GEP (Life Maintinance) Week 1 Flashcards
Name these anatomical structures
● Digestion begins via mastication (chewing)
and amylase secreted in saliva by salivary
glands
● Floor attaches to the tongue
● Lateral walls known as buccal region (cheek).
Formed by the buccinator muscles
● Roof contains hard palate (bony) and soft
palate (muscular)
○ Soft palate separates oropharynx from
nasopharynx
The mouth is richly innervated by several cranial
nerves → jaw and dental pain hurts A LOT
Name the anatomical structures, innervation and sensation of the tounge
Apex = mobile tip
Body = anterior 2/3rds; mobile
Root = attachment to mandible and hyoid
bone
Sulcum terminalis = v-shaped groove at
body-root boundary
What is the oesophagus and the anatomical structures around it
● Fibromuscular tube (~25cm)
responsible for food transit to stomach
● Posterior to trachea and airways
● Pharynx to cardiac orifice (C6 - T11)
● Vascular supply split in thirds
downwards inferior thyroid, thoracic
aorta and left gastric arteries
● Venous drainage via inferior thyroid and
azygos veins
What is the anatomical positions of the stomach and its function
● Acidic, digestive zone ● Fundus - gas-filled, rounded section ● Greater and lesser curvatures are
attached by greater and lesser
omentum (double folds of peritoneum)
● Contains rugae - folds allowing for
distension
● Pyloric sphincter lies at L1; this forms
the transpyloric plane at which the
superior mesenteric artery arises
What are the anatomical structures and functions of the duodenum
- Most proximal part of small intestine
● Receives chyme from pylorus, bile from
liver + gallbladder and pancreatic
secretions
● 4 sections forming a ‘C’ shape: superior,
descending, inferior, ascending (or D1-4)
● D1 is a common site of duodenal ulcers ○ Gastroduodenal artery lies posterior
to D1 - ulcers may lead to severe
haemorrhage of this artery
● D2 contains major duodenal papilla -
entry pt of bile and pancreatic secretions
● D3 - start of the midgut; crosses IVC and
aorta
● D4 - duodenum ends and jejunum begins
What is a sphincter, how does it work and name main sphicters around the stomach
**Sphincter: **circular muscle separating GI tract regions. Open
(relax) and close (contract) to control bodily functions and only
allow single direction flow.
**Upper Oesophageal Sphincter: **pharynx- upper oesophagus
**Lower Oesophageal Sphincter (LOS) : **oesphagus- stomach
-important in stopping acidic stomach contents passing back up
the oesophagus (reflux)
Vertebral Levels of Diaphragm apertures:
T8 - VENA CAVA
T10 – OESOPHAGUS
T12 – AORTIC HIATUS
What are the 3 anti-reflux barrier
- Angle of his
- Crural Diaphragm
- Phrenoesophageal ligament
What are the layers of the oesophagus
Structure of the oesophagus
Adventitia
- Connects Oesophagus to surrounding
structures.
- Similar to Serosa
Muscularis propia/externa (muscle)
- Upper = Skeletal muscle
- Mid = Mix
- Lower = Smooth muscle
- Becomes thicker at both ends for sphincters
Submucosa:
- Areola Connective tissue
- Blood vessels
- Mucous Glands
Mucosa:
- Mucularis Mucosae
- Lamina Propria
- Non-keratinized stratified squamous
epithelium (abrasion protection
How does the Oesophagus allow motility
Contraction & relaxation of GI walls and
sphincters.
In the oesophagus the proximal 1/3 = skeletal
muscle while the distal ⅔ = smooth muscle.
The muscle fibers of the esophagus are
bi-directional, with the external layer running
longitudinally and the internal layer comprising
of circular fibers.
Contraction and relaxation of these muscles is
called peristalsis.
Circular:
- Contract superior to bolus
- Compresses food downwards
Longitudinal
- Contract inferior to bolus
- Shortens + opens oesophagus to receive
food.
What are the layers of the stomach
- Serosa – connective tissue
- Muscularis – outer longitudinal, middle circular,
inner oblique, plexus - Submucosa – plexus
- Mucosa – simple columnar epithelium and cells
for digestion
Why do we produce stomach acid
● Food breakdown - activates pepsinogen (secreted by chief cells at fundus and
body); this converts it into pepsin, an enzyme that breaks proteins into amino
acids and peptides
● Kills pathogens (beware H. Pylori)
● Neck cells secrete a blanket of mucus → protects stomach wall from
contents
● Bicarbonate buffer secreted by epithelial cells; stimulated by PGs
What are the 3 methods that promote stomach acid production
All 3 stimulate proton pump
(H+/K+ ATPase) activity
1) Vagal activity: directly at M3 receptors of parietal
cells - “rest and digest”
2) Gastrin: secreted by G cells - stimulated by 1).
Gastrin binds to CCK receptors on parietal cells
3) Histamines: secreted by enterochromaffin-like
(ECL) cells; they bind to H2 receptors on parietal
cells. Stimulated by 1) and 2).
What are the 3 phases of acid secretion
- CEPHALIC - activated when see or chew food → stimulated vagal activity + gastrin
- GASTRIC - food inside stomach (mechanical distention and increased peptide conc.) → stimulates vagal activity + gastrin
- DUODENAL - chyme reaches duodenum → release of CCK and secretin → inhibit acid secretion
CCK: Cholecystokinin
What is the role of somatostatin in the stomach
the drop in pH → secretion of somatostatin
from D cells in antrum → inhibits acid
secretion
What pharmological interventions are used for stomach acid production
○ Proton pump inhibitors (PPIs) - taken orally
(eg. omeprazole, lansoprazole)
○ H2-receptor antagonists - taken orally (eg.
ranitidine, cimetidine)
What is peptic ulcer disease and how does it occur
-This occurs due to the Imbalance of protective vs.
damaging factors
-Can lead to damage to mucosal layers causing pepsin and HCl to
-come into contact with epithelial cells → inflammation and fibrosis
-Erosion → ulcer (>5mm diameter)
Common sites:
● Stomach antrum & body
● Duodenum (95% in 1st part)
● Distal oesophagus, Meckel’s
diverticulum (less common)
Different types of peptic ulcer disease location
DUODENAL
● x4 more common
● Pain - relieved by food (hence, worse at
night)
● Vomiting less common
● Malignancy less common
● Less prone to bleeds (but if so, melaena)
GASTRIC
● Less common
● Pain - worse after eating
● Vomiting more common
● Malignant changes are possible
● More prone to bleeds (and more likely to
present as haematemesis)
● Often on lesser curvature; malignant
changes are highly likely if elsewhere
What are the complication of peptic ulcer disease
1) acute bleeding (remember NSAIDs),
2) perforation into peritoneal cavity (surgical
emergency; prostration, shock, peritonitic pain +++; rigidity/guarding, bowel sounds nil),
3) malignancy,
4) reduced gastric outflow
What are the investigations for peptic ulcer disease
First take a Hx of presenting symptoms!
(incl. review of medications)
● Test for H. Pylori → C13 breath test,
stool antigen or biopsy
● FBC, CRP, serum amylase/lipase,
LFTs
● Imaging: CXR, CT
● Endoscopy
○ Perform if dysphagia OR >55yrs +
red flag (persistent anaemia/upper
abdominal pain/N+V/reflux/weight
loss)
○ Take biopsies if appropriate
How do you treat H-pylori
a) Lifestyle modification (smoking, alcohol and other precipitating factors)
b) Remove medication if ulcers are drug-induced
Triple therapy: if H-pylori positve
7 day course of oral PPI + 2
antibiotics (metronidazole, amoxicillin
or clarithromycin)
Retest in 6-8 wks; proceed as for -ve
or repeat triple therapy
If H-pylori negative
4-8 week course of PPI or H2-blocker
If no improvement, add H2-blocker or
PPI; consider endoscopy or rarer causes
What are the symptoms and features of Peptic ulcer disease
Asymptomatic, dyspepsia, epigastric pain (relieved by antacids), weight loss, anaemia, melaena
What is H-pylori and how does it affect humans
● Gram -ve spiral bacillus
● Evades stomach acid effectively by
creating an alkaline microenvironment
● Uses flagella for motility → invasion of
gastric mucosa
● Leads to inflammation and ulceration
● Highly virulent: mucinase, ureases,
vacuolating toxin A, Cag A, among
others
What ulceration risk factors are there
● NSAIDs are a major risk factor for peptic ulceration
○ Long-term NSAIDs should be co-prescribed with a
PPI to protect gastric mucosa
● Corticosteroids, bisphosphonates, SSRIs
● Other RFs: gastric acid secretion, alcohol, smoking,
delayed gastric emptying/duodenal reflux, Z-E syndrome
What are the quadrants and abdomiopelvic regions
**Quadrants: **Right upper, and lower/ Left upper and lower.
Causes to be aware of abdominal pain
-GORD
-eosinophilic oesophagitis
-achalasia
What is GORD
Gastro-oesophageal reflux disease
- Acid & stomach contents reflux into the oesophagus causing symptoms.
- Sx: -heart burn; after meals (typical), worse when lying down/bending over, can happen at night
-acid regurgitation; acid in the mouth after food, sour/bitter taste
Less common; dysphagia, bloating, halitosis, laryngitis
Red flag symptoms
-weight loss
-night sweats
-anaemia
-loss of appetite
-dyspepsia
-abdominal mass
-dysphagia
How is GORD diagnosed
Clinical diagnosis; can be diagnosed without investigation with
above symptoms but without red flag symptoms
What are the risk factors for GORD
● Family history
● Obesity
● Older age
● Hiatus hernia
● TLOSRs (transient lower oesophageal sphincter
relaxations)
● Stress
● Medications
● Smoking
● Alcohol consumption
● Pregnancy
What is a hiatus hernia
some upper part of the stomach bulges up into the thorax through the LOS.
Allows gastric contents to reflux into the distal oesophagus more easily, is closely related with GORD development and aggravation.
LOS: lower oesophogeal sphincter
What are the two types of Hiatus Hernia
- Sliding: stomach and section of oesophagus slide up through the hiatus. More common.
- Paraesophageal: part of the stomach squeezes through. Less common, more concern.
Can also get mixed.
What are the treatment for Hiatus Hernia
Treatment: weight loss, treat GORD; surgery is indicated when symptoms/complications of GORD do not resolve
What are the complications of GORD
Barrett’s Oesophagus; change in the normal non-keritanized squamous epithelium of the oesophagus to specialised intestinal metaplasia (columnar mucosa)
- the presence of Barrett’s esophagus is important because those who have it are at
greater than normal risk of developing cancer of the esophagus.
What are the different types of cells changes that can occur from GORD.
Dysplasia: **tissue develops a large number of immature cells (reversible)
Metaplasia: mature differentiated cell transforms into new mature cell type (often caused by environmental stressor) (reversible)
Neoplasia: Uncontrolled, irreversible abnormal growth. Literally means “new tissue”. May or may not be malignant – used synonymously with cancer.
What are the investigations for GORD
1st line: therapeutic 8-week trial of a PPI (clinical diagnosis; PPI= investigation & management)
Further investigations; indicated if above shows no improvement, for alarm symptoms or complicated disease symptoms
PPI’s stopped before these procedures
* OGD (oesophagogastroduodenoscopy) (endoscopy); normal or may show
oesophagitis (erosion, ulcerations, strictures) or Barrett’s oesophagus
* Ambulatory pH monitoring; pH <4 more than 4% of the time is abnormal
- NICE Guidelines = Dysphagia OR > 55 + weight loss + (upper abdominal pain or
reflux or dyspepsia; refer for urgent endoscopy
What are the management of GORD
1) Lifestyle changes - reduce spicy/fatty foods, small+regular meals, lose weight,
reduce alcohol intake, reduce caffeine intake, elevate head at night, avoid
eating < 3hrs before bed, smoking cessation
2) Review medication (NSAIDs, CCBs, etc)
3) Antacids can help reduce symptoms
4) + PPI
5) + H2-blocker OR twice-daily PPI
6) Surgery (in severe cases)
a) Fundoplication
b) Magnetic bead band
What are the fundoplication methods
What is Upper GI endoscopy and what are the uses
Used diagnostically and therapeutically.
Diagnostic indications:
melaena/haematemesis, dysphagia,
>55yrs + red flag Sx, suspect Coeliac
(duodenal biopsy), Fe deficiency,
persistent vomiting
Therapeutic indications:
Treating bleeds, variceal banding,
stent insertion, stricture dilatation,
polyp resection
What are the 4 grades of LA classification of erosive oesophagistis
