GIT RPA Flashcards
Which sphincter is implicated in GORD
lower oesophageal sphincter transient relaxation
What absorption is impacted by PPI
calcium/vitamin D - contributes to osteoporosis
other medications
Alarm symptoms in GORD (3)
dysphagia, weight loss, haematemasis
Lifestyle management of GORD
weight loss (!!!)
smoking cessation
avoid precipitants (ETOH, coffee, chocolate, spicy food)
Behaviour (nocturnal head elevation)
effective in 20-30%
Classification of Barrett’s
short vs long segment
Is malignancy risk high with short or long segment Barrett’s
long segment
What is the appearance of Barrett’s in g-scope
salmon coloured
What is the pathological change in Barrett’s
smoking - squamous
now, mostly adenocarcinoma
change to intestinal mucosa
Management of high grade dysplasia for Barrett’s
endoscopic ablative therapy
Barrett’s oesophagus and no dysplasia subsequent management
repeat endoscopy in 6 months
maintained on PPIs (but not much evidence)
Barrett’s oesophagus and low grade dysplasia subsequent management
Repeat endoscopy in 3 months
Moving towards the same management as high grade dysplasia
G-scope appearance of eosinophilic oesophagitiis
Ringed appearance + furrows
What other conditions are eosinophilic oesophagitiis associated with
atopic conditions
What is the management of eosinophilic oesophagitis
1st line - PPIs
2nd line - topic corticosteroids (ingested fluticasone)
Elimination diets in children (in adults it’s often airborne)
oesophageal dilatation is only performed if there is a single dominant stricture in the oesophagus
Achalasia barium swallow appearance
Bird’s beak
Achalasia diagnosis
Endoscopy to rule out malignancy
Manometry is for diagnosis
Management of achalasia
young patients - pneumatic dilatation of LOS; surgery (laparoscopic Heller’s myotome)
old patients - nitrates, CCB, botox
Portal pressure to develop GO varices
> 12mmHg
Portal pressure to have bleeding GO varices
> 18 mmHg
Pathogenesis of GO varices
Increase portal pressure due to scarred liver
Shunts bleed towards other directions -> spleen (splenomegaly, thrombocytopenia etc)
When is the first endoscopy for cirrhotic patients
at diagnosis
Primary prophylaxis for GO varices
non-selective BB
- propanolol (decreases risk of first bleed by 50%); need to drop pulse by 25%
Grade 2 +
- banding program
(higher grade do better with banding cf medical therapy)
Acute haematemesis and varices - which of the following does not improve mortality rates: A - terlipression B - octreotide C - IV antibiotics D - IV PPIs E- Early endoscopy
IV PPIs
MOA of terlipressin
powerful vasopressin
SE of terlipressin (or what conditions should one be more careful with its use or consider octreotide)
Strokes, cardiac events, pulmonary oedema due to powerful vasoconstriction of vessels
Management of uncontrolled variceal haemorrhage
Danis stent (large self-expanding metal stent that applies direct circumferential pressure) - used if the patient is being bridged to something else
Sengstaken-Blakemore or Linton tube
- more likely to cause ischaemia so can only leave for 48 hr (cf Danis stent which is 7-14 days and a better choice who is being bridged)
TIPSS MOA
Decreases portal hypertension
Contraindication for TIPSS
encephalopathy as it facilitates increased ammonia to CNS
Secondary prophylaxis to oesophageal varices
Beta blockers + band ligation
TIPSS if recurrent bleeding
Await liver transplant
Which condition cannot get TIPSS
Primary sclerosis cholangitis
Increased rate of cholangitis due to blocked/dilated ducts
Which is not a risk factor for PUD:
- enteric coated aspirin
- alcohol
- COX-2 inhibitors
- smoking
- Helicobacter
ETOH
what transplant med causes PUD
mycophenolate
and steroids through poor healing - not much evidence
Regimen for people with no allergies for H. Pylori eradiacation
amoxicillin 1g bd
clarithromycin 500mg bd
esomeprazole 40mg
most common cause of resistance to H. Pylori
Clarithromycin resistance
When should urea breath test be done after treatment H. Pylori
8 weeks + after treatment
Urease breath test - what kind of false results can you get
only false negatives, can’t get false positives
Pathogenesis of H. Pylori
H pylori produces ammonia to survive the gastric acidic environment
