Session 8

Question 1

Describe the gross & microscopic anatomy of the large intestines and relate these it͛s function LO

1. What are the main sections in the large intestine?
2. The large intestine can be distinguished from the small intestine by:

Answer 1

1. Caecum, Appendix, Ascending, Transverse, Descending and sigmoid colon, Rectum and Anal Canal
2. o Omental Appendices
   - Small, fatty, omentum-like projections
   o Teniae Coli
   - Three distinct longitudinal bands of muscle
   - Begin at the appendix, where it͛s 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
   o Haustra
   - Sacculations of the wall of the colon between teniae
   o Diameter
   - Much larger than that of the small intestine

Question 2

1. What are haustra?

Answer 2

1. sacculations caused by contraction of teniae coli

muscularis mucosae is indistinct at this magnification

Question 3

Describe the functions of the large intestine LO

What ion channel is used for absorption

Which hormon eallows for further reabsorption of water

Answer 3

• Removes water (less than SI) - mostly ascending colon
• Turns chyme into a semi solid
• synthesis of vitamins K, B12, thiamine and riboflavine
• breakdown of 10 to 20 bile acids
• conversion of bilirubin to non-pigmented metabolites - (all readily absorbed)
• temporary storage until defaecation (distal)

ENaC

Question 4

Describe the motility of the colon and rectum LO

Answer 4

Small intestine:

Slow caudal progression of contents due to an intestinal gradient (higher frequency of pacemakers proximally)

Segmentation (mixes the contents back and forth) (following meals)

Peristalsis

Large Intestine:

Segmentation agitates and mixes the contents forming haustra by bunching up (haustral
shuttling)

Mass movements (3xday) (generally after a meal) and move contents from transverse colon to rectum

Rectum:

25% full we get the urge to defecate:

o Internal sphincter (smooth muscle) relaxes due to parasympathetic control

o External sphincter (striated) relaxes due to voluntary control and intra- abdominal pressure rises and there is expulsion of faeces

Question 5

Describe the mechanisms of defaecation LO

Answer 5

Distal colon where we store out feaces

Rapid peristalsis in distal large bowel moves stuff into the rectum

Rectum becomes distended and we defecate -> mass movement (25%)

Higher centre control overrides reflex – reverse peristalsis

Large bowel lots of tight junction further along guy get more tight/robust don’t want water we have absorbed to escape out into the lumen

Question 6

Describe the causes of intestinal inflammation and infection LO

Answer 6

Inflammation: Inflammatory bowel disease (idiopathic

2 common types:
• Crohns disease (affects 15-30 yrolds & 60 yrolds)
• Ulcerative colitis (young adults)
• Diversion colitis
• Pouchitis
• Microscopic colitis

Infection: cholera salmonella c.diff

Question 7

Complete the table for Chrons & UC

Answer 7

Perinatal relating to the time, usually a number of weeks, immediately before and after birth

Question 8

Endoscopic features & investigations

Answer 8

Question 9

Further investigations not mentioned before and what you would see

Answer 9

Question 10

Further investigations

Answer 10

History

Chronic inflammation of lamina propria in mucosa

Crypt abscesses – crypts become distorted due to inflammation (can be seen in crohn͛s too but more common UC)

Less goblet cells

Question 11

Signs & symptoms, patients, causes

Answer 11

Question 12

Complications for UC and Chrons

Answer 12

Cholangitis - charcots -> fever, cholangitis, RUQ pain

Question 13

Treatment of UC and Chrons

Answer 13

Question 14

1. Gross pathology - Crohns
2. Granulomas arise with:

Answer 14

1. •Discrete superficial ulcers
   •Deeper ulcers
   •Transmural inflammation
   • Thickening of bowel wall
   • Narrowing of lumen
2. • Persistent, low-grade antigenic stimulation -> infections -> Mycobacteria: Tuberculosis, leprosy – Other infections e.g. some fungi

• Hypersensitivity -> Mildly irritant foreign material

Question 15

1. Why does granulomas arise with Chrons?
2. What is a fistula?
3. What is a stricture?
4. How do you know there is a stenosis when looking at a radiograph??
5. Even after diagnostic evaluation, 10% have disorders that cannot be classified thus is diagnosed as?

