GI and Liver Flashcards
Give 4 functions of the liver.
- Glucose and fat metabolism.
- Detoxification and excretion.
- Protein synthesis e.g. albumin, clotting factors.
- Defence against infection.
Name 3 things that liver function tests measure.
- Serum bilirubin.
- Serum albumin.
- Pro-thrombin time.
Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease).
Alkaline phosphatase.
What enzymes increase in the serum in hepatocellular liver disease?
Transaminases e.g. AST and ALT.
Name two hepatocellular enzymes.
Transaminases e.g. AST and ALT.
Name a cholestatic enzyme.
Alkaline phosphatase.
What are the potential consequences of hepatocyte regeneration in someone with liver cirrhosis?
Neoplasia and therefore HCC. Hepatocyte regeneration is liable to errors.
Give 3 causes of iron overload.
- Genetic disorders e.g. haemochromatosis.
- Multiple blood transfusions.
- Haemolysis.
- Alcoholic liver disease.
What protein is responsible for controlling iron absorption?
Hepcidin.
Levels of this protein are decreased in haemochromatosis.
Give 3 causes of duct obstruction.
- Gallstones.
- Stricture (narrowing) e.g. malignant, inflammatory.
- Carcinoma.
- Blocked stent.
What can cause peritonitis?
- Bacterial infection due to a perforated organ; spontaneous bacterial peritonitis; infection secondary to peritoneal dialysis.
- Non-infective causes e.g. bile leak; blood from ruptured ectopic pregnancy.
Name a cause of pelvic inflammatory disease.
A complication of chlamydial infection.
Give 4 reasons why liver patients are vulnerable to infection.
- They have impaired reticulo-endothelial function.
- Reduced opsonic activity.
- Leukocyte function is reduced.
- Permeable gut wall.
Give 5 causes of diarrhoeal infection.
- Traveller’s diarrhoea.
- Viral e.g. rotavirus, norovirus.
- Bacterial e.g. E.coli.
- Parasites e.g. helminths.
- Nosocomial e.g. c.diff.
Give 5 causes of non-diarrhoeal infection.
- Gastritis/peptic ulcer disease e.g. h.pylori.
- Acute cholecystitis.
- Peritonitis.
- Typhoid/paratyphoid.
- Amoebic liver disease.
Give 3 ways in which diarrhoea can be prevented.
- Access to clean water.
- Good sanitation.
- Hand hygiene.
What is the diagnostic criteria for traveller’s diarrhoea?
> 3 unformed stools per day and at least one of:
- Abdominal pain.
- Cramps.
- Nausea.
- Vomiting.
It occurs within 3 days of arrival in a new country.
Give 3 causes of traveller’s diarrhoea.
- Enterotoxigenic e.coli (ETEC).
- Campylobacter.
- Norovirus.
Describe the pathophysiology of traveller’s diarrhoea.
Heat labile ETEC modifies Gs and it is in a permanent ‘locked on’ state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient -> diarrhoea.
Which type of e.coli can cause bloody diarrhoea and has a shiga like toxin?
Enterohaemorrhagic e.coli (EHEC) aka e.coli 0157.
What does EIEC stand for?
Enteroinvasive e.coli.
Which type of e.coli is responsible for causing large volumes of watery diarrhoea?
Enteropathogenic e.coli (EPEC).
What does EAEC stand for?
Enteroaggregative e.coli.
What does DAEC stand for?
Diffusely adherent e.coli.
What is the leading cause of diarrhoeal illness in young children?
Rotavirus.
There is a vaccine - rotarix.
Name a helminth responsible for causing diarrhoeal infection.
Schistosomiasis.
Give 5 symptoms of helminth infection.
- Fever.
- Eosinophilia.
- Diarrhoea.
- Cough.
- Wheeze.
Briefly describe the reproductive cycle of schistosomiasis.
- Fluke matures in blood vessels and reproduces sexually in human host.
- Eggs expelled in faeces and enter water source.
- Asexual reproduction in an intermediate host.
- Larvae expelled and penetrate back into human host.
Why is c.diff highly infectious?
It is a spore forming bacteria.
Gram positive
Give 5 risk factors for c.diff infection.
- Increasing age.
- Co-morbidities.
- Antibiotic use.
- PPI.
- Long hospital stays.
Describe the treatment for c.diff infection.
Metronidazole and vancomyocin (PO).
Name 5 antibiotics prone to causing c.diff infection.
- Ciprofloxacin.
- Co-amoxiclav.
- Clindamycin.
- Cephlasporins.
- Carbapenems.
RULE OF C’s!
What can helicobacter pylori infection cause?
H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.
Describe h.pylori.
A gram negative bacilli with a flagellum.
Describe the treatment for H.pylori infection.
Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromyocin and amoxicillin.
Who is most likely to be affected by diverticular disease?
Older patients and those with low fibre diets.
Describe the pathophysiology of diverticulitis.
Out-pouching of bowel mucosa -> faeces can get trapped here and obstruct the diverticula -> abscess and inflammation -> diverticulitis.
What part of the bowel is most likely to be affected by diverticulitis?
The descending colon.
What is acute diverticulitis?
A sudden attack of swelling in the diverticula. Can be due to surgical causes.
Describe the signs of acute diverticulitis.
Similar to the signs of appendicitis but on the left side e.g. pain in the left iliac fossa region, fever, tachycardia.
Name the 3 broad categories that describe the causes of intestinal obstruction.
- Blockage.
- Contraction.
- Pressure.
Intestinal obstruction: give 3 causes of blockage.
- Tumour.
- Diaphragm disease.
- Gallstones in ileum (rare).
Intestinal obstruction: what is thought to cause diaphragm disease?
NSAIDS.
Intestinal obstruction: give 3 causes of contraction.
- Inflammation.
- Intramural tumours.
- Hirschprung’s disease.
Describe how Crohn’s disease can cause intestinal obstruction.
Crohn’s disease -> fibrosis -> contraction -> obstruction.
Describe how Diverticular disease can cause intestinal obstruction.
Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.
What is Hirschprung’s disease?
A congenital condition where there is a lack of nerves in the bowel and so motility is affected. This leads to obstruction and gross dilatation of the bowel.
Intestinal obstruction: give 3 causes of pressure.
- Adhesions.
- Volvulus.
- Peritoneal tumour.
Intestinal obstruction: what are adhesions?
Adhesions often form secondary to abdominal surgery. Loops of bowel stick together and the bowel is pulled and distorted. 40% of intestinal obstructions are due to adhesions.
Intestinal obstruction: what causes adhesions?
Adhesions often form secondary to abdominal surgery.
Intestinal obstruction: what is volvulus?
Volvulus is a twist/rotation in the bowel; closed loop obstruction. There is a risk of necrosis.
Intestinal obstruction: which areas of the bowel are most likely to be affected by volvulus?
Volvulus occurs in free floating areas of the bowel e.g. bowel with mesentery. The sigmoid colon has a long mesentery and so can twist on itself.
Give 4 common causes of small bowel obstruction in adults.
- Adhesions.
- Hernias.
- Crohn’s disease.
- Malignancy.
Which is more common: small bowel obstruction or large bowel obstruction?
Small bowel obstruction is more common; it makes up 75% of intestinal obstruction.
Give 3 common causes of small bowel obstruction in children.
- Appendicitis.
- Volvulus.
- Intussusception.
Intestinal obstruction: what is intussusception?
Intussusception is when part of the intestine invaginates into another section of the intestine -> telescoping. It is caused by force in-balances.
Define hernia.
The abnormal protrusion of an organ into a body cavity it doesn’t normally belong.
What are the risks of hernia’s if left untreated?
They can become strangulated and you may not be able to return them into their correct body cavity - irreducible.
Give 2 symptoms of hernia.
- Pain.
2. Palpable lump.
Give 5 symptoms of small bowel obstruction.
- Vomiting.
- Pain.
- Constipation.
- Distension.
- Tenderness.
Would dilatation, distension and increased secretions be seen proximal or distal to an intestinal obstruction?
Proximal.
Give 4 signs of small bowel obstruction.
- Vital signs e.g. increased HR, hypotension, raised temperature.
- Tenderness and swelling.
- Resonance.
- Bowel sounds.
What investigations might you do in someone who you suspect to have a small bowel obstruction?
