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Z YEAR 1 BRS Gastroentology > Pancreas and Small Bowel > Flashcards

Pancreas and Small Bowel Flashcards

1
Q

What is part of the endocrine secretion?

A

Endocrine - 2% of gland
•Islets of Langerhans
•Secrete hormones into blood - Insulin & Glucagon (also Somatostatin and Pancreatic Polypeptide)
-Regulation of blood glucose, metabolism & growth effects - (Endocrine course)

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2
Q

What is part of the exocrine secretion?

A

Exocrine - 98% of gland
•Secretes pancreatic juice into duodenum via MPD/sphincter of Oddi/ampulla
•Digestive function (covered in this lecture)

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3
Q

What is Acini?

A
  • Ducts
  • Acini are grape-like clusters of secretory units
  • Acinar cells secrete pro-enzymes into ducts
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4
Q

What is Islets?

A
  • Derived from the branching duct system
  • Lose contact with ducts – become islets
  • Differentiate into α- and β-cells secreting into blood
  • Tail > head
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5
Q

What is the composition of islets?

A
  • α-cells (A) form about 15-20% of islet tissue and secrete glucagon
  • β-cells (B) form about 60-70% of islet tissue and secrete insulin
  • δ-cells (D) form about 5-10% of islet tissue and secrete somatostatin
  • Acini (2)
  • The islets are highly vascular, ensuring that all endocrine cells have close access to a site for secretion
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6
Q

What are secretory acinar cells?

A

-Large with apical secretion granules

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7
Q

What are duct cells?

A

Small and pale

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8
Q

What is endocrine?

A

secretion into the blood stream to have effect on distant target organ (autocrine/paracrine): ductless gland

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9
Q

What is exocrine?

A

secretion into a duct to have direct local effect

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10
Q

What are the main endocrine secretion of the pancreas and their actions?

A
  1. Insulin: anabolic hormone
    - Promotes glucose transport into cell and storage as glycogen
    - Decrease blood glucose
    - Promotes protein synthesis and lipogensis
  2. Glucagon
    - increase gluconeogensis and glycogenolysis (increases blood glucose)
  3. Somatostatin: Endocrine cyanide
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11
Q

What are the two components of pancreatic juice?

A
  • ↓ vol, viscous, enzyme-rich - Acinar cells

* ↑ vol, watery, HCO3- rich - Duct & Centroacinar cells

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12
Q

What is pancreatic juice with bicarbonate secretion?

A

Pancreatic juice: Bicarbonate secretion:
•Produced by duct & centroacinar cells
•Pancreatic Juice = ↑ bicarbonate
•~ 120 mM (mmol/L) - (plasma ~25 mM)
•pH 7.5-8.0

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13
Q

What is the function of pancreatic juice?

A

•Neutralises acid chyme from stomach
-prevents damage to duodenal mucosa
-Raises pH to optimum range for pancreatic enzymes to work
•Washes low volume enzyme secretion out of pancreas into duodenum

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14
Q

What happens to rate of bicarbonate secretion to Duodenum pH?

A

Duodenal pH < 5 → linear ↑ in pancreatic HCO3- secretion

Duodenal pH <3 → not much more ↑ in HCO3- secretion

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15
Q

Why does HCO3- secretions stop when pH is still acid?

A
  • Bile also contains HCO3- and helps neutralise acid chyme

- Brunners glands secrete alkaline fluid

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16
Q

What is the second step in pancreatic HCO3- secretion?

A

• Cl-/HCO3- exchange at lumen (anion exchanger [AE])
• Na+/H+ exchange at basolateral membrane into bloodstream (sodium-hydrogen exchanger (antiporter) type 1 [NHE-1])
-Exchange driven by electrochemical gradients
•High EC (blood) Na+ compared to IC (duct cell)
•High Cl- in lumen compared to IC (duct cell)

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17
Q

What is the third step in pancreatic HCO3- secretion?

A
  1. Pancreatic HCO3- Secretion
    • Na+ gradient into cell from blood maintained by Na+/K+ exchange pump
    •Uses ATP - Primary active transport
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18
Q

What is the fourth step in pancreatic HCO3- secretion?

A
  1. Pancreatic HCO3- Secretion
    • K+ returns to blood via K+-channel
    • Cl- returns to lumen via Cl-channel (cystic fibrosis transmembrane conductance regulator [CFTR])
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19
Q

What happens in gastric parietal cell (acid) and pancreatic duct cells (alkaline)?

A
  • Same reaction but:
  • Stomach:
    1. H+ goes to gastric juice
    2. HCO3- goes to blood
    3. Gastric venous blood is lakline
  • Pancreas:
    1. HCO3- secreted into juice
    2. H+ into blood
    3. Pancreatic venous blood is acidic
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20
Q

What are enzyme of digestion of? Where are they made?

A 
Enzymes for digestion of:
• fat (lipases)
• protein (proteases) 
•carbohydrates (amylase)
→ synthesised &amp; stored in zymogen granules
•Zymogens = pro-enzymes
-Made in acinar cell
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21
Q

How does pancreases try to stop digesting itself/pancreatitis?

A
  • Proteases are released as inactive pro-enzymes
  • protects acini & ducts from auto-digestion
  • Pancreas also contains a trypsin inhibitor to prevent trypsin activation
  • Enzymes only activated in duodenum
  • Blockage of MPD may overload protection → auto-digestion (= acute pancreatitis)
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22
Q

How does pancreases try to stop digesting itself/pancreatitis?

A

•Proteases are released as inactive pro-enzymes
-Protects acini & ducts from auto-digestion
•Pancreas also contains a trypsin inhibitor to prevent trypsin activation
•Enzymes only activated in duodenum
•Blockage of MPD may overload protection → auto-digestion (= acute pancreatitis)

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23
Q

What does enterokinase do?

A
  • Duodenal mucosa secretes an enzyme - Enterokinase (enteropeptidase)
  • converts trypsinogen → trypsin.
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24
Q

What does trypsin do?

A

-Trypsin then converts all other proteolytic & some lipolytic enzymes
-NB: Lipase secreted in active form but requires colipase (i.e. secreted as precursor)
0NB: lipases require presence of bile salts for effective action - see liver sessions

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25
Q

What is altered pancreatic enzyme function?

A

-Pancreatic secretions adapt to diet:
•e.g. ↑ protein, ↓ carbs → ↑s proportion of proteases & ↓ proportion of amylases
-Pancreatic enzymes (+ bile) essential for normal digestion of a meal:
• Lack of these can → malnutrition even if dietary input is OK.
•(unlike salivary, gastric enzymes)

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26
Q

What does Orlisatat do?

A
  • Inhibits pancreatic lipase
  • Causes statorhea (increase faecel fat
  • Occurs when pancreatic lipase secretion
  • E.g. cystic fibrosis, chronic pancreatitis, orlistat (decreases intestinal fat absorption)
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27
Q

How is pancreatic juice secretion controlled with cephalic phase?

A
  • Reflex response to sight/smell/taste of food
  • Enzyme-rich component only.
  • Low volume - “mobilises” enzymes
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28
Q

How is pancreatic juice secretion controlled with gastric phase?

A
  • Stimulation of pancreatic secretion originating from food arriving in the stomach
  • Same mechanisms involved as for cephalic phase
29
Q

How is pancreatic juice secretion controlled with intestinal phase?

A
  • Hormonally mediated when gastric chyme enters duodenum.
  • BOTH components of pancreatic juice stimulated
  • enzymes & HCO3- juice flows into duodenum
30
Q

How is pancreatic juice enzyme secretion controlled in acini ?

A
  1. Vagus nerve –
    • Cholinergic
    • Vagal stimulation of enzyme secretn (& communicates information from gut to brain)
  2. Cholecystokinin (CCK) (Ca2+/PLC)
31
Q

How is pancreatic juice bicarbonate controlled on duct and centroacinar. cells?

A

• Secretin (cAMP)

32
Q

Describe control of enzyme secretion in acini?

A
  1. Vagus nerve (acetylcholine {Ach})
  2. Mechanisms responsible for controlling release of CCK from duodenal I cells
    - CCK - relaying peptide (CCK-RP)
    - Gastrin-releasing peptide (GRP)
33
Q

What is the control of HCO3 - secretion in Acini?

A
  • Acinar fluid is isotonic
  • resembles plasma in its concs of Na+, K+, Cl− & HCO3−.
  • Secretion of acinar fluid & proteins it contains is stimulated primarily by CCK
34
Q

What is the control of HCO3 - secretion in ducts?

A
  • S cells Secretin stimulates secretion of H2O & HCO3- from cells lining extralobular ducts.
  • Secretin-stimulated secretion is richer in HCO3−cf acinar secretion because of Cl−/HCO3−exchange
35
Q

What is the negative feedback in control of HCO3- secretion in ducts?

A

•Secretin and HCO3−secretion
•Classic negative-feedback loop
Responds to ↓in luminal pH in duodenum

36
Q

What is. the stimulus interaction?

A
  • CCK alone - no effect on HCO3− secretion
  • CCK can markedly ↑ HCO3− secretion that has been stimulated by secretin
  • Vagus nerve has similar effect to CCK
  • Secretin NO EFFECT on enzyme secretion
37
Q

Summarise what happens in a meal

A
  1. Food mixed, digested in stomach pH 2
  2. Chyme squirted into duodenum
  3. •H+ ions in duodenum → ↑secretin → ↑pancreatic juice
    •+ bile & Brunner’s gland secretions
    -(↑s pH to neutral/alkaline)
  4. •Peptides & fat in duodenum cause sharp ↑ in CCK & vagal nerve stimulation
    • → stimulates pancreatic enzyme release
    •Peaks by 30 mins, continues until stomach empty.
  5. •CCK potentiates effects of secretin on aqueous component
    •Necessary as most of duodenum not at ↓pH
38
Q

What is the structure of the small bowel?

A

-Approx. 6m long & 3.5cm in diameter.
•Duodenum: 25 cm
•Jejunum: 2.5 m
•Ileum: 3.75 m
•No suddentransition between them
•All have same basic histological organisation

39
Q

What is the function of the mesentery?

A

•Suspends small & large bowel from posterior abdominal wall
-anchoring them in place
-whilst still allowing some movement
•Provides a conduitfor blood vessels, nerves & lymphatic vessels.

40
Q

what are the villi in small bowl like?

A
  • only occur in the small intestine
  • Motile
  • Have a rich blood supply & lymph drainage for absorption of digested nutrients
  • Have good innervation from the submucosal plexus.
  • Have simple epithelium
  • 1 cell thick
  • dominated by enterocytes (columnar absorptive cells)
41
Q

What are Villi (mucosa) lined with?

A
  • simple columnar epithelium consisting of:
  • primarily enterocytes (absorptive cells)
  • scattered goblet cells
  • enteroendocrine cells
42
Q

What does Crypts of Lieberkühn - epithelium include?

A
  • Paneth cells

* Stem cells

43
Q

What are enterocytes?

A
  • Most abundant cells in small bowel
  • Tall columnar cells with microvilli & a basal nucleus.
  • Specialised for absorption & transport of substances.
  • Short lifespan of 1-6 days.
44
Q

What is the surface area of enterocytes like?

A

Surface area
•Cylindrical internal surface area of small bowel is 0.4m2.
•Folds, villi & microvilli ↑ surface area to ~200m2 (size of a tennis court)
•At least a 500 fold ↑

45
Q

What are microvilli?

A
  • Microvilli (~0.5-1.5mm high) make up the “brush border”.
  • Several thousand microvilli per cell
  • Surface of microvilli covered with glycocalyx
46
Q

What is glycocalyx?

A
  • rich carbohydrate layer on apical membrane
  • serves as protection from digestional lumen yet allows for absorption.
  • traps a layer of water & mucous known as “unstirred layer”
  • regulates rate of absorption from intestinal lumen
47
Q

What are goblet cells?

A
  • 2nd most abundant epithelial cell type
  • Mucous containing granules accumulate at apical end of cell, causing ‘goblet’ shape.
  • Mucous → large glycoprotein that facilitates passage of material through bowel.
  • ­ abundance of goblet cells along entire length of bowel
  • ↓ in duodenum
  • ↑ in colon
48
Q

What are Enteroendocrine Cells?

A
  • Columnar epithelial cells
  • scattered among enterocytes
  • most often found in lower part of crypts.
  • Hormone secreting
  • e.g. to influence gut motility (see Regulation of function lecture)
  • In older text books → referred to as chromaffin cells (affinity for chromium/silver salts).
49
Q

What are Paneth Cells?

A
  • Found only in the bases of crypts
  • Contain large, acidophilic granules
  • Granules contain:
  • antibacterial enzyme lysozyme (protects stem cells)
  • Glycoproteins & zinc (essential trace metal for a no. of enzymes)
  • Also engulf some bacteria & protozoa
  • May have a role in regulating intestinal flora
50
Q

What are stem cells?

A
  • Undifferentiated cells which remain capable of cell division to replace cells which die
  • Epithelial stem cells are essential in the GI tract to continually replenish the surface epithelium
  • Continually divide by mitosis
  • Migrate up to tip of villus, replacing older cells that die by apoptosis
  • -> digested and reabsorbed
  • Differentiate into various cell types (pluripotent)
51
Q

Why do enterocytes and goblet cells of small bowel have short life span (36 hours)?

A
  1. Enterocytes are first line of defence against GI pathogens and may be directly affected by toxic substances in diet
  2. Effects of agents which interfere with cell function, metabolic rate etc will be diminished
  3. Any lesions will be short-lived
  4. If escalator-like transit of enterocytes is interrupted through impaired production of new cells (e.g. radiation) severe intestinal dysfunction will occur
52
Q

What is the transition like in small bowel?

A
  • No suddentransition between duodenum, jejunum, ileum
  • All have same basic histological organisation.
  • But – some general differences
53
Q

Describe the duodenum

A

•Distinguished by presence of Brunner’s glands
•Submucosal coiled tubular mucous glands secreting alkaline fluid
•Open into the base of the crypts
•Alkaline secretions of Brunner’s glands
-Neutralizes acidic chyme from stomach, protecting proximal small bowel
-Help optimise pH for action of pancreatic digestive enzymes.

54
Q

What are the function of small intestine motility?

A
  • To mix ingested food with digestive secretions & enzymes
  • To facilitate contact between contents of intestine & the intestinal mucosa
  • To propel intestinal contents along alimentary tract
55
Q

What is segmentation?

A

1.Segmentation (mixing)
•Mixes contents of lumen
•Occurs by stationary contraction of circular muscles at intervals.
•More frequent contractions in duodenum cf. ileum
•allow pancreatic enzymes & bile to mix with chyme
•Although chyme moves in both directions, net effect is movement → colon

56
Q

What peristalsis?

A
  1. Peristalsis (propelling)
    •Involves sequential contraction of adjacent rings of smooth muscle
    •Propels chyme towards colon
    •Most waves of peristalsis only travel about 10cm
    •Segmentation & peristalsis result in chyme being segmented, mixed & propelled → colon
57
Q

What is migrating motor complex?

A
  1. Migrating Motor Complex
    •Cycles of smooth muscle contractions sweeping through gut
    •Begin in stomach → small intestine → colon → next wave starts in duodenum
    •Prevents migration of colonic bacteria into ileum
58
Q

What is digestion in duodenum like?

A
  1. Digestion in small bowel occurs in an alkaline environment
  2. Pancreatic digestive enzymes & bile enter duodenum from MPD & CBD
  3. Duodenal epithelium also produces its own digestive enzymes
  4. Digestion occurs in lumen & in contact with the membrane
59
Q

Describe digestion of carbohydrates

A
  • Carbohydrates contain ~50% of ingested calories in western diet.
  • Digestion begins in mouth by salivary a-amylase (destroyed in stomach (acid pH)
  • Most of digestion of carbohydrates occurs in small intestine
60
Q

What are simple carbohydrates?

A
  • Simple carbohydrates
  • monosaccharides - glucose & fructose
  • disaccharides - sucrose & maltose
61
Q

What are complex carbohydrates?

A
  • Complex carbohydrates
  • starch, cellulose, pectins
  • → sugars bonded together to form a chain
62
Q

What is pancreatic alpha amylase?

A
  • Secreted into duodenum in response to a meal
  • Continues digestion of starch & glycogen in small bowel (started by salivary amylase)
  • Needs Cl- for optimum activity & neutral/slightly alkaline pH
  • Acts mainly in lumen (some also adsorbs to brush border)
  • Digestion of amylase products & simple carbohydrates occurs at the brush border
63
Q

How are carbs digested?

A
  1. Absorption of glucose & galactose is by 2o
    active transport
    -Carrier protein = SGLT-1 on apical membrane
  2. Absorption of fructose is by facilitated diffusion.
    -Carrier protein = GLUT-5 on apical membrane
  3. GLUT-2 facilitates exit at basolateral membrane
  4. Human small intestine can absorb 10kg of simple sugars/day
64
Q

How are proteins digested?

A
  • Protein digestion begins in lumen of stomach by pepsin
  • pepsin then inactivated in alkaline duodenum
  • 5x pancreatic proteases secreted as precursors → lumen of small bowel (e.g. trypsinogen)
  • Trypsin activated by enterokinase
  • an enzyme located on duodenal brush border
  • Trypsin → activates other proteases
  • hydrolyse proteins → single amino acids (AA) & oligopeptides (AA)n
65
Q

What is the Action of luminal, brush-border & cytosolic peptidases

A
  1. Variety of peptidases at brush borders of enterocytes progressively hydrolyse (AA)n → AAs
  2. Enterocytes directly absorb some of small (AA)n via action of H+/oligopeptide cotransporter PepT1
  3. These small peptides are digested to AAs by peptidases in cytoplasm of enterocytes
66
Q

Describe digestion of lipids

A

•Lipids are poorly soluble in water
•more complicated to digest.
•4 stage process in small bowel:
1. Secretion of bile salts & pancreatic lipases
2. Emulsification (↑s surface area for digestion)
3. Enzymatic hydrolysis of ester linkages
-Colipase complexes with lipase – prevents bile salts displacing lipase from fat droplet
4. Solubilisation of lipolytic products in bile salt micelles

67
Q

How are lipids absorbed?

A

-Unlike AAs & simple sugars → lipids transformed as absorbed via enterocytes
-Fatty acids (FAs) & monoglycerides (MG) leave micelles and enter enterocytes
-FAs & MG resynthesized into tri-glycerides (TGS) by 2x pathways:
Monoglyceride acylation (major)
Phosphatidic acid pathway (minor)
-Chylomicrons - lipoprotein particles synthesised as an emulsion (80-90% TGs, 8-9% phospholipids, 2% cholesterol, 2% protein, trace carbohydrate) in Golgi apparatus
-Chylomicrons secreted across basement membrane by exocytosis
Chylomicrons enter a lacteal (lymph capillary) → lymph transports them away from bowel

68
Q

What is the iloecaecal valve?

A
  • Ileum is separated from the colon by the ileocaecal valve
  • Relaxation & contraction controls passage of material into colon
  • Also prevents back flow of bacteria into ileum

Z YEAR 1 BRS Gastroentology (11 decks)

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