Metabolic and Endocrine Function
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Transcript of Metabolic and Endocrine Function
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Metabolic and Endocrine Function
Larry Santiago, MSN, RN
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Assessment and Management of Patients With Hepatic
Disorders
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Assessment
• Health History–Exposure to hepatotoxins–Alcohol and drug use–Lifestyle behaviors
• Physical Examination–Skin inspection–Abdominal assessment–Liver palpation
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Diagnostic Evaluation
• Liver Function Tests – page 1079• Liver Biopsy-removal of a small amount of liver tissue through needle aspiration
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Diagnostic Evaluation 2
–Ultrasonography
–Computed
Tomography
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Diagnostic Evaluation 3
- Magnetic resonance imaging (MRI)
- Laparoscopy
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Hepatic Dysfunction
• Jaundice- hemolytic, hepatocellular, obstructive, and hereditary hyperbilirubinemia
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Hepatic Dysfunction 2
• Portal Hypertension
• Ascites
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Ascites
• Pathophysiology
• Clinical manifestations
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Ascites 2
• Medical/Nursing management
- Dietary Modification – strict sodium restriction
- Diuretics
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Ascites 3
- Bed Rest
- Paracentesis
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Esophageal Varices
• - dilated, tortuous veins found in the submucosa of the esophagus or even the stomach
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Hepatic Encephalopathy and Coma
• Results from accumulation of ammonia and other toxic metabolites in the blood
• Hepatic coma represents most advanced stage of hepatic encephalopathy
• Clinical manifestations include: mental changes, motor disturbances, asterixis and constructional apraxia
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Hepatic Encephalopathy
- RN is responsible for maintaining a safe environment to prevent injury, bleeding, and infection
- Assess neuro status frequently
- Strict I & O
- Assess for symptoms of infection
- Monitor serum ammonia level and electrolytes
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Management of Patients With Viral Hepatic Disorders
• Viral Hepatitis
- Systemic viral infection in which necrosis and inflammation of the liver cells produce a cluster of changes
- Includes Hepatitis A,B,C,D, and E
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Hepatitis A
• Mode of transmission
- fecal/oral
Signs & Symptoms:
Headache, malaise,
fatigue, later on dark
urine, jaundice, tender
liver
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Hepatitis B
• Mode of transmission:
- sex, either by intercourse
or oral contact
- Perinatal tranmission
- Health care personnel
- Long incubation period (70-80 days)
- Signs/symptoms insidious and variable
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Hepatitis B 2
• Active Immunization: Hepatitis B Vaccine
• Passive Immunity: Hepatitis B Immune Globulin
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Hepatitis B 3
• Medical/Nursing management
- Antiviral agents – Epvir and Hepsera
- Bed rest, activity restriction
- Adequate nutrition
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Hepatitis C
• Mode of transmission:- Blood transfusion- Risk increased with STDSigns and Symptoms:Similar to HBV, but less severe and anicteric- Increased risk of chronic liver disease and
hepatic cancer- Hepatitis G risk factors similar to HCV
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Hepatitis D
• Mode of transmission:
- same as HBV
Signs and Symptoms:
Similar to HBV
Outcome:
Greater likelihood of carrier state, chronic active hepatitis, and cirrhosis
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Hepatitis E
Mode of transmission:Fecal-oralSigns and Symptoms:Similar to HAVVery severe in PG womenOutcome:Similar to HAV except very severe in PG
women
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Management of Patients With Nonviral Hepatic Disorders
• Toxic Hepatitis
- Exposure to
hepatotoxic chemicals or meds
- Symptoms include vomiting, abnormal clotting, delirium, coma, seizures, death
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Hepatic Cirrhosis
• Types of cirrhosis:
- Alcoholic cirrhosis – most common
- Postnecrotic cirrhosis – broad bands of scar tissue from previous acute viral hepatitis
- Biliary cirrhosis – result of chronic biliary obstruction and infection – much less common
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Hepatic Cirrhosis 2
• Pathophysiology
- Alcohol consumption major
causative factor
- Characterized by episodes
of necrosis involving the liver cells
- Destroyed liver cells are replaced by scar tissue
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Hepatic Cirrhosis 3
• Clinical manifestations- Hepatomegaly- Portal Obstruction and Ascites- Infection and Peritonitis- Gastrointestinal varices- Edema- Vitamin deficiency and anemia- Mental deterioration
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Hepatic Cirrhosis 4
• Assessment and Diagnostic Findings
• Medical Management
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Assessment and Management of Patients With Biliary Disorders
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Diseases of the Gallbladder
• Cholecystitis- acute inflammation, calculous cholecystitis
• Cholelithiasis-
gallstones
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Cholelithiasis
• Medical Management- lithotripsy, UDCA and CDCA, MTBE, ERCP
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• ERCP
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Cholelithiasis 2
• Surgical Management- cholecystectomy
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Cholelithiasis 3
• Nursing Management- relieve pain, promote biliary drainage, improve nutritional status
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Diseases of the Pancreas
• Acute Pancreatitis- mild, self- limiting to fatal, self-digestion of pancreas by proteolytic enzymes
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Acute Pancreatitis
Gerontologic considerations – mortality increases with advancing age
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Acute Pancreatitis 2
• Pathophysiology
- Caused by self-digestion of the pancreas
- Long-term use of alcohol is commonly associated
- Mortality rate is high (10%)
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Acute Pancreatitis 3
• Clinical Manifestations
- Severe abdominal pain
- Nausea/vomiting
- Hypotension
- Respiratory distress
- Tachycardia
- Cyanosis
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Acute Pancreatitis 4
• Medical Management directed at relief of symptoms, prevention and treatment of complications, and managing exocrine and endocrine insufficiency of pancreatitis
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Chronic Pancreatitis
- Characterized by progressive anatomic and functional destruction of the pancreas
- End result is mechanical obstruction of the pancreatic and common bile ducts and the duodenum
- Major causes are alcoholism and malnutrition
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Chronic Pancreatitis 2
• Clinical Manifestations
- Recurring attacks of severe abdominal and back pain
- Vomiting
- Opioids often do not provide relief
- Weight loss
- Steatorrhea
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Chronic Pancreatitis 3
• Medical Management
- Pain management
- Diabetes Mellitus
- Pancreatico-
jejunostomy
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• Assessment and Management of Patients With Diabetes Mellitus
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Diabetes Mellitus
• Type 1- destruction of pancreatic beta cells
- Combined genetic, immunologic, and environmental factors contribute to beta cell destruction
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Diabetes Mellitus 2
• Type 2- insulin resistance and impaired insulin secretion
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Diabetes Mellitus 2
• Gestational Diabetes- glucose intolerance with onset during pregnancy
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Assessment and Diagnostic Findings
• 3 P’s- polyuria, polydipsia, polyphagia
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Assessment and Diagnostic Findings 2
• Fasting Plasma Glucose > 126 mg/dL
• Random Plasma Glucose > 200 mg/dL
• 2-hour Postload Glucose > 200 mg/dL
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Diabetes Management
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Diabetes Management
• Complications- retinopathy, nephropathy, and neuropathy
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Diabetes Management 2
• Hypoglycemia
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Nutrition
• Nutrition, diet, and weight control are the foundation of diabetes management
• Meal Planning and Related Teaching
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Meal Planning• Caloric Requirements- To promote a 1-2 lb.
weight loss per week, 500
to 1,000 calories are
subtracted from the daily
total
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Caloric Distribution
• Carbohydrates
• Fats
• Fiber
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Exercise
• Benefits
• Exercise precautions
• Exercise recommendations
• Gerontologic considerations
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Monitoring Glucose Levels
Glycosated Hemoglobin – HgbA1c
- Reflects average blood glucose levels over 2-3 months
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Pharmacologic Therapy
• Insulin Therapy and Insulin Preparations
- Grouped into several categories based on the onset, peak,
and duration of action
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Categories of Insulin
• Rapid actingAgent – Lispro (Humalog) - Aspart (Novolog)Onset – 10-15minPeak – 1 hour - 40-50min (Aspart)Duration – 3 hours - 4-6 hours (Aspart)
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Categories of Insulin 2
• Short-acting
• Agent – Regular (Humalog R, Novolin R)
• Onset – ½ - 1 hour
• Peak – 2-3 hours
• Duration – 4-6 hours
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Categories of Insulin 3
• Intermediate-acting
- NPH
- Humulin N, Novolin N
Onset – 3-4 hours
Peak – 6-12 hours
Duration – 16-20 hours
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Categories of Insulin 4
• Long-acting
• Agent
- Ultralente
Onset – 6-8 hours
Peak – 12-16 hours
Duration – 20-30 hours
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Categories of Insulin 5
• Very long-acting
Agent – Lantus
Onset – 1 hour
Peak – Continuous
Duration – 24 hours
Indications – Used primarily to control fasting glucose level
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Insulin Regimens• Conventional Regimen- One or more injections of a
mixture of short and intermediate acting insulins per day
- Patients may have blood glucose levels well above normal
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Insulin Regimens 2
• Intensive Regimen
- Keeps blood glucose
Levels as close to normal
as possible
Example – Insulin Sliding
Scale
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Complications of Insulin Therapy
• Complications- allergic reactions, lipodystrophy, resistance, hyperglycemia
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Methods of DeliveryInsulin pens –
Jet injectors –
Insulin pumps -
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Oral Antidiabetic Agents1) Sulfonylureas
- Directly stimulate the pancreas to secrete insulin
- Side effects – GI symptoms and dermatologic reactions
2) Biguanides
- Facilitates insulin’s action on
peripheral receptor sites
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Oral Antidiabetic Agents 2
• Thiazolidinediones
- Enhance insulin action at the receptor site
without increasing insulin secretion from the beta cells of the pancreas
- May affect liver function
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Oral Antidiabetic Agents 3
• Meglitinides
- Lowers blood glucose level by stimulating insulin release from the pancreatic beta cells
- Principal side effect is hypoglycemia
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Nursing Management
• Diabetic Teaching Plan
- Self-Administration of Insulin
Storing Insulin
Selecting Syringes
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Nursing Management 2
• Preparing the Injection: Mixing Insulins
• Selecting and Rotating the Injection Site
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Acute Complications• HypoglyemiaClinical Manifestations- Mild hypoglycemia – sweating, tremor,
tachycardia, palpitations, nervousness, hunger
- Moderate – inability to concentrate, headache, lightheadedness, confusion, memory lapses, numbness of lips and tonuge
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Hypoglycemia 2
• Severe hypoglycemia
Clinical manifestations – disoriented behavior, seizures, difficulty arousing from sleep, loss of consciousness
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Management of Hypoglycemia
3-4 commercially prepared glucose tablets
4-6 oz. of fruit juice or regular soda
6-10 Life Savers or other hard candies
2-3 teaspoons of sugar or honey
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Emergency Measures
• Patients who are unconscious or cannot swallow
- 25-50 mL 50% Dextrose in Water (D50W) administered IV
- Effect usually seen within minutes
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Diabetic Ketoacidosis• 3 Main Features:
1) Hyperglycemia
2) Dehydration and
electrolyte loss
3) Acidosis
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Pathophysiology
• 3 Main Causes
- Decreased or missed dose of insulin
- Illness or infection
- Undiagnosed and
untreated diabetes
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Diabetic Ketoacidosis 2
• Clinical manifestations – Polyuria, polydipsia, blurred vision, headache, anorexia, nausea, vomiting, abdominal pain, acetone or “fruity” breath, hyperventilation (Kussmaul respirations)
• Diagnostic Findings
Blood glucose levels vary from 300-800 mg/dL
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Diabetic Ketoacidosis 3
• Prevention
- Patients must be taught “sick day” rules:
Do not eleminate insulin when nausea/vomiting occurs
If patients cannot take fluids without
vomiting, the MD must be
notified
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Diabetic Ketoacidosis 4
• Medical/Nursing management
- Rehydration
- Restoring Electrolytes
- Reversing Acidosis
- Monitor EKG
- Patient Teaching
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HHMS
• Hyperglycemic Hyperosmolar Nonketotic Syndrome
- Serious condition with alterations of the sensorium
- Ketosis is minimal or absent
- Occurs most often in older people with no history of DM or mild Type 2 DM
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HHMS 2
• Clinical manifestations
- Hypotension, profound dehydration, tachycardia, variable neurologic signs (coma, seizures, hemiparesis)
- Mortality rate – 10-40%
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HHMS 3
• Assessment and Diagnostic Findings
- Blood glucose level 600-1200 mg/dL
- Electrolyte levels consistent with dehydration
- Mental status changes
- Hallucinations
- Postural hypotension
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HHMS 4
• Medical Management
- Fluid replacement
- Correction of electrolyte imbalances
- Insulin administration
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Long-Term Complications
• Macrovascular Complications- MI, CAD, Stroke
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Long-Term Complications 2
• Microvascular Complications and Diabetic Retinopathy
- Leading cause of blindness between 20-74 years old
- Most diabetics have some degree of retinopathy after 20 years (especially Type 1 diabetics)
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Long-Term Complications 3
• Retinopathy – Deterioration of small blood vessels that nourish the retina
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Long Term Complications 4
• Cataracts – Opacity of the lens of the eye; cataracts occur at an earlier age in diabetics
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Long Term Complications 5
• Glaucoma
- Results from occlusion of the outflow channels by new blood vessels. May occur with slightly higher frequency in the diabetic population
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Nephropathy
• 20-30% of people with Type 1 or Type 2 diabetes develop nephropathy
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Nephropathy 2
• Assessment and diagostic findings
- Urine dipstick test consistently positive for significant amounts of albumin
- Serum creatinine and BUN
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Nephropathy 3
• Medical Management
- Control of Hypertension
- Prevention or vigorous treatment of UTI
- Avoidance of nephrotoxic substances
- Adjustment of meds as renal function changes
- Low sodium, low protein diet
![Page 102: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/102.jpg)
Diabetic Neuropathy
• Peripheral
- Symptoms include paresthesias and burning sensations
- Decreased pain and temperature sensation
- Foot deformities
- Lower extremity pain
![Page 103: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/103.jpg)
Peripheral Neuropathy
• Management
- Intensive insulin therapy and good blood glucose control delays onset and slows progression
- Pain management
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Autonomic Neuropathy
• Hypoglycemic Unawareness
- Autonomic neuropathy of the adrenal medulla is responsible for diminished symptoms of hypoglycemia
• Sexual Dysfunction
- Impotence occurs with greater
frequency in diabetic men
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Foot and Leg Problems
• Neuropathy – Increased dryness and fissuring of the skin
• Peripheral Vascular Disease –
Poor circulation of the lower
extremities contributes to poor
wound healing/gangrene
• Immunocompromise – Impaired ability of leukocytes to destroy bacteria
![Page 106: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/106.jpg)
• Assessment and Management of Patients With Endocrine Disorders
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Pituitary Disorders
• Diabetes Insipidus- deficiency of antidiuretic hormone
- Clinical Manifestations –
Enormous daily output of
very dilute urine
Spec Grav 1.001-1.005
![Page 110: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/110.jpg)
Diabetes Insipidus
• Medical Management
- To replace ADH
- Ensure adequate fluid replacement
- Identify and correct the underlying intracranial pathology
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Diabetes Insipidus 2
• Pharmacologic Therapy
- DDAVP – synthetic
vasopresin without the
Vascular effects of natural
ADH
- Intranasal
- IM ADH
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Syndrome of Inappropriate Antidiuretic Hormone Secretion
