Endocrine Disorders

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Information about Endocrine Disorders
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Published on February 12, 2009

Author: nionoveno

Source: slideshare.net

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Slideshow presentatin of Endocrine Disorders

MAJOR DISORDERS OF THE ENDOCRINE SYSTEM Nio C. Noveno, RN, MAN

 

HORMONE REGULATION: NEGATIVE FEEDBACK MECHANISM If the client is healthy, the concentration of hormones is maintained at a constant level. When the hormone concentration rises, further production of that hormone is inhibited. When the hormone concentration falls, the rate of production of that hormone increases.

If the client is healthy,

the concentration of hormones

is maintained at a constant level.

When the hormone concentration rises,

further production of that hormone is inhibited.

When the hormone concentration falls,

the rate of production of that hormone increases.

HORMONE REGULATION: NEGATIVE FEEDBACK MECHANISM

DISORDERS OF THE ENDOCRINE SYSTEM Primary Problem in the target gland; autonomous Secondary Problem in the pituitary Tertiary Problem in the hypothalamus

Primary

Problem in the target gland; autonomous

Secondary

Problem in the pituitary

Tertiary

Problem in the hypothalamus

ANTERIOR PITUITARY DISORDERS

 

 

HYPERPITUITARISM May be due to overactivity of gland or the result of an adenoma Characterized by: Excessive serum concentration of pituitary hormones (GH, ACTH, PRL) Morphologic and functional changes in the anterior pituitary

May be due to overactivity of gland

or the result of an adenoma

Characterized by:

Excessive serum concentration

of pituitary hormones (GH, ACTH, PRL)

Morphologic and functional changes

in the anterior pituitary

GROWTH HORMONE HYPERSECRETION Gigantism Prior to closure of the epiphyses; proportional growth Acromegaly After closure of the epiphyses; disproportional growth

Gigantism

Prior to closure

of the epiphyses;

proportional growth

Acromegaly

After closure

of the epiphyses;

disproportional

growth

HYPERPITUITARISM: CLINICAL MANIFESTATIONS A rthritis C hest: barrel-shaped R ough facial features O dd sensations: hands and feet M uscle weakness & fatigue E nlargement of organs G rowth of coarse hair A menorrhea; breast milk production L oss of vision; headaches I mpotence; increased perspiration S noring

A rthritis

HYPERPITUITARISM: CLINICAL MANIFESTATIONS

HYPERPITUITARISM: MANAGEMENT Medication Bromocriptine- Cabergoline (dopamine agonists) GH hypersecretion and prolactinoma Ocreotide (somatostatin) GH hypersecretion Radiation Indicated for larger tumors Surgery Trans-sphenoidal hypophysectomy

Medication

Bromocriptine-

Cabergoline

(dopamine agonists)

GH hypersecretion

and prolactinoma

Ocreotide

(somatostatin)

GH hypersecretion

Radiation

Indicated for larger

tumors

Surgery

Trans-sphenoidal

hypophysectomy

TRANS-SPHENOIDAL HYPOPHYSECTOMY Post-surgery nursing care Semi- to high- Fowler’s position Protect from infection and stressful situations Hormone replacement Constant neurologic checks MIOW to check for DI WOF CSF leak Encourage deep-breathing, but not coughing Institute measures to prevent constipation [straining increases ICP]

Post-surgery nursing care

Semi- to high- Fowler’s position

Protect from infection and stressful situations

Hormone replacement

Constant neurologic checks

MIOW to check for DI

WOF CSF leak

Encourage deep-breathing, but not coughing

Institute measures to prevent constipation

[straining increases ICP]

HYPOPITUITARISM Deficiency of one or more anterior pituitary hormones Causes Infections / Inflammatory disorders Autoimmune diseases Congenital absence Tumor Surgery / Radiation therapy

Deficiency of one or more

anterior pituitary hormones

Causes

Infections / Inflammatory disorders

Autoimmune diseases

Congenital absence

Tumor

Surgery / Radiation therapy

HYPOPITUITARISM Simmonds' disease [Panhypopituitarism] Complete absence of pituitary hormones Cachexia: most prominent feature Follows destruction of the pituitary by surgery, infection, injury, or a tumor Sheehan’s syndrome [Post-partum pituitary necrosis] A complication of delivery Results from severe blood loss and hypovolemia  Pituitary ischemia

Simmonds' disease

[Panhypopituitarism]

Complete absence

of pituitary hormones

Cachexia:

most prominent feature

Follows destruction

of the pituitary

by surgery, infection,

injury, or a tumor

HYPOPITUITARISM: CLINICAL MANIFESTATIONS Hypo -thermia, -glycemia, -tension Loss of vision, strength, libido, & secondary sexual characteristics

Hypo -thermia, -glycemia, -tension

HYPOPITUITARISM: MANAGEMENT Medication Hormonal substitution [maybe for life] Corticosteroids Levothyroxine Androgen / Estrogen Growth hormone Radiation Indicated for larger tumors Surgery Trans-sphenoidal hypophysectomy

Medication

Hormonal substitution

[maybe for life]

Corticosteroids

Levothyroxine

Androgen / Estrogen

Growth hormone

Radiation

Indicated for larger

tumors

Surgery

Trans-sphenoidal

hypophysectomy

POSTERIOR PITUITARY DISORDERS

 

 

DIABETES INSIPIDUS Characterized by massive polyuria due to either lack of ADH or renal insensitivity Central DI Due to a deficiency in ADH production Nephrogenic DI Due to a defect in the kidney tubules that interferes with water absorption Polyuria is unresponsive to ADH, which is secreted normally.

