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1b. GASTROINTESTINAL > Gastrointestinal Science > Flashcards

Gastrointestinal Science Flashcards

1
Q

Name the two directions of food movement in the GI tract.

A

Aboral (oral to anal) and oral (anal to oral)

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2
Q

Name the organs of the alimentary tract and the accessory GI organs.

A

Tongue, pharynx, oesophagus, stomach, liver, gall bladder, pancreas, duodenum, jejunum, ileum, caecum, colon, appendix, rectum, anus, salivary glands, biliary tree

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3
Q

What is the purpose of the mouth and oropharynx?

A

Chops and lubricates food, and begins digestion of carbohydrates

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4
Q

What are the two main purposes of the stomach?

A

Physical and chemical digestion

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5
Q

Describe the makeup of the small intestine.

A

Duodenum, jejunum, ileum. Connects by the caecum

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6
Q

Describe the makeup of the large intestine.

A

Connects by caecum. Then appendix, colon

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7
Q

Name the two components of the rectum and describe the purpose of the rectum and anus.

A

Sigmoid and descending.

Regulates expulsion of faeces

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8
Q

What are the accessory structures of the GI tract?

A

Liver, gallbladder, salivary glands, pancreas

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9
Q

Name the histological layers of the GI tract.

A

Mucosa (epithelium (NOT endo), lamina propria), submucosa, muscularis externa (circular and longitudinal muscle)

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10
Q

Name the two nerve plexuses of the GI tract. Where are they located?

A

Submucous (submucosal), myenteric (muscularis externa)

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11
Q

What are the four functions of the GI tract?

A

Motility (movement), secretion, digestion, absorption

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12
Q

Describe the muscle makeup of the alimentary tract.

A

Smooth muscle except at the extreme ends of the tract (oral and anal) where it is skeletal

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13
Q

Describe how muscle in the GI tract allows motility.

A

By circular muscle (makes lumen longer/narrower), longitudinal (shorter/fatter), very outer musclaris externa (change in absorptive area, mixing)

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14
Q

What is the name of food when it reaches the duodenum?

A

Chyme

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15
Q

What is the name of the pacemaker cells of the alimentary canal?

A

Interstital cells of Cajal

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16
Q

Which cellular component allows spread of action potential in the gut?

A

Gap junctions

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17
Q

Describe how an action potential is created in the gut.

A

‘Slow waves’ are constantly being created by pacemaker cells. When they reach above the membrane potential threshold they fire calcium APs

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18
Q

Describe the effect of prolonged firing of APs.

A

Greater force, which means greater muscle tension

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19
Q

Which stimuli increase the ‘resting potential’ of ICC action potentials, making it more likely for the threshold to be reached?

A

Neuronal, hormonal, mechanical

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20
Q

Describe the parasympathetic supply of the gut.

A

Vagus nerve, and sacral nerves S2 - S4

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21
Q

Describe the effects of parasympathetic and sympathetic supply to the alimentary tract.

A

Parasympathetic - increases digestion/secretion, relaxes sphincters/stomach.
Sympathetic - increases sphincter tone, decreases blood flow/secretion

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22
Q

What are the main purposes of the GI plexuses?

A

Myenteric - motility and sphincter control

Submucous - epithelium, blood vessels

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23
Q

Name the three components of GI reflex circuits.

A

Sensory, interneurons, effectors

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24
Q

Name the three types of GI reflex circuit.

A

Local, short, long

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25
Q

What is the name of a reflex which takes place entirely within the vagus nerve?

A

Vaso-vagal

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26
Q

What is glycogenesis?

A

Formation of glycogen

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27
Q

What is glycogenolysis?

A

Splitting of glycogen to form glucose

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28
Q

What is gluconeogenesis?

A

Formation of glucose from amino acid, glycerol, or lactic acid precursors

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29
Q

Describe the difference between glycogen stored in the liver and muscle cells.

A

In the liver it is used to regulate blood sugar. In muscle it is not available to the blood stream, just for glycolysis

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30
Q

Name and describe the two types of link in glycogen.

A

Alpha 1-4 glycosidic = straight chain

Alpha 1-6 glycosidic = branches

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31
Q

Which enzyme attaches primers to glucose residues for binding to glycogen?

A

Glycogenin

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32
Q

Name the intermediates of the metabolic pathway for glycogenesis.

A

G6P, G1P, UDP-glucose, [glucose]n+1

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33
Q

Name the three main enzymes in glycogenesis.

A

Glucophosphomutase, UTP-glucose phosphorylase, glycogen synthase

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34
Q

Name the main enzyme in glycogenolysis.

A

Glycogen phosphorylase (although many other enzymes are required to debranch glycogen)

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35
Q

Name the three main enzymes in gluconeogenesis, and which reactions they catalyse.

A

Phosphenol pyruvate carboxy kinase (PEPCK); pyruvate -> phosphenol pyruvate
Fructose-1,6-phosphatase (F1,6bP -> F6P)
Glucose-6-phosphatase (G6P -> glucose)

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36
Q

Which enzymes do the gluconeogenesis enzymes bypass?

A

Pyruvate kinase, phosphofructokinase, hexokinase

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37
Q

What is the name of the cycle which converts muscle lactic acid back to glucose?

A

Cori cycle

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38
Q

Why is fat an essential energy source?

A

Stores lots of energy, provides essential fatty acids, and for fat-soluble vitamins (A, D, E, K)

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39
Q

What is an essential fatty acid?

A

One the body needs but cannot synthesise

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40
Q

What are the chemical properties of lipids, TAGs, and fatty acids?

A

Non-polar, usually straight chain, usually cis, compact, alipathic (doesn’t form rings)

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41
Q

Name the three main fatty acids and their configuration.

A

Palmitic acid (16:0), Stearic acid (18:0), Oleic acid (18:1)

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42
Q

What are the alpha, beta, and omega carbons of fatty acids?

