Digestive System Flashcards
Functions of the Digestive System
- Ingestion – active process
- Mechanical processing - structural
- Digestion – chemical breakdown
- Secretion – H 2 O, enzymes, buffers, acid
- Absorption - CHO, lipid, protein, ions, vitamins, water, minerals
- Excretion - Removal of waste
Peritoneum
- A serous membrane encapsulating with peritioneal fluid
- Outer parietal membrane lines the inner surface of the body wall
- Inner visceral membrane covering the organs of the peritioneal cavity (aka serosa)
- 7 L of fluid is moved in/out of
peritoneum each day, only small volume (20 ml) there at any one time
Peritoneum & Disease
Peritonitis
* Abnormal accumulation of peritoneal fluid associated with liver disease/cirrhosis, renal disease, heart failure & infection (laparoscopy)
Clinical signs
* Abdominal swelling/redness
Clinical symptoms
* Severe abdominal pain
* Heartburn/indigestion
Mesentery
- Doubled sheets of “sandwiched”
peritoneum - Forms access route for
blood/lymph vessels & nerves - Organs of GIT suspended/fixed by
mesentery’s within peritoneal cavity
Layers of the GIT (alimentary canal)
- Mucosa
- Submucosa
- Muscularis Externa
- Adventitia / Serosa
Mucosa
- Inner lining; epithelium (enterocytes) & underlying lamina
propria - Epithelium; simple or stratified
- Lamina propria; loose irregular CT, blood/lymph vessels, nerves &
muscularis mucosa
Submucosa
- Dense irregular connective tissue
- Larger blood/lymph vessels
- Exocrine glands (buffers & mucus)
- Submucosal nerve plexus
Muscularis Externa
- Transverse (circular) & longitudinal layers of SM
- Peristalsis (motility) & segmentation
- Myenteric intrinsic nerve plexus
- Regional differences
Muscle layers in the Muscularis
The combination of circular and
longitudinal smooth muscle gives
the tube an ability to perform
complex movements that squeeze
and propel ingesta in the lumen
Serosa
- Outermost layer
- Visceral peritoneum
- Loose irregular CT covered by simple squamous epithelia
- Double layered mesentery, houses vascular and nervous supplies to the GIT
- Adventitia at oesophagus Martini
Control of digestive function
- Motility
- Rate of digestion / absorption
Coordinated via: - Enteric nervous system
- Submucosal & Myenteric
- Long & Short reflexes
- Enterogasterones
- Hormone “like” chemicals secreted locally that impact digestion/absorption
Motility
Rhythmic cycles of contraction induced by pace-setter cells within the muscularis externa (basal electrical rhythm; BER)
* Peristalsis
Esophagus, stomach & SI
* Segmentation
SI - mixing bolus with intestinal secretions
* Haustral
LI - compaction
Controls of Movement in the Digestive System
- Local mechanisms
– Coordinate response to changes in pH or chemical stimuli - Neural mechanisms
– Parasympathetic and local nervous reflexes - Hormonal mechanisms
– Enhance or inhibit smooth muscle
contraction
Short reflexes
- Local stimulus & local effectors (smooth muscle & glands)
- Enterogasterones (gastrin, secretin, CCK, motilin, ghrelin)
Long reflexes
- Cephalic reflexes (smell etc)
- Afferents from GIT to CNS (chemo/mechano/osmo etc)
Cholecystokinin (CCK) Stimulus
Arrival of chyme containing lipids and partially digestive proteins.
Cholecystokinin (CCK) Origin
Duodenum
Cholecystokinin (CCK) Target
-Pancreas
-Gallbladder
-Duodenum
-Stomach
-CNS
Cholecystokinin (CCK) Effects
-Stimulates production of pancreatic enzymes
-Stimulates contraction of gallbladder
-Causes relaxation of hepatopancreatic sphincter
-Inhibits gastric secretion and motion
- May reduce hunger
Enterocrinin Stimulus
Arrival of chyme in duodenum
Enterocrinin Origin
Duodenum
Enterocrinin Target
Duodenum
Enterocrinin Effects
Stimulates mucin production
Gastric Inhibitory Peptide (GIP) Stimulus
Arrival of chyme containing large quantities of fat and glucose
Gastric Inhibitory Peptide (GIP) Origin
Duodenum
Gastric Inhibitory Peptide (GIP) Target
-Pancreas
-Stomach
-Apidose Tissue
-Skeletal Muscle
Gastric Inhibitory Peptide (GIP) Effects
-Stimulates release in insulin by pancreatic islets
-Inhibits gastric secretion and motility
-Stimulates lipid synthesis
-Stimulates glucose use
Gastrin Stimulus
Vagus nerve stimulation or arrival of food in the stomach.
