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Phase 1 > GI > Flashcards

GI Flashcards

1
Q

How is swallowing initiated?

A

When pressure receptors in the wall of the pharynx are stimulated by food or drink, and forced into the rear of the mouth by the tongue

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2
Q

What is the nervous supply to the nasopharynx?

A

Maxillary nerve (V2- second branch of trigeminal nerve V)

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3
Q

What is the nervous supply to the oropharynx?

A

Glossopharyngeal nerve (IX)

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4
Q

What is the nervous supply to the laryngopharynx?

A

Vagus nerve X

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5
Q

What muscles manipulate food during chewing and elevate the hyoid bone?

A

The buccinator and supra hyoid

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6
Q

How is the pharynx shortened and widened during swallowing?

A

Elevation of the hyoid bone via actions of the muscles of the floor of the palate

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7
Q

How is food prevented from entering the trachea?

A

Impulses from the swallowing centre close the glottis. Food tilts the epiglottis over the closed glottis.

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8
Q

What is the nervous supply to the pharyngeal constrictor muscles?

A

Vagus X

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9
Q

Is the upper third of the oesophagus skeletal or smooth muscle?

A

Skeletal

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10
Q

Is the lower two thirds of the oesophagus skeletal or smooth muscle?

A

Smooth

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11
Q

What is the ring of skeletal muscle around the oesophagus just below the pharynx?

A

The upper oesophageal sphincter

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12
Q

What is the ring of smooth muscle surrounding the oesophagus in the last portion of the oesophagus?

A

The lower oesophageal sphincter

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13
Q

What is a peristaltic wave?

A

Waves of muscle contractions that proceed along the oesophagus, compressing the lumen and forcing the food ahead

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14
Q

How long does one oesophageal peristaltic wave take to reach the stomach?

A

9 seconds

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15
Q

What is the nervous supply that allows the gag reflex?

A

A reflex arc between the glossopharyngeal (IX) and Vagus (X) nerves

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16
Q

What are the functions of saliva?

A

Lubricant for mastication
Maintaining oral pH (maintained at 7.4) by the bicarbonate/carbonate buffer system
Release digestive enzyme- salivary alpha amylase released from parotid gland

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17
Q

What is the daily secretion of saliva?

A

800-1500 ml

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18
Q

What is serous secretion?

A

Alpha amylase for starch digestion

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19
Q

What is mucous secretion?

A

Mucins for lubrication of mucosal surfaces

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20
Q

What secretion does parotid glands release?

A

Serous

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21
Q

What secretion does submandibular glands secrete?

A

Mucous and serous

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22
Q

What secretion does sublingual glands secrete?

A

Mucous and serous but mainly mucous

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23
Q

What secretion does minor glands secrete?

A

Predominantly mucous but some serous

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24
Q

What factors 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 
Time of day
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25
Q

What are the defences of the oral cavity provided by?

A

The mucosa
The salivary glands
Palatine tonsils

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26
Q

Which salivary glands are continuously active?

A

Submandibular, sublingual and minor glands

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27
Q

What are the epithelial tissues present in salivary glands?

A

Acinar Cells and ducts

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28
Q

What do the ducts do in salivary glands?

A

Collect to form the large cut entering the mouth. Equipped with channels and transporters in the apical and basolateral membranes enabling transport of fluid and electrolytes

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29
Q

What are the two types of acini?

A

Serous and mucous

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30
Q

What do serous acini secrete?

A

Water and alpha amylase

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31
Q

Where are serous acini mainly found?

A

Parotid glands

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32
Q

What do mucous acini secrete?

A

Mucous (water and glycoproteins)

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33
Q

Where are mucous acini found?

A

Submandibular and sublingual glands

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34
Q

What are the two types of intralobular ducts?

A

Intercalated and striated

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35
Q

Describe intercalated ducts

A

Short narrow duct segments with cuboidal cells that connect acini to larger striated ducts

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36
Q

Describe striated ducts

A

Striated like a thick lawn, and major site for reabsorption of NaCl. Appear striated at the basal end. Basal membrane is highly folded into microvilli for active transport of HCO3 against conc gradient.

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37
Q

What ions do ducts secrete?

A

K+ and HCO3-

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38
Q

What ions do ducts reabsorb?

A

Na+ and Cl-

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39
Q

Why is saliva hypotonic?

A

The epithelium of the ducts reabsorb water

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40
Q

How much of the salivary flow are from the major glands?

A

80%

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41
Q

Where are the minor saliva glands found?

A

The submucosa or oral mucosa of the lips, cheeks, hard and soft plate and the tongue

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42
Q

Where is the parotid gland?

A

Superficial triangular outline between the zygomatic arch, sternocleidomastoid and ramus of mandible

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43
Q

Where does the parotid gland enter the mouth?

A

Near the second upper molar

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44
Q

What is the sympathetic sensory innervation of the parotid gland?

A

Auriculo-temporal nerve which is a branch of the mandibular nerve

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45
Q

What is the parasympathetic innervation of the parotid gland?

A

Glossopharyngeal nerve (stimulates secretion)

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46
Q

What are the structures that pass through the parotid gland?

A

External carotid artery, retromandibular vein and facial nerve

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47
Q

What are the two lobes of the submandibular gland, and how are they seperated?

A

Seperated by the mylohyoid muscle, larger superficial lobe and a smaller deep lobe

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48
Q

Where does the submadibular gland empty into the oral cavity?

A

The sublingual papillae- under tongue

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49
Q

What is the parasympathetic innervation of the submandibular gland?

A

Chorda tympani branch of facial nerve VII

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50
Q

What is the sympathetic innervation of the submandibular gland?

A

Lingual nerve which is derived from the facial nerve VII

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51
Q

Where is the sublingual gland?

A

Located on the floor of the mouth between mylohyoid muscles and oral mucosa of the floor of the mouth

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52
Q

What is the parasympathetic innervation of the sublingual gland?

