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GI Flashcards

1
Q

What are NSAIDs?

A

Non-steroidal anti-inflammatory drugs

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2
Q

What are the major salivary glands?

A

Parotid gland (serous); submandibular salivary gland (mixed serous and mucinous); sublingual salivary gland (mucinous)

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3
Q

What are the cells in the GI tract?

A

There is lymphoid tissue, exocrine glands, endocrine glands, layers of muscle. It has a large surface area.

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4
Q

What is the mucosa of the GI tract?

A

The structure depends on the site within GI tract. It is specialised to provide a variety of functions. It may include endocrine and exocrine cells.

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5
Q

What is the submucosa of the GI tract?

A

It is loose connective tissue. It contains nerve plexuses.

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6
Q

What are the layers of the muscularis propria?

A

It has an inner circular layer at an outer longitudinal layer.

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7
Q

What epithelium does the mouth have and why?

A

It has stratified squamous epithelium to resist stress and infection.

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8
Q

What immune defence does the mouth have?

A

It has lymphoid tissue to resist infection, along with lysozyme and IgA.

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9
Q

Where is keratin in the mouth?

A

It is on the lips to resist dessication

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10
Q

What glands are in the mouth?

A

There are mucinous and seromucinous glands to initiate digestion and facilitate movement

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11
Q

What enzyme is secreted in saliva?

A

Amylase to initiate digestion.

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12
Q

What is in the oral cavity?

A

Buccal mucosa, the tongue, gums and the roof and floor of the mouth.

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13
Q

What are the three taste buds in the mouth?

A

Circumvallate papillae; filiform papillae; fungiform papillae

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14
Q

Where are circumvallate papillae?

A

They are taste buds prominent in the walls of the surrounding ‘moats’. They form a V-shaped line demarcating the anterior 2/3rds and the posterior 1/3rd of the tongue. It detects bitter taste.

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15
Q

Where are the filiform papillae?

A

They are located in the anterior 2/3rds of the tongue, they aren’t taste buds.

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16
Q

Where are the fungiform papillae?

A

They are randomly scattered, mushroom-like shape. They taste sweet taste at the top of the tongue and salty taste is at the lateral sides.

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17
Q

What is the function of the mucosa in the mouth?

A

The mucosa is a physical barrier so acts as a defence mechanism.

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18
Q

What is the defence function of the salivary glands?

A

Salivary glands secrete saliva that washes away food particles, bacteria and viruses. They are surrounded by lymphatic systems, which are linked to the thoracic duct and blood vessels.

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19
Q

What is the defence function of the palatine tonsils?

A

They contain lymphocyte subsets and dendritic cells.

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20
Q

Where is saliva produced?

A

Unstimulated saliva is mainly from the submandibular glands. Stimulated saliva is mainly parotid secretion.

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21
Q

What is the function of saliva?

A

It is a lubricant for mastication, swallowing and speech. It acts as a bicarbonate/carbonate buffer for rapid neutralisation of acids so the pH is 7.2

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22
Q

What glands secrete saliva?

A

The serous glands secrete alpha amylase and the mucous glands secrete mucins for lubrication of mucosal surfaces. Most minor glands are mucous

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23
Q

What are the saliva flow statistics?

A

Daily secretion of 800-1500ml in adults. The pH ranges from 6.2-7.4. The flow rate is 0.3-7ml/minute

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24
Q

How do salivary glands transport electrolytes?

A

They are equipped with channels and transporters in the apical and basolateral membranes enabling transport of fluid and electrolytes.

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25
Q

What cells are salivary ducts made of?

A

They are composed of two types of epithelial tissues: acinar cells and ducts. These two form a large duct entering the mouth.

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26
Q

What are the two types of acinar cells?

A

There are serous and mucous acinar cells.

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27
Q

What are serous acinar cells?

A

They are small central ducts, that secrete water and alpha amylose. They are dark staining and have a nucleus in the basal third.

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28
Q

What are mucous acinar cells?

A

They are large central ducts that secrete mucous. They are pale staining and have the nucleus at the base of the cell.

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29
Q

What are the types of ducts in salivary glands?

A

There are interlobular ducts and a main excretory duct.

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30
Q

What are interlobular ducts split into?

A

They are intercalated and striated.

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31
Q

What are intercalated intralobular ducts?

A

They are short narrow duct segments with cuboidal cells that connect acini to larger striated ducts.

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32
Q

What are striated intralobular ducts?

A

They are the major site for reabsorption of NaCl. The basal membrane is highly folded into microvilli for active transport of HCO3- against the concentration gradient. They are filled with mitochondria.

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33
Q

What is primary saliva?

A

It is an NaCl rich isotonic plasma-like fluid secreted by acini cells.

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34
Q

What do the salivary ducts excrete?

A

They secrete K+ and HCO3- and reabsorb Na+ and Cl-. The epithelium of the duct doesn’t allow any water movement so the final saliva becomes hypotonic.

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35
Q

What is the predominant pathway for protein excretion from the salivary gland?

A

It is mucosal and leads to the saliva across the apical membrane.

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36
Q

What is the constitutive pathway for protein excretion from the salivary gland?

A

It is serousal and leads mainly towards the interstitium and the blood stream across the basolateral membrane

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37
Q

What is the first stage of swallowing?

A

It is voluntary. Food is compressed against the roof of the mouth and pushed towards the oropharynx by the tongue.

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38
Q

What is stage 2 of swallowing?

A

It is involuntary. The nasopharynx is closed off by the soft palate. The pharynx is shortened and widened by elevation of the hyoid bone.

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39
Q

What is the third stage of swallowing?

A

It is involuntary. It is sequential contraction of the constrictor muscles, followed by the return of the hyoid bone and the pharynx.

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40
Q

What are the problems with swallowing?

A

The gag reflex, choking, obstruction of the airway, impactation of food within the laryngopharynx.

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41
Q

What happens during the gag reflex?

A

There is reflex elevation of the pharynx, caused by irritation of the oropharynx. The reflex arc is between CN IX and X

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42
Q

How does choking happen?

A

Failure to co-ordinate swallowing actions.

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43
Q

What is the foregut?

A

It consists of the pharynx, oesophagus, stomach, the proximal half of the duodenum, liver, pancreas and biliary tract.

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44
Q

What artery supplies the foregut?

A

It is supplied by the celiac artery.

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45
Q

What is midgut?

A

It consists of the small intestine, caecum, vermiform appendix, ascending colon and the left 2/3rds of the transverse colon.

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46
Q

What supplied the midgut?

A

The superior mesenteric artery

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47
Q

What is the hindgut?

A

The right 1/3rd of the transverse colon, the descending colon, sigmoid colon, rectum and anal canal.

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48
Q

What is the hindgut supplied by?

A

The inferior mesenteric artery

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49
Q

What is screening?

A

A process which sorts out apparently well people who probably have a disease from those who probably don’t

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50
Q

What are the three types of disease prevention?

A

Primary, secondary and tertiary

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51
Q

What is primary prevention?

A

Prevention when there is no disease

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52
Q

What is secondary prevention?

A

Prevention when there are no symptoms

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53
Q

What is tertiary prevention?

A

Prevention when the patient already has a clinical disease

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54
Q

What is the definition of sensitivity?

A

The proportion of people with the disease who are correctly identified by screening.

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55
Q

What is specifity?

A

The proportion of people who don’t have the disease who are correctly excluded by screening.

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56
Q

What causes Barrett’s oesophagus?

A

It is caused by reflux of reflux gastric acid into the oesophagus

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57
Q

What happens when the patient has Barrett’s oesophagus?

A

Squamous epithelium undergoes metaplasia to become columnar epithelium (more suitable to the environment)

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58
Q

What is the role of pepsin?

A

It accelerates protein digestion. It accounts for approx 20% of protein digestion. It breaks down collagen in meat, which helps provide a larger SA for digestion

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59
Q

What is the function of the oesophagus?

A

It conveys food from mouth to the stomach

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60
Q

What epithelium is in the oesophagus?

A

Stratified squamous non-keratinised epithelium that can resist sheer stress

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61
Q

What is mucosa of the oesophagus?

A

It is made up of the lamina propria, muscularis propria, and muscularis mucosae.

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62
Q

What is the muscularis mucosae?

A

It is a thin layer of smooth muscle

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63
Q

What is the adventitia of the oesophagus?

A

It is a loose fibrous connective tissue.

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64
Q

Which part of the oesophagus is covered by peritoneum?

A

The intrabdominal 2-3cm of the oesophagus is covered by the peritoneum

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65
Q

What is gastric emptying?

A

When the capacity of the stomach is greater than the capacity of the duodenum

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66
Q

What does overfilling of the duodenum cause?

A

It causes dumping syndrome. The symptoms are D&V, cramping and bloating.

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67
Q

What does gastric emptying cause?

A

Gastroparesis. It is idiopathic. It causes nausea, GORD, vomiting and undigested food.

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68
Q

What regulates gastric emptying?

A

It is regulated by the same factors that regulate HCl production

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69
Q

How are proteases activation?

A

Chief cells secrete pepsinogen, which is converted into pepsin by the presence of HCl. Pepsin catalysed the breakdown of proteins into peptides.

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70
Q

What effects protease activation?

A

Pepsinogen to pepsin is pH dependant. It is most effective when pH is less than 2. Pepsin is only active at low pH.

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71
Q

Where is pepsin inactivated?

A

There is irreversible inactivation in the small intestine by HCO3-

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72
Q

What is the feedback mechanism of protease activation?

A

There is a positive feedback loop because pepsin also catalyses the reaction

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73
Q

What happens during protease secretion?

A

Chief cells produce pepsinogen. It is synthesised as a zymogen.

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74
Q

Why do chief cells produce pepsinogen not pepsin?

A

Because pepsin is active and pepsinogen isn’t.

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75
Q

What is a zymogen?

A

An inactive substance, which is converted to an enzyme when activated by another enzyme.

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76
Q

What regulates protease secretion?

A

The secretion parallels HCl secretion. It is activated by the stomach lumen. The pepsinogen secretion is mediated by input from the enteric nervous system (ACh)

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77
Q

What are the causes of peptic ulcers?

A

Helicobacter pylori, NSAIDs and bile salts.

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78
Q

How does helicobacter pylori?

A

It lives in the gastric mucus and secretes urease, which splits urea into CO2+ and ammonia. Ammonia and H+ makes ammonium, which secretes proteases and phospholipids that damage gastric epithelium, reducing mucosal defence

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79
Q

How does NSAIDs cause peptic ulcers?

A

It inhibits cyclo-oxygenase 1, which is needed for prostaglandin synthesis, which secretes mucus so there is reduced mucosal defence because you don’t make glucose.

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80
Q

How do bile salts cause peptic ulcers?

A

Bile salts cause duodeno-gastric reflux. Regurgitated bile strips away mucus layer, so there is reduced mucosal defence.

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81
Q

What is a peptic ulcer?

A

An ulcer is a breach in a mucosal surface (a gap in the epithelial cells) (the stomach digests itself)

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82
Q

When does a stomach ulcer occur?

A

If there is a increased mucosal attack or a reduced mucosal defence

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83
Q

What is the mucosal defence made up of?

A

It consists of: alkaline mucus; tight junctions between epithelial cells; replacement of damaged cells (stem cells from the bottom of the gastric loop) and negative feedback loops

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84
Q

What do parietal cells secrete?

A

Parietal cells actively transport H+ out of their cells, creating approx 2L of HCl/day. It also secretes K+ and Cl- into the stomach lumen through ion channels.

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85
Q

What do parietal cells absorb to secrete gastric acid?

A

They receive Cl- from the capillary. They actively absorb K+ from the stomach lumen.

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86
Q

How is the H+ needed for gastric acid replenished?

A

The H+ comes from hydrolysis in the cell. CO2 and H2O replenish the H+ and also the HCO3- excreted into the capillary

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87
Q

What organs regulate gastric acid secretion?

A

The brain, stomach and duodenum.

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88
Q

What neurotransmitter affects gastric acid secretion?

A

The parasympathetic neurotransmitter ACh activates secretion.

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89
Q

What hormone affects gastric acid secretion?

A

The hormone gastrin activates secretion

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90
Q

How do paracrine factors affect gastric acid secretion?

A

The paracrine factor histamine activates secretion and somatostatin inhibits secretion

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91
Q

How do enterogastrones affect gastric acid secretion?

A

The enterogastrones secretin inhibits secretion and CCK inhibits secretion

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92
Q

What makes up the muscularis externa of the stomach?

A

It is made up of 3 layers of smooth muscle: an outer longitudinal layer; a middle circular layer and an inner oblique layer of smooth muscle

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93
Q

What is the function of the cardia of the stomach?

A

It controls the entry of the bolts into the stomach and prevents reflux.

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94
Q

What cells make up the cardia of the stomach?

A

It has a non-specialised glandular mucosa.

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95
Q

What cells make up the fundus and body of the stomach?

A

They have straight glands, parietal cells and chief cells and APUD (secretes gastrin).

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96
Q

What cells make up the Antrum of the stomach?

A

It has straight mucous glands and no parietal cells.

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97
Q

What cells make up the pylorus of the stomach?

A

They have mucous glands. It is a prominent superficial zone.

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98
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 proteases in an inactive form; secrete intrinsic factors; activate proteases; lubrication; mucosal production

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99
Q

What are the key cell types in the stomach?

A

Parietal cells, chief cells, enteroendocrine cells and mucous cells on the surface of the gastric epithelium

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100
Q

What is qualitative research?

A

A methodological approach to research that emphasis words, exploration and interpretation rather than numbers.

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101
Q

What are the barriers preventing lots of qualitative research?

A

The dominance of clinical epidemiology and lack of method transparency

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102
Q

What is qualitative research used for?

A

To quantify the likelihood of participating; compare the characteristics of participants who participate or not

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103
Q

Where does the greater omentum hang down from?

A

The greater curvature of the stomach. The posterior layer also fuses with the mesentary of the transverse colon.

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104
Q

How does the spleen develop?

A

The spleen develops as a mesodermal proliferation in the left layer of stomach dorsal mesentary

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105
Q

What is the spleen attached to?

A

The spleen is attached to the posterior abdominal wall in the region of the left kidney by the lienorenal ligament and it is connected to the stomach by the gastrolienal ligament.

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106
Q

How if the lesser sac formed?

A

Longitudinal rotation of the stomach pulls the dorsal mesentery to the left, creating a space behind the stomach, which is the lesser sac. At the same time, the anterior mesentery is pulled to the right

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107
Q

Where is the dorsal mesentery?

A

It extends from the lower part of the oesophagus to the cloacal region.

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108
Q

Where is the ventral mesentery?

A

The ventral mesentary is present only in the region of the foregut. So the foregut is the only region of the gut that contains both ventral and dorsal mesentary.

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109
Q

What is the ventral mesentary derived from?

