Metabolic and Endocrine Function Larry Santiago, MSN, RN

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