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Semester 4 > Case 3 - The pancreas > Flashcards

Case 3 - The pancreas Flashcards

1
Q

What if the function of B5, B6 transporters

A
  • B5 - involved in calcium absorption in the kidney
  • B6 - involved in calcium absorption in the small intestine
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2
Q

What are the end products of polysaccharide digestion and where does it occur?

A
  • Polysaccharides are digested to:
    • Monosaccharides
  • Occurs in:
    • Saliva
    • pancreas
    • brush border
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3
Q

What causes pathological secretion of ions by the gut

A
  • Caused by E.coli and rotavirus
  • toxins produced by bacteria hijack nromal celullar processes
  • intestinal cells normally secrete H2O together with mucus and HCO3- (2L per day)
  • In cholera secretion exceeds 20 L per day
  • Some toxins also inhibit sodium absorption but not SGLT1 (oral rehydration therapy)
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4
Q

What are the water soluble vitamins

A
  • B group
  • C
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5
Q

What are the mechanical causes of acute pancreatitis?

A
  • Gall stones
  • trauma
  • latrogenic injury
    • operative injury
    • endoscopic procedures with dye injection
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6
Q

Explan how cholesterol is absorbed?

A
  • Occurs in the duodenum
  • receptor mediated endocytosis
  • Ezetimibe inhibits endocytosis = decreases plasma cholesterol
  • Nieman - Pick Cl-like (NPCIL1) PROTEIN
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7
Q

What ar ethe effects of alcohol abuse in the mouth/upper GI?

A
  • Increase incidence of cancer especially
    • tongue
    • buccal mucosa
    • gums
    • pharynx
    • upper oesophagus (cigarrettes and spirits)
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8
Q

How is iron absorbed into the cell?

A
  • Iron is transported through the DMT as ferrous (reduced form) Fe2+ at the same time as it transports protons (secondary active transport) leading to the accumulation of ferrous ions
  • Iron is absorbed as haem protein, haem is oxidised releasing iron in the form of ferric ions Fe2+which are reduced to ferrous ions, the remainder of the haem protein forms biliverdin a precursor of bilirubin
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9
Q

What does a decrease in SI surface area such as in Crohns or Coeliac lead to

A
  • Malabsorption
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10
Q

How does CCK control pancreatic secretion?

A
  • Stimulates secretion of enzyme component
  • produced by APUD cells in the duodenal mucosa in response to food constituents in the duodenal chyme
  • CCK and gastrin compete for the same receptors on acinar cells
  • CCK, gastrin and Ach all increase enzyme protein synthesis and secretion via increasing intracellular calcium and increase in phosphatidylinositol turnover
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11
Q

How is calcium absorped?

A
  • Calcium absorption can be paracellular or intracellular down a concentration gradient

Transcellular route

  • Calcium enters the cell via the apical using a channel TRPV6
  • In the cell cytoplasm it binds to the protein calbindin to prevent calcium acting as an intracellular signal
  • at the basolateral membrane calcium is removed by a calcium pump Ca2+ - ATPase in exchange for H+ antiporter

Paracellular route

  • Ca2+ travels down a concentration gradient through the tight functions of the cells
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12
Q

What is absorbed in the ileum?

A
  • Vitamin B12
  • Bile salts
  • Potassium
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13
Q

Explain the pathogenesisi of defective intracellular transport of proenzymes within acinar cells.

A
  • In normal acinar cells, digestive enzymes and lysosomal hydrolases are transported in separate pathways
  • In acinar injury they are transported to the same place leading to activation of proenzymes
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14
Q

What are the end products of protein digestion and where does it occur?

A
  • Proteins are digested to
    • Amino acids
    • dipeptides
    • tripeptides
  • Occurs in the:
    • stomach
    • pancreas
    • bursh border
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15
Q

What is chronic pancreatitis?

A
  • Prolonged inflammation of the pancreas,
  • irreversible destruction of exocrine parenchyma,
  • fibrosis in the later stages
  • destruction of endocrine parencyma
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16
Q

What are the mechanisms to preventthe pancreas from autodigestion from its own enzyme?

A
  • Enzymes secreted by the pancreas are inactive proenzymes packaged in zymogens which are secretory granules
  • The packaged proenzymes are activated by trypsin which is activated by duodenal enteropeptidase in the SI therefore intrapancreatic activation of proenzymes is minimal
  • acinar and ductal cells secrete trypsin inhibitors e.g. serine protease inhibitor Kazal type I (SPINKI) which limit intrapancreatic trypsina activity
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17
Q

Explain how short chain fatty acids?

give examples of SCFA

A
  • Butyrate, propionate, acetate
  • SCFA are not a major component of the diet, but produced by bacterial fermentaion in the colon
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18
Q

Explain how amino acids are absorbed from the lumen to isf.

