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Digestive System Module > Lecture 27 > Flashcards

Lecture 27 Flashcards

1
Q

2nd part of Duodenum

A

Where ampulla opens
Ampulla= medial wall of duodenum
-where pancreatic secretions and bile will meet intestinal contents

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2
Q

Central role of duodenum

A

Role:
1. Inhibition of gastric emptying
2. Inhibition of acid secretion
3. Stimulation of pancreatic and biliary secretion
Mechanism: Duodenum has sensory function
-Endocrine cells response to nutrients
(Sensory function: around duodenum have multiple sensory cells and receptors which mediate release of pancreatic and biliary secretions)
-Vagal afferents respond to luminal contents (sense certain contents and duodenum distention)

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3
Q

Intestinal phase

A

last phase of a meal
Digestive fats and proteins have reached duodenum + excessive amount of gastric acid into duodenum
Duodenal Fats and proteins –> CCK cholecystokinen release simulated
Duodenal HCl –> Secretin release stimulated

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4
Q

Enteroendocrine cells

A

Specialised endocrine cells in GI tract and pancreas:
(role in pancreatic an biliary secretion)
-I cells (secretes cholecystokinin)
-S cells (secretes secretin)
-Enterochromaffin cells
–NB:do NOT confuse with enterochromaffin like cells in the stomach (ECL) that secrete histamine

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5
Q

Functions of Enteroendocrine cel surfaces

A

Apical surface: Faces gut lumen (internally)

Basolateral surface: Faces circulation

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6
Q

I cells

A

Apical surface of cell senses (apical sensory receptors) partially digested fats and proteins (in 2nd part of duodenum)
Stimulates release of cholecystokinin (CKK) from basolateral surface of cell
-as CCK has to enter circulation

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7
Q

S cells

A

Apical surface of cells senses low pH (acidic) in duodenum
(excessive acid in duodenum needs to be neutralised)
Stimulates release of secretin from basolateral surface of cell

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8
Q

Roles of CCK and secretin

A

Inhibit gastric emptying
-slows transit of food from stomach –> duodenum. as duodenum becomes distended with chyme(fats, proteins, HCl), want to slow down process, to allow absoprtion to occur distally
Inhibit gastric secretion
-need negative feedback loop to turn off system

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9
Q

Enterochromaffin cells

A

Apical surface of cell senses food or irritant (chemo drugs, potent side effects of nasuea/vomitting. chemo oral medication irritate SI and stimulate enterochromaffin cells)
Stimulates serotonin release from basolateral surface of cell
Note: Serotonin:
-stimulates gut motility (why irritating medications can cause diarrohea)
-high levels in blood activates receptors in medulla leading to vomiting

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10
Q

Roles of pancreas in digestion

A

2x functions
Endo and Exocrine function
-Digestion: Exocrine. release of enzymes and bicarbonate function for digestion
-cluster of cells, ducts b/w. Acinar cells for release of digestive enzymes.
-Acinar cells bought together by Ductles and interlobular ducts –> pancreatic duct –> secreted into duodenum
-Endocrine: hormones (insulin)

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11
Q

Exocrine pancreas

A

Secretes into small intestine:
-Digestive enzymes for fat and protein digestion- Acinar cells
-Bicarbonate ions to neutralize acidic pH (in SI from stomach) -Ductal cells
Acinar cells: digestive enzymes
Ductal cells: alkaline solution containing bicarbonate

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12
Q

Acinar cells of Pancreas

A

Filled with secretory granules containing precursor enzymes (also known as Zymogens/Proenzymes)
-not active/inactive form
Granules are released into small intestine via pancreatic duct
-some enzymes are activated in small intestine to prevent auto-degradation of pancreas
-protection
Lots of RER Rough endoplasmic reticulum for production of enzymes

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13
Q

Pancreatic enzymes: Proteases

A

Proteases: digest proteins
Pancreas –> Duodenum
1. Trypsinogen (inactive)(stored in pancreas) – (released under CCK simulation) cleaves peptide bond/ SI Enteropeptidases –> Trypsin (active)
2. Chymotrypsinogen (inactive) –cleaves peptide bond/Trypsin –> Chymotrypsin (active)

