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
