THE ENDOCRINE

SYSTEM & ITS

DISTURBANCES

PREPARED BY: MARJORIE C. CABUAL, RN, MN

 PITUITARY GLAND
• ANTERIOR PITITUARY GLAND
– TSH, ACTH, LH, FSH, MSH
– GROWTH HORMONE, PROLACTIN

• POSTERIOR PITUITARY GLAND

– ADH OR VASOPRESSIN
– OXYTOCIN
 THYROID GLAND

– THYROXINE (T4)
– TRIIODOTHYRONINE (T3)
– THYROCALCITONIN
 PARATHROID GLAND
• PARATHYROID HORMONE (PTH) OR
PARATHORMONE
– Regulates calcium and phosphorus blood levels
– Increases intestinal absorption of calcium
 PANCREAS
• ALPHA CELLS
– GLUCAGON

• BETA CELLS
– INSULIN

• DELTA CELLS
– SOMATOSTATIN

• F CELLS
– PANCREATIC POLYPEPTIDE
 ADRENAL GLANDS
• ADRENAL CORTEX
– GLUCOCORTICOIDS e.g. Cortisol
– MINERALOCORTICOIDS e.g. Aldosterone
– SEX HORMONES or ANDROGENS e.g.
Testosterone and Estrogen

• ADRENAL MEDULLA
– EPINEPRINE (Adrenaline)
– NOREPINEPHRINE
 Gonads
• OVARIES
– Estrogen
– Progesterone
• TESTES
– Testosterone
Assessment of the Endocrine System
 Health history
• Subjective data
– Past health history
– Diet history
– Medications
– Surgery or treatments
– Functional health patterns (Gordon’s)
• Objective data
– V/S
– Height and weight
– Mental-emotional status
– Head-to-toe physical examination
 Lab/Diagnostic studies
• Serum studies
• Radiologic studies
• Urine studies
DIABETES MELLITUS

A chronic disease of absolute or relative

insulin deficiency characterized by
alteration in metabolism of CHO.
 Etiology
• Genetic
• Autoimmune
• Race/ethnicity
• Obesity/hypertension
• Environmental factor e.g. stress
• Lifestyle and diet
 Incidence
• Higher among African-American and
Hispanics than whites.
 2 TYPES
• TYPE I (IDDM/JUVENILE
• TYPE II (NIDDM/MATURE-ONSET DM
• Feedback mechanism between blood glucose
and insulin
• Normal insulin production
 TYPE I
• ABRUPT ONSET
• OCCURS BEFORE 35 Y.O.
• ABSOLUTE INSULIN DEFICIENCY
 Risk factors
• Genetic predisposition for increased
susceptibility
• Environmental triggers stimulate an
autoimmune response e.g. viral infections,
chemical toxins
 Manifestations
• Polyuria
• Polydipsia
• Polyphagia
• Glycosuria
• Weight loss
• Fatigue, malaise
• Visual changes
• Abnormal discomfort and pain
 Pathophysiology
• Autoimmune reaction- beta cells are destroyed
– Beta cell destruction occurs slowly
– Hyperglycemia occurs when 80-90% are destroyed

• Alpha cells produce excess glucagons causing

hyperglycemia
 Diagnostic tests
• Blood glucose greater than 250mg/dl
Ketones in blood and urine
Glucose present in urine
Electrolyte abnormalities (Na, K, Cl)
Opthalmologic exam may show diabetic
retinopathy
 Treatment
• Blood glucose monitoring
• Insulin subcutaneous/IV
• Restore fluid balance: initially 0.9% saline at
500 – 1000 mL/hr
• Correct electrolyte imbalance- potassium is
monitored frequently
• Assess risk for dysrrhythmias
• Treat underlying condition precipitating DKA
 TYPE II
• INSIDOUS ONSET
• OCCURS 40 Y.O. &
ABOVE
• USUALLY AFFECTS
OBESE PERSON
• LACK OF INSULIN
RECEPTORS
 Pathophysiology
• insulin insufficiency
• insulin resistance, poor utilization of tissues,
inappropriate glucose production by the liver
RISK FACTORS:
1. History of diabetes
2. Obesity (especially of upper body)
3. Physical inactivity
4. Race/ethnicity: African American, Hispanic,
or American Indian origin
5. Women: history of gestational diabetes
6. Clients with hypertension
 Complications of DM
• Hyperglycemia
– DKA
– HHNS
• Hypoglycemia
• Dawn phenomenon: rise in blood sugar
between 4 am and 8 am, not associated with
hypoglycemia (associated with Diabetes Type
1 and 2)
• Somogyi effect: combination of hypoglycemia
during night with a rebound morning
hyperglycemia that may lead to insulin
resistance for 12 to 48 hours
• Complications Affecting System/Organ
Function
A. Coronary Artery Disease
B. Hypertension
C. Stroke: Type 2 diabetics are 2 – 6
times more likely to have stroke
D. Peripheral Vascular Disease
E. Diabetic Retinopathy
F. Diabetic Nephropathy
G. Peripheral (Somatic) Neuropathies
H. Visceral (Autonomic) Neuropathies
 ASSESSMENT
Clinical manifestations
• Classic symptoms associated with Type 1
• Weight loss
• Malaise/Fatigue
• Recurrent infections
• Prolonged wound healing
• Visual changes
• Glycosuria
 Diagnostic studies
• Fasting plasma glucose level ↑126 mg/dl
• RBS 200mg/dl
• 2-hour OGTT ↑ 200mg/dl
• Glycosylated hgb or hemoglobin A1c
(HgbA1C)
– Indicates overall glucose control for the
previous 90-120 days.
– Goal: 7% or less
 PLANNING/NURSING DX
• Deficient knowledge
• Ineffective renal tissue perfusion
• Imbalanced nutrition
• Pain
• Impaired oral mucous membrane
• Impaired urinary elimination
• Constipation/diarrhea
• Overflow incontinence
• Risk for impaired skin integrity
• Risk for infection
• Risk for deficient fluid volume
• Risk for injury
• Risk for ineffective sexuality patterns
• Sexual dysfunction
• Situational low self-esteem
• Anxiety
• Fear
• Powerlessness
• Social isolation
• Noncompliance
• Ineffective health maintenance
 NURSING INTERVENTIONS
Collaborative Care
Goals:
• Reduce symptoms
• Promote well-being
• Prevent acute complications
• Delay the onset and progression of long term
complications
 Diabetes Management
• Drug therapy
• Nutritional therapy
• SMBG or urine ketone
testing
• Exercise
 DRUG THERAPY
• INSULIN injections • ORAL AGENTS
– Rapid- acting – Sulfonylureas
– Short-acting – Meglitinides
– Intermediate – Biguanides
– Long-acting – a-Glucosidase
– Mixed type inhibitors
– Thiazolidinediones
1. Sulfonylureas – stimulate insulin release from
the pancreas (Glipizide)
2. Meglitinide – acts like sulfonylureas at a faster
rate
3. Biguanide – reduces hepatic glucose
production and enhances tissue response to
insulin (metformin-Glucophage)
4. Alpha-glucosidase Inhibitors – limits the
absorption of carbohydrates from the small
intestine (Acarbose)
5. Thiazolidinediones – increase insulin
sensitivity at receptor sites on cells
(rosiglitazone-Avandia)
6. D-phenylalanine (Amino Acid) Derivative :
stimulates very rapid and short insulin
secretion to decrease spikes in glucose
following meals; reduces overall glucose level
 Nutritional Therapy
Over-all Goal
To assist in making changes in nutrition and exercise
habits
Specific Goals
1. Maintain blood glucose levels as near normal.
2. Achieve lipid profiles and BP levels that reduce the
risk for ♥ disease.
3. Modify lifestyle
4. Improve health through healthy food choices &
physical activity
5. Address individual nutritional needs while taking into
account personal and cultural preferences and
respecting the individual’s willingness to change.
 Nutritional therapy

