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Kofi: Pure clinical conditions 2 > GI > Flashcards

GI Flashcards

1
Q

What are the implications of the external environment?

A
  • You have to ingest food, digest food, absorb food and egest what not needed
  • Stop toxin/infection entering
  • Very thin epithelium
  • Need water in gut lumen for chemical reactions and cant lose to external world
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2
Q

What are the waste products that are not ingested in the gut?

A
  • Bilirubin

- Cholesterol

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3
Q

What are the areas of mechanical disruptions in the GI tract?

A
  • Mouth/Teeth

- Stomach

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4
Q

What are the muscular actions of the stomach?

A
  • Vigorous contractions of the stomach cause food to be liquefied.
  • Upper area create basal tone (tonic)
  • Lower area has powerful peristaltic contractions that effectively grind food and mix stomach contents. Every 20 seconds proximal to distal
  • Has additional inner oblique layer of muscle
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5
Q

How does the stomach resist rise in intraluminal pressure?

A

Eat quicker that digest

  • Stomach can distend due to rugae (temporary folds)
  • Receptive relaxation occurs to allow food to enter stomach without raising intragastric pressure to much and prevents reflux of stomach content during swallow
  • Vagally stimulated relaxation
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6
Q

What is the purpose of the colon?

A
  • Contents are only evacuated several times a day
  • Acts as a temporary storage
  • Gastrocolic reflex
  • Mass movements to rectum which is normally empty
  • Final water absorption
  • Final electrolyte absorption
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7
Q

What are the contents of the stomach for chemical digestion?

A
  • Acid

- Pepsin

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8
Q

What are the defences of the GI tract?

A
  • Saliva
  • HCl
  • Liver (kupffer cells)
  • Peyer’s Patches (Lymphoid follicles, Submucosa, mainly in terminal ileum)
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9
Q

What are broad functions of the oesophagus?

A
  • Rapid transport of bolus to stomach through thorax
  • Upper oesophageal sphicnter prevents air from entering GI tract
  • Lower oesophageal sphincter prevents reflux into the oesaphagus
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10
Q

What are broad functions of the the stomach?

A
  • Storage facility
  • Produce chyme
  • Infections control (HCL)
  • Secrete intrinsic factor (Vit B12)
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11
Q

What are broad functions of the the stomach?

A
  • Storage facility (receptive relaxation)
  • Produce chyme
  • Infections control (HCL)
  • Secrete intrinsic factor (Vit B12)
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12
Q

What are the broad functions of the duodenum?

A
  • Start of small intestine
  • Neutralisation/osmotic stabilisation of chyme (HCO3 secretions)
  • Digestion wrapping up (pancreatic secretions, bile)
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13
Q

What are broad functions of Jejunum/ileum?

A
  • Final digestion
  • Nutrient absorption mainly in the jejunum
  • Water/electrolyte absorption mainly in ileum
  • Bile recirculation in ileum
  • B12 absorption in the terminal ileum
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14
Q

What is the structure of the peritoneum?

A
  • Parietal peritoneum in contact with abdomen
  • Visceral in contact with organs
  • Space between parietal and visceral peritoneum with fluid
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15
Q

How is the gut controlled?

A
  • Autonomic nervous system
  • Enteric nervous system
  • Hormones and paracrine
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16
Q

What presynaptic nerves formed by the sympathetic nervous system to supply the Gut?

A
  • Greater splanchnic nerve (T5-T9)
  • Lesser splanchnic nerve (T10-T11)
  • Least (T12)
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17
Q

What is the purpose of the splanchnic nerves?

A

-Synapse with pre-vertebral ganglia
(Coeliac, Renal, superior mesenteric, inferior mesenteric and others)
-Mainly innervate blood vessels
-Generally inhibits GI function
-Post ganglionic fibres extend to myenteric and submucosal plexus and release norepinephrine
-Reduces motility

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18
Q

What are the nerves from he parasymapthic nervous system to the gut?

A
  • Vagus nerve

- Pelvic splachnic nerves (S2-S4)

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19
Q

What does the right and left vagus become in the gut?

A
  • Right vagus becomes posterior vagal trunk

- Left vagus becomes anterior vagal trunk

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20
Q

What is the functions of the parasymapathetic system on the gut?

A
  • Pre ganglionic fibres (long) synapse in walls of the viscera
  • Post ganglionic fibres (short) release Acetylcholine and peptides (GIP and VIP)
  • Innervate smooth muscle/endocrine and secretory
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21
Q

Which parts of the GI tract does the Pelvic nerve innervate?

A
  • Transverse colon

- Anal canal

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22
Q

Which parts of the GI tract does the vagus nerve innervate?

A
  • Oesaphagus

- Transverse colon

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23
Q

What are the features of the enteric nervous system?

A
  • Divisions of the nervous system
  • Can operate completely independently
  • Exists from the oesophagus to anus
  • It has 2 main plexuses: Submucosal and Myenteric
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24
Q

What is another name for the submucosal plexus?

A

-Meissner’s Plexus

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25
Q

What is another name for the myenteric plexus?

A

-Auerbach’s

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26
Q

What is the function of the submucosal and myenteric plexuses?

A

Submucosal

  • Secretions
  • Blood flow

Myenteric
-Motility

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27
Q

What is the route that hormones take in the GI tract?

A
  • Released from endocrine cells
  • Pass into portal circulation
  • Pass through the liver
  • Enter systemic circulation to end up close to their release point
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28
Q

How is Hal production inhibited?

A

Somatostatin

  • Released by D cells in antrum of stomach and pancreas
  • Stimulated by H+ (low pH) on stomach lumen. Food is buffer so when it leaves the stomach pH drops
  • Inhibits G cells
  • Stomach distension reduces due to reduced vagal activity
  • Inhibits histamine release
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29
Q

What is the action of Gastrin in the gut?

A
  • Acts on G cells in antrum of stomach

- Increase gastric acid secretion

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30
Q

What is the action of cholecystokinin?

A
  • I cells in duodenum and jejunum

- Increases pancreatic/gallbladder secretions

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31
Q

What is the control of the release of CCK?

A
  • Stimulated by fat and protein
  • Gall bladder contracts
  • Pancreas stimulated
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32
Q

What is the action of secretin?

A
  • Increases HCO3 from pancreas/gallbladder

- Decrease gastric acid secretion

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33
Q

What is the control of release of secretin?

A
  • Release stimulated by H+ and fatty acids

- Released from S cells in the duodenum

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34
Q

What is the action of GIP?

A
  • Increases insulin

- Decreases gastric acid secretion

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35
Q

What is the control of GIP release?

A
  • Cells in the duodenum and jejunum

- Stimulated by sugars, amino acids and fatty acids

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36
Q

Why does appendicitis present with central abdominal pain initially?

A
  • Visceral peritoneum involved

- Visceral afferents accompany sympathetic motor fibres back to spinal sensory ganglia

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37
Q

Why does pain localise to the Right iliac fossa (suprapubic region)?

A
  • Involvement of the parietal peritoneum
  • Due to somatic sensory pain
  • Pain is localised
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38
Q

Where can visceral pain from foregut, midgut and handout structures be felt?

A

Foregut - Epigastric
Midgut - Periumbilical
Hindgut - Suprapubic/hypogastric

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39
Q

Which muscles in the GI tract are not smooth muscle and instead skeletal muscle?

A
  • Pharynx
  • Upper 1/3 of oesaphagus
  • External anal sphincter (voluntary control)
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40
Q

What are the types of motility that occur in the GI tract?

A

Peristalsis

  • Contraction proximal to contents and relaxation distal
  • Propels contents in one direction

Segmentation

  • Contraction splits contents then releaxes
  • To and fro movement that mix contents

Mass movement

  • Occurs in distal colon
  • Rapid movement of contents into rectum
  • Gastrocolic reflex
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41
Q

What is paralytic ileus?

A

Loss of GI contractility

-Can occur following GI surgery

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42
Q

What is achalasia?

A

Failure of LOS to relax

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43
Q

What is Hirschsprung’s disease?

A
  • Lack of myenteric and submucosal plexus

- Results in function obstruction

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44
Q

What is secreted in the GI tract?

A
  • Water
  • Acid
  • Alkali
  • Enzymes
  • Mucus
  • Waste products
  • Emulsifiers
  • Intrinsic factor
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45
Q

Where do secretion come from in the GI tract?

A
  • Saliva (acini of salivary glands)
  • Gastric (gastric glands)
  • Intestinal (Brunner’s glands, intestinal glands, Goblet cells)
  • Liver (hepatocytes)
  • Pancreas (exocrine pancreas)
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46
Q

What are the purposes of stomach acid?

