WEEK 2 Flashcards
What is the difference between children and young people?
CHILDREN = people who are probably not mature enough to make important decisions themselves
YOUNG PERSON = those who are mature enough to make important decisions about themselves
As well as clinical best interests, what other things should be considered? (HINT: there’s 6 things)
- The views of the child or young person (so far as they can express them)
- Views of the parents
- Views of others close to child/young person
- Cultural, religoud or other beliefs and values of child/parents
- Views of other healthcare professionals who have an interest in their welfare
- Which choice (if more than one) will LEAST restrict the child/YP’s future options
Gillick competence is when a young person under 16 has the capacity to make a relevant decision. How is said competence determined?
If they can understaind, retain, use/weigh and communicate this decision
Why is consent more easily accepted than refusal?
As Dr only needs 1 ‘key’ to unlock consent
3 keys potentially exist in the case of the mature minor
- mature minor
- parents
- courts
What is the current law for minors being organ donors?
SCOTLAND - anyone under age of 16 cannot
ENG, WALES and N.IRE - solid organ donation by living children permitted
BMA used to be opposed but now support so long as young person competent to give valid consent
What is the current law with regards to minors and euthanasia?
NETHERLANDS - legal for those over 12 y.o
(Dutch paeds association want age limit to be lifted altogether)
BELGIUM lifted all age restrictions in 2014
Define (i) generic substitution (ii) therapeutic substitution.
(i) occurs when a different formulation of the same drug is substituted. All generic variation sof a drug are considered by the licensing authority to be equivalent to each other and to the originator drug.
(ii) the replacement of the originally-prescribed drug with an alternative molecule with assumed equivalent therapeutic effect. the alaternative drug may be within the same class or from another class with assumed therapeutic equivalence
What are the (i) advantages and (ii) disadvantages of the oral route?
(i) cheap, safe and convenient
(ii) patient compliance, variation in bioavailability of drug
What are the 5 types of oral routes that can be used to administer a drug?
- BUCCAL/SUBLINGUAL MUCOSA
- direct absorption into blood
- avoids 1st pass metabolism
- not ideal surface for absorption - GASTRIC MUCOSA
- enteric coating to prevent absorption before reaching SI - SMALL INTESTINE
- this is the main site of drug absorption
- large S.A, more neutral pH - LARGE INTESTINE/COLON
- poor absorption, long transit times - RECTAL MUCOSA
- direct to systemic circulation
What are the 4 ways that small molecules cross cell membranes?
- Diffusing directly through the lipid
- lipid solubility is highly important for this - Diffusing though aqueous pores
- mostly for diffusion of gases - Transmembrane carrier protein e.g. solute carriers
- Pinocytosis
- mostly macromolecules, not drugs
In general what does food tend to do to the rate of gastric emptying?
Slows it
What are the reasons for a drug to have (i) decreased absorption (ii) delayed absorption (iii) increased absorption?
(i) intestinal motility, interactions with food acids, pre-systemic metabolism
(ii) gastric emptying
(iii) poorly water soluble drugs, increased solubilisation and decreased pre-systemic metabolism
Describe/explain the first pass metabolism of Levodopa, a prodrug used to treat Parkinson’s disease.
Rapidly taken up from stomach and small intestine by a large neutral amino acid transport carrier (LNAA)
- DOPA decarboxylase is present in gastric mucosa
What effect do the following drugs have on absorption: (i) Antacids, proton pump inhibs (ii) laxatives, anticholinergics (iii) vasodilators (iv) neomycin (v) tetracycline, calcium, Mg (vi) cholestyramine (vii) charcoal.
(i) change is gastric or intestinal pH
(ii) change in GI motility
(iii) change in GI perfusion
(iv) interference with mucosal function
(v) chelation
(vi) resin binding
(vii) adsorption
What is the effect of intestinal disease on Gi motility?
Altered rate of drug absorption due to the diseases state
e. g. increased motility, compromised GI integrity
- Crohn’s, coeliac.
What are the 6 factors which affect oral absorptions?
- Particle size and formulation
- GI motility
- 1st pass metabolism (by gut wall or hepatic enzymes)
- Physiochemical factors (direct drug interactions, dietary factors, varying pH)
- Splanchnic blood flow (increased flow decreases absorption)
- Efflux pumps
What are the (i) key biological factors (ii) key drug factors?
(i) blood flow, surface area, metabolic enzymes, compartment pH
(ii) lipid solubility, weak acid/base, charge, size
THE FOREGUT: (i) where does it lie? (ii) What is it supplied by (referred pain)? (iii) What does it give rise to?
(i) Extends from the mouth to just distal to the developing liver
(ii) Coeliac trunk - refers pain to epigastrium (T7-9)
(iii) oesophagus, stomach, proximal duodenum, liver and biliary system, pancreas and spleen
By what week of development does the stomach appear? Describe its various ways of rotation.
4th week
- 90 degrees clockwise around longitudinal axis so that the left side faces anteriorly, the lesser curve faces to the right and greater curve faces left
- AP axis so pyloric part lies on right and oesophago-gastric junction slightly left so that the greater curve faces left and anterior
Initially the duodenum is found in the midline, what happens to it during embryological development?
The rotations of the stomach also cause the duodenum to rotate and swing to the right (mainly AP rotation)
- then ‘falls’ on the posterior abdominal wall and becomes retroperitoneal
When does the liver develop? What does it develop from? What 2 things does it give rise to?
During the 3rd week from an endodermal bud
- gives rise to the hepatic ducts and gall bladder
What does the pancreas form from? How is it that it comes to lie in the curve of the duodenum?
Forms from dorsal and ventral endodermal buds from duodenum
- rotation of duodenum causes ventral bud to migrate around to lie behind and fuse with the dorsal bud => lying in the curve
What is an annular pancreas?
the ventral pancreas may form as 2 lobes, which then form an obstructive Annular Pancreas.
What makes up the ventral mesentery with regards to the stomach? When the stomach rotates longitudinally, what way does the mesentery shift?
Lesser omentum
Falciform ligament
- shifts to the right (dorsal mesentery shifts to left)
When the stomach rotates antero-posteriorly, what happens to the (i) liver (ii) free edge of the lesser omentum?
(i) thrown upwards under the diaphragm
(ii) lies almost vertically between the liver and the duodenum
What are the boundaries of the opening into the lesser sac (epiploic foramen)? (anterior. posterior, superior and inferior)
ANTERIOR - free border of lesser omentum, with the bile duct, hepatic artery proper and the portal vein
POSTERIORLY - IVC
SUPERIORLY - caudate process of caudate lobe of liver
INFERIORLY - 1st part of duodenum.
What are the boundaries/relations of the lesser sac?
ANTERIOR - caudate lobe of liver, lesser omentum, stomach
POSTERIOR - pancreas
LATERALLY - left kidney and adrenal gland; on the right epiploic foramen
- extends up as far as diaphragm and down, it may extend a little way between the layers of greater omentum.
How is the greater omentum formed to hang off of the greater curve of the stomach?
As the stomach rotates on its AP axis and the greater curve faces inferiorly, the dorsal mesentery is dragged with it so that a big, double-layered fold of mesentery (greater omentum) hangs off the greater curve
How is the extent of the lesser sac decreased?
From the fact that the layers of the greater omentum and the transverse colon fuse with each other
What mesentery does the spleen form within?
dorsal
What is the (i) lienorenal ligament (ii) gastrolineal/gastrosplenic ligament?
(i) mesentery (double layers) of peritoneum between the spleen and posterior abdominal wall (close to kidney)
(ii) double layer between the spleen and stomach
In adults, what does the tail of the pancreas extend into?
The lienorenal ligament
THE MIDGUT: (i) where does it lie? (ii) What is it supplied by (referred pain)?
(i) commences immediately distal to the entrance of the bile duct into the duodenum and ends 2/3 along the transverse colon
(ii) Superior mesenteric artery - pain refers to peri-unbilical region (T10)
How is the midgut connected to the yolk sac during embryological development?
By the vitelline duct
What are the various types of rotation which occur to the primary intestinal loop?
Rotates in a counter clockwise direction - 90 degrees in physiological hernia
- then another 180 degrees as the loop drops back into the abdomen at about 70 days (10 weeks)
- overall there is about 270 degrees of rotation around the axis of the superior mesenteric artery
What types of congenital abnormalities can occur in the midgut region?
Vitelline duct fistula - faecal discharge at imbilicus
Gastroschisis
Omphalocele
Umbilical hernia
- failure of recanalisation may lead to narrowing or even complete obstruction of the GI tract at any point
THE HINDGUT: (i) What is it supplied by (referred pain)? (ii) What does it give rise to?
(i) inferior mesenteric artery - pain to suprapubic region (T12)
(ii) distal end of transverse colon (1/3), descending colon, sigmoid colon, rectum and upper 2/3 anal canal
What does the most inferior part of the hindgut develop from? What is said structure divided by? What does said structure divide into (i) anteriorly (ii) posteriorly?
From the cloaca, which is divided by the mesodermal uro-rectal septum
(i) urogenital system
(ii) anorectal canal
What are 2 cases where the doctors and parents disagree? Describe these cases and their outcomes.
CASE 1:
- S (parents = Jehovah’s witnesses), 4.5 years old with T cell leukaemia
- undergoing chemo and blood transfusion would improve recover but parents refused (religious and safety reasons) BUT their refusal was overrules
CASE 2:
- A (Jodie and Mary, conjoined twins)
- if remained together, would both die
- if separated, Jodie would live and Mary would die
- Drs wanted to act to separate but parents did not allow
- high court, then court of appeal. Separation took place.
What are the 2 cases with regards to the mature minor? Describe their outcomes.
CASE1 : refusal of life saving blood transfusion on religous grounds - overrules
- 15 y.o boy, jehovah’s witness that refused blood transfusion for his leukaemia
- not enough to know he would die but must understand the ‘manner of his death and the extent of his and his family’s suffering’
(on turning 18, he refused further transfusions and dies
CASE2: Hannah Jones (refusal of heart transplant - upheld)
- PCT sought court order for heart transplant for 13 y.o (had refused and parents agreed)
- CPO said hannah was adamant and refusal was respected
(agreed to transplant the following year and is currently doing well)
Describe the formation of the anal canal.
The distal aspect of the cloaca is closed by a membrane
- as the surrounding mesoderm and ectoderm proliferate, the anal part of the membrane sinks in to the anal pit
- the membrane breaks down at 8 weeks, so that the proximal 2/3 of the anal canal is derived from the hindgut endoderm while the distal 1/3 is derived from rectoderm
What is Hirchsprung disease?
Lack of normal development of the colonic innervation leads to a constricted, agangionic segment of bowel, with a distended segment proximally (of which its innervation is normal)
What are the psychosomatic disorders?
Disorders where emotional or psychological factors can impact on the symptoms
Give 5 examples of psychosomatic disorders.
Asthma Atopic dermatitis Tension-type headaches Chronic fatigue syndrome IBS
What do psychosomatic disorders challenge?
Biomedical model of illness
What is IBS?
A common digestive condition
- your GP may be able to identify IBS based on your symptoms, although blood tests may be needed to rule out other conditions
What are the some of the symptoms and signs of IBS?
- Abdominal pain and cramping - may be relieved by defecation
- Change in bowel habits (diarrhoea or constipation)
- Bloating and swelling of your stomach
- Excessive wind (flatulence)
- Occasionally experiencing an urgent need to go to the toilet
- Feeling that you haven’t fully emptied your bowels after going to toilet
- Passing mucus from your bottom
What is the occurrence of IBS?
20 - 30 years old
more so in women
10-20% of the population
What are the 4 way to manage IBS?
- Diet/lifestyle changes approach
- Drug treatments
- Psychological approach
- Complementary therapies approach
What are the (i) first line (ii) second line drugs used to treat IBS?
(i) - antidiarrhoeal e.g. loperamide
- laxatives (not lactulose)
- antispasmodics
(ii)
- laxatives e.g. linaclotide
- antidepressants: TCAs if first line ineffective, then SSRIs if TCAs ineffective
What are the 3 types of complementary therapies used to treat IBS?
Nutraceuticals
Chinese herbal medicine
Probiotics
What are the 3 types of psychological approaches used after 12 months of IBS treatment?
Cognitive behavioural therapy
Hypnotherapy
Psychological therapy
What are the 5 parenteral routes for drug absorption?
- Subcutaneous
- Intramuscular
- Inhalation
- Intranasal
- Topical
Describe the anatomical location of the oesophagus.
Starts in the midline as the continuation of the pharynx at C6
25cm long x 2cm diameter
Passes immediately posterior to the trachea, anterior to vertebral column, with arch of the aorta to its left in superior mediastinum
Inferiorly it swings forwards and to the left before piercing the diaphragm at T10
Other than sphincters, what can indent the oesophagus and shows up with Ba swallow? Describe.