A

Alpha - adjacent to the carbon of the carboxyl group
Beta - adjacent to alpha
Omega - furthest from carboxyl group

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43
Q

Describe the process by which fat is absorbed into the mucosa.

A

TAGs degraded by lipases to fatty acids. These bind with monoacylglycerols, crossing the membrane to form TAGs again. These bind with other lipids/proteins to form chylomicrons

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44
Q

Describe the first stage of energy release from fatty acids (i.e. cytoplasmic).

A

Fatty acid + CoA -> acyl-CoA.
Acyl-CoA + carnatine -> acyl-carnatine + CoA
Acyl-carnatine crosses the mitochondrial matrix

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45
Q

Describe the second stage of energy release from fatty acids (i.e. mitochondrial matrix).

A

Acyl-carnatine + CoA -> acyl-CoA + carnatine

Acyl-CoA -> acetyl-CoA, FADH2, NADH, shortened acyl-CoA

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46
Q

Name the process by which acyl-CoA is transported into the mitochondrial matrix.

A

The carnatine shuttle

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47
Q

By which process is acyl-CoA broken down in the mitochondrial matrix?

A

Beta oxidation

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48
Q

What is the main purpose of ketones in respiration?

A

Can be converted to acetyl-CoA in starvation/diabetes

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49
Q

What are the clinical signs of ketone use in respiration?

A

Severe acidosis, breath smells of acetone

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50
Q

How are fatty acids created from acetyl-CoA?

A

Citrate transports to cytoplasm. Acetyl-CoA carboxylase converts to malonyl-CoA. This, plus NADH and fatty acid synthase creates fatty acids.

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51
Q

Which two substances promote acetyl-CoA carboxylase?

A

Insulin and citrate

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52
Q

Which three substances inhibit acetyl-CoA carboxylase?

A

Glucagon, adrenaline, palmitoyl-CoA

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53
Q

Under which conditions is lipogenesis most likely to occur?

A

The fed state, with a supply of carbohydrates, energy, and citrate

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54
Q

How are excess fatty acids stored?

A

In adipose, by VLDL

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55
Q

Why are amino acids that are not in use degraded?

A

There is no way to store them

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56
Q

Where in the GI tract are proteins degraded, how, and what into?

A

Stomach - proteolytic enzymes, and single amino acids or di-/tripeptides

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57
Q

When may degradation of proteins pose a problem to the liver?

A

High concentrations of nitrogen in side groups - NH4+/NH3 is toxic

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58
Q

Describe the transamination stage of amino acid catabolism.

A

An alpha-amino acid transfers the alpha-group to ketoglutarate, forming an alpha-keto acid. Also formed is glutamic acid

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59
Q

How is glutamic acid (the product of deamination) tranferred to the liver?

A

As alanine (w/ pyruvate) or glutamine (with NH4+)

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60
Q

Describe the de-amination step of amino acid catabolism.

A

Glutamate breaks off NH4+ (NAD accepting an electron to become NADH). A ketoglutarate is also formed

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61
Q

Describe the reactants and products of the urea cycle.

A

Reactants - NH4+, aspartic acid, ATP

Products - urea, fumerate, carbon skeletons

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62
Q

Describe how carbon skeletons of the urea cycle may be used.

A

Ketogenic - forms acetyl-CoA or fatty acids

Glucogenic - forms pyruvate or glucose

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63
Q

What is the name of the condition that blocks degradation of phenylalanine and tyrosine?

A

Alcaptonuria

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64
Q

Describe maple syrup urine disease.

A

Urine smells of maple syrup. Blocks valine, isoleucine, and leucine. Treated by diet, otherwise mental/physical retardation occurs

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65
Q

Describe phenylketouria.

A

Buildup of phenylalanine. Can cause severe mental retardation. Limit phenylalanine in the diet

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66
Q

How may a urea cycle defect be treated?

A

Drugs that remove nitrogen, gene therapy, low protein diet

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67
Q

What is the epithelium of the oral cavity and oropharynx?

A

Stratified squamous

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68
Q

What is the epithelium of the nasal cavity and nasopharynx?

A

Respiratory - keratinized pseudostratified columnar

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69
Q

Name the four papillae of the tongue.

A

Fungiform, circumvallate, foliale, filiform

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70
Q

Name the main feature of the posterior 1/3 of the tongue.

A

Associated with lymphoid aggregates

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71
Q

Name the four tonsils.

A

Palatine, lingual, tubual, pharyngeal

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72
Q

Name the three areas of the stomach.

A

Cardia, body, pylorus

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73
Q

Describe the difference between the epithelium of the isthmus and fundus of the stomach.

A

Isthmus mostly parietal cells

Fundus mostly chief cells

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74
Q

Describe the gastric pits of the cardia, fundus, and pylorus.

A

Cardia - deep, loose, tortous
Fundus, shallow, straight, long
Pylorus - deep, branched, coiled, high density

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75
Q

Describe how the pyloric sphincter differs from the pylorus.

A

More smooth muscle

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76
Q

Describe the two main features of the small intestine’s epithelium.

A

Microvili, crypts of Lieberkuhn

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77
Q

Where are Brunner’s glands, and what do they do?

A

Duodenum. Protect duodenum from gastric juices and neutralise chyme

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78
Q

What are Peyer’s patches?

A

Gut-associated lymphoid tissue (GALT)

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79
Q

Name two unique cells found in the crypts of Lieberkuhn.

A

Paneth cells - immune role

Stem cells - replenish the epithelium

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80
Q

Name the five main type of cell found in the small intestine.

A

Enterocyte, enteroendocrine, goblet, Paneth, stem

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81
Q

What two main types of cell are found in the colon?

A

Absorptive and goblet (lubricates)

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82
Q

Describe the smooth muscle alignment in the colon.

