Auer Ch 36 Small Intestine

Front 1

Duodenum length:

Back 1

1 meter in length

Front 2

Location of duodenum:

Back 2

right of midline, extends caudally and dorsally right abdomen, passes root of mesentery and right kidney, related to the transverse colon by duodenocolic fold, caudal to right kidney turns medially to left abdomen, to duodenojejunal flexure

Front 3

Major duodenal papilla:

Back 3

opening from the bile duct, pancreatic duct

Front 4

Minor duodenal papilla:

Back 4

opening to the accessory pancreatic duct. More distally the duodenum is.

Front 5

Location of jejunum:

Back 5

left dorsal abdomen

Front 6

Distinguishing feature of ileum:

Back 6

anti-mesenteric band, a continuation of the dorsal cecal band, can be referred to as ileocecal fold

Front 7

Composition of ileocecal orifice:

Back 7

3 muscular layers: inner circular layer, middle longitudinal layer continguous with longitudinal layer of ileum, outer layer continguous with circular layer of cecum

Front 8

Duodenal blood supply:

Back 8

gastroduodenal artery, a branch of the celiac artery

Front 9

Jejunal arterial supply:

Back 9

multiple jejunal arteries, branch from the cranial mesenteric artery

Front 10

Arrangement of jejunal arteries:

Back 10

comprise arcades within the mesojejunum, each arcade consists of a major jejunal artery, an arcuate vessel that forms a loop with the next jejunal vessel, and several vasa recta that pass from the arcuate vessel to the intestinal wall

Front 11

Ileal blood supply:

Back 11

ileal artery, a branch of the ileocecal artery, which is a branch of the cranial mesenteric artery

Front 12

Location of digestion and absorption of nutrients:

Back 12

predominately proximal half of small intestine

Front 13

Location of absorption of water:

Back 13

predominately distal third of the small intestine

Front 14

How does small intestinal mucosal anatomy differs from other regions?

Back 14

presence of villi, which are finger-like projections of epithelium

Front 15

How crypts related to villi?

Back 15

Villi are surrounded by crypts. After several cellular divisions, columnar cells in the crypts migrate to the villus

Front 16

What stimulates release of digestive enzymes?

Back 16

Hydrogen ions, protein, and fat in the duodenum stimulate the pancreas and liver to secrete digestive enzymes, secretin, and bile acids

Front 17

Secretin:

Back 17

released from S cells and results in secretion of water and HCO3 into the lumen

Front 18

Role of HCO3 secretion:

Back 18

neutralizes hydrogen ions preventing duodenal mucosal injury, provides functional pH for enzymes, and increases solubility of bile and fatty acids

Front 19

What do protein and fat stimulate the release of?

Back 19

cholecystokinin (CCK) from I cells

Front 20

Function of CCK?

Back 20

stimulates the pancreas to release amylase for carbohydrate digestion, lipase for fat digestion, and several enzymes for protein digestion

Front 21

What are the enzymes for protein digestion secreted from the pancreas:

Back 21

trypsin, chymotrypsin, carboxypeptidase, and elastase

Front 22

What cells comprise the mucosal epithelium?

Back 22

predominately enterocytes, goblet cells, enteroendocrine cells, paneth cells, and undifferentiated columnar cells

Front 23

Arrangement of enterocytes:

Back 23

microvilli, forming a brush border

Front 24

Function of brush border enterocytes:

Back 24

further digest nutrients, after initial breakdown by pancreatic enzymes, and absorb digestive products

Front 25

Enzymes used by microvilli enterocytes for digestion:

Back 25

disaccharidases to digest carbohydrates and peptidases to digest proteins

Front 26

How does water and ion movement occurs?

Back 26

transcellular and paracellular mechanisms

Front 27

Sodium movement:

Back 27

from lumen to cell down electrochemical gradient and from cell to circulation against its electrochemical gradient, using Na/K-ATPase pumps

Front 28

Benefit of Na electrochemical gradient:

Back 28

sufficient to move chloride, glucose, AA, and B vitamins into the cell against electrochemical gradients

Front 29

Primary mechanism for water movement:

Back 29

paracellular

Front 30

Benefits of paracellular water movement:

Back 30

pulls low molecular weight substances, such as Ca, Mg, AA, and glucose with it

Front 31

What is transcellular water movement linked to?

Back 31

osmotic gradient produced by pumping of Na out of cell, gradient pulls water into the cell, increasing intracellular hydrostatic pressure, which forces water across the membrane into the capillary bed

Front 32

Pancreatic amylase products:

Back 32

oligo- and disaccharides

Front 33

How are oligo- and disaccharides digested?

