Endocrine Disorders

MAJOR DISORDERS MAJOR DISORDERS OF THE ENDOCRINE OF THE ENDOCRINE

SYSTEMSYSTEMNio C. Noveno, RN, MANNio C. Noveno, RN, MAN

HORMONE REGULATION:HORMONE REGULATION:NEGATIVE FEEDBACK NEGATIVE FEEDBACK MECHANISMMECHANISM

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 NEGATIVE FEEDBACK MECHANISMMECHANISM

DISORDERS OF THE DISORDERS OF THE ENDOCRINE SYSTEMENDOCRINE SYSTEM

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 feature

Follows destructionof the pituitary

by surgery, infection, injury, or a tumor

Sheehan’s Sheehan’s syndromesyndrome

[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 polyuriadue to either lack of ADH or renal

insensitivity

Central DICentral DI

Due to a deficiency in ADH production

Nephrogenic DINephrogenic DI

Due 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 creatinine

Serum 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 SYNDROME OF INAPPROPRIATE ADHADH

Disorder due to excessive ADH release

Clinical Manifestations

Persistent excretion of concentrated urineSigns of fluid overload

HyponatremiaLOC changes

No 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

Fine-needle aspiration biopsyFine-needle aspiration biopsy

Sampling of thyroid tissue to detect malignancy

Initial test for evaluation of thyroid massesResults

Negative [benign]Positive [malignant]

Indeterminate [suspicious]Inadequate [non-diagnostic]

THYROID FUNCTION TESTSTHYROID 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.

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 hypermotility

RRapid weight lossAApprehension

VVolume deficit; voracious appetiteEExophthalmos; erratic menses

SSystolic BP elevated; sweating

[tremors, tachycardia, palpitations]

in secondary disease

in primary diseaseTSTSHH

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 thyroidectomy

Treatment 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

AAutoimmuneDDevelopment

alDDietary

IIodine deficiencyOOncologic

DDrugsIIatrogenicNNon-

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-limiting

Hypothyroidism without myxedemaHypothyroidism without myxedemaMild thyroid failure in older children and adults

Hypothyroidism with myxedemaHypothyroidism with myxedemaSevere thyroid failure in older individuals

HYPOTHYROIDISM:HYPOTHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

DDry, brittle hair; dry, coarse skin

EEdema (periorbital)RReduced BMR [bradycardia,

bradypnea]AApathy; anorexia; anemiaIIncreased weight; intolerance to

coldLLethargy; loss of libido

in secondary disease

in primary diseaseTSTSHH

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-calorie

Encourage activityMaintain 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, corticosteroids

IV fluid replacementWrap patient in blanket

Treat infectionor any underlying illness

PARATHYROID PARATHYROID DISORDERSDISORDERS

HYPERPARATHYROIDISMHYPERPARATHYROIDISM

PrimaryPrimary

Single adenomaGenetic disorders

Multiple endocrine neoplasias

SecondarySecondary

RicketsVitamin D deficiencyChronic renal failure

Phenytoin or laxative abuse

HYPERPARATHYROIDISM:HYPERPARATHYROIDISM:CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

CConstipation

AApathyLLordosisCCardiac

dysrhythmiasUUpset GITLLow energylevelsIIncreased BP

PO4PTHCalcium

Alkaline 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; dysrhythmias

EExtremities: tinglingFFotophobia

IIncreased bone densityCChvostek sign; crampsIIrritability

TTrousseau sign; tetany

PO4PTHCalcium

Alkaline 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

Trousseau’s & Chvostek’sElevated serum PO4; low Ca2+TinglingAlkalosis; ArrhythmiasNarrowing 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]

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 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

GlucocorticoidsCortisol, corticosteroneIncrease blood glucose levels by

increasing rate of gluconeogenesisIncrease protein catabolismIncrease mobilization of fatty acidsPromote sodium and water retentionAnti-inflammatory effectAid the body in coping with stress


MineralocorticoidsAldosterone, Corticosterone,

DeoxycorticosteroneRegulate fluid and electrolyte balanceStimulate reabsorption of sodium,

chloride and waterStimulate potassium excretion

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


Sex hormonesAndrogens, EstrogensInfluences 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;

FludrocortisonePNSS (0.9 NaCl)

Dextrose Diet:

High-CHO & CHONLow 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 antacid

Avoid: Contacts & Stress

CUSHING'S SYNDROME

CUSHING'S DISEASE

AAdrenal drenal hyperplasia / tumorhyperplasia / tumor

CCushing’s diseaseushing’s diseaseTTumor-secreting umor-secreting

ACTHACTHHHypothalamicypothalamic

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 elevated

MMenstrual irregularities

PPorosity 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 supplements

High-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 productionBlockage of insulin supply

Autoimmune responseExcess 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

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 olyuriolyuriaaolydipsiolydipsiaaolypholyph

agiaagiaruritururitussaresthesaresthes

iaiaoor oor healinghealingoor oor

eyesighteyesight

NormalNormal ImpairedImpaired DMDM

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

2H 2H OGTOGT

TT<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 Insulin dose adjustments

depend ondepend 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 pump1) Basal doses of regular insulin

delivered every few minutes bolus doses delivered pc

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

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

DIABETES MELLITUS

Client teaching points:1. Proper insulin preparation

using aseptic technique2. When to remove the pump

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

3. 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 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

BiguanidesBiguanidesReduces 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 Alpha-glucosidase inhibitorsinhibitors

Inhibits alpha-glucosidase enzymes in the small intestine and alpha

amylase in the pancreasDecreases 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 resistance

Agents:

Pioglitazone (Actos)Rosiglitazone (Avandia)

Rosiglitazone + Metformin (Avandamet)

GLYCOSYLATED HEMOGLOBIN (HBA1C)

Reflects Reflects effectiveness of effectiveness of

treatmenttreatment

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

> 9% (poor control)

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 Hypoglycemia: <50 mg/dLmg/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 icing4 oz. orange juice6 oz. regular soda6-8 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

MAJOR DISORDERS MAJOR DISORDERS OF THE ENDOCRINE OF THE ENDOCRINE SYSTEMSYSTEMTHANK YOU!

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

Education

Endocrine Disorders