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Summary of Metabolism and Endocrine - Medical Surgical Nursing

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The metabolism and endocrine section of Medical-Surgical Nursing focuses on the regulation of body processes through hormones secreted by glands such as the pituitary, thyroid, parathyroid, adrenal glands, and pancreas. It covers common disorders including diabetes mellitus, thyroid imbalances (hypo- and hyperthyroidism), adrenal conditions like Addison’s disease and Cushing’s syndrome, and pituitary disorders such as acromegaly and diabetes insipidus. Emphasis is placed on diagnostic procedures (blood tests, imaging, and hormone stimulation tests), treatment plans, and nursing responsibilities. Nursing care includes monitoring hormone levels, managing medications, educating patients on lifestyle modifications, and recognizing complications like hypoglycemia or electrolyte imbalances. The goal is to support patient safety, promote adherence to treatment, and provide holistic, coordinated care

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MS RLE

Liver  The liver synthesizes most plasma proteins,
 Largest gland of the body and a major organ including albumin, globulins, clotting factors,
 Receives nutrient-rich blood directly from the GI tract and transport proteins.
 Stores or transforms nutrients into chemical  It requires Vitamin K for the synthesis of
substances clotting factors, such as prothrombin.
 Manufactures and secretes bile  Amino acids are used for protein synthesis in
 Removes waste products from the bloodstream and the liver.
secretes them into the bile
 Fat Metabolism
 Bile produced by the liver is stored temporarily in the
 The liver breaks down fatty acids for energy
gallbladder
and produces ketone bodies (acetoacetic acid,
 When needed for digestion, the gallbladder empties
beta-hydroxybutyric acid, acetone) during
and bile enters the intestine
times of limited glucose (e.g., starvation or
Important in the regulation of glucose and protein diabetes).
 Fatty acids also help in synthesizing
cholesterol, lecithin, lipoproteins, and other
lipids.
 Vitamin and Iron Storage
 The liver stores vitamins A, B, D, and B-
complex vitamins, as well as iron and copper.
 Bile Formation
 Bile is continuously produced by hepatocytes
and stored in the gallbladder for digestion.
 Bile aids in fat emulsification and the excretion
of waste products like bilirubin.
Anatomy of the Liver
 The liver is a large, vascular organ located behind the  Bilirubin Excretion
ribs in the upper right abdomen, weighing 1200-  Bilirubin, from the breakdown of hemoglobin, is
1500 g and divided into four lobes. processed in the liver and excreted in bile.
 Each lobe is divided into functional units called  In the intestine, bilirubin is converted to
lobules, surrounded by connective tissue. urobilinogen, partially excreted in feces, and
 Blood enters the liver from two sources: 80% from the reabsorbed into portal blood for reuse or
nutrient-rich but oxygen-poor portal vein, and the excretion through the kidneys.
rest from the oxygen-rich hepatic artery.  Drug Metabolism
 These blood vessels form sinusoids, which bathe  The liver metabolizes many drugs (e.g.,
liver cells (hepatocytes) in a mixture of venous and barbiturates, opioids, sedatives) by
arterial blood. conjugating them with compounds for
 The sinusoids drain into central veins, which join to excretion.
form the hepatic vein, draining into the inferior vena  First-pass metabolism reduces the
cava near the diaphragm. bioavailability of some oral drugs, meaning
 Kupffer cells, a type of phagocyte, engulf bacteria larger doses may be needed to achieve the
and other particles from portal blood. desired effect compared to parenteral routes.
 The smallest bile ducts, called canaliculi, carry
secretions from hepatocytes to larger bile ducts, Assessment of Liver
forming the hepatic duct.  Health History
 The hepatic duct and cystic duct from the gallbladder  Past Medical History: Check for liver diseases
merge to form the common bile duct, which or past issues (e.g., hepatitis, cirrhosis).
empties into the small intestine.  Lifestyle: Look at alcohol use, diet, exercise,
 -The sphincter of Oddi controls bile flow from the and toxin exposure.
common bile duct into the duodenum.  Medications: Review drugs that may affect
liver health.
Functions of the Liver  Family History: Ask about liver problems or
 Glucose Metabolism genetic liver conditions.
 The liver regulates blood glucose levels by
converting glucose into glycogen (stored in  Physical Assessment
hepatocytes) after meals.  Skin: Look for jaundice (yellow skin/eyes),
 When needed, glycogen is converted back to swelling (edema), or spider veins.
glucose (glycogenolysis) and released into the  Tremor and Asterixis: Check for hand tremors
bloodstream. or involuntary hand flapping (signs of liver
 When glycogen stores are insufficient, the liver issues).
produces glucose via gluconeogenesis, using  Abdominal Assessment
amino acids or lactate, especially during  Fluid Wave: Check for fluid buildup in the
hypoglycemia. abdomen (ascites).
 Ammonia Conversion  Palpation:
 Ammonia, a by-product of amino acid  Liver Size: Feel for the liver in the right
breakdown, is converted into urea by the liver. upper abdomen.
 Ammonia from intestinal bacteria is also  Tenderness: Look for pain when touching
removed from portal blood and converted into the liver.
 Palpable Liver: If the liver is enlarged, it

