Portal Hypertension Flashcards
Why does portal hypertension occur?
What drugs can be used to decrease the pressure across the portal system?
Increased intrahepatic resistance due to fibrosis leading to increased intrahepatic venou pressure
-> leads to back pressure into the portal system
Decreased bioavailability of vasodilators
Increased sensitivity to vasoconstrictors
Drugs:
-Non-selectibe beta-blockers= decreased intra-hepatic resistance and splanchnic blood flow and decrease CO to decrease the flow which can lead to decreased pressure across systemic circ
Eg Carvedilol/propranolol/nadolol
What are the possible complications of portal hypertension?
Variceal formation and haemorrhage
Ascites
Myocardial hypertrophy
Encephalopathy
Sepsis
-increased gut permeability due to increased production of vasodilators etc-> leads to translocation of bacteria
What is ascites and how might a patient present?
Besides portal hypertension, what are other causes of ascites?
Fluid within the peritoneal cavity
Px:
- pain and discomfort
- abdominal distension
- weight gain
- breathlessness
Other causes:
- malignancy
- HF
- nephrotic syndrome
- infection i.e. TB
What is the mechanisms underlying ascites?
Vasodilators released from splanchnic circulation in response to portal hypertension and travel to systemic circulation to reduce the effective circulating volume
Decreased circulating volume leads to RAAS activation and salt retention
Hydrostatic pressure and increased capillary permeability in abdo compilaries
Lymph formation> return
Leads to ascites and hyperdynamic circulation
What are the 2 different forms of ascites?
What is measured to differentiate between them?
Transudative= high gradient -> due to PHTN Exudative= low gradient-> NOT due to PHTN
[Serum albumin] - [ascites albumin] = SAAG
High gradient= >1.1g/dL
-means that there is greater concentration of albumin in serum than ascites
Low gradient= <1.1g/dL
-means there is similar level of albumin in serum to ascites= associated with secretory aetiology which leads to higher level of protein in ascitic fluid
How can ascites be managed?
Duiretics
- Loop diuretics (frusemide)
- aldosterone competitors (spironolactone)
Salt restriction
Paracentesis= ascitic tap or ascitis drain
Prophylactic antibiotics -> prevents against SBP
TIPS or transplant if refractory ascites
What are the possible complications of diuretiuc therapy?
Renal dysfunction
Hyponatraemia
Encephalopathy
-reduced circulating volume leads to decreased renal ammonia clearance
Muscle cramps
Electrolyte disturbance
Anti-androgenic SE with spironolactone metabolites
What is refractory ascites?
What are the 2 management options when a patient has refractory ascites?
Patient is requiring regular paracentisis in order to manage their ascites i.e. medical management not working
Transplant (should be considered before TIPS)
Transjugular-intrahepatic portosystemic shunt (TIPS)
-acts to decrease portal pressure by shunting blood from the portal vein to the hepatic vein
What is spontaneous bacterial peritonitis and why does it occur?
What organisms is it associated with?
Infection of ascitis fluid and peritoneal lining
Combination of:
- increased bowel permeability
- jejunal overgrowth and floral change
- reduced innate immunity
E coli
Klebsiella pneumoniae
Gram +ve cocci (staphylococcus + enterococcus)
How might someone with SBP present?
How are these patients managed?
- Can be asymptomatic-> low threshold for bacteria to culture in fluid
- Fever
- Abdo pain
- Deranged bloods i.e. WCC/CRP/Creatinine
- Ileus
- Hypotension
Ascitic culture to determine Abx sensitivity
IV Abx -> based on culture results
What is hepatorenal syndrome?
Why is associated with portal hypertension?
How are these patients managed?
Hypertension in portal system causes dilation of portal blood vessels leading to loss of circulating volume -> decreased blood flow to kidneys
Leads to hypotension in kidneys and activation of RAAS -> leads to renal vasoconstriction
I.e. leads to under perfusion of the kidneys
Consequently= RAPID deterioration in kidney function and can be fatal w/i week w/o liver transplant
Why do varices form and what are the common sites?
Back-pressure across the portal system leads to vessels at sites of anastomoses between systemic and portal veins to become swollen + tortuous
Gastro-oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein
How are stable varices managed?
Propranolol-> reduces the portal hypertension
Elastic band ligation
Injection of sclerosant (less effective)
TIPS
-if medical/endoscopic measures to reduce stable varices doesn’t work OR if bleeding varcies cannot be controlled in other ways
Why are bleeding varices a medical emergency?
High blood flow through the varices can mean that patient can exsanguinate very quickly once they start bleeding
How is someone present with bleeding varices managed?
A-E
Initiate major haemorrhage protocol (2222)
Resuscitation:
-Vasopressin analogues (Terlipressin) to cause vasocontriction and slow the bleeding
-Vit K and FFP to correct any coagulopathy
(IV Vit K or Beriplex)
-Cross match
-INR
-FBC
-Tranfuse with blood
-prophylactic broad spectrum antibiotics i.e. shown to reduce mortality
Urgent endoscopy
- elastic band ligation
- injection of sclerosant
- Sengstaken-Blakemore tube
