Lecture 5 Flashcards
What are the 4 concentric tunics/layers of the gut tube?
- Mucosa
a) Epithelium
b) Lamina Propria
c) Muscularis Mucosae - Submucosa
- Muscularis Externa
- Adventitia/Serosa (Visceral Peritoneum)
+series of glands outside of tube proper (empty secretions into tube)
What is located outside of the 4x concentric tunics/layers of the gut tube?
Outside tube proper, is series of glands, which empty secretions into the tube
What is the function of the mucosa’s epithelium?
- Protection- multiple layers (if you lose superficial wont bleed/sacrificial layer)
oesophagus, stomach, salivary glands, pancreas, liver, small intestines - Secretion
- Absorption
-combination dependant on area
What is the function of the mucosa’s lamina propria?
- Support-
a) mechanical support through CT/collagen (structural and physical support)
b) functional support (BV nerves lymphatics embedded in CT)
What is the function of the muscularis mucosae?
Boundary between mucosa and submucosa
1. Movement: “muscle of the mucosa”. allows movement Independent of peristalsis to occur
What is the function of the submucosa?
Loosely arranged in gut to allow expansion when bolus of food moves through gut tube
(Same function as Lamina Propria)
1. Support-
a) mechanical support through CT/collagen (structural and physical support)
b) functional support (BV nerves lymphatics embedded in CT)
What is the function of the Muscularis Externa?
- IC/OL usually (Inner Circular and Outer Longitudinal)
Exception: Stomach (additional inner oblique) - INvoluntary Control of Smooth muscle
Exception: a) Oesophagus when swallowing voluntary b) anal sphincter
Sphincters= usually thickening of IC inner Circular layer of Muscularis Externa
What is the role of sphincters?
Gate keepers
control flow and direction and timing and amount of substance
going from one end of the tube to another
-usually thickening of IC (inner circular) layer of Muscularis Externa
Adventitia
Outer most CT connective tissue covering
of any organ, vessel or other structure
-(vessel): Tunica Adventitia outer most layer of BV, connecting BV to adjacent structures
Serosa
“Visceral Peritoneum”
Slippery outer covering for gut tube
2x layered
outer mesothelium sits on a bed of CT connective tissue
Production of Serous Fluid
Peritoneum produces 7Litres of serous fluid every day
Is reabsorbed and Recycled
Aberent/changes to serous fluid production= Ascites and Peritonitis
Ascites
Unusual conditions (e.g. liver disease, heart failure, electrolyte imbalance)
(esp. with cirrhosus/other liver diseases)
- can be drained/managed
- cancer patients can also display ascites
a) (change in blood hydrostatic pressure causes) Accumulation of fluid (in peritoneal space)
b) abdominal swelling
c) distortion of visceral organs
- distented obvious superficial BV (portal hypertension)
Peritonitis
Physical damage, chemical irritation, bacterial invasion (complication from surgery)
Inflammation interferes with normal function
Nervous control of gut
Enteric System Nervous Plexi:
a) Submucosal (Meissner’s) nerve plexus (embedded in submucosa)
b) Myenteric (Auerbach’s) nerve plexus (b/w IC and OL of muscularis externa)
- Gut’s own Enteric NS (controls itself/second brain). Own afferent and efferent nerves
-heavily under Autonomic NS influence (ANS) (each salivary gland receives both sympathetic and parasympathetic stimulation)
Increase:
a) sight and thought of food (preparation, presentation, smell, taste, chewing)
b) nausea
Decrease:
a) Fatigue, Sleep, Fear, Dehydration, Exercise
Sympathetic N S
