Week 11: HEPATIC DISORDERS Flashcards
Liver
- Supports digestion of proteins and fats
- Located in RUQ
- Regenerative
- Produces bile
- Made up of four lobes
- Functional unit: lobules (highly vascularized)
- Hepatocytes – cells of liver, found in lobules
Key functions:
- Protein metabolism
- Storage (carbs, fats)
- Detoxification
- Bile production
- Clotting factors
Gallbladder
Stores bile:
o Dark yellow/green fluid
o Produced by liver, stores and concentrated in gallbladder
o Makes stool brown, emesis yellow
o Contains: water, lytes, fatty acids, cholesterol, bilirubin, bile salts
Pancreas
- Exocrine functions:
o Amylase to carbs
o Trypsin to proteins
o Lipase to fats
o Increase pH of digestive system to normal amount
Endocrine functions:
- Secrete hormones that assist with blood glucose levels
Liver Disease
Disturbance in liver function (acute or chronic)
Stressors include:
- Fats (non-alcoholic fatty liver disease)
- Alcohol (fatty liver, cirrhosis)
- Viruses (hep c)
- Hepatotoxic substances (Tylenol overdose)
Stages of liver disease:
Inflammation
- Stress causes inflammation in the liver, damaging hepatocytes
Necrosis
- Poor perfusion destroys hepatocytes
Fibrosis and scarring
- Tissue is replaced with fibrous scar tissue and abnormal lobules, irreversible
Damaged hepatocytes:
- Can’t filter or absorb/store
- Increased waste buildup in the body
- Increased pressure through CV system (bp)
- Poor nutrition (cannot break down nutrients)
Disrupted liver perfusion:
Blood cannot move through hepatic vessels
Pressure increases through hepatic vessels
Pressure backs up into GI system, can cause varices, edema, bleeding, and
ruptures
Disrupted production of albumin
Fluid is not retained in the intravascular space (exits out of the capillaries, edema, congestion think traffic, less exits to get off highway)
Edema, ascites
Health History: Liver disease
Risk factors:
Medication use – hepatotoxicity
Infectious diseases – hepatitis, HIV
Comorbidities – jaundice, hepatitis, biliary tract disorders
Family history – increase risk for diagnosis in immediate family
Genetics – may impact liver function
Lifestyle – diet, exercise, smoking, alcohol
Physical assessment: Liver disease Nutritional deficiencies
- Fat-soluble vitamins (A, D, E, K)
Low vitamin K – bleeding risk
Liver is enlarged from inflammation and cannot filter, waste builds up,
pressure builds, fluid moves out, pressure backs up into GI vessels, varices
Physical assessment: liver disease cardiovascular
Cardiovascular – blood flow is obstructed through the liver, and pressure rises:
- Hepatic portal hypertension
- Splepnomegaly
- Ascites
- Collateral circulation – varices
- Cardiac dysrhythmias
- Abnormal angiogenesis (new blood vessel formation)
Nursing Assessment: liver disease Integumentary
Integumentary – cause of waste buildup, pressure buildup:
Jaundice
Edema
Petechiae, ecchymosis
Spider angiomas
Palmer erythema
Pruritis
Nursing assessment: liver disease neuro - waste buildup
Confusion
Sleepiness
Tremor (asterixis)
Hyperactive deep tendon reflex
Hepatic encephalopathy
Nursing assessment: liver disease Respiratory
pressure rises and backs up through vessels:
Platypnea (SOB relieved by laying)
Dyspnea
Clubbing fingers
Cyanosis
Decrease SpO2
Nursing assessment: liver disease Renal
pressure rises and backs up through vessels, decreased perfusion:
Symptoms of hypoperfusion
Cognitive changes
U/O changes
Weight gain
Ascites
Fluid/lytes imbalances
Nursing assessment: liver disease other findings
Palpitation for hepatomegaly – extended liver, tender/hard
Ascites – fluid in abdomen
Stool – clay coloured, blood
Hematemesis – esophageal varices
Complications of Liver Disorders
Ascites- Abnormal build-up of fluid in the peritoneal space
Causes of Ascites
Hepatic portal hypertension
Increased aldosterone, decreased albumin
S&S of Ascites
Increased abdominal girth
Increased weight
Abdominal discomfort
SOB
Fluid & lyte imbalances
Umbilical herniation
Nursing Management: Ascites
Nutritional therapy – low Na diet
Pharmacologic therapy – diuretic therapy (spironolactone, IV albumin)
Paracentesis
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
- Treatment in patients with ascites needing frequent paracentesis
- A tract is creased between the higher-pressure portal vein and the
lower-pressure hepatic vein – decreasing the portal venous
pressure causes a decrease in ascites
Pharmacological treatment: Ascites
spironolactone or furosemide or norfloxacin
Esophageal Varices
Esophageal Varices
Enlarged and additional veins with poor integrity in esophagus and stomach o Risk – GI bleeding
Can be an emergency – depending on size of bleed
Nursing management:
Monitor for S&S of GI hemorrhage
Pharmacologic therapy
Endoscopy Banding Therapy (Ligation)
- Treats varices
- Endoscope is loaded with rubber bands to wrap the varices – shrink and fall off over time
- TIPS
Esophageal Varices pharmacological intervention
vit K or OLOLs (metor-, Carvedi-)
Hepatic encephalopathy
Depressed CNS causes neurological changes - EMERGENCY
Causes:
Elevated ammonia levels leads to increased GABA, worsening the CNS depression
S&S:
Mental status changes
Disturbed sleep
Asterixis (tremors)
Difficulty handwriting
Hyperactive deep tendon reflexes
Flaccidity and coma
Nursing Assessment: Hepatic encephalopathy
Monitor – VS, neuro status, serum ammonia, respiratory depression
Nutritional therapy – low protein diet (avoid meat and eggs)
Pharmacologic therapy – lactulose and antibiotic therapy
Pharmacologic therapy Hepatic encephalopathy
rifaximin or lactulose
Nursing priorities: Hepatic encephalopathy
Monitor for progression & complications
Ascites, bleeding, hepatic encephalopathy, hepatopulmonary syndrome
Medical management
Medications for symptoms management, complications
Health teaching
Lifestyle, treatment
Alcohol
Infection prevention
Bleeding precautions
Pancreatitis
Inflammation of the pancreas (acute or chronic)
Can lead to autodigestion of the pancreas
Causes of pancreatitis
o Excessive alcohol use
o Viral/bacterial infections (mumps)
o Gallstones
o Trauma/tumors
o Hypercalcemia, hypercholesterolemia
o Cystic fibrosis
Health history – risk factors: Pancreatitis
Infectious diseases – mumps
Genetics – cystic fibrosis
Comorbidities – gallstones, tumours
Lifestyle – smoking, alcohol
Signs and symptoms of disorder
Labs & Investigations: Pancreatitis
Increased amylase and lipase
Increased blood glucose (not making insulin)
Pancreatitis Pain
Pain:
LUQ
Lef side of back
Pain worsens when laying down, better when sitting up and bent forward
Pain can be worse with eating or drinking
Pancreatitis: GI
Pain location, tenderness, guarding on palpation
N/V
Decreased bowel sounds
Weight loss, diarrhea, steatorrhea (increase in fat in stool), diabetes
development (long-term)
Pancreatitis: CV
Hemodynamic instability
Increased HR – pain
Decreased BP – dehydration, bleeding
Pancreatitis Integumentary:
Cullen’s sign (bruising near belly button)
Grey Turners sign (bruising on one or both sides (waist) of body)
Nursing Priorities of Pancreatitis
Monitor for progression & complications
- Respiratory, nutritional, lyte imbalances, hemorrhagic necrosis (shock risk)
Medical management
- Pain management
- Health teaching
Pharmacological Interventions: Pancreatitis
opioids
Cholecystitis
- Inflammation of gallbladder
- Causes:
o Cholelithiasis (gall stones, 80%)
o Bile flow obstruction - Risk factors:
o Comorbidities – gall stones, sickle cell disease
o Lifestyle – smoking, alcohol, obesity
o S&S of disorder
Physical assessment: Cholecystitis
o Pain:
RUQ
Right side of back, lower part of scapula
Worsens with eating or drinking
Constant or colicky
o GI:
Pain location, tenderness, guarding on palpation
N/V
Avoids deep breathing – pain
Pale coloured stool
o Integumentary
Jaundice
o Murphy’s Sign
Acute cholecytitis
Labs & Investigations: Cholecystitis
Endoscopic retrograde cholangiopancreatography
Nursing priorities: Cholecystitis
Surgical intervention care – surgical pre and post care
o Health teaching – lifestyle (diet)
