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Phase 1 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Name the 5 digestive functions of the stomach:

A

-Store and mix food
-Dissolve and continue digestion
-Regulate emptying into the duodenum
-Secrete proteases
-Secrete intrinsic factor

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2
Q

Name 4 other functions of the stomach:

A

-Kill microbes
-Lubrication
-Activate proteases
-Mucosal protection

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3
Q

What are the key cell types in the stomach?

A

-Mucous cells
-Parietal cells - mainly in fundus
-Chief cells - protease production
-Enteroendocrine cells - hormone production

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4
Q

What is gastric acid secretion?

A

-Hydrochloric acid
-Approx 2 litres/day
-[H+] > 150mM
-Secreted by parietal cells

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5
Q

What is gastric acid secretion dependant on?

A

-Energy dependant as it is active transport (ATP required)
-Neurohormonal regulation

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6
Q

Explain the process of gastric acid secretion:

A

-H+/K+ ATPase transporter protein in parietal cell membrane
-Transports 1 H+ out of the cell into the stomach lumen and 1 K+ into the cell
-Active transport of the hydrogen, passive movement of potassium ions
-K+ transported out of cell into stomach lumen through transport protein
-Cl- transported out of cell into stomach lumen via transporter protein

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7
Q

Explain the process of gastric acid secretion:

A

-H+/K+ ATPase transporter protein in parietal cell membrane
-Transports 1 H+ out of the cell into the stomach lumen and 1 K+ into the cell -> requires energy from ATP hydrolysis
-Active transport of the hydrogen, passive movement of potassium ions
-K+ transported out of cell into stomach lumen through transport protein
-Cl- transported out of cell into stomach lumen via transporter protein

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8
Q

Where do H+ come from in parietal cells to be transported into the stomach lumen?

A

Breakdown of H2O into H+ and OH-

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9
Q

Where do Cl- come from in parietal cells?

A

-Transported from the blood into the parietal cells through a transporter protein
-HCO3- is transported out of the cell into the blood via the same transporter

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10
Q

How is water reformed in parietal cells?

A

-CO2 + H2O -> H2CO3
-Via carbonic anhydrase enzyme
-H2O -> H2CO3 -> HCO3- + H+
-H+ + OH- -> H2O

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11
Q

Label this diagram:
What does it show?

A

Gastric acid secretion

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12
Q

What 3 things turn on gastric acid secretion during cephalic phase?

A

-Parasympathetic nervous system (vagus)
-Sight, smell, taste of food and chewing
-Acetylcholine (ACh) release

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13
Q

What is the effect of ACh on gastric acid secretion and how?

A

-Acts directly on parietal cells
-Triggers release of gastrin and histamine
-Net effect = increased gastric acid production

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14
Q

What 4 things turn on gastric acid secretion during gastric phase?

A

-Gastric acid distension
-Presence of peptides and amino acids
-Gastrin release

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15
Q

How does gastrin affect gastric acid secretion?

A

-Acts directly on parietal cells
-Gastrin triggers release of histamine
-Histamine acts directly on parietal cells
-Net effect = increased gastric acid production

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16
Q

Why is histamine important in gastric acid secretion?

A

-Acts directly
-Mediates effects of gastrin and acetylcholine

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17
Q

By what mechanism does protein in the stomach affect gastric acid secretion?

A

-Direct stimulus for gastrin release
-Proteins in lumen act as a buffer - mopping up H+ ions, causing pH to rise
-Causes decreased secretion of somatostatin
-More parietal cell activity - lack of inhibition

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18
Q

How does pH affect the turning off of gastric acid secretion during gastric phase?

A

-Low luminal pH (high H+
-Directly inhibits gastrin secretion
-Indirectly inhibits histamine release vi gastrin
-Stimulates somatostatin release - inhibits parietal cell activity

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19
Q

What 4 things in the duodenum affect gastric acid secretion in intestinal phase?

A

-Duodenal distension
-Low luminal pH
-Hypertonic luminal contents
-Presence of amino acids and fatty acids

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20
Q

How does the intestinal phase affect gastric aid secretion (mechanism)?

A

-Trigger release of enterogastrones:
-Secretin - inhibits gastrin release, promotes somatostatin release
-Cholecystokinin (CCk)
-Short and long neural pathways, reducing ACh release

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21
Q

Label this diagram:
What does it show?

A

Which substances affect the transporter protein of gastric acid secretion through secondary messengers

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22
Q

Label this diagram:

A
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23
Q

What is a peptic ulcer and some causes?

A

-An ulcer is a breach in a mucosal surface
-Causes:
-Helicobacter pylori infection
-Drugs - NSAIDS
-Chemical irritants - alcohol, bile salts, dietary factors
-Gastrinoma

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24
Q

what are 4 ways that a gastric mucosa can defend itself?

A

-Alkaline mucus
-Tight junctions between epithelial cells
-Replacement of damaged cells
-Feedback loops

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25
Q

Describe what most commonly causes a peptic ulcer:

A

-Helicobacter pylori
-Lives in gastric mucus
-Secretes urease - splits urea into CO2 + ammonia
-Ammonia + H+ = ammonium
-Ammonium, secreted proteases, phospholipases and vacuolating cytotoxin A damage gastric epithelium
-Inflammatory response
-Reduced mucosal defence

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26
Q

What are NSAIDs and how do they cause peptic ulcers?

A

-Non-steroidal anti-inflammatory drugs
-Mucus secretion stimulated by prostaglandins
-Cyclo-oxygenase 1 needed for prostaglandin synthesis
-NSAIDs inhibit cyclo-oxygenase 1
-Reduced mucosal defence

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27
Q

What is needed for prostaglandin synthesis and what does a lack of this cause?

A

-Cyclo-oxygenase 1
-NSAIDs inhibit cyclo-oxygenase 1
-reduced mucosal defence as mucus secretion is secreted by prostaglandins

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28
Q

How do bile salts cause peptic ulcers?

A

-Duodeno-gastric reflux
-Regurgitated bile strips away mucus layer
-reduced mucosal defence

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29
Q

How do you treat peptic ulcers caused by Helicobacter pylori?

A

-Eradicate the organism
-Triple therapy: 1 - proton pump inhibitor
2 - antibiotics

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30
Q

What cells produce pepsinogen and what mediates its production?

A

-Chief cells
-Mediated by input from enteric nervous system (ACh)
-Secretion parallels HCl secretion

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31
Q

What is pepsinogen?
What is the science name for this?

A

Inactive form (zymogen) of pepsin enzyme

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32
Q

Where is pepsinogen activated?

A

Luminal activation to pepsin

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33
Q

What is pepsinogen activation dependant on?

A

-pH dependant
-Most efficient when pH<2
-Positive feedback loop - pepsin also catalyses the reaction

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34
Q

Under what conditions is pepsin active?
When is it inactivated?

A

-Pepsin is only active at low pH
-Irreversible inactivation in small intestine by HCO3-

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35
Q

Label this diagram:
What does it show?

A
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36
Q

What is pepsin’s role in protein digestion?

A

-Accelerates protein digestion
-Breaks down collagen in meat - helps shred meat into smaller pieces with greater surface area for digestion

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37
Q

Is pepsin essential for protein digestion, why?

A

-Not essential - protein digestion can occur if the stomach is removed
-Normally accounts for around 20% of total protein digestion

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38
Q

What is the stomach volume when empty and full?

A

-Empty stomach has volume of around 50mL
-When eating it can accommodate around 1.5L with little luminal pressure increase

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39
Q

What does smooth muscle in the stomach body and fundus undergo when empty/full?

A

Receptive relaxation

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40
Q

What is gastric motility coordinated by?

A

-Receptive relaxation mediated by parasympathetic nervous system acting on enteric nerve plexus
-Coordination - afferent input via vagus nerve
-Nitric oxide and serotonin released by enteric nerves mediate relaxation

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41
Q

What is peristalsis?

A

Wave like muscle contractions that move food through the digestive tract

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42
Q

Where does peristalsis begin?

A

-Peristaltic waves begin in gastric body
-Weak contraction in body - little mixing

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43
Q

What is the second stage of peristalsis?

A

-More powerful contraction in gastric antrum
-Pylorus closes as peristaltic waves reach it

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44
Q

What is the third stage of peristalsis?

A

-Little chyme enters duodenum
-Antral contents forced back towards body (mixing)

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45
Q

What determines the frequency of peristaltic waves?

A

-Determined by pacemaker cells in muscularis propria and is constant (3/minute)
-Interstitial cells of Cajal

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46
Q

Describe the basic electrical rhythm of the stomach:

A

-Pacemaker cells undergo slow depolarisation-repolarisation cycles
-Depolarisation waves transmitted through gap junctions to adjacent smooth muscle cells
-Do not cause significant contraction in empty stomach

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47
Q

Do the strength of peristaltic contractions vary, why?

A

-Yes
-Excitatory neurotransmitters and hormones further depolarise membranes
-Action potential generated when threshold reached

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48
Q

What two things can increase the strength of peristaltic contractions?

A

-Gastrin
-Gastric distension (mediated by mechanoreceptors)

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49
Q

Name six things that decrease the strength of peristaltic contractions:

A

-Duodenal distension
-Increase in duodenal luminal fat
-Increase in duodenal osmolarity
-Decrease in duodenal luminal pH
-Increase in sympathetic NS action
-Decrease in parasympathetic NS action

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50
Q

When does gastric emptying happen?

A

Capacity of stomach > capacity of duodenum

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51
Q

What causes dumping syndrome?
Name some symptoms:

A

-Overfilling of duodenum by a hypertonic solution
-Vomiting
-Bloating
-Cramps
-Diarrhoea
-Dizziness
-Fatigue
-Weakness
-Sweating

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52
Q

Label this diagram:

A
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53
Q

What is gastroparesis and what can cause it?

A

-Delayed gastric emptying
-Drugs
-Abdominal surgery
-Parkinson’s disease
-Multiple sclerosis
-Scleroderma
-Amyloidosis
-Female gender

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54
Q

What is the term for delayed gastric emptying?

A

Gastroparesis

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55
Q

What are 6 symptoms of gastroparesis?

A

-Nausea
-Early satiety
-Vomiting undigested food
-GORD
-Abdo pain/ bloating
-Anorexia

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56
Q

What does the bilaminar disc develop from?

A

The inner cell mass

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57
Q

Describe gastrulation:

A

-Primitive streak forms on epiblast
-Epiblast cells migrate to primitive streak and invaginate through it
-Some cells displace hypoblast and form endoderm
-Some cells create new layer between the epiblast and endoderm = mesoderm
-Epiblast = ectoderm

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58
Q

What structures develop from the ectoderm?

A

-CNS and PNS
-Skin, hair and nails
-Pituitary gland, sweat glands, tooth enamel

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59
Q

What structures develop from the mesoderm?

A

-Muscle, cartilage and bone
-Urogenital system, spleen and adrenal cortex
-Connective tissue of gut wall, pancreas and liver
-Visceral peritoneum

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60
Q

What structures develop from the endoderm?

A

-Epithelium of Gi tract, respiratory tract
-Hepatocytes (liver cells)
-Endocrine and exocrine cells of pancreas

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61
Q

What does this diagram show?

A

-Lateral folding

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62
Q

what does this diagram show?

A

-Cephalo-caudal folding
-Close of gut tube along its length except for connection that remains between midgut and yolk sac - vitelline duct > narrows and degenerates during gestation
-Closure of ventral body wall complete except at connecting stalk > umbilical cord

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63
Q

Label the mesoderm on this diagram:

A
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64
Q

What are three conditions due to failure of ventral body wall to close?

A

-Thoracic region: Ectopia cordis
-Abdomen: Gastroschisis
-Pelvic region: Bladder exstrophy

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65
Q

When does the gut tube start to differentiate?

A

-Whilst lateral folding is bringing the ventral body wall together

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66
Q

What specifies the different parts of the gut tube?

A

-Concentration gradient of retinoic acid
-Lowest cranially
-Highest distally
-Differential expression of transcription factors and genes along the tube specify how regions will develop

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67
Q

Label this diagram:
What does it show?

A

Differentiation of the gut tube

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68
Q

What is in the foregut and its derivatives?

A

-Foregut:
-Oesophagus
-Stomach
-First half of duodenum
-Derivatives:
-Liver
-Pancreas
-Mesenteries:
-Dorsal mesentery
-Ventral mesentery

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69
Q

Describe the ventral mesentery (embryology):

A

-Arises from septum transversum
-Liver grows into it and splits it into 2:
-Lesser omentum - connects liver to stomach and duodenum
-Falciform ligament - connects liver to anterior abdominal wall

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70
Q

Describe the oesophagus (embryology):
What is the difference in nerve innervation?

A

-Upper 2/3 - striated muscle innervated by vagus nerve
-Lower 1/3 - smooth muscle innervated by splanchnic nerves
-Lung bud appears at ventral wall of foregut in the 4th week - become separated from each other

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71
Q

What abnormal development can occur during oesophageal development?

A

-Oesophageal atresia
- +/- tracheoesophageal fistula (abnormal connection)

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72
Q

How and when does the stomach form?

A

-This section of gut tube starts to dilate in week 4
-Changes shape due to different rate of growth of different parts
-Changes position - rotates 90 degrees clockwise around its long axis: left side to lie anteriorly and right side posteriorly
-Brings duodenum to right

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73
Q

How does the liver develop (first stage)?

A

-Liver bud is an outgrowth from the distal foregut (endoderm epithelium)
-Appears in week 3
-Cells proliferate - grow into septum transversum
-Connection between liver bud and foregut (duodenum) narrows > bile duct

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74
Q

How does the liver develop (second stage)?

A

-Small outgrowth from the bile duct > gallbladder
-As liver grows, remaining mesoderm either side becomes membranous > falciform ligament and lesser omentum

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75
Q

How does the pancreas develop?

A

-Dorsal and ventral buds arise from duodenum
-Dorsal bud develops in dorsal mesentery
-Rotation of the stomach swings ventral bud posteriorly
-Dorsal and ventral buds fuse

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76
Q

How does the lesser sac form?

A

Rotation forms small space behind the stomach - lesser sac

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77
Q

Stomach

Dorsal mesentery
Rotation
Posterior abdominal wall
Lesser sac

What are the final positions of the foregut viscera?

A

-Rotation of the stomach brings it to left side and anterior and swings duodenum to right
-Dorsal mesentery along greater curvature bulges down and grows - greater omentum - becomes fixed to mesentery of transverse colon (and posterior wall)
-Rotation alters the position of mesenteries, omenta and peritoneal ligaments
-Some organs brought into contact with posterior abdominal wall - pancreas and duodenum and become retroperitoneal
-Small space behind stomach is formed - lesser sac

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78
Q

What does the spleen develop from?

A

Dorsal mesentery

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79
Q

What are the functions of saliva?

A

-Lubricant for mastication, swallowing and speech
-Oral hygiene
-Wash
-Immunity - antibacterial/antiviral/antifungal
-Buffer

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80
Q

What pH does the oral cavity need to be maintained at and how?

A

-Around 7.2
-Range of around 6.2-7.4
-Bicarbonate/carbonate buffer system for rapid neutralisation of acids

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81
Q

What is needed for taste?

A

Aqueous solvent for digestive enzymes required for taste

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82
Q

What does dysfunction of the salivary glands associate with?

A

-Oral pain
-Infections
-Increased risk of dental caries

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83
Q

What is the flow rate of saliva production?

A

0.3 to 0.7ml per minute

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84
Q

What volume of saliva is secreted in adults and from where?

A

-Daily secretion of 800-1500ml in adults
-From major and minor glands

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85
Q

What is in the serous secretion of saliva?

A

-Alpha amylase
-Starch digestion

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86
Q

What is in the mucus secretion of saliva?

A

-Mucins
-Lubrication of mucosal surfaces

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87
Q

What kind of secretion does the parotid gland produce?

A

Serous

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88
Q

What kind of secretion is produced by submandibular and sublingual glands?

A

Both mucous and serous

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89
Q

What kind of secretion do minor salivary glands produce?

A

Mainly mucous

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90
Q

What 8 things affect the composition and amount of saliva produced?

A

-Flow rate
-Circadian rhythm
-Type and size of gland
-Duration and type of stimulus
-Diet
-Drugs
-Age
-Gender

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91
Q

What is saliva?

A

Secretion of proteins and glycoproteins in a buffered electrolyte solution

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92
Q

What are the major contributions of saliva to oral health?

A

-Lubrication - mucous coat
-Mechanical coat - flow
-Buffering salts - neutralise acids
-Remineralisation - Ca2+ and PO43-
-Defensive and digestive function - proteins

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93
Q

How many proteins and peptides have been detected in saliva?

A

-3652 proteins
-12,562 peptides

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94
Q

What proportion of salivary proteins and peptides are also contained in serum?

A

-51% of proteins
-79% of peptides

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95
Q

What 3 things provide defence in the mouth?

A

-The mucosa - physical barrier
-Palatine tonsils - lymphocyte subsets + dendritic cells - immune surveillance and resistance to infection
-Salivary glands - saliva washes away food particles, bacteria or viruses might use for metabolic support

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96
Q

How do salivary glands link to immunity?

A

-Salivary glands are surrounded by lymphatic system - linked to thoracic duct and blood
-Broad range of immune cells
-Oral mucosa and glands have high blood flow rate

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97
Q

Which glands are continuously active and which aren’t?

A

-Continuously active - Submandibular, sublingual and minor glands
-Not - Parotid

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98
Q

What becomes the main source of saliva and when?

A

-Parotid gland
-No measurable unstimulated secretion
-Main source of saliva when stimulated
-SMG glands main source of unstimulated saliva

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99
Q

What does whole saliva contain?

A

-Salivary gland secretions
-Blood
-Oral tissues
-Microorganisms
-Food remnants

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100
Q

What could saliva be used for and how?

A

-Diagnosis instead of blood samples
-salivary TB biomarkers are worth the search to evaluate their ability to differentiate between TB disease states

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101
Q

What is the basic structure of salivary glands?

A

-Composed of two morphologically and distinct epithelial tissue
-Acinar cells around
-Ducts - collect to form large duct entering the mouth

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102
Q

What are salivary glands equipped with (similar to other glands)?

A

Channels and transporters in the apical and basolateral membranes enabling transport of fluid and electrolytes

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103
Q

What are the two types of acini?

A

Serous and mucous acini

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104
Q

Describe serous acini:

A

-Dark staining
-Nucleus in basal third
-Small central duct
-Secrete water + alpha amylase

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105
Q

Describe mucous acini:

A

-Pail staining - “foamy”
-Nucleus at base
-Large central duct
-Secrete mucous (water + glycoproteins)

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106
Q

What are the two larger ducts of the salivary glands?

A

-Intralobular ducts
-main excretory duct

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107
Q

What do intralobular ducts divide into?

A

-Intercalated:
-Short narrow duct segments
-Cuboidal cells that connect acini to larger striated ducts
-Striated:
-Striated like a thick lawn
-Major site for reabsorption of NaCl

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108
Q

Label this diagram:
What does it show?

A

Salivary gland

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109
Q

Label this diagram:

A
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110
Q

Describe 3 things about striated salivary ducts:

A

-Appear striated at basal end
-Basal membrane highly folded into microvilli for active transport of HCO3 against concentration gradient
-Microvilli filled with mitochondria for energy to facilitate active transport

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111
Q

What is this?

A

Striated salivary duct

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112
Q

Do the salivary ducts just facilitate the transport of saliva?

A

No

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113
Q

what is the function of the salivary ducts?

A

-Primary saliva - Rich in NaCl and isotonic plasma-like fluid secreted by acini
-Electrolyte composition is modified in duct system
-Ducts secrete K+ and HCO3- and reabsorb Na+ and Cl-
-epithelium of duct doesnt allow any water movement so final saliva becomes saliva

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114
Q

What does epithelium of salivary ducts not allow and why?

A

-Not allow any water movement
-Final saliva becomes hypotonic

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115
Q

What are salivary glands a good target for?

A

Valuable target tissue for both systemic and upper GI tract gene therapeutic applications

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116
Q

What are the advantages of salivary glands (6)?

A

-Well encapsulated - limit undesirable vector spread
-Nearly every luminal membrane easy to access - non-invasive
-Ductal access of SG uses limited fluid volume - not diluted or disseminate during deliver - low vector dose
-Epithelium well differentiated and slowly dividing - stable cell-population for vectors
-Large protein export production
-Single Sg not crucial to life and can be removed

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117
Q

What are the 2 general pathways for protein secretion of salivary glands?

A

-Predominant leading to saliva (mucosal; across apical membrane)
-Constitutive leading mainly towads interstitium and bloodstream (serosal; across basolateral membrane)

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118
Q

What can entry into regulated salivary secretion be saturated by and how is it overcome??

A

Overexpression of transgene product and “overflow” can exit via constitutive into bloodstream

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119
Q

How can salivary hypofunction be overcome?

A

-hAQP-1 cDNA transfer into duct epithelial cells
-Codes water channel - plasma membrane protein that facilitates rapid transmembrane water movement in response to osmotic gradient
-Duct cells generate osmotic gradient (lumen>interstitium) that water could follow

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120
Q

What can cause salivary hypofunction?

A

-Radiation therapy
-RT damage - fluid secreting acinar cells leaves water-impermeable duct cells
-Normal saliva duct reabsorbs NaCl secreted by acinar cells in isotonic primary salivary fluid

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121
Q

How many main salivary glands are there?

A

-Three pairs of main salivary glands
-Parotid
-Submandibular
-Sublingual

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122
Q

What percentage of salivary flow do main salivary glands provide?

A

80%

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123
Q

Where are minor salivary glands?

A

-Submucosa of oral mucosa
-Lips
-Cheeks
-Hard and soft palate
-Tongue

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124
Q

What percentage of salivary flow is provided by minor salivary glands?

A

20%

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125
Q

What do parotid glands contain?

A

Serous acini

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126
Q

What do submandibular salivary glands contain?

A

-Mixed
-Serous and mucous acinini
-referred to as seromucous

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127
Q

What do sublingual salivary glands contain?

A

-Mixed
-More mucous acini

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128
Q

Where are parotid salivary glands?

A

-Superficial triangle outline between:
-Zygomatic arch
-Sternocleidomastoid
-Ramus of mandible + masseter and med pterygoid

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129
Q

Where is the parotid duct?

A

-Stenson’s duct
-Crosses masseter
-Pierces buccinator and enters oral cavity at 7/7
-Palpate a finger’s breadth below zygomatic arch

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130
Q

Label this diagram:

A
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131
Q

What does the parotid salivary gland look like horizontally?

A

triangular outline with apex on carotid sheath

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132
Q

What 3 things pass through the parotid salivary gland?

A

-External carotid artery + terminal branches
-Retromandibular vein
-Facial nerve + branches to muscles of facial expression (MFE)
-(PAROTID CAPSULE VERY TOUGH)

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133
Q

What are parotid glands almost entirely made of?

A

-Serous acini
-Ducts interspersed

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134
Q

What are the two lobes of the submandibular salivary gland separated by?

A

Mylohyoid muscle

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135
Q

What are the two lobes of the submandibular salivary gland?

A

-Larger superficial lobe
-Smaller deep lobe in floor of mouth

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136
Q

What is the path of the submandibular duct?

A

-Wharton’s duct
-Begins in superficial lobe
-Wraps around free posterior border of mylohyoid
-runs along floor of mouth and empties into oral cavity at sublingual papillae

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137
Q

Label this diagram:
What does it show?

A

Opening of ducts at sublingual papillae

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138
Q

What is the histology of the submandibular salivary gland?

A

-Mixed gland of serous and mucous acini
-Some serous acini arranged as crescent-shaped groups of glandular cells at bases of mucous acini
-Referred to as serous demilunes

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139
Q

Where is the sublingual salivary gland?

A

Between mylohyoid muscle and oral mucosa of the floor of the mouth

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140
Q

Label this diagram:

A
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141
Q

Describe sublingual salivary glands and their drainage:

A

-Variable in size with mixed acini
-Mainly mucous acini
-No large duct - drains into submandibular duct and/or small ducts that pierce oral mucosa on the floor of the mouth

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142
Q

Label this diagram:

A
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143
Q

Where are minor salivary glands found?

A

-Concentrated in bucal labial, palatal and lingual regions
-Also found:
-Superior pole of tonsils (Weber’s glands)
-Tonsillar pillars
-Base of tongue (von Ebner’s glands)

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144
Q

What is the histology of minor salivary glands?

A

-All minor salivary glands are mucous except serous glands of von Ebner
-Lack branching network of draining ducts - each salivary unit has its own simple duct

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145
Q

What stimulation causes the production of saliva?

A

-Parasympathetic nerve stimulation causes production of a copious flow of saliva
-Sympathetic stimulation causes secretion of protein and glycoprotein

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146
Q

What are 5 causes of salivary gland disease and dysfunction?

A

-Obstructive
-Inflammatory
-Degenerative
-Drug side effects
-Cancer

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147
Q

What is xerostomia and causes?

A

-Dry mouth
-May be consequence of CF or Sjogrens syndrome
-Most common causes:
-Medication
-Irradiation for head and neck cancers
-High prevelence of caries and candida infections

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148
Q

What is obstruction to salivary glands?

A

-Saliva contains calcium and phosphate ions that can form salivary calculi (stones)
-Most often in submandibular glands (80%)
-Block duct at bend round mylohyoid or at exit at sublingual papillae

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149
Q

What is inflammation of salivary gland and causes?

A

-Infection secondary to blockage
-Causes:
-Mumps (viral infection):
-Fever, malaise
-Swelling of glands
-Pain especially over parotid because capsule does not allow much enlargement

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150
Q

What is degenerative condition of salivary glands?

A

-Complications of radiotherapy to head and neck for cancer treatment
-Sjogren’s syndrome
-Mainly post-menopausal females
-Also affects lacrimal glands
-rheumatoid arthritis may also be present

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151
Q

Describe drug side effects on salivary glands:

A

-Most common dysfunction encountered
-500 prescription drugs have sympatheticomimetic effect
-Act on NA receptors or inhibit parasympathetic action at ACh receptors

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152
Q

At what point will a patient experience xerostomia?

A

If salivary output falls to <50% of normal flow

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153
Q

What are the consequences of salivary gland dysfunction?

A

-Low lubrication - oral function difficult
-Low (natural) oral hygiene - poor pH control
-Accumulation of plaque -> rampant dental caries, gingivitis and periodontal disease
-Opportunistic infections esp. fungal infections (candida = thrush)

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154
Q

Label this diagram:
What does it show?

A

Movement of glucose

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155
Q

Label this diagram:
What does this show?

A

Processing of glucose in the liver

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156
Q

Label this diagram:
What does it show?

A

Movement and process of glucose in skeletal muscles

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157
Q

Label this diagram:
What does it show?

A

Glucose processing in the brain

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158
Q

Label this diagram:
What does it show?

A

Metabolism of glucose in RBC

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159
Q

Label this diagram:
What does it show?

A

Metabolism of glucose in adipocytes

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160
Q

Label this diagram:
What does it show?

A

Metabolism of amino acids

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161
Q

Label this diagram:
What does it show?

A

Absorption of lipids

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162
Q

Summarise the metabolism of fuels in the fed state:

A

-Fuels oxidised for energy
-Any excess stored:
-Triglycerides in adipose
-Glycogen in liver and muscle

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163
Q

Label this diagram:
What does it show?

A

Glucose metabolism during short fasting

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164
Q

Label this diagram:
What does it show?

A

Glucose metabolism during long fasting

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165
Q

Label this diagram:
What does it show?

A

Fat metabolism during fasting

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166
Q

Label this diagram:
What does it show?

A

Prolonged fasting

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167
Q

What substances to do with energy metabolism can be measured?

A
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168
Q

How can you describe insulin and glucagon and what processes show this?

A

-Insulin is anabolic
-Glucagon is catabolic

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169
Q

What are the effects of cortisol on fuel metabolism?

A

Preparation for stress response

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170
Q

What are the effects of adrenaline on fuel metabolism?

A

Fight or flight response

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171
Q

What are the effects of thyroxine on fuel metabolism?

A
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172
Q

What are the effects of growth hormone on fuel metabolism?

A
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173
Q

Describe the energy balance for fuel metabolism:

A
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174
Q

What would each of these energy balances produce?

A
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175
Q

What 3 things contribute to obesity?

A
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176
Q

What does this describe and how does it change with obesity?

A

-Leptin
-Released by adipocytes

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177
Q

What does this describe?

A

-Ghrelin
-Produced by stomach

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178
Q

What two hormones control apetite?

A

-Ghrelin increases apetite
-Leptin decreases apetite

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179
Q

What are 4 diseases associated with metabolic problems?

A

-Diabetes
-Lipid disorders
-Malabsorption / processing of nutrients
-Obesity

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180
Q

What are 7 functions that the liver performs?

A

-Carbohydrate metabolism
-Fat metabolism
-Protein metabolism
-Hormone metabolism
-Toxin/drug metabolism and excretion
-Storage
-Bilirubin metabolism and excretion

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181
Q

Label this diagram:
What does it show?

A

Iron metabolism

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182
Q

What is ferritin?

A

-Large spherical protein
-Consists of 24 noncovalently linked subunits
-Subunits form a shell surrounding a central core

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183
Q

How many atoms of iron are in a ferritin core?

A

Up to 5000 atoms of iron

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184
Q

Where is ferritin found?

A

-Cytoplasm of cells
-Also found in serum

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185
Q

What is the concentration of ferritin related to?

A

Concentration of ferritin is directly proportional to the total iron stores in the body

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186
Q

What two groups of disorders can cause ferritin excess?

A

-Excess iron storage disorders
-Non-iron overload

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187
Q

What are 5 examples of excess iron storage disorders that can cause ferritin excess?

A

-Hereditary haemochromatosis
-Haemolytic anaemia
-Sideroblastic anaemia
-Mulitple blood transfusions
-Iron replacement therapy

188
Q

What are 4 non-iron overload disorders that can cause ferritin excess?

A

-Liver disease
-Some malignancies
-Significant tissue destruction
-Acute phase response:
-Inflammation
-Infection
-Autoimmune disorders

189
Q

What is the only known cause of ferritin deficiency and what can it result in?

A

-Iron deficiency
-Can result in anaemia:
-Ferritin less than 20ug/L indicated depletion
-Ferritin less than 12ug/L suggests a complete absence of stored iron

190
Q

How are vitamins usually provided?

A

In the diet

191
Q

What is RDA?

A

Recommended daily allowance

192
Q

What is AI?

A

-Adequate intake
-Where no evidence to determine RDA

193
Q

What are 3 things that vitamins can act as?

A

-Gene activators
-Free-radical scavengers
-Coenzymes or cofactors in metabolic reactions

194
Q

What can excess vitamin ingestion cause?

A

Can result in toxicity

195
Q

What is the difference between water-soluble and fat-soluble vitamins?

A

-Water soluble vitamins pass more readily through the body
-They require more regular intake than fat-soluble vitamins

196
Q

What are 4 examples of fat-soluble vitamins?

197
Q

What are 2 examples of water-soluble vitamins?

198
Q

How do we source retinal?

A

-Ingest directly from meat
-Produce retinal from carotenes

199
Q

What is the chemical name group of vitamin A?

200
Q

What are 5 sources of retinols?

A

-Meat (liver)
-Dairy
-Egga
-Supplements
-Fortified cereals

201
Q

What are 4 sources of carotenoids?

A

-carrots
-Spinach
-Swede
-Tomatoes

202
Q

What is the daily requirement for intake of vitamin A?

A

-Men: 0.6 mg/day
-Women: 0.7mg/day

203
Q

What are 4 functions of vitamin A?

A

-Vision
-Used to form rhodopsin in rod cells of retina
-Reproduction
-Spermatogenesis in males
-Prevention of foetal resorption of female
-Growth
-Stabilisation of cellular membranes

204
Q

Describe vitamin A deficiency:

A

-Rare in affluent countries as vitamin A levels drop when liver stores severely depleted
-Fat malabsorption can cause it
-Clinical features:
-Night blindness
-Xeropthalmia
-Blindness

205
Q

What are symptoms of acute vitamin A excess?

A

-Abdominal pain, nausea and vomiting
-Severe headaches, dizziness, sluggishness and irritability
-Desquamation of skin

206
Q

What are symptoms of chronic vitamin A excess?

A

-Joint and bone pain
-Hair loss, dryness of the lips
-Anorexia
-Weight loss and hepatomegaly

207
Q

What is carotenemia and what is it a cause of?

A

-Reversible yellowing of the skin
-Does not cause toxicity
-Vitamin A excess

208
Q

What are 3 functions of vitamin D?

A

-Increased intestinal absorption of calcium
-Reabsorption and formation of bone
-Reduced renal excretion of calcium

209
Q

What does a vitamin D deficiency cause?

A

-Demineralisation of bone:
-Rickets in children
-Osteomalacia in adults

210
Q

Where is vitamin E stored?

A

-Non-adipose cells such as liver and plasma
-Labile (readily available) and fixed pool

211
Q

Is vitamin E important?

A

-Yes
-Important antioxidant

212
Q

What are the daily intake requirements of vitamin e?

A

-Men: 4 mg/day
-Women: 3 mg/day

213
Q

What 3 things can cause a vitamin E deficiency?

A

-Fat malabsorption (e.g. cystic fibrosis)
-Premature infants
-rare congenital defects in fat metabolism (e.g. abetalipoproteinanaemia)

214
Q

What are 5 clinical manifestations of vitamin E deficiency?

A

-Haemolytic anaemia
-Myopathy
-Retinopathy
-Ataxia
-Neuropathy

215
Q

What are the symptoms of vitamin E excess?

A

-None
-Vitamin E excess is relatively safe in excess

216
Q

How is vitamin K absorbed and stored?

A

-Rapidly taken up by the liver
-Transferred to very low-density lipoproteins and low density lipoproteins which carry it in the plasma

217
Q

What are 3 sources of vitamin K?

A

-Vitamin K1 (phylloquinone)
-Synthesised by plants and present in food
-Vitamin K2 (menaquinone)
-Synthesised in humans by intestinal bacteria
-Synthetic vitamin K’s
-K3 (menadione)
-K4 (menadiol)

218
Q

What are 2 functions of vitamin K and how is it assessed?

A

-Responsible for activation of some blood clotting factors
-Needed for liver synthesis of plasma clotting factors:
-II
-VII
-IX
-X
-Assessed by measuring prothrombin time

219
Q

What are 2 causes of vitamin K deficiency?

A

-Haemorrhagic disease of newborn
-Vitamin K injection given to newborn babies
-Rare is adults, unless on warfarin

220
Q

What are consequences of vitamin K excess?

A

-K1 relatively safe in excess
-Synthetic forms are more toxic
-Can result in oxidative damage, red cell fragility and formation of methaemoglobin

221
Q

What are common sources of vitamin C?

A

Fresh fruit and vegetables

222
Q

What is the daily recommended intake of vitamin C for adults?

223
Q

What are 3 functions of vitamin C?

A

-Collagen synthesis
-Antioxidant
-Iron absorption

224
Q

What does vitamin C deficiency cause?

A

-Scurvy
-Easy bruising and bleeding
-Teeth and gum disease
-Hair loss

225
Q

Describe vitamin c treatment:

A

-Improves symptoms quickly
-Joint pain gone within 48 hours
-Full recovery within two weeks

226
Q

What can excess vitamin C cause?

A

-Doses > 1g/day can cause Gi side effects
-No evidence that increased vitamin C reduces the incidence or duration of colds

227
Q

What did the first clinical trial look at?

A

Different daily treatments that contain vitamin C and their outcomes

228
Q

What is another name for vitamin B12?

A

Cobalamins

229
Q

What are the two active forms of vitamin B12?

A

-Methylcobalamin
-5-deoxyadenosylcobalamin

230
Q

How is vitamin B12 digested and absorbed in the body?

A

-Released from food by acid and enzymes in the stomach
-Binds to R protein to protect it from stomach acid
-Released from R proteins by pancreatic polypeptide
-Intrinsic factor (IF) produced by the stomach needed for absorption
-IF-B12 complex absorbed in terminal ileum
-B12 stored in liver

231
Q

What are 3 potential causes of vitamin B12 deficiency?

A

-Pernicious anaemia
-Autoimmune destruction of IF-producing cells in stomach
-Malabsorption
-Lack of stomach acid
-Pancreatic disease
-Small bowel disease
-Veganism

232
Q

What are 2 symptoms of vitamin B12 deficiency?

A

-Macrocytic anaemia
-Peripheral neuropathy in prolonged deficiency

233
Q

What are common dietary sources of folate?

A

Found in many foods fortified with folic acid

234
Q

Who has higher requirements of folate intake?

A

Pregnant women

235
Q

What are 3 functions of folate?

A

-Coenzyme in methylation reactions
-DNA synthesis
-Synthesis of methionine from homocysteine

236
Q

What are 3 causes of folate deficiency?

A

-Malabsorption
-Drugs that interfere with folic acid metabolism (anticonvulsants, methotrexate)
-Disease states that increase cell turnover (leukemia, haemolytic anaemia, psoriasis)

237
Q

What are 3 symptoms of folate deficiency?

A

-High homocysteine levels
-Macrocytic anaemia
-Foetal development abnormalities (neural tube defects)

238
Q

What is the intrinsic pathway activated by?

239
Q

What activates the extrinsic pathway?

A

FVII coming into contact with tissue factor

240
Q

What does the coagulation cascade eventually result in?

A

Fibrin clot formation

241
Q

Which 6 clotting factors are produced in the liver?

A

-I (fibrinogen)
-II (prothrombin)
-IV
-V
-VI
-VII

242
Q

What 3 things can be measured to test the performance of the clotting pathways?

A

-Prothrombin time (PT) (extrinsic pathway)
-International normalised ratio (INR)
-Activated partial thromboplastin time (aPTT) (intrinsic pathway)

243
Q

What can a prolonged PT indicate?

A

Deficiency in the synthetic capacity of the liver

244
Q

Is prolonged PT specific to liver disease?

A

-No, other causes:
-DIC
-Severe GI bleed
-Some drugs
-Vitamin K deficiency

245
Q

Label this diagram of hormones regulating fuel metabolism:

246
Q

What are xenobiotics?

A

-Foreign substances with no nutritional value
-Serve no purpose
-Need to be excreted, may be toxic if not excreted in time
-Can cause damage to cell protein, lipids or DNA

247
Q

Give a brief description of liver detoxification:

A

-Oxidation in phase I reactions - Cytochrome P450 enzymes
-Conjugation in phase II reaction (for renal excretion)
-Active metabolites of a drug
-Ethanol detoxification

248
Q

What group of enzymes have been found to play a large part in detoxification?

A

Cytochrome P450 enzymes

249
Q

What are the 2 main types of xenobiotic biotransformation reactions and what are their functions?

A

-Phase I and phase II
-Purpose of making the compounds non-toxic and water -soluble

250
Q

What kind of reactions happen in phase I and phase II reactions?

251
Q

What kind of reactions happen in phase I and phase II reactions and how is hydrophillicity affected?

252
Q

What is this?
Describe its structure:

A

-Paracetemol
-Acetyl group attached to amine group attacked to phenol in the para-position
-para-acetylaminophenol

253
Q

What does this show?
What are its properties?

A

-para-acetylaminophenol glucuronide
-glucoronyl group has many OH groups making it polar to facilitate excretion in the urine

254
Q

Where does most detoxification take place?

255
Q

What are 4 mechanisms of detoxification in the liver?

A

-Inactivation and facilitated elimination of drugs and other xenobiotics
-Formation of active metabolites with similar or occasionally enhanced activity
-Activation of pro-drugs
-Toxification of less toxic xenobiotics

256
Q

Where does most biotransformation in the liver take place?

A

-Within the endoplasmic reticulum
-Often SER

257
Q

How many groups of cytochrome P450 enzymes are there and by how many genes are they coded by (superfamily)?

A

-10 main groups of cytochrome P450 enzymes
-55 genes

258
Q

What features do all P450 enzymes have in common?

A

-All present in the SER - hence called microsomal enzymes
-Oxidise the substrate and reduce oxygen
-Have reductase subunit which uses NADPH
-They are inducible - enzyme activity may be increased by certain drugs, some dietary components and some environmental toxins
-Generate a reactive free radical compound

259
Q

How are cytochrome P450 enzymes subdivided into families?

A

-According to amino acid similarity
-Important: CYP3A4, CYP2D6

260
Q

Why is CYP3A4 important?

A

-Involved in metabolism of about 50% of clinically prescribed drugs
-Accounts for 1/3 of cytochrome enzymes in liver

261
Q

Explain induction and genetics in terms of cytochrome P450 enzymes:

A

-Induction - one drugs can induce numerous cytochrome isoenzymes
-Genetics - note genetic variation especially in CYP2D6

262
Q

What 3 medications are metabolised by CYP3A4?

A

-Paracetemol
-Codeine
-Diazepam

263
Q

What 2 medications are metabolised by CYP2D6?

A

-Amitriptyline
-Codeine

264
Q

Can a medication be metabolised by more than one cytochrome enzyme?

A

-YES (important)
-Codeine is an important example

265
Q

What do reactions catalysed by cytochrome P450 enzymes start with?

A

-Start with cytochrome P450 reductase (auxillary enzyme)
-It transfers hydrogen (and e-) from NADPH to cytochrome P450

266
Q

In drug and alcohol metabolism, where is cytochrome P450 bound?

A

-Phospholipid membrane (SER)
-Attached to a reductase
-Cytochrome P450 has active site and haem component for oxygen binding

267
Q

What is the second stage of cytochrome P450 reactions?

A

-Elemental O2 enters the reaction and oxygen is the electron acceptor
-2 oxygen molecules have different fate
-Hydrogen used by cytochrome P450 to reduce one of the oxygen atoms to water
-Other oxygen retained in a highly reactive form, used to force one or the other reaction on the substrate
-Most commonly forms a OH group

268
Q

What is this?

A

Fe-heme group of cytochrome P450

269
Q

What is one of the most commonest mechanisms of drug interactions?

A

Via cytochrome P450

270
Q

What may accelerate or inhibit the breakdown of some medications?

A

-Induction of cytochrome P450 enzymes due to drug interactions
-Enzymes may be inhibited by various drugs and foodstuffs (usually take quicker effect than induction)
-Can result in increased blood concentrations of certain medications
-Drugs can compete for the active site on cytochrome P450 enzymes
-Drugs with higher affinity will be metabolised faster

271
Q

What does this show?

A

-Cytochrome P450 (CYP3A4) induction via phenobarbital
-Phenolbab binds to a receptor in the cytoplasm
-Receptor migrates to the nucleus while bound to suitable compound (phenolbarb)
-Enhances mRNA formation

272
Q

What does this show?

A

-Clozapine inducers can affect cytochrome P450
-Clozapine levels increase after cessation of smoking and decrease for smokers
-Dose of clozapine may need to be altered to avoid toxicity or for it to be affected
-Shows how factors such as smoking affect liver metabolism

273
Q

What inducers affect clozapine?

A

-Barbiturates
-Carbamazepine
-Primidone
-Rifampicin
-Cruciferous vegetables, e.g. cabbage, broccoli
-Grilled meat
-Smoking
(Increased metabolism of drugs)

274
Q

What agents inhibit cytochrome P450, increasing concentrations of medications such as clozapine?

A

Ciproflaxacin

275
Q

Why is grapefruit juice significant in cytochrome P450 enzymes?

A

-Cytochrome P450 enzymes inhibited by dietary components
-A lot of medications metabolised in phase I by CYP3A4
-Most statins metabolised by CYP3A4
-Inhibiting metabolism of simvastatin and atorvastatin, grapefruit juice causes increased blood levels with increased side effects

276
Q

What are 4 common pathways of detoxification including drug metabolism and what do they show?

A

-Active drug to inactive metabolite
-Active drug to active metabolite
-Inactive drug to active metabolite
-Active drug to reactive intermediate
(Products have been neutralised)

277
Q

What does this show?

A

-Inactivation of a xenobiotic (Active drug to inactive metabolite)
-OH group added
-OH group conjugated with glucuronic acid or sulphate resulting in product sufficiently polar to be excreted by kidneys
-Due to the fact excretion of unmodified drug id very slow as it is non-polar and mainly dissolves in fat with little in the plasma

278
Q

Describe active drug to active metabolite conversion:

A

-Active drug may be converted to another active form
-Codeine metabolised into morphine
-Codeine is morphine molecule with one hydroxyl group replaced by methyl group making it less susceptible to first pass metabolism
-Codeine is active and is de-methylated in the liver to morphine which is also active

279
Q

What does this show?

A

-Active drug to active metabolite
-CYP3A4 de-methylates to active metabolite norcodeine
-5-10% acted on by CYP2D6 to produce morphine

280
Q

Describe pro-drug to active drug metabolism:

A

-Inactive drug or pro-drug may be converted in liver to active agent
-Loratadine is pro-drug of desloratadine - largely responsible for antihistaminergic effects of parent compound

281
Q

Describe active drug to reactive intermediate metabolism:

A

-Drug converted into possibly toxic intermediate
-Benzopyrenes (incomplete combustion of organic matter) converted into epoxides
-Subsequent reaction with DNA is major mechanism of carcinogenesis in smokers
-Reaction is of benzopyrenes with CYP1A1to produce epoxides

282
Q

What is paracetamol metabolism an example of?

A

-Active drug to reactive intermediate
-Active drug metabolised into harmful reactive intermediate
-Also called acetaminophen
-CYP2E1 produces harmful intermediates

283
Q

Describe paracetamol metabolism at therapeutic doses:

A

-Usually only 5-10% is metabolised via the cytochrome P450 system to NAPQI
-Then metabolised to harmless products that can be excreted in the urine
-At therapeutic dose, NAPQI is quickly metabolised and inactivated by G-SH

284
Q

Describe paracetamol metabolism at overdose:

A

-G-SH overwhelmed
-Well over 5-10% is metabolised by cytochrome enzymes producing excess NAPQI
-Toxic NAPQI builds up, causing liver cell damage

285
Q

Describe 6 Phase II reactions:

A

-Glycoside conjugation - glucuronidation
-Sulphate - sulphation
-Glutathione
-Methylation
-Acylation
-Phosphate conjugation
-TOP TWO MOST COMMON

286
Q

What are phase II reactions?

A

-Conjugation reactions
-Make the compound more water-soluble
-Glucuronyl, sulphate and phosphate groups are polar and make the molecule ready for excretion via urine

287
Q

What are responsible for most phase II reactions?

A

-Transferase enzymes
-Uridine diphosphoglucuronosyl transferase (UGT)
-N-acetyl transferase (NAT)
-Glutathione S-transferae (GST)
-Sulphotransferase (ST)

288
Q

Describe microsomal enzymes:
-Location
-Sites
-Enzymes
-Reactions
-Note

A

-Location - SER
-Sites - Liver the kidney, lungs, intestinal mucosa
-Enzymes - mono-oxygenases (CYPs, FMOs); UGTs
-Reactions - majority of drug biotransformation reaction; oxidative, reductive and hydrolytic and gluronidation
-Note - INDUCIBLE by drugs, diet

289
Q

Describe non microsomal enzymes:
-Location
-Sites
-Enzymes
-Reactions
-Note

A

-Location - cytoplasm and mitochondria of hepatocytes, other tissues
-Sites - protein oxidases, esterases, amidases, conjugases
-Enzymes - protein oxidases, esterases, amidases, conjugases
-Reactions - non-specific enzymes that catalyse few oxidative, a number of reductive and hydrolytic - conjugation other than glucuronidation
-Note - not inducible but having polymorphism

290
Q

Is ethanol metabolised via phase I or II

A

-Doesn’t fit either
-Doesn’t need to be conjugated for excretion
-2% to 10% is excreted in urine - used in liver as dietary fuel
-Major route via alcohol dehydrogenase (ADH)

291
Q

What is the role of the microsomal system of ethanol metabolism?

A

-Microsomal Ethanol Oxidising System (MEOS)
-Predominantly CYP2E1
-Produces acetaldehyde as intermediate (toxic)
-CYP2E1 has high affinity for alcohol (MEOS is combined ethanol-oxidising activity of all CYP450 enzymes)

292
Q

How does ethanol cause liver damage?

A

-If liver’s ability to oxidise acetaldehyde is overwhelmed, it accumulates in the liver
-Contributes to alcohol-induced hepatitis by forming adducts with amino acids
-Also binds to glutathione and predisposes cells to damage by peroxides and other free radicals

293
Q

What is acetaldheyde metabolised to in the liver and by what?

A

-Acetate
-Acetaldehyde dehydrogenase producing NADH

294
Q

What are the 3 functions of the colon?

A

-Absorption of water and electrolytes (osmosis)
-Excretion of waste (motility)
-Production of vitamins (microbiome)

295
Q

Label this diagram of the large intestine:

296
Q

Label this diagram:
What does it show?

A

Different layers of the colon

297
Q

What are the muscular layers to the colon?

A

-Continuous circular muscle
-3 “ribbons” of longitudinal muscle - taeniae coli

298
Q

What are the 3 “ribbons” of longitudinal muscle of the colon called?

A

Taeniae coli

299
Q

What is the basic histology of the colon?

A

-Simple columnar epithelium
-Goblet cells

300
Q

What is the nerve supply of the colon?

A

-Enteric nervous system (Intrinsic)
-Myenteric plexus
-Submucosal plexus
-Extrinsic nervous system
-Parasympathetic
-Sympathetic

301
Q

What makes up the enteric nervous system of the colon?

A

-Myenteric plexus
-Submucosal plexus

302
Q

Label this diagram:
What does it show?

A

The anal sphincter

303
Q

What are the 4 basic phases of defecation?

A
  1. Basal
  2. Pre-expulsive
  3. Expulsive
  4. Termination
304
Q

Describe the basal phase of defecation:

A

-Colon - segmental contractions (mixing)
-Rectum - motor complexes (keeps rectum empty)
-“braking mechanism”
-Anal sphincter - tonic contraction
-Puborectalis - contracted (90o angle)

305
Q

Describe the pre-expulsive phase of defecation:

A

-Colon - high amplitude propagating contractions
-Mass movement of stool (8 times a day)
-Gastro-colic reflex
-Rectum - fills causing distension
-Rectal compliance (adaptive relaxation)
-Anal sphincter - EAS maintains contraction
-Reflex relaxation of IAS - stool sampling
-Puborectalis - remains contracted

306
Q

Describe the expulsive phase of defecation:

A

-Rectum contracts
-IAS, EAS and PR relax
-Valsalva manoeuvre/posture aid emptying

307
Q

Describe the termination phase of defecation:

A

-Traction loss causes sudden contractions of EAS
-“closing reflex”
-Valsalva ceases
-Change in posture (to standing)

308
Q

Label this diagram:
What does it show?

A

Parasympathetic defecation reflex

309
Q

What are 4 disorders of defecation causing constipation?

A

-Consistency of stool
-Bowel motility
-Physical blockage to the bowel
-Pelvic floor disorders

310
Q

What are 4 disorders of defecation that cause diarrhoea?

A

-Consistency of stool or frequency of movements
-Diseased bowel mucosa
-Reduced rectal capacity
-Pelvic floor disorder

311
Q

Why are plain abdominal x-rays of limited use?

A

-Abdominal anatomy is more complex than thoracic anatomy
-Most abdominal tissue is of similar density - difficult to differentiate
-Equivalent ionising radiation as 4 months of background radiation

312
Q

What are common uses of abdominal x-rays?

A

-Looking for foreign bodies
-Dilated loops of bowel (sign of intestinal obstruction)

313
Q

How does Computed Tomography (CT) work?

A

-Directing very large dose of x-rays at patient from various angles
-Reproduce images digitally producing 3D images
-Scroll through series of images to see each part of the abdomen

314
Q

Is CT commonly used, any drawbacks?

A

-Frequently used
-Much greater dose of ionising radiation
-CT of abdomen and pelvis exposes patient to equivalent of approximately 4.5 years of background radiation

315
Q

What are common uses of CT scans?

A

-Widely used in abdominal imaging for many pathologies
-Very often used with contrast

316
Q

What is contrast (abdominal imaging)?

A

-Contrast agents are radio-opaque liquids
-Increase differentiation between different tissues
-Iodine and barium (x-rays/CT)
-Gadolinium (MRI)

317
Q

How can contrast agents enter the body?

A

-Swallowed
-Inserted into the GI tract via rectum before x-rays or CT scan
-Not absorbed - later excreted via the anus

318
Q

How can contrast agents visualise blood vessels?

A

-Injected into veins or arteries during x-rays, CTs or MRIs
-Help radiologist to identify inflammation, cancer, blockage of blood vessels and bleeding
-Filtered out of blood by kidneys and excreted in urine

319
Q

What are common uses of contrast in abdominal imaging?

A

-Barium swallow
-Barium enema
-CT abdomen with contrast
-CT aortogram
-Trauma CT

320
Q

Are ultrasound (US) scans useful?

A

-Very frequently used
-Images not as useful as CT as they are 2D images
-Less detailed

321
Q

How does ultrasound work?

A

-Sounds waves of higher frequency than human hearing
-Directed from probe towards target structure
-Reflected off structure and received back at probe
-Time taken and amplitude of rebound detected and used to calculate densities and depths of structures
-Images viewed in real-time and probe can be placed where needed to view desired organ

322
Q

What are the advantages and disadvantages of ultrasound?

A

-Non-ionising so theoretically cause no harm to the patient
-fairly difficult to perform and interpret, specialist training is needed

323
Q

What are common abdominal uses of ultrasound?

A

-Liver
-Gallbladder
-biliary tree
-Aorta
-Kidneys
-Bladder volume
-Vascular access
-Fluid in abdomen

324
Q

Describe endoscopy:

A

-Very frequently used
-Visualise lumen of hollow organs using camera
-Non-ionising but may need sedation and risk of perforation
-Capsule endoscopy - pill-sized camera swallowed

325
Q

What are common uses of endoscopy?

A

-Visualise lumen and walls of oesophagus
-Stomach
-Small and large intestine
-Looking for bleeding or foreign bodies

326
Q

What is laparoscopy?

A

-Keyhole surgery
-Small finger sized holes in anterior abdominal wall and inserting cameras to visualise peritoneal cavity
-Can be used to just have a look but can be procedural
-Commonly used to visualise abdominal and pelvic organs

327
Q

Label the small and large bowel:

328
Q

What are the maximum ‘normal’ diameters of the small intestine, large intestine and caecum?

A

-3,6,9 rule
-SI - 3cm
-LI - 6cm
-Caecum - 9cm
-Larger suggests dilated bowel and possible obstruction

329
Q

What is different about CT scans?

A

-Produced a series of images, not a single image like a plain x-ray
-May need to scroll through images to view different planes

330
Q

Label these abdominal CT scans:

331
Q

Label this diagram:

332
Q

What does terrestrial mean?

A

-Not living in an aqueous solution filled with nutrients
-Humans are terrestrial

333
Q

What have humans adapted for optimum nutrient absorption?

A

-Specialised gut tube through the body for getting nutrients to the circulatory system for delivery to tissues
-Organisation of shapes that maximise surface area for exchange

334
Q

Label this diagram:
What does it show?

A

Overview of GI processes

335
Q

What is the function of the GI tract?

A

-Take relatively large solids and digest them into smaller molecules that can be absorbed as nutrients
-Serve as a barrier to toxins, bacteria, parasites, etc.

336
Q

What is the functional anatomy of the GI system (5)?

A

-GI system is a hollow organ - tube through body
-Lumen is ‘outside’ the body’s tissues but its environment is tightly controlled by the body
-Specialised organs for secretion of enzymes and bile
-Epithelial cells line entire GI and serve as primary barrier
-Structure maximises surface area for secretion and absorption (folds, villi, crypts)

337
Q

What is a key feature of the GI tract?

A

-Transport of fluid and electrolyte is a key function of the GI tract
-Epithelial cells may:
-Secrete water and electrolytes
-Absorb water and electrolytes

338
Q

Label this diagram of daily gut fluid balance:

339
Q

How are H2O and electrolytes moved in the GI system?

A

-Water moves down osmotic gradient
-Electrolytes move down electrochemical gradient
-To move against a conc gradient = energy
-Energy is supplied by sodium gradients (generated by sodium pumps) and by proton gradients

340
Q

What does this diagram show?

A

-Paracellular = in between cells
-Transcellular = through cells
-Even though there are tight junctions, movement of water and ions can still occur in between cells
-Majority is transcellular

341
Q

How much fluid does the small intestine absorb a day?

342
Q

How long is the small intestine?

343
Q

Where in the small intestine does net absorption and net secretion take place?

A

-Net absorption = villi
-Net secretion = crypts

344
Q

What does this show?

A

Normal villi

345
Q

Label this diagram of nutrient absorption:
How does it work?

A

-Na+ couples nutrient absorption
-2 stage transcellular process:
-1st stage - membrane transport protein
-2nd stage - Na+/K+ ATPase transporter
-Water follows due to osmosis

346
Q

Label this diagram:
what does it show?

A

intestinal secretion

347
Q

What 4 things affect absorption in the GI system?

A

-Number and structure of enterocytes
-Blood and lymph flows
-Nutrient intake
-GI motility

348
Q

What 3 things affect the secretion in the GI system?

A

-Irritants
-Bile
-Bacterial toxins

349
Q

What 2 factors can affect Gi motility and secretion in the GI system?

A

-Hormonal
-Neural

350
Q

What are 3 clinical manifestations of disorders affecting GI absorption and secretion?

A

-Diarrhoea
-Weight loss
-Failure to thrive

351
Q

What does this show and what can cause it?

A

-Damaged villi
-Coeliac disease

352
Q

Describe toxin-induced diarrhoea:

A

-Cholera toxin released from bacteria into infected intestine
-Binds to intestinal cells
-Stimulates adenylate cyclase to produce cAMP
-Dramatic efflux of ions and water
-Watery diarrhoea

353
Q

How do oral rehydration salts work?

A

-Water passively follows the osmotic gradient
-SGLT1- sodium glucose co-transporter moves Na and glucose from luminal membrane into enterocyte
-Water follows

354
Q

What is the definition of digestion and its two parts?

A

-Breakdown of large, complex organic molecules that can be used by the body
-Mechanical - chewing, churning
-Chemical - enzymes

355
Q

What three groups of macronutrients are digested?

A

-Carbohydrates -> monosaccharides
-Protein -> amino acids
-Fats - > fatty acids/glycerol

356
Q

Where is the primary site for digestion and absorption of food?

A

Small intestine

357
Q

How does digestion occur in the GI lumen?

A

By secreted enzymes and on the surface of enterocytes by membrane-bound enzymes

358
Q

How does absorption occur in the small intestine?

A

-Simple diffusion
-Facilitated diffusion
-Active transport
-Endocytosis
-Paracellular transport

359
Q

How is the surface area of the small intestine increased?

A

-Greatly increased by extensive folding
-Projection of fingerlike villi covered with microvilli

360
Q

Label this diagram:
What does it show?

A

Digestion of carbohydrates

361
Q

Label this diagram:
What does it show?

A

-Absorption of digested carbohydrates
-Enterocytes absorb glucose and galactose
-Through an Na-dependent secondary active transport process
-Fructose is absorbed through facilitated diffusion

362
Q

Label this diagram:

363
Q

Label this diagram:

364
Q

How are fats digested?

A

-Fat and water tend to separate
-Enzymes in water can’t get at the fat

-Bile (emulsifier) arrives
-Has affinity for both fat and water and can therefore bring fat into the water

-After emulsification, fat is mixed in the water solution
-Fat-digesting enzymes have access to it

365
Q

Where are bile acids released and moved?

A

-Released into the small intestine
-After function performed - recycled back to the liver
-97% recycled

366
Q

Label this diagram of fat absorption in the small intestine:

371
Q

What are 4 functions of saliva?

A

-Lubricates, cleans oral cavity
-Dissolves chemicals
-Suppresses bacterial growth
-Digest starch by amylase

372
Q

Label this diagram:

373
Q

Label this diagram:

374
Q

Label this diagram:

375
Q

What do mucous neck cells produce + function?

376
Q

What do parietal cells produce + function?

377
Q

What do enterochromaffin-like cells produce + function?

378
Q

What do chief cells produce + function?

379
Q

What do D cells produce + function?

380
Q

What do g cells produce + function?

381
Q

Describe the first phase of gastric secretion regulation:

A

Cephalic phase

382
Q

Describe the second stage of gastric secretion regulation:

383
Q

Describe the third stage of gastric secretion regulation:

384
Q

What are the 2 functions of the pancreas?

A

-Endocrine function:
-Secretes insulin and glucagon from islets of Langerhans
-Exocrine function:
-Secretion of pancreatic juice

385
Q

What 3 things regulate pancreatic secretions?

386
Q

What are the main components of the exocrine secretion of the pancreas?

A

-Aqueous bicarbonate secretion
-Enzyme secretion

387
Q

What. are the average diameters of the pancreatic duct in each section of the pancreas?

A

-Tail - 1mm
-Middle - 2mm
-Head - 3-4mm
DISTENSION SUGGESTS BLOCKAGE IN THE PANCREATIC DUCT

388
Q

Label this diagram of pancreatic cells:

389
Q

Label the different cell types of the pancreas:

390
Q

Label the different functions of the different parts of the pancreas:

391
Q

What is the rate of bicarbonate secretion in the pancreas and by what cells?

A

-1 litre/24 hours
-Epithelial cells in pancreatic duct produce HCO3- and H2O
-Resting phase maintains a low flow - predominantly Na+ and Cl-
-High flow rates Na+ and HCO3-

392
Q

What is the function of the bicarbonate secretion produced by the pancreas?

A

-Protects duodenal mucosa by neutralising stomach acid
-Buffers duodenal contents to optimise pH for enzyme digestion

393
Q

What initiates protein digestion?

A

Initiated by pepsin in the stomach

394
Q

Where does a majority of protein digestion occur and by what?

A

-Small intestine
-Pancreatic proteases: trypsin and chymotrypsin

395
Q

How are trypsin and chymotrypsin stored?

A

-Stored as proenzymes:
-trypsinogen
-chymotrypsinogen
-Trypsinogen activated by enterokinase
-Trypsin activates chymotrypsinogen and additional trypsinogen

396
Q

Can triglycerides be absorbed across intestinal mucosa?

397
Q

How are lipids digested?

A

-Lipases hydrolyse triglycerides to monoglycerides and free fatty acids
-Bile salts aid triglyceride digestion and absorption of monoglycerides and free fatty acids

398
Q

What is fat digestion dependent on?

A

Pancreatic and hepatic secretion

399
Q

What is orlistat?

A

Pancreatic lipase inhibitor

400
Q

Describe the role of amylase:

A

-Hydrolyses starch to maltose (glucose-glucose disaccharide) and maltotriose (trisaccharide) and limit dextrins
-Pancreas is major source of amylase
-salivary amylase has a small role

401
Q

What are 4 other examples of digestive enzymes?

A

-Ribonuclease
-Deoxyribonuclease
-Gelatinase
-Elastase

402
Q

What is pancreatic enzyme secretion like during cephalic stage?

A

-Vagal innervation and gastrin
-Low level stimulus in anticipation of a meal
-Water, bicarbonate and enzymes released

403
Q

What is pancreatic secretion like during intestinal stage?

A

-Secretin
-Cholecystokinin
-Gastrin
-Release water, bicarbonate and enzymes

407
Q

What three hormones control pancreatic secretion?

A

-Cholecystokinin
-Secretin
-Gastrin

408
Q

What is the endocrine function of the pancreas and why is it important?

A

-Insulin and glucagon secretion
-Vital for carbohydrate and lipid metabolism

409
Q

What are 4 symptoms on pancreatic exocrine insufficiency?

A

-Maldigestion
-Diarrhoea
-Steatorrhoea
-Weight loss

410
Q

What are 4 consequences of pancreatic exocrine insufficiency?

A

-Malnutrition
-Oesteoporosis
-Increased cardiovascular morbidity
-Symptom burden

411
Q

What are 4 factors in an assessment of pancreatic function?

A

-History, risk factors
-Imaging
-Faecal elastase
-Markers of malnutrition

412
Q

What is the treatment of PEI?
(pancreatic exocrine insufficiency)

A

-Pancreatic enzyme replacement therapy
-STOP smoking
-Bone health assessment
-Treat underlying cause

413
Q

Why is bile important (3)?

A

-Lipid digestion and absorption
-Cholesterol homeostasis
-Excretion of lipid soluble xenobiotics/drug metabolites/heavy metals

414
Q

What is bile?

A

-Complex lipid-rich micellular solution
-Water
-Inorganic electrolytes
-Organic solutes (bile acids, phospholipids, cholesterol, bile pigment)

415
Q

What is the daily production of bile?

A

500-600mls per day

416
Q

What does formation of bile depend on?

A

-Hepatic synthesis and cannalicular secretion of bile acids
-Bile acids = major organic anion in bile

417
Q

What is the maintenance of hepatic bile formation essential for?

A

Normal liver function

418
Q

What is the turnover rate of bile?

A

-Most bile acids (95%) secreted by hepatocytes have been previously secreted into intestine
-Enterohepatic circulation

419
Q

Label this diagram:

420
Q

What are bile acids synthesised from and where?

A

-Cholesterol
-Hepatocytes of the acini

421
Q

What are the primary bile acids and what are they synthesised from + their properties?

A

-Cholic acid (CA) - water soluble
-Chenodeoxycholic acid (CDCA) - water soluble
-Cholesterol - lipophilic

422
Q

What happens to primary bile acids before secretion and why?

A

-Cholic acid (AC) and Chenodeoxycholic acid (CDCA) are conjugated before secretion into bile canaliculus
-N-acyl amidated with glycine or taurine
-Enhances hydrophilicity and acidic strength of side chain
-pKa = 5.0 unconjugated
-pKa = 3.9 glycine conjugate, 2.0 taurine conjugate

423
Q

What does conjugation do to the movement of bile acids?

A

Decreases passive diffusion of bile acids across membranes during transit through EHC (keeps intraluminal)

424
Q

Describe the classical pathway of bile acids:

425
Q

What properties do bile acids have and what does this do?

A

-Amphipathic - hydrophilic and hydrophobic parts
-Reduce surface tension and aid emulsification

426
Q

l=Label the parts of the bile acid:

427
Q

Describe emulsification:

A

-Fat is insoluble in water
-Emulsification increases surface area for lipolysis
-Stable emulsion important for close apposition of lipase and triglycerides
-Lipases act at surface of emulsified droplet and liberate FA from glycerol backbone (lipolysis)

428
Q

Explain the process of absorption of fatty acids and glycerol:

429
Q

Explain the emulsification and digestion of lipids

430
Q

What is the pathway of chylomicrons?

431
Q

What are the first 3 functions of bile acids?

A

-Induce bile flow (osmotic effect) and secretion of biliary lipids (Pl and cholesterol)
-Digestion of dietary fats - solubilising lipids and lipid digestion products as mixed micelles facilitating aqueous diffusion across intestinal mucosa
-Facilitates protein absorption - accelerating hydrolysis by pancreatic proteases

432
Q

What are the second 3 functions of bile acids?

A

-Cholesterol homeostasis - facilitates dietary absorption/elimination as BA are water-soluble end-products of cholesterol catabolism, indice bile flow and solubilise cholesterol enabling movement from hepatocytes -> lumen of intestine
-Antimicrobial (physiochemical + inducing anti-microbial genes)
-Prevents calcium gallstones and oxalate renal stones

433
Q

Label this diagram of nitrogen metabolism:

434
Q

Label this diagram of nitrogen metabolism:

435
Q

Label this inputs and outputs of this system in the liver:

436
Q

What are the most common donor/acceptor pairs?

437
Q

Label this diagram of the movement of amine groups:
Describe it:

A

Alpha-keto-acid can be used in citric acid cycle for glucose production (GLUCONEOGENESIS)

438
Q

Label the inputs and outputs of the glucose alanine cycle:

439
Q

Label the glucose alanine cycle:
What does it do?

A

-Alanine principal ammonia transporter
-Pyruvate recycled into glucose
-Gluconeogenesis takes place in liver and not muscle to conserve ATP for contraction

440
Q

What enzymes are used as an indicator for liver cell damage?

A

-Aminotransferase enzymes
-AST, ALT
-Higher levels = higher leakage from cells

441
Q

Label the urea cycle:
Describe it:

A

-One turn of cycle consumes 3 ATP equivalents and 4 high energy nucleotides (PO4-)
-Urea is only compound generated all others are regenerated

442
Q

What is the name for this?
Label it:

A

Kreb’s bicycle

443
Q

Label the diagram of the movement of amine during the glucose-alanine cycle:

A

-Alanine transaminated
-Pyruvate can be used in krebs for gluconeogenesis
-Glutamate can be oxidatively deaminated

444
Q

What happens to glutamate cycles during low energy times?
Why?

A

-alpha-ketoglutarate can be fed into citric acid cycle so hepatocytes can upregulate GDH in times of energy depletion
-ADP drives reaction due to energy depletion
-Reverse when ATP is in excess
-NH3 can be converted into urea for excretion

445
Q

Label the glutamine synthase reaction:
Why is it done?

A

-Produces amino acid
-Suitable for incorporation into proteins
-Principal role is principal ammonia carrier
-Mostly found in blood, non-toxic

446
Q

Label the glutaminase reaction:
Why is it done?

A

-Mitochondrial enzyme so seperate to glutamate synthesis
-Liver is neither net consumer or producer of glutamine
-Liver can scavenge ammonia that hasn’t been incorporated into urea
-Ammonia is controlled by incorporation into either glutamine. orurea

447
Q

What is transamination?

A

Chemical reaction transferring an amine group from an amino acid to a ketoacid to form a new amino acid

448
Q

What does this show?

A

-High levels of ammonia associated with neurotoxicity
-Ammonia can cross blood-brain barrier very easily
-Converted to glutamate by glutamate dehydrogenase
-Alpha-ketoglutarate depletes and so does Krebs
-Irreparable cell damage and cell death

449
Q

How is the embryonic gut tube formed?

A

-Connection between gut and yolk sac
-Dorsal mesentery forms

450
Q

What are the 5 stages of midgut development?

A
  1. Elongation
  2. Physiological herniation
  3. Rotation
  4. Retraction
  5. Fixation
451
Q

Describe the first step of midgut development:

A

-Elongation
-Elongation -> formation of primary intestinal loop
-Connection to yolk sac (vitelline dict) maintained but narrows

452
Q

What are the two parts of the primary intestinal loop?

A

-Cephalic limb
-Caudal limb

453
Q

What does the cephalic limb go on to form?

A

-Distal part of duodenum
-Jejunum
-Part of ileum

454
Q

What does the caudal limb go on to form?

A

-Distal part of ileum
-Caecum
-Appendix
-Ascending colon
-Proximal 2/3 transverse colon

455
Q

Describe the second part of midgut development:

A

-Intestinal loops herniate (move into) into umbilical cord - 6th week
-Abdominal cavity too small for gut loops and liver
-Gut loop starts to rotate
-90o anticlockwise at axis of SMA

456
Q

Describe the third stage of midgut development:

A

-Rotation
-Anticlockwise from front
-First 90o during herniation
-Brings caudal limb more cranially

457
Q

What happens at the end of the third stage of midgut development?

A

-Continued elongation
-Elongation continues
-Part destined to become small intestine develops coils
-Large intestine part elongates but doesn’t coil

458
Q

Describe the fourth stage of midgut formation:

A

-10th week gut loop returns to abdomen
-Gut loop roates further 180o anticlockwise
-Total rotation = 270o

459
Q

What does retraction lead to in midgut development?

A

-Starts to position gut
-Jejunum 1st to left side
-Ileum follows to right
-Caecum returns LUQ
-Caecum descends to RIF, ascending colon to right

460
Q

Describe the fifth stage of midgut development:

A

-Some mesenteries close contact with posterior abdominal wall and fuse/fix
-Considered ‘retroperitoneal’
-fascial layer (toldt fascia) develops between parietal peritoneum on posterior body wall and visceral peritoneum on organ

461
Q

What is this?

462
Q

What are the final positions of midgut viscera after development?

A

-Jejunum + ileum central, jejunum UL, ileum LR
-Ileum enter caecum on right
-Caecum descend RIF
-Ascending + Descending colon fix posterior body wall
-Dorsal mesentery SI rotate around SMA with gut loop

463
Q

Describe the movement of the caecal bud and appendix:

A

-Once gut returns to abdomen, caecal bud first in RUQ
-Descends to RIF and ascending colon lengthens
-Appendix develops during descent - comes to lie in a variety of postions

464
Q

Describe appendicitis referred pain:

A

-Umbilicus, T10
-Part of midgut so sympathetic supply (motor) from lesser splanchnic nerve - T10-11 spinal cord levels
-Visceral sensory fibres return to cord and brain from midgut to same levels
-Brain interprets pain as coming from umbilicus skin

465
Q

Describe the first part of hindgut formation:

A

-Boundary between endoderm lining cloaca and surface ectoderm is cloacal membrane
-urorectal septum grows towards cloacal membrane and separates allantois from cloaca

466
Q

Describe the second stage of hindgut formation:

A

-Ectoderm of cloacal membrane invaginates to form anal pit - lower part of anal canal
-Cloacal (anal) membrane ruptures - upper and lower anal canal continuous
-Upper and lower different blood supplies due to different origins

Phase 1 (23 decks)

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