- Take a good history - ask about previous surgery (adhesions)!
- FBC, U+E, lactate.
- X-ray.
- CT, ultrasound, MRI.
What is the management/treatment for small bowel obstruction?
- Fluid resuscitation.
- Bowel decompression.
- Analgesia and anti-emetics.
- Antibiotics.
- Surgery e.g. laparotomy, bypass segment, resection.
Give 2 common causes of large bowel obstruction.
- Colorectal malignancy.
2. Volvulus (especially in the developing world).
Give 5 symptoms of large bowel obstruction.
- Tenesmus.
- Constipation.
- Abdominal discomfort.
- Bloating.
- Vomiting.
- Weight loss.
What investigations might you do in someone who you suspect to have a large bowel obstruction?
- Digital rectal examination.
- Sigmoidoscopy.
- Plain X-ray.
- CT scan.
Describe the management for a large bowel obstruction.
- Fast the patient.
- Supplement O2.
- IV fluids to replace losses and correct electrolyte imbalance.
- Urinary catheterisation to monitor urine output.
Give 3 consequences of untreated intestinal obstructions.
- Ischaemia.
- Necrosis.
- Perforation.
Describe the progression from normal epithelium to colorectal cancer.
- Normal epithelium.
- Adenoma.
- Colorectal adenocarcinoma.
- Metastatic colorectal adenocarcinoma.
Define adenocarcinoma.
A malignant tumour of glandular epithelium.
What is familial adenomatous polyposis?
Familial adenomatous polyposis is a genetic condition where you develop thousands of polyps in your teens.
Describe the pathophysiology of familial adenomatous polyposis.
There is a mutation in apc protein and so the apc/GSK complex isn’t formed -> beta catenin levels increase -> up-regulation of adenomatous gene transcription.
Describe the pathophysiology of HNPCC.
There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.
How can adenoma formation be prevented?
NSAIDS are believed to prevent adenoma formation.
What is the treatment for adenoma?
Endoscopic resection.
What is the treatment for colorectal adenocarcinoma?
Surgical resection can be done when there is no spread. Remember to balance risks v benefits. The patient has a pre-op assessment.
What is the treatment for metastatic colorectal adenocarcinoma?
Chemotherapy and palliative care.
Give 3 reasons why bowel cancer survival has increased over recent years.
- Introduction of the bowel cancer screening programme.
- Colonoscopic techniques.
- Improvements in treatment options.
Give 5 risk factors for colorectal cancer.
- Low fibre diet.
- Diet high in red meat.
- Alcohol.
- Smoking.
- A PMH of adenoma or ulcerative colitis.
- A family history of colorectal cancer; FAP or HNPCC.
What can affect the clinical presentation of a colorectal cancer?
How close the cancer is to the rectum affects its clinical presentation.
Give 3 signs of rectal cancer.
- PR bleeding.
- Mucus.
- Thin stools.
- Tenesmus.
Give 2 signs of a left sided/sigmoid cancer.
- Change of bowel habit e.g. diarrhoea, constipation.
2. PR bleeding.
Give 3 signs of a right sided cancer.
- Anaemia.
- Mass.
- Diarrhoea that doesn’t settle.
Describe the emergency presentation of a left sided colon cancer.
The LHS of the colon is narrow and so the patient is likely to present with signs of obstruction e.g. constipation; colicky abdominal pain; abdominal distension; vomiting.
Describe the emergency presentation of a right sided colon cancer.
The RHS of the colon is wide and so the patient is likely to present with signs of perforation.
What investigations might you do in someone who you suspect might have colorectal cancer?
Colonoscopy = gold standard!
It permits biopsy and removal of small polyps.
- Tumour markers are good for monitoring progress.
- Faecal occult blood is used in screening but not diagnosis.
Give 5 non-infective causes of diarrhoea.
- Neoplasm.
- Inflammatory.
- Irritable bowel.
- Anatomical.
- Chemical.
- Hormonal.
- Radiation.
Give 3 infective causes of dysentery.
- Shigella.
- Salmonella.
- Campylobacter.
- E.coli 0157.
Give 2 infective causes of non-bloody diarrhoea.
- Rotavirus.
2. Norovirus.
Describe the chain of infection.
Reservoir -> agent -> transmission -> host -> person to person spread.
Give 3 ways in which infection can be transmitted.
- Direct e.g. faeco-oral.
- Indirect e.g. vectorborne (malaria).
- Airborne e.g. respiratory route.
What is the treatment for vibrio cholerae infection?
HYDRATE e.g. ORS. What goes out must be replaced.
Describe the management of c.diff infection.
- Control antibiotic use.
- Infection control measures.
- Isolate the case.
- Case finding.
- Test stool samples for toxin.
Give 4 groups at risk of diarrhoeal infection.
- Food handlers.
- Health care workers.
- Children who attend nursery.
- Persons of doubtful personal hygiene.
Give 3 causes of peptic ulcers.
- Prolonged NSAID use -> decreased mucin production.
- H.pylori infection.
- Hyper-acidity.
Give 3 symptoms of peptic ulcers.
Often acute onset of symptoms:
- Pain.
- Bleeding.
- Perforation.
What investigations might you do in someone who you suspect to have peptic ulcers?
- H.pylori test e.g. urease breath test and faecal antigen test.
- Gastroscopy.
- Barium meal.
Give 3 treatments for peptic ulcers.
- Stop NSAIDS.
- PPI’s e.g. omeprazole.
- H.pylori eradication.
Give 2 potential complications of oesophago-gastroduodenoscopy (OGD).
- Cardiopulmonary.
2. Small risk of bleeding or perforation.
Give 3 indications for OGD.
- Dyspepsia.
- Dysphagia.
- Anaemia.
- Suspected coeliac disease.
Give 3 indications for colonoscopy.
- Altered bowel habit.
- Diarrhoea +/- dysentery.
- Anaemia.
Give 3 symptoms of GORD.
- Heart burn.
- Acid reflux.
- Dysphagia.
Describe the pathophysiology of coeliac disease.
Gliadin (product of gluten digestion) = immunogenic. It can have direct toxic effects by up-regulating the innate immune system or HLADQ2 can present it to T helper cells in the lamina propria -> inflammation -> villi atrophy -> malabsorption.
Give 5 symptoms of coeliac disease.
- Diarrhoea.
- Weight loss.
- Irritable bowel.
- Iron deficiency anaemia.
- Mouth ulcers.
- Abnormal liver function.
What investigations might you do in someone who you suspect to have coeliac disease?
- Serology - look for auto-antibodies - TTG and EMA.
2. Gastroscopy - duodenal biopsies.
What part of the bowel is commonly affected by Crohn’s disease?
Can affect anywhere from the mouth to anus.
What part of the bowel is commonly affected by ulcerative colitis?
It only affects the rectum. It spreads proximally but only affects the colon.
Give 5 complications of Crohn’s disease.
- Malabsorption.
- Fistula.
- Obstruction.
- Perforation.
- Anal fissures.
- Neoplasia.
- Amyloidosis (rare).
Give 5 complications of ulcerative colitis.
- Colon: blood loss and colorectal cancer.
- Arthritis.
- Iritis and episcleritis.
- Fatty liver and primary sclerosing cholangitis.
- Erythema nodosum.
Give an example of a functional bowel disorder.
IBS.
Describe the multi-factorial pathophysiology of IBS.
The following factors can all contribute to IBS:
- Psychological morbidity e.g. trauma in early life.
- Abnormal gut motility.
- Genetics.
- Altered gut signalling (visceral hypersensitivity).
Give 3 symptoms of IBS.
- ABDOMINAL PAIN!
- Pain is relieved on defecation.
- Bloating.
- Change in bowel habit.
- Mucus.
- Fatigue.
Give an example of a differential diagnosis for IBS.
- Coeliac disease.
- Lactose intolerance.
- Bile acid malabsorption.
- IBD.
- Colorectal cancer.
What investigations might you do in someone who you suspect has IBS?
- Bloods - FBC, U+E, LFT.
- CRP.
- Coeliac serology.
Describe the treatment for mild IBS.
Education, reassurance, dietary modification e.g. FODMAP.
Describe the treatment for moderate IBS.
Pharmacotherapy and psychological treatments:
- Antispasmodics for pain.
- Laxatives for constipation.
- Anti-motility agents for diarrhoea.
- CBT and hypnotherapy.
Describe the treatment for severe IBS.
MDT approach, referral to specialist pain treatment centres.
- Tri-cyclic anti-depressants.
Why are all gastric ulcers re-scoped 6-8 weeks after treatment?
All peptic ulcers are re-scoped to ensure they’ve healed. If they haven’t healed it could be a sign of malignancy.
What is the criteria for dyspepsia?
> 1 of the following:
- Postprandial fullness.
- Early satiation.
- Epigastric pain/burning.
Give 5 causes of dyspepsia.
- Excess acid.
- Prolonged NSAIDS.
- Large volume meals.
- Obesity.
- Smoking/alcohol.
- Pregnancy.
Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.
- Unexplained weight loss.
- Anaemia.
- Dysphagia.
- Upper abdominal mass.
- Persistent vomiting.
What investigations might you do in someone with dyspepsia?
- Endoscopy.
- Gastroscopy.
- Barium swallow.
- Capsule endoscopy.
What is the management for dyspepsia if the red flag criteria has been met?
- Suspend NSAID use and review medication.
- Endoscopy.
- Refer malignancy to specialist.
What is the management for dyspepsia without red flag symptoms?
- Review medication.
- Lifestyle advice.
- Full dose PPI for 1 month.
- Test and treat h.pylori infection.
What kind of lifestyle advice might you give to someone with dyspepsia?
- Lose weight.
- Stop smoking.
- Cut down alcohol.
- Dietary modification.
Describe the treatment for GORD.
- PPI.
- Lifestyle modification.
- Anti-reflux surgery.
Give a potential consequence of anterior ulcer haemorrhage.
Acute peritonitis.
Give a potential consequence of posterior ulcer haemorrhage.
Pancreatitis.
Name 5 things that can break down the mucin layer in the stomach and cause gastritis.
- Not enough blood - mucosal ischaemia.
- H.pylori.
- Aspirin, NSAIDS.
- Increased acid - stress.
- Bile reflux - direct irritant.
- Alcohol.
Describe the treatment for gastritis.
- Reduced mucosal ischaemia.
- PPI.
- H2RA.
- Enteric coated aspirin.
Give 5 broad causes of malabsorption.
- Defective intra-luminal digestion.
- Insufficient absorptive area.
- Lack of digestive enzymes.
- Defective epithelial transport.
- Lymphatic obstruction.
Malabsorption: what can cause defective intra-luminal digestion?
- Pancreatic insufficiency due to pancreatitis, CF. There is a lack of digestive enzymes.
- Defective bile secretion due to biliary obstruction or ileal resection.
- Bacterial overgrowth.
Why can pancreatitis cause malabsorption?
Pancreatitis results in pancreatic insufficiency and so a lack of pancreatic digestive enzymes. There is defective intra-luminal digestion which leads to malabsorption.
Malabsorption: what can cause insufficient absorptive area?
- Coeliac disease.
- Crohn’s disease.
- Extensive parasitisation.
- Small intestine resection.
Malabsorption: give an example of when there is a lack of digestive enzymes.
Lactose intolerance - disaccharide enzyme deficiency.
Malabsorption: what can cause lymphatic obstruction?
- Lymphoma.
2. TB.
Describe the distribution of inflammation seen in Crohn’s disease.
Patchy, granulomatous, transmural inflammation (can affect just the mucosa or go through the bowel wall).
Describe the distribution of inflammation seen in ulcerative colitis.
Continuous inflammation affecting only the mucosa.
Histologically, what part of the bowel wall is affected in ulcerative colitis?
Just the mucosa.
Histologically, what part of the bowel wall is affected in crohn’s disease?
Can affect just the mucosa or can go all the way through to the bowel wall -> transmural inflammation.
What is the treatment for crohn’s disease and ulcerative colitis?
Anti-inflammatories.
Name the break down product of gluten that can trigger coeliac disease.
Gliadin.
What part of the small intestine is mainly affected by coeliac disease?
Duodenum.
What disorders might be associated with coeliac disease?
Other autoimmune disorders:
- T1 diabetes.
- Thyroxoicosis.
- Hypothyroidism.
- Addisons disease.
Osteoporosis is also commonly seen in people with coeliac disease.
What is the prevalence of coeliac disease?
1%.
What cells normally line the oesophagus?
Stratified squamous non-keratinising cells.
What is Barrett’s oesophagus?
When squamous cells undergo metaplastic changes and become columnar cells.
What can cause Barrett’s oesophagus?
- GORD.
2. Obesity.
Give a potential consequence of Barrett’s oesophagus.
Adenocarcinoma.
Describe how Barrett’s oesophagus can lead to oesophageal adenocarcinoma.
- GORD damages normal oesophageal squamous cells.
- Glandular columnar epithelial cells replace squamous cells (metaplasia).
- Continuing reflux leads to dysplastic oesophageal glandular epithelium.
- Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
Give 5 symptoms of oesophageal carcinoma.
- Dysphagia.
- Odynophagia (painful swallowing).
People often present very late. - Vomiting.
- Weight loss.
- Anaemia.
- GI bleed.
- Reflux.
Give 3 causes of squamous cell carcinoma.
- Smoking.
- Alcohol.
- Poor diet.
What can cause oesophageal adenocarcinoma?
Barrett’s oesophagus.
Give 3 causes of gastric cancer.
- Smoked foods.
- Pickles.
- H.pylori infection.
- Pernicious anaemia.
Describe how gastric cancer can develop from normal gastric mucosa.
Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.
Give 3 causes of oesophageal carcinoma.
- GORD -> Barrett’s.
- Smoking.
- Alcohol.
What investigations might you do in someone who you suspect to have oesophageal carcinoma?
- Barium swallow.
2. Endoscopy.
Describe the 2 treatment options for oesophageal cancer.
- Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
- Medically unfit and metastases = palliative care. Stents can help with dysphagia.
Give 3 signs of gastric cancer.
- Weight loss.
- Anaemia.
- Vomiting blood.
- Melaena.
- Dyspepsia.
A mutation in what gene can cause familial diffuse gastric cancer?
CDH1 - 80% chance of gastric cancer.
Prophylactic gastrectomy is done in these patients.
What investigations might you do in someone who you suspect has gastric cancer?
- Endoscopy.
- CT.
- Laparoscopy.
What is the advantage of doing a laparoscopy in someone with gastric cancer?
It can detect metastatic disease that may not be detected on ultrasound/endoscopy.
What is the treatment for proximal gastric cancers that have no spread?
3 cycles of chemo and then a full gastrectomy. Lymph node removal too.
What is the treatment for distal gastric cancers that have no spread?
3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.
What vitamin supplement will a patient need following gastrectomy?
They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.
Where in the colon do the majority of colon cancers occur?
In the descending/sigmoid colon and rectum.
Why do proximal colon cancers have a worse prognosis?
They have fewer signs and so people often present with them at a very advanced and late stage.
What 3 histological features are needed in order to make a diagnosis of coeliac disease?
- Raised intraepithelial lymphocytes.
- Crypt hyperplasia.
- Villous atrophy.
What would be raised in the blood tests taken from someone with primary biliary cirrhosis?
- Raised IgM.
- Raised ALP.
- Positive AMA.
Name 4 fat soluble vitamins.
A, D, E and K.
Why might someone with primary biliary cirrhosis experience itching as a symptom?
Because there is a build up of bilirubin.
Are most liver cancers primary or secondary?
Secondary - they have metastasised to the liver from the GI tract, breast and bronchus.
Where have most secondary liver cancers arisen from?
- The Gi tract.
- Breast.
- Bronchus.
Describe the aetiology of HCC.
Most HCC is in patients with cirrhosis. This is often due to HBV/HCV and alcohol.
Give 5 symptoms of HCC.
- Weight loss.
- Anorexia.
- Fever.
- Malaise.
- Ascites.
What investigations might you do on someone who you suspect has HCC?
- Bloods: serum AFP may be raised.
- US or CT to identify lesions.
- MRI.
- Biopsy if diagnostic doubt.
Describe the treatment for HCC.
- Surgical resection of solitary tumours.
- Liver transplant.
- Percutaneous ablation.
How long after infection with hepatitis B virus is HBsAg present in the serum for?
HBsAg will be present in the serum from 6 weeks - 3 months after infection.
