Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DEMS I > liver tests > Flashcards

liver tests Flashcards

1
Q
  1. Recognize common liver chemistry tests and their clinical implications when abnormal, including AST and ALT, Alkaline phosphatase, and Bilirubin.
A

AST: hepatocellular damage. ALT: hepatocellular damage. Bilirubin: cholestasis, impaired conjugation or biliary obstruction. Alkaline phosphatase: cholestasis, infiltrative disease or biliary obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

prothrombin time

A

•Assesses the extrinsic clotting pathway. When combined with serum albumin can assess synthetic function aka hepatic function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of Prothrombin time prolongation

A

hepatocellular dysfunction or Vitamin K deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Non hepatic causes of low albumin levels

A

poor nutrition, nephrosis, malabsorption, severe illness with catabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Non hepatic causes of elevated prothrombin time

A

malabsorption, genetic causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

compare half lives of albumin and coagulation factors

A

albumin half life is 19-21 days. Coag factors half lives may be less than a day. These tests can be used to determine acute vs chronic components of hepatic function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Test to assess hepatic dysfunction vs Vit K deficiency with prolonged prothrombin time

A

Administer subcutaneous vitamin K and assess response. No correction indicates liver dysfunction. Normalization indicates vitamin K deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Characterize patterns of liver chemistry test abnormalities for hepatocellular and cholestatic liver diseases.
A

Hepatocellular injury or necrosis: predominantly AST and ALT elevation. Cholestatic pattern: predominantly alk phos elevation. Can also have a mixed pattern which indicates synthetic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Function of AST and ALT

A

Both are aminotransferases which catalyze transfer of aa groups to form hepatic metabolites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

compare location in hepatocyte and organ expression of AST and ALT

A

AST: cytosol and mitochondria, liver, heart, muscle and blood. ALT: cytosol, liver only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

AST:ALT ratio

A

normally 1 b/c impaired plasma clearance of AST by sinusoidal cells. Alcoholic liver disease is >2 b/c hepatic deficiency of B6 which is cofactor for ALT activity and alcohol induced injury to mitochondria enriched in AST.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hepatic causes of mild (< 5X) AST and ALT elevations

A

Chronic HBV and HCV, acute viral hepatitis (A-E, EBV, CMV), steatohepatitis, alcohol related liver injury, hemochromatosis, autoimmune hepatitis, alpha1- antitrypsin deficiency, Wilsons dz, celiac dz and cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NON hepatic causes of mild (< 5X) AST and ALT elevations

A

hemolysis, myopathy, thyroid dz, strenous exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of severe (>15X) AST and ALT elevations

A

acute viral hepatitis (A-E, herpes), meds/toxins, ischemic hepatitis, autoimmune hepatitis, Wilsons dz, acute Budd-Chiari syndrome, hepatic artery ligation or thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Alkaline phosphatase function

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tissue location of alk phos

A

Nearly all tissues: liver (microvilli of bile canaliculus), bone, placenta, intestine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of elevated alk phos

A

Cholestatic or infiltrative diseases of liver, Obstruction of biliary system, Bone disease, Pregnancy, renal failure, CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

List infiltrative dz of liver that cause elevation in alkaline phosphatase

A

sarcoidosis, tuberculosis, fungal, granulomatous dz, amyloidosis, lymphoma, metastatic malignancy, hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do you differentiate hepatobiliary vs nonhepatobiliary origin of elevated alk phos?

A
  1. 5’-nucleotidease: Significantly elevated only in liver disease, highest levels in cholestatic diseases. 2. gamma-glutamyltransferase (GGT): Not present in bone, Elevated after alcohol consumption and almost all types of liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Bilirubin metabolism

A

Normal heme degradation product. Requires conjugation (glucuronidation) into water soluble forms before biliary excretion. Heme > heme oxygenase converts to biliverdin in kupffer cells of liver > biliverdin reductase converts to bilirubin > UDP glucuronyl transferase conjugates bilirubin into water soluble form in hepatocytes > bile canaliculus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Indirect vs direct bilirubin

A

indirect: measures unconjugated bilirubin before entering hepatocyte. Direct: measures conjugated bilirubin that has exited hepatocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hemolytic jaundice

A

overwhelmed conjugation: indirect bilirubin increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Biliary obstruction- effect on direct and indirect bilirubin

A

obstruction leads to conjugated hyperbilirubinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Gilberts syndrome

A

dimished bilirubin-UGT (enzyme that conjugates bilirubin) leads to unconjugated hyperbilirubinemia with normal AST, ALT and alk phosph

25
Q

Crigler-Najjar syndrome

A

rare autosomal recessive UDP-GT deficiency causes impaired bilirubin conjugation. Leads to unconjugated hyperbilirubinemia. Type I: severe jaundice, neuro impairment. Type 2: lower serum bilirubin, no neuro problems

26
Q

Dubin-Johnson syndrome

A

defective secretion of conjugated bilirubin due to mutation of MRP-2 gene (responsible for transporting conjugated bilirubin from hepatocyte into bile canaliculus). Leads to conjugated hyperbilirubinemia

27
Q

bilirubin levels in cirrhosis

A

conjugated hyperbilirubinemia- impairment of hepatocellular bilirubin secretion into bile, but bilirubin conjugation is preserved. Also, increased peripheral RBC destruction occurs

28
Q

sites of cholestasis, detection method and examples

A
  1. lesion in canaliculus/ biliary ductules: detected by labs or liver biopsy. Includes cholestatic drugs, PBC and pregnancy. 2. intra/extra hepatic bile duct lesion: detected by imaging (US, ERCP, MRCP). Includes biliary atresia, PSC, gallstones, malignancy of pancreas or bile duct.
29
Q

List diseases that cuase indirect hyperbilirubinemia

A

gilberts syndrome (nl LFTs), hemolysis (nl LFTs) , and crigler-Najjar syndrome

30
Q

list diseases that cause direct hyperbilirubinemia

A

extrahepatic obstruction of bile flow, intrahepatic cholestasis, hepatitis, cirrhosis

31
Q

Chronic Hepatitis B diagnosis

A

hepatitis B surface antigen (HBsAg) for >6 months

32
Q

When is treatment considered in chronic hep B

A

1) HBsAg positive >6 months, 2) serum HBV DNA >10^5 copies/mL and 3) persistent or intermittent elevation in ALT and AST levels. OR if cirrhosis and positive HBV DNA (regardless of AST/ALT)

33
Q

Benefits of chronic Hep B treatment

A

reduces the risk of progressive chronic liver disease and long-term complications of cirrhosis and hepatocellular carcinoma (HCC). prevent decompensation of liver disease (development of jaundice, ascites, variceal bleeding).

34
Q

Hep B treatment results/goal

A

Although treatment can lead to viral suppression in HBeAg positive patients with normal ALT, the likelihood of HBeAg seroconversion (loss of HBeAg and developemend of HBeAb) is low. Goal is HBeAg seroconversion which is associated with negative HBV DNA when treatment is stopped. Goal is NOT to achieve loss of HBsAg

35
Q

Chronic Hep B treatment

A
  1. Interferon (standard and pegylated): finite duration of treatment, absence of resistant mutants and more durable response. Interferon should not be used in patients with advanced liver disease. 2. nucleoside/tide analogs (lamivudine, adefovir, entecavir or tenofovir): less side effects
36
Q

compare the Hep B antigens

A

HBsAg: surface antigen, marker of active infection. HBeAg: e antigen, surrogate marker of high viral load. HBcAg: core antibody, marker of active infection

37
Q

Diagnosis of chronic Hep C

A

HCV RNA in the blood

38
Q

Goal of HCV therapy

A

sustained virological response: eradicate HCV RNA and to remain HCV RNA negative 12 weeks after antiviral therapy is stopped

