endocrine disorders 09
TRANSCRIPT
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Dennis Christopher D. So Chan RNTUA-SLCN
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Endocrine System The endocrine system
integrates body functions by the synthesis and release of hormones
The functions of the endocrine and the nervous system are interrelated.
Hypothalamus: link between the nervous system and the endocrine system.
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Endocrine Glands Pituitary Gland Adrenal Glands Thyroid Glands Parathyroid Glands Gonads
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Endocrine SystemEndocrine Glands
secrete their products directly to the blood stream
different from exocrine glands
Exocrine glands: secrete through ducts onto epithelial surfaces or into the GI tract
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Overview of the Endocrine SystemThe body’s second great controlling system
which influences metabolic activities of cells by means of hormones, which are produced by endocrine glands Endocrine glands: pituitary, thyroid,
parathyroid, adrenal, pineal, and thymus The pancreas and gonads produce both
hormones and exocrine productsThe hypothalamus has both neural functions and
releases hormonesOther tissues and organs that produce
hormones: adipose cells, pockets of cells in the walls of the small intestine, stomach, kidneys, and heart
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Functions of Endocrine System1. Metabolism and tissue maturation2. Ion regulation3. Water Balance4. Immune system regulation5. Heart rate and blood pressure regulation6. Control of blood glucose and other
nutrients7. Control of reproductive function8. Uterine contractions and milk release
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Hormones Are chemical substances that are secreted by
the endocrine glands. Can travel moderate to long distances or very
short distances. Acts only to cells or tissues that have
receptors for the specific hormone. Target organ: the cell or tissue that responds
to a particular hormone.
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Hormones are dissolved in plasma or bind to plasma proteins
Water-soluble hormonesProteins, epinephrine, and norepinephrineDo not bind to plasma proteins or readily diffuse out of
the bloodThey are quickly broken down by enzymes or are taken
up by tissuesThese hormones regulate activities that have a rapid
onset and a short durationLipid-soluble hormones and thyroid hormones
Not quickly removed from the bloodProduce a prolonged effect
Hormones leave the blood to reach target tissues or are excreted by the kidneys or liver
Hormone Transport and Excretion
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Regulation of Hormones If the client is healthy, the concentration or
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 the production of that hormone increases.
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Diseases of the Endocrine System Primary Disease- problem in target gland;
autonomous
Secondary Disease-problem outside the target gland; most often due to a problem in pituitary gland
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HypopituitarismHyperpituitatism
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Hypopituitarism Caused by low levels of one or more anterior
pituitary hormones.
Lack of the hormone leads to loss of function in the gland or organ that it controls.
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Causes of Primary Hypopituitarism Pituitary tumors Inadequate blood supply to the pituitary gland
o e.g. Sheehan’s syndrome Infections and or inflammatory diseases
o sarcoidosiso amyloidosis
Radiation therapy Surgical removal of pituitary tissue Autoimmune diseases Congenital absence
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Causes of 2° Hypopituitarism Tumors of the hypothalamus Inflammatory disease Head injuries Surgical damage to the pituitary and/or blood
vessels or nerves leading to it.
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Signs and Symptoms Tumor: bitemporal
hemianopsia on visual confrontation
Varying signs of hormonal disturbances depending on which hormones are being under secreted
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Signs and Symptoms Gonadotropin Deficiency
Congenital Onset Delayed or absent secondary sexual
characteristics May have micropenis, cryptorchidism
Acquired Loss of body hair Infertility, decrease libido, impotence in males,
amenorrhea in females Prolactin Deficiency
Failure to lactate
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Signs and Symptoms TSH (Thyroid Stimulating hormone) Deficiency
causes hypothyroidism with manifesations such as fatigue, weakness, weight change, and hyperlipidemia
Adrenocorticotropic (ACTH) hormone deficiency
• results in diminished cortisol secretion.• symptoms include weakness, fatigue, weight
loss, and hypotension
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Signs and Symptoms
Growth hormone (GH) deficiency
In childhood: failure to grow
In adulthood: mild to moderate central obesity, increased systolic BP and increases in LDL cholesterol
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Diagnostics X-ray, MRI or CT
scan: pituitary tumor
Plasma hormone levels: decreased
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Therapeutics Hormonal Substitution: may be for life
corticosteroids levothyroxine androgen for males estrogen for females Growth hormone
Radiation therapy for tumorsSurgery for tumors: Transphenoidal Hypophysectomy
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Hyperpituitarism Hyperfunction of the anterior pituitary
gland=oversecretion of one or more of the pituitary hormones
Usually caused by benign pituitary adenoma 2 most common hormones affected:
Prolactin growth hormone
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Prolactinoma vs.Somatotropinoma
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Prolactinoma Female: galactorrhea menstrual
disturbances, infertility, signs of estrogen deficit (vaginal mucosal atrophy, decreased vaginal lubrication and libido)
Male: Decreased libido and possible impotence, reduced sperm count and infertility, gynecomastia
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Growth Hormone Hypersecretion Gigantism: GH hypersecretion prior to
closure of epiphyses; proportional growth
Acromegaly: GH hypersecretion after closure of epiphyses; disproportional growth
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Gigantism vs. Acromegaly
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Growth Homone Hypersecretion:Signs and Symptoms Enlarged hand and feet; carpal tunnel syndrome
common Coarsening of features esp. in Acromegaly;
prominent mandible, tooth spacing widens, Macroglossia leading to OSA Hypertension, cardiomegaly, heart failure Insulin resistance leading to type 2 DM Visual field defects: bitemporal hemianopsia-
>complete blindness Headaches Arthritis Hypogonadism
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Therapeutics Medication
bromocriptine and cabergoline (dopamine agonist) For prolactinoma and GH hypersecretion
Octreotide (somatostatin) for GH hypersecretion Sx
surgical remission is achieved in about 70% of patients followed over 3 years
Growth hormone levels fall immediately; diaphoresis and carpal tunnel syndrome often improve within a day post-Sx
Radiation Therapy for large tumors Diet
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Nursing Interventions Provide emotional support=striking body
change can cause psychological stress. Perform or assist with range of motion
exercises to promote maximum joint mobility and prevent injury.
