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P2 - Gastrointestinal system > Pancreas, small intestine, iron metabolism and hepatitis > Flashcards

Pancreas, small intestine, iron metabolism and hepatitis Flashcards

1
Q

What are the 2 forms of cellular iron storage

A

Ferriting and Haemosiderin

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2
Q

What are the properties of ferritin?

A

Soluble, stores iron, but readily available from reticuloendothelial system, small amounts in serum used to test overall iron stores

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3
Q

What is haemosiderin?

A

Insoluble conglomerates of ferritin, iron is only slowly available

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4
Q

In what condition does serum ferritin decrease?

A

Iron deficiency anemia

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5
Q

When does serum ferritin increases?

A

In iron overload, and in tissue inflammation as it is acute phase protein

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6
Q

What protein transfers iron in plasma?

A

Transferrin (Tf)

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7
Q

What type of protein is transferrin?

A

Glycoprotein with 2 iron binding domains, shaped as Y

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8
Q

Where is transferrin synthesized?

A

In hepatocytes

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9
Q

What is the normal saturation of transferrin with Fe and how is its concentration controlled?

A

30% saturated with Fe3+, if iron decreases levels of Tf increase and vice versa

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10
Q

What is the body content of iron?

A

4 mg

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11
Q

What is the daily iron need and what is the intake on Western diet?

A

Daily iron need is 1 - 2 mg/d and in Western diet the intake is 15 - 20 mg/d

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12
Q

How much iron is lost per day during menstruation?

A

1 - 2 mg/d

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13
Q

How does the iron end up stored in RES?

A

Iron is absorbed and bound to Tf, then used in Myoglobin enzymes and absorbed into RBCs from which it is stored in the RES

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14
Q

How are the bodily levels of iron controlled?

A

By absorption as there is no excretory mechanism

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15
Q

What types of iron exist and in which foods it can be found?

A

Haem iron - red meat; Non-haem iron - white meat, green vegetables, cereals

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16
Q

Where is iron absorbed in the GI?

A

Predominantly in duodenum

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17
Q

What cells absorb iron?

A

Duodenal enterocytes

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18
Q

How is Haem transported absorbed into the enterocyte?

A

Diffuses into the cell and is broken down by Haem oxygenase into Fe2+, biliverdin and CO2 and moves into the labile iron pool in the cell

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19
Q

How is non-haem iron absorbed into the enterocyte?

A

Released from food and must be reduced from the ferric acid to ferrous (Fe2+) by duodenal cytochrome b1 (dCytb1), influenced by Vit C; Fe2+ is than transported by divalent metal transporter 1 (DMT1) and then taken into the labile iron pool

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20
Q

What happens to Fe2+ inside the duodenal enterocyte?

A

Either binds to Ferritin, moves to mitochondria or is transported out by Ferroportin and Hepcidin

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21
Q

What is Ferroportin?

A

A transmembrane protein releasing Fe2+ out of the cell during absorption but also from its store in macrophages

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22
Q

What is Hepcidin?

A

Protein which inhibits iron transport by binding to ferroportin, resulting in breakdown of the transporter - the interaction is the most important regulator of GI iron absorption

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23
Q

What happens to Fe2+ as it is released from the enterocyte?

A

Oxidized into Fe3+ and binds to Transferrin

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24
Q

How is iron stored in RES?

A

RES macrophages get iron from effete RBCs, store iron as ferritin or haemosiderin and release it by controlled Ferroportin and Hepcidin

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25
Q

How much iron does RES store?

A

500 mg of iron

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26
Q

How is Tf-iron taken up into cells and into which ones?

A

Taken up via Tf receptors on erythroblasts, hepatocytes and others

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27
Q

Where is transferrin synthesised?

A

In the liver

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28
Q

What is the total amount of iron transported per day?

A

Up to 50 mg of iron can be transported, although only 4 mg can be bound to Tf at any one time

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29
Q

What produces Haem in the erythroblast?

A

Mitochondria, first step in the pathway is mediated by ALA-S2

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30
Q

What are the properties of Haem

A

Able to reversibly bind O2 without undergoing oxidization or reduction

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31
Q

Describe iron metabolism regulation by Hepcidin

A

‘Low iron’ hormone - reduces levels of iron in plasma by binding ferroportin and thus reducing iron absorption and iron release by macrophages

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32
Q

Where is Hepcidin synthesised

A

In the liver

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33
Q

What are the results of Hepcidin loss?

