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my esa 3 > GI > Flashcards

GI Flashcards

1
Q

What does kellikrein do, and why is it necessary?

A

Aids the production of bradykinin, which helps manage large blood supply when working maximally.

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2
Q

What are the 4 layers of the gut wall? (Innermost to outermost)

A

Mucosa
Submucosa
External muscular layers (muscularis externae)
Serosa

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3
Q

What is mucosa comprised of?

A

Epithelium
Lamina propria
Muscularis mucosa

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4
Q

What is often a feature of the lamina propria?

A

Payers patches (aggregations of lymphocytes)

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5
Q

What is submucosa comprised of?

A

A layer of connective tissue bearing glands, arteries, veins and nerves

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6
Q

What is the muscularis external comprised of in the gut?

A

2 layers of smooth muscle (outer longitudinal and an inner circular layer)
Creates peristaltic waves to move luminal contents

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7
Q

What is the serosa?

A

A serous membrane comprised of connective tissue and simple squamous epithelium (mesothelium)

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8
Q

What enzymes does saliva contain?

A

Amylase and lipase

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9
Q

How is saliva bacteriostatic?

A

Contains immunoglobulin A, antibody IgA

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10
Q

Why does saliva have a high calcium content?

A

To help protect the teeth

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11
Q

How does the stomach help prevent rises in pressure as it fills?

A

It’s walls relax

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12
Q

What are the 3 layers of muscle in the stomach?

A

Oblique, circular and longitudinal

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13
Q

Is the chyme leaving the stomach hypotonic, isotonic, or hypertonic?

A

Hypertonic

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14
Q

What happens to the hypertonic chyme in the duodenum?

A

Water is drawn from the ECF to render the hypertonic solution isotonic.
Liver secretes vile (containing water, alkali and bile salts to emulsify fats)
Pancreas secretes alkali to help neutralise acidic chyme, along with enzymes to digest food

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15
Q

What is plicae circulares, and where are they found?

A

Protrusions with villi on them to further increase surface area. Found in the jejunum

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16
Q

Where is the small intestine most active?

A

Proximal

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17
Q

List the components of the colon in order

A

Caecum, ascending, transverse, descending, sigmoid

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18
Q

What are the 2 neural plexuses of the gut wall?

A 
Submucosal plexus (plexus of Meissner)
Myenteric plexus
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19
Q

What effect does histamine have in the stomach?

A

Helps control the production of acid

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20
Q

What approximate pH is saliva?

A

~pH8

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21
Q

Is saliva hypertonic, isotonic, or hypotonic?

A

Hypotonic (more isotonic if high flow rate)

Rich in K+ and HCO3

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22
Q

What causes secretion of saliva?

A

Contraction of myoepithelial cells in salivary glands

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23
Q

List some immune proteins present in saliva

A

IgA, lysozyme, lactoferrin

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24
Q

How does lactoferrin function as an immune protein?

A

Sequesters iron away from bacteria

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25
Q

How does saliva aid bolus formation?

A

Moistens and lubricates forming bolus

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26
Q

Approximately how much saliva is formed a day?

A

~1.5 litres

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27
Q

What are some consequences of xerostomia?

A

Lack of ability to taste (saliva is the solvent for taste molecules)
Sore lips, inflamed tongue

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28
Q

What are the 3 salivary gland pairs

A

Parotid glands
Sublingual glands
Submandibular glands

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29
Q

Which of the salivary glands isn’t easily palpable?

A

Sublingual glands

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30
Q

Which nerve innovates the parotid glands?

A

Glossopharangeal nerve

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31
Q

Which nerve innovates the sublingual and submandibular glands?

A

Facial nerve

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32
Q

What sort of saliva does the parotid gland produce?

A

Rich in water, electrolytes and enzymes

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33
Q

What percentage of saliva production comes from the parotid glands?

A

~25%

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34
Q

What sort of saliva do the sublingual glands produce?

A

Rich in mucus

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35
Q

Approximately what percentage of saliva is produced by the sublingual glands?

A

~5%

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36
Q

What sort of saliva do the submandibular glands produce?

A

Serous and mucus

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37
Q

Approximately what percentage of saliva is produced by the submandibular glands?

A

~70%

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38
Q

What effect does the sympathetic nervous system have on the salivary glands?

A

Reduces blood flow to salivary glands (hence dry mouth when nervous)

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39
Q

Is the solution secreted by the acinar cells of the salivary glands hypertonic, isotonic or hypotonic?

A

Isotonic. Solution is made hypotonic as it travels along ducts, hence why solution is more isotonic when there is a high flow rate

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40
Q

Salivary glands above the aural fissure are innervated by what nerve?

A

Greater petrosal of VII

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41
Q

Salivary glands below the aural fissure are innervated by what nerve?

A

Chorda tympani of VII

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42
Q

What is one clinical effect of the path the chorda tympani of VII takes?

A

Runs through the middle ear, so can be cut off by infection

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43
Q

Name and describe the 3 phases of swallowing

A
  1. Voluntary - bolus moved towards pharynx, once it touches the pharyngeal wall, the next phase begins
  2. Pharyngeal - afferent info from receptors in pharynx reaches swallowing centre in brain. Soft pallet seals off nasopharynx. Pharyngeal constrictors push bolus downwards. Larynx elevates, closing epiglottis. Vocal cords addict, breathing temporarily ceases. Opening of upper oesophageal sphincter.
  3. Oesophageal- closing of upper oesophageal sphincter. Peristaltic waves carries bolus downwards into oesophagus.
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44
Q

How is muscle in the oesophagus distributed?

A

Upper 1/3 - voluntary striated muscle, under control of somatic nerves.
Lower 2/3 - smooth muscle under control of the parasympathetic nervous system

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45
Q

What may cause dysphasia?

A

Neurological flaw
Luminal obstruction
External obstruction

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46
Q

What facters help prevent gastro-oesophageal reflux?

A

Functional sphincter formed formed from smooth muscle of distal oesophagus
Diaphragm
Intra-abdominal oesophagus which gets compressed when intra-abdominal pressure rises
Mucosal ‘rosette’ at cardia
Acute angle of entry of oesophagus

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47
Q

What is the function of the greater omentum?

A

Limits infection, forms localised abscess instead of peritiniumitis (which has a very poor mortality)

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48
Q

What can a weakened linea alba result in?

A

Divarication of recti (not a hernia)

Common in woman who have had many kids

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49
Q

Why is a rectum sheath hernia so very painful?

A

No room for blood to accumulate as muscle is entrapped in the linea alba

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50
Q

How does one tell the difference between a patent urachus and a patent vitellointestinal duct?

A

Inject dye

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51
Q

What is exampholos?

A

Umbilical defect. Visceral covered by peritoneum and amnion

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52
Q

What is referred pain?

A

Pain received at a site distant from the site causing the pain

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53
Q

What is somatic referred pain?

A

Pain caused by a noxious stimulus to the proximal part of a somatic nerve that is perceived in the distal dermatome of the nerve. (Brain thinks pain is coming from the end of the nerve/where nerve goes to)

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54
Q

What is visceral referred pain?

A

In the thorax and abdomen, visceral afferent pain fibres follow sympathetic fibres back to the same spinal segments that gave rise to the preganglionic sympathetic fibres.
CNS perceives visceral pain as coming from the somatic portion of the body supplied by the relevant spinal cord segments

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55
Q

What may cause visceral pain?

A 
Iscaemia
Abnormally strong muscle contraction
Inflammation
Stretch
NOT touch, burning, cutting, crushing
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56
Q

What may cause referred left shoulder pain?

A

Diaphragmatic irritation, e.g. By ruptured spleen, ectopic pregnancy, perforated ulcer…

Only left shoulder as liver is in the way of the right side of the diaphragm

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57
Q

Define hernia

A

A protrusion of part of the abdominal contents beyond the normal confines of the abdominal wall/its containing cavity.

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58
Q

What 3 components make up a hernia?

A

The sac
The contents of the sac
The coverings of the sac

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59
Q

What constitutes the sac of a hernia?

A

A pouch of peritoneum

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60
Q

What constitutes the contents of a hernia?

A

Anything found in abdominal cavity (commonly loop of bowel, omentum)

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61
Q

What constitutes the coverings of a hernia?

A

Layers of the abdominal wall through which the hernia has passed

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62
Q

List 4 weaknesses in the abdominal wall

A

Inguinal canal
Femoral canal
Umbilicus
Any previous incisions

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63
Q

List the borders of the inguinal canal

A

Roof - transversalis fascia, internal oblique muscle, transversus abdominus
Posterior wall - transversalis fascia
Anterior wall - aponeurosis of the external oblique, internal oblique muscle
Floor - inguinal ligament, lacunar ligament

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64
Q

What are the 2 openings to the inguinal canal? Where are they found?

A

Deep (internal) ring - found above the midpoint of the inguinal ligament, lateral to the epigastric vessels.
Superficial (external) ring - marks the end of the inguinal canal, lies just superior to the pubic tubercle

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65
Q

How is the deep (internal) ring of the inguinal canal created?

A

Ring is created by the transversalis fascia which invaginates to form a covering of the contents of the inguinal canal.

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66
Q

How was the superficial (external) ring of the inguinal canal formed?

A

Formed by the evagination of the external oblique, which forms another covering of the inguinal canal contents

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67
Q

What does the inguinal canal contain?

A

In men, the spermatic cord, to supply and drain the tested.

