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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.
HYPERTHYROIDISM:HYPERTHYROIDISM:MANAGEMENTMANAGEMENT
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
HYPERTHYROIDISM:HYPERTHYROIDISM:MANAGEMENTMANAGEMENT
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
HYPERTHYROIDISM:HYPERTHYROIDISM:MANAGEMENTMANAGEMENT
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
ADRENAL CORTEX HORMONES
MineralocorticoidsAldosterone, Corticosterone,
DeoxycorticosteroneRegulate fluid and electrolyte balanceStimulate reabsorption of sodium,
chloride and waterStimulate potassium excretion
Under the control of Renin-Angiotensin-Aldosterone system (RAAS)
ADRENAL CORTEX HORMONES
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