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Semester 4 (NME) > Stomach > Flashcards

Stomach Flashcards

1
Q

What are the 4 functions of the stomach?

A

Storage
Mechanical breakdown
Chemical breakdown
Produces intrinsic factor

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2
Q

What is intrinsic factor?

A

A glycoprotein used to absorb vitB12 in the small intestine

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3
Q

What is chyme?

A

A mix of ingested substances and secretions of glands

A viscious, very acidic mixture

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4
Q

Between which vertebral levels does the stomach lie?

A

T7 and L3

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5
Q

What are the three layers of the muscular externa in the stomach?

A

Longitudinal layer (superficial)
Circular layer
Oblique layer (deepest)
Serosa of stomach lining

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6
Q

What type of epithelium lines the stomach and how is it protected?

A

Simple columnar epithelum

Produces alkaline mucus layer

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7
Q

What are rugae in the stomach?

A

Prominant folds in the mucosa which allow expansion (upto 50x)

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8
Q

What type of secretions dominate in the cardia?

A

Lots of mucous to coat oesophagus and protect

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9
Q

What are gastric pits?

A

Shallow depressions with cells at the base dividing to replace superficial cells (shed within 3-7days). Alcohol or chemicals can increase turnover

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10
Q

What are gastric glands?

A

Each pit communicates with several gastric glands which go deep into the lamina propria (between epithelum and muscle layer). These glands have parietal and chief cells which secrete 1.6L gastric juice per day

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11
Q

Which cells lie in the proximal/ base of the gastric glands?

A

Proximal- Parietal (secrete HCL/ IF)

Base: Chief cells (secrete pepsinogen)

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12
Q

How does the parietal cell secrete HCl?

A

1) Carbonic anhydrase converts CO2+H2O into H2CO3
2) It dissociates into H+ and bicarbonate
3) Antiport exchanger swaps HCO3- for Cl-
H+ and Cl- secreted seperately to prevent damage to cell

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13
Q

What pH is the stomach kept at and why is it at this level?

A

pH 1.5-2

Kills microorganisms, activates pepsin, denatures enzymes, breaks down cell wall and connective tissue

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14
Q

Name one major function which vitB12 is needed for?

A

Erythropoeisis

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15
Q

What is pernicious anemia?

A

An autoimmune disease in which parietal cells of the stomach responsible for secreting intrinsic factor are destroyed

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16
Q

What is pepsinogen?

A

A proenzyme secreted by chief cells, in pH 1.5-2 it is converted to pepsin (protein digesting enzyme)

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17
Q

Name two functions of chief cells present in infants but not in adults?

A

Produces renin to coagulate milk proteins

Produces gastric lipase- To digest milk fats

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18
Q

Parietal and chief cells are each more prevalent where?

A

Parietal cells- Fundus and body

Chief cells- Antrum

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19
Q

What do the pyloric glands do?

A

Secrete mucus (not enzymes or acid)

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20
Q

What are enteroendocrine cells?

A

Scattered amounst pyloric cells

Release several hormones (Gastrin/ somatostatin/ ghrelin/ obestatin)

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21
Q

What is Ghrelin?

Where is it secreted from?

A

Secreted by P/D cells in fundus
Levels rise before a meal to indicate hunger, levels fall to indicate satiety
Also antagonises leptin

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22
Q

What is leptin?

A

Produced by adipose tissue

High levels give feeling of fullness

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23
Q

Where do leptin and Ghrelin act?

A

Receptors in the arcuate nucleus of the hypothalamus to regulate appetite
HIGH LEPTIN = Feel full
HIGH GHRELIN= Feel hungry

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24
Q

What is the function of obestatin?

A

It causes feelings of fullness when in high levels

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25
Q

How are proteins digested in the stomach?

A

Pepsin enzyme

Done slowly at first, rate of digestion increases as stomach pH falls

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26
Q

How are starch and fats digested in the stomach?

A

For 1-2 hours salivary amylase and lingual lipase continue to work (until pH drops below 4.5ish). Then these enzymes become denatured

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27
Q

Why is food not absorbed in the stomach?

A

1) Incomplete digestion
2) Mucus barrier
3) No transport mechanisms

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28
Q

Name 2 things which can cross stomach linining?

A

Alcohol (absorption decreased with fatty meal as alcohol is lipid soluble)
Aspirin (CI in gastric ulcers as changes mucus layer)

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29
Q

What blood vessels supply the stomach?

A

Lesser curvature/ cardia = R/L gastric
Greater curvature = R gastro-omental (inf)/ L gastro-omental (sup)
Fundus= Short gastric artery (from splenic)

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30
Q

What does mucus comprise of?

A

90%- water and ions
5-10%- Glycoproteins
1-5%- Mucins

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31
Q

What are mucins?

A

Very large specific glycoproteins (glycans are sugars) they form cross links and gels, helping them stop pathogens. Glycans can stop proteases from pathogens breaking the mucin down

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32
Q

What are the two layers of mucus in the GI tract?

A

Loose (contains good bacteria which release nutrients)
Adherant- Close to cell

Loose layer can be shed if infiltrated for protection

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33
Q

What is the glycocalyx?

A

A sugar layer which surrounds to the cell and links extracellular mucins with the cell membrane
Extra defense layer

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34
Q

What are MUC6 and MUC5AC?

A

MUC6- In adherant mucus layer, binds pathogens like H.Pylori and inhibits their cell wall synth
MUC5AC- In mucus layer under MUC6, if pathogens get past MUC6 it allows the layer above to be shed

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35
Q

From where is mucus secreted in the GI tract?

A

Foveolar cells

(GI equivalent of goblet cells). They line gastric mucosa and form simple columnar epithelium

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36
Q

What are secretory canaliculi?

A

Within parietal cells, secrete H+ and Cl-. Enlarge to secrete then return to rest phase

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37
Q

Through where do secretin and gastrin travel?

A

Through the blood

Gastrin gets you ready to digest

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38
Q

What effect does low pH have on gastrin secretion

A

Lower pH = less gastrin secretion

39
Q

What are the stimuli for gastrin/secretin and CCK release?

A 
Gastrin = Food in stomach 
Secretin= H+ in duodenum  
CCK= Fats in duodenum
40
Q

What is a hiatal hernia?

A

Protrusion of the stomach into the thorax due to separation of the diaphragmatic crura

41
Q

What is the major symptom of GORD?

A

Heartburn, pain made worse by bending, stopping or lying. Pain relieved by antacids. Pain made worse when drinking hot liquids or alcohol.

42
Q

What is the pathophysiology of GORD?

A

Transient relaxation of LES independent of swallow

43
Q

What is dyspepsia?

A

Inexact term used to describe upper adbo symptoms such a heartburn, pain or discomfort, wind, belching, nausea or fullness. Px tend to refer to these as ‘indigestion’.

44
Q

What are the risk factors for PUD disease?

A

NSAIDS, H.Pylori infection, smoking, genetics, blood group O

45
Q

What GI disturbances can be caused by NSAIDS?

A

Discomfort, dyspepsia, diarrhoea or constipation, N+V, bleeding and ulceration

46
Q

What effects do prostaglandins have on the GI tract?

A

Increase bicarbonate and mucin release
Reduce gastric acid release by acting on ECL cells
Prevent vasoconstriction (and thus mucosa damage) which normally follows injury

47
Q

How do NSAIDS affect the GI tract?

A

Inhibition of COX-1 prevents prostaglandin synthesis which is needed to regulate release of normal mucus and bicarbonate in the GI tract. Inhibition of this leads to lower secretion.

48
Q

What are the COX enzymes?

A

Control the rate limiting step in prostaglandin synthesis. Inhibition of COX-2 gives anti-inflammatry effects. Inhibition of COX-1 causes toxicity and SE’s

49
Q

What are the malignancy risks with DU’s and GU’s?

A

DU’s carry a very low malignancy risk
GU’s can represent malignancy and should always be biopsied (GU’s tend to present later in life and often remain silent until complications occur)

50
Q

Which is more common, duodenal ulcers or gastric ulcers?

A

Duodenal

51
Q

Which portion of the duodenum do DU’s normally affect?

A

First portion (>95%). Most are within 3cm of the pylorus

52
Q

What is the clinical definition of an ulcer?

A

Break in the mucosal surface greater than 5mm in size, with depth to the muscularis mucosa (submucosa)

53
Q

What is the lifetime prevalence of PUD?

A

12% in M

10% in F

54
Q

What is the main symptom of PUD?

A

Burning/ gnawing epigastric pain exacerbated by fasting/ improved with meals

55
Q

When is endoscopy or a biopsy more likely to be indicated in suspected H.pylori infections?

A

In older patients or those with alarm symptoms to exclude malignancy

56
Q

Name 3 non-invasive tests which could be done to look for H.Pylori infection?

A

Serum IgG antibodies/ stool antigen test / 13C urea breath test

57
Q

When a H.Pylori infection begins to colonise the stomach which is normally the first area of the stomach it grows in?

A

Antrum

58
Q

What % of duodenal and what % of gastric ulcers are due to h.pylori infection?

A

Duodenal- 80%

Gastric- 60%

59
Q

How does infection with H.pylori cause increased acid secretion (and further damage)?

A

Inflammaton diminishes number of somatostatin producing D-cells. These means gastric (therefore HCl) release is less inhibited. This leads to gastric metaplasia which when inflamed and infected can become ulcerated

60
Q

Name two genes which when expressed in H.pylori can increase risk of PUD?

A

CagA and VacA

61
Q

How do immune cells recognise when an epithelial cell has been infiltrated by H.pylori?

A

The CagA gene is trans located into epithelial cells by the infection. This causes changes in the cell which are detected by the Nod1 receptor which stimulates an inflammatory response

62
Q

What does H.Pylori infection do to the stomach lining?

A

Infiltration of the mucosa causes a chronic persistent immune response, which is ineffective at clearing infection but damages stomach lining.

63
Q

Colonisation of H.pylori can cause what?

A

Gastritis, PUD, gastric adenocarcinoma

Can protect against GERD and oesophageal carcinoma

64
Q

Helicobacter Pylori colonises the stomachs of what % of the worlds population?

A

50%

65
Q

What is the role of brunners glands?

A

Secrete alkaline mucus to neutralise acid contents in the duodenum. Located in duodenal submucosa

66
Q

What sort of mixture does the stomach secrete during interdigestive periods?

A

Very small amount of gastric juice, mainly mucus and small amount of pepsin but almost no acid. However emotional stimuli can cause acid secretion (PUD RF)

67
Q

How does chime in the intestines inhibit gastric secretion?

A

Reverse enterogastric reflex/ GIP/ VIP and somatostatin

68
Q

Each phase of gastric secretion accounts for what % of total secretion?

A

Cephalic- 30% Gastric- 60% Intestinal- 10%

69
Q

What are the three phases of gastric secretion?

A

Cephalic (PNS vagal stimulation from appetite centres in hypothalamus)
Gastric (Vagovagal reflexes, local enteric reflexes and gastrin mechanism)
Intestinal (Presence of food in duodenum causes stomach gastric juice secretion)

70
Q

Which cells secrete histamine and how does this act?

A

Enterochromaffin-like cells. Found deep in the recess of oxynitic glands, they release histamine directly onto the parietal cells to increase HCl secretion. The rate of histamine formation is controlled by levels of Gastrin

71
Q

What are surface mucus cells?

A

Cover entire surface of stomach mucosa between glands to leave a continuous coating layer of mucus

72
Q

Where is vitamin B12 absorbed, what else is needed?

A

Absorbed in ileum

With co-factor IF

73
Q

What cleaves pepsinogen into pepsin?

A

HCl

74
Q

At what pH is pepsin inactivated?

A

pH5

75
Q

Name three things which can stimulate parietal cells to secrete acid?

A

Gastrin/ histamine/ acetylcholine from PNS of enteric NS

76
Q

What is the vasovagal reflex?

A

Food stretches stomach so contractions begin

77
Q

Gastric glands are also known as X glands. What cell types reside in them?

A

X= Oxynitic

Contain mucus neck cells, chief cells (pepsinogen and gastric lipase) and parietal cells (HCl and IF)

78
Q

What effect does nitric oxide have on the lower oesophageal sphincter?

A

Relaxes it

79
Q

What is a migrating motor complex?

A

Cycles of motor activity which migrate from the stomach to the distal ileum. It’s initiated by motilin. Clear stomach and SI of luminal contents in preparation for next meal

80
Q

What is the physiology of proton pumps?

A

On apical membrane of parietal cell. Make H+ from H2CO3 in the blood and swaps it for a K+ (in) using one ATP
The antiporter undergoes a conformation change driven by phosphorylation (from the ATP binding)

81
Q

How does bicarbonate leave a parietal cell and why?

A

On basolateral membrane, one HCO3- goes out and one Cl- comes in
This balances H+ and Cl- extrusion on the apical membrane

82
Q

What happens to the pancreas when it’s stimulated by secretin?

A

Releases NaHCO3 from centroacinar cells

83
Q

What is the function of CCK?

A

FROM I CELLS IN DUODENUM/ JEJUNUM
Inhibits gastric emptying and acid secretion
Causes release of pancreatic enzymes from acinar cells

84
Q

What type of bacteria is H.pylori?

A

Gram -ve (doesn’t stain, no thick peptidoglycan wall)

Curved rod

85
Q

How does H.Pylori live in acid?

A

It metabolizes urea so the NH3 keeps local pH around the bacteria high

86
Q

How does H.Pylori damage mainly affect the stomach?

A

Damage to D-cells, so less somatostatin release and more damage by acid

87
Q

Which prostaglandin is crucial in mucus but has it’s synthesis inhibited by NSAIDS?

A

PGE2

88
Q

What adhesion molecules help bind H.Pylori to the mucosal cells?

A

BabA on h.pylori binds with the lewis antigen on gastric mucosal cells

89
Q

How is urea used by H.pylori to damage cells?

A

Urease converts urea to ammonium which is toxic to cells

90
Q

How can duodenal ulcers be classified?

A

T1 to T4

Based on location

91
Q

Food affects pain levels from DU’s and GU’s how?

A

DU: Pain worse with hunger, better by eating, with pain onset ~2hrs after meals
GU: Pain worse with meals. immediate pain when eating

92
Q

What is the epidemiology of peritonitis in PUD and how does it occur?

A

1 in 350 PUD patients

Lining splits so stomach bacteria enter peritoneum

93
Q

What is the diverticular disease?

A 
Small buldges (diverticula) develop in lining of intestine, presenting with lower abdo pain and bloating 
50% of pop by age 80
94
Q

What is the difference between diverticulosis and diverticulitis?

A

Diverticulosis: Diverticular disease is present but no symptx
Diverticulitis: Diverticula become inflamed

Semester 4 (NME) (24 decks)

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