Arthritic osteophytes
- may cause pain on swallowing
- will be associated with thickening of the anterior longitudinal ligament
What is the (i) arterial (ii) venous (iii) nervous and (iv) lymphatic supply of the SUPERIOR/CERVICAL third of the oesophagus?
(i) inferior thyroid arteries
(ii) brachiocephalic veins
(iii) branches of vagus (RLN)
(iv) deep cervical nodes
What is the (i) arterial (ii) venous (iii) nervous and (iv) lymphatic supply of the MIDDLE/THORACIC third of the oesophagus?
(i) thoracic aorta and bronchial arteries
(ii) azygous system
(iii) oesophageal plexus
(iv) Tracheobronchial nodes
What is the (i) arterial (ii) venous (iii) nervous and (iv) lymphatic supply of the INFERIOR/ABDOMINAL third of the oesophagus?
(i) left gastric
(ii) left gastric veins (=> to portal vein)
(iii) branches of oesophageal plexus
(iv) left gastric and coeliac nodes
Where are the 4 oesophageal constrictors located?
- Upper oesophageal sphincter
- Arch of aorta
- Left main bronchus
- Diaphragm (lower oesophageal sphincter
What structures are (i) anterior (ii) posterior to the oesophagus?
(i) trachea, right PA, left main bronchus, left atrium, diaphragm
(ii) vertebral bodies (C6-T12), thoracic duct, thoracic aorta (inferiorly)
What epithelium lines the ‘abdominal’ oesophagus?
Stratified squamous epithelium with submucosal mucous glands
What occurs if someone has cirrhotic liver disease?
It raises the portal venous pressure (portal hypertension)
- blood escapes via the submucosal veins in the oesophagus and into the systemic azygous vein
- veins therefore become dilated and tortuous… oesophageal varices (may cause fatal haemorrhage)
There is no anatomical sphincter at the lower end of the oesophagus, instead, reflux is prevented by a ‘physiological’ cardiac sphincter. Give the 3 movements that result in this sphincter.
- Contraction of right crus of diaphragm
- Tonic contraction of the circular layer of smooth muscle in the lower oesophagus
- The ‘valvular’ effect of the oblique entry of the oesophagus into the stomach, augmented by the oblique muscle layer
What is the Z-line?
The transition from stratified squamous (oesophageal) to columnar (gastric) epithelium
What region(s) does the stomach lie in?
Across the epigastric region
- but extends to the umbilical and left hypogastric regions
What is the stomach related to (i) anteriorly (ii) posteriorly?
(i) anterior abdominal wall, left costal margin, left pleura and lung (above diaphragm), diaphragm itself, left lobe of liver
(ii) lesser sac, diaphragm, spleen, left suprarenal gland, upper part of left kidney, splenic artery, pancreas, transverse mesocolon, transverse colon
Describe the mucous membrane of the stomach. How is the pyloric sphincter formed and what is its function?
Mucous membrane is thick and vascular. It is thrown into numerous folds, or rugae, that flatten on distension
Circular muscle coat thickened in pyloric region to form sphincter that controls the outflow of gastric contents into the duodenum
What is the role of the stomach?
It receives and stores food and fluid
- adds more fluid plus acid and enzymes to create chyme and carry out digestion
Describe the left gastric artery. What does it supply?
Arises from coeliac artery
- passes upward and to the left to reach the oesophagus, then descends along the lesser curvature of the stomach
Supplies: lower 1/3 oesophagus and proximal part of lesser curve and adjacent body of stomach
Describe the right gastric artery. What does it supply?
Arises from the hepatic artery at the upper border of the pylorus and runs to the left along the lesser curvature
- supplies distal part of lesser curve and adjacent body of stomach
Where do the short gastric arteries arise from? What is their path within the body? What do they supply?
Arise from splenic artery at the hilum of the spleen
- pass forward in the gastrosplenic ligament to supply the fundus
Describe the origin, pathway adn what it supplies of the (i) left and (ii) right gastro-epiploic.
(i) arises form splenic artery at spleen hilum, passes forward in gastrosplenic ligament to supply stomach along proximal part of greater curvature and adjacent body
(ii) arises from gastroduodenal branch of hepatic artery, passes to left and supplies stomach along distal part of greater curvature and adjacent body
Where do the following veins drain to; (i) left and right gastric (ii) short gastric and left gastroepiploic (iii) right gastroepiploic ?
(i) directly into portal vein
(ii) splenic vein
(iii) superior mesenteric vein
What is the lymph drainage of the stomach?
Lymph passes to the nodes that lie along the arteries that supply the stomach
- all lymph from stomach eventually passes to coeliac nodes located around the root of the coeliac trunk on the posterior abdominal wall
What is the nerve supply of the stomach?
Includes:
- sympathetic fibres derived from T5-9 via the greater splanchnic nerves and the coeliac plexus
- parasympathetic fibres from right and left vagus
What is the stomach bed formed by? What is its boundaries superiorly and inferiorly?
Formed by the posterior wall of the lesser sac, and retroperitoneal structures between it and the posterior abdominal wall
SUPERIOR = left crus of diaphragm, spleen, left suprarenal gland and upper pole of L. kidney
INFERIOR = body and tail of pancreas, transverse mesocolon, left colic flexure, splenic artery
What (approximately) is the total length of the duodenum?
6-7m long
Where is the duodenum located? What structures does it receive? What is its functions?
Found adjacent to the head of the pancreas
Receives the openings of the bile and pancreatic ducts
FUNCTIONS: continued digestion (especially of fats) and absorption
Describe the 4 parts of the duodenum.
1st (superior) part begins at pylorus and runs up, back and to the right, starting on the transpyloric plane at L1 level
2nd (descending) part runs vertically down infront of r.kidneys hikum on right side of L2 and L3
- about halfways down its medial border the bile duct and main pancreatic duct pierce the duodenal wall at major duodenal papilla (ampulla of Vater)
3rd (horizontal) part runs horizontally to the left on the subcostal plane, infront of L3 and following the lower margins of the head of the pancreas
4th (ascending) part runs up and to the left to the duodenojejunal flexure at L2
What is the arterial blood supply of the (i) upper half (ii) lower half of the duodenum?
(i) Supraduodenal and gastroduodenal branches of common hepatic artery (coeliac trunk, foregut)
- gastroduodenal gives anterior and posterior superior pancreaticoduodenal branches
(ii) Superior mesenteric artery that gives inferior pancreaticoduodenal artery
- which quickly divides into anterior and posterior branches
What is the (i) venous (ii) lymphatic and (iii) nervous supply of the duodenum?
(i) superior pancreaticoduodenal vein drains to portal vein, the inferior pancreaticoduodenal joins the superior mesenteric vein
(ii) Coeliac and Sup Mesenteric nodes
(iii) Sympathetic greater (T5-9) and lesser splanchnic (T10/11)
Parasympathetic (vagus) nerves via coeliac and sup. mesenteric plexuses
What are the 3 major functions of gastric motility?
- Allows stomach to act as a reservoir for the large volume of food ingested at a single meal (receptive relaxation)
- Breaks food into smaller particles and mixes with gastric secretions
- Empties gastric contents into duodenum at a controlled rate
What are the 3 types of smooth muscle layers within the stomach?
Outer = longitudinal Middle = circular Inner = oblique
What is the innervation from the (i) Extrinsic nerves (ii) enteric nervous system (myenteric plexus)? What are the sensory afferent fibres?
(i) PS = stimulate gastric smooth muscle motility and secretions
S = inhibit motility and secretions
(ii) PS via vagus
S via coeliac ganglion
- between sensory receptors and the ENS and centrally via the vagus and splanchnic nerves
What does distension of the lower oesophagus induce?
Relaxation of the lower oesophageal sphincter and the orad region of the stomach
- this reduces pressure and increases the volume inside the stomach (1.5 litres)
What is the vagovagal reflex? What is the (i) afferent (ii) efferent information?
Afferent and efferent nerve fibres in the vagus
(i) mechanoreceptors associated with chewing, oesophageal and stomach distension relay information to CNS via sensory neurons
(ii) VIP released from postganglion peptidergic vagal neurons is responsible for orad relaxation
Where does mixing occur in the stomach? Explain the anatomical features as to why this is the case.
Muscle layers in the fundus and body are thin, therefore weak contractions are produced and the contents settle into layers based on their density
Because of this, the thick muscular wall of the caudad region is responsible for mixing
- contraction waves begin in the middle of the body and move distally with increasing strength towards the pylorus
What is retropulsion?
It propels the gastric contents back for further mixing in the stomach
What effect do the following have on the action potential frequency; (i) parasympathetic stimulation, gastrin and motilin (ii) sympathetic stimulation and secretin?
(i) INCREASE
(ii) DECREASE
How many waves in the stomach per minute?
3 - 5
What are MMCs? When do they occur? What do they do?
They are periodic gastric contractions known as Migrating Myoelectric Complexes
- mediated by motilin (released from endocrine in upper GI)
- 90 min intervals
It clears the stomach of residue remaining from previous meal
Occurs during fasting activity
After a meal what does the stomach contain?
1.5 litres of solids, liquids and gastric secretions
How long does emptying of the gastric contents take?
About 3 hours
Why is the rate of gastric emptying regulated?
To ensure that gastric H+ is neutralised in the duodenum and that there is adequate time for digestion and absorption of nutrients
What are the 3 physical factors affecting emptying?
- Liquids empty more rapidly than solids
- Isotonic fluids empty more rapidly than hypo- or (especially) hypertonic fluids
- Solids must be reduced to particles smaller than 1mm^3 or less - retropulsion continues until this is achieved
What 2 chemical factors inhibit gastric emptying? Describe/Explain.
The presence of fat and of H+ ions in the duodenum
- FAT - mediated by cholecystokinin (which is secreted when fat reaches the duodenum)
- H+ - mediated by reflexes in the enteric nervous system. H+ receptors in duodenum detect a low pH and relay info to gastric smooth muscle via interneurons in myenteric plexus
What are the 3 functions of the small intestine motility?
- Mixes chyme with digestive enzymes and pancreatic secretions
- Exposes nutrients to the intestinal mucosa for absorption
- Propels unabsorbed chyme into the large intestine
How many slow waves occur in the (i) duodenum (ii) ileum per minute?
(i) 12
(ii) 9
How often do MMCs occur in the small intestine? What is their function in the small intestine?
Every 90 minutes to clear the small intestine of residual chyme
What type of contractions are responsible for (i) mixing (ii) forward movement?
(i) segmental contractions
(ii) peristaltic contractions
What is the structure and innervation of the colon?
Longitudinal muscle concentrated in 3 bands - Taeniae (tenia) coli
PARASYMP
- vagus = caecum, asc and transverse colon. Stimulation causes segmental contractions of proximal colon
- pelvic nerves = desc and sigmoid colon, rectum and anal canal. Stimulation causes expulsive contractions of colon
SYMP
- stimulation stops colonic movements
What do contractions of the caecum and proximal colon do?
They mix the contents
- reverse peristalsis and segmental propulsion towards the caecum can occur
(note: retention favours sodium and water absorption)
What happens after the contents of the small intestine enter the caecum and proximal colon?
The ileoceacal sphincter contracts
- faecal material moves from the caecum, through the colon to the rectum and on to the anal canal
Roughly, how much chyme does the colon receive per day? How much of this is lost daily in faeces?
500 - 1500ml
- but most of the salt and water are absorbed
- 100ml per day lost in faeces
What does poor motility cause in the large intestine?
Greater absorption and hard faeces in the transverse colon
- causing constipation
What does excess motility cause in the large intestine?
Less absorption and diarrhoea or loose faeces
What are mass movements in the colon?
Movement of contents of large intestine over long distances (20cm) and occur 1-3x per day
The final mass movement propels faecal content into the rectum, what is this caused by?
gastrocolic and duodenocolic reflexes
What is the gastrocolic reflex? What is the (i) afferent and (ii) efferent limb of the reflex?
Distension of the stomach by food increases the motility of the colon and the frequency of mass movements in the large intestine
(i) A: in stomach, mediated by PS system
(ii) E: increasing colon motility - mediated by CCK(cholecystokinin) and gastrin
How does defecation occur?
As the rectum fills with faeces, the smooth muscle of the rectum contracts and the internal anal sphincter relaxes = RECTOSPHINCTERIC REFLEX
The external anal sphincter remains tonically contracted
- it is relaxed voluntarily, the smooth muscle of the rectum contracts and the pressure forces faeces through the anal canal
Where is the vomiting centre located?
In the medulla
What is the afferent information for vomiting? (HINT: there’s 4 points)
- Vestibular system
- Back of throat
- GI tract
- Chemoreceptor trigger zone in the 4th ventricle
What is the efferent response for vomiting? (HINT: there’s 5 points)
- Reverse peristalsis in small intestine
- Relaxation of stomach and pylorus
- Forced inspiration to increase abdominal pressure
- Relaxation of lower oesophageal sphincter
- Forceful expulsion of gastric and duodenal contents
What is the name of the 3 movement patterns that occur in the stomach?
- Propulsion
- Grinding
- Retropulsion
What are the 3 levels of gut defences?
- Physical
- Innate immunity
- Acquired immunity
What are the host defences found within the mouth? (HINT: there’s 4)
- Flow of liquids
- Saliva
- Antimicrobials (found in saliva) - lactoferrin, lysozyme
- Normal microbiota
What are the 2 host defences found in the oesophagus?
Flow of liquids
Peristalsis
What are the 3 host defences found in the stomach?
- Acidic pH
- Antimicrobials - beta defensins
- Mucus - prevents bugs being able to attach to epithelial cells and also protects us from our own acid
What are the host defences found within the small intestine? (HINT: there’s 7)
- Flow of gut contents
- Peristalsis
- Mucus
- Bile
- Secretory IgA
- Antimicrobial peptides - alpha defensins
- Normal bacterial microbiota
What are the 4 host defences of the large intestine?
- Normal microbiota
- Peristalsis
- Mucus
- Shedding and replication of epithelium
What is the host-bacteria relationship for the following types of bacteria; (i) commensal (ii) symbiotic (iii) parasitic?
(i) host = ok bacteria = good (ii) host and bacteria = good (iii) host = bad bacteria = good
What are the 3 types of bacteria found in probiotics? What is their function?
- Lactobacillus spp.
- Bifidobacterium spp.
- Bacteroides spp.
- alter the pH by producing lactic acid and tip the balance just enough so that some pathogenic bacteria will not be able to grow and divide
What are prebiotics? What do they do?
They are non-digestible food ingredients
- stimulate the growth/activity of gut microbiota
What 6 things do prebiotics and probiotics do for the guts immune system?
- Development of mucosal barrier
- Synthesis of vitamins
- Metabolism of bile acids
- Production of short-chain fatty acids
- Reduction in pH in large bowel
- Immune system activation
What is the role(s) of gut microbiota? (HINT: there’s 5)
- Prevent colonisation by pathogens
- Excrete useful metabolites
- Ferment unused energy substrates
- Synthesise and excrete vitamins
- Produce hormones
What are the 3 ways to maintain a healthy gut microbiota?
Probiotics
Prebiotics
Bacteriotherapy
What are the factors controlling Gut Microbiota? (HINT: there’s 7)
Physiological status Underlying disease Intestinal secretions Intestinal motility Immune mechanisms Environmental factors Use of antibiotics
What is the primary immune organ in the body?
GI tract
What does GI microbiota have a strong influence on?
The development of the local and systemic immunity and in the regulation of immune functions
What are MAMPs?
Microbe associated molecular patterns
What do they following stand for; (i) TLRs (ii) NODs (iii) NLRs? What, collectively, are they? hat do they do?
(i) Toll-like receptors
(ii) Numcleotide-binding oligomerization domain-containing proteins
(iii) NOD-like receptors
- they are pattern recognition receptors which recognise the MAMPs
What is NF kappa B? What is its function?
It is a transcription factor
- it switches other genes on or off
Results in the transcription of pro inflammatory genes which secrete cytokines and chemokines such as TNF and IFNgamma which recruit immune cells to the site of infection
How are most infections of the GI tract acquired?
Via the faecal-oral route
When does an infection of the GI tract occur?
when the micro-organism causes ill-health
What are the 3 ways to acquire an intestinal infection?
- Ingestion of infected food and water
- Ingestion of bacterial toxins
- Use of oral antibiotics
What are the 4 characteristics of Gastroenteritis?
Nausea
Vomiting
Diarrhoea
Abdominal discomfort
What is enterocolitis?
Inflammation involving the mucosa of both the small and large intestine
What is diarrhoea defined as? What does it occur as a result of? What does it involve?
Abnormal faecal discharge characterised by frequent and/or fluid stool
- is as a result of disease in the small intestine
- involves increased fluid and electrolyte loss
What is dysentry? What is it a result of? What is it associated with?
Inflammation disorder of the GI tract
- resulting from disease of large intestine
- associated with blood and pus in faeces
- accompanied usually by pain, fever and abdominal cramps
What are the clinical effects of pathogenic invasion of the GI tract? (HINT: there’s 7)
- Diarrhoea/dysentry
- Malaena
- Blood in faeces
- Pus in faeces
- Abdominal cramps
- Fever
- Sepsis
Secretion is the addition of fluids, enzymes and mucous to the lumen of the GI tract. What are the 4 sources of secretions?
- Produced by salivary glands (saliva)
- Cells of gastric mucosa (gastric secretion)
- Exocrine cells of the pancreas (pancreatic secretion)
- Liver (bile)
What are the characteristics of saliva? (HINT: there’s 4 points)
High HCO3-
High K+
Hypotonic
alpha-amylase and lingual lipase
What are the factors that (i) increase (ii) decrease the secretion of saliva?
(i) parasympathetic primarily and also sympathetic
(ii) sleep, dehydration, atropine
How much saliva do you secrete daily? What are the 3 functions of saliva?
1 litre per day
- initial digestion of starches and lipids
- dilution and buffering of ingested foods
- lubrication of ingested foods with mucous (mucin)
Name and describe the structure of the 3 groups of paired salivary glands.
PAROTID - serous cells secreting an aqueous fluid composed of water, ions and enzymes
SUBLINGUAL - mostly mucous cells
SUBMANDIBULAR - mixed glands containing serous and mucous cells, mucin glycoprotein for lubrication
What is the blood flow like of the salivary glands?
High blood flow
- 10 times that of exercising muscle
What are (i) acinar cells (ii) myoepithelial cells (iii) ductal cells?
(i) produce an initial isotonic saliva composed of water, ions, enzymes and mucus
(ii) in (and near) the acini are stimulated by neural input to eject saliva
(iii) modify the initial saliva by altering electrolyte concentrations
How is the salivary secretion modified?
It is a combined action of the following:
- absorption of Na+ and Cl-
- secretion of K+ and HCO3-
- because more NaCl is absorbed than KHCO3 secreted there is net absorption of solute
- the low water permeability of ductal cells means that the final saliva is hypotonic
What are the 4 types of acinar cell secretions?
