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BMS2031 > GUT > Flashcards

GUT Flashcards

1
Q

What is the rough general pathway for food?

A
  • Macstication–> Bolus –> pharynx–> larynx–> Oesophagus–> Stomach–> small intestine –> large intestine–> anus
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2
Q

What are the accessory glands?

A
  • Salivary glands
  • Liver (bile)
  • tongue
  • Pancreas (enzymes breaking down foods)
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3
Q

What is the inner lining of the gut called?

A
  • Mucosa
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4
Q

What are 4 functions of the GI system?

A
  1. Nutrient absorption
  2. release/removal of waster
  3. Regulation of H2O and electrolytes to MAINTAIN BODY FLUID osmolarity
  4. Immune function (mucosa contains macrophages-IgA)
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5
Q

What moves food through the gut?

A
  • MOTILITY –> propulsion through gut

- Smooth muscle contracts

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6
Q

How do we get muscle cells to contract?

A
  • Excitation (APs)

- Smooth muscle cells at each section of the gut are COUPLED

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7
Q

What connects each smooth muscle cell?

A
  • Gap junctions (one AP spreads through the whole unit)

- Via wave of excitation

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8
Q

What does the gut tube do when circular muscle contracts?

A
  • It is CONSTRICTED (get narrower)
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9
Q

What does the gut tube do when the longitudinal muscle contracts?

A
  • It SHORTENS
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10
Q

Before the bolus in the gut tube there is ___________ (type of constriction)

A

Before the bolus there is circular constrction

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11
Q

After the bolus in the gut tube there is ______ (type of constriction)

A

Longitudinal shortening

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12
Q

What is oesophageal peristaliss?

A
  • Contraction and relaxation of circular and smooth longitudinal muscle layers–> motility
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13
Q

Which two sphincters are made up of skeletal muscle?

A 
Upper oesophageal (1) 
- External anal sphincter (7)
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14
Q

Which spincters are made up of smooth muscle ?-

A
  1. Lower oesphageal
  2. Pyloric Sphincter (b/w bottom of stomach and start of small intestine)
  3. Sphincter of Oddi (hepatopancreatic)
  4. Ileocecal (b/w ileum and cecum)
  5. Internal anal sphincter
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15
Q

What are the internal sphincters in a constant state of?

A
  • Constant state of constriction (maintained by SNS)

- Maintained by BOTH intrinsic enteric nerves and extrinsic nerves

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16
Q

What does the relaxation of these 5 sphincters result from?

A

ACTIVATION of parasympathetic nerves and INTRINSIC INHIBITORY nerves in myenteric plexus

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17
Q

Which types of nerves innervate the gut?

A
  • SENSORY NERVES–> Chemoreceptors and mechanireceptors
  • SOMATIC MOTOR NERVES –> Skeletal muscle (upper oesophageal and sphincter)
  • AUTONOMIC NERVES–> Innervate glands and smooth muscle
  • ENTERIC NERVES–> Also innervate glands and smooth muscle
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18
Q

In times of extreme stress what happens to the neuronal controls?

A
  • They all go!!
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19
Q

What are the two intrinsic nerve plexuses that the enteric nervous system is comprised of?

A
  1. Myenteric Plexux

2. Submucosal plexus

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20
Q

What is the myenteric part of the ENS involved with?

A
  • b/w circular and longitudinal muscle layers and runs along ENTIRE length of GUT (control MOTILITY)
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21
Q

What is the submucosal plexus involved with?

A
  • in submucosal connective tissue, only in CERTAIN REGIONS, controls SECRETIONS, localised blood flow –> nutrient absorption
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22
Q

What happens to the motility with the sympathetic system and parasympathetic system respecitvely?

A
  • Motility decreases (Sympathetic) and increases (parasympathetic)
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23
Q

What happens to the motility in the submucosal phase?

A
  • There is NO CHANGE
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24
Q

What happens to motility in the myenteric system?

A
  • EXCITATORY
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25
Q

What is the effect of the Sympathetic nervous system for secretions?

A
  • Decrease
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26
Q

What is the effect of the parasympathetic system for the Secretions?

A
  • Increase
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27
Q

What is the effect of the myenteric ENS on secretions ?

A
  • NO change
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28
Q

What is the effect of the Submucosal ENS on the Secretions

A
  • Can be an increase in secretion (excitatory)
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29
Q

What is the effect of the sympathetic nervous system on the smooth muscle sphincters?

A
  • Constriction
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30
Q

What is the effect of the parasympathetic nervous systyem on the smooth muscle sphincters?

A
  • Relaxation
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31
Q

What is the effect of the myenteric ENS on smooth muscle sphincters?

A
  • but can be inhibitory–> via NO- (relaxation)
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32
Q

What is the effect of the submucosal system on smooth muscle sphincters?

A
  • No change
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33
Q

What does the ileocecal valve depend on ?

A
  • The pressure
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34
Q

What is chyme and where is it first found?

A
  • Found in small intestine
  • Semi fluid pulp
  • Mixture of food and gastric secretions
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35
Q

Where does most of the chemical digestion occur?

A
  • in the duodenum (also almost all nutrient absorption)
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36
Q

How is small intestine motility stimulated?

A
  • food enters, fills stomach–> stretch receptors go to CNS –> PNS efferent nerves–> to small intestine to stimulate motility
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37
Q

What are segmenting contractions and when do they occur?

A
  • “CHOP” food up –> localised constrictions
  • Slosh (mix) food backwards and forwards with digestive enzymes
  • NO net movement of material
  • Chyme broken down into smaller sections
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38
Q

After most of the meal has been absorbed, what are segmenting contractions replaced by?

A
  • Replaced by the MIGRATING MOTOR COMPLEX
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39
Q

What is the migrating motor complex (MMC)?

A

-Peristaltic contractions of several adjacent segments from stomach –> large intestine

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40
Q

When is the MMC inhibited?

A
  • Inhibited when food enters the stomach –> becasue segmenting contractions need to occur first to let food be broken down
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41
Q

What is the MMC initiated by and modulated by?

A
  • INCREASE in chyme pH or the MOTILIN plasma hormone concentration (stimulating motility)
  • Modulated by enteric (via stretch receptors) or autonomic nervous system
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42
Q

What happens when you have no MMC?

A
  • Large overgrowth of bacteria
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43
Q

What are 4 processes that occur in the large intestine?

A
  • Haustral (mixing) contractions
  • Chemical digestion –> enteric bacteria
  • H2O and electrolyte absorption
  • Propulsive actions (mass movements)
  • Excretion (via defication)
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44
Q

In a normal person, how long does it take for food to pass through the small intestine–> large intestine and excretion?

A
  • It takes 12-24 hours
  • Ileocelcal sphincter–> cecum–> ascending colon–> transverse colon–> descending colon–> sigmoid colon–> anal canal
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45
Q

What type of muscle are the haustra in the large intestine?

A

Circular muscle, have a sac like appearance

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46
Q

What type of muscle is the tenia colae in the large intestine?

A
  • Longitudinal muscle
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47
Q

What is the rough pathway for haustral contractions?

A
  • Chyme moves to lumen of large intestine–> stretch receptors ACTIVATED–> myenteric nerves activated–> shortening/activation of longitudinal muscle layer strips AND localised constriction of circular smooth muscle
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48
Q

What are the haustral contracitons in the large intestine replaced by and what is the rough mechanism (also where do they occur in large intestine)?

A
  • MASS movements (peristaltic contractions) –> power propulsions
  • Constrctive ring forms and there is LOSS OF HAUSTRA–> VERY LONG CONTRACTIONS (30 seconds) and 3-4 per day)
  • occur from cecum to sigmoidal colon
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49
Q

What triggers the mass movements of the large intestine and what is it mediated by?

A
  • Gastrocolic and duodeno-colic reflexes –> activated by DISTENSION of the stomach (stretch receptors) OR duodenum
  • ANS mediation –> PNS (mass movement stimulation)
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50
Q

What are the two key functions of the colon?

A
  1. Absorption of fluids/electrolytes

2. Storage

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51
Q

What happens if the transit is too slow through the large intestine?

A
  • More time for water absorption, so hard stool–> constipation
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52
Q

What happens if the transit time is too fast?

A
  • NOT enough time for absorption–> diarrhea and loose feces
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53
Q

What is the definition of constipation?

A
  • Pass stools less than 2 times a week and straining 25% of the time, hard stools and incomplete evacuation
54
Q

What are the main causes of constipation?

A
  • gastrointestinal disease (intestinal obstruction) , slow transit, and rectal prolapse
55
Q

How come increasing the fibre content (generally in low severity cases) can lead to softening of stools?

A
  • the fibre absorbs the fluids, swells and activates the stretch receptors + stimulates motility
56
Q

What is diarrhea?

A
  • Rapid movement of fecal matter through the large intestine
57
Q

What are the two main causes of diarrhea?

A
  1. ORGANIC–> Inflammation of the lining of the large intestine (ulcerative collitis)
  2. FUNCTIONAL–> e.g. Lactose intolerance –> can’t be chemically broken down (soluble globules sitting in large intestine–> H2O is OSMOTICALLY drawn in)
58
Q

What is the treatment for diarrhea?

A
  • Treating underlying cause

- Oral fluid and electrolyte replacement

59
Q

What is stetorrhea?

A
  • Fat malabsorption

- Can’t digest fats–> results in smelly, pale and fatty stools

60
Q

What triggers the defication reflex and what is the pathway?

A
  • MASS movement triggers peristaltic wave from sigmoidal colon –> rectum –> stretch receptors activated in wall of sigmoidal colon
  • Synapse on S.C–> activation of PNS + myenteric nerves (contractions) innervating rectal wall and internal anal sphincter–> stool moves into anal canal–> SUBMUCOSAL NERVES ACTIVATED–> MUCOUS lubricates stools
  • Internal anal sphincter RELAXES
61
Q

When is the submucosal part of the enteric nervous system active?

A
  • In the defication reflex when mucous is secreted to lubricate the stool and in the gastric phase of HCl secretion
62
Q

What is retrograde peristalsis and when does it occur?

A
  • When feces move back up to sigmoidal colon

- Occurs when you hold on from doing poo

63
Q

When holding onto stool, which 3 events occur?

A
  1. Relaxation of the internal anal sphincter
  2. Contraction of the external anal sphincter
  3. Contraction of the rectum
64
Q

What is the default mode of the external anal sphincter?

A
  • Closed (contracted)
  • Get signals from cerebral cortex (inhibition of somatic motor nerves) innervating external anal sphincter–> relaxation of the external anal sphincter
65
Q

What are the 5 digestive processes that occur in the stomach?

A
  1. Acts as a STORAGE AREA
  2. Mechanical digestion and propulsion –> peristaltic waves (churning/pyloric pump)–> mixes food with gastric secretions to form CHYME –> chyme empties into the duodenum
  3. PROTEIN digestion initiated (pepsin)
  4. INTRINSIC FACTOR (needed to ABSORB vit B12) –> maturation of RBCs
  5. Absorption of a few FAT SOLUBLE substances–> fats slowly emptied from stomach –> 20% of alcohol absorbed (fat slows alcohol absorption)
66
Q

Where do stomach secretions come from in stomach?

A
  • GASTRIC glands

- 4 main secretory cells

67
Q

What are the 4 types of secretory cells?

A
  1. Mucous cells
  2. Parietal cells
  3. Chief cells
  4. Enteroendocrine cells
68
Q

What is the general function of mucous cells?

A
  • Lubricating food
69
Q

What is the general function of parietal cells?

A

Secrete H+ (as HCl) and intrinsic factor

70
Q

What is the general function of chief cells?

A
  • Secretes pepsinogen (inactive form of pepsin)
71
Q

What is the general function of enteroendocrine cells?

A
  • Secreting histamine and gastrin
72
Q

Which two factors stimualte acid secretion ?

A
  • HISTAMINE (ECL cells) and Gastrin
73
Q

what is the optimum pH for pepsinogen–> pepsin?

A
  • 2-4
74
Q

What are three reasons why gastric juices are so acidic?

A
  1. To activate pepsin (pepsinogen –> pepsin)
  2. To KILL pathogens (steralise meal)
  3. To break down cellulose
75
Q

What do the parietal cells secrete H+ ions against?

A
  • their concnetration gradient

- [H+} in cytosol of parietal cells

76
Q

What feature do parietal cells have that indicate they would undergo active transport?

A
  • MANY mitochondria –> active transport–> lumen (secreted into lumen)
77
Q

What is the process that is occurring all the time in the parietal cells (cytoplasm)?

A

Co2 + H2O–> H2Co3–> H+ + HCO3-

78
Q

What does the anion exchanger do in parietal cells?

A
  • Ecxchanges HCO3-(goes into veins of stomach) for Cl- ions (veins of stomach going INTO parietal cells)
79
Q

Why are the veins draining the stomach more alkaline than the arteries supplying the stomach?

A
  • “alkaline tide”

- HIGH [HCO3-] –> acts as a buffer and mops up free H+ ions –> pH increases

80
Q

How do we INCREASE acid secretion through a meal?

A
  • Gastrin (G type receptor), Histamine (H type receptor), Ach (PNS + enteric secrete Ach (muscarinic receptors)
  • these cause (via 2nd messenger) INSERTION of proton pumps into luminal membrane
81
Q

What happens when you eat a juicy hamburger and delicious chips?

A
  • Parietal HCl secretion is activated by nerves and hormones when ingesting meal and there are different stages we go through
82
Q

Which stages is the digestion of a meal composed of? -

A
  1. Cephallic stage
  2. Gastric Phase
  3. Intestinal phase
83
Q

What occurs in the cephallic phase of HCl secretion?

A
  • Stimuli: Smell, taste, vision, sound (food cooking/frying), mastication
  • Pathway: From the brainstem–> medulla oblongata–> activation of the vagus nerve (PNS)–> inervate parietal cells and G cells –> Gatrin and Ach secretion
  • Ach causes direct H+ secretion
  • Gastrin acts on ECL to release HISTAMINE –> acts on receptors on parietal cells to INCREASE ACID SECRETION
  • peptides and amino acids stimulate G cells to secrete gastrin
84
Q

What are the stimuli for the cephallic phase?

A

Stimuli: Smell, taste, vision, sound (food cooking/frying), mastication

85
Q

What is the pathway for the cephallic phase?

A
  • Pathway: From the brainstem–> medulla oblongata–> activation of the vagus nerve (PNS)–> inervate parietal cells and G cells –> Gatrin and Ach secretion
  • Ach causes direct H+ secretion
  • Gastrin acts on ECL to release HISTAMINE –> acts on receptors on parietal cells to INCREASE ACID SECRETION
  • peptides and amino acids stimulate G cells to secrete gastrin
86
Q

What occurs in the gastric phase of HCl secretion?

A

Stimuli: Stretch of stomach wall, INCREASE in pH, partially digested proteins
PATHWAY: Enteric (local) submucosal secretions + ONS nerves (vagal) –> innervate parietal cells and G cells –> release gastrin and Ach –> Gastrin acts on ECL–> histamine release–> acts on receptors of parietal cells to INCREASE hydrogen secretion

87
Q

What are the stimuli for the gastric phase of HCl secretion?

A
  • Stimuli: Stretch of stomach wall, INCREASE in pH, partially digested proteins
88
Q

What is the pathway for gastric phase of HCl secretion?

A

PATHWAY: Enteric (local) submucosal secretions + ONS nerves (vagal) –> innervate parietal cells and G cells –> release gastrin and Ach –> Gastrin acts on ECL–> histamine release–> acts on receptors of parietal cells to INCREASE hydrogen secretion

89
Q

What occurs in the intestinal phase of HCl secretion?