Characterized by massive polyuria

due to either lack of ADH or renal insensitivity

Central DI

Due to a deficiency in ADH production

Nephrogenic DI

Due to a defect in the kidney tubules

that interferes with water absorption

Polyuria is unresponsive to ADH,

which is secreted normally.

DIABETES INSIPIDUS: DIAGNOSTICS Fluid deprivation test Administration of desmopressin 24-hour urine collection for volume, glucose, and creatinine Serum for glucose, urea nitrogen, calcium, uric acid, potassium, sodium

Fluid deprivation test

Administration of desmopressin

24-hour urine collection

for volume, glucose, and creatinine

Serum for glucose, urea nitrogen, calcium, uric acid, potassium, sodium

DIABETES INSIPIDUS: MANAGEMENT Central DI : Desmopressin, Lypressin [intranasal] Vasopressin tannate in oil [IM] Nephrogenic DI : Indomethacin- -hydrochlorothiazide -desmopressin -amiloride Clofibrate, chlorpropamide

Central DI :

Desmopressin, Lypressin [intranasal]

Vasopressin tannate in oil [IM]

Nephrogenic DI :

Indomethacin-

-hydrochlorothiazide

-desmopressin

-amiloride

Clofibrate, chlorpropamide

SYNDROME OF INAPPROPRIATE ADH Disorder due to excessive ADH release Clinical Manifestations Persistent excretion of concentrated urine Signs of fluid overload Hyponatremia LOC changes No edema

Disorder due to excessive ADH release

Clinical Manifestations

Persistent excretion of concentrated urine

Signs of fluid overload

Hyponatremia

LOC changes

No edema

SIADH: DIAGNOSTICS Low serum sodium [<135 mEq/L] Low serum osmolality High urine osmolality [>100 mOsmol/kg] High urine sodium excretion [>20 mmol/L] Normal renal function: low BUN [<10 mg/dL]

Low serum sodium [<135 mEq/L]

Low serum osmolality

High urine osmolality [>100 mOsmol/kg]

High urine sodium excretion [>20 mmol/L]

Normal renal function: low BUN [<10 mg/dL]

SIADH: MANAGEMENT Maintain fluid balance MIOW Fluid restriction Loop diuretic [If with evidence of fluid overload] Lithium or demeclocycline [Chronic treatment] Maintain Na balance Increased Na intake Emergency treatment of 3% NaCl, followed by furosemide [If serum Na <120, or if patient is seizing] Excessively rapid correction of hyponatremia may cause central pontine myelinolysis!

Maintain fluid balance

MIOW

Fluid restriction

Loop diuretic

[If with evidence of fluid overload]

Lithium or demeclocycline

[Chronic treatment]

Maintain Na balance

Increased Na intake

Emergency treatment of 3% NaCl, followed by furosemide

[If serum Na <120, or if patient is seizing]

Excessively rapid correction of hyponatremia may cause central pontine myelinolysis!

THYROID DISORDERS

 

 

THYROID FUNCTION TESTS Serum TSH Single best screening test [high sensitivity] 0.38 – 6.15 mcU/mL If TSH is normal, fT 4 should be normal. Screening required beginning 35 years, then q 5 years thereafter Also used for monitoring thyroid hormone replacement therapy

Serum TSH

Single best screening test [high sensitivity]

0.38 – 6.15 mcU/mL

If TSH is normal, fT 4 should be normal.

Screening required beginning 35 years,

then q 5 years thereafter

Also used for monitoring thyroid hormone

replacement therapy

THYROID FUNCTION TESTS Serum fT 4 A direct measurement of free thyroxine, the only metabolic fraction of T 4 0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L) Used to confirm an abnormal TSH

Serum fT 4

A direct measurement of free thyroxine,

the only metabolic fraction of T 4

0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L)

Used to confirm an abnormal TSH

THYROID FUNCTION TESTS Total serum T 3 and T 4 T 3 70 to 220 ng/dL (1.15 to 3.10 nmol/L) T 4 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L) T 3 levels appear to be a more accurate indicator of hyperthyroidism.

Total serum T 3 and T 4

T 3 70 to 220 ng/dL (1.15 to 3.10 nmol/L)

T 4 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L)

T 3 levels appear to be a more accurate

indicator of hyperthyroidism.

THYROID FUNCTION TESTS T 3 resin uptake test Indirect measurement of unsaturated thyroid-binding globulin (TBG) 25 – 35% uptake Thyroid antibodies 5 – 10% of the population Grave’s: 80% Hashimoto’s: 100%

T 3 resin uptake test

Indirect measurement of unsaturated

thyroid-binding globulin (TBG)

25 – 35% uptake

Thyroid antibodies

5 – 10% of the population

Grave’s: 80%

Hashimoto’s: 100%

THYROID FUNCTION TESTS Thyroid scan / Radioscan / Scintiscan Utilizes a gamma camera and radioisotopes 123 I, thallium, americium, technetium-99m [ 99m Tc] pertechnetate Results Hot areas: increased activity Cold areas: decreased activity

Thyroid scan / Radioscan / Scintiscan

Utilizes a gamma camera and radioisotopes

123 I, thallium, americium,

technetium-99m [ 99m Tc] pertechnetate

Results

Hot areas: increased activity

Cold areas: decreased activity

THYROID FUNCTION TESTS Radioactive iodine uptake (RAIU) Measures the proportion of administered tracer dose of ¹²³I present in the thyroid gland at a specific time after administration Results Hyper: high uptake Hypo: low uptake

