Lecture 14 Flashcards

1
Q

What does gastric motility result from?

A

Contraction/relaxation of layers of muscle in stomach (myenteric plexus)

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2
Q

How does gastric motility occur?

A

Myenteric plexus receives input from ANS: parasympathetic stimulation increases motility, sympathetic input decreases motility

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3
Q

Zymogen?

A

Inactive form of enzyme

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4
Q

Role of pepsin?

A

Hydrolyses proteins to polypeptide/amino acids which stimulates acid production

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5
Q

When is pepsin inactivated?

A

At pH higher than 6 (can be reactivated upon re-acidification)

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6
Q

Role of salivary amylase?

A

acts on carbohydrate if pH~6 (mouth) so far less active in stomach (acidic)

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7
Q

What increases antral contraction?

A

Distension (swelling from pressure inside) of stomach + increased gastrin levels

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8
Q

What does stomach emptying involve?

A

Constriction of lower oesophageal sphincter, contraction of gastric muscularis, relaxation of pyloric sphincter

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9
Q

What inhibits gastric emptying (entry to duodenum)?

A

Distension of duodenum, presence of fat, increased HCl concentration

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10
Q

Role of enterogastric reflex?

A

Prevents too much chyme entering duodenum all at once/aids digestion

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11
Q

What occurs when there’s fat in duodenum?

A

Fundus relaxes lowering intragastric pressure (high fat meal = full for longer)

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12
Q

Absorption in stomach?

A

Limited (some water/electrolytes/alcohol/drug, stomach wall impermeable to most materials

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13
Q

When does absorption properly start?

A

When contents reach small intestine, food acted upon by products of pancreas/liver/gallbladder

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14
Q

Gastric ulcer?

A

Erosion of mucosal layer causing inflammation/damage to underlying tissue (acid not necessarily the main damaging feature)

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15
Q

Causes of gastric ulcers?

A

Associated with H. Pylori infection, NSAID uses, smoking, alcohol…

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16
Q

Managing gastric ulcers?

A

Dietary control, drug therapy (control of acid production) eradication of H. Pylori

17
Q
A