A

Not continuous - three strips teniae coli

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83
Q

How does the appendix’s histology differ from the colon?

A

Fewer crypts. Circular lymphoid tissue

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84
Q

Describe the epithelium of the anal canal.

A

Non-keratinized stratified squamous (becomes keratinized after the anus)

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85
Q

What is the main endothelium of the liver?

A

Simple squamous, fenestrated

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86
Q

Name the main components of the hepatic lobules.

A

Portal tracts/triads, sinusoids, space of Disse, Kupffer cells, hepatocytes, hepatic stellate cells

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87
Q

Describe the composition of the portal tract/triad.

A

Hepatic artery, portal vein, and bile duct

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88
Q

What is the purpose of hepatic stellate cells?

A

Makes connective tissue and stores vitamin A

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89
Q

What are Kupffer cells?

A

Macrophages in the liver

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90
Q

Describe the composition of bile.

A

Bilrubin (pigment of Hb that makes faeces brown), and bile salts

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91
Q

Which liver cells modify bile?

A

Cholangiocytes

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92
Q

Which cellular structures allow movement of bile?

A

Bile canaliculi

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93
Q

Describe the epithelium of the gall bladder.

A

Simple columnar

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94
Q

How does the gall bladder get rid of bile?

A

Pumps Na/Cl between epithelial cells. Osmotic pressure change causes water to rush in and remove bile

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95
Q

Which two main factors stimulate gallbladder action?

A

Vagus nerve, hormone cholecystokinin

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96
Q

What is the name for gallstones?

A

Cholecystitis

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97
Q

Describe the white blood cell components at each end of the pancreas. Why is this the case?

A

Basal end - basophilic, due to much RER

Apical end - eosinophilic, due to zymogen

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98
Q

How does the digestive cascade begin?

A

An enteropeptidase converts trypsinogen to trypsin

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99
Q

What is the name of pancreatic duct cells in the cavity (acini)?

A

Centroacinar cells

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100
Q

Where does the pancreas join the duodenum?

A

Hepatopancreatic ampulla (of Vater)

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101
Q

Which group of joints open the mouth?

A

Temporomandibular joints (TMJs)

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102
Q

Name the four TMJs. Which opens the mouth?

A

Medial pterygoid, lateral pterygoid, temporous, masseter. Lateral pterygoid opens

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103
Q

Describe the classification of teeth.

A

Upper jaw is maxillary, lower is mandibular.

1, 2: Incisors. 3: canine. 4, 5: premolar. 6,7,8: molar.

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104
Q

Which cranial nerves supply general sensation of the mouth?

A

CN V2 (maxillary trigeminal) and CN V3 (mandibular trigeminal)

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105
Q

Name the three salivary glands.

A

Parotid, sublingual, submandibular.

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106
Q

What is the name for the gums?

A

Gingiva

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107
Q

Describe the routes of the 2nd and 3rd division of the trigeminal nerve.

A

2 -> pons, foramen rotundum, face

3 -> pons, foramen ovale, TMJs

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108
Q

Name the four tongue muscles.

A

Palatoglossus, styloglossus, hypoglossus, genioglossus

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109
Q

Describe the nerve supply of the tongue.

A

Anterior 2/3: general sens V3, special sens VII
Posterior 1/3: general & special sens both IX
Tongue muscles (except palatoglossus) supplied by XII

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110
Q

Describe the route taken by cranial nerve VII, the facial nerve.

A

Pontomedullary junction, temporal bone via internal acoustic meatus, stylomastoid foramen, anterior tongue with muscles for facial expression and mouth

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111
Q

Name CN IX and XII.

A

IX - glossopharyngeal (tongue and pharynx)

XII - hypoglossal (tongue muscle)

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112
Q

Describe the muscle and nerve anatomy of the oesophagus.

A

Circular constrictor muscles overlap each other. All connect to the midline raphe. X supplies voluntary. IX and X supply involuntary. Plexus is present

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113
Q

Name the three types of GI contraction.

A

Cervical (head), thoracic, diaphragmatic

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114
Q

Describe the two sphincters of the oesophagus.

A

Top sphincter - anatomical. Bottom - z line, physiological. Intragastric pressure < intrathoracic pressure

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115
Q

Which condition will reduce efficacy of the oesophageal lower sphincter?

A

A hernia

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116
Q

Describe how food is swallowed. Also give the cranial nerves involved.

A

Lips close (VII), bolus pushed to oesophagus (XII), soft palate and larynx elevate (X), oesophagus contracts (IX, X), the pharynx raises and shortens, and peristalsis occurs

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117
Q

What are the three general areas of the GI tract, derived from embryological origin?

A

Foregut (up to pylorus, 1/2 pancreas), midgut (to proximal end of transverse colon, 1/2 pancreas), hindgut (descending colon to anus)

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118
Q

Name the nine areas on the ‘chest grid’.

A

Top row - hypochondrium, epigastric (RH, E, LH)
Middle - lumber (flank), umbilical (RL, U, LL)
Bottom - iliac fossa, pelvic (RI, P, LI)

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119
Q

Give descriptive words for the peritoneum.

A

Thin, transparent, semi-permeable

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120
Q

Name the three categories of peritoneal organ.

A

Intraperitoneal (entirely visceral), retroperitoneal (visceral in anterior only), mesentery (double visceral wrap)

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121
Q

Where does communication between the greater and lesser stomach sac occur?

A

Omental foramen

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122
Q

Which nerve fibres do visceral afferents travel back to the CNS with?

A

Sympathetic

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123
Q

Name the visceral afferent spinal outlets for the three Gi categories.

A

Foregut - T6-9, Midgut - T 8-12, Hindgut - T10 - L2

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124
Q

Name the four fibres in which somatic motor, somatic sensory, and sympathetic fibres are conveyed in.

A

Thoracoabdominal, subcostal, iliohypogastric, ilioinguinal (7-11th ICs, T12. two halves of L1)

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125
Q

Describe the progression of pain felt in appendicitis.

