Pathophysiology, Signs and Symptoms of Liver Cirrhosis

Symptom Pathophysiology
o Development of collateral Hepatomegaly  obstruction of the portal circulation  backflow
vessels of blood to:
– Esophageal varices - esophageal veins  (rupture possible)
– Caput medusae - gastric veins
– Hemorrhoids - anal veins

o Portal hypertension Increase in hydrostatic pressure  escape of fluids to the

– Ascites abdominal cavity

– Decreased albumin Decrease in colloidal osmotic pressure  escape of fluids all

production: Anasarca around the body
o Splenomegaly: Pancytopenia Due to destruction of the liver, the spleen will compensate leading
to its enlargement  destruction of RBC, WBC, platelets

o Impaired bile synthesis Inability of the liver to produce bile  lack of fatty acids
– Malabsorption of fat- - inability to transport ADEK
soluble vitamins
– Impaired metabolism of - inability to stimulate Adrenal Cortex  lack of:
sex hormones
– Female: menstrual Estrogen and Progesterone  Amenorrhea
disorders
– Male: testicular atrophy, Androgen
gynecomastia
– Steatorrhea Fats goes with the feces
o Decreased clotting factor Lack of vitamin K for clotting factor synthesis
synthesis: Bleeding
tendencies

o Failure to conjugate bilirubin Inability of the liver to conjugate bilirubin  increase in total
– Jaundice bilirubin  ejection of unconjugate bilirubin (dark yellow) in the
– Icterus blood
– Tea-colored urine
– Pruritus Bilirubin ejection can cause drying of the skin  irritable itchiness

o Loss of liver glycogen:

Hypoglycemia Inability of the liver to store glycogen

o Loss of detoxification Inability of the liver to detoxify ammonia  build up of ammonia

properties outside the blood brain barrier  cerebral dehydration 
– Hepatorenal syndrome: symptoms:
azotemia 1. Asterixis
– Hepatic encephalopathy 2.
 PANCREATITIS

• Is acute / chronic inflammation of the pancreas.

Etiology and Incidence:

Cause: Unknown

Predisposing Fators
• Male
• Middle-age
• Medicine / substance
• Meat /meal intake
• Midnight attack

Pathophysiology

Disruptions of pancreatic ducts

Hyperglycemia Spill of pancreatic enzymes

Hypocalcemia
Autodigestion

Incapacitating Hemorrhage Peritoneal

pain Spill

Release of chemical Hypovolemic Peritonitis

mediators shock

Respiratory Septic
Neurogenic Distress shock
shock

Manifestations:

• Abdominal tenderness and distention

• Abrupt pain
– burning, stabbing or pressing
– epigastric area
– radiates to the shoulder, substernal area, back and flank
– Relieved knee-chest position
• Cullen’s sign
– Sign of hemorrhage
– Bluish discoloration of the periumbilical area
• Dyspnea
• Tachycardia
• Hypotension
• Fever
• Jaundice
• Nausea and vomiting
• Pain upon eating
• Steatorrhea
• Weight loss

Nursing Interventions:

• Assess:
– abdominal, cardiac, and respiratory status
– fluid balance
• Monitor and record:
– vital signs
– intake and output
– laboratory studies
– central venous pressure (CVP)
– daily weight
– urine and stool for color
– blood glucose level

• Administer the following, as ordered:

• Demerol for pain. Morphine Sulfate is contraindicated
• IVF
• Diet: NPO
• to rest the pancreas
• prevent nausea and vomiting.
• Keep the patient in Semi-Fowler’s position
• Environment:
• Quiet
• Restful

Pathophysiology, Signs and Symptoms of Renal Failure

Excretory Problems:
 Middle molecule accumulation or urea  trapping of:
 Glucose – hyperglycemia
 Keratin  sallow, yellow discoloration of the hair; split ends
 Lipids  hyperlipidemia  atherosclerosis  ASHD
• Inability of lipids / fatty acids to stimulate adrenal cortex to release sex hormones 
amenorrhea, infertility, impotence

 Travel of urea around the body:

 Surface to the skin  uremic frost  pruritus
 Surface to GI tract  PUD  gastric bleeding
 Surface to pericardium  percarditis
 Build up outside the blood brain barrier  CNS depression, psychological changes

 Inability to remove uric acid  inability of the kidneys to produce HCO3  metabolic acidosis 
destruction of WBC  infection tendencies

 Inability to remove uric acid  GOUT

 Inability to remove potassium  HYPERKALEMIA  cardiac arrest

Endocrine Problems:

 Inability to produce REF  decreased BM stimulation  decreased precursor cell production 

decreased RBC  anemia  anorexia, N/V

 Inability to produce hydroxyl:

o Decreased vitamin D  hypocalcemia  bleeding tendencies (calcium is a clotting
factor)
o Decreased vitamin D  hypocalcemia  parathyroid gland compensation 
hyperparathyroidism  ejection of calcium to the blood  renal osteodystrophy 
osteoporosis  risk for fracture

 Decreased urine output  false activation of RAAS  hypertension, CHF, pulmonary edema