Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

GI block 2 > Lecture 4 - Liver 1 > Flashcards

Lecture 4 - Liver 1 Flashcards

1
Q

LFTs commonly include?

hepatic panel = LFT

A 
Bilirubin
Albumin
ALT
AST
ALP
Total Protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Less commonly included in LFTs?

A

GGT
LDH
PTT/INR
Platelets

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

Review: ALT is found primarily in the liver whereas AST is found in skeletal muscles and erythrocytes. So?

A

ALT elevations are generally more specific for hepatic injury

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

Transaminitis?

A

Elevation of transaminases (ALT/AST), often discovered on routine labs in otherwise asymptomatic pt

DDx is vast (so requires a thorough history, PE, repeat labs, hepatitis panel, hepatitis US, GI referral)

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

2:1 elevation in AST:ALT often indicates what? (particularly in light of elevated GGT)

A

alcohol-related liver disease

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

AST/ALT catalyze transfer of a-amino groups from aspartate/alanine to a-keto group of ketoglutaric acid to generate oxalacetic/pyruvic acids.

Both enzymes require what?

A

pyridoxal-5’-phosphate (Vit B6) (a deficiency which has a greater effect on ALT, hence the 2:1 ratio)

(alcoholic liver disease = pyridoxal-5’-phosphate deficiency)

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

GGT is an enzyme that is present in hepatocytes, biliary epithelial cells, renal tubules, pancreas, intestine (mechanisms of alteration are similar to ALP).

A

Note that GGT levels can also be observed in a variety of non-hepatic diseases as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Many diseases of the liver, regardless of cause, may be responsible for altered GGT serum levels.

Because of lack of specificity, but HIGH SENSITIVITY, GGT can be useful for IDing causes of altered ALP levels

A

GGT elevated, with AST/ALT ratio > 2, may support the diagnosis of alcoholic liver disease

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

Disproportionate elevation in alkaline phosphatase (ALP) compared to ALT/AST…

A

LFT w/ cholestatic pattern

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

Most common causes of pathological elevation of ALP?

A

Liver/bone disease

Hepatic ALP is present on the surface of bile duct epithelium. Cholestasis enhances the synthesis and release of ALP, and accumulating bile salts increase its release from the cell surface

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

Pathologic increase in portal pressure indicated by?

A

pressure gradient b/w portal vein and IVC > 10 mm HG

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

Most common etiology of portal HTN?

A

Cirrhosis

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

Jaundice is result of accumulation of bilirubin in body tissue but isn’t clinically apparent until what level?

A

greater than 2 mg/dL

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

Unconjugated bilirubin (+albumin) is found where?

A

Found in the blood… then… arrives at the liver where it becomes conjugated and moved through the biliary system to the small intestine for excretion

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

Prehepatic jaundice is shown by elevated levels of unconjugated (indirect) bilirubin, most commonly due to?

A
  1. overproduction of bilirubin
  2. impaired bilirubin uptake by the liver
  3. abnormalities of bilirubin conjugation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Unconjugated hyperbilirubinemia causes?

A

Increased bili production: Hemolytic anemias, hemolytics rxns, hematomas, pulm infarct

Impaired bili uptake/storage: posthepatitis hyperbilirubinemia, Gilbert syndrome, Crigler-Najjar syndrome, drug rxns (TMP-SMX)

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

Plasma elevation of BOTH unconjugated and conjugated bilirubin can be to?

(this is often referred to as conjugated hyperbilirubinemia, even though both fractions of bilirubin are elevated)

A

Hepatocellular disease

Impaired canalicular disease

Biliary obstruction

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

Conjugated hyperbilirubinemia from hepatocellular dysfunction could be caused by?

A

hepatitis

cirrhosis

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

Examples of conditions of biliary obstructions causing hyperbilirubinemia are?

A

choledocholithiasis

biliary atresia

carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical findings of unconjugated hyperbilirubinemia (prehepatic jaundice)?

A

Mild jaundice (maybe only scleral icterus)

Normal stool/urine color

Splenomegaly if etiology is hemolytic disorder (note that sickle cell anemia will likely NOT present w/ splenomegaly)

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

Clinical findings of hepatic/conjugated jaundice (hepatocellular disease)?

So, cirrhosis and hepatitis

A

Malaise, anorexia

Low grade fever

RUQ pn

Dark urine

amenorrhea

enlarged/tender liver

spider teleangiectasias

palmar erythema

ascites

gynecomastia

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

Clinical findings of conjugated jaundice from cholestatic syndromes?

A

Jaundice

Pruritus

light colored stool

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

Clinical findings of conjugated-biliary obstruction jaundice?

(post hepatic)

A

RUQ pn

wt loss (suggestive of carcinoma)

pruritus

dark urine

light-colored (acholic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  1. Lab studies for jaundice?
  2. Radiographs for jaundice?
  3. What else can you do, for bile ducts maybe?
A
  1. Hepatic labs, CBC, CMP, UA
  2. Hepatic US
  3. ERCP, if biliary obstruction is suspected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Endoscopic technique in which a specialized side-viewing upper endoscope is guided into duodenum, allowing for instruments to be passed into the bile and pancreatic ducts... Indicated for?
ERCP indicated in jaundiced patient suspected of having biliary obstruction
26
Tx approach for jaundice?
Aimed at underlying etiology SHould be referred (GI) for underlying etiology
27
Parameters for acute liver failure?
Severe acute liver injury w: encephalopathy AND impaired synthetic fx (INR>1.5) (w/in 8 weeks of onset of dz, in a pt w/o preexisting liver dz)
28
Most common cause of acute liver failure?
Acetaminophen (45%) risk increased in pts w/ DM
29
By definition, pts w/ acute liver failure have severe acute liver injury (hepatic encelopathy, INR>1.5) Other ssx?
``` Fatigue/malaise/lethargy anorexia N/V RUQ pn pruritus jaundice abd distension (from ascites) ```
30
Lab finding for acute liver failure?
* INR>1.5 * markedly elevated aminotransferase levels * Elevated bilirubin and ALK PHOS * Low platelet count (<150,000) elevated ammonia elevated amylase/lipase elevated BUN/Cr
31
Acute liver failure admission/in patient mgmt parameters?
IV fluid/electrolyte replacement Dietary monitoring Gastroprotective measures (IV PPI, H2 to prevent stress gastropathy) (and of course other tx as indicaated by etiology)
32
Most common causes of viral hepatitis in US?
Hep A Hep B Hep C
33
The hepatropic viruses follow a similar pathologic pattern... what is it?
Viral replication Prodromal Icteric Convalescent
34
What would you see during phase 1 of viral hepatitis?
(viral replication phase) Pts typically asymptomatic Labs show serologic and enzyme markers of hepatitis
35
What would you see during phase 2 of viral hepatitis?
Prodromal phase ``` Anorexia/Nausea/Vomiting Arthralgias Malaise/Fatigue Urticaria Pruritus Alterations in taste (aversion to cig smoke) ```
36
What would you see during phase 3 of viral hepatitis?
(Icteric phase) Predominant GI symptoms Jaundice Dark urine -> pale-colored stools Malaise (maybe RUQ w/ hepatomegaly)
37
What might you see during phase 4 of viral hepatitis?
Convalescent phase symptoms/jaundice resolve liver enzymes return to normal
38
Most common cause of viral hepatitis in US? Route/transmission?
Hep A (fecal oral transmission) Associated w/ localized outbreaks/contaminated food/water
39
30 day incubation period Viral shedding in feces of infected host for up to two weeks prior to onset of clinical syndrome Low mortality (progression to fulminant disease is rare unless?)
acute hepatitis A | unless coinfection w/ HCV
40
Acute Hep A ssx: ``` Malaise/myalgia/arthralgia easy fatigability Upper resp. ssx Nausea/Vomiting Anorexia (smokes develop distaste for cigs) Low grade fever ``` When do the ssx start and what's the deal with the fever?
Ssx begin ~4 weeks post-exposure (so, get a good hx) Low grade fever... once it breaks expect an onset of jaundice 5-10 days after (presentation may be initially mistaken for viral gastroenteritis or viral URI)
41
In acute Hep A, what can you expect to see when jaundice develops? How long is Hep A course of illness typically?
Dark urine ->acholic stools Clinical ssx initially worsen, followed by progressive improvement Course of illness is typically 2-3 weeks (self-limiting w/ no progression to chronic carrier state)
42
Lab findings for Acute Hep A?
Markedly elevated AST/ALT Moderately elevated bilirubin/ALP Anti-HAV antibodies appear
43
The presence of what is diagnostic for acute Hep A illness?
presence of IgM anti-HAV
44
Tx for HAV?
Bedrest if needed Symptomatic care (antiemetic, antidiarrheals, fluids) Avoid strenous work/exercise NO ALCOHOL/HEPATOTOXIC MEDS
45
Mode of infection for HBV?
Inoculation of infected blood Sexual contact (saliva, semen, vaginal secretions) HBsAg positive mothers may transmit to newborn during delivery
46
Acute Hep B has variable presentation, but has a risk of?
conversion to chronic hepatitis
47
Groups at risk for Hep B?
Healthcare workers (including staff at hemodialysis centers) IV drug users Prisoners
48
Incubation period for Hep B?
6 weeks to 6 months
49
Chronic Hep B patients have a substantial risk for?
cirrhosis and hepatocellular carcinoma | men moreso than women
50
Ssx of acute Hep B?
Simiilar to Hep A... (see below) ``` Malaise/myalgia/arthralgia easy fatigability Upper resp. ssx Nausea/Vomiting Anorexia (smokes develop distaste for cigs) Low grade fever ``` Ssx begin ~4 weeks post-exposure Low grade fever... once it breaks expect an onset of jaundice 5-10 days after (presentation may be initially mistaken for viral gastroenteritis or viral URI)
