DSA Jaundice Part 2 Flashcards
1
Q
What type of emphemysa does A1 AT cause and when?
A
Panacinar emphsema (lower lobes) at a young age.
2
Q
Who goes Chronic HepB
A
- 90% of infants with maternal transmission in endemic areas (Africa/Asia)
- Asymptomatic heathy carriers
3
Q
What is important to note about AST and ALT levels in Chronic HepC?
A
Fluctuate, and can be NORMAL
4
Q
Most cases of Hep___ is curable.
A
C
5
Q
What does right heart failure cause?
A
=> passive congestion of the liver => nutmeg liver (centrilobular congestion)
6
Q
What conditions do we see nutmeg liver in?
A
- 1. R HF
- 2. Budd-Chiari Syndrome
7
Q
How does R HF damage the liver?
A
Nutmeg liver:
-
ischemic hepatitis =>
- ischemic hepatopathy,
- hypoxic hepatitic,
- shock liver,
- acute cardiogenic liver injury.
8
Q
In patient with RHF, what can we see in H&P?
A
1. Pulsatile liver due to: Hepatojugular reflex + triscupid regurg
9
Q
How do Diagnoose RHF?
A
1. Increase in serum N-terminal BNP or BNP
10
Q
Shock liver in RHF can cause what lab levels?
A
- Rapid and striking ↑ AST/ALT (>5000)
- ↑ LDH occurs early
- Mild ↑ in ASP/Br
11
Q
____ is the development of fibrosis.
A
Cirrhosis
12
Q
What are the 3 types of cirrhosis?
A
- Compensated
- Compensated with varices
- Decompensated (ascites, varices, encephalopathy or jaundice)
13
Q
What reduces the risk of cirrhosis?
A
Drinking coffee and tea
14
Q
MCC of cirrhosis?
A
- Alcohol
- Chronic Hep C
- NAFLD
- Hep B
15
Q
Clinical manifestations of Cirrhosis
A
May be absent, with cirrhosis only accidently found during surgery.
16
Q
Signs of Cirrhosis? (7)
A
- Jaundice
- Spider telangectasis
- Palmar erythema
- Dupuytren contractures.
- Vit def (glossitis and cheliosis)
- Caput madesea
- Asterxis
17
Q
Cirrhosis
- CBC
- INR
- CMP
A
- CBC: Anemia, pancytopenia (low platets)
- Prolonged PT (INR)
- CMP => typically a cholestatic pattern
- ↑ BR/ALP
- Glucose disturbances
- Hypoalbumenia
18
Q
Cirrhosis due to _____ will show (x) in serum
- Viral
- Hemochromatosis
- Primary Biliary Cirrhosis
- AI
- Wilsons
- A1 AT Defiency
A
- u already know-
- Fe, total iron-binding capacity, ferritin
- AMA (anti-mT antibody)
- ASMA (anti- smoothMusc AB); Anti-LKM, ANA
- ↓ Ceruloplasm
- ↓ a1 AT and phenotype!
19
Q
What imaging can we do in Cirrhosis patients that tells us size of the liver, detect ascites, or hepatic nodules?
A
Abdominal US
20
Q
What imaging can we do in Cirrhosis patients to diagnose Budd-Chiari Syndrome?
What are we looking at.
A
-
Abdominal US + doppler
- patency of splenic, portal and hepatic vein
21
Q
What will CT+ contrast or MRI show us in patients with Cirrhosis?
A
- Cirrhotic liver
- splenomegaly
- collaterals
- venous thrombosis
- characterizing hepatic nodules
22
Q
How do we DEFINITIVELY diagnose Cirrhosis?
A
- LIVER BIOPSY => histologically classify grade and stage
23
Q
In Cirrhotic patients, what can be done to look for varices?
A
EGD
24
Q
Treatments for Cirrhosis?
which is most important
A
- ***** NO ALCOHOL
- Vaccines: HepA/B, Pneumococca, yearly influenza
- NSAIDS (CI); ACE-I/ANG-II ANT => Avoid
25
How do we treat **ascites** and **edema** in **Cirrhosis**?
1. **TIPSS (transjugular intrahepatic portosystemic shunt) =\> treats portal HTN \*\*\***
1. can cause: hepatic encepathlogy, infection, shunt stenosis/occlusion
2. Spironolactone and furosemide
26
what predicts the **severity of cirrhosis** and **risk of complications?**
What labs should we order and what may we see on PE?
**_Child-Pugh Scoring System_**
* CMP or **hepatic function panel (BR, albumin) PT/INR**
* **Ascites** and **encephalopathy**
27
Purpose of **MELD/MELD-NA** for **end-stage liver disease?**
* Scores are based on what factors?
* **Predict survival** in patients with cirrhosis
* **Bilirubin, Cr, INR** and **Na+**
28
Complications of **Cirrhosis** (4)
1. **HCC**
2. **Increase risk of getting DM \*\*\*\***
3. **Vit D deficiency**
4. **UGIB (GE varices, Portal HTN)**
29
What is defined as **portal HTN?**
What causes it?
**↑ of hepatic venous pressure \>5 mmg, due to cirrhosis.**
Caused by:
1. Cirrhosis causes: increased intrahepatic resistance to blood flow through the liver
2. Increased splanchinic blood flow due to vasodilation
30
What is SAAG?
SAAG = serum ascites albumin gradient and it tells us what the **etiology of the ascites is.**
31
SAAG **\> 1.1 g/dL**
* Ascites is due to **portal HTN** caused by
1. **Hepatic congestion** (RHF/ constrictive pericariditis, Budd-Chiari Sundrome (hepatic vein thrombosis)
2. **Liver disease**
3. **Portal Vein occlusion**
4. **\* Myxedema**
32
What are signs of **cirrhosis**? (ones not mentioned before)
1. Testicular atrophy
2. Muscle wasting
3. Dupuytrens Contracture
4. Umbilical hernia
5. Esophageal varices
33
How do we establish a diagnosis of ascites?
**Abdominal US**
We can then do a **paracentesis** (diagnostic and therepeutic) =\> run a **SAAG** to tell us the CAUSE of ascites.
34
SAAG \<1.1 g/dL
Ascites is due to
1. Hypoalbuminemia
2. Diseased periteum
35
What electrolyte problem will people with ascites see?
**Hyponatremia** because free water excretion is impaired
36
What are our categories of causes of **ascites**?
What is the MCC of ascites?
1. NL peritoneum
2. Diseased peritoneum (MCC is due to portal HTN due to chronic liver disease)
37
H&P in Ascites
1. Increase waists (feel pregnant/pants dont fit
2. Ask about RF for liver disease: alcohol, transfusions, tattoos, IV drug use, a hx of viral hepatitis or jaundice, and birth in an area endemic for hepatitis
3. Cancer =\> could mean malignant ascites
4. Fevers =\> could mean bacterial peritonitis (spont or secondary)
5. immigant, immunocomproised, malnourish alcoholic: Tuberculosis peritonitis
38
PE on pt with ascites
1. **Large liver** due to thrombosis of hepatic vein (BCS)
2. **Asterixis**
3. **Shifting dullness** = changes in percusion dep on position; must have at least 1500 ml.
39
When is an **abdominal parecentesis** done in a patients?
1. **ANY pt with acites**, esp sx, **to rule out SBP (spontaneous bacterial peritonitis**)
2. All patient with new onset ascites
3. All patients admitted to hospital with cirrhosis and ascites.
40
Once a paracentesis is done, what routine studies should be done on ascites fluid?
\*which is the most important
1. **WBC count with differential** =\> suggests SPB if (\>250 mcL; neutrocytic ascites) _MOST IMPORTANT\*\*\*_
2. **Albumin** and **total protein (=\>** calculate SAAG)
3. Culture and gram stain
41
Abdominal US + doppler studies in a patient with ascites diagnoses \_\_\_\_\_\_
Budd Chiari Syndrome
42
Typical patient presenting with **hepatic encelopathy?**
What will we do if we suspect?
How do we treat
* Patient with a **hx of liver disease** presenting with **AMS; could have asterixis in PE**
1. **Check ammonia levels** and **diagnose clinically**
2. **Treat: Lactulose** (if cant tolerate; neomycin, metronidazole, rifaximin)
3. =\> DO **NOT** monitor ammonia levels**, check to see if symptoms resolve** bc ammonia levels & severity do not correlate well
43
What can precipitate Hepatic encephalopathy?
**1. GI bleed**
2. **Constipation** bc not pooping out and holding ammonia in
44
What is the cause of **SPONTANEOUS BACTERIAL PERITONITIS?**
* Bacterial infection of ascites that occurs in the absence of a intra-abdominal source of infection.
* **Enteric bacteria translocate** and cause a **monomicrobial infection.**
45
Common pathogens that cause SPONTANEOUS BACTERIAL PERITONITIS
which does NOT cause
1. **Enteric gram (-) bacteria**: E.coli, klebsiella
2. **Gram (+) bacteria:** Strep pneumo, vridinans, enterococci)
**Anaerobic bacteria** is NOT associated.
46
Symptoms of SPONTANEOUS BACTERIAL PERITONITIS
* Many cases are subtle, but MC symptoms are
* **Abdominal pain + feve**r ++++ [change in mental status and worsening kidney function]
47
How do we diagnose SBP?
Do cultures establish the organism
* WBC count of fluid shows ascites has neutrophil count (PMN) \>250 cells/mcL.
* No
48
Treatmnt of reccurent **SBP**
1. Liver transplant
2. Empirical ABX
49
Patients with SBP have a high-risk of \_\_\_\_\_\_\_.
Major cause of death?
* **Nephrotoxicity**
* **Kidney injury** (increase albumin)
50
Prevent and prognosis of SBP
1. Prevent: oral once a day prophylactic therapy
2. Prgnosis
1. \>30% die ; if treated early \<10%
51
Difference between spontaneous bacterial peritonitis and **secondary bacterial peritonitis**
## Footnote
**Treatment?**
Secondary bacterial peritonitis =\> asciticf luid has become infected by an intra-abdominal infection.
* On ascitic fluid gram stain/culture =\> MANY organisms =\> diagnositic.
Treat: broad specture coverge of bacteria
52
Diagnosis of **Hepatocellular Carcinoma** in a pt with known liver disease
Treatment?
Screen?
1. **Abnormal US**
2. **↑ AFP**
**Treat:**
1. **Radiofrequency ablation**
2. **TACE (Transcathetic arterial embolization)**
3. **Surgical resention and liver transplant = rarely successful**
**Screen:** US + AFP in at risk pts/6months (conflicting restults
53
**Obstructive c**auses of jaundice
* 1. Gallstones
* 2. ACute Cholecystistis =\> impacted cystic duct
* 3. Choledocholithiasis =\> stones in CBD
* 4/ Ascending cholangitis
54
**Acute Cholecystitis**
* Signs
* Imaging
* Some jaundice + RUQ/epigastric tenderness **(+ Murphys sign)**
* Imaging
* **1. HIDA scan** =\> obstructed cystic duct
* **2. RUQ abdominal US** =\>
* thick GB wall, pericholecystic fluid, sonographic murphys sign
55
Diagnose and treat **Choledocolithiasis**.
1. Laparoscopic cholecystemoy + ERCP
2. **IF suspect stones before cholesctectomy:** ECRP with sphincterectomy and stone extration or stent replacement.
56
Bacteria that cause Ascending cholangitis
1. **Ecoli**
2. **Klebiella**
3. **Enterococcus**
57
Charcot and Reynold Triads in Ascending Cholantiis
* **Charcots triad:** RUQ pain + fever/chills + jaundice
* **Reynolds**: +++++ **AMS** + **hypotension** =\> indicates *suppuration* an*d endoscopic MRGNC*
58
Cholelithiasis Treatment
1. **Laparascopic cholestectomy**
1. if asymptomic, risk of needing surgey is SMALL
2. **Ursodeoxycholic acid**
59
**ACUTE CHOLECYSTITIS**
Treatment
1. **Urgent cholecystectomy** =\> suspected or confirmed complication.
2. **Delayed surgery** =\> pts with high risk of emergent surgery and where the diagnosis is in doubt.
60
**Cholangitis** treatment
Treated like acute cholecystitis;
* No oral intake, hydration, analgesia, and antibiotics are the mainstays
* Stones should be removed surgically or endoscopically
61
**PRIMARY SCLEROSING CHOLANGITIS (PSC)**
Treatment
1. **No treatment**
1. Cholestyramine to control puritis
2. Uresodeoxycholic acid =\> improves liver tests but not survial
3. Liver transplant =\> end stage cirrhosis
62
What is **Primary Billiary Cirrhosis/Cholangitis (PBC)**
* **MC in?**
* **Sx?**
* **Serology**
* **Duct lesions**
* **Treatment**
* AI destruction of the small intrahepatic bile ducts, causing cholestasis
* 50 YO F
* Asymptomatic, with only ↑ **ALP/GGT, birubin, cholesterol and IgM**
* Anti-mT AB (AMA) in 90-95%
* Liver biopsy =\> florid duct lesion
* Ursodeoxycholic acid
63
On H & P, people with **PBC** may have
1. **Jaundice**
2. **Prutitis**
3. **Xanthelasma**
64
What are risk factors of **PBC**?
1. UTI (e.coli or lactobacl)
2. Smoking
3. Hormone replacement therapy
4. Hair dye
65
PRognosis of PBC depends on
1. Age
2. BR
3. Albumin,
4. PT
5. Edema
66
What is **Primary Sclerosing Cholangitis (PSC)**
## Footnote
MC in?
Sx?
Serology
Radiology
Duct lesions
Treatment
***AI disorder*** where **inflammation**, **fibrosis** and **strictures** form in **intra- AND extra-hepatic** bile ducts. Found in 70% of patients with **IBD** (primarily UC)
* **20-50YO M**
* Prutitis + jaundice + fatigue
* 65% ANCA (+)
* Beads on a string: strictures and beading of large bile ducts; pruning of smaller ducts
* Extrahepatic/large intrahepatic =\> neutrophil inflammatory destruction of epithelium, superimposed on chronic inflamm;
* Med/small intrahepatic ducts =\> onion skin fibrosis around degenerating bile duct =\> tombstone scare
* No therapy
* Sx treatment: steroids, bile salt chelators for puritis; liver transplant
67
Complications of PSC
Increase risk of **cholangiocarcinoma**
68
\_\_\_\_\_\_ is associated with **xanthelsma**
**PBC**
69
What is **Budd Chiari Syndrome**
**Thrombosis (obstruction**) in 2 or more **hepatic veins =\>**
* Tender, painful hepatomegaly (red and purple), jaundice, ascites, splenomegaly
* Nutmeg liver (RHF), caval webs
70
What is the most common cause of the heptic vein obstruction =\> Budd Chiari Syndrome
* **Hypercoagulable sates (75%);**
* 50% have polycythemia vera
71
In \_\_\_\_\_\_\_\_, Budd Chiari is asosciated with a poor standard of living.
1. **India**
2. **China**
3. **S. Africa**
72
Imaging studies for Budd-Chiari sundrome will show what?
1. **Occlusion/absence of flow in the hepatic vein/ IVC**
2. Prominant caudate liver lobe d/t congestion.
73
Image test of choice for Budd-Chiari Syndrome.
Other?
* **CEUS (contrast-enhanced) US \*\*\*\***
1. Color or pulse doppler US
2. Direct venography: delineat caval webs vs occluded hepatic veins (spider web patter)
74
What will biopsy of liver show in Budd Chiari Syndrome
- Treatment and Management
* **Nutmeg liver (centrilobular necrosis/CONGESTION)**
* Treamtent
* **1. Symptomatic treatment**
* In some cases
* 2. Anticoagulation
* 3. Thrombolytic therapy
* liver transplant
75
How is **Budd-Chiari Syndrome** and **Hepatocellular carcinoma** related?
* HCC can complicate by causing hypercoagulable state
* BCS can also cause HCC
76
**PAncreatic cancer**
* Sx
* Signs
* Diagnostics
* Painless jaundice and WL; if pain, hurts most at night from laying back and improves when bending forward
* Trousseau sign of maliginancy and Courviosier isgn
* **Ca 19-9 \>100 U/mL**
77
**Dubin Johnson syndrome**
* Nature of defect
* Type of Hyperbili
* Characteristics
* prognosis
* Reduced excretory function of hepatocytes
* Conjugated
* Benign, asx jaundice;
* black liver; biopsy = centrilobular brown pgiment
* GB is **NOT** seen on oral cholecystopgraphy
* great
78
**Rotor Syndrome**
1. Nature of defect
2. Type of Hyperbili
3. Characteristics
4. prognosis
1. Reduced hepatocyte uptake of BR conjugates
2. Conjugated
3. Similar to DJ, except; liver is not black, GB **is** seen on oral choleystopgrapgy
4. Great
