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Flashcards in Stomach Deck (49):
1

Give 4 functions of the stomach.

1. Stores and mixes food
2. Digests food
3. Kills microbes
4. Offers mucosal protection

2

Which cells of the stomach produce gastric acid (HCL) and intrinsic factor?

Parietal cells

3

What do the chief cells of the stomach produce?

Pepsinogen

4

What do enterochromaffin-like (ECL) cells release?

Histamine

5

Which cells release gastrin?

G cells

6

What do D cells release?

Somatostatin

7

What is the lower portion of the stomach called?

Antrum

8

What is the role of the antrum?

Mixing the stomach contents

9

Describe how parietal cells produce HCL.

1. Water breaks down into OH- and H+
2. CO2 from respiration is converted into H2O3 via carbonic anhydrase
3. H2CO3 rapidly dissociates into HCO3- and H+
4. H+ react with OH- ions from the breakdown of water to regenerate H2O
5. H+ from the breakdown of H2O are pumped into the stomach lumen via the H+/K+ ATPase pump in the luminal membrane of the parietal cells. 1 K+ ion is pumped in to the parietal cell for every 1H+ ion pumped out into the stomach
6. HCO3- is secreted into the capillary for the exchange of Cl- ions
7. Cl- ions diffuse into the stomach and combine with H+ to form HCL.

10

What inhibits the release of HCL from parietal cells?

1. D cells, by releasing somatostatin - stimulated by low PH
2. Prostaglandins

11

What protects the stomach from its own acid?

Mucus

12

What stimulates the parietal cells to release HCL?

1. ECL cells releasing histamine
2. Gastrin binds to receptors on parietal cells which also stimulates the release of HCL
3. Parasympathetic stimulation from the vagus nerve: acetylcholine binds to muscaranic receptors on both ECL and parietal cells.

Both gastrin and histamine increase the number of H+/K+ ATPase pumps on the plasma membrane of parietal cells

13

Name the phases of gastric acid secretion.

Cephalic phase - during meal, eating
Gastric phase - once food has reached stomach

14

Name the phases of turning off gastric acid secretion.

Gastric phase - low PH stimulates somatostatin release
Intestinal phase - in duodenum

15

Describe the intestinal phase of turning off gastric acid secretion.

Initiated by duodenal distension, low PH, hypertonic solutions. Causes release of enterogastrones e.g. secretin and cholecystokinin (CKK). Secretin inhibits gastrin release and promotes somatostatin release.

16

What is an ulcer?

A breach in a mucosal surface.

17

Which infection is the biggest cause of peptic ulcers?

Helicobacter pylori infection.

18

How does helicobacter pylori cause peptic ulcers?

The bacteria lives in the gastric mucus.
1. It secretes urease, splitting urea into CO2 and ammonia
2. Ammonia combines with H+ to form ammonium which is toxic and results in less mucous production
3. Proteases and cytotoxin A released from the bacteria attack the gastric epithelium, further reducing mucous production

19

What is the treatment for infection by helicobacter pylori?

Triple therapy: proton pump inhibitor - inhibits H+ ions being pumped into lumen, increasing gastric PH to make conditions inhospitable for the bacteria.
Antibiotics are given as well.

20

Which drugs cause peptic ulcers?

NSAIDs: non-steroidal anti-inflammatory drugs. e.g. aspirin, ibuprofen

21

How do NSAIDs cause peptic ulcers?

Mucous secretion is stimulated by prostaglandins. Cyclo-oxygenase 1 is needed for prostaglandin synthesis. NSAIDs inhibit cyclo-oxygenase 1, reducing mucosal production and defence

22

What is the treatment for peptic ulcers caused by NSAIDs?

Use prostaglandin analogues (mimic effect of prostaglandins) to reduce acid secretion.

23

How do bile salts cause peptic ulcers?

Alkaline bile strips away gastric mucous layer of the stomach, resulting in reduced mucosal defence.

24

What are tumours of parietal cells called?

Gastrinoma. Caused by excessive gastric release causing attack on mucosa.

25

Describe two synthetic ways to reduce gastric acid secretion.

1. Proton pump inhibitors: inhibits pumps pumping H+ into stomach lumen e.g. lansoprazole
2. H2 receptor agonists: block receptors for histamine thereby reducing acid secretion

26

Describe the protective mechanisms of the gastric mucosa.

1. Alkaline mucus on luminal surface
2. Tight junctions between epithelial cells
3. Stem cells at base of pits to replace damaged cells

27

Which cells produce pepsinogen?

Chief cells

28

Why is pepsin stored as pepsinogen?

In order to prevent it digesting chief cells

29

What is pepsinogen mediated by?

Input from the enteric nervous system via Ach (parasympathetic)

30

What is the role of pepsin in protein digestion?

Accelerates protein digestion.
Accounts for 20% of protein digestion.
Breaks down collagen.

31

What stimulates pepsinogen conversion to pepsin?

Low PH generated by HCL activates the conversion of pepsinogen into pepsin. Positive feedback occurs as once pepsin is produced, it can cleave pepsinogen itself to produce more pepsin.

32

What is the empty stomach volume?

50mL

33

What volume can the stomach accommodate when eating? How does it accommodate for a larger volume?

1.5L. Does this by smooth muscle and fundus receptive relaxation.

34

What is released by enteric nerves to receptively relax the stomach?

Nitric oxide and serotonin. ACh activates parietal and chief cells to initiate receptive relaxation.

35

Describe how peristalsis drives food down the stomach.

1. Each wave begins in the body of the stomach. These initial contractions are too weak to produce much mixing of luminal contents with acid and pepsin.
2. More powerful contractions occur in the antrum, which enables better mixing of luminal contents
3. Pyloric sphincter between antrum and duodenum closes as peristaltic waves reach it. This ensures little chyme enters the duodenum.

36

Which cells determine the frequency of peristaltic waves?

Interstitial cells of Cajal in the muscular propria. These are pacemaker cells.

37

The pacemaker cells (Cajal) undergo slow depolarisation-repolarisation cycles. How are the waves of depolarisation transmitted to adjacent smooth muscle cells?

Through gap junctions

38

Name the factors that increase peristaltic contraction.

Gastrin
Gastric distension (mediated by mechanoreceptors)
Increase in parasympathetic stimulation

39

Name the factors that decrease peristaltic contraction.

Duodenal distension
Increase in duodenal fat
Increase in duodenal osmolarity
Decrease in duodenal PH
Increase in sympathetic stimulation

40

What is dumping syndrome?

Overfilling the duodenum by a hypertonic solution

41

What is the clinical term for delayed gastric emptying?

Gastroparesis

42

What causes gastroparesis?

1. Idiopathic (unknown cause)
2. MS
3. Diabetes mellitus

43

What are the symptoms of gastroparesis?

Causes matter in stomach to rot and smell and have a similar appearance to that of faeces.

Symptoms: nausea, feeling full early (early satiety), vomiting undigested food

44

What does GORD stand for?

Gastro-oesophageal reflux disease

45

Name some causes of GORD.

Pregnancy, hiatus hernia (stomach moves above oesophagus), obesity + smoking

46

Which structure allows for communication between the greater and lesser omental sac?

Foramen of Winslow

47

What is the most common position of the appendix?

Retrocaecal

48

Name structures found within the peritoneum.

Stomach, spleen, liver, transverse colon

49

Name retroperitoneal structures.

Kidneys, adrenal glands, pancreas, oesophagus, rectum, aorta, duodenum