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Medicine > GI case > Flashcards

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
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2
Q

Energy requirements:

  • Man
  • Woman
A
  • 2,500 calories a day

- 2,000 calories a day

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3
Q

Overweight/Obesity statistics among adults:

A
  • 7/10 men are overweight/obese

- 6/10 women are overweight/obese

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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
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5
Q

BMI classifications:

  • Underweight
  • Normal
  • Overweight
  • Obese
  • Morbidly obese
A
  • < 18.5
  • 18.5-24.9
  • 25-29.9
  • 30-39.9
  • > /= 40
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6
Q

Obesity Aetiology: (7)

A

Many potential factors:

  • Psychological
  • Cultural
  • Psychiatric
  • Environmental factors
  • Genetics
  • Medications
  • Endocrine disorders
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7
Q

Obesity consequences:

A
  • A modifiable risk factor for disease
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8
Q

Obesity: treatment options

A
  • Lifestyle changes
  • Pharmacotherapy
  • Bariatric surgery
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9
Q

Consequences of malnutrition:

A
  • Literally everything is negatively effected
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10
Q

Malnutrition in hospital

A
  • Significant proportion of patients admitted to hospitals, care homes and mental health units are at risk of malnutrition
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11
Q

Functions of the liver and gallbladder: (3)

A
  • Metabolism
  • Synthetic function
  • Biliary circulation
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12
Q

Liver metabolism: carbohydrates (3)

  • Description
  • 2 functions
A
  • Liver is an ‘altruistic’ organ - releases glucose into the blood stream
  • Glycogen storage
  • Gluconeogenesis
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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)
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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
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15
Q

Urea cycle:

A
  • Removes ammonia from the liver

- May be affected by liver damage

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16
Q

Hyperammonaemia

A 
Elevated levels of ammonia.
Mostly caused by a defect in the urea cycle, causes:
- Confusion 
- Excessive sleepiness 
- Hand tremors 
- Coma
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17
Q

Hyperammonaemia:

A
  • Excess ammonia in the blood stream

- May be seen in urea cycle disorders, other inborn metabolic errors and liver failure

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18
Q

Liver metabolism: lipids

A
  • Essential in lipid metabolism

- Liver problems may disrupt lipid levels (cholesterol, triglyceride)

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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
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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
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21
Q

Liver disease and bleeding: (3)

A
  • Clotting factors synthesised in the liver
  • Cholestasis: malabsorption of Vitamin K
  • Decreased platelet count
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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
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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
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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
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25
Q

What can go wrong with bilirubin?:

  • Increase in unconjugated bilirubin
  • Fault in conjugation system
  • Fault in biliary system
A
  • 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)
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26
Q

Use of blood tests in biliary problems:

A
  • 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)
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27
Q

Bile salts:

  • Synthesis
  • Role
A
  • Synthesised from cholesterol

- Emulsify lipids prior to intestinal absorption

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28
Q

Enterohepatic circulation:

A
  • ## Bile salts continuously recirculated via hepatic portal vein from gut
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29
Q

Liver failure:

  • Carbohydrate metabolism:
  • Protein synthesis:
  • Protein metabolism:
  • Lipid metabolism:
  • Drug metabolism:
  • Haem catabolism:
  • Bile acid metabolism:
A
  • 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
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30
Q

GENERAL layered structure of GI tract: (4)

A
  • Mucosa
  • Submucosa
  • Muscularis externa
  • Serosa
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31
Q

Mucosa structures: interior to exterior (3)

A
  • Epithelium: specialised polarised cells, sight of cell absorption
  • Lamina propria: loose connective tissue
  • Muscularis mucosae: responsible for local movement (squeezing glands)
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32
Q

Muscularis externa structure: (2)

A
  • Circular muscle: inner layer, circles the lumen

- Longitudal muscle: outer layer, runs length of tube

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33
Q

Submucosa:

A
  • connective tissue containing organelles
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34
Q

Serosa:

A
  • Connective tissue, keeps the GI tract together
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35
Q

Gut associated lymphoid tissue (GALT):

