Lecture 70/72 - Liver Diseases 1 and 2 Flashcards

1
Q

what is the relationship between cirrhosis and portal HTN?

A

Cirrhosis – -Increased Intra-hepatic resistance due to scarring; initial mechanism leading to portal HTN

Distorted Sinusoidal Architecture
Sinusoids are usually nice and orderly
But now distorted, increased pressures
Leading to increased resistance

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2
Q

what are some signs and symptoms of cirrhosis and portal HTN?

A
Spider Angiomata -- 
	Pectoral Alopecia
	Palpable liver 
	Caput Medusae 
	Ascites 
	Clubbing of the Fingers 
	Muscle wasting 
	Gynocomastia 
	Splenomegaly
	Testicular atrophy  and Low testosterone 
	Female escutcheon -- male pubic hair shape (rhomboid) becomes more feminine (triangular) 
	Palmar erythmea 
	Purpura and Petechia -- bleedings
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3
Q

what are complications (potential manifestions) of portal HTN?

A

varices

Hepatic Encephalopathy

Ascites

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4
Q

what are two common sites for varices?

what is the name of the sign for a bleeding site on endoscopy

A

gastric and esophageal

red whale sign

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5
Q

Describe three methods for bleeding management of varices?

A

Hemostasis of Bleeding Esophageal Varices

Sclerotherapy
Endoscopic Ligation
Transjugular Intrahepatic Portal-Systemic Shunt (TIPS Procedure)

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6
Q

What is the a Transjugular Intrahepatic Portal-Systemic Shunt (TIPS Procedure) ?

A

Use needle to connect hepatic vein system (normal pressure) to the portal system (High pressure in a cirrhotic)
Create a conduit with catheter and expandable metal stent to reduce the pressures in the portal System

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7
Q

Hepatic Encephalopathy – what is the mechanism of onset?

A

diverting a lot of blood around the liver; therefore unable to metabolize a lot of neurotoxic substances, such as ammonia

can be spontaneous or in the setting of TIPs for example

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8
Q

what are the 4 stages of Hepatic Encephalopathy

A

Stage 1 – confusion; can be very subtle
□ Have patient draw a clock, ask about date, etc

§ Stage 2 – drowsiness
□ Typically exhibit asterixis (flapping tremor)

§ Stage 3 – somnolence
□ Also exhibit asterixis

§ Stage 4 – Coma
□ Usually have to intubate

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9
Q

what is the best management for hepatic encephalopathy?

A

Lactulose
Decreases the pH in the colon
-converting the ammonia (NH3) to ammonium (NH4+), which does not cross the mucosa and excreted

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10
Q

Ascites — what is it?

A

Accumulation of fluid in the abdomen

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11
Q

what is the difference between uncomplicated and refractory ascites ?

A

§ Uncomplicated Ascites —
Can be controlled with salt restriction +/- Diuretics

§ Refractory Ascites
Cannot be handled with diuresis

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12
Q

how is uncomplicated ascites managed ?

how is refractory ascities managed ?

A

Uncomplicated: salt restirction, diuresis, Large volume paracentesis + albumin supplment

Refractory: LVP + albumin, TIPS, Portal vein shunt

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13
Q

what are the common Complications of Ascites?

A

Infection: Spontaneous Bacterial Peritonitis

§ Tense Ascities –
So much pressure, its pushing on the base of the lungs

Umbilical Hernia – if rupture, can lead to hypotension

Hydrothorax – Fluid leaking form the abdominal cavity to above the diaphragm

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14
Q

Hepatocellular Carcinoma –

describe some infectious risk factors? where are these endemic?

describe some non infectious risk factors?

A

§ Alcoholism and Hep C – US

§ Hepatitis B – World wide (asia and africa)

  • Cirrhosis

Hemochromatosis

Wilson’s disease

DMT2 + obesity === NAFLD

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15
Q

what are some indications for liver transplant?

A

Decompensated cirrhosis, fulminant liver failure, HCC (Milan criteria)

Viral liver disease, auto-immune, inherited, autoimmune, cholestatic, malignancy, NAFLD, Vascular

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16
Q

in general … what is the Milan Criteria ?

A

Milan criteria are applied as a basis for selecting patients with cirrhosis and hepatocellular carcinoma for liver transplantation.

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17
Q

in general what is the MELD score?

what is it used to determine?

what labs are taken into consideration in the calculation?

A

Model for End-Stage Liver Disease — used to assess severity of liver disease

bilirubin, creatinine and INR

18
Q

what are some contra-indications for liver Tx ?

A

severe Cardiopulmonary disease

hepatic malignancy with vascular invasion

Extrahepatic malignancy

Active infection

active substance abuse, poor compliance, social support

19
Q

what is the difference between acute liver failure and fulminant liver failure ?

A

Acute Liver Failurefocus of today – liver injury without AMS

Fulminant liver failure – liver injury with AMS

20
Q

what are the different classes of etiologies of acute liver failure ?

A

Toxic – acetaminophen (intrinsic), other idiosyncratic iatrogenic, death cap mushroom

Alcoholic

Viral – Hep A, B, D, E, C

Auto Immune

Hereditary

Pregnancy

Ischemic

21
Q

what is the most common cause of acute liver failure

A

Acetominophen Overdose

22
Q

Acetominophen Overdose – what is the mechanism of liver damage?

Symptoms?

Labs?

treatment? (early vs late)

A
    • When the system is overloaded, cytochrome P450 kicks in and metabolizes acetaminophen to NAPQI, a toxic reactive Intermediate.
    • NAPQI reacts with glutathione to yield a non -toxic intermediate. If glutathione stores depleted, NAPQI toxic build up, which may take 2-3 days

Symptoms: Nausea, vomiting, hepatomegaly, abdominal pain, anorexia, encephalopathy

Labs?
Extremely high AST/ALTs (1000s), with possible kidney injury

Treatment:
early (3 hours of ingestion) – Activated Charcoal

up to 48 hours or more – N AcetylCysteine

23
Q

what is king’s criteria?

A

Predicts prognosis of acetaminophen toxicity based on < arterial pH 7.3 vs

PTT > 100, AND High Creatinine AND grade 3,4 Encephalopathy

24
Q

why are alcoholics at greater risk (ie need only lower dose) to see acetaminophen toxicity?

A

Alcoholics – may be eating less food. therefore low glutathione stores. therefore easier to overload the system and achieve NAPQI toxicitiy

25
Mushroom Poisoning name of mushroom? Symptms? Labs? Treatment?
Amanita Phalloides (Death Cap Muschroom) Severe abd pain, nausea, vomiting Historically do not survive without transplant very high ALT/AST Possible Treatment: PCN G; or Milk Thistle vs transplant
26
Idiosyncratic Hepatotoxins (other iatrogenic liver injury) - what drugs most commonly? - Diagnosis? - Treatment ?
can occur with almost any drug Idiosyncratic drug reaction within the first 6 months of use Treatment: stop the drug Diagnosis -- Dx of exclusion; determining causality is difficult
27
what viruses can lead to acute liver failure? what are the typical LFT values?
Labs: High ALT/AST (3K - 5K) Hepatitis A -- rare in the US Hepatitis B -- Most common worldwide Hepatitis D - Hepatitis E - Hepatitis C -- most common cause of chronic liver disease, but not acute scenario
28
Hepatitis A -- - how is it transmitted? sources? Diagnostic lab ?
Fecal/oral transmission; Shellfish, polluted water, poor sanitary conditions Dx -- Hepatitis A IgM (for acute)
29
Hepatitis B -- - how is it transmitted? Diagnostic labs?
transmitted via infectious blood, bodily fluids Child birth transmission Check both surface and core antibody IgM surface antigen persists in persons with the chronic infection acute setting -- Surface and core IgM
30
Delta Hepatitis - unique feature about this infection? Diagnositic labs?
Requires a previously existing or concurrent Hepatitis B infection HD antibody IgM -
31
Hepatitis E how is it transmitted? diagnostic test?
fecal, oral transmission Self-limiting disease Dx -- No great test; HE Ab IgM
32
Acute alcoholic hepatitis -- Epi and describe the mortality... Lab findings? Symptoms ? Histology Treatment?
Not really considered acute liver failure assocaiated with poor outcomes (high 6 month mortality w/o transplant) Labs: ALT/ASTs do not exceed 500 AST:ALT ratio -- 2:1 histology: hepatocytes; microsteatosis; macrosteatois; Mallory Bodies treatment: : Glucocorticoids, Pentoxifyline
33
``` Wilson's Disease: - demographics at risk? - how is it acquired? - symptoms - ```
Autosomal recessive young women Symptoms: Neurologic, psychiatric symptoms, motor function; acute liver failure; refractory coagulation, hemolytic anemia, renal failure
34
Diagnosis of Wilsons? Labs? pathognomic occular finding on physical exam for wilson's disease?
24 hour urine or plasma copper collection Alk Phosph : Total Bilirubin ratio < 4 Kayser Fleishcer rings
35
Autoimmune Hepatitis: mechanism of disease ? labs? histo? Diagnostic test?
cell mediated immune response against the liver More a chronic disease Uncommonly presents as acute, fulminant hepatitis Labs -- mixed elevation of AST/ALT and high alk phosph/bilirubin Histology -- can be severe with massive liver necrosis Dx: Autoantibodies
36
Liver disease in Pregnanccy and Post Partum? -- when during pregnacny course is this most likely to develop? - what is the treatment?
Confined to third trimester, and after delivery Increased fetal and maternal mortality Treatment: deliver the baby and stabilize mom and baby
37
causes of Liver disease in Pregnanccy and Post Partum? (what is HELP syndrome?) lab range
Acute Fatty Liver Disease of Pregnancy HELP Syndrome -- Hemolysis, Elevated Liver Enzymes, Low Platelets AST/ALT -- 300-500 range
38
Ischemic Hepatitis -- ("shock liver") - what is it? - causes? - what is a concerning pattern of lab findings?
Liver cells necrosis due to diminished perfusion - Cardiac arrest, hypotension, thrombosis Rapid increase of AST/ALT with rapid resolution (this means that the hepatocytes are damaged and not even releasing AST/ALT anymore)
39
what is Budd Chiari Syndrome what is it? what is the presentation triad? Diagnosis methods? Underlying causes? Treatment?
Hepatic Vein thrombosis triad: severe abdominal pain, massive hepatomegaly, new ascites Diagnosis -- look for the clot on Ultrasound, CT or MRI Underlying Causes: malignacy, hypercoagulable states, myeloproliferative, women on OCPs Thrombolytics, anticoagulation, TIPS, surgery, and liver Transplant
40
HCC -- what are the risk factors? what are 2 methods for screening? Imaging ?
any patient with cirrhosis Imaging, AFP CT with contrast
41
HCC -- | Treatment methods?
Chemo-embolization; direct chemotherapy Radio-frequency ablation Sorafenib -- anti VEGF; but only extends live by about 2 months Transplant