Endocrine disorders
Transcript of 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.
DISORDERS OF THE ENDOCRINE DISORDERS OF THE ENDOCRINE SYSTEMSYSTEM
PrimaryPrimaryProblem in the target gland; autonomous
SecondarySecondaryProblem in the pituitary
TertiaryTertiaryProblem in the hypothalamus
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: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
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 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
THYROID FUNCTION TESTSTHYROID FUNCTION TESTS
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
THYROID FUNCTION TESTSTHYROID FUNCTION TESTS
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.
THYROID FUNCTION TESTSTHYROID FUNCTION TESTS
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 FUNCTION TESTSTHYROID FUNCTION TESTS
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
THYROID FUNCTION TESTSTHYROID FUNCTION TESTS
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
THYROID FUNCTION TESTSTHYROID FUNCTION TESTS
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]
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 hypermotilityRRapid weight lossAApprehension
VVolume deficit; voracious appetiteEExophthalmos; erratic mensesSSystolic BP elevated; sweating
[tremors, tachycardia, palpitations]
in secondary disease in primary diseaseTSHTSH
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 thyroidectomyTreatment 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
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
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
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
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
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
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
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
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)
ADRENAL CORTEX HORMONES
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
MVS [4x / day]Infection, Addisonian crisis,
dehydrationMIOW / MBP / MBG
Give steroids with milk or an antacidAvoid: Contacts & Stress
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
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
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]
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
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]