Acute and Chronic Liver Failure Flashcards
Liver Chemistries
AST
ALT
GGT
Alk Phosphate
Bilirubin (direct and indirect)
INR
platelets
albumin
AST and ALT: released when the hepatocytes are damaged, thus a marker picked up to indicated liver damang
ALT is more specific to the liver than AST, but both are from other tissues as well
AST: think more along the lines of alcoholic disease in the liver
Alk Phophaste: when elevated on its own you want to consider gallbladder disease in relation to the liver
- alk phoasphate is not specific to jsut the liver though, so getting a GGT will help specific if the alk phos is high and the GGT is high then its more liekly a liver cause (vs. the bone or placenta, etc.)
Bilirubin
indirect (unconjugated bilirubin) : is associated with an increased in hemolysis –> a pre-liver issue where there is som uch unconjugated (pre-liver conjugation) that the lvier cant keep up
Direct (conjugated bilirubin): is associated with an intra-hepatic issue if elevated or there is an issue–> there is a buildp buecase no enoguh of it is being excreted through the bile (problem in the liver and the ducts)
Albumin: made in the liver ONLY; thus a god marker of synthetic liver function (can order this)
INR: is a good read on the livers ability to create and produce clotting factors –> if the liver cannot produce these; there will be a decrease in them; leading to prolonged bleeding which is reflected in an increase in INR
Platelets: are most commonly assocaited with the liver function; if there is a decrease in platelets (think a result of decrease TPO which is made in the liver) therefore you have a problem with the liver
Acute Liver Injury
lab patterns for…
- hepatocellular
- cholestatic
- isolated hyperbilirubinemia
Hepatocellular
- disproportinately elevated AST/ALT when compared to how elevated the alk phosphate is elevated
Cholestatic
- a disproportiate elevation in the alk. phos more than the AST/ALT elevation
Isolated Hyperbili
think hemolysis due to elevated bili but no changes with alt/ast and alk phosphate
can also have mixed disease states
Cirrhotic liver: low albumin, high INR, low platelets with any of the above
Acute Liver Failure
- Etiology
- Symptoms
- Diagnosis
Treatment
Etiology
- can be a result of a wide variety of liver injures (most commonly think acetominophen toxicity, but shock/sepsis, hepatitis, fatty liver, etc.)
- the result is liver fulminant: aka severe, sudden deterioration of the liver
- fulminant: symptoms occuring within 8 weeks of the acute liver disease
- subfulminent: occuring > 8 weeks after acute liver disease onset
- prognosis of this is POOR; most need a transplant
Symptoms
- GI (N/V)
- Jaundice
- pruritus
- lethargy
- fatigue
- neuro: confusion, disodered sleep, coma, unresponsive
- asterixis on exam!!!
- the key symptoms: hepathic encephalopathy (AMS), INR > 1.5 & elevated AST/ALT = for dx.
Diagnosis
- the INR > 1.5, AST/ALT elevated, with Hepatic encephalopathy is the key
other labs
- elevated bilirubin
- low platlets
- elevated ast/alt (Markedly)
- elevated INR
Treatment
- ICU admission for intubation if the HE continues
- monitor for worsening liver failure
- treat complications or underlying
- nutrtional support
- transplant list
Chronic Liver Disease (Cirrhosis)
Etiology
Causes (of cirrhosis)
Symptoms
Etiology
- cirrhosis is a late stage finding in hepatic fiberosis; irreversible damage
- fiberosis of the hepatocytes leads to interhepatic vascualr resistance (the blood cant travel) and then overtime the liver fails to work
Causes of Cirrhosis
- Most Common = chronic viral hepatits (in other countries) , alcohol-associated liver disease, hemochromatosis, NAFLD
- others include = autoimmue hepatitis, Wilson’’s disease, A1A deficiency, neoplasms of the liver, Budd-Chiari
Symptoms
- nonspecific: anoerxia, weight loss, weakness, and fituge
- puritis, signs of upper GI bleeding (secondary to complications), abd. distention, confusion
- Jaundice, spider angiomas/telangiectasisas, acites caput medusa, hepao/splenomegaly, palmar erythema, clubbing
Cirrhosis (Chronic Liver Diseae)
Diagnosis
Treatment
Diagnosis
- abdominal US done (see cirrhosis)
- gold standard= liver bopsy to confirm the dx. but not generally needed if all other signs point to it
you will see evidence of liver failure on exam, clinical signs, complications likae varices, ascites, SBP & HE
MELD Score - model for End Stage Liver Failure
- used to calculate spot on transplant list; higher mortality risk = higher MELD
- TIPS: best with MELD < 14
- alcoholic hepatitis: MELD > 20
- hepatorenal : MELD > 20
Treatment is transplant
Varices and Variceal Hemorrhage
Etiology
Symptoms
Treatment
Etiology
- pts. usually have increased portal HTN in an attempt to decompress the HTN and return blood to circulation, carices form (common in esophagus)
Symptoms
- commonly, they will bleed: hematemisis or melanea
Treatment
- fluid resusications and blood product support
- ceftriaxone prophlyatically to decreased risk
- ocreotide to decrease splanchininc blood flow
- endoscopic control of the bleeding via banding of th evarices
- TIPS proceudre to solve the portal HTN and reduce recurrance of varices
assocaited with high mortality rates
Ascites
Etiology
Symotoms
Diagnosis
Treatment
Etiology
- buildup of the fluid in the peritoneal cavity secondary to an edematous state usually
- most common complicatin of cirrhosis
Symptoms and SIgns
- shifting dullness: change in location of dullness to percussion when pt. turns to side (shows that it si free flowing fluid)
Diagnosis
- shifting dullness on PE
- US or CT can be done
Treatment
- paracentesis
diuretics (spirnolactone + lasix 2:1 ratio)
reduce sodium
therapeduic paracentesis
TIPS
Indications for Paracentesis
- new ascites
- clinical deterioration of the pt. (fever, AMS< hypotension)
- lab studies that may say infected fluid
How is the etiology of Ascites determined?
SAAG v PMN
- the fluid from a paracentesis should be sent out for testing
to find out if its infect = need to calculate the PMN
PMN: polymorphic neutrophils: WBC x PMN = total PNM
PMN > 250 = theyre at criteria for spontaneous bacterial peritonitit (SBP)
to find out if the ascites is due to portal hypertension… = SAAG
- serum ascites albumin gradient (albumin in serum to ascites fluid ratio)
- if difference > 1.1 = portal hypertension
- if difference is < 1.1 = not portal hypertension
what is SBP in the setting of chronic liver failure & ascites
etiology
symptoms
diagnosis
treatment
SBP: sponteanous bacterial peritonitis
- ascites infection in the fluid not due to an intra-abdominal issue – no surgically treatable source
e. coli is most common pathogen
Risk Factors
- advanced cirrhoiss
- prior SBP
- variceal hemorhage
Symptoms
- fever
- abd. pain/tenderness
- AMS
- dirrhea, hypotension, hypothermia
Diagnosis
- PMN count > 250
- positive asecitc fluid bacterial culutre
Treatment
- ceftriaxone or cefotaxime
- good prognosis if treated prior to shock
pts. at high risk of SBP or had it before should be on prophylatic bactrum or cipro for life)
Hepatorenal Syndrome
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- a severe hepatic injury resulting in eventually a reduced perfusion to the kidneys, resulting in an AKI due to hepatic failure
- the portal HTN –> triggers aterial vasodilation in the splachnic circulation –> decreases blood flow to the kidenys & triggers RAAS system and an AKI develops due to the poor flow
Diagnosis
- Diagnosis of exclusion: rule out all other possible causes of an AKI in these pts. first before you blame it on the bad liver
- can use US to rule things out
Treatment
- improvement will be from improving the hepatic failure
- discontinue all HTN agents —- these are vasodialtion and messing with kidneys
- in ICU: pressors + albumin
- non-ICu: midodrin, octreotide, albumin
givein albumin will help pull luid back into the vessels through oncotic pressure
Hepatic Encephalopathy
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- ammonia from the gut goes to the lvier –> but the liver is failing so it cant conver the ammonia to glutamine
- ammoina enters the blood stream & it goes to the brain and interferes with brain function
- this is seen dueing Acute liver failure
- can be seen in cirrhosis
Symptoms: a Scale to determine severity (Grade I-IV)
- behavior changes, confusion, slurred speech
- lethargy
- stupor, incoherant speech
- coma and unresponsive to pain
Diagnosis
- a clinical diagnosis cannot be made on the amount of ammonia in the blood stream because it does not direclty correlated with severity of disease
- use H&PE: asterxis signs
- exculde all other AMS reasons
- elvaulate what might be the precipatating factor = alkalosis, renal failure, low volume, etc.
