Gastro Flashcards
(93 cards)
1
Q
Causes of acute liver failure
A
ParacetamolMushroom poisoningDrug induced - esctasty, metamphet, valproate, isnoniazindViral Hep - A, B, EEBV, CMV, Ischaeamic hepBudd ChiariWilsonsPost resection
2
Q
Causes of chronic liver failure
A
Viral B, CAlcoholic liver diseaseNon alcoholic steatohepHaemachromatosisVeno-occlusive diseaseRight side failure??Autoimmune - hepatitis, PSC, PBS
3
Q
Defining trial of ALF
A
CoagulopathyJaundice (hyperbili)Enceph (with raised ICP)
4
Q
Defining features of chronic failure/cirrhosis
A
JaundiceAscites and SBPVariceal diseaseEncephalopathy WITHOUT raised ICPHepatorenal syndRisk of HCC
5
Q
Define ALF
A
RareLife threatning disease With risk of MOF and DeathTriad of Encephalopathy Coag Jaundice
6
Q
Timing of ALF
A
Onset from jaundice to encephHyperacute - <7 daysAcute 7-28 daysSub acute 5-12 weeks
7
Q
Manifestations of ALF
A
Haemodynamic instability - high output vasodilationAKICoagulapathyEncephalopathy and coma (higher ammonia, higher risk of ICP)Infection - sepsis
8
Q
Grade encephalopathy
A
West Haven systemGrades 1 -41 - Lack of awareness, euphoria, anxiety, impaired addition2 - Lethargy, apathy, suble persona change, impaired subtraction, inapprpriate 3 - Somnolence —> semi stupour, confusion, disorientation, responds to voice4 - Coma
9
Q
Management feaures
A
Specialist input —> transfer to liver centreSpecific therapies —> NACSupportive - ABC and RRTManage enceph and ICPManage coagTransplant
10
Q
Features of treating enceph and ICP
A
1) remove ammonia Lactulose, LOLA, rifaxmine RRT
2) manage oedema Temperature Sedation 30 degree head up nursing Loose ties Optimise CPP
11
Q
Features of coagulapthy management in ALF
A
Routine correction - afffects PT and therefore transplant decisionsOnly if needing cover for procedures
12
Q
Contra indictations to liver transplant in ALF
A
Severe cerebral oedemaRising vasopressor needsUncontrolled sepsisMajor psych co-morbidity
13
Q
Kings Criteria - Paracetamol
A
Ph< 7.3 (24 hours post admission AND following fluid resus)ORGrade 3 to 4 encephPT >100sCr>300ORArterial lactate >3,5 at 4 hoursOR>3 at 12 hours
14
Q
Kings Criteria for non paracetamol
A
PT>100OR3 of
PT>50Non hep A/B aetiologyAge <10 or >40Bili > 300Duration of jaudice prior to enceph > 7 days
15
Q
Why would chronic liver failure get into ITU
A
Variceal haemorrhageManagement of encephalopathyRenal/metabolic dysfunction Ascites and hepato renal syndromeExtra hepatic —> sepsis, resp failure
16
Q
CVS changes in cirrhosis
A
Hyperdynamic circ —> low PVR, inc CO, decreased BPCirrhotic cardiomypoathy —> diastolic dysfunctionAlterations in hepatic/splanchnic flow —> hepatic resistance—> portal congestion, varicesVascular changes to other organs - pulmonary vasodilation, VQ mismatch Renal vasoconstriction —-> hepato renal
17
Q
Mortality scoring systems in CLD
A
Child-Pugh ScoreMELDUKELDGeneral systems - SOFA better than APACHE II in cirrhosis CLIF - SOFA
18
Q
Features of Child Pugh score
A
Graded 1-3 per category
BilirubinAlbuminINRAscitesEncephA - 5-6B - 7-9 C - >9
19
Q
Feautres of MELD
A
Creatinine, INR and BilirubinPlaced in eqn.UKELD , adds in sodium
20
Q
Why is renal dysfunction common in cirrhotivcd
A
Hypovolaemia —-> laxatives, blood loss from GI, sepsis, loop/spiro often usedSepsisNephrotoxic agents - diureticsHRS
21
Q
Types of HRS
A
Type 1 - Higher mortality —> two fold increase in Cr in 2 weeksType 2 - Ascites refractory to dieurtetic therapy
22
Q
Diagnosis of HRS
A
Cirrhosis with ascitesNo improvement in creatinine after 2 days of diuretic withdrawel AND volume explansion Albumin 1g/kg per day to a max of 100gNo shockNo current or recent nephrotoxicsAbsence of parenchymasl kidney disease (Proteinurial 4500mg/day, microhaematuria +/- abnormal renal US
23
Q
Management of renal dysfunction in HRS
A
Volume replacement HAS is colloid of choice 1g/kg load then 20-40g/day May bind cytokines Where sepsis predominates over HRS —> crystalloid
Vasoconstriction Terlipressin Splanchnic vasoconstriction —> renal perfusion increases and effective volume Avoid with high dose norad Can be given outside of ITU 1mg 4-6 hoursNon-responders - 50% RRT as bridge to trasnsplant Livefr support devices not in use
