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
