Alimentary System Flashcards
1
Q
What are the organs of the gastrointestinal tract?
A
Mouth, oesophagus, stomach, small intestine, liver, biliary system, pancreas, large intestine
2
Q
What does the colon consist of?
A
Caecum, appendix, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending flexure, sigmoid colon
3
Q
What are the components of the burden of disease?
A
Patient burden, Health costs, Morbidity, Mortality, Incidence and prevalence
4
Q
What are the general symptoms of GI diseases?
A
Anorexia, Weight Loss, Anaemia
5
Q
What are the symptoms of diseases in the upper GI tract?
A
Haematemesis, Malena, Vomiting, Nausea, Dysphagia, Odynophagia, Heart burn, Acid regurgitation, Chest pain, Belching, Epigastric Pain
6
Q
What are the symptoms of disease of the liver and biliary system?
A
Right upper quadrant pain, biliary colic, Icterus (jaundice), Pruritus (dark urine), Cholestasis (pale stool) Ascities (abdominal distension)
7
Q
What are the symptoms of disease of the Mid GI tract and pancreas?
A
Abdominal pain, diarrhoea, Steatorrhoea, Distension
8
Q
What are the symptoms of disease of the lower GI tract?
A
Abdominal pain, diarrhoea, bleeding, constipation, incontinence (inappropriate passing of urine)
9
Q
What are general signs of GI disease?
A
Cachexia, Obesity, Lymphadenopathy, Anaemia, Jaundice
10
Q
What are the signs of GI disease in the hands?
A
Koilinychia (thin, brittle, concave nails.
Leuconychia (white discolouration of nails)
Clubbing
Tachycardia
Tremor
Dupytrens contracture (flexion deformity of fingers)
11
Q
What are the signs of GI disease in the abdomen?
A
Organ enlargement
Mass
Tenderness
Distension
12
Q
What are the signs of GI disease in the anus and rectum?
A
Haemorrhoids (enlargement of blood filled spongy cushions in the anus)
Fistula (abnormal communication between two organs)
Fissure (break in skin lining anal canal)
Rectal masses
Proctitis (inflammation of the rectum)
13
Q
General statistics about GI disease
A
1/8 Hospital Admissions Responsible for 12% Deaths in the UK 1/4 Main operations Drug prescriptions>£4 billion 5% adults suffer chronic illness
14
Q
Major GI Diseases
A
Worldwide- Malnutrition, enteric infections, gastric cancer, viral hepatitis
UK- dyspepsia, liver disease, colon cancer
15
Q
What are the three areas of the small intestine?
A
Jejunum, Ileum, Duodenum
16
Q
What are the roles of the areas of the small intestine?
A
Absorption of blood, nutrients and water from the lumen to the blood
17
Q
What is the size of the small intestine and its components?
A
Small intestine: 6m long, 3.5 cm diameter
Duodenum: 25 cm
Jejunum: 2.5m
Ileum: 3.75 m
18
Q
What is the function of the mesentery?
A
It surrounds the small intestine and is folded and has a large blood supply to support the metabolic functions of the cell as well as aid absorption
19
Q
Describe the digestive epithelium
A
It lies on the external muscular wall (consisting of circular and longitudinal muscles) and has an internal folded mucosa which are covered in villi (around 1mm long) and have invaginations called crypts of leiberkuhn)
20
Q
Describe the intestinal epithelium
A
Simple epithelium (1 cell thick) consists of columnar absorptive cells (enterocytes) and are interspersed with goblet and enteroendocrine cells)
21
Q
What are the properties of villi?
A
Motile
Large Blood Supply
Good Lymphatic Drainage
Innervation from submucosal plexus
22
Q
What do crypts of Lieberkun consist of?
A
Paneth Cells
Stem Cells
23
Q
What is the most abundant cell in the small intestine?
A
Enterocytes
24
Q
What are the properties of enterocytes?
A
Tall columnar
Apical microvilli
Basal nuclei
25
What is the life span of an enterocyte?
1-6 days
26
What is the use of tight junctions between cells?
Intercellular communication
27
What is the size of the microvilli?
0.5-1.5 micrometres
28
Which membrane of enterocytes do the microvilli overly?
Apical membrane
29
Where does the glycocalyx reside?
On the apical membrane of the enterocytes and is a rich carbohydrate layer
30
What is the function of the glycocalyx?
Protects microvilli and enterocytes from digestion from digestive enzymes.
Provides environment for digestion to take place
31
How does the glycocalyx provide an environment for absorption?
Traps a layer of mucous and water known as the 'unstirred layer' which contains many enzymes and regulates the rate of absorption from the lumen
32
To what extent does the villi, microvilli and mucosal folds increase the surface area of the small intestine?
By 500x. From 0.4 m 2 to 200 m2
33
What is the second most abundant epithelial cell type in the small intestine?
Goblet cell
34
What is the reason for the characteristic shape of the goblet cell?
Mucous filled granules accumulate at the apical end
35
How does the position of granules in the goblet cell aid secretion?
Secretion is unidirectional
| Products go into lumen, NOT blood
36
What is mucous?
A large glycoprotein that facilitates the movement of digested material through the bowel
37
Describe the abundance of goblet cells in the small intestine
Fewer in duodenum compared to colon. Number increases along length of small intestine.
38
What type of cell are enteroendocrine cells?
Columnar epithelial cells found mainly in the lower part of the crypts
Hormone secreting cells (chromaffin cells)
39
Where are paneth cells found?
In the base of the crypts
40
What do paneth cells contains?
Acidophilic granules which contain lyzozomes (protect cell from bacterial pathogens), glycoproteins and zinc
41
How do pluripotent cells replace goblet cells and enterocytes?
Divide by mitosis and migrate to villus tip
42
How do pluripotent cells die?
Senescence (shed off into lumen and digested)- escalator of epithelial migration, first line of defence against GI diseases
43
What can effect the escalator of epithelial migration?
Radiation
44
How can the cholera toxin lead to dehydration and death?
Results in prolonged opening of chloride channels in small intestine so more water goes into lumen resulting in water diarrhoea
45
How is a person with cholera treated?
Oral rehydration therapy
46
Why is treatment for the bacteria not required?
The body will expel the bacteria and enterotoxin due to rapid turnover of the cells
47
Describe the differences in appearance of the different areas of the small intestine
Duodenum- Brunners glands which have alkaline secretions
Jejunum- taller and thinner plicae circulars (valves of Kerckring)
Ileum- Peyers patches (like large intestine)
48
What is the cause of the frilly interior of the jejunum?
The circular folds of the mucosa
49
How do peyers Patches protect the body?
Prime the immune system and prevent bacteria from migrating into the small intestine from the colon due to its position
50
What are the functions of small intestine motility?
Neutralise stomach chime and mix food with digestive enzymes
Facilitate contact between intestine and intestinal mucosa
Propel intestinal contents along the alimentary tract
51
What are the processes of small intestine motility?
Segmentation
Peristalsis
Migrating Motor Complex
52
What is segmentation
Frequent stationary contractions of circular muscles at intervals to mix contents of lumen
53
What is peristalsis
Propels chime towards colon due to sequential contraction of smooth muscle, waves are about 10cm apart
54
What is the migrating motor complex recognised as
Rumbling stomach
55
What is the migrating motor complex?
Waves of smooth muscle contractions which during fasting which prevents the movement of colonic bacteria into the ileum and clears the intestine of residual food.
Waves begin in colon, and when they reach terminal ileum they start in the duodenum
56
What are the four mechanism of absorption?
Passive diffusion
Facilitated diffusion
Primary active transport
Secondary active transport
57
What is the source of energy for primary and secondary active transport
Primary active transport: hydrolysis of ATP
| Secondary active transport: electrochemical gradient
58
How much of ingested calories is owed to carbohydrates?
50%
59
Where does most digestion of carbohydrates occur?
Small intestine, primarily on the unstirred layer
60
What happens in the intestine in response to a meal for carbohydrate digestion?
Pancreatic alpha-amylase is secreted into the duodenum which requires Cl- and an alkaline environment which is provided by the Brunner's glands
61
How are the different sugar molecules absorbed?
Glucose & Galactose- Secondary active transport on carrier protein SGLT-1 on apical membrane
Fructose- Facilitated diffusion on carrier protein GLUT-5 on apical membrane
62
How do sugar molecules exit the carrier protein
GLUT-2 on basolateral membrane
63
Where does digestion of proteins begin?
In stomach due to pepsin
64
How are pancreatic proteases involved in digestion
They are secreted into the small intestine (trypsinogen) then converted on the duodenal brush border into trypsin by the action of enterokinase.
Trypsin carries on digestion and activates other proteases.
65
How are proteins broken down?
After being broken down into large polypeptides, brush border peptidases break them down further into di/tri peptides and free amino acids
66
How are the products of protein digestion absorbed?
Di/tri peptides: facilitated diffusion and secondary active transport
Free amino acids: carrier proteins followed by breakdown into amino acids by cytoplasmic peptidases before they cross the basolateral membrane
67
What are the stages of digestion of lipids?
Secretion of bile and lipase's
Emulsification
Enzymatic hydrolysis of ester linkages
Solubilisation of lipolytic products in micelles
68
What is the purpose of emulsification?
Lipids are poorly soluble therefore the surface area of fat for digestion is increased
69
Describe the structure of bile salts
Amphipathic with steroid nucleus
Bile acid Hydrophobic face
Hydrophilic face with OH groups on carboxyl/sulfonic acid
Hydrophobic face dissolves in fat and hydrophilic face dissolves in water
70
What is the function of bile salts?
Facilitate emulsification into suspension of lipid droplets which allows pancreatic lipase to split triglycerides into two fatty acids and a monoglyceride.
71
What prevents bile salts from displacing lipase from the micelle?
Pancreatic lipase forms complexes with colipase
72
What is the function of phospholipase A2
hydrolyses fatty acids at the 2 position of phospholipids which forms lyso-phospholipids and free fatty acids
73
What is the function of pancreatic cholesterol esterase
Hydrolyses cholesterol esters to free cholesterol and fatty acids
74
How are lipid digestion products absorbed
Micelles can be transported across the unstirred layer and present monoglycerides and fatty acids to the brush border. Bile salts are absorbed in ileum but lipid aborption is complete by mid-jejunum.
75
How are bile salts recylced
Transported back to liver via enterohepatic circulation
76
What does lipid metabolism involve
Re-synthesis of triglycerides in enterocytes
77
What are the two pathways of lipid metabolism
```
Monoglyceride acylation (major)
Phosphatidic acid (minor)
```
78
What is monoglyceride acylation?
Fatty acids bind to the apical membrane and fatty acid binding proteins transfer them to the smooth endoplasmic reticulum where they are esterified to triglycerides
79
What is the phosphatidic acid pathway?
Triglycerides are synthesised from CoA fatty acid and alpha- phosphoglycerate
80
What are chylomicrons?
```
After triglyceride synthesis, lipoproteins are synthesised as an emulsion consisting of :-
80-90% triglycerides
8-9% phospholipids
2% cholesterol
2% proteins and trace carbohydrates
```
They are transported to basolateral membrane of golgi and secreted by exocytosis and enter lacteals due to large size
81
What prevents back flow of bacteria from colon to ileum
Ileocaecal sphincter
82
What causes undernutrition
Inadequate consumption, poor absorption, excessive loss of nutrients
83
Why is BMI less relevant in undernourished patients?
Severely undernourished people may have fluid imbalance which will affect weight
84
What are surrogate measurements for undernourished patients?
Arm circumference and arm skin-folds
85
What are nutrient requirements?
The amount needed to be consumed by an individual in order to maintain optimal health and function and avoid deficiency
86
Which hormones regulate feeding
PYY- GI hormone with anorexic effect
Ghrelin- stomach and pancreatic hormone with orexigenic effect
Leptin- Long term effects, released from adipocytes with anorexic effect
87
What are the effects of leptin
Cessation of menstrual cycles
| Obesity leads to leptin resistance
88
What is BERIBERI?
thiamine deficiency
89
What is thiamine
Occurs as free thiamine and various phosphorylated forms (monophosphate, triphosphate and pyrophosphate)
Needed for the release and utilisation of energy from food and nerve function (found on neurone membranes)
Found in unrefined cereals and fresh foods
90
What are the properties of BERI BERI
Ailment of nervous system
Lethargy and fatigue
Effects cardiovascular, nervous, muscular and GI systems
Found in people with diet of polished white rice
Alcoholics
Post-gastric bypass patients
91
PELLAGRA
Niacin deficiency
92
Why is niacin important
Nicotinamide is derivative of niacin and forms coenzymes NAD and NADP
Niacin coenzymes are needed
93
What are the signs of undernutrition?
```
Muscle wasting
Weight loss
Loss of subcutaneous fat (loose skin on extremities)
Glossitis
Har loss
Infections
Peripheral oedema (no cardiac disease)
Listless
Poor wound healing
Recurrent pulmonary infections
```
94
What is the passive response to energy restriction/starvation to decrease resting metabolic rate?
