Lecture 14 Liver Disease 2 Flashcards
What are varices?
collateral vessels that form at esophagus and stomach - as blood flows through them they become enlarged and they aren’t built to withstand the pressure
they may remain stable, or increase or decrease in size (depending on liver fxn)
with progression of liver disease and lack of tx these will increase in size and have increased tension of the vessel wall = increased probability of rupture and bleed
How do we screen/risk assess for varices?
correlated with disease severity (20% risk of mortality per episode)
Risk fx: depends on severity of liver disease, size and thickness of varices, hx of bleeding (rebleeding occurs at rate of 60%)
risk of variceal bleeding associated with Child-Pugh score,, bleeding can occur once portal venous pressure > 10 mmHg
Screening: all pt diagnosed with cirrhosis should be screened upon diagnosis with endoscopy ⇒ upper endoscopy with insertion of think flexible tube with camera ⇒ should repeat imaging every 1-3 years,, if varix present but <5 mmHg = prophylaxis with BBs
if varix present and >5 mmHg = BBs and EVL
How do varices present?
they are asymptomatic until they rupture and bleed
GI bleeding ⇒ hematemesis, melena, hematochezia
lightheadedness, bloating, tachycardia, decreased BP
BB usage for tx of varices (MOA, drugs/dose, monitoring)
MOA: reduction in portal blood flow,, Drugs: non-selective ones are preferred ⇒ B1 blockade = decreased CO = decreased portal perfusion, B2 blockade = unopposed alpha-adrenergic vasoconstriction = decreased splanchnic perfusion
Propranolol 10-20 mg BID (max 160-320/day), Nadolol 20-40 mg QD (max 80-160/day), Carvedilol 3.125 mg BID (max 6.25 BID)
titrate to a decreased HR by 25% or to 55-60 bpm while maintaining > 90 mmHg
Monitoring: HR, absence of bleeding, bradycardia, hypotension (>90 mmHg), hyponatremia, AKI
What are the methods of endoscopic intervention for varices?
Endoscopic variceal ligation (EVL) - using an endoscope provider uses suction to pull varices into scope, rubber bands deployed from scope which wrap the vein and prevent further bleeding
Endoscopic injection sclerotherapy (EIS) - more complications than EVL, not as effective as BB + EVL
What are ways to manage acutely bleeding varices?
Supportive: ABC - protecting airway, O2
blood transfusions, fresh frozen plasma, Vit K, platelets, fluids
Pharm: prophylactic antibiotics, octreotide IV infusions, somatostatin, vasopressin
Endoscopic: EVL, EIS
Surgical: transjugular intrahepatic portosystemic shunt
What is involved in the secondary prevention of variceal bleeding?
very high risk of recurrent bleeding after episode already happened
Tx: non-selective BBs and EVL if eligible (start as soon as hemodynamically stable after episode), can consider transjugular intrahepatic portosystemic shunt if pt has recurrent bleeding on BB + EVL
What is ascites?
accumulation of protein containing fluid in abdomen - fluid leaks from surface of liver and intestine and accumulates in peritoneal cavity due to activation of RAAS, reduced hepatic synthetic fxn leads to hypoalbuminemia which can further exacerbate fluid accumulation
Sx: ab distension, weight gain, dyspnea, early satiety
How is ascites managed?
Non-Pharm: low sodium ⇒ <2 g/day,, fluid restriction ⇒ <1.5 L/day
removal of fluid (paracentesis if respiratory distress)
Pharm: diuretics, spironolactone, furosemide,, Surgical: surgery to reroute blood flow, creation of transjugular intrahepatic portosystemic shunt, liver transplantation
Diuretics for tx of ascites (Drugs/dose, efficacy, AE/monitoring)
Drugs: spironolactone - 100-200 mg/day titrate Q5-7D to response ⇒ is 1st line tx
furosemide - 40 mg/day titrate by 20-40 mg/day to response ⇒ if adding to spironolactone add at ratio of 40:100 to prevent electrolyte disturbance,, Metolazone ‒ 2.5 mg/day ⇒ can be added if refractory to prior two
Amiloride - 5 mg/day ⇒ can be used instead of spironolactone if intolerable to AE like gyno, hyperkalemia
Efficacy: weight - aim for 1-1.5 kg/day loss in pt with peripheral edema and 0.5-1 kg/day if not
ab girth, urine output - should be around 500 mL/day
AE/Monitor: electrolytes (K+, Na+, Mg2+), SCr, BUN, BP
with furosemide and metolazone ⇒ uric acid, volume depletion
with spironolactone ⇒ gyno, hyperkalemia
What is spontaneous bacterial peritonitis?
infection of the ascitic fluid, can be life threatening, Sx: presence of ascites, fever, ad tenderness
may be caused by enterobacterales, less commonly strep species
Tx: 3rd-gen cephalosporin or ciprofloxacin F5-7D
Prophylaxis: TMP/SMX, norfloxacin, ciprofloxacin ⇒ these only used in high risk pt due to risk of resistance, consider in pt with GI bleed, CP score >/= 9, consider deprescribing PPIs
What is hepatic encephalopathy?
deterioration of brain fxn due to liver insufficiency or portosystemic shunt
occurs due to accumulation of gut-derived nitrogenous substances (ex. ammonia), due to liver fxn they aren’t removed and reach the CNS where they alter neurotransmission
Sx: changes in cognition, behaviour, consciousness, mild confusion to coma
is reversible
What are the different classifications of hepatic encephalopathy?
Type A: associated with Acute liver failure - has potential for cerebral edema and herniations
Type B: due to portal-systemic Bypass without associated intrinsic liver disease
Type C: occurs in pt with Cirrhosis - episodic ⇒ may be precipitated, spontaneous or recurrent
persistent ⇒ may be mild, severe, tx-dependent
minimal
What is asterixis?
clinical sign showing inability to maintain a sustained posture of muscle contraction
What are risk factors/triggers for hepatic encephalopathy?
constipation, portosystemic shunts, TIPS, portal vein thrombosis, infections (particularly SBP), AKI, electrolyte derangements (particularly hypokalemia), GI bleed, excess dietary protein, hypoxemia, hypercapnia
Lactulose for hepatic encephalopathy (MOA, dose, AE)
1st line, nonabsorbable fructose + galactose
MOA: removes nitrogenous waste products from GI tract through laxative action ⇒ further metabolized into short chain organic acids in colon which inhibits growth of ammonia producing bacteria
Dose: 45 mL Q1h PO until pt has bowel movement and clinical improvement, then maintain 15-45 mL 1-4 x/day, titrate to produce 2-3 loose bowel movements/day
AE: bloating flatulence, cramps, diarrhea
Rifaximin for hepatic encephalopathy (MOA, Dose, AE)
2nd line, use if refractory to lactulose or intolerable, or if recurrence of this, if added to lactulose remission is maintained better, is expensive though
MOA: reduces urease producing bacteria in intestines which decreases ammonia in blood,, Dose: 550 mg PO BID WITHOUT food
AE: not sig absorbed from GI tract