A

The septum transversum

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110
Q

What does the free lower margin of the ventral mesentary contain?

A

The hepatic artery, the portal vein and the bile duct.

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111
Q

Where does the liver develop from?

A

It develops in the free lower margin of the ventral mesentary. It divides it into the lesser omentum and the falciform ligament

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112
Q

How does the stomach rotate around the longitudinal axis whilst being an embryo?

A

The stomach rotates 90degrees around he axis so the left side is anterior and the right side is posterior, the nerves move simultaneously.

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113
Q

How do the lesser and greater curvature of the stomach form?

A

During rotation around the longitude like axis the left side grows faster than the right and gives rise to the greater and lesser curvatures.

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114
Q

What happens when the stomach rotates around the posterior axis?

A

The stomach rotates so it’s pyloric end moves right and upwards and it’s cardiac end moves to the left and downwards

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115
Q

When does the respiratory diverticulum (lung bud) develop in a foetus?

A

At 4 weeks the respiratory diverticulum appears at the beginning of the oesophagus.

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116
Q

What does the tracheoesophageal septum do?

A

It gradually develops and separates the diverticulum from the dorsal part of the foregut. The ventral part is the respiratory primordium.

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117
Q

What is an intraperitoneal organ?

A

An organ that is surrounded and connected to the body wall by mesentary.

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118
Q

What are ligaments?

A

Double layers of peritoneum that pass from an organ to another organ or to the body wall.

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119
Q

What are the functions of the mesentary and ligaments?

A

They provide a pathway for blood vessels, lymphatics and nerves to go to and from the abdominal viscera

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120
Q

How many pharyngeal pouches are there?

A

There are 4.

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121
Q

What weeks does the pharynx develop in?

A

It develops in week 4/5.

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122
Q

What are the pharyngeal arches made from?

A

They are formed of masses of mesenchymal tissue which are invaded by the cranial neural crest cells. Each arch is covered externally by ectoderm and internally by endoderm.

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123
Q

What are the pharyngeal pouches?

A

They are envaginations in the endoderm that lines the internal pharyngeal arches.

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124
Q

What are the pharyngeal clefts?

A

They appear on the external pharyngeal wall in the ectoderm of the pharyngeal arches.

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125
Q

What is the greater omentum?

A

It is part of the dorsal mesentery of the stomach, which is hanging down from its greater curvature.

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126
Q

What is the lesser omentum?

A

It is part of the ventral mesentary of the stomach, it is attached superiority to the liver and to the lesser curvature of the stomach inferiorly

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127
Q

What is the greater sac?

A

It is the part of the peritoneal cavity that you enter when you open the anterior abdominal wall and the parietal peritoneum

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128
Q

What is the lesser sac?

A

It is the part of the peritoneal cavity, which is trapped behind the stomach and the liver

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129
Q

What are the four categories of carbohydrates?

A

Free sugars (mono & disaccharides); short chain carbohydrates (oligosaccharides); starch; non-starch polysaccharides

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130
Q

What do buccinator and suprahyoid muscles do?

A

They manipulate food during chewing. They elevate the hyoid bone and flatten the floor of the mouth

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131
Q

What muscles are used in the first stage of swallowing?

A

The buccinator and suprahyoid muscles

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132
Q

What are the muscles of the palate used to do in swallowing?

A

They help to form the bolus of food and close off the nasopharynx during swallowing

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133
Q

What do the muscles of the floor of the mouth do during swallowing?

A

They lower the mandible if the hyoid bone is fixed. They raise the hyoid bone and larynx if the mandible is fixed

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134
Q

What muscles are used is the second phase of swallowing?

A

The muscles of the floor of the mouth

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135
Q

What does the infrahyoid muscle of the neck do?

A

If fixes the hyoid bone, enabling opening of the mouth. They draw down the hyoid bone and larynx.

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136
Q

What muscles are used in the third phase of swallowing?

A

The infrahyoid muscles

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137
Q

What are the pharyngeal constrictor muscles?

A

They are three overlapping muscles that form the posterior and lateral sides of the pharynx.

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138
Q

What innervates the pharyngeal constrictor muscles?

A

The pharyngeal plexus (CN X, XI)

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139
Q

What order do the pharyngeal constrictor muscles contract in?

A

They contract sequentially, from above down, to drive to bolus into the oesophagus during the third phase

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140
Q

What does the parasympathetic nervous system do to the gastric acid secretion?

A

It turns it on. Acetylcholine is released from the parasympathetic nerve ends in the stomach.

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141
Q

What activates parasympathetic nervous system of gastric acid secretion?

A

It is activated by sight, smell, taste of food and chewing.

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142
Q

What affect does acetylcholine have on gastric acid secretion?

A

It acts directly on parietal cells and stimulates proton cells. It triggers the release of gastrin and histamine, which both turn on parietal cells

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143
Q

What does gastrin do during gastric acid secretion?

A

It acts directly on the parietal cells and triggers the release of histamine

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144
Q

What does histamine do during gastric acid secretion?

A

It acts directly on the parietal cells but it also mediates the effects of gastrin and ACh

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145
Q

What do proteins in the stomach do?

A

They are a direct stimulus for gastrin release. They also act as a buffer, mopping up H+ ions, causing the pH to rise.

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146
Q

What does a rise in pH of the stomach cause?

A

It causes a decreased secretion of somatostatin

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147
Q

What does somatostatin do?

A

It turns off the stomach

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148
Q

What is a xenobiotic?

A

A foreign substance that is not meant to be in the body. They are absorbed either unintentionally as compounds pr sent in food and drink or deliberately as drugs for therapeutic purposes

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149
Q

What is an exogenous xenobiotics?

A

Ingested but not meant to be there like drugs and pollutants

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150
Q

What is an endogenous xenobiotics?

A

Things created in the body that aren’t meant to be there like urea

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151
Q

What is cytochrome P450?

A

It is an enzyme that catalyses phase 1 reactions in liver detoxification

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152
Q

What does phase 1 in liver detoxification do?

A

Adds or exposes functional groups to make the xenobiotics functional

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153
Q

What happens during phase 2 in liver detoxification?

A

It is conjugation with endogenous molecules

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154
Q

What is the aim of liver detoxification?

A

To make xenobiotics soluble so they can be excreted in the urea. They do this by making them polar so they are dissolved in water

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155
Q

Where is cytochrome P450 found?

A

In all of your body, but there is a high concentration of it in the liver

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156
Q

How much of iron ingested is anyone’s each day?

A

10%

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157
Q

How do you loose iron?

A

Urine, faeces, menstrual blood, sweat

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158
Q

Where is ingested ion actively transported to?

A

Intestinal epithelium cells

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159
Q

What is ferretin?

A

It is an iron complex that acts as an intracellular iron store

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160
Q

What happens to iron bound to ferretin?

A

It is either transferred to transferrin or it is excreted back into the intestinal lumen, where it is excreted as faeces

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161
Q

What happens to ferretin levels when there is an iron increase?

A

It increases the ferretin level, by activating the transcription factors, increasing the amount of iron stored

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162
Q

How is ferritin in the liver formed?

A

Iron from transferring is transported to the liver and combines with apoferritin to form ferritin

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163
Q

What happens if you have too much B12?

A

Your red blood cells swell and stop working

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164
Q

Deficiency of B12 causes what?

A

Pernitcious anaemia, when RBC don’t concave so they have smaller surface area

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165
Q

Is vitamin B12 water soluble?

A

Yes

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166
Q

What vitamins are water soluble?

A

B12

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167
Q

What vitamins are fat soluble?

A

A, D, E, K

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168
Q

Where is vitamin A stored?

A

In the stellate cells of the space of Disse in the liver

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169
Q

What does vitamin A do?

A

It regulates the contraction of the sinusoids because it is in the space of Disse

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170
Q

What does too much vitamin A cause?

A

Portal hypertension, liver cirrhosis

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171
Q

What happens during prenylation?

A

Adding of a hydrophilic groups to a protein

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172
Q

What is the function of the urea?

A

It turns ammonia into urea

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173
Q

How much of what acid does the stomach secrete everyday?

A

2L of HCl

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174
Q

What does a low luminal stomach pH do?

A

It inhibits gastrin secretion, which indirectly inhibits histamine release. It also stimulates somatostatin release, which inhibits parietal cell activity

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175
Q

What does duodenal distension do to parietal cells?

A

It turns them off

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176
Q

What causes a low luminal pH in the duodenum?

A

Hypertonic luminal contents, because of the presence of amino acids and fatty acids

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177
Q

What does a low duodenum luminal pH trigger?

A

The release of enterogastrones: secretin and cholecystokinin (CKK)

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178
Q

What are enterogastrones?

A

Hormones secretes by the mucosa of the duodenum in response to dietary lipids that inhibit the caudal motion of the contents

179
Q

What does secretin do?

A

Inhibits gastrin release and promotes somatostatin release

180
Q

What is the volume of the stomach?

A

An empty stomach has a volume of approx 50ml but when eating is can accommodate approx 1.5L

181
Q

What happens to the pressure when the volume of the stomach changes?

A

Nothing, there is relatively little change in luminal pressure

182
Q

Why is there little change in luminal pressure when the stomach volume increases?

A

Because the smooth muscle in the body and fundus undergoes receptive relaxation

183
Q

What mediates receptive relaxation?

A

It is mediated by the parasympathetic nervous system acting on enteric nerve plexus.

184
Q

Is there an afferent input to receptive relaxation?

A

Yes, it is via the vagus nerve so the brain knows what is happening in the stomach

185
Q

What do the enteric nerves release to mediate relaxation of the stomach?

A

Nitric oxide and serotonin

186
Q

What are the peristaltic waves like in the gastric body?

A

They begin here, there are weak contractions and there is little mixing

187
Q

How do the contractions in the stomach antrum compare with the gastric body?

A

They are more powerful in the gastric antrum

188
Q

When does the pylorus close?

A

As the peristaltic wave reaches it so the fluid moves back into the stomach body and is churned.

189
Q

Where are the pacemaker cells of the stomach?

A

In the muscularis propria.

190
Q

What is the rate of peristaltic waves?

A

It is at a constant rate of 3/minute

191
Q

How long are depolarisation repolarisation cycles in the stomach pacemaker cells?

A

Slow

192
Q

How are depolarisation waves transmitted between cells?

A

Through gap junctions to adjacent smooth muscle cells

193
Q

Are there peristaltic waves when the stomach in empty?

A

No, there is not significant contraction in an empty stomach because the stomach doesn’t have enough power to release a peristaltic wave

194
Q

What does gastrin do to receptors?

A

It makes the stomach more receptive to the signals so strengthens the contractions, as does gastric distension

195
Q

What mediates the gastric distension?

A

Mechanoreceptors

196
Q

What decreases the strength of stomach contraction?

A

Duodenal distension; an increase in duodenal luminal fat and osmolarity; a decrease in duodenal pH; increase in sympathetic innervation; decrease in parasympathetic innervation

197
Q

Does water move across the gastric mucosa?

A

Only a small amount of water moves across because of the high osmotic load of secretes HCl

198
Q

Does water move across the small intestine?

A

Yes, it moves freely according to the osmotic gradients and aquaporins (both solute driven)

199
Q

Does sodium move in or out of the ileum and jejunum lumen?

A

It is actively transported out of the lumen by pumps located in the membranes

200
Q

Does sodium move in or out of the colon lumen?

A

It is actively pumped into the lumen and water follows

201
Q

How is potassium moved across the membranes in the GI tract?

A

In general, it is by passive diffusion, so it is determined by the potential different between the lumen and the interstitial capillary

202
Q

Where is potassium movement greatest in the GI tract?

A

In the colon, then the ileum, then the jejunum

203
Q

Where is Chloride and Bicarbonate reabsorbed?

A

In the ileum and the colon

204
Q

What artery supplies the foregut?

A

The celiac artery

205
Q

What artery supplies the midgut?

A

The superior mesenteric artery

206
Q

Where do the celiac artery and superior mesenteric artery anastomose?

A

Around the entrance of the common bile duct

207
Q

What are the five stages of midgut formation?

A

(1) stage of elongation; (2) stage of physiological umbilical herniation; (3) stage of rotation (4) stage of refraction; (5) stage of fixation

208
Q

Name two oligosaccharides? The

A

Lactose and sucrose

209
Q

Name three monosaccharides

A

Glucose, fructose, and galactose

210
Q

Name two polysaccharides

A

Starch and glycogen

211
Q

Are D or L isomers utilised in metabolism?

A

D-isomers

212
Q

What is glycogen?

A

It is from animal sources. It is a polymer of glucose molecules joined by 1,4 alpha glycosidic links, with some chain branches at alpha 1,6 linkages

213
Q

What enzymes breaks down starch?

A

Alpha amylase in saliva

214
Q

What is the optimum pH for amylase and how does it affect where it works

A

The optimum pH is 6.7 so activity is terminated by gastric acidity

215
Q

What type of bonds does pancreatic alpha amylase catalyse?

A

Alpha 1,4 links but not alpha 1,6 branches, terminal alpha 1,4 linkages or ones next to branch parts

216
Q

What are the end products of carbohydrate digestion?

A

Maltose (disaccharide); maltotriose (trisaccharide); larger polymers with glucose of alpha 1,4 linkages and branched polymers

217
Q

Where are hextoses and pentoses absorbed?

A

Across the intestinal mucosa, they then enter the capillaries, which drain into the portal vein

218
Q

How does Na concentration affect glucose absorption?

A

They share the same transporter, so a high Na concentration at the mucosal facilitates glucose absorption.

219
Q

How is galactose absorbed?

A

It is a glucose isomer, it is transported from the lumen by the same channel as glucose.

220
Q

How does Na concentration affect fructose absorption?

A

It doesn’t. Fructose utilises a different carrier and it’s absorption is independent of luminal Na facilitated diffusion

221
Q

Where and how does protein digestion begin?

A

In the stomach, where pepsins cleave some of the peptide bonds

222
Q

What activates pepsins ?

A

They are secretes as pepsinogen sand are activated by the low luminal pH, which changes the tertiary structure.

223
Q

What are the two types of pepsinogen?

A

Pepsinogen 1 (only in HCl secreting region) and pepsinogen 2 (only in the pyloric region)

224
Q

What do pepsins do?

A

They hydrolyse bonds between aromatic amino acids, such as tyrosine or phenylamine and a second amino acid. They products are peptides

225
Q

What is the optimum pH for pepsins and how does it affect where it works?

A

The optimum pH is 1.6-3.2 therefore action is terminated on exit from the stomach.

226
Q

Where are small peptides broken down and what by?

A

They are broken down in the small intestine by proteolytic enzymes of the pancreas

227
Q

What are the different types of proteolytic enzymes of the pancreas?

A

Endopeptidases and exopeptidases

228
Q

Where are di and tripeptides absorbed and what by?

