cirrhosis Flashcards
(28 cards)
consequences of cirrhosis
1) block blood flow
2) impede hepatocyte perfusion
3) impair liver synthetic function (e.g. produce albumin)
aetiology of cirrhosis
1) alcohol
2) chronic Hep B & C
3) metabolic liver syndrome
- hemochromatomasis: body cannot process iron properly, accumulate
4) drug induced: isoniazid, methyldopa, amiodarone, diclofenac, methotrexate
progression of cirrhosis
1) compensated
- silent, asymptomatic, generally good QoL
2) decompensated
- 1st clinical symptoms: ascites, bleeding, encephalopathy, jaundice
- progression due to development of complications
- end stage: death or liver transplant
complications of cirrhosis
1) variceal bleeding
2) hepatic encephalopathy
3) cirrhotic cardiomyopathy
4) hepatopulmonary syndrome, portopulmonary syndrome
5) hepatorenal syndrome, AKI
6) ascites
general ascites
- accumulation of excess fluid in peritoneal cavity
- prone to complications: bacterial infection, nutrient & electrolyte imbalance, HRS
pathogenesis of ascites
structural component
- cirrhosis -> development of nodules surrounded by fibrotic material -> impede blood flow to liver
functional component
- increase in vascular tone (constriction) -> portal HTN -> sphlanic vasodilation (body detect increase in portal pressure)
- portal HTN -> increase in hydrostatic pressure
- lower albumin synthesis -> lesser albumin to maintain oncotic pressure -> lower intravascular oncotic pressure
- portal HTN + vasodilation -> underfilling & lesser aldosterone in liver -> further activation of RAAS -> further Na & H2O retention
- sphlanic vasodilation: lymph formation > lymph return
- end of day: fluid from portal circulation into peritoneal cavity
ascites related sypmtoms
1) dyspnoea: difficulty breathing cuz stomach distended
2) abdominal distention & pain
goals of therapy of ascites
1) control ascites
2) prevent/relieve ascites related symptoms
3) prevent life threatening conditions: SBP, HRS
treatment of ascites
1) abdominal paracentesis
- insert needle into abdominal cavity to aspirate ascitic fluid
- send ascitic fluid for analysis: cell count w differential, ascitic fluid total protein, signs for bacterial infection, serum ascitic albumin gradient (SAAG, SAAG >/= 11 means portal HTN)
2) dietary
- no alcohol
- Na retention (2000mg/day) to prevent further fluid retention
3) spironolactone (aldosterone agonist) 100mg + frusemide 40mg (loop) OM PO
- titrate every 3-5 days with 100:40 ratio until adequate natriuresis & weight loss
- frusemide lower risk of hyperkaliemia & prevent water retention
4) antibiotics for SBP: long term prophylaxis
5) tie rubber band/BP lowering meds to prevent bleeding
caution for treatment of ascites
1) no NSAIDs cuz worsen
2) no ACEi/ARB cuz risk of AKI and HRS
3) no need for fluid retention
- patient already in state of hypovolemia
- fluid retention further activate RAAS -> further water retention
general varices
- swelling of veins around stomach & oesophagus -> burst & bleed
- asymptomatic until burst
- diagnosis: endoscopy to find swollen veins around stomach & oesophagus
hepatic venous pressure gradient (HVPG)
. pressure difference between portal and central venin
. HVPG > 5 mmHg = portal HTN
. HVPG > 10 mmHg = variceal bleeding
coagulation defects
. decrease synthesis of procoagulation factors and naturally occurring anticoagulants, antithrombin, protein C & S
. increase in anticoagulant factor VII & von Willdebrand
- state of rebalanced hemostasis
- balance can be tipped anytime (risk of bleeding/thrombosis)
. thrombocytopenia common
diagnosis for cirrhosis - history taking
1) identifying symptoms
- asymptomatic: compensated
- initial symptoms (non-specific): fatigue, loss of appetite, weight loss
- signs of decompensated cirrhosis
2) determine cause of cirrhosis
- alcohol/drug abuse
- obesity, diabetes, NAFLD
- risk factors for Hep B & C
- personal/family history of immune/hepatic disease
- drugs that can cause cirrhosis