A
  • STIMULI: Stretch of the duodenal wall, DECREASE in pH
  • PATHWAY: Intestinal endocrine secretions (enterogastrones: secretin, GIP)–> decrease Ach, Gastrinm Secretion of HCl to INCREASE pH
  • Inhibition of vagal nuclei in medulla and local neuronal reflexes
90
Q

Why are proton pump inhibitors better to treat excessive HCl secretion than having a drug that blocks the histamine receptor?

A
  • Because you are blocking GASTRIN, HISTAMINE, and Ach all in one SO MORE EFFECTIVE RESULT!!
91
Q

What are the causes of gastric ulcers?

A
  • High acid/pepsin content
  • Irritation
  • Poor blood supply (lacks oxygen)
  • Poor mucous secretion (HCO3- is in mucous)
  • Helicobacter pylori
92
Q

treatment for gastric ulcers?

A
  • PPIs + antibiotics (if for H.pylori)
93
Q

What is the pH of bile roughly?

A
  • Neutral (7.8)
94
Q

Where is bile synthesized and secreted from?

A
  • Synthesized and secreted from LIVER
95
Q

Where is bile stored between meal?

A
  • Gallbladder via the cystic duct
96
Q

What is the rough pathway for the emptying of bile into the duodenum?

A
  • Made in LIVER
  • 2 bile ducts in liver join to make the COMMON HEPATIC DUCT
  • Bile empties via a common BILE duct
  • empties into duodenum via sphincter of Oddi
97
Q

What do bile salts do?

A
  • Help in emulsifying the fats in small intestine
98
Q

What is the precursor of bile salts?

A
  • Cholesterol
99
Q

What does lecithin do?

A
  • combines with bile salts to emulsify fats
100
Q

What is the composition of bile?

A
  • bile salts
  • cholesterol
  • Lecithin
  • Electrolytes anad H2O (HCO3- very high)
  • Bile pigments (from breakdown of haem)
101
Q

Why is bile green?

A
  • biliverdin pigment
102
Q

What is the main enzyme that breaks down fat in the body?

A
  • PANCREATIC LIPASE
103
Q

What can pancreatic lipase work on?

A
  • Only on the surface of fats
104
Q

What do bile salts and lecithin do to help pancreatic liapse?

A
  • They emulsify fats (into smaller bits) so pancreatic lipase can get access to the fats
105
Q

What is a property of pancreatic lipase?

A
  • It is amphipathic (both hyrophobic and hydrophillic parts)
106
Q

What allows for the emulsification of fats (physically)?

A
  • HUGE fat globules EMPTY into the duodenum –> SEGMENTING contractions of small intestine will churn fat into smaller droplets (1mm diameter)
107
Q

What is inside the emulsification droplets?

A
  • Triglycerides
  • Fat soluble vitamins
  • Phospholipids
  • Emulfisying agents
108
Q

What does the bile salts wrapping around the outside of the emulsion droplets prevent?

A
  • Bc. is-ve charge, prevents droplets from coming back together
109
Q

How does pancreatic lipase break down fat droplets?

A
  • Co-lipase (pancreas) also released with pancreatic lipase
  • Co-lipase binds to pancreatic lipase and FORCES BILE SALTS OFF allowing the pancreatic lipase to access the tryclycerides to BREAK DOWN
  • triglyceride–(lipase)–> monoglyceride + FAs –> diffuse across intestinal epithelial cells (across gut wall)
110
Q

What is a potential drug for obestiy?

A
  • Xenical (pancreatic lipase inhibitor)
  • bit side effects are steathorrhea, and blocks uptake of fat soluble vitamines (A,E,K)
  • Also people regain weight after 9-12 months
111
Q

What does acidity cause in the regulation of bile secretion? *

A
  • Acidity causes the gut hormone cells lining the duodenum to secrete SECRETIN (natures antacid) –> this goes to the liver and causes a secretion of alkaline fluid from bile ductal cells
112
Q

What do fats cause in the regualtion of bile secretion?

