Gastro Flashcards
What is the primary factor leading to accumulation of ascities in patients with cirrhosis?
Splanchnic dilatation
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: clear yellow brown turbid milky 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?
MCS
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?
- 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 - Amiloride 10-20 mg OD if pt cannot tolerate spironolactone
what is the Tx fro severe and refractory ascites sue to liver cirrhosis?
- 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.
MOA Azathioprine?
Immunosuppressive drug.
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?
6
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:
without dysplasia
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)?
Colonoscopy
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 Endocrine Neurocrine Paracrine
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? Gastrin CCK Secretin Glucagon Gastric inhibitory peptide VIP Serotonin Substance P
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?
H/K/ATPase pump
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
Renal failure
Hypercalcaemia
Hyperlipidaemia
Vagotomy/SB resection
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.
Secretin provocation
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 Paraneoplastic dysmotlity Crohn's disease Achalasia of LES
What are the acute causes of pancreatitis?
Alcohol Gallstones Drugs Infection metabolic ERCP, post Ischaemia - rare, after prolonged Sx in prone position
Causes of chronic pancreatitis?
EtOH Genetic Duct obstruction Tropical Systemic disease AI Idiopathic
Have studies shown statins reduce risk of pancreatitis?
Yes.
Fibrates no.
How do you treat post ERCP pancreatitis?
NSAIDs
Acute Mesenteric ischaemia. Cause, Presentation, Ix, Tx?
Causes:
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
Presentation: >50 y Underlying cardiac disease Acute onset of severe ado pain AS, tender, pain out of proportion to examination
Ix:
Gold standard is mesenteric angiography
Tx:
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?
Intestinal angina.
Manifestation of mesenteric arthersclerosis.
Presentation:
Abdo pain 30 minutes after eating - due to diversion of small bowel blood flow to gut after eating.
Leads to sitophobia - fear of eating
Ix:
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.
Tx:
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.
Presentation: Fatigue Dry eyes Dry mouth Pruritis Jaundice and cutaneous hyperpigmentation rarely observed.
Ix:
High Bili
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.
Tx:
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.
Cease EtOH
Supportive care
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 score: Total Bilirubin Serum albumin INR Ascites Hepatic encephalopathy
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
Tx:
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 Small HCC Liver disease that would result in a 2 year mortality rate of >50% without liver tranplantation Diuretic resistnat ascites recurrent HE recurrent SBP recurrent or persistent GI haem Intractable cholangitis HPS Portopulmonary HT Metabolic syndromes curable with lvier tranplant e.g. falilial amyloidosis, urea cycle disorders, oxalosis
Most common indication for liver transplant?
Hepatoma
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.
Tx?
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?
NAFLD
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
False.
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?
Liver resection
However many patients are ineligible due to extent of tumour nor liver dysfuntion.
Non surgical candidates: Local tumour ablation TACE RTx Systemic Tx
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
False.
Do not benefit from ERCP with or without sphincterotomy.
What are the causes of pseudo-obstruction?
Hypothyroidism (bradycardia, hypothermia) Hypokalaemis Diabtes Uraemia Hypocalcaemia and hyperparathyroidism
Fistulae occur in 20-25% of Crohn’s pts. T/F
True
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?
35%
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
Renal impairment
1,25 (OH) Vitmain D - the bioactive form
C. difficile Tx?
Orla metronidazole
Oral Metro x 2
Oral vanc (can include IV metronidazole with vanc)
Faecal transplant, may need more than one infusion
Exclusions for faecal tranplant:
ICU
Immunocompromised
Mx of bloating in IBS?
Trial low FODMAPs diet:
Fermentable
Oligosachharides - frutans, galacto-oligosaccharides
Disacchardies e.g. lactose
Monosaccharides - fructose in excess of glucose
Polyols - sorbitol, mannitol, maltitol, xylitol and isomalt
peppermint oil
- antispasmotic and anti-flatulent effects
Iberogast (STW5)
- herbal agent containing extracts if the plant Iberis amara that increases motility.
Symptoms of IBS?
Abdo pain
Bloating
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?
Dx:
bubble study. TTE with microbuble contrast. Left heart will usually not have microbubbles unless there us a intracardiac or intrapulmonary shunt.
Tx:
Liver tranplant
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.
Dx:
Endoscopy and biopsies demonstrating > 15/hpf
Tx:
Trial pts on PPI first to see if response
1st line
- 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
Elimination diets
Endoscopic dilatation
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
Tx
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
Tx:
Prednisone
+/- Azathioprine
Hepatocellular derangement for the following: EtOH hepatitis Viral Drugs Iscahemic Hepatitis
EtOH
- AST> ALT (S for schooner)
Viral
-ALT > AST
Drugs
- temporal relationship is key
- Drugs can cause any pattern
- common are abx, NSAIDs, MTX, AZA, paracetamol
Ischaemic hepatitis
- 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 HR>90 Hb 30 CRP > 45 Severe inflammation on colonoscopy
Tx:
Colorectal surgical consult D3 onwards if no improvement with steroids
rescues drugs
- cyclosporin or
- infliximab
D5-6, no clinical response than colectomy in rescue failure
What is IgG4 related disease? What organs are affected?
Tx
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
Tx:
Steroids
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
Rifaximin.
MOA
Indication
AE
minimally absorbed oral antibiotic -> alteration of bacterial flora.
Indication:
Hepatic encephalopathy
- 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
Empirical Antibiotics
WH diuretics as dehydrated
What is the used in the prevention and Tx of encephalopathy?
Nutrition
- 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)?
Antibiotics, 60%
Doxy and tetracyclines in particular
Bisphosphonates - oral alendronate
NSAIDs
Which protease inhibitors are indicated in HCV Tx?
AE
Telepravir - anaemia, rash, pruritis Bocepravir - 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:
Endoscopic US
- 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?
Diagnostic: Choledocholithiasis pancreatic head assessment pancreatic cysts Oesophageal tumour staging Mediastinal masses
Therapeutic:
draining of pancreatic pseudocysts
drainage of biliary obstruction
Child Pugh Score classification of liver cirrhosis.
Components to score - Pour another beer at eleven
Classes
Prothrombin time Ascites Bilirubin mg/dL Albumin Encephalopathy
Class A 5-6 points:
Severenliver disease
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:
Small varices
No varices
Small varices
- yearly
No varices
- 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
True
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
Terlipresin. MOA
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?
AE?
Cyclasporine/Tacrolimus
- HTN, nephrotoxic, DM, lipids, tremor, Hirsutism, neurological
MMF:
diarrhoea
nausea
GI intolerance
Azathioprine: Hepatitis Pneumonitis/pancreatitis GI disturbance leukopenia
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
Biliary stricture
Renal/DM/Cosmetic
Post liver tranplant:
Late complications post transplant, > 3 months
Cancer:
PTLD - post tranplant lymphoproliferative disorder
Skin
Vascular- AMI
Renal (15% Cr >0.15, 5% Cr>0.25)
Recurrent disease
OP
Post liver tranplant:
When does acute rejection occur?
% of rejections
Tx
7-10 days
- cholestatic LFTs due to portal based inflammation
30%
Bolus steroids
Post liver tranplant:
When does chronic rejection occur?
% of rejections
Tx
Months to years post tx
- cholestatic LFTs due to vanishing bile duct syndrome
3%
Tx: increase immunosuppression, tacrolimus
may not be treatable
Recurrent disease post liver transplant. Recurrence rates for following: HCV HBV PSC PBC
HCV:
Universal recurrence
Mean time to recurrent cirrhosis is 7 years
HBV:
Without prophylaxis recurrence is very common
Long life antivirals with Entecavir
PSC:
30% develop recurrence
Morbidity common
Mortality rare
PBC:
Mortality rare
University of California, San Francisco criteria for liver transplant in HCC.
Single nodule
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?
20%
Which colonic poly has the highest potential for malignant transformation?
Villous
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?
Barrett’s oseophagus
What are the 4 types of Inherited pancreatits?
Hereditary: AD 80% penetrance recurrent mild attacks from > 5 yo Chromosoem 7q35 Trypsinogen gene PRSS1 Increased risk of cancer
SPINK1 mutation:
adolescents with pancreatitis and normal tripsinogen activity
1/4 pts have no FHX
CFTR gene mutation:
idiopathic chronic pancreatitis
male infertility
AI pancreatitis:
IgG4 disease, mild currents attacks, presents with mass
achalasia:
Manometry finding
Tx
Failure of LES relaxation with swallowing
Tx
Botulinum toxin
-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:
Manometric finding
Barium swallow
Tx
Dysphagia to solid and liquids, chest pain
Mannometry:
intermittent, 20% or more simultaneous contractions with high amplitude > 30 mmHg.
Non peristaltic contracions in response to swallowing.
Barium swallow:
Cork screw oesophagus
Tx:
CCB
Nut cracker oesophagus aka hypertensive peristalsis:
Presenation
Manometric finding
Tx
Asymptomatic
Manometric finding of average distal pressures > 220 mmHg during 10 x 5 ml liquid swallows.
Tx:
CCB
What is dumping syndrome?
Early vs. late
Tx
Caused by destruction or bypass of the pyloric sphincter
Occurs 20% of pts post pyloroplasty or distal gastrectomy.
Eraly: 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.
Late dumping:
Same symptoms as above a couple of hours after eating.
Due to hyoglycaemic following postprandial insulin peak.
Tx:
Dietary changes
Avoid carbs
When to suspect factitious diarrhoea? Presentation Electrolyte abnormality Appearance of colon Ix to confirm
Long standing blaoting and watery diarrhoea
Postural drop
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?
EUS
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?
Valve replacement CABS Cardiac transplantation Transcatheter aortic valve implantation (TAVI) Insertion of ventricular assist devices - cephazolin Add vanc if MRSA
Barrett’s oesophagus:
Changes on endoscopy
Tx
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.
Tx:
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
Barrett’s oesophagus.
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
Presbyoesophagus: What? Age group Presenatation Manometry
Manifestations of degenerating motor function in the aging oesophagus.
Pts > 80 yo
Asymptomatic but may complain of chest pain or dysphagia.
Mannometry: tertiary contractions (ranging from minor to severe) Decreased amplitude
Oesophageal ca:
Types
Types:
Adenocarcinoma - more common in western world, affects distal
Squamous cell - 90% overall, more common in developing world, affects proximal oesophagous.
M>F
RF:
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
Presentation:
Progressive solid food dysphagia most common and reduced oral intake.
Anaemia from GI bleeding.
Staging: Endoscopy diagnostic Endoscopic US- used for staging and accurate for establishing tumour stage CT for distant mets PET- changes staging in 20%
Staging: O = tumour in mucosa 1 = tumour in submucosa 2a = into muscle 2b = into lymph nodes 3 = beyond muscle 4 = mets
Tx:
Stage 0
-endoscopic mucosal ressection
Stage I
- 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
Stage IV:
Symptom control
- 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:
I-IV
Tx phase II and IV, when ALT is persis or intermittently elevated
Phase 1: immune tolerance HBsAg > 6 months HBeAg +ve Anti-HBe ab +ve ALT normal HBV DNA >= 20 000 Liver histo normal Mx: Montior q 3-6 months
Phase 2: Immune clearance
HBsAg > 6 months
HBeAg +ve
Spontaneous conversion to anti-HBe may occur
ALT persistently or intermittently elevated
HBV DNA >= 20 000
Liver histo moderate to severe heaptitis
Mx:
Tx
Phase 3: Immune control HbsAg > 6 months HbeAg -ve Anti-Hbe ab +ve ALT normal DNA 6 months HbeAg -ve Anti-Hbe ab +ve ALT elevated inter or persist DNA >2000 Liver histo mod to severe hep Mx: Tx
Tx for decompensated cirrhosis (HbeAg +ve or -ve) secondary to Hep B?
Screen for AFP and US for HCC q 6-12 months Treat early 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
- Treat
- 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
False. CI.
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
Hbe Ag +ve mother. Risk of chronic HCC to child?
90%
HbeAg -ve mother =
