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My DEMS I > LFTs > Flashcards

LFTs Flashcards

1
Q

AST locationin hepatocyte/organ exp

A

cytosol and mitochondria

liver, heart, muscle, blood

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2
Q

ALT location in hepatocyte/organ exp

A

cytosol

liver only

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3
Q

AST:ALT ratio

A

Typically ratio is 1 seen in cirrhosis
Impaired plasma clearance of AST by sinusoidal cells?

Ratio >2 suggestive of alcoholic liver disease
Lower ALT from hepatic deficiency of pyridoxine (B6) in alcoholics which is cofactor for enzymatic activity of ALT
Preferential alcohol-induced injury to mitochondria enriched in AST

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4
Q

etiology of mild (

A 
Hepatic: 
Chronic HBV and HCV
Acute viral hepatitis (A-E, EBV, CMV)
Steatohepatitis
Alcohol-related liver injury (AST predominant)
Hemochromotosis
Autoimmune Hepatitis
Alpha1-Antitrypsin deficiency
Wilson’s disease
Celiac disease
Cirrhosis
Non-Hepatic:
Hemolysis
Myopathy
Thyroid disease
Strenuous exercise
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5
Q

increased AST and ALT

A

H&P
D.c hepatotoxic meds
Alk phos, bilirubin, INR, albumin, viral hepatitis serologies, iron studies

Neg serologies, w sx
Ultrasound, ANA, anti-smooth muscle antibody, ceruloplasmin, alpha 1-antitrypsin
liver biopsy

Negative serologies, asx
Lifestyle modification
repeat liver chem in 3-6 mo

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6
Q

Etiology of sever (>15x nml) AST and ALT elevations

A 
Acute viral hepatitis (A-E, herpes)
Medications/toxins
Ischemic hepatitis
Autoimmune hepatitis
Wilson’s disease
Acute Budd-Chiari syndrome
Hepatic artery ligation or thrombosis
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7
Q

Alkaline phosphatase: action, location in tiss, elev in

A

Hydrolase enzyme responsible for removing phosphate groups from nucleotides, proteins and alkaloids

Present in nearly all tissues:
Liver, localized to microvilli of bile canaliculus
Bone
Placenta
Intestine
Elevated in
Cholestatic or infiltrative diseases of liver
Obstruction of biliary system
Bone disease
Pregnancy
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8
Q

Alk phos hepatobiliary vs nonhepatobiliary origin

A

Isoenzyme determination (helps w/ location)

5’-nucleotidease
Significantly elevated only in liver disease, highest levels in cholestatic diseases

gamma-glutamyltransferase (GGT)
Not present in bone
Elevated after alcohol consumption and almost all types of LIVER disease (can be elevated in a number of conditions)

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9
Q

Causes of elevated alk phos: hepatobiliary

A 
Bile duct obstruction
Primary biliary cirrhosis (PBC)
Primary sclerosing cholangitis (PSC)
Medications
Hepatitis
Cirrhosis
Infiltrating disease of liver
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10
Q

nonhepatic causes for elevated alk phos

A 
Bone disease
Pregnancy
Chronic renal failure
Lymphoma and other malignancies
Congestive heart failure
Infection and inflammation
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11
Q

Infiltrating diseases of liver causing elevation in alk phos

A 
Sarcoidosis
Tuberculosis
Fungal infection
Other granulomatous diseases
Amyloidosis
Lymphoma
Metastatic malignancy
Hepatocellular carcinoma
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12
Q

elevated Alk phos algorithm

A 
H&P
liver chem
normal AST and ALT?
gamaGGT or 5'nucleotidase (if elevated move to RUQ US below)
normal?
etiology is not hepatobiliary
Abnormal AST and ALT?
RUQ US to assess for biliary duct dilatation
yes:
ERCP or MRCP
No:
AMA:
Positive? PBC
Negative?*Evaluation for elevated ALT, liver biopsy and/or ERCP or MRCP (ie eval for
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13
Q

Bilirubin

A

Normal heme degradation product

Excreted from body via secretion into bile

Insoluble in water

Requires conjugation (glucuronidation) into water-soluble forms before biliary excretion

  • Unconjugated (indirect) bilirubin
  • Conjugated (direct) bilirubin
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14
Q

Location of conj/unconj bili

A 
unconjugated bili in blood
to liver (ER), conjugated, and put in bile canaliculus
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15
Q

Biliary obstruction and bilirubin

A

can’t get conjugate bili out, ends up back in blood: increased conjugated bilirubin

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16
Q

Gilbert’s disease

A

decreased bilirubin uptake

Most common inherited disorder of bilirubin glucuronidation
Mutation in promoter region of gene encoding for UDP-GT resulting in reduced activity

5-10% Western population homozygous for condition

Conditions associated with elevated bilirubin
Hemolysis
Fasting
Febrile illness
Physical stress

delay in moving unconjugated bilirubin to liver (elevated total bili)

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17
Q

Crigler-Najjar Syndrome

A

impaired bilirubin conjugation

Rare, autosomal recessive
UDP-GT deficiency or low levels of enzyme
Type I: severe jaundice, neurologic impairment
Type II: lower serum bilirubin, no neurologic impairment

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18
Q

Dubin-Johnson syndrome*

A

defective secretion of conjugated bilirubin

rare
Impairment of biliary excretion
Mutation of MRP-2 gene
Protein responsible for transporting conjugated bilirubin from hepatocyte into bile canaliculus
Most defects in ATP binding region
Benign, no Rx needed
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19
Q

bili and cirrhosis

A
  • RBC membranes less stable
  • RBC removed more frequently (so increased unconjugated bili)
  • scarring: hard to get bili in and out
  • reduced liver mass (Scar tissue)

Hard to process

20
Q

Classification of cholestasis (decreased bile flow

A

site of lesion: canaliculus or biliary ductules
detection: lab tests or liver biopsy
common ex: cholestatic drugs rxns, PBC preg

site: intra/extrahepatic bile ducts

Detectin: imaging: US ERCP MRCP
ex: Biliary atresia, PSC, gallstones, malignancy of pancreas or bile duct

21
Q

unconj (indir) hyperbili

A

Gilbert’s syndrome
Hemolysis (increased heme breakdown)
Crigler-Najjar syndrome

22
Q

conjugated (direct) hyperbili

A

Extrahepatic obstruction of bile flow
Intrahepatic cholestasis
Hepatitis
Cirrhosis

23
Q

elevated bili algorithm

A

H&P, liver chem

unconj bili, nml AST & ALT and alk phos:
Gilbert’s syndrome, hemolysis studies

or

Conjugated bili, abnorm AST and ALT and alk phos:
RUQ US to assess for ductal dilatation
Present: ERCP or MRCP
Absent: Elevated ALT evaluation, AMA, ERCP or MRCP and/or liver biopsy

24
Q

Common Liver chem tests and implications of abnormality

A

AST: hepatocell damage
ALT: hepatocell damage
Bilirubin: cholestasis, impaired conjugation, or biliary obstruction
Alk phos: cholestasis, infiltrative disease, or biliary obstruction
Albumin: synthetic dysfunction
–
PTT: synthetic dysfunc

25
Q

PAtterns of liver chem abnormalities

A

predom AST/ALT elev: hepatocellular injury or necrosis

Cholestatic pattern: predom alk phos elev

26
Q

Look up bili metabolism and review handout**

A

–

27
Q

Reasons to treat chronic hepatitis

A

Prevent liver failure and development of cirrhosis and associated complications:
Varices
Ascites
Hepatic encephalopathy

Reduce risk of hepatocellular carcinoma

28
Q

HBsAg

A

hep B surface antigen:
marker of active infection
presence for>6 mo defines chronic hep B infection

29
Q

HBsAB

A

(or anti-HBs)
antibody to HBsAG
-marker of immunity to hepatitis B

30
Q

HBcAB

A

hep B core antibody
-marker of active or prior infection
(can’t tell if chronic or new)

31
Q

HBeAg

A

hep B “e” antigen

-marker of high viral load

32
Q

HBeAB (or anti-Hbe)

