Digestion 5

Question 1

what tends to fall within the rumen and what tends to fall within the reticulum

Answer 1

rumen - lighter materials - grass and hay

reticulum - heavier material like nails, grains, rocks

Question 2

volatile fatty acids, can they move across mucosa, how much energy do they provide why transport important

Answer 2

can be directly absorbed across the mucosa into blood
provide more than 70% of dietary energy
continuous removal of VFA prevents acidification of the ruminal pH

Question 3

what receptors in rumen involved with contractions and via what innervation

Answer 3

stretch receptors and chemoreceptors modulate contractions via vagul axons that reply signals to brainstem

Question 4

what papillae found in newborns, what does exposure to roughage do to the papillae
what compounds stimulate papillary growth

Answer 4

rudimentary in newborn and suckling ruminants - exposure to roughage promotes development of papillae
proprionate, butyrate - produced by fermentation and possibly insulin-like growth factor-1

Question 5

what does a high plane of nutrition, poor plane of nutrition and adequate fibre do to the ruminal papillae

Answer 5

high plane - production of abundant VFA - larger papillae to promote absorption
poor plane - small blunt papillae
fibre - 15% of diet - long slender papillae

Question 6

High concentration rations with inadequate roughage what is the result for papillae and why, what else causes this

Answer 6

tumpy, club-shaped papillae that tend to form clumps, nodules and rosettes, especially in the ventral sac of the rumen
1) mucosa undergoes hyperplasia, hyperkeratosis and often hyperpigmentation
2) clumping is encouraged by hyperplasia of secondary papillae
Vitamin A deficiency in calvs can also cause hyperkeratosis of the forestomach mucosa.

Question 7

what occurs when plant fibre or animal hairs adhere to forestomach mucosa - what is the disease called

Answer 7

contribute to mattered appearance may penetrate mucosa and cause inflammation - barley beef rumenitis in feedlot cattle

Question 8

what is an appropriate pH for the ruminal fluid

Answer 8

5.5 - 7.5

Question 9

what does overly dry ruminal content, excessively watery ruminal content, voluminous frothy content and acidic pH

Answer 9

1) dehydration
2) vagal indigestion or grain overload
3) primary bloat
4) grain overload (lactic acidosis)

Question 10

what does ammoniacal odour and alkaline pH, ordour of cooked turnips or pugent insecticida smell, rancid odour and puterfied milk say about the animal during post mortem

Answer 10

1) urea toxicity
2) organophosphate poisoning
3) failure of the oesophageal groove reflex

Question 11

what does lead flakes or motor oil, aromatic ordour and pine needles mean for the animal during post mortem and what other plant poisonings are there

Answer 11

1) lead poisoning
2) yew posioning - toxic alkaloids
runus spp. (plums, cherries, peaches, apricots, almonds) all contain hydrogen cyanide)

Question 12

other things to look at during post mortem

Answer 12

the papillae, if any erosin, ulceration or scarring and how well the mucosa can be peeled away - adherence of the mucosa is abnormal and may reflec rumenitis or ruminal fibrosis

Question 13

Bloat what is it, what are the types, mortality rate, what does it occur

Answer 13

dilation of the rumen, ruminal tympany
primary (acute) or secondary (chronic)
up to 50% mortality rate
rumen generates high amount of gas 30-50L per hour cows 5L per hour sheep and goat and if anything interferes with eructation can cause bloat

Question 14

primary bloat what other name, what occurs, what most often associated with and what is the mechanisms

Answer 14

frothy bloat
acute condition of rumen in which stable foam forms preventing the eructation of gas - generally only small volume of unstable foam forms
often associated with succulent legumes (e.g. alfalfa and clover) (pasture bloat) -bloat within 1-3 days
1) succulents stimulate less saliva production
]2) increased viscosity of ruminal fluid -promotion of foam formation
3) soluble proteins released from legume chloroplasts are degraded by ruminal flora
4) rise to the surface of the ruminal fluid and become denatured and insoluble - stabilisation of the foam
5) legume acids also drop the ruminal pH to 5.4-6 (optimal for formation of stable foam)
6) failure of eructation
7) distension of the rumen
8) massive increase in intra-abdominal pressure 9) pressure on the diaphragm and lungs - dyspnoea - hypoxaemia
10) high intra-abdominal pressure +/- direct compression of the intra-abdominal caudal vena cava by the rumen also causes impaired venous return to the heart
11) circulatory failure with congestion of the distal hindlimbs

Question 15

what other causes for primary bloat and mechanism

Answer 15

1) genetically predisposed because produce less saliva
2) in feedlot cattle feed on high concentrate and low roughage diets - onset of feedlot bloat is usually more gradual than that of pasture bloat
1) high concentrate/low roughage diets
2) decreased saliva production
3) a gradual change in the ruminal flora
4) increased bacterial production of polysaccharides
5) increased viscosity of the fluid - stable foam formation
6) as said before - failure of eructation etc.

Question 16

post mortem findings of animals with primary bloat

Answer 16

1) sudden death - laying on back sawhorse posture
2) abdomen markedly distended by gas
3) dark, poorly clotted blood from orifices
4) pale muscles of proximal hindlimbs
5) bloat line in the oesophagus at the level of thoracic inlet
6) bulging diaphragm
7) lungs pale and compressed
8) bulky forthy contents in rumen however may disappear more than 10-12 hours after death

Question 17

secondary bloat what is it why occurs and causes

Answer 17

usually chronic condition - episodes of acute - physical or functional obstruction preventing eructation of gas

1) physical obstruction of oesophagus by tumour, foreign body, stricture
2) fibrous adhesions, tumours, abseceses or peritonitis interfering with contraction rumem and reticulum
3) functional obstruction of oesophagus due to vagal nerve injury or organophosphate poisoning
4) excess indigestible roughage
5) failure of oesophageal groove reflex in bucket-feed calves

Question 18

what are the post mortem findings for secondary bloat and what are the mechanisms behind the cause of excess indigestible roughage and failure of the oesophageal groove reflex for second what clinical signs and where may else see

Answer 18

as per primary but without stable foam formation and possible presence of physical obstruction

1) if digestible nutrients (starch, sugars) in the diet are inadequate, excess roughage cannot be digested and accumulates in the rumen and reticulum - distension - inhibition of contractions - failure of eructation
2) ruminal drinkers”) milk or milk replacer flows into the rumen - putrefaction - mild rumenitis and hyperkeratosis
- clinical signs include inappetence, recurrent bloat, abdominal pain and passage of clay-like faeces
- may see a similar problem in calves fed by stomach tube

Question 19

what are the 3 main groups of foreign bodies that get lodges in rumen or reticulum, why- what species most common in

Answer 19

cows due to non-selective eating habits

1) trichobezoars = spherical masses largely composed of hair or wool
- more common in younger animals
- may be associated with inadequate dietary fibre, boredom, pica or skin disease (e.g. lice)
- may become impregnated with mineral
- usually incidental
2) phytobezoars = spherical masses largely composed of plant fibres
- may be due to rough feed or oral or dental disease that impairs mastication
- may become impregnated with mineral
- usually incidental
3) bezoars are only of importance if they are regurgitated to obstruct the oesophagus or if they obstruct the reticulo-omasal orifice, the abomasal pylorus or the intestines

Question 20

what can foreign bodies, sharp objects and wood shavings or straw lead to

Answer 20

1) lead poisoning when dissolved
2) traumatic reticuloperitonitis
3) may cause diffuse mixed bacterial cellulitits

Question 21

traumatic reticuloperitontitis what occurs what if incomplete perforation and penetration through the wall

Answer 21

sharp bodies may move into reticulum during contractions generally cranioventral direction, bacteria extend alon perforation track from reticulum
incomplete - often inconsequential but may cause focal suppurative or granulomatous inflammation in the wall of reticulum with minor overlying peritonitis
complete - acute local peritonitis - chronic local fibrosis - sometimes can be drawn back into reticulum

Question 22

traumatic reticuloperitontitis what occurs if penetrate diaphragm, pericardial sac and what are some other sequels

Answer 22

diaphragm - pleuritis and pneumonia
heart - florid suppurative pericarditis and eventual right sided congestive heart failure
1) pentration of myocardium or artery - haemorrhage
2) penetration liver or spleen - abscessation
3) penetration reticulum wall - chronic suppurative inflammation in grooves resulting in vagus indigestion

Question 23

Vagus indigestion what is it and what are the clinical signs

Answer 23

a clinical syndrome resulting from a physical or functional outflow obstruction of the forestomach or abomasum - distension of the rumen and reticulum
- characterised by persistent ruminal atony or irregular motility, gradual bilateral abdominal distension, inappetence and decreased milk production

Question 24

List 6 causes of vagus indigestion

Answer 24

1) traumatic reticuloperitonitis
2) physical obstruction of outflow from the rumen/reticulum, omasum or abomasum
- e.g. foreign bodies, neoplasms, abscesses adjacent to the reticulo-omasal orifice
3) damage to the vagus nerve anywhere along its length (neck, pharynx, intra-thoracic, intra-abdominal)
4) degeneration of muscle in the wall of the oesophageal groove - flaccidity
5) pregnancy
- possibly due to displacement of the abomasum by the uterus
6) idiopathic

Question 25

what are the post mortem findings of vagus indigestion and what is rumenitis

Answer 25

- rumen distended with watery fluid lacking odour; unmacerated food particles float on the surface of the fluid - omasum can be very large and impacted with dry feed - abomasum may be distended and impacted with dry feed inflammation of the rumen

Question 26

lactic acidosis what is it, where does it occur, what may it trigger, what what are survivors predisposed to

Answer 26

ruminal acidosis, grain overload, rumen overload, carbohydrate engorgement most common cause of rumenitis occurs in dairy and feedlot cattle, sheep and goats - due to dietary overload with rapidly fermentable carbohydrate (e.g. grain, bread, root crops) or a sudden increase in the amount of carbohydrate in the diet - the amount of carbohydrate consumed is less important than the rapidity of the dietary change - may trigger a severe acute metabolic disease - high morbidity and mortality - survivors have chemical rumenitis and are predisposed to development of secondary infections with Fusobacterium necrophorum and/or fungi

Question 27

what is the mechanism behind lactic acidosis

Answer 27

1) fermentation of the carbohydrate 2) increased VFA production 3) decreased ruminal pH ○ at a pH of ≤ 5.0, ruminal Gram-negative bacteria (which predominate in health) and protozoa die ○ streptococci (especially Streptococcus bovis) begin to proliferate and produce lactic acid - further decrease in the pH ○ at a pH of 4.5-5.0, streptococci then decline and lactobacilli proliferate 4) low pH  ruminal atony and reduced secretion of saliva ( decreased buffering of ruminal acid by salivary bicarbonate) 5) lactic acid acts osmotically 6) fluid moves from circulation into the ruminal lumen 7) ruminal distension and then diarrhoea 8) profound dehydration and hypovolaemic shock 9) death

Question 28

post mortem findings of lactic acidosis what is diagnostic

Answer 28

1) a rumen pH

Question 29

Secondary Bacterial Rumenitis (Necrobacillary Rumenitis) | when does it occur what occurs

Answer 29

- ruminants that survive a mild episode of lactic acidosis may develop secondary bacterial infection of the damaged ruminal mucosa 1) the necrotic lesions slough - ulcers 2) healing by granulation tissue - white stellate scars lacking papillae 3) embolism of infection via portal vein branches to the liver 4) multiple foci of coagulative necrosis that ultimately liquefy to form conventional hepatic abscesses (= hepatic necrobacillosis)

Question 30

Secondary Fungal Rumenitis | what is it, how severe is it, what occurs, when to suspect

Answer 30

- mycotic infection of the rumen is most often a complication of lactic acidosis - much more severe than necrobacillary rumenitis and often fatal - fungal hyphae invade blood vessels of the ruminal wall - vasculitis, thrombosis and infarction, lesions are typically circular - always suspect fungal infection if fibrinohaemorrhagic lesions extend from the ruminal mucosa to the serosal surface - in fatal cases, most of the ventral sac of the rumen and parts of the reticulum and omasum are involved

Question 31

Secondary Fungal Rumenitis may develop secondary to mucosal ulceration cause by - list 4 causes

Answer 31

1) broad spectrum antibiotic administration with disruption of normal flora - especially in calves 2) septicaemia 3) reflux of abomasal contents 4) primary viral infection – especially bovine viral diarrhoea virus (BVDV) infection

Question 32

viral rumenitis what occurs and list some examples of diseases that cause this

Answer 32

``` - the following viral infections may cause lesions in the mucosa of the forestomach compartments: • bovine herpesvirus-1 • bovine papular stomatitis • contagious ecthyma (scabby mouth, orf) • BVDV/mucosal disease • bluetongue • rinderpest • foot and mouth disease • bovine adenovirus ```

Question 33

toxic rumenitis what occurs and how

Answer 33

- e.g. accidental consumption of excess urea as a non-protein nitrogen supplement or in fertiliser production of ammonia in the rumen - caustic injury to the mucosa

Question 34

parasites gongylonema and paramphistomum what do they cuase

Answer 34

Gongylonema spp. – nematodes found in the oesophageal and ruminal mucosa +/- lamina propria - red blood-filled serpentine tracks - heal by scar tissue Paramphistomum and related spp. – conical flukes - found in the rumen and reticulum of cattle, sheep and wild ruminants - reside between the ruminal papillae - usually non-pathogenic but large numbers may cause atrophy and hyperkeratosis of the papillae

Question 35

Neoplasia what is clinicl significance and may it call and list the 5 types

Answer 35

- most neoplasms of the ruminant forestomach are of no clinical significance - large lesions in strategic locations may cause secondary bloat or vagus indigestion 1) papilloma 2) fibropapilloma 3) squamous cell carcinoma 4) lymphoma 5) fibroma

Question 36

describe papilloma what type of neoplasia, which species common with what fibropapilloma - what type of neoplasa what caused by

Answer 36

papilloma - a benign neoplasm of squamous epithelial cells - rare in sheep - common in cattle in some areas due to infection with bovine papillomavirus type 4 fibropapilloma - a benign neoplasm of squamous epithelial cells lamina proprial fibrocytes/fibroblasts - due to infection with bovine papillomavirus 2

Question 37

describe squamous cell carcinoma, lymphoma and fibroma what type of neoplasia and what species found in

Answer 37

1) squamous cell carcinoma – a malignant neoplasm of squamous epithelial cells - rare in sheep and most cattle - can be common in cattle in some locations (e.g. Scotland, northern England, (Kenya) due to exposure to bovine papillomavirus 4 and carcinogens in bracken fern (Pteridium aqulinum) or other native plants 2) lymphoma - a malignant neoplasm of lymphocytes - rare in cattle, and usually as an extension from lymphoma involving the abomasum 3) fibroma - a rare benign neoplasm of fibrocytes/fibroblasts

Question 38

how much of the pancreas in composed of exocrine tissue | define the terms parenchyma and stroma

Answer 38

80-85% - Parenchyma - term for the functional tissue within an organ - Stroma - connective or supporting tissue with no functional unit

Question 39

clinical signs for diseases of the exocrine pancreas

Answer 39

○ Maldigestion - weight loss, small intestine diarrhoea ○ Jaundice - can get blockage in the bile duct so build-up of bile secretions causing jaundice ○ Metabolic disturbance - weight loss despite normal or increased appetite ○ Acute signs - abdominal pain, vomiting, shock - significant inflammation and loss of tissue - pain

Question 40

List and describe the 7 safeguards in place to prevent pancreatic auto-digestion

Answer 40

1) Inactive proenzymes - Not secreted in active form only really lipase and amylase and trypsin generally activates the rest 2) Zymogen secretion - Store the enzymes and protect the cell 3) Proenzyme secretion - Only secrete when have enough material to digest and can secrete into duodenum 4) Activation of trypsinogen in the duodenal lumen - Protect the pancreas be activating in the duodenum - done as enterokinase activates trypsinogen and is secreted by the duodenal mucosal cells 5) Pancreatic duct sphincters - Prevent backflow into the pancreas from the duodenum 6) Trypsin inhibitors - Within the pancreas - pancreatic inhibitory trypsin inhibitor 7) Acinar cell hydrolases - Break down active enzymes that may have been prematurely released from the granules

Question 41

Regenerative capacity and repair of the pancreas

Answer 41

