Flashcards in Gastro Deck (139):
What is the primary factor leading to accumulation of ascities in patients with cirrhosis?
What is the pathophysiology of ascites in cirrhosis?
Cirrhosis -> portal hypertension (sinusoidal pressure > 12 mmHg)-> splanchnic dilatation-> increase splanchnic pressure -> formation of ascities
Splanchnic dilatation also results in arterial underfilling -> activation of vasoconstriction and antinatriuretic factors -> sodium retention -> plasma volume expansion -> ascites
what is the serum to ascites albumin gradient (SAAG)? What is it used to identify?
SAAG = serum albumin - ascites albumin
Used to identify the presence of portal hypertension
> 11 = portal HT (cirrhosis, HF, bud chiari, alcholic hepatitis)
what does the appearance of the following ascitic fluid suggest:
pink or bloody
Clear yellow = normal bili and protein
brown = high bili
turbid = infection
milky = elevated triglyceride concentration usually secondary to lymphoma
Pink or bloody = traumatic tap, malignancy, cirrhosis, punctured vessel
What Ix do you order for an ascitic fluid?
Protein; if >=2.5 or 3 gldL then exudate, if 1.0 = malignancy
Amylase, lipase- elevated if due to pancreatitis or gut perforation
Tb- Tb PCR
Cytology - malignant cells
what is the treatment for ascites due to cirrhosis?
1. Spironolactone50-100 mg PO OD, increase by 100 mg q 4 days up to 400 mg OD.
2, Can add Frusemide40 mg PO. Increase by 40 mg q 4 days up to 160 mg OD
3. Amiloride 10-20 mg OD if pt cannot tolerate spironolactone
what is the Tx fro severe and refractory ascites sue to liver cirrhosis?
1. Transplant only definitive therapeutic option
2. TIPS to shunt between hepatic and portal veins
what does B12 deficiency lead to?
Pernicious anaemia identified by macrocytosis, intramedullary haemolysis and peripheral neuropathy
Where is our source of Vit B12?
Where is Vitamin B12 stored?
How is Vitamin B12 absorbed?
Meat and dairy is the only source of Vit B12
Total body stores are 2-5 mg with half of stores in the liver
Cobalamin is liberated from food by acid and pepsin. Binds to R-factors in the saliva and gastric juice.
In the duodenum, cobalmin freed from R-proteins due to actions of PANCREATIC proteases. Then binds to intrinsic factor.
The IF-Cbl complex binds to ileal receptors in the terminal ileum.
A purine anti-metabolite.
Metabolised via mercaptopurine to thioguinine metabolites which interfere with purine synthesis imparing with lymphocyte proliferation, celluluar immunity and anti-body responses.
Indications for Azathioprine
Prevention of post transplant rejection
immune and inflammatory diseases
What is the significance of TMPT testing when starting azathioprine?
1 in 300 ppl have low or no TPMT activity and are at severe risk of myelosuppresion. Avoid use or reduce dose to 1/10.
What is the interaction of azathioprine and allopurinol?
Allopurinol reduces azathioprine metabolism increasing the risk of severe bone marrow toxicity
What results would you expect in a pt with azathioprine resistance?
high 6MMP, low 6-TGN
Describe the pathway of azathioprine metabolism
AZA -> 6-MP -> 6 - MMP via TPMT
AZA -> 6-MP -> 6-TIMP -> 6-TXMP -> 6- TGN
What is the recommended treatment for Hepatitis C Genotype 1?
Sofosbuvir (Nucleotide polymerase inhibitor) + ribavirin + PEG for 12 weeks or
Olysio for 12 weeks + ribavirin + PEG for 24 weeks
If not elgible to receive interferon:
Solvadi + Olysio +/- ribavirin for 12 weeks or
Solvadi + ribavirin for 24 weeks
How many Hep C genotypes are there?
What is the treatment for Hep C Genotype 2?
Solvadi + ribavirin for 12 weeks
What is the treatment for Hep C Genotype 3?
Solvadi + ribavirin for 24 weeks
What is the treatment for Hep C Genetoype 4?
Solvadi + ribavirin + PEG for 12 weeks or
Olysio fro 12 weeks + ribavirin + PEG for 24-28 weeks
If not eligible for interferon:
Solvadi + ribavirin for 24 weeks
what is the treatment for Hep C genotype 5 or 6?
