liver

patho end stage liver disease

Liver is unable to conjugate proteins

Leads to poor wound wound healing, peripheral edema, anemia

Extra circulating hormones

Hyoernatermia

Hirstusim

Hypokalemia

Excess estrogen

Glycenomastera,

Itchy red palms,

spider angiomas

Related to livers inability to store raw materials

Bleeding

Anemia

Hypoglycemia

Nitrogen build up leads to

Hepatic encephalopathy

work of the liver

carbohydrate metabolism

fat metabolism

bile production

blood coagulation

removal of drugs and hormones

storage

dx test

ALT, AST, LDH

Alk phos

bilirubin

total protein, albumin

glucose

coags-PT

cholesterol

Low plts risk for

Bleeding out

liver biopsy

monitor for bleeding

frequent vital signs

positioning

Positioning for a liver biopsy

flat on right side

cirrhosis

chronic and progressive

degeneration and destruction of hepatocytes

regeneration is abnormal and disorganized

changes in size, shape and function of liver

types of cirrhosis

fatty liver disease

post necrotic

biliary

cardiac

fatty liver disease cirrhosis

alcoholic, obesity, DM2

Post necrotic cirrhosis

viral, toxic, or idiopathic

biliary cirrhosis

obstruction

jaundice is main feature

cardiac cirrhosis

R/T

heart failure dilated and congested hepatic venules and small hepatic veins

early manifestations of cirrhosis

GI: nausea/vomiting, anorexia, change in bowel habits, dull, heavy feeling in abdomen

vague, RUQ pain

fever, fatigue

later manifestations of cirrhosis

jaundice

spider angiomas

coagulopathies

anemia

hormonal irregularities

fluid retention

peripheral neuropathy

nursing assessment

history reconciliation

mental status

fluid status: daily weights, I&O, abd girth

Skin: jaundice, bruising, petechiae, pruritis

neuro status

monitor labs: liver enzymes, CBC, albumin, NH3, lytes, PT/PTT, glucose, BUN, creatinine, bilirubin

nursing interventions

rest: decreases metabolism

position: improves ventilation

diet: high calorie, high carbs, vit. sup., protien based on mental status (NH3 production rate)

skin care: hydroxyzine, cholestyramine, relieve pressure, protect from injury

safety: bleeding precautions, fall precautions

patient education: written, significant others

stages of development

destruction by virus, ETOH, toxin

inflammation/hepatomegaly

fibrotic regeneration

hepatic insufficiency

portal hypertension

due to structural changes in the liver that increase resistance of blood flow through the liver

increased resistance causes development of collateral circulation and thinning of venous vessels

esophageal varices

results from portal hypertension

varices can occur anywhere but most common in GI tract

bleeding varices are life threatening and may be triggered by any increase in intraabdominal pressure or trauma to the area

management of varices

GOAL: prevent rupture and tears

PPI

diet: thorough chewing, avoid rough/uncut food, avoid large food bolus

minimize URIs: avoid exposure, treat early, suppress coughing

prompt treatment of bleeding

medications for esophageal varices

vasopressin

octreotide

nitroglycerin gtt

beta-blockers

Spironolactone

Spares K

blocks aldosterone

Lactolose

Orange liquid that binds NH3 in gut to be pooped out

Hyper aldosterone results in

Increases of fluid

vasopressin

constricts vessels to stop bleeding

octreotide

Decreases circulation of blood

nitroglycerine gtt

Dilates other blood vessels to get other places rather than varices opening

Lowers bp

beta blockers

Slows HR and BP

tamponade

tube down throat to stop bleeding

airway precautions: cut balloons, aspiration protection

TIPS procedure

non surgical approach to insert stent

diverts blood from portal to systemic venous system

increased incidence of encephalopathy

Ascites

result of increased portal pressure, low albumin state, and fluid retention

decreasing oncotic pressure and increase venous pressure causes fluid to shift into interstitial and third spaces

increased fluid retention also related to hyperaldosteronism

management of ascites

diet: low sodium, normal protein intake (or sl increase)

diuretics: spironolactone and furosemide

removes/redirects fluid: paracentesis and shunt

paracentesis

used for compromised patients

can be done at bedside

cautious removal of fluid

fluid re-accumulates

albumin

laveen shunts

one way valve between abdomen and vena cava

as pressure in abdomen increases, forces valve to open to allow fluid into vena cava

vascular fluid overload can be problematic

increased risk for infection, DIC, thrombosis

encephalopathy

liver is unable to metabolize ammonia that is created during digestion

NH3 crosses blood brain barrier

neurological changes reflect increasing levels of NH3

terminal complication of hepatic failure

management of encephalopathy

lactulose

rifaximin

LOLA

remove old blood from GI tract

prevent constipation

hepatorenal syndrome

functional renal failure

most probably related to decreasing perfusion to kidney

also increased burden of metabolites

may follow GI hemorrhage, diuretic therapy or paracentesis