You are on page 1of 177
The ENDOCRINE SYSTEM
The ENDOCRINE SYSTEM
Anatomy and physiologic Overview  Endocrines: Without ducts : Ductless glands .  A group of

Anatomy and physiologic Overview

  • Endocrines: Without ducts: Ductless glands.

  • A group of glands all of which lack ducts or specific channels to release their secretions.

  • All of them secrete or produce “Chemical

Messengers” or Hormones.

  • Hormones by definition bring metabolic changes in target tissues.

  • The target tissues are usually far away from the

endocrine glands.

WHY ENDOCRINE SYSTEM? 4 MOST IMPORTANT PURPOSES 2. 1. HOMEOSTASIS. COMBATING STRESS. GROWTH & DEVELOPMENT. REPRODUCTION.

WHY ENDOCRINE SYSTEM?

4 MOST IMPORTANT PURPOSES

WHY ENDOCRINE SYSTEM? 4 MOST IMPORTANT PURPOSES 2. 1. HOMEOSTASIS. COMBATING STRESS. GROWTH & DEVELOPMENT. REPRODUCTION.
  • 2.

1. HOMEOSTASIS.

COMBATING STRESS.

GROWTH & DEVELOPMENT.

REPRODUCTION.

WHY ENDOCRINE SYSTEM? 4 MOST IMPORTANT PURPOSES 2. 1. HOMEOSTASIS. COMBATING STRESS. GROWTH & DEVELOPMENT. REPRODUCTION.
  • 3.

WHY ENDOCRINE SYSTEM? 4 MOST IMPORTANT PURPOSES 2. 1. HOMEOSTASIS. COMBATING STRESS. GROWTH & DEVELOPMENT. REPRODUCTION.
  • 4.

WHY ENDOCRINE SYSTEM? 4 MOST IMPORTANT PURPOSES 2. 1. HOMEOSTASIS. COMBATING STRESS. GROWTH & DEVELOPMENT. REPRODUCTION.
ENDOCRINES ARE USEFUL FOR… 1. HOMEOSTASIS  Endocrines help us in maintaining the homeostasis of: 

ENDOCRINES ARE USEFUL FOR…

1. HOMEOSTASIS

  • Endocrines help us in maintaining the homeostasis of:

    • Temperature: Thermoregulation or thermostasis.

    • Metabolism

    • Nutrition: Glucostasis

    • Acid Base Balance

ENDOCRINES ARE USEFUL FOR… 1. HOMEOSTASIS  Endocrines help us in maintaining the homeostasis of: 
ENDOCRINES ARE USEFUL IN… 2. COMBATING STRESS  INFECTION  TRAUMA  SHOCK

ENDOCRINES ARE USEFUL IN…

2. COMBATING STRESS

ENDOCRINES ARE USEFUL IN… 2. COMBATING STRESS  INFECTION  TRAUMA  SHOCK
  • INFECTION

  • TRAUMA

  • SHOCK

ENDOCRINES ARE USEFUL FOR… 3. GROWTH & DEVELOPMENT  Increase in the cell number: Hyperplasia 

ENDOCRINES ARE USEFUL FOR…

3. GROWTH & DEVELOPMENT

  • Increase in the cell number: Hyperplasia

  • Increase in cell SIZE:

Hypertrophy.

ENDOCRINES ARE USEFUL FOR… 3. GROWTH & DEVELOPMENT  Increase in the cell number: Hyperplasia 
ENDOCRINES ARE USEFUL FOR… 4. REPRODUCTION  The Male and female Gonads secrete:  Sex Hormones

ENDOCRINES ARE USEFUL FOR… 4.

REPRODUCTION

ENDOCRINES ARE USEFUL FOR… 4. REPRODUCTION  The Male and female Gonads secrete:  Sex Hormones
  • The Male and female

Gonads secrete:

  • Sex Hormones

  • These sex hormones cause the development of

    • Primary sex organs

    • Secondary sexual characteristics.

HORMONES  It is important in regulation of the internal environment of the body and effect

HORMONES

  • It is important in regulation of the internal

environment of the body and effect every aspect of life.

  • Natural chemicals that exert their effects on specific tissues known as

target tissues

  • The mechanism for regulating hormone in the blood stream is called negative feedback

Target Tissues  usually located some distance from endocrine glands with no direct physical connection between

Target Tissues

  • usually located some distance from endocrine glands with no direct

physical connection between the endocrine

glands and its target tissue

Glands Of The Endocrine System 1. Pituitary glands 2. Thyroid glands 3. Parathyroid glands 4. Pancreatic

Glands Of The Endocrine System

  • 1. Pituitary glands

  • 2. Thyroid glands

  • 3. Parathyroid glands

  • 4. Pancreatic islets

  • 5. Ovaries

  • 6. Testes

  • 7. Adrenal glands

HORMONES PRODUCED IN THE BODY  HYPOTHALAMUS:  CRH, TRH, GHRH, GHIH, GnRH, PIH.  ANTERIOR

HORMONES PRODUCED IN THE

BODY

  • HYPOTHALAMUS:

    • CRH, TRH, GHRH, GHIH, GnRH, PIH.

  • ANTERIOR PITUITARY GLAND:

    • GH, ACTH, TSH, FSH, LH, Prolactin.

  • POSTERIOR PITUITARY GLAND:

    • ADH, & Oxytocin.

  • THYROID GLAND:

    • Thyroxin, T 3, Calcitonin.

HORMONES PRODUCED IN THE BODY  ADRENAL CORTEX:  Aldosterone, Cortisol, Sex steroids.  ADRENAL MEDULLA:

HORMONES PRODUCED IN THE

BODY

  • ADRENAL CORTEX:

    • Aldosterone, Cortisol, Sex steroids.

  • ADRENAL MEDULLA:

    • Epinephrine, Norepinephrine, Dopamine.

  • ENDOCRINE PANCREAS:

    • Glucagon, Insulin, Somatostatin, Pan polypeptide.