A

They are absorbed and finally broken down by intracellular peptidases so the final digestion of peptides occurs in the lumen, the brush border or within the cell

229
Q

What is linked to di and tripeptides transportation?

A

Na+. It is facilitated by an increase in luminal Na+ concentration

230
Q

How do amino acids move into the portal blood?

A

By passive diffusion

231
Q

Where does protein in the stools come from?

A

Only 2-5% is from the small intestine, most is found there due to bacteria and cellular debris from the colon

232
Q

Where does far digestion begin and with what?

A

It begins in the duodenum with pancreatic lipase

233
Q

What does pancreatic lipase do?

A

It hydrolyses the bonds of the triglycerides. The 1&3 bonds are easier than the second bond.

234
Q

What protein does lipase need to bind to to work?

A

Lipase only works on emulsified fats and cannot work without the protein co-lipase

235
Q

What does co-lipase do?

A

It binds to the surface of the fat droplet, displacing the emulsified agents and anchoring the lipase.

236
Q

What is the most common form of cholesterol and how is it broken down?

A

Most of the dietary cholesterol is in the form of cholesterol esters and pancreatic esterase hydrolyses these in the lumen

237
Q

Where are fats emulsified?

A

In the small intestine, by the detergent action of bile salts and monoglycerides, producing particles of between 200-500nm in size

238
Q

What are micelles formed from

A

Lipids and bile salts, they generally contain free fatty acids, monoglycerides and cholesterol

239
Q

What does micellar formation do?

A

It further solubilises the lipids and provides a mechanism for their transport to the brush border by diffusion

240
Q

How do lipids enter the cells?

A

By passive diffusion, they are rapidly esterified, maintaining the concentration gradient for diffusion

241
Q

What is vitamin A used for?

A

Cellular growth and differentiation; process of vision; reproduction; embryonic development; maintenance of mucous membranes; production of lymphocytes

242
Q

What is vitamin A found in?

A

Dairy products, livers, oily fish, margarine. 70% of UK intake is from pre-formed vitamin A

243
Q

What does vitamin C do?

A

It aids with the synthesis of collagen, neurotransmitters and carnitine

244
Q

What does vitamin C have an antioxidant ability?

A

Because it can donate electrons to radical O2 compounds

245
Q

How does vitamin C help absorb non-haem (plant-based) iron?

A

In the intestine is prevents the formation of insoluble ferric hydroxide. Patients with wounds and needs need a lot of it

246
Q

Where is vitamin C found?

A

In citrus fruits and green leafy vegetables. Potatoes are a very important source in the UK. Kidney os the only animal source

247
Q

How does vitamins C’s solubility affect it?

A

It means it is easily lost when it is boiled

248
Q

What are the signs of vitamin C deficiency?

A

Bleeding gums (hyperkeratosis); a decrease in skeletal strength; long term deficiency causes scurvy

249
Q

Are B vitamins water or fat soluble?

A

They are 8 water soluble vitamins

250
Q

What are B vitamins important for?

A

They are important in cell metabolism and energy production. They have distinct roles but act synergistically

251
Q

Where are B vitamins stored in the body?

A

Body storage is often limited because they have low stability .

252
Q

Is the risk of toxicity higher in water soluble or fat soluble vitamins?

A

Water soluble vitamins

253
Q

What is a macronutrients?

A

A complex energy source that we take in as food. Usually fats, proteins and carbohydrates

254
Q

What is BMR?

A

A measure of the total amount of energy produced by unit time. It is roughly equivalent to ATP usage, which is produced as required.

255
Q

Which organs require the most energy at rest?

A

The brain and liver require approx 40% of body energy at rest

256
Q

How is BMR measured?

A

By O2 consumption in a person who is awake, restful and fasted for 12 hours.

257
Q

What are the units of BMR?

A

Kcal/hr/m2 of body surface

258
Q

Are starches soluble or insoluble?

A

They are mainly found as insoluble granules. Cooking in moist heat denatures the granules so that they unfold and absorb water and become soluble. On cooling they return to their natural state

259
Q

What are starches clinically used for?

A

Either as polymers or partially digested starch molecules for external feeding of patients who are unable to take food orally

260
Q

What causes lactose intolerance?

A

Deficiency of the enzyme lactase. It can be acquired or congenital.

261
Q

How does lactose intolerance affect the body?

A

It affects the osmotic effect, which means that large amounts of water and ferment able sugar enters the large intestine

262
Q

What is the main element in protein?

A

Nitrogen. Nitrogen metabolism is often synonymous with protein metabolism

263
Q

How many amino acids are essential?

A

Out of the 20 amino acids 8/9 are essential

264
Q

What does the liver do to amino acids, triglycerides and glucose?

A

These molecules are transported to the liver for the conversion to storage molecules, they are the transported to the special storage areas

265
Q

Where is fat stored?

A

Adipose tissue

266
Q

Where is glycogen stored?

A

In muscle

267
Q

Why is leptin and what does it do?

A

It is a hormone that keeps the appetite centres in the brain informed about the nutritional state of the individual

268
Q

Where does the liver receive blood from?

A

25% of the blood supply to the liver is arterial blood from the hepatic artery (oxygenated) 75% of the blood entering the liver is venous blood from the hepatic portal vein (deoxygenated)

269
Q

Why does blood go to the liver before the heart?

A

The intestine contains lots of viruses so the liver filters it before it goes to the heart

270
Q

Where do the hepatic portal vein and hepatic artery empty?

A

The terminal branches empty together in sinusoids surrounding the hepatic cells.

271
Q

How does the blood leave the liver?

A

Via the hepatic veins, which end in the inferior vena cava. This blood is deoxygenated, detoxified, and containing normal nutrient levels

272
Q

What is a liver lobule?

A

The liver is divided into thousands of small units called lobules by thin layers of connective tissue. It is composed of radiating double plates of hepatocytes, separated by a vascular sinosoidal network

273
Q

What is the size and shape of a liver lobule?

A

Each lobule is about 1mm in diameter and is roughly hexagonal in shape

274
Q

What vessels are in each liver lobule?

A

Each lobule has a central vein in the middle and a portal triad at each vertices.

275
Q

What does a portal triad consist of?

A

A branch of the hepatic artery, the portal vein and the common bile duct.

276
Q

What are sinusoids made up of?

A

They have an incomplete lining of highly fenestrated endothelial cells, some of these cells are macrophagic (Kupffer cells)

277
Q

What is the space of Disse?

A

The space between the endothelium and hepatocytes.

278
Q

How is lymph collected in the liver?

A

It is collected and delivered to the lymphatic capillaries in the space of Disse. Lymph is collected in the hepatic duct outside the liver.

279
Q

How is blood drained out of the liver?

A

Blood from the branches of the hepatic artery and portal vein in the portal triad, drains into sinusoids and then to the central vein, which goes to the hepatic veins, which end in the inferior vena cava

280
Q

Where does bile formed by the liver cells go?

A

It is discharged into the bile canaliculi within the layers of the cell plates and the drains into bile ducts of the triads

281
Q

What causes negative nitrogen balance?

A

Malnutrition, head injuries and multiple trauma

282
Q

What are the two types of malnutrition?

A

Marasmus (insufficient calorie intake) and kwashiorkor (insufficient protein intake but adequate calorie intake)

283
Q

What is a cause of positive nitrogen balance?

A

Pregnancy because pregnant women need more nitrogen

284
Q

What is the main input of nitrogen?

A

Amino acids in protein

285
Q

What is the most common output of nitrogen?

A

The NH3 molecule, which is toxic so most species convert it to a non-toxic excretory product

286
Q

What are lipids?

A

Esters of fatty acids

287
Q

How are triacylglycerides and fatty acids transported in the body?

A

By attaching to albumin

288
Q

Where are lipids stored?

A

Stored anywhere in the body

289
Q

Can fatty acids diffuse through the phospholipid bilayer of the cell?

A

Yes, through a channel protein using facilitated diffusion, not through the actual bilayer because they’re too big

290
Q

What are the transported systems of lipids?

A

They cannot be transported as lipids, they are broken down into fatty acids and glycerol by lipase

291
Q

What is the catabolism of lipids?

A

Oxidation of fatty acids to supply energy for bodily functions

292
Q

What is anabolism of lipids?

A

Synthesis of cholesterol and fatty acids or synthesis of fat from proteins and carbohydrates

293
Q

Where is insulin stored?

A

It fat storage in adipocyte

294
Q

What does insulin do?

A

Stimulates lipoprotein lipase, which breaks down the triglycerides in lipoproteins to store fatty acids in triglyceride in adipocytes

295
Q

How does insulin get to the liver?

A

It travels in the blood

296
Q

Why are fatty acids brought into the cell?

A

To be broken down into acetyl coA in the mitochondria

297
Q

What do chylomicrons do?

A

They carry lipids from the gut to muscle (used) and adipose tissue (stored)

298
Q

Where does lipid breakdown start?

A

In the stomach by lingual lipase or gastric lipase

299
Q

What do lipoproteins do?

A

Carry lipids

300
Q

What is bile salt?

A

Amphiphilic steroid (hydrophobic)

301
Q

What do bile salts do?

A

Emulsify ingested fat

302
Q

What is a micelles?

A

A lipid cell with lots of bile salts around it. It increases the surface area of the fat so lipase can break it down quicker. The bile salts bind to stop the little bits of fat joining together again and also make it soluble

303
Q

What stimulates bile salt production?

A

CCK, it stimulates the gallbladder to release bile salts so the lipids are emulsified

304
Q

What are the interstitial cells of cajal?

A

Pacemaker cells of the gut

305
Q

Where is the pancreas?

A

It is retroperitoneally across the posterior abdominal wall. It sits behind the stomach across the back of the abdomen

306
Q

Where does the head of the pancreas lie?

A

The head is disc-shaped and lies within the concavity of the duodenum.

307
Q

What is the uncinate process of the pancreas?

A

It is part of the head that extends to the left behind the superior mesenteric vessels.

308
Q

Where does the pancreas develop from?

A

The endodermal lining of the duodenum as a dorsal and ventral buds

309
Q

What is the main pancreatic duct formed from?

A

It is formed from the Union of the ventral pancreatic duct with the distal part of the duct of dorsal bud.

310
Q

What enters the ampulla of Vater?

A

The main pancreatic duct and the common bile duct

311
Q

Where is the ampulla of Vater?

A

It enters the posteromedial wall of the duodenum at the site of the major papilla

312
Q

What are the islets of langerhans develop from?

A

The paraenchyma of the pancreas

313
Q

What do microsomal enzymes do?

A

They do the majority of drug biotransformation reactions as well as doing oxidative, reductive and hydrolytic and glucoronidation.

314
Q

Where are microsomal enzymes?

A

They are in the smooth endoplasmic reticulum. They are made in the liver then transported to the kidney, lungs and intestinal mucosa

315
Q

What are non-microsomal enzymes?

A

They are non-specific enzymes and hat catalyse few oxidative, a number of reductive and hydrolytic reactions and also conjugation reactions other than glucunonidation

316
Q

What happens during phase 1 in biotransformation reactions?

A

Functional groups are added or exposed that has a small increase in hydrophilicity

317
Q

What happens during phase 2 of biotransformation reactions?

A

They are conjugated with endogenous molecules which causes a large increase in hydrophilicity

318
Q

Where does iron metabolism take place?

A

In the liver

319
Q

What vitamins are stored in the liver?

A

Vitamins A/D/B12

320
Q

What is dietary iron taken up by?

A

Transferring in the plasma in the duodenum. It is then used or stored

321
Q

Where is iron used in the body?

A

By myoglobin in the muscle or haemoglobin in erythrocytes in the Bon marrow

322
Q

Where is dietary iron stored?

A

In the liver parenchyma

323
Q

How is iron absorbed into the duodenum epithelial cell?

A

It either binds to heme and moves through a heme transporter or is reduced to Fe2+ by duodenal cytochrome B so it can pass though the DMT1 transporter.

324
Q

How is iron transferred into the blood from the duodenal epithelium cell.

A

It moves through a ferroportin 1 channel either directly or indirectly (by binding to mucosal ferritin)

325
Q

What happens to an iron molecule once it passes through the ferroportin 1 channel in the blood?

A

It is oxidised into Fe3+ by cytochrome B so it can bind to transferrin

326
Q

What does hepcidin do?

A

It binds to the ferroportin 1 transporter so iron cannot be transported out of the intestinal lumen or the hepatocytes so it can’t bind to transferrin in the plasma

327
Q

What regulates hepcidin levels?

A

Transferrin receptor 2 creates and therefore regulates hepcidin production

328
Q

How does iron get transported into cells that need to use it?

A

Transferrin receptors 1 & 2 transport iron from the transferrin into the cell

329
Q

Where are R-proteins produced and what do they do?

A

They are produced by the stomach and salivary glands. They bind to dietary B12 to protect it from the effects of HCl exposure in the stomach

330
Q

What releases vitamin B12 from the R-protein?

A

Pancreatic protease a

331
Q

Where is intrinsic factor produced and what does it do?

A

It is produced in the parietal cells of the stomach. It binds to vitamin B12 for it to be absorbed in the ileum.

332
Q

What is vitamin B12 needed for?

A

It increases the levels of methylation reaction. It is needed to produce H4 folate, which is the only folate that can synthesise nucleic acid so it increases nucleic acid synthesis

333
Q

What is protein turnover?

A

The continuous degradation and re-synthesis of all cellular proteins

334
Q

What is the ratio of liberated amino acids used to the ones excreted?

A

70-80% of liberated amino acids are re-utilised into proteins and 20-25% and turn d into urea for excretion

335
Q

Where are high rates of protein turnover?

A

Organs that are undergoing high rates of structural rearrangement

336
Q

What are the two types of protein degradation?

A

Lysosomal and non-lysosomal

337
Q

What cells are used in lysosomal degradation?

A

The sinusoidal endothelial cells, kuppfer cells and pit cells

338
Q

Where does lysosomal degradation take place?

A

In the reticulo-endothelial system of the liver

339
Q

What do sinusoidal endothelial cells do?

A

They remove soluble proteins and fragments through the fenestrations on their luminal surface. They remove fibrin and fibrin degradation products, collagen and IgG complexes

340
Q

What do Kuppfer cells do?

A

They are the liver resident macrophages and perform a phagocytose particulate matter

341
Q

What are pest sequences?

A

Target proteins for degradation. They are hydrophilic regions containing either proline, glutamic acid, serine or threonine.

342
Q

What does ubiquitin mediate?

A

Non-lysosomal degradation

343
Q

How does ubiquitin mediate non-lysosomal degradation?

A

It is convalently linked to a protein slated for destruction via a 3 stage ATP dependant enzymatic pathway. This attachment triggers other ubiquitinations.

344
Q

What do proteosomes do?

A

They bind to polyubiquitin protein, unfold them and then digest them hydrolytically

345
Q

Where are amino acids stored?

