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E&E > SI function & digestion/absorption (Songster) > Flashcards

SI function & digestion/absorption (Songster) Flashcards

1
Q

GIT MOTILITY

5 layers of GIT

A
  1. serosa
  2. longitudinal smoooth muscle
  3. circular smooth muscle
  4. submucosa
  5. mucosa
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2
Q

GIT MOTILITY

Two phases of GIT motility

A
  1. Digestive: promotes digestion by mixing contents w/ enzymes and maximizes mucosal contact (for absorption into bloodstream)
  2. Interdigestive: housekeeping phase. Strong contractions driven by migrating motor complex (electrical waves that migrate in SI that move contents along in response to motilin hormone).
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3
Q

GIT MOTILITY

Segmentation contractions versus peristaltic waves

A

Segmentation = “chops” the chyme//back-and-forth mixing of chyme w/ secretions

Peristaltic waves = propulsive mixing that move chyme toward ileocolic junction / spread chyme along intestinal mucosa

chyme, a thick semifluid mass of partially digested food and digestive secretions that is formed in the stomach and intestine during digestion. In the stomach, digestive juices are formed by the gastric glands; these secretions include the enzyme pepsin, which breaks down proteins, and hydrochloric acid.

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4
Q

GIT MOTILITY

How are contractions coordinated?

A

Via intrinsic (enteric) and extrinsic (autonomic – para/symp.) nervous systems

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5
Q

GIT MOTILITY

Two plexuses of enteric nervous sytem and their functions

A
  1. Myenteric: motility
  2. Submucosal: blood flow and GI secretion
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6
Q

GIT MOTILITY

Peptide hormones that enhance SI motility

A
  • gastrin, CCK (digestive phase)
  • motilin (interdigestive)
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7
Q

GIT MOTILITY

peptide hormones that inhibit SI motility

A

secretin & glucagon (GIP)

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8
Q

GIT MOTILITY

CCK (Cholecystokinin)
- cell type of origin/stimulator
- sites of action + major functions

A
  • Stimulated by I cells in the duodenum
  • gall bladder contractions++; stimulates pancreatic growth and enzyme secretion (e.g., insulin); inhibits gastric emptying
  • stimulated by duodenal fatty acids; amino acids; high levels of duodenal acid

pushes bile from gall bladder into SI –> stomach relaxes

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9
Q

GIT MOTILITY

Secretin
- cell type of origin
- sites of action + major functions
- stimulators

A
  • stimulated by S cells in duodenum/jejunum in response to acid presence
  • stimulates secretion of bicarbonate-rich pancreatic fluids and of bile bicarbonate
  • relaxes duodenal papilla
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10
Q

GIT MOTILITY

3 Consequences of dysmotility of GIT (hypo- and hypermotility)

A
  • Ileus (hypomotility)
  • Diarrhea (either hypo or hypermotility)
  • Constipation (hypomotility)
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11
Q

CHO DIGESTION

What species can digest insoluble CHOs and how?

A

Herbivores (both soluble & insoluble) -> via FERMENTATION insoluble CHOs broken down by host microbes in rumen and/or cecum

True symbiotic rlstp. b/w microbes & insoluble CHOs

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12
Q

CHO DIGESTION

CHO digestion steps (luminal and mucosal phases)

A

Two phases: LUMINAL phase (part of digestive phase) and MUCOSAL (membranous) phase

  1. LUMINAL: pancreatic & digestive enzymes
    - CHOs get mechanically digested in the stomach
    - Chyme from stomach empties into duodenum & mixes with pancreatic juice (pancreatic amylase) -> majority of CHOs digested
    - Leftover CHOs (mainly di- and tri-saccharrides) b/c too big to enter enterocytes
  2. MUCOSAL (membranous): only small intestine enzymes
    - di/trisacharides too big to enter enterocytes get further digested
    - occurs on the BRUSH BORDER (microvili) of the SI

Chyme = the partially digested food expelled by stomach into duodenum

Pancreas and liver both produce “juices” that aid with digestion. The pancreas has a ductal system that drains its pancreatic juices into the duodenum. The liver produces biliary juices (bile) in its tissues (parenchyma) that pass into the biliary ductal system, where its ducts meet to form the common bile duct that then drain into the duodenum. Common bile duct + pancreatic duct drain into duodenum via major duodenal papilla

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13
Q

CHO DIGESTION

How do the products of luminal digestion get absorbed?

A

PRODUCTS = THE CHOS TOO BIG TO BE ABSORBED IN LUMINAL PHASE -> get absorbed in the MUCOSAL PHASE (in the jejunum) instead:

  • enterocytic enzymes (maltase, sucrase, lactase, isomaltase) cleave the di/trisaccharides into monosaccharides via hydrolysis, allowing for their absorption into enterocytes thru active 2º transport or facilitated diffusion
  • The monosaccharides within enterocytes then get absorbed into the bloodstream
monosaccharides get absorbed into enterocytes

These enzymes line jejunal walls & form the brush border (chemical barrier which food must pass ino order to be absorbed), and are bound to microvilli

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14
Q

PROTEIN DIGESTION

Describe the GASTRIC luminal phase in protein digestion

A

STOMACH
- Pepsin + acidic stomach (2-3 pH) break down protein into proteoses (large polypeptides) –> proteoses move into SI

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15
Q

PROTEIN DIGESTION

Describe the enteric luminal phase in protein digestion

A
  • In the Small Intestine
  • Pancreatic peptidases break the proteases (large polypeptides) into di/tripeptides, and a few amino acids
  • the AAs can be absorbed into the enterocytes, as well as some of the di/tripeptides can be absorbed into them
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16
Q

PROTEIN DIGESTION

Describe the mucosal phase in protein digestion

A

Occurs in the SI

  • Aminopeptidases cleave any remaining polypeptides into absorbale di/tripeptides and/or into absorbable individual amino acids
  • Absorbed peptides//AAs then can be absorbed into BOTH the bloodstream and lymphatic circulation

enter both blood and lymph circulation once absorbed

Intracellular proteases: there are also intracellular di/tripeptidases within enterocytes that will further break down any absorbed di/tripeptiddes into individual AAs
- Di and tripeptides can also be absorbed directly into circulation and don’t have to be cleaved into individual AAs!

