liver cirrhosis Flashcards
cirrhosis definition
fibrosis(progressive scarring) of hepatic parenchyma forming nodules, which disrupt the hepatic function, restriced venous ouflow and portal hypertention
Scarring is accompanied by loss of viable hepatocytes (the functional cells of the liver).
Complications of cirrhosis and the associated portal hypertension include:
Cirrhosis is irreversible and leads to portal hypertension
* esophageal varices
* gastric varices
* ascites
* spontaneous bacterial peritonitis
* hepatic encephalopathy
* hepatorenal syndrome
Most common causes of Cirrhosis:
- Alcohol ingestion: decades of heavy driking more quickly develope in woemn thn men
- Viral hepatitis B & C infection: acute reversible hepatic inflammation chronic B OR C cause cirrhosis
both b and c transmitted through iv drugs and sexual route more common in B
normal portal vein pressure and portal hypertention
Normal portal vein pressure is 5 - 10 mm Hg
portal hypertension, which is a consequence of increased resistance to hepatic blood flow, occurs when portal pressure exceeds 10 - 12 mm Hg
Portal hypertension can result from
pre-hepatic, intrahepatic, or post-hepatic damage. The most common cause is intrahepatic damage.
symtoms of cirrhosis
The liver processes metabolic waste products for excretion; in cirrhosis, bilirubin (from the enzymatic breakdown of heme) can accumulate, causing jaundice (yellowing of the skin), scleral icterus (yellowing of the sclera), and tea-colored urine (urinary bilirubin excreted as urobilinogen).
Pathophysiology of portal HTN
Portal hypertension results from fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature.
Ascites
Ascites is the accumulation of fluid in the peritonium.
It is the most common condition associated with cirrhosis and indicates a poor prognosis
ascites pathophysiology
- cirrohtic changes and decrease in synthetic function lead to hypoalbumin
- low albumin, increase hydrostatic pressure and capillary permialbility allow fluid to leak from the vascular space into body tissues
- Lowered effective intravascular volume kidney perfusion cause activation of aldoestron, RAAS system which retain water and salt
varices definition
and caused by?
- varices are weak superficial vessels that product into gastric lumen and may rupture and bleed due to increase in pressure
- varices are most imp result of increase portal hypertention
- they are caused by devleopment of another route to blood flow to overcome resistance to drainage from the originating organ.
- Patients with cirrhosis are at risk for varices?
- varices location
- hemmorage and death rate in varices
- when portal pressure exceed the vena cava pressure by ≥ 12 mm Hg
- Varices may develop in the esophagus, stomach, and rectum to compensate for the increased blood volume.
- Hemorrhage from varices occurs in 25% to 40% of patients with cirrhosis
- Each episode of variceal bleeding carries a 25% to 30% risk of death.
.
hepatorenal syndrome
decrease in renal function due to cirrhosis that is not caused by intrusic renal disease
* if not treated fetal with mortility rate 50 % in 14 days
kidney compensation to HRS
The kidneys attempt to counteract the drop in renal perfusion by: RAAS activation which causes fluid retention and renal vasoconstriction in an attempt to increase renal blood flow.
Spontaneous Bacterial Peritonitis (SBP)
SBP is an acute bacterial infection of peritoneal (ascitic) fluid in the absence of intra-abdominal infection or intestinal perforation
Up to 30% of patients with ascites develop SBP
The most common bacteria isolated from patients with SBP are:
Gram-negative aerobes e.g. Escherichia coli, Klebsiella pneumoniae
Gram-positive pathogen e.g. Streptococcus pneumoniae.
Hepatic Encephalopathy (HE)
- In cirrhosis, there is impaired clearance of ammonia due to reduced conversion of ammonia to urea by the liver resulting in encephalopathy.
- Ammonia accumulates in the bloodstream because circulation bypasses the liver, preventing the metabolism of nitrogenous waste products.
- Ammonia is produced from protein catabolism and generated by bacteria in the gastrointestinal tract.
Hepatic Encephalopathy and CNS effect
Patients with HE commonly have elevated serum ammonia concentrations, but ammonia levels do not correlate with the degree of CNS impairment (because other toxins are involved).
factors that are involved in the development of HE
oesophageal bleeding, PUD, Excessive protein intake, Sedatives & Opioids.