• Reduction in caloric intake

• Low-fat diet
• Consistency of CHO for weight reduction
• Uniform timing of meals desirable but not essential
• Intermeal and bedtime snacks not usually
recommended
• Nutritional supplement for exercise programs may be
necessary if patient controlled on sulfonylyurea or
insulin
• Food composition:
• Protein 15-20%
• Fat less than 10%
• CHO 60-70%
• Alcohol- high in calories
• Diet teaching- nurse works with dietician; Food
Guide Pyramid as teaching tool or (food exhange
list)
• Exercise- regular and consistent (Guidelines on
exercise for patients with DM)
• Fiber: 20 to 35 grams/day; promotes intestinal
motility and gives feeling of fullness
• Sodium: recommended intake 1000 mg per
1000 kcal
• Sweeteners approved by FDA
• Limited use of alcohol: potentiates
hypoglycemic effect of insulin and oral
hypoglycemics
 Self-monitoring of Blood Glucose
(SMBG)
• Provides current blood
glucose readings
• Enables the patient to
make self-management
decisions
• Detects episodic
hyperglycemia and
hypoglycemia
• Portable glucose
meters
• G2 Biographer from
GlucoWatch
 Exercise
• Increases uptake of
glucose by muscle cells
• Decreases cholesterol
and triglyceride levels
• Clients should consult
with health care
provider before
beginning or changing
exercise program
• Knowledge deficit
– Teach patient that exercise will decrease bld. sugar
level and results in weight loss
– Keep a diary of food intake and exercise, a graph
of body measurements & blood sugar level.
– Ask exercise preference
– Ascertain action of oral hypoglycemic agents
– Meal 1-3 hours before exercise
– Monitor blood sugar level before exercise.
 Surgical Management
• Pancreas
Transplantation (Type 1
DM)
 New Developments in Diabetic
Therapy
• Inhaled insulin
• Skin patch
• Oral spray
• Insulin pills
 Nursing management
• Asssessment
• Planning
Goals : The patient to:
1. be active participant in the management
2. experience few or no episodes of acute
hyper/hypoglycemic emergencies
3. maintain blood glucose levels at normal or near
normal
4. prevent, minimize or delay occurrence of chronic
complications
• Nursing implementation
– Health promotion and maintenance
• ADA recommends routine screening for all overweight
adults over age 45.
– Acute interventions
• Hypoglycemia
• DKA (Diabetic Ketoacidosis)
• HHNS (Hyperosmolar Hyperglycemic Nonketotic
Syndrome)
– Stress of acute illness and surgery
– Ambulatory and Home Care
• Insulin therapy, oral agents, personal hygiene, medical
identification and travel, patient and family teaching
(empowerment approach)
 Organizations
• American Diabetes Associations
– Affiliates located in all states (1-800-DIABETES)
– Publishes materials
– Sponsors conferences for healthcare professionals
– Research and management of patients.
• American Associations of Diabetes Educators
– Pamphlets
– Booklets
– Bimonthly magazine e.g. Diabetes Forecast
• Drug Companies
 Organizations/resources
American Diabetes American Associations of
Associations (ADA) Diabetes Educators
Affiliates located in all Pamphlets
states (1-800- Booklets
DIABETES)
Bimonthly magazine
Publishes materials e.g. Diabetes Forecast
Sponsors conferences for
healthcare professionals Drug Companies
Research and
management of patients.
 COMPLICATIONS & NURSING
MANAGEMENT
• HYPOGLYCEMIA

