Week 2- Objectives Flashcards

1
Q
  1. What are the two main physiological functions of the respiratory system?
A

Two obtain oxygen from the external environment and supply it to the cells and to remove from the body the carbon dioxide produced by cellular metabolism

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2
Q
  1. How does one of these functions affect the acid-base balance of the body?
A

Removing carbon dioxide from the body can contribute to the acid-base balance by effecting the amount of CO2 and water that is converted to carbonic acid

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3
Q
  1. How do the concentrations of oxygen and carbon dioxide in the right ventricular blood compare with those concentrations in left ventricular blood?
A

Right ventricular blood has much less oxygen and much more carbon dioxide than left ventricular blood since it returning from systemic circulation

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4
Q
  1. Describe some non-CO2/O2-exchange functions of the respiratory system?
A

phonation, immune function, ace-base balance and create intrathoracic

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5
Q
  1. What happens to inhaled air as it passes through the nasal sinuses before entering the trachea?
A

Warms, humidifies and cleans the air coming into the body to protect the respiratory system

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6
Q

L1-1. How much blood flows through the lung per minute at rest? How much air is cycled into and out of the lung per minute at rest?

A

Blood through lung 5 L/min; Air flow 5 L/min, measured in volume of expired air in L/min

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7
Q

L1-2. Under resting conditions, how many milliliters of CO2 are carried by each liter of blood flowing into the lung, and how many milliliters of O2 are carried by each liter of blood leaving the lung?

A

O2 250 mL/min flowing from the lung ; CO2 200 mL/min flowing to the lung

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8
Q

L1-3. What is the function of alveolar macrophages?

A

Wander around on the alveolar surfaces and phagocytose bacteria, particulates, foreign bodies

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9
Q
  1. What is meant by the term “gas exchange?” What is an “acinus” and how does its role in gas exchange compare to that of the airways that supply it?
A

Gas exchange is the carrying of oxygen and carbon dioxide in and out of the body respectively which is exchanged between the blood supply via capillaries to alveolar sacs which allow for interface with air. The portion of the lung supplied by a primary respiratory bronchiole is called an acinus (all of the airways of an acinus participated in gas exchange

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10
Q
  1. What do you call an airway that is not surrounded by cartilage?
A

bronchiole

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11
Q
  1. What is the “mucociliary escalator” and what is its function?
A

Secretion and movement of mucus that functions as a protective element in the respiratory tract by trapping and expelling particulates

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12
Q
  1. How many alveoli are present in the average human lung, and what is their total surface area?
A

Estimated at 300 million in the adult, resulting in 50-100 sq. meters of surface area for gas exchange via diffusion

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13
Q
  1. What is a type I alveolar epithelial cell? What is a type II alveolar epithelial cell? What is the function of the alveolar macrophage?
A

Type I: squamous epithelial cell (large surface area)
Type II: larger cuboidal cells that produce surfactant and lung stem cell
Alveolar macrophages: patrol the alveolar surface and phagocytize inspired particles such as bacteria

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14
Q
  1. What structures compose the barrier to gas exchange between alveolar gas and alveolar capillary blood? What is the average thickness of this barrier?
A

Surfactant on lung lining, Alveolar epithelium (type I cell), fused basement membrane, capillary endothelium; usually 0.2-.5 um thick; transport is completely by passive diffusion both in the lung and in the systemic tissues

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15
Q
  1. What force is responsible for moving air from the atmosphere into the lungs? How does this force vary between inspiration and expiration?
A

differences in transmural pressure between the thorax and lung; Normally the difference in atmospheric pressure and thoracic pressure created by respiration muscle (negative-pressure breathing) causes distending pressure across the alveolar wall causing air to enter the lung during inspiration, during expiration the intrathoracic space is smaller, creating greater pressure on the alveoli than atmospheric pressure coming into the lung and a net movement out of the lung; during expiration there exists the force of elastic recoil of the alveoli that assist in expiration