```
Decrease insulin
Decrease thyroxine and T3
Release glucagon
Release growth hormone
Substrate mobilisation of free fatty acid and amino acid leading to weight loss
```
95
What is the active response to reduced energy flux?
Decreased SNS activity
Increase catecholamine production
Decreased metabolic flux and energy expenditure
96
What are the effects of short and long fasts?
Short fasts: Loss of glycogen and associated water from liver and gut weight
Long fasts: Further gut and liver weight and muscle weight and fat loss
97
Normal metabolic rate
25-30kcal/kg/d
98
What does the pancreatic bud form?
The dorsal and ventral mesenteries of the foregut in function with the midgut
Dorsal bud expands on left to form head neck body and tail
Duodenum rotates and forms C-shape, ventral bud forms rest of head and uncinate process
99
Where are islets of Langerhans most prevalent in the pancreas
Tail
100
How does pancreatic juice reach the duodenum?
Main and accessory pancreatic ducts which fuse with the common bile duct to enter the duodenum
101
What forms of imaging is used to assess pancreatic tumours and disease?
MRI- tumours
| Angiography- disease
102
What do pancreatic juices consist of?
Digestive enzymes and HC03-
103
How are endocrine cells formed?
From the branching duct system (tail of pancreas) then lose contact and differentiate further
104
How is the major pancreatic duct formed?
Connective tissue between exocrine acinar cells and endocrine islet cells with columnar epithelium and minor pancreatic duct fuse
105
What are the components of pancreatic juice
Low volume, viscous rich in digestive enzymes secreted by acinar cells
High volume, water solution rich in HC03 secreted by centroacinar and duct cells
106
What are the differences between acinar and duct cells?
Acinar cells are large with apical secretory granules (containing inactive precursors protecting the cells from auto digestion)
Duct cells are small with few granules
107
What is the concentration and pH of bicarbonate secretion
120 mM
| 7.5-8 pH
108
What is the mechanism of secretion
Separation of H+ and HC03-
Transport of H+ and HC03- out of the duct cell
Mainenance of Na+ gradient
Movement of K+ into blood and Cl- into duct cell
109
How is the NA+ gradient maintained
Na/K pump
110
What are zymogens?
Pro enzymes which store lipases, amylases and proteases and protect the acini and ducts from auto digestion
111
Why can acute pancreatitis lead to auto-digestion
Blockage can lead to overload of zymogen protection
112
How does the pancreas ensure protein digestion only occurs in duodenum
Secrets trypsin inhibitor
113
How does enterokinase activate tryspin
Cleaves trysinogen between valine and isoleucine
114
What is an anti-obesity drug
ORLISTAT- pancreatic lipase inhibitor
115
What are the phases of pancreatic secretion
Cephalic
Gastric
Intestinal
116
How is the cephalic phase initiated
Pancreatic secretion enters before food enters the duodenum via the vagal reflex in response to taste and smell. Cholinergic synapses resulting in enzymes.
117
What initiates the intestinal phase
When acid chime enters the duodenum from the stomach, the duodenal mucosa secretes secretin and CCK into the blood
118
What is secretin and CCK
Secretin is formed in response to acidic pH and stimulates bicarbonate secretion- involves cAMP
CCk is formed in response to fats/proteins and stimulated enzyme production. Involves calcium ions and PLC via vagus reflex
119
What ends the cephalic phase
The meal being eaten
120
What ends the intestinal phase
The absorption of fats/proteins therefore the removal of the stimulus for CCK production
121
What are the roles of bile?
Cholesterol homeostasis
Dietary lipid/vitamin absorption
Removal of xenobiotic/drugs/waste products
122
Which GI Pathogens affects the mouth?
Oral Candidiasis
123
Give examples of gastric pathogens
Hectobacter pylori, e.coli, noravirus, cholera
124
What innate GI Defence mechanisms are there?
Gastric acid
| Oral commensal flora,
125
What innate GI Defence mechanisms are there?
```
Gastric acid
Oral commensal flora
Peristalsis
Mucous from goblet cells
Proteases
Brush border
```
126
What is rich in MALT
Oral cavity
| Tongue, palatine, lingual and pharyngeal tonsils
127
What are the differences between organised and unorganised GALT
Not organised: lamina propria lymphocytes and intra-epithelial lymphocytes
Organised: cryptopatches, Peyers patches, isolates lymphoid follicles, mesenteric lymph nodes
128
Within the gut mucosa, what is dome epithelium?