Back 33

to monosaccharides by brush border oligosaccharidases and disaccharidases

Front 34

Examples of monosaccharides:

Back 34

fructose, glucose, and galactose

Front 35

How are glucose and glactose moved from the lumen to the cell?

Back 35

by Na- dependent cotransporters

Front 36

How is fructose moved from lumen to cell?

Back 36

cellular diffusion and does not require Na

Front 37

How are monosaccharides moved from cell to capillary bed?

Back 37

occurs through passive transport down a concentration gradient

Front 38

Pancreatic peptidases products:

Back 38

small neutral peptides

Front 39

How are small neutral peptides digested?

Back 39

broken down to dipeptides, tripeptides, or AA by brush border oligopeptidases, Intracellular enterocyte oligopeptidases reduce peptides to AA

Front 40

How are AA transported to the capillary?

Back 40

down a concentration gradient

Front 41

Pancreatic lipase products:

Back 41

fatty acids and monoglycerides from long and medium chain triglycerides

Front 42

How do fatty acids, monoglycerides, fat-soluble vitamins, and cholesterol move from lumen to cell?

Back 42

combine with bile acids to form a water soluble micelle. Micelles carry these substances to brush border for release and absorption, from the lumen to the cell, down a concentration gradient

Front 43

How do fatty acids and monoglycerides move out of the cell?

Back 43

formed to chylomicrons in cell, which are released to lymphatics

Front 44

How is iron absorbed?

Back 44

If systemic stores are low, Fe enters the cell from the lumen, remains unbound, and is transported out of the cell by transferrin receptors. If systemic stores are adequate, enterocytes are high in an iron-binding protein called apoferritin. After entering the cell from the lumen, iron is bound to apoferritin to form ferritin. Ferritin remains stored in the cell and is lost when the brush border enterocyte exfoliates at the end of its life span

Front 45

Where does Ca absorption occur?

Back 45

predominately in the duodenum

Front 46

How does Ca move from lumen to enterocyte?

Back 46

down a concentration gradient using a transporter and complexed to a Ca- specific binding protein

Front 47

What regulates Ca-specific binding protein?

Back 47

Vitamin D bioactive form, 1,25-dihydroxycholecalciferol

Front 48

How is Ca transported from the cell to the capillary bed?

Back 48

against its electrochemical gradient using Ca-ATPase pumps

Front 49

What do crypt cells secrete?

Back 49

chime, secretory IgA, and noxious or infectious agents, mucus

Front 50

Layers of smooth muscle of the small intestine:

Back 50

outer longitudinal layer, inner circular layer

Front 51

Function of outer longitudinal muscle layer:

Back 51

responsible for synchronous shortening and widening of segemnts

Front 52

Function of inner circular layers:

Back 52

responsible for rhythmic segmentation, lengthening and narrowing the lumen

Front 53

What controls longitudinal shortening?

Back 53

interstitial cells of cajal (ICC)

Front 54

What are ICC?

Back 54

pacemaker cells

Front 55

Where are ICC located?

Back 55

either associated with the muscle or are within myenteric plexuses

Front 56

Types of myoelectric activity of the smooth muscle:

Back 56

slow wave or an action potential

Front 57

What are slow waves?

Back 57

phasic oscillations of the smooth muscle resting potential, responsible for the rhythmicity of muscular contractions

Front 58

What are smooth muscle action potentials?

Back 58

created when threshold of muscle cells is lowered and the phasic slow wave depolarizes

Front 59

Phases of migrating motor complex:

Back 59

Phase 1 only slow waves without any action potentials, phase 2 has slow waves with occasional or intermittent action potentials, phase 3 has an action potential for every slow wave

Front 60

Benefits of MMC?

Back 60

reduces bacterial colonization in the small intestine and phase 2 is responsible for moving most of a digested meal through the small intestine

Front 61

Neural control of motility:

Back 61

Sympathetic input (cranial and caudal mesenteric plexuses), parasympathetic input (vagus nerve), enteric nervous system

Front 62

What is the enteric nervous system composed of?

Back 62

ganglia in the myenteric plexus and the submucosal plexus

Front 63

What do myenteric neurons innervate?

Back 63

longitudinal muscular layers and the outer circular layer

Front 64

What do submucosal plexus neurons innervate?

Back 64

inner circular musculature

Front 65

How does ileal motility control differ from other portions of the small intestine?

Back 65

ileum also has migrating action potential complex (MAPC), serotonin & presence of intraluminal fatty acids increase peristalsis

Front 66

What can small intestinal injury result from?

Back 66

small intestinal distention or ischemia or both

Front 67

MOA of distention injury:

Back 67

Gas distention or intraluminal ingesta can compress mural veins, compression increases capillary pressure results in filtration of fluid from the vessel into the interstitium, causing tissue edema, fluid moves from the tissues into the intestinal lumen, arterial compression leads to complete ischemia of the tissues, mucosal injury results in loss of the epithelial barrier, endotoxin exposure

Front 68

What injury can result after decompression of distended intestine?

Back 68

Serosal edema and serosal infiltration by RBC and WBC

Front 69

Restitution:

Back 69

migration of crypt cells to cover the villus tip in early healing

Front 70

Examples of non-strangulating disease:

Back 70

ileal impaction, ileal muscular hypertrophy, ascarid impaction, proximal enteritis, neoplasia, gastroduodenal obstruction, and inflammatory diseases

Front 71

Risk factors for ileal impactions:

Back 71

coastal Bermuda grass hay, especially in southwest US, seasonal predilection may be present, with many cases occurring in the fall, tapeworm (anaplocephala perfoliata) infestation

Front 72

Reasons for post-operative failure with parascaris equorum infestation:

Back 72

undetected intestinal damage, release of toxins or antigenic proteins from dead worms, pre-existing debilitation, pre-exisiting pneumonia, and failure to remove a significant portion of worms at surgery

Front 73

Ascarid control:

Back 73

use of anthelmintics effective against parascaris, deworming no sooner than 60 days of age, retreating at interval sufficient to prevent pasture contamination, allowing passage of a modest amount of worms to decrease selection pressure for anthelmintic resistance

Front 74

Results of inflammation associated with proximal enteritis:

Back 74

disruption of mucosal barrier, endotoxemia, liver injury results when duodenal contents are refluxed into the common bile duct, resulting in ascending infection and absorption of endotoxemia

Front 75

Treatment goals of proximal enteritis:

Back 75

frequent gastric decompression, maintain fluid and electrolyte balances, and restore normal intestinal function, prevention or attenuation of endotoxemia

Front 76

Inflammatory intestinal diseases:

Back 76

proliferative enteropathy caused by lawsonia intercellularis, eosinophilic gastroenteritis, idiopathic focal eosinophilic enteritis, and intestinal pythiosis.

Front 77

Examples of strangulating obstruction:

Back 77

volvulus, epiploric foramen entrapment, pedunculated lipoma, intussusception, mesenteric rents, inguinal herniation, gastro-splenic ligament entrapment, vitalline anomalies, umbilical herniation, and digphragmatic herniation

Front 78

Volvulus:

Back 78

rotation of jejunum or jejunum and ileum around the mesentery into distinct spirals

Front 79

Volvulus nodulus:

Back 79

occurs when the jejunum and ileum undergo a 360 rotation and form a mesenteric pouch which traps prestenotic jejunum, pulling the ileum into the pouch, to form a loop that knots the entrapment

Front 80

Borders of epiploic foramen:

Back 80

dorsal and craniodorsal caudate process of the right liver, cranioventral border is the portal vein, and the gastropancreatic fold is the ventral border

Front 81

Factors associated with the development of EFE:

Back 81

increased periods of stabling (i.e. in fall and winter), cribbing behavior, history of colic in the previous year, and an increased height of the individual horse

Front 82

Anatomy of most EFE:

Back 82

occur from small intestine located on the left traversing to the right abdomen through the foramen

Front 83

Locations of intussusception:

Back 83

jejunojejunal, jejunoileal, ileoileal, and ileocecal

Front 84

intussuscipien :

Back 84

outer, exposed portion of the intussusception

Front 85

intussesceptum :

Back 85

inner, unexposed, entrapped portion

Front 86

Surgical correction of ileoileal and ileocecal intussusceptions:

Back 86

reduction, reduction with myotomy, incomplete bypass

Front 87

Describe typhlotomy technique to remove non-reducible intussusception:

Back 87

distal jejunum transected with stapling devise close to ileocecal junction, stab incision made into cecum, intussuscption pulled through cecal incision, incision made into wall of intussescipien and intussusceptum exteriorized through incision until transected end of jejunum is distal to final transection site, final transection of ileum made within lumen of cecum using a stapling devise

Front 88

Complications of typhlotomy technique to remove intussusception:

Back 88

hemorrhage if mesenteric vessels tear when pulling the damaged bowel through the cecum

Front 89

Types of inguinal hernias:

Back 89

indirect or direct, congenital or acquired

Front 90

Indirect hernia:

Back 90

bowel within vaginal tunic after passing through the vaginal ring

Front 91

Direct hernia:

Back 91

vaginal tunic ruptured, bowel is in direct contact with the subcutaneous space of the scrotum

Front 92

What congenital hernias require surgical intervention?

