gastric motility and the pancreas Flashcards

1
Q

where do peristaltic waves travel from in the stomach and what occurs at each area

A

from the body to antrum

body - thin muscle so weak contractions (no mixing)

antrum - thick muscle so powerful contractions (mixing occurs)

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2
Q

what happens when the peristaltic wave reaches the antrum

A

contraction of the pyloric sphincter

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3
Q

what does contraction of the pyloric sphincter allow

A
  1. only a small quantity of gastric content (chyme) enters the duodenum
  2. rest of contents pushed back up to body so allows of further mixing/grinding with acid
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4
Q

what produces gastric peristaltic waves

A

peristaltic rhythm (~3/min) is generated by pacemaker cells in the longitudinal muscle

they are SLOW waves

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5
Q

briefly describe how the pacemaker cells make the slow peristaltic waves

A

slow waves:

  • occur from spontaneous depolarisation/repolarisation
  • conducted through gap junctions along longitudinal muscle layer
  • depolarisation is sub-threshold so require further depolarisation to induce action potentials and contractions

slow wave rhythm is from basic electrical rhythm (BER)

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6
Q

what determines the strength of contractions

A

number of action potentials

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7
Q

what determines the frequency of the contractions

A

basic electrical rhythm (BER)

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8
Q

what neural/hormonal controls can affect gastric peristalsis and how

A

gastrin - increases contractions

distension of stomach wall - long/short reflexes - increases contractions

fat/amino acid/hypertonicity in duodenum - inhibits motility

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9
Q

what neutralises the acid in the duodenum

A

bicarbonate (HCO3) secretions from brunners gland duct cells (submucosal glands)

bicarb rises up from the duodenum to meet the acid coming in from the stomach

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10
Q

what is the reaction for neutralisation of the acid

A
H+ + HCO3-
=
H2CO3
= 
H2O + CO2
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11
Q

what are the two controls for duodenal HCO3 secretion that are triggered by the presence of acid

A
  1. long (vagal) and short (ENS) reflexes - increases HCO3 secretion
  2. release of secretin from S cells - increases HCO3 secretion
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12
Q

what does secretin also cause

A

HCO3 secretion from the pancreas and liver

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13
Q

how is secretin secretion controlled

A

self limiting negative feedback loop - when acid neutralisation occurs - secretin release inhibited

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14
Q

what are the three main parts of the pancreas

A

Head (located within curvature of duodenum),

body,

tail (extends to spleen)

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15
Q

what comprises the endocrine portion of the pancreas (i.e. material into circulatory system)

A

pancreatic islets (islets of Langerhans)

islet cells produce:

  • insulin
  • glucagon (control [glucose]blood )
  • somatostatin (controls secretion of insulin and glucagon)
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16
Q

what comprises the exocrine portion of the pancreas (i.e. material to outside the body)

A

acinar cells that contain lobules

17
Q

what is the primary exocrine route out of the pancreas

A
  • acinar cells
  • lobules connected by intercalated ducts
  • interlobular ducts
  • main pancreatic duct
  • common bile duct
  • hepatopancreatic ampulla (SPHINCTER OF ODDI)
  • duodenum
18
Q

what is the secondary exocrine route out of the pancreas

A

the accessory pancreatic duct - also goes to the duodenum

19
Q

what is the function of the exocrine pancreas

A

digestive fucntion

  • secretion of bicarbonate by duct cells
  • secretion of digestive ezymes by acinar cells
20
Q

what is the basic anatomical structure of the exocrine pancreas

A

acini - ducts - pancreatic duct

21
Q

what kind of cells make up duct cells

A

cuboidal epithelium

22
Q

why is nothing digested by the secreted enzymes as it goes down the pancreatic ducts

A

if it did pancreas would essentially be digesting itself

23
Q

what are zymogens and where are they stored

A

digestive enzymes that are stored as inactive granules (zymogens)

stored in the acinar cells

24
Q

what does having inactive forms of the enzymes prevent

A

autodigestion of the pancreas

25
Q

what converts zymogens to their active forms

A

trypsin

26
Q

what does trypsin come from

A

trypsinogen

27
Q

what converts trypsinogen into trypsin

A

enterokinase bound to the brush border of the duodenum

28
Q

what are the 6 categories of pancreatic enzymes

A
  1. proteases
  2. nucleases
  3. elastases
  4. phospholipases
  5. lipases
  6. a-amylse
29
Q

what do each of the categories of pancreatic enzymes do

A
  1. proteases - cleave peptide bonds
  2. nucleases - hydrplyse DNA/RNA
  3. elastases - collagen digestion
  4. phospholipases - phospholipids to fatty acids
  5. lipases - triglycerides to fatty acids + glycerol
  6. a-amylse - starch to maltose and glucose
30
Q

what stimulates secretion of bicarbonate

A

secretin

31
Q

what is secretin rekeased in response to

A

acid in the duodenum

32
Q

what stimulates secretion of zymogens

A

cholecystokinin (CCK)

33
Q

what is CCK released in response to

A

fat/amino acids in the duodenum

also under neural control (vagal/local reflexes) - triggered by arrival of organic nutrients in the duodenum

34
Q

summarise the negative feedback loop of secretin secretion

A
  1. increased acid in stomach
  2. increased secretin secretion in small intestine
  3. increased plasma secretin
  4. increased bicarbonate secretion in pancreas
  5. increased flow of bicarbonate to small intestine
  6. increased neutralisation of intestinal acid in small intestine
  7. TIGGERS NEGATIVE FEEDBACK TO REDUCE SECRETIN SECRETION AT STEP 2
35
Q

summarise the negative feedback loop of cholecystokinin secretion

A
  1. increased fatty acids and amino acids
  2. increased CCK secretion in small intestine
  3. increased plasma CCK
  4. increased enzyme secretion in pancreas
  5. increased flow of enzymes to small intestine
  6. increased digestion of fats and proteins in small intestine
  7. TRIGGERS NEGATIVE FEEDBACK TO REDUCE CCK SECRETION AT STEP 2