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14
Q

Site of zymogen activation

A

Activation of inactive proenzymes takes place in the duodenal lumen (brush border) via proteolytic cleavage
Trypsin can cleave:
-trypsinogen (i.e. autocatalytic) (can cleave itself from trypsinogen to tripson, and can also cleave other proenzymes in second part of duodenums)-cycle of activation
-chymotrypsinogen
-other proenzymes

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15
Q

Pancreatic enzymes: Active form storage

A
  1. Pancreatic lipase - converts triglycerides into monoglycerides + free fatty acids. Active
  2. Amylase - converts starch into sugars. Active
    - important in pancreatitis - inflammation. these active enzymes become elevated in serum and can be measured as indication of pancreatitis
    - can also cause further damage as are in active form and released directly into pancreas
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16
Q

Release of pancreatic enzymes

A

Controlled by cholecystokinin (CCK)
-CCK stimulates pancreatic enzymes via 2x pathways:
(alongside action on stomach CCK is main hormone responsible for pancreas stimulation)
Fat/proteins
1. -Enters blood circulation directly form basolaterla surface to get to acinar cells of pancreas –> stimulates release of pancreatic enzymes
2. -Sends message/excites via afferent fibres next to I cells to Vagus nerve in brain stem - efferent fibres of vagus nerve transmit message to pancreas –> stimulates release of pancreatic enzymes

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17
Q

Ductal cells

A

Intercalated duct and centro-acinar cells release bicarbonate secretion into small intestine via pancreatic duct –> SI
Neutralises gastric acid in duodenum
Needs to be neutral pH (neutralise acidic chyme entering SI) from optimal function of pancreatic enzymes

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18
Q

Importance of maintaining small intestinal pH Near neutrality

A
  1. Inactive pepsin
  2. Prevent mucosal damage (stomach has increase mucous and goblet cell production. these adaptation not in SI)
  3. Increase fatty acid and bile acid solubility
  4. Optimise pH of pancreatic and duodenal enterocyte brush border enzymes
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19
Q

Ion transporters involved in bicarbonate secretion

A
  1. HCO3- is taken up into ductal cell from the basolateral surface
  2. Carbonic anhydrase (catalyst) forms HCO3- from H2O and CO2
    - cell itself makes bicarbonate
  3. HCO3- secretion into duct lumen involves:
    a) Cl-/HCO3- exchanger
    - -maintains ionic neutral charge and osmotic pressure (lose -ve ion)
    b) CFTR transporter (located next to exchanger. Pumps Cl- into duct, then recycled back into cell as part of exchange with bicarbonate)
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20
Q

Release of pancreatic bicarbonate secretion

A

Controlled by secretin
Secretin:
-enters blood circulation to get to ductal cells of pancreas –> binds receptors on pancreatic ductal cells (binds to receptors) –> increases levels of cyclic AMP in cell –> activates CFTS –> stimulates release of alkaline secretion
-no vagus nerve pathway

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21
Q

Regulation of Pancreatic Secretion

A
  1. (FFA, peptides, amino acids, releasing peptides) Fats and proteins in the duodenum stimulate I cells to release CCK
    CCK stimulates pancreatic acinar cells to release digestive enzymes (via 2x pathways)
  2. (Acid, FFa, releasing peptides) HCl in the duodenum stimulate S cells to release secretin
    Secretin stimulates pancreatic ductal cells to release secretions rich in bicarbonate for acid neutralisaiton
22
Q

Other factors influencing the regulation of pancreatic secretion

A
  1. Gastrin: secreted during a meal, also stimulates pancreatic acinar cells to release digestive enzymes
  2. The vagus nerve innervates the pancreas:
    - Vagal stimulation and ACh Acetylcholine release during a meal also applies a low-level stimulus to the pancreas (for release of digestive enzymes and bicarbonate secretion)
23
Q

Other actions of CCK

A

Stimulates bile production in liver
Gall bladder contraction
Sphincter of Oddi relaxation to deliver more bile into duodenum