, MS RLE

 Liver function tests may not show abnormal  Bilirubin and Urobilinogen: Serum bilirubin and
results until more than 70% of liver tissue is urine urobilinogen levels may be elevated.
damaged.  Liver Enzymes: AST and ALT levels increase,
 Tests measure enzyme activity and serum indicating liver cell damage.
levels of proteins, bilirubin, ammonia, clotting  Other Symptoms: Headache, chills, and fever,
factors, and lipids. particularly if the cause is infectious.
 Prognosis: Hepatocellular jaundice may be
 ALT (Alanine Aminotransferase): Increased in liver
reversible depending on the cause and extent
disorders, used to monitor conditions like hepatitis,
of liver damage.
cirrhosis, or liver damage from medications.
 AST (Aspartate Aminotransferase): Elevated levels  Obstructive Jaundice
can indicate damage to organs like the heart, liver,  Cause:
muscles, or kidneys. Not specific to liver disease  Extrahepatic Obstruction: Blockage
but may increase in cirrhosis, hepatitis, or liver outside the liver (e.g., gallstones,
cancer. inflammation, tumors, or pressure from an
 GGT (Gamma Glutamyl Transferase): High levels enlarged organ).
are linked to cholestasis and alcoholic liver  Intrahepatic Obstruction: Blockage inside
disease. the liver’s small bile ducts (e.g.,
inflammation or certain medications like
 Liver Biopsy
some antibiotics and hormones).
 A liver biopsy involves removing a small
 Effects:
sample of liver tissue for examination.
 Bile backs up into the liver and enters the
 It helps diagnose liver conditions when clinical
bloodstream, causing jaundice (yellowing
findings and lab tests aren’t enough.
of skin, mucous membranes, and eyes).
 Often used to evaluate liver disorders or detect
 Urine turns deep orange and foamy due to
lesions
bilirubin.
.
 Stools become light or clay-colored
Other Diagnostic test
because of a lack of bile in the intestine.
 Ultrasonography, CT Scans, and MRI: Used to
 Symptoms:
identify normal liver structures and abnormalities in
 Itching from bile buildup in the skin.
the liver and biliary tree.
 Fatty food intolerance and indigestion due
 Radioisotope Liver Scan: Assesses liver size, blood
to impaired fat digestion.
flow, and possible obstructions.
 Lab Results:
 Laparoscopy: A fiberoptic endoscope is inserted
 Moderate increase in AST, ALT, and
through a small abdominal incision to:
GGT.
Jaundice  High bilirubin and alkaline phosphatase
 Occurs when bilirubin concentration in the blood levels.
increases due to liver disease, bile flow obstruction  Hyperbilirubinemia (high bilirubin levels) can be
(e.g., gallstones), or excessive red blood cell caused by inherited disorders, leading to jaundice.
destruction.  Gilbert Syndrome:
 With bile duct obstruction, bilirubin cannot enter the  Increased unconjugated bilirubin causes
intestine, leading to a decrease in urobilinogen in jaundice.
the stool and absence in the urine.  Liver function and histology are normal, with
 Jaundice becomes visible when serum bilirubin no hemolysis.
exceeds 2.0 mg/dL, resulting in a yellow or  Affects 3-8% of the population, mostly males.
greenish-yellow tint to the skin and sclerae (the
Other Inherited Conditions:
white part of the eyes).
 Dubin-Johnson Syndrome: Chronic jaundice with liver
Types of Jaundice pigment.
 Hemolytic Jaundice  Rotor Syndrome: Chronic conjugated
 Cause: Increased red blood cell destruction, hyperbilirubinemia, no liver pigment.
leading to excess bilirubin in the blood.  Benign Cholestatic Jaundice of Pregnancy: Due to
 Bilirubin: Predominantly unconjugated (free) sensitivity to pregnancy hormones.
bilirubin.  Benign Recurrent Intrahepatic Cholestasis: A genetic
 Fecal and Urine Urobilinogen: Increased, but condition affecting bile flow.
urine is free of bilirubin.
Portal Hypertension
 Symptoms: Mild jaundice, unless bilirubin
 increased pressure in the portal venous system due
levels are extremely high (over 20-25 mg/dL),
to liver damage, commonly caused by cirrhosis but
which can lead to central nervous system
can occur in non-cirrhotic liver disease.
effects.
 Complications: Long-term mild jaundice can Key Features:
lead to pigment stones in the gallbladder.  Splenomegaly (enlarged spleen) with possible
hypersplenism (overactive spleen).
 Hepatocellular Jaundice
 Major complications include ascites (fluid buildup in
 Cause: Liver cell damage prevents proper
the abdomen) and varices (enlarged veins, often in
clearance of bilirubin from the blood. Common
the esophagus, which can bleed).
causes include hepatitis, viral infections,
alcohol abuse, and chemical toxins. Ascites
 Associated with: Cirrhosis (often due to  is the buildup of fluid in the abdomen, often due to
excessive alcohol intake or viral infections). liver problems.