A

antibody to hep B “e” antigen

33
Q

HBV DNA

A

presence means active viral replication

34
Q

Goal of HBV treatment

A

HBeAg seroconversion:
Loss of HBeAg and development of HBeAb associated with negative HBV DNA when treatment stopped

Prevention of decompensated cirrhosis in those with advanced fibrosis

Note: Loss of HBsAg rarely occurs

35
Q

Chronic HBV infection indications for tx

A
  1. HBsAg(+) > 6 months*
  2. Serum HBV DNA >105 copies/mL
  3. Persistent or intermittent elevation in ALT and AST levels
    - Liklihood of HBeAg seroconversion with normal ALT is very low

-treat pts w/ advanced liver disease

36
Q

Treatment options for HBV

A

Interferon

  • Finite duration of therapy (1 year)
  • Absence of resistant mutations
  • More durable response
  • feel like you have flu

Nucleoside/tide analoges
Fewer side effects
Resistant mutations
(people choose this option)

37
Q

If undergo tx for HBV, and still have HBs Ag… risk of

A

liver cancer still.

tx prevented virus replication, but you still technically have hepatitis B

38
Q

Look at cases 10/27 8a

A

–

39
Q

chronic HCV and goal of tx

A

defined as presence of HCV RNA in blood >6mo after infection

Goal of antiviral therapy is to clear HCV RNA: HCV RNA negative 12 weeks after stopping therapy
Sustained virological response (SVR) = cure

(HCV antibody often positive, but definition of infection is HCV RNA >6mo)

40
Q

tx of HCV

A

Tx: pills, but very expensive ($1,000/d)

41
Q

Hereditary hemochromatosis

A

Inherited disorder: increased intestinal iron absorption

Consider w/ elevated AST and ALT

Tx: therapeutic phlebotomy:
500 mL of whole blood = 200-250 mg iron
Endpoint is serum ferritin 50 ng/mL
Maintenance phlebotomy to keep ferritin 50-100 ng/mL

For anemic patients not able to tolerate phlebotomy, chelation therapy with desfuroxamine

Gene: C282Y

look at case!

42
Q

Autoimmune hepatitis

A

Chronic hepatitis characterized by immunologic and autoimmune features

Treatment based on immune suppression:
Corticosteroids
Azathioprine

Relapse typically occurs if treatment stopped after liver enzymes normalized

50% chance of flair with cessation of therapy 2 year after achieving remission

Often see plasma cells on histology, bridging necrosis, etc.

43
Q

***Primary biliary cirrhosis

A

Immune mediated disease causing damage to SMALL (micro) intrahepatic bile ducts

Tx: ursodeoxycolic acid (UDCA):
Secondary bile acid, metabolic byproduct of intestinal bacteria
Improves bile acid transport, “detoxifies” bile and providing cytoprotection

Use of UDCA:
Improved liver biochemistries
Improve survival
Reduce need for liver transplantation

Alk phos more elevated than ALT

Dx: antimitochondrial Ab
Check DEXA for osteoporosis

44
Q

PSC

A

Inflammatory disease of the intra- and extrahepatic LARGE bile ducts
Leads to strictures and obstruction of bile ducts and can ultimately result in cirrhosis

No effective medical therapy

Treatment focused on management of complications of bile duct obstruction:

  • Stenting strictures
  • Antibiotics for cholangitis

Risk for cholangiocarcinoma

Most with this have UC (20% w/ UC have this)

45
Q

Wilson Disease

A

AR
Decreased hepatocullar copper excretion –> hepatic copper accumulation and injury

Tx: copper chelation:
D-penicillamine
Trientine

Maintenance therapy with zinc

Might see Kayser-Fleisher rings (Cu rings around iris)

46
Q

Non-alcoholic steatohepatitis

A 
NASH is presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning with or without fibrosis)
Tx:  modifying risk factors
-Obesity
-Diabetes mellitus type 2
-Dyslipidemia

Investigational therapies
Diabetes medications – even if not diabetic
Vitamin E - antioxidant

no real effective tx currently

My DEMS I (26 decks)

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