GI Flashcards
1
Q
Is stage 1 of swallowing voluntary or involuntary?
A
Voluntary.
2
Q
What happens in stage 1 of swallowing?
A
Food is compressed against the roof of the mouth and is pushed to the oropharynx by the tongue.
3
Q
Is stage 2 of swallowing voluntary or involuntary?
A
Involuntary.
4
Q
What happens in stage 2 of swallowing?
A
The nasopharynx closes off due to soft palate elevation. The trachea is closed off by the epiglottis. Elevation of the hyoid bone shortens and widens the pharynx.
5
Q
Is stage 3 of swallowing voluntary or involuntary?
A
Involuntary.
6
Q
What happens in stage 3 of swallowing?
A
The pharyngeal constrictor muscles sequentially contract producing peristaltic waves. This propels the bolus of food down the Oesophagus. This is followed by depression of the hyoid bone.
7
Q
Name 6 muscles/groups of muscles that are involved in swallowing.
A
- Buccinator.2. Suprahyoids.3. Muscles of the palate.4. Muscles of the floor of the mouth. 5. Infrahyoids. 6. Pharyngeal constrictor muscles.
8
Q
Which muscle(s) manipulate food in chewing. Elevate the hyoid bone and flatten the floor of the mouth?
A
Buccinator and Suprahyoids.
9
Q
What is the function of the muscles of the soft palate in swallowing?
A
They act to tense and elevate the soft palate.
10
Q
What is the function of the muscles of the floor of the mouth in swallowing?
A
They raise the hyoid bone and larynx.
11
Q
What is the function of the infrahyoids?
A
To depress the hyoid bone and larynx.
12
Q
What is the function of the pharyngeal constrictor muscles?
A
They contract sequentially producing peristaltic waves which drive food into the oesophagus.
13
Q
Do parotid glands have mainly serous or mainly mucous acini?
A
Mainly serous acini.
14
Q
What is serous acini secretion composed of?
A
alpha amylase - this is needed for starch digestion.
15
Q
Do sublingual glands have mainly serous or mainly mucous acini?
A
Mainly mucous acini.
16
Q
What is mucous acini secretion composed of?
A
Mucin - needed for lubrication.
17
Q
Do submandibular glands have mainly serous or mainly mucous acini?
A
They have serous and mucus acini.
18
Q
Which of the main salivary glands is constantly active?
A
Submandibular.
19
Q
What is the function of saliva?
A
It acts as a lubricant for chewing, swallowing and speech. It is important in oral hygiene; has a role in immunity, wash and it can also act as a buffer.
20
Q
What is the optimum oral pH?
A
7.2
21
Q
What is the pH range of saliva?
A
6.2 - 7.4
22
Q
Name 4 factors that can affect the composition of saliva.
A
- Stimulus. 2. Age. 3. Gender. 4. Drugs.
23
Q
Are serous acini dark staining or pale staining on a histological slide?
A
Dark staining. (Mucus acini = pale staining).
24
Q
What is the epithelium lining of intercalated ducts?
A
Simple cuboidal epithelium.
25
What is the function of intercalated ducts?
They connect acini to larger striated ducts.
26
What ions are reabsorbed at striated ducts?
Na+ and Cl-
27
Is saliva hypotonic or hypertonic?
Hypotonic - water reabsorption and ion secretion.
28
What is the importance of the striated duct basal membrane being highly folded?
It is folded into microvilli for the active transport of HCO3- against its concentration gradient.
29
What organelle is abundant in striated ducts and why?
Mitochondria. For the active transport of ions.
30
Name 2 ions that striated ducts secrete.
K+ and HCO3-
31
Name 2 ions that striated ducts reabsorb.
Na+ and Cl-
32
What ducts do striated ducts lead on to?
Interlobular (excretory) ducts.
33
What is the epithelium lining of interlobular ducts?
Simple columnar epithelium.
34
What is the parasympathetic innervation of the Parotid gland?
Cn 9 - glossopharyngeal.
35
What is the parasympathetic innervation of the Sublingual gland?
Cn 7 - facial.
36
What is the parasympathetic innervation of the Submandibular gland?
Cn 7 - facial.
37
What nerve passes through the parotid gland but does not innervate it?
The facial nerve (Cn 7) gives rise to its 5 terminal branches in the parotid gland.
38
What artery ascends through the parotid gland?
The external carotid artery.
39
Does parasympathetic innervation stimulate or inhibit salivary secretion?
Stimulates.
40
What is the volume of an empty stomach?
50ml
41
What is the maximum volume of the stomach?
1.5L
42
What is receptive relaxation?
Smooth muscle in the body and fundus of the stomach relaxes prior to the arrival of food, this allows the stomach volume to increase. There is afferent input from Cn 10. NO and serotonin also influence relaxation.
43
Where do peristaltic waves begin?
In the gastric body.
44
Where in the stomach are peristaltic contractions the most powerful?
In the gastric antrum.
45
Why is the pyloric sphincter closed as the peristaltic wave reaches it?
This prevents chyme entering the duodenum and so the gastric contents are forced back and mixed together in the body of the stomach.
46
On average, how many peristaltic waves are there a minute?
3 (slow repol/depol cycles).
47
Name 2 factors that can increase the strength of peristaltic contractions.
1. Gastrin.2. Gastric distension.
48
Name 5 factors that can decrease the strength of peristaltic contractions.
1. Duodenal distension. 2. Low pH in duodenum lumen. 3. Increased duodenal osmolarity. 4. Increased sympathetic action.5. Decreased parasympathetic action.
49
What do parietal cells secrete?
HCl and intrinsic factor.
50
What do chief cells secrete?
Pepsinogen and gastric lipase.
51
What cells secrete Gastrin?
Enteroendocrine cells / G cells.
52
What cells secrete somatostatin?
D cells.
53
What cells secrete histamine?
Enterochromaffin like cells.
54
On average, how much gastric acid do we secrete a day?
2L
55
What is the hydrogen ion concentration of gastric acid?
>150mM
56
Where does the H+ come from in gastric acid?
In parietal cells: H2O + CO2 = HCO3- + H+
57
What is the mechanism of the H+/K+ ATPase proton pump?
It pumps H+ into the stomach lumen and K+ into the parietal cell via primary active transport
58
What ions are exchanged on the side of the parietal cell in contact with the capillaries?
Cl- is pumped into the parietal cell and HCO3- moves out of the parietal cell into the capillary.
59
What is the importance of HCO3- being exchanged for Cl-?
HCO3- moving out of the cell increases the rate of the forward reaction and so more H+ are produced. Cl- moving into the cell then moves into the stomach lumen via Cl- channels and combines with H+ to form HCl.
60
What are the 4 phases important in regulating gastric acid secretion? Do these phases turn secretion on or off?
1. Cephalic phase - turning ON.2. Gastric phase - turning ON.3. Gastric phase - turning OFF.4. Intestinal phase - turning OFF.
61
Regulating gastric acid secretion: What stimuli are involved in the cephalic phase?
Sight, smell, taste of food. Chewing.
62
Regulating gastric acid secretion: What stimuli are involved in the gastric ON phase?
Gastric distension, presence of peptides and amino acids in the stomach.
63
Regulating gastric acid secretion: What stimuli are involved in the gastric OFF phase?
Low pH in gastric lumen.
64
Regulating gastric acid secretion: What stimuli are involved in the intestinal phase?
Low pH in duodenal lumen, duodenal distension, presence of amino acids and fatty acids in the duodenum.
65
Briefly describe the cephalic phase.
The parasympathetic nervous system is triggered by stimuli. This releases Ach. Ach acts on parietal cells and on gastrin and histamine. HCl secretion increases.
66
Briefly describe the gastric ON phase.
Gastrin is released in response to the stimuli. This acts on parietal cells and triggers release of histamine (histamine then acts on parietal cells too). HCl secretion increases.
67
Briefly describe the gastric OFF phase.
Gastrin is inhibited in response to stimuli and histamine is therefore indirectly inhibited. Somatostatin is also released and this inhibits parietal cells. HCl secretion decreases.
68
Briefly describe the intestinal phase.
The enterogastrones secretin and CCK are released in response to stimuli. Secretin inhibits gastrin and stimulates further somatostatin release. HCl secretion decreases.
69
What neurotransmitter is involved in regulating gastric acid secretion?
Ach.
70
What hormone is involved in regulating gastric acid secretion?
Gastrin.
71
What paracrine factors are involved in regulating gastric acid secretion?
Histamine and Somatostatin.
72
What enterogastrones are involved in regulating gastric acid secretion?
Secretin and CCK.
73
Name the 4 main defence mechanisms against gastric acid secretion.
1. Alkaline mucous. 2. Tight junctions between epithelial cells. 3. Replacing damaged cells. 4. Feedback loops.
74
Define ulcer.
A breach in a mucosal surface.
75
Name 3 things that can cause peptic ulcers.
1. Helicobacter pylori. 2. NSAIDS.3. Chemical irritants.
76
Why do NSAIDS cause peptic ulcers?
They inhibit cycle-oxygenase 1. Cycle-oxygenase 1 is needed for prostaglandin synthesis, prostaglandins stimulate mucus secretion. Without cycle-oxygenase 1 there is less mucus and so the mucosal defence is reduced.
77
Why does helicobacter pylori cause peptic ulcers?
