Gastrointestinal System Flashcards

1
Q

What are the functions of the gastrointestinal tract (GIT)

A

Transfers digested organic nutrients, minerals, and water from the external environment to internal environment. Plays a role in digestion and absorption.

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2
Q

What occurs during digestion in the gastrointestinal tract

A

Chemical alteration of food into absorbable molecules. GI motility, pH changes, biological detergents, and enzymes.

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3
Q

What occurs during absorption of the gastrointestinal tract

A

Movement of digested food from the intestine into the blood or lymphatic system.

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4
Q

What is excretion of the gastrointestinal tract

A

Non-absorbable components of food, bacteria, intestinal cells, hydrophobic molecules (drugs, cholesterol, and steroids).

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5
Q

How does host defense occur for the gastrointestinal system

A

GIT is continuous with the exterior of the body. It is a potential portal for harmful substances and microorganisms. We develop a highly developed immune system due to this.

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6
Q

What are the components of the gastrointestinal tract

A

Mouth, Pharynx, Esophagus, Stomach, Small intestine (Duodenum, Jejunum, Ileum), and the Large Intestine

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7
Q

What are the accessory organs are made of the gastrointestinal system

A

Pancreas, Liver, and Gall Bladder.

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8
Q

What is the structure of the GIT

A

Long muscular tube stretching from mouth to anus. It’s composition from mid-esophagus to anus is very similar with some exceptions.

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9
Q

What are the layers of the mucosa

A
Epithelial layer
Lamina propria
Muscularis mucosa
Submucosa
Muscularis externa 
Serosa
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10
Q

What is the epithelial layer of the mucosa

A

Epithelium is the layer of cells that lines all body cavities and surfaces. “Polarized” meaning that it is different at one surface compared to the other. Basolateral and apical arrangement. Different transport proteins at the apical structure compared to basolateral. Tight junctions confine transport proteins to specific membrane regions. Provides selective uptake of nutrients, electrolytes, and water. Prevents passage of harmful substances. Surface area is amplified by villi and crypts (+ microvilli). Stem cells in crypts divide and daughter cells migrate upwards toward the villous.

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11
Q

What is the lamina propria layer of the mucosa

A

Connective tissue, small blood vessels, nerve fibers, lymphatic vessels, and immune and inflammatory cells.

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12
Q

What is the muscularis mucosa layer

A

Thin layer of smooth muscle. Not involved in the contraction of the GIT. May be important in villi movement.

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13
Q

What is the submucosa layer of the mucosa

A

Plexus of nerve cell bodies. Relays information to and away from the mucosa. Also composed of connective tissue, blood, and lymphatic vessels.

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14
Q

What is the muscularis externa layer of mucosa

A

Thick inner layer of circular muscle which has fibers oriented to cause narrowing of lumen. Myenteric nerve plexus which has a network of nerve cells, which regulate muscle function. Thinner outer layer of longitudinal muscle which has fibers oriented to shorten muscle.

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15
Q

What is the serosa layer of the mucosa

A

Connective tissue, encases intestine and forms connection point to the abdominal wall.

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16
Q

What is the paracellular pathway

A

It is limited by the tight junction seal and water and small ions can diffuse through it.

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17
Q

What is the transcellular pathway.

A

It is a two-step process that requires a transport protein on the apical and basolateral surface of the cell.

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18
Q

How is blood supplied to the GIT

A

It is critical for carrying away water soluble absorbed nutrients for usage at other sites in the body. Blood perfuses intestine and then flows to the liver via the portal vein.

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19
Q

What is portal circulation

A

The portal vein drains blood from the digestive tract and empties directly into the liver. It is a circulation of nutrient-rich blood between the gut and the liver. This allows the liver to remove harmful substances and process nutrients.

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20
Q

Why is the liver an unusual organ

A

Liver is an unusual organ because it receives blood from both venous (portal) and arterial circulation. Liver receives less oxygenated blood, more nutrient rich blood than other organs.

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21
Q

How is the gastrointestinal processes regulated

A

Governed by the volume and composition of lumen

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22
Q

What are the reflexes of the GI tract initiated by

A

Distension of wall by volume of luminal contents, osmolarity of contents, pH of contents, and concentrations of specific digestion contents such as (monosaccharides, fatty acids, peptides, and amino acids).

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23
Q

What are the regulations of the GI processes propagated by

A

Mechanoreceptors: Activated by mechanical stimuli such as pressure and stretch
Osmoreceptors: Activated by changes in osmolarity
Chemoreceptors: Activated by the binding of specific chemicals.

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24
Q

What is the intrinsic neural regulation of the GI Processes

A

Enteric nervous system. Controls the activity of the secretomotor neurons; such as motility and secretory function. Contained completely within the walls of the GIT. Dense and complex network of neurons. Brain of the gut and can function independently of the CNS.

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25
Q

What are the nerve networks the intrinsic neural regulation

A

Myenteric plexus influences smooth muscle

Submucosal plexus influences secretion

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26
Q

What does the extrinsic neuronal regulation of the GI processes

A

There is parasympathetic and sympathetic processes

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27
Q

What does the extrinsic neuronal regulation of GI processes influences

A

Hunger, Sight/smell of food, and emotional state.

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28
Q

What is the parasympathetic reaction of the mouth

A

Stimulates flow of saliva

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29
Q

What is the parasympathetic reaction of the stomach

A

Stimulates peristalsis and secretion

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30
Q

What is the parasympathetic reaction of the liver

A

Stimulates releases of bile

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31
Q

What is the sympathetic reaction of the mouth

A

Stimulates flow of saliva

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32
Q

What is the sympathetic reaction of the stomach

A

Inhibits peristalsis and secretion

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33
Q

What is the sympathetic reaction of the liver

A

Conversion of glycogen to glucose

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34
Q

What are endocrine chemical messengers in the GI tract

A

Endocrines are hormone-secreting gland cell. They release hormones in the blood vessels. They target cells in one or more distant places in one body.

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35
Q

What are neurocrine chemical messengers in the GI tract

A

It impacts the nerve cell, releases a neurotransmitters. Neuron or effector cell near site of neurotransmitter release.

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36
Q

What are paracrine chemical messengers in the GI tract

A

Impacts the local cell. Releases a paracrine substance. Target cells near site of release of paracrine substance.

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37
Q

What are autocrine chemical messengers in the GI tract

A

Impacts the local cell. Releases the autocrine substances. Autocrine substances acts on the same cell that secreted the substance.

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38
Q

How do endocrine chemical messengers control GI activity

A

Chemical messenger passes from cell which produced it into blood and is carried blood to it (relatively distant) target

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39
Q

How do neurocrine chemical messengers control GI activity

A

Chemical messenger is released from a nerve, travels across a synapse and acts on a post-synaptic cell.

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40
Q

How do paracrine chemical messengers control the GI activity

A

Chemical messenger diffuses through intestinal fluid to nearby cells.

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41
Q

How do autocrine chemical messengers control GI activity

A

Chemical messenger acts on the cell which produced it.

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42
Q

What is the hormonal control of the GI activity

A

Endocrine cells are scattered throughout the epithelium of the stomach and small intestine. One surface each endocrine cell exposed to the GI lumen. The chemical substances in lumen stimulate cell to release hormones across opposite surface of the cell into blood vessels in lamina propria. Hormones travel through blood to target cells.

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43
Q

What are the best understood GI hormones

A

Secretin, Cholecystokinin (CCK), Gastrin, and Glucose-dependent insulinotropic peptide (GIP). Each participates in a feedback control system that regulates some aspect of the GI lumen. Most GI hormones affect more than one type of target cell.

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44
Q

What does Gastrin do

A

Major release site: Stomach antrum (G cells)
Major stimuli for release: Peptides/amino acids in stomach, parasympathetic nerves.
Major actions: Increase in HCl, and an increase in motility (stomach, ileum, and large intestine)

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45
Q

What does Secretin do

A

Major release site: Small intestine (S cells)
Major stimuli for release: Acid in small intestines (pH < 4.5)
Major actions: Decrease in HCl, decrease in stomach motility, and an increase in HCO3-/H2O from pancreas and in bile.

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46
Q

What does Cholecystokinin (CCK) do

A

Major release site: Small intestine (I cells)
Major stimuli for release: Digested fat/protein in small intestine
Major actions: Decrease in HCl, decrease in stomach motility, and an increase in enzymes from the pancreas and bile expulsion.

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47
Q

What does Glucose-dependent insulinotropic peptide (GIP) do

A

Major release site: Small intestine (K cells)
Major stimuli for release: Glucose or fat in the small intestine
Major actions: Increase in insulin

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48
Q

What is intestinal motility

A

Contraction and relaxation of the two outer smooth muscle layers of the GIT allows the movement of contents from one site to another. Two forms peristalsis and segmentation

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49
Q

What is peristalsis (propulsion)

A

Circular muscle contracts on the oral site of a bolus of food (longitudinal layer relaxes). Circular muscle contracts and moves toward the anus, propelling the contents of the lumen in that direction, as the ring moves, the circular muscle on the other side of the distended area relaxes (longitudinal muscle contracts), facilitating smooth passage of the bolus.

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50
Q

What is segmentation (mixing)

A

Contraction and relaxation of intestinal segments with little net movement of contents towards the large intestine. Mostly occurs in the small intestine. Allows mixing of contents with digestive enzymes. Slows transit time to allow absorption of nutrients and water.

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51
Q

What is the basic electrical rhythm of the GIT

A

GIT has pacemaker cells throughout the smooth muscle cells. Constantly undergoing spontaneous depolarization-repolarization cycles (slow waves). These slow waves are the basic electrical rhythm

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52
Q

What are the slow waves of the basic electrical rhythm

A

Slow waves propagated through the circular and longitudinal muscle layer through gap junctions. In the absence of neural/hormonal input spontaneous slow waves don’t result in significant contractions. Excitatory hormones/neurotransmitters further depolarize the membrane and bring it close to threshold.

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53
Q

How does the force and frequency of contractions are seen in the GI tract

A

The number of action potentials fired proportional to force of contraction. Frequency of contraction maintained by the basic electrical rhythm. Force of contraction mediated by neuronal and hormonal input.

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54
Q

What are the phases of the gastrointestinal control

A
  1. Cephalic (head)
  2. Gastric (stomach)
  3. Intestinal
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55
Q

What is the cephalic phase of the gastrointestinal control

A

Receptors in the heads are stimulated by sight, smell, taste, chewing of food, and emotional state. The parasympathetic fibers activate neurons int he GI nerve plexi.

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56
Q

What is the gastric phase of the gastrointestinal control

A

Receptors in the stomach stimulated by distension, acidity, amino acids, and peptides. Short and long neural reflexes mediate the response (gastrin and acetylcholine).

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57
Q

What is the intestinal phase of gastrointestinal phase

A

Receptors in intestine stimulated by distension, acidity, osmolarity, and digestive products. Mediated by short and long neural reflexes by hormones secretin, cholecystokinin, and glucose-dependent insulinotropic peptide (GIP). All of these are secreted by endocrine cells in the small intestine.

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58
Q

What controls food intake

A

Hypothalamus which contains the feeding and satiety centers.

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59
Q

What is the feeding center

A

Found in the hypothalamus, found in the lateral region. Activation of this region increase hunger. Animals with lesions in this area become anorexic and lose weight.

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60
Q

What is the satiety center

A

Found in the hypothalamus in the ventromedial region. Activation of this region makes you feel full. Animals with lesions in this area overeat and become obsese.

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61
Q

What are orexigenic factors

A

These increase intake. Neuropeptide Y, NPY will stimulate hunger. Ghrelin which synthesizes and releases from endocrine cells in the stomach during fasting, and stimulates the release of NPY and other neuropeptides in hypothalamus feeding center.

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62
Q

What are the anorexigenic factors

A

They decrease intake. Leptin (from adipose), insulin (from pancreas), peptide YY (from intestines), and melanocortin (from hypothalamus)

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63
Q

How is Water Intake regulated

A
  1. Increased plasma osmolarity
  2. Decrease plasma volume
  3. Dry mouth and throat will stimulate thirst
  4. Prevention of over-hydration
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64
Q

How does an increased plasma osmolarity impact water intake

A

Most important under physiological conditions. Osmoreceptors in thirst center within the hypothalamus. Vasopressin (antidiuretic hormone is released) causing a conservation of water at the kidneys

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65
Q

How can a decrease in plasma volume impact water intake

A

Stimulation of baroreceptors in cardiovascular system. Baroreceptors in kidney afferent arteries leading to activation of renin angiotensin system. Result is production of angiotension 2 which as a direct effect on the hypothalamus to increase thirst.

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66
Q

How can prevention of over-hydration impact water intake

A

Person stops drinking well before water is absorbed by GIT. Probably mediated by stimulus from mouth, throat, and GIT.

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67
Q

What are the three main salivary glands

A

Parotid glands which produce a serous secretion
Submandibular glands which produce a serous/mucous secretion
Sublingual glands which produce a mucous secretion

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68
Q

What composes Saliva

A

Water (96-99.5%, hypotonic, and slightly alkaline)
Electrolytes (Relatively rich in K+ and HCO3-, and relatively poor in Na+ and Cl-)
Digestive enzymes (amylase, lipase)
Glycoproteins (Mucin [mucin + water = mucuous]
Other components (Anti-microbial factors like lysozyme, lactoferrin, and others)

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69
Q

What are the functions of saliva

A

Moistens and lubricates food. Initiates digestion with amylase and lingual lipase. Dissolves a small amount of food to allow diffusion to taste buds which affects appetites and food intake. Antibacterial actions which prevents microbial colonization. Aids in speech. Buffering action which contains HCO3- which helps to neutralize acids.

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70
Q

How do acinar cells form saliva

A

With water, electrolytes, and proteins. The proteins are released by exocytosis. Cl-, bicarbonate and potassium ions are actively secreted. Na+ and H2O follow paracellularly via the (leaky) tight junctions. Initial secretion is isotonic (ionic composition comparable to plasma) due to leakiness of acinar cell layer. Myoepithelial cells contract and expel formed saliva from acinus into the duct.

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71
Q

How do ductal cells form saliva.

A

Ductal cells modify the initial saliva to a hypotonic and alkaline state. Net loss of Na+ and Cl- (active reabsorption). Addition of K+ and HCO3- (active secretion) - to a lesser extent. Duct cells are tightly joined and impermeable to H2O.

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72
Q

What is the role of saliva in digestion

A

Starch digestion is initiated in the mouth by amylase. Inhibited at acidic pH in stomach. 95% of carbohydrates digested in the small intestine by pancreatic amylase. Plant starch made up of glucose polymers-amylose and amylopectin. Lingual lipase causes the acid to stable and therefore active in stomach. Overall amylase and lingual lipase are minor pathways for digestion which may be important during pathological conditions and neonates.

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73
Q

What is salivary pathophysiology

A

Variety of conditions where salivary secretion is impaired through congenitally, autoimmune processes, side effects of drugs, and radiation treatments.

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74
Q

What are some consequences of salivary pathophysiology

A

Dry mouth, decrease oral pH (tooth decay, esophageal erosions), difficulty in lubricating and swallowing food (poor nutrition).

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75
Q

How to treat salivary pathophysiology

A

Frequent sips of water and fluoride

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76
Q

What is swallowing

A

Complex reflex initiated by pressure receptors in the walls of the pharynx. Stimulated by food/liquid entering the pharynx. Receptors send signals to the swallowing center in the brainstem. In turn signals to muscles in the: pharynx - throat passage common to food and air, esophagus, and respiratory muscles.

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77
Q

What is the larynx

A

Voice box, located between the pharynx and trachea.

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78
Q

What is the glottis

A

Area around the vocal cords - where air travels through

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79
Q

What is the epiglottis

A

Tissue flap that covers larynx and trachea during swallowing

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80
Q

What is the steps of swallowing

A
  1. Tongue pushes food bolus to the back of the pharynx
  2. Soft palate elevates to prevent food from entering the nasal passages. Impulses from the swallowing center. Inhibits respiration, raises the larynx and closes the glottis.
  3. Epiglottis covers the glottis to prevent food or liquid entering trachea
  4. Food descends into the esophagus.
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81
Q

What is the esophagus

A

Transfers food from mouth to stomach. 18-25 cm long tube. Skeletal muscle surrounds the upper third, smooth muscles surround the lower two-thirds. Food passes very rapidly, no absorption, mucous glands for lubrication. Exposed to rough/abrasive food contents but there is specialized epithelium to protect the esophagus.

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82
Q

What are the esophageal sphincters

A

Upper esophageal sphincter: Ring of skeletal muscle just below the pharynx
Lower esophageal sphincter: Ring of smooth muscle at the stomach.
The sphincters are closed when swallowing, vomiting, and burping

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83
Q

What are the esophageal phase of swallowing

A
  1. Relaxation of the upper esophageal sphincter
  2. Peristaltic waves move food bolus down the esophagus (one wave takes 5-9 seconds from the top to the stomach).
  3. Lower sphincter opens and allows food to pass into stomach
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84
Q

What happens when the upper esophageal sphincter relaxes

A

Food passes through, sphincter closes, glottis opens breathing resumes.

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85
Q

What happens when the lower sphincter opens and food enters the stomach

A

Once the food passes the sphincter the sphincter closes

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86
Q

What is the main driving force of swallowing

A

Peristalsis is along with gravity that assist but it is not necessary because you can swallow in zero gravity and when hanging upside down.

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87
Q

What is heart burn

A

The lower esophageal sphincter prevents gastric contents from reaching the esophagus.

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88
Q

What happens when acid reaches the esophagus

A

Stimulates peristalsis, increases salivary secretion, and results in neutralization and clearance.

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89
Q

How can heart burn occur

A

Due to an insufficient sphincter, after a big meal, and during pregnancy.

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90
Q

What is the stomach

A

Muscular saclike organ located between the esophagus and the small intestine

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91
Q

What are the functions of the stomach

A

Storage of food. Mechanical breakdown of food. Chemical breakdown of food. Reduces food to fragments of proteins, polysaccharides, droplets of fat, salt, and water “chyme.” Control the rate at which food enters the small intestine. Secretes “intrinsic factor” critical for absorption of Vitamin B12 in the ileum. Very little absorption across the stomach

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92
Q

How is food chemically broken down in the stomach

A

The stomach secretes pepsinogen which converts to pepsin which is the protein digesting enzyme. The stomach also secretes HCl for dissolving food, partially digesting macromolecules in food and sterilization of food.

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93
Q

Why is the intrinsic factor important in the stomach

A

Vitamin B12 is required for normal red blood cell formation. Lack of intrinsic factor results in pernicious anemia which is a red blood cell deficiency.

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94
Q

What are the components of the stomach

A

Fundus, Body and Antrum

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95
Q

What do the fundus and body do in the stomach

A

They are the thinner layers of smooth muscle and they secrete mucous, pepsinogen, and HCl

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96
Q

What does the antrum do in the stomach

A

It is the thicker smooth muscle layer and it secretes mucous, pepsinogen, and gastrin

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97
Q

What are the major exocrine secretions of the stomach

A

Substances secreted into ducts then on to an epithelial surface without passing into blood. They are mucuous, HCl and pepsinogen

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98
Q

What is the mucous secretion of the stomach

A

It is the protective coating over stomach epithelium to avoid “self-digesting”

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99
Q

What is the HCl secretion of the stomach

A

Hydrolysis of proteins

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100
Q

What is the Pepsinogen secretion of the stomach

A

Digestion of proteins

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101
Q

What are the minor secretions of the stomach

A

Intrinsic factor, gastrin, histamine, and somatostatin

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102
Q

What is the intrinsic factor secretion of the stomach

A

Responsible for Vitamin B12 absorption

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103
Q

What is the gastrin secretion of the stomach

A

Endocrine and it stimulates HCl production and stomach motility

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104
Q

What is the histamine secretion of the stomach

A

Paracrine, stimulates HCl production

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105
Q

What is the somatostatin secretion of the stomach

A

Paracrine, and it inhibts HCl production

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106
Q

What are the different types of cells in the stomach

A
Chief Cells
Enteroendocrine Cells
Enterochromaffin-like Cells
D-Cells
Parietal Cell
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107
Q

What are chief cells in the stomach

A

Gastric glands in all regions of the stomach. They secrete pepsinogen which is an inactive precursor to pepsin (zymogen), pepsinogen cleaved by acid to pepsin, and pepsin accelerates protein digestion

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108
Q

What are enteroendocrine cells in the stomach

A

Gastric glands in the antrum. Also known as G-cell. Secretes gastrin which is responsible for stimulating HCl production by parietal cell and stimulating GI motility.

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109
Q

What are enterochromaffin-like cells in the stomach

A

Gastric glands in all regions (more in antrum). It secretes histamine and stimulates HCl release.

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110
Q

What are D-cells in the stomach

A

Gastric glands in all regions (more in antrum). Secretes somatostatin and it has negative regulation of HCl secretion

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111
Q

What is a parietal cell in the stomach

A

Found in gastric glands contained in the fundus/body regions. Also known as an oxyntic cell. Secretes HCl and intrinsic factors. Canaliculi increase the surface area of the cells and maximize secretion to the stomach lumen.

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112
Q

What is the role of the parietal cell in the stomach

A

Responsible for acid secretion, acid secretion requires energy-lots of mitochondria, and actively secreting cell has better defined “canaliculus”

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113
Q

What ensures the acidification of the stomach lumen

A
  1. H+/K+ ATPase
  2. Carbonic anhydrase (CA)
  3. Cl-/HCO3- exchanger - responsible for secondary active transport
  4. K+ channels
  5. Cl- channels
114
Q

What is the role of H+/K+ ATPase in the acidification of the stomach lumen

A

It is in the luminal membrane, it pumps H+ into the lumen exchange for K+ into the cell. It did this through active transport and it was electroneutral.

115
Q

What is the role of carbonic anhydrase in the acidification of the lumen

A

Catalyses the formation of H2CO3 from H2O and CO2. H2CO3 dissociates into H+ (for secretion into lumen) and HCO3-

116
Q

What is the role of the Cl-/HCO3- exchanger in the acidification of the stomach lumen

A

Excess HO- is effluxed from the cell as HCO3- in exchange for Cl-. This is a critical step (in conjunction with carbonic anhydrase) for maintenance of neutral cellular pH

117
Q

What is the role of K+ channels in the acidification of the stomach lumen

A

K+ is recycled back into the stomach lumen. This is done through diffusion through a channel and there is a loss of positive charge (which is compensated by Cl- secretion)

118
Q

What is the role of the Cl- channels of the acidification of the stomach lumen

A

Cl- leaks back into the stomach lumen. There is diffusion through the channel and it compensates for loss of positive charge through K+ channels.

119
Q

What are the four chemical messengers that regulate acid secretion of the parietal cell

A

Gastrin (gastric hormone)
Acetylcholine (neurotransmitter)
Histamine (paracrine)
Somatostatin (paracrine) - the only messenger that inhibits the release of HCl, gastrin, and histamine.

120
Q

How is pepsinogen secreted by chief cells

A

Stimulation by enteric nervous system and there is parallels release of HCl.

121
Q

What is advantage of inactive precursor secretion

A

Makes sure that we don’t go through with self-digestion. Pepsin is active only at low pH - irreversibly inactivated when it enters the small intestine.

122
Q

What aer the Phases of the Gastric Secretion

A
  1. Cephalic Phase - Anticipatory, excitatory, and mainly via the vagus nerve.
  2. Gastric Phase - Major phase, excitatory, and mainly via gastrin
  3. Intestinal phase - Mainly inhibitory, due to the presence of acid, fat, digestion productions and hypertonic solutions in the duodenum
123
Q

How does acetylcholine regulate gastric secretions

A

Acetylcholine also increases acid secretion by the parietal cell by stimulating the release of gastrin from G-cells, and stimulating the release of histamine from enterochromaffin like cells, and inhibiting somatostatin release from D-cells.

124
Q

How does somatostain regulate gastric secretion

A

Somatostatin inhibits acid secretion by parietal cell.

125
Q

How does gastrin regulate gastric secretion

A

Gastrin also increases acid secretion by the parietal cell by stimulating histamine release

126
Q

What happens when acid secretion happens at a high rate

A

Parasympathetic input will be reduced during the cephalic phase. Negative feedback occurs for gastrin production and the acid inhibits release. Somatostatin release increases due to reduced parasympathetic inhibition of D-cell and direction stimulation of somatostatin release by acid. Somatostatin then directly inhibits acid secretion from parietal cell, inhibits histamine release from enterochromaffin-like cells, and inhibits gastrin release from G-cell.

127
Q

How is the stomach flexible

A

Empty stomach is small (50 mL) diameter larger than the small intestine. Consumption of meal will lead to smooth muscle relexation which will lead to stomach increasing to about 1.5 L without increasing pressure.

128
Q

How does gastric motility occur

A

Food stimulates peristaltic waves whcih are weak contraction in the body of the stomach. This causes a powerful contraction in the antrum which mixes luminal contents and causes the closure of the pyloric sphincter

129
Q

What happens when the pyloric sphincter is closed in the stomach

A

Small amounts of stomach contents released to the duodenum, and most antral contents are forced backward towards the body of the stomach resulting in mixing of contents with enzymes and acid.

130
Q

What is the electrical basis of stomach motility

A

The stomach has pacemaker cells in the smooth muscle layers which causes spontaneous slow waves of depolarization and replorization. Excitatory hormones and neurotransmitters further depolarize and determine the strength of a stomach contraction

131
Q

What can trigger the vomiting center in the medulla

A

Psychogenic factors such as sights and smells
GIT disturbances such as infection, distension, and obstruction
Motion sickness or an inner ear infection
Alcohol and toxins which trigger chemoreceptors in the GIT or brain
Pressure on the central nervous system

132
Q

What happens when the vomiting center is triggered in the medulla.

A
  1. Nausa, Salivation, and breath held in mid-inspiration
  2. Glottis closes off trachea
  3. Lower esophageal sphincter and esophagus relaxes
  4. Diaphgram and abdominal muscles contract
  5. Reverse peristalsis moves upper intestinal contents into the stomach
  6. Stomach contents move up through esophagus and out through the mouth
  7. The soft palate is raised to avoid vomit coming out of the nose
133
Q

What are the benefits of vomitting

A

Removal of harmful substances prior to absorption such as bacteria and toxins. Nausea and feeling bad should prevent individual from consuming noxious substances again.

134
Q

What are the consequences of vomiting

A

Dehydration, loss of salts (electrolyte imbalance), metabolic alkalosis due to loss of H+, and acid erosion of tooth enamel.

135
Q

What are ulcers

A

A damaged/eroded area of GIT mucosa, usually in acidic regions. This can occur in the esophagus, stomach, or most commonly in the duodenum.

136
Q

What can cause ulcers

A

Imbalance between “agressive” factors (acid, pepsin), and “protective” factors (mucus, HCO3-)
Helicobacter pylori infection - causes chronic inflammation and erosion
NSAIDS (aspirin, ibuprofen) - decreases prostaglandin production
Smoking
Excessive alcohol
Stress
Gastrinomas

137
Q

How can you treat ulcers

A

Antibiotics
H+/K+ ATPase inhibitor
Histamine (H2) antagonist
Prostaglandin type drugs

138
Q

What is gastric bypass surgery

A

In extremely obese patients a surgery will be performed that results in the bypassing of the stomach and rooting the food directly to the small intestine.

139
Q

What are the problems that can occur with gastric bypass surgery

A

Lack of intrinsic factor release, less acid treatment with food, and difficulty regulating the amount of food reaching the small intestine

140
Q

How do patients ensure that gastric bypass surgery is successful

A

Vitamin B12 injections and eating smaller meals.

141
Q

What does the exocrine pancreas do

A

Produces secretions that go into gut. Source for most enzymes required for meal digestion such as carbohydrates, protein, fat, and nucleic acid. Enzymes are produced in excess and this is notably because problems with digestion and absorption will occur if this function falls below 10%. Critical for secreting HCO3- into the duodenum for the neutralization of stomach acid which is critical for enzyme function

142
Q

What does the endocrine pancres do

A

It is non-digestive and produces hormones that regulate the entire body. It’s primary hormone release is insulin

143
Q

What is the anatomy of the exocrine pancreas

A

Secretion of substances into ducts that drain onto an epithelial surface

144
Q

What is the anatomy of the endocrine pancreas

A

Ductless gland, secretion occurs across epithelial basolateral surface for diffusion into blood.

145
Q

What are the pancreatic ducts

A

Very similar to salivary glands, they are acinar cells that produce and secrete digestive enzymes through exocytosis. The duct cells secrete H2O and HCO3-.

146
Q

What are pancreatic juices

A

Isotonic, alkaline, and 1-2 L made per day. It contains electrolytes and digestive enzymes.

147
Q

What are the electrolytes in pancreatic juices

A

High HCO3-, low Cl-.

HCO3- and H2O was secreted mainly but the duct cells. HCO3- neutralizes gastric acid in the duodenum

148
Q

What are the digestive enzymes responsible for in pancreatic juices

A

Essential for digestion of proteins, carbohydrates, fats, and nucleic acids. Secreted by acinar cells. Proteolytic enzymes stored and secreted in inactive forms; activation occurs in the duodenum,

149
Q

How is HCO3- made in the pancreatic duct cells

A
  1. Chloride channel (CFTR) opens
  2. Cl- in lumen exchanged for HCO3- in cell
  3. H2O and Na+ follow paracellularly in response to electrochemical gradient across epithelium
  4. Neutral pH of cytosol is maintained by exchange of H+ (exported from cell) for Na+ (imported) - this is used in combination with carbonic anhydrase
150
Q

What happens to the alkaline and acid tides after you consume a big meal

A

Parietal cell in the stomach are producing lots of acid, large amount of HCO3- pumped across the basolateral surface into blood stream. This referred to as alkaline tide.
Duct cells in pancreas are producing and secreting HCO3-, large amounts of H+ being pumped across the basolater surface into blood stream. This is referred to as acid tide.
HCO3- from stomach and H+ from pancreas eventually meet up in the portal vein

151
Q

What is the digestive function of the pancreas

A

Source for most enzymes required for meal digestion, acinar cells synthesize and pack pro-enzymes into zymogen granules that are stored at the apical pore of the cell, and appropriate neurohormonal input results in their exocytosis into the lumen of the duct.

152
Q

What would happen if we didn’t have a pancreas

A

Starvation would occur without the pancreas

153
Q

What do amylolytic enzymes do

A

Digest starches into sugars

154
Q

What do lipases do

A

Digest triglycerides into free fatty acids and monoglycerides

155
Q

What do nucleases do

A

Digest nucleic acids into free molecules

156
Q

How are digestive enzymes secreted from the pancreas

A

Most enzymes secreted as inactive forms that are activated in the duodenum. Enterokinase-enzyme embedded in the luminal membrane of the duodenum. It cleaves trypsinogen to trypsin. Trypsin is a protease and activates other proteases.

157
Q

How is autodigestion prevented

A

Storage of digestive enzymes as inactive proforms and these can’t normally be activated unless they reach the intestine. Pancreas also secretes a variety of trypsin inhibitors to antagonize any prematurely activated trypsin. Trypsin can degrade itself if activated prior to reaching the intestine.

158
Q

How is the pancreas related to cystic fibrosis

A

The Cl- channel involved in HCO3- secretion in the pancreas is the channel that is mutated in the disease cystic fibrosis. CF patients can suffer from “pancreatic insufficiency”

159
Q

What is “pancreatic insufficiency” in cystic fibrosis

A

Still produce all the digestive enzymes. HCO3- and H2O secretion is minimal, and enzymes do not get flushed from ducts and therefore do not reach the intestine. Retained proteolytic enzymes can result in pancreatic autodigestion. Must receive supplements of digestive enzymes and antacids to allow for adequate nutrition.

160
Q

What is trypsinogen

A

It is an inactive enzyme
Activated by: Enterokinase
Active Enzyme: Trypsin
Action: Endopeptidases (hydrolyze interior peptide bones of proteins and polypeptides)
End-products: Mixture of peptides and amino acids

161
Q

What is Chymotrypsinogen

A

An inactive enzyme
Activated by: Trypsin
Active enzyme: Chymotrypsin
Action: Endopeptidases (hydrolyze interior peptide bonds of proteins and polypeptides)
End-products: Mixture of peptides and amino acids

162
Q

What is Pro-elastase

A

An inactive enzyme
Activated by: Trypsin
Active enzyme: Elastase
Action: Endopeptidases (hydrolyze interior peptide bondes of proteins and polypeptides)
End-products: Mixture of peptides and amino acids

163
Q

Whati s Pro-carboxy peptidases A and B

A

An inactive enzyme
Activated by Trypsin
Active enzyme: Carboxypeptidase A and B
Action: Exopeptidases (hydrolyze bonds at C-terminal end)
End-products: Mixture of peptides and amino acids

164
Q

What is amylase

A

An active enzyme
Action: Cleaves starches to sugars (same as salivary amylase)
End-Products: Maltose, maltotriose, and alpha-limit dextrins

165
Q

What is lipase

A

An active enzyme
Action: Hydrolyze triglycerides
End-products: Free fatty acids and 2-monoglycerides

166
Q

What is Prephospholipase A2

A

An inactive enzyme
Activated by: Trypsin
Action: Hydrolyzes phospholipids
End-products: Free fatty acids and lysophospholipids

167
Q

What is cholesterolesterase

A

An active enzyme
Action: Hydrolyzes cholesterol-esters
End-products: Free fatty acids and cholesterol

168
Q

How can CCK regulate pancreatic juice secretion

A

Fatty acids and amino acids in the small intestine triggers CCK secretion from cells in small intestine into blood. The CCK stimulates when the pancreas to increase digestive enzyme secretion and gall bladder contraction. Fats and amino acids are absorbed and stimulation of CCK release is stopped - due to the removal

169
Q

What happens during gall bladder contraction

A

Release of bile acids for fat breakdown. Relaxation of the sphincter of Oddi.

170
Q

How does secretin regulate pancreatic HCO3- secretion

A

Acid enters the duodenum from the stomach. Reduced pH triggers secretin secretion from cells in small intestine into blood. The secretin stimualtes pancreas (duct cells) to increase HCO3- secretion and liver (duct cells) to increase HCO3- secretion. The stomach acid is neutralized, and stimulation of secretin release is stopped.

171
Q

What are the phases of pancreatic secretion

A
  1. Cephalic Phase
  2. Gastric Phase
  3. Intestinal Phase
172
Q

What is the cephalic phase of pancreatic secretion

A

Minor phase but sight, smell, taste and any other sense will stimulate pancreatic secretion via the parasympathetic nerves

173
Q

What is the gastric phase of pancreatic secretion

A

Minor phase but distension of stomach will stimulate pancreatic secretion via the parasympathetic nerves

174
Q

What is the intestinal phase of pancreatic secretion

A

Major phase of regulation. Acid from stomach in duodenum in secretin release. Digested fat and protein duodenum results in CCK release.

175
Q

What is the liver

A

The largest internal organ of the body, receives 25% of the cardiac out, contains 4 different lobes, and extends across the entire abdominal cavity

176
Q

What is the structure of a hepatic lobule in a liver

A

Hexagonal structure with a central vein running through the center, and portal triads at each corner

177
Q

What is the structure of a portal triad of a liver

A

Portal triad composed of branches of hepatic artery, portal vein, and bile duct

178
Q

What are the cell types that are present in the liver

A

Epithelial cells
Kupffer cells
Endothelial cells

179
Q

What are the epithelial cells in the liver

A

Hepatocytes and Bile duct epithelium or cholangiocytes

180
Q

What do hepatocytes do in the liver

A

Account for ~70% of the cells in the liver and is important for synthesizing many different components of bile

181
Q

What do bile duct epithelium cells do in the liver

A

Account for 3-5% of the cells in the liver and they modify the components of the bile

182
Q

What are Kupffer cells in the liver

A

They act as macrophages

183
Q

What do endothelial cells do in the liver

A

They are lining the sinusoids and they are “fenestrated” and are thus very leaky

184
Q

What are the major functions of the liver

A

Exocrine Gland - Formation and secretion of bile
Metabolism and storage of nutrients - Liver matches supply to demand
Deactivation and detoxification - Drugs, hormones, waste products, toxicants
Production of circulating proteins - Blood coagulation factors, lipoproteins

185
Q

What are the constituents of bile

A
  1. Bile acids
  2. Cholesterol
  3. Salts and water
  4. Phospholipids
  5. Bile pigments
  6. Trace metals.
186
Q

What is the role of bile in fat digestion

A

Pancreatic lipase is a water-soluble enzyme and can only work at the surface of lipid droplets. Large lipid droplets need to be made smaller for efficient access by lipase. This process is called emulsification.

187
Q

What does emulsification require

A

Mechanical disruption to make droplets smaller through GI motility, and emulsifying agent to prevent droplets from re-aggregating into amphipathic bile acids and phospholipids

188
Q

What are the micelles that can be formed in fat digestion

A

Bile acids can also form “mixed micelles” with phospholipids and products of lipase digestion (free fatty acids and monoglycerides). “Micelle” is a soluble cluster of amphipathic molecules with nonpolar groups in the middle and polar groups on the outer layer

189
Q

What is the micelle function

A

Fatty acids and monoglycerides are insoluble in water. Micelles keep monoglycerides and fatty acids in small soluble aggregates. The equilibrium between the micelle and free fatty acid monoglycerides. Micelles are like a “holding station” for small non-soluble lipids.

190
Q

Where is bile formed

A

Hepatocytes, Bile duct cells and Gall bladder

191
Q

What role does hepatocytes form in bile formation

A

Produce and secrete bile acids, also secrete phospholipids, bile pigments, and all the components are secreted through primary active transport

192
Q

How is bile formed in the bile duct cells

A

They add HCO3- (and other salts) and H2O to bile

193
Q

How is bile formed in gall bladder

A

Stores and concentrates the bile between meals then expels it into the duodenum after a meal.

194
Q

What is the enterohepatic circulation of bile acids

A

There is 20-40g of bile acids are released into the intestine each day, ~0.5g is lost in the feces. This recycling of bile acids occurs through the enterohepatic circulation. This allows for the secretion rate to greatly exceed the synthesis rate.

195
Q

What are the steps of the bile acid recycling

A
  1. Bile acids are released by the liver/gall bladder into the duodenum for fat digestion
  2. Bile acids are reabsorbed across the small intestine (ileum) into the portal circulation
  3. Bile acids are transported back into hepatocytes
196
Q

What factors can impact the enterohepatic circulation

A

Dietary fiber can squester the bile acids preventing the cycling back to the liver resulting in them being lost in feces. Certain drugs and toxins can also undergo enterohepatic circulation.

197
Q

How does secretin impact the hepatobiliary secretion during intestinal phase

A

Secretin is produced and released by S-cells in the duodenum which are stimulated by acid in the duodenum. Secretin increases HCO3- secretion by the bile duct cells (and the pancreas)

198
Q

How does cholecystokinin (CCK) impact the hepatobiliary secretion during intestinal phase

A

Produced by the I-cells in the duodenum and jejunum which is stimulated by digested fats/proteins in the upper small intestine. CCK increases the contraction of the gall bladder and relaxes the sphincter of Oddi and bile is released into the duodenum.

199
Q

What are gallstones

A

Majority are “cholesterol stones”. Cholesterol is water insoluble and only kept in solution in bile through the formation of micelles with bile acids and phospholipids. If the concentration of cholesterol in bile becomes high relative to bile acids, cholesterol starts to precipitate out, “nucleating” agent also required.

200
Q

What are pigment stones

A

Less common and caused by excessive hemolysis (red blood cell breakdown) which increases the concentration in bile, and pigments form precipitages with Ca2+

201
Q

What are the consequences of gallstones

A

Depends on location of stones; may cause obstruction/infection of gallbladder, liver, or pancreas. Pain, nausea, jaundice, malabsorption of fats and fat-soluble vitamins.

202
Q

What is the treatment of gallstones

A

Cholecystectomy (removal of gallbladder)
Removal of stones
Drugs to dissolve gallstones

203
Q

What is the small intestine

A

Located between the stomach and the large intestine. Tube of 2.4cm in diameter, 3m in length. It is divided into three sections the duodenum, jejunum, and ileum.

204
Q

What are the major functions of the small intestine

A

Digestion and absorption of protein, fat, carbohydrate, electrolytes, water, minerals, and vitamins.

205
Q

What is the duodenum responsible for

A

Mixing of pancreatic digestive enzymes and bile with food. Absorption of nutrients, iron, and calcium. Release of endocrine hormones secretin and CCK.

206
Q

What is the jejunum responsible for

A

Digestion and absorption

207
Q

What is the ileum responsible for

A

Digestion and absorption primarily of bile acids and vitamin B12

208
Q

What happens to chyme in the small intestine

A

Most of the chyme entering the small intestine is digested and absorbed in the first 25% of the small intestine (duodenum and jejunum)

209
Q

How is the surface area of the small intestine increased

A

There is folds that increase surface area of the intestine. Villi, Crypts, Microvilli, and Enterocytes will further increase the surface area.

210
Q

What makes up the structure of a villus in the small intestine

A

These stem cells differentiate into Paneth cells, Endocrine cells, Enterocytes, and Goblet cells. Once they reach the top of the villus they will be sloughed off and released into feces.

211
Q

What do enterocytes do

A

They are an absorptive cell which are responsible for absorbing nutrients. They will have things coming from the intestinal lumen into cell for absorption to take place. They contain brush border enzymes.

212
Q

What are goblet cells in the small intestine

A

Scattered through the small intestines epithelial layer. It is full of bubbles of exocytic vesicles filled with mucin.

213
Q

What are the enteroendocrine cells in the small intestine

A

Scattered through the small intestine epithelial layer. Responsible for releasing hormones such as secretin and CCK. Across the basolateral layer across the interstitial space and into circulation

214
Q

What do Paneth cells do in the small intestine

A

They have exocytic vesicles that are filled with antibacterial proteins. These antibacterial proteins that are released into the gastrointestinal lumen to reduce bacterial growth in the small intestine.

215
Q

What is a brush border enzyme

A

Enzyme is anchored to the brush border with catalytic activities in the lumen. This is important for breaking down carbohydrates and peptides into sugars and amino acids prior to transport across the enterocyte.

216
Q

What does brush border mean

A

Small projections (Microvilli) of epithelial cells covering the villi of the small intestine, major absorptive surface of the small intestine.

217
Q

How are carbohydrates digested

A

Starch is broken down into maltose, maltotriose, and alpha-limit dextrins by salivary and pancreatic amylases. These are broken down to monosaccharide glucose by brush border enzymes. Other sugars in diet table sugar (sucrose) and milk sugar (lactose) are also broken down by brush border enzymes.

218
Q

How is Glucose and Galactose absorbed internally

A

These sugars work their way from the intestinal lumen with the help of transporters into the epithelial cells. From the epithelial cells it using enterocytes to transport it into the blood.

219
Q

How is Fructose internally absorbed

A

This is facilitated compared to other sugars and it easily makes it way from the intestinal lumen, epithelial cells, and blood.

220
Q

What is lactose

A

The milk sugar lactose is digested by brush border enzyme lactase in the small intestine into the monosaccharide’s glucose and galactose.

221
Q

What causes lactose intolerance.

A

All mammals including humans lose lactase expression (to varying degrees) post-weaning from milk. So they can’t completely digest lactose.

222
Q

What happens when someone is lactose intolerant

A

Results in decreased water absorption in the gut (presence of lactose produces an osmotic gradient). Lactose-containing fluid passes on to large intestines and bacteria digest lactose. This will cause gas (colon distension, pain) and diarrhea.

223
Q

How can you treat lactose intolerance

A

Can come lactase pills with meal or ingest “lactose free” dairy products that has been pre-treated with lactase.

224
Q

How is protein digested into the small intestine

A

Proteins are broken down by pepsin in the stomach, and in the small intestine by pancreatic proteases. Once digested, free amino acids are absorbed by secondary active transport coupled to Na+. Small peptides can also be absorbed by different secondary active transport proteins coupled to H+. Amino acids then undergo facilitated diffusion across the basolateral surface of the enterocyte.

225
Q

What are carboxypeptidases

A

Enzyme that is pancreatic protease

226
Q

What is aminopeptidases

A

A brush border enzyme that is in the small intestine

227
Q

How is fat digested into the small intestine

A

Products of lipase are incorporated into micelles which are in dynamic state-breaking down and reforming. As micelles breakdown, they will release fatty acids and monoglycerides that can then go across the small intestine epithelium. Once absorbed by the enterocyte fatty acids and monoglycerides are processed by the endoplasmic reticulum back into triglycerides

228
Q

What happens to fat once it makes into into the endoplasmic reticulum

A

Within the endoplasmic reticulum triglycerides aggregate into lipid droplets coated with amphipathic proteins. Lipid droplets packaged in the Golgi and secreted via exocytosis. Extracellular fat droplets know as “chylomicrons”

229
Q

What is chylomicron

A

Chylomicron contains triglycerides, phospholipids, fat soluble vitamins, and cholesterol. The large chylomicron enters the lymphatic system.

230
Q

How is iron absorbed into the small intestine

A

Iron is the oxygen binding component in red blood cells and a key component of many enzymes. Iron (as Fe2+) is actively transported into the enterocyte and incorporated into the protein ferritin.

231
Q

What happens to iron that is not stored from the small intestine

A

Iron that is not stored is released on the blood side of the enterocyte and transported through the blood attached to the plasma protein transferrin.

232
Q

What happens to iron when it is bound to ferritin

A

Iron that remains in the enterocyte bound to ferritin is excreted from the body when the enterocytes slough off the villi tips.

233
Q

What happens when iron supplies are ample

A

When iron stores are ample in the body expression of ferritin protein is upregulated resulting in a reduced absorption of iron.

234
Q

What happens when irons stores are depelted

A

When iron stores are depleted the production of intestinal ferritin decrease resulting in increased absorption

235
Q

What happens when you have iron toxicity

A

When the body has excess iron this can result in toxicity, including skin pigmentation, and heart failure. This can be caused by genetic defects in absorption control pathways, adult males/post-menopausal women excessively supplementing, poisoned children.

236
Q

What is the treatment of iron toxicity

A

Bloodletting and sometimes self-imposed vomiting and diarrhea through use of laxatives

237
Q

What is iron-reduced anemia

A

Redcued number and/or size of red blood cells. The symptoms are tiredness, light-headedness, and headaches. It is caused by not enough iron in the diet, loss of iron through blood loss, poor iron absorption and intestinal diseases.

238
Q

What is the treatments for iron-deficiency anemia

A

Iron supplements, iron infusions, iron salts, vitamin B12, heme iron, and iron in its Fe2+ form

239
Q

Why are water and electrolytes important for the small intestine

A

Control of fluid in intestine is critical for GI function which permits contact between food and digestive enzymes. Diffusion of digested nutrients to absorption. Fluidity provides for transmit without damage to the epithelium.

240
Q

How does the small intestine handles fluid

A

Intestine handles large quantities of fluids each day, some of it front the diet. Majority from the intestine and organs is drained and reabsorbed by the small intestine

241
Q

How much fluid is handled by the GI tract each day?

A

8-9 liters each day. Only 100 mL is lost in feces. The majority of the fluid is absorbed into the blood from the small intestines

242
Q

How is water absorbed into the small intestine

A

Predominantly depends on Na+ gradients generated during secondary active nutrient uptake of glucose and galactose

243
Q

How is water secreted from the small intestine

A

Predominantly depends on Cl- gradients generated by the secondary active Na+/K+/2Cl- transporter. Generally, this happens in the crypt cells

244
Q

What is Cholera

A

Occurs after eating food or drinking water contaminated with Vibrio cholerae bacteria. It causes vomiting and excessive diarrhea - upwards of 20 litres of stool per day versus the normal 0.1 litre). This can lead to dehydration, electrolyte imbalance and death if left untreated

245
Q

How does the bacteria Vibrio cholerae impact the intestines

A

Vibrio cholerae produce a toxin that drastically increases the production of cAMP in the cyrpt epithelium of the small intestine. This results in the activation of the Cl- channel and excessive secretion of Cl- in the gut lumen, water follows leading to diarrhea.

246
Q

How is cholerae treated

A

Consumption of clean water containing salt and glucose through fluid replacement. Intravenous fluids.

247
Q

How does the small intestine move during digestion

A

Most common motion in small intestine during digestion is “segmentation? There is continuous division and subdivision of intestinal contents. The frequency of contraction set by basic electrical rhythm. Contraction force is determined by neurohormonal input. There is a slow net migration towards the large intestine

248
Q

How is the continuous division and subdivision of intestinal contents during digestion

A

Mechanical breakdown of food which increases surface area and mixing of food with digestive enzymes.

249
Q

What is the frequency of contractions in the small intestine during digestion

A

12 contractions per minute in the duodenum

9 contractions per minute in the ileum

250
Q

What is the motility of the small intestine after absorption

A

The contractions of the small intestine stops and is replaced by a pattern of peristaltic activity called the migrating myoelectric complex. This begins in lower portion of the stomach travels about 2 feet along the small intestine and then dies out. Next overlapping wave starts further down the small intestine, and this is repeated along the small intestine which takes roughly 2 hours and then repeats.

251
Q

What is the purpose of the migrating myoelectric complex

A

It pushes any undigested material from the small to the large intestne and prevents from remaining in the small intestine

252
Q

How is the migrating myoelectric complex regulated

A

The intestinal hormone motilitn which is released by cells in the small intestine through tone initiated the migrating myoelectric complex. When you eat it inhibits the release of motilin and the MMC will cease when next meal is consumed.

253
Q

What is the large intestine

A

Tube of approximately 6.5 centimetres in diameter and 1.5 metes in length. It was made up of the cecum/appendix, ascending/transverse/descending/sigmoidal colon, rectum, and anus

254
Q

What is the ileocecal valve

A

The valve between the large and small intestine, the sphincter between the cecum and ileum. It opens when the ileum contracts (post-meal), and closes when intestine is distended. It retains large intestine contents including bacteria

255
Q

What is the cecum/appendix in the large intestine

A

No apparent function in humans. In some other species it is well developed and contains commensal bacteria important for digesting complex carbohydrates.

256
Q

What is the major functions of the colon

A

Reabsorption, reservoir for the storage of wastes and indigestible materials prior to elimination by defecation, and absorption of products of bacterial metabolism

257
Q

What does the rectum do

A

Reservoir for feces

258
Q

What does the anus do

A

It has two sphincters (inner and outer) to control defecation

259
Q

What are the large intestine cell types

A

Large intestine only contains crypts (no villi) so the surface area is much lower than the small intestine. The cells that make up the large intestine are absorptive cells/enterocytes, goblet cells, paneth cells, and endocrine cells.

260
Q

What are the stem cells in the large intestine

A

Stem cells are found in the crypts and they will differentiate into one of the four different epithelial cell types.

261
Q

What is the ecosystem of bacteria in the large intestine

A

It is the “gut microbiome” and the healthy adult gut contains over 1000 species of bacteria. They can liberate short chain fatty acids from dietary fibre that are absorbed. They can also absorb vitamines that are. The ecosystem can be influenced by diet, medications, and bowel function. It had a large implication on health.

262
Q

What can cause problems in the ecosystem of the large intestine

A

Obesity, allergies, clostridium difficile infection, inflammatory bowel disease, toxicant metabolism and malabsorption

263
Q

What is Clostridium difficile infection

A

It is an antibiotic-resistant infection that can lead to issues with integrity in the gastrointestinal tract wall and it is treated with a poop transplant

264
Q

How is water absorbed in the large intestine

A

Predominantly depends on Na+ gradients generated by Na+/K+ ATPase

265
Q

What is the secretion of water in the large intestine

A

Predominantly depends on Cl- gradients generated by secondary Na+/K+/2Cl-

266
Q

What is motility in the large intestine

A

Mixing the contents and retaining them for optimal salvage of fluid and bacterial products.

267
Q

What is mixing in the large intestine

A

Segmentation that is much slower with the basic electrical rhythm and allows for retention in the colon for 18-24 hours.

268
Q

What is propulsion of the large intestine

A

Occurs three to four times a day there is a wave of intense contraction known as a “mass movement” spreads rapidly over the large intestine, pushing content towards the anus. Occurs after eating and prior to defecation

269
Q

What is feces

A

Feces made up of water, undigested food, bacteria, and sloughed epithelial cells.

270
Q

What is defecation

A

Initiating by the mass movement of large intestine contents into the rectum. They rectum distends and mechanoreceptor activated.

271
Q

What is the reflex of defecation

A

Rectum contracts, internal anal sphincter relaxes and the outer anal sphincter contracts. There is an increased peristaltic activity in the sigmoid colon, increasing pressures results in reflex relaxation of the external anal sphincter. The feces is then voided.

272
Q

How can the brain override the reflex of defecation

A

After toilet training, brain can override the reflex relaxation of the outer sphincter resulting in delayed defecation. This causes reverse peristalsis then occurs, and rectal contents move back into the sigmoidal colon.

273
Q

What happens during water secretion in the large intestine

A

Water secretion depends on the Cl- gradient generated by the secondary active transport by NKCC1 (Na+/K+/2Cl- transporter)

274
Q

What is aminopeptidase

A

Brush border enzyme

275
Q

Where are chylomicrons found during fat digestion and absorption

A

Chylomicrons are released across the basolateral surface of the enterocyte, and enters the lymphatic system by diffusing into lacteals.

276
Q

What is true about acetylcholine and acid secretion

A

Acetylcholine can increase acid secretion by inhibiting somatostatin release

277
Q

What hormones make a person feel hungry and therefore increase food intake

A

Neuropeptide Y

278
Q

What does gastrointestinal motility do during segmentation

A

Segmentation slows the transit time of the small intestine contents to allow for the absorption of nutrients

279
Q

How is secretin stimulated

A

Secretin release is stimulated mainly by acid in duodenum

280
Q

How is the extrinsic neuronal regulation of the gastrointestinal tract influenced

A

Influences the gastrointestinal tract through the autonomic nervous system

281
Q

Which enzyme is responsible for activating trypsinogen to trypsin and where does it occur

A

Enterokinase is responsible for activating trypsinogen to trypsin in the duodenum