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16
Q
  1. What pressure is responsible for causing the alveoli to expand during inspiration?
A

Transmural pressure gradient is the between the intraplural pressure and the alveolar pressure which is created by the contracting and relaxing of muscles of inspiration; the transmural pressure gradient distends the alveolar wall (also called transpulmonary pressure)

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17
Q
  1. Why is it easier to inflate a saline-filled lung than an air-filled lung (Fig. 32-8)?
A

When the lung is filled with saline there is no surface tension at the air-liquid border as there would be if the lung was filled with air; surface tension plays a large role in the recoil of lungs; more pressure is required to inflate with air because you must overcome the surface tension at the air-liquid border

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18
Q
  1. If two alveoli of unequal size but equal surface tension were connected to a common airway (Fig. 32-10), the smaller one would empty into the larger one. Why?
A

According to laplace law Pressure= 2 surface tension/ radius P=2T/r (which gives the relation between the pressure inside the alveolus and the wall tension of the alveolus) the pressure in the smaller (smaller radius) one would be greater and by that pressure gradient cause air to flow from the larger to the smaller; normally the surface tension of most liquids (such as water) is constant and not dependent on the area of the air-liquid surface

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19
Q
  1. What is lung surfactant, where does it come from, and what does it do?
A

Surfactant produced by type II alveolar cells, it decreases surface tension, and increases the compliance of the lungs above that predicted by an air-water interface and decreasing the inspiratory work of breathing, it also decreases the surface tension of small alveoli and helps to equalize alveolar pressure throughout the lung; Surfactant lowers T as r decreases so T/r is therefore nearly equal for all alveoli accomplished by the distribution of surfactant within the alveolae- the closer molecules of surfactant the more reduction of surface area

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20
Q

L2-1. What is the alveolar liquid lining layer, and what effect does it have on the forces needed for breathing?

A

The liquid layer is water and it causes an increase on surface pressure of the inside of the lung, a surface area which surfactant works to reduce

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21
Q
  1. What physical forces are responsible for the resting lung volume at Functional Residual Capacity (FRC)?
A

The inward elastic recoil of the lung normally opposes the outward elastic recoil of the chest wall, functional residual capacity occurs at the end a of a normal tidal expiration, when no respiratory muscles are actively contracting; this is the volume at which the recoil of the lung and the recoil of the chest are equal and opposite

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22
Q
  1. At FRC, how does the transmural pressure across the thoracic wall compare to the transmural pressure across the lung?
A

At FRC, transmural pressure across the lung is approximately equal and opposite of the transmural pressure across the thoracic wall; the magnitude is approximately +/- 5 mmHg

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23
Q
  1. Why is alveolar pressure zero at the end of inspiration (Fig. 32-5)? Why does intrapleural pressure reach its most negative value at the end of inspiration?
A

As alveoli fill with air their pressure increases and returns to atmospheric pressure (zero); At the end of inspiration air is neither going in or out of the lung, intrapleural pressure reaches its most negative value at the end of inspiration because the alveolae have deflated and the alveolar distending pressure is lowest because the inspiratory muscles are relaxing and causing the thoracic cavity to become smaller

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24
Q
  1. What causes the characteristic noise of wheezing?
A

Narrowing of airways that causes turbulent air flow and characteristic wheezing noise

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25
Q
  1. Why do airways collapse during a forced expiration?
A

Forced expiration by intercostal and abdominal muscles creates a positive intrapleural pressure which allows the elastic recoil of the alveolae to collapse the airway

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26
Q
  1. In a series of expiratory flow-volume loops (Fig. 32-16), why is the left side effort-dependent, while the right side is effort-independent?
A

At high volumes, the air flow rate is effort-dependent, at low lung volumes air flow rate is effort independent

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27
Q
  1. How do changes in the shape of a flow-volume curve help to diagnose airway obstructions?
A