SIADH – excessive growth hormone secretion from the pituitary gland
- Important to eliminate the underlying cause – example: lung CA
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Thyroid Disorders
HypothyroidismMyxedema – advancedthyroid deficiencyHashimoto’s Disease –AKA autoimmune thyroiditis is the most common cause of
hypothyroidism
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Hypothyroidism
• Pathophysiology
- >95% have primary or thyroidal hypothyroidism, which refers to dysfunction of the
thyroid gland itself
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Hypothyroidism 2
• Clinical Manifestations
- Extreme fatigue
- Hair loss, brittle nails, dry skin
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Hypothyroidism 3
• Affects women five times more frequently then men, occurs most often between 30-60 years old
• Low temperature and
pulse rate
- Weight gain, thickened
skin, personality changes
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Hypothyroidism 4
• Medical Management- Pharmacologic TherapySynthroid or Levothroid- Prevention of Medication Interactions- Gerontologic Considerations- Modifying Activity- Monitoring Physical Status- Promoting Physical Comfort
![Page 118: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/118.jpg)
Hyperthyroidism
• Second most common endocrine disorder after DM
Grave’s disease - most common type
- Results from an excessive output of thyroid hormones caused by abnormal stimulation of the thyroid gland
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Hyperthyroidism 2
• Clinical manifestations
- Nervousness
- Palpitations
- Poor heat tolerance, diaphoresis
- Elderly – dry skin and pruritis
- Exophthalmos
- Increased appetite
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Hyperthyroidism 4
• Diagnostic Findings – increase in serum T4
• Medical Management
- Pharmacologic therapy –
Use of irradiation by
administration of the
radioisotope 123I
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Hyperthyoidism 5
• Antithyroid medications
- Propacil or Tapazole
- Blocks the utilization of iodine
by interfering with the
Iodothyrosines in the synthesis of thyroid
hormones
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Thyroid Storm
• Form of severe hyperthyroidism
• Almost always fatal without treatment
• Critically ill and requires astute observation and aggressive care
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Thyroid Storm 2
• Clinical Manifestations
- High fever (above 101.3F)
- Extreme tachycardia (>130)
- Exaggerated hyperthryoid sx
- Delirium psychosis, coma
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Thyroid Storm 3
• Management- Hypothermia mattress or blanket- Humidified oxygen- IV fluids- PTU or methimazole- Hydrocortizone – treat shock/adrenal
insuffciency- Iodine – decrease output of T4 from the thyroid
gland
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Hyperthyroidism 6
• Surgical Management
- Reserved for special circumstances
Examples – PG with allergy to antithyroid meds, large goiters
- Subtotal thyroidectomy –
Removal of 5/6 of thyroid
tissue
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Thyroid Tumors
Endemic Goiter
- Most common type of goiter
- Encountered where natural
iodine supply is deficient
- Represents a compensatory hypertrophy of the thyroid gland
- Recedes after iodine imbalance is corrected
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Nodular Goiter
• Areas of hyperplasia
• Nodules can descend into the thorax and cause local pressure symptoms
• Can become malignant
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Thyroid Cancer
• Assessment and
Diagnostic Findings
- Lesions that are single,
hard, fixed on palpation
- Diagnose with needle
biopsy, MRI, CT,
Thyroid scan
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Thyroid Cancer 2
• Surgical Management- Total or near-total thyroidectomy- Thyroid hormone administered in suppressive doses after surgery- Radiation – oral administration of radioactive
iodine, external administration of radiation therapy
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Nursing Management
• Preoperative Care
- Diet high in carbohydrates and proteins
- Demonstrate raising the elbows and placing the hands behind the neck to provide support
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Nursing Management 2
• Postoperative Care
- Assess surgical dsg and reinforce PRN
- Monitor for respiratory distress
- Pain management
- IV fluids
- Discourage talking
- OOB same day
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Parathyroid Disorders
• Parathyroid Function
- Regulates Calcium and
Phosphorus metabolism
- Increased secretion of parathormone results in increased calcium absorption from kidney, intestine, and bones
- Excess parathormone can result in elevated levels of serum calcium
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Hyperparathyroidism
• Caused by overproduction of parathyroid hormone by the parathyroid glands