A
  • Innate barrier to infection
  • Prepares proteins for digestion
  • Activate enzymes
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47
Q

What are the emulsifiers in the GI tract and their purpose ?

A
  • Bile salts
  • Increase surface area of lipids
  • Aids digestion by lipases
  • Allows lipid breakdown products to be transported in the gut
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48
Q

What is the purpose of mucus in the GI tract?

A
  • Protects against chemical damage due to acidic environment in stomach
  • Protects against bacteria in small intestine
  • Habours bacteria in large intestine
  • Lubricates to reduce friction
  • Forms physical barrier against bacterial inflammation
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49
Q

What are the principles of absorption in the GI tract?

A
  • Movement across enterocyte

- Movement paracellularly

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50
Q

How is the large surface in the Gi tract created?

A
  • Plica circulares (Permanent folds in small intestine)
  • Villi
  • Microvilli
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51
Q

What are the effects of disrupting surface area in the gut?

A
  • Diarrhoea
  • Malnutrition
  • Anaemia (Crohn’s, Coeliac)
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52
Q

What is absorbed in the GI tract?

A
  • Nutrients (carbohydrates, proteins, lipids, fat soluble vitamins, Vitamin B12, Bile salts, Ca2+, Fe2+)
  • Electrolytes
  • Water
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53
Q

How is water reabsorbed in the GI tract?

A

Passive
-After a meal, water uptake is driven by nutrients coupled with Na+ (sodium co-transporters)

In between meals
-Na+ and Cl- absorbed (sodium/hydrogen & chloride/bicarbonate exchangers)

In colon
-Additional mechanism so that stool can be desiccated (ENaC)

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54
Q

What are the layers of the gut tube?

A
  • Mucosa
  • Submucosa
  • External muscle layers
  • Serosa
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55
Q

What are the regions of the mucosa?

A

Epithelial layer

  • Selectively permeable barrier
  • Facilitate transport and digestion of food
  • Promote absorption
  • Produce hormones
  • Produce mucus

Lamina propria

  • Lots of lymphoid nodules and macropahes
  • Produces antibodies to protect against bacteria/viral invasion

Muscularis mucosa
-Layer of smooth muscle in different direction to help keep crypt contents dynamic and epithelium in contact with gut contents

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56
Q

What are the contents of the submucosa?

A
  • Contains dense connective tissue, blood vessels, glands, lymphoid tissue
  • Contain submucosal plexus (Meissner’s)
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57
Q

What are the contents inner circular muscle?

A

-Myenteric plexus

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58
Q

What are the contents of the serosa?

A
  • Blood and lymph vessels and adipose tissue

- Continuous with mesenteries

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59
Q

What are the epithelial regions of the gut?

A
  • Stratified squamous in oesaphagus and distal anus

- Everything in between is simple columnar

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60
Q

What is an enterocyte?

A
  • Simple columnar epithelial that absorbs
  • Predominant cell of small intestine and colon
  • One cell thick
  • Has microvilli
  • Blood vessels/lymphatics lie immediately below the basolateral membrane of the enterocyte
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61
Q

What is the purpose of the enterocyte?

A
  • Apical membrane (faces the lumen)

- Basolateral membrane (faces blood vessels)

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62
Q

What is the structure of the goblet cells?

A
  • Has a wide top and pushed down base nucleus
  • Has a terminal bar, mucus droplet and basal nucleus
  • Produces mucus to protect the epithelia against pathogens and keeps some bacteria alive
  • Scattered in between enterocytes in intestinal epithelia
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63
Q

What the defences of the stomach?

A
  • Surface mucus cells line gastric mucosa/gastric pits in stomach and secrete mucus/HCO3 that forms thick alkaline viscous layer that adheres to stomach epithelium acid to protect the stomach and keep the epithelial surface at a higher pH
  • High turnover of epithelial cells to help keep epithelia intact
  • Prostagladins to maintain mucosal blood flow to supply epithelium with nutrients
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64
Q

What are crypts of lieberkuhn (intestinal gland) and what do they contain?

A

Intestinal glands

  • Stem cells
  • Paneth cells
  • Enteroendocrine cells
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65
Q

What is the purpose of the cells in the crypts of lieberkuhn?

A

Stem cells

  • Constantly divide to replace epithelia (2-4 days)
  • Mature as they migrate to surface

Paneth cells

  • Located at base of crypts
  • Secrete antibacterial proteins to protect stem cells

Enteroendocrine cells

  • Secrete hormones to control functions of the gut
  • Hormones such as gastrin, CCK and secretin
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66
Q

What are the effects of inflammatory bowel disease on crypts?

A
  • Crypt alteration
  • Cryptitis (inflammation of wall)
  • Crypt abscess (neutrophils in lumen)
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67
Q

What do the acini glands tend to secrete?

A
  • Serous (+enzymes) secretions
  • Tubules tend to secrete mucous (Brunner’s glands)

*salivary glands can be mixed

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68
Q

What is ulceration in the GI tract?

A
  • Erosion through muscularis mucosae

- Failure of protective merchiasnm such as mucus production

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69
Q

What is coeliac disease?

A
  • Inability to tolerate gliadin found in gluten.
  • Gluten is found in wheat, rye and barley
  • Results in immune response which damages the mucosa leading to poor digestion and malabsorption
  • Causs absence of intestinal villi and causes lengthening of intestinal crypts.
  • Lymphocytes infiltrate epithelium
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70
Q

What are the layers of the abdominal wall?

A
  • Skin
  • Fascia/Fat (superficial and deep)
  • 3X anterolateral muscles
  • Peritoneum
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71
Q

Which muscle is enveloped by the aponeurosis of the lateral muscles?

A

Rectus abdominus

Forms the rectus sheath

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72
Q

What are the 3 anterolateral muscles?

A
  • External oblique
  • Internal oblique, transverse abdominis, Rectus abdominis)
  • Transversalis fascia
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73
Q

What is the arcuate line?

A
  • Lower limit of the posterior layer of rectus sheath
  • Point at which inferior epigastric vessels pierce rectus abdominus
  • Roughly half way between umbilicus and pubic crest
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74
Q

What is mesentery?

A

Double fold of peritoneum that teaches the viscera to the posterior abdominal wall

Contains blood vessels, lymph vessels, nerves and fat

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75
Q

What are the organs that are connected by mesentery?

A
  • Jejenum
  • Ileum
  • Appendix
  • Transverse Colon
  • Sigmoid Colon
  • Rectum
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76
Q

What is the peritoneal ligament?

A

Double fold of peritoneum that connect two viscera together
or

Double fold of peritoneum that connects viscera to the abdominal wall

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77
Q

What are the examples of peritoneal ligaments?

A
  • Gastrocolic ligament (Stomach to transverse colon)
  • Gastrosplenic ligament (Stomach to spleen)
  • Falciform ligament (liver ot anterior abdominal wall)
  • Triangular ligaments (liver to diaphragm)
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78
Q

What are the omenta?

A
  • Double folds of peritoneum
  • Greater omentum hangs off the greater curve of the stomach and folds back up and attaches to the anterior surface of the transverse colon
  • Lesser omentum connects lesser curve of the stomach to the liver
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79
Q

What is the blood supply to the GI tract?

A

Arterial is from branches of the aorta

  • Coeliac trunk
  • Superior mesenteric artery
  • Inferior mesenteric

Venous drainage goes to the liver via the Hepatic Portal Vein
-Portal system

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80
Q

What is the composition of saliva?

A
  • Mostly water (Hypotonic)
  • Rich in potassium and bicarbonate
  • Mucins to help with lubrication
  • Enzymes: Amylase, Lingual lipase
  • Diversity of immune proteins
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81
Q

What are functions of saliva?

A
  • Creation of bolus
  • Initaite process of digestion
  • Oral hygiene
  • Transmitting disease
  • Protection of mouth
  • Speech
  • Solvent for taste
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82
Q

What is xerostomia?

A

-Dry mouth

Can lead to dental cavities, mouth ulcers, bad breath and oral thrush

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83
Q

What are the 3 pairs of salivary glands?

A
  • Parotid gland
  • Sub lingual gland
  • Sub mandibular gland
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84
Q

What is the oral preparatory phase?

A
  • Voluntary
  • Pushes the bolus towards the pharynx
  • Once bolus touches the pharyngeal wall, pharyngeal phase begins
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85
Q

Describe the structure of the oesophagus and outline its functions

A
  • Muscular layers

- Transport of bolus from oral cavity to the stomach by peristalsis

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86
Q

Outline the pharyngeal phase of swallowing?

