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Flashcards in Physio Phinal Deck (141):
1

Motility

Movements that mix GI contents and propels them along the length

2

Secretion

Processes by which glands secrete water, enzymes, ions, etc. into the GI tract

3

Digestion

Processes by which large ingested molecules are degraded by enzymes to smaller and absorbable molecules

4

Absorption

Processes by which nutrients are absorbed by the GI tract and enter blood

5

Excretion

Excretion of undigested or waste products

6

Mucosa

Inner Most Layer of Gut Wall Containing:
-Single layer epithelium
-Lamina Propia
-Muscularis Mucosae

7

Lamina Propia

loose con. tissue (collagen, elastin fibrils), lymph nodes, capillaries found w/in the MUCOSA

8

Muscularis Mucosae

thin innermost layer of intestinal smooth muscle

9

Submucosa

Beneath the Mucosa, loose con. tissue, glands, large nerve trunks and blood vessels. Includes melssner's plexus.

10

Tight Junction

Located between cells, create a seal which prevents leaking and maintains cell gradients. Under physiological conditions they are mildly leaky

11

Villi

ABSORPTION: Increase SA, covered mostly in mature absorptive enterocytes and some mucus secreting cells, live only for a few days, die then shed into the lumen

12

Crypts (of Lieberkuhn)

SECRETION: invaginations around the villi, usually contain younger epithelial cells, stem cells at the base, generally found in colon

13

Muscularis Externa

Responsible for motility, located under the Submucosa, contains myenteric plexus

14

Serosa

Outermost layer of gut, mainly con. tissue, a layer of mesothelial cells which form mysentary

15

Regulatory Mechanisms (III)

I. Paracrine
II. Endocrine
III. Neural

16

Process Endocrine Regulation

I. Sensor Cell (EEC) receives stimulus, secretes hormone into the blood stream
II. Target cell (remotely located) receives signal, responds accordingly

17

Enteroendocrine Cells (EEC)

Open Type: apical membrane touching lumen, basolateral which secretes hormone
Closed Type: apical not in touch with lumen,

18

Process Paracrine Regulation

I. Sensor Cell (EEC) receives stimulus
II. EEC acts on target cell (located nearby) via diffusion through interstitial space
III. uses histamine, serotonin

19

Gastrin**

Source: Gastric antrum (G Cells)
Stimulus: Oligopeptides
Pathway: Endocrine
Targets: ECL cells and parietal cells of the gastric corpus
Effect: parietal cells secrete acid, ECL histamine

20

Secretin**

Source: Duodenum (S Cells)
Stimulus: Protons
Pathway: Endocrine, Paracrine
Targets: Vagal afferent terminals, pancreatic duct cells
Effect: Stimulation Pancreatic ductile secretion

21

Gluco-Insulinotropic Peptide (GIP)**

Source: Intestine (K Cells)
Stimulus: Fatty acids, glucose
Pathway: Endocrine
Targets: beta cells in pancreas
Effect: Stimulation insulin secretion

22

Peptide YY**

Source: Intestine (L Cells)
Stimulus: Fatty Acids, glucose, hydrolyzed protein
Pathway: Endocrine, Paracrine
Targets: neurons, smooth muscle
Effect: Inhibits gastric, pancreatic, gastric acid secretion, intestinal motility, food uptake

23

Cholecystokinin (CCK)**

Source: Duodenum (I Cells)
Stimulus: Fatty Acids, hydrolyzed proteins
Pathway: Paracrine, Endocrine
Target: vagal afferent terminals, pancreatic acinar cells
Effect: inhibits gastric emptying, acid secretion; stimulates pancreatic enzyme secretion, gallbladder contraction, inhibition food intake

24

Proglucagon-derived peptides 1/2 (GLP-1/2)**

Source: Intestine (L cells)
Stimulus: fatty acids, glucose, hydrolyzed proteins
Pathway: endocrine, paracrine
Targets: neurons, epithelial cells
Effect: glucose homeostasis, epithelial cell proliferation

25

Post-translational Modification of Hormones in GI Tract

modifications are used to move inactive peptides to their active forms, this mech prevents inappropriate digestion during times when no food is present

26

Neurocrine Regulation GI Tract

I. Afferent nerve senses stimulus
II. Signal propagates to the CNS
III. Efferent nerve relays signal to target cell

27

Innervation GI Tract

I. Extrinsic (cell bodies outside gut)
II. Intrinsic/Enteric (cell bodies in gut wall)

28

Enteric Nervous System (ENS)

-Responsible for motility, secretion, blood flow within the gut
-Independent of the CNS
-Myenteric Plexus (motility)
-Submucosal Plexus (secretions)

29

Extrinsic Nervous System (Parasympathetic)

-Stimulates the GI secretion and activity
-Acetylcholine is the key neurotransmitter
-Vasovagal Pathway, Gastric receptive relaxation pathway

30

Extrinsic Nervous System (Sympathetic)

-Plays an important role in regulation of blood flow in the GI tract
-Inhibits smooth muscle function, closes sphincters, decreases secretions

31

Cephalic Phase (Stimulation)

thinking about/anticipating eating
smelling (olfactory input)
seeing food (visual input)

32

Cephalic Phase (Response)

INC parasympathetic input:
-salivary, gastric acid, pancreatic enzyme secretion inc.
-contraction and relaxation of sphincter oddi (bile duct sphincter)

33

Oral Phase (Stimulation)

Ingested food is in contact with the surface of the GI tract

34

Oral Phase (Response)

In Mouth: initiation digestion via chewing, salivary enzymes (amylase and lingual lipase) and glycoprotein mucin

35

Functions GI Secretions

-Degradation macronutrients
-facilitate absorption
-lubricate food bolus
-maintain a proper ionic/osmotic milieu
-aid in repair/replacement of barrier functions
-contribute to body fluid homeostasis
-immunological functions

36

Functions Saliva

-Alkaline substance
-Lubrication/Moistening food for swallowing
-Solubilization for taste
-Produce intraluminal stimuli in stomach
-Neutralize refluxed acid in esophagus
-Clean mouth, antibacterial action
-Aid in speech

37

Duct Cells (II)

I. Ductal Cells (squat shape)
II. Myoepithelial Cells (elongated shape)

38

Ductal Cells

Modify ionic composition and osmolarity of saliva before it is excreted into the mouth. water impermeable.

39

Myoepithelial Cells

Stimulated by neural input, contract to eject the saliva

40

Acinar Cells (II)

I. Serous Cells
II. Mucous Cells

41

Serous Cells

secrete aqueous fluid: water, ions, enzymes

42

Mucous Cells

Secrete mucin glycoproteins

43

Submandibular Salivary Gland

Has both mucous and serous cells, produces 70% of total daily salivary secretion

44

Parotid Salivary Gland

Has only serous cells, produces 25% of total daily salivary secretion

45

Sublingual Gland

has only mucous cells, produces 5% of total daily salivary secretion

46

Saliva contains?

alpha-amylase, lipase, mucin glycoproteins, IgA

47

Saliva production is stimulated by?

BOTH parasympathetic and sympathetic nervous systems

48

Modification of saliva occurs when?

flow rate is low, it will take the Na, Cl out of the saliva and secrete K and HCO3 into it.

49

Process Saliva Production

I. Acinar cells make saliva (isotonic plasma-like solution)
II. When flow rate is low, ductal cells modify (makes hypotonic saliva)
III. Ducts absorb Na, CL and secrete K, HCO3
IV. Final saliva ejected into the mouth

50

High Flow Rate Saliva Composition

NO MODIFICATION
Na: High
Cl: High
K: Low
HCO3: same in both

51

Low Flow Rate Saliva Composition

MODIFICATION
Na: Low
Cl: Low
K: High
HCO3: same in both

52

Exchanger Vs. Transporter**

Exchanger = no net charge
Transporter = net charge is not 0

53

Transporters/Exchangers Apical Side Acinar Cells**

K Channels-- send K into lumen
HCO3, Cl channels-- send HCO3, Cl into lumen
Tight Junctions: allow Na and H2O into lumen

54

Transporters/Exchangers Basal Side Acinar Cells**

Na/K ATPase-- use ATP to force Na out of cell, K into cell
K Channel-- K flows out of cell
Na/H+ Exchanger-- Na comes in, H+ goes out
Na/2Cl/K Cotransporter-- pumps all three into the cell
Tight Junctions: allow Na and H2O into cell

55

Transporters/Exchangers Apical Side Ductal Cells**

Na Channel-- allows Na into Cell
Cl/HCO3 Exchanger-- sends HCO3 out to lumen, Cl in
Na/H+ Exchanger-- sends Na in, H+ out to lumen
H+/K Exchanger-- sends K out to lumen, H+ in
Tight Junctions: allow H2O to flow

56

Transporters/Exchangers Basal Side Ductal Cells**

Na/K ATPase-- Na out, K in
K Channels-- K out
Cl Channels-- Cl out
H+/Na Exchanger-- Na in, H+ out

57

Regulation Salivary Secretion (parasympathetic)

I. Parasympathetic Stimulation
II. Intracellular calcium increases due to Ach acting on muscarinic receptors
III. Acinar or Ductal Cells produce Saliva

58

Regulation Salivary Secretion (sympathetic)

I. Sympathetic Stimulation
II. Norepinephrine acts on Beta receptors, cAMP is released
III. Acinar or Ductal Cells produce saliva

59

Swallowing

-Propels food from mouth-->pharynx-->stomach
-Inhibits respiration (NO CHOKING)
-Initially voluntary, then involuntary

60

Esophageal Phase

I. Presence bolus initiates primary peristalsis, UES will relax and open to admit food then close
II. Wave moves slowly, distention triggers secondary peristalsis, LES will relax and open to accept food into the stomach.

61

Receptive Relaxation

LES and the proximal stomach relax in order to accept food w/out inc pressure in the stomach significantly

62

GERD

Gastroesophogeal Reflux Disease
-acid is allowed back through LES into throat
-acid causes pain and discomfort
-treat w/ omeprazole or ranitidine

63

Functions of the Stomach

-temporary storage
-secretion acid (kills microorganisms, converts pepsinogen to pepsin)
-secrete intrinsic factor (vit B12 absorption)
-secrete water for lubrication, aqueous environment
-motor activity for mixing/moving food

64

LES and Cardia of Stomach

Secretions: Mucus, HCO3
Purpose: prevent reflux, allow entry of food, regulation of belching

65

Fundus and Body of Stomach

Parietal Glands here
Secretions: H+, intrinsic factor, mucus, HCO3, pepsinogens, lipase
Purpose: reservoir, tonic force during emptying

66

Antrum and Pylorus of Stomach

Endocrine cells here
Secretions: Mucus, HCO3
Purpose: mixing, grinding, sleving, regulation of emptying

67

Anatomy of Gastric Pit (in fundus)

Neck Region: parietal cells, neck mucous cell
Base Cells: Chief Cells (secrete pepsinogen), connective tissue, parietal cell w/ several nuclei, capillary

68

At what pH does pepsinogen get converted into pepsin?

3.0 -- 3.5

69

Superficial Epithelial Cells (gastric pit)

located near the top, secrete bicarb

70

Mucous Neck Cell (gastric pit)

located under the superficial epithelial cells (still near top), secrete mucin

71

Stem Cells (gastric pit)

under the mucous neck cells, make new cells

72

Parietal Cells (gastric pit)

Located in the center, secrete acid (H+) and intrinsic factor

73

Chief Cells (gastric pit)

located as near the bottom, secrete pepsinogen which is converted to pepsin at low pH

74

Endocrine Cells (gastric pit)

located in the very bottom, these are enterochromaffin-like (ECL) cells which release histamine

75

Antrum

Contains no parietal cells, but does release gastrin (g cells) and somatostatin (d cells) from endocrine cells.

76

Resting Parietal Cells

tublovesiclles, intracellular canaliculi present in cytoplasm-- near to apical membrane, they have a low rate of secretion

77

Activated Parietal Cells

50-100 fold increase in surface areas, tublovesiciles fused with membranes of intracellular canaliculi which open to cell lumen of gland, they have a high rate of secretion

78

Mechanism of Acid Secretion (basal side)

-Bicarb/Cl exchanger pumps bicarb out and Cl into cell
-K Channels allow K to leave cell
-Na/K ATPase pumps Na out and K in

79

Mechanism of Acid Secretion (apical side)

H+/K ATPase pumps H+ into the cell lumen, K goes into the cell
-Cl Channels -- allow Cl to enter the lumen

80

Mechanism Proton Pump Inhibitors (PPI's)

These stop the K/H+ ATPase from functioning, which in turn prohibits acid secretion into the stomach

81

Regulation Gastric Secretion (Neural)

I. Distention sends afferent signals to CNS
II. Efferent signals trigger increased secretions of H+, Pepsinogen, gastrin

82

Regulation Gastric Secretion (Endocrine)

I. Proteins, Oligopeptides trigger gastrin secretion by g-cells
II. H+ and Pepsinogen secretion increases

83

Protection Gastric Epithelium

Ach activates the gastric epithelial cells to secrete bicarb and mucus which keeps the pH at the cellular level around 7, whereas in the body of the stomach pH is closer to 2

84

Damaging Agents to Mucosal Integrity

NSAIDs, Helicobacter pylori, alcohol, tobacco, caffeine, bile --> all can lead to an ulcer

85

Functions of the Pancreas

Exocrine--secretes pancreatic juice, bicarb rich, pH close to 8
Endocrine-- secretes insulin and glucagon

86

exocytosis

towards apical membrane

87

endocytosis

towards basal membrane

88

Zymogen Granules

Located in pancreas, contain a lot of digestive enzymes

89

Precursor of Proteases

ALWAYS SECRETED IN INACTIVE FORM
Trypsinogen
Chymotrypsinogen
Proelastase
Procarboxypeptidase A
Procarboxypeptidase B

90

Starch digesting enzymes

Amylase

91

Lipid-digesting enzymes

lipase
prophospholipase A2
Nonspecific esterase

92

Regulatory Factors

procolipase
trypsin inhibitors

93

Acinar Fluid**

-Isotonic, resembles plasma in conc. of Na, K, Cl, HCO3
-Secretion of it stimulated by CCK

94

Secretin**

-Stimulates secretion H2O and bicarb in the extrolobular region

95

Acinar Fluid vs. Secretin Stimulated Secretion**

secretin stimulated is richer in bicarb than acinar secretion due to Cl/HCO3 exchange

96

Low Flow Rate Modifications Pancreatic Secretions**

No modification occurs, secretions are isotonic, similar to plasma concentrations

97

High flow rate modifications pancreatic secretions**

modifications occur, secretin causes the bicarb and H2O concentrations to be higher under high flow

98

Control Ductular Secretions (Pancreas)

I. low pH food bolus enters the small intestine
II. Low pH stimulates the S-Cells which release secretin
III. Secretin increases ductular bicarb secretion
IV. pH reaches 7 then the cycle stops

99

Cystic Fibrosis (Mutations)**

-Most common lethal genetic disease
-Mutations: deletion of the phenylalanine (F508), deletion of three consecutive base pairs in the nucleotide-binding domain

100

How does Bicarb get into the lumen of the duct?

Via AE Exchanger, CFTR Channel

101

AE Exchanger

Anion Exchanger that sends bicarb out and takes Cl in
SLC26A3: DRA
SLC26A6: PAT-1

102

CFTR Channel

-Cystic Fibrosis Transmembrane Regulator
-sends Cl out of the cell

103

How is HCO3 produced?

Via the NBC-1 or a process involving the combination of CO2 and H2O

104

NBC-1

cotransporter on the basilar ductal membrane which pumps 2HCO3 molecules and a sodium into the cell. The 2HCO3 is hydrolyzed and the H+ is pumped out of the cell in exchange for a Na

105

Carbohydrate Digestion occurs where?

Initially in the mouth (amylase)
In the lumen of the intestine
On the surface of enterocytes

106

Sucrase

Specificity: alpha 1,4 bonds of maltose, maltrotriose and sucrose
Products: glucose, fructose

107

Isomaltase

Specificity: alpha 1,4 bonds of maltose, maltotriose, alpha 1,6 bonds of alpha limit dextrins
Products: Glucose

108

Glucoamylase

Specificity: alpha 1,4 bonds of maltose, maltotriose
Products: Glucose

109

Lactase

Specificity: lactose
Products: glucose, galactose

110

Uptake of Carbs (II) [transport in]

-SGLT1 (sodium dependent glucose transporter one) transports glucose and galactose into cell with Na.
-GLUT5 transports fructose into the cell

111

Carb uptake inefficiency

leads to diarrhea :(

112

Uptake of Carbs (III) transport out]

-Na/K ATPase -- transports the Na out, K comes in
-GLUT2 sends glucose, galactose and fructose out of cell
-??? a mystery mechanism also removes just fructose

113

Digestion Protiens

Carboxypeptidase A targets neutral amino acids
B targets basic amino acids
Endopeptidase targets basic amino acids

114

Uptake Peptides

PEPT1-- peptide one protein dependent transporters which take di and tri peptides in along with H+

115

Hartnup's Disease**

Mutations in Na dependent transporter of neutral amino acids, basic transporters remains intact
effects seen in the brain and skin

116

Cysteinuria**

Mutations in Na dependent transporters of basic amino acids, neutral transporters remain intact.
Kidney stones form, cysteine is seen in the urine

117

Digestion Lipids

-Gastric lipase cant break down ester bond @ position 2
-co-lipase stops bile acids from digesting lipid lipase
-bile acids digest the lipids
-once digested transport through lymph nodes, then into blood

118

Bowel Movements Frequency

Mean number varies, but overall generally 1

119

Patterns of Daily Evacuations (BM's)

vary, more water means diarrhea

120

fluid absorbed in intestine

duodenum/jejunum: ~5.5 L
Ileum: ~2 L
Colon/rectum: ~1.3 L
Maximum Capacity: D,J,I ~12 L
C/R ~4-6 L

121

Villi (digestive/transport)

Brush Border Hydrolases: abundant
Nutrient Transport: high
Net Water/Ion Transport: Absorption
Permeability: Low

122

Crypt (digestive/transport)

Brush Border Hydrolases: sparse
Nutrient Transport: low
Net Water/Ion Transport: secretion
Permeability: high

123

Intestinal Absorption (Duodenum)

Fe

124

Intestinal Absorption (Jejunum)

Fe, Ca, Folate, Carbs, proteins, lipids, vitamins

125

Intestinal Absorption (Ileum)

Bile salts, vitamin B12

126

Causes Diarrhea

I. dec brush border hydrolases
II. Villus Atrophy
III. Crypt hyperplasia
IV. Inflammation induced secretion

127

Pathogens which cause diarrhea

cryptosporidia
giardia
e. coli

128

When does diarrhea occur?

When colonic water load exceeds absorptive capacity

129

Mechanisms which cause diarrhea (III) [inhibit fluid/electrolyte absorption]

I. inhibited or defective enterocyte absorption of fluid and electrolytes
II. Luminal presence of osmotically active agents
III. Increased propulsive activity causing decreased contact time

130

Mechanisms which cause diarrhea (II) [increase fluid/electrolyte secretion]

I. Stimulated anion secretion
II. Secretion from hyperplastic crypts

131

Acute Diarrhea

-lasts 2-3 weeks
-usually infectious
-usually self-limiting

132

Chronic Diarrhea

-lasts longer than 3 weeks
-usually multiple causes
-course length varies

133

Treat Diarrhea

Glucocorticoids
Mineralocorticoids

134

Ductal Anatomy Pancreas

main pancreatic duct joins common bile duct and drains through major papilla into duodenum

135

Histology Pancreas

Exocrine 80% (digestion)
Endocrine 20% (carb/glucose digestion)

136

Enzyme Secretion

Most enzymes secreted as proenzymes, trypsin (active form of trypsinogen) will activate them

137

Acute Pancreatitis

Inflammation of the pancreas
Caused by autodigestion due to premature activation digestive enzymes
Clinical course : mild - life threatening

138

Drug Induced Pancreatitis

Uncommon
Many drugs implicated
May occur after many years of being on drug
more often found in elderly, HIV infected, those on multiple medications

139

Etiology (part I)

Hypercalcemia
Trauma
Abdominal Operations
Hypertriglyceridemia
Pregnancy
Organ Transplantation

140

Etiology (part II)

Pancreatic Duct Obstruction
Toxins
Infections
ERCP
Autoimmune
Vasculitis
Hereditary Causes
Idiopathic

141

Diagnosis

Need Two of the following:
I. abdominal pain characteristic AP
II. serum amylase and/or lipase greater than or equal to 3x the upper limit of normal
III. findings characteristic of AP on CT scan