Evaluate muscle weakness, especially in the patient with late stage Acromegaly.
Keep the skin dry. Avoid using an oily lotion because the skin is already oily.
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Nursing Interventions Be aware that pituitary tumor cause visual
problems. If there is hemianopsia, stand where he can see you.
Warn relatives that hyperpituitarism can cause inexplicable mood changes.
If the patient is a child, explain to the parents that surgery prevents permanent soft-tissue deformities but won’t correct bone changes that have already occurred.
After an operation, emphasize the importance of continuing hormone replacement therapy.
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Transphenoidal Hypophysectomy
Endoscopic, transnasal, transsphenoidal pituitary microsurgery.
Removal of adenoma while preserving anterior pituitary function in most patients.
Surgery is usually well tolerated, but complication occur in about 10%.
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Postoperative care WOF: Bleeding
operative site is patched with muscle or fat-> sutures easily disrupted.
keep the patient on bed rest for 24 hours after surgery and encourage ambulation thereafter
keep the head of bed elevated (30°) to avoid placing tension or pressure on the suture line.
Instruct the patient not to sneeze, cough, blow his nose, or bend over for several days to avoid disturbing the suture line.
Arrange for visual field testing as soon as possible because visual defects can indicate hemorrhage.
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Postoperative Care WOF: CSF leak and infection
reinforce measures to prevent increased ICP oral care, BUT the patient should not brush his
teeth for 2 weeks to avoid suture line disruption Signs of CSF leak
Frequent clearing of the throat and swallowing Presence of halo ring on gauze Test for glucose Signs of infection Fever, headache, nuchal rigidity
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Postoperative Care WOF: Post-Op pain
Mild analgesics for headache caused by CSF loss during surgery or paranasal pain.
Paranasal pain typically subsides when the catheters and packing are removed, usually 24 to 72 hours after surgery
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Postoperative Care WOF: Diabetes Insipidus
due to inadequate release of ADH usually happens 24 to 48 hours after surgery and
may resolve within 72 hours. be alert for increased thirst and increased specific
gravity. Management I & O, urine sp. Gravity and daily weight monitoring Fluid replacement Aqueous vasopressin, sublingual desmopressin
acetate.
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Postoperative Care WOF: S/Sx of hypopituitarism
patient may need hormonal replacement therapy due to decreased pituitary secretion of tropic hormones.
Necessary: cortisol immediate post-op Maintenance hormonal replacement as needed
o Cortisolo Thyroxineo Estrogen or Testosteroneo Vasopressin
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Diabetes InsipidusSIADH
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Vasopressin or Antidiuretic Hormone
Regulates water metabolism
Released during stress or in response to an increase plasma osmolality to stimulate reabsorption of water and decreased urine output.
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Diabetes Insipidus Disorder characterized by massive polyuria
due to either lack of ADH or kidney’s insensitivity to it.
Types:Central DINephrogenic DI
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Diabetes Insipidus Central Diabetes Insipidus: Deficiency of
vasopressinPrimary diabetes Insipidus ( without an identifiable
organic lesion noted on MRI of the pituitary and hypothalamus) May be familial, occurring as a dominant trait, or
(“idiopathic”)Secondary diabetes insipidus
Due to damage to the hypothalamus or pituitary stalk by tumor, anoxic encephalopathy, surgical or accidental trauma, infection (encephalitis, tuberculosis, syphilis), sarcoidosis, or multifocal langerhans cell (eosinophilic) granulomatosis (“histiocytosis X”)
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Diabetes Insipidus “Nephrogenic Diabetes Insipidus”
Due to defect in the kidney tubules that interferes with water reabsorption
Polyuria is unresponsive to vasopressinPatients have normal secretion of vasopressin
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Diabetes InsipidusSigns and Symptoms Polyuria-> enormous daily output of very dilute
urine, water-like urine with specific gravity of 1.001 to 1.005
Intense thirst (patient tends to drink 4 to 40liters of fluid daily), especially with a craving for ice water,
Dehydration-> weight loss, poor tissue turgor, dry mucous membranes, constipation, muscle weakness, dizziness.
Inadequate water replacement results in Hyperosmolality (irritability, mental dullness,
coma, hyperthermia) because of dehydration and hypernatremia
Hypovolemia (hypotension, tachycardia and shock eventually)
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Diabetes Insipidus Diagnostics
Fluid deprivation test-> to differentiate between psychogenic polydipsia and DI
Administration of desmopressin->to differentiate between central DI and nephrogenic DI
24 hour urine collection of volume, glucose, and creatinine
Serum for glucose, urea nitrogen, calcium, uric acid, potassium and sodium.
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TherapeuticsMedications
For central DI Desmopressin (DDAVP): intranasal Lypressin: intrasanal Vasopressin tannate in oil: IM
For nephrogenic DI: Indomethacin-hydrochlorthiazide (with potassium
supplementation) Indomethacin-demopressin Indomethacin-amiloride
Clofibrate, chlorpropamide and thiazide diuretics (mild DI)
Psychotherapy
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DI: Nursing ManagementMaintain fluid and Sodium balance
Record I & O. Weigh patient daily.Maintain fluid intake to prevent dehydration.WOF: dehydration and shockKeep the side rails up and assist with walking if
the patient is dizzy or has muscle weakness.Monitor urine specific gravity between doses.
Watch for decreased specific gravity with increased urine output->need for the next dose or a dosage increase.
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DI: Nursing Management Add more bulk foods and fruit juices to the diet-
>to prevent constipation. Laxative (milk of magnesia PRN).
Provide meticulous skin and mouth care, and apply a lubricant to cracked or sore lips.
Diet: low in sodium Carry out drug therapy
caution must be used with administration of vasopressin if coronary artery disease is present->causes vasoconstriction
assist in searching for the underlying pathology
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Syndrome of Inappropriate Antiduretic Hormone (SIADH) Disorder due to
excessive ADH release Signs and Symptoms
persistent excretion of concentrated urine
signs of fluid overload change in level of
consciousness NO EDEMA HYPONATREMIA
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Causes of SIADH Tumors: bronchogenic carcinoma, lymphoma,
pancreatic cancer, mesothelioma Pulmonary: TB, pneumonia, lung abscess, COPD,
pneumothorax, HIV secretion CNS: meningitis, head injury, subdural hematoma,
subarachnoid hemorrhage, neurosurgery Drugs: some medications (vincristine,
phenotiazines, tricylic antidepressants, thiazide diuretics, and others) and nicotine have been implicated in SIADH; they either directly stimulate the pituitary gland or increase the sensitivity of renal tubules to circulating ADH.
