GI- the last hurdle Flashcards

1
Q

define acute hepatic failure

A

severe lver injury for fewer than 26 weeks duration. + encephalopathy + impaired synthetic function (inr > 1.5) - in a patient without chirrosis or preexisting liver disease.

high morbid + mortality but getting better as ICU gets better

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2
Q

causes of acute hepatic failure + signs and symptoms

A

hepatitis (viral OR drug induced)hypoxia induced liver injury, budd-chiari syndrome, veno-occlusive disease, mushroom ingestion etc etc etc - long list .

paracetamol toxicity is the most comon cause. A+E are the most common viruses

S+S: jaundice, fetor hepaticus- strong sweet breath
asterixis
drowsy + confused + slurred speech.

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3
Q

pathology of hepatic encephalopoathy

A

accumulation of glutammine 2’ to ammonia crossing the BBB.
accumulation of oxidative stress
depletion of ATP and GTP meaning astrocites swell and edema formation.

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4
Q

investigation and treatment of acute hepatic failure

A

Ix:
INR > 1.5
elevated bili, aminotransferases, thrombocytopenia + anaemia, hypoglycaemia, inc ammonia

could also show acute renal injury.

CT chest abdo pelvis.
USS +/- doppler can be considred if vascular concern.
Brain CT/MRI to rule out chronic aetiology of neuro manifestations.

Rx: supportive care + management of complications untill cause known.

if paracetamol- NAC of activated charcoal (if within 4 hrs)

rising aminotransferases + or worsening + coaulopathy indicates hepatic nercosis.

consider liver transplantation.

if grade 3 encephalopothy- intubate and sedate with minimal suctioning and stimulation.

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5
Q

discuss alcoholic hepatitis

A

inflmmation of the liver due to excessive intake of alcohol.- probably about 10 years worth (8-10 a day)

found in association with fatty liver.

can present acutely- after big binge - or chronically. - but within 60 days of a big one.

important- alcoholic steatohepatitis- is a histological diagnosis
alcoholic hepatitis is a clinical diag.

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6
Q

signs and symptoms + Ixof alcoholic hepatitis

A

mild- fever, RUQ pain, elevates aminotransferases- normalising with sobriety,

severe- jaundice, ascites, hepatic encephalopathy, coagulopathy.

Ix:
should have imaging to rule out obstruction + other liver disease.—–> USS

LFTs- inc AST: ALT 2:1 (opposite of other liver disorder)
Carbohydrate-deficient transferrin- most reliable marker for chronic alcoholism.
CRP is a good marker of alcoholic hepatitis.

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7
Q

management of alcoholic hepatitis

A

classify using child-pugh score.

abstinance + adequate nutritional support

short course pred 40mg/day 28 days.
- if no response in a week stop.
pentoxifylline
NAC
transplantation

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8
Q

discuss child-pugh score

A

measures bili
albumin
inr
ascites
encephalopathy

scores them all-
5-6 points- 100% one year survival- 85% 2 year

7-9- 80% one year survival- 60% 2 year

10-15- 45% one year- 35% 2 year

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9
Q

discuss chirrosis

A

chronic- irreversable liver damage.

hepatocites replaced with fibrosis/ scar tissue.

nodules of fibrosis form shrinking the liver.
structural change affects flow through the liver- increacing resistance in vessels + portal hypertension

ccauses: booze, drugs. inflammation (thiink Hep A + B etc)
metabolic (NAFLD, A1 antitrypsin)

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10
Q

signs and symptoms of Chirrosis + invstigations

A

hepatic jaundice
hepatomegaly
splenomealy
spider naevi- sign of inc oestrogen
palmer erythaema
gynecomastia + testicular atrophy.
bruising
ascites
asterixis (ammonia build up)

Ix:
LFT- raised ALT, AST, ALP
coagulation- raised prothrombin
fibroscan- helps assess the elasticitty of the liver. - ax degree of fibrosis

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11
Q

how to examine the extent of fibrosis in chirrosis and NAFLD

A

FIB4 score

age X AST/PLT X root ALT

less than 1.45- no chirrohsis
abover 3.25- chirrosis

between is inconclusive.

