2009

Endocrine System

RAJ PARIHAAR
4/14/2009

Table of Contents
1. Overview of Anatomy & Physiology of Endocrine System ......................................................3
2. Pancreatic Disorder ...................................................................................................................9
Diabetes Mellitus (DM) .................................................................................................. 9
Diabetic Ketoacidosis (DKA) ........................................................................................ 22
Hyperglycemic Hyperosmolar Non-Ketotic Coma (HHNKC) ........................................ 24
3. Pituitary Disorder .................................................................................................................... 26
Diabetes Incipidus (DI) ............................................................................................... 26
Syndrome of Inappropriate Anti-diuretic Hormone Secretion (SIADH) ..................... 28
4. Thyroid Disorder...................................................................................................................... 30
Goiter ........................................................................................................................... 30
Hypothyroidism (Myxedema) ...................................................................................... 34
Hyperthyroidism .......................................................................................................... 38
5. peraThyroid Disorder .............................................................................................................. 41
hypoperathyroidism..................................................................................................... 41
Hyperparathyroidism ................................................................................................... 45
6. Adrenal Disorder ..................................................................................................................... 48
Pheochromocytoma ..................................................................................................... 48
Cushing Syndrome ....................................................................................................... 51
Addisons disease......................................................................................................... 54
Addisonian Crisis ......................................................................................................... 57
Corticosteroid Therapy ................................................................................................ 58

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Overview of Anatomy & Physiology of

Endocrine System

ENDOCRINE SYSTEM
Is composed of an interrelated complex of glands (Pituitary G, Adrenal G, Thyroid G,
Parathyroid G, Islets of langerhans of the pancreas, Ovaries & Testes) that secretes a variety
of hormones directly into the bloodstream.
Its major function, together with the nervous system: is to regulate body function
HORMONES REGULATION
1. Hormones: chemical substance that acts s messenger to specific cells & organs (target
organs), stimulating & inhibiting various processes
Two Major Categories
a. Local: hormones with specific effect in the area of secretion (ex. Secretin,
cholecystokinin, panceozymin [CCK-PZ])
b. General: hormones transported in the blood to distant sites where they exert their
effects (ex. Cortisol)
2. Negative Feedback Mechanisms:
a. Decreased concentration of a circulating hormones triggers production of a stimulating
hormones from pituitary gland; this hormones in turn stimulates its target organ to
produce hormones
b. Increased concentration of a hormones inhibits production of the stimulating hormone,
resulting in decreased secretion of the target organ hormone
3. Positive Feedback Mechanisms:
c. Increased concentration of a circulating hormones triggers production of a stimulating
hormones from pituitary gland; this hormones in turn stimulates its target organ to
produce hormones
d. Decreased concentration of a hormones inhibits production of the stimulating hormone,
resulting in decreased secretion of the target organ hormone
4. Some hormones are controlled by changing blood levels of specific substances (ex. Calcium,
glucose)

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5. Certain hormones (ex. Cortisol or female reproductive hormones) follow rhythmic patterns
of secretion
6. Autonomic & CNS control (pituitary-hypothalamic axis): hypothalamus controls release of
the hormones of the anterior pituitary gland through releasing & inhibiting factors that
stimulate or inhibits hormone secretions
HORMONE FUNCTION
Endocrine G

Hormone

Functions

Pituitary G
Anterior lobe

TSH

Stimulate thyroid G to release thyroid hormones

ACTH

Stimulate adrenal cortex to produce & release

adrenocoticoids

FSH, LH

Stimulate growth, maturation, & function of primary

& secondary sex organ

GH, Somatotropin

Stimulate growth of body tissues & bones

Prolactin or LTH

Stimulate development of mammary gland &

Lactation

Posterior lobe

ADH

Regulates H2O metabolism; release during stress

or in response to an increase in plasma osmolality
To stimulate reabsorption of H2O & decrease urine
Output
Stimulate uterine contractions during delivery & the

Oxytocin

Release of milk in lactation

Affects skin pigmentation

Intermediate lobe

MSH

Adrenal G

Mineralocorticoid

Adrenal Cortex

(ex. Aldosterone)

Regulate fluid & electrolyte balance; stimulate

reabsoption of sodium, chloride, & H2O; stimulate
potassium excretion

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Glucocorticoids

Increase blood glucose level by increasing rate of

(ex. Cortisol,

glyconeogenesis; increase CHON catabolism;

corticosterone)

increase mobilization of fatty acid; promote sodium

& H2O retention; anti-inflammatory effect; aid body
in coping with stress

Sex Hormones
(androgens,

Influence development of secondary sex

Characteristics

estrogens
progesterones)

Adrenal Medulla

Epinephrine,
Norepinephrine

Function in acute stress; increase HR, BP; dilates

bronchioles; convert glycogen to glucose when
Needed by the muscles for energy

Thyroid G

: T3, T4
: Thyrocalcitonin

Regulate metabolic rate; CHO, fats, & CHON

Metabolism; aid in regulating physical & mental
Growth & development
Lowers serum calcium & phosphate levels

Parathyroid G

: PTH

Regulates serum calcium & phosphate levels

Insulin

Allows glucose to diffuse across cell membrane;

Pancreas
(islets of Langerhans)
Beta Cells

Converts glucose to glycogen

Alpha Cells

Glucagon

Increase blood glucose by causing glyconeogenisis &

glycogenolysis in the liver; secreted in response to
low blood sugar

Ovaries

: Estrogen,
Progesterone

Development of secondary sex characteristics in the

Female, maturation of sex organ, sexual functioning ,
Maintenance of pregnancy

Testes

: Testosterone

Development of secondary sex characteristics in the

Male maturation of the sex organs, sexual
functioning

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PITUITARY GLAND (HYPOPHYSIS)

Located in sella turcica at the base of brain
Controls all metabolic function of body
3 Lobes of Pituitary Gland
1. Anterior Lobe PG (Adenohypophysis)
a. Secretes tropic hormones (hormones that stimulate target glands to produce their
hormones): adrenocorticotropic H (ACTH), thyroid-stimulating H (TSH), folliclestimulating H (FSH), luteinizing H (LH)
ACTH: promotes development of adrenal cortex
LH: secretes estrogen
FSH: secretes progesterone
b. Also secretes hormones that have direct effects on tissues: somatotropic or growth H,
prolactin
Somatotropic / GH: promotes elongation of long bones
Hyposecretion of GH: among children results to dwarfism
Hypersecretion of GH: among children results to gigantism
Hypersecretion of GH: among adults results to acromegaly (square face)
DOC: Ocreotide (Sandostatin)
Prolactin: promotes development of mammary gland; with help of oxytocin it
initiates milk let down reflex
c. Regulated by hypothalamic releasing & inhibiting factors & by negative feedback system
2. Posterior Lobe PG (Neurohypophysis)
Does not produce hormones
Store & release anti-diuretic hormones (ADH) & oxytocin produced by hypothalamus
Secretes hormones oxytocin (promotes uterine contractions preventing bleeding or
hemorrhage)
Administer oxytocin immediately after delivery to prevent uterine atony.
Initiates milk let down reflex with help of hormone prolactin
3. Intermediate Lobe PG
Secretes melanocytes stimulating H (MSH)
MSH: for skin pigmentation
Hyposecretion of MSH: results to albinism
Hypersecretion of MSH: results to vitiligo
2 feared complications of albinism:
1. Lead to blindness due to severe photophobia
2. Prone to skin cancer

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ADRENAL GLANDS
Two small glands, one above each kidney; Located at top of each kidney
2 Sections of Adrenal Glands
1. Adrenal Cortex (outer portion): produces mineralocorticoids, glucocorticoids, sex
hormones
3 Zones/Layers
Zona Fasciculata: secretes glucocortocoids (cortisol): controls glucose metabolism:
Sugar
Zona Reticularis: secretes traces of glucocorticoids & androgenic hormones:
promotes secondary sex characteristics: Sex
Zona Glumerulosa: secretes mineralocorticoids (aldosterone): promotes sodium and
water reabsorption and excretion of potassium: Salt
2. Adrenal Medulla (inner portion): produces epinephrine, norepinephrine (secretes
catecholamines a power hormone): vasoconstrictor
2 Types of Catecholamines:
Epinephrine (vasoconstrictor)
Norepinephrine (vasoconstrictor)
o

Pheochromocytoma (adrenal medulla): Increase secretion of norepinephrine:

Leading to hypertension which is resistant to pharmacological agents leading to
CVA: Use beta-blockers

THYROID GLAND
Located in anterior portion of the neck
Consist of 2 lobes connected by a narrow isthmus
Produces thyroxine (T4), triiodothyronine (T3), thyrocalcitonin
3 Hormones Secreted:
T3: 3 molecules of iodine (more potent)
T4: 4 molecule of iodine
T3 and T4 are metabolic hormone: increase brain activity; promotes cerebration
(thinking); increase V/S
Thyrocalcitonin: antagonizes the effects of parathormone to promote calcium
reabsorption.
PARATHYROID GLAND
4 small glands located in pairs behind the thyroid gland
Produce parathormone (PTH)

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 Promotes calcium reabsorption

PANCREAS
Located behind the stomach
Has both endocrine & exocrine function (mixed gland)
Consist of Acinar Cells (exocrine gland): which secretes pancreatic juices: that aids in
digestion
Islets of langerhans (alpha & beta cells) involved in endocrine function:
Alpha Cell: produce glucagons: (function: hyperglycemia)
Beta Cell: produce insulin: (function: hypoglycemia)
Delta Cells: produce somatostatin: (function: antagonizes the effects of growth
hormones)
GONADS
Ovaries: located in pelvic cavity; produce estrogen & progesterone
Testes: located in scrotum; produces testosterone
PINEAL GLAND
Secretes melatonin
Inhibits LH secretion
It controls & regulates circadian rhythm (body clock)

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Pancreatic Disorder
DIABETES MELLITUS (DM)
DEFINITION
Diabetes Mellitus represent a group of chronic metabolic disorders characterized by
hyperglycemia due to total or partial insulin deficiency or insensitivity of the cells to insulin
as a result of defect in insulin secretion, insulin action or both.

