Abdomen Flashcards
Abdominal pain (differentials)
RUQ - biliary colic, cholecystitis, ascending cholangitis, acute hepatitis
Epigastric - gastritis, perforated peptic ulcer, cholecystitis, pancreatitis, AMI (referred)
LUQ - splenic rupture, LL pneumonia
Hypochondrium - renal colic, pyelonephritis, testicular torsion
Umbilical - SBO, gastroenteritis, early appendicitis, ruptured AA, mesenteric ischaemia.
RIF - appendicitis, Crohn disease, Meckel diverticulitis, mesenteric adenitis, ovarian torsion, ruptured R) ectopic pregnancy
Suprapubic - large bowel obstruction, cystitis, PID
LIF - diverticulitis, ruptured L) ectopic pregnancy
Jaundice (differentials)
Probability diagnosis - hepatitis A/B/C, cholelithiasis, alcoholic hepatitis/cirrhosis
Serious diagnoses - malignancy (pancreas, biliary tract, hepatocellular), severe infections (sepsis, ascending cholangitis), rarities (Wilson)
Pitfalls - Gilbert, cardiac failure, primary biliary cirrhosis, haemochromatosis, CMV/EBV
Key points for assessment and management of hepatitis C
Key steps
1. Confirm current hepatitis infection (viral RNA)
2. Ascertain whether patient is treatment naive or has previously been treated but not cured
3. Assess for presence of cirrhosis
4. Consider if the patient has hepatitis B or HIV co-infection
5. Review medications for potential drug interactions with direct-acting antiviral drugs
6. Consider pregnancy
7. Consider whether the patient has decompensated liver disease
How to test for hepatitis C
Perform hepatitis C antibody testing
Follow up with HCV RNA
● Genotyping is not required for treatment but is funded by MBS
● Useful if there is reinfection or if there is a change in genotype
Acute liver failure (definition, differentials, evaluation)
Characterised by: liver tests more than 10 times the upper limit of normal, hepatic encephalopathy, and a prolonged prothrombin time. Note: Marked elevation without liver failure may indicate underlying chronic liver disease. Differentials: ● Paracetamol toxicity ● Acute viral hepatitis ● Alcoholic hepatitis ● Autoimmune hepatitis ● Wilson disease ● Ischaemic hepatitis ● Budd-Chiari syndrome ● HELLP syndrome ● Malignant infiltration ● Toxin exposure ● Sepsis ● Heat stroke ● Muscle disorders Evaluation: ● Paracetamol level ● Toxicology screen ● Acute viral hepatitis serologies ● Autoimmune markers (ANA, anti-smooth muscle antibodies, anti-liver/kidney microsomal antibodies type 1, IgG) ● Transabdominal ultrasonography
Coeliac disease (screening, diagnosis)
Screening
Antibody screening:
● First line - IgA, anti-tissue transglutaminase, anti-deamidated gliadin antibody.
● Reserved for those on gluten-free diet - HLA DQ2 or DQ8.
Micronutrient deficiencies: iron, B12, folate, vitamin D
Diagnosis
Gold standard: Confirmed on duodenal biopsy (blunting of villi)
Deranged LFTs - evaluation (history, examination)
History
Aim is to screen for risk factors:
● ETOH
● Medications
● Viral hepatitis
● Occupational or recreational exposure to hepatotoxins (e.g. mushroom picking)
● Associated medical conditions (e.g. RHF, diabetes mellitus, arthritis, obesity, pregnancy, IBD etc.)
Examination
● Temporal and proximal muscle wasting
● Stigmata of liver disease (spider naevi, palmar erythema, gynaecomastia, and caput medusae).