diagnosis for cirrhosis - history taking
1) identifying symptoms
- asymptomatic: compensated
- 1st clinical sypmtoms (non-specific): fatigue, weight loss, loss of appetitie
- signs of decompensated cirrhosis
2) determine cause of cirrhosis
- alcohol/drug abuse
- obesity, diabetes, NAFLD
- risk factor for Hep B & C
- personal/family history of immune/hepatic disease
- drug induced
diagnosis for cirrhosis - physical examination
1) jaundice: yellowing of skin/eyes
2) pruritus
3) plamar erythema
4) spider angiomata
5) hyperpigmentation
6) metabolic problems: gynaecomastia, testicular atrophy, axillary hair loss (lower oestrogen produced by liver)
diagnosis for cirrhosis - lab test
1) assessment
- LFT: hepatocellular/cholestatic
- coagulation test (PT, aPTT, INR): synthetic function of liver
- complete blood count + platelet
2) other causes of cirrhosis
- Hep B/C: serologic test for viral load
- autoimmune disease: antinuclear antibody titer
- haemochromasis: serum Fe & transferrin saturation, genotype testing (maybe)
- alpha-1 antitrypsin deficiency: alpha-1 antitrypsin levels & genotyping
diagnosis for cirrhosis - imaging test
1) ultrasound
- presence of varices, portal HTN, cirrhosis
2) elastography
- if ultrasound cmi
diagnosis for cirrhosis - tissue biopsy
if non-invasive cmi
general approach to treating cirrhosis
A) identify and eliminate (if possible) causes for cirrhosis
B) assess risk for variceal bleeding and benign pharmacological prophylaxis when indicated
. prophylactic endoscopic therapy
- for patients with high risk medium-large size varices
- for patients CI/intolerant of BB
- tie rubber band around varices
. variceal obliteration w endoscopic techniques
- for acute bleeding
C) monitor for patient for ascites + pharmacotherapy + paracentesis
- monitor for spontaneous bacterial peritonitis (SBP) & acute deterioration of clinical status
D) monitor for other causes of HE
- pharmacotherapy (diet, lactulose, ribavirin)
E) monitor for other liver complications
- HRS, pulmonary insufficiencies, endocrine dysfunction
levels of treatment of cirrhosis
1) primary prophylaxis
- compensated, HVPG >/= 10 mmHg
- presence of varices
- goal: prevent decompensation
2) treat acute variceal bleeding
- first blood, presence of variceal haemorrhage
- goal: control bleeding, prevent early rebleeding and death
3) secondary prophylaxis
- goal: prevent rebleeding
primary prophylaxis
. for high risk varices
- small + red wales + Child-Pugh score C
- medium/large irregardless of Child-Pugh
. BB
- MOA:
1) B1 blockade: lower cardiac output
2) B2 blockade: lower splanchnic blood flow
- carvedilol: alpha blockade as well to increase release of NO
- target HR: 55-60bpm
- caution
1) systolic BP needs to be > 90 mmHg
2) refractory/tense ascites
3) other complications (AKI, bleeding)
- SE: pulmonary bronchospasms, bradycardia
. endoscopy variceal ligation
- tie rubber band around varices
- goal: eradication (until no further ligation possible)
- dose: every 2-3 wks until eradication
treatment for acute variceal bleeding
1) stabilise patient
- ABC
- volume replacement: crystalloids, transfusion (Hb < 7)
2) drug therapy
. vasoactive drug
- splanchnic dilation -> lower blood flow -> reduce bleeding
- doesnt stop bleeding, still require ligation
- osteopresin: hyperglycemia, HTN, bradycardia
- vasopressin, somatostatin
. antibiotics
- prevent risk of infection
3) endoscopic techniques
- within 12 hrs of bleed
- confirm site of bleed, ligation
4) continue drug therapy
- vasoactive: 3-5 days
- antibiotics: 5-7 days
5) after continuing drug therapy
. controlled: secondary prophylaxis
. bleeding
- transjugular intrahepatic portosystemic shunt (TIPS): insert stent between portal and hepatic vein to relieve pressure off varices, don’t need secondary prophylaxis but refer for transplant
- balloon tamponade: insert & inflate balloon tamponade, last 24 hrs
secondary prophylaxis
. BB + EVL
. TIPS if above cmi
