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Gastrointestinal System > Week 2 > Flashcards

Week 2 Flashcards

1
Q

what do mucus neck cells of the stomach secrete?

A

Mucus

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2
Q

what do chief cells secrete?

A

pepsinogens

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3
Q

what do parietal cells secrete?

A

HCl
Intrinsic factor

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4
Q

what is the pH of the stomach lumen?

A

pH < 2

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5
Q

what are the three phases that cause the gastric mucosa to secrete gastric juice?

A

cephalic phase
gastric phase
intestinal phase

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6
Q

what happens in the cephalic phase (1st phase of gastric secretion)?

A

occurs before food enters the stomach and is stimulated by the sight, smell, thought or taste of food.

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7
Q

what happens during the gastric phase (2nd phase of gastric secretion)?

A

the gastric phase stimulates gastric activity by stretching the stomach and raising the pH of its contents which leads to the release of HCl by the parietal cells.

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8
Q

what happens during the intestinal phase (3rd phase of gastric secretion)?

A

intestinal phase is stimulated by stretching of the duodenum due to chyme entering from the stomach.

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9
Q

what factors increase HCl secretion?

A

vagal stimulation (neurocrine)
gastrin (endocrine)
histamine (paracrine)

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10
Q

what factors decrease HCl production?

A

sympathetic nervous system e.g. anxiety
low gastric pH
CCK
gastric inhibitory peptide
secretin
proton pump inhibitors e.g. omeprazole
H2 receptor antagonists
ACh receptor antagonists

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11
Q

what are enterogastrones? and give examples.

A

hormones released from gland cells in duodenal mucosa.
e.g. secretin, cholecystokinin (CCK), GIP.

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12
Q

What stimulated the release of enterogastrones?

A

acid
hypertonic solutions
fatty acids
monoglycerides

in duodenum

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13
Q

what is the function of enterogastrones in gastric secretion?

A

act collectively to prevent further acid build up in the duodenum by either:

  • inhibiting gastric secretion.
  • reducing gastric emptying (inhibit motility/contract pyloric sphincter).
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14
Q

what is the inactive form of pepsinogen?

A

zymogen

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15
Q

what happens to pepsinogen at a low pH < 3.

A

pepsinogen > pepsin.

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16
Q

describe the cytoprotective role of gastric mucus.

A
  • protects mucosal surface from mechanical injury.
  • gastric mucus has a neutral ph (HCO3) protects against gastric acid corrosion and pepsin digestion.
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17
Q

describe why the production of intrinsic factore is an essential function of the stomach.

A

required for vitamin B12 absorption.
intrinsic factor/B12 complex absorbed from ileum

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18
Q

function of pepsin?

A

enzyme involved in protein digestion

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19
Q

control of pepsinogen secretion follows the same process as

A

HCl secretion

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20
Q

what part of the stomach has the most gastric motility?

A

antrum
peristaltic waves from body > antrum

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21
Q

what does the antrum do?

A

thick muscle > powerful contraction
Mixing
Contraction of pyloric sphincter:
- only small amounts of chyme entering duodenum.

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22
Q

what generates peristaltic rhythm?

A

pacemaker cells (longitudinal muscle layer).

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23
Q

what is the effect of gastrin on motility?

A

increases contraction

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24
Q

what is the effect of distension of the stomach wall on motility?

A

increase contraction

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25
Q

what is the effect of fatr/acid/amino acid/hypertonicity in duodenum on motility?

A

inhibiton of motility

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26
Q

how is acid in the duodenum neutralised?

A

bicarbonate (HCO3) secretion from Brunner’s gland duct cell (submucosal glands).

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27
Q

what does acid in the duodenum trigger?

A
  • long (vagal) and short (ENS) reflexes > HCO3 secretion.
  • release of secretin from S cells > HCO3 secretion.
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28
Q

what does secretin do?

A

stimulates HCO3 secretion from pancreas and liver

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29
Q

describe the negative feedback control mechanism in secretin release.

A

acid in duodenum > secretin release
acid neutralisation > inhibits secretin release

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30
Q

describe the endocrine portion of the pancreas and its function

A

islets of Langerhans:
- produce insulin, glucagon and somatostatin.

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31
Q

describe the anatomical structure of the exocrine pancreas.

A

acinar cells > ducts > pancreatic ducts.

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32
Q

what is the function of the exocrine pancreas? what cells are involved?

A

responsible for digestive function of pancreas:
- secretion of bicarbonate by duct cells.
- secretion of digestive enzymes by acinar cells.

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33
Q

label this portion of pancreas

A
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34
Q

what are zymogens and what is their function

A

digestive enzyme in inactive form.
stored as zymogen to prevent autodigestion of pancreas.

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35
Q

how is trypsin activated?

A

an enterokinase catalyses the conversion of trypsinogen to trypsin.

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36
Q

what enzyme activates zymogens?

A

trypsin

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37
Q

del

A

del

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38
Q

control of pancreatic function

A
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39
Q

control of pancreatic function

A
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40
Q

control of pancreatic function

A
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41
Q

control of pancreatic function

A
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42
Q

control of pancreatic function

A
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43
Q

control of pancreatic function

A
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44
Q

control of pancreatic function

A
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45
Q

control of pancreatic function

A
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46
Q

control of pancreatic function

A
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47
Q

control of pancreatic function

A
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48
Q

control of pancreatic function

A
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49
Q

control of pancreatic function

A
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50
Q

what is the pathology of oesophageal reflux?

A
  • reflux of gastric acid into osophagus - hiatus hernia.
  • thickening of squamous epithelium.
  • ulceration of oesophageal epithelium when severe reflux.
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51
Q

what are complication of oesophageal reflux?

A

fibrosis:
- stricture formation.
- impaired motility.
- obstruction.

Barrett’s oesophagus.

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52
Q

what is Barrett’s oesophagus?

A
  • a type of metaplasia caused by the transformation from squamous epithelium to glandular epithelium. - pre-malignant condition.
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53
Q

what is the 3rd most common cancer of alimentary tract?

A

oesophageal cancer

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54
Q

what are the two histological types of oesophageal cancer?

A
  • squamous carcinoma.
  • adenocarcinoma (develops from Barrett’s oesophagus).
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55
Q

what are risk factors from each type of oesophageal cancer?

A

squamous carcinoma:
- smoking.
- alcohol.
- dietary carcinogens.

adenocarcinoma:
- Barrett’s metaplasia.
- Obesity.

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56
Q

what are some local effects of oesophageal cancer?

A

obstruction
ulceration
perforation

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57
Q

what are ways in which oesophageal cancer can spread?

A

direct:
- to surrounding tissues.

lymphatic spread:
- to regional lymph nodes.

blood spread:
- liver.

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58
Q

what is the prognosis of oesophageal cancer?

A

very poor
- 5 year survival rate less than 15%.

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59
Q

Types of gastritis pathology (ABC ACRONYM).

A
  • autoimmune (type A).
  • bacterial (type B).
  • chemical injury (type C).
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60
Q

describe autoimmune gastritis.

A
  • organ-specific autoimmune disease.
  • autoantibodies to parietal cells and intrinsic factor.
  • associated with other autoimmune diseases.
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61
Q

pathology of autoimmune gastritis

A
  • auto-antibodies that react to parietal cells and intrinsic factor.
  • causes chronic inflammation.
  • decreased acid secretion.
  • loss of intrinsic factor > vitamin B12 deficiency (pernicious anaemia).
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62
Q

what is the most common type of gastritis?

A

bacterial gastritis.

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63
Q

what bacteria is implicated in bacterial gastritis?

A

helicobacter pylori

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64
Q

describe helicobacter pylori, where its found and its effects in bacterial gastritis.

A
  • gram negative bacerium.
  • found in gastric mucus on surface of gastric epithelium.
  • produces acute and chronic inflammatory response.
  • increased acid production.
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65
Q

what causes chemical gastritis and how does it differ in appearance.

A

drugs - NSAIDs
alcohol
bile reflux.

no inflammation, no organisms. Corkscrewing (reactive features).

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66
Q

what causes peptic ulceration?

A

an imbalance beween acid secretion and mucosal barrier.

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67
Q

what areas can peptic ulceration affect?

A

lower oesophagus
body and antrum of stomach
first and second parts of duodenum

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68
Q

what are peptic ulcers usually associated with?

A

H. pylori > increased gastric acid.

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69
Q

complications of peptic ulceration

A

bleeding:
- acute = haemorrhage.
- chronic = anaemia.

perforation > peritonitis

healing by fibrosis > obstruction

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70
Q

what is the second most common cancer of the alimentary tract?

A

stomach cancer

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71
Q

how does stomach cancer developed and what is it associated with?

A

develops through phases of intestinal metaplasia and dysplasia (in stomach).
associated with previous H.pylori infection.

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72
Q

what type of cancer is stomach cancer?

A

adenocarcinoma.

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73
Q

describe the different ways stomach cancer can spread

A
  • direct > surrounding tissues.
  • lymphatic.
  • blood > liver.
  • transcoelomic spread . within peritoneal cavity.
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74
Q

what is the prognosis of stomach cancer?

A

5 year survival rate less than 20%

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75
Q

what is a hiatus hernia

A

when part of the stomach squeezes up into the chest through an opening (‘hiatus’) in the diaphragm.

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76
Q

what are the functions of the liver?

A

protein synthesis
metabolism of fat and carbs
detoxification of drugs and toxins including alcohol

77
Q

what is liver failure a complication of?

A

acute liver injury
chronic liver injury i.e. cirrhosis

78
Q

what are some causes of acute liver injury?

A

hepatitis:
- viruses
- alcohol
- drugs

bile duct obstruction

79
Q

what is the pathology of viral hepatitis?

A

-inflammation of the liver.
-liver cell damage and death of individual liver cells.

80
Q

discuss the three outcomes of acute inflammation caused by viral hepatitis

A
  • resolution > liver returns to normal (hepatitis A, E).
  • liver failure if severe damage to liver (Hepatitis A, B, E).
  • progression to chronic hepatitis and cirrhosis (Hepatitis B, C).
81
Q

discuss the changes to the liver in alcoholic liver disease

A
  • fatty change.
  • alcoholic hepatitis > acute inflammation, liver cell death and liver failure.
  • progress to cirrhosis.
82
Q

what is jaundice and how is it caused?

A
  • increased circulating bilirubin.
  • caused by altered metabolism of bilirubin.
83
Q

discuss the pre-hepatic pathway of bilirubin metabolism.

A
  • occurs due to haemolysis.
  • breakdown of haemoglobin in spleen to form haem and globin.
  • haem converted to bilirubin in liver.
  • release of bilirubin into circulation.
84
Q

discuss the hepatic pathway of bilirubin metabolism

A
  • uptake of bilirubin by hepatocytes.
  • conjugation of bilirubin in hepatocytes.
  • excretion of conjugated bilirubin into biliary system.
85
Q

discuss the post-hepatic pathway of bilirubin metabolism.

A
  • transport of conjugated bilirubin in biliary system.
  • breakdown of bilirubin conjugate in intestine.
  • reabsorption of bilirubin > entero-hepatic circulation of bilirubin.
86
Q

what are the three classes of jaundince?

A

pre-hepatic
hepatic
post-hepatic

87
Q

describe pre-hepatic jaundice blood

A

high levels of unconjugated bilirubin present in the blood which is not water soluble so cannot enter the urine

88
Q

what are hepatic causes of jaundice?

A

cholestasis.
intra-hepatic bile obstruction.

89
Q

what is cholestasis?

A

Cholestasis is defined as a decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow through intra-or extrahepatic bile ducts.

  • accumulation of bile within hepatocytes of bile canaliculi.
90
Q

what are causes of cholestasis?

A

viral hepatitis
alcoholic hepatitis
liver failure
drugs > therapeutic and recreational.

91
Q

what can cause intra-hepatic bile duct obstruction?

A
  • primary biliary cholangitis.
  • primary sclerosing cholangitis.
  • tumours of liver.
92
Q

del

A

del

93
Q

describe the pathology of primary biliary cholangitis

A
  • autoimmune disease
  • granulomatous inflammation and scarring involving bile ducts.
  • loss of intra-hepatic bile ducts.
  • progression to cirrhosis.
94
Q

what is the pathology of primary sclerosing cholangitis

A
  • chronic inflammation and fibrous obliteration of bile ducts.
  • loss of intra-hepatic bile ducts.
  • associated with inflammatory bowel disease.
95
Q

describe complications of primary sclerosing cholangitis

A
  • progression to cirrhosis
  • increased risk of developing cholangiocarcinoma.
96
Q

what is hepatic cirrhosis a response to?

A

end stage chronic liver disease > response of liver to chronic injury.

97
Q

causes of cirrhosis

A
  • alcohol.
  • hepatitis B, c.
  • immune mediated liver disease > auto-immune hepatitis, primary biliary cholangitis.
  • metabolic disorders > excess iron or copper.
  • obesity > diabetes mellitus.
98
Q

name of excess iron disorder?

A

primary haemochromatosis

99
Q

name of excess copper disorder?

A

Wilson’s disease

100
Q

pathology of cirrhosis

A

diffuse process involving whole liver.
- loss of normal liver structure.
- replaced by nodules of hepatocytes and fibrous tissue.

101
Q

complications of cirrhosis

A
  • liver failure.
  • portal hypertension.
  • increased risk of hepatocellular carcinoma.
102
Q

what is hepatocellular carcinoma?

A

malignant tumour of hepatocytes

103
Q

what is a cholangiocarcinoma?

A

malignant tumour of bile duct epithelium

104
Q

causes of post-hepatic jaundice?

A
  • cholelithiasis (gall stones).
  • diseases of gall bladder.
  • extra-hepatic duct obstruction.
105
Q

risk factors for gallstones?

A

obesity
diabetes

106
Q

pathology of gallstones

A

inflammation:
- acute cholecystitis
- chronic cholecystitis

107
Q

pathology of acute cholecystitis

A
  • acute inflammation of gall bladder:
    > empyema : perforation of gallbladder, biliary peritonitis.
  • progression to chronic inflammation.
108
Q

what is chronic cholecystitis?

A

chronic inflammation and fibrosis of gall bladder

109
Q

causes of common bile duct obstruction

A
  • gallstones.
  • tumours of bile duct.
  • benign stricture.
  • external compression (tumours).
110
Q

effects of common bile duct obstruction

A
  • jaundice
  • no bile excreted into duodenum.
  • ascending cholangitis.
  • secondary biliary cirrhosis if prolonged.
111
Q

what nerve controls peristalsis of oesophagus and relaxation of the LOS?

A

vagus nerve

112
Q

what causes gastro-oesophageal reflux disease (GORD)?

A

persistent reflux and heartburn.

113
Q

symptoms of dysphagia

A

subjective sensation of difficulty in swallowing food.
- may also be accompanied by odynophagia > pain with swallowing.

114
Q

what are the different causes of oesophageal dysphagia?

A
  • benign stricture
  • malignant stricture
  • motility disorders (e.g. achalasia, presbyoesophagus)
  • eosinophilic oesophagitis
  • extrinsic compression (e.g. in lung cancer).
115
Q

what carcinoma affects the top of the oesophagus?

A

squamous carcinoma

116
Q

what carcinoma affects the bottom of the oesophagus?

A

adenocarcinoma

117
Q

dysphagia or reflux symptoms with alarm features investigation?

A

endoscopy:
- oesophago-gastro-duodenoscopy (OGD).
- upper GI endoscopy (UGIE).

118
Q

when would a barium swallow (contrast radiology) be used?

A

primary indication is investigation of dysphagia (however endoscopy is preferred test).
- can exclude pharyngeal pouch or post-cricoid web prior to endoscopy.

119
Q

refractory heartburn/reflux investigation?

A

pH-metry
- nasal catheter containing pH sensors at both sphincter (UOS and LOS) placed in oesophagus to measure pH levels over a period of time.

120
Q

what is manometry and when is it used?

A

nasal catheter containing multiple pressure sensors placed in oesophagus.

  • used in investigation of dysphagia/suspected motility disorder (usually after endoscopy). ACHALASIA!!!
121
Q

what does manometry assess?

A
  • sphincter tonicity, relaxation of sphincters and oesophageal motility.
122
Q

oesophageal hypermotility symptom

A
  • severe, episodic chest pain +/- dysphagia.
123
Q

what is the appearance of oesophageal hypermotility on Ba swallow?

A

‘corkscrew appearance’.

124
Q

what does manometry of oesophageal hypermotility show?

A

exaggerated, uncoordinates, hypertonic contractions.

125
Q

what are symptoms of oesophageal hypomotility?

A
  • heartburn and reflux due to failure of LOS mechanism.
126
Q

what conditions is oesophageal hypomotility associated with?

A
  • connective tissue disease.
  • diabetes.
  • neuropathy.
127
Q

what is achalasia?

A

Achalasia is a rare neuromuscular disorder of the oesophagus characterized by the inability of the lower oesophageal sphincter (LES) to relax, often resulting in difficulty swallowing and other associated symptoms.

128
Q

signs and symptoms of achalasia?

A

Dysphagia – usually has a gradual onset, over a period of months to years
Regurgitation of undigested food
Aspiration pneumonia (secondary to regurgitation)
Retrosternal chest pain or heartburn – often unresponsive to proton pump inhibitors (PPI)
Weight loss – typically mild but can be severe in advanced cases

129
Q

manometry results in achalasia

A
  • high pressure LOS at rest.
  • failure of the LOS to relax after swallowing.
  • an absence of peristaltic contractions in the lower oesophagus.
130
Q

treatment of achalasia? (pharmacological, endoscopic, radiological, surgical)

A

-pharmacological: nitrates, CCBs.
-endoscopic: botulinum toxin pneumatic balloon dilation.
-radiological: pneumatic balloon dilation.
-surgery: myotomy, oesophageal dilation.

131
Q

complications of achalasia?

A

aspiration pneumonia and lung disease.
increased risk of squamous cell oesophageal carcinoma.

132
Q

GORD symptoms?

A

heartburn
cough
water brash (excessive saliva mixes with stomach acids and gives a foul taste in the mouth)
sleep disturbance

133
Q

GORD risk factors

A

pregnancy
obesity
drugs lowering LOS pressure
smoking
alcoholism
hypomotility

134
Q

what are the alarm features of GORD in which endoscopy should be performed?

A

dysphagia
weight loss
vomiting

135
Q

GORD aetiology

A

GORD is caused by a defective lower oesophageal sphincter, which enables the reflux of gastric contents into the oesophagus.

136
Q

GORD aetiology due to hiatus hernia

A

anatomical distortion of the OG junction

137
Q

GORD pathophysiology

A
  • mucosa exposed to acid-pepsin and bile.
  • increased cell loss and regenerative activity (i.e. inflammation).
  • erosive oesophagitis.
138
Q

GORD complications

A
  • ulceration (5%)
  • stricture (8-15%)
  • glandular metaplasia (Barrett’s oesophagus).
  • carcinoma.
139
Q

Barretts oesophagus treatment

A
  • endoscopic mucosal resection (EMR).
  • radio-frequency ablation (RFA).
  • oesophagectomy rarely (mortality 10%).
140
Q

GORD treatment

A
  • lifestyle measures.
    Pharmacological:
  • alginates (gaviscon).
  • H2RA (ranitidine).
  • PPI (omeprazole, lansoprazole).

for refractory disease/symptoms:
- anti-reflux surgery (fundoplication).

141
Q

oesophageal cancer signs and symptoms

A
  • progressive dysphagia.
  • anorexia and weight loss.
  • odynophagia.
  • chest pain.
  • cough.
  • pneumonia.
  • vocal cord paralysis.
  • haematemesis.
142
Q

how is oesophageal cancer diagnosed?

A

endoscopy
biopsy

143
Q

how is oesophageal cancer staged?

A

CT scan
endoscopic US
PET scan
Bone scan

TNM classification

144
Q

oesophageal cancer treatment

A

only potential cure is surgical oesophagectomy +/- adjuvant or neoadjuvant chemotherapy.

palliative care: chemotherapy, radiotherapy etc.

145
Q

describe eosinophili oesophagitis

A

chronic immune/allergen mediated condition defined clinically by symptoms of oesophageal dysfunction by an eosinophilic infiltration of the oesophageal epithelium in the absence of secondary caused of local or systemic eosinophilia,.

146
Q

eosinophilic oesophagitis presentation

A

dysphagia and food bolus obstruction

147
Q

eosinophilic oesophagitis treatment

A
  • topical/swallowed corticosteroids.
  • dietary elimination.
  • endoscopic dilatation.
148
Q

dyspepsia symptoms and duration criteria

A
  • upper abdominal discomfort, retrosternal pain, anorexia, nausea, vomiting, bloating, fullness, early satiety and heartburn.
  • for 4 weeks.
149
Q

what are some upper GI causes of dyspepsia?

A

GORD
peptic ulcer
gastritis
non ulcer dyspepsia
gastric cancer

150
Q

what are red flag symptoms of dyspepsia that should be referred for endoscopy? use ALARMS 55 mnemonic

A
  • Anorexia
  • Loss of weight
  • Anaemia
  • Recent onset or persistent despite treatment.
  • Melaena/haematemesis (GI bleeding) or mass.
  • Swallowing problems - dysphagia.
  • > 55 years old.
151
Q

discuss H.pylori infection

A
  • colonises gastric type mucosa.
  • resides in the surface mucous layer and does not penetrate the epithelial layer.
  • evokes immune response in underlying mucosa - dependent on host genetic factors.
152
Q

what are the clinical outcomes of H.pylori infections?

A
  • asymptomatic or chronic gastritis (>80%).
  • chronic atrophic gastritis and intestinal metaplasia (15-20%).
  • gastric or duodenal ulcer (15-20%).
  • gastric cancer and MALT lymphoma (<1%).
153
Q

describe the difference in responses to chronic H.pylori infection

A

antral predominant gastritis:
- increased acid, low risk of gastric cancer > DU disease.

corpus predominant gastritis:
- decreased acid, gastric atrophy > gastric cancer.

mild mixed gastritis:
- normal acid > no significant disease.

154
Q

how is H.pylori infection diagnosed? NON-INVASIVE METHOD

A

non-invasive:
- serology: IgG against H.pylori.
- 13C/14 labelled CO2 urea breath test.
- stool antigen test- ELISA - need to be off omeprazole for two weeks.

155
Q

how is H.pylori infection diagnosed? INVASIVE METHOD

A

invasive: requires endoscopy
- histology: gastric biopsies stained for the bacteria.
- culture of gastric biopsies.
- rapid slide urease test (CLO) - ammonia (NH3).

156
Q

how are peptic ulcers treated?

A
  • eradication of H.pylori.
  • antacid medication - PPI (omeprazole) or H2 receptor antagonists (ranitidine).
  • NSAID cessation.
157
Q

discuss the eradication of H.pylori infection

A

Triple therapy for 7 days:
- clarithromycin 500mg bd.
- Amoxycillin 1g bd or Metronidazole 400mgbd.
- in case of penicillin allergy > tetracycline.
- PPI e.g. omeprazole 20mg bd.

158
Q

what are symptoms and signs of gastric outlet obstruction?

A
  • vomiting > lacks bile, fermented foodstuffs.
  • early satiety.
  • abdominal distension.
  • weight loss.
  • dehydration.
  • metabolic alkalosis.
159
Q

how is gastric outlet obstruction treated?

A

endoscopic balloon dilation
surgery

160
Q

what are treatment options for oesophageal cancer when it is metastatic and the patient is unfit?

A
  • stenting.
  • palliative radiotherapy.
  • palliative chemotherapy.
161
Q

what are treatment options for oesophageal cancer that is resectable and the patient is fit?

A
  • oesophagectomy + chemotherapy > 5 year survival approx 45%.
    or
  • chemo/radiotherapy > 5 year survival approx 30%.
162
Q

what happens in oesophagectomy?

A
  • the cancerous part of the oesophagus is removed and the stomach is pulled up into the chest and reattached to the remaining oesophagus.
163
Q

what are modifiable risk factors in stomach cancer?

A
  • infection with H.pylori.
  • alcohol.
  • smoking.
  • excessive consumption of salted fish, pickled vegetables and cured meats.
164
Q

what are surgery options for gastric cancer?

A

subtotal gastrectomy - portion of stomach removed.

total gastrectomy and Roux en Y reconstruction - whole stomach removed and eosophago-jejunostomy perfomed.

165
Q

when is bariatric surgery for obesity indicated?

A

BMI:
- 35 - 39.9 obese
- >/= 40 morbidly obese

166
Q

where is the liver located?

A

upper right quadrant of abdomen.
right hypochondriac region

167
Q

what is found in the portal triad of the liver?

A

Porta:
- hepatic artery.
- hepatic portal vein.
- hepatic duct (bile duct).

168
Q

what are the four lobes of the liver called?

A

right
left
quadrate
caudate

169
Q

what are the parenchymal cells of the liver called?

A

hepatocytes

170
Q

what are the non- parenchymal cells of the liver called?

A

LSEC, HSC, Kupffer cells, pit cells.

171
Q

what are the cholangiocytes of the liver called?

A

biliary epithelial cells.

172
Q

label this hepatic lobule

A
173
Q

label this hepatic lobule

A
174
Q

what are the six components of bile?

A

bile acids
lecithin
cholesterol
bile pigments (bilirubin)
toxic metals (detoxified in liver)
bicarbonate (neutralization of acid chyme), secreted by duct cells

175
Q

why are faeces brown?

A

bilirubin modified by bacterial enzymes > brown pigments

176
Q

pathway of bile salts movement

A

liver > bile duct > duodenum > ileum > hepatic portal vein > liver etc.

177
Q

describe the gallbladder

A

saclike structure on interior surface of liver.

178
Q

what is the function of the sphincter of oddi?

A

controls release of bile and pancreatic juice into duodenum.

179
Q

give the sequence of events in bile secretion from gallbladder.

A
  • sphincter of oddi contracted (closed) > bile forced back into gallbladder.
  • fat in duodenum > release of CCK.
  • CCK > relaxation of sphincter of oddi and gallbladder contraction.
  • discharge of bile into duodenum > fat solubilisation.
180
Q

role of CCK in digestion

A

inhibits gastric emptying
stimulates pancreatic enzyme secretion and bile secretion

181
Q

role of secretin in neutralisation

A
  • decreases gastric acid secretion
  • decreases gastric emptying
  • increases duodenal, pancreatic and bile duct HCO3 secretion.
182
Q

what does this barium swallow show?

A

achalasia > can see failure of oesophageal sphincter relaxation

183
Q

what is ascending cholangitis?

A

Ascending cholangitis is a severe, acute infection and inflammation of the biliary tree, often resulting from a blockage that facilitates bacterial ascent from the duodenum.

184
Q

what is charcot’s triad?
and Reynold’s pentad?

A

three primary symptoms of ascending cholangitis (charcot’s);
- right upper quadrant pain.
- fever.
- jaundice.

two additional symptoms in severe cases (Reynold’s pentad):
- hypotension.
- mental confusion.

185
Q

what bonds link glucose monomers present in starch and how are they cleaved?

A

beta-1,4 glycosidic bonds
alpha-amylase cleaves the bonds

186
Q

what inhibits gastrin secretion?

A

lowering pH in stomach as gastrin stimulates HCl secretion so this is a negative feedback loop

187
Q

what component of saliva determines its tonicity>?

A

electrolytes

188
Q

what ligament contains the portal triad?

A

hepatoduodenal ligament

Gastrointestinal System (16 decks)

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