Areas with no mucosa epithelium, but rather M cells, act as portal of entry for antigens to be transferred to lymphocytes, macrophages and dendritic cells
129
How is IgA transported from submucosa to the lumen?
Transyctosis
130
What are the groups of CD4 cells
Th1- cellular immunity
Th2- humoral immunity
Treg- immunoregulatory function
Th17- inflammation and autoimmunity
131
What are the symptoms of Crohns disease
Structuring
Ulceration
Inflammation
132
What are the symptoms of Crohns disease
Structuring
Ulceration
Inflammation
133
Where does the liver lie?
The right upper quadrant, superior border at 5th costal cartilage
134
How to percuss liver
Percuss chest inferiorly, percuss abdomen superiorly and dull area is liver
135
What separates the two lobes of the liver
Falciform ligament
136
Why is the gallbladder not palpable
Lies inferior to arch of liver, if palpable then an enlargement is indicated
137
How much of cardiac output is received by the liver
25%
138
Explain the dual supply of the liver
20% is artery blood from left and right branches of hepatic artery and is oxygen rich.
80% is venous blood from gut from the hepatic portal vein and is nutrient rich
139
Why is the liver protected from acute ischemia if an embolus is present.
It has a direct and indirect blood supply
140
What are the function of the liver
```
Synthesise bile pigments
Breakdown over-dated RBC
Secrete bile into duodenum
Secrete bile pigments into bile
Site of insulin dependent glycogen storage
```
141
Where does the liver arise from?
Septum transversum
142
Where may the common bile duct join the pancreatic duct?
The ampulla
143
What can be used to view the biliary tree?
ERCP
144
What are the resident liver macrophages?
Kupffer cells which reside in the space
145
How could hepatic stellate cells cause cirrhosis?
They contain vitamin a which if due to toxic insult may deposit fibrous tissue and lead to fibrosis
146
What is the Space of Disse
Space between hepatocyte and associated sinusoid epithelium
147
Why is the endothelium fenestrated?
To allow movement of substances
148
What are the characteristics of a diseased liver?
Endothelium lose fenestrae, stellate cells deposit into space of Disse, Kupffer cells unregulated and produce free radicals which cause further damage and hepatocytes lose microvilli
149
What are common causes of acute pancreatitis?
Alcoholism and cholelithiasis
150
What is classified obese with regards to waist circumference?
Men> 102 Women >88
151
What is classified obese with regards to hypertension?
bp> 135/80
152
What is classified obese with regards to HDL count?
Men> 1 Women>1.3
153
What is classified obese with regards to Fasting glucose?
>6mmol
154
Explain gastric bypass surgery
Stops calories coming into contact with duodenum so reduces fat absorption
155
How can acute liver failure be subdivided
Hyperacute : Less than 7 days between jaundice and encephalopathy
Acute: Between 1 to 4 weeks
Subacute: Between 5 and 28 weeks
156
What are the causes of acute liver failure
Hyperacute: paracetamol, Hep A Hep B
Acute: Hep A, B, E idiosyncratic drug toxicity
Subacute: Non A Non B heptatitis
157
What are the causes of chronic liver disease?
Alcoholism
Chronic viral hep b and c
Sclerosing cholangitis
Primary biliary cirrhosis
158
What are the clinical features of chronic liver disease
Portal hypertension
Oesophageal varices
Ascites
159
What are the plexi in the GIT
Meyenteric
Submucosal
Minor
160
What is the submucosal plexus continuous with
Duodenum and large intestine
161
What is the purpose of the submucosal plexus
Senses environment within lumen and then controls gut secretion, gut endocrine and epithelial function and blood flow
162
Where is gastrin synthesised
Antrum and upper small intestine
163
What inhibits gastrin secretion
pH
164
Where is secretin synthesised
S cells of upper duodenum and jejunum
165
What stimulates secretin
pH of less than 4.5 in duodenum
166
Where is Gastric Inhibtory Peptide synthesised
K cells of duonedum and jejunum
167
What does GIP stimulate
Secretin
168
Where is PYY synthesised
L cells in ileum, rectum, colon
169
When is PYY stimulated?
After eating
170
What are the main functions of the liver
Digestion
Energy metabolism
Detoxification
171
Where does the biliary system drain into?
From ductules into right and left hepatic ducts into the common hepatic duct, which joins the cystic duct to drain into the common bile duct
172
What is gluconeogenesis?
Process of forming glucose from non-carbohydrate sources
173
What is the cori cycle?
