GI Flashcards

0
Q

What are the overall processes involved in GI function?

A

Initial physical disruption –> Ingestion and transport to storage –> Initial chemic disruption and creation of suspension (chyme) –> Disinfection –> Controlled release of Chyme –> Dilution and neutralisation –> Completion of chemical breakdown –> Absorption of nutrients and electrolytes –> Final absorption of water and electrolytes –> Producing faeces for controlled excretion.

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1
Q

What is the purpose and reasoning for the functions of the GI tract?

A

Metabolic processes need a specific, range of small molecules. Food has a wide range of mostly large molecules locked into complex structures. It may also be contaminated with pathogens.
Digestion makes food into a sterile, neutral, and isotonic solution of small sugars, amino acids and small peptides, small particles of lipids and other small molecules. This is now ready for absorption and excretion.

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2
Q

What are the broad functions of the mouth and oesophagus?

A
  1. Mastication
  2. Saliva
    o Protects mouth
    • Wets / Bacteriostatic / Alkaline / High Ca2+
    o Lubricates food for mastication and swallowing
    • Wet / Mucus
    o Starts digestion
    • Sugars​ - amylase
  3. Swallowing
    o Formation of bolus
    o Rapid oesophageal transport
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3
Q

What are the broad functions of the stomach?

A

o Storage
- Relaxes to accommodate food
o Initial disruption
- Contracts rhythmically to mix and disrupt
- Secretes acid and Proteolytic enzymes to break down tissues and disinfect
- Now known as Chyme
o Delivers Chyme slowly into the Duodenum

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4
Q

What are the broad functions of the duodenum?

A

o Dilution and neutralisation of Chyme

  • Water drawn in from ECF. Stomach impermeable, Duodenum permeable.
  • Alkali (bile) added from Liver and Pancreas
  • Enzymes added from pancreas and intestine
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5
Q

What are the broad functions of the small intestine?

A

o Absorption of nutrients and electrolytes
- Fluid passes very slowly through the small intestine
- Large surface area
- Epithelial cells absorb molecules, some actively some passive
• Often coupled to Na+ absorption
- Pass into hepatic portal circulation (First pass…)
o Absorbs the majority of water (1.5L vs. 0.15L large intestine)

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6
Q

What are the broad functions of the large intestine?

A

o Final absorption of water (0.15)
o Very slow transit
o Faeces form and accumulate in the descending and sigmoid colon

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7
Q

What are the broad functions of the rectum ?

A

o Faeces propelled periodically into rectum
o Urge to defecate
o Controlled relaxation of sphincters and expulsion of faeces

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8
Q

What four histological layers does the alimentary canal consist of?

A

From the oral cavity to the anus the alimentary canal consists of four layers:
o Mucosa
• Epithelial lining and thin layer of smooth muscle
o Submucosa
• Fibroelastic tissue with vessels, nerves, leucocytes and fat cells
o Muscularis Externa
• Inner circular and outer longitudinal layer of smooth muscle with the myenteric plexus lying in between the layers.
o Serosa/Adventitia
• Thin outer covering of connective tissue
A variation in the cellular composition of these layers provides adaptations for specific functions whilst remaining a continuous hollow tube of variable diameter and shape

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9
Q

Describe the fluid balance of the Gut

A

Each day we ingest about 1kg of food and about a litre of liquids. The food is mixed with 1.5L of Saliva and about 2.5L of gastric secretions to form chyme. Chyme is very hypertonic (has a high osmotic strength) and is very acidic.
When chyme is slowly released from the stomach, around 9L of water (and alkali) moves into it from the ECF via osmosis.
The small intestine then absorbs about 12.5L of the fluid, and the large intestine absorbs about 1.35L.

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10
Q

What are some properties of the enteric system and how is it related to the Autonomic nervous system?

A

The enteric nervous system is a subdivision of the autonomic nervous system that directly controls the GI system. It is made up of two nerve plexuses in the wall of the gut that may act independently of the CNS (short reflex pathway). This activity may be modified by both branches of the ANS (long reflex pathway). Parasympathetic control however is the most significant. It coordinates both secretion and motility using a range of neurotransmitters, not just Ach as you may expect (parasympathetic).

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11
Q

How are hormones involved in the motility and secretion of the gut?

A

Endocrine cells in the walls of the gut release a dozen or more peptide hormones. These include both hormones with endocrine action and paracrine action. The hormones comprise two structurally related groups – the Gastrin group and the Secretin group. These hormones are released from one part of the gut to affect the secretions or the motility of other parts.

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12
Q

What is dysphagia?

A

Difficultly swallowing. May be caused by problems with the oesophagus, e.g. musculature, obstruction by tumour or neurological, e.g. a stroke. Tumours of the oesophagus, high up are Squamous Cell Carcinoma, lower down are Adenocarcinomas.

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13
Q

What is acid reflux?

A

Sphincter between the oesophagus and the stomach is weak, acid refluxes into the oesophagus and causes irritation and pain (heartburn).

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14
Q

What is Barrett’s oesophagus?

A

Metaplasia of the lower oesophageal squamous epithelium to gastric columnar. This is to protect against acid reflux.

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15
Q

What are oesophageal varices?

A

Portal venous system is overloaded due to cirrhosis, blood is diverted to the oesophagus through connecting vessels. This leads to the dilation of sub mucosal veins in the lower part of the oesophagus

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16
Q

What is a peptic ulcer?

A

Area of damage to the inner mucosa of the stomach or duodenum, usually due to irritation from gastric acid.

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17
Q

What is pancreatitis?

A

Inflamed pancreas, causes considerable pain. Characterised by the release of amylases into the blood stream.

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18
Q

What is jaundice?

A

Liver cannot excrete bilirubin, which accumulates in the blood. If build up of bilirubin is due to excess haemoglobin breakdown it is Pre-hepatic Jaundice. If build up of bilirubin is due to bile duct obstruction and back up of bile causing liver damage it is Post-hepatic or Obstructive Jaundice

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19
Q

What are gallstones?

A

Precipitation of bile acids and cholesterol in the bladder forms gall stones. Often asymptomatic, but may move within the gall bladder causing painful Biliary Colic, or move to obstruct biliary outflow. Tumours of the pancreas may also obstruct outflow

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20
Q

What is malabsorption?

A

Several conditions affect how well the intestines can absorb things

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21
Q

What is appendicitis?

A

Inflammation of the appendix, presents as a sharp pain in the side at the same level as T10, which then localises to the right lower quadrant.

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22
Q

What is peritonitis?

A

Inflammation of the peritoneum

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23
Q

What is IBS?

A

Inflammatory Bowel Syndrome – E.g. ulcerative colitis and Crohn’s disease

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24
Q

What is acute blockage of the small intestine?

A

Present with Pain (in their back), vomiting and bloating

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25
Q

What are haemorrhoids?

A

Vascular structures in the anal canal that aid with stool control. When they become swollen and inflamed they are painful, itchy and blood may be present in stool.

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26
Q

What is a prolapse?

A

Literally means ‘to fall out of place’. Prolapse is a condition where organs fall down or slip out of place. E.g. the rectum can prolapse.

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27
Q

What is a diverticula?

A

Pressure is too high in the colon, producing an abnormal ‘outpouching’ to form a hollow. The sigmoid colon is the area most prone as the blood supply causes an area of weakness (?)

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28
Q

What is Meckels’ diverticulum?

A

A pouch in the lower part of the small intestine, a vestigial remnant of the yolk sac. It can produce ectopic gastric mucosa that may then produce gastric acid, causing irritation.

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29
Q

What is colo rectal cancer?

A

The large intestine is a common site of malignancies, and colo-rectal cancer is a major cause of mortality.

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30
Q

What is the mouth and it’s purpose?

A

The mouth is the entrance to the GI tract. It serves to disrupt foodstuffs and mix them with saliva to form boluses to be swallowed.

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31
Q

What is the purpose of the teeth?

A

The teeth cut (incisors), crush (molars) and mix food with saliva.

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32
Q

What powerful muscles generate the force behind the teeth movement and what innervates these?

A

The powerful muscles of mastication, the Masseter, generate the force behind teeth. A branch of the trigeminal nerve innervates the Masseter.
.

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33
Q

How many muscles make up the tongue? What is the purpose of the tongue?

A

The tongue is a collection of 8 muscles that work to manipulate food for mastication and form it into a bolus. It also aids in swallowing by pushing the bolus to the back of the mouth

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34
Q

What is the oropharynx? And some of its features? What is the relevance of the glottis

A

The oropharynx lies behind the oral cavity, and forms the portion of the pharynx below the nasopharynx but above the laryngopharynx.
It extends from the uvula, which is the end of the palate, to the level of the hyoid bone/ epiglottis
Because both food and air pass through the oropharynx, a flap of tissue called the epiglottis closes over the glottis to prevent aspiration.

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35
Q

What is the oesophagus?

A

The oesophagus is a muscular tube that passes food from the pharynx to the stomach. It is continuous with the lower part of the laryngopharynx.

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36
Q

What are the histological layers of the oesophagus?

A

The oesophagus has several layers, from inside to out:
o Mucosa composed of non-keratinized stratified squamous epithelium, lamina propria and a layer of smooth muscle (Muscularis Mucosa)
o Submucosa containing the mucous secreting glands
o Mucularis externa. Upper third of oesophagus is striated, skeletal muscle under conscious control for swallowing. The lower two thirds are smooth muscle under autonomic control (peristalsis).

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37
Q

How much saliva is produced every day?

A

1.5 litres of saliva is produced each day.

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38
Q

What are the functions of saliva?

A
It has several functions:
1. Lubricates and wets food
2. Starts the digestion of carbohydrates (Amylase)
3. Protects oral environment
o Keeps mucosa moist
o Washes teeth
o Maintains alkaline environment
• Neutralises acid produced by bacteria
o High Ca2+ concentration
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39
Q

What is zerostomia?

A

Insufficient Saliva production. You are still able to eat provided food is moist, but teeth and mucosa degrade very quickly.

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40
Q

What are the main constituents of saliva?

A

o Water
• Hypotonic solution
o Electrolytes
• Na+, Cl-, usually at a lower concentration than plasma
• Ca2+, K+, I- (iodide) usually at a higher concentration than plasma
o Alkali
• HCO3- at a higher concentration than plasma
o Bacteriostats
o Mucus - (Mixture of mucopolysaccharides)
o Enzymes - Salivary amylase (can live without it, relatively minor)

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41
Q

Describe the 3 types of salivary glands and their functions

A

There are three paired salivary glands. They are all ducted, exocrine glands, but do not all excrete the same thing.
Exocrine glands are made up of blind-ended tubes (Acini), lined with acinar cells. The acini are connected via a system of ducts to a single outlet, lined by duct cells. Acinar cells and duct cells have different functions.
o Parotid Glands
• Watery secretion, rich in enzymes but little mucus
• Serous saliva
• 25% of volume secreted
o Sub-lingual glands
• Viscous secretion, no enzymes but lots of mucus
• Mucus saliva
• 5% of volume secreted
o Sub-maxillary glands
• All components of saliva (mixed serous and mucus)
• Mixture of serous and mucus acini leading to a common duct
• 70% of volume secreted

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42
Q

How is serous saliva secreted?

A

Saliva is a hypotonic solution, but there is no cellular mechanism to secrete water. Therefore more concentrated solution is secreted, and solute is then reabsorbed from it to leave the final hypotonic solution.
Acinar Cells secrete an isotonic fluid containing enzymes. Duct Cells then remove Na+ and Cl- and add HCO3-. The gaps between duct cells are tight, so water does not follow the resulting osmotic gradient and so saliva remains hypotonic.

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43
Q

At a low flow rate of saliva how hypotonic is saliva?

A

At a low flow rate, the duct cells have the opportunity to remove most Na+, so saliva is very hypotonic.

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44
Q

At a high flow rate of saliva, how hypotonic is saliva? How is pH affected?

A

The rate at which duct cells can modify saliva is limited, so at a high flow rate a smaller fraction is removed and the saliva becomes less hypotonic. However, the stimulus for secretion promotes HCO3- secretion, so saliva becomes more alkaline. (At a high flow rate)

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45
Q

How does acinar secretion occur (re: saliva)?

A

Cl- ions are actively secreted from Acinar cells into the lumen of the duct. Water and other ions (Na+) will then follow passively.

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46
Q

How does ductal modification occur (re: saliva)?

A

The action of the Na/K-ATPase Antiporter in the Basolateral membrane of duct cells lowers the [Na+] inside the cell. This means there is a concentration gradient, where [Na+] is high in the duct lumen and low in the duct cells. Na+ diffuses passively back into the Duct cells.
The action of the Na/K-ATPase Antiporter also increases the [K+] concentration in side the cell. The resulting concentration gradient drives the expulsion of Cl- from the duct cells into the ECF. Again, a concentration gradient is set up between the duct lumen and cells, with [Cl-] low inside and [Cl-] high outside. This gradient drives the expulsion of HCO3- into the duct lumen.

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47
Q

How is salivary secretion controlled?

A

Salivary secretion is mostly controlled by the autonomic nervous system.

Parasympathetic
Parasympathetic stimulation increases the production of primary secretion (Acinar cells) and increases the addition of HCO3- (Duct cells)
o Parotid Gland
• Glossopharyngeal Nerve (9th cranial nerve)
• Otic ganglion
o Submandibular and Sublingual Glands
• Facial Nerve (7th cranial nerve)
• Submandibular ganglion
o Muscarinic receptors
• Blocked by atropine like drugs
o Co-transmitters stimulate extra blood flow

Outflow is mediated by:
o From centres in the medulla
o Afferent information from:
• Mouth and tongue
o Taste receptors, especially acid
• Nose
• Conditioned reflexes
o Pavlov’s dogs

Sympathetic
Sympathetic stimulation reduces the blood flow to the salivary glands, limiting salivary flow and producing the typical dry mouth of anxiety.
o Superior cervical ganglion

The rate of ductal recovery of Na+ is also increased by the release of aldosterone from the adrenal cortex. ( high ENaC, high Na/K/ATPase), making saliva even more hypotonic.

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48
Q

What are the three phases of swallowing?

A

Once food has been masticated and mixed with saliva to form a bolus, it must be swallowed. Swallowing is in three phases:
1. Voluntary Phase

  1. Pharyngeal Phase
  2. Oesophageal Phase
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49
Q

Describe the voluntary phase of swallowing

A

o Tongue moves the bolus back onto the pharynx

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50
Q

Describe the pharyngeal phase of swallowing

A

o Afferent information from pressure receptors in the palate and anterior pharynx reaches the swallowing centre in the brain stem.
o A set of movements is triggered
• Inhibition of breathing
• Raising of the larynx
• Closure of the glottis
• Opening of the upper oesophageal ‘sphincter’

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51
Q

Describe the oesophageal phase of swallowing

A

o The muscle in the upper third of the oesophagus is voluntary striated muscle under somatic control
o The muscle of the lower two thirds is smooth muscle under control of the parasympathetic nervous system.
o A wave of peristalsis sweeps down the oesophagus, propelling the bolus to the stomach in ~9 seconds.
o Coordinated by extrinsic nerves from the swallowing centre of the brain
o Lower oesophageal ‘sphincter’ opens

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52
Q

What is dysphagia?

A

Dysphagia – The symptom of difficulty in swallowing

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53
Q

What are some causes of dysphagia?

A

Dysphagia may result as a consequence of a primary oesophageal disorder, for example motility problems of the smooth muscle preventing peristalsis. The name for this condition is achalasia.
Dysphagia may also result as a secondary consequence of another issue, E.g. obstruction or compression of the oesophagus due to a tumour.

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54
Q

What is odynophagia?

A

Odynophagia – The symptom of pain whilst swallowing

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55
Q

What is oesophageal dysphagia?

A

o Dysphagia for Solids

• Investigate with a barium swallow/endoscopy

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56
Q

What is oropharyngeal dysphagia?

A

o Dysphagia for liquids
• Investigate with a flexible endoscopy evaluation of swallowing. This will allow you to view the entire trachea/oesophagus.
• Most commonly due to a stroke

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57
Q

How is the body adapted to prevent acid reflux from the stomach?

A

The stomach produces strong acids (HCl) and enzymes (pepsin) to aid in the digestion of food. The mucosa of the stomach provides protection from it’s harmful content, but the mucosa of the oesophagus does not have this protection.
The oesophagus is protected from these acids by a one way valve mechanism at it’s junction with the stomach.
This one way valve is called the lower oesophageal sphincter. This coupled with the angle of His that is formed at this point prevents the contents of the stomach refluxing back into the oesophagus.
The crus of the diaphragm helps with the sphincteric action.

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58
Q

What are some consequences of free gastro-oesophageal reflux?

A

Barrett’s oesophagus

Gastro-oesophageal Reflux Disease (GORD)

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59
Q

What is Barrett’s oesophagus?

A

An abnormal change of the epithelial cells of the oesophagus.
This is a metaplasia from non-keratinised stratified squamous epithelia to columnar epithelium and goblet cells. This is in an attempt to better resist the harmful contents of the stomach.
Barrett’s oesophagus is strongly associated with adenocarcinoma, a particularly lethal cancer.

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60
Q

What is GORD?

A

The reflux of the stomach’s contents into the oesophagus and pharynx causes several symptoms, including a cough, hoarseness and asthma.

All of the symptoms result from the acidic contents of the stomach refluxing back out.

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61
Q

Describe the structure of the abdominal wall and it’s boundaries

A

Although it is continuous, the abdominal wall is subdivided into the anterior wall, right and left lateral walls and the posterior wall. The boundary between the anterior and the lateral walls is indefinite; therefore the term anterolateral abdominal wall is used.
The anterolateral abdominal wall is bounded superiorly by the cartilages of the 7th-10th ribs, and the xiphoid process of the sternum, and inferiorly by the inguinal ligament and the superior margins of the anterolateral aspects of the pelvic girdle (iliac crests, pubic crests and pubic symphysis).

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62
Q

What does the anterolateral abdominal wall consist of?

A

The anterolateral abdominal wall consists of skin, subcutaneous tissue (superficial fascia/fat), muscles and their aponeuroses, deep fascia, extraperitoneal fat and parietal peritoneum.

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63
Q

What are the major landmarks of the abdominal wall?

A
Umbilicus
Epigastric Fossa (Pit of the stomach)
Linea Alba
Pubic Crest and Symphysis
Inguinal Groove
Semilunar lines
Tendinous Intersections of Rectus Abdominis
Arcuate Line (aka Douglas’ line)
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64
Q

What is the umbilicus?

A

Obvious feature of the anterolateral abdominal wall at Spinal Level L3

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65
Q

What is the epigastric fossa? (Pit of the stomach)

A

Slight depression in the epigastric region, just inferior to the xiphoid process. Particularly noticeable when a person is in the supine position because the abdominal organs spread out. Heartburn is commonly felt at this site.

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66
Q

What is linea alba?

A

Aponeuroses of abdominal muscles, separating the left and right rectus abdominis. Visible in lean individuals because of the vertical skin groove superficial to it. If the linea alba is lax, when the rectus abdominis contract the muscles spread apart. This is called divarication of recti.

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67
Q

What is the pubic crest and symphysis?

A

The upper margins of the pubic bones and the cartilaginous joint that unite them. Can be felt at the inferior end of the linea alba.

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68
Q

What is the inguinal groove?

A

A skin crease that is parallel and just inferior to the inguinal ligament (runs between ASIS and pubic tubercle). Marks the division between the abdominal wall and the thigh.

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69
Q

What are the semilunar lines?

A

Slightly curved, Tendinous line on either side of the rectus abdominis.

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70
Q

What are the tendinous interjections of rectus abdominis?

A

Clearly visible in persons with well-developed rectus muscles. The interdigitating bellies of the serratus anterior and external oblique muscles are also visible.

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71
Q

What is the arcuate line (aka Douglas line)?

A

Where the fibrous sheath stops (inferior limit of the posterior layer of the rectus sheath). 1/3 of the way from the umbilicus to the pubic crest.

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72
Q

Describe the abdominal musculature

A

There are five (bilaterally paired) muscles in the anterolateral abdominal wall, three flat muscles and two vertical muscles.
Flat Muscles – External Oblique, Internal Oblique and Transversus Abdominis
Vertical Muscles – Rectus Abdominis and Pyramidalis
The three flat muscles’ fibres have varying orientations, with the fibres of the Obliques running diagonally and perpendicular to each other, and the fibres of the Transversus running transversely.
All three flat muscles are continued anteriorly and medially as strong, sheet-like aponeuroses. Between the mid-clavicular line and the midline, the aponeuroses form the tough, aponeurotic, tendinous rectus sheath that encloses the Rectus Abdominis.
The aponeuroses then interweave with their fellows of the opposite side, forming the linea alba, which extends from the xiphoid process to the pubic symphysis. The interweaving is not only between right and left sides, but also between intermediate and deep layers.
The two vertical muscles of the anterolateral abdominal wall are contained within the rectus sheath, the large Rectus Abdominis and small Pyramidalis.

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73
Q

What are the most important features to consider when designing an incision and why?

A

When designing an incision, we want one that we can close and provide long-lasting strength, thus minimising the incidence of incisional herniae. If we try to sew muscle together, the sutures will ‘cut out’.

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74
Q

What is a midline incision?

A

Surgeons suture the linea alba together to provide a strong closure.

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75
Q

What is a transverse incision?

A

Surgeons suture the external oblique aponeuroses together to provide a strong closure

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76
Q

What incision is used for an appendicectomy?

A

o Incision at McBurney’s point
o 2/3rds of the distance between the umbilicus and ASIS
o Through a ‘gridiron’ muscle-splitting incision

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77
Q

What is a gridiron incision?

A

Put scissors in and open and close them to separate out the muscle fibres, followed by the next two layers. Have to separate out the fibres of the external and internal oblique’s and the transversalis.

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78
Q

What is a patent Urachus?

A

Can present at birth or in later life in men when they develop bladder outflow obstruction due to benign prostatic hypertrophy.

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79
Q

What is the Vitelline duct?

A

Vitelline Duct – omphalomesenteric duct- attaches the yolk sac (via the umbilicus) to the midgut lumen of the developing foetus
Can persist resulting in a number of different abnormalities- Meckel’s diverticulum in particular

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80
Q

What is Meckels’ diverticulum?

A
Also known as Ilieal Diverticulum, and is the most common GI abnormality. It is a ‘cul-de-sac’ in the ileum. Meckel’s Diverticulum follows a Rule of 2’s:
o 2% of the population affected
o 2 feet from the ileocecal valve
o 2 inches long
o Usually detected in under 2’s
• Can be asymptomatic
o 2:1 Male:Female
The diverticulum can contain ectopic gastric or pancreatic tissue. The ectopic tissue will secrete enzymes and acids into tissue not protected from them, causing ulceration. The reason for this is not clear.
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81
Q

What is a Vitelline cyst?

A

The vitelline duct forms fibrous strands at either end.

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82
Q

What is a Vitelline fistula?

A

There is direct communication between the umbilicus and the intestinal tract. This results in faecal matter coming out of the umbilicus

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83
Q

What is omphalocoele?

A

Omphalocoele is the persistence of physiological herniation. A part of the gut tube fails to return to the abdominal cavity following its normal herniation into the umbilical cord. Since the umbilical cord is covered by a reflection of the amnion, this epithelial layer covers the defect.
Compare but DO NOT CONFUSE WITH umbilical hernia.

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84
Q

What is gastroschisis?

A

Gastroschisis is the failure of closure of the abdominal wall during folding of the embryo, leaving the gut tube and its derivatives outside the body cavity.
There is no covering over the gut tube/derivatives as they herniate through the abdominal wall directly into the amniotic cavity.

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85
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.
E.g. Shingles affects nerves; pain is felt distally along the nerves from the problem.

Source - tissues such as skin, muscle, joints, bones, and ligaments - often known as musculo-skeletal pain.
Receptors activated - specific receptors (nociceptors) for heat, cold, vibration, stretch (muscles), inflammation (e.g. cuts and sprains which cause tissue disruption), and oxygen starvation (ischaemic muscle cramps).
Characteristics - often sharp and well localised, and can often be reproduced by touching or moving the area or tissue involved.

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86
Q

What is visceral referred pain?

A

In the thorax and abdomen, visceral afferent pain fibres follow sympathetic fibres back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibres.
The CNS perceives visceral pain as coming from the somatic portion of the body supplied by the relevant spinal cord segments.
Visceral pain is caused by ischaemia, abnormally strong muscle contraction, inflammation and stretch.
Touch, burning, cutting and crushing does not cause visceral pain.

Source - internal organs of the main body cavities. There are three main cavities - thorax (heart and lungs), abdomen (liver, kidneys, spleen and bowels), pelvis (bladder, womb, and ovaries).
Receptors activated - specific receptors (nociceptors) for stretch, inflammation, and oxygen starvation (ischaemia).
Characteristics - often poorly localised, and may feel like a vague deep ache, sometimes being cramping or colicky in nature. It frequently produces referred pain to the back, with pelvic pain referring pain to the lower back, abdominal pain referring pain to the mid-back, and thoracic pain referring pain to the upper back.

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87
Q

How is visceral referred pain related to the embryological development of the heart?

A

Foregut Pain – Epigastric region
Midgut pain – Periumbilical region
Hindgut Pain – Suprapubic region

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88
Q

Where do retro peritoneal organs produce pain?

A

Retroperitoneal structures can cause central back pain, e.g. pancreas and abdominal aorta.

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89
Q

Were are the common sites of pain in acute appendicitis?

A

In early appendicitis the pain begins at the umbilicus, since the innervation of the appendix enters the spine at that Level (T10).
Later, as the appendix becomes more inflamed it irritates the surrounding bowel wall, localising the pain to the right lower quadrant (irritation to somatic nerve).

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90
Q

Where is pain felt in small/ large bowel colic?

A

Doubled over in pain.

Small bowel colic Periumbilical (midgut)

Large bowel colic Suprapubic (hindgut)

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91
Q

Where is pain felt in Renal colic?

A

Patient rolls around on the floor.

Pain is “worse than child birth”.

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92
Q

What are some causes of Referred Diaphragmatic irritation and where is pain felt?

A

o Ruptured spleen
o Ectopic Pregnancy
o Perforated ulcer
Blood pools in pelvis, giving pain. The patient feels faint due to the loss of blood, so lies down causing the blood to rush up to the diaphragm (C3/4/5). The presence of blood here results in referred pain to the left shoulder (Liver is in the way of the blood at the right diaphragm).

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93
Q

Describe the peritoneal cavity as a potential space

A

The peritoneal cavity is a potential space of capillary thinness between the parietal and visceral layers of peritoneum. It contains no organs, but contains a thin film of peritoneal fluid. Lymphatic vessels, particularly on the interior surface of the diaphragm absorb the peritoneal fluid.

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94
Q

How does the peritoneal cavity differ in females and males?

A

In males the peritoneal cavity is completely closed, but in females there is a communication pathway to the exterior of the body through the uterine tubes, cavity and vagina. The communication constitutes a potential pathway of infection from the exterior.

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95
Q

Describe the structure of the peritoneum

A

The peritoneum is a continuous, two layered membrane - the parietal peritoneum, which lines the internal surface of the abdominal wall and the visceral peritoneum, which invests viscera such as the stomach and intestines.
Both layers of the peritoneum consist of mesothelium, a layer of simple squamous epithelial cells.

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96
Q

Describe some features of the parietal peritoneum

A

The parietal peritoneum is served by the same blood, lymphatic and somatic nerve supply as the region of the wall it lines. Therefore, like the overlying skin, the interior of the body wall is sensitive to pressure, pain, heat and cold and laceration. Pain is generally well localised, apart from on the inferior surface of the central part of the diaphragm, which is innervated by the phrenic nerve (C3/4/5, referred pain to shoulder). This explains why the pain from appendicitis shifts to over the appendix, as the parietal peritoneum becomes inflamed, localising the pain.

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97
Q

Describe some features of the visceral peritoneum

A

The visceral peritoneum shares the same blood, lymphatic and visceral nerve supply as the organs it covers. Also, like the organs it covers the visceral peritoneum is insensitive to touch, heat and cold and laceration; it is stimulated primarily by stretching and chemical irritation. The pain produced is poorly localised, being referred to the dermatomes of the spinal ganglia providing the sensory fibres.

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98
Q

What is a mesentery?

A

A mesentery is a double layer of peritoneum that occurs as a result of the invagination of the peritoneum by an organ and constitutes a continuity of the visceral and parietal peritoneum. A mesentery connects an intraperitoneal organ to the body wall (usually the posterior abdominal wall)

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99
Q

What is an omentum?

A

An omentum is a double-layered extension or fold of peritoneum that passes from the stomach and proximal part of the duodenum to adjacent organs in the abdominal cavity

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100
Q

What is the greater omentum?

A

A prominent, four-layered peritoneal fold that hands down like an apron from the greater curve of the stomach. After descending it folds back and attaches to the anterior surface of the transverse colon and its mesentery.

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101
Q

What is the lesser omentum?

A

A much smaller, double-layered peritoneal fold that connects the lesser curvature of the stomach and the proximal part of the duodenum to the liver. It also connects the stomach to the portal triad.

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102
Q

What is a peritoneal ligament?

A

A double layer of peritoneum that connects an organ with another organ or to the abdominal wall

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103
Q

Where do peritoneal ligaments connect the liver to?

A

Peritoneal Ligaments Connect the Liver to:
o Anterior abdominal wall – Falciform Ligament
o Stomach – Hepatogastric Ligament (membranous portion of lesser omentum)
o Duodenum – Hepatoduodenal Ligament (the thickened free edge of the lesser omentum, which conducts the portal triad – portal vein, hepatic artery, bile duct)

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104
Q

Where do peritoneal ligaments connect the stomach to?

A

Peritoneal Ligaments Connect the Stomach to:
o Inferior surface of the diaphragm – Gastrophrenic Ligament
o Spleen – Gastrosplenic ligament
o Transverse colon – Gastrocolic ligament (greater omentum)

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105
Q

In what 2 ways can structures of the peritoneum be classified?

A

o Intraperitoneal are completely covered by peritoneum, however not completely enclosed due to the mesentery (think of the concept of a fist in the balloon).
o Retroperitoneal / extraperitoneal are outside the peritoneal cavity and thus are only partially covered by the parietal peritoneum, for example the kidneys lie between parietal peritoneum (only found on the anterior surface) and the posterior abdominal wall.
• Kidneys, ureters, and the bladder
• The aorta and the IVC,
• The oesophagus
• The duodenum (except for the proximal part)
• Most of the pancreas,
• The ascending and descending colon, and the rectum.

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106
Q

What planes divide the abdominal wall and what 9 surface regions are there?

A

The abdomen is divided by the midclavicular lines vertically and the subcoastal and transtubercular lines horizontally.

Right hypochondriac, epigastric, left hypochondriac
Right lumbar, umbilical, left lumbar
Right iliac, suprapubic, left iliac

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107
Q

Explain the relationship between the transverse mesocolon and the supra and infra colic compartments

A

The Transverse Mesocolon (mesentery of the transverse colon) divides the abdominal cavity into a Supracolic Compartment, containing the stomach, liver, and spleen, and an Infracolic Compartment, containing the small intestine and ascending and descending colon.
The Infracolic Compartment lies posterior to the greater omentum and is divided into the right and left Infracolic spaces by the mesentery of the small intestine.

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108
Q

By what means does the supra and infra colic compartments communicate?

A

Free communication occurs between the Supracolic and the Infracolic compartments through the Paracolic Gutters, the groves between the lateral aspect of the ascending or descending colon and the posterolateral abdominal wall.

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109
Q

What is the greater sac?

A

The Greater Sac is made up of the Supracolic and Infracolic compartments

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110
Q

What is the lesser sac?

A

The Lesser Sac, or Omental bursa, is an extensive sac-like cavity that lies posterior to the stomach, lesser omentum, and adjacent structures. It has a superior recess, limited superiorly by the diaphragm and the posterior layers of the coronary ligament of the liver, and an inferior recess between the superior parts of the layers of the greater omentum. Most of the inferior recess becomes sealed off from the main part (posterior to the stomach) after adhesion of the anterior and posterior layers of the greater omentum.
The Lesser Sac/Omental bursa permits free movement of the stomach on the structures posterior and inferior to it because it’s anterior and posterior walls slide smoothly over one another.

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111
Q

By what means do the greater and lesser sac communicate with one another?

A

The Greater and Lesser (omental bursa) Sacs communicate through the omental foramen (epiploic foramen), an opening situated posterior to the free edge of the less omentum (hepatoduodenal ligament – see above). The omental foramen can located by running a finger along the gall bladder to free the edge of the lesser omentum, and usually admits two fingers.

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112
Q

What is the right subphrenic space?

A

The Right Subphrenic Space lies between the diaphragm and the anterior, superior and right lateral surfaces of the right lobe of the liver.
It is bounded on the left side by the falciform ligament and behind by the upper layer of the coronary ligament. It is a relatively common site for collections of fluid after right-sided abdominal inflammation.

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113
Q

What is the left subphrenic space?

A

The Left Subphrenic Space lies between the diaphragm, the anterior and superior surfaces of the left lobe of the liver, the anterosuperior surface of the stomach and the diaphragmatic surface of the spleen.
It is bounded to the right by the falciform ligament and behind by the anterior layer of the left triangular ligament. It is much enlarged in the absence of the spleen and is a common site for fluid collection, particularly after a splenectomy.

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114
Q

Which subphrenic space is larger than the other? And why?

A

The left Subphrenic space is substantially larger than the right (liver is on the right).

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115
Q

What are the Recto-uterine and Vesico-Uterine Pouches?

A

In females the peritoneum passes from the rectum to the posterior vaginal fornix and then back to the uterine cervix and body as the recto-uterine fold, which descends to form the recto-uterine pouch (of Douglas).
The peritoneum spreads over the uterine fundus to its anterior surface as far as the junction of the body and cervix, from which it is reflected forwards to the upper surface of the bladder, forming a shallow Vesico-uterine pouch.

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116
Q

What is the Recto-vesicle Pouch?

A

In males the peritoneum leaves the junction of the middle and lower thirds of the rectum, passing forwards to the upper poles of the seminal vesicles and superior aspect of the bladder. Between the rectum and bladder it forms the rectovesical pouch.

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117
Q

Describe the mesentery of the small intestine

A

A broad, fan shaped fold, connecting the coils of the jejunum and ileum to the posterior abdominal wall. Between the two sheets of peritoneum are blood vessels, lymph vessels are nerves. This allows these part of the intestine to move relatively freely within the abdominal cavity.
The attached, parietal border is the root of the mesentery about 15 cm from the duodenojejunal flexture at the level of left side L2, obliquely (towards inferior right) to the ileocaecal junction.
The root of the mesentery crosses the second and third parts of the duodenum, abdominal aorta, inferior vena cava, right ureter, right psoas major muscle and right gonadal artery.

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118
Q

Describe the sigmoid mesocolon

A

This is a peritoneal fold attaching the sigmoid colon to the pelvic wall, the attachment being an inverted V with an apex near the division of the left common iliac artery.
The left limb descends medial to the left psoas major and the right passes into the pelvis to end in the midline at the level of the third sacral vertebra. Sigmoid and superior rectal vessels run between its layers and the left ureter descends into the pelvis behind its apex.

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119
Q

Where are the four most common sites of hernia formation?

A

Inguinal
Femoral
Umbilical
Epigastric

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120
Q

Describe the structure of the inguinal canal

A

The inguinal canal is an oblique passage that extends in a downward and medial direction. It begins at the deep (internal) inguinal ring and continues for approximately 4cm, ending at the superficial (external) inguinal ring. The canal lies in between the muscles of the anterior abdominal wall and runs parallel and superior to the medial half of the inguinal ligament (the inguinal ligament is the inferior border of the aponeurosis of the external oblique muscle, attached between the ASIS and the pubic tubercle).

The spermatic cord in men and the round ligament of the uterus in women passes through the canal. Additionally, in both sexes the ilioinguinal nerve passes through part of the canal.

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121
Q

What is an inguinal hernia?

A

An inguinal hernia is a protrusion of the abdominal cavity contents through the inguinal canal. They are very common (Lifetime risk 27% for men, 3% for women).

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122
Q

What is a direct inguinal hernia?

A

Protrudes into the inguinal canal through a weakened area in the transversalis fascia near the medial inguinal fossa within an anatomical region known as the Inguinal / Hesselbach’s triangle.

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123
Q

What is an indirect inguinal hernia?

A

Protrudes through the deep inguinal ring, within the diverging arms of the transversalis fascial sling. Most indirect inguinal hernias are the result of the failure of embryonic closure of the deep inguinal ring after the testicle has passed through it.

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124
Q

Describe epigastric hernias

A

Epigastric Hernias occur in the epigastric region, in the midline between the xiphoid process and the umbilicus, through the linea alba.
The primary risk factors are obesity and pregnancy.

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125
Q

Describe umbilical hernias

A

Umbilical Hernias occur through the umbilical ring. They are usually small and result from increased intra-abdominal pressure in the presence of weakness and incomplete closure of the anterior abdominal wall after ligation of the umbilical cord at birth.
Acquired umbilical hernias occur in adults, most commonly in women and obese people.

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126
Q

What is a femoral hernia?

A

Femoral Hernias are a protrusion of abdominal viscera into the femoral canal, occurring through the femoral ring.

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127
Q

What is an umbilical hernia?

A

A protrusion of the abdominal cavity contents through the umbilical ring

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128
Q

What is an epigastric hernia?

A

A protrusion of the abdominal cavity contents in the midline between the xiphoid process and the umbilicus- through the linea alba

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129
Q

Describe a femoral hernia

A

Femoral Hernias are a protrusion of abdominal viscera into the femoral canal, occurring through the femoral ring. A femoral hernia appears as a mass, often tender, in the femoral triangle.

Femoral Hernias are bounded by the femoral vein laterally and the lacunar ligament medially. The hernia compresses the contents of the femoral canal (loose connective tissue, fat and lymphatics) and distends the wall of the canal.

Initially femoral hernias are small, as they are contained within the canal, but they can enlarge by passing inferiorly through the saphenous opening into the subcutaneous tissue of the thigh.

Femoral Hernias are more common in females as they have wider pelves.
Strangulation of femoral hernias may occur because of the sharp, rigid boundaries of the femoral ring.

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130
Q

What is a strangulation of a hernia?

A

The constriction of blood vessels, preventing the flow of blood to tissue

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131
Q

What is incarceration of a hernia?

A

Hernia cannot be reduced, or pushed back into place, at least not without very much external effort.

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132
Q

What parasympathetically innervates the parotid gland?

A
Glossopharangeal nerve (CN9)
Otic ganglion
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133
Q

What parasympathetically innervates the submaxillary and sublingual glands?

A
Facial nerve (CN7)
Submandibular ganglion (submaxillary)
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134
Q

What is the sympathetic innervation of the salivary glands?

A

Superior cervical ganglion

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135
Q

What is released from the adrenal cortex that increases the rate of ductal recovery of Na+? How does it do this?

A

Aldosterone
Increases activity of ENaC and Na/K ATPase
Makes saliva very very hypotonic

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136
Q

Describe the structure of the oesophagus

A

Muscular tube connecting pharynx to the stomach
About 8 inches long
Lined by mucosa- non keratinised stratified squamous
Runs posteriorly to trachea and heart
Runs anteriorly to spine
Just before entering the stomach it passes through the diaphragm
Upper 1/3 - voluntary striated muscle
Lower 2/3 - smooth muscle under control of PSNS

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137
Q

What is the function of the oesophagus?

A

Carries food, liquids, and saliva (bolus) from mouth to stomach

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138
Q

What are the borders of Hesselbachs triangle?

A

The borders of Hesselbach’s triangle are:
o Inferiorly – Medial half of the inguinal ligament
o Medially – Lower lateral border of rectus abdominis
o Laterally – Inferior epigastric artery

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139
Q
Oesophagus
Stomach - function
Stomach - anatomy
Gastric disease
Liver 
Biliary tree
Pancreas
Gall bladder
Spleen
A

E

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140
Q

How long is the oesophagus?

A

25cm

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141
Q

What is the average diameter of the oesophagus?

A

2cm

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142
Q

What are the three constrictions of the oesophagus?

A

Normally has 3 constrictions where adjacent structures produce impressions

  • cervical constriction (upper oesophageal spinchter) - at its beginning at the pharyngo-oesophageal junction; approx. 15cm from incisor teeth; caused by cricopharyngeus muscle
  • thoracic (broncho-aortic) constriction- compound constriction where it is first crossed by the arch of the aorta 22.5cm from incisor teeth, and then where it is crossed by the left main bronchus 27.5cm from the incisor teeth
  • diaphragmatic constriction- where it passes through oesophageal hiatus of diaphragm, approx. 40cm from incisor teeth
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143
Q

How many layers of muscle does the oesophagus have and how does it vary along the oesophagus?

A

Has internal circular and external longitudinal layers of muscle
Superior 1/3 - voluntary striated muscle
Middle 1/3 - both
Inferior 1/3 - smooth muscle

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144
Q

What part of the diaphragm does the oesophagus pass through?

A

Passes through elliptical oesophageal hiatus in the muscular right crus of the diaphragm, just to the left of the median plane at level of T10 vertebra

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145
Q

Where in the stomach does the oesophagus terminate?

A

Terminates by entering the stomach at the cardial orifice of the stomach to the left of the midline at the level of the 7th left costal cartilage and T11 vertebra

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146
Q

What nerve plexus is the oesophagus encircled by distally?

A

Oesophageal (nerve) plexus

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147
Q

How does food move rapidly through the oesophagus?

A

Food passes through rapidly because of the peristaltic action if it’s musculature aided but not dependent on gravity

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148
Q

How is the oesophagus attached to the diaphragm? What does this allow?

A

Oesophagus attached to margins of oesophageal hiatus in the diaphragm by the phrenico- oesophageal ligament - extension of inferior diaphragmatic fascia
Permits independent movement of the diaphragm and oesophagus during respiration and swallowing

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149
Q

Where is the oesophagus trumpet shaped and why?

A

Abdominal part of the oesophagus only 1.25cm long passes from oesophageal hiatus pin the right crus of the diaphragm to the cardial orifice of the stomach, widening as it approaches, passing anteriorly and to the left as it descends inferiorly

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150
Q

Describe the peritoneum around the oesophagus

A

Anterior surface covered with peritoneum of the greater sac, continuous with that covering the anterior surface of the stomach
Posterior part of abdominal part of oesophagus is covered with peritoneum of the omental bursa, continuous with that covering the posterior surface of the stomach

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151
Q

Describe the oesophagus’ location in relation to the stomach

A

Right border- Continuous with the lesser curvature of the stomach
Left border- separated from fundus of stomach by cardiac notch between oesophagus and fundus

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152
Q

Describe the oesophagus’ location in relation to the liver

A

Fits into a groove on the posterior surface of the liver

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153
Q

What is the arterial supply to the oesophagus?

A

Abdominal oesophagus- left gastric artery, (branch of coeliac trunk) and left phrenic artery

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154
Q

Describe the venous drainage of the oesophagus

A

Submucosal veins - portal venous sytem via left gastric veins
Submucosa veins - systemic venous system via the oesophageal veins entering the azygous system

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155
Q

Describe the lymphatic drainage of the oesophagus

A

Of abdominal part is to left gastric lymph nodes - efferent lymphatic vessels from these nodes drain mainly to celiac lymph nodes

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156
Q

What are the functions of the stomach?

A

Stores food
Disinfects food
Breaks food down into chyme- chemical disruption (acid and enzymes) and physical disruption (motility)

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157
Q

Where in the stomach do secretions come from?

A

From gastric pits (contain neck cells) -indentations in stomach mucosa that are openings to gastric glands (contain parietal, chief and G cells (& smooth muscle cells))

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158
Q

What cells in the stomach produce hydrochloric acid? What’s the importance of HCl?

A

Parietal cells

Acid keeps the pH<2

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159
Q

What cells in the stomach produce proteolytic enzymes (pepsin)? What’s the importance of these enzymes?

A

Chief cells

Non specifically breaks down proteins - > peptides

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160
Q

What cells in the stomach produce mucus? What is the importance of this mucus?

A

Neck cells

Sticky so that it’s not easily removed from the stomach lining and basic, due to amine group on the proteins

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161
Q

What cells in the stomach produce HCO3-? What is the importance of HCO3-?

A

Neck cells

Secreted by neck cells into the mucus and provide a buffer for H+ ions

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162
Q

What cells in the stomach produce Gastrin? What is the importance of gastrin?

A

Binds to surface receptor on the parietal cell stimulating acid and intrinsic factor (B12- anaemia)

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163
Q

How is stomach acid produced and secreted into the stomach from the parietal cells?

A

In mitochondria of parietal cells, water is split into H+ and OH- ions- generating lots of H+ ions
Generated OH- ions combine with CO2 fro metabolism to form HCO3- which is exported to the blood (for every mole of H+ secreted into the stomach, 1 mole of HCO3- enters the blood)
H+ produced at a fast rate as parietal cells have lots of mitochondria - but can’t be allowed to accumulate in the cells
Parietal cells have canaliculi (invaginations of the cell wall) which have proton pumps - expel H+ against a high concentration gradient
As concentration gradient is very high, it’s a very energy intensive process

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164
Q

What are the three main factors that stimulate parietal cells to release acid in the stomach?

A

Gastrin
Histamine
Acetyl chlorine

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165
Q

What triggers gastrin to be produced in the stomach?

A

Peptides

Acetyl choline from intrinsic neurones - after they have detected distension (ACh also acts directly in parietal cells)

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166
Q

How does gastrin stimulate acid secretion in the stomach?

A

Hormone is secreted by G cells in stomach
Polypeptide, main form is 17AAs long
Binds to surface receptor on parietal cell
Stimulates acid and intrinsic factor secretion via second messenger pathway

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167
Q

What inhibits gastrin being produced in the stomach?

A

Low pH in stomach - negative feedback

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168
Q

What stimulates histamine production in the stomach?

A

Gastrin and ACh stimulate mast cells to secrete histamine

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169
Q

How does histamine stimulate acid secretion from parietal cells in the stomach?

A

Released from mast cells
Binds to H2 surface receptors on parietal cells, locally
Acid secretion stimulated via c-amp
Works as an amplifier

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170
Q

How does acetyl choline stimulate acid secretion in the stomach?

A

Released from postganglionic parasympathetic neurones
Acts on muscarinic receptor in the parietal cell
Stimulates acid secretion by second messenger pathway

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171
Q

What stimulates ACh secretion in the stomach?

A

Distension

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172
Q

What are the 3 phases of gastric secretion?

A

Cephalic phase
Gastric phase
Intestinal phase

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173
Q

Describe the cephalic phase of gastric secretion

A

The ‘brain led’ phase. The sight and smell of food, and the act of swallowing, activates the parasympathetic nervous system, which stimulates the release of Ach. This stimulates parietal cells directly and via histamine (increases Acid).

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174
Q

Describe the gastric phase of gastric secretion

A

Once food reaches the stomach, it causes distension, further stimulating Ach release, and subsequently parietal cells (increases Acid).
The arrival of food will also buffer the small amount of stomach acid in the stomach in between meals, causing luminal pH to rise. This disinhibits Gastrin (increases Acid).
Acid and enzymes will then act on proteins to produce peptides, further stimulating Gastrin release as the pH falls and the initial disinhibition is removed (increases Acid).

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175
Q

Describe the intestinal phase of gastric secretion

A

Once chyme leaves the stomach in significant quantities, it stimulates the release of the hormones Cholecystokinin and Gastric Inhibitory Polypeptide from the intestines that antagonise Gastrin (decreases Acid). Coupled with this, the small amount of acid left in the stomach is no longer being buffered by food, and the low pH inhibits Gastrin (decreases Acid).

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176
Q

What drugs affect acid secretion?

A

Acid secretion may be reduced by inhibition of:
o Histamine at H2 Receptors
E.g. Cimetidine
Removes the amplification of Gastrin/Ach signal
o Proton Pump Inhibitors (PPIs)
E.g. Omeprazole
Prevents H+ ions being pumped into parietal cell canaliculi
o also treat ulcers by eliminTing H pylori with antibiotics

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177
Q

Describe the stomachs defences to acid

A

The luminal pH of the stomach is usually below 2. Without any protection, this would dissolve mucosa. Neck cells secrete mucus to protect the mucosa.
Mucus is Sticky, so is not easily removed from the stomach lining. It is also Basic, due to Amine groups on the proteins.
The mucus forms a ‘unstirred layer’ that ions cannot move through easily.
H+ ions slowly diffuse in and react with the basic groups on mucus and with HCO3- that is secreted by surface epithelial cells.
Because of the unstirred layer, HCO3- stays close to the surface cells. This means the pH at the surface cells is well above 6.
Mucus and HCO3- secretion from neck cells and surface cells respectively is stimulated by prostaglandins, which are promoted by most factors that stimulate acid secretion.

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178
Q

How are the stomachs defences breached?

A

o Alcohol
• Dissolves the mucus, allowing the acid to attack the stomach
o H. Pylori
• Surface cells become infected, inhibiting mucus/HCO3- production
o NSAIDS
• Inhibit prostaglandins, therefore reducing defences
• Some, like aspirin are converted to a non-ionised form by stomach acid, allowing them to pass through the mucus layer into cells before they re-ionise.

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179
Q

What are the two mechanisms of stomach motility?

A

Receptive relaxation

Rhythmic contractions

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180
Q

What is receptive relaxation of the stomach?

A

As food travels down the oesophagus, a neural reflex carried out by the vagus nerve triggers the relaxation of the muscle in the stomach’s wall, so pressure does not increase. This means that pressure in the stomach does not increase as it fills limiting reflux and allowing us to consume large meals (but not if there is damage to the vagus nerve).

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181
Q

What are the rhythmic contractions of the stomach?

A

The stomach has longitudinal and circular muscle that is driven by a pacemaker in the cardiac region. The pacemaker fires ~3 times a minute, causing regular, accelerating peristaltic contractions from the Cardia to Pylorus.
This, combined with the stomach’s funnel shape both mixes the contents of the stomach and moves liquid chyme into the pyloric region. This occurs as the accelerating peristaltic wave overtakes larger lumps, driving them back into the fundus. Chyme however is decanted into the pyloric region.

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182
Q

Describe gastric emptying

A

Accelerating, rhythmic, peristaltic contraction moving solid lumps backwards into the fundus of the stomach whilst letting liquid chyme moving forwards
As chyme enter pyloric region, a small squirt is ejected before the peristaltic wave reaches the Pylorus and shits it - so rest of chyme returns to stomach

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183
Q

How is gastric emptying controlled?

A

3 peristaltic waves - 3 ejected squirts of chyme a minute
Squirt volume affected by rate of acceleration of peristaltic wave and hormones from the intestine
Gastric emptying slowed by fat, low pH and hypertonicity in the duodenum

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184
Q

What is the stomach?

A

Expanded part of the GI tract between the oesophagus and duodenum

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185
Q

What is the stomach specialised for?

A

Specialised for accumulation of ingested food

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186
Q

How much food can the adult stomach hold?

A

2-3litres

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187
Q

What are the 5 recognisable parts of the stomach?

A
Cardia 
Fundus
Body
Antrum
Pylorus
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188
Q

What are the 2 curvatures of the stomach?

A

Greater and lesser

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189
Q

Which part of the stomach releases HCl and pepsinogen generally?

A

Upper 2/3

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190
Q

What part of the stomach releases mucus and gastrin generally?

A

Lower 1/3

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191
Q

What two spinchters are found at the entrance and exit of the stomach?

A

Inferior oesophageal spinchter

Pyloric spinchter

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192
Q

Describe the inferior oesophageal spinchter

A

Lies to left of T11 vertebral on horizontal plane through tip of xiphoid process
Immediately superior to Z line diaphragmatic musculature forming the oesophageal hiatus functions as a physiological spinchter that contracts and relaxes
This coupled with the cardiac notch prevents reflux

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193
Q

What is the Z line?

A

Line where the mucosa abruptly changes from oesophageal to gastric is the Z line

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194
Q

Describe the pyloric spinchter

A

At pyloric end of stomach, circular muscle coat is thickened to produce the pyloric spinchter
This controls the discharge of stomach contents through the pyloric orifice into the duodenum

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195
Q

What’s the macroscopic structure of the gastric mucosa?

A

When empty the gastric mucosa is thrown into longitudinal folds called RUGAE
Gastric canal forms temporarily between gastric folds along lesser curvature of stomach to allow saliva and other fluids (and small amounts of chewed food) to pass along to the pylorus

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196
Q

What’s the microscopic structure of the gastric mucosa?

A

Columnar type epithelia
Cardia- neck cells–> mucus
Fundus and body- neck cells –> mucus ; parietal cells –> acid ; chief cells –> pepsinogen
Pylorus - neck cells–> mucus ; G cells –> gastrin

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197
Q

What are 4 features in the abdomen associated with the stomach?

A

Greater omentum
Lesser omentum
Epiploic foramen
Coeliac trunk

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198
Q

What is the greater omentum?

A

A prominent, four-layered peritoneal fold that hands down like an apron from the Greater Curve of the Stomach. After descending it folds back and attaches to the anterior surface of the Transverse Colon and its mesentery

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199
Q

What is the lesser omentum?

A

A much smaller, double-layered peritoneal fold that connects the Lesser Curvature of the Stomach and the Proximal part of the Duodenum to the Liver. It also connects the stomach to the portal triad.

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200
Q

What is the epiploic foramen?

A

The Greater and Lesser (omental bursa) Sacs communicate through the omental foramen (epiploic foramen), an opening situated posterior to the free edge of the less omentum (hepatoduodenal ligament – see above). The omental foramen can located by running a finger along the gall bladder to free the edge of the lesser omentum, and usually admits two fingers.

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201
Q

What is the coeliac trunk?

A

Originates from the abdominal aorta, giving rise to left gastric, splenic and common hepatic arteries

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202
Q

Describe the blood supply to the stomach

A

Lesser curvature - supplied by left gastric artery and common hepatic artery leading to the right gastric artery // drained by left and right gastric veins that drain to the hepatic portal vein
Greater curvature - supplied by splenic artery leading to the left epiploic artery and the common hepatic artery leading to the gastroduodenal artery and the right epiploic artery // drained by left epiploic vein that drains to the splenic vein and the right epiploic vein that drains to the SMV- splenic vein and SMV drain into hepatic portal vein
Fundus and body- supplied by splenic artery leading to the posterior gastric/ small gastric artery // drained by small gastric vein that drains into the splenic vein which drains into the hepatic portal vein

203
Q

What are the normal anti reflux mechanisms that prevent reflux of acid into the lower oesophagus?

A

o Lower oesophageal sphincter – which is usually closed and transiently relaxes as part of physiology of swallowing to allow bolus to move into stomach
o Oesophagus enters stomach in abdominal cavity
o Pressure in abdominal cavity is higher than that of thoracic
o Right crus of diaphragm acts as sling around the lower oesophagus

204
Q

A small amount of acid reflux is normal- what is this normally controlled by?

A

Some acid reflux is normal and this is normally dealt with by secondary peristaltic waves, gravity and salivary bicarbonate.

205
Q

What is GORD?

A

Clinical features of GORD occur when antireflux mechanisms fail and there is prolonged contact of gastric juices with lower oesophageal mucosa.
Gastro-oesophageal reflux disease (GORD)

206
Q

What is the main clinical feature of GORD?

A
o Dyspepsia (heartburn)
• Worse on lying down, bending over and drinking hot drinks.
207
Q

What investigations are usually involved in the diagnosis of GORD?

A

Usually clinical diagnosis made without investigation on symptoms alone, no need to investigate unless alarming symptoms (such as dysphagia) or hiatus hernia is suspected (which would be investigated by endoscopy.

208
Q

How is GORD generally managed?

A

o Lifestyle
• Lose weight, stop smoking, reduce alcohol consumption, reduce consumption of food groups known to aggravate (e.g. chocolate, fatty foods)
o Medication
• Simple antacids – e.g. calcium carbonate (neutralisies acid)
• Raft antacids (alginates) – e.g. Gaviscon liquid, taken after eating which creates protective raft that sits on top of stomach contents to prevent reflux
• PPIs – e.g. omeprazole – reduction in acid secretion by parietal cells
• H2 antagonists – e.g. ranitidine – blocks H2 receptors which reduced acid secretion

209
Q

What is a potential complication of GORD?

A

Continual contact of gastric juices with oesophageal mucosa can lead to metaplastic change to Barrett’s oesophagus

210
Q

What is PUD?

A

Peptic ulcer is break in superficial epithelial cells penetrating down into Muscularis mucosa of either stomach (GU) or duodenum (DU). Most DUs are found in duodenal cap and GUs are most commonly seen in lesser curvature of stomach

211
Q

What are the main causes of PUD?

A

Leading cause in developed world is use of NSAIDs, which inhibit production of prostaglandins, prevents production of protective unstirred layer (innate protection against gastric acid). 50% of patients taking long term NSAIDs have mucosal damage and 30% when endoscoped have peptic ulceration but only 5% will be symptomatic and only 1-2% will have complication such as GI bleed.
Also caused most commonly in developing countries by Helicobacter Pylori

212
Q

What are the main clinical features of PUD?

A

o Recurrent, burning epigastric pain (pain is often worse at night and when hungry with Duodenal Ulcers and relieved when eating). Pain may subside with antacids
• Persistent, severe pain suggest penetration of ulcer into other organs
• Back pain suggest penetrating posterior ulcer
o Can also get nausea, vomiting (though less common)
o With GUs can get weight loss and anorexia
o May be asymptomatic and present for first time with hematemesis when ulcer has perforated blood vessel(s)

213
Q

What investigations are involved in the diagnosis of PUD?

A

o Investigate H pylori infection

o In older patients (over 55y/o) or with other alarming symptoms à endoscopy to exclude cancer

214
Q

What is the general management for PUD?

A

o If due to H pylori infection à Triple Therapy
• Proton Pump Inhibitor – Omeprazole
• Antibiotics – Clarithromycin / Amoxicillin
• H2 Antagonist – Cimetidine
o If taking NSAIDs – stop or review – use alternatives (NSAIDs with lower risk of causing PUD), or use prophylactic PPI as well as NSAID
• PPI – e.g. omeprazole

215
Q

What are some complications of PUD?

A

o Haemorrhage of blood vessel which ulcer has eroded à presents with hematemesis and melena
o Perforation of the ulcer – more common in DUs than GUs – usually perforate into peritoneal cavity
o Gastric outlet obstruction à can be pre-pyloric, pyloric or duodenal. Occurs either because of active ulcer with oedema or due to healing of an ulcer with associated fibrosis (scarring). Gastric outlet obstruction normally presents as vomiting without pain.

216
Q

Describe Helicobacter pylori and its mechanism of action

A

o H pylori is a gram negative, aerobic, helical, urease producing bacterium that resides in the stomach of infected individuals.
o Production of urease produces ammonia, which neutralises acidic environment, which allows bacterium to survive.
o It colonises gastric epithelium – in mucous layer or just beneath. Damage to epithelia occurs through enzymes released and through induction of apoptosis. Damage also occurs due to the inflammatory response to the infection (inflammatory cells and mediators)

217
Q

What investigations are involved in the diagnosis of helicobacter pylori infection?

A

o IgG detected in serum (relatively good sensitivity and specificity)
o 13C-urea breath test (13C-urea ingested – if H pylori present the urease produced will break down 13C-urea to NH3 and CO2 – CO2 (where the carbon is 13C) will be exhaled on breath and detected).
o Can also take gastric sample by endoscopy and detect by histology and culture

218
Q

What is the general treatment of helicobacter pylori infection?

A

o Triple therapy.
• Proton Pump Inhibitor – Omeprazole
• Two Antibiotics – Clarithromycin / Amoxicillin
• H2 Antagonist (if severe)
o This standard eradication therapy, depending on local resistance, is successful at eradicating infection in 90% of patients.
• 7-14 day treatment – 14 days more effective but side-effects of treatment may put patients off finishing two week course

219
Q

What 4 sequelae can result from an infection by helicobacter pylori?

A

o Gastritis
• Usual effect of infection, which is usually asymptomatic.
• Chronic gastritis causes hypergastrinaemia due to gastrin release from astral G cells à this increased acid production is usually asymptomatic but can lead to duodenal ulceration (which will eventually produce symptoms)
o Peptic ulcer disease
• Duodenal ulcers (DUs) à prevalence of DU due to H pylori is falling due to decreased prevalence of H pylori infection. If ulcers due to H pylori infection, eradication of infection relieves symptoms and decreases chances of recurrence. The precise mechanism of ulceration is unclear (only occurs in 15% of infected people) à factors implicated though are genetic predispositions, bacterial virulence, increased gastrin secretion and smoking
• Gastric ulcers (GUs) à associated with gastritis affecting the body as well as antrum, which can cause parietal cell loss à reduction in acid production. Ulceration thought to occur due to reduction in gastric mucosal resistance due to cytokine production as a result of infection
o Gastric cancer

220
Q

How may gastric acid secretion be reduced by drugs?

A

Acid secretion may be reduced by inhibition of:
o Histamine at H2 Receptors
E.g. Cimetidine
Removes the amplification of Gastrin/Ach signal
o Proton Pump Inhibitors (PPIs)
E.g. Omeprazole
Prevents H+ ions being pumped into parietal cell canaliculi

221
Q

What is the condition of chyme when it’s emptied into the duodenum? And how is this generally corrected?

A

Acidic- corrected by HCO3- secreted from the pancreas, liver and duodenal mucosa
Hypertonic- corrected by osmotic movement of water across the duodenal wall
Partly digested- completed by enzymes from pancreas and small intestinal mucosa and bile acids from liver

222
Q

What is the pancreas?

A

Exocrine and endocrine gland

223
Q

What two substances does the exocrine pancreas secrete?

A

Alkaline juice

Enzymes

224
Q

Where are the enzymes secreted from in the pancreas?

A

Acini

225
Q

Where is the alkaline juice secreted from in the exocrine pancreas?

A

Ducts

226
Q

What enzymes are secreted from the acini in the exocrine pancreas?

A

Proteases- trypsin(ogen), chymotrypsin(ogen), (pro)elastase, (pro)carboxypeptidase
Amylases
Lipases

227
Q

How are enzymes secreted from the acinar cells in the pancreas?

A

Enzymes are synthesised on ribosomes- mostly as inactive precursors
They are packaged into condensing vacuoles the Golgi complex to form zymogen granules
Zymogen granules are secreted by exocytosis (incorporated into a sac in the membrane that everts)
Activated in intestine by enzymatic cleavage

228
Q

What stimulates acinar secretion of enzymes in the pancreas?

A

Acinar secretion is stimulated by:
CCK- released from duodenal APUD cells in response to hypertonicity and fats in the chyme being detected (often called the intestinal phase)
Gastrin- G cells in stomach
ACh- stimulated release by vagus nerve (cephalic phase- pancreas begins to make enzymes when food is first smelt etc.)

229
Q

How does CCK affect acinar cells of the pancreas, the stomach and e gall bladder?

A

Acinar cells of pancreas- stimulates enzyme secretion
Stomach- inhibits acid secretion
Gall bladder- stimulates contraction

230
Q

What family of hormones does CCK belong to?

A

Gastrin

231
Q

What inhibits acid secretion in the stomach?

A

Cholecystokinin (CCK)

232
Q

What is the liver?

A

Largest single organ with many functions

233
Q

What are the main functions of the liver?

A

Blood- energy metabolism, detoxification, plasma proteins

Gut- bile secretion 0.25-1l /day (bile acid and alkaline juice for digestion// excretion of bile pigment- bilirubin)

234
Q

Describe the microscopic structure of the liver and relate this to its function

A

The microscopic structure of the liver supports its function. The basic functional unit is a lobule surrounding a central vein, which drains blood from the liver to the systemic veins. Blood from the hepatic portal vein and hepatic arteries enters vessels at the periphery of the lobule, and flows through sinusoids lined by hepatocytes to the central vein.
Hepatocytes are very complex cells that support most of liver functions.
Bile is formed in canaliculi, and flows towards the periphery into bile ducts.

235
Q

Bile has two components- what are they?

A

Bile acid dependent component

Bile acid independent component

236
Q

Where is the bile acid dependent component of bile secreted from? And what does it consist of?

A

Secreted into canaliculi by hepatocytes

Consists of bile acid and pigment (bilirubin)

237
Q

Where is the bile acid independent component of bile secreted from? And what does it consist of?

A

Secreted from the hepatic duct cells

Consists of alkaline juice which is practically identical to that from pancreas (HCO3-, ions and water)

238
Q

Describe the digestion of fats with the help of bile in the duodenum?

A

Fats are relatively insoluble in water, making them tend to aggregate into large globules, preventing the effective action of digestive enzymes. Acid in the stomach exacerbates this.

In the duodenum, bile acids enable fats to be incorporated into small (4-6nm) micelles, with fats in the middle and the polar components of bile acids on the outside. These micelles generate a high surface area for the action of lipases, which cleave the fatty acids from glycerol. The micelles also carry these products into the ‘unstirred layer’ immediately next to the mucosa, where fatty acids can be released to slowly diffuse into the epithelial cells.

Once inside the epithelial cells they are reconstituted into triacylglycerols and re-expelled as chylomicrons, structured small particles made up of lipids covered in phospholipids, which facilitate the transport of fat in the lymphatic system from the gut to systemic veins.

239
Q

How are gall stones formed?

A

Bile acids return to the liver in between meals and are secreted by canaliculi cell walls a long time before they are next needed. Until they are needed, they are stored in the gall bladder.
To reduce the volume that needs to be stored, bile acids are concentrated by the transport of salt and water across the gall bladder epithelium. However, the concentration process increases the risks of precipitation, leading to Gall Stones.
Gallstones are often asymptomatic, but they can move into the neck of the gall bladder or biliary tree, causing very painful biliary colic or even obstruction. This is often followed by inflammation (Cholecystitis) and infection of the Gall Bladder.

240
Q

Why is pain from gall stones usually worse after eating?

A

Pain from Gallstones can be worse after eating, as the secretion of Cholecystokinin (CCK) will cause the gall bladder to contract

241
Q

Gall stones found in the cystic duct can lead to what?

A

Cholecystitis

242
Q

Gall stones found in the common bile duct can lead to what?

A

Ascending cholangitis

243
Q

Gall stones found in the terminal duct / ampulla of varta can lead to what?

A

Pancreatitis

244
Q

What are the two most common causes of pancreatitis?

A

Chronic alcohol abuse

Gall stone in ampulla of varta/ terminal duct

245
Q

What is steatorrhoea?

A

If bile acids or pancreatic enzymes (Lipases) are not secreted in adequate amounts, fat appears in faeces. This makes them pale, float and smell foul. This is relatively common, and is called Steatorrhoea, or ‘Fatty Faeces’.

246
Q

What is jaundice?

A

Bile pigments are excretory products. The most common bile pigment is Bilirubin, produced as a product of haemoglobin breakdown.

Bilirubin is conjugated in the liver and secreted in the bile to be excreted in faces.

If it cannot be excreted it accumulates in the blood, giving the condition known as Jaundice.

247
Q

What is the pancreas?

A

Elongated accessory digestive exocrine and endocrine gland

248
Q

Describe the location of the pancreas

A

Lies retroperitoneally
Overlies and transversely crosses bodies of L1 and L2 vertebra along the transpyloric plane pm the posterior abdominal wall
Lies posterior to stomach, between duodenum on right and spleen on left
Transverse mesocolon attaches to its anterior margin

249
Q

What are the exocrine secretions of the pancreas?

A

Pancreatic juice from Acinar cells (enzymes) and duct cells (alkaline juice)
- enters the duodenum through the main and accessory pancreatic ducts

250
Q

What are the endocrine secretions of the pancreas?

A

Glucagon and insulin from pancreatic islets of langerhans

- enter the blood

251
Q

What are the four regions of the pancreas?

A

Head
Neck
Body
Tail

252
Q

Describe the head of the pancreas

A

The expanded part of the gland, embraced by the C-shaped curve of the duodenum, to the right of the superior mesenteric vessels and just inferior to the transpyloric plane.
Firmly attaches to medial aspect of descending and horizontal part of duodenum.
Ulcinate process- projection from inferior part of head, extends medially to left, posterior to SMA.
Rests posteriorly on IVC, tight renal artery and vein and left renal vein.
Bile duct en route to opening in descending part of duodenum - lies in groove on posterio-superior surface of the head (or is embedded in it)

253
Q

Describe the neck of the pancreas

A

Short (1.5-2cm), and overlies the superior mesenteric vessels, which form a groove in it’s posterior surface.
The anterior surface of the neck is covered with peritoneum and adjacent to the pylorus of the stomach.
The SMV joins the splenic vein posterior to the neck to form the hepatic portal vein.

254
Q

Describe the body of the pancreas

A

Continues from the neck and lies to the left of the superior mesenteric vessels, passing over the aorta and L2 vertebra, continuing just above the transpyloric plane posterior to the omental bursa.
The anterior surface is covered with peritoneum and forms part of the stomach bed.
The posterior surface is devoid of peritoneum and is in contact with the aorta, SMA, left suprarenal gland, left kidney and renal vessels.

255
Q

Describe the tail of the pancreas

A

Lies anterior to the left kidney, where it is closely related to the splenic hilum and the left colic flexure. The tail is relatively mobile and passes between the layers of the splenorenal ligament with the splenic vessels.

256
Q

Describe the main pancreatic duct

A

The main pancreatic duct begins at the tail of the pancreas and runs through the gland to the head. It then turns inferiorly, and is closely related to the bile duct. The two usually unite to form to short, dilated hepatopancreatic Ampulla of Vater, which opens into the descending part of the duodenum at summit of major duodenal papilla.
3 spinchters- spinchter of pancreatic duct, spinchter of bile duct, hepatopancreatic spinchter

257
Q

What is the accessory pancreatic duct?

A

Opens into duodenum at summit of minor duodenal papilla.
Usually communicates with main pancreatic duct.
Sometime main pancreatic duct is smaller than the accessory duct and so two are not connected and the accessory duct will carry more pancreatic juice.

258
Q

What is the arterial supply of the pancreas?

A

The arterial supply of the pancreas is derived mainly from the branches of the Splenic Artery. Multiple Pancreatic arteries that form arches with pancreatic branches of the Gastroduodenal and Superior Mesenteric arteries.
The Anterior and Posterior Superior Pancreaticoduodenal Arteries (branches of the Gastroduodenal Artery) and the Anterior and Posterior Inferior Pancreaticoduodenal Arteries (branches of the SMA) form anteriorly and posteriorly placed arches that supply the head.

259
Q

What is the venous drainage of the pancreas?

A

Venous drainage from the pancreas occurs via a corresponding Pancreatic Veins. The head of the pancreas has corresponding Superior and Inferior Pancreaticoduodenal Veins.

Most pancreatic veins empty into the splenic vein, but some empty into the SMV.

260
Q

What is the nervous supply of the pancreas?

A

Derived from vagus and abdominal splanchnic nerves- passing through the diaphragm
PSNS and SNS fibres also distributed to acinar cells and islets
PSNS fibres are secretomotor but pancreatic secretions are primarily mediated by CCK and secretin (hormones formed by epithelia cells of duodenum and proximal intestinal mucosa under stimulus of acid contents from stomach)

261
Q

What is the liver?

A

The liver is the largest gland in the body, and after the skin, the largest single organ. Except for fat, all nutrients absorbed from the digestive tract are initially conveyed to the liver by the portal venous system.

262
Q

Describe the location of the liver in the body

A

The liver lies mainly in the right upper quadrant of the abdomen where it is protected by the rib cage and diaphragm. The normal liver lies deep to ribs 7-11 on the right side and cross the midline towards the left nipple. Consequently, the liver occupies most of the right hypochondrium and upper epigastrium and extends into the left hypochondrium.

263
Q

How does the livers position in the body change with movement of the diaphragm and gravity?

A

The liver moves with the excursions of the diaphragm and is located more inferiorly when standing due to gravity.

264
Q

Describe some of the surfaces and borders of the liver

A

The liver has a convex Diaphragmatic surface (anterior, superior and some posterior) and a relatively flat or even concave Visceral surface (posteroinferior), where are separated anteriorly by its sharp Inferior border that follows the right costal margin inferior to the diaphragm.

265
Q

What are the subphrenic recesses? The falciform ligament? Sub hepatic space?

A
Subphrenic recesses (superior extensions of the peritoneal cavity (great sac) exist between the diaphragm and the anterior and superior aspects of the diaphragmatic surface of the liver.
The Subphrenic recesses are separated into right and left recesses by the Falciform ligament, which extends between the liver and the anterior abdominal wall. The attachment of the Falciform ligament divides the Right Lobe from the much smaller Left Lobe. The portion of the Supracolic compartment of the peritoneal cavity immediately inferior to the liver is called the subhepatic space.
266
Q

What is ligamentum teres?

A

The round ligament, or ligamentum teres is contained within the Falciform ligament. (Liver) It is the embryonic remnant of the umbilical vein.

267
Q

What is the bare area of the liver? What vessel lies in this area?

A

The Diaphragmatic surface of the liver is covered with visceral peritoneum, except posteriorly in the Bare Area of the liver, where it lies in direct contact with the diaphragm. There is a deep groove in the bare area, where the inferior vena cava travels.

268
Q

Link the bare area of the liver to the coronary ligament and triangular ligaments

A

The bare are is marked out by the reflection of the peritoneum from the diaphragm to it as the anterior (upper) and poster (lower) layers of the Coronary Ligament.

These layers met on the right to form the Right Triangular Ligament and diverge towards the left to enclose the triangular bare area.
Near the apex of the wedge-shaped liver, the layers meet on the left to form the Left Triangular Ligament.

269
Q

What is the fossa of the gallbladder on the liver? And the porta hepatis?

A

The visceral surface of the liver is covered with peritoneum, except at the fossa for the gallbladder and the porta hepatis (like a hilum) a transverse fissure where vessels (hepatic portal vein, hepatic artery and lymphatics) that supply and drain the liver enter and leave it.
In contrast to the smooth diaphragmatic surface, the visceral surface bears multiples fissures and impressions from contact with other organs.

270
Q

Describe the lobes of the liver

A

The liver is split into two anatomical and two accessory lobes by the reflections of peritoneum from its surface, the fissures formed in relation to those reflections and the vessels serving the liver and the gallbladder.
Left lobe
Right lobe- contains within it the caudate and quadrate lobes

Liver has 8 functional lobes but 4 anatomical lobes

271
Q

What are the caudate and quadrate lobes of the liver?

A

On the visceral surface, the right and left sagittal fissures split the right lobe with the porta hepatis into the Quadrate Lobe (gallbladder) anteriorly and inferiorly and the Caudate Lobe (IVC) posteriorly and superiorly.

272
Q

Describe the gall bladder

A

The Gallbladder is 7-10cm long and lies in the fossa for the gallbladder on the visceral surface of the liver. This fossa lies at the junction of the right and left lobes of the liver.
The Gallbladder is pear-shaped and can hold up to 50ml of bile. Peritoneum completely surrounds it’s fundus and binds it’s body and neck to the liver.
The hepatic surface of the gallbladder is attached to the liver by connective tissue of the fibrous capsule of the liver.
The gallbladder has three parts:
o Fundus
o Body
o Neck
The neck of the gallbladder joins the cystic duct

273
Q

Describe the biliary tree

A

The Biliary Ducts convey bile from the liver to the duodenum.
Hepatocytes produce bile continuously, secreting it into canaliculi.
The canaliculi drain into the small interlobular biliary ducts and then into the large collecting bile ducts, which in turn merge to form the right and left hepatic ducts.
Shortly after leaving the porta hepatis, these hepatic ducts unite to form the common hepatic duct, which is joined on the right side by the cystic duct to form the common bile duct, which conveys the bile to the duodenum, through the Ampulla of Vater (spinchter of Oddi). Shortly before this, the Pancreatic Duct joins the common bile duct.

274
Q

What’s the arterial supply to the gallbladder and biliary tree?

A

The arterial supply of the gallbladder and cystic duct is from the Cystic Artery, which commonly arises in the triangle between the common hepatic duct, cystic duct and visceral surface of the liver, the cystohepatic triangle (of Calot).

275
Q

What’s the venous drainage from the gallbladder and biliary tree?

A

The venous drainage from the neck of the gallbladder and cystic duct flows via the Cystic Veins. These small and usually multiple veins enter the liver directly or drain through the hepatic portal vein.

The venous drainage from the fundus and body of the gallbladder pass directly into the visceral surface of the liver and drain into the hepatic sinusoids.

276
Q

What is the spleen?

A

The spleen is an ovoid, usually purplish, pulpy mass about the size and shape of a fist. It is relatively delicate and considered the most vulnerable abdominal organ.

277
Q

Where is the spleen located?

A

The spleen is located in the Upper Left Quadrant (ULQ) or hypochondrium of the abdomen, resting on the left colic flexure. It is entirely covered by a layer of visceral peritoneum, except at the splenic hilum, where the splenic branches of the splenic artery and vein enter and leave.

278
Q

How is the spleen related to its surrounding structures?

A
The relations of the spleen are:
o Anteriorly
The stomach
Attached by the Gastrosplenic Ligament
o Posteriorly
The left part of the diaphragm, which separates it from the pleura, lung and ribs 9-11
o Inferiorly
The left colic flexure
o Medially
The left kidney
Attached by the Splenorenal ligament
279
Q

What’s the arterial supply to the spleen?

A

The arterial supply of the spleen is from the Splenic Artery, the largest branch of the coeliac trunk. It follows a tortuous course posterior to the omental bursa, anterior to the left kidney and along the superior border of the pancreas.
Between the layers of the splenorenal ligament, the splenic artery divides into five or more branches that enter the hilum, supplying the different vascular segments of the spleen.

280
Q

What is the venous drainage of the spleen?

A

The venous drainage of the spleen flows via the Splenic Vein, formed by several tributaries that emerge from the hilum.
It is joined by the Inferior Mesenteric Vein and runs posterior to the body and tail of the pancreas throughout most of its course.
The splenic vein unites with the Superior Mesenteric Vein posterior to the neck of the pancreas to form the Hepatic Portal Vein.

281
Q

What are the range of toxins that the GI tract and liver may be exposed to?

A
Inevitably, when we ingest food and water we also risk ingesting toxins. These include:
o Chemical
o Bacteria
o Viruses
o Protozoa
o Nematodes (Roundworms)
o Cestodes (Tapeworms)
o Trematodes (Flukes)
282
Q

What are the physical innate mechanisms of defence against toxins?

A

o Sight / Smell
• If food looks or smells bad you don’t eat it
o Memory
• If food tastes bad, you don’t eat it next time
o Saliva
• pH 7.0
• Contains lysozyme, lactoperoxidase, complement, IgA and polymorphs
• Washes toxins down into the stomach
o Stomach Acid
• Low pH kills the majority of bacteria and viruses
o Small Intestine Secretions
• Bile
• Proteolytic enzymes
• Lack of nutrients
• Shedding of epithelial cells
o Colonic mucus
• Protects the colonic epithelium from it’s contents
o Anaerobic environment (Small bowel, colon)
o Peristalsis/Segmentation
• Normal intestinal transit time is 12 – 18hrs. If peristalsis is slowed, gut infections are prolonged. E.g. shigellosis.

283
Q

What is xerostomia?

A

Severe illness and/or dehydration results in a reduced salivary flow (xerostomia) and dry mouth, which then leads to microbial overgrowth in the mouth and dental caries
Can lead to parotitis caused by infection by staphylococcus aureus (mortality of 25%)

284
Q

What is achlorhydria?

A

Condition where patients don’t produce enough gastric acid in the stomach
Usually have pernicious anaemia, and are on drugs such as H2 antagonists and proton pump inhibitors
Usually makes the patient more susceptible to shigellosis, cholera and salmonella infections

285
Q

If a patient is taking PPIs in a hospital, what are they at more risk of acquiring?

A

C. Difficile

286
Q

What bacteria and viruses are resistant to gastric acid?

A

MTB is resistant to gastric acid (acid and alcohol fast bacterium AAFB)- so gastric washings can be used to collect the bacteria for diagnostic purposes
H. Pylori produces urease which acts in urea to produce a protective cloud of ammonia
Enteroviruses such as HEPATITIS A, POLIO and COXSACKIEVIRUS are resistant to gastric acid

287
Q

What are the cellular innate defences to toxins?

A

Cellular Innate Defences
o Neutrophils- trap and kill bacteria
o Macrophages- circulating monocytes –> tissue macrophages ; lungs liver and spleen
• Kupffer cells in the Liver
o Natural Killer cells (Kill virus infected cells)
o Tissue Mast Cells- from basophils in blood; release histamine - vasodilator causing lots of fluid loss
o Eosinophils
• Parasitic infections

288
Q

How are tissue mast cells related to water loss?

A

Gut infections which activate complement recruit mast cells which release histamine- causes vasodilation and increased capillary permeability –> massive fluid loss

289
Q

How much fluid loss may you get in cholera?

A

1l/hour

50% mortality (untreated)

290
Q

What are some symptoms of cholera?

A

Sunken eyes
Dehydration
Washer woman hands (wrinkly)
Rice water urine (mucus and enterocytes)

291
Q

When may eosinophilia be seen?

A

Asthma
Hay fever
Parasitic infections (worms)

292
Q

What are the cellular adaptive defences to toxins?

A

Adaptive Defences (Cellular)
o B Lymphocytes
o Produce antibodies including IgA and IgE that are particularly effective against extracellular microbes
o T Lymphocytes
o Directed against intracellular organisms
o Lymphatic Tissues
o Mucosal Associated Lymphoid Tissue (MALT) in the GI tract is called Gut Associated Lymphoid Tissue (GALT)
o GALT is diffusely distributed by also nodular in three locations:
• Tonsils (mouth is high risk oxen and so needs a large amount of lymphatic tissue at back of throat- palatine, Ingush and nasopharyngeal tonsil)
• Peyer’s patches
• Appendix

293
Q

What is tonsillitis?

A

Inflammation of tonsils

294
Q

What is mesenteric adenitis?

A

o Ileocaecal lymphatic tissue
o Mesenteric adenitis is a common cause of right iliac fossa pain in children, and can easily be mistaken for appendicitis
o Caused mostly by adenovirus/coxsackie virus
o Typhoid fever causes inflamed Peyer’s patches in terminal ileum, which can perforated and kill patients

295
Q

What is appendicitis?

A

Many cases arise from lymphoid hyperplasia at the appendix base leading to an obstructed outflow
o Stasis à Infection
• Purulent appendicitis is commoner during epidemics of chickenpox in children
• Appendix may be obstructed by a faecolith
o Calcified faecal matter, visible on an X-ray
• Appendix may be obstructed by a worm

296
Q

What is gut Ischaemia?

A

Gut Ischaemia
The GI tract’s defence mechanisms require the GI tract itself to have an intact blood supply.
Intestinal/hepatic ischaemia due to arterial disease, systemic hypotension, or intestinal venous thrombosis can (frequently does) lead to overwhelming sepsis and rapid death (within hours)

297
Q

What is liver failure? And it’s causes?

A

Liver Failure
Liver failure gives an increased susceptibility to infections, toxins, drugs and hormones. There is also increased blood ammonia due to the failure of the urea cycle. Ammonia is produced by colonic bacteria and the deamination of amino acids, and can cause hepatic encephalopathy.

Causes of Liver Failure:
o Viral hepatitis
• Main cause worldwide
o Alcohol
• Main cause in the UK
o Drugs
• Paracetamol, halothane
o Industrial solvents
o Mushroom poisoning
298
Q

What is cirrhosis?

A

Cirrhosis (Hepatic Fibrosis)
Hepatic fibrosis leads to portal venous hypertension, leading to porosytemic shunting and therefore toxin shunting.
Portosystemic shunting leads to oesophageal varices, haemorrhoids and caput medusa.

299
Q

What does the liver do to bile pigments?

A

Bile Pigments
Bile pigments are excretory products. The most common bile pigment is Bilirubin, produced as a product of haemoglobin breakdown.
Bilirubin is conjugated in the liver and secreted in the bile to be excreted in faces.
If it cannot be excreted it accumulates in the blood, giving the condition known as Jaundice.

300
Q

What does the liver do to hormones?

A

Hormones

The liver breaks down many hormones, notably insulin.

301
Q

What does the liver do to albumin?

A

Albumin
Albumin is the most abundant plasma protein. Albumin is essential in maintaining the oncotic pressure needed for proper distribution of body fluids.

302
Q

What does the liver do to coagulation factors?

A
The liver produces several coagulation factors:
o I – Fibrinogen
o II – Prothrombin
o V
o VII
o IX
o X
o XI
As well as Protein C, Protein S and Antithrombin.
303
Q

What does the liver do to thrombopoeitin?

A

Thombopoietin

A glycoprotein hormone that regulates the production of platelets by bone marrow.

304
Q

What does the liver do to amino acids?

A

Amino Acid Synthesis

o Transamination

305
Q

How would you investigate a basic liver function test?

A

Hepatocellular Damage
If hepatocytes are damaged, their ruptured membranes will allow Aminotransferases into the blood stream. Their presence there is indicative of liver damage (ALT/AST).

Cholestasis (Bile ducts)
Bilirubin – Unable to excrete bilirubin, plasma concentration rises
Alkaline Phosphatase – Enzyme in cells lining the liver’s biliary ducts. Plasma levels rise with an obstruction.

Synthetic function
Albumin – Levels reduced in chronic liver disease
Prothrombin time (Clotting) – Measures the clotting tendency of blood
306
Q

What are the causes and effects of jaundice?

A

Damaged hepatocytes have a reduced capacity to excrete bilirubin. This leads to bilirubin accumulating in the blood, giving Jaundice.

The increased levels of bilirubin (Hyperbilirubinaemia) results in a yellowish pigmentation of the skin, conjunctival membranes over the scleae and other mucus membranes.

Jaundice is clinically detectable at >40mmol/L (Normal range <22mmol/L)

307
Q

What is prehepatic jaundice?

A

Pre-Hepatic Jaundice
Excessive Bilirubin Production, usually due to an increased breakdown of red blood cells (haemolysis)
o Liver unable to cope with excess bilirubin

308
Q

What are the lab findings with pre hepatic jaundice?

A
Lab Findings:
o Unconjugated hyperbilirubinaemia
o Reticulocytosis
o Anaemia
o increase LDH
o decrease Haptoglobin
309
Q

What are the inherited and acquired causes of pre hepatic jaundice?

A
Causes:
o Inherited
• Red Cell Membrane defects
• Haemoglobin abnormalities
• Metabolic defects
o Congenital Hyperbilirubinaemias
• Gilbert’s syndrome ß 10% of the population
• Crigler-Najjar syndrome ß Rare
• Dublin-Johnson syndrome ß Rare
o Acquired
• Immune
• Mechanical ß E.g. RBC’s running across metal heart valves
• Acquired membrane defects
• Infections
• Drugs
• Burns
310
Q

What is hepatic jaundice?

A

Hepatic Jaundice

Reduced capacity of liver cells to secrete conjugated bilirubin into the blood

311
Q

What are the lab findings with hepatic jaundice?

A

Lab Findings:
o Mixed unconjugated and conjugated hyperbilirubinaemia
o increased Liver enzymes (ALT/AST)
o Abnormal Clotting

312
Q

What are the causes of hepatic jaundice?

A
Causes
o Congenital
• Gilbert’s Syndrome
• Crigler-Najjar syndrome
o Hepatic Inflammation
• Viral (Hepatitis A, B, C and E, Epstein Barr Virus (EBV))
• Autoimune hepatitis
• Alcohol
• Haemochromotosis
• Wilson’s disease
o Drugs
• Paracetamol
o Cirrhosis
• Alocohol
• Chronic hepatitis
• Metabolic disorders
o Hepatic tumours
• Hepatocellular carcinoma
• Metastases
313
Q

What is post hepatic jaundice?

A

Post-Hepatic Jaundice
Obstruction to drainage of bile, causing a back up of bile acids into the liver. Can be intrahepatic or extrahepatic. The passage of conjugated bilirubin is blocked.

314
Q

What are the lab findings with post hepatic jaundice?

A
Lab Findings
o Conjugated hyperbilirubinaemia
o Bilirubin in urine (dark)
o increased Canalicular enzymes (ALP)
o -/increased liver enzymes (ALT/AST)
315
Q

What are the causes of post hepatic jaundice?

A
Causes
o Intrahepatic
• Hepatitis
• Drugs
• Cirrhosis
• Primary biliary colic
o Extrahepatic
• Gallstones/Biliary stricture
• Carcinoma
o Head of pancreas
o Ampulla
o Bile duct
o Porta hepatis lymph nodes
o Liver metastases
• Pancreatitis
• Sclerosing cholangitis
316
Q

Describe how alcohol abuse can lead to fatty liver, hepatitis and cirrhosis

A

Fatty liver
o Alcohol metabolism generates NADH from NAD+
• increase NADH induces fatty acid synthesis
• decrease NAD+ results in decrease fatty acid oxidation
o Accumulation of fatty acids in the liver
• Glycerol à TAGs
o TAGs accumulate, giving fatty liver
Alcoholic Hepatitis
o Inflammation of hepatocytes
Cirrhosis
Liver cell necrosis followed by nodular regeneration and fibrosis, resulting in increased resistance to blood flow and deranged liver function.

317
Q

What are some complications of alcohol abuse?

A
o Hepatocellular carcinoma
o Liver failure
o Wernicke-Korsakoff syndrome
o Encephalopathy
o Dementia
o Epilepsy
318
Q

What are some causes of cirrhosis of the liver?

A
Causes
o Alcohol
o Wilson’s Disease
o a1-antitrypsin deficiency
o Biliary cirrhosis
o Haemochromotosis
o Hepatitis B or C
o Autoimmune hepatitis
319
Q

What are some clinical features of liver cirrhosis?

A
Clinical Features
o Liver dysfunction
o Jaundice
o Anaemia
o Bruising
o Palmar erythema
o Dupuytren’s contracture
320
Q

What lab findings would you expect for a patient with liver cirrhosis?

A
Investigations
o - / increase ALT/AST
o increase ALP
o increase Bilirubin
o decrease Albumin
o Deranged clotting
321
Q

How would you manage a patient with cirrhosis?

A

The management of Cirrhosis includes stopping drinking, treating complications and transplantation.

322
Q

What is portal hypertension?

A

Portal hypertension is defined as portal venous pressure > 20mmHg

323
Q

What may cause portal hypertension?

A

o Obstruction of the portal vein
• Congenital, thrombosis or extrinsic compression
o Obstruction of flow within the liver
• Cirrhosis, hepatoportal sclerosis, Schistosomiasis, sarcoidosis)

324
Q

How may portal hypertension lead to ascites?

A

Ascites
The high pressure in the portal venous system means blood is backed up into the abdomen. The increase in hydrostatic pressure in the abdomen means less fluid is reabsorbed into blood vessels at the end of capillary beds.
If the liver is damaged, reduced oncotic pressure inside the vessels, due to lack of plasma proteins, may also contribute.

325
Q

How may portal hypertension lead to splenomegaly?

A

Splenomegaly – Due to subsequent increased B.P. in the spleen

326
Q

What are the portal systemic anastamoses and how may they result in varices and other clinical problems?

A

There are several anastomoses between the hepatic portal and systemic veins. As such, when the pressure is increased in the portal venous system, blood is backed up through these anastomoses. The increased blood pressure causes the vessels to dilate, protrude into the lumen, rupture/ulcerate and haemorrhage.
o Oesophageal varices
o Rectal varices
o Caput Medusae

Portal to Systemic
. Left Gastric to Azygous/Oesophageal

Oesophageal Varices
. Superior rectal to Inferior rectal

Rectal Varices
. Paraumbilical to Small epigastric of abdominal wall

Caput Medusae
. Colic/Splenic/Portal to Retroperitoneal veins of posterior abdominal wall or diaphragm

Portal veins here are on the posterior aspects (bare areas) of secondarily retroperitoneal viscera or the liver.

327
Q

What are some causes and consequences of gallstones?

A

Bile acids return to the liver in between meals and are secreted by canaliculi cell walls a long time before they are next needed. Until they are needed, they are stored in the gall bladder.
To reduce the volume that needs to be stored, bile acids are concentrated by the transport of salt and water across the gall bladder epithelium. However, the concentration process increases the risks of precipitation, leading to Gall Stones.

Gallstones are often asymptomatic, but they can move into the neck of the gall bladder or biliary tree, causing very painful biliary colic or even obstruction. This is often followed by inflammation (Cholecystitis) and infection of the Gall Bladder.
Pain from Gallstones can be worse after eating, as the secretion of Cholecystokinin (CCK) will cause the gall bladder to contract.

328
Q

What is pancreatitis?

A

Pancreatitis is an inflammatory process, caused by the effects of enzymes released from pancreatic Acini

329
Q

What are some features of acute pancreatitis?

A

Acute
o Oedema, Haemorrhage, Necrosis
o Severe pain, vomiting, dehydration, Shock
o increased Amylase, Glycaemia, ALP/Bilirubin
o decreased Ca2+

330
Q

What are some features of chronic pancreatitis?

A

Chronic
o Fibrosis, Calcification
o Pain, Malabsorption (Steatorrhoea, decreased albumin, weight loss)

331
Q

What are the causes of pancreatitis?

A
Causes of Pacreatitis – GET SMASHED
o Gallstones (Block Pancreatic duct/Amuplla of Vater)
o Ethanol (Hyper-stimulation of pancreatic secretions)
o Trauma
o Steroids
o Mumps
o Autoimmune
o Scorpion bite
o Hyperlipidaemia
o ERCP/Iatrogenic
o Drugs
332
Q

Describe pancreatic carcinomas

A

90% of pancreatic carcinomas are Ductal Adenocarcinomas, and they account for ~5% of cancer deaths.

Clinical Presentation:
Initially symptomless, but then lots of symptoms all at the same time:
o Obstructive jaundice, pain, vomiting, Malabsorption, diabetes

333
Q

Describe the enterohepatic cycle of bile acids

A

In response to Gastric emptying, the duodenum secretes Cholecystokinin (CCK). This stimulates the contraction of the Gall Bladder, ejecting concentrated bile acids together with enzymes from the pancreas.
Alkali from the Pancreas and Liver is also released in response to Secretin.
Bile acids are released through the Ampulla of Vater, and aid with the digestion and absorption of fats. They continue to the terminal ileum, where they are actively absorbed by the epithelium.
The venous return from the gut enters the hepatic portal blood, where hepatocytes actively take up Bile Acids and re-secrete them into Canaliculi.
Most bile acids are recovered, but some are unconjugated by the action of gut bacteria and are lost. Hepatocytes subsequently replace it by synthesising more.

334
Q

What is the purpose of the gall bladder?

A

Bile acids return to the liver in between meals and are secreted by canaliculi cell walls a long time before they are next needed. Until they are needed, they are stored in the gall bladder.

335
Q

Describe bile acids

A

Related to cholesterol
Relatively insoluble in water- amphipathic - travel in bile as micelles (bile acids, cholesterol and phospholipids)
Two main bile acids- cholic acid, chenodeoxycholic acid
Conjugated to amino acids
Needed for digestion and absorption of fats- emulsification of large fat globules into smaller globules, increasing surface area over which enzymes can act on fat and break it down

336
Q

How is alkaline juice secreted from the ductal cells in the pancreas?

A

HCO3- is present in the blood at elevated concentrations due to gastric acid secretion. The pancreatic duct cells secrete the HCO3- using the same cellular mechanism as other HCO3- secreting cells:
o Na-K-ATPase sets up a Na+ concentration gradient
o Hydrogen ions are exported from the duct cell into ECF using the Na+ concentration gradient via NHE (normally on apical membrane in kidney- but here on by membrane!)
o H+ ions combine with HCO3- to form H2O and CO2, which are taken up into the cell
o H2O and CO2 reform H+ and HCO3- inside the cell
o HCO3- is exported into the duct lumen
o H+ ion is recycled, ‘going around in a circle’ to carry more HCO3- from the ECF to the Lumen

337
Q

What stimulates ductal secretion of alkaline juices in the pancreas?

A

Duct secretion is stimulated by Secretin, which is released from Jejunal cells in response to low pH caused by acid from stomach. Cholecystokinin (CCK) facilitates secretin’s action.

338
Q

What 3 parts can the small intestine be divided into?

A

Duodenum
Jejunum
Ileum

339
Q

What is the structure of the duodenum?

A
25 cm long
Breadth of 1w fingers
First and shortest segment
Widest and most fixed part 
C shaped around head of pancreas
340
Q

What is the location of the duodenum?

A

C shaped around the head of pancreas
Begins at Pylorus (RHS) and ends at duodenojejunal flexure on LHS
Most is fixed to structures on posterior abdominal wall by peritoneum
Partly retroperitoneal

341
Q

Describe the duodenal cap/ ampulla

A

The first 2cm of the superior part of the duodenum, immediately distal to the pylorus is known as the ampulla or duodenal cap. It has a mesentery and is mobile. In contrast, the rest of the duodenum is retroperitoneal and immobile.

342
Q

Why is the duodenal cap/ ampulla a common site of ulceration?

A

As the duodenal cap is immediately distal to the pylorus, this is a common site of ulceration. If the ulcer erodes backwards through the Gastroduodenal artery, blood loss can be severe (“Like turning on a tap”).

343
Q

Describe the superior part of the duodenum

A

The superior part of the duodenum ascends from the pylorus and is overlapped by the liver and gallbladder. Peritoneum covers its anterior aspect, but it is bare of peritoneum posteriorly (except for the duodenal cap). The proximal part has the hepatoduodenal ligament (part of the lesser omentum) attached superiorly, and the greater omentum attached inferiorly.

344
Q

Describe the descending part of the duodenum

A

The descending part of the duodenum runs inferiorly, curving around the head of the pancreas. The Bile and Main pancreatic ducts enter its posteromedial wall via the Ampulla of Vater. The descending part of the duodenum is entirely retroperitoneal. The anterior surface of its proximal and distal thirds is covered with peritoneum; however the peritoneum reflects in its middle third to form the double-layered mesentery of the transverse colon, the Transverse Mesocolon.

345
Q

Describe the inferior part of duodenum

A

The inferior (horizontal) part of the duodenum runs transversely right à left, passing over the IBC, aorta and L3 vertebra. The Superior Mesenteric Artery and Vein and the root of the mesentery of the jejunum and ileum cross it. Where these structures cross is the only part of its anterior surface not covered with peritoneum. Posteriorly it is separated from the vertebral column by the right psoas major, IVC, aorta and the right testicular/ovarian vessels.

346
Q

Describe the ascending part of the duodenum

A

The ascending part of the duodenum runs superiorly and along the left side of the aorta to reach the inferior border of the body of the pancreas. Here it curves anterior to join the jejunum at the duodenojejunal flexure, supported by the attachment of a suspensory muscle of the duodenum (Ligament of Treitz). Contraction of this muscle widens the flexure, facilitating movement.

347
Q

Describe the jejunum

A

The jejunum is the second part of the small intestine, beginning at the duodenojejunal flexure where the digestive tract resumes an intraperitoneal course.
Together, the jejunum and ileum are 6-7 metres long, the jejunum constituting approximately two fifths and the ileum three fifths of the intraperitoneal section of the small intestine.
Most of the Jejunum lies in the left upper quadrant (LUQ) of the Infracolic compartment.

348
Q

Describe the ileum

A

The third part of the small intestine, the ileum, ends at the ileocaecal junction.
Together, the jejunum and ileum are 6-7 metres long, the jejunum constituting approximately two fifths and the ileum three fifths of the intraperitoneal section of the small intestine.
Most of the ileum lies in the right lower quadrant (RLQ).
The terminal ileum usually lies in the pelvis, from which it ascends, ending in the medial aspect of the cecum.

349
Q

Describe the mesentery of the jejunum and ileum

A

The mesentery is a fan-shaped fold of peritoneum that attaches the jejunum and ileum to the posterior abdominal wall. Between its two layers are the superior mesenteric vessels, lymph nodes, a variable amount of fat and autonomic nerves.
The root of the mesentery crosses the ascending and inferior parts of the duodenum, abdominal aorta, IVC, right ureter, right psoas major, and right testicular/ovarian vessels.

350
Q

What are some features of the jejunum?

A
Deep red
Large diameter 2-4 cm
Thick and heavy wall
Large vascularity
Long vasa recta
A few large arcades
Little fat in mesentery
Large, tall and closely packed plicae circulares
Few Peyers patches
351
Q

What are some features of the ileum?

A
Pale pink
Small diameter (2-3cm)
Thin and light wall
Little vascularity
Short vasa recta
Many small short arcades
Lots of fat in mesentery
Low and sparse plicae circulares 
Many Peyers patches
352
Q

What is the blood supply to the duodenum proximal to the bile duct?

A

Foregut derivative
Coeliac trunk
Coeliac Trunk –> Gastroduodenal –> Superior Pancreaticoduodenal

353
Q

What is the blood supply to the duodenum distal to the bile duct?

A

Midgut derivative
Superior mesenteric artery
Abdominal Aorta –> SMA –> Inferior Pancreaticoduodenal

354
Q

What is the venous drainage of the duodenum?

A

The Veins of the Duodenum follow the arteries and drain into the Hepatic Portal Vein, some directly, some through the Superior Mesenteric and Splenic Veins.

355
Q

What is the blood supply to the jejunum and ileum?

A

The Jejunum and Ileum are both derived from the Midgut.

Abdominal Aorta –> SMA –> Jejunal
Abdominal Aorta –> SMA –> Ileal

The SMA usually arises from the abdominal aorta at the level of the L1 vertebra, approximately 1cm inferior to the celiac trunk, and runs between the layers of mesentery, sending 15-18 branches to the jejunum and ileum.
These arteries unite to form loops or arches called arterial arcades, which gives rise to straight arteries called vasa recta.

356
Q

What are the eight sections of the large intestine?

A

The large intestine consists of the Caecum, Appendix, Ascending, Transverse, Descending and sigmoid colon, Rectum and Anal Canal.

357
Q

What are the four main structural ways that the large intestine can be distinguished from the small intestine?

A

The large intestine can be distinguished from the small intestine by:
o Omental Appendices
o Teniae Coli
o Haustra
o Diameter
• Much larger than that of the small intestine

358
Q

What are omental appendices of the large intestine?

A

Small, fatty, omentum-like projections

359
Q

What are taenia coli of the large intestine?

A
  • Three distinct longitudinal bands of muscle
  • Begin at the appendix, where it’s longitudinal muscle splits into 3 bands
  • Run the length of the large intestine
  • Merge together again at the rectosigmoid junction into a continuous layer around the rectum
360
Q

What are haustra of the large intestine?

A

• Sacculations of the wall of the colon between teniae

361
Q

Describe the caecum

A

The Caecum is the first part of the large intestine and is continuous with the ascending colon. It is a blind intestinal pouch, approximately 7.5cm in both length and breadth.

It lies in the Iliac Fossa of the Right Lower Quadrant of the abdomen, inferior to the junction of the terminal ileum and caecum (ileocaecal junction).
If distended with faeces or gas, the caecum may be palpable through the anterolateral abdominal wall.

The caecum usually lies within 2.5cm of the inguinal ligament, is almost entirely enveloped by peritoneum and is mobile. However, the caecum has no mesentery. Because of this relative freedom, it may be displaced from the iliac fossa, but is commonly bound to the lateral abdominal wall by one or more cecal folds of peritoneum.

362
Q

Describe the appendix

A

The appendix is a blind intestinal diverticulum (6-10cm in length) that contains masses of lymphoid tissue.
The appendix arises from the posteromedial aspect of the caecum inferior to the ileocaecal junction. It is usually retrocaecal, but its position is variable.
The appendix has a short, triangular mesentery, the Mesoappendix, which derived from the posterior side of the mesentery of the terminal ileum. The mesoappendix attaches to the caecum and the proximal part of the appendix.

363
Q

What is the blood supply of the caecum?

A

Midgut derivative

Abdominal Aorta –> SMA –> Ileocolic

364
Q

What is the blood supply of the appendix?

A

Midgut derivative

Abdominal Aorta –> SMA –> Ileocolic –> Appendicular

365
Q

What is the venous drainage of the caecum and appendix?

A

Venous drainage from the Caecum and Appendix flows through a tributary of the SMV, the Ileocolic vein.

366
Q

What are the 4 parts of the colon called?

A

Ascending colon
Transverse colon
Descending colon
Sigmoid colon

367
Q

Describe the ascending colon

A

o The ascending colon passes superiorly on the right side of the abdominal cavity from the Caecum to the right lobe of the liver, where it turns to the left at the Right Colic Flexure (hepatic flexure). The flexure lies deep to the 9th and 10th ribs and is overlapped by the inferior part of the liver.
o The ascending colon is narrower than the caecum and is secondarily retroperitoneal along the right side of the posterior abdominal wall, covered by peritoneum anteriorly and on its sides. It is separated from the anterolateral abdominal wall by the greater omentum.
o The ascending colon has a short mesentery in 25% of people.
o A deep vertical groove lined with parietal peritoneum, the Right Paracolic Gutter, lies between the lateral aspect of the ascending colon and the adjacent abdominal wall.

368
Q

Describe the transverse colon

A

o The transverse colon is the third, longest and most mobile part of the large intestine. It crosses the abdomen from the Right to Left colic flexures, where it turns inferior to become the descending colon.
o The Left Colic Flexure (splenic flexure) is usually more superior, more acute and less mobile than the right. It lies anterior to the inferior part of the left kidney and attaches to the diaphragm through the Phrenicocolic Ligament.
o The transverse colon and its mesentery, the Transverse Mesocolon, loops down often inferior to the level of the iliac crests. The mesentery is adherent to or fused with the posterior wall of the omental bursa. The root of the transverse Mesocolon lies along the inferior border of the pancreas and is continuous with the parietal peritoneum posteriorly.
o Being freely movable, the transverse colon is variable in position, usually handing to the level of the umbilicus (L3), but in tall, thin people it may extend down into the pelvis.

369
Q

Describe the descending colon

A

o The descending colon occupies a secondarily retroperitoneal position (covered by peritoneum anteriorly and laterally, binding it to the posterior abdominal wall), between the Left Colic Flexure to the Left Iliac Fossa, where it is continuous with the sigmoid colon.
o As it descends, the colon passes anterior to the lateral border of the left kidney.
o The descending colon has a short mesentery in 33% of people.
o As with the ascending colon, a deep vertical groove lined with parietal peritoneum, the Left Paracolic Gutter, lies between the lateral aspect of the ascending colon and the adjacent abdominal wall.

370
Q

Describe the sigmoid colon

A

The sigmoid colon, characterised by its S-Shaped loop of variable length, links the Descending Colon and the Rectum, running from the iliac fossa to the S3 vertebra.
o The termination of teniae coli, approximately 15cm from the anus, indicates the rectosigmoid junction.
o The Sigmoid Colon usually has a long mesentery, the Sigmoid Mesocolon, and therefore has considerable mobility, especially it’s middle part. This can lead to Volvulus of the Sigmoid Colon.
o The root of the sigmoid Mesocolon has an inverted V-shaped attachment, extending medially and superiorly along the external iliac vessels to the anterior aspect of the sacrum.
o The left ureter and the division of the left common iliac artery lie Retroperitoneally, posterior to the apex of the root of the sigmoid Mesocolon.

371
Q

What is the blood supply to the ascending colon?

A

Midgut derivative

Abdominal aorta –> SMA –> ileocolic –> right colic

372
Q

What is the blood supply to the right colic flexure?

A

Midgut derivative
Abdominal Aorta –> SMA –> Right Colic
Abdominal aorta –> SMA –> middle colic –> right middle colic

Anastamoses of right colic and right middle colic artery

373
Q

What is the blood supply to the transverse colon?

A

Midgut and hindgut derivative
R + L middle colic artery
Abdominal aorta –> middle colic –> L+R middle colic

374
Q

What is the blood supply to the left colic flexure?

A

Hindgut derivative
Abdominal aorta –> SMA –> middle colic –> left middle colic
Abdominal aorta –> IMA –> left colic

Anastamoses of left middle colic and left colic

375
Q

What is the blood supply of the descending colon?

A

Hind gut derivative

Abdominal aorta –> IMA –> left colic

376
Q

What is the blood supply to the sigmoid colon?

A

Hind gut derivative

Abdominal aorta –> IMA –> sigmoidal branches

377
Q

What is the blood supply to the rectum?

A

Hind gut derivative
Abdominal aorta –> IMA –> Rectal branches of IMA

Aorta –> IMA –> Superior Rectal –> R+L Branch
Aorta –> Common Iliac –> R+L Internal Iliac –> R+L Middle Rectal
Aorta –> Common Iliac –> R+L Internal Iliac –> Inferior Pudendal –> R + L Inferior Rectal

378
Q

What is the venous drainage of the ascending colon and right colic flexure?

A

Venous drainage of the ascending colon and right colic flexure is through the Ileocolic and Right Colic Veins, which drain into the SMV and subsequently the portal vein.

379
Q

What is the venous drainage of the transverse colon?

A

Venous drainage of the transverse colon is through the Middle Colic Vein, which drains into the SMV and subsequently the portal vein.

380
Q

What is the venous drainage of the descending and sigmoid colon?

A

Venous drainage of the descending and sigmoid colon is through the Left Colic and Sigmoid Veins, which drain into the IMV and subsequently the Splenic and Portal Veins.

381
Q

Describe the rectum

A

The Rectum is the fixed, primarily retroperitoneal and subperitoneal, terminal part of the large intestine.
o First Third
• Peritoneum covers the anterior and lateral surfaces
o Middle Third
• Peritoneum only covers the anterior surface
o Final third
• No covering, as it is subperitoneal
The rectum is continuous with the sigmoid colon at the level of S3 vertebra. At this point, the rectosigmoid junction, the teniae coli of the sigmoid colon spread to form a continuous outer longitudinal layer of smooth muscle.

382
Q

What is the venous drainage of the rectum?

A

Venous drainage of the rectum is through the Superior, Middle and Inferior Rectal Veins.
The Superior Rectal Vein drains into the IMV, then the Splenic and Portal vein
The Middle and Inferior Rectal veins drain into the systemic system.

383
Q

When are the anastamoses in the venous system around the rectus clinically important?

A

The anastomoses between the Portal and Systemic venous systems in the Rectum/Anal Canal are clinically important in Portal Hypertension (varices).

384
Q

Describe the anal canal

A

The anal canal is the terminal part of the large intestine and of the entire digestive canal. The canal begins where the Rectal Ampulla narrows at the level of the U-shaped sling formed by the puborectalis muscle, and ends at the Anus.
The anal canal, surrounded by internal and external anal sphincters, descends posteroinferiorly between the anococcygeal ligament and the perineal body.
The canal is collapsed, except during the passage of faeces. Both sphincters must relax before defecation can occur.
Internally, the superior half of the mucous membrane of the anal canal is characterised by a series of longitudinal ridges called anal columns. These columns contain the terminal branches of the superior rectal artery and vein (see above).
The anorectal junction, indicated by the superior end of the anal columns is where the rectum joins the anal canal. At this point the rectal ampulla abruptly narrows as it traverses the pelvic diaphragm. The inferior ends of the anal columns are joined by anal valves and superior to the vales are Anal Sinuses.
When compressed by faeces, anal sinuses exude mucus, which aids in evacuation of faeces from the anal canal. The inferior comb like shape of the anal valves forms an irregular line, the Pectinate line.
The anal canal superior to the Pectinate line differs from the part inferior to the Pectinate line in its arterial supply, innervation and lymphatic drainage. These differences result from their different embryological origins.

385
Q

What is the blood supply to the anal canal?

A

Above the Pectinate line, the Anal Canal is derived from the Hindgut, thus its blood supply is from the IMA, via the Superior Rectal artery

Below the Pectinate line, the Anal Canal is derived from Endoderm and gains its blood supply from the two Inferior Rectal Arteries.

The Middle Rectal Arteries assist with the blood supply to the anal canal by forming anastomoses with the Superior and Inferior Rectal Arteries.

386
Q

What is the nerve supply of the anal canal?

A

Above the Pectinate line, nerve supply is visceral. Therefore superior to the Pectinate line, the anal canal is sensitive only to stretching. All visceral afferents travel with the parasympathetic fibres to spinal sensory ganglia S2-S4 (referred pain).
Below the Pectinate line, nerve supply is somatic, derived from the Inferior Anal Nerves, branches of the Pudendal Nerve. Therefore, below the Pectinate line, the Anal Canal is sensitive to pain, touch and temperature, and pain is well localised.

387
Q

What’s the recto vesical pouch in males?

A

In males, after the second third of the rectum, the peritoneum reflects onto the posterior wall of the bladder, forming the floor of the rectovesical pouch.

388
Q

What’s the Rectouterine Pouch (Pouch of Douglas) in females?

A

In females, after the second third of the rectum, the peritoneum reflects onto the posterior part of the fornix of the Vagina, forming the floor of the rectouterine pouch.

389
Q

What’s the Vesicouterine Pouch in females?

A

The peritoneal reflection in females between the Uterus and Urinary Bladder

390
Q

What are the three features of chyme when it enters the duodenum from the stomach?

A

The stomach empties chyme into the duodenum, where it is conditioned:
o Acidic
• Corrected by HCO3- secreted from the pancreas, liver and Duodenal mucosa
• HCO3- produced during the production of Gastric Acid
o Hypertonic
• Corrected by the osmotic movement of water into the duodenum across its wall
o Partly digested
• Digestion completed by enzymes from the pancreas and Duodenal mucosa, with bile acids from the liver.

391
Q

How is the small intestine adapted for absorption and it’s function?

A
Absorption requires a large surface area, to which the luminal contents of the small intestine need to be exposed to through gentle agitation for hours.
The small intestine is very long and the surface area for absorption is increased by millions of villi projecting into the lumen.
Epithelial cells (enterocytes) arise by rapid division in the crypts between the villi, and migrate towards the tips, from which they are shed. They mature as they migrate and their luminal surface is covered with millions of micro villi, further increasing the surface area and forming the brush border.
The brush border forms an ‘unstirred layer’ where nutrients meet and react with enzymes secreted by the enterocytes, completing digestion prior to absorption.
392
Q

How is the large intestine adapted for its function?

A

The large intestines absorb water from the indigestible residues of chyme, converting it into semi-solid stool or faeces that is stored temporarily and allowed to accumulate until defecation occurs.
The large intestines have teniae coli (thickened bands of smooth muscle, representing most of the longitudinal coat). They run the length of the large intestine, and because their tonic contraction shortens the part of the wall with which they are associated, the colon becomes sacculated or ‘baggy’ between the teniae, forming Haustra.

393
Q

What do all sections of the small intestine secrete?

A
o Secrete protease / carbohydrase enzymes to complete digestion
o Secrete Hormones
• Secretin
• Gastrin
• Cholecystokinin
394
Q

What are the main functions of the duodenum?

A
o Bile and Pancreatic Secretions added
• Ampulla of Vater
o Secretes HCO3- to neutralise Chyme
o Osmotic movement of water into the Duodenum, making Chyme more hypotonic
o Absorption
• Iron
395
Q

What are the main functions of the jejunum?

A
o Absorption
• Carbohydrates
• Amino Acids
o Small enough to soak through the villi
• Fatty acids
• Vitamins
• Minerals
• Electrolytes
• Water
396
Q

What are the main functions of the ileum?

A

o Absorption
• Vitamin B12
• Bile
• Anything not absorbed by the jejunum

397
Q

What are the main functions of the large intestine?

A

Takes about 16 hours to finish the digestion of food.
o Absorption
• Water
• Any remaining absorbable nutrients
• Vitamins created by colonic bacteria
o Vitamin K, B12, Thiamine, riboflavin
o Sends indigestible matter to the rectum

398
Q

What are the main functions of the rectum?

A

o Faeces

• Stores and compacts faecal matter

399
Q

Describe the breakdown of sugars

A

Carbohydrates are ingested in the form of amyloses, amylopectins or disaccharides such as sucrose.
o Amylose – Straight chain a-1,4 bonds
o Amylopectin – Branched with a-1,6 bonds at branches
a-Amylases act on a-1,4 bonds, and are secreted in saliva and by the pancreas. They yield glucose and maltose from amyloses, and a-limit dextrins from amylopectins.

Brush Border Enzymes complete breakdown to glucose.
o Isomaltase
• Breaks down branched molecules at a-1,6 bonds
o Maltase- Maltose to Glucose
o Sucrase- Sucrose to Glucose/Fructose diamer
o Lactase- Lactose to Glucose/Galactose diamer

400
Q

Describe absorption of sugars in the small intestine

A

Glucose is absorbed actively using the energy from a Na+ gradient set up by Na/K/ATPase in the basolateral membrane.
Glucose enters the epithelial cell across its apical membrane via a Na+/Glucose Symporter, SGLT1. This transporter also transports Galactose.
Glucose then leaves the epithelia cell into the bloodstream across its basolateral membrane via facilitated diffusion through the GLUT2 transporter.
Fructose enters the cell from the lumen via facilitated diffusion

401
Q

Describe the breakdown of amino acids

A

Proteins are digested to short peptides, 10-20 AA’s long (oligopeptides) in the stomach by Pepsin secreted from chief cells.
In the Duodenum, Peptidases are secreted from the pancreas.
Different enzymes ‘prefer’ breaking different bonds:
o Pepsin- Bonds near aromatic AA side chains
o Trypsin- Bonds near basic AA side chains
o Chymotrypsin- Bonds near aromatic AA side chains
o Carboxypeptidase- C-terminal AA’s with basic side chains

Both amino acids and small peptides (2/3 AA’s) are absorbed. Further to this, in neonates our guts are ‘open’, so they are able to pick up whole proteins. This allows breast milk to confer passive immunity on babies via IgA absorption.

402
Q

Describe absorption of amino acids in small intestine

A

Active Uptake of Amino Acids
There are at least five Na+/Amino acid Co-transporters (below), which work in a similar way to the uptake of glucose by using the Na+ gradient set up by Na-K-ATPase.
o Small, neutral AA’s
o Neutral AA’s, Basic AA’s and Cystine
o Acidic AA’s
o Imuno-AA’s
o B-AA’s (Mainly Taurine)
Some AA uptake is by facilitated passive diffusion.
Dipeptides and tripeptides are taken up by an active mechanisms associated with pumping H+ into the lumen, which then returns by co-transport with the peptide.

403
Q

Describe the breakdown and absorption of fats in small intestine

A

Fats are relatively insoluble in water, making them tend to aggregate into large globules, preventing the effective action of digestive enzymes. Acid in the stomach exacerbates this.

In the duodenum, bile acids enable fats to be incorporated into small (4-6nm) micelles, with fats in the middle and the polar components of bile acids on the outside. These micelles generate a high surface area for the action of lipases, which cleave the fatty acids from glycerol.
The micelles also carry these products into the ‘unstirred layer’ immediately next to the mucosa, where fatty acids can be released to slowly diffuse into the epithelial cells.

Once inside the epithelial cells they are reconstituted into triacylglycerols and re-expelled as chylomicrons, structured small particles made up of lipids covered in phospholipids, which facilitate the transport of fat in the lymphatic system from the gut to systemic veins.

404
Q

Describe the absorption of salts and water in the small intestine

A

Sodium is taken up via diffusion into the cell, and actively transported across the basolateral membrane by Na-K-ATPase. This provides the driving force for the majority of absorption (see above).
Chloride follows the movement of Na+.
The movement of the two ions, coupled with all of the absorption, gives an Osmotic Gradient leading to the uptake of water.

405
Q

Describe the absorption of calcium in small intestine

A

o 700mg/day absorbed out of 6g consumed (Just > 10%)
o Enters the cell by facilitated diffusion
• Low Intracellular concentration
o Pumped out of basolateral membrane by Ca2+-ATPase
o Both processes require Vitamin D
o Stimulated by Parathyroid Hormone (PTH)

406
Q

Describe the absorption of iron in small intestine

A

o 20mg a day of Iron is consumed
• Mostly haem
o Iron can only be absorbed in it’s ferrous form (Fe2+)
• Gastric acid solubises iron complexes (Makes it ferrous)
• Stomach also secretes Gastroferrin (Binds iron and keeps it ferrous)
Intestinal mucosal cells secrete transferrin, which finds to ferrous iron (Fe2+) in the lumen. The complex is taken into cells by endocytosis, split and the iron is exported to the blood, where it binds again to transferrin.

407
Q

Describe the absorption of vitamins in the small intestine

A

Water-soluble vitamins are absorbed via passive diffusion
• Vitamin C, B vitamins
o Vitamin B12 is absorbed with a co-factor in the terminal ileum only
• Intrinsic Factor – Binds to B12 in the stomach to keep it soluble
• Secreted by the stomach mucosa
Pernicious anaemia occurs with Vitamin B12 deficiency. It occurs when there is damage to the stomach, preventing it from secreting intrinsic factor, or the terminal ileum has been damaged (e.g. Crohn’s) or removed.

408
Q

What is the basis of oral rehydration therapy?

A

o The uptake of Na+ generates an osmotic gradient, which water follows.
o Glucose uptake stimulates Na+ uptake, plus generates its own osmotic gradient
So a mixture of glucose and NaCl will stimulate maximum water uptake.
This is known as Oral Rehydration Fluid.

409
Q

What is segmenting in the small intestine?

A

Intestinal contents must move very slowly (transit time in hours), whilst being gently agitated for effective absorption.
This is achieved by a pattern of motility called Segmenting, which is very different to peristalsis.
The small intestine is divided into sections, each with a pacemaker. The frequency of the pacemaker gets less from the duodenum to the terminal ileum (12 times a minute à 8), a phenomenon known as the intestinal gradient.
Each pacemaker drives a small section of intestine, causing intermitted contraction of smooth muscle along its length.
These contractions separate the intestine into segments where the muscle is not contracted, whose contents are effectively mixed by movement from the portions that do contract. After a few seconds he contractions relax, and at the next pacemaker firing different areas contract.
Segmenting itself does not propel contents along the intestine, merely mixes the contents. The intestinal gradient however means that there is a net movement, albeit slow, in a caudal direction.

410
Q

What is haustral shuffling in the large intestine?

A

The large intestine is divided naturally into segments known as Haustra, as the circular muscles are more complete than the longitudinal, which have been reduced to taenia coli (thick circular muscle, thin longitudinal – only 3 layers).
Contraction of the smooth muscle in the walls of the Haustra shuffles the contents back and forth, as the slow absorption of remaining water and salts forms faeces. The contents slowly progresses towards the sigmoid colon, with control like segmenting.

411
Q

Describe the mass movement in the large intestine

A

Mass Movement
Infrequently (once or twice a day), there is a Peristaltic, propelling pattern from the transverse through to the descending colon. This forces faeces rapidly into the rectum, which is normally empty, inducing the urge to defecate.
Mass movement is often triggered by eating, the Gastro-colic reflex. They often also happen at certain times of the day, as “people like to be regular”.

412
Q

Describe the mechanism of defecation and the anal sphincters involved

A

Once mass movement has filled the rectum, the urge to defecate arises due to pressure receptors. Waves of contraction in the rectal muscle then force faeces towards the anus.

Anal Sphincters
Internal
o Smooth Muscle
o Parasympathetic control
• Relaxes

External
o Voluntary Striated Muscle
o Voluntary (normally) control
• Relaxes

Once both sphincters are relaxes, intra-abdominal pressure is increased (forces expiration) and there is an expulsion of faeces.
The voluntary control of the external sphincter is overridden if rectal pressure becomes too high.

413
Q

What are 5 causes of inflammatory bowel disease?

A
o Ulcerative Colitis
o Crohn’s Disease
o Diversion Colitis
o Diverticular colitis
o Radiation, Drug, Infectious, Ischaemic Colitis
414
Q

What are the risk factors / triggers of IBD?

A

X

415
Q

What are the general investigations involved in diagnosing IBD?

A

X

416
Q

What is ulcerative colitis?

A

X

417
Q

What is the clinical presentation of an individual with ulcerative colitis? And their symptoms?

A

X

418
Q

What are the macroscopic changes seen with Ulcerative colitis?

A

X

419
Q

What are the microscopic changes seen with Ulcerative colitis?

A

X

420
Q

What are some radiological abnormalities seen with Ulcerative colitis?

A

X

421
Q

What treatment options are available for individuals with ulcerative colitis?

A

X

422
Q

What is Crohn’s disease?

A

X

423
Q

What is the clinical presentation of an individual with Crohn’s disease? And their symptoms?

A

X

424
Q

What are the macroscopic changes seen with Crohn’s disease?

A

X

425
Q

What are the microscopic changes seen with Crohn’s disease?

A

X

426
Q

What are some radiological abnormalities seen with Crohn’s disease?

A

X

427
Q

What treatment options are available for individuals with Crohn’s disease?

A

X

428
Q

What are the beneficial roles of normal flora in the GI tract?

A
o Synthesise and excrete vitamins
• Vitamin K, Vitamin B12, Thiamine
o Prevent colonisation by pathogens
• Space, Bacteriosides
o Kill non-indigenous bacteria
• Bacteriosides
o Stimulate the development of GALT
o Stimulate production of natural antibodies
429
Q

Which parts of the GI tract are anaerobic?

A

o Parts of the mouth
o Tongue, deep in taste buds, biofilm between teeth, gingival crevice areas
o Small Bowel
o Colon

430
Q

What bacteria and fungi are found in the mouth?

A

The mouth has many Anaerobic bacteria, therefore can cause very nasty/fatal infections
o Streptococci
• Streptococcus mutans cause dental caries/gingivitis (dental plaque)
o Staphylococci
• Staphylococcus aureus can cause Parotitis
o Candida
• Oral Thrush, caused by Candida Albicans
o Lactobacillus
o Enterococcus

431
Q

When can the bacteria in the mouth cause disease?

A

In a malnourished, dehydrated, immunocompromised or systemically unwell patient, these bacteria can cause tissue destruction, known as Noma / Cancrum Oris.

432
Q

What bacteria are found in the nose?

A

The nose has Staphylococcus and Streptococcus amongst many others. The nose is one of three sites for MRSA screening swabs (Nose, Throat, Perineum), as these are the three sites where Staphylococci are normally found.

433
Q

What bacteria and fungi are found in the throat?

A
o Strep. Viridans
• 100% of people
• Non-pathogenic throat commensal
• During teeth brushing, dental procedures and general anaesthesia may enter the blood stream (Bacteraemia)
o Strep. Pyogenes
• Tonsillitis (30%, 70% is viral)
o Strep. Pneumoniae
• Community acquired pneumonia (30%)
o Staphylococci
• 100% of people
o Neisseria Meningitidis
• 100% of people
o Haemophilus Influenzea
• Community acquired pneumonia (13%)
o Lactobacilli
• Makes vagina acidic, so Candida Albicans can’t grow (Thrush)
o Corynebacterium Diptheriae
o Candida Albicans
• Oral/vagina thrush
434
Q

What bacteria and viruses cause tonsillitis and in what proportion?

A

o 70% Viral
• Adenovirus, Rhinovirus, Epstein-Barr Virus (EBV)
o 30% Bacterial
• Step. Pyogenes

435
Q

What bacteria commonly causes ulceration in the stomach?

A

o Helicobacter Pylori
• At least 50% of the worlds population is infected
• Only 10-20% infected develop gastric/duodenal ulcers
• Associated with 90% of Duodenal and 70% of Gastric ulcers

436
Q

What bacteria are found in the colon normally?

A
More than 100 species regularly exist in the colon of humans, 95-99% of which are anaerobes, particularly Bacteroides and Clostridial species.
o Always present in the colon
• Bacteroides fragillis
• Bacteroides oralis
• Bacteroides melaninogenicus
• E. Coli – Most common cause of UTI
• Enterococcus faecalis – Second most common cause of UTI
o Other Colonic Bacilli (Gram –‘ve Enteric Bacilli)
• Pseudomonas
• Proteus
• Klebsiella
• Salmonella
• Shigella
• Vibrio cholera
• Campylobacter
437
Q

What is dirty surgery and how can it be prevented?

A

Although it is only the colon that normally contains large numbers of bacteria, if we are operating on the small bowel it will be abnormal. This all gut surgery is viewed as ‘dirty surgery’ with a high risk of wound infection.
To reduce surgical wound infection, antibiotics are given prophylactically. They need to be able to cover Anaerobes, Gram –‘ve Bacilli and Gram +’ve Bacilli.
Metronidazole kills anaerobes, so it is given with a broad-spectrum antibiotic such as Gentamicin or Cephalosporin.

438
Q

What is facial peritonitis?

A

When faeces containing huge amounts of bacteria gains entry to the otherwise sterile peritoneum.
Has a high mortality rate, even in young fit people, due to the huge numbers of bacteria floating free in the peritoneum.

439
Q

What is a perianal abscess?

A

Glands in the anal canal produce mucus for lubrication to aid with passing faeces. Infection of them leads to abscess around the anus – perianal abscess.

440
Q

What bacteria are normally found in the vagina?

A

Lactobacillus (Gram +’ve Bacilli) is a normal vaginal flora organism. It converts glycogen into lactic acid, providing an acidic environment to prevent other bacteria and candida albicans from growing (Thrush).

441
Q

What bacteria are usually found in the perianal area?

A

o Bacteroides –> Cannot survive O2 –> Not present
o E. Coli –> Can survive O2 –> Present
o Enterococcus faecalis –> Can survive O2 –> Present
o Lactobacillus –> Can survive O2 –> Present

442
Q

What bacteria commonly cause UTIs?

A

90% of UTIs occur in women, as there is a much shorter distance from the anus to the urethra.
The commonest causative organism is E. coli, followed by Enterococcus faecalis and thereafter various Gram –‘ve enteric bacilli (Klebsiella, Proteus, Pseudomonas).

443
Q

Briefly describe the three clostridia bacteria

A

Tetani – Tetanus
o Neonatal tetanus kills 60,000 a year
Difficile – Pseuomembranous colitis
o Severe inflammation of the colon
o Often arises after antibiotic treatment
o Produces spores, which are present in hospitals
Perfringens – Gas/wet gangrene
o Anaerobic digestion of glucose leads to ethanol + CO2 (Fluid plus gas), thus wet or gas gangrene

444
Q

Describe Norovirus

A

Every year there are epidemics of viral infections, often noro-viruses that produce a short period of vomiting and diarrhoea.

445
Q

What is gastroenteritis?

A

Gastroenteritis (Food Poisoning) may follow consumption of food or drink contaminated with organisms or toxins, often of bacterial origin but already present in food.
In both cases there is vomiting and diarrhoea. Onset is very rapid if toxins are ingested, within a very small number of hours, but may take up to 48 hours if caused by organisms.
The most common organisms are strains of Salmonella, Campylobacter and Listeria. Toxins may come from Staphylococcus and Clostridium.

446
Q

What is cholera?

A

Cholera is a severe acute infection, which is endemic in many parts of the world and periodically occurs in epidemics that are a real risk after natural disasters.
The organism responsible, Vibrio Cholerae survives in water supplies and has a very specific effect on the ileum, leading to massive movement of water and salt into the lumen by active secretion.
This leads to very serious diarrhoea, which after initial evacuation has a characteristic ‘rice-water’ appearance made up of intestinal secretions plus mucus.
Rapid, severe dehydration follows, which is severely life threatening. Management must replace lost water and electrolytes with appropriate replacement fluids.

447
Q

What are some intestinal parasites?

A

Intestinal parasites are common around the world and can cause a variety of effects. Some protozoans such as Giardia and Cryptosporidium cause Gastroenteritis. Other Helminth infestations may lead to Malabsorption amongst other effects.

448
Q

What is bacteraemia?

A

In Bacteraemia, the bacteria are rapidly cleared from the bloodstream (by liver/spleen macrophages). No symptoms are produced.

449
Q

What is septicaemia?

A

In Septicaemia, bacteria are not cleared and multiply in the blood stream. Sepsis symptoms develop.

450
Q

What is the main cause of travellers diarrhoea?

A

Enterotoxinogenic E. Coli (ETEC) is a major cause of Travellers’ diarrhoea in developing countries, caused by heat stable or labile toxins produced from this serotype, which results in severe, cholera-like watery diarrhoea.
There is no inflammation and the condition is usually self-limiting.

451
Q

How is oesophageal candidiasis usually treated?

A

Amphotericin lozenges

452
Q

What is Quinsy?

A

Extremely enlarged tonsil on one side due to an abscess

  • deviates uvula
  • struggle to inhale
  • pop quinsy with scalpel
  • patients swallow pus
  • -> but internal carotid artery lies just behind
453
Q

Epidemiology of oesophageal cancer

A

o Wide Geographical variation
• Incidence low in USA, and high around Caspian sea and parts of China
o 2% of malignancies in the UK
• Males > Females

454
Q

Clinical features of oesophageal cancer

A

o Dysphagia
• Progressively worsening as tumour grows and occludes lumen
o Weight loss

455
Q

Investigations for oesophageal cancer

A

Endoscopy
Biopsy
Barium swallow

456
Q

Pathological features of oesophageal cancer

A
o Squamous cell carcinoma
• Commonest type
• May occur at any level
o Adenocarcinoma
• Uncommon
• Lower third
• Association with Barrett’s oesophagus
457
Q

Prognosis of oesophageal cancer

A

Advanced disease at presentation in most cases
o Direct spread through the oesophageal wall
o Only 40% resectable
o 5% five year survival

458
Q

Epidemiology of gastric cancer

A
Gastric cancer is the second most common GI malignancy, with approximately 11,000 new cases in England and Wales each year.
o Common
• 15% of Cancer deaths worldwide
o Men > Women
o Geographical variation
• Common in Japan, Columbia, Finland
o Associated with Gastritis
o Commoner in Blood Group A
459
Q

Clinical features of gastric cancer

A

o Symptoms often vague

• Epigastric pain, vomiting, weight loss

460
Q

Investigations for gastric cancer

A

Endoscopy
Biopsy
Barium swallow

461
Q

Macroscopic features of gastric cancer

A

o Fungating
o Ulcerating
o Infiltrative
• Linitis plastica

462
Q

Microscopic features of gastric cancer

A

o Intestinal
• Variable degree of gland formation
o Diffuse
• Single cells and small groups, signet ring cells

463
Q

Early vs Advanced gastric cancer

A
Early Gastric Cancer
o Confined to mucosa/sub-mucosa
o Good Prognosis
Advanced Gastric Cancer
o Further spread
o Common in the UK
o ~10% 5 year survival
464
Q

Metastases of gastric cancer

A
Spread
o Direct
• Through gastric wall into duodenum, transverse colon, pancreas
o Lymph nodes
o Liver
o Trans-Coelomic
• Peritoneum
• Ovaries
465
Q

H pylori and gastric cancer

A

There is a general association of chronic inflammation with cancer. Gastric cancer is common in countries with high H. Pylori prevalence, e.g. Columbia. The association is supported by serological and epidemiological evidence.

466
Q

Gastric lymphoma

A

o The commonest GI Lymphoma
o Starts as a low-grade lesion
o Strong association with H. Pylori
o Eradication of H. Pylori may lead to regression of tumour
o Prognosis much better than gastric cancer

467
Q

Gastrointestinal stromal tumour

A

o Uncommon
o Derived from interstitial cells of Cajal
o The causative mutation, C-kit (CD117) makes it vulnerable to targeted treatment
o Unpredictable behaviour
• Pleomorphism
• Mitoses
• Necrosis

468
Q

Large intestine tumours

A
o Adenomas
• Benign, neoplastic lesions in the large bowel (Dysplasia)
• Familial Adenomatous Polyposis (FAP)
• Gardner’s Syndrome
o Adenocarcinomas
o Polyps
o Anal Carcinoma
469
Q

Familial adenomatous polyposis

A

FAP An autosomal dominant condition on Chromosome 5. By the time the patient is 20 there are thousands of adenomas in the large intestine, giving a high risk of cancer.

470
Q

Gardner’s syndrome

A

Gardner’s is similar to FAP, with bone and soft tissue tumours.

471
Q

Large intestine adenomas

A

Benign, neoplastic lesions in the large bowel (Dysplasia)
o Macroscopic
• Sessile or pedunculated
o Microscopic
• Variable degree of dysplasia
o Malignant Potential
o Incidence increases with age in western population
o Genetic Syndromes- Familial Adenomatous Polyposis (FAP), Gardner’s Syndrome

472
Q

Colorectal adenocarcinoma

A
473
Q

Carcinoid tumour in large intestine

A

Rare and unpredictable neuro-endocrine tumour

474
Q

Lymphoma in large intestine

A

Rare, may be primary or spread from elsewhere

475
Q

Smooth muscle/stromal tumours of large intestine

A

Rare and unpredictable

476
Q

Carcinoma of pancreas

A
Morphology
o 2/3 in the head
o Firm pale mass with a necrotic centre
o May infiltrate adjacent structures, e.g. the spleen
Histology
o 80% are ductal adenocarcinomas
o Well formed glands
o Some acinar tumours contain zymogen granules
o All types have poor prognosis
477
Q

Carcinoma of ampulla of vater

A

The bile duct is blocked with only a small tumour, leading to jaundice and early presentation when the tumour is still treatable.

478
Q

Islet cell tumour

A
o Rare
o Insulinoma
-Hypoglycaemia
o Glycagonoma
-Characteristic skin rash
o Vasoactive Intestinal Peptideoma (VIPoma)
-Werner Morrison syndrome
o Gastrinoma
-Zollinger-Ellison syndrome
479
Q

Liver tumours

A
Benign tumours are fairly rare
o Hepatic adenoma
o Bile duct adenoma/hamartoma
o Haemangioma
Malignant
o Hepatocellular carcinoma
o Cholangiocarcinoma
o Hepatoblastoma
480
Q

Describe contrast studies used to investigate the GI tract

A
Contrast is used to define hollow viscera. Examples of contrast that is used include Barium and water soluble contrast (typically using iodine).
• Barium swallow
• Barium enema
• Barium meal/follow through
• Water soluble contrast studies

A Barium Enema is a Barium study where the contrast medium is inserted rectally. This study enables the colon to be visualized.

481
Q

Describe ultrasounds used to investigate the GI tract

A

o Use of sound waves to generate image
• Frequency above audible range of human hearing (20 KHz)
• Usually 2-18 MHz
o Cheap compared to CT and MRI
o Portable
o Highly user dependent
Can be used to determine if a patient has Gallstones, or to see if the common bile duct is dilated (an indicator that there is an impacted gallstone in the duct).
Abdominal ultrasound scan can also view the Liver and portal vein, even the Appendix.
These scans are often difficult to interpret and the usefulness of a scan is often down to who is doing and interpreting the scan.

482
Q

Describe GI angiography used to investigate the GI tract

A

For both bleeding and ischaemia, being able to visualise the Blood supply to the GI tract is very useful.
This is done by injecting a radio-opaque contrast agent intravenously and then using various modalities to capture the images.

483
Q

Describe abdominal x rays used to investigate GI tract problems

A

Features of an AXR
o Stomach
o Small and Large Bowel
o Soft Tissues
o Liver, spleen, kidneys, psoas muscles, bladder, lung bases
o Bones
Any part of a hollow tube is visible on an X-ray if it is filled with gas (Low density gas acts as a contrast).
Fully fluid filled lumens are not visible.
You can visualise the stomach (if gas filled) but more commonly we use this to visualise the small bowel.

484
Q

What are some reasons for requesting an abdominal x ray?

A

o Acute abdominal pain
o Small or large bowel obstruction
o Acute exacerbation of IBD
o Renal colic

485
Q

Compare what the small and large bowel look like on an AXR

A

The small bowel
Usually occupies a central position on the Abdominal X-ray and can display its ‘circular folds’ or Valvulae conniventes, which appear as lines that appear to cross the whole of the bowel lumen

Large bowel
In contrast to the small bowel, this usually occupies a more peripheral position on the abdominal X-ray.
It is often possible to see the Haustra on the X-ray, which appear as incomplete lines going across the lumen.
Faeces can also appear on the X-ray and this can look like clouds in the lumen.

486
Q

How can you tell if a small or large bowel obstruction had caused dilation?

A

Small and large bowel obstruction can be noted and follow the rule of 3/6/9.
o The small bowel is said to be dilated when it is greater than 3cm diameter.
o The large bowel when it is greater than 6cm
o The Caecum (when the ileocaecal valve is working) is said to be dilated when it is greater than 9cm
o This only applies when the X-ray shown is to scale. You can’t tell on these pictures!

487
Q

How does a person with small bowel obstruction present?

A

Small bowel usually presents with vomiting (early) and mild distension. Absolute constipation (not passing anything per rectum, even flatus) is a late feature.
You vomit early simply because the obstruction is nearer the mouth than a large bowel obstruction. For the same reason constipation is a late feature in small bowel obstruction.
There will be colicky pain that presents every 2-3 minutes.

488
Q

What are some causes of small bowel obstruction?

A
o Adhesions
o Hernias
• Inguinal, Femoral, Incisional
o Tumours
o Inflammation
489
Q

How does a person with large bowel obstruction present?

A

This presents with abdominal pain and distension with constipation as an early feature (nothing can pass into the rectum and out).
The pain is also colicky but not as frequent as small bowel obstruction (every 10-15 minutes).
Vomiting is a late feature of large bowel obstruction (it has further to travel to the mouth) and can be faeculant.

490
Q

What are some causes of large bowel obstruction?

A
o Colorectal carcinoma
o Diverticular stricture
o Hernia
o Volvulus
o Pseudo-obstruction
491
Q

What is a volvulus?

A

This is when a viscera twists around itself or more commonly when it twists around its mesentery. Most common is a Sigmoid volvulus or more rarely Caecal volvulus.
When this twisting occurs the enclosed loop of bowel dilates and is at risk of perforating or cutting of its blood supply (which runs in the mesentery).
At this stage we would not expect you to be comfortable interpreting a volvulus on an abdominal X-ray. I would like you to be aware that it can happen though and what it means

492
Q

What more peculiar abnormalities can be seen on an AXR?

A
o Pancreatitis (chronic)
o Aneurysms with calcification
o Nodes
o Bones
o Artifact
o Foreign body
o Kidney Stones
493
Q

What can an erect chest x ray be useful in diagnosing?

A

An Erect Chest X-ray can be useful in diagnosing perforated bowel.

494
Q

What can cause a perforated bowel?

A
o Peptic ulcer
o Diverticular disease
o Tumor
o Obstruction
o Trauma
o Iatrogenic
495
Q

Why does a CXR in GI studies have to be erect?

A

The CXR needs to be erect because you are looking for the diaphragm to be elevated away from any other viscera (the Liver on the right) by the presence of air/gas in the peritoneal cavity.
The air/gas will rise to the top of the cavity and so the patient needs to be sat up for 10 minutes prior to the X-ray to ensure this happens.
The peritoneal cavity only normally contains a small amount of fluid, so the presence of air/gas is abnormal and could be the result of perforated bowel.

496
Q

Describe an abdominal CT

A

Abdominal CT
o High dose radiation
o Good spatial resolution (poor contrast resolution vs MRI)
o Use of IV or oral/rectal contrast

Can be done in a variety of anatomical planes

497
Q

Describe MRI of the abdomen

A
Magnetic resonance imaging (MRI)
o Magnetic resonance imaging
o First human MRI scan 1977 (in the US)
• However developed by Sir Peter Mansfield (University of Nottingham)
o No radiation
o Good spatial and contrast resolution
o Time consuming
498
Q

Describe a Magnetic resonance cholangio-pancreatogram (MRCP),

A

Magnetic resonance cholangio-pancreatogram (MRCP) is an MRI scan that can visualize the Gallbladder and biliary tree.

499
Q

What enzyme is responsible for bilirubin conjugation in the liver?

A

UDP- Glucuronyl transferase

500
Q

What is Gilbert’s syndrome?

A

Congenital disease
Deficiency in UDP- glucuronyl transferase deficiency
Bilirubin can’t be conjugated (made soluble) in liver
High concentration of unconjugated bilirubin in blood

501
Q

Pernicious anaemia

A

Private study session 8

502
Q

What are 4 features of pernicious anaemia?

A

Increased mean cell volume (MCV)
hypersegmented neutrophils
hemolysis with reticulocytosis
leukopenia and thrombocytopenia.

503
Q

What is VIPoma?

A

Werner Morrisons syndrome
Vasoactive intestinal polypeptide
Stimulates bowel muscle
Diarrhoea

504
Q

What is Gastrinoma?

A

Zollinger-Ellison syndrome
Produce acid in excess
Prolonged gastric irritation