Ms Adds

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

Pathophysiology Hepatomegaly  obstruction of the portal circulation  backflow of blood to: - esophageal veins  (rupture possible) - gastric veins - anal veins

o Portal hypertension – Ascites

Increase in hydrostatic pressure  escape of fluids to the abdominal cavity

Decreased albumin production: Anasarca o Splenomegaly: Pancytopenia

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

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

Inability of the liver to produce bile  lack of fatty acids - inability to transport ADEK

o Failure to conjugate bilirubin – Jaundice – Icterus – Tea-colored urine – Pruritus

Inability of the liver to conjugate bilirubin  increase in total bilirubin  ejection of unconjugate bilirubin (dark yellow) in the blood

–

- 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

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 properties – Hepatorenal syndrome: azotemia – Hepatic encephalopathy

Inability of the liver to detoxify ammonia  build up of ammonia outside the blood brain barrier  cerebral dehydration  symptoms: 1. Asterixis 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 Hypocalcemia

Spill of pancreatic enzymes Autodigestion

Incapacitating pain

Hemorrhage

Peritoneal Spill

Release of chemical mediators

Hypovolemic shock

Peritonitis

Neurogenic shock

Respiratory Distress

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

Septic shock

• • •

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