Laboratory tests
of Cirrhosis
Hypoalbuminemia
Elevated prothrombin time
Thrombocytopenia
Increased bilirubin concentration
Elevated liver enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ -glutamyl transpeptidase (GGT)
Non-pharmacological Treatment
- Avoiding additional hepatic insult
- Lifestyle modifications
- abstain from alocol regardless of etiology is liver or not
- with ascitis: avoid sodium diet
- Hepatically metabolized medications avoided/ monitored due to risk of accumulation
- temporary protein restriction in HE
Non-pharmacological Treatment
device
Endoscopic band ligation (application of a stricture around the varix) is used to stop acutely bleeding varices.
Band ligation is the preferred endoscopic treatment and is effective in stopping acute variceal bleeding in up to 90% of patients.
Treatment goals for an acute bleeding are:
Volume resuscitation
Acute treatment of bleeding
Prevention of recurrence.
Risk factors for early re-bleeding are:
Age >60 years
Acute renal failure
Severe initial bleeding (defined as hemoglobin <8 mg/dL).
Risk factors for late re-bleeding are:
Severe liver failure
Continued alcohol abuse
Large variceal size
Renal failure
Hepatocellular carcinoma.
Hepatic Encephalopathy
treatment
Treatment is then aimed at reducing the amount of ammonia & nitrogenous products in the blood
Daily intake of 35 - 40 kcal/kg of body weight & protein intake of 1.2 - 1.5 g/kg body weight has been recommended for patients awaiting transplantation.
Hepatic Encephalopathy lactulose
dose?
route?
why lactulose?
Lactulose is effective for acute and chronic hepatic encephalopathy
* For acute encephalopathy, 30 - 45 mL every hour until evacuation, with the dose then titrated to give 2 - 4 loose stools daily and full recovery of consciousness
* Administration via NGT or rectal retention enema are options in patients who cannot take oral therapy
* Lactulose is the preferred for HE because: increases osmotic pressure in the colon and also undergoes fermentation by gut flora resulting in production of organic acids which lower colonic pH.
Neomycin & metronidazole for HE treatment
Neomycin & metronidazole (should be used for short period to avoid nephrotoxicity) are other options to reduce ammonia production by bacterial normal flora.
Neomycin to be used only if satisfactory results are not obtained with lactulose
If both agents fail as monotherapy, the combination of lactulose and neomycin may be considered
flumazenil in HE treatment
A theory was raised that false transmitters are the cause of encephalopathy. This has been demonstrated by functional improvement after administering flumazenil (a benzodiazepine antagonist).
Unfortunately, long-term benefit of flumazenil has not been demonstrated, and because of its parenteral administration, flumazenil is not an appropriate choice for clinical use.
Spontaneous Bacterial peritonitis (SBP) treatment
third-generation cephalosporin prophylactic antibiotic therapy during acute variceal bleeding.
why?
* bcz its cover against most commonly encountered pathogens.
* reduces in-hospital infections
* mortality in patients hospitalized for variceal bleeding
*
If SBP is suspected, empirical antibiotic therapy should be initiated with a broad-spectrum antibiotic after ascitic fluid collection, pending cultures and susceptibilities
Treatment options for varices:
- Splanchnic vasoconstrictors e.g. Somatostatin or octreotide
- Endoscopic Interventions:
* Sclerotherapy (injecting sclerosing agent e.g. ethanolamine into the varix)
* Band Ligation (placement of rubber bands around the varix)
how to stop bleeding in vercise
- Combination of vasoconstrictor and variceal ligation to manage bleeding is recommended.
- Balloon tamponade is used as a temporary measure (maximum of 24 hours) to stop massive bleeding.
- Surgical intervention: in patients who have failed repeated endoscopy and vasoactive drug therapy.
Goals of treatment of ascites are:
- Mobilize ascitic fluid
- Diminish abdominal discomfort, back pain, and difficulty in movement
- Prevent complications (bacterial peritonitis & respiratory distress).
Treatment should be done gradually to permit ascitic fluid to equilibrate with intravascular fluid