24
Q

Other actions of Secretin

A

Stimulates bile duct to release bicarbonate solution

25
Q

Cystic Fibrosis

A

Autosomal recessive (genetic condition) (must have 2x abnormal copies-both parents)
Various mutations of the CFTR gene described (Cl- pump. Regulates Bicarbonate-located close)
Defective CFTR ion channel - very little to no function
Secretions - become extremely thick. Occurs in a number of organ systems, throughout entire body.
Thick, sticky mucous clogs passage (not watery bicarbonate secretions). Buildup blocks up airways/nasal passages, pancreatic duct. thick and sticky leading to bacterial infection
Affects mostly the lungs but also:
1. Sinuses (infections)
2. Lungs (thick, sticky mucous buildup, bacterial infection and widened airways)
3. Skin (sweat glands produce slaty sweat)
4. Liver (blocked biliary ducts)
5. Pancreas (blocked pancreatic ducts)
6. Intestines (cannot fully absorb nutrients)
7. Reproductive organs (male and female) complications
Airway with cystic fibrosis:
-bacterial infections. thick mucous airway. sticky blocks, widened airway. Blood in mucous.

26
Q

CFTR

A

CFTR= Cystic Fibrosis Transmembrane Conductance Regulator
Chloride channel (present throughout body, therefore defect effects multiple body systems)
Lung, Liver, Pancreas, GI tract, Reproductive tract, Sweat glands
Involved in Production of sweat, mucus, digestive fluids
CFTR also plays an important part in secretion of HCO3- working alongside the Cl-/HCO3- exchanger

27
Q

The pancreas is CF

A

Ducts blocked up and plugged with mucous –> episodes of inflammation which damages pancreas

  1. Cystic Fibrosis CF can lead to pancreatic insufficiency (exocrine and endocrine both effected)
    - analogous to liver failure. Pancreas stops producing enzymes and stops working normally.
  2. Defective CFTR transporter in pancreas
  3. -Cl- accumulates in ductal cells (excess amount inside)
  4. -Cells become more negatively charged, drawing Na+ (+ve charge to compensate and counteract) and then H2O from ductal lumen into cells (due to increased osmotic gradient)
  5. -ducts become dried up/ as water is sucked back into cell
  6. -Pancreatic secretions become hyper-viscous (i.e. too thick)
  7. Pancreatic ducts become blocked
  8. Insufficient pancreatic enzymes released
  9. Build up of enzymes n pancreas. Inappropriately activated in pancreas - auto-digestion of pancreas - pancreatitis - pancreas becomes damaged and replaced by fibrosis
28
Q

Pancreatitis

A

Acute
-acute inflammation
-abdominal pain
-elevated pancreatic enzymes in serum (amylase and lipase- as released from adamaged acinar pancreatic cells)
-self limiting (cells will recover)
Chronic: (ongoing insult)
-Chronic inflammation
-Chronic abdominal pain (not severe, but more grumbling pain)
–> leads to fibrosis
-Progressive loss of pancreatic endocrine and exocrine function

29
Q

Causes of Pancreatitis

A

**Alcohol
**Gallstones (bilicholic. maybe jaundice aswell on Blood test)
-causes 80%. Easy to find out by taking history
Autoimmune (autoimmune pancreatitis. antibodies which target specific receptors on pancreatic cells)
Drugs
Trauma (abdominal trauma which ruptures pancreas –> pancreatitis)
Post-ERCP
-endoscopic retrograde cholangiopancreatography
-done on people typically with gallstones.
Structural anomalis (e.g. pancreas divisum)
Metabolic e.g. Hypertriglyceridaemia/hypercalcaemia
-excessive trigylceride (not mildly elevated like in most of people)
Viral infections e.g. mumps
Cystic fibrosis
Hereditary/Familial

30
Q

Pancreas Divisum

A

Common congenital anomaly (born with this condition)
In the embryo. pancreas starts off in 2x parts - dorsal and ventral, each with own duct
During normal development, these 2 parts fuse to form one main pancreatic duct (opens into ampulla)
In the pancreas divisum, failure of ducts to fuse
-2x separate ducts
-accessory duct larger
-dont know why occurs

31
Q

Recovery of Acute and chronic Pancreatitis

A 
Acute pancreatitis recovery:
-acutely inflamed pancreas
-can fully recover
Chronic pancreatitis recovery:
-Long term or repeated episodes of inflammation causes irreversible damage leading to fibrosis and calcification of pancreas
-exocrine insufficiency
-endocrine insufficiency
32
Q