• DIABETIC ACIDOSIS OR COMA

• DIABETIC FOOT
 Hypoglycemia
• Also referred to as insulin
reaction or low blood
glucose <45-60mg/dl
• S/S:
a. Cool, clammy skin
b. Rapid heartbeat
c. Hunger
d. Nervousness, tremor
e. Faintness, dizziness
f. Unsteady gait, slurred
and/or incoherent speech
g. Vision changes
h. Seizures, coma
 HYPOGLYCEMIA
INTERVENTIONS
Conscious Patient: Worsening
– administer 15-20g of quick symptoms/unconscious:
–acting CHO e.g. soda,
• Subcutaneous or IM
juice, low-fat milk
glucagon
– Repetition of treatment in
15min. • IV 50ml 50% glucose
– Administration of long-
acting CHO e.g. slice of • Determine cause of
bread, crackers hypoglycemia (after
– Immediate notification of correction of condition)
provider/emergency service.
 Diabetic ketoacidoses (DKA)
(mainly associated with DM type 1)
• Profound deficiency of • ETIOLOGY
insulin characterized by – Undiagnosed DM
hyperglycemia, ketosis, – Inadequate treatment
acidosis, and
– Insulin not taken as
dehydration.
prescribed
• Occurs in people with
– Infection
type1 but may be seen
in type 2 DM. – Change in diet,
insulin or exercise
regimen
 DKA
• S/S: Lab findings:
– Manifestations of Glucose level ↑250 mg/dl
dehydration Arterial blood pH 7.35
– Lethargy and
Serum bicarbonate ↓15mEq/L
weakness
Ketones in blood & urine
– Abdominal pain
– Anorexia and vomiting
– Kussmaul respirations
– Acetone breath
 DKA
Interventions
Initial: Ongoing monitoring:
– Patent airway • Monitor V/S, LOC,
– O2 cardiac rhythm, O2 sat.,
– IV access u.o.
– Fluid resucitation of 0.9 • Assess breath sounds
NaCL sol. • monitor serum glucose
– Continous regular and K
insulin drip 0.1 u/kg/hr. • Administer K to correct
– Identify hx of diabetes, hypokalemia
time of last food, time • Administer Na
& amount of insulin Bicarbonate if severe
injection acidosis (pH <7.0).
 HHNS
(mainly associated with DM type 2)
• A life-threatening • ETIOLOGY:
syndrome that can occur – Fluid vol. deficit
in patient with DM who
is unable to produce – Mental depression
enough insulin to prevent
DKA but not enough to
prevent severe
hyperglycemia, osmotic
diuresis, & extracellular
fluid depletion.
• Occurs in type 2
 HHNS
• S/S: • Lab findings:
– Somnolence – Blood sugar
– Coma ↑400mg/dl
– Seizures – Marked increased in
– Hemiparesis serum osmolality
– Ketone bodies absent
– aphasia
or minimal in both
blood and urine
 DKA & HHNS
COLLABORATIVE CARE
• IV
• IV INSULIN
• ELECTROLYTE REPLACEMENT
• ASSESSMENT OF MENTAL STATUS
• RECORDING OF I & O
• CVP if indiccated
• ASSESSMENT OF GLUCOSE LEVELS AND
KETONES
• ECG MONITORING
• ASSESSMENT OF C/P STATUS
 HYPERTHYROIDISM
• Definition: excessive delivery of thyroid hormone to
peripheral tissues
• Also known as thyrotoxicosis

• Pathophysiology
a. Autoimmune reactions (Grave’s disease)
b. Excess secretion of TSH from pituitary gland
c. Neoplasms (toxic multinodular goiter)
d. Thyroiditis
e. Excessive intake of thyroid medications
 Etiology
• Genetic factors
• Excessive dietary iodine intake
• Medications e.g. lithium, amniodarone
• Toxic nodules or tumors
 S/S
• Enlarged goiter
• Nervousness
• Heat intolerance and sweating
• Weight loss, ↑ appetite
• Frequent bowel movements
• Tremor and palpitations, hypertension
• Exophthalmos
• Difficulty concentrating
• Fine tremor, shaky handwriting, clumsiness
• Pretibial myxedema
• Ackopachy, clubbing of the fingers and toes
• Thyroid storm
– Hypertension, tachycardia, vomiting, high fever
– Pulmonary edema, shock, tremors, emotional
lability,
– Confusion, delirium, psychosis, apathy, stupor,
coma, diarrhea, abdominal pain, nausea and
vomiting, jaundice, and hyperglycemia
 Complications
• Muscle wasting, atrophy, and paralysis
• Vision loss or diplopia
• Heart failure, arrhythmias
• Hypoparathyroidism after thyroidectomy
• Hypothyroidism after radioactive iodine
treatment
 Diagnostic test findings
• Radioimmunoassay: ↑ serum T4 and T3
• Blood testing: ↓ TSH level
• Thyroid scan: ↑ uptake of 131I in Graves’ dse.
• Electrocardiography: shows tachycardia
 Management
• V/S q4
• Rest
• Quiet environment
• Frequent bed linen changes, sponge baths, and
cool environment
• Drug therapy:
– Antithyroid drugs
• Propylthioucil (PTU)
• Methimazole (Tapazole)

