Wednesday [stomach/bowel anatomy, Chiari malformation, bowel obstruction]]

Question 1

how long is the oesophagus?

Answer 1

25cm

Question 2

Where does the oesophagus originate/terminate?

Answer 2

Oringates inferior border of cricoid [C6] and extends to the cardiac orifice stomach [T11]

Question 3

Anatomical structure of the oesophagus

Answer 3

The oesophagus shares a similar structure with many of the organs in the alimentary tract:

Adventitia – outer layer of connective tissue.
Note: The very distal and intraperitoneal portion of the oesophagus has an outer covering of serosa, instead of adventitia.
Muscle layer – external layer of longitudinal muscle and inner layer of circular muscle. The external layer is composed of different muscle types in each third:
Superior third – voluntary striated muscle
Middle third – voluntary striated and smooth muscle
Inferior third – smooth muscle
Submucosa
Mucosa – non-keratinised stratified squamous epithelium (contiguous with columnar epithelium of the stomach).

Question 4

how is the upper oesophageal sphincter produced?

Answer 4

Striated cricopharyngeus muscle.

Normally contracted to prevent entrance air to oesophagus.

Question 5

Location and how the LES is maintained

Answer 5

The lower oesophageal sphincter is located at the gastro-oesophageal junction (between the stomach and oesophagus). The gastro-oesophageal junction is situated to the left of the T11 vertebra, and is marked by the change from oesophageal to gastric mucosa.

The sphincter is classified as a physiological (or functional) sphincter, as it does not have any specific sphincteric muscle. Instead, the sphincter is maintained by four factors:

Oesophagus enters the stomach at an acute angle.
Walls of the intra-abdominal section of the oesophagus are compressed when there is a positive intra-abdominal pressure.
Prominent mucosal folds at the gastro-oesophageal junction aid in occluding the lumen.
Right crus of the diaphragm has a “pinch-cock” effect.

Question 6

What are the four physiological contractions in the oesophagus’ lumen?

Answer 6

The anatomical relations of the oesophagus give rise to four physiological constrictions in its lumen – it is these areas where food/foreign objects are most likely to become impacted. They can be remembered using the acronym ‘ABCD‘:

Arch of aorta
Bronchus (left main stem)
Cricoid cartilage
Diaphragmatic hiatus

Question 7

Thoracic and abdominal vasculature of the oesophagus

Answer 7

Thoracic

The thoracic part of the oesophagus receives its arterial supply from the branches of the thoracic aorta and the inferior thyroid artery (a branch of the thyrocervical trunk).

Venous drainage into the systemic circulation occurs via branches of the azygous veins and the inferior thyroid vein.

Abdominal

The abdominal oesophagus is supplied by the left gastric artery (a branch of the coeliac trunk) and left inferior phrenic artery. This part of the oesophagus has a mixed venous drainage via two routes:

To the portal circulation via left gastric vein
To the systemic circulation via the azygous vein.
These two routes form a porto-systemic anastomosis, a connection between the portal and systemic venous systems.

Question 8

How is the oesophagus innervated?

Answer 8

The oesophagus is innervated by the oesophageal plexus, which is formed by a combination of the parasympathetic vagal trunks and sympathetic fibres from the cervical and thoracic sympathetic trunks.

Two different types of nerve fibre run in the vagal trunks. The upper oesophageal sphincter and upper striated muscle is supplied by fibres originating from the nucleus ambiguus. Fibres supplying the lower oesophageal sphincter and smooth muscle of the lower oesophagus arise from the dorsal motor nucleus

Question 9

Lymphatics of the oesophagus

Answer 9

The lymphatic drainage of the oesophagus is divided into thirds:

Superior third – deep cervical lymph nodes.
Middle third – superior and posterior mediastinal nodes.
Lower third – left gastric and celiac nodes.

Question 10

Type of cell change does Barrett’s oesophagus refer to? And how can this be detected?

Answer 10

Barrett’s oesophagus refers to the metaplasia (reversible change from one differentiated cell type to another) of lower oesophageal squamous epithelium to gastric columnar epithelium. It is usually caused by chronic acid exposure as a result of a malfunctioning lower oesophageal sphincter. The acid irritates the oesophageal epithelium, leading to a metaplastic change.

The most common symptom is a long-term burning sensation of indigestion.

It can be detected via endoscopy of the oesophagus. Patients who are found to have it will be monitored for any cancerous changes

Question 11

How common are oesophageal carincomas? Clinical features, and two main types of oesophageal carcinomas.

Answer 11

Around 2% of malignancies in the UK are oesophageal carcinomas. The clinical features of this carcinoma are:

Dysphagia – difficulty swallowing. It becomes progressively worse over time as the tumour increases in size, restricting the passage of food.
Weight loss
There are two major types of oesophageal carcinomas: squamous cell carcinoma and adenocarcinoma.

Squamous cell carcinoma – the most common subtype of oesophagus cancer. It can occur at any level of the oesophagus.
Adenocarcinoma – only occurs in the inferior third of the oesophagus and is associated with Barrett’s oesophagus. It usually originates in the metaplastic epithelium of Barrett’s oesophagus.

Question 12

Why, how and when does oesophageal varices present?

Answer 12

The abdominal oesophagus drains into both the systemic and portal circulation, forming an anastomosis between the two.

Oesophageal varices are abnormally dilated sub-mucosal veins (in the wall of the oesophagus) that lie within this anastomosis. They are usually produced when the pressure in the portal system increases beyond normal, a state known as portal hypertension. Portal hypertension most commonly occurs secondary to chronic liver disease, such as cirrhosis or an obstruction in the portal vein.

The varices are predisposed to bleeding, with most patients presenting with haematemesis (vomiting of blood). Alcoholics are at a high risk of developing oesophageal varices.

Question 13

How long is the small intestine and where does it extend from?

Answer 13

approx 6.5m average person

Pylorus of the stomach to the ileocaceal junction

Question 14

How long is the duodenum?

Answer 14

The most proximal portion of the small intestine is the duodenum. Its name is derived from the Latin ‘duodenum digitorum’, meaning twelve fingers length. It runs from the pylorus of the stomach to the duodenojejunal junction.

The duodenum can be divided into four parts: superior, descending, inferior and ascending. Together these parts form a ‘C’ shape, that is around 25cm long, and which wraps around the head of the pancreas

Question 15

What is marked by teh major duodenal papilla? Which duodenal part crosses over at the IVC and the aorta? Which has the duodenal flexure> Which aprt has the hepatoduoudenal ligament?

Answer 15

D1 – Superior (Spinal level L1)

The first section of the duodenum is known as ‘the cap’. It ascends upwards from the pylorus of the stomach, and is connected to the liver by the hepatoduodenal ligament. This area is most common site of duodenal ulceration.

The initial 3cm of the superior duodenum is covered anteriorly and posteriorly by visceral peritoneum, with the remainder retroperitoneal (only covered anteriorly).

D2 – Descending (L1-L3)

The descending portion curves inferiorly around the head of the pancreas. It lies posteriorly to the transverse colon, and anterior to the right kidney.

Internally, the descending duodenum is marked by the major duodenal papilla – the opening at which bile and pancreatic secretions to enter from the ampulla of Vater (hepatopancreatic ampulla).

D3 – Inferior (L3)

The inferior duodenum travels laterally to the left, crossing over the inferior vena cava and aorta. It is located inferiorly to the pancreas, and posteriorly to the superior mesenteric artery and vein.

D4 – Ascending (L3-L2)

After the duodenum crosses the aorta, it ascends and curves anteriorly to join the jejunum at a sharp turn known as the duodenojejunal flexure.

Located at the duodenojejunal junction is a slip of muscle called the suspensory muscle of the duodenum. Contraction of this muscle widens the angle of the flexure, and aids movement of the intestinal contents into the jejunum

Question 16

Where is the most common part of the duodenum to ulcerated? What is an ulcer? Most comon cause of ulceration?

Answer 16

A duodenal ulcer is the erosion of the mucosa in the duodenum. It may also be described as a peptic ulcer (although this term can also be used to refer to ulcerations in the stomach). Duodenal ulcers are most likely to occur in the superior portion of the duodenum.

The most common causes of duodenal ulcers are Helicobacter pylori infection and chronic NSAID therapy

Question 17

Tx and Cx of duodenal ulceration

Answer 17

An ulcer in itself can be painful, but is not particularly troublesome and can be treated medically. However, if the ulcer progresses to create a complete perforation through the bowel wall, this is a surgical emergency, and usually warrants immediate repair. A perforation may be complicated by:

Inflammation of the peritoneum(peritonitis) – causing damage to the surrounding viscera, such as the liver, pancreas and gall bladder.
Erosion of the gastroduodenal artery – causing haemorrhage and potential hypovolaemia shock.

Question 18

Which parts of the small intestine is intraperitoneal?

Answer 18

The jejunum and ileum are the distal two parts of the small intestine. In contrast to the duodenum, they are intraperitoneal.

Question 19

Where does the jejunum begin?

Answer 19

The jejunum begins at the duodenojejunal flexure. There is no clear external demarcation between the jejunum and ileum – although the two parts are macroscopically different. The ileum ends at the ileocaecal junction.

At this junction, the ileum invaginates into the cecum to form the ileocecal valve. Although it is not developed enough to control movement of material from the ileum to the cecum, it can prevent reflux of material back into the ileum (if patent, see below).

Question 20

Location, intestinal wall thickness, vasa recta, arcades, colour comparison of the jejunum as compared to the ilieum

Answer 20

image

Question 21

Arterial supply duodenum and why this is important [bonus: lymphatic and venous]

Answer 21

Duodenum
The arterial supply of the duodenum is derived from two sources:

Proximal to the major duodenal papilla – supplied by the gastroduodenal artery (branch of the common hepatic artery from the coeliac trunk).
Distal to the major duodenal papilla – supplied by the inferior pancreaticoduodenal artery (branch of superior mesenteric artery).
This transition is important – it marks the change from the embryological foregut to midgut. The veins of the duodenum follow the major arteries and drain into the hepatic portal vein.

Lymphatic drainage is to the pancreatoduodenal and superior mesenteric nodes.

Question 22

Arterial supply jejunum [B: venous and lyphatics]

Answer 22

The arterial supply to the jejunoileum is from the superior mesenteric artery.

The superior mesenteric artery arises from the aorta at the level of the L1 vertebrae, immediately inferior to the coeliac trunk. It moves in between layers of mesentery, splitting into approximately 20 branches. These branches anastomose to form loops, called arcades. From the arcades, long and straight arteries arise, called vasa recta.

The venous drainage is via the superior mesenteric vein. It unites with the splenic vein at the neck of the pancreas to form the hepatic portal vein.

Lymphatic drainage is into the superior mesenteric nodes.

Question 23

What separates the large and small intestine? Why is this important?

Answer 23

The ileocaecal valve represents the separation between the small and large intestine. Its main function is to prevent the reflux of enteric fluid from the colon into the small intestine. It is also used as an landmark during colonoscopy, indicating that the limit of the colon has been reached and that a complete colonoscopy has been performed.

The ileocaecal valve is also important in the setting of large bowel obstruction. Should the ileocaecal valve be competent, a closed loop obstruction can occur and cause bowel perforation. Should the ileocaecal valve be incompetent (i.e. allow backflow of enteric contents into the small bowel) then the situation is less emergent and the trajectory of the obstruction less rapid.

Question 24

Anatomical structure and relations of the cecum

Answer 24

The cecum is the most proximal part of the large intestine and can be found in the right iliac fossa of the abdomen. It lies inferiorly to the ileocecal junction and can be palpated if enlarged due to faeces, inflammation, or malignancy.

The cecum derives its name from its inferior blind-end (‘cecum’ is derived from the Latin word ‘caecus’, meaning ‘blind’). Superiorly, the cecum is continuous with the ascending colon. Unlike the ascending colon, the cecum is intraperitoneal and has a variable mesentery.

Between the cecum and ileum is the ileocecal valve. This structure prevents reflux of large bowel contents into the ileum during peristalsis and is thought to function passively, as opposed to a defined muscular sphincter.

Note: In cases of large bowel obstruction, an incompetent ileocecal valve is paradoxically advantageous as it allows the retrograde passage of bowel contents back into the ileum. This helps to decompress the cecum and prevent “closed loop” obstructions and perforations.

Question 25

Lymphatic drainage of the cecum

Answer 25

Lymph from the cecum drains into the ileocolic lymph nodes (which surround the ileocolic artery).

Question 26

How common are volvulus?

Answer 26

A volvulus occurs when part of the intestine ‘twists’ on itself, causing obstruction of the lumen. Cecal volvulus represents approximately 10% of all intestinal volvuluses (the most common location is the sigmoid colon)

Question 27

CF and Tx of cecal volvulus

Answer 27

Common clinical features include colicky abdominal pain, abdominal distension, and absolute constipation. Abdominal x-ray typically demonstrates a distended loop of large bowel that originates from the right lower quadrant.

Treatment involves decompression of the volvulus. In cases when bowel perforation has occurred, the affected area is usually surgically resected.

Question 28

Main function of bile, how much is produced by the liver each day?

Answer 28

Bile is an aqueous, alkaline, greenish-yellow liquid whose main function is to emulsify fats in the small intestine and to eliminate substances from the liver. The liver produces 0.25-1L of bile per day.

Question 29

What is bile up of?

Answer 29

Bile is made up of bile acids, cholesterol, phospholipids, bile pigments (such as bilirubin and biliverdin), electrolytes and water.

Question 30

Two main groups of bile constituents

[B: where do they drain into]

Answer 30

The bile acid-dependent component is produced by hepatocytes. The hepatocytes secrete bile acids, bile pigments and cholesterol into canaliculi, which are small channels that transport the bile acid dependent portion towards the bile ducts.
The bile acid-independent component is made by the ductal cells that line the bile ducts. These cells secrete an alkaline solution – similar to the fluid made by pancreatic duct cells. The hormone secretin stimulates this secretion.

Question 31

What stimulates bile production?

Answer 31

Bile is continuously produced, but we only need it during and after meals. Therefore the gallbladder concentrates and stores bile, by removing the water and ions. After eating, the hormone cholecystokinin is released from the duodenum. This stimulates gallbladder contraction and relaxes the sphincter of Oddi, thus allowing bile to flow into the duodenum.

Question 32

What are the two primary bile acids?

Answer 32

Cholic acid

Chenodeoxycholic acid

Question 33

How are bile salts formed?

Answer 33

Bile acids + When these bile acids are conjugated with the amino acids glycine and taurine, they form bile salts. Bile salts are more soluble than bile acids and act as detergents to emulsify lipids.

Question 34

Properties of bile salts

Answer 34

Bile salts are amphipathic which means they have a hydrophobic end which is lipid-soluble and a hydrophilic end which is water-soluble. This structure allows bile salts to emulsify fats into smaller droplets, increasing the surface area for lipids to be broken down by duodenal lipases.

Question 35

What are micelles?

Answer 35

The bile acids coat the products of lipid breakdown as well as cholesterol and phospholipids to form spherical structures known as micelles. Micelles play an important role in the digestion of fats and transport their contents to the intestinal epithelium where they can be absorbed. However, the bile acids don’t enter the gut epithelial cells with the lipids, rather they recirculate back to the liver, via the enterohepatic circulation.

Question 36

Go through bile pigments

Answer 36

Bile also contains bile pigments which are excretory products of the liver and include biliverdin and bilirubin. Bilirubin is a breakdown product of haemoglobin and is conjugated in the liver and secreted into bile. Bile pigments are normally excreted in the faeces and make the faeces appear brown. Problems in the liver or biliary tree often result in the accumulation of bilirubin in the blood, which manifests as jaundice

Question 37

Enterohepatic circulation of bile acids

Answer 37

Bile passes out of the liver through the bile ducts and is concentrated and stored in the gallbladder. During and after a meal, bile is excreted from the gall bladder by contraction and passes into the duodenum through the common bile duct. Most of the bile acids are reabsorbed in the terminal ileum and returned to the liver via the hepatic portal vein. The liver then extracts the bile salts

Question 38

What does the enteropathic circulation of bile allow?

Answer 38

The enterohepatic circulation allows the liver to recycle and preserve a pool of bile acids

Question 39

What are gallstones? RF, Sx, Cx too.

Answer 39

Gallstones are small lumps of solid material that form in the gall bladder. Abnormal concentrations of bile acids can increase the risk of precipitation of bile out of solution to form stones. They can be made up entirely of cholesterol, bile pigments or a mixture of the two. Risk factors for gallstone formation include being female, obesity, age >40, and poor diet.

Gallstones are often asymptomatic but can cause painful biliary colic if they move to occlude the neck of the gall bladder or the biliary tree. Biliary colic is intermittent pain in the right upper quadrant, typically precipitated by the consumption of a fatty meal and subsequent contractions of the gallbladder. This can lead to further complications such as cholecystitis (inflammation of the gallbladder) or ascending cholangitis (inflammation of the bile ducts). Associated symptoms include nausea/vomiting, abdominal pain, jaundice and fever.

Question 40

Size and location of the spleen

Answer 40

The spleen is an organ the size of a fist found in the left upper quadrant (LUQ) of the abdomen, under the protection of the inferior thoracic cage.

Question 41

Two types of tissue in the spleen

Answer 41

White pulp and red pulp

Question 42

What nodules do the white part of the spleen contain?

Answer 42

Malpighian corpuscles

Question 43

What do malpighan corpuscles contain?

Answer 43

Periarteriolar lymphoid sheaths rich in T-lymphocytes and macrophages.
A marginal zone, rich in macrophages
Lymphoid follicles, rich in naive B-lymphocytes

Question 44

Function of the white pulp and how it does this

Answer 44

Because of this, the white pulp of the spleen has a very important role in the normal immune response to infection. Antigen presenting cells may enter the white pulp, resulting in activation of the T-lymphocytes stored there. These in turn, activate the B-lymphocytes in the follicles, converting them to plasma cells which then produce of IgM antibodies initially and eventually IgG antibodies.

Pathogens may also enter the follicles directly. B-lymphocytes detect this and can then present the antigen to the T-lymphocytes. This leads to a process known as co-stimulation, in which the two cell types activate each other – so the B-lymphocyte is then able to become a plasma cell and produce antibodies against the pathogen.

The white pulp is also important in how the body deals with encapsulated bacteria e.g. Neisseria meningitidis, Haemophilus influenzae and Streptococcus pneumoniae. Encapsulated bacteria tend to have a very smooth surface with a negative charge which therefore reduces the ability of phagocytes to attach and engulf the bacteria. The B-lymphocytes in the white pulp help opsonise these bacteria.

Question 45

How much does the red pulp of the spleen?

Answer 45

Roughly 80% of the spleen parenchyma

Question 46

What is the red pulp made up of?

Answer 46

It is separated from the white pulp by the marginal zone. The red pulp is primarily made up of tissue known as the cords, which is rich in macrophages, and the venous sinus.

Question 47

Functions fo the red pulp

Answer 47

Removal of old, damaged and dead red blood cells along with antigens and microorganisms – the venous sinuses have gaps in the endothelial lining which allows normal cells to pass through, abnormal cells remain in the cords and are phagocytosed by macrophages
Phagocytosis of opsonised bacteria by macrophages
Sequestration of platelets.
Storage of red blood cells in case of hypovolaemia, these can then be released following an injury resulting in blood loss
Prenatally, it is haematopoietic until about the fifth month of gestation when bone marrow becomes the main site for haematopoiesis

Question 48

Cause of splenomegaly

Answer 48

Splenomegaly is an enlarged spleen which can be caused by infection, portal hypertension, granulocytic leukaemia (increased lymphocyte and white blood cells), haemolytic and granulocytic anaemias etc.

Question 49

When is spleen palpable

Answer 49

splenomegaly

Question 50

How to assess and treat splenomegaly

Answer 50

To assess the size of the spleen, a patient’s abdomen should be palpated diagonally from right iliac fossa (RIF) to LUQ as it tends to enlarge towards the RIF. Underlying cause for the splenomegaly should be treated and in some cases a splenectomy (removing the spleen) may be suggested.

Question 51

Cause and Tx for asplenia

Answer 51

Asplenia is the lack of a functional spleen. It can be congenital or acquired (due to splenectomy). Patients are left immunocompromised and therefore are at a higher risk of acquiring infection from encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis.

To reduce this risk, these patients are given lifelong prophylactic antibiotics; immunisation for the above mentioned organisms and annual flu vaccines. They should seek expert advice at first signs of infection.

