Gastro (NEW) Flashcards
1
Q
Hep A overview
A
Epidemiology
- sporadic and epidemic
- vaccine available
Aetiology
- faecal oral transmission
- > contaminated food and water
Pathophys
-1 month incubation period
Clinical manifestations
- symptomatic in 70%
- initially
- > nausea/vomiting
- > anorexia/fever/malaise
- > abdo pain
- after days to a week
- > pale stools/dark urine/jaundice/pruritus
- > tender hepatomegaly/spenomegaly
- > rash/arthlagia
- jaundice peaks within two weeks
- recovery within 2-3 months
- > longer in cholestatic
- > relapses may occur
- > rarely fulminant
- > chronic/cancer does not occur
LFTS
- elevated transaminases
- > over 1000
- > peak 1 month after infection
- elevated bili
- elevated al phos
- elevated CRP
Serology
- anti-HAV IgM
- > appears with clinical features
- > lasts approx 3-6 months
- > represents acute
- anti-HAV IgG
- > appear early in convalescence
- > lasts decades
- > protective antibody
- > represents vaccinations/immunity
Treatment
- supportive
- infection prevention
- > infective during incubation/ 1 week after jaundice
2
Q
acute Hep B background
A
Epidemiology
- HBVsAg prevalence varies by region
- > low risk = <2%
- > high risk = >8%
Aetiology
- B’s
- > baby making (sexually transmitted)
- > babies (vertical/not breastfeeding)
- > blood (needles/transfusions/tattoo/piercing
- HCV/HDV coinfection/superinfection
- > suppresses HBV replication (lower transaminases)
- > fulminant hepatitis/cirrhosis/cancer more likely
Pathophys
- HBsAg
- > envelope protein/indicates viral load
- > first to appear
- > dissapears 1-2 months post icteral phase with appearance of anti-HBs
- Anti-HBs
- > protective antibody (prevents re-infection)
- IgM anti-HBc
- > appears early before anti-HBs
- > present during window phase
- > lasts approx 6 months/indicates acute infection
- IgG anti-HBc
- > appears after 6 months/indicates previous infection
- > IgG not present with vaccination
- HBeAg
- > nucleocapsid protein/same gene as core
- > secreted into circulation/HBcAg is not
- > reflects infectivity
- > appears early with HBsAg
- HBV DNA
- > indicates viral load and infectivity
- > more useful for prognosis than HBeAg
3
Q
Acute Hep B evaluation
A
Clinical manifestations
- 70% are asymptomatic
- rarely fulminant
- incubation of up to 4 months
- then serum-like sickness
- then constitutional symptoms
- > anorexia
- > nausea/vomiting
- > jaundice
- > RUQ pain
- recovery after 1-3 months
- > ongoing fibrosis after seroconversion
- > reactivation possible with immunosuppression
LFTs
- elevated transaminases
- > over 1000
- > normalises within by 6 months (otherwise chronic)
- raised bili
Serology
- HBsAg+
- > acute infection
- > reactivation of chronic
- > during HBeAg seroconversion
- > superinfection
- > hepatitis due to other cause in HB+ patient
- Also present initially
- > IgM anti-HBc
- > HBV DNA
- > HBeAg
- Window period
- > no HBsAg or anti HBsAg
- > more common in fulminant
- > only marker of infection = IgM anti HBcAg
4
Q
Chronic hep B background
A
Epidemiology
-more common in developing countries
Aetiology
- neonatal infections
- > 90%
- adult infections
- > 5%
Pathophys
- immune tolerance phase in neonatal infection
- > high HBV DNA
- > high HBeAg
- > low LFTs
- converts to immune active after 10-30 years
- > annual spontaneous resolution rate low
- immune active phase
- > ALT raised
- > decreased DNA
- > may have anti-HBc IgM
- > may have α fetoprotein elevation
- > possibly with symptoms
- seroconversion of HBeAg more common with immune activation
- > approx 15% overall
- inactive carrier phase
- > HBsAg+
- > no HBeAg
- > anti-HBeAg present
- > DNA may be undetectable as intrahepatacyte
- > LFTs low
- resolution
- > annual resolution rate approx 2%
- > anti-HBs present
- > risk of cirrhosis decreased but HCC remains
5
Q
Chronic hep B evaluation
A
Clinical manifestations
- often no hx of acute elicited
- generally asymptomatic
- > some fatigue
- > acute symptoms with exacerbations
- stigmata of chronic liver disease if cirrhotic
- extrahepatic manifestations
- > polarteritis nodosa
- > membranous GN
- > aplastic anaemia
- 5 year progression
- > chronic to cirrhosis in 15%
- > cirrhosis to HCC in 10%
LFTs
- aminotransferases moderately elevated