Radioactive iodine uptake (RAIU)

Measures the proportion of administered tracer

dose of ¹²³I present in the thyroid gland

at a specific time after administration

Results

Hyper: high uptake

Hypo: low uptake

THYROID FUNCTION TESTS Fine-needle aspiration biopsy Sampling of thyroid tissue to detect malignancy Initial test for evaluation of thyroid masses Results Negative [benign] Positive [malignant] Indeterminate [suspicious] Inadequate [non-diagnostic]

Fine-needle aspiration biopsy

Sampling of thyroid tissue to detect malignancy

Initial test for evaluation of thyroid masses

Results

Negative [benign]

Positive [malignant]

Indeterminate [suspicious]

Inadequate [non-diagnostic]

THYROID FUNCTION TESTS Nursing Implications Determine whether the patient has taken medications or agents that contain iodine [antiseptics, multivitamins, cough syrup, amiodarone] because these may alter the test results. Assess for allergy to iodine or shellfish. For scans, tell patient that radiation is only minimal.

Nursing Implications

Determine whether the patient has taken medications or agents that contain iodine [antiseptics, multivitamins, cough syrup, amiodarone] because these may alter the test results.

Assess for allergy to iodine or shellfish.

For scans, tell patient that radiation is only minimal.

HYPERTHYROIDISM Increased basal metabolic rate (BMR) Causes Grave’s disease (autoimmune) Initial manifestation of thyroiditis TSH-screening pituitary tumor Toxic adenoma Factitious thyrotoxicosis Amiodarone therapy

Increased basal metabolic rate (BMR)

Causes

Grave’s disease (autoimmune)

Initial manifestation of thyroiditis

TSH-screening pituitary tumor

Toxic adenoma

Factitious thyrotoxicosis

Amiodarone therapy

HYPERTHYROIDISM: CLINICAL MANIFESTATIONS G I hypermotility R apid weight loss A pprehension V olume deficit; voracious appetite E xophthalmos; erratic menses S ystolic BP elevated; sweating [tremors, tachycardia, palpitations]  in secondary disease  in primary disease TSH

G I hypermotility

HYPERTHYROIDISM: CLINICAL MANIFESTATIONS

THYROID STORM / THYROTOXIC CRISIS Marked delirium Severe tachycardia Vomiting Diarrhea Dehydration High fever Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid surgery, RAI Increased systemic adrenergic activity: Severe hypermetabolism

Marked delirium

Severe tachycardia

Vomiting

Diarrhea

Dehydration

High fever

HYPERTHYROIDISM: MANAGEMENT Anti-thyroid drugs Propylthiouracil (PTU); methimazole Blocks thyroid hormone (TH) synthesis Used for pregnant women and patients who have refused surgery or RAI treatment During pregnancy, PTU is DOC. 1% of infants born to mothers on anti- thyroid therapy will be hypothyroid. WOF agranulocytosis.

Anti-thyroid drugs

Propylthiouracil (PTU); methimazole

Blocks thyroid hormone (TH) synthesis

Used for pregnant women and patients

who have refused surgery or RAI treatment

During pregnancy, PTU is DOC.

1% of infants born to mothers on anti-

thyroid therapy will be hypothyroid.

WOF agranulocytosis.

HYPERTHYROIDISM: MANAGEMENT RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s) Adjunct to other anti-thyroid drugs in preparation for thyroidectomy Treatment for thyrotoxic crisis Inhibit release and synthesis of TH Decrease vascularity of the thyroid gland Decrease thyroidal uptake of RAI

RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s)

Adjunct to other anti-thyroid drugs

in preparation for thyroidectomy

Treatment for thyrotoxic crisis

Inhibit release and synthesis of TH

Decrease vascularity of the thyroid gland

Decrease thyroidal uptake of RAI

HYPERTHYROIDISM: MANAGEMENT Medications to relieve the symptoms related to the increased metabolic rate: Digitalis, propranolol (Inderal), phenobarbital Well-balanced, high-calorie diet with vitamin and mineral supplements Subtotal or total thyroidectomy

Medications to relieve the symptoms

related to the increased metabolic rate:

Digitalis, propranolol (Inderal), phenobarbital

Well-balanced, high-calorie diet

with vitamin and mineral supplements

Subtotal or total thyroidectomy

RAI THERAPY : NURSING IMPLICATIONS NPO post-midnight prior to administration [Food may delay absorption] After initial dose: Urine and saliva slightly radioactive x 24H Vomitus highly radioactive x 6-8H Institute full radiation precautions. Instruct the patient to use appropriate disposal methods when coughing and expectorating.

NPO post-midnight prior to administration

[Food may delay absorption]

After initial dose:

Urine and saliva slightly radioactive x 24H

Vomitus highly radioactive x 6-8H

Institute full radiation precautions.

Instruct the patient to use appropriate disposal methods when coughing and expectorating.

K OR NA IODIDE, SSKI (LUGOL’S) : NURSING IMPLICATIONS Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste. Give iodides through a straw to avoid teeth discoloration. Force fluids to prevent fluid volume deficit. Warn patient that sudden withdrawal may precipitate a thyrotoxic crisis. Store in a light-resistant container.

Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste.

Give iodides through a straw to avoid teeth discoloration.

Force fluids to prevent fluid volume deficit.

Warn patient that sudden withdrawal may precipitate a thyrotoxic crisis.

Store in a light-resistant container.

