Week 2 Flashcards
1
Q
what do mucus neck cells of the stomach secrete?
A
Mucus
2
Q
what do chief cells secrete?
A
pepsinogens
3
Q
what do parietal cells secrete?
A
HCl
Intrinsic factor
4
Q
what is the pH of the stomach lumen?
A
pH < 2
5
Q
what are the three phases that cause the gastric mucosa to secrete gastric juice?
A
cephalic phase
gastric phase
intestinal phase
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.
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.
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.
9
Q
what factors increase HCl secretion?
A
vagal stimulation (neurocrine)
gastrin (endocrine)
histamine (paracrine)
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
11
Q
what are enterogastrones? and give examples.
A
hormones released from gland cells in duodenal mucosa.
e.g. secretin, cholecystokinin (CCK), GIP.
12
Q
What stimulated the release of enterogastrones?
A
acid
hypertonic solutions
fatty acids
monoglycerides
in duodenum
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).
14
Q
what is the inactive form of pepsinogen?
A
zymogen
15
Q
what happens to pepsinogen at a low pH < 3.
A
pepsinogen > pepsin.
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.
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
18
Q
function of pepsin?
A
enzyme involved in protein digestion
19
Q
control of pepsinogen secretion follows the same process as
A
HCl secretion
20
Q
what part of the stomach has the most gastric motility?
A
antrum
peristaltic waves from body > antrum
21
Q
what does the antrum do?
A
thick muscle > powerful contraction
Mixing
Contraction of pyloric sphincter:
- only small amounts of chyme entering duodenum.
22
Q
what generates peristaltic rhythm?
A
pacemaker cells (longitudinal muscle layer).
23
Q
what is the effect of gastrin on motility?
A
increases contraction
24
Q
what is the effect of distension of the stomach wall on motility?
A
increase contraction
25
what is the effect of fatr/acid/amino acid/hypertonicity in duodenum on motility?
inhibiton of motility
26
how is acid in the duodenum neutralised?
bicarbonate (HCO3) secretion from Brunner's gland duct cell (submucosal glands).
27
what does acid in the duodenum trigger?
- long (vagal) and short (ENS) reflexes > HCO3 secretion.
- release of secretin from S cells > HCO3 secretion.
28
what does secretin do?
stimulates HCO3 secretion from pancreas and liver
29
describe the negative feedback control mechanism in secretin release.
acid in duodenum > secretin release
acid neutralisation > inhibits secretin release
30
describe the endocrine portion of the pancreas and its function
islets of Langerhans:
- produce insulin, glucagon and somatostatin.
31
describe the anatomical structure of the exocrine pancreas.
acinar cells > ducts > pancreatic ducts.
32
what is the function of the exocrine pancreas? what cells are involved?
responsible for digestive function of pancreas:
- secretion of bicarbonate by duct cells.
- secretion of digestive enzymes by acinar cells.
33
label this portion of pancreas
34
what are zymogens and what is their function
digestive enzyme in inactive form.
stored as zymogen to prevent autodigestion of pancreas.
35
how is trypsin activated?
an enterokinase catalyses the conversion of trypsinogen to trypsin.
36
what enzyme activates zymogens?
trypsin
37
del
del
38
control of pancreatic function
39
control of pancreatic function
40
control of pancreatic function
41
control of pancreatic function
42
control of pancreatic function
43
control of pancreatic function
44
control of pancreatic function
45
control of pancreatic function
46
control of pancreatic function
47
control of pancreatic function
48
control of pancreatic function
49
control of pancreatic function
50
what is the pathology of oesophageal reflux?
- reflux of gastric acid into osophagus - hiatus hernia.
- thickening of squamous epithelium.
- ulceration of oesophageal epithelium when severe reflux.
51
what are complication of oesophageal reflux?
fibrosis:
- stricture formation.
- impaired motility.
- obstruction.
Barrett's oesophagus.
52
what is Barrett's oesophagus?
- a type of metaplasia caused by the transformation from squamous epithelium to glandular epithelium. - pre-malignant condition.
53
what is the 3rd most common cancer of alimentary tract?
oesophageal cancer
54
what are the two histological types of oesophageal cancer?
- squamous carcinoma.
