Gi Flashcards
(106 cards)
1
Q
recognise the gastrointestinal tract as an external environment and discuss the implications of this.
A
2
Q
describe the overall processes of the GI tract
A
3
Q
- outline the broad functions of the various regions of the GI tract
A
Mouth
◦ Physical breakdown of food
◦ Initial digestive enzymes released ◦ Infection control
Oesophagus
◦ Rapid transport of bolus to stomach through thorax
◦ UOS
◦ Prevents air from entering GI tract
◦ LOS
◦ helps prevents reflux into oesophagus
Stomach
◦ Storage
◦ To produce chyme (gastric secretions and partially digested food)
◦Muscle contractions
◦Proteases
◦ Digestion started
◦ Infection control (HCL)
◦ Secrete intrinsic factor(Vit B12)
Duodenum
◦ Start of small intestine
◦ Neutralisation/osmotic stabilisation of chyme with bile and pancreatic secretions
Jejunum/ileum
◦ Final digestion
◦ Nutrient absorption in Mainly jejunum
◦ Ileum - B12 absorption
Large bowel
◦ Final water absorption
◦ Temporary storage
◦ Final electrolyte absorption
◦ Some bile salt absorption
◦ Production of some SCFAs
Rectum/anus
◦ defaecation
4
Q
- describe the general structural plan of the alimentary canal
A
5
Q
describe the anatomy and function of the peritoneal cavity
A
6
Q
- Describe the organisation and function of mesenteries
A
-Double folds of peritoneum that connect retro and intra
Ligaments are double folds that connect intra
7
Q
describe the muscles of the anterolateral abdominal wall and their innervation
A
Nerve innervation = anterior rami of T7-T12
External oblique
Origin = 5th to 12th rib
Insertion = iliac crest, inguinal ligament and linea alba (which is midline)
Goes from out to in
Connects via aponeurosis
Compress abdominal viscera, flex the trunk, rotate trunk.
These 2 also get L1 supply
Internal oblique
Origin = lateral portion of inguinal ligament, iliac crest, thoracolumbar fascia.
Direction of fibres perpendicular to EO at top
Insertion = lower 3-4 ribs, linea alba, pubic crest
Action = compress abdominal viscera, flex the trunk, ipsilateral rotator
Transverse abdominus
Origin = lower ribs costal cartilage, thoracolumbar fascia, medial lip of iliac crest, portion of inguinal ligament
Fibres are transverse
Insertion = aponeurosis of linea alba and pubic crest
Action = compress abdominal viscera
Rectus abdominus
Vertically
Pubic crest, pubic tubercle and pubic crest and insert into costal cartilage of ribs 5 to 7 and xiphoid process
Breaks which are tenderness intersections
8
Q
describe the anatomy of the rectus sheath above and below the arcuate line
A
Aponeuroses of the 3 muscles envelope rectus abdominus - go anterior and posterior, then blend in with linea alba.
The enveloping is called rectus sheath.
Arcuate line is halfway between umbilicus and pubic symphysis.
Below it aponeuroses is only anterior. Posterior is transversalis fascia and parietal peritoneum.
9
Q
Describe the layers of the gut and the most prominent features of each
A
- Mucosa (innermost);
Epithelial layer
• Selectively permeable barrier
• Facilitate transport and digestion of food
• Promote absorption
• Produce hormones
• Produce mucus
Lamina propria
• Lots of lymphoid nodules and macrophages
• Produce antibodies (mainly IgA which is resistant to
proteases)
• Protect against bacterial/viral invasion
Stratified squamous in oesophagus and distal anus
Everything in between is simple columnar.
Muscularis mucosa
Layers of smooth muscle orientated in different
directions
• Keeps epithelium in contact with gut contents
• Helps keep crypt contents dynamic
- Submucosa
Contains dense connective tissue, blood vessels,
glands, lymphoid tissue
• Contains submucosal plexus (Meissner’s)
- External muscle layers
Inner circular muscle
• Myenteric (Auerbach’s) plexus
• Outer longitudinal muscle
- Serosa (outermost)
Blood and lymph vessels and adipose tissue
• Continuous with mesenteries
10
Q
compare the regional variation in macro- and microstructure of each of the major divisions of the alimentary canal and relate it to functional adaptations for transport, storage, digestion and absorption
A
11
Q
describe the epithelial cell types of the major divisions of the alimentary tract
A
Stomach
12
Q
describe the specialised cells types of the alimentary tract and their function
A
Stomach
Surface mucous cells
• Line gastric mucosa/gastric pits
• Secrete mucus/HCO3 that forms barrier to stomach acid
Small intestine + colon
Enterocyte
• Predominant cell, One cell thick
• Need to transport nutrients through Apical membrane + Basolateral membrane
• Blood vessels/lymphatics lie immediately below the enterocyte (in LP)
• Microvilli
Goblet cells
Scattered in between enterocytes
Mucus compresses nucleus to its base
• Mucus protects epithelia from:
• Friction (acts as lubricant)
• Chemical damage (acidic environment)
• Bacterial inflammation (forms physical
barrier)
13
Q
compare the broad function of the intestinal villi and the intestinal crypts
A
Villi have enterocytes and goblet cells
Crypts have:
Enteroendocrine cells - Secrete hormones that control the function of the gut eg • Gastrin
• Cholecystokinin • Secretin
Stem cells - replace epithelia every 2-4 days
Paneth cells - Located at base
• Secrete antibacterial proteins
• Protect stem cells
14
Q
describe the basic structure of the autonomic nervous system in relation to its influence on the gastrointestinal tract
A
Parasympathetic
Vagus nerve
Pelvic Sphlanic Nerve (S2-S4)
Post release Ach, peptides, GIP, Vaso inhibitory peptide
Pre synapse in walls of viscera
Innervate smooth muscle/endocrine and secretory
Sym
T5-L2
• Pass through (paravertebral) sympathetic trunk without synapsing
• Form (abdominopelvic) presynaptic splanchnic nerves
• Greater (T5-9)
• Lesser (T10-11)
• Least (T12)
• These splanchnic nerves synapse with prevertebral ganglia
• Coeliac, renal, superior mesenteric, inferior mesenteric and others
• Mainly innervate blood vessels
Post ganglionic fibres extend to myenteric and
submucosal plexuses
• Release norepinephrine
• Generally inhibits GI function
15
Q
describe the properties of the enteric nervous system, and its relationship to the autonomic nervous system
A
16
Q
Describe the role of the major hormones of the gut (gastrin, cholecystokinin, secretin, GIP and somatostatin)
A
Gastrin
Neurocrine - gastrin releasing peptide
• G cells in antrum of stomach
• Increases gastric acid secretion
Cholecystokinin (CCK)
• I cells in duodenum and jejunum
• Increases pancreatic/gallbladder
secretions
• Stimulated by fat and protein
• Gall bladder contracts
• Pancreas stimulated
Secretin
• S cells in the duodenum
• Stimulated by H+ and fatty acids
• Increases HCO3 from
pancreas/gallbladder
• Decreases gastric acid secretion
Gastric inhibitory polypeptide (GIP)
• Cells in the duodenum and jejunum
• Stimulated by sugars, amino acids and fatty
acids
• Increases insulin
• Decreased gastric acid secretion
17
Q
- describe the anatomy of the inguinal canal
A
Oblique passage through lower part of the abdominal wall, connecting the
peritoneal cavity to the scrotum in males.
Floor = inguinal
ligament, a thickened and rolled edge of the aponeurosis of the external oblique muscle.
The roof =arching fibres of
the internal oblique and transverse abdominis muscles.
The posterior wall of the inguinal canal is composed of the transversalis fascia, which is the deepest layer of fascia.
The entrance = deep ring, which is located within the transversalis fascia.
The anterior wall =aponeurosis of the external oblique muscle, and it contains the
superficial ring, which serves as the exit point.
Exit = towards scrotum or labia major
18
Q
- Explain how inguinal hernias develop (embryologically) and
relate this to the descent of the testis in the male.
A
Testis descend (7 th-8th month)
Processus vaginalis - point of peritoneum that descends before testis. Then obliterates. Covers testis as tunica vaginalis.
Gubernaculum
◦ Condensed band of mesenchyme that links inferior portion of testis to scrotum. Condenses so testis descends.
19
Q
- describe the anatomy and clinical presentation of inguinal
hernias
A
Inguinal hernias are divided into two types: indirect (50% of
hernias) and direct (25% of hernias). More common in males.
Indirect can extend into the scrotum if the processus vaginalis doesn’t obliterate - go through inguinal canal.
Direct = through a natural weakness in the abdominal wall called Hesselbach’s triangle.
They appear to come out through the superficial inguinal ring but are not inside the inguinal canal.
Signs and symptoms:
Swelling
Discomfort
Nausea/vomiting
Necrotic bowel
20
Q
- describe and compare the relevant anatomy associated with
direct and indirect inguinal hernias (to include the conjoint
tendon)
A
Indirect:
Passes through the deep Inguinal ring
§ The inguinal canal
§ The superficial Inguinal ring
Then depending on where the Processus Vaginalis was obliterated can potentially descend into the scrotum
Borders = floor is inguinal + lacunar ligament
Roof = interior oblique and transverse abdominus = conjoint tendon
Anterior wall = external oblique aponeuroses
Posterior wall = transverse facialis
Direct:
Lateral to rectus abdominus
Medial to inferior epigastric
Superior to inguinal lig
21
Q
- describe the relationship between the femoral canal and the inguinal ligament. Explain how femoral hernias develop including the anatomy and clinical presentation of such hernias.
A
More common in females
Herniates through femoral ring and femoral canal so becomes inferior to inguinal ligament.
NAVEL - it is medial to femoral vein
Lateral to lacunar ligament
Femoral canal is small so more likely to become incarcerated - blocks venous flow. Venous pressure inc and blocks arterial flow - contents of hernia ischaemic - strangulated hernia
22
Q
- describe the anatomy and clinical presentation of umbilical and para umbilical
hernias
A
Inc incidence if premature, African descent and low birthweight.
Not usually painful and spontaneously resolve/ close by 3-4 age
Surgery is effective
Hernia goes through umbilical ring - this is a defect in linea alba which umbilical cord passes through - should close after birth.
Para umbilical is in adults - females more and risk factor is obesity
Goes through defect in linea alba - near umbilicus
Risk of strangulation as defect is small.
23
Q
- describe the common incisional sites used for abdominal surgery and incisional hernias.
A
- Midline incision - through linea alba avoiding umbilicus, avascular
Extendable if need bigger operating field
High post op pain - Paramedian - are either side of midline (can follow rectus border)
poor cosmetics, can damage nerves/structures (right side has falciform ligament and can disrupt nerve supply to rectus muscles) - Gridiron - 2/3 way from umbilicus to ASIS
appendicectomy - Pfannenstial- obs and urology
- Kocher - open cholecystectomy- fro removing gallbladder
Parallel to subcostal margin
Incisional hernias
Risk factors - emergency surgery, advancing age, chemo, pregnancy, obesity, midline, wound infection.
24
Q
Describe epigastric, in relation to their relevant anatomy
A
25
Explain why visceral pain is perceived in the epigastric, umbilical and suprapubic regions of the
abdomen
Pain that results from:
Visceral stretching/inflammation / ischaemia
Pain is - Diffuse/poorly defined, Often midline
Nausea, vomiting, sweating
Pain from a:
•Foregut viscera- Epigastric area- Foregut referred pain felt in T5-T9 dermatomes - Associated with Greater splanchnic nerve
•Midgut viscera- Peri umbilical - referred pain felt in T10-T11
dermatomes - Associated with Lesser splanchnic nerve
•Hindgut viscera- Supra-pubic - referred pain felt in T12-
L1/L2 dermatomes - Associated with Least splanchnic nerve/lumbar splanchnic nerves
26
Hernia
hernia is a protrusion of part of the abdominal contents beyond the normal confines of the abdominal wall.
3 parts - sac (peritoneum pouch), contents(loops of bowel, omentum etc) and covering.
Hernias that are not stuck
◦ Fullness or swelling
◦ Gets larger when intra-abdominal pressure increases
◦ Aches
Hernias that are stuck (incarcerated)
◦ Pain ◦ Cannot be moved
◦ Nausea and vomiting (and other signs of bowel obstruction) ◦ Systemic problems if bowel has become ischaemic
Causes - Weakness in the containing cavity
Congenitally
o Post surgery where wounds have not healed adequately (incisional hernia)
o Normal points of weakness
Anything that increases intra-abdominal pressure - o Obesity
o Weightlifting
o Chronic constipation/coughing
27
explain how the process of folding in the embryo during the 4th and 5th week creates the primitive gut, the abdominal wall
Primitive gut tube and Abdominal wall formed by lateral folding:
Somatic mesoderm grows ventrally to form lateral body walls.
Each body wall folds towards midline to form cylindrical shape.
Splanchnic mesoderm and endoderm fold in from lateral side and endoderm goes into inner part of the embryo to form gut tube.
Foregut = oesophagus to duodenum 2nd part + lower resp
Midgut = duodenum to 2/3 of transverse colon
Hindgut = 1/3 + rest of colon (descending and sigmoid) till cloaca
Foregut = coeliac artery
Mid = SMA
Hind = IMA
28
describe how the coelomic cavity and peritoneal cavity develop
The mesoderm surrounding the gut splits into layers; somatic (develops into the abdominal wall) and splanchnic (smooth muscles of the gut wall).
The space created by the split is the coelomic cavity which begins as one large cavity (the forerunner of the pleural cavity and peritoneal cavity).
29
describe the fate of the embryonic dorsal and ventral
mesenteries
The dorsal and ventral mesenteries become the various peritoneal folds and reflections that suspend the gut and give passage to vessels and nerves in the adult.
the greater omentum is derived from the dorsal mesentery and the lesser omentum from the ventral mesentery.
30
explain how the greater and lesser omenta and the mesentery of
the small intestine develop and relate this to their arrangements
in the neonate and the adult 5.
31
describe the basic development of the foregut structures
(stomach, liver, pancreas, and duodenum)
When the stomach develops the dorsal border develops faster giving the stomach its characteristic shape (greater curve).
The liver develops within the ventral mesentery along with the biliary system and uncinated process of the pancreas.
The pancreas is a foregut structure which develops from two portions (a dorsal portion forming most of the gland and a ventral portion forming most of the duct system).
The liver grows into the ventral mesentery dividing it into two
parts (the falciform ligament and the lesser omentum).
32
describe the functions of saliva
Lubrication -mucins
Protection - cooling effect, buffers acid, antibacterial (lysosomes), lactoferrin reduces iron availability to bacteria.