Obstructive diseases interfere with airflow (often high lung volume), restrictive diseases restrict the expansion of the lung (descreased peak expiratory flow); these curves can also help differentiate between fixed and variable obstructions (and whether the obstruction is extrathoracic or intrathoracic)

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28
Q
  1. What feature of lipids makes their assimilation into the body different from that of carbohydrates and proteins?
A

Lipids are hydrophobic and thus more soluble in the organic solvents (includes fat soluble vitamins)

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29
Q
  1. How does the quantity of dietary lipid processed by the GI tract per day compare with the quantity of endogenous lipid processed?
A

Dietary lipids (120-150g) and 40-50g of endogenous lipids

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30
Q
  1. How does the quantity of endogenous cholesterol secreted daily compare to the quantity of consumed cholesterol in an average diet?
A

The endogenous secretion of cholesterol of 1-2g per day usually exceeds dietary intake of 200-500mg that is typical of most individuals

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31
Q
  1. Gastric lipase is responsible for what proportion of total GI tract lipolysis? How do the hydrolysis products of gastric lipase differ from those of pancreatic lipase?
A

10-30% in a healthy adult and gastric lipase acts preferentially to hydrolyze the first position of a triglyceride which is different than the action of pancreatic lipase

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32
Q
  1. What is the role of CCK in lipid digestion?
A

What is the role of CCK in lipid digestion?

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33
Q
  1. What is the function of colipase?
A

Colipase binds to bile acids and lipase which stabilizes the presence of lipase on the surface of oil droplets, with lipase alone bile salts are able to displace lipase from the surface of oil droplets

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34
Q
  1. Why is cholesterol esterase important in triglyceride hydrolysis?
A

Cholesterol esterase is capable of degrading not only esters of cholesterol derived from dietary sources but also the esters of vitamins A, D and E; its broad specificity renders it capable of hydrolyzing the 2- position of the fatty acids

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35
Q
  1. Why are bile acids important for the assimilation of lipolysis products out of the gut lumen? How do bile acids solubilize lipolysis products?
A

Bile helps the micelle formation and lipolytic products that are captured in micelles are truly in solution, bile acts as a detergent (it ampiphillic)

36
Q
  1. Why is a bile deficiency likely to lead to a vitamin deficiency?
A

Inability to break up fat droplets and absorb lipid soluble vitamins

37
Q
  1. How are medium chain fatty acids (6-12 carbon atoms) absorbed out of the gut lumen differently from long chain fatty acids?
A

Have measurable absorption via the paracellular route, with increased water solubility, and therefore appear to bypass the intracellular processing events that are encountered by long-chain fatty acids and are exported largely by portal circulation not the lacteal system

38
Q
  1. What are chylomicrons, how are they made, and what is their role in lipid assimilation into the body?
A

After absorption into enterocytes, triglycerides are resterified and trafficked with proteins together as chylomicrons (core of triglyceride surrounded by phospholipids, cholesterol esters and the apoproteins); chylomicrons are the structure used to transport dietary lipids to other locations in the body

39
Q
  1. Describe the liver’s role in maintaining blood glucose concentration.
A

It preforms glycogen storage, conversion of galactose and fructose to glucose, gluconeogenesis and the formation of many important biochemical compounds from the intermediate products of carbohydrate metabolism; liver removes excess glucose from the blood and returns it as needed in glucose buffer function

40
Q
  1. Describe the liver’s role in fat metabolism and absorption.
A

Liver supports an especially high rate of oxidation of fatty acids to supply energy for other body functions

41
Q
  1. What is the liver’s role in protein synthesis and metabolism?
A

Converts amino acids and two-carbon fragments derived from carbohydrates to fats that can be transported to adipose tissue for storage

42
Q
  1. What are xenobiotics, and what is the liver’s connection to them?
A

Xenobiotics (foreign chemicals) can be converted (via cytochrome P450 and other enzymes) to inactive, less lipophilic metabolites that can be excreted into bile and excreted