CLASSIFICATION
1. TYPE 1 - INSULIN-DEPENDENT DIABETES MELLITUS (IDDM) OR JUVENILE DIABETES (BRITTLE
DISEASE) - Insulin-producing pancreatic beta cells in the islets of langerhans are
destroyed by an autoimmune process resulting in little of no insulin production (Absolute
insulin deficiency). 10% general population has Type I DM
2. TYPE 2 (NON- INSULIN-DEPENDENT DIABETES MELLITUS (NIDDM) OR MATURITY ONSET
DIABETES -It May result to partial deficiency of insulin production &/or an insensitivity of
the cells to insulin. 90% of general population has Type II DM
3. GESTATIONAL DIABETES - Gestational diabetes is appearance of diabetes for the first time
during pregnancy and disappears postpartum.

ETIOLOGY

Type 1 diabetes is thought to be the result of an autoimmune response against beta

cells in the islets of langerhans in the pancreas.

Type 2 diabetes occurs as a result of a variety of risk factors including obesity,

sedentary life style, increasing age, past history of gestational diabetes, past history of
glucose intolerance, and ethnicity.

PREDISPOSING FACTORS
A. TYPE 1 DIABETES
1. Autoimmune disease such as Graves disease, hashimotos thyroiditis and addisions
disease
2. Due to viral infections mumps, rubella ect.
3. Drugs: diuretics (Lasix), Steroids, oral contraceptives
4. Related to carbon tetrachloride toxicity

B. TYPE 2 DIABETES
1. Genetic factors
2. Obesity: because obese persons lack insulin receptor binding sites

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PATHOPHYSIOLOGY

TYPE 1 DIABETES
DUE TO PREDISPOSING FECTORS
DEVOLOP IMMUNOLOGICAL RESPONSE
AUTOIMMUNITY AGAINST THE CELL
RESPONSE
DESTRUCTION OF CELL
RESPONSE
INSULIN DEFICIENCY
RESPONSE
CELLULAR STARVATION

CLINICAL TYPE 1 DM

HYPERGLYCEMIA

STIMULATES THE APPETITE CENTER (HYPOTHALAMUS)

POLYPHAGIA

INCREASE
CATABOLISM

LYPOLYSIS IN ADIPOSE TISSUE

INCREASE OSMOTIC DIURETICS

GLYCOSURIA

GLYCOGENESIS
GLYCOGENOLYSIS

POLYUREA

CELLULAR DEHYDRATION

WEIGHT LOSS

INCREASE FATTY ACID &

CHOLESTIROL IN PLASMA

INCOMPLATE OXIDATION
IN LIVER

STIMULATES THE THIRST

CENTER (HYPOTHALAMUS)

ATHEROSCLEROSIS

KETONES

POLYDYPSIA

HYPERTENSION; MI & CVA

DIABETIC KETO ACIDOSIS

THIS LEADS TO KETONEMIA, KETONURIA & METABOLIC ACIDOSIS

KETONE SACTS AS CNS DEPRESSANTS

DIABETIC COMA

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TYPE 2 DIABETES

DUE TO PREDISPOSING FECTORS

DICERASE INSULINE PRODUCTION

OR
INSULIN RESISTANCE

CELLULAR STARVATION

CLINICAL TYPE 1 DM

STIMULATES THE APPETITE CENTER (HYPOTHALAMUS)

POLYPHAGIA

INCREASE
CATABOLISM

GLYCOGENESIS
GLYCOGENOLYSIS

LYPOLYSIS IN ADIPOSE TISSUE

INCREASE FATTY ACID &
CHOLESTIROL IN PLASMA

COMPLATE OXIDATION IN
LIVER

HYPERGLYCEMIA
INCREASE OSMOTIC DIURETICS
GLYCOSURIA

POLYUREA

CELLULAR DEHYDRATION

STIMULATES THE THIRST

CENTER (HYPOTHALAMUS)

ATHEROSCLEROSIS

POLYDYPSIA

WEIGHT LOSS
HYPERTENSION; MI & CVA

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CLINICAL MANIFESTATION
1. Polyuria

7. Anorexia

2. Polydipsia

8. Nausea and vomiting

3. Polyphagia

9. Blurring of vision

4. Glucosuria

10. Increase susceptibility to infection

5. Weight loss

11. Delayed / poor wound healing

6. Fatigue

INVESTIGATION
1. Fasting Blood Sugar:
a. FBS of greater than or equal to 126 mg/dL at two occasions confirms DM
b. May be normal in Type II DM
2. Random blood glucose of greater than or equal to 200 mg/dL with classic symptoms
(polyuria, polydipsia, polyphagia, weight loss)
3. Oral Glucose Tolerance Test: elevated [insulin level <5 micro gm / ml]
4. Glycosolated Hemoglobin (hemoglobin A1c): elevated [>6%]
5. Uineanalysis
6. Islet cell antibody
7. WBC Count. And urine culture for infection.

MEDICAL MANAGEMENT
TREATMENT GOAL
The main principle aim of the management is to establish and maintains metabolic
control.
The main therapeutic aims are

Normalize insulin activity

Achieve normal blood glucose levels

Maintain patient diet

Life style modification

Prevent complications

According to these therapeutic goals the DM management is divided into 5 components1. Nutritional management
2. Activity and exercise
3. Monitoring
4. Pharmacological therapy
5. Education

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NUTRITIONAL MANAGEMENT
Nutrition, diet and weight control are the foundation of diabetes management and it is
the first line treatment of the DM type-2.

The goal of meal planning is to control blood glucose and lipid levels

Weight loss and maintenance is a primary treatment for type 2 diabetes.

NUTRITIONAL MANAGEMENT GUIDELINES

PRINCIPLE
1.

Each meal should consist of a

balance of carbohydrates, proteins,
and fats.

5060% carbohydrates

2030% fats

1020% proteins

ACTION
Carbohydrates should be varied to include
fruits, starches, and vegetables.
Protein selections that are lean will help
reduce fat and cholesterol intake.
Fats should be used low in total calories.
High in calories, fats contribute to weight
gain.

2.

Consistency in timing of meals and

Avoid skipping or delaying meals.

amounts of food eaten on a day-to-

Measure portion sizes using a scale or

day basis help regulate blood

glucose levels.

measuring cups.
Know the equivalent amounts of commonly
used foods within a food group, eg, 1 slice
of bread = cup cooked pasta.

3.

Increase the intake of soluble and

insoluble fiber.

Substitute foods high in fiber for processed

foods when possible, eg, whole-grain bread
in place of white bread.
Eat fresh fruit and vegetables in place of
juices.

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4.

Avoid salt whenever possible.

Do not season foods with salt or saltcontaining spices.

Limit use of foods with hidden sodium
content (e.g., crackers, pickled foods,
cheese, processed meats).
Use salt-containing condiments sparingly
(ketchup, soy sauce, gravies, bouillon).

5.

Prepare foods to retain vitamins

Do not uses fry foods.

and minerals and reduce fats.

Bake, broil, or boil foods and discard fat.

Eat raw fruits and vegetables or steam
vegetables to retain fiber.
Avoid adding calories with butter or cream
sauces, fat back, and bacon.
Trim all visible fat from meat; skim off fat
from stews or other prepared dishes.

6.

Distribute snacks in the meal plan

depending on insulin/medication
regimens, physical activity, and
lifestyle.

7.

Use alcohol only in moderation.

Smaller, more frequent meals may

enhance glucose control in type 2 DM.
Unplanned activity may call for an
additional snack to avoid hypoglycemia.
Always consume alcohol with food to avoid
hypoglycemia.
Do not omit food from meal plan in
exchange for alcohol.
Limit intake to 1-2 drinks per week (4 oz
dry wine, 12 oz beer, or 1.5 oz distilled
liquor = 1 alcohol serving).

8.

Use alternative nonnutritive,

Limit diet soda intake to 2 L/day.

noncaloric sweeteners in

Avoid frequent use of foods and beverages

moderation.

with concentrated sucrose.

EXERCISE
Regularly scheduled, moderate exercise performed for at least 30 minutes most days of
the week to

Promotes the utilization of carbohydrates,

Assists with weight control,

Improving insulin utilization, and

Improves cardiovascular fitness.

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NOTE Clients should not begin exercising if glucose is above 250mg/dl and ketones are present
in the urine.
Clients are encouraged to exercise daily at the same time, using the same type of
activity if exercise is used to control blood sugar.
Clients should be encouraged to monitor blood sugar before, during, and after exercise
particularly if there is a potential for hypoglycemia (particularly so for clients using
insulin therapy and sulfonylurea treatment).

MONITORING
1. Self-monitoring of blood glucose

Two to four times daily if insulin is required.

Three times daily if insulin is required before all meals.

Two to three times per week if insulin is not required, including one test that is done
after meals (2 hours is suggested time).

Whenever hypoglycemia or hyperglycemia is suspected.

Increase frequency of testing with changes in medications, activity, or diet and with
stress or illness.

2. Glycosylated hemoglobin (HgbA1c)

HgbA1c contains glucose molecules, which attach to red blood cells; RBCs live in
body for 23 months; therefore, the HgbA1c reflects the average blood glucose level
over 23 months.

Normal ranges are usually 46% and indicate an almost normal blood glucose
control.

Levels over seven would indicate less than optimal control, putting the client at risk
for complications.

Every decline of one in HgbA1c produces up to a 40% risk reduction; for example
decrease in level from 8 to 7.

3. Urine Testing

for Glucose and Ketones

Ketone bodies in the urine indicate that control of type 1 diabetes is deteriorating
and the risk of diabetic ketoacidosis (DKA) is high.

PHARMACOLOGICAL THERAPY
Insulin therapy for patients with type 1 diabetes to control initial hyperglycemia.
Oral antidiabetic agents for patients with type 2 diabetes who do not achieve glucose
control with diet and exercise only.

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INSULIN THERAPY
Insulin injected subcutaneously is the first line therapy in the treatment of type 1
diabetes. The different type of insulin are biased their time of onset and duration of
action, rapid, short, intermediate, long acting insulin and mixed insulin.

TYPES OF THE INSULIN

INSULIN

ONSET

PEAK

DURATION

INDICATION

Rapid-acting
Lispro(Humalog)

10-15

Aspart (Novolin)

min

0.5-1 hour

3-6 hours

For rapid reduction of glucose

level, to treat postprandial
hyperglycemia, and/or

To prevent nocturnal
hypoglycemia.

Short-acting
Humalog R

0.5-1

Novolin R

hour

2-3 hours

4-6 hours

used in treating ketoacidosis;

during surgery, infection,

(R Regular)

trauma;

management of poorly
controlled diabetes;

to supplement long-acting
insulin

Intermediate-acting
NPH (neutral

1-4

protamine

hours

6-12 hours

16-20 hours

used for maintenance therapy

Usually taken after food

Used primarily to control

Hagedorn)
Lente
Long-acting
Ultralente

6-8

12-16

hours

hours

20-30 hours

fasting glucose level

used for maintenance therapy

in clients who experience
hyperglycemia during the
night with intermediate-acting
insulin

Very Long-acting
Glargine (Lantus)

1 hour

Continuous

24 hours

Used for basal dose

(no peak)

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Mixtures of insulin

Mixtures of insulin preparations with different onsets and durations of action

frequently are administered in a single injection by drawing measured doses of 2
preparations into the same syringe immediately before use.

The exception is glargine insulin, which should not be mixed with any other form of
insulin.

Preparations that contain a mixture of 70% NPH and 30% regular human insulin (ie,
Novolin 70/30, Humulin 70/30) are available, as is Humulin 50/50, but the fixed
ratios of intermediate-acting to rapid-acting insulin may restrict their use. In
addition, a 25/75 mixture of NPH and lispro insulin is available.

Complications of insulin therapy

Hypoglycemia

Local allergic reactions at the injection site including local itching, erythematous and
indurate lesions, and discrete subcutaneous nodules.

Rarely, patients may develop systemic reactions, including generalised urticaria and
anaphylactic reactions.

Fat atrophy or fat hypertrophy may develop at the injection sites.

Fat atrophy is usually due to impurities in the insulin preparation.

Fat hypertrophy is attributed to the local lipogenic effects of the injected insulin.

Formation of anti-insulin antibodies.

MORNING HYPERGLYCEMIA

Insulin waning

Progressive rise in blood glucose from bedtime to morning

Rx - Increase evening dose of intermediate or long-acting Insulin

Dawn phenomenon

Relatively normal blood glucose until about 3 AM, when the level begins to rise
result of normal nighttime release of hormones, which are counter regulatory to
insulin and cause an increase in blood sugar level

Rx - Change time of injection of evening intermediate acting insulin from

dinnertime to bedtime

Somogyi effect

Normal or elevated blood glucose at bedtime, a decrease at 23 AM to

hypoglycemic levels, and a subsequent increase result of medications acting at
the wrong time, blood sugar drops during night, liver attempts to correct
hypoglycemia and client arises with high blood sugar levels.

Rx-Decrease evening (predinner or bedtime) dose of intermediate-acting insulin

or increase bedtime snack.

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NOTE in type 2 DM insulin therapy is given when the diet, exercise and oral antidiabetes
therapy is unresponsive.
ORAL HYPOGLYCEMIC AGENT
Oral antidiabetic agents used in addition to other treatment modalities in type 2 DM.
Sulfonylureas

Glucotrol

Diabeta

Amaryl

Increase insulin secretion

side effects include weight gain and hypoglycemia

Biguanides

Glucophage

Metformin

Insulin sensitizer does not cause hypoglycemia

Some clients lose weight

GI side effects are usually self-limiting to 2 weeks

Alpha glucosidase inhibitors

Acarbose and glycet

Inhibit glucose absorption

Major deterrent severe flatulence

Thiazolidinediones (glitonones)

Avandia

Actos

Insulin sensitizers

Meglitinides

Prandin

Starlix

Insulin secretagogues

EDUCATION
1.

Regarding Disease process

2.

Diet

3.

Client should be able to plan a meal using exchange lists before discharge

Emphasize importance of regularity of meals; never skip meals

Insulin

How to draw up into syringe

Use insulin at room temp
Gently roll the vial between palms
Draw up insulin using sterile technique

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 If mixing insulin, draw up clear insulin, before cloudy insulin

Injection technique
Systematically rotate the site: to prevent lipodystrophy: (hypertrophy or atrophy
of tissue)
Insert needle at a 45 (skinny clients) or 90 (fat or obese clients) degree angle
depending on amount of adipose tissue
May store current vial of insulin at room temperature; refrigerate extra supplies

Somogyis phenomenon: hypoglycemia followed by periods of hyperglycemia or

rebound effect of insulin.

4.

Provide many opportunities for return demonstration

Oral hypoglycemic agent

Stress importance of taking the drug regularly

Avoid alcohol intake while on medication: it can lead to severe hypoglycemia reaction

Instruct the client to take it with meals: to lessen GIT irritation & prevent
hypoglycemia

5.

Urine testing (not very accurate reflection of blood glucose level)

May be satisfactory for Type II diabetics since they are more stable

Use clinitest, tes-tape, diastix, for glucose testing

Perform test before meals & at bedtime

Use freshly voided specimen

Be consistent in brand of urine test used

Report results in percentage

Report result to physician if results are greater that 1%, especially if experiencing
symptoms of hyperglycemia

Urine testing for ketones should be done by Type I diabetic clients when there is
persistent glycosuria, increase blood glucose level or if the client is not feeling well
(acetest, ketostix)

6.

Blood glucose monitoring

Use for Type I diabetic client: since it gives exact blood glucose level & also detects
hypoglycemia

Instruct client in finger stick technique: use of monitor device (if used), & recording
& utilization of test results

7.

General care

Perform good oral hygiene & have regular dental exam

Have regular eye exam

Care for sick days (ex. Cold or flu)

Do not omit insulin or oral hypoglycemic agent: since infection causes increase
blood sugar

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 Notify physician
Monitor urine or blood glucose level & urine ketones frequently
If N/V occurs: sip on clear liquid with simple sugar
8.

9.

Foot care

Wash foot with mild soap & water & pat dry

Apply lanolin lotion to feet: to prevent drying & cracking

Cut toenail straight across

Avoid constrictive garments such as garters

Wear clean, absorbent socks (cotton or wool)

Purchase properly fitting shoes & break new shoes in gradually

Never go barefoot

Inspect foot daily & notify physician: if cut, blister, or break in skin occurs

Exercise

Undertake regular exercise; avoid sporadic, vigorous exercise

Food intake may need to be increased before exercising

Exercise is best performed after meals when the blood sugar is rising

10. Complication

Learn to recognized S/sx of hypo/hyperglycemia: for hypoglycemia (cold and

clammy skin), for hyperglycemia (dry and warm skin): administer simple sugars

Eat candy or drink orange juice with sugar added for insulin reaction (hypoglycemia)

Monitor signs of DKA & HONKC

11. Need to wear a Medic-Alert bracelet

COMPLICATIONS
Complications can be acute or chronic.

Acute complications include the followinq:

Hypoglycemia (insulin reaction)
Local allergic reaction
OKA
Diabetic hyperglycemic hyperosmolar coma

Chronic complications are further subdivided into macrovascular, microvascular, and

Miscellaneous.
Macro vascular complications

Atherosclerosis

Cerebrovescular disease

Ischemic heart disease

Ischemia of lower limb (ie, gangrene)

Micro vascular complications

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Peripheral neuropathy

Peripheral neuropathy

Diabetic retinopathy,

Diabetic nephropathy

Miscellaneous complications

Skin infections

Necrobiosis Iipoidica

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DIABETIC KETOACIDOSIS (DKA)

DKA is acute complication of Type I DM characterized by hyperglycemia, ketonurea,

dehydration & accumulation of ketones in the body that leads to metabolic acidosis
and severe CNS depression

PREDISPOSING FACTORS
1. Undiagnosed DM
2. Neglect to treatment
3. Infection
4. cardiovascular disorder
5. Hyperglycemia

CLINICAL MANIFESTATION
1. Polyuria

12. Blurring of vision

2. Polydipsia

13. PS: Acetone breath odor

3. Polyphagia

14. PS: Kussmauls Respiration

4. Glucosuria

(rapid shallow breathing) or

5. ketonurea

tachypnea

6. Weight loss

15. Alteration in LOC

7. Anorexia

16. Hypotension

8. N/V

17. Tachycardia

9. Abdominal pain

18. CNS depression leading to

10. Skin warm, dry & flushed

coma

11. Dry mucous membrane; soft

eyeballs

INVESTIGATION
1. FBS: is increased
2. Serum glucose & ketones level: elevated
3. BUN (normal value: 10 20): elevated: due to dehydration
4. Creatinine (normal value: .8 1): elevated: due to dehydration
5. Hct (normal value: female 36 42, male 42 48): elevated: due to dehydration
6. Serum Na: decrease
7. Serum K: maybe normal or elevated at first
8. ABG: metabolic acidosis with compensatory respiratory alkalosis

MANAGEMENT & NURSING INTERVENTION

1. Maintain patent airway
2. Assist in mechanical ventilation

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3. Maintain F&E balance:

a. Administer IV therapy as ordered:

Normal saline (0.9% NaCl), followed by hypotonic solutions (.45% NaCl)

sodium chloride: to counteract dehydration & shock

When blood sugar drops to 250 mg/dl: may add 5% dextrose to IV

Potassium will be added: when the urine output is adequate

b. Observe for F&E imbalance, especially fluid overload, hyperkalemia &

hypokalemia
4. Administer insulin as ordered: regular acting insulin/rapid acting insulin
a. Regular insulin IV (drip or push) & / or subcutaneously (SC)
b. If given IV drip: give small amount of albumin since insulin adheres to IV
tubing
c. Monitor blood glucose level frequently
5. Administer medications as ordered:
a. Sodium Bicarbonate: to counteract acidosis
b. Antibiotics: to prevent infection
6. Check urine output every hour
7. Monitor V/S, I&O & blood sugar levels
8. Assist client with self-care
9. Provide care for unconscious client if in a coma
10. Discuss with client the reasons ketosis developed & provide additional diabetic
teaching if indicated

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HYPERGLYCEMIC HYPEROSMOLAR NON-KETOTIC COMA (HHNKC)

Hyperglycemic Hyperosmolar Non-Ketotic Coma (HHNKC) is an acute complication of type 2
DM Characterized by extremely high blood sugar level & a hyperosmolar state without
ketosis.

PREDISPOSING FACTORS
1. Undiagnosed diabetes
2. Infection or other stress
3. Certain medications (ex. dilantin, thiazide, diuretics)
4. Dialysis
5. Hyperalimentation
6. Major burns
7. Pancreatic disease

CLINICAL MANIFESTATION
1. Polyuria
2. Polydipsia

10. Dry

mucous

membrane;

soft

eyeballs

3. Polyphagia

11. Blurring of vision

4. Glucosuria

12. Hypotension

5. Weight loss

13. Tachycardia

6. Anorexia

14. Headache and dizziness

7. N/V

15. Restlessness

8. Abdominal pain

16. Seizure activity

9. Skin warm, dry & flushed

17. Alteration / Decrease LOC: diabetic

coma

INVESTIGATION
1. Blood glucose level: extremely elevated
2. BUN: elevated: due to dehydration
3. Creatinine: elevted: due to dehydration
4. Hct: elevated: due to dehydration
5. Urine: (+) for glucose

MANAGEMENT & NURSING INTERVENTION

1. Maintain patent airway
2. Assist in mechanical ventilation
3. Maintain F&E balance:
c. Administer IV therapy as ordered:

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Normal saline (0.9% NaCl), followed by hypotonic solutions (.45% NaCl)

sodium chloride: to counteract dehydration & shock

When blood sugar drops to 250 mg/dl: may add 5% dextrose to IV

Potassium will be added: when the urine output is adequate

d. Observe for F&E imbalance, especially fluid overload, hyperkalemia &

hypokalemia
4. Administer insulin as ordered: regular acting insulin/rapid acting insulin
d. Regular insulin IV (drip or push) & / or subcutaneously (SC)
e. If given IV drip: give small amount of albumin since insulin adheres to IV
tubing
f.

Monitor blood glucose level frequently

5. Administer medications as ordered:

c. Sodium Bicarbonate: to counteract acidosis
d. Antibiotics: to prevent infection
6. Check urine output every hour
7. Monitor V/S, I&O & blood sugar levels
8. Assist client with self-care
9. Provide care for unconscious client if in a coma
10. Discuss with client the reasons ketosis developed & provide additional diabetic
teaching if indicated

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Pituitary Disorder
DIABETES INCIPIDUS (DI)
Diabetes insipidus (DI) is a condition characterized by excretion of large amounts of
severely diluted urine and excessive thirst, caused by a deficiency of vasopressin, also
known as antidiuretic hormone (ADH) [central diabetes insipidus] and insensitivity of the
kidneys to ADH [nephrogenic diabetes insipidus].

ETIOLOGY & PATHOPHYSIOLOGY

1.

Primary:

2.

Idiopathic.

Secondary:

head trauma,

Neurosurgery, Related to pituitary surgery

Presence of tumor
intracranial or metastatic

3.

Vascular disease (aneurysms, infarct),

Infection (meningitis, encephalitis).

Inflammation

Nephrogenic DI:

long-standing renal disease,

hypokalemia,

some medications

CLINICAL MANIFESTATION
1. Severe polyuria with low specific gravity
2. Polydipsia (excessive thirst)
3. Fatigue
4. Muscle weakness
5. Irritability
6. Weight loss
7. Hypotension
8. Signs of dehydration
a. Adult: thirst; Children: tachycardia
b. Agitation
c. Poor Skin turgor
d. Dry mucous membrane
9. Tachycardia, eventually shock if fluids is not replaced

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10. If left untreated results to hypovolemic shock (late sign anuria)

INVESTIGATION
1. Urine Specific Gravity (NV: 1.015 1.030): less than 1.004
2. Serum Na: increase resulting to hypernatremia
3. H2O deprivation test: reveals inability to concentrate urine

MANAGEMENT WITH NURSING INTERVENTION

1. Maintain F&E balance / Force fluids 2000-3000 ml/day
a. Keep accurate I&O
b. Weigh daily
c. Administer IV/oral fluids as ordered to replace fluid loss
2. Monitor strictly V/S & observe for signs of dehydration & hypovolemia
3. Administer hormone replacement as ordered:
a. Desmopressin acetate (DDAVP) vasopressin derivative administered into the
nose through a soft, flexible nasal tube or by nasal spray.
i. Duration of action 12 to 24 hours.
ii. Use

For

patients

who

have

some

residual

hypothalamic

ADH

(determined by low levels of circulating ADH).

b. Chlorpropamide (Diabinese) potentiates action of vasopressin on renalconcentrating mechanism.
c. Clofibrate (Atromid-S) probably acts by augmenting ADH secretion from
posterior pituitary.
d. Carbamazepine (Tegretol) potentiates action of endogenous vasopressin.
e. For patients with nephrogenic DI chlorpropamide (Diabinese) may be of used.
f.

Reversible by discontinuing causative medication if cause is drug related.

4. Prevent complications: hypovolemic shock is the most feared complication

5. Provide client teaching & discharge planning concerning:
a. Lifelong hormone replacement: Lypressin (Diapid) as needed to control polyuria
& polydipsia
b. Need to wear medic-alert bracelet

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SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE SECRETION

(SIADH)
The SIADH is a syndrome characterized by hyper secretion of anti-diuretic hormone
(ADH) from the posterior pituitary gland resulting hyponatremia, and sometimes fluid
overload.

ETIOLOGY & PATHOPHYSIOLOGY

1.

Some common causes of SIADH include:

meningitis (treated with fluid restriction and diuretics)

Head injury

Related to hyperplasia of pituitary gland (increase size of organ brought about by

increase of number of cells)

Cancers
Lung

cancer

cancer,

as

(especially
well

as

small
other

cell

lung

small-cell

The release of ADH is not inhibited &

Individual ingests water

malignancies of other organs)

Infections
Brain abscess

Plasma osmolality drops.

Pneumonia
Lung abscess

Low sodium level

Drugs
Chlorpropamide

Abnormal handling of water loading

Clofibrate
Phenothiazine

SIADH

Cyclophosphamide
Carbamazepine
Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants)
Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy)

CLINICAL MANIFESTATION
1.

Person with SIADH cannot excrete dilute urine

2.

Fluid retention & Na deficiency

3.

Hypertension

Edema

Weight gain

Water intoxication: may lead to cerebral edema: lead to increase ICP; may lead to
seizure activity.

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INVESTIGATION
Laboratory findings in diagnosis of SIADH include1) Hyponatremia <130 mEq/L, and POsm <270 mOsm/kg.
2) Urine sodium concentration >20 mEqlL (inappropriate natriuresis)
3) Urine specific gravity is increase
4) Low blood urea nitrogen (BUN)
5) Low creatinine
6) Low uric acid
7) Low albumin

MEDICAL MANAGEMENT
1.

Treat underlying cause if possible

2.

Diuretics & fluid restriction

Fluid restriction to 800-1,000 ml/day should be obtained to increase serum sodium.

Intravenous saline - For very symptomatic patients (severe confusion, convulsions,

or coma) hypertonic saline (3%) 200-300 ml IV in 3-4 h should be given.

3.

4.

Drugs

Demeclocycline can be used in chronic situations to inhibitor of ADH action.

Conivaptan - an approved antagonist of both V1A and V2 vasopressin receptors.

Tolvaptan - an unapproved oral antagonist of the V2 vasopressin receptor.

Care must be taken when correcting hyponatremia. A rapid rise in the sodium level may
cause central pontine myelinolysis.

NURSING INTERVENTION
1) Restrict fluid: to promote fluid loss & gradual increase in serum Na
2) Administer medications as ordered:
a. Loop diuretics (Lasix)
b. Osmotic diuretics (Mannitol)
3) Monitor strictly V/S, I&O & neuro check
4) Weigh patient daily and assess for pitting edema
5) Monitor serum electrolytes & blood chemistries carefully
6) Provide meticulous skin care
7) Prevent complications

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Thyroid Disorder
GOITER
Goiter also is enlargement in the thyroid gland due to iodine deficiency, which can lead
to a swelling of the neck or larynx.

CLASSIFICATION
They are classified in different ways:
1. Diffuse goiter - Diffuse goiter is a goiter that has spread through the entire thyroid.
2. Nodular goiter Nodular goiter is the goiter of the one node of the thyroid. If the
goiter is spread more then one node is called multinodular goiter.
1. Toxic goiter - Toxic goiter refers to goiter with hyperthyroidism. These most commonly
due to Graves' disease, but can be caused by inflammation or a multinodular goiter.
2. Nontoxic goiter - Nontoxic goiter is a diffuse or nodular enlargement of the thyroid
gland that does not result from an inflammatory or neoplastic process and is not
associated with abnormal thyroid function.

1.

Endemic: caused by nutritional iodine deficiency, most common in the goiter belt
area, areas where soil & H2O are deficient in iodine; occurs most frequently during
adolescence & pregnancy

Goiter belt area:

Midwest, northwest & great lakes region
Places far from sea
Mountainous regions

2.

Sporadic: caused by

Increase intake of goitrogenic foods (contains agent that decrease the thyroxine
production: pro-goitrin an anti-thyroid agent that has no iodine).

Ex. cabbage, turnips, radish, strawberry, carrots, sweet potato, rutabagas, peaches,
peas, spinach, broccoli, all nuts

Soil erosion washes away iodine

Goitrogenic drugs:
Anti-Thyroid Agent:
Propylthiouracil (PTU)

Para-amino salicylic acid

Lithium Carbonate

Large doses of iodine

PASA (Aspirin)

Phenylbutazone

Cobalt

Genetic defects that prevents synthesis of thyroid hormones

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ETIOLOGY
Worldwide, the most common cause for goiter is iodine deficiency.
In countries that use iodized salt, Hashimoto's thyroiditis becomes the most common
cause.
Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease
where the body's own T-cells attack the cells of the thyroid. It was the first disease to be
recognized as an autoimmune disease
Other causes are:

Hypothyroid

Hyperthyroid

congenital hypothyroidism

Graves' disease

Ingestion of goitrogens

Thyroiditis (acute, chronic)

Side-effects

Thyroid cancer

of

pharmacological

therapy

PATHOPHYSIOLOGY
When

levels

of

thyroid

hormones

fall,

thyrotropin-releasing
hormone

(TRH)

produced

is

by

the

hypothalamus.
TRH

then

prompts

the

pituitary gland to make

thyrotropin

or

stimulating

thyroid
hormone

(TSH), which stimulates

the

thyroid

glands

production of T4 and T3.

Causes the thyroid gland
to

grow

in

size

by

increasing cell division.

CLINICAL MANIFESTATION
1. Enlarged thyroid gland
2. Dysphasia
3. Respiratory distress
4. Mild restlessness

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INVESTIGATION
1. Serum T4: reveals normal or below normal
2. Thyroid Scan: reveals enlarged thyroid gland.
3. Serum Thyroid Stimulating Hormone (TSH): is increased (confirmatory diagnostic
test)
4. RAIU (Radio Active Iodine Uptake): normal or increased

MEDICAL MANAGEMENT
1. Drug Therapy:
a. Hormone replacement with levothyroxine (Synthroid) (T4), liothyronine
(Cytomel) (T3)
b. Small dose of iodine (Lugols or potassium iodide solution): for goiter
resulting from iodine deficiency
2. Avoidance of goitrogenic food or drugs in sporadic goiter
3. Surgery:
a. Subtotal thyroidectomy: (if goiter is large) to relieve pressure symptoms & for
cosmetic reasons

NURSING INTERVENTION
1. Administer Replacement therapy as ordered:
a. Lugols Solution / SSKI (Saturated Solution of Potassium Iodine)

Color purple or violet and administered via straw to prevent staining of teeth.

4 Medications to be taken via straw: Lugols, Iron, Tetracycline, Nitrofurantoin

(DOC: for pyelonephritis)

b. Thyroid Hormones:

Levothyroxine (Synthroid)

Liothyronine (Cytomel)

Thyroid Extracts

Nursing Intervention when giving Thyroid Hormones:

1. Instruct client to take in the morning to prevent insomnia
2. Monitor vital signs especially heart rate because drug causes tachycardia and
palpitations
3. Monitor side effects:

Insomnia

Tachycardia and palpitations

Hypertension

Heat intolerance

2. Increase dietary intake of foods rich in iodine:

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Seaweeds

Seafoods like oyster, crabs, clams and lobster but not shrimps because it
contains lesser amount of iodine.

Iodized salt: best taken raw because it is easily destroyed by heat

3. Assist in surgical procedure of subtotal thyroidectomy

4. Provide client teaching & discharge planning concerning:

Used of iodized salt in preventing & treating endemic goiter

Thyroid hormone replacement

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HYPOTHYROIDISM (MYXEDEMA)
Hypothyroidism is the disease state that caused by insufficient production of thyroid
hormone by the thyroid gland.
Cretinism is a form of hypothyroidism found in Children. That can lead to mental
retardation.
Myxedema is a form of hypothyroidism found in Adults. That can lead to non pitting
edema

ETIOLOGY & CLASSIFICATION

Hypothyroidism is often classified by the organ of origin

Primary or thyroidal hypothyroidism - refers to dysfunction of the thyroid gland

itself. The most common forms include Hashimoto's thyroiditis (an autoimmune
disease), Iodine deficiency and radioiodine therapy for hyperthyroidism

Central hypothyroidism - When thyroid dysfunction is caused by failure of the

pituitary gland, the hypothalamus, or both, it is known as central hypothyroidism.

Pituitary or secondary hypothyroidism - It is caused entirely by a pituitary

disorder. Occurs if the pituitary gland does not create enough thyroid stimulating
hormone (TSH) to induce the thyroid gland to produce enough thyroxine and
triiodothyronine. Although not every case of secondary hypothyroidism has a
clear-cut cause, it is usually caused by damage to the pituitary gland, as by a
tumor, radiation, or surgery. and

Hypothalamic or tertiary hypothyroidism - if it is attributable to a disorder of

the hypothalamus resulting

the hypothalamus fails to produce

sufficient

thyrotropin-releasing hormone (TRH). TRH prompts the pituitary gland to

produce thyrotropin (TSH). Hence may also be termed hypothalamic-pituitaryaxis hypothyroidism.

Iatrogenic - surgical removal of the gland or over treatment of hyperthyroidism

with drugs or radioactive iodine; disease caused by medical intervention such as
surgery

Cretinism - When thyroid deficiency is present at birth, the condition is known as

cretinism. In such instances, the mother may also suffer from thyroid deficiency.

Myxedema

The

term

myxedema

refers

to

the

accumulation

of

mucopolysaccharides in subcutaneous and other interstitial tissues. Although

myxedema occurs in long-standing hypothyroidism in adult, the term is used
appropriately only to describe the extreme symptoms of severe hypothyroidism.

In severe or untreated cases myxedema coma may occur:

Characterized

by

intensification

of

S/sx

of

hypothyroidism

&

neurologic

impairment leading to coma

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Mortality rate high; prompt recognition & treatment essential

Precipitating factors: failure to take prescribed medications; infection; trauma;

exposure to cold; use of sedatives, narcotics or anesthetics

CLINICAL MANIFESTATION
In adults, hypothyroidism is associated with the following clinical manifestation

Early symptoms

Poor muscle tone (muscle hypotonia)

Fatigue

Cold intolerance, increased sensitivity to cold

Depression

Muscle cramps and joint pain

Goiter

Thin, brittle fingernails

Thin, brittle hair

Paleness

Decreased sweating

Dry, itchy skin

Weight gain and water retention

Bradycardia (low heart rate less than sixty beats per minute)

Constipation

Late symptoms

Slowed mental processes

Slow speech and a hoarse, breaking voice deepening of the voice can also be
noticed

Dry puffy skin, especially on the face (Dull look)

Thinning of the outer third of the eyebrows (sign of Hertoghe)

Abnormal menstrual cycles

Low basal body temperature

Generalized interstitial non-pitting edema (Myxedema)

Decrease libido

Memory impairment

Psychosis

INVESTIGATION
1. Serum T3 and T4: is decreased
2. Serum Cholesterol: is increased
3. Serum Thyroid Stimulating Hormone (TSH): is increased

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4. RAIU (Radio Active Iodine Uptake): is decreased

MEDICAL MANAGEMENT
1. Drug Therapy:

Levothyroxine (Synthroid)

Thyroglobulin (Proloid)

Dessicated thyroid

Liothyronine (Cytomel)

2. Myxedema coma is a medical emergency:

IV thyroid hormones

Correction of hypothermina

Maintenance of vital function

Treatment of precipitating cause

NURSING INTERVENTION
1. Monitor strictly V/S & I&O, daily weights; observe for edema & signs of
cardiovascular complication & to determine presence of myxedema coma
2. Administer thyroid hormone replacement therapy as ordered & monitor effects:
a. Observe signs of thyrotoxicosis:

Tachycardia & palpitation

N/V

Diarrhea

Sweating

Tremors

Agitation

Dyspnea

b. Increase dosage gradually, especially in clients with cardiac complication

3. Provide comfortable and warm environment: due to cold intolerance
4. Provide a low calorie diet
5. Avoid the use of sedatives; reduce the dose of any sedatives, narcotics, or
anesthetic agent by half as ordered
6.

Provide meticulous skin care: to prevent skin breakdown

7. Increase fluid & food high in fiber: to prevent constipation; administer stool
softener as ordered
8. Observe for signs of myxedema coma; provide appropriate nursing care
a. Administer medication as ordered
b. Maintain vital functions:

Correct hypothermia

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Maintain adequate ventilation

9. Myxedema coma:

A complication of hypothyroidism & an emergency case

A severe form of hypothyroidism is characterized by:

Severe hypotension

Bradycardia

Bradypnea

Hypoventilation

Hyponatremia

Hypoglycemia

Hypothermia

Leading to progressive stupor and coma

Nursing Management for Myxedema Coma

1. Assist in mechanical ventilation
2. Administer thyroid hormones as ordered
3. Administer IVF replacement isotonic fluid solution as ordered / Force fluids

10. Provide client health teaching and discharge planning concerning:

a. Thyroid hormone replacement
b. Importance of regular follow-up care
c. Need in additional protection in cold weather
d. Measures to prevent constipation
e. Avoid precipitating factors leading to myxedema coma & hypovolemic shock
f.

Stress & infection

g. Use of anesthetics, narcotics, and sedatives

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HYPERTHYROIDISM
Hyperthyroidism is the disease state that caused by overactive tissue within the thyroid
gland, resulting in overproduction and thus an excessive amount of thyroid hormone in
the blood causes an increase in metabolic process.
Hyperthyroidism is the second most prevalent endocrine disorder, after diabetes
mellitus.
Graves disease, the most common type of hyperthyroidism, results from an excessive
output of thyroid hormones caused by abnormal stimulation of the thyroid gland by
circulating immunoglobulins.

ETIOLOGY
The major causes in humans are

Graves' disease (the most common etiology with 70-80%)

Toxic thyroid adenoma

Toxic multinodular goiter

CLINICAL MANIFESTATION
Increase appetite (hyperphagia): but there is weight loss
Heat intolerance
Weight loss
Diarrhea: increase motility
Increased in all V/S: except wt & menses

Tachycardia

Increase systolic BP

Palpitation

Warm smooth skin

Fine soft hair
Pliable nails
CNS involvement

Irritability & agitation

Restlessness

Tremors

Insomnia

Hallucinations

Sweating

Hyperactive movement

Goiter
PS: Exopthalmus (protrusion of eyeballs)

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 Amenorrhea

INVESTIGATION
Serum T3 and T4: is increased
RAIU (Radio Active Iodine Uptake): is increased
Thyroid Scan: reveals an enlarged thyroid gland

MEDICAL MANAGEMENT
1. Drug Therap:
a. Anti-thyroid

drugs:

Propylthiouracil

(PTU)

&

methimazole

(Tapazole):

blocke

synthesis of thyroid hormone; toxic effect include agranulocytosis

b. Adrenergic Blocking Agent: Propranolol (Inderal): used to decrease sympathetic
activity & alleviate symptoms such as tachycardia
2. Radioactive Iodine Therapy
a. Radioactive isotope of iodine (ex. 131I): given to destroy the thyroid gland, thereby
decreasing production of thyroid hormone
b. Used in middle-aged or older clients who are resistant to, or develop toxicity from
drug therapy
c. Hypothyroidism is a potential complication
3. Surgery: Thyroidectomy performed in younger client for whom drug therapy has not
been effective

NURSING INTERVENTION
1. Monitor strictly V/s & I&O, daily weight
2. Administer anti-thyroid medications as ordered:
a. Propylthiouracil (PTU)
b. Methimazole (Tapazole)
3. Provide for period of uninterrupted rest:
a. Assign a private room away from excessive activity
b. Administer medication to promote sleep as ordered
4. Provide comfortable and cold environment
5. Minimized stress in the environment
6. Encourage quiet, relaxing diversional activities
7. Provide dietary intake that is high in CHO, CHON, calories, vitamin & minerals with
supplemental feeding between meals & at bedtime; omit stimulant
8. Observe for & prevent complication
a. Exophthalmos: protects eyes with dark glasses & artificial tears as ordered
b. Thyroid Storm
9. Provide meticulous skin care

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10. Maintain side rails

11. Provide bilateral eye patch to prevent drying of the eyes
12. Assist in surgical procedures subtotal Thyroidectomy:
13. Provide client teaching & discharge planning concerning:
a. Need to recognized & report S/sx of agranulocytosis (fever, sore throat, skin
rash): if taking anti-thyroid drugs
b. S/sx of hyperthyroidism & hypothyroidism

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peraThyroid Disorder
HYPOPERATHYROIDISM
Hypoparathyroidism is decreased function of the parathyroid glands, leading to
decreased levels of parathyroid hormone (PTH); characterized by hypocalcaemia,
hyperphosphatemia and neuromuscular hyper-excitability.

ETIOLOGY
IDIOPATHIC HYPOPARATHYROIDISM - it may result from autoimmune, genetic disorder, or
congenital absence of parathyroid gland (Di George Syndrome)
IATROGENIC OR ACQUIRED HYPOPARATHYROIDISM - Typically resulting from accidental
damage to or removal of parathyroid gland during thyroidectomy or any neck surgery. It
may also due to the ischemic infraction of parathyroid gland during surgery,
hemochromatosis, sarchoidotrauma, amyloidosis, tuberculosis, neoplasm, Trauma or
massive thyroid irritation.
REVERSIBLE HYPOPARATHYROIDISM it may result from hypomagnesaemia induced
impairment of hormone synthesis.

PATHOPHYSIOLOGY

NORMAL PHYSIOLOGY OF THE PARATHYROID HORMONE

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PATHOPHYSIOLOGY OF HYPOPARATHYROIDISM
CLINICAL MANIFESTATION
1. ACUTE HYPOCALCEMIA (TETANY)

Parenthesis: tingling sensation of finger & around lip

Muscle spasm

Laryngospasm/bronchospasm

Dysphagia

Seizure: feared complications

Cardiac arrhythmia: feared complications

Numbness

Positive trousseaus sign: carpopedal spasm

Positive chvostek sign

2. CHRONIC HYPOCALCEMIA (TETANY)

Fatigue

Loss of tooth enamel

Weakness

Tremors

Muscle cramps

Cardiac arrhythmias

Personality changes

Cataract formation

Irritability

Photophobia

Memory impairment

Anorexia

Agitation

N/V

Dry scaly skin

Longitudinal ridges on finger nail

Hair loss

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INVESTIGATION
TROUSSEAUS SIGN (CARPOPEDAL SPASM):- positive when corpopedal spasm is induced by
occluding the blood flow to the arm for 3 min with a blood pressure cuff.
CHVOSTEK SIGN:- positive when a sharp tapping over the facial nerve just in front of the
parotid gland and anterior to the ear causes spasm or twitching of the mouth, nose and
eye.

LAB STUDIES

Serum Calcium level: decreased (Normal value: 8.5 11 mg/100 ml)

Serum Phosphate level: increased (Normal value: 2.5 4.5 mg/100 ml)

Skeletal X-ray of long bones: reveals an increased in bone density

Serum PTH: low

MEDICAL MANAGEMENT
ACUTE TETANY
1. Maintain patient airway.
2. 10% Calcium Gluconate slow IV drip as ordered
3. Administer anticonvulsant (phenytoin or phenorbital) to control seizures.
4. Alert: - Avoid the drug phenothiazine because of possible inducement of sever
dyskinesia.
5. Monitor serum calcium or phosphate level
6. Provide quite environment free from excessive stimuli

CHRONIC TETANY
1. Oral calcium preparation: Calcium Gluconate, Calcium Lactate, Calcium Carbonate
2. Large dose of vitamin D (Calciferol): to help absorption of calcium
3. If patient is not tolerating the pure form of the vitaminD, alternatives are
(Dihydrotachystrol if renal functions are adequate; If not ok then calcitriol.
4. Phosphate Binder: Aluminum Hydroxide Gel (Amphogel) or aluminum carbonate gel,
basic (basaljel): to decrease phosphate levels

NURSING MANAGEMENT
1. Administer medications as ordered
2. Institute seizure & safety precaution
3. Provide quite environment free from excessive stimuli
4. Avoid precipitating stimulus such as glaring lights and noise
5. Monitor signs of hoarseness or stridor; check for signs for Chvosteks & Trousseaus sign
6. Keep emergency equipment (tracheostomy set, injectable Calcium Gluconate) at
bedside: for presence of laryngospasm

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7. For Tetany or generalized muscle cramp: may use rebreathing bag or paper bag to
produce mild respiratory acidosis: to promote Increase ionized Ca levels
8. Monitor serum calcium & phosphate level
9. Provide high-calcium & low-phosphorus diet
10. Provide client teaching:

Medication regimen: oral calcium preparation & vit D to be taken with meal to
increase absorption

Need to recognized & report S/sx of hypo / hyperkalemia

Importance of follow-up care with periodic serum calcium level

Prevent complications

Hormonal replacement therapy for lifetime

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HYPERPARATHYROIDISM
Hyperparathyroidism is caused by overproduction of parathyroid glands that result in an
alter state of calcium; phosphate and bone metabolism. It is characterized by bone
decalcification and the development of renal calcium and other body stone.

ETIOLOGY
PRIMARY HYPERPARATHYROIDISM: caused by tumor & hyperplasia of parathyroid gland;
most commonly affects women especially in post-menopausal women
SECONDARY HYPERPARATHYROIDISM: cause by compensatory over secretion of PTH in
response to hypocalcaemia from:

Children: Ricketts

Adults: Osteomalacia

Chronic renal disease

Malabsorption syndrome

PATHOPHYSIOLOGY

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CLINICAL MANIFESTATION
Patient may have no specific symptoms or may experiences sign and symptoms.
SKELETAL AND ARTICULAR SYSTEM RELATED: -Bone pain (especially at back); Bone
demineralization; Pathologic fracture
RENAL SYSTEM RELATED: - Kidney stones; renal colic; Polyuria; Polydipsia; Cool moist skin
GIT RELATED: -Anorexia; N/V; Gastric Ulcer; Constipation
CNS RELATED: - Irritability / Agitation; Personality changes; Depression; Memory
impairment; psychosis; stupor and coma.
CVS RELATED: - Cardiac arrhythmias; Hypertension
OTHER: - cataract; subcutaneous calcification; Muscle weakness; Fatigue

COMPLICATION
Formation of renal stones, calcification of kidney parenchyma, renal shutdown
Ulceration of upper GI tract leading to hemorrhage and perforation
Demineralization of bones, cysts, and fibrosis of marrow leads to fractures, especially of
vertebral bodies and ribs
Hypoparathyroidism after surgery

INVESTIGATION
Serum Calcium level: is increased (Normal value: 8.5 11 mg/100 ml)
Serum Phosphate level: is decreased (Normal value: 2.5 4.5 mg/100 ml)
Skeletal X-ray of long bones: reveals bone demineralization and ed in bone density
Serum PTH: high

MANAGEMENT
1.

Administer Hydration (I.V. saline) and diuretics-furosemide (Lasix) to increase urinary

excretion of calcium to prevent renal stone and renal failure.

2.

Dietary calcium is restricted, and all drugs that might cause hyperkalemia (thiazides,
vitamin D) are discontinued.

3.

Monitoring of daily serum calcium, blood urea nitrogen (BUN), potassium, and
magnesium levels

4.

If medical management is not effective Surgical removal of abnormal parathyroid

tissue.

NURSING MANAGEMENT
1.

Administer IV infusions of normal saline solution & give diuretics as ordered

2.

Monitor I&O & observe fluid overload & electrolytes imbalance

3.

Assist client with self-care: Provide careful handling, Moving, Ambulation - to prevent
pathologic fracture

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4.

Monitor V/S: report irregularities

5.

Force fluids 2000-3000 L/day: to prevent kidney stones

6.

Provide acid-ash juices (ex. Cranberry, orange juice): to acidify urine & prevent bacterial
growth

7.

Strain urine: using gauze pad: for stone analysis

8.

Provide low-calcium & high-phosphorus diet

9.

Provide warm sitz bath: for comfort

10. Maintain side rails

11. Assist in surgical procedure: Parathyroidectomy
12. Provide client teaching

Need to engage in progressive ambulatory activities

Increase fluid intake

Use

of

calcium

preparation

&

importance

of

high-calcium

diet

following

parathyroidectomy

Prevent complications: renal failure

Hormonal replacement therapy for lifetime

Importance of follow up care

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Adrenal Disorder
PHEOCHROMOCYTOMA
Pheochromocytoma is a tumor that is usually benign and originates from the chromaffin
cells of the adrenal medulla, so it is also known as chromaffin tumor.
It is characterized by paroxysmal or sustained hypertension due to overs creation of the
catecholamine epinephrine or nor-epinephrine. (Hyper function of the adrenal medulla)

ETIOLOGY
The cause of pheochromocytoma is unknown; about 5% of cases are hereditary
It May occur as component of multiple endocrine neoplasia, an autosomal-dominant
syndrome, thyroid cancer, hyperparathyroidism, and Cushing's syndrome with excess
ACTH.
It can occur at any age, but is most common between the ages of 40 and 60
It is uncommon in people older than age 65.
Most pheochromocytoma tumors are benign; 10% are malignant with metastasis.

CLINICAL MANIFESTATIONS
5 H Hypertension, Headaches, hyperhidrosis, hyper metabolism, and hyperglycemia

The nature and severity of signs and symptoms depends on the predominance of
norepinephrine or epinephrine secretion and on whether secretion is continuous or
intermittent.
Excess secretion of norepinephrine and epinephrine produces hypertension, hyper
metabolism, and hyperglycemia
The cardinal sign is Hypertension may be paroxysmal (intermittent) or persistent
(chronic); anti-hypertensive are not effective.
Headaches and vision disturbances are common.
The hyper metabolic and hyperglycemic effects produce excessive perspiration, tremor,
pallor or face flushing, nervousness, elevated blood glucose levels, polyuria, nausea,
vomiting, diarrhea, abdominal pain, and paresthesia.
Emotional changes, including psychotic behavior, may occur.
Symptoms may be triggered by allergic reactions, physical exertion, emotional upset, or
may occur without identifiable stimulus.

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INVESTIGATION
These signs can be associated with the five Hs: hypertension, headache, hyperhidrosis
(excessive sweating), hypermetabolism, and hyperglycemia.
Measurements of urine and plasma levels of catecholamines

Urine catecholamines levels - metanephrines [MN] and vanillylmandelic acid [VMA]

(metabolites of epinephrine and norepinephrine) are elevated in 24-hour urine
sample.

Plasma catecholamines levels elevated (it is measured with the patient supine and
at rest for 30 minutes. To prevent elevation of catecholamine levels by the stress of
venipuncture, a butterfly needle, or cannula inserted 30 minutes before the blood
specimen is obtained.)

CT scan and MRI of the adrenal glands or of the entire abdomen are done to identify
tumor.
Clonidine suppression test drug does not suppress the Plasma catecholamines levels

MANAGEMENT
MEDICAL MANAGEMENT
Admitted in the intensive care unit for close monitoring of ECG changes
Administration of alpha-adrenergic blocking agents (e.g., phentolamine [Regitine]) or
smooth muscle relaxants (e.g., sodium nitroprusside [Nipride]) to lower the blood
pressure quickly.
Long-acting alpha-blocker (Phenoxybenzamine (Dibenzyline)) may be used when the
blood pressure is stable to prepare the patient for surgery.
Beta-adrenergic blocking agents, such as propranolol (Inderal), may be used in patients
with cardiac dysrhythmias or those not responsive to alpha-blockers.
Catecholamine synthesis inhibitors, such as alpha-methyl-p-tyrosine (metyrosine) are
occasionally used when adrenergic blocking agents do not reduce the effects of
catecholamines.

SURGICAL MANAGEMENT
The definitive treatment of pheochromocytoma is surgical removal of the tumor, usually
with adrenalectomy.
Bilateral adrenalectomy may be necessary if tumors are present in both adrenal glands.

NURSING MANAGEMENT
Ensure bed rest and elevate the head of bed 45 degrees during severe hypertension.
Carry out tasks and procedures in calm, unhurried manner when with the patient.
Instruct the patient about use of relaxation exercises.
Reduce environmental stressors by providing calm, quiet environment. Restrict visitors.

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 Eliminate stimulants (coffee, tea, cola) from the diet.

Reduce events that precipitate episodes of severe hypertension palpation of the tumor,
physical exertion, emotional upset.
Administer sedatives as prescribed to promote relaxation and rest.
Monitor for orthostatic hypotension after administration of phentolamine (Regitine).
Encourage oral fluids and maintain I.V. infusion preoperatively to ensure adequate
volume expansion going into surgery.

POSTOPERATIVE CARE
Monitor vital signs, ECG, arterial BP, neurologic status, and urine output closely
postoperatively.
Assess for and report complications of hypertension, hypotension, and hyperglycemia.
Maintain adequate hydration with I.V. infusion to prevent hypotension. (Because
reduction of catecholamines immediately postoperatively causes vasodilation and
enlargement of vascular space, hypotension may occur.)
Monitor intake and output and laboratory results for BUN, creatinine, and glucose.
Corticosteroid replacement is required if bilateral adrenalectomy

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CUSHING SYNDROME
Cushing Syndrome is the condition resulting from excessive secretion of corticosteroids,
particularly glucocorticoid cortisol by the adrenal cortex. It is also as hypercrtisolism.

ETIOLOGY
PRIMARY CUSHINGS SYNDROME: - The most common cause of Cushings syndrome is
bilateral adrenal hyperplasia or adrenocortical tumors.
SECONDARY CUSHINGS SYNDROME (also called Cushings disease): caused by functioning
pituitary or non-pituitary neoplasm secreting.

Hyper-secretion of ACTH by the pituitary or from ectopic sources such as small cell
carcinoma of lungs, medullary carcinoma of thyroid, or tumor of thymus or pancreas
tumor

IATROGENIC: cause by prolonged use of corticosteroids

CLINICAL MANIFESTATION
Central obesity weight gain and altered
fat distribution with round (moon) face,
buffalo hump, and pendulous abdomen.
Hypertension
Physiological
weakness;

distribution
Muscle

Hypernatremia;

wasting;

Muscle
Fatigue;

hypocalcaemia;

constipation etc.
Decrease resistance to infection
Skin changes - Purple striae on trunk;
Acne; Thin skin; Easy bruising
Signs

of

masculinization

in

women:

menstrual dysfunction, decrease libido

Osteoporosis
Edema
Metabolic acidosis

INVESTIGATION
FBS: is increased
Plasma Cortisol: is increased
Serum Sodium: is increased
Serum Potassium: is decreased
Abnormal dexamethasone suppression test positive

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MANAGEMENT
Surgical excision of the adenoma
Metastatic and un-resectable adrenal carcinoma treated with mitotane, ketoconazole
metyrapone aminoglutethimide and adrenal enzyme inhibitor etc.
Ectopic tumors are resected by the surgery.
If the sources of ACTH cannot be resected or in case of uncontrolled adrenal hyperplasia
is treated with adrenalectomy.

NURSING MANAGEMENT
Maintain muscle tone

Provide ROM exercise

Assist in ambulation

Prevent accidents fall & provide adequate rest

Protect client from exposure to infection
Maintain skin integrity

Provide meticulous skin care

Prevent tearing of the skin: use paper tape if necessary

Minimize stress in the environment

Monitor V/S: observe for hypertension & edema
Monitor I & O & daily weight: assess for pitting edema: Measure abdominal girth: notify
physician
Provide diet low in Calorie & Na & high in CHON, K, Ca, and Vitamin D
Monitor urine: for glucose & acetone; administer insulin as ordered
Provide psychological support & acceptance
Prepare client for hypophysectomy or radiation: if condition is caused by a pituitary
tumor
Prepare client for Adrenalectomy: if condition is caused by an adrenal tumor or
hyperplasia
Restrict sodium intake
Administer medications as ordered: Spironolactone (Aldactone): potassium sparring
diuretics
Provide client teaching

Diet modification

Importance of adequate rest

Need to avoid stress & infection

Change in medication regimen (alternate day therapy or reduce dosage): if caused of

condition is prolonged corticosteroid therapy

Prevent complications (DM)

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Hormonal replacement for lifetime

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ADDISONS DISEASE
Addisons disease is caused by deficiency of the mineralocorticoids, glucocorticoids, &
sex hormones (androgens) due to the hypo-functioning of the adrenal cortex, which
leads to metabolic disturbance (hypoglycemia); Fluid and electrolyte imbalance (Na,
H2O, K) and Deficiency of neuromuscular function

ETIOLOGY
Relatively rare disease caused by:

Idiopathic atrophy of the adrenal cortex - due to an autoimmune process

Destruction of the gland secondary to TB or fungal infections

Inadequate secretions of the ACTH from the pituitary gland

Iatrogenic - Surgical removal of both adrenal glands (bilateral Adrenelectomy)

CLINICAL MANIFESTATIONS
Fatigue, Muscle weakness
Anorexia, N/V, abdominal pain, weight loss
Symptoms of hypoglycemic reaction / Hypoglycemia

Tremors,

Tachycardia,

Irritability,

Restlessness,

Extreme fatigue,

Diaphoresis and

Depression

Hyponatremia - hypotension, signs of dehydration, weight loss, weak pulse

Hyperkalemia: agitation, diarrhea, arrhythmia
Decrease tolerance to stress
Decrease libido
Loss of pubic and axillary hair
Bronze like skin pigmentation

INVESTIGATION
FBS: is decreased (normal value: 80 100 mg/dl)
Plasma Cortisol: is decreased
Serum Sodium: is decrease (normal value: 135 145 meq/L)
Serum Potassium: is increased (normal value: 3.5 4.5 meq/L)

MANAGEMENT
Administer hormone replacement therapy as ordered:

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Glucocorticoids: stimulate diurnal rhythm of cortisol release, give 2/3 of dose in early
morning & 1/3 of dose in afternoon

Dexamethasone

Hydrocortisone

Prednisone

Mineralocorticoids

Fludrocortisone Acetate (Florinef)

Fluid replacement therapy for restore and maintain the fluid and electrolyte balance.
Antibiotics may be given if any sign of infection.

NURSING MANAGEMENT
Administer hormone replacement therapy as ordered
Care when we are giving steroid therapy

Instruct client to take 2/3 dose in the morning and 1/3 dose in the afternoon to
mimic the normal diurnal rhythm

Taper dose (withdraw gradually from drug)

Monitor side effects:

Hypertension

Edema

Hirsutism

Increase susceptibility to infection

Moon face appearance

Monitor V/S
Decrease stress in the environment
Prevent exposure to infection
Provide rest period: prevent fatigue
Weight daily
Provide small frequent feeding of diet: decrease in K, increase cal, CHO, CHON, Na: to
prevent hypoglycemia, & hyponatremia & provide proper nutrition
Monitor I&O: to determine presence of addisonian crisis (complication of addisons
disease)
Provide meticulous skin care
Provide client teaching regarding

Disease process: signs of adrenal insufficiency

Use of prescribe medication for lifelong replacement therapy: never omit medication

Need to avoid stress, trauma & infection: notify the physician if these occurs as
medication dosage may need to be adjusted

Stress management technique

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Diet modification

Use of salt tablet (if prescribe) or ingestion of salty foods (potato chips): if
experiencing increase sweating

Importance of alternating regular exercise with rest periods

Avoidance of strenuous exercise especially in hot weather

Avoid precipitating factor: leading to addisonian crisis: stress, infection, sudden

withdrawal to steroids

Prevent complications: addisonian crisis, hypovolemic shock

Importance of follow up care

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ADDISONIAN CRISIS
Severe exacerbation of Addisons disease caused by acute adrenal insufficiency
Acute medical emergency due to extreme and sudden depletion of corticosteroid
production in body.

PREDISPOSING FACTORS
Strenuous activity
Stress
Trauma
Infection
Failure to take prescribe medicine
Iatrogenic:

Surgery of pituitary gland or adrenal gland

Rapid withdrawal of exogenous steroids in a client on long-term steroid therapy

CLINICAL MANIFESTATIONS
Generalized muscle weakness
Severe hypotension
Hypovolemic shock; vascular collapse
Hyponatremia: leading to progressive stupor and coma

INVESTIGATION
FBS: is decreased (normal value: 80 100 mg/dl)
Plasma Cortisol: is decreased
Serum Sodium: is decrease (normal value: 135 145 meq/L)
Serum Potassium: is increased (normal value: 3.5 4.5 meq/L)

NURSING INTERVENTION
Assist in mechanical ventilation
Administer IV fluids (5% dextrose in saline, plasma) as ordered: to treat vascular
collapse
Administer IV glucocorticoids: Hydrocortisone & vasopressors as ordered
Force fluids Administration
If crisis precipitate by infection: administer antibiotics as ordered
Maintain strict bed rest & eliminate all forms of stressful stimuli
Monitor V/S, I&O & daily weight
Protect client from infection
Provide client teaching same as Addisons disease

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CORTICOSTEROID THERAPY
Corticosteroids are a class of natural and synthetic analogues of the hormones secreted
by the adrenal gland.
Corticosteroids include:

The anti-inflammatory glucocorticoid compounds

The mineralocorticoids, which control water and salt balance through their effects on
the kidneys corticotrophins, which control the secretion of hormones by the pituitary
gland

Synthetic

corticosteroid

preparations

having

the

both

glucocorticoid

and

mineralocorticoid properties.

INDICATION
Commonly used in

Addisons disease,

Adrenal insufficiency,

Allergic reactions,

Arthritis,

Asthma,

Autoimmune disease.

Brain tumors,

Dermatitis,

Hepatitis,

Idiopathic thrombocytopenic purpura (ITP),

Inflammatory bowel disease,

Joint pain,

Systemic lupus erythematous (SLE)

Uveitis,

CORTICOSTEROID MEDICATIONS
Corticosteroids are available in injections, oral medications, topical medications, nasal
medications, rectal foams, and ear and eye drops.
Corticosteroids suppress the bodys natural production of corticosteroids by inhibiting the
release of adrenorticotropic hormone.
Corticosteroid medications include:

Beclomethasone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Betamethasone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Cortisone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Dexamethasone - Exclusively a glucocorticoid in its actions.

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Fludrocortisone (Florinef) - Mineralocorticoid available only in oral form.

Hydrocortisone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Methylprednisolone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Prednisolone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Prednisone - Primarily a glucocorticoid with mild mineralocorticoid effects.

Triamcinolone - Primarily a glucocorticoid with mild mineralocorticoid effects.

DOSE

The administration of pharmacologic doses of steroids once-daily or every-other-day.

In keeping with the natural secretion of cortisol, the best time of the day for the total
corticosteroid dose is in the early morning from 7 to 8 am or the dose is divided and
give 2/3 dose in the morning and 1/3 dose in the afternoon to produce the normal
diurnal rhythm.

Large-dose therapy give in the morning (at 8 am) when the gland is most active,
produces maximal suppression of the gland. A large morning dose is more
physiologic because it allows the body to escape effects of the steroids from evening
to next morning, when serum levels are normally low, hence minimizing cushingoid
effects.

TAPER DOSE (REDUCING CORTICOSTEROIDS)

Corticosteroids inhibit the bodys ability to produce natural corticosteroids; the dose
of Corticosteroid dosages are reduced gradually (tapered) over a period of weeks or
even months to allow normal adrenal function to return and to prevent steroidinduced adrenal insufficiency. Up to 1 year or more after use of corticosteroids, the
patient is still at risk for adrenal insufficiency in times of stress.

If

the

dose

is

reduced

too

quickly,

side

effects

of

fatigue,

body

aches,

lightheadedness and difficulty recovering from minor illnesses, may occur.

SIDE EFFECTS OF CORTICOSTEROIDS

Chronic high doses of glucocorticoids leads to adrenal excess or Cushings syndrome.
Symptoms vary, but most people have upper body obesity, a round face, increased fat
around the neck, and thinning of the arms and legs. In its later stages, this condition
can cause weakening of bones and muscles with rib and spinal column fractures.
Short-term effects of corticosteroids are usually mild and include

Fluid retention,

Increased appetite,

Increased blood pressure,

Increased blood sugar,

Increased eye pressure that can lead to glaucoma,

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Indigestion,

Insomnia and

Menstrual irregularities,

Mood swings,

Nervousness

Stomach pain,

Weight gain,

Infrequent adverse reactions include

Drug-induced paranoia,

Delirium,

Depression, and

Increased facial hair growth.

Topical corticosteroids can lead to

Thin skin

Red lesions and

Acne

Injected corticosteroids can cause irritation near the site of injection.

Long-term use of corticosteroids can cause

Thinning of the skin,

Bone loss,

Glaucoma,

Liver disease, and

Susceptibility to infection.

Allergies to corticosteroids can develop,

Causing rash,

Itching,

Hives, and

Respiratory problems.

NOTE - Any adverse effects that develop after starting corticosteroids should be reported to
ones healthcare provider as soon as possible.

NURSING CARE
Instruct client to take 2/3 dose in the morning and 1/3 dose in the afternoon to mimic
the normal diurnal rhythm
Taper dose (withdraw gradually from drug)
Monitor side effects
Monitor V/S
Decrease stress in the environment

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 Prevent exposure to infection

Provide rest period: prevent fatigue
Weight daily
Provide proper nutrition
Monitor I&O
Provide meticulous skin care
Provide client teaching

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