In women, the round ligament of uterus traverses through the canal

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68
Q

What usually prevents structures potentially entering the inguinal canal?

A

The wall are usually collapsed

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69
Q

What does the superficial (external) ring of the inguinal canal contain to prevent the ring from widening?

A

Intercrural fibres, which run perpendicular to the aponeurosis of the external oblique

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70
Q

What are the borders of the femoral canal?

A

Medical - lacunar ligament
Lateral - femoral vein
Anterior - inguinal ligament
Posterior - pectineal ligament, superior ramus of pubic bone, pectineus muscle

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71
Q

What is processus vaginalis?

A

Embryological developmental out pouching of the parietal peritoneum. Precedes the testes in their descent down within the gubernaculum. Closes, remaining portion around the testes becomes the tunica vaginalis

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72
Q

What is the gubernaculum?

A

Condensed band of mesenchyme that links inferior portion of testes (gonad) to labioscrotal swelling

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73
Q

Which border of the inguinal canal contains the deep ring?

A

Posterior wall

Transversalis fascia

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74
Q

Which border of the inguinal canal contains the superficial ring?

A

Anterior wall

Aponeurosis of external oblique

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75
Q

What are the 2 types of inguinal hernia?

A

Indirect and direct

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76
Q

Describe an indirect inguinal hernia

A

Passes through deep inguinal ring. Goes through inguinal canal, and out superficial inguinal ring. Then, depending on where processus vaginalis was obliterated, can potentially descend into the scrotum
Superior source to femoral vessels

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77
Q

Describe an direct inguinal hernia

A

Bulges through Hesselbach’s triangle, generally in the vicinity of the superficial inguinal ring

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78
Q

What are the boundaries of Hesselbach’s triangle/inguinal triangle?

A

Medial - lateral margin of rectus sheath (also called linea semilunaris)
Superolateral border - inferior epigastric vessels
Inferior border - inguinal ligament

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79
Q

What differentiates between a direct or an indirect inguinal hernia?

A

Direct - lateral/superior to inferior epigastric vessels

Indirect - medial/inferior to inferior epigastric vessels

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80
Q

What is omphalocele?

A

Abdominal contents herniated into umbilical cord. Has peritoneal covering.

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81
Q

Where does an epigastric hernia occur?

A

Occurs through the linea alba, between xiphoid process and umbilicus.

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82
Q

What is an ‘incarcerated’ hernia?

A

Stuck, irreducible (can’t be pushed back through)

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83
Q

What is a ‘strangulated’ hernia?

A

Blood supply is disrupted, can lead to necrosis

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84
Q

What is a diaphragmatic hernia?

A

Defects in diaphragm may allow any viscus to herniate into chest

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85
Q

What are the basic functions of the stomach?

A

Disinfection
Short term store of food
Continue digestion
Disrupt food

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86
Q

What type of epithelium lines stomach walls?

A

Columnar epithelium

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87
Q

What type of epithelium lines the oesophagus?

A

Stratified squamous

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88
Q

What are gastric pits?

A

Little ‘holes’ in the stomach wall with gastric glands at their base

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89
Q

What types of cells are present in the stomach?

A

Mucous, parietal, chief, G-cells

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90
Q

What is special about the stomachs smooth muscle compared to the rest of the GI tract?

A

Extra oblique layer of muscle

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91
Q

Describe the action of the upper stomach muscle

A

Sustained contractions, creates basal tone

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92
Q

Describe the action of the lower stomach muscle

A

Strong peristalsis mixes contents. Coordinated movements, every 20s or so, moving contents proximal to distal

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93
Q

How does the shape of the stomach effect its contents passage through it?

A

Funnel shape accelerates food towards duodenum. Sphincter there only lets liquid chyme through, lumps are left behind for further digestion

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94
Q

How does vagally mediated relaxation of the stomach as it fills aid it’s ability to act as a store of food?

A

Allows food to enter stomach without raising intra-gastric pressures too much
Prevents reflux of contents during swallowing
Gastric mucosal foods (rugae) allows distension

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95
Q

What enables distension of the stomach?

A

Gastric mucosal folds (rugae)

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96
Q

What functions does stomach acid have?

A

Disinfects stomach contents
Helps untraveled proteins
Activates proteases (pepsinogen to pepsin)

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97
Q

What secretions are secreted by the stomach wall?

A

HCl, mucus, HCO3-, pepsinogen, intrinsic factor

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98
Q

What does a parietal cell in the stomach secrete?

A

HCl and intrinsic factor

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99
Q

What does a G cell in the stomach secrete?

A

Gastrin

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100
Q

What does a enterochromaffin like cell (ECL) in the stomach secrete?

A

Histamine

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101
Q

What does a Chief cell in the stomach secrete?

A

Pepsinogen

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102
Q

What does a D cell in the stomach secrete?

A

Somatostatin

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103
Q

What does a Mucous cell in the stomach (surface and neck) secrete?

A

Mucous

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104
Q

Where are the majority of gastric glands located?

A

At the base of gastric pits

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105
Q

What does the cardia of the stomach predominantly secrete?

A

Mucus

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106
Q

What does the fundus/body of the stomach predominantly secrete?

A

Mucus, HCl, pepsinogen

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107
Q

What does the pylorus of the stomach predominantly secrete?

A

Gastrin, somatostatin

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108
Q

What effect does gastrin have parietal cells?

A

‘Normal’ stimulus

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109
Q

What effect does histamine have parietal cells?

A

‘Amplifier’ (alone wouldn’t have much effect)

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110
Q

What effect does ACh have parietal cells?

A

Increases secretion (from nervous system, especially when combined with histamine)

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111
Q

What stimulates gastrin secretion by G cells in the Antrum of the stomach?

A 
Peptides/amino acids in stomach lumen
Vagal stimulation (acetylcholine, gastrin-releasing peptide GRP)
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112
Q

What inhibits HCl production?

A 
Low pH (i.e. When food, which acts as buffer, leaves stomach) activates D cells, which secrete somatostatin, which inhibits G cells (& ECL cells).
Stomach distension reduces, reduced vagal activity
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113
Q

What does somatostatin do in the stomach?

A

Inhibits G cells (& ECL cells), reducing gastrin and histamine secretion.

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114
Q

Describe the process of HCl production in the stomach

A 
Water is split (H+ and OH-)
H+ moved into stomach lumen
Cl- moved into stomach lumen
CO2 combines with OH- forming HCO3-, which is moved into the bloodstream (alkaline tide)
Very energy intensive!
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115
Q

What is the proton pump used to produce HCl in the stomach?

A

H+/K+ ATPase

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116
Q

What are the 3 phases of digestion?

A

Cephalic (pre-stomach)
Gastric (stomach)
Intestinal (post-stomach)

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117
Q

Describe the cephalic portion of digestion

A

Smelling, tasting, chewing, swallowing, parasympathetic stimuli. Direct stimulation of parietal cell by vagus nerve. Stimulation of G cells by vagus nerve (GRP) released)
Anticipation of food - increases gastric motility

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118
Q

Describe the gastric phase of digestion

A

Distension of stomach stimulates vagus nerve, which then stimulates parietal and G cells. Presence of amino acids and small peptides stimulates G cells. Food acts as buffer, removes inhibition on gastrin production. Enteric NS and gastrin causes smooth muscle contractions

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119
Q

Describe the intestinal phase of digestion

A

Chyme initially stimulates gastrin secretion - partially digested proteins detected in duodenum, short phase. Soon overtaken by inhibition of G cells. Presence of lipids activates enterogastric reflex - reduces vagal stimulation. Chyme stimulates CCK and secretin (helps suppress secretion)

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120
Q

What are the defences the stomach has to protect against digesting itself?

A

Mucins and HCO3-, release by surface mucosal cells, neck cells in gastric glands. Forms thick alkaline viscous layer that adheres to epithelium
High turnover of epithelial cells
Prostaglandins - maintains mucosal bloodflow, supplying epithelium with nutrients

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121
Q

What things might breach the stomach defences?

A

Alcohol - dissolves mucus layer
Helicobacter pylori - chronic active gastritis
NSAIDs - inhibits prostaglandins

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122
Q

What does breaches in stomach defences lead to?

A

Gastritis (inflammation), ulceration, reflux disease

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123
Q

What pharmacological intervention could you use if the stomachs defences have been breached?

A 
H2 blockers (cimetidine, ranitidine)
Proton pump inhibitors (omeprazole)
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124
Q

What are the stomachs defences against its gastric acid?

A

Mucins/HCO3-: released by surface mucus cells in gastric glands. Forms thick alkaline viscous layer that adheres to epithelium (epithelial surface maintained at higher pH)
High turnover of epithelial cells
Postaglandins: maintains mucosal bloodflow, supplying epithelium with nutrients

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125
Q

List some things which might breach the stomachs defences to its own gastric acid

A

Alcohol - dissolves mucus layer
Helicobacter pylori - chronic active gastritis
NSAIDs - inhibits postaglandins

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126
Q

What can breaches in the stomachs defences against its own gastric acid lead to?

A

Gastritis (inflammation), ulceration, reflux disease

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127
Q

What pharmacological interventions can be used when the stomachs defences to its own gastric acid are compromised?

A 
H2 blockers (cimetidine, ranitidine)
Proton pump inhibitors (omeprazole)
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128
Q

Name a proton pump inhibitor

A

Omeprazole

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129
Q

Name a H2 blocker

A

Cimetidine

Ranitidine

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130
Q

What is dyspepsia?

A

Upper GI symptoms

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131
Q

What does GORD stand for?

A

Gastro oesophageal reflux disease

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132
Q

What are the symptoms of GORD?

A

Gastro oesophageal reflux disease

Heartburn, cough, sore throat, dysphagia

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133
Q

What can cause GORD?

A

Gastro oesophageal reflux disease
Lower oesophageal sphincter problems, delayed gastric emptying (raised intracellular-gastric pressure), hiatus hernia, obesity

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134
Q

What are some problems that may occur with GORD?

A

Oesophigitis, strictures, Barrets oesophagus (metaplasia of squamous epithelium to columnar), increased risk of developing Adenocarcinoma

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135
Q

What metaplasia occurs in barrets oesophagus?

A

Metaplasia of squamous epithelium to columnar

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136
Q

What treatment can be used to GORD?

A

Lifestyle modifications
Pharmacological (antacids, proton pump inhibitors, H2 antacids)
Surgery (rare)

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137
Q

What is the most common cause of gastritis?

A

H. Pylori infection

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138
Q

What could cause chronic gastritis?

A

Bacterial - H pylori infection
Autoimmune - antibodies to gastric parietal cells, can lead to pernicious anaemia
Chemical/reactive - alcohol, NSAIDs, bile reflex (minimal inflammation)

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139
Q

What are the symptoms of chronic gastritis due to H pylori infection?

A

Asymptomatic, or pain, nausea, vomiting ect. Others may develop due to complications e.g. Peptic ulcers, Adenocarcinoma

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140
Q

What are the symptoms of chronic gastritis due to autoimmunity?

A

Anaemic symptoms (tired, breathless…), glossitis, anorexia, neurological symptoms

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141
Q

What is glossitis?

A

Inflammation of the tongue

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142
Q

What is peptic ulcer disease?

A

Defects in gastric/duodenal mucosa. Must extend through muscularis mucosa.

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143
Q

Where is peptic ulcer disease most common?

A

1st part of duodenum, lesser curve of the stomach

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144
Q

What are the normal defence mechanisms against peptic ulcer disease?

A

Mucus, bicarbonate, prostaglandins, epithelial renewal, adequate mucosal bloodflow (can remove acid that diffuses through injured mucosa)

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145
Q

What are the symptoms of peptic ulcer disease?

A

Epigastric pain (sometimes back pain), burning/gnawing following meals, bleeding, anaemia, satiety early, weight loss

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146
Q

What is functional dyspepsia?

A

Symptoms of ulcer disease, but no physical evidence of organic disease

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147
Q

How might peptic ulcer disease be diagnosed?

A

Upper GI endoscopy, biopsies (benign/malignant ulceration, H-pylori), urease breath test, errect CXR (perforation), bloodtests (anaemia)

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148
Q

How would you treat peptic ulcer disease caused by H-pylori?

A

Eradicate organism - triple therapy:
PPI
Clarithromycin
Amoxicillin

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149
Q

What treatment might you use for peptic ulcer disease?

A

Stop NSAIDs
Endoscopy for bleeding ulcers (and follow up for gastric ulcers)
PPIs

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150
Q

What sort of bacteria is helicobacter pylori?

A

Helix shaped
Gram negative
Microaerophilic
Has a flagellum

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151
Q

What is a microaerophilic organism?

A

Requires O2 to survive, but prefers a lower concentration of O2 than present normally in the atmosphere

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152
Q

How does h pylori produce urease?

A

Converts urea to urease and ammonium

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153
Q

How does h pylori survive the stomachs low pH?

A

Converts urea to urease and ammonium, using the NH4+ to produce a less acidic cloud in which it lives within the mucus layer of stomach

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154
Q

How does h pylori damage the stomach?

A 
Releases cytotoxins
Direct epithelial injury
Ammonia produced is toxic to epithelia 
Promotes inflammation response
Possibly degrades mucus layer
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155
Q

What is the effects of H pylori dependent on?

A

Location of colonisation within the stomach

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156
Q

What are the effects of H pylori if it colonises in the antrum?

A

Home of G cells
Increased gastrin secretion (or decreased D cell activity)
Increased parietal cell acid secretion, duodenal epithelium metaplasia - colonisation of duodenum - duodenal ulceration

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157
Q

What are the effects of H pylori if it colonises in the body of stomach?

A

Atrophic effect. Gastric ulcer - leads to intestinal metaplasia, dysplasia, cancer.

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158
Q

What is Zollinger-Ellison syndrome?

A

No beta islet cell gastrin secreting tumour of the pancreas. Can be a part of MEN1. Proliferation of parietal cells - lots of acid production. Severe ulceration of the stomach and small bowel. Abdominal pain, diarrhoea

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159
Q

What is stress ulceration?

A

Symptoms of gastritis/ulceration following severe burns, raised intercranial pressure, sepsis, severe trauma, multiple organ failure ect.

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160
Q

How might stomach cancer present?

A

Dysphagia, anorexia, malaena, weight loss, nausea/vomiting, virchovs nodes enlarged
Has to be quite large before symptoms present

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161
Q

What are some risk factors for stomach cancer?

A

Male, H-pylori, dietary factors, smoking

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162
Q

What sort of cancer is the majority of stomach cancers?

A

Adenocarcinomas

Small number of lymphomas, carcinoid, stromal

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163
Q

How might one diagnose stomach cancer?

A

Bloods, upper GI endoscopy, CT, Rx, surgery, chemotherapy, radiation

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164
Q

What osmotic state is the chyme that enters the duodenum from the stomach?

A

Hypertonic

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165
Q

What corrects the hypertonicity of chyme leaving the stomach?

A

Osmotic movement of large quantities of water across the permeable duodenal wall

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166
Q

How is the acidity of the chyme leaving the stomach corrected?

A

The addition of alkali secreted by pancreas and liver, derived from the excess HCO3- added to the blood as a result of gastric acid secretion

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167
Q

Why is chyme leaving the stomach hypertonic?

A

Lots of solute from food dissolved in gastric juice - the stomach wall is largely impermeable to water (so it can’t dilute chyme)

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168
Q

What proportion of the pancreas is exocrine?

A

~90%

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169
Q

What is the result of sympathetic stimulation of the pancreas?

A

Inhibition

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170
Q

What is the result of parasympathetic stimulation of the pancreas?

A

Stimulation

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171
Q

What hormone can stimulate a pancreatic acinus?

A

Cholecystokinin CCK

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172
Q

What proteases does the pancreas secrete?

A

Trypsin(ogen)
Chymotrypsin
Elastase
Carboxypeptidase

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173
Q

How are enzymes formed in the pancreas?

A

Formed on ribosomes on RER, packaged via golgi apparatus into zymogen granules, which are released by exocytosis with appropriate stimulus - parasympathetic/CCK

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174
Q

What might be found in the bloodstream if the pancreas is damaged?

A

Enzymes (notably amylase)

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175
Q

What are zymogen granules?

A

Membrane bound vesicles containing zymogens (inactive precursors to enzymes). Avoids digestion of pancreas

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176
Q

What do duct cells in the pancreas do to help produce alkali?

A

Secrete alkali by pumping HCO3- actively from extracellular fluid into lumen. H+ ions expelled across basolateral membrane using energy derived from the inward movement of Na+. This combines with HCO3- to generate CO2 which enters the cells, and reacts with H2O to form HCO3- and H+.

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177
Q

What osmotic state is the exogenous excretions from the pancreas?

A

Isotonic

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178
Q

What does secretin do?

A

Controls secretion of enzymatic juice from pancreas

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179
Q

Where is secretin produced?

A

S cells in the jejunum in response to acidity of the jejunal contents

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180
Q

What potentiates the action of secretin?

A

CCK

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181
Q

What happens to the concentration of HCO3- in pancreatic secretions at faster flow rates?

A

Increased secretion of HCO3-, so increased conc. of HCO3-

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182
Q

List some of the livers functions

A

Metabolism, detoxification, plasma protein production, secretion of bile

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183
Q

Approximately how much bile is secreted by the liver a day?

A

~250ml

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184
Q

What are the gut related functions of the liver?

A

Secretion of bile acids and alkaline juice

Excretion of bile pigments - especially bilirubin

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185
Q

What is the chief functioning cell of the liver?

A

Hepatocytes (~80% of mass of liver)

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186
Q

Describe hepatocytes

A

Very active at producing proteins/lipids for export. Contain lots of rough/smooth ER and stacks of golgi membranes. Contain lots of glycogen.

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187
Q

What is the structural unit of the liver?

A

A lobule

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188
Q

What is a liver lobule?

A

Structural unit of the liver - hexagon surrounding a central vein which drains the blood.
Blood from hepatic arteries and portal vein enters vessels on the periphery of lobule, and flows through sinusoids lined by hepatocytes to the central vein.

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189
Q

Describe the flow of blood in a hepatic lobule

A

Blood from hepatic arteries and portal vein enters vessels on the periphery of lobule, and flows through sinusoids lined by hepatocytes to the central vein.

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190
Q

Where is bile formed?

A

In the canaliculi, then flows towards the periphery where it then drains into bile ducts

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191
Q

What are the 2 components of bile?

A

Bile acid dependent fraction (secreted by cells lining the canaliculi) - bile salts, cholesterol, bile pigments
Bile independent fraction (secreted by cells lining the intro-hepatic bile ducts, stimulated by secretin) - alkaline

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192
Q

Where is the bile acid dependent fraction of bile secreted?

A

Cells lining the canaliculi

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193
Q

Where is the bile acid independent fraction secreted from?

A

Cells lining the intro-hepatic bile ducts

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194
Q

What stimulates secretion of the bile acid independent fraction?

A

Secretin

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195
Q

What are the 2 main bile salts?

A

Cholic acid

Chenodeoxycholic acid

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196
Q

What are the 2 main bile salts derivatives of?

A

Cholesterol

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197
Q

What amino acids are conjugated with bile salts in bile?

A

Glycine or taurine

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198
Q

How are bile salts composed in bile?

A

Conjugated to amino acids, then travel in bile in micro particles (micelles made up of bile acids, cholesterol and phospholipids)

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199
Q

What are bile pigments?

A

Secretory products conjugated in the liver and secreted in bile (major one is bilirubin - breakdown product of haemoglobin)

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200
Q

What is the function a micelle?

A

A vehicle to carry hydrophobic molecules through an aqueous medium e.g. Products of lipid digestion (cholesterol, monoglycerides, free fatty acids)

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201
Q

What happens to micelles?

A

Diffuse with products of the brush border of epithelial cells, can be released slowly and diffuse into epithelial cells.
Once inside, fats are reconstituted into triglycerides, phospholipids, cholesterol ect, and re expelled as chylomicrons (facilitate transport of fat in the lymphatic system from gut to systemic veins)

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202
Q

What do chylomicrons do?

A

facilitate transport of fat in the lymphatic system from gut to systemic veins

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203
Q

What is around the surface of a chylomicron?

A

Apoproteins around the external surface

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204
Q

Why can chylomicrons only enter lymph capillaries (lacteal)?

A

Too large to enter ‘normal’ capillaries

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205
Q

How do chylomicrons leave the basement membrane of gut epithelial cells?

A

Exocytosis

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206
Q

Where do chylomicrons renter vascular circulation?

A

Via thoracic duct

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207
Q

Where are bile acids absorbed?

A

The terminal ileum (apart from a small proportion deconjugated by bacterial action)

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208
Q

How are bile acids returned to the liver?

A

Absorbed in the terminal ilium and returned via portal vein

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209
Q

How are losses of bile acids replaced?

A

Hepatic synthesis

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210
Q

What does the gall bladder do?

A

Concentrates bile (removes H2O/ions), reducing its volume

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211
Q

What is a consequence of the gall bladder concentrating bile?

A

Increasing the risk of gallstones, which can move into neck of gall bladder/biliary tree, causing painful biliary colic or obstruction (followed by inflammation and infection)

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212
Q

How is bile released?

A

Smooth muscle contraction, stimulated by CCK (cholecystokinin) released from the duodenum

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213
Q

What stimulates smooth muscle contraction, leading to the secretion of bile?

A

Stimulated by CCK (cholecystokinin) released from the duodenum

214
Q

How can cirrhosis lead to portal hypertension?

A

Fibrous tissue surrounds intrahepatic vessels, impeding circulation

215
Q

List some physical adaptations of the GI system against toxins/infection

A

Gastric acid, saliva, sight, smell, memory…

216
Q

What does saliva contain to help defend against infection?

A

Lysozyme, lactoperoxidase, complement, IgA, polymorph

217
Q

Approximately how much gastric juice is produced each day?

A

2.5l

218
Q

What is the lowest pH gastric juice can be?

A

0.87

219
Q

What is achlorhydria?

A

Low (or absent) production of hydrochloric acid in gastric secretions of the stomach and other digestive organs

220
Q

What are patients with achlorhydria more susceptible to?

A

Infection from shingellosis, cholera, salmonella, C. difficile

221
Q

What might cause achlorhydria?

A

Drugs e.g. PPI, H2 antagonists

222
Q

What is an AAFB?

A

Acid and Alcohol Fast Bacterium

223
Q

Of what clinical relevance is mycobacterium tuberculosis being AAFB?

A

It is resistant to gastric acid, therefore washings can be used to collect the bacteria for diagnostic purposes

224
Q

List some pathogens that are resistant to gastric acid?

A

Enteroviruses e.g. Hep A, polio, coxsackie,
Helicobacter pylori
Mycobacterium tuberculosis

225
Q

What must bacteria be able to resist in or due to survive in the small intestine?

A

Bile (detergents), proteolytic enzymes, lack of nutrients, anaerobic environment, shedding of epithelial cells and rapid transit (peristalisis)

226
Q

Is the small bowel normally sterile?

A

Yes

227
Q

What is the main role of the colon?

A

Water absorption

228
Q

Is the colon an aerobic or anaerobic environment?

A

Anaerobic

229
Q

What protects the colonic epithelium from its contents?

A

Mucus layer

230
Q

What is eosinophillia?

A

A raised number of eosinphils

231
Q

What might cause eosinophillia?

A

Asthma, hay fever or parasite infections (more common in Africa)

232
Q

What do mast cell granules contain?

A

Histamine

233
Q

What is a consequence of gut infections that activate complement?

A

Recruitment of mast cells, which release histamine. This causes vasodilation and increased capillary permeability - and can result in massive fluid loss e.g. In cholera

234
Q

Where are most mast cells located in the body?

A

Lungs, liver and spleen.

Monocytes are in the blood circulating, become macrophages in tissue

235
Q

Where does all of the venous drainage of the gut from the duodenum down end up?

A

In the hepatic portal vein, into the hilum of the liver

236
Q

What is the portal system?

A

2 capillary systems in series - the hepatic portal system and the hypothalamo-hypophyseal portal system

237
Q

What is a kupffer cell?

A

A macrophage in the liver

238
Q

What might cause liver failure?

A

Viral hepatitis, alcohol, overdose of drugs such as paracetamol, halothane, industrial solvents, mushroom poisoning

239
Q

What does liver failure lead to increased susceptibility of?

A

Bacterial and fungal infections, toxins, drugs and hormones. High mortality

240
Q

How is ammonia produced in the body?

A

By colonic bacteria and deamination of amino acids.

241
Q

What can increased blood ammonia cause?

A

Encephalopathy (bad, very difficult to treat)

242
Q

Why may there be increased blood ammonia in liver failure?

A

Failure to clear ammonia via urea cycle

243
Q

What can portal venous hypertension lead to?

A

Portosystemic shunting, and therefore toxin shunting. Portosystemic shunting leads to oesophageal varices, haemorrhoids, and capt medusa

244
Q

What can portosystemic shunting lead to?

A

Oesophageal varices, haemorrhoids, and capt medusa

245
Q

What are the adaptive cellular defences of the GIT?

A

B-lymphocytes - produce antibodies including IgA and IgE that are particularly effective against extracellular microbes
T-lymphocytes - are directed against Intracellular organisms

246
Q

What is the adaptive defences of the GIT lymphatic tissue?

A

Gut associated lymphoid tissue (GALT) is diffusely distributed, but also nodular at the tonsils, at payers patches and at the appendix

247
Q

What is MALT ?

A

Mucosal associated lymphoid tissue

248
Q

What is ileocaecal lymphatic tissue there for?

A

Patches at terminal ileum in case of reflux of bacteria in colon to ileum

249
Q

What is a common cause of right iliac fossa pain in children that might be mistaken for appendicitis?

A

Mesenteric adenitis - caused mostly by adenovirus/coxsackie virus

250
Q

What is the result of lymphoid hyperplasia at the appendix base?

A

Obstructed outflow of appendix, stasis and infection - appendicitis

251
Q

When is purulent appendicitis commoner?

A

During epidemics of chickenpox in children

252
Q

What might cause obstructive appendicitis

A

Fecolith (worm)

Lymphoid hyperplasia

253
Q

What might cause intestinal/hepatic ischaemia?

A

Arterial disease, systemic hypotension, intestinal Venus thrombosis

254
Q

What can intestinal/hepatic ischaemic lead to?

A

Over whelming sepsis and rapid death

255
Q

Why can liver disease present in many different ways?

A

Many different functions of the liver

256
Q

List some possible symptoms of liver disease

A

Bleeding/poor clotting, oedema/ascites/ankle swelling, skin irritation, jaundice, abdominal pain, jaundice, asymptomatic, encephalopathy, nausea, vomiting….

257
Q

What must happen to bilirubin in order for it to get into the liver?

A

Must be attached to albumin

258
Q

What happens to biliruben once if gets into the liver?

A

Biliruben is then conjugated to make it water soluble - urobilingen which is a bile pigment

259
Q

Describe how pre-hepatic jaundice occurs

A

Increased biliruben load to the liver e.g. Haemolytic anaemia. Liver can’t conjugate all this amount fast enough, any unconjugated biliruben remains in blood circulation

260
Q

Describe the process by which hepatic jaundice might occur

A

Decreased rate of conjugation of biliruben e.g. Injury/damage to the liver
Defects in conjugation e.g. Gilbert’s syndrome
Unconjugated biliruben and conjugated bacteria

261
Q

Describe the process by which post hepatic jaundice occurs

A

Obstruction to bile drainage into duodenum e.g. Gallstones, pancreatic cancer, intrahepatic obstruction to drainage (hepatocyte swelling)
Biliruben in the bile is conjugated (water soluble), cannot leave biliary drainage system, refluxes into circulation but doesn’t make it into stool (which is thus pale and floats)

262
Q

What do LFTs give an indication of?

A

Traditional ones give an indication of liver damage, rather than function

263
Q

What 4 enzymes might leak from the liver if damaged?

A

Alanine Aminotransferase ALT
Aspartate Aminotransferase AST
Alkaline Phosphodiesterase ALP
Gamma-glutamyltransferase GGT

264
Q

In what cells might alkaline phosphodiesterase ALP be found in?

A

Cells lining the bile ducts

265
Q

How would you take a true measure of liver function?

A

Measuring proteins synthesised by liver e.g. Albumin, clotting factors

266
Q

What precisely is hepatitis?

A

Inflammation of the liver

267
Q

What is steatosis, steatohepatitits?

A

Fatty liver

268
Q

What might cause steatohepatitis?

A

Alcoholic-related fatty liver disease

Non-alcoholic related fatty liver disease

269
Q

What might cause hepatitis (liver inflammation)?

A

Viral e.g. Hep A, B, C…
Autoimmune
Drugs e.g. Alcohol, paracetamol
Hereditary disorder e.g. Haemochromatosis and Wilson’s disease
Fatty liver disease (alcoholic and non-alcoholic)
Malignancy (metastases, or primary malignancy)

270
Q

What is the most common kind of primary malignancy present in the liver?

A

Hepatocellular carcinoma

271
Q

What can chronic liver disease lead to?

A

Cirrhosis
Inflammation of the liver (chronic or recurrent e.g. Alcohol abuse)
Ongoing liver cell damage/necrosis
Nodular regeneration and fibrosis (scarring). Architectural change to liver
Increased resistance to blood flow
Portal hypertension (clinical features ascites, and porto-systemic shunting)

272
Q

Where are the major sites for porto-systemic anastomoses (distended engorged veins can appear here in portal hypertension)

A

Oesophageal varies - left gastric, oesophageal branches of azygous
Anorectal varies - superior rectal vein, middle and inferior rectal vein
Caput medusa - paraumbilical veins, superior and inferior epigastric vein

273
Q

What can portal hypertension cause along with distended engorged veins at sites of porto-systemic anastomoses?

A

Ascites

Splenomegaly

274
Q

What does the biliary tree do?

A

Provides drainage system for bile

275
Q

What can abnormal contractions of the gall bladder lead to?

A

Precipitation of bile constituents, leading to gall stones

276
Q

What can gallstones be constituted of?

A

Mixed (most common)

Pure cholesterol or pigment (calcium bilirubinate)

277
Q

What can the of impaction of gallstones in biliary tree cause?

A

Biliary colic and/or cholecystitis

278
Q

What are the symptoms of impaction of gallstones in biliary tree?

A

Nausea/vomiting
Abdominal pain (intermittent Vs constant)
Jaundice
Fever and RUQ tenderness (cholecystitis)

279
Q

What imaging might you use to identify symptomatic gallstones?

A

Ultrasound

280
Q

What is acute pancreatitis?

A

Damage to acinar cells releases enzymes, inflammation of pancreatic tissue

281
Q

What is the most common cause of pancreatitis?

A

Gallstones, alcohol

282
Q

How does pancreatitis present?

A

Severe pain, vomiting, hypotension. Significant mortality.

283
Q

What is the treatment of pancreatitis?

A

Supportive - analgesics and fluids

284
Q

What is the majority of pancreatic cancer?

A

Ductal adenocarcinoma (90%)

285
Q

What is the major risk factor for pancreatic cancer?

A

Smoking

286
Q

What are the symptoms of pancreatic cancer?

A 
Initially symptomless, then develop:
Obstructive jaundice (head of pancreas sooner than body or tail)
Pain (referred to back)
Weight loss
Vomiting
Malabsorption
Diabetes
287
Q

What constitution is chyme in the intestines?

A

Isotonic and neutral

288
Q

What is the function of the intestines?

A

Absorb nutrients, water and electrolytes

289
Q

What is the paracellular route?

A

The gaps between cells

290
Q

What are plicae circulares?

A

Permanent circular folds in the intestine

291
Q

How is the intestine adapted to have a large surface area?

A

Mucosa folded into villi. Surface is covered in micovilli. Plicae circulares.

292
Q

What is the ‘unstirred layer’ in the intestine?

A

Layer of contents formed by the brush border where nutrients meet and react with enzymes secreted by the enterocytes, so completing digestion prior to absorption

293
Q

What type of cells make up the intestinal epithelia?

A

Enterocytes and goblet cells (mucus producing)

294
Q

What makes up an intestinal gland (crypt)?

A

Stem cells at base, migrate to surface, maturing as they migrate. Also enteroendocrine glands, paneth cells (part of the immune system)

295
Q

What are paneth cells a part of?

A

The immune system

296
Q

What constitutes a micelle?

A

Outer bile salts, inner lipids

297
Q

How many sugars chained together can the body absorb?

A

Only single sugars!

298
Q

How is glucose absorbed?

A

Alongside Na+

299
Q

Where does final breakdown of molecules occur?

A

In the brush border, by ‘brush border hydrolases’

300
Q

What are the ‘goal’ monosaccharides which the body can absorb? The end points of carbohydrate digestion

A

Glucose
Fructose
Galactose

301
Q

What sort of carbohydrate is starch?

A

Polysaccharide

302
Q

What sort of carbohydrate is lactose?

A

Disaccharide

303
Q

What sort of carbohydrate is sucrose?

A

Disaccharide

304
Q

What bonds do alpha amylases cleave?

A

Alpha 1,4 bonds of straight chain amyloses

305
Q

What can alpha amylases yield?

A

Cleave alpha 1,4 bonds of straight chains amyloses to yield glucose/maltose in a straight chain, or alpha limit dextrins in branched chains

306
Q

What bonds does isomaltase break?

A

Branching points, alpha 1,6 bonds

307
Q

What does isomaltase yield?

A

Breaks branching point alpha 1,6 bonds to yield glucose

308
Q

What is starch digested into?

A

Glucose

309
Q

What is maltose digested into?

A

Glucose (x2!)

310
Q

What breaks maltose down into glucose?

A

Maltase

311
Q

What are alpha dextrins broken down into?

A

Glucose

312
Q

What breaks down alpha dextrins?

A

Isomaltase

313
Q

What is lactose broken down by?

A

Lactase

314
Q

What is lactose broken down into?

A

Glucose and galactose

315
Q

What breaks down sucrose?

A

Sucrase

316
Q

What is sucrose broken down into?

A

Glucose and fructose

317
Q

Where does sodium glucose transporter 1 move contents from/to?

A

Glucose lumen to cell

318
Q

Where does GLUT 2 move glucose from/to?

A

Cell to blood

319
Q

Where does GLUT 5 move fructose from/to?

A

Into cell

320
Q

What does GLUT 5 transport?

A

Fructose

321
Q

How does Na/K ATPase aid absorption of glucose?

A

It’s activity on basolateral membrane maintains a low Intracellular Na+

322
Q

What must happen first before glucose can bind to sodium glucose transporter 1?

A

Na+ must bind to transporter

323
Q

What does GLUT 2 transport?

A

Glucose

324
Q

Where does GLUT 2 transport glucose from/to?

A

Out of enterocyte. Diffuses down gradient into capillary blood.

325
Q

How does fructose enter enterocytes?

A

Facilitated diffusion via GLUT 5

326
Q

What is the principle behind oral rehydration therapy?

A

Uptake of Na+ generates osmotic gradient - water follows. Glucose uptake stimulates Na+ uptake - mixture of glucose and salt will stimulate maximum water uptake.

327
Q

What constituents of proteins can be absorbed?

A

Amino acids, dipeptides and tripeptides

328
Q

What cells release pepsinogen in the stomach?

A

Chief cells

329
Q

What converts pepsinogen to pepsin?

A

HCl

330
Q

What, with regards to proteins, is enters the intestine from the stomach?

A

Oligopeptides/amino acids

331
Q

What converts trypsinogen (released by the pancreas) to trypsin?

A

Enteropeptidase

332
Q

What effect does trypsin have on other pancreatic proteases?

A

Activates them! E.g. Chymotrypsinogen –> chymotrypsin

333
Q

What sort of peptide bonds does trypsin cleave?

A

Peptide bonds next to basic amino acids

334
Q

What sort of peptide bonds does chymotrypsin cleave?

A

Peptide bonds next to aromatic amino acids

335
Q

What sort of peptide bonds does carboxypeptidase cleave?

A

Cleaves c-terminal amino acids

336
Q

What does exopeptidase do?

A

Breaks bonds at ends of polypeptide to produce dipeptides or individual amino acids e.g. Carboxypeptidase

337
Q

What does endopeptidase do?

A

Breaks bonds in middle of polypeptide to produce shorter polypeptides e.g. Trypsin, chymotrypsin, elastase

338
Q

How are amino acids absorbed?

A

Via sodium-amino acid cotransporters

Different ones for different amino acids - neutral, basic, acidic…

339
Q

How are most protein products ingested?

A

As dipeptides/tripeptides (not AA)

340
Q

What transports dipeptides/tripeptides?

A

H+ co-transporter peptide transporter 1 (PepT1)

341
Q

What happens to dipeptides/tripeptides once they have been transported inside the intestinal cell?

A

They are converted to amino acids by cytosolic peotidases

342
Q

What is the basis for Na+/water uptake?

A

Na+ is moved by active transport out of cell on basolateral membrane. Na+ diffuses into epithelial cells. Water can now also move into intracellular space.

343
Q

How is Na+ taken up in the small intestine?

