GI Flashcards

1
Q
  1. What are the 3 different parts of the pharynx?
A

Oropharynx, nasopharynx, laryngopharynx

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2
Q
  1. What sort of muscle is present in the pharynx? What control is it under?
A

There are circular and longitudinal muscles in the pharynx, they are under control of branches of the vagus and glossopharyngeal nerves

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3
Q
  1. What is the muscle composition of the different parts of the oesophagus?
A

Upper third: voluntary striated muscle
Middle third: a mixture of voluntary striated muscle and smooth muscle
Lower third: smooth muscle under autonomic control

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4
Q
  1. What sort of epithelium does the oesophagus have?
A

Non-keratinised stratified squamous epithelium that resists injury

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5
Q
  1. What are the 4 main regions of the stomach?
A

Fundus, body, antrum, pylorus

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6
Q
  1. What sort of cells comprise the gastric glands? Exocrine or endocrine?
A

Gastric glands are exocrine.

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7
Q
  1. What do parietal cells in the stomach secrete?
A

Parietal cells secrete HCl and intrinsic factor

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8
Q

What do chief cells in the stomach secrete?

A

Chief cells secrete pepsinogen

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9
Q
  1. What do G cells in the stomach secrete?
A

G cells secrete gastrin

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10
Q
  1. What do D cells in the stomach secrete?
A

D cells secrete somatostatin

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11
Q
  1. What is the fundus of the stomach mainly for?
A

Storage – it can stretch a lot to accommodate lots of food

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12
Q
  1. What is the role of gastrin?
A

Gastrin increases stomach acid secretion by stimulating parietal cells to secrete HCl. It is stimulated by the presence of peptides and amino acids in the stomach.

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13
Q
  1. What is the role of intrinsic factor?
A

Intrinsic factor is secreted by parietal cells in the stomach and it is essential for the absorption of vitamin B12 in the small intestine.

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14
Q
  1. How is HCl secreted by parietal cells in the stomach?
A

Proton pumps, powered by ATP pump H+ into the stomach lumen in exchange for K+ that enters the parietal cell. K+ and Cl- diffuse into the stomach lumen in through channels in the parietal cell membrane – the net result is H+ and Cl- in the stomach lumen. The enzyme carbonic anhydrase in parietal cells catalyses the formation of carbonic acid from water and CO2 which then dissociates, providing a good source of H+ ions for stomach secretion and also HCO3-. HCO3- is exchanged for Cl- by antiporters in the basolateral membrane so Cl- can enter the stomach lumen too.

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15
Q
  1. Gastric acid is secreted by parietal cells in the fundus of the stomach in a process involving active pumping of protons (H+ ions) on the luminal surface.
    Which ion is exchanged for H+ at the proton pump?
A

K+

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16
Q
  1. What is the role of the HCl in the stomach?
A

HCl in the stomach is needed to break down proteins, as pepsinogen is activated to its active form pepsin in a low pH.

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17
Q
  1. What are the 3 phases of gastric acid regulation?
A

Cephalic – taste/smell of food stimulates secretion of pepsinogen + HCl in stomach by vagal nerve activity. Gastrin secretion in lower part of stomach.
Gastric – Food has entered and distended the stomach, stomach has stretched which activates the parasympathetic reflex and has a direct effect on gastric glands, increasing secretion.
Intestinal – chime has already entered the duodenum so gastric secretions are no longer needed. When chyme has loads of lipids in or its just acid then gastric secretion is inhibited. This ensures absorption of the SI matches the stomach digestion rate. Secretin, CCK and GIP inhibit gastric secretion.

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18
Q
  1. How does histamine influence secretion of gastric acid? What cells does it bind to?
A

Histamine is released from entero-chromaffin-like cells and binds to H2 receptors on parietal cells to stimulate gastric acid secretion.

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19
Q
  1. Why do NSAIDs pose a risk of gastric ulceration?
A

The release of protective mucus (which protects the stomach from its own acid) from stomach epithelium is a prostaglandin dependent process. When NSAIDs are taken, they inhibit prostaglandins so inhibit mucus production, which can lead to damage of the epithelium by the stomach acid, causing ulcers.

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20
Q

What are the 3 regions of the small intestine called?

