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Gastroenterology Flashcards

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1
Q

Why is calbindin important

A

Binds to calcium and moves it from apical membrane of enterocyte to basolateral membrane of enterocyte. This maintains a low intracellular conc of Ca2+ which is important in preventing calcium’s action as an intracellular signal

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2
Q

Which enzyme liberates Fe2+ from erythrocytes

A

Haem oxygenase

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3
Q

What reduces Fe2+ to Fe3+

A

Vitamin C

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4
Q

How is dietary haem absorbed into enterocytes

A

Via haem carrier protein 1 (HCP 1) and receptor mediated endocytosis

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5
Q

How is the absorption of too much iron prevented

A

Via storage as ferritin molecules in enterocytes (fe 2+ is oxidised to fe 3+ and binds to apoferritin to form a ferritin micelle, this iron is not available for transport in plasma and is lost in the intestinal lumen by shedding of the epithelial cells and excrete in faeces)
And
By action of hepcidin - suppresses ferroportin function to decrease iron absorption from enterocyte into blood

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6
Q

How is denaturation of Vit B12 in the stomach avoided

A

Attaches itself to haptocorrin (R protein) which is released in saliva and from parietal cells

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7
Q

Where is the greatest amount of water absorbed

A

Small bowel esp jejunum

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8
Q

Which protein facilitates the transport of Ca2+ through the cytoskeleton of the enterocyte

A

Calbindin

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9
Q

What does the transverse colon hang off the stomach by

A

A wide band of tissue called the greater omentum

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10
Q

Start and end of the ascending colon

A

Caecum to hepatic flexure

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11
Q

Blood supply of the transverse colon

A

Proximal transverse colon - mid colic artery (a branch of the superior mesenteric artery) COLIC NOT COLONIC
Distal 1/3 transverse colon - inferior mesenteric artery
The space between them is not very well perfused so is vulnerable to ischaemia

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12
Q

Function of taeniae coli

A

Facilitate large intestine motility

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13
Q

What are the lymphoid tissues in the walls if the small intestine and in the large intestines

A

Small intestine - layers patches

Large intestine - solitary nodules

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14
Q

How does the rectum differ from the colon

A

Has transverse recital folds in its submucosa

Has no taeniae coli in its muscularis extrema

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15
Q

Does the large bowel have villi

A

No

But the enterocytes have small irregular microvilli for the absorption of water and ions

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16
Q

Describe the contractions of the proximal colon, and the transverse and descending colon

A

Proximal colon = antipropulsive patterns, retain the chyme form allow more time for absorption of water and electrolytes
Transverse and descending colon = local segmental contractions of circular muscle - haustral contractions, allow back and forth mixing to occur

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17
Q

3 types of imaging for pancreas

A

CT scan
MRCP (magnetic resonance cholangio pancreatography)
Angiography (dye in arteries)

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18
Q

What does the coeliac axis/artery split into

A

Left gastric artery
Splenic artery
Common Hepatic artery

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19
Q

Difference between a endocrine and exocrine secretions in the pancreas

A

In general, endocrine is ductless gland secretion into the blood to act on distant target
Exocrine is secretion from gland into a duct to have a direct local effect

In pancreas, endocrine has a glucose regulatory and growth effects function (insulin, glucagon and somatostatin from islets). 2% of pancreatic secretions
Exocrine has a digestive function, secrets pancreatic juices into main pancreatic duct. 98% of pancreatic secretions

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20
Q

Are there more islets at the tail or head of pancreas

A

Tail

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21
Q

What do acinar cells secrete into ducts in pancreas

A

Pro enzymes

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22
Q

Why are the islets highly vascular

A

To ensure all the endocrine cells (alpha, beta, delta) have closed access to a site for secretion

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23
Q

Describe the pancreatic micro anatomy of an acinus

A

Small pancreatic ducts are surrounded by cells.
Closest to them are a few centroacinar cells, then as you go further out there is a cluster of lost of acinar cells
Intracellular Canaliculi separate the acinar cells and drain into the pancreatic duct
The pancreatic duct then gets larger as it moves away from the acinus, and becomes an intercalated duct
This then joins to form an intralobular duct which later joints with the main pancreatic duct