A
  • Involuntary
  • Soft palate seals of the nasopharynx
  • Pharyngeal constrictors push bolus downwards
  • Larynx elevates closing epiglottis
  • Vocal cords duct to protect the airway and breathing temporarily ceases
  • The upper oesophageal sphincter opens
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87
Q

Outline the anatomical relationships of the oesophagus

A
  • Originates in the neck at 6th cervical vertebrae
  • Sits posteriorly the larynx and trachea
  • Closely related to the aorta (right hand side)
  • Pierces the diaphragm at T10 (oesophageal hiatus)
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88
Q

What are causes of dysphagia?

A

Dysphagia is difficulty swallowing

Causes are

  • Stroke that affect nerves controlling swallowing
  • Oesophageal tumour (solid are a problem)
  • Hardening of muscular layers
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89
Q

Describe the anatomical mechanisms that prevent gastro-oesophageal reflux.

A
  • Lower oesophageal sphincter (diaphragm)
  • Intra-abdominal oesophagus which gets compressed when intra-abdominal pressure rises
  • Mucosal rosette at cardia to prevent back flow
  • Acute angle of entry of oesophagus
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90
Q

Give an overview of the control of saliva production.

A

-Autonomic control
-Mainly parasympathetically controlled to stimulate salivary secretion
-Sympathetic also causes small amounts of saliva
secretion and can also vasoconstrict blood vessels

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91
Q

What is the structure of a salivary cell?

A
  • Acinus line with acinus cells
  • Ductal portion with ductal cells
  • Myoepithelial cells
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92
Q

Outline the production of saliva.

A
  • Acinus produces initial saliva which is isotonic and releases it into the ductal portion
  • Ductal cells modify the initial solution to produce hypotonic saliva.
  • Myoepithelial cells which help move saliva from the structure into the mouth
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93
Q

What is the purpose of kallikrein released in the saliva?

A

-Helps to produces bradykinin to vasodilate in the mouth in periods of maximum activity to allow blood flow to get to salivary glands

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94
Q

How does saliva flow rate affect its modification by duct cells?

A
  • Increased flow rate of saliva results in less modification
  • Decreased flow rate of saliva results in more modification by duct cells

*Bicarbonate gets excreted more at higher flow rates as an exception

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95
Q

How do duct cells form hypotonic saliva?

A
  • Exchanging increased amounts of sodium, chloride from the saliva in the lumen into the cell compared to excreting bicarbonate and potassium back into the lumen.
  • This results in a hypotonic solution
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96
Q

What are the nervous supply for the submandibular and sublingual?

A

-Parasympathetic from the facial nerve

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97
Q

What is the nervous supply fo rate parotid gland?

A
  • Parasympathetic fibres from the glossopharyngeal fibres

- Increases production of saliva

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98
Q

Which drugs could have an effect of the parasympathetic innervation of the salivary glands?

A
  • Anti muscurinic

- Can cause xerostomia

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99
Q

Outline the oesohaphgeal phase of swallowing?

A
  • Involuntary
  • Closure of the upper oesophageal sphincter
  • Peristaltic wave carries bolus downwards into oesophagus
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100
Q

Outline the neural control of swallowing and the gag reflex?

A
  • Mechanoreceptors in wall of pharynx detect the bolus
  • Glossopharyngeal nerve carries sensory impulses to medulla
  • Vagus nerve carries impulses to the Pharyngeal constrictors which contract to cause an effect
  • Pushes the bolus inferiorly

*Gag reflex works the same. Psychological possibly

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101
Q

What are the narrowings found in the oesophagus?

A
  • Tightest narrowing is the junction between the pharynx and oesophagus
  • Second narrowing is when the arch of aorta crosses the oesophagus
  • Third narrowing is when the left main bronchus crosses the oesophagus
  • Final narrowing is when oesophagus passes through diaphragm (T10)
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102
Q

Outline some of the clinical consequences of free gastro-oesophageal reflux.

A

-Barrett’s oesaphagus

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103
Q

Describe the protective mechanisms of the nasal cavity and the larynx during swallowing.

A
  • The nasal cavity is protected by elevation of the soft palate
  • The respiratory tract is protected by elevation of the larynx (which closes epiglottis) and adduction of the vocal cords.
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104
Q

Describe areas of potential weakness in the abdominal wall

A
  • Inguinal canal
  • Femoral canal
  • Umbilicus
  • Previous incisions
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105
Q

What is the inguinal canal and where does it pass in males and females?

A

Oblique passage through lower part of the abdominal wall

Males
-Structures pass through abdomen to testis

Females
-Round ligament goes through Uterus - Labium majus

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106
Q

Distinguish direct and indirect inguinal hernias

A

Indirect

  • Lateral to the inferior epigastric vessels
  • Goes through deep ring, inguinal canal and superficial ring

Direct Inguinal Hernia

  • Bulges through Hesselbach’s triangle
  • Medial to inferior epigastric vessels
  • Goes through the inguinal canal and superficial ring
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107
Q

Where can the deep and superficial ring be found?

A
  • Deep ring in the posterior wall of inguinal canal

- Superficial ring in the anterior wall of inguinal canal

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108
Q

Describe the structure of a hernia

A

Sac - Pouch of peritoneum

Contents of the Sac - Commonly loops of bowel, omentum but other structures as well

Covering of the Sac - Layers of abdominal wall through which the hernia has passed.

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109
Q

What can occur if the processus vaginalis doesn’t close after the gubernaculum causes the testis to descend?

A
  • Inguinal hernia (indirect)

- Scrotal hernia

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110
Q

What are the borders of the inguinal canal?

A

Floor

  • Inguinal ligament
  • Lacunar ligament medially

Roof

  • Internal oblique
  • Transverse abdominus

Posterior wall

  • Transversalis fascia
  • Conjoint tendon medially

Anterior wall
-Aponeurosis of external oblique

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111
Q

Why are femoral hernias more common in females?

A
  • Pelvic anatomy different. Femoral ring entrance is bigger in females
  • Can get easily stuck
  • If Stuck, can lead to strangulation of the hernia due to loss of blood supply. Ischaemia can result.
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112
Q

What are the borders of the femoral canal?

A

Medial border – Lacunar ligament.
Lateral border – Femoral vein.
Anterior border – Inguinal ligament.
Posterior border – Pectineal ligament, superior ramus of the pubic bone, and the pectineus muscle

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113
Q

What is an omphalocele?

A
  • Congenital umbilical hernia
  • Content herniate into umbilical cord
  • Has peritoneal covering
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114
Q

What an acquired infantile hernia?

A
  • Type of umbilical hernia

- Contents herniate through weakness in scar of umbilicus

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115
Q

What is an acquired adult hernia?

A
  • Type of umbilical hernia
  • Herniation through linea alba in region of umbilicus
  • More in females than males
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116
Q

What is an epigastric hernia?

A
  • Occurs through linea alba
  • Occurs between Xiphoid process to umbilicus
  • Usually start with small hernia
  • Chronic straining forces more fat out which can eventually pull peritoneum through
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117
Q

What are symptoms of hernias?

A

Varied. Based around what happens if loops of bowel get trapped

  • Pain
  • Vomiting
  • Sepsis
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118
Q

What cell cover the surface of the stomach and extend into gastric pits/glands?

A
  • Parietal cells
  • Mucous cells
  • Chief cells
  • G cells
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119
Q

How does the stomach continue digestion?

A

Acidic conditions

  • Helps unravel protein
  • Activates proteases (pepsinogen to pepsin)
  • Disinfects stomach contents
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120
Q

What does the stomach secrete?

A
  • HCl
  • Intrinsic factor
  • Mucus/HCO3-
  • Pepsinogen
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121
Q

What are the regions of the stomach proximal to distal?

A
  • Cardia (below LOS)
  • Fundus (Upper region)
  • Body
  • Pylorus
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122
Q

How is HCl production in the stomach controlled?

A

Parietal cells stimulated by

  • Gastrin
  • Histmaine
  • ACh
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123
Q

How is gastrin production controlled?

A

G cells in antrum stimulated by

  • Peptides/amino acid in stomach lumen
  • Vagal stimulation by acetyl choline and GRP
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124
Q

What are examples of things that breach stomach defences?

A
  • Alcohol dissolves the mucus layer
  • Helicobacter pylori which can cause chronic active gastritis
  • NSAIDS inhibit prostaglandin
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125
Q

What is gastrooesophageal reflux disease?

A

-Reflux of stomach contents into the oesophagus

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126
Q

What are the symptoms of gastro-oesophageal reflux?