● Ascites or encephalopathy (decompensated cirrhosis)
● Dupuytren’s contractures, testicular atrophy (advanced cirrhosis)
● Abdominal examination:
○ Hepatomegaly
○ Splenomegaly
○ Ascites
Abnormal bilirubin - unconjugated vs. conjugated
Unconjugated
- Overproduction (haemolysis, significant bruising, polycythaemia)
- Impaired uptake (breastfeeding, ileus, sepsis, congested heart failure)
- Impaired conjugation (Gilbert, breastmilk jaundice)
Conjugated
- Intrahepatic process (obstruction, cystic fibrosis, total parenteral nutrition)
- Extrahepatic obstruction (cholelithiasis, primary sclerosing cholangitis, primary biliary cirrhosis)
- Hepatocellular injury (infection, Wilson, ETOH, autoimmune hepatitis)
Deranged LFTs - patterns
Hepatocellular
- Disproportionate elevation of aminotransferases compared to ALP
- Serum bilirubin may be elevated
- Test of synthetic function may be abnormal
Cholestatic
- Disproportionate elevation of ALP compared to aminotransferases
- Serum bilirubin may be elevated
- Test of synthetic function may be abnormal
Isolated hyperbilirubinaemia
- Nil other derangement apart from bilirubin
** Refer to page 117 of GP Study Notes
Deranged LFTs - mild to moderate causes
Less than 15x upper limit of normal. Associated with CLD, and mild hepatic insults. Differentials: ● Medication use ● Chronic viral hepatitis ● Alcoholic liver disease ● Haemochromatosis ● NAFLD ● Autoimmune hepatitis ● Wilson disease ● Alpha-1 antitrypsin deficiency ● Thyroid disorders ● Coeliac disease ● Anorexia nervosa
Deranged LFTs - cholestasis causes
Intrahepatic
- Drug toxicity
- PBC
- Primary sclerosing cholangitis
- Viral hepatitis
- Cholestasis of pregnancy
- Benign postoperative cholestasis
- Infiltrative disease
- Total parenteral nutrition
Extrahepatic
- Choledocholithiasis
- Malignant obstruction
- Primary sclerosing cholangitis with an extrahepatic bile
duct stricture
- Chronic pancreatitis with stricturing of the distal bile
duct
Deranged LFTs - when to refer
● Unexplained, persistent liver test elevations
● Patients who are being considered for a liver biopsy
40M with lethargy. Denies ETOH. O/E Abdo normal. Taking paracetamol 4-6 hourly for L) knee pain. LFT: ALT and AST 10x upper limit, ALP and GGT above 100.
Differentials
Initial investigations
Differentials ● Paracetamol overdose/poisoning ● Nonalcoholic steatohepatitis ● Haemochromatosis ● Viral hepatitis ● Autoimmune hepatitis ● Wilson’s disease ● Alpha-1 antitrypsin deficiency
Initial investigations : Liver ultrasound, hepatitis B serology, hepatitis C serology, iron studies, paracetamol level
Food protein-induced allergic proctocolitis (trigger, diagnosis, examination, treatment)
Characterised by: inflammation of the distal colon.
Trigger: commonly cow’s milk protein. Occasionally so or other foods.
Diagnosis: clinical. Confirmed after resolution of symptoms upon withdrawal of presumed food antigen.
Examination: anal fissures in otherwise health baby.
Treatment: Empiric. Complete elimination of cow’s milk or suspected antigen from diet. If breast-feeding, the mother
must eliminate it from her diet.
H.pylori (key point, test of cure)
Key point
● For uncomplicated duodenal ulcer disease, eradication therapy is usually all that is required
● If complicated, PPI for 8 weeks is appropriate
Test of cure: Urea breath test.
● At least 4 weeks after triple therapy
● PPI should be withheld for at least 1 week prior
57M, lawyer, presenting with bouts of nausea with bloating sensations and sense of fullness in the upper abdomen.
Pain worse after meals and usually resolves with OTC antacids. Heavy smoker. Stressed about work and has been
taking aspirin for a headache.
- Apart for H.pylori infection and peptic ulcer, what other differentials would you consider?
- Patient has small duodenal ulcer due to H. Pylori infection. What are five aspects of his management?
Apart for H.pylori infection and peptic ulcer, what other differentials would you consider? ● Gastro-oesophageal reflux disease ● Aspirin-induced gastritis ● Functional dyspepsia ● Gastric cancer ● Oesophagitis ● Oesophageal cancer ● Myocardial ischaemia
Patient has small duodenal ulcer due to H. Pylori infection. What are five aspects of his management?
- Esomeprazole 20 mg + clarithromycin 500 mg + amoxicillin 1 g BD for a week
- Repeat urea breath test 4 weeks after treatment
- Not to use aspirin for headache
- Stop smoking
- Avoid triggering food
- Stress management