A

Chorda tympani branch of the facial nerve VII

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53
Q

What is the sympathetic innervation of the sublingual gland?

A

The lingual nerve which is derived from the facial nerve VII

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54
Q

Does sympathetic or parasympathetic stimulation inhibit salivary secretion in the minor glands?

A

Sympathetic

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55
Q

What is xerostomia?

A

Dry mouth

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56
Q

Where do salivary calculi (stones) normally form?

A

Submandibular gland

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57
Q

What are the functions of the stomach?

A 
Store and mix food
Dissolve and continue digestion
Regulate emptying into the duodenum
Kill microbes
Secrete protease
Secrete intrinsic factor
Activate proteases
Lubrication
Mucosal Protection
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58
Q

What do parietal cells produce?

A

Gastric acid and intrinsic factor

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59
Q

What do chief cells produce?

A

Pepsinogen

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60
Q

What do ECL cells release?

A

Histamine

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61
Q

What do G cells release?

A

Gastrin

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62
Q

What do D cells release?

A

Somatostatin

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63
Q

What do glands in the thin walled upper portions of the body of the stomach secrete?

A

Mucous, hydrochloric acid and pepsinogen

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64
Q

What do the glands in the thick walled antrum secrete?

A

A little acid, mainly gastrin

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65
Q

How much hydrochloric acid is produced per day?

A

2 litres

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66
Q

Describe how HCl is made in the stomach

A

H2O in the parietal cell breaks down into OH- and H+
H2CO3 rapidly disassociates into HCO3- and H+
The H+ ions produced can then react with OH- to regenerate H2O
The H+ ions are actively pumped into the stomach lumen. They pump 1 k+ into the cell for every 1 H+ out.
The K+ ions diffuse back out through K+ channels.
The HCO3- is secreted into the capillary for the exchange of Cl- ions. These Cl- ions then enter the stomach through Cl- channels. In the stomach the H+ ions and Cl- ions react to form HCl.

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67
Q

How is H2CO3 produced?

A

CO2 and H2O from respiration are converted via the enzyme carbonic anhydrase

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68
Q

Describe the cephalic phase to increase gastric acid production

A

This is a parasympathetic response initiated by sight, smell, taste or chewing. Acetyl choline is released and it acts indirectly in parietal cells, triggering the release of gastrin and histamine. These both increase the number of H+/K+ATPase pumps, to increase gastric acid production

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69
Q

Describe the gastric phase to increase gastric acid production

A

Gastrin is released which acts directly on parietal cells, and triggers the release of histamine. These both increase the number of H+/K+ATPase pumps on the membrane of parietal cells, increasing gastric acid production

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70
Q

How is the cephalic phase to increase gastric acid production initiated?

A

Smell, sight, taste or chewing

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71
Q

How is the gastric phase to increase gastric acid production initiated?

A

Gastric distension from the volume of ingested material and the presence of peptides and amino acids

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72
Q

How do proteins in the stomach increase acid production?

A

The proteins act as a buffer thereby reducing the amount of H+ ions, increasing the pH, resulting in decreased secretion of somatostatin which increases parietal cell activity, increasing gastric acid production

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73
Q

What is the gastric phase to decrease gastric acid secretion?

A

A low luminal pH directly inhibits gastrin secretion thereby indirectly inhibiting histamine release. The pH also stimulates somatostatin release which inhibits parietal cell activity.

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74
Q

What does somatostatin do?

A

Inhibit parietal cell activity- less gastric acid secretion

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75
Q

What initiates the intestinal phase to decrease gastric acid secretion?

A

Duodenal distension, low pH, hypertonic solutions, the presense of amino acids and fatty acids

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76
Q

What is the intestinal phase to decrease gastric acid secretion?

A

Locally produced chemical messengers called enterogastrones such as secretin and cholecystokinin (CCK) are released. They also trigger short and long neural pathways which reduce ACh release.

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77
Q

What is secretin?

A

A enterogastrone which inhibits gastrin release and promotes somatostatin release

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78
Q

What is an ulcer?

A

A breach in a mucosal surface

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79
Q

Describe helicobacter pylori infection

A

A bacteria that lives in gastric mucus. It secretes urease which splits urea into CO2 and ammonia. The ammonia reacts with H+ to produce ammonium, which is toxic to gastric mucosa resulting in less mucous being produced. Secreted proteases, phospholipase and vacuolating cytotoxin A can then begin attacking the gastric epithelium, further reducing mucous production. Results in inflammatory response.

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80
Q

What is the treatment for helicobacter pylori infection?

A

Eradicate organism using triple therapy; proton pump inhibitor (increases gastric pH making conditions inhospitable), and antibiotics

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81
Q

What does NSAID stand for?

A

Non-steroidal anti-inflammatory drugs

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82
Q

How can NSAIDs cause a stomach ulcer?

A

NSAIDs inhibit cyclo-oxygenase 1 thus reducing mucosal defence?

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83
Q

How is mucous secretion stimulated?

A

Prostaglandins (cyclo-oxygenase 1 is needed for prostaglandin synthesis)

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84
Q

What are the chemical irritants that can cause gastric ulcers?

A

Alcohol, bile salts (can be refluxed from duodenum)

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85
Q

What is a gastrinoma?

A

A rare tumour of parietal cells causing excessive gastrin release (can cause increased attack on gastric mucosa causing gastric ulcers)

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86
Q

What are the synthetic ways to reduce gastric acid secretion?

A

Proton-pump inhibitors or H2 receptor agonists

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87
Q

What are examples of proton-pump inhibitors?

A

Omeprazole, lasoprazole and esomeprazole

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88
Q

What are examples of H2 receptor agonists?

A

Cimetidine and ranitidine

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89
Q

What do H2 receptor agonists do?

A

Block the receptors for histamine thereby reducing acid secretion

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90
Q

What are the protective mechanisms of gastric mucosa?