, MS RLE

 Widening blood vessels in the digestive system  Sodium intake may be further reduced to 500
adds to fluid buildup. mg/day
 The liver’s inability to process aldosterone  Rarely used (not well tolerated by most
causes the kidneys to keep too much water and patients)
salt.  Diuretics may be prescribed
 Low albumin levels from liver damage make fluid
Pharmacologic Therapy
leak into the abdomen.
 Main Treatment
 Effect: The body keeps retaining more fluid, making
 Diuretics + low-sodium diet = works in 90% of
the problem worse.
patients
 Other Causes: Conditions like cancer, kidney
 First Choice Diuretic
disease, and heart failure can also cause ascites.
 Spironolactone
 Blocks aldosterone
 Helps keep potassium levels normal
 Best for ascites due to cirrhosis
 Furosemide
 May be added to spironolactone
 Use carefully — can cause low sodium
(hyponatremia) if used long-term
 Drugs to Avoid
 Ammonium chloride
 Acetazolamide
 These can trigger hepatic encephalopathy
(brain dysfunction)
 Safe Weight Loss (per day)
 With edema: Max 1 kg (2.2 lbs)
 Without edema: Max 0.5–0.75 kg(1.1–1.65 lbs)
 Fluid Restriction - Only if sodium levels are very low
 Possible Side Effects
Clinical Manifestations of Ascites
 Fluid and electrolyte problems:
 Increased abdominal size and rapid weight
gain.Shortness of breath and discomfort from the  Dehydration (hypovolemia)
enlarged abdomen.  Low potassium (hypokalemia)
 Visible striae (stretch marks) and distended veins on
 Low sodium (hyponatremia)
the abdomen.  Alkalosis (↑ blood pH)
 Umbilical hernias may occur, especially in patients
 Encephalopathy
 Caused by dehydration or low potassium
with cirrhosis.
 Fluid and electrolyte imbalances are common.
Low potassium → ↑ ammonia in blood → brain
problems
Assessment and Diagnostic Findings
 Physical Exam:
Paracentesis
 Procedure to remove ascitic fluid from the peritoneal
 Percussion of the abdomen is used to check
for fluid buildup. cavity
 Done through a puncture or small surgical incision in
 When the patient lies down, the flanks of the
abdomen may bulge, indicating fluid. the abdominal wall
 Performed under sterile conditions
 Shifting dullness or a fluid wave confirms the
 Not a routine treatment for ascites anymore
presence of fluid (a large amount is needed for
 Now mainly used for:
fluid wave).
 Monitoring:
 Diagnostic examination of ascitic fluid
 Regular measurement of abdominal girth and  Treatment of massive, resistant ascites causing
body weight helps track the progress of ascites serious problems
and response to treatment.  Preparation for: Diagnostic imaging, Peritoneal
 Medical Management Treatment Includes:
dialysis, Surgery
 Paracentesis gives only temporary relief
 Dietary changes.
 Medications. Ultrasound Guidance
 In patients at high risk for bleeding (abnormal
 Bed rest.
 Paracentesis (removal of fluid from the coagulation)
 In patients with previous abdominal surgery (risk of
abdomen).
 Shunts and other treatments as needed. adhesions)

Nutritional Therapy for Ascites Lab Tests on Ascitic Fluid
 Cell count
 Treatment Goal is to achieve negative sodium
 Albumin level
balance to reduce fluid retention.
 Total protein level
 Foods to Avoid
 Culture
 Table salt
 Other diagnostic tests as needed
 Salty foods/snacks
 Salted butter and margarine Large-Volume Paracentesis
 Canned and frozen foods (unless low-  Removal of 5–6 liters of fluid is considered safe
sodium/2g sodium labeled)  Effective treatment for severe ascites
 Adapting to Low-Sodium Diet, taste buds may take  Should be considered early, not just for patients who

2–3 months to adjust. fail diuretic therapy

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Geschreven in
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