A
  • Cause CCK (cholecystokinin) to be secreted which causes the constriciton of the gall bladder and relaxes the sphincter of Oddi
113
Q

What is the pathway for the regulation of bile secretion?

A
  1. Acidic fatty chyme entering duodenum causes release of CCK and secretin from duodenal wall enteroendocrine cells
  2. CCK and secretin enter bloodstream
  3. Bile salts and secretin (via bloodstream) stimulate liver to produce bile more rapidly
  4. Vagal stimulation causes weak contractions of galbladder
  5. CCK (via bloodstream) causes gallbladder to contract and sphincter of Oddi to relax (bile enters duodenum)
  6. bile salts are reabsorbed into the blood
114
Q

What are 5 actions of CCK?

A
  1. Contracts the gall bladder
  2. Relaxes sphincter of Oddi
  3. Acts on enzyme synthesising cells –> secretes pancreatic lipase
  4. Acts on STOMACH to inhibit churning (fat needs to empty slowly)
  5. CONSTRICTS the pyloric sphincter (slows the emptying of fatty chyme)
115
Q

Where is CCK secreted from ?

A
  • enteroendocrine cells
116
Q

Are the majority of bile salts absorbed in the body?

A
  • YES! 95% reabsorbed/recycled via the Hepatic Portal vein
117
Q

Where is amylase active?

A
  • In the MOUTH and at the start of duodenum to end of ileum
118
Q

Why does the amount of starch stay the same from the end of oesophagus to the start of duodenum?

A
  • becasue otherwise proteases will break it down!!
119
Q

What will a partient with pancreatitis show for the breakdown of starch?

A
  • Some breakdown of starch in the mouth but after that there will be no activity
120
Q

Which enzyme do pancreatic secretions and salivary glands contain?

A

-Amylase

121
Q

Where are the protein digesting enzymes the most active?

A
  • At the end of the oesophagus/start of stomach (pepsinogen–> pepsin) –> end of ileum (small intestine)
122
Q

Which parts of the digestive system contain the protein digesting enzymes?

A
  • Stomach and duodenal secretions
123
Q

Where is trypsin most active?

A
  • at the start of the duodenum (top of the duodenum)
124
Q

How is acidic chyme released from the stomach, neutralised in the duodenum and why is it necessary for protein digestion?

A
  • Trypsin released via Sphincter of Oddi to TOP OF DUODENUM
  • trypsin needs an ALKALINE environment
  • Chemoreceptors DETECT H+ ions and enteroendocrine cells can RELEASE SECRETIN (natures antacid) into the bloodstream
  • Goes to liver and causes the release of bile (bile ductal cells rich in bicarb)
  • Also acts on pancreatic ductal cells (exocrine function) to RELEASE PANCREATIC SECRETIONS (which neutralise)
125
Q

What kind of environment does trypsin need for optimal activity?

A
  • Alkaline environment
126
Q

What does membrane bound enterokinase do?

A
  • Converts trypsinogen–> active trypsin
127
Q

how is bile beneficial for chemical digestion of lipids?

A
  • Lecithin and bile salts break down fat

- Allows more SA for pancreatic lipase to break down triglycerides (get access to them to make FA + glycerol)

128
Q

How is bile triggered following the digestion of a meal?

A
  • CCK released from enteroendocrine cells in response to detection of fat
  • RELAXATION of sphincter of Oddi and more contractions of gall bladder –> to allow more bile and secretions to come through
129
Q

Where is lipase the most active from?

A
  • The end of stomach to end of ileum as it is in more contact with fats
130
Q

if a baby is suspected to have hirschprungs disease, what symptoms would there be and what would you do to test for it?

A
  • If baby doesn’t pass stool in the first 48 hours

- to test for it: stain for meconium (substance in newborn poo) OR do a biopsy and stain for Ach precursors

131
Q

What is the treatment for Hirschprungs disease?

A
  • Until the age of 5 not much is done, but after then, the section can be removed and they may have to ahve a colonic bag–> bc. loss of all intrinsic nerves

BMS2031 (7 decks)

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