A

Alkaline mucus on luminal surface, tight junctions between epithelial cells, replacement of damaged cells, feedback loops

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91
Q

Why is pepsin secreted as pepsionogen?

A

To prevent it digesting the chief cells

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92
Q

What ion irreversibly inactivates pepsin?

A

HCO3-

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93
Q

What is essential for vitamin B-12 absorption?

A

Intrinsic factor

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94
Q

What percentage of total protein digestion does pepsin account for?

A

20%

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95
Q

What is the volume of an empty stomach?

A

50ml

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96
Q

What volume can a full stomach accommodate?

A

1.5L

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97
Q

How does the stomach increase in volume?

A

The smooth muscles in the body and fundus receptive relax

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98
Q

What is the nervous supply mediating receptive relaxation?

A

Parasympathetic nervous system acting on the enteric nerve plexuses with co-ordination provided by afferent input from the stomach via the vagus nerve and the swallowing centre

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99
Q

What chemicals mediate receptive relaxation?

A

Nitric oxide and serotonin

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100
Q

What is the direction of the peristaltic waves in the stomach?

A

From the body towards the antrum

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101
Q

What is the pyloric sphincter?

A

A ring of smooth muscle and connective tissue between the antrum and the duodenum

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102
Q

What is the frequency of peristaltic gastric waves determined by?

A

Pacemaker cells -interstitial cells of cajal, in the muscular propria

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103
Q

What is the frequency of peristaltic gastric waves?

A

3 per minute

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104
Q

What can increase the strength of gastric contractions?

A

Gastrin, gastrin distension

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105
Q

What can decrease strength of gastric contractions?

A

Duodenal distension, increase in duodenal fat, increase in duodenal osmolarity, increase in duodenal pH, increase in sympathetic stimulation, decrease in parasympathetic stimulation

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106
Q

What are the symptoms of dumping syndrome?

A

Vomiting, bloating, cramps, diarrhoea, dizziness, fatigue, weakness, sweating

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107
Q

What causes dumping syndrome?

A

Overfilling of the duodenum by a hypertonic solution

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108
Q

What is gastroparesis?

A

Delayed gastric emptying

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109
Q

What happens to the pH of the duodenum, when gastric contents enter?

A

Duodenal pH falls

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110
Q

What are the symptoms of gastroparesis?

A

Nausea, early satiety, vomiting undigested food, GORD, abdominal pain, anorexia

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111
Q

What drugs can cause gastroparesis?

A

H2 receptor antagonists, proton pump inhibitors, opiod analgesics, diphenhydramine, beta-adrenergic receptor agonists, calcium channel blockers, levodopa

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112
Q

What can cause GORD?

A

Pregnancy, Hiatus hernia, obesity and smoking

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113
Q

What percentage of water is absorbed in the small intestine?

A

80%

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114
Q

Which part of the small intestine absorbs the most amount of water?

A

The jejunum

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115
Q

How much of the fluid load is reabsorbed?

A

98%

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116
Q

How is potassium reabsorbed?

A

K+ is absorbed by passive diffusion in the colon

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117
Q

How is chloride reabsorbed?

A

Cl- is actively reabsorbed in exchange for bicarbonate resulting in the intestinal contents becoming more alkaline

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118
Q

What is the absorpitive state?

A

Ingested nutrients enter the blood from the GI tract. During this state, some of the ingested nutrients provide the energy requirements of the body and the remainder is added to the body’s energy stores to be called upon during the post absorptive state

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119
Q

What is the postabsorptive state?

A

The GI tract is empty of nutrients and the body’s own stores must supply energy

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120
Q

What is the average daily intake of lipid?

A

70 to 100 ml per day

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121
Q

What are the three main important fatty acids we absorb?

A

Palmitic, stearic and oleic acid

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122
Q

Where does triglyceride digestion begin?

A

In the mouth

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123
Q

Where is lipase synthesised?

A

Pancreas

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124
Q

What are triglycerides seperated into under the action of lipase?

A

Monoglycerides and fatty acids

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125
Q

What are examples of emulsifying agents?

A

Phospholipids, bile salts

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126
Q

What does the process of emulsification require?

A

Mechanical distruption of the large droplets into smaller droplets, and an emulsifying agent

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127
Q

How are bile salts formed?

A

Formed from cholesterol in the liver

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128
Q

What are bile salts formed from?

A

Bile salts, fat soluble vitamins, cholesterol, fatty acids, monoglycerides, and phospholipids

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129
Q

What are chylomicrons formed from?

A

Phospholipids, cholesterol and fat-soluble vitamins

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130
Q

What are the three main sources of fatty acids for triglyceride synthesis?

A

Glucose that enters adipose tissue and is broken down to synthesise fatty acids
Glucose that is used in the liver to form VLDL triglycerides
Ingested triglycerides transported in the blood in chylomicrons and taken up by adipocytes

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131
Q

What vitamins are fat soluble?

A

Vitamin A, D, E and K

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132
Q

Where is vitamin C and B (not B12) absorbed and how?

A

They are absorbed by diffusion in the jejunum

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133
Q

Where is vitamin B12 absorbed and how?

A

It is bound to intrinsic factor and absorbed in the lower portion of the ileum via endocytosis

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134
Q

Where is the main site of protein digestion and absorption of protein?

A

The duodenum

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135
Q

How many amino acids are essential?

A

8

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136
Q

Where does protein digestion begin?

A

The stomach

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137
Q

Where is pepsinogen I found?

A

The HCl secreting region of the stomach

138
Q

Where is pepsinogen II found?

A

The pyloric region

139
Q

What is the pH of the duodenal cap?

A

2-4

140
Q

What is the pH in the duodenum?

A

6.5

141
Q

Where are endopeptidases and exopeptidases produced?

A

The pancreas

142
Q

What are examples of endopeptidases?

A

Trypsin, Chymotrypsin and elastase

143
Q

What are examples of exopeptidases?