A

Increased GI absorption, increased RES iron release, increased TF% saturation and parenchymal iron overload

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34
Q

What is parenchyma?

A

The functional tissue of an organ as distinguished from the connective and supporting tissue

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35
Q

What is the most likely cause of iron deficiency anaemia in males and post-menopausal women?

A

GI blood loss

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36
Q

What is the most likely cause of iron deficiency anaemia in young women?

A

Menstrual blood loss or pregnancy

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37
Q

What is celiac disease and how does it affect iron absorption?

A

Blunting of villi, villus atrophy, enlarged hyperplastic crypts and increased infiltration of lymphoid cells in the lamina propria and epithelium, results in abnormal absorption

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38
Q

What are the haematinic deficiencies in Coeliac disease in order from the most to least likely

A

Folate deficiency, iron deficiency, vitamin B12 deficiency

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39
Q

What is Sideroblastic anaemia

A

Erythroblasts take in iron but do not change it into haem, mitochondria become paralysed around the nucleus

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40
Q

What is Hereditary Haemochromatosis

A

An autosomal recessive disorder of iron metabolism causing iron overload

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41
Q

What are the causes of Hereditary Haemochromatosis

A

Abnormalities of the HFE gene, most commonly homozygous C282Y mutation of the HFE gene

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42
Q

What is the relationship between HFE mutation and HH?

A

Reduce hepsidin production and thus Tf can become 100% saturated while there is free serum iron

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43
Q

What are the laboratory findings in Hereditary haemochromatosis?

A

Increased Transferrin saturation, increased iron and increased Ferritin

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44
Q

What are the consequences of Hereditary haemochromatosis?

A

Fibrosis/cirrhosis of the liver, diabetes, arthritis, cardiomyopathy, skin bronzing

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45
Q

What is the treatment of Hereditary Haemochromatosis?

A

Venesection weekly, than at increased periods; monitoring ferritin and transferrin saturation

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46
Q

What is the estimated total body iron in somebody with HH?

A

20 mg or more

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47
Q

Define acute hepatitis

A

Inflammation of the liver,

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48
Q

What would be the clinical findings in acute hepatitis, including LFTS

A

Raised ALT and AST, jaundice and clotting derangement

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49
Q

What are the causes of acute hepatitis?

A

Infections: Hep A, B, C, D, E, Malaria, Syphilis

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50
Q

Define chronic hepatitis

A

Hepatitis virus present for more than 6 months, variable changes in liver function

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51
Q

Outline characteristics of hepatitis A

A

RNA virus, survives for months in contaminated water, virus is shed via billiary tree into gut, no chronic carriage and good immunity after infection

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52
Q

How is hepatitis A virus transmitted?

A

Faeco-oral transmission, contaminated water and food, person-person, humans only reservoir

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53
Q

How is hepatitis A diagnosed?

A

Test blood and stool for IgM or RNA; deranged liver function tests

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54
Q

What is the incubation period of hepatitis A?

A

30 days

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55
Q

What are the symptoms of hepatitis A?

A

Fever, abdominal pain, diarrhea, jaundice, itch, muscle pains

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56
Q

What is the severity of hepatitis A and what are its determinants?

A

Self-limiting illness, age is main determinant of severity - symptoms and mortality rate increases with age, low mortality overall

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57
Q

What is the treatment for hepatitis A?

A

No specific treatment, maintain hydration and avoid alcohol

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58
Q

Outline the hepatitis A vaccine

A

Inactivated virus, 95% efficacy, protection for 4 weeks after 1st dose, 2nd dose gives life protection

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59
Q

To whom is hepatitis A vaccine given?

A

Pre-exposure - travellers, homosexual men, chronic liver disease patients, IVDU
Post exposure - outbreak control

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60
Q

What is hepatitis A immune globulin?

A

Pooled immunoglobulin giving 3-6 months immunity, given pre-exposure if allergic to vaccine, <4 weeks till travel, or to control outbreak

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61
Q

Describe features of hepatitis E

A

RNA virus with 4 genotypes, more common than Hep A

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62
Q

What is the incubation period of Hep E?

A

40 days

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63
Q

How is Hep E transmitted?

A

Faeco-oral, pork products, minimal person to person transmission

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64
Q

What does Hep A virus look like?

A

Closely packed colony of rounded viruses

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65
Q

What does Hep E virus look like?

A

Loosely packed rounded viruses

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66
Q

What are the symptoms of Hep E?

A

Similar to Hep A plus rare reports of neurological effects

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67
Q

What is the fatality rate of Hep E?

A

1-3%, higher in pregnant women

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68
Q

What is the treatment for Hep E?

A

Supportive, no vaccine

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69
Q

What are the neurological manifestations of Hep E?

A

Guillaine Barre syndrome, encephalitis, ataxia, myopathy

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70
Q

Define encephalitis

A

Inflammation and swelling of brain

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71
Q

Define ataxia

A

A neurological sign consisting of lack of voluntary coordination of muscle movements that includes gait abnormality

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72
Q

Define myopathy

A

A disease of the muscle in which the muscle fibers do not function properly. This results in muscular weakness.

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73
Q

Define Guillaine Barre syndrome

A

A rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system

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74
Q

What is the type causing Hep B?

A

Hepadnavirus - DNA virus

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75
Q

What is the estimated number of people that die due to Hep B

A

2 million deaths per year

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76
Q

What are the consequences of Hep B?

A

Chronic liver inflammation, as the virus constantly replicates it causes liver cirrhosis and failure, upper GI haemorrhages, hepatoma - hepatic cancer

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77
Q

What does Hep B virus looks like?

A

Rod like shaped single viruses

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78
Q

How is Hep B transmitted?

A

By blood (transfusion, transplants, contaminated needles. mother to baby), by bodily fluids (sexual intercourse)

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79
Q

What is the incubation period of Hep B?

A

2-6 months

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80
Q

What are the symptoms of Hep B?

A

Fever, fatigue, jaundice, myalgia, joint pains

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81
Q

What role does age play in Hep B?

A

Determines severity of illness and risk of chronic infection

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82
Q

What is the common outcome if a newborn or young child compared to adult is infected with Hep B?

A

Usually asymptomatic, but this leads to chronic infection, adults are symptomatic but can clear the infection

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83
Q

What are the complications of Hep B?

A

Weight loss, abdo pain, fever, cachexia, bloody ascites, enlarged liver

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84
Q

What are the problems in chronic Hep B?

A

Development of chronic liver disease in 25%, cirrhosis, decompensation, Hepatocellular carcinoma, death

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85
Q

What is the natural course of Hep B infection?

A

After infection HBeAG positive and period of immune tolerance, than ALT increases and HBv DNA decreases this process is associated with liver inflammation and fibrosis - immune clearance, then low replicative state and lastly reactivation, HBeAg negative and further liver damage

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86
Q

How many people with chronic Hep B will be identified by sAg?

A

more than 6/12

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87
Q

What are the 2 groups that Hep B carrier are divided into?

A

eAg +ve (early disease) and eAG -ne (late disease)

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88
Q

What are characteristics of eAg +ve Hep B patients?

A

High viral load, high risk of chronic liver damage and HCC, highly infectious

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89
Q

What are characteristics of eAg -ve Hep B patients?

A

Low viral load, lower risk of CLD and HCC, less infectious

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90
Q

What is the treatment for acute Hep B?

A

No treatment

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91
Q

What is the treatment for chronic Hep B?

A

Treat those with liver inflammation, aim is to suppress viral replication, some with clear sAg spontaneously

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92
Q

What are the 2 types of therapy for chronic Hep B?

A

Immunological and antiviral drugs

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93
Q

Describe the immunological treatment of chronic Hep B

A

Pegylated interferon alpha - increased cellular immune response, lots of side-effects

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94
Q

Describe the antiviral drugs in treatment of chronic Hep B

A

Suppress viral replication

Tenofovir and Entecavir

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95
Q

How is hep B prevented?

A

Education, screening of pregnant women and doctors, immunisation, protect blood supply and hospital supplies

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96
Q

Describe basic characteristics of Hep D

A

ssRNA virus, requires HBV to replicate so need to either catch them at the same time or already be infected with D

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97
Q

How is Hep D transmitted?

A

Same as for Hep B - bodily fluids

98
Q

How is Hep D treated?

A

Peg IFN

99
Q

What does Hep D virus looks like?

A

Rounded single compartments, RNA with protein coat

100
Q

Outline Hep C

A

ss RNA virus, multiple genotypes, no vaccine and no reliable immunity after infection

101
Q

How is Hep C transmitted?

A

Injecting drugs, transfusion and transplant, sexual and vertical transmission is rare

102
Q

What is the incubation period of Hep C?

A

6 - 7 weeks

103
Q

How many patients with acute Hep C will be symptomatic?

A

25%

104
Q

How many patients infected with Hep C will develop chronic infection?

A

70%

105
Q

How many percent of patients with Hep C will develop cirrhosis or hepatocellular carcinoma?

A

25% cirrhosis, up to 5% HCC

106
Q

How is Hep C diagnosed?

A

By screening of high risk groups, anti HCV IgG positive = chronic infection or cleared infection, PCR or antigen positive = current infection/viraemia

107
Q

How is Hep C treated?

A

Pegylated interferon alpha and ribavarin; direct acting antiviral (stop replication and assembly of virus, 95% success rate)

108
Q

What is sAg and what it signify?

A

Surface antigen - marker of infection, if positive then now infected

109
Q

What is sAb and what it signify?

A

Surface antibody - marker of immunity, cleared but have antibody, or vaccinated

110
Q

What is cAB and what does it signify?

A

Core antibody - either have the infection or had it in the past

111
Q

What is eAg and what does it signify?

A

E antigen - suggests high infectivity, how far into the infection a patient is, more antigen, more infected

112
Q

What is eAb and what does it signify?

A

E antibody - suggests low infectivity, more antibody less infected

113
Q

When is HBV infection diagnosed?

A

If sAg or DNA are detectable

114
Q

Where is pancreas located?

A

Posterior to stomach, extending from duodenum to spleen

115
Q

What parts of pancreas are peritoneal?

A

The tail of pancreas, rest is retroperitoneal

116
Q

Where does the head of pancreas lies?

A

Within the C shaped space created by duodenum

117
Q

What is uncinate process and where does it lie?

A

Projection from the lower part of the head of pancreas, passes posterior to the superior mesenteric vessels

118
Q

Where does neck of pancreas lie in relation to the superior mesenteric vessels?

A

Anteriorly

119
Q

What are the parts of the pancreas?

A

Uncinate process, head, neck, body and tail

120
Q

Where does the tail of pancreas lie?

A

Between layers of the splenorenal ligament

121
Q

What is the covering of pancreas?

A

Thin collagenous capsule which extends as a delicate septa between lobules; contains vasculature, lymphatic vessels, nerves and excretory ducts

122
Q

Describe the course of the pancreatic duct

A

Begins in the tail, enters the head and turns inferiorly, in the lower part of the head joins the bile duct and forms the hepatopancreatic ampulla (ampulla of Vater) which enters the duodenum at the major duodenal papilla

123
Q

Where does the Accessory pancreatic duct empty?

A

At the Lesser duodenal papilla

124
Q

What is the blood supply of pancreas?

A

Gastroduodenal artery, anterior and posterior superior pancreaticoduodenal artery, dorsal pancreatic artery, anterior and posterior inferior pancreaticoduodenal artery

125
Q

Which arteries that supply the pancreas have common origin in Celiac trunk?

A

Gastroduodenal which gives rise also to ant.+post. superior pancreaticoduodenal arteries, dorsal pancreatic artery and great pancreatic artery

126
Q

Which artery supplying the pancreas originates in the superior mesenteric artery?

A

Anterior and posterior inferior pancreaticoduodenal artery

127
Q

Which vein drains the pancreas?

A

Splenic vein

128
Q

What nerves supply the pancreas?

A

Vagus nerve and thoracic splanchnic nerve fibres from the superior mesenteric and celiac plexuses

129
Q

Name the 2 functional components of the pancreas

A

Exocrine and endocrine components

130
Q

Outline the structure of the exocrine component

A

Closely packed secretory acini that drain into a highly branched duct system

131
Q

How is the stucture of exocrine component of the pancreas suported?

A

By interlobular ducts and their supporting tissue

132
Q

What is each acinus made up of?

A

An irregular cluster of pyramid shaped secretory cells

133
Q

Describe the coure of exocrine ducts

A

Begins as a central lumen surrounded by accinus, this continues as intercalated ducts which drain into intralobular ducts and then interlobular ducts in the septa of the gland

134
Q

What epithelium can found in the pancreatic ducts of the exocrine component?

A

Simple cuboidal epithelium which becomes stratified cuboidal epithelium in the larger ducts

135
Q

Is the acinar vascular system connected with the endocrine system?

A

No, it is independet

136
Q

Describe acinar cells

A

Typical protein secreting cells, triangular shape with apices projected into the central lumen, have loads of rough ER and eosinophilic secretory vesicles, produce zymogen granules which are released by exocytosis

137
Q

Describe centroacinar cells

A

Pale nuclei, terminal lining cells of intercalated ducts, secrete water, Na+ and bicarbonate ions

138
Q

What maintains the secretion of bicarbonate by the centroacinar cells?

A

Cystic fibrosis transmembrane conductance regulator that also provides Cl-

139
Q

What are the cells of the exocrine component of pancreas?

A

Acinar cells, Centroacinar cells, goblet cells, enteroendocrine cells, myoepithelial cells and serous cells

140
Q

Describe the endocrine component of the pancreas

A

Composed of Islets of Langerhans and Insuloacinar portal system; mainly to regulate glucose metabolism

141
Q

Describe the insuloacinar system of the endocrine component of the pancreas

A

Each islet is supplied by different arteriole forming a capillary network, leaving venules supply blood to the acini and thus locally control the exocrine component

142
Q

How much volume has each component of the pancreas?

A

Endocrine - 2% and exorcine 98%

143
Q

Name the beginning and end point of the small intestine

A

Pyloric orifice and ileocecal fold

144
Q

How long is the small intestine?

A

3 - 7 m

145
Q

How long is the duodenum?

A

26 cm

146
Q

How long is the jejunum?

A

3.5 m

147
Q

How long is the Ileum

A

1.5 m

148
Q

How does the diameter changes across the small intestine?

A

Narrows

149
Q

What is the shape of duodenum?

A

C-shaped

150
Q

Where is duodenum located?

A

Above the level of umbilicus, retroperitoneal

151
Q

By which ligament is the duodenum connected to the liver?

A

Hepatoduodenal ligament

152
Q

How is the duodenum divided and what vertebral level are they on?

A

Superior - L1, descending - L3, inferior - L3 and ascending - L2 part; also D1 to D4

153
Q

Describe the superior part of the duodenum

A

From pyloric orifice to the neck of the gallbladder, passes anteriorly to the bile duct, gastroduodenal artery, portal vein and inferior vena cava, common place for duodenal ulcer

154
Q

Describe the descending part of duodenum

A

From the neck of the gallbladder to the lower border of the vertebra L3, anterior surface is crossed by the transverse colon, contains the major and minor duodenal papilla

155
Q

Where is the junction of midgut and foregut?

A

Below the major duodenal papilla

156
Q

Describe the inferior part of the duodenum

A

Longest, crosses the inferior vena cava, the aorta and the vertebral column, crossed anteriorly by the mesenteric vessels

157
Q

Describe the ascending part of the duodenum

A

Goes up and terminates at the duodenojejunal flexure, passes to the left of aorta

158
Q

Describe the duodenojejunal flexure

A

Surrounded by a fold of peritoneum containing muscle fibres called suspensory muscle ligament of duodenum

159
Q

Name the arteries that supply duodenum

A

Branches from the gastroduodenal artery:
supraduodenal artery;

duodenal branches of ant, and post. superior pancreaticoduodenal a.,

duodenal branches of the ant. and post. inferior pancreaticoduodenal a.,

first jejunal branch from the superior mesenteric artery

160
Q

What are the characteristics of jejunum?

A

Larger and thicker walls then ileum, prominent folds that circle the lumen = plicae circulates; less promiment arterial arcades and longer vasa recta

161
Q

Where is jejunum located?

A

In the left upper quadrant - left hypochondrium

162
Q

What is the blood supply of jejunum?

A

Jejunal arteries - from superior mesenteric artery

163
Q

Where is Ileum located?

A

In the right iliac region

164
Q

What are the characteristics of ileum

A

Thinner walls, fewer less prominent plicae circulares, shorter vasa recta, more mesenteric fat and arterial arcades, Peyer’s patches

165
Q

Where does the ileum open to?

A

To the large intestine where cecum and ascending colon join together

166
Q

Describe the ileocecal folds

A

Surround the iliac opening, 2 flaps projecting into the lumen, come together at the ends to form ridges, musculature continues into the flap to make a sphincter, controls reflux and regulates passage into the cecum

167
Q

Describe the blood supply of ileum

A

Ileal arteries from the superior mesenteric artery, ileal branch from the ileocolic artery

168
Q

Describe the microstructure of small intestine

A

Mucosa and submucosa are arranged into plicae circulares/valves of Kerckring, mucosal surface is made up of villi and the surface of columnar enterocytesis covered with microvilli

169
Q

Where does the muscularis mucosae lie in the small intestine?

A

Beneath the mucosal crytps, separating mucosa from submucosa

170
Q

How is the muscle organised within the muscularis of the small intestine?

A

Inner circular layer and outer longitudinal layer

171
Q

What covers the peritoneal aspect of the muscularis of small intestine?

A

Loose collagenous serosa which is lined by mesothelium

172
Q

What are Peyer’s patches and where they are found?

A

Lymphoid aggregations within the lamina propria, mostly in ileum

173
Q

What are Brunner’s glands and where they are found?

A

Occupy entire submucosa and some in lamina propria mainly in duodenum, secrete alkaline mucins into the lumen of the small into the base of mucosal crypts

174
Q

What is the epithelium of the small intestine

A

Villi lined by simple columnar epithelium continuous with the epithelium of the crypts

175
Q

What are the cell types found in the small intestine?

A

Enterocytes, goblet cells, paneth cells, neuroendorine cells, stem cells, Intraepithelial lymphocytes, plasma cells

176
Q

Describe enterocytes of the small intestine

A

Tall columnar cells, most numerous and main absorptive cells, have surface microvilli making up the brush border, contain large no of free ribosomes and mitochondria; 3-5 days lifespan

177
Q

Describe the goblet cells within the small intestine

A

Scattered among enterocytes, produce mucins for lubrication and protection, 3-5 days lifespan

178
Q

Describe the Paneth cells of the small intestine

A

At the base of the crypts, distinguished by their prominent eosinophilic apical granules, defensive function, contain antimicrobial peptides and protective enzymes like lysozyme and phospholipase A, weeks life span

179
Q

Describe the neuroendocrine cells of the small intestine

A

Produce locally acting hormones that regulate gastrointestinal motility and secretion, different type for different hormone: secretin, somatostatin, serotonin

180
Q

Describe the stem cells of the small intestine

A

At the base of the crypts, can differentiate into all of the cell types

181
Q

Describe the intraepithelial lymphocytes of the small intestine

A

Mostly T cells, defense against invasive organisms

182
Q

Describe the plasma cells of the small intestine

A

In the villous core, secrete IgA into the intestinal lumen by transcytosis

183
Q

What is transcytosis?

A

Endocytosis with transfer to the extracellular fluid at the base of the cell

184
Q

What is contained within the lamina propria of the small intestine

A

At core of each villus, contains rich vascular and lymphatic network - lacteal

185
Q

What covers the surface of the microvilli?

A

Thick glycocalyx to aid absorption of pancreatic digestine enzymes and mucous layer

186
Q

What type of cytoskeleton supports the microvilli?

A

Microfilament cytoskeleton

187
Q

What is the basal lamina densa of an enterocyte like?

A

Discontinuous

188
Q

What is found in the crypts of Lieberkuhn?

A

Mostly stem cells

189
Q

What is the function of endocrine pancreas?

A

To secrete glucagon, insulin, somatostatin and pancreatic polypeptide

190
Q

Name and describe the cells that produce glucagon

A

Alpha cells, 20% of each islet; low blood glucose stimulates release of glucagon

191
Q

What cells produce insulin and what percentage of the islet do they make?

A

Beta cells, 75%

192
Q

Describe characteristics of delta cells

A

4% of the islet, secrete somatostatin (also released by hypothalamus, stomach and intestine)

193
Q

What is the role of somatostatin?

A

Inhibiting hormone - pancreatic somatostatin inhibits the release of both glucagon and insulin

194
Q

Describe the characteristics of a PP cell

A

1% of islet cells, secretes pancreatic polypeptide hormone, role in appetite and regulation of pancreatic secretions

195
Q

Describe the secretion s of acinar pancreatic cells

A

Secrete the inactive forms of the enzymes trypsin, chymotrypsin and carboxylpeptidases; active amylase, lipase, cholesterol esterase and phospholipase; trypsin inhibitor

196
Q

What does the epithelial cells of the intercalated duct secrete?

A

Water and bicarbonate

197
Q

What is a zymogen?

A

Inactive version of an enzyme

198
Q

What triggers release of pancreatic enzymes?

A

Vagal stimulation (Ach release onto the acinar cells), Acidic gastric chyme which stimulates release of secreting and cholecystokinin - these then act on acinar cells and intercalated duct cells

199
Q

What stimulates the pancreas to release bicarbonate ions and water?

A

Secretin

200
Q

Name the enzymes that aid digestion of carbohydrates

A

Pancreatic and salivary amylase, lactase, sucrase, maltase, alpha-dextrinase

201
Q

What is the role of pancreatic amylase

A

More powerful than salivary amylase, converts all carbohydrates to maltose and/or other small glucose polymers within 15 to 30 minutes

202
Q

What are the common features of the intestinal epithelial enzymes?

A

Hydrolysis of disaccharides and polymers to monosaccharides, on the microvilli of enterocytes make up the brush border

203
Q

What are the properties of lactase?

A

Splits lactose into glucose and galactose

204
Q

What are the properties of sucrase?

A

Splits sucrose into fructose and glucose

205
Q

What are the properties of maltase?

A

Splits maltose and glucose polymers to glucose

206
Q

What are the properties of alpha-dextrinase?

A

Splits maltose and glucose polymers into glucose

207
Q

How are glucose and galactose absorbed into the portal blood?

A

By sodium co-transport mechanism; Na+ is actively transported out of the enterocyte to blood which depletes the enterocyte of Na+ and the cell activates the secondary active transport, Na+ combines with transport protein at the lumen and once it also combines with glucose it is transported into the enterocyte, facilitated diffusion gets glucose from the cell to blood

208
Q

How is fructose absorbed into the portal blood?

A

By facilitated diffusion and after entering the cell becomes phosphorylated and converted to glucose

209
Q

Where does digestion of proteins occur?

A

Mostly in duodenum and jejunum, but begins in the stomach

210
Q

What are the major pancreatic proteolytic enzymes?

A

Trypsin, chymotripsin, carboxypolypeptidase, elastase

211
Q

What is the role of peptidases?

A

Aminopolypeptidases and dipeptidases on the brush border broke proteins further down

212
Q

Describe the absorption of protein in the small intestine

A

Only aa, di and tripeptides are transported by sodium co-transporter, some amino acids are transported by faciliated diffusion

213
Q

How do proteins move from enterocyte to blood?

A

Have to be broken down by specific peptidases into amino acids which than diffuse into the blood stream

214
Q

Outline the digestion of fats in the small intestine

A

Emulsification by bile acids and lecithin, triglyceride digestion by pancreatic and enteric lipase, micelles formation by bile salts

215
Q

What are the enzymes that digest cholesterol and phospholipids?

A

Cholester ester hydrolase, phospholipase A2

216
Q

How are fats absorbed?

A

Micelles move to the brush border where they dissolve and its components dissolve across the plasma membrane, inside the cell the lipids are taken up by smooth endoplasmic reticulum and converted to new triglycerides, released as chylomicrons

217
Q

How is water absorbed?

A

By osmosis between tight junctions and through the cells and creates flow of fluid

218
Q

How is sodium absorbed in the small intestine?

A

By active transport (sodium-glucose co-transporter, sodium-amino acid co-transporter, sodium-hydrogen exchanger), then actively exported out of the cell, chloride ions are passively drag with sodium

219
Q

What is aldosterone enhancement in the small intestine?

A

In response to dehydration released, acts to enhance enzymes and transporters to increase absorption of sodium, and thus also water and minerals

220
Q

What are the 2 ways by which chloride ions can be absorbed?