  • Location
  • Role
A
  • Lymph nodes found throughout the lamina propria

- Recognise food stuffs and defend against pathogens

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36
Q

Crypts and villi:

A
  • Villi: finger like projections of the epithelium. Responsible for absorption
  • Crypts: Innermost gaps between, secretion
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37
Q

Epithelial cells in the GI tract:

A
  • Specialised polarised cells
  • Absorptive cells: Small intestine
  • Secretory cells: stomach
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38
Q

Five major sites of secretion in the GI tract:

A
  • Salivary glands
  • Gastric glands
  • Exocrine pancreas
  • Liver-billiary system
  • Small intestine
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39
Q

GI tract secretion:

  • Daily total:
  • Contains:
  • Function:
A
  • 6-7 Litres/day
  • Enzymes, ions, water and mucus
  • Breakdown large compounds, regulate pH, dilute and protect
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40
Q

Basic Regulatory mechanisms control GI function: (3)

A
  • Endocrine
  • Paracrine
  • Neuronal
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41
Q

Gastrointestinal hormones that regulate secretion and motility (2)

A
  • Gastrin: gastric secretion, gastric motility

- CCK: Gallbladder contraction and pancreatic secretion

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42
Q

GI hormones: That regulate blood flow

A
  • CCK: stimulates blood flow
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43
Q

Innervation of GI tract:

  • structure
  • Sensors
  • Neuronal plexus
  • Effectors
A
  • Intrinsic to the GI tract (short-range)
  • Monitored by chemo and mechanoreceptors
  • Submucosal and myenteric plexus (neurones)
  • Effectors: smooth muscle, secretory cell, blood vessel
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44
Q

Innervation of GI tract: extrinsic nervous system

A
  • Intrinsic receptors send signals to CNS
  • ANS nerves innervate intrinsic effectors
  • Vasovagal reflex
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45
Q

Functions of GI tract musculature 3:

A
  • Non-propulsive movements (segmentation)
  • Peristaltic movements (propulsive)
  • Reservoir functions
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46
Q

GI tract muscle contraction time frames:

A
  • Phasic (seconds)

- Tonic (minutes-hours)

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47
Q

GI smooth muscle properties: (2)

A
  • Single-unit action (function as one)

- Membrane potential oscillates (slow waves), frequency of slow waves controls frequency of contractions

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48
Q

location of sphincters: (6)

A
  • 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
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49
Q

Pyloric sphincter:

  • Junction
  • Type of sphincter
A
  • Gastro-duodenal

- Anatomical sphincter: formed by large inwards bulge of circular muscle

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50
Q

Lower oesophageal sphincter:

  • Junction:
  • Type of sphincter:
A
  • Gastro-oesophageal
  • Physiological sphincter (only): no bulging of circular muscle
  • Epithelium changes from stratified squamous to simple columnar
51
Q

The swallowing reflex: (5)

  • Initiation
  • Food triggers ….
  • Signal sent to ….
  • ……. nerves send motor signals to ……
  • …….. nerves innervate pharynx and ……
A
  • 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
Q

Process of swallowing:

  1. Oral/voluntary phase (2)
  2. Pharyngeal phase (3)
  3. Oesophageal phase (1)
A
  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
Q

The stomach and swallowing:

  • Orad role
  • Orad and caudad role:
  • During swallowing
A
  • Orad: accommodation of food
  • Orad and caudad: gastric emptying
  • During swallowing the orad relaxes
54
Q

Vomiting:

  1. Reverse ….
  2. relaxation of
  3. forced inspiration
  4. Sharply elevated
  5. Reflex relaxation
A
  • 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
Q

Stomach Peristalsis: (4)

  • Contractions begin in the …. and travel to the ……
  • Increases in …
  • Mixing occurs in the …..
  • Retropulsion
A
  • 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
Q

Small intestine motility: Non-propulsive movements:

  • Caused by
  • Effect
A
  • Non-propulsive movements: caused by rhythmic contraction and relaxation of the muscular external
  • Mixes chyme and brings nutrients to mucosal surface
57
Q

Small intestine motility: peristalsis

  • Frequency
  • Cause
  • Allows
A
  • 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
Q