A
  • 50% are absorbed by the co-transporter (symporter) Pep T1 as di and tripeptides with H+
  • Hydrolysed to amino acids in enterocytes
  • absorbed via secondary active transporter
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19
Q

How are triacyglcerides resynthesised?

A
  • Resynthesised in SER and packaged in chylomicrons
  • exocytosis of chylomicrons which are then transported in lymphatic to the liver
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20
Q

Which pancreatic enzymes are released as enzyme precursors?

A
  • Trypsin
  • Chymotrypsin
  • Carboxypeptidase
  • Elastase
  • Phospholipase A
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21
Q

What are the effects of alcohol abuse in the pancreas

A

acute and chronic pancreatitis

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22
Q

How does alcohol consumption lead to acute pancreatitis?

A
  • Alcohol activates all the methods that cause acute pancreatitis
  • it increases contraction of the sphincter of Oddi
  • Chronic consumption leads to production of protein rich pancreatic fluid causing obstruction of small pancreatic ducts
  • Leads to alcohol induced oxidative stress which may promote the fusion of zymogens and lysosomes and alter intracellular calcium levels due to mitochondrial damage
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23
Q

Name all the fat soluble vitamines

A
  • A
  • D
  • E
  • K
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24
Q

What are the common causes of pancreatic obstruction?

A
  • Gallstones
  • biliary sludge
  • periampullary neoplasms
  • choledochoceles
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25
Q

How does somatostatin control pancreatic secretion?

A
  • Inhibits
    • pancreatic secretion
    • release of exocrine enzyme
    • alkaline secretion
    • insulin
    • glucagon
    • CCK
    • secretin
    • gastrin
  • Release from D cells in iselts is stimulated by gastrin, cck, secretin release
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26
Q

Explain the intestinal phase of pancreatic secretion

A
  • Vhyme enters the proximal region of the SI and stimulates pancreatic secretion
  • Lipids and peptones timulate duodenal I cells - release CCCK - stimulate acinar cells - digestive enzyme release
  • Lipids and peptones activate vagovagal enteropancreatic reflex - stimultaes acinar cells
  • Gatric acid entering the duodenum and bile acids and lipids stimulate duodenal S cells to release secretin, stiumlating duct cells to secrete HCO3- and fluid
  • Duodenal pH must be 4.5 to activate S cell secretion
27
Q

What are the end products of triglycerides digestion and where does it occur?

A
  • tryglycerides are digested to form
    • Free fatty acids
    • monoglycerides
28
Q

Describe the secretion of enzymes and precursors?

A
  • Enzymes and precursosrs are synthesized in RER
  • Released into cisternae of endoplasmic reticulum
  • Buds continaing enzymes break of cisternae and form vacuoles in region of golgi
  • Vacuoles migrate to lminal membrane and exocytosis occurs
  • Same enzymes are packaged together in each xymogen granule and released together
  • Zymogen granule membrane is recycled from cell membrane
29
Q

Explain the process of fat digestion

A
  • Dependendent on bile salts
  • Bile is released due to sensinf fat in the duodenum
  • bile emulsifies fat - making large fat droplets smaller increasing the surface are for the action of pancreatic lipase
  • pancreatic lipases breaks down triacyglycerol to form monoacyglycerol and 2x free fatty acids these products are stabilised due to the formation of mixed micelles as they are transported to the apical membrane
30
Q

What are the effects of alcohol abuse in the stomach?

A
  • Peptic ulcers
  • acute gastritis
  • chronic peptic ulceration
  • portal gatropathy
31
Q

What is the function of the XAG- transporter?

A
  • Co transportert (Na+ and other)
  • glutamate
  • H+
  • K+ (extruded out the cell)
    *
32
Q

How are the fat soluble vitamins absorbed

A
  • Facilitated diffusion/endocytosis at physiological concentrations (low concentrations)
  • Require optimal fat digestion
  • deficiences with pancreatic and biliary disease
33
Q

What leads to diarrhoea?

