Gastrointestinal Function Flashcards

1
Q

Digestive Enzymes

A

Amylase, Lipase, Pepsin, Collapse, Phospholipase, Trypsin, Chymotrypsin, Enterokinase, Disaccharides, Dipeptidases

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2
Q

Salivary Glands

A

Enzymes: amylase, lipase
Targets: starch, TGLs

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3
Q

Stomach

A

Enzymes: pepsin, lipase
Targets: proteins, TGLs

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4
Q

Pancreas

A

Enzymes: amylase, lipase/colipase, phospholipase, trypsin, chymotrypsin
Targets: starch, TGLs, phospholipids, peptides,

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5
Q

Intestine

A

Enzymes: enterokinase, disaccharides, dipeptides
Targets: activates trypsin, complex sugars, peptides

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6
Q

“entero”

A

= gut

enterocyte: absorbs nutrients - lipids in the SI

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7
Q

GI tract anatomy

A

Mesentery - OUTER layer containing blood vessels

Mucosa - Epithelial, lamina propria, muscularis mucosa
Submucosa - Meisseners plexus
Muscular Propria - circular muscle (auerbachs myenteric plexus), longitudinal muscle
Serosa - cell lining around the mesentery

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8
Q

Trypsin

A

attracts:
lys (+) - aromatic won’t fit
arg (+) - activates chymotrypsin & collapse

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9
Q

Epithelial vs. Endothelial

A

Epithelial - in contact with outside world

Endothelial - inside only (i.e.: blood vessels)

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10
Q

How to make food usable?

A

1) Mechanical disruption (mastication in mouth and churning in stomach)
2) Chemical digestion (lipids, aa, carbs)

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11
Q

Pepsin

A

ONLY zygomen that is is not activated by cleavage - activated by LOW pH

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12
Q

Enterokinase

A

enteropeptidase that activates trypsinogen by converting it to trypsin

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13
Q

GI peptides/modulators

A

1) Endocrine - SLOW
- ALL GI endocrine hormones are peptides

2) Paracrine
- peptides: somatostatin
- non-peptides: histamine

3) Neurocrine - FAST
- peptides: VIP
- non-peptides: ACh, NE
- nerve release diffuse to target cells

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14
Q

GI Hormones

A
Secretin
Gastrin
Cholecystokinin (CCK)
Glucose-Dependent Insulinotropic Peptide
Motilin
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15
Q

Hormonal Control of Digestion

A

1) Physiological even in one part that alters activity in another
2) Effect persists after denervation
3) Eliminating source tissue prevents response
4) Isolated substance produces response when injected into blood at proper dose

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16
Q

Gastrin

A

ANTRUM! (duodenum & jejunum too)

  • related to CCK (Trp-Met-Asp-Phe-NH3)
  • G cells
  • gastric acid secretion is 1,500x MORE potent than histamine
  • trophic activity: stimulates growth of oxyntic mucosa of stomach, duodenal mucosa, and colon mucosa
  • surgical removal of antrum causes atrophy
  • patients with gastrin-secreting tumors have mucosal hyperplasia and hypertrophy
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17
Q

Tyrosine

A

MUST be sulfated in Gastrin & CCK

18
Q

CCK

A
  • related to Gastrin (Trp-Met-Asp-Phe-NH3)
  • digests fat and slows down chyme to slow gastric emptying
  • emptying of gallbladder
  • pancreatic exocrine enzymatic secretion
  • inhibits gastric emptying
  • delivery of pancreatic enzymes and bile into small intestine
  • trophic effects: exocrine pancreas and gallbladder mucosa
19
Q

Secretin

A
  • natures antacid
  • requires ALL 27 AA for activity
  • released from S cells of duodenal mucosa
  • stimulates bicarb and pepsin to inhibit gastric secretion
  • acid (less than 4.5pH) and fatty acids cause release
  • trophic effect on exocrine pancreas
20
Q

GIP (gastric inhibitory polypeptide)

A
  • released from K cells of the duodenum and proximal jejunum
  • oral glucose
  • all food (protein, carb, fat)
  • fat MUST be hydrolyzed
  • stimulates insulin release
  • inhibits gastric acid secretion
21
Q

Motilin

A
  • released from M cells of duodenum and proximal jejunum during FASTING (100+ min)
  • peptide family
  • Neural controls release
  • stimulates upper GI motility
  • “housekeeping contractions”
22
Q

Hypertrophy vs. Hyperplasia

A

trophy - cell size

plasia - replication

23
Q

Zollinger-Ellison Syndrome

A

Gastrinoma!!!
- ChiRhoStim (synthetic secretin) used to inhibit gastric secretions! if gastrin production doesn’t stop, indicative of a gastrinoma (NOT a peptic ulcer)
- Loss of K+ in stool
- increase in parietal cell mass: increase acid production
- intestinal hyperacidity leads to peptic ulcer
- decrease in bile salts and lipase activity
= diarrhea, steatorrhea, hypokalemia

24
Q

Low pH

A
  • inactivates pancreatic lipase
  • bile salts precipitate
    = steatorrhea
25
Q

Hypokalemia

A
  • results from loss of K+ GI secretions in stool

IMPORTANT for movement - nerve/muscle

26
Q

Histamine

A
  • acid secretion
  • Gastrin and ACh cause histamine release from cells in stomach
  • histamine H2 receptor blockers decrease acid secretion! (ex: cimetidine (tagamet) and ranitidine (zantac))
27
Q

Cimetidine

A

ie: Tagamet

histamine H2 blocker that decreases acid secretion

28
Q

Ranitidine

A

ie: Zantac

histamine H2 blocker that decreases acid secretion

29
Q

Paracrines

A

Somatostatin (peptide) and Histamine

30
Q

Somatostatin

A
  • release stimulated by acid
  • inhibited by ACh
  • directly inhibits parietal cell acid secretion
  • mediates acid induced inhibition of gastric release
31
Q

Parietal Cell

A
  • secretes acid
32
Q

Neurocrines

A

VIP, GRP (Bombesin), Enkephalins

33
Q

VIP

A
  • decrease in Ca++ relaxes gut smooth muscle

- located in gut mucosa and smooth muscle

34
Q

GRP (Bombesin)

A
  • gastrin releasing peptide from G cells
  • located in gastric mucosa
  • with CCK, stops hunger signals
35
Q

Enkephalins

A
  • increases smooth muscle tone

- located in gut mucosa and smooth muscle

36
Q

Enteric Nervous System

A
  • intrinsic nervous system
  • network of neurons that control GI system
  • second brain: MORE neurons than spinal cord and can operate independently of the brain
  • myenteric auerbach’s plexus
  • submucosal meissner’s plexus
37
Q

Autonomic Nervous System

A
  • extrinsic nervous system
  • parasympathetic stimulates ACh (preganglionic) & VAGUS NERVE
  • sympathetic inhibits NE (postganglionic)
38
Q

Mast Cell

A
  • immune control of GI function
  • resting mast cell and activated mast cell

1) GI tract - increased fluid secretion and increased peristalsis lead to expulsion of GI tract content (diarrhea/vomitting)
2) Airway - decreased diameter and increased mucous secretion leads to expulsion of airway contents (phlegm/coughing)
3) Blood Vessels - increased blood flow and increased permeability lead to edema, inflammation, increased lymph flow and carriage of antigen to lymph nodes

39
Q

Cytokine

A

TNF-a promotes inflammation, stimulates cytokine production bu many cell types and activates endothelium

40
Q

Tryptase, Chemise, Cathespin G & Carboxypeptidase

A

enzymes that remodel connective tissue matrix

41
Q

Toxic Mediators

A

Histamine and herapin are toxic to parasites to increase vascular permeability and cause smooth muscle contraction

42
Q

Heparin

A

toxic mediator that is toxic to parasites to increase vascular permeability and cause smooth muscle contraction