Functions of colonic contractions: (3)n

  • Chyme
  • Semi-solid contents
  • Moves to
A
  • Mixes chyme, improves absorption of water and salts from the colon
  • Kneading semi-solid contents
  • Moves contents toward anus
59
Q

Mass peristalsis:

  • Effect
  • Controlled by
A
  • Specialised type of movement, 1-3/day, moves the colonic contents towards the anus
  • Directly controlled by enteric nervous system (gastrocolic reflex)
60
Q

Defaecation: Rectosphincteric reflex (internal)

A
  • 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
Q

Defaecation: external process (3)

A
  • Rectospinteric reflex
  • Relaxation of external anal sphincter
  • Contraction of abdominal wall muscles and relaxation of pelvic wall muscles
62
Q

Glands around the mouth:

A
  • Parotid glands: serous (watery) secretion rich in alpha-amylase
  • Submandibular and sublingual glands: seromucous secretion
  • Minor salivary glands: mucous secretion rich in glycoproteins
63
Q

Salivary secretion Stats:

  • Quantity/day
  • Osmolarity
  • pH
  • Composition
A
  • 1.5 litres a day
  • Hypotonic (only one in GI tract)
  • pH: 7
  • Composition: mucin glycoproteins, lysosome, a-amylase
64
Q

Functions of saliva: (3)

  • Mucin glycoproteins, water
  • Lysozome
  • A-amylase
A
  • Lubricate the food to aid swallowing (mucin glycoproteins, water)
  • Clean and protect mouth cavity (lysosome)
  • Reduce starch to oligosaccharides (a-amylase)
65
Q

Role of stomach in digestion: (3)

A
  • Reservoir: gastric motility
  • Digests proteins (pepsins)
  • Essential for the absorption of vitamin B12 (intrinsic factor)
66
Q

Gastric (acid) secretion

  • Amount/day
  • Composition
  • pH
A
  • 2.0 L/day
  • HCl, pepsins, intrinsic factor, mucus HCO3-
  • 0.9-1.5
67
Q

Structure of gastric mucosa:

  • Description
  • Secretory cells (5) top to bottom
  • HCO3-
  • Mucous
  • HCL, IF
  • Pepsinogens
  • Histamine, somatostatin
A
  • 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
Q

Secretion of pepsins:

  • Origin
  • Role
  • Optimal pH
  • Reason for pH
A
  • secreted by chief cells
  • Digest proteins
  • Optimal pH: < 3
  • Low pH required for pepsinogen activation and pepsin activity
69
Q

Functions of HCl: (3)

A
  • Promotes activation and activity of pepsins
  • Kills or inhibits microorganisms
  • Stimulates secretions in the small intestine
70
Q

Morphological changes that accompany HCl secretion:

  • Parietal cells contain….
  • Stimuli causes ….. to surface, forming ……
  • Increases ……
A
  • 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
Q

Cellular mechanism for HCl secretion: stages 1-4

  • ATP hydrolysis
  • K+ movements
  • Carbonic anhydrase
  • HCO3- movements
A

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
Q

Cellular mechanism of HCL secretion: (5-8)

  • Alkaline tide
  • Cl- movement
  • Na+/K+ATPase
  • K+ CL- relation
A
  1. HCO3- ions that exit the cell across the basolateral membrane cause the alkalinisation of local blood vessels termed “alkaline tide”
  2. 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
  3. The Na+-K+-ATPase creates the inwardly directed Na+ gradient across the basolateral membrane.
  4. Basolateral membrane K+ channels maintain the driving force for Cl- exit across the apical membrane
73
Q

Secretion of mucus and bicarbonate:

  • Secretes mucous
  • Secretes HCO3-
  • Regulatory ligands (2)
A
  • Surface epithelial cells and mucous neck cells
  • Surface epithelial cells (majority)
  • Acetylcholine: via calcium signalling
  • Prostoglandins: stimulates mucous and HCO3-. Inhibits acid secretion
74
Q

Gastric mucosal barrier:

  • Reliant on: (2)
  • Neutralisation zone
A
  • 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
Q

