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GI Block > Cirrhosis & PHTN > Flashcards

Cirrhosis & PHTN Flashcards

1
Q

Phase 1 vs. 2 of liver drug metabolism

A

Phase 1: changes lipophilic molecules into water soluble ones via Cytochrome
Phase 2: attachment of large molecules to improve water solubility (glucuronidate, methyl, acetic acid, etc.)

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2
Q

In liver injury, _____________ cell activation lead to the accumulation of scar (fibril-forming) matrix

A

Stellate

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3
Q

In liver injury, ____________ cell (macrophage) activation leads to activation of Stellate cells

A

Kupffer

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4
Q

Potential etiologies of Cirrhosis

A 
Viral (Hep B and C)
Toxic (Alcohol, drugs)
Metabolic (fatty liver)
Biliary (PCS and PBC)
Genetic (Hemachromatosis, Wilson's Disease, Alpha-1 Antitrypsin)
Cystic Fibrosis
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5
Q

What are some pathophysiologic changes that occur during cirrhosis

A 
Unable to process bile (distributes to skin and eyes/scleral icterus)
Coagulopathy
Less albumin (ascites/edema)
Hypoglycemia
Portal HTN
Longer drug half-lives
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6
Q

consequence of liver cirrhosis; root cause of many complications of cirrhosis; increased pressure in the portal system

A

Portal HTN

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7
Q

Portal HTN will cause a backup of blood through what veins?

A 
Left gastric vein (esophageal varices)
Rectal vein (hemorrhoids)
Umbilical vein (caput medusae)
Splenic vein (splenomegaly)
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8
Q

Once a patient develops complications (below )of cirrhosis, they have________

Variceal hemorrhage
Ascites
Spontaneous Bacterial Peritonitis
HRS
HPS
Portopulmonary HTN
Hepatocellular carcinoma
Hepatic encephalopathy
A

Decompensated Cirrhosis

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9
Q

MOST devastating complication of cirrhosis and portal HTN; prevention includes endoscopy, non-selective b-blockers and band ligation

A

Variceal Hemorrhage

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10
Q

Prevention/treatments for Variceal Hemorrhage

A

Upper Endoscopy
Non-slective b-blockers
Band ligation

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11
Q

The most common cause of ascites is…

A

cirrhosis

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12
Q

most common complication of cirrhosis;

A

Ascites

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13
Q

used to help determine the cause of ascites

A

SAAG

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14
Q

A SAAG score of >1.1 g/dL is indicative of…

A

Cirrhosis, liver disease

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15
Q

Treatment for Ascites

A

Low sodium diet
Diuretics
Surgical Shunt (Denver shunt/TIPS)
LVP (Large Volume Paracentesis)

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16
Q

When using diuretics for ascites, you need to carefully monitor the levels of…

A

sodium (hyponatremia)

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17
Q

complication of cirrhosis; peritoneal fluid >250 neutrophils; due to bacterial translocation from gut (E. coli)

A

Spontaneous Bacterial Peritonitis (SBP)

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18
Q

With Spontaneous Bacterial Peritonitis, which gut microbe is usually the etiologic agent?

A

E. coli

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19
Q

complication of cirrhosis; development of acute renal failure due to blood stagnating in mesenteric system instead of the systemic circulation; presents with oliguria, low urine sodium and systemic hypotension

A

Hepatorenal Syndrome

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20
Q

Oliguria, low urine Na+, and systemic hypotension are clinical presentation of

A

Hepatorenal Syndrome (HRS)

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21
Q

What are the diagnostic criteria for Hepatorenal Syndrome

A
  • Cirrhosis w/ ascites

- Increased Serum creatinine >1.5 mg/dl

22
Q

Hepatorenal Syndrome Type (1 or 2) is defined as being RAPIDLY FATAL, 50% reduction of clearance (or doubling of serum creatinine) in <2 weeks

A

Type 1

23
Q

Hepatorenal Syndrome Type (1 or 2) is defined as less severe, slower and characterized by diuretic refractory ascities

A

Type 2

24
Q

Liver transplant, in the setting of Hepatorenal Syndrome, will result in an improvement of renal function (True or False)

A

True

25
Q

The most common causes of Hepatocellular Carcinoma (worldwide vs. Western)

A
  • Worldwide: HBV (Hep. B)
  • Western:
    1. HCV (Hep. C)
    2. Non-alcoholic fatty liver disease
    3. Alcohol
26
Q

How can you potentially diagnose Hepatocellular Carcinoma w/o biopsy

A

MRI

  • AFP can be helpful
27
Q

Although not sensitive or specific, but if AFP (Alpha Feto Protein) is >200, _______ highly suscipicious

A

HCC

28
Q

procedure done for cirrhotic liver; shunt is placed between hepatic and portal veins with the goal of reducing portal HTN; used for varices and ascites; complications include hepatic encephalopathy and hepatic failure (toxins bypass liver into systemic circulation)

A

TIPS

29
Q

complication of cirrhosis, and possibly TIPS; disturbance of CNS function due to hepatic insufficiency and toxic buildup (ammonia); patients will present with AMS (altered mental status)

A

Hepatic Encephalopathy

30
Q

What neurotoxin can accumulate and cross BBB causing hepatic encphalopathy?

A

Ammonia

31
Q

How to diagnose Hepatic Encephalopathy

A
  • Diagnosis of exclusion

- Elevated ammonia (helpful, but not sensitive/specific)

32
Q

Live-saving intervention for decompensated cirrhosis; shows ~90% 5 year survival

A

Liver Transplant

33
Q

The most common cause of acute liver failure is…

A

Drugs

34
Q

Drug-induced liver injury can be caused by either…

A

1) toxic reaction to drug/metabolite

2) immune-mediated inflammatory reaction to the drug

35
Q

What are the two patterns of hepatotoxicity due to drugs

A

Intrinsic: predictable, dose-depending injury (higher dose= more injury)

Idiosyncratic: injury not predictable (not dose-dependent)

36
Q

Acetaminophen is metabolized in the liver via what three pathways?

A

1) Glucoronidation*
2) Sulfation*
3) Cytochrome P-450 (phase 1; produces toxic NAPQI)

  • are the main metabolizers (phase II) and produce non-toxic products
37
Q

Which drug is the single most common cause of Acute Liver Failure, usually due to overdosing

A

Acetaminophen

38
Q

Examples of etiologies for Chronic Liver Failure

A

Hep B and C (both are viral etiologies –> cirrhosis –> CLF)

39
Q

Cirrhosis requires that what two anatomic alterations take place?

A

1) thick fibrosis of septa

2) Regenerative nodules

40
Q

Fibrosis stage is _______ but cirrhosis is not _______

A

reversible

41
Q

What will a cirrhotic liver look like on CT?

A

Shrunken liver

Bumpy/nodular texture

42
Q

Why might the spleen be enlarged with liver cirrhosis?

A

Portal HTN causes back-pressure of blood into the celiac trunk and into the splenic vein

43
Q

The repetitive injury and repair that leads to cirrhosis can make someone more prone to…

A

HCC

44
Q

What will hepatocellular carcinoma look like on a slice of liver tissue?

A

Nodular

Darker and more bile-stained (Greenish)

45
Q

If you wanted to see the severe fibrosis in liver cirrhosis, which stain would you use on a tissue sample?

A

Trichrome stain

46
Q

What aspects of the “healing process” in the liver contributes to the development of cirrhosis?

A
  1. Loss of vessel fenestrations
  2. Deposition of basement membrane
  3. Fibrosis (collagen deposition) in Space of Disse
47
Q

How can cirrhosis result is hematemesis?

A

Cirrhosis—> Portal HTN—> Esophageal/gastric varices—> Rupture with massive bleeding

Also note that cirrhosis can cause diminished clotting factors, further worsening bleeding

48
Q

What is prehepatic cause of PHTN in non-cirrhotic CLF?

A

Portal Vein Thrombosis

  • Normal liver tissue and functions (until severe) b/c patient don’t have cirrhosis, and their liver is provided adequate blood flow by proper hepatic artery.
49
Q

What is intra-hepatic cause of PHTN in non-cirrhotic CLF?

A

Amyloidosis (accumulation of abnormal proteins)

  • Congo red stain + (amyloid appears orange-red color)
  • Apple-green under polarized light
50
Q

What is post-hepatic cause of PHTN in non-cirrhotic CLF?

A

Budd-Chiari Syndrome

*Thrombotic occlusion of the hepatic vein causing venous back pressure to damage liver

51
Q

What is the histologic hallmarks of Budd-Chiari Syndrome?

A

Hepatocytes are congested with RBCs

  • looks bloody
52
Q

Why might the caudate lobe not be effected by a Budd-Chiari Syndrome clot?

A

Caudate lobe is drained by small veins that directly enter IVC (bypasses thrombosed hepatic vein); compensatory hypertrophy (caudate hypertrophy) occurs

GI Block (9 decks)

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