hepatic disorders Flashcards
largest gland
liver
blood supply to liver
portal vein, and it’s unoxygenated. gets oxygenated blood from hepatic artery.
functions of the liver
Bile production and excretion
Excretion of bilirubin, cholesterol, hormones, and drugs
Metabolism of fats, proteins, and carbohydrates
Enzyme activation
Storage of glycogen, vitamins, and minerals
Synthesis of plasma proteins, such as albumin, and clotting factors
Blood detoxification and purification
fats break down into
ketones
albumin
without it leaking
ammonia?
ammonia conversion to urea
liver can store how much blood?
1 liter
liver Storages what vitamins?
Storage-fat-soluble vitamins (A,D, E, K) and minerals
Synthesis of
Synthesis-serum proteins, phospholipids, cholesterol, clotting factors
liver immunity (my kupffer is immune to my liver)
filters blood via Kupffer cells
increased resistance within the portal venous system results in
decreased blood flow through and out of the liver. Collateral circulation develops to help relieve pressure. doesn’t help splanchnic (digestive) circulation.
blood backed up in the livers backs up in
splenic vein and collaterals
portal HTN will cause (varicose)
varices in GI tract and rectum (hemorrhoids)
portal HTN - symptoms (just if the liver doesn’t work) and what do ppl look like?
Hepatomegaly, splenomegaly
Esophageal, gastric, rectal varices (hemorrhoids)
Alterations in
Production & secretion of bile
can’t process CHO, protein, lipid fat (skinny arms and legs, big belly) metabolism
can’t clear Hormones
Detoxification
liver labs
if liver problems - Enzyme elevation
ALT, AST, alkaline phosphatase
Bilirubin elevations
Total , indirect, direct, urine bilirubin
Protein reduced
Serum albumin, total protein low
Ammonia elevated
Coagulation prolonged PT, PTT, INR
liver diagnostics (tips for the liver)
Liver biopsy
TIPS (rerouting)
Paracentesis
CT
MRI
PET (for liver cancer)
gall bladder diagnostics (Erp is a good gal)
MRCP
ERCP
Ultrasonography
Cholesintigraphy
Cholangiography (dye into ducts to view biliary tract)
liver problems - exam for resp CV renal
fluid volume deficit (3rd spacing) - flat neck veins - fluid leaks out
Edema (crackles)
Adventitious BS
BP low, pulse - high and weak
BUN, Cr, urine sodium, UO, and I & O (hepatorenal syndrome, low survival rate and can’t get a transplant)
put them in reverse trendelenberg
liver disease - neurologic
GCS (hepatic encephalopathy) aspiration
MS
Coordination
Reflexes
Movement
Seizures
liver disease - GI assessment
N, V, anorexia
Diarrhea or constipation, color of stool, volume, consistency
Lactulose?
Ascites- enlarging abd girth, abd fluid wave, ***if fluid it will be dullness on percussion, protruding umbilicus, assess BS, visible collateral veins on abdominal wall
Bleeding esophageal varices, CBC, hematemesis, melena
Hepatic tenderness and enlargement
liver problems - integumentary system (liver spiders and medusa)
Jaundice
Pruritus
Spider angioma (red and purple marks)
Edema
Dry, flaky skin
Poor skin turgor
Caput medusa (circulation around belly button)
Poor wound healing, ecchymosis, petechiae, bleeding gums
NAFLD (non-alcholic fatty liver disease)
Steatohepatitis (fatty hepatitis)
Accumulation of fat in liver causes scarring and damage leading to liver failure
NAFLD - symptoms (just 3, fatty liver is FAR)
Symptoms include RUQ pain, fatigue and anorexia
NAFLD - risk factors (Kel and predinsone make my liver not fat)
Gastric bypass surgery, hyperlipidemia, rapid weight loss, obesity, toxic chemicals, medications
Prednisone, amiodarone, tamoxifin, diltiazem, methotrexate
cirrohosis
Liver cells are destroyed and replaced by connective/scar tissue that alters circulation/flow within the liver.
Diffuse, fibrotic changes
Destruction of hepatocytes
Congested/obstructed flow
Blood, lymph, bile
Chronic & progressive
All body systems are affected
Can progress to hepatic encephalopathy/coma. only cure is transplant.
general s/sx of cirrohosis - breathing?
Firm nodular liver to palpation
Abdominal pain RRQ
Chronic dyspnea,
Change in bowel habits
Anemia/ bruising
SGOT/AST and SGPT/ALT rise
early s/sx of cirrhosis (pain in RUQ and gi problems cirrose early in the morning)
Generalized weakness, malaise
RUQ pain
Wt. loss, A/N/V, flatulence, GI disturbances, indigestion, change in BM
late s/sx of cirrhosis (spiders cirrhose late at night)
Change in mental status, memory
Spider angiomas (face, neck, shoulders) , jaundice, esophageal varices, GIB, ascites edema
Coagulopathy, bruising, thrombocytopenia
Splenomegaly, hepatomegaly
Peripheral neuropathy
lanecc’s cirrhosis (lance the drinker has cirrhosis)
ETOH induced, about 20% of alcoholics develop
billiary obstruction cirrhosis
Retention of bile/inflammation of ducts-jaundice
Obstruction of common bile duct
post necrotic cirrhosis (art has necrosis)
hepatic artery is blocked and causes necrosis. shock or trauma.