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12
Q

management of chirrosis + list some complications

A

meals every 2-3 hours
low sodium- minimise fluid retention
avoid alcohol
steroids in severe disease

in ascited- reduce sodium before giving spironolactone + then loop diuretics.

Complications-
malnutrition- no ability to store glycogen
cannot metabolise proteins
portal htn + splenomegaly

hepatocellular carcinoma
spontaneous bacterial peritoniti- caused by E.Coli —> ciproflaxin mx.

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13
Q

discuss chronic liver disease

A

progressive deterioration of liver function over more than 6 months.

chirrosis is the final stage of liver function decline.

continuous cycle of inflammation, destruction, regeneration- fibrosis and chirrosis.

caued by alcohol, NAFLD, genetic causes, autoimmune etc etc.

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14
Q

pathology of liver fibrosis

A

hepatic stellate cells - activated by liver injury, rtransform into myofibroblast like cells. – lay down extracellular matrix- collagen.

General signs and symptoms-
fatigue, anorexia, weight loss– or condition dependant

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15
Q

stages of hepatic encephalopathy

A

0- sub clinical with normal mental status

1- trivial lack of awareness- euphoria/ anxiety + shortenend attention span. impaied additino + subtraction

2- letargy, apathy, disorientation to time, inappropriate behaviour

3- semi stupor- responsive to stimuli, confusion + gross disorientation

4- coma

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16
Q

investigations of chronic liver disease + staging of chronic liver disease + preventative care.

A

CT/ USS

elastography. biopsy

Lab findings:
inc AST, ALT, ALP, GGT,– 2-3 x normal limit

bili conjugated > non conjugated

raised PT/INR

Stages:
hepatitis/ steatosis
fibrosis
chirrhosis
hepatocellular carcinoma

preventative care in CLD:
no alcohol
screen for Hep B+C
vaccinate A+B
avoid iron supplimentation
avoid over thr counter painkillers
maintain good lipid profile.

17
Q

discuss Non alcoholic fatty liver disease + its stages.

A

an umbrella term- covers liver disease without classical causes (alcohol, drug)

often diagnosed incidentally.
20-30% prevalence in western countries.

– generally the liver manifestation of metabolid syndrome

simple steatosis
statohepatitis
fibrosis
chirrosis
carcinoma

18
Q

risk factors for NAFLD + pathologenesis

A

obesity, diabetus, insulin resistance, metabolic syndrome.
1st degree relly with it.
arsenic exposure

accumulation of fat droplets due to insulin resistance in cytoplasm of hepatocites

excess delivery of free fatty acid and triglycerides to the liver + decreaced excretion leading to accumulation.
excess carbs is also a stimuus for denovo fatty acid synth in the liver.

multifactoral 2nd hit.
some infflammatory xdative stress is then applied to the already prone to injury liver.

hepatocites- baloon, aggregation, aPOPtosie and necrose.

19
Q

investigation of NAFLD

A

biopsy- more than 10% of hepatocites with fat droplets on biopsy- gold standard.
mildly elevated aminotransferases AST:ALT less than 1.

USS abdo

S+S: nausea, vom, jaundice, prrirotis, ascites, memory impairment, easy bleed, loss of appetite.
mild – moderate hepatomegaly.

20
Q

Rx of NAFLD + staging

A

lifestyle changes
3-5% weight loss, or 7-10% in NASH

survey for carcinoma
treat complications

Staging::
Grade1: steatosis up to 66%, occasional balooning zone 3 (most hypoxic) - mild/ no portal inflam

Grade 2: any degree of steatosis + obvious balooning, inflammation with polymorphs

Grade 3: panacinar steatosis, balooning, disarray inflam, polymorphs, chronic moderate portal inflam.