- adenocarcinoma (develops from Barrett's oesophagus).
55
what are risk factors from each type of oesophageal cancer?
squamous carcinoma:
- smoking.
- alcohol.
- dietary carcinogens.
adenocarcinoma:
- Barrett's metaplasia.
- Obesity.
56
what are some local effects of oesophageal cancer?
obstruction
ulceration
perforation
57
what are ways in which oesophageal cancer can spread?
direct:
- to surrounding tissues.
lymphatic spread:
- to regional lymph nodes.
blood spread:
- liver.
58
what is the prognosis of oesophageal cancer?
very poor
- 5 year survival rate less than 15%.
59
Types of gastritis pathology (ABC ACRONYM).
- autoimmune (type A).
- bacterial (type B).
- chemical injury (type C).
60
describe autoimmune gastritis.
- organ-specific autoimmune disease.
- autoantibodies to parietal cells and intrinsic factor.
- associated with other autoimmune diseases.
61
pathology of autoimmune gastritis
- 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).
62
what is the most common type of gastritis?
bacterial gastritis.
63
what bacteria is implicated in bacterial gastritis?
helicobacter pylori
64
describe helicobacter pylori, where its found and its effects in bacterial gastritis.
- gram negative bacerium.
- found in gastric mucus on surface of gastric epithelium.
- produces acute and chronic inflammatory response.
- increased acid production.
65
what causes chemical gastritis and how does it differ in appearance.
drugs - NSAIDs
alcohol
bile reflux.
no inflammation, no organisms. Corkscrewing (reactive features).
66
what causes peptic ulceration?
an imbalance beween acid secretion and mucosal barrier.
67
what areas can peptic ulceration affect?
lower oesophagus
body and antrum of stomach
first and second parts of duodenum
68
what are peptic ulcers usually associated with?
H. pylori > increased gastric acid.
69
complications of peptic ulceration
bleeding:
- acute = haemorrhage.
- chronic = anaemia.
perforation > peritonitis
healing by fibrosis > obstruction
70
what is the second most common cancer of the alimentary tract?
stomach cancer
71
how does stomach cancer developed and what is it associated with?
develops through phases of intestinal metaplasia and dysplasia (in stomach).
associated with previous H.pylori infection.
72
what type of cancer is stomach cancer?
adenocarcinoma.
73
describe the different ways stomach cancer can spread
- direct > surrounding tissues.
- lymphatic.
- blood > liver.
- transcoelomic spread . within peritoneal cavity.
74
what is the prognosis of stomach cancer?
5 year survival rate less than 20%
75
what is a hiatus hernia
when part of the stomach squeezes up into the chest through an opening ('hiatus') in the diaphragm.
76
what are the functions of the liver?
protein synthesis
metabolism of fat and carbs
detoxification of drugs and toxins including alcohol
77
what is liver failure a complication of?
acute liver injury
chronic liver injury i.e. cirrhosis
78
what are some causes of acute liver injury?
hepatitis:
- viruses
- alcohol
- drugs
bile duct obstruction
79
what is the pathology of viral hepatitis?
-inflammation of the liver.
-liver cell damage and death of individual liver cells.
80
discuss the three outcomes of acute inflammation caused by viral hepatitis
- 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
discuss the changes to the liver in alcoholic liver disease
- fatty change.
- alcoholic hepatitis > acute inflammation, liver cell death and liver failure.
- progress to cirrhosis.
82
what is jaundice and how is it caused?
- increased circulating bilirubin.
- caused by altered metabolism of bilirubin.
83
discuss the pre-hepatic pathway of bilirubin metabolism.
- 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
discuss the hepatic pathway of bilirubin metabolism
- uptake of bilirubin by hepatocytes.
- conjugation of bilirubin in hepatocytes.
- excretion of conjugated bilirubin into biliary system.
85
discuss the post-hepatic pathway of bilirubin metabolism.
- transport of conjugated bilirubin in biliary system.
- breakdown of bilirubin conjugate in intestine.
- reabsorption of bilirubin > entero-hepatic circulation of bilirubin.
