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GI II Exam II > DSA Jaundice > Flashcards

DSA Jaundice Flashcards

1
Q

CMP measures what?

A
  1. AST/ALT
  2. Albumin
  3. BR
  4. ALP
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2
Q

Jaundice is yellow skin pigmentation caused by ________.

A

↑ serum bilirubin

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3
Q

Causes of hyperbilirubinemia (3)

A
    1. Overproduction
    1. Impaired uptake, conjugation or excretion of BR
    1. Regurgitation of UCB or CB from damaged hepatocytes or bile ducts
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4
Q

Bilirubin is the major breakdown product of _________, released from ___________.

A
  • Hemoglobin
  • Released from senscent erythrocytes
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5
Q

What are the first signs of jaundice?

A

Yellowing of the eyes, oral mucosa and palms

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6
Q

What changes will we see in:

  • Hepatocellular damage => damage to hepatocytes.
  • Which is MORE specific?
A

↑ AST/ALT

*ALT = more specific

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7
Q

What changes will we see in:

  • Cholestatic damage => damage to bile ducts, causing ______.
A
  • Damage to the bile ducts =>
    • cholestasis, thus, the bile cannot reach the duodenum.
  • ↑ in
    • ↑ alkaline phoshatase
    • ↑ bilirubin
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8
Q

Cholestatic damage (↑ ALP and bilirubin) can cause what symptoms?

A
  1. Jaundice
  2. Pruritis
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9
Q

1st thing to do when we have jaundice is what?

A

Determine if:

  • 1. Unconjugated/indirect or Conjugated/direct hyperbilirubinemia
    1. Other biochemical liver tests are abnormal
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10
Q

DDX

Unconjugated Hyperbilirubinemia => Jaundice

A
  1. Hemolytic syndrome (anemia or reaction)
  2. Gilbert Syndrome
  3. Crigler-Najar Syndrome
  4. Viral Hepattitis (can be both))
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11
Q

DDX

Conjugated Hyperbilirubinemia => Jaundice

A
  1. Hepatitis
  2. Cirrhosis
  3. Obstruction
    1. Choledocolithiasis, Cholangitis,
    2. PBC, PSC,
    3. Budd-Chiari
    4. Pancreatic cancer
  4. Dubin-Johnson Syndrome
  5. Rotor syndrome
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12
Q

1st diagnostic studies to get in a patient with jaundice

A
    1. CBC: to look for hemolysis => anemia and thrombocytopenia (prehepatic sources that cause unconjugated hyperbilrubinemia).
    1. Chemistry labs:
      * ​AST/ALT, ALP, Total BR (+ fractionated BR to tell if indirect vs direct)
      * Fractionate ALP by ordering GGT
    1. US to see if obstructive jaundice (conjugated)
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13
Q
  • Jaundice due to unconjugated/indirect hyperbilirubinemia
    • ↑ bilrubin production

DX???

A
  1. Hemolysis
  2. Hematoma
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14
Q

Jaundice due to unconjugated/indirect hyperbilirubinemia

  • Due to impaired bilirubin uptake and storage

DX???

A
  1. Post-hep
  2. Gilbert
  3. CN Syndrome
  4. Drug reaction
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15
Q

Jaundice due to conjugated/direct hyperbilirubinemia

  • Due to impaired excretion

DX???

A
  1. Dubin Johnson Syndrome
  2. Rotor Syndrome
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16
Q

Jaundice due to conjugated/direct hyperbilirubinemia

  • Due to Hepatocellular dysfunction

DX???

A
  1. Hepatitis/ Cirrhosis
  2. Drugs/ biliary cirrhosis
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17
Q

Hemolyis causes ______ hyperbilirubinema.

What diagnostic test do we run and what are we looking for?

A
  • Hemolysis => unconjugated hyperbilirubinemia
  • CBC
    • Anemia and thrombocytopenia by looking for (↓) haptoglobin and (↑) LDH
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18
Q

What is Gilbert Syndrome?

  • Pathophys
  • Labs
  • Treatment
A
  • Benign, asymptomatic AR jaundice seen after fasting, post-exercise
  • ↓ activity of UDGT => isolated ↑ bilirubin (unconjugated hyperbilirubinemia); however NL when not in those conditions
  • No treatment needed
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19
Q

Gilbert syndrome is associated with reduced mortality from __________.

A

CV disease

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20
Q

CN Syndrome 1 and 2 and Gilbert => unconjugated hyperbilrubinemia

Differentiate them based on

  • Inheritance
  • Defect
  • Liver histology

Clinical course

A
  • CN Syndrome Type 1
    • AR
    • ABSENT UGT1A1 activity
    • NL
    • Kills bb in neonatal
  • CN Syndrome Type 2
    • AD with variable penetrance
    • Decrease UGT1A1 activity
    • NL
    • Mild; occasional kernicterus
  • Gilbert
    • AR
    • Decrease UGT1A1 Acticity
    • NL
    • Innocous
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21
Q

Which indicated acute and chronic infection: IgM and IgG

A
  • IgM = acute
  • IgG = chronic
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22
Q

How long is chronic hepatitis?

A

> 3- 6 months

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23
Q

How can we tell is fibrosis/cirrhosis is occuring in chronic liver disease?

A
  1. Serum FibroSure
  2. US elastography
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24
Q

It is important to ask about _________, because they can cause transminitis/LF or hepatitis

A

MEDICATIONSS1

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25
Q

Acute Heptitis can be caused by: ____________

What may the patient report?

PE?

A
  • Viral, drugs or ischemia
  • Acolic stools, suddenly grossed out by smoking
  • Tender hepatomegaly, jaundice
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26
Q

When a patient comes in with acute hepatisis, what diagnostic test is IMPORTANT to run?

Generally, how it is treated?

A
  • Acetominophen levels via Rumack Matthew Nomogram
  • Generally, self-limited and supportive
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27
Q

Complication of acute hepatitis? (3)

A
  1. Cirrhosis
  2. HCC
  3. Fulminant liver failure => death
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28
Q

What is the course of HepA virus?

A
  • Never chronic; self-limited; pt recovers
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29
Q

_________ can cause an aversion to smoking.

A

Hep A

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30
Q

HepA

  • RF:
  • Symptoms
  • What pattern of injury is seen and how does this affect labs:
A
  • RF: International travel!
  • Symptoms: Jaundice + tender hepatomegaly + acholic stools
  • Labs: Hepatocellular AND cholestatic pattern
    • ↑ AST/ALT
    • ↑ BR/ALP
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31
Q
  • ________ is seen in the serum in HepA soon after onset.
  • Diagnosis = Detection of _______
  • What indicates that the persion was PREVIOUSLY exposed to HAV, is non-infected and immune?
A
  • IgM and IgG Anti-HAV
  • Diagnosis = IgM anti- HAV
  • Previously exposed (not infected/ immune) = IgG anti-HAV w/o IgM anti-HAV.
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32
Q

Is there a vaccine for Hep A?

A

Yes

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33
Q

Hep B

  • Acute/chronic or both?
  • Symptoms?
  • Transmission?
  • What pattern of injury is seen and how does this affect labs?
  • Vaccine?
A
  • Mainly acute, but chronic 5-10% of cases
  • Jaundice + tender hepatomegaly, low-grade fever + POLYARTERITIS NODOSA
  • Parenteral, sexual or perinatal (mom => bb)
  • Hepatocellular pattern; NO cholestasis pattern
    • MARKEDLY ↑ AST/ALT early in the course (higher than HepA)
    • If severe enough = prlong PT and INR => bleeding
  • Yes: protects against B and D
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34
Q

Where is HepB endemic and how is is passed down?

A

Africa and SE ASia

=> HBsAg (+) mom passes Hep B to BB => causing the risk of chronic infection to be 90%

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35
Q

How can we prevent Hep B before exposure and AFTER exposure in an unvaccinated person??

A
  • Before: 3 dose vaccine
  • After exposure in an unvaccinated person: Vaccine + HepB immune globulin (HBIG) immediately- 14 days after sex or birth (maternal transmission)
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36
Q

The window period is between HBsAg disappearing and HBsAb appearing, which may be several weeks, but the patient is still considered to have ______. To detect, we must measure ______. This is very important when screening blood donations.

A
  • Acute HepB
  • IgM HBcAg
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37
Q

What is very important when screening blood donations?

A

Screen for IgM HBcAg to see if patient has acute HepB

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38
Q

HepB

  1. Window period
  2. Acute infection
  3. Chronic infeciton
  4. Prior infection
  5. Immunization
A
  1. Window period: IgM HBcAg
  2. Acute infection: HBsAg, IgM HBcAg, HBe Ag and HBV DNA (if replicating)
  3. Chronic infeciton: same + [IgG anti-HBcAg]
  4. Prior infection (2): Anti-HBsAg and IgG anti-HBcAg
  5. Immunization: ONLY AntiHBsAg
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39
Q

________ typically parellaels prescee of HBeAg.

A

HBV DNA

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40
Q

If ______ persists >6 months after the acute illness => chronic hepatitis B.

A

HBsAg

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41
Q

When is Anti-HBsAg increased?

A

1. After clearance of HBsAg

2. Vaccination

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42
Q

____ indicates ACUTE hep B infection

A

IgM anti-HBcAg

***IgG also appears but persists FOREVER

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43
Q

________ may reappear during flares of previously inactive chronic hepatitis B

A

IgM anti-HBcAg

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44
Q

______ is the secretory form of HBcAg and if it persists longer than _____ => increase liklihood of chronic HepB

A

HBeAg

> 3months => chronic HepB

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45
Q

Hep D

  • Endemic areas in HepB ( _________), spreads via _________
  • In non-endemic areas (__________), spreads via __________.
A
  • Endemic = Mediterranean Basin = spread non-percutaneously
  • Nonendemic areas = N europe and US = percutaneously in HBsAg+ IV drug users or transfusion.
46
Q

What is a ssRNA genome with 7 genotypes and is most commonly CHRONIC?

A

HepC

47
Q
  • 30% of people with _____ are co-infected with HepC
  • >90% of patients got hepatitis from ________, have HepC
  • >50% of people with HepC get it from via _______, with ________ being a risk factor.
A
  • 30% of people with HIV are co-infected with HepC
  • >90% of patients got hepatitis from transfusion, have HepC
  • >50% of people with HepC get it from via IV drug use, with intranasal cocaine being a risk factor.
48
Q
  • Hep C aquired in the hostpital and outpatient clinics have received it via _________
  • In the developing world, ____________ => leads to ↑ HepC cases
  • Covert transmission of HepC has occured via ______.
A
  • multidose vials of saline used to flush catheters
  • unsafe medical practies
  • Bloody fisticuffs
49
Q

HepC

  • What pattern of injury is seen and how does this affect labs?
  • Complications

Prevention?

A
  • Hepatcellular: marked FLUCTUATING ↑ of AST/ALT
  • Cirrhosis, HCC, HIV co-infection, mixed cryoglobinemia, membranoproliferative Gnephritis, lichin platus
  • If infected =>SAFE SEX
50
Q

What is the most SENSITIVE indicator of HepC infection?

How do we properly dx?

A

HCV RNA

  1. Screen => check for Anti HCV in the serum
  2. If (+) => HCV RNA => most sensitive
51
Q

When has a person recovered from prior HepC infection?

A
    • anti-HCV w/o HCV RNA
52
Q

Which viral hepatisis is associated with ↓ serum cholesterol?

A

Chronic HepC infection

53
Q

CDC and USPSTF recommend screening persons born between _______ for HepC

A

1945-65 (Baby Boomers)

54
Q

New recommendation say that who should be screened for HepC?

A
  1. Once in all adults over 18YO, except in areas where prev is infectoin is less than 0.1%
  2. All pregnant W in each pregnancy, except in areas where prev of infection is less than 0.1%
55
Q

HepE

  • RF
  • Where is it epidemic?
  • Transmission
  • Vaccine?
  • Acute with no carrier state, however, what group of people have seen Chronic HepE infection that progresses to Cirrhosis?
A
  • Immunocompromised ppl
  • Asia, Middle East, N. Africa, C. America, India
  • Enterically fecal-oral from water; spread by SWINE
  • Clinical trials are testing one that is promissing
  • Transplant patients treated with tacrolimus
56
Q

What are dose-dependent direct hepatotoxins that can cause hepatitis?

A

1. Mushroom poisoining

2. Acetominophein

57
Q

What are idiosyncratic drugs/toxins (sporadic and not related to dose) that can cause hepatitis?

A
  1. Isoniazid
  2. Sulfonamides
58
Q

How do we treat toxic/drug- induced hepatitis?

A
  1. Supportive:
    1. stop taking drug/toxin
    2. Gastric lavage and give oral charcoal & cholestyramine
59
Q

Acute Liver Failure

  • MCC
  • Patients will have ________ and _________.
  • Diagnostics: _____________
  • Complication?
A
  • Acetominophin OD
  • Hepatic encephalopthy + coagulopathies
  • Acetominophen level via Rumak Matthew Nomogram
  • Not reco/treated => multiorgan failure and death.
60
Q

Tyelonal/ acetominophen OD is detected by the Rumack- Matthew Nomogram (measures the acetominophen plasma concetration after (x) hours of ingestion) to determine in patient has hepatoxicity).

  • It is important to obtain _______.
  • How do we treat
A
  • 4 hour acetominophen level
  • NAC (N-acetylcystine) within 8 hours of ingestion (but can be effective if 24-36 hours later) provides sulfhydrl groups to bind toxins
61
Q
  • What is fulminant hepatic failure?
  • Subfulimant?
A
  • Fulminant hepatic failure => pt gets hepatic encephalopthy within 8 weeks of onset of acute liver disease
  • Subfulminant => pt gets hepatic encephalopathy between 8 weeks - 6 months.
62
Q

Fulminant Hepatitis

  • What is this? Assx symptoms?
  • Diagnosis and
A
  • LF + encephalopathy: Massive hepatic necrosis + hepatic encepholapthy (impaired consciousness) that occurs within 8 weeks of the onset of an illness.
    • Rapidly shrinking liver + ascites + edema
  • [Rapidly ↑ bilirubin] & [marked prolongation of PT] EVEN as AST/ALT ↓
63
Q

What type of edema is most common in Fulminant Hepatitis?

A

Cerebral edema

64
Q

How do we treat Fulminant Hepatitis?

A
  1. Support patient
    1. Maintain fluids, circulation and respiration
    2. Control bleeding, fix hypoglycemia, tx other complications
  2. No proteins
  3. Consider liver transplant
65
Q

How can we treat encephalopthy seen in fulminant hepatitis?

A
  1. Oral lactulose
  2. Neomycin
66
Q

What is the KEY to improving survival in patients with Fulminant Hepatitis?

A
  1. Meticulous intensive care +
  2. Prophylatic ABX
67
Q

Mortality rate in Fulmanant Hep is _______.

A

VERY HIGH!

68
Q

______ is the most common cause of chronic liver disaese in the US.

A

NAFLD

69
Q

What is chronic hepatitis?

A

Chronic inflammtion of the liver for at LEAST 6 months.

70
Q

Which 3 hepaittis can cause chronic Hep, key signs and how are they mediated?

A
  • Chronic HepB, C, Autoimmune => IMMUNE COMPLEX MEDIATED
  • HBV: polyarteritis nodsa
  • HCV: mixed cryoglobenimia
71
Q

In Chronic Hepatitis, ______ is used to histologically classify by _________ and _______.

A
  • BIOPSY
    • Grade & Stage
72
Q

What are the causes of Chronic Hepatitis?

A
  1. HBV +/- HDV
  2. HCV
  3. AI Hep
  4. Wilsons
  5. Hemochromatosis
  6. A1-antitrypsin deficiency
73
Q

What is the most common type of AIH, which can lead to chronic Hep?

Who does it occur in

Serology?

What do we see on exam?

A
  • Type 1:
    • 30-50YO W
    • (+) ASMA ab*** and (+) ANA ab and hypergammaglobulinemia
    • Healthy young W with stigmata of cirrhosis
74
Q

In AIH,

  1. Serum AST/ALT levels will be ___________
  2. _________ is usually increased
A
  1. AST/ALT: > 1000 units/L
  2. Total bilirubin
75
Q

What is Stigmata of cirrhosis?

A
  1. Multiple spider telangiectasias
  2. Cutaneous striae
  3. Acne
  4. Hirsutism
  5. Hepatomegaly
76
Q

What is a complication of Autoimmune Hepatitis?

Treatment?

A
  1. Cirrhosis
  2. HCC
  • Treat: glucocorticoids
77
Q

_______ if the most common precursor to cirrhosis.

A

Alcohol liver disease

78
Q

How much alcohol must be drinken to classify as Alcohol Liver Disease?

When doing an H&P, what is ONE thing we need tp be catious be?

A
  • M: > 80g/day
  • W: > 30-40 g/day

bitchez lie and wont admit too much alcohol use

79
Q
  • Alcoholic Fatty Liver Disease (Steatosis) is often _____________.
  • In Alcoholic hepatitis, you will see what 2 key characterstics .
A
  • Steatosis: Asymptomic hepatomegaly
  • AH:
    • 2:1 AST: ALT ratio (not above 300 u/L)
    • Mallory Denk Bodies: alcoholic hyaline
80
Q

Think alcohol when you see ____________.

A

2:1 AST: ALT ratio (not >300 u/L)

81
Q

What increases our risk of developing alcoholic cirrhosis?

A

>50grams/day for >10 years

82
Q

In alcoholic liver disease, what will you see on CMP?

A
  1. 2:1 ratio of AST/ALT (not above 300/L)
  2. ↓ albumin; ↑ gamma-globulin level
  3. ↑ bilirubin
  4. ↑ ALP and GGT
83
Q

In alcoholic liver disease, what will you see on CBC?

A
  1. Macrocytic/megaloblastic anemia
  2. Leukocytosis
  3. Lerkopenia
  4. Thrombobocytopenia
84
Q

PT/PTT/INR will be ________ in alcohol liver disease.

A

increase

85
Q

______ deficiency can be seen in alcohol liver disease

A

Folic acid deficiency

86
Q

Alchol Liver Diseease

  • Imaging
  • Biopsy of Liver
  • Treatment
A
  • US Fibrosure to see if cirrhosis
  • Biopsy findings are SAME as NASH: mallor bodies (alcoholic hyaline)
  • Tx
    1. STOP alcochol
    2. Daily mutlivitamin + 100 mg of thiamine + 1 mg folic acid + zinc
    3. Liver transplant if end-stage, but must abstain alcohol for 6 months
87
Q

When treatming Alcohol Liver Disease, what must be done to prevent Wernicke-Korsakoff Syndrome?

A
  • Before giving glucose to a patient, replace thiamine (vitamins) 1st. Otherwise, patient can get Wernickes
88
Q

Wernickes encepalopthy Triad

  • Diagnosis?
  • Treat:
A
  • 1. Confusion
  • 2. Ataxia-staggering/ no coordination
  • 3. Involuntary eye movements (horizontal nystagmus

Dx: clinical suspicion

Treat: thiamine

89
Q

Korsakoff Syndrome sx

A
  1. REALLY bad Wernickes => that causes permenant and severe memory issues, so will make up shit to fill in gaps
90
Q

50% of critically ill pts with _________ will die in 30 days

A

alcoholic hepatitis

91
Q

Alcohol Liver Disease

  1. Maddrey’s discriminant function: ?
    1. _____ = poor prognosis and tx with ______
  2. A Model for End-Stage Liver Disease (MELD/MELD-Na) score
    1. _______ = significant mortality in alcoholic hepatitis.
  3. Glasgow Alcoholic Hepatitis Score: predicts mortality based on a multivariable model
    1. _____= who got glucocorticoids had higher survial rates than those who did not
A
  • Maddrey’s discriminant function: severity and mortality in pts w alcoholic hepatis by measuring PT and serum bilirubin
    • ​> 32 = high short term death and treat w glucocorticoids
  • (MELD/MELD-Na)
    • > 21 = significant chance of death from alcoholic heaptitis
  • Glasgow Alcholic HEpatitis Score = predicts death based on many variables
    • > than or equal to 9
92
Q

Fatty liver aka Hepatic steatosis can be caused by what 2 things?

A
  1. Acoholic fatty liver diasease
  2. NAFLD
93
Q

How much alcohol must someone drink to be dx with NAFLD?

A
  • M: < 30 mg/day
  • W: < 20 mg/ day
94
Q

NAFLD

What are the main causes of NAFLD?

what do these increase risk of? (3 C’s)

Most commonly occur in ___________

What protects AGAINST NAFLD?

Who is unlkely to get cirrhosis caused by NASH?

A
  1. Metabolic syndrome
    1. obesity, DM, hyperTAG + insulin resistance
  2. Increase risk for: CV disease, CKD, colorectal cancer
  3. Hispanics
  4. Protects: coffee and physical activity
  5. AA
95
Q

NAFLD

  • Sx?
  • Serum levels?
  • Liver Biopsy = diagnostic
A
  • Asx or mild RUQ pain + hepatomegaly, but all you may see is INC AST/ALT/ALP
    • ​however, NL in 80% w hepatic steatosis
  • Biopsy
    • Focal infiltration of polymorphonuclear neutrophils
    • Mallory hyaline
    • LOOKS EXACLTY LIKE ALCOHOLIC HEPATITIS => NASH
96
Q

Vinyl Chloride is a weird cause of _______

A

Fatty LIVER

97
Q

Hemochromatosis = increased iron ab from duodenum

  1. What causes us to suspect hemochromatosis?
  2. Rarely recognized before patient is ______
  3. Overall mortality is __________.
  4. Risk factors for developing advanced fibrosis: ____, _____, ____
A
  1. ↑ iron saturation; ↑ serum ferritin or FH
  2. 50s
  3. slightly incrased
  4. M; DM; excess alcohol consumption
98
Q

Describe sx of patient with Hemochromatosis

A
  • Mostly asymptomatic. Early, sx are non-specific. L
  • Later, as iron starts to deposit, patient can get
    1. skin pigmentation
    2. DM and complication
    3. erectile dysfunction
    4. ARthritis
99
Q

Patients with Hemochromatiss are at INCREASED RISK FOR ____

A

Yersinia enterocolitica

100
Q

Hemochromatosis

  • Labs
  • Who do we screen?
A

Labs

  1. HFE gene mutation
  2. Mild abnl AST/ALT/ASP
  3. ↑ plasma iron with > 45% transferrin saturation
  4. ↑ serum ferritin

Screen

  1. Anyone w iron overload
  2. All first degree family members
101
Q

Hemochromatisis Tx

A
  1. Avoid foods with iron
  2. Weekly phlebotomies***
  3. PPI to decrease iron absorbtion
  4. if you get a liver transplant => nl levels and no more phleb
102
Q

If patients have [hemochromatosis + anemia] or secondary iron overload due to thalassemia who cannot tolerate plebotomies, how do we treat?

A

Chelating agent deferoxamine

103
Q

Wilsons disease is a AR disorder than can cause cirrhosis and organ toxicity due to mutation in _____ and dx at age ______, causing _____

A
  • ATP7B mutation
  • Dx under 40 YO
  • too much absoprtion of Cu from SI, but impaired copper excretion in bile and failure to put it in ceruloplasm
104
Q

Sx seen in Wilsons

which is the pathogomeunomic sign

A
    1. Hemolytic anemia (Cu toxic to RBC_
  • 2. Kayser Fleischer rings - brown green ring around eye ***** pathomneumonic sign
    1. Neuro defects (migrains, insomnia, seizures)
    1. Psych features (behavior and personality changes)
      * can occur b4 neuro
105
Q

Wilsons Disease is a __________ in adolescents; but a _______ in young adults

A

liver disease = adolescents

neuropsych = young adults

106
Q

When should we consider wilsons diasese as a dx

A

Child/young adult wiht

  1. hepatitis
  2. splenomegaly with hypersplenism
  3. Coombs neg hemolytic anemia
  4. Portal HTN
  5. NEuro/psych problems
107
Q

Wilsons Diagnosists

Labs and which imaging study should we do?

A
  1. Low serum ceruloplasm
  2. High concentation of copper in liver; increased urine excretion of copper
  3. MRI of the brain show copper deposts
108
Q

ALPHA 1 ANTITRYPSIN DEFICIENCY

  • The most commonly diagnosed inherited hepatic disorder in infants and children.

Develop what 2 problems?

  • Diagnositcs?
A
  • Pulmonary emphysema at a young age in lower lobes (if smoker = upper lobes)
  • Liver disease due to acc of misfolded protein
  • Check A1-AT phenotype (homozygous PIZZ)
109
Q

ALPHA 1 ANTITRYPSIN DEFICIENCY

Tx:

A
  1. Smoking abstinence/cessation
  2. Liver transplant
    1. MC genetic cause requiring liver transplant in children
110
Q
A

GI II Exam II (10 decks)

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