A

Carboxyl dipeptidases and the amino peptidases of the brush border

144
Q

Where does the final digestion of peptides occur?

A

The intestinal lumen
The brush border
Within the cell

145
Q

Describe the digestion of lactose

A

Forms beta linkages sinse OH groups lies above the plane of the molecule thus it requires its own enzyme to be broken down.

146
Q

Why are people lactose-intolerant?

A

They do not have sufficient amounts of beta enzymes

147
Q

What is the most common disaccharide?

A

Sucrose

148
Q

Which type of isomer of amino acids are found in the proteins we utilise?

A

L forms

149
Q

Which type of isomer of sugar molecules are utilised in metabolism?

A

D forms

150
Q

What type of glycosidic linkages are found in glycogen?

A

Alpha 1-4, and alpha 1-6

151
Q

What type of linkages are found it starch?

A

Mainly alpha 1-4 and some alpha 1-6 glycosidic linkages

152
Q

What type of linkages are found in cellulose?

A

Beta 1-4 glycosidic

153
Q

How is starch first degraded?

A

Ptalin - alpha amylase in the mouth

154
Q

What is the optimal pH for ptyalin?

A

6.7

155
Q

Where is olgiosaccharidases?

A

The outer portion of the membrane of the microvilli

156
Q

What are examples of olgiosaccharidases?

A

Maltase
Lactase
Sucrase
Alpha-Limit dextrinase

157
Q

How is glucose absorbed?

A

Sodium-glocose cotransporter (facilitated diffusion)

158
Q

What are the roles of liver in the conversion of glucose?

A

Glucose can be converted to glycogen or alpha-glycerol phosphate/fatty acids

159
Q

Where is lipoprotein lipase located?

A

The blood-facing surface of the capillary endothelial cells, especially those in adipose tissue

160
Q

What is the equation for BMI?

A

Weight (KG)/ Height ^2(m)

161
Q

What classifies as obese on BMI?

A

> 30

162
Q

What classifies as overweight on BMI?

A

> 25

163
Q

What classifies as underweight on BMI?

A

<18.5

164
Q

How long can an adult male last with only glycogen stores?

A

12 Hours

165
Q

How long can an adult male last with lipid stores?

A

3 Months

166
Q

What fuels are used by the brain?

A

Glucose, ketone bodies

167
Q

What fuels are used by muscle?

A

Glucose, ketone bodies (in starvation), triacyglycerola, branched-chain amino acids

168
Q

What fuels are used by the liver?

A

Amino acids, fatty acids, glucose and alcohol

169
Q

What fuels are used by the kidney?

A

Glucose, ketone bodies (cortex), glucose (medulla)

170
Q

What fuels are used by the small intestine?

A

Ketone bodies (mainly in starvation), glutamine (amino acid)

171
Q

What fuels are used by the large intestine?

A

Short chain fatty acids, glutamine

172
Q

What is the basal metabolic rate?

A

Minimum amount of energy required to keep the body alive- decreases with age

173
Q

Where is vitamin A stored?

A

Ito cells in the space of Disse of the liver

174
Q

What are the functions of vitamin A?

A 
Cellular growth and differentiation
Process of vision
Healthy skin
Reproduction
Embryonic development 
Maintenance of bodies mucus membranes 
Immune system
175
Q

What are the sources of vitamin A?

A

Liver
Dairy products
Oily fish
Margarine

176
Q

What can happen in vitamin A deficiency?

A 
Night blindness
Xerophthalmia 
Growth retardation
Keratinisation of epithelia 
Impaired hearing, tase and smell
Increases susceptibility to infection
177
Q

What are the functions of vitamin C?

A

Synthesis of collagen, neurotransmitters, and carnitine
Antioxidant ability
Absorption of non-haem iron

178
Q

What are the sources of vitamin C?

A

Citrus fruits
Green leafy vegetables
Potatoes
Kidney

179
Q

What happens in vitamin C deficiency?

A

Weakness
Bleeding gums
Hyperkeratosis
Scurvy

180
Q

What is the function of B vitamins?

A

Cell metabolism

Energy production

181
Q

Where is vitamin B-12 found?

A

Fish
Poultry
Meat
Eggs

182
Q

What happens in vitamin B deficiency?

A

Pernicious anaemia

183
Q

Where is vitamin D found?

A

Vitamin D3- UV radiation

Vitamin D2- Plants

184
Q

What is the function of active vitamin D?

A

Stimulates intestinal absorption of Ca2+ and phosphate

185
Q

When is PTH released?

A

If there is a decrease in calcium ions (low vitamin D)

186
Q

What are the actions of PTH?

A

Increases reabsorption of bone by osteoclasts- can lead to osteoporosis
Stimulates the formation of 1,25-dihydroxyvitamin D
Directly increases Ca2+ and decreases phosphate ions reabsorption in the kidneys

187
Q

What is the function of vitamin E?

A

Antioxidant

188
Q

What is the function of vitamin K?

A

Production of clotting factors (2,7,9,10) in the liver

189
Q

What is giardiasis?

A

Infection which causes the villi to atrophy thus reducing absorption capacity

190
Q

How does coeliac disease occur?

A

Autoimmune condition whereby Gluten is partially degraded triggering an immune response whereby the system attacks the villi and microvilli resulting in a loss of brush border surface area, resulting in decreased absorption

191
Q

What are Xenobiotics?

A

Foreign chemical substance not normally found or produced in the body which cannot be used for energy requirements. Can be absorbed across lungs, skin or ingested. Excreted in bile, urine, sweat and breath.

192
Q

What are the properties of pharmacologically active compounds?

A

Lipophilic
Non-ionised at pH 7.4
Bound to plasma proteins to be transported in the blood

193
Q

What is a microsome?

A

A small particle consisting of a piece of endoplasmic reticulum to which ribosomes are attached

194
Q

What is a microsomal enzyme?

A

Enzymes which can be found in microsomes

195
Q

What type of reactions can microsomal enzymes do?

A

Mainly phase I reactions but can do phase II

196
Q

Where are microsomal enzymes found?

A

Mainly in liver hepatocytes but can be found in the kidneys and lungs too

197
Q

What are examples of microsomal enzymes?

A

Cytochrome P450, FMOs, UGT

198
Q

What happens in a phase I reaction for a microsomal enzyme?

A

Biotransforming substances

199
Q

What happens in a phase II reaction for a microsomal enzyme?

A

Glucuronidation

200
Q

What reactions can non-microsomal enzymes do?

A

Mainly phase II reactions- all conjugation reactions except glucuronidation

201
Q

What is the aim of drug metabolism?

A

To make the drugs more polar so they cannot get across membranes and thus are easily excreted

202
Q

Where does drug metabolism mainly occur?

A

The liver

203
Q

What is the aim of a phase I reaction?

A

To make the drug more hydrophilic so it can be excreted by the kidneys

204
Q

What type of group is introduced or exposed in a phase I reaction and why?

A

A hydroxyl group or other reactive site that can be used for conjugation reactions

205
Q

What are the non-synthetic catabolic reactions for a phase I reaction?

A

Oxidation, reduction and hydrolysis

206
Q

What is functionalisation as part of a phase I reaction?

A

Introduces a reactive group to a drug
Product is usually more reactive
Small increase in hydrophilicity

207
Q

How are phase I reactions normally catalysed?

A

Cytochrome P450

208
Q

What is a cytochrome P450 enzyme?

A

Type of microsomal enzyme involved in Phase I reactions. Uses heme group to oxidise substances. Products of P450 enzymes are more water soluble.

209
Q

What is the overall reaction for a phase I reaction?

A

NADPH+ H+ +O2 + RH = NADP + +H2O +ROH

210
Q

What are phase II reactions?

A

Sythetic anabolic reactions known as conjugation reaction. Aims to significantly increase hydrophilicity for renal excretion

211
Q

What is a conjugation reaction?

A

Attachment of substituent groups to a molecule. Usually inactive products catalysed by transferases.

212
Q

What is a glucuronidation reaction?

A

Addition of a glucuronic acid group to the drug to make it more hydrophilic. Uses UGT enzyme, and UDPGA co-enzyme to conjugate glucuronic acid. Process forms covalent bonds

213
Q

What are the reactions of asprin?

A

Phase I: It is a pro-drug so activated upon metabolism by a hydrolysis reaction to salcylic acid.
Phase II: Conjugated with glycine or glucuronic acid, forming a range fof ionised metabolite.

214
Q

What are the reactions of paracetamol?

A

Predominantly metabolised via a phase II reaction- conjugated with glucuronic acid and sulphate.
If stores of glucuronic acid and sulphate are low, paracetamol will undergo phase I metabolism via oxidation to produce toxic NAPQI.

215
Q

What enzymes are used in the metabolism of alcohol?

A

Alcohol dehydrognase

Aldehyde dehydrogenase

216
Q

Where does the homeostatic control of iron balance occur?

A

The intestinal epithelium in the duodenum- actively absorbs iron from ingested foods

217
Q

What percentage of ingested iron is absorbed into the blood each day?

A

10%

218
Q

What is ferritin?

A

A protein-iron complex that acts as as intracellular store for iron

219
Q

What happens when the body stores of iron are low?

A

The production of intestinal ferritin decreases resulting in a decrease in the amount of iron bound to ferritin thus increasing the unbound iron released into the blood. The absorbed iron that does not bind to ferritin is released into the blood where it is able to circulate around the body bound to the plasma protein transferrin. It transports iron in the blood plasma to the bone marrow to be incorporated into new erythrocytes.

220
Q

Where is most of the iron stored?

A

In the liver in liver ferritin within kupffer cells

221
Q

What types of proteins does the liver produce?

A

Plasma proteins, clotting factors and complement factors

222
Q

What are the functions of albumin?

A

Binding and transport of large hydrophobic compounds

Maintenance of colloid osmotic pressure

223
Q

What is colloid osmotic pressure?

A

The effective osmotic pressure across blood vessel walls which are permeable to electrolytes but not large molecules

224
Q

How does albumin maintain osmotic pressure?

A

Its presence in the plasma means that the water concentration of blood plasma is slightly lower than that of the interstitial fluid meaning there is a net flow of water out of the interstitial fluid into the blood plasma

225
Q

What are Starling forces?

A
  1. Capillary hydrostatic pressure
  2. Interstitial hydrostatic pressure
  3. Osmotic force due to plasma protein concentration
  4. Osmotic force due to interstitial fluid protein concentration
226
Q

How does liver failure cause oedema?

A

There is a reduction in albumin so less albumin in the blood. This will decrease oncotic pressure and there will be an accumulation of water in interstitial fluid

227
Q

What conditions can cause a decrease in albumin?

A

Nephrotic syndrome
Haemorrhage
Gut Loss
Burns

228
Q

What do globulins transport?

A

Lipids by lipoproteins
Iron by transferrin
Copper by caeruloplasmin

229
Q

Where are globulins produced?

A

Gamma-globulins are not made in the liver, but alpha/beta globulins are made in the liver

230
Q

Which clotting factors are NOT produced in the liver?

A

Calcium (IV) and von Willebrand factor (VIII)

231
Q

What are complement factors?

A

A plasma protein which sticks to pathogens. It is recognised by neutrophils and help mark which pathogens to kill

232
Q

What are the 2 primary methods of protein breakdown?

A

Lysosomal and ubiquitin-proteasome

233
Q

Describe the lysosomal method of protein breakdown

A

Carried out in the reticulo-endothelial system of the liver which is comprised of sinusoidal endothelial cells, kupffer cells and pit cells. Sinusoidal endothelial cells remove soluble proteins and fragments from the blood through the fenestrations known as sieve plates on their luminal surface. Once in the liver these proteins are then fused into lysosomes. Kupffer cells perform a similar function except they package into phagosomes. Both contain hydrolytic enzymes to break down the protein into amino acids.

234
Q

Describe the ubiquitin-proteasome pathway of protein degradation

A

Occurs in the cytoplasm. Different proteins degrade at different rates. Proteins can be targeted for degradation by the attachment of a small peptide called ubiquitin to the protein. This peptide directs the protein to a protein complex called a proteasome which unfolds the protein and breaks it down to smaller peptides.

235
Q

Where does amino acid degradation and catabolism occur?

A

The hepatocytes of the liver

236
Q

What does amino acid catabolism produce?

A

Nitrogen, and a carbon skeleton

237
Q

What are the two main catabolism processes?

A

Oxidative deamination and transamination

238
Q

Describe oxidative deamination

A

Results in the liberation of an amino group as free ammonia. Glutamate is the only amino acid that undergoes rapid oxidative deamination. Amino acid gives rise to ammonia molecule and is replaced by an oxygen atom from water to form an alpha-keto acid. The alpha keto-acid can then be used in the Krebs cycle for use in glucose production- gluconeogenesis. The co-enzyme involved is NAD+ (forward reaction), and NADPH (backward reaction). The enzyme that catalyses the reaction is glutamate dehydrogenase.

239
Q

How are high levels of ammonia associated with neurotoxicity?

A

Ammonia is able to cross the blood brain barrier very easily. Once inside it is converted to glutamate. This means there is a depletion in alpha-ketoglutarate. This results in the Kreb’s cycle coming to a halt. This results in irreparable cell damage and neural cell death.

240
Q

Describe transamination

A

Transfer of an alpha-amino group from amino acid to a keto-acid to form an alpha-keto- acid. If the amino acid alanine is transaminated then the amino group from it is transferred to a keto acid, and results in the formation of pyruvate and glutamate. The enzyme involved for these reactions is aminotransferase and they are found in cytosol of mitochondria. This reaction is readily reversible.

241
Q

What is the most common cause of a positive nitrogen balance?

A

Pregnancy

242
Q

What is the most common cause of a negative nitrogen balance?

A

Malnutrition

243
Q

What are the steps of the urea cycle?

A

Argenine is cleaved by arginase generating urea and ornithine. Then ammonia and CO2 is built up on the ornithine to form citrulline. Another molecule of ammonia is then added to citrulline to regenerate arginine and enable the cycle to go around again.

244
Q

What happens in the post-absorptive state?

A

Nutrients are no longer absorbed from the GI tract. Nutrients stores must supply the energy requirements of the body

245
Q

What are the three main sources of glucose in the post-absorptive state?

A

Glycogenolysis
Lipolysis
Protein

246
Q

Where does glycogenolysis occur?

A

Occurs in the liver and skeletal muscles.

247
Q

How does glycogenolysis in the liver occur?

A

Glycose-6-phosphate in enzymatically converted to glucose which then enters the blood. Hepatic glycogenolysis begins within seconds of an appropriate stimulus, such as sympathetic nervous system activation. Consequently it is the first line of defence in maintaining the plasma glucose concentration within a homeostatic range. The amount of glucose available here can only supply the bodies requirements for only several hours.

248
Q

How does glycogenolysis occur in skeletal muscle?

A

Glucose-6-phosphate undergoes glycolysis within muscle to yield ATP, pyruvate and lactate. The ATP and pyruvate are used directly by the muscle cell. However, some of the lactate enters the blood and circulates to the liver and is converted into glucose which can then leave the liver cells to enter the blood. Thus muscle glycogen contributes to blood glucose indirectly by way of the livers, processing of lactate.

249
Q

How does lipolysis occur?

A

The catabolism of triglycerides in adipose tissue via the hydrolysis of triglycerides to produce glycerol and fatty acids. Glycerol and fatty acids enter the blood via diffusion. The glycerol enters the liver which in turn enzymatically converts it through a series of steps into glucose

250
Q

How does gluconeogenesis occur?

A

Large quantities of protein in muscle and tissues can be catabolised without significant cellular malfunction. There are limits however, and continued protein loss during a prolonged fast ultimately means disruption of cell function, sickness and eventually death. The proteins supply amino acids, which enter the blood and are taken up by the liver, where they are converted via the alpha-keto acid pathway to glucose, which can then be released into the blood.

251
Q

Which cells store most of the bodies fat?

A

Adipocytes and hepatocytes

252
Q

What percentage of the bodies energy is stored in triglycerides?

A

78%

253
Q

What percentage of the bodies energy is stored in proteins?

A

21%

254
Q

What are the functions of lipids?

A

Energy reserves
Structural part of cell membrane
Hormone metabolism

255
Q

Where are HDLs formed?

A

The liver

256
Q

Where are LDLs formed?

A

The plasma

257
Q

What is the role of HDLs?

A

Remove excess cholesterol from blood and tissue. They then deliver this cholesterol to the liver which secretes it into the bile or converts it into bile salts

258
Q

What are the roles of LDLs?

A

The main cholesterol carriers and they deliver cholesterol to cells throughout the body. LDLs bind to plasma membrane receptors specific for a protein component of the LDLs and are taken up by the cells via endocytosis.

259
Q

Why is LDL cholesterol said to be “bad”?

A

High plasma concentrations can be associated with increased deposition of cholesterol in arterial walls and a higher incidence of heart attacks.

260
Q

What is the role of VLDLs?

A

Carry triglycerides from glucose in the liver to adipocytes

261
Q

Where are VLDLs synthsised?

A

Hepatocytes

262
Q

What is the function of adipocytes?

A

To synthesise and store triglycerides during periods of food uptake and then, when food is not being absorbed from the small intestine, to release fatty acids and glycerol into the blood for uptake and use by other cells in order to provide the energy required for ATP formation

263
Q

How are ATP molecules produced from fatty acids?