XMX eXercise eMotion eXcitement Inhibits gut function • Predominates at times of activity/stress • Diverts blood to brain and muscles -secretion of a small volume of viscous saliva containing high enzyme concentrations (not mucous to lubricate) -reduced volume produces sensation of dry mouth -blood vessels are constricted (restricts blood flow and secretion)
Parasympathetic N S
PSL rePletion reSt reLaxation Promotes gut function • During and after mealtimes • Stimulate secretion and transportation in the gut tube -accelerates secretion (make saliva), resulting in the production of large amounts of watery saliva -myoepithelial cells contract -increased blood flow (sustains demand for metabolism)
Magnified histological slide of lobule (40x)
Cross section through alveoli/acini of gland (sea of acini)
2x predominant different cell populations
Dark and lightly staining
Three major salivary glands
- Parotid. ~25% of saliva. Serous only (dark) - Munks virus preferential target
- Submandibular. ~70% Serous and Mucous
- Sublingual. ~5% Serous and Mucous
- proportion of 2x cell populations determines whether secretions are watery/serous or sticky/mucousy/viscous
Serous Acinus
- Watery
- Central darkly staining nuclei
- Dark staining acini = Zymogen Granules in cytoplasm of cells (in serous acini)
Zymogen granule = enzyme
b) Predominant enzyme= Amylase (CHO)- particularly in salivary gland.- helps to break down carbohydrates and sugars -good substrate for bacterial growth - Myoepithelial cells: surrounding base of acini cells. Modified epithelial cells. Contractile- help to squeeze acini contents into lumen/propel secretions along
Mucous Acinus
- Viscous/sticky
- Peripheral flattened nuclei
- Lightly staining acini: (peripheral flattened nuclei as) Light staining mucous granules occupying most of cytoplasm (pushing nuclei to periphery)
- Myoepithelial cells: surrounding base of acini cells. Modified epithelial cells. Contractile- help to squeeze acini contents into lumen/propel secretions along
Striated Ducts
Intralobular
Basal infoldings of membranes
Aligned Mitochondria (gives striated appearance)
-Metabolically active
- Active transport
Function: Exchange Na and Cl of K and HCO3-(Bicarbonate)
What are the 7x key components of Saliva?
- Enzyme (serous acini)
- Mucous (mucous acini)
- carbohydrate-rich glycoproteins (mucins) - Bicarbonate (striated ducts)
- 99% water
- assortment of ions, buffers, metabolites, enzymes
What are the 3x key functions of saliva?
- Lubrication
- Protection
a) bacterial adhesion(mucous) and secretion(acidic) (bicarbonate ions HCO3- help counteract bacterial acidic secretions)
b) vomit (acidic) (bicarbonate ions HCO3- help counteract regurgitated gastric contents) - Digestion
Salivary Mucous
Carbohydrate-rich glycoproteins
- help lubrication
- prevent bacterial adhesion
Puking
Oral cavity water rash/influx of saliva
- Reflex protective mechanism
- influx of alkaline basic saliva as last line of defence against acidic regurgitation
Salivary Bicarbonate
Helps counteract
- bacterial acidic secretions
- acidic vomit/regurgitated gastric contents
- Puking:Oral cavity water rash/influx of saliva
- Reflex protective mechanism
- influx of alkaline basic saliva as last line of defence against acidic regurgitation
Salivary Lysozyme
Break down bacterial cell walls
Salivary Lactoferin
Ion Kelater
-helps fight ion dependant bacteria
IgA
Immunoglobulin A
Helps fight bacteria and viruses
Salivary Amylase Enzyme
Amylase: Active range ph 4-11 (optimal ph in middle)
-breaks down sugars into monomers/basic units.
-sugars good substrate for bacterial growth.
therefore breaking down sugars: 1. aiding digestion.
2. indirectly reducing substrate available for bacterial consumption
Salivary Lypase Enzyme
Lipase: optimal ph 4.0
- fat break down.
relatively lower pH
-therefore more active in stomach than oral cavity
Salivary Kallikrein Enzyme
Protease
not really involved in enzyme
-cleave and activate another pro-enzyme
-eventually increases blood flow/supply to salivary glands
(need to increase blood flow to sustain demand for metabolism)
Xerostomia
dry mouth
- Mumps (virus which preferentially targets parotid glands)
- Salivary duct calculi (stones)
- Salivary gland tumours (usually benign)
- Sjogern’s syndrome (SHOH-grinz)- autoimmune condition/generalised dryness
- Medications
Hypersalivation
Watery brash
- Associated with many conditions (inc. peptic ulceration & IBD)
- Medications
- Toxins
Meth mouth
bad teeth
destruction of salivary glands (protection and digestive functions)
a)loss of protective features (amylase, mucous, bacteria in oral cavity etc)
Function of Oesophagus
Rapid transport (peristalsis) of food bolus to the stomach
Straight tube about 25cm long
Thick muscular walls
Protective lining
Contains glands
Collapsed outline with submucosal folds when empty-only expands when bolus travels through
-folds stretch out flat as food descends to the stomach
Epithelium of Oesophagus
Thick sacrificial stratified squamous epithelium (6-8 layers)
Non-keritinized in humans
-small number of keratohyalin granules, not dont undergo true cornification
–>
Transitions into Cuboidal/columnar (as approaches stomach)
Muscularis Mucosae of Oesophagus
Upper: Absent/rare
Near stomach: developed
Longitudinal smooth muscle + elastic network (discontinuous in places)
Permits independant movement and folding of mucosa- which aids digestion and absorption
-poorly preserved(not well definied)/discontinuous in some places
Muscular Externa of Oesophagus
2x thick coats -inner and outer
-Not always circular and longitudinal respectively
-Inner= many spiral and oblique bundles
Outer= also irregularly arranged in many places
Top 1/3 =mostly skeletal (myocites and striations) (voluntary control, voluntary contractions)
Middle 1/3= mixed skeletal and smooth
Inferior 1/3= mostly smooth
Peristalsis vs Segmentation
Sphincters - upper and lower.
-physiological > anatomical.
-NO obvious muscle thickening
-Lower sphincter area has some increase in inner muscle coat
-Tonal contraction
Peristalsis
- Contraction of circular muscles behind bolus
- Contraction of longitudinal muscles ahead of bolus
- Contraction in circular muscle layer forces muscle forward
- peristalsis propels materials along the length of the digestive tract by co-ordinated contractions of the circular and longitudinal layers
Segmentation
Segmentation movements primarily involve the Circular muscle layers
- these activities churn and mix the contents of the digestive tract
- but do NOT produce net movement in a particular direction
Oesophageal covering
Adventitia
-Not lined by mesothelial cells
-b/w trachea and oesophagus
-except for 1-2cm b/w diaphragm and stomach
Retroperitoneal: Anterior and Left Lateral surfaces covered by peritoneum/serosa
Oesophageal Nerves
ANS
Autonomic NS
Co-ordinates movements involved in swallowing
5x Gastrooesophageal diseases
- Achalasia - aperistalsis of oesophagus with a failure of the lower oesophageal sphincter to relax on swallowing
- Neurological disorders (brainstem), neuromuscular disorders, extreme old age
- Gastro-oesophageal disease (GORD)
- Reflux oesophagiti
- Barett’s oesophagus
Swallowing
If swallowing goes down wrong tube
-cough- lungs trying to expel fluid from airtube/trachea
Epiglottis prevents choking whilst ingesting. Covers glottis/entrance to trachea. Helps redirect food down correct tube
“Barium swallow”
Trachea-normally open. Anterior to oesophagus
Trachea
Normally open
C-shaped cartilage ring- helps to keep it permenantly open -even when -ve pressure allowing us to breath in and out
-Trachealis muscle
Anterior to oesophagus
Adventitia (not lined by mesothelial cells) b/w itself and oesophagus
Oesopageal Submucosa
- Loosely packed= can expand an compress as required
- if densely packed= little flexibility for movement
Chronic Oesophagitis –> Barretts Oesophagus
Gastric Oesophageal Reflux reduce
gastric juices reflux back into oesophagus
normally lower oesophageal sphincter prevents (but not fool proof)
-chronic gastric acid exposure= lead to pesophagitis (oesophagus inflammation)
-stratified squamous epithelium protects against Physical abrasion Not Chemical
Ulcer = epithelium digested away
Chronic acid Exposure: Transformation/Metaplasia from stratified squamous –> glandular/stomach like epithelium
-Precursor to oesophageal cancer
Adenocarcinoma (from Barrett’s Oesophagus)
Oesophageal Varices
Portal hypertension due to elevated pressure in liver, due to obstruction chirrosus
=Backflow of blood into Dilated BV
-Weak veins, over worked andover filled
Very dangerous- bleed and heamorahage easily
-massive blood loss (with serious consequences)
Stomach
Storage tank Secretion, Sterilisation and Digestion -some absoportion J-shaped bag approx 1.5L capacity 4x key (3x histologically distinct) regions - Cardia, fundus, Body, Pylorus 2x Sphincters: LOS Lower Oesophageal Sphincter + Pyloric Sphincter Additional Inner Oblique layer
Rugae
Transient folds of the stomach
Empty= prominant
Full/contracting = less
Cardia
cardiac glands
Mucus
“buffer zone”
Body
Parietal (Oxyntic) glands -HCL -Intrinsic Factor -Pepsinogen -Somatostatin "business end" -where Acid is produced -fundus and body is often where most activities are restricted to -digestion + chewing to produce Chyme
Pylorus
Pyloric Glands
- Pepsinogen
- Mucus (predominant)
- Gastrin
- Somatostatin
- dont want chyme to be conc. acid, therefore mucus production
Simple columnar mucous cells of the stomach
Of surface and pits
Elongated nucleus
Insoluble, Alkaline/neutral glycoprotein
forms a protective mucous bicarbonate barrier sheet above the epithelium
1. -Produces mucous coat/gel layer. a) Mechanism of defence to stop stomach from digesting itself.
b) helps trap bicarbonate HCO3-, to counteract acidic lumenal contents
2. -Protects itself by high rate of differentiation and replacement by Undifferentiated stem cells when damaged
3. -enriched phospholipids in membrane, acting as additional barrier
4. -Prostaglandins: derivatives of fatty acids. Hormone like activity. E2 especially is protective, stimulating production of mucous and phospholipds
5. Helicobacterum Pylori= Major cuase of stomach ulcers, a) produces urease, which converts blood’s urea into ammonia, which attacks and degrades mucous coat. b) produces toxins damages epithelial cells c) releases ulcerogens (PAF Platelet Activating Factor) which is negative.
Mucous Neck cells of the stomach
of gastric glands Expanded apex Basal Nucleus Soluble Acidic glycoproteins secreted when food is present (like dissolves like, when there is active digestion the slighlty acidic mucous helps it to digest better Mucous granules are less densely packed
Undifferentiated stem cells of the stomach
Simple columnar Epithelium protects itself by high rate of differentiation and replacement by Undifferentiated stem cells when damaged
+
Differentiates into specialised Parietal/Oxyntic cells
Parietal cells of the stomach
Oxyntic cells
Releases HCl, intrinsic factor
Intracellular canaliculi
1. HCl: a) Sterilise food b) acidify environment.
-chief cell’s Pepsinogen pre-enzymes are converted by acidic environment (created by parietal cell’s HCl) into active pepsin
-aberent/insufficent parital cell activity/insufficient HCl production = Decreased Digestion + LEss bacteria killes leading to Gastroenteritus
2. Intrinsic Factor: Vit B12 absorption = needed for RBC heamatopoiesis (aberent parietal acitivity can lead to Pernicious Anaemia (autoimmune diseases that attack parietal cells themselves))
OH- converted to HCO3-. exchanged for Cl-. diffuses into venous blood leaving that stomach
-Produces protective bicarbonate ion
Chief cells of the stomach
Zymogenic cells
Pepsinogen (inactive form of pepsin enzyme) secreted into gland’s lumen
-Pepsin= helps cleave proteins
Zymogen granules
Enteroendocrine cells
Secretory granules G cells= gastrin ECL cells= histamine D cells= somatostatin Hormone liberated through basal lamina into capillaries of lamina propria