43
Q
  1. How does the arterial blood supply to the liver compare to its portal venous supply?
A

1,300 mL/min blood flow via the portal vein and 500 mL/min supplied by the hepatic artery (portal blood flow may increase to almost 90% in the period following a meal)

44
Q
  1. How do the liver sinusoids affect liver blood flow?
A

Sinusoids are low resistance cavities, as portal blood flow increases, sinusoids are gradually recruited to allow the perfusion of the liver with much greater volume per unit time

45
Q
  1. What is the hepatic triad?
A

Portal vein branches (hepatic venules), hepatic artery branches and bile ducts

46
Q
  1. Approximately how many cells are in an adult liver, and what percentage of them are hepatocytes?
A

Hepatocytes (80%, approximately 100 billion); nonparenchymal cells include stellate cells, sinusoidal endothelial cells and kupfer cells

47
Q
  1. What are bile canaliculi and what is their function?
A

Specialized grooves between hepatocytes that form a continuous network that drains eventually into the bile ductules (apical side)

48
Q
  1. What is the function of Kuppfer cells?
A

Arise from macrophage and line the sinusoidal epithelium, playing a major role in host defense and can be used to internalize foreign proteins or microorganizms that have been coated with host antibodies

49
Q
  1. What is the role of stellate cells in liver fibrosis?
A

Stellate cells produce extracelluar matrix materials such as collagen, deposited in the space of Disse and impairs hepatic function

50
Q
  1. What is the function of cholangiocytes and where are they found?
A

Make up the walls of biliary ducts as columnar epithelial cells, which absorb and secrete various substances into and out of the bile

51
Q
  1. What is bile and what is its function?
A

Bile is a lipid-rich solution designed to promote the elimination of hydrophobic solutes, it is a micellar solution in which bile acids, cholesterol metabolites forming micelles with phophatidylcholine; plays an important role in the digestion and absorption of dietary lipids (process more efficient) and insoluble dietary lipids and fat soluble vitamins are depend on micellar solubilization for absorption

52
Q
  1. Bile acids are synthesized from what precursor molecule? Bile acids are said to be amphipathic. What does that mean and why is it important? At what rate are bile acids synthesized per day?
A

Bile is made from cholesterol by changing its steroid nucleus and alkyl side chain, is amphaipathic (having both hydrophilic and hydrophobic face it allows bile to act as a solvent for both hydrophobic and hydrophilic molecules; bile acids are kinked molecules that are highly water soluble when ionized and synthesized at a rate of 200-400mg/day

53
Q
  1. What is lithocholic acid and where is it formed?
A

Lithocholic acid is a secondary bile acid that is converted from chenodeoxycholic acid by bacterial enzymes in the colon and it is particularly cytotoxic if present at high concentrations

54
Q
  1. Why are bile acids conjugated to form bile salts? Where does this happen?
A

Primary and secondary bile acids are modified in the liver by conjugating them to an amino group of glycine or taurine; bile salts are more water soluble and are substrates for active transport across the canalicular membrane

55
Q
  1. What happens when bile acids exceed the critical micellar concentration in the intestinal lumen?
A

a concentration at which bile acid molecules are spontaneously self-associated into micelles, hiding their hydrophobic portions from the aqueous environment

56
Q
  1. What is the function of mixed micelles?
A

Serves as the solvent for hydrophobic waste products

57
Q
  1. Why is bile brown?
A

Conjugated billirubin is what gives bile its brown color

58
Q
  1. How is bile modified by bile ductules?
A

Smallest bile ductules are lined by cholangiocytes which are columnar epithelial cells specialized to modify bile composition

59
Q
  1. Why is the amount of bile secreted per day roughly 10-fold greater than the amount of bile synthesized by the liver per day?
A

The constant circulation of bile salts from the intestine to the liver re-uses the bile salts

60
Q

140 . What are apical sodium-dependent bile salt transporters (asbt), what is there function, and where are they found?

A

The sodium coupled transporter that recognizes bile acid conjugates and reabsorbs them, they are found in the epithelial cells of the terminal ileum

61
Q
  1. How much bile lost in the feces each day, and how does it compare to the amount of bile synthesized by the liver per day?
A

Bile lost in the feces is equal to input, between 1-1.2g/day

62
Q
  1. What is the function of gall bladder, and what is its capacity in an adult human?
A

The gall bladder stores and concentrates bile coming form the liver in the period between meals; approximately 50mL in an adult human

63
Q
  1. What happens to bile synthesis and circulation if the gall bladder is removed?
A

The bile acid pool continues to cycle through the enterohepatic circulation and the majority of the bile acid pool is stored in the small intestine

64
Q
  1. The gall bladder has two functional layers. What are they and what do they do?
A

Epithelium: columnar epithelium that are connected by very tight junctions that concentrates bile
Musculature: smooth muscle that controls the volume of the gall bladder

65
Q
  1. Gall bladder contraction is brought about by what neural and hormonal pathways? What stimulus activates these pathways?
A

Via cholinergic input from the vagus nerve as well as CCK via CCK receptors and via gallbladder nerves

66
Q
  1. How can the bile acid concentration in the gall bladder increase ten-fold, while the bile itself remains isotonic with plasma?
A

Bile and cations like sodium increase concentration while chloride and bicarbonate decrease in concentration; the majority of the bile acid molecules are physically in the form of mixed micelles that contain cholesterol and phophatidylcholine (once CMC is reached, monomeric concentration of bile is reached, that single molecule whether Na or micelle has the same osmotic pull)

67
Q
  1. What is bilirubin, and where does the majority of it come from?
A

Bilirubin is a metabolite of heme and serves to coordinate iron in various proteins as well as an antioxidant and means to excrete unwanted heme; majority of bilirubin comes from heme released by senescent RBC

68
Q
  1. Bilirubin is nearly insoluble in water. How then is it circulated around the body?
A

It is taken up by albumin when it is released into the blood as its affinity for unconjugated bilirubin for albumin is extremely high

69
Q
  1. When bilirubin enters the hepatic circulation, which cells take it up? What happens to the bilirubin within these cells, and how is it then excreted?
A

Hepatocytes take up bilirubin in the liver, bilirubin inside the cells binds to a variety of intracellular proteins that maintain its solubility and traffic it appropriately ; bile exits cells via a membrane transport protein known as MRP2, only conjugated bile is able to enter the bile through MRP2. Conjugation to a molecule of glucuronic acid is catalyzed by UDP glucuronyl transferase and result in the sequential esterification of two glucouronide to bilirubin

70
Q
  1. What effect does conjugation of bilirubin have on its transport along the intestinal lumen?
A

Conjugation of bile increases the water solubility of the bile allowing it to travel without a protein carrier, it also promotes the elimination of the metabolic waste products contained in bilirubin

71
Q
  1. How is bilirubin responsible for the normal color of the stool?
A

Metabolism of by deconjugation by enteric flora produces molecules like urobiliogens and stercobilinogens which are further metabolized to urobilins and stercobilins and these give color to the stool

72
Q
  1. What is the normal transit time for food substances to move from the mouth to the ileocal valve?
A

In the small intestine, substances move from the mouth to the ileocecal valve in a little under 2 hours in a healthy adult

73
Q
  1. What is the normal transit time for substances to move from the cecum to the rectum?
A

Normal transit from the cecum to the rectum is 1-2 days

74
Q
  1. What are the roles migrating motor complexes (MMC’s) in intestinal motor function, and when do they typically occur? Describe characteristics of MMC phases I, II, & III.
A

During fasting, small intestine exhibits MMC when the meal has been emptied from the intestine, the MMC resumes with characteristic phases, after a meal is ingested, the motility event in the small intestine become more frequent and the pattern rests on the BER
Phase I is quiescence, during phase II, contractile activity increases but with irregular contractions that fail to propel luminal contents, in phase II involves a 5-10 min period of intense, luminally occlusive contractions that sweep from the body of the beginning to

75
Q
  1. What is the function of segmental propulsion in the colon? What colonic muscle layers are involved in these?
A

Segmentation serves to move contents of the intestine back and forth as a result of “programed” enteric neural circuitry to allow for proper re-absorption of liquid; short contractions are initiated by the circular muscles and long duration contractions last for 20-60 seconds which may be stationary or propagate for a short distance and are attributed to contraction of the longitudinal muscles

76
Q
  1. What is the function of high-amplitude propagating contractions in the colon? How often do they occur?
A

Propagate exclusively aborally and provide for mass movement of the feces over long distances, they precede the need to defecate and occur about 10 times per day and are associated with rising in the morning and with eating; sweep from the cecum to the colon to the rectum and result in relaxation of the internal anal sphincter

77
Q
  1. What colonic muscles are involved in defecation? How does the activity of these muscles differ between expulsion of solids (defecation) and gases (flatus)?
A

Defecation is assisted by the relaxation of the puborectalis muscle which results in a less acute rectoanal angle, rectal contraction produces the propulsive force enhanced by recus abdominus, diaphragm and other levator ani muscles. Contractile actions of expulsion of flatulus includes all of the same movements except the puborectalis muscle does not relax and does not change the retro anal angle (preventing loss of feces)

78
Q
  1. What is the largest immunological organ in the body? Why do you think it is this one?
A

Mucosal immune system (along with mucosa-associated lymphoid tissues) due to its large surface area and susceptibility to foreign invasion, including developed tolerance

79
Q
  1. What are M cells, where are they found, and what is their role in gut immunity?
A

Specialized epithelial cells overlie organized lymphoid aggregates known as Peyer’s patches, and their role is to present antigens to immunological cells

80
Q
  1. What is IgA, what does it do, and where does it originate in the GI system?
A

IgA plasma cells in the lamina propria secrete two IgA molecules that are bound together by a short poly pepetide sequence; IgA exerts protection in the intestine via several mechanism: bind microbial antigens, food antigens and viruses to prevent their uptake by intestinal epithelial cells; bound IgA destined for the apical membrane can traffic antigens back to the cell apex, or may sequester antigens that are able to penetrate to the lamina propria

81
Q
  1. Which segment of the GI tract contains the largest number of bacteria? How many bacteria are found there, and what kinds are they?
A

The largest number of microbes occur in the colon, (number of bacteria exceeds the number of cells in the body) at least 400 different bacterial species; major anerobic spcies include bacteriodes, bifidobacteria, clostridia, eubacteria and anerobic stretococcci, aerobes include E. coli, streptococci and staphylococci

82
Q
  1. What effects do antibiotics have on the colonic bacterial population?
A

Antibiotics can kill off the colonic bacterial population and they may lead to overgrowth of harmful bacteria ie. C. Diff.

83
Q
  1. What are some of the beneficial effects of colonic bacteria?
A

Helps development of the mucosal immune system by providing a stimulus to drive its development and maturation of intestinal lymphoid populations, it also helps in epithelial proliferation and differentiation; colonic bacterial convert bilirubin into urobiliogen and salvage nutrients that cannot be degraded by pancreatic or other digestive enzymes (fermentation can provide short chain fatty acids which can be used by colonic cells as fuel); furthermore they protect the intestine against colonization of harmful bacteria

84
Q
  1. On average, how much flatulent gas does the GI tract release each day, and what are its two greatest components?
A

On average 1L/day mostly consisting of N2 (65%) and hydrogen (20%)

85
Q
  1. What are borborygmi?
A

Bowel sounds, produced by gas moving back and forth by motility patterns