liver top tier Flashcards
liver failure =
types
key features
- Liver failure= liver loses ability to repair
- Acute failure = acute liver injury, previously normal liver
- Acute- on-chronic failure = liver failure as a result of decompensation of chronic liver disease
- Key features = encephalopathy, jaundice, coagulopathy, ascites
liver failure pathophysiology
- injury/death to hepatocytes
- Particular damage in zone 3 around central vein - least blood supply
- Neutrophils kill them
- Apoptosis (due to damage)
- Autoimmune
- Inflammation
- Fibrosis - cirrhosis is irreversible , but fatty liver damage is reversible
- Function decline
fatty liver disease pathophysiology
- two states + their features
- two causes
simple steatosis
- Hepatocytes balloon due to fat accumulation
- perivenular fibrosis (small amounts)
–> inflammation –>
steatohepatitis (= fatty liver disease)
- Hepatocytes balloon due to fat accumulation
- inflammation and fibrosis
- Hepatocytes accumulate cytoskeleton protein as unable to use it due to dysfunction (mallory bodies)
- Neutrophils come to kill em - hepatocyte necrosis
both reversible
this is the case for both causes : alcoholic and non-alcoholic
encephalopathy
- pathophysiology
wernickes’s
- pathophysiology inc cause
- triad presentation
- treatment
- Ammonia not cleared by the liver, builds up in the circulation and passes to the brain
- Astrocytes try to clear ammonia by converting glutamate → glutamine. Excess glutamine causes imbalance in osmotic pressure so fluid into cells → cerebral oedema
- Permanent brain damage as ammonia is neurotoxic (halts Krebs cycle, less ATP)
wernicke’s encephalopathy:
- Thiamine reserves exhausted - malnutrition, alcoholism
- Triad (most don’t have all 3)
- – Ataxia
- – Nystagmus (involuntary eye movements)/ ophthalmoplegia (paralysis / weakness of eye muscles)
- – Confusion
- Acute onset
- Reversible : treat with IV thiamine
causes of acute liver failure
Viral hepatitis +other infections eg, bacteria, parasites
- Rarely C (mainly chronic)
- Cytomegalovirus
- EBV
- Herpes
Drugs
- Drugs started recently are the relevant ones
- Paracetamol overdose is common
- Alcohol,
- antidepressant -amitriptyline
- NSAIDs
- ecstasy , cocaine
- Antibiotics -ciprofloxacin, doxycycline, erythromycin
Vascular
- Congestion (venous congestion from right sided heart failure or obstruction of the hepatic vein)
- Obstruction
chronic causes of liver failure
chronic triggers - acute deterioriation of chronic disease
- Viral hepatitis (not A/e - acute)
- Non alcoholic/ alcholic steatohepatitis
- Autoimmune
- Metabolic liver disease – Genetic - wilsons and A1AT deficiency
- Cancer - hepatocellular carcinoma
- Vascular
Chronic triggers (acute deterioration of chronic disease)
- Constipation
- Drugs
- Infection
- GI bleed
- Alcohol withdrawal
- Low Na, K, glucose
risk factors for non-alc liver failure (conditions, not patient characteristics)
Obesity
Diabetes
Hyperlipidemia
High risk of thrombosis
encephalopathy presentation and test for it
Test: count down in 7s form 100, count animal in a min, spell World backwards, dot-dot, draw 5 point star
1) Altered mood/behaviour, sleep disturbance
2) Drowsy, Confusion, slurred speech, +/- asterixis
3) incoherent, restless, asterixis, stupor
4) Coma
(Liver flap = asterixis – flapping tremor with wrist extended)
liver failure signs
Jaundice Encephalopathy Fever Hypertension Hyper-reflexia Fetor hepaticus = patient smells like pear drops Small liver
acute liver failure symptoms
Jaundice \+ Itching (bile salt collects under skin) \+ Unusual stool/urine Bleeding (coagulopathy) Myalgia GI/abdominal pain Lethargy malaise
chronic liver failure symptoms
Ascites is rare Spider naevus (red vessel skin mark, 5+ is pathological) Bruising Wasting Clubbing (nails) Palmar erythara - red hands jaundice is rare
paracetomol overdose - signs/investigations
Increased prothrombin time ALT/AST rly high - 1000 Metabolic acidosis Raised creatinine Hypoglycaemia -gluconeogenesis is inhibited
liver failure investigations
Bloods
- High bilirubin
- Low albumin
- Long prothrombin time, high INR
- LFTs = enzymes released from hepatocytes due to damage… High AST/ALT
- U/Es
- Low glucose - no gluconeogenesis
- Blood culture
- Lipids
ultrasound/MRI/CT
- look for biliary obstruction
- Nodular outline=cirrhosis
- tumours
- varices
- Liver/Spleen size
- Grades encephalopathy - electroencephalogram
- dopple
Microbiology- determine cause (is it infection)
- Ascites fluid
- Urine culture
- Blood culture
- Viral serology/ immunology - Look for antigen/ antibodies of virus, and autoantibodies
biopsy
liver failure management
- Symptom management
- – Eg analgesia - opiates paracetamol, be careful
- Treat underlying cause
- – N-acetyl cystine (NAC) for paracetamol poisoning - and glucose if hypoglycemic
- – Gallstone removal/crushing/dissolution
- – Cancer treatment
- – Antivirals
- Electrolyte balance, acid base balance
- Correct clotting defects - give IV platelets, vitamin K, plasma
- Liver transplant
- Careful with drug prescription (eg hypoglycaemic/constipation/blood thinned effects)
- Antihypertensives - not ACEi
- Proton pump inhibitors to reduce GI bleed risk
- Mannitol for raised intercranial pressure
- Monitor glucose and give IV if necessary
what drug is given for paracetamol poisoning
N-acetyl cystine (NAC
liver failure complications
Hypoglycaemia Bleeding (coagulopathy) Encephalopathy Varices Vulnerable to infection Malnutrition Impotence Amenorrhea
risk factors/ causes for pancreatitis
I GET SMASHED Idiopathic Gallstones (f) Ethanol - alcohol (m) Trauma (kids) Steroid Mumps Autoimmune Scorpion venom Hyperlipidemia ERCP - endoscopic retrograde cholangiopancreatography (following this) Drugs (eg corticosteroids, NSAIDs, diuretics)
Pregnancy
neoplasia/malignancy
pancreatitis pathophysiology
- Inflammation of pancreatic gland, initiated by acute injury
- Premature activation of pancreatic enzymes (eg amylase!) which cause pancreatic inflammation by enzyme mediated autodigestion
- Prematurely activated enzymes digest vessel walls in pancreas, causing leakage of fluid into tissues → oedema, inflammation, hypovolemia, potential haemorrhage
- Destruction of islet of langerhans → less beta cells → less insulin→ hyperglycaemia
- Lipolytic enzymes cause fat necrosis → skin discolouration (Cullen’s Grey turner’s local, bruise-like).
- The released fatty acids bind to Ca → white precipitates in fat and potentially hypocalcemia
Chronic = irreversible fibrosis
pancreatitis signs
Hypovolemia Tachycardia Jaundice Fever Dehydration Hypotension Cullen’s sign = periumbilical bruising Grey Turner’s sign = left flank bruising
pancreatitis symptoms
Oedema Pain - Upper abdominal / epigastric/central abdominal - Radiates to back - Relieved by sitting forward Anorexia nausea/ vomiting Tetany = intermittent muscle spasms (due to hypocalcaemia)
pancreatitis invesitgations
Bloods
- Inflammation - high wbc
- High glucose
- Raised serum amylase - 3x! But drops quite quickly
- Raised serum lipase
- Cultures -see if infection
Temperature
HR
BP
Urine
- Raised urine amylase
Imaging
- CXR/Ultrasound – Maybe gallstones (cause)
- CT/MRI- see necrosis extent
- CXR - excludes perforation differential diagnosis
how is pancreatitis scored
and why
Glasgow + Ranson /APACHE 2 scoring systems
Factors = age, neutrophils, calcium, glucose (obesity/conditions too in APACHE2 ) in first 48/24 h
for prognosis and treatment
pancreatitis management
- Nil by mouth. Nasogastric tube for supplements – reduce pancreatic enzyme release
- fluid replacement (Crystalloid / saline IV) - (lost in third-space sequestration = goes somewhere in body, not balancing with ECF)… to increase urine flow rate and stabilise vital signs (Temp, HR, breathing rate, BP)
- Analgesia - opiates
- Antibiotics - if proven infection (blood cultures)
- Surgical drainage of fluid collections/cysts
- Insulin - in glucose needs correcting (Take over liver functions)
- Calcium correction (liver function impaired)
- Cholecystectomy - may cause recurrent episodes
- Stop risk factors (alcohol, smoking)
- Enzyme replacement ? if chronic
- LMW heparin = DVT/PE prophylaxis
complications of pancreatitis
Hyperglycaemia Hemorrhage - shock Hypocalcemia Renal failure ARDS - acute respiratory distress Coagulopathy , thrombosis Fistulae
If bursts → digests insides = necrosis
Bile duct strictures
Steatorrhea
Low insulin- diabetes
how bad is alcoholic liver disease.
main cause of liver death
alcoholic liver disease risk factors/ cause
alcohol - do not need to be alcoholic / dependent
some genetic component
how does fibrosis cause portal hypertension
due to increased vascular resistance which is due to cirrhosis and architectural distortion (decreased outflow) and splanchnic vasodilation (increased inflow)
how does portal hypertension cause varices
New vessels form + small vessels vasodilate
Shunts
