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