GI Topic 3 - Small Intestine, Exocrine Pancreas, Pancreatitis Flashcards

1
Q

Where do pancreatic juices drain?

A
  • Pancreatic duct runs the full length of the pancreas, unites with the common bile duct to form the pancreatic ampulla of Vater
  • The ampulla opens into the 2nd part of the duodenum via the major duodenal papilla, controlled by the sphincter of Oddi
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2
Q

List the risk factors for chronic pancreatitis

A
  • Male
  • Middle aged
  • Afro-carribean
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3
Q

Describe the epidemiology of Haemachromatosis

A
  • Males affected more severely than females - lose iron through menstruation/pregnancy
  • Most prevelant in celtic (Northern Europe) population
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4
Q

Describe the functional adaptations of the walls of the duodenum

A
  • Submucosal Brunner’s glands - produce alkaline mucous in the crypts of Leiberkuhn to neutralise acidic chyme
  • Villi and microvilli increase the surface area for absorption
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5
Q

Describe movement of fluid in the jejunum and ileum

A
  • Enterocytes responsible for fluid movement - pump sodium into the intestinal lumen, water follows - aids digestion
    • Enterocytes are CFTR dependents and cAMP modulated
    • Cl-, Na+ and K+ move in, CFTR pumps Cl- out, Na+ follows
  • Water also moves by passive diffusion - there is increasing osmotic activity with advancing digestion
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6
Q

What is the normal daily iron requirement? Is this usually fulfilled?

A

1-2mg/day, western diet is 15-20mg/day

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7
Q

How are Ferroportin and Hepcidin involved in iron balance?

A
  • Ferroportin - transmembrane protein, essential for release of iron from macrophages
  • Hepcidin - responsible for iron homeostasis
    • Decreases GI absorption of iron, decreases RES release of iron - decreases iron levels
    • Binds to and degrades ferroportin
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8
Q

Describe the structure of the exocrine pancreas

A
  • Lobulated, serous gland
  • Composed of approx 1 milion clusters called acini, connected by short intercalated ducts (1 per lobe)
  • Intercalated ducts drain to intralobular collecting ducts which drain to the main pancreatic duct
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9
Q

Describe the parts of the duodenum

A

4 parts - superior/1st part, descending/2nd part, transverse/horizontal/3rd part, ascending/4th part

  • 1st part - intraperitoneal, level L1, attached to liver by hepatoduodenal ligament
  • 2nd - 4th - retroperitoneal
  • 2nd part has major duodenal papilla - bile and pancreatic secretions enter from ampulla of Vater
  • 3rd crosses vena cava and aorta, posterior to superior mesenteric artery and vein
  • 4th - joins jejunum at duodenojejunal flexure
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10
Q

Describe carbohydrate absorption in the jejunum and ileum

A
  • Carbohydrates broken down from polysaccharides to monosaccharides
    • Glucose and galactose - absorbed by active transport if concentration is low, facilitated transport if concentration is high
    • Fructose - limited absorption, co-absorption with glucose
    • Protein - amino acids absorbed by sodium-gradient facilitated diffusion, small amount of di/tripeptides by active transport
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11
Q

List the symptoms of chronic intestinal pseudo-obstruction

A

Abdominal pain, constipation, vomiting, weight loss

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12
Q

What are plicae circularis?

A

Folds circling the lumen of the jejunum - increase surface area

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13
Q

List the enzymes which contain iron

A
  • Cytochromes
  • Perioxidases
  • Xanthine oxidase
  • Catalases
  • RNA reductase
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14
Q

Describe the gross structure of the small intestine

A
  1. Duodenum
  2. Jejunum
  3. Ileum
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15
Q

What is the function of Gastrin?

A

Increases stomach motility and gastric acid/enzyme secretion

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16
Q

Describe the histological changes which occur in coeliac disease and the affect this has

A
  • Loss of villous height
  • Elongation of crypts of Leiberkuhn
  • Increased proinflammatory cells
  • Decreased surface area of intestine walls
  • Decreased absorptive capacity
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17
Q

List the endocrine secretions of the jejunum and ileum

A
  • VIP
  • GLP-1 and 2
  • GHRF
  • Neuropeptide Y
  • Peptide YY
  • Substance P
  • Bombesin
  • Serotonin (from enterochromaffin cells)
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18
Q

What are arcades?

A

Arterial loops of the small intestines

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19
Q

Compare sources of haem and non-haem iron

A

Haem iron - red meat

Non-haem iron - white meat, green vegetables, cereals

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20
Q

Compare normal RBCs to anaemic RBCs

A
  • Normal - healthy outer rim of haemoglobin, paler in the middle
  • Anaemic - paler (hypochromic), smaller (microcytic), pencil-like
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21
Q

Describe small intestinal motility when fasting

A

Migrating motor complex

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22
Q

Describe the dietary changes which are made in the management of chronic pancreatitis

A
  • Low fat, high protein, high calorie diet
  • Fat soluble vitamin supplementation
  • Pancreatic enzyme supplementation for steatorrhoea or poor nutritional status
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23
Q

How does the pancreas produce bicarbonate?

A

Secreted by centracinar cells and the epithelial lining of intercalated ducts, supply maintained by cystic fibrosis transmembrane conductance regulator (CFTR)

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24
Q

Describe the gross structure of the pancreas

A

Head, neck, body and tail

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25
Q

Describe the iron content of the body

A
  • Total body = 4g
    • RBC = 3g
    • Reticuloendothelial system = 200-500mg
    • Myoglobin = 200-300mg
    • Enzymes = 100mg
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26
Q

What are the consequences of iron overload in haemochromatosis?

A

Extra 20g of iron - distributed to other tissues:

  • Liver - causes cirrhosis, nodules and fibrosis
  • Pancreas - causes diabetes
  • Skin - causes bronzing
  • Joints - causes arthritis, especially of metacarpophalangeal joint of middle finger
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27
Q

Where is the spleen in relation to the pancreas?

A

Hilum of the spleen sits on the tail of the pancreas

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28
Q

Describe the risk of infection associated with coeliac disease

A
  • Increased risk of infection from encapsulated organisms
    • Pneumoccocal
    • Haemophilus influenzae
    • Meningoccocus
  • Vaccination important
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29
Q

What causes haemochromatosis?

A
  • Autosomal recessive disorder, causes iron overload
  • Abnormalities of HFE gene (needed for Hepcidin production) usually cause - homozygous C282Y most common
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30
Q

What is the function of secretin?

A
  • Increases bile secretion
  • Increases buffer secretion by the pancreas
  • Decreases gastric motility and secretion
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31
Q

What is refractory coeliac disease?

A
  • Persistance malabsorption/villous atrophy after 6-12 months gluten-free diet
  • Type 1 - normal immunophenotype
    • 96% 5 year survival
    • Treatment - steroids, immunosuppressants
  • Type 2 - abnormal immunophenotype
    • Ulcerative jejunitis, ulceration in jejunum/ileum
    • 58% 5 year survival
    • 60-80% progression to enteropathy-associated T-cell lymphoma
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32
Q

What is the exocrine function of the pancreas?

A

Produces pancreatic juices - aid digestion

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33
Q

Describe the venous drainage of the pancreas

A
  • Head - superior mesenteric vein, drains to HPV
  • Rest - pancreatic veins which drain to the splenic vein (joins the superior mesenteric vein to form the HPV)
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34
Q

How do erythroblasts use iron?

A
  • Transferrin-iron complex binds to Tf receptor on cell surface
  • RBC precursor mitochondria use Iron to produce Haem using ALA-S2
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35
Q

List the differences between the jejunum and ileum

A
  • Jejunum
    • Upper L quadrant
    • Thick intestinal wall
    • Longer vasa recta
    • Less arcades
    • Red in colour
    • Inner mucosal lining has plicae circularis
  • Ileum
    • Lower R quadrant
    • Thin intestinal wall
    • Short vasa recta
    • More arcades
    • Pink in colour
    • No plicae circularis
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36
Q

What causes bile acid malabsorption and how is it treated?

A
  • Caused by ileal resection/malabsorption
  • Treat with bile acid sequestrants
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37
Q

Define chronic pancreatitis

A

Continuing inflammatory disease of the pancreas characterised by morphological changes - pain and loss of exocrine and endocrine functions

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38
Q

Describe the location of the jejunum and ileum

A
  • Intraperitoneal
  • Attached to posterior abdominal wall by mesentery
  • Jejunum begins at duodenojejunal flexure
  • No clear demarcation between the jejunum and ileum
  • Ileum ends at the ileocaecal valve
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39
Q

List the diseases associated with coeliac disease

A
  • Dermatitis herpetiformis
    • Itchy rash on extensor surfaces, occurs after 90% villous atrophy
  • Other AI diseases - Type 1 diabetes, thyrotoxicosis, Addison’s disease
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40
Q

How can the risk of coeliac-related malignancy be reduced?

A

Adherance to a gluten-free diet

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41
Q

Describe the innervation of the pancreas

A
  • Parasympathetic - vagus
  • Sympathetic - thoracic splanchnic nerves from superior mesenteric and coeliac plexuses
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42
Q

How is iron balance regulated?

A

Altering GI iron absorption/excretion is the only mechanism for regulating iron balance

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43
Q

Describe the treatment of chronic pancreatitis

A
  • Lifestyle - quit smoking and drinking alcohol
  • Endoscopic removal of stones/dilate strictures
  • Coeliac axis block - manage pain
  • Screen for diabetes mellitus
  • Analgesia - paracetamol, NSAIDs, opiods
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44
Q

What is acute post-operative ileus?

A
  • Constipation and intolerance of oral intake (no mechanical obstruction) after surgery
  • Physiological ileus:
    • Small intestine - 0-24 hours
    • Stomach - 24-68 hours
    • Colon - 48-72 hours
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45
Q

List disorders of iron metabolism

A
  1. Iron deficiency anaemia
  2. Iron malabsorption e.g. coeliac disease
  3. Haemochromatosis
  4. Sideroblast anaemia
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46
Q

What is the function of VIP?

A

Reduces acid secretion in the stomach

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47
Q

Describe the venous drainage of the jejunum and ileum

A
  • Superior mesenteric vein
    • splenic vein at neck of pancreas - drains to hepatic portal vein
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48
Q

How does recurrent acute pancreatitis cause chronic pancreatitis?

A
  • Inflammatory changes and necrosis - scarring in periductular areas
  • Ductules become obstructed - stone formation
49
Q

Describe the functional adaptations of the ileum

A
  • Lymphoid follicles (Peyer’s patches) in submucosa, extends to lamina propria - produce lymphocytes in response to ingested foreign molecules
  • Enteroendocrine cells especially in crypts
  • Paneth cells deep in crypts - immune granules to destroy microorganisms
50
Q

Describe the arterial supply of the jejunum and ileum

A
  • Superior mesenteric artery
  • Arises from aorta at level of L1, immediately inferior to coeliac trunk
  • Moves between layers of mesentery, splits into approximately 20 branches
  • Branches anastomose to form loops - arcades
  • Arcades form long, straight vasa recta
51
Q

Describe the innervation of the duodenum

A
  • Sympathetic - intestinal plexuses along pancreaticoduodenal arteries
  • Parasympathetic - coeliac and superior mesenteric plexuses (vagus nerve)
52
Q

Describe the anatomical position of the pancreas

A
  • Mostly posterior to stomach, retroperitoneal
  • Extends across posterior abdominal wall from duodenum to spleen
  • Epigastric and L hypochondrium regions
  • Head is in the ‘C’ of the duodenum
53
Q

Describe steatorrhoea

A

Fatty stool - loose, pale, floating

54
Q

Describe the presentation of coeliac disease in adults

A
  • Symptomatic - diarrhoea, bloating, flatulence, abdominal pain/discomfort (may be constipated)
  • Chronic/recurrent iron deficiency anaemia
  • Nutritional deficiency
  • Reduced fertility/amenorrhoea
  • Osteoporosis
  • Elevated AST/ALT
  • Neurological/psychiatric symptoms
55
Q

How is iron absorbed in the small intestines?

A
  • Ferrous iron absorbed by mucosal cells into the blood/ECM bound to ferritin
  • Low pH aids absorption
  • Only absorbed in duodenum and jejunum
  • Rate of absorption proportional to requirement
56
Q

How is iron transported in plasma?

A
  • Transferrin - glycoprotein, made in hepatocytes
  • High concentration when iron concentration is low
  • Low concentration when iron concentration is high
  • Two iron atoms per molecule of ferritin
  • Normally - 30% saturated with iron, 70% free
57
Q

How is iron stored within cells?

A

Ferritin (soluble) or Haemosiderin (insoluble)

58
Q

List the zymogens produced by the pancreas and describe their activation

A
  • Trypsinogen, activated to trypsin by enterkinase
  • Chymotrypsin, activated to chymotrypsin by trypsin
  • Lipase/co-lipase/phospholipase
  • Amylase - digests alpha 1-4 glucose to glucose bonds only
  • Lipase - digests triglycerides to free fatty acids and monoglycerides
59
Q

What is the consequence of bile acid malabsorption?

A

Unable to absorb fat soluble vitamins - A, D, E, K

60
Q

Describe the presentation of coeliac disease in infants

A
  • 4-24 months - introduction of cereals
  • Impaired growth, diarrhoea, vomiting, abdominal distention
61
Q

How does hereditary pancreatitis develop?

A
  • Gene coding for trypsin overactive, cannot be inactivated
  • Autodigestion of pancreatic tissue
  • Acute pancreatitis leading to chronic pancreatitis
62
Q

Describe the functional adaptations of the jejunum

A
  • Tallest villi
  • No Brunner’s glands
63
Q

How does HFE gene mutation cause iron overload in haemochromatosis?

A

Mutation causes decreased hepcidin production, increased GI absorption of iron

64
Q

How is coeliac disease diagnosed?

A
  • Serology
    • High IgA tTG - sensitive
    • High IgA EMA (antiendomysial antibody) - specific
  • Endoscopy
    • Scalloping, lack of folds
    • Mosaic pattern
    • Prominent submucosal BVs
    • Nodular muscoa
  • Biopsy
    • Distal duodenum - 4x, must be on gluten-rich diet
65
Q

List the risks factors for coeliac disease

A
  • Female
  • 1st degree relative with coeliac
  • HLA-DQ2/DQ8 gene
66
Q

What is the function of GIP?

A

Decreases gastric activity

67
Q

List the symptoms and treatment of enteropathy-associated T-cell lymphoma

A
  • Weight loss, night sweats, itch, GI bleeding
  • Often advanced and incurable
68
Q

What is chronic intestinal pseudo-obstruction?

A

Signs of mechanical obstruction of the intestines without actual occlusion

69
Q

List the risk factors for acute post-operative ileus

A
  • Open surgery
  • Prolonged abdominal/pelvic surgery
  • Delayed enteral nutrition
  • Peri-operative complications
  • Peri-operative opiates
70
Q

Describe the treatment of coeliac disease

A

Gluten-free diet - avoid wheat, barley, rye

71
Q

How are haem and non-haem iron absorbed?

A
  • Haem iron is easily absorbed
  • Non-haem
    • Released by acidic digestion and proteolytic gastric enzymes
    • Converted from ferric to ferrous form by duodenal cytochrome b1
    • Influenced by Vitamin C
  • Absorbed into enterocytes by divalent metal transporter 1 (DMT1)
72
Q

How long are the jejunum and ileum?

A

Jejunum = 2.5m

Ileum = 3.5m

73
Q

What happens if an individual with Haemochromatosis is treated with a blood transfusion?

A

Causes iron overload - bone marrow failure

74
Q

Define coeliac disease and describe its cause

A
  • Gluten-sensitive enteropathy
  • Small intestinal villous atrophy - resolves when gluten is withdrawn from diet
  • Innappropriate T-cell mediated immune response in the genetically susceptible
  • Alpha-gliadin is the most toxic moiety
75
Q

How is Vitamin B12 absorbed in the small intestines?

A
  • Dependent on B12 from diet although intestinal microflora produce B12
  • Need low pH, gastric enzymes and intrinsic factor from parietal cells for absorption
  • IF-B12 complex is absorbed in the terminal ileum
76
Q

Describe the morphological changes which occur in chronic pancreatitis

A
  • Dilated pancreatic ducts, filled with protein plugs (may be calcified)
  • Atrophy of acini and fibrosis - relative preservation of islets
  • Increasing concentration of pancreatic proteins and increasing duct pressure = formation of protein plugs with calcium carbonate, leading to calculi formation
  • Lack of lipases in advanced disease - malabsorption of fat, reduced absorption of vitamins A, D, E and K, steatorrhoea
  • Islets can be lost in advanced disease leading to diabetes mellitus
77
Q

How do contractions of the small intestine change after a meal?

A

Entry of chyme to duodenum stimulates the gastroenteric reflex - along with vagal stimulation, myenteric plexus action, gastrin, CCK, insulin and serotonin release causes increased intestinal motility

78
Q

List diseases of malabsorption

A
  1. Coeliac disease
  2. Pancreatic exocrine insufficiency
  3. Steatorrhoea (post-hepatic jaundice)
  4. Bile acid malabsorption
  5. Zollinger-Ellison Syndrome
79
Q

Describe the histology of the exocrine pancreas

A
  • Functional unit - acinus
    • Lined by pyramidal cells joined by apical junction complexes
      • centroacinar cells, continuous with low cudoidal epithelium of intercalated duct
80
Q

What is the function of CCK?

A
  • Increases pancreatic secretions
  • Increases bile and pancreatic secretions release into the duodenum
  • Reduces gastric activity
  • Reduces hunger
81
Q

Describe the arterial supply of the duodenum

A
  • Before ampulla of Vater - gastroduodenal artery (from coeliac trunk)
  • After ampulla of Vater - inferior pancreaticoduodenal artery (branch of super mesenteric artery)
  • Change marks the transition from foregut to midgut
82
Q

What is a peristaltic rush and why does it occur?

A
  • If intestinal mucosa is irritated
  • Enteric nervous initiation of contraction
  • Sweeps chyme from the small intestines into the colon - relieves irritation of the small intestines
83
Q

Name the secretions of the duodenum

A
  • CCK
  • Secretin
  • GIP
  • VIP
  • Gastrin
  • Alkaline mucous from Brunner’s glands
84
Q

Describe the release of iron from the RES

A
  • Macrophages get iron from breakdown of RBCs
  • RES iron stored as ferritin/haemosidin
  • Ferroportin/hepcidin control RES macrophage iron release
  • If cells don’t require iron - stored as ferritin
  • If cells require iron - bound to transferrin, taken to tissues
  • RBC recycle iron - released on breakdown, transferrin iron taken up by erythroblasts if they have the transferrin receptor
85
Q

List the symptoms of chronic pancreatitis

A
  • Chronic/recurrent upper or generalised abdominal pain
  • Nausea
  • Vomiting
  • Bloating
  • Weight loss
  • Steatorrhoea
  • Jaundice
  • Chronic liver disease
86
Q

Describe Sideroblastic anaemia

A

RBC takes in iron but iron is trapped in ring sideroblast - can’t synthesise haem

87
Q

Describe the presentation of coeliac in older children

A

Anaemia, short, pubertal delay, recurrent abdominal pain, behavioural disturbance

88
Q

How is chronic pancreatitis diagnosed?

A
  • Transabdominal ultrasound - shows inflammation of pancreas and gallstones
  • MRCP - radiolabelled isotope injected to show pancreas, gallbladder and the pancreatic/bile ducts
  • CT
  • Blood tests -
    • IgG4 - autoimmune
    • Serum amylase, lipase and trypsinogen (will be high in pancreatitis)
89
Q

Which cells are resposible for iron absorption?

A

Enterocytes

90
Q

What causes chronic pancreatitis?

A

T - toxic and metabolic (alcohol, smoking, hypercalcaemia, hyperlipidaemia)

I - idiopathic

G - genetic (HP, CFTR, SPINK-1)

A - autoimmune

R - Recurrent and severe acute pancreatitis

O - obstructive (gallstones)

91
Q

Describe the shape and size of the duodenum

A
  • Shortest and widest part - 0.25m long
  • C-shaped curve around the head of the pancreas
92
Q

Where does exocrine secretion occur in the jejunum and ileum?

A

Crypts of Leiberkuhn

93
Q

How quickly do liquids and solids pass through the small intestines?

A
  • Transports liquids and solids at same rate
  • Liquids reach caecum earlier due to faster gastric emptying
  • Liquids - 30 minutes, solid chyme - 150 minutes
94
Q

How does coeliac disease cause iron malabsorption?

A

Infiltration of small lymphocytes into the lamina propria of the GI tract causes blunting of villi, causes ineffective absorption

95
Q

Describe the general function of the small intestines

A

Majority of digestion/absorption, relatively little secretion

96
Q

Describe the arterial supply of the pancreas

A
  • Head - superior and inferior pancreaticoduodenal arteries, branches of the gastroduodenal artery (from the coeliac trunk) and superior mesenteric arteries
  • Rest - pancreatic branches of splenic artery
97
Q

Describe the Marsh Classification of Coeliac disease

A

0 = No changes - <40 lymphocytes per 100 enterocytes, crypts and villi normal

1 = >40 lymphocytes per 100 enterocytes, crypts and villi normal

2 = >40 lymphocytes per 100 enterocytes, crypts elongated, villi normal

3a = >40 lymphocytes per 100 enterocytes, crypts elongated, mild villous atropy

3b = >40 lymphocytes per 100 enterocytes, crypts elongated, marked villous atrophy

3c = >40 lymphocytes per 100 enterocytes, crypts elongated, absent villi

98
Q

List disorders of small bowel transit

A
  1. Chronic intestinal pseudo-obstruction
  2. Acute post-operative ileus
99
Q

How is Haemochromatosis treated?

A
  • Venesection (initially up to weekly)
    • Monitor ferritin and transferrin saturation
    • Prevent/limit organ damage
100
Q

Describe the layers of the walls of the small intestines

A
  • Mucosa - columnar epithelium, lamina propria, muscularis mucosae
  • Submucosa - Brunners glands (produce mucous)
  • Muscularis propria - circular and longitudinal smooth muscle
  • Serosa - forms visceral peritoneum
101
Q

What is Zollinger-Ellison disease?

A
  • Hyperplasia/tumour - gastrinoma
  • Constant hypersecretion of gastrin
  • Aggressive recurrent peptic ulcer disease
  • Diagnosis - stimulated gastrin level
  • Treat with v high doses of PPI, surgery to remove tumour
102
Q

List the potential complications of coeliac disease

A
  • Infection
  • Osteoporosis
  • Refractory coeliac disease
  • Malignancy
103
Q

Describe the contractions which occur in the small intestine

A
  • Prolonged propagated contractions move the chyme intermittently from the ileum to the colon in boluses
  • Mixing contractions - segmentation, propulsive contractions due to peristalsis
  • Peristalsis is weak in the small intestine - contractile ring around gut moves chyme forwards
104
Q

How does obstruction e.g. due to gallstones cause pancreatitis?

