Digestive System 3 Flashcards

1
Q

What are Parietal Cells?

A

Parietal Cells Form hydrogen and bicarbonate from water and carbon dioxide

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2
Q

In the Parietal cell

What happens to the H+ once Carbonic Acid is broken down?

A

Hydrogen crosses into stomach lumen via primary active transport (hydrogen- potassium pump)

Apical Membrane

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3
Q

In the Parietal cell

What happens to the HCO3- (Bircarbonate) once Carbonic Acid is broken down?

A

Bicarbonate crosses into bloodstream and chloride crosses into parietal cell
(secondary active transport - counter transport)

Basolateral Membrane

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4
Q

In the Parietal cell

Once Chloride enters the Parietal Cell, where does it go?

A

Chloride flows into the stomach lumen via facilitated diffusion on the Apical Membrane

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5
Q

Once in the Stomach Lumen, what happens to Chloride?

A

The Hydrogen that left the parietal cell via primary active transport and the chloride that left the parietal cell via facilitated diffusion combine in the stomach lumen to form HCl

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6
Q

In the Parietal cell

What moves via facilitated transport?

A

K+ & Cl- on apical membrane
move in to stomach lumen

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7
Q

In the Parietal Cell

What moves via Primary Active Transport?

A

H+ and K+ via counter transport
H+ moves from Parietal cell to Stomach Lumen
K+ moves into Parietal Cell from Stomach Lumen
(On the Apical Membrane)

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8
Q

In the Parietal Cell

What moves via Secondary Active Trasnport?

A

HCO3- and Cl- via counter transport
HCO3- moves from Parietal Cell into Bloodstream
Cl- moves into Parietal Cell from Bloodstream
(On the Basolateral Membrane)

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9
Q

What Controls how much acid is released into the Stomach Lumen?

A

Secondary messengers regulate how many hydrogen-potassium pumps inserted on apical membrane.

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10
Q

What Increases Secondary Messengers?
(effectively increasing H+/K+ Pumps on Apical Membrane and releasing more acid)

A

Gastrin - Hormone
Histamine - Paracrine
Acetycholine (Ach) - Neurotransmitter
can release binded target cells to increase secondary messengers

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11
Q

gastrin (hormone), histamine (paracrine), and/or acetylcholine (neurotransmitter) are classified as what

A

Inhibitors (increase # of Secondary Messengers)

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12
Q

Which Hormone is Excitatory?

A

Somatostatin decrease the # of secondary messngers when target cells is released.

Resulting in less pumps on apical membrane and less acis in Lumen

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13
Q

Gastrin, Histamine and Acetycholine target cell release results in what?

A

increases secondary messengers

more pumps on apical membrane

more acid in lumen

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14
Q

What responds in both directions (pro-acid and anti-acid)?

A

chemoreceptors

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15
Q

What is Pro-Acid?

A
  1. Chemoreceptors detect a decrease in acidity
  2. Neural, Parasympathetic and Enteric work to increase acid formation
  3. Secretion of Gastrin (H), Histamine (P), Acetylcholine (NT)
  4. Increase in Secondary Messengers, Apical Pumps & Acid Formation
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16
Q

What is Anti-Acid?

A
  1. Chemoreceptors detect an increase in acidity
  2. Neural and Sympathetic work to decrease acid formation
  3. Secretion of Somatostatin (H)
  4. Decrease in Secondary Messengers, Apical Pumps & Acid Formation
  5. Negative Feedback
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17
Q

What is the negative feedback in the Anti Acid Response?

A

if acidity increases, gastrin won’t be released, meaning less secondary messengers

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18
Q

What is the Intestinal phase?

A

Intestinal phase – food arrives in duodenum –
receptors detect increased acidity, fats, amino
acids, distension

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19
Q

What is the Short (Neural) Reflex of the Enterogastric Reflex once food enters the Duodenum?

A

Short reflexes – directly on stomach
decreases Gastric Emptying

20
Q

What is the Long (Neural) Reflex of the Enterogastric Reflex once food enters the Duodenum?

A

Long reflexes – CNS changes on stomach
The CNS increases Sympathetic firing and decreases paraysympathetic firing which decreases gastric emptying in the stomach

21
Q

What is the Hormonal Reflex once food enters the Duodenum?

A

Hormonal – Increased CCK / secretin secretion
Leads to Plasma Levels increasing and a decrease in Gastric Emptying

22
Q

What is the Overall Goal Of the Neural and Hormonal Responses once food enters the Duodenum?

A

Overall – neural and hormonal responses:

  • Decreased gastric motility
  • increased contraction of pyloric sphincter.
  • Decreased gastric emptying
  • Trying to match gastric emptying to small intestine digestion/absorption
23
Q

What happens in the Duodenum is Overloaded?

A

Overload duodenum – dumping syndrome – nausea, sweating, dizziness, diarrhea, vomiting

24
Q

How can Emotions affect Gastric Emptying?

2

A

Emotions

  • Sadness, fear, body pain – inhibit.
  • Anger, aggression (fight or flight response) – stimulate
25
Q

How can Excerisize affect Gastric Emptying?

A
  • moderate intensity = stimulate
  • high intensity = inhibit
26
Q

Why could Inhibiting Gastric Emptying be Harmful?

A

Inhibiting gastric emptying, can limit the absorption of nutrients and water in the small intestine as they remain in the stomach. This limitation can impact the availability of essential substances to the tissues actively engaged in physical activity.

27
Q

What is Bile Composed of?

6

A

Bile contains bicarbonate, bile salts, bile pigments,
phospholipids, organic wastes, cholesterol

28
Q

Where is Bile Produced?

A

The Liver

29
Q

Where is Bile Stored when not needed?

A

flows to gallbladder for storage

30
Q

What is the Bodys Response when Bile is Needed?

A

When Bile is Needed:
Fatty Acids in Duodenum Release Cholecystokinin (CCK),
Gallbladder Contrats- Bile flows into Common Bile Duct
Sphinter of Oddi Relaxes- Bile Flows into Duodenum

CCK = Cholecystokinin

31
Q

What is Bicarbonate used for?

A

helps neutralize acidic chyme coming out of stomach.

32
Q

Where are Bile Salts Found?

A

Bile salts – enterohepatic circulation – release and recycling

33
Q

What is the Role of Bile Salts?

A

Enter duodenum to aid in fat digestion
Forms cyclic pathway between liver and small intestine.

34
Q

What happens to Bile Salts once they Reach the ileum?

A

Once they reach the Ileum, they are absorbed into the portal vein and return to the liver

95% recycled so only small amount (5%) lost in feces
needs to be synthesized by liver to replace

35
Q

Bile Pathway

A
36
Q

What Neutralizes the Chyme that is entering The duodenum? Why does it need to be neutralized?

A

Bicarbonate is the Key Acid Neutralizer

Acid must be neutralized to create alkaline environment preferred by enzymes released into small intestine.

37
Q

Where is Bicarbonate Released from?

2

A

Small amount – liver/gallbladder
Large amount – pancreas – pancreatic juice (collective name for pancreatic secretions)

38
Q

How does the Pancrease Produce Bicarbonate?

A
  • Pancreatic duct cell forms hydrogen and bicarbonate from water and carbon dioxide.
  • Hydrogen enters bloodstream.
  • Bicarbonate released into pancreatic duct lumen as part of pancreatic juice.
  • Pancreatic duct carries pancreatic juice to duodenum where it can enter and neutralize acidic chyme
39
Q

What Enzymes are Found in the Pancreatic Juice?

5

A

Trypsin
Chymotrypsin
Carboxypeptidase
Pancreatic Lipase
Pancreatic Amylase

40
Q

What is the Fuction of Trypsin and Chemotrypsin?

A

Trypsin, Chymotrypsin
Splits proteins to peptide fragments

41
Q

What is the Function of Carboxypeptidase?

A

Carboxypeptidase
Splits terminal amino acid from end of protein.

42
Q

What is the Function of Pancreatic Lipase?

A

Pancreatic Lipase
Splits triglycerides to fatty acids and monoglycerides.

43
Q

What is the Function of Pancreatic Amylase?

A

Pancreatic Amylase
Splits polysaccharides to maltose

44
Q

The pancrease secretes inactive enzymes, what activated Trypsin, Chemotrypsin and Carbocypeptidase in the Small Intenstine?

A
  • Trypsinogen
    → trypsin activated by enterokinase (a brush border enzyme).
  • Chymotrypsinogen
    → chymotrypsin activated by trypsin.
  • Procarboxypeptidase
    → carboxypeptidase activated by trypsin
45
Q

Hormonal

What happens when Acid from stomach in small intestine increases production?

5

A
46
Q

Hormonal

What happened when Intestinal fatty acid and amino acid production increases in the Small Intestine?

A