Jaundice Flashcards
(97 cards)
1
Q
What is the normal pathway of BR metabolism?
A
Initially it is bound to albumin, transported to the liver, conjugated ti a water-soluble form (glucuronide), excreted into bile and converted to urobilinogen in the colon
2
Q
Which enzymes are elevated in hepatocellular disease?
Which is more specific for liver injury?
A
AST/ALT
ALT is more specific than AST for liver injury
3
Q
Which enzymes are elevated in cholestatic disease?
A
ALP and BR
4
Q
“True” liver function tests include (4)
A
PT/INR
Albumin
Cholesterol
Ammonia
5
Q
DDx considerations for diseases with unconjugated jaundice (3)
A
Hemolytic syndrome
Gilbert syndrome
Crigler-Najjar syndrome
***possibly viral hepatitis (can be both)
6
Q
DDx considerations for diseases with conjugated jaundice (5)
A
Hepatitis
Cirrhosis
Obstruction
Dubin-Johnson syndrome
Rotor syndrome
7
Q
What should be evaluated for on a CBC in a patient with jaundice?
A
Anemia and thrombocytopenia
8
Q
What chemistry labs should be ordered for a patient presenting with jaundice? (3)
A
AST/ALT, total BR, ALP
9
Q
Diagnosing obstructive jaundice (conjugated) typically begins with what?
A
US
10
Q
Which antibodies suggest an acute vs. chronic viral hepatitis: IgM and IgG?
A
IgM: acute
IgG: chronic
11
Q
Stool appearance in acute hepatitis:
A
Acholic stools
12
Q
What are 3 staples of labs that should be done in a patient presenting with acute hepatitis?
A
CMP (AST/ALT, BR, ALP, albumin, renal function)
PT/INR
Acetaminophen level
13
Q
What is the #1 risk factor for HAV?
A
International travel
14
Q
“Aversion to smoking” =
A
HAV
15
Q
Unique symptoms of HAV (3)
A
Enlarged and tender liver
Jaundice
Acholic stools
16
Q
What liver enzymes are markedly elevated in HAV?
Elevation of which labs indicate cholestasis?
What is the best test for diagnosing acute hepatitis A?
A
AST/ALT
Elevated BR and ALP
IgM anti-HAV Abs
17
Q
What is the duration/progression of HBV?
A
Acute illness usually subsides over 2-3 weeks -> complete clinical and laboratory recovery by 16 weeks
5-10% will become chronic
18
Q
Marked cholestasis is not a feature in…
A
HBV
19
Q
When are aminotransferases highest in HBV?
A
Early in the course
20
Q
Positive serology in the window period in HBV (1)
A
IgM Abs
21
Q
Positive serology in acute infection in HBV (4)
A
HBsAg
IgM Abs
HBeAg
HBV DNA
22
Q
Positive serology in prior infection of HBV (2)
A
Anti-HBsAg
IgG Abs
23
Q
Positive serology in chronic infection of HBV (5)
A
HBsAg IgM Abs IgG Abs HBeAg HBV DNA
24
Q
What does HBeAg indicate?
If it persists past 3 mo…
A
Viral replication and infectivity
There is an increased likelihood of chronic HBV
25
What does HDV require for its replication?
Requires HBV for replication
26
Co-infection of HCV has been found in at least 30% of...
Patients with HIV infections
27
How does cholesterol levels change in chronic HCV?
Decrease in serum cholesterol
28
What is the recommendation for HCV screening?
Screen people born between 1945-1965 (baby boomers)
29
HEV is most commonly known to infect:
What is the route of transmission? What spreads the virus?
Immunocompromised hosts
F-O route, spread by swine
30
What is the treatment for toxic and drug induced hepatitis?
Supportive treatment: withdraw suspected agent; include use of gastric lavage and oral admin of charcoal or cholestryamine
31
What is used to evaluate acetaminophen level?
Rumack-Matthew nomogram
32
What happens if acute liver failure is not recognized/treated?
Multiorgan failure and death
33
When should therapy for acetaminophen overdose begin?
Within 8 hrs. of ingestion, but can be effective even as late as 24-36 hrs.
34
What is fulminant hepatic failure?
When does subfulminant hepatic failure begin?
Hepatic encephalopathy development within 8 weeks of onset of ALD with presence of coagulopathy.
Subfulminant hepatic failure begins between 8 wks. and 6 mo.
35
Etiology of fulminant hepatitis
Massive hepatic necrosis with impaired consciousness occurring within 8 wks. of onset of the illness
36
Clinical manifestations of fulminant hepatitis include: (3)
Encephalopathy that may evolve to deep coma.
Liver changes: rapidly shrinking liver + rapidly rising BR + prolongation of PT + signs of confusion, disorientation, etc.
Cerebral edema.
37
What are labs/diagnostics used in fulminant hepatitis?
Rapidly increasing BR and marked prolongation of the PT even as the aminotransferases fall
38
What is the treatment for fulminant hepatitis? (4)
Supportive: maintain fluid balance, circulation, respiration
Restrict protein intake
Oral lactulose or neomycin
*Prophylactic abx (one factor that improves survival)
....maybe consider liver transplant
39
What are the terminal events in fulminant hepatitis?
What is the mortality rate?
GI bleeding, sepsis, respiratory failure, RF, CV damage, etc.
Mortality rate is high: >80% in patients with deep coma
40
Chronic hepatitis must last longer than:
6 mo.
41
Which extra-hepatic manifestation occurs in chronic hepatitis in a patient with HBV?
PAN
42
Which extra-hepatic manifestation occurs in chronic hepatitis in a patient with HCV?
Mixed cryoglobinemia
43
What age does AIH commonly present?
How do these patients appear?
F>M (80%); 30-50 y/o
Progressive jaundice, anorexia, hepatomegaly. abdominal pain. epistaxis, fever, amenorrhea.
Exam reveals a healthy-looking young woman with stigmata of cirrhosis.
44
What lab changes occur in AIH?
Serum ALT > 1000, usually elevated BR
45
Major treatment for AIH?
What complications may ensue?
Glucocorticoids
Cirrhosis
-> risk of HCC
46
Alcoholic liver disease occurs most often in consumption of how much liquor daily?
80 g/day in men and 30-40 g/day in women
```
Daily:
-4 oz of 100-proof whiskey
-15 oz wine
-4 12-oz cans of beer
...all for 10+ years
```
47
What ratio of LFTs should make you think alcohol-related?
2:1 AST to ALT
48
Lab findings in alcoholic liver disease on CMP (5)
CBC
PT/INR
```
CMP:
2x AST > ALT
Low albumin
Elevated ALP and GGT
Increased BR
```
```
CBC:
Anemia
Left shift leukocytosis
Leukopenia
Thrombocytopenia in 10%
```
PT/INR:
Prolonged PT/INR
49
What imaging is good for alcoholic liver disease?
US elastography which can show absence of fibrosis
50
What can precipitate Wernicke-Korsakoff syndrome in patients with alcoholic liver disease?
Glucose administration (increases thiamine needs) and can cause W-K syndrome if thiamine is not also given with it.
51
Aside from abstinence from alcohol, what is given to patients with alcoholic liver disease? (5)
Daily multivitamin, thiamine 100 mg, folic acid, Zn
Transfusions of RBC or plasma if needed
52
Wernicke encephalopathy triad =
What is the treatment?
Confusion, ataxia, abnormal eye movements
Thiamine
53
Korsakoff syndrome =
Permanent severe memory issues, confabulation (make-up stories, fabrication, etc.)
54
What is needed to calculate Maddrey's discriminant function? (2)
What value suggests a poor prognosis?
What is a beneficial therapy?
PT and serum BR
>32 is poor prognosis (short-term mortality)
Glucocorticoids
55
Glasgow alcoholic hepatitis score predicts:
| What does it evaluate?
Mortality in alcoholic hepatitis
GAH >9 who received glucocorticoids had higher survival rates than those who did no get glucocorticoids.
GAH <9 shows no benefit with glucocorticoids.
56
How little alcohol should be consumed to make the diagnosis of NAFLD?
<20 g of alcohol in women and <30 g in men
57
Most common cause of chronic liver disease =
Increased risk in which ethnicity?
NAFLD
Hispanics
58
Classic tetrad in Hemochromatosis
What age is the onset?
Cirrhosis w/ hepatomegaly
Abnormal skin pigmentation
DM
Cardiac dysfunction
Rarely onsets before 50 y/o
59
What are risks for advanced fibrosis in Hemochromatosis? (3)
What processes may suggest an increased mortality? (3)
Male sex
Excess alcohol consumption
DM
Hepatic and pancreatic insufficiency
HF
Hypogonadism (ED can develop in men)
60
Lab/genetic abnormalities in Hemochromatosis (4)
HFE mutation
Mildly abnormal LFTs (AST, ALP)
Elevated plasma iron with >45% transferrin saturation
Elevated serum ferritin
61
What imaging is helpful in Hemochromatosis?
MRI or CT
62
Iron studies and HFE testing is recommended for which patients?
All first-degree family memers with Hemochromatosis
63
What are some treatments/management strategies for patients with Hemochromatosis? (4)
Weekly phlebotomy therapy
Iron-rich food avoidance
PPI once iron store depletion is done
Deferoxamine (a chelating agent for patients with hemochromatosis and anemia)
64
What age does Wilson disease occur?
When does liver disease in Wilson's present?
When does neuropsychiatric disease present?
What imaging can be helpful?
<40 y/o
Liver Dz - adolescents
Neuropsychiatric disease - young adults
MRI of brain
65
Biopsy shows Kayser-Fleischer rings. Diagnosis?
Wilson disease
66
ATP7B mutation =
Wilson disease
67
Most commonly diagnosed inherited hepatic disorder in infants and children =
a1-ATD
68
Chronic HBV is endemic in which parts of the world?
Many infants can it via...
It is asymptomatic when...
Endemic in Asia and sub-Saharan Africa
90% of infants with maternal transmission
Asymptomatic healthy carrier state
69
Which Abs are positive in chronic HBV?
```
HBsAg
Anti-HBc (IgM)
Anti-HBc (IgG)
HBeAg
HBV DNA
```
70
Chronic HCV may lead to cirrhosis progression in which patients?
```
Men after 20 years of disease
Drink >50g of EtOH daily
Become infected post 40 y/o
Immunocompromised
Tobacco, cannabis and fatty liver promotes fibrosis
```
71
Coffee slows the progression of what?
Chronic HCV
72
Patients can have normal AST/ALT in which infection?
HCV
73
Which viral hepatitis is curable?
HCV
74
Passive congestion of the liver (nutmeg liver) can cause:
Ischemic hepatitis - ischemic hetopathy, hypoxic hepatitis, shock liver, acute cardiogenic liver injury
75
What meds may help prior to admission in a patient with passive liver congestion against ischemic hepatitis?
What symptoms is associated with a worse prognosis?
Statin therapy
Jaundice
76
The hepatojugular reflex evaluates...
| What pathology is it associated with?
Right heart function
| Nutmeg liver
77
What lab is markedly elevated in right heart failure with liver involvement?
What is present is hepatic ischemia is onvolved?
Elevation in proBNP or BNP
Rapid and striking elevation of serum aminotransferase and LDH
78
Findings on CBC in cirrhosis (2)
Chemistry findings in cirrhosis (2)
Anemia, pancytopenia
Glucose distrubances, hypoalbuminemia
79
Definitive diagnosis of cirrhosis requires:
Bx
80
Serum ascites albumin gradient (SAAG) =
Serum albumin - ascites album = SAAG
81
Hyponatremia occurs in:
Ascites
82
3 categories of routine studies of ascites fluid
1. Cell count: WBC ct. with diff is most important test
2. Albumin and total protein: SAAG is best test to classify ascites
3. Culture and Gram stain
83
Best imaging for diagnosing ascites
Abdominal US
84
Hepatic encephalopathy =
What specific lab is elevated?
ALteration in mental status and cognitive function in the presence of liver failure
Ammonia, but the correlation between severity and ammonia is not that helpful
85
4 stages of overt hepatic encephalopathy
1. mild confusion
2. drowsiness
3. stupor
4. coma
86
2 major precipitants of hepatic encephalopathy
2 most common symptoms:
GI bleeding, constipation
Fever and abdominal pain
87
Which bugs are NOT associated with spontaneous bacterial peritonitis?
Anaerobic bacteria
88
What is the most important test to run on ascitic fluid in SBP? What level allows a diagnosis?
WBC ct. - >250 WBC/mcL
89
What is the best treatment for recurrent SBP?
What is the best antibiotic?
What is a major cause of death?
Liver transplant
3rd-gen cephalosporin IV or a beta-lactam agent
Kidney injury, which develops in 40% of patients
90
3 treatment options in HCC
Trasplant/resection
Radiofrequency ablation
Transcatheter arterial embolization (TACE)
91
No satisfactory therapy exists in...
Primary sclerosing cholangitis
92
Major treatment option for primary biliary cirrhosis:
Ursodeoxycholic acid
93
What can occur as a consequence of hepatic v. obstruction (Budd-Chiari syndrome)?
What is associated with it?
What are the symptoms?
RSHF -> nutmeg liver
Hypercoagulibility
RUQ pain, jaundice, splenomegaly and ascites
94
What is the screening test of choice for Budd-Chiari?
Contrast-enhanced US (CEUS)
95
Window period of HBV
What test must be done if you suspect this?
Period between HBsAg disappearing ad HBsAb appearing. May last a few weeks, but the patient is still considered to have acute HBV.
Both tests may be negative, but disease is still there. Must check IgM!
96
Positive serology in immunization of HBV (1)
Anti-HBs (HBsAb)
97
When you see “pyogenic gangrenosum” you should think of...
Ulcerative colitis