Treatment
- correct underlying condition
- lower the blood ammonia via GI binders: Lactulose & Rifaximin to get bowels to 2/3 a day
Hepatocellular Carcinoma (HCC)
Etiology
Symptoms
Etiology
- a primary tumor of the liver, due to chronic cirrhosis (usually), alchol use, hepatitis, NASH
Symptoms
- cirrhosis in 90%
- symptoms common a result of th eunderlying cirrhosis (varices, ascites, etc.) rather thant the tumor
- those with advanced dx. = weight loss, mass, early satiety
Diagnosis
- CT/MRI: can show the mass without the need to biopsy
- if imaging not helping; biopsy can be done
- not diagnosis: but using AFP can help surveillence of disase progress
Treatment
- if eligibale: surgical ressection of the tumor is best
- can do abaltion if they cant do surgery
- can do systemic treatmetn with immunotherapy, chemotherapy, etc.
can do a combo of chemo, surgery, etc.
transplant can be considered
Portal Vein Thormbosis (PVT)
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- the most common cause of EXTRAHEPATIC portal vein obstruction
- can lead to portal hypertension
- common in cirrhosis, showing the imbalance in the hemostatsis and slowed portal flow = increased risk of clotting
- non cirrhotic pts. can be due to clotting conditions
acute
- a sudden onset of the venous occlusion due to the thrombus formation
- these pt. dont have collateral cirulation as a reuslt of a previosu protal HTN, thus no where for blood to go
Diagnosis: CT or MRI
Treatment: anticoag. 6 months
chronic
- can occur in those who had acute and it never resolved (treated or not)
- they have collateral blood vessels here, so the blood flows around
Diagnosis: CT or MRI can us US with doppler
Treatment: not ususally a need for anticoags. becuase no risk of PE –> rather treat and screen for varices and portal HTN treatment (Bblocker)
complications = ischmiea, sepsis, HTN, ascites, varices
Budd-Chiari Syndrome
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- any process which results in an inturruption of bloow flood OUT of the liver – thus a problem of the hepativ vein flow into the IVC
Causes: 5 Ps
- Polycythemia Vera
- Pills: OCPs
- PNH: paroxysaml nocturnal hemoglobinuria
- Protein C&S def.
- PRegnant
Triad od Symptoms
- abdominal pain
- ascites
- hepatomegaly
Diagnosis
- doppler US: look for thrombosis
- rarely do you need bx.
Treatment
- correct the underlying condition
- anticoag. them
consider…
- thrombolysis if acute presention
- angioplasy/stenting
- liver transplant
Non-alcoholic Fatty Liver Disease (NAFLD)
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- hepatic steatosis and fat accumulation NOT due to alcohol consumption
- progresses to cirrhosis
NAFLD and NASH
NAFL: steatosis without inflammation
NASH: steatosis with inflammation
due to western diet, T2DM, cetrnal obesity, metabolic syndrome
Symptoms
- hepatomegaly
- mildly elevated AST/ALT
Diagnosis
- hepatic steatosis found (via bx. or imaging)
- excluded alcohol causes
- excluded other causes
- no chronic liver disease
Treament
- avoid alcohol, get hepatits vax. & modify life style = prevent progression
- weight loss
- glycemic control
- monitor AST/ALT and alk. phos every 3-6 months
- monitor for fiberosis with US every 3-4 years
