Liver, pancreas, skin Flashcards
What is the function of the pancreas? What does it house?
Produces hormones and digestive enzymes. Houses:
Alpha cells: glucagon
Beta cells: insulin
Delta cells: somatostatin and gastrin
Explain the pathophysiology of acute pancreatitis?
Inflammation from an insult or injury activates pancreatic enzymes, which auto-digest and cause fibrosis. Leads to thrombi and necrosis of tissue. Vasodilation from vessel damage, fat necrosis occurs, fatty acids bind to CA, results in hypocalcemia.
What factors lead to acute pancreatitis?
Biliary tract disease with gallstones is the leading cause. Alcoholism, ab surgery or diagnostics, trauma. Mostly middle aged men, medication toxicities, viral infections, gastric or duodenal ulcers leading to peritonitis.
Clinical manifestations of acute pancreatitis?
Abdominal pain: severe, sudden-often after large mean and/or alcohol intake. Weight loss, n/v, ab distention. Ad guarding, rigid abdomen. Cullen’s and turner’s sign.
Gray-blue discoloration of the abdomen and peri-umbilical area.
Gray-blue discoloration of the flanks.
Cullen’s sign
Turner’s sign
What does elevated amylase (serum and urine), lipase, trypsin, and elastase indicated?
Elevated glucose indicates?
Pancreatic cell injury.
Glucose indicates pancreatic cell injury, impaired carb metabolism, decreased insulin release.
What do elevated bilirubin and ALT indicated?
Hypocalcemia and hypomagnesia?
Hepatobiliary involvement
Enzymatic fat necrosis
Clinical management of acute pancreatitis?
Fluid resuscitation, NPO during acute period, electrolyte replacement, NGT to suction (n/v, ileum). Pain control (morphine or dilaudid). H2 blocker or PPI, anitemetics.
Comfort and nutrition for acute pancreatitis?
Comfort measures: semi-fowler’s, decrease anxiety, skin integrity, oral care
Enteral feeding, TPN (severe and continued NPO). NPO 24-48 hours, then clear fluids, then low fat, low protein. Bland, no spices. Avoid GI stimulants, no alcohol. Surgery usually isn’t indicated.
Progressive, destructive disease. Remission and exacerbations. Pancreatic insufficiency, decreased function.
Chronic pancreatitis. Chronic calcifying: alcohol induced. Chronic obstructive: gallstones. Autoimmune Idiopathic and hereditary chronic.
What are some of the s/s of chronic pancreatitis?
Intense ab pain that is continuous, burning, or gnawing. Ab tenderness, ascites, vomiting, weight loss, jaundice, dark urine, 3 P’s, steatorrhea or clay-colored stools.
Respiratory compromise: adventitious or decreased breath sounds, dyspnea, orthopnea
Diagnosing chronic pancreatitis?
Endoscopic retrograde cholangiopancreatography (ERCP). MRI, CT, US. Glucose tolerance test which evaluates pancreatic islet cell function. Amylase and lipase levels may be elevated.
Non-surgical management of chronic pancreatitis?
Medication: pain relief, pancreatic enzyme replacement therapy. Insulin or other anti-diabetic agents.
Nutrition therapy: Monitor foods that cause pain/discomfort. Avoid fats, which leads to diarrhea. Avoid alcohol and smoking. Vitamin and mineral replacements
Administration of pancreatic-enzyme replacement therapy?
PERT. Take immediately before or with meals and snacks. Administer after antacid or H2 blockers. Swallow tab, no chewing, to help decrease oral irritation. Mix powdered enzymes in juice/applesauce. Do not crush enteric coated preparations.
Surgery for chronic pancreatitis?
Persistent pain and/or restore drainage. Pancreaticojejunostomy. Stent placement, removal of pancreas, often endoscopic or laparoscopic procedures.
What is the pathophysiology of chronic pancreatitis?
Usually epithelial cells of the pancreatic ducts. Discovered late so has spread throughout organ. Rapid growth and spread in the surrounding tissue. Most site is the heart of the pancreas. Necrotic pancreatic tumors increase thromboplastin factors: VTE is a common complication
Clinical manifestations and diagnosis of pancreatic cancer?
