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Patho 2 Exam 2 > Normal Physiology of the Digestive System > Flashcards

Normal Physiology of the Digestive System Flashcards

1
Q

Digestive System (4)

A
  1. Two most important organs: pancreas and liver (secretory organs necessary for GI function)
  2. Digestive system is DISASSEMBLY LINE; we digest food as solid masses and get it down to fine liquid then ingested in form of macromolecules consisting of individual units
  3. Need to break down macromolecules into units so we can then absorb the nutrients
  4. Breakdown of medications, take down water, electrolytes, foods, etc.
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2
Q

Wall of GI Tract Layers (5)

A
  1. Mucosa: innermost layer of tract
  2. Submucous plexus: thick connective tissue layer
  3. Muscularis externa: double layer of smooth muscle
  4. Serosa: layer of connective tissue over tract wall
  5. Mesentary: serous membrane connected to tract
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3
Q

Mucosa Layer of GI tract (3)

A

Innermost layer

  1. Starts with mucous membrane → lamina propria → muscularis mucosa
  2. Sheep of epithelial tissue that is perpetually moistened by production of mucous
  3. The interface between interior and exterior environment
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4
Q

Muscularis Externa Layer of GI Tract (3)

A

Double layer of smooth muscle

  1. The two layers are oriented in different directions
  2. Inner circular muscle layer: muscle cells run in circumference around the tube
    * When muscle cells contract they squeeze and get smaller in diameter
  3. Outer longitudinal muscle: muscle fibers run longitudinally down the tube; when they contract the tube gets shorter
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5
Q

Mesentary Layer of GI Tract (3)

A
  1. Serous membrane connected to tract
  2. There is a double layer of mesentery that allows the membranes to connect over the tube
  3. The mesentery lines the interior of the body cavity and comes off and then covers all the visceral organs
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6
Q

Basic Properties of Epithelial Cells (3)

A
  1. Same properties of mucosal layer
  2. Epithelial cells with tight junctions between them so that nothing can get between them
    * Anything that wants to move from lumen of GI tract to underlying capillaries (the blood) has to cross the epithelial cells
  3. Interspersed between these epithelial cells are secretory cells: mucous cells, endocrine cells, and exocrine cells
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7
Q

Secretory Cells within Epithelial cells (3)

A
  1. Mucous cells or goblet cells produce mucous
  2. Endocrine cells produce hormones that regulate the function; goes into underlying vascular tissue and enters bloodstream
  3. Exocrine cells digestive enzymes that are released in lumen of GI tract
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8
Q

Esophagus Mucosal Anatomy

A

Most of the wall is muscle

This is because esophagus: has one function, which is for transport; quickly gets food from mouth to stomach
*No digestion or absorption here

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9
Q

Small Intestine Mucosal Anatomy

A
  1. Function is digestion and absorption; before food leaves small intestine, all digestible things will be absorbed
  2. Muscle layer is very small, because we want things to move slowly through it for maximal absorption
  3. Mucosal layer is in vili shape; this maximizes absorption by maximizing surface area available for absorption
    * The cells lining the villi have microvili
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10
Q

Four Basic Digestive Properties

A
  1. Motility
  2. Secretion
  3. Digestion
  4. Absorption
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11
Q

Motility (4)

A

Movement through GI tract accomplishes two things:

  1. Need propulsive movements to move things forward
  2. Have mixing movements to mix food with digestive enzymes
  3. Mixing and propulsive movement
  4. Timing of these muscle contractions (peristalsis and segmentation contraction) determines how quickly things move through the GI tract and how quickly you can absorb things
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12
Q

Mixing Motility

A

Primary movement: Segmentation Contractions

*Random contractions of circular muscles that help mix the contents of the GI tract

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13
Q

Propulsive Motility

A

Most common propulsive movement is peristalsis

*Waves of muscle contractions that move down the tube; extremely effective way of moving things down the tract

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14
Q

Secretion (7, what it is, digestion, timing, product, etc.)

A
  1. Mucus is secreted throughout GI tract (everywhere)
    * Wherever it is secreted, it plays a key role in keeping food hydrated and moist, which is necessary to digest things
  2. Digestion = hydrolysis reactions, so we need a lot of water to maintain them
  3. The mucous that stomach produces is very thick and highly alkaline; it represents a critical protective barrier on the lining of the stomach
    * Without mucous, stomach would digest itself very quickly
  4. Also have secretion of acid, digestive enzymes, and bile salts
  5. Different structures are responsible for secreting different things
  6. Timing of secretion is highly controlled and most of the time, secretion is anticipatory
    * Timing of Secretion controlled via the nervous and endocrine system
  7. The product secreted dependent on location within digestive tract
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15
Q

Digestion (2)

A

Chemical breakdown of food

  1. Process of chemical digestion is the breakdown of macromolecules into absorptive subunits
  2. Three categories of foods (carbohydrates, proteins, fats)
    * All are consumed in form of macromolecules and need to be broken down into subunits
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16
Q

Carbohydrate Digestion (6)

A

Consumed in two macromolecule forms
1.Polysaccharides

  1. Disaccharides
  2. The individual subunits (what makes up poly and disaccharides) are glucose, galactose, and fructose (sugars)
    * Of these three, the one that we are capable of breaking down for energy is glucose
  3. Galactose and fructose first needs to be converted into glucose before we can break it down and use it for energy
  4. We need multiple enzymes to breakdown carbohydrates, maltose/maltase is just one of them
  5. Can absorb them in monosacaccharide form
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17
Q

Polysaacharides

A

Long chains of sugars: starch (plant form) and glycogen (produced by us)
*Starch= dietary source

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18
Q

Disaccharides

A

Sweet carbohydrates: sucrose (table sugar) and lactose (dairy products) and maltose

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19
Q

Protein Digestion (3)

A
  1. Long chains of amino acids
  2. Greatest number of digestive enzymes dedicated to breaking down proteins
  3. Can absorb them in amino acids form
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20
Q

Fat Digestion (5)

A
  1. Most complex digestive process
  2. Have a lipid that needs to be digested in an aqueous solution, which is challenging
  3. Consume them in the form of triglycerides (3 fatty acid chains attached to glycerol backbone)
  4. When we breakdown triglycerides we produce 2 fatty acids and 1 monoglyceride
    * In the form of fatty acids + monoglyceride = state that we can absorb
  5. Only enzyme that breaks down fat is LIPASE
    * Only organ that produces lipase = pancreas
    * People with pancreatic disease/impaired pancreatic function can’t breakdown fat; have body wasting and get very skinny and produce stools that are all fat
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21
Q

Absorption (4)

A
  1. Small intestine is main organ of absorption; where we absorb all food, water, etc.
    * Small intestine has a specific mechanism for transporting water, monosaccharides, fatty acids, and amino acids across mucosal wall and into blood vessels
  2. Malabsorption (impaired absorption) is often called by maldigestion
  3. Anything that affects overall absorptive surface area will affect absorption
  4. It is the most important process in the digestive tract
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22
Q

Excretion

A

A non-digestive function of the GI tract; Gut responsible for excreting waste

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23
Q

Fluid/Electrolyte Balance

A
  1. A non-digestive function of the GI tract
  2. Small Intestine reabsorbs up to 9-11 liters/day
  3. Where we absorb water and all of our electrolytes
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24
Q

Immunity (3)

A

A non-digestive function of the GI tract

  1. Gut Associated Lymph (GALT)
    * Immune cells lining GI tract wall
  2. Lymphocytes and mast cells located in between epithelial cells and in the lamina Propria
  3. The Hepatic Phagocytic System
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25
Q

Liver and immune function (5)

A

Hepatic Phagocitic System

  1. Liver system of phagocytic cells called Kupffer cells
  2. Lots of macrophages in liver to protect us from what our gut absorbs
  3. Liver can neutralize the ammonia produced by gut bacteria and surveys everything for immune cells
  4. t metabolizes a large chunk of the stuff we absorb, like drugs or environmental toxins
  5. Liver filters everything our GI tract absorbs
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26
Q

Enteric System (7)

A
  1. Network of autonomic nerves found in the wall of the GI tract
  2. Very complex; represents postganglionic fibers of the parasympathetic nervous system
    * Technically part of PNS, but operates autonomously
  3. Postganglionic fibers of the parasympathetic nervous system that innervate the gut
  4. Considered the 3rd branch of the autonomic nervous system
  5. Autonomous closed loops: sensory – efferent – negative feedback
    * Has it’s own sensors, effectors, etc.
  6. Controls: Motility, Secretion, Digestion, and Absorption
  7. Lives in gut
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27
Q

Sympathetic Control of Gut (extrinsic)

A

Sympathetic stimulation slows digestion (inhibits secretion and motility)
*SNS tends to inhibit digestion and slow down motility

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28
Q

Parasympathetic Control of Gut (extrinsic)

A

Vagal stimulation promotes digestion (stimulates secretion and motility)
*Vagus control with gut function: everything anticipatory (anticipates food entering GI tract) will come from the brain

*People with spinal cord injuries will have adequate digestion but no anticipatory stimulation of gut function

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29
Q

The Enteric Endocrine System (3)

A
  1. Set of endocrine cells and hormones in GI tract to coordinate and regulate digestion
  2. Regulates function by secreting hormones; secrete hormones in response to specific stimuli
  3. Single hormone-secreting cells are scattered among other types of epithelial cells mucosa of stomach and small intestine
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30
Q

Enteric Endocrine System Targets

A

Smooth muscle, exocrine glands, endocrine glands

  • Directly control motility, secretion, digestion, absorption
  • Controlled by local short loop and influenced by longer loops (the global control)
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31
Q

Chewing Food (3)

A
  1. Incredibly important; maximizes ability for stomach and large intestine to breakdown food
  2. Reduces likelihood of indigestion
  3. Motility is chewing

No food is absorbed in the mouth!

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32
Q

Salivary Glands

A
  1. Salivary glands associated with lots of mucous; salivary amylase is an enzyme that breaks down polysaccharides
  2. So carbohydrate digestion begins in the mouth with the intro of salivary amylase
    * The more you chew, the more salivary amylase gets into the food you chew
  3. Lysoszome
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33
Q

Lysozyme

A

breaks down bacterial walls

*Reason why animals lick their wounds; because it is applying natural anti-microbial agent

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34
Q

Swallowing (2)

A

Push food to the back of our throat and it presses on the area of our throat just before the upper esophageal sphincter

  • So we swallow food, it gets pushed back, and causes stretching above the upper esophageal sphincter
  • This triggers the opening of the upper esophageal sphincter and a waive of peristalsis down the esophagus

*As long as there is still food in the back of the throat, peristalsis still gets triggered

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35
Q

Swallowing Reflex

A

swallowing reflex opens and quickly closes the upper esophageal sphincter and lower esophageal sphincter

We want to keep it closed because it minimizes the amount of the air that we swallow

Want to keep lower esophageal closed so that stomach acid doesn’t leak into esophagus

36
Q

Stomach (3)

A
  1. Food enters stomach from esophagus, and then body of stomach and incorporates digestive enzymes and gastric juices before food then gets fully mixed in lower stomach
    * Lower stomach has more muscle in it for this mixing
  2. By the time food moves into duodenum, it no longer looks like food
  3. Digestive enzyme in the stomach = pepsin
37
Q

Mucosal Lining of Stomach (3)

A
  1. Has deep invaginations called gastric pits
    * At very bottom of gastric pits is where we find cells that produce gastric juices, acids, and enzymes that breakdown food
  2. The gastric pit (lumen) and surface lining has thick alkaline mucous that fills the pits and forms a thick layer on the surface of the stomach
    * Represents critical protective layer for the cells lining the stomach
  3. Two major areas of stomach: body and fundus vs. antrum
    * Cells that make up mucosal lining are very different in the bodies of the stomach vs. the antrum
38
Q