• Occurs 2-4 times more often in women, common between 60-70 year old
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Hyperparathyroidism 2
• Clinical Manifestations
- May be asymptomatic
- Fatigue, muscle
weakness, nausea,
constipation cardiac dysrythmias – related to hypercalcemia
- Skeletal pain and tenderness, esp. back and joints; pathologic fx or deformities
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Hyperparathyroidism 3
• Assessment and Diagnostic Findings
- Diagnosed by persistent elevation of serum calcium levels and elevated parathormone level
- Double antibody parathyroid hormone test
- Ultrasound, MRI, thallium scan, fine-needle biopsy
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Hypercalcemic Crisis
• Serum calcium greater than 15 mg/dL
• Life-threatening! – neurologic,
cardiovascular, renal symptoms
Treatment: rehydration with
large amt. of IV fluids, diuretics
to excrete calcium, phosphate
supplements
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Hyperparathyroidism 4
• Medical Management
- Hydration Therapy
- Mobility
- Diet and Medications
- Important to follow up to ensure return of calcium levels to normal
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Hypoparathyroidism
• occurs frequently with thryoidectomy or radical
neck dissection
• Caused by a deficiency of parathormone that results in elevated blood phosphate
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Hypoparathyroidism 2
• Clinical manifestations- Chief symptom – TETANY(tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movements)- Broncho or laryngeal spasm, carpopedal spasm,
dysphagia, photophobia, dysrhythmias, seizures
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Hypoparathyroidism 3
• Assessment and Diagnostic Findings
- Tetany develops at calcium levels of 5-6 mg/dL
Trousseau’s sign – carpal spasms Chvostek’s sign – cheek twitching
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Hypoparathyroidism 4
• Medical Management
- Goal of therapy to raise serum calcium level to 9-10 mg/dL
- IV Calcium gluconate
- IV Parathormone
(high incidence of allergies)
- Environment free of noise, drafts, bright lights, or sudden movement
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Nursing Management
• Post-op thyroidectomy care
• Keep Calcium gluconate at bedside
• Watch for potentially fatal dysrhythmias
• Teach about high calcium and low phosphate intake
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Adrenal Disorders
• Addison’s disease AKA adrenocortical insufficiency
- Adrenal cortex function is inadequate to meet patient’s need for cortical hormones
- 80% of cases caused by autoimmunity or idiopathic
![Page 145: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/145.jpg)
Addison’s disease
• Clinical manifestations
- Characterized by muscle weakness, anorexia, GI symptoms, fatigue, emaciation, dark pigmentation, hypotension, hypoglycemia,
hyponatremia,
hyperkalemia
![Page 146: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/146.jpg)
Addisonian crisis
- Characterized by cyanosis and classic signs of circulatory shock:
Pallor, apprehension, rapid and weak pulse, rapid respirations, low BP, headache, nausea, abd pain, diarrhea
- Complication of Addison’s
disease
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Addison’s disease 2
• Diagnostic findings
- Low levels of adrenocortical hormones in the blood or urine
- Decreased cortisol levels
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Addison’s disease 3 – Medical managment
• Combating circulatory shock:
- Restoring blood circulation
- Administering fluids and corticosteroids
- IV Hydrocortisone
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Nursing Management
• Assessing the patient
• Monitoring and Managing Addisonian Crisis
• Restoring Fluid Balance
• Improving Activity Tolerance
![Page 150: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/150.jpg)
Cushing’s Syndrome
• Results from excessive adrenocortical activity
• Commonly caused by use of corticosteroid medications
• Also caused by overproduction of endogenous corticosteroids
![Page 151: Metabolic and Endocrine Function](https://reader036.fdocuments.in/reader036/viewer/2022062410/5681553b550346895dc31176/html5/thumbnails/151.jpg)
Clinical Manifestations
• Central-type obesity, with a fatty “buffalo hump” neck and supraclavicular areas, heavy trunk, and relatively thin extremities
• Skin is thin, fragile and easily traumatized• Ecchymosis and striae develop• Muscle wasting, osteoporosis• Moon faced appearance• Women 20-40 years are 5x more likely than men to get Cushing’s
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Medical Management
• If cause is pituitary tumors, surgical removal by transsphenoidal hypophysectomy
• Symptoms of adrenal insufficiency may begin 12-48 hours after surgery
• Hydrocortisone for temporary replacement
• Reduce or taper corticosteroids to the minimum dosage need to treat the disease