Arrival of chyme containing large quantities of undigested proteins.
Gastrin Origin
Stomach
Duodenum
Gastrin Target
Stomach
Gastrin Effects
-Stimulates production of acids and enzymes; increases mobility
Secretin Stimulus
Arrival of chyme in the duodenum
Secretin Origin
Duodenum
Secretin Target
-Pancreas
-Stomach
-Liver
Secretin Effects
-Stimulus production of alkaline buffers
-Inhibits gastric secretion and mobility
-Increases rate of bile secretion
Vasoactive Intestinal Peptide (VIP) Stimulus
Arrival of chyme in the duodenum
Vasoactive Intestinal Peptide (VIP) Origin
Duodenum
Vasoactive Intestinal Peptide (VIP) Target
-Duodenal glands
-Stomach
Vasoactive Intestinal Peptide (VIP) Effects
Stimulates buffer secretion; inhibits acid production; dilates intestinal capillaries
Function of Oral/Buccal cavity
- Analysis of food
- sensory analysis of food
- Mechanical digestion
- through the actions of the teeth,
tongue, and palatal surfaces; - includes mechanical processing
and mastication
- through the actions of the teeth,
- Lubrication
- by mixing with mucus and saliva
- Limited digestion
- limited chemical digestion of
carbohydrates and lipids
- limited chemical digestion of
The Oesophagus
- Anatomically and functionally, the Oesophagus is the least complex section of the digestive tube.
- The oesophagus begins as an extension of the pharynx in the back of the oral cavity:
– It then courses down the neck
behind the trachea,
– through the thoracic cavity,
– penetrates the diaphragm to
connect with the stomach in the
abdominal cavity
Function of the Oesophagus
– to convey boluses of food from the pharynx to the stomach
- Carries solids and liquids from the pharynx (mouth) to the stomach.
Histology of the Oesophagus
Distinctive features of the oesophageal wall include:
– Non-keratinized, stratified squamous epithelium
– Folded mucosa and submucosa
– Mucous secretions by oesophageal glands
– A muscularis with both smooth and skeletal muscle portions
– Lacks serosa
– Anchored by an adventitia
Muscle Layers in the Oesophagus
Muscular tube from pharynx to stomach:
-Upper 1/3 ; Skeletal Muscle
-Lower 2/3; Smooth Muscle
Upper oesophageal sphincter:
-Skeletal Muscle
-Between pharynx and
oesophagus
Lower oesophageal sphincter:
-Smooth Muscle
-Between oesophagus and
stomach
Deglutition
- 2400 times per day
- every 40s !
- Voluntary & involuntary
1. Buccal phase
2. Pharyngeal phase
3. Oesophageal phase
Deglutition- Buccal Phase
- Voluntary
- Compression of bolus (hard palate)
- Tongue pushes bolus posteriorly
- Soft palate lifts (nasopharanx)
- Bolus enters oropharynx
Deglutition- Pharyngeal Phase
- Involuntary/reflex
- Pre-programmed all or none
sequence - Bolus contacts palatal arches
and uvula - Receptors relay afferents via
trigeminal & glossopharyngeal
nerves to swallowing centre in
medulla. - Efferents to pharyngeal constrictor muscles move the bolus into the oesophagus by constricting the pharyngeal wall
- Elevation of larynx, folding of epiglottis direct bolus past trachea
- Respiration inhibited
Deglutition- Oesophageal Phase
- Involuntary/reflex
- Primary peristaltic waves drives bolus down esophagus (10 s).
- Secondary stronger peristaltic
waves may be required. - Local stretch receptors detect
distension and peristaltic contractions are modified (submucosal & myenteric plexus)
Dysphagia
- Difficulty swallowing
- Oropharyngeal / oesophageal
– Genetic (cleft palate)
– Obstructive (tumor)
– Neurological (stroke)
– Muscular (scleroderma) - Nasogastric tube
- PEG (percutaneous endoscopic gastrostomy) tube
Gastroesophageal reflux disease (GERD)
- Caused by adaptation to chronic acid exposure from reflux oesophagitis
- Mucosa replaced by metaplastic
columnar epithelium - Strong association with oesophageal cancer
Functions of the stomach
- Stores ingested food
- Mechanical breakdown
- Secretes enzymes and acid to break chemical bonds of ingested
food - Secretes intrinsic factor (IF)
Location of the stomach
- Located in the upper left abdomen, inferior to the diaphragm
- The stomach is an expanded
section of the digestive tract
between the Oesophagus and
Small intestine
Anatomy of the stomach
- The most distal and narrow section of the stomach is termed the Pylorus
- As food is liquefied in the stomach it passes through the pyloric canal into the small intestine
- The wall of the stomach is
structurally similar to other parts of the digestive tube - HOWEVER, the stomach has an extra, oblique layer of smooth muscle inside the circular layer
- This aids in the performance of complex grinding motions
Pylorus Location (Stomach)
antrum and pyloric canal adjacent to the duodenum
Cardia Location (Stomach)
superior, medial portion
Fundus Location (Stomach)
portion superior to stomach- oesophageal junction
Body Location (Stomach)
area between the fundus and the curve of the J
Pyloric Sphincterm Location (Stomach)
Guards exit from stomach
Rugae (Stomach)
– Ridges and folds in relaxed stomach
– In the empty state, the stomach is
contracted and its mucosa and submucosa are thrown up into distinct folds called Rugae
– when distended with food, the rugae are “ironed out” and flat
Stomach histology
- Epithelial cells in the mucosa of the stomach are: Simple Columnar cells
- A simple columnar epithelium is a single layer of columnar cells attached to the basement membrane, with oval-shaped nuclei located in the basal region.
- Epithelium is towards the top of the mucosal layer of the stomach.
- Mucosa of the stomach contains many other types of secretory cells.
Stomach layers
- Mucosa
- Simple columnar epithelium - Submucosa
- Muscularis externa
- Oblique fibres
- Circular fibres
- Longitudinal fibres - Serosa
Pyloric glands (Stomach)
Mucous secretion containing
several hormones
Gastric glands (Stomach)
– Parietal cells
– Chief cells
-G Cells (Enteroendocrine cells)
P/D1 cells- fundus (Stomach)
Produce ghrelin; ghrelin increases
before meals to initiate hunger, and decreases shortly after eating to curb hunger
Enteroendocrine cells (Stomach)
G cells: Produce gastrin- stimulates secretion by parietal and chief cells, and contractions of the gastric wall that mix and stir the gastric contents
Chief cells (Stomach)
Secrete pepsinogen – inactive proenzyme; acid in gastric lumen converts pepsinogen to pepsin
(protein digesting enzyme)
Parietal cells (Stomach)
– Intrinsic factor (IF) and HCl
– IF: secreted in stomach; glycoprotein that helps absorb vitamin B12 across intestinal lining
– HCl – denatures proteins, breaks down cell walls, connective tissues, protection, activation of pepsin
Formation of gastric juice (HCL)
–Alkaline Tide
-Gastric juice pH 1.5
1. H+ produced in parietal cell by reduction of CO2 + H2O
2. H+ transported into gastric gland
3. HCO-3 diffuses into interstitial fluid via counter transport with Cl -
4. HCO-3 diffuses into circ, raising blood pH (alkaline tide)
5. Cl- diffuses into gastric gland via Cl- channels
Stomach secretions- Mucous
The most abundant epithelial cells are mucous cells, which cover the entire lumenal surface
–These cells secrete a bicarbonate-rich mucous that coats and lubricates the gastric surface
–Protecting the epithelium from acid and other chemical insults
Stomach secretions- Acid
Hydrochloric acid is secreted from parietal cells into the lumen where it establishes an extremely acidic environment
– Activates pepsinogen
–Inactivation of ingested microorganisms such as bacteria
Stomach secretions- Proteases
Pepsinogen, is secreted into gastric juice from both mucous cells and chief cells