Helicobacter pylori lives in gastric mucus. It secretes urease. Urease breaks into CO2 and NH3. The NH3 combines with H+ to form NH4+. NH4+ damages the gastric epithelium, an inflammatory response is triggered and mucosal defence is reduced.
78
Name 2 drugs that can be used to reduce gastric acid secretion.
1. Proton pump inhibitors. 2. H2 receptor antagonists.
79
If water input is 9L, how much is reabsorbed and how much is excreted in the faeces?
8.8L is reabsorbed and 0.2L is excreted in the faeces.
80
How does water move across the small intestine?
It moves freely by osmosis and also via aquaporins.
81
How does Na+ move across the small intestine?
Na+ is actively transported from the lumen by pumps located in the cell membranes in the ileum and jejunum.
82
How does K+ move across the small intestine?
Via passive diffusion. Movement is determined by the potential difference between lumen and capillaries.
83
Where does Cl- and HCO3- reabsorption mainly take place?
In the ileum and colon.
84
What is the mechanism for Cl- and HCO3- reabsorption?
Cl- is actively reabsorbed in exchage for HCO3-. The intestinal contents therefore become more alkaline.
85
What enzyme digests starch in the small intestine?
Pancreatic amylase.
86
What bonds does pancreatic amylase break?
alpha 1-4 linkages.
87
What are the end products of starch digestion?
Maltose!Also maltotriose, glucose polymers and alpha-dextrins.
88
Where in the small intestine are bile salts absorbed?
Terminal Ileum
89
What enzyme(s) hydrolyse peptide bonds in the stomach?
Pepsins.
90
What is the optimum pH for pepsins?
1.6-3.2
91
Why is pepsin action terminated in the small intestine?
The pH in the small intestine is too alkaline and so it denatures.
92
What enzyme(s) further break down peptides in the small intestine?
Pancreatic proteases.
93
What is the precursor molecule for pepsin?
Pepsinogen.
94
What activates pepsinogen?
Low pH.
95
What 2 groups can pancreatic proteases be divided into?
1. Endopeptidases e.g. trypsin.2. Exopeptidases e.g. carboxy dipeptidases.
96
How do amino acids get absorbed into the blood?
Passive diffusion.
97
What enzyme(s) hydrolyse cholesterol esters in the intestinal lumen?
Pancreatic esterases.
98
What emulsifies lipids?
Bile salts.
99
What is the advantage of emulsifying lipids?
It increases the SA for digestion and so digestion is more efficient.
100
What digests lipids in the small intestine?
Pancreatic lipases.
101
Are lipids hydrophobic or hydrophilic?
Hydrophobic.
102
What are the end products of fat digestion?
Free fatty acids and monoglycerides.
103
What triglyceride bonds is pancreatic lipase able to hydrolyse with ease?
1 and 3 bonds (the 2 bond is hydrolysed at a slower rate).
104
What protein binds pancreatic lipase to the surface of the lipid?
Co-lipase. This is essential, pancreatic lipase can not work without it.
105
The end products of fat digestion combine with bile salts and cholesterol to form what?
Mixed micelles.
106
What is the function of mixed micelles?
Lipid transport systems.
107
How are chylomicrons formed?
Triglycerides, phospholipids and cholesterol combine with proteins inside the epithelial cell forming chylomicrons.
108
Is vitamin A fat or water soluble?
Fat soluble.
109
What are the functions of vitamin A?
Vitamin A is needed for cellular growth and differentiation. It is also important for eyesight and lymphocyte production.
110
Name 3 sources of vitamin A.
1. Oily fish.2. Dairy.3. Liver
111
What is the recommended daily intake of vitamin A for men and women?
Women - 600µg. Men - 700µg.
112
What are the consequences of vitamin A deficiency?
Night blindness, growth retardation, increased susceptibility to infection.
113
What are the consequences of vitamin A toxicity?
Anorexia, vomiting, headache, reduced bone density, conjunctivitis.
114
Is vitamin C fat or water soluble?
Water soluble (easily lost when boiled).
115
What are the functions of vitamin C?
Synthesis of collagen, neurotransmitters and carnitine. It has an antioxidant ability and can absorb non-haem iron.
116
Name 4 sources of vitamin C.
1. Citrus fruits. 2. Green leafy veg.3. Potatoes.4. Kidney.
117
What is the recommended daily intake of vitamin C?
40mg.
118
What are the consequences of vitamin C deficiency?
Weakness, shortness of breath, aching, bleeding gums, thickening of skin.
119
What are the consequences of vitamin C toxicity?
Diarrhoea, nausea, renal stone formation.
120
Are B vitamins fat or water soluble?
Water soluble.
121
How many B vitamins are there?
8
122
What are B vitamins important for?
Cell metabolism and energy production.
123
How long do glycogen stores in a 70Kg adult last?
About 12 hours.
124
How long do lipid stores in a 70Kg adult last?
3 months.
125
What percentage of BMR do these organs use?a) Brain.b) Liver.c) Muscle.
a) 20%.b) 21%.c) 22%.
126
What fuels does the brain use?
Glucose and ketone bodies.
127
What fuels does the liver use?
Glucose, amino acids, fatty acids.
128
What fuels does muscle use?
Glucose, ketone bodies, amino acids and triacylglycerol.
129
What are free sugars and starch associated with effecting?
They can cause shifts in blood glucose and insulin due to their rapid absorption. This can strain the pancreas.
130
What type of starch is the most desirable and why?
Slowly digestible starch. It is slowly digested and absorbed and so has little influence on blood glucose and insulin.
131
What is the cause of lactose intolerance?
A deficiency in lactase.
132
Give 3 symptoms of lactose intolerance.
1. Bloating. 2. Diarrhoea. 3. Pain.
133
Explain the mechanism that produces the symptoms of lactose intolerance.
Lactose intolerance has an osmotic effect. H2O and fermentable sugars enter the the large intestine lumen and cause diarrhoea, bloating and pain.
134
Why might someone with enterocyte loss be unable to break down lactose?
Enterocytes at villi contain lactase. If the enterocytes are lost they may have lactase deficiency.
135
Define BMR.
The energy needed to stay alive at rest, usually 24kcal/kg/day.
136
Where does the foregut begin and end?
Mouth to the major duodenal papilla. (In the embryo - oropharyngeal membrane to the liver bud).
137
Where does the midgut begin and end?
Major duodenal papilla to 2/3 along the TC. (In embryo - liver bud to 2/3 along TC).
138
Where does the hindgut begin and end?
Distal 1/3 of TC to anal canal. (In embryo - distal 1/3 of TC to cloacal membrane).
139
Why are the foregut, midgut and hindgut divisions different in the adult compared to in the embryo?
It changes due to the formation of the ampulla of vater.
140
Are the pharyngeal clefts formed in the endoderm or ectoderm?
Ectoderm.
141
Are the pharyngeal pouches formed in the endoderm or ectoderm?
Endoderm.
142
How many pharyngeal arches are there?
5 (4 pharyngeal clefts and pouches).
143
What does the first pharyngeal arch form?
Muscles for mastication. Innervation: Cn 5.
144
What does the second pharyngeal arch form?
Muscles for facial expression. Innervation: Cn 7.
145
What does the third pharyngeal arch form?
Stylopharyngeus muscle. Innervation: Cn 9.
146
What does the fourth pharyngeal arch form?
Cricothyroid muscle. Innervation: External branch of superior laryngeal nerve (Cn 10).
147
What does the sixth pharyngeal arch form?
Intrinsic muscles of the Larynx. Innervation: Recurrent laryngeal nerve (Cn 10).
148
Why is the stomach the shape it is?
Due to differences in growth rates. The greater curvature grows faster than the lesser curvature.
149
Why does the left vagus nerve become the anterior vagal trunk and the right vagus become the posterior vagal trunk?
Due to the 90 degrees clockwise rotation of the stomach in its longitudinal axis.
150
What are the axis of stomach rotation?
Longitudinal and anteroposterior.
151
What does the dorsal mesentery become?
The greater omentum.
152
What does the ventral mesentery become?
The lesser omentum.
153
What are the 5 stages of midgut development?
1. Elongation. 2. Herniation.3. Rotation. 4. Retraction. 5. Fixation.
154
What connects the midgut to the yolk sac?
The Vitelline duct.
155
What happens in the elongation stage of midgut development?
Rapid elongation forms the primary intestinal loop. The proximal part of the loop forms the small intestine and the distal part forms the large intestine up to 2/3 TC.
156
What happens in the herniation stage of midgut development?
The rapid growth of the intestinal loop means it is pushed into the extra embryonic cavity in the umbilical cord.
157
What happens in the rotation stage of midgut development?
The elongated intestinal loop rotates 270 degrees anticlockwise.
158
What happens in the retraction stage of midgut development?
In the 10th week the herniated midgut returns into the expanded abdominal cavity. Th jejunum is first to return.
159
What happens in fixation of midgut organs?
This is when some regions of the gut lose their dorsal mesentery. These regions become retroperitoneal.
160
What are the 4 layers of the GI tract?
1. An innermost mucosa.2. A sub-mucosa.3. An external muscle coat (muscularis externa) 4. A serosa.
161
What is the innermost mucosa layer composed of?
- A folded epithelium. - Lamina propria (connective tissue).- Muscularis mucosa (ring of smooth muscle).
162
What is the submucosa layer composed of?
Loose connective tissue containing glands and lymph tissue. Many blood vessels and a rich plexus of nerves that is part of the enteric nervous system (Meissner's plexus) are also found in the submucosa.
163
What is the muscular externa composed of? What is its function?
Composed of 2 layers of smooth muscle: circular and longitudinal. Nerves that are part of the enteric nerve plexus are also present here (Aurebach's plexus). Contraction of the muscle helps to break down and food and propel it along the GI tract.
164
What is the serous layer composed of?
Composed of a simple squamous epithelium that covers the outside surface of the gut tube facing the peritoneal cavity.
165
What enzyme are parietal cells abundant in?
Carbonic anhydrase.
166
Give 5 functions of hepatocytes.
1. Creation and storage of energy in the form of glycogen. 2. Synthesise and secrete plasma proteins.3. Remove amino groups from amino acids for the production of urea. (Deamination). 4. Uptake, synthesis and excretion of bilirubin and bile acids. 5. Detoxification and inactivation of drugs and toxins.
167
What are the 2 key stages for fat digestion?
1. Emulsification. 2. Triglyceride hydrolysis.
168
What clinical feature would you see in a patient with fat malabsorption?
Pale and smelly faeces.
169
What clinical feature would you see in a patient with vitamin K malabsorption?
Bruising.
170
What clinical feature would you see in a patient with protein malabsorption?
Swollen ankles.
171
Where in the layers of the GI tract would Meissner's plexus be found?
In the submucosa.
172
Where in the layers of the GI tract would Auerbach's plexus be found?
In the muscularis externa between the circular and longitudinal layers of muscle.
173
Name the abdominal retroperitoneal organs.
Supradrenal glands, Aorta, IVC, Duodenum (except cap), Pancreas (except tail), Ureters, Colon (ascending and descending), Kidneys, Oesophagus, Rectum.
174
Name the abdominal intraperitoneal organs.
Spleen, Small intestine, Appendix, Liver, Transverse colon, Stomach, Sigmoid colon.
175
What is the arcuate line?
The lower limit of the posterior rectus sheath.
176
What happens to the posterior rectus sheath below the arcuate line?
It is absent. The rectus abdominis is in direct contact with the transversalis fascia.
177
What envelopes the rectus abdominis above the arcuate line?
It is enveloped by the internal oblique aponeurosis.
178
What is the anterior layer of rectus sheath formed from?
External oblique aponeurosis and the anterior lamina of the internal oblique aponeurosis.
179
What is the posterior layer of the rectus sheath formed from?
The posterior lamina of the internal oblique aponeurosis and the transversus abdominis aponeurosis.
180
What forms the anterior rectus sheath below the rectus abdominis?
The external oblique, internal oblique and transversus abdominis aponeurosis' all form the anterior rectus sheath. There is no posterior rectus sheath.
181
What vertebral level does the umbilicus mark when lying down?
L3.
182
What abdominal plane would you refer to when carrying out a lumbar puncture?
The intercristal plane. It joins the highest points of the pelvis posteriorly and marks the space between L4 and L5.
183
Describe 2 ways in which the transpyloric plane can be drawn.
1. The midpoint between the suprasternal notch and the pubic symphysis. 2. Connects the two points marked by the insertion of the rectus sheath into the costal margin.
184
Name 3 structures that cross the transpyloric plane.
1. The pylorus of the stomach. 2. The gall bladder. 3. The pancreas.
185
At what vertebral level is the transpyloric plane?
L1.
186
What is the intercristal plane?
It connects the highest points of the pelvis at the lower back.
187
At what vertebral level is the intercristal plane?
L4/5.
188
What is the intertubercular plane?
A line that joins the tubercles of the iliac crests.
189
At what vertebral level is the intertubercular plane?
L5
190
What is the subcostal plane?
A plane parallel to the lowest points of the costal margins.
191
At what vertebral level is the subcostal plane?
L2.
192
Where is the swallowing centre found?
Medulla oblongata.
193
What molecule is responsible for the activation of pepsinogen into pepsin?
HCl.
194
Give 3 functions of HCl in the stomach.
1. Solubilisation of food particles. 2. Kills microbes. 3. Activates pepsinogen forming pepsin.
195
Histamine is secreted by enterchromaffin like cells. What are enterochromaffin cells?
Enterchromaffin cells are located in the intestine and secrete serotonin, not histamine.
196
What type of cells are secretin and CCK?
Enterogastrones.
197
Chief cells secrete pepsinogen and and an enzyme. What is the enzyme?
Gastric lipase.
198
Name 3 monosaccharides.
1. Glucose. 2. Fructose. 3. Galactose.
199
Name 3 disaccharides.
1. Sucrose (glucose and fructose).2. Lactose (glucose and galactose).3. Maltose (glucose and glucose).
200
Name 3 polysaccharides.
1. Starch. 2. Cellulose. 3. Glycogen.
201
Where does the majority of complex polysaccharide digestion occur?
In the large intestine via gut bacteria.
202
Where is the first site of starch digestion?
In the mouth via salivary amylase.
203
Briefly describe starch digestion.
Begins in the mouth via salivary amylase. In the small intestine pancreatic amylases catalyse alpha 1-4 linkages forming maltose. The end products are further broken down by enzymes e.g. maltase on the luminal membrane; this forms monosaccharides. The products diffuse into the blood.
204
What are proteins digested into?
Dipeptides, tripeptides and amino acids.
205
What enzyme is responsible for protein digestion in the stomach?
Pepsin.
206
What is the optimum pH for pepsin action?
1.6 - 3.2
207
What does pepsin break proteins into?
Peptide fragments.
208
What enzymes are responsible for protein digestion in the small intestine?
Pancreatic proteases.
209
What are the 2 types of pancreatic proteases?
1. Endopeptidases. 2. Exopeptidases.
210
Give 2 examples of an endopeptidase.
1. Trypsin. 2. Chymotrypsin.
211
Give 2 examples of an exopeptidase.
1. Carboxypeptidases. 2. Aminopeptidases.
212
What is the function of endopeptidases?
They break peptide bonds between non-terminal amino acids.
213
What is the function of exopeptidases?
They break peptide bonds between terminal amino acids and so form monomers.
214
Which type of pancreatic protease can form monomers?
Exopeptidases.
215
By what process are the products of protein digestion absorbed into the intestinal epithelial cells?
Secondary active transport coupled to H+ or Na+.
216
What molecules make up phospholipids?
1 glycerol backbone, 2 fatty acids and 1 phosphate group.
217
What are triglycerides broken down into?
Monoglycerides and free fatty acids.
218
What enzyme is needed for fat digestion?
Pancreatic lipase.
219
What mechanism speeds up the digestion of fats?
Emulsification - the surface area for lipase action is increased.
220
What substances emulsify lipids?
Bile salts and phospholipids.
221
What enzyme anchors lipase to the surface of an emulsified lipid droplet?
Colipase.
222
Name 4 molecules to make up micelles.
1. Fatty acids. 2. Monoglycerides. 3. Bile salts. 4. Phospholipids.
223
What molecule is produced that aids absorption?
Micelles.
224
What is the function of micelles?
They are lipid transport systems. They move to the epithelial brush border and release the fatty acids and monoglycerides for absorption.
225
What happens to the fatty acids and monoglycerides inside the intestinal epithelial cells?
They are re-synthesised into triglycerides in the smooth ER.
226
Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the intestinal epithelial cells?
To maintain the concentration gradient for further absorption of fatty acids and monoglycerides.
227
Inside the intestinal epithelial cell, triglycerides combine with other lipids e.g. cholesterol to form what molecules?
Chylomicrons.
228
What are the functions of chylomicrons?
Chylomicrons move through the lymphatics and the blood stream to tissues.
229
How is vitamin B12 absorbed?
It binds to a protein, intrinsic factor. It is then absorbed in the terminal ileum via endocytosis.
230
What can cause pernicious anaemia?
If you have low levels of intrinsic factor you will have B12 deficiency. This will mean fewer RBC's will be formed leading to pernicious anaemia.
231
What can cause Barrett's oesophagus?
GORD.
232
Describe Barrett's oesophagus.
When the stratified squamous oesophageal epithelium changes to a simple columnar one at the lower end of the oesophagus. This can be caused by prolonged acid reflux from the stomach.
233
What is the function of the Vagus nerve in regards to parietal cells?
The vagus nerve stimulates the release of Ach which then acts on the parietal cells to increase HCl production.
234
Give 4 risk factors for GORD.
1. Obesity. 2. Pregnancy. 3. Hiatal hernia. 4. Smoking. (Sedentary lifestyle is not a risk factor).
235
Where in the stomach are G cells most numerous?
In the antrum.
236
Name 2 areas of the body with a low pH to combat bacteria.
Stomach and vagina.
237
Name 3 organs that secrete digestive enzymes.
1. Stomach. 2. Pancreas.3. Salivary glands.
238
What structure, visible microscopically, is primarily responsible for absorption?
Villi.
239
Name 3 physical mechanisms of absorption.
1. Endocytosis. 2. Diffusion/facilitated diffusion. 3. Active transport.
240
Name 2 diseases that can cause malabsorption.
1. Crohn's disease - loss of plicae circulares.2. Coeliac disease - vili atrophy.
241
Define malnutrition.
A lack of nutrition due to not eating enough, being unable to absorb nutrients, eating the wrong things.
242
Why might an elderly person be at risk of malnutrition?
1. Immobility - unable to cook and eat.2. Dental problems meaning its difficult to chew foods. 3. Decreased appetite. 4. Not eating the right things.
243
Name 3 physical tests for malnutrition.
1. BMI.2. Amount of body fat.3. Height.
244
Give 4 complications of malnutrition.
1. Apathy.2. Depression. 3. Increased risk of infection. 4. Anaemia.
245
Why is endoscopy preferred to a barium meal?
Produces a better image and is more accurate. Also prevents exposure to radiation as a barium meal requires an X-ray.
246
What muscles contributes to the upper oesophageal sphincter?
Cricopharyngeus.
247
Where are the stem cells that replace the epithelium located?
The base of crypts.
248
What are the pacemaker cells of the small intestine called?
Interstitial cells of Cajal.
249
Name 2 endocrine secretions from the duodenum?
1. Secretin. 2. CCK.
250
Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the epithelial cell?
To maintain a diffusion gradient allowing for further reabsorption.
251
Which papillae do not bear taste buds?
Filiform papillae.
252
Does the oesophagus have a serosa layer?
No!
253
What is refeeding syndrome?
Metabolic disturbances (hypokalemia, hypomagnesemia etc) that occur due to reinstitution of nutrition to patients who are starved/severley malnourished.
254
What are the functions of the stomach?
To store and mix food, dissolve and continue digestion, kill microbes, regulate flow of food, secrete proeases, secrete intrinsic factor, Lubrication.
255
Where is B12 absorbed?
Terminal ilium
256
What is chyme?
chewed up food that leaves the stomach.
257
What are the areas of the stomach?
cardia where the oesophagus joins, fundus at the top, body main top bit, antrum bottom main and pylorus the bit near the sphincter.
258
What are the key cells of the stomach?
Mucous cells, parietal cells, chief cells and enteroendocrine cells
259
Where are most of the mucous cells?
On the surface of the wall lining.
260
What are gastric pits?
The dips in the surface of the stomach. where you get parietal chief and enteroendocrine.
261
Where are you most likely to find parietal cells?
In the pits of the fundus and body not antrum
262
Where are you most likely to find chief cells?
In the pits of the antrum
263
What is Gastric acid?
Hydrochloric acid, about 2 litres a day, more than 150nM H+ concentration
264
Which cells produce gastric acid?
Parietal cells
265
How is gastric acid produced?
Chloride diffuses into the stomach passively to keep it electrically neutral by having potassium leaving. To increase H+ there is a hydrogen potassium pump ATP is used here. the comes from water. to replenish hydrogen ions carbonic andydrase converts CO2 into carbonic acid and the bicarbonate is released and the let into the blood by swapping with a chloride
266
What is an effect of vomiting ?
Low potassium
267
What is the turning on cephalic phase?
Initiated by the parasympathetic nervous system. this happens when we see smell or taste food. it causes Acetylcholine to be released onto parietal cells and triggers the release of gastrin and histamine which increases acid production
268
What is the gastric phase turning it on?
Gastric distension and the presence of pepties and amino acids stimulates release of gastrin, and this acts on parietal cells. Gastrin triggers the release of histamine which also acts on parietal cells which increase acid production
269
Why is histamine important?
It acts directly on parietal cells but also mediates the effects of gastrin and acetylcholine. which make this a good target for drugs
270
Why does protein in the stomach initiate acid release?
It is a direct stimulus for gastrin release, the protein acts as a buffer increasing pH by absorbing H+ ions, this leads to decreased somatostatin and more parietal cell activity
271
How is gastric acid secretion reduces in the gastric phase?
Low pH directly inhibits gastrin selection, it indirectly inhibits histamine release via gastrin and stimulates somatostatin release which inhibits parietal cell activity
272
How is gastric acid secretion turned off in the intestinal phase?
Distension in the duodenum, low luminal pH, hypertonic luminal contents and presenece of amino acids and fatty acids, these lead to enterogastrones being released such as secretin, which inhibits gastrin release and promotes somatostatin, it also releases choecystokinin and reduces ACh release
273
What type of signalling cells are gastrin, acetylcholine, histamine and somato statin?
Gastrin is a hormone, Histamin and somatostatin are paracrine chemicals, Acetylcholine is a neurotransmitter
274
How do the chemical act on the parietal cells?
Causes the more of the pumps to be put on the surface of the cells
275
What are peptic ulcers?
an ulcer is a breach in a mucosal surface.
276
What are the causes of peptic ulcers?
Helicobacter pylori infection, Drugs-NSAIDS, Chemical irritants alcohol and bile salts, dietary factors and gastrinoma.
277
What are the mechanisms of peptic ulcers?
Too much acid, or weakened mucosal defence
278
How is the stomach lining protected from the acid it produces?
Alkaline mucus, tight junctions between epithelial cells, replacement of damaged cells and feedback loops
279
How can helicobacter pylori cause an ulcer?
They live in the mucus, secreat urease splitting urea into ammonia and this can bind to hydrogen ions and proteases phospholipases and vacuolating cytotoxin A can damage the gastric epithelium and cause an inflamatory response which reduces mucus production
280
What are NSAIDs responsible for in the stomach?
Mucus secretion is stimulated by prostaglandins and Cyclo-oxygenase 1 needed for the synthesis of this, NSAIDS inhibit cyco-oxygenases and this reduces the mucosal defence
281
How can bile salts case ulcers?
Duodeno-gastric refux, regurgitated bile strips away mucus layer, reduce mucosal defence
282
How can Helicobacter pylori induced ulcers be treated?
Proton pump inhibitor for the acids, and two types of antibiotic to reduce numebrs of bateria
283
How can NSAID ulcers be treated?
Give the a proton pump inhibitor or histamine blocker, give them a prostaglandin analogue
284
Which cells secrete intrinsic factor?
Parietal cells
285
Which cells produce pepsin?
None
286
Which cell produces pepsinogen?
The chief cells
287
What is a zymogen?
An inactive form of an enzyme
288
What stimulates chief cells?
Same as for gastric acid
289
What activates pepsinogen?
Hydrochloric acid and pepsin can make it into pepsin
290
How is pepsinogen modified into pepsin?
it is cleaved into smaller parts
291
What allows for protease activation?
Low pH
292
How can pepsin be inactivated?
By reacting with the HCO3 in the small intestine
293
How much of protein digestion is the stomach responsible for?
abour 20%
294
What is the role of pepsin?
Not essential but accelerates protein digestion. Breaks collagen in meat
295
What is the volume of the stomach?
50mL
296
What is the maximum volume of the stomach?
1.5L
297
What is receptive relaxation?
Passive relaxation of the muscularis propria to increase the volume of the stomach
298
What helps gastric receptive relaxation?
Vagus parasympathetic innervation. NO and seretonin and enteric nerve plexuses
299
What is peristalsis?
Rhythmic wave like contractions in the walls of the stomach.
300
What are the pacemakers of the stomach?
Interstitial cells of khal also in intestines
301
Describe the contraction of the stomach?
Weak in fundus and body. forces food to pylorus and it closes the sphincter and squeezes food against it.
302
How is food let out of the stomach?
Small letting out of chyme into duodenum
303
How frequent is the basic electrical rhythm?
3 times per minute
304
How are gastricdepolarisations transmitted to other cells?
through gap junctions
305
How are the pacemakers able to generate action potentials?
ACh stimulus and other hormones to stimulate an action potential gastrin can do it and mechano receptors release gastrin
306
What duodenal factors decrease gastric motility?
increased duodenal luminal fat duodenal distension, duodenal osmolarity, decreased luminal pH
307
What is the importance of controlling gastric emptying?
The capacity of the duodenum is less than the capacity of the stomach
308
What is dumping syndrome?
When too much hypertonic solution goes into the duodenum.
309
What are the symptoms of dumping syndrome?
Vomiting, bloating, cramps, diarrhoes, dizziness, fatigue, weakness, sweating, dizziness, tachycardia
310
What is gastroparesis and its causes?
Delayed gastric emptying, no known cause, can be autonomic neuropathies, drugs, abdominal sugeries, parkinsons, MS scleroderma, amyloidosi, Female gender
311
What drugs can cause gastroparesis?
GI agents H2 antagonists, proton pump inhibitors, Anti cholinergic medications, Dephenhydramine, Opiod analgesics, Tricyclic antidepressantsOthers Beta adregenergic agonits, calcium channek blockers, interfereon alpha
312
What are symptoms of gastroparesis?
Nausea, early satiety, comiting undigested food, GORD, Abdominal pain, Bloating anorexia
313
What is special about the circulation in the liver?
There is the normal blood supply from the hepatic artery and blood returns to the heart by the hepatic veins and the IVC. Blood also comes from the small intestine via the superior and inferior mesenteric vein.
314
What are some of the main functions of the liver?
Detoxification- Filters and cleans blood of waste productsImmune functions- fights infections and diseasesSynthesis- of clotting factors proteins enzymes, glycogen and fatsProduction of bile- and breakdown of biirubinEnergy storage- glycogen and fatRegulation of fat metabolism Ability to regenerate
315
Describe the metabolic role of the liver
Continuous supply of energy for the body by controlling the metabolism of carbohydrates and fats
316
What regulates the liver metabolic activity?
Nerves and endocrine glands like the pancreas thyroid and adrenal glands
317
Where are lipides stored?
in adipocytes in hepatocytes and elsewhere
318
Which are more fluid saturated or unsaturated fatty acids?
Unsaturaes as they need more space due to their bent shape
319
What are the functions of lipids?
Part of cell membranes, Energy reserve, Integral to form cells, can be part of inflamatory cascades(arachadonic acid)Hormone metabolism like sx hormones and vitamin D
320
Where does energy in the body come from?
The oxidation of lipids or carbohydrates. 30-40 days of lipid energy lipid reserve 100000kcal
321
Where is the main storage f glycogen?
In the liver
322
Where do lipids come from to the liver?
The portal vein hepatic artery and lymphatics
323
In what form are lipids brought into the liver?
As free fatty acids
324
How can fatty acid storage be increased?
Eat more fatty acids.
325
How are lipids transported in the body?
As tryglycerides or fatty acids bound to albumin or within lipoproteins. Triglycerides cant pass through membranes by fatty acids can
326
What are the ways that fatty acids can be taken up by the liver?
Fatty acid binding proteins, Fatty acid translocase and fatty acid transport polypeptide
327
What is the name of the enzyme that can convert triglycerides into free fatty acids?
Lipoprotein lipase
328
What enzyme releases fatty acids from adipocytes?
Hormone sensitive lipase
329
What does insulin do in terms of fat storage?
Fat storage in adipocytes, stimulates lipoprotein lipase to break down TG to release FFA to be stored in the adipocytes. it reduces the activity of HSL so there is reduced export of lipids from the adipocytes
330
What are the effects of insulin resistance on fats?
Increased lipolysis in adipocytes leading to lots of TG in circulation, Increased offer of fatty acids to the liver so their uptake increases. increased glucose levels in blood mean less demand for lipids so used to store energy.
331
What is de novo lipogenesis?
Happens in the liver and is the sequential extension of an alkaoic chain starting from Acetyl-CoA via serial decarboxylative condensation reactions.
332
What is the rate limiting step of de novo lipogenesis?
Aecetyl-CoA to Malonyl-CoA catalysed by Acetyl-CoA carboxylase
333
What affects the rate of de novo lipogenesis?
Rate is related to Fatty acid sythetase which is activated by insulin and inactivated by catecholamines and glucagon, it has negative feedback on itself
334
What are lipoproteins?
A core of triglycerides and cholesterol-esters and a surface monolayer of phospholipids colesteral and specific proteins(apoproteins)
335
What determines the type of lipoprotein?
the ratio of protein to lipid defined by their density LDL HDL VLDL and chylomicrons
336
What do chylomicrons do?
Carry lipids from the gut to muscle and adipose tissue
337
What happens to chylomicron remnants?
They are taken up in the liver
338
What percentage of cholesterol comes from food?
10%
339
Where is cholesterol processed?
In the liver
340
How is cholesterol excreted?
Through the bile. it taken by lipoproteins in the circulation to the liver
341
How is fats and cholesterol exported from the liver?
As bile acids and VLDL
342
What is the process to export a fatty acid?
Apoprotein B100 is synthesised in the rER
the lipid compnent is synthesised in the sER
they are added by TAG proteins to ApoB.
They are sent to the Golgi apparatus where ApoB is glycosylated
and then migrates to the sinusoidal membrane and exocytosed as a VLDL
343
What affects Fatty acid oxidation?
Periperal fatty acid availablility increased by glucagon and decreased by insulin.
344
What are the 3 locations for oxidation of fatty acids in the liver?
Peroxisomal Beta oxidation
Mitochondrial beta-oxidation
ER Microsomal omega oxidation
345
What is mitochondrial beta-oxidation and what is it regulated by?
Oxidation of FAs of various chain lengths.
Progressive shortening of FAs in to acteyl-CoA
Condensed into ketone bodies which can be oxidised and enter the TCA cycle
Regulated by:
CPT (Carnitine Palmitosyl Transferase)
Carnitine concentration
Malonyl-CoA (Inhibits CPT)
346
What is peroxisomal beta oxidation?
Main Role in detoxification of:
very long chain FAs
2-methyl branched chain FAs
Dicarbolic acids - very toxic
4 step repeated process to shorten the FAs
By two acyl-CoA oxidases and two Thiolases
347
What is steatosis?
Fat gathering in the liver cells
348
What is microsomal omega oxidation?
Normally minor but increased pathway in Fat overload.
CYP4A enzymes oxidise saturated and unsaturated fatty acids.
Omega oxidation in the ER
Decarboxylation of omega hydroxyl FAs in cytosol
enter Beta oxidation pathway
349
How are Fatty acids able to regulate actions?
Gene expresson by controlling transcription factors. the control metabolic machinary for metabolic machinery for fatty acid metabolism
350
What are PPAR? and what would reduced PPAR sensing lead to?
Peroxisome Proliferator-Activated Receptor:
```
nuclear Receptors important for lipid metabolism
alpha, beta, gamma, delta
all involved in lipid homeostasis,
gamma is for energy storage
alpha is for gene transcription
```
Reduced PPAR sensing leads to steatosis and increased induction of CYP2E1 and proinflammatory cytokines.
351
What happens in defective metabolism of fats?
Less oxidation (so fat is overloaded) so microsomal omega oxidation increases
more dicarboxylic acids which inhibit other pathways of oxidation
leads to lipotoxicity and steatohepatitis
352
What are the deaseases reated to fat in the liver?
NAFLD non-alcoholic fattty liver diseas and NASH non-alcoholic steatohepatitis.
353
What are the stages of liver damage?
Fatty liver (deposits of fat cause enlargement), liver fibrosis (scar tissue forms) and cirrhosis ( growth of connective tissue destroys liver structure .
354
What causes fatty liver?
Increased TG in plasma from excess diarary intake and caloric intake. Also increased flux of FA increase releae of FA and uptake by hepatocytes. Decreased FA oxidation which decreased demand for lipids and increases storage.
355
What is steathepatitis?
Too much fat in the liver. Leads to large release of TG and FA overload increase Reactive Oxygen species production, It causes inflamation from kupffercells ad ethanol can activate stellate cells for fibrogeneseis. lipidperoxidation products cause inflamation
356
How do you manage fatty liver diseas?
Reduce calories, increase demant for consumption. usually will burn the fat off
357
How does alcohol cause fatty liver?
The high calorific values cause fat storage.
358
How does alcochol get procesed?
Alcohol is metabolised Alcohol dehydrogenase (under normal levels) or by the microsomal ethanol oxidising system using CYP2E1 (in excess) which produces acetaldehyde.
This can be further metabolised to acetate by aldehyde dehydrogenase.
Acetate can be used in the kerbs cycle
In excess, acetaldehyde is produced quicker and in more quantities which is toxic and damages the Hepatocytes from the production of free radicals
359
Which of the layers in the trilamina disk form the mid and hind gut?
Endoderm forms the mucosa of the bowl some layers are from mesoderm
360
What types of folding happens in the embryo?
Lateral the mesoderm and endoderm come round to make boweltube and is surrunded by the mesoderm to form the mesentry and peritoneal membrane
361
What deos the endoderm give rise to in the GI tract?
The endothelium of the bowel the hepatocytes of the liver and exo and endocrine pancreas
362
What does the visceral mesoderm give rise to?
The muscular wall connective tissue and cisceral peritonium
363
What is interesting about innervation of parietial peritonium?
It is the same as the overlying skin
364
What is interesting about innervation of visceral peritoneum?
It is supplied by separate nerves the greater for foregut lesser for mid and least for hind and causes refered pain
365
Where do the lungs develop from?
The foregut
366
Where is the boundary of the foregut and midgut?
Where the pancreatic duct joins the bowel.
367
What is the first stage of the GI developmen?
There is a forward looping supplied by the superior mesenteric artery
368
Where is refered pain for the heart and lungs?
T1-T5 inside of forarm and upper arm and on chest
369
Where is referred pain for the Foregut?
T5-T9 below nipples and umbilicus
370
Where is referred pain for the midgut?
T10-T11 the umbilicus
371
Where is referred pain for the Hindgut?
T12 just above hair bearing area
372
Describe the stages of the primitive Gut tube development.
Elongation, physiological herniation, rotation, retraction and fixation
373
What happens in elongation and herniation?
it elongates and then most of midgut loop passes through the umbilicus. elongates in the cephalic limb close to the head. it has rapid growth while the liver and pancreas grows in week 6
374
Describe the rotation of the tube?
the caecum rotates infront of the bowl clockwise from above to put it in the right lower part.
375
Describe retraction?
the abdominal area is big enough the mesentry facilitates this as it doesnt extend/ the transverse colon and the duodenum comes in first.
376
Where is the appendix?
In a variable position which leads to variable presentation of diseases.
377
What is the fixation stage?
on organs that are retroperitoneal the two layers fuse together and fix it to the wall
378
Which parts of the GI tract are fixed?
The duodenum apart from very first part. Ascending colon and descending and rectum
379
Where is the mesentry for the transverse colon passing?
Above the duodenum and across.
380
Where is the small intestine mesentry running from?
The duodena jejunal flecture to the illio cecal valve.
381
How can you look at the bowel?
Barium ennema and pump air in to xray it.
382
What embryological faults can happen?
rotation- caecum not in right place
| retraction- part of bowl in the umbilical cord or can rupture the cord.
383
What is the function of saliva?
Lubricant for mastication, swallowing and speechOral hygiene to wash the mouth buffer the acidity, and offer immune defenceAdds digestive enzyme and aids taste and without it can lead to infection and pain
384
What is the flow rate of saliva?
0.3-7ml per minute arount 1-1.5L over a day
385
What is the pH of saliva?
6.2-7.4
386
What is in the saliva?
Water serous secretion of amylase alpha and mucus secretion other enzymes such as water etc
387
Which salivary gland only produces serous secretions?
Parotid gland
388
What factors affect the composition of the saliva?
Flow rate, circadian rhythm, type and size of gland, duration and type of stimulus, diet, drugs, age ,gender
389
What defenses are there in the mouth?
The mucous provides a physical barrier. the palatie tonsils that have lymohocutes and dendritic cells, salivary glands wash away food and bacteria
390
Which glands continuously produce saliva?
Submandibular, sublingual and minor glands are continuously producing
391
Which gland only produces secretions when stimulated?
The parotid
392
What is the balance between mucous and serous secretions?
Unstimulates is mixedstimulated is mainly serous
393
What is whole saliva?
Saivary gland secretions, blood, oral tissue, microorganisms and food reminants
394
What are Exosomes?
Cell specific lipid microvesicles, can migrate through the vasculature. reside in a number of biofluids eg urin blood breast milk and saliva and we don't yet know their function but could be to do with immune response and contain DNA
395
What type of tests could the saliva be used for?
Diagnostic or prognostic tests
396
What are the structure of the salivary glands?
They have two distinct epithelial layers. Acinar cells which surround ducts which form a large duct enterig the mouth. There are many channels and transporters in the apical and basolateral mebranes enabling transport of fluid and electrolytes.
397
What are the two types of acinus?
Serous and mucous.
398
Describe the two types of acinar cells histologically
serous are dark staining nucleus in basal third and small central ducts secrete water and alpha amylase.
mucous are pale staining nucleus at the base large central duct and secrete water and glycoproteins.
399
What are the types of ducts in the glands?
Intralobular ducts and main excretory
400
What are the two divisions of intralobular ducts?
Intercalated short and narrow segments with cuboidal cells that connect acini to striated ducts. And striated ducts are major site for sodium chloride reabsorption
401
What is the appearace of striated ducts histologically?
Look striated
basal membrane has many microvilli for transport
many mitochondria for transport
402
Other than conduction what are the fuctnios of the ducts?
Primary saliver has lots of NaCL and is isotonic but it becomes hypotonic and NaCl also have secretions of potassium and HCO3
403
Which glands are the major salivary glands?
Parotid submandibular and sublingual.
404
Where are the parotid glands?
just in fron of the ear it has a capusule
405
What structures pass through the parotid gland?
The external carotid and termial branches, retromandibular vein, facial nerve.
406
Where is the outlet of the duct for the parotid?
above top of the molar on top
407
Where is the submandibular gland?
under the manduble bone there are two lobes.
408
What is wharton's duct?
it secretes the saliva from the submandibular and sublingual glands into the mouth. It is positioned in the sublingual papillae
409
Where are the sublingual gland?
Between mylohyoid muscle and oral mucosa
410
What does sublingual gland secrete??
mixed but mainly mucous
411
What are some of the minor glands?
around Buccal labial palatal and lingual regions. at base of tounge von ebner glands that secrete serous. all other minor are mucous producers
412
Which nerve innervates parotid?
the 9th cranial nerve does parasympathetic
413
What is Xerostomia?
Dry mouth
414
What are the main causes for dry mouth?
Radio treatment of cancer, CF sjogrens syndrome and often medications
415
What are other problems with glands?
Obstructed glands with stones, infections with them from mumps and parotid has the capsules which causes painDegenerative from radiotherapy.
416
What is Sjogren's syndrome?
An autoimmune condition that affects areas that produce fluids such as the salivary glands and the tear ducts resulting in dryness
Manly post-menopausal females, affects eyes, could be linked to arthritis
417
What is the effects of salivary gland dysfunction?
Low lubrication poor hygiene accumulation of plaque and caries gingivitis and periodontal disease and opportunistic infections
418
What is the effects of salivary gland dysfunction?
Low lubrication poor hygiene accumulation of plaque and caries gingivitis and periodontal disease and opportunistic infections
419
What is the function of bile?
Lipid emulsification and absorption, Cholesterol homeostasis, excretion of lipid soluble xenobiotics drug metabolites and heavy metals
420
What is bile?
A complex lipid-rich micellar solution containing water inorganic electrolytes, organic solutes, bile acids, phospholipids, cholesterol, bile pigments)
421
How much bile is produced a day?
500-600ml
422
How much of bile acids are lost each time?
5%
423
What makes up most of bile?
Bile acids then phospholipids cholestrol and protein small bilirubin
424
What are the types of bile acid?
Primary: Cholic and Chenodeoxycholic
Secondary: Deoxycholic and lithocholic acids
425
What produces secondary bile acids?
Bacterial conversion
426
What is the precursor for bile acids?
Cholesterol is used to produce it
427
What is the purpose of bile acid prodction?
the primary bile acids are water soluble unlike cholesterol
428
What happens the bile acids before the are secreted?
They are conjugated with taurine or glycine to make them lionised at physiological pH and therefore able to produce mixed micelles
429
What is amphipathic?
Like water and fat to reduce surface tension and aid emulsification
430
what is the function of emulsofication?
gives a large SA for lipolysis enzymes
431
What is colipase?
an enzyme that facilitates binding of lipase to the droplet
432
How do the fatty acids and monoglycerides get into the enterocyte?
They form micells with bile acids
433
What happens in an enterocyte to the fats?
Packaged into the lipoproteins for transport.
434
What are the functions of bile acids?
Induce bile flow through osmotic effect.
they are involved in the digestion of dietary fats,
facilitates protein absorption by accelerating hydrolysis,
involved in cholesterol homeostasis
antimicrobial can induce genes
prevents calcium gallstones and renal stones
435
describe the movement of cholesterol from the liver
It passes into the duodenum and 50% of all cholesterol including dietary is reabsorbed
436
What do statins do?
THey inhibit HMG CoA reductase to prevent cholesterol being formed
437
What does Exetimibe do?
Block protein mediated transport of cholesterol across the membrane of the small intestine
438
What happens to bile acids during the fasted state?
Bile acids go down the billary tract to gall bladder and get concentrated to 10x
439
What happens to the bile during the fed state?
CCK is released from duodenal mucosa which causes the sphincter of oddi to open and contract the gall bladder
440
What happens to bile acids in the small intestine
They stay intraluminal, they are reabsorbed in the terminal illium via the apical sodium bile acid transporter. and re enter the liver via portal circulation
441
How often does the circulation happen per meal?
2-3 times
442
What is the feedback mechanism for bile acid?
bile acids inhibit cholesterol 7 aloha hydroxylase
443
What is farnacoid X receptor?
Bile acids are ligands for it. this causes synthesis of Endocrine polypeptide hormen FGF19 to inhibit CYP7A1
444
what can go wrong in the circulation?
Inherited defects, deconjugation of bile acids from small bowel bacterial overgrowth, cholecystectomy can cause diarrhoea as it is just stored in duodenum.Ileal resection where absorbed bile acids ebter colon where they inhibit water absorption/ induce secretion resulting in bile salt diarrhoea
445
What happens in biliary obstruction and what are some clinical symptoms?
A stone blocks it, pancreatic carcinoma can cause malabsorption of fat soluble vitamins and fat resulting in steatorrhoea
446
What happens in biliary obstruction?
A stone blocks it, pancreatic carcinoma can cause malabsorption of fat soluble vitamins and fat resulting in steatorrhoea
447
What is the function of the colon?
Production of vitamins, absorption of water and electrolytes and excretion.
448
What makes faeces brown?
Stercobilin
449
What are the layers of the colonic wall?
Mucosa submucosa, muscularis mucosae and muscularis propria and serosae which encapsulatied
450
What is the muscular layer of the colon like?
continuous circular muscle, 3 stripes of longditudinal muscle taeniae coli
451
What are haustrations?
bumps in and out of the surface on the large bowel. (the bumps)
452
What is the epithelium in the bowel?
Columnar epithelium with goblet cells crypts of leibercoum
453
What is absorbed in the colon?
Water by osmosis, sodium is actively transported out of it
454
How are vitamins produced in the colon?
By bacteria produce them
455
What is the intrinsic nerve supply in the colon?
Meissners and Auerbach's plexus this contraction continues on its own and is stimulated by faecal matter in the tube.
456
What is the extrinsic innervation to the rectum
Parasympathetic - pelvic splanchnic nerves (S2-4)
| Sympathetic, Lumbar splanchnic nerves and hypogastric plexus
457
What is the gastro-colic reflex?
The stomach stretching and food in the jejunum leading to mass movement of the colon.
458
What is the structure of the anal sphincter?
There are many muscles such as levator ani internal and external anal sphincter. The internal is smooth muscle. the external anal sphincter is skeletal muscle
459
What happens when the rectum is empty?
both sphincters are contracted puborectalis (a sling that keeps the angle of the rectum acute) muscle is contracted
460
What happens when the rectum fills?
the external sphincter is relaxed, puborectalis relaxes, rectum contracts and do a valsalva maneuver (increases abdominal pressure by closing glottis and squeezing muscles
461
How do we know when we need to daefacate?
Pressure sensors in the rectum relax the anal sphincter, it is a sampling reflex
462
What could lead to constipation defaecation?
Consistency of stool, Bowel motility, physical blockage to the bowel, pelvic floor disorders
463
How can constipation be cured?
Drink more water, more dietary fibre, exercise, way sit on the toiletMedical- Laxative,
464
What can cause diarrhoea?
Consistency of stool or frequency of movements, diseased bowel mucosa, reduced rectal capacity, pelvic floor disorder
465
What diseases are associated with metabilic problems?
Diabetes, obesity, high cholesterol, aorexia.
466
What can happen to proteins in the body?
The enter the nitrogen pool and can become tissue protein, enter the urea cycle then citric acid cycle or excreted, or can be put into pyruvate and into the TCA cycle
467
What can happen to carbohydrates?
glycolysis to Pyruvate or acetyl CoA and then TCA cycle.
468
What happens to lipds in the body?
They undergo beta oxidation to enter TCA cycle
469
What comes from carbohydrates?
Glucose
470
What are proteins brokendown into?
Amino acids
471
What does fat become?
triglycerides
472
Where is glucose absorbed?
The intestines
473
Where glucose used?
Muscles, Brain, RBC and adipocytes to be stored
474
What happens to glucose in the liver?
Insulin promotes the uptake of glucose into cells, here it can be stored as glycogen. or it can be Acetyl CoA for energy production. With excess can be converted into triglycerides can be exported by LDL
475
What happens to glucose in the muscle?
Stored as glycogen, or used for respiration
476
How is glucose used in the brain?
It is used directly for energy
477
How is glucose used in RBCs?
Glucose is converted into pyruvate in glycolysis and then to lactate as cant do aerobic respiration
478
What happens in adipicytes to glucose?
Stored as triglycerides in the cells mediated by glucose
479
What happens to amino acids in the bloodstream?
They enter cells and are used to construct proteins, they can makehormones or they can feed into the krebs cycle
480
What happens to triglycerides in the body?
can be joined to proteins to be transported to the other parts of the body chylomicrons travel in the lymphatics
481
What happens in the fed state?
Fuels are oxidesed to energy. excess is stored as triglycerides in adipose tissue, glycogen in the liver and muscle
482
What happens in the body during fasting short term?
Energy stores are broken down to produce glucose. glycogen is broken down from the liver glucagon promotes this. the glucose goes to the brain and muscles and RBCs. this is called glycogenolysis
483
What happens in a longer fast initially?
All glycogen is used up in stores, amino acids are used preferentially by muscle protein. lactate from RBCs and glycerol can be released from adipocytes. this is all sent to the liver where these molecules produce glucose. Gluconeogenesis
484
What happens in a longer fast to the fats?
Triglycerides are split into glycerol that goes to the liver for conversion to glucose, Fatty acids can be used by the kidney and muscle as a source of energy. the fatty acids can produce ketones in an emergency. this is lipolysis and is driven by glucagon
485
What happens in prolonged fasting?
cant break down all of the muscles as can't move. so after a while it preserves muscles. this is when fatty acids are used and ketogenesis often takes place.
486
Which substances can be measured in the blood?
Glucose, ketones, insulin, lactate and triglycerides
487
Which hormones that regulate fuel metabolism?
Insulin and glucagon, cortisol, Adrenaline and noradrenaline, thyroxine, growth hormone and somatostatin
488
What does insulin do?
It is anabolic it promotes glycogen storage, fat storage and protein synthesie?
489
What does glucagon do?
It is catabolic it promotes glycogenolysis, gluconeogenesis and ketogenesis
490
What is the effect of cortisol?
Lipolysis, protein breakdown, gluconeogenesis and glycogen storage it is a preparation for a stress response
491
What are the effects of adrenaline?
Glycogenolysis, gluconeogenesis and lipolysis it is fight or flight hormone
492
What does thyroxine do?
It controls glycolysis, cholesterol synthesis, glucose uptake, protein synthesis and sensitises cells to adrenaline
493
What does growth hormone do?
Gluconeogenesis glycoge syntheis lipolysis, protein synthesis, decreased glucose use
494
What is Diet induced thermogensis?
The heat energy produced from the breakdown of food into its constituent nutrients
495
How is appetite controlled?
Ghrelin increases appetite and Leptin decreases hunger. high lipids gives high leptin but in obesity the body becomes desensitised
496
What are the foregut derivatives?
oesophagus stomach first half of duodenum pancreas liver, biliary system and dorsal and ventral mesentery ommentum
497
What is the dorsal mesentery?
the greater omentum
498
what is the ventral mesentry?
the lesser omentum
499
Which artery supplies the foregut?
The coealiac axis
500
What is the falciform ligamaent?
The free edge of the lesser ommentum that contains the ligamentum teres
501
What is the falciform ligament?
The free edge of the lesser ommentum that contains the ligamentum teres
502
Which mesentery does the liver grow in?
the lesser omentum/ventral
503
What are the outgrowths of the duodenum?
Two into the ventral mesentery( one pancreas the other liver) and one into the dorsal mesentery
504
describe the liver out pouching?
The bile ducts grow then some separate to form the liver in the ventral mesntery.it develops to the right of the midline and has overlapping mesentery and there is a bare area.
505
What is the portal triad like?
Has peritoneum surrounding it all they are at the edge of the lesser omentum
506
What is the rotation of the pancreas?
The dorsal rotates90 degrees to the left side. the ventral rotates to the same position bringing the bile ductwith it to the other pancrease.
507
What areas of the pancreas are formed from the ventral bud and dorsal bud?
Ventral bud:
Uncinate process
Head
Main pancreatic duct
Dorsal Bud:
Neck body and tail of the pancreas
508
Whar happen to the superior mesenteric artery and vein?
They get sandwiched between the two pancreases
509
Where is the head of the pancreas?
right by the duodenum
510
Where is the neck of the pancrease?
the bit that overlies the blood vessels
511
Where does the spleen develop?
The dorsal mesentry
512
Describe the rotation of the stomach
It rotates 90 degrees clockwise so the left side lies anteriorly and the right side lies posteriorly
513
where is the lesser sac?
The lesser omentum and greater omentum, posteria of it is the pancreas
514
When does the omentum grow the most?
In puberty
515
What happens in iron metabolism?
comes in to duodenum put into transferrin and can be made into blood cells muscles or in the liver. it is stored in the liver cells and reticuloendothelal macrophages
516
What is ferritin?
Large spherical protein with 24 units, it can contain 50000 atoms of iron an is in the cytoplasm and in the serum, the amout in the serum tells us how much iron in the body.
517
What is ferritin excess?
excess iron storage disorder, hereditary haemochromatosis, haemolytic anaemia, multiple blood transfusions, iron suppliments. can be non-iron overload like liver disease
518
What causes ferritin deficiency?
Not enough iron
519
What are vitamins used for?
Gene activators, free-radical scavengers, coenzymes or cofactors in metabolic reactions
520
Which vitamins are fat soluble?
ADEK
521
Which vitamins are water soluble?
B and C
522
How long do water soluble vitamin stores last?
Not long as easily washed out of body
523
What is vitamin A used for?
Used for help in eye function, comes from carrots and meat. it forms rhodopsin in rods of the eye and for spermatogenesis for growth and membranes
524
What is a defficiency in vitamin A?
Rare in affluent countries can lead to blindness night blindness can happen in fat malabsorption.
525
What happens with excess vitamin A?
Not very very bad but can lead to nausea vomiting headaches, can get yellowing of the skin
526
What is vitamin D used for?
increased intestinal absorption of calcium, resorption and formation of bone, reduced renal excretion of calcium.
527
What is the problem with vitamin D deficiency?
Rickets in children osteomalacia in adults
528
What is the role of sunlight in vitamin D?
sunlight converts it from 7dehydrocholesterol, into cholecalciferol, can come from others and its stored as 25 hydroxyvitamin D then converted to 1,25 dihydroxy to be used
529
What is vitamin E used for?
In antioxidants
530
How is vitamin E stored?
In adipose as fixed pool, and in licer and plasma as a labile store
531
What is defficiency and excess of vitamin E like?
Caused by fat malabsorption CF, premature infants, get haemolytic anaemia, myopathy, retinopathy ataxia and neuropathy in excess its not too harmful
532
What is vitamin K used for?
It is stored in licer but then given to LDL. it is used for clotting factors 2,7,9,10 it activates some.
533
What does a defficincy in vitamin K
Haemorragic disease of the nowborn not usually a problem in adults.
534
What happens in excess vitamin K?
K1 is safe, synthetic forms are more toxic, oxidative damage and red cell fragility
535
What is the use of vitamin C?
Collagen synthesis, antioxidant and iron absorption
536
What happens in vitamin C deficiency?
Scurvy easy bruising and bleeding teath and gum disease hair loss, quick treatment
537
What happens in excess?
Can cause GI side effects
538
What is vitamin B12 deffiecinecy?
caused by Pernicious anaemia, autoimmune destruction of IF producing cells in stomach.
malabsorption by lack of acid pancreatic disease or veganism
causes macrocytic anaemia and peripheral neuropathy in prolongued deficiency
539
What are the forms of B12?
methylcobalamin and 5-deoxyadenosylcobalamin
540
How is B12 absorbed?
Binds to R protein to protect from acid, then binds to intrinsic factor to be absorbed in the terminal ilium
541
What is folate?
Found in lots of fortified foods involved in coenzymes for DNA synthesis
542
What is the folate deficiency like?
malabsorption taking drugs can cause it, symptoms are high homocystine levels macrocytic anaemia and foetal abnormalites
543
What are the two clotting pathways?
intrinsic which is activated by contact, the extrinsic pathway activated by CF7 touching tissue factor.