A

Na+ is cotransported

344
Q

How is Na+ taken up in the large intestine?

A

Na+ channels, induced by aldosterone (aquaporin)

345
Q

What happens to Ca2+ uptake when Ca2+ intake is low?

A

Active transcellular absorption. Enters cell via facilitated diffusion. Ca2+ATPase removes Ca2+ from basolateral membrane. This process requires Vit. D (calbindin), stimulated by PTH.
Ca2+ enters cells by facilitated diffusion and is then expelled actively across the basolateral membrane.

346
Q

Approximately how much as a percentage of ingested Ca2+ is normally absorbed?

A

~10%

347
Q

What does the active absorption of Ca2+ by Ca2+ ATPase require?

A

Vitamin D

348
Q

How is Ca2+ absorbed when Ca2+ levels are normal/high?

A

Passive paracellular absorption

349
Q

In which state is most iron absorbed?

A

Fe2+

350
Q

What is important in the absorption of iron?

A

Gastric acid - iron is cotransported with H+ across apical membrane

351
Q

Describe what happens to iron absorption when iron levels in the body are low

A

Iron binds to transferrin secreted by enterocytes. Once in cell, Fe2+ is liberated and exported to blood, where it again binds to transferrin.

352
Q

Describe what happens to iron absorption when iron levels in the body are high

A

Iron contained in ferritin complexes (trapped in cell). Lost when enterocyte is replaced

353
Q

Which vitamins are water soluble?

A

C, B

354
Q

How are water soluble Vitamins absorbed?

A

Mostly absorbed by Na+ cotransport (Vit C/B)

355
Q

How is Vitamin B12 absorbed?

A

Absorbed in the terminal ileum, bound to intrinsic factor, secreted by gastric parietal cells.

356
Q

What could is a possible consequence of gastritis/terminal ileal removal?

A

Pernicious anaemia due to Vit B12 deficiency (essential for erythropoiesis)

357
Q

Describe the motility of the small intestine

A

Slow, caudal progression of food. Intestinal pacemakers have higher frequency proximally, driving slow caudal progression of contents via segmentation - back and forth, mixing of contents, does not propel contents along intestine.

358
Q

Describe the distribution of pacemakers in the small intestine

A

Higher frequency proximally, driving slow caudal progression of contents via segmentation. Firing of pacemakers decreases caudally (~12times/min in duodenum to ~8times/min in terminal ilium).

359
Q

How do pacemakers drive segmentation in the small intestine?

A

Firing of pacemakers decreases caudally (~12times/min in duodenum to ~8times/min in terminal ilium). Pacemakers sends activity through the nerve plexuses which cause contraction of the smooth muscle at intervals along its length. This separates intestine into segments where muscle is not contracted - mixing contents (gradient helps also).

360
Q

What are ‘haustra’?

A

The large intestine is naturally divided up into segments, known as hausta, as circular muscles are more complete than the longitudinal, which have been reduced to the taenia coli.

361
Q

What is ‘haustral shuttling’?

A

The mechanism by which colonic contents are agitated and propelled along in the proximal colon.

362
Q

What does haustral shuttling do?

A

Mixes contents, allowing most of the remaining water to be absorbed, forming faecaes

363
Q

What is a mass movement?

A

Occurs 1-3 times a day. Can move contents rapidly from transverse colon to rectum. Often triggered by eating (gastro-colic reflex). Initiated by stretch receptors in the rectum.

364
Q

How does a mass movement occur?

A

Coordinated peristalsis like movement from transverse colon to rectum.

365
Q

What gives the urge to dedicate?

A

Faeces in the rectum (which is usually empty)

366
Q

Describe the process by which a mass movement occurs voluntarily

A

Enhanced contraction of rectal smooth muscle, relaxation of the smooth muscle internal anal sphincter, and skeletal muscle external sphincter, combined with expiration against a closed glottis and abdominal muscle contraction to increase infra abdominal pressure, thus expelling faeces.

367
Q

What happens if voluntary dedication doesn’t occur?

A

Sacral reflexes will eventually trigger it to involuntarily trigger dedication as rectal pressure rises.

368
Q

What is inflammatory bowel disease?

A

A group of conditions characterised by idiopathic inflammation of the GI tract, effecting gut function

369
Q

What are the 2 common types of inflammatory bowel disease?

A

Chrons disease and ulcerative colitis

370
Q

How might inflammatory bowel disease present extra-intestinally?

A

Extra-intestinal problems, e.g. MSK pain, arthritis, skin (erythema nodosum/pyoderma gangrenosum/psoriasis), liver/biliary tree - primary sclerosing cholangitis, eye problems

371
Q

What causes inflammatory bowel disease?

A

Genetic - 1st degree relative increased risk. Gut organisms (altered interaction). Immune response -trigger e.g. Antibiotics, infections, diet, smoking.

372
Q

How might crohns disease present?

A

Tender mass, mild perinatal inflammation/ulceration, low grade fever, mildly anaemic

373
Q

What is the pathology of Crohn’s disease?

A

Hyperaemia, mucosal oedema, descrete superficial ulcers, deeper ulcers, transmural inflammation, thickening of bowel wall, narrowing of lumen. Cobblestone appearance (if severe), fistulae - bowel/bladder/vagina/skin. Granuloma formation

374
Q

What investigations might you do for Crohn’s disease?

A

Bloods (anaemia), CT/MRI scans (bowel wall thickening, obstruction, extramural problems). Barium enema/follow through (used less. Strictures/fistulae). Colonoscopy.

375
Q

How might ulcerative colitis present?

A

Multiple stools with mucus in. Mild lower abdominal pain/cramping. No perinatal disease, normal temp.

376
Q

What pathological changes might be seen in ulcerative colitis?

A

Chronic inflammatory infiltrate of lamina propria. Crypt abscesses, crypt distortion. Decreased goblet cells. Pseudopolyps. Loss of haustra

377
Q

What investigations would you do for ulcerative colitis?

A

Bloods - anaemia, serum markers. Stool cultures. Plain abdominal radiographs. Barium enema (mild cases only). CT/MRI - less useful in diagnosing uncomplicated UC. Colonoscopy

378
Q

Would there be rectal involvement in Crohn’s disease and/or ulcerative colitis?

A

Crohns - no

UC - yes

379
Q

Would there be gross bleeding in Crohn’s disease and/or ulcerative colitis?

A

Crohns - 25%

UC - Yes

380
Q

Would there be perianal disease in Crohn’s disease and/or ulcerative colitis?

A

Crohns - 75%

UC - rare

381
Q

Would there be fistula formation in Crohn’s disease and/or ulcerative colitis?

A

Crohns - yes

UC - no

382
Q

Would there be malnutrition in Crohn’s disease and/or ulcerative colitis?

A

Crohns - potentially

UC - no

383
Q

Would there be transmural inflammation in Crohn’s disease and/or ulcerative colitis?

A

Crohns - yes

UC - rare

384
Q

Would there be granulomas in Crohn’s disease and/or ulcerative colitis?

A

Crohns - up to 75%

UC - no

385
Q

Would there be fibrosis in Crohn’s disease and/or ulcerative colitis?

A

Crohns - common

UC - no

386
Q

Would there be crypt abscesses in Crohn’s disease and/or ulcerative colitis?

A

Crohns - rare

UC - common

387
Q

Would there be mucosal involvement in Crohn’s disease and/or ulcerative colitis?

A

Crohns - skip lesions

UC - continuous

388
Q

Would there be aphthous ulcers in Crohn’s disease and/or ulcerative colitis?

A

Crohns - yes

UC - rare

389
Q

Would there be linea ulcers in Crohn’s disease and/or ulcerative colitis?

A

Crohns - yes

UC - rare

390
Q

Would there be friable mucosa in Crohn’s disease and/or ulcerative colitis?

A

Crohns - rare

UC - yes

391
Q

Would there be cobblestone appearance in Crohn’s disease and/or ulcerative colitis?

A

Crohns - Yes (severe cases)

UC - no

392
Q

Would there be fistula in Crohn’s disease and/or ulcerative colitis?

A

Crohns - yes

UC - no

393
Q

Would there be narrowing in Crohn’s disease and/or ulcerative colitis?

A

Crohns - yes

UC - rare

394
Q

List some features of Crohn’s disease, that are not present in ulcerative colitis

A

Fistula formation, malnutrition, granulomas, fibrosis, skip lesions, cobblestone appearance

395
Q

In what disease might a ‘lead pipe colon’ (with no visible ridges) be seen?

A

Ulcerative colitis

396
Q

What is the medical treatment of inflammatory bowel disease?

A

Stepwise approach
1 - Aminosalicylates (sulfasalazine 5-ASA preparations, for flares and remission)
2 - Corticosteroids (prednisolone - flares only)
3 - Immunomodulators (azathioprine - fistulas/maintenance of remission)

397
Q

What is the surgical treatment of Crohn’s disease?

A

Not curative, strictures/fistulas. As little bowel removed as possible.

398
Q

What is the surgical treatment of UC?

A

Curable (colectomy). Inflammation not settling. Precancerous changes, toxic megacolon.

399
Q

Where re the majority of the bacteria in our bodies?

A

In the colon

400
Q

How may bacteria be classified?

A 
Cocci/bacilli
Gram positive/gram negative
Aerobic/anaerobic obligate/facultative
Spore forming
Pili/slime - ability to stick to a surface
401
Q

What are obligate aerobes?