A
  • Increase in osmotic load in the colon therefore water follows the osmotic load leading to increase in fluid in faeces
  • Osmotic load is causes by incmplete digestion and absorption of food
    • Lack of enzymes/transporters due to genetic causes or decrease of pancreas and biliary systems
    • damage to mucosal cells
      • autoimmune
      • infections
  • Osmotic load may be increased by secretions of ions by gut
34
Q

How many ml/g of ethanol are equvalent to one unit

A
  • 10ml
  • 8g
35
Q

Explain the pathogensis of primary acinar cell injury

A
  • Release of digestive enzymes causes inglammation and autodigestion
  • Leads to oxidative stress and the release of free radicals in acinar cells
  • leading to me,brane lipid oxidation that activates API and NF-KB inducing chemokines which induce other cells
  • Increase in calcium triggers activation of digestive enzymes and a decrease in calcium levles causes trypsin to cleave and inactivate itself
  • increase in calcium lebels result in activation of trypsin favoured therefore increase in calcium levels ina cinar may lead to excessive activation of trypsin
36
Q

What are the hereditary factors leading to acute pancreatitis

A
  • Characterised by recurrent attacks of sever acute pancreatitis often beginning in childhood ultimately leading to chronic pancreatitis. Defect increases or sustains trypsin activity
    • PRSSI: Dominat leads to trypsin resistant to self activation or more prone to activation
    • SPINK1: Recessive leads to inhibitor of trypsin therefore mutation leads to increase of trypsin activity
    • CFTR: Decresases bicarbonate secretion by pancreatic ductal cells, promoting plugging, duct obstruction and development of pancreatitis
37
Q

Explain the process of fat absorption.

A
  • Simple diffusion - limited with few free fatty acids in the undissociated state
  • FFA transporters such as CD36 and SCFA transporters are present in the colon
  • Monoacyglycerol transport is via carrier mediated mechanisms
38
Q

Which pancreatic enzymes are released as active enzymes?

A
  • Lipase
  • alpha amylase
  • ribonuclease
  • deoxyribonuclease
39
Q

What is the main site of absorption?

A

Duodenum and jejunum

40
Q

What is the function of a pept 1 transporter?

A
  • Co-transporter of:
    • H+
    • di/tri - peptide
41
Q

What causes a lack of enxymes and transporters

A
  • Congenital (neonate) = watery
    • glucose - galactose malabsorption (SGLT1)
    • lactase deficiency
  • Decrease of pancreas and biliary systems = steatorrhoea
    • pancreatitis
    • cystic fibrosis
    • hepatitis
    • gall stones
42
Q

Explain how H2O is absorbed?

A
  • H2O moves down an osmotic gradient which is created by absorption of nutrients
  • Route for H2O absorption:
    • Via junctional complexes between cells
    • via SGLT1 and amino acid transporters
    • not aquaporin channels
    • leaky tight junctions in the ileum but not in the stomach
43
Q

What does incomplete digestion lead to?

A

Malabsorption

44
Q

Which vitamin regulates calcium absorption?

A
  • Vitamin D
  • Vitamin D binds to intracellular receptors and triggers transcription of mRNA which codes for
    • TRPV6
    • PMCA
    • calbindin
45
Q

How are the water soluble vitamins absorbed?

A
  • Specific transporters (facilitated and secondary active transport)
  • B12 endocytosis
  • B12 requires intrinsic factor from parietal cells
46
Q

Explain how carbohydrates are absorbed from the lumen into the isf

A
  • on the basolateral membrane
    • Sodium x3 and potassium x2 antiporter which moves sodium out of the cell creating a gradient that drives sodium from the lumen into the cell
    • GLUT2 receptor trasports glucose out of the cell into the isf
  • On the apical memebrane
    • SGLT1 - transports sodium and glucose into the cell following the sodium gradient created by the sodium potassium antiporter
    • glucose is absorbed by facilitated diffusion by the GLUT5 when glucose accumulates it leads it to be removed from the cell via basal membrane
47
Q

What are the signs and symptoms of alcohol poisoning

A
  • Signs:
    • confusion
    • comiting
    • seizures
    • loss of coordination
    • irregular
    • slow breathing
    • blue tinged or pale skin
    • hypothermia (low body temp)
  • symptoms:
    • irregular slow breathing
    • stupor
    • unconscious but unresponsive
    • inhale vomit leading to fatal lung damage
    • severe dehydration may cause permanent brain damage
    • seizures are due to lowered blood sugar levels
48
Q

What are the infectious causes if the acute pancreatitis?

A
  • Mumps
49
Q

How does secretin control pancreatic secretion?

A
  • Released from the duodenal mucosa, stimulated by low pH of chyme from stomach
  • Stimulates secretion of alkaline aqueous component of the pancreatic juice secretion
  • secretin acts to increase cAMP intracellularly of ductal cells stimulating the chloride channel
  • the increase in cAMP potentiates the effect of CCK, gastin and Ach
50
Q

Explain the pathogenesis of pancreatic duct obstructtion.

A
  • Obstruction increases intrapancreatic ductal pressure and leads to accumulation of enzyme rich fluid in the interstitium
  • Pancreatic lipase is released in an active form therefore causes local fat necrosis
  • Death of adipocytes produces danger signals locally stimulating periacinar myofibroblasts and leukocytes to release pro inflammatory cytokines and other inflammtory mediators that initiate local inflammation and promote interstitial oedema through a leaky microvasculature
  • oedema compromises blood flow, causing vascular insufficiency and ischemic injury to acinar cells
51
Q

Describe the mechanism of pancreatic juice secretion from the acinus and duct cells?

A
52
Q

What causes damage to the mucosa?

A
  • Immune/autoimmune - coeliac, Crohn’s disease
  • infections (water and hygiene)
    • bacteria Shigella and campylobacter leads to destruction of intestinal wall leading to a decrease in surface area leads to blood in faeces (dysentry)
    • Bacteria salmonella leading to inflammation
    • Protozoa giardia, entamoeba
53
Q

Why is it important for the pancreatic juice to neutralise the acidic chyme from the stomach?

A
  • Pancreatic enzymes work at neutral and slightly alkaline pH for optimum action
  • Absorption of fat depends on formation in the intestinal lumen of micelles, a process which only takes place at neutral or slightly alkaline pH
  • Protection of the intestinal mucosa from excess acid which can damage it, leading to formation of micelles
54
Q

What are the effects of alcohol abuse in the oesophagus?

A
  • squamous carcinoma cancers
  • varicosities in lower oesophageal are prone to bleeding, gut bacteria will turn the blood into malena
55
Q

Describe the activation of enzyme precursors!

A
  • Trypisonegen is converted to trypsin its active proteolytic form by enterokinase which is presnet in the SI brush border
  • Once a small amount of activated tryspin has been formed it can catalyse the conversion of more trypsinigen to trypsin
  • Trypsin is a proteolytic enzyme that converts the following to their activated forms
    • chymotrypsinogen
    • procarboxylase peptidase
    • proelastase
    • phospholipase A
  • In acute pancreatitis activated enzymes are present in the pancreatic ducts leading to the destruction of the pancreatic tissue
56
Q

What are the genetic causes of acute pancreatitis?

A
  • Mutations in genes encoding
    • Trypsin
    • trypsin regulators
    • proteins that regulate calcium metabolism
57
Q

What are the clinical features of acute pancreatitis?

A
  • Pain is attributed to release of toxic enzymes, cytokines and other mediators into the circulation and explosive activation of a sysetmic inflammatory response
    • Abdominal pain - pain is constant(epigastrium) and intense and is referred to the upper back and occasionally to the left shoulder
    • Anorexia, nausea and vovmittingfrequently accompany the pain
    • elevated plasma levels of amylase and lipase support the diagnosis of acute pancreatitis
    • nausea and vomitting
    • circulatory colapse - tachycardia and poor peripheral perfusion
    • epigastric upper abdominal tenderness
    • bruising in the flank 1 - 2 days after intial presentation
58
Q

What are the metabolic causes of acute pancreatitis?

A
  • Alcoholism
  • Hypolipoproteinaemia
  • Hyperclacemia
  • Drugs
    • azathioprine
    • furosemide
    • oestrogens
59
Q

How is potassium absorbed in the SI?

A
  • Paracellular diffusion in the ileum
  • colon - predominantly secretion
60
Q

What is the function of a Bo transporter?

A
  • Co-transporter (Na+)
  • specific to alanine
61
Q

What are the vascular causes of acute pancreatitis?

A
  • Shock
  • atheroembolism
  • vasculitis
62
Q

What are the clinical features of chronic pancreatitis?

A
  • Repeated episodes of acute pancreatitis
  • Repeated attacks of mild to moderate sever abdominal pain or persistent abdominal and back pain
  • Attacks may be precipitated by alchol abuse, overeating (increases demands of the pancreas, use of opiates and other drugs that increase the tone of the sphincter of Oddi)
  • steatorrhoea - requires loss of 90% of pancreatic exocrine function
  • weight loss - due to reduced oral intake secondary to symptoms or related complications such as pancreatic exocrine insufficiency
63
Q

What is absorbed in the colon?

A
  • H20
  • Na
  • SCFA - short chain fatty acids

Semester 4 (15 decks)

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