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Cirrhosis
- chronic, progressive
- widespread fibrosis & nodule formation
- alter/destroyed hepatocytes unable to be fully regenerated
- leaves liver scarred, nodular and inefficient
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cirrhosis 2
- 9th leading cause of death in US
- 4th when considering only 34-54 to
- highest incidence b/t 40-60 yrs
- 2x as common in men than women
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Cirrhosis
types
- alcoholic (Laennec's portal, micronodular)
- postnecrotic
- billary
- cardiac
- cause can't always be identity- sometimes overlapping
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alcoholic cirrhosis
- alcohol- primary risk factor
- - increased risk: if daily drinking, poor nutrition
- with excessive alcohol, fat accumulates in hepatocytes (infiltration of fat, replace hepatocyte)
- with abstinence at this level, changes may be reversible
- if not, widespread scarring occurs- not reversible, loss of function, necrosis- sepsis
- (daily drinking is a greater risk- not what u drinking. adding with poor nutrition)
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Postnecrotic cirrhosis
- most common worldwide form
- massive loss of liver cells with irregular patterns of regenration
- - broad bands of scar tissue
- complication of hepatitis (esp B & C)
- liver becomes small and nodular
- most common reason is hepatitis
- virus cause scar tissue
- hep + alc- inc risk
- not + alc- inc risk
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Bilary Cirrhosis
- result of chronic obstructed bile flow and infection (cholangitis)- infection/inflamm common bile duct
- damage hepatocytes
- inflammatory process causescell necrosis and scar tissue formation
- - diffuse fibrosis and scarring of liver
- less common than other forms
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Cardiac cirrhosis
- chronic liver disease from severe, long term right side heart failure
- progressive fibrosis due to prolonged venous blood retention
- - hepatic vein
- congested hepatopathy- venous congestion in liver which causes fibrosis. cause inflammation cell contents leak out = end in scar tissue
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Cirrohosis 3
- final stage in many liver injury
- extensive hepatocyte necrosis & scarring
- results in changes in vascular, bile, lymphatic flow- r/t to fibrosis
- liver becomes nodular
- attempts to regenerate may work at first but eventually are exhausted
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cirrhosis 4
- liver is left scarred, nodular, unable to function properly
- 2 clinical problems
- - decreased liver function
- - portal hypertension (severe cirrhosis)- can't get blood into liver so it backs up
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cirrhosis 5
- onset usually insidious
- slow progression initially
- may be reversed if insults stop early enough
- - liver can regenerate itself
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cirrohosis
early s/s
- GI: anorexia, dyspepsia, flatuence, n/v. change in bowel patterns
- - changes in cho, protein fat metabolism
- Pain: dull, heavy RUQ or epigastric area
- - stretching/swelling of liver capsule, spasm of billary ducts (maybe obstructed at sphrincter), vascular spasms
- fever, malaise, weight loss
- enlarged firm liver
- - liver is enlarged with fat
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cirrhosis
advance symptoms
- many system wide manifestation
- often are severe and due to:
- liver failure- inability to synthesis, and clotting factors
- portal htn
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cirrhosis
other advance symptoms
- jaudice/pruritis
- - dec ability to conjugate and execrete bilirubin
- - bile salts deposit in skin
- peripheral edema
- - reduced plasma albumin
- - often generalized, more likely LE
- ascites
- - fluid in the peritoneal space due to reduced plasma protein with changes in hydrostatic pressure
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cirrhosis
advance symptoms
skin lesions
- spider angiomas: small dilated blood vessels with a bright read center and spiderlife branches
- - occur on nose, cheeks, upper truck and neck
- - due to inc circulating estrogen
- Palmer erthema: redness that blanches with pressure on palms
- due to incre circulating estrogen
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Cirrhosis
advance symptoms
hematologic problems
- thrombocytopenia, anemia, leukopenia
- - due to splenomegaly from back up of blood from portal vein into the spleen
- - the spleen incr activity and incre removal of blood cell from circulation
- - other causes: poor nutrition, poor absorbtion of FA, bleeding (chronic alcohol use dec absorption of vitamins, mineral, nutrients
- alcohol dec absorption of nutrition
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hematological problems
- leukopenia
- - incre removal of blood cells by spleen
- - decre production, function and movement of wbc
- - incr risk of infection
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advanced symptoms
coagulation problems
- liver's inability to produce prothrombin and other clotting factors
- epitaxis, purpura, petechiae, easy bruising, gingival bleeding, heavy menses
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advanced symptoms
vitamin and mineral deficiency
- Vita K
- folic acid, thiamine
- Fe, calcium, vita D
- chronic alcoholism: decr absorption of FA, vita B12, B6, thiamine, vita C
- venous congestion and add alcohol (down absorption)
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Advance symptoms
endocrine changes
- due to liver's inability to metabolize and inactivate hormones- excessive estrogen
- - men- skin lesions and gynecomastia, loss of axillary and pubic hair, testicular atrophy, impotence
- - women- amenorrgea, vaginal bleeding in older women
- failure to metabolize aldosterone- hyperaldosteronism (Na/H2O retention with postassium loss)-- edema
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Advance symptoms
peripheral neuropathy
- esp w/alcoholic cirrhosis
- likely due to thiamine, folic acid and vita b12 def
- most likely sensory deficits
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