Back 92

Those that rupture, or do not resolve spontaneously

Front 93

Approach to congenital hernia repair:

Back 93

inguinal incision, bowel returned to abdomen, closed castration performed, with a transfixation ligature through the vaginal tunic

Front 94

Approach to direct hernia repair:

Back 94

edges of the tunic are identified, bowel is reduced, castration is performed and the tunic closed

Front 95

Acquired hernia correction:

Back 95

manual massage standing, in dorsal recumbancy, or by laparoscopic guidance, should have hernioplasty performed to prevent reherniation, hernias that are not amenable to correction by these methods can be approached through an inguinal incision with or without a ventral midline approach

Front 96

How is hernioplasty performed?

Back 96

laparoscopically in the recumbent or standing horse and ring closure or coverage can be by graft, mesh, or mesh plug

Front 97

Benefits of unilateral castration after acquired inguinal hernia:

Back 97

more complete closure of the tunic and eliminate risk of recurrence

Front 98

How is small intestine incarcerated through a rent in the gastrosplenic ligament?

Back 98

passes from caudal to cranial such that the entrapped loop is situated lateral to the stomach and cranial lateral to the spleen

Front 99

Examples of Vitelline anomalies:

Back 99

mesodivericular bands or meckel diverticula

Front 100

Mesodiverticular band:

Back 100

develop when the vitelline artery and its mesentery do not atrophy during embryonic development

Front 101

Meckel diverticula:

Back 101

remnants of the omphalomesenteric (vitelline) duct, which was a communication between the yolk sac and the early embryonic gut

Front 102

Parietal hernia:

Back 102

occurs when only the antimesenteric portion of the wall of the ileum is incarcerated

Front 103

What does successful small intestinal surgery require?

Back 103

identification & correction of the primary insult, decompression of small intestine, resection of non-viable intestine, preservation of anatomic and physiologic continuity, rapid completion of surgery, early return of intestinal function, and appropriate post-operative support

Front 104

Intra-operative criteria for judging viability:

Back 104

serosal color, improvement in color after correction, mesenteric arterial pulse, intestinal motility either spontaneous or evoked

Front 105

Freeman’s viability grades:

Back 105

Grade I: Improves within 15 minutes after correction of the lesion and is similar to healthy adjacent bowel, but slightly darker pink, with mild edema and rare ecchymoses. Motility spontaneous or induced by snapping a finger against the intestinal wall; Grade II: Improves within 15 minutes after correction of the lesion and has marked edema, with extensive ecchymoses, coalescing into diffuse patches of red against a background of dark pink, and no circumferential constrictions at points of strangulation. Motility weak or induced by snapping a finger against the intestinal wall; Grade III: Similar to Grade II, with some circumferential constriction in the wall and/or black patches or stripes against a red background; Grade IV: Improves slightly or not at all within 15 minutes after correction of the lesion and predominantly dark red, blue or purple, with bowel wall thickness ranging from thin to thick, a flaccid wall, little or no motility and with or without black striations, a necrotic odor or constrictions at points of strangulation; Grade V: Diffusely grey, black, or green amotile bowel with or without a necrotic odor.

Front 106

Describe decompression of the bowel through a proposed resected portion:

Back 106

mesenteric vessel ligated 2-3 times or ligated and transected with a LDS , leaving a tail of suture, mesentery cut a set distance from bowel, ligating vessels in mesentery as reached, bowel exteriorized and emptied away from the surgical field, proximal and distal aspects of freed bowel can be anastomosed, ends of mesenteric suture gathered and tied

Front 107

Options for anastomosis involving the jejunum:

Back 107

hand sewn end to end jejunojejunostomy, stapled side to side jejunojejunostomy, or stapled functional end to end jejunojejunostomy

Front 108

Describe hand sewn EE JJO:

Back 108

large stoma should be created by cutting intestine at 50 to 60 degree angle or by creating S shaped curve, single suture placed first through mesenteric ends and antimesenteric ends to align the ends properly, closed in single or double layer closure

Front 109

Benefits of cushings pattern:

Back 109

less exposure of suture material

Front 110

Disadvantage of cushing pattern:

Back 110

more likely to purse string the bowel

Front 111

Disadvantages of double layer closure:

Back 111

excessive seromuscular inversion, stomal constriction, and post-operative obstruction