These patients also carry an asplenia card/pendant/bracelet to alert healthcare professionals about their condition.

Question 52

How much of the pancreas is enodrine?

Answer 52

When we consider the functions of the pancreas, it is simpler to view it as a mix of two glands. We can divide the pancreas into an exocrine gland, containing the acinar and duct tissue, and the endocrine gland containing the islets of Langerhans.

The majority of the pancreas is made up of the exocrine portion (85% by mass) and secretes digestive enzymes, water and bicarbonate to assist in digestion

Question 53

Why is bicarb important to the pancreas?

Answer 53

The bicarbonate helps in neutralising the stomach acid. This is a vital part of digestion as the small intestine is not specialised to withstand the strong acids from the stomach. This is because the small intestine, unlike the stomach, lacks a thick protective mucous layer. Additionally, the digestive enzymes secreted by the pancreas reach their optimum function at a basic pH. This is achieved by the bicarbonate secretions of the pancreas

Question 54

What is the functional unit of the exocrine pancreas

Answer 54

The functional unit of the exocrine pancreas includes the acinus and its duct system. The word acinus is from the Latin term for “berry in a cluster”. These acinar cells are specialised in enzyme synthesis, storage and secretion. The duct system modifies the aqueous secretions. This mechanism is stimulated by the parasympathetic system and inhibited by the sympathetic system.

Question 55

how are digestive enzymes secreted by teh pancreas

Answer 55

The acinar cells produce digestive enzymes on the rough endoplasmic reticulum. They are then moved to the Golgi complex where they form condensing vacuoles. These condensing vacuoles are then concentrated into inactive zymogen granules in pancreatic acinar cells and stored for secretion. They are secreted into the main pancreatic duct, which merges with the bile duct at the head of the pancreas and forms the Ampulla of Vater. From here it enters the duodenum

Question 56

Which enzymes are secreted by the pancreas?

Answer 56

Enzymes secreted:

Proteases
Chymotrypsinogen and Trypsinogen
Digest proteins and peptides to single amino acids
Pancreatic lipase
Digests triglycerides, monoglyceride and free fatty acids
Amylase
Starch and maltose (disaccharides)
Other enzymes include ribonuclease, gelatinase, elastase etc.

Question 57

How is bicarbonate secreted?

Answer 57

Water and carbon dioxide combine in a reaction catalysed by the enzyme carbonic anhydrase. The product formed is carbonic acid (H2CO3).

H2O + CO2 -> H2CO3

Carbonic acid then dissociates into hydrogen ions (H+) and bicarbonate ions (HCO3–)

H2CO3 -> H+ + HCO3–

H+ ions are transported out of the pancreatic ductal cells into the blood in exchange for Na+ ions by an H+/Na+ antiporter. The Na+ ions that enter the cell are then removed by the Na+/H+/ATPase.

The HCO3– produced from the dissociation of carbonic acid is then transported into the intercalated ducts of the pancreas in exchange for Cl–. An intracellular build up of Cl– is avoided by a chloride channel which allows chloride ions to return to the lumen of the intercalated ducts.

The bicarbonate ions, Na+ ions and water then move through the intercalated ducts and end up at the main pancreatic duct ready for secretion into the duodenum upon an appropriate stimulus.

Question 58

What is vagal innervation to the pancreas?

Answer 58

There are a number of factors involved in triggering the pancreas to release its secretions. Vagal innervation to the pancreas stimulates the secretion of enzymes. This stimulation occurs when we see, smell or taste food, or when the stomach wall is stretched

Question 59

How does the body encourage pancreatic secretions?

Answer 59

There are also other ways in which the body encourages pancreatic secretions. Besides the vagal stimulation, acidic chyme entering the duodenum stimulates S cells to release secretin. Secretin is a hormone that causes the pancreatic cells to secrete the alkaline parts of the pancreatic juices

Question 60

How does fatty acids and protein present in the chyme combine with the acidic pH to release which hormone?

Answer 60

The fatty acids and protein present in the chyme, combined with the acidic pH, trigger I cells in the duodenum to release the hormone cholecystokinin (CCK). This hormone also leads to secretion of digestive enzymes in the pancreatic juices. In addition, CCK stimulates bile secretion via gallbladder contraction.