HYPOTHYROIDISM A state of low serum TH levels or cellular resistance to TH A utoimmune D evelopmental D ietary I odine deficiency O ncologic D rugs I atrogenic N on-thyroidal E ndocrine

A state of low serum TH levels

or cellular resistance to TH

HYPOTHYROIDISM Causes Chronic autoimmune [Hashimoto’s] thyroiditis Hypothalamic failure to produce TRH Pituitary failure to produce TSH Inborn errors of TH synthesis Thyroidectomy / Radiation therapy Anti-thyroid therapy Iodine deficiency

Causes

Chronic autoimmune [Hashimoto’s] thyroiditis

Hypothalamic failure to produce TRH

Pituitary failure to produce TSH

Inborn errors of TH synthesis

Thyroidectomy / Radiation therapy

Anti-thyroid therapy

Iodine deficiency

HYPOTHYROIDISM Classified according to the time of life in which it occurs Cretinism In infants and young children Lymphocytic thyroiditis Appears after 6 years of age and peaks during adolescence; self-limiting Hypothyroidism without myxedema Mild thyroid failure in older children and adults Hypothyroidism with myxedema Severe thyroid failure in older individuals

Classified according to the time of life in which it occurs

Cretinism

In infants and young children

Lymphocytic thyroiditis

Appears after 6 years of age

and peaks during adolescence; self-limiting

Hypothyroidism without myxedema

Mild thyroid failure in older children and adults

Hypothyroidism with myxedema

Severe thyroid failure in older individuals

HYPOTHYROIDISM: CLINICAL MANIFESTATIONS D ry, brittle hair; dry, coarse skin E dema (periorbital) R educed BMR [bradycardia, bradypnea] A pathy; anorexia; anemia I ncreased weight; intolerance to cold L ethargy; loss of libido E nlarged tongue D rooling  in secondary disease  in primary disease TSH

D ry, brittle hair; dry, coarse skin

MYXEDEMA COMA Hypotension Bradycardia Hypothermia Hyponatremia Hypoglycemia Respiratory failure Coma Precipitating Factors Acute illness Rapid withdrawal of thyroid medication Anesthesia / Surgery Hypothermia Opioid use

Hypotension

Bradycardia

Hypothermia

Hyponatremia

Hypoglycemia

Respiratory failure

Coma

HYPOTHYROIDISM: MANAGEMENT Prevention Prophylactic iodine supplements to decrease the incidence of iodine-deficient goiter Symptomatic cases Hormonal replacement Levothyroxine (Synthroid) Liothyronine (Cytomel) Liotrix (Thyrolar) Dosage increased q 2-3 weeks especially in elderly patients

Prevention

Prophylactic iodine supplements to decrease

the incidence of iodine-deficient goiter

Symptomatic cases

Hormonal replacement

Levothyroxine (Synthroid)

Liothyronine (Cytomel)

Liotrix (Thyrolar)

Dosage increased q 2-3 weeks

especially in elderly patients

HYPOTHYROIDISM: MANAGEMENT Tell patient to WOF: Chest pain, palpitations, sweating, nervousness, and other S/S of overdosage Instruct the patient to take TH at the same time each day to maintain constant hormone levels. Suggest a morning dosage to prevent insomnia. Monitor apical pulse and BP. If pulse >100 bpm, withhold drug.

Tell patient to WOF:

Chest pain, palpitations, sweating,

nervousness, and other S/S of overdosage

Instruct the patient to take TH at the same time

each day to maintain constant hormone levels.

Suggest a morning dosage to prevent insomnia.

Monitor apical pulse and BP.

If pulse >100 bpm, withhold drug.

HYPOTHYROIDISM: NURSING INTERVENTIONS Diet : high-bulk, low-calorie Encourage activity Maintain warm environment Administer cathartics and stool softeners To prevent myxedema coma , tell patient to continue course of thyroid medication even if symptoms subside. Maintain patent airway Administer medications: Synthroid, glucose, corticosteroids IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness

Diet : high-bulk, low-calorie

Encourage activity

Maintain warm environment

Administer cathartics

and stool softeners

To prevent

myxedema coma ,

tell patient to continue

course of thyroid

medication even if

symptoms subside.

PARATHYROID DISORDERS

 

 

HYPERPARATHYROIDISM Primary Single adenoma Genetic disorders Multiple endocrine neoplasias Secondary Rickets Vitamin D deficiency Chronic renal failure Phenytoin or laxative abuse

Primary

Single adenoma

Genetic disorders

Multiple endocrine neoplasias

Secondary

Rickets

Vitamin D deficiency

Chronic renal failure

Phenytoin or laxative abuse

HYPERPARATHYROIDISM: CLINICAL MANIFESTATIONS C onstipation A pathy L ordosis C ardiac dysrhythmias U pset GIT L ow energylevels I ncreased BP  PO 4  PTH Calcium Alkaline phospatase

C onstipation

HYPERPARATHYROIDISM: MANAGEMENT Surgery to remove adenoma Force fluids; limit dietary calcium intake For life-threatening hypercalcemia: Furosemide Bisphosphonates [Etidroanate (Didrodinel), pamidronate] Calcitonin (Cibacalcin, Miacalcin) Plicamycin (Mithracin) + glucocorticoid Mithramycin

Surgery to remove adenoma

Force fluids; limit dietary calcium intake

For life-threatening hypercalcemia:

Furosemide

Bisphosphonates

[Etidroanate (Didrodinel), pamidronate]

Calcitonin (Cibacalcin, Miacalcin)

Plicamycin (Mithracin) + glucocorticoid

Mithramycin

HYPOPARATHYROIDISM Causes Congenital absence or malfunction of the parathyroids Autoimmune destruction Removal or injury to one or more parathyroids during neck surgery Massive thyroid radiation therapy Ischemic parathyroid infarction during surgery

Causes

Congenital absence

or malfunction of the parathyroids

Autoimmune destruction

Removal or injury to one or more

parathyroids during neck surgery

Massive thyroid radiation therapy

Ischemic parathyroid infarction during surgery

HYPOPARATHYROIDISM: CLINICAL MANIFESTATIONS D yspnea; dysrhythmias E xtremities: tingling F otophobia I ncreased bone density C hvostek sign; cramps I rritability T rousseau sign; tetany  PO 4  PTH Calcium Alkaline phospatase

D yspnea; dysrhythmias

HYPERTHYROIDISM: MANAGEMENT IV Ca chloride or gluconate [emergency treatment] DOC post-thyroidectomy Oral Ca salts (Ca carbonate or gluconate) Vitamin D supplementation Increase intestinal Ca absorption Dihydrotachysterol, ergocalciferol

IV Ca chloride or gluconate [emergency treatment]

DOC post-thyroidectomy

Oral Ca salts (Ca carbonate or gluconate)

Vitamin D supplementation

Increase intestinal Ca absorption

Dihydrotachysterol, ergocalciferol

T rousseau’s & Chvostek’s E levated serum PO 4 ; low Ca 2+ T ingling A lkalosis; Arrhythmias N arrowing of airway I rritability C ramps

HYPOPARATHYROIDISM Parathormone injections [in acute attacks] WOF allergies Diet: High-calcium [spinach], low-phosphate [milk, cheese, egg yolks] Al(OH) 2 , Gelusil, Amphogel p.c. Pentobarbital (Nembutal) [calm environment]

Parathormone injections [in acute attacks]

WOF allergies

Diet: High-calcium [spinach], low-phosphate [milk, cheese, egg yolks]

Al(OH) 2 , Gelusil, Amphogel p.c.

Pentobarbital (Nembutal)

[calm environment]

T C AKE ARE ETANY RACHEOSTOMY ALCIUM GLUCONATE ALCIUM 8.6 – 10.6 mg / dL

PHEOCHROMOCYTOMA

ADRENAL GLANDS

ADRENAL MEDULLA Release cathecholamines Epinephrine Norephinephrine Released during “fight or flight” situations (sympathetic effect)

Release cathecholamines

Epinephrine

Norephinephrine

Released during “fight or flight” situations (sympathetic effect)

PHEOCHROMOCYTOMA Adrenal tumor Increased Epi and NEpi Heredity

Adrenal tumor

Increased Epi and NEpi

Heredity

PHEOCHROMOCYTOMA H eadache A nxiety N ausea E ye disturbances S evere hypertension

H eadache

A nxiety

N ausea

E ye disturbances

S evere hypertension

PHEOCHROMOCYTOMA BP HR Diaphoresis BMR VMA Glucose

PHEOCHROMOCYTOMA Adrenalectomy Steroid treatment Antihypertensive and antidysrhythmic nitroprusside (Nipride) propranolol (Inderal) phentolamine (Regitine)

Adrenalectomy

Steroid treatment

Antihypertensive and antidysrhythmic

nitroprusside (Nipride)

propranolol (Inderal)

phentolamine (Regitine)

PHEOCHROMOCYTOMA MBP / MIO Fluid replacements Decrease environmental stimulation Maintenance doses of steroids Follow-up check up 24-hour urine specimens [VMA and catecholamine studies] Avoid : coffee, chocolate, beer, wine, citrus fruit, bananas, and vanilla 24h before test

MBP / MIO

Fluid replacements

Decrease environmental stimulation

Maintenance doses of steroids

Follow-up check up

24-hour urine specimens

[VMA and catecholamine studies]

Avoid : coffee, chocolate, beer, wine, citrus fruit, bananas, and vanilla 24h before test

ADDISON'S DISEASE

ADRENAL CORTEX HORMONES Glucocorticoids Cortisol, corticosterone Increase blood glucose levels by increasing rate of gluconeogenesis Increase protein catabolism Increase mobilization of fatty acids Promote sodium and water retention Anti-inflammatory effect Aid the body in coping with stress

Glucocorticoids

Cortisol, corticosterone

Increase blood glucose levels by increasing rate of gluconeogenesis

Increase protein catabolism

Increase mobilization of fatty acids

Promote sodium and water retention

Anti-inflammatory effect

Aid the body in coping with stress

ADRENAL CORTEX HORMONES Mineralocorticoids Aldosterone, Corticosterone, Deoxycorticosterone Regulate fluid and electrolyte balance Stimulate reabsorption of sodium, chloride and water Stimulate potassium excretion Under the control of Renin-Angiotensin-Aldosterone system (RAAS)

Mineralocorticoids

Aldosterone, Corticosterone, Deoxycorticosterone

Regulate fluid and electrolyte balance

Stimulate reabsorption of sodium, chloride and water

Stimulate potassium excretion

Under the control of Renin-Angiotensin-Aldosterone system (RAAS)

 

ADRENAL CORTEX HORMONES Sex hormones Androgens, Estrogens Influences the development of sexual characteristics

Sex hormones

Androgens, Estrogens

Influences the development of sexual characteristics

 

ADDISON'S DISEASE Hyposecretion of adrenocortical hormones Destruction of the cortex Idiopathic atrophy

Hyposecretion of adrenocortical hormones

Destruction of the cortex

Idiopathic atrophy

ADDISON'S DISEASE W eakness E xcess stress A / N / V / D K & ACTH elevation; Low Na, BP, cortisol, glucose

W eakness

E xcess stress

A / N / V / D

K & ACTH elevation; Low Na, BP, cortisol, glucose

 

ADDISON'S DISEASE Replacement of hormones Hydrocortisone; Fludrocortisone PNSS (0.9 NaCl) Dextrose Diet : High-CHO & CHON Low potassium, high sodium

Replacement of hormones

Hydrocortisone; Fludrocortisone

PNSS (0.9 NaCl)

Dextrose

Diet :

High-CHO & CHON

Low potassium, high sodium

ADDISON'S DISEASE VS, weight, and serum glucose level 24-hour urine specimens [LOW 17- hydroxycorticosteroids & 17-ketosteroids] Electrolyte levels:  K;  Na Bronze-skin Changes in energy or activity

VS, weight, and serum glucose level

24-hour urine specimens

[LOW 17- hydroxycorticosteroids & 17-ketosteroids]

Electrolyte levels:  K;  Na

Bronze-skin

Changes in energy or activity

ADDISON’S DISEASE

ADDISON'S DISEASE MVS [4x / day] Infection, Addisonian crisis, dehydration MIOW / MBP / MBG Give steroids with milk or an antacid Avoid : Contacts & Stress

MVS [4x / day]

Infection, Addisonian crisis, dehydration

MIOW / MBP / MBG

Give steroids with milk or an antacid

Avoid : Contacts & Stress

CUSHING'S SYNDROME

CUSHING'S DISEASE A drenal hyperplasia / tumor C ushing’s disease T umor-secreting ACTH H ypothalamic

A drenal hyperplasia / tumor

C ushing’s disease

T umor-secreting ACTH

H ypothalamic

B uffalo hump U nusual behavior (depression, personality changes, fatigability) F acial features (moonface, hirsutism in women) F at (truncal obesity) A CTH and cortisol in blood elevated; L oss of muscle mass O verextended skin (abdominal striae with easy bruisability)

B uffalo hump

U nusual behavior (depression, personality changes, fatigability)

F acial features (moonface, hirsutism in women)

F at (truncal obesity)

A CTH and cortisol in blood elevated;

L oss of muscle mass

O verextended skin (abdominal striae with easy bruisability)

H ypertension, hyperglycemia, hypernatremia U rinary cortisol elevated M enstrual irregularities P orosity of bones (osteoporosis)

H ypertension, hyperglycemia, hypernatremia

U rinary cortisol elevated

M enstrual irregularities

P orosity of bones (osteoporosis)

CUSHING’S SYNDROME

CUSHING'S SYNDROME Remove exogenous steroids Hypophysectomy or irradiation Adrenalectomy

Remove exogenous steroids

Hypophysectomy or irradiation

Adrenalectomy

CUSHING'S SYNDROME Cyproheptadine (Periactin) Metyrapone Mitotane (Lysodren) Aminoglutethamide (Cytadren) Potassium supplements High-CHON; Low Na

Cyproheptadine (Periactin)

Metyrapone

Mitotane (Lysodren)

Aminoglutethamide (Cytadren)

Potassium supplements

High-CHON; Low Na

CUSHING'S SYNDROME MVS, MIOW, MBP, MBG Electrolyte levels: Na & K Urine specimens [LOW 17- hydroxycorticosteroids & 17-ketosteroids] Physical appearance Changes in coping & sexuality [verbalization] Stress reduction

MVS, MIOW, MBP, MBG

Electrolyte levels: Na & K

Urine specimens

[LOW 17- hydroxycorticosteroids & 17-ketosteroids]

Physical appearance

Changes in coping & sexuality

[verbalization]

Stress reduction

DIABETES MELLITUS

DIABETES MELLITUS Insulin resistance [GDM, age] Failure in production Blockage of insulin supply Autoimmune response Excess body fat Heredity

Insulin resistance [GDM, age]

Failure in production

Blockage of insulin supply

Autoimmune response

Excess body fat

Heredity

DIABETES MELLITUS Type I [juvenile ]/IDDM Type II [adult- onset type]/ NIDDM gradual onset diet and exercise obesity Pancreatectomy, Cushing's syndrome, drugs

Type I [juvenile ]/IDDM

Type II [adult- onset type]/ NIDDM

gradual onset

diet and exercise obesity

Pancreatectomy, Cushing's syndrome, drugs

DIABETES MELLITUS Low insulin leads to : Hyperglycemia Glucosuria Polyuria Gluconeogenesis

Low insulin leads to :

Hyperglycemia

Glucosuria

Polyuria

Gluconeogenesis

DIABETES MELLITUS Complications Microvascular Retinopathy & Renal failure Macrovascular CV and PVD Peripheral neuropathy

Complications

Microvascular

Retinopathy & Renal failure

Macrovascular

CV and PVD

Peripheral neuropathy

P olyuria olydipsia olyphagia ruritus aresthesia oor healing oor eyesight

Normal Impaired DM FBS <110mg/dl 110-125mg/dl ≥ 126mg/dl 2H OGTT <140mg/dl ≥ 140; <200mg/dl ≥ 200 mg/dl

DIABETES MELLITUS Diet complex CHO [50% to 60%] water-soluble fiber oat, bran, peas, beans, pectin-rich FV CHON [12% to 20%] 60 and 85 g CHOO [<30%] 70 to 90 g/day / MUFA

Diet

complex CHO [50% to 60%]

water-soluble fiber

oat, bran, peas, beans, pectin-rich FV

CHON [12% to 20%]

60 and 85 g

CHOO [<30%]

70 to 90 g/day / MUFA

DIABETES MELLITUS Insulin dose adjustments depend on : physical and emotional stresses specific type of insulin condition and needs of the client

Insulin dose adjustments depend on :

physical and emotional stresses

specific type of insulin

condition and needs of the client

Insulin Onset Peak Duration Ultra rapid acting insulin analog (humalog) 10-15 min 1 H 3 H SAI (humulin regular) ½ - 1 H 2-4 H 4-6 (8) H IAI (humulin lente, Humulin NPH) 3-4 H 4-12 H 16-20 H LAI (Protamine zinc, humulin ultralente) 6-8 H 12-16 H 20-30 H Premixed insulin (NPH-regular [80-20, 70-30, 50-50]) ½-1 H 2-12 H 18-24 hrs Insulin glargine (Lantus ) Slower than NPH No Peak 24 H

DIABETES MELLITUS Somogyi effect Epinephrine & Glucagon Glycogenolysis [iatrogenically-induced hyperglycemia] Lowering insulin dosage at night MBG

Somogyi effect

Epinephrine & Glucagon

Glycogenolysis

[iatrogenically-induced hyperglycemia]

Lowering insulin dosage at night

MBG

DIABETES MELLITUS Insulin pump Basal doses of regular insulin delivered every few minutes bolus doses delivered pc Appropriate amount of insulin for 24 hours plus priming is drawn into syringe The administration set is primed and needle inserted aseptically, usually into abdomen

Insulin pump

Basal doses of regular insulin delivered every few minutes bolus doses delivered pc

Appropriate amount of insulin for 24 hours plus priming is drawn into syringe

The administration set is primed and needle inserted aseptically, usually into abdomen

DIABETES MELLITUS Client teaching points: Proper insulin preparation using aseptic technique When to remove the pump (e.g., before showering or sexual relations) MBG at home

Client teaching points:

Proper insulin preparation using aseptic technique

When to remove the pump (e.g., before showering or sexual relations)

MBG at home

INSULIN ADMINISTRATION Increases the hypoglycemic effects of insulin Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs Increases blood glucose levels Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives Increase the need for increased insulin dose Illness, infection, and stress

Increases the hypoglycemic effects of insulin

Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs

ORAL HYPOGLYCEMIC AGENTS Sulfonylureas Promotes increase insulin secretion from pancreatic beta cells through direct stimulation First Generation Agents : Acetohexamide Tolbutamide (Orinase) Tolzamide (Tolinase) Chlorpropamide (Diabenese) Second Generation Agents : Glipizide (Minidiab, Glucotrol) Glyburide (DiaBeta, Glynase, Micronase) Glimepiride (Amaryl)

Sulfonylureas

Promotes increase insulin secretion from pancreatic beta cells through direct stimulation

First Generation Agents :

Acetohexamide

Tolbutamide (Orinase)

Tolzamide (Tolinase)

Chlorpropamide (Diabenese)

Second Generation Agents :

Glipizide (Minidiab, Glucotrol)

Glyburide (DiaBeta, Glynase, Micronase)

Glimepiride (Amaryl)

ORAL HYPOGLYCEMICS Biguanides Reduces hepatic production of glucose by inhibiting glycogenolysis Decrease the intestinal absorption of glucose and improving lipid profile Agents : Phenformin Metformin (Glucophage, Glucophage XR) Buformin

Biguanides

Reduces hepatic production of glucose by inhibiting glycogenolysis

Decrease the intestinal absorption of glucose and improving lipid profile

Agents :

Phenformin

Metformin (Glucophage, Glucophage XR)

Buformin

ORAL HYPOGLYCEMICS Alpha-glucosidase inhibitors Inhibits alpha-glucosidase enzymes in the small intestine and alpha amylase in the pancreas Decreases rate of complex carbohydrate metabolism resulting to a reduced rate postprandially Agents : Acarbose (Precose, Gluconase, Glucobay) Miglitol (Glyset)

Alpha-glucosidase inhibitors

Inhibits alpha-glucosidase enzymes in the small intestine and alpha amylase in the pancreas

Decreases rate of complex carbohydrate metabolism resulting to a reduced rate postprandially

Agents :

Acarbose (Precose, Gluconase, Glucobay)

Miglitol (Glyset)

ORAL HYPOGLYCEMICS Thiazolidinediones Enhances insulin action at the cell and post-receptor site and decreasing insulin resistance Agents : Pioglitazone (Actos) Rosiglitazone (Avandia) Rosiglitazone + Metformin (Avandamet)

Thiazolidinediones

Enhances insulin action at the cell and post-receptor site and decreasing insulin resistance

Agents :

Pioglitazone (Actos)

Rosiglitazone (Avandia)

Rosiglitazone + Metformin (Avandamet)

DIABETES MELLITUS Other therapies include: pancreas islet cell grafts pancreas transplants implantable insulin pumps cyclosporin [Sandimmune, Neoral]

Other therapies include:

pancreas islet cell grafts

pancreas transplants

implantable insulin pumps

cyclosporin [Sandimmune, Neoral]

DIABETES MELLITUS MBG [done pc and hs ] + HbA1C MBP + weight Renal function + MIO Eye examination