Types of Cells in Gastric Pits (4)

A
  1. mucosal cells –> produce mucous
  2. chief cells
  3. parietal cells
  4. ECL cells
39
Q

Chief Cells in Gastric Pits

A

Breaks down protein

  • Any enzyme that breaks down protein will be released in it’s inactive form first, otherwise it will kill the cell that is producing it
  • Pepcinogen (activated pepcin) is activated by acid
40
Q

Parietal Cells in Gastric Pits

A

Produce hydrochloric acid and intrinsic factor

41
Q

Intrinsic Factor

A

A substance that binds to Vitamin B12 and allows for absorption of Vitamin B12 by the small intestine

  • Without it, you wouldn’t absorb B12, which is critical for RBC production
  • Pernicious anemia: Vitamin B12 deficiency due to intrinsic factor deficiency
42
Q

ECL Cells in Gastric Pits

A

Produce histamine

  • The histamine goes into the blood stream locally and is designed to stimulate the parietal cells and the chief cells (especially parietal cells)
  • Enhances HCl production
43
Q

G Cells

A

Type of endocrine cell

Produces gastrin, which stimulates acid production

44
Q

Gastrin (3)

A
  1. Stimulates acid production
    * Stimulates chief cells and parietal cells → production of HCl
  2. Stimulates motility throughout GI tract
    * If you feel hungry, gastrin stimulates motility and stomach grumbles
    * Gastrin is significantly stimulated by coffee and nicotine
  3. Released at the earliest point in the digestive process
    * Released even with anticipation of food (smelling, chewing, tasting, swallowing)
45
Q

D Cells

A

Produce somatostatin

46
Q

Somatostatin

A

Somatostatin turns things off

*As things move out of the stomach, somatostatin gets released and decreases HCl production and motility

47
Q

Phases of control of digestion

A

Four phases control Digestive activity (gastric secretion, gastric motility, small and large bowel motility, and the initiation of the events of overall digestion)

  1. Interdigestive Phase –> circadian rhythm
  2. Cephalic Phase
  3. Gastric Phase
  4. Intestinal Phase
48
Q

Cephalic Phase of Digestion (3)

A
  1. Anticipatory
  2. Anticipating food entering the stomach
  3. Wakes everything up, stimulates secretion and motility
49
Q

Gastric phase of Digestion

A

Happens when food enters stomach

*Food in the stomach; further stimulates everything going on in stomach and in rest of GI tract

50
Q

Intestinal Phase of Digestion (2)

A
  1. Food in the intestines
    * Phase where food enters small intestine
  2. We are focused on starting to shut down secretion and motility in the stomach and focusing on coordinating what we need for digestion and absorption in the small intestine
51
Q

What occurs when food moves from stomach to duodenum? (2 things)

A
  1. Food from stomach is extremely acidic, and duodenum doesn’t have thick alkaline mucous to protect it → sodium bicarbonate produced by the pancreas neutralizes the acid
    * Critical thing that has to happen: we have to coordinate with pancreas to produce sodium bicarbonate to neutralize the acid
  2. Fat digestion
    * Fat digestion begins and ends in the duodenum
    * Digesting fat requires pancreatic secretion of lipase and secretion of bile from the liver
52
Q

Pancreatic Juices (3)

A
  1. Produced by exocrine portion of pancreas
    * Cells of these individual ducts can either produce digestive enzymes or produce sodium bicarbonate
  2. Enzymes mix with solution and you get pancreatic juices
    * Pancreatic juices get made and then are released into duodenum
  3. CCK and Secretin coordinate this to stimulate the secretion
53
Q

Actions that must happen in the upper GI Tract for food to proceed to the GI Tract (2 with explanation)

A
  1. Food enters of the Stomach – HCL and pepsin section, gastric mixing, food turned into Chyme
    * Rate at which stomach enters gets slowed down dramatically to buy duodenum some time to coordinate with pancreas and liver
    * Two enzymes critical for this: CCK and secretin
  2. Food begins to move into the Doudenum – this slows down gastric motility to allow time for the release of pancreatic juices and bile from the liver. The digestion of fat begins and ends in the duodenum (major bottleneck). The release of CCK and Secretin from the duodenum are critical to the process.
    * CCK and Secretin act on liver and pancreas to stimulate secretion of bile and juices
54
Q

Types of Pancreatic Enzymes (3)

A
  1. Proteolytic Enzymes
  2. Pancreatic amylase
  3. Pancreatic Lipase
55
Q

Proteolytic Enzymes (3)

A
  1. Trypsinogen → Trypsin
    A. First to get activated
    B. The enzyme that activates it is aminopeptidase, which is found attached to the plasma membrane of the mucosal cells in the small intestine
    C. Only acts on proteins that bind to aminopeptidase, so it won’t digest the cell it’s attached to
  2. Chymotrypsinogen → Chymotrypsin
    A. Activated by Trypsin
  3. Procarboxypeptidase → carboxypeptidase
    A. Activated by Trypsin

**These are released in the inactive form and → to active form

56
Q

Pancreatic amylase

A

Breaks down carbohydrates

salivary amylase in the mouth also breaks down carbohydrates

57
Q

Pancreatic lipase

A

Breaks down fats
*Our only source of lipase

  • We need bile from the liver and pancreatic lipase to enter the duodenum and digest our fat
  • This slows the overall digestive time down the most
58
Q

Bile Composition (3)

A
  1. Aqueous alkaline fluid
  2. Organic compounds - bile salts, cholesterol, lecithin, bilirubin
  • Play a major role in aiding fat digestion
  • Through “fat emulsification;” bile emulsifies fat
  • Secreted into the duodenum
  1. Bile salts have an amphipathic structure, meaning that one end of the structure is lipid soluble and the other end is water soluble
    * When bile salts interact with fat, they create lipid emulsion droplets
59
Q

Bile Emulsification (3 steps)

A

OCCURS IN THE DUODENUM

1st: Take fat and create smaller droplets of fat and prevent them from reforming

2nd: Once you form the smaller droplets through intestinal mixing, the bile salts surround the individual droplets and put their hydrophobic ends in them and point the hydrophilic ends into the solution to prevent the droplets from recombining
* This is very important because it increases the surface area that lipase can now act on these droplets*

3rd: Bile surrounds small droplets of fat and prevents them from reforming

60
Q

Indigestion (6)

A
  1. Consume a rich meal high in fat and “bottle neck;” food is sitting in stomach waiting for the fat to get digested and emptied
  2. As it sits in the stomach, the amount of food that is undigested goes down unprocessed, so there is less buffering of the acid
  3. The actual acidity level of the contents of the stomach get higher and you get sour acid feeling and then begin to feel nauseous
  4. If food stays in stomach for too long, the stomach wants to either vomit or stool
  5. Can’t stool because down route is clogged, so people vomit
  6. Can be caused by many things, but it is often the result of impaired or overwhelmed fat digestion
61
Q

Liver (3)

A
  1. Contributes bile salts to digestion
  2. Important for fat digestion and absorption
  3. Two types of cells that make up the liver: Hepatocytes and Kupffer cells
62
Q

Three Mechanisms that Control Bile Secretion

A
  1. Chemical – cholerectics
  2. Hormonal – secretin
  3. Neural – vagal stimulation
63
Q

Bile Release

A

Presence of Chyme in Small Intestine → release of CCK, which:

  • Stimulates liver to produce Oddi
  • Contracts gall bladder
  • Relaxes and opens sphincter of oddi
64
Q

Bile production and sphincter of Oddi

A
  1. Bile is produced by the liver (converted from cholesterol) and leave the liver through the common bile duct
    * In this duct there is the sphincter of Oddi
  2. When we aren’t actively digesting food that contains fat, the sphincter of Oddi is tightly closed
    * So the bile that is produced by the liver tends to back up and get stored in the gall bladder
65
Q

CCK (4)

A
  1. When we consume fat, we release CCK
  2. CCK opens the sphincter of Oddi, in addition to triggering bile production, and contracts the gallbladder
  3. So now you get flow of bile into the duodenum and the bile starts to emulsify fat
  4. Some of the bile will get reabsorbed in the terminal portions of the small intestine (about 50%) and will get absorbed and go back to the liver
66
Q

Positive Feedback Loop of Bile Production (explanation and 3 points about it)

A

When the bile salts come back to the liver, it is a very strong signal for the liver to make even more bile…

  1. We eat fat → we release CCK → CCK triggers liver to produce bile, it relaxes sphincter of Oddi, contracts gallbladder → bile enters duodenum and does fat emulsification and digestion → 50% of the bile salts released get reabsorbed in the terminal portions of the small intestine and go back to the liver → when bile comes back to the liver it is a strong signal for the liver to produce even more bile → more bile is produced and the cycle starts over

THIS IS A POSITIVE FEEDBACK LOOP

  1. What shuts off this feedback loop is when fat digestion is complete and CCK is no longer released, which constricts the sphincter of Oddi and bile no longer enters the duodenum or gets reabsorbed
  2. Any bile that is produced by the liver in this interim is stored in the gall bladder
67
Q

Small Intestine (4)

A
  1. Divided into three segments: Duodenum, Jejunum, Ileum
  2. Small intestine is where all of our food digestion and absorption is going to be completed
  3. Also have majority of water, electrolytes vitamin, and mineral absorption happening
  4. Primary motility in small intestine is segmentation as both mixing movements and propulsion movements
68
Q

Segmentation Contractions in Small Intestine (2)

A
  1. Segmentation contractions in the small intestine are very powerful mixing movements, in addition to mixing food with digestion enzymes it also increases the contact that the food has with the surface area (enhances absorption)
  2. Segmentation helps propulsion because we have a higher frequency of segmentation contractions in the early portions of the small intestine compared to the lower, so we are contracting faster in the upper part creating a very gentle and slow movement forward
69
Q

Mucous membrane of small intestine (6)

A
  1. The mucous membrane of the small intestine is unique compared to the rest of the GI tract; it is different in terms of structure (villi) and they have membrane bound digestive enzymes
  2. The villi structure enhances surface area
  3. We also have micorvilli, so each individual cell along the villi has an apical surface
  4. Mucosal membrane = “brush border membrane” because the apical membrane look like brissles of brushes
  5. Along this brush border is where we have the membrane bound enzymes –> “brush border enzymes”
  6. All of the villi and microvilli expand the surface area for digestion by 600x compared to a flat mucosal lining
    * Anything that affects this lining can greatly affect nutrition and hydration
70
Q

Enzymes in mucous membrane of small intestine (3)

A
  1. Enterokinase,
  2. Aminopeptidase,
  3. Diascharidases (enzymes that breakdown disaccharides into monosacharadies)
    - –maltase, sucrase, lactase

*The brush border membrane contains these three categories of membrane-bound digestive enzymes

71
Q

Enzyme –> Disaccharide –> monosaacharides (3)

A
  1. Maltase –> breaks down Maltose –> into Glucose
  2. Sucrase –> breaks down Sucrose –> into Fructose
  3. Lactase –> breaks down Lactose –> into Galactose
72
Q

Aminopeptidase

A

The brush border enzyme that breaks down polypeptide fragments into individual amino acids
*Will activate trypsin, etc.

73
Q

Process of Fat Digestion

A

1st: Pancreatic lipase comes in and breaks down the triglycerides into free fatty acids and monoglycerides
2nd: free fatty acids and monoglycerides reorganize with the bile salts, so now the bile salts are surrounding free fatty acids and monoglycerides, which creates the Micele structure
3rd: The micelle is what gets absorbed into the brush border cell
4th: Within the small intestine mucosal cell, the micelle reforms triglycerides
5th: The triglycerides are repackaged and creates a lipoprotein chylomicron

74
Q

Chylomicron

A

Chylomicrons are packages of triglycerides produced by the small intestine cell that can then enter the central lacteal and eventually enter the bloodstream

75
Q

Micele structure

A

ABSORBABLE FORM OF DIGESTED FAT

The free fatty acids and monoglycerides reorganize with the bile salts, so now the bile salts are surrounding free fatty acids and monoglycerides, which creates the MICELLE structure

*Inside a micelle is monoglycerides and free fatty acids

76
Q

Pancreatic Lipase

A

Breaks triglycerides to form micelle structure

77
Q

Large Intestine (4)

A
  1. By the time we get to the large intestine we should have digested and absorbed all of our food
  2. Now we have feces/waste
  3. Within the feces is some amount of water, electrolytes, and minerals that we want to take back
  4. Before the feces leaves the body we want to reabsorb a certain amount of the water, electrolytes, and minerals
78
Q

Motility in Colon: Haustraul Contractions (5)

A
  1. A type of segmentation contraction that are designed to mix up the feces and increase the contact of feces with colon wall to enhance absorption
  2. Slow and non-proulsive
  3. Result of autonomous rhythmicity of colon smooth muscle
  4. Mixing movment
  5. Controlled by local reflexes via intrinsic nerve plexuses
79
Q

Motility in Colon: Mass Movements (7)

A
  1. Strong propulsive movement
  2. Capable of driving feces down 3/4th of the colon in seconds
  3. Usually occurs after meals
  4. Occur 3-4 times per day – usually after meals
  5. Drive feces 1-3/4’s length of colon in a few seconds
  6. Stimulation - gastrocolic reflex - via Gastrin
  7. If mass movements triggered by gastrin push feces in rectum, it will trigger the sensation of defecation
80
Q

Defecation Reflex (3 steps)

A

1st: Distention on the rectal wall triggers the stretch receptors on the wall to cause a reflexive relaxation of the internal anal sphincter
2nd: The internal anal sphincter, composed of smooth muscle, reflexively relaxes when there is distention on the rectal wall
3rd: This moves feces down a little further

81
Q

External anal sphincter

A

Composed of skeletal muscle, controlled voluntarily so we can control the timing of defecation reflex

82
Q

What happens if defecation is delayed? (2)

A
  1. If defecation is delayed too long, the mass movements will slow down and feces can move back out of the rectum and decrease distention and you can loose the desire to defecate
  2. Drawback to this: delaying defecation too much causes you to absorb more and more water from the feces in the colon, and the more water you absorb, the harder the stool becomes, which is more difficult to pass
    * Increased risk of constipation
83
Q

Diarrhea (4)

A
  1. The things that cause diarrhea include colonic motility that is too rapid, so you don’t have enough time to absorb water
  2. Can happen due to bacteria → leading to speedy motility in GI tract to get rid of it quickly, so with no time to absorb the water there is loose stool
  3. The other mechanism for diarrhea is osmotic diarrhea, which occurs when the osmolarity of feces is elevated, especially with undigested material in the colon
  4. Undigested material can be caused by some sort of enzyme deficiency (ex: lactose intolerant) or fiber
84
Q

Fiber (3)

A
  1. Fiber is defined by the fact that we don’t have a mechanism for digesting it
  2. We can’t digest fiber so it enters the large intestine undigested and raises the osmolarity of stool and then softens it by drawing water in
  3. Too much fiber → osmotic diarrhea
85
Q

What’s so great about fiber? (3)

A
  1. Aids in digestion in a few ways
  2. Adds volume to chyme and eventually feces
  3. Increases the osmolarity of chyme

Patho 2 Exam 2 (8 decks)

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