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Y2B1 - GIT 📕 > Physiology 🫁 > Flashcards

Physiology 🫁 Flashcards

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1
Q

What is the main function of the GIT?

A

The functions of the gastrointestinal tract (GIT) are digestion and absorption of nutrients.

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2
Q

What are the major activities needed to serve the functions of GIT?

A

➢ Motility
➢ Secretions
➢ Digestion
➢ Absorption.

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3
Q

What are the organs of the GIT?

A

• The GIT is arranged as mouth, esophagus, stomach, small intestine (duodenum, jejunum, and ileum), large intestine, and anus. “The alimentary duct”

• Other structures of the gastrointestinal tract are the salivary glands, pancreas, liver, and gall bladder, all have secretory functions

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4
Q

How is gastrointestinal function regulated?

A

1-Nervous regulation

2-Hormonal regulation.

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5
Q

Nervous regulation of GIT functions

A

It is carried out by the autonomic nervous system which has an extrinsic and an intrinsic component.

A: Intrinsic innervation by the enteric nervous system (ENS)

B: Extrinsic innervation: (parasympathetic and sympathetic nervous systems)

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6
Q

What is the site enteric nervous system?

A

located in the wall of the whole length of the gut

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7
Q

What is the function of the enteric nervous system?

A

It controls most functions of the GI tract, even in the absence of extrinsic innervation

“but at a constant rate”

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8
Q

What are the nerve plexuses of the enteric nervous system?

A

It contains 2 nerve plexuses:

  1. Myenteric plexus (Auerbach’s plexus): primarily controls the motility of the GI smooth muscle.
  2. Submucosal plexus (Meissner’s plexus): primarily controls secretion and blood flow of GIT.
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9
Q

Innervation and connection of enteric nervous system

A
  • Both plexuses are connected by interneurons, secretes acetyl choline, serotonin, Large number of polypeptides
  • Both plexuses receive sensory information directly from mechano-receptors and chemoreceptors in the mucosa and send motor information directly to smooth muscle, secretory and endocrine cells to control their functions.
  • Also receive input from the parasympathetic and sympathetic nervous system which modulate their activity.
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10
Q

What is the extrinsic innervation of GIT mediated by?

A

parasympathetic and sympathetic nervous systems

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11
Q

What is the parasympathetic innervation of the GIT carried by?

A

is carried via the vagus and pelvic nerves.

  1. Parasympathetic nervous system:

➢ The vagus nerve innervates the esophagus, stomach, pancreas, and upper large intestine.

➢ The pelvic nerve (sacral 2,3,4) innervates the lower large intestine, rectum, and anus.

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12
Q

What is the course of parasympathetic fibers to GIT?

A

Parasympathetic fibers synapse in the plexuses. The plexuses then send information to the smooth muscle, secretory cells, and endocrine cells of the GI tract.

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13
Q

What are vagovagal reflexes?

A

Reflexes in which both afferent and efferent pathways are contained in the vagus nerve are called vagovagal reflexes.

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14
Q

What is the nature of parasympathetic neurons to the GIT?

A

The parasympathetic neurons to the GIT may be cholinergic, releasing acetylcholine or peptidergic, releasing peptides eg. substance P, and vasoactive intestinal polypeptides (VIP).

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15
Q

What is the function of the parasympathetic neurons to the GIT?

A

Stimulation of parasympathetic nerves stimulates all functions of the gut.

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16
Q

What is the origin of the sympathetic nervous system to GIT?

A

➢ Its fibers originate in the spinal cord between T-5 and L-2.

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17
Q

What is the course of the sympathetic adrenergic fibers to the GIT?

A
  • The sympathetic adrenergic fibers synapse in nerve plexuses
  • The plexuses then send information to the smooth muscle, secretory cells, and endocrine cells of the GI tract.
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18
Q

What is the function of sympathetic nerves concerning GIT?

A

Stimulation of sympathetic nerves produce inhibition of all functions of the gut and vasoconstriction of blood vessels.

“Either indirectly by inhibition of acetylcholine or directly”

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19
Q

What are the types of reflexes that happen in nervous regulation of GIT?

A

1- Short (local) reflexes

2- Long reflexes

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20
Q

Short (local) reflexes

A

❖ They occur entirely inside ENS.

❖ All the components of these reflexes are located in the gut’s wall.

❖ These reflexes are responsible for self -regulation of GI functions.

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21
Q

Long reflexes

A

❖ They are mediated through extrinsic autonomic nerves (sympath. &parasymp.)

❖ They involve centers in the CNS.

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22
Q

Where are GIT hormones released from? And what is their route to the site of action?

A

GIT hormones are released from endocrine cells in the GI mucosa into the portal circulation, to the liver, then through the inferior vena cava to the heart, and then back again to the digestive system to exert their actions on target cells.

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23
Q

What is the chemical structure of GIT Hormones?

A

All GIT hormones are polypeptides

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24
Q

Give examples for GIT Hormones

A
  1. Gastrin
  2. CCK
  3. Secretin
  4. GIP
  5. VIP
  6. Somatostatin
  7. GRP
  8. Motilin
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25
Q

What are GIT Hormones classified into?

A

(According to structural similarity):

1-Gastrin family: Gastrin, Cholecystokinin.

2-Secretin family: Secretin, Vaso-active intestinal peptide (VIP), Glucose- dependent insulinotropic peptide (GIP).

3- Others

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26
Q

Where is gastrin secreted from?

A

Gastrin is secreted from the G cells of the gastric antrum & duodenal bulb, and TG cells: in the stomach and small intestine.

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27
Q

What is the stimuli for gastrin secretion?

A

After taking a meal, gastrin is released in response to the following:

  1. Small peptides and amino acids in the lumen of the stomach.
  2. Distention of the stomach by food
  3. Vagal stimulation, mediated by gastrin-releasing peptide (GRP)
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28
Q

Does atropine block vagally mediated gastrin secretion?

A

No, because the mediator of the vagal effect is GRP, not acetylcholine (Ach).

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29
Q

What is the action of gastrin?

A

✓ Stimulates the secretion of HCl and pepsin from the stomach.

✓ Stimulates gastric motility.

✓ Stimulates growth of gastric mucosa. «For protection»

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30
Q

What happens when the acidity increases in the GIT?

A

acidity will inhibit gastrin secretion. So, there is -ve feedback relation between the degree of acidity and the secretion of the gastrin.

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31
Q

What inhibits gastrin secretion?

A
  1. H+ in the lumen of the stomach, ie (↓ PH)
    - The high acidity of the stomach inhibits gastrin release by negative feedback control to protect the gastric mucosa from high acidity
  2. Somatostatin, secretin, and GIP
    - inhibit gastrin release.
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32
Q

What is Zollinger–Ellison syndrome (gastrinoma)?

A

Is gastrin secreting tumor commonly develops peptic ulcer

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33
Q

What is the source of CCK?

A

CCK is released from the I cells of the upper GIT mucosa (duodenum, jejunum)

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34
Q

What stimulates the secretion of CCK?

A

Small peptides and amino acids. Also Fatty acids and monoglycerides in the upper part of the small intestine

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35
Q

What are the actions of CCK?

A
  1. Stimulates bile secretion by contraction of the gallbladder and relaxation of Oddi’s sphincter. «Cholagogue»
  2. Stimulates pancreatic enzyme secretion.
  3. Potentiates secretin-induced stimulation of pancreatic HCO3– secretion.
  4. Stimulates growth of the exocrine pancreas.
  5. Inhibits gastric emptying. Thus, meals containing fat stimulate CCK secretion, which slows gastric emptying, allows more digestion and absorption time. “To avoid piling up of food in the duodenum”
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36
Q

What is the source of secretin?

A

Secretin is released by the S cells of the duodenum.

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37
Q

What stimulates the release of secretin?

A

Secretin is released in response to H+ and fatty acids & products of protein digestion in the duodenum

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38
Q

What are the actions of secretin?

A

Its functions are coordinated to reduce the amount of H+ in the lumen of the small intestine So:

  1. Stimulates pancreatic HCO3– secretion and increases the growth of the exocrine pancreas. The bicarbonate causes neutralization of acidity and provides alkaline medium needed for the action of pancreatic enzymes.
  2. Stimulates bile, HCO3– and H2O secretion by the liver.
  3. Inhibits H+ secretion by gastric parietal cells.
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39
Q

How does nicotine affect the secretion of secretin?

A

Nicotine (present in cigarettes) inhibits the secretion of secretin. So heavy smokers have hyperacidity which may lead to peptic ulcers.

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40
Q

Where is GIP (Glucose-Dependent Insulinotropic Peptide) secreted from?

A

Secreted by duodenum and jejunum in response to fat, protein, and carbohydrate.

«Especially glucose»

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41
Q

What is the action of GIP (Glucose-Dependent Insulinotropic Peptide)?

A
  1. Stimulates insulin release.
  2. Inhibits H+ secretion by gastric parietal cells.
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42
Q

Where is VIP (Vaso-active intestinal peptide) Released from?

A

It is released from neurons in GI tract.

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43
Q

What is the action of VIP (Vaso-active intestinal peptide)?

A

• produces relaxation of GI smooth muscle.

• Stimulates pancreatic HCO3– secretion, secretion of water and electrolytes from the intestine

• It inhibits gastric H+ secretion. In these actions, it resembles secretin.

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44
Q

What is the function of motilin?

A
  • Regulates intestinal motility between meals preparing it for the next meal.
  • Responsible for migrating motor complex of intestinal motility between meals.
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45
Q

What is the action of GRP (bombesin)?

A

Stimulates gastrin release from G cells.

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46
Q

What is somatostatin?

“Inhibitory hormone”

A

It is the growth-hormone –inhibiting-hormone.

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47
Q

What is the source of somatostatin?

A

It is secreted by D cells in the pancreas and GI mucosa.

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48
Q

What is the stimulus for somatostatin secretion?

A

It is secreted by cells throughout the GI tract in response to H+ in the lumen.

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49
Q

What inhibits somatostatin secretion?

A

Its secretion is inhibited by vagal stimulation.

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50
Q

What is the action of somatostatin?

A

It inhibits the release of all GI hormones and gastric H+ secretion.

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51
Q

what is Mastication (Chewing)?

A

It is the act by which food is broken down into small particles to be swallowed easily.

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52
Q

what does the process of mastication involve?

A
  • It involves movements of the mandible, lips, cheeks, and tongue.
  • These movements are performed by mastication muscles. (Inervated by the trigeminal nerve)
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53
Q

what is the mechanism of mastication?

A

It is a reflex:

  1. Presence of food in the mouth causes reflex inhibition of mastication muscles. → drop of the lower jaw.
  2. The jaw drop initiates stretch reflex of the jaw muscles → Rebound contraction of these muscles → Elevation of the jaw and closure of the mouth.
  3. The bolus of food is compressed against the linings of the mouth → inhibits the jaw muscles → drop the jaw, and the process is repeated again and again.
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54
Q

what are the functions of mastication?

A
  1. Breakdown of the food into small particles → easy swallowing, decrease the mechanical damage of the mucosa.
  2. It stimulates salivary secretion, also taste and smell receptors
  3. Help digestion, especially fruits and vegetables which contain undigestible cellulose “they are only digested mechanically”
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55
Q

enumerate the salivary glands in the human body

A

The principal salivary glands are Parotid, submandibular and sublingual glands. Small glands are scattered in the mucous membrane of the buccal cavity.

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56
Q

what is the nature and type of secretion of salivary glands?

A

Parotid gland: Secretes 25% of the total secretion, contains only serous fluid- secreting cells.

Sublingual gland: Secretes 5% of the total secretion, and contains only mucous secreting cells.

Submandibular gland: Secretes 70% of the total secretion, contains serous and mucous cells.

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57
Q

what is the characters of saliva?

A
  • Volume: 800-1500 ml/day.
  • PH: Slightly above 7 during rest.
  • Saliva is composed of 99% water. and 1% solids.
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58
Q

what are the solids found in saliva?

A

Organic:
- Mucin
- Enzymes: Digestive enzymes (α-amylase and lingual lipase) and lysozyme
- IgA.

Inorganic: Na+, K+, Cl- & HCO3-, and thiocyanate ions

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59
Q

what are the stages of formation of saliva?

A

The formation of saliva is an active secretory process. It occurs in two stages.

A) First stage
B) Second stage

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60
Q

first stage of saliva formation

A
  • The acini secrete primary secretion which is isotonic. “conc. like plasma” That means, the concentrations of Na+, K+, Cl-, and HCO3- are close to those in plasma.
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61
Q

second stage of saliva formation

A
  • It occurs in the salivary duct, where: The following modify the initial saliva by the following processes:
  1. The ducts reabsorb Na+ and Cl–; therefore, the concentrations of these ions are lower than their plasma concentrations.
  2. The ducts secrete K+ and HCO3–; therefore, the concentrations of these ions are higher than their plasma concentrations.
  3. Saliva becomes hypotonic in the ducts.
  4. At high flow rates, saliva is like the initial secretion from the acinus; it has the highest Na+ and Cl–concentrations and the lowest K+ concentration. “During eating”
  5. At low flow rates, saliva has the lowest Na+ and Cl– and the highest K+ concentration. “during rest”

This is the only hypotonic fluid secreted by the GI tract.

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62
Q

what is the mechanism of salivation?

A
  • Salivary secretion is a rapid process, so it is under nervous control only.
  • increased by both sympathetic and parasympathetic stimulation, Parasympathetic is dominant.
  • Parasympathetic stimulation (cranial nerves VII and IX) increases saliva which is watery and little in enzymes (true secretion)
  • Sympathetic stimulation increases saliva secretion which is little in amount, and rich in enzymes (trophic secretion),
  • Salivary secretion occurs in 3 phases
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63
Q

what are the phases of salivation?

A

A) Cephalic phase
B) Buccal phase
C) Gastroesophageal phase

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64
Q

characters of Cephalic phase of salivation

A
  • Occurs before food enters the mouth.
  • It is caused by conditioned (psychic) reflex
  • It is acquired not an inherent reflex. It needs training. Seeing the food, smelling, and or even thinking of it, stimulate salivation.
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65
Q

what is the mechanism of cephalic phase of salivation?

A
  • Auditory and visual centers send impulses to salivary nuclei.
  • Salivary nuclei send sympathetic and parasympathetic efferent fibers to the salivary glands to secrete. By training, new functional connections develop between these centers in the cerebral cortex and the salivary nuclei.
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66
Q

what are the charachters of buccal phase of salivation?

A
  • Salivary secretion occurs when food enters the mouth.
  • It is caused by unconditioned reflex, which is inherent and not an acquired reflex. It does not need training or an intact cerebral cortex.
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67
Q

what is the mechanism of buccal phase of salivation?

A
  • Chemical (eg. food) or mechanical (e.g. chewing gum or dentist’s instrument) stimulation excites the taste receptors in the tongue.
  • It sends impulses to the salivary nuclei in the medulla oblongata. Which send efferent sympathetic and parasympathetic to salivary glands to secrete.
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67
Q

what is the mechanism of Gastroesophageal phase of salivation?

A
  • Irritation of the lower end of the esophagus & stomach or upper intestine → will cause salivation by esophago-salivary reflex and gastro-salivary reflex.
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68
Q

what are the functions of saliva?

A
  1. Starts the digestion of the starch by salivary α- amylase enzyme.
  2. It keeps the buccal cavity wet→ helps speech processing
  3. It acts as a solvent for food particles → effective stimulus to taste receptors.
  4. It acts as a diluting medium for irritating substances.
  5. Regulate body temperature in panting animals.
  6. Facilitates swallowing by lubricant action of mucin.
  7. It keeps the PH of the mouth at about 7:
    - This alkalinity preserves calcium in the teeth.
    - Acidity of the buccal cavity (e.g. by bacterial action on food remnant) will cause dissolution of Ca++ from teeth. → Dental caries.
  8. Role of saliva in oral hygiene:
    - Flow of saliva wash away the pathogenic bacteria and the food particles.
    - It contains IgA → immunological defense against bacteria and viruses.
    - Thiocyanate ions, which are bactericidal.
    - It contains lysozymes that destroy bacteria.
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69
Q

what is Deglutition (Swallowing)?

A
  • It is the process by which food is transferred from the mouth cavity to the stomach.
  • It is divided into three stages.
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70
Q

what are the stages of deglutition?

A
  1. Buccal (voluntary) stage
  2. Pharyngeal (involuntary) stage
  3. Esophageal (Involuntary) stage
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71
Q

Buccal (voluntary) stage of swallowing

A
  • The tongue moves upward and backward against the palate pushing the food into the pharynx.
  • Once the food reaches the pharynx, the process of swallowing becomes entirely automatic and cannot be stopped.
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72
Q

pharyngeal (involuntary) phase of swallowing

A

Involuntary phase (reflex in nature in which) :

  • Stimulus → presence of food at the back of the mouth
  • Receptors→ swallowing receptor area at the back of mouth.
  • Afferent fibers→ 5th, 9th , and 10th cranial nerves.
  • Center→ swallowing center in the medulla oblongata.
  • Efferent fibers→5th, 9th, 10th, 12th cranial n. →Series of muscle contraction
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73
Q

what are the functions of efferent impulses sent by the swallowing center in pharygeal phase?

A

1- Prevent food entrance to the nose through:
- Pulling the soft palate upward to close the posterior nasal cavity

2- Prevent food entrance to the trachea through:
- The vocal cords are approximated strongly.
- The epiglottis swings to close the laryngeal opening.
- Inhibition of the respiratory center→ deglutition apnea

3- Allow passage of food to the stomach through:
- Relaxation of the upper esophageal sphincter. So the food moves to the esophagus.
- Contraction of the superior constrictor muscle of the pharynx, This contraction spreads downward as rapid peristalsis along the esophagus.
- Relaxation of the lower esophageal sphincter and stomach to receive food (Receptive relaxation).

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74
Q

Esophageal stage

A

Involuntary stage, conduct food from the esophagus to the stomach

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75
Q

what are the types of peristalitic movements of the esophagus?

A

1- Primary peristalsis: It is a continuation of the contraction of the superior constrictor muscle of the pharynx.

2- Secondary peristalsis: It is caused by presence of food in the esophagus due to failure of primary peristalsis to move all food.

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76
Q

what is the length of the esophagus?

A

20cm long

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77
Q

what are the sphincters of the esophagus?

A
  • The upper end of the esophagus is guarded by the upper esophageal sphincter.
  • The lower end is guarded by the lower esophageal sphincter.
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78
Q

what is the Upper esophageal sphincter (UES)?

A

It is striated muscle thickening in the upper 3 cm segment of the esophagus.

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79
Q

activity of Upper esophageal sphincter (UES)

A

During rest, the UES contracts, prevents entrance of air into the stomach during breathing and relaxes during swallowing until food passes then it
contracts again.

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80
Q

what is the site of the lower esophageal sphincter (LES)?

A

It extends 2-5cm above the gastro-esophageal junction.

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81
Q

activity of the Lower esophageal sphincter (LES)

A
  • During rest the LES contracted to prevent regurgitation of the acidic gastric contents into the lower end of the esophagus.
  • It relaxes during swallowing to pass food into the stomach.
  • If its tone is decreased, the acidic gastric contents will regurgitate (reflux) into the esophagus causing heartburn (Reflux esophagitis).
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82
Q

what are the factors that decrease the tone of LES?

A
  1. Food: e.g. Fat, tea, coffee, chocolate.
  2. Abnormal position of the sphincter. As in case of hiatus hernia, in which the LES is present intrathoracic (It is normally in the abdominal cavity). “due to negative intrathoracic pressure”
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83
Q

what are the factors that increase the tone of LES?

A
  • Large doses of gastrin (as occur after meals) increase the tone of LES.
  • This effect is important since gastrin increases HCL secretion and by increasing the tone of LES, also limits the reflux of this acid into the esophagus.
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84
Q

what is achalasia of the cardia?

A

Achalasia may occur if the lower esophageal sphincter does not relax during swallowing and food accumulates in the esophagus.

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85
Q

what is the stomach divided into functionally? and what is its function?

A

Functionally, the stomach is divided into:
1- Proximal motor unit: Consists of the body and fundus.
2- Distal motor unit: Consists of the antrum, pyloric canal, and pyloric sphincter.

  • The stomach function is storage, mixing of food with gastric secretion, and slow emptying of food into the small intestine.
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86
Q

what are the types of cells that are found in the glands of gastic mucosa?

A

1) Parietal (oxyntic) cells: Secrete HCl and intrinsic factor.

2) Peptic (chief) cells: Secrete proteolytic enzymes ——> pepsinogens.

3) Mucous cells: secrete mucus

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87
Q

what are the phases of gastric secretions?

A

1- Cephalic (psychic) phase responsible for 20% of secretion

2- Gastric phase: It accounts for 60%-70%

3- Intestinal phase: accounts for 10%

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88
Q

what are the characters of the Cephalic (psychic) phase of gastric secretion?

A
  • Occurs before food reaches the stomach.
  • It is caused by 2 reflexes.
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89
Q

what are the two reflexes of the Cephalic (psychic) phase of gastric secretion?

A
  • Conditioned reflex
  • Unconditioned reflex
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90
Q

explain the mechanism of conitioned reflex of cephalic phase of gastric secretion

A
  • Seeing the food, smelling, send afferent from visual to the vagal nucleus in the medulla.
  • Efferent vagal fibers go to the stomach to stimulate its secretion.
  • It is an acquired reflex
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91
Q

explain the mechanism of unconitioned reflex of cephalic phase of gastric secretion

A
  • Presence of food in the mouth stimulate taste receptors, send afferent to the vagal nucleus.
  • The vagal nucleus sends efferents to stimulate gastric secretion.
  • It is an inherent reflex, These reflexes also stimulate pancreatic secretion and evacuation of the gallbladder through efferent vagal fibers.
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92
Q

explain the mechanism of gastric phase of gastric secretion

A
  • Begins with food entering the stomach.
  • It occurs through long and short reflexes
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93
Q

explain the mechanism of intestinal phase of gastric secretion

A
  • The presence of chyme in the duodenum causes some gastric secretion. This may be due to the duodenal release of gastrin.
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94
Q

what are the characters of gastric juice?

A
  • It is the most acidic fluid in the body (PH is 1).
  • The volume: 2.5 - 3 L/day.
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95
Q

what is the composition of gastric juice?

A

1)Water:- 99%

2)HCL:- 0.5%.

3)Inorganic constituents: e.g. Na, K, Ca, Mg (0.1%).

4)Organic constituents: e.g. Enzymes: pepsinogens, gastric lipase, gelatinase, and gastric amylase, mucus, and intrinsic factor.

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96
Q

what secretes HCL? and what are its receptors?

A

It is formed by the oxyntic (parietal) cells. The cells have 5 types of receptors:-

1- Muscarinic receptors

2- Gastrin receptors

3- Histaminic receptors: (H2 receptors).

4- Prostaglandin receptors: through which prostaglandins inhibit acid secretion. Anti-inflammatory drugs inhibit prostaglandin synthesis. so, it increases the incidence of peptic ulcers

5- Somatostatin receptor: Through which somatostatin inhibits HCl.

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97
Q

cellular mechanism of HCL secretion

A

1- Cl-is actively transported into the lumen of the canaliculus. This creates negative potential in the canaliculus.

2- Passive diffusion of K+ to the canaliculus aided by this negative potential.

3- H+ (derived from the dissociation of H2CO3 by carbonic anhydrase enzyme C.A.) is actively pumped into the canaliculus in exchange with K+ with the aid of H+-K+ ATPase enzyme

4- HCO-3, in exchange with Cl-, diffuse out of the cell to the extracellular fluid: This efflux of HCO3- will raise the pH of blood and this is called alkaline tide. For every H+ pumped there is one HCO3-found as an alkaline tide.

5- Water diffuses through the cell into the canaliculus by osmosis.

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98
Q

what is H2CO3 derived from?

“In HCL Secretion”

A

(H2CO3 is derived from combination of H2O and CO2 with the aid of the carbonic anhydrase enzyme (C.A). The CO2 is formed during the metabolism of the cell or entered from the blood. H2CO3 is dissociated by C.A. into H+ and HCO3-)

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98
Q

Control of HCI secretion

A

1- HCL is inhibited by:
- GIP, secretin, VIP and somatostatin, Prostaglandins.
- Increased acidity of gastric content, Fear and depression.

2- HCL is stimulated by:
- Acetylcholine, Gastrin, and Histamine, Anger.

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99
Q

what are the functions of HCL?

very important

A

1- It activates pepsinogens into pepsin and provides an acidic medium for their actions.

2- It kills many ingested bacteria.

3- It stimulates the flow of bile and pancreatic juice by stimulating CCK and secretin.

4- It helps Ca++ and iron absorption.

5- Control gastric emptying, excessive duodenal acidity delays gastric emptying.

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100
Q

what is pepsinogen? and what activates it?

A
  • pepsinogen is a proteolytic enzyme secreted by the peptic cells in an inactive form and activated by HCl to active pepsin. Then pepsin activates the rest of pepsinogens (autoactivation).
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101
Q

what stimulates the release of pepsinogen?

A

Its release is stimulated by gastrin, histamine, and acetylcholine.

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102
Q

what media does pepsinogen need?

A

Pepsin needs a highly acidic medium, so it becomes inactive in the duodenum. the acidity is neutralized by pancreatic alkaline secretion

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103
Q

what secretes the intrinsic factor? and what is its importance?

A

It is secreted by the oxyntic cells. It is essential for absorption of vitamin B12.

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104
Q

what do The mucous secreting cells in the stomach produce?

A
  1. large quantities of thin mucous
  2. Large quantities of more viscid mucous form a gel that coats the mucosa.
  3. They also secrete HCO3- which is trapped in the mucous gel.
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105
Q

how does the stomach protect itself from the harmful effects of HCL & pepsin?

A

The stomach protects itself from the harmful effects of HCl and pepsin by what is called the gastric mucosal barrier (GMB)

  1. The thick mucus gel coat is more than 1mm thick, containing HCO3- which provides major protection.
  2. HCl secreted by the oxyntic cells cross this barrier in finger-like channels leaving the gel layer intact.
  3. The gastric mucosal cells are tightly joined by a tight junction.
  4. Integrity of the membrane of the mucosal cells.
  5. The presence of trefoil peptides in the mucosa. These peptides resist the acid effect and autodigestion of gastric mucosa.
105
Q

how do prostaglandins affect the GMB?

A

Prostaglandins strengthen the GMB by stimulating mucous secretion, inhibits HCL secretion and Increases mucosal blood flow.

106
Q

how do Alcohol, salts, sugar at high concentration, vinegar, aspirin, and anti- inflammatory drugs affect GMB?

A

break down the GMB.

107
Q

what is peptic ulcer?

A

It is an excoriated area of the mucosa of the stomach

108
Q

what causes peptic ulcer?

A
  1. Breakdown of GMB.
  2. Excessive acid secretion. which may be due to:
    - Higher gastrin response to feeding.
    - Hypersensitivity of the oxyntic cells to gastrin.
  3. The gram-negative bacterium (Helicobacter pylori).
    - H. pylori colonizes the gastric mucous, attaches to gastric epithelial cells and release cytotoxins that attack and break down the protective mucous barrier and underlying cells.
109
Q

what are the motor functions of the stomach?

A
  • Storage function of the stomach
  • Mixing movements (Peristalsis)
  • Emptying of the stomach
  • Motility of the fasted stomach
110
Q

Storage function of the stomach

A

It is relaxation of the fundus and upper portion of the body relax (receptive relaxation) when food enters the stomach. Its volume can increase from 50 ml. to 1.5L without a marked increase in pressure.

111
Q

Mixing movements (Peristalsis)

A

When the stomach is filled → weak peristaltic waves (mixing waves) move along the stomach toward the antrum. They are controlled by the basal electrical rhythm BER

112
Q

what is BER?

A
  • BER is a wave of depolarization and repolarization originating from the pacemaker region. It occurs at a rate of once /20 seconds.
  • Normally, the wave is subthreshold to elicit gastric contraction. If neural or hormonal factors are present, the potential can increase to a threshold level and action potential is generated and produce a gastric contraction.
113
Q

what increases peristalsis?

A

gastrin, vagal stimulation, and gastric distension

114
Q

what decreases peristalsis?

A

sympathetic stimulation, duodenal distension, fats, acids, and hypertonicity.

115
Q

what does peristalitic movements lead to?

A
  • They mix the food with the gastric secretion and provide weak propulsion of food toward the antrum (propulsion)
  • When this movement reaches the pyloric opening, It will open passing a small amount of the most fluid part of the food contents to the duodenum. the sphincter closes again when the movement fades.
  • But when the gastric contents reach the closed sphincter, the contents move back toward the body of the stomach. This backward movement is called retropulsion.
115
Q

what are pyloric mills?

A

Repeated propulsion and retropulsion, because they cause complete grinding and mixing of food with gastric juice.

116
Q

what are the characteristics of food resulting from peristalisis?

A

murky, milky, semifluid called “chyme”.

117
Q

Emptying of the stomach

A
  • Gastric emptying is a slow process, to avoid distension of the duodenum. Once peristalsis occurs, the pressure in the pyloric antrum exceeds that in the duodenum.
  • So the gastric contents pass to the duodenum till the pylorus closes preventing more evacuation and also preventing regurgitation of the duodenal contents into the stomach, which is repeated with the new wave.
118
Q

what regulates gastric emptying?

A

Gastric emptying is regulated by gastric & duodenal factors.

119
Q

How do gastric factors affect gastric emptying?

A

All gastric factors increase gastric emptying

120
Q

gastric factors affecting gastric emptying

A

1) Nervous: Distension of the stomach by food will stimulate mechanoreceptors in the wall of the stomach →long vago-vagal and short reflexes → Increase pyloric pump and inhibit the pyloric sphincter.

2) Hormonal: Gastrin hormone → Increase pyloric pump. Inhibit pyloric sphincter.

3) Consistency of gastric contents: Soft food emptied quicker than hard food.

121
Q

how do doudenal factors affect gastric emptying?

A

All duodenal factors inhibit gastric emptying.

122
Q

doudenal factors affecting gastric emptying

A

1) Nervous signals:
- Distension and acidity of the duodenum (caused by presence of gastric contents) → initiate enterogastric reflex which inhibits gastric emptying.

2) Hormonal signals:
- Fat entering the duodenum → releases CCK from the upper intestine, which inhibits gastric emptying.→ allows the time for fat to be digested.

123
Q

how is enterogastric reflex elicited?

A

1) Distension or irritation to the duodenal mucosa.

2) Decreased PH of the duodenum inhibits gastric emptying until the acidity is neutralized by pancreatic secretion.

3) Products of protein digestion: to insure sufficient time for its digestion

124
Q

what is Migrating motor complex (MMR)?

A

MMR is periodic episodes of contractions that occur, once every 90 minutes in fasted stomach. It is regulated by motulin hormone

125
Q

what is the role of Migrating motor complex (MMR)?

A
  • It clears the stomach and the small intestine from the undigestible residues. It Inhibits migration of colonic bacteria into the terminal ileum.
126
Q

what are Hunger contractions?

A

These are rhythmic peristaltic contractions in an empty stomach after a long time of fasting.

127
Q

what are the charachters of hunger contractions?

A

They may be very strong → pain (hunger pangs) which starts after 12-24h. after the last meal. reach the maximum intensity in 3-4 days then gradually decrease and fasting can be continued without pain.

128
Q

what is the definition of vomiting?

A

Vomiting is an outward expulsion of gastric contents through the esophagus, pharynx, and mouth

129
Q

what coordinates vomiting?

A

It is coordinated by the vomiting center in the medulla oblongata.

130
Q

what are the afferent impulses responsible for vomiting?

A

from different parts of the body to the vomiting center.

130
Q

what are the efferent impulses responsible for vomiting?

A
  • 5th, 7th, 9th, 10th,and 12th to the GIT.
  • Spinal nerves to the diaphragm and abdominal muscles.
131
Q

what are the actions done by the efferent impulses? concerning vomiting

A

i) Relaxation of the cardiac sphincter (LES)

ii) Strong contraction of the diaphragm and all abdominal muscles→ ↑ intra-abdominal pressure squeezes the stomach and expels its contents into the esophagus and not in the direction of the pylorus.

iii) The stomach is passive in the process of vomiting and its wall is relaxed.

iv) Elevation of the soft palate to close the posterior nasal cavity. The glottis is also closed.

132
Q

what are the causes of vomiting?

A

The vomiting center may be stimulated by impulses from many parts of the body:

  1. Mechanical stimulation of the posterior part of the tongue.
  2. Irritation of the mucosa of the stomach and duodenum e.g. gastritis.
  3. Visceral pain e.g. acute peritonitis.
  4. Motion sickness. They arise from the organ of equilibrium in the internal ear.
  5. Stimulation of trigger zone area by toxins or drugs, and Increase intracranial tension.
133
Q

what is the definition of food absorbtion?

A

It is the passage of digested food from the lumen of GIT through mucosa to blood stream.

134
Q

what are the routes of food absorbtion?

A

The absorbed substances reach blood through blood capillaries or lymph vessels

135
Q

what are the sites of food Absorbtion?

A

1) Mainly small intestine: because of the large mucosal absorptive surface (250m2 or more).

2) Stomach: alcohol and some drugs which are highly lipid soluble are absorbed from stomach.

3) Large intestine: can absorb water, electrolytes, glucose, amino acids and drugs.

136
Q

absorbtion of water

A
  • By passive diffusion from diluted to concentrated solutions (i.e by osmosis).
  • The amount of water ingested is about 2 L/d and the secretions of GIT are about 7L/d 7.5L/d are absorbed from small intestine and approximately 1.5liters fluid passes to the large intestine. 95% is absorbed so about 100 ml/d water is excreted in stool.
137
Q

Absorbtion of Na ions

A
  • Na+ ions are transported across the basolateral border of the enterocyte by Na+- K+ pump located at this border.
  • This decreases Na+ concentration inside the enterocyte and helps transport of Na+ from the lumen into the enterocyte by the following ways :-
    1) About 30% are transported by Na+-glucose, Na+- amino acid and Na+- H+ transporters.
    2) About 30% by neutral Na+- Cl- co-transporter.
    3) The remainder(40%) is transported through special Na+ channels.
138
Q

what is the basis for the manufacture of oral rehydration therapy?

(How oral rehydration therapy works)

A

✓ The presence of glucose in intestinal lumen facilitates Na+ absorption because of the presence of common carrier.

✓ This is the basis for treatment of Na+ and water loss in diarrhea by oral administration of solution containing NaCl and glucose.

139
Q

Absorption of Cl- ions

A
  • Cl-ions are absorbed in small intestine by two secondary active transport mechanisms :-
    1. By Na+ or K+- Cl- co-transporter.
    2. By Cl– HCO3 exchanger (in ileum and colon).
    3. Cl- ions also diffuse through the leaky tight junction between the enterocytes following Na+ ions .
140
Q

Absorption of HCO3-ions

A

Are absorbed actively and by an indirect way:

  • Some Na+ ions are absorbed coupled with counter-transport of H+ ions.
  • H+ ions combine with HCO3 to form carbonic acid which dissociates into water and CO2.
  • CO2 diffuses to blood to be expired through lungs or binds with water intracellular to form carbonic acid again which dissociated to H+ and HCO3 -, the latter diffuses to blood
141
Q

Absorption of Ca++ Ions

A
  • They are actively transported mainly in upper small intestine.
  • They are absorbed according to the body needs:
    1. when plasma calcium level decreases, it stimulates parathyroid hormone secretion which activates vitamin D in kidney (to 1,25 dihydroxy cholecalciferol).
  1. This active metabolite increases calcium absorption from intestine by:-
    1) stimulating formation of calcium binding proteins at the apical border
    2) calcium ATP ase, at the basolateral border.
142
Q

what decreases the absorbtion of ca ions?

A

Their absorption decreases by factors which form insoluble calcium salts in intestine as oxalates, phosphates, phytates, increase PH and much fatty acids.

143
Q

what does Vitamin D deficiency or chronic renal failure lead to? (concerning ca absorbtion)

A

results in inadequate intestinal Ca2+ absorption, causing rickets in children and osteomalacia in adults.

144
Q

Absorption of iron

A

▪ It is actively transported mainly in upper small intestine and according to body needs :-

  1. is absorbed as heme iron (iron bound to hemoglobin or myoglobin) or as free Fe2+. In the intestinal cells, “heme iron” is degraded and free Fe2+ is released.
  2. The free Fe2+ binds to apoferritin and is transported into the blood.
  3. Free Fe2+ circulates in the blood bound to transferrin, which transports it from the small intestine to its storage sites in the liver, and from the liver to the bone marrow for the synthesis of hemoglobin.
145
Q

what is the most common cause of anemia?

A

Iron deficiency is the most common cause of anemia.

146
Q

what effect does insulin have on intestinal absorbtion?

A

Insulin has little effect on intestinal transport of sugars.

147
Q

is the absorbtion of monosaccharides regulated?

A

No, Absorption of monosaccharides is not regulated; the intestine can absorb over 5 kg of sucrose each day.

148
Q

Absorption of glucose and galactose

A
  • Glucose and galactose are absorbed by
    ✓ Na+ dependent secondary active transport at the brush border (the transporter is SGLT1)
    ✓ leave the basolateral border to blood by facilitated diffusion (the carrier is GLUT2).
  • SGLT1 has 2 receptor sites:- one for Na+ & the other for glucose or galactose. As a result of active transport of Na+ through the basolateral membrane, the concentration of Na+ decreases inside the cell.
  • This favors facilitated cotransport of Na+ and glucose or galactose. The increase in concentration of glucose or galactose helps their facilitated diffusion out of the cell into blood capillaries.
149
Q

absorbtion of fructose

A

❖ Is absorbed by facilitated diffusion at the brush border and also the basolateral membrane (the transporters are GLUT5 and GLUT2 respectively).

❖ Its absorption is independent of Na+ .

❖ Most of it is converted into glucose within the intestinal cell, so its concentration is continuously decreased maintaining a high concentration gradient for diffusion of fructose from the lumen.

150
Q

absorbtion of pentose

A

are absorbed by simple diffusion.

151
Q

what is the cause of lactose intolerance?

A

Lactose intolerance results from the absence of brush border lactase enzyme and, thus, the inability to hydrolyze lactose to glucose and galactose for absorption. Non absorbed lactose and H2O remain in the lumen of the GI tract and cause osmotic diarrhea.

152
Q

Absorption of amino acids

A
  • Almost all proteins are absorbed as amino acids
  • Amino acids are absorbed by Na+ dependent secondary active transport and leave cell by facilitated diffusion into portal blood.
153
Q

absorbtion of small peptides

A
  • small quantities of small (di & tri) peptides are also absorbed
  • Di and tripeptides are absorbed by
    1. H+ dependent co-transporter in apical membrane.
    2. Then intracellurally most of them are hydrolysed to amino acids (by cytosolic peptidase) which exit the cell by facilitated diffusion.
    3. The remaining di and tripeptides are absorbed unchanged.
  • Separate carriers are present for absorption of basic, acidic, neutral, di- and- tripeptides.
154
Q

absorbtion of whole proteins

A

Extremely minute quantities of whole proteins can be absorbed by pinocytosis e.g maternal antibodies in clostrum and foreign proteins producing allergic symptoms after eating certain foods.

155
Q

absorbtion of bases of nucleotides

A

absorbed by active transport.

156
Q

absorbtion of lipids

A

❖ Micelles bring the products of lipid digestion into contact with the absorptive surface of the intestinal cells.

❖ Then, fatty acids, monoglycerides, and cholesterol diffuse across the luminal membrane into the cells.

❖ Glycerol is hydrophilic and is not contained in the micelles.

❖ In the intestinal cells, the products of lipid digestion are re-esterified to triglycerides,cholesterol ester, and phospholipids and, with apoproteins, form chylomicrons.

❖ Chylomicrons are transported out of the intestinal cells by exocytosis. Because chylomicrons are too large to enter the capillaries, they are transferred to lymph vessels and are added to the bloodstream via the thoracic duct.

157
Q

wha does Lack of apoprotein B result in?

A

Lack of apoprotein B results in the inability to transport chylomicrons out of the intestinal cells and causes abetalipoproteinemia.

158
Q

Absorption of Vitamins

A

❖ Fat soluble vitamins: are absorbed with fat by the same mechanism.

❖ All water soluble vitamins except vitamin B12 are absorbed by Na+ dependent active transport mechanism.

❖ Absorption of vitamin B12: Vitamin B12 binds to the intrinsic factor, secreted by gastric mucosa, to form a complex which binds to specific receptors in ileum and is absorbed by endocytosis

159
Q

what does gastrectomy lead to? (concerning vitamin absorbtion)

A
  • Gastrectomy results in the loss of gastric parietal cells, which are the source of intrinsic factor, leading to pernicious anemia.
  • Injection of vitamin B12 is required to prevent pernicious anemia.
160
Q

Anatomy of the pancreas

A
  • The pancreas is both an endocrine and exocrine gland.

a. Endocrine part → islets of Langerhans that secretes hormones e.g. insulin

b. Exocrine part → compound alveolar gland that secretes the pancreatic juice

161
Q

How are the pancreatic secretions conducted to the duodenum?

A
  • through a system of ducts. The small ducts drain into a single large duct which usually joins the common bile duct forming the ampulla of Vater.
  • This opens through the duodenal papilla and its opening is encircled by the sphincter of Oddi.
162
Q

what is the nerve supply of the pancreas?

A
  1. Parasympathetic supply →from vagus N.
  2. Sympathetic supply →from the greater splanchic N.
163
Q

what are the charachters of pancreatic juice?

A
  • This juice is the most important digestive juice
  • Volume →1.5 L/day.
  • pH → alkaline secretion (about 8) → due to its high bicarbonate content
  • Composition:
    a) 98.5% Water
    b) 1.5% Solids;
164
Q

what are the main parts of pancreatic juice?

A

A) Aqueous part
B) Enzymatic part

165
Q

what is the aqueous part of the pancreatic juice? and what secretes it?

A

This is a watery juice rich in bicarbonates, It is secreted by duct cells.

166
Q

what is the function of the aqueous part of the pancreatic juice?

A
  • Neutralizes the acid chyme which enters the duodenum, this:
    1. Protects the delicate duodenal mucosa from excess acidity → prevents development of duodenal ulcer.
    2. Adjusts pH for action of pancreatic enzymes.
  • Washes out the thick viscid enzymatic part secreted by the alveoli
167
Q

what is the mechanism of HCO3 secretion in the pancreas?

A
  • In the ductal cells of pancreatic glands
  1. CO2 and H2O combine in ductal cells to form H2CO3
  2. H2CO3 dissociates into H+ and HCO3-
  3. H+ is transported into blood by Na+-H+ exchanger at basolateral membrane of ductal cells
  4. HCO3- is secreted into pancreatic juice by Cl–HCO3- exchanger at apical membrane of ductal cells (followed by osmotic flow of water)
  5. Absorption of H+ causes acidification of pancreatic
    venous blood
168
Q

what are the components of the enzymatic part of the pancreatic secretions?

A

A) Proteolytic Enzymes:
1. Trypsin
2. Chymotrypsin, carboxypeptidases and elastase
3. DNases and RNAses

B) Lipolytic Enzymes:
1. Pancreatic lipase
2. Cholesterol esterase
3. Phospholipase A

C) Alpha amylase

169
Q

what form is trypsin secreted in? and what activates it?

A
  • Is secreted in the form of trypsinogen and activated by enterokinase, then by trypsin
170
Q

what is the function of trypsin?

A
  • Acts on proteins, proteoses and peptones to form polypeptides and dipeptides.
171
Q

what is the function of trypsin inhibitor?

A

prevents premature activation of trypsin in the pancreatic ducts, so protect the pancreas from autodigestion.

172
Q

what activates chymotrypsin, carboxypeptidase & elastase?

A

Are activated by trypsin

173
Q

what is the function of Chymotrypsin, carboxypeptidases and elastase?

A

- Chymotrypsin: splits proteins, proteoses and peptones into polypeptides and dipeptides

- Carboxypeptidases: split polypeptides into amino acids and lower peptides

- Elastase: split elastin protein into peptides

174
Q

what is the function of DNases and RNAse?

A

Split DNA and RNA into nucleotides.

175
Q

what activates pancreatic lipase?

A

Is activated by bile salts and colipase.

176
Q

what is the function of pancreatic lipase?

A

Acts on triglycerides to form fatty acids, glycerol and monoglycerides.

177
Q

what is the function of cholesterol esterase?

A

Split cholesterol esters into cholesterol and fatty acids.

178
Q

what is the function of Phospholipase A?

A

Splits phospholipids into lysophospholipids and fatty acids.

179
Q

what is the function of alpha amylase?

A

Acts on cooked and uncooked starch, glycogen and most other carbohydrates, except cellulose, to convert them into dextrin, maltose and maltotriose.

180
Q

control of pancreatic secretion

A

1) Nervous Control (or Vagal stimulation)

2) Hormonal Control (by GIT hormones)
- Secretin
- Cholecystokinin
- Other hormones

181
Q

nervous control of pancreatic secretions

A

It is done through:

a) Conditioned reflexes initiated by sight, smell, or thinking of food.
b) Unconditioned reflexes initiated by presence of food in mouth, stomach and small intestine.

  • It causes VD and stimulation of pancreatic secretion (small in volume, rich in enzymes and poor in bicarbonate).
182
Q

secretin (control of pancreatic secretions)

A

Secretion:
- Secreted from S cells of duodenal mucosa in response to gastric acid chyme

Action:
- Stimulates the secretion of the aqueous part of the pancreatic juice.
- Stimulates the secretion of watery bile rich in NaHCO3

183
Q

CCK (control of pancreatic secretions)

A

Secretion:
- Secreted from I cell of duodenal mucosa in response to digestive products of proteins and fats

Action:
- It stimulates the secretion of the enzymatic part of the pancreatic juice.

184
Q

how do other hormones affect the pancreatic secretions?

A

i. Gastrin, VIP, motilin and insulin → stimulate pancreatic secretions

ii. Somatostatin, glucagon and enkephalin → inhibit pancreatic secretions

185
Q

what are the phases of pancreatic secretion?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
186
Q

Cephalic phase of pancreatic secretions

A
  • before food reach the stomach
  • Accounts for about 20% of secretion after meal.
  • Is induced by vagal stimulation (via conditioned and unconditioned reflexes) and gastrin.
  • Causes stimulation of secretion rich in enzymes.
187
Q

gastric phase of pancreatic secretions

A
  • when food reach the stomach
  • Accounts for about 5-10% of secretion after meal.
  • Is induced by vagal stimulation (via gastropancreatic reflex) and gastrin.
  • Causes stimulation of secretion rich in enzymes.
188
Q

intestinal phase of ancreatic secretions

A
  • when food reach the intestine
  • Accounts for about 60-70% of secretion after meal
  • Is due to secretin and CCK release and vagal stimulation (entero-pancreatic reflex).
  • Causes stimulation of secretion which is large in volume, rich in HCO3 and enzymes.
189
Q

what is the largest gland in the body?

A

the liver (weighing about 3 pounds).

190
Q

liver regenerating ability

A

Liver is capable of regenerating itself and this capacity can be seriously impaired by repeated or extensive damage.

191
Q

what are the functions of the liver?

A
  1. Metabolic functions
  2. Synthetic functions
  3. Storage functions
  4. Regulation of body temp
  5. Detoxification functions
  6. Circulatory and hematologic functions
  7. Excretory functions
192
Q

metabolic functions of the liver

A
  • Liver performs more than 500 metabolic reactions involved in ;

a) CHO metabolism e.g. glycogenesis, glycogenolysis,
b) Fat metabolism e.g. beta oxidation of fatty acids, cholesterol synthesis
c) Protein metabolism e.g. deamination, urea formation

193
Q

synthetic functions of the liver

A

a) Urea, uric acid and bile salts.
b) Alkaline phosphatase, transaminases, lactic dehydrogenase
c) Vitamin D3
d) Vitamin A from carotene

194
Q

storage functions of the liver

A
  • Stores variable amounts of glycogen, proteins, fats, vitamins, metals as iron and copper
195
Q

how does the liver regulate body temperature?

A

heat production by metabolic reactions in the liver

196
Q

excretory functions of the liver

A
  • Liver excretes bile pigments, toxins, drugs and heavy metals
197
Q

detoxification functions of the liver

A
  • Liver degrades hormones e.g. insulin, drugs and other toxic substances
198
Q

circulatory and hematologic functions of the liver

A

Reservoir functions of liver:
- the liver stores about 500 ml.

RBCs formation:
- During fetal life, the red cells are formed in the liver
- In adults, liver stores vitamin B12, iron, copper which are essential for erythropoiesis

Formation of:
- Synthesis of coagulation clotting e.g. fibrinogen and prothrombin.

Member of the reticuloendothelial system:
- cleans the blood from bacteria and destroy old RBCs

Formation of:
- about 1/2 of the body lymph.

199
Q

what are the charachters of bile? and what is responsible for its secretion?

A
  • Bile is an important digestive juice that is secreted by the liver and stored in the gallbladder.
  • Hepatocytes are responsible for 75% of bile secretion → canalicular bile.
  • Cholangiocytes of bile ducts are responsible for 25% of bile secretion → ductular bile.
200
Q

compare between hepatic bile and gallbladder bile

A
201
Q

what are the functions of bile?

A
  1. Bile contains bile salts that are essential for fat digestion and absorption.
  2. The alkali content of bile helps neutralization of gastric HCl.
  3. The mucin in bile acts as a lubricant in the small intestine.
  4. A route of excretion of bile pigments, cholesterol, drugs and toxins.
202
Q

what is the definition of bile salts?

A

They are the Na and K salts of bile acids conjugated with glycine or taurine e.g. Na taurocholate, Na glycocholate

203
Q

what are the types of bile acids?

A

The bile acids are 2 types:

  • 1ry bile acids → are formed in liver e.g. cholic and chenodoxycholic acids.
  • 2ry bile acids→ are formed from the 1ry acids e.g. deoxycholic and lithocholic acids.
204
Q

What is the fate of bile salts?

A

Entero-hepatic Circulation:

  • After doing their action in intestine, bile salts either;

1) 90-95% of bile salts are absorbed from the terminal ileum and pass in portal circulation to the liver to be resecreted in bile→ entero-hepatic circulation of bile salts.

2) 5-10% of bile salts passes to the colon: → excreted with the feces

  • The circulating pool of bile salts is about 3.5 gm→ so it circulates twice during a meal and 6-8 times per day.
205
Q

what are the functions of bile salts?

A

1) Help digestion of fat
2) Help absorption of fat and fat soluble vitamins (hydrotropic action)
3) Help absorption of Ca, Mg and iron
4) Solvent action
5) Laxative action
6) Antiputrefactive action
7) Choleretic action

206
Q

Digestion function of bile salts

A

Help digestion of fat by:

1) Activation of lipase

2) Emulsification of fat i.e. converting it into fine globules by reducing surface tension → ↑ surface area for action of lipase.

3) Dissolving fatty acids → expose deeper layers of fat for action of lipase.

207
Q

absorbtion function of bile salts

A

Help absorption of fat and fat soluble vitamins (hydrotropic action):
- Bile salts form with fat digestion products and fat soluble vitamins soluble and easily diffusible particles→ called micelles.

Help absorption of Ca, Mg and iron:
- This because the nonabsorbed fat ↓es their absorption.

208
Q

solvent action of bile salts

A
  • They keep cholesterol in solution forming micelles→ prevent its precipitation in gallbladder and formation of gall stones.
209
Q

Laxative actions of bile salts

A

They stimulate intestinal movements.

210
Q

antiputrefactive action of bile salts

A
  • In absence of bile salts, the undigested fat envelops protein particles preventing their digestion→ intestinal bacteria attack the undigested protein and cause putrifcation.
211
Q

choleretic action of bile salts

A
  • They stimulate bile secretion by liver.
  • About 50% of canalicular bile secretion is dependent on bile salts.
212
Q

control of bile secretion

A

1) Bile salts
2) Hormonal control
3) Nervous control
4) Hepatic blood flow

213
Q

How do bile salts control the secretion of bile?

A

Bile salts are the most powerful stimulants of bile secretion → major choleretics (50% of canalicular bile flow is bile salt dependent).So the more the bile salts in the enterohepatic circulation the more the bile flow (as during meals).

214
Q

hormonal control of bile secretion

A

a) Secretin: stimulates HCO3 secretion by the Cholangiocytes →hydrocholeretic.

b) Gastrin: stimulates bile secretion

c) CCK: stimulates bile secretion

d) Other hormones stimulating bile secretion include: insulin, glucagon and bombesin.

e) Hormones inhibit bile secretion include: somatostatin, estrogen and progesterone.

215
Q

nervous control of bile secretion

A

i) Vagal stimulation:
- It stimulates bile secretion due to choleretic effect of acetyl choline and ↑ hepatic blood flow by VD.

ii) Sympathetic stimulation:
- It ↓es bile secretion 2ry to ↓ hepatic blood flow due to VC of hepatic blood vessels.

216
Q

how does hepatic blood flow control bile secretion?

A
  • Bile secretion is directly proportional to the liver blood flow, when it is ↑ed (as during meals) bile secretion ↑es.
217
Q

what are the functions of gall bladder?

A

1) Storage of bile
2) Concentration of bile
3) Acidification of bile
4) Biliary pressure buffer
5) Secretion of mucus (white bile)
6) Emptying of bile

218
Q

Storage function of gall bladder

A
  • GB capacity is 20-60 ml.
  • In between meals GB is flaccid and sphincter of Oddi is closed so bile flow through cystic duct to GB.
  • During meals bile secretion by liver passes directly to the duodenum.
219
Q

concentration function of gall bladder

A
  • Bile is normally concentrated about 5 fold but it can be concentrated up to 12-20 fold.
220
Q

acidification function of gall bladder

A
  • It is done by absorption of NaHCO3→ GB bile is relatively acidic.
  • This prevents precipitation of Ca and formation of gall stones.
221
Q

how does the gall bladder prevent excessive pressure in the biliary passages?

A
  • GB prevents excessive rise of pressure in the biliary passages by accommodation and concentration of large volume of bile → prevents stoppage of bile secretion and protects hepatocytes from damage.
222
Q

mucus secretion function of gall bladder

A
  • It protects GB from the highly concentrated bile.
  • It gives bile its semifluid consistency.
  • It lubricates and protects intestinal mucosa from chemical and mechanical damage.
223
Q

emptying function of gall bladder

A

During meals, CCK and vagal stimulation causes contraction of GB and relaxation of sphincter of Oddi →bile is evacuated into the duodenum.

224
Q

what do the large intestine consist of (physiologically)?

A

✓ Proximal colon (absorbing colon) involving cecum, ascending colon and right half of the transverse colon.

✓ Distal colon (storage colon) which involves the left half the transverse colon, descending colon and sigmoid colon.

✓ Rectum and anal canal (anorectal segment).

225
Q

what is the length of the colon?

A

The length of colon is:

  • about 1m in living adult
  • about 1.5m at autopsy.
226
Q

what is the nerve supply of the large intestine?

A
227
Q

what are the functions of the large intestine?

A

1) Absorption of water, electrolytes, glucose, amino acids and drugs.

2) Secretory function:
- Secretion of some GIT hormones as VIP and somatostatin.
- Colonic secretion

3) Excretion of heavy metals as mercury, lead, arsenic, bismuth.

4) Synthesis of vitamin K and some members of vitamin B complex by bacteria of large intestine.

5) Motor functions of large intestine:
- Storage of feces till time of defection. It is the principal function of distal colon.
- Mixing and propelling the contents by movements of large intestine.
- Defecation and continence which are the motor functions of anorectal segment.

228
Q

what are the characters of colonic secretions?

A
  • It is viscous alkaline secretion rich in mucus, HCO3- and K++
  • Alkaline (PH 8) because of active secretion of HCO3-ions (in exchange for Cl-) which neutralizes acids produced by bacteria.
229
Q

what is the function of mucus in the large intestine?

A
  • Mucus protects the wall against injury and bacteria, adheres fecal material together, lubricates passage of feces and facilitates the process of defection.
230
Q

what stimulates/inhibits colonic secretions?

A

Colonic secretion is:
- stimulated by direct tactile stimulation, local myenteric reflex and by parasympathetic stimulation
- inhibited by sympathetic stimulation.

231
Q

what are the types of movements in the large intestine?

A
  1. Segmental contractions
  2. Peristaltic contractions
  3. Antiperistaltic contractions
  4. Mass movements (mass peristalsis)
232
Q

what are the characters of segmental contractions of the large intestine?

“happens by the contraction of circular muscles”

A
  • They are called haustral contractions as the segments formed are sac-like segments.
  • They are controlled by BER whose frequency increases along the colon from 9/min at cecum to 16/min at sigmoid colon. “myogenic”
  • It is irregular and variable.
  • The frequency of contractions is greater in rectum than sigmoid colon causing retrograde movement of fecal material. Thus the rectum is normally empty and suppositories placed in rectum are pushed up into the colon.
233
Q

what are the functions of segmental contractions of the large intestine?

A

1) they mix the colonic contents and by exposing more of the contents to the mucosa help absorption.

2) They produce minor forward propulsion of contents in cecum and ascending colon, 8-15 hours are required to move chyme from cecum through the colon.

234
Q

what are the characters and functions of peristalitic movements in the large intestine?

“By contraction of longitudinal muscles”

A
  • They are weak and rare.
  • They move the colonic contents very slowly towards the rectum.
235
Q

what are the charachters and functions of the anti-peristalitic movements of the large intestine?

A
  • Sometimes seen in the colon.
  • They facilitate absorption in large intestine.
236
Q

what is the mass peristalisis of the large intestine?

A
  • They are modified type of peristalsis, the contraction involves a greater length of colon 20 cm or more forcing a mass of feces down the colon.
237
Q

where do the mass movements of the large intestine start? and how often do they occur?

A
  • They usually start in the middle of the transverse colon preceded by:-
    1) relaxation of circular muscle
    2) disappearance of haustral contractions.
  • They occur once or twice per day (often after meal).
238
Q

what is the function of mass movements of the large intestine?

A

They serve to empty the colon rapidly into the rectum.

239
Q

” 2 distention + 2 I + CR”

what initiates the mass movements of the large intestine?

A

1) Distension of stomach and duodenum by meal through
▪ gastro-colic reflexes
▪ duodeno-colic reflexes
▪ gastrin hormone.

2) Irritation of the colon (as in ulcerative colitis). “ulcerative colitis may be treated by cigarettes!”

3) Overdistension of a segment of the colon.

4) Intense parasympathetic stimulation.

5) Conditioned reflex which occurs at the usual times of defecation.

240
Q

regulation of colonic motility

A

nervous & hormonal

241
Q

nervous regulation of colonic motility

A
242
Q

hormonal regulation of colonic motility

A
243
Q

what is the definition of defecation?

A

It is the act of emptying the colon through anus to outside.

244
Q

Is defecation controlled voluntarily or involutarily?

A

voluntarily controlled

(but not in infants)

245
Q

what is the mechanism of defectation?

A
  1. As the rectum fills with fecal material, it contracts and the internal anal sphincter relaxes (rectosphincteric reflex).
  2. Once the rectum is filled to about 25% of its capacity, there is an urge to defecate. However, defecation is prevented because the external anal sphincter is tonically contracted.
  3. When it is convenient to defecate, the external anal sphincter is relaxed voluntarily. The smooth muscle of the rectum contracts, forcing the feces out of the body.
  4. Intra-abdominal pressure is increased by expiring against a closed glottis (Valsalva maneuver). (Straining helps defecation)

——-OR——

Stimulus: Presence of more than 25% of fecal capacity in rectum

Receptor: Strech receptors (Mechano & Chemo)

Afferent: Pelvic nerve

Center: S2,3,4 of Spinal cord

Efferent: Pelvic nerve

Action: Contraction of the wall of rectum and relaxation of internal anal spinchter

246
Q

characters of the gastrocolic reflex

A
  • The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements.
  1. The gastrocolic reflex has a rapid parasympathetic component that is initiated when the stomach is stretched by food.
  2. A slower, hormonal component is mediated by CCK and gastrin.
247
Q

what are the disorders of large intestine motility?

A

1) Irritable bowel syndrome
2) Megacolon (Hirschsprung’s disease)

248
Q

how could emotional factors affect large intestine motility?

A
  • Emotional factors strongly influence large intestinal motility via the extrinsic ANS. It may occur during periods of stress and may result in:
    1. constipation (increased segmentation contractions)
    2. diarrhea (decreased segmentation contractions).
249
Q

what are the characters of hirshsprung’s disease?

A
  • the absence of the colonic enteric nervous system, results in constriction of the involved segment, marked dilatation and accumulation of intestinal contents proximal to the constriction, and severe constipation.
250
Q

what is fecal continence?

A

It is the ability to control elimination of rectal contents during rest and during sudden increase intra-abdominal pressure (as during cough and sneezing).

251
Q

what are the mechanisms of fecal continence?

A
  1. Tone of internal and external anal sphincters
  2. Tone of puborectalis muscle
  3. Anal sensation
  4. Rectal sensation, compliance and motility
  5. Intact innervation of anorectal region
  6. Consistency of stool
252
Q

role of Tone of internal and external anal sphincters in fecal continence

A
  1. They maintain anal canal closure. The resting anal pressure (about 60 mmHg) is higher than the rectal pressure (about 6 mmHg):-
    - 80% of it is due to the resting tone of internal anal sphincter .
    - 20% of it is due to the tone of external anal sphincter.
  2. Anal canal has also spongy tissue pads which expand securing complete closure.
253
Q

role of Tone of puborectalis muscle in fecal continence

A

It maintains the ano-rectal angle which forms important barrier to passage of stool from rectum to anal canal.

254
Q

what is the anal canal mucosa sensitive to?

A

pain, touch and temperature.

255
Q

role of anal sensation in fecal continence

A
  • Anal canal mucosa is sensitive to pain, touch and temperature.
  • This allows differentiation between solid and liquid stool from gases.
  • This is important because solid and liquid feces are expelled only in the toilet.
256
Q

what is rectum sensitive to?

A

only to stretch, giving the desire to defecate and triggering reflex and voluntary contraction of external anal sphincter and puborectalis muscle. This preserve continence in stress situations caused by rise in rectal pressure as their resting tone alone is not sufficient in such conditions.

257
Q

role of rectum compliance in fecal continence

A

Rectum has the ability to accommodate different fecal volumes without high intrarectal pressure. The reservoir function maintains continence and allows for appropriate times of defecation.

258
Q

role of rectum motility in fecal continence

A

The basal electrical rhythm in rectum is higher than sigmoid colon. This acts as a barrier to fecal flow and makes rectum empty in the interdefecatory periods.

259
Q

role of consisteny of stool in fecal continence

A

Solid consistency of stool is important because continence becomes difficult with large volume of liquid stool.

260
Q

Some notes about defecation

A
  • Mass movements of the colon cause rectal distension
  • defecation reflex is integrated in the Spinal Cord
  • the cause of colonic peristalisis by meal is gastrocolic reflex

Y2B1 - GIT 📕 (9 decks)

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