Answer 15

1. Unknown

– Sarcoid (abnormal collections of inflammatory cells that form lumps)

– Wegeners granulomatosis (blood vessels become inflamed)

– Crohns disease

2. abnormal connection between two epithelium-lined organs
3. Narrowing
4. Dilatation of colon before to stenosis
5. Indeterminate Colitis

Question 16

H&E what does this stand for and what does each stain for and the colour

Answer 16

Haematoxylin -> DNA -> purple
Eosin -> cytoplasm & CT-> pink

Question 17

1. What type of inflammation is Chrons & UC ?
2. How Does Chronic Inflammation Arise?
3. What main cell type is present in chronic inflammation

Answer 17

1. Chronic inflammation (Chronic response to injury with associated fibrosis)
2. Take over’ from acute inflammation
   …if damage is too severe to be resolved within a few days
   de novo
   – Some autoimmune conditions (e.g. RA)
   – Some chronic infections (e.g. viral hepatitis)
   - chronic low-level irritation͟
   Alongside acute inflammation
   …in severe persistent or repeated irritation
3. Macrophages, lymphocytes, (plasma cells, eosinophils) (vary in different conditions)

Question 18

1. Functions:
2. Difference between cytokine and chemokine
3. What are giant cells? What are the three types?

Answer 18

1. – Phagocytosis

– Processing and presentation of antigen to immune system

– Synthesis of not only cytokines, but also complement components, blood clotting factors & proteases

– Control of other cells by cytokine release

2. Cytokines: proteins that have effect on cells around them
   Chemokine: ability to induce directed chemotaxis
3. • Multinucleate cells made by fusion of macrophages
   • Frustrated phagocytosis

Langhans giant cells – the nuclei are arranged around the periphery of the giant cell, they are often (but not exclusively) seen in tuberculosis,

Foreign body giant cells – the nuclei are arranged randomly in the cell.

Touton giant cells – Nuclei ring towards the centre of the cell

Fat necrosis and xanthomas (xanthomas are discussed in the session on atherosclerosis). Foam cells which are simply macrophages whose cytoplasm appears foamy as they have phagocytised a lot of lipid.

Question 19

Q. No. Of different cell types can vary in different conditions for example?

RA:
Chronic gastritis:
Leishmaniasis:

Answer 19

– Rheumatoid arthritis: Mainly plasma cells
– Chronic gastritis: Mainly lymphocytes
– Leishmaniasis (a protozoal infection): Mainly macrophages

diagnosis

Question 20

EFFECTS OF CHRONIC INFLAMMATION

Answer 20

• Fibrosis e.g. gall bladder (chronic cholecystitis), chronic peptic ulcers, cirrhosis

• Impaired function (as normal tissue replaced with fibrous tissue) e.g. chronic inflammatory bowel disease, cirrhosis
– Rarely increased function e.g. mucus secretion, thyrotoxicosis e.g. Graves͛ disease

• Atrophy
– gastric mucosa, adrenal glands

• Stimulation of immune response
– Macrophage
- lymphocyte interactions

Question 21

UC &/ Chrons
• Discontinuous distribution
• Affects any part of the gastrointestinal system
• Inflammation is limited to mucosa and submucosa
• ͚Cobblestone͛ appearance to bowel mucosa classically seen
• Granulomas often present
• Crypt abscesses common
• Distorted crypt architecture very common
• Anal lesions common
• Bowel fistulae more likely
• Significant increased risk of colon cancer
• Often most severe in distal colon
• Colectomy often indicated Patients with ulcerative colitis may develop complications in organs or
tissues other than the gastrointestinal system. Which organs/tissues can be involved and what
complications can occur in them?

Answer 21

Question 22

1. Motor innervation of the peritoneum? & sensory
2. What is the nerve root which supplies dermatomal innervation to the umbilical region & suprapubic region?
3. What provides motor innervation to foregut midgut and hindgut

Answer 22

1. Parietal peritoneum: nerves of the abdominal wall & somatic (sensory)

Visceral peritoneum: ANS (motor) & splanchnic (sensory)

2. Afferent fibres T10 & T12
3. Foregut: vagus (para), greater splanchnic nerve (T5-T9 symp)

Midgut: vagus (para), lesser splanchnic nerve (T10-T11 symp)

hindgut: 1/2 vagus 1/2 pelvic, least splanchnic nerve (T12 symp)

Question 23

1. What is reffered pain?
2. What is somatic reffered pain?
3. Give an example of somatic reffered pain

Answer 23

1. Pain perceived at a site distant from the site causing the pain
2. Pain caused by a noxious stimulus to the proximal part of a somatic nerve that is perceived in the distal dermatome of the nerve
3. The diaphragm has 2 motor nerves innervating it. Phrenic centrally and intercostal. Irritation of the intercostal nerve (T9/t10?). Phrenic has motor of C3,4,5, but dermatomes are not in the region of diaphragm as decent of diaphragm during birth. Dermatomes in tip of shoulder.

Question 24

What is this image showing?

Answer 24

Even when you have irritation of T10 somatic nerve brain will usually localise the pain to the whole T10 dermatome

Question 25

What will happen if you have shingles in the T12 dermatome?

Answer 25

Pain proceeds rash. Will fell pain in the whole T12 dermatome. Can be confused with appendicitis. SOMATIC REFERRED PAIN.

Question 26

1. What is visceral referred pain? 2. Give an example

Answer 26

**Thorax & abdomen:** **visceral** (splanchnic) 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 segment(s)

Question 27

What causes visceral pain?

Answer 27

* Abnormally strong muscle contraction & stretch * Inflammation * Ischaemia **WHERE is the VISCERAL PAIN? CSI!**

Question 28

If you have a peptic ulcer where would you fell pain and why? Where would you feel pain in your foregut, midgut and hindgut?

Answer 28

In stomach thus visceral afferent effected. Stomach is part of the foregut. Foregut is innervated by parasymapthetic (vagus) and sympathetic (greater) T5-T9. The visceral afferent travels with the sympathetic efferent, it enters the spinal cord of the sympathetic efferents. Due to this the brain perceives the visceral pain as somatic pain of the spinal levels it enters. Thus pain is epigastric.

Question 29

Where would you feel pain in cholecystitis?

Answer 29

Gall bladder will have visceral afferents. It will have motor efferents from the vagus nerve (para) & the **greater splanchnic nerve (sympathetic T5-T9) coeliac trunk.** The viscerals travel with the greater splanchnic efferents and enter the vertebrae at the same levels. The brain perceives the visceral pain as somatic pain at the vertebral levels the visceral afferents enter (T5-T9). Epigastric pain. The gall bladder can inflame so much that it can irritate the peritoneum overlying the gall bladder. Causing localised sharp pain. The gall bladder can also irritate the diaphragm. The diaphragm has dual motor innervation -\> phrenic and splanchnic (motor nerves). It has sensory innervation from somatic nerves, which travel to the anterior ramus (which has both sensory & motor nerves) & goes through mixed nerve, then goes through the dorsal nerve root. The brain perceives this pain (that is irritating the proximal somatic nerve) to the dermatome which the proximal somatic nerve innervates. Thus shoulder pain. The intercostal nerves can also be irritated (proximal motor nerve) (T1-T11 branch of the anterior rami) brain perceives pain in the dermatome. T8/9/10 innervate the dermatome near the scapula.

Question 30

Where do we feel pain from the spleen?

Answer 30

Spleen is in the **PERITONEUM** right flank

Question 31

Acute appendicitis

Answer 31

Appendix is part of the midgut. Visceral afferents enter the spinal cord with sympathetic (T10-T11 lesser splanchnic) brain perceives the pain as somatic pain from the spinal levels the afferents enter the spinal cord. Thus pain is in T10/11 paraumbilical. Later the parietal peritoneum cna become impinged. The sensory afferents of the parietal peritoneum travel through the anterior ramus, mixed spinal nerve, dorsal root ganglion then nerve, to brain. Brain relays the pain to the dermatome which the proximal part of the somatic nerve was irritated.

Question 32

Pancreatic & abdominal aorta pain

Answer 32

Question 33

Small bowel colic where would you feel pain and how frequent?

Answer 33

Every 90s part of the midgut para umbilical

Question 34

Small bowel colic: where do we feel pain and how frequently?

Answer 34

Question 35

Renal ureteric pain location?

Answer 35

Loin to groin loin: kidneys retropertioneal, impinges on somatic nerve, localised pain groin: stone moving down ureters, ureters are retroperitoneal move to the pelvic brim, groin pain patients with **URETERIC COLIC ROLL AROUND ON THE FLOOR**

Question 36

Where do you feel pain in peritonitis?

Answer 36

Pain caused by a noxious stimulus to the proximal part of a somatic nerve that is perceived in the distal dermatome of the nerve

Question 37

Where does a patient with peritonitis experience pain?

Answer 37

Severe **pain all over** abdomen which may be referred to the **shoulder tips** * ‘Rigid abdomen’. Diaphragmatic and abdominal wall movement greatly increase pain. Therefore often **shallow rapid breathing** * Very **tender** on examination of the abdomen * In the early stages patients may have ‘**rebound tenderness’**

Question 38

**_The peritoneum_** * Surface area is 2 square metres * Peritoneal blood flow is normally 150 ml/min * Peritoneal cavity normally contains 100 ml of serous fluid * Peritoneal fluid is drained by the lymphatic system * So, because of its large surface area an inflamed peritoneal cavity can exude litres of fluid!!

Question 39

Why do we become dehydrated in bowel obstruction?

Answer 39

secretion into GI tract, isotonic solution is secreted, this comes from the ECF we vomit up the fluid, allows for more fluid to be sequestered, increase in haematocrit, weight loss, **dry mucous membranes**, sunken-appearing eyes, **decreased skin turgor,** increased capillary refill time, hypotension and postural hypotension, tachycardia, weak and thready peripheral pulses,

Question 40

1. Where can we get bleeding in the abdomen? 2. Give causes for each

Answer 40

**GUT** - oesophageal varices (Haematemesis & melaena (enzymes/ bacteria, mouth-caecum) - peptic ulcer (Haematemesis & melaena) - diverticular disease (Bright red bleeding per rectum called **haematochezia**) **RETROPERITONEUM** AAA (\>65, smoker, CT disorders) -\> tamponades bleed, compensatory mechanisms **PERITONEAL CAVITY** Ectopic pregnancy, trauma,

Question 41

What are the complications of having a duodenal ulcer (clue: draw the coeliac trunk)

Answer 41

Posterior duodenal ulcer that has eroded into the **gastroduodenal artery**

Question 42

What can cause bleeding per rectum?

Answer 42

Peptic ulcer -\> melaena (dark due to bac/enzymes) oesophageal varices (dark due to bac/ enzymes) IBS - melaena adenocarcinoma Haemorrhosids infective gastroenteritis

Question 43

1. Patients taking oral iron have black stools, how would we know the difference? 2. If a patient has haematemesis and haematochezia then they are bleeding massively from the? 3. How to test if there is an upper GI bleed

Answer 43

1. Smell 2. upper GIT 3. - bleeding from the stomach/ oesophagus - arge protein meal to the small bowel - converted by the liver into urea - **if the serum creatinine is normal then a rise in blood urea in a patient with oesophago/gastric bleeding will help to indicate:** **– The source of bleeding** – The **higher the blood urea rise the larger the bleed**

Question 44

What is this image showing

Answer 44

Diverticular: pockets/protrusions that normally occur in the colon (usually in the elderly) cause haematochezia

Question 45

Retroperitoneal bleeding Commonest causes:

Answer 45

– Ruptured abdominal aortic aneurysm (AAA) – Patients on anticoagulants may bleed from torn retroperitoneal veins. INR usually \> 5.0 can track retroperitoneally through muscle

Question 46

1. Typical presentation of ruptured AAA 2. Outcome of ruptured AAA

Answer 46

1. • Sudden death (50%) • Sudden onset of severe abdominal and back/loin pain • Sudden collapse • Presents to the emergency department with ‘shock’ 2. • In the 50% that make it to hospital, 70% are operable & the survival in that 35% of the total is 50%. Therefore overall survival is about 17%. Overall mortality is 83%

Question 47

What are the symptoms/signs of a ruptured ectopic pregnancy

Answer 47

Bleeding into the peritoneal cavity: - R**eproductive age** **- lower abdominal pain** **- vaginal bleeding** **- collapse and left shoulder tip pain on lying down (C3,4,5)** - Every year 12,000 women in the UK develop an ectopic pregnancy and 6 women a year die from ectopic pregnancy

Question 48

Perforation of a viscus. Which viscus perforation is most likely to lead to bleeding in the peritoneum?

Answer 48

Duodenal ulcer more common than gastric ulcer perforation

Question 49

Complication of gastric ulcer perforation

Answer 49

Question 50

* **Perforated** **peptic ulceration** leads to a ? * Perforated diverticular disease leads to ?

Answer 50

chemical peritonitis. Mortality 10% peritoneal sepsis & septicemia. Mortality rate 50%.

Question 51

What would the person on the right present with

Answer 51

* Patient has severe generalised abdominal pain * Patient lies still, shallow breathing * Patient will be hypovolaemic * Patient may be septic * Needs treatment URGENTLY rebound tenderness?

Question 52

1. What is this image showing? What can cause it? 2. Anaesthetic agents dramatically reduce sympathetic tone and many have a negative inotropic effect. Why is this important if the person is dehydrated?

Answer 52

1. Pneumoperitoneum - perforated viscus 2. • In a patient who is dehydrated the sympathetic nervous system is maximally activated to maintain vital organ perfusion. If the dehydration is not corrected prior to anaesthesia then the patient may become profoundly hypotensive and die at the induction of anaesthesia • Because many anaesthetic agents affect cardiac muscle/conduction function, correction of either hypokalemia or hyperkalemia is also very important prior to anaesthesia e.g. Bowel obstruction - sigmoid volvulus, adhesions from previous surgery?

Question 53

Bowel obstruction 1. What is this type of hypovolaemia caleld? 2. How would this effect the electrolyte balance? 3. How would this effect the acid base balance?

Answer 53

1. Isotonic hypovolaemia (from ECF) 2. **Vomiting** leads to loss of **hydrogen and chloride (HCl) ions** which leads to a **metabolic alkalosis** • **Renal compensation** for this metabolic alkalosis (loss of H+ ions) is to preserve H+ at the **expense of potassium** -\> **hypokalemia** 3. The end result is **hypochloremic, hypokalemic metabolic alkalosis** **correct hypovolaemia and serum potassium abnormalities** **saline sodium/choroid 0.9%**

Question 54

Acute pancreatitis 1. What type of bleeding does this cause? 2. Aetiology? 3. Prognosis 4. Management 5. Diagnosis

Answer 54

1. Autodigestion by proteases of the retroperitoneum 2. – Alcohol – Gallstones 3. • 10% mortality irrespective of age 4. • No specific treatment • Management is **supportive -\>** significant dehydration (vomiting and fluid sequestration in retroperitoneum) 5. **Raised serum amylase**

Question 55

**_Acute gut ischaemia_** 1. Commonest cause? 2. Patients present with?

Answer 55

1. Embolism (atrial fibrillation) 2. **Severe abdominal pain** - **tender over the ischaemic gut** - Patients rapidly become ‘toxic’ and **hypotensive** - An important clue is a very **high white cell count (\>20 x109/l – normal is 4-11)** - Treatment is **urgent laparotomy** (in the next hour!) & resection of dead bowel - Shock phase: fluids start to leak through the damaged colon lining. Metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion. Patients who progress to this phase are often critically ill and require intensive care.

Question 56

**_Acute cholangitis_** 1. What is it? 2. Commonest cause? 3. Prognosis? 4. Presentation 5. Treatment

Answer 56

1. **Infection** of bile ducts (**e.coli** -\> bile ducts have lots of E.coli in general) 2. Cholelithiasis (jaundice, bilary stasis) (others: head of pancreas - adenocarcinoma, intervention, stents) 3. 10% mortality (decreased significantly) There is not usually a history of biliary colic 4. Image 5. **Endoscopic retrograde cholangiography (ERCP),** sphincterotomy and stone extraction

Question 57

What is the structure of the liver?

Answer 57