found and what are the 4 main cell types?

Answer 178

Islets of Langerhans = clumps of endocrine pancreas 4 major cell types in these islets Alpha cells - glucagon ß cells - insulin Delta cell - somatostatin and gastrin PP cell - pancreatic polypeptide

Question 179

(VI) where are the exocrine Pancreatic Secretions ( Enzymatic Portion) formed? What enzymes are produced? Where are the enzymes stored?

Answer 179

1) Enzymatic component of pancreatic secretion made by acinar cells a)Amylase - secreted active i) Hydrolyzes starches b) Lipases / Phospholipases - secreted active i) Lipase = hydrolyzes triglycerides ii) Phospholipase = hydrolyzes phospholipids c) Proteases - secreted inactive and activated in duodenum i) Hydrolyzes proteins ii) Ex: trypsinogen → trypsin 2) Enzymes concentrated and stored in zymogen granules until stimulated to secrete (mainly parasympathetic and CCK) a) ENTEROKINASE activates trypsinogen to trypsin which then activates all the other zymogens

Question 180

describe the Formation of Pancreatic Secretions (Aqueous Component)?

Answer 180

Aqueous component is made by the ductal cells 1) Contains Na, Cl, K, HCO3 2) Na and K similar to plasma concentrations 3) Cl and HCO3 vary w/ flow rate i) High flow rate = high concentration of HCO3 and low Cl- concentration ii)Low flow rate = low concentration of HCO3 and high concentration of Cl- 4) Net result = secretion of HCO3 and absorption of H+

Question 181

(VI) what part of the pancrea produces the aqueous component?

Answer 181

Ductal cells

Question 182

What is the net result of production of the aqueous component of pancreatic solutions?

Answer 182

secretion of HCO3 and absorption of H+

Question 183

(VI) what regulates the secretion fo the aqueous and enzymatic proportion of the pancreatic secretions?

Answer 183

Aqueous portion - Stimulated by arrival of H+ in the duodenum, secretin, and VIP Enzyme portion - Stimulated by digestion products in the duodenum (peptides, AAs, FAs) - ***3 major agonists of enzyme secretion = ACh, gastrin, CCK (need to reduce acid)`

Question 184

what are the phases of pancreatic secretion ?

Answer 184

1) Cephalic = stimulated by smell, taste, conditioning via vagus; enzymes a) ACh -> H+ secretion by parietal cells -> secretin release in duodenum -> pancreatic fluid and bicarb secretion b) vagal stimulation -> gastrin from G cells -> pancreatic enzymes (gastrin like CCK in dogs ) 2) gastric= stimulated by distension of stomach by vagus; enzymes a) protein products in stomach -> gastrin -> pancreatic enzymes and gastric acid secretion REMEBER THIS NEXT ONE - MOST IMPORTANT 3) Intestinal = MOST IMPORTANT, enzymes and aqueous portions secreted a) 80% of secretion b) H+ triggers release of SECRETIN → HCO3- secretion i. Secretin also inhibits gastric secretions and emptying and gastrin release c) CCK → ENZYME secretion i. CCK released in response to AAs and FAs in SI ii. Also potentiates effect of secretin on ductal cells

Question 185

(VI) what are the most important enzymatic secretions from acinar cells?

Answer 185

-CCK is MOST IMPORTANT signaler for enzyme secretion -AAs, peptides, FAs→ I cells→ CCK secretion→ CCKa receptors on acinar cells → enzymes!

Question 186

(VI) which is the most important enzyme in increasing the secretion of aqueous portion of the liver enzymes?

Answer 186

-Secretin is the MOST IMPORTANT signaler for aqueous secretion -H+ in duodenum → S cells → secretin → ductal cells → bicarb rich aqueous secretion

Question 187

draw a diagram depicting the regulation of pancreatic secretion;

Answer 187

Question 188

what controls bile secretion when chyme reaches the SI?

Answer 188

CCK secreted (by I cells) → CCK causes contraction of GB and relaxation of sphincter of Oddi → bile flows from GB into duodenum

Question 189

once lipid absorbtion is complete what occurs to bile salts?

Answer 189

90% bile salts are recirculated to the liver via enterohepatic circulation 10% go into the colon where part is lost in the faeces as stercobilin and some is modified into secondary bile acids from colonic bacteria

Question 190

decribe the main steps in bile salts enterohepatic recirculation ?

Answer 190

- Absorption bile salts from the ileum into portal circulation - Delivered back to liver - Hepatocytes extract bile salts from portal blood - Allows for conservation of bile salts--liver only has to replace the small amount that is lost in the feces

Question 191

what is the composition of bile?

Answer 191

bile salts, bile pigments (bilirubin), cholesterol, phospholipids

Question 192

How are bile salts formed?

Answer 192

Bile acids; a) Primary Bile Acids = synthesized from cholesterol (cholic acid) b) Secondary Bile Acids = made from primary BAs that are modified by intestinal bacteria (deoxycholic acid are conjugated in the liver with glycine or taurine to form bile salts

Question 193

why are bile acids converter to salts instead of being secreted to digest solutes

Answer 193

Bile salts are amphipathic which allows for lipids to be solubilized and they are more water soluble

Question 194

what is billirubin and what is its life cycle ?

Answer 194

Byproduct of hemoglobin metabolism which is combined with bile acids, phospholipids and cholesterole to form bile. Reticuloendothelial system degrades hemoglobin resulting in bilirubin -> transported into the liver by albumin -> live conjugates billirubin with glucoronic acid to form conjugated billirubin (this is yellow - also known as billirubin glucoronide) -> conjugated billirubin is unconjugated in the intestines and made into urobillinogen by bacteria -> urobillinogen is reticulated to the liver, some excreted in urine, some oxidised to urobillin and stercobilin (dark colour of faeces) Note, while in the gallbladder the bile is concentrated by epithelial cells thar remove water and other ions.

Question 195

what cell population is responsible for depositing bile in the gallbladder for future use

Answer 195

hepatocytes and ductal cells to make bile which is deposited in the gallbladder

Question 196

what are the stimuli for bile ejection ?

Answer 196

Ejection of bile: occurs after a meal is ingested - MAJOR STIMULUS = CCK → secreted by I cells in response to AAs, peptides, FAs - CCK causes contraction of GB and relaxation of sphincter of Oddi

Question 197

what ion channels are reponsible for bile salt re-absorbtion and where are these found?

Answer 197

Na-bile salt cotransporters in the Ileum re-absorb bile salts from the lumen of the intestine and eject them into the portal system

Question 198

how does the liver determine how much bile acid to produce for the formation of bile salts?

Answer 198

The system is under negative feedback controle by bile salts which inhibite cholesterole-7-alpha hydroxylase (CYP7A1) which catalyses the first rate limiting step in bile acid synthesis where cholesterole is converted to 7a-hydroxycholesterole, a precurdor of by acid

Question 199

CYP7A1 is what and what family of enzymes does it bellong to?

Answer 199

CYP7A1 is cholesterole 7 alpha-hydroxylase which is the enzyme that catalyzes cholesterole into 7alpha-hydroxycholesterole, a precursor of bile acids. It belongs to the p450 enzyme family

Question 200

In the following table, determine if the substance results in increased or decreased HCL secretion

Answer 200

Question 201

where is somatostatin secreted by?

Answer 201

Somatostatin is secreted by delta cells at several locations in the digestive system, namely the pyloric antrum, the duodenum and the pancreatic islets

Question 202

what is the effect of somatostatin on HCL secretion?

Answer 202

n the stomach, somatostatin acts directly on the acid-producing parietal cells via a G-protein coupled receptor (which inhibits adenylate cyclase, thus effectively antagonising the stimulatory effect of histamine) to reduce acid secretion.[14] Somatostatin can also indirectly decrease stomach acid production by preventing the release of other hormones, including gastrin and histamine which effectively slows down the digestive process.

Question 203

fill in the table regarding bile salts

Answer 203

Question 204

List the 4 fat soluble vitamins.

Answer 204

A,D,E,K

Question 205

In the jejunum, ileum and colon, what electrolytes are absorbed and what electrolytes are secreted ?

Answer 205

Question 206

All ingested carbohydrates must be broken down to _______ in order to be absorbed. Disaccharides Monosaccharides Peptides Polysaccharides

Answer 206

Monosacharides

Question 207

Pancreatic secretions are made of 2 main components: the aqueous portion and the enzymatic portion. The aqueous portion is made by ______ and the enzymatic portion is made by ______. Acinar cells, ductal cells Ductal cells, acinar cells Acinar cells, Zymogen cells Ductal cells, Zymogen cells

Answer 207

Ductal cells, acinar cells

Question 208

During peristaltic contractions in the small intestine, what substance contributes to relaxation of the intestinal smooth muscle in front of (aborad) the food bolus? Acetylcholine Neuropeptide Y Substance P VIP

Answer 208

VIP

Question 209

Please label if the below substances increase or decrease the frequency of action potentials and force of gastric contractions.

Answer 209

Question 210

In the gastrointestinal tract, slow waves are a unique characteristic that provides tonic contraction of the smooth muscle. At the peak of the slow wave, if the membrane potential is maximally depolarized and meets threshold, an action potential occurs. Depolarization is caused by opening of what channels? Calcium channels Chloride channels Potassium channels Sodium channels

Answer 210

Calcium channels

Question 211

Pick the correct neurotransmitter. Postganglionic neurons of the parasympathetic NS within the GI tract release peptides or (ACETYLCHOLINE / NOREPINEPHRINE) Postganglionic neurons of the sympathetic NS within the GI tract release (ACETYLCHOLINE / NOREPINEPHRINE)

Answer 211

Postganglionic neurons of the parasympathetic NS within the GI tract release peptides or (ACETYLCHOLINE) Postganglionic neurons of the sympathetic NS within the GI tract release (NOREPINEPHRINE)

Question 212

Pick if the below substances increase or decrease appetite. Leptin: DECREASES/INCREASES appetite Insulin: DECREASES /INCREASES appetite GLP-1: DECREASES/INCREASES appetite Ghrelin: DECREASES/INCREASES appetite a Peptide YY (PYY): DECREASES/INCREASES appetite

Answer 212

Leptin: DECREASESappetite Insulin: DECREASES appetite GLP-1: DECREASES appetite Ghrelin: INCREASES appetite a Peptide YY (PYY): DECREASES appetite

Question 213

fill in the table

Answer 213

Question 214

what occurs when there is disruption of water and electrolyte absorbtion?

Answer 214

diarrhoea -> what is not absorbed is secreted

Question 215

what electrolytes does the jejunum absorb?

Answer 215

major Na absorption site in SI Net absorption of NaHCO3

Question 216

what electrolytes does the ileum absorb?

Answer 216

Net absorption of NaCl

Question 217

what are the main molecules absorbed by the colon ?

Answer 217

- Na (this is how it is the principal absorber of water) - Ammonia (product of ammino acid metabolism - produced by colonic bacteria) - Volatile fatty acids (VFAs -> acetate, proprionate, butyrate [made by microbial fermentation in the colon])

Question 218

what electrolyte is the colon responsible for secreting?

Answer 218

K

Question 219

what effects does aldosterone have in the colon ?

Answer 219

it increases Na re-absobrtion which in turns re-absorbs water

Question 220

what are the 2 major types of salivary secretion

Answer 220

1) serous - alpha-amylase to start digestion of starches, water ions and electrolytes 2) mucous = lubrucation

Question 221

what secretions are produced by the 3 salivary glands ?

Answer 221

1) parotid - serous only 2) submandibular - mixed 3) sublingual - mixed

Question 222

what is the first enzyme that has to be secreted by the pancreatic acinar cells and why ?

Answer 222

Enterokinase This is the enzyme that activates proteases. Ie converts trypsinogen to trypsin ! if this is not secreted first then proteins cannot be broken down

Question 223

what are the key differences between the aqueous component and enzymatic component of the pancreas?

Answer 223

The aqueous component contrains everything that is neutralizing (e.g. HCO3) - hence H+ in the duodenum is a stimualtor for secretin which then results in bicarb release The enzyme portion is everything that digests - hence it is stimulated by the arrival of AA, FA and carb (CCK is released In response to these) neutralization happens first and then the enzyme breakdown

Question 224

where are the villi of the intestine the longest and shortest ? Why

Answer 224

Longested in the duodenum and shortest in the illeum This is due to absorbtion, most is absorbed in the duodenum and the least in the illeum

Question 225

what is the brush border?

Answer 225

the apicak surface of the epithelial cells is further increased with microvilli which are the brush border (increase surface area)

Question 226

What cell types make up the villi?

Answer 226

The surface of the villi are covered with epithelial cells (enterocytes) and interspersed with goblet cells (which secrete mucous)

Question 227

What are the 3 subcrups of carbohydrates and what suggar belongs to each group?

Answer 227

1) polysacharidsease 2) disacharides (sucrose, lactose, maltose, trehalose) 3) monosacharides (glucose, fructose)

Question 228

what type of sugar is absorbed by the intestinal epithelial cells ?

Answer 228

Only monosacharides can be absorbed. So glucose, galactose and fructose

Question 229

What is starch? How is it metabolised and what are the enzymes involved

Answer 229

most important dietary carb in animals and is digested by pancreatic amylase -> becomes a disacharide which the intestinal brush border breakes it down into monosachardised The intestinal brush border enzymes are maltase, isomaltase, lactase and surase

Question 230

what are the two pathways of nutrient absorbtion?

Answer 230

1) cellular 2) paracellular

Question 231

How are the monosacharides transported into the cells? how are they transported out into the blood?