- alpha amylase
- begins the initial digestion of carbohydrates - Lingual lipase
- begins the initial digestion of lipdis - Mucus
- lubricant - Kallikrein
- enzymatic cleavage of kininogen to bradykinin (potent vasodilator)
- allows for a good blood supply to the salivary glands
Salivary secretion is exclusively under neural control by the ANS (i.e. no hormonal regulation). What does neural stimulation result in?
Increased saliva production, HCO3- production, enzyme secretion and myoepithelial cell contraction
Gastric secretion is known as gastric juice. What is it composed of?
HCl - protein digestion
Pepsinogen - protein digestion
Intrinsic factor - vit B12 absorption (in the ileum)
Mucus - protects gastric mucosa and lubricates food
What are the characteristics of gastric secretions?
HCl
Pepsinogen
Intrinsic factor
What factors (i) increase (ii) decrease gastric secretion?
(i) Gastrin, ACh, Histamine, Parasympathetic
(ii) H+ in stomach, Chyme in duodenum, Somatostatin, Atropine, Cimetidine, Omeprazole
What are the 3 types of gastric cells? What do they secrete and where are they located?
PARIETAL CELLS - proximal body of stomach - secrete intrinsic factor and HCl
CHIEF CELLS - body of stomach - secretes pepsinogen
G CELLS - antrum of stomach - secretes gastrin (to circulation)
In the stomach, how is the surface area increased?
By gastric glands
Describe the importance of HCl secretion.
Parietal cells increase HCl which acidifies the gastric contents to pH 1-2
- low gastric pH converts inactive pepsinogen to pepsin (active form)
What is pepsin? What is its function?
A protease which initiates protein digestion
What is the role of carbonic anhydrase?
Catalyses the combination of metabolic CO2 and H2O to eventually become H+ and HCO3-
Describe the HCl secretion on the apical surface of the gastric parietal cells.
H+ secreted into the lumen via the H+-K+ ATPase
CL- follows by diffusion through an apical channel
Describe the HCl secretion on the basolateral surface of the gastric parietal cells.
HCO3- exhanged for CL- via the chloride-bicarbonate exchanger (alkaline tide)
- eventually HCO3- is secreted back into the GI tract in pancreatic secretions
What is the cephalic phase of gastric HCl release? What is it stimulated by (i) directly (ii) indirectly?
Contributes to 30% of secretion
- smell, taste, chewing, swallowing, conditioned reflex in anticipation of food
(i) parietal cells by the vagus
(ii) parietal cells by gastrin - vagal gastrin releasing peptide stimulates gastrin release from G cells
- gastrin hormone enters the circulation and stimulates parietal cells to release HCl
What is the gastric phase of gastric HCl release?
Contributes to 60% of secretion
- is distension of stomach and the presence of breakdown products of proteins, amino acids and small peptides in the stomach
What does distension cause? (HINT: there’s 3 points)
- Direct vagal stimulation of parietal cells
- Indirect stimulation via gastrin
- Local reflexes in the antrum that stimulate gastrin release
What is the (i) Direct and (ii) indirect stimulation used to regulate HCl secretion?
(i) VAGAL PATHWAY
- vagal release of ACh activates parietal cells
(ii) VAGAL PATHWAY
- vagal stimulated release of gastrin from G cells (by GRP neuropeptide transmitter)
What is the intestinal phase of gastric HCl release?
Contributes to 10% of secretion
- presence of breakdown products of proteins in the duodenum
What is the (i) origin (ii) action (iii) second messenger of ACETYLCHOLINE (neurocrine)?
(i) vagus nerve
(ii) binds to the muscarinic (M3) receptors on parietal cells
(iii) IP3/Ca2+
What is the (i) origin (ii) action (iii) second messenger of HISTAMINE (paracrine)?
(i) Enterochromaffin like cells (ECL) in the gastric mucosa
(ii) Diffuses to and binds to H2 receptors on parietal cells
(iii) Cyclic AMP
What is the (i) origin (ii) action (iii) second messenger of GASTRIN (hormone)?
(i) G cells in stomach antrum
(ii) Binds to CCK(B) receptors on parietal cells
(iii) IP3/Ca2+
When is HCl secretion inhibited? WHEN does this occur?
When HCl is no longer needed to conver pepsinogen to pepsin
- Occurs after the chyme moves into the small intestine and the H+ buffering capacity of the food is no longer a factor
What is the (i) direct (ii) indirect pathway of somatostatin?
(i) binds to receptors on parietal cells and inhibits adenylate cyclase via Gi protein
(ii) inhibits histamine release from ECL cells and gastrin release from G cells
What is pepsinogen secreted by? In response to what?
By chief and mucous cells in the oxyntic glands in response to vagal stimulation
What does H+ trigger?
local reflexes
- which stimulate chief cells to secrete pepsinogen
Where is mucoprotein released from? Why is it important?
Released from parietal cells required for vit B12 absorption in the ileum
- it is the only ESSENTIAL secretion of the stomach
What does lack of intrinsic factor cause?
Pernicious anaemia
- autoimmune condition
Following a gastectomy, what do patients receive? Why is this the case?
Injections of vit B12
- to bypass the absorption defect
What is Zollinger-Ellison syndrome?
Is a rare condition that is an endocrine tumour known as a Gastrinoma (gastrin secreting tumour)
- non beta cells of the pancreas
- get a high circulating levels of gastrin
What effect does the high levels of gastrin in Zollinger-Ellison syndrome?
- Increased H+ secretion by parietal cells
- Hypertrophy of gastric mucosa
- Duodenal ulcers (constant secretion of gastric H+)
- Acidification of intestinal lumen - inactivation of pancreatic lipases.
How long are the jejunum and ileum?
About 6 metres long
2/5 jejunum and 3/5 ileum
Where does the jejunum begin?
jejunum begins at duodenojejunal flexure
Where does the ileum end?
Ileocaecal junction in the right iliac fossa
How/why are the jejunum and ileum freely mobile?
As they are suspended from the posterior abdominal wall by the fan-shaped mesentery of the small intestine that carries the blood, lymph and nerve supply
Where does the (i) jejunum (ii) ileum lie within the body?
(i) upper left abdomen
(ii) lower right and also in the pelvis
What are the structural differences that allow you to distinguish the jejunum from the ileum?
Jejunum is wider bored, thicker walled, and redder than the ileum
- its wall feels thicker because the permanent infoldings of the submucosa, the plicae circulares, are larger, more numerous, and more closely set in the jejunum
- whereas in the upper part of the ileum they are smaller and more widely separated, in the lower part they are absent
What are the structural differences between the MESENTERY of the (i) jejunum (ii) ileum?