Gastric mucosa protection: anatomical:

A
  • Apical membrane impermeable to H+

- Tight junctions don’t allow H+ paracellular movement

76
Q

Viscous fingering:

A
  • Acid is shot out of gastric glands into the lumen
77
Q

Direct Regulation of HCl secretion: Histamine

  • Originates from
  • Binds to
  • Action
A
  • ECL cell
  • H2 receptor
  • Acts on cAMP
78
Q

Indirect HCl regulation:

A
  • Nerves and gastrin both stimulate the ECL cell, increasing histamine production
79
Q

control of gastric secretion: cephalic phase

  • Secretory signals
  • Dependant on:
  • Total % volume of secretion
  • Occurs when?
A
  • Sight, smell, taste, chewing
  • Entirely dependant on vagus nerve
  • 30% of total secretion volume
  • Occurs before food enters stomach
79
Q

Control of gastric acid secretion: mechanisms

  • Distention
  • Amino acids
  • Inhibition
A
  • 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
Q

Control of gastric acid secretion: gastric phase stats

  • Controlled by
  • Amount
A
  • controlled by vasovagal reflexes, hormones and paracrine factors
  • Accounts for >50% of gastric secretion
81
Q 
Control of gastric secretion: intestinal phase:
- Early in gastric emptying 
- Later in gastric emptying 
Distension:
Digested proteins
A
  • 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
Q

Control of gastric secretion: intestinal phase

- Stimulation of secretion: mechanism

A
  • Distension of duodenum: mechanoreceptors stimulated, vasovagal reflex initiated, stims G cell and parietal cell
  • Digested proteins: chemoreceptors stimulated, causes indirect stimulation
83
Q

Control of gastric secretion: intestinal phase: inhibition (HCl detected)

  • Detection, secretion
  • Secretin action (1)
  • Secretin action (2)
A
  • 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
Q

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 …
A
  • 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
Q

Gastric emptying:

  • Definition
  • Speed varies by food type
  • Rate of GE does not exceed:(4)
A
  • 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
Q

Mechanisms of digestion and absorption: brush-border hydrolysis

A
  • brush-border hydrolysis of oligomer (sucrose) to monomer (glucose)
86
Q

Mechanisms of digestion and absorption: Luminal hydrolysis

A
  • Polymer (protein) is hydrolysed in the lumen, then the monomer (amino acid) is absorbed
87
Q

Mechanisms of digestion and absorption: Intracellular hydrolysis

A
  • Peptide absorbed into the apical membrane then hydrolysed to its monomer (amino acid)
88
Q

Mechanisms of digestion and absorption: Lunminal hydrolysis followed by intracellular resynthesis

A
  • Triglyceride hydrolysed into monomers, Absorbed vial apical membrane
  • Re-synthesised to triglyceride in the cell
89
Q

Digestion and absorption: carbohydrates

  • Pathway (2)
  • Transport mechanisms (3)
A
  • 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
Q

Digestion and absorption of proteins: 3 routes

  • Simple
  • Brush-border
  • Intracellular
A
  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
Q

Digestion and absorption of proteins facts: (2)

  • Apical membrane
  • Absorption varies in intestine
A
  • Amino acids cross apical membrane by Na+ dependant and independent mechanisms
  • Amino acid and peptide absorption: duodenum>jejunum»ileum
92
Q

Digestion and absorption of fat: part 1

  • emulsification
  • Pancreatic lipase
  • Products
A
  • 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
Q

Digestion and absorption of fats: part 2

  • Mixed micelle formation
  • Mixed micelle breakdown/diffusion
  • Chylomicron formation
A
  • 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
Q

Digestion and absorption of fat simplified: (4)

A
  • 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
Q

Substances used in glucose synthesis: (3)

A
  • Lactate to Pyruvate
  • Triglycerides to Glycerol
  • Glucogenic Amino acids
96
Q

Difference between gluconeogenesis (GNG) and glycolysis

A
  • 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
Q

Gluconeogenesis transversing the mitochondria: (3)

A
  • 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
Q

glycogen synthesis;

