Gastro Flashcards
What is acute cholecystitis?
inflammation of the gallbladder caused by a blockage of the cystic duct
usually caused by gallstones
What causes cholecystitis? What are the risk factors?
usually a gallstone in the neck of the gallbladder or the cystic duct
rarely can be acalculous where the gallbladder isn’t being stimulated by food to regularly empty, resulting in a build-up of pressure
How does cholecystitis present?
right upper quadrant pain which may radiate to the right shoulder
- may have fever, nausea, vomiting, tachycardia and tachypnoea, right upper quadrant tenderness, murphy’s sign, raised inflammatory markers and WBCs
Investigation for suspected cholecystitis?
- FBC, LFTs, blood cultures, amylase
- abdominal US
- look for thickened gallbladder wall, stones in gb or fluid around gb
- MRCP to visualise biliary tree
How is cholecystitis managed?
- nil by mouth
- IV fluids
- antibiotics
- NG tube if required for vomiting
- ERCP if stone in common bile duct
- Cholecystectomy is definitive management
Complications of cholecystitis
- sepsis
- gallbladder empyema
- gangrenous gallbladder
- perforation
Risk factors for gallstones
female fat fair forty fertile
Main causes of acute cholangitis
- gallstone in the bile duct
- infection after an ERCP
Which organisms cause acute cholangitis?
- Escherichia coli
- Klebsiella species
- Enterococcus species
How does acute cholangitis present?
Charcot’s triad of RUQ pain, fever and jaundice
How is acute cholangitis managed?
- nil by mouth
- IV fluids
- blood cultures
- IV antibiotics
- abdominal US
- ERCP to remove stone
- Percutaneous transhepatic cholangiogram if ERCP isn’t suitable/failed
What is haemochromatosis?
- iron storage disorder that results in excessive total body iron and deposition of iron in tissues
What causes haemochromatosis?
- human haemochromatosis gene on chromosome 6
- mutation of this gene
- autosomal recessive
Symptoms of haemochromatosis
- presents after age of 40
- later in females due to menstruation acting to regularly eliminate iron from the body
- chronic tiredness
- joint pain
- pigmentation
- hair loss
- erectile dysfunction
- amenorrhoea
- cognitive symptoms
How is haemochromatosis diagnosed?
- serum ferritin level should be high
- transferrin saturation (high means iron overload,, normal suggests inflammation or non-alcohol fatty liver disease)
- if high serum ferritin and transferrin saturation then do genetic testing to confirm haemochromatosis
Complications of haemochromatosis
- type 1 diabetes (iron affects pancreas function)
- liver cirrhosis
- iron deposits in pituitary and gonads lead to endocrine and sexual problems
- cardiomyopathy (deposits in heart)
- hepatocellular carcinoma
- hypothyroidism
- chondrocalcinosis/pseudogout
How is haemochromatosis managed?
- venesection
- monitoring serum ferritin
- avoid alcohol
- genetic counselling
- monitoring and treatment of complications
What causes appendicitis and what can it lead to?
- gut organisms invade the appendix wall after lumen obstruction
- can lead to oedema, ischaemic necrosis and perforation
Presenting symptoms of appendicitis
- periumbilical pain that moves to the right iliac fossa
- anorexia
- vomiting
- constipation
- diarrhoea
Signs of appendicitis on examination
- tachycardia
- fever
- lying still
- coughing hurts
- shallow breaths
- RIF: guarding, rebound and percussion tenderness
- Rovsing’s sign positive
- psoas sign (extension of hip)
- cope sign (flexion ad extension of the hip)
How is appendicitis diagnosed?
- based on clinical presentation and raised inflammatory markers
- CT to confirm, US in women to exclude ovarian and gynaecological pathology
- diagnostic laparoscopy if investigations are negative
Differentials of appendicitis
- ectopic pregnancy - do serum or urine hCG
2. ovarian cysts
How is appendicitis managed? What are the complications?
- appendicectomy
- bleeding, infection, pain, scars
- removal of a normal appendix
- anaesthetic risks
- venous thromboembolism
What is cholangiocarcinoma?
bile duct cancer
majority are adenocarcinomas
Risk factors for cholangiocarcinoma
- primary sclerosing cholangitis
- liver flukes (parasitic infection)
How does cholangiocarcinoma present?
- obstructive jaundice is key
- with pale stools, dark urine and pruritis
- could have weight loss, RUQ pain, palpable gallbladder, hepatomegaly
What is Courvoisier’s law?
palpable gallbladder with jaundice is unlikely to be gallstones
either cholangiocarcinoma or pancreatic cancer
Investigations for suspected cholangiocarcinoma
- based on imaging plus biopsy
- CT TAP to look for other cancers
- CA 19-9 is a tumour marker that is raised
- MRCP to view biliary tree
- ERCP to put a stent in and relieve the obstruction
How is cholangiocarcinoma treated?
- curative surgery in early cases combined with radiotherapy and chemotherapy
- palliative treatment may involve stents, surgery, chemo, radio, end of life care
What is pancreatitis?
inflammation of the pancreas
What are the possible causes of pancreatitis?
- gallstones
- alcohol
- post ERCP
I GET SMASHED
How does acute pancreatitis present?
- severe epigastric pain
- radiates to the back
- vomiting
- tenderness
- low-grade fever, tachycardia
- relieved by sitting forward
- anorexia
Signs of pancreatitis on examination
- epigastric tenderness
- fever
- shock
- decreased bowel sounds
- possibly cullen’s sign and grey-turners sign
Investigations for pancreatitis
- serum amylase and lipase
- high WCC
- U&Es
- high CRP
- LFTs
- ABG
- US to look at gallbladder and stones
- erect CXR to look for perforation or plerual effusion
What is the Glasgow score?
- severity of pancreatitis
- 0 or 1 is mild
- 2 is moderate
- 3 or more is severe
PANCREAS
PaO2 less than 8 Age over 55 Neutrophils over 15 Calcium less than 2 Urea over 16 Enzymes (high liver) Albumin less than 32 Sugar (glucose over 10)
How is acute pancreatitis managed?
- ABCDE
- IV fluids
- NG tube if vomiting
- catheter
- analgesia
- blood sugar control
- antibiotics but only if indicated
- ERCP for gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct
- necrosectomy if necrotic tissue
Complications of acute pancreatitis
- necrosis
- infection of necrotic area
- abscess formation
- chronic pancreatitis
What is diverticular disease?
Diverticulosis with symptoms (diverticulitis, inflammation and infection)
What are the risk factors for diverticular disease?
- increased age
- low fibre diets
- obesity
- NSAIDs
How is diverticular disease diagnosed?
- colonoscopy or CT scan
- if acute then erect chest x-ray
Signs of acute diverticulitis
- pain and tenderness in left iliac fossa
- fever
- diarrhoea
- nausea and vomiting
- rectal bleeding
- raised CRP and WCC
How should acute diverticulitis be treated?
- oral co-amoxiclav
- analgesia
- avoid NSAIDs
- take clear liquids until symptoms improve
- increased fibre
severe pain or complications: - NBM
- IV Abx
- IV fluids
- analgesia
- CT scans
- urgent surgery
What is liver cirrhosis?
result of chronic inflammation and damage to liver cells
when the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver
affects structure and blood flow of liver, causing increased resistance in vessels leading into the liver (portal hypertension)
4 common causes of liver cirrhosis
- alcoholic liver disease
- non-alcoholic liver disease
- hepatitis B
- hepatitis C
What are some rarer causes of liver cirrhosis
- autoimmune hepatitis
- primary biliary cirrhosis
- haemochromatosis
- Wilsons Disease
- alpha 1 antitrypsin deficiency
- CF
- drugs (amiodarone, methotrexate, sodium valproate)
Signs of cirrhosis
- jaundice
- hepatomegaly (can shrink as it becomes more cirrhotic)
- splenomegaly (portal hypertension)
- spider naevi
- palmar erythema
- gynaecomastia and testicular atrophy (reduced testosterone and raised oestrogen)
- bruising
- ascites
- caput medusae
- asterixis
Investigations of cirrhosis
- Liver biochemistry is often normal but in decompensated cirrhosis all the markers (ALT, AST, ALP, bilirubin)
- Albumin and PT time are good markers of ‘synthetic’ function of the liver, albumin level drops and PT time increases
- Hyponatraemia indicated fluid retention
- Urea and creatinine becomes deranged in hepatorenal syndrome
- Viral markers and autoantibodies to identify the cause
- Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma and can be checked every 6 months as a screening test in patients with cirrhosis along with US
- Enhanced liver fibrosis test is first-line for assessing fibrosis in non-alcoholic fatty liver disease
What is the enhanced liver fibrosis test?
- First line investigation for non-alcoholic fatty liver disease
- measures HA, PIIINP and TIMP-1 markers and makes a score
<7.7 = none to mild fibrosis
- 7 to 9.8 = moderate fibrosis
- 8 or above = severe fibrosis
Signs of cirrhosis on US
- nodularity of surface of liver
- ‘corkscrew’ appearance of the arteries with increased flow as they compensate for reduced portal flow
- enlarged portal vein with reduced flow
- ascites
- splenomegaly
Patients with cirrhosis should be screened for _______ every 6 months
hepatocellular carcinoma
What is a fibroscan?
checks elasticity of the liver to assess degree of cirrhosis
A fibroscan should be done every 2 years in patients with
- hepatitis C
- heavy drinkers (over 50 units or 35)
- alcoholic liver disease
- chronic hepatitis B
What is the Child-Pugh score?
for cirrhosis severity
- takes into account bilirubin, albumin, INR, ascites and encephalopathy
What is the MELD score?
used every 6 months for patients with compensated cirrhosis
- takes into account bilirubin, creatinine, INR and sodium to determine whether they need dialysis or liver transplant
How should cirrhosis be managed?
US and alpha-fetoprotein every 6 months for HCC
Endoscopy every 3 years without known varices
High protein, low sodium
MELD score every 6 months
Liver transplant consideration
Managing complications
What are some complications of cirrhosis? How should each complication be managed?
- Malnutrition due to increased use of muscle tissue as fuel and increased metabolism of proteins in the liver. Also leads to reduced ability to store glucose as glycogen and release it when required
- regular meals, low sodium diet (minimise fluid retention), high protein and high calorie, avoid alcohol - Portal hypertension and varices. Varices occur at gastro-oesophageal junction, ileocecal junction, rectum and anterior abdominal wall (caput medusae). Varices can bleed very quickly so that’s why they’re concerning.
- Propanolol reduces portal hypertension by acting as a non-selective beta blocker
- elastic ligation of varices
- injection of sclerosant
- Transjugular intra-hepatic portosystemic shunt allows blood to flow from portal vein to hepatic vein
- bleeding varices require vasopressin analogues (terlipressin), coagulopathy correction with vitamin K and FFP, broad spectrum antibiotics and possibly intubation.
- bleeding varices require urgent endoscopy, injection of sclerosant or elastic band ligation - Ascites is caused by portal hypertension causing liquid to leak out of capillaries. Reduction of blood pressure into the liver causes renin to be released which leads to aldosterone and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative ascites.
- low sodium diet, anti-aldosterone diuretics, prophylactic antibiotics - Spontaneous bacterial peritonitis is infection of the ascitic fluid and peritoneal lining
- fever, abdominal pain, deranged bloods, ileus, hypotension
- E.coli, klebisella, gram positive cocci
- ascitic culture and then antibiotics, usually IV cephalosporin such as cefotaxime - Hepatorenal syndrome is hypotension in kidney and activation of the renin-angiotensin system causing renal vasoconstriction, which combined with low circulating volume leads to starvation of blood to the kidney. Rapid kidney deterioration. Can be fatal within a week so give a liver transplant.
- Hepatic encephalopathy is build up of ammonia due to impaired metabolism in liver and also a lot of ammonia bypasses the liver altogether.
- laxatives to clear the ammonia, antibiotics, rifaximin, nutritional support
- acute reduced consciousness, confusion
- precipitated by constipation, electrolyte disturbance, infection, GI bleed, high protein diet, medications
What are the causes of an upper GI bleed?
- oesophageal varices
- Mallory-Weiss tear
- ulcers of stomach or duodenum
- cancers of the stomach or duodenum
How does an upper GI bleed present?
- haematemesis
- ‘coffee ground’ vomit
- melaena
- haemodynamic instability
- possibly epigastric pain and dyspepsia in peptic ulcers
- jaundice for ascites in liver disease with oesophageal varices
What is the Glasgow-Blatchford scale?
- risk of having an upper GI bleed
- over 0 = high risk
- drop in Hb, rise in urea, blood pressure, heart rate, melaena, syncopy
Why does urea rise in upper GI bleeds?
blood in GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea in then absorbed in the intestines
What is the Rockall score?
risk of re-bleeding and overall mortality in upper GI bleed patients post-endoscopy
- age, shock features, co-morbidities, cause of bleeding, endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels
How should an upper GI bleed be managed?
ABCDE
Bloods (FBC, U&Es,
Coagulation, LFTs, crossmatch 2 units)
Access (2 large bore cannula)
Transfuse (blood, platelets
and FFP if big haemorrhage, platelets for active bleeding and thrombocytopenia, prothrombin complex concentrate for patients taking warfarin)
Endoscopy within 24 hours
Drugs (stop anticoagulants and NSAIDs)
Terlipressin and prophylactic broad spectrum antibiotics if oesophageal varices are suspected (in chronic liver disease)
OGD to provide interventions that stop bleeding e.g. banding of varices or cauterisation of bleeding vessel
What are the typical features of all hernias?
- soft lump protruding from the abdominal wall
- lump may be reducible
- may protrude on coughing
- aching, pulling or dragging sensation
What are the 3 complications of hernias
- Incarceration: when the hernia cannot be reduced back. Bowel is trapped back in the herniated position. This can lead to obstruction and strangulation.
- Obstruction is where a hernia causes a blockage in the passage of faeces through the bowel. Presents with vomiting, generalised abdominal pain and absolute constipation.
- Strangulation is where a hernia non-reducible and the base of the hernia becomes so tight that is cuts off the blood supply causing ischaemia. Significant pain and tenderness. Surgical emergency.
What is Richter’s hernia?
- specific situation that can occur in any abdominal hernia
- where only part of the bowel wall and lumen herniate, other side of that section remains within the peritoneal cavity
- can become strangulated
What is Maydl’s hernia?
- specific situation where two different loops of bowel are contained within the hernia
What are the general principles of management for hernias?
- Conservative management: leave it alone. Suitable when the hernia has a wide neck and in patients with co-morbidities
- Tension-free repair: place a mesh over the defect in the abdominal wall. Mesh is sutured to the muscles and tissues on either side of the defect.
- Tension repair: surgical operation to suture the muscles and tissue on either side of the defect back together. Rarely performed and have been largely replaced by tension-free repair.
How to differentiate indirect and direct inguinal hernias
When you reduce an indirect inguinal hernia and then place pressure on the deep inguinal ring, the hernia will remain reduced.
What is Hasselbach’s triangle?
- rectus abdominis muscle (medial)
- inferior epigastric vessels (superior and lateral)
- inguinal ligament (inferior)
Where do femoral hernias occur?
- through the femoral canal, which is below the inguinal ligament, at the top of the thigh
- femoral vein laterally
- lacunar ligament medially
- inguinal ligament anteriorly
- pectineal ligament posteriorly
What are incisional hernias?
occur at site of incision from previous surgery
- due to weakness where muscles and tissues were closed after a surgical incision
- bigger the incision, the greater the risk
Umbilical hernias are common in ______ and _______
neonates and older adults
What is a Spigelian hernia?
- occurs between lateral border of rectus abdominis muscle and the linea semilunaris
- this is the site of the spigelian fascia which is an aponeurosis between the muscles of the abdominal wall
- US used to help establish the diagnosis
What are diastasis recti?
- widening of the linea alba, the connective tissue that separates the rectus abdominis muscle.
Who is commonly affected by obturator hernias?
older women, especially after multiple vaginal deliveries
- often asymptomatic but may present with irritation to the obturator nerve, causing pain in the groin or medial thigh
What is a hiatus hernia, what are the different types and how are they treated? What are the symptoms and complications?
- stomach up through the diaphragm
- Type 1 = sliding
- Type 2 = rolling
- Type 3 = rolling and sliding
- Type 4 = large opening with additional organs entering the thorax
- increasing age, obesity and pregnancy
- heartburn, acid reflux, reflux of food, burping, bloating, halitosis
- CXR, CT scan, endoscopy, barium swallow test
- conservative
- surgical by laparoscopic fundoplication
What is volvulus?
conditions where the bowel twists around itself and the mesentery that it is attached to
- leads to a closed-loop obstruction where a section of bowel is isolated by obstruction on either side
- can lead to bowel ischaemia, leading to necrosis and bowel perforation
What are the 2 main types of volvulus? Who’s affected by them?
sigmoid = older patients caecal = younger
Risk factors for volvulus
- neuropsychiatric disorders (e.g. parkinson’s)
- nursing home residents
- chronic constipation
- high fibre diet
- pregnancy
- adhesions
Presentations of volvulus
- similar to bowel obstruction
- green bilious vomiting
- abdominal distention
- diffuse abdominal pain
- absolute constipation and lack of flatulence
How is volvulus diagnosed?
- abdominal x-ray shows coffee bean sign
- contrast CT to confirm and look for other pathology
How is volvulus managed?
- NBM, NG tube, IV fluids
- Conservative management = for sigmoid volvulus without peritonitis, flexible sigmoidoscope is inserted to correct the volvulus
surgical = laparotomy, hartmann’s procedure(remove rectosigmoid colon and form a colostomy), ileocecal resection or right hemicolectomy for caecal volvulus
What is hepatitis and what are the different types?
- inflammation of the liver
- can be chronic low level inflammation to acute and severe inflammation leading to large areas of necrosis and liver failure
- alcoholic, non-alcoholic, viral, autoimmune, drug induced
Presentation of hepatitis
- can be asymptomatic or could present with non-specific symptoms
- abdominal pain
- fatigue
- pruritus
- muscle and joint aches
- nausea and vomiting
- jaundice
- fever (viral hepatitis)
Typical biochemical findings of hepatitis
deranged LFTs, high AST and ALT with proportionally less of a rise in ALP, possible rise in bilirubin due to inflammation
Tell me about hepatitis A
- most common viral cause
- rare in UK
- RNA virus
- faecal-oral route
- Causes cholestasis with dark urine and pale stools and moderately hepatomegaly
- resolves with treatment in 1-3 months
- treated with analgesia
Tell me about hepatitis B
- DNA virus
- spreads via direct contact or blood/bodily fluids
- can also spread via pregnancy and delivery
- most recover within 2 months but 10% become carriers
What viral markers do we look for in viral hepatitis?
- when screening for hep B, test HBcAb (for previous infection) and HBsAg (for active infection)
- If these are positive then do further testing for HBeAGg (viral replication and high infectivity) and viral load
- HBsAb demonstrates an immune response to HBsAg so need to test for other viral markers to distinguish between previous infection or vaccination
- HBcAb helps to distinguish between acute, chronic or past infection. We can measure IgM and IgG versions. IgM implies active infection and will give higher titre in acute infection and lower in chronic infection. IgG indicates a past infection where HBsAg is negative
- HBeAg helps see how infective it is and high much it’s replicating
Describe the hep B vaccination
- hepatitis B surface antigen is injected
- vaccinated patients are tested for HBsAb to confirm the response
- vaccine requires 3 doses at different intervals
How is viral hepatitis managed?
- low threshold for screening at risk patients
- screen for other blood born viruses and STIs
- refer to gastro, hepatology or infectious diseases
- notify public health
- stop smoking and alcohol
- education
- test for complication
- fibroscan for cirrhosis and US for HCC
- antiviral medication
- liver transplant in end-stage liver disease
What is hepatitis C, how is it tested for and how is it managed?
- RNA virus
- spread by blood and bodily fluids
- no vaccine but antiviral meds are available
- 3 in 4 become chronic
- can cause cirrhosis and HCC
- hep c antibody screened for
- RNA testing to confirm diagnosis
- treatment same as hep B
What is hepatitis D?
- RNA virus
- only survives in patients with hep B infection
- attaches itself to the HBsAg to survive.
What is hepatitis E?
RNA virus
faecal oral route
- usually cleared within a month and no treatment
What are the 2 types of autoimmune hepatitis?
type 1 in adults (usually women in late 40s or 50s)
type 2 in kids (teenage or early twenties, acute raised transaminases and jaundice)
Which antibodies are associated with autoimmune hepatitis?
Type 1: ANA, anti-actin, anti-SLA/LP
Type 2: anti-LKM1, anti-LC1
How is autoimmune hepatitis treated?
- prednisolone and azathioprine
What is coeliac disease?
- exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel, usually develops in early childhood but can start at any age
How does coeliac present? In what other conditions do we always test for coeliac?
- failure to thrive
- diarrhoea
- weight loss
- mouth ulcers
- anaemia
- dermatitis herpertiformis
- rarely: peripheral neuropathy, cerebella ataxia, epilepsy
- always test for coeliac in new diagnosis of T1DM
Which genes are associated with coeliac?
HLA-DQ2
HLA-DQ8
Which auto-antibodies are associated with coeliac?
- anti-TTG tissue transglutaminase)
- anti-EMA (endomysial)
- anti-DGP
Why do you test for IgA deficiency in coeliac?
Anti-TTG and anti-EMA are IgA
So if you have IgA deficiency you might miss coeliac disease
In this case test for IgG versions or just do an endoscopy with biopsy
How is coeliac disease diagnosed?
- investigate when they’re still eating gluten
- check total IgA
- check for anti-TTG and anti-EMA
- endoscopy and intestinal biopsy show crypt hypertrophy and villous atrophy
What are the associated conditions of coeliac?
T1D Thyroid disease Autoimmune hepatitis Primary biliary cirrhosis Primary sclerosing cholangitis
Complications of untreated coeliac disease
- vitamin deficiency
- anaemia
- osteoporosis
- ulcerative jejunitis
- lymphoma of the intestine
- non-Hodgkin lymphoma
- small bowel adenocarcinoma
What are the differences between Crohn’s and UC?
- Crohn’s - no blood or mucus, entire GI tract, skip lesions, terminal ileum most affected, transmural inflammation, smoking is a risk factor, associated with weight loss, strictures and fistulas
- UC - continuous inflammation, limited to colon and rectum, only superficial mucosa affected, smoking is protective, excrete blood and mucus, use aminosalicylates, primary sclerosing cholangitis
How does inflammatory bowel disease present?
- diarrhoea, abdominal pain, passing blood, weight loss
How should you test for inflammatory bowel disease?
- routine bloods for anaemia, infection, thyroid, kidney and liver function
- CRP raised
- faecal calprotectin is a useful screening test (sensitive and specific to IBD)
- endoscopy with biopsy is diagnostic
- imaging with CT and MRI to look for fistulas, abscesses and strictures
How should Crohn’s be managed?
First-line to induce remission: steroids (oral prednisolone or IV hydrocortisone)
To induce remission: If steroids alone don’t work then consider adding an immunosuppressant: azathioprine, mercaptopurine, methotrexate, infliximab, adalimumab
To maintain remission:
First-line = azathioprine or mercaptopurine
Alternatives = methotrexate, infliximab, adalimumab
Surgery:
When the disease only affects the distal ileum it’s possible to resect this area and prevent further disease
Also used to treat strictures and fistulas caused by Crohn’s
How should UC be managed?
- To induce remission in moderate disease:
- First-line = aminosalicylate (e.g.mesalazine oral or rectal)
- Second-line = corticosteroids (e.g. prednisolone)
- To induce remission in severe disease:
- Fist-line = IV corticosteroids (e.g. hydrocortisone)
- Second line = IV ciclosporin
- Maintaining remission
- aminosalicylate
- azathioprine
- mercaptopurine - Surgery
- panproctocolectomy with permanent ileostomy or ileo-anal anstomosis (J-pouch)(removal of rectum and colon)
What is third spacing?
- when you have a bowel obstruction
- GI tract keeps secreting fluids that would normally be reabsorbed in the colon
- but if the fluid can’t be reabsorbed due to an obstruction then you get hypovolaemia and shock
What are the 3 big causes of bowel obstruction?
- adhesions (90% of small bowel)
- hernias (small bowel)
- malignancy (large bowel)
What are some less common causes of bowel obstruction?
volvulus (large bowel)
diverticular disease
strictures (secondary to crohn’s)
intussusception (young kids aged 6 months to 2 years)
What are adhesions of the bowel and what causes them?
- pieces of scar tissue that bind the abdominal contents together
- cause kinking or squeezing of the bowel
- usually in small bowel rather than large bowel
- abdominal or pelvic surgery
- peritonitis
- abdominal or pelvic infections
- endometriosis
What are closed-loop obstructions?
- two points of obstructions along the bowel meaning that there is a middle section sandwiched between two points of obstruction
What can cause closed-loop bowel obstruction
- adhesions that compress two areas of bowel
- hernias that isolate a section of bowel blocking either end
- volvulus
- single point of obstruction in the large bowel with an ileocecal valve that is competent
What do we mean by a competent ileocecal valve?
- a valve that doesn’t allow any movement back into the ileum from the caecum
How does a bowel obstruction present?
- green bilious vomiting
- abdominal distention
- diffuse abdominal pain
- absolute constipation and lack of flatulence
- tinkling bowel sounds may be heard early on
What are the normal limits for bowel diameter?
3cm for small bowel
6cm for colon
9cm for caecum
How should bowel obstructions be managed?
- ABCDE approach - hypovolaemic shock, bowel ischaemia, bowel perforation, sepsis
- Bloods - electrolyte imbalance, metabolic alkalosis (due to vomiting), bowel ischaemia (raised lactate)
- NBM, IV fluids, NG tube with free drainage to allow stomach contents to freely drain and reduce the risk of vomiting and aspiration
- Abdominal x ray
- erect CXR to look for air under the diaphragm
- Contrast abdominal CT scan to confirm the diagnosis
What surgical options are there for bowel obstruction?
- Conservative = stable patients with obstruction secondary to adhesions of volvulus
- Laparoscopy or laparotomy - explorative, adhesiolysis, hernia repair, emergency resection of obstructing tumour, stents
What is ileus?
- condition affecting the small bowel, where the normal peristalsis that pushes the contents along the length of the intestines, temporarily stops
- may also be known as paralytic or adynamic ileus
What is a pseudo-obstruction?
functional obstruction of the large bowel where the patients present with intestinal obstruction, but no mechanical cause is found
What are some common causes of ileus?
- injury to the bowel
- handling of the bowel during surgery
- inflammation or infection in, or nearby the bowel (peritonitis, appendicitis, pancreatitis, pneumonia)
- electrolyte imbalance (hypokalaemia, hyponatraemia)
Signs and symptoms of ileus?
- green bilious vomiting
- abdominal distension
- diffuse abdominal pain
- absolute constipation and lack of flatulence
- absent bowel sounds
How should ileus be managed?
- usually resolves with treatment of underlying cause
- supportive care
- NBM
- NG tube if vomiting
- IV fluids
- mobilisation
- total parenteral nutrition may be required while waiting for bowel to regain function
What is irritable bowel syndrome?
no identifiable cause of abnormal functioning of a normal bowel
Symptoms of irritable bowel syndrome
- diarrhoea
- constipation
- fluctuating bowel habit
- abdominal pain
- bloating
- worse after eating
- improved by opening bowels
Criteria for diagnosis of IBS
- normal FBC, ESR, CRP
- faecal calprotectin negative
- negative coeliac serology
- cancer not suspected or excluded
Symptoms should suggest: abdominal pain/discomfort which is relieved on opening bowels OR associated with a change in bowel habit AND 2 of: abnormal stool passage, bloating, worse symptoms after eating, PR mucus
How should IBS be treated?
- adequate fluid intake
- regular small meals
- reduced processed foods
- limit caffeine or alcohol
- trial of probiotic supplements for 4 weeks
- Medication
- First-line = loperamide for diarrhoea
- Laxatives for constipation
- Avoid lactulose as it can cause bloating
- Use linaclotide as a specialist laxative for IBS if not responding to first-line laxative
- Antispasmodics for cramps (buscopan)
- Second-line = tricylic antidepressants (amitriptyline)
- Third-line = SSRIs antidepressants
- CBT for psychological help to reduce distress
What is infectious mononucleosis?
- condition caused by infection with the EBV
- aka glandular fever
- virus is found in saliva of infected individuals
- spread by kissing, sharing cups, toothbrushes and other equipment that transmits saliva
How doe infectious mononucleosis respond to amoxicillin?
- intensely itchy maculopapular rash in response to amoxicillin or cefalosporins
What are the key features of infectious mononucleosis?
- fever
- sore throat
- fatigue
- lymphadenopathy
- tonsillar enlargement
- splenomegaly
What types of antibody does the body produce in infectious mononucleosis?
- heterophile antibodies
- takes up to 6 weeks for them to be produced
How do we test for heterophile antibodies? Comment on the specificity and sensitivity
- Monospot test = introduce RBCs from horses, heterophile antibodies will react to those horse cells
- Paul_bunnell test = uses sheep RBCs
- 100% specific for infectious mononucelosis but only 70-80% sensitive as it takes up to 6 weeks for the antibodies to be produced
What are some specific antibody tests for EBV antibodies? What do EBV antibodies target?
- these antibodies target viral capsid antigen
- IgM antibody rises early and suggests acute infection
- IgG antibody persists after the condition and suggests immunity
How should infectious mononucleosis be managed?
- lasts around 2-3 weeks but can leave you fatigued for several months
- avoid alcohol
- avoid contact sports
What are the complications of infectious mononucleosis?
- splenic rupture
- glomerulonephritis
- haemolytic anaemia
- thrombocytopenia
- chronic fatigue
- associated with Burkitt’s lymphoma
What are haemorrhoids?
enlarged anal vascular cushions
Haemorrhoids are more common in:
pregnancy, obesity, increased age, increased abdominal pressure
Why do haemorrhoids occur in pregnancy?
due to constipation, pressure from the baby in the pelvis and the effects of hormones that relax the connective tissues
What are anal cushions?
- specialised submucosal tissue that contain connections between the arteries and veins
- supported by smooth muscle and connective tissue
- help control anal continence, along with the internal and external sphincters
Where do the enlarged anal cushions usually form in haemorrhoids?
3,7 and 11 o’clock
How can we classify haemorrhoids?
- depends on size and whether they prolapse from the anus
- 1st degree = no prolapse
- 2nd degree = prolapse when straining and return on relaxing
- 3rd degree = prolapse when straining, do not return on relaxing but can be pushed back
- 4th degree = prolapsed permanently
What are the symptoms of haemorrhoids?
- often associated with constipation and straining
- may be asymptomatic
- painless, bright red bleeding, typically on the toilet tissue or seen after opening the bowels
- blood is not mixes with the stool
- sore, itchy anus, feeling a lump around or inside the anus
How should you examine for haemorrhoids?
- External haemorrhoids are visible in inspection as swellings
- Internal haemorrhoids may be felt on a PR exam
- Prolapse may appear if te patient is asked to bear down
- Proctoscopy is used for proper visualisation
How should haemorrhoids be managed?
- rule out anal fissures, diverticulosis, IBD and colorectal cancer
- consider testing for anaemia if there is prolonged bleeding or clinical signs of anaemia
- topical treatments for symptomatic relief and to help reduce swelling: anusol to shrink it or anusol HC (with hydrocortisone), germoloids cream (local anaesthetic), proctosedyl ointment (short term only steroid)
- constipation treated with more fibre, good fluid intake, using laxatives, avoid straining
- rubber band ligation to cut off blood supply to haemorrhoid
- injection sclerotherapy to cause sclerosis and atrophy
- infra-red coagulation to damage the blood supply
- bipolar diathermy
- surgery = haemorrhoidal artery ligation, haemorrhoidectomy, stapled haemorrhoidectomy
What causes thrombosed haemorrhoids?
- caused by strangulation at the base of the haemorrhoid resulting in thrombosis
- can be very painful
- appear as purplish, very tender, swollen lumps around the anus
- PR exam too painful
- resolve in time but can take several weeks
- may benefit from surgical management
What are the causes of peritonitis?