Solvadi + ribavirin + PEG for 12 weeks or
Ribavirin + PEG for 48 weeks
If not eligible to receive Interferon there are no recommended treatment options
What are the American Gastro Association guidelines for a pt with Barrett's oesophagus:
low grade dysplasia
High-grade dysplasia in the absence of eradication therapy
No dysplasia : 3-5 years
Low grade: 6-12 months
High grade dysplasia in the absence of eradication therapy: 3 months
What is the treatment for recurrent C. diff infection?
Duodenal infusion of faeces.
Sig more effective than the use of vancomycin
What is the recommended guidelines for colorectal ca screening for average or slightly increased risk (Asymptomatic or one first or second degree relative with CRC diagnosed at 55 years or older)
FOBT every 2 years from age 50 years
What is the recommended guidelines for colorectal ca screening for moderately increased risk (1-2% of population) (asymptomatic with 1 first degree relative with CRC diagnosed before 55 years or 2 first degree or 1 first degree and one second degree on the same side of the family with CRC diagnosed at any age without high risk features)?
Sigmoidoscopy plus double contrast barium enema or CT colonography if colonoscopy CI.
Every 5 years from age 50 years or at an age 10 years younger than the age of 1st diagnosis of CRC in the family. Whichever comes first.
Consider offerring FOBT in intervening years.
What is the recommended guidelines for colorectal ca screening for high risk (=3 1st degree or second degree relatives on the same side of the family diagnosed with CRC (suspected Lynch syndrome, also known as HNPCC) or other Lynch syndrome related cancers or
- >=2 first or second degree relatives on the same side of the family Dx with CRC, including any of the following high risk features: multiple CRC in one person, CRC before 50 y, family member who has or had Lynch syndrome related cancer or
- 1 fist degree or second degree relative with CRC, with suspected FAP or
- somebody in the family whom the presence of a high risk mutation in the adenomatous polyposis coli (APC) or one of the mismatch repair genes has been identified
- refer to genrtic screening of affected relatives.
- FAP: flexible sigmoidoscopy or
- Colonoscopy in attentuated FAP
Those at risk for FAP
what do the following mean?
Autocrine - self communicating e.g. NO, IGF
Endocrine - hormones
Neurocrine - Vagus nerve e.g. Ach, VIP
Paracrine - parallel, talking next door e.g. somatostatin
Where are the following peptide hormones produced? Function?
Gastric inhibitory peptide
Gastrin - Antral G cells. Regulates gastric H+.
CCK - Intestinal I cells. Regulates pancreatic enzyme regulation.
Secretin - Intestinal S cells. Regulation of HCO3.
Glucagon - Intestinal L cells. Regulation of Insulin.
Gastric inhibitory peptide - Intestinal K cells. Reg of insulin release. Inhibitor of H+.
VIP - Myenteric inhibitory motorneurons/submucosal neurons. Neural inhibitor of of motility/stimulant of fluid secretion.
Serotonin - EC cell of digestive tract. Stimulus of peristalsis.
Substance P - Neurotransmitter.
what is the rate limiting step in acid production?
What are some of the AE of PPIs in studies?
Increased risk of Pneumonia, Gastroenteritris e.g. Campylobacter, Salmonella, OP.
Significant risk of C. diff in meta analysis.
What are the causes of Hypergastrinaemia?
Atrophic gastritis - pericious anaemia, H. pylori
Gastrin secreting tumour
Prolonged acid inhibition e.g. PPI, H2RAs
What is Zollinger-Ellison Syndrome?
Gastrin secreting tumour -> ulcer disease.
1/3 of pts have MEN1
How do you Dx ZES?
Gastrinoma triangle - bound by junction of cystic and CBD, junction of 2nd-3rd parts of duodenum and junction of neck and body of pancreas.
Step 1 - Fasting gastrin > 1000 pg/mL in absence of PPI.
If eelvated gastrin, confirm with basal acid output test.
Step 2 - BAO = acid output > 10 mEq/ hr.
Step 3 - secretin provocation test to confirm Dx.
Should expect increase of gastrin>200pg/ml above baseline within 15 minutes of infusion.
Which cells control persitalsis?