A
  • glycogen synthase activated when blood glucose levels are high (via insulin)
99
Q

glycogen breakdown

A
  • Glycogen phosphorylate activated by AMP and Ca2+ in muscle, converts glycogen to glucose-1-phosphate
100
Q

Gluconeogenesis (GNG): costs

A
  • 4 ATP, 2 GTP and 2 NADH per glucose
101
Q

Relationship between rate of reaction and conc. substrates: (2)

A
  • Rates are more sensitive to concentrations at concentrations near or below their Km
  • Rate becomes insensitive at high substrate concentrations
102
Q

[ATP], [ADP] and [AMP] in regulation for glycolysis and GNG
- Glycolysis:

A
  • Glycolysis: Phosphofructokinase

- inhibited by ATP and citrate, stimulated by ADP and AMP

103
Q

[ATP], [ADP] and [AMP] in regulation for glycolysis and GNG

- GNG

A
  • GNG: fructose-1,6-phosphatase

- Inhibited by AMP

104
Q

AMPK: AMP-acttivated protein kinase

  • Effects on:
  • extrahepatic tissue: AMPK shifts metabolism to
  • Liver: Triggers ……… to provide glucose for the brain
  • Brain: stimulates
A
  • 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
Q

Acetyl CoA role in metabolism: (3)

A
  • Regulates the fate of pyruvate
  • Stimulates GNG: activates Pyruvate carboxylase
  • Inhibits citric acid cycle: inhibits PDC (pyruvate dehydrogenase complex)
106
Q

Pyruvate can be a source of new glucose:

A
  • Used to store energy as glycogen

- Generates NADPH for lipid synthesis

107
Q

Pyruvate can be a source of Acetyl-CoA:

A
  • Used to store energy as body fat

- Used to make ATP via citric acid cycle

108
Q

Fatty acid oxidation:

  1. Beta oxidation
  2. Citric acid cycle
  3. oxidative phosphorylation
A

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
Q
  • Energy yield from Beta-oxidation of palmitic acid (C16);
  • Acetyl CoA inCitric acid cycle:
  • Oxidative phosphorylation:
  • TOTALS
A
  • 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
Q

Acetyl CoA produces three types of ketone: (3)

A
  • Acetone
  • Acetoacetate
  • D-beta-Hydroxybutate
111
Q

Ketone body function:

A
  • Mobile acetyl-CoA, ketone bodies used to form acetyl-CoA

- Acetyl-CoA then enters the citric acid cycle and produce ATP as normal

112
Q

Metabolism in the liver during starvation:

  • Preference for GNG
  • Ketone bodies
  • Use of ketone bodies
A
  • 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
Q

Functions of ATP:

A
  • Carrying energy
  • Building block of DNA, RNA
  • Part of CoA, VitB also required
  • As cyclic AMP (signalling)
  • Synthesise NADH
114
Q

NADH and NADPH: (4)

  • Synthesised from
  • Form
  • Oxidised form
  • Role
  • Pathways (2)
A
  • 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
Q

Vitamin facts:

  • Definition
  • Deficiency
  • Roles
A
  • Organic molecules that cannot be synthesised
  • Deficiency leads to disease
  • Most act as coenzymes or antioxidants
116
Q

Vitamin facts:

A
  • Measured in micro/milligrams

- RDA’s don’t vary much with age or sex

117
Q

Consequence of dietary deficiency: Vit.A

A
  • Impaired vision and more
117
Q

Consequence of dietary deficiency: Vit c

A
  • Scurvy
118
Q

Direct Regulation of HCl secretion: Gastrin

  • Originates from
  • Binds to
  • Action
A
  • G cell
  • CCK-B receptor
  • Ca2+
119
Q

Direct Regulation of HCl secretion: Acetylcholine (neuronal)

  • Originates from
  • Binds to
  • Action
A
  • Enteric neuron
  • M3 receptor
  • Ca2+
120
Q

Indirect regulation of HCl secretion:

A
  • Gastrin and Acetylcholine can both stimulate the ECL cell, increasing the amount of Histamine secreted

Medicine (18 decks)

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