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gastrointestinal tract Flashcards

1
Q

What does the GI tract consist of?

A

Alimentary canal and accessory organs

Mucosa- epithelium, lamina propria, muscularis mucosae
Submucosa- glands
Muscularis- circular/longitudinal muscle layer
Serosa- c.tissue layer, peritoneum

+ ducts, lymph nodes, good blood supply, nervous tissue

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2
Q

What is the intramural plexus?

A

Myenteric plexus

Submucosal plexus

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3
Q

What does the GI tract do?

A

Breaks down ingested food into small molecules to be taken into body tissue by digestion (chemical/mechanical) and absorption

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4
Q

What are the normal transit times in the GI tract?

A 
Mouth- 1 min
Oesophagus- 10s
Stomach- ~2hrs
Small intestine- 3-6hrs
Large intestine- 1-2 days
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5
Q

What is swallowing?

A
  1. Oral phase (voluntary)
    Tongue compresses bolus against hard palate, respiration inhibited, retraction of tongue forces bolus into pharynx
  2. Pharyngeal phase (involuntary)
    Bolus pushed from pharynx into oesophagus, soft palate reflected backwards closing nasal pharynx
  3. Oesophageal phase (25cm by 2cm)
    Gravity + upper sphincter relaxes and bolus moved into oesophagus, vagus nerve triggers start primary peristaltic wave, enteric nervous system mediates secondary peristaltic wave, lower oesophageal sphincter relaxes (prevents reflux)
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6
Q

What is the stomach?

A

Two openings-
Oesophagus and duodenum

4 regions-
Fundus, cardia, body, pylorus

  1. Reservoir- stores food
  2. Prep chamber- begins mechanical digestion
  3. Emptying regulator- feedback response from duodenum, controls rate of release of calorie, H+ and particles into duodenum
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7
Q

What are the gastric functions?

A

Motility-
~gastric accom- temporary storage
~trituration- dissolve/mix/grind
~gastric emptying- controls delivery to small intestine

Digestion- initiates via gastric juice

Protection- from foreign invasion/mechanical abrasion/prevents autodigestion

Absorption- alcohol and fat soluble drugs

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8
Q

What is stomach lining composed of?

A 
Rugae (allowing stretch)
Lamina propria (ducts from gastric glands to pits on surface for gastric juice)
Muscularis mucosae
Submucosa
Muscularis externa
Peritoneum (serosa)
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9
Q

What is gastric juice?

A

Water ions
HCl-
~low pH, prevents bacterial growth, catalyses cleavage of pepsinogens to pepsin
Pepsinogens
Intrinsic factor (glycoproteins binds to Vit B12 to allow digestion in the ilium)
Mucus
Gastric (hormone produced from G cells, regulates acid secretion)

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10
Q

What are pepsinogens?

A

Proenzyme of pepsin

Breaks proteins into peptides

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11
Q

What are the gastric glands?

A

Cardiac glands- mucus/HCl
Oxyntic glands (acid secreting)- mucus/HCl/pepsinogens/intrinsic factor (aka parietal)
Pyloric glands- mucus/pepsinogens

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12
Q

What is the gastric secretory response?

A

Cephalic phase- sight/smell/thought of food triggers secretion and motility via vagus nerve (parasympathetic)

Gastric phase- physical presence of bolus triggers long (vagal) and short (myentric) reflexes causing peristalsis and gastrin release

Intestinal phase- intestinal gastrin release in response to distention of duodenum +/ products of protein digestion, hormones released to inhibit motility

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13
Q

What is the small intestine composed of?

A

Duodenum
Jejunum
Ilium

Highly coiled, folded and long
Most absorption takes place here

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14
Q

What are the three strata of folding?

A

Plicae- x5
Villi- x10 (light microscope)
Microvilli- x600 (electron microscope)

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15
Q

What does the large intestine consist of?

A

Chyme passes through (water/salt/sugar/vitamins)
~cecum
~ascending colon
~transverse colon
~descending colon
~sigmoid colon
Tenia coli- 3 bands of longitudinal muscle
Haustra- pockets undergoing segmentation (mixing of contents)
Sphincters- internal and external
Tightly packed mucosa- goblet cells- mucus
Peyers patches- local immune protection
Lots of bacteria- fermenting fibre and communicating w host cells

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16
Q

What are the control mechanisms?

