Cirrhosis Flashcards

1
Q

Differential diagnosis of Cirrhosis?

A
  • Alcoholism
  • Chronic Viral Hepatitis (B,C)
  • Non-alcohlic statohepatitis (NASH) due to obesity epidemic
    • now, most common cause in use due to obesity epidemic
  • Biliary Cirrhosis
    • primary biliary cirrhosis (PBC)
    • Primary Sclerosing Cholangiitis (PSC)
    • Auotimmune cholangiopathy
  • Cardiac Cirrhosis
  • Inherited Metabolic Liver diseases
    • heriditary hemochromatosis
    • Wilson’s disease
    • Alpha-1-antitrypsin deficiency
    • cystic fibrosis
    • rare disorders
      • porphyria, urea cycle defects, etc.
  • cryptogenic cirrhosis
    • we don’t have any idea why they have it
  • Drugs
    • methotrexate
    • isoniazid
    • alpha-methyldopa
    • vitamin A
    • amiodarone
  • Weird stuff
    • brucellosis
    • echinococcosis
    • congenital or tertiary syphilis
    • indian childhood cirrhosis
    • granulomatous liver disease
    • polycystic liver disease
    • schistosomiasis (presinusoidal fibrosis)
    • acute fatty liver of pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

check this out

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

check this out

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Areas with what tyep of innervation are more susecptible to vascular complications?

A

vascular complications tend to localize around areas of dual circulation and dual venosu drainage

where portal venous circulation in close proximity to systemic circulation – shared areas can expeience hypertension & varicosities will form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Complications of Cirrhosis?

A
  • anascarca = genera swelling of whole body
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do ascites happen?

What are 3 factors that lead to it?

A

Increased hydrostatic pressure in the mesenteric circulation resulting in serous effusion (fluid) into the serosa resulting in aggregation of fluid in the peritoneum

  • hydrostatic pressure from the cirrhosis causing portal venous hypertension
  • part due to decreased circulating plasma protein
  • in part due to vasodilation in

this leads to activation fo vasoconstrictors–> leads to sodium retention–> edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Differential diagnosis of ascites?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What tests are performed every time you do a pericentisis?

A
  • glucose
    • if you think its peritonitis
    • lower glucose & simultaneous glucose in serum would indicate bacterial consumption of glucose in fluid
  • LDH
    • infectious stuff
  • amylase
    • pancreatitis
  • cytology
    • if suspect cancer
  • triglycerides
    • if mesenteric lymphpatic link
  • bilirubin
    • if damage to biliary tree
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is ascites concerning?

A
  • risk spontaneous bacterial peritonitis
    • protein rich fluid – outstanding culture media
    • rough to get antibiotics to the site
  • hernia formation
  • fluid leakage – impaired healing
  • abdominal compartment syndrome
    • can occlude venous return
  • ileus
    • functional equivalent bowel obstruction (bowel goest on strike)
  • SAAG >= 1.1 indicates portal hypertension with 97% accuracy
    • serum albumin ascites gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you treat ascites?

Why can’t you just drain it?

A

If you just drain it, it will keep coming back

  • dietary sodium restriction
    • <2000 mgday
    • education
    • constant reinforcement
  • dieuretics (get kidney to restrict sodium)
    • spironalactone
    • furosemide
    • 100:40 ratio
    • can titrate every 2 weeks
  • occasional paracentesis
    • when diuretics don’t work well enough
    • at admition to hospital or symptomatic control abdominal distention
    • need to give 5g albumin/liter you remove
  • serial therapeutic paracentesis
  • TIPS
    • long catheter through jugular into superior vena cava into inferior vena cava into hepatic vein radical & shoeve a needle through wall to portal vein. Creating a tunnel through hepatic portal vein & hepatic systemic vein so portal venous drain can decombress.
    • without going through hepatic first pass metabolism
  • liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What structure leaks to cause ascites?

A
  • capillary driven
  • coming from gut, omentum, other serosa surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the most common varices?

Specific risks?

Treatment?

A

Esophageal varices

  • high bleeding risk
  • treatment
    • banding
    • sclerotherapy injections
    • propanolol or nadolol (no selective beta blockers) - reduce portal venous pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are gastric varices treated?

A
  • cyanoacrylate
  • splenectomy
    • remove circulation through short gastric
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does hepatic encephalopathy occur?

A
  • Urea splitting organisms in the GI flora produce ammonia
  • normally protal circulation first pases nitrogenous waste through the liver
  • hepatocytes process it via the urea
    • ammonia will diffuse intot he CNS
    • astrocytes use ammonia to make glutamate from glutamine (a cytotoxin)
    • benzodiazepine-like effect (GABA mediated)
    • unabated, in the increased CNS edema can cause herniation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

At what westhave critera do astrices start showing up & disappearing?

A

grade 2 – major risk factor for automobile accidents

disappear grade 3/4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for hepatic encephalopathy?

A
  • lactulose
    • osmotic laxative
    • trying to decrease amout of microbiota hanging out inside your colon
  • rifamixin
    • topical (non-absorbed) antibiotic, supresses urea splittes
    • decrease risk of relapse vs. lactulose alone
      *
17
Q

What is the result of coagulopathy of liver failure? How do you treat it?

A
  • Synthetic deficit of (liver produced) coagulation factors (INR elecates first)
  • Thrombocytopenia due to sequestration (in liver/spleen) from portal hypertension
  • marrow suppressin
  • included in MELD score (INR)
  • can make minor trauma life threatening – b/c they can bleed a lot
  • Treat
    • surgical hemostasis is still required
    • transfuse platelets
    • transfuse FFP / Crypoprecipitate
    • factor IIa concentrate for life threatening bleeding
18
Q

Cirrhosis increases the risk for what cancers?

Screening procedures?

A
  • hepatocellular carcinoma (20x increased risk)
  • melanoma
  • colon/rectal
  • hematologic
  • esophageal
  • gastric
  • Screening
    • screened for HCCA
    • image every 6 months -1 yr
    • MRI > 3 phase CT > ultrasound
      • cost & sensitivity
    • alpha-fetoprotein (with ultrasound) every 6 months
      • 20ng/ml sensitivity is 60%
      • PPV 9-50%
19
Q

Infectious complications of portal hypertension?

Why are they particularly at risk?

A
  • functionally aspleinc
  • listeria
  • Yersinia enterocolitica
  • Vibrio vulnificus
    • requires iron
  • iron overloadedm acrophages show decreased phagocytosis