Pain, jaundice, weight loss. Usually present at the advanced stage. Malignant cells to peritoneal cavity: metastatic disease, ascites.
Diagnosed with CT, MRI, ERCP
Clinical management of pancreatic cancer?
Goal is to prevent spread of tumor and palliative care. Chemo with combo agents.
External beam radiation for pain relief. Shrinks the tumor cells to alleviate destruction and improve food absorption.
Pain control with high doses of opioids (Morphine), biliary stents
Surgical management of pancreatic cancer?
Pre-op: Poor surgical risk, malnutrition and debilitation. Tube feeding: jejunostomy. TPN.
Total pancreatectomy. Pancreaticoduodenectomy: Whipple procedure or resection.
Radical pancreaticoduodenectomy?
Whipple. Removal of pancreas head, duodenum, stomach (partial), portion of jejunum, gallbladder, distal common bile duct
What does monitoring NGT drainage after surgery for pancreatic cancer do? Semi-fowler’s positioning?
Prevents pressure buildup. Reduces stimulation of remaining pancreatic tissue.
Reduces stress on the suture line and anastomosis sites. Improves lung expansion
Fluid and electrolytes and glucose after pancreatic cancer surgery?
Significant blood loss during the procedure. NG drainage.
Glucose monitoring because of transient hyper or hypoglycemia.
What is the function of the liver?
Detoxify drugs, toxins, hormones, virus, bacteria. Converts fat soluble waste into water soluble waste and urea. Metabolizes, or breaks down nutrients from food to produce energy when needed. Prevents shortages of nutrients by storing certain vitamins, minerals, and sugar. Produces bile (700-1200mL), a compound needed to digest fat and absorb A, D, E, K.
Venous blood from the Gi tract empties in to the portal vein and travels through the liver before moving into the general circulation. Explain portal HTN?
Obstruction of blood flow in the portal vein produces an increase in the hydrostatic pressure within the peritoneal capillaries contributing to the development of ascites, splenic enlargement, shunting of blood to collateral venous channels causing varicosity’s of the hemorrhoidal and esophageal veins.
Accumulation of plasma in the peritoneal cavity caused by increased pressure forcing fluid out of the intravascular space into the cavity.
Ascites. Plasma contains albumin so circulating proteins are decreased. Decreased serum osmotic pressure. Intravascular fluid depletion stimulates kidney to conserve Na and water, which leads to increased hydrostatic pressure and creates more ascites.
Explain a paracentesis?
Ultrasound guided. Relief of acute symptoms. Usually drain 1-4L. Rapid removal leads to vasodilation and shock. Client care.
Ascites management?
Monitor I/O. Daily weight and ab girth, low Na diet, monitor dyspnea, HOB above 30. Diuretic therapy (furosemide, spironolactone). Paracentesis, shunts
Explain a three shunts for ascites?
Transjugular intrahepatic portal-systemic shunt (TIPS): between portal and hepatic vein to decrease pressure, decreases risk of bleeding.
Peritovenous shunt is a one-way valve that drains ascites fluid into the superior vena cava
Portacaval diverts portal venous blood flow from the liver
Decreased of synthesis of bile in the liver.
Prevents the absorption of vitamin K. Without the K clotting factors are not produced in sufficient numbers. Abnormal prothrombin times, prolonged or elevated.
Backup of blood in the spleen.
Splenomegaly. Enlarged spleen destroys platelets. Thrombocytopenia is often the first clinical sign of liver dysfunction.
Usually due to hepatocellular disease (cannot metabolize bilirubin so it builds up) or intrahepatic obstruction (clogs bile duct so secretion is not possible). s/s?
Jaundice. Hemolytic. Hereditary hyperbilirubinemia.
Skin is yellow-orange and pruritic. Schlera and secretions are tinged yellow. Urine is dark and tea-colored brown. Stools are clay-colored.
Systemic, viral infection that causes necrosis and inflammation of the liver cells.
Viral hepatitis. Six types, A, B, C, D, E, G. All cause cause acute hepatitis.
B, C, D can cause chronic hepatitis.
Acute hepatitis?
Lasts less than 6 months and resolves spontaneously.
RUQ pain, arthralgia, myalgia, leathery, fever, chills, malaise, anorexia, n/v, diarrhea/constipation, jaundice, dark urine, clay-colored stool, pruritic
Hepatitis that is spread via the fecal-oral route through person to person or contaminated food.