A
  • Heart burn
  • Cough
  • Sore throat
  • Dysphagia
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127
Q

What are causes of gastro-oesophageal reflux?

A
  • Lower oesophageal problems
  • Delayed gastric emptying
  • Hiatus hernia
  • Obesity
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128
Q

What are complications that arise from gastro-oesophageal reflux disease?

A
  • Barrett’s oesophagus which is metaplasia of squamous epithelium to columnar. Increased risk of developing adenocarcinoma
  • Oesophagitis
  • Strictures
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129
Q

What is the treatment for gastro-oesophageal reflux disease?

A

-Lifestyle modifications

Pharmacological

  • Antacids
  • H2 antagonists (block histamine)
  • Proton Pump Inhibitors

Surgery(rare)

130
Q

What is acute gastritis?

A

Acute mucosal inflammatory process. Caused by:

  • Heavy use of NSAIDS
  • Lots of alcohol
  • Chemotherapy
  • Bile reflux
131
Q

What are the symptoms of acute gastritis?

A

Asymptomatic most of the time but can present with

  • Pain
  • Nausua
  • Vomiting
  • Occasionally bleeding
132
Q

What are the common causes of chronic gastritis?

A

Bacterial
-H pylori infection

Autoimmune

  • Antibodies to gastric parietal cells
  • Can lead to pernicious anemia

Chemical/reactive (minimal inflammation)

  • Chronic alcohol abuse
  • NSAIDS
  • Reflux of bile
133
Q

What are symptoms of chronic gastritis caused by H.pylori?

A

Asymptomatic or similar to acute gastritis

-Symptoms may develop due to complications (peptic ulcers, adenocarcinoma, MALT lymphoma)

134
Q

What are symptoms of chronic gastritis caused by an autoimmune disorder?

A
  • Symptoms of anaemia
  • Glossitis
  • Anorexia
  • Neurological symptoms
135
Q

What is peptic ulcer disease?

A

Defects in gastric/duodenal mucosa that extend through the muscular mucosa
-Commonly in first part of duodenum and lesser curve of the stomach

136
Q

What are the causes of peptic ulcer disease?

A
  • Stomach acid
  • H pylori
  • NSAIDS
  • Smoking
  • Massive physiological stress
137
Q

What are the symptoms of peptic ulcer disease?

A

Epigastric pain

  • Burning/Gnawing
  • Follows meal times
  • Often at night

Serious symptoms

  • Bleeding/anaemia
  • Satiety (early)
  • Weight loss
138
Q

What is functional dyspepsia?

A
  • Symptoms of ulcer disease
  • No physical evidence
  • Diagnosis of exclusion
139
Q

What are the methods used to diagnose gastric pathology?

A
  • Upper GI endoscopy (biopsies)
  • Urease breath test
  • Erect chest X-ray (perforation)
  • Blood test (anaemia)
140
Q

What is the treatment for peptic ulcer disease?

A
  • Eradicate H-pylori
  • Stop NSAIDS
  • Endoscopy for bleeding ulcers and follow up fro treated gastric ulcers
  • PPIs
141
Q

How do H2 blockers work?

A

-Stop histamine components which stimulate parietal cells

142
Q

Describe the pathogenesis of helicobacter-pylori?

A
  • Spread via faecal-oral route
  • Helix shaped gram negative
  • Produces urease which covers urea to ammonium to increase local pH
  • Has flagellum for good motility. It lives in mucus layer/adheres to gastric epithelia
143
Q

How does helicobacter pylori cause problems?

A
  • Relase cytotoxins to cause direct epithelial injury
  • Expresses urease which can form ammonia which is toxic to epithelium
  • Possibly degrades mucus layer
  • Promotes inflammatory response which can cause self injury
144
Q

What is the pathological result of the location of H-pylori colonisation?

A

In antrum
-Duodenal ulceration

In antrum and body
-Asymptomatic

Predominantly in body
-Can lead to cancer

145
Q

What are causes of stress ulceration?

A
  • Severe burns
  • Raised intracranial pressure
  • Sepsis
  • Severe trauma
  • Multiple organ failure
146
Q

Describe the key properties of chyme leaving the stomach

A
  • Hypertonic
  • Low pH
  • Partially digested
147
Q

List the secretions of the exocrine pancreas

A

Acini

  • Amylases
  • Lipases
  • Proteases (trypsin, chymotrypsin, Elastase, Carboxypeptidase

Duct cells

  • Aqueous compenent
  • Bicarbonate
148
Q

What stimulates pancreatic and biliary secretions?

A

Secretin
CCK (enzymes)
Autonomic (PNS stimulates, SNS inhibits)

149
Q

Describe the mechanism of secretion of alkaline juice

A
  • Stimulated by secretin
  • Release of aqueous bicarbonate component of pracretuc secretions by duct cells to neutralise chyme. Also released as part of bile
150
Q

Describe how the microscopic structure of the liver relates to its functions

A
  • Hexgonal arrangement
  • Triad of structures at each corner (portal vein, hepatic artery, bile duct)
  • Substance brought liver start at periphery and work towards middle
  • Central vein in the middle
  • Blood enter lobule via hepatic artery and portal vein
  • Blood flows toward central vein via sinusoids (low pressure)
  • Bile flows out alone canaliculi then bile duct into duodenum
151
Q

Why are pancreatic proteases release in inactive forms?

A
  • Inactive protease enzymes (zymogen) produced within acinar cells and are concentrated and stored in zymogen granules
  • The enzymes are converted to active forms where they need to be used
152
Q

Describe the digestive functions of the liver and the components of bile

A

Liver secretes bile into duodenum to emulsify fat so they can be readily digested by lipases secreted by pancreas

Bile consists of

  • Bile acids and bile pigments
  • Alkaline solution
153
Q

The liver acinus is divided in zone 1, 2, 3 starting from the periphery towards the centre. Where is toxic and ischaemic damage likely to have a greater effect?

A

Toxic
-Zone 1. Last region to receive blood supply

Ischaemic
-Zone 3. Last region to receive blood supply

154
Q

Describe the function of the gall bladder and the relationship to the formation of gallstones

A
  • Bile is stored in the gallbladder

- Concentrates bile which can lead to gallstones

155
Q

Describe the secretion of bile acids and the entero-hepatic circulation of bile acids

A

-CCK stimulates bile release by causing gallbladder contraction

156
Q

What are bile salts?

A

Two primary acids

  • Cholic acid
  • Chenodeoxycolic acid

Bile salts are bile acids conjugated with amino acids

157
Q

Why are bile acids conjugated?

A
  • Not always soluble at duodenal pHs

- Bile salts have amphipathic structure so can fact at oil/water interface

158
Q

Describe the mechanisms of digestion of fats

A
  • Lipids tend to form large globules by time reached duodenum which results in small surface area for enzymes to act
  • Bile salts emulsify fat into smaller units to increase surface area and allow lipases to act
  • Bile salts then create micelles with product of lipid breakdown
  • Micell transports digested lipids to luminal membrane of enterocyte
  • Lipids diffuse into intestinal epithelial cells
159
Q

What is the enter-hepatic circulation of bile acids?

A
  • Bile salts remain in gut
  • Reabsorbed in terminal ileum
  • Returned to liver in portal blood

Liver recycle bile acids

160
Q

How are digested fat transported to the blood circulation?

A
  • Inside the enterocyte, lipid molecules are built back up again into triglycerides, phospholipids and cholesterol
  • Lipids packed with apoproteins within enterocyte into chylomicrons
  • Chylomicrons exocytosed from basolateral membrane of enterocyte ad enter lymph capillaries into thoracic duct
161
Q

What is steatorrhoea?

A
  • Certain pathologies may cause bile acids or pancreatic lipases to not be secreted in adequate amounts
  • Undigested fat appears in faeces. It is pale, floating and foul smelling
162
Q

What are the symptoms of coeliac disease?

A
  • Diarhoea

- Flatulence

163
Q

How does chyme becomes isotonic as it leaves the duodenum?

A
  • Stomach is impermeable to water
  • Duodenum is relatively permeable to water
  • Hypertonic chyme draws movement of water from ECF/circulation into duodenum
164
Q

What are the key points of carbohydrate digestion?

A
  • Carbohydrates are chains of sugars (Polysaccharides, Disaccharides, Monosaccharides)
  • Only monosaccharides can be absorbed (Fructose, Galactose, Glucose)
  • Final breakdown occurs in brush border by brush border hydrolases
  • Glucose can only enter with Na+
  • Fructose can enter from lumen through GLUT-5
165
Q

How is starch digested?

A
  • Amylase
  • Break in the middle results in maltose. Maltase can digest maltose
  • Break at the end results in glucose
  • Isomaltase can disrupt branching chains to form glucose from alpha dextrin
166
Q

How are monosaccharides absorbed?

A
  • Na+/K+ ATPase on basolateral membrane maintains aa low intracellular Na+
  • SGLT1 bind to Na+. Allows glucose to bind which allows Na+ and glucose to move into cell
  • GLUT2 transports glucose out of enterocyte as the basolateral membrane. Diffuses down gradient into capillary blood
167
Q

What are the principles of oral rehydration?

A
  • Uptake of Na+ generate osmotic gradient and water follows
  • Glucose uptake stimulate Na+ uptake
  • Mixture of glucose and salt will stimulate maximum water uptake
168
Q

What are the principles of protein digestion in stomach?

A
  • Only amino acids, dipeptides and tripeptides absorbed
  • Pepsinogen released from chief cells which gets converted to pepsin by HCl
  • Pepsin acts on protein to form oligopeptides /amino acids which move to the small intestine
169
Q

What are the principles of protein digestion in small intestine?

A
  • Pancreas release proteases as zymogens
  • Trypsinogen conver to trypsin by enteropeptidase. Trypsin then activates other proteases
  • Endopeptidases (Trypsin, Chymotrypsin, Elastase) produce shorter polypeptides
  • Exopeptidases (carboxypeptidase A & B) produce dipeptides and amino acids
170
Q

How are protein product absorbed?

A
  • Amino acids are transported into cell by Na+-amino acid co-transporters (neutral, acidic, basic, imino)
  • Dipeptides/tripeptides moved by H+ co-transporter called peptide transporter 1 into the cell where they are converted to amino acids by systolic peptidases
171
Q

Describe the basis of electrolyte and water uptake in the GI tract?

A
  • Na+ moved by activ transport of the cell on basolateral membrane
  • Na+ diffuses into epithelial cells
  • Osmoic gradient from all bsoritpn leads to uptake of water. The fluid absorbed is isoosmotic
172
Q

What are the similarities and differences in electrolyte/water uptake in small intestine vs the large intestine?

A

-Both have Na+-K+ ATPase on basolateral membrane

Apical membrane

  • Na+ is co-transported in the small intestine
  • Na+ channels in the large intestine which is induced by aldosterone (ENaC)
173
Q

Describe uptake of calcium in the intestine?

A

When calcium intake is low

  • Active transcellular absorption so it enters cell via facilitated diffusion
  • Ca+ ATPase removes Ca+ from basolateral membrane
  • Process requires Vitamin D and is stimulated by parathyroid hormone.

When calcium intake is normal/high
-Passive paracellular absorption

174
Q

Describe the uptake of iron in the GI tract?

A
  • Mostly in haem/Fe2+
  • Gastric acid is important in the process
  • Iron absorbed across apical membrane. This is via co-trasnport with H+
  • If iron levels are low, iron binds to transferrin to be transported to stores
  • If iron levels are high, iron contained in ferritin complexes and trapped in cells. Lost when enterocyte is replaced
175
Q

How are water soluble vitamins absorbed?

A

Absorbed by Na+ co-transport (Vitamin C/B)
-Vitamin B12 absorbed in terminal ileum bound to intrinsic factor which is secreted by gastric parietal cells. Removal of terminal ileum and gastritis can cause B12 deficiency

176
Q

What investigations done for coeliac disease?

A
  • Upper GI endoscopy and biopsies. Checks for mucosal pathology and whether villli are reduced or absent
  • Bloods (Serology, Electrolyte imbalances and Anaemia)
  • Treatment (diet)
177
Q

Describe red cell breakdown.

A
  • 120 days
  • Occurs extravascularly in macrophages in spleen and liver
  • Bilirubin released by heme breakdown. It is hydrophobic and therefore bound to albumin before being carried to the liver
  • Bilirubin conjugated with glucoronic acid by UDP glucoronyl transferase
  • Conjuaged bilirubin is water soluble and secreted by hepatocyte into bile canaculi
178
Q

Describe bilirubin transport?

A
  • Conjuagted bilirubin is converted to urobiligoen in the intestine and kidney
  • In the intestine urobilinogen is converted to stercobilin
  • In the kidneys urobilinogen is converted to urobilin which is light yellow
179
Q

How do we measure liver dysfunction?

A
  • Failure of anabolism (albumin, glycogen, numerous coagulation factors, Haematopoiesis in fetus)
  • Failure to catabolise and excrete (drugs, hormones, haemaglobin, poisons, can take over removal of aged red cells after splenectomy)
  • Markers of hepatocyte damage
180
Q

What is the results of failure of anabolism?

A
  • Prolonged prothrombin time (inr)
  • Signifies serious liver damage
  • Hypoalbuminaemia reflects severe liver dysfunction
  • Signs of severe liver damage
181
Q

What is pre-hepatic jaundice?

A

-Too much bilirubin

Caused by haemolytic anaemia for example

182
Q

What is intra-hepatic jaundice?

A

-Failure of hepatocytes to conjugate and/or secrete most of the bilirubin presented to them. Stasis within the liver is called cholestasis.

Caused by hepatitis, cirrhosis for example

183
Q

What is post-hepatic jaundice?

A

-Failure of the biliary tree to convert the conjugated bilirubin to the duodenum.

Caused by biliary tree obstruction such as gallstones or carcinoma of the head of pancreas

184
Q

What is result of increased serum levels of conjugated bilirubin?

A

-Water soluble so will be excreted in the urine and turn the urine dark yellow. Can be measured with a dipstick

185
Q

What is the result of increased level of urobilinogen?

A

Will not noticeable colour the urine but can be measured with a dipstick

186
Q

Why does pruritus occur in post-hepatic jaundice?

A

-Inability to secrete bile salts leading to itching

187
Q

What are the signs of pre-hepatic jaundice?

A
  • Dark stools
  • Normal urine colour
  • Mild jaundice
  • No prurities
188
Q

What are the signs of intra-hepatic jaundice?

A
  • Moderate jaundice
  • Stools normal
  • Urine is dark
  • No pruritus usually
189
Q

What are features of post-hepatic jaundice?

A
  • Raised serum bilirubin
  • Decreased urinary urobiliogen
  • Conjuagted bilirubin present in urine
190
Q

What are features of intra-hepatic jaundice?

A
  • Raised serum biliruibin
  • Normal urinary urobiliogen
  • Conjugated bilirubin present in urine
191
Q

What are features of pre-hepatic jaundice?

A
  • Raised serum bilirubin
  • Increased urinary urobiliogen
  • No conjugated bilirubin present in urine
192
Q

What are signs of post-hepatic jaundice?

A
  • Severe jaundice
  • Stools pale
  • Urine is dark
  • Pruritis
193
Q

What are markers of liver damage?

A
  • ALT
  • AST
  • Alk Phos
  • Gamma GT (alcohol induced so can indicate alcoholism)
194
Q

What are the causes of increased Alk Phos?

A

Bone disease

  • Bone metastases
  • Bone fracture
  • Osteomalacia
  • Hyperparathyroidism
  • Paget’s disease of bone

Liver disease with cholestasis

  • Biliary obstruction
  • Cirrhosis
  • Liver metastases
  • Drugs

*Normally high in growing bone

195
Q

What are causes of Raised ALT?

A

Hepatitis

  • Viral
  • Acute alcohol intake
  • Fatty liver disease
  • Drugs/toxins
196
Q

What are causes of raised Gamma GT?

A
  • Biliary duct obstruction
  • Cirrhosis
  • Liver metastases
  • Drugs
  • Alcoholism
197
Q

What are common liver and bile duct disease?

A
  • Hepatitis
  • Cirrhosis
  • Gallstones and biliary tract obstruction
  • Liver metastases
198
Q

What is pathology underlying hepatitis?

A

-Inflamed and/or necrotic hepatocytes that cannot function normally

199
Q

What are the implications of liver failure?

A
  • Increased susceptibility to infections (bacterial mostly)
  • Increases susceptilibit to toxins and drugs
  • Increased blood ammonia due to failure to clear ammonia via urea cycle
  • Ammonia is produced by colonic bacteria and deamination of amino acids. this can causes hepatic encephalopathy
200
Q

What are symptoms of hepatitis?

A
  • Feeling generally unwell
  • Anorexia
  • Fever
  • Right upper quadrant pain
  • Dark urine
  • Jaundice
201
Q

What are typical blood test findings in acute hepatitis?