A

Bacteria that must have oxygen to survive

402
Q

Give some examples of obligate aerobes

A

Pseudomonas

Mycobacterium TB

403
Q

What are obligate anaerobes?

A

Die in the presence of O2.

404
Q

Give some examples of obligate aerobes

A

Bacteroides fragilis

Clostridium (although not its spores)

405
Q

Where are anaerobic areas of the GIT?

A

Mouth - on tongue deep in taste buds, fluid films including biofilm in between teeth, gingival crevice areas and people with periodontal disease in periodontal pockets
Small bowel
Colon

406
Q

How do human colonic bacteria help their host?

A

Synthesise and excrete vitamins that are absorbed by host e.g. Vit K, b12, thiamine and other B vitamins
Prevent colonisation by pathogens
Kill non-indigenous bacteria
Stimulate development of MALT (in caecum and peters patches)
Stimulate production of natural antibiotics

407
Q

What are some consequences of ‘germ free’ animals?

A

Vitamin deficiencies, especially Vit K and Vit B12
Increased susceptibility to infectious disease
Poorly developed immune system, especially in GI tract
Lack of natural antibody, or natural immunity to bacterial infection

408
Q

List some aerobic, gram positive cocci

A

Staphylococci
Streptococci
Enterococci

409
Q

List some gram negative aerobic cocci

A

Neisseria meningitidis

Neisseria gonorrhoeae

410
Q

List a gram positive anaerobic bacilli

A

Clostridia (tetani, perfringens, difficile)

411
Q

List some gram positive aerobic bacilli

A

Corynebacterium diphtheria
Bacillus anthrax
Lactobacillus
Mycobacterium TB

412
Q

Is mycobacterium TB gram positive or negative?

A

Positive

413
Q

List some gram negative, aerobic, non-enteric bacilli

A

Haemophilus influenzae
Bordetella pertussis
Brucella

414
Q

What is the causative organism of whooping cough?

A

Bordetella pertussis

Gram-negative, aerobic

415
Q

List some gram negative anaerobic enteric bacilli

A

Bacteriodes fragilis

416
Q

List some gram negative, aerobic, enteric bacilli

A 
E. coli
Pseudomonas
Proteus
Klebsiella
Salmonella
Shigella 
Vibrio cholera
Campylobacter
Helicobacter pylori
417
Q

Why can bites cause nasty/fatal infections?

A

Mouth contains many anaerobes

418
Q

What might appear in the mouth if an individual is particularly unwell/malnourished/immunocompromised?

A

Mouth bacteria can cause tissue destruction; noma/cancrum oris

419
Q

What causes oral thrush?

A

Candida albicans

420
Q

What might induce oral thrush?

A 
Oral antibiotics (which kill off other bacteria)
Candida albicans is causative organism
421
Q

What are the risk factors for oral thrush (caused by Candida albicans)?

A

Newborns, antibiotics, diabetes, inhaled steroids, immune deficiency

422
Q

What is the treatment for oral thrush?

A

Amphotericin lozenges

Nystatin suspension

423
Q

What is dental caries/gingivitis?

A

The teeth are colonised by the mouth bacteria plus streptococcus mutans (can cause plaque)

424
Q

What is ludwigs angina?

A

Swollen, sore throat, usually streptococcal. Laryngeal oedema can be fatal.

425
Q

Whee are the 3 sites used for MRSA screening swabs?

A

Nose, threat, perineum

426
Q

What sort of organisms are found in the nose normally?

A

Staphylococcus and streptococcus amongst others

427
Q

What bacteria are usually found in the throat?

A 
Strep viridans
Strep pyogenes
Strep pneumoniae
Staphylococci
Neisseria meningitidis
Haemophilus influenzae
Lactobacilli
Corynebacterium diptheriae 
Candida albicans
428
Q

How might strep viridans cause infection of prostheses?

A

Non-pathogenic throat commensal. May enter blood stream (bacteraemia) during teeth brushing, general anaethesia, dental procedures. May stick to prostheses such as heart valves, vascular grafts, orthopaedic implants ect. and cause infection. Prostheses don’t have the ‘antibacterial sticking’ armour cells do.

429
Q

Why are prostheses particularly susceptible to infection?

A

Prostheses don’t have the ‘antibacterial sticking’ armour cells do.

430
Q

What is bacteraemia?

A

Bacteria in blood but are rapidly cleared from the bloodstream (by liver/spleen macrophages). Asymptomatic.

431
Q

What is septicaemia?

A

Bacteria in bloodstream and are not cleared. Multiply in the bloodstream. Sepsis symptoms develop. (Bacteria are proliferating, not just passing). High mortality.

432
Q

What causes tonsillitis?

A

70% viral - adenovirus, rhinovirus, epstein-barr

30% bacterial - mainly strep. Pyogenes (beta haemolytic)

433
Q

What proportion of people infected with H pylori develop gastric ulcers/duodenal ulcers?

A

Only 10-20%

434
Q

What proportion of colonic bacteria are anaerobes?

A

95-99% of over 100 species

435
Q

What species of bacteria of particularly prevalent in the colon?

A

Bacteroides and clostridium species

436
Q

List types of bacteria that are always present in the colon

A

Bacteroides (fragilis, oralis, melaninogenicus)
Eschericia coli
Enterococcus faecalis

437
Q

List some common gram negative bacteria of the colon

A 
Pseudomonas
Proteus
Klebsiella
Salmonella
Shigella
Vibrio cholera
Campylobacter
438
Q

List a common gram positive colonic bacterium

A

Lactobacillus

439
Q

What precautions might you take when performing ‘dirty’ surgery (e.g. On the colon)

A

Prophylactic antibiotics to reduce risk of wound infection. Needs to cover anaerobes, gram negative bacilli and gram positive cocci.

440
Q

What does prophylactic antibiotics for intestinal surgery need to cover?

A

Needs to cover anaerobes, gram negative bacilli and gram positive cocci.

441
Q

What antibiotics might you use for prophylactic treatment of intestinal surgery?

A

Metroniadazole - kills anaerobes
Along with a broad spectrum antibiotic e.g. Gentamicin or cephalosporin.
Alternatively is co-amoxiclav augmentin - but this is a penicillin (allergy!)
Adhere to local policy

442
Q

What mortality is faecal peritonitis?

A

50% mortality even in young fit people.

443
Q

Can bacteriodes survive O2 on perianal skin?

A

Nope

444
Q

Can E. coli survive the O2 on perineal skin?

A

Yes

445
Q

Can enterococcus faecalis survive the O2 on perineal skin?

A

Yes

446
Q

Can lactobacillus survive the O2 on perineal skin?

A

Yes

447
Q

Where is lactobacillus a normal commensal?

A

Vagina

448
Q

How does lactobacillus aid its host?

A

Converts glycogen to lactic acid. Acidic environment prevents other bacteria and candida from colonating vagina

449
Q

What is a potential complication of lactobacillus acidophilus?

A

Broad spectrum antibiotic treatment kills lactobacilli and can lead to vaginal thrush

450
Q

What is the commonest causative organism of UTI?

A

E. Coli (~75%)

451
Q

What organisms generally cause UTI

A

Commonest - E. Coli (75%)
Next common - enterococcus faecalis
Thereafter various gram negative enteric bacilli (klebsiella, proteus, pseudomonas)

452
Q

What does clostridia tetani cause?

A

Tetanus

453
Q

What does clostridia perfringens cause?

A

Gas/wet gangrene

454
Q

What are the classical symptoms of tetenus?

A

‘Lock jaw’, opisthotonus

Acts like acetylcholine, causing muscle spasm

455
Q

Who does tetanus generally infect news days?

A

Neonate

Old people without a recent vaccine update

456
Q

How does clostridium perfringens cause gas/wet gangrene?

A

Anaerobic digestion of glucose, producing ethanol and CO2 (fluid plus gas)

457
Q

What is the treatment of gas/wet gangrene, as caused by clostridium perfringens?

A

Remove effected flesh/amputate ASAP

458
Q

What are the clinical features of oesophageal carcinoma?

A

Progressive dysphagia, weight loss

459
Q

What investigations might you do for oesophageal carcinoma?

A

Endoscopy, biopsy, barium

460
Q

What are the possible types of oesophageal carcinoma?

A

Squamous cell carcinoma (most common type)

Adenocarcinoma (associated with Barrett’s oesophagus, lower 1/3)

461
Q

What is the prognosis of oesophageal carcinoma?

A

Advanced disease usually at presentation
Direct spread though oesophageal wall
Only 40% resectable, 5% 5yr survival
Many patients have a tube passed though tumour to facilitate swallowing

462
Q

What is the prognosis of gastric cancer?

A

Poor, 20% 5yr survival

463
Q

What is gastric cancer associated with?

A

Gastritis

Commoner in blood group A

464
Q

What are the clinical features of gastric cancer?

A

Symptoms often vague. Epigastric pain, vomiting, weight loss

465
Q

What investigations might you do for gastric cancer?

A

Endoscopy, biopsy, barium

466
Q

What microscopic features might be present in gastric cancer?

A

Fungating, ulcerating, infiltrative (linitis plastica) early.
Intestinal - varying degree of gland formation. Diffuse - single cells and small groups, signet ring cells.

467
Q

What are the features of early gastric cancer?

A

Confined to mucosa/submucosa, good prognosis

468
Q

What are the features of advanced gastric cancer?

A

Further spread, 10% 5yr survival

Common in the U.K.

469
Q

Where does gastric cancer generally spread to?

