Pathophysiology, Signs and Symptoms of Liver Cirrhosis Symptom o Development of collateral vessels – Esophageal varices – Caput medusae – Hemorrhoids

o Portal hypertension – Ascites Decreased albumin production: Anasarca o Splenomegaly: Pancytopenia – o Impaired bile synthesis – Malabsorption of fatsoluble vitamins – Impaired metabolism of sex hormones – Female: menstrual disorders – Male: testicular atrophy, gynecomastia – Steatorrhea o Decreased clotting factor synthesis: Bleeding tendencies o Failure to conjugate bilirubin – Jaundice – Icterus – Tea-colored urine – Pruritus o Loss of liver glycogen: Hypoglycemia o Loss of detoxification properties – Hepatorenal syndrome: azotemia – Hepatic encephalopathy Pathophysiology Hepatomegaly  obstruction of the portal circulation  backflow of blood to: - esophageal veins  (rupture possible) - gastric veins - anal veins Increase in hydrostatic pressure  escape of fluids to the abdominal cavity Decrease in colloidal osmotic pressure  escape of fluids all around the body Due to destruction of the liver, the spleen will compensate leading to its enlargement  destruction of RBC, WBC, platelets Inability of the liver to produce bile  lack of fatty acids - inability to transport ADEK - inability to stimulate Adrenal Cortex  lack of: Estrogen and Progesterone  Amenorrhea Androgen Fats goes with the feces Lack of vitamin K for clotting factor synthesis

Inability of the liver to conjugate bilirubin  increase in total bilirubin  ejection of unconjugate bilirubin (dark yellow) in the blood Bilirubin ejection can cause drying of the skin  irritable itchiness Inability of the liver to store glycogen Inability of the liver to detoxify ammonia  build up of ammonia outside the blood brain barrier  cerebral dehydration  symptoms: 1. Asterixis 2.

PANCREATITIS • Etiology and Incidence: Cause: Unknown Predisposing Fators • Male • Middle-age • Medicine / substance • Meat /meal intake • Midnight attack Pathophysiology Is acute / chronic inflammation of the pancreas.

Disruptions of pancreatic ducts

H erg em yp lyc ia H o lc ia yp ca em

Spill of pancreatic enzymes Autodigestion

Incapacitating pain Release of chemical mediators Neurogenic shock
Manifestations: • •

Hemorrhage

Peritoneal Spill Peritonitis Respiratory Distress Septic shock

Hypovolemic shock

• • • • • • •

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

Sign up to vote on this title
UsefulNot useful