Cirrhosis Flashcards

1
Q

Cirrhosis

A

Irreversible scarring and inflammation of fibrotic liver disease

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2
Q

Death rate of cirrhosis

A

26%

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3
Q

Causes of cirrhosis

A

structural changes from injury (alc, viral) and fibrosis

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4
Q

Cirrhosis patho

A

chaotic fibrosis causes obstructive biliary channels and obstructed blood flow leading to jaundice, portal HTN

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5
Q

Fibrosis

A

connective tissue from infiltrates of leukocytes that release inflammatory mediators and activate fibrotic processes

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6
Q

What stops the liver from regenerating with cirrhosis?

A

hypoxia, necrosis, atrophy, liver failure

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7
Q

Does cirrhosis develop quickly?

A

NO - often slow, but alc can be very fast

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8
Q

What can stop progression of cirrhosis?

A

removal of the toxin (won’t reverse it tho)

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9
Q

Causes of cirrhosis

A
  • hep b & c
  • excess alc intake
  • idiopathic,
  • non-alcoholic fatty liver disease (NASH & NAFLD)
  • autoimmune
  • hereditary metabolic conditions
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10
Q

alcoholic cirrhosis

A
  • alcohol is converted to acetaldehyde which activates hepatic stellate cells in excess (involved in fibrosis);
  • acetaldehyde inhibits export of proteins from the liver, alters vitamin metabolism, induces malnutrition
  • Kupffer cells attract neutrophils which cause toxins to accumulate from gut bacteria and cause suppressed cell-immunity
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11
Q

Alcoholic fatty liver leads to…

A

Alcohol steatohepatitis which leads to alcoholic cirrhosis

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12
Q

Alcohol fatty liver

A
  • mild or asymptomatic
  • reversible
  • fatty accumulation from inc lipogenesis
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13
Q

Alcoholic steatohepatitis

A
  • inflammatory degeneration of hepatocytes, WBCs infiltrate, stimulates irreversible fibrosis
  • anorexia, nausea, edema, jaundice
  • inc hepatic fat storage
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14
Q

Alcoholic cirrhosis

A
  • immunological problem
  • inflammation, oxidative stress, cell damage, cell necrosis, fibrosis and scarring
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15
Q

Patho of cirrhosis

A

Liver cells are destroyed - try to regenerate - disorganization - abnormal growth - poor BF and scarring - hypoxia - liver failure

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16
Q

CM of cirrhosis

A

Insidious
- N/V, anorexia, flatulence, change bowel habits
- fever, wt loss
- palpable liver

17
Q

Late CM of cirrhosis (often diagnostic)

A
  • jaundice from bili build up
  • peripheral edema
  • dec albumin
  • inc PT
  • ascites from portal HTN
  • skin lesions like spider angiomas
  • anemia from lacking clotting fx
  • esophageal and anorectal varices
  • encephalopathy from inc ammonia
18
Q

Endocrine SE of cirrhosis

A
  • chronic amenorrhea
  • hypogonadism
  • fertility problems
19
Q

Varices

A

Distended veins that can cause high mortality and bleeding if they burst

20
Q

Portal HTN

A

Resistant portal BF causing varices and ascites

21
Q

Fx of portal HTN

A

systemic hypotension, vascular underfilling, stimulation of RAS system (vasoconstriction), plasma volume expansion, inc CO–ascites

22
Q

Portal HTN CM

A

asymptomatic until complications - variceal hemorrhage, ascites, peritonitis, cardiomyopathy, hepatorenal syndrome–kidney/liver failure, heart failure

23
Q

Tx for portal HTN

A

Prevent/tx complications
- liver transplant

24
Q

Protein’s role in HTN

A

Lack pro to keep fluid in the vessels

25
Q

Hepatic encephalopathy

A
  • 30-45% cirrhosis patients
  • LOC is primary driver of dx
  • graded by severity
  • toxins build up in the brain, especially inc ammonia (neurotoxins)
  • not dx by ammonia levels tho
26
Q

Acute liver failure aka fulminant liver failure

A
  • not r/t cirrhosis or fibrosis
  • often Tylenol OD (tx with acetylcysteine)
  • 6-8W after viral hepatitis or metabolic liver disease
  • 5d-8W after tylenol OD
27
Q

Fulminant liver failure patho

A

Edematous hepatocytes and patchy area of necrosis and inflammatory cell infiltrates that disrupt liver tissue

28
Q

S/s fulminant liver failure

A

Like late cirrhosis but without cellular changesT

29
Q

Tx for fulminant liver failure

A

Liver transplant
- catch early, stop toxins