MBG [done pc and hs ] + HbA1C

MBP + weight

Renal function + MIO

Eye examination

GLYCOSYLATED HEMOGLOBIN (HBA 1C ) Reflects effectiveness of treatment < 7.5% (good control) 7.6% - 8.9% (fair control) > 9% (poor control)

Reflects effectiveness of treatment

< 7.5% (good control)

7.6% - 8.9% (fair control)

> 9% (poor control)

DIABETES MELLITUS diet & weight ketonuria note infection legs / feet / toenails check [keep in between toes dry] acceptance & understanding

diet & weight

ketonuria

note infection

legs / feet / toenails check

[keep in between toes dry]

acceptance & understanding

DIABETES MELLITUS Administer insulin sterile technique rotating injection sites dosage / types / strengths / peak CHO source Avoid : tight shoes; smoking; heat

Administer insulin

sterile technique

rotating injection sites

dosage / types / strengths / peak

CHO source

Avoid : tight shoes; smoking; heat

DIABETES MELLITUS hypoglycemia Headache Nervousness Diaphoresis Rapid, thready pulse Slurred speech

hypoglycemia

Headache

Nervousness

Diaphoresis

Rapid, thready pulse

Slurred speech

THE CLIENT IS TIRED! T I rritability R estlessness E D iaphoresis Hypoglycemia: <50 mg/dL Causes: Overtreated hyperglycemia Increased exercise β -blockers Gastric paresis Alcohol intake Erratic insulin absorption achycardia xcessive hunger xcitability remors

T

I rritability

R estlessness

E

D iaphoresis

Hypoglycemia: <50 mg/dL

Causes:

Overtreated hyperglycemia

Increased exercise

β -blockers

Gastric paresis

Alcohol intake

Erratic insulin absorption

Mild : S hakiness T remors E xcessive hunger P aresthesias P allor D iaphoresis Rx : 10-15 gm carbohydrate 2 oz. (1 small tube of) cake icing 4 oz. orange juice 6 oz. regular soda 6-8 oz 2% skim milk (4 to) 10 pieces of hard candy

Mild :

S hakiness

T remors

E xcessive hunger

P aresthesias

P allor

D iaphoresis

Rx :

10-15 gm carbohydrate

2 oz. (1 small tube of) cake icing

4 oz. orange juice

6 oz. regular soda

6-8 oz 2% skim milk

(4 to) 10 pieces of hard candy

Moderate : D rowsiness I mpaired judgment D ouble or blurred vision H eadache I nability to concentrate M ood swings I rritability S lurred speech Rx : 20-30 gm carbohydrate Glucagon 1 mg SQ/IM

Moderate :

D rowsiness

I mpaired judgment

D ouble or blurred vision

H eadache

I nability to concentrate

M ood swings

I rritability

S lurred speech

Rx :

20-30 gm carbohydrate

Glucagon 1 mg SQ/IM

Severe : S eizures U nconsciousness D isorientation Rx : 25 gm D 50 dextrose IV Glucagon 1 mg IM/IV

Severe :

S eizures

U nconsciousness

D isorientation

Rx :

25 gm D 50 dextrose IV

Glucagon 1 mg IM/IV

DIABETES MELLITUS diabetic coma Restlessness Hot, dry, flushed skin Thirst Rapid pulse Nausea Fruity odor to breath

diabetic coma

Restlessness

Hot, dry, flushed skin

Thirst

Rapid pulse

Nausea

Fruity odor to breath

K etoacidosis U rinary changes S unken eyeballs S kin is warm & flushed M embranes are dry A rrhythmias U pset GI system L ow BP S aline solution Rx : Regular insulin drip 0.9% or 0.45% NSS 1:1 [100U:100cc] Nursing care: Check glucose 250-300 mg/dL [q30-60mins] 250 mg/dL DC the drip

K etoacidosis

U rinary changes

S unken eyeballs

S kin is warm & flushed

M embranes are dry

A rrhythmias

U pset GI system

L ow BP

S aline solution

Rx :

Regular insulin drip

0.9% or 0.45% NSS

1:1 [100U:100cc]

Nursing care:

Check glucose

250-300 mg/dL [q30-60mins]

250 mg/dL

DC the drip

NON K etosis is absent E lectrolyte imbalance [K + decrease] T hirst O btundation T reat with regular insulin drip I nitiate diet C orrect hyperglycemia

NON

K etosis is absent

E lectrolyte imbalance [K + decrease]

T hirst

O btundation

T reat with regular insulin drip

I nitiate diet

C orrect hyperglycemia

N ormal creatinine? E rythrocyte sedimentation rate [ESR: 0-20 mm/hr] P oor glycemic control H emodialysis R estrict: Na + , CHON, K + , weight O utput & input (MIO) N o symptoms

N ormal creatinine?

E rythrocyte sedimentation rate [ESR: 0-20 mm/hr]

P oor glycemic control

H emodialysis

R estrict: Na + , CHON, K + , weight

O utput & input (MIO)

N o symptoms

R educed O 2 in the eye E levated sugar & BP T ension is high in the retina I ncreased lens opacity N O eyesight A nnual eye exam [every 6-12 months]

R educed O 2 in the eye

E levated sugar & BP

T ension is high in the retina

I ncreased lens opacity

N O eyesight

A nnual eye exam [every 6-12 months]

MAJOR DISORDERS OF THE ENDOCRINE SYSTEM THANK YOU! Nio C. Noveno, RN, MAN

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