Pancreatic Insufficiency

A
  1. Pancreatic Endocrine insufficiency:
    * the pancreas produces hormones that regulate blood sugar. Insulin, Glucagon, Somatostatin, Pancreatic Polypeptide
    - impaired insulin production (insulin deficiency)
    - diabetes (treat as per diabetes)
    - take insulin supplements
33
Q

Pancreatic Insufficiency: Exocrine

A
  1. Pancreatic Exocrine insufficiency
    *the pancreas produces enzymes that help digest our food. Amylase, Protease, Lipase
    -fatabsoprtion and bicarbonate nuetalisaiton of acidic pH
    -impaired digestive enzyme production
    -fat malabsoprtion
    Need to lose >90% of exocrine function (before develop symptoms)
    Loss of lipase most critical
    Fat malabsoprtion:
    -Weight loss (due to fat not being absorbed)
    -Steatorrheoa
    -pale, bulky, floating stools, difficult to flush, oil droplets
    -Pancreatic enzyme supplements can be taken by mouth
34
Q

Chronic Pancreatitis Pancreatogram

A

Dilate main duct
Irregular side branches (coming off main duct)
Calcification (white shiny areas- indicated previous damage/inflammation)
- head or tail

35
Q

Bile

A

400-800mL/day produced

  1. Water
  2. Electrolytes
  3. Organic molecules:
    - bile acids(salts) - most important
    - cholesterol
    - phospholipids
    - Bilirubin
36
Q

Bile location re liver

A

Bile made in hepatocytes

  • canaliculi (b/w liver cells) drain bile from liver
  • meet in larger bile ducts (in portal triad) –> common bile ducts
  • major bile ducts (Right, Left and Common hepatic
37
Q

Enterohepatic circulation

A
  1. Secreted bile salts consist of 95% old, recycled bile salts, and 5% newly synthesized bile salts
    - common bile duct –> ampulla –> duodenum –> SI
  2. 95% of bile salts are reabsorbed by the Terminal Ileum of the small intestine
    - Terminal Illeum has specialised receptors that pick up bile.–> portal venous circulation
  3. Reabsorbed bile salts are recycled by enterohepatic circulation
  4. 5% of bile salts are lost in feces
38
Q

Functions of Bile

A
  1. Carrier bile acids
    - critical for digestion and absorption of fats and fat soluble vitamins (DrAKE)
  2. Elimination of waste products including bilirubin
    - secreted into bile–> faeces
39
Q

Source of bile acids

A

Hepatocytes contain bile acids from two sources

  1. 5% newly synthesized in liver from cholesterol
  2. 95% reabsorbed from terminal ileum
    - Bile in terminal ileum –> enterohepatic circulation –> portal vein –> sinusoids –> hepatocyte
    - Uptake of bile salts in the terminal ileum involved bile acid/Na+ transporter (Na+K+ATPase pump)
40
Q

Bile flow through Biliary tree

A

Hepatocytes secrete bile
(flows through in natural fashion, no pump)
-large quantities of bile acids, cholesterol, other organic molecules
Bile enters canaliculi and flows into larger bile ducts
As it flows through, watery secretion rich in bicarbonate is added to the bile by ductal epithelial cells (keeps neutral pH)
Bile leaves the liver, flowing down common hepatic duct and enters cystic duct into the gallbladder
Bile flow is deiven by the following mechanisms:
1. Bile flow into canaliculi
a)Bile acid dependant pathway: Active transport of bile acids from blood into canaliculi draws water with it (osmotic effect) (aids bile secretion)
b) bile acid-independant (transport of other solutes and electrolytes)-drawing fluids into bile ducts
2. Reabsorption and secretion of water and electrolytes by ductules and ducts
-secretion occurs in response to secretin
-bile isnt in constant state before final product

41
Q

Gall bladder

A

Bile from the liver enters gallbladder as a result of closure of the sphincter of oddi
Gall bladder stores and concentrates bile when not eating
-unlike in ducts (watery)
-partially why gallstones develop
When eating, fat in duodenum stimulates CCK release, which:
-causes gall bladder to contract, delivering bile to duodenum
-relaxes sphincter of Oddi
Autonomic NS ANS (vagus)also has influence on gallbladder function