HORMONES PRODUCED IN THE BODY  TESTES:  Testosterone, Estrogen, Inhibin.  OVARY:  Estrogens, Progesterone,

HORMONES PRODUCED IN THE

BODY

  • TESTES:

    • Testosterone, Estrogen, Inhibin.

  • OVARY:

    • Estrogens, Progesterone, Relaxin.

  • PLACENTA:

    • Estrogens, Progesterone, HCG, HPL.

  • THYMUS:

    • Thymosin.

  • PINEAL GLAND:

    • Melatonin

HYPERSECRETION:  Excessive Production of hormones due to:  Tumors in the gland.  Excess tropic

HYPERSECRETION:

  • Excessive Production of hormones due to:

    • Tumors in the gland.

    • Excess tropic influence.

  • Results in:

    • Clinical syndromes with signs/symptoms due to:

      • Increased blood levels of the hormone

  • Example: Hyperthyroidism: Thyroxin levels

  • Clinical features: Fine tremor, Anxiety, PR, BMR

  • Acromegaly: Growth Hormone.

  • HYPOSECRETION:  Drop in the production of hormones due to:  Excision of gland: Eg: Parathyroids.

    HYPOSECRETION:

    • Drop in the production of hormones due

    to:

    • Excision of gland: Eg: Parathyroids.

    • Hypofunctioning of gland cells: Eg: Diabetes mellitus.

    • Decreased tropic influence.

    • Results in:

      • Clinical features/ syndromes due to

      • blood levels of the hormone

    ENDOCRINE DISORDERS
    ENDOCRINE DISORDERS
    Thyroid Hyperfunction Disorder  1. Graves disease: immunological factors, genetic predisposition, infection, stress, excessive intake of

    Thyroid Hyperfunction Disorder

    • 1. Graves disease: immunological factors,

    genetic predisposition, infection, stress, excessive intake of thyroid medication; occurs

    8 times more frequently in females

    • 2. Goiter: inadequate intake of iodine, increase in thyroid demand

    • 3.Thyroid storm: Stress, injury, infection, surgery

    Causes of Hyperthyroid Disorder  Auto immune response  Neoplasm  Excessive intake of thyroid medication

    Causes of Hyperthyroid Disorder

    • Auto immune response

    • Neoplasm

    • Excessive intake of thyroid medication

    • Excess secretion of TSH from the anterior pituitary glands

    Pathophysiology THYROID HYPERFUNCTION DISORDERS  1. Production of thyroid hormone (TH) is dependent on adequate secretion

    Pathophysiology

    THYROID HYPERFUNCTION DISORDERS

    • 1. Production of thyroid hormone (TH) is

    dependent on adequate secretion of

    thyroid stimulating hormone (TSH) from

    the anterior pituitary gland; The hypothalamus regulates pituitary

    secretion of TSH by negative feedback

    Hyperthyroidism  Hyper function of the thyroid gland  Leads to an excess of thyroid hormone

    Hyperthyroidism

    • Hyper function of the thyroid gland

    • Leads to an excess of thyroid hormone in the body

    • The presence of excess TH leads to hyper

    metabolic state

    • Which causes increase in metabolic function

    • Increase in oxygen consumption by tissue,

    • And heat production

    Graves’ Disease  The most common cause of hyperthyroidism, is seen most often in woman under

    Graves’ Disease

    • The most common cause of hyperthyroidism,

    is seen most often in woman under age of 40.

    • The exact cause is unknown, it is considered

    an autoimmune disorder to stimulation of

    the thyroid gland from a long acting thyroid stimulator (LATS)

    • The result in an excess production of TH, Which leads to hypermetabolic state

    GOITER  It is describes the enlargement or hypertropy of the thyroid gland in attempt to

    GOITER

    • It is describes the enlargement or hypertropy of the

    thyroid gland in attempt to compensate for inadequate TH

    • It may be present in hyperthyroidism or hypothyroidism

    • Goiter may be result of response to excess TSH stimulation, excess growth stimulating immunoglobulins, or presence of substance that inhibit thyroid hormone synthesis

    • The goiter may become enlarge that compress the neck and chest

    Toxic Multinodular Goiter  It exist when small, independently functioning nodules in the thyroid gland tissue

    Toxic Multinodular Goiter

    • It exist when small, independently

    functioning nodules in the thyroid gland tissue are present and secrete TH hormone

    • The nodule may be benign or malignant

    • The manifestation developed more slowly than graves’ disease.

    • Toxic goiter is most often seen in woman age

    60 or older who had goiter for several years.

    Thyroid Storm  Also known as thyroid crisis or thyrotoxicosis  It is life threatening condition

    Thyroid Storm

    • Also known as thyroid crisis or thyrotoxicosis

    • It is life threatening condition which describes an extreme state of hyperthyroidism

    • The presence of excessive TH causes a rapid increase in metabolic rate

    • Immediate treatment is necessary to avoid

    death

    Nursing assessment for Hyperthyroidism  1. eyes, vital sign, cardiac monitor for rhythm changes, sign of

    Nursing assessment for

    Hyperthyroidism

    • 1. eyes, vital sign, cardiac monitor for rhythm

    changes, sign of congestive heart failure, nutritional assessment, complaints of GI distress, muscle strength and appearance, presence of goiter, reproductive history, integument assessment, weight, fluid status

    • 2. Assessment findings for thyroid storm include elevated temperature, symptoms of pain, bowel/GI complaints, neurological, development of seizures, changes in VS, respiratory status

    Nursing management for Hyperthyroidism 1. Medication A. Antithyroid medication to reduce TH production  1. Methimazole

    Nursing management for

    Hyperthyroidism

    1. Medication

    • A. Antithyroid medication to reduce TH production

      • 1. Methimazole (Tapazole)

      • 2. Propylthioracil (PTU, Propyl-Thracil)

    B. Propanolol (Inderal) to treat dysrhythmias

    • C. Glucocorticoids: interfere with conversion of T3 and

    T4

    D. Lugol’s Solution (iodine) to decrease vascularity and

    size of thyroid E. Antipyretic if needed

    Nursing management for Hyperthyroidism Educate the client that it may take several weeks before the therapeutic

    Nursing management for

    Hyperthyroidism

    Educate the client that it may take several weeks before the therapeutic effects of antithyroid medications are noticed

    • a. Instruct to take medication as prescribe and not abruptly discontinue medication

    • b. Educate about the signs of hypothyroidism,

    which may occur if to much medicine is

    taken or dose needs adjusting

    Nursing management for hyperthyroidisn  3. Monitor for cardiac dysthythmias  4.Implement antipyretic measures  5.

    Nursing management for

    hyperthyroidisn

    • 3. Monitor for cardiac dysthythmias

    • 4.Implement antipyretic measures

    • 5. Elevate head of the bed to decrease eye pressure

    • 6. Teach eye care and monitor for vision changes if exophthalmos occurs, since it will not change even after medication have been started.

    Nursing management for hyperthyroidism  7. Monitor dietary intake: Client may require up to 4,000 to

    Nursing management for

    hyperthyroidism

    • 7. Monitor dietary intake: Client may require up to 4,000 to 5,000 calories a day during hypermetabolic state

    • 8. Monitor intake and output

    • 9. Monitor weight

    • 10. Keep the environment cool and quiet because of the symptoms

    Nursing management for Hyperthyroidism 11. Radioactive therapy may be recommended to destroy thyroid cells in order

    Nursing management for

    Hyperthyroidism

    11. Radioactive therapy may be recommended to

    destroy thyroid cells in order to reduce production of TH

    A. Give radioactive iodine orally; expect result in 6 to 8 weeks

    B. Does not require hospitalization or radiation precaution

    C. Contraindicated in pregnant woman

    D. Monitor for sign and symptoms of hyperthyroidism

    Nursing management for Hyperthyroidism 12. Preoperative and postoperative care for surgical intervention to remove all or

    Nursing management for

    Hyperthyroidism

    12. Preoperative and postoperative care for surgical intervention

    to remove all or part of the thyroid (thyroidectomy)

    • A. subtotal thyroidectomy leaves part of the thyroid gland intact in order to produce adequate amounts of TH

    • B. For total thyroidectomy life long thyroid hormone replacement is necessary; educate for strict compliance with medication regimen

    • C. Preoperative care include administering antithyroid medications to promote euthyroid state, and iodine preparation to decrease vascularity of the glands. Teach the client how to support the neck to reduce strain in the suture line

    Nursing management for hyperthyroidism  Post operative care includes monitoring for complication of hemorrhage, respiratory distress,

    Nursing management for

    hyperthyroidism

    • Post operative care includes monitoring for

    complication of hemorrhage, respiratory distress, laryngeal nerve damage, and tetany

    • 13. Priority nursing diagnosis for thyroid

    hyperfunction disorders: Activity intolerance; altered nutrition; hyperthermia; risk for

    injury

    Thyroid Hypofunction Disorder A. Overview 1. Hypofunction of the thyroid glands leads to an insufficient amount

    Thyroid Hypofunction Disorder

    A.

    Overview

    • 1. Hypofunction of the thyroid glands leads to an insufficient amount of thyroid hormone (TH), a condition known as hypothyroidism

    • 2. Decrease TH result in a hypometabolic state manifested by a decrease in metabolic

    function, a decrease in oxygen consumption

    by tissue, and decrease in heat production

    Thyroid hypofunction Disorder A. Hypothyroidism B. Myxedema C. Myxedema coma

    Thyroid hypofunction Disorder

    • A. Hypothyroidism B. Myxedema

    • C. Myxedema coma

    MYXEDEMA HYPOTHYROIDISM

    MYXEDEMA

    HYPOTHYROIDISM

    MYXEDEMA HYPOTHYROIDISM
    Classified as primary and secondary A. Causes of primary hypothyroidism include congenital defects, loss of thyroid

    Classified as primary and secondary

    A. Causes of primary hypothyroidism include

    congenital defects, loss of thyroid tissue from surgery or radiation, antithyroid medication,

    endemic iodine deficiency, or thyroiditis

    B. Causes of secondary hyperthyroidism include peripheral resistance to TH or pituitary TSH

    deficiency

    Pathophysiology 1. Hypothyroidism describe an insufficient amount of TH which leads to a decrease in metabolic

    Pathophysiology

    1. Hypothyroidism describe an insufficient amount of

    TH which leads to a decrease in metabolic rate; manifestation developed slowly over months or years

    2. Myxedema describes a generalized hypometabolic state occurring with untreated hypothyroidism

    • A. Accumulation of proteins in the interstitial space result in an increase of interstitial fluid, causing

    mucinous edema, (myxedema)

    • B. This non-pitting edema is most commonly found in the pretibial and facial area

    Pathophysiology of Myxedema coma  Also known as hypothyroid crisis  It is the result of

    Pathophysiology of Myxedema coma

    • Also known as hypothyroid crisis

    • It is the result of extreme or prolonged hypothyroidism; though rare, it is life threatening condition

    • A. Characterized by severe metabolic state: lactic acid acidosis, hypoglycemia, hyponatremia, hypotension, bradycardia, cardiovascular collapse, hypothermia, hypoventilation, coma

    • B. Precipitated by inadequate thyroid replacement,

    infection, trauma, exposure to cold temperature, CNS depressant

    Pathophysiology Iodine deficiency: iodine is necessary for TH synthesis and secretion A. Iodine deficiency occurs as

    Pathophysiology

    Iodine deficiency: iodine is necessary for TH

    synthesis and secretion

    • A. Iodine deficiency occurs as a result of

    antithyroid drugs, and lithium or iodine

    intake

    • B. In US , thyroid deficiency because of in

    adequate iodine intake is rare with the use

    of iodized salt

    Myxedema Coma Signs and symptoms:  Hypothermia  Cardiovascular collapse  Coma  Hyponatremia  Hypoglycemia

    Myxedema Coma

    Signs and symptoms:

    • Hypothermia

    • Cardiovascular collapse

    • Coma

    • Hyponatremia

    • Hypoglycemia

    • Lactic acidosis

    Nursing Assessment 1. Assessment of hypothyroidism include neurological assessment, presence of periorbital edema, presence of goiter,

    Nursing Assessment

    • 1. Assessment of hypothyroidism include

    neurological assessment, presence of periorbital edema, presence of goiter,

    reproductive history, fluid status, weight,

    activity tolerance, respiratory status

    • 2. Assessment in myxedema coma include cardiac assessment, and other assessment

    performed for hypothyroidism

    Priority nursing diagnosis for thyroid hypofunction disorder  Activity intolerance  Altered nutrition  Decrease Cardiac

    Priority nursing diagnosis for thyroid

    hypofunction disorder

    • Activity intolerance

    • Altered nutrition

    • Decrease Cardiac output

    • Hypothermia

    • Risk for skin integrity

    • Risk for injury

    Parathyroid disorder 1. The parathyroid glands are located posterior to the thyroid glands a. Their major

    Parathyroid disorder

    • 1. The parathyroid glands are located posterior to the thyroid glands

      • a. Their major function is to maintain normal serum calcium levels by secreting TH, which increases bone reabsorption of calcium

      • b. PTH respond to decrease calcium levels by increasing calcium absorption from bone, kidneys,

    and intestine

    Hyperparathyroidism  It is an Increase in PTH, which leads to hypercalcemia, hyperposphatemia, bone damage, and

    Hyperparathyroidism

    • It is an Increase in PTH, which leads to hypercalcemia, hyperposphatemia, bone

    damage, and renal damage

    Nursing assessment for Hyperparathyroidism 1. Includes neurological assessment including LOC, VS , heart rhythm, GI assessment,

    Nursing assessment for

    Hyperparathyroidism

    • 1. Includes neurological assessment including LOC, VS , heart rhythm, GI

    assessment, complain of pain, muscle

    strength, weight , I and O

    Hypoparathyroidism  It is a decrease in PTH, Which leads to hypocalcemia, hyperreflexia, and altered sensorium

    Hypoparathyroidism

    • It is a decrease in PTH, Which leads to

    hypocalcemia, hyperreflexia, and altered sensorium

    • The most common cause of hypoparathyroidism is damage or removal of the parathyroid gland during surgery

    Nursing Assessment for hypoparathyroidism

    Nursing Assessment for

    hypoparathyroidism

    Nursing Assessment for hypoparathyroidism
    NURSING MANAGEMENT

    NURSING MANAGEMENT

    Priority nursing diagnosis for parathyroid disorder  Impaired physical mobility  Risk for injury  Altered

    Priority nursing diagnosis for

    parathyroid disorder

    • Impaired physical mobility

    • Risk for injury

    • Altered urinary elimination

    • Altered nutrition

    Adrenal Cortex Hyperfunction Disorder A. Overview 1. The adrenal glands are located superior to each kidney

    Adrenal Cortex Hyperfunction

    Disorder

    A.

    Overview

    • 1. The adrenal glands are located superior to each kidney and composed of the adrenal medulla (the inner layer of adrenal gland) and the adrenal cortex (the outer layer of adrenal gland

      • a. The adrenal medulla secretes the catecholomines:

    epinephrine, norepinephrine and dopamine

    • b. The adrenal cortex secretes mineralcorticoids

    (aldosterone), glucocorticoids (cortisol, androgen, andestrogens (sex hormone)

    ADRENAL CORTEX HYPERFUNCTION DISORDER 2. The function of epinephrine and norepinephrine (catecholamines) include increasing metabolic rate,

    ADRENAL CORTEX HYPERFUNCTION DISORDER

    • 2. The function of epinephrine and norepinephrine

    (catecholamines) include increasing metabolic rate, increasing alertness, increasing insulin levels and

    the “fight or flight response

    • 3. The functions of glucocorticoids (cortisol) includes

    assisting the body’s response to stress, suppression

    of inflammation, increasing serum glucose by acting

    as insulin antagonist, it regulates CHO, fat’ and

    protein metabolism, enhancing protein synthesis,

    and increasing breakdown of protein and fatty acid

    Functions 4. The function of adrenocorticotropic hormone is for growth and development 5. The function mineralcorticoids

    Functions

    • 4. The function of adrenocorticotropic hormone

    is for growth and development

    • 5. The function mineralcorticoids (aldosterone)

    includes sodium (Na) and water retention

    and potassium excretion

    • 6. Androgens and estrogens contribute to

    growth and development

    ADRENAL CORTEX HYPERFUNCTION DISORDER  Cushing’s Syndrome or hypercortisolism result in excess production of cortisol (glucocorticoids).

    ADRENAL CORTEX HYPERFUNCTION

    DISORDER

    • Cushing’s Syndrome or hypercortisolism result in excess production of cortisol (glucocorticoids).

    • Conn’s Syndrome or Hyperaldosteronism result in excess production of aldosterone

    Cause of Hypercortisolism ( Cushing’s syndrome)  Include Adrenal tumors  Adrenal hyperplasia  Or exogenous

    Cause of Hypercortisolism

    ( Cushing’s syndrome)

    • Include Adrenal tumors

    • Adrenal hyperplasia

    • Or exogenous glucocorticoids

    Causes of hyperaldosteronism ( conn’s syndrome)  Include adrenal lesion  Or condition that stimulate overproduction

    Causes of hyperaldosteronism

    ( conn’s syndrome)

    • Include adrenal lesion

    • Or condition that stimulate overproduction of aldosterone: heart

    failure, cirrhosis of liver, dehydration, renal disease

    CUSHING’S SYNDROME

    CUSHING’S SYNDROME

    Pathophysiology of Hypercortisolism A. The functions of glucocorticoids (cortisol, ACTH) include promoting gluconeogenesis, maintaining serum glucose

    Pathophysiology of Hypercortisolism

    • A. The functions of glucocorticoids (cortisol, ACTH) include promoting gluconeogenesis, maintaining serum glucose levels,

    adaptation to stress, and augmenting

    release of catelectomines to increase blood pressure

    S/S of Hypersecretion of cortisol

    S/S of Hypersecretion of cortisol

    Nursing management for Cushing’s Syndrome  Includes vital sign: increase BP/ arrhythmias  Neurological assessment 

    Nursing management for Cushing’s

    Syndrome

    • Includes vital sign: increase BP/ arrhythmias

    • Neurological assessment

    • History of GI, renal, and reproductive problem

    • Muscle strength

    • Integument assessment

    • Weight ; presence of edema, I and O

    Nursing management for Cushing’s syndrome

    Nursing management for Cushing’s

    syndrome

    Nursing management for Cushing’s syndrome
    Nursing management for Cushing’s syndrome

    Nursing management for Cushing’s

    syndrome

    Nursing management for Cushing’s syndrome B. Preoperative and postoperative care is for adrenalectomy if performed C.

    Nursing management for Cushing’s

    syndrome

    B. Preoperative and postoperative care is for

    adrenalectomy if performed

    C. Assist in monitoring effects of radiation if

    performed

    D. Monitor for addisonian crisis cause by drug therapy

    Priority Nursing diagnosis for Cushing’s Syndrome  Fluid volume in excess  Risk for infection 

    Priority Nursing diagnosis for Cushing’s

    Syndrome

    • Fluid volume in excess

    • Risk for infection

    • Activity intolerance

    • anxiety

    • Knowledge deficit

    • Risk for impaired skin integrity

    CONN’S SYNDROME/ HYPERALDOSTERONISM

    CONN’S SYNDROME/

    HYPERALDOSTERONISM

    Causes of Conn’s Syndrome or Hyperaldosteronism  Adrenal lesion  Any condition that stimulates overproduction of

    Causes of Conn’s Syndrome or

    Hyperaldosteronism

    • Adrenal lesion

    • Any condition that stimulates overproduction of aldosterone: heart failure, cirrhosis of liver, dehydration, renal disease.

    Pathophysiology of Conn’s syndrome a. Role of aldosterone ( a mineralcorticoid) is soduim and water retention

    Pathophysiology of Conn’s syndrome

    • a. Role of aldosterone ( a mineralcorticoid) is

    soduim and water retention

    • b. Aldosterone affects tubular reabsorption of sodium and water also has role in excretion of potassium and hydrogen ions

    S/S for Conn’s Syndrome  In secondary hyperaldosteronism hypertension is uncommon  Visual disturbance  Paresthesia

    S/S for Conn’s Syndrome

    • In secondary hyperaldosteronism hypertension is uncommon

    • Visual disturbance

    • Paresthesia

    • Dysarrythmias

    • Fluid retention, renal damage, polyuria

    • Muscle weakness, tetany

    • Electrolyte and acid-base imbalance

    Nursing management for Conn’s Syndrome a. Medication 1. Spironolactone (aldactone) to treat hypertension and hypokalemia for

    Nursing management for Conn’s

    Syndrome

    a. Medication

    • 1. Spironolactone (aldactone) to treat hypertension and hypokalemia for clients who will not treat surgically

    • 2. Amiloride (midamor) for those clients unable to tolerate aldactone

    • 3. Administer glucocorticoids preoperatively as

    prescribed to prevent adrenal hyperfunction

    Nursing management for Conn’s Syndrome B. Preoperative and postoperative care for adrenalectomy C. If bilateral adrenalectomy

    Nursing management for Conn’s

    Syndrome

    B. Preoperative and postoperative care for

    adrenalectomy

    C. If bilateral adrenalectomy is performed, life

    time replacement of glucocorticoid is

    necessary D. Monitor BP, Urine output, electrolytes

    E. Low sodium diet

    F Teach side effects of medications

    Priority nursing diagnosis for Conn’s syndrome  Altered urinary elimination  Fluid volume in excess 

    Priority nursing diagnosis for Conn’s

    syndrome

    • Altered urinary elimination

    • Fluid volume in excess

    • Risk for injury

    Addison’s Crisis  It can occur, which is an acute insufficiency of adenocortical hormone from lack

    Addison’s Crisis

    • It can occur, which is an acute insufficiency of

    adenocortical hormone from lack of cortisol during stress , such as surgery or pregnancy,

    or exogenous corticosteroid therapy is

    abruptly discontinue

    • If not treated immediately, circulatory

    collapse, shock, and death may occur

    Nursing Management 1. Medication A. Addison’s Disease: administer cortisone, prednisone, fludcortisone acetate (florinef) asprescribe B, Addisonian

    Nursing Management

    1. Medication

    A. Addison’s Disease: administer cortisone,

    prednisone, fludcortisone acetate (florinef)

    asprescribe

    B, Addisonian Crisis, immediate intravenous glucocticoid replacement and fluids with

    sodium

    Anterior Pituitary Disorder A. Overview 1. The pituitary gland referred to as master gland is located

    Anterior Pituitary Disorder

    A.

    Overview

    1. The pituitary gland referred to as master gland is located at the base of the brain

    adjacent to hypothalamus, it is responsible

    for regulating endocrine function by producing hormone that affect body system

    and stimulating other endocrine glands to

    secrete hormone

    Hormones Secreted By the Pituitary glands a. Growth Hormone (GH) b. Thyroid stimulating hormone (TSH) c.

    Hormones Secreted By the Pituitary

    glands

    • a. Growth Hormone (GH)

    • b. Thyroid stimulating hormone (TSH)

    • c. Adenocorticotropic hormone (ACTH)

    • d. FSH

    • e. LH

    • f. Prolactin (PRL)

    Anterior Pituitary Disorder 3. Disorder of the anterior pituitary gland result in excessive or insufficient pituitary

    Anterior Pituitary Disorder

    3. Disorder of the anterior pituitary gland result

    in excessive or insufficient pituitary hormone disorder are as not common than other endocrine disorder

    4. Growth hormone is the hormone necessary for growth that regulates cell division and the synthesis of protein, exerts other metabolic effects on endocrine organs, skin. Skeletal muscle, cardiac muscle, and connective issue

    Hyperfunction of the Anterior Pituitary (Hyperpituitarism)  It is the result of excess production and secretion

    Hyperfunction of the Anterior

    Pituitary (Hyperpituitarism)

    • It is the result of excess production and

    secretion of one or more hormones: (GH), FSH, TSH, LH, ACTH: Leading to Tissue over

    growth.

    • The most comm0n cause of hyperpituitarism is benign adenoma

    Hypofunction of the Pituitary Gland (hypopituitarism) 1. It is aresult in a deficiency of one or

    Hypofunction of the Pituitary Gland

    (hypopituitarism)

    • 1. It is aresult in a deficiency of one or more pituitary hormones: GH, follicle stimulating hormone (FSH), TSH, LH, ACTH

    • 2. Causes include surgical removal of the pituitary gland, pituitary tumors, infection, trauma, congenital defects, radiation

    Common Disorder a. Hyperpituitarism ; Giantism and acromegaly b. Hyporpituitarism: dwarfism

    Common Disorder

    • a. Hyperpituitarism ; Giantism

    and acromegaly b. Hyporpituitarism: dwarfism

    dwarfism giantism CRETINISM

    dwarfism

    giantism

    dwarfism giantism CRETINISM

    CRETINISM

    Hyperpituitarism Giantism Acromegaly

    Hyperpituitarism

    Hyperpituitarism Giantism Acromegaly
    Hyperpituitarism Giantism Acromegaly

    Giantism

    Acromegaly

    Pathophysiology of Giantism a. Giantism is the result of growth hormone hypersecretion that begins before the

    Pathophysiology of Giantism

    • a. Giantism is the result of growth hormone hypersecretion that begins before the closure of the epiphysicial plates

      • 1. This hypersecretion leads the person to become abnormally tall reaching 7 to 8 ft. in height

      • 2. The body proportion are generally normal

      • 3. Early detection, diagnosis, and treatment has made this disorder rare in occurrence

      • 4. Common cause is tumor

    Acromegaly  It is the result of GH over secretion during continue to grow, leading to

    Acromegaly

    • It is the result of GH over secretion during continue

    to grow, leading to adulthood, bone connective tissue continue to grow , leading to disproportionate enlargement of tissue.

    • Most common cause is tumor

    • S/S include large hands and feet, protrusion of the lower jaw, coarse facial features, sign of osteoporosis, change in hand and shoe and glove size that slowly progress; systemic symptoms hypertension, CAD, CHF, enlarge adrenal gland, thyroid and parathyroid gland

    Dwarfism  Result from deficient secretion of anterior pituitary hormones  Inadequate secretion of these hormones

    Dwarfism

    • Result from deficient secretion of anterior pituitary hormones

    • Inadequate secretion of these hormones leads to growth retardation and

    accompanying metabolic disorder

    • S/S include short stature, obesity, short pitch voice, slow measuring skeletal system ,

    hyperlipidemia, hypercholesteremia

    Nursing assessment a. Assessment of gigantism includes growth chart for height and weight by age and

    Nursing assessment

    • a. Assessment of gigantism includes growth chart for

    height and weight by age and visual exam.

    • b. Assessment of acromegaly includes VS, Visual disturbances, S/S of CHF or diabetes, growth and development, symptoms and analysis of pain

    • c. Assessment for dwarfism include growth chart and development of sex organ

    • d. Diagnostic test : bone scan, cholesterol, lipid funnel

    , hormone levels

    TRANSSPHENOIDAL HYPOPHYSECTOMY

    TRANSSPHENOIDAL HYPOPHYSECTOMY

    Nursing diagnosis  Activity intolerance, body image disturbance, sexual dysfunction, anticipatory grieving, ineffective individual coping; altered

    Nursing diagnosis

    • Activity intolerance, body image

    disturbance, sexual dysfunction, anticipatory grieving, ineffective

    individual coping; altered growth

    and development

    Posterior pituitary disorder A. Overview  1. The posterior pituitary gland secrete hormones oxytoxin and antidiuretic

    Posterior pituitary disorder

    A. Overview

    • 1. The posterior pituitary gland secrete hormones oxytoxin and antidiuretic hormone (vasopressin), the purpose of antidiuretic hormone is to control serum osmolarity

    • Disorder of the posterior pituitary gland are primarily result of excessive or deficient ADH

    secretion

    DISORDER OF THE POSTERIOR PITUITARY GLAND A. DIABETES INSIPIDUS (DI ) is the result of ADH

    DISORDER OF THE POSTERIOR

    PITUITARY GLAND

    • A. DIABETES INSIPIDUS (DI) is the result of ADH insufficiency, resulting to excessive fluid excretion

      • B. SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION (SIADH) is the result of excessive secretion of ADH and water retention

    CAUSES  Diabetes Insipidus: unknown etiology in most cases, head trauma with damage to the pituitary

    CAUSES

    • Diabetes Insipidus: unknown etiology in most

    cases, head trauma with damage to the pituitary or tumor

    • SIADH: occurs most often as the result of ectopic production of ADH by malignant tumors , but may also occur as the result of

    pituitary surgery, head injury, or medications

    such as diuretics, anesthetics and barbiturates

    Nursing assessment for DI  I and O  Complain of thirst  Dry skin 

    Nursing assessment for DI

    • I and O

    • Complain of thirst

    • Dry skin

    • Sunken eyeball weakness,

    • Decreased urinary output

    • Dry mucous membrane

    S/S of DI  Polyuria  Excessive Thirst  Polydipsia  Dehydration in event the client

    S/S of DI

    • Polyuria

    • Excessive Thirst

    • Polydipsia

    • Dehydration in event the client is unable to replace fluid loss

    DI and its classification  ADH insufficiency leads to the excretion of large amount of urine

    DI and its classification

    • ADH insufficiency leads to the excretion of large amount of urine (polyuria), up to 12 L/day

    • Neurogenic DI occurs when there is a decrease in the synthesis and excretion of ADH : may be idiopathic, or may result from trauma or dysfunction of the hypothalamus or pituitary gland

    • Nephrogenic DI occurs when the renal tubules is not

    sensitive to ADH

    Nursing Management For DI a. Medications include vasopressin (pitressin, pressyn) for treatment of nuerogenic DI b.

    Nursing Management For DI

    • a. Medications include vasopressin (pitressin, pressyn) for treatment of nuerogenic DI

    • b. Administration of hypotonic solution

    • c. Increase fluid intake

    • d. Treatment is life long for chronic DI

    • e. Monitor daily weigh

    • f. Low NA diet and to avoid caffeine since this increases urine output

    • g. Educate client for medic alert bracelet

    S/S of (SIADH)  Lethargy  Confusion  Changes in neurological status  Cerebral edema 

    S/S of (SIADH)

    • Lethargy

    • Confusion

    • Changes in neurological status

    • Cerebral edema

    • Muscle cramps weakness, decrease urine

    output, fluid retention, weight gain

    Assessment of SIADH  Assess for nuerological indicator like LOC  I and O  weight

    Assessment of SIADH

    • Assess for nuerological indicator like LOC

    • I and O

    • weight

    Nursing Management For (SIADH)  Medications include diuretics, demeclocycline (declomycin)  Administration of hypertonic saline fluids

    Nursing Management For (SIADH)

    • Medications include diuretics,

    demeclocycline (declomycin)

    • Administration of hypertonic saline fluids

    • Oral fluid restriction

    • I and O and daily weight

    • Monitor for neurological changes and water retention

    Nursing Diagnosis for disorder of posterior pituitary disorder  Fluid volume in excess  Fluid volume

    Nursing Diagnosis for disorder of

    posterior pituitary disorder

    • Fluid volume in excess

    • Fluid volume deficit

    • Altered urinary elimination

    • Risk for Injury

    • Knowledge deficit

    DIABETES MELLITUS

    DIABETES MELLITUS

    CAUSES OF DM a. Type 1 DM: occurs as a result of genetic, environmental or immunological

    CAUSES OF DM

    • a. Type 1 DM: occurs as a result of genetic,

    environmental or immunological factors that may damage the pancreatic beta cells

    • b. Type 2 DM Etiology is unknown: however, obesity is the single most important risk factor

    S/S of DM a. Early manifestation of type 1 DM; polyuria, polydispia, polypaghia, glycosuria, fatigue, weight

    S/S of DM

    • a. Early manifestation of type 1 DM; polyuria,

    polydispia, polypaghia, glycosuria, fatigue, weight loss, nausea, vomiting, abdominal

    pain

    • b. Early manifestation ofin type 2 Dm : polyuria, polydipsia, blurring of vision,

    weight gain

    S/S of DM General multisystem findings 1. Sensory/ neurological: diabetic retinopathy, cataracts, glaucoma, paresthesias, loss of

    S/S of DM

    General multisystem findings

    • 1. Sensory/ neurological: diabetic retinopathy, cataracts, glaucoma, paresthesias, loss of sensation, peripheral neuropathy

    • 2. Cardiovascular assessment: coronary artery disease, peripheral vascular disease, hypertension

    • 3. G I: constipation or diarrhea

    • 4. Musculoskeletal : contractures

    S/S of DM General multisystem findings 5. Integumentary : atrophy, foot ulcer, poor wound healing, chronic

    S/S of DM

    General multisystem findings

    • 5. Integumentary : atrophy, foot ulcer, poor

    wound healing, chronic skin infections

    • 6. Renal: edema, chronic renal failure,

    albuminuria, UTI

    • 7. Reproductive assessment: Sexual dysfunction, Vaginitis

    • 8. Metabolic: hypergycemia, hypokalemia, metabolic acidosis

    Symptoms of DKA  Abdominal pain , nausea and vomiting  Metabolic acidosis  Fruity breath

    Symptoms of DKA

    • Abdominal pain , nausea and vomiting

    • Metabolic acidosis

    • Fruity breath odor

    • Kaussmaul’s respiration

    • Altered LOC

    • Coma and death if not untreated

    Complication of DKA  Hypoglycemia  Atherosclerosis  CVA, PVD  Retinopathy  Paresthesia (especially feet)

    Complication of DKA

    • Hypoglycemia

    • Atherosclerosis

    • CVA, PVD

    • Retinopathy

    • Paresthesia (especially feet)

    • Renal failure

    • Carpal tunnel syndrome,

    • Peridontal disease

    • Gangrene, amputation, inability to heal

    Diagnostic test for DM  Serum fasting sugar Increase (hyperglycemia) increase to 126 mg/dl  Serum

    Diagnostic test for DM

    • Serum fasting sugar Increase (hyperglycemia) increase to 126 mg/dl

    • Serum glycosylated hemoglobin levels; increase to 7 percent

    • Urine for glucose, and ketones positive

    • Urine for protein is positive

    • Serum potassium is decrease

    • 2- hours plasma glucose (after meal) is increase to 200 mg/ dl

    • Cholesterol and triglyceride levels is elevated

    Nursing management for DM 1. Medication include insulin and hypoglycemic agent a. Type 1 diabetes: regular

    Nursing management for DM

    • 1. Medication include insulin and hypoglycemic agent

      • a. Type 1 diabetes: regular insulin, NPH insulin such as 70/30

      • b. Type 2 diabetes: oral agents such as glipizide (glocotrol), glyburide (micronase), tolazamide (tolomide), Metformin (glucophage) etc.

        • 2. Monitor I and O, serum glucose, electrolytes

    Client education for DM A. Teach sign and symptoms of hypoglycemia (irritability, fatigue, weakness, tremors, headache,

    Client education for DM

    • A. Teach sign and symptoms of hypoglycemia

    (irritability, fatigue, weakness, tremors, headache, possible coma) and

    hyperglycemia with appropriate

    interventions

    • B. Teach for self administration of insulin or

    hypoglycemic agent

    Insulin therapy and insulin preparation  In type I DM exogenous insulin must be administered for

    Insulin therapy and insulin preparation

    • In type I DM exogenous insulin must be

    administered for life because the body loses the ability to produce insulin

    • Reaction time of most common insulin preparation

    • Rapid-acting insulin

    • Short acting insulin

    • Intermediate- acting

    • Long acting insulin

    • Very long acting insulin

    Categories of insulin preparation  Rapid acting it is indicated for rapid reduction of glucose level,

    Categories of insulin preparation

    • Rapid acting it is indicated for rapid reduction of glucose level, to treat postprandial hyperglycemia, and/or to prevent nocturnal hyperglycemia

    • Agent: lispro (humalog)- onset 10-15 min, peak 1 hour, duration 2-4 hours

    • Apart (novolog) onset 5 to 15 min, peak 40- 50 min duration 2-4 hours

    Categories of insulin preparation  Short acting usually administered 20-30 min before meal; may be taken

    Categories of insulin preparation

    • Short acting usually administered 20-30 min before meal; may be taken alone or in combination with long acting insulin

    • Agent : Regular (humalog R), Novolin R, Iletin

    II regular)

    • Onset ½ -1 hours, peak 1 hour, duration 4-6 hours

    Categories of insulin preparation  Intermediate Acting it is usually taken after food  Agent: NPH(

    Categories of insulin preparation

    • Intermediate Acting it is usually taken after food

    • Agent: NPH( neutral protamine hagadorn)

    • Onset: 2-4 hours, peak: 4-12 hours, Duration 16 to

      • 20 hours

    • Agent: Humalin N, Iletin II lente, Iletin II NPH, Novolin L (lente) , Iletin II (NPH), Novolin Lente, Novolin (NPH)

    • Onset: 3-4 hours , Peak: 4-12 hours, Duration:16 -

      • 20 Hours

    Categories of insulin preparation  Long Acting Insulin it is used to control fasting glucose level

    Categories of insulin preparation

    • Long Acting Insulin it is used to control fasting glucose level

    • Agent: Ultra lente ( “UL”)

    • Onset: 6-8 h, Peak:12-16 h, Duration: 20-30 h

    • Very Long Acting it is used for basal dose (“Peakless”) that is the insulin is absorbed slowly for

    24 hours and can be given once a day and given HS originally, however it is now approved to be given

    once a day at any time of the day but at same time to prevent overlap of action. It should not mix with other insulin preparation to avoid precipitation

    because of each PH of 4

    Complication of insulin therapy  Local allergic reaction ( readiness, swelling , tenderness and indurations or

    Complication of insulin therapy

    • Local allergic reaction ( readiness, swelling ,

    tenderness and indurations or 2-4 cm wheal) may appear at the injection site

    • Systemic allergic reaction it is rare, when occur there is local skin reaction that gradually spreads to generalized urticaria, treatment desensitization.

    • Insulin lipodystrophy it refers to a localized reaction in form of lipoatrophy or lipohypertrophy at the injection site

    • Resistance to insulin injection.

    Complication of insulin therapy  Morning hyperglycemia a. Insulin Wanning it is progressive rise in blood

    Complication of insulin therapy

    • Morning hyperglycemia

      • a. Insulin Wanning it is progressive rise in blood glucose from bedtime to morning

      • b. Dawn Phenomenom it is relatively normal blood

    glucose until about 3 Am, when the levels begins to

    rise

    • c. Somogyi Effect it is normal or elevated blood glucose at bedtime, a decrease at 2-3 AM to

    hypoglycemic levels, and a subsequent increase

    cause by the production of counterregulatory hormones

    Patient Education Self injection of insulin  Insulin injection are self administered into subcutaneous tissue with

    Patient Education

    Self injection of insulin

    • Insulin injection are self administered into

    subcutaneous tissue with the use of special insulin syringe.

    Self Injection

    • 1. With on hand , stabilize the skin by spreading it or pinching large area

    • 2. Pick up syringe with the other hand and hold it as you would a pencil. Insert needle straight into the skin.

    Self injection of insulin 3. To inject the insulin, push the plunger all way in 4.

    Self injection of insulin

    3. To inject the insulin, push the plunger all way

    in

    4. Pull needle straight out of skin. Press cotton

    ball over the injection site for several seconds

    5 Use disposable syringe only once and discard into hard plastic container (with a tight-fitting

    top) such as empty bleach container. Follow

    state regulations for disposal of needle

    Selecting and Rotating the injection site Four main areas for injection 1. Abdomen 2. Upper arms

    Selecting and Rotating the injection site

    Four main areas for injection

    • 1. Abdomen

    • 2. Upper arms (posterior surface)

    • 3. Thighs (anterior surface)

    • 4. Hips

    Note: The speed of absorption is greatest in the

    abdomen and decreases progressively in the

    arm, thight and hip respectively

    Patient Education  Teach the patient how to get CBG or self monitoring glucose  Teach

    Patient Education

    • Teach the patient how to get CBG or self

    monitoring glucose

    • Teach the client about proper dietary

    management for diabetes

    • Teach proper diabetic foot care and wound care

    • Teach for proper exercise for diabetes