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MRCS Part B > General Surgery > Flashcards

General Surgery Flashcards

1
Q

What causes a hernia?

A

Increased Intra-abdominal pressure:
- chronic cough
- abdominal distension (pregnancy, ascitis, obesity)
- straining (chronic constipation, weight lifting)
- kyphoscoliosis

Weakened Abdo Wall Tissue:
- congenital defects (patent umbilical ring or processus vaginalis)
- Collagen disorders
- Trauma
- Ageing
- malnutrition
- steroid use

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2
Q

What is pus?

A

Pus is a mixture of living, dead and dying bacteria and neutrophils with cellular debris and liquefied tissue.
It may become surrounded by a membrane in which case is becomes and abscess.

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3
Q

Why do adhesions occur following inflammation in the abdomen?

A

Following acute inflammation the inflamed tissues undergo organisation with growth of capillaries. Fibroblasts proliferate and cause fibrosis.
The exudate that covers the bowel and loops sticks together in a fibrinous adhesion and failure to remove it results in fibroblast proliferation and collegen laid down causing permanent adhesions.

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4
Q

Which is more common in women: inguinal or femoral hernia?

A

Inguinal hernia are more common in both M and F, however in the case of a femoral hernia its more common in females than males.

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5
Q

What are the principles of tissue sampling on suspicion of malignancy?

A
  • aim enough suspicious tissue to make a diagnosis whilst not contaminating the surrounding field
  • sample should be placed in a fixative for preservation
  • sample should be labelled with patient details, time, date, sample type and location, and relevant history
  • various methods: biopsy, FNAC,
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6
Q

How does immunohistochemistry work?

A

Antibody labelled with dye is used to detect a specific antigen in the tissue. When bound it causes a coloured stain.

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7
Q

How can the site of a metastatic tumour be accurately determined?

A

Sometimes this is difficult. But you can look for tumour specific antigens E.g. PSA

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8
Q

What are the principles of frozen section?

A

Obtaining a fresh tissue sample and then frozen to maintain histological characteristics then rapid lab analysis,

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9
Q

What are the hallmarks of cancerous cells?

A
  • self sufficiency in growth signals
  • insensitivity to anti-growth
  • evade apoptosis
  • limitless replication potential
  • induce angiogenesis
  • evade detection by the immune system
  • genomic instability
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10
Q

What is the hayflick hypothesis?

A

That normal cells have a limit on how many times they can divide before undergoing apoptosis. It’s approximately 50 times and is due to shortening of the telomere.

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11
Q

How do cancerous cells obtain immortality?

A

They utilise the enzyme telomerase to rebuild the telomere on each division therefore no shortening occurs

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12
Q

What is the difference between grading and staging?

A

Grading is the description of the lesion and how differentiated the cell types are.
Staging is a classification according to size and spread around the body.

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13
Q

What are the branches of the abdominal aorta and the levels at which they arise?

A

T12- inferior phrenic
L1 (upper) - coeliac trunk
L1- suprarenal
L1 (lower) - SMA
L1-L2 - renal
L2 - gonadal
L1,2,3,4 - 4x paired lumbar
L3 - IMA
L4 - median sacral
L4 - CIA

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14
Q

Describe the tributaries, relations and course of the portal vein.

A

Formed by the confluence of the superior mesenteric and the splenic vein. It lies anterior to the IVC and posterior to the head of the pancreas and first part of duodenum.
Other tributaries include:
R&L gastric veins
Superior pancreaticoduodenal
Cystic vein
Peri-umbilical vein in the ligamentum teres

It ascends in the free edge of the lesser omentum posterior to the bile duct and hepatic artery
At the porta hepatis it divides into two and supplied the respective halves of the liver

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15
Q

What causes abdominal compartment syndrome?

A

Bleeding, post op AAA repair/rupture, pancreatitis, BO or ileus, burns, abdo wall closure too tight.

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16
Q

What are the symptoms of abdominal compartment syndrome?

A

Difficult ventilation, ABG showing high lactate due to ischaemia, decreased urine output.
Can measure the intra-abdominal pressure via the bladder (>20mmHg is diagnostic).

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17
Q

Describe the gross anatomy of the oesophagus?

A

This is a fibromuscular tube, approximately 25cm long, originating at the cricoid cartilage(C6) and terminating at the cardiac orifice (T11).
It has 3 parts:
1. Cervical: cricopharyngeus - thoracic inlet
2. Thoracic: thoracic inlet - T10 diaphragmatic hiatus
3. Abdominal: T10- GOJ (T11).

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18
Q

What are the anatomical relations to the oesophagus?

A

Anterior:
- Trachea
- L recurrent laryngeal nerve
- Pericardium/heart
- L vagus nerve

Posterior:
- Thoracic vertebra
- thoracic duct
- azygous vein
- descending aorta
- R vagus
- L crus of the diaphragm

Right:
- pleura
- terminal azygous vein

Left:
- subclavian artery
- aortic arch
- thoracic duct
- pleura

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19
Q

What are the areas of physiological constriction of the oesophagus?

A

Arch of the aorta (T4)
Left main bronchus
Cricoid cartilage (C6)
Diaphragmatic hiatus (T10)

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20
Q

What are the layers of the oesophageal wall?

A

Internal - External:
1. Mucosa (non-keratinised stratefied squamous epithelium)
2. Submucosa (contains nerves and blood vessels)
3. Muscularis circular and longitudinal (the upper third is striated muscle and the lower third is smooth muscle, the middle third is mixed).
4. Adventitia (NOT serosa)

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21
Q

Describe the anatomy of the oesophageal sphincters?

A

Upper Sphincter: striated muscle sphincter at the junction between the pharynx and the oesophagus. Produced by the cricopharyngeus muscle.

Lower: this is located at the GOJ at around T11. This is a physiological sphincter due to its high pressure. 4 factors contribute to it:
- Acute angle of entry to the stomach
- Walls are compressed due to intraluminal plexus giving the smooth muscle high resting tone
- Prominent mucosal folds
- R crus of the diaphragm acting as a sling.
It is controlled hormonally - Gastrin and Ach cause contraction and CCK, secretin, VIP, NO cause relaxation.

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22
Q

What is the blood supply to the oesophagus?

A

Superior - Inferior thyroid
Middle - branches of the thoracic aorta
Inferior - branches from the L gastric

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23
Q

What is the venous drainage of the oesophagus?

A

Azygous vein and inferior thyroid vein which go to the systemic circulation, and to the L gastric which is portal.
Therefore it is an area of porto-systemic anastamosis.

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24
Q

Where is the lymph drainage of the oesophagus?

A

Superior - deep cervical nodes
Middle - superior and posterior mediastinal nodes
Inferior - coeliac nodes.

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25
Q

What is the innervation of the oesophagus?

A

Innervated by the oesophageal plexus, formed by the vagal trunks and sympathetic thoracic and cervical trunks.

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26
Q

What is the thoracic duct? and what is its anatomical course?

A

This structure drains lymph from all structures below the diaphragm, Left hemithorax and left head and neck.
It begins at T12 (the cisterna chyli) and ascends via the oesophageal hiatus (T10) where is crosses the midline posterior to the oesophagus at T5. It drains into the L brachiocephalic vein.

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27
Q

What are the risk factors for GORD?

A

Obesity
Pregnancy
Diabetes
Smoking
Age
Hiatus hernia
Oesophageal dysmotility

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28
Q

What are the normal anti-reflux mechanisms of the oesophagus?

A

High pressure oesophageal sphincter, angle of His, mucosal rosette at the GOJ, sling of the R crus of the diaphragm.
Acid receptors in the distal oesophagus also cause peristalsis.

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29
Q

What are the indications for endoscopy?

A
  • Dysphagia
  • Odonophagia
  • Anaemia and bleeding
  • Previous Barret’s
  • Weight loss
  • Recurrance/no resolution after PPI therapy
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30
Q

Describe a classification system for GORD on endoscopy.

A

The Los Angeles classification system:
A= mucosal breaks <5mm
B= mucosal breaks >5m
C= mucosal breaks extending over the muscosal folds but <75% of the circumference
D = as above but >75%

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31
Q

How would you manage GORD?

A

Conservative: Lifestyle modification
Medical: PPI/ H2 antagonists
Surgical: Nissen Fundoplication

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32
Q

What are the complications of Nissen Fundoplication?

A

Dysphagia
Gas retention
Inability to vomit
Recurrence
Bilobed stomach

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33
Q

What is Barret’s oesophagus?

A

Metaplasia of the stratefied squamous epithelium to columnar with goblet cells, occurs secondary to GORD.

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34
Q

What is metaplasia?

A

This is the reversible change from one cell type to another.

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35
Q

What is the surveillance program for Barret’s oesophagus?

A
  • Short segment <3cm with NO dysplasia = repeat endoscopy in 3-5 years.
  • Larger segment >3cm with NO dysplasia = repeat in 2 years.
  • Indeterminate or low grade dysplasia = PPI and repeat in 3-6 months.
  • High grade dysplasia = PPI, MDT discussion, Endoscopic mucosal ablation or resection (7% risk of developing adenocarcinoma at 1 year).
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36
Q

What are the features of oesophageal cancer?

A

Progressive dysphagia
GORD
Weight loss
May have signs of liver metastases/supraclavicular lymph nodes.

*50% have unresectable disease at presentation

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37
Q

What are the subtypes of oesophageal cancer?

A

Adenocarcinoma (most common) at the distal oesophagus due to Barret’s. Normally positive for PAS and CK7.

Squamous cell carcinoma (mid oesophagus), associated with HPV16/18, achalasia and corrosive injury. There are keratin whirls and cytological atypia.

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38
Q

What are the resection options for oesophageal Ca?

A

Ivor Lewis Procedure: mid-distal tumours: 2x incision.

McKewen Procedure: proximal tumours: 3x incision.

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39
Q

What are the complications of oesophageal resection?

A

Mortality (1-2%)
Morbidity (60%)
Anastomotic leak
Conduit necrosis
Pneumonia
Chyle leak
AF
Recurrent laryngeal nerve injury

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40
Q

What is achalasia?

A

Lack of effective peristalsis of the oesophagus with incomplete or no relaxation of the oesophageal sphincter. Typically due to degeneration of the myenteric plexus of Walbach.
It causes progressive dysphagia

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41
Q

What investigations would be useful for diagnosis of achalasia?

A

Barium swallow - giving a “bird beak” appearance.
Manometry
Endoscopy (to rule out cancer)

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42
Q

How do you manage achalasia?

A

Medical: CCB
Endoscopic botox - gives 6 months of relief but causes fibrosis so only suitable for elderly or unfit.
Pneumatic dilatation - temporary and has risks of recurrence and perforation.
Myotomy

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43
Q

What are the causes of oesophagitis?