Hepatitis A. Incubation is 15-50 days, not life-threatening. May not know if infected. Mild flu-like upper respiratory infection, low-grade fever. Prevention is the HAV vaccine.
Hepatitis that is spread via blood and body fluids. Unprotected sex, sharing needles/sticks, mother to baby during birth, contact with open sores, hemodialysis, imunnosuppressed.
Hepatitis B. Symptoms occur within 25-180 days of exposure and are vague. Loss of appetite, generalized aching, malaise, weakness. Most adults recover and develop immunity.
Prevention of hepatitis B?
Vaccine.
Immediate post-exposure treatment. Give HBIG within 7 days percutaneous exposure and within 2 weeks of sexual exposure.
HBV vaccine given within 12-24 hours gives about 70-905 success
Hepatitis that is spread blood to blood via sex, IV’s, transfusions, HCW, blood, needles, tattoos, blood products prior to 1992.
Hepatitis C. Incubation is 15-160 days. May not know if infected. Long term leads to cirrhosis which needs a liver transplant.
Hepatitis that only occurs with HVB. Spread via parenteral or sexual contact.
Hepatitis D. Incubation is 28-160 days.
Hepatitis that occurs in large outbreaks with floods. Self-limiting and resolves on its own. Spread via fecal-oral.
Hepatitis E. Incubation is 28-35 days. Jaundice. No chronic version.
Associated with hepB and C, chronic liver disease, cirrhosis. Smoking, alcohol.
Liver cancer. Toxins incude arsenic and vinyl chloride. Usually originates outside the liver in the lungs, breasts, and digestive tract.
Health history assessment for skin disorders?
Often from an underlying disease (syphilis, kaposi’s sarcoma, rash of lupus). Where did it start and how long has it been present? Has it spread? Any travel or recent exposure to the environment? New meds? Occupation (hands in water, latex, etc). Sun exposure, tanning booths, sunscreen? Overuse of soaps, especially in the elderly?
What is visually assessed in the skin
Color: pigmentation, blood supply (pallor, erythema, cyanosis, jaundice). Temperature, odor. Moisture, turgor. Texture.
Reactivation of the dormant virus, from previous chickenpox. Cluster of vesicles follow peripheral sensory nerves that do not cross the midline. Causes intense pain in 50% of people and symptoms last from months to years.
Herpes zoster (shingles). 2/3 of lesions over the thoracic area. Remainder usually trigeminal nerve involvement (face, eye, scalp).
Treatment and prevention of herpes zoster?
Treatment is often nothing. Antivirals, analgesics (long term management).
Prevention involves Zostavax for those 60 years or older, unless they’re immunocompromised. Protection from the vaccine decreases within the first 5 years after vaccination, beyond 5 years is uncertain.
What are two types of pre-cancerous skin lesions?
Seborrheic keratosis, rarely develops into malignancy.
Actinic keratosis: 0.25%-1% annually develop into squamous cell carcinoma.
May be normal age-related changes.
Skin which is sun exposed or chronic irrigation. Irregular, soft, red, ulcerative.
Squamous cell carcinoma.
Metastasis is possible.
Sun exposed areas of older, fair individuals. Pearly raised lesions with depressed centers.
Basal cells carcinomas. Rarely metastasizes.
This has an increased incidence due to sun exposure and thinning ozone. High rate of metastasis.
Melanoma. Always excised. Virotherapy.
ABCDEF
ABCDEF of melanoma?
Asymmetry Border irregularity Color variation Diameter Evolution Feeling
Types of treatment for skin cancer?
Excision, freezing, topical agents (chemo), systemic chemo (melanoma), biotherapy (interferon for melanoma)
Family and pt teaching for skin cancer?
Avoid direct sunlight, tanning booths. Sunscreen and reply q2hr. Balanced diet for intact and healthy skin.
Monthly skin checks using a mirror. Look for pigmented areas, moles, newly acquired skin growths, changes in lesions, itching, pain. Dermatologists.
Examples of cholestatic medications?
Phenothiazines, antithyroids, sulfonylureas, tricyclic antidepressants, nitrofurantoin, androgens, estrogens, some antibiotics