A
  • Uncontrolled activation of trypsin - tissue damage due to autodigestion
  • Stones cause scarring, ulceration, obstruction, stasis and atrophy of pancreatic tissue
105
Q

Describe the management of chronic intestinal pseudo-obstruction

A
  • Nutritional - enteral/parenteral feeding
  • Antibiotics for small intestinal bacterial overgrowth
  • Refractory - small bowel transplantation
106
Q

What causes chronic intestinal pseudo-obstruction?

A

Primary or secondary to other diseases

  • Myopathic - scleroderma, amyloidosis
  • Neuropathic - Parkinson’s
  • Endocrine - Diabetes mellitus, servere hypothyroidism
  • Drugs - Phenothiazines, Parkinson’s drugs
107
Q

What reduces intestinal motility?

A

Secretin and glucagon

108
Q

What causes iron deficiency anaemia?

A
  • Young women (20%) - menstruation/pregnancy
  • Males + post-menopausal females - due to GI blood loss until proven otherwise
109
Q

How are fats absorbed in the small intestine?

A

Bile acid circulation

110
Q

List the exocrine pancreatic secretions

A
  • Bicarbonate (neutralises chyme)
  • Zymogens - enzyme precursors, activated to give functional digestive enzymes
111
Q

Compare transferrin saturation in iron deficiency anaemia and Haemachromotosis to normal

A
  • Normal = 30% saturation
  • IDA - high transferrin, low iron
  • Haemochromatosis - low transferrin, high iron - up to 100% saturation
112
Q

Describe the pathophysiology of coeliac disease

A
  • Genetic susceptibility and adenovirus 12 infection
  • Peptide on alpha-gliadin similar to E1b portion of virus
  • Cross reactivity = inappropriate immune response to alpha-gliadin
113
Q

Describe the innervation of the jejunum and ileum

A
  • Sympathetic - T5-9 form the coeliac and superior mesenteric ganglia - gives off greater and lesser splanchnic nerves
  • Parasympathetic - preganglionic from posterior vagal trunks, synapse on postganglionic cells in myenteric + submucosal plexus of intestinal wall
114
Q

Which important vascular structures are associated anatomically with the pancreas?

A
  • Splenic vein and superior mesenteric vein unite behind the neck of the pancreas to form the portal vein
  • The inferior mesenteric vein joins the splenic vein behind the body of the pancreas
  • The aorta becomes the superior mesenteric artery behind the neck of the pancreas
  • The splenic artery and vein follow behind the pancreas to the spleen
115
Q

What is absorbed in the jejunum and ileum?

A
  • Carbohydrates
  • Peptides
  • Fat
  • Water
  • Vitamins
  • Electrolytes
  • Minerals
116
Q

Describe the venous drainage of the duodenum

A
  • Follow major arteries, drain into portal vein
  • 1st part - prepyloric vein drains into HPV
  • 2nd - 4th parts - superior pancreaticoduodenal vein drains into superior mesenteric vein
117
Q

What causes small bowel adenocarcinoma?

A

Rare - coeliac or Crohn’s disease

118
Q

Describe the pathogenesis of Coeliac disease

A
  1. Alpha gliadin digested and absorbed
  2. Exposed to tissue transglutaminase (TTG) which causes deamination, making it more immunogenic
  3. Enables binding to HLA-DQ2 and activation of pro-inflammatory T cell response
  4. CD4 T cells cause villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis
  5. B cellls produce antibodies e.g. antigliadin, antiendomysial and anti-TTG antibodies