– Iodine preparations decrease blood flow to the

thyroid gland.
– Lithium Carbonate-inhibits thyroid hormone release.
– Beta-adrenegic blocking drugs e.g. Propanolol
– Radioactive Iodine therapy
• Surgical
– Total thyroidectomy
• Client must take lifelong thyroid replacement
– Subtotal thyroidectomy
• Pre-op care:
– Drug therapy to achieve euthyroid state before
surgery with iodine preparations
– Control of cardiac problems
– High protein, high CHO diet
– Deep breathing and coughing exercises
• Post-op care:
– V/S
– Sandbags or pillows to support the neck
– Semi-fowlers position when awake
– Avoid neck extension
– Pain meds
– Humidification of air
– Exercises and suction when needed
– Watch for complications
• Post-op complications
– Hemorrhage
– Respiratory distress
– Hypocalcemia and tetany
– Larengyl nerve damage
– Thyroid storm
 Hypothyroidism
• The result of decreased metabolism from low
levels of thyroid hormones
 Pathophysiology
• Thyroid cells may fail to produce sufficient
levels of thyroid hormones
• The cells themselves are damaged and no
longer function normally
• Other times thyroid cells are functional but the
person does not ingest enough substances
needed to make thyroid hormones
• TH is too low or absent, the blood levels of
TH are very low and the client
↓
decreased BMR
↓
The hypothalamus and Anterior Pit. G make
stimulatory hormones (TSH) as compensation
↓
TSH binds to thyroid cells and causes the
Thyroid gland to enlarged, forming a goiter.
• Cellular energy production is decreased &
metabolites build up
↓
Myxedema; tongue thickened and edema to form in the
larynx, making the voice more husky; Mxedema face-
dull puffy skin, course hair

Myxedema Coma (decreased in metabolism in cardiac

tissue causes the heart muscle to become flabby and
chamber size to increase; ↓
Decreased perfusion results in tissue and organ failure
 Etiology
• Most causes occur as a result of thyroid
surgery and radioactive iodine treatment of
hyperthyroidism
• Common in areas where soil and water have
little natural iodide (endemic goiter)
 Incidence/prevalence
• Women 30-60 years old
• Women are affected 7-10x more often than
men.
 Assessment
• Increase in time spent sleeping (14-16hrs/day)
• Generalized weakness, anorexia, muscle
aches, and paresthesias, constipation
• Cold intolerance
• Decrease in libido
• Infertility, changes in menses
• For men, impotence and fertility
 Nursing Diagnosis
• Hypothermia
• Imbalanced nutrition
• Constipation
• Activity intolerance
• Disturbed thought process
 Management
• Provision of extra clothing, warm environment
• Low-calorie, high protein diet
• Assess bowel pattern, provide 2-3L of
fluids/day
• Foods high in bulk and roughage
• Encourage activity
• Laxatives
• Thyroid replacement
• Rest periods
• Assess thingking process, repeat information
to patient
• Provide clock and calendar to maintain
orientation to time and day
• Provide handouts with all instructions
 Addison’s Disease
(Adrenal gland hypofunction)

• ↓ adrenocortical steriods as a result of ↓

production of ACTH
• Dysfunction of hypothalamic-pituitary control
mechanism
• Complete or partial destruction of the adrenal
glands
 Pathophysiology
• Insufficiency of adrenocortical steroids through
the loss of mineralocorticoid (aldosterone) and
glucocorticoid (cortisol) action.
• Effects of ↓ aldosterone- ↑water excretion, ECF
volume depletion, hypotension, ↓ cardiac output
• Impaired secretion of cortisol results in
decreased gluconeogenesis- hypoglycemia,
weakness, anorexia, emotional disturbances,
↓resistance to stress
 Assessment
Health history/PA
• Lethargy, fatigue, muscle weakness
• Salt craving
• Gastrointestinal symptoms
• Weight loss
• Menstrual changes; male clients may report
impotence
• Meds-steriods, anticoagulants, cytotoxic drugs
• Hyperkalemia (elevated blood levels of K)
• Hyperpigmentation of hand r/t adrenocortical
deficiency
• Decreased energy level
• Mood swings
• Client is forgetful
 Diagnostic assessment
• Low serum cortisol
• Low FBS
• Low Na
• Elevated K
• Plasma cortisol levels fail to rise during stimulation
tests
• glucocorticoid metabolites in urine
• Radiologic exams- may show atrophy of the gland
• ACTH stimulation test- the most definitive test for
adrenal insufficiency
• ACTH stimulation test can be done on
outpatient basis
– Cosyntropin 0.25-1mg given IM or IV
– Plasma cortisol levels are obtained at 30-min and 1
hr interval after the baseline value is established.
– Result:
• absent or markedly decreased cortisol- primary
insufficiency
 Management
• V/S
• Promote fluid balance
• Weight daily
• I and O
• Monitor lab values
• Replacement therapy:
– Hydrocortisone
– Fludrocortisone (Florinef)
• Salt additives for excess heat or humidity
• Teach patient symptoms of steroid overdose