The stomach increases gastric pH to compensate and causes ulcers
What kind of ulcers are most frequent in H Pylori
duodenum > gastric
H. Pylori eradication treatment in patients with penicillin allergy
clarithromycin, metronidazole, PPI
60% successful eradication vs 80% w amoxicillin
Next line in resistant H Pylori
Rifabutin, doxycycline, tetracycline PPI
nexium HP7 for 1 week, then levofloxacin based combo therapy for another 10-14 days (din’t se in patients >70 due to risk of C. Diff)
Which NSAID is most likely to cause gastric ulceration
aspirin
COX2s are slightly better
MOA of NSAID related ulceration
Decreases prostaglandins and inhibition of COX-1 and COX 2
and epithelial proliferation
(see slides)
Management of incidental gastric ulcer, negative for H Pylori and investigations for other causes are negative
PPI 40mg bd for 8 weeks then repeat gastroscopy
must biopsy the area if the ulcer is still present
gastric ulcers have malignant potential unlike duodenal ulcers
Approach to anti platelets in PUD
only stop for 3-4 days due to increased risk for cardiovascular events
can consider changing aspirin to clopidogrel
Amount of bleeding required to produce melena
150mL
Amount of bleeding from upper GI source required to cause bright red PR bleeding
high volume >500mL
Management of bleeding duodenal ulcer
multiple therapies simultaneously:
- injection w adrenaline, clipping, coagulation w heat probe
Forrest classification in ulcers
stigmata in endoscopic appearance to assess risk of rebreeding
Acute hemorrhage
Forrest I a (Spurting hemorrhage)
Forrest I b (Oozing hemorrhage)
Signs of recent hemorrhage
Forrest II a (Non bleeding Visible vessel)
Forrest II b (Adherent clot)
Forrest II c (Flat pigmented haematin (coffee ground base) on ulcer base)
Lesions without active bleeding
Forrest III (Lesions without signs of recent hemorrhage or fibrin-covered clean ulcer base)[2]
Duration of PPI infusion for bleeding ulcer
72hr from TIME of endoscopy
Rebleeding after 72hr of PPI infusion after first endoscopy for bleeding ulcer
repeat endoscopy and endoscopic therapy and have another PPI infusion
options if ongoing bleeding:
interventional radiology
surgery last line
Insidious presentation of coeliac’s
irone deficiency anaemia
osteoporosis
infertility and miscarriages
which family members of coeliac patients to screen
first degree relatives
Diagnosis of coeliac’s
Small bowel biopsy
antibody testing - tTF and anti-endomysial Ab (>90% sensitivity) not diagnostic however
What autoimmune conditions are associated with coeliac’s
autoimmune thyroiditis
dermatitis herpetiformis (80% will have coeliac)
T1DM
and many more..
what malignancy is associated w coeliac disease
small bowel lymphoma
first line test to do in compliant coeliac disease who after many years of dietary compliance develops new weight loss and diarrhoea
CT abdo pelvis
risk factors for NH lymphoma in coeliac patients
gluten
refractory disease
IgG 4 disease - most common presentation
systemic fibroinflammatory condition
autoimmune pancreatitis
mostly affects pancreas and biliary tree
Diagnosis of IgG4 disease
IgG4 serum levels
Tumefactive lesions
Histology - dense lymhoplasmacytic infiltrate, storiform fibrosis
IgG positive staining on immunohistochemistry
Treatment of IgG4 disease
Mostly monitoring
Otherwise:
Immunosuppression - steroids, azathioprine methotrexate
Rituximab for refractory disease
Prophylaxis for complications of ERCP - pancreatitis
indomethacin suppository 100mg
ERCP indications
These days used for therapeutic not just diagnostic due to high complication rate (except PSC)
1) obstructed bile duct confirmed on CT angio, MRCP, USS
2) gallstone pancreatitis AND cholangitis
3) PSC if inadequate imaging or evidence of biliary obstruction
4) Sphincter of odds dysfunction (Type I; usually don’t perform for type II - biliary colic + 1 of abnormall bloods or imaging)
Type 1 sphincter of Oddi dysfunction
biliary colic
abnormal LFT/pancreatic enzymes
abnormal dilated ducts
tests should return to normal after 1 week of episode
must satisfy all 3 criteria to get ERCP - as pancreatic rates are +++
Investigation for younger patients with recurrent IDA w clear recurrent scopes
