4. Stomach, abdominal wall & hernias

Question 0

Name 2 substances released in the stomach that help prevent ulceration

Answer 0

Mucus

HCO3-

Question 1

Name 2 substances the stomach releases to break down food & state which cells release these substances

Answer 1

Pepsinogen - chief cells

HCL (activates pro-enzymes) - parietal cells

Question 2

During the gastric phase, what effect does food entering the stomach have on the production of gastrin & why?

Answer 2

Gastrin production increases when food enters stomach:

Because stomach distension stimulates release of Ach from vagal preganglionic nerve fibres. Stimulates Gastrin releasing hormone, stimulates G cells to release Gastrin

Dietary peptides in stomach lumen also stimulate G cells

Food buffers stomach & acid. pH rises. Releases G cells from inhibition of somatostatin

Question 3

During intestinal phase, what mechanisms reduce production of Gastrin?

Answer 3

Fall of pH due to unbuffered HCL in stomach stimulates D cells to produce somatostatin

Somatostatin inhibits G cells from producing Gastri

Question 4

Name 3 things that when detected in duodenum, slow rate of gastric emptying

Answer 4

Fatty acids

Low pH

Hypertonicity

Question 5

Draw a cross sectional diagram of the anterior abdominal wall

Answer 5

http://thehealthscience.com/showthread.php?844706-Rectus-Sheath-Hematoma

Question 6

What potential organ damage might occur from a stab wound to the following areas:
Umbilical
Left hypochondrium
Right flank

Answer 6

Small bowel

Small bowel, large bowel, spleen

Large bowel (ascending colon)

Question 7

What muscle layers would be penetrated if a stab wound occurs either side of the right or left flank?

Answer 7

External oblique
Internal oblique
Transversus abdominus

Question 8

Name 2 consequences of an abdominal stab wound, other than death

Answer 8

Blood loss = shock

Peritonitis due to blood or gut contents entering peritoneal cavity. Causes irritation (inflammation) of peritoneum & infection (leading to peritonitis)

Question 9

Discuss the mechanisms of diffuse & localised pain

Answer 9

Diffuse = visceral pain:
Can be linked to embryological foregut, midgut & hindgut structures.
Due to viscera not having dedicated pain fibres; instead use sympathetic afferents.
Pain felt from viscera usually felt in midline and in either:
Epigastrium (foregut)
Umbilicus (midgut)
Suprapubic region (hindgut)

Localised = parietal pain:
Parietal peritoneum stimulated (derived from somatic mesoderm).
Somatic neurones relate pain to dorsal root ganglions in spinal cord.
Pain localised to dermatome nearest to pathological process; more specific than visceral pain

Question 10

Describe a direct inguinal hernia

Answer 10

Result from weakening in abdominal wall in Hesselbach’s triangle.
Hernia bulges outwards & medial to inferior epigastric vessels.
Pushes into superficial inguinal ring (a further area of weakness)

Question 11

Describe the boundaries of Hesselbach’s triangle

Answer 11

Rectus abdominus
Inguinal ligament
Inferior epigastric artery

Question 12

Describe an indirect inguinal hernia

Answer 12

Passes into deep inguinal ring (lateral to inferior epigastric vessels) & into inguinal canal.
Passes through canal or out through superficial ring

Question 13

Can you easily distinguish the different inguinal hernias in a clinical setting?

Answer 13

No.

2 types of hernias can present in similar ways

Question 14

Whats the difference between an incarcerated & strangulated hernia

Answer 14

Incarcerated: irreducible

Strangulated: compromised blood supply

Question 15

Draw a diagram of the femoral canal

Answer 15

https://www.studyblue.com/notes/note/n/lecture-10-antmed-thighknee/deck/1019399

Question 16

Why is a femoral hernia more likely to be incarcerated than an inguinal hernia?

Answer 16

Femoral canal has a tighter entrance: harder for things to get in, but also more likely for things to get stuck

Question 17

What are the potential clinical consequences of an incarcerated hernia?

Answer 17

If bowel become herniated, can become obstructed = vomiting (esp small bowel), electrolyte imbalance, perforated bowel, colicky abdo pain.

Herniated tissue may also become strangulated; blood supply compromised = tissue death. High mortality rate

Question 18

What are the boundaries of an umbilical hernia?

Answer 18

Same as boundaries of the umbilicus:

Gap in linea alba, bounded on either side by rectus abdominus muscles

Question 19

Explain why an umbilical hernia is commonly seen as a congenital disorder

Answer 19

During embryological dev, midgut herniates out of umbilical ring before returning a few weeks later.
Failure to properly close the defect in abdominal wall provides route for abdominal contents to herniate out through umbilicus.
Mostly resolve in children
Can occur in adults esp if regularly increase intra-abdominal pressure (e.g. Chronic cough, constipation)

Question 20

Define dyspepsia

Answer 20

Includes a variety of symptoms including:

Upper abdominal pain, heart burn, acid reflux, nausea, vomiting

Question 21

Define gastro-oesophageal reflux disease

Answer 21

A digestive disorder characterised by Ineffective LOS.

Results in reflux of stomach contents into oesophagus

Question 22

What is H.Pylori?

Answer 22

A gram negative, helical, aerobic, urease-producing bacteria

A major cause of peptic ulcerations

Question 23

How does H.Pylori survive the acidic conditions of the stomach?

Answer 23

Using its flagellum & chemotaxis, maintains preferred position within mucus layer of stomach, avoiding more acidic lumen.

Produces enzyme urease: converts urea (found in stomach) to ammonia & CO2.
Ammonia then converts to Ammonium.
Ammonium uses H+ ion to create NH4.

Neutralises acidic conditions surrounding bacteria

Question 24

How do you confirm the presence of H Pylori in a patient?

Answer 24

Urease breath test

Swallow radio-labelled urea
If can detect radio-labelled CO2, demonstrates that urea was split by urease.
Indirectly indicates presence of H.P

Question 25

Give an example of a common H. pylori eradication therapy

Answer 25

1-2 weeks of antibiotics (Amoxycillin, Clarithromycin / Metronidazole)
Proton Pump Inhibitor (Omeprazole)

Question 26

Why are PPIs more effective then H2 antagonists at reducing stomach acid production?

Answer 26

Blocking H2 receptors: still other inputs on parietal cells that will result in acid secretion

PPIs: blocks all receptor inputs - common path ends at this point

Question 27

Give an example of a PPI and a H2 antagonist

Answer 27

PPI: Omeprazole, Lansoprazole

H2 antagonist: Cimetidine, Ranitidine

Question 28

List 3 potential causes for burning upper abdo pain, worsening at night and relieved by eating

Answer 28

Duodenal ulcer
Gastric ulcer
Gastritis

Question 29

What group of pain killers may be responsible for gastric/duodenal ulcers or gastritis?

How?

Answer 29

NSAIDS

Cox1 inhibitors:
Cox converts arachidonic acid into prostaglandin.
PGe protective of duodenal mucosa: increases mucus production & HCO3- & increase mucosal blood flow

Question 30

How might you remove the Ach stimulation of the parietal cell?

Answer 30

Vagotony

But depending on where takes place, will also have other effects (i.e. Decreasing gastric motility & gastric emptying)

Question 31

Explain the symptom of dark, tarry stools as well as a gastric/duodenal ulcer

Answer 31

Upper GI bleed from ulceration
Haem portion of blood oxidised as travels thru gut
Pigments the stool & gives it tarry consistency

Question 32

What tests might be carried out on a suspected upper GI bleed from ulceration?

Answer 32

Upper GI endoscopy to directly visualise oesophagus, stomach & duodenum