A

Trick question! They’re not! They are either used in proteins straight away or are excreted

346
Q

What is the most common reason for phosphorylation of proteins?

A

As a mechanism to regulate the biological activity of a protein (they are usually reversible)

347
Q

How does phosphorylation affect glucose synthase and glucose phosphorylase?

A

It inhibits the activity of glucose synthase but activates the activity of glucose phosphorylase

348
Q

What stimulates phosporylation of glucose synthase and phosphorylase and what is the effect?

A

They are stimulaed by glucagon release from the pancrease. They can cause increased hepatic glucose to the blood

349
Q

What do kinases do?

A

They phosphorylate proteins

350
Q

What are the enzymes that remove phosphate groups called?

A

Phosphatases

351
Q

Why is the break down and synthesis of proteins from amino acids reversible?

A

So that the proteins can circulate free amino acids in a continuous cycle of synthesis of breakdown

352
Q

What are excess amino acids metabolised into?

A

NH4+ and alpha-keto acids

353
Q

What are alpha keto acids used for?

A

They are fed into the Kreb’s cycle to be incorporated into glucose production

354
Q

What happens to ammonia produced by amino acid metabolism?

A

Most of it is excreted, but some is used in the biosynthesis of amine containing substances

355
Q

What is the main input of amine groups into the liver?

A

It is from dietary amino acids

356
Q

What are serum levels of aminotransferase clinically used for?

A

Indicators of liver cell damage because these enzymes are used in the hepatocytes so high levels indicate hepatocyte leakage

357
Q

What is the glutamate dehydrogenase reaction?

A

It a reversible reaction. The forward reaction uses NAD and ADP/GDP to generate alpha-ketoglutarate. The backwards reaction forms glutamate.

358
Q

What is the alpha ketoglutarate formed by the glutamate dehydrogenase reaction used for?

A

It is fed into the Kreb’s cycle to produce ATP so hepatocytes are capable of increasing ATP production at time of energy depletion.

359
Q

What drives the glutamate dehydrogenase reaction?

A

ADP/GDP drive the reaction forward because they represent low “energy”/ATP levels

360
Q

What is glutamate used for?

A

It is an amino acid that is available for incorporation into a protein

361
Q

What is the glutamine synthesase reaction?

A

A reaction which produces glutamine, which is an amino acid that can incorporated into a protein

362
Q

What is the function of glutamine?

A

It’s main function is to be a circulating ammonia carrier. In this state it is a neutral, non-toxic compound which passes readily through cell membranes

363
Q

What is the most common amino acid in the blood?

A

glutamine

364
Q

What is the function of glutaminase?

A

It breaks down glutamine in the mitochondria so the nitrogen is released.

365
Q

What is the difference in locations between glutamine synthetase and glutaminase?

A

Glutamine synthetase is a cytosolic enzyme and glutaminase is a mitochondrial enzyme, which ensures that the liver is neither a net consumer or producer of glutamine.

366
Q

What is the principal transporter and scavenger of ammonia in muscle?

A

Alanine

367
Q

How does the glutamate alanine cycle work?

A

Glutamate picks up ammonia. The enzyme alanine aminotransferase then forms alpha-ketoglutarate and the amino acid gets attached to pyruvate making alanine, which gets transported in the blood to the liver, where urea is produced and pyruvate is released

368
Q

What is our source of arginine and what is it broken down into?

A

Arginine is either from our diet or protein breakdown. It is cleave by arginase into urea and ornithine.

369
Q

How is citrulline formed?

A

A new urea is built from ammonia and CO2 on the ornithine. It is reconfigured into arginine using enzymes in the cytosol and mitochondria.

370
Q

What are used in the urea cycle?

A

There is a net consumption of 3 ATP and 4 high energy nucleotide PO4. Urea is the only component generated by the cycle, the others are all recycled.

371
Q

What provides the energy for the urea cycle?

A

The production of the cycle intermediates.

372
Q

What regulate the urea cycle?

A

The regulation of the enzymes resposible for urea production

373
Q

What causes an increase in the rate of the urea cycle?

A

Increased intake of protein. Long periods of starvation because protein is used as an energy source

374
Q

What causes a rise in ammonia levels?

A

The blood doesn’t get exposed to enough liver parenchymal cells to have the ammonia removed. It is a sign of sever liver failure.

375
Q

What is the effect of raised ammonia levels?

A

It crosses the blood brain barrier. Once inside it produces glutamate throught the glutamate dehydrogenase reaction so there is less alpha-ketoglutarate so the Kreb’s cycle happens less.

376
Q

What is albumin?

A

It is a highly negatively charged, highly soluble single polypeptide protein.

377
Q

What controls the rate of albumin production?

A

Changes in colloid osmotic pressure and osmolality of the extravascular liver space. Production can be increased by 2 to 3 fold when necessary

378
Q

How does albumin enter and leave the circulation?

A

It leaves via the interstitium to the lymph system and back into the circulation via the thoracic duct.

379
Q

What is the Transcapillart Escape rate?

A

The rate of albumin extravasates (how quick it leaves the circulation) per hour

380
Q

What determines the Transcapillary escape rate?

A

(1) the capillary and interstitial free albumin concentration; (2) the capillary permeability to albumin; (3) the movement of solute/solvent; (4) electrical charges across the capillary wall

381
Q

How many binding sites does an albumin molcule have?

A

It is important for binding and transport. It has 4 binding sites and competitive binding at one site could cause a conformational change in another one

382
Q

Does albumin control colloid osmotic pressure?

A

Yes, it maintains the effective osmotic pressure across blood vessel walls

383
Q

How does albumin affect radicals?

A

It has a large number of sulphydryl groups which can scavange free radicals, which is important in sepsis.

384
Q

How does albumin affect coagulation?

A

It has anticoagulant and antithrombotic effects

385
Q

What are the causes of a decrease in albumin?

A

Liver disease, large resections or renal failure, heammorrage or exudative loss, it burns through damaged capillary walls

386
Q

What are the consequences of an albumin decrease?

A

Decreased colloid osmotic pressure and oedema formation. Decreased ligand binding and hormone transport

387
Q

What is the metabolic role of the liver?

A

It maintains a continuous supple of energy for the body by controlling the metabolism of CHO and fats.

388
Q

What regulates the liver?

A

Endocrine glands (pancreas, adrenal and thyroid) and nerves

389
Q
A
390
Q

What are lipids?

A

Esters of fatty acids and certain alcohol compounds (glycerol) and other compounds (cholesterol). They are insoluble in water

391
Q

What are the properties of saturated fatty acids?

A

They line up close together and are their esters are solid at room temperature (fats)

392
Q

What are the properties of unsaturated fatty acids?

A

They need more space and are less tightly packed. Their esters are liquid at room temperature (oils)

393
Q

What are triacylglycerides?

A

A single glycerol molecule esterified to 3 fatty acids. They are stored as fat in adipocytes, hepatocytes and elsewhere

394
Q

What are lipids used in?

A

Cell membranes; inflammatory cascades; cholesterol (sex hormones); vitamin D

395
Q

How are lipids transported?

A

As triacylglycerides or fatty acids bound to albumin or within lipoproteins.

396
Q

How do lipids cross the cell membrane?

A

Triacylglycerides cannot diffuse through cell membranes so lipases releases the fatty acids to facilitate transport into the cells, where they are re-esterified to triacylglycerides

397
Q

What does insulin do?