A

Dull and aching to sharp stabbing in right inguinal area

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126
Q

What is ascites?

A

Collection of fluid in the peritoneal cavity.

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127
Q

Which procedure should be used to treat ascites? Why must care be taken?

A

Paracentesis (‘abdominocentesis’). Must drain lateral to rectus sheath, to avoid inferior epigastric artery

128
Q

What is the name for pain that comes and goes?

A

Colicky pain

129
Q

Which four factors should be considered when assessing pain?

A

Location, character (visceral, somatic), referral pattern, and timing

130
Q

At which levels are the abdominal organs supplied by sympathetic nerves?

A

T5 - L2

131
Q

Describe how the sympathetic supply reaches the organs of the abdomen from the CNS.

A

Abdominopelvic splanchnic nerves -> prevertebral ganglia -> periarterial plexus (hitches a ride)

132
Q

How does the adrenal gland’s sympathetic innervation differ from normal sympathetic supply? Where?

A

No synapse at the ganglia, synapses directly with cells. T10 - L1

133
Q

Where are foregut, midgut, and hindgut pain typically felt?

A

Epigastric, umbillical, pelvic

134
Q

Name the main regions of the stomach. What are the two halves called?

A

Fundus, body, antrum, pylorus. Orad, caudad

135
Q

How does activity of the orad stomach break down food?

A

Weak tonic contractions with low amplitude. Minimal mixing.

136
Q

What may increase or decrease rate of orad contractions?

A

Vagal increases, gastrin decreases

137
Q

How does activity of the caudad stomach break down food?

A

Slow waves that reach potential. Retropulsion against the pylorus breaks down food (faster velocity) and allows it to pass through

138
Q

What is the name for the wave that passes from caudad stomach through to the duodenum?

A

The antral wave (/pump)

139
Q

Which three factors change rate of caudad stomach antral waves?

A

Rate of emptying, distension, consistency

140
Q

Which factors decrease rate of stomach emptying?

A

Neurons and hormones (fat, acid), hypertonicity, distention

141
Q

Name the two types of epithelium in the stomach regions and which cells they primarily are composed of.

A

Orad - oxyntic, parietal

Caudad - pyloric, chief

142
Q

Which chemicals may the orad stomach epithelium secrete?

A

HCl, peptinogen and pepsin, intrinsic factors, gastroferrin, mucus

143
Q

Which chemicals may the pyloric stomach epithelium secrete?

A

Gastrin (increasing HCl), somatostatin (decreasing HCl),mucus

144
Q

There are two pathways of secreting H for HCl in the stomach - direct and indirect. Briefly describe them.

A

Direct - ACh, gastrin, or histamine may act directly on mucosal cells, or ACh/gastrin may act on ECLs to activate histamin release

145
Q

What is the name of a chemical which promotes secretion from a cell?

A

A secretagogue

146
Q

Which chemicals prevent H+ secretion from the stomach epithelium?

A

Somatostatin and prostaglandin

147
Q

By which chemical pathways do the secretagogues for H+ in the stomach epithelium act?

A

ACh/gastrin - IP3 and PIP2

Histamine - adenylyl cyclase

148
Q

Name the three secretory phases. Describe them.

A

Cephalic - ACh, gastrin, and histamine released
Gastric - distension causes secretion.
Intestinal

149
Q

Which factors will decrease acid secretion in the stomach?

A

Food buffers, pH, D cell inhibition

150
Q

Which channels are involved for H+ secretion in the stomach?

A

K+, Cl- (CFTR), Na/K ATPase, H/K ATPase, Cl-/HCO3 symporter

151
Q

What is segmentation?

A

Contraction of the circular muscle in the intestine to divide chyme into segments, breaking it down

152
Q

What is the mechanism of segmentation? What may affect its rate?

A

Slow wave thresholds - gastroileal reflex, or autonomic innervation triggers and increases/decreases respectively

153
Q

Which two main hormones trigger H+ release in the stomach?

A

Gastrin and secretin

154
Q

Which two main hormones inhibit gastric emptying?

A

Gastric inhibitory peptide (GIP), and glucose-like protein 1 (GLP1).

155
Q

Which hormones trigger the MMR, and appetite respectively?

A

Motilitin, ghrelin

156
Q

Describe the actions of the stomach hormone cholecystokinin (CCK).

A

Inhibits gastric emptying, pancreatic enzymes, and Oddi sphincter tone. Promotes secretion and bile

157
Q

Which factors promote succus entericus, and which inhibits it?

A

Distension, irritation, gastrin, CCK, secretin, vagal activity increase, sympathetic activity decreases

158
Q

What are the two components of succus entericus, and where do they come from?

A

Mucus, aqueous salt

Goblet cells, crypts of Lieberkuhn

159
Q

Which channel proteins are mainly associated with succus entericus release?

A

Na/K ATPase, Na/K/2Cl cotransporter, CFTR

160
Q

What is the name of the electrical activity of peristalsis?

A

Migrating motor complex

161
Q

What is the main purpose of the migrating motor complex?

A

A housekeeping function - cleans up

162
Q

Which factors may promote peristalsis, and which supress or inhibit it?

A

Promotes - motilitin
Suppresses - gastrin, CCK
Inhibits - vagus, eating

163
Q

Describe the difference between the exocrine and endocrine pancreas.

A

Exocrine - digestive juices containing proteases, lipases, amylases etc from acinar (centroacinar) cells
Endocrine - glucagon/insulin from islets of Langerhans

164
Q

What is the purpose of pancreatic duct cells?

A

Secrete alkaline HCO3-, neutralising chyme and protecting the mucosa from self-digestion

165
Q

Name the five main proteases.

A

Elastin, chymotrypsin, trypsin, carboxypeptidase A & B

166
Q

Name the two stages of assimilation.

A

Digestion and absorption

167
Q

Briefly describe the breakdown of carbohydrate.

A

Starch -> oligosaccharides (alpha-amylase) -> monosaccharides (oligosaccharidase)

168
Q

Describe the actions of the carbohydrate-lytic enzymes.

A

Alpha-amylase breaks alpha 1-4 glycosidic links internally. Oligosaccharidases break terminal a 1-4 links

169
Q

Name four of the main oligodendrocytes.

A

Maltose, sucrose, isomaltase (all faster than absorption) lactase (slower than absorption)

170
Q

Name the main entry and exit channels of glucose in enterocytes.

A

Entry - SGLT1 (Na/glucose symporter), GLUT5 (fructose entry), GLUT2 (all exit)

171
Q

Briefly describe the breakdown of protein.

A

Protein -> peptides (HCl, pepsin) -> oligopeptides (trypsin, chymotrypsin, elastase, carboxypeptidase A/B) -> amino acids (membrane protein)

172
Q

Describe the difference between endopeptidases and exopeptidases.

A

Endo- break down to 2-6 peptide chain
Exo- break down to single amino acids.
Trypsin, chymotryspin, elastase are endo
Carboxypeptidase A/B are exo-

173
Q

Describe the movement of amino acids in enterocytes at the apical and basolateral membranes.

A

Apical - 7 methods (5 require Na)

Basolateral - bidirectional. 3 efflux 2 influx

174
Q

How are di/tri/tetrapeptides absorbed in the enterocyte?

A

Absorbed by H+ methods, degraded within the cell

175
Q

Name the two main enzymes associated with lipolysis.

A

Gastric and pancreatic lipase

176
Q

Describe how most lipids/fats are broken down outside enterocytes.

A

Micelle formation. Outer lipids hydrolysed by pancreatic lipase, replaced by inner lipids, shrinking micelle

177
Q

When fats have been broken down, they typically have around 12 carbons. What happens to those > 12, and < 12?

A

< 12 - diffusion

> 12 - chylomicron storage

178
Q

Describe the role of bile salts in fat degradation.

A

Bile salts increase surface area, but block access by lipases - colipase fixes this

179
Q

Describe the problems that may arise from lack of bile salts.

A

Steahorroea (fat in stool), and fat-soluble vitamin deficiency

180
Q

Which drugs should be used to treat hypercholesterolaemia?

A

Ezetimbe - NPC1LP1, statins

181
Q

Why is iron important physiologically?

A

Component of Hb (2/3 of body store)

182
Q

How is iron absorption/degradation matched?

A

By the duodenum

183
Q

Describe the problems caused by a lack/excess of iron.

A

Anaemia, toxicity to the liver, heart, pancreas

184
Q

Describe briefly the absorption of Fe3+ into enterocytes.

A

Absorped by channel protein, (can be stored by apoferratin), exits by ferraportin. Transported across by mobilfarrin. Reduced by a factor to Fe2+

185
Q

Name the reduction factors for Fe3+.

A

HCl, vitamin C, Dctyb (duodenal cytochrome B), gastroferrin

186
Q

Describe how haem may be degraded in enterocytes.

A

Degradation to Fe2+ and bilverdin by haem oxidase

187
Q

Which factor increases absorption of iron, and which decreases ferraportin expression?

A

Absorption - blood loss

Ferraportin - hepcidin

188
Q

Describe vitamin B12.

A

Not water soluble. Not in vegetables - vegans may suffer from insufficiency

189
Q

Which three factors do fat-soluble vitamins require to be absorbed?

A

Bile secretion, intact mucosa, mixed micelles

190
Q

Describe the absorption of calcium in enterocytes.

A

Passively absorbed (paracellular), actively (transcellular). Mostly active in chyme. Regulated by 1,25-dihydroxyvitamin D (calcitrol) and parathyroid

191
Q

Describe where each layer of GI histology originates embryologically.

A

Visceral mesoderm - lamina propria, muscularis mucosae, muscularis externa, CTs
Endoderm - epithelium, associated ducts/glands
Neural crest - ENS, Meissner’s, Auerbach’s plexuses

192
Q

Which embryo landmarks does the intestinal mesentry originate from?

A

(Ventral) falciform ligament, lesser omentum

(Dorsal) mesogastrium, mesoduodenum, mesocolon

193
Q

When are the oesophagus, circular muscle, and longitudinal muscle formed?

A

Week 4, 5, 8

194
Q

Describe what occurs during week 4 of gastrointestinal development.

A

Caudal foregut dilates. Dorsal border grows and rotates 90 degrees
Duodenum formed from caudal foregut (1, 2) and cranial midgut (3, 4)

195
Q

Describe how the liver is developed during embryological growth.

A

Liver bud -> mesoderm of the septum transversum, which forms haematopoetic, Kupffer, and connective cells
Endoderm -> hepatocytes, biliary tree

196
Q

Describe how the pancreas is developed during embryological development.

A

Dorsal pancreatic bud -> dorsal duct -> main duct
Ventral swaps sides (R->L) and becomes retroperitoneal
Ventral is bilobed, wrapping round and forming the annular pancreas

197
Q

Describe the formation and development of the spleen during embryological development.

A

W5, from mesoderm. Haemopoetic then lymphatic

Lobes becomes notches

198
Q

Describe the development of the midgut through embryological growth.

A

(bottom half of duodenum to proximal 2/3 colon)
w4 - yolk sac communicates with midgut. YS narrows to form the vitelline duct.
Rotates out as an outgrowth to form structures
w10 - re-entry (small intestine first, caecum last)

199
Q

Name the main defects that can occur with midgut development.

A

Meckel’s diverticulum

Vitelline cyst/fistula

200
Q

Which embryological structure forms the perineal body, anal membrane, and anorectal canal?

A

The cloaca and cloacal membrane (hindgut)

201
Q

Name the main defects that can occur with anal formation.

A

Urorectal, rectovaginal, and rectoperineal fistulas.

202
Q

Name the three main organs associated with bile and their role in this system.

A

Spleen (formation of bilirubin), liver (converts to bile), gallbladder (stores/concentrates bile)

203
Q

Why is bile important?

A

To aid in absorption of fats in the small intestine.

204
Q

What is the name of the major artery which supplies the foregut organs? How does it divide?

A

The celiac trunk - splenic, left gastric, hepatic trifurcation

205
Q

The celiac trunk trifurcates. What does each division then bifurcate to?

A

Gastroduodenal and superior pancreatico-duodenal

206
Q

Describe the spleen.

A

Intraperitoneal. Pain felt in left hypogastric region. Ribs 9-11. Moves with respiration

207
Q

Describe the blood supply of the stomach.

A

L/R gastric arteries (lesser curvature)
L/R gastro-omental arteries (greater curvature)
Both sets anastamose.

208
Q

What is the name of the vessel that supplies the gallbladder with blood? Where does it arise?

A

The cystic artery. The right hepatic artery

209
Q

Describe the pain supply around the gallbladder.

A

Visceral afferents T6-9. Pain felt in epigastic/hypogastric regions (+/- referral to right shoulder)

210
Q

Describe the division of the liver.

A 
4 anatomical (L/R/quadrate/caudate)
8 functional (I-VIII), each with own vessel set
Segmentectomy can be performed
211
Q

Describe the most common cause of hepatomegaly.

A

Increased central venous pressure means backup through IVC and hepatic veins. No valves

212
Q

Name the two pouches surrounding the liver.

A

Hepatorenal (Morison’s), subphrenic

213
Q

Name the main veins surrounding the liver.

A

Splenic, inferior/superior mesenteric, hepatic portal vein, IVC (see notes for assembly)

214
Q

Name the three main ligaments surrounding the liver, and what they attach to.

A

Coronary - diaphragm
Falciform - anterior abdominal wall
Ligamentum teres - umbilical vein remnant

215
Q

What is the difference between paracellular and transcellular transport?

A

Transcellular occurs through cells, paracellular through tight junctions

216
Q

Lymphoid tissue is typically found in two different types in GI tissue. Describe these.

A

Scattered - typically crypts

Organised - Peyer’s patches

217
Q

Describe the process by which T cell activation of dendritic cells causes them to migrate to the lumen.

A 
T cells (guided by CCR7, L-selectin)
Paracellular transport
Maturation of dendrites (a4B2, CCR9)
Drains to thoracic duct
Attaches by MaDCAM1
218
Q

Which feature of dendrites allows greater neutralisation of pathogens in the GI tract?

A

Extension across cells into the lumen

219
Q

Describe the composition of the humoural response in the GI mucosa.

A

80% IgA (a J dimer), 15% IgM, 5% IgG

220
Q

Describe, in general, non-specific terms, the role of commensals in the GI tract.

A

Assist in hyporegulation of immune/T cells, prevents maturation of dendrites

221
Q

Describe the specific pathway in which T cells cause genetic transcription of immune factors.

A

T cells activate IKK pathway
This phosphorylates IaB
This moves NFaB into the nucleus to bind to DNA

222
Q

Which specific chemicals do commensal organisms in the GI tract release to downregulate NFaB and dendrite maturation?

A

NFaB -> PPARgamma
IaB -> don’t need to know (just be aware)
Dendrites -> PGE2, TGF-B, TSLP

223
Q

How can T cells destroy virally infected GI mucosal cells?

A

MHC class I, perforin/granzyme/FAS-ligand paths

224
Q

How can non-specific (innate) immune cells stimulate a response locally in the GI tract?

A

PRRs trigger the NFkB path, releasing chemokines, cytokines, and defensins

225
Q

Describe the relationship between dendrites and activation of T cells.

A

Immature dendrites activate TH3/Treg

Mature dendrites activate TH1/TH2

226
Q

Describe the role of TH2 cells in GI mucosal immunity.

A

Activates eosinophils, mast cells, and stimulates B cells to release IgE. Can also stimulate repair/mucus secretion in mucosal cells

227
Q

Describe the role of TH1 cells in GI mucosal immunity.

A

Stimulates B cells to produce IgG2a, activates macrophages

228
Q

Describe what occurs when mucosal immunity is disregulated.

A

Infected macrophages travel to lymph nodes, infecting CD4 cells, spreading the infection.

229
Q

Describe the mechanism of food allergy.

A

Type I hypersensitivity. Cross-linking of IgE on mast cells with specific food antigens.

230
Q

Describe the effects of general and local histamine release.

A

General -> systematic anaphylaxis

Local -> acute uritcaria (hives)/wheal and flare

231
Q

What is the primary GI response to asthma and seasonal rhinoconjunctivitis?

A

Mucus secretion

232
Q

How does Coeliac’s cause malnutrition? Which specific immune components does this involve?

A

Damage to the small intestine

Gamma interferon from gluten specific T cells -> IL-15 -> proliferating IEL, killing epithelial cells

233
Q

What two tests should be used for diagnosing of Coelic’s disease?

A

Biopsy (gold standard, especially in paeds)

Serology useful for IgA levels

234
Q

Describe the immunologic effects of Crohn’s disease.

A

Distal ileum/colon (although all GI tract can be affected)

Focal/discontinous inflammation with deep, eroding fissures (+/- granulomas)

235
Q

Which specific immune components are present in Crohn’s disease?

A

TH1, gamma interferon, IL-12, TNF alpha

236
Q

Describe the immunologic effects of ulcerative colitis.

A

Starts at rectum, moves proximally
Can result in arthritis/uveitis/skin lesions
Distorted crypts, monocyte/neutrophil/plasma cell infiltration

237
Q

How should Crohn’s and ulcerative colitis be treated?

A

With NSAIDs and immunosupressive drugs

238
Q

What do the following crypt cells secrete: chief, D cell, G cell, enterochromoffin-like cell (ECL), parietal, mucus?

A

Chief - pepsinogen, D - somatostatin, G - gastrin, ECL - histamine, parietal - HCl, mucus - mucus and bicarbonate

239
Q

Describe how the crypts of Lieberkuhn are kept at a pH of 6-7 while the stomach is at a pH of 1.

A

Mucus/bicarbonate layer secreted by mucus cells

240
Q

Is crypt secretion typically paracrine, exocrine, or endocrine?

A

Paracrine

241
Q

Name the receptors that histamine, ACh, gastrin, and somatostatin affect.

A

H2, M3, CCK2, SSRT2

242
Q

Describe the mechanism by which antacids can reduce indigestion.

A

Binds H+/HCO3- to form H2O/CO2, buffering HCl

243
Q

Describe the mechanism of, indication of, and effects of misoprostol.

A

Prostaglandin E1 analogue.
Indicated for peptic ulcers.
Can cause abdominal pain, diarrhoea, and induce labour

244
Q

Name three prostaglandin E1 analogues, other than misoprostol.

A

Lanzoprasole, ameprazole, pantoprazole

245
Q

Describe the mechanism and effects of proton pump inhibitors.

A

Irreversibly binds H+/K+ ATPase.
Indicated for peptic ulcers.
Can increase pH, leading to impaired stomach defences

246
Q

Describe how the treatment of H. pylori should occur with benign peptic ulcer formation.

A

PPIs and abx

clarithromycin, amoxicillin/metronidazole

247
Q

Name the five types of anti-emetic, and which receptor they target.

A

Anti-histamines (H1, brain). Anti-muscarinics (M1, brain). 5-HT3 antagonists (5-HT3 receptor). Dopamine antagonists (D2). Neurokinin-1 antagonists (NK1)

248
Q

Describe anti-diarrhoeal drugs.

A

Electrolyte replacment. Binds to u-opiate receptors.

Can be combined with atropine.

249
Q

Name the three main laxatives.

A

Lspagula husk, lactulose, senna-stimulant purgative

250
Q

How is the iliocaecal sphincter opened?

A

The gastroileal reflex, driven by CCK and gastrin. Opened when duodenum is distended (and closed when colon distended).

251
Q

Name the main cause of appendicits.

A

Faecalith

252
Q

Name the ions secreted and absorbed by the colon.

A

Absorbed - Na, Cl, H2O

Secreted - K, HCO3, mucus

253
Q

Which features of the colon assist in absorption of ions?

A

Folds, crypts, microvilli.

Goblet cells, which secrete trefoil protein and glycosaminoglycans (host defence)

254
Q

Which three methods does the colon have to move material along its length?

A

Haustration (like segmentation, but slower, to allow absorption). Peristalsis-like movement 1-3 times a day (gastrocolic response), defaecation

255
Q

What are the main advantages of colon commensal bacteria?

A

Competes with pathogens, motility/mucosal integrity, vitamin K synthesis, activates some IBD drugs

256
Q

What is the name of air expelled through the anus? Where can it arise from?

A

Flatus - swallowed air or indigestable carbohydrates

257
Q

Give the main symptoms and treatment of IBS.

A 
Diarrhoea, constipation, abdominal pain.
Symptomatic relief (linaclotide constipation, amitriptyline for pain)
258
Q

Give the five main functions of the liver.

A

Metabolism of carbohydrates, fats, and proteins. Stores vitamins and glycogen. Kupffer cells - immunity/bilirubin breakdown

259
Q

Name the many components of liver primary juice.

A

Cholic, chenodeoxycholic acids, electrolytes (Na/K/Ca/Cl/HCO3), lipids, phospholipids, cholesterol, IgA, bilirubin, metabolic waste

260
Q

What is the name of the ducts in which liver primary juice run to bile ducts?

A

Canaliculi

261
Q

Cholelithiasis is formation of gallstones in the liver tracts. Describe treatment.

A

Laparascopic cholecystectomy, analgesia, atropine/GTN for biliary spasm

262
Q

By which process do bile salts/acids return to the liver?

A

Enterohepatic recycling

263
Q

Describe how some bile salts may be degraded to bile acids in the GI tract.

A

Bacteria can dehydroxylate

264
Q

What are bile salt/acid sequestrants?

A

Resins. Stop bile salt/acid being reabsorbed by binding.

265
Q

Name the three main bile acid/salt sequestrants/resins.

A

Colveselam, colestepol, colestyramine

266
Q

Name the set of enzymes in the liver responsible for most metabolism reactions.

A

Cytochrome P450 (CCY)

267
Q

Describe cytochrome P450 enzymes.

A

A family of monooxygenases in the liver ER

268
Q

What is hepatic encephalopathy?

A

Failure of the urea cycle to degrade ammonia. Toxic buildup leads to incoordination, drowsiness, coma, cerebral oedema, and death.

269
Q

Describe the metabolism of aspirin in the liver.

A

Aspirin (drug) -> salicylic acid (derivative) -> glucuronide (conjugate)

270
Q

How should hepatic encephalopathy be treated?

A

With lactulose or antibiotics

271
Q

Describe the bile flow from liver and gallbladder to the duodenum.

A

R + L hepatic ducts -> common hepatic
CH + cystic -> common bile duct
CBD + common pancreatic -> ampulla of Vater

272
Q

Name the three main sphincters in the bile flow.

A

Bile duct sphincter, pancreatic sphincter, sphincter of Oddi

273
Q

Which investigation may be used to visualise the biliary tree?

A

Endoscopic retrograde cholangiopancreatotography

274
Q

Describe the main cause of extra/post-hepatic obstructive jaundice.