- Localised = appendicitis, cholecystitis, diverticulitis, salpingitis
- Primary generalised peritonitis = bacterial infection of peritoneal cavity without an obvious source, could be via haematogenous or lymphatic spread
Risk factors are ascites and nephrotic syndrome
- Secondary generalised peritonitis = bacterial translocation from a localised focus or non-bacterial due to a spillage of bowel contents, bile and blood
Presenting symptoms of peritonitis
- sharp, continuous, localised pain
- worse on movement and coughing
- symptoms may be vague in those with liver disease and ascites due to confusion caused by encephalopathy
Signs of peritonitis on examination
- check vital signs and look for signs of dehydration or compromised perfusion
- Localised = tenderness, guarding, rebound tenderness
- Generalised = very unwell, lie still, shallow breathing, rigid abdomen, tenderness reduced bowel sounds
Management for peritonitis
- Localised = depends on cause, some causes may require surgery, some causes treated with antibiotics
- Generalised = risk of death from sepsis or shock, fluids, antibiotics, catheter, NG tube, central venous line, laparotomy to remove infected or necrotic tissue, treat cause
What are the possible liver issues caused by excessive alcohol intake?
- Alcoholic fatty liver disease
- Alcoholic hepatitis
- Chronic cirrhosis
Main presenting symptoms of alcoholic hepatitis
- may remain asymptomatic and undetected
- nausea
- malaise
- epigastric pain
- right hypochondrial pain
- low-grade fever
- possibly jaundice, abdominal discomfort or swelling, swollen ankles, GI bleeding
- same signs on examination as hepatitis
How should alcoholic hepatitis be managed?
- thiamine
- vitamin C
- monitor urine output
- treat encephalopathy with oral lactulose or phosphate enemas
- diuretics for ascites
Where does GI perforation usually occur?
- Large bowel: diverticulitis, colorectal cancer, appendicitis, volvulus, UC
- Gastroduodenal: perforated duodenal or gastric ulcer, gastric cancer
- Small bowel: small bowel trauma or infection, Crohn’s
- Oesophagus: Boerhaave’s
- NSAIDs, steroids, bisphosphonates
Presenting symptoms of GI perforation
- Large bowel = peritonitic abdominal pain, rule out ruptured AAA
- Gastroduodenal = sudden epigastric pain which becomes generalised
- Oesophageal = severe pain following vomiting
How should GI perforation be managed?
- resuscitation
- Large bowel = resection of section (hartmann’s)
- Gastroduodenal = laparotomy to close perforation with omental patch
What is GORD?
- inflammation of the oesophagus caused by reflux of gastric acid and/or bile
What causes GORD?
- disruption of mechanisms to prevent reflux
- issue with lower oesophageal sphincter, angle of junction, mucosa or intra-abdominal portion of oesophagus
Presenting symptoms of GORD
- heartburn
- worse on lying down, bending, large meals, alcohol
- relieved by antacids
- waterbrash
- dysphagia if peptic stricture forms
Investigations for GORD
- clinical diagnosis
- upper GI endoscopy to exclude malignancy or confirm oesophagitis
- barium swallow to detect a hiatus hernia, peptic stricture
How should GORD be managed?
- weight loss
- elevate the bed
- avoid provoking factors
- stop smoking
- lower fat meals
- antacids
- H2 antagonists
- PPIs
- annual endoscopy to check for Barrett’s
What is infectious colitis, what causes it? What are the presenting symptoms? Investigations?
- inflammation of the colon due to bacteria, parasites or viruses
- lack of sanitation, drinking contaminated water, antibiotic use
- diarrhoea, blood and mucus in the stools, lower abdominal pain, malaise, low-grade fever
- diagnosis is clinical, stool culture may help
Where are anal fissures?
90% are posterior
- anterior tends to occur after childbirth
What causes anal fissures?
hard faeces
rare causes = syphillis, herpes, trauma, crohn’s, anal cancer, psoriasis
Presenting symptoms of anal fissure
- tearing pain when passing faeces
- little bit of blood on paper perhaps
- anal itching
How should anal fissures be treated?
- high fibre diet, soften the stools (laxatives), hydration
- lidocaine ointment, GTN ointment, dilitiazem (relax sphincter)
- lateral sphincterotomy to rleax sphincter and promote healing (given if intolerant or non-responsive to medication)
What is liver failure?
severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy
How is liver failure classified?
- Hyper-acute = less than 7 days
- Acute = 1-4 weeks
- Subacute = 4-12 weeks
- Acute-on-chronic in those with chronic liver disease
What are the causes of liver failure?
- Viral = hepatitis A,B,C,D and E
- Drugs = paracetamol overdose
- Less common = autoimmune, budd-chiari, pregnancy related, malignancy, haemochromatosis, mushroom poisoning, wilson’s disease
What causes the jaundice, encephalopathy and coagulopathy in liver failure?
- Jaundice = decreased secretion of conjugated bilirubin
- Encephalopathy = failure to excrete ammonia properly
- Coagulopathy = reduced synthesis of clotting factors, reduced platelets
Presenting symptoms of liver failure and signs on examination
- fever
- nausea
- jaundice (not always)
- jaundice
- encephalopathy
- asterixis
- fetor hepaticus
- ascites ad splenomegaly
- bruising or bleeding
Investigations for liver failure
- Identify the cause: viral serology, paracetamol levels, autoantibodies, ferritin
- Bloods: FBC, U&Es, Glucose, LFTs, CRP, coagulation screen, group and save
- Liver US/CT
- Ascitic tap - neutrophils over 250/mm^3 = spontaneous bacterial peritonitis
Management plan for liver failure
- ABCDE
- N-acetylcysteine for paracetamol overdose
- treat and prevent the complication
- treat any renal failure
- liver transplant
What is peptic ulcer disease?
ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin
- usually gastric and duodenal but can occur in the oesophagus and Meckel’s diverticulum
What causes peptic ulcer disease?
imbalance between the damaging action of acid and pepsin and the the mucosal protective mechanism
- common causes are helicobacter pylori and NSAIDs
- rarer causes is Zollinger-Ellison syndrome (gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas)
Presenting symptoms of peptic ulcer disease
epigastric pain relieved by antacids
- gastric ulcer pain is worse soon after eating
- duodenal ulcer pain is worse several hours after eating
Investigations for peptic ulcer disease
- Bloods -the usual plus IV secretin causes a rise in serum gastrin in ZE patients
- Endoscopy
- Rockall scoring if there’s a bleed
- Test for H.pylori
How can we test for H.pylori?
- C13 urea breath test - C13 is detected in expelled air
- Serology - IgG antibody against H.pylori confirms exposure to H.pylori
- Campylobacter-like organism test (CLO) - gastric biopsy placed with urea and a pH indicator, if H.pylori is present, ammonia is produced from the urea and colour change from yellow to red
How should we manage peptic ulcer disease?
- Acute - fluids if bleeding, close monitoring, endoscopy, surgical treatment
- Endoscopy - injection sclerotherapy, laser coagulation, electrocoagulation
- Surgery - if perforated or bleeding can’t be controlled
- H.pylori eradication - 2 antibiotics + PPI
- Stop NSAIDs
What causes anal abscesses and fistulae? What are the risk factors?
- bacterial infection
- fistulae are a complication of an abscess
- fistulae can also develop secondary to Crohn’s
- Crohn’s
- Diabetes
- malignancy
Presenting symptoms of anal abscess/fistulae?
- constant throbbing pain in the perineum
- intermittent discharge near the anal region
- personal or family history of IBD
Signs of anal abscesses on examination
- localised tender perineal mass
- small skin lesion near the anus
- thickened area over the abscess/fistula may be felt on DRE
How are anal abscesses and fistulae treated?
- surgery
- open drainage of abscess
- laying open of fistula or dye inserted into external opening to find internal opening
- Antibiotics
What is pernicious anaemia? How is it linked to vitamin B12?
- most common cause of vitamin B12 deficiency
- autoimmune condition which causes the immune system to attack the stomach lining meaning no intrinsic factor is produced
- we need intrinsic factor to absorb B12 in the terminal ileum
What are some causes of B12 deficiency?
- pernicious anaemia
- gastrectomy, atrophic gastritis
- malabsorption, ilieal resection, Crohn’s affecting the terminal ileum
- colchicine, metformin
Who is affected by vitamin B12 deficiency?
- peak = 60 years
- vegans have a higher risk of dietary vitamin B12 deficiency
Signs and symptoms of B12 deficiency
- fatigue
- lethargy
- dyspnoea
- faintness
- palpitations
- headache
- paraesthesia, numbness, cognitive changes, visual disturbances
- pallor
- glossitis, angular stomatitis, irritability, dementia, depression
How should B12 deficiency be investigated?
- no gold standard
- FBC and blood film show hyper-segmented neutrophils, oval macrocytes, circulating megaloblasts
- test for pernicious anaemia with anti-intrinsic factor antibodies, anti-parietal cell antibodies
What is the most common type of colorectal cancer and where would you find it?
- adenocarcinoma
- 60% rectum and sigmoid
- 30% descending colon
- 10% rest of colon
What are the risk factors for colorectal cancer?
- environmental and genetic
- sequence of genetic changes that go from normal bowel epithelium to cancer
- western diet
- colorectal polyps
- previous colorectal cancer
- family history
- IBD
Presenting symptoms of colorectal cancer
- left-sided colon and rectum = change in bowel habit, rectal bleeding (mixed with stool), tenesmus (due to SOL in rectum)
- Right-sided colon = presents later, anaemia symptoms, weight loss, non-specific malaise
20% of tumours will present as an emergency via large bowel obstruction or haemorrhage/peritonitis due to perforation
Investigations for colorectal cancer
- Bloods - FBC, LFTs, Tumour markers (CEA)
- Stools (Faecal occult blood test)
- Endoscopy - sigmoidoscopy, colonoscopy, used to biopsy the tumour
- Double-contrast barium enema shows apple core strictures
- Contrast CT for staging
What is the main type of gastric cancer?
adenocarcinoma
Risk factors for gastric cancer
- smoked and processed foods
- smoking
- alcohol
- H.pylori infection
- atrophic gastritis
- pernicious anaemia
- partial gastrectomy
- gastric polyps
Presenting symptoms of gastric cancer
- often asymptomatic early
- early satiety
- epigastric discomfort
- weight loss, anorexia, nausea/vomiting
- dysphagia
Signs of gastric cancer on examination?
- epigastric mass
- abdominal tenderness
- ascites
- signs of anaemia
- Virchow’s Node
- sister mary joseph’s nodule
- krukenberg’s tumour
Investigations for gastric cancer
- endoscopy
- bloods
- CT/MRI
- endoscopic USS to assess depth of gastric invasion and lymph node involvement
Most common types of oesophageal cancer
- squamous cell carcinoma (developing)
- adenocarcinoma (western)
Causes of oesophageal cancer
Adeno = GORD + Barrett’s
Squamous cell = alcohol, tumour, achalasia, scleroderma, coeliac disease, nutritional deficiencies, dietary toxins
Presenting symptoms of oesophageal cancer
- often asymptomatic
- progressive dysphagia
- regurgitation
- cough
- voice hoarseness
- odynophagia
- weight loss
- fatigue
Investigations for oesophageal cancer
- endoscopy
- barium swallow and CXR
- staging CT