Interstitial cells of Cajal in myenteric plexus. Serves as pacemaker cells leading to slow waves potential -> contraction of smooth muscle
Which motility disorders are associated with loss of interstitial cells of Cajal?
Slow transit constipatiomn/chronic idiopathic constipation
Internal anal sphincter achalasia
Gastroparesis (idiopathic and diabetic)
Afferent loop syndrome
Megacolon and megaduodenum
Achalasia of LES
What are the acute causes of pancreatitis?
Ischaemia - rare, after prolonged Sx in prone position
Causes of chronic pancreatitis?
Have studies shown statins reduce risk of pancreatitis?
How do you treat post ERCP pancreatitis?
Acute Mesenteric ischaemia. Cause, Presentation, Ix, Tx?
occlusive (85-95%) or non occlusive (20-30%) obstruction of arterial or venous flow.
SMA embolism in 50%
SMA thrombosis 15-25%
Non occlusive - usually due to splanchnic vasoconstriction
Mesenteric venous occlusion 5%
Focal segmental inschaemia
SMA embolism from LA or ventricular mural thrombus is the most common cause
Underlying cardiac disease
Acute onset of severe ado pain
AS, tender, pain out of proportion to examination
Gold standard is mesenteric angiography
Papaverine- phosphodiesterase inhibitor can be used at the time of angiography to relieve mesenteric vasoconstriction in pts with embolic and non embolic arterial occlusion as well as nonexclusive ischaemia.
Laparotomy and embolectomy
Mesenteric artery thrombus - Surgical revascularisation
Mesenteric venous thrombus - anitcoag and resection of infarcted bowel
Non- occlusive - Tx cause, resection is ischaemia present
Chronic Mesenteric Ischaemia. Cause, Presentation, Ix, Tx?
Manifestation of mesenteric arthersclerosis.
Abdo pain 30 minutes after eating - due to diversion of small bowel blood flow to gut after eating.
Leads to sitophobia - fear of eating
Splanchnic angiography - occlusion of at least 2 of the major splanchnic arteries
Doppler US a screening test but cannot confirm Dx
MR and CT angiography useful but abnormal study still warrants a splanchnic angiography.
Surgical revascularisation is the definitive Tx
Percutaneous angioplasty with or without stunting can be attempted in pts who are poor surgical candidates for bypass Sx.
Primary Biliary Cirrhosis: What, Presentation, Ix, Tx?
Chronic cholestatic liver disease of unknown cause. Ongoing immunologic attack on interlobular bile ducts eventually lead to cirrhosis and liver failure.
Affects middle aged F, median onset 50y.
Jaundice and cutaneous hyperpigmentation rarely observed.
ALP 1.5 x ULN
AST and ALT 5xULN
Mitochondrial antibody present in 90-95% at titres > 1:40
Liver bx if ab -ve
Histo - focal duct obliteration with granuloma formation known as florid duct lesion is pathognomonic.
Ursodeoxycholic acid , offers survival benefit
Symptomatic Tx of dry eyes, dry mouth and pruritis
Liver transplant highly effective for end stage PBC
What test has the most NPV in coeliac disease?
HLA DQ2/8 negative
Very unlikely to have disease
Consider testing in non dx histo or negative serology
PUD: most common cause? Common site? Dx?
H. pylori and NSAIDs cause > 90%
Duodenum most common, 95% in bulb or pyloric channel.
In the stomach most are in the antrum.
Duodenal ulcers have increased acid secretion compared with gastric.
Dx confimed by upper endoscopy with rapid urease test and histo.
If Bx not taken, then urea breath test or faecal antigen test
PPIs can casue false negatives and should be stopped 7-14 days prior
Where are the following absorbed in the GIT? Iron, folate, B12/bile salts
iron - duodenum
folate - jejunum
absorption > in proximal then distal jejunum
B12/bile salts - ileum
Tx of alcoholic hepatitis?
Based on Maddrey discriminant function score (MDF)
MDF ≥32 = severe alcoholic hepatitis. Tx with prednisone or pentoxifylline.
Pentoxyfylline used when pt has fever (SBP), bleeding, RF as prednisone CI.
How do you calculate the Maddrey discriminant function score (MDF)?
4.6 [PT (s) - control PT (s)] + total bilirubin.
>= 32 suggest severe alcoholic hepatitis with short term mortality risk of 50%
What is the MELD score? How do you calculate it?
Prognostic Index to assess mortality in pts with ALD
MELD 5-6 = 100% 1 y survival
MELD 7-9 = 81% 1 y survival
MELD 10-15 = 45% 1 yr survival
Biggest predictor of varices?
Portal pressure (hepatic venous portal pressure)
> 10 suggest high risk of bleeding
HVPG is the only measurable factor
Child Pugh score C = 70% risk of bleed
NAFLD. What, Dx, Tx?
Usually results fro insulin resistance and metabolic syndrome.
Inflammation and fibrosis associated with NAFLD is referred to as NASH.
10% progress to cirrhosis.
Dx: US, VT, MRI can confirm heaptic steatosis but cannot indetify inflammtion and fibrosis. Liver Bx confirms NASH
Weight loss and managment of co-morbidities
What is the criteria for liver transplantation in fulminant hepatic failure?
PT > 100 sec irrespective of grade of encephalotpathy OR
any 3 of the following
- Age 40 y
- non A-B hepatitis, halaothane of drug reaction
- Jaundice to encephalopathy > 7 d
- PT > 50 s
- serum bilirubin > 300
What is the criteria for liver transplantation in fulminant hepatic failure in paracetamol overdose?
pH 100 and
serum Cr > 300
in pts with grade III or IV encephalopathy
CI to liver transplant?
Ongoing smoking and EtOH
Indications for liver transplant?
MELD score> 15 in adult
Liver disease that would result in a 2 year mortality rate of >50% without liver tranplantation
Diuretic resistnat ascites
recurrent or persistent GI haem
Metabolic syndromes curable with lvier tranplant e.g. falilial amyloidosis, urea cycle disorders, oxalosis
Most common indication for liver transplant?
Why do you perform weekly CMV levels post transplant for 7 months?
High risk of CMV infection.
High titres indicate high dose immunosuppression.
Decrease immunosuppressive doses and start valganciclovir
How common is liver rejection post transplant?
Signs of liver rejection.
30-40%. Can occur at 1 week.
Elevated liver enzymes.
Biliary stricture or rejection. Perform MRCP and if negative then liver biopsy.
Responsive to steroids.
What is the most common cause of deranged LFTs?
How do you distinguish between achalasia and peptic stricture?
In achalasia - acute onset, days to both solids and liquids
In Oesophageal peptic stricture - chronic, progressive to solids and then liquids
What is Plummer Vinson syndrome?
Dysphagia with Fe def anaemia associated with oseophageal web (thin membranes located in the middle or upper oesophagus)
A biopsy is always indicated in the Dx of HCC. T/F
In the setting of CLD and elevated AFP the characteristic findings of HCC is sufficient.
Dedicated 4 phase mulit-detector CT or dynamic contrast MRI is sufficient with late arterial phase imaging is recommended.
Manifest as enhancing mass with hyper-vascularity during the arterial phase and washout dueing the venous phase.
When is a percutaneous image-guided biopsy indicated?
Liver met > 1 cm when imaging findings not characteristic of HCC or hemangioma
What is the Tx for HCC?
However many patients are ineligible due to extent of tumour nor liver dysfuntion.
Non surgical candidates:
Local tumour ablation
What are the indications for an ERCP?
Stone in CBD
Co-exiting cholangitis (fever, jaundice, septic shock)
Persistent biliary obstruction (conjugated bili > 5 mg per deciliter)
Clinical deterioration and increasing LFTs
In the absence of cholangitis and biliary obstruction, ERCP within 24-72h does not lead to reduction in mortality
ERCP is indicated in biliary/gallstone pancreatitis. T/F
Do not benefit from ERCP with or without sphincterotomy.
What are the causes of pseudo-obstruction?
Hypothyroidism (bradycardia, hypothermia)
Hypocalcaemia and hyperparathyroidism
Fistulae occur in 20-25% of Crohn's pts. T/F
Metronidazoel and cipro are effectivein fistulising Crohn's. T/F
True however long term therapy have adverse effects.
Cipro is used although no more effective.
How many pts remain fistula free after Infliximab at 1 year?
Heals > 50% of fistulae
Tacrlimus is more effective than other therapies at healing fistulas in crohn's disease?
