Abdominal pain- quizlet Flashcards
Mallory Weiss tear
A tear in the lower oesophageal mucosa
Often secondary to violent coughing or vomiting
Presents as severe vomiting, blood in vomit, retching, abdominal pain
Therapeutic endoscopy to inject with adrenaline
Peptic ulcer disease
A break or ulceration in the protective mucosal lining of the stomach or duodenum
Causes 35-50% of upper GI bleeds
Typically presents as epigastric/chest pain, heartburn, malaena, upper GI bleeding
Risk factors for peptic ulcers
> 65
H.pylori infection
High dose NSAIDS
Smoker
Alcohol consumption
Blood group O (duodenal)
Increased gastric emptying (duodenal)
Decreased gastric emptying (gastric)
Gastric ulcers
20% of ulcers
Peptic ulcers in the stomach mucosa typically due to medications/ H.pylori
Signs and symptoms of gastric ulcers
Epigastric pain
Pain is not relieved by food - it is made worse
Pain occurs 30m-1hr after food
May cause early satiety and weight loss
Not as common
More likely to get vomiting
More likely to be malignant than duodenal ulcers
Signs and symptoms of duodenal ulcers
Epigastric pain
Pain is relieved by food
Pain peaks 2-3 hours after a meal
Pain is more likely to wake a patient at night
95% are due to H.pylori
High reoccurrence rate
Vomiting is less common
Investigations into peptic ulcers
Lab tests for H.pylori- CLO can be done after endoscopy
Upper GI endoscopy
Management of peptic ulcer
No stigmata of haemorrhage:
- start a PPI for 4-8 weeks with repeat endoscopy after 6-8 weeks
- stop any NSAIDs / aspirin
- eradicate H.pylori if confirmed via antibiotics
- antacids (not long-term use)
Stigmata of haemorrhage:
- application of heat
- injection of ulcers
- clips
Perforated peptic ulcer
Creates free air
Air under the diaphragm causes pain in the left shoulder
Peritonism
Absent bowel sounds
Do a laparotomy to repair
Gastroesophageal varices
Abnormal, enlarged veins within the oesophagus
Develop when blood flow to the liver is blocked causing portal hypertension and pushing blood through smaller vessels which are weaker so become swollen/ leaky/ prone to rupture
Risk factors: Portal hypertensions, large varices, Liver failure/cirrhosis, chronic alcohol use
Symptoms of gastroesophageal varices
Lots of blood in the vomit
Malaena
Dizziness
Loss of conscious in severe cases
May also be signs of liver disease i.e. jaundice/itchy/skin.ascites
Treatment of gastroesophageal varices
Hypotensive drugs e.g. propranolol for prevention
IV Terlipressin 2mg
Endoscopy to tie elastic bands to stop the bleeding (band ligation)
Transjugular intrahepatic portosytemic shunt to direct blood away from the portal vein
Liver transplant
Prophylactic broad spectrum antibiotics reduce mortality
Indications for a transjugular intrahepatic portosystemic shunt
Secondary prophylaxis for gastroesophageal varices
Refractory ascites
Treating portal hypertension in Budd-Chiari syndrome
Can cause or worsen hepatic encephalopathy though
Heart failure is an absolute contraindication
Symptoms of oesophageal cancer
Dysphagia - progressive from solids to liquids
Odynophagia
Indigestion
Reflux
Nausea
Vomiting
Hoarse voice - in upper oesophageal cancer due to involvement of the recurrent laryngeal nerve
Weight loss
Risk factors for oesophageal cancer
Long term acid refflux
Obesity
Male gender
Age >40
Smoking
Alcohol use
Previous cancer
Diet high in fat and cholesterol
High intake of hot foods
Types of oesophageal cancer
Squamous cell carcinoma: most common worldwide, seen in the top two thirds of the oesophagus
Adenocarcinoma- lower third of the oesophagus, associated with obesity and GORD
Haemorrhoids
Varicosities in the lower rectum or anus
Associated with constipation / straining / pregnancy / obesity / raised intra-abdominal pressure
These may bleed
Haemorrhoids: symptoms and management
Get tenesmus, perianal itch, constipation, pain is very rare, bright red blood in the stool that is not mixed in
Manage with topical corticosteroids - rubber band ligation if prolapsing - haemorrhoidectomy if severe
Anal fissure
A small tear in the lining of the anus
Risk factors include IBD / constipation / pregnancy and childbirth
Pain on defecation
Red flag ESR level
50- cancer until proven otherwise
Management of acute upper GI bleeding
Stabilise the patient with the ABCDE approach
Insert 2 large bore IV cannula
Take FBC, UE, LFT, clotting, cross match
Give fluids if hypotensive
Catheterise
Correct clotting if needed / reverse anticoagulation with prothrombin complex (works quicker than vitamin K)
Risk stratification based on Rockall and Blatchford score
Endoscopic management in due course - within 24 hours
Rockall score
Score for upper GI bleeds after endoscopy
Estimates the risk of re-bleeding and mortality based on clinical presentation and endoscopy findings:
- signs of shock
- age
- co-morbidities
- diagnosis e.g. cause of bleeding
- visible stigmata of recent haemorrhage e.g. clots / visible bleeding vessels
Glasgow-Blatchford bleeding score
Stratifies high and low risk patients with upper GI bleeds at their initial presentation to help make a management plan
Used prior to endoscopy
0 = low chance of medical intervention requirement
>0 = high risk GI bleed likely to require medical intervention
Intervention may be transfusion / endoscopy / surgery
Features of the Glasgow-Blatchford bleeding score
Features:
- drop in Hb
- rise in urea (due to blood being broken down by digestive enzymes)
- bp
- hr
- melaena
- syncope
H.pylori: tests and antibiotics
Urea breath test: accuracy of >95%, preferred non invasive technique
Raid urease test: less accurate
Antibiotics: amoxicillin and either clarithromycin or metronidazole
Pathology of jaundice
Haemoglobin is broken down in to unconjugated bilirubin
This binds to albumin in the blood and is taken to the liver
In the liver it is taken up by hepatocytes
It is then conjugated with glucuronic acid to make it water soluble
The conjugated bilirubin is then excreted in bile in to the duodenum
Here is it metabolised by bacteria to form urobillinogen
Some urobillogen is excreted in faeces, some undergoes enterohepatic circulation
Jaundice occurs when this pathway is disrupted and the liver cant get rid of the bilirubin
Unconjugated hyperbilirubinaemia
Classification:
Pre-hepatic - due to increased bilirubin production
Hepatocellular - due to reduced hepatocyte uptake of bilirubin
Causes:
- haemolysis e.g. haemolytic anaemia or malaria
- Gilbert disease (conjugation disorder)
- drugs e.g. chloramphenicol, gentamicin
- physiology e.g. neonatal jaundice
Conjugated hyperbilirbunemia
Classification:
Hepatocellular - diminished ability to conjugate
Intrahepatic obstruction
Extrahepatic obstruction
Causes:
- hepatitis
- cirrhosis
- drugs e.g. halothane, paracetamol, MAOI
- Dublin-Johnson syndrome
- tumour
- gallstones
- alcohol
Post hepatic jaundice
Impaired excretion of conjugated bilirubin - leading to cholestasis
This makes the urine dark and the stools pale as less reaches the gut
Get pruritis
Causes:
- primary biliary cirrhosis
- primary sclerosing cholangitis
- bile duct gallstones
- drugs e.g. steroids / some antibiotics
- malignancy
Urine urobilinogen
Normally 1-4mg/day
Absence= biliary obstruction/hepatic disease
Increased levels: haemolytic disease
Hepatitis symptoms
Temperature
RUQ pain
Muscle and joint pain
Nausea and vomiting
Fatigue
Loss of appetite
Dark urine
Pale stools
Itchy skin
Jaundice
Hepatitis A
Faecal-oral route (Ends in a vowel, comes from the bowel)
RNA virus
Causes jaundice, N&V, fever
Resolves within months
Manage with basic analgesia
Most common hepatitis worldwide but rare in the UK - usually due to contaminated water or food
Notifiable disease
Hepatitis B
Blood borne / vertical transmission
DNA virus
Most common worldwide cause of chronic liver disease - likely to develop to cirrhosis and hepatocellular carcinoma
Vaccination is available in 3 doses - part of the 6 in 1
Hepatitis C
Blood borne
RNA virus
1 in 4 fight off the infection
3 in 4 becomes chronic - can lead to cirrhosis, liver failure and liver cancer
Screen with anti-HCV antibody
Treat with direct acting antivirals which cure the infection in 90% of patients
No vaccine is available
Hepatitis D
Blood borne
RNA virus
Can develop in to chronic hepatitis
Only affects people who have hepatitis B as it requires hep B for its replication
Can be prevented by hepatitis B immunisation
Hepatitis E
Faecal-oral
RNA
Very mild disease which improves within a month
No vaccination
Type 1 autoimmune hepatitis
In adults
- get anti-nuclear antibodies
- anti-smooth muscle antibodies
- anti-soluble liver antigen
- presents around / after the menopause with fatigue and features of liver disease
Type 2 autoimmune hepatitis
In children
- anti-liver kidney microsomes 1
- anti-liver cytosol antigen type 1
- presents in teens / early twenties with acute hepatitis with high transaminase and jaundice
Treat with prednisolone
Gilberts syndrome
Autosomal recessive non-haemolytic jaundice
Causes a deficiency in the bilirubin uridine diphosphate glucuronosyltransferase enzyme - therefore get decreased processing of bilirubin so hyperbilirubinemia
It is harmless
Tends to become apparent due to stressors e.g. illness, fasting, dehydration, mensturation, exercise, lack of sleep
Only complication is increased risk of gallstones
No treatment - fluctuations tend to resolve
Non alcoholic fatty liver disease
The development of a fatty liver resulting from excessive quantities of fats being deposited from causes that exclude alcohol
Most likely asymptomatic unless it develops to NASH
May get some mild fatigue and discomfort in the upper right abdomen
Causes: Obesity, Insulin resistance and type 2 diabetes, Hypercholesterolaemia, Metabolic syndrome
Non alcoholic steatohepatitis
The aggressive form of non alcoholic fatty liver disease which can develop in people with non alcoholic fatty liver disease
Symptoms include ascites, jaundice, weight loss, right upper quadrant pain, fatigue
Liver fibrosis
The excessive accumulation of extracellular matrix proteins e.g. collagen which causes the liver tissue to become scarred
This is the step before liver cirrhosis
Doesnt cause many symptoms but it does cause problems
Causes: NAFLD/NASH, Autoimmune hepatitis, Alcoholic liver disease, Biliary obstruction
Cirrhosis
Severe scarring of the liver which leads to non-reversible architectural damage
The liver is now severely damaged and cant function normally
This is when symptoms really start to show e.g. decreased appetite, weakness, fatigue, weight loss, nausea and vomiting, RUQ pain
Decompensated liver disease
An acute deterioration in liver function in a patient with known cirrhosis
The symptoms come on suddenly and are very bad:
- jaundice
- ascites
- hepatic encephalopathy
- hepatorenal syndrome
Occurs due to stressors in the life
Hepatic encephalopathy
Caused in liver damage due to accumulated toxin i.e. ammonia in the blood
Symptoms include confusion, personality/mood changes, poor concentration, tremor, seizures, slow movement, slurred speech
Can give laxatives to try get rid of ammonia
ALT, AST, ALP, GGT
ALT, AST: released in hepatocyte damage
ALP: released in liver pathology in response to cholestasis, marker of bile duct pathology
A raised ALP and GGT: indicative of a non-hepatobiliary pathology i.e. bone metastasis/fractures
GGT: raised in bile flow obstruction/bile duct damage
Bilirubin, albumin, PT time
Bilirubin- raised in liver damage, anaemia, cholestasis
Albumin- low in liver disease
PT- time it takes for blood to clot, raised in liver disease
Inhibitors of the p450 system
Antibiotics e.g. erythromycin / ciprofloxacin
Isoniazid
Omeprazole
Amiodarone
Allopurinol
SSRIs
Sodium valproate
Acute alcohol intake
Caution with these if a patient takes warfarin - will cause increased risk of bleeding - cause INR levels to be higher
Inducers of the p450 system
Antiepileptics
Barbiturates
Rifampicin
St joins wort
Chronic alcohol intake
Smoking
Cause INR levels to be lower
Cholangitis
Inflammation of the biliary tree
Caused by a stone blocking one of the ducts
Therefore bile flow is obstructed
This becomes. a medium for bacteria to grow - most commonly E.coli
Can also be caused by pancreatitis / tumour / clots
Can be autoimmune - anti-mitochondrial antibodies causing interlobular bile duct granulomatous destruction
Cholangitis: symptoms, investigations and treatment
Get Charcot’s triad:
- RUQ pain
- Fever
- Jaundice
Reynolds pentad- contains Charcot’s triad alongside confusion and signs of septic shock
May also get itchy skin / pale stool / dark urine
On bloods there will be raised ALP, raised GGT and raised bilirubin
USS should be done
MRCP
Treatment:
- fluids
- antibiotics
- biliary drainage
- ERCP
- assessment of the cause (if gallstones consider a cholecystectomy)
Coeliac disease
A T cell mediated autoimmune disease due to the immune system reacting to gluten (prolamin)
Can cause villus atrophy which is atrophy of the villi in the small intestine due to coeliac disease which can lead to severe malabsorption which includes anaemia
Symptoms of coeliac disease
Abdominal pain
Constipation
Diarrhoea
Weight loss
Fatigue
Nausea and vomiting
Bloating
Dermatitis herpetiformis
Steatorrhoea
Investigations into coeliac disease
Patients must be eating gluten before diagnosis for at least 6 weeks as negative results in the above will occur if they have cut it out
BEDSIDE: stool culture to exclude IBD and infection
BLOODS:
- FBC - may see IDA
- CRP
- first line measurement = anti-TTG- IgA i.e. tissue transglutamine antibodies
IMAGING:
- gold standard = endoscopy and biopsy of the duodenum/jejunal (will see villus atrophy, crypt hyperplasia, intra-epithelial lymphocytes)
- DEXA scan
- jejunal biopsies are of better quality
Associated with the HLA-DQ2 allele
Complications of coeliac disease
Macrocytic anaemia - either iron deficiency or B12 / folate
Osteoporosis
Lactose intolerance
Enteropathy associated T cell lymphoma - the more a patient eats gluten the higher the chance of developing this
Hyposplenism and therefore increased infection risk - seen by Howell-jolly bodies on film - these patients need annual influenza vaccine and pneumococcal booster every 5 years
Difference between MRCP and ERCP
ERCP- treatment and imaging
MRCP- imaging only
Coffee bean sign
Shows sigmoid volvulus