Digestion - salivary amylase, lingual lipase
• Maintenance of oral hygiene
Protection from infection
• Taste
• (transmission of infection)
33
list the components of saliva secreted by each pair of salivary
glands
Link to body log
Amylase (secreted by salivary glands)
Lingual lipase (secreted by lingual glands)
Parotid gland - 25%, enzymes, serous
Anterior border = Masseter
Superior = zygomatic arch
Inferior = mandible
Posterior = ear
From under tongue Submandibular - serous and mucus, 70%
Sublingual - mucus, less enzymes, 5%
34
explain the mechanisms of secretion of (hypotonic) serous
saliva
Link to body log
Acinar cells produce ISOTONIC saliva
Myoepithelial cells contract
Ductal cells move sodium + Cl out of solution while being impermeable to h2o
Pumps in potassium and bicarbonate(b highest at high flow rate)
Becomes HYPOTONIC (depending on flow rate - less hypotonic during high )
35
describe the control of salivary secretion
Link to CNS
Pathologies
Autonomic
Sympathetic stimulates
secretion of small amounts of
less watery saliva, but also causes vasoconstriction
Parasympathetic = glossophyrangeal nerve - parotid gland
Facial nerve - submandibular + lingual glands
Xerostomia - not enough saliva
Causes= Medications, autoimmune, dementia, readiotherapy, dehydration
Symptoms = infections, tooth decay, halitosis
Infections that affect salivary glands
Viral - Mumps - parotid - MMR
Autoimmune = Sjogrens - dry mouth c swollen/painful salivary glands
Salivary stones = sialoliths- calcified - pain associated with eating - commonly submandibular Wharton’s duct
36
describe the processes of swallowing
Oral phase = bolus touches pharyngeal wall
• Voluntary
Tongue movements move bolus to touch hard palate na towards pharynx.
Pharyngeal phase
• Involuntary
• Soft palate seals off nasopharynx
• Pharyngeal constrictors push bolus downwards
• Larynx elevates, closing epiglottis
• Vocal cords adduct (protecting airway) and breathing temporarily ceases
• Opening of the upper oesophageal sphincter
Oesophageal phase
• Involuntary
• Closure of the upper oesophageal sphincter
• Peristaltic wave carries bolus downwards into oesophagus
Neural control
Mechanoreceptors
Glossopharyngeal nerve
Goes to medulla
Vagus nerve
Pharyngeal constrictors
37
outline the anatomical relationships of the oesophagus and
how disordered swallowing may occur as a consequence of a primary oesophageal disorder or a condition in a closely related structure
38
categorise different types of dysphagia based on the
underlying pathology
Problems with swallowing
Dribbling
Material can enter resp tract and cause choking
Fluid swallowing harder to control
Causes - Parkinson’s, MS etc
Blockage to passage of food
Fibrous rings
Oesophageal cancer - progressive (eventually blocks food and fluid) - above 55 with this and other red flag symptoms means investigate
Achalasia- failure of LOS to relax.
39
describe the position and functional anatomy of the stomach, its parts, sphincters, vascular and nerve supply, and key relations to other abdominal organs
Below diaphragm
Top = fundus
Body
Antrum
LOS stops reflux.
Intrinsic smooth muscle and crural part of diaphragm closes it when inc intra abdominal pressure.
Muscular - intrinsic + diaphragm
Right crus
Acute angle coming into stomach
Pyloric sphincter controls release of chyme into duodenum.
40
• describe the macro and microscopic structure of the gastric mucosa
Muscles:
Oblique
Circular
Longitudinal
Epithelia = surface mucus cells
Invaginations of epithelia = gastric pits which lead to gastric glands
Contain parietal cells that produce acid (lot in body)
Also chief (lot in body) and enteroendocrine cells(eg G cells in antral).
41
• describe the components of gastric secretion and their cellular origins
Call CCK receptor Gastrin receptor
HCl from parietal:
H+/K+ ATPase/proton pumps in tubulovesicles in resting phase.
In stimulation phase - H+ out and K+ in as tubulovesicles bind to apical membrane.
Carbonic acid broken down to H+ and bicarb by CA
Bicarbonate/Cl antiporter allows Cl into cell and then leaves cell to go into lumen through Cl channels
HCl formed in lumen
Has K+ channels which allows it to leave.
Have canaliculi and microvilli.
Gastrin from G cells
Gastrin released when:
# peptides sensed in lumen
# sensory triggers cause vagus nerves to release ach which binds to muscarinic receptors
# GRP released by stretch by vagus nerves
Gastrin binds to CCK receptors on parietal cell
Histamine released by entero-chromaffin like cell
by vagal stimulation or CCK receptor (which Gastrin binds to)
Which binds to histamine receptor on parietal cell
Pepsinogen from chief cells
D cells produce somatostatin which inhibits production of Gastrin by binding to receptor of G cell.
42
• describe the mechanisms that exist to protect the stomach epithelia against an acidic environment
Mucus secretion from surface mucus cells
Secret bicarbonate onto epithelia so alkaline layer
Rich blood supply- take away acid quickly
Prostaglandins = inc blood flow, mucus
Epithelial cells replaced regularly
43
• describe the patterns of motility of the stomach, including receptive relaxation and peristalsis
Stimulation of acid production in stomach
Peristalsis in oesophagus
Reflex relaxation of proximal stomach - receptive relaxation
Rugae means fundus can distend
Fill without sig rise in pressure
Stimulation:
1st = triggers
Sensory - cephalic - 30%
Gastric - food enters so stretch, food raises pH, amino acids +small peptides - 60%
Intestinal - chyme in duodenum - 10%
Gastrin binds to CCK receptors on parietal
Vagal stimulation
Ach binds to Mcr receptors on parietal
Histamine binds to CCK resceptors
44
• describe the process of gastric emptying and its control
45
describe the overall functions of the stomach
Storage facility
Start digestion of protein - chyme
Little bit carb + fat digestion
Disinfects
46
Describe the origins, courses and major branches of the abdominal aorta (coeliac trunk, superior mesenteric artery and inferior mesenteric artery)
Describe the origins, courses and major branches of the superior mesenteric artery.
Abdominal aorta - coeliac trunk at T12
gives off SMA at L1 which supplies midgut.
Branches to left to ileum and jejunum.
SMA gives off right colic artery (to ascending colon) and middle colic artery (to transverse colon) and iliocolic artery (to terminal ileum and caecum at right lower quadrant).
Anastomoses linking blood supply to colon is marginal artery.
IMA at L3 which supplies hindgut
Gives off left colic artery for descending colon.
Sigmoid arteries come off and supply sigmoid.
IMA becomes superior rectal artery as it passes pelvis.
Splenic flexure where midgut and hindgut anastomoses meet - weakest area.
47
Dyspepsia def
GORD ( symptoms, risk factors, complications, treatment)
Dyspepsia - 4 weeks of upper GI symptoms
GORD
Symptoms - heart burn, acidic taste, dental erosion, cough
Risk factors - inc intra abdominal pressure = obesity, pregnancy
LOS dysfunction
Hiatus hernia - LOS herniates into thorax
Delayed gastric emptying
Complications:
Oesphagsitis, ulceration, haemorrhage, strictures, barrets (stratified squamous to columnar so adenocarcinoma)
Treatment- weight loss, avoid trigger foos, PPIs, H2 receptor antagonists, fundoplication
48
Gastritis def and histology
Acute and chronic causes
Symptoms for autoimmune and H pylori
Transmission, path, colonise, diagnose, treatment for h.pylori
Inflammation of stomach mucosa
Acute = NSAIDs, alcohol, chemo, bile reflux
Chronic = infection with H.pylori (g -ve), autoimmune
Transmission = H.pylori from faeco-oral or oral-oral
Pathophysiology = Flagella, chemotaxis, adhesins.
Then damage epithelia by:
urea to ammonia (toxic) to inc pH.
CAG A (cytotoxin associated gene) into cell which causes inflammation and inc stomach cancer risk.
VAG A inc cell permeability and is toxic.
Mucinase damages mucus layer.
Colonisation:
Antrum = inc Gastrin = inc acid = damage to duodenum = colonisation of this and ulcers
Fundus = atrophy of parietal cells = cancerous
Diagnosis = urea breath test (patients ingest urea with radioactive carbon 13 so if lot exhaled then they are infected), stool antigen test, endoscopy with biopsy
Treatment = PPI + clarithromycin (can be resistant) + metronidazole for 7 days. SE = diarrhoea + nausea.
Antibodies to parietal cells so dec acid and IF
Symptoms - Vit B12 def so glossitis and megaloblastic anaemia. Also neurological symptoms such as anorexia.
Atrophy of body of stomach as this is where most parietal cells are.
Histology:
Epithelial damage, Neutrophil response, vasodilation, hyperplasia
Lymphocytes, glandular atrophy, fibrotic, metaplasia
49
Peptic ulcer disease
Compare gastric and duodenal
Link to body log
Link to NSAIDs in path pro
Defect in gastric or duodenal mucosa that extends through Muscularis mucosa
Usually lesser curve and antrum and duodenum (3x)
Duodenal - O, risk inc with age after 35yrs, high acid, higher majority due to H.pylori due to colonisation of antrum then inc Gastrin then inc acid then acidic chyme.
Gastric - A, social class, risk inc with age, low acid
Risk factors
H.pylori, NSAIDs due to dec prostaglandin synthesis, smoking, stress eg massive burns
Complications = necrotic and scar tissue replaces Muscularis externa can cause pyloric stenosis so vomiting.
Perforation -go through wall of gut. Leads to peritonitis.
Ulceration into other organs
Haemorrhage so malaena (slow) - black stool
If into gastro-duodenal artery then haematemesis
Malignancy
Symptoms- burning/gnawing pain, epigastric pain, back pain, following meals (duodenal can have momentary release), early satiety, weight loss
Treatment
Eliminate H.pylori
Stop NSAIDs
If bleeding then endoscopically inject around ulcer. If perforated repair surgically.
50
1. describe the key properties of chyme leaving the stomach
2. list the secretions of the exocrine pancreas
3. relate the structure of the endocrine pancreas to its secretions
1. Hypertonic, acidic, partially digested
Then in duodenum becomes isotonic
2. Enzymes - amylase + lipase. Inactive proteases = trypsinogen, chymotrypsin, elastase, carboxypeptidase which are activated by trypsin. Also, bicarbonate ions
3.
4.
51
4. describe the mechanism of secretion of alkaline juice
5. describe the control of pancreatic and biliary secretion
5. Sympathetic inhibits pancreatic secretion
Para - vagus stimulates, hormones - CCK.
Enzymes concentrated into membrane bound zymogen granules and released with stimulus.
52
2. describe the digestive functions of the liver and the components of bile
3. describe the secretion of bile acids and the entero-hepatic circulation of bile acids
5. describe the mechanisms of digestion of fats
2. 2 primary bile acids are cholic acid and chenodeoxycholic acid
Bile acids conjugate with glycine and taurine to form bile salts.
3. Bile drains from liver to duodenum.
Bile acid dependant is secreted into canaliculi by hepatocytes and contains bile acids and pigments.
Independent is secreted by duct cells and stimulated by secretin.
Bile salts after delivering lipids are reabsorbed in terminal ileum and liver extracts it from portal blood.
5. Bile salts emulsify fats
Form micelles
Carry cholesterol, monoglycerides and FFA by diffusion into epithelial cells.
Re-esterified into triglycerides, phospholipids, cholesterol
Packaged with apoproteins to form Chylomicrons.
Exocytosis from basolateral membrane into lymphatic system.
53
1. describe how the microscopic structure of the liver relates to its functions
4. describe the function of the gall bladder and the relationship to the formation of gallstones
4. Stores bile, concentrates it which can lead to gallstones
54
• describe digestion of carbohydrates and proteins
• describe absorption of sugars, amino acids, salts in small intestine
Digestion:
Starch made up of amylose and amylopectin
Alpha 1-4 bonds broken by amylase
So glucose + maltose + alpha dextrin(from amylopectin)
Then isomaltase breaks 1-6 alpha bonds
So glucose + maltose
Lactose = glucose + galactose by lactase which is brush border enzyme
Sucrose = glucose + fructose by sucrase
Absorption:
SGLT1 in apical membrane cotransports glucose/galactose by gradient of Na+ in cell as it is pumped out by Na+/K+ ATPase
Fructose comes in by GLUT5
Then in basolateral all leave by GLUT2 into blood
Digestion:
Stomach activates pepsinogen into pepsin so makes small peptides + amino acids
In duodenum - zymogens are present as secreted from pancreas. Trypsinogen converted to trypsin by Enteropeptidase.
Trypsin activates other proteases - chymotrypsinogen, proelastase (endopeptidase - middle) procarboxypeptidase A and B (exo).
Absorption:
By co-transport with Na+ or PEPT1
Cystolic peptidases break down small peptides or go into blood like amino acids.
55
• describe the basis of oral rehydration therapy by absorption of water
Describe water secretion
Water follows Na+:
Absorbed via paracellular as Na+ pumped out and gathers there. Or intracellular as Na+ goes in by co-transport.
Oral rehydration packet has sugar, salt and water as water is absorbed as it goes down osmotic gradient.
Secretion
Cl- moves into cell from blood via Na+/K+/Cl- transporter.
When cAMP rises then Cl- goes out via CFTR
Na+ goes out via tight junction and forms NaCl
Draws H2O out
56
• describe the common causes for vitamin B12 deficiency
Vit B12 def
Causes = lack of IF, hypochlorhydria (lack of stomach acid)/PPI/gastric atrophy means less release cobalamin, dietary, inflammatory disease of terminal ileum where B12 is absorbed (eg Crohs)
57
• describe the pathological basis and symptoms of lactose intolerance
Deficiency of lactase
Lactose not broken down - high osmotic pressure in lumen which draws H2O in - diarrhoea
Fermented in colon - flatus + bloating
58
• describe the symptoms of irritable bowel syndrome (IBS)
Symptoms
Abdo pain
Bloating
Flatulence
Diarrhoea/constipation
Rectal urgency
Female to male = 2:1
20-40
Psychological disorders
59
• describe the pathological basis, symptoms, investigation, and
treatment of coeliac disease
Immune response to gluten
Gliadian fraction = wheat, rye, barley
Damages mucosa
Flattening of villi
Hypertrophy of crypts
Lymphocytes in epithelium
Causes
Genetic
Malabsorption = Diarrhoea, weight loss, flatulence, abdo pain, anaemia as dec Fe absorption, neuro as dec Ca
Investigations
Blood test - IgA to smooth muscle Endomysium and tissue transglutaminase
Endoscopy + duodenal biopsy
Treatment- gluten free diet
60
1. outline the main roles of the liver and explain how this may be impaired by common liver pathology
1. Storage = glycogen, fat-soluble vitamins (A,D,E, K and B12), iron, copper
2. Synthesis - glucose through gluconeogenesis, lipids and cholesterol for cell membrane and hormones, bile, clotting factors, albumin (maintains blood vol and transports substances).
3. Metabolism - glycogenolysis, gluconeogenesis, detoxification- removes bilirubin, ammonia, drugs, and alcohol. Also lipid breakdown and synthesis of fats.
61
2. To describe the pathophysiology and clinical presentation of common
hepatic pathology (cirrhosis, alcoholic and non-alcoholic liver disease, hepatitis and autoimmune conditions)
Alcoholic liver disease
Takes years (this is initially reversible).
Fatty liver (steatosis), then alcoholic hepatitis and end point is cirrhosis which is irreversible.
Presentation - jaundice with tender hepatomegaly.
Non-alcoholic fatty liver disease (NAFLD) - accumulation of fat which can progress to inflammation and liver cell injury, and then cirrhosis.