cardiac passive congestion d/t CHF cirrhosis
scar tissue forms
metabolic cirrhosis (glycogen is metabolic)
glycogen storage disease, wilson’s disease (copper)
primary cirrhosis (it’s primary autoimmune for cirrhosis)
autoimmune disease destroys bile ducts, usually middle-aged women. main complaint is fatigue and they are jaundice.
atrophic/hypertrophic cirrhosis (it’s in the name)
decrease in size, or connective tissue hyperplasia
treatment for cirrhosis - and avoid what meds (bummer if you get cirrohsis)
Antacids, vitamins and diuretics (neutralize stomach acid)
NO MORE ALCOHOL
Avoid narcotics
I & O and daily weights
REST
Prevent bleeding
Measure abdominal girth
Monitor jaundice
Good skin care
cirrhosis diet (think - too much hurts the brain)
Diet
Decrease protein
Low sodium
cirrhosis causes (coag in the vein causes cirrhosis)
hypercoagulability in the portal vein
Esophageal Varicies
Most common portal HTN
Esophageal Varicies - Pathophysiology
Portal HTN >obstruction > collateral circulation in esophagus/venous > increased pressure > ulceration and hemorrhage
esophageal varicies - Assessment - what does vomit look like?
Hematemesis, melena, hepatic encephalopathy, dilated abdominal veins, ascites
Endoscopy, ultrasound
esophageal varicies - treatment
Fluid resuscitation, correct coagulopathies, sclerotherapy, banding, Sengstaken-Blakemore tube, vasopressin, TIPS, Warren Shunt, Partial Mesocaval Shunt
shunt
where it orginates is first word, and where it ends is the last word.
ascites
Increase in hydrostatic pressure & lymph formation
ascites - 2 main causes (think pressure)
portal HTN and decreased colloid osmotic pressure. Then Na retention and the kidneys get involved causing hepatorenal syndrome
ascites - s/sx - what about flanks?
Bulging flanks, protruding umbilicus, fluid wave, shifting dullness to percussion
ascites - treatment
Sodium restriction, diuretics, aquaretics (vasopressin V2 receptor agonists), water restriction, administration of albumin/colloids, therapeutic paracentesis, TIPS (transjugular intrahepatic porto systemic shunt, automated low flow pump system (Alfapump)
Hepatorenal Syndrome (HRS) - type 1 (#1 dies fast and first)
Severe rapidly progressing renal failure with a doubling of creatinine in 2 weeks
Usually follows a precipitating event
Most patient die within 2 weeks of onset
Hepatorenal Syndrome (HRS) - type 2 (too (2) slow)
Slower, chronic, more progressive increase in creatinine
Patient exhibit signs of liver failure and arterial HTN
Severe ascites refractory to diuretics
Predisposed to developing Type 1
hepatorenal syndrome - s/sx (basic renal stuff)
Clinical characteristics
Presence of liver failure
Decreased GFR
Reduced urine sodium
Azotemia (high BUN)
Oliguria or anuria
High BUN/creatinine ratio
Hepatic Encephalopathy
Protein-breaks down to ammonia-liver converts to urea-excreted by kidneys
hepatic encephalopathy - s/sx (smell and energy level?)
***more and more sleepy over time. reflexes go down. Slow EEG. Foul odor - fetor. AMS, alteration in behavior, LOC changes
hepatic encephalopathy - causes
Infection, elevated protein intake, worsening hepatic function, constipation, azotemia, GI bleeding, hypovolemia, hypoxia, CNS depressants, overuse of diuretics
hepatic encephalopathy - stages 1 - 4 (don’t need to memorize this)
1 - mild confusion
2 - lethargy, blindness
3 - incoordination, inactive but arousable
4 - coma, death, unresponsive
hepatitis A (A fecal)
Transmission through fecal-oral route
High risk groups
hepatitis patho
Inflammation of the liver caused by a viral infection or toxins
Inflammatory cells/fluid/lymphocytes > congestion > enlargement > distortion of lobular pattern > necrosis
Distortion > increase pressure > portal HTN
Edema of bile channels > increased bilirubin
hepatitis B (B sexually active, or virus)
DNA virus
Sexually transmitted, perinatal, blood. treatment Interferon, lamivudine
Hep C
Blood, sexually, perinatal. treatment Interferon, ribavirin
need to know this - stages of hepatitis (pre ick, post)
Preicteric, Icteric, Posticteric
preicteric (P for preicteric, P for prodromal)
Prodromal (infection to start of signs and symptoms)
One week
Flu like
Malaise, fatigue, H/A, myalgia
A/N/V, diarrhea, low-grade fever, conjunctivitis, cough
Aversion to odors, avoidance of protein foods
Elevated LFT’s
Severe
Urticaria, rashes, polyarthritis, arthralgia
icteric (Ick, you have jaundice for 4 weeks?)
starts with jaundice. 4-6 week
Jaundice, dark urine, light colored stools
Tender enlarged liver
Elevated LFT’s
Severe puritis
Preicteric symptoms subside
Posticteric - how long? (think of mom at 4)
recovery. Up to four months
transplant criteria
End-stage organ failure
Short life expectancy
Severe functional disability
No other serious health problems
Psychological readiness
Support in place