86
what are the three classes of jaundince?
pre-hepatic
hepatic
post-hepatic
87
describe pre-hepatic jaundice blood
high levels of unconjugated bilirubin present in the blood which is not water soluble so cannot enter the urine
88
what are hepatic causes of jaundice?
cholestasis.
intra-hepatic bile obstruction.
89
what is cholestasis?
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
what are causes of cholestasis?
viral hepatitis
alcoholic hepatitis
liver failure
drugs > therapeutic and recreational.
91
what can cause intra-hepatic bile duct obstruction?
- primary biliary cholangitis.
- primary sclerosing cholangitis.
- tumours of liver.
92
del
del
93
describe the pathology of primary biliary cholangitis
- autoimmune disease
- granulomatous inflammation and scarring involving bile ducts.
- loss of intra-hepatic bile ducts.
- progression to cirrhosis.
94
what is the pathology of primary sclerosing cholangitis
- chronic inflammation and fibrous obliteration of bile ducts.
- loss of intra-hepatic bile ducts.
- associated with inflammatory bowel disease.
95
describe complications of primary sclerosing cholangitis
- progression to cirrhosis
- increased risk of developing cholangiocarcinoma.
96
what is hepatic cirrhosis a response to?
end stage chronic liver disease > response of liver to chronic injury.
97
causes of cirrhosis
- alcohol.
- hepatitis B, c.
- immune mediated liver disease > auto-immune hepatitis, primary biliary cholangitis.
- metabolic disorders > excess iron or copper.
- obesity > diabetes mellitus.
98
name of excess iron disorder?
primary haemochromatosis
99
name of excess copper disorder?
Wilson's disease
100
pathology of cirrhosis
diffuse process involving whole liver.
- loss of normal liver structure.
- replaced by nodules of hepatocytes and fibrous tissue.
101
complications of cirrhosis
- liver failure.
- portal hypertension.
- increased risk of hepatocellular carcinoma.
102
what is hepatocellular carcinoma?
malignant tumour of hepatocytes
103
what is a cholangiocarcinoma?
malignant tumour of bile duct epithelium
104
causes of post-hepatic jaundice?
- cholelithiasis (gall stones).
- diseases of gall bladder.
- extra-hepatic duct obstruction.
105
risk factors for gallstones?
obesity
diabetes
106
pathology of gallstones
inflammation:
- acute cholecystitis
- chronic cholecystitis
107
pathology of acute cholecystitis
- acute inflammation of gall bladder:
> empyema : perforation of gallbladder, biliary peritonitis.
- progression to chronic inflammation.
108
what is chronic cholecystitis?
chronic inflammation and fibrosis of gall bladder
109
causes of common bile duct obstruction
- gallstones.
- tumours of bile duct.
- benign stricture.
- external compression (tumours).
110
effects of common bile duct obstruction
- jaundice
- no bile excreted into duodenum.
- ascending cholangitis.
- secondary biliary cirrhosis if prolonged.
111
what nerve controls peristalsis of oesophagus and relaxation of the LOS?
vagus nerve
112
what causes gastro-oesophageal reflux disease (GORD)?
persistent reflux and heartburn.
113
symptoms of dysphagia
subjective sensation of difficulty in swallowing food.
- may also be accompanied by odynophagia > pain with swallowing.
114
what are the different causes of oesophageal dysphagia?
- benign stricture
- malignant stricture
- motility disorders (e.g. achalasia, presbyoesophagus)
- eosinophilic oesophagitis
- extrinsic compression (e.g. in lung cancer).
115
what carcinoma affects the top of the oesophagus?
squamous carcinoma
116
what carcinoma affects the bottom of the oesophagus?
adenocarcinoma
117
dysphagia or reflux symptoms with alarm features investigation?
endoscopy:
- oesophago-gastro-duodenoscopy (OGD).
- upper GI endoscopy (UGIE).
118
when would a barium swallow (contrast radiology) be used?
primary indication is investigation of dysphagia (however endoscopy is preferred test).
- can exclude pharyngeal pouch or post-cricoid web prior to endoscopy.
119
refractory heartburn/reflux investigation?
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
what is manometry and when is it used?
nasal catheter containing multiple pressure sensors placed in oesophagus.
- used in investigation of dysphagia/suspected motility disorder (usually after endoscopy). ACHALASIA!!!
121
what does manometry assess?
- sphincter tonicity, relaxation of sphincters and oesophageal motility.
122
oesophageal hypermotility symptom
- severe, episodic chest pain +/- dysphagia.
123
what is the appearance of oesophageal hypermotility on Ba swallow?
'corkscrew appearance'.
124
what does manometry of oesophageal hypermotility show?
exaggerated, uncoordinates, hypertonic contractions.
125
what are symptoms of oesophageal hypomotility?
- heartburn and reflux due to failure of LOS mechanism.
126
what conditions is oesophageal hypomotility associated with?
- connective tissue disease.
- diabetes.
- neuropathy.
127
what is achalasia?
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
signs and symptoms of achalasia?
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
manometry results in achalasia
- high pressure LOS at rest.
- failure of the LOS to relax after swallowing.
- an absence of peristaltic contractions in the lower oesophagus.
130
treatment of achalasia? (pharmacological, endoscopic, radiological, surgical)
-pharmacological: nitrates, CCBs.
-endoscopic: botulinum toxin pneumatic balloon dilation.
-radiological: pneumatic balloon dilation.
-surgery: myotomy, oesophageal dilation.
131
complications of achalasia?
aspiration pneumonia and lung disease.
increased risk of squamous cell oesophageal carcinoma.
132
GORD symptoms?
heartburn
cough
water brash (excessive saliva mixes with stomach acids and gives a foul taste in the mouth)
sleep disturbance
133
GORD risk factors
pregnancy
obesity
drugs lowering LOS pressure
smoking
alcoholism
hypomotility
134
what are the alarm features of GORD in which endoscopy should be performed?
dysphagia
weight loss
vomiting
135
GORD aetiology
GORD is caused by a defective lower oesophageal sphincter, which enables the reflux of gastric contents into the oesophagus.
136
GORD aetiology due to hiatus hernia
anatomical distortion of the OG junction
137
GORD pathophysiology
- mucosa exposed to acid-pepsin and bile.
- increased cell loss and regenerative activity (i.e. inflammation).
- erosive oesophagitis.
138
GORD complications
- ulceration (5%)
- stricture (8-15%)
- glandular metaplasia (Barrett's oesophagus).
- carcinoma.
139
Barretts oesophagus treatment
- endoscopic mucosal resection (EMR).
- radio-frequency ablation (RFA).
- oesophagectomy rarely (mortality 10%).
140
GORD treatment
- lifestyle measures.
Pharmacological:
- alginates (gaviscon).
- H2RA (ranitidine).
- PPI (omeprazole, lansoprazole).
for refractory disease/symptoms:
- anti-reflux surgery (fundoplication).
141
oesophageal cancer signs and symptoms
- progressive dysphagia.
- anorexia and weight loss.
- odynophagia.
- chest pain.
- cough.
- pneumonia.
- vocal cord paralysis.
- haematemesis.
142
how is oesophageal cancer diagnosed?
endoscopy
biopsy
143
how is oesophageal cancer staged?
CT scan
endoscopic US
PET scan
Bone scan
TNM classification
144
oesophageal cancer treatment
only potential cure is surgical oesophagectomy +/- adjuvant or neoadjuvant chemotherapy.
palliative care: chemotherapy, radiotherapy etc.
145
describe eosinophili oesophagitis
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
eosinophilic oesophagitis presentation
dysphagia and food bolus obstruction
147
eosinophilic oesophagitis treatment
- topical/swallowed corticosteroids.
- dietary elimination.
- endoscopic dilatation.
148
dyspepsia symptoms and duration criteria
- upper abdominal discomfort, retrosternal pain, anorexia, nausea, vomiting, bloating, fullness, early satiety and heartburn.
- for 4 weeks.
149
what are some upper GI causes of dyspepsia?
GORD
peptic ulcer
gastritis
non ulcer dyspepsia
gastric cancer
150
what are red flag symptoms of dyspepsia that should be referred for endoscopy? use ALARMS 55 mnemonic
- Anorexia
- Loss of weight
- Anaemia
- Recent onset or persistent despite treatment.
- Melaena/haematemesis (GI bleeding) or mass.
- Swallowing problems - dysphagia.
- > 55 years old.
151
discuss H.pylori infection
- 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
what are the clinical outcomes of H.pylori infections?
- 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
describe the difference in responses to chronic H.pylori infection
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
how is H.pylori infection diagnosed? NON-INVASIVE METHOD
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
how is H.pylori infection diagnosed? INVASIVE METHOD
invasive: requires endoscopy
- histology: gastric biopsies stained for the bacteria.
- culture of gastric biopsies.
- rapid slide urease test (CLO) - ammonia (NH3).
156
how are peptic ulcers treated?
- eradication of H.pylori.
- antacid medication - PPI (omeprazole) or H2 receptor antagonists (ranitidine).
- NSAID cessation.
157
discuss the eradication of H.pylori infection
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
what are symptoms and signs of gastric outlet obstruction?
- vomiting > lacks bile, fermented foodstuffs.
- early satiety.
- abdominal distension.
- weight loss.
- dehydration.
- metabolic alkalosis.
159
how is gastric outlet obstruction treated?
endoscopic balloon dilation
surgery
160
what are treatment options for oesophageal cancer when it is metastatic and the patient is unfit?
- stenting.
- palliative radiotherapy.
- palliative chemotherapy.
161
what are treatment options for oesophageal cancer that is resectable and the patient is fit?
- oesophagectomy + chemotherapy > 5 year survival approx 45%.
or
- chemo/radiotherapy > 5 year survival approx 30%.
162
what happens in oesophagectomy?
- the cancerous part of the oesophagus is removed and the stomach is pulled up into the chest and reattached to the remaining oesophagus.
163
what are modifiable risk factors in stomach cancer?
- infection with H.pylori.
- alcohol.
- smoking.
- excessive consumption of salted fish, pickled vegetables and cured meats.
164
what are surgery options for gastric cancer?
subtotal gastrectomy - portion of stomach removed.
total gastrectomy and Roux en Y reconstruction - whole stomach removed and eosophago-jejunostomy perfomed.
165
when is bariatric surgery for obesity indicated?
BMI:
- 35 - 39.9 obese
- >/= 40 morbidly obese
166
where is the liver located?
upper right quadrant of abdomen.
right hypochondriac region
167
what is found in the portal triad of the liver?
Porta:
- hepatic artery.
- hepatic portal vein.
- hepatic duct (bile duct).
168
what are the four lobes of the liver called?
right
left
quadrate
caudate
169
what are the parenchymal cells of the liver called?
hepatocytes
170
what are the non- parenchymal cells of the liver called?
LSEC, HSC, Kupffer cells, pit cells.
171
what are the cholangiocytes of the liver called?
biliary epithelial cells.
172
label this hepatic lobule
173
label this hepatic lobule
174
what are the six components of bile?
bile acids
lecithin
cholesterol
bile pigments (bilirubin)
toxic metals (detoxified in liver)
bicarbonate (neutralization of acid chyme), secreted by duct cells
175
why are faeces brown?
bilirubin modified by bacterial enzymes > brown pigments
176
pathway of bile salts movement
liver > bile duct > duodenum > ileum > hepatic portal vein > liver etc.
177
describe the gallbladder
saclike structure on interior surface of liver.
178
what is the function of the sphincter of oddi?
controls release of bile and pancreatic juice into duodenum.
179
give the sequence of events in bile secretion from gallbladder.
- 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
role of CCK in digestion
inhibits gastric emptying
stimulates pancreatic enzyme secretion and bile secretion
181
role of secretin in neutralisation
- decreases gastric acid secretion
- decreases gastric emptying
- increases duodenal, pancreatic and bile duct HCO3 secretion.
182
what does this barium swallow show?
achalasia > can see failure of oesophageal sphincter relaxation
183
what is ascending cholangitis?
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
what is charcot's triad?
and Reynold's pentad?
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
what bonds link glucose monomers present in starch and how are they cleaved?
beta-1,4 glycosidic bonds
alpha-amylase cleaves the bonds
186
what inhibits gastrin secretion?
lowering pH in stomach as gastrin stimulates HCl secretion so this is a negative feedback loop
187
what component of saliva determines its tonicity>?
electrolytes
188
what ligament contains the portal triad?
hepatoduodenal ligament
