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
Q

Mushroom Poisoning

name of mushroom?
Symptms?

Labs?
Treatment?

A

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
Q

Idiosyncratic Hepatotoxins (other iatrogenic liver injury)

  • what drugs most commonly?
  • Diagnosis?
  • Treatment ?
A

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
Q

what viruses can lead to acute liver failure?

what are the typical LFT values?

A

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
Q

Hepatitis A –
- how is it transmitted? sources?

Diagnostic lab ?

A

Fecal/oral transmission; Shellfish, polluted water, poor sanitary conditions

Dx – Hepatitis A IgM (for acute)

29
Q

Hepatitis B –
- how is it transmitted?
Diagnostic labs?

A

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
Q

Delta Hepatitis
- unique feature about this infection?

Diagnositic labs?

A

Requires a previously existing or concurrent Hepatitis B infection

HD antibody IgM -

31
Q

Hepatitis E

how is it transmitted?

diagnostic test?

A

fecal, oral transmission
Self-limiting disease

Dx – No great test; HE Ab IgM

32
Q

Acute alcoholic hepatitis –

Epi and describe the mortality…

Lab findings?

Symptoms ?

Histology

Treatment?

A

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
Q
Wilson's Disease: 
- demographics at risk? 
- how is it acquired? 
- symptoms 
-
A

Autosomal recessive
young women

Symptoms: Neurologic, psychiatric symptoms, motor function; acute liver failure; refractory coagulation, hemolytic anemia, renal failure

34
Q

Diagnosis of Wilsons?

Labs?

pathognomic occular finding on physical exam for wilson’s disease?

A

24 hour urine or plasma copper collection

Alk Phosph : Total Bilirubin ratio < 4

Kayser Fleishcer rings

35
Q

Autoimmune Hepatitis:
mechanism of disease ?

labs?

histo?

Diagnostic test?

A

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
Q

Liver disease in Pregnanccy and Post Partum?
– when during pregnacny course is this most likely to develop?

  • what is the treatment?
A

Confined to third trimester, and after delivery

Increased fetal and maternal mortality

Treatment: deliver the baby and stabilize mom and baby

37
Q

causes of Liver disease in Pregnanccy and Post Partum?

(what is HELP syndrome?)

lab range

A

Acute Fatty Liver Disease of Pregnancy

HELP Syndrome – Hemolysis, Elevated Liver Enzymes, Low Platelets

AST/ALT – 300-500 range

38
Q

Ischemic Hepatitis – (“shock liver”)

  • what is it?
  • causes?
  • what is a concerning pattern of lab findings?
A

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
Q

what is Budd Chiari Syndrome

what is it?
what is the presentation triad?

Diagnosis methods?

Underlying causes?

Treatment?

A

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
Q

HCC –
what are the risk factors?

what are 2 methods for screening?

Imaging ?

A

any patient with cirrhosis

Imaging, AFP

CT with contrast

41
Q

HCC –

Treatment methods?

A

Chemo-embolization; direct chemotherapy

Radio-frequency ablation

	Sorafenib -- anti VEGF; but only extends live by about 2 months 

Transplant