How long after infection with hepatitis B virus is anti-HBV core (IgM) present in the serum for?
Anti-HBV core (IgM) slowly rises from 6 weeks after infection and its serum level peaks at about 4 months.
Name 3 diseases that lead to heamolytic anaemia and so a raised unconjugated bilirubin and pre-hepatic jaundice.
Causes of haemolytic anaemia:
- Sickle cell disease.
- Hereditary spherocytosis/elliptocytosis.
- GP6D deficiency.
- Hypersplenism.
How would you know if an individual had been vaccinated against hepatitis B?
They would have anti-HBVs IgG in their serum.
What type of anaemia do you associate with alcoholic liver disease?
Macrocytic anaemia.
Name a protozoa that can cause amoebic liver abscess?
Entemoeba histolytica.
What are the symptoms of entemoeba histolytica?
- RUQ pain.
- Bloody diarrhoea.
- Fever and malaise.
Often the patient has a history of foreign/rural travel.
What is the treatment for entemoeba histolytica?
Metronidazole.
What is the treatment for mild/moderate UC?
Mesalazine.
A 4-year-old girl presents with diarrhoea and is hypotensive. What is the physiological reason that fluid moves from the interstitium to the vascular compartment in this case?
Reduced hydrostatic pressure.
Fluid will move from the interstitium into the plasma if there is an increase in osmotic pressure or a decrease in hydrostatic pressure. As this patient is hypotensive it is more likely to be the latter.
What is a potential consequence of h.pylori infection in a person with decreased gastric acid?
Gastric cancer.
What is a potential consequence of h.pylori infection in a person with increased gastric acid?
Duodenal ulcer.
Give 2 indications for the need of immediate surgical intervention in someone with a small bowel obstruction.
- Signs of perforation (peritonitis).
2. Signs of strangulation.
Where is folate absorbed?
In the jejunum.
Where is vitamin B12 absorbed?
In the terminal ileum.
Where is iron absorbed?
In the duodenum.
In someone with coeliac disease, what are they most likely to be deficient in - iron, folate, or B12?
Iron.
Coeliac disease mainly affects the duodenum and iron is absorbed in the duodenum. Folate is absorbed in the jejunum and B12 in the terminal ileum.
Give 5 histological features of a malignant neoplasm.
- High mitotic activity.
- Rapid growth.
- Border irregularity.
- Necrosis.
- Poor resemblance to normal tissues.
What lymph nodes can oesophageal carcinoma commonly metastasise to?
Para-oesophageal lymph nodes.
What hormone is responsible for the production of gastric acid?
Gastrin.
A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.
Hypoalbuminaemia.
List 5 important questions a GP should ask when taking a history to establish a cause of diarrhoea.
- Blood or mucus in the stools.
- Family history of bowel problems?
- Abdominal pain.
- Recent foreign travel history.
- Bloating.
- Weight loss.
List two blood tests a GP might perform to help differentiate between the different causes of diarrhoea.
- FBC.
2. ESR/CRP.
List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.
- Stool culture.
2. Faecal calprotectin.
State one histological feature that will be seen in ulcerative colitis.
- Crypt abscess.
2. Increase in plasma cells in the lamina propria.
What investigations might you do in someone with inflammatory bowel disease?
- Bloods - FBC, ESR, CRP.
- Faecal calprotectin - shows inflammation but is not specific for IBD.
- Flexible sigmoidoscopy.
- Colonoscopy.
What 2 products does haem break down in to?
Haem -> Fe2+ and biliverdin.
What enzyme converts biliverdin to unconjugated bilirubin?
Biliverdin reductase.
What is the function of glucuronosyltransferase?
It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.
What protein does unconjugated bilirubin bind to and why?
Albumin.
It isn’t H2O soluble therefore it binds to albumin so it can travel in the blood to the liver.
What does conjugated bilirubin form?
Urobilinogen.
What is responsible for the conversion of conjugated bilirubin into urobilinogen?
Intestinal bacteria.
What can urobilinogen form?
- It can go back to the liver via the enterohepatic system.
- It can go to the kidneys forming urinary urobilin.
- It can form stercobilin which is excreted in the faeces.
What disease could be caused by a non-functioning mutation in NOD2?
Crohn’s.