A

Duodenum, jejunum, ileum

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21
Q
  1. What do S cells in the small intestine secrete and what does this substance do?
A

S cells in the small intestine secrete the hormone secretin, which stimulates the secretion of water and bicarbonate from the pancreas and bile ducts, due to an acidic pH in the small intestine.

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22
Q
  1. What do I cells in the duodenum secrete and what does this substance do?
A

Entero-endocrine cells secrete cholecystokinin which is a hormone that increases pancreatic enzyme secretion and gall bladder emptying in response to fatty acids and amino acids present in the SI.

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23
Q

What do K cells of the small intestine secrete and what does this substance do?

A

K cells secrete Gastric inhibitory polypeptide or glucose dependent insulinotropic polypeptide which inhibits gastrin secretion and helps release of insulin from the pancreas in response to raised blood glucose. Its release is stimulated by the presence of fat and glucose in the SI.

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24
Q
  1. What sort of vessels does a villi contain in the small intestine?
A

Lacteal, capillary bed

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25
Q

How are glucose and galactose absorbed in the small intestine?

A

Glucose and galactose are absorbed via a secondary active transport mechanism in the small intestine. More sodium wants to flow into the intestinal cells down its concentration gradient, so it does, and with it it brings glucose and galactose that enter the cell via SGLUT1 channel.

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26
Q
  1. How are amino acids absorbed in the small intestine?
A

Amino acids tend to be absorbed via active transport. Some are via a secondary active transport mechanism with sodium, similar to how glucose and galactose are transported, others are actively transported by themselves.

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27
Q
  1. How are lipids absorbed in the small intestine?
A

Micelles help ferry lipids towards intestinal cells where they are absorbed by simple diffusion. Here they become coated with proteins and form chylomicrons, then via exocytosis from the absorptive cell they enter the lacteals and via the lymphatic system get put into the venous circulation, from here they are transported to the liver and adipose tissues.

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28
Q
  1. At what vertebral level is the transpyloric plane? What structures cross this plane?
A

L1

Pylorus 
Pancreatic neck
Duodenojejunal flexure
Fundus of gall bladder
9th costal cartilage
Hila of kidneys
Origin of portal vein
Transverse mesocolon
- double fold of peritoneum which connects the transverse colon to the posterior abdominal wall
2nd part of duodenum 
Superior mesenteric artery origin
Hilum of spleen 
Termination of spinal cord
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29
Q
  1. What is the blood supply to the pancreas?
A

Branches of the splenic artery and branches of the superior and inferior pancreaticoduodenal arteries, which are branches of the gastroduodenal and superior mesenteric arteries.

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30
Q
  1. Why does pain from appendicitis originate at the umbilicus and move to the right iliac fossa?
A

It starts off generalised as it is only visceral peritoneum which is affected, it moves to the right as it becomes more inflamed and the parietal peritoneum is affected.

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31
Q
  1. What vitamins does the large intestine produce?
A

Vitamin K and vitamin B

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32
Q

What are the two types of nerve supply in the GI tract?

A

Myenteric and submucosal plexus – enteric nerve supply

Autonomic innervation – vagus fibres

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33
Q
  1. What two plexuses are present in the GI tract? Where are they found in the histological layers and what do they do?
A

Myenteric plexus – controls muscular contractions to propel mixing waves in the stomach, present in the muscularis layer.
Submucosal plexus – controls gastric secretions, found in the submucosal layer.

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34
Q
  1. What does the hormone grehlin do?
A

Grehlin increases your appetite- the hunger hormone, and increases GH secretion.

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35
Q
  1. What does the hormone motilin do?
A

Motilin increases motility in the stomach and small intestine.

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36
Q
  1. What does the hormone gastric inhibitory polypeptide (aka glucose-dependent insulinotropic polypeptide) do? When is it released?
A

Inhibits gastric secretion and stimulates insulin release from the pancreas in response to a rise in blood glucose, its release is stimulated by the presence of glucose and fats in the SI.

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37
Q
  1. What is the difference between oncogenes and proto-oncogenes?
A

Oncogenes generally cause neoplastic transformation by interfering with normal cell growth or differentiation, often disrupting the control of the cell cycle.
Proto-oncogenes are normal genes that are involved in normal growth control. Proto-oncogenes may become oncogenes through mutation, which confers a specific selective advantage.

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38
Q
  1. How might oncogenes cause cancer?
A
  1. Oncogenes generally cause neoplastic transformation by interfering with normal cell growth or differentiation, often disrupting the control of the cell cycle. They can increase progression through the cell cycle, causing cellular proliferation. Oncogenes can code for a variety of proteins that could make this happen, such as cell surface receptors, signal transducers, transcription factors, growth factors or epigenetic modifiers (that affect transcription).
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39
Q
  1. What is EGFR and how might it cause cancer?
A

EGFR stands for epidermal growth factor receptor, it is a member of the protein kinase family – activation of it can cause increased levels of phosphorylation and increased progression through the cell cycle. It has been linked to lung cancer.

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40
Q
  1. What type of protein is RAS and how might it cause cancer?
A

There are 3 subtypes of RAS – KRAS, NRAS, HRAS. RAS encodes a signalling protein that conveys an extracellular signal to effector molecules in the cell; it is a signalling transducer. When RAS is wild type, it causes overactive signalling within the cell.

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41
Q
  1. How does Rb (retinoblastoma) normally work to stop tumours forming?
A

Rb is a tumour suppressor protein. It prevents excessive cellular proliferation by inhibiting cell cycle progression until a cell is ready to divide. Only one working allele of the gene is necessary for it to illicit its tumour suppressive function (the mutated gene is recessive). So a patient would need to be homozygous in defective Rb genes for the tumour suppressor function to be affected.

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42
Q
  1. What does TP53 normally do?
A

TP53 is a tumour suppressor gene. It regulates genome expression by the creation of proteins that bind to DNA and regulate transcription. People who inherit only ONE copy of a defective TP53 are likely to get tumours at a young age – the defect is dominant.

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43
Q
  1. What is APC and what does it normally do?
A

APC is a tumour suppressor gene. Mutations in the APC gene may lead to colorectal cancer. In order for cancer to develop, most alleles must be defective.

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44
Q
  1. What are the arteries that come off the celiac trunk?
A

Splenic artery, left gastric artery, common hepatic artery

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45
Q

What vertebral levels are the celiac trunk, SMA and IMA?

A

Celiac trunk: T12
SMA: L1
IMA: L3

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46
Q
  1. What parts of the body feed signals into the vomiting centre in the brain?
A

Vestibular system
Heart and gastrointestinal tract
CNS
Chemoreceptor trigger zone

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47
Q
  1. Name some neurotransmitters and their respective receptors that can trigger vomiting.
A

Histamine and H1 receptor
Acetylcholine and Muscarinic ACh receptors
Dopamine and D2 receptors
Serotonin and 5-HT3 receptors

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48
Q
  1. Therefore, what receptors can be targeted for anti-emitic therapy?
A

H1 receptor, MACh receptors, D2 receptors, 5-HT3 receptors

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49
Q
  1. Name a D2 dopamine antagonist, H1 histamine antagonist, Muscarinic ACh antagonist, and a 5-HT3 antagonist.
A

H1 receptor antagonist: cyclizine
MACh receptor antagonist: hyoscine
D2 receptor antagonist: metoclopramide
5-HT3 receptors: ondasteron

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50
Q
  1. Name a proton pump inhibitor, H2 antagonist, synthetic prostaglandin and antacid.
A

PPI: omeprazole
H2 antagonist: ranitidine
synthetic prostaglandin: misoprostol
Antacid: aluminium hydroxide

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51
Q
  1. What condition might cause painful obstructive jaundice, and what might cause painless obstructive jaundice?
A

Painful obstructive jaundice: gallstones

Painless obstructive jaundice: pancreatic cancer

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52
Q
  1. What happens to the majority of bile salts after they are used?
A

They are reabsorbed into the liver via the hepatic portal vein for reuse

53
Q
  1. What is the difference between HDL and LDL cholesterol? Which one is ‘good’ and which one is ‘bad’ and why?
A

HDL cholesterol is ‘good’ for you as it transports LDL cholesterol from the walls of arteries back to the liver for breakdown. LDL cholesterol is ‘bad’ for you as it builds up in the walls of arteries.

54
Q

What is the general organisation of the intestinal wall? From outside to inside

A
Adventitia AKA serosa
Longitudinal muscle layer
Circular muscle layer
Submucosal layer
Muscularis mucosae 
Mucosa composed of
- Epithelial layer
- Lamina propria
55
Q

What type of epithelium is found after the gastro-oesophageal junction of the oesophagus

A

Non-stratified columnar epithelium

56
Q

What is the innervation of the oesophagus?

A

Vagus nerve innervates oesophageal muscle directly

Also via the intrinsic nerves in the Myenteric nerve plexus

  • Located between the longitudinal and circular muscle layers
  • Submucosal plexus
57
Q

What are the 2 types of ganglia in the enteric nervous system?

A

Myenteric AKA Auerbach’s plexus

Submucosal AKA Meissner’s plexus
- S and S

58
Q

What is the arterial supply of the oesophagus?

A

Cervical portion
- Inferior thyroid artery

Thoracic portion
- Bronchial and oesophageal branches of thoracic artery

Abdominal portion
- Ascending branches of the left phrenic and left gastric arteries

59
Q

How do oesophageal varices form?

A

In portal hypertension collateral veins divert gastric blood to the oesophageal veins (instead of to the hepatic portal vein).
As a result the oesophageal veins enlarge and forms varies.

60
Q

Is peristalsis voluntary or involuntary?

A

Involuntary

61
Q

What are the anatomical relations of the stomach?

A

Spleen lies to the left

Pancreas lies inferiorly and posteriorly

Liver lies to the right

62
Q

Which cells produce HCL?

A

Parietal

Oxyntic

63
Q

Which cells produce pepsinogen?

A

Chief cells

64
Q

Which cells produce mucus?

A

Goblet cells

65
Q

What is the function of intrinsic factor?

A
  • Facilitates absorption of vitamin B12
  • Intrinsic factor binds to vitamin B12, allowing it to escape degradation in the stomach and the intestine and to be safely transported to the terminal ileum where it is absorbed
66
Q

What is the function of gastroferrin?

A
  • Facilitates absorption of iron

* Gastroferrin binds to Fe2+, facilitating absorption in the duodenum

67
Q

What do entero-chromaffin-like cells produce?

A

Histamine

68
Q

Where is CCK produced and what is its’ function?

A

CCK = Cholecystokinin
Released by I cells in the small intestine
Stimulates pancreatic secretions
Stimulates gall bladder contraction (stimulates greater release of bile into duodenum)
Major stimulus for this is the presence of fats in the duodenum

69
Q

Where is Secretin produced and what is its function?

A

Released by S cells
Stimulated by low pH
Becoming more acidic due to more gastric acid entering
Releases more bicarbonate from the pancreas and through bile

70
Q

What are enterocytes and what is their function?

A

Simple columnar epithelial cells
Round or oblong nucleus located centrally
Synthesise digestive enzymes and secrete them to apical brush border

71
Q

What are paneth cells and what is their function?

A

Paneth cells are found at the base of the small intestinal crypts
Specialised for protein synthesis and secretion
Contain antibacterial proteins
- Lysozyme
- Phospholipase A2
- Defensins

72
Q

Which molecules are actively absorbed into the small intestine?

A
  • Sugars
  • Amino acids
  • Electrolytes
73
Q

What molecules enter the enterocytes of the small intestine by diffusion?

A

Fatty acids and cholesterol

  • They are re-esterified intracellularly
  • Complexed with apolipoproteins to form chylomicrons
  • Released at the basolateral surface
74
Q

Where are the major digestive surfaces of the intestine?

A

Jejunum and ileum

75
Q

What is the arterial supply to the duodenum?

A

Coeliac artery

76
Q

What is the venous drainage of the duodenum?

A

Superior mesenteric vein

77
Q

Which organs are retroperitoneal?

A
S – Suprarenal (adrenal) glands
A – Aorta/IVC
D – Duodenum (except the duodenal cap – first 2cm)
P – Pancreas (except the tail)
U – Ureters 
C – Colon (ascending and descending parts)
K - Kidneys
E – (O)esophagus
R – Rectum
78
Q

How might appendicitis present?

A
  • Initially pain from the appendix (midgut structure) and visceral peritoneum is referred to the umbilical region
  • As the appendix becomes inflamed and irritates the parietal peritoneum the pain becomes localised to the right lower quadrant
79
Q

Where does the splenic vein run in relation to the pancreas?

A

Along the superior border

80
Q

Where does the pancreas drain into the duodenum?

A

The main pancreatic duct extends along the length of the gland
- A smaller accessory duct drains the superior part of the head and may open separately into the duodenum

The main duct joins the common bile duct before opening into the duodenum through the ampulla of Vater

81
Q

What is the function of pancreatic acini?

A

To secrete pancreatic enzymes and fluid into the ducts

82
Q

Where is insulin made?

A

Insulin is made by beta cells in the islets of the pancreas.

Insulin secretion is stimulated by hyperglycaemia

83
Q

Where is glucagon made?

A

Glucagon is made by alpha cells in the islets of the pancreas.
Glucagon secretion is stimulated by hypoglycaemia

84
Q

What do D cells secrete?

A

D cells of the pancreas secrete somatostatin and gastrin

85
Q

What stimulates pancreatic secretion?

A

Cholecystokinin which is released when food enters the duodenum

86
Q

How does pancreatic insufficiency occur in Cystic Fibrosis?

A

Cento-acinar and duct cells secrete most of the fluid and alkali
By exchanging HCO3- for Cl- ions
Using the cystic fibrosis transmembrane regulator (CFTR) protein
- Pancreatic insufficiency therefore occurs in cystic fibrosis, where an abnormal CFTR gene is inherited

87
Q

What is the arterial supply to the pancreas?

A

Branches of the coeliac and superior mesenteric arteries supply the pancreas

88
Q

What is the venous drainage of the pancreas?

A

Hepatic portal vein

89
Q

What nerves supply the pancreas?

A

Vagus and splanchnic nerves

90
Q

What does the falciform ligament traverse

A

The liver - divides it into L and R lobes

91
Q

What is found within the hilum of the liver?

A

Portal vein
Hepatic artery
Common bile duct

92
Q

What is contained within the portal triad?

A

Hepatic artery
Hepatic portal vein
Bile duct

93
Q

What is the function of the liver?

A
Regulating metabolism
Storing nutrients 
- glycogen 
- vitamin B12
Producing and secreting
- clotting factors 
- plasma proteins
Synthesising 
- bile acids
Detoxifying 
- bilirubin
- drugs
- toxins
94
Q

What does the splenic vein drain?

A

Stomach
Pancreas
Spleen

95
Q

What does the superior mesenteric vein drain?

A

Small intestine

Most of the large intestine

96
Q

What drains the remaining part of the large intestine that is not drained by the superior mesenteric vein?

A

Inferior mesenteric vein

97
Q

Where is the main absorptive surface of the GI tract?

A

Jejunum and ileum

98
Q

What are Peyer’s patches?

A

Organised lymphoid follicles
Contain macrophages, dendritic cells, B and T lymphocytes
Provide immune response against ingested pathogen

99
Q

Where is vitamin B12 digested?

A

Terminal ileum

100
Q

What supplies the jejunum and ileum?

A

Superior mesenteric artery

101
Q

What is contained within the foregut?

A

Please Oh Pretty Please Stop Being Loud

POPPSBL
P - Pharynx
O - Oesophagus
P - Pancreas
P - Proximal duodenum 
- D1 and proximal half of D2
S - Stomach
B - Biliary system 
L - Liver
102
Q

What is produced in pancreatic islets and the pancreatic acini?

A

Islets - hormones (insulin and glucagon)

Acini - digestive enzymes

103
Q

What structures are found within the hindgut?

A
Distal 1/3 of transverse colon
Rectum 
Sigmoid colon
Descending colon 
Splenic flexure
104
Q

What structures are found within the midgut?

A
Duodenum 
- Distal 1/2 of D2
- All of D3 and D4
Jejunum 
Ileum 
Caecum 
Appendix
Ascending colon
Hepatic flexure
Transverse colon 
- Proximal 2/3
105
Q

What is the arterial supply and venous drainage of the foregut?