A

Idiopathic (IgE mediated)
Systemic sclerosis
Polymositis
SLE
Parkinsons
Myasthenia GravisW

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44
Q

What are the endoscopic features of oesophagitis?

A

Concentric rings
Focal strictures
Yellow papules/exudate
Longitudinal furrows

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45
Q

What are some causes of oesophageal strictures?

A

Upper:
- Mediastinal Radiation
- Congenital
- Pemphigoid
- Oesophagitis

Lower:
- Peptic stricture
- Oesophagitis
- Scleroderma
- Zollinger Ellison
- Oesophageal rings A/B (if at the GOJ then considered a Schatzi ring).

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46
Q

What are the 4 physiological points of oesophageal narrowing?

A

Arch of the Aorta
Bronchus
Cricophayngeus muscle
R crus of the diaphragm

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47
Q

Indications for urgent intervention with oesophageal foreign body?

A
  • airway compromise
  • complete dysphagia (unable to swallow saliva)
  • sharp object
  • button battery
  • magnets

Or if failure to pass in 3 weeks or a large object (>5cm long or >2.5cm wide)

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48
Q

What is Macler’s triad?

A

This is a triad of symptoms of oesophageal perforation:
Vomiting
Chest pain
Subcut emphysema

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49
Q

What are the causes of oesophageal perforation?

A

Iatrogenic
Boerharves syndrome
Foreign body
Corrosive disease
Malignancy
Neoadjuvent chemo
Trauma

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50
Q

How would you manage an oesophageal perforation?

A

Endoscopic clipping or stent
Surgical primary repair, drainage and T tube, resection and diversion with delayed reconstruction.

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51
Q

What is the Rockall score?

A

This score predicts mortality with UGI bleed.
Age, BP, Co-morbidities, Diagnosis, Evidence of bleed

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52
Q

What is the greater omentum?

A

This is a double layer of peritoneum which hangs down from greater curve of the stomach and folds back to attach to the transverse mesocolon. It contains lymph nodes, gastro-omental arteries and the gastrosplenic ligament (containing the short gastrics).

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53
Q

Where does the lesser omentum sit?

A

This is continuous with the peritoneum of the stomach and D1 an it attaches to the liver. It contains the L and R gastric arteries.

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54
Q

What are the anatomical relations of the stomach?

A

Superior: oesophagus and diaphragm (left side)
Inferior: small bowel
Anterior: greater omentum, anterior abdominal wall, L lobe of the liver
Posterior: lesser sac, pancreas, left kidney, splenic artery, left adrenal and transverse mesocolon.

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55
Q

What is the vascular supply to the stomach?

A

Short gastrics (from the splenic) supply the fundus.
R gastric is a branch of the common hepatic, L gastric from the coeliac trunk.
L gastro-omental is a branch of the splenic
R gastro-omental is a branch of the gastroduodenal.

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56
Q

What is the neurological supply of the stomach?

A

Parasympathetic innervation is via the vagal trunks (this increases motility and secretions).
Sympathetic is via the T6-T9 coeliac plexus.
There is also a submucosal Meissner’s plexus which has secretomotor neurons which supply glandular tissue and exocrine cells, and a Auberchs plexus which acts on the smooth muscle via Ach receptors.

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57
Q

What is the lymphatic drainage?

A

Lesser curve nodes; 1,3,5 –> R and L gasrtic
Greater curve nodes; 2,4,6 –> splenic

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58
Q

Describe the gastric secretions and what cells produce them.

A

Gastric acid:
Secreted by parietal cells.
The pH is maintained at around 2 via the H+/K+ATPase.
It acts to activate pepsinogen into pepsin.
It is increased in response to vagal stimulation, gastrin and histamine, it is decreased in response to somatostatin, CCK and secretin.

Intrinsic factor is produced by parietal cells in response to vagal stimulation, gastrin and histamine.
It acts to bind to B12 to allow absorption.

Histamine is produced by EC cells in response to vagal stimulation.

Gastrin is produced by G cells in the antrum.
It acts to stimulate secretion of gastric acid, intrinsic factor and increase gastric secretions.
It is stimulated by stomach distension and products of digestion. It is inhibited by low pH and a somatostatin.

Mucus - lubricates and protects underlying mucosa.

Pepsinogen - produced by chief cells.

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59
Q

Describe the secretions from the small intestine and where they are secreted from?

A

Secretin: S cells in the duodenum in response to acid/fatty acids.
It increases bicarbonate secretions from the pancreas and decreases gastric acid production.

VIP is produced in the small intestine in response to neuronal stimulation. It inhibits pepsinogen and increases pancreatic secretions.

Somatostatin is produced by the D cells in the pancreas and stomach, in response to fat, bile and glucose.
it causes reduced gastrin, insulin and pancreatic secretions.

Cholecystokinin: I cells in the duodenum.
Causes increase in GB contraction, contraction of pyloric sphincter and increased bile production, as well as relaxation of sphincter of oddi and reduced appetite.

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60
Q

How do H2 antagonists work?

A

Block histamine receptors of the acid producing parietal cells and therefore reduce acid secretion.

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61
Q

How do PPI work?

A

Block the H+/K+ ATPase pump, preventing acid production being effective?

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62
Q

How do NSAIDs cause gastric ulceration?

A

Reduce prostaglandins which decrease the mucosal integrity.

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63
Q

How does smoking increase risk of gastric ulceration?

A

Reduces gastric emptying, increases acid production and reduces bicarbonate.

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64
Q

What are some causes of malabsorption?

A

Intestinal:
- coeliac
- crohns
- topical spruce
- Whipples disease (gram +ve bacterium which causes villous atrophy)
- giardiasis

Pancreatic:
- chronic pancreatitis
- cystic fibrosis
- pancreatic cancer

Biliary:
- biliary obstruction
- PBC

Other:
- short gut syndrome
- anorexia
- systemic sclerosis

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65
Q

What are the classifications of hiatus hernia?

A

1 - Sliding
Cardia herniates proximally with movement of the sphincter into the thorax

2- Para-oesophageal
OGJ remains in place but the fundus herniates.

  1. OGJ and fundus and cardia herniate into the thorax
  2. Transverse colon herniates into the thorax.
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66
Q

What are the indications for surgery in hiatus hernia?

A
  • Symptomatic reflux that has failed conservative management
  • Aspiration/chest symptoms i.e. asthma
  • Risk of strangulation or volvulus
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67
Q

What is the pathophysiology of acute gastric volvulus?

A

Organo-axial rotation (around a line drawn from the cardia to the pylorus).
Mesenterico-axial (around a transverse line between the lesser and greater curvature).

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68
Q

What is Barchardt triad?

A

This is the symptoms of acute gastric volvulus:
- severe epigastric pain
- inability to vomit
- inability to pass an NG tube

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69
Q

How would you manage an acute gastric volvulus?

A

Attempt decompression via NG
If fails then gastroscopy
If fails then surgical

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70
Q

What are the risk factors for gastric cancer?

A

Low socioeconomic status
Low fibre diet
Obesity
Smoking
Polyps
Li-Fraumini syndrome
HNPCC
H.Pylori
Prior gastric surgery
EBV
Atrophic gastritis
Anaemia

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71
Q

What are the histological subtypes of gastric cancer?

A

95% are adenocarcinoma
They may be intestinal (mass forming). These are more likely to be tubular or papillary and metastasise to bone and liver.
They can also be diffuse type which are more likely to be mucinous or signet ring and these are more likely to cause ulceration and peritoneal mets.

72
Q

How would you stage gastric cancer?

A

Early= limited to the mucosa/submucosa, with no lymphatic spread
Late= invades muscularis propria or has lymph node involvement.

73
Q

How would you manage a gastric cancer?

A

If mucosa only you could consider endoscopic mucosal resection.
If further then resection:
- Cardia/proximal: total gastrectomy and roux-en-y bypass
- Distal; subtotal gastrectomy with removal of greater omentum and gastric artery

74
Q

What is a GIST tumour?

A

This is cancer arising from the intestinal cells of Cajal. These are the pacemaker cells of the myenteric plexus.
They are normally spindle cell shaped and are +ve for CKIT and CD34.
They cause smooth surfaced lesions with a central depression.
There is NO role for chemo or radiotherapy and therefore must undergo resection with wide macroscopic margins due to the psuedocapsule.

75
Q

Where is the most common site of extra-nodal lymphoma?

A

Gastric lymphoma: MALT

76
Q

What are the risk factors for gastric lymphoma?

A

H Pylori, campylobacter, HIV, EBV, Hep B

77
Q

What are the macroscopic features of MALT lymphoma?

A

Ill defined thickening, contact bleeding with lymphocytic infiltration. It causes Peyer’s patches.
It is diagnosed when there is:
- normal bone marrow/peripheral blood
- no palpable lymph nodes
- no mediastinal lymph nodes
- disease in 1 GI segment ONLY

78
Q

How would you manage a patient with MALT?

A

H Pylori eradication
Rituximab
Chemo/radiotherapy

79
Q

What deficiencies may be present post-gastrectomy?

A

Iron - due to the loss of gastric acid which is vital to convert Fe2+ > Fe3+ which can be absorbed in the small bowel.

Vitamin B12 - due to the loss of the R protein and intrinsic factor

Calcium - relies on acid for absorption

80
Q

What is dumping syndrome?

A

This is due to a short transit time in the gut. It has two phases:
Early: gastric contents flood the small bowel causing an influx or bile, pancreatic juices causing a large fluid shift (therefore sweating, increased HR and palpitations).
Late: rebound hypoglycaemia due to the increased levels of bicarb and this causes a rapid insulin production initially.

81
Q

What are the normal protective factors of the GI tract against peptic ulcer disease?

A
  1. Mucus cap
  2. Prostoglandins maintain mucosal integrity
  3. Microcirculation acts to neutralise acid.
82
Q

What is the most common cause of peptic ulcer disease?

A

H.Pylori

83
Q

What is H.Pylori?

A

This is the most common cause of peptic ulcer disease.
It is a gram -ve spiral-rod shaped bacterium with a flagellum. It produces urease enzyme which in turn produces ammonia which is toxic to the epithelium.
It therefore causes increased gastrin, decreased mucus production and decreased bicarbonate.
It also causes VacA and CagA which propogate cytokine release and therefore inflammation.
It is spread via the faeco-oral route.

84
Q

How would you diagnose H.Pylori?

A

Urease breath test, serum test of stool antigen.
The gold standard is the Clo test which is a campylobacter-like organism test via biopsy.

85
Q

What is H.Pylori associated with?

A

Gastric ulceration/duodenal ulceration
Chronic gastritis
Lymphoma (MALT)
Gastric adenocarcinoma

86
Q

How would you manage H.Pylori?

A

Triple therapy (2x abx and omeprazole) for 14 days then repeat test to ensure eradication.

87
Q

How do peptic ulcers present?

A
  • Upper abdominal pain
  • Gastric; pain worse after eating, duodenal; pain relieved by eating.
  • bleeding (posterior)
  • perforation/peritonitis (anterior)
  • cancer
88
Q

What is the forest classification of a bleeding ulcer?

A

1a - arterial bleed
1b - venous bleed
2a - visible vessel with no bleed
2b - clot
2c - evidence of a recent bleed
3 - clean based ulcer

89
Q

How would you manage a bleeding peptic ulcer?

A
  1. IV PPI
  2. Gastroscopy (diagnostic and theraputic)
    - adrenaline injection
    - diathermy
    - clipping
    - haemostatic spray
  3. Surgery
    - underunning of the ulcer
    - resection
    - embolisation
90
Q

What are the indications for surgery in management of a peptic ulcer?

A
  • failure of medical management
  • ongoing bleed
  • 2x rebleed in <60 or 1x rebleed in >60
  • transfusion requirement of over 4 units in 24 hours.
91
Q

Other than H.Pylori, what are some other causes of gastritis?

A

Curlings ulcer (burns)
Cushings ulcer (head injury due to vagal stimulation and increased acid)
Alcohol
NSAIDs
Trauma
Auto-immune gastritis (TYPE A) due to antibodies against parietal cells.
Type B gastritis secondary to duodenal reflux

92
Q

When is bariatric surgery indicated?

A

BMI>40
BMI > 35 with T2DM and HTN

93
Q

What are some examples of bariatric surgical options?

A
  1. Gastric banding: adjustable band around proximal stomach and inflated to affect satiety. This is reversible however takes longer to achieve target weight.
    Complications include: slipping. erosion, loosening.
  2. Sleeve gastrectomy: resection of body and fundus.
  3. Roux-en-y-bypass
    Gastric pouch is formed and connected to the jejunum, the remaining stomach and duodenum is left in situ and attached distally. This is irreversible. 50% become B12 deficient.
94
Q

What is metabolic syndrome?

A

5/5 of:
- obesity
- HTN
- Hypertriglyceridemia
- Hypercholesterolaemia
- T2DM

95
Q

What scoring system can be used to assess nutrition?

A

MUST: uses BMI, unplanned weight loss, acute illness and NBM status.
Can also use mid-arm circumference and triceps skin fold as other assessments.

96
Q

What are the indications of paraenteral feeding?

A

SBO, ileus, severe diarrhoea/vomiting, enterocutaneous fistula, >5 days of NBM status.

97
Q

What does TPN contain?

A

water, carbohydrates, protein, lipids, vitamins and trace elements.

98
Q

What are the complications of para-enteral nutrition?

A

Central line: pneumothorax, IE, haemothorax, blood clots, infection

Metabolic: hyperglycaemia, electrolyte disturbances, deranged LFT, refeeding syndrome.W

99
Q

What is refeeding syndrome?

A

shifts in fluids and electrolytes resulting in hormonal and metabolic changes, particularly phosphate which is required for ATP and structural integrity of cell membranes.
It causes symptoms of: confusion, seizure, cardiac arrhythmia, failure and death.

100
Q

What are the fat soluble vitamins and why are they important?

A

Vitamin A: retinal function and membrane stabilisation
Vitamin D: calcium homeostasis
Vitamin E: free radical scavenger
Vitamin K: clotting factor synthesis

101
Q

Why does TPN have to be delivered via a central line?

A

High osmolality leads to thrombophlebitis of the peripheral veins.

102
Q

What would you differentials for gastric outlet obstruction include?

A

Duodenal atresia
Volvulus
Intussusception
Pyloric stenosis
Mass
Hernia

103
Q

What blood gas picture would you expect to see with a gastric outlet obstruction?

A

Chronic vomiting will cause a hypochloraemic, hypokalaemic, metabolis alkalosis.

They also get a hypocalcaemia due to the excessive binding to albumin.

104
Q

What is the pathophysiology behind thehypochloraemic, hypokalaemic, metabolic alkalosis in gastric outlet obstruction?

A
  • Low K+ due to the H+ loss, therefore K+ is exchanged in the kidneys to try and conserve H+
  • K+ is also lost from salivary and gastric contents
  • K+ shifts intracellularly in exchange for H+
  • The volume loss causes activation of RAAS which causes K+ loss to exchange for Na+
105
Q

Why does vomiting cause an increased anion gap?

A

Because there is a volume depletion which leads to a greater concentration of albumin which is an anion but is not included in the equation.

106
Q

What causes a normal anion gap metabolic acidosis?

A

Overhydration of NaCl
Renal tubular acidosis (due to lack of reabsorption of bicarb)
Diarrhoea (loss of bicarb)
Carbonic anhydrase inhibitors

When bicarb is lost, it is replaced by Chloride and therefore anion gap remains the same.

107
Q

What are the causes of a raised anion gap metabolic acidosis?

A

Increased anion gap due to dissociation of H+ from an acid with an anion (ie. lactic acid > H+ and lactate). The H+ then combines to HCO3 to be blown off and CO2, but the dissociated anion adds to the negative charge, but isn’t in the equation and therefore the gap increases.

Examples include:
- Lactic acidosis: ischaemia, DKA
- Uraemia
- Methanol or salicylate poisoning.

108
Q

Describe the parts of the duodenum.

A

D1: Superior
This is at the L1 level, only intraperitoneal section. It is connected to the liver by the hepatoduodenal ligament.

D2: Descending
This runs vertically down L1-L3 levels, curving around the head of the pancreas, parallel to the IVC. The bile duct and pancreatic duct enter on its postero-medial wall.

D3: Inferior
Crosses the IVC and aorta at the level of L3, posterior to the SMV and SMA.

D4: Ascending
This turns superiorly after crossing the aorta (the duodenojejunal flexure). It is supported by the ligament of Trietz.

109
Q

What is the blood supply to the duodenum?

A

Parts 1 and 2 are supplied by the gastroduodenal artery and its branches (superior pancreaticoduodenal) and parts 3 and 4 by the inferior pancreaticoduodenal artery (from the SMA).

110
Q

What are the differences between the jejunum and the ileum?

A

Jejunum: thicker walls, redder, larger diameter, larger valvular conivente, thinner mesentery with longer vessels.

Ileum: thinner walled, pink, smaller diameter, with thicker mesentery with shorter but more vessels.

111
Q

What features of the small bowel cause an increase in the surface area?

A

Long length, valvulae conniventes, villi and microvilli

112
Q

What is the function of the small bowel?

A
  1. Digestion of carbohydrates: via salivary and pancreatic amylase.
  2. Digestion of proteins and fats that are broken down by stomach/pancreatic enzymes but absorbed in the small bowel.
  3. Absorption of water (mainly in the jejunum)
  4. Absorption of iron, B12, bile salts, calcium and K+
113
Q

What is Peutz-Jeghers disorder?

A

This is an autosomal dominant mutation of the STK11 gene, causing harmatomatous polyps in the jejunum and melanin spots in the mucosal regions.
It is benign but increases the risk of intussusception.

114
Q

What is a polyp?

A

A polyp is an overgrowth causing a pedunculated lesion from the normal epithelial surface.

115
Q

What is a harmatoma?

A

A hamartoma is a tumour-like malformation composed of a disorganised arrangement of
different amounts of tissue normally found at that site. It grows under normal growth
controls.

116
Q

What is carcinoid syndrome?

A

Carcinoid tumours are neuroendocrine tumours that secrete serotonin. They often occur in the ileum.
They get liver and lymphatic mets which results in serotonin being released into the systemic system and this is what causes the syndrome of flushing, diarrhoea and bronchospasm.

117
Q

How does radiotherapy cause small bowel injury?

A

Because the small bowel has rapidly dividing epithelium it is highly susceptible to radiation injury. It causes sloughing of dead cells, causing abdominal cramps, nausea and vomiting. In the chronic stage it causes vessel damage and ischaemia leading to malabsorption, ischaemia, and fistulae/stricture formation.

118
Q

What are the signs and what is the pathophysiology of mesenteric vein thrombosis?

A

Causes slow onset, non-specific abdominal pain.
Increasing oedema causes venous compromise, which then causes arterial compromise, which then causes patchy necrosis.
Underlying causes include idiopathic, protein C and S deficiency, antithrombin III deficiency, portal HTN and sepsis.

119
Q

What malabsorption syndromes may you see after resection of the jejunum?

A

Reduced absorption of water, electrolytes, fats, proteins and carbohydrates.
Typically folic acid deficiency.
However, symptoms are normally transient due to ileum compensation.

120
Q

What malabsorption syndromes may you see after resection of the terminal ileum?

A

Megaloblastic anaemia due to loss of B12.
Gallstones due to reduction in bile salt reabsorption.
Loss of absorption of fat soluble vitamins.

121
Q

What is short bowel syndrome?

A

Occurs when >80% of the small bowel has been resected. It causes an increased water loss and electrolyte disturbance.
Management is via; fluid replacement, opiate/loperamide control of diarrhoea until hyperplasia and compensation of the remaining bowel occurs.

122
Q

What is the function of the ileocecal valve?

A

Prevents reflux of large bowel contents during peristalsis.

123
Q

What are the anatomical locations of the appendix?

A

75% Retrocecal
Others include: subcecal, pelvic, post-ileal and pre-ileal.

124
Q

Which parts of the colon are retroperitoneal?

A

Ascending and descending colon, inferior rectum.

125
Q

What are some of the features of the large bowel?

A

Omental appendages: small peritoneal pouches containing fat on the surface.
Teniae Coli: 3 longitudinal muscle strips (mesocolic, free and omental).
Hasutra: caused by the contraction if teniae coli.

126
Q

What is the nerve supply to the colon?

A

Midgut: superior mesenteric plexus (para and sympathetic)
Hindgut: parasympathetic is via the inferior mesenteric plexus and sympathetic is via the lumbar plexus.

127
Q

What are the anatomical relations of the ascending colon?

A

Anterior: small intestine, greater omentum
Posterior: iliacus and quadratus lumborum, R kidney, iliohypogastric and ilioinguinal nerve.

128
Q

What are the anatomical relations of the transverse colon?

A

Anterior: greater omentum.
Posterior: duodenum, small bowel, pancreas.

129
Q

What are the anatomical relations of the descending colon?

A

Ant: small intestine and greater omentum
Posterior: iliacus, quadratus lumborum, left kidney, iliohypogastric and ilioinguinal.

130
Q

What are the anatomical relations of the sigmoid colon?

A

Anterior: bladder and uterus
Posterior: rectum, sacrum and ileum.

131
Q

What spinal level does the rectum begin?

A

S3 (where the teniae coli merge)

132
Q

Does the rectum have a mesentery?

A

No but it has a fascial layer called the mesorectum.

133
Q

Describe the peritoneal coverings of the rectum.

A

Proximal 1/3 is covered anteriorly and laterally by the peritoneum.
The middle 1/3 is covered anteriorly by peritoneum
The distal 1/3 is fully extraperitoneal.

134
Q

What are the anatomical relations of the rectum in a male?

A

Anterior:
- Devonvilliers fascia (separates from prostate)
- Ileum
- Bladder
- Rectovesicular pouch
- Sigmoid
- Seminal vesicles.

Posterior:
- Waldayers fascia
- Coccygeus muscle
- Levator ani
- Sacral plexus
- Sacrum, coccyx and piriformis.

135
Q

What is the arterial supply to the rectum?

A

Superior rectal artery (from IMA)
Middle rectal artery (from IIA)
Inferior rectal artery (from internal pudendal)

136
Q

What is the venous drainage of the rectum?

A

Superior rectal artery > portal venous system
Middle and inferior > systemic venous system.

137
Q

What is the nerve supply to the rectum?

A

Sympathetic is via the lumbar splanchnic nerves and the hypogastric plexus.
The parasympathetic is via the pelvic splanchnic s2-s4

138
Q

How can polyps be classified?

A

Sessile (flat)
Pedunculated (fibro-vascular stalk)
Neoplastic (adenomatous/serrated)
Non-neoplastic (Juvenile, harmatoma, psuedopolyp)

139
Q

Where do adenomatous polyps arise from? How can they be further subclassified?

A

They arise from the mucus producing cells. They are premalignant.
They can be further divided into tubular, tubulo-villous and villous.

140
Q

What is the adenoma>carcinoma pathway?

A

This is dysplasia due to high mitotic figures, nuclear pleomoprhism and loss of polarity.
1. Inactivation of the APC gene
2. Mutation of KRAS
3. Mutation of SMAD4
4. Mutation of TP53.

141
Q

Can you give some examples of genetic colon cancers?

A

Polyposis syndromes:
FAP
Peutz-Jeghers
Juvenile polyposis
PTEN Harmatoma

Non-polyposis:
HNPCC

142
Q

What is mutated in FAP?

A

Mutation of the APC gene.W

143
Q

What is the lifetime risk of cancer in FAP? And therefore how are these patients managed?

A

100% risk.
They should have annual flexible sigmoidoscopy from age 10, if polyps then colonoscopy until colectomy undertaken in young adults.
Procedure of choice is a proctocolectomy and ilio-anal anastomosis.

144
Q

What is Juvenile Polyposis Syndrome? How is it diagnosed?

A

Mutation of the SMAD4 gene causing benign polyps. It causes bleeding and intussusception.
To be diagnosed you must have 3-5 polyps of a family history.
The lifetime risk of cancer is about 40% as they undergo malignant transformation via the adenoma to carcinoma pathway.

145
Q

What is Cowdens syndrome? What other tumours does it predispose to?

A

Mutation in the PTEN gene, causing harmatomatous polyps.
They calso get mucocutaneous lesions, thyroid goitres and cystic lesions in the breast/uterus.

146
Q

What are the features of FAP?

A

This causes 100s of adenomatous polyps in the colon.
Extra-intestinal: desmoid tumours, dark patches of the retina and osteoma in the mandible/skull.

147
Q

What causes HNPCC?

A

This is a mutation in the mismatch repair genes. Typically causes right sided tumours.
It is diagnosed via the Amsterdam criteria:
- exclusion of FAP
- Mismatch repair gene mutation
- 3 cases of HNPCC related cancers (colorectal, endometrial or renal in relatives of 2 generations of <45 years).

148
Q

What are the features of colorectal cancer?

A

Acute:
- PR bleed
- Obstruction
- Perforation
- Fistula

Non-acute:
- pain
- anaemia
- hepatomegaly
- ascites
- weight loss
- tenesmus
- change to bowel habits
- PR bleed

149
Q

What is the screening process for colorectal cancer in the UK?

A

FIT test: 59-69yo get bi-annual stool test. If +ve (around 2%) they then undergo colonoscopy.

150
Q

What are synchronous and metanchrononous tumours?

A

Synchronous: growth of another tumour at the same time of within 6 months.
Metanchrononous: growth of another tumour after 6 months.

151
Q

How can colorectal cancer spread?

A

Direct: duodenum, pancreas, genitourinary
Lymph: mesenteric nodes
Haematogenous: liver, lungs
Peritoneal/Ovarian: Krukenberg tumours.

152
Q

Describe Duke’s criteria.

A

A- not breaching the muscularis propria
B - no lymph node involvement
C - invades regional lymph nodes
D - metastases

153
Q

How would you manage colon cancer?

A

Resectable and Non-metastatic:
- resection with 5cm margins above and below.
Options include:
- R hemi (ligation of the ileocolic and R colic) for caecal/ascending colon tumours.
- Extended R hemi (ligation of above + middle colic) for hepatic flexure tumours.
- Subtotal colectomy (ligation of above + left colic) for transverse colon tumours.
- Left hemi (ligation of left colic) for splenic flexure tumours.
- Anterior resection (ligation of the IMA) for sigmoid tumours.

Resectable and Metastatic:
- Neoadjuvant chemo and resection of colorectal Ca, followed by resection of liver mets.

Unresectable:
- palliative chemo
- Vgef treatment/ rituximab to inhibit vascular growth
- RFA for liver mets
- Symptomatic resection if required.

154
Q

How would you surgically manage a obstructing left sided tumour?

A

Proximal loop colostomy or hartman’s with an end colostomy.

155
Q

How are rectal tumours managed?

A

Tumours sitting above the anterior peritoneal reflection should be managed as colon cancer, below the anterior peritoneal reflection as rectal cancer.

Rectal cancer can have chemo-radiotherapy which may reduce tumour size.
They can be managed either via a low anterior resection (mid level rectal tumour) or via an AP resection (lower rectal tumour).
They should have chemo after for 6 months.

156
Q

What are the complications of radiotherapy for rectal Ca?

A

May cause proctitis, sexual dysfunction, poor wound healing

157
Q

How would you manage an acutely presenting rectal Ca?

A

These have a high mortality and morbidity in regards to resection in acute settings, therefore you should consider a loop colostomy to decompress, neoadjuvant chemo/radiotherapy and formal resection at a later date.

158
Q

What are the symptoms and signs of ulcerative colitis?

A

Intestinal:
- Bloody diarrhoea
- Urgency/Tenesmus
- Abdominal pain
- Weight loss

Extra-intestinal:
- Spondylitis
- PSC
- Pyoderma gangrenosum
- Scleritis/Uveitis
- Clubbing
- Arthritis
- Episcleritis
- Erythema nodosum
- Osteoporosis

159
Q

How would you grade a flare of UC?

A

Mild = 4 or less stools a day, normal WCC and no systemic signs.

Moderate: 4-7 stools a day with minimal systemic upset.

Severe: >7 stools a day with systemic upset.

160
Q

What are the macroscopic and microscopic features you may see with UC?

A

Macroscopic:
- pseudopolyps
- loss of vascular pattern
- contact bleeding
- “featureless colon”
- continuous inflammation

Microscopic:
- Goblet cell depletion
- Crypt abscesses
- Superficial inflammation
- Ulceration

161
Q

How would you medically manage UC?

A

If it is mild and limited to the rectum then you can give rectal mesalazine and steroids.

If it is moderate or beyond the rectum then oral sulfasalazine, oral steroids or infliximab.

If it is severe: IVI, IV steroids, abx or ciclosporin.

162
Q

What are the indications for surgery in UC?

A

Toxic megacolon
Refractory bleeding
Perforation
Irretractable disease
Malignancy

163
Q

What is the emergency surgical procedure of choice in UC?

A

Subtotal colectomy and ileostomy.
OR if controlled then proctocolectomy and ileal pouch formation.

164
Q

What is toxic megacolon?

A

This is dilatation of the colon >6cm with systemic toxicity.
It may be due to inflammatory bowel disease, C-diff, Bechet’s, campylobater, CMV or ischaemia.
It is managed by IV abx, IV steroids and surgical resection.

165
Q

What factors increase risk of cancer in UC?

A

Family Hx, Pancolitis, prolonged disease time, PSC

166
Q

What is sulfasalazine?

A

This is an aminosalicylate which acts to inhibit inflammatory mediators.
It can be given PO or PR
Used in UC but not in Crohn’sW

167
Q

What is azothioprine?

A

This is a thiopurine. These inhibit T cell proliferation and natural killer cells. They are immune modulators and take 2-3 months to work. They can prevent recurrence, however you must check TMPT enzyme, otherwise will cause bone marrow suppression.

168
Q

What are the features of Crohn’s disease?

A

Intestinal:
Abdominal pain
Fistula
Stricture
Ileitis
GS
Perianal disease
Apthous ulcers
Weight loss
Loose stool

Extraintestinal:
B12 deficiency
Arthritis
Erythema nodosum
Pyoderma gangrenosum
Uveitis
Ank Spond
PSC
Cirrhosis

169
Q

What are the macro and microscopic features of Crohn’s?

A

Macroscopic:
- cobblestone appearance
- Skip lesions
- thick inflammation
- ulceration
- strictures
- mesenteric fat wrapping

Microscopic:
- granulomatous inflammation (non-caseating)
- Full thickness inflammation
- normal goblet cells
- vasculitis

170
Q

How do you manage Crohn’s?

A

Mainstay is steroids and TNF alpha inhibitors such as infliximab.
Surgery should be last resort due to risk of short bowel syndrome.

171
Q

What is C-diff?

A

This is a spore forming anaerobic gram +ve bacteria, resistant to the gastric acid.
It produces toxins - enterotoxin and cytotoxin which cause local and systemic inflammation.
It causes a pseudomembranous colitis.

172
Q

How would you manage C-diff?

A

Oral metro for 10-14 days.
If recurrence add Vanc PO or IV

173
Q

What are the risk factors for development of ischaemic gut?

A

CVD, Age, AF, COPD, Smoking, Hypercoaguable state, COCP, CCB, Cocaine, post-op, constipation.

174
Q

What is a diverticulum?

A

Sac-like protrusions through the muscle wall occurring at weak points in the muscularis (normally where the vasa recta perforate).

175
Q

Describe the Hinchey Classification of Diverticulitis?

A
  1. Pericolic abscess
  2. Pelvic abscess
  3. Purulent peritonitis
  4. Faecal peritonitis
176
Q

What are some of the complications of diveriticulitis?

A

Abscess
Bleeding
Strictures
Fistula
Perforation

177
Q

What are the anterior relations of the aorta?

A

Celiac trunk and branches
Body of pancreas
SMA
3rd part of the duodenum
Root of mesentery
Splenic vein
Left renal vein

MRCS Part B (14 decks)

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