51
Lab findings for Acute Hep B?
Similar to HAV Greater elevations in AST/ALT (serology findings are imprtant markers for different clinical states of HBV.... see next notecards)
52
Serologic hallmark of HBV INFECTION?
Hepatitis B surface Antigen (HBsAg)
53
Appears in most individuals AFTER CLEARANCE of HBsAg and after successful vaccination against Hep B?
anti-HBs (antibody to HBsAg)
54
Intracellular antigen expressed in infected hepatocytes NOT DETECTABLE IN SERUM
Hepatitis B core antigen (HBcAg)
55
Appears shortly after HBsAg is detected During acute infection, this antibody is predominantly of IgM class...?
Anti-HBc
56
Detection of what is typically regarded as an indication of acute HBV infection?
IgM anti-HBc
57
What persists in patients who recover from acute HBV and those who progress to chronic HBV?
IgG anti-HBc
58
A secretory protein that is processed from the pre-core protein... Indicates viral replication and infectivity
HBeAg (hepatitis B e antigen)
59
Persistence of ____ beyond 3 months indicates increased likelihood of chronic HBV?
HBeAg | HBV DNA parallels the presence of HBeAg
60
Treatment for acute HBV?
Supportive (as in HAV) Antiviral tx is reserved for those who develop severe disease
61
In acute HBV, what indicates severe disease requiring inpatient mgmt?
encephalopathy or coagulopathy
62
Acute HBV timelines for illness and recovery?
clinical illness lasts 2-3 weeks complete recovery by 16 weeks
63
Prevention measures for HBV?
screening of donated blood serologic testing in pregnancy safe sex practices safe handling of blood/body fluids/contaminated material vaccination
64
What would you administer for known exposure?
Hep B immune globulin | followed by vaccination series
65
HCV modes of infection?
50% by injection drug use Transfusion Body piercing/tattoo/hemodialysis (STI/maternal transmission possible, but low risk)
66
Vaccine available for HCV?
Negative (co-infection in HIV positive pts is common) (also, high risk of conversion to chronic state w/ an accompanying increase in risk of cirrhosis and carcinoma)
67
Incubation period for Hep C?
6-7 weeks | clinical illness is mild, or can be totally asymptomatic
68
Lab findings for Acute Hep C? What is confirmatory for Hep C?
Hep Panel similar to HAV, HBV If Anti-HCV EIA is positive or ambiguous, obtain HCV RNA test...presence of HCV RNA is confirmatory
69
If HCV is confirmed... obtain renal panel and UA to observe for what?
Observe for proteineuria, hematuria, and/or reduction of GFR
70
Medical treatment for Acute Hepatitis C is typically initiated after sufficient time to evaluate for for spontaneous clearance. Recheck HCV RNA when?
12 weeks after exposure | or after diagnosis if exposure is uncertain
71
Tx decision for acute HCV are made by a hepatologist and are based on pt risk factors A typical course of pharmacotherapy might include?
peginterferon weekly for 12-24 weeks (depending on viral genotype)
72
Acute HCV pts typically recover in?
3-6 mos Up to 80% covert to chronic disease 30% develop cirrhosis (meaning an increased risk of hepatocellular carcinoma)
73
Causes infection only in assocation with HBV infection, specifically the HBsAg?
Hepatitis D should therefore test in patients w/ acute HBV infxn (usual route = IV drug use)
74
Hep E is a major cause of hepatitis in what areas? | and therefore should be a consideration in patients who have traveled to these areas
Central/SE Asia, middle east, North Africa | fecal-oral transmission, water-borne outbreaks
75
Hep E is a mild-moderate illness, but in certain patients it commonly progresses from severe to fulminant hepatitis?
Pregnant patients
76
Chronic viral hepatitis is an infection w/ HBV or HCV for greater than 3 mos, with what parameters?
Persistent elevated AST/ALT Persistent presence of HBsAg/anti-HBc or anti-HCV Or histologic findings on liver biopsy (in the absence of concomitant cirrhosis, pts may be asymptomatic)
77
Treatment of chronic HBV (and HDV) is? [not super important... GI doc will do this]
``` Nucleoside or nucleoside analogs: Lamivudine Adefovir Telbivudine Tenofovir Entecavir ``` OR pegylated interferon
78
chronic HCV tx?
Direct-acting and host-targeting antiviral agents (with regimens based upon viral genotype) Ledipasvir + sofosbuivir (super expesnive though)
79
Form of chronic hepatitis due to autoantibodies, more common in whom?
more common in women varying clinical presentation (may be incidental finding)
80
Autoimmune hepatitis has varying clinical presentation (may be incidental finding)... ssx may include?
Transaminitis fatigue/lethargy/malaise/anorexia/nausea/abd pain/itching/small joint arthralgia More severe = profound jaundice, elevated PT, marked AST/ALT (>1000)
81
WHat are some common extrahepatitic manifestions of autoimmune hepatitis? (increased risk of cirrhosis and cancer)
Arthritis Sjogren syndrome thyroiditis nepthritis UC Coombs-pos hemolytic anemia

GI block 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions