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FFICM > Definitions, Tables, Facts - Gastro > Flashcards

Definitions, Tables, Facts - Gastro Flashcards

1
Q

Causes of acute liver failure

A 
Paracetamol
Mushroom poisoning
Drug induced - esctasty, metamphet, valproate, isnoniazind
Viral Hep - A, B, E
EBV, CMV, 
Ischaeamic hep
Budd Chiari
Wilsons
Post resection
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2
Q

Causes of chronic liver failure

A 
Viral B, C
Alcoholic liver disease
Non alcoholic steatohep
Haemachromatosis
Veno-occlusive disease
Right side failure??

Autoimmune - hepatitis, PSC, PBS

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3
Q

Defining trial of ALF

A

Coagulopathy
Jaundice (hyperbili)
Enceph (with raised ICP)

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4
Q

Defining features of chronic failure/cirrhosis

A 
Jaundice
Ascites and SBP
Variceal disease
Encephalopathy WITHOUT raised ICP
Hepatorenal synd
Risk of HCC
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5
Q

Define ALF

A

Rare
Life threatning disease
With risk of MOF and Death

Triad of
Encephalopathy
Coag
Jaundice

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6
Q

Timing of ALF

A

Onset from jaundice to enceph

Hyperacute - <7 days
Acute 7-28 days
Sub acute 5-12 weeks

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7
Q

Manifestations of ALF

A

Haemodynamic instability - high output vasodilation
AKI
Coagulapathy
Encephalopathy and coma (higher ammonia, higher risk of ICP)
Infection - sepsis

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8
Q

Grade encephalopathy

A

West Haven system

Grades 1 -4

1 - Lack of awareness, euphoria, anxiety, impaired addition

2 - Lethargy, apathy, suble persona change, impaired subtraction, inapprpriate

3 - Somnolence —> semi stupour, confusion, disorientation, responds to voice

4 - Coma

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9
Q

Management feaures

A 
Specialist input —> transfer to liver centre
Specific therapies —> NAC
Supportive - ABC and RRT
Manage enceph and ICP
Manage coag
Transplant
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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 decisions

Only if needing cover for procedures

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12
Q

Contra indictations to liver transplant in ALF

A

Severe cerebral oedema
Rising vasopressor needs
Uncontrolled sepsis
Major psych co-morbidity

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13
Q

Kings Criteria - Paracetamol

A

Ph< 7.3 (24 hours post admission AND following fluid resus)

OR

Grade 3 to 4 enceph
PT >100s
Cr>300

OR

Arterial lactate >3,5 at 4 hours
OR
>3 at 12 hours

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14
Q

Kings Criteria for non paracetamol

A

PT>100

OR

3 of

PT>50
Non hep A/B aetiology
Age <10 or >40
Bili > 300
Duration of jaudice prior to enceph > 7 days
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15
Q

Why would chronic liver failure get into ITU

A

Variceal haemorrhage
Management of encephalopathy
Renal/metabolic dysfunction
Ascites and hepato renal syndrome

Extra hepatic —> sepsis, resp failure

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16
Q

CVS changes in cirrhosis

A

Hyperdynamic circ —> low PVR, inc CO, decreased BP

Cirrhotic cardiomypoathy —> diastolic dysfunction

Alterations in hepatic/splanchnic flow —> hepatic resistance—> portal congestion, varices

Vascular 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 Score

MELD

UKELD

General 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

Bilirubin
Albumin
INR
Ascites
Enceph

A - 5-6
B - 7-9
C - >9

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19
Q

Feautres of MELD

A

Creatinine, INR and Bilirubin

Placed 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 used

Sepsis

Nephrotoxic agents - diuretics

HRS

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21
Q

Types of HRS

A

Type 1 - Higher mortality —> two fold increase in Cr in 2 weeks

Type 2 - Ascites refractory to dieurtetic therapy

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22
Q

Diagnosis of HRS

A

Cirrhosis with ascites

No improvement in creatinine after 2 days of diuretic withdrawel AND volume explansion
Albumin 1g/kg per day to a max of 100g

No shock

No current or recent nephrotoxics

Absence 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 Failure

Hypoalbuminaemia —> nephrotic, malnutirion

Peritonal disesae —> infection, ovarian Ca, mesothelioma

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25
Q

Consequences of ascites

A

Pressure —> ACS
Resp comprimise

SBP

Hepatic hydrothorax

HRS

PAIN

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26
Q

Treatment of ascites

A

Sodium restriction

Furosemide and spiro

Paracentesis
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

Benefits

Reduce intra abdominal pressure
Improved organ blood flow
Improved lung compliance
Patient comfort

Risk
Cutaenous or abdominal infection
Haemodyamic collapse
Renal dysfunction from low BP
Viscous 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 ALF
B - related to porto-systemic bypass
C - relates to cirrhosis

Difference 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,
Constipation
Electroylte disturbance
GI bleed
Meds - benzos, propanolol (portal hypertension)
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32
Q

Management of hepatic enceph

A

Lactulose
Phosphate enemas
LOLA
RRT - indicated in hyperammonia

Gut -
Rifaximin
TIPPS —> reduce calibre

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33
Q

Indications for Liver trasnplanbt

A 
ALF
HCC
Decompensated CLD
ACquired or chronic biliary disease
Metabolic disease
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34
Q

Peri-transplant issues

A

3 phases
Resection
Anhepatic phase
Reperfusion

Monitoring
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, coag

Hep artery thrombosis
Doppler at 24 huors
If weak, triple phase CT
Revascularise, or regraft

Venous 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.pylori
Peptic ulcer disease
NSAIDs

NG tube trauma
Erosive tumour
Vascular ectasia
Mallery Weiss
Angiodysplasia
Dieulafoy 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 
ABCDE
Early aggressive resus
Correct coag
Transfuse to 70
Risk stratify
PPI - Hong Kong
40
Q

Name the risk stratifying scores in non variceal bleeds

A

Glascow Blatchford Score

Rockall (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

Age
Shock
Co-morbidities
Diagnosis (mallery, other, GI cancer)
Evidence of bleeding
43
Q

Endotherapy options in non-variceal bleeds

A

Submucosal adrenlaine 1:10000

Biploar diathermy

Aluminium clipping

Haemostatic sprays

44
Q

Differences between stress ulcers and peptic

A

Stress more likely to appear in gastric fundus
Bleeding is a diffuse ooze
Often related to reduced splanchnic flow

45
Q

Risks or features associated with stress ulcer

A 
Mechanical vent for more than 48 hours
Coagulopathy
MOF
History of GI bleeds
Trauma or burns
Steroids
Renal 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 same
Sucrafate not as effective as either - second line

Sucrafate - inhibit digoxin and warfain, phenytoin
PPI - interact with anti-platelets

Risk 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 resuce

Pre - Non variceal - iv PPI, variceal —> terlipressin and Abx

Endo - Adrenaline, diathermy, clips. VERSUS endoscopic band ligation and sclerotherapy

Rescue - 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 value

Value at which haemorrhage occurs

A

Greater than 5mmHg

Greater than 10mmHg

50
Q

Places where varices can form

A 
Oesophagus —> retrograde splenic/long gastric vein flow
Gastric fungus
Rectum
Retroperitoneal
Abdominal wall
Liver bare area
51
Q

Grade of varices

A

3 grades

1 - Small, disappear on insufflation of oesophagus

2 - between 2 and 3

3 - Large varices, occluding lumen

52
Q

Management options of a variceal bleed

A

Antibiotics
Secondary infections
Prophylaxis reduces mortality
Cipro/ceftriaxone

Vasoactive
Terlipressin - constricts mesenteric arterioles

Sengstaken

Endoscopy
1 - no tx
2 and 3 beta blockade and band ligation

TIPPS

53
Q

Features of risk of rebleeding in varices

A

High Child-Pugh score

Increasing portal pressure

High risk endoscopic features

54
Q

Indications for TIPSS

A

Refractory variceal haemorrhage

Recurrent/refractory ascites

Hepatopulmonary syndrome

Hepatic hydrothorax

55
Q

Things to do before TIPSS

A

Doppler of portal / biliary system
Relieve biliary obstruction before TIPSS

Echo - RH —> TIPPS causes increased RV preload

EEG - TIPPS can cause HE (not really in practise)

56
Q

Describe a TIPPS

A

Venous access - RIJ

Catheter down SVC to hepatic vein

Portal vein identified —> needle directed from hep vein to portal vein

Guidewire and stent deployed

57
Q

Contra-indications to TIPSS

A

Severe tricuspid regurgitation

Severe pulmonary hypertension

CCF

58
Q

Complications of TIPPS

A

Access —> liver capsule rupture, biliary rupture and fistula, hepatic infarct

Stent —> thrombsis, migration

Shunt —> encephalopathy

59
Q

Define diarrhoea

A

WHO —> 3 or more loose or watery stools a day

BGS —> 200g a day

Bristol - 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 chloride

Inflammatory
Loss of muscles integrity
?bloody
IBD or infection — E. coli, shigella, salmonella

Dysmotile
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, clinicamycin

Long standing IBD

Intestinal surgery

PPI

Long hospital stay

Cancer, immunosuppresion, DM

63
Q

Diagnosis of C.diff

A

PCR —> colonisation/carrier

CDT (toxin B) —> active infection

Colonoscopy —> pseudomembranes

64
Q

Complications of c.diff

A

Bowel Perf

Toxic 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 iv

Vancomycin —-> oral only

Fidaxomicin —> non inferior to vanc but less SE

Faecal transplant

Surgery
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 abuse
ERCP
Gallstones
Trauma
Metabolic - hyperlipids, hyper algae Mia
Drugs - Azathioprine, steroids
Infection -CMV, mumps
68
Q

Diagnostic criteria of pacnreatitis

A

2 out of 3 of

Upper abdominal pain
Amylase of lipase >3 x upper range of normal
CT 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 complications

Mod - transient (<48hours) organ failure, OR complications

Severe - persistant organ failure or complication > 48 hours

71
Q

What are the local complications of pancreatitis

A

Necrosis of the pancreas or peri-panic tissue

CT and FNAC

72
Q

Systemic determinants of acute panc

A

Present and persistent organ failure

Sofa score >2

Transient —> less than 48 hours

73
Q

New panc definitions building on Atlanta

A

Mild - absence of necrosis and organ failure

Mod - sterile necrosis+/- transient failure

Severe - infected necrosis +/- persistent failure

Critical - infected AND persistent failure

74
Q

Pancreatitis scoring systems

A 
Ransom Score
Glasgow Imrie Score
APACHE II
SOFA
Balthazar
CT severity Index
75
Q

Describe Ransons score

A

Risk stratifies and predict mortality

Half 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 severe

0-2: 2%
3-4 15%
5-6 40%
7-8 100%

77
Q

What’s on the Glasgow Imrie Score

A 
Age
PaO2
WCC
Calcium
Urea
LDH
Albumin
Glucose

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 disease

Organ failure —> ARDS, effusions, atectasis
Shock
AKI
Ileus, metabolic issues, ACS

79
Q

Management principles of acute pancreatitist

A

Admit if Ranson >3

Supportive - 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 early

Antibiotics - no. Only in infected necrosis after FNAC.
Probiotics - harmful, increased ischaemia

ERCP - 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 infected

Infected —> positive bacterial/fungal/culture on FNAC
Gas in pancreatic bed on imaging

Tx —> 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 12mmHg

1 - 12-15
2 - 16-20
3 - 21-25
4 >25 mmHg

83
Q

How to measure IAP

A

Direct - laparoscopic port

Indirect - 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 closure

Medical - peritoneal dialysis, intra-abdominal infection, pancreatitis, intestinal oedema

Trauma

Burns

Obesity

87
Q

Consequences of ACS

A

Resp - splinting, reduced compliance, Adele tasks, decreased FRC. Hypoxaemia and infection

CVS - reduced venous return, SV and CO

Renal - reduced renal perf pressure at >15, anuria at >30

GI - hepatic dysfunction

Nervous - rising ICP

88
Q

Measuring energy requirements

A

Indirect calorimetry - gold standard.
Calories on basis of oxygen consumption. No really done

Measure CO2 productio - needs stable conditions, and over feed overestimates expenditure

Estimation - Scholfied eqn, Harris Benedict eqns.
By weight - 25kcal/kg

89
Q

Daily needs

A

Under 65 - 25kcal/kg, over 65, 20kcal/kg

Carbs - 60% of non protein calories
3.-4g/kg

Protein 1 to 1.5 g/kg
Increase for burns, trauma

Lipid 40% of noon protein
0.7-1.5G

Water 30mls/kg

Na 1-2mmol/kg
K 0.7-1
Ca 0.1
Mg 0.1
Phos 0.4
90
Q

Pros and con of enteral nutrition

A

Cheaper
Easier to do
Lower risk of infection
Gut protective (maintains integrity)

BUT

Needs functioning GI tract
?VAP
Less reliable delivery of energy

91
Q

Complications of PN

A

Access - needs a CVP and of that

Liver - hepatic steatosis, cholestasis, failure

Sepsis

Increased 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

FFICM (59 decks)

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