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24
Q

What are enzymes of the pancreatic acinar cells synthesised and stored in

A

Zymogen molecules - stores of pro enzymes

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25
What converts tripsinogen to trypsin and where is it released
Enterokinase | Secreted by duodenal mucosa
26
What is the role of trypsin
Converts all proteases and some lipases into their active form NB: lipases are already secrete in active form but need to be bound to colipase which is secreted in its precursor inactive form (Lipase also needs bile to work)
27
How does pancreas protect itself against auto digestion and how can these protective mechanisms be overcome
Proteases are secreted in their inactive precursor form Enzymes only become active when they reach the duodenum Pancreas also secrets a trypsin inhibitor Blockage of the main pancreatic duct can overcome these and cause auto digestion and acute pancreatitis
28
Anti obesity drug orlistat inhibits pancreatic lipases. What side effects might you expect and where else could you see these affects
Can’t digest lipids So more lipids enter faces Get fatty stool - steatorrhea Also see this is people with cystic fibrosis and chronic pancreatitis as they also have problems producing pancreatic enzymes such as lipases
29
How do pancreatic enzyme secretions and diet relate
Secretions adapt to your diet Eg if you eat more carbs and less proteins Your pancreas secretes more amylase and less protease
30
What happens if you have a lack of pancreatic enzymes and bile but good dietary input
``` You get malnourished Pancreatic enzymes (and bile) are essential for digestion, unlike gastric and salivary enzymes ```
31
Which molecules stimulate and inhibit production of cholecystokinin from duodenal I cells
Amino acids and fatty acids stimulate CCK production | Trypsin inhibits CCK production
32
What controls enzymatic pancreatic juice secretion
``` Vagus nerve (cholinergic) Cholecystokinin hormone (CCK) ```
33
What controls bicarbonate pancreatic juice secretion
Secretin hormone
34
Describe the control of bicarbonate secretion in pancreatic ducts
``` Decrease in duodenal pH Stimulates S cells S cells produce secretin Secretin causes pancreas to secrete bicarbonate rich fluid Increase in duodenal pH ```
35
What is the effect of CCK on bicarbonate pancreatic secretion
Has no effect on its own But when combined with secretin, can increase bicarbonate secretion more than if it was just secretin alone Vagus nerve has a similar effect (But secretin has NO EFFECT on enzyme secretion)
36
What is the innervation of the villi from
The submucosal plexus
37
What cells line the villi
Mostly enterocytes | But also have scattered goblet cells and enteroendocrine cells
38
What cells are found in the crypts
Paneth cells and stem cells
39
What is the brush border made of
Microvilli covered with glycocalyx
40
Describe distribution of goblet cells in the bowel
Increases along the length in the bowel - more in colon (bc of hard solidified contents, needs more lubrication)
41
Roel of enteroendocrine cells
Secret hormones to regulate gut motility
42
What is the role of paneth cells and where are they found
Found only at the base of the crypts of villi Contain large acidophilic granules Granules contain - antibacterial enzyme lysozymes (protects stem cells) - glycoproteins - zinc (essential trace metal for the function of many enzymes) Engulfs some bacteria and Protozoa May have a role in regulating intestinal flora
43
What can radiation cause in small intestine
Can cause impaired production of new cells (stem cells in the crypts) so erythrocytes lining the villi can’t be replaced. This is very bad as erythrocytes have a rapid turnover and short life span So you get severe intestinal dysfunction
44
Why do erythrocytes and goblet cells lining the villi have very short life spans
They are the first line of defence against GI pathogens and may be directly affected by toxic substances from the food you ingest Their rapid turnover means that the effects are less likely to be able to spread to rest of body and also means that lesions and DNA damage for example, as short lived
45
How is duodenum distinguished from the ileum and jejunum
Has Brunners glands which secret alkaline fluid Neutralises acidic chyme - protects duodenal lining - provides optimum ph for pancreatic enzymes to work
46
What does pancreatic amylase need for optimum activity
Cl- | And a neutral or slightly alkaline pH
47
How do enterocytes directly absorb small peptides/oligopeptides
H+/oligopeptide cotransporter PepT1
48
Role of colipase
Prevents bile salts displacing lipase from fat droplets
49
Role of ileocecal valve
Prevents backflow of bacteria into ileum
50
Describe lipid digestion and absorption
1) secretion of bile and pancreatic enzymes (lipases) 2) emulsification 3) hydrolysis of ester linkages breaking triglycerides into monoglycerides and fatty acids by lipase bound to colipase (colipase prevents the bile salts removing lipase from the fat droplet) 4) solubilisation of lipolytic products by formation of the monoglycerdeis and fatty acids into a bile salt micelle 5) fatty acids and monoglycerides leave micelle and enter enterocyte 6) triglyceride is re synthesised in enterocyte by major pathway (monoglyceride acylation) or minor pathway (phosphatidic acid pathway) 7) formation of chylomicrons in Golgi 8) chylomicrons leave cell by exocytosis across basement membrane and enter lacteals of lymphatic system
51
Symptoms of acute pancreatitis
Epigastric pain - radiating to back, lean forward to relieve pain Nausea and vomiting Fever
52
Clinical signs of acute pancreatitis
Haemodynamic instability - perfusion failure: tachycardia and hypotension Peritonism - inflammation of the peritoneum, abdomen is tender on examination Seen in haemorrhagic acute pancreatitis: Grey turners sign - bruising on sides - between lower rip and top of hip Cullens sign - brushing around the umbilicus
53
3 types of acute pancreatitis
Haemorrhagic pancreatitis Oedematous pancreatitis Necrotic pancreatitis
54
3 other differential diagnoses for acute pancreatitis
Gall stone disease or associated complications Peptic ulcer or perforation (can puncture pancreas) Leaky/ruptured aortic aneurysms (aorta is behind pancreas so can push on it and rip it)
55
4 principles of management of acute pancreatitis
Fluid resuscitation: IV fluids, urinary catheter, strict fluid balance monitoring using central venous pressure lines Analgesia Pancreatic rest (nutritional support: NJ (nasojejunum) or TNP (total parenteral nutritional), bypass pancreas and GI tract) Determine the underlying cause
56
When are antibiotics used for acute pancreatitis
If necrotic tissue becomes infected
57
List some systemic complications of acute pancreatitis
Hypocalcaemia Hyperglycaemia SIRS (systemic inflammatory response syndrome) ARF (acute renal failure) DIC (disseminated intravascular coagulation) ARDS (adult respiratory distress syndrome) MOF (multi organ failure) and death
58
List some local complications of acute pancreatitis
Pancreatic abscess Pancreatic pseudo cyst Pancreatic necrosis (could become infected necrosis too) Bleeding: small vessel= haemorrhagic pancreatitis (Cullen’s or grey turners sign), large vessel = life threatening bleed Thrombosis Chronic pancreatitis
59
Management of infected necrosis (in pancreatitis)
Antibiotics and percutaneous drainage
60
What is a pancreatic pseudocyst
Peri-pancreatic fluid collection within a fibrous capsule (real cyst has epithelial capsule) Arises 6 weeks after pancreatitis
61
What is the management of a pancreatic pseudo cyst
Most resolve by themselves after 6 months But if 1) it’s symptomatic (causing pain) Or 2) it’s compressing structures around it Or 3) it’s infected Then you drain it 1) percutaneously: through skin Or 2) endoscopically: insert stent between stomach and cyst, so cyst drains into stomach (best option) Or 3) surgery, open/laparoscopically: pseudocystgastrostomy (hole between stomach and cyst pseudocystjejunostomy (drain into jejunum)
62
What 2 conditions can chronic pancreatitis cause
IDDM: insulin dependent diabetes mellitus (type 1 diabetes) | Steatorrhea
63
Describe briefly chronic pancreatitis pathophysiology
Alcohol abuse causes increase in proenzyme concentration and calcium salt precipitation Proenzyme concentration increase causes protein plug formation Protein plug formation and calcium salt precipitation cause calcium deposition Calcium deposition causes epithelial lesions Epithelial lesions causes enzyme activation
64
3 ways to intervene to treat chronic pancreatic
Endoscopic management: take out or crush the gall stone Surgical drainage: stitch part of bowel onto pancreas so pancreatic juices drain into bowel Surgical resection: total or partial taking out of pancreas
65
How does a radiologists provide the radiological tumour stage
Using the TNM system T = size of tumour N = lymph node involvement M = metastases
66
What does the pathologist do in GI cancer MDT
diagnose the cancer Do histology typing - see what cells the cancer is eg glandular cells, adenocarcinoma Do molecular typing - see what mutations the cancer cells have, helps to decide which treatment is best Determine the tumour grade - how aggressive the tumour is
67
What are the 2 types of oesophageal cancers
Squamous cell carcinoma = upper 2/3 of oesophagus | Adenocarcinoma = lower 1/3 of oesophagus, when squamous cells become columnar, associated with acid reflux
68
Most common symptom of oesophageal cancer
Dysphagia (difficulty swallowing)
69
Why are most patients with oesophageal cancer deemed unfit for the surgery
Because they are malnourished, the tumour blocked their oesophagus making it difficult for them to eat
70
Describe how oesophageal cancer arises
30% of uk population has oesophagitis (inflammation of oesophageal lining) due to GORD (gastro oesophageal reflux disease) 5% of these people will develop Barrett’s oesophagus This metaplasia can become dysplastic 0.5%-11% of people with Barrett’s oesophagus will develop an adenocarcinoma
71
How is oesophageal cancer diagnosed and staged
Diagnosis: upper GI endoscopy, if lesion is found do a biopsy (pathologist will diagnose) Staging: chest and abdomen CT scan, PET-CT scan, laparoscopy, ultrasound (sees of has metastasised to lymph nodes)
72
Treatment options for oesophageal cancer
Is the patient fit enough to undergo treatment? Is the cancer treatable? Yes: treat radically/with curative intent - neoadjuvent chemotherapy - surgery No: palliative therapy - palliative chemotherapy - steroid to reduce oedema around tumour - oesophageal stent
73
Causes of gastric cancer
Main cause = chronic gastritis (inflammation of stomach lining) Due to - H pylori infected - causes chronic acid overproduction - pernicious anaemia - auto antibodies against the parietal cells - parietal gastrectomy - distal part of stomach (including pylorus) is removed and some bowel is stitched there, but this causes pancreatic and biliary juice to flow into the stench which is going to cause irritation - Epstein Barr virus - Family history - High salt diet - Smoking
74
Most common symptom of gastric cancer
Dyspepsia (upper abdominal discomfort after eating or drinking)
75
What are the red flags to look our for about gastric cancer
ALARMS55 Anaemia Loss of weight or appetite Abdominal mass upon examination Recent progressive onset of symptoms Melaena (black smelly faeces, has blood from upper GI which ash been digested) or Haematemesis (blood in vomit) Swallowing difficulty (dysphagia) 55 years or older
76
Diagnosis and staging of gastric cancer
``` Diagnosis: endoscopy and biopsy Staging: CT of chest, abdomen and pelvis PET-CT scan Laparoscopy Ultrasound ```
77
What treatments could you recommend to someone with type 2 diabetes
Glucose lowering medication (metformin, gliclazide) Weight loss Lifestyle changes
78
3 possible consequences if type 2 diabetes is left untreated
Retinopathy Nephropathy Foot ulcers
79
Treatments for gastro oesophgeal reflux disease
Protein pump inhibitor (omeprazole, lansoprazole) H2 receptor blocker (ranitidine) Somatostatin analogues
80
Exercise tolerance test?
Incremental exercise bike/treadmill test to precipitate symptoms as a diagnostic tool

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