Front 112

Advantages of stapled JJO:

Back 112

speed, reduced tissue handling, improved tissue blood flow, and reduced contamination risk

Front 113

Disadvantage of stapled anastomoses:

Back 113

cost

Front 114

Benefit of EE anastomoses:

Back 114

maintain normal anatomic positioning and physiologic continuity

Front 115

Disadvantages of SS anastomoses:

Back 115

increase the number of raw edges, suture lines, and staple lines, which may increase focal inflammation

Front 116

Describe SS JJO:

Back 116

proximal and distal jejunum blind end stumps are created with either a TA90 or cut and closed manually with Parker-Kerr technique, 2 ends aligned side by side along the antimesenteric border, stay sutures placed in each segment, stab incision made into each portion of jejunum, GIA or ILA introduced into stab incision, fired to create a stoma and place 2 lines of staples on either side of the stoma, stab incisions are oversewn in inverted pattern

Front 117

Describe function EE JJO:

Back 117

exposed ends of the transected jejunal stumps are not closed, but aligned with each open end next to each other, GIA or ILA fired between the 2 segments from the open end, then the open portion is closed

Front 118

Types of Jejunocecal or ileocecal anastomosis:

Back 118

side to side or end to side

Front 119

Benefits of SS JCO:

Back 119

creates a larger stoma

Front 120

Complications of ES JCO:

Back 120

bowel kinking, adhesion formation, impaction, intusseception of the anastomosis, and torsion

Front 121

Describe ES JCO:

Back 121

stoma created between dorsal and medial cecal bands, transected end of intestine directed toward the cecal base, region of stoma creation on cecum elevated with babcock forceps, mesenteric and antimesenteric ends of attached to cecum with single sutures, lembert or cushings pattern used on 1 side to appose seromuscular layer of intestine to seromuscular layer of cecum, incision made in cecum, exposed edges of cecum and intestine apposed with simple continuous full thickness suture pattern on both sides of stoma, final side apposed with lembert or cushings inverted pattern, free intestinal mesentery sewn to cecum, following to ileocecal fold, ileal stump, and previously gathered mesentery

Front 122

Descrbe SS JCO:

Back 122

free end of jejunum or ileum is oversewn in Parker-Kerr technique or transected with TA90, placement of intestinal end is between dorsal and medial cecal bands, directed toward the base, hand sewn or can be created with stapling devises

Front 123

Advantages of JIO over JCO:

Back 123

preservation of anatomic and physiologic conditions, especially function of the ileocecal valve

Front 124

Disadvantages of JIO:

Back 124

obstruction of the anastomosis

Front 125

Surgical approach to the duodenum in the adult horse:

Back 125

cranial ventral midline to J shaped incision, with the table tilted to elevate the front end of the horse

Front 126

Post-operative small intestinal diet:

Back 126

small amounts of a high fiber diet

Front 127

Benefits of high fiber diet:

Back 127

stimulates propulsive motility and enhanced healing of anastomosis by flow of intestinal content through the region

Front 128

Indications for repeat celiotomy:

Back 128

post-operative colic

Front 129

Common findings on repeat celiotomy:

Back 129

Ileus, obstruction of the anastomosis, and intestinal ischemia

Front 130

Disadvantages of repeat celiotomy:

Back 130

increased risk of incisional infection and cost

Front 131

Post-operative small intestinal surgical complications:

Back 131

anastomotic obstruction, pain, endotoxemia, ileus, adhesions, and short bowel syndrome

Front 132

Causes of mechanical obstruction of the anastomosis:

Back 132

impaction of feed material, hematoma formation, constriction, and shortening of the mesentery

Front 133

Result of prolonged anastomotic obstruction:

Back 133

peritonitis and adhesion formation

Front 134

What increases risks of anastomotic obstruction?

Back 134

JCO and failure to decompress small intestine

Front 135

Why is anastomotic obstruction risk greater with JCO?

Back 135

when the small intestinal segment is directed toward the cecal apex, bypass of the function of the ileocecal valve, and the sharp transition between intestinal segments with differing functions, and devitalized ileal stump creating a focus for adhesions

Front 136

Factors that may contribute to post-operative ileus:

Back 136

increased PCV and heart rate, length of intestinal segment affected and or resected, duration of surgery, duration of anesthesia, segment affected, and increasing age

Front 137

Factors that may contribute to the formation of adhesions:

Back 137

ileus, ischemia, foreign material, serosal abrasion, excessive handling, and large suture material

Front 138

Most common location of intussesception:

Back 138

ileocecal