Answer 231

glucose and galactose are absorbed by Na-dependent cotransporters = SGLT1 Fructose is absorbed via facilitated diffusion = GLUT5 ________________ glucose and galactose are Transported from the cell to blood by facilitated diffusion = GLUT 2 Fructose is transported from cell to blood by GLUT 2

Question 232

what is the galactose and glucose (from lumen to cell) transported name and what does it use as a co-transport? What other receptor has to be present to to allow for the above cotransporter to function?

Answer 232

SGL1 and it uses Na as a cotransport? Becuase Na has to enter the cell to allow glucose and galactose in, it has to do this down a concentration gradient. As a result, there is a Na:K ATPase on the blood side which pumps out Na from the cell to create that gradient

Question 233

where does protein digestion start and finish and what are the enzymes involved in each section?

Answer 233

Starts in the stomach with Pepsin (activated from pepsinogen by low pH) Finished in the small SI with pancreatic and brush border proteases. The proteases are; - trypsin, chymptrypsin, elastase, carboxypeptidase A and B

Question 234

Describe the pathway of pepsin production, activation and deactivation.

Answer 234

Pepsinogen is produced by the Chief cells in the stomach. It is activated by low pH (acid - remeber dilation of stomach and other promoters increase gastrin from G cells which then promotes HCL secretion by parietal cells) which converts it to pepsin. Pepsin breaks down proteins. The pepsin in the SI is then deactivated by HCO3

Question 235

what are important enzymes for protein digestion in the SI ? Which ones are active and which ones need activation ? How does activation happen?

Answer 235

Pancreatic and brush border enzymes are secreted inactive and then have to be activated; Inactive enzymes; Trypsinogen, chymotrypsinogen, preoelastase, procarboxypeptidase A and B Trypsinogen become trypsin by brush border enzyme enterokinase . Trypsin activates the remained of the pancreatic and brush border enxymes to chymotrypsin, elastase, carboxypeptidase A and B

Question 236

what protein components can be digested by the intestine ? which ones are too big and how are these processed ?

Answer 236

Amino acids, dipeptides, tripeptides Proteins and oligopeptides are too big and they are just further processed by peptidases

Question 237

How do pancreatic peptides deactivate ?

Answer 237

They digest each other to turn each other off when the food has been absorbed

Question 238

How are amino acids, dipeptides and tripeptides uptaken into the blood stream?

Answer 238

Aminoacids are cotransported with Na via the Na-aminoacid contrasporter into the cell, then secreted by an amino acid transorter into the blood Dipeptides and tripeptides are uptaken by a H+ cotransported. In the cell, these ether diffuse across the membrane or they are further broken down into AA by peptidase and then they use the same amino acide transporter as stated above

Question 239

What non-amino acid channel is essential for the amino acid transporter's proper function in the small intestine's epithelial cells?

Answer 239

The Na:K ATPase. This pumps Na out of the cell, which is essential to form a concentration gradient. If there were no concentration gradient, the amino acid transporter would pump Na into the cell which cannot leave, ether reversing the action of the pump or stalling it preventing amino acid absorbtion

Question 240

what are dietary lipids?

Answer 240

cholesterole, tricglycerised, phospholipids.

Question 241

why are lipids the hardest to absorb and what is the first step that has to occur to allow for the absorption of these ?

Answer 241

Lipids are not water soluble, and the content of the SI and stomach is aqueous. These have to have to be emulsified for them to be absorbed.

Question 242

What are the key steps in fat digestion ?

Answer 242

1) Stomach; breaks up lipids into smaller pieces, gastric lipases start digestion of triglycerides to glycerol and free fatty acids 2) small intestine (major player) - Bile salts + lysolecithin surround the lipids and emulsify dietary lipids - Pancreatic enzymes -> hydrolyze (aka digest) the fat

Question 243

If the SI does most of the digestive work for lipids, what are the roles of the stomach? and how these achieved ?

Answer 243

The stomach breaks down lipids into smaller pieces, gastric lipase starts digestion of triglycerides to glycerol and free FA. BUT the MOST important role, is the SLOWING of gastric EMPTYING medicated by CCK

Question 244

what are the major pancreatic enzymes in fat digestion and what is their role? Are these secreted as active or inactive enzymes

Answer 244

1) pancreatic lipase; ACTIVE -> hydrolyzes 1 trygliceride to 1 monoglycerideand 2 FA 2) cholesterole ester hydrolase; ACTIVE -> hydrolizes cholesterole ester to free cholesterole and FA 3) Phospholipase A2; PROENZYME activated by trypsin -> hydrolyzes phospholipids to lysolectin and FA

Question 245

what is colipase?

Answer 245

it essential for pancreatic enzyme funciton. Colipase is secreted as Procolipase and activated by trypsin. Colipase, displaces bile salts which is important because pancreatic lipase is inactivated by bile salts. Colipase by displacing these, will allow pancreatic enzyme to bind and work

Question 246

Once pancreatic enzymes have broken down the fats, how are these absorbed ?

Answer 246

they have to be solubilised in the lumen in Micelles. Milecces then diffuse to brush border and diffuse across the cells (bile salts stay in the lumen and are recycled), mostly in the mid jejunum. In the intestinal epithelial cells, lipids are re-esterified with free FA to what they were originally (triglycerides, cholesterol ester, phospholipids). Lipids atre then packed with apoproteins into particles called chylomicrons. These are packaged into vesicles which migrate to the basolaterla membrane -> exocytosed -> enter lactelas -> lymph circulation -> carries chylomicrosn to thoracic duct -> enter blood stream

Question 247

what are micelles ?

Answer 247

they are solubilised lipids which have; a) Core = lipid digestion products b) shell = bile salts And are mainly absorbed in the mid-jejunum

Question 248

what are chylomicrons?

Answer 248

these are tryclicerides and cholesterole cores which have phospholipids and apoprotein on the outside. These are formed when fats are re-esterified with FA inside the enterocytes

Question 249

what pathological conditions affects fat digestion?

Answer 249

Pancreatic insufficiency -> no pancreatic enzymes, NO FAT DIGESTION Excessive acidity in duodenum -> excess H+ by parietal cells vs inadequate pancreatic bicarb production Bile salt deficiency = ileal resection Bacterial overgrowth -> deconjucate bile salts and makes fat digestion less effective

Question 250

what are water soluble vitamins

Answer 250

B1, B2, B6, B12, C, biotin, Folic acid, nicotinic acid

Question 251

How fat soluble vitamins absorbed ?

Answer 251

just like lipids. They are incorporated into micelles, then made into chylomychrons and extruded in the lymph

Question 252

what abnormalities in absorbtion do we see with lymphanjactasia ?

Answer 252

issues absorbing fat and fat solumble vitamins so you may see issues like vitamin D deficiency or coagulopathes

Question 253

What are water-soluble vitamins absorbed by in the intestines ? What is the one exception and how is this absorbed?

Answer 253

Na contransporter in the small intestine. The exception is B12 which needs intrinsic factor; B12 binds to R proteins ->proteases degrade R proteins -> B12 transferred to intrinsic factor -> B12+ intrinsic factor is resistant to degradation by proteases -> absorbed in the illeum

Question 254

What is unusual about the absorption of B12 compared to other water-soluble vitamins ?