A
  1. Autonomic nervous system
  2. Enteric nervous system
  3. Gut peptides (paracrine and endocrine)

-long and short reflexes, peristalsis and motility, secretion and absorption

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17
Q

How does the ANS play a role?

A 
Stimulates digestion- parasympathetic nerves (vagus and pelvic)
Inhibits digestion- sympathetic nerves
Speeds up and slows down
Flight or flight via rest and digest
Controls some secretions
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18
Q

How does the ENS play a role?

A 
Myenteric plexus and submucosal plexus
Sense luminal contents
Controls muscle and glands
100 million neurons
Contains sensory/motor/interneurone/muscle/glands
Motility and secretion
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19
Q

What are long reflexes?

A

External stimuli
Involves CNS
Alters activity of ENS
Causes changes in motility and secretion

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20
Q

What are short reflexes?

A

Internal stimuli
ENS
Local neural circuits
Cause changes in motility and secretion

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21
Q

What is Hirschprungs disease?

A

Partly/unformed ENS
Congenital disorder
Must be surgically removed

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22
Q

How do hormones play a role?

A

22 hormones secreted by enteroendocrine cells in mucosa

S- stomach, D- duodenum, J- jejunum, I- ilium, C- colon

Gastrin- SDJ
Secretin- DJI
Cholecystokinin- DJI
Glucagon-like- SDJIC
Somatostatin-like- SDJIC

Stimulated by chemical, osmotic and pH
Negative feedback mechanisms

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23
Q

What are enteroendocrine cells?

A

Single cells scattered throughout
Link between luminal contents and capillaries
Densely packed w vesicles
Sense contents and respond via release of hormones into bloodstream

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24
Q

What is the stomach motility like after a meal?