A
  • Normal albumin and INR
  • High serum bilirubin
  • Conjugated bilirubin present in the urine
  • Very high serum ALT
  • Normal/Silghtly raised Alk Phos
  • Normal/Silghtly raised Gamma GT
202
Q

What is liver cirrhosis and causes?

A

-Liver fibrosis producing a shrunken hard nodular liver

Caused by alcohol, Viral hepatitis, Fatty liver disease and Idiopathic

203
Q

What are the effects of liver fibrosis?

A
  • Pressure and occlusion of the hepatic sinusoids leads to portal hypertension which leads to portosystemic shunting, including oesophageal varices, diverting nutrient-carrying blood away from the liver.
  • Pressure on the bile canaliculi and therefore reduced ability to excrete toxins, bilirubin.
  • Replacement of hepatocytes by fibrous tissue which leads to reduced albumin and clotting factor production
204
Q

What are the sites of portosystemic anastomoses?

A
  • Anorectal juction
  • Ligamentum teres of falciform ligament
  • Oesophagogastric junction
205
Q

What are symptoms of cirrhosis?

A
  • Fatigue/Weakness
  • Bleeding and bruising early
  • Swollen abdomen
  • Swollen legs
  • Weight loss
  • Jaundice
  • Haematemesis and/or malena
  • Confusion, drowsiness and slurred speech
206
Q

How can cirrhosis be treated?

A
  • Not possible to reverse
  • Treatment aimed at dealing with complications
  • Only cure is liver transplantation
207
Q

What is cholangitis?

A

Life threatening complication of bile duct obstruction as a result of infection in the bile ducts. Commonest bacteria is E.Coli
-Obstruction is common due to to gall stones in common bile duct

208
Q

What is a biliary colic?

A
  • Not a true colic. Pain is constant
  • Pain in the right upper quadrant that radiates to the tip of the right scapula/shoulder due to irritation of diaphragm
  • Often precipitated by eating a fatty meal and can last up to 6 hours
209
Q

What is acute cholecystitis?

A
  • Gallstone obstructs the cystic duct then there is stasis of the gallbladder contents which is an infection risk
  • Infecting organism is E.Coli
210
Q

What are the symptoms of acute cholecystitis?

A
  • Severe gall bladder pain
  • Systemically unwell and toxic
  • Pyrexial
  • Tender over gall bladder
211
Q

What is acute pancreatitis?

A

-Premature activation of pancreatic proteases in the pancreas itself rather than the duodenum. Protease then auto digest the pancreases and retroperitoneum

212
Q

What is chronic pancreatitis?

A
  • Rare and due to repeated low grade pancreatitis that causes pancreatic fibrosis.
  • Due to alcohol abuse
  • Pancreas become calcified and patients suffer severe epigastric and back pain that leads to opiate addiction and not infrequently suicide.
213
Q

What is the aetiology of acute pancreatitis?

A
  • Alcohol alters the balance between proteolytic enzymes and protease inhibitors thus triggering enzyme activation, auto digestion and cell destruction
  • Gallstones blocking the ampulla of vater lead to outflow obstruction with pancreatic duct hypertension and a toxic effect of bile salts contribute to activation of pancreatic proteases.
214
Q

What are symptoms of acute pancreatitis?

A
  • Epigastric pain that goes through the back
  • Vomiting
  • Dehydration
215
Q

How is acute pancreatitis diagnosed and treated?

A

Investigations

  • Raised serum amylase or serum lipase
  • CT scan may be used in moderate/severe cases to look for pancreatic necrosis/pseudocyst. Necrosed pancreas is non-enhancing with contrast

Treatment of acute pancreatitis

  • No specific treatment
  • Analgesis, supportive treatment
  • Fluid resuscitation as patient can sequester litres of fluid in their retropeiritoneum
216
Q

What is clinical presentation of pancreas cancer?

A
  • Anorexia, Malaise, Fatigue
  • Significant weight loss
  • Epigastric and/or back pain
  • Dark urine
  • Pale Stools
  • Pruritis
217
Q

What is clinical presentation of an AAA?

A
  • Sudden death
  • Sudden onset of severe abdominal and back/loin pain
  • Sudden collapse
  • Presents to the emergency department with shock. 83% mortality. Most patient die of multi-organ failure on the ITU
218
Q

What are 2 common types of inflammatory bowel disease?

A
  • Crohn’s disease

- Ulcerative colitis

219
Q

What are the gross pathological features of Crohn’s disease?

A
  • Affects anywhere in the GI tract. Ileum in most cases
  • Skip lesions
  • Cobblestone appearance
  • Transmural inflammation
  • Fistulae
  • Mucosal oedema
  • Discrete superficial ulcers
  • Thickening of bowel wall
  • Narrowing of lumen
220
Q

What are the gross pathological features features of ulcerative colitis?

A
  • Begins in rectum
  • Can extend to involve entire colon
  • Continuous pattern
  • Mucosal inflammation
  • Loss of haustra
  • Pseudopolyps
221
Q

What are the causes of intestinal inflammation and infection?

A
  • Genetic
  • Gut organism
  • Immune response (Triggered by Antibiotics, Infections, Diet, Smoking)
222
Q

What is the presentation of Crohn’s disease?

A
  • Weight loss
  • Right lower quadrant pain
  • Joint pains
  • Young patient
  • Tender mass
  • Mild perianal inflammation/ulceration
  • Low grade fever
  • Mildly anaemic
223
Q

What is the presentation of Ulcerative Colitis?

A
  • Bloody stool
  • Mucus in stool
  • Weight loss
  • Mild lower abdominal pain/cramping
  • Painful red eye
  • Mildly tender abdomen
224
Q

What are microscopic features of Crohn’s disease?

A

-Granuloma formation

225
Q

How is Crohn’s disease investigated?

A
  • Bloods (Anaemia)
  • CT/MRI scans (Bowel wall thickening, Obstruction, Extramural problems)
  • Barium enema/follow through (Used less, Strictures/fistulae, Colonoscopy)
226
Q

What are microscopic features of Ulcerative colitis?

A
  • Crypt abscesses
  • Crypt distortion
  • Goblet cells
  • Chronic inflammatory infiltrate of lamina propria
227
Q

How is ulcerative colitis investigated?

A
  • Stool cultures
  • CT/MRI – less useful in diagnosing uncomplicated UC
  • Plain abdominal radiographs
  • Bloods (Anaemia, Serum markers)
  • Barium enema (mild cases only)
  • Colonoscopy
228
Q

What are radiological features of Crohn’s and Ulcerative Colitis?

A

Crohn’s
-String sign of cantor. Normal size lumen that becomes thinner due to strictures

ULcerative colitis

  • Lots of ulceration between contrast
  • Loss of haustra leading to featureless colon. Lead pipe colon
229
Q

What are the medical treatment options of inflammatory bowel diseases?

A
  • Aminosalicylates
  • Corticosteroids
  • Immunomodulators
230
Q

What are the surgical treatment options of inflammatory bowel diseases?

A

Crohn’s

  • Not curative
  • Strictures/fistulae
  • As little bowel removed as possible

Ulcerative colitis

  • Curable (colectomy)
  • Inflammation not settling
  • Pre-cancerous changes
  • Toxic megacolon
231
Q

What is the nerve supply of the peritoneum?

A
  • Parietal peritoneum is supplied by the same nerve that supply skin of abdomen. Perceives inflammation as pain at the site of the inflammation
  • Visceral peritoneum is supplied by the nerve supply of the viscera it invests. This produces referred pain
232
Q

What are the symptoms of peritonitis?

A
  • Severe pain all over abdomen which may refer to the shoulder tips
  • Rigid abdomen as diaphragmatic and abdominal wall movement greatly increases pain.
  • Shallow rapid breathing
  • Very tender on examination of abdomen
  • Rebound tenderness may occur in early stages
233
Q

Describe the common life threatening events occurring in the abdominal cavity

A

Blood loss

  • Into the gut
  • Into the retro-peritoneum (AAA, patients on anticoagulants may bleed from torn retroperitoneal veins)
  • Into the peritoneal cavity

Perforation of a viscus
-Allows the outside world to enter the peritoneal cavity causing inflammation, hypovolaemia and sepsis

Autodigestion of the retroperitoneum due to acute pancreatitis

Acute cholangitis

Acute gut ischaemia

234
Q

What is the clinical presentation of bowel perforation?

A
  • Severe generalised abdominal pain
  • Patient lies still, shallow breathing
  • Patients will be hypovolemic
  • Patient may be septic

Symptoms of peritonitis

235
Q

What is the clinical presentation of bowel ischaemia?

