GI case Flashcards
1
Q
Healthy Diet: (2)
A
A diet containing:
- An appropriate balance of food groups to obtain appropriate nutrients
- The right amount of energy to maintain an energy balance
2
Q
Energy requirements:
- Man
- Woman
A
- 2,500 calories a day
- 2,000 calories a day
3
Q
Overweight/Obesity statistics among adults:
A
- 7/10 men are overweight/obese
- 6/10 women are overweight/obese
4
Q
Obesity definition:
A
- Generally a result of energy intake being greater than energy expenditure
- Determined by Body Mass Index (BMI), 30 or higher
5
Q
BMI classifications:
- Underweight
- Normal
- Overweight
- Obese
- Morbidly obese
A
- < 18.5
- 18.5-24.9
- 25-29.9
- 30-39.9
- > /= 40
6
Q
Obesity Aetiology: (7)
A
Many potential factors:
- Psychological
- Cultural
- Psychiatric
- Environmental factors
- Genetics
- Medications
- Endocrine disorders
7
Q
Obesity consequences:
A
- A modifiable risk factor for disease
8
Q
Obesity: treatment options
A
- Lifestyle changes
- Pharmacotherapy
- Bariatric surgery
9
Q
Consequences of malnutrition:
A
- Literally everything is negatively effected
10
Q
Malnutrition in hospital
A
- Significant proportion of patients admitted to hospitals, care homes and mental health units are at risk of malnutrition
11
Q
Functions of the liver and gallbladder: (3)
A
- Metabolism
- Synthetic function
- Biliary circulation
12
Q
Liver metabolism: carbohydrates (3)
- Description
- 2 functions
A
- Liver is an ‘altruistic’ organ - releases glucose into the blood stream
- Glycogen storage
- Gluconeogenesis
13
Q
Liver metabolism: proteins
A
- Transamination: Aminotransferases break the amino acid down to glutamic acid
- Oxidative deamination produces carboxylic acid and ammonia (which needs to be removed)
14
Q
Aminotransferases:
- Location
- Indication
- Clinical
A
- Should be in the hepatocytes, not the bloodstream
- Large quantities in bloodstream indicates hepatocyte damage
- ALT monitored clinically for hepatocyte damage
15
Q
Urea cycle:
A
- Removes ammonia from the liver
- May be affected by liver damage
16
Q
Hyperammonaemia
A
Elevated levels of ammonia. Mostly caused by a defect in the urea cycle, causes: - Confusion - Excessive sleepiness - Hand tremors - Coma
17
Q
Hyperammonaemia:
A
- Excess ammonia in the blood stream
- May be seen in urea cycle disorders, other inborn metabolic errors and liver failure
18
Q
Liver metabolism: lipids
A
- Essential in lipid metabolism
- Liver problems may disrupt lipid levels (cholesterol, triglyceride)
19
Q
Synthetic function of the liver: albumin:
- % of plasma proteins
- Maintains:
- Also acts as:
A
- Makes up 50% of plasma proteins
- Main factor in maintaining osmotic pressure
- Also acts as a carrier protein: calcium, bilirubin
20
Q
Hypoalbuminaemia:
- Definition
- Cause
- Effect
A
- Low levels off albumin in the blood
- Caused by liver disease, nephrotic syndrome, malnutrition and burns
- causes Peripheral oedema
21
Q
Liver disease and bleeding: (3)
A
- Clotting factors synthesised in the liver
- Cholestasis: malabsorption of Vitamin K
- Decreased platelet count
22
Q
Biliary system:
- Globin route
- Haem route
A
Breaks down old/damaged RBCs:
- First into Haem and globin (protein)
- Globin broken down to amino acids
- Haem is then broken down to Biliverdin and iron by Haemoxygenase
- Biliverdin to bilirubin via biliverdin reductase
23
Q
Biliary system:
- Globin route
- Haem route
A
Spleen breaks down old/damaged RBCs:
- First into Haem and globin (protein)
- Globin broken down to amino acids
- Haem is then broken down to Biliverdin and iron by Haemoxygenase
- Biliverdin (soluble) to bilirubin (non-soluble) via biliverdin reductase
24
Q
Conjugation of bilirubin:
A
- Bilirubin transported to liver bound to albumin
- Bilirubin taken up by the liver via facilitated diffusion: conjugated to glucuronic acid
- Conjugated bilirubin released into bile
25
What can go wrong with bilirubin?:
- Increase in unconjugated bilirubin
- Fault in conjugation system
- Fault in biliary system
- Increase in unconjugated bilirubin:
result: inc. in unconjugated bilirubin
- Fault in conjungation system: benign for the most part
- Fault in biliary system (cancer, gallstone): Excess CONJUGATED bilirubin, leaks into circulation, no urobilinogen in faeces (pale)
26
Use of blood tests in biliary problems:
- state of excess bilirubin helps to figure out where a problem is located
- Liver isoenzyme alkaline phosphatase (ALP) found in the biliary ducts
- Raised ALP suggests CHOLESTASIS (biliary system blockage)
27
Bile salts:
- Synthesis
- Role
- Synthesised from cholesterol
| - Emulsify lipids prior to intestinal absorption
28
Enterohepatic circulation:
- Bile salts continuously recirculated via hepatic portal vein from gut
-
29
Liver failure:
- Carbohydrate metabolism:
- Protein synthesis:
- Protein metabolism:
- Lipid metabolism:
- Drug metabolism:
- Haem catabolism:
- Bile acid metabolism:
- Carbohydrate metabolism: hypoglycaemia
- Protein synthesis: hypoalbuminaemia, clotting problems
- Protein metabolism: hyper ammonaemia
- Lipid metabolism: Increased TG and cholesterol
- Drug metabolism: altered drug half life
- Haem catabolism: incr. bilirubin
- Bile acid metabolism: increase bile acids
30
GENERAL layered structure of GI tract: (4)
- Mucosa
- Submucosa
- Muscularis externa
- Serosa
31
Mucosa structures: interior to exterior (3)
- Epithelium: specialised polarised cells, sight of cell absorption
- Lamina propria: loose connective tissue
- Muscularis mucosae: responsible for local movement (squeezing glands)
32
Muscularis externa structure: (2)
- Circular muscle: inner layer, circles the lumen
| - Longitudal muscle: outer layer, runs length of tube
33
Submucosa:
- connective tissue containing organelles
34
Serosa:
- Connective tissue, keeps the GI tract together
35
Gut associated lymphoid tissue (GALT):
- Location
- Role
- Lymph nodes found throughout the lamina propria
| - Recognise food stuffs and defend against pathogens
36
Crypts and villi:
- Villi: finger like projections of the epithelium. Responsible for absorption
- Crypts: Innermost gaps between, secretion
37
Epithelial cells in the GI tract:
- Specialised polarised cells
- Absorptive cells: Small intestine
- Secretory cells: stomach
38
Five major sites of secretion in the GI tract:
- Salivary glands
- Gastric glands
- Exocrine pancreas
- Liver-billiary system
- Small intestine
39
GI tract secretion:
- Daily total:
- Contains:
- Function:
- 6-7 Litres/day
- Enzymes, ions, water and mucus
- Breakdown large compounds, regulate pH, dilute and protect
40
Basic Regulatory mechanisms control GI function: (3)
- Endocrine
- Paracrine
- Neuronal
41
Gastrointestinal hormones that regulate secretion and motility (2)
- Gastrin: gastric secretion, gastric motility
| - CCK: Gallbladder contraction and pancreatic secretion
42
GI hormones: That regulate blood flow
- CCK: stimulates blood flow
43
Innervation of GI tract:
- structure
- Sensors
- Neuronal plexus
- Effectors
- Intrinsic to the GI tract (short-range)
- Monitored by chemo and mechanoreceptors
- Submucosal and myenteric plexus (neurones)
- Effectors: smooth muscle, secretory cell, blood vessel
44
Innervation of GI tract: extrinsic nervous system
- Intrinsic receptors send signals to CNS
- ANS nerves innervate intrinsic effectors
- Vasovagal reflex
45
Functions of GI tract musculature 3:
- Non-propulsive movements (segmentation)
- Peristaltic movements (propulsive)
- Reservoir functions
46
GI tract muscle contraction time frames:
- Phasic (seconds)
| - Tonic (minutes-hours)
47
GI smooth muscle properties: (2)
- Single-unit action (function as one)
| - Membrane potential oscillates (slow waves), frequency of slow waves controls frequency of contractions
48
location of sphincters: (6)
- Upper oesophageal sphincter (UES)
- Lower oesophageal sphincter: (LOS)
- Pyloric sphincter
- Sphincter of oddi (bile duct to pancreatic)
- Ileoceacal sphincter (small to large intestine)
- Internal and external anal sphincters
49
Pyloric sphincter:
- Junction
- Type of sphincter
- Gastro-duodenal
| - Anatomical sphincter: formed by large inwards bulge of circular muscle
50
Lower oesophageal sphincter:
- Junction:
- Type of sphincter:
- Gastro-oesophageal
- Physiological sphincter (only): no bulging of circular muscle
- Epithelium changes from stratified squamous to simple columnar
51
The swallowing reflex: (5)
- Initiation
- Food triggers ....
- Signal sent to ....
- ....... nerves send motor signals to ......
- ........ nerves innervate pharynx and ......
- Initiated voluntarily, then entirely under reflex control
- Food triggers touch receptors near the pharyngeal opening
- Signal sent to medulla and lower pons
- Vagal nerves send motor signal to oesophagus
- Cranial nerves innervate the pharynx and upper oesophagus
52
Process of swallowing:
1. Oral/voluntary phase (2)
2. Pharyngeal phase (3)
3. Oesophageal phase (1)
1. Oral/voluntary phase:
- Tongue presses food against the hard pallet
- Bolus forced into pharynx, stimulating touch receptors
2. Pharyngeal phase:
- Soft palate elevates
- Epiglottis closes trachea
- Upper oesophageal sphincter relaxes
3. Oesophageal phase
- Upper oesophageal sphincter closed, peristalsis starts
53
The stomach and swallowing:
- Orad role
- Orad and caudad role:
- During swallowing
- Orad: accommodation of food
- Orad and caudad: gastric emptying
- During swallowing the orad relaxes
54
Vomiting:
1. Reverse ....
2. relaxation of
3. forced inspiration
4. Sharply elevated
5. Reflex relaxation
- Reverse peristalsis
- Pyloric sphincter and stomach relax
- Forced inspiration against a closed epiglottis
- Sharply elevated intra-abdominal pressure
- Reflex relaxation of upper oesophageal sphincter
55
Stomach Peristalsis: (4)
- Contractions begin in the .... and travel to the ......
- Increases in ...
- Mixing occurs in the .....
- Retropulsion
- Contractions begin in the corpus and travel to the pylorus
- They increase in force and velocity as they approach the gastroduodenal junction
- Mixing occurs in the antrum
- Retropulsion is effective at mixing and breaking down contents
56
Small intestine motility: Non-propulsive movements:
- Caused by
- Effect
- Non-propulsive movements: caused by rhythmic contraction and relaxation of the muscular external
- Mixes chyme and brings nutrients to mucosal surface
57
Small intestine motility: peristalsis
- Frequency
- Cause
- Allows
- Occurs at low frequency
- Caused by contraction of successive sections of muscularis externa
- Propels chyme for a short distance, allowing time for digestion/absorption
58
Functions of colonic contractions: (3)n
- Chyme
- Semi-solid contents
- Moves to
- Mixes chyme, improves absorption of water and salts from the colon
- Kneading semi-solid contents
- Moves contents toward anus
59
Mass peristalsis:
- Effect
- Controlled by
- Specialised type of movement, 1-3/day, moves the colonic contents towards the anus
- Directly controlled by enteric nervous system (gastrocolic reflex)
60
Defaecation: Rectosphincteric reflex (internal)
- Distension in the sigmoid colon triggers afferent nerves to send a signal to the sacral spinal cord
- Efferent pelvic nerves cause relaxation of the internal anal sphincter
61
Defaecation: external process (3)
- Rectospinteric reflex
- Relaxation of external anal sphincter
- Contraction of abdominal wall muscles and relaxation of pelvic wall muscles
62
Glands around the mouth:
- Parotid glands: serous (watery) secretion rich in alpha-amylase
- Submandibular and sublingual glands: seromucous secretion
- Minor salivary glands: mucous secretion rich in glycoproteins
63
Salivary secretion Stats:
- Quantity/day
- Osmolarity
- pH
- Composition
- 1.5 litres a day
- Hypotonic (only one in GI tract)
- pH: 7
- Composition: mucin glycoproteins, lysosome, a-amylase
64
Functions of saliva: (3)
- Mucin glycoproteins, water
- Lysozome
- A-amylase
- Lubricate the food to aid swallowing (mucin glycoproteins, water)
- Clean and protect mouth cavity (lysosome)
- Reduce starch to oligosaccharides (a-amylase)
65
Role of stomach in digestion: (3)
- Reservoir: gastric motility
- Digests proteins (pepsins)
- Essential for the absorption of vitamin B12 (intrinsic factor)
66
Gastric (acid) secretion
- Amount/day
- Composition
- pH
- 2.0 L/day
- HCl, pepsins, intrinsic factor, mucus HCO3-
- 0.9-1.5
67
Structure of gastric mucosa:
- Description
- Secretory cells (5) top to bottom
- HCO3-
- Mucous
- HCL, IF
- Pepsinogens
- Histamine, somatostatin
- Arranged into gastric pits, lined by different secretory cells
- Surface epithelium cell: HCO3-
- Mucous neck cell: Mucus
- Parietal cell: HCL, IF
- Chief cell, pepsinogens
- Endocrine cell, Histamine, somatostatin
68
Secretion of pepsins:
- Origin
- Role
- Optimal pH
- Reason for pH
- secreted by chief cells
- Digest proteins
- Optimal pH: < 3
- Low pH required for pepsinogen activation and pepsin activity
69
Functions of HCl: (3)
- Promotes activation and activity of pepsins
- Kills or inhibits microorganisms
- Stimulates secretions in the small intestine
70
Morphological changes that accompany HCl secretion:
- Parietal cells contain....
- Stimuli causes ..... to surface, forming ......
- Increases ......
- Parietal cell contains tubulovesicles containing H+ pumps and K+, Cl- channels
- Stimuli causes tubulovesicles to surface, forming canaliculus
- Increases secretory membrane SA (50-100X) with more H+ pumps, K+ channels and Cl- channels
71
Cellular mechanism for HCl secretion: stages 1-4
- ATP hydrolysis
- K+ movements
- Carbonic anhydrase
- HCO3- movements
1- Energy from ATP hydrolysis used to pump H+ into the lumen and K+ into the cell
2- Apical membrane K+ channels recycle K+ ions across the apical membrane
3- H+ secretion causes intracellular pH to rise, triggering passive uptake of CO2 and H2O across the basolateral membrane. Carbonic anhydrase catalyses their conversion to H+ and HCO3-
4- HCO3- ions are then removed across the basolateral membrane by the anion (CL-/HCO3-) exchanger
72
Cellular mechanism of HCL secretion: (5-8)
- Alkaline tide
- Cl- movement
- Na+/K+ATPase
- K+ CL- relation
5. HCO3- ions that exit the cell across the basolateral membrane cause the alkalinisation of local blood vessels termed “alkaline tide”
6. The Cl- ions that enter the cell across the basolateral membrane via the Cl-/HCO3- exchanger exit passively across the apical membrane via a Cl- channel to complete the process of acid (HCl) secretion
7. The Na+-K+-ATPase creates the inwardly directed Na+ gradient across the basolateral membrane.
8. Basolateral membrane K+ channels maintain the driving force for Cl- exit across the apical membrane
73
Secretion of mucus and bicarbonate:
- Secretes mucous
- Secretes HCO3-
- Regulatory ligands (2)
- Surface epithelial cells and mucous neck cells
- Surface epithelial cells (majority)
- Acetylcholine: via calcium signalling
- Prostoglandins: stimulates mucous and HCO3-. Inhibits acid secretion
74
Gastric mucosal barrier:
- Reliant on: (2)
- Neutralisation zone
- A HCO3- rich mucous blanket covers the epithelial cells (pH 7)
- Gastric lumen has pH 1.5
- Mucus gel neutralisation zone: zone between the two layers that is neutral due to opposing flows of H+ and HCO3-
75
Gastric mucosa protection: anatomical:
- Apical membrane impermeable to H+
| - Tight junctions don't allow H+ paracellular movement
76
Viscous fingering:
- Acid is shot out of gastric glands into the lumen
77
Direct Regulation of HCl secretion: Histamine
- Originates from
- Binds to
- Action
- ECL cell
- H2 receptor
- Acts on cAMP
78
Indirect HCl regulation:
- Nerves and gastrin both stimulate the ECL cell, increasing histamine production
79
control of gastric secretion: cephalic phase
- Secretory signals
- Dependant on:
- Total % volume of secretion
- Occurs when?
- Sight, smell, taste, chewing
- Entirely dependant on vagus nerve
- 30% of total secretion volume
- Occurs before food enters stomach
79
Control of gastric acid secretion: mechanisms
- Distention
- Amino acids
- Inhibition
- Distension: triggers mechanoreceptors, triggering vagovagal reflex
- Amino acids: trigger chemoreceptors on G cells, releasing gastrin, stimulating parietal cells
- Inhibition: Chemoreceptors on D cell detect HCL, releasing somatostatin, shutting down G cells and parietal cells
80
Control of gastric acid secretion: gastric phase stats
- Controlled by
- Amount
- controlled by vasovagal reflexes, hormones and paracrine factors
- Accounts for >50% of gastric secretion
81
```
Control of gastric secretion: intestinal phase:
- Early in gastric emptying
- Later in gastric emptying
Distension:
Digested proteins
```
- Early in gastric emptying: gastric chyme pH>3, STIMULATION predominates
- Later in gastric emptying: gastric chyme pH<3, INHIBITION predominates
- Distension of duodenum: mechanoreceptors stimulated, vasovagal reflex initiated, stims G cell and parietal cell
- Digested proteins: chemoreceptors stimulated, causes indirect stimulation
82
Control of gastric secretion: intestinal phase
| - Stimulation of secretion: mechanism
- Distension of duodenum: mechanoreceptors stimulated, vasovagal reflex initiated, stims G cell and parietal cell
- Digested proteins: chemoreceptors stimulated, causes indirect stimulation
83
Control of gastric secretion: intestinal phase: inhibition (HCl detected)
- Detection, secretion
- Secretin action (1)
- Secretin action (2)
- HCl detected in duodenum by S cell chemoreceptor, S cell then secretes secretin.
- Secretin travels via blood vessels to stomach. Inhibits parietal cells and G cells (antrum)
- Secretin also stimulates D cells to release somatostatin (direct or hormonal)
83
Control of gastric secretion: intestinal phase: inhibition (HCl detected)
- HCl detected in ....... by S cell, S cell secretes .....
- .......... inhibition route, targets .... cells, .... cells
- Also stimulates D cells to release ...
- HCl detected in duodenum by S cell chemoreceptor, S cell then secretes secretin.
- Secretin travels via blood vessels to stomach. Inhibits parietal cells and G cells (antrum)
- Secretin also stimulates D cells to release somatostatin (direct or hormonal)
84
Gastric emptying:
- Definition
- Speed varies by food type
- Rate of GE does not exceed:(4)
- Delivery of chyme from stomach to duodenum
- Speed varies: carbs>proteins>fats>indigestibe solids
- Rate of GE does not exceed:
. Acid neutralisation rate
. Fat emulsification rate
. Time for small intestine to process chyme
85
Mechanisms of digestion and absorption: brush-border hydrolysis
- brush-border hydrolysis of oligomer (sucrose) to monomer (glucose)
86
Mechanisms of digestion and absorption: Luminal hydrolysis
- Polymer (protein) is hydrolysed in the lumen, then the monomer (amino acid) is absorbed
87
Mechanisms of digestion and absorption: Intracellular hydrolysis
- Peptide absorbed into the apical membrane then hydrolysed to its monomer (amino acid)
88
Mechanisms of digestion and absorption: Lunminal hydrolysis followed by intracellular resynthesis
- Triglyceride hydrolysed into monomers, Absorbed vial apical membrane
- Re-synthesised to triglyceride in the cell
89
Digestion and absorption: carbohydrates
- Pathway (2)
- Transport mechanisms (3)
- Starch converted to maltose via alpha amylase
- Maltose converted to glucose via maltase
- SGLT1: Na+ coupled glucose transporter (apical)
- GLUT2: Glucose transporter 2 (basolateral)
- GLUT5: transports fructose (apical)
90
Digestion and absorption of proteins: 3 routes
- Simple
- Brush-border
- Intracellular
1. Proteins broken down to amino acids by proteases and absorbed
2. Dipeptides hydrolysed by peptidases (brush-border hydrolysis)
3. Dipeptides and tripeptides undergo intracellular hydrolysis
91
Digestion and absorption of proteins facts: (2)
- Apical membrane
- Absorption varies in intestine
- Amino acids cross apical membrane by Na+ dependant and independent mechanisms
- Amino acid and peptide absorption: duodenum>jejunum>>ileum
92
Digestion and absorption of fat: part 1
- emulsification
- Pancreatic lipase
- Products
- Triglycerides grouped and emulsified, creating emulsion droplets
- Pancreatic lipase works at the interphase between the lipid environment and aqueous environment,
- produces fatty acid and monoglyceride
93
Digestion and absorption of fats: part 2
- Mixed micelle formation
- Mixed micelle breakdown/diffusion
- Chylomicron formation
- Phospholipid cholesterol and bile salt micelle bind to fatty acids and monoglycerides, forming a mixed micelle
- Mixed micelle enters unstirred layer (acid), fatty acids and monoglycerides leave mixed micelle and diffuse across the apical membrane
- Chylomicrons form in SER and leave the cell via exocytosis into lymph duct
94
Digestion and absorption of fat simplified: (4)
- Emulsion droplet key step in fat digestion
- Fatty acid and monoglyceride diffuse across the apical membrane; no transport proteins required
- Triglyceride reformed in villus epithelial cells, delivered to lacteals
-
95
Substances used in glucose synthesis: (3)
- Lactate to Pyruvate
- Triglycerides to Glycerol
- Glucogenic Amino acids
96
Difference between gluconeogenesis (GNG) and glycolysis
- GNG (anabolic) is almost the reverse of glycolysis (catabolic)
- 3/10 glycolysis steps (1,3,10) are irreversible so glycolysis and GNG use different enzymes for these steps
97
Gluconeogenesis transversing the mitochondria: (3)
- Inner mitochondrial membrane not permeable to oxaloacetate
- Oxaloacetate converted into PEP or malate
- Lactate precursor prefers conversion to PEP
- Oxaloacetate converted to PEP within the inner mitochondrial membrane, malate leaves mitochondria before converting to oxaloacetate then PEP
98
glycogen synthesis;
- glycogen synthase activated when blood glucose levels are high (via insulin)
99
glycogen breakdown
- Glycogen phosphorylate activated by AMP and Ca2+ in muscle, converts glycogen to glucose-1-phosphate
100
Gluconeogenesis (GNG): costs
- 4 ATP, 2 GTP and 2 NADH per glucose
101
Relationship between rate of reaction and conc. substrates: (2)