Question 61

Anatomically, what is the main pancreatic duct?

Answer 61

Anatomically, the main pancreatic duct merges with the bile duct, which leads to the Ampulla of Vater. It is here that these secretions pour into the duodenum and help neutralise and digest chyme.

Question 62

What is the most common tumour of the pancreas?

Answer 62

The most common cancer of the pancreas occurs in the exocrine portion and are called ductal adenocarcinomas

Question 63

Cx, Dx and Tx of pancreatic tumours

Answer 63

Ductal adenocarcinomas can disrupt exocrine secretions, causing patients to develop pancreatitis and pain. Digestive enzymes are secreted into the pancreas instead of the duodenum. As key digestive enzymes are not reaching the duodenum effectively, this can lead to diarrhoea and incomplete digestion of food.

Pancreatic cancers are mostly diagnosed at a very late stage, as symptoms will only present once the cancer reaches a certain size. At this point it is often too late for surgery, which is the only curative treatment option available. This type of cancer is very difficult to treat and as such has a poor prognosis.

Question 64

How can pancreatitis be detected?

Answer 64

An inflammation of the pancreas is known as pancreatitis. Pancreatitis can be diagnosed by detection of pancreatic amylase and lipase in a blood test.

Question 65

Common presentation pancreatitis

Answer 65

A common presentation would be intense pain in the central abdomen radiating to the back. Patients may complain of pale stools and dark urine. In pancreatitis, the digestive enzymes of the pancreas damage the tissue and structure of the pancreas.

Question 66

Why do fatty stools occur in pancreatitis?

Answer 66

The digestive enzymes do not reach the duodenum, leading to incomplete digestion of fatty acids. This results in fatty stools (steatorrhoea), which have a pungent smell and float in water.

Question 67

Which disease leads to inappropriate zymogen activation?

Answer 67

Bicarbonate secretion in ductal cells depends on the protein CFTR. This is both a chloride channel and a bicarbonate channel. When the CFTR protein is defective, as it is in Cystic Fibrosis, the secretion of bicarbonate by duct cells is affected. This leads to a blockage in the pancreatic ducts and inappropriate zymogen activation. This causes damage to acinar and duct cells.

Patients suffering from a complete lack of CFTR function are usually born with pancreatic insufficiency. This means their pancreas releases an inadequate amount of digestive enzymes. These patients require constant treatment with digestive enzyme supplements.

To a lesser degree, patients with less severe mutations in CFTR proteins with some limited channel function still have an increased risk of developing pancreatitis.

Question 68

What is the Chiari malformation?

Answer 68

Chiari malformation (CM) is a structural defect in the cerebellum, characterized by a downward displacement of one or both cerebellar tonsils through the foramen magnum (the opening at the base of the skull).

Question 69

Common Sx of CM

Answer 69

CMs can cause headaches, difficulty swallowing, vomiting, dizziness, neck pain, unsteady gait, poor hand coordination, numbness and tingling of the hands and feet, and speech problems.

Question 70

Less common Sx of CM

Answer 70

Less often, people may experience ringing or buzzing in the ears, weakness, slow heart rhythm, or fast heart rhythm, curvature of the spine (scoliosis) related to spinal cord impairment, abnormal breathing, such as central sleep apnea, characterized by periods of breathing cessation during sleep, and, in severe cases, paralysis

Question 71

What can Chiari malformation lead to?

Answer 71

This can sometimes lead to non-communicating hydrocephalus[4] as a result of obstruction of cerebrospinal fluid (CSF) outflow.

Question 72

What is the CSF outflow caused by?

Answer 72

The cerebrospinal fluid outflow is caused by phase difference in outflow and influx of blood in the vasculature of the brain.

Question 73

What is type 2 CM also known as?

Answer 73

Arnold-Chiari malformation

Question 74

Difference in Sx between adults and children

Answer 74

Findings are due to brain stem and lower cranial nerve dysfunction. Onset of symptoms are less likely to be present during adulthood in most patients. Younger children generally have a substantially different presentation of clinical symptoms from older children. Younger children are more likely to have a more rapid neurological degeneration with profound brain stem dysfunction over several days.

Question 75

What may the blockage of CSF in CM lead to [and hand weakness etc.]?