(i) attached to posterior abdominal wall above and to the left of the aorta at L2
- the mesenteric vessels form only one or two arcades, with long and less frequent branches passing to the intestinal wall
- fat is deposited near the root and is less obvious near the intestinal wall
(ii) attached below and to the right of the aorta at the SI joint
- receives numerous short terminal vessels that arise from a series of 3/4 or even more arcades
- the fat is deposited throughout so that it extends from the root to the intestinal wall
What are Peyer’s patches? Where are these patches found?
Aggregations of lymphoid tissue
- present in the mucous membrane of the lower ileum along the antimesenteric border
- in the living these may be visible through the wall of the ileum from the outside
What is the ileocaecal valve? What is its function?
2 horizontal folds of mucosu membrane that project around the orifice of the epithelium
- situated at the junction of the small intestine and the large intestine
FUNCTION = limit reflux of colonic contents into the caecum
What is the arterial and venous blood supply of the jejunum and ileum?
ARTERY - jejunal and ileal arteries from the SMA and its ileocaecal branch
VEINS - correspond to the branches of the SMA and drain into the SMV, which joins with the splenic vein to form the portal vein
What is the (i) lymph drainage (ii) nerve supply of the jejunum and ileum?
(i) SM nodes which are situated around origin of SMA
(ii) Sympathetic, lesser splanchnic nerve T10/11 and parasympathetic (vagus) nerves via the superior mesenteric plexus
Where does the SMA arise? What does it carry? What does it supply?
From the aorta at L1
- carries nerves (sympathetic) derived from T10 and T11
- supplies the midgut (ampulla of Vater in duodenum to 2/3 along transverse colon)
Describe (in detail) the intestinal lymph drainage via the mesentery.
There’s a lacteal centre in the centre of each villus for the absorption of digested fat and lipids (chyle)
- chyle passes from lacteals into mesenteric lymph channels that DON’T pass through lymph nodes but converge on the cisterna chyli that lies in the upper abdomen and passes through the diaphragm as the thoracic duct
What happens to the lymph absorbed from the intestinal wall?
Passes into mesenteric lymph channels, but these filter through the mesenteric nodes
- afferents from the mesenteric nodes converge on nodes at the route of the SMA
- afferents from the nodes on the SMA pass to the cisterna chyli
What is a Merkel’s Diverticulum? What disease does it get mistaken for as it has similar signs and symptoms?
A remnant of the vitello - intestinal duct that may ulcerate causing signs and symptoms similar to appendicitis
(it is 2 inches long, 2 feet from the end of the ileum, in 2% of people)
What main symptom arises from a patent vitelline duct (vitelline fistula)?
Faecal discharge at the umbilicus
How long is the colon/large intestine? What does it consist of?
- 5 metres long
- caecum
- ascending colon
- hepatic (right) flexure
- transverse colon
- splenic (left) flexure
- descending and sigmoid colon
- rectum and finally anal canal
What parts of the large intestine are (i) retroperitoneal (ii) intraperitoneal?
(i) ascending and descending
ii) transverse and sigmoid (as on a mesentery
What are the external differences of the large intestine compared to the small intestine?
Larger in diameter
- has tags of fat known as omental appendices (appendices epiploicae)
- has 3 tenia coli i.e. condensations of the longitudinal muscle layer
- has (sacculations) haustra of the colon
What are the internal differences of the large intestine compared to the small intestine (ileum)? (HINT: what are 3 things the large intestine lacks which the ileum has?)
LACKS:
- plicae circularis
- villi
- peyers patches
Where is the caecum located? Describe its anatomical appearance.
Lies below the level of the junction of the ileum with the large intestine and is continuous with the ascending colon
- a pouch about 7.5cm wide and lies covered by peritoneum, but NOT on a mesentery, in the right iliac fossa
Where do the 3 taeniae coli converge? Why is this significant clinically?
In the caecum at the root of the appendix
- may be a guide to its location during surgery
Where is the root of the appendix found?
At McBurney’s point
- 1/3 up from ASIS to umbilicus
What is the appendix? What is it suspended on?
A narrow blind ended tube hanging from the caecum
- submucosa is packed full of lymphoid tissue
- suspended on a short but highly variable meso-appendix that transmits the appendicular vessels.
What are all the possible positions of the appendix? - WHY are these various positions possible?
Retrocaecal (64%) - pelvic (32%) - subcaecal (2%) - pre-ileal (1%) - retro-ileal (0.5%) Due to the variable peritoneal recesses formed adjacent to the caecum
What can be affected by an inflamed appendix? Why is this the case?
Appendicular artery
- it is close and parallel to the appendix distally
- becomes obstructed causing gangrene and rupture of the appendix
Where is the appendicular artery derived from?
The ileocolic branch of the SMA from the aorta at L1 with nerves derived from T10/11
Where does early appendicitis refer pain to? Where does this pain then move to (explain)?
Refers pain to peri-umbilical region
- pain moves to right inguinal region later when the parietal peritoneum is involved
What is the arterial supply of the caecum and appendix?
All derived from the ileocolic artery from the SMA
- anterior caecal artery
- posterior caecal artery
- appendicular artery (from post. caecal)
What is the lymph drainage of the caecum and appendix?
Nodes on the SMA
How long is the ascending colon? In what region is it found?
13cm long
- R. lumbar region
Where does the ascending colon become the transverse colon?
At the hepatic flexure (related to liver)
How long is the transverse colon? Where is it located anatomically?
38cm long
- hanging downward, on its mesentery, posterior to the greater omentum and across the umbilical region
- then ascends to splenic flexure where it turns posteriorly and inferiorly and loses its mesentery to become retroperitoneal
How long is the descending colon? Where does it lie in the body?
25cm long
- left lumbar region
- extends down towards pelvic brim where it becomes the sigmoid colon
How long is the sigmoid colon? How is it mobile? Where does it become the rectum?
25-38cm long
- mobile on a fan-shaped mesentery and hangs down into the pelvic cavity in the form of a loop
- becomes continuous with the rectum in front of S3
What is sigmoid volvulus? What can this result in?
When the sigmoid rotates upon itself
- colonic diverticulae may become obstructed and mimic left sided ‘appendicitis’
What are the following related to (organ wise) (i) root of transverse mesocolon (ii) ascending colon (iii) descending colon?
(i) crosses the lower pancreas
(ii) right kidney and duodenum, with ureter and major vessels medially
(iii) left kidney with the duodeno-jejunal flexure, with ureter and major vessels medially
What parts of the colon does the (i) SMA (ii) IMA supply? Note what branches are supplying these organs.