Acinar cells replacement via mitotic division from surviving cells or duct epithelium ○ Dependent on adequate blood supply and adequate duct drainage Hampered by fibrosis as release collagen fibres causing scar tissue and restricting the area for regrowth of functional tissue Stellate cells - contribute to fibrosis as they sit around acinar cells are if damaged release the collagen for fibrosis

Question 42

congenital abnormalities list 3 types

Answer 42

1) Ectopic pancreatic tissue - Pancreatic tissue found in the wall of the duodenum 2) Abnormalities of the pancreatic duct: 1. Variations in duct pattern 2. Pancreatic bladders - reported in cats are formed by duct dilation and grossly resemble gall bladders 3. Cystic pancreatic ducts - generally don't occur in isolation but also occur in the liver and kidney 4. Congenital stenosis of ducts (narrowing of the ducts) 3) Exocrine pancreatic hypoplasia Hypoplasia - underdevelopment - tissue never grew in the first place - Incomplete growth/development of exocrine parenchyma - acinar cells - Islets and ducts are generally normal Occurs sporadically in calves and affected calves have clincial signs of exocrine pancreatic insufficiency

Question 43

exocrine pancreatic atrophy what types

Answer 43

Atrophy - degeneration of tissue - tissue mass decreases after growth to the normal size has been achieved 1) Primary atrophy 2) secondary atrophy

Question 44

primary atrophy, what is it, due to what, what occurs, is it reversible if so how

Answer 44

- Diffuse change - Due to starvation, anorexia, chronic disease, nutritional deficiencies - Depletion of zymogen granules, then acinar cells shrink ○ Acinar architecture lost ○ Chronic - eventually lose all RER so function capacity is gone - no longer create enzymes - May be reversible by acinar cell hypertrophy (enlargement of individual cells) and hyperplasia (increased number of cells following mitotic division)

Question 45

secondary atrophy results from what occurs

Answer 45

- almost all acinar parenchyma has disappeared - Resulting from pancreatic disease ○ Eg duct obstruction and fibrosis - Often non-uniform distribution - May see cocurrent inflammation/fibrosis which may extend to the islets

Question 46

Juvenile pancreatic atrophy what breed more likely at what age, what type of disease, what does it do, what is the result

Answer 46

Dogs – esp. German Shepherds - inherited autosomal recessive trait - 6-12 months old - Autoimmune mechanism - multifocal lymphocytic pancreatitis - destroys pancreatic tissue, causing multifocal lymphocytic pancreatitis - barely any pancreatic tissue remaining Manifests as exocrine pancreatic insufficiency - cannot digest food and losing weight - Lots of sugars, carbohydrates aren't being digested and absorbed so act as solute and drag out water changing the osmotic pressure and causing watery osmotic diarrhoea

Question 47

exocrine pancreatic insufficiency what cause, clinical signs,

Answer 47

- due to the large functional reserve, > 90% of exocrine pancreatic secretory function must be lost before clinical signs of nutrient maldigestion emerge - Chronic weight loss (voracious appetite) - Pale voluminous faeces (soft, smelly, more water as osmotic diarrhoea - Undigested food particles (steatorrhoea (fat droplets), creatorrhoea (muscle fibres), amylorrhoea (starch particles)) - May have diarrhoea due to maldigestion, + occasionally small intestinal bacterial overgrowth which results in diarrhoea

Question 48

Define 1) steatorrhoea 2) creatorrhoea 3) amylorrhoea

Answer 48

undigested found in faeces 1) fat droplets 2) muscle fibres 3) starch particles

Question 49

exocrine pancreatic insufficiency where seen, what result in, diagnostic and treatment

Answer 49

- Mainly seen in dogs, usually resulting from juvenile pancreatic atrophy - May result from pancreatic necrosis or pancreatitis - TLI - expect low levels - Trypsin like immunoreactivity test treatment Need to give pancreatic enzyme supplementation for the rest of its life Avoid fatty foods and give highly digestible food - once vomiting has ceased May need to give some antibiotics if get bacterial overgrowth

Question 50

actue pancreatic necrosis how severe what usually thought to be, what occurs

Answer 50