A

Coeliac trunk

Splenic vein

106
Q

What is the arterial supply and venous drainage of the midgut?

A

Superior mesenteric artery

Superior mesenteric vein

107
Q

What is the arterial supply and venous drainage of the midgut?

A

Inferior mesenteric artery

Inferior mesenteric vein

108
Q

How many Kcalories per gram are found in; carbohydrate, fat and protein

A
Carbohydrate = 4kcal/g
Fat = 9kcal/g
Protein = 4kcal/g
109
Q

Which vitamins are fat-soluble?

A

A, D, E, K

- therefore all other vitamins are water-soluble

110
Q

Which microorganism is responsible for gastric ulcers?

A

Helicobacter pylori

- 80%

111
Q

What treatment is given for a bacterial-caused gastric ulcer?

A

Triple therapy

  • proton pump inhibitor
  • 2 antibiotics
  • Amoxicillin plus one of either clarithromycin or metronidazole
112
Q

Name some NSAIDS

A

Ibuprofen
Diclofenac
Naproxen

113
Q

What is the first line treatment for minor GI reflux

A

Omeprazole

If omeprazole is not tolerated, give ranitidine

114
Q

What are the 4 main classes of laxatives and how do they work? Name an example in each category

A

Bulk forming laxative - increase faecal mass - Fibrogel

Osmotic laxative - increase fluid in large bowel - lactulose

Stimulant laxatives - increase intestinal motility - Senna

Faecal softeners - lubricate and soften - arachis oil (peanut)

115
Q

What drug is given prior to colonoscopy?

A

Picolax

- made from sodium picosulphate and magnesium citrate

116
Q

What drug can be given to prevent diarrhoea?

A

Ispaghula

  • a bulking agent
  • absorbs water
117
Q

What is the most likely diagnosis?

Presentation:
Haematemesis
Drinks 10 units of alcohol per day
Pain on swallowing

A

Oesophageal varices

118
Q

What is the most likely diagnosis?

Presentation:
24y/o 
Female 
Stressed
Altered bowel habits 
- constiapation and diarrhoea
Mucus in stools
A

Irritable Bowel Syndrome
- less severe than IBD

Treat stress firstly and GI symptoms should ease

119
Q

What are the common presentations of Coeliac disease?

A

Coeliac disease is caused by an adverse reaction to gluten

Diarrhoea
Constipation
Fatty stools
- Float
- Very smelly
Abdominal pain
Bloating
Flatulence 
Indigestion
Fatigue
Weight loss
120
Q

What is the most likely diagnosis?

Heartburn
Acid reflux
Bad breath
Nausea
Tooth decay
A

Gastro-oesophageal reflux disease

121
Q

What is the most likely diagnosis?

Presentation:
Heartburn
Burning stomach pain
Fatty food intolerance
Vomiting 
Pain between 15-30 minutes after meals
Pain relieved by vomiting
A

Gastric ulcer

122
Q

What is the most likely diagnosis?

Presentation:
Indigestion
Nausea
Heartburn
Burning stomach pain 
Fatty food intolerance 
Pain relieved by meals
A

Duodenal ulcer

123
Q

What are the common presentations of diverticular disease?

A
Left lower quadrant pain - left iliac fossa
Crampy pain 
Change in bowel habits
Nausea 
Vomiting
124
Q

What are the two types of Inflammatory Bowel Disease?

A

Ulcerative Colitis

Crohn’s disease

125
Q

What is the pattern of inflammation in Crohn’s disease?

A

Asymmetrical inflammation
- one part of the GI tract will be inflamed and the next part won’t

Can affect any part of the digestive tract from mouth and anus

126
Q

What is the pattern of inflammation of Ulcerative Colitis?

A

Symmetrical inflammation
- long stretch of inflammation

Affects the large intestine

127
Q

What is the most likely clinical diagnosis?

Thin
Diarrhoea
Abdominal mass common

A

Crohn’s disease

128
Q

What is the most likely clinical diagnosis?

Bloody diarrhoea
No abdominal mass

A

Ulcerative colitis

129
Q

What are the symptoms of pancreatitis?

A

Fever

Upper abdominal pain