(i) Ileocolic, right colic and middle colic branches to the caecum, ascending colon, hepatic flexure and 2/3 of transverse colon
(ii) left colic and sigmoid branches to 1/3 of transverse colon, splenic flexure, descending and sigmoid colon
Where/what does the IMA end as?
The superior rectal artery supplying the rectum and anal canal
Where does the IMA arise from? What nerves does it carry?
Aorta at L3
- carries sympathetic nerves derived from T12 (least splanchnic nerves) and parasympathetics from S2,3,4 (NOT vagus)
What is the marginal artery of Drummond?
The IMA and SMA anastamose, forming a collateral circulation should the IMA be obstructed
Why does referred pain exist within the abdomen?
Due to afferents running with the efferent sympathetic nerves derived from T7 - 12
- the brain cannot localise visceral pain; localisation occurs with the involvement of overlying, parietal peritoneum
What is Hirchsprung disease?
Lack of normal development of the colonic innervation leads to a constricted, aganglionic segment of bowel, with a distended segment proximally (the innervation of which is normal)
How long is the rectum? What is its route in the body? What is its function?
13cm long
- begins in front of S3
- passes downward, following the curve of the sacrum and coccyx, it ends in front of the tip of the coccyx by piercing the pelvic diaphragm and becoming continuous with the anal canal
- it stores faeces
How long is the anal canal? Where does it lie? What is its function?
4cm (retroperitoneal)
- passes down and back from the rectal ampulla to the anus
- it is a conduit to the outside world
What are the characteristics of pancreatic secretion?
High HCO3- (isotonic)
Pancreatic lipase, amylase and proteases
What are the 3 factors that increase pancreatic secretion?
- Secretin
- Cholecystokinin (CCK) - potentiates secretin
- Parasympathetic supply
How much fluid does the exocrine pancreas excrete daily? What is pancreatic secretion composed of?
1L of fluid per day into the duodenum
- composed of an aqueous solution containing enzymes and high HCO3-
What is the function of the HCO3- (bicarbonate)?
to neutralise the stomach H+
What effect does (i) parasympathetic (ii) sympathetic innervation of the pancreas have on its secretion?
(i) from vagus, stimulates secretion
(ii) inhibits secretion
Where are pancreatic enzymes stored?
In condensed zymogen granules until release
Where is the aqueous component of pancreatic secretion released from?
Centroacinar cells and ductal cells
What ions does pancreatic fluid contain?
It is an isotonic fluid containing:
- Na+
- K+
- Cl-
- HCO3-
What does modification of the composition of pancreatic secretion by the ductal cells result in?
A fluid secretion rich in HCO3- (bicarb)
Describe the ezymatic component of pancreatic secretion.
Released from acinar cells
- pancreatic amylase and lipases are secreted as active enzymes
- pancreatic proteases are secreted in the inactive form and activated in the duodenum (enterokinase)
What are the 3 phases to regulate pancreatic secretions? Describe each one.
- CEPHALIC PHASE
- initiated by taste, smell and conditioning, mediated by the vagus nerve (mainly enzymatic secretion) - GASTRIC PHASE
- initiated by distension of the stomach and mediated by vagus nerve (mainly enzymatic secretion) - INTESTINAL PHASE
- accounts for 80% of pancreatic secretion
- both enzymatic and aqueous secretions are stimulated
How are acinar cells regulated?
- Duodenal I cells secrete CCK in response to the presence of amino acids, small peptide and fatty acids in the intestinal lumen
- vagal release of ACh potentiated CCK action
How are ductal cells regulated?
Secretin released by the S cells of the duodenum is the major stimulus for aqueous rich HCO3- secretion
- secretin release is triggered by the arrival of acidic chyme in the duodenum
- ACh and CCK potentiate secretin action
What is bile? What is it essential for? Where is it produced and then stored?
It is a mix of bile salts (50%), bile pigments (2%), cholesterol (4%) and phospholipids (40%)
- is essential for the digestion and absorption of lipids (water insoluble)
- produced and secreted by the liver and stored in the gallbladder
What do bile salts do to lipids?
They emulsify them to prepare them for digestion and solubilise the products of digestion into ‘packets’ called micelles
What are the 3 functions of the gall bladder?
- RESERVOIR FOR BILE
- stores bile that’s continually produced by hepatocytes and flows to gallbladder through bile ducts - CONCENTRATION OF BILE
- epithelial cells lining the gallbladder absorb ions and water isomatically - EJECTION OF BILE
- begins 30mins after a meal. Major stimulus for ejection is release of CCK from the I cells in duodenum and jejunum
What is CCK (cholecystokinin)? Where is it secreted from and in response to what?
A 33 amino acid peptide hormone related to gastrin
- secreted from I cells of duodenal and jejunal mucosa in response to the presence of monoglycerides, fatty acids, small peptides and amino acids
What are the 5 hormonal actions of CCK?
- Contraction of gall bladder and relaxation of sphincter of Oddi to eject bile (emulsification and solubilisation of dietary fat)
- Secretion of pancreatic enzymes (both lipases and proteases)
- Secretion of pancreatic HCO3
- Growth of exocrine pancreas and gall bladder
- Inhibition of gastric emptying
What are mixed micelles?
Products of lipid digestion (cholesterol, mononglycerides, lysolecithin and free fatty acids) are solubilised in mixed micelles
- core contains products of lipid digestion
- surface coating of bile salts which are amphipathic
What is (i) digestion (ii) absorption?
(i) the chamical breakdown of ingested food into absorbable molecules
(ii) movement of nutrients, water and electrolytes from the lumen of the intestine to the blood.
- 2 pathways: cellular and paracellular
What does chyme in the small intestine trigger? What 2 things does this stimulate?
Triggers CCK release
- stimulates gall bladder contraction and relaxation of the sphincter of oddi
When lipid absorption is complete, what happens to the complete bile salts?
They are recirculated to the liver by the enterohepatic portal circulation
How are bile salts extracted from the portal blood? How many daily (as a percentage)?
By hepatocytes
- 20% loss per day
Describe the structure of the intestinal mucosa.
The structure of the small intestine is arranged in circular folds of Keckring
- villi project from the folds. The surface of villi are covered with epithelial cells (enterocytes) with mucus secreting cells (goblet cells)
What is the ‘brush border’?
The apical surface of epithelial cells in the intestinal mucosa is covered by microvilli