A

Gallstones/carcinoma in the head of the pancreas, causing bile to back up to the liver (forcing bilirubin into the blood)

275
Q

Name the four areas of the pancreas.

A

Head, uncinate process, body, tail

276
Q

Name the main cause of pancreatic pain. Where does it present in the patient?

A

Pancreatitis - epigastric/umbillical regions

277
Q

The duodenum and pancreas have an intimate relationship. Describe the vasculature between them.

A

Superior and inferior gastropancreatic arteries (from common hepatic and superior mesenteric respectively)

278
Q

Name the four areas of the duodenum.

A

Superior -> descending -> horizontal -> ascending

279
Q

Describe the main difference between the epithelium of the jejunum and the ileum.

A

Jejunum -> plicae circularis

Ileum -> much smoother

280
Q

Where does the duodenum become the jejunum?

A

At the duodenaljejunal (one word) fixture

281
Q

Describe how chylomicrons are transported to venous circulation.

A

Through lacteals -> left venous angle

282
Q

Name the four main lymphatic systems of the GI tract.

A

Celiac, superior mesenteric (midgut), inferior mesenteric (hindgut), lumbar

283
Q

Name the eight main components of the liver function test.

A 
Liver - AST/ALT
Biliary - ALP/GGT
Pancreas -amylase/lipase
Prothrombin time (PT)
Bilirubin (conjugated/unconjugated)
284
Q

Of the enzymes in the liver function test, which are more specific? To where?

A

ALT - liver/hepatocytes
GGT - biliary tree
Lipase - pancreas (amylase also salivary)

285
Q

Which clotting factors does the liver produce?

A

I, II, V, VII, IX, X, XII, XIII (1, 2, 5, 7, 9, 10, 12, 13)

286
Q

What are the three causes of malabsorption?

A

Luminal digestion, mucosal disease, structural disease

287
Q

Name the specific disease states that cause malabsorption.

A

Coeliac, lactase malabsorption, tropical sprue, Whipple’s, Crohn’s, Parasites, bacterial overgrowth

288
Q

Name some causes of malnutrition.

A

Disease, hospital admission, chronic, acute, psychosocial

289
Q

What are the symptoms of malnutrition?

A

Impaired immune response, fatigue, water/electrolyte disturbances, thinness, history weight loss, loose clothes, swallowing

290
Q

What is the main tool for malnutrition, and describe it?

A

MUST - BMI/% weight loss/acute effects

291
Q

Name the two types of tube feeding.

A

Enteral (nasogastric, nasojejunal, percutaneous)

Parenteral (specialist and expensive)

292
Q

What is the name of the site where fluid can collect next to the colon?

A

Paracolic gutters

293
Q

Name the three main cavities in the peritoneal cavity.

A

Supracolic, infracolic, paracolic gutters

294
Q

The position of the appendix is variable. In which position is it usually found?

A

Retrocaecal

295
Q

What is the name of the point at which the appendicel orifice can be palpated?

A

McBurney’s point

296
Q

Which component allows movement of the sigmoid colon?

A

Mesentery

297
Q

Describe the arterial supply of the GI tract from the abdominal aorta.

A

Celiac trunk, SMA, IMA
Splits into left common iliac, right common iliac
Lateral branches to kidneys/adrenal glands etc.

298
Q

What is the name of the anastamosis between the SMA and IMA?

A

Anastomosis of Drummond

299
Q

Name the three venous anastamoses between hepatic and systemic flow.

A

Ligamentum teres, distal oesophagus, rectum/anal canal

300
Q

What is the name of the muscle which forms the pelvic floor? Which three muscles are these split into?

A

Levator ani -> iliococcygeus, pubococcygeus, puborectalis

301
Q

Describe the two nerve supplies to the levator ani.

A

Nerve to levator ani

Pudendal (S2, 3, 4)

302
Q

What is the name of the division between the colon and rectum? What anatomical level does it occur?

A

Rectosigmoid junction, S3

303
Q

What is the name of the division between the rectum and anus?

A

Pectinate line

304
Q

Describe the three main sphincters of the anal canal.

A

Internal -> sup 2/3 -> symp/para
External -> inf 1/3 -> pudendal/distension
Puborectalis -> voluntary

305
Q

Give the anatomical landmarks of the 1. sympathetic supply, 2. somatic motor supply, 3. parasympathetic.

A
  1. T12-L2, 2. S2-4, 3. S2-4
306
Q

Describe the course of the pudendal nerves.

A

Branch of sacral plexus -> greater sciatic foramen

307
Q

Describe the embryonic layers as divided by the pectinate line.

A

Visceral and parietal

308
Q

Name the three main abdominal lymph nodes.

A

Internal, external, and common iliac

309
Q

Name the fat and loose connective tissue around the anus that communicates posteriorly.

A

Ischioanal fossae

310
Q

Describe the linea alba and linea semilunaris.

A

Linea alba - from xiphoid to pubic symphesis

Linea semilunaris - lateral to anterior abdomen

311
Q

Name the five layers of muscle in the abdomen and their muscle fibre orientation.

A

External oblique (hands in pockets), internal oblique (hands on chest), transversalis abdominus (horizontal), transversalis fascia, parietal peritoneum

312
Q

Where are the sites of direct and indirect inguinal hernias?

A

Direct - Hesselbach’s triangle

Indirect - inguinal canal

313
Q

What is the name of the structure that connects the inguinal canal to the skin?

A

The gubernaculum

314
Q

What is the name of the area of innate weakness in femoral hernias?

A

Myopectineal orifice

315
Q

Name the dimensions of the inguinal canal.

A

Superior - conjoint tendon (internal oblique + transversus abdominus)
Inferior - inguinal ligament
Anterior - external oblique
Posterior - transversalis fascia

316
Q

When does a hernia become a medical emergency?

A

When it becomes strangulated.

1b. GASTROINTESTINAL (10 decks)

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