A
  • Severe abdominal pain
  • Tender over ischaemic gut
  • Becomes rapidly toxic and hypotensive
  • Very high white cell count
236
Q

What is the clinical presentation of pancreatitis?

A
  • Significant dehydration due to vomiting and fluid sequestration in retroperitoneum
  • Raised serum amylase
237
Q

What is the clinical presentation of cholangitis?

A 
Charcots triad
-Jaundice
-Fever
-Right upper quadrant pain
May also have Reynold pentad
-Hypotension 
-Confusion
-Rigors

May develop septic shock due to the bile duct being blocked by bacteria. This leads to canaliculi backing up into the central vein and this is a huge area of contact between the infected area and the blood.

238
Q

What is the underlying pathology in relation to abdominal aortic aneurysm?

A

-Sudden Blood loss

239
Q

What is the underlying pathology in relation to bowel perforation?

A
  • Perforated peptic ulcer can leads to chemical peritonitis. 10% mortality
  • Perforated diverticular disease can lead to peritoneal sepsis and septicaemia. 50% mortality
  • Posterior perforation of gastric ulcer initially allows gastric contents to enter the lesser sac. Thereafter the fluid can track into the greater sac via the epiploic foramen.
  • Faecal peritonitis can occur with perforation of large bowel
240
Q

What is the underlying pathology in relation to bowel ischaemia?

A

-Embolism (atrial fibrillation)

241
Q

What is the clinical presentation of bleeding oesophageal varices?

A
  • Haematemesis

- Malaena

242
Q

What is the clinical presentation of bleeding peptic ulcer disease?

A
  • Haematemesis

- Malaena

243
Q

What is the clinical presentation of bleeding diverticular disease?

A

-Bright red bleeding per rectum (haematochezia)

244
Q

What is malaena?

A
  • Melaena is due to alteration of blood by digestive enzymes and can occur with bleeding from anywhere from the mouth to caecum
  • Patients taking oral iron can have black stools. The smell reveals the difference
245
Q

What is haematemesis?

A

Vomiting blood

246
Q

What is the significance of urea measurement for GI bleeds?

A
  • Bleeding from the stomach or oesophagus presents with a large protein meal to the small bowel.
  • The protein is converted by the liver into urea.
  • Rise in blood urea in patient with oesophageal/gastric bleeding will help indicate (if the creatinine is normal) source of bleeding and size of the bleed
247
Q
  1. describe the key features of the gut immune response to infection, including the Gut-associated lymphoid tissue (GALT)
  2. describe the importance of the gut microbiome and the role of commensal organisms
  3. Describe an approach to a patient presenting with traveller’s diarrhea and
    consider protozoa such as Giardia and Entamoeba
A

ggggg

248
Q

Describe an clinical approach, with regard to history, examination and investigation of a patient presenting with gastroenteritis

A
  • History
  • Physical examination of hydration status
  • Abdominal examination
  • Take appropriate samples and request right test
249
Q

What is the main example of a viral cause of gastroenteritis?

A
  • Norovirus
  • PEak incidence in the winter and affects all ages
  • Immunity is short-lived and reinfections can occur
  • Resits freeing, disinfection with alcohol and temperature up to 60 C
250
Q

How is norovirus transmitted?

A
  • Faeco-oral person to person transmission
  • 24 hour incubation period
  • Viral particles shed in stool and vomit and fomites can contaminate environment
251
Q

What is route of infection for shigella infection?

A
  • Faecal oral route

- Direct person to person

252
Q

Describe Shigella.

A
  • Gram negative facultative anaerobic
  • Rod shaped
  • Non-spore forming
  • Non motile
253
Q

What are the virulence factors of Shigella?

A
  • Plasmid

- Shinga toxin (exotoxin)

254
Q

How does shigella cause diarrhoea?

A
  • Enters the interstitial epithelial cells by endocytosis
  • Escapes from the endocytic vesicle and multiplies inside the cell
  • Mucosal abscesses from leading to cell death and this results in diarrhoea with blood and mucus
255
Q

Describe the key features of Cryptosporidium

A

-Microscopic parasite

256
Q

What is the route of infection for cryptosporidium?

A

-Faecal oral route

257
Q

How can salmonella cause gastroenteritis?

A
  • Salmonella invade epithelial cells of the small intestine.
  • Disease may remain localized or become systemic, sometimes with disseminated foci.
  • The organisms are facultative, intracellular parasites that survive in phagocytic cells
258
Q

Describe salmonella

A
  • Gram negative baccili
  • Spore forming
  • Motile
259
Q

What are some virulence factors of salmonella?

A
  • Endotoxins

- Fimbraie

260
Q

Recognise and describe the importance of infection prevention and infection
control measures with regard to GI infections

A
  • Handwashing
  • Isolation
  • Environmental cleaning
  • 48 hour rule especially for healthcare professional, childcare, schools and food handlers
261
Q

How are GI infections treated?

A
  • Fluid resuscitation
  • Antibiotics if immunocompromised
  • Treatment of underlying conditions
262
Q

Describe how G.I. cancers may spread within the body

A
  • Blood stream

- Lymph

263
Q

What are risk factors of oesophageal carcinomas?

A
  • Smoking
  • Obesity
  • Barrett’s
264
Q

What are histological features of malignancies in the oesophagus?

A
  • Squamous cell carcinoma

- Lower third can develop adenocarcinoma from Barretts

265
Q

What is the incidence of GI cancer from most common to least common?

A
  1. Bowel
  2. Pancreas
  3. Oesophagus
  4. Stomach
  5. Liver
266
Q

What is the clinical presentation of Gastric Cancer?

A
  • Similar pain to peptic ulcer

- 50% have palpable mass

267
Q

What are risk factors of Gastric Cancer?

A
  • Smoking
  • High salt diet
  • Family history
  • Chronic inflammation (chronic gastritis by H.Pylori)
268
Q

What is the most important environment factor for stomach cancer?

A

-H.Pylori

269
Q

Which part of the GI tract is the most common site for a primary gastrointestinal lymphoma?

A
  • Stomach
  • MALT tissue
  • Most associated with H.Pylori
  • Similar presentation to gastric carcinoma but prognosis better
270
Q

What are the histological features of stomach cancers?

A
  • Adenocarcinomas
  • Arise from chronic gastritis common or metaplasia.

Stomach ulcers potentially malignant

271
Q

Why does gastric cancer have a poor prognosis?

A

-Present late and are therefore advanced

272
Q

How does pancreatic cancer present?

A

Head

  • Painless jaundice (Interferes with biliary flow into duodenum. )
  • Persistent pain
  • Weight loss anorexia
  • Fatigue

Body/Tail
-Symptoms more vague

273
Q

What are the risk factors for pancreatic cancer?

A
  • Family history
  • Smoking
  • Chronic pancreatitis
  • Men more than women
  • Incidence increases with age. Typical over 60 years
274
Q

What is the histological features of pancreatic cancer?

A
  • Commonly (80%) are ductal adenocarcinomas

- Commonly affects head of pancreas

275
Q

What is the clinical presentation of small bowel cancer?

A
  • Per rectum bleeding
  • Change in bowel habit (frequency, consistency, discomfort)
  • Weight loss
  • Abdominal pain
276
Q

What are risk factors of small bowel cancer?

A
  • Inflammatory bowel disease
  • Coeliac disease
  • Familial adenomatous polypoids
  • Diet
277
Q

What are risk factors of large bowel cancer?

A
  • Family history
  • Inflammatory bowel disease
  • Polyposis syndromes (FAP)
  • Diet and lifestyle
278
Q

What the histological features of small bowel cancer?

A

Rare!

  • Stromal
  • Lymphoma
  • Adenocarcinoma
  • Sarcoma
  • Carcinoid tumours
279
Q

What are the histological features of large bowel cancer?

A

-Adenocarcinoma (mostly in rectum and sigmoid colon)

Most can be viewed with sigmoidoscope

280
Q

What is the basis for most colorectal cancer?

A
  • Adenomas are the basis of most colorectal cancers.
  • Demonstrated by 
familial adenomatous polyposis, an inherited condition where invariably the 
numerous adenomas present will undergo malignant change.
281
Q

What genetic events are coleorectal cancers related to?

A
  • Activation of oncogene
  • Ineffective DNA repair
  • Loss of tumour suppressor genes
282
Q

What are the features of rectal cancers?

A

Usually ulcerating and therefore give PR bleeding. They 
can also produce the symptom of tenesmus due to distension of the rectum.

283
Q

What is the clinical presentation of left sided colon cancer?