42
Q

Cholestasis

A

Can be benign and malignant causes
Obstruction to bile flow i.e. cholestasis will lead to: (mechanical or function/physiological)
-Increased pressure in the biliary tract and liver
Leads to rupture of tight junctions and leakage of bile
Bile contents spill back into circulation causing jaundice - (hyperbilirubinaemia) (yellowing of skin)
-one of most common causes of cholestasis is Gall stones

43
Q

Gall stones

A
  1. Cholestrol stones are most common
    -form due to cholesterol precipitating (of high bile conc)in gall bladder
  2. Pigment stones
    -made up of bilirubin from the bile
    Most gallstones are asymptomatic/no problems
    -If gallstones falls out of gallbladder and too large to pas through bile duct –> biliary obstruction
    -stretching/distention of bile duct = Results in pain, sometimes jaundice (if obstruction is long enough and hepatocyte damage), liver test abnormality
44
Q

Gallstone diagnosis

A

Ultrasound probe scanning gallbladder through body wall
Right upper quadrant scan
Normally Well seen on ultra sound
-benign cause?
white opaque stones on bottom of black pocket (gall bladder)
-not nescessarily troublesome
-only troublesome if drop out of gallbladder and block
-e.g. cystic duct
-common bile duct =Choledocolysisis = jaundice
Intraoperative cholangiogram

45
Q

Gallstone removal

A

Telescope in duodenum
Basket to remove stones
-fine wire around gallbladder
- stones removed then dropped into small intestine

46
Q

Biliary strictures

A 
either benign (usually) or malignant (cancer)
-can cause obstruction
-i.e. cholestasis and jaundice
narrowing of bile duct
Common cause:
-repeated infection
- primary sclerosing cholangitis
47
Q

Malignant causes of biliary obstruction

A

Dilation of biliary tract
Tight stricture (typically leads to jaundice) - probably cholangiocarcinoma (cancer of bile duct)
-fairly rare
-typically distal bile duct
-or hepatic duct bifurcation - obstruction of the common hepatic duct choangiocarcinoma - dilated bile ducts

48
Q

Pancreatic cancer

A

a cancer in the head of the pancreas can cause narrowing of the common bile duct, obstructing flow
-tail don’t causes many symptoms

49
Q

Effect of prolonged bile duct obstruction (malignancy)

A

Gallstones typically acute presentation. quick jaundice onset and pain due to b d distention.
Cancer typically prolonged obstruction, therefore not much pain as degree of slow adaptation and stretching
1. (painless) Jaundice: Yellow discolouration of skin/sclera from excess bilirubin in blood
2. Itching: Probably from bile salts accumulation in skin
3. Nausea: Probably from bile salts (excessive)
4. Malabsorption of fat and fat-soluble vitamins (no/insufficent release of bile into GI tract. weight loss and steatorea)
5. Effects of renal perfusion
-Mechanism ? - can lead to renal failure

50
Q

Man with characteristic Pancreatic Malignancy

A

Yellow sclera
Skin scratch marks (severe itching)
Ecchymoses (bruising)- bruising tendency due to malabsorption of vit K (fat soluble vitamin)- for clotting factor production
Palpable gallbladder (gradual obstruction, allows gall bladder to compensate, tends to distend over time. unlikely to be related to benign (stones))-signs assoc. with malignancy
(Courvioser’s sign: enlarged gallbladder with jaundice - unlikely to be stones)
Pancreatic mass (epigastri region. hard)
Palpable lymph node in left supraclavicular fossa
-Virchow’s node: intra-abdominal malignancy
Pale stools (not by itself a sign of malignancy. but often long history of pale stools and steatorea

51
Q

Treatment of malignancy/ strictures in patients with inoperable cancers

A

Alot of cancers present as inoperable due to late presentation

  • Plastic Biliary Stent in Papilla
  • Tube which opens up stricture in pancreatic or common bile duct
  • pokes just out of ampulla
  • internal part lies along common bile duct to keep stricture patent and allow bile to flow through

Digestive System Module (38 decks)

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