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Pete FFICM SOE/OSCE > Gastro > Flashcards

Gastro Flashcards

1
Q

Causes of acute liver failure

A 
ParacetamolMushroom poisoningDrug induced - esctasty, metamphet, valproate, isnoniazindViral Hep - A, B, EEBV, CMV, Ischaeamic hepBudd ChiariWilsonsPost resection
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2
Q

Causes of chronic liver failure

A 
Viral B, CAlcoholic liver diseaseNon alcoholic steatohepHaemachromatosisVeno-occlusive diseaseRight side failure??
Autoimmune - hepatitis, PSC, PBS
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3
Q

Defining trial of ALF

A

CoagulopathyJaundice (hyperbili)Enceph (with raised ICP)

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4
Q

Defining features of chronic failure/cirrhosis

A 
JaundiceAscites and SBPVariceal diseaseEncephalopathy WITHOUT raised ICPHepatorenal syndRisk of HCC
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5
Q

Define ALF

A

RareLife threatning disease With risk of MOF and DeathTriad of Encephalopathy Coag Jaundice

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6
Q

Timing of ALF

A

Onset from jaundice to encephHyperacute - <7 daysAcute 7-28 daysSub acute 5-12 weeks

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7
Q

Manifestations of ALF

A

Haemodynamic instability - high output vasodilationAKICoagulapathyEncephalopathy and coma (higher ammonia, higher risk of ICP)Infection - sepsis

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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

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9
Q

Management feaures

A 
Specialist input —> transfer to liver centreSpecific therapies —> NACSupportive - ABC and RRTManage enceph and ICPManage coagTransplant
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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
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11
Q

Features of coagulapthy management in ALF

A

Routine correction - afffects PT and therefore transplant decisionsOnly if needing cover for procedures

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12
Q

Contra indictations to liver transplant in ALF

A

Severe cerebral oedemaRising vasopressor needsUncontrolled sepsisMajor psych co-morbidity

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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

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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
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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

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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

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17
Q

Mortality scoring systems in CLD

A

Child-Pugh ScoreMELDUKELDGeneral systems - SOFA better than APACHE II in cirrhosis CLIF - SOFA

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18
Q

Features of Child Pugh score

A

Graded 1-3 per category

BilirubinAlbuminINRAscitesEnceph
A - 5-6B - 7-9 C - >9
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19
Q

Feautres of MELD

A

Creatinine, INR and BilirubinPlaced in eqn.UKELD , adds in sodium

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20
Q

Why is renal dysfunction common in cirrhotivcd

A

Hypovolaemia —-> laxatives, blood loss from GI, sepsis, loop/spiro often usedSepsisNephrotoxic agents - diureticsHRS

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21
Q

Types of HRS

A

Type 1 - Higher mortality —> two fold increase in Cr in 2 weeksType 2 - Ascites refractory to dieurtetic therapy

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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

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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 hours
Non-responders - 50% RRT as bridge to trasnsplant Livefr support devices not in use
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24
Q

Causes of ascites

A

Portal hypertension —> cirrhosis, Budd Chiari, Heart FailureHypoalbuminaemia —> nephrotic, malnutirionPeritonal disesae —> infection, ovarian Ca, mesothelioma

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25
Q

Consequences of ascites

A

Pressure —> ACS Resp comprimiseSBPHepatic hydrothoraxHRSPAIN

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26
Q

Treatment of ascites

A

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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27
Q

Benefits and risk of paracentesis

A

BenefitsReduce intra abdominal pressureImproved organ blood flowImproved lung compliancePatient comfort

RiskCutaenous or abdominal infectionHaemodyamic collapseRenal dysfunction from low BPViscous perf
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28
Q

How long should an ascitic drain be left in

A

6 hours - infection risk

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29
Q

How much HAS after draining ascites

A

100mls of 20% for every 1-2 litres

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30
Q

Classification of hepatic encephalopathy (in terms of causes)Not the ALF criteria

A

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

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31
Q

Causes of hep enceph in cirrhosis

A 
Sepsis,ConstipationElectroylte disturbanceGI bleedMeds - benzos, propanolol (portal hypertension)
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32
Q

Management of hepatic enceph

A

LactulosePhosphate enemasLOLARRT - indicated in hyperammoniaGut - Rifaximin TIPPS —> reduce calibre

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33
Q

Indications for Liver trasnplanbt

A 
ALFHCCDecompensated CLDACquired or chronic biliary diseaseMetabolic disease
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34
Q

Peri-transplant issues

A

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

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35
Q

Post transplant complications

A

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
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36
Q

Define upper GI haemorrhage

A

Any bleed from the pharynx to the ligament of Treitz

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37
Q

Causes of non-variceal bleeds

A

H.pyloriPeptic ulcer diseaseNSAIDs

NG tube traumaErosive tumourVascular ectasiaMallery WeissAngiodysplasiaDieulafoy lesions
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38
Q

Transfusion target in non variceal bleed

A

70g/dL reduced mort compared to 90

39
Q

Features of non variceal bleed management

A 
ABCDEEarly aggressive resusCorrect coagTransfuse to 70Risk stratifyPPI - Hong Kong
40
Q

Name the risk stratifying scores in non variceal bleeds

A

Glascow Blatchford ScoreRockall (but needs endoscopy to be done to complete the score)

41
Q

Feautres of Glascow Blatchford Score

A 
On admission	Blood Urea	Hb (different scores for men and women)	Systolic BP	Other (pulse>100)			Melanea			Syncope			Liver disese			Heart failrue
42
Q

Features of Rockall Score

A

Score 0-3

AgeShockCo-morbiditiesDiagnosis (mallery, other, GI cancer)Evidence of bleeding
43
Q

Endotherapy options in non-variceal bleeds

A

Submucosal adrenlaine 1:10000Biploar diathermyAluminium clippingHaemostatic sprays

44
Q

Differences between stress ulcers and peptic

A

Stress more likely to appear in gastric fundusBleeding is a diffuse oozeOften related to reduced splanchnic flow

45
Q

Risks or features associated with stress ulcer

A 
Mechanical vent for more than 48 hoursCoagulopathyMOFHistory of GI bleedsTrauma or burnsSteroidsRenal failure
46
Q

Stress ulcer prophylaxis

A

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
Q

Compare non variceal to variceal treatments

A

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
Q

Normal portal pressure in a non-cirrhosis

A

Less than 5mmHg

49
Q

Portal hypertension valueValue at which haemorrhage occurs

A

Greater than 5mmHgGreater than 10mmHg

50
Q

Places where varices can form

A 
Oesophagus —> retrograde splenic/long gastric vein flowGastric fungusRectumRetroperitonealAbdominal wallLiver bare area
51
Q

Grade of varices

A

3 grades1 - Small, disappear on insufflation of oesophagus2 - between 2 and 33 - Large varices, occluding lumen

52
Q

Management options of a variceal bleed

A

Antibiotics Secondary infections Prophylaxis reduces mortality Cipro/ceftriaxoneVasoactive Terlipressin - constricts mesenteric arteriolesSengstakenEndoscopy 1 - no tx 2 and 3 beta blockade and band ligationTIPPS

53
Q

Features of risk of rebleeding in varices

A

High Child-Pugh scoreIncreasing portal pressureHigh risk endoscopic features

54
Q

Indications for TIPSS

A

Refractory variceal haemorrhageRecurrent/refractory ascitesHepatopulmonary syndromeHepatic hydrothorax

55
Q

Things to do before TIPSS

A

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
Q

Describe a TIPPS

A

Venous access - RIJCatheter down SVC to hepatic veinPortal vein identified —> needle directed from hep vein to portal veinGuidewire and stent deployed

57
Q

Contra-indications to TIPSS

A

Severe tricuspid regurgitationSevere pulmonary hypertensionCCF

58
Q

Complications of TIPPS

A

Access —> liver capsule rupture, biliary rupture and fistula, hepatic infarctStent —> thrombsis, migrationShunt —> encephalopathy

59
Q

Define diarrhoea

A

WHO —> 3 or more loose or watery stools a dayBGS —> 200g a dayBristol - types 6 or 7

60
Q

Types of diarrhoea

A 
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
Q

What is c.diff

A

Gram negative anaerobe, spore forming

62
Q

Risk factors for c.diff

A

Use of Abx —> penicillins cephalosporins, clinicamycinLong standing IBDIntestinal surgeryPPILong hospital stayCancer, immunosuppresion, DM

63
Q

Diagnosis of C.diff

A

PCR —> colonisation/carrierCDT (toxin B) —> active infectionColonoscopy —> pseudomembranes

64
Q

Complications of c.diff

A

Bowel PerfToxic mega colon —> colonic dilation >7cm

Fulminant colitis	severe abdo pain, lactic acidosis	hypovolaemia	fever	raised WCC
65
Q

Tx of c.diff

A

Metronidazole —> oral or ivVancomycin —-> oral onlyFidaxomicin —> non inferior to vanc but less SEFaecal transplantSurgery colectomy

66
Q

Other infective agents in diarrhoea

A 
Inflammatory	E.coli	Shigella (cipro/ceftriaxone)	Campylobacter (cipro)	Salmonella (cipro)
Cholera (cipro/doxy)Viral - Noro, rota, adeno ,CMV (ganciclovir)Parasite - giardia, entamoeba (metronidiazole)
67
Q

Causes of acute pancreatitis

A 
Alcohol abuseERCPGallstonesTraumaMetabolic - hyperlipids, hyper algae MiaDrugs - Azathioprine, steroidsInfection -CMV, mumps
68
Q

Diagnostic criteria of pacnreatitis

A

2 out of 3 ofUpper abdominal painAmylase of lipase >3 x upper range of normalCT findings

69
Q

Types of CT finding of pancreatitis

A

Acute interstitial oedematous 85%Necrotic 15%

70
Q

Severity class of pancreatitis Atlanta

A

Mild - no organ failure, no local/systemic complicationsMod - transient (<48hours) organ failure, OR complicationsSevere - persistant organ failure or complication > 48 hours

71
Q

What are the local complications of pancreatitis

A

Necrosis of the pancreas or peri-panic tissueCT and FNAC

72
Q

Systemic determinants of acute panc

A

Present and persistent organ failureSofa score >2Transient —> less than 48 hours

73
Q

New panc definitions building on Atlanta

A

Mild - absence of necrosis and organ failureMod - sterile necrosis+/- transient failureSevere - infected necrosis +/- persistent failureCritical - infected AND persistent failure

74
Q

Pancreatitis scoring systems

A 
Ransom ScoreGlasgow Imrie ScoreAPACHE IISOFABalthazarCT severity Index
75
Q

Describe Ransons score

A

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
Q

Ransons score indicates:

A

3 is severe0-2: 2%3-4 15%5-6 40%7-8 100%

77
Q

What’s on the Glasgow Imrie Score

A 
AgePaO2WCCCalciumUreaLDHAlbuminGlucose
3 or more —> critical care
78
Q

Complications of pancreatitis

A 
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
Q

Management principles of acute pancreatitist

A

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
Q

Principles of necrotic pancreatitis, diag and management

A

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
Q

Normal IAP

A

5-7mmHg

82
Q

Define and grade IAH

A

Greater than 12mmHg1 - 12-152 - 16-203 - 21-254 >25 mmHg

83
Q

How to measure IAP

A

Direct - laparoscopic portIndirect - ballon tipped catheter in stomach or bladder attached to transducer Zero vesicular transducer to pubic symph

84
Q

APP eqn

A

APP = MAP - IAP

85
Q

Define ACS

A

IAP >20mmHg with associated organ failure +/- an APP<60

86
Q

Causes of ACS

A

Surgical - haemorrhage, collection, ileus, large hernia, tight abdominal closureMedical - peritoneal dialysis, intra-abdominal infection, pancreatitis, intestinal oedemaTraumaBurnsObesity

87
Q

Consequences of ACS

A

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
Q

Measuring energy requirements

A

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
Q

Daily needs

A

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
90
Q

Pros and con of enteral nutrition

A

CheaperEasier to doLower risk of infectionGut protective (maintains integrity)BUTNeeds functioning GI tract?VAPLess reliable delivery of energy

91
Q

Complications of PN

A

Access - needs a CVP and of thatLiver - hepatic steatosis, cholestasis, failureSepsisIncreased hyperglycaemia

92
Q

EN versus PN evidence

A

CALORIES - no diff in 30 day mort. EN, more vomiting and hypo

93
Q

Timing of nutrition

A

Early less than 48 hours, concenus is start early

Pete FFICM SOE/OSCE (199 decks)

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