pill cam
Investigation for older patients (80+) with recurrent IDA w clear recurrent scopes
Abdo CT scan for malignancy
What DAA for HCV is contraindicated in decompensated cirrhosis
protease inhibitors
What DAA is not recommended in eGFR <30
sofosbuvir (oral nucleoside analogue)
What genotypes in HBV are associated with better response to IFN
A and B respond better than C and D
What is genotype F associated with in HBV
fulminant liver failure
Where is universal screening for HBV performed
B cell therapy / immunotherapy for malignancy
antenatal
What are the predictors used in most models for HBV cirrhosis/HCC
ALT, HbeAg, male, age
HbsAg -ve
anti-HBc -ve
anti-HBs -ve
susceptible, no current or prior infection
HbsAg -ve
anti-HBc +ve
anti-HBs +ve
resolved infection but could reactivate
HbsAg -ve
anti-HBc -ve
anti-HBs +ve
vaccinated
HbsAg +ve
anti-HBc +ve
anti-HBs -ve
ImG anti-nbc high titre
acute HBV infection
Isolated
anti-HBc positive
escape mutant or occult infection
What phases of HBV should get treatment
immune escape
immune clearance
essentially when LFTs are abnormal
where in the viral replication cycle does the antivirals work in HBV
RNA replication
the cccDNA is not targeted currently
hence why patients remain HbSAg positive
only viral suppression is achieved
What antivirals are used in chronic HBV
oral nucleotide analogues
entecavir and tenofovir (ETC + TDF)
Peg interferon might sometimes be used as it’s finite therapy for 1 year (more side effects)
TAF vs TDF
TAF is tenofovir alafenamide - a novel prodrug of tenofovir
TAF has better bone and kidney SE profiles
Management of ladies of HbsAG + mothers
HBIG + HB Vax x3
Management of women planning pregnancy already on antiviral
stop prior vs continue - tenofovir ok to continue
Who should get antiviral prophylaxis (pregnant women)
high viral load >10^6 IU/mL wet 30 to 2-3 months post delivery
Extrahepatic manifestation of HEV
neurological complications e.g. gillian barre, (see slides)
Lipophilic vs hydrophilic statin in HCC
lipophilic statins reduce HCC (simvastatin + atorvastatin)
Liver nodule <1cm in cirrhotic patient on screening next step
Repeat US at 4 months
Liver nodule >1cm in cirrhotic patient on screening
Multiphasic contrast-enhanced CT or multiphase contrast-enhanced MRI
If classic features on imaging, don’t need biopsy, can treat as HCC
classic features:
- 4 phase multi-slice CT: arterial enhancement, washout on portal and delayed phase
Early stage HCC w 2-3 nodules <3cm treatment
transplant (or ablation if not transplant candidate)
Intermediate stage HCC w multi nodular unresectable + preserved liver function treatment
chemoembolization (considered palliative)
Small solitary HCC in resectable patients <5cm treatment
resection or transplant
resection has better long term survival
recurrence rate is 50-60% at 5 years with probably a new tumour
SIRT for HCC
selective internal radiation therapy
very small beads delivered into the tumour selectively
Systemic therapies for HCC - 2 first lines on PBS
sorafenib (kinase inhibitor drug)
lenvatinib
Acute liver failure key features (4)
severe acute failure
liver injury AST/ALT >2-3 ULN
and impaired liver function
must have hepatic encephalopathy within 12 weeks of onset of jaundice
if there is no hepatic encephalopathy, it’s just acute liver injury
King’s college criteria for paracetamol ALF and transplantation
pH < 7.3
or
In a 24h period, all 3 of:
INR > 6 (PT > 100s) +
Cr > 300mmol/L +
grade III or IV encephalopathy
Child pugh scoring
ascites, encephalopathy, bilirubin, serum albumin, INR
Higher mortality out of decompensation w ascites vs decompensation w bleeding
decompensation w bleeding
Acute-on-chronic liver failure
characterised by acute decompensation of chronic liver disease associated with organ failures and high short-term mortality. Alcohol and chronic viral hepatitis are the most common underlying liver diseases. Up to 40%–50% of the cases of ACLF have no identifiable trigger; in the remaining patients, sepsis, active alcoholism and relapse of chronic viral hepatitis are the most common reported precipitating factors. An excessive systemic inflammatory response seems to play a crucial role in the development of ACLF.