Causes - obesity, diabetes, and metabolic syndrome
Autoimmune Diseases:
Autoimmune Hepatitis - immune system mistakenly attacks the liver, causing inflammation and damage. Leads to cirrhosis.
Primary Biliary Cirrhosis - progressive destruction of bile ducts in the liver - lead to cirrhosis.
Primary Sclerosing Cholangitis - inflammation and scarring of the bile ducts - leading to cirrhosis.
Presentation:
Non-specific - Nausea, vomiting, loss of appetite, abdo pain, fatigue
Specific - jaundice, oedema (dec albumin), bleeding(dec clotting factors), confusin(build up of ammonia)
62
Cirrhosis and causes
3. describe the portal circulation
Cirrhosis - formation of scar tissue, becomes nodular and hardened, disrupts function. Causes:
alcohol misuse, certain
medications, deposition of fat, iron (haemochromatosis) or copper(Wilson’s disease - due to dec secretion within biliary system), autoimmune causes, chronic hepatitis (B or C - inc risk of hepatocellular carcinoma).
Portal circulation - drains into liver before reaching IVC, includes IMV,SMV, splenic vein. Join together to form portal vein.
Responsible for carrying nutrient- rich blood from stomach, intestines, and spleen, to liver for removing toxins and metabolising nutrients.
63
4. describe how liver pathology can lead to portal hypertension and how
this may present clinically
Portal hypertension = blood flow into liver from portal vein is restricted due to fibrotic changes (cirrhosis) in liver so inc hydrostatic pressure within portal venous system.
Presentation:
Varices - Fibrotic liver - blood cannot flow to hepatic sinusoid - inc portal pressure. Blood can flow through normally unused connections to relieve pressure - porto-systemic anastomoses.
Form varices (dilated veins) in oesophagus (can rupture), around the umbilicus (Caput medusa - can be seen) or in the anorectal region (rectal bleeding, anaemia, and discomfort).
Ascites - accumulation of fluid in the abdominal cavity.
Splenomegaly - inc pressure within splenic circulation
64
5. describe how liver pathology can cause hepatorenal syndrome
When acute kidney injury can result from cirrhosis.
This is related to:
portal hypertension
Splanchnic vasodilation - cirrhosis and portal hypertension inc nitric oxide in gut vessels
Activation of RAAS - blood pools in gut so need systemic vasoconstriction
This dec renal blood flow and causes kidney injury.
65
Describe biliary tree
6. describe the formation and composition of gallstones
The common hepatic duct and cystic duct join to form the common bile duct, which releases bile into the duodenum. The pancreatic duct also joins the common bile duct, allowing pancreatic enzymes to enter the duodenum.
Gallstones = certain components of bile, esp bilirubin and cholesterol, come out of solution to form a solid.
Risk factors - diet, lifestyle, gender (more common in women), and pregnancy.
66
7. describe the pathology and clinical presentation of the common complications of gallstones (biliary colic, acute cholecystitis,
ascending cholangitis, and acute pancreatitis
Biliary colic occurs due to a temporary obstruction of the cystic duct which causes sudden onset RUQ pain. There is no associated
inflammation. Pain relief and cholecystectomy.
Acute cholecystitis occurs if a gallstone becomes impacted within the cystic duct. Inflammation, RUQ pain and fever. Same with antibiotics. No jaundice.
Acute ascending cholangitis is - infection of the biliary tree caused by a stone blocking the common bile duct. Charcot’s triad (jaundice, fever and RUQ pain) often results. Same as above with fluid management.
acute pancreatitis - gallstone obstructs the distal common bile duct at the same location as the major pancreatic duct joins it.
Pro-enzymes in pancreatic secretions prematurely activated within the ductal system.
Auto-digestion = inflammatory reaction.
epigastric pain that may radiate to the back.
Identify elevated amylase and lipase in blood tests, rule out other causes of epigastric pain and supportive care. Treat underlying cause.
67
1. define jaundice
Jaundice is the clinical manifestation of raised plasma bilirubin
68
2. describe how jaundice relates to haem/bilirubin metabolism
Bilirubin is a breakdown product of the haem component of RBCs.
1st Spleen - Hb into haem and globin. Then biliverdin and then unconjugated bilirubin.
Pre-hepatic - caused by too much haem breakdown - raised unconjugated bilirubin
levels
2nd Liver - unconjugated bilirubin is transported by albumin to liver. Combined with glucuronic acid, making it conjugated so water-soluble and suitable for excretion.
Hepatic -dec liver function - mixed levels
Post-hepatic is caused by obstruction of the biliary tree - conjugated
69
3. describe the clinical presentation of jaundice
yellow discoloration of the skin and the whites of the eyes
Post- hepatic = blocked pathway for bilirubin excretion so absence of bilirubin in the gut - pale stools
Present in urine - dark urine
70
4. describe common pathology that can cause jaundice (pre-hepatic,
hepatic, and post-hepatic)
Pre - Haemolytic anaemias (e.g., sickle cell anaemia, thalassemia)
• Hereditary conditions affecting red blood cell
• Blood transfusion reactions
• Certain infections (e.g., malaria)
• Medications or toxins that cause haemolysis
Hep - • Acute viral hepatitis
• Paracetamol toxicity
• infections affecting the liver
• Chronic liver diseases
• Genetic disorders affecting bilirubin metabolism within the liver
Post - • Gallstones blocking the common bile duct
• Inflammation or scarring of the bile ducts (e.g., primary sclerosing cholangitis)
• Pancreatic tumours causing compression of the biliary tree
• Biliary atresia (a congenital condition where bile ducts are absent or underdeveloped)
71
5. describe how malignancy in the head of the pancreas can cause
jaundice
72
state which tests are included in the liver function tests (LFTs) and
describe what each of them can measure
Albumin levels - liver produces it so in liver disease it falls
ALT and AST levels = enzymes present in the hepatocytes.
When there is hepatocyte damage they are raised in plasma.
ALT - more specific and in acute liver damage is raised more.
ALP levels = found in cells lining the biliary tree, raised in pathology leading to cholestasis (e.g., gallstones).
Gamma-Glutamyl Transferase (GGT): GGT is found in liver cells so elevated when there is damage in the bile ducts. Measuring GGT can help confirm whether elevated ALP levels are due to liver-related issues.
5. Bilirubin
73
7. interpret abnormal LFTs in the context of jaundice
74
Describe the incidence of common cancers of the G.I. tract
Bowel, pancreas, stomach, oesophagus, liver inn order of most to least- quarter of 20 most common cancers
75
(oesophageal cancer
pathology, clinical presentation, basic understanding of diagnosis and treatment
Pathology
Clinical presentation:
Progressive dysphagia - Initially solids more difficult to swallow (physical obstruction)
• Odynophagia (pain on swallowing)
Anaemia
Loss of weight
Aorexia - loss of appetite
Recent onset of progressive symptoms
Malaena
Diagnosis
1. Blood tests- FBC - • Anaemia
2. (OGD) with biopsy
• Can help determine whether benign or cancerous cause
3. CT thorax and abdomen
• Size of primary, local invasion, metastatic spread
Treatment (dependent on stage)
• Endoscopic therapies (for limited disease) • Oesophagectomy (removal of oesophagus) • Chemoradiotherapy
Risk Factors
Squamous Cell Carcinomas- smoking, alcohol use, dietary intake e.g. hot beverages
Adenocarcinomas- obesity, reflux disease, Barrett’s oesophagus
Prognosis- 5% survival at 5 years
76
• Describe the basic histology of common gastro-intestinal cancers
Oesophageal
Most commonly squamous cell carcinomas - Generally upper 2/3rd
Adenocarcinomas from columnar epithelium can occur in the lower 1/3rd - Barrett’s oesophagus (change of epithelium)
Gastric
Histology • Most commonly adenocarcinomas • Can get lymphoma, leiomyosarcoma,
neuroendocrine tumours
gastric cardia (31%), followed by the antrum (26%), and body of the stomach (14%)
Pancreatic ductal adenocarcinoma is the
main type
• Pancreatic neuroendocrine tumours are rare and originate from the endocrine cells in the pancreas
• They may be non-functional, or they may secrete hormones e.g.
insulin
Hepatocellular carcinoma (HCC) - Primary cancer arising from hepatocytes
Choloangicarcinoma
Adenocarcinoma, can be intra or extra-hepatic
Colorectal
Adenocarcinomas which progress from normal epithelium in a classical
pattern
Anal
squamous cell carcinomas
77
stomach,
pathology, clinical presentation, basic understanding of diagnosis and treatment
Classification
Location
• Cardia gastric cancer- similar presentation to oesophageal cancer
• Non-cardia gastric cancer- in other parts of the stomach
Type
• Lauren classification
➢Diffuse (occurs more often in young patients and has a worse prognosis than intestinal type)
➢Intestinal
Clinical Presentation:
➢ Unexplained weight loss
➢ Epigastric abdominal pain
➢ Lymphadenopathy- Virchow’s node
➢ Dysphagia (if cancer is located around the cardia)
Prognosis- 70% 5-year survival for local disease • 5% if distant metastasis
Risk factors:
General - Age (50-70), Male
Strong
• Pernicious anaemia
• H-Pylori
• N-nitroso compounds
Weak - Family history, High salt (weakens gastric mucosa and enhances negative effects of N-nitroso compounds), Smoking
Investigations • Bloods- anaemia • Upper GI endoscopy and biopsy- for tissue diagnosis
• CT CAP (chest, abdomen and pelvis)- for determining extent of disease
Management:
Superficial- endoscopic mucosal resection
Localised- surgery to remove all or part of the stomach (gastrectomy) BUT if not suitable
for surgery then chemoradiation Metastatic- chemotherapy/immunotherapy and supportive care
78
pancreas,
pathology, clinical presentation, basic understanding of diagnosis and treatment
Risk Factors
• Smoking • Chronic pancreatitis
• Inherited mutations in BRCA1 , BRCA2 ,
and PALB2 and with familial syndromes
• Men, increasing age
Clinical Presentation
• Painless jaundice, unexplained weight loss, can present with abdominal/back pain
• New-onset type 2 diabetes mellitus in an adult over 50 years of age without any obesity-related risk factors
Investigations
• Bloods- LFTs if jaundiced, CA 19-9
• CT- focused on pancreas can give very high diagnostic accuracy
• USS- Can detect cancer arising in the head with reasonable accuracy but not in the body
or tail
• May biopsy (EUS-FNA)
Management
• 10-15% are suitable for surgical resection (followed by pancreatic enzyme replacement)
• Biliary stenting for jaundice
• Chemotherapy, potentially radiotherapy, and symptom management
20% 5 year survival
79
hepatocellular,
pathology, clinical presentation, basic understanding of diagnosis and treatment
Risk Factors
Causes of cirrhosis - alcohol, Hep B&C
Clinical Presentation - underlying liver
disease so those symptoms can mask the malignancye.g. ascites, fatigue
Acute hepatic decompensation or right upper quadrant pain can be signs of the development of HCC
Prognosis
5-year survival rate= approx. 50% with complete surgical resection or liver transplantation
Advanced HCC= median overall survival time with treatment is approx. 1 year
Investigations -Blood tests:
➢ LFTs, Prothrombin time/INR (check synthetic function of the liver), Viral hepatitis panel
• USS- Non invasive and a good way to screen high risk individuals - CT/MRI abdomen, Liver Biopsy
Treatment - If suitable then ablation, resection or transplantation. If not then chemotherapy/immunotherapy
80
Cholangiocarcinoma (Bile Duct Cancers)
pathology, clinical presentation, basic understanding of diagnosis and treatment
Risk Factors
Liver and bile duct diseases- cirrhosis,
alcoholic liver disease, bile duct diseases (e.g. bile duct adenoma), gallstones,
PSC
• Infections
• Exposure to certain toxins/medications
Clinical Presentation - painless jaundice, pruritus, dark urine,
and light colour stool in extrahepatic due to biliary obstruction
Prognosis- five-year survival rate in metastatic disease is 2%
81
Colorectal cancer - link to path pro
pathology, clinical presentation, basic understanding of diagnosis and treatment
Risk Factors
• Dietary- high dietary fat, high red meat consumption, low dietary fibre, alcohol intake
• history of IBD
• Genetic - familial adenomatous polyposis (FAP) and hereditary
nonpolyposis colorectal cancer (HNPCC)
Clinical Presentation
Red flags:
In right side occult bleeding in stool, left is rectal bleeding.
Change in bowel habit (in right it’s late and left it’s early).
Iron deficiency anaemia
Tenesmus
Mass on rectal examination (right and left iliac fossa).
Both sides- Unexplained weight loss
Other:
• Advanced (more likely in right) - bowel obstruction (in left more likely) or perforation
symptoms due to hepatic or peritoneal metastases e.g. abdominal pain and ascites
Prognosis - For non-metastatic - 5-year survival rate is 50-
95%
82
CC 2 - link to pass
Investigations
• Stool tests- e.g. FIT*
• Blood tests- FBC for anaemia, CEA
• Colonoscopy and biopsy
• Imaging- CT, MRI
Management
• Surgery with pre or post-operative chemotherapy/immunotherapy
Screening
83
Anal cancer
pathology, clinical presentation, basic understanding of diagnosis and treatment
Risk Factors
• Strongly associated with HPV infection, HIV infection
• Engaging in anal-receptive sexual intercourse
• Chronic local inflammation due to IBD or recurrent anal fissures
Clinical Presentation
• local symptoms such as perianal pruritus or pain, bleeding, discharge, and a mass like sensation
Prognosis - More than 70% of cases can be cured with chemoradiation
Management
• Pap smears in high-risk populations
Better prevention and
treatment of HIV infection
84
Describe how G.I. cancers may spread within the body - notion for all cancers that go to liver
Liver is a common site for
metastases
• Haematological e.g. portal
spread from other GI viscera
• Lymphatic
• Spread via other routes e.g.
ovarian= transcoelomic
Eg - colorectal, pancreatic, gastric cancer
85
• Describe the adeno-carcinoma sequence relating to colorectal cancer
Series of genetic and epigenetic mutations leading to activation of oncogenes and inactivation of tumour suppressor genes. Hereditary Non-Polyposis Colon Cancer (HNPCC) Syndrome - autosomal dominant - Germline mutation affects one of several DNA mismatch repair genes eg MSH2,MSH6.
Normal Glandular Cells -> Adenomas (Benign neoplasms) -> Invasive Carcinoma
86
1. describe the normal anatomy of the rectum + blood supply
Rectum - 12-15cm long passes through the pelvic floor
Has a continuous band of outer longitudinal muscles unlike the taeniae coli of the rest of the colon
Temporary storage of faeces prior to defaecation
Stretching of rectum stimulates urge to defaecate
Arteries/veins
Superior rectal artery -continuation of Inferior mesenteric artery
Middle rectal artery- internal iliac
Inferior rectal- pudendal artery
Venous drainage
Portal drainage through superior rectal vein
Systemic drainage through internal iliac vein
Forms porto-systemic anastomosis
87
Anatomy of anal canal
The anal canal continues on from the rectum
Starts at proximal border of the anal sphincter complex
Rectum points anteriorly - Pubo-rectalis sling changes the direction of the anatomy - Anal canal points posteriorly - continence mechanism
Anal sphincter complex
• Internal involuntary sphincter - Thickening of circular smooth muscle - autonomic control (80% of resting anal pressure)
• External anal sphincter is striated muscle (20% of resting pressure). Nerve supply from pudendal nerve.