544
What do the clotting pathways lead to?
Common pathway of thrombin turning fibrinogin into fibrin clot
545
What is prothrombin time?
The clotting time via extrinsic pathway
546
What is the activated partial thromoplastin time?
measures intrinsic pathway measurement
547
What does prolongues PT mean?
Prolongued PT may be deficiency in the synthetic capacity of the liver
548
What are the two phase of biotransformations of waste products?
Add or expose functional groups to the molecules such as OH SH NH2 or COOH to try and increase hydrophilicity slightly
Phase 2 i biosynthetic where the molecules are conjugated with endogenous molecules like glucoronic acids. it forms covalent bnds and increases hydrophilicity
549
What is glucuronidies?
is any substance produced by linking glucuronic acid to another substance via a glycosidic bond which makes substances more water soluble
550
what is the purpose of the drugs being detoxified
to make it more hydrophilic so it can be excreted
551
What is Cytochrome P450?
There are 10 moan groups encoded by about 60 genes they all are present in sER hence microsomal enzymes, the oxidise substrates and reduce water. they use NADPH they are indicible and can be modified by drigs and generate fre radicals
552
Why is Cytochrom P450 important?
It is involved in lots of drug drug reactions one durg can eaffect metabolism of another. they can also be inhibited by food. this can cause overdose
553
What can affect clozapine?
Barbituates rafamoicin and smoking can induce it and ciproflaxin are known to inhibit the cytochrome enzyme.
554
What are the clinical uses of this proses of biotransformation?
Some drugs are converted into inactive forms quickly, others are changed to another chemical with the same effect, some got from inactive drugs to active drugs, others could cause toxic products during breakdown
555
How are opiates being metabolised?
Codine molecule is morphone with OH replaced by methyl, so better distributed around the drug, this is then changed to morphine a useful product also
556
What happens to paracetamol?
Paracetamol is glucuronidated or sulohonated to make it more easily excreted but alternatively, some is excreted as NAPQI which can build up in overdose
557
What are some phase two reactions?
Glucoronidation sulphation, Glutatione, Methylation, Acylation, Phosphate conjucation
558
What is special about ethanol?
It doesn't fit phase one or phase 2, it is reduced to acetaldehyde, which can be harmful.
this can be done from microsomal systems as well this is worse in frequent drinkers.
it is converted to acetate in the liver but with the liver is overwhelmed it causes a bulid up of acetaldehyde this buildup causes damage
559
What are the parts of an amino acid?
Amino group NH2 acid group COOH and a sidechain
560
What is the difference between dipeptides, polypeptides, proteins?
Dipeptide is two AA polypeptide is less than 50AA protein is more than 50AA
561
How is nitrogen excreted in the kidney?
Not as protein but as urea
562
When might you have a negatice nitrogen balance?
Protein malnutrition, severe illness or sepsis, corticosteroids, cancer or deficiency
563
What is Kwashiorkor?
Protein-energy malnutrition
564
What happens to amino acid in the fed state?
Dietary protein is absorbed as amino acids in the gut. it is take to the liver where it can be conerted into proteins which travel to cells or go as lipoproteins or amino acids in the blood stream.can be converted to glucose
565
How is amino acid absorbed?
co transport with sodium and amino acids
566
What are essential amino acids?
Ones that the body cannot synthesis on its own
567
What are conditionally essential amino acids?
alanine is used to produce tyrosine. so can be produced but only in the presence of others
568
Non essential amino acids?
They are substances that are very easily produced by the body
569
What are glucogenic amino acids?
Carbon backbone can be used to produce glucose
570
What is a ketogenic amino acid?
is one that the backbone can be used for acetyl CoA
571
What are the two ketogenic amino acids?
Leucine and lysine
572
What is the way amino acids can be joined with the respitation?
They can enter at many stages, becoming pyruvate or CoA
573
What is transamination?
conversion of an amino acid and an alpa ketoacid into a different alphaketo acid and producing another amino acid. swappin the amino goup
574
What is the clinical use of transamination?
It is a good identifier of liver function
575
What is transamination of alanine?
Alanine+ alphaketoglutarate---> pyruvate+ glutamate
576
What is the use of transamination of alanine?
it is a shuttle for ammonia to the liver where it can be processed
577
How is ammonia excreted?
it is bound with bicarbonate to carbamyl phosphate which enters the urea cycle.
578
What happens to amino acids in the fasting state?
protein is broken into AA in the muscle and then put into TCA cycle and sent out to the other organs to be used.
579
Where can the urea cycle happen?
In
580
Where can the urea cycle happen?
In the liver only
581
Why do some proteins have bigger lifetimes?
Degredation factors: faulty ageing or obsolete, signal transduction, flexible system to meet protein/ energy requirements of environment.
582
What are the two main means of protein breakdown?
Proteasomes(ubiquitin) and lysosomes
583
What is ubiquitin?
A small protein that marks proteins for destructions it uses lysine residues. there are three enzymes that are used.
584
What is a proteasome?
Reacts to ubiquiting and contains proteolytic enzymes
585
What is the N-terminal rules?
The group at the end of the protein chane determins if it is destroyed. eg PEST or cyclin destruction box
586
What is the alanine glucose cycle?
Glucose can be sent to the cells and there it turns into pyruvate that can accept amine group from then the alanine can go to the liver and be turned back into glucose alphaketo-glutamate is made from glutamate
587
What is the aim of the urea cycle?
To turn ammonia to urea
588
What is the ornithine cycle?
Ammonia is added to citrulline to produce arginine and urea then ornithing has ammonia and CO2 to make citrulline
589
What can the urea cycle be linked to ?
the aspartate argininocuccinate shunt of the citric acid cycle
590
Where do the different parts of the urea cycle take place?
Ornithine and citruline parts in the mitochondrion. the rest in the cytoplasm.
591
How can you test for inherited metabolic disease?
test for bulidup of things in the cycle.
592
What happens to carbamoyl phosphate when it is not removed?
It prodcues oratate that can be picked up in urine of patiens with ornithine transcarbamalase problems
593
What is a good test for liver problems?
Ammonia testing
594
What is the role of the epithelial cells in the GI tract?
To absorb water and ions and secrete them
595
How long is the small intestine?
6m aprox
596
What increases the surface area of the small bowel?
The vili and the crypts
597
What is the function of the crypts?
they secret substances mainly
598
how is the trans cellular process facilitated?
The sodium potassium pump pumps sodium into the blood and potassium into the cell. Sodium moves from the intestinal lumen into the cell bringing other substances with it
599
What facilitates secretion in the intestine?
Chloride secretion coming into the cell it infuences cAMP which influences the chloride into the lumen and secretion of water.
600
What are the symptoms of digestive system conditions?
Diarrhoea, weight loss and failure to thrive
601
What happens in coelia disease?
the villi become dammaged?
602
What is prevalence in UK?
1 in 100
603
What is gluten?
protein is in wheat barley and rye
604
Why are rehydration drinks very salty?
The salts are absorbed and draw water into the body
605
Where is carbohydrates broken down first?
In the mouth
606
What breaks starch into sugar?
amylase to maltose then maltase to glucose
607
What is sucrose made of?
Glucose and fructose
608
What is lactose made of?
Glucose and galactose
609
How is glucose absorbed?
secondary active transport
610
How is fructose absorbed?
Facilitated diffusion
611
What molecules are broken down in the mouth?
carbohydrates and fats
612
How are amino acids absorbed?
They are absorbed by facilitated diffusion.
613
How do fats get absorbed?
As free fatty acids through the membrane
614
What enzymes are present in the stomach?
Pepsin and Lipase
615
What enzymes are released by the pancreas?
Amylase, lipase and colipate, phospholipase, trypsin and chymotrypsin
616
What enzymes are in the small intestine?
Disaccaridases enterokinase(activates trypsin) peptidases
617
What do chief cells do?
gastric lipases and pepsinogen
618
What are the pancreatic fuctions?
Endocrine (insulin glucagon)
| Exocrine- bicarbonate and enzymes
619
What is a pancreatic islet?
Alpha cells and beta cells and the acini what secrete enzymes into the pancreatic duct.
620
What happens at the different parts of the salivary duct?
Acinar Cell: NaCl rich secretions along with main salivary enzymes
Intercalated duct cells: Join acini to larger striated ducts
Striated duct cells: secrete HCO3- and K+ and reabsorb Na and Cl
621
Where is CF involved in the pancreas?
It is responsible for chloride and bicarbonate secretion protein
622
What chemicals stimulate the pancreas?
Secretin and cholecystokinin
623
Where is CCK produced?
In the duodenum and jejunum by the I cells
624
Why is bicarbonate secreted?
It buffers the acid from the stomach.
625
What helps activation/production of trypsin?
Trypsin and enterokinase
626
What activates chymotripsin?
Trypsin
627
How can you divide diseases of the panceas?
Intrinsic problems CF Cancer Autoimmune, Not linked directly could be under stimulation of pancreas, post surgical gastric resection whipple's
628
How do you image it?
MRI and CT as ultrasound doesn't work well externally? Ultrasound through the stomach
629
How can pancreatic insufficiency be treated?
Enzyme replacement, bone health assessment stop smoking treat underlying cause
630
What hormone has the strongest effect in inhibiting gastric empyting
Cholecystokinin
631
What are the major control mechanisms for gastric emptying?
Duodenal gastric feedback
hormones such as CCK
neural control