17
Q

PROTEIN DIGESTION

Exocrine Pancreatic Insufficiency (EPI – malabsorption)
- pathogenesis
- clinical signs
- etiology

A
  • Pathogenesis: Failure of production of normal pancreatic enzymes –> proteins and carbs cannot be digested like normal -> therefore, the lack normal nutritional subunits that would typically get absorbed by enterocytes (malabsorption)
  • Clinical signs: weight loss/emaciated even though presence of ravenous appetite; very laege/soft stool with tan/yellow color due to excessive fat in stool
  • Etiology: atropy of the pancreas, often genetic or autoimmune condition

german shepherds; rough-coated collies

Tx = life-long via supplementing the missing pancreatic enzymes

18
Q

FAT DIGESTION

Enteric Fat Digestion
Describe the secretion of bile into the duodenal lumen + its role in fat digestion, and describe the roles of CCK and Secretin

A

BILE BREAKS DOWN FAT (TRIGLYCERIDES) INTO FATTY ACIDS via emulsification
- Bile is made in liver, stored in gallbladder, and secreted into duodenum via common bile duct
- Presence of fat + AAs in duodenum -> signal release of CCK -> CCK stimulates gallbladder contractions -> bile (acid + salts) gets released into lumen of SI//duodenum
- Secretin acts on pancreas to open up the duodenal papillae to allow for relase of bile into duodenum

bile salts = BA but with taurine or glycine attached, lowering PKA

lower pka allows for bile salts to be more soluble in water

19
Q

FAT DIGESTION

Emulsification

A

Required to transform insoluble triglycerides into soluble forms for absorption

  • occurs in the LUMEN of the duodenum, under the influence of bile
  • bile salts break the large fat globules down into smaller particles: fat droplets // soluble triglycerides

bile salts = BA but with taurine or glycine attached, lowering PKA; lower pka allows for bile salts to be more soluble in water

20
Q

FAT DIGESTION

Steps of fat absorption:

A
  1. Once emulsification occurs in duodenal lumen, the emulsified fat droplets (soluble triglycerides) are hydrolized (via pancreatic lipase) into fatty acids and monoglycerides in a micelle formation in the jejunum
  2. The micelle components (all bile components except for bile acids) are absorbed into enterocytes, then reassembled BACK into insoluble triglycerides
  3. The insoluble triglycerides are transported out of the enterocyte via combining with cholesterol & phospholipids -> transport vehicle (chylomicron)
  4. The chylomicrons are transported out into lymphatic circulation (never bloodstream!)

PANCREATIC LIPASE ACT ON MICELLES IN THE JEJUNUM!!

Micelles = in jejunal LUMEN
Chylomicron = in enterocyte

21
Q

FAT DIGESTION

Steps for the Bile Acids test

A
  1. Fast for 12 hours
  2. Obtain a pre blood sample
  3. Feed a fatty meal
  4. Obtain a post blood sample 2 hours later (after gallbladder has been able to contract/secrete bile into duodenum)

if liver is not functioning properly, will have high bile acids

Normal liver function: reabsorbs bile acids in distal ileum vasculature via portal circulation (enterohepatic circulation)

Abnormal liver function: Bile acids accumulate in portal circulation, spill over into systemic circulation -> high bile acids

22
Q

FAT DIGESTION

Bile composition

A

bile acids, water, electrolytes, choelsterol, phospholipids, proteins, fatty acids, bilirubin

synthesized by hepatocytes from cholesterol; stored in gallbaldder

23
Q

FAT DIGESTION

What stimulates gallbladder contraction in the interdigestive phase versus the post-prandial phase?

A

Interdigestive phase: GI contractions occur in response to the gallbladder’s response to the migrating motor complex (MMC) via motilin –> induces

Post-prandial: vagal stimulation (stomach distends with food), CCK, and Secretin (–> relaxtion of duodenal papilla)

Neuroendocrine controls GB contraction in post-prandial state especially

24
Q

FAT DIGESTION

Micelle

A
  • are smaller than emulsified fat droplets
  • are water-soluble -> CAN move thru watery SI luminal contents
  • diffue to apical surface of enterocytes (all components of bile MINUS bile acid)

bile acid gets reabsorded in distal ileus

25
Q

FAT DIGESTION

Why isn’t fat absorbed into systemic circulation immediately after GI absorption?

A

Chylomicrons are too big to enter into capillaries -> enter lymphatic system via lacteals, eventually entering systemic circulation via the thoracic ducts

arrows = thoracic ducts
26
Q

FAT DIGESTION

Lipemia

A

excessive amount of chylomicrons in systemic circulation

27
Q

FAT DIGESTION

Bile duct obstruction and vitamin K deficiency

A

Bile duct obstruction -> no bile in intestinal tract -> not able to digest fats or absorb fat-soluble vitamins (Vitamin K!!)
Vitamin K is necessary for clotting -> Check PT/PTT prior to surgery for bile duct obstruction and if abnormal, inject VitK parentally so it can be absorbed into systemic circulation//bypass intestinal absoprtion phase

E&E (30 decks)

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