A
  1. Fasting state- quiescent
  2. Meal enters, lower oesophageal sphincter relaxes- fungus + body relaxes=accommodation
  3. Peristalsis- waves push towards pylorus, mixing occurs in antrum
  4. Antral systole- retropulsion pushes some contents back into body and some chyme into duodenum, pyloric sphincter also regulates
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25
What hormones are released to inhibit gastric motility and why?
Gastroinhibitory peptide Cholecystokinin (CCK) Secretin Protects small intestine from being overloaded Keeps food in stomach long enough to be broken down efficiently
26
What is the rate of gastric emptying?
Liquids- 2-3 mins, 80% in half an hour | Solids- lag due to time to reduce particle size (1mm diameter), ~few hours
27
What are peptic ulcers?
Break in mucosal barrier to expose underlying tissue to corrosive action (acid, proteolytic enzymes) Symptoms- abdominal pain, bloating, nausea, vomiting, bleeding (haemorrhage and anaemia)
28
How are peptic ulcers formed?
Endogenous- ~anxiety (parasympathetic output [more Ach, Gastrin] so more acid) ~stress (sympathetic output [more Ad] so less HCO3/mucus] Exogenous- ~diet (alcohol [damages cells, stimulate parietal cell] and coffee [stimulate parietal cell]) Non-steroidal anti-inflammatory drugs (NSAIDs) eg. Ibuprofen ~limits prostaglandin production so less inhibition of acid Helicobacter pylori- bacteria producing proteases and endotoxins which break down tissue and produce inflammatory responses
29
What secretions come from accessory organs into the duodenum?
Pancreas (exocrine gland 85% [acinar cells], endocrine gland 2%[Islets of Langerhans]) Acinus releases water/ions, HCO3 (bicarbonate) and enzymes Islets release alpha cells (glucagon) and beta cells (insulin)
30
What is the pancreas composed of?
``` Acinar cells- polarised epithelial cells Centroancinar cells- mainly HCO3 Islets of Langerhans Intercellular canaliculi Intercalated ducts Intralobular duct ```
31
What do acinar cells consist of?
``` Nucleus Mitochondria RER Golgi body Zygomen granules (vesicles with enzymes) ```
32
What enzymes do the zymogen granules contain?
``` Proteins digested by- ~Trypsinogen- trypsin ~Chymotrypsinogen- chymotrypsin ~Proelastase- elastase ~Procarboxypeptidase- carboxypeptidase ``` Fats digested by- Lipases and phospholipases Nucleic acids digested by- Nucleases Carbohydrates digested by- Alpha-amylase
33
What duodenal feedback mechanisms exist?
Cholecystokinin release into bloodstream in response to proteins and fat= pancreatic acinar cell secretion Secretin release into bloodstream in response to pH<5= pancreatic centroacinar cell secretion (HCO3)
34
Why is the liver important?
Protein synthesis- esp. albumin and clotting factors Storage- triglycerides, glycogen and some vitamins Gluconeogenesis- lipids/AAs into glucose Toxins- conjugation and breakdown Bile synthesis and secretion of bile acids and bilirubin
35
What is bile composed of?
Water/ions- alkaline Bile acids- digestion/absorption of fats and micelles formation Proteins- antibacterial, protect against infection Bile pigments- breakdown products of Hg (bilirubin) Organic molecules- cholesterol, phospholipids etc
36
What does the gall bladder do?
Reservoir, regulates delivery and alters bile composition Absorption- concentrates bile (Na+, Cl-, H2O) Secretion- neutralises and protects (H+, mucin) Motor- expand to accommodate and contract to deliver bile, regulated by- Ach (cephalic phase) 20% CCK (intestinal phase) 80%
37
How is bile delivery regulated?
Secretin- stimulates secretion | CCK- releases by relaxing sphincter of Oddi and contracting gall bladder
38
What are gallstones?
Disruption of balance Calcified stones of cholesterol, bilirubin and calcium Cause sharp pain, infection and inflammation Causes- genetics, body weight, decreased mobility of gall bladder, diet and other diseases such as liver cirrhosis or sickle cell anaemia
39
What is the microvilli brush border?
Large surface area Glycocalyx (unstirred layer) contains enzymes- Maltase, lactase, sucrase, dipeptidases Absorbed pancreatic enzymes
40
How are carbs transported across the border?
Glucose/galactose carrier ~co transport- Na+ dependent via SGLT1 ~energy required to maintain Na+ gradient Fructose ~facilitated diffusion via GLUT2 Lead to capillaries to hepatic portal vein
41
How are proteins digested?
Stomach- gastric pepsin turns it into polypeptides and small peptides Duodenum- pancreatic proteases turns it into polypeptides, small peptides and AAs Jejunum (brush border)- peptidases turns large peptides into small peptides and AAs
42
How are proteins transported across the border?
Peptidase in border breaks down any large peptides Carrier proteins take small peptides and AAs across via active transport Intracellular proteases break down small peptides into AAs The AAs enter capillaries via facilitated diffusion
43
How are lipids digested?
Pancreatic lipase generate monoglycerides, fatty acids and glycerol Bile salts emulsify fats Micelles transported across glycocalyx
44
How are fats transported across the border?
Intracellularly products are reconstituted and packaged into chylomicrons These are exocytosed into the lateral space These are diffused into lacteals which return to system circulation via thoracic lymph duct
45
Why might malabsorption occur?