A

Diffusion with Na+ and by membrane chloride-bicarbonate exchanger, exits the cell through chloride channels

221
Q

How is bicarbonate absorbed in the small intestine?

A

Bicarbonate combines with H+ to form carbonic acid and then H20 and CO2, CO2 diffuses into the cell and into the blood, CO2 from blood is taken back in and converted to H+ and HCO3-

222
Q

How are potassium, magnesium and phosphate absorbed?

A

Active transport, easier for monovalent than bivalent ions

223
Q

How is calcium absorbed?

A

By Calcium-stimulated ATPase and Calcium-binding protein (calbindin) - controlled by PTH and vit D

224
Q

List at least 5 causes of chronic pancreatitis

A

Alcohol, Chronic kidney disease, recurrent acute pancreatitis, hypercalcaemia, autoimmune, obstructive, tropical, hereditary: cystic fibrosis, trypsinogen and inhibitory protein defects

225
Q

What type of pain is typical in chronic pancreatitis?

A

Epigastric pain radiating towards the back, episodic pattern, short periods of severe pain or chronic pain, increased after alcohol or fatty meal consumption

226
Q

What are the signs and symptoms of chronic pancreatitis?

A

Pain, anorexia, weight loss, diabetes, exocrine insufficiency, jaundice

227
Q

Define chronic pancreatitis

A

Long standing inflammation of the pancrea

228
Q

List the initial investigations for chronic pancreatitis

A

Transabdominal ultrasound

229
Q

List the further assessments for chronic pancreatits

A 
Contrast-enhanced CT scanning (can see pancreatic calcification and dilated ducts)
MRI with MRCP
Serum amylase and lipase
Serum IgM levels
Faecal elastase
Gene mutation analysis
Endoscopic ultrasound
230
Q

Describe the pathogenesis of chronic pancreatitis

A

Increase in activated trypsin within the pancreas, this leads to precipitation of proteins and plug formation; the plug is a nidus for calcification and causes ductal obstruction; leading to ductal hypertension and further damage

231
Q

What are the 2 possible ways of increase in activated trypsin in pancreas during chronic pancreatitis?

A
  1. increased/premature activation of trypsinogen to trypsin

2. impaired inactivation/clearance of the activated enzyme from the pancreas

232
Q

What are the main histological changes in chronic pancreatitis?

A

Loss of acini and replacement by fibrosis, Islets of Langerhans may or may not be destroyed

233
Q

Name genes that can be related to chronic pancreatitis

A 
PRS1 gene (encodes trypsinogen)
Calcium-sensing receptor (role in trypsinogen activation, alcohol interaction)
SPINK-1 (serine protease inhibitor)
Cystic fibrosis transmembrane conductance regulator - CTFR (bicarbonate secretions which flush activated trypsin to duodenum)
234
Q

Describe type 1 autoimmune chronic pancreatitis

A

Middle-aged men, associated with raised serum and tissue levels of IgG4, may be independent from trypsin pathways; other organs involved: billiary tree, thyroid, salivary gland and renal tissues

235
Q

Describe type 2 autoimmune chronic pancreatitis

A

Early in mid-life, equal sex distribution, no autoimmune IgG4-positive cells, 30% of cases associated with inflammatory bowel disease

236
Q

Describe the management of chronic pancreatitis

A

No treatment mostly symptom management:
Abdominal pain - NSAIDs and an opiate (tramadol), tricyclic antidepressants (amitriptyline), pregabalin; extracorporeal shock wave lithotripsy to fragment stones

237
Q

What are the surgical treatments for chronic pancreatitis?

A

Duct drainage and partial resection of the pancreas

238
Q

How do you manage malabsorption in chronic pancreatitis?

A

Pancreatic enzyme supplements in the form of microspheres, plus and acid suppressor like H2 receptor antagonist of proton pump inhibitor

239
Q

How do you manage autoimmune chronic pancreatitis?

A

Glucocorticoid therapy and azathioprine for relapses

240
Q

How should the diet be modified in chronic pancreatitis?

A

Abstain from alcohol, smoking and greasy/fried foods; drink plenty of fluids and eat high vitamin low fat diet

P2 - Gastrointestinal system (5 decks)

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