- Rates are more sensitive to concentrations at concentrations near or below their Km
- Rate becomes insensitive at high substrate concentrations
102
[ATP], [ADP] and [AMP] in regulation for glycolysis and GNG
- Glycolysis:
- Glycolysis: Phosphofructokinase
| - inhibited by ATP and citrate, stimulated by ADP and AMP
103
[ATP], [ADP] and [AMP] in regulation for glycolysis and GNG
| - GNG
- GNG: fructose-1,6-phosphatase
| - Inhibited by AMP
104
AMPK: AMP-acttivated protein kinase
- Effects on:
- extrahepatic tissue: AMPK shifts metabolism to
- Liver: Triggers ......... to provide glucose for the brain
- Brain: stimulates
- AMP-activated Protein kinase is activated by AMP via sympathetic NS
Effects on:
- extrahepatic tissue: AMPK shifts metabolism towards the use of fatty acids for fuel
- Liver: triggers gluconeoenesis to provide glucose for the brain
- Brain: stimulates feeding behaviour
105
Acetyl CoA role in metabolism: (3)
- Regulates the fate of pyruvate
- Stimulates GNG: activates Pyruvate carboxylase
- Inhibits citric acid cycle: inhibits PDC (pyruvate dehydrogenase complex)
106
Pyruvate can be a source of new glucose:
- Used to store energy as glycogen
| - Generates NADPH for lipid synthesis
107
Pyruvate can be a source of Acetyl-CoA:
- Used to store energy as body fat
| - Used to make ATP via citric acid cycle
108
Fatty acid oxidation:
1. Beta oxidation
2. Citric acid cycle
3. oxidative phosphorylation
1- Beta oxidation. FA's are oxidised two carbons at a time and combine with CoA
2- acetyl CoA enters the citric acid cycle and is used to form NADH and FADH2
3- high energy electrons in NADH and FADH2 are used to synthesise ATP in oxidative phosphorylation
109
- Energy yield from Beta-oxidation of palmitic acid (C16);
- Acetyl CoA inCitric acid cycle:
- Oxidative phosphorylation:
- TOTALS
- Beta-oxidation: 8 acetyl CoA, 7NADH, 7 FADH2
- Acetyl CoA: 3 NADH, 1 FADH2 and 1 GTP
- Oxidative phosphorylation:
- 1 NADH = 2.5 ATP
- 1 FADH2 = 1.5 ATP
- TOTALS: 106 ATP
NADH = 7 + (8X3) = 31 = 77.5 ATP
FADH2 = 7 + (8X1) = 15 = 22.5 ATP
GTP = 8 = 8 ATP
110
Acetyl CoA produces three types of ketone: (3)
- Acetone
- Acetoacetate
- D-beta-Hydroxybutate
111
Ketone body function:
- Mobile acetyl-CoA, ketone bodies used to form acetyl-CoA
| - Acetyl-CoA then enters the citric acid cycle and produce ATP as normal
112
Metabolism in the liver during starvation:
- Preference for GNG
- Ketone bodies
- Use of ketone bodies
- Oxaloacetate is preferentially used for GNG to maintain [glucose]
- This slows the citric acid cycle in the liver, enhancing the formation of ketone bodies, releasing CoA to allow b-oxidation to continue
- Ketone bodies used as extra source of fuel as glucose is low
113
Functions of ATP:
- Carrying energy
- Building block of DNA, RNA
- Part of CoA, VitB also required
- As cyclic AMP (signalling)
- Synthesise NADH
114
NADH and NADPH: (4)
- Synthesised from
- Form
- Oxidised form
- Role
- Pathways (2)
- Both are synthesised for vitamin. B3 and ATP
- Both are activated carrier molecules
- NADH and NADPH are both reduced forms. NAD+ and NADP+ are the oxidised forms
- Both transfer high energy electrons between molecules
- NADH: catabolic pathways
- NADPH: anabolic pathways
115
Vitamin facts:
- Definition
- Deficiency
- Roles
- Organic molecules that cannot be synthesised
- Deficiency leads to disease
- Most act as coenzymes or antioxidants
116
Vitamin facts:
- Measured in micro/milligrams
| - RDA's don't vary much with age or sex
117
Consequence of dietary deficiency: Vit.A
- Impaired vision and more
117
Consequence of dietary deficiency: Vit c
- Scurvy
118
Direct Regulation of HCl secretion: Gastrin
- Originates from
- Binds to
- Action
- G cell
- CCK-B receptor
- Ca2+
119
Direct Regulation of HCl secretion: Acetylcholine (neuronal)
- Originates from
- Binds to
- Action
- Enteric neuron
- M3 receptor
- Ca2+
120
Indirect regulation of HCl secretion:
- Gastrin and Acetylcholine can both stimulate the ECL cell, increasing the amount of Histamine secreted