–Once secreted, pepsinogen is activated by stomach acid into the active protease pepsin, which is largely responsible for the stomach’s ability to initiate digestion of proteins
–In the young, chief cells also secrete chymosin (rennin)
*a protease that coagulates milk
protein allowing it to be
retained more than briefly in
the stomach
Stomach secretions- Hormones
The principle hormone secreted from the gastric epithelium is Gastrin
–A peptide that is important in control of acid secretion and gastric motility
–Stimulates secretion by parietal and chief cells, and contractions of the gastric wall that mix the gastric contents
Regulation of gastric activity
Cephalic phase
Gastric phase
Intestinal phase
Cephalic phase
- Prepares stomach to receive ingested material
- Seeing, smelling and anticipating food perceived in the brain and the brain informs the stomach that it
should prepare for receipt of a meal– directed by the central nervous system (CNS) - Parasympathetic nervous system sends a stimulus to the vagus nerve:
–Resulting in release of acetylcholine (Ach) in the vicinity of G cells and parietal cells.
–Binding of Ach to its receptor on G cells induces secretion of the hormone Gastrin (enteroendocrine)
–Acetylcholine, histamine and Gastrin, stimulates parietal cells to secrete small amounts of acid - Additionally, a low level of gastric motility is induced
Gastric phase
- Begins with the arrival of food in the stomach:
– Stomach wall distension and mucosal irritation - Activation of the enteric nervous system and release of gastrin cause vigorous smooth muscle contractions.
–The net result is that secretory and motor functions of the stomach are fully turned on
–lots of acid and pepsinogen are secreted
–pepsinogen is converted into pepsin
–vigorous grinding and mixing contractions take place - However, there is a mechanism in place in the stomach to prevent excessive acid secretion - if lumenal pH drops low enough (less than about 2)
–motility and secretion are temporarily suspended
Intestinal phase
- Controls the rate of gastric emptying
- As food is liquefied in the stomach, it is emptied into the small intestine
- The small intestine needs to be able to slow down gastric emptying, to allow it time to neutralize the acid and efficiently absorb incoming nutrients
- Hence, this phase of gastric function is dominated by the small intestine sending inhibitory signals to the stomach to slow secretion and motility
–Two types of signals are used: nervous (neural responses) and endocrine (hormonal responses). - Distension of the small intestine, as well as irritation of the mucosa leads to gastric-inhibitory impulses in the nervous system - this nervous pathway is called the enterogastric reflex.
- Secondly, enteric hormones are released from cells in the small intestine and contribute to suppression of gastric activity.
Regulation of Gastric Activity - Summary
- Brain alerts the stomach that it should expect arrival of a meal
- Stomach comes out of its inter-digestive resting and begins low level motor and secretory activity (cephalic phase)
- After a meal is consumed, the gastric motor and secretory activity is fully turned on (gastric phase)
- If the meal is at all substantial, the gastric phase is periodically suppressed by signals from the small intestine (intestinal phase)
- Eventually, the meal is fully liquefied and emptied, and the stomach falls back into a state of very low motor and secretory activity, where it remains until the next cephalic phase
Digestion and absorption in the stomach
- Ingested food reaches stomach- salivary amylase and lingual lipase continue the digestion of carbohydrates and lipids
- Preliminary digestion of proteins
–Pepsin: breaks down proteins into smaller peptide and polypeptide chains
–Protein digestion not completed in the stomach - Carbohydrates, lipids, and proteins only partially broken down
- Very little absorption of nutrients because:
1. the mucus covering the epithelial cells means that they are not directly exposed to chyme
2. the epithelial cells lack the specialized transport mechanisms of cells that line the small intestine
3. the gastric lining is somewhat impermeable to water
4. digestion has not been completed by the time chyme leaves the stomach - Some drugs (aspirin, anti inflammatory) are absorbed