True. Becoming second line therapy after TNF (infliximab)
What is the main circulating form of Vit D?
If you suspect renal impairment in Vit D def, which form of Vit D do you measure?
Main is 25(OH) Vitamin D
1,25 (OH) Vitmain D - the bioactive form
C. difficile Tx?
Oral Metro x 2
Oral vanc (can include IV metronidazole with vanc)
Faecal transplant, may need more than one infusion
Exclusions for faecal tranplant:
Mx of bloating in IBS?
Trial low FODMAPs diet:
Oligosachharides - frutans, galacto-oligosaccharides
Disacchardies e.g. lactose
Monosaccharides - fructose in excess of glucose
Polyols - sorbitol, mannitol, maltitol, xylitol and isomalt
- antispasmotic and anti-flatulent effects
- herbal agent containing extracts if the plant Iberis amara that increases motility.
Symptoms of IBS?
Abnormal bowel habits e.g. intermittent diarrhoea and constipation
What is the pathophysiology of hepatopulmonary renal syndrome?
A vascular disorder of the lung which occurs in the setting of chronic liver disease.
- dilatation of pulmonary capillaries
- Pleural and pulmonary AV malformations/shunts
- arterial hypoxaemia and orthodeoxia (reduction in arterial oxygen tension from supine to upright position). Due to a preferential perfusion of lung bases in an upright position where the vascular abnormalities are typically found. This is called PLATYPNOEA.
How do you Dx and Mx Heptopulmonary syndrome?
bubble study. TTE with microbuble contrast. Left heart will usually not have microbubbles unless there us a intracardiac or intrapulmonary shunt.
No medical therapy
Tx of NAFLD?
1st line - weight loss
Vitamin E may help, doses > 400IU associated with increased mortality
Pioglitazone can improve histology however AE are weight gain, oedema and HF.
What is a common presentation of Eosinophilic oesophagitis? Dx, Tx
Food bolus obstruction is common.
Young male with Hx of atopy.
Endoscopy and biopsies demonstrating > 15/hpf
Trial pts on PPI first to see if response
- diet therapy and avoidance of allergens
- SFED for 8 weeks then reintroduce 1 at a time (no milk, wheat, soy, seafood, eggs)
Topical inhaled corticosteroid or systemic corticosteroids provide short term relief.
PPI - 30% will respond
How are bile salts synthesised?
In liver from cholesterol and conjugated.
Transported into bile ducts ad stored in gallbladder.
Released into doudenum post prandially.
Reabsorbed in the terminal ileum.
What is bile salt diarrhoea? Tx
If biles salts are not reabsorbed in the terminal ileum, they enter the colon ancause diarrhoea by:
- inducing secretion of Na and H2O
- increasing colonic motility and stimulating defacation
- Increasing mucous secretion
- muscosal damage
Cholestyramine - oral bile acid sequestion
What is the criteria for Dx of AIH? Tx?
ANA or SMA >=1:40 or >=1:80 = 1 point OR
LKM = 2 points OR
SLA +ve = 2 points
IgG > upper limit normal 1 point
IgG > 1.10 x ULN = 2points
Liver histology compatible with AIH = 1 point
Liver histo typical AIH = 2 points
Absence of viral hepatitis = 2 points
Points >=6 probable AIH
Points >= 7 definite AIH
Hepatocellular derangement for the following:
- AST> ALT (S for schooner)
-ALT > AST
- temporal relationship is key
- Drugs can cause any pattern
- common are abx, NSAIDs, MTX, AZA, paracetamol
- AST, ALT in 1000s
- AST settles quicker than ALT which drops slowly
- can get subsequent rise in Bilirubin
UC: What are the markers of severity? Tx?
No of bloody stools > 6/d + 1 or more of the following:
Febrile > 37.8
CRP > 45
Severe inflammation on colonoscopy
Colorectal surgical consult D3 onwards if no improvement with steroids
- cyclosporin or
D5-6, no clinical response than colectomy in rescue failure
What is IgG4 related disease? What organs are affected?
Fibroinflammatory disease characterised by:
- Tumefactive lesions
- dense lymphoplasmacytic infiltrate on Bx
- storiform fibrosis
- similar histopathological features in all tissues
Often but not always an elevated IgG4
Can affect all organs
- pancreas and biliary tree
- salivary glands, lymph nodes
- retroperitoneal fibrosis also common
What are the RF for Hep B reactvation with immunosuppression?
Previous or active disease are at risk of reactivation
sAg +ve > sAg -ve, cAB -ve
Rituximab and anthracyclines
Who should receive Hep B prophylaxis Tx during immunosuppression?
All pts sAg +ve
All pts sAg-ve and HbcAb +ve and receive rituximab
Prophylaxis should continue for 6-12 months post CTx
12 months post Rituximab
HbcAb +ve and HbsAg -ve. Should they receive Hep B prophylaxis prior to CTx?
Controversial and guideline varies.
Definitely in pts receiving Rituximab
minimally absorbed oral antibiotic -> alteration of bacterial flora.
- maintains remission from encephalopathy
- reduces the risk of hospitalisation with encephalopathy
What is the acute Mx of hepatic encephalopathy?
Treat underlying precipitant
Lactulose titrated to 3-4 bowel motions/d
WH diuretics as dehydrated
What is the used in the prevention and Tx of encephalopathy?
- high energy, high protein
Branch amino acids
- hepatamine (restricted to tranplant centres)
- lactulose(non-absorbable oral disaccharides)
- Rifaximin (on PBS if pt is on lactulose)
How can you distinguish between NASH and alcoholic hepatitis on histo?
Neutrophils present in alcoholic hepatitis.
Neutrophilic infiltration is most specific for EtOH hepatitis.
Not present in NASH.
Which medication is most associated with oesophageal ulceration (pill induced oesophagitis)?
Doxy and tetracyclines in particular
Bisphosphonates - oral alendronate
Which protease inhibitors are indicated in HCV Tx?
- anaemia, rash, pruritis
- anaemia, rash, dysgeusia
Improved SVR from 40-70%
Genotype 1 only
What is the best imaging for choledocholithiasis?
If stone undetected, next best imaging?
ERCP GOLD standard - high specificity and sensitivity.
If ERCP -ve then:
- minimally invasive
Can be performed prior to ERCP, done in same procedure. Reduce risk of invasive Mx.
- good views of CBB and has an advantage over cross sectional imaging for small stones.
Indications for Endoscopic US?
pancreatic head assessment
Oesophageal tumour staging
draining of pancreatic pseudocysts
drainage of biliary obstruction
Child Pugh Score classification of liver cirrhosis.
Components to score - Pour another beer at eleven
Class A 5-6 points:
Class B 7-9:
Moderateraly severe liver disease
CLass C 10-15 points:
Most severe liver disease
Pts with cirrhosis.
What is the screening recommendation for:
- 2nd yearly
Recommended primary prophylaxis against variceal bleed.
Medication vs. Surgical
Medications: does not improve mortality but reduces bleeding rates compared to placebo
Propanolol or nadolol
- aim HR 55bpm
Endoscopic ligation - reduces mortality
Every 2-4 weeks until varices obliterated
FU endcoscopy 1-3 months after obliteration then every 6-12 months indefinitely
BB can be ceased when varices erradicated
Mx of acute variceal bleed?
Non aggressive resus
Octreotide and terlipressin (glypressin) to control bleeding in 80% of cases
Endoscopy with banding
Ceftriaxone followed by norfloxacin
TIPS has been shown to increase survival in patients with cirrhosis and variceal bleeding. T/F
Early use of TIPS associated with sig reduction in Tx failure and mortality in pts with cirrhosis who were hospitalised for acute variceal bleed and at high risk of Tx failure
When should a Dx of Hepatorenal syndrome 1 be considered?
When there is an increase in SCr of 150% or more from baseline.
HRS1 is acute
HRS2 is chronic, over months
Long acting vasopressin analog.
Mediates vassoconstriction by activation of vasopressin receptor on vascular smooth muscle cells within the splanchnic bed.
Reverse splanchnic vasodilation.
Optimal duration of therapy is >3 days.
SBP. What prophylaxis is recommended after the 1st episode?
Norfloxacin 400 mg OR bactrim DS equally effective.
SBP spontaneously recurs in 70%.
First episode is often a trigger for OLTx referral
How may PMN is Dx of SBP?
> 250 PMN/ml
Which immunosuppressive therapy is used post liver transplant?
- HTN, nephrotoxic, DM, lipids, tremor, Hirsutism, neurological
Post liver tranplant:
Early complications post transplant,
Graft failure, rare
Infection - bacterial, CMV, fungal
- PJP proph with bactrim 1/2 DS tablet OD for 6/12
- CMV proph with valganciclovir for 3/12
- if requires CMV Tx, use Ganciclovir IV for 10-14/7
Post liver tranplant:
Late complications post transplant, > 3 months
PTLD - post tranplant lymphoproliferative disorder
Renal (15% Cr >0.15, 5% Cr>0.25)
Post liver tranplant:
When does acute rejection occur?
% of rejections
- cholestatic LFTs due to portal based inflammation
Post liver tranplant:
When does chronic rejection occur?
% of rejections
Months to years post tx
- cholestatic LFTs due to vanishing bile duct syndrome
Tx: increase immunosuppression, tacrolimus
may not be treatable
Recurrent disease post liver transplant. Recurrence rates for following:
Mean time to recurrent cirrhosis is 7 years
Without prophylaxis recurrence is very common
Long life antivirals with Entecavir
30% develop recurrence
University of California, San Francisco criteria for liver transplant in HCC.
Best serological marker for acute infection?
Hep B core IgM
In pts untreated post transfusion Hep C, what is the lifetime risk of progression to cirrhosis?
Which colonic poly has the highest potential for malignant transformation?
What is the most common mechanism for malignant ascites?
Obstruction of abdo lymphatics
The risk factor with the greatest impact on the development of oesophageal cancer is?
What are the 4 types of Inherited pancreatits?
recurrent mild attacks from > 5 yo
Trypsinogen gene PRSS1
Increased risk of cancer
adolescents with pancreatitis and normal tripsinogen activity
1/4 pts have no FHX
CFTR gene mutation:
idiopathic chronic pancreatitis
IgG4 disease, mild currents attacks, presents with mass
Failure of LES relaxation with swallowing
-similiar efficacy to dilatation and safer
-median effect for 12 months
In the liver which are is most prone to ischaemia?
Zone 3 (around central vein)
Zone 1 - affected PBC
Diffuse oesophageal spasm:
Dysphagia to solid and liquids, chest pain
intermittent, 20% or more simultaneous contractions with high amplitude > 30 mmHg.
Non peristaltic contracions in response to swallowing.
Cork screw oesophagus
Nut cracker oesophagus aka hypertensive peristalsis:
Manometric finding of average distal pressures > 220 mmHg during 10 x 5 ml liquid swallows.
What is dumping syndrome?
Early vs. late
Caused by destruction or bypass of the pyloric sphincter
Occurs 20% of pts post pyloroplasty or distal gastrectomy.
Occurs 15-30 minutes after meal
N/V/D, cramps, vomiting
Diaphoresis, palpitations and flushing
Due to rapid emptying of hyperosmolar chyme (particularly carbs) into the small bowel leading to fluid retention due to osmotic gradient and release of serotonin and VIP.
Same symptoms as above a couple of hours after eating.
Due to hyoglycaemic following postprandial insulin peak.
When to suspect factitious diarrhoea?
Appearance of colon
Ix to confirm
Long standing blaoting and watery diarrhoea
serum K low
Urine Na low = 2
Urinary potassium higher 50
Melanosis coli is the appearance of colon
Confirm with stool and urine testing for laxatives using thin later chromatography (bisacodyl or senna)
What is a small bowel series aka small bowel enema, enteroclysis?
contrast travelling through the small bowel to Ix obstruction, stricture.
What is a pooled red blood cell scan?
Ix whether liver mass on CT/US is benign or malignant, and to exclude haemangioma in case a liver biopsy is required because the haemangioma will actively bleed if it undergoes biopsy.
Haemangioma of the liver will accumulate the radioactive tracer to a greater degree than the surrounding liver tissue.
Which Ix provides the most information for staging in Oesophageal cancer?
Which gastro procedures require antibiotic prophylaxis?
Percutaneous gastrostomy or jejunostomy tube insertion wither endoscopic or radiologically
- Cephazolin reduces risk of peristomal infective complications
- add Vanc is MRSA
EUS or EUS with FNA if:
adjacent to GIT and may be considered for solid lesions adjacent to the lower GIT. Not recommended if lesion is adjacent to the upper GIT.
In a ERCP if:
- complete biliary drainage may not be achieved or
- communicating pancreatic cysts or pseudocysts
- before tranpapillary or transmural drainage of pseudocyst
Cardiac procedures requiring antibiotic prophylaxis?
Transcatheter aortic valve implantation (TAVI)
Insertion of ventricular assist devices
Add vanc if MRSA
Changes on endoscopy
metaplasia of the squamous epithelium of the lower oesophagus to a columnar epithelium of intestinal type
Premalignant condition associated with 40-125 fold increase in the incidence of adenocarcinoma of the oseophagus.
High grade dysplasia
- endoscopic mucosal resection for Dx and staging AND/OR ablation followed by high dose acid suppression
- Further Mx: Oesophagectomy, endoscopic ablation (photodynamic or radiofrequency)
Surveillance every 3 months
Pt has erosive oesophagitis above squamocolumnar junction and is not on a PPI and endoscopy reveals dysplastic epithelium with features of active inflammation. Next step?
Repeat biopsies after 2 months of Tx with PPI
Manifestations of degenerating motor function in the aging oesophagus.
Pts > 80 yo
Asymptomatic but may complain of chest pain or dysphagia.
tertiary contractions (ranging from minor to severe)
Adenocarcinoma - more common in western world, affects distal
Squamous cell - 90% overall, more common in developing world, affects proximal oesophagous.
SCC- alcohol, tobacco, corsive injury to oesophagus, HPV not proven, precursor is squmouse dysplasia, no proven role fo
Adeno - Smoking, OBESITY, H. pylori, GORD and BE
Progressive solid food dysphagia most common and reduced oral intake.
Anaemia from GI bleeding.
Endoscopic US- used for staging and accurate for establishing tumour stage
CT for distant mets
PET- changes staging in 20%
O = tumour in mucosa
1 = tumour in submucosa
2a = into muscle
2b = into lymph nodes
3 = beyond muscle
4 = mets
-endoscopic mucosal ressection
- oesophagectomy + lymph node clearance
Stage II and III
- oesophagectomy alone, 5-34% 5 year survival
Neoadjuvant = pre-op CTx and RTx improves survival compared to Sx alone for both cancers
Role of adjuvant CT and RT unclear
- stent or RTx
CTx controversial, not sown to be superior to supportive care
- 2 drugs (5-FU and cisplatin) is SD
- 3 drugs (epi, cis + 5FU) is alternative with increased toxicity.
No survival benefit.
Stages of Hep B infection and Tx options:
Tx phase II and IV, when ALT is persis or intermittently elevated
Phase 1: immune tolerance
HBsAg > 6 months
Anti-HBe ab +ve
HBV DNA >= 20 000
Liver histo normal
Mx: Montior q 3-6 months
Phase 2: Immune clearance
HBsAg > 6 months
Spontaneous conversion to anti-HBe may occur
ALT persistently or intermittently elevated
HBV DNA >= 20 000
Liver histo moderate to severe heaptitis
Phase 3: Immune control
HbsAg > 6 months
Anti-Hbe ab +ve
DNA 6 months
Anti-Hbe ab +ve
ALT elevated inter or persist
Liver histo mod to severe hep
Tx for decompensated cirrhosis (HbeAg +ve or -ve) secondary to Hep B?
Screen for AFP and US for HCC q 6-12 months
Combination with Tenofavir and Entacavir
PegInterferon is CONTRAINDICATED
Life long Tx required
Refer for OLT
Tx of compensated (HbeAg +ve or -ve) liver cirrhosis in Hep B?
Screen for HCC with US and AFP every 6-12 months.
HBV DNA 2000 IU/ml
- Tenof or Entec
- to avoid flares, PEGInterferon should be used in early well copensated liver failure
Mx of infants of mothers with HBSAg +ve?
All infants should recieve vaccine and HBIG
PEG interferon can be given in pregnancy? T/F
Monitoring of Hep B?
Confirm Antiviral response to Tx at 12 weeks
Monitor at 24,36 and 48 weeks
Complete response, 2000 IU/ml
- Consider add on therapy and monitor q 3 months