Endocrine disorders

MAJOR DISORDERS MAJOR DISORDERS OF THE ENDOCRINE SYSTEMOF THE ENDOCRINE SYSTEM

Nio C. Noveno, RN, MANNio C. Noveno, RN, MAN

HORMONE REGULATION:HORMONE REGULATION:NEGATIVE FEEDBACK MECHANISMNEGATIVE 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.

HORMONE REGULATION:HORMONE REGULATION:NEGATIVE FEEDBACK MECHANISMNEGATIVE FEEDBACK MECHANISM

DISORDERS OF THE ENDOCRINE DISORDERS OF THE ENDOCRINE SYSTEMSYSTEM

PrimaryPrimaryProblem in the target gland; autonomous

SecondarySecondaryProblem in the pituitary

TertiaryTertiaryProblem in the hypothalamus

ANTERIOR PITUITARY ANTERIOR PITUITARY DISORDERSDISORDERS

HYPERPITUITARISMHYPERPITUITARISMMay 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 GROWTH HORMONE HYPERSECRETIONHYPERSECRETION

GigantismGigantismPrior to closure

of the epiphyses; proportional growth

AcromegalyAcromegalyAfter closure

of the epiphyses; disproportional

growth

HYPERPITUITARISM:HYPERPITUITARISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

AArthritisCChest: barrel-shapedRRough facial featuresOOdd sensations: hands and feetMMuscle weakness & fatigueEEnlargement of organsGGrowth of coarse hairAAmenorrhea; breast milk productionLLoss of vision; headachesIImpotence; increased perspiration SSnoring

HYPERPITUITARISM:HYPERPITUITARISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

HYPERPITUITARISM:HYPERPITUITARISM:MANAGEMENTMANAGEMENT

MedicationMedicationBromocriptine-Cabergoline

(dopamine agonists) GH hypersecretionand prolactinoma

Ocreotide (somatostatin)

GH hypersecretion

RadiationRadiationIndicated for larger

tumors

SurgerySurgeryTrans-sphenoidal hypophysectomy

TRANS-SPHENOIDAL TRANS-SPHENOIDAL HYPOPHYSECTOMYHYPOPHYSECTOMY

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]

HYPOPITUITARISMHYPOPITUITARISM

Deficiency of one or moreanterior pituitary hormones

CausesInfections / Inflammatory disorders

Autoimmune diseasesCongenital absence

TumorSurgery / Radiation therapy

HYPOPITUITARISMHYPOPITUITARISMSimmonds' diseaseSimmonds' disease

[Panhypopituitarism]Complete absence

of pituitary hormones Cachexia:

most prominent featureFollows destruction

of the pituitaryby surgery, infection,

injury, or a tumor

Sheehan’s syndromeSheehan’s syndrome[Post-partum

pituitary necrosis]

A complicationof delivery

Results from severe blood loss and hypovolemia

Pituitary ischemia

HYPOPITUITARISM:HYPOPITUITARISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

HypoHypo -thermia, -glycemia, -tension

LossLoss of vision, strength, libido, & secondary sexual characteristics

HYPOPITUITARISM:HYPOPITUITARISM:MANAGEMENTMANAGEMENT

MedicationMedicationHormonal substitution

[maybe for life]

CorticosteroidsLevothyroxine

Androgen / EstrogenGrowth hormone

RadiationRadiationIndicated for larger

tumors

SurgerySurgeryTrans-sphenoidal hypophysectomy

POSTERIOR PITUITARY POSTERIOR PITUITARY DISORDERSDISORDERS

DIABETES INSIPIDUSDIABETES INSIPIDUSCharacterized by massive polyuria

due to either lack of ADH or renal insensitivity

Central DICentral DIDue to a deficiency in ADH production

Nephrogenic DINephrogenic DIDue to a defect in the kidney tubulesthat interferes with water absorption

Polyuria is unresponsive to ADH,which is secreted normally.

DIABETES INSIPIDUS:DIABETES INSIPIDUS:DIAGNOSTICSDIAGNOSTICS

Fluid deprivation testAdministration of desmopressin24-hour urine collection

for volume, glucose, and creatinineSerum for glucose, urea nitrogen,

calcium, uric acid, potassium, sodium

DIABETES INSIPIDUS:DIABETES INSIPIDUS:MANAGEMENTMANAGEMENT

Central DI:Desmopressin, Lypressin [intranasal]Vasopressin tannate in oil [IM]

Nephrogenic DI:Indomethacin-

-hydrochlorothiazide-desmopressin-amiloride

Clofibrate, chlorpropamide

SYNDROME OF INAPPROPRIATE ADHSYNDROME OF INAPPROPRIATE ADH

Disorder due to excessive ADH release

Clinical Manifestations

Persistent excretion of concentrated urineSigns of fluid overload

HyponatremiaLOC changesNo edema

SIADH: DIAGNOSTICSSIADH: 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]

SIADH: MANAGEMENTSIADH: MANAGEMENTMaintain 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 DISORDERSTHYROID DISORDERS

THYROID FUNCTION TESTSTHYROID FUNCTION TESTS

Serum TSHSerum TSHSingle best screening test [high sensitivity]

0.38 – 6.15 mcU/mLIf TSH is normal, fT4 should be normal.Screening required beginning 35 years,

then q 5 years thereafterAlso used for monitoring thyroid hormone

replacement therapy


Serum fTSerum fT 44A direct measurement of free

thyroxine, the only metabolic fraction of T4

0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L)Used to confirm an abnormal TSH


Total serum TTotal serum T 33 and T and T 44TT33 70 to 220 ng/dL (1.15 to 3.10 nmol/L)

TT44 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L)

T3 levels appear to be a more accurate

indicator of hyperthyroidism.


TT 33 resin uptake test resin uptake testIndirect measurement of unsaturated

thyroid-binding globulin (TBG)25 – 35% uptake

Thyroid antibodiesThyroid antibodies5 – 10% of the population

Grave’s: 80%Hashimoto’s: 100%


Thyroid scan / Radioscan / ScintiscanThyroid scan / Radioscan / ScintiscanUtilizes a gamma camera and

radioisotopes123I, thallium, americium,

technetium-99m [99mTc] pertechnetateResults

Hot areas: increased activityCold areas: decreased activity


Radioactive iodine uptake (RAIU)Radioactive iodine uptake (RAIU)

Measures the proportion of administered tracer

dose of ¹²³I present in the thyroid glandat a specific time after administration

ResultsHyper: high uptakeHypo: low uptake


Fine-needle aspiration biopsyFine-needle aspiration biopsy

Sampling of thyroid tissue to detect malignancyInitial test for evaluation of thyroid masses

ResultsNegative [benign]

Positive [malignant]Indeterminate [suspicious]

Inadequate [non-diagnostic]


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.

HYPERTHYROIDISMHYPERTHYROIDISM

Increased basal metabolic rate (BMR)Increased basal metabolic rate (BMR)

CausesGrave’s disease (autoimmune)

Initial manifestation of thyroiditisTSH-screening pituitary tumor

Toxic adenomaFactitious thyrotoxicosis

Amiodarone therapy

HYPERTHYROIDISM:HYPERTHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

GGI hypermotilityRRapid weight lossAApprehension

VVolume deficit; voracious appetiteEExophthalmos; erratic mensesSSystolic BP elevated; sweating

[tremors, tachycardia, palpitations]

in secondary disease in primary diseaseTSHTSH

HYPERTHYROIDISM:HYPERTHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

THYROID STORM / THYROTOXIC THYROID STORM / THYROTOXIC CRISISCRISIS

Marked deliriumSevere tachycardia

VomitingDiarrhea

DehydrationHigh fever

Occurs in patientswith existing

but unrecognized thyrotoxicosis,

stressful illness,thyroid surgery, RAI

Increased systemic adrenergic activity:

Severehypermetabolism

HYPERTHYROIDISM:HYPERTHYROIDISM:MANAGEMENTMANAGEMENT

Anti-thyroid drugsAnti-thyroid drugsPropylthiouracil (PTU); methimazolePropylthiouracil (PTU); methimazole

Blocks thyroid hormone (TH) synthesis

Used for pregnant women and patientswho 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.


RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s)RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s)Adjunct to other anti-thyroid drugsin preparation for thyroidectomyTreatment for thyrotoxic crisis

Inhibit release and synthesis of THDecrease vascularity of the thyroid gland

Decrease thyroidal uptake of RAI


Medications to relieve the symptomsrelated to the increased metabolic rate:

Digitalis, propranolol (Inderal), phenobarbitalDigitalis, propranolol (Inderal), phenobarbital

Well-balanced, high-calorie dietwith vitamin and mineral supplements

Subtotal or total thyroidectomy

RAI THERAPYRAI THERAPY::

NURSING IMPLICATIONSNURSING IMPLICATIONS NPO post-midnight prior to administration

[Food may delay absorption]

After initial dose:Urine and saliva slightly radioactive x 24HVomitus highly radioactive x 6-8HInstitute full radiation precautions.

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

K OR NA IODIDE, SSKI (LUGOL’S)K OR NA IODIDE, SSKI (LUGOL’S)::

NURSING IMPLICATIONSNURSING 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.

HYPOTHYROIDISMHYPOTHYROIDISMA state of low serum TH levels

or cellular resistance to TH

AAutoimmuneDDevelopmentalDDietary

IIodine deficiencyOOncologicDDrugsIIatrogenicNNon-thyroidalEEndocrine

HYPOTHYROIDISMHYPOTHYROIDISM

CausesChronic autoimmune [Hashimoto’s]

thyroiditisHypothalamic failure to produce TRH

Pituitary failure to produce TSHInborn errors of TH synthesis

Thyroidectomy / Radiation therapyAnti-thyroid therapy

Iodine deficiency

HYPOTHYROIDISMHYPOTHYROIDISMClassified according to the time of life in which it occurs

CretinismCretinismIn infants and young children

Lymphocytic thyroiditisLymphocytic thyroiditisAppears after 6 years of age

and peaks during adolescence; self-limitingHypothyroidism without myxedemaHypothyroidism without myxedema

Mild thyroid failure in older children and adultsHypothyroidism with myxedemaHypothyroidism with myxedema

Severe thyroid failure in older individuals

HYPOTHYROIDISM:HYPOTHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

DDry, brittle hair; dry, coarse skinEEdema (periorbital)RReduced BMR [bradycardia, bradypnea]AApathy; anorexia; anemiaIIncreased weight; intolerance to coldLLethargy; loss of libido

in secondary disease in primary diseaseTSHTSH

EEnlarged tongueDDrooling

MYXEDEMA COMAMYXEDEMA COMA

Hypotension

Bradycardia

Hypothermia

Hyponatremia

Hypoglycemia

Respiratory failure

Coma

Precipitating Factors

Acute illness

Rapid withdrawalof thyroid medication

Anesthesia / Surgery

Hypothermia

Opioid use

HYPOTHYROIDISM:HYPOTHYROIDISM:MANAGEMENTMANAGEMENT

PreventionProphylactic iodine supplements to decrease

the incidence of iodine-deficient goiter

Symptomatic casesHormonal replacement

Levothyroxine (Synthroid)Levothyroxine (Synthroid)Liothyronine (Cytomel)Liothyronine (Cytomel)

Liotrix (Thyrolar)Liotrix (Thyrolar)Dosage increased q 2-3 weeksespecially in elderly patients

HYPOTHYROIDISM:HYPOTHYROIDISM:MANAGEMENTMANAGEMENT

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:HYPOTHYROIDISM:NURSING INTERVENTIONSNURSING INTERVENTIONS

Diet: high-bulk, low-calorieEncourage activity

Maintain warm environmentAdminister catharticsand stool softeners

To preventmyxedema coma,

tell patient to continue course of thyroid

medication even if symptoms subside.

Maintain patent airwayAdminister medications:

Synthroid, glucose,

corticosteroidsIV fluid replacement

Wrap patient in blanketTreat infection

or any underlying illness

PARATHYROID DISORDERSPARATHYROID DISORDERS

HYPERPARATHYROIDISMHYPERPARATHYROIDISM

PrimaryPrimarySingle adenoma

Genetic disordersMultiple endocrine neoplasias

SecondarySecondaryRickets

Vitamin D deficiencyChronic renal failure

Phenytoin or laxative abuse

HYPERPARATHYROIDISM:HYPERPARATHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

CConstipationAApathyLLordosisCCardiac dysrhythmiasUUpset GITLLow energylevelsIIncreased BP

PO4PTHCalciumAlkaline phospatase

HYPERPARATHYROIDISM:HYPERPARATHYROIDISM:MANAGEMENTMANAGEMENT

Surgery to remove adenoma

Force fluids; limit dietary calcium intake

For life-threatening hypercalcemia:Furosemide

Bisphosphonates[Etidroanate (Didrodinel), pamidronate]

Calcitonin (Cibacalcin, Miacalcin)

Plicamycin (Mithracin) + glucocorticoidMithramycin

HYPOPARATHYROIDISMHYPOPARATHYROIDISM

Causes

Congenital absenceor malfunction of the parathyroids

Autoimmune destruction

Removal or injury to one or moreparathyroids during neck surgery

Massive thyroid radiation therapy

Ischemic parathyroid infarction during surgery

HYPOPARATHYROIDISM:HYPOPARATHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

DDyspnea; dysrhythmiasEExtremities: tinglingFFotophobiaIIncreased bone densityCChvostek sign; crampsIIrritabilityTTrousseau sign; tetany

PO4PTHCalciumAlkaline phospatase


IV Ca chloride or gluconate [emergency treatment]

DOC post-thyroidectomy

Oral Ca salts (Ca carbonate or gluconate)

Vitamin D supplementationIncrease intestinal Ca absorption

Dihydrotachysterol, ergocalciferol

T ’ ’rous s eau s &Chvos tek sE levated s erum PO4; low Ca2+

Ting lingA ; lkalos is ArrhythmiasN arrowing of airwayIrritabilityCramps

HYPOPARATHYROIDISM

Parathormone injections [in acute attacks]

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

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

Pentobarbital (Nembutal) [calm environment]

T C

AKE

ARE

ETANYETANY

RACHEOSTOMRACHEOSTOMYY

ALCIUM GLUCONATEALCIUM GLUCONATE

ALCIUM 8.6 – 10.6 ALCIUM 8.6 – 10.6 mg / dLmg / dL

PHEOCHROMOCYTOMA

ADRENAL GLANDS

ADRENAL MEDULLA

Release cathecholamines Epinephrine Norephinephrine

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

PHEOCHROMOCYTOMA

Adrenal tumorAdrenal tumor

Increased Epi and NEpiIncreased Epi and NEpi

HeredityHeredity

PHEOCHROMOCYTOMA

HHeadache

AAnxiety

NNausea

EEye disturbances

SSevere hypertension

PHEOCHROMOCYTOMA

BPBP

HRHR

DiaphoresisDiaphoresis

BMRBMR

VMAVMA

GlucoseGlucose

PHEOCHROMOCYTOMAAdrenalectomy

Steroid treatment

Antihypertensive and antidysrhythmic

nitroprusside (Nipride) propranolol (Inderal)

phentolamine (Regitine)

PHEOCHROMOCYTOMA

MBP / MIOFluid replacements

Decrease environmental stimulationMaintenance doses of steroids

Follow-up check up24-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


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)


Sex hormonesAndrogens, Estrogens Influences the development of sexual characteristics

ADDISON'S DISEASE

Hyposecretion of adrenocortical hormones

Destruction of the cortex

Idiopathic atrophy

ADDISON'S DISEASE

WWeakness

EExcess stress

AA / N / V / D

KK & 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

ADDISON'S DISEASE

VS, weight, and serum glucose level

24-hour urine specimens[LOW 17- hydroxycorticosteroids &

17-ketosteroids]Electrolyte levels: K; Na

Bronze-skinChanges in energy or activity

ADDISON’S DISEASE

ADDISON'S DISEASE

MVS [4x / day]Infection, Addisonian crisis,

dehydrationMIOW / MBP / MBG

Give steroids with milk or an antacidAvoid: Contacts & Stress

CUSHING'S SYNDROME

CUSHING'S DISEASE

AAdrenal hyperplasia / drenal hyperplasia / tumortumor

CCushing’s diseaseushing’s diseaseTTumor-secreting ACTHumor-secreting ACTHHHypothalamicypothalamic