Has deep section that starts at upper anal canal. Mixes with fibres from levator ani. Joins with pubo-rectalis to form sling
Also has superficial section
Anal canal contains the Dentate line
Above the dentate line - Visceral pain receptors.- Columnar epithelium - Hindgut
Below the dentate line - Somatic pain receptors • Stratified squamous epithelia - sharp, localised - ectoderm
88
Process of continence
The anal canal is involved in continence
Factors required:
Distensible rectum (inc pressure would overcome sphincter)•
Firm bulky faeces (easier for sphincter)•
Normal anorectal angle (puborectalis sling)
Anal cushions (blood vessels that distend and help sphincter)
Normal anal sphincters
1. Mass movement
2. Defecation reflex
Stimulus - rectum distends
Response - Contraction in rectum and sigmoid colon. internal anal sphincter relaxes. External contracts.
3. Inc rectum pressure
4. Delay
Contraction of EAS, puborectalis muscle, reverse peristalsis of sigmoid colon. In defecation opp and Valsalva manoeuvre which is inc intra abdominal pressure.
89
describe common causes of haematochezia - haemorrhoids, anal fissure,
- look at notion for grading and image of haemorrhoid
Haemorrhoids - Internal - most common - Above dentate line
• Caused by loss of connective tissue support around anal cushions
Relatively painless as above the line
Enlarge and prolapse through anal canal so can go below line
Bleed bright red blood/pruritis
Treatment
• Increased hydration/ high fibre diet
• Avoid straining
• Rubber band ligation - necrosis and fall off
• Surgery
External
• Swelling of the anal cushions which may then thrombose
• Painful++
• Surgery
Anal fissure
Linear tear in the anoderm(it is the ectoderm) usually posterior midline.
Due to - Due to passing of hard stool, High internal anal sphincter tone (inc risk of tear), Reduced blood flow to anal mucosa.
• Pain on defaecation (passing razor blades)
Treatment
• Hydration, dietary fibre, analgesia
• Warm baths
• Medication trying to relax the internal anal sphincter
90
differentiate between the common causes and clinical presentation of melaena and haematochezia
Haematochezia - bright red blood
Rough order of frequency :
Diverticulitis
Angiodysplasia (small vascular malformation in bowel wall)
Colitis - IBD, infective
Colorectal cancer (erodes through blood vessels)
Anorectal disease - haemorrhoids and anal fissure
Upper GI bleeding - Large bleed with fast transit
Melaena - Black tarry stools
Offensive smelling
Due to the haemoglobin being altered by digestive enzymes and gut bacteria
Common causes
•Upper GI bleeding
• Peptic ulcer disease
• Variceal bleeds
• Upper GI malignancy - Oesophageal/ gastric cancer
Uncommon causes
• Gastritis • Meckel’s diverticulum • Iron supplements
91
Describe the importance of the gut microbiome and the role of commensal organisms
Benefits:
Harmful bacteria cannot compete for nutrients
Produce antimicrobial substances
Help to develop newborn’s immune system
Produce certain nutrients eg Vit K
Bacteria in colon produce SCFAs - acetate(cholesterol metabolism), propionate(regulate satiety), butyrate(energy source for colonocytes, regulate gut environment)
Diversity lowers risk of obesity, IBD, affects response to chemotherapy and insulin.
Need high-fibre diet, prebiotics. No artificial sweeteners.
Proximal gut - relatively sterile other than H.pylori (stomach is aerophillic- lower pO2)
More distal = more bacteria - anaerobic
Faeces - 20% bacteria
Faecal microbiota transplant for pseudomembranous colitis (C.difficile), IBD - administered through NG tube, upper Gi endoscopy, colonoscopy, enemas - Need healthy 10-25yr olds.
92
Describe the clinical features and aetiology of gastrointestinal infections caused by common bacterial agents -gram -ve rods - link with infection
Salmonella
Nausea, vomiting, non-boddy diarrhoea, fever, cramping
Ingesting contaminated food and water
2-3days
Pathophysiology of systemic disease:
Salmonella gain access to enterocytes and move to submucosa
Macrophages there transfer it to reticuloendothelial system Multiply inside cells and cause lymphoid hyperplasia. Liver and gallbladder infection.
Re-enter gut from liver
Campylobacter - spiral
Fever, cramping, bloody diarrhoea
Faeco-oral route (chickens)
Multiply within host (incubation 1-7 days), releases cytotoxin
Self-limiting - just need fluids (sometimes antibiotics)
Shigella
5yrs or younger
Spread from infected stools, person-person
Bloody diarrhoea with mucus, cramping
Small dose
Invades LI colonocytes, multiplies and invades neighbouring cells, kills them, forms abscesses in mucosa
Resolves in week
Enterotoxigenic E.coli
Commensal but also pathogen
Faecal-oral in contaminated water
Traveller’s diarrhoea - watery diarrhoea
Adheres to enterocytes, produce enterotoxins, hypersecretion of Cl-, water leaves cells into lumen
93
Gram negative rods comparison
Bloody diarrhoea - shigella, campylobacter - colon
Watery - salmonella, ETEC - SI
Haemolytic uraemia syndrome (anaemia, thrombocytopenia, AKI) - shigella, campylobacter
Duration short to long
ETEC, Salmonella, shigella, camp
94
Describe the clinical features and aetiology of gastrointestinal infections caused by common bacterial agents -gram +ve - link with infection
+ve, anaerobic (fine for colon), spore forming bacillus
Faecal-oral
Following antibiotics (esp broad spectrum - for some can be asymptomatic) can colonise and release A (enterotoxin - hypersecretion - diarrhoea) & B (cytotoxin - kills colonocytes) toxins. Cramping.
Complications:
Pseudomembranous colitis - elevated yellow plaques join to form pseudomembrane - stop offending antibiotics, fluids, metronidazole/vancomycin, probiotics
Toxic megacolon - surgery
95
Describe the clinical features and aetiology of gastrointestinal infections caused by virus
Rotavirus - double-stranded RNA virus
Under 5s
Fascia-oral route low dose
Vomiting with fever, diarrhoea
Chloride secretion - virus inc cyclic ANP so opens CFTR channels so Na+ and water into lumen, SGLT1 disruption - dec glucose and Na+ into cell , reduced brush border enzyme function - malabsorption
Manage dehydration
Norovirus - RNA
Any age
Low dose
Vomiting due to delayed gastric emptying. Diarrhoea due to anion secretion. Infects SI, damges microvilli - disruption of brush border enzyme
Incubation 1-2 days and symptoms 1-3 days
Oral rehydration
96
Describe the clinical features and aetiology of gastrointestinal infections caused by Protozoa
Cryptosporidium- sporozoan- non-motile
Faeco-oral route, water
Risk factors - swimmers, backpackers, petting zoos, child-care workers
Ingestion of Oocyst , multiplication in distal SI epithelial cells, brush border enzyme disruption, chloride excretion - watery diarrhoea. Oocyst excreted in faeces.
Fluids- with AIDS need anti-parasitic treatment
Giardia - flagella
Children (adults asymptomatic)
Faecal -oral route (picked up from surface and swallowed, contaminated food), water
Cyst ingested, stomach acid/pancreatic enzymes release cyst, multiplies ( incubation 10+days), proximal SI villus atrophy, (persistent diarrhoea, lactose deficiency), back to cyst in colon and excreted.
Cramping (up to 6weeks)
Antibiotics and fluids
Entamoeba- extending cytoplasmic projections
Mostly asymptomatic
Developing countries, poor sanitary conditions, men who have sex with men
Faeco-oral route
Excystation, trophozoites (active feeding stage) invade colon mucosa and cause bloody diarrhoea + inflammatory changes. Then excreted. Cause liver abscesses.
Anti-protozoal/metronidazole
Colitis or toxic megacolon require surgery
97
1. Describe the aetiology and clinical presentation of primary peritonitis (ascites, cirrhosis, perforated appendicitis, perforated peptic ulcer, perforated diverticulitis, volvulus, cancer)
Peritonitis
Inflammation of the serosal membrane that lines the abdominal cavity
Primary - Spontaneous eg Spontaneous bacterial peritonitis - infection of ascitic fluid that cannot be attributed to any ongoing inflammatory condition
Most common in patients with end stage liver disease
Clinical Presentation
• Abdominal pain, fever, vomiting
Diagnostic Investigations
• Aspirating ascitic fluid- neutrophil count >250 cells/mm3
98
Secondary peritonitis
Secondary - Breakdown of the peritoneal membranes (secondary to inflammation, perforation, or gangrene of an intra-abdominal structure) leading to ‘foreign’ substances entering cavity
Bacterial
•Peptic ulcer disease (perforated)
•Appendicitis (perforated) •Diverticulitis (perforated)
•Post surgery
Non- Bacterial
•Tubal pregnancy that bleeds (the peritoneal cavity is not enclosed in females)
•Ovarian cyst
Clinical Presentation
• Abdominal pain
• Diffuse abdominal pain is common in perforated viscera
• Patients often lie very still as any movement makes the pain worse
• O/E guarding and rebound tenderness
Treatment approaches
• Control the infectious source - Surgery
• Eliminate bacteria and toxins - Antibacterial therapy
• Maintain organ system function - Intensive care
99
2. Describe the aetiology of small and large bowel obstruction (SB-adhesions, hernias, malignancy, IBD, volvulus, LB- colon cancer, volvulus, intussusception)
Bowel obstruction is a mechanical or functional problem that inhibits the normal movement of gut contents.
Small bowel:
Common causes in children:
• Intussusception
when one part of the gut tube telescopes into an adjacent section
‘Lead point’ (a mass that precipitates the telescoping action)
When lymphatic and venous drainage is impaired you get oedema - can impede arterial supply (infarction)
Abdominal pain, vomiting and haematochezia
Treatment - Air enema, Surgery
• Intestinal atresia
Common causes in adults include:
• Adhesions - fibrous bands between organs or tissues - Arise after abdominal surgeries
• Incarcerated hernias - can narrow lumen enough to cause obstruction - Incarcerated groin hernias most common
Other causes:
• IBD eg Crohn’s as repeated episodes of inflammation/healing causes narrowing
Clinical Presentation of small bowel obstruction
• Nausea and vomiting (bilious, early)
• Abdominal pain (colicky pain) and distension
• Absolute constipation (late)
Other consequences of adhesions e.g. infertility)
Diagnosis
• History
• Physical examination- abdominal distension - tympanic on percussion, increased/absent bowel sounds, presence of hernia
• Imaging
100
Large bowel obstruction - notion for imaging
Occurs in older patients
Causes include:
• Colon cancer (60% of mechanical obstructions)
• Diverticular disease (20%)
• Volvulus- Sigmoid (60%), Caecal:
Part of colon twists around its mesentery
Can result from overloaded sigmoid colon (constipation), high fibre diets.
Coffee bean sign usually in sigmoid volvulus
Clinical Presentation
Gradual if caused by cancer but abrupt with volvulus
• Change in bowel habit
• Abdominal distension - tympanic on percussion
• Crampy abdominal pain
• Nausea/vomiting (later)
Tinkling bowel sounds
Diagnosis
• History
• Physical examination
• Imaging - look for transition point, air
Competence of the ileo-caecal valve - colon cannot decompress proximally = closed loop obstruction - Ischaemia and perforation
101
3. Compare and contrast the clinical presentation of small and large bowel obstruction
Small
Abdominal pain - Colicky (3-4 mins)
Vomiting - Relatively early Constipation - Relatively late
Age of patient - Younger age group
Large
Colicky (10-15 mins)
Relatively late
Relatively early
Older age group
102
4. Describe the underlying causes of acute mesenteric ischaemia (emboli, atherosclerosis, aortic aneurysm, hypotension) and its clinical presentation
More common in females (75%) and in patients with a history of peripheral vascular disease.
Consequences:
Arterial Compromise
Acute occlusion - Arterial embolism in SMA, Vasculitis
Non occlusive - low cardiac output
Venous compromise
Mesenteric venous thrombosis - Systemic coagulopathy, malignancy
Clinical Presentation
• Elderly patients with a cardiovascular risk factors
• Abdominal pain is disproportionate to the clinical
findings
• Classically pain comes on 30 minutes after eating (and last 4
hours)
• Nausea and vomiting
• Pain often left sided because blood supply to the splenic
flexure is most fragile
Investigations
• Blood tests - Metabolic acidosis/increased lactate levels
• Erect chest x-ray (to check for perforation)
• CT angiography
Treatment
• Surgery- resection of ischaemic bowel - bypass graft • Thrombolysis/angioplasty
103
5. Describe the aetiology and clinical presentation of major upper GI bleeding (oesophageal varices, perforated peptic ulcer)
Peptic ulceration
Disruption in the gastric/duodenal mucosa
Usually greater then 5mm diameter
Going through to submucosa (through muscularis mucosa)
First part of the duodenum most commonly has ulcers -
Gastro-duodenal artery lies behind first part of duodenum
Gastric ulcers
• Lesser curve and antrum common
Splenic artery
Oesophageal varices - Porto-systemic anastomoses:
Portal drainage- Oesophageal veins drain into left gastric vein, drains into portal vein
Systemic drainage- Oesophageal veins drain into azygous vein, drains into SVC
Treatment
Endoscopy & band ligation Blood transfusion
If bleeding is still not controlled:
• TIPS (Transjugular intrahepatic portosystemic shunt) - An expandable metal is placed within the liver, Bridges the portal vein to hepatic vein, Decompresses portal vein pressure so dec variceal pressure and ascites
• Terlipressin- reduces portal venous pressure
Other cause:
Upper - Mallory Weiss tear, oesophagitidis
Lower - colitis, diverticular
Vomit fresh blood - oesophageal varicose
Coffee ground - bleeding ulcer
Malena - ulcer
Dark blood - diverticular
Fresh blood - haemorrhoids
104
6. Describe the risk factors and clinical presentation of a ruptured abdominal aortic aneurysm (AAA)
What - dilation of abdominal aorta of 3cm or more
Where - infrarenal
Mechanism - degradation of media layer of arterial wall - degradation of elastin and collagen
Risk factors - smoking, male, inc age, inherited risk
Symptoms - compression of surrounding structures causes vomiting, back pain, urinary frequency. Syncope due to transient hypotension. Cardiovascular collapse.
Diagnosis - pulsating abdominal mass
Treatment - stop smoking, control hypertension, surgery - clamp aorta, open aorta, add graft
105
describe the imaging for GI tract - x-rays, fluoroscopy studies such as barium swallows, ultrasound, CT, MRI, and angiography
106
Retroperitoneal organs
S = Suprarenal (adrenal) Glands
A = Aorta/IVC
D =Duodenum (except the proximal 2cm, the duodenal cap)
P = Pancreas (except the tail)
U = Ureters
C = Colon (ascending and descending parts) - so not transverse
K = Kidneys
E = (O)esophagus
R = Rectum