Management of ascites
1st line
dietary manipulation (low salt)
spiro
up to 400mg/day
2nd line
diuretics large volume paracentesis + IV albumin
refractory ascites
2nd line
TIPSS
Transplant
Nutritional support for all
Non transplant treatment that improves survival for refractory ascites
TIPSS
Ascites PMN for SBP
> 250/mcL
Type 1 vs 2 HRS
type 1 is a form of AKI - really poor early survival
creatinine doubles to >220
type 2 is a form of acute on chronic kidney injury of chronic kidney disease (patients w declining renal function over 6 to 12 months)
Cr >133
Management of AKI in cirrhosis
Withdrawal diretics
treat infection
plasmave volume expansion w diuretics
vasoconstriction
dialysis
transplant
what BB is preferred for primary prophylaxis of variceal bleeding
carvedilol
cancel 2019 paper carvedilol prevents deaths in ascites
Which pulmonary complication is a contraindication to liver transplant in cirrhosis
Portopulmonary hypertension
compared with hepatopulmonary syndrome which is an indication for transplantation
what type of diet (aside from low salt) in liver disease
high protein high energy
what are the histological manifestations of NASH
hepatic steatosis w either lobular inflammation, hepatocyte ballooning with or without fibrosis
PNPLA3
genetic driver of NAFLD in hispanics
Most important determinant of outcome in NAFLD
fibrosis (can only be determined by biopsy)
What other malignancies are associated with NALFD (Aside from HCC)
breast ca
colorectal ca
HCC surveillance in NASH
6 monthly US in NASH cirrhosis
Hyperferritinaemia in NAFLD
Not a marker of iron overload - rather of inflammation
Associated w fibrosis in NAFLD
phlebotomy is not associated w improvement
liver enzynes pattern in alcoholic hepatitis
AST>ALT
<1000
> 1000 more likely paracetamol, ischaemic etc
treatment of alcoholic hepatitis
pred
Autoimmune hepatitis type I vs II
type I - ANCE, ANA, Anti Smooth muscle, anti-actin anti soluble liver antigen
type II - anti LKM, anti-liver cytosol
Autoimmune hepatitis treatment
Pred
Azathioprine
Primary biliary cholangitis serological findings
positive AMA >95%
+ANA
AMA titre does not correlate to disease stage
Which IBD has preserved goblet cells
crohn’s has preserved goblet cells where as UC has depleted goblet cells
mechanism of action of faecal calprotectin
calcium binding protein found in cytosol of neutrophils
released w cell damage in GI tract
good for distinguishing IBD and IBS
role in following disease course
Anti-Saccharomyces cerevisiae antibody (ASCA) in IBD
specific but not very sensitive in Crohn’s
when to consider thiopurines in crown’s and UC
Crohn’s: at diagnosis
UC: use 5ASA first and if it doesn’t work then aza
Use of cyclosporin in IBD
rescue therapy in UC (not crown’s)
What has been proven to stop post op recurrence in crohn’s disease
metronidazole
aza
TNF-alpha
stopping smoking
Not responding to first line immunomodulator in IBD
combination therapy with biologic
how long to wait to immunosuppress after live vaccine
3 weeks before starting immunosuppression
have to wait 3 months after immunosuppression before giving live vaccines
Colon cancer screening if have both PSC and UC
yearly C-scopes
Who/when to screen for colon cancer in UC and Crohn’s
UC beyond sigmoid colon
CD >1/3 colon involved
from 8 yr after diagnosis
start earlier if strong FHx of CRC
yearly in active disease, strong 1st degree relative family history
3 yearly in inactive UC/CD or 1st degree relative >50yr
what’s greatest risk to pregnancy in IBD
flare of IBD
Follow up of PUD - gastric and duodenal
8 weeks of PPI should heal any ulcer - EXCEPT if it’s malignant
If gastric, should rescope after to look for malignancy
If duodenal don’t need to rescope
Also do not ned to continue PPI
What ulcers are more associated with H Pylori
duodenal (90% caused by H Pylori)
Second line for H Pylori after 1st line failed
Amoxycillin 1g
Levofloxacin 500mg bd
PPI
10 days
HCV SVR rates for pan genotypic agents
95%
Options for HCV treatment failure
Sofosbuvir/velpatasvir/voxilaprevir (VOSEVI)
pathophysiology of hepatorenal syndrome
due to marked splanchnic arterial vasodilatation causing markedly decreased effective arterial blood volume
overcoming the RAS system
causing renal perfusion
hence why there is no intrinsic renal disease
terlipressin in hepatorenal syndrome
for transplant candidates as it only causes a temporary constriction in the splanchnic arteries
hence as bridging therapy
least common side effect of lenvatinib
rash
lenvatinib
multi-kinase inhibitor
rash is much less than sorafenib
for advanced metastatic disease + child pugh A
advanced metastatic disease HCC + child pugh B/C
palliate
pathophysiology of alpha1-antitrypsin deficiency
There are different types of alpha1-antitripsin mutations
z mutation results in the production of an abnormal protein which is trapped in the endoplasmic reticulum of hepatocytes. The protein is toxic to the hepatocytes.
the null null mutation results in no liver disease because there’s no abnormal protein in hepatocytes