BBuffalo humpUUnusual behavior (depression, personality

changes, fatigability)

FFacial features (moonface, hirsutism in women)

FFat (truncal obesity)AACTH and cortisol in blood elevated;

LLoss of muscle massOOverextended skin (abdominal striae with easy bruisability)

HHypertension, hyperglycemia, hypernatremia

UUrinary cortisol elevatedMMenstrual irregularitiesPPorosity of bones (osteoporosis)

CUSHING’S SYNDROME

CUSHING'S SYNDROME

Remove exogenous steroids

Hypophysectomy or irradiation

Adrenalectomy

CUSHING'S SYNDROME

Cyproheptadine (Periactin)Metyrapone

Mitotane (Lysodren)Aminoglutethamide (Cytadren)

Potassium supplementsHigh-CHON; Low Na

CUSHING'S SYNDROME

MVS, MIOW, MBP, MBGElectrolyte 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 supplyAutoimmune response

Excess body fatHeredity

DIABETES MELLITUS

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 toLow insulin leads to:

Hyperglycemia Glucosuria Polyuria

Gluconeogenesis

DIABETES MELLITUS

ComplicationsMicrovascular

Retinopathy & Renal failureMacrovascular

CV and PVDPeripheral neuropathy

P P olyuriaolyuriaolydipsiaolydipsia

olyphagiolyphagiaa

ruritusruritusaresthesiaaresthesia

oor healingoor healingoor eyesightoor eyesight

NormalNormal ImpairedImpaired DMDM

FBSFBS <110mg/dl 110-125mg/dl ≥126mg/dl

2H 2H OGTTOGTT <140mg/dl

≥140; <200mg/dl

≥ 200 mg/dl

DIABETES MELLITUS

DietDietcomplex CHO [50% to 60%]

water-soluble fiberoat, bran, peas, beans, pectin-rich

FVCHON [12% to 20%]

60 and 85 gCHOO [<30%]

70 to 90 g/day / MUFA

DIABETES MELLITUS

Insulin dose adjustments depend onInsulin dose adjustments depend on:physical and emotional

stressesspecific type of insulin

condition and needs of the client

InsulinInsulin OnsetOnset PeakPeak DurationDuration

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 effectSomogyi effectEpinephrine & Glucagon

Glycogenolysis [iatrogenically-induced hyperglycemia]

Lowering insulin dosage at night MBG

DIABETES MELLITUS

Insulin pumpInsulin pumpI Basal doses of regular insulin delivered

every few minutes bolus doses delivered pc

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

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

DIABETES MELLITUS

Client teaching points:2. Proper insulin preparation using

aseptic technique3. When to remove the pump

(e.g., before showering or sexual relations)

4. MBG at home

INSULIN ADMINISTRATIONIncreases the hypoglycemic effects of insulinAspirin, alcohol, oral anticoagulants, oral

hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs

Increases blood glucose levelsGlucocorticoids, thiazide diuretics, thyroid

agents, oral contraceptives

Increase the need for increased insulin dose

Illness, infection, and stress

ORAL HYPOGLYCEMIC AGENTS

SulfonylureasSulfonylureasPromotes increase insulin secretion from pancreatic

beta cells through direct stimulationFirst Generation Agents:

Acetohexamide Tolbutamide (Orinase)Tolzamide (Tolinase)

Chlorpropamide (Diabenese)Second Generation Agents:

Glipizide (Minidiab, Glucotrol)Glyburide (DiaBeta, Glynase, Micronase)

Glimepiride (Amaryl)

ORAL HYPOGLYCEMICS

BiguanidesBiguanidesReduces hepatic production of glucose

by inhibiting glycogenolysisDecrease the intestinal absorption of

glucose and improving lipid profileAgents:

PhenforminMetformin (Glucophage, Glucophage XR)

Buformin

ORAL HYPOGLYCEMICS

Alpha-glucosidase inhibitorsAlpha-glucosidase inhibitorsInhibits 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

ThiazolidinedionesThiazolidinedionesEnhances insulin action at the cell and post-

receptor site and decreasing insulin resistanceAgents:

Pioglitazone (Actos)Rosiglitazone (Avandia)

Rosiglitazone + Metformin (Avandamet)

DIABETES MELLITUS

Other therapies include:2. pancreas islet cell grafts3. pancreas transplants4. implantable insulin pumps5. cyclosporin [Sandimmune,

Neoral]

DIABETES MELLITUS

MBG [done pc and hs] + HbA1C

MBP + weightRenal function + MIO

Eye examination

GLYCOSYLATED HEMOGLOBIN (HBA1C)

Reflects effectiveness of Reflects effectiveness of treatmenttreatment

< 7.5% (good control)7.6% - 8.9% (fair control)

> 9% (poor control)

DIABETES MELLITUS

diet & weightketonuria

note infection legs / feet / toenails check[keep in between toes dry]

acceptance & understanding acceptance & understanding

DIABETES MELLITUS

Administer insulinAdminister insulinsterile technique

rotating injection sitesdosage / types / strengths / peak

CHO source

AvoidAvoid: tight shoes; smoking; heat

DIABETES MELLITUS

hypoglycemiahypoglycemiaHeadache

NervousnessDiaphoresis

Rapid, thready pulseSlurred speech

THE CLIENT IS TIRED!

TIrritability

Restlessness

EDiaphoresis

Hypoglycemia: <50 mg/dLHypoglycemia: <50 mg/dL

Causes: Overtreated hyperglycemia Increased exercise β-blockers Gastric paresis Alcohol intake Erratic insulin absorption

achycardia

xcessive hungerxcitability

remors

Mild:ShakinessTremorsExcessive

hungerParesthesiasPallorDiaphoresis

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:Drowsiness Impaired judgmentDouble or blurred vision

Headache Inability to concentrate

Mood swings Irritability Slurred speech

Rx:

20-30 gm carbohydrate

Glucagon 1 mg SQ/IM

Severe:

Seizures

Unconsciousness

Disorientation

Rx:

25 gm D50 dextrose IV

Glucagon 1 mg IM/IV

DIABETES MELLITUS

diabetic comadiabetic comaRestlessness

Hot, dry, flushed skinThirst

Rapid pulseNausea

Fruity odor to breath

KK etoacidosisetoacidosisUU rinary rinary

changeschangesSS unken eyeballsunken eyeballsSS kin is warm & kin is warm &

flushedflushedMM embranes are embranes are

drydryAA rrhythmiasrrhythmiasUU pset GI pset GI

systemsystemLL ow BPow BPSS aline solutionaline solution

Rx: Regular insulin drip

0.9% 0.45% or NSS 1:1 [100 :100 ]U cc

:Nursing care Check glucose

250-300 / mg dL[ 30-60 ]q mins

250 / mg dL DC the drip

NONNONKK etos is is abs ent etos is is abs entEE [lec tro lyte imbalance K [lec tro lyte imbalance K++

]decreas e]decreas eTThirs thirs tOObtundationbtundationTT reat with regular ins ulin drip reat with regular ins ulin dripII nitiate die t nitiate die tCC orrect hyperglycemia orrect hyperglycemia

Normal creatinine?

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

Poor glycemic control

HemodialysisRestrict: Na+, CHON, K+, weight

Output & input (MIO)

No symptoms

Reduced O2 in the eye

Elevated sugar & BP

Tension is high in the retina

Increased lens opacity

NO eyesight

Annual eye exam [every 6-12 months]

MAJOR DISORDERS MAJOR DISORDERS OF THE ENDOCRINE OF THE ENDOCRINE SYSTEMSYSTEM

!THANK YOU

Nio C. Noveno, RN, MANNio C. Noveno, RN, MAN

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Endocrine disorders