Answer 75

The blockage of cerebrospinal fluid (CSF) flow may also cause a syrinx to form, eventually leading to syringomyelia. Central cord symptoms such as hand weakness, dissociated sensory loss, and, in severe cases, paralysis may occur
This is a fluid-filled cyst in the spinal cord.

Question 76

Most widely accepted cause for chiari malformations

Answer 76

The most widely accepted pathophysiological mechanism by which Chiari type I malformations occur is by a reduction or lack of development of the posterior fossa as a result of congenital or acquired disorders. Congenital causes include hydrocephalus, craniosynostosis (especially of the lambdoid suture), hyperostosis (such as craniometaphyseal dysplasia, osteopetrosis, erythroid hyperplasia), X-linked vitamin D-resistant rickets, and neurofibromatosis type I. Acquired disorders include space occupying lesions due to one of several potential causes ranging from brain tumors to hematomas.[13] Traumatic brain injury may cause delayed acquired Chiari malformation, but the pathophysiology of this is unknown.[14] Additionally, ectopia may be present but asymptomatic until a whiplash injury causes it to become symptomatic

Question 77

Dx of CM

Answer 77

Neuro exam, patient history, medical imaging, MRI

Dx of Chiari II can be made prenantlly through USS

Question 78

What are the types of CM

Answer 78

image

Question 79

Tx for volvulus

Answer 79

Sigmoidoscopy, barium enema, bowel resection

Question 80

What is volvullus?

Answer 80

volvulus is when a loop of intestine twists around itself and the mesentery that supports it, resulting in a bowel obstruction.

Question 81

Sx and onset of volvuusu

Answer 81

Symptoms include abdominal pain, abdominal bloating, vomiting, constipation, and bloody stool.[1][2] Onset of symptoms may be rapid or more gradual.[2] The mesentery may become so tightly twisted that blood flow to part of the intestine is cut off, resulting in ischemic bowel.[1] In this situation there may be fever or significant pain when the abdomen is touched.

Question 82

Sx and Sx bowel obstruction

Answer 82

N+V, vomiting, crmaping, constipation, diarrhoea, distended abdomen, fever, tachycardia

Question 83

Categorisation of bowel obstruction

Answer 83

Mechanical obstruction

1. adhesion
2. tumour [cancer]
3. intersussectpion
4. hernia [protrusion intestine]
5. volvulus [twisting of the bowel]

Pseudoobstruction

Question 84

Most common cause mechanical obstruction?

Answer 84

Adhesions after surgery

Question 85

What are adhesions and what can they cause?

Answer 85

Fibrous brudges between bowel segments, adhesions cause extrinsic compression of the bowel

Question 86

Common cause tumours obstructions, RF as well

Answer 86

COlorectal cancer, RF = Fhx, age, obesity, IBD, diet

Question 87

intersusscpetion common, where is this common

Answer 87

1-5% mechical bowel obstruction, common site is the ileocaecal valve

Question 88

hernia define

Answer 88

defined as progressive bulging of an organ or an organ through the body wall that normally onctained it

Question 89

What can hernias be

Answer 89

internal or external

Question 90

where volvulus commonly?

Answer 90

Caeceum and sigmoid

Question 91

What can adhesions lead to?

Answer 91

Volvulus

Question 92

What are the types of pseudoobstruction

Answer 92

Myopathy and neuropathy, and also Hirschprung disease

Question 93

Where nerves missing in Hirschprung disease

Answer 93

congenital condition where nerve mssinig distal end of the colon -> no-abndmorla peristalisis -> bowel obstruction

Question 94

What is bowel death be caused by in obstruction?

Answer 94

Food left in bowel for a time -> bowel distnetion _. venous compression -> decrease oxygenation -> cells of intestine die [and also less peristalisis so more distention]

Question 95

Why can bowel distension lead to hypotension

Answer 95

Bowel distention -> venous compression -> fluid secretion _. loss of H20 -> loss of electrolytes -> hypotension shock

Question 96

Why can sepsis result from?

Answer 96

Bowel distention or toxins in bacteria of obstructed bowel

Question 97

Cx of bowel obstruction

Answer 97

1. Bowel ischemia
2. perforation
3. sepsis