A
  1. Molecule of coenzyme A link to the carboxyl at the end of a fatty acid
  2. This step is followed by the breakdown of ATP —> AMP + 2Pi
  3. The coenzyme A derivative of fatty acid then proceeds through beta-
    oxidation reactions
  4. A molecule of acetyl coenzyme A is split off from the fatty acid and two pairs of hydrogen atoms are transferred to coenzymes (one pair to FAD and the
    other pair to NAD+)
  5. The hydrogen atoms from the coenzymes then enter the oxidative
    phosphorylation pathway to form ATP
  6. Another coenzyme A attaches to the fatty acid and the cycle is repeated
  7. Each passage through this sequence shortens the fatty acid chain by two
    carbons atoms until all the carbon atoms have transferred to coenzyme A
    molecules
  8. These molecules then lead to the production of CO2 & ATP via the Kreb’s
    cycle & oxidative phosphorylation
264
Q

What is the role of lipoprotein lipase?

A

Hydrolyses triglycerides in lipoproteins (chylomicrons and VLDLs) into 2 free fatty acids and 1 glycerol molecule

265
Q

Where is hepatic lipase expressed?

A

In the liver and adrenal glands

266
Q

What is the role of hepatic lipase?

A

Converts IDL (intermediate density lipoprotein) into LDL thereby packaging it with more triglycerides to be released in the body

267
Q

What are the roles of bile?

A

Used to emulsify fats, serves as an excretory pathway for most steroid hormones, many drugs as well as some toxins metabolised by the liver

268
Q

Where does the gall bladder lie?

A

At the junction of the right mid-clavicular line and costal margin

269
Q

Where does the portal vein collect blood from?

A

The superior mesenteric vein

270
Q

What does the portal triad consist of?

A

A hepatic portal vein, hepatic artery, bile duct

271
Q

What is the space of disse?

A

Where hepatocytes are seperated from the sinusoids

272
Q

Where do substances absorbed from the small intestine end up?

A

The hepatic sinusoid

273
Q

What is the blood supply to the liver?

A

80% Portal vein, 20% hepatic artery

274
Q

What are the role of stellate cells?

A

They are responsible for producing the extracellular matrix in the space of disse

275
Q

How are bile canaliculi bound together?

A

Tight junctions, gap junctions and desmosomes

276
Q

How is bile pumped towards bile ducts from bile canaliculi?

A

Actin filaments

277
Q

What does the common bile duct consist of?

A

Bile ducts which join to form the common hepatic duct. The cystic duct then joins allowing bile to collect in the gall bladder. This then becomes the common bile duct

278
Q

What is the ampulla of vater?

A

The point at which the pancreatic duct joins the common bile duct

279
Q

Where do the pancreatic duct and common bile duct enter the duodenum?

A

The major duodenal papilla

280
Q

What is the sphincter of Oddi?

A

The sphincter around the common bile duct and pancreatic duct to regulate entry of bile into the duodenum

281
Q

What are the six major ingredients of bile?

A 
Bile salts 
Lecithin 
HCO3- and other salts
Cholesterol
Bile pigments
Trace metals
282
Q

Where are bile salts manufactured?

A

Hepatocytes

283
Q

Why are bile salts, cholesterol and lecithin aggregated into mixed micelles?

A

Bile salts are powerful detergents for their fat emulsification function. However they are also capable of damaging cell membranes and so they are seperated in micelles to reduce damage until they are required.

284
Q

Why is HCO3- needed in bile?

A

To help neutralise the acids in the duodenum

285
Q

How is the HCO3- rich bile solution secreted?

A

Via epithelial cells lining the bile ducts

286
Q

How is secretion of the HCO3- rich solution stimulated?

A

Secretin in response to the presence of acid in the duodenum

287
Q

What stimulates the gallbladder to contract?

A

Cholecystokin- released due to amino and fatty acids in the duodenum

288
Q

What is enterohepatic circulation?

A

During the digestion of a fatty meal, most of the bile salts entering the intestinal tract are absorbed by specific Na+ coupled transporters in the jejunum and terminal ileum. These bile salts are returned via the portal vein to the liver where they are once again secreted into the bile. This is driven by secondary active transport coupled to Na+

289
Q

What are bile pigments formed from?

A

The haem portion of haemoglobin when old/ damaged erythrocytes are broken down in the spleen and liver

290
Q

What colour is bilirubin?

A

Yellow

291
Q

How is haem broken down?

A

Under the action of hemoxygenase into biliverdin and Fe2+ and CO

292
Q

How is biliverdin reduced?

A

Under the action of biliverdin reductase into unconjugated bilirubin

293
Q

What is unconjugated bilirubin bound to to be transported to the liver?

A

Albumin

294
Q

How is unconjugated bilirubin made conjugated?

A

Glucuronidation in the liver under the action of UDP glucuronyl transferase

295
Q

How is conjugated bilirubin converted to urobilinogen?

A

It is reduced through a hydrolysis reaction under the action of intestinal bacteria in the ilium

296
Q

What happens to urobilinogen that is reabsorbed?

A

It is bound to albumin and transported back to the liver. It is oxidised to urobilin and either recycled into bile or transported to the kidneys where it is excreted in urine- responsible for the yellowish colour of urine.

297
Q

What happens to urobilinogen that is not reabsorbed into the blood?

A

It is oxidised by another type of intestinal bacteria to form stercobilin and then excreted into the faeces- responsible for its brownish colour

298
Q

What is jaundice?

A

A yellow discolouration of the skin caused by a high serum bilirubin level (clinically detectable when bilirubin is above 50 micromol/L)

299
Q

What are three main types of jaundice?

A

Pre-hepatic
Hepatic
Post hepatic

300
Q

What is pre-hepatic jaundice?

A

Increased breakdown of erythrocytes resulting in increased levels of unconjugated bilirubin. This causes an increased serum unconjugated bilirubin

301
Q

What are the clinical syptoms of pre-hepatic jaundice?

A

Normal stools and urine
Yellow skin
Enlarged spleen

302
Q

What are the causes of pre-hepatic jaundice?

A

Malaria, sickle cell anaemia, thalassaemia, physiological jaundice of the newborn

303
Q

What is hepatic jaundice?

A

The result of hepatocellular celling. Impaired cellular uptake, defective conjugation or abnormal secretion of bilirubin by hepatocytes. The liver is damaged so unable to metabolise the unconjugated bilirubin, resulting in a buildup in serum unconjugated bilirubin. Damage could also mean that conjugated bilirubin is unable to be secreted resulting in a raised serum conjugated bilirubin as well. Increased conjugated and unconjugated bilirubin, decreased urobilinogen.

304
Q

What are the clinical symptoms of hepatic jaundice?

A

Dark urine
Normal or pale stools
Enlargement of the spleen
Yellow skin

305
Q

What causes hepatic jaundice?

A

Viral hepatitis, drugs, alcohol hepatitis, cirrhosis, and jaundice of the newborn

306
Q

What is post-hepatic jaundice?

A

When biliary system is damaged, inflamed or obstructed. Elevated serum conjugated bilirubin.

307
Q

What are the clinical symptoms of post-hepatic jaundice?

A 
Dark urine
Pale stools
Normal levels of unconjugated bilirubin
No enlargement of the spleen
Yellow skin
308
Q

What causes post-hepatic jaundice?

A

Gallstones, pancreatic cancer, gallbladder cancer, bile duct cancer, pancreatitis

309
Q

Why can cancer or inflammation of the pancreas cause jaundice?

A

The head of the pancreas is situated in the duodenal loop which is near the common bile duct, thus any inflammation or cancer of the pancreas can eventually cause obstruction to the duct, causing jaundice

310
Q

Where will pain from acute pancreatitis radiate from?

A

The back

311
Q

What is gilbert syndrome?

A

Where there is a shortage of UDP glycerol transferase, meaning only small amounts of conjugation can occur. There will be a normal conjugated bilirubin level but a raised unconjugated bilirubin level

312
Q

How are gall stones formed?

A

When the concentration of cholesterol in bile becomes high in relation to the concentrations of phospholipids and bile salts, the cholsterol will crystalise out of solution forming gall stones

313
Q

Why do gall stones cause decreased fat digestion and absorption?

A

The stone may become lodged in the common bile duct, thus preventing the bile from entering the intestines

314
Q

Why can gall stones cause clotting problems or calcium malabsorption?

A

Decreased absorption of fat soluble vitamins A D K and E.

315
Q

Why can gall stones cause diarrhoea and fluid and nutrient loss?

A

Some excess fat in the large intestine will be converted into fatty acid derivatives by bacteria that alter salt and water movements leading to a net flow of fluid into the large intestine

316
Q

Is the pacreas retroperitoneal or intraperitoneal?

A

All retroperitoneal apart from the tail which is attached to the spleen and is intraperitoneal

317
Q

Where does the uncinate process arise from?

A

The ventral bud

318
Q

What vessels lie inbetween the uncinate process and the head of the pancreas?

A

The superior mesenteric vein and artery

319
Q

What is the main blood supply to the pancreas?

A

The coelic trunk

320
Q

What are the divisions of the coeliac trunk at the coeliac axis?

A

Gastric arteries, hepatic artery, and splenic artery

321
Q

What is the venous drainage of the pancreas?

A

Mainly the splenic vein which then joins the superior mesenteric vein to form the portal vein

322
Q

What does the exocrine pancreas secrete?

A

HCO3-

Digestive enzymes

323
Q

Where do the secretions from the exocrine pancreas arise from?

A

The acinar tissue of the pancreas

324
Q

What will bile reflux down the pancreatic duct cause and why?

A

Acute inflammation due to its detergent properties

325
Q

What cells secrete HCO3- in the pancreatic duct?

A

Duct cells

326
Q

Why is HCO3- secreted in the pancreatic duct?

A

To protect the duodenal mucosa from the gastric acid and buffer the material entering the duodenum to a pH that is suitable for enzyme action

327
Q

How is the secretion of HCO3- from the pancreas and liver stimulated?

A

The release of the gastrointestinal hormone secretin in response to the presence of acid in the duodenum

328
Q

What exchanger allows the pancreatic duct cells to pump out HCO3-?

A

Cl-/HCO3-

329
Q

What cells secrete digestive enzymes at the pancreatic end of the duct system?

A

Gland cells

330
Q

What does the release of CCK do?

A

Stimulates the secretion of digestive enzymes and also potentiates the actions of secretin. Stimulates the contraction of the gall bladder and relaxes the sphincter of Oddi

331
Q

Where is CCK produced?

A

The small intestine

332
Q

What are the naturally active digestive enzymes?

A

Alpha-amylase and lipase

333
Q

Where is enterokinase found?

A

Embedded in the luminal plasma membranes of the intestinal epithelial cells

334
Q

What is enterokinase?

A

A proteolyic enzyme that splits off a peptide from pancreatic trypsinogen forming the active enzyme trypsin

335
Q

What is the role of trypsin?

A

Activate other pancreatic zymogens by splitting off peptide fragments

336
Q

What is chymotrypsinogen activated into?

A

Chymotrypsin enzyme

337
Q

What is produced by delta cells in the pancreatic islets?

A

Somatostatin

338
Q

What do alpha cells in the islets of langerhans produce?

A

Glycagon

339
Q

What do beta cells in the islets of langerhans produce?

A

Insulin and amylin

340
Q

What do PP cells in the islets of langerhans produce?

A

Pancreatic polypeptide

341
Q

What is the blood supply to the liver?

A

25% from hepatic artery (oxygenated)

75% from portal vein (deoxygenated but nutrients)

342
Q

How does blood leave the liver?

A

The hepatic vein which eventually drains into the inferior vena cava

Phase 1 (41 decks)

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