A

Direct - lymph nodes, liver, trans-coelomic (peritoneum, ovaries)

470
Q

What are the treatment options for gastric cancer?

A

Surgery, chemotherapy, herceptin

471
Q

What is H. Pylori associated with?

A

Association of chronic inflammation with cancer

472
Q

What is the commonest form of GI lymphoma?

A

Gastric lymphoma

473
Q

Describe gastric lymphoma

A

Starts as a low grade lesion, strong association with h pylori. Eradication of H. Pylori may lead to regression of tumour. Prognosis better than gastric cancer.

474
Q

Describe GI stromal tumours

A

Uncommon. Derived from interstitial cells of cajal c-kit. Specific targeted treatment - imatinib. Unpredictable behaviour - pleomorphism, mitosis, necrosis

475
Q

What types of tumours may be present in the intestine?

A

Adenomas, adenocarcinoma, polyps, anal carcinoma

476
Q

What are the features of an adenoma of intestines?

A

Macroscopic - sessile or pedunculated
Microscopic - variable degree of dysplasia
Behaviour - definitive malignant potential
Incidence - increases with age in western populations, genetic syndrome.

477
Q

What is familial adenomatous polypossis?

A

Autosomal dominant (chromosome 5). Thousands of adenomas by 20s - high risk of cancer.

478
Q

What is gardeners syndrome?

A

Similar to FAP. Bone and soft tissue tumours

479
Q

Describe the adenoma carcinoma sequence

A

Synchronous lesions, metachronous lesions, adenomas with invasion

480
Q

What are the macroscopic features of adenocarcinoma?

A

60-70% rectosigmoid. Fungating (especially right side), stenotic (especially left side)

481
Q

What are the microscopic features of colorectal adenocarinoma?

A

Moderately differentiated adenocarinoma, occ mucinous, occ signet ring cell type

482
Q

Describe the spread of colorectal adenocarcinoma

A

Direct through bowel wall to adjacent organs e.g. Bladder. Via lymphatics to mesenteric lymph nodes. Via portal system to liver.

483
Q

Describe dukes staging for adenocarcinoma

A

A - confined to bowel wall
B - through wall, lymph nodes clear
C - lymph nodes involved
C1/C2 - highest node clear/involved

484
Q

How is a k-ras mutation relevant for treatment of colorectal cancer?

A

Enables treatment with cetuximab (only works if pathway activated)

485
Q

How is an 18q DCC mutation relevant to colorectal cancer?

A

18q DCC - deleted in colorectal cancer

486
Q

What lifestyle factors might predispose a person to colorectal cancer?

A

Low residue diet - noxious substances are in the bowel longer, so are in contact with the bowel wall longer. Slow transit time, high fat intake.

487
Q

What is the outcome of colorectal cancer?

A

Survival decreases with increased dukes staging. Liver metastases common in advanced disease. Chemotherapy (palliative), resection of liver deposits, local radiotherapy.

488
Q

Where does colorectal cancer often metastase to?

A

The liver

489
Q

List some large intestinal tumours (other than colorectal adenocarcinoma)

A

Carcinoid tumour - rare endocrine tumour, difficult to predict behaviour
Lymphoma - rare, may be primary or spread from elsewhere
Smooth muscle/stromal tumours - rare and unpredictable

490
Q

Describe carcinoma of the pancreas

A

Early symptoms vague. Diagnosis is usually delayed. Weight loss, jaundice, trousseau’s sign. Imaging enables diagnosis 2/3 in head (firm pale mass). Cut surface, necrotic, haemorrhagic, cystic. May infiltrate adjacent structures e.g. Spleen.

491
Q

What can insulinoma (islet cell tumour) cause?

A

Hypoglycaemia

492
Q

What can glucagonoma (islet cell tumour) cause?

A

Characteristic skin rash

493
Q

What can VIPoma (islet cell tumour) cause?

A

Werner Morrison syndrome

494
Q

What can gastrinoma (islet cell tumour) cause?

A

Zollinger-Ellison syndrome

495
Q

List some benign tumours of the liver

A

Hepatic adenoma
Bile duct adenoma/hamartoma
Haemangioma

496
Q

List some malignant (primary) tumours of the liver

A

Hepatocellular carcinoma
Cholangiocarcinoma
Hepatoblastoma

497
Q

What are the available mechanisms to image the GIT?

A 
Plain X-Rays - abdominal AXR, chest CXR
Contrast studies - barium swallow/enema/meal + follow through. Water soluble contrast studies
Ultrasound
Cross sectional imaging - CT, MRI
Angiography
498
Q

When might someone request an AXR?

A

Acute abdominal pain. Small or large bowel obstruction. Acute exacerbation of IBD. Renal colic (although CT better)

499
Q

List the features of an AXR

A

ABC

Air, bowel, calcification/bones+stones

500
Q

When is bowel visible on an AXR?

A

If gas filled, or gas and fluid filled (need low density contrast to show up)

501
Q

Describe how the transit time effects ability to see parts of the bowel on an AXR

A 
Slow colon (faeces and gas) visible
Medium stomach (fluid and lots of gas) visible
Fast small bowel (fluid) not so visible
502
Q

Describe what the small bowel looks like on an AXR

A

Central position, often not seen (fast transit time, fluid filled). Valvulae conniventes. Gross entire wall thin.

503
Q

Descibe what the large bowel looks like on an AXR

A

Peripheral position. Frames small bowel loop. Haustra. Faeces and gas, slow transit time.
Transverse colon can hang down to pelvis. Sigmoid colon can loop and be long.

504
Q

What might show up on an AXR with regrants to the bowel?

A

Mucosal thickening, featureless colon, bowel wall oedema. Acute or chronic changes.

505
Q

What is the rule of 3s for when analysing an AXR?

A 
Of note if:
Small bowel obstruction >3cm
Large bowel obstruction >3cm
Competent ileocaecal valve (caecum>9cm)
Incompetent ileocaecal valve
506
Q

What should you be able to recognise on an AXR

A 
Paralytic ileum
Volvulus
Toxic megacolon
'The rule of 3s'
Small bowel obstruction >3cm
Large bowel obstruction >3cm
Competent ileocaecal valve (caecum>9cm)
Incompetent ileocaecal valve
507
Q

How might a small bowel obstruction present?

A

Vomiting (early), distension (mild), absolute constipation (late), colicky pain

508
Q

What might cause a small bowel obstruction?

A

Adhesions, hernias (inguinal, femoral, incisional), tumours, inflammation

509
Q

How might a large bowel obstruction present?

A

Vomiting (late, faeculant), distension (significant), paint absolute constipation

510
Q

What might cause a large bowel obstruction?

A

Colorectal carcinoma, diverticular stricture, hernia, volvulus, pseudo-obstruction

511
Q

What is a volvulus?

A

Twisting around the mesentery. Encased bowel loop dilates (perforation, ischaemia). Common in sigmoid (uncommon in caecal, anatomical defect)

512
Q

Where is volvulus common?

A

Sigmoid colon. Starts in LIF. Coffee bean sign towards RUQ. Dilation of proximal bowel - obstructed.

513
Q

What is a toxic megacolon?

A

Acute deteriation with UC or colitis. Colonic dilation. Oedema pseudopolyps. Toxic implies patient is unwell!

514
Q

What is a ‘leadpipe colon’?

A

Featureless colon, loss of haustra. Ulcerative colitis - chronic inflammation.

515
Q

Describe what ‘thumb printing’ is in an AXR

A

Oedematous thickened haustra. Thickened wall. Active inflammation, often UC. Can see in other processes with oedema.

516
Q

What other abnormalities might be present in an AXR?

A

Stones, organs/masses, calcification (pancreatitis, vasculature nodes), bones, artefacts, foreign body

517
Q

What might cause perforation - pneumoperitpneum?

A

Peptic ulcer, diverticulum, tumour, obstruction, trauma, latrogenic-laparoscopy 3-6 days.

518
Q

What would be the initial imaging of choice for a bowel perforation/pneumoperitoneum?

A

CXR (air collects under the diaphragm so is easy to see

519
Q

When might you use a contrast study for the GIT?

A

Used to define hollow viscera - barium/water soluble

520
Q

List some common GI contrast studies

A

Swallow, meal, small bowel enema/follow through, enema

521
Q

Describe an abdominal CT?

A

Computerised axial tomography. High dose radiation. Gives good spatial resolution (poor constant resolution Vs MRI). Use of IV or oral contrast. Can be done to produce a virtual colonoscopy.

522
Q

Describe an abdominal MRI

A

Magnetic resonance imaging. No radiation. Good spatial and contrast resolution. Time consuming.

523
Q

Describe an abdominal USS

A

Use of sound waves to generate image (above human audible range frequency). Cheap compared to CT and MRI. Portable, so fast. However highly user dependent.

524
Q

What is a GI angiography?

A

Catheter into artery + contrast

525
Q

What is odynophagia?

A

Painful swallowing

526
Q

What is colicky pain every 2-3mins likely to be?

A

Small bowel obstruction

527
Q

What is colicky pain every 10-15mins likely to be?

A

Large bowel obstruction

528
Q

What sort of pain is caused by an ulcer?

A

Dull, burning

529
Q

What causes malaena?

A

Upper GI bleeding

530
Q

What is alkalaemia?

A

Blood pH of 7.45 or greater

531
Q

What is acidaemia?

A

Blood pH of 7.35 or less

my esa 3 (6 decks)

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