endocrine new edition
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ENDOCRINESYSTEM AND MAJOR
DISORDERS
By: MISS SHENELL A. DELFIN, RN
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FUNCTION:Endocrine system consist of a series of glands
“ductless” that function individually or conjointly to integrate and control innumerable metabolic activities in the body.
These glands automatically regulate various body processes by releasing chemical messengers called hormones.
OVERACTIVITY OR UNDERACTIVITY of any one of them affects the whole system.
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FUNCTION:Control and coordination of the processes
which are wide spread in the body such as:Response to stress or injuryGrowth and developmentReproductionFluids and electrolytesAcid base-balanceEnergy metabolism
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ENDOCRINE GLANDSENDOCRINE GLAND
HORMONES FUNCTIONS
PITUITARYANTERIOR
TSH Thyroid to release hormones
LOBE ACTH Adrenal cortex to release hormones
FSH,LH Growth, maturation & function of sex organs
GH/SOMATOTROPIN
Growth of body tissues & bones
PROLACTIN/LTH
Development of mammary glands & lactation
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ENDOCRINE GLANDSENDOCRINE GLAND
HORMONE FUNCTION
PITUITARYPOSTERIOR
LOBE
ADH Regulates water metabolism
OXYTOCIN Stimulate uterine contractions release of milk
INTERME- DIATE LOBE
MSH Affects skin pigmentation
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ENDOCRINE GLANDSENDOCRINE GLAND
HORMONES FUNCTION
ADRENAL CORTEX
ALDOSTERONE Fluid & electrolyte balance; Na reabsorption; K excretion
CORTISOL Glycogenolysis;GluconeogenesisNa & water reabsorptionAntiinflammatoryStress hormone
SEXHORMONES
Slightly significant
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ENDOCRINEGLAND
HORMONE FUNCTION
ADRENAL MEDULLA
EPINEPHRINENOR-EPINEPHRINE
Increase heart rate & BPBronchodilation, GlycogenolysisStress hormone
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ENDOCRINE GLANDSENDOCRINE GLAND
HORMONE FUNCTION
THYROID T3 & T4’ Regulate metabolic rateRegulate physical & mental
growth & development
THYRO- CALCITONIN
Decrease serum Ca by increasing bone deposition
PARA- THYROID
PTH Increase serum calcium by promoting bone decalcification
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ENDOCRINE GLANDSENDOCRINEGLAND
HORMONE FUNCTION
PANCREAS BETA
CELLS
INSULIN Decrease blood glucose by: Glucose diffusion across cell
membrane;Converts glucose to
glycogen
ALPHA CELLS
GLUCAGON Increase blood glucose by:GluconeogenesisGlycogenolysis
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ENDOCRINE GLANDSENDOCRINEGLAND
HORMONES FUNCTION
OVARIES ESTROGEN &PROGES- TERONE
Development of secondary sex charac in female
Maturation of sex organsSexual functioningMaintenance of pregnancy
TESTES TESTOS- TERONE
Development of secondary sex charac in male
Maturation of sex organsSexual functioning
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HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISM
CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)
RHYTHMIC PATTERNS OF SECRETION (e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)
AUTONOMIC & C.N.S. CONTROL(PITUITARY-HYPOTHALAMIC AXIS,
ADRENAL MEDULLA HORMONES)
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NEGATIVE FEEDBACK MECHANISM
DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)
PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g. TSH)
STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE
(e.g. Thyroid gland release of Thyroxine)
RETURN OF THE NORMAL CONCENTRATION OF HORMONE
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NEGATIVE FEEDBACK MECHANISM
INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)
PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)
DECREASED PRODUCTION & SECRETION OF TARGET ORGAN OF THE HORMONE
(e.g. Thyroid gland release of Thyroxine)
RETURN OF THE NORMAL CONCENTRATION OF HORMONE
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Endocrine Disorders
If you can remember what each hormone does in the body, it will be easier to remember what results from imbalances of that hormone. Most symptoms of hormone HYPERACTIVITY are the
opposite of symptoms of that hormones HYPOACTIVITY.
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ANTERIOR PITUITARY DISTURBANCES
HYPOPITUITARISM
HYPERPITUITARISM
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PITUITARY ANTERIOR LOBEHORMONE HYPO FXN HYPER FXN
GH Dwarfism – youngCachexia - adult
Gigantism – youngAcromegaly - adult
ACTH Atrophy of adrenal cortex
Cushing’s dse
TSH Atrophy & depressed thyroid fxn
Grave’s dse
FSH Atrophy & infertility Exaggerated fxn of sex organs
PROLACTIN Underdevelopment of mammary glands
Decreased milk production
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HyperpituitarismMay 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
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Manifestations of acromegaly. Progressive alterations in facial appearance include enlargement of the cheekbones and jaw along with thickening of soft-tissue structures such as the nose, lips, cheeks, and the flesh above the brows. (Courtesy of Clinical Pathological Conference, American Journal of Medicine.)
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Hyperpituitarism:Clinical Manifestations
ArthritisChest: barrel-shapedRough facial featuresOdd sensations: hands and
feetMuscle weakness & fatigueEnlargement of organsGrowth of coarse hairAmenorrhea; breast milk
productionLoss of vision; headachesImpotence; increased
perspiration Snoring
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Hyperpituitarism:Clinical Manifestations
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Hypopituitarism
Deficiency of one or moreanterior pituitary hormones
CausesInfections / Inflammatory disorders
Autoimmune diseasesCongenital absence
TumorSurgery / Radiation therapy
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Hypopituitarism:Clinical Manifestations
Hypo -thermia, -glycemia, -tension
Loss of vision, strength, libido, & secondary sexual
characteristics
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DWARFISM
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MANAGEMENTHYPOPITUITARISM
SURGICAL REMOVAL / IRRADIATIONREPLACEMENT THERAPY
THYROID HORMONES STEROIDS SEX & GROWTH HORMONES GONADOTROPINS (restore fertility)
HYPERPITUITARISMSURGICAL REMOVAL / IRRADIATIONMONITOR FOR HYPERGLYCEMIA &
CARDIOVASCULAR PROBLEMS
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Trans-sphenoidal hypophysectomy
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POSTERIOR PITUITARY DISTURBANCES
DIABETES INSIPIDUS
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
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FUNCTION:WHEN THERE IS A OF SERUM
OSMOLALITY, THE NORMAL BODY RESPONSE IS TO THE SECRETION OF ADH.
WHEN THE NORMAL FEEDBACK MECHANISM FOR ADH IS SUSTAINED, THERE IS EXCESSIVE WATER RETENTION IN THE BODY
WHEN THERE IS OR INADEQUATE AMOUNT OF ADH, THE BODY IS UNABLE TO CONCENTRATE URINE, & EXCESSIVE H2O LOSS OCCURS
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DIABETES INSIPIDUSCHARACTERIZED BY A DEFICIENCY OF ADH. WHEN IT OCCURS, IT IS MOST OFTEN
ASSOCIATED WITH :NEUROLOGICAL CONDITIONS, SURGERY, TUMORS, HEAD INJURY, OR INFLAMMATORY PROBLEMS
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DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN
S/SX:POLYURIA
15-29L/ DAYPOLYDIPSIASG OF URINE IS <1.010S/SX OF DHNSHOCK
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DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN
MANAGEMENTHORMONAL REPLACEMENT – FOR LIFE
VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAY
NON-HORMONAL THERAPYCHLORPROPRAMIDE – INCREASE RESPONSE OF THE
BODY TO DECREASED VASOPRESSIN
INCREASE FLUIDSMONITOR I&O + WEIGHT (MIOW)MAINTAIN FLUID & ELECTROLYTE
BALANCE
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SYNDROME OF INAPPROPRIATE ADH
(SIADH)ELEVATED ADHS/SX:DECREASED SERUM SODIUM
CX IN LOC TO UNCONSCIOUSNESSSEIZURES
WATER INTOXICATIONN/VMENTAL CONFUSIONPersistent excretion of concentrated urineSigns of fluid overloadHyponatremia
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SYNDROME OF INAPPROPRIATE ADH
MANAGEMENT:WATER INTAKE RESTRICTIONADMINISTER AS ORDERED:
NaClDiureticsDemeclocycline (declamycin) – a tetracycline
analogue that interferes with the action of ADH on the collecting tubules
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THYROID DISORDERS
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Hypothyroidism underactive state of the thyroid gland hyposecretion of thyroid hormone most common in women, middle-age primary function is to control the level of cellular
metabolism by secreting thyroxin (T4) and triiodothyronine (T3)
DX: decreased T3, T4 Elevated TSH, cholesterol
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HypothyroidismA state of low serum TH levels
or cellular resistance to TH
AutoimmuneDevelopment
alDietary
Iodine deficiencyOncologic
DrugsIatrogenicNon-
thyroidalEndocrine
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Pathophysiology inadequate secretion of thyroid hormone
general slowing of all physical and mental process
metabolic rate oxidation of nutrients for energy heat production
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Complications :• Cretinism – severe physical and mental
retardation resulting from severe deficiency of thyroid function in infancy or childhood (congenital hypothyroidism)
requires lifetime hormone replacement• Myxedema – occur from prolonged severe
disease accelerated devt. of coronary artery disease coma – rapid dev’t. of impaired consciousness and suppression of vital functions
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MYXEDEMA COMA- a condition resulting from persistent low thyroid production.
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Med. Mgt. – thyroid replacement therapy Levothyroxine (Synthyroid) , liothyronine Expected effects: diuresis, puffiness, improved reflexes and muscle tone, PR
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Nsg. Interventions provide a warm environment, conducive to
rest avoid use of all sedatives assist client in choosing calorie, cholesterol
diet fluid and fiber to relieve constipation physical activity and sensory stimulation
gradually as condition improves monitor cardiovascular response to increased
hormone levels carefully provide info. about prescribed medications
(name, dosage, side effects) and importance of lifelong medical supervision
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Hyperthyroidism
over-secretion of the thyroid gland also called thyrotoxicosis or graves disease, tissues are stimulated by excessive thyroid hormone a recurrent syndrome, may appear after emotional
stress or infection occurs mostly in women 20-50 yrs old
Causes : adenoma, goiter, viral inflammation, auto-immune glandular stimulation, grave’s disease - most common cause
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Hyperthyroidism (cont.)
DX: > elevated T3, T4 valuesT4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/L• abnormal findings in the thyroid scan
Goiter – enlargement of the thyroid gland • due to stimulation of the thyroid gland by TSH
Simple goiter – enlarged thyroid gland• due to iodine deficiency, intake of goitrogenic
foods cabbage, turnips, soybeans• may be hereditary
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Grave’s Disease disorder char. by one or more of the ff:
diffuse goiter
hyperthyroidism
infiltrative opthalmopathy exophthalmos seen in females under age 40 result from stimulation of the thyroid gland by thyroid-stimulating immunoglobulins (TSI) cause is unknown, may be hereditary, gender-
related, often occurs after severe emotional stress or infection
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Complications :
cardiovascular disease (HPN, Angina, CHF) Exophthalmos – abnormal protrusion of the eyeballs
- caused by abnormal deposits of fat and fluid in the retroocular tissue
Corneal abrasion Thyroid storm or crisis life-threatening hypermetabolism and excessive adrenergic response (HR, RR, BP)
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Thyroid Storm or Crisis
a medical emergency pts. develop severe manifestation of hyperthyroidism
temp., tachycardia, dysrhythmias worsening tremors, restlessness delirious or psychotic state or coma abdominal pain BP and RR
Precipitated by a major stressor: infection trauma or surgery (thyroidectomy) inadequate treatment
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Do you take this woman as your wife…. In sickness and
in health…
TAKE ME! TAKE ME!!
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Anxiety Flushed, smooth skin Heat intolerance Mood swings Diaphoresis Tachycardia Palpitations Dyspnea Delirium, coma Heart failure
Assessment Findings: Thyroid storm
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Med. Mgt.• Medications
Propylthiouracil (PTU) – antithyroid drug - blocks thyroid hormone production- can cause agranulocytosis- monitor pt. CBC
Methimazole (Tapazole) – blocks TH prod. Iodine preparations – the size and vascularity of the thyroid gland; inhibit release of thyroid hormones 1.) Lugol’s solution
can be given with milk or fruit juice should be taken with a straw – may stain the teeth complications : brassy taste in the mouth, sore teeth and gums
2.) Saturated solution of potassium iodide (SSKI)
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Med. Mgt.• Medications
Propanolal (Inderal) and other adrenergic blockers• relieve the adrenergic effects of excess thyroid
hormone (sweating, palpitations, tremors)
• Radioactive iodine – limits the secretion of the
hormone by damaging or destroying thyroid tissue
• Surgical intervention (performed only when pt. is in a
euthyroid state) subtotal thyroidectomy (large goiter) total thyroidectomy (if carcinoma is present)
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Nsg. Interventions: Provide calm, restful envt.
1. physical comfort, cool envt. temp., bathe frequently w/ cool water
2. provide adequate rest, avoid muscle fatigue3. stressors in the envt.— noise and lights4. relaxation techniques
Provide adequate nutrients1. calorie, protein, balanced diet (4,000-5,000
cal/day)2. fluid intake3. Restrict stimulants (tea, coffee, alcohol)4. small, frequent feedings if hypermotility is
present5. Daily wt.
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Nsg. Interventions:
Provide emotional support
Provide eye care1. eye drops, dark glasses, patch eyes if
necessary2. elevate head of bed for sleep3. restrict dietary sodium4. assess adequacy of lid closure
Be alert for complications
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Post-op care after Thyroidectomy
O2 therapy, suction secretions Monitor for signs of bleeding and excessive edema elevate head of bed 30o, support head and neck –
to avoid tension on suturescheck dressing frequently, check behind the neck
for bleeding assess for signs of resp. distress, hoarseness (laryngeal edema or damage) keep tracheostomy set in patient’s room for
emergency use
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Post-op Complications: be alert for the possibility of:
1. Tetany (due to hypocalcemia caused by accidental removal of parathyroid glands)
assess for numbness, tingling or muscle twitching
Chvostek’s sign and Trousseau’s sign Ca+ gluconate IV
2. HemorrhageWOF: hypotension, tachycardia, other signs of
hypovolemiaWOF: irregular breathing, swelling, choking---
possible hemorrhage and tracheal compressionWOF: early signs of hemorrhage: repeated
clearing of the throat, difficulty swallowing
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Post-op Complications: be alert for the possibility of:
3. Thyroid storm - life-threatening- sudden release of thyroid hormone- fever, tachycardia, increasing restlessness
and agitation, delirium
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PARATHYROID GLAND DISORDERS
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Hypoparathyroidism is characterized by decrease in
the PTH level
PARATHYROID HORMONE
Mobilization of calcium and phosphorous
from bone
Promotes resorption of calcium from
bone to maintain normal serum calcium levels
Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).
Renal: increases calcium
reabsorption and phosphate excretion
Function of calcium: maintains N muscle
and neuromuscular responses.
Necessary component for blood coagulation mechanisms
CALCIUM STAYS IN THE BONE
CALCIUM DEPOSITED
IN THE BONE
EXCRETION OF CALCIUM
HYPOCALCEMIA
• TINGLING OF FINGERS• CHVOSTEKS/
TROUSSEAU’S• FATIGUE, WEAKNESS• CARDIAC
ARRHYTHMIAS• SEIZURE• BRONCHOSPASM
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TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY
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PARATHYROID DISORDERS
DIAGNOSTIC TESTS:HEMATOLOGICAL
SERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASE
URINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR
REABSORPTION OF PHOSPHATE
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HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITYMANAGEMENT:Ca SUPPLEMENTVIT D SUPPLEMENT – LIQ FORM: WITH WATER,
JUICE OR MILK, pc
SEIZURE precLISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDE
CaGLUCONATE @ BEDSIDE
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T C
AKE
ARE
ETANY
RACHEOSTOMY
ALCIUM GLUCONATE
ALCIUM 8.6 – 10.6 mg / dL
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Hyperparathyroidism is characterized by excesssive
secretion of PTH
PARATHYROID HORMONE
Mobilization of calcium and phosphorous
from bone
Promotes resorption of calcium from
bone to maintain normal serum calcium levels
Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).
Renal: increases calcium
reabsorption and phosphate excretion
Function of calcium: maintains N muscle
and neuromuscular responses.
Necessary component for blood coagulation
mechanisms
CALCIUM RELEASED INTO
THE BLOOD LEADS TO BONE
DAMAGE
HYPERCALCEMIA, LACK OF RESORPTION OF CALCIUM INTO THE
BONE( BONE CYST AND PATHOLOGIC
FRACTURE)
TUBULAR CALCIUM DEPOSIT- KIDNEY
STONES, AZOTEMIA, HPN BY RF, RENAL
FAILURE
ANOREXIAN/V
CONSTIPATIONPEPTIC ULCER DSE
MUSCLE WEAKNESS
PERSONALITY CHANGESCARDIAC
ARRHYTHMIAS
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HYPERPARATHYROIDISMINCREASED PTH PRODUCTIONHYPERCALCEMIAHYPOPHOSPHATEMIAPRIMARY – TUMOR OR HYPERPLASIA OF THE
PARATHYROID GLAND
SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:CHRONIC RENAL DSEMALABSORPTION SYNDROMEOSTEOMALACIA
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HYPERPARATHYROIDISMMANAGEMENT:
TX OF CHOICE : SURGICAL REMOVAL OF HYPERPLASTIC TISSUE
IV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)LOW CaSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY
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DISORDERS OF THE PANCREAS
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DIABETES MELLITUS(TYPE I, TYPE II)
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TWO TYPES OF DIABETES
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Diabetes Mellitus
is a chronic disorder of carbohydrate, protein, and fat metabolism resulting from insulin deficiency or abnormality in the use of insulinPredisposing factors:
exact cause of diabetes mellitus remain unknown
genetic / hereditary predisposition viruses pancreatitis pancreatic tumor autoimmune disorder obesity (overweight people require more insulin
to metabolize the food they eat or the number of insulin receptor sites in cells is decreased)
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Types1.Insulin – Dependent Diabetes Mellitus (IDDM) or
Type I destruction of beta cells of the pancreas little or no
insulin production requires daily insulin admin. may occur at any age, usually appears below age 15
2.Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type II probably caused by:
disturbance in insulin reception in the cells number of insulin receptors loss of beta cell responsiveness to glucose leading
to slow or insulin release by the pancreas
occurs over age 40 but can occur in children common in overweight or obese w/ some circulating insulin present, often do not
require insulin
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P olyuriaolydipsiaolyph
agiaruritusaresthes
iaoor healingoor
eyesight
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DIAGNOSTIC TEST FOR DM
1. Fasting Blood Sugar (FBS) NPO for 12 hours Normal value= 80-120 mg/dl 140 mg/dl or more – diagnostic of DM
2. Postprandial blood sugar Blood is withdrawn 2 hrs. after a meal N value = < 120mg/dl 200 mg/dl or more is diagnostic of DM
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3. Oral Glucose Tolerance Test (OGTT) NPO 12 hrs, no smoking, coffee or tea,
minimize activity, minimize stress obtain FBS, administer 100 gm. Glucose by
mouth diluted in juice; obtain blood and urine specimen after 1, 2 and 3 hrs.
N value = blood glucose rise to 140 mg/dl in the 1st hour and returns to normal by 2nd and 3rd hrs.
Abnormal = blood glucose does not return to normal by 2nd and 3rd hrs.; all urine specimen positive for glucose
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Diagnostic Tests for DM
4. Glycosylated hemoglobin Provides information about blood glucose
level during the previous 3 months bec. glucose in the bloodstream attaches to
some of the hemoglobin and stay attached during the 120-day lifespan of the RBC
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D-I-A-B-E-T-E-SD- DIET: 50-60% CHO, 20-30% FATS,
10-20% CHONI- INSULIN– TYPE 1A- ANTIDIABETIC AGENTS– TYPE 2B- BLOOD SUGAR MONITORINGE- EXERCISET- TRANSPLANT OF PANCREASE- ENSURE ADEQUATE FOOD INTAKES- SCRUPULOUS FOOT CARE
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Management of Hypoglycemia
1. Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar
2. Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth
3. As soon as pt. regains consciousness, he should be given carbohydrate by mouth
4. If pt. does not respond to the above measures, he is given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10% glucose in water I.V.
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Oral Antidiabetic AgentsClassification &
ExamplesMechanism of Action
Sulfonylureas-Tolbutamide (Orinase)- Chlorpropamide (Diabinese)- Glipizide (Glucatrol)- Glimepiride (Amaryl)- Glibenclamide
stimulate beta cells of the pancreas to secrete insulin improve binding bet. insulin and insulin receptors no. of insulin receptors
Biguanides- Metformin (Glucophage)
body tissues’ sensitivity to insulin glucose uptake inhibit glucose prod. by the liver
Alpha-Glucosidase Inhibitors- Acarbose (Precose)- Miglitol (Glyset)
delay absorption of glucose in the intestine
Thiazolidinediones- Rosiglitazone (Avandia)- Pioglitazone (Actos)
enhance insulin action at the receptor sites
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Oral Antidiabetic Agents
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DIABETES MILLETUSINSULIN THERAPYDISPENSED IN “U”/ml : eg 100, 80REFRIGERATEGIVEN @ ROOM TEMPGENTLY ROTATED, NOT SHAKENROUTE : SQ ; IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND
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INSULIN ONSET PEAK
DURATION
Ultra rapid acting Insulin analog (Humalog)
15 mins.
2-4 hrs.
6-8 hrs.
Rapid acting: Regular (Semilente)
½-1 hr 2-4 hrs.
6-8 hrs.
Intermediate: NPH (Lente)
1-2 hrs. 7-12 hrs.
24-30 hrs.
Long acting: Protamine Zinc (Ultralente)
4-6 hrs. 18 + hrs
30-36 hrs.
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DIABETES MILLETUSINSULIN THERAPY:SITE OF INJECTION:
ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS
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B. Teach pt. on correct administration of insulin and other hypoglycemic agents.
1. insulin in current use may be stored at room temp., all others in ref. or cool area
2. avoid injecting cold insulin lead to tissue reaction3. roll insulin vial to mix, do not shake, remove air
bubbles from syringe4. press (do not rub) the site after injection (rubbing
may alter the rate of absorption of insulin)5. avoid smoking for 30 mins. after injection (cigarette
smoking absorption)6. Rotate sites Failure to rotate sites may lead to Lipodystrophy Lipodystrophy – localized disturbance of fat
metabolism Ex. Lipohypertrophy – thickening of subcutaneous
tissue at injection site, feel lumpy or hard, spongy result to absorption of insulin making it
difficult to control the pt.’s blood glucose
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Teach pt. to estabilish and maintain a pattern of regular exercise Benefits of exercise :
promotes use of CHO & enhances action of insulin blood glucose levels need for insulin the no. of functioning receptor sites for insulin
perform exercise after meals to ensure an adequate level of blood glucose
carry a rapid-acting source of glucose during exercise
excessive or unplanned exercise may trigger hypoglycemia
take insulin and food before active exercise
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ACUTE COMPLICATIONS OF DIABETES MILLETUS
DIABETIC KETO-ACIDOSIS (DKA)
INSULIN SHOCK
HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA
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Diabetic Ketoacidosis (DKA) Coma
S/Sx:polyuria, thirstnausea, vomiting, abdominal pain –-- due to acidosisweakness, headache, fatigue --- due to acidosis and F/E imbalancedim visiondehydration, hypovolemic shock (PR, BP, dry skin, wt. loss)hyperpnea (Kussmaul’s breathing)acetone breath (fruity odor)lethargy COMABlood glucose level > 250-350 mg/100 ml.
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Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC)
can occur when the action of insulin is severely inhibitedseen in pts. w/ NIDDM, elderly persons w/ NIDDM
Precipitating factors:infection, renal failure, MI, CVA, GI hemorrhage, pancreatitis, CHF, TPN, surgery, dialysis, steroids
S/Sx: polyuria oliguria (renal insufficiency) lethargy temp, PR, BP, signs of severe fluid deficit Confusion, seizure, coma Blood glucose level > 600 mg/100 ml.
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HHONKS/SX:S/SX OF DKA WITHOUT:
KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA
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Interventions for DKA and Hyperosmolar Coma
Regular insulin IV push or IV drip 0.9% NaCl IV – 1 L during the 1st hr, 2-8 L over 24 hrs. administer sodium bicarbonate IV to correct acidosis Monitor electrolyte levels, esp. serum K+ levels administer K+, monitor UO hourly (30ml/hr)
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Long-term Complications of DM
1. Vascular Changesa. ) Macroangiopathy – hardening and damage of the
walls of large arteriesCoronary Artery DiseaseCVA (Stroke)Peripheral vascular disease – foot ulcers and gangrene
b. ) Microangiopathy – destruction of small blood vesselsRetinopathy – damage to retinal capillaries; hemorrhage, blindnessNephropathy – damage microcirculation of kidneys; CRF
2. Neuropathy Damage to the neurons caused by vascular insufficiency and blood glucoseSensory and motor impairmentNumbness, tingling, pain in extremities Painless neuropathy
Impotence!!
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DISORDERS OF THE ADRENAL GLANDS
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ADRENAL GLANDSTIMULATED BY ACTHADRENAL MEDULLA- SECRETES
CATECOLAMINE, (EPINEPHRINE, & NOREPINEPHRINE).
ADRENAL CORTEX- MAIN BODY; RESP FOR SECRETION OF GLUCO,MINERALO, SEX HORMONES (ANDRO & ESTRO)
FUNCTION IS TO CONTROL THE (-) FEEDBACK MECHANISMS REGULATING HORMONE RELEASE
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ADRENAL CORTEX DISORERS
ADRENAL INSUFFICIENCY ( ADDISON’S DSE)
CUSHING’S SYNDROME
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ADRENAL INSUFFICIENCY
ADDISON’S DISEASE
INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO
STRESS
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Addison's DiseaseReplacement of hormones
Hydrocortisone; Fludrocortisone
PNSS (0.9 NaCl)Dextrose
Diet:High-CHO & CHON
Low potassium, high sodium
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Addison’s disease
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Addison's DiseaseMVS [4x / day]
Infection, Addisonian crisis, dehydration
MIOW / MBP / MBGGive steroids with milk or an
antacidAvoid: Contacts & Stress
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CUSHING’S SYNDROMECAUSE:SUSTAINED OVER-PRODUCTION OF
GLUCOCORTICOIDS BY ADRENAL GLAND FROM ACTH BY PITUITARY TUMOR
EXCESSIVE GLUCORTICOID ADMINISTRATION
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CUSHING’S SYNDROMES/SX:TRUNCAL OBESITYBUFFALO HUMPMOON-FACEWT GAINSODIUM RETENTIONTHINNING OF EXTREMITIES – FROM LOSS OF
MUSCLE TISSUE DUE TO PROTEIN CATABOLISM
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CUSHING’S SYNDROME
PURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:
OLIGOMENORRHEAHIRSUTISMGYNECOMASTIA
HYPERTENSION FROM S. Na
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CUSHING’S SYNDROME
TREATMENT & NURSING CARE:
PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE
RESPONSE ARE SUPPRESSEDPROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMYTreat HPN
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ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE
CONN’S SYNDROME
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CONN’S SYNDROMEPRIMARY ALDOSTERONISMCAUSE:ADRENAL ADENOMAS/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPNMANAGEMENT:SURGERYALDACTONE – ALDOSTERONE ANTAGONIST
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ADRENAL MEDULLA
HORMONES : EPINEPHRINE NOREPINEPHRINE
EFFECTS
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PHEOCHROMOCYTOMATUMOR OF ADRENAL MEDULLA SECRETES INCREASED
AMOUNT OF CATECHOLAMINES
A small tumor in the adrenal gland that secretes large amounts of epinephrine and norepinephrine.
S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE- VANILLYMANDALIC
ACID
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VMA IN 24H URINEEND PRODUCT OF CATECHOLAMINE
METABOLISMDRUGS & FOOD TO BE WITHHELD 24H B4 THE
TEST:COFFEE & TEABANANAVANILLACHOCOLATES
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PHEOCHROMOCYTOMAMANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING
AGENTS: PHENTOLAMINE
NURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUCOSE &
ACETONE
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THE AGING EFFECTS OF ENDOCRINE SYSTEM
DECREASE IN TSH,TH & INSULIN
DECREASE BMR & ENERGY
DECREASE GLUCOSE TOLERANCE
DECREASE IN GHDECREASE IN MUSCLE MASS & INCREASE FAT
STORAGE
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RECAP:ANTERIOR PITUITARY:GIGANTISM, ACROMEGALLY, DWARFISM
POSTERIOR PITUITARY:DIABETES INSIPIDUS, SIADHLOCATION: BASE OF THE BRAIN
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RECAPADRENAL GLAND:ADDISON’S DSECUSHING SYNDROMEALADOSTERONISM
ADRENAL MEDULLA:PHEOCHROMOCYTOMA
LOCATION: ON TOP OF THE KIDNEY
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RECAPPANCREAS:DMLOCATION: POSTERIOR TO LIVER
PARATHYROID:HYPORATHYROIDISMHYPERPARATHYROIDISMLOCATION: NEAR THYROID
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RECAPTHYROID:HYPOTHYROIDISMCRETINISMMYXEDEMAHYPERTHYROIDISM (GRAVE’S DSE)
LOCATION: ANTERIOR PART OF NECK
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QUESTION NO. 1A CLIENT IS FOUND TO BE COMATOSE &
HYPOGLYCEMIC W/ A BLOOD SUGAR OF 50 MG/DL. WHAT NURSING ACTION IS IMPLEMENTED FIRST?
A. INFUSE 1L OF D5W OVER A 12 HR PERIOD.B. ADMIN. 50% GLUCOSE IVC. CHECK THE CLIENT’S URINE FOR THE
PRESENCE OF SUGAR AND ACETONED. ENCOURAGE THE CLIENT TO DRINK ORANGE
JUICE W/ ADDED SUGAR
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QUESTION NO.2WHAT IS THE PRIMARY ACTION OF INSULIN IN
THE BODY?A. ENHANCES THE TRANSPORT OF GLUCOSE
ACROSS THE CELL WALLSB. AIDS IN THE PROCESS OF
GLUCONEOGENESISC. STIMULATES THE PANCREATIC BETA CELLSD. DECREASE THE INTESTINAL ABSORPTION OF
GLUCOSE
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QUESTION NO.3POSTOPERATIVE THYROIDECTOMY NURSING
CARE INCLUDES WHICH MEASURES?A. HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF
HOARSENESS IS PRESENTB. PROVIDE LOW-CALCIUM DIET TO PREVENT
HYPERCALCEMIAC. CHECK THE DRESSING AT THE BACK OF THE
NECK FOR BLEEDINGD. APPLY SOFT CERVICAL COLLAR TO RESTRICT
MOVEMENT
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