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SIADH: diagnostic tests Low serum sodium (<135meqs/L) Low serum osmolality High urine sodium osmolality (urine
osmolality >100 mosmol/kg) High urine sodium excretion (>20 mmol/L) Normal renal function (low
BUN<10mg/dL),absence of hypothyroidism and glucocorticoid deficiency and recent diuretic therapy.
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SIADH: Management Maintain fluid balance
Restriction or water intake (<1,000ml/day). (takes 3-10 days to work) If the patient has evidence of fluid
overloading, a history of CHF, or is resistant to treatment, loop diuretics (furosemide) may be added as well.
Chronic treatment: lithium or demeclocycline which inhibit ADH action.
Monitoring of body weight.
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SIADH: Management Maintain sodium balance
Increase sodium intake if the serum sodium is below 120 or if the
patient is seizing, emergency treatment: 3% NaCL. May be followed by furosemide.
Excessively rapid correction of hyponatemia may cause central pontine myelinolysis.
Patients with a plasma sodium concentration greater then 125 mmol/L rarely need specific therapy for hyponatremia.
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Adrenal InsufficiencyCushing’s SyndromeHyperaldosteronsimPheochromocytoma
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Adrenal Cortex Hormones Glucocorticoids
Cortisol, corticosterone Increased blood glucose levels by increasing
the rate of gluconeogenesis. Increase protein catabolism Increasing mobilization of fatty acids promote
Na and H2O retention Anti-inflammatory effect Aid the body in coping with stress
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Adrenal Cortex Hormones Mineralocorticoids
Aldosterone, corticosterone, Deoxycorticosterone
Regulate fluid and electrolyte balanceStimulate reabsorption of sodium, chloride and
waterStimulate potassium excretion.
Under the control of the Renin-Angiotensin-aldosterone system
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Adrenal cortex hormones Sex hormones
Androgens, EstrogensInfluences the development of sexual
characteristics
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Adrenal Medulla Release catecholamines
EpinephrineNorepinephrine
Released during “fight or flight” situations-> SYMPATHETIC effect
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Hypercortisolism (Cushing’s Syndrome)Cluster of physical
abnormalities due to excessive cortisol release
Cortisol excess is due either to: Autonomous steroid
release from adrenal Increased ACTH release
from pituitary complication of
exogenous steroid therapy
Pic of hympy dumpty
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Hypercortisolism (Cushing’s Syndrome)Altered metabolism of
CHO: hyperglycemiaCHON: muscle wasting, thin, fragile skin,
impaired wound healingFats: central obesity, moon face, buffalo humpNa and water retentionHypokalemia, hypocalcemiaAcne, hirsutism, menstrual changes, decreased
libidoWeakness, emotional lability
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Cushing’s Syndrome
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Complications Osteoporosis
Peptic Ulcer
Immune and inflammatory response is also compromised
Other complications include HPN, and sexual and psychological complications
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Cushing’s Syndrome: Diagnostics ACTH levels-> determine whether the
syndrome is ACTH dependent. 24-hour urine collection for cortisol, midnight
serum cortisol Dexamethasone suppression test-> 1mg
dexamethasone given at 11 pm and serum cortisol taken at 8am the next day.Cortisol level <5ug/dl excludes Cushing’s
syndrome with 98% certainty Radiologic evaluation
Tumor in the pituitary or adrenal gland
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Cushing’s Syndorme: Management Transsphenoidal resection of pituitary tumor Medications:
o Aminogluthetimide: adrenal enzyme inhibitoro Metyrapone and ketoconazole: suppress
hypercortisolism in unresectable adrenal tumor Antihypertensives Adrenalectomy as needed
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Cushing’s Syndome: Nursing ConsiderationsMonitor VS, WOF for HPNSafety Precaution:
Maintain muscle tone Prevent accidents or falls and provide adequate rest
Protect client from exposure to infection, monitor WBC
Maintain skin integrityMinimize stressProvide diet low in calories, sodium and high
in protein, potassium, calcium and vitamin DMonitor for urine glucose and acetone, administer
insulin if necessaryPrepare client for adrenalectomy if needed
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HyperaldosteronismHypersecretion of aldosterone from the
adrenal cortex
Two types: Primary disease of the adrenal cortex Secondary condition due to increased plasma
renin activityCauses:
Excessive reabsorption of sodium and water Excessive renal excretion of potassium
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Hyperaldosteronism: CausesPrimary hyperaldosteronism: Autonomous
secretion of aldosterone from the adrenals Benign adrenal adenoma (Conn’s syndrome)
Secondary hyperaldosteronism: High renin state-> stimulating aldosterone release Renal artery stenosis Wilm’s tumor Pregnancy Oral Contraceptive use Nephritic syndrome Cirrhosis with ascites Heart failure
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Hyperaldosteronism: signs and sypmtoms Hypertension
Headache and visual disturbance Hypokalemia
Muscle weakness and fatigueParesthesia and ArrhytmiasPolyuria and PolydipsiaTetany from alkalosis
Hypernatremia
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Hyperaldosteronism: DiagnosticsHypokalemiaHypernatremiaElevated serum bicarbonate and pHHypomagnesemiaElevated plasma and urinary aldosteroneDecreased Renin in 1° hyperaldosteronismIncreased Renin in 2° hyperaldosteronismLow specific gravity urine (diluted urine)
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Hyperaldosteronism: TreatmentPrimary hyperaldosteronism:
Unilateral adrenalectomy After aderenalectomy, WOF: signs of adrenal insufficiency.
• Potassium-sparing diuretic (such as spironolactone or amiloride)-> may lead to decreased libido, gynecomastia, impotence
• Antihypertensives• Aminogluthetimide-> inhibits synthesis of
aldosterone.• Diet: sodium restriction, increased potassium• Treatment of secondary hyperaldosteronism:
include correction of the underlying cause.
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Adrenal Insufficiency• 1° adrenal insufficiency: Addison’s disease
The most common form of adrenal hypofunction-> occurs when more than 90% of the adrenal gland is destroyed
Autoimmune process-> decreased secretion of androgen, glucocorticoids, and mineralocorticoids.
• 2 ° adrenal Insufficiency: It may also be caused by a disorder outside the gland Aldosterone secretion frequently continues.Nursing Alert! Adrenal crisis (addisonian crisis) is
a medical emergency requiring immediate, vigorous treatment.
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Adrenal Insufficiency:causesAutoimmune destruction of the adrenal gland,
tuberculosis, bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, or fungal infections.
Secondary adrenal hypofunction is caused by Hypopituitarism Abrupt withdrawal of long term corticosteroid
therapy• In a patient with adrenal hypofunction, adrenal
crisis occurs when the body’s stores of glucocorticoids are exhausted by trauma, infection, surgery, or other physiologic stressors.
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Adrenal Insufficiency: signs and symptomsWeakness, fatigue
Weight loss, nausea and vomiting, anorexia
Chronic constipation or diarrhea
Cardiovascular abnormalities Postural hypotension, decreased cardiac output Weak, irregular pulse Decreased tolerance for even minor stress
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Adrenal Insufficiency: signs and symptomsConspicuous bronze skin coloration,
especially in hand creases and over the metacarpophalangeal joints, elbows, and knees.
Poor coordinationFasting hypoglycemia; and craving for salty
food.AmenorrheaAdrenal crisis
Profound weakness and fatigue, shock, severe nausea and vomiting, hypotension, dehydration and high fever.
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POMC: the “Big Momma”MSH is produced when the ACTH production
is increased-> hyperpigmentation
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Adrenal Insufficiency
Decreased plasma cortisol levels and serum sodium levels.
Increased ACTH (in addison’s), serum potassium, and BUN level.
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Adrenal Insufficiency: TreatmentCorticosteroid replacement, usually with
cortisone or hydrocortisone-> primary lifelong treatment
Fludrocortisone acetate: acts as a mineralocorticoid to prevent dehydration and hypotension.
Adrenal Crisis: prompt IV bolus of corticosteroids, 3 to 5 L of IV fluids, dextrose
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Adrenal Insufficiency: Nursing ManagementWOF: adrenal crisis
Hypotension and signs of shock (decreased level of consciousness and urine output)
Watch for hyperkalemia before treatment and for hypokalemia after treatment (from excessive mineralocorticoid effect)
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Adrenal Insufficiency: Nursing Management
If patient has diabetes, check blood glucose levels periodically because steroid replacement may necessitate changing the insulin dosage.
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Adrenal Insufficiency: Nursing Management Diet: maintain sodium and potassium balance,
high protein and carbohydrates
If the patient is anorexic, suggest six small meals per day to increase calorie intake.
Observe the patient receiving steroids for cushingoid signs, such as fluid retention around the eyes and face.
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Adrenal Insufficiency: Nursing Management Instruct on lifelong cortisone replacement
therapy: “ Do not omit medications” Give 2/3 of dose in AM and 1/3 in PM
Instruct the patient that he’ll need to increase the dosage during times of stress.
Warn that infection, injury, or profuse sweating in hot weather may precipitate crisis.
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Pheochromocytoma Rare disorder, a chromaffin-cell tumor of the
sympathetic nervous system, usually in the adrenal medulla, secretes an excess of the catecholamines epinephrine and norepinephrine.
This causes episodes of hypotension and symptoms of catecholamine excess.
The tumor is usually benign but may be malignant in as many as 10% of patient.
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Pheochromocytoma
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Pheochromocytoma: Signs and Symptoms Think sympathetic!!!
Persistent or paroxysmal HPN Palpitations, tachycardia,
headache, visual disturbances, diaphoresis, pallor, warmth or fluting, paresthesia, tremor, and excitation.
Anxiety, fright, nervousness, feelings of impending doom, abdominal or chest pain, tachypnea, N&V, fatigue, wt. loss, constipation, postural hypotension, paradoxical response to antiHPNs(common), hyperglycemia
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Pheochromocytoma:Diagnostic tests:
Increased plasma levels of catecholamines, elevated blood sugar, glucosuria
Elevated urinary catecholamines and urinary VMA Nursing considerations! Avoid coffee, nuts,
chocolate, banana, vanilla.
Tumor on CT scan.
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Pheochromocytoma: TreatmentSurgical removal of the tumor with sparing of
the normal adrenals, if possible WOF: hypo or hypertension post-op
Anti-hypertensives: Alpha-adrenergic blocker ( phentolamine,
prazosin, or phenoxybenzamines) A beta-blocker (propanolol)
Metyrosine may be used to block catecholamine synthesis.
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AdrenalectomyResection or removal of one or both adrenal
glands.
The treatment of choiceFor adrenal hyperfunction and
hyperaldosteronismAdrenal tumors, such as adenomas and
pheochromocytomas.
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Adrenalectomy: Pre-opCorrect electrolyte imbalance
Potassium, sodium, calcium
• Manage hypertension
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Adrenalectomy: Post-Op careMonitor vital signsWOF: shock and hemorrhageKeep in mind that postoperative hypertension
is common because handling of the adrenal glands stimulates catecholamine release.
WOF: adrenal crisis-> hypotension, hyponatremia, hyperkalemia
Remember, glucocorticoids from the adrenal cortex are essential to life and must be replaced to prevent adrenal crisis until the hypothalamic, pituitary, and adrenal axis resumes functioning.
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Adrenalectomy: Nursing interventionsInstruct the patient to take prescribed
medication as directed.
If patient had unilateral adrenalectomy, explain that he may be able to taper his medication in a few months.
Inform patient that sudden withdrawal of steroids can precipitate adrenal crisis.
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HyperthyroidismHypothyroidsim
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The Thyroid GlandThyroid gland is a butterfly-shaped organ located in the lower neck anterior to the trachea
It consists of two lateral lobes connected by an isthmus
The gland is about 5cm long and 3cm wide and weighs about 30g
It produces 3 hormones: T3, T4, and calcitonin
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Functions of Thyroid HormonesT3
T4
Calcitonin
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Tests of Thyroid FunctionThyroid-Stimulating Hormone
Single best screening test of thyroid function because of its high sensitivity
Values above the normal range of 0.38 to 6.15 uU/mL are indicative of primary hypothyroidism, and low values indicate hyperthyroidism
If TSH is normal, there is a 98% chance that the free thyroxine (FT4) is also normal.
Used for monitoring thyroid hormone replacement therapy and for differentiating between disorders of the thyroid gland and disorders of the pituitary or hypothalamus.
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Tests of Thyroid FunctionSerum Free Thyroxine
Test used to confirm an abnormal TSH is FT4 FT4 is a direct measurement of free (unbound)
thyroxine, the only metabolically active fraction of T4.
Normal value: 0.9 and 1.7ng/L (11.5 to 21.8pmol/L)Serum T3 and T4
Normal range for T4 is between 4.5 and 11.5ug/dL (58.5 to 150 nmol/L)
Although serum T3 and T4 levels generally increase or decrease together, the T3 level appears to be a more accurate indicator of hyperthyroidism, which causes a greater rise in T3 than T4 levels.
Normal range for serum T3 is 70 to 220ng/dL (1.15 to 3.10 nmo/L)
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Tests of Thyroid FunctionThyroid scan, Radioscan, or Scintiscan
In a thyroid scan, a scintillation detector or gamma camera moves back and forth across the area to be studied and a visual image is made of the distribution of radioactivity in the area being scanned.
• Isotopes used: 123I->most commonly used isotope. Technetium-99m pertechnetate, thallium,
thallium and americanium Scans are helpful in determining location, size, shape,
and anatomic function of the thyroid gland, particularly when thyroid tissue is substernal or large.
Identifying areas of increased function (“Hot”areas) or decreased function (“cold” areas) can assist in diagnosis.
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Tests of Thyroid FunctionRadioactive Iodine Uptake
Measures the rate of iodine uptake by the thyroid gland.
The patient is administered a tracer dose of iodine-123
Measures the proportion of the administered dose present in the thyroid gland at a specific time after its administration.
Affected by the patient’s intake of iodine or thyroid hormone; therefore, a careful preliminary clinical history is essential in evaluating results.
Hyperthyroidism-> high uptake of the 123I Hypothyroidism-> very low uptake.
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Tests of Thyroid FunctionFine-Needle
Aspiration Biopsy Sampling Thyroid
Tissue to: detect malignancy
Initial test for evaluation of thyroid masses.
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Tests of Thyroid Function
Nursing Implications of Thyroid TestsIt is necessary to determine whether the
patient has taken medications or agents that contain iodine because these alter the results of some of the schedule tests.
Assess for allergy to iodine or shellfishFor the scans, tell patient that radiation is
minimal
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Plummer’s nails
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HyperthyroidismOr thyrotoxicosisIncreased metabolic rateCauses:
o Grave’s diseaseo Initial manifestations of thyroiditis (hashimoto’s
and subacute thyroiditis)o Toxic adenomao TSH-secreting pituitary tumoro Factitious thyrotoxicosiso Jodbasedow diseaseo Amiodarone-induced
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Hyperthyroid: Signs and SymptomsEnlarged thyroid glandTachycardia-> atrial fibrillation, heart failureHypertensionHeat intolerance, diaphoresisSmooth, soft, warm skinFine Soft HairDiarrhea, weight loss inspite of increased appetiteNervousness and fine tremors of hands.Hyperactive reflexes, body weaknessPersonality changes, mood swingsOsteoporosisClubbing and swelling of fingers, Plummer’s nailsMenstrual disturbances, decreased fertility
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Signs and Symptom’s of Grave’s DiseaseAll s/s of thyrotoxicosis
Grave’s exopthalmos-> vision loss, diplopia
Pretibial Edema
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Hyperthyroidism
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Thyroid StormA medical emergency: high mortality
Marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, high fever
Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid surgery, RAI administration
Increased systemic adrenergic activity->epinephrine overproduction and severe hypermetabolism
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Hyperthyroidism: DiagnosticsRadioimmunoassay test shows elevated T4
and T3.Thyroid scan reveals increased radioactive
iodine (123I) uptake.↓TSH in 1° hyperthyroidism↑TSH in 2° hyperthyroidismOrbital sonography and CT scan confirm
subclinical ophthalmopathy
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Hyperthyroidism: ManagementPropylthiouracil (PTU) and methimazoleUsed for pregnant women and patient who refuse
surgery or 131I treatment.During pregnancy PTU, is the preferred
therapyA few (1%) of the infants born to mothers
receiving antithyroid medication will be hypothyroid.
Mechanism of actionBlocks thyroid hormone synthesis
• WOF: Agranulocytosis
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Hyperthyroidism: ManagementRadioactive iodine (131I), potassium or
sodium iodide (Potassium iodide SSKI), strong iodine solution (Lugol’s solution)
Adjunct with other antithyroid drugs in preparation for thyroidectomy
Treatment for thyrotoxic crisis: Inhibits the release and synthesis of thyroid
hormonesDecreases the vascularity of the thyroid glandDecreases thyroidal uptake of radioactive iodine
following radiation emergencies or administration of radioactive isotopes of iodine.
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Hyperthyroidism: Nursing ManagementPotassium, or sodium iodide, (potassium iodide
solution, SSKI) strong iodine solution (Lugol’s solution) Category D
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
Warn the patient that sudden withdrawal may precipitate thyrotoxicosis
Store in a light-resistant containerGive iodides through a straw to avoid tooth
discolorationForce fluids to prevent fluid volume deficit
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Hyperthyroidism: Nursing Management of RAI treatmentRadioactive iodine (sodium iodide or 131I)-cat. X
Food may delay absorption. The patient should fast overnight before administration
After dose for hyperthyroidism, the patient’s urine and saliva are slightly radioactive for 24 hours; vomitus is highly radioactive for 6 to8 hours.
Institute full radiation precautions during this time
Instruct the patient to use appropriate disposal methods when coughing and expectorating.
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Hyperthyroidism: Nursing Management of RAI Tx After dose for thyroid cancer, isolate the
patient and observe the following precations:Pregnant personnel shouldn't take care of the
clientDisposable eating utensils and linens should be
usedInstruct the patient to save all urine in lead
containers for 24 to 48 hours so amount of radioactive material excreted can be determined
Or flush the toilet twice after urination
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Hyperthyroidism: Nursing Management of RAI Treatment
The patient should drink as much fluid as possible for 48 hours after drug administration to facilitate excretion.
Limit contact with the patient to 30 minutes per shift per person the 1st day; may increase time to 1 hour on 2nd day and longer on the 3rd day.
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Hyperthyroidism: Nursing Management of RAI treatment If the patient is discharged less than 7 days
after 131I dose for thyroid cancer, warn patient:To avoid close, prolonged contact with small
childrenNot to sleep in the same room with his spouse
for 7 days after treatment-> increased risk of thyroid cancer in persons exposed to 131I.
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Hyperthyroidism B- blockers, Digoxin, anticoagulation Prednisone for opthalmopathy Treatment for thyroid storm:
o PTUo I.V. propanolol to block sympathetic effectso Corticosteroids to replace depleted cortisol
levelso Iodide to block release of thyroid hormone
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Hyperthyroidism: ManagementSurgery: ThyroidectomyFor exopthalmos
Suggest sunglasses or eye patches to protect his eyes from light
Moisten the conjunctivae often with artificial tears Warn the patient with severe lid retraction to avoid
sudden physical movement that might cause the lid to slip behind the eyeball.
Elevate the head of bed to reduce periorbital edema Stress the importance of regular medical follow-up
after discharge because hypothyroidism may develop from 2 to 4 weeks pot-op
Drug therapy and 131I therapy require careful monitoring and comprehensive teaching
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Hypothyroidism A state of low serum thyroid hormone levels or cellular
resistance to thyroid hormoneCauses May result from thyroidectomy Radiation therapy Chronic autoimmune thyroiditis ( Hashimoto’s Thyroiditis) Inflammatory conditions such as amyloidosis and
sarcoidosis Pituitary failure to produce TSH Hypothalamic failure to produce thyrotropin-releasing
hormone(TRH) Inborn errors of thyroid hormone synthesis An inability to synthesize thyroid hormone because of
iodine deficiency. Use of antithyroid medications such as PTU.
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Hypothyroidism Weakness Fatigue Forgetfulness Cold intolerance Unexplained weight gain Constipation Goiter Slow speech Decreasing mental
stability
Cool, dry, coarse, flaky inelastic skin.
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HypothyroidismPuffy face, hands and feetDry, sparse hairThick, brittle nailsSlow pulse rateAnorexiaAbdominal distentionMenorrhagia Decreased libidoInfertilityAtaxiaIntentional tremor
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Myxedema Coma Manifests as hypotension, bradycardia,
hypothermia, hyponatremia, hypoglycemia, respiratory failure, coma
Can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia, surgery, hypothermia, use of opioids
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Hypothyroidism : Diagnostics Radioimmunoassay tests: ↓ T3 & T4 ↑TSH level with 1° hypothyroidism ↓TSH in 2 ° hypothyroidism Serum cholesterol and triglyceride levels are
increased
In myxedema coma Low serum Na levels Respiratory acidosis because of hypoventilation
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ManagementPrevention: Prophylactic iodine
supplements to decrease the incidence of iodine deficient goiter
Symptomatic cases:Hormonal replacement: synthroid
(synthetic hormone (levothyroxine))-dosage is increased q 2-3weeks
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Nursing Management of replacement therapy Warn the patient (especially the elderly) to
tell the doctor if withChest pain, palpitations, sweating,
nervousness, or other signs or symptoms of overdosage
Signs and symptoms of aggravated cardiovascular disease (chest pain, dyspnea and tachycardia)
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Nursing Management of replacement therapy Instruct the patient to take thyroid hormones
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 is >100bpm, withhold the drug. Assess to tachyarrhythmia and chest pain.
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Nursing Management of Replacement therapy Thyroid hormones alter thyroid function test
results.For 123I uptake studiesD/C levothyroxine 4 weeks before the test.D/C liothyronine 7 to 10 days before the test.
Monitor prothrombin time; a patient taking these hormones usually requires less anticoagulant WOF: unusual bleeding and bruising
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Hypothyroidism: Nursing InterventionsDiet: High bulk, low-calorie dietEncourage activityMaintain warm environmentAdminister cathartics and stool softeners, as needed.To prevent myxedema coma, tell the patient to
continue his course of thyroid medication even if his symptoms subside: Maintain patent airway Administer meds-synthroid, glucose, corticosteroids. IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness
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HyperparathyroidismCharacterized by
excess activity or one more of the four parathyroid glands, resulting in excessive secretion of parathyroid hormone(PTH)
Maybe primary or secondary
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Hyperparathyroidism: causes1° hyperparathyroidism:
Single adenoma, genetic disorders, or MEN
• 2 ° hyperparathyroidism:Rickets, vitamin D deficiency, chronic renal
failure, phenytoin or laxative abuse.
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HyperparathyroidismEffect of PTH secretion: ↑Calcium
Through increased bone resorption, increased GI and renal absorption of calcium
• Complications Renal calculi-> renal failure Osteoporosis Pancreatitis Peptic ulcer
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HyperparathyroidismTHINK OF HYPERCALCEMIA: CNS: psychomotor and personality disturbances,
loss of memory for recent event, depression, overt psychosis, stupor and possibly, coma.
GI: anorexia, N&V dyspepsia, and constipation.
Neuromuscular: fatigue; marked muscle weakness and atrophy, particularly in the legs.
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Hyperparathyroidism:Signs and Symptoms Renal: symptoms of recurring nephrolithiasis-
>renal insufficiency
Skeletal and articular: chronic lower back pain and easy fracturing from bone degeneration, bone tenderness, joint pain
Others: skin pruritus, vision impairment, subcutaneous calcification.
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Hyperparathyroidism: Dx ↑ serum PTH levels ↑ serum Ca and decreased Phosphorus
levels. X-rays may show diffuse demineralization of
bones Elevated alkaline phosphatase
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Hyperparathyroidism: Treatment Surgery to remove the adenoma Force fluids; limiting dietary calcium intake For life threatening hypercalcemia: promote
sodium and calcium excretion, using normal saline solution (up to 6L in life-threatening situations), furosemide, and administering oral sodium or potassium phosphate, Calcitonin
Postmenopausal women: estrogen supplements
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Hypoparathyroidism A deficiency of PTH PTH primarily regulates calcium balance; hypoparathyroidism leads to
hypocalcemia and produces neuromuscular symptoms ranging from paresthesia to tetany.
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Hypoparathyroidism Congenital absence or malfunction of the parathyroid
glands. Autoimmune destruction Removal of or injury to one or more parathyroid glands
during neck surgery Rarely, from massive thyroid radiation therapy. Ischemic infarction of the parathyroids during Sx. Diseases, such as amyloidosis or neoplasms Suppression of normal gland function caused by
hypercalcemia(reversible) Hypomagnesemia-induced impairment of hormone
secretion(reversible)
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Hypoparathyroidism: Signs and Sypmtoms Neuromuscular irritability Increased deep tendon reflexes, (+) chvostek’s and Trousseau’s
signs Dysphagia Paresthesia Psychosis Mental deficiency in children Tetany seizures Arrhythmias Abdominal pain Dry, lusterless hair, spontaneous hair loss Brittle fingernails that develop ridges or fall out. Dry scaly skin Weakened tooth enamel may cause teeth to stain, crack, and
decay easily.
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Hypoparathyroidism
Decreased PTH and serum calcium levels
Elevated serum phosphorus levels
X-rays reveal increased bone density
ECG: prolonged Qti, QRS-complex ST-elevation changes.
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Diabetes Mellitus
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Hormones of the PancreasInsulin
Decreases blood sugar: Stimulating active transport of glucose into muscle
and adipose tissue Promoting the conversion of glucose to glycogen for
storage Promoting conversion of fatty acids into fat Stimulating protein synthesis
Secreted in response to high blood sugarFound in βcells of the islets of langerhans
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Hormones of the PancreasGlucagon
Increases blood glucose by Causing glycogenolysis and gluconeogenesis in the
liver
Secreted in response to low blood sugar Found in the α-cells of the islets of langerhans
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Diabetes MellitusChronic disease characterized by
hyperglycemiaIt is due to total or partial insulin deficiency or
insensitivity of the cells to insulin
Characterized by disorders in the metabolism of CHO, FAT and CHON as well changes in the structure and function of blood vessels.
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Types of DM Type 1 or IDDM
Usually occurs in children or in non-obese adults
Type 2 or NIDDM Usually occurs in obese adult over age 40
Gestational DM Secondary DM
Induced by trauma, surgery, pancreatic disease or medications
Can be treated as either type 1 or type 2
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Comparison Bet Type 1 and Type II Diabetes Mellitus
Type 1 Type 2
Onset- SuddenAge at Onset- Any age
(typically young)Body Habitus- Usually
thinKetosis- commonAutoantibodies-present
in most casesEndogenous insulin- low
or absent
GradualMostly in adults
Frequently obeseRareAbsent
Can be normal, decreased, or increased.
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PathophysiologyHyperglycemia Lack of insulin causes
hyperglycemia (insulin is necessary for the transport across the membrane)
Body excretes excess glucose through kidneys ->osmotic diuresis->polyuria->dehydration->polydipsia
Cellular starvation-> polyphagia
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Cont. pathophysiology
The body turns to fats and protein for energy; but in the absence of glucose in the cell, fats cannot be completely metabolized and ketones are produced
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Chronic Complications
Microangiopathy: retinopathy, nephropathy
Macroangiopathy: peripheral vascular disease: peripheral vascular disease, atheroscelrosis, CAD
Neuropathy
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Pathophysiology of Diabetic Nephropathy
Hyperglycemia
↑GFR Microalbuminuria
Proteinuria
↓GFR
ESRD
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Diabetic Foot
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Instruction in the care of the FeetHygiene of the feet
Wash feet daily with mild soap and lukewarm water. Dry thoroughly between toes by pressure. DO NOT RUB vigorously, as this is apt to break the delicate skin
Rub well with vegetable oil to keep them soft, prevent excess friction, remove scales, and prevent dryness.
If the feet become too soft and tender, rub them with alcohol about once a week.
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Instruction in the Care of the FeetHygiene of the feet When rubbing the feet, always rub upward from the
tips of the toes. If varicose veins are present, massage the feet very gently; never massage the legs.
If the toenails are brittle and dry, soften them by soaking for 1 ½ hr each night in lukewarm water containing 1 tsbp of powdered sodium borate (borax) per quart. Clean around nails become too long, file them with an emery board. File them straight across and no shorter than the underlying soft tissue of the toes. Never cut the corner of the nails.
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Instruction in the care of the Feet Wear low-heeled shoes of soft leather that fit the
shape of the feet correctly. The shoes should have wide toes that will cause no pressure, fit close in the arch, and grip the heels snugly. Wear new shoes one-half hour on the first day and increase by 1 hour each day following. Wear thick, warm, loose stockings.
Treatment of Corns and Calluses Corns and calluses are due to friction and pressure,
most often from improperly fitted shoes and stockings. Wear shoes that fit properly and cause no friction or pressure.
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Instructions in the Care of the Feet To remove excess calluses or corns, soak the
feet in lukewarm (not hot) water, using a mild soap, for about 10 minutes and then rub off the excess tissue with a towel or file. Do not tear it off. Under no circumstances must the skin become irritated.
Do not cut corns or calluses. If they need attention it is safer to see a podiatrist.
Prevent callus formation under the ball of the foot (a) by exercise, such as curling and stretching the toes several times a day; (b) by finishing each step on the toes and not on the ball of the foot. And (c) by wearing shoes that are not too short and that do not have high heels
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Diagnostics: FBS, OGTT and RBSNormalGlucoseTolerance
Impaired GlucoseTolerance
DiabetesMellitus
FastingPlasmaGlucose
< 110 mg/dl 11o-125 mg/dl ≥ 126 mg/dl on 2 occassions
2 hours after glucose
< 140 mg/dl ≥ 140 but <200 ≥ 200 mg/dl
Random Blood Glucose
--------- --------- >200 mg/dl plus diabetic symptoms
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Diagnostics: Glycosylated HemoglobinNV= 7.5% or less good control
7.6%--8.9% fair control
9% or greater, poor control
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Therapeutic interventions Lifestyle changes
Weight control and exercise
Planned diet 50-60% of calories are
complex carbohydrates, high fiber
12-20% of daily calories is protein, 60-85g/day
Fat intake not to exceed 30% of daily calories, more of polyunsaturated/ monounsaturated fats
Basic tools: food exchange groups
Self monitoring of blood glucose
Moderation in alcohol intake
Using artificial sweetener is acceptable
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Cont: therapeutic interventionsInsulin administration:
For type 1 and type 2 dm when diet and weight control therapy failed.
Aspirin, alcohol, oral anticoagulants, oral hypoglycemics beta blockers, TCA’s, tetracycline, MAOI’s increase the hypoglycemic effect of insulin
Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives increase glucose levels
Illness, infection and stress increase the need for insulin
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Insulin Onset Peak Duration
Ultra rapid acting insulin analog(humalog)
10- 15 mins 1 hour 3 hours
Short acting insulin(Human regular insulin)
30 minutes- 1 hour
2-4 hours 4-6 hours
Intermediate acting insulin(Humulin lente, Humulin NPH)
3-4 hours 4-12 hours 16-20 hours
Long acting Insulin(Protamine zinc, humulin ultralente)
6-8 hours 12-16 hours 20-30 hours
Premixed insulin(70% NPH, 30% regular)
30min-1 hour 2-12 hours 18-24 hours
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Example Order for Typical Sliding Scale (HR)
CBG Insulin Dose150-200 201-250 251-300301-350351-400>400
2 units4 units6 units8 units10 unitsRefer to MROD, EFOD
or Diabetology Fellow.
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Complications of Insulin TherapyLocal allergic reaction, lipodystrophy, insulin
resistance
“Dawn Phenomenon”- increase in blood sugar because of release of GH at around 3am;Tx: give NPH at 10 pm
• “Somogyi effect”-rebound hyperglycemia at 7am after a bout of hypoglycemia at 2-3am.Tx: Decrease the evening dose of intermediate
acting insulin
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Diabetes Mellitus: Complication of Insulin
Dawn Phenomenon
Somogyi Phenomenon
S/SxHyperglycemia at dawn
Rebound Hyperglycemia at early morning
Cause Growth hormone release at 3 AM
Hypoglycemia at dawn
Mgt Give IAI at 10 PM (or adjust dose)
Decrease dose of IAI at 10 PM
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Complications of insulin therapyHypoglycemia Hypoglycemia
If awake, give 10-15 g of fast acting simple carbohydrate (glucose tablets, fruit juice, and soda)
If unconscious, glucagon SQ or IM
If in the hospital, 25-5o cc of D5050 (50% dextrose in 50cc vial)
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Oral Hypoglycemic Agents For DM type 2
May have to be shifted to insulin when sick, under stress, during surgery.
Necessary to shift to insulin when pregnant
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Oral Hypoglycemicso Sulfonyureas
Promotes increase insulin secretion from pancreatic beta cells through the stimulation( requires at least 30% normally functioning beta cells)
1st gen-agents: Tolbutamide, acetohexamide, tolzamide,
chlorpropamide2nd gen-agents:
Glypizide, Glyburide
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Oral HypoglycemicsBiguanides
Reduces hepatic production of glucose by inhibiting glucogenolysis
Decrease the intestinal absorption of glucose and improves lipid profile
Agents Phenformin, Metformin, Buformin
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Oral HypoglycemicsThiazolidinediones-enhances action at the cell
and post receptor site decreasing insulin resistance
Agents: Pioglitazone (actos), Rosiglitazone (avandia)
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Acute Complication: DKAo Characterized by hyperglycemia and
accumulation of ketones in the body causing metabolic acidosis
o Occurs in insulin dependent Diabetic cliento Precipitating factors: Undiagnosed DM,
neglect of treatment, infection, other physical or emotional stress
o Onset slow, maybe hours to days
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DKA: Signs and Symptoms Polydipsia, polyphagia, polyuria Nausea and vomiting, abdominal pain Skin warm, dry and flushed Dry mucous membranes Kussmaul’s respirations or hyperventilation;
acetone breath Alterations in LOC Hypotension, tachycardia
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Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)Characterized by hyperglycemia and a
hyperosmolar state w/o ketosis
Occurs in NIDDM or non-diabetic persons (typically elderly persons
Precipitating factors: undiagnosed DM, infection or other stress; certain medications, dialysis, hyperalimentation, major burns
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Emergency ManagementFor both DKA and HHNK, treat dehydration first
with 0.9% or .45% saline Shift to d5w when glucose levels are down to 250-
300mg/dl WOF too rapid correction, it can cause rapid fluid
shifts (brain edema and increased ICP, ARDS) IV regular insulin 0.1 unit/kg bolus then 0.1 u/kg/hr
drip Correcting electrolyte imbalance. WOF hypoK as a
result of treatment. For severe acidosis (pH <7.1), DKA patients may have to be given NaHCO3
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DKA HHNK
Lab Findings
•Hyperglycemia (>250)
•Metabolic Acidosis ph <7.3
•Ketosis
•Hyperglycemia (>600mg/dl)
•Hyperosmolarity(>320 mOsm/L)
•pH >7.3 (no acidosis)
S/sx HyperglycemiaPolyuriaDehydrationAcidosis
HyperglycemiaHyperosmolarityPolyuria (osmotic diuresis)Dehydration
Type of patients DM type I
DM type IIElderlyPatients on TPN, burn
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DKA HHNK
Treatment HydrationInsulinNaHCO3
HydrationInsulin
Mortality
rate
5% to 10% 10% to 20%
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“Always strive for excellence in everything that you do.”
Thank You Very MuchDCSC RN