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Gastroenterology Flashcards

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
Q

What converts tripsinogen to trypsin and where is it released

A

Enterokinase

Secreted by duodenal mucosa

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26
Q

What is the role of trypsin

A

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)

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27
Q

How does pancreas protect itself against auto digestion and how can these protective mechanisms be overcome

A

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

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28
Q

Anti obesity drug orlistat inhibits pancreatic lipases. What side effects might you expect and where else could you see these affects

A

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

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29
Q

How do pancreatic enzyme secretions and diet relate

A

Secretions adapt to your diet
Eg if you eat more carbs and less proteins
Your pancreas secretes more amylase and less protease

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30
Q

What happens if you have a lack of pancreatic enzymes and bile but good dietary input

A 
You get malnourished
Pancreatic enzymes (and bile) are essential for digestion, unlike gastric and salivary enzymes
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31
Q

Which molecules stimulate and inhibit production of cholecystokinin from duodenal I cells

A

Amino acids and fatty acids stimulate CCK production

Trypsin inhibits CCK production

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32
Q

What controls enzymatic pancreatic juice secretion

A 
Vagus nerve (cholinergic)
Cholecystokinin hormone (CCK)
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33
Q

What controls bicarbonate pancreatic juice secretion

A

Secretin hormone

34
Q

Describe the control of bicarbonate secretion in pancreatic ducts

A 
Decrease in duodenal pH 
Stimulates S cells
S cells produce secretin 
Secretin causes pancreas to secrete bicarbonate rich fluid 
Increase in duodenal pH
35
Q

What is the effect of CCK on bicarbonate pancreatic secretion

A

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
Q

What is the innervation of the villi from

A

The submucosal plexus

37
Q

What cells line the villi

A

Mostly enterocytes

But also have scattered goblet cells and enteroendocrine cells

38
Q

What cells are found in the crypts

A

Paneth cells and stem cells

39
Q

What is the brush border made of

A

Microvilli covered with glycocalyx

40
Q

Describe distribution of goblet cells in the bowel

A

Increases along the length in the bowel - more in colon (bc of hard solidified contents, needs more lubrication)

41
Q

Roel of enteroendocrine cells

A

Secret hormones to regulate gut motility

42
Q

What is the role of paneth cells and where are they found

A

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
Q

What can radiation cause in small intestine

A

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
Q

Why do erythrocytes and goblet cells lining the villi have very short life spans

A

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
Q

How is duodenum distinguished from the ileum and jejunum

A

Has Brunners glands which secret alkaline fluid
Neutralises acidic chyme
- protects duodenal lining
- provides optimum ph for pancreatic enzymes to work

46
Q

What does pancreatic amylase need for optimum activity

A

Cl-

And a neutral or slightly alkaline pH

47
Q

How do enterocytes directly absorb small peptides/oligopeptides

A

H+/oligopeptide cotransporter PepT1

48
Q

Role of colipase

A

Prevents bile salts displacing lipase from fat droplets

49
Q

Role of ileocecal valve

A

Prevents backflow of bacteria into ileum

50
Q

Describe lipid digestion and absorption

A

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
Q

Symptoms of acute pancreatitis

A

Epigastric pain - radiating to back, lean forward to relieve pain
Nausea and vomiting
Fever

52
Q

Clinical signs of acute pancreatitis

A

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
Q

3 types of acute pancreatitis

A

Haemorrhagic pancreatitis
Oedematous pancreatitis
Necrotic pancreatitis

54
Q

3 other differential diagnoses for acute pancreatitis

A

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
Q

4 principles of management of acute pancreatitis

A

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
Q

When are antibiotics used for acute pancreatitis

A

If necrotic tissue becomes infected

57
Q

List some systemic complications of acute pancreatitis

A

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
Q

List some local complications of acute pancreatitis

A

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
Q

Management of infected necrosis (in pancreatitis)

A

Antibiotics and percutaneous drainage

60
Q

What is a pancreatic pseudocyst

A

Peri-pancreatic fluid collection within a fibrous capsule (real cyst has epithelial capsule)
Arises 6 weeks after pancreatitis

61
Q

What is the management of a pancreatic pseudo cyst

A

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
Q

What 2 conditions can chronic pancreatitis cause

A

IDDM: insulin dependent diabetes mellitus (type 1 diabetes)

Steatorrhea

63
Q

Describe briefly chronic pancreatitis pathophysiology

A

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
Q

3 ways to intervene to treat chronic pancreatic

A

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
Q

How does a radiologists provide the radiological tumour stage

A

Using the TNM system
T = size of tumour
N = lymph node involvement
M = metastases

66
Q

What does the pathologist do in GI cancer MDT

A

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
Q

What are the 2 types of oesophageal cancers

A

Squamous cell carcinoma = upper 2/3 of oesophagus

Adenocarcinoma = lower 1/3 of oesophagus, when squamous cells become columnar, associated with acid reflux

68
Q

Most common symptom of oesophageal cancer

A

Dysphagia (difficulty swallowing)

69
Q

Why are most patients with oesophageal cancer deemed unfit for the surgery

A

Because they are malnourished, the tumour blocked their oesophagus making it difficult for them to eat

70
Q

Describe how oesophageal cancer arises

A

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
Q

How is oesophageal cancer diagnosed and staged

A

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
Q

Treatment options for oesophageal cancer

A

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
Q

Causes of gastric cancer

A

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
Q

Most common symptom of gastric cancer

A

Dyspepsia (upper abdominal discomfort after eating or drinking)

75
Q

What are the red flags to look our for about gastric cancer

A

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
Q

Diagnosis and staging of gastric cancer

A 
Diagnosis: endoscopy and biopsy
Staging: CT of chest, abdomen and pelvis
PET-CT scan 
Laparoscopy 
Ultrasound
77
Q

What treatments could you recommend to someone with type 2 diabetes

A

Glucose lowering medication (metformin, gliclazide)
Weight loss
Lifestyle changes

78
Q

3 possible consequences if type 2 diabetes is left untreated

A

Retinopathy
Nephropathy
Foot ulcers

79
Q

Treatments for gastro oesophgeal reflux disease

A

Protein pump inhibitor (omeprazole, lansoprazole)
H2 receptor blocker (ranitidine)
Somatostatin analogues

80
Q

Exercise tolerance test?

A

Incremental exercise bike/treadmill test to precipitate symptoms as a diagnostic tool

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