24
Q
Causes of ascites
A
Portal hypertension —> cirrhosis, Budd Chiari, Heart FailureHypoalbuminaemia —> nephrotic, malnutirionPeritonal disesae —> infection, ovarian Ca, mesothelioma
25
Consequences of ascites
Pressure —> ACS Resp comprimiseSBPHepatic hydrothoraxHRSPAIN
26
Treatment of ascites
Sodium restrictionFurosemide and spiroParacentesis Total abdominal paracent —> remove ALL fluid in a time frame Limited paracent —> remove to an end point (e.g. IAP <20mmHg)
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Benefits and risk of paracentesis
BenefitsReduce intra abdominal pressureImproved organ blood flowImproved lung compliancePatient comfort```RiskCutaenous or abdominal infectionHaemodyamic collapseRenal dysfunction from low BPViscous perf```
28
How long should an ascitic drain be left in
6 hours - infection risk
29
How much HAS after draining ascites
100mls of 20% for every 1-2 litres
30
Classification of hepatic encephalopathy (in terms of causes)Not the ALF criteria
A - related to ALFB - related to porto-systemic bypassC - relates to cirrhosisDifference from ALF is it happens for different reasons, and there is no rise in ICP
31
Causes of hep enceph in cirrhosis
```Sepsis,ConstipationElectroylte disturbanceGI bleedMeds - benzos, propanolol (portal hypertension)```
32
Management of hepatic enceph
LactulosePhosphate enemasLOLARRT - indicated in hyperammoniaGut - Rifaximin TIPPS —> reduce calibre
33
Indications for Liver trasnplanbt
```ALFHCCDecompensated CLDACquired or chronic biliary diseaseMetabolic disease```
34
Peri-transplant issues
3 phases Resection Anhepatic phase ReperfusionMonitoring Plasma lactate, normalises in first 6 hours Monitor coag and gluconeogeneis (rising plasma glucose)Immunosuppresion iv Abx and antifungal Peri op hydrocort/m-pred Enteral early - tacrolimus, cyclosporin, azathioprine If renal dysfunction - low dose tacrolimus and alternatives given basiluxamab
35
Post transplant complications
Primary Non Function Failure to start enzymatic procceses Transaminases dont normalise or rebound hyperbili, coagHep artery thrombosis Doppler at 24 huors If weak, triple phase CT Revascularise, or regraftVenous thrombosis```Biliary Issues Bile leak/obstruction Rising bili and ALP ERCP?? Beware biliary peritonitis, drain/repair biliary```Sepsis
36
Define upper GI haemorrhage
Any bleed from the pharynx to the ligament of Treitz
37
Causes of non-variceal bleeds
H.pyloriPeptic ulcer diseaseNSAIDs```NG tube traumaErosive tumourVascular ectasiaMallery WeissAngiodysplasiaDieulafoy lesions```
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Transfusion target in non variceal bleed
70g/dL reduced mort compared to 90
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Features of non variceal bleed management
```ABCDEEarly aggressive resusCorrect coagTransfuse to 70Risk stratifyPPI - Hong Kong```
40
Name the risk stratifying scores in non variceal bleeds
Glascow Blatchford ScoreRockall (but needs endoscopy to be done to complete the score)
41
Feautres of Glascow Blatchford Score
```On admission Blood Urea Hb (different scores for men and women) Systolic BP Other (pulse>100) Melanea Syncope Liver disese Heart failrue```
42
Features of Rockall Score
Score 0-3```AgeShockCo-morbiditiesDiagnosis (mallery, other, GI cancer)Evidence of bleeding```
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Endotherapy options in non-variceal bleeds
Submucosal adrenlaine 1:10000Biploar diathermyAluminium clippingHaemostatic sprays
44
Differences between stress ulcers and peptic
Stress more likely to appear in gastric fundusBleeding is a diffuse oozeOften related to reduced splanchnic flow
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Risks or features associated with stress ulcer
```Mechanical vent for more than 48 hoursCoagulopathyMOFHistory of GI bleedsTrauma or burnsSteroidsRenal failure```
46
Stress ulcer prophylaxis
Enteral feed early —> improves splanchnic flow```Drugs: PPI H2 antag Sucrafate - protect mucosa Antacids```PPI superior to H2, but mortality sameSucrafate not as effective as either - second lineSucrafate - inhibit digoxin and warfain, phenytoinPPI - interact with anti-plateletsRisk of nosocomial pneumonia through acid suppresion (poor evidence)Association between c.diff and acid suppresion
47
Compare non variceal to variceal treatments
Pre-endo, endoscopic, and resucePre - Non variceal - iv PPI, variceal —> terlipressin and AbxEndo - Adrenaline, diathermy, clips. VERSUS endoscopic band ligation and sclerotherapyRescue - Repeat, mesentertic angio and embolise, surgery VERSUS repeat, Sangstaken Blackmore, Stent, TIPPS, transplant
48
Normal portal pressure in a non-cirrhosis
Less than 5mmHg
49
Portal hypertension valueValue at which haemorrhage occurs
Greater than 5mmHgGreater than 10mmHg
50
Places where varices can form
```Oesophagus —> retrograde splenic/long gastric vein flowGastric fungusRectumRetroperitonealAbdominal wallLiver bare area```
51
Grade of varices
3 grades1 - Small, disappear on insufflation of oesophagus2 - between 2 and 33 - Large varices, occluding lumen
52
Management options of a variceal bleed
Antibiotics Secondary infections Prophylaxis reduces mortality Cipro/ceftriaxoneVasoactive Terlipressin - constricts mesenteric arteriolesSengstakenEndoscopy 1 - no tx 2 and 3 beta blockade and band ligationTIPPS
53
Features of risk of rebleeding in varices
High Child-Pugh scoreIncreasing portal pressureHigh risk endoscopic features
54
Indications for TIPSS
Refractory variceal haemorrhageRecurrent/refractory ascitesHepatopulmonary syndromeHepatic hydrothorax
55
Things to do before TIPSS
Doppler of portal / biliary system Relieve biliary obstruction before TIPSSEcho - RH —> TIPPS causes increased RV preloadEEG - TIPPS can cause HE (not really in practise)
56
Describe a TIPPS
Venous access - RIJCatheter down SVC to hepatic veinPortal vein identified —> needle directed from hep vein to portal veinGuidewire and stent deployed
57
Contra-indications to TIPSS
Severe tricuspid regurgitationSevere pulmonary hypertensionCCF
58
Complications of TIPPS
Access —> liver capsule rupture, biliary rupture and fistula, hepatic infarctStent —> thrombsis, migrationShunt —> encephalopathy
59
Define diarrhoea
WHO —> 3 or more loose or watery stools a dayBGS —> 200g a dayBristol - types 6 or 7
60
Types of diarrhoea
```Osmotic Can’t absorb osmotically active substances Mg, Bile salt, lactulose Malapbsorptiopn —> coeliac STOP WITH STARVATION```Secretory Increased secretion from mucosa Decreased absorption Infective diarrhoea and example —Cholera…secretes chlorideInflammatory Loss of muscles integrity ?bloody IBD or infection — E. coli, shigella, salmonellaDysmotile After ileus for example
61
What is c.diff
Gram negative anaerobe, spore forming
62
Risk factors for c.diff
Use of Abx —> penicillins cephalosporins, clinicamycinLong standing IBDIntestinal surgeryPPILong hospital stayCancer, immunosuppresion, DM
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Diagnosis of C.diff
PCR —> colonisation/carrierCDT (toxin B) —> active infectionColonoscopy —> pseudomembranes
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Complications of c.diff
Bowel PerfToxic mega colon —> colonic dilation >7cm```Fulminant colitis severe abdo pain, lactic acidosis hypovolaemia fever raised WCC```
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Tx of c.diff
Metronidazole —> oral or ivVancomycin —-> oral onlyFidaxomicin —> non inferior to vanc but less SEFaecal transplantSurgery colectomy
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Other infective agents in diarrhoea
```Inflammatory E.coli Shigella (cipro/ceftriaxone) Campylobacter (cipro) Salmonella (cipro)``` Cholera (cipro/doxy)Viral - Noro, rota, adeno ,CMV (ganciclovir)Parasite - giardia, entamoeba (metronidiazole)
67
Causes of acute pancreatitis
```Alcohol abuseERCPGallstonesTraumaMetabolic - hyperlipids, hyper algae MiaDrugs - Azathioprine, steroidsInfection -CMV, mumps```
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Diagnostic criteria of pacnreatitis
2 out of 3 ofUpper abdominal painAmylase of lipase >3 x upper range of normalCT findings
69
Types of CT finding of pancreatitis
Acute interstitial oedematous 85%Necrotic 15%
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Severity class of pancreatitis Atlanta
Mild - no organ failure, no local/systemic complicationsMod - transient (<48hours) organ failure, OR complicationsSevere - persistant organ failure or complication > 48 hours
71
What are the local complications of pancreatitis
Necrosis of the pancreas or peri-panic tissueCT and FNAC
72
Systemic determinants of acute panc
Present and persistent organ failureSofa score >2Transient —> less than 48 hours
73
New panc definitions building on Atlanta
Mild - absence of necrosis and organ failureMod - sterile necrosis+/- transient failureSevere - infected necrosis +/- persistent failureCritical - infected AND persistent failure
74
Pancreatitis scoring systems
```Ransom ScoreGlasgow Imrie ScoreAPACHE IISOFABalthazarCT severity Index```
75
Describe Ransons score
Risk stratifies and predict mortalityHalf on admission, half 24 hours later```Admission —> Age>55 AST>250 Glucose >11.2 WCC>16 LDH >350``````24 hours —>. Fall in Hct>10% PaO2<8 Base def >4 Fluid sequest > 6 litres Urea rise >1.8```
76
Ransons score indicates:
3 is severe0-2: 2%3-4 15%5-6 40%7-8 100%
77
What’s on the Glasgow Imrie Score
```AgePaO2WCCCalciumUreaLDHAlbuminGlucose```3 or more —> critical care
78
Complications of pancreatitis
```Local Necrosis Pseudocyst (>4 weeks) Peri-pancreatic collections (early) Pseudoaneurysm Mesenterinc vein thrombus```Systemic —> exacerbation of co-existing diseaseOrgan failure —> ARDS, effusions, atectasis Shock AKI Ileus, metabolic issues, ACS
79
Management principles of acute pancreatitist
Admit if Ranson >3Supportive - fluid resus, analgesia, organ support (drip and suck no more)Nutrition - no gut rest. Attempt NG feed. If not, try NJ. PN only for people who fail altogether Feed earlyAntibiotics - no. Only in infected necrosis after FNAC.Probiotics - harmful, increased ischaemiaERCP - gallstone pancreatitis In presence of cholangitis Cholestasis Predicted severe Do not do if mild.
80
Principles of necrotic pancreatitis, diag and management
Can be sterile or infectedInfected —> positive bacterial/fungal/culture on FNAC Gas in pancreatic bed on imagingTx —> iv. Broad spec (carbapenem) Wait for necrosis to wall off (4 weeks) Percutaneous or endoscopic drainage OR minimally invasive necrosectomy Whipples…
81
Normal IAP
5-7mmHg
82
Define and grade IAH
Greater than 12mmHg1 - 12-152 - 16-203 - 21-254 >25 mmHg
83
How to measure IAP
Direct - laparoscopic portIndirect - ballon tipped catheter in stomach or bladder attached to transducer Zero vesicular transducer to pubic symph
84
APP eqn
APP = MAP - IAP
85
Define ACS
IAP >20mmHg with associated organ failure +/- an APP<60
86
Causes of ACS
Surgical - haemorrhage, collection, ileus, large hernia, tight abdominal closureMedical - peritoneal dialysis, intra-abdominal infection, pancreatitis, intestinal oedemaTraumaBurnsObesity
87
Consequences of ACS
Resp - splinting, reduced compliance, Adele tasks, decreased FRC. Hypoxaemia and infectionCVS - reduced venous return, SV and CORenal - reduced renal perf pressure at >15, anuria at >30GI - hepatic dysfunctionNervous - rising ICP
88
Measuring energy requirements
Indirect calorimetry - gold standard. Calories on basis of oxygen consumption. No really doneMeasure CO2 productio - needs stable conditions, and over feed overestimates expenditureEstimation - Scholfied eqn, Harris Benedict eqns. By weight - 25kcal/kg
89
Daily needs
Under 65 - 25kcal/kg, over 65, 20kcal/kgCarbs - 60% of non protein calories 3.-4g/kgProtein 1 to 1.5 g/kg Increase for burns, traumaLipid 40% of noon protein 0.7-1.5GWater 30mls/kg```Na 1-2mmol/kgK 0.7-1Ca 0.1Mg 0.1Phos 0.4```
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Pros and con of enteral nutrition
CheaperEasier to doLower risk of infectionGut protective (maintains integrity)BUTNeeds functioning GI tract?VAPLess reliable delivery of energy
91
Complications of PN
Access - needs a CVP and of thatLiver - hepatic steatosis, cholestasis, failureSepsisIncreased hyperglycaemia
92
EN versus PN evidence
CALORIES - no diff in 30 day mort. EN, more vomiting and hypo
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Timing of nutrition
Early less than 48 hours, concenus is start early