Glucose is broken down anaerobically by muscles into lactate which is then converted into glucose in the liver
174
How can glucose be formed from triglycerides or deamination?
Triglycerides- glycerol- glucose
| Alanine- pyruvate- glucose
175
How much of plasma proteins are synthesised by the liver?
90%
176
What is transamination?
The production of non essential amino acids from an alpha-keto precursor. Involved an amino group from one amino acid and a ketone group from another.
177
What is deamination?
Conversion of an amino acid into its corresponding leto acid by removing the amine group as ammonia and replacing it with a ketone group
178
What is urea?
NH2C(O)NH2
179
How is urea formed?
Liver converts ammonia into urea using carbon dioxide which is then excreted in the urine
180
What are the the properties of urea?
Soluble
Metabolically inert
Non toxic
181
How can fats be used as an energy source?
Fatty acids can be converted into acetyl coA which can then enter the TCA cycle
182
What do lipoproteins consist of?
Triglycerides, cholesterol core, phospholipid and protein coat
183
What are the various types of lipoproteins
```
VDL= lots of triglycerides
IDL= intermediate density lipoproteins
LDL= Lots of cholesterol and phospholipids
HDL= High protein coat
```
184
Which is the most dense lipoprotein
HDL- the lower the density, the larger the diameter
185
Why is CETP of interest to drug companies?
It shuttles cholesterol of HDL's to LDL's. High HDL:LDL ratio is significant in the prevention of atherosclerosis.
186
What is a phospholipid?
Fatty acid, phosphoric acid and nitrogenous base
187
What is cholesterol?
Sterol nucleus synthesised from acetyl coa and dietary intake
188
Where does secretion of bile occur?
Through canniculi between adjacent hepatocytes into the biliary system
189
How are cholic and chenodeoxycholic acids formed?
Oxidation of cholesterol. Carboxyl and hydroxyl groups are then added to make the acids soluble
190
What are the products of conjugated primary bile acids?
taurcholic and glycocholic acid
191
How are secondary bile salts formed?
Primary bile salts are deconjugated and dehydroxylated and converted with GI bacteria
192
What dothe hydrophobic and hydrophilic faces of bile salts consist of?
Hydrophobic- nuceus and methyl groups
| Hydrophilic- hydroxyl and carboxyl groups
193
Where is the ampulla of Vater located?
2nd part of duodenum
194
How is bile released?
Released into the ampulla of cater during digestion. Some is released during the cephalic and gastric stages as a result of the vagal nerve and gastrin secretion. However most bile is released during the intestinal phase as a result of CCK secretion causing the gallbladder to contract and relaxation of the sphincter of Oddi
195
What happens to bile salts when they enter hepatic circulation?
Bile salts are actively absorbed in the terminal ileum. They are de-hydroxylated and de-conjugated with colonic bacteria to make them more lipid soluble
They are sent back to the liver via the hepatic portal vein.
Hepatocytes remove all bile salts from the hepatic portal vein and they a re-conjugated and re-hydroxylated
196
How many times during a meal is the bile salt pool secreted?
Twice
197
Why is lecithin useful for excess cholesterol
Allows more cholesterol into micelles
198
How is bilirubin produced
Porphirin group of harm is broken down to bilirubin in the spleen. In the liver it is conjugated to glucoronic acid and excreted in the bile
199
Which fat soluble vitamins does the liver store?
A, D, E, K. Stores last for 6-12 months except the small store of Vit K which poses a problem as Vit K is needed for blood clotting
200
What does the Liver store
Vitamins A,D,E,K
Iron as ferritin, available for erythropoeisis
Vitamin B12- lack leads to pernicious anaemia and nerve demyelation
Fat and glycogen
201
How is the liver protected from pathogens
Kupffer cells which are resident macrophages in liver sinusoids destroy pathogens which enter enterohepatic circulation from the lumen of the gut
This will prevent the pathogen from entering the rest of the body
202
How is vitamin D formed
UV light is required to convert cholesterol into a Vitamin D precursor.
The precursor then requires double hydroxylation to convert it into Vitamin D.
The first hydroxylation occurs in the liver and the second occurs in the kidneys.
203
What are the layers of the gut wall?
Mucosa
Submucosa
Muscularis
Serous/adventitia
204
How does food reach the pharynx?
Tongue pushes food into pharynx from mouth which is under neural control
205
Where does the pharynx become the oesophagus?
C5- ending at t10
206
How is the oesophagus protected from wear and tear?