39
Q

HCV standard of care

A

The current standard of care for treating HCV genotype 1 has been pegylated interferon, ribavirin and an NS3/4a protease inhibitor (boceprevir or telaprevir) for 24-48 weeks. Patients with other genotypes are currently treated with pegylated interferon and ribavirin

40
Q

Unfavorable and favorable predictors of sustained virological response with HCV therapy

A

unfavorable: high baseline HCV RNA, genotype 1. black/hispanic, age, body weight, insulin resistance, more severe liver histology or steatosis. Favorable: low baseline HCV RNA, genotype 2/3, white

41
Q

New Hep C treatments

A

target HCV encoded proteins vital to replication and life cycle of virus

42
Q

Hereditary hemochromatosis benefits of treatment

A

prevent major causes of death in HH including decompensated cirrhosis, hepatocellular carcinoma, diabetes and cardiomyopathy. Survival is normal in patients in whom treatment is initiated before the development of cirrhosis or diabetes

43
Q

Hereditary hemochromatosis treatment

A

Therapeutic phlebotomy (Each 500 mL of whole blood removed contains 200-250 mg of iron) once per week for one year then once every 2-4 months for maintenance. OR chelation with desferoxamine if anemic patient

44
Q

Hereditary hemochromatosis treatment endpoint

A

serum ferritin of 50 ng/mL

45
Q

Autoimmune hepatitis treatment

A

primary: Prednisone to suppress overactive immune system. Secondary: azathioprine, allows for lower doses of prednisone to be used. Stopping therapy results in a flair

46
Q

Azathioprine side effects

A

reduction in the white blood cell count, nausea and rarely pancreatitis

47
Q

corticosteroids side effects

A

weight gain, anxiety, osteoporosis, diabetes, high blood pressure and cataracts.

48
Q

Primary biliary cirrhosis diagnosis

A

anti-mitochondrial antibody

49
Q

Primary biliary cirrhosis treatment

A

Ursodiol (ursodeoxycholic acid)- a secondary bile acid which is a metabolic byproduct of intestinal bacteria. Improves bile acid transport/detox, cytoprotection and anti-apoptosis

50
Q

Primary sclerosing cholangitis treatment

A

stent strictures with endoscopic retrograde cholangioscopy, treat cholangitis with antibiotics. Liver transplant is only long term treatment

51
Q

Wilson disease treatment

A

general chelators that induce cupria (loss of copper in the urine) such as D-penicillamine and trientine, then zinc which interferes with uptake of copper from GI tract and induces enterocyte chelation of metals.

52
Q

how do you monitor treatment of Wilson disease

A

24-hour urinary copper excretion. With chronic (maintenance) treatment, urinary copper excretion should run in the vicinity of 200-500 mcg per day on treatment. Values of urine copper excretion <200 mcg/day may indicate either non-adherence to theapy or overtreatment and excess copper removal

53
Q

Non-alcoholic steatohepatitis treatment

A

Modifying risk factors for NASH: 1) Obesity, 2) Type II diabetes mellitus, and 3) Dyslipidemia. Investigational therapies have included use of diabetes drugs (even if not associated with diabetes) and vitamin E – an antioxidant.

54
Q

what causes syphilis and what happens

A

treponema pallidum- causes demyelination of posterior columns in spinal cord and sclerosing of posterior roots. Results in decreased reflexes, decreased pain and proprioception.

55
Q

microglia develop from what

A

monocytes- mesoderm derived

56
Q

structures arising from surface ectoderm

A

lens of eye, epidermis and anterior pituitary

57
Q

structures from neuroectoderm

A

CNS neurons, oligodendrocytes, astrocytes, ependymal cells,

58
Q

internuclear ophthalmoplegia

A

seen in MS- demyelination of ipsilateral medial longitudinal fasciculus results innormal lateral rectus movement of eyes, but contralateral CN III does not stimulate medial rectus to fire. Abducting eye gets nystagmus

DEMS I (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions