View
44
Download
0
Category
Preview:
DESCRIPTION
Metabolic and Endocrine Function. Larry Santiago, MSN, RN. Assessment and Management of Patients With Hepatic Disorders. Assessment. Health History Exposure to hepatotoxins Alcohol and drug use Lifestyle behaviors Physical Examination Skin inspection Abdominal assessment Liver palpation. - PowerPoint PPT Presentation
Citation preview
Metabolic and Endocrine Function
Larry Santiago, MSN, RN
Assessment and Management of Patients With Hepatic
Disorders
Assessment
• Health History–Exposure to hepatotoxins–Alcohol and drug use–Lifestyle behaviors
• Physical Examination–Skin inspection–Abdominal assessment–Liver palpation
Diagnostic Evaluation
• Liver Function Tests – page 1079• Liver Biopsy-removal of a small amount of liver tissue through needle aspiration
Diagnostic Evaluation 2
–Ultrasonography
–Computed
Tomography
Diagnostic Evaluation 3
- Magnetic resonance imaging (MRI)
- Laparoscopy
Hepatic Dysfunction
• Jaundice- hemolytic, hepatocellular, obstructive, and hereditary hyperbilirubinemia
Hepatic Dysfunction 2
• Portal Hypertension
• Ascites
Ascites
• Pathophysiology
• Clinical manifestations
Ascites 2
• Medical/Nursing management
- Dietary Modification – strict sodium restriction
- Diuretics
Ascites 3
- Bed Rest
- Paracentesis
Esophageal Varices
• - dilated, tortuous veins found in the submucosa of the esophagus or even the stomach
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
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
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
Hepatitis A
• Mode of transmission
- fecal/oral
Signs & Symptoms:
Headache, malaise,
fatigue, later on dark
urine, jaundice, tender
liver
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
Hepatitis B 2
• Active Immunization: Hepatitis B Vaccine
• Passive Immunity: Hepatitis B Immune Globulin
Hepatitis B 3
• Medical/Nursing management
- Antiviral agents – Epvir and Hepsera
- Bed rest, activity restriction
- Adequate nutrition
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
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
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
Management of Patients With Nonviral Hepatic Disorders
• Toxic Hepatitis
- Exposure to
hepatotoxic chemicals or meds
- Symptoms include vomiting, abnormal clotting, delirium, coma, seizures, death
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
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
Hepatic Cirrhosis 3
• Clinical manifestations- Hepatomegaly- Portal Obstruction and Ascites- Infection and Peritonitis- Gastrointestinal varices- Edema- Vitamin deficiency and anemia- Mental deterioration
Hepatic Cirrhosis 4
• Assessment and Diagnostic Findings
• Medical Management
Assessment and Management of Patients With Biliary Disorders
Diseases of the Gallbladder
• Cholecystitis- acute inflammation, calculous cholecystitis
• Cholelithiasis-
gallstones
Cholelithiasis
• Medical Management- lithotripsy, UDCA and CDCA, MTBE, ERCP
• ERCP
Cholelithiasis 2
• Surgical Management- cholecystectomy
Cholelithiasis 3
• Nursing Management- relieve pain, promote biliary drainage, improve nutritional status
Diseases of the Pancreas
• Acute Pancreatitis- mild, self- limiting to fatal, self-digestion of pancreas by proteolytic enzymes
Acute Pancreatitis
Gerontologic considerations – mortality increases with advancing age
Acute Pancreatitis 2
• Pathophysiology
- Caused by self-digestion of the pancreas
- Long-term use of alcohol is commonly associated
- Mortality rate is high (10%)
Acute Pancreatitis 3
• Clinical Manifestations
- Severe abdominal pain
- Nausea/vomiting
- Hypotension
- Respiratory distress
- Tachycardia
- Cyanosis
Acute Pancreatitis 4
• Medical Management directed at relief of symptoms, prevention and treatment of complications, and managing exocrine and endocrine insufficiency of pancreatitis
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
Chronic Pancreatitis 2
• Clinical Manifestations
- Recurring attacks of severe abdominal and back pain
- Vomiting
- Opioids often do not provide relief
- Weight loss
- Steatorrhea
Chronic Pancreatitis 3
• Medical Management
- Pain management
- Diabetes Mellitus
- Pancreatico-
jejunostomy
• Assessment and Management of Patients With Diabetes Mellitus
Diabetes Mellitus
• Type 1- destruction of pancreatic beta cells
- Combined genetic, immunologic, and environmental factors contribute to beta cell destruction
Diabetes Mellitus 2
• Type 2- insulin resistance and impaired insulin secretion
Diabetes Mellitus 2
• Gestational Diabetes- glucose intolerance with onset during pregnancy
Assessment and Diagnostic Findings
• 3 P’s- polyuria, polydipsia, polyphagia
Assessment and Diagnostic Findings 2
• Fasting Plasma Glucose > 126 mg/dL
• Random Plasma Glucose > 200 mg/dL
• 2-hour Postload Glucose > 200 mg/dL
Diabetes Management
Diabetes Management
• Complications- retinopathy, nephropathy, and neuropathy
Diabetes Management 2
• Hypoglycemia
Nutrition
• Nutrition, diet, and weight control are the foundation of diabetes management
• Meal Planning and Related Teaching
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
Caloric Distribution
• Carbohydrates
• Fats
• Fiber
Exercise
• Benefits
• Exercise precautions
• Exercise recommendations
• Gerontologic considerations
Monitoring Glucose Levels
Glycosated Hemoglobin – HgbA1c
- Reflects average blood glucose levels over 2-3 months
Pharmacologic Therapy
• Insulin Therapy and Insulin Preparations
- Grouped into several categories based on the onset, peak,
and duration of action
Categories of Insulin
• Rapid actingAgent – Lispro (Humalog) - Aspart (Novolog)Onset – 10-15minPeak – 1 hour - 40-50min (Aspart)Duration – 3 hours - 4-6 hours (Aspart)
Categories of Insulin 2
• Short-acting
• Agent – Regular (Humalog R, Novolin R)
• Onset – ½ - 1 hour
• Peak – 2-3 hours
• Duration – 4-6 hours
Categories of Insulin 3
• Intermediate-acting
- NPH
- Humulin N, Novolin N
Onset – 3-4 hours
Peak – 6-12 hours
Duration – 16-20 hours
Categories of Insulin 4
• Long-acting
• Agent
- Ultralente
Onset – 6-8 hours
Peak – 12-16 hours
Duration – 20-30 hours
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
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
Insulin Regimens 2
• Intensive Regimen
- Keeps blood glucose
Levels as close to normal
as possible
Example – Insulin Sliding
Scale
Complications of Insulin Therapy
• Complications- allergic reactions, lipodystrophy, resistance, hyperglycemia
Methods of DeliveryInsulin pens –
Jet injectors –
Insulin pumps -
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
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
Oral Antidiabetic Agents 3
• Meglitinides
- Lowers blood glucose level by stimulating insulin release from the pancreatic beta cells
- Principal side effect is hypoglycemia
Nursing Management
• Diabetic Teaching Plan
- Self-Administration of Insulin
Storing Insulin
Selecting Syringes
Nursing Management 2
• Preparing the Injection: Mixing Insulins
• Selecting and Rotating the Injection Site
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
Hypoglycemia 2
• Severe hypoglycemia
Clinical manifestations – disoriented behavior, seizures, difficulty arousing from sleep, loss of consciousness
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
Emergency Measures
• Patients who are unconscious or cannot swallow
- 25-50 mL 50% Dextrose in Water (D50W) administered IV
- Effect usually seen within minutes
Diabetic Ketoacidosis• 3 Main Features:
1) Hyperglycemia
2) Dehydration and
electrolyte loss
3) Acidosis
Pathophysiology
• 3 Main Causes
- Decreased or missed dose of insulin
- Illness or infection
- Undiagnosed and
untreated diabetes
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
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
Diabetic Ketoacidosis 4
• Medical/Nursing management
- Rehydration
- Restoring Electrolytes
- Reversing Acidosis
- Monitor EKG
- Patient Teaching
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
HHMS 2
• Clinical manifestations
- Hypotension, profound dehydration, tachycardia, variable neurologic signs (coma, seizures, hemiparesis)
- Mortality rate – 10-40%
HHMS 3
• Assessment and Diagnostic Findings
- Blood glucose level 600-1200 mg/dL
- Electrolyte levels consistent with dehydration
- Mental status changes
- Hallucinations
- Postural hypotension
HHMS 4
• Medical Management
- Fluid replacement
- Correction of electrolyte imbalances
- Insulin administration
Long-Term Complications
• Macrovascular Complications- MI, CAD, Stroke
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)
Long-Term Complications 3
• Retinopathy – Deterioration of small blood vessels that nourish the retina
Long Term Complications 4
• Cataracts – Opacity of the lens of the eye; cataracts occur at an earlier age in diabetics
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
Nephropathy
• 20-30% of people with Type 1 or Type 2 diabetes develop nephropathy
Nephropathy 2
• Assessment and diagostic findings
- Urine dipstick test consistently positive for significant amounts of albumin
- Serum creatinine and BUN
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
Diabetic Neuropathy
• Peripheral
- Symptoms include paresthesias and burning sensations
- Decreased pain and temperature sensation
- Foot deformities
- Lower extremity pain
Peripheral Neuropathy
• Management
- Intensive insulin therapy and good blood glucose control delays onset and slows progression
- Pain management
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
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
• Assessment and Management of Patients With Endocrine Disorders
Pituitary Disorders
• Diabetes Insipidus- deficiency of antidiuretic hormone
- Clinical Manifestations –
Enormous daily output of
very dilute urine
Spec Grav 1.001-1.005
Diabetes Insipidus
• Medical Management
- To replace ADH
- Ensure adequate fluid replacement
- Identify and correct the underlying intracranial pathology
Diabetes Insipidus 2
• Pharmacologic Therapy
- DDAVP – synthetic
vasopresin without the
Vascular effects of natural
ADH
- Intranasal
- IM ADH
Syndrome of Inappropriate Antidiuretic Hormone Secretion
SIADH – excessive growth hormone secretion from the pituitary gland
- Important to eliminate the underlying cause – example: lung CA
Thyroid Disorders
HypothyroidismMyxedema – advancedthyroid deficiencyHashimoto’s Disease –AKA autoimmune thyroiditis is the most common cause of
hypothyroidism
Hypothyroidism
• Pathophysiology
- >95% have primary or thyroidal hypothyroidism, which refers to dysfunction of the
thyroid gland itself
Hypothyroidism 2
• Clinical Manifestations
- Extreme fatigue
- Hair loss, brittle nails, dry skin
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
Hypothyroidism 4
• Medical Management- Pharmacologic TherapySynthroid or Levothroid- Prevention of Medication Interactions- Gerontologic Considerations- Modifying Activity- Monitoring Physical Status- Promoting Physical Comfort
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
Hyperthyroidism 2
• Clinical manifestations
- Nervousness
- Palpitations
- Poor heat tolerance, diaphoresis
- Elderly – dry skin and pruritis
- Exophthalmos
- Increased appetite
Hyperthyroidism 4
• Diagnostic Findings – increase in serum T4
• Medical Management
- Pharmacologic therapy –
Use of irradiation by
administration of the
radioisotope 123I
Hyperthyoidism 5
• Antithyroid medications
- Propacil or Tapazole
- Blocks the utilization of iodine
by interfering with the
Iodothyrosines in the synthesis of thyroid
hormones
Thyroid Storm
• Form of severe hyperthyroidism
• Almost always fatal without treatment
• Critically ill and requires astute observation and aggressive care
Thyroid Storm 2
• Clinical Manifestations
- High fever (above 101.3F)
- Extreme tachycardia (>130)
- Exaggerated hyperthryoid sx
- Delirium psychosis, coma
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
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
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
Nodular Goiter
• Areas of hyperplasia
• Nodules can descend into the thorax and cause local pressure symptoms
• Can become malignant
Thyroid Cancer
• Assessment and
Diagnostic Findings
- Lesions that are single,
hard, fixed on palpation
- Diagnose with needle
biopsy, MRI, CT,
Thyroid scan
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
Nursing Management
• Preoperative Care
- Diet high in carbohydrates and proteins
- Demonstrate raising the elbows and placing the hands behind the neck to provide support
Nursing Management 2
• Postoperative Care
- Assess surgical dsg and reinforce PRN
- Monitor for respiratory distress
- Pain management
- IV fluids
- Discourage talking
- OOB same day
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
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
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
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
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
Hyperparathyroidism 4
• Medical Management
- Hydration Therapy
- Mobility
- Diet and Medications
- Important to follow up to ensure return of calcium levels to normal
Hypoparathyroidism
• occurs frequently with thryoidectomy or radical
neck dissection
• Caused by a deficiency of parathormone that results in elevated blood phosphate
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
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
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
Nursing Management
• Post-op thyroidectomy care
• Keep Calcium gluconate at bedside
• Watch for potentially fatal dysrhythmias
• Teach about high calcium and low phosphate intake
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
Addison’s disease
• Clinical manifestations
- Characterized by muscle weakness, anorexia, GI symptoms, fatigue, emaciation, dark pigmentation, hypotension, hypoglycemia,
hyponatremia,
hyperkalemia
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
Addison’s disease 2
• Diagnostic findings
- Low levels of adrenocortical hormones in the blood or urine
- Decreased cortisol levels
Addison’s disease 3 – Medical managment
• Combating circulatory shock:
- Restoring blood circulation
- Administering fluids and corticosteroids
- IV Hydrocortisone
Nursing Management
• Assessing the patient
• Monitoring and Managing Addisonian Crisis
• Restoring Fluid Balance
• Improving Activity Tolerance
Cushing’s Syndrome
• Results from excessive adrenocortical activity
• Commonly caused by use of corticosteroid medications
• Also caused by overproduction of endogenous corticosteroids
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
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
Recommended