Absent or defective enzymes Defects in transported proteins Diseases/infections of small intestine Symptoms- steatorrhea (frothy/greasy stool), diarrhoea, weight loss Lactase deficiency- lactose intolerant Coeliac disease- abnormal immune response to gluten, loss of mucosal epithelium Pernicious anaemia- malabsorption of Vit B12 in ileum due to production of antibodies to intrinsic factors
46
What are the main functions of the large intestine?
High mucus secretion to help passage of stool Water reabsorption aided by Cl- absorption in exchange for HCO3- (osmotic gradient) HCO3- buffers acid produced by bacterial fermentation
47
What is the GI tract flora?
ORAL Commensalism bacteria, pathogens eg. Porphyromonas gingivalis STOMACH Helicobacter pylori ``` GUT/LARGE INTESTINE 10^14 microorganisms Primes gut immune system Fibre fermentation Symbiosis between host and bacteria Synthesis of essential nutrients- folic acid, Vit K Aids absorption of Vit B12 ```
48
Why is dietary fibre important?
Regulates motility ~slows gastric emptying ~increase motility of colon-intestine Absorption ~holds water ~slows absorption of nutrients Colonic bacterial substrate Prevents/treats constipation, haemorrhoids and diverticulosis
49
What is gastrointestinal gas?
1-4 pints a day Via swallowed air, neutralised acid or bacterial metabolism, diffusion from blood Esp. Beans (stachyose), onions, cabbage, prunes and nuts Components- Hydrogen, methane (ammonia, hydrogen, sulphide, indole, skatole, volatile amines)
50
What is excreted?
``` Indigestible fibre Bacteria Inorganic material Fat derivatives Desquamated cells Mucus ```
51
What is the normal balance between absorption and secretion like?
Volume moving from blood to gut lumen is less than lumen to blood So absorption is greater than secretion
52
What are the reasons for diarrhoea?
1. Osmotic ~increased solutes in lumen- less water reabsorption ~poorly absorbed substrate ~malabsorption disorder eg. Lactose intolerance ``` 2. Secretory ~increased secretion of water into lumen ~eg. cholera toxin- opens Cl- channel ~laxatives, hormones, drugs (antidepressants), caffeine ~bile acid malabsorption ``` 3. Inflammatory/infectious ~damages absorptive epithelium ~clostridium difficile ~invasive parasites 4. Deranged motility ~altered transit time so less time for water reabsorption ~irritable bowel syndrome
53
What is colon motility like?
The haustra form pockets that contract contents into the next pockets where mixing occurs It can be pushed forwards and backwards Fermentation and water absorption occurs 2-3 times a day a gastro-colic response happens- ~mass movement of matter into aboral end of colon for defecation
54
How is defecation/emptying regulated?
Faeces in rectum cause distension Stretch receptors are activated and afferent signals are sent to the spinal cord Voluntary somatic motor nerves are inhibited allowing external anal sphincter to relax Autonomic symp/para symp stimulate contraction of rectum and relaxation of internal anal sphincter
55
What is continence, incontinence and defecation failure?
Continence- storage- rectal accommodation and sphincter contraction Incontinence- pelvic floor damage, pudental nerve damage Defecation failure- spinal injury, outlet obstruction (eg tumours)
56
What is emesis?
Protective mechanisms to prevent damage to GI tract and ingestion of contaminated/toxic substances Vomiting
57
How are toxins detected?
1. Pre ingestion- smell, sight, taste 2. Pre absorption- toxin detection in lumen, mechanoreceptors and chemoreceptors trigger expulsion (vomiting) Rapid before ends up in bloodstream 3. Post absorption- chemoreceptive trigger zone, in postrema (in medulla oblongata) and outside blood brain barrier which samples blood toxins ~induces nausea to prevent further ingestion ~activates vomit centres —can be activated w emetic drugs
58
What are some appropriate and inappropriate vomiting?
Food poisoning Bowel obstruction Bowel disease Pregnancy Motion sickness Cancer therapy
59
What is nausea?
``` Pallor Sweating Salivation Irregular breathing Increased heart rate Several increased force of retching ```
60
How is nausea conducted in the GI tract?
Retrograde giant contractions into stomach Proximal stomach relaxes to allow Antral motility inhibited to prevent emptying Saliva protects oral cavity/oesophagus Deep inspiration Glottis closure to protect airways Air/saliva drawn into oesophagus- decrease oesophageal pressure Soft palate elevated to prevent entry into nasopharynx Expiration and diaphragm/abdominal contraction- increase intra abdominal pressure Lower oesophageal sphincter relaxes Contents pass into oesophagus Upper oesophageal sphincter relaxes
61
What is the vomiting centre?
Chemoreceptor trigger zone or direct nerve impulses Inputs may be- Higher CNS- pain, injury, sight, smell, fear, memory Vestibular system- motion sickness Via cranial nerve IX and X Irradiance of abdomen- highly emetogenic, indicating that trigger lies within
62
What are enterochromaffin cells?
Releases 5-HT (serotonin) in gut which activates 5-HT3 receptors on vagus nerve This triggers emesis and also enters circulation and acts on chemoreceptor trigger zone
63
How does anti cancer chemotherapy involve vomiting?
Anticipatory- conditioned Acute- enterochromaffin cells release 5HT Delayed- damage to epithelial/cell breakdown products evoke mediator release (5HT again)
64
What are anti-emetics?
Block activation of vomiting centre Ondanstron- 5HT3 antagonist- competes w 5HT For motion sickness- antihistamines eg. hyoscine

growth, development, ageing, nutrition (40 decks)

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