- > higher during exacerbation
Serology
- diagnosis
- > HBsAg >6 mnths
- > anti HBs Ag undetectable
- > anti HBc is IgG
- position in natural history determined by
- > HBsAg/anti HBsAg
- > HBeAg/anti HBeAg
- > HBV DNA
- > ALT
Cirrhosis
- FBC
- > thrombocytopaenia/leukopaenia
- Coags
- > prolonged INR/PT
- hypoalbuminaemia
- LFTs
- > hyperbilirubinaemia
- > transaminases may be relatively normal
Diagnosis
- HBsAg > 6 months
- anti-HBsAg undetectable
- anti-HBc is IgG
Monitor disease progression
- aminotransferases usually moderately elevated
- during exacerabtion
- > sig increase in aminotransferase
- > α fetoprotein elevated
- decompensated cirrhosis
- > decreased WCC and platelets
- > hypoalbuminaemia
- > prolonged prothrombin/INR
- > hyperbilirubinaemia
- position in natural history determined by
- > HBsAg/anti HBsAg
- > HBeAg/anti HBeAg
- > HBV DNA
- > ALT
6
Q
Peptic ulcer disease background
A
Epidemiology
- prevalence = approx 5%
- > increases with age
- h pylori = 30%
- > 20% get peptic ulcers
- > 2% get gastric cancer
Aetiology
- predominately
- > H pylori
- > NSAIDs
- occassionaly
- > zollinger ellison (gastrin secreting neuroendocrine)
- > bisphosphonates
Pathophys
- imbalance between protective/destructive forces
- > protective = bicarb rich mucin/epithelial tight junctions
- > destructive = HCL/pepsin/h pylori/bile acids
- duodenal ulcer
- > associated with gastric acid hypersecretion
- > impaired somatostatin secretion or ZE
- gastric ulcer
- > gastric secretion normal
- > h pylori inflammation degrades mucin/tight junctions
- NSAIDs
- > direct injury with hydrogen trapping
- > impair protection and repair through COX
- > promote bleeding through anti-platelet
Complications
- bleeding
- penetration
- perforation
- gastric outlet obstruction
- gastric adenocarcinoma
- > antral then diffuse atrophic gastritis
- > intestinal metaplasia
- > neoplasia
- MALT lymphoma
- > T and B cell aggregation/activation in lamina propria
- > forms follicle similar to Peyers patch
- > aberrant activation -> neoplasia
7
Q
Peptic ulcer evaluation
A
Clinical manifestations
- dyspepsia
- epigastric pain
- > may radiate to back
- nausea/vomiting
- > if immediately after food = ?gastric outlet obstruction
- diarrhoea
- > may indicate ZE
- epigastric tenderness
- > pointing sign
- severe disease
- > anaemia
- > haematemesis/malaena
- > shock
Endoscopy
- gold standard for diagnosis
- histology
- > diagnose h pylori
- > ddx neoplasia/gastric metaplasia/MALT lymphoma
- biopsy
- > rapid ureas test
Non invasive H pylori testing
- urea breath test/stool antigen
- > highly sensitive/specific
- > sensitivity decreased by PPI/bismuth/antibiotics
- > switch to H2 antagonist 2 weeks before testing
ZE testing
- indication
- > multiple/refractory ulcers
- > ulcers distal to duodenum
- > family hx
- fasting serum gastrin
- > cease PPI before test
8
Q
Peptic ulcer management
A
H pylori negative
- cease NSAIDs if possible
- > switch to COX2 inhibitor if possible
- > consider misoprostol 100-200mcg QD
- PPI treatment
- > esomeprazole 20mg BD once daily
- > continue for 4-8 weeks
- H2 antagonist
- > less effect/consider if resistant
- > famotidine 20mg BD
H pylori positive
- Cease NSAIDs
- Triple therapy (Antibiotics Cure Pylori) = 80% effective
- > amoxicillin 1g BD for 7 days
- > clarithromycin 500mg BD for 7 days
- > esomeprazole 20mg BD for 7 days
- metronidazole vs amoxicillin triple therapy
- > amoxicillin resistance extremely rare in Aus
- > metronidazole resistance approx 50% in Aus
- Quadruple therapy (Please Boost My Therapy)
- > failure/previous macrolide exposure/penicillin allergy
- > esomeprazole 20mg BD 14 days
- > bismuth 120mg QD 14days
- > metronidazole 400mg TDS 14 days
- > doxycycline 500mg QD 14 days
- Eradication testing
- > with urea breath test
- > cease bismuth/antibiotics for 4 weeks
- > cease PPI for 2 weeks
Benefits of H pylori eradication
- peptic ulcer
- > promotes ulcer healing/reduces risk of relapse
- dyspepsia
- > improves symptoms
- NSAID users
- > peptic ulcer risk 60 fold
- > bleeding risk 6 fold
- atrophic gastritis/intestinal metaplasia
- > reduce progression to gastric carcinoma
- long term acid suppression
- > reduce progression to metaplasia
- low grade MALT lymphoma
- > induce regression