```
Stratified squamous epithelium
Non keratinising- therefore is moist
Mucous secreting glands
Protective layers
2 sphincters- pressure in oesophagus is less than the atmosphere so they prevent the backtracking of food
```
207
What causes the upper oesophageal sphincter to open?
The swallowing centre in the medulla under parasympathetic control via the vagus nerve
208
What happens if the bolus of food gets stuck?
A second wave of peristalsis is initiated
209
What is the mechanism of the lower sphincter?
Resides at the Z-line of gastro-oesophageal junction
Not a sphincter as such
Due to pressure difference between stomach and oesophagus
Contraction of the diaphragm
When stomach expands, it compressed the Z-line
210
What is heartburn
Because the lower sphincter is not foolproof, acid from stomach can go up into the oesophagus
211
Why may the lower sphincter not be efficient in pregnancy?
Stomach is forced upwards, and sphincter is forced into thorax. Pressure difference is lost as is the contractility of the diaphragm.
212
What is the function of the stomach?
To break down the bolus of food and hold food and release it periodically into duodenum and kill bacteria/parasites.
213
What are the secretions of the stomach
Cardia and pyloris- mucous
Body and fundus- mucous, acid, pepsinogen
Antrum- gastrin
214
What do the parietal and and endocrine cells in the stomach produce?
Parietal- HCl
| Endocrine- gastrin
215
What is the pH of the epithelium and lumen?
Epithelium- 6-7 (neutralised by bicarbonate ions trapped in the mucus)
Lumen- 1-2
216
What is a chief cell?
Cell that produces pepsinogen
| Well adapted for protein synthesis, contains large amounts of RER, Golgi and secretory granules
217
What is the appearance of the parietal cell in the resting state?
Lots of mitochondria, concentrating the H+ ions is a very active process requiring much ATP
Internal reservoirs and canaliculi
218
What is the appearance of the parietal cell in the active state?
Tubular vesicles fuse with canaliculi which fuse to form reservoirs that extend to the apical membrane.
On the basolateral membrane there is an Na/K pump. K+ diffuses across lumen.
H+ is actively exchange into the cell for K+.
Bicarbonate ions are exchanged for Cl- ion which diffuse into the cell
Cl- and H+ join to form HCl
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How is pepsin formed
Pepsinogen has an internalised active site which is protected
Acid of the stomach exposes the active site. Hcl reacts with pepsinogen to form pepsin.
Via positive feedback, Pepsin catalyses its own production.
Pepsin is a protease
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What are the functions of gastrin
Produced in antrum of stomach
Stimulates histamine release from chromaffin cells of lamina propria
Together, these two things cause the increase of acid in the stomach.
Negative feedback- more acidic stomach gets, the more gastrin secretion is inhibited
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How does a protein rich meal lessen gastrin inhibition?
Protein acts as a good buffer for acid
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How does Ach prepare for arrival of food?
Stimulates parietal cells to produce acid and chromaffin cells to release histamine indirectly
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What causes gastrin and Ach to be released in the gastric phase?
Food enters stomach and distension stimulates stretch receptors.
Contents stimulates chemoreceptors leading to a local enteric response
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What effect does the intestinal phase have on the production of gastrin?
Inhibitory
| Food enters small intestine, more alkaline environment is required.
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What does the large intestine consist of?
Caecum, appendix, rectum, colon, anal canal
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What are the dimensions of the colon?
1.5 m long
| 6cm diameter
227
What are the main functions of the colon?
Reabsorption of electrolytes/water and elimination of undigested food/waste
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What are the structural features of the colon?
Appendicies Epiploicae
Taeni coli
Haustra
Solitary nodules
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What are taeni coli?
3 longitudinal bands running along the length of the colon
| Needed for large intestine motility
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Where does most electrolyte water reabsorption occur?
Proximial colon
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What is the mechanism of reabsorption?
Na+ and Cl- ions are absorbed by exchange mechanisms and ion channel.
Water follows by osmosis.
K+ diffuses in passively
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How much water can the large intestine absorb?
Up to 4.5 l - above this diarrhoea will occur
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What is the rectum?
The dilated distal portion of the alimentary canal
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How is the rectum distinguished from the colon?
Has transverse folds in the submucosa and no taeni coli in muscular is externa
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How many goblet cells are in the large intestine in comparison to the small intestine?
More goblet cells in large intestine, predominantly in the crypts. Required for mucous secretion to move solid contents of intestine.
Acetylcholine stimulate goblet cells secretion
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What cell type is present in the small intestine but not the large intestine?
Paneth cells
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What is the difference between the glycocalyx of the small intestine and large intestine?
It does not contain digestive enzymes in the large intestine
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What is haustra
When the longitudinal layers of taeni coli penetrate the circular layers of muscle at intervals.
They contracts individually
239
Why is motility important?
Promotes the reabsorption of electrolytes and water
240
Which type of food promotes mass movement in the large intestine?
Food with a lot of fibre
241
Describe the parasympathetic innervation of the large intestine
Vagus nerve innervates the ascending colon and most of the transverse colon
Pelvic nerve innervates more distally
242
Describe the sympathetic innervation of the large intestine
Thoracocolumnar outlflow
243
What is the external anal sphincter controlled by?
Somatic motor fibres in the pudendal nerve
244
What is the defecation reflex controlled by?
Sacral spinal chord
| Includes reflex on voluntary actions
245
Describe defecation
Filling of the rectum causes a reflex in response to distension of the walls
Pressure receptors send signals via the meyenteric plexus to start peristaltic waves in the descending colon, sigmoid colon and rectum.
The internal anal sphincter is inhibited.
The external anal spinster is under voluntary control.
The urger can be resisted and feeling can subside.
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What is the social part of the rectum
The last few cm which can distinguish between solid, liquid and gas
247
How much faeces is produced in a day
150 g
| 2/3 water
248
What gives the odour to faeces
Bacterial fermentation
249
What solids are contain in faeces?
Bacteria, bile pigments, salts, cellulose and cell debris
250
What is microbiome
The symbiotic relationship that mammals have with their gut microbial community
251
What is the role of the flora?
Synthesise and secrete vitamins
Prevent bacteria from colonising by competing for areas of nutrients
Produce cross reactive antibodies
Antagonise bacteria by producing substances to inhibit or kill
Stimulate production of certain tissue such as caecum and lympathic
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What are the types of flora?
Bacteroides- non sporeforming, anaerobic, gram negative
| Bifidobacteria- non sporeforming, gram positive, lactic acid bacteria
253
Which type of flora is the most prevalent?
Bacteroides
254
Which type of flora is implicated in the initiation of colitis and colon cancer?
Bacteroides
255
Which type of flora is thought to prevent the colonisation of certain pathogens?
Bifidobacteria
256
What is a normal weight of bowel movement?
200g a day
257
What are two presenting features of malabsorption?
Diarrhoea/ Steatorrhoea
Weight loss
Growth failure
258
What would you assess for malnutrition?
Loss of fat
Muscle wasting
Ascites
Oedema
259
What causes maldigestion?
Reduced gastric tissue/secretions
Reduced pancreatic tissue
Reduced bile secretion
Reduced brush border enzymes
260
What causes malabsorption?
Loss of enterocyte function
Pre & post mucosal effects
Single gene disorders
261
What is Coeliac disease?
Inflammatory disease of the upper intestine due to gluten ingestion in susceptible individuals
262
What does coeliac disease present as?
Subtotal villus atrophy
263
What is the main gene involved in coeliac disease?
HLA-DQ2
264
What is ethanol insoluble in?
Fats and oil
265
How is ethanol metabolised?
Ethanol converted into acetaldehyde by alcohol dehydrogenase
Acetaldehyde converted into carbon dioxide and water by acetaldehyde dehydrogenase
266
Why can Asians not metabolise alcohol efficiently?
They are deficient in aldehyde dehydrogenase
267
What alternative pathways are present for metabolising alcohol?
CYP2E1 and catalase
268
How can tolerance be explained?
The more alcohol consumed, the more CYP2E1 that can be produced
269
What problems can CYP2E1 cause?
Free radicals are a bi-product of this pathway and can lead to inflammation
270
What are the long term effects of alcohol?
```
Pancreatic damage
Myocardial damage
Enhanced toxicity
Fatty liver
Ongoing liver damage
Carcinogenesis
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271
What is steatosis
fatty liver
272
What is steatohepatitis
Fatty liver with inflammation
273
What are the consequences of steatosis and steatohepatitis
Fibrosis
274
How can alcoholism lead to hepatocyte fibrosis
Chronic inflammation can lead to hepatic stellate cells within the space of Disse to turn into fibroblasts. These will lay down collagen fibres that will condense into fibrous bands
275
What are the types of diarrhoea
Secretory
Osmotic
Inflammatory
Hypermotility