A
  • Weight loss
  • Bowel obstruction (Contents are more solid on left side)
  • Tenesmus
  • Early change in bowel habit
  • Less advanced disease at presentation
  • Rectal bleeding
  • Abdominal pain
  • Mass in left illiac fossa
284
Q

What is the clinical presentation right sided colon cancer?

A
  • Weight loss
  • Anaemia
  • Occult bleeding
  • Mass in right iliac fossa
  • Disease more likely to be advanced at presentation
  • Caecum and colon are more distensible so obstruction doesn’t occur early
285
Q

Describe the adenoma-carcinoma sequence

A

Benign growth derived from genetic changes

  • Become hyperplastic
  • Abnormal differential leads to dysplasia of the cells
  • Dysplastic cells have potential to become cancerous
286
Q

What are the contents of the external muscle layers?

A
  • Inner circular muscle

- Outer longitudinal muscle

287
Q

What are the ligament of the liver and their attachments?

A

Falciform ligament
-Attaches the anterior surface of the liver to the anterior abdominal wall. Free edge contains the ligamentum teres

Coronary ligament
-Attaches the superior surface of the liver to the diaphragm

Right and Left Triangular ligament
-Attaches the superior surface of the liver to the diaphragm

Inferior vena cava – Secures to the posterior surface of the liver through hepatic veins and fibrous tissue

Lesser omentum

288
Q

What are the parts of the lesser omentum

A

Hepatic duodenal ligament which extends form the duodenum to the liver

Hepatogastric ligament which extends from the stomach to the liver

289
Q

What are the macroscopic features of the liver?

A

4 lobes

  • Divided into right and left lobes by the falciform ligament
  • Caudate lobe on the upper aspect of the visceral surface. Lies between inferior vena cava and a fossa produced by the Ligamentum Venosum
  • Quadrate lobe located on the lower aspect of the visceral surface. Lies between gallbladder and a fossa produced by the Ligamentum Teres
290
Q

What are the main branches of the coeliac trunk and their path?

A
  • Left gastric which travels along the lesser curve of the stomach where it anastomose with the right gastric artery
  • Splenic artery which travels towards the spleen running posteriorly to the stomach and along the superior margin of the pancreas. Terminates to supply the spleen
  • Common hepatic arteries which travels past the superior aspect of the duodenum
291
Q

What are the branches of the splenic artery and area of supply ?

A
  • Pancreatic branches which supply the body and tails of the pancreas
  • Left gastroepiploic which supplies the greater curvature of the stomach
  • Short gastric which supplies the fundus of the stomach
292
Q

What are the branches of the common hepatic artery and path?

A
  • Proper hepatic artery ascends through lesser omentum

- Gastroduodenal artery descends posterior o the superior portion of the duodenum

293
Q

What are the branches of the gastroduodenal artery and area of supply?

A
  • Right gastroepiploic which supplies the greater curvature and greater omentum
  • Superior pancreatoduodenal artery which supplies the head of the pancreas
294
Q

What are the branches of the proper hepatic artery and their area of supply?

A
  • Right gastric to supply the pylorus and lesser curvature of the stomach
  • Right and left hepatic artery which divide inferior to porta hepatis to supply the respective lobes of the liver
  • Cystic which is a branch of the right hepatic which supplies the gallbladder
295
Q

What are the regions of the peritoneal cavity?

A
  • Greater sac (larger portion)

- Lesser sac

296
Q

What are the areas of the greater peritoneal sac separated by?

A

Transverse colon

  • Supracolic
  • Infracolic
297
Q

How are the colics connected by?

A

Paracolic gutters

298
Q

Where does the lesser peritoneal sac lie?

A
  • Lies posterior to the stomach
  • Known as omental bursa
  • Allows stomach to move freely against the structures inferior and posterior to it
299
Q

What connect the greater and lesser sac?

A

-Epiploic foramen which lies posterior to the ligamentum teres

300
Q

Where does the rectovesical pouch lie?

A

Double folding of peritoneum between the rectum and the bladder. The peritoneal cavity is completely closed in males.

301
Q

Where does the pouch of Douglas lie?

A

Rectouterine Pouch

Double folded extension of the peritoneum between the rectum and the posterior wall of the uterus.

302
Q

Where does the vesicouterine pouch lie?

A

The vesicouterine pouch is a double fold of peritoneum between the anterior surface of the uterus and the bladder.

303
Q

What are the primarily retroperitoneal organs?

A
  • Oesophagus
  • Rectum
  • Kidneys
304
Q

What are the secondarily retroperitoneal organs?

A
  • Ascending colon

- Descending colon

305
Q

Describe the surface anatomy of foregut organs on the abdominal wall.

A

Stomach - Epigastrium
Duodenum - Epigastrium
Liver – Lies in the dome of the right diaphragm. Right hypochondrium and epigastric region
Pancreas – Lies in C shape of duodenum. Behind the stomach. Tail in left Hypochodnrium
Spleen – Lies near 10th rib and posterior

306
Q

Describe the surface anatomy of the midgut organs on the abdominal wall.

A

Jejunum - Left lumbar and umbilical regions of abdomen
Ileum – terminate in right inguinal region and mainly lower portion of abdomen
Caecum – Appendix arise here. Right inguinal region
Ascending Colon – Arise from right inguinal region to right lumber region

307
Q

Describe the surface anatomy of the hindgut organs on the abdominal wall.

A

Transverse colon – Arise from the ascending colon and travels transversely across abdomen
Descending colon – Left lumber region to Left inguinal
Sigmoid colon – Arises from left inguinal
Rectum

308
Q

What is formed by the aponeuroses of all the flat muscle in the midline?

A

Linea alba

309
Q

Which muscle is located in the middle of the abdominal wall?

A
  • Rectus abdominus
  • Split into 2 by the linea alba
  • Lateral border is the linea semilunares
  • Tendinous intersections form the six pack
310
Q

What forms the anterior wall of the rectus sheath?

A

-Aponeuroses of the external oblique and half of the internal oblique

311
Q

What forms the posterior wall of the rectus sheath?

A

-Aponeuroses of half the internal oblique and transverse abdoniums

At Arcuate line the apoenurses all become anterior

312
Q

What is the path of the superior mesenteric artery?

A
  • Arises at L1 anteriorly to the abdominal aorta
  • Descends down the posterior aspect of the abdomen.
  • Supplies the midgut
313
Q

What are the anatomical relations with the superior mesenteric artery?

A

Anterior to the SMA

  • Pyloric part of the stomach Splenic vein
  • Neck of the pancreas

Posterior to the SMA

  • Left renal vein
  • Uncinate process of the pancreas – hooks around the back of the SMA
  • Inferior part of the duodenum
314
Q

What are the major branches of SMA?

A

Inferior Pancreaticoduodenal – Inferior region of the dad of the pancreas, uncinate process, duodenum

Right colic – Supplies the ascending colon

Illeocolic artery – Ascending colon, Appendix, Caecum, Ileum

Middle colic artery – Supplies the transverse colon

Jejununal arteries – Supplies the jejunum. Smaller number of arterial arcades but longer vasa recta than illegal arteries

Ileal arteries – Supplies the ileum

315
Q

What is unique about the superior mesenteric artery blood supply?

A

Formation of arcade to supply the parts of the GUT

316
Q

What is the path of the inferior mesenteric artery?

A

Arise at L3 near the inferior border of the duodenum
Depends anteriorly then moves to the left side and it is a retroperitoneal
Supplies the hindgut

317
Q

What are the major branches of the inferior mesenteric artery?

A

Left colic artery

  • Ascending branch which supplies the distal 1/3 of the transverse colon, and the upper aspect of the descending colon.
  • Descending branch – moves inferiorly to supply the lower part of the descending colon. It anastamoses with the superior sigmoid artery.

Sigmoid arteries - supply descending colon and the sigmoid colon

Superior Rectal artery -

318
Q

What is the marginal artery?

A

Continuous arterial circle along the inner border of the colon. Straight vessels arise form the artery to supply the colon.

319
Q

What makes up the marginal artery?

A
  • Illeocolic, right colic and middle colic of superior mesenteric artery.
  • Left colic and sigmoid branches of the inferior mesenteric artery
320
Q

What is the arc of riolan?

A

Anastomosis between the middle colic branch of superior mesenteric artery and left colic branch of inferior mesenteric artery.

321
Q

Which artery can a horseshoe kidney hook onto?

A

Inferior mesenteric artery

322
Q

What is the venous drainage of the gut?

A

Hepatic portal vein

Kofi: Pure clinical conditions 2 (5 decks)

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