A

It helps with fat storage in adipocytes. It stimulates lipoprotein lipase, which breaks down triglycerides in lipoproteins to store fatty acids

398
Q

How does insulin affect hormone sensitive lipase in adipocytes?

A

It reduces the activity of hormone sensitive lipase, leading to reduced fatty acids export from adipocytes

399
Q

What does insulin resistance do?

A

Increases lipolysis in adipocytes -> increased number of fatty acids in circulation and therefore hepatocytes-> increase uptake of fatty acids -> increased glucose levels -> less demand for lipids as an energy source

400
Q

What is de novo lipogenesis?

A

The enzyme pathway for converting dietary carbohydrate into fat. It is dependant on insulin concentration and sensitivity

401
Q

What is the function of the hepatic de novo lipogenesis?

A

It is primarily for export in lipoproteins, which are used as an energy source and as a structural components for membranes.

402
Q

What affects de novo lipogenesis?

A

HIgh levels of carbohydrate increases it. Fasting and fat feeding inibits it.

403
Q

What is a lipoprotein made of?

A

It consists of a core containing triglycerides and cholesterol esters and a surface monolayer of phospholipids, cholesterol and apoproteins

404
Q

What are apoproteins?

A

Specific proteins

405
Q

What is the ratio of proteins to lipids in lipoproteins?

A

It varies. They are defined by their density (HDL, LDL, VLDL and chylomicrons)

406
Q

What is the function of chylomicrons?

A

They carry lipids from the gut to muscle and adipose tissue.

407
Q

How are chylomicrons taken up by and what organ are they taken up into?

A

They are taken up by the liver via receptor mediated endocytosis

408
Q

Why are chylomicrons easily absorbed?

A

Because of their recognition of ApoE by hepatocyte surface receptors

409
Q

How and where is cholesterol processed?

A

It is esterified intracellularly by Acyl CoA, cholesterol acyltransferase (in lipoproteins) or by lecithin. The liver is where most cholesterol is processed

410
Q

How are cholesterol molecules transported in the blood?

A

Lipoproteins carry both tryglycerides andcholesterol through the circulatory system

411
Q

How is cholesterol excreted?

A

Through bile

412
Q

How does ApoB used in fatty acid transport to the golgi apparatus?

A

Apoprotein B is synthesised in the RER. Lipid compouns (triglycerides and cholesterol) are synthesis in the smooth ER. They are added together by triacylglycerides transfer proteins. This is transported in a vesicle to the golgi apparatus, where ApoB is glycosylated.

413
Q

What happens to the fatty acid-ApoB complex in the golgi apparatus?

A

The glycosylated ApoB with lipid component buds off the golgi apparatus and migrate through the sinusoidal membrane of the hepatocytes. The vesicles fuse with the membranes and the VLDL is released

414
Q

How does peripheral fatty acid metabolism affect glucagon and insulin?

A

It decreases glucagon levels and increases insulin levels

415
Q

What are the three types of fatty acid oxidation in the liver?

A

There is beta oxidation in the mitochondria and peroxisomes and gamma oxidation in the endoplasmic reticulum.

416
Q

Where is bile created?

A

It is secreted by hepatocytes, but is relatively dilute so it is stored and concentrated in the gall bladder

417
Q

What is the function of bile?

A

It’s function in fat absorption is as an emulsifier, this is due to the anionic detergent properties of the bile acids, which constitute about 50% of the dissolved constituents

418
Q

How does bile enter the gall bladder?

A

It receives bile through the cystic duct from the common hepatic duct, which is formed from the left and right hepatic ducts from their respective sides of the liver.

419
Q

How is bile expelled from the gall bladder?

A

CKK causes the gall bladder to contract. Expulsion occurs throught the cystic duct, when the bile travels down the common bile duct and exits via the ampulla

420
Q

What is the blood supply of the gall bladder?

A

It is supplied by the cystic artery but it has no venous drainage, the blood drains from the gallbladder directly into the liver with no identifiable pathway

421
Q

What do hepatic sinusoids contain?

A

It contains mixed portal vein/ hepatic artery blood as opposed to having a discrete arterial/venous blood supply.

422
Q

What is the blood supply of the liver?

A

75% of the blood comes from the portal vein and only 25% of the blood comes from the hepatic artery.

423
Q

How does the sinusoid blood leave the liver?

A

It flows towards the centre of the lobule and exits via the centrolobular vein.

424
Q

What is the structure of hepatic sinusoids?

A

They are lined with a continuous layer of specialised cells, interspersed with Kuppfer cells. On the undersurface there are stellate cells

425
Q

What do stellate cells do?

A

They are responsible for producing the extra-cellular matrix in the space of Disse.

426
Q

Where are the bile canaliculi?

A

They are between adjacent hepatocytes. They don’t have specialised walls but they are like a groove running along the side of the hepatocyte. They are bound together by tight junctions, gap junctions and desmosomes.

427
Q

How does bile get transported into the bile canaliculi?

A

Actin filaments are found in the areas around the canaliculi and ‘pump’ the formed bile towards the ducts. Transport into the canaliculus is via specialised export pumps or transporters

428
Q

Where are bile salts produced and what from?

A

They are produced in the liver from cholesterol, but they are re-circulated from the gut

429
Q

How are bile salts and toxins absorbed into the liver?

A

Via the portal vein. They are usually conjugated to amino acids

430
Q

What are micelles formed from?

A

Secondary bile acids (produced by gut bacteria), lecithin and cholesterol. They are aggregated together in soluble units making the mixed micelle. They maintain this aggregation in the gall bladder even in concentrated bile

431
Q

Why are bile salts turned into micelles?

A

Because they are powerful emulsifying agents, which is good for their function but can damage cell membranes, so the micelle reduces the actions until it is appropriate.

432
Q

Is the sphincter of Oddi open or closed during the inter-digestive period?

A

It is closed to faciliatate the entry of bile into the gallbladder

433
Q

What is adaptive relaxation?

A

When the size of the organ increases but the pressure within it doesn’t

434
Q

Why does the gall bladder exhibit adaptive relaxation?

A

Because the whole system is a low pressure, low flow system

435
Q

Is the sphincter of Oddi open or closed after a meal?

A

When food enter the duodenum CKK is released, causing the gallbladder to contract and the sphincter of Oddi to open so bile flow into the duodenum.

436
Q

Where are bile salts reabsorbed?

A

They start to be reabsorbed in the jejunum but the greatest amount being reabsorbed in the terminal ileum

437
Q

What is bilirubin?

A

It is the heam-breakdown pigment responsible for the colour of bile

438
Q

How is bilirubin reduced to urobilinogen?

A

Being fairly water soluble, it is conjugated to glucuronic acid and excreted in the bile. In the interstine, bacterial action can reduce this to urobilinogen

439
Q

What happens to urobilinogen?

A

Most of it passes in the faeces, but some is reabsorbed into the portal circulation and either recycled into the bile or filtered by the kidneys and passed into the urine

440
Q

What is the blood supply of the duodenum?

A

Foregut part: superior pancreaticoduodenal artery

Midgut part: inferior pancreaticoduodenal artery

441
Q

What is segementation and where is it?

A

Stationary contraction and relaxation of the small intestinal segements. Mixes the chyme and allows it to come into contact with the intestinal wall.

Only in the small intestine

442
Q

What is the main function of the large intestine? How does it achieve this?

A

To store and concentrate faeces by absorbing water. Active transport of sodium out of the lumen so that water follows

443
Q

What does hypertonic mean?

A

Having a higher osmotic pressure than a particular fluid, typically an intracellular fluid

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