Answer 254

The exception is B12, which needs an intrinsic factor; B12 binds to R proteins ->proteases degrade R proteins -> B12 is transferred to intrinsic factor -> B12+ intrinsic factor is resistant to degradation by proteases -> absorbed in the ileum

Question 255

How is Ca absorbed in the small intestine? What regulates increased or decreased absorbtion

Answer 255

Absorbed in the SI. Dietary is cholecalciferol (D3 which is inactive). D3-> 25 (OH) D -> 1.25(OH)D Calcium absorption is promoted by the SI when there is induced synthesis of Calbindin D-28K. When this increases vit D is increased

Question 256

How is iron absobed in the liver ?

Answer 256

Absorbed across intestinal epithelial cells as free iron (Fe2+) and heme iron (bound to hemoglobin or myoglobin) which is then digested releasing free iron) Free iron -> vinds apoferritin -> goes into the blood -> binds ß-globulin transferrin -> transported from SI to liver for storage -> then goes to bone marrow where it us used to make haemoglobin TRANSferrin TRANSports ferrin

Question 257

in regards to water and electrolyte transport, what is absorbed in the jejunum, ileum and colon?

Answer 257

Jejunum -> major Na absorbtion site in SI. Net absorbtion of NaHCO3 Ileum -> Net absorbtion of NaCL Colon -> Na absorption and K secretion (aldesterone), but also absorbs ammonia (product of AA metabolism by colonic bacteria) and volatile Fa (acetate, proprionate, butyrate - made by microbial fermentation in the colon)

Question 258

How doe the intestine SECRETE electroytes ?

Answer 258

Via the CRYPTS - secrete fluid and electrolytes - Importantn channels are NaKATPase, Na-K-2Cl cotransporter and CL channels

Question 259

What is GALT? why is this important in development? How does it develop?

Answer 259

gut associated lymphoid tissue Early B cell development occurs in the intestinal mucosa, detal liver and bone marrow This becomes the Peyers patches, where IgA mucosal immunity is stimulated by commensal bacterial. Additionally, specific clostridial and bacteroidies spp will induce t-reg cells in these sytes (butyrate produced by gut bacteria is important for T reg differentiation

Question 260

bacteria are responsible for the synthesis of what major essential nutrients in the colon?

Answer 260

Vitamin K B12 Biotin Folic Acid Pantothenate

Question 261

Colonic bacteria are involved in the absorbtion of what 3 key ions?

Answer 261

Calcium Magnesium Iron

Question 262

what metabolic processing pathways are gut microbes essential for?

Answer 262

- breakdown indigestible carbs (e.g Butyrate ->reduction seen with IBD) - Breakdown proteins to amino acids (signaling molecules and antimicrobial peptides) - Prevention and promotion of obesity (Short chain fatty acids affect lipid, glucose and cholesterole metabolism)

Question 263

what are short chain fatty acids and where do these come from?

Answer 263

Acetate Proprionate Butyrate These are main metabolites of dietary fibers by starch fermentation in the colon. Butyrate also dervice from protein Improtat in the gut for local immunity but also for kidney and brain health

Question 264

what are secondary bile acids? How are these produced?

Answer 264

Deoxycholic acid Lithocoid acid Bile salts undergo hepatic recirculation for the most part. Those that do not, can undergo a 2 step process for secondary bile acid productiion 1) deconjugation ->bile acid 2) dehydroxylation -> primary bile salt to secondary bile salt

Question 265

why is Clostridium hiranosis important for gut health? What is a common cause of C Hiranosis depletion in the gut?

Answer 265

They play a significant role in formation of secondary bile acids. Without these, we see a marked decrease in secondary bioacids which help prevent proliferation of pathogenic bacteria E.coli and C difficile Treatment with metronidazole

Question 266

what is dysbiosis? What are the more common changes seen?

Answer 266

Decreased bacterial diversity and decreased beneficial bacteria ( clostridium hiranosis, Fusobacteria, Bacteriodes, some firmicutes) We also see an increase in negative bacteria such as Proteobacteria (e.coli - associated with IBD), C. perfringens (and e.coli) which cause acute D+, and decreased overal function of the microbiota

Question 267

how do you measure dysbiosis? Explain the results? what is a major cause of change?

Answer 267

Dysbiosis index by texas A&M where they cross the sample with what is classified as normal. Anything >0 us dysbiosis while negative numbers are normal microbiota. Antimicrobials - in humans that this can persist for 1 year (fluoroquinilones)

Question 268

If you give dogs with diarrhoea metronidazole, and in another population a placebo, what is the difference in time to resolution of disease? What about when given compared to populations on probiotics?

Answer 268

There is no signficant difference Even with a left shift it will not make a difference. The only time they should be given is with a degenerative left shift or sepsis Also no difference in time to improvement on probiotics

Question 269

what a re prebiotics, probiotics and postbiotics. Which ones engraft and become part of the population ?

Answer 269

Prebiotics -> AKA fiber (feed microbiome) Probiotics -> good backteria Postbiotics -> metabolites, short chain fatty acids (SCFS - are essential energy for colonocyte) functional proteins etc. Non of them engraft. Not even probiotics

Question 270

what are indications for a fecal microbiota transplant? How is this given

Answer 270

- refractory C perfringens or C difficile infections - refractory IBD - Parvovirus Given via nasoduodenal tube or trans colon. A fresh or frozen sample can be given but it may need to be repeated.

Question 271

hydrolized diets have been shown to increase what gut bacterial populaitons?

Answer 271

C hiranosis and E. coli

Question 272

How many lobes does the liver have and what are their names? What is the site of vessel exit and what vesses?

Answer 272

6 (both dog and cat) Left lateral and medial Right lateral and medial Quadrate Caudate Porta hepatis is where the protal vein, hepatic artery and bile duct exit the liver

Question 273

Describe the bile tract

Answer 273

Bile canaliculi in the liver combine to form the hepatic ducts (~3-5). These drain into the gallbladder, which has an exeting vessel called the cystic duct which then joins the common bile duct which enters the duodenum at the major duodenal papilla. Dog has a major pancreatic duct entering here too, but they also have an accessory pancreatic duct (which is the largest) which enters at a minor papilla. Cats, only 20% have an accessory so most them have a largfer major pancreatic duct.

Question 274

what is a hepatic lobule? Why is this important ?

Answer 274

region with a central vein circumferiatiated by protal tracts (each has a portal vein, bile duct, hepatic artery and lympathc plate - this is surrounded by a plate of hepatic cells) this is important as toxicities can spread centrally- > outward dependin g on the toxins and the size of the vessels can change depending on the disease

Question 275

in which zone of the liver would you expect copper accumolation in primary copper hepatopathy?

Answer 275

zone 3 - central lobular

Question 276

in which zone of the liver would you expect copper accumolation in secondary copper hepatopathy?

Answer 276

zone 2

Question 277

what are the main cells of the liver? what are their main family type?

Answer 277

Hepatocytes -> parenchymal cells Kupffer cells -> resident macrophages Stellate cells (lipocytes, Ito cells) -> cells that can differentiate inot others like collagen producing cells Others; Cholangiocytes (the parenchyal cells of the billiary system), Dendritic cells (antigen presenting), inlfammatory cells maybe present, endothelial cells.

Question 278

what are the roles of hepatocytes?

Answer 278

metabolic cells responsible for nutrient processing, drug processing et.

Question 279

what is the role of kupfer cells

Answer 279

these are resident liver macrophages with phagocytic properties. Essential as the liver is exposed to poratal blood draining the GIT where there is significant bacterial translocation risk

Question 280

what is the role of stellate cells?

Answer 280

these are often involved in fibrosis. they can differentiate into collagen producing myofibroblasts and have an essential role as antigen presenters. They also store Vitamin A in the liver

Question 281

where is vitamin A stored in the liver?

Answer 281

stellate cells

Question 282

How does the hepatic circulatory system differ from other organs?

Answer 282

70-75% of blood is venous and portal. Per unit of blood, it is poorly oxygenated but becuase so much of it goes to the liver, it actually contributes 50% of O2 supply. 20-25% of blood is from hepatic artery and provides 50% of the O2. Blood flows through portal, into hepatic sinusoids (distensible channels imbetween hepatocytes) from zone 1->3 and drains in the central vein (outwars to inwards). The artery does the same. this is why Zone 1 gets more O2 and you get CENTRIlobular necrosis in hypoxia. Also, there is a larger volume of hepatocites in zone 1 to metabolise whatever it needs to.

Question 283

what is the space of Disse?

Answer 283

Space beteween the endothelial cells of the sinusoid lumen and the hepatocitoes. Plasma filtrate filters out of the sinusoid (supplied by blood from the portal and hepatic arteries). A large component of this plasma will end up forming lymph. This space drains into the central vein.

Question 284

where are kupfer cells?

Answer 284

They sit in the fenestrated endothelium and extend their limbs into the sinusoids. This allows them to filter everything from the GIT blood (portal) and systemic)

Question 285

why are the bile cannaliculi infiltrating the layers of hepatocytes?

Answer 285

Hepatocites use the nutrients from the portal flow to produce bile which they drain into the bile cananiculi which then drains into the bile duct

Question 286

What is the difference in flow between arterieal and portal blood and bile?

Answer 286

Arterial and portal blood flow from the vessles -> sinuids -> central vein, so from zone 1-> 3 Bile is produced by hepatocityes once they have received flood, and they drain this into the bile cannaniculi that merge into the bile duct - i.e. from Zone 3-> (bile duct + hepatic artery + portal are all within the limiting plate

Question 287

when there is decreased synthetic liver function, the formation of what producst maybe decreased?

Answer 287

Liver synthesizes many proteins, including albumin and fibrinogen, most alpha-globulins, and some of the beta-globulins. Prothrombin and clotting factors V, VII, VIII, IX, and X are produced in the liver, as well as ceruoplasmin, ferritin, and many serum enzymes.

Question 288

when proteins are catabolised what is the major by product and what is this converted to?

Answer 288

Ammonia -> Urea

Question 289

what are are acute phase proteins? which are produced by the liver

Answer 289

a group of serum proteins whose levels increase or decrease in response to inflammation or infection Positive AFP - C-reactive protein (CRP) - Fibrinogen Negative AFP - Albumin - Transferrin - Haptoglobin - Alpha-1-antitrypsin

Question 290

deficiencies in which essential amino acid can occur from cats fed dog foods for prolonged periods of time? How does this affect the liver?

Answer 290

taurine It used by cats to conjugate bile acids. They also get GIT upset, DCM and hyperlucency of tapetum

Question 291

describe bile secretion

Answer 291

Bile salts are synthesized from cholesterol and conjugated to an amino acid (usually taurine or glycine). They are secreted into the biliary tract where they undergo storage in the gallbladder and are subsequently delivered to the small intestine. Intestinal bacteria may transform some of these primary bile acids into secondary bile acids. Ileal re-absorption of bile salts permits enterohepatic re-circulation; portal blood returns the bile acids to the liver for re-uptake re-conjugation, and re-secretion

Question 292

what hormone allows bile secretion ?

Answer 292

CCK stimulated by food in the SI stimulates gallbaldder compression and relaxation of the sphincter of Odi

Question 293

fill in the diagram

Answer 293

Question 294

how does bile acid synthesis occur?

Answer 294

cholesterole is unconjugated to produce cholic acid and chenodeoxycholic acid. These are then re-onjugted with glycine or taurine to form conjugated bile aids

Question 295

What happens to conjugated bile acids in the GIT?

Answer 295

secreted into the duodenum where they aid digestion . Conjugated (90%) undergo entero-hepatic recyrculation (absorbtion by IBAT in the ileum) where they are re-used, or 5% enter systemic circulation. ~10% will be go into the cholon, where it is unconjugated and absorbed into the portal systelm, lost in faexes (stercobilin) or a processed by the bacterial into secondary bile acids (deoxycholic and lithocoic acid)

Question 296

what clinical implications does a lack of secondary bile acids have?

Answer 296

secondary have anti-inflammatory properties. With dysbiosis, where primary are not being converted you can see inflammatory responses or bile acid diarrhoea.

Question 297

Name a key bacterial involved in converting primary to secondary bile acids in dogs?

Answer 297

Clostridium hiranonis

Question 298

Liver metabolism is essential in metabolising what type of drugs and why?

Answer 298

Essential for lipophilic drug metabolism, where it tries to male these more polar. If it did not do this, then these drugs would be re-absorbed by the kidneys

Question 299

what is the role of the liver in processing nitrogenous waste? Give an example

Answer 299

This is toxic waste such which is processed by the urea cycle. Key is ammonia produced by GIT bacteria. This is absorbed in the portal cystem, enters hepatocytes where it is placed in the urea cycle and made into urea for excretion or energy metabolism

Question 300

explain the mechanism of why bedesonide may have less systemic side effects compared to other oral steroid formulations?

Answer 300

undergoes HIGH first pass metablism in the liver. Aprox 90% is converted into metabolites with low corticosteroid activity, thus has minimal system side effects

Question 301

How does the liver process bilirubin?

Answer 301

bilrubin bound to albumin is absorbed into hepatocytes. This is then Conjugate with glucoronic acid via the enzyme UDP glucoronyl trnasferase. Conjugated bilirubin is water soluble so it can then be excreted in urine or bile.

Question 302

6m old yorkie presents pre-neutre lab work. You see low BUN and performe bile acids which are elevated. Is this dog in liver failiure? Why or why not?

Answer 302

No. you can have changes consistent with dysfunction without failiure. E.g. PSS have less functional mass and may have lower BUN without having liver failiure. PSS dogs can have high bile acids without failiure. They do not receive the same trophic substances supplied by the protal vein, and they can atrophy/lose functional mass witout being in failiure

Question 303

where is VIP secreted from and what does it do?

Answer 303

Vasoactive intestinal peptide is secreted by nervous cells of the enteric nervous system Relaxation of smooth muscle: VIP relaxes both vascular and non-vascular smooth muscle, contributing to gastrointestinal motility. Secretion stimulation: It stimulates the secretion of water and electrolytes from the pancreas and intestine, influencing digestion and nutrient absorption. Inhibition of gastric acid secretion: VIP helps regulate gastric acid secretion, preventing excessive acidity. Blood flow regulation: VIP plays a role in regulating blood flow within the gastrointestinal tract.

Question 304

what is the definition of chronic hepatitis?

Answer 304

Key histo changes of the presence of lymphocytic, plasmacytic, or granulomatous inflammation (portal, multifocal, zonal orpanlobular) or some combination of these along with hepatocyte death and variable severity of fibrosis and degeneration

Question 305

what are infectious causes of chronic hepatitis

Answer 305

No strong evidence for infection. Leptospirosis can cause acute hepatitis and chronic pylogranumalotous response. Bacillus piliformis, helicobacter, and Bartonella spp have been identified in dogs with CH. Leishmania has been associated with CH, also causing granulomatous lesions

Question 306

what toxin/drugs are most commonly associated with CH

Answer 306

Carprofen, oxubendazole, amiodarone, aflatoxin and cycasin. MOST COMMON TOXIC CAUSE OF CH is CHRONIC COPPER EXCESS

Question 307

what breeds are over represented for chronic copper excess

Answer 307

Bedlington, Dalmation, labrador, Doberman and Westy

Question 308

Why does abnormal hepatic copper accumolation occur?

Answer 308

Due to decreased bile loss (chronic cholestasis) or increased dietary intake (high copper chalate premixes in food)

Question 309

Altered copper excretion, causing a hepatopathy, is associated with genetic mutation and protein change

Answer 309

Autosomal recessive deletions in exon 2 of the ATP7B-associated protein COMMD1 Potential gene candidate includes ABCA12, which has also been associated with Cu tox independently of COMMD1

Question 310

at what concentration does copper become toxic?

Answer 310

We do not know. ALT rises have been shown with [Cu] of 1000ug/g DW and almost all patients are toxic >1500ug/g DW. There is strong phenotypic variability

Question 311

what are the challenges associated with diagnosing CuCH What are the 3 diagntic criteria for diagnosing CuCh

Answer 311

1) Histiological evidence of Chronic hepatitis associated with hepatic copper accumulation located in centrilobular areas (zone 3) 2) Histochemical copper staining showing hepatocyte copper staining showing accumolation in centrilobular areas 3) Hepatic copper quantitation with concrenatrations >1000 ug/g DW liver

Question 312

What are metabolic conditions associated with chronic hepatopathy?

Answer 312

Alpha-1-antitrypsin (ATT) deficiency caused by abnormal hepatic processing of AAT, results in hepatocyte retention of abnormally folded proteins causing CH -> seen in American and English cocker spaniels Porphyrin metabolism, erythropoietic protoporphyria results in abnormal accumulation of perphyrins

Question 313

How can you diagnose an autoimmune chronic hepatopathy?

Answer 313

There is no test, and there are no specific criterial. The consensus states that you need to rule out other causes and then look for evidence of the following; Presence of lymphocytic infiltrates in the liver, abnormal expression of major histocompatibility complex class II proteins, positive serum autoantibodies, familial history of liver diseases, association with other immune-mediated disorders, dermal predisposition and favourable response to immunosuppression

Question 314

what are the most common clinical signs associated with chronic liver hepatopathy?

Answer 314

Decreased appetite 61% Lethargy 56% Icterus 34% Ascities 32% Pu/Pd 30% Vomiting 24% Diarrhora 20% Hepatic encephalopathy 7%

Question 315

How common is hepatic encephalopathy with chronic liver disease?

Answer 315

it is not common at 7% of clinical signs

Question 316

How do ALT and ALP raise in relation to each other during the progression of chronic hepatopathy ?

Answer 316

Initially, ALT raises and is the most common blood work change. Then ALP, but ALT is usually orders of magnitude higher. However, as hepatocytes are lost we can see ALP increase above ALT. GGT will also increase beyond ALT.

Question 317

what is the prognostic utility of ALT, ALP, BIL and GGT in chronic liver disease?

Answer 317

There is none for ALT, GGT and ALP . ALT, though, can give us an idea of the severity of the disease. BIL is elevated in 50% of CH dogs and is a NEGATIVE prognostic indicator.

Question 318

what is a key blood test change which can tell you that your hepatopathy is chronic?

Answer 318

Hypoalbuminemia. There are large hepatic reserves, so there is a lag in the loss of this. When it starts going down, it indicates that hepatic function is insufficient to keep up with production needs.

Question 319

What is the most sensitive test for hepatic function?

Answer 319

Total serum bile acids (TBSA). Not sensitive for the early stage of CH, so used as a screening tool and should be used as a confirmatory tool to determine the need for biopsy. However, they are uniformily increases when PSS are present, so their use in diagnosis PSS and cirrhosis are high.

Question 320

What is the role of ammonium blood testS?

Answer 320

Sensitive for diagnosing cirrhosis and PSS, with both being high and being as sensitive as bile acids for this. However, it is also more specific as it is not affected by cholestasis. However, it is technically more difficult to measure

Question 321

what does ammonium butyrate crystalluria suggest in a dog?

Answer 321

presence of episodic hyperammonemia

Question 322

when may you see Fanconi like syndrome in liver disease?

Answer 322

with CuCH or other toxin induced hepatopathies. This is mostly due to concurrent AKI

Question 323

what are pre-biopsy considerations ?

Answer 323

Check for coagulation abnormalities (PT, APTT, BMBT, Firbinogen, PLT count) Check for anemia Check for thrombocytopaenia

Question 324

Why is it challenging to assess the bleeding risk in patients with chronic hepatopathies ?

Answer 324

liver has both a role in forming clotting facotors to promote bleeding, but also a role in creating clot breakdown enzymes.

Question 325

why would chronic liver disease cause thrombocytopaenia and how often is this seen ?

Answer 325

23% of late chronic cases Causes are consumptive (e.g. duodenal ulceration) vs decreased production of thrombopoietin by hepatocytes. May occur in moderate CH is there is synthetic failiure or vitamin K deficiency

Question 326

If you are to perform a liver biopsy in a patient with abnormal clotting parameters/platelets what is the evidence of prophylactic treatment and what could you give?

Answer 326

There is no evidence of the benefits of Vit K, plasma, transfusion, or protease inhibitors.

Question 327

what are sampling methods for liver biopsieS?

Answer 327

Want 12-15 portal triads. Laparoscopic - 5mm cup Laparatomy - wedge from center, not just the margin FNA have no useful role Trucut with 14-16g percutaneous US guide can provide adequate samples. Surgical biopsies from 2 liver lobes, shob be obtained for histo, aerobic and anaerobic culture and quantitative copper. The lap should be put in a casset to prevent crushing.

Question 328

why is copper hepatopathy toxic?

Answer 328

increased oxidative membrane injury, generating injurious hydroxyl and superoxide radicals.

Question 329

how to treat copper hepatopathy?

Answer 329

Chelation key - copper diet can aid chelation D-penicillamine (D-pen) is the Cu chelator of choice. Binds the urine and it eliminates it in the urine Copper-restricted diets (<0.12mg/100kcal of Cu)

Question 330

How does D-Pen worK?

Answer 330

D-penicillamine increases metallothionein in hepatocytes, which detoxify by increasing excretion of Cu from enterocytes (facilitating faecal elimination). It subsequently binds Cu in the blood stream where it can help eliminate it in the urine Must be given on an empty stomach; otherwise it will be bound by Cu in the food..

Question 331

D-pen is expensive. What are alternatives for owners?

Answer 331

It can be compounded for less. Tetrathimobylate and trietine in dogs is limited. Zinc interferes with enteric Cu uptake via metallothionein induction. However, Zinc reduces copper accumulation slowly which is not appropriate for toxic treatment.

Question 332

how do hepatoprotectants work?

Answer 332

Necroinflammatory hepatic diseases are associated with the depletion of antioxidant defence mechanisms Ursodeoxycholic acid: Bile acid which has choleretic, immunomodulatory, antioxidant, anti-inflammatory, cytoprotective and antiapoptotic properties. Indicated for dogs with manifesting evidence of cholestasis, inflammation involving bile ductules SAMe: intermediate metabolite of hepatic transsulfuration, transmethylation, and decarboxylation reactions. SAMe/Sylmarin has been shown to protect agains hepatoxicity of lomustine-associated hepatotoxicity

Question 333

when are NON dietary supplements indicated in liver disease ?

Answer 333

Protein restricted duet to 2.1-2.5g/protein/kg. titrate diet with protein soruces if there is muscle loss. Vit K not warranted unless there is acholic faeces and chronically hyperbillirubuneic with prolongaion of PT.

Question 334

what is the survival time for chronic hepatoparhy

Answer 334

Median 561 +/- 268

Question 335

what are signs of hepatic encephalopathy? How do you treat>

Answer 335

blindess, circling, headshaking, ptyalism which can lead to obtundation and coma. Dietary protein medulation, lactulose, antibiotics. Support secondary signs (eg PPI and sucralfate for ulceration etc)

Question 336

what is hepatic microvascular dyspasia? Where is it most commonly seen?

Answer 336

Hypoplasia of the portal vein (also known as microvascular dysplasia, or MVD) is a microscopic intrahepatic vascular abnormality in which portal venous blood is diverted into the hepatic veins within the intrahepatic microcirculation. Reported in small breed dogs yorkies etc) and these are usually secondary to portal vein hypoplasia and the disease results in hepatic parenchymal hypoperfusion

Question 337

How can biliary diseases be classified as as?

Answer 337

(1) biliary cystic disease, (2) cholestatic disease, (3) cholangitis, (4) disorders of the GB.

Question 338

how can cholecystitis be charachterised as? What diagnostic is used to identify these?

Answer 338

Type I; Necrotising Type II; Acute Type III; Chronic Emphysematous Ultrasound is highly sensitive for identifying GB rupture, emphysema, etc.

Question 339

What are most choleolyths made of? How are they made?

Answer 339

Calcium carbonate, bilirubin (pigment stones), and cholesterol. exact mechanism is unknown, cholelith formation is a multifactorial process involving bile stasis, bile supersaturation, nidus formation, and alterations in crystallization inhibitors. Choleliths generally are formed in the GB; however, formation can occur within bile ducts or the CBD (choledocholithiasis) as a consequence of bile stasis, inflammation, or infection

Question 340

what is the medical treatment of choleolythiasis?

Answer 340

includes broad-spectrum antibiotics and choleretic therapy to facilitate clearance of biliary aggregates (by promoting flow of lower viscosity bile). Treatment with ursodeoxycholic acid may have an advantage for choledocholiths lodged in small intrahepatic bile ducts that are not amenable to surgical intervention. Surgery is usually warranted with obstruction and is necessary if there is perforation. During the procedure, it is essential to get a sample of bile for culture and to retrograde inject saline up the bile duct to confirm patency.

Question 341

what are clinical signs of cholelithiasis?

Answer 341

progressive vomiting, dehydration, anorexia, icterus, and lethargy.

Question 342

What is a biliary mucocele?

Answer 342

characterized histologically by hyperplasia of mucus-secreting glands within the GB mucosa, which results in an abnormal accumulation of mucus within the GB lumen. Extension of bile-laden mucus into the EHBT may result in various degrees of EHBO. Marked GB distention can result in GB rupture

Question 343

How do biliary mucoceles occur? gene involvement?

Answer 343

pathogenesis remains un- known; however, a mutation in the canine gene ABCB4 (which functions exclusively as a phospholipid transloca- tor) has been identified recently in Shetland sheepdogs (and other breeds) with confirmed mucoceles. A weak association exists between mucocele formation and endo- crine disease (hyperadrenocorticism and hypothyroid- ism) and exogenous steroid administration.

Question 344

How do you treat biliary mucocele?

Answer 344

if non-clinical; ombination of choleretic therapy (UDCA) and antibiotic therapy has been suggested. S-adenosylmethionine (SAMe; Denosyl) can provide hepatoprotective and anti- oxidant benefits. Sequential biochemical and ultrasound evaluations are necessary to monitor response to therapy. Clinical; Surgical intervention Cholecystectomy is preferred in the literature because of the excellent long-term results in patient’s survival of the perioperative period Concerns regarding the potential for mucocele recurrence and concerns regarding the integrity of the GB wall also question the validity of cholecystoenterostomy in the management of GB mucocele

Question 345

what is vavuolar hepatopathy ?

Answer 345

syndrome in which hepatocytes are swollen secondary to cytoplasmic accumulation of fat, glycogen or water.The etiopathogenesis is unclear. Numerous underlying causes have been reported: exogenous steroids and hyperadrenocorticism lead to glycogen accumulation in the hepatocytes, while diabetes mellitus and hypothyroidism may lead to fat accumulation in the hepatocytes (i.e. steatosis). These parenchymal changes do not progress to clinical liver disease/failure.

Question 346

what is hepatocutaneous syndrome?

Answer 346

Also known as superficial necrolytic dermatitis, metabolic epidermal necrosis, necrolytic migratory erythema. Affected dogs have crusting skin lesions, particularly on the extremities (paw pads, nose, periorbital, perianal regions). Concurrent signs of diabetes mellitus are frequent (PUPD, polyphagia, weight loss) altough the pathogenesis for this is unclear.

Question 347

what is the cause of hepatocutaneous lesions?

Answer 347

characterized by severe degenerative vacuolar hepatopathy secondary to an underlying metabolic disorder which is unidentified in most of the cases. Glucagonoma, insulinoma and phenobarbital have been described as causes of hepatocutaneous syndrome. Nutritional deficiencies (amino acids, essential fatty acids, zinc) are suspected to play a role in the disease pathogenesis.

Question 348

what clinical pathological findings do you have with vacuolar hepatopathy ?

Answer 348

levated serum liver enzyme activities, hypoalbuminemia, hyperglycaemia, glucosuria. US shows swiss-cheese like partenchyma appearance. Pacreatic mass caused by glugagonoma may be present

Question 349

What is the difference between acute and chronic pancreatitis?

Answer 349

Acute- reversible Chronic- irreversible (can be a sequel of untreated acute)

Question 350

what are the forms of acute pancreatitis in cats? Which one is worse? How do you differentiate the two?

Answer 350

acute necrotising pancreatitis, where there is a lot of fat necrosis and acute suppurative without fat necrosis. Acute necrotizing pancreatitis generally carries a poor prognosis. Would need biopsies to distinguish but these are seldom done in pratice

Question 351

what are causes of pancreatitis in dogs?

Answer 351

Breed predisposed to hyperlipedemia (schanauzer). history of recent surgery, dietary indiscretion, drug therapy (azathioprine, potassium bromide with phenobarbitone, organophosphates, etc.); hyperlipidemia, obesity, hypercalcemia, endocrine diseases (diabetes mellitus, hyperadrenocorticism, hypothyroidism); ischemia secondary to any disorder; hemolysis, canine babesiosis and leishmaniosis.

Question 352

What changes do you see on blood work with chronic hepatitis and what non routine testing is available and how good is this?

Answer 352

Bloodwork may show leukocytosis, azotemia (dehydration, concurrent renal injury), elevated liver enzyme activities, or hypocalcemia which is a negative prognostic indicator. Serum lipase and amylase are not specific of pancreatitis. They may be increased with gastroenteritis, hepatopathy or renal disease.In addition, their concentration is normal in up to 20% of dogs with acute pancreatitis. Trypsin-like immunoreactivity (TLI) is specific for exocrine pancreatic function but it is not sensitive for pancreatitis and is therefore not used clinically. Canine pancreatic lipase (cPL) is more specific for pancreatitis than serum total lipase because it detects lipase that is only secreted by the pancreas.

Question 353

what diagnostic test can aid in the diagnosis of exocrine pancreatic insufficiency ?

Answer 353

Trypsin-like immunoreactivity (TLI) is specific for exocrine pancreatic function but it is not sensitive for pancreatitis and is therefore not used clinically.

Question 354

what is lymphangiactasia?

Answer 354

Lymphangiectasia is defined by a marked dilation and dysfunction of the intestinal lymphatics (i.e. lacteals) secondary to lymphatic obstruction (either physical or physiologic).

Question 355

What are the clinical pathologica; findings of lymphangiectasia?

Answer 355

- Hypoproteinemia – abnormal lacteals rupture and proteins from the lymph are lost into the intestines - Lymphopenia +/- immunodeficiency – lymphocytes are also lost through lymph leakage into the intestinal lumen putting patients at increased risk for inflammatory or neoplastic disorder (e.g. Lundehund and gastric lymphocytes carcinoma). Endoscopic findings are very characteristic with the presence of milky white droplets and dilated lacteals. Diagnosis is confirmed with biopsies and histopathology.

Question 356

Is lymphangiactasia primary or secondary in origin? Explain how it/they happen

Answer 356

Both Primary lymphangiectasia is congenital and has been described in various breeds such as small terrier breeds (Yorkshire, Maltese), Rottweilers, Norwegian Lundehund. It has not been described in cats. The disease is usually restricted to the intestines (thoracic lymphatics are more variably involved) and is characterized by inflammation of the intestinal mucosa and development of lipogranulomas in the intestinal wall or mesentery as a consequence of lymphatic leakage. As lipogranulomas enlarge and coalesce, they participate to the lymphatic obstruction. Secondary lymphangiectasia develop following obstruction of lymphatics by inflammatory, fibrosing or neoplastic diseases. Thoracic duct obstruction and right heart failure are physiological mechanisms of lymphatic obstruction.

Question 357

How do yout treat lymphangiactasia?

Answer 357

-Dietary management – ultra low fat diet, calorie dense and highly digestible. Supplementation with fat- soluble vitamins may be needed. Dietary modifications may be sufficient for treatment if it is started before the development of lipogranulomas. - Reduction of the intestinal inflammation secondary to lymph leakage and crypt damage and particularly indicated in case of lipogranulomas - antiinflammatory doses of predni(so)lone. Cyclosporine treatment may be effective. - Treating complications of PLE if present (cf. PLE treatment)

Question 358

Define IBD?

Answer 358

IBD is a group of diseases of the GI tract characterized by chronic GI signs and idiopathic intestinal inflammation identified by histology. The inflammation can occur in the stomach and/or SI and/or LI and can be classified as lymphoplasmacytic (the most common), eosinophilic, granulomatous or neutrophilic (infrequent).

Question 359

what are the clinical sings of IBD ?

Answer 359

Major clinical signs are chronic +/- intermittent vomiting and diarrhea (SI, LI or mixed). Hematochezia, melena, weight loss, anorexia, polyphagia may be observed. Triaditis syndrome, which is characterized by concurrent IBD, cholangitis and pancreatitis in cats, has been described in about 1/3 of cats with severe signs of IBD.

Question 360

what is the etiopathogenesis of IBD? what do you see on blood work?

Answer 360

The exact etiopathogenesis of IBD is unknown. It is suspected to be associated with a loss of oral tolerance secondary to disruption of the mucosal barrier, inappropriate response of the immune system and changes in the microbiome. IBD is a diagnosis of exclusion and a full diagnostic work-up is required to rule out other etiologies. Blood work results are not specific. Mild elevation in liver enzyme activities is frequently seen in dogs as a marker of reactive hepatopathy secondary to the on-going intestinal inflammation. Liver enzyme elevations in cats always suggest a primary hepatic disease due to their short half-life. both diHuseintlamm Low serum folate and/or cobalamin concentration reflect inflammation in the corresponding GI portions. Anemia maybe seen

Question 361

How do you treat IBD?

Answer 361

- Treatment trial of parasiticides for occult parasitism - Exclusion diet trial - highly digestible diet, novel antigen or hydrolyzed diet (cf. chronic gastritis for more details). Note: an elimination diet trial can be performed prior endoscopy. - Antimicrobial trial - tylosin for 28d (SIBO) - Immunosupressive treatment -> Chlorambucil-prednisolone has been shown to be more effective than a prednisolone- azathioprine combination for dogs. Cyclosporine effective but expensive -> prednisone alone in cats (cannot use anzathioprine. Budesonide can be used - Cobalamin-folate supplementation - GIT scope and biopsies