severly sick also called acute pancreatitis but necrosis with secondary inflammation - Perilobular distribution (occur around the edges of the lobules) – widespread or scattered foci throughout the organ - Involvement of surrounding fibrofatty connective tissues - fat cell destruction - Ducts and centrilobular parenchyma not involved in acute stages - Neutrophils are drawn in via necrosis of cells and they produce free radicals that can cause widespread tissue destruction

Question 51

clinical signs of acute pancreatic necrosis and causes

Answer 51

- Older/middle aged dogs - Overweight, onset sometimes after large fatty meal - Anorexia, depression, vague abdominal pain - Or severe abdominal pain, acute vomiting, dehydration, jaundice - Adopt the "prayer stance" in attempt to relieve cranial abdominal pain (could be liver or stomach as well) - May be subclinical/unnoticed or severe causing shock and death - Cats: non-specific signs causes - Local release of activated proteolytic and lipolytic enzymes ○ Premature and innappropraite activation of enzymes, once effect blood flow and oxygenation of acinar cells go into shock and can release contents ○ Thought that fat droplets can block capillaries and cause acinar to go into shock Miniature schnauzers have genetics that lead to excess fat in blood - abdominal trauma - cats falling

Question 52

acute pancreatic necrosis possible causes of hypoxia, duct pressure mechanism

Answer 52

1) Acinar cells respond with increased intracellular Ca2+ → lysosome activation (contain destructive enzymes that can break down granules and activate enzymes within) releases granule contents 2) Trypsinogen → trypsin → other enzymes activated 3) Activated enzymes cause local tissue and vascular injury 4) Oedema (swelling of tissue), haemorrhage, thrombosis (blot clotting) and necrosis 5) Further damage from leukocytes - produce free radicals and enzymes

Question 53

acute pancreatic necrosis if severe what occurs

Answer 53

Activated enzymes and inflammatory mediators can get into the systemic circulation and cause: - Necrosis of hepatocyte - secondary liver failure - Pulmonary oedema - damage to alveolar tissue - Heart muscle and kidney damage 1) Serum protease inhibitors overwhelmed 2) Activation of coagulation and complement system 3) Intravascular coagulation, vasodilation and shock 4) Multiple organ failure and death

Question 54

acute pancreatic necrosis secondary problems

Answer 54

1) Bile duct obstruction - jaundice 2) Secondary bacterial infection 3) Ongoing necrosis and fibrosis of pancreas may cause destruction of islet cells leading to diabetes mellitus

Question 55

acute haemorrhagic pancreatic necrosis what species seen, what causes and what occurs

Answer 55

- Important in humans (bile duct calculi [stones] or alcohol abuse) - Occasionally seen in cats and dogs, maybe due to severe vomiting. - Caused by reflux of duodenal contents up the pancreatic ducts ○ Centrilobular and periductal necrosis - within the ducts - Severe haemorrhage and secondary infection/abscessation

Question 56

List the 3 types of pancreatitis

Answer 56

1) focal pancreatitis 2) multifocal pancreatitis 3) interstitial pancreatitis

Question 57

describe focal pancreatitis and what caused by

Answer 57

- Focal suppurative pancreatitis or pancreatic abscessation - Local or blood-borne spread of bacteria - Maybe caused by encysted nematode larvae in pigs

Question 58

Multifocal pancreatitis what involved, what causes, what diseases display this

Answer 58

- Multifocal necrosis with lymphocytic inflammation - Certain viral infections, e.g. canine distemper, parvovirus, adenovirus ○ Inflammation is secondary and occurs in other organs as well such as liver, spleen - Foot and mouth disease in ruminants - Toxoplasmosis in cats

Question 59

interstitial pancreatitis where inflammation, what causes, what occurs, what species important what is the result

Answer 59

- Inflammation of the interstitial connective tissues of the pancreas (esp. around the ducts) - Bacteria or parasites cause inflammation in the ducts which spreads. - Cats and horses: one pancreatic duct with bile duct – concurrent colangiohepatitis ○ Horses have two but the minor duct is so small occurs if this affects the major duct - In horses heavy scarring and enlargement of the pancreas due to irregular dilation of the ducts - End up with nodules in the pancreas due to fibrosis

Question 60

pancreatic duct calculi what is it, how often and pancreatic duct parasites what types and what causes

Answer 60

``` Pancreatic litiasis (balls) - Rare and occasionally seen in cattle - Line the main pancreatic duct Some flukes - May cause inflammation, fibrosis as try to wall off the parasite and obstruction ```

Question 61

pancreatic neoplasia what are they two types for exocrine and what occurs

Answer 61

1) Exocrine pancreatic adenoma - Rare, benign 2) Exocrine pancreatic adenocarcinoma - Malignant, arising from acinar cells or duct cells - spontaneous change - Nodules with haemorrhage and necrosis - Can spread from pancreas to the liver - Older dogs, may show signs of anorexia and weight loss, or signs of pancreatic necrosis

Question 62

The crypt-villus unit how related, where blood vessels and what are the cell types within the villus and the crypt

Answer 62

- Crypt is continuous with the villus - Cells undergo upward migration from the crypt to the villus - Blood vessels are very close to the intestinal lumen - only one cell distance Villus cell types - As cells migrate from crypts differentiate into the following 1) Goblet cells 2) Columnar absorptive cells Crypt cell types 1) Columnar cells 2) Paneth cells 3) Stem cells - origin of all cells that make up the crypt and villi

Question 63

List and describe the 4 differences of the jejunum and ileum compared to the duodenum

Answer 63

1) Villi are longer in the duodenum however they are longer relative to the crypts in the jejunum and ileum 2) Density of goblet cells increases caudally 3) No Brunners glands 4) Peyer's patches are present - Aggregated lymphoid nodules in submucosa - Most obvious in the ileum

Question 64

brunner's glands where found, what type of gland which what secretory units, where do duct penetrate and open

Answer 64

- Glands present in submucosa of duodenum - Tubulacinar glands - Mucus secretion or mixed serous/mucus - species variation - mucus in dogs and ruminants, serous is horses and pigs - Ducts penetrate muscularis mucosa - Ducts open into base of intestinal mucosal glands

Question 65

where are the capillaries in the villus and what is the lacteal

Answer 65

capillary in lamina propria | lacteal is the lymphatic in the lamina propria

Question 66

What is secreted and from what cells in the mucosa of the small intestine that are specialized for digestion

Answer 66

1) Digestive enzymes- - membrane bound in columnar absorptive cells - Paneth cells ( ruminants and horses only) ○ secrete peptidase & lysozyme 2) Mucus- - from goblet cells on villi - from submucosal glands (Brunner’s glands - duodenum only) - submucosal glands- mucous in dogs & ruminants ○ serous (proteinaceous) in pigs & horses 3) Chloride - From columnar cells of crypts

Question 67

paneth cells where located, what shape, what species present and what role

Answer 67

- At the base of mucosal glands - Pyramidal shape ○ Prominent eosinophilic granules and basal nucleus - Antibacterial role ○ Secretes peptidase and lysozyme - Ruminants and horses

Question 68

columnar cells what triggers chloride secretion and how to increase chloride secretion, what does increase result in

Answer 68

- Increased cAMP & increased cGMP--> increased chloride secretion ○ Can occur due to different toxins as well - how they exert their effects § Cholera toxin - cAMP increase § E.coli - cGMP increase - Increase in chloride means increase in secretory diarrhoea ○ Increase osmotic pressure due to increase in salts which increases loss from the gut resulting in secretory diarrhoea

Question 69

list 4 specilisation for absorption in small intestine

Answer 69

1) Sheer length of the tube 2) Mucosal/submucosa folds - plicae 3) Finger-like projections of mucosa - villi 4) Folding of apical cell membrane - microvilli - brush boarder

Question 70

enterocytes what type of epithelial cells, function and special characteristic

Answer 70

- Simple columnar epithelial cells - most numerous - Absorptive cells - Prominent microvilli on apical border Glycocalyx - mucus layer firmly attached to cell surface

Question 71

where does most of the reabsorption of water occur but what is most efficient also list 2 important molecules absorbed from ileum and what can result

Answer 71

Most of the reabsorption of water occurs in the duodenum and jejunum however in colon water absorption still really important and higher efficiency Ileum absorption 1) Bile salts 2) Fat soluble vitamins - vitamin B12 - Vitamin B12 deficiency can result from ileal resection

Question 72

Oral rehydration therapy how used with Na+

Answer 72

- Clinical use for osmotic diarrhoea as increase glucose load so Na+ will be absorbed will help reserve the osmotic pressure and stop the water loss from the tissues ○ The Na/glucose cotransport system is unaffected by some diarrhoea causing organisms - like E.coli

Question 73

List the 3 factors that decrease sodium absorption and what causes these

Answer 73

1) cAMP- increased by prostaglandins, cholera toxin 2) cGMP- increased by E Coli toxic agent (tourist diarrheoa) 3) intracellular Calcium- increased by acetyl choline

Question 74

carbohydrate digestion and absorption in the intestines

Answer 74

- Dietary CHO presented to brush border as disaccharides - Disaccharidases located in brush border ( maltase, sucrase, lactase) • Co-transport of Na and glucose (driven by active transport of Na across basolateral border)

Question 75

protein digestion and absorption in intestines

Answer 75

* Presented to intestinal epithelium as small peptides and amino acids * Peptidases located in apical membrane (brush border) breakdown protein into amino acids * Amino acids absorbed by secondary active transport * Each amino acid has a specific carrier mediated Na dependent transport system

Question 76

folate and cobalamin (Vit B12) absorption in intestines

Answer 76

* Specific folate carriers located in mid small intestine * Specific cobalamin carriers located in distal SI (ileum) * Requires binding to intrinsic factor (compound) that is secreted by parietal cells of the stomach

Question 77

Where is the dysfunction in the following scenarios 1) sudden onset of profuse watery diarrhoea 2) chronic diarrhoea with pale fluid faeces 3) increase volume of pale faces 4) increased frequency of soft mucoid faeces

Answer 77

1) small intestine greatest proportion of water reabsorbed 2) pancreas - pale suggest fat may relate to low lipase production 3) liver/bilary system - primary bile salt deficiency 4) colon problem - inflammation of colon

Question 78

2 main roles of intestinal bacteria in carnivores

Answer 78

1. Promote proliferation of intestinal epithelial cells - compounds produced help stimulate 2. Help prevent the colonisation and proliferation of harmful bacterial species

Question 79

why do herbivores need bacteria for digestion

Answer 79

1) cellulose has mainly beta -1,4-linked polysacchardies that cannot be broken down from mammalian enzymes (amylase) 2) microorganisms synthesis essential amino acids that may not be present in diet 3) bacteria net producers water soluble vitamins (B group and vit K) - not in diet

Question 80

advantages and disavantages of foregut fermenters

Answer 80

Advantages 1) Large quantities of food can be stored rapidly for later mastication and fermentation. 2) Bacterial cell contents (a source of protein) are released at an early stage in digestion. 3) The main products of fermentation have ample opportunity to be absorbed in the remainder of the tract Disadvantages: 1) All food constituents are exposed to bacterial breakdown

Question 81

3 advantages of hindgut fermenters

Answer 81

1) Not all food constituents are exposed to bacterial breakdown; 2) Dietary protein, fats and non-structural carbohydrates can be digested and utilized by the animal in a similar way to the carnivores and omnivores. 3) The amount of easily digestible substrates such as starch reaching the hindgut is much reduced and it is mainly the indigestible fibre which is acted on by the bacteria.

Question 82

3 disadvantages of hingut fermenters

Answer 82

1) Only one opportunity to chew the food and therefore animal must chew it thoroughly as it ingests it. 2) Digesta may not be held in the GI tract for sufficient time to allow optimal/complete bacterial action 3) Not all of the products of bacterial action will get absorbed (e.g. decreased amounts of bacterial amino acids absorbed).

Question 83

how is food digested in fermentation

Answer 83

1) fermented into volatile fatty acids - absorbed through rumen wall 2) hydrolyses food into peptides and amino acids used by microbes to synthesize microbial protein 3) lipid digestion is limited and some bacterial lipids are generated

Question 84

Kangaroos how ferment food and what is special about their waste products

Answer 84

- Expanded foregut where bacteria and fungi ferment food - Not true ruminant as greatly expanded forestomach with sacculated (non-glandular) and tubular regions - Instead of releasing high amounts of methane kangaroos virtually none ○ Hydrogen by-product is instead converted into acetate which is then used for further energy ○ Bacteria have yet been isolated - want to possibly but in cow to reduce greenhouse emissions

Question 85

rabbits how do they ferment food and what special behavioral adaptation is present, what animal similar

Answer 85

- Large caecum with 10 times capacity of the stomach - don’t have large ascending colon - Overcome problem of lost productions of digestion through faeces by coprophagy ○ Produces two type of faeces the normal hard pellets (which are not eaten) and the soft faeces or caecotrophs, which contain well-fermented material from the caecum, and which are consumed. Guinea pigs

Question 86

birds how do they ferment food and what occurs on commercial concentrate diet

Answer 86

- Have two caeca like poultry and colon which ferments food (65% of GI content) - Gain little or nothing from fermentation when on commercial concentrate diet

Question 87

ruminal acidosis in cow cause and what occurs and what result in

Answer 87

cause - too much dietary carbohydrate entering rumen starch is easily fermentable by streptococci and lactobacilli and this leads to the production of lactic acid within the rumen, which lowers the pH below 5.5 and starts to kill off other bacteria result in inflammation of rumen mucosa, impaired FVA absorption and motility of rumen

Question 88

carbohydrate overload in horse cause

Answer 88

- Normally little starch escapes digestion in small intestine and reach bacteria in large intestine - If too much grain-based carbohydrate then mammalian digestive enzyme overwhelmed and most of starch available for hindgut microbes - same as ruminal acidosis - larger problem as inflammation increase permeability of colon wall so bacteria may enter blood stream - endotoxaemia (toxic shock)