digestive system lecture 7 Flashcards

1
Q

What are the principles of secretion?
What is the salivary gland secretion?

A

requires energy and blood flow
-glands, saliva (ONLY hypotonic secretion in GIT;
ptyalin, a salivary amylase (active at neutral pH); mucin)

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2
Q

What is regulating salvation?
What is secreted in gastric section?

A

ANS (parasympathetic – ALL Neural, NO hormonal regulation)
-different glandular cells in different locations composition of Mixed Gastric Juice
a) HCl b) Pepsinogen c) Mucin

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3
Q

Where are surface epithelila cells present?
What are the 4 functions of HCl?

A

-everwhere in the GIT
Precipitates Soluble Proteins :allows the proteins to remain longer in the stomach
-Denatures Proteins more readily digested
-Activates Pepsin
-Provides Optimal pH for Pepsin activity

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4
Q

What does the gastric mucosal barrier (GMB) do?
Where is it found

A

-it is the main protective layer and it has a specialization of tight junctions and sruface which makes them permeable to H+ on apical side (only found in stomach)

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5
Q

What does H+ions interact with?
What does the muci-bicarb layer adsorb?
What does muci bicard layer secreted?

A

H+ can freely pass across mucous gel but interact with bicarbonae and are neutralized (pH of 7 after it passes layer)
-bicarbonate layers
-secretes mucous and bicarbonate

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6
Q

What does rapid cell turnover (re-epthelization) produce

A

-produces up to 1 million new epithelilal cells per day specifically in the stoamch +SI

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7
Q

What are the factors that contribute to ulcers for a normal HCl ouput but weak input?
What are the drugs/bacteria?

A

normal HCl but weak barrier caused by: Aspirin & NSAIDs (can weaken barrier)
Helicobacter pylori (bacteria that burrows itself in layers between the mucous of these cells and produces toxins which damage mucousal layer

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8
Q

What factors contribute to a normal barrier but excessive hcl output?

A

gastrin producing tumors can cause this

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9
Q

What is part of the nervous vs hormonal input?

A

-vagus and sympathetic
-hormonal=gastrin, histamine, somatostatin

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10
Q

What are the 3 phases of gastric secretion?

A

cephalic=psychic and gustatory
gastric (when food is in stomach)
intestinal (when food is in intestine)

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11
Q

what do the neurons smooth muscle of GIT synapse on?

A

-they synapse on the secreting cell

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12
Q

What does the ENS do in neural regulation of secretion?
How can it be activated

A

-sends excitatory input onto secretory cells
-ENS can be activated when we have stretch in the stomach or when we think of food to send efferents in preparation for food

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13
Q

What does cephalic phase lead to and what is it mediated by?

A

-it is vagally mediated and leads to vasodilation

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14
Q

What does the sympathetic input for secretion regulation do?

A

inhibits secretion and leads to vasoconstriciton

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15
Q

What does the local enteric reflex do?
WHat do the vago-vagal reflex do?

A

it causes distention
-can reinforce stimulus

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16
Q

What do secretagogues act on?
What are secretagogues

A

act on gastrin secreting g-cell which leads to gastrin release in stomach, leading to increase in HCl by parietal cell
-amino acids or partially digested proteins which act on gatrin-releasing cells G-cells

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17
Q

What are secretagogues producing?
What are local enteric reflexes doing?
What is gastrin?
What are the vagally mediated reflexes?

A

GASTRIN (a peptide hormone) released by endocrine cells in the antrum (G-Cells) in response to:
Secretagogues (products of protein digestion)
Local enteric reflexes (distention in antrum)
-vago-vagal reflexes

18
Q

What does the cephalic phase do?

A

-it prepares enzymes to be ready for when the meal arrives

19
Q

What occurs when there is an increase in secretagogues?
To the g cell, parietal cell?
What type of loop is this?

A

-increased secretagogue causes increase in g-cell (gastrin release) which causes an increase in paritela cell–>increase in HCl
-this actiavtes pepsinogen to pepsin (more protein break down)
-this is a positive feedback

20
Q

What does a low pH cause in the gastrin regulation cycle?
What does the g-cell have to sense the ph?
What type of feedback is this?

A

-it causes a release of somatostain which inhibts the g-cell and the parietal cell
-it has receptors to detect the pH which reduces number of secretagogues
-negative feedback

21
Q

What is gastrin
what does gastrin stimulate?
What is the trophic effect?

A

-a hormone released by G cells in the stomach and duodenum
Stimulates HCl Secretion
-Trophic Effect – stimulates production of
more parietal cells

22
Q

When is gastrin present?
WHat stimulates release of gastrin during which phase?
What 2 things stimulates it?

A

Gastrin release precedes and accompanies the meal.
Release occurs as part of the cephalic phase.
Release is stimulated by stretch in the stomach.
Release is stimulated by the presence of secretagogues in the stomach.
The latter two contribute to positive feedback of gastrin secretion.

23
Q

when 2 things cause gastrin release inhibited?
what do these contribute to?

A

Gastrin release is inhibited by low pH in the stomach.
Gastrin release is inhibited by somatostatin.
These contribute to negative feedback on gastrin secretion

24
Q

when does somatostain release occur in the presence of?
What 2 cells does it inhibit?

A

Release occurs in the presence of low pH in the stomach.
Inhibits gastrin release from G-cells
Inhibits HCl secretion from parietal cell

25
Q

Where is there alot of histamine?
What does histamine elicit?

A

-Lots of Histamine in Gastric Mucosa
Histamine administration elicits large volumes of gastric juice with lots of HCl

26
Q

What 3 things does the parietal cell have a receptor for?
what does an histamine inhibitor do vs proton pump for ulcers/

A

-gastrin, histamine and Ach
-histamine inhibitor blocks about 70% where proton pump blocks about 90-95% of hcl secretion

27
Q

What does a blockade or stimulation of one of the parietal cell receptors do?
What happens to sensitivity when you block vs when you stimulate histamine?

A

-changes the properties of one or both of the other 2 receptors
-blocked histamine means Ach and gastrin are less sensitive
-stimulation of histamine increases Ach/gastrin sensitivity

28
Q

WHat is the permissive hypothesis for histamine?
WHat does blocking the tonic/background release do?

A

Histamine is constantly released and presented to the Parietal Cells as a tonic background, sensitizing them to other stimuli
-inhibits acid secretion in response to ACh and Gastrin

29
Q

WHat do H2-receptor blockers do?

A

are widely used to decrease HCl secretion
Recall, also use H+/K+ ATPase blockers

30
Q

What does the intestinal phase (duodenal excitatory component do)?

A

-it activates secretagogues to activate cells in the duodenum which releases gastirn to increase HCl

31
Q

What are the factors that lead to inhibition of gastric secretion?

A

-distention
ph<3.5
high osmolarity
chemical compostion
fat»proteins»carbs
-they all produce negative feedback

32
Q

What is inhibitory 1 for intestinal phase?

A

-it is the enterogastric reflex (factors controlling antral peristalsis)

33
Q

WHat do motor and secretory activities in the stomach reflect a balance between?

A

Both MOTOR and SECRETORY activities of
the stomach (at any moment in time) reflect a balance between EXCITATORY and INHIBITORY influences on the MUSCULAR and GLANDULAR cells in the gastric wall

34
Q

What are the pre intesintal changed (when food is still in stomach)?
What is meal reduced to?

A

Meal reduced to semi-liquid consistency
Acidified, osmotic pressure is unchanged
Limited Digestion

35
Q

What breaks down polysaccharides?
proteins?
and some lipids in the preintestinal changes?

A

salivary amylase ptyalin (neutral mouth pH) breaks them down in disaccharides
-gastric pepsin breaks down proteins into polypeptides
-lipids broken down by lingual lipase into di-,monoglycerides and fatty acids

36
Q

What are the 4 upper intestinal functions at the levels of the SI?

A

-CHYME NEUTRALIZATION
-OSMOTIC EQUILIBRATION will be isotonic by the time it reaches the colon
-DIGESTION continues
-ABSORPTION begins

37
Q

What does the cystic duct join?

A

joins the gallbladder

38
Q

What is the volume of pancreatic juice?
What are the mosm?
What are the main electrolytes?
What is its pH?

A

-Volume: 0.5 – 1.5 liters/day
Isotonic: ~300 mOsm
Main Electrolytes: Na+, K+, Cl-, HCO3- (has neutral pH)
pH: 7.2 – 8.2

39
Q

WHat does the pancrease produce?

A

Pancreas produces the largest quantities and the most powerful Digestive
ENZYMES: Amylases
Proteases
Lipases

40
Q

What do disacharides need to be converted into for absorption?

A

need to converted to monosaccharides by amylase

41
Q

What are the pancreatic proteases?
when is proenzyme active?

A

proenzyme not active untile cleaved at level of SI when converted to an enzyme
-trypsinogen uses enterokinase to convert into trypsin in SI

42
Q

What other products can trypsin be used to cleave?
What does trypsin inhibitor do, what secretes it?

A

chymotrypsinogen into chymotrypsin
-protease